E-LEARNING RESOURCES IN VETERINARY PARASITOLOGY

1. DIAGNOSIS OF VETERINARY ENDOPARASITIC INFECTIONS

2.LIFE CYCLES OF SOME IMPORTANT PARASITES

3. Parasites and Parasitism in Livestock

4. Laboratory Demonstrations in Parasitology Useful Biological Prefixes and Suffixes

Diagnosis of Veterinary Endo-parasitic Infections
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Laboratory techniques - Fecal Samples Laboratory techniques - Blood Samples Parasitological Drug Index

As per Hosts
Click on the host of choice: Domesticated Mammals Poultry and other birds Reptiles top

As per Diagnostic Techniques Click on the procedure for further details:
Techniques for Fecal Samples

Comparison of Fecal Examination Techniques Frequently found artifacts in fecal smears Direct Smear Zinc Sulfate Flotation Ethyl Acetate Sedimentation Baermannization
Modified Wisconsin Sugar Flotation Method

Stoll Egg Counting Technique McMaster Egg Counting Technique Saturated salt flotation method top

Techniques for Blood Samples

Filtration Method Smears Procedure for concentration of blood (Knott's Test)

Therapeutic Index Index of common drugs used in treatment endoparasitic infections of Animals top

This section is intended to reinforce important principles

in the diagnosis, epidemiology, pathology, and treatment and control of selected parasites of significance in veterinary medicine. This is not intended to be a primary source of information about any of the parasites, but rather serve as a reference and reminder of the application of the life cycle to the practice of veterinary medicine.

Parasites and Parasitism in Livestock

Contents
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Introduction to Parasitology Introduction to Nematodes Trichostrongyloidea Strongyloidea Ascaridoidea Oxyuroidea Trematodes Siphonaptera (fleas) Anthelmintics & their Uses Heartworm

Veterinary Parasitology Laboratory Demonstrations

In each Parasitology lab, the teaching staff will put out numerous displays of the parasites which you are required to know. Next to each display is a card that explains the display. Photocopies of all these cards are available in the library. In the past, students would make a photocopy and then use it to make notes on as they progressed through each lab station. The only problem was that some of the twice photocopied cards were of poor quality. Therefore, we have made the contents of these cards available on this web site.

Laboratory 1 - Introduction to the Parasitology Laboratory Nematode Taxonomy Laboratory 2 - Strongyles Laboratory 3 - Hookworms, Lungworms and Strongyloides Laboratory 4 - Ascarids, Oxyuris, and Trichocephalids Laboratory 5 - Spirurids and Filariids LAB EXAM 1 Laboratory 6 - Trematodes Laboratory 7 - Cestodes, Acanthocephalans Laboratory 8 - The Arachnids Laboratory 9 - Insects of Veterinary Importance Laboratory 10 - Protozoa

Useful Biological Prefixes and Suffixes
Prefix or suffix aabacantho-adalbi-algia ambyl- or amblyo amylananaancyloangioanteanti- (ant) apoaqua-ase autobibiobrachyMeaning not, without from, away spine to, toward white pain blunt starch not, without up, upon bent vessel before, in front of against, opposed to off, from, away from water designating an enzyme self two, twice life short Examples atypical abnormal Acanthocephala dorsad, adhere albicans neuralgia Ambylocera amylopsin anhydrous anabolism ancylostoma angiocarditis anterior antitoxin, anthelmintic apoplexy aquatic amylase autosuggestion biceps, bifocal biology brachycardia

bradycalor-cara -cardia-cephalus -cera -cerca cerebrochrom-cidal corpuscteno-cyst -cyte, cyto-dermic didiadys-ectomy em-, en-, endo-emia enteroepi-

slow heat head heart head horn tail brain color killing body like a cockle bladder cell skin two, twice through, between bad, difficult cut out in, into blood intestine on, above, upon

bradycardia calorimeter Toxocara bradycardia Ctenocephalides brachycera Onchocerca cerebrospinal chromosome bacteriocidal corpuscle Ctenocephalides oocyst cytoplasm hypodermic dichromic diaphragm dyspepsia appendectomy embolism, endoskeleton anemia enterokinase epiglottis

erythro-fer-fract-gastro-gen-glossoglyc-gnath-gnosis -graph -helminth hemoheterohomohydrohyperhypo-iasis interintrairischn or ischno -itis kata-, cata-

red to carry, to transport to break stomach to produce, to begin tongue glucose, sugar jaw, cheek knowledge, to know to write worm blood different, other alike, same water over, more than under, less than infestation between, together within not long, thin inflammation down

erythrocyte afferent, efferent fracture, refraction pneumogastric genetics, glycogen hypoglossal glycosuria gnathostoma diagnosis cardiograph anthelminthic hemorrhage heterozygous homozygous hydrolytic hypersecretion hyposecretion onchocerciasis intercostal intrathoracic irregular Ischnocera appendicitis catabolism

kin-lacleuco-, leuko-ology lymph-, lympho-lysin, -lysis, -lytic macro-meter micromonomyonemaneurnephr-oid -ole -oma onchooncooo-opia -osis os-, oste-, osteoovi-

to move or activate milk white science, knowledge lymph dissolve, destroy large measure small one muscle thread relating to nerves kidneys like small swelling, tumor hook mass, bulk egg sight condition or process bone egg

kinetic lactase, prolactin leucocyte physiology lymphocyte hemolysis macrophage manometer microorganism

monocyte, monosacchar myosin, myoglobin nematode neurilemma nephritis lymphoid, ameboid bronchiole sarcoma Onchocerca oncosphere oocyst myopia, hyperopia cyanosis, phagocytosis osteology, osteocyte oviducy, ovipositor

parapathoperiphago-phil-plasmplaty-pnea pneumo-ped polypostpropropriopseudopsychopulmo-renal -rrhea sarco-

near, by, beside disease, suffering around, near to eat loving substance broad breathing air, lungs foot many after, behind before, giving rise to one's own false mind lung kidney flow flesh, muscle

parathyroid pathology pericardium phagocyte basophil, eosinophil cytoplasm, plasmolysis Platyhelminthes dyspnea pneumonia pseudoped polysaccharide postganglionic proenzyme proprioceptors pseudoped psychology pulmonary adrenal diarrhea sarcoplasm

soma-some stoma-

body body mouth

somatic cell chromosome ancylostoma

-strongyle -thrombo-tode -tome, -tomy toxi-, toxotricho-trophic -tropic -ule -uria -uris vaso-

cylinder clot, coagulation like to cut poison hair-like feeding attached to small pertains to urine tail pertains to blood vessel

trichostrongylus thrombosis nematode tonsillectomy toxin trichostrongylus autotrophic phototropic saccule glycosuria trichuris vasodilation

Index of Commonly Used Pharmaceuticals in the Treatment of Veterinary Parasitic Infections
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Drug
trade names.)

Trade names
(may also be available under other

Amprolium Butamisole Hyrdochloride Clindamycin Dichlorvos

Corid Styquin Antirobe Task

Diethylcarbamazine
Disophenol Sodium Epsiprantel Febantel Fenbendazole Imidocarb dipropionate

Nemacide
DNP Cestex Drontal Plus Panacur

Imizol

Ivermectin
Plus, etc.

Ivomec, Heartgard, Heartgard

Mebendazole
Melarsomine dihydrochloride

Telminic

Immiticide
Flagyl Interceptor ProHeart, ProHeart 6 Navigator

Metronidazole Milbemycin oxime Moxidectin Nitazoxanide Piperazine Praziquantel Pyrantel Pamoate Pyrantel embonate Selamectin Sulfadimethoxine Thiacetarsamide sodium

Pipa-tabs, Tasty Paste, WRM Rid, etc.

Droncit, Drontal, Drontal Plus
Nemex, Heartgard plus, Strongid T, etc.

Drontal, Drontal Plus Revolution Albon, Bactrovet

Carparsolate

Web-link
www.fda.gov/cvm/greenbook/greenbook.html of currently approved drugs. The FDA's searchable list

Diagnosis of Veterinary Endoparasitic Infections

Domesticated Mammals
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Cat Dog Cow Ferret Goats Sheep Horse Llama Pig Rabbit

Birds
Robin - Turdus migratorius

Reptiles

Loggerhead turtle - Caretta caretta

Comparison of Fecal Examination Techniques

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TECHNIQUE
Direct Smear

ADVANTAGES
Quick to prepare. No distortion of parasites if isotonic saline is used as diluent. Only way to see live trophozoites (isotonic saline must be used as the diluent). Useful for examining feces of small birds and reptiles (where trematode eggs are common). Procedure floats the most common helminth ova and coccidian oocyst . Solutions are inexpensive. There is little debris to obscure the view of the parasite.

DISADVANTAGES
Can miss parasite if concentration is too low or if too much debris or fat is present. Sand, seeds, or other fecal debris can make apposition of coverslip onto slide difficult. May take a long time to examine.

Saturated Sucrose or Salt

Procedure will not float trematode ova and some tapeworm (pseudophyllidian) ova. Distorts Giardia cysts. Time consuming if centrifugation not performed. Unsuitable for fatty stool samples.

Zinc Sulfate Flotation

Recommended procedure for most fecal exams Procedure floats most helminth eggs. Best method for protozoan cysts, especially Giardia. There is little debris to obscure view of parasites. Procedure recovers ALL types of helminth ova, larvae, and most protozoan cysts. It is the best technique for formalin - fixed samples and for stools with high fat content.

Procedure will not float some trematode ova, and some tapeworm (pseudophyllidian) ova. Unsuitable for fatty stool samples. ZnSO4 is expensive and a hydrometer should be used to make up the solution.

Ethyl Acetate Sedimentation

It is more difficult to perform than other techniques. Ethyl acetate is flammable and expensive. There is more debris in preparation preps than in flotation preps - therefore it will take longer to read.

Artifacts

Scroll down to see an assortment of artifacts commonly found in fecal smears and floats of dogs and cats.

Free living mite and mite egg (dog feces)

Above: Stained with iodine Below: unstained and at a higher magnification

Yeast (Saccharomycopsis gutulatus): this is a normal inhabitant of the gut of rabbits, it is commonly found in fecal floats done on dogs that ate rabbit feces. It is not pathogenic and it just passes through the dog.

Plant cells

Free living mites and mite egg (dog feces)

Monocystis sp. sporocyst and plant nematode in dog feces (10X).

Monocystis sp. sporocyst (40X)

(100X)

Monocystis sp. is a protozoan parasite of earthworms. The sporocysts appear in the feces of animals (usually dogs and turtles) that have eaten infected earthworms. The sporocysts are not infectious to dogs and the dog is not infected with the parasite. Plant nematodes also just "pass through" the dog; they can be identified as a plant nematode if the "spears" they use to puncture plant cell-walls can be seen in the buccal cavity.

Pollen in dog feces

Pine pollen in dog feces

Air bubble

Eimeria sp. oocyst in dog feces. Eimeria spp. do not infect dogs, this oocyst (~ 40 µm) was ingested with something the dog ate (maybe horse or cattle manure!) and just passed through the dog. (Photo by Terri Jarratt and used with permission.)

Plant spine Fiber

Plant

Plant cell

Fungal spores

Note the small piece of the hypha still attached to one end of each of the spores.

Direct Fecal Smear Examination

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Direct Smear Fecal Exam
1. Place a small amount of feces on a microscope slide. 2. Add a drop of liquid to the feces and mix thoroughly. The type of liquid added depends on what you hope to accomplish with the technique. If you are examining a liquid fecal sample for the presence of protozoan trophozoites (live active protozoa) then use saline (if any extra liquid is needed). If you are looking for helminth eggs and protozoan cysts in a small sample (bird droppings, rectal smear, etc) then either water or iodine may be used. 3. Cover with a cover slip. Move the cover slip around until it lays flat. You should be able to read through the smear (light from the microscope must be able to pass through the sample in order for you to examine it). 4. Examine the slide using the 10X objective, and then go over it with the 40X objective. Because this technique examines only a very small amount of feces, it should only be used in the following circumstances: a. Liquid feces where protozoan trophozoites may be present. b. Fecal samples where the amount of feces obtained is too small to handle with any other technique. c. As an adjunct to a flotation technique where you are looking for eggs that do not float. (In this case you probably would be better off running an ethyl acetate sedimentation and examining the resultant pellet using the direct smear method.) Note: Circumstances "b" and "c" occur frequently when dealing with small fish, birds, amphibians and reptiles and thus the direct smear has some utility in dealing with fecal samples from these

.animals.

remove a sample from the surface of the solution and place on a microscope slide. Centrifuge as in step 5. Using a tongue depressor. Add a drop of iodine (to stain the cysts and the ova) and a coverslip. The mixture should be checked with a hydrometer and adjusted to 1.18 specific gravity) is made by adding 386 grams of ZnSO4 to 1 liter of water.Fecal Examination Using the Zinc Sulfate Centrifugal Flotation Method || Root || Main || Below is a description of how to test fecal samples using the Zinc Sulfate Centrifugal Flotation Method: Fill a 15 ml centrifuge tube with ZnSO4 solution (1. To do this. the eggs will sink but the fat will remain afloat as the eggs are heavier than water. * ZnSO4 solution (1. pour the ZnSO4-fecal mixture back into the centrifuge tube. Note: If the sample contains a large amount of fat or other material that floats in water. start at step 1 but use water instead of ZnSO4. After centrifugation pour off the supernatant and add the ZnSO4 solution . Using a funnel. you may want to wash the sample before doing the flotation.. You may have to take several samples with the rod or loop to get enough material to examine .mix well. When you centrifuge the water-fecal mixture.18 specific gravity. Centrifuge for 2 minutes at high speed (1500 .you want the equivalent of a large drop on the slide. Using a headed-rod or loop. The ZnSO 4 solution should be stored tightly capped to prevent evaporation (and the resulting change in specific . Examine at 10X on a microscope.2000 rpm).18 specific gravity)* and pour into a glass dish. push the feces (2 to 3 grams about 1 cm in diameter) through a strainer into the ZnSO4 solution in the dish.

.gravity of the solution).

then pour solution into a 15 ml centrifuge tube. and then centrifuge it. Shake the tube vigorously. being careful to leave the pellet at the bottom of the tube intact. and plug the tube with a rubber stopper. Using a stick. CAUTION: Test materials before placing Ethyl Acetate into them. This solvent will dissolve many types of plastic!! The white plastic centrifuge tubes (Polypropylene) used in the lab are OK. "ring" the plug of fat at the water-ethyl acetate interface (the plug adheres to the side of the tube and must be detached before the liquid contents of the tube can be poured off). Pour off the supernatant.Fecal Examination Using the Ethyl Acetate Sedimentation Method || Root || Main || Below is description of how to test a fecal sample using the Ethyl Acetate Sedimentation Method: Pass a piece of feces (about 5x5 mm) through a sieve into about 9 ml of water. . but clear plastic tubes (polystyrene) and the disposable polystyrene cups will dissolve. Add about 3 ml of ethyl acetate.

centrifuge. you can re-suspend the pellet in flotation solution. A pellet of sediment at the bottom. .Transfer some of the sediment from the bottom of the tube to a slide and examine. The sediment can be transferred in several ways: 1)If some liquid remains. the pellet can be resuspended and a drop transferred with a pipette. An ethyl acetate layer on top. 3) Use a stick to remove some of the pellet and smear it on a slide as you would when making a direct smear. D. B. Because formalin fixed eggs and cysts may not float (they may now have a specific gravity of greater than 1. A plug of dissolved fat in the middle.2) this technique is preferred for formalin fixed samples. NOTE:When removed from the centrifuge. C. and remove the material from the top of the float to examine for eggs. A layer of water. your tube will have clearly defined layers: A. NOTE: If you did this technique just to remove fat. 2) Add a drop of iodine to the pellet to resuspend it and then transfer with a pipette.

Most parasitic larval nematodes are poor swimmers. Second. Let sit for 20 minutes Using a Pasteur pipette. Therefore. some of them will migrate through the tissue paper and fall into the water. the warmer it is. you do not want to over heat them! . Because the larvae can't . the more active the larva will be (however. The Baermannization method is used for the extraction of live larval stages of nematode parasites from the feces.Fecal Examination Using The Baermannization Method Below is description of how to test a fecal sample using Baermannization Method. The larvae will move around in a random fashion and within time.37 to 40oC is the upper limit). Spread about one gram of feces on a piece of tissue paper and place it into the sieve Place warm* water in the dish until it just covers the feces. Place a sieve in a custard dish or other similar container. * This procedure makes use of two characteristics of parasitic larval nematode behavior. remove a drop of sediment at the bottom of the tube and place it on a microscope slide for examination. Be careful not to disrupt the feces. Be careful not to resuspend the sediment before you take a sample from it. First. the following events take place when the sieve is placed in the water. Allow mixture to sit for one hour** Lift off sieve Pour liquid into a 50 ml centrifuge tube.

they sink to the bottom of the dish and accumulate there. but with time the fecal sample breaks down and begins to pass through the paper tissue leading to an accumulation of sediment along with the larvae. ** The longer you wait the more larvae will accumulate at the bottom of the dish. .swim.

The number of eggs counted is the number per 3 grams of feces. 8. Fill a 15 ml test tube with 10 ml of Sheather’s* solution. 5. 3. Fill the tube to just over the top and place a cover slip onto the meniscus. . Pour the Sheather’s solution from the test tube into the cup and mix well. It is the most accurate as it counts all the eggs in 3 grams of feces and because it is a flotation method it has little debris to interfere with the count. Weigh 3 grams of feces and place into a cup. 4. 1. then remove the cover slip and place on a slide.Modified Wisconsin Sugar Flotation Method This method of determining the EPG is probably the most commonly used method. Let sit for about 5 minutes. so keep refrigerated and use quickly. This solution will grow mold if left out. 7. there may be too many eggs to count. if the EPG is high. Examine the entire cover slip and count the number of eggs that you find. Stir until dissolved and allow to cool. place a strainer into the funnel and pour the fecal-sugar solution mixture through the strainer into the test tube. 9. Centrifuge the tube for 2 to 4 minutes. Place a funnel into the test tube tube. squeeze the liquid out of the feces that is left in the strainer. so divide by 3 to find the EPG. 2. 6. Using a tongue depressor. * Sheather’s Solution: Add 454 gm (1 lb) of table sugar to 355 ml of very hot water. However.

Lift the sieve and hold over the dish.15 ml X 100 is equal to 1/3 of the total number of eggs in the original 3 grams (and thus equal to eggs per gram = EPG).15 ml is 1/300 of 45 ml (42 ml water and 3 grams of feces) so the number of eggs in 0.15 of the suspension and spread over 2 slides. take 0. The mathematics: 0. While stirring the water-feces mixture. Weigh out 3 grams of feces Measure out 42 ml of water and place it into a dish. . Examine both slides for worm eggs. The total amount of eggs counted X 100 represents the number of eggs per gram of feces. The disadvantage is that the counting takes a long time because of the amount of extra (non-egg) material on the slides. Push out any remaining water from the feces. Using a tongue depressor. push the 3 grams of feces through a sieve into the water.Fecal Examination Using the Stoll Egg Counting Method The Stoll Egg Counting Technique is a method for determining the number of nematode eggs per gram of feces in order to estimate the worm burden in an animal. Cover each slide with a long coverslip (or 2 regular coverslips). The advantage of this technique is that it requires no specialized equipment.

take a sample of the mixture with a pipette and transfer it to one of the chambers of the McMaster slide. Repeat the procedure and fill the other chamber. The mathematics: The volume under the etched area of each chamber is 0. this is the eggs per gram (EPG). The disadvantage is that you must use a special counting chamber. This is 1/200 of 60 ml. Weigh out 2 grams of feces Pass the feces through a sieve into a dish containing 60 ml of ZnSO4 or saturated salt solution. Push out any remaining solution from the feces. Multiple the total number of eggs in the 2 chambers by 100.Fecal Examination Using the McMaster Egg Method The McMaster Egg Counting Technique is a method for determining the number of nematode eggs per gram of feces in order to estimate the worm burden in an animal.15 cm deep).3 ml. so the volume examined is 0. the final result is "eggs per gram of feces". Wait 30 seconds then count the total number of eggs under both of the etched areas on the slide. . Lift the sieve and hold over the dish. Since you started with 2 grams of feces and then multiplied by 100. While stirring vigorously (you may want to put the solution in a flask to prevent spillage). The advantage of this technique is that it is quick as the eggs are floated free of debris before counting.15 ml (the etched area is 1 cm X 1 cm and the chamber is 0.

Some people make the bottom piece a little wider than the top piece to make it easier to load. 3.mii. e-mail: helmint@ktl. South Africa (http://www.5 cm by 7. Focal Point.com/ .mcmaster. The etched lines should be as thin as possible so eggs are not hidden under them. . See the photo above. fax: +370 5 2729727. Onderstepoort.lt. WA. 2. USA 98029 http://www. M.: +370 698 87699.15 cm thick) placed at both edges and in the center between the etched boxes. Antanas Vysniauskas.vetslides. Lithuania Tel.Marcinkeviciaus No 17-14. The 2 pieces are separated by pieces (0. If you want to have one of these slides made for you here are the particulars: They are usually made of Glass or Plexiglass: 2 pieces (2.5 cm) with 2 etched boxes (1 cm by 1 cm) on the under side of the top piece. Chalex Corporation 5004-228th Ave SE. Issaquah. The etched boxes usually have 5 additional etched lines (subdividing the box into 6 sections) to make counting easier. Vilnius LT-08412.co.za/) Prof.Above: McMaster slide Sources for McMaster slides are: 1.

Below are a few examples.Fecal Examination Using the Saturated Salt Flotation Method Saturated Salt Flotation There are numerous devices for doing this type of flotation now in use in local veterinary hospitals. Ovatector system Ovassay Plus Fecalyzer .

. 1 liter of water. Collect a 1 ml blood sample into EDTA or heparin and add to 10 ml lysing solution within a syringe. (Lysing solution consists of 5.) 2. Mix thoroughly.0 ml Triton X-100.Filtration Method to Detect Microfilariae in Blood 1. The lysed blood solution is pushed through an 8 um pore filter membrane. Attach syringe to a filter unit (see drawing below). Remove the filter from the filter holder. 8. place it on a microscope slide and add one drop of 1:10.000 Methylene Blue Stain. 3.0 grams of NaCo3. Cover filter with a cover glass and examine under microscope.

Procedure for Making Blood Smears

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Procedure for making Blood smears (thin films) : To do a blood smear you need two slides. On one slide the blood sample is placed - this is the "sample" slide. The second slide is used to smear the drop of blood - this the "spreader" slide. Clean the sample slide by wiping it with alcohol. Handle slides by edges only. (any grease on the slide will cause the dried blood to flake off during staining). Place a very small drop of blood near the end of the sample slide. Place the end of the spreader slide on the sample slide so that the short sided edge of the spreader is just below the drop of blood. The next two steps should be done quickly to avoid smears that are too thick. Holding the spreader at an angle of 30 o (relative to the sample slide), push the spreader so that the edge just barely touches the drop of blood. By capillary action, a thin line of blood will spread along the edge of the spreader . Quickly drag the spreader along the entire length of the sample slide in one fluid motion. Note that the blood is being dragged by the spreader. To view a Quick Time Video of the procedure click here. If the correct amount of blood was used, and the technique was performed correctly, the smear should end before the end of the sample slide. The smear should also end in a "feathered edge" - a region where the blood cells are well separated. Air dry the sample slide. Fix and stain the slide. Various methods may be used. Normally a commercial staining kit is utilized following the manufacturer's instructions.

Modified Knott Method

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Add 1 ml of freshly drawn blood to 9 ml of 2% formalin (aqueous) in a centrifuge tube. Mix well to lyse red blood cells. Centrifuge for 5 minutes at 1500 rpm. Pour off the supernatant fluid. Note: Invert the tube completely when decanting the supernatant. Add a drop of 1% aqueous methylene blue. Adjust the amount to suit yourself, it stains the microfilariae blue and makes them easier to view). Then stir or mix up the sediment in the bottom of the tube. Place a drop of the stained mixture on a microscope slide and add a cover slip. Examine under a microscope.

Please choose a parasite: Ancylostoma caninum Dictyocaulus viviparus Dirofilaria immitis Echinococcus granulosus Eimeria bovis Giardia Haemonchus contortus Toxocara canis

Directions for site us

You may navigate between c tab. Click on the appropriate life cycle for that category. For more information about highlighted item. This will po one) containing pertinent inf diagrams, or other informati windows using the 'Close W clicking the appropriate butt otherwise, you will be lost in uncertain terms, please see

A|B|C|D|E|F| G|H|I |J |K|L|M |N|O |P|Q |R|S| T|U|V|W|X|Y -AAlae: Flattened, wing-like expansions of the cuticle of nematodes (cervical, caudal or lateral).

Apical complex: A complex set of organelles found at the anterior end of the protozoans of the Ph has a role in the penetration of host cells. Arrested development: See hypobiosis. Return to top of page

-B-

Bradyzoite: A stage in the life cycle of protozoa of the family Sarcocystidae (tissue-cyst-forming c to describe the merozoite which forms within the tissue cyst in the intermediate host (and rarely wit stage rarely infects new cells within the intermediate host, rather it is the infectious stage for the de Return to top of page

-C-

Cercaria: In the trematode life cycle, the cercaria is a larval trematode (which may or may not have cercaria develops from the germinal cells of the sporocyst or redia and emerges from the snail (int species) the metacercaria.

Coenurus: Larva of Taenia multiceps which is a fluid filled cyst containing many invaginated scole

Control: Reduction of disease incidence, prevalence, morbidity or mortality to a locally acceptable Continued intervention measures are required to maintain the reduction. Cysticercoid: A single, evaginated scolex that is embedded in a small solid cyst that are typically arthropods (Cyclophyllidian tapeworms).

Cysticercus: Larval stage in the cestode life cycle which is a fluid filled cyst containing an attache in mammal intermediate hosts (cyclophyllidian tapeworms) Return to top of page

-D-

Definitive Host: Found in all parasitic life cycles. The definitive host is the host in which the sexual If there are no sexual stages in the life cycle, then the definitive host is the host in the life cycle con

-D-

Definitive Host: Found in all parasitic life cycles. The definitive host is the host in which the sexual If there are no sexual stages in the life cycle, then the definitive host is the host in the life cycle con

Direct Parasite Life Cycle: A life cycle of a parasite in which the pre-parasitic larvae develop in the which the eggs will EITHER hatch and the pre-parasitic larvae are entirely free-living (e.g. Ostertag usually an L3 and infection occurs via ingestion of infective stage or skin penetration OR the eggs d develop inside their eggs (e.g. Ascaris suum) and infective stage is usually the egg containing the definitive host occurs via ingestion of the infective stage. Return to top of page

-E-

Embryonated egg: (Also called a "Larvated egg"): A nematode egg with a developed larva insi in the morula stage and develop in the environment to the embryonated stage (the stage just befor Strongyloides spp., Dictyocaulus arnfieldi) are embryonated at the time they leave the host. Ensheathed: A larval nematode that is within the retained cuticle of the previous stage.

Eradication: Permanent reduction to zero of the worldwide incidence of infection caused by a spec Intervention measures are no longer needed. Exsheathment: The final step in molting of the infective stage when the old cuticle (sheath) is lost inside the definitive host. It is a requirement for the establishment for infection in the host. Extinction: The specific organism no longer exists in nature or the laboratory. Return to top of page

-FReturn to top of page

-G-

Gametocyte: The stage in the life cycle of some protozoa (Apicomplexa) which is destined to beco Return to top of page

-H-

Helminths: A general term referring to the nematodes (roundworms), trematodes (flat worms, fluke acanthocephalans (thorny-headed worms).

Hydatid Cyst: Larva of Echinococcus spp. which is a large fluid filled cyst containing many invagin also contain many invaginated scolecies. There are two types of hydatid cysts: E. granulosus has multilocularis has a multi-locular (many chambered) cyst.

Hypobiosis: In parasitology: A temporary halt in nematode development within the host at an early cycle in nematodes with direct life cycles only. Nematodes arrest as immature forms in the definitiv

Hydatid Cyst: Larva of Echinococcus spp. which is a large fluid filled cyst containing many invagin also contain many invaginated scolecies. There are two types of hydatid cysts: E. granulosus has multilocularis has a multi-locular (many chambered) cyst.

Hypobiosis: In parasitology: A temporary halt in nematode development within the host at an early cycle in nematodes with direct life cycles only. Nematodes arrest as immature forms in the definitiv external environment pose a hazard to survival of free living pre-parasitic stages (usually in winter o more favorable, the arrested development resume their development to adults the life cycle continu Return to top of page

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Intermediate host: A stage in the life cycle that is essential to parasite development (with some ex of the parasite to the definitive host is usually by predation. Intermediate hosts are not required for

Indirect Life Cycle: A life cycle of a parasite in which the pre-parasitic larvae develop inside an ap Return to top of page

-JReturn to top of page

-KReturn to top of page

-L-

Life cycle: The stages an organism goes through over time containing a possible pre-parasitic and as a circle beginning with the formation of a individual and ending with the production of the next ge the parasite gives the investigator predictive value for understanding pathogenesis and clinical sign and control of the parasite. Life cycles can either be direct or indirect. Return to top of page

-MMeront: See schizont. Merozoite: The invasive stage that is the end result of schizogony.

Metacercaria: Stage of trematode life cycle that the cercaria after invading the second intermediat develop into. When ingested by the definitive host, the metacercaria will develop to the adult stage Metacestode: Mature tapeworm larvae.

Miracidium: The pyriform, ciliated larva of a trematode that developed in and hatched from the egg and undergo development to the next stage in the lifecycle. Myiasis: Infestation of organs and tissues of vertebrates by larval dipterans (true flies).

Miracidium: The pyriform, ciliated larva of a trematode that developed in and hatched from the egg and undergo development to the next stage in the lifecycle. Myiasis: Infestation of organs and tissues of vertebrates by larval dipterans (true flies). Return to top of page

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Occult infection: An infection with adult worms but no corresponding diagnostic stage. For exam (heartworm) some hosts may not have circulating microfilaria (this may be a result of immune-medi single-sex infection, chemosterilization of the adult worms by drug treatment, or senescent adults). heartworm infection".

Oncosphere: In a cestode life cycle, the oncosphere is the hexacanth (6-hooked) embryo found in

Oviparous: Laying eggs in which the embryos have developed little or not at all. Seen, for examp Ancylostoma caninum.

Ovoviviparous: Condition in which the organism develops in an egg and hatches within the adult emerges from the adult female. Seen, for example, in the nematode Dirofilaria immitis and in some Return to top of page

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Paedogenesis: A process in the molluscan intermediate host which involves the production of new which one trematode egg may eventually develop into hundreds of adults.

Parasite: Organisms that live temporarily or permanently on or within other living organisms (plant obtaining food.

Parasitic Phase of Life Cycle: The development and maturation to adult males and females occu cycle.

Parasitism: A two species association in which one species, the parasite, lives on or in a second s its life and obtains nourishment from it. The parasite may or may not cause disease in the host.

Parasitology: The study of host-parasite relationships. Traditionally this area of study has focused helminths and arthropods.

Paratenic host (transport host): A type of intermediate host in which immature helminths may su undergo development. Further parasitic development depends upon infection of the definitive host, paratenic host. Completion of a life cycle may happen with or without a paratenic host, but the pres make infection of the definitive host by the parasite more efficient.

Periparturient Rise in Fecal Egg Counts (PPR): An increase in the number of parasite eggs in th This can be pronounced in ewes, sows, and goats.

paratenic host. Completion of a life cycle may happen with or without a paratenic host, but the pres make infection of the definitive host by the parasite more efficient.

Periparturient Rise in Fecal Egg Counts (PPR): An increase in the number of parasite eggs in th This can be pronounced in ewes, sows, and goats. Phagolysosome: A phagosome that has fused with a lysosome within the phagocyte. Phagosome: A vacuole within a cell that was formed during phagocytosis.

Pre-parasitic Phase of Life Cycle: The development to the infective stage occurring outside the d second (intermediate) host of the parasite life cycle. Predilection site: The site within a host where the parasite is normally found.

Prepatent Period (PPP): The period of time from infection until mature adult parasites are produci

Procercoid: The larvae of Pseudophyllidian tapeworms in which after a crustacean ingests a ciliate the body cavity of the crustacean.

Pleurocercoid: Second larval type in Pseudophyllidian tapeworms in which after the crustacean is procercoid is liberated, the pleurocercoid is develops in the muscles of the new host and possesse stage which is infective to final host.

Procercoid: The larvae of Pseudophyllidian tapeworms in which after a crustacean ingests a ciliate the body cavity of the crustacean.

Proglottid: One segment of the body (strobila) of a tapeworm. Proglottids may be immature, matu present) or gravid (full of eggs). . Return to top of page

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Redia: In the trematode life cycle, the redia is the larval form (possessing an oral sucker) that deve give rise to the cercariae in the snail (intermediate host). Return to top of page

-SSchizont (meront): An asexual reproducing stage of some protozoa. It reproduces by schizogony.

Schizogony: In schizogony the nucleus of the original invading protozoan undergoes repeated divisions to form man

becomes surrounded by cytoplasm and a cell membrane forms around each new organism. These new stages within t

Scolex: The anterior end ("head") of the adult cestode, it is the hold-fast organ that anchors the w

Somatic Migration: Migration in the host by a parasite through the lungs into the systemic circulat

Schizogony: In schizogony the nucleus of the original invading protozoan undergoes repeated divisions to form man

becomes surrounded by cytoplasm and a cell membrane forms around each new organism. These new stages within t

Scolex: The anterior end ("head") of the adult cestode, it is the hold-fast organ that anchors the w

Somatic Migration: Migration in the host by a parasite through the lungs into the systemic circulat encyst in the tissues.

Spicules: Chitinous structures found in male nematodes, usually paired. They are inserted in the f

Sporocyst: In the trematode life cycle, the miracidium will invade a snail, lose the cilia and develo sporocyst, from which the redia will develop (in some species the sporocyst gives rise to a daught Sporozoite: The initial invasive stage of most of the Apicompexan protozoa. Strobila: The string of proglottides which make up the "body" of a tapeworm.

Strobilocercus: A type of larva of cyclophyllidian tapeworms (i.e. the larva of Taenia taeniaeformi Return to top of page

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Tachyzoite: Extra-intestinal stage of Toxoplasma that are found in in vacuoles muscle, liver, brain, definitive hosts. Sporulated oocysts are ingested and liberated sporozoites rapidly penetrate the in the invasive and proliferative stage of Toxoplasma. Tetrathyridium: Worm like larva with an invaginated scolex found only in Mesocestoididae.

Tracheal Migration: Migration in the host by a parasite into alveoli up the respiratory tree and then intestine. Transport host: See paratenic host.

Trophozoite: The stage of the protozoa in the host which feeds and grows until division commence

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Vector: An intermediate host in a parasitic life cycle, that may or may not (paratenic host) be esse A vector will seek out the definitive host in the life cycle to prey on it, whereas other intermediate h

Visceral Larva Migrans: Nematode larvae migration in hosts that are suitable for long survival but adult stage. The larva worms wander for a time in the hosts tissues.

Viviparous: Condition in which the embryo develops within the female and is nourished by the mo example: mammals.

Visceral Larva Migrans: Nematode larvae migration in hosts that are suitable for long survival but adult stage. The larva worms wander for a time in the hosts tissues.

Viviparous: Condition in which the embryo develops within the female and is nourished by the mo example: mammals. Return to top of page

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Links to online Parasitology resources:
http://www.biosci.ohio-state.edu/~parasite/home.html--Parasites and Parasitological Resources: A site maintained by The Ohio State University with images and descriptions of over 500 parasites. www.ivis.org--Another source of information on veterinary parasites is "Companion and Exotic Animal Parasitology" (Last updated: 29-June-00) edited by D. D. Bowman. This web based text can be found on the site maintained by The International Veterinary Information Service (IVIS). http://asp.unl.edu/--The American Society of Parasitologists web site www.heartwormsociety.org--The American Heartworm Society web site www.aavp.org--The American Association of Veterinary Parasitologists web site

Introduction to Parasitology
Topics
Parasites and parasitism The spectrum of parasitism Parasite life cycles Defined stages in life cycles The importance of life cycles - pathogenesis The importance of life cycles - epidemiology Important questions about life cycles Table 1 Table 2 The concepts of infection and disease Parasitism and disease

The Nematodes
Topics
Introduction Classification - overview External Morphology - cuticle modifications Internal Morphology - general anatomy Digestive System Reproductive System Basic Nematode Life Cycle Life Cycle Variations Exsheathment The Infective and Diagnostic Stages Arrested Development Table 1 - Classification of Nematodes of Veterinary Importance

The Trichostrongyloidea
Topics
The Order Strongylida The Superfamily Trichostrongyloidea Classification Life cycles of the family Trichostrongylidae Arrested Development and the Periparturient Rise Genus Trichostrongylus Morphology and species Life cycles Pathogenesis and clinical signs Epidemiology and diagnosis Genus Haemonchus Morphology and species Life cycle Pathogenesis Epidemiology Clinical signs and diagnosis Genus Ostertagia Morphology and species Abomasal nematodes - male spicules Life cycle Pathogenesis Epidemiology Clinical signs and diagnosis Genus Nematodirus Life cycle Genus Cooperia Life cycle Genus Hyostrongylus Life cycle Genus Dictyocaulus Morphology and species Life cycle Pathogenesis Epidemiology Clinical signs and diagnosis

The Strongyloidea
Topics
The Order Strongylida The Superfamily Strongyloidea The Syngamidae Stephanurus dentatus Morphology Life cycles Pathogenesis Epidemiology, clinical signs and diagnosis Syngamus trachea Morphology, pathogenesis, epidemiology, clinical signs, diagnosis Life cycle The Chabertiidae Chabertia ovina Morphology, pathogenesis, epidemiology, clinical signs, diagnosis Genus Oesophagostomum Morphology and species Life cycles Pathogenesis and epidemiology Clinical signs and diagnosis Intestinal strongyles of horses - The strongylidae The large strongyles Morphology and species Life cycles - Strongylus vulgaris Life cycles - Strongylus edentatus and Strongylus equinus Pathogenesis - adults feeding in the cecum and colon Pathogenesis - migrating stages of Strongylus vulgaris Pathogenesis - migrating stages of Strongylus equinus and Strongylus edentatus The small strongyles Morphology and species Life cycles Pathogenesis Epidemiology of equine strongyles Hatching, development of larvae and arrested development Seasonal changes in strongyle egg counts and pasture L3 levels Development of strongyle infections in foals Treatment and control of equine strongyles The use of anthelmintics to control strongyle infections Control of small strongyles with anthelmintics

The Ascaridoidea
Topics
Introduction to the Ascarids Species, hosts and importance Ascarids of dogs and cats Toxocara canis Toxocara cati Toxascaris leonina Ascaris suum Introduction and description Life cycle Pathogenesis and disease Epidemiology and diagnosis Parascaris equorum Introduction and description Life cycle Pathogenesis and disease Epidemiology and diagnosis Schematic life cycles Toxocara canis Toxocara cati Toxascaris leonina

The Oxyuroidea
Topics

Introduction and description Oxyuris equi Life cycle Pathogenesis and disease Epidemiology and diagnosis Treatment and control

PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS

The Siphonaptera - Fleas
Topics
Life cycles

PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS
Parasiticides - the Anthelmintics
Topics
Terminology, Introduction and Properties Spectrum of activity Safety considerations The issues of cost and residues Routes of administration Anthelmintic groups Macrocyclic Lactones Ivermectin

PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS
Heartworm
Topics
Dirofilaria immitis The Worm and its Life Cycle Host Species Epidemiology Pathophysiology of Heartworm in Dogs Cardiopulmonary Disease Caval Syndrome Secondary Complications: Renal and Hepatic Disease Ectopic Infections Hypersensitivity Reactions and Occult Infections Diagnosis Clinical Signs and Laboratory Findings Radiographic Findings Parasitological Examination and Immunodiagnostics Another Filarial Infection : Dipetalonema reconditum Treatment and Prevention in Dogs Pharmaceuticals Surgery Heartworm Disease in Cats

Laboratory 1

INTRODUCTION TO PARASITOLOGY

Click on the text below to jump down to the desired section of this page. Taxonomy scheme Nematodes Trematodes Cestodes Arthropods Protozoa Techniques Review Question

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The taxonomy scheme on the card above is the one we will use in

this course as it is the one used in the text book. Note that it differs from the one given in the introductory lectures in that the protozoa are listed in the animal kingdom and not in the Protista. Taxonomists are not in agreement as to the number of kingdoms and how organisms are divided among them, as can be seen by a the third scheme shown below where the prokaryotes are divided into two kingdoms and the eukaryotes are lumped into one.

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Members of the Phylum NEMATHELMINTHES have a straight intestine, composed of only epithelial cells, with a posterior anus. The body cavity is a pseudocoel (i.e. lacking a mesodermal lining).

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The nematodes (phylum NEMATHELMINTHES, Class NEMATODA) are cylindrical in shape tapering at both ends and have a complete digestive system. The body is covered by an acellular cuticle. These helminths (worms) are commonly known as "roundworms" because of the shape of their cross-section

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Ascaris suum - Adult nematodes from the small intestine of a pig. This species is one of the larger nematodes.

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Ascaris suum - The diagnostic stage of this nematode is the egg which is passed out in the feces. The eggs will float in a saturated salt solution, therefore a standard fecal floatation can be used to diagnose an infection with this worm.

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Dirofilaria immitis ("Heartworm") - These adult nematodes are found primarily in the pulmonary arteries and sometimes in the right ventricle. Large numbers of adult heart worms (as seen here) can so damage the lining of the pulmonary vasculature that pulmonary hypertension and right-sided heart failure can result.

This museum specimen represents the classic picture of heartworm. In actual fact, a large mass of worms in the right ventricle is an artifact of death. In the living animal the worms are usually forced down into the pulmonary arteries by the blood flow.

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Members of the Phylum PLATYHELMINTHES (the "flatworms") are usually flattened dorso-ventrally and are bilaterally symmetrical. They lack true body segmentation, a body cavity and an anus.

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The Trematodes (Phylum PLATYHELMINTHES, Class TREMATODA), as adults, are flattened dorso-ventrally, have a blind gut and no coelom. They also have suckers for attachment to the host. They are commonly referred to as "flukes".

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Dicrocoelium dendriticum - This small trematode is found in the bile ducts of sheep and cattle.

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Dicrocoelium dendriticum - The egg, which passes in the feces, is the diagnostic stage of this trematode. This egg, like many trematode ova, is operculate (has a cap on one end) and contains the next life-cycle stage, the miracidium.

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Fasciola hepatica - An adult specimen taken from the bile duct of an infected sheep. Note the size, distinct cone at the anterior end, "shoulders", and the "leaf-shaped" outline.

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Fasciola hepatica - The adults of this trematode are found in the bile ducts of the liver. This specimen is from a cow, but these flatworms may also infect sheep, man, and most other mammals. Note the thickening of the bile ducts caused by the parasite infection.

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Fasciola hepatica - The diagnostic stage of this trematode is the egg which is passed in the feces. Like many fluke eggs it has an operculum (cap) at one end and does not float in the standard saturated salt solution. You must use a sedimentation method to concentrate the feces in order to diagnose an infection with this parasite.

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The Cestodes (Phylum PLATYHELMINTHES, Class CESTODA), as adults, are ribbon shaped organisms whose "body" is made up of many repeating segments. They have no digestive tract or coelom and the adults are always found in some part of the host's digestive

Card 1:20 Taenia saginata .The adult is found in the small intestine of humans and may be quite long. Card 1:19 Taenia saginata . The cysticerci appear as white. fluid-filled bodies throughout the muscle tissue.The diagnostic stage for an infection caused by the adult tapeworm in humans is usually the gravid proglottid (an egg filled segment of the worm) which passes out with the feces. saginata in the muscle of a cow. The larva is a cysticercus. Card 1:18 Taenia saginata . This slide shows an egg which was removed from a proglottid (although these eggs sometimes may be found in the feces by a standard fecal flotation).This gross specimen shows the larval stages of T. Return to top of page . Identification of the type of tapeworm can be made by examining the morphology of the proglottid and the eggs it contains.tract.

and . non-cellular material (usually chitin or calcium carbonate). Card 1:23 Card 1:24 Class HEXAPODA (INSECTA) Insects have all of the characteristics of the phylum Arthropoda. thorax. multi-jointed appendages and an exoskeleton (outer covering) of secreted. Their bodies are more or less segmented. The veterinary medical importance of these animals stems from their ability to act as pathogenic ecto. and their bodies are divided into three segments: head.Card 1:21 Card 1:22 Phylum ARTHROPODA Arthropods are bilaterally symmetrical animals with paired. They have a dorsal heart and a ventral nerve cord. their exoskeletons are composed of chitin and cross-linked proteins. Specifically. The adult stages have three pairs of legs.and endoparasites and from their ability to transmit other parasites or microbial pathogens. and they are cold-blooded.

The larva.abdomen. pupa. and the larvae live attached to the wall of the horse's stomach. The adult flies are free-living. the fleas. This mosquito is an insect that may act as a vector and intermediate host for several different parasites. and male and female adults are seen here. We will study three groups or orders of insects in this course. (This museum specimen shows the larvae attached to the mucosa of a horse's stomach. These insects are the larval stage of a fly. Card 1:25 Gasterophilus sp. Card 1:27 Card 1:28 .) Card 1:26 Culex sp. These orders are constituted by the true flies. and the lice.

but differ from those animals in that they have four pairs of legs in the adult stage. Note the damage that this skin burrowing mite (arachnid) has caused to this cat's head. the Order ACARINA. their bodies exhibit fusion of two of the insect segments.Class ARACHNIDA Arachnids have all the characteristics of the phylum Arthropoda. into a single body region known as the cephalothorax. which includes the ticks and mites. They share a chitinous exoskelton with the insects. the head and thorax. Also. We will deal with only one Order in the class Arachnida. Card 1:31 . Card 1:30 Notoedres sp. Card 1:29 Notoedres cati This tiny skin burrowing mite was recovered in a skin scraping from a cat exhibiting symptoms of mange as illustrated in the museum specimen to the right.

pseudopodium. The white nodules you see in this rabbit's liver are part of the pathology caused by this parasite.Dermacentor variabilis ("American Dog Tick") These adult ticks (arachnids) were removed from the skin of a dog. they also are vectors for several parasitic diseases. Ticks not only suck blood from their hosts. . Card 1:34 Eimeria stieda This protozoan infects the liver of rabbits. and cilia) or the lack of such structures. Most of the protozoa are microscopic. Return to top of page Card 1:32 Card 1:33 The protozoa (Phylum PROTOZOA) are single cell animals which fall into several classes. In general the classes of protozoa are organized around structures used for locomotion (flagellum. such as Rocky Mountain Spotted Fever.

it will float in a standard salt solution.Card 1: 35 Eimeria stieda The diagnostic stage of this coccidian is the oocyst which passes in the feces. Return to top of page Card 1:37 . Card 1: 36 Haemoproteus The stage of the protozoan seen in this red blood cell of a pigeon is one of the sexual forms of the parasite. This parasite is in the same group of protozoans as malaria.

(right: modified Baermann apparatus.BAERMANN APPARATUS This device is used to recover nematode larvae from a fecal sample.) Which of the diagnostic methods learned in today's laboratory would be the best one to use to detect the eggs of this parasite in the deer's feces. Click here for the answer. left: Baermann apparatus). A. Return to top of page Review Question This parasite was recovered from the bile duct of a deer. Its eggs (the diagnostic stage) are found in the host's feces. Return to top of page . The larvae under the microscope at the right were recovered using a Baermann apparatus.) To what Phylum and Class does this parasite belong? B.

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Nematode Taxonomy Back to Index Class: Nematoda Superfamily: Trichostrongyloidea Strongyloidea Metastrongyloidea Rhabditoidea Oxyuroidea Ascaridoidea Subuluroidea Spiruoidea Filarioidea Trichuroidea Dioctophymatoidea Back to Index .

Laboratory 2 THE STRONGYLES Click on the text below to jump down to the desired section of this page. Nematodirus sp. Oesophagostomum dentatum Stephanurus dentatus Strongylus sp. Haemonchus sp. Ostertagia sp. Syngamus trachea Review Question Return to top of page Card 2:1 . Cyathostomum sp. Cooperia sp Chabertia sp. Trichostrongylus sp.

Haemonchus sp. Note the spirally wound ovaries in the female worms which gives them their common name the "Barber pole worm". Size 20 to 30 mm (this is the largest of the abomasal trichostrongyles) Card 2:2 Haemonchus contortus This is the common "barber pole" worm of the abomasum of sheep. This nematode is common in the abomasum of sheep. This slide shows the bursa of a male worm. and other ruminants. goat. cattle. Card 2:3 Haemonchus contortus This slide shows the vulva flap of a female worm. . Note the asymmetrical dorsal ray which is characteristic of this genus.

5 to 8. This trichostrongyle of the abomasum is intermediate in size (smaller than Haemonchus and larger than Trichostrongylus).Return to top of page Card 2:4 Ostertagia sp. Note the very small size of the worm. Male 7.5 mm Female 10 to 12 mm Return to top of page Card 2:5 Trichostrongylus sp. One of the many species of Trichostrongylus found in horses and ruminants. Male 4 to 5 mm Female 5 to 7 mm Return to top of page Card 2:6 .

Male 4.5 to 5.2 mm Card 2:7 Cooperia curticei This female specimen demonstrates the characteristic "watch spring" appearance of the parasite.5 mm Female 5.8 to 7. This worm is commonly found in the small intestine of sheep. Note the small size of these nematodes and their coiled ("watch spring") appearance. Return to top of page Card 2:8 . The anterior end shows the cervical inflation which is finely striated.Cooperia curticei Male and Female worms.

Note the buccal capsule can be seen with the naked eye Male 13 mm Female 18 mm Card 2:9 Chabertia ovina Mounted specimen to show the large buccal capsule which is directed ventrally.Chabertia ovina This parasite is commonly found in the large intestine of sheep and cattle. Return to top of page Card 2:10 . Note the leaf crowns.

egg B = typical strongyle egg . A = Nematodirus sp. This is a relatively long trichostrongyle found in the intestine of ruminants. Male 7.5 mm Female 10 to 12 mm Card 2:12 Nematodirus sp. This slide shows the bursa of the male worm. Note that the anterior end of this worm is thinner than the posterior. Egg Because of its size (200 X 90 um. Note the long spicules which are joined together at the tip by a narrow membrane. this egg is easily identifiable to genus. about twice as large as other strongyle-type eggs) and shape. Also note the size: Male 10 to 15 mm Female 15 to 23 mm Card 2:11 Nematodirus sp. These characteristic spicules can be used to identify this nematode as Nematodirus sp.Nematodirus sp.5 to 8.

5 to 8.(Return to top of page) Card 2:13 Oesophagostomum dentatum One of the species of nodular worms of pigs. dentatum. Card 2:15 Oesophagostomum dentatum This is a section through a nodule produced in the intestine of a pig by O.5 mm Female 10 to 12 mm Card 2:14 Oesophagostomum dentatum Note the small buccal capsule (A). which is terminated by a ventral groove. leaf crowns (B) and a definite cephalic vesicle (C). . Note the size: Male 7.

Note the thin cuticle and visible internal organs. Male 25 mm Female 35 mm Return to top of page Card 2:18 Strongylus vulgaris Whole worms. Note the thickened intestinal wall and the many nodules. Return to top of page Card 2:17 Stephanurus dentatus This is the kidney worm of swine and is found in cysts which open to the hilus of the kidney and the ureters. The females have pointed tails while the males have a bursa at the caudal end. . Note the robust nature of these nematodes and their size (smaller than the other species of Strongylus).Card 2:16 Sheep colon infected with Oesophagostomum sp.

Note the size and the robust nature of these nematodes. Card 2:20 Parasitic thrombi of the arteries of a horse due to the larval stages of Strongylus vulgaris. Card 2:22 . Note the large buccal capsule (A) and the leaf crowns at the anterior end. Card 2:21 Strongylus equinus Whole worms.Card 2:19 Strongylus vulgaris A common nematode of the large intestine of horses. Two ear shaped teeth (B) are in the buccal capsule and a dorsal "gutter" (C) runs down the dorsal side of the buccal capsule. Note the marked thickening of the arterial wall and the thrombus formation.

Note the leaf crowns (A) surrounding the mouth.) Card 2:23 Strongylus edentatus Whole worms.Strongylus equinus Note the large buccal capsule and the leaf crowns (C) at the anterior end. There is a dorsal "gutter" (D) with a bifid dorsal tooth (B) at its base and two smaller ventral teeth (A) at the base of the buccal capsule. The purpose of this gutter is to allow enzymes secreted by glands in the esophagus to make their way into the buccal capsule which would be filled with host tissue while the worm is feeding. There are no teeth in the buccal capsule of this species. however a dorsal "gutter" (C) is present. Return to top of page . Note the size and the robust nature of these nematodes. Card 2:24 Strongylus edentatus One of the largest of the nematodes of the large intestine of the horse. which opens into a large buccal capsule (B). (You will have to focus up and down to see both ventral teeth.

The males may have large bursa. The sexes are found in permanent copulation. Trichonema spp.. fowl and various wild birds. hence the "Y"-shaped appearance of the worm pair. goose.) A large number of genera and species exist and they vary in size from 5 mm to 15 mm. Note the size (much smaller than Strongylus spp. Male 2 to 6 mm Female 5 to 20 mm Return to top of page Card 2:26 . etc.) Whole worms.Card 2:25 Small strongyles (Cyathostomum spp. Return to top of page Card 2:26 Syngamus trachea Occurs in the trachea of turkey.

Indicate which is the more important pathogen. if possible. Give the genus and.Review Question A. CLICK HERE FOR THE ANSWER Return to top of page . B. the species of each. The worms in the dish were removed from the colon of a horse which died with severe colic.

Compare the size of these worms (10 to 16 mm) with the smaller U. LUNGWORMS AND STRONGYLOIDES Click on the text below to jump down to the desired section of this page. stenocephala. . A fresh specimen of A. . Ancylostoma caninum Ancylostoma braziliense Uncinaria stenocephala Bunostomum trigonocephalum Oslerus (Filaroides) osleri Muellerius capillaris Dictyocaulus viviparus Metastrongylus apri Strongyloides spp.Laboratory 3 HOOKWORMS. caninum is often colored red by the blood in its gut (the color fades on fixation in alcohol). Review Question Return to top of page Card 3:1 Ancylostoma caninum Whole worms.

Card 3:4 Ancylostoma caninum First-stage larva. bulbed rhabditiform esophagus and straight tail (no genital rudiment is visible). It is the major etiological agent of cutaneous larval migrans in humans in the United States. . and the pair of large lateral teeth. Return to top of page Card 3:6 Ancylostoma braziliense This hookworm occurs in both cats and dogs.Card 3:2 Ancylostoma caninum Specimen showing the mouth capsule. which is bent dorsally. but may be transported north in pets that travel with their owners. Note the deep mouth (buccal) capsule. Note the mouth tube. It is endemic in the gulf coast states. Note the deep capsule (bent dorsally) and 3 pairs of teeth (3 on each side of the ventral margin).

Because the head is bent to the dorsal side.5 mm Female 7 to 12 mm Card 3:8 Uncinaria stenocephala This adult worm is mounted to show the buccal capsule. Note that these hookworms are smaller and thinner than A. the ventral surface appears to be the anterior end of the worm.Return to top of page Card 3:7 Uncinaria stenocephala Whole worms. Male 5 to 8. caninum but instead of teeth there are cutting plates. Remember that this nematode is similar to A. Return to top of page Card 3:9 . caninum. one on each side of the ventral surface of the mouth.

This species occurs in sheep and is similar in size and appearance to the cattle hookworm (B. phlebotomum). Note the cutting plates seen on the ventral aspect of the mouth.Bunostomum trigonocephalum Whole worms. Return to top of page Card 3:11 . identification of the hookworms will depend on seeing the buccal capsule and cutting plates. Male 14 mm Female 24 mm Card 3:10 Bunostomum trigonocephalum Specimen mounted to show the buccal capsule. Because there are other bursate nematodes in the small intestine of sheep and cattle.

Note the kinked tail (A). Numerous L1 can be seen within the uteri of the female worms. osleri. Card 3:13 Oslerus (Filaroides) osleri This is a preserved specimen of a trachea of a dog infected with O. Card 3:14 . Note the numerous wart-like nodules present at the bifurcation of the trachea and extending into the bronchi. Note the accumulation of fibrous tissue around numerous nematodes (seen in cross-section). Card 3:12 Oslerus (Filaroides) osleri This slide is a cross-section of one of several nodules removed from the trachea of a dog.Oslerus (Filaroides) osleri L1 The first stage larvae of this lungworm can be found in the feces or tracheal washes of infected dogs.

Decreased lung sounds on the right side. Readmitted 11/10. Taken to 3 different veterinarians who diagnosed: 1) allergy 2) pneumonia 3) normal dog. PHYSICAL EXAMINATION: Dog sits on front elbows abducted. 5. HISTORY: During the last 2-3 weeks there was periodic respiratory distress. radiographs indicated a pneumothorax. Re-examined 11/23: Breathing normally. Wall of trachea weakened due to Oslerus osleri infection. . NOTE: At the time this dog was seen there were no anthelmintics which were active against O. the dog would have labored breathing. A thoracotomy (10/27) showed nothing abnormal. removed several nodules from trachea. COURSE OF THERAPY: 1. 4.Oslerus (Filaroides) osleri PATIENT: 1 1/2 year old male schnauzer. Pathology indicated granulomas containing numerous nematodes. 3) Allergy. Re-examined 12/17: Dog normal. Several were large enough to obstruct bronchi during deep inspiration. Hospitalized for 8 days (10/24 to 11/2). 3. *This indicated that the dog had heartworm in addition to the Oslerus osleri infection. 2. and pass out. Dog sent home 1/2. Radiographs indicated air in the mediastinum (possibly leaking from trachea). During attacks the dog became cyanotic. become cyanotic. TENTATIVE DIAGNOSIS: 1) Diaphragmatic hernia. Removed enough to make a patent opening. DIAGNOSIS: Pneumothorax due to leakage of air from the trachea. 2) Tension pneumothorax. given antibiotics and had air removed from thorax periodically. Returned 11/5 for removal of more air from thorax. A blood smear showed many microfilariae*. (Several nodules sent to pathology). "gasping for breath". Broncoscopy showed numerous nodular growths (1 to 5 mm) from the mid-trachea into both main stem bronchi. Dog was sent home. osleri. Today we have several effective drugs to kill this worm and one of them would have been used in this dog along with the surgery. Radiographs indicated a spherical density of the ventral aspect of the trachea at the level of the right cardiac border.

The worm is associated with small. (Return to top of page) Card 3:18 Metastrongylus apri Whole specimens. Return to top of page Card 3:16 Dictyocaulus viviparous Whole specimens. . nodular lung lesions which contain adult worms and larvae. white nematodes found in the bronchi of pigs. Note the large size (4 to 8 cm) and the white color (the intestine may show through as a dark line). slender. These nematodes occur in the bronchi of cattle.Return to top of page Card 3:15 Muellerius capillaris This slide shows this lungworm in the lung of a goat. Note they are long (up to 6 cm).

(see card3:23 for comparable image) Card 3:23 Strongyloides stercoralis This is a parasitic (parthenogenic) female recovered from a mucosal scraping of the small intestine of a dog. Note the small size. and long esophagus. Note the presence of several worms (seen in cross-section) in the bronchi and the normal lung tissue surrounding the bronchi. Return to top of page Card 3:22 Strongyloides ransomi Adult females from the intestine of a pig. There are no males in the parasitic portion of the life-cycle. Card 3:24 .Card 3:20 Metastrongylus apri This is an autopsy specimen from a pig infected with Metastrongylus apri.

) Note also the simple pointed tail (this separates these larvae from lungworm L1). Return to top of page Card 3:26 . The length of the esophagus and the notch in the tail allow you to distinguish between the L3 and the L1. Note the filariform esophagus which extends to 40% of the body length. (The latter 2 characteristics distinguish these larvae from those of the hookworms. and the large genital rudiment (GR). Card 3:25 Strongyloides stercoralis Infective L3. L3 can sometimes be found in tracheal washes of an infected dog. which is short (much less than 40% of the body) and distinctly bulbed. these occur on the soil surface or in fecal cultures. Note the rhabditiform esophagus. Focus carefully and notice the notched tail. primates and humans.Strongyloides stercoralis This is a first-stage larva as passed in the feces. Living L3 are infectious for dogs. the short mouth capsule.

A. B.Review Question These worms were some of the many removed from the small intestine of a 6 week old puppy that died of severe anemia. How did the puppy most likely acquire this infection? Click here for the answer Return to top of page . Identify the nematode (Genus and species).

Laboratory 4 ASCARIDS. Ascaris suum Parascaris equorum Toxocara canis Toxascaris leonina Toxocara cati Baylisascaris procyonis Ascaridia galli Heterakis gallinarum Oxyuris equi Trichinella spiralis Trichuris vulpis Capillaria spp. AND TRICHOCEPHALIDS Click on the text below to jump down to the desired section of this page. Dioctophyma renale Review Question Return to top of page Card 4:1 . OXYURIS.

Card 4:3b . Card 4:2 Ascaris suum This slide shows the 3 lips at the anterior of the worm.Ascaris suum This is the ascarid of swine. In addition. Note its size and shape. (Focus up and down to see all 3.) Card 4:3a Pig lung infected with Ascaris suum Note the marked degree of hemorrhage in the lung. most of the air spaces are filled with blood. there is edema and cellular infiltration. . The male is smaller than the female and has a curved tail with spicules.

) Card 4:5 . (three lips are a characteristic of all ascarids. Note its size and the 3 large lips at the anterior end.All of the ascarids in this 1 gallon jar came from one foal. Return to top of page Card 4:4 Parascaris equorum This is the ascarid of horses.

cati end abruptly. In both of these worms the alae merge gradually into the cuticle. the alae of T. Note the 3 lips (focus up and down to see all 3) and the cervical alae. The alae are clear cuticular flanges running along the lateral margins of the worm. canis. Return to top of page Card 4:6 Toxocara canis This is the common ascarid of dogs. Focus up and down to see all three. In contrast.Parascaris equorum This slide shows the 3 lips (1 dorsal and 2 ventral). They are similar in shape to those of Toxascaris leonina. Return to top of page Card 4:7 Toxascaris leonina The cervical alae of this ascarid of dogs and cats is similar to those of the dog ascarid T. .

puppy described in the case report. Toxascaris leonina Toxocara canis Card 4:9 Toxocara canis The worms in this bottle were recovered from the 3 lb. Recall the biological differences between the two species: Host(s).Card 4:8 Toxocara canis and Toxascaris leonina Adult worms. the males measure up to 10 cm and the females up to 18 cm long T. transmission options. canis is much larger. leonina males are up to 7 cm and the females are up to 10 cm. Return to top of page . T. Are both equally significant in public health. larval migration (or not) and the resulting differences in pathogenesis.

. leonina the other ascarid of cats. unlike those of T. Thus.Card 4:10 Toxocara cati These are the adults of the common ascarid of cats. Card 4:11 Toxocara cati Note that the cervical alae of this ascarid terminate abruptly. ascarids that are expelled in the feces of cats can be easily distinguished. Note that the cervical alae can be seen with the naked eye. Return to top of page Card 4:12 .

causing this species to be especially pathogenic. This worm lacks cervical alae. and many wild birds (e.g. As has been pointed out in the lecture. canis. geese. crows). The larvae (not adults) occur in humans (and other mammals and birds) where they are one of several causative agents of "larval migrans".Baylisascaris procyonis Adults from the small intestine of a raccoon. This parasite occurs in the small intestine of chickens.116 mm Return to top of page Card 4:14 . this is an increasingly important parasite in veterinary public health. Males 50 . Return to top of page Card 4:13 Ascaridia galli Adult worms. they are large and highly neurotropic. Although its larvae are not as prevalent in humans as those of T. turkeys.76 mm Females 72 .

its susceptibility to modern anthelmintics has all but eliminated this nematode from horses in this part of the country. The females are larger than the males. Note its size. This is the most common caecal worm of ground-reared poultry. Note the females have long thin tails (a characteristic of the family) while the males have a blunt tail with caudal alae and a single spicule. Return to top of page Card 4:16 . Return to top of page Card 4:15 Oxyuris equi These are adults of the pinworm of horses. Formerly a very common parasite of the large intestine.Heterakis gallinarum These are adults.

Trichinella spiralis This is a section of muscle from a Trichinella spiralis infected mouse in the acute phase. whereas the thick posterior end protrudes into the lumen. Note that the thin anterior end is embedded in the mucosa. the common name: "whipworm". Note the size and the long. Card 4:18 Trichuris vulpis This museum specimen demonstrates an infection with the whipworm of dogs. Trichinella spiralis is unique among the nematodes because the same individual serves as the definitive and intermediate host. Return to top of page Card 4:17 Trichuris vulpis These are adult dog whipworms. It is these larvae that cause the most characteristic symptoms of trichinosis. Hence. Card 4:19 . thin anterior end (the "lash") and the short. Observe the abundant inflammation. thick posterior end (the "whip-handle") of the worm.

Capillaria spp. Card 4:21 . The posterior portion of the body is not conspicuously thicker than the anterior as in the case of the whipworms. In some species. larvae may occur in invertebrates as well. with a smooth surface and possesses a plug at each pole. but they are small and slender. lemon-shaped.Trichuris vulpis The egg of Trichuris sp. It is unembryonated when passed in the feces. thick shelled. mammals and other vertebrates. It measures 80 X 40 um. Note: Focus up and down to see the texture of the outer surface of the eggshell. These nematodes are closely related to Trichuris. occur in many species of birds. is brown in color. Return to top of page Card 4:20 Capillaria spp.

The easiest way to distinguish this egg from that of a whipworm is to examine the surface of the egg. Note: Focus up and down to see the texture of the outer surface of the eggshell. Capillaria spp. Note the very large size and its location (within the kidney). Card 4:23 . Return to top of page Card 4:22 Dioctophyma renale This nematode is one of the largest known and is found in the kidney of dogs and wild carnivores (especially fish eating carnivores. e.Capillaria aerophila The sides of this egg are usually parallel and the polar plugs tend to be asymmetrical.g. only one kidney is usually parasitized. eggs have a rough surface while Trichuris spp. It causes destruction of the kidney tissue until only a fibrous shell is left. eggs have a smooth surface. Fortunately. mink).

thick shelled. A) Name the parasite(s) present on the slide.g. elevated respiratory rate. coughing. pitted (except at the poles) and are unsegmented (unembryonated) when passed in the urine. some two weeks prior. e. had shown clinical signs of pneumonia.. (Note : Please do not move the slide. Return to top of page Card 4:24 Review Question This slide under the microscope contains the product of a fecal exam on a young pup from Philadelphia which. They are barrel shaped.Dioctophyma renale This slide shows the egg of the kidney worm of dogs and other carnivores. foamy nasal discharge.) B) Which parasite(s) could have accounted for the pulmonary signs? Click here for Answer . etc.

aegypti Onchocerca lienalis Setaria equina Gongylonema pulchrum Physaloptera sp.Laboratory 5 SPIRURIDS AND FILARIDS Click on the text below to jump down to the desired section of this page. "Horse hair worm" Review Question Return to top of page Card 5:1 Spirocerca lupi The esophageal worm of dogs. Spirocerca lupi Dracunculus insignis Dirofilaria immitis Dipetalonema reconditum Ae. . . Living specimens are pink to bright red in color. These worms are large and usually coiled.

Card 5:2 Spirocerca lupi The eggs of this worm are small (40 X 15 um). . Card 5:4 Spirocerca lupi Radiographs Note the granulomatous mass surrounding the esophagus (difficult to see here) in both the general survey and in the angiogram on the right. When passed in the feces they contain a larva bent in the shape of an "U". Note the fibrous nodule or tumor with the worms coiled inside. Card 5:3 Spirocerca lupi Mounted specimen showing the esophageal lesion caused by the worm. vertebrae (red arrows). Tissues in these nodules have been known to undergo malignant transformation. oval. . Some students have told us that these look like miniature paperclips. Also note that in the survey you can see the thickening of the bodies of the thoracic . . thick shelled with parallel sides. The angiogram clearly shows an aneurysm in the descending aorta.

Cyclops sp. Card 5:6 Dracunculus insignis This slide shows the L1 of the "guinea worm" of wildlife.. . The female worm will make a hole through the skin (usually of the leg) in order to deposit L1 when the skin gets wet. L1 will be discharged into the tube and can be used to diagnose the infection. . If a tube of water is placed over the skin ulcer formed by the female worm. Return to top of page Card 5:5 Dracunculus insignis This is an adult spirurid worm removed from a dog. This parasite of wildlife lives subcutaneously in its host. . This is the stage that is infective to the intermediate host.

Females reach a size of 25-30 cm long. and are slender. .This slide shows the adult female worm discharging L1 into a test tube. . Card 5:8 . in the right atrium. Return to top of page Card 5:7 Dirofilaria immitis These worms are found mainly in the pulmonary arteries and. with heavy infections. Males are shorter (12-16 cm) and the tail (right) is spirally coiled.

microfilaria Note the tapered anterior end. From a Knott preparation. Card 5:8a Dirofilaria immitis Ultrasound showing caval syndrome. Numerous white spots can be seen in the uppermost section.Dirofilaria immitis . Return to top of page . Card 5:8b Dirofilaria immitis Ultrasound showing two adult worms in the pulmonary arteries. The presence of the worms is easily identified. In most specimens you will see a straight body and straight (or slightly curved) tail. These spots represent adult worms in the right ventricle. . . Each worm is seen as parallel white lines. . The width is > 6 um.

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Dipetalonema reconditum microfilaria
Note the "blunt" anterior end (the cephalic hook may or may not be seen). The tail is curved (usually). The width (4.7 to 5.8 um) is less than D. immitis.
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Dirofilaria immitis
Microfilariae stained by the acid phosphatase technique. NOTE that staining is "zonal". These zones correspond to the excretory (anterior) and anal (posterior) pores of the microfilariae.

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Dipetalonema reconditum
Microfilaria stained by the acid phosphatase technique. Note that the staining is uniform in these microfilariae.

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Females of Aedes aegypti mosquitoes feeding on blood containing microfilariae of Dirofilaria immitis via artificial membrane feeding apparatus.

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Digestive tract of blood-engorged female Ae. aegypti. A: Midgut with blood. B: Hindgut (may be pulsating). C: Malphigian tubules (white in color). Note: You can actually see the giant 1o cells of the tubules under the dissecting scope.

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Gut contents of female Ae. aegypti showing microfilariae of D. immitis.

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Larvae of D. immitis from malphigian tubules 6 days after infection. (Focus up and down). A: 2nd stage D. immitis larvae. B: Malphigian tubule.
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Third stage larvae (infective) in mouthparts (labial sheath) 13 days after infection.

Arrows point to emerging L3 from proboscis.

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This museum specimen is from a dog with D. immitis infection. The pulmonary arteries have been dissected open to reveal the primary predilection site of the adult parasite. This museum specimen also shows adults of D. immitis in the right atrium. Retrograde movement of large numbers of adults into the right heart, as seen here, is usually an artifact of death, but may occur in vivo in cases of caval syndrome. .

Card 5:18

This model depicts the primary predilection site of adult D. immitis - the pulmonary arteries. Note that the model also represents the formation of rough villus-like plaques in the arterial lining, a response to injury by the worms and the primary lesion responsible for pulmonary . hypertension in heartworm disease.

Card 5:19

This model depicts D. immitis adults in the right atrium of the canine heart. Such a situation may occur in caval syndrome when decreased cardiac output permits retrograde migration of adult worms from the pulmonary arteries. In many cases, finding adult worms in this location at necropsy is simply an artifact of death. When pulmonary blood flow ceases, the worms move into the right heart.
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Onchocerca lienalis - microfilariae from a bovine skin biopsy
To see the microfilariae, carefully remove the petri dish top and focus on the bottom of the dish. The worms often congregate around the edges of the dish or around the skin biopsy itself. They are tiny, less than 300 um in length, and should be highly motile.

Please do not readjust the microscope or light.

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Card 5:22

Setaria equina
Removed from the peritoneal cavity of a horse. Males: 4 to 8 cm. Females: 7 to 14 cm.
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Setaria sp. microfilaria
These microfilariae are sheathed.

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Gongylonema pulchrum
The sinusoidal tracks on the mucus membrane of this sheep's esophagus indicates where the adult of this spirurid worm is located. This worm uses dung beetles as the intermediate host. This nematode is a non-pathogenic parasite of many domestic mammals.
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Physaloptera sp.
These spirurid nematodes are parasites of the stomach of carnivores. They are normally found in opossums and raccoons but can occasionally be found in dogs and cats. This parasite uses a coprophagous beetle as an intermediate . host.

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"Horse hair worms" Adult found in swimming pool
Phylum Nematomorpha Class Gordioidea Adults are free living inhabitants of fresh water. Larvae are parasitic in insects. The larvae mature to the adult stage in the insect and when the insect is in . contact with water the adult emerges. This is why the adult worm can be found swimming in a pet's water dish or the family swimming pool.

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Card 5:27

Review Question
A dog was presented to a local veterinarian for a routine heartworm exam. The dog was not showing any clinical signs of infection. The results of a Knott concentration test are seen in the compound scope at the right. (Please do not move the specimen!) The results of . a serologic test for Dirofilaria immitis antigen are also seen at this station. This test is showing a negative. A. Based on the information you have and on the appearance of the specimen under the scope, what would be your diagnosis? B. What further testing might you do to confirm your diagnosis? C. What are the implications of this

B. What further testing might you do to confirm your diagnosis? C. What are the implications of this finding for the dog's health? Click here for the answers

PARASITOLOGY LAB EXAM
(This is an actual examination paper for your reference) (Click on the question to see the picture that goes with the question) Question 1. A. A local dairy farmer has just acquired some livestock and is concerned that they may have liver flukes (the trematode Fasciola hepatica). What fecal examination method will give you the best chance of finding the eggs of this parasite? (3 pts.) B. A 3-week-old puppy has watery diarrhea. Given its age and clinical signs you suspect a Giardia infection. What fecal examination method will give you the best chance of detecting this parasite? (3 pts.) C. A 4-year-old dog has a chronic cough and you have included the nematodes that live in the lungs on your list of possible causes. What fecal examination method(s) will give you enough information to rule out (or in) the presence of these "lungworms"? (3 pts.)

Question 2. A. The fecal sample in the device at your place came from a 4-year-old male Rottweiler as part of his yearly check-up. Examine the sample and identify the eggs of the parasite (give Genus and species). (7 pts.) B. What other similar looking egg could appear in dog feces and how could You tell it apart from the egg you identified in part A? (3 pts.) Question 3. A. The sample of meat in the dish at your place is beef hamburger that is thought to have been contaminated with pork. Is it likely that the hamburger has pork in it (yes, no, can't tell)? (4 pts.) B. Explain your answer to part A. (3 pts.)

Question 4. A. A saturated salt flotation was done on a fecal sample from a 4 month old Puppy which has been brought to you for its first check-up. The results of this test are shown under the microscope at Station #4. Identify the parasite egg (give Genus and species). (7 pts.) B. What other similar looking egg may be found the feces of a dog and how could you tell it apart from the egg you identified in part A? (3 pts.) Question 5. A. A 6-year-old male mix breed dog was brought in to your practice with the complaint that it had chronic vomiting. The results of a saturated salt flotation fecal examination is shown under the microscope at Station #5. Identify the egg (give Genus and species). (6 pts.) B. What pathologic changes may have been caused by this parasite and what other procedures would you do to determine if this dog had these pathologic conditions?

(3 pts.) Question 6. A. The egg seen under the microscope at Station #6 was recovered from the feces of a 1 month old foal which has diarrhea. Many of these eggs are present on the slide. Identify the parasite (give Genus and species). (6 pts.) B. Why would you expect to see eggs of this parasite in a young foal rather than in a mature horse? (3 pts.) Question 7. A. The egg seen under the microscope at Station #7 was recovered during a urine analysis of a pig. Identify the parasite (give Genus and species). (6 pts.) B. In what organ does the adult worm reside? (3 pts.)

Question 8. A. The worms seen under the microscope at Station #8 were recovered from the small intestine of a sheep which died of bacterial pneumonia. Identify the parasite (give Genus only). (6 pts.) B. Describe the egg you would expect to find in the feces. (3 pts.) Question 9. A. A number of adult nematodes, each about 1.5 cm long, were recovered from the large intestine of a horse which died suddenly. The anterior end of the worm is shown on the kodachromes at Station #9. Identify the parasite (give Genus and species). (6 pts.) B. Where in the horse would the fourth-stage larvae (L4) of this worm be found? (3 pts.) Question 10. A. The dish under the microscope at Station #10 contains a skin biopsy in saline. The biopsy was taken from the ventral midline of a horse with itching dermatitis in this area. Identify the parasite (give Genus only). (6 pts.) B. How is this parasite transmitted? (3 pts.)

Laboratory 6

TREMATODES

Click on the text below to jump down to the desired section of this page. Gyrodactylus sp. Fasciola hepatica Fascioloides magna Dicrocoelium dendriticum Paramphistomum cervi Paragonimus kellicotti Heterobilharzia americana

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Gyrodactylus sp.
This monogenean trematode is an ectoparasite of fish. Note the haptor ("holdfast organ") at the posterior of the worm.

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Fasciola hepatica - Eggs
Note the size, shape, color, and the operculum.

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Fasciola - miracidium
Note the cilia, eye-spots and the germ cells.

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Limnea spp.
One of the many snail intermediates hosts suitable for the development of Fasciola stages.

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Fasciola - Redia
Characterized by a primitive digestive tract made up of a pharynx and intestine. Note the developing cercariae within the redia.

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Fasciola - cercaria
Note the oral and ventral suckers. Also note the tail for swimming.

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Fasciola hepatica - metacercaria
The encysted metacercaria would normally be found on vegetation.

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Fasciola hepatica
Adult specimen taken from the bile duct of an infected animal. Note the size, distinct cone at the anterior end, " shoulders" and broad outline.

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Model of a Sheep Liver infected with Fasciola hepatica
Note the thickened, calcified bile ducts and the adult worms in the bile ducts (difficult to see in this photo).
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Fascioloides magna
Very large liver fluke. Indigenous to North Americana. Normal Host Deer: Adults encapsulated but eggs passed into bile ducts. Abnormal Host Cattle: Adults encapsulated, no eggs passed. Sheep: Uninterrupted migration in liver parenchyma. Host usually dies.
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Dicrocoelium dendriticum - Eggs
These eggs are small, dark brown and asymmetrical, they are thick walled with an indistinct operculum.

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Dicrocoelium dendriticum
Adult specimen taken from the bile duct of an infected animal. Note the small size, lancet shape, absence of distinct cone at the anterior end, no "shoulders", narrow outline. Compare with Fasciola hepatica
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Paramphistomum cervi
The rumen fluke of sheep and cattle. Note the thick, circular fleshy character of the specimens in the bottom of the jar. Also the flukes buried in the rumen papillae.

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Paragonimus kellicotti
This trematode occurs in the lungs of dogs, cats, and wild carnivores and is found in fibrotic lung cysts. The second intermediate host is a crayfish. (What is the first intermediate host?)

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Paragonimus kellicotti - Eggs
These are large yellowish-brown operculated eggs that are found in the feces (or demonstrated in the sputum). They measure 75-118 u X 42-67 u and have a marked "shoulder" or "ridge" surrounding the operculum. .

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Heterobilharzia americana
Adult worms from the mesenteric veins of a dog. The male is the larger of the two, and has the gynaecophoral groove where the female resides following mating. Separate sexes are the distinguishing feature of the schistosomes.
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Review Question: The worms at the left were recovered from the bile duct of a deer in upper New York state. A. Identify the worms (Genus and species) B. How did the deer acquire the infection? CLICK HERE FOR THE ANSWER

Comments: please e-mail Dr. Nolan at parasit@vet.upenn.edu

Laboratory 7

CESTODES AND ACANTHOCEPHALANS

Click on the text below to jump down to the desired section of this page. Diphyllobothrium latum Spirometra mansonoides Mesocestoides Dipylidium caninum Taenia taeniaeformis Taenia pisiformis Cysticercus of Taenia Taenia multiceps Echinococcus granulosus Echinococcus multilocularis Taenia sp. egg Anoplocephala Moniezia Macracanthorhynchus hiridinaceus Review question

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Diphyllobothrium latum
(Cestoda: Pseudophyllidea) Segments of the broad fish tapeworm of man and dogs.

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Diphyllobothrium latum - eggs
Note the light brown color, shape, size (approximately 60 X 45 microns), and they are operculated (the operculum is indistinct in a fresh preparation). The eggs are not embryonated when passed in the feces.
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Spirometra mansonoides
(Cestoda: Pseudophyllidea) Portions of an adult worm. Note the line of brown spots going up the center of the worm. These are the uteri of the proglottids filled with brown eggs. Eggs . (not segments) are found in the feces. From the small intestine of a cat.

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Mesocestoides - gravid proglottid
(Cestoda: Cyclophyllidea) Uterus lies in the mid-line of the proglottid. The eggs pass from this to be stored in the parauterine organ which can be seen as a thick-walled structure at one end of the proglottid.
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Mesocestoides sp.
Tetrathyridia removed from the peritoneal cavity of a dog. Note the size, and gross appearance (resemble "cream of wheat" particles).
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Dipylidium caninum proglottid
(Cestoda: Cyclophyllidea) Found in the small intestine of the dog, cat, and occasionally man. Note the two sets of reproductive organs in each segment. The gravid segments contain numerous "egg packets", the other reproductive organs having degenerated.

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Dipylidium caninum - egg packets
The egg packets contain 15-20 eggs in each and are seldom seen free in the feces. They may, however, be readily expressed from the gravid proglottids.

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Cysticercoid
This tapeworm larval stage is found in arthropods. It is the metacestode stage of Dipylidium caninum, Anoplocephala spp., and Moniezia spp.

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Taenia taeniaeformis - adults
(Cestoda: Cyclophyllidea) This is known as the "broad necked' tapeworm of cats. The neck is almost as broad as the scolex and segmentation begins immediately behind the scolex.

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Strobilocercus
This is the larval stage of Taenia taeniaformis which has been removed from the intermediate host (a mouse).

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Taenia taeniaeformis - Strobilocercus
Note the pea-sized nodules containing the larval worms embedded in the liver. These are young larvae and the protoscoleces are still invaginated.

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Taenia pisiformis - Adult
(Cestoda: Cyclophyllidea) Adult from the small intestine of a dog. Note the lateral genital pore on the gravid proglottids and how it alternates sides irregularly.
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Card 7:13

Cysticercus
This is the larval stage of members of the genus Taenia. Note in this specimen the protoscolex is everted. Normally it would be found inside of the "bladder".

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Taenia crassiceps
(Cestoda: Cyclophyllidea) Cysticercus of T. crassiceps (left) from the peritoneal cavity of a groundhog. (Note the fluid filled bladder with protoscolex at one end). Cysticercus of T. pisiformis from a rabbit peritoneal cavity is similar to T. crassiceps, but larger (not shown). Image on right is a bottle filled with Taenia cysticerci from the peritoneal cavity of a groundhog.
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Card 7:15

Taenia saginata- cysticercus
(Cestoda: Cyclophyllidea) Cysticercus of Taenia saginata in the skeletal muscle of a cow. Note the pea-sized cysts.
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Taenia multiceps - coenurus
(Cestoda: Cyclophyllidea) This slide shows a cross section through the larva (coenurus). Note the many protoscolecies growing from the germinal layer.
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Return to top of page Card 7:17

Echinococcus granulosus
(Cestoda: Cyclophyllidea) Note the size and number of segments in this adult tapeworm. There is a scolex, and one immature, one mature, and one gravid proglottid.
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Card 7:18

Echinococcus granulosus
(Cestoda: Cyclophyllidea) Numerous hydatid cysts in the liver of a horse. A horse may become infected with a number of cysts at one time (each . egg ingested will result in one cyst).

Card 7:19 Hydatid cyst This is the larval stage of Echinococcus granulosus. (Intermediate stage of Echinococcus granulosus). . . Also note the daughter cyst with protoscolices within the main cyst. Note the thick laminated cyst wall and the fibrous host response outside the cyst wall. Note the myriad of small cysts produced by exogenous budding of the mother cysts. Return to top of page Card 7:20 Echinococcus multilocularis (Cestoda: Cyclophyllidea) This animal was infected 9 weeks ago. Card 7:21 . . Diagram of structure associated with the Hydatid Cyst.

many protoscolices. Return to top of page Card 7:23 . . Note the thin walls. radially striated eggs. and the lack of a host response. eggs Thick-shelled. light brown in color and measures about 34 X 38 um.Alveolar hydatid cyst This is the larval stage of Echinococcus multilocularis. . Return to top of page Card 7:22 Taenia sp.

perfoliata is characterized by 4 lappets. one behind each sucker. Note: 1) A. 2) A. intermediate host is an orbatid mite in which the cysticercoids develop. magna. Return to top of page Card 7:25 . The intermediate hosts are . There are no lappets on A.Anoplocephala magna and Anoplocephala perfoliata (Cestoda: Cyclophyllidea) These tapeworms are found in the small and large intestine (respectively) of the horse. The scolex has 4 prominent suckers and the segments are broader than long. The . perfoliata is smaller than A. Return to top of page Card 7:24 Moniezia expansa (Cestoda: Cyclophyllidea) Found in the small intestine of sheep (particularly lambs) and other ruminants. magna. oribatid mites.

They contain a larval stage. pitted and ellipsoidal. . Note the recurved hooks on the proboscis in which assist in the anchoring of the parasite to the intestinal wall. . Return to top of page Card 7:27 . The eggs are thick shelled (4 shells in fact) dark brown.Macracanthorhynchus hiridinaceus (Phylum: Acanthocephala) Proboscis of the Thorny-Headed worm (Acanthocephala) of pigs. the acanthor. Card 7:26 Macracanthorhynchus hiridinaceus This slide shows the eggs of the thorny-headed worm of pigs.

A. . Based on the shape of the proglottids (wide and short) to what family of ruminate cestodes are they related? B. What do you expect the eggs to look like? Click here for answer .Review question This worm was found in a pronghorn antelope at the zoo.

Argas persicus Otobius megnini Ixodes sp. Chorioptes bovis Otodectes cyanotis Sarcoptes sp. Demodex sp. Amblyomma americanum Dermacentor variabilis Rhipicephalus sangiuneus Review Question Return to top of page Card 9:1 .Laboratory 8 THE ARACHNIDS Click on the text below to jump down to the desired section of this page. Ornithonyssus sylvarium Pneumonyssus caninum Cheyletiella parasitivorax Psorptes sp. Notoedres cati Knemidocoptes sp. Haemaphysalis sp.

This parasite is extremely common in this area. Australia. Pale color (yellow-white when alive) 2.9 mm 4. it is more successful than Dermanyssus gallinae. larvae and nymphs in the feathers of a leghorn pullet which died from blood loss. Well-developed legs (large for the body size) terminated by claws 3. It is very capable of transferring from wild birds into the chicken houses and is transferred from farm to .Ornithonyssus sylvarium"The northern fowl mite" Here you see masses of eggs. shaking of head. 1. Size: 1 . farm when eggs are collected. Palps have 5 segments 5. Africa. adults. Note: . Very small chelicerae (mouth parts) Return to top of page . Hawaii. but it also has the option of being a temporary parasite. Distribution: USA. sneezing.. in that its entire life cycle can occur on the host.1.5 X 6 . Once in a "chicken" house. the "red mite of poultry". nose rubbing. Return to top of page Card 9:2 Pneumonyssus caninum Predilection site: Nasal cavity and sinuses. S. Effects: From none to hyperemia of mucosa.

. coxae II and III are widely separated as in Sarcoptes. and 4th pairs of legs but absent from the 3rd pair of legs. Card 9:5 . the segmented pedicles are present on the 1st. Note that the legs are elongated. the stylet-like chelicerae and the large palps with pincers . Return to top of page Card 9:4 Psorptes ovis spp.Card 9:3 Cheyletiella parasitivorax "Rabbit Mite" Note the oval body with a "waist" at mid-section. 2nd.

A: Pretarsus B: Segmented stalk . the copulatory suckers and the bell-shaped suckers on the first three pairs of legs. Note that the pretarsal sucker is on a segmented stalk. Card 9:6 Psorptic mange Ear of rabbit . . (Yellow arrow points to an epimere). Return to top of page Card 9:7 Chorioptes bovis Note the ribbon-like setae on the anal tubercles. .Psorptes sp. Note also that unlike Otodectes the anterior epimeres run more or less parallel.

stalked pedicel and the suckers on 1st and 2nd pairs of legs. Also note the presence of long trailing setae. . the simple. Card 9:10 . Return to top of page Card 9:9 Sarcoptes scabei Note the globular body shape. coxae II and III are widely separated.Return to top of page Card 9:8 Otodectes cyanotis "The auricular mite" of dogs and cats Note the general outline and the fact that the epimeres (the grooves in the cuticle which extend from the base of each leg) converge toward each other. .

.Sarcoptes sp. . Anus postero-dorsal in position. Card 9:11 Sarcoptic mange Leg of fox. Note that the pretarsal sucker is on a non-segmented stalk. Return to top of page Card 9:12 Notoedres cati Similar to Sarcoptes but considerably smaller and more globose. (PLEASE DO NOT MOVE THE SLIDE) . .

burrows. show the mite. Note the absence of scales and spines on the dorsal surface. and causes thickening of the skin and loss of hair. suckers. and Notoedres sp. Like Sarcoptes sp. The "scaly-leg" mite of chickens Compare with Sarcoptes sp. Return to top of page Card 9:15 . A skin scraping examined under the microscope would . this mite lives in the skin.Card 9:13 Head of Cat with Mange This cat was suffering from infection with burrowing sarcoptid Notoedres cati. The tarsal segments have claw-like structures and tactile hairs instead of pediculated . Return to top of page Card 9:14 Knemidocoptes sp.

Also note the annular rings on abdominal cuticle. The top picture is the adult. the thorax bearing 4 pairs of stumpy legs. composed of: the head. The cuticle has a leathery texture .Demodex sp. The scutum is lacking in the family ARGASIDAE 3. and the cigar-shaped abdomen. The mouth parts are ventral on the body 4. the bottom picture is the egg. The oval shape of the tick 2. Note the elongate shape. Return to top of page Card 9:17 . Return to top of page Card 9:16 Argas persicus Note: 1. PLEASE DO NOT MOVE .

Adult Note the posteriorly directed spine on 1st coxa (Fig. Card 9:19 . there are no festoons on the posterior margin of the body. The genital pore is present and . 6) and pre-anal groove (yellow arrow). Return to top of page Card 9:18 Ixodes scapularis .Otobius megnini "The spinose ear tick" Note: ARGASIDAE characters Spines on dorsum Mouth parts on ventral surface of body .

During lab (not seen in these pics).Nymph This is the stage most commonly encountered on middle-sized mammals (dogs and cats) and on humans. Return to top of page Card 9:20 Haemaphysalis sp. . especially the 2nd palpal segment which is laterally produced. Females and Nymphal Stages Note the characteristics of the genus. note the convergent palpi. . The coxal spine is not as elongate as in the adult and the genital pore is absent (sexually immature). Return to top of page Card 9:21 .Ixodes scapularis .

Return to top of page Card 9:22 Dermacentor variabilis Examine specimens for characters of genus. Also note the coxae on the ventral aspect of the males: Coxae I are deeply cleft.Amblyomma americanum "The Lone Star Tick" Males and Females Note the ornate scutum with a central white mark on the female and the long mouth parts (the 2nd palpal segment is elongated). Coxae IV are larger than coxae I. The eyes are on the lateral margin of the scutum. . . Return to top of page Card 9:23 . Especially note the rectangular basis capitulum and the palpal segments of more or less uniform length and shape.

Festoons are present along the posterior margin. 3. There is a marked hexagonal angulation in the basal part of the basis capituli.Rhipicephalus sanguineus The "Brown Dog Tick" Note: 1. PA. . In the genus Rhipicephalus all of the coxae are of approximately the same size. 4. 5. Knowing the ticks that occur commonly on dogs. A. The anal groove surrounds the anus posteriorly. would your identification lead you to caution the clients about any public health concern? Click here for answer . 2. The hypostome and palpi are short. . Identify the specimen to Genus B. Return to top of page Card 9:24 Review Question The specimen in the dish was removed from the skin of a dog in southern Montgomery County.

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Sarcophaga and Calliphora adults Wing veins Antenna of Cyclorrapha Oestrus ovis Cuterebra Hypoderma Melophagus ovinus Ctenocephalides spp. (fleas) Trichodectes canis Damalina caprae Linognathus setosus Hematopinus spp. Tabanus spp. Gasterophilus spp.Laboratory 9 INSECTS OF VETERINARY IMPORTANCE Click on the text below to jump down to the desired section of this page. Phthirus pubis Pediculus humanus Review Question Return to top of page Card 8:1 . Lucilia. Simulian spp.

B) Compare the size of this early larval stage with a later larval stage in the dish next to the microscope. 4) The ventral proleg is armed with hooks on its anterior end. It is used as a holdfast to anchor the larva in fast moving streams. A) Under the microscope is an early larval stage.Simulium spp. Card 8:3 . Card 8:2 Simulium spp. 3) It has an anterior pair of mouth brushes. "Black Fly" Eggs . . It is used to migrate in "inchworm" fashion. 1) It is cylindrical 2) It has a posterior sucker-like organ armed with hooks.

(eg. (eg. C) Short proboscis. that is. . Card 8:4 Simulium spp. B) The multisegmeted antennae. A) The humpbacked appearance. C) It has respiratory filaments on the anterior end. Return to top of page Card 8:5 .Simulium spp. PUPA A) It is enclosed in a cocoon which is spun by the salivary glands of the last larval stage. Culicoides). Cyclorrhapa). . Simulium. A pupa covered by the hardened 3rd larval skin is known as a coarctate pupa. it is not covered by the 3rd larval skin. Tabanus. . B) It is an exarate pupa.

. .Tabanus Wing veins are important in identifying flies. you are not responsible for knowing the different wing vein patterns. however. . . Card 8:6 Tabanus spp. But you should know the antenna types. Return to top of page Card 8:7 Gasterophilus intestinalis and G. nasalis Distinguish between the larvae using the key provided (figure #5 in lab book). . LARVA Note the fleshy tubercles on each segment.

Card 8:8 Gasterophilus intestinalis Larvae attached to the mucosa of the stomach of a horse. Note the rings of inflammatory thickening with eroded centers where the larvae were . attached. You can see lesions where the larvae have detached. Card 8:9 .. .

Gasterophilus sp. Return to top of page Card 8:12 . Adult . Card 8:10 Gasterophilus sp. Right: bottle filled with horse hairs and attached eggs. . Left: egg on the hair of a horse leg.

.Lucilia. Return to top of page Card 8. But you should know the antenna types. .13A . however. Return to top of page Card 8:13 Wing veins are important in identifying flies. Sarcophaga. and Calliphora adults See lab handout. you are not responsible for knowing the different wing vein patterns.

sheep nasal bot These were removed from the nasal cavities and frontal sinuses of sheep at New Bolton Center on post-mortem examination at the beginning of March. As the larvae matures it develops the brown bands on the dorsal surface of its segments. Morphology of spiracular plate 5. Posterior spiracles 4. Bands of spines on the ventral surface 6. Return to top of page Card 8:14 Oestris ovis larvae . . Large black oral hooks 3. Note: 1. Shape and size 2.Cyclorrhapha: Fly head (enface) Note the typical club-shaped antennae laying in the groove between the eyes.

Note: 1. . Return to top of page Card 8:15 Cuterebra larva This is a mature larva which would be found in a dermal pocket in the host. Morphology of spiracular plate. The larva is covered with spines. 3. Return to top of page Card 8:16 . The dark color of the mature larva. 2..

Ventral surface of penultimate segment unarmed. opening narrow. Card 8:17 Hypoderma sp. Ventral surface of penultimate segment armed with spines Return to top of page Card 8:18 . opening wide.Mature larvae H. spiracle button small. light spots which . more pointed at ends Spiracle plates kidney-shaped. The scars lower the price received for the hide. When the lesions heal. .Leather damage due to Hypoderma This piece of leather shows the lesions following the emergence of Hypoderma sp. bovis 28 mm Barrel shaped Spiracle plates ear shaped. spiracle button well defined. Surface level. are scars form. surface depressed. larvae from the back of a bovine. lineatum 25 mm Thinner. H.

The female lays mature larvae and cements them to the wool. Card 8:20 . Return to top of page Card 8:19 Flea Life-Cycle Egg . The larvae immediately pupate. This is a wingless fly (order: Diptera). Wool is damaged when the sheep scratch and rub themselves.adult .pupa .sheep ked (Fam: Hippoboscidae) Collected from lambs at New Bolton Center Note: 1. Sac-like abdomen The adults live in the wool of sheep. 2. .Melophagus ovinus .larva . The adults irritate sheep by their bites and soil the fleece with feces and blood. Strong legs 3.

and the human flea can act as intermediate hosts for Dipylidium caninum. C. caninum eggs. and cystercercoids then develop within the flea.Ctenocephalides felis . The head is longer (less blunt) than that of the dog flea. the dog flea.the cat flea The cat flea. Note: 1. canis. Card 8:21 Ctenocephalides felis . 2. man) acquire the infection by swallowing the infected adult .larvae These larvae are free-living. The final host (dogs. The first two spines on the genal ctenidium are almost the same size. Live larvae may have a red color from feeding on the adult flea's feces and dried blood. . Note the tuft of strong bristles at the posterior end. The larval stage of the flea becomes infected eating D. cats. flea. Card 8:22 .

The head is more rounded than that of C. felis. . Return to top of page Card 8:23 Trichodectes canis. abdomen and 3 pairs of legs.Antennae extend laterally from head (Suborder Ischnocera) . abdomen dorsoventrally flattened -Three pairs of legs with 1 claw at the end of each leg . Presence of both genal and pronotal ctenidia (combs). Short first tooth on the genal ctenidium. thorax. thorax.biting louse of dogs Note: General structure .Head: anterior end is broad and flat: characteristic of the biting lice Return to top of page Card 8:24 .head.Ctenocephalides canis Note: General structure . .Head.

goats. . . Card 8:26 Linognathus sp. Sucking lice of this genus are found on cattle.Damalinia caprae Adult on goat hair This louse belongs to the suborder Ischnocera (see the characteristics of Trichodectes canis). sheep and dog. . .Nit (egg) Egg glued to the hair of a dog. Return to top of page Card 8:25 Linognathus setosus .

a sucking louse (Anoplura).Narrow. thorax. Return to top of page . .) 3. Return to top of page Card 8:28 Phthirus pubis . pointed head with recessed stylets (adapted for sucking).Antennae extend laterally from head . . Thorax with 3 pairs of legs.sucking louse Note: General structure . Broad abdomen. Head bearing antennae 2.crab or pubic louse of humans . abdomen dorsoventrally flattened . .Head.Three pairs of strong legs each with a claw . Note: 1.Return to top of page Card 8:27 Haematopinus spp. (The first pair of legs is slender compared to the others.5 segments .

Oval abdomen The nymphs are smaller but have a very similar structure to the adults. A. B. Could the dog have gotten the tapeworm from this louse? Click here for answer . 2. . Thorax with 3 pairs of legs 4. The body is longer than that of Phthirus pubis. .Card 8:29 Pediculus humanis head or body louse of humans .a sucking louse (Anoplura) Note: 1. Return to top of page Card 8:30 Review Question This louse was removed from a dog that had tapeworm segments in its feces. Head bearing antennae 3. Identify the louse (be specific as possible).

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Trichomonas muris Trypanosoma brucei Leishmania donovani Babesia canis Haemoproteus columbae Leucocytozoon smithi Eimeria spp. Entamoeba histolytica Giardia sp. Toxoplasma gondii Cryptosporidium parvum Review Question Return to top of page Card 10:1 .Laboratory 10 THE PROTOZOA Click on the text below to jump down to the desired section of this page. Isospora spp. Sarcocystis sp.

. spherical.trophozoite Note the single. In dogs the trophozoite is the diagnostic stage. but are almost never seen in infected dogs. vesicular nucleus (containing an endosome). .cysts Cysts measure about 10 to 12 um in length and each contains two to four nuclei. an axostyles and a median body. Return to top of page Card 10:2 Giardia .Entamoeba histolytica . Card 10:3 . The cyst is the diagnostic stage in monkeys and humans.

Giardia .) and there are 8 . Return to top of page Card 10:4 Trichomonas muris This flagellate is similar in appearance to T.trophozoites This trophozoite was found in the watery feces of an infected dog by a direct smear. foetus of cattle. . The internal organelles are doubled (i. 2 median bodies. etc. flagella. Note the undulating membrane and free flagella. Normally only cysts are found in the feces. two nuclei. Return to top of page Card 10:5 .e. and the size (10 to 18 um in length). Note the shape (pear shaped).

Trypansoma brucei Pathogenic trypanosome of domestic animals in tropical Africa. leaving behind nuclear material (green arrows). The spleen cells have ruptured during the making of the slide. . . Return to top of page Card 10:5a Leishmania donovani This slide is a tissue impression of the spleen (stained with Giemsa) of an infected dog. Return to top of page Card 10:6 . Note the nucleus and kinetoplast that are present in each amastigote. kinetoplast. Note the nucleus. The Leishmania amastigotes however are too small to be effected by the forces that ruptured the spleen cells so they remain intact (yellow arrows). undulating membrane and the free flagellum.

Remember that the schizonts are not found in the blood cells. Return to top of page Card 10:7 Haemoproteus columbae This blood smear shows a gametocyte which is wrapped around the nucleus of an erythrocyte (which is not distorted). . . Return to top of page Card 10:8 . They generally contain a vacuole and multiple infection of the erythrocytes is common. or amoeboid 2 to 4 um in diameter.Babesia canis The trophozoites are pyriform and 4 to 5 um long.

In this species the 2nd generation schizont is large and subepithial in position. tenella. Little evidence of the white blood cell morphology remains. Note the many merozoites within the mature schizonts. Note that no schizonts appear in the blood. . . . note that each contains 4 sporocysts each with 2 sporozoites.Leucocytozoon smithi . .gametocyte This slide shows a typical gametocyte which has distorted the white blood cell into an elongate. Return to top of page Card 10:9 Eimeria tenella These are sporulated oocysts. Card 10:10 Eimeria tenella This slide shows the 2nd generation schizonts E. elliptical body.

this is the micropyle. The small granules within the macrogametes are assumed to form the oocyst wall after fertilization has occured. Note the thinning of the wall (arrows) at one pole of the oocyst . . The top image shows the swollen. Diagnosis of coccidiosis in poultry is done by showing the presence of oocysts in the feces or other stages in the intestinal epithelium.This illustration shows the lesion site of E. The majority of these gametes are macrogametes (female). Species identification is made by determining the location and type of lesions in the intestine. Unporulated oocyst from the feces of a goat. tenella in the chicken . Card 10:11 Eimeria sp. . and the bottom illustration shows the location of the caeca in the intestinal tract.the ceca. thickened ceca found in an affected chicken. . This section shows the gametes in the epithelial cells. Return to top of page . Card 10:12 Eimeria sp. This is a cross section of the intestine of a goat infected with Eimeria sp.

about 20 µm). rivolta (cat). felis (cat) and the oocyst of I. This is a sporocyst recovered from the feces of a dog. A mature cyst in the muscle of the intermediate host. . canis (dog) looks like that of I. . . Return to top of page Card 10:13 Sarcocystis sp. unsporulated. Card 10:14 Sarcocystis sp. . about 40 µm) and a sporulated Isospora rivolta oocyst (red arrow.Card 10:12a Isospora felis oocyst (blue arrow. The oocyst of I. ohioensis (dog) is similar to that of I.

Oocysts sporulate within 48 hours after being passed from the cat. . Note the small size (9 to 14 um) and the round shape.Return to top of page Card 10:15 Toxoplasma gondii Sporulated and unsporulated oocyst. . Card 10:16 Toxoplasma gondii The tachyzoites are elongate and crescent-shaped. Card 10:17 Toxoplasma gondii Note that this cyst contains many bradyzoites. . They measure 4 to 6 um in length. .

Note the tachyzoites radiating from the center of the schizont. Return to top of page Card 10:19 Cryptosporidium parvum This is a fecal smear stained by the acid fast technique. The oocysts are acid-fast and therefore stain red.Card 10:18 Toxoplasma gondii Schizonts in the intestinal cells of a cat. . Yeasts (which are about the same size as the oocysts. . 5 um) stain a light blue or green (depending on the counter-stain used). Return to top of page Card 10:20 .

B. A. Identify the parasite (Genus only). The client's dog ate some of the kittens's feces just before this sample was collected from the litter box. . Is the stage seen on this slide (red arrow) infectious to dogs? Click here for answer .Review Question This slide shows the result of a zinc sulfate flotation of a fecal sample from an asymptomatic kitten. The object shown is 14 X 9 um.

The coccidia are 50 times as sensitive to this inhibition as is the host. SID for 5 days or 110 to 220 mg/kg SID for 7 to 12 days.Amprolium Chemical group: thiamine analog Trade names: Corid. Eimeria in cattle and poultry. Dose: In dogs and cats: "extra label use": 300 to 400 mg/kg. In chickens: For prevention of coccidiosis: 36. Amprol Mode of action: thiamine analog. .5 g/ton in the feed or in the drinking water at 0. Toxicity: May cause thiamine deficiency if given at high rates. Pharmacokinetics: Freely soluble in water.113. competitively inhibits the active transport of thiamine. Parasite Targets: Isospora in dogs and cats.012%.3 . No withdrawal is needed.

Butamisole hydrochloride Chemical group: Imidazothiazole Trade names: Styquin (no longer sold in the United States) Mode of action: Probably similar to other imidazothiazoles. Toxicity: Incoordination. Ancylostoma caninum . convulsions. LD50 in dogs is 11.25 mg/kg Parasite Targets: Trichuris vulpis.e. tremors. i. and death were seen in dogs given 3 to 4 times the recommended dose. emesis.4 mg/kg (SC) Use in dogs over 8 weeks of age.: Acetylcholine agonist and depolarizing neuromuscular blocking agent Pharmacokinetics: ? Dose: 2.

Dose: Dogs: T. binds to plasma proteins. 1997. (ME Fichera & DS Roos.: 25 mg/kg (PO) divided BID until cured or immunity develops. Dogs receiving 600 mg/kg/day developed anorexia and vomiting. It will pass in the milk. Babesiaspp. Cats: 25 mg/kg divided BID or TID for 28 days (PO) Toxicity: Dogs tolerated 300 mg/kg daily for up to a year. in protozoa it is linked to the loss of the 35 kb plastid DNA which is necessary for production of the vacuole in which the parasites lives.) Pharmacokinetics: Rapidly absorbed from the gut. Parasite Targets: Toxoplasma gondii. exits body in urine and bile (feces). A plastid organelle as a drug target in apicomplexan parasites.Clindamycin Chemical group: Trade name: Lincosamide antibiotic Antirobe Mode of action: Binds to ribosomes in bacteria. partially metabolized in the liver. . gondii: 10 to 40 mg/kg/day (PO) divided TID or QID. Babesia spp. Nature 389:407-409.

Dichlorvous Chemical group: Organophosphate Trade names: Task Mode of action: Cholinesterase inhibitor Pharmacokinetics: Rapidly metabolized and excreted.. Toxicity: Minimum toxic dose in horses and sheep is 25 mg/kg. the LD1 for formulated Dichlorvous is 182 mg/kg. . hookworms. Dose: 10 to 12 mg/kg (PO) Use in dogs and cats over 2 weeks of age and over 2 lbs. and Trichuris vulpis. LD50 in dogs is between 28 and 45 mg/kg for drug grade. Parasite Targets: Ascarids.

Toxicity: Shock-like reactions in dogs with circulating microfilaria. causes hyperpolarization of nerve membrane and flaccid paralysis of the nematode. Vomiting common when given on an empty stomach. Elimination is virtually complete by 48 hours. Dose: 11. Parasite Targets: Ascarids .4 to 22.7 mg/kg (25 to 50 mg/lb). LD50 in rodents is 660 mg/kg (mice) and 1380 mg/kg (rats). PO. worms are removed by normal peristalsis. Pharmacokinetics: Rapidly absorbed from the gut and excreted in the urine. Eliminated through the urine as metabolites.Diethylcarbamazine Chemical group: Piperazine Trade names: Nemacide Mode of action: GABA agonist.

has a half life in the dog of about 2 Pharmacokinetics: weeks.Disophenol Sodium Chemical group: Trade name: Mode of action: Substituted phenol DNP . and death are seen with overdoses. hyperventilation.no longer being sold in the United States Uncoupler of oxidative phosphorylation Binds to red blood cells. convulsions. Dose: 9 mg/kg (SC) in dogs and cats Toxicity: Narrow safety range. Parasite Targets: Hookworms. Spirocerca lupi . Blindness.

5 mg/kg (Use in dogs over 7 weeks of age) Toxicity: Minimum lethal dose in rats was greater than 5000 mg/kg. No adverse reactions seen in kittens given 29.Epsiprantel Chemical group: Trade name: Isoquinoline-pyrazine Cestex Mode of action: Unknown. Leaves host in feces as parent Cat: 2.9 mg/kg and none in puppies given 100 mg/kg. may interfere with calcium metabolism leading to detachment and disruption of the tegument. Dose: Poorly absorbed from gut.) Dog: 5. Parasite Targets: Tapeworms .75 mg/kg (Use in cats over 7 weeks of age. Pharmacokinetics: compound.

oxfendazole sulphone and at least 7 other metabolites.. hookworms. oxfendazole.000 mg/kg..Febantel Chemical group: Trade name: Mode of action: Pro-benzimidazole Drontal Plus* Binds to tubulin subunit and interferes with microtubule formation Pharmacokinetics: Metabolized in the liver to fenbendazole. Taenia sp. but most leave in the bile. These may circulate in the blood. Dose: 25 mg/kg (PO) (Drontal Plus) one dose (3 doses (SID) for Giardia). * also contains pyrantel pamoate and praziquantel . Oxfendazole is teratogenic in rats and sheep. Toxicity: Acute toxicity: LD50 in dogs is over 10. Giardia sp. Parasite Targets: Ascarids. Trichuris vulpis.

Capillaria sp. Paragonimus kellicotti. 250 mg/kg daily for 30 days was not toxic to dogs. hookworms. (PO) SID. and returns to gut in bile. . Totally eliminated in 48 hours. probably in liver. Aelurostrongylus abstrusus. most leaves the dog in the feces as fenbendazole. some is metabolized to oxfendazole.. Parasite Targets: Ascarids. Trichuris vulpis. Toxicity: Toxic dose not found.Fenbendazole Chemical group: Trade names: Mode of action: benzimidazole Panacur Binds to tubulin subunit and interferes with microtubule formation.. Taenia sp.. Giardia sp. Dose: 50 mg/kg. 500 mg/kg not toxic in a single dose. Pharmacokinetics: Poorly absorbed from the gut. Filaroides sp. For Giardia use for 5 days. Strongyloides sp. Use in dogs and cats (use in cats is prohibited in some countries like the US) over 2 weeks of age.. for 3 days.

2 weeks apart.9 mg/kg. .6 mg/kg.) Dose: 6. Parasite Targets: Babesia spp. Causes pain upon injection.Imidocarb dipropionate Chemical group: N. Acute toxicity symptoms are consistent with a cholinesterase inhibitor activity. Residues were found mainly in the liver and some in the kidney (it seems to be eliminated through the urine and feces. Safe in dogs up to 9.N'-bis (3-(4. Toxicity: LD50 in rats was 450 .5-Dihydro-1H-imidazol-2-yl)phenyl) urea Trade names: IMIZOL Mode of action: May interfere with polyamine synthesis and function. IM or subcutaneous injection. Pharmacokinetics: In dogs given an intravenous bolus. 2 doses. the plasma half-life was 207 min and 80% was eliminated in 8 hours.1200 mg/kg.

4 mg/kg (PO [SQ in cats]). repeat as needed. Pigs: 10mg /75 lb body wt. Heartgard for Mode of action: Binds to glutamate gated chloride channels in the parasites’ nervous system. Australian sheepdogs and some collie mixes: toxic signs (lethargy. Iverheart Plus. Ivomec. coma) appear above 0. less rapidly from a subcutaneous site. etc. For other nematodes and for mites: 0.006 mg/kg (PO). Half life in dogs is about 24 to 36 hours.024 mg/kg (PO) given monthly. Higher doses not recommended for puppies. in puppies 6 weeks of age and older. causing them to open. Heartgard Plus also contains Pyrantel Pamoate 2. Toxicity: In collies. toxic signs are seen at doses at and above 0. Leaves the body in the feces as ivermectin. In other dogs.8 mg/kg. given monthly.Ivermectin Chemical group: Trade names: Cats.2 to 0. Avermectin. 1. Heartgard Plus*. Heartworm L4. (Cats probably about the same as dogs). pig and cattle preparations to dogs or cats may cause local problems due to the vehicle. Prolonged monthly use may shorten the life span of the adult heartworm. ataxia. most nematodes (except adult heartworms2). Cats: 0. Pharmacokinetics: Rapidly absorbed from the gut. . Parasite Targets: and mites.1 mg/kg. (Macrocyclic Lactone) Heartgard 30. Subcutaneous administration of horse. Dose: For heartworm prevention: Dogs: 0.

Trichuris vulpis. Pharmacokinetics: Poorly absorbed. thus action limited to gut. (Stomach worm in dogs). Taenia sp. Toxicity: Acute toxic dose not found (above 1000 mg/kg in dogs and cats). . Dose: 22 mg/kg (PO). for 3 days. SID.. Echinococcus granulosus. Parasite Targets: Hookworms. Ascarids.Mebendazole Chemical group: benzimidazole Trade name: Telmintic Powder Mode of action: Binds to tubulin and interferes with microtubule formation. Physaloptera sp.

24 hours apart.) Toxicity: LD50 in rats (IM) was 24 to 33 mg/kg. The drug is rapidly cleared from the body. Dose: 2.Melarsomine dihydrochloride Chemical group: arsenical Trade name: Immiticide Mode of action: Unknown. 2002. Wildl. vomiting and anorexia.5 mg/kg (IM) twice. J. presumably due to the arsenic’s effect on glycolysis. (A 10% death rate can be expected in dogs with class 3 disease when 2 doses are given initially.5 mg/kg and 2. et al. Injection site reactions are common.5 mg/kg.7 mg/kg were fatal to Heartworm infected river otters (Lontra canadensis) and red pandas (Ailurus fulgens fulgens) [Neiffer. Med 33(3)242-248]. some metabolites and the parent compound are eliminated in the bile and other metabolites are passed in the urine. Pharmacokinetics: Absorbed very rapidly from the injections site. Zoo. as are lethargy. (Dogs with class 3 disease should receive one dose and allowed to recover for a few months before receiving the complete set of 2 doses.) Doses between 2. Parasite Targets: Heartworm adults . some mortality seen in dogs given 7..

. ataxia. for 5 days (PO) Toxicity: Dog can tolerate doses of 100 mg/kg per day for a month. Higher doses produce neurological signs (tremors. most is excreted in the urine.) Parasite Targets: Giardia spp. Some returns to the gut in the bile and through the colon. SID. Pharmacokinetics: Rapidly and completely absorbed from gut. . Will pass in the milk. etc.Metronidazole Chemical group: 5-nitroimidazole Trade name: Flagyl Mode of action: Reduced in anaerobic organisms to reactive metabolites which release superoxide anions. Dose: 30 mg/kg. Trichomonas spp.

Cleared from blood by 120 hours. Dose: 0.5 mg/kg (PO). Sentinel* Mode of action: Opens chloride channels in the nerve cells. most nematodes (except adult heartworm and Uncinaria stenocephala). Pharmacokinetics: Rapidly absorbed from the gut. Use in dogs over 4 weeks of age (Interceptor). some mites. Toxicity: Toxic dose is above 10 mg/kg.Milbemycin Oxime Chemical group: Macrocyclic lactone Trade names: Interceptor. Parasite Targets: Heartworm L4. * Sentinel contains Milbemycin and Lufenuron .

ProHeart6 will kill hookworms for up to 2 weeks after it is injected. ProHeart6: 0.17mg/kg. causing paralysis. salivation and mild depression were seen. [microspheres] once every 6 months (SQ) For use in dogs over 6 months of age. Toxicity: Dog: Safe at up to 5 to 10 times the recommended dose. once a month. For use in dogs over 8 weeks of age.Moxidectin Chemical group: Macrocyclic lactone Trade name: ProHeart. ProHeart6 Mode of action: Probably works like other macrocyclic lactones and opens chloride channels in the nerve cells. ataxia. Pharmacokinetics: Dog: ProHeart6: Peak blood levels by 7 to 14 days post-injection. Parasite Targets: Dirofilaria immitis L3 and young L4. in a collie given 30 times the recommended dose. (PO). by 6 months post-injection little drug remains in the dog. Dose: Dog: ProHeart: 3 µg/kg. .

Nitazoxanide Chemical group: benzamide Trade names: Navigator (Idexx Pharmaceuticals. It is important to monitor the horse for adverse signs during the course of treatment. (The above information came from the Navigator® package insert) . Toxicity: A single dose at 5X the regular dose lead to transient depressed appetite.36 mg/lb once a day on days 1 to 5. The drug can disrupt the normal microbial flora of the GI tract leading to enterocolitis even at the normal dose. Parasite Targets: Sarcocystis neurona in horses.72mg/lb dose: Cmax = 0.) Mode of action: Target organisms are able to reduce nitazoxanide’s nitro group to a toxic free radical which interferes with cellular respiration. Multiple (4) 5X doses lead to the death of 5 of 8 horses.72 mg/lb once a day on days 6 to 28. Inc. loose stools and lethargy for 11 to 14 days post treatment. Pharmacokinetics: Given a single 22. then 22.13 hr. Dose: 11. The active metabolite (deacetynitazoxanide) is undetectable in plasma by 24 hrs post dosing. Tmax = 2.51 ppm.

therefore not safe to use in microfilaria positive dogs. Parasite Targets: Toxocara spp. Use in animals over 6 weeks of age. Toxascaris leonina . Elimination is virtually complete by 24 hours. WRM Rid. Signs: Depression. Toxicity: Acute oral: About 800 mg/kg. actual dose varies with the salt. Mode of action: GABA agonist. Pharmacokinetics: Rapidly absorbed from the gut and excreted in the urine. causes hyperpolarization of nerve membrane and flaccid paralysis of the nematode. Will kill microfilaria.. Tasty Paste. worms are removed by normal peristalsis.Piperazine Chemical group: Piperazine Trade names: Pipa-tabs. etc. (100 mg/kg of piperazine adipate) (PO). Dose: About 60 mg/kg of piperazine base. Side effects apparently common in cats and dogs. hind leg weakness or incoordination.

T. 1977. Sakamoto. Drontal Plus2 Mode of action: Modulates cell membrane permeability (calcium dependent). Veterinary Medical Review. Drontal1. Journal of the American Veterinary Medical Association. metabolites and unchanged parent compound pass out in the feces. 1. 4 Toxicity: LD50 in rats is between 2000 and 3000 mg/kg. 4.Praziquantel Chemical group: Acylated quinoline-pyrazine Trade names: Droncit. 1:64-74. Pyrantel Pamoate and Febantel. 1985. metabolized in the liver. No clinical effects seen in dogs or cats dosed with 100 mg/kg. Kirkpatrick and Shelly. . Drontal contains Praziquantel and Pyrantel Pamoate. 3. TID for 2 days. Pharmacokinetics: Rapidly absorbed from the gut. Parasite Targets: Tapeworms and trematodes. Drontal Plus contains Praziquantel. Tape Worm Tabs. Dose: Cyclophyllidean Tapeworms: 3 to 5 mg/kg (PO or SC) Pseudopyllidean Tapeworms: 35 mg/kg (SC)3 Intestinal Trematodes: 30 mg/kg (PO) Lung flukes in dogs: 25 mg/kg. 187(1):75-6. leads to a disintegration of the tapeworm’s tegument. 2.

Heartgard Plus3. Drontal contains Pyrantel and Praziquantel 2. Sure Shot. Pyratabs. It produces rigid contraction of the muscles.6 mg/kg produced vomiting and diarrhea in 2/92 cats. although dogs given 50 mg/kg for the same length of time did have signs of toxicity.Pyrantel Pamoate. Parasite Targets: hookworms. Most of the pamoate/embonate salts remains in the gut and will pass in the feces. It appears to act on the nerve ganglia and nematode muscle cell membranes. Drontal1. ascarids. Strongid T. a single dose of 230. Drontal Plus2. etc. the rest passes in the feces unchanged. Mode of action: Acetylcholine agonist and depolarizing neuromuscular blocking agent. Dose: 5 mg/kg (PO) Use in animals over 2 weeks of age. (Stomach worm in cats and dogs) 1. Heartgard Plus contains Ivermectin and Pyrantel . D-Worm. Pharmacokinetics: 40% of soluble salts (pyrantel citrate) passes in urine as metabolites. Dogs: Acute LD50 dose is over 690 mg/kg. Febantel and Praziquantel 3. Physaloptera sp. Toxicity: Cats: 100 mg/kg daily for 3 days produced no side effects. dogs given 20 mg/kg daily for 3 months had no problems. Pyrantel embonate Chemical group: Imidazothiazole Trade names: Nemex II. Drontal Plus contains Pyrantel. Evict Liquid wormer.

Parasitol. 91:393-403. (See: Novotny.4. Active concentrations are found in the plasma for at least 30 days. fleas. 2000. Toxicity: Cats: 60 mg/kg (10 X dose) produced no adverse reactions when given to kittens (initially 6 wks old) for 7 monthly treatments. Safety of Selamectin in Cats. Parasitol. Humans: Has a 279 fold safety range. et al.) Dogs: 60 mg/kg (10 X dose) produced no adverse reactions when give to puppies (initially 6 wks old) for 7 monthly treatments. Parasite Targets: hookworms. heartworm L3. Pharmacokinetics: Absorbed through the skin and distributed via the blood. ticks. Safety of Selamectin in Dogs. Otodectes . 18 mg/kg (3 X dose) produced no effect on reproduction in females or males and no problems in heartworm positive dogs (but it did reduce the levels of microfilaria to nil by the 3 rd monthly treatment).Selamectin Chemical group: Macrocyclic lactone Trade name: Revolution Mode of action: Binds to glutamate gated chloride channels in the parasites’ nervous system. causing them to open. ascarids. Vet. 18 mg/kg (3 X dose) produced no effect on reproduction in females or males and no problems in heartworm positive cats. Dose: 6 mg/kg (topical) Use in animals over 6 weeks of age. scabies. MJ. 2000. 3 monthly doses of 30 mg/kg produced no adverse effects in avermectin sensitive collies. 91:377-391). Vet. and a small amount in the urine. Orally a 6 mg/kg dose caused 2 of 6 cats to vomit (probably due to the alcohol carrier). et al. Concentrates in sebaceous glands. MJ. Most excreted unmetabolized in the feces. (See: Krautmann.

then 27. SID for 10 to 14 days (PO) Toxicity: low Parasite Targets : Isospora spp. . Dose: 55 mg/kg the first day. coccidiastatic. eliminated in the urine (dog) or metabolized in the liver and excreted as acetylsulfadimethoxine in the bile (cat and other species). Bactrovet Mode of action: Folic acid synthesis inhibitor. Pharmacokinetics: Readily absorbed from the gut.5 mg/kg.Sulfadimethoxine Chemical group: Sulfonamide Trade names: Albon.

presumably due to the arsenic’s effect on glycolysis. Toxicity: 3.7 mg/kg daily for 3 days produced serious side-effects in 1/3 of the dogs tested.2 mg/kg BID for two days (IV). Side-effects at the standard dose increase with the clinical severity of the heartworm disease. . it is metabolized by the liver. Parasite Targets: Dirofilaria immitis adults. Dose: 2. Pharmacokinetics: Elimination half life in dogs is about 46 min.Thiacetarsamide sodium Chemical group: Arsenical Trade names: Carparsolate Sodium .no longer sold in the United States Mode of action: Unknown.

Diagnosis of Veterinary Endoparasitic Infections || Root || Main || Cat Homepage List of feline endoparasites Feline parasitology Quiz Image library of feline parasite diagnostic stages (Felis catus) Class : Mammalia Order : Carnivora Family: Felidae Genus: Felis Species: catus .

Diagnosis Quiz Choose a case a below to test your knowledge Quiz Case 1 Quiz Case 2 Quiz Case 3 Quiz Case 4 Quiz Case 5 Egg Quiz .

Dog Homepage Here is a comprehensive list of canine endoparasites Try the Quiz below on this page Go to an image library of canine parasite diagnostic stages Dog (Canis familiaris) Class : Mammalia Order : Carnivora Family: Canidae Genus: Canis Species: familiaris .

Diagnosis Quiz Choose a case a below to test your knowledge Quiz Case 1 Quiz Case 2 Quiz Case 3 Quiz Case 4 Quiz on Eggs. larvae and cysts .

Cow Homepage (Bos taurus) Class : Mammalia Order : Artiodactyla Family: Bovidae Genus: Bos Species: taurus .

Ferret Homepage (Mustella putorius furo) Click here for a list of Class : Mammalia Order : Carnivora Family: Mustelidae Genus: Mustella Species: putorius Subspecies: furo .

Goat Homepage (Capra hircus) Class : Mammalia Order : Artiodactyla Family: Bovidae Genus: Capra Species: hircus .

Sheep Homepage (Ovis aries) Sheep and Goat share almost the same parasite classes to view their parasites click here Class : Mammalia Order : Artiodactyla Family: Bovidae Genus: Ovis Species: aries .

Horse Homepage (Equus caballus) Class : Mammalia Order : Perissodactyla Family: Equidae Genus: Equus Species: caballus Horse parasite list .

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Llama Homepage (Lama glama) Class : Mammalia Order : Artiodactyla Family: Camelidae Genus: Lama Species: glama .

Pig Homepage (Sus scrofa) Class : Mammalia Order :Artiodactyla Family: Suidae Genus: Sus Species: scrofa .

Rabbit Homepage (Oryctolagus cuniculus) Class : Mammalia Order : Lagomorpha Family: Leporidae Genus: Oryctolagus Species: cuniculus .

Robin Homepage (Turdus migratorius) Class : Aves Order : Passeriformes Family: Turdidae Genus: Turdus Species: migratorius .

Loggerhead Turtle (Caretta caretta) Parasite List Sulcascaris sulcata (Ascarid) Ozobranchus margoi (leech) .

Fecal Examination Using "Ovatector" brand Fecal Float .

Fecal Examination Using "Ovassay Plus" brand Fecal Float .

Fecal Examination Using "Fecalyzer" brand Fecal Float .

Also note the thin feathered edge that is left at the far end of the smear.You will need Quick Time® in order to view this video. The video will loop until you hit the Blood Smear Instructions button to return to the Blood Smear Page. . Note that the spreader slide is pulled up against the small drop of blood and then quickly pushed to the other end of the slide pulling the blood behind it.

Ancylostoma caninum .

Dictyocaulus viviparus (Directions for Use) .

Dirofilaria immitis .

Echinococcus granulosus (Directions for Use) .

Eimeria bovis (Directions for Use)

Giardia (Directions for Use)

Haemonchus contortus (Directions for Use)

Toxocara canis (Directions for Use)

Introduction to Parasitology
Key definitions
1. Veterinary Parasitology Veterinary Parasitology is the science that deals with the parasites of domestic animals. More specifically, it is the science that deals with the interactions between a host and the population of parasites that are found on or in that host. A more encompassing point of view, from an epidemiological perspective, would define Veterinary Parasitology as the science that deals with the interactions between host populations and the parasites that infect them. This broad definition means that Veterinary Parasitology covers many aspects of parasites of domestic animals and their hosts including: the morphology, biochemistry, physiology and life cycles of parasites, the immunological, pathological and clinical responses of the host to the presence of parasites, all aspects of treatment and control of parasitic infections and diseases and the public health aspects of parasites of domestic animals that may also infect humans. 2. Parasitism The term parasitism may be defined as a two-species association in which one species, the parasite, lives on or in a second species, the host, for a significant period of its life and obtains nourishment from it. This is a commonly accepted working definition of parasitism and using it we can emphasize several important features of the host-parasite relationship. a. Parasitism always involves two species, the parasite and the host. b. Many of these parasitic associations produce pathological changes in hosts that may result in disease. c. Successful treatment and control of parasitic diseases requires not only comprehensive information about the parasite itself but also a good understanding of the nature of parasites' interactions with their hosts. d. The parasite is always the beneficiary and the host is always the provider in any host-parasite relationship. This definition of parasitism is a general one but it tells us nothing about parasites themselves. It does not address which particular infectious organisms of domestic animals we might include in the realm of parasitology. The protozoa, arthropods and helminths are traditionally defined as parasites. However, there are members of the scientific community who designate all infectious agents of animals as parasites including viruses, bacteria and fungi. This broader definition of parasites includes viruses, bacteria and fungi as well as the arthropods, helminths and protozoa. Within this broad definition, parasites are further divided into microparasites and macroparasites. The following table summarizes their salient characteristics.

Microparasites

Macroparasites

Bacteria, Viruses, Fungi, Protozoa Unicellular or acellular organisms Usually multiply in the host so that a few infecting organisms may give rise to many in a non-immune host. Short generation time - hours or days Acute infections most commonly seen. Infected animals may succumb, may recover and show significant protective immunity or the infection may, in some cases revert to a chronic state

Arthropods, Helmi Multicellular organisms Rarely multiply in a host

Long generation time - usually w months

Chronic infections are most com acute infections may be seen in susceptible animals. Recovery infections does not necessarily protection on the host.

However, the consensus among parasitologists is to view the subjects of the discipline as including only the arthropods, helminths and protozoa.

Introduction to Parasitology
The Spectrum of Parasitism
Parasites are an extremely varied group. They range from flies, such as the blood-sucking mosquitoes, nematodes such as the heartworm of dogs, liver flukes of cattle and sheep, fleas commonly found on dogs and cats, lice and ticks found on almost all domestic animals and protozoa such as Giardia which are found in most domestic animals but are of particular significance in cattle and dogs. The table below illustrates some of these parasites.

A female mosquito blood feeding. Mosquitoes serve as intermediate hosts of other parasites such as Dirofilaria immitis the dog and cat heartworm and Plasmodium species causing malaria in humans and birds. They are also vectors of viruses causing yellow fever and encephalitis.

A cluster of nematodes, the roundworm of dogs, Toxoca This parasite is common in puppies and may be transmi transplacentally as well as to nursing pups in their mothe This parasite has public health importance as a cause of larva migrans in man.

Fleas are common parasites of dogs and cats. They bite their hosts and feed on blood. Fleas are intermediate hosts of the tapeworm Dipylidium caninum and the filarid nematode Dipetalonema reconditum. The cat flea is a vector of feline parvovirus.

Fasciola hepatica, the liver fluke of ruminants. The para complex life cycle involving snail intermediate hosts. Mig developing flukes in the host liver provokes an intense in reaction with severe liver damage.

Hematopinus suis, the blood-sucking louse of swine is common in pigs raised indoors with transmission readily occurring from pig to pig. Infested pigs are restless and rub their skin frequently to relieve the itching.

Anoplocephala perfoliata, a tapeworm of horses, is oft clusters at the ileo-cecal junction. It is widespread in dist usually benign. However, cecal abscesses, and intussus have been reported.

The nematode Dirofilaria immitis, the heartworm has a complex life cycle involving mosquitoes as intermediate hosts. These worms are found in the cardio-pulmonary circulation and may cause severe heart disease in dogs and cats.

The protozoan Giardia is important as a cause of diarrh and cattle but is also found in other domestic animals as The trophozoite stage, shown here, attaches to the muco epithelium cells of the small intestine.

An important feature to note about parasites is that they are not equally parasitic. Parasitism is seen as a spectrum. It includes organisms at one of the spectrum that spend most or all of their lives as independent free-living creatures, seeking a host only to feed. The other end of the spectrum includes parasites that spend their entire lives in or on a host and cannot survive at any stage of their life cycles without a host. Between these two extremes we see a whole host of parasitic configurations with differing degrees of host dependency.
At one end of the spectrum, we see flies such as mosquitoes which are the least parasitic and visit their hosts only to feed. Fleas are slightly more parasitic in that they feed and often lay eggs on the host. Coccidial protozoans are even more parasitic with all the life cycle stages except two occurring inside a host. Ascaris suum, a nematode of pigs has two well defined phases to its life cycle - a parasitic phase in the swine host and a preparasitic phase consisting of three stages found free-living in the external environment. At the other

end of the spectrum, we find the lice which spend their entire lives on the hair or feathers of their hosts. Off the host they will surviv most one or two days. Dirofilaria immitis, the dog heartworm is entirely parasitic with all stages of the life cycle occurring either in th mosquito intermediate host.

Introduction to Parasitology
Parasite Life Cycles
Despite their diversity, parasites do have some common features: all of them have unique life cycles and each major parasite group (arthropods, nematodes, cestodes, trematodes and protozoa) includes a set of well-defined and recognizable stages unique to each group. The multicellular nematodes, for example, have life cycles which include adult males and females. They reproduce sexually and eggs are laid by the female. Larvae develop, in these eggs, hatch and progress through a series of developing larval stages until they reach adulthood as sexually mature males and females and the cycle begins again. Most nematodes follow this basic life cycle pattern, although some may also include variations and additional complexities. Click here to view the life cycle of the small strongyles of horses, an uncomplicated cycle. Remember to use the back button of your browser to return to this page. Click here to view the life cycle of Dirofilaria immitis, the heartworm of dogs. This pattern is complicated by the inclusion of required intermediate hosts, mosquitos. Use the back button of your browser to return directly to this page. The protozoa are unicellular organisms. Most of them have a phase of sexual reproduction in their life cycles and also include an asexual reproductive phase. They lack recognizable male and female adult stages as we see in the nematodes but they do have male and female stages that are analogous to eggs and sperm. For example, the coccidia have the following stages in their life cycles: oocysts, sporozoites, schizonts, merozoites, microgamets, macrogametes, zygotes. In a simple coccidian life cycle, a host is infecte by an oocyst containgin sporozoites which leave the oocyst and infect host cells. Asexual multiplication occurs resulting in an intracellular schizont containing many merozoites. Asexual reproduction (schizogony) may be repeated several times and ends with the beginning of sexual reproduction. Merozoites transform into micro or macro gametocytes. Macrogametocytes are female and grow to occupy a single host cell when they are usually called macrogametes. Microgametocytes are male and divide to produce microgametes which leave the host cell in search of a macrogamete. The latter is penetrated by a microgamete, fusion of their nuclei occurs and a zygote is formed. A cyst wall is formed around the zygote resulting in an oocyst which sporulates, forming sporozoites. This sporulated occyst is the infective form for the host. Click here to view the life cycle of Eimeria bovis, a coccidian of cattle. (Use the back button of your browser to return to this page). The arthropods have different life cycles but like the others they also have distinct and recognizable life cycle stages.

A female louse lays eggs which attach to the hair or feathers of a host A miniature adult called a nymph hatches from each egg and grows to an adult. The whole life cycle takes approximately one month.

Fleas are also arthropods and although they have distinct life cycle stages they are different to those of their lice cousins. Female fleas lay eggs from which larvae hatch. Each larva metamorphoses first into a pupa which in turn transforms into an adult.

Introduction to Parasitology
The Importance of Life Cycles
Life cycles of parasites may provide two important pieces of information. 1. Information that has predictive value with respect to the pathogenic importance of each particular parasite. 2. Information of epidemiological significance that is indispensable to developing effective control programs.

Pathogenesis If we know the migration patterns of a parasite's life cycle in its host, this information can be used to predict the parasite's involvement in disease. For example by knowing the migratory pathways of Ascaris suum in pigs we can predict where the significant pathological changes will occur. Ascaris suum larvae migrate from the small intestine (F) to the liver (G) via the hepatic portal vein and then to the lungs (H) via the heart. Knowing this, we can predict that important pathological changes will be found in the liver and lungs. Migrating larvae in the liver cause an inflammatory reaction, intralobular tissue destruction and hemorrhage. This is followed by an intense infiltration of eosinophils and collagen production. These lesions are visible at necropsy on liver surfaces as whitish areas and are commonly called "milk spots" since they resemble splashes of milk. Migration of larvae in the lungs also produces hemorrhagic lesions and intense infiltrations of eosinophils around alveoli into which larvae are migrating on their way up the bronchial tree. Repeated infections will produce more widespread hemorrhages, edema and emphysema. The image to the right shows significant hemorrhagic lesions in the apical and cardiac lobes of Ascaris- infected lungs.

Introduction to Parasitology
The Importance of Life Cycles
Life cycles of parasites may provide two important pieces of information. 1. Information that has predictive value with respect to the pathogenic importance of each particular parasite. 2. Information of epidemiological significance that is indispensable to developing effective control programs.

Epidemiology
We can make generalizations about the epidemiology and control of many parasites from information about their life cycles, in particular the requirements for transmission. For example the strongyles of horses are transmitted directly by ingestion of infective third stage larvae from pasture while horses are grazing. The survival of these infective larvae as well as their development for eggs is controlled primarily by temperature combined with humidity. This is true, not only of the horse strongyles, but also of all nematodes with direct life cycles.

Below 8'C, horse strongyle eggs will not hatch and above 38'C, they die. The image to the right shows that between these two extremes, the proportion of eggs developing through to third stage infective larvae is directly dependent on temperature with the maximum number of L3s developing at 26'C. Not only is 26'C the temperature at which the maximum number of L3s will develop from eggs but it is also the temperature at which eggs will develop to L3s in the shortest possible time. In the case of horse strongyles this will be approximately 72 hours. % of infective stage larvae developing from viable eggs at various temperatures

As a result of this influence of temperature and moisture on the survival and development of preparasitic life cycle stages, the strongyles of horses show seasonal patterns of development in temperate areas of the world with distinct seasonal changes in weather. These effects are shown in this graph of seasonal changes in strongyle eggs in the feces of grazing horses This graph shows that maximum transmission of horse strongyles occurs in spring, summer and early fall(autumn) when temperatures are optimum for rapid development of infective L3s from strongyle eggs passed in horse feces. In winter minimum development occurs and the majority of eggs and larvae will not survive. The great majority (95%) of eggs passed are from the cyathostomes with only a small small contribution from the large strongyles such as Strongylus vulgaris. This reflects the number of cyathostomes (tens of thousands) present compared with the large strongyles (hundreds) in naturally infected horses. These cyclical patterns occur regularly from year to year, from grazing season to grazing season and are predictable because of the effects of temperature and moisture on the life cycles of these nematodes. Their predictability is valuable because it allows us to focus control programs at strategic times of the year with the maximum possible benefits.

Introduction to Parasitology
Information from Life Cycles
The key to understanding Parasitology lies in a thorough knowledge of the life cycles whether the parasites are nematodes, cestodes, trematodes, arthropods or protozoa. However, these life cycles are extremely varied, ranging from the simple to the very complex. Learning them can be daunting to many veterinary students but it helps to distill them down to a few common questions as listed below. 1. How does an animal host acquire a parasitic infection? For example, does the host become infected by direct ingestion of an infective stage, by ingestion of an intermediate host or transport host containing infective stages, by skin penetration of an infective stage, by direct contact with an infected host, or via the bite of an intermediate host serving as a vector. An important question in the case of many parasites is whether the host can be infected by transmission from mother to fetus across the placenta or to nursing offspring via colostrum or milk. 2. The second question asks what the predilection site of the parasite is in its definitive host. The predilection site is the place in the host where adult males and females are found. In those parasites without recognizable male and female forms, it's the site(s) where sexual and/or asexual reproduction occurs. 3. A related third question asks how the parasite reaches the predilections site since this may involve extensive migration through the body of a host. 4. The fourth questions asks how a parasite leaves its definitive host to return either to the environment or to its intermediate host. 5. The fifth and final question asks for the identity two life cycle stages; the (infective) stage entering the host and the stage leaving the host. The latter is often called the diagnostic stage if it is valuable in diagnosing parasitic infections. The following tables answer these questions for eight different parasites across the spectrum of Parasitology. Table 1 - Toxocara canis, Dirofilaria immitis, Fasciola hepatica, Haemonchus contortus Table 2 - Dipylidium caninum, Isospora suis, Hematopinus suis, Babesia species If you go to these tables, please use the back button on your browser to return to this page.

Introduction to Parasitology
Summary of important information about specific life cycles

Table 1

Toxocara canis

Dirofilaria immitis

Fasciola hepatica

Haemonchus contortus

Route(s) of 1. Ingestion of entry to the infective eggs 2. Ingestion of host mouse hosts (paratenic) 3. Transplacental migration of L2s to fetal liver 4. Transmammary transmission of L3s to nursing pups Predilection Small intestine site

1. Injection of 1. Ingestion of 1. Ingestion L3s by metacercariae of infective blood-feeding larvae female mosquitos (intermediate hosts)

Right Bile ducts of ventricle and the liver pulmonary arteries Migration through the body and vascular system Migration from the small intestine across the peritoneal cavity to the liver

Abomasum

Route to the predilection site

Direct development in the small intestine after ingestion of paratenic hosts and L3s from the mammary gland. Otherwise by tracheal migration. In the feces of the host

Direct development in the abomasum after ingestion

Route of exit from the host

In the blood meal taken by a mosquito feeding on the host. L3

In the feces of In the feces the host of the host

Life cycle stage(s) entering the host

Egg, L2 or L3 depending on the route of transmission

Encysted metacercaria

Ensheathed L3

Stage Egg leaving the host (diagnostic stage)

Microfilaria

Egg

Egg

Introduction to Parasitology
Summary of important information about specific life cycles

Table 2

Dipylidium caninum - dog & cat tapeworm

Eimeria bovis - coccidian of cattle

Hematopinus Babesis canis suis - dogs - pig louse 1. Injection of sporozoites by feeding female ticks (Rhipicephalus)

Route(s) of 1. Ingestion 1. Ingestion Direct contact of sporulated with an entry to the of intermediate oocysts infested host host hosts (fleas and lice) containing cysticercoids. Predilection Small intestine site in the definitive host Small Skin and hair intestine coat (Asexual reproduction) Large intestine (sexual reproduction) Direct development in the intestine None -all life cycle stages occur on the host

Red cells (asexual reproduction)

Route to the predilection site

Direct development in the small intestine after ingestion of intermediate hosts. In the feces of the host

Invasion of red cells by sporozoites

Route of exit from the host

In the feces of the host

None - all life cycle stages occur on the host. Adults and nymphs move to another host via direct contact All stages except eggs

Infected red cells are ingested by feeding ticks

Stage Cysticercoid entering the host (infective stage)

Sporulated oocyst

Sporozoites

Stage Egg leaving the host (diagnostic stage)

oocyst

All stages except eggs

Trophozoite in host red blood cells

Introduction to Parasitology
Infection and disease
The terms infection and disease are not synonymous. While an animal must be infected with a parasite to produce disease it does not necessarily follow that all infected animals will show clinical signs of disease. When susceptible animals are infected with viruses, bacteria and protozoa, the host's lack of immunity usually results in clinically obvious disease. The outcome of these infections will depend on an interaction of factors including the virulence of the organism and how rapidly and successfully the host can mount an effective immune response. Protozoa are unique among the parasites in that they multiply rapidly in their hosts such that they may overwhelm them. This is particularly true of susceptible animals such as the young or older animals whose immune system has been compromised in some way. For example in congenital infections with Toxoplasma and Neospora, the disease is usually more severe because the fetus lacks a fully developed immune system and the outcome is likely to be fetal death. In cats receiving kidney transplants their immune system will be compromised because they are being treated with immunosuppresive drugs like corticosteroids. These cats are at high risk for being overwhelmed by acute Toxoplasmosis, an infection that has lain dormant in these transplant recipients and kept in check by cell mediated immunity. Suppression of cmi by immunosuppressive drugs allows these dormant organisms to begin mutiplying again producing acute infections that may be severe enough to overwhelm transplant recipients causing their death. This example illustrates another possible outcome to parasitic diseases namely that the immune response allows a host to successfully overcome acute clinical disease but the infection is either not totally cleared or the animal remains susceptible to low level infections. In both cases, the animal may harbor chronic subclinical infections throughout its life. Subsequent events during its lifetime may compromise the immune response and allow these chronic infections to flare up as potentially life-threatening acute diseases or make the anima, once more, susceptible to a new infection with a parasite. Parturition and lactation are events that, in some cases, appear to make animals more susceptible to parasite infections probably resulting from compromise of the immune response. For example, it is well established that parturient and lactating ewes are more susceptible to infections with Haemonchus contortus and post- partum dairy cattle are more susceptible to coccidial infections. Nematodes are more complicated than protozoa partly because they do not multiply inside their hosts. One nematode egg can only produce one infective larvae that develops into one adult worm. Therefore the development of clinical disease in hosts infected with nematodes depends almost entirely on the actual number of larvae infecting a susceptible host. I other words, the outcome of nematode infections is generally more dependent on the parasite burden and that is, in turn, directly related to the infecting dose. Generally speaking there is a direct correlation between the number of infecting larvae and the severity of any disease produced; a small number of infective larvae will produce minor pathological changes and generally no obvious clinical disease. It will often take many larvae (thousands or even tens of thousands) to incite pathological changes severe enough to produce serious clinical signs. For example, a foal infected with 100 Parascaris equorum will show either no clinical signs or at worst some coughing and minor nasal discharge. Conversely, a foal infected with 5,000 P. equorum will show severe clinical signs and may succumb to the infection. However, like all general rules there are often exceptions. Within the nematodes there are some whose anatomical locations, in a host, are such that even a small number of nematodes will incite pathological changes that can have devastating consequences for

a host. One example is Strongylus vulgaris in horses. Migration of even a few larvae in the mesenteric arterial tree can produce pathological changes (thrombi and emboli) severe enough to block blood supply to significant portions of the large intestine. The outcome is often acute colic that may be fatal. These changes are shown in the images below.

Images illustrating the pathogenesis of Strongylus vulgaris infections in horses

The celiac axis and its branches and the cranial mesenteric artery and its branches showing thrombosis and thickening of arterial walls due to Strongylus vulgaris larval migrations. Image courtesy of Dr. Owen Slocombe and Merial Inc.

Necrosis of the cecum and ventral colon of a horse resulting from ischemis and infarctions due to lesions produced by migrating larvae of Strongylus vulgaris. Image courtesy of Dr. Harold Drudge and Hoechst-Roussel

The dorsal aorta of a horse showing fibrin tracks due to migrations of Strongylus vulgaris larvae beyond the root of the cranial mesenteric artery. Image courtesy of Merial Inc.

Arteriographic picture of the abdomen of a foal 30 days after infection with 50 third stage larvae of Strongylus vulgaris. Image courtesy of Dr Jay Georgi. The mesenteric artery and its branches show minor changes

Arteriographic picture of the abdomen of a foal 60 days after infection with 50 third stage larvae of Strongylus vulgaris. Image courtesy of Dr Jay Georgi. The mesenteric artery and its branches show extensive changes.

Arteriographic picture of the abdomen of a foal 60 days after infection with 50 third stage larvae of Strongylus vulgaris and treatment at 30 days with a larvicidal anthelmintic. The mesenteric artery is essentially normal. Image courtesy of Dr Jay Georgi

A second exception is Dirofilaria immitis (the heartworm) in cats. Infections with even one or two adult heartworms may cause severe pathophysiological changes and life-threatening disease.

Introduction to Parasitology
Parasites and disease
Many parasites have complex life cycles that involve extensive migrations in their hosts. Others have simple life cycles with little or no migrations. The propensity of a parasite to cause disease (its pathogenic potential) is not a simple prediction since it may depend on a number of factors including the examples listed below. Factors influencing the pathogenic potential of a parasite 1. The migratory pathway in a host 2. The anatomical site where a parasite develops if it does not migrate in its host. 3. Feeding habits 4. The predilection site 5. The propensity to stimulate hyperactive immunological responses in the host that may lead to immunopathological changes such as fibrosis, granulomas, cachexia, autoimmuine reactions, allergic reactions and splenomegaly. 6. The potential of the parasite to transmit other infectious agents. This property is especially relevant to the arthropods. Despite the complexities of parasite interactions with their hosts, we can make certain predictions about the pathogenic potential of a parasite and the likely clinical signs if we know certain details about its life cycle, its predilection site and its feeding habits. The following table summarizes the relevant information about Ostertagia ostertagi, a nematode parasite of cattle found commonly throughout temperate areas of the world, and Haemonchus contortus a nematode of sheep found throughout the world in warm temperate and subtropical areas.

Factors influencing the pathogenic potential of parasites Migratory pathway Site of parasite development Predilection site Feeding habits Immunopathological changes Transmission of other infectious agents

Ostertagia ostertagi None Gastric glands Abomasum Ingestion of abomasal contents None None

Haemo

In close apposit mucosa Abomasum Blood feeder None None

With this information, we can make certain assumptions and predictions about the pathophysiological changes and the clinical signs in these infections.

Ostertagia ostertagi. The nematode grows and develops in the gastric glands of
the abomasum which it leaves just before it becomes an adult, approximately 17-21 days after infection. During its time in a gastric gland, the nematode grows about 100 fold. Therefore we can predict that this growth will result in erosion of the secretory epithelium and also that swelling of the gland will occur. In heavy infections these erosive effects can be widespread resulting in heavy losses of secretory cells and significant reductions in the output of HCL and pepsinogen. These changes are summarized in the table below.

Pathogenesis of Ostertagia ostertagi Morphological Biochemical changes changes Loss of chief cells Reduction in HCl in the abomasum and a rise in the pH of abomasal contents Physiological consequences Failure to convert pepsinogen to pepsin. Loss of the bacteriostatic effect of an acid pH Results Protein digestion impaired. Bacterial accumulation in the g.i. tract Loss of protein digestion

Loss of peptic Reduction in secretion of cells pepsinogen

These changes will result in the collection of osmotically active materials in the intestine (undigested protein and bacteria) and these, in turn, will promote the transfer of fluid from the extracellular spaces into the gut lumen and diarrhea (watery feces) will be the outcome of this process. Diarrhea is, in fact, the primary clinical sign in acute ostertagiosis and we can make this prediction from a small, but critical, amount of information about the parasitic phase of the nematode's life cycle.

Haemonchus contortus. In this example, unlike Ostertagia, the parasite matures
on the mucosal surface of the the abomasum. Therefore its growth and development has little effect on the mucosa and makes no contribution to its pathogenic potential. Despite the fact that adult Haemonchus are no more than 1cm long, they are voracious blood feeders and it is this blood loss that is entirely responsible for the pathophysiological changes and clinical signs we see in Haemonchosis.

Pathogenesis of Haemonchus contortus Feeding Impact of Biochemical Physiological habits feeding changes consequences Blood Severe blood Loss of red cells Anemia feeding by loss. A worm = drop in the PCV L4s and burden of adults may 1,000 worms Loss of plasma Edema remove may remove proteins 0.05ml 50ml blood = hypoproteinemia blood per per day from (hypoalbuminemia) worm. an infected host.
The magnitude of the red cells losses due to the feeding habits of this parasite makes it easy to predict that anemia of varying degrees of severity will be a constant feature of these infections and will usually be seen clinically as pale mucous membranes and lethargy. The latter can be explained by the reduced oxygen carrying capacity of the blood due to the loss of Hemoglobin along with red cells and a resultant reduction in oxygen perfusion of tissues such as muscles. Edema is usually seen in live sheep as a gathering of fluid in the submandibular space,

between the mandibles and for this reason is often called "bottle jaw". At necropsy a Haemonchus-infected sheep would show a general wetness of the tissues as well as fluid in the peritoneal (ascites) and thoracic (hydrothorax) cavities. Edema has a more complicated explanation than anemia and requires an understanding of the forces controlling fluid flow in tissues at the capillary level.

The exchange of fluid between blood and the interstitial spaces, at the capillary level, is controlled by the opposing effect of two forces, Hydrostatic Pressure (HP) and Plasma Colloid Osmotic Pressure (COP). HP tends to force fluid out of the capillaries and COP tends to draw fluid into the capillaries. The balance of these two forces will determine what occurs. At the arterial end of a capillary HP is greater than COP and fluid will leave the capillary to perfuse the interstitial spaces. At the venous end of a capillary, HP is lower than COP and fluid will return to the capillary from the interstitial spaces. The concentration of albumin in plasma is the most important contributor to colloid osmotic pressure and is, therefore, the most important determinant in regulating fluid flow at the capillary level. A reduction in the level of albumin, because of blood loss, in Haemonchosis will result in a corresponding reduction in the COP with a net outflow of fluid from blood, its accumulation in the interstitial spaces and this is called edema. We know that Haemonchus is a blood sucking parasite and causes significant blood loss including plasma proteins. Our knowledge of the physiological forces governing fluid flow at the capillary level (Starling's Principles) leads us to predict that edema will be a logical and likely outcome of Haemonchus infections

The Nematodes
Introduction
Nematodes are commonly called roundworms because, as the name suggests, they are round when viewed in cross section. However, they are in fact cylindrical in structure and taper towards their anterior and posterior ends. They are bilaterally symmetrical, and while the sexes are separate in most species, a few are hermaphrodite. Nematodes that parasitize our domestic animals are found in all parts of the body but are most commonly found in the digestive and respiratory tracts and the circulatory system. Nematode parasites of domestic animals vary greatly in size ranging from small hair-like worms (up to 2 cm long) in the Superfamily Trichostrongyloidea to large, robust worms ( up to 40cm long) in the Superfamily Ascaridoidea. The following six examples show the considerable variations in size and appearance seen among the nematodes

Species:

Toxocara canis

Dirofilaria immitis Filarioidea Spirurida Right heart, pulmonary arteries Dogs, cats, ferrets 23 - 30 cm

Trichostrongylus axei Trichostrongyloidea Strongylida Abomasum/stomach

Superfamily: Ascaridoidea Order: Location: Hosts: Size: Ascaridida Small intestine Dogs 10 - 18 cm

Ruminants, horses, swine 0.7 cm

Species: Superfamily: Order: Location: Hosts:

Parascaris equorum Ascaridoidea Ascaridida Small intestine Horses, donkeys

Syngamus trachea Strongyloidea Strongylida Trachea Fowl, game birds

Size:

15 - 40cm

0.5 - 2 cm

The Nematodes
Classification
All living organisms, plants and animals, are organized into a hierarchy of groups called taxa. This structure is based primarily on the degrees of similarity among members of the same group and also shows the contrasts among members of different taxa. The highest level of classification considered here is the Phylum and the lowest is the Species. Nematodes belong to the Animal Kingdom and their taxonomic hierarchy is expressed as follows: KINGDOM PHYLUM CLASS ORDER SUPERFAMILY FAMILY SUBFAMILY GENUS SPECIES Species are named using the binomial system of Linnaeus (1753) and are written in italics. A species is defined as a collection of similar organisms that will only interbreed among themselves. Examples of nematode species include Strongylus vulgaris in horses, Toxocara canis in dogs, and Haemonchus contortus in sheep. Even though many different species are morphologically similar and may share the same habitat in the same host they are still distinct species because they do not interbreed. For example, three members of the genus Strongylus inhabit the large intestines of horses: Strongylus vulgaris, Strongylus equinus, and Strongylus edentatus. They are similar in size and appearance and without the aid of a microscope they are not readily distinguishable from each other. Although they share the same host and the same habitat within that host, they do not breed with each other. However, their similarities (as species) allow us to group them in the same hierarchical tree of classification. In addition, these similarities allow us to conclude that the three Strongylus species share common ancestors and this phylogenetic relationship is also recognized by placing them in the same taxonomic hierarchical tree.

CLASSIFICATION
Strongylus species
Phylum: Nematoda Family: Strongylidae

The two images below show nematodes with and without a copulatory . Examples are shown in the following table.Order: Strongylida Subfamily: Strongylinae Genus: Strongylus Superfamily: Strongyloidea Within the nematodes. Order Superfamily Strongyloidea Ancylostomatoidea Metastrongyloidea Comments Strongylida Trichostrongyloidea "Bursate" nematodes Ascaridida Oxyurida Rhabditida Spirurida Ascaridoidea Oxyuroidea Rhabditoidea Spiruroidea Thelazioidea Filarioidea Habronematoidea Trichuroidea (Trichinelloidea) Dioctophymatoidea "Non-bursate" nematodes Enoplida Nematodes in the order Strongylida are also called "bursate nematodes". some of the taxonomic groups have suffixes (endings) that are specific for the particular group. a descriptive term referring to the fact that each male has a pronounced copulatory bursa at the tail (posterior) end. SUFFIX ida oidea idae inae TAXONOMIC GROUP ORDER SUPERFAMILY FAMILY SUBFAMILY Most of the nematodes of veterinary importance are found in the six orders and thirteen superfamilies listed in the table below.

Click here to view a table showing a more complete classification of nematodes of veterinary importance. taxonomy database is maintained by "NCBI/Gen Bank" and includes a searchable index. Tail end of male showing copulatory bursa.bursa. Fig. Male without a copulatory bursa showing spicule (A). 2 Heterakis (Order Ascaridida. . spicules and bursal rays. A second. Fig. caudal ala (B) and pre-cloacal sucker (C). 1 Cooperia (Order Strongylida. more comprehensive. Sources There are several good sources on the Internet that describe taxonomic hierarchy. Superfamily Trichostrongyloidea). One can be found on the Web site maintained by the Royal (Dick) School of Veterinary Medicine at the University of Edinburgh in Scotland. Superfamily Ascaridoidea).

Since the body cavities of nematodes contain pressurized fluids the cuticle apparently serves to maintain the body at a constant diameter by resisting the internal pressure of these fluids.soluble ions. alae and papillae. vagina. ascorbic acid. Cuticular modifications at the anterior ends of many nematodes may include leaf crowns. A variety of organic compounds have been identified in the cuticles of many nematodes. lipids. allowing only the passage of water molecules and certain small water.cuticle Nematodes are covered by a protective outer skin called a cuticle which is naturally colorless and partly translucent.cephalic (B) and the anterior . Leaf crowns (A) are rows of finger-like projections surrounding the rim of the opening to the buccal cavity. The cuticle also lines the buccal cavity. In many nematodes the cuticle is a smooth outer layer but in others the cuticle may have longitudinal and circular striations and may be modified to produce a variety of structures that can be useful in identification of specific nematodes. cloaca and rectum. in fact. These include amino acids. metabolically activity most of the time. The cuticle also appears to function as part of what Noble et al describe as the "hydrostatic skeleton of nematodes". The patterns of the several cuticular layers and their contents appear to allow simultaneous radial strength and longitudinal flexibility. Vesicles are inflations of the cuticle around the mouth . excretory pore. It is also known that the cuticle is antigenic and may play an important role in eliciting the immune responses of infected hosts. ATP and hemoglobin. carbohydrates.The Nematodes External Structures . the cuticle therefore maintains a nematode's form and structure and also provides an anchor for muscles. They are particularly obvious in the strongyles of horses. at the same time. esophagus. In other words. Their presence and variety suggests that the cuticle is far from inert and is. In keeping this fluid contained. RNA. allowing the nematode to stretch longitudinally. proteins. the cuticle layers are arranged so as to maintain a constant body diameter while. The cuticle is also resistant to host digestive enzymes and in most nematodes is relatively impervious. vesicles.

esophagus -cervical (C). Click here to see a set of images of specific nematodes showing modifications to the cuticle at their posterior ends. A bursa has two lateral lobes and in some species. The bursa is supported by finger-like structures called rays which are caudal papillae with associated muscle tissue. Each lateral lobe usually contains six rays and the dorsal lobe has one ray. folded hand but during copulation it is greatly expanded and used to grasp the female. caudal alae are greatly expanded to form a structure called a copulatory bursa . Cervical papillae (E) are paired spine-like projections found in the esophageal region. as the name suggests. a third dorsal lobe. Caudal papillae are cuticular protuberances believed to be sensory in function. They vary in shape from small "button-like" protuberances to longer "stalk-like" structures. Click here to see a set of images showing specific nematodes with cuticle modifications of their anterior ends. Cervical alae (D) are located in the terminal half of the esophageal region when cervical vesicles are also present and cover most of the esophageal region in the absence of vesicles.so called because it is used by the male to grasp the female during copulation. In male nematodes. When resting. Their function is believed to be tactile or sensory.posterior end Cuticle modifications at the posterior ends of nematodes may include caudal papillae and caudal alae. Cuticle modifications .The number and shape of these rays may be valuable characteristics for species identification of nematodes in the order Strongylida. Alae are. Caudal alae are wing-like expansions of the cuticle and may be found at the tail ends of nematodes. of species belonging to the order Strongylida. . the bursa looks like a relaxed. "wing-like" expansions of the cuticle.

.

The nematode stage (usually an egg or L1) that passes from a definitive host must develop through to a stage (usually the L3) that can then infect another host. Exsheathment . At this point further growth is possible only if the larva grows a new. At this stage the larva. with a new cuticle is completely enclosed by its old cuticle. This pattern is illustrated by the adjacent figure and consists of two phases. Initiation of the hatching process is controlled by several factors including temperature and moisture levels in the external environment. an egg. These eggs must pass through the three developmental stages (L1. L2. all of them can be related to the same basic pattern. This is an important point to emphasize . Hatching occurs only when environmental conditions are favorable for survival of hatched larvae. This process is called molting and involves two steps. The parasitic phase takes place inside the definitive host while the pre-parasitic phase occurs either as a freeliving phase in the external environment or inside a second host.a process by which the old cuticle is loosened and ruptured . Sometimes the sexually immature adult stages are called L5's In most species sexual reproduction by adult nematodes is the norm and occurs within an infected definitive host. 1. parasitic and pre-parasitic. L2. Synthesis of a new cuticle by the hypodermis. This newly hatched L1 feeds on bacteria and grows until constrained by its outer skin or cuticle. L4) and two adult stages comprising separate males and females. Eggs are laid by the female and pass from this host into the external environment. 2. then hatches. called an intermediate host. These conditions stimulate the enclosed larvae to assume its own role in hatching by secreting enzymes to digest the surrounding egg membranes. more flexible.The Nematodes Basic Nematode Life Cycle Despite the diversity and complexity of many nematode life cycles. A first stage larva develops inside an egg. This basic life cycle also consists of seven stages. and L3) before the nematode is again infective for another host.In the vast majority of nematode life cycles the stage that passes from the definitive host is not the same stage that is infective for another definitive host. L3. cuticle and casts off its old outer cuticle. then exerting pressure against the weakened membranes to rupture them and escape. four larval stages (L2.

Nematodes molt four times during each life cycle with a molt occurring at the end of each larval stage. This developmental cycle can be represented by a growth curve as shown in the following figure. . An (L1) develops inside the egg. This second stage larva also shows a rapid spurt of growth followed by a second molt (M2) to a third stage larva (L3) the infective stage for many nematode species. This final larval stage grows and undertakes a final molt (M4) to an immature adult (L5). the third and fourth larval stages (L3 and L4) and also the fourth larval stages and immature adults (L4 and L5). grows rapidly then molts (M1) to an L2. The L5 grows to the limit of its new cuticle. the second and third larval stages (L2 and L3). hatches (H). at the same time developing into a sexually mature adult male or female. Therefore. molts separate the first and second larval stages (L1 and L2). This (L3) grows then molts(M3) inside the host to an L4.followed by the larva wriggling out of the casing of the old cuticle. These L5's pass through a final growth phase to become sexually mature adult males and females.

Hatching will take place after these eggs are eaten by another host and the infective larva escapes.larvae develop to the infective stage inside an appropriate intermediate host. in addition to the definitive host. In nematodes where first stage larvae hatch from their eggs subsequent development takes place in the environment and the third stage larva is the infective stage.The Nematodes Life cycle variations Although the basic nematode life cycle described previously holds true for many nematode species. In these cases transmission of infective nematode larvae occurs during feeding on the definitive host. the roundworm of pigs. In these life cycles there are two possible methods of transmission of infective larvae to the definitive host. Example: Parelaphostrongylus tenuis. . There are two types of life cycle in nematodes infecting domestic animals . Example: Dirofilaria immitis. may play a role in the life cycle. Most of these variations are concerned with the infective stage and whether other hosts. Example: Ascaris suum. The intermediate host is a biting or sucking arthropod.all preparasitic stages are found free-living in the environment and their development may take place either inside the egg or after hatching. Examples of this type of direct life cycle occur among members of the family Trichostrongylidae In nematodes where eggs do not hatch. The intermediate host is ingested by the definitive host and infective larvae are released by digestion in the alimentary tract. Direct life cycles . the heartworm of dogs and cats. preparasitic larvae develop inside their eggs so that the infective stage is an egg containing an infective larva.Direct and Indirect. the brainworm of white-tailed deer. Indirect life cycles . it is also true that other species show a number of variations and complications in their life cycle patterns.

These activated neurosecretory cells release hormones (including nor adrenaline) which act directly on the excretory cell to stimulate the uptake of water which. temperature and reducing agents) activate neurosecretory cells in the nerve ring. in turn. because it completely encloses the larva. The cuticle breaks at this point and the anterior end detaches as a cap (B). are released into the excretory duct and pass into the space between the two cuticles.primarily levels of dissolved carbon dioxide (influenced by pH. The actual exsheathment of Haemonchus third stage larvae takes place in the rumen and appears to be a three-stage process. . The exsheathment process in Haemonchus contortus in ruminants has been reasonably well delineated. The exsheathed L3 (C) wriggles out leaving the sheath (D) (second stage cuticle) behind. This outer sheath plays a protective role for these larvae but. The infective stage for most stronglyid species is a third stage larva still enclosed in the loosely-fitting cuticle (sheath) from the preceding second stage. In species infecting grazing ruminants transmission occurs by ingestion of ensheathed third stage larvae during grazing. including leucine aminopeptidase. 2. The first process to occur is exsheathment since without it. and final. it also prevents feeding. activates enzymes present in crystalline form. The process of exsheathment is particularly important in the order Strongylida since it plays a vital role in transmission to the definitive host. Activated enzymes.The Nematodes Exsheathment The molting process in nematode growth and development involves two steps: synthesis of a new cuticle and exsheathment or shedding of the old. Environmental conditions in the rumen . Enzyme action weakens the cuticle (A). The accompanying diagram shows the third. at the base of the esophagus. 1. stage in the exsheathment process. 3. infection can not proceed.

Without exsheathment. . The accompanying image shows Haemonchus larvae exsheathing in a petri dish after stimulation with carbon dioxide. Larva A still retains its sheath while larva B is wriggling out of its sheath (C). Haemonchus contortus will not infect horses because they lack a rumen and therefore infective Haemonchus larvae ingested by horses will not receive the necessary stimulus to begin the infective process. This ensures that nematodes will not exsheath when ingested by abnormal hosts. The process of exsheathment during infection is not only host specific but is also site specific within the host. infection would not occur. For example. is labeled D. its larva having escaped. in nematodes like Haemonchus. empty sheath. A cast.The importance of exsheathment is because it initiates infection.

Arrested development can only be diagnosed by examining the population of worms in a host animal at necropsy. Synonyms include the terms hypobiosis. It is of particular importance in the order Strongylida especially the Trichostrongyles of grazing ruminants. However. Arrested larvae not only fail to grow but also their metabolic rate decreases significantly and they stop moving. In this state they can survive for weeks or months before resuming development and may also be resistant to some anthelmintics at doses that are usually lethal to adults and normally developing larval populations. inhibited larval development and arrested larval development Arrested development may be defined as a temporary halt in the parasitic phase of development at a specific point in the nematode life cycle. . Under normal circumstances when a host is infected with a nematode. This image shows a histological section of an abomasum with an arrested larva (early L4) of Ostertagia ostertagi contained within a gastric gland.The Nematodes Arrested Development Arrested development is an important feature of the life cycles of a number of nematode species. larval inhibition. If arrested stages are present. parasitic development begins immediately and continues through to adult males and females in the normal prepatent period characteristic of the species. the worm population will show the following characteristics. under certain circumstances larval development will be halted or arrested at a specific stage (usually L3 or L4) and the prepatent period is prolonged sometimes for weeks or months. the small strongyles of horses and the hookworms of dogs and humans.

A significant percentage of larvae will be at the same stage of development. The most recent exposure of the host animal to infection will be at least prior to the prepatent periods of the nematode species present. An overcrowding effect whereby the presence of adult worms causes the "feedback" inhibition of incoming infective larvae which go into arrest until the adult worm population decreases in number or is eliminated. In other words hypobiosis occurs inside the definitive host but results from . Host immune responses inhibiting the normal development of the parasitic phase of the life cycle. Initiating factors in arrested development Epidemiological and experimental evidence has identified three factors responsible for the initiation of arrested development. 1.03 mm wide). and the larger group will be mature adults. Merial Inc arrested larvae. they do not develop continuously through to adults but instead arrest in host tissues either as exsheathed L3s or as early L4s. When these L3s subsequently infect a host. 2. Seasonal Arrest Hypobiosis is the term most often used for arrested development that has a seasonal basis. The image shows the relative sizes of an arrested L4 and a mature adult male). The smaller group will be Image courtesy of Dr.12 mm wide) . adult females (~ 10 mm long and 0. 3.1.14 mm wide) and arrested larvae in the early L4 stage (~ 1 mm long & 0. In these species hypobiosis is initiated by an environmental signal received by free-living L3s. Jorge Guerrero. 3. the nematode population will include adult males (~ 7 mm long & 0. 2. It is a biologically important feature since it seems to be of particular importance in nematodes with relatively short adult life spans. (In the case of Ostertagia ostertagi. The sizes of recovered worms will show a bimodal distribution. Seasonal influences on infective larvae on pasture.

Argentina and South Africa. In Northern Nigeria. In the southern United States. hospitable to the survival and development of free-living stages. for example. for example. Brazil. infected with a "winter-arresting" strain of Ostertagia ostertagi were moved to Louisiana ( a region where hypobiosis occurs in Spring) and grazed on Ostertagia-free pastures thus contaminating them with free-living stages of the "winter-arresting" strain. by arresting as immature stages until conditions improve to the point where free-living larval stages can again grow and develop to the infective stage. hypobiosis occurs in Haemonchus contortus and Cooperia species in cattle. Peru. Similarly. as early L4's. with the onset of falling temperatures signaling the approach of winter. the time for hypobiosis in their new environment. only a proportion of such ingested larvae (usually no more than 60%) will arrest since England's milder winters will often allow preparasitic stages to survive on pasture. Several studies have shown that the propensity for hypobiosis is genetically based.e. Chile. In contrast. hypobiosis occurs in Spring in regions of the southern hemisphere where summers are also hot and dry. hostile to survival of their progeny. cattle from Ohio. dry summer. Hypobiosis is clearly genetically controlled but is not an "all or none" phenomenon. Ostertagia ostertagi arrests during spring and remains arrested during the following hot. For example. The converse was also true. temperate climates and pronounced seasonal changes. This evidence confirmed other observations that several different strains exist in populations of nematodes where hypobiosis is a significant feature of the life cycle. in late fall (autumn). In cold temperate climates such as are found in Maine and Eastern Canada. Resumption of development begins at the onset of the rainy season when the environment is. for example southern England. suitable for preparasitic development of the next generation of eggs and larvae. In milder climates. with a six-month dry season. The resumption of development of these hypobiotic larvae occurs in late winter or early spring when environmental conditions are. The resumption of development (to adults) of these arrested larvae occurs once the environment is. Calves grazed on this newly contaminated pasture were subsequently shown to contain hypobiotic larvae in the fall (autumn). arrested larvae accumulate inside grazing animals during the fall/autumn.environmental signals received by free-living infective larvae. once again. a season that is usually threatening to the survival of free-living stages on pasture. Hypobiosis in Spring thus allows Ostertagia to survive within the host. the great majority of trichostrongyle larvae ingested by grazing ruminants. In warm temperate regions of the northern hemisphere. again. hypobiosis appears to be linked to the onset of a dry season since dry conditions also threaten both the survival and development of free-living stages. will undergo hypobiosis. These regions include parts of Australia (coastal and adjoining tablelands). i. protected from the inhospitable external environment. the season for hypobiosis in their original Ohio environment rather than Spring. Ostertagia in cattle transferred from Louisiana to Ohio continued to show hypobiosis in the Spring. In tropical regions. once again. The triggering mechanisms responsible for ending hypobiosis and allowing larvae to resume . It is a mechanism for nematodes to survive a period of harsh climatic conditions. conducive to survival and development of free-living preparasitic stages. hypobiosis has been recorded at the onset of dry seasons. hypobiosis is much less important in Southern Nigeria and Southern Ghana where the dry season is short. In regions of the northern hemisphere with cool.

For example. and worm burdens are usually expelled as a consequence of the restored immune response. . As the grazing season progresses these animals develop a strong immune response to nematode infections and one of the manifestations of the immune response is the inhibition of larvae inside the host. As animals graze. It also has considerable epidemiological implications to nematode hosts and must be considered when devising methods for prevention and control of nematode infections and disease. An inhibition of the immune response. Trichostrongylus. If so. There are several reasons why arrested development is important. is not an option and is not triggered by extraneous influences. particularly ruminants. Larvae infecting a host are more likely to arrest if there is already an established population of adult worms in that host. the phenomenon has considerable biological importance to nematodes that incorporate it into their life cycle options. Immune competence is restored when prolactin levels drop. However. Evidence for this comes from New Zealand studies where it was found that hypobiotic larvae mature at the same rate as they undergo arrest leading to the conclusion that arrested larvae resume their development at a set time after they become arrested in the host. the small strongyles of horses. Immune arrest Another form of arrested development is also recognized and is due to the influence of the immune response. particularly the ascarids and spirurids. are not really known.development. is related to serum levels of prolactin. then some type of genetically programmed clock would trigger the ending of hypobiosis at a set time after induction. we can assume that hypobiotic larvae begin to accumulate in September in cattle grazing pastures in cool temperate regions of the northern hemisphere and this accumulation ends when these cattle are housed for the winter at the end of November. they continually ingest infective third stage larvae which develop to adults in the normal prepatent period. This is particularly true of the Trichostrongyles such as Ostertagia. it has been hypothesized that seasonally arrested larvae are in a similar state to diapause in insects. Haemonchus. In sheep. Biological importance of arrested development Whatever the triggering mechanisms are that initiate developmental arrest and induce resumption of development. also. If we further assume that these larvae will remain arrested for 4 months then resumption of development will begin in January and continue until the end of March. at weaning. Cooperia and Dictyocaulus as well as Oesophagostomum and. goats and pigs maturation of these immunologically arrested larvae appears to be linked with parturition. It appears that seasonal hypobiosis is an important option for the life cycles of a number of nematodes of grazing animals. This form of arrested development is often called quiescence since it is an intrinsic part of the life cycle. Quiescence Hypobiosis and immunological arrest of parasitic larvae should be distinguished from other forms of developmental arrest seen in paratenic and intermediate hosts during the life cycles of many nematodes. specifically associated with gut-dwelling nematodes.

Clearly the choice of drugs to be used in a nematode control program will be influenced by the role of arrested development in specific nematode life cycles and by the susceptibility of arrested larvae to the range of available anthelmintics. Development of adults from arrested larvae will produce significant contamination of pastures with nematode eggs at a time when environmental conditions are. 2. Resumption of development of large numbers of larvae in a host may produce serious outbreaks of disease. immunologically naive animals grazing pastures for the first time. 4. Hypobiotic larvae are depressed metabolically and hence may be less susceptible to some anthelmintics. Arrested development ensures survival of nematodes during times when conditions are hostile to their survival in the external environment. 3. favorable for development of preparasitic stages to infective larvae. .1. once again. This contamination which begins at the start of the grazing season and reaches a peak several weeks later is particularly dangerous for young.

CLASSIFICATION OF NEMATODES OF VETERINARY IMPORTANCE ORDER STRONGYLIDA SUPERFAMILY TRICHOSTRONGYLOIDEA FAMILY TRICHOSTRONGYLIDAE DICTYOCAULIDAE STRONGYLOIDEA STRONGYLIDAE CHABERTIIDAE SYNGAMIDAE ANCYLOSTOMATOIDEA ANCYLOSTOMATIDAE METASTRONGYLOIDEA METASTRONGYLIDAE PROTOSTRONGYLIDAE FILAROIDIDAE .

ANGIOSTRONGYLIDAE ASCARIDIDA ASCARIDOIDEA ASCARIDIDAE OXYURIDA RHABDITIDA SPIRURIDA OXYUROIDEA RHABDITOIDEA SPIRUROIDEA THELAZIOIDEA FILARIOIDEA OXYURIDAE STRONGYLOIDIDAE SPIROCERCIDAE THELAZIIDAE ONCHOCERCIDAE HABRONEMATOIDEA ENOPLIDA TRICHUROIDEA (TRICHINELLOIDEA) HABRONEMATIDAE TRICHINELLIDAE TRICHURIDAE DIOCTOPHYMATOIDEA DIOCTOPHYMATIDAE .

Examples of direct (free living larvae) and indirect (intermediate host) life cycles can be found among the members of this order. Notice the difference between these eggs and the whipworm (Trichuris) egg (C). horses. as well as the lungworms of ruminants and. the hookworms of dogs and cats. whose species produce eggs that are approximately twice the size of "strongyle-type eggs (B).The Trichostrongyloidea Strongylida The order Strongylida includes many of the important nematodes found in the gastrointestinal tracts of ruminants. There are four superfamilies of importance in domestic animals: Trichostrongyloidea Strongyloidea Ancylostomatoidea Metastrongyloidea Females belonging to the superfamilies Trichostrongyloidea. Strongyloidea and Ancylostomatoidea produce smooth. ellipsoidal "strongyle-type" eggs (A). thin-shelled. and swine. . Their distinguishing features include a copulatory bursa in males and a buccal capsule of variable shape and size. approximately 80-100 microns long and 40-50 microns wide. One exception to this rule is Nematodirus. The following table gives an overview of the classification of this order with an emphasis on the superfamily Trichostrongyloidea.

There are two genera and thirty three species in this superfamily. Females pass a "strongyle-type" egg and their life cycles are direct and similar to the Trichostrongyloidea but it is also believed that paratenic hosts (snails and slugs) may play a role in their life cycles.A fifth (minor) superfamily. are bursate nematodes found in the digestive tracts of terrestrial snakes and occasionally lizards. . the Diaphanocephaloidea.

with an extremely small buccal capsule. Hypobiosis (seasonal arrested development) is an important feature of the life cycles of the trichostrongylids and is therefore an important factor when devising appropriate methods of controlling infection and disease caused by these nematodes. Superfamily Family Genera Trichostrongylus Haemonchus Ostertagia Nematodirus Cooperia Hyostrongylus Dictyocaulus Trichostrongyloidea Trichostrongylidae Dictyocaulidae Trichostrongylidae Members of the family Trichostrongylidae are widely found in large domestic animals especially cattle. All species have direct life cycles (no intermediate hosts). and a pronounced copulatory bursa. There is no migration within the definitive host. In domestic animals they are common and important parasites of ruminants but a few species are also found in horses and swine. . swine and. to a lesser extent. They are found in all terrestrial vertebrates especially mammals. Classification The following table shows the classification of the trichostrongloidea of domestic animals to the genus level.The Trichostrongyloidea Members of this superfamily are widespread throughout the world in all major stock raising areas. horses. They are small (~1/2 to 3cm long). and infection is by ingestion of ensheathed third stage larvae (L3's). and hair-like. goats. Their predilection sites are the stomach/abomasum or small intestine. sheep.

In the 1960s. Immunological constraints on egg production by existing female worms will be suspended. the primary lactogenic hormone. Incoming larvae ( either previously arrested or newly ingested from pasture) will develop to egg-laying adults without any constraints from the host's immune response. Hence the term was re-named the "periparturient rise" or "PPR" to more accurately describe its association with parturition and lactation. 2. The end result will be a rise in the output of nematode eggs which will be seen as an increase in fecal nematode egg counts of ewes in late pregnancy and lactation. also associated with hormonal changes in late pregnancy and lactation. 1. a process often called self cure. The population of adult nematodes (responsible for the PPR) is expelled. arrested development and the subsequent maturation of arrested larvae has particular significance in pregnant and lactating female hosts. in turn. Since this occurred regularly in the spring. appears to interfere (directly or indirectly) with the immunological mechanisms responsible for expulsion of gut-dwelling nematodes in sheep and goats. lambing occurred between January 1st . Terminating lactation by weaning nursing lambs has four sequential results in the mother ewes.The Trichostrongyloidea Arrested Development and the Periparturient Rise (PPR) In the trichostrongyles of ruminants. especially sheep and goats. it was named the "spring rise". Experimental observations in sheep have shown that the PPR is associated with a periparturient relaxation of immunity that is. and also illustrates how the PPR can be controlled by appropriate anthelmintic treatments. However. 4. several authors described a rise in nematode egg counts in the feces of lactating ewes. 1. Their circulating levels of prolactin drop. which begins to rise in late pregnancy and is maintained at high levels during lactation. Fecal nematode egg counts drop to zero This graph depicts the PPR as it occurs naturally in a flock of sheep. 2. This suspension of parasite-specific immune responsiveness has the following consequences. it was later concluded that these observations were related to the reproductive status of the ewes rather than the season of the year since the same rise in egg counts was observed in ewes in which parturition and lactation occurred in other seasons. 3. In this particular flock. Prolactin. Immunological responsiveness is restored.

the day of weaning.and February 15th. developed from eggs deposited on the pasture by ewes showing a PPR. reflecting a self cure of their worm population. Both groups of ewes continued to graze on pastures after their lambs were weaned and showed a typical summer rise in egg counts. At that point the fecal egg counts of these ewes dropped precipitously. Clearly. at parturition. These resulted from the acquisition of infections from grazing pasture contaminated by third stage larvae which. . in turn. The ewes were divided into two groups: one was left untreated (yellow line) while the other (green line) was treated.a drug effective against both adult worms and arrested larvae. a PPR did not occur. Ewes and their lambs were kept indoors until weaning on April 29th. the fecal egg counts of untreated ewes started to rise (the PPR) and peaked on April 29th. Six weeks after lambing began. this was a reflection that the Ivermectin treatment eliminated those worms responsible for the eventual PPR (arrested larvae and existing adults). In treated ewes. with Ivermectin .

Infective larvae of ruminant species tend to migrate onto vegetation where they are available. . Males are readily identified by their spicules. for grazing animals. Nematode Species Host Species Predilection site Trichostrongylus axei ruminants. horses. Females have a tapered tail and are missing a vulva flap. enclosed in a film of moisture. There are four important species animals and these are listed in the table below.The Trichostrongyloidea Genus Trichostrongylus Trichostrongylus spp are widely distributed throughout the world. there is no buccal capsule (A) and the opening of the excretory pore (B) is easily seen in the anterior esophageal region of adult worms. The life cycles of all three species are similar and follow the family pattern with a strongyle-type egg and a free living preparasitic phase. They are thin and with a length of 7 mm or less are difficult to see without a microscope As the accompanying image shows. and pigs Abomasum/stomach Trichostrongylus colubriformis ruminants small intestine Trichostrongylus vitrinus ruminants small intestine Trichostrongylus capricola goats and sheep small intestine Trichostrongylus species are the smallest members of the family Trichostrongylidae.

Adult worms may survive in birds for at least two years. The prepatent period is 7-8 days and hypobiosis occurs during winter at the exsheathed L3 stage. produces a "Spring Rise" in strongyle-type egg output from the resulting adult worm population and is also responsible for the seasonal occurrence of grouse disease and associated mortality in red grouse during spring time. Grouse chicks appear to acquire their infections early in life as their diet changes to heather from insects as the birds approach maturity. and development to adults takes place in the mucosa of the abomasum or small intestine. Prevalence rates in adult grouse can reach 100% and worm burdens have been reported to reach as high as 10. axei). .The parasitic phase is non-migratory. and approximately 25 days in horses (T. in spring. is found in the small intestine and ceca of birds especially geese and grouse and is widely distributed throughout the world.000 in adult birds. depending on the species. The prepatent period is 2-3 weeks in ruminants. Trichostrongylus tenuis. One other important species. Synchronized resumption of development of arrested L3s. It is particularly common in red grouse in Britain where it is the causative agent of "grouse disease". Field studies have shown that ensheathed infective L3s accumulate in films of moisture on the outer tips of heather.

exsheathed L3s penetrate between the epithelial glands with formation of tunnels between the epithelium and the lamina propria. axei infections in horses may produce a hyperemic gastritis . especially in ruminants. However. heavy infections (10. Clinical signs Light infections are usually asymptomatic but but may contribute to poor appetites. . In the duodenum. villi are distorted and stunted thereby reducing the intestinal surface area for absorption. In the stomach/abomasum nodular lesions containing developing worms may be seen.Trichostrongylus species Pathogenesis In Trichostrongylus axei infections. diminished growth rates and soft feces. In the case of infections with intestinal species. exsheathed L3s penetrate between the gastric glands and their subsequent growth and development cause nodular lesions similar to those produced by Ostertagia in sheep and cattle. The accompanying image shows a dead sheep which succumbed to trichostrongylosis. The fecal lumps attached to the hind quarters typically result from diarrhea due to Trichostrongylus infections and can be a source of attraction for blowflies producing a myiasis.a rise in the pH of abomasal contents and increased permeability of the mucosa.000+ worms) will produce a diarrhea that is serious and can be debilitating. The term "black scours" is sometimes used to describe the diarrhea because it is often watery and dark green (almost black) in color. T. emergence of immature adults some 10-12 days later cause erosions of mucosal surfaces accompanied by hemorrhage and loss of plasma proteins into the intestinal tract. Erosion of glandular epithelium with replacement by immature undifferentiated cells results in changes similar to ostertagiosis .

clinical infections may be seen after the dry season or a period of drought. axei to cross-infect between horses and ruminants may lead to amplification of T. large numbers of L3s survive drought by becoming desiccated and are re-hydrated by subsequent rains. infections will be seen only during the grazing season. In temperate zones of both hemispheres enough L3s may survive winter and produce clinical outbreaks of trichostrongylosis in grazing ruminants in early spring. In Australia and Brazil. as such. They are readily identified with a microscope with males having uniquely shaped spicules. nematodes that produce similar eggs. Survival of preparasitic stages . clinical signs of a watery diarrhea and weight loss will be present in a variable number of animals. Trichostrongylus adults are too small to be readily observed in situ at necropsy.Eggs and infective L3s are able to survive both heat and cold.i. nematodes may also be the cause of diarrhea and weight loss. from early spring through to late autumn (fall). The ability of T. In subtropical areas.000 or more worms per animal are not unusual in clinical outbreaks. clinical outbreaks of trichostrongylosis have occurred when rain followed a dry period. Diagnosis A diagnosis of trichostrongylosis is made on the basis of a combination of factors Clinical signs Seasonal occurrence of disease Necropsy findings Presence of Strongyle-type eggs in the feces of infected animals Fecal cultures to identify Trichostronglyus L3s In herds or flocks with heavy infections. in warmer subtropical areas Trichostrongylus species are important pathogens in grazing ruminants and counts of 10. However. In temperate areas. Hypobiosis occurs at the L3 stage and is an important controlling feature of life cycles in temperate areas of the world. although these signs are only suggestive of a diagnosis since other g. are not distinguishable from other g. . L3s may survive winter in sufficient numbers to produce clinical infections soon after the start of the grazing season.i. axei infections in horses when mixed grazing of pastures with horses and ruminants is used as a parasite control measure. In these cases. Their role is usually contributory to parasitic gastroenteritis in which Ostertagia or Haemonchus are the primary pathogens in ruminants.Trichostrongylus species Epidemiology Trichostrongylus species are not usually primary pathogens in temperate regions of the world. Trichostrongylus eggs are "strongyle-type" and.

.

The copulatory bursa (A) of the male is distinct because it has an asymmetrical dorsal lobe with a Y-shaped dorsal ray (B). looking like a barber pole because the white ovaries wind around the red blood filled intestine. which is sometimes confused with the spicules (C). Because they feed on blood. the female has a striking appearance. Within the genus Haemonchus there are two important species: Nematode Species Host Species Predilection site Haemonchus contortus sheep and goats Abomasum Haemonchus placei cattle Abomasum . They achieve this by using a tiny lancet in their small buccal capsule.The Trichostrongyloidea Haemonchus species Haemonchus species are the largest of the nematodes found in the abomasum of ruminants (10-30mm). They range from 10-30mm in length and are reddish when fresh because they are blood suckers.

anywhere from 20. death is the usual outcome. grazing sheep develop a sudden onset anemia. As a result. Anywhere from 2. Fourth stage larvae as well as adults are blood suckers which means that blood losses. In acute haemonchosis. large numbers of worms are found in the abomasum . these animals are unable to replace all their lost serum proteins fom their deficient diet. At necropsy.pathogenesis Haemonchosis is characterized by a hemorrhagic anemia attributable to blood loss via the blood-sucking activities of worms in the abomasum. and if grazing continues. It often follows a period of warm. Without treatment. At necropsy. This syndrome results from ingestion of large numbers of infective larvae by sheep grazing on a heavily contaminated pasture. In the absence of treatment. Consequently. Haemonchus contortus In hyperacute haemonchosis. . plateaus. sufficient to cause a clinically obvious anemia.000 worms may be found and the abomasal contents will be brown due to the presence of blood. these animals will be pale and edematous and longitudinal sections of the long bones will show expansion of red marrow into the medullary cavity. wet weather during which massive numbers of Haemonchus eggs develop rapidly to infective stages. Worms also secrete an anticoagulant into the bleeding lesion ensuring that these lesions will continue to bleed after the worm is replete and has moved away. They ingest blood flowing from these slit capillaries.The Nematodes Haemonchus . sudden deaths in a flock of previously healthy sheep are seen. Hemorrhagic lesions will usually be present on the abomasal mucosa . The PCV drops initially. Chronic haemonchosis in a sheep flock usually results from a combination of infections with small numbers of worms and poor nutrition that persist for a prolonged period of time (several weeks or months).000 have been reported. these animals will progressively worsen. The actual mechanism of blood sucking involves the worm attaching to the mucosa and extruding its oral lancet to slit capillaries in the abomasal mucosa.000 to as many as 50. signaling exhaustion of the erythropoietic system.000 to 20. they lose weight as they mobilize muscle proteins to provide the amino acids necessary to synthesize vitally important proteins such as plasma proteins and hemoglobin. may occur before an infection is patent. Infected sheep suffer a chronic daily loss of small amounts of blood but this loss is exacerbated by a diet poor in protein. then falls even further.

. The accompanying image shows how body weights and growth rates of sheep are affected by chronic haemonchosis. It is clearly important that infected sheep maintain physiological levels of important plasma proteins and Hb.Another form of chronic haemonchosis may also be seen in sheep flocks where mild to moderate infections occur and where nutrition is good. in the face of blood losses due to the infecting worms. these animals appear to be clinically healthy but their weight gains are approximately half those of controls. They do this by diverting available dietary proteins away from muscle synthesis and towards vital organs such as the liver and bone marrow where plasma proteins are synthesized and red cells are produced. chronic haemonchosis of this type will clearly have financial consequences due to poor weight gains combined with increased feed intake. After 16 weeks of infection. These reduced growth rates cannot be accounted for by loss of appetite since nitrogen (N) intake values show that infected sheep were consuming more protein than the control sheep.

severe edema (ascites and submandibular edema "bottle jaw"). weakness. edema may or may not be present. Fecal egg counts Necropsy . expansion of red bone marrow in the long bones.The Nematodes Haemonchus contortus Clinical signs Sudden death from hemorrhagic gastritis in the hyperacute form. . mild anemia. edema. pale mucous membranes.worms in the abomasum. Diagnosis Clinical signs. dark feces. Acute haemonchosis .weight loss.anemia (pale mucous membranes). lethargy. loss of wool. Chronic haemonchosis .

All parasitic larval stages are found in the gastric glands of the abomasum which must be digested in order to release the larvae for observation with a microscope. On a global basis they are the major cause of parasitic gastritis (Ostertagiosis) of ruminants in temperate climates. . lyrata. leptospicularis found in cattle. although tiny. Morphology Adult worms are small (approximately 1 cm long) and brownish in color. Ostertagia species are found throughout temperate and subtropical areas of the world. They are difficult to see at necropsy unless they are present in large numbers (thousands). and O. The spicules of males are fairly similar in size and shape but are quite distinguishable from spicules of males in other abomasal nematodes (Trichostrongylus axei and Haemonchus). The following table lists the three major species. sheep and goats. less common species include O. Nematode Species Host Species Predilection site Ostertagia ostertagi cattle Abomasum Ostertagia circumcincta sheep and goats Abomasum (Teladorsagia) Ostertagia trifurcata sheep and goats Abomasum Other. Ostertagia ostertagi is particularly important in temperate areas wherever cattle are raised.Ostertagia Species These are small (~10mm) reddish brown worms found in the abomasum of ruminants. kolchida in cattle plus O. as shown by the linked images from light microscopy and scanning electron microscopy. A buccal cavity is present. The cattle species.

Trichostrongyles of the abomasum Male spicules Haemonchus placei .tail end of male showing paired spicules (B) Trichostrongylus axei .tail end of male showing paired spicules (A) Ostertagia ostertagi.tail end of male showing paired spicules (C) .

winters characteristic of the north. seasonal arrested development or hypobiosis is the most significant factor controlling transmission patterns of Ostertagia ostertagi because it occurs regularly from year to year. 3. cold (sometimes harsh). (Source US Veterinary Services. 1. Although there are two distinct patterns to hypobiosis and transmission of Ostertagia ostertagi the divisions are not entirely absolute because weather patterns do not fall readily into two distinctive northern and southern regions and also because weather . hypobiosis begins in autumn. signaling the approach of winter. 2005). 2. Temperature and moisture The most important factors controlling the preparasitic phase of the life cycle of Ostertagia species are temperature and moisture. The influence of seasonal arrested development (hypobiosis) on the parasitic phase of the life cycle. The stimulus for larvae to arrest is falling temperatures in early autumn. In the northern states. 1. There are also four common features that influence these epidemiological patterns despite the wide range of climates and management conditions under which cattle are raised. wet. Although the climate in the continental United States is predominantly temperate there are significant variations ranging from cool and wet in the pacific Northwest to hot and dry in the southwest and a warm. enabling Ostertagia to survive the long. The image shows the approximate lines of demarcation between the geographical areas where Ostertagia arrests over winter and where it arrests over summer.Ostertagia Epidemiology (for US only) The epidemiological patterns of ostertagiosis have been well defined in most areas of the world. The different ways in which pasture is used to raise dairy replacement heifers and beef calves. 4. Arrested development In the United States. L3s so stimulated will arrest if they are ingested by grazing cattle and will remain arrested throughout the subsequent winter. The influence of temperature and moisture on the survival and development of preparasitic stages of the life cycle. as in other temperate areas of the world. 2. Temperature determines the rate of development and moisture is essential for development to occur in the first place. The influence of the immune response on infection and disease. almost subtropical climate in the southeast.

sometimes very humid with variable amounts amounts of rain usually as of rain usually as thunder thunderstorms. . often severely so. Type II disease always results from arrested L4's resuming their development to immature adults and leaving the gastric glands approximately 7-10 days after development resumes. Southern United States Mild and warm. which lies approximately between the two broken white lines. storms. hypobiosis may begin in autumn. and March. Precipitation mostly rain with very occasional sleet or snow showers. in spring or not at all depending on the locality. Type I disease occurs most commonly in young cattle grazing contaminated pastures for their first time. Here. Ostertagiosis is seen as two distinct clinical entities. a hot summer and a mild winter. Pasture A minor wave is seen in April Pasture levels of L3s usually and May. Precipitation most often as snow. Type I Outbreaks may be seen in Outbreaks may be seen anytime late spring but occur more from mid December through the disease commonly between late end of May but the most severe summer and mid autumn outbreaks usually occur in the due to the peak levels of months of January. The table below summarizes the major influences on transmission of Ostertagia ostertagi and the times of year when the disease and hypobiosis generally occur in the two major regions of the United States. This is followed by a steady again in August through decline through the hot summer October. occasional cool Winter or cold periods of short duration. Feature Northern United States Cold. February. hypobiosis begins in the spring and lasts over the hot summers with resumption of development of arrested larvae in late summer and early fall. Southern areas of the United Sates are characterized by a warm spring and autumn. In the transition zone. This dips in June peak from March through mid L3s and July but rises to peak May. February pasture L3s at this time. The influence of climate on the epidemiology of Ostertagia and other nematodes of the gi tract will be discussed more extensively in a later chapter. In these cases the pathological insults and clinical signs are always due to immature adults leaving gastric glands after developing from L3s ingested approximately 3 weeks before.conditions vary from year to year in many localities. sleet and freezing rain. These L3s begin to decline in late begin to rise again slowly in October and reaches low November and a more rapid rise levels in December through to peak levels begins in March. Pasture levels of months to low levels . The stimulus for larvae to arrest in these areas is not precisely known but is thought to be either rising temperatures or possibly declining moisture levels that are usually seen in late winter-early spring. Type I and Type II. Very hot and humid with variable Summer Warm. but weeks or months after first being ingested as L3s.

November and December. In general. For example dairy calves raised in confinement housing will have limited exposure to Ostertagia infections and will not develop a strong immune response. The periparturient relaxation of immunity allows these larvae to resume development and cause severe enough pathological changes in gastric glands to result in clinical disease. It is speculated that these animals are probably harboring large numbers of Ostertagia larvae in arrested development because of the host's immune response. Management practices that limit the acquisition of immunity will also affect the the patterns of ostertagiosis. Immunity Significant immunity does not develop in grazing cattle until after a full grazing season and that immunity will decline when animals are not exposed to infective L3s for several months during their first winter housing. Dry cows and replacement heifers are usually turned out to pasture during the growing season in northern but may be pastured year for most of the year in some southeastern states and the Pacific northwest.Hypobiosis Significant numbers of arrested larvae may be found anytime between mid October and the end of March with peak numbers between mid December and mid February. Pasture use in cattle management In the United States there are wide regional variations in the methods by which dairy cattle are raised. These regional and climatic influences on the epidemiology of Ostertagia infections will be considered in more detail along with other gastrointestinal nematodes in the later chapter on Parasites of Cattle. Ostertagia in sheep and goats Ostertagiosis in small ruminants appears to be much less important in the United States . 3. October. Clearly the epidemiology of ostertagiosis in beef calves will differ depending on whether they are spring-born or autumn-born and also in which region of the United States they are raised. Type II ostertagiosis may be seen in the months of September. most beef calves are born either in the spring or autumn. calves are often sent directly to feed lots for finishing or are kept at their herd of origin as replacements or as "stocker cattle" raised on pasture for several more months before being sent to feed lots for finishing. These variations depend to a large extent on the prevailing regional climate which. Cow herds and their calves tend to be on pastures for most of the year in all regions of the United States with supplementary feeding only when pastures are limited due to weather that is either too hot or too cold. Significant numbers of arrested larvae may be found between early April and the end of September with peak numbers in the months of May. Immunity tends to be strong in adult cattle and clinical ostertagiosis tends to be uncommon in cattle over two years old. These animals will be susceptible to infection and disease throughout their lives if they are ever exposed to pastures contaminated with Ostertagia infective larvae. July and August. Type II Outbreaks of Type II ostertagiosis may be seen disease anytime between early February and early May. Their is some evidence that a periparturient relaxation of immunity may occur in first calving heifers and this may lead to significant infections and disease outbreaks in these animals. There are fewer variations in the management and grazing of beef cow herds. June. in turn determines the seasonal availability of pastures for grazing. After weaning. In general adult lactating dairy cattle are kept in confinement housing with access to dry lots or pastures only for exercise during mild weather periods. 4.

the more temperate climate allows Ostertagia circumcincta and Ostertagia trifurcata to thrive more readily than the United States and clinical outbreaks of diarrhea may be seen in late summer and early autumn in grazing lambs. However.S. In Europe. Ostertagia circumcincta is the dominant nematode of sheep and goats. it is not usually cited as a major cause of disease probably because it is present in relatively small numbers. Oregon and Northern California. wetter.than in cooler parts of the world such as Northern Europe and the British Isles. Ostertagia circumcincta is quite prevalent in sheep and goats along with Haemonchus contortus and Trichostrongylus colubriformis but its significance in disease is considerably less than Haemonchus even though it is often found in greater numbers at necropsies. In the southern United States. unlike its bovine counterpart. particularly the cooler. circumcinta. In the western U. This is because small numbers of Haemonchus may cause significant problems as a result of its propensity for sucking blood. Hypobiosis is a generally recognized phenomenon in Ostertagia species of sheep and allows survival of the nematode over winter. Ostertagia circumcincta is of no real significance in small ruminants because the hot and often dry summers are hostile to the survival of its preparasitic stages and it would appear that O. . has not developed hypobiosis as a mechanism for survival. coastal areas of Washington. Type II ostertagiosis has been reported in yearling sheep that grazed pastures the previous years. In the northern and central United States.

Ostertagia ostertagi Clinical signs The range of recorded clinical signs in bovine ostertagiosis is as follows. in the absence of adequate treatment and control measures. Ostertagiosis in lactating adults Although grazing animals remain susceptible to O. A more substantial description and explanation of hypoproteinemia and edema is given in the later chapter on pathophysiology. Reports in the literature have provided evidence that anthelmintic treatments of adults cows at or near parturition will produce increases in milk yields with attendant financial . especially in Type II ostertagiosis. their growth rates will be retarded and the costs of rearing such animals will increase substantially. but with appropriate treatment they will recover quickly and resume their normal growth patterns. but its significance and cause is unknown. dehydration and thirst. Animals infected with fewer worms may still show clinical signs. Submandibular edema (commonly called "bottle jaw") may also be seen and this directly results from a hypoproteinemia that is. a reflection of the severe protein loss through the damaged gastric glands. rough coats and their hindquartes are always soiled with feces as a result of the profuse diarrhea. A low grade anemia may be seen. losing up to 20% of their body weight in 10 days or less. Affected animals are usually depressed with dull. in heavy infections with severe diarrhea and anorexia. especially diarrhea. animals may become rapidly emaciated. ostertagi throughout their lives. in turn. Ostertagiosis can be a serious disease especially in young cattle and unless sick animals are removed from contaminated pastures and treated with appropriate anthelmintics they will likely die. Weight loss may be significant and. Diarrhea Anorexia or reduced appetite Dehydration Thirst Weight loss Submandibular edema Anemia The primary clinical sign in bovine ostertagiosis is diarrhea which is often described as "profuse and watery" and is usually accompanied by anorexia. The results will be significant economic penalties to affected farms or ranches whether ostertagiosis manifests as subclinical or clinical disease. infections in mature animals are usually light in terms of worm burdens. Animals with lighter Ostertagia infections may not show any clinical signs but.

In this event. In severe Type II disease the same clinical signs in older animals with a previous history of grazing contaminated pastures is also highly suggestive of ostertagiosis. the clinical sign of diarrhea accompanied by losses of appetite and weight in calves that are currently grazing known contaminated pastures is highly suggestive of a diagnosis of ostertagiosis. The effects of these suggested benefits are shown in the accompanying image. The presumption and the claim is that anthelmintic treatment at parturition offers substantial benefits in terms of increased milk production during the subsequent lactation and this will be translated directly into significant economic benefits to the milk producer. egg counts greater than 1. In severe Type I disease. In these animals clinical signs will only subside if they are treated with an anthelmintic effective against arrested larvae as well as adult worms.i.000 epg are usually seen but counts are much more variable in Type II disease. The presence of strongyle-type eggs in the feces of affected animals will merely confirm the presence of adult strongyle nematodes in the g. ostertagi and removing them from pastures will confirm the diagnosis if the clinical signs subside. The red line represents the milk production curve of a cow that is untreated with any anthelmintics at all during its production life beginning with the first parturition. In Type I disease. time is also important and for this reason treatment is sometimes implemented before ostertagioisis is confirmed as a definitive diagnosis. at or near parturition. The green line represents the production curve of a cow that is treated with an anthelmintic approximately 3-4 months after parturition. Under field conditions such action is often warranted even before a diagnosis is confirmed because in seriously ill cattle. It has been postulated that hypersensitivity reactions to even small numbers of developing larvae will produce changes in the gastric glands that are significant enough to result in mucosal permeability of the kind usually seen only in heavy infections. The presumption is that this anthelmintic would be one with a zero withdrawal time so that milk from treated cows would not have to be discarded or otherwise kept from the human food supply. it is theorized that even low burdens of Ostertagia ostertagi will produce pathological changes in the abomasum and severe enough derangements in protein metabolism that milk production will be affected. tract. The blue line represents the production curve following treatment. Diagnosis A diagnosis of ostertagiosis is usually made on the basis of several characteristics. Other reports have denied such benefits and still others have shown substantial increases only in the milk yields of lactating heifers following treatment at their first parturition but not in adult cows in later lactations. Treating these animals with an anthelmintic effective against O. with a drug whose withdrawal time does not exceed 96 hours .benefits to the producer. Although adult cows harbor substantially lower worm burdens than growing calves and heifers. . time is of the essence.the time of colostrum production when such milk would be kept from the human food supply anyway.

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Nematodirus These are slender. in Oregon in 1985 and has since been identified in Washington and several New England and Mid Atlantic States (Vermont. The image above shows the tail end of a Nematodirus battus male. The image above shows the tail end of a Nematodirus battus female. filicollis are commonly seen in sheep throughout the United State. As the accompanying image shows. battus. In N.S. New York. each bursal lobe has one pair of parallel rays (B) while all the other species have two.5 cm long). t are distinguished morphologically by an inflated cuticle around the anterior end which may also sho transverse striations. spathiger and N. battus was first recorded in the U. The species occurring in North America are listed in the table below Nematode Species Nematodirus battus Nematodirus spathiger Nematodirus filicollis Nematodirus helvetianus Nematodirus abnormalis Host Species Predilection site sheep small intestine sheep and goats small intestine sheep and goats small intestine cattle small intestine sheep and goats small intestine N. Large numbers of these long slender worms are usually seen at necropsy. pointed tail which in other Nematodirus species ends bluntly and has a small spine attached. relatively long worms (up to 2. Maryland) . Spicules of all species are paired and long and the tips are fused (A). The black arrow shows the long. N. in small intestine. as clumps resembling cotton wool.

However. Combined with the short prepatent period this will lead to sudden outbreaks of diarrhea in young lambs during the period before and after weaning. In N.As the accompanying image shows. it is also claimed that larval arrest in Nematodirus species is entirely due to host resistance since in Britain there appears to be no obvious seasonal pattern to its occurrence. battus infections in Britain the special hatching requirements ensure that lambs will be invariably exposed to heavily contaminated pastures in late spring. There is no migration within the definitive host and the prepatent period is approximately 15 days. taking as long as 2 months in temperate climates. Its importance therefore is as an additive affect in mixed infections of nematodes causing parasitic gastroenteritis. Nematodirus battus does cause significant disease in lambs in Britain because its unusual hatching requirements may result in heavy contamination of pastures with newly hatched L3s just as lambs are close to weaning and are beginning to graze pastures more in late spring (May and early June in Britain). However. Pathogenesis and clinical signs Nematodirus is not usually a primary pathogen in ruminants in North America. Life-cycle The most important feature of the life cycle is that L3's develop within the protective egg shell. Arrested development has been recorded in sheep in Canada and the northern United States and has been attributed to hypobiosis at the L4 stage as a mechanism for survival over winter. Diagnosis . Adult ewes have developed a strong immunity to Nematodirus and are usually unaffected. Diarrhea followed rapidly by dehydration are the primary clinical signs. Epidemiology The most important factor influencing transmission of Nematodirus species is the ability of L3s to survive from year to year enclosed inside their protective egg shells. the eggs (B) of Nematodirus are approximately twice as large as the typical strongyle-type egg (A). Development is slow.

Nematodirus infections in North America are usually subclinical and the presence of the nematode is diagnosed by detecting the characteristic eggs (A) in fecal floats along with strongyle-type eggs (B) of other trichostrongylid nematodes. However. . diarrhea will often occur before patency and eggs will often be absent in feces.In acute outbreaks of disease in lambs (in Britain).

Species in domestic animals are usually 5-9mm long and males have a prominent bursa in relation to their size. The most distinguishing morphological feature of the genus is the cephalic vesicle. found in all the species. Nematode Species Cooperia curticei Cooperia oncophora Cooperia pectinata Host Species sheep and goats cattle cattle Predilection small intestine small intestine small intestine Cooperia punctata Cooperia surnabada cattle cattle and sheep small intestine small intestine . as shown in the accompanying image of a female. There are five important species in ruminants. Cooperia curticei is easily recognized on microscopic examination by its coiled appearance that has been described as like a "watch spring". In addition the anterior cuticle has transverse striations and these can be seen by clicking on the image or here.. Male spicules are short and their shapes may be used to identify the different species. giving the head end a slightly bulbous appearance when worms are examined under a dissecting microscope or under the low power of a compound microscope. The image on the right shows the tail end of Cooperia oncophora with a prominent bursa typical of the genus and paired spicules whose shape is characteristic of the species.Cooperia Cooperia species are nematodes of the small intestine of ruminants.

Diagnosis Cooperia infections are usually secondary contributors to parasitic gastroenteritis caused by the more important nematodes. Therefore. they are rarely diagnosed as monospecific infections. anorexia and poor weight gains. Ostertagia and Haemonchus. Arrested development is an important feature of the life cycle. Clinical signs A variety of clinical signs have been attributed to Cooperia species and these include diarrhea. The image to the right shows strongyle-type eggs (including Cooperia) and a Nematodirus egg (A) in a fecal sample. Epidemiology Patterns of transmission are different depending on the species. females pass strongyle-type eggs that may be found in host feces. In subtropical areas the patterns of transmission follow those of Haemonchus with hypobiosis during the dry seasons. pectinata and suranabada are believed to be more pathogenic since they penetrate the mucosa during larval development causing changes similar to those of intestinal species of Trichostrongylus.Life cycle The life cycle is direct and similar to the other Trichostrongyles. Pathogenesis Cooperia are generally considered to be mild pathogens. They contribute secondary effects to the primary pathogens Ostertagia and Haemonchus in parasitic gastroenteritis. . However. However. Cooperia punctata. In temperate climates the patterns follow Ostertagia with winter hypobiosis at the L4 stage in the northern hemisphere. weight loss. like most other trichostrongyles.

It seems likely that the reddish appearance of the worms may be due to passive ingestion of hemorrhagic stomach contents during feeding by adults. commonly called the "red stomach worm" of pigs. Seasonal hypobiosis is an important feature of the life cycle in temperate areas of the world. It is a slender worm. anorexia and sometimes diarrhea. 5-10mm in length. loss of condition. The prepatent period is approximately 3 weeks. Infected animals pass "strongyle type eggs" which cannot be distinguished morphologically from Oesophagostomum dentatum and Trichostrongylus axei except by larval cultivation. . parietal cells are replaced by proliferating immature cells that produce nodules (as shown in the accompanying image) similar to those in ostertagiosis. However. Since L3s invade the gastric glands and emerge as immature adults as in ostertagiosis. Life cycle The life cycle is similar to other members of the family Trichostrongylidae. Because of the free-living larval requirements.Hyostrongylus The only species of importance in domestic animals is Hyostrongylus rubidus . transmission has been recorded in pigs raised totally in confinement. infection is mostly seen in pigs with access to pasture. Its reddish color when fresh has led to the assumption that the worm is an active blood feeder although this claim is disputed because its parasitic phase in the host is very similar to Ostertagia species. Heavy infections may produce ulceration of the gastric mucosa with excessive bleeding from ruptured blood vessels giving rise to a hemorrhagic gastritis. It is a common nematode of adult swine. with access to pasture and has a world wide distribution in areas with temperate climates. It causes a hemorrhagic gastritis and usually presents as a chronic wasting disease with anemia. The image on the right shows fresh specimens in the stomach at necropsy. Pathogenesis and clinical signs Pathogenic effects of Hyostrongylus infections are similar to Ostertagia in cattle.

Dictyocaulus head end showing the small mouth opening (arrow). . A summary will be given on this page. The males have a prominent copulatory bursa. especially the bronchi of the diaphragmatic lobes and the trachea. from 3 to 8 cm long. tip(arrow) There are three Dictyocaulus species of importance in domestic anmials. Dictyocaulus showing the dark spicules and one mouth opening surrounded dorsal ray with a trilobed by lips. swallowed and pass out from infected cattle in their feces. Life cycle A fuller description of the life cycle may be viewed by clicking here. They are found throughout the world but are more common and clinically important in temperate areas particularly when summer rainfall is above average. They are thin. L1s migrate up the trachea. are coughed up. The mouth is surrounded by 4 lips and the mouth opening leads into a small buccal capsule. thread-like worms. Scanning electron Dictyocaulus male bursa micrograph of showing the short. Nematode Species Dictyocaulus filaria Dictyocaulus viviparus Dictyocaulus arnfeldi Host Species sheep and goats cattle and deer donkeys and horses Predilection site trachea and bronchi trachea and bronchi trachea and bronchi Dictyocaulus viviparus Dictyocaulus viviparus is the most pathogenic and will be discussed in detail. These hatch immediately.Dictyocaulus Members of the family Dictyocaulidae are unusual among the Trichostrongyloidea in that they parasitize the lungs. Females are ovoviviparus which means that they lay eggs that are already embryonated. fat.

then continue via the lymphatics and blood to the lungs where they migrate through the capillary walls into the alveoli.The preparasitic phase of the life cycle is similar to the other Trichostrongyles. with one exception. they have evolved a method of facilitating their dispersal from the fecal pad to the surrounding grass where they can be ingested by susceptible grazing animals. The final molt occurs and the immature adults move up the bronchioles to the bronchi. Larvae migrate onto the sporangia of the fungus Pilobolus that commonly grows in cattle feces. Image courtesy of Merial Inc Ingested L3s migrate through the intestinal wall to the mesenteric lymph nodes. molt to L4. releasing their spores into the surrounding environment. The prepatent period is 3 to 4 weeks. Because the L3's are not particularly motile. This is shown in the image cartoon on the right. the larvae of Dictyocaulus are also released. as shown in the image to the right. . Image courtesy of Merial Inc When the sporangia explode.

Patent disease is associated with adult worms in the bronchi and manifests as a bronchitis with a mucus exudate followed by pneumonia due to aspiration of eggs and L1's into the alveoli where they are surrounded by inflammatory cells. 3. including macrophages and giant cells. However. permeable alveolar epithelium into a thickened layer of cells that is much less permeable to the passage of oxygen and carbon dioxide. Alveoli fill with transuded fluid and the alveolar walls become lined with protein "hyaline membranes" as water in the transuded fluid evaporates or is reaborbed. 2. postpatent parasitic bronchitis. Eosinophilic plug in a small bronchiole and collapse of surrounding alveoli. Interstitial emphysema and pulmonary edema are common complications of this syndrome and when this stage is reached. Pulmonary edema results from the onset of cardiac failure in animals with dyspnea. . is unknown but is due to a proliferation of alveolar epithelial cells converting the thin. during this recovery phase a small number of animals may succumb to a postpatent parasitic bronchitis or a secondary bacterial pneumonia. These membranes further compromise gas exchange at the alveolar epithelial surfaces and lead to a significant deterioration in clinical condition. bronchioles and bronchi and inducing an inflammatory response. and ingested. death is almost certain. In moderate to heavy infections. Images showing the development of parasitic bronchitis in cattle due to Dictyocaulus viviparus Dictyocaulus viviparus 1. The severity of these lesions is directly related to the degree of infection such that heavy infections may lead to interstitial emphysema and pulmonary edema that is often fatal. The bronchial epithelium is infiltrated by inflammatory cells and becomes hyperplastic.Dictyocaulus viviparus Pathogenesis Severe pathological changes can occur before patency due to larvae and immature adults migrating through the alveoli. Air present in the alveoli is absorbed into the blood and the alveoli collapse because new air cannot pass the eosinophilic plug. In lightly infected animals. the bronchial lesions may take several weeks or months to recover. Heavy infections may progress to emphysema and edema. The etiology of the syndrome. Bronchiolar passages become clogged with inflammatory cells. Larva migrating up a bronchus. Adults in a bronchus with exudation and intense cellular infiltration surrounding the bronchus. including eosinophils. macrophages and neutrophils and if severe enough may result in collapse of alveoli distal to these cellular infiltrates because air cannot pass through these plugs. thereby compromising gaseous exchange at the alveolar surfaces. recovery will occur following expulsion of the adult worm population.

Post patent parasitic bronchitis . Reinfection lesion dead worm surrounded by an eosinophilic necrotic area and proliferating lymphoid tissue. 10.parasitic pneumonia with giant cells and macrophages engulfing aspirated eggs and newly hatched larvae 8. Adult worms in the diaphragmatic bronchi. Many macrophages are present in the lumen of these epithelialized alveoli 9. Gross picture of emphysema 11. 5. Hyaline membranes lining the alveolar surfaces . 6. Parasitic pneumonia with giant cells and macrophages engulfing aspirated eggs and newly hatched larvae 7. Distribution of lung worm lesions in the diaphragmatic lobes.diffuse epithelialization (swelling and proliferation of type II pneumocytes).4. High power . Pulmonary edema emphysema 13. Microscopic picture of 12.

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viviparus is less common than in Europe and often goes undiagnosed because veterinarians are generally unfamiliar with the nematode and the methods used to diagnose infections. viviparus has been reported sporadically in North America during the last 50 years. to the point where disease outbreaks may be seen in susceptible unvaccinated cattle (of all ages).either as fully mature or hypobiotic immature adults . These animals clearly lacked immunity to D. Epidemiological investigations in Britain have concluded that survival of Dictyocaulus and its transmission are dependent on two conditions 1. parasitic bronchitis went undiagnosed and untreated for several weeks after the initial reporting of clinical signs (usually sporadic coughing in animals on pasture) because sick animals were usually treated initially for pneumonia of either viral or bacterial origin. These conditions have resulted . These observations reinforce the point that calfhood vaccination programs must be continued every year with every new group of susceptible calves. In areas of the world where cattle are primarily raised on pasture. Britain and eastern Canada. Contamination levels of L3s eventually build up. although its precise role in transmission has not been determined as yet.sufficient to maintain low level contamination of pastures. These animals often had small numbers of adult Dictyocaulus in their lungs and passed small numbers of L1s . Weather patterns in Britain seem to have changed during the last 10-15 years with dry. viviparus and we can safely conclude that they received little or no exposure to the parasite during their growing phase and so were still susceptible to infections as adults.Dictyocaulus viviparus Epidemiology Calves and yearlings turned out to pasture for the first time are highly susceptible to infections with Dictyocaulus viviparus since their lack of previous exposure means they have not developed an immune response. adult animals will have been already exposed to the parasite during their growing phase and will therefore have a strong acquired immunity. Older animals (yearlings and adults) may serve as carriers over winter in that some adult worms . These areas are mostly in northern Europe including the British Isles. viviparus is endemic in temperate areas of the northern hemisphere with mild summers and high rainfall. warmer summers being more frequent. 2. In the United States. D. D. Use of the lungworm vaccine (Dictol) in Britain was high in the early years after its introduction in 1965. the Pacific northwest and Eastern Canada. The recent increases in cases of parasitic bronchitis in adult cattle. Parasitic bronchitis due to D. Third stage larvae(L3s) may survive over winter on pasture in enough numbers to cause infections and perhaps disease in susceptible animals turned out to pasture in early spring.will survive in the bronchi. in Britain may be attributed to several factors 1. Hypobiosis at the immature adult stage (L5) as been documented in mainland Europe. Cases have been consistently reported from the northeast United States. It is common in cattle-raising areas with permanent pastures used for seasonal grazing. The small numbers of L3s on pasture serve to boost the immune response of vaccinated calves throughout their lives but may produce clinical parasitic bronchitis in susceptible animals. on pasture. vaccinated animals are still susceptible to infection at a low level even though they are protected against disease. Many of these more recent cases were reported in adult lactating dairy cows and all occurred in animals managed on intensive grazing systems. the mid west. However. Over time the annual use-levels of the vaccine in susceptible calves tapered off. Some of these unvaccinated animals would not be exposed to sufficient levels of infections to initiate a protective immune response and would therefore remain susceptible to infections even as adults. 2. In a number of cases reported in the literature.

These kinds of changeable weather patterns make it more likely that calves will grow to adults without significant exposure to D. In warm or hot and dry summers. outbreaks of parasitic bronchitis will be seen more frequently. There is also evidence that deer may serve as reservoirs of infection. This behavior may allow larvae to survive periods of inclement weather that would be hostile to their survival and return to the surface pasture when conditions are more favorable. The vaccine used in western Europe consists of third stage larvae partly attenuated by irradiation and administered orally to calves at least two months old and before they are exposed to infection by turning them out to pasture. There is some evidence that Dictyocaulus larvae may burrow into the soil where it is cooler than on the surface pasture. Two doses of the vaccine are given 4 weeks apart and vaccinated animals should not be placed on pasture until two weeks after the second dose. . In areas of the United States where Dictyocaulus is prevalent. maintaining L3s on pasture at sufficient levels to produce clinical disease in grazing cattle. Dictyocaulus infections and disease will rarely be seen. However. summers are not consistently cool and wet leading to variable levels of pasture contamination with L3s depending on temperature and moisture.in fewer larvae on pasture so that grazing calves have not only experienced fewer outbreaks of parasitic bronchitis but also have not developed strong immune responses to the parasite. As a result they remain susceptible to the parasite through to their lives as adults. viviparus and will therefore remain susceptible to infections. when summers are cooler and wetter than normal.

Mild Moderate Severe infections infections infections Intermittent.head and neck held straight out horizontally with tongue protruded. Salivation. crackles. In adult cattle milk production will be affected. loss of appetite. .Dictyocaulus viviparus Clinical signs In herd outbreaks of parasitic bronchitis. Respiratory distress is characterized by animals assuming the "air hunger" position . They are 310-360 microns long and 16-19 microns wide and the latter two thirds of the body contains prominent dark brown food granules present in the intestinal cells. Confirmation of the diagnosis comes from finding characteristic first stage larvae(L1s) in the feces of animals with patent infections by using a Baerman apparatus. anorexia. Diaphragmatic Diaphragmatic auscultation sometimes lobes lobes .coughing. cough pronounced on exercise Respiratory Often normal Tachypnea 40. Clinical signs in parasitic bronchitis are associated with a progressively developing bronchitis and pneumonia . Frequent even A deep. fever. tachypnea. loss of weight and dyspnea. fever. Other signs None Usually none Respiratory distress (dyspnea). The image on the right shows such a larva. Since D.pronounced occasional pronounced squeaks and squeaks squeaks and crackles. harsh More at rest. a spectrum of clinical signs may be seen as illustrated in the following table.Severe tachypnea rate 60/minute >80/minute Lung Often normal. Clinical sign Coughing Diagnosis The clinical signs of coughing in cattle either on pasture or with a recent history of grazing is usually strongly indicative of parasitic bronchitis due to Dictyocaulus viviparus. gasping for air with head and neck outstretched.

finding these L1s in cattle feces is diagnostic. temperate areas where heavily contaminated pastures with Dictyocaulus L3s may produce severe outbreaks in calves soon after turnout to pasture in the spring. This is particularly true in cooler. At necropsy. with large numbers of developing larvae being destroyed by the immune response. In a herd outbreak of suspected parasitic bronchitis repeat fecal samples should be taken and examined for L1s since clinical signs in heavy infections are usually first seen during the prepatent period. . adult worms may be easily seen in the bronchi of infected lungs. The absence of L1s in the feces of animals with severe clinical signs of parasitic bronchitis usually means that these cattle are strongly immune but are undergoing a severe challenge infection.viviparus is the only lungworm of cattle.

The following table gives an overview of the classification of this order with an emphasis on the superfamily Strongyloidea.The Strongyloidea Strongylida The order Strongylida includes many of the important nematodes found in the gastrointestinal tracts of ruminants. horses.examples Strongylida Trichostrongyloidea Trichostrongylidae Dictyocaulidae Strongyloidea Strongylidae Strongylinae Strongylus Triodontophorus Cyathostominae Cyathostomum Cylicostephanus Cylicocyclus Cylicodontophorus Poteriostomum Gyalocephalus Chabertiidae Chabertiinae Oesophagostominae Chabertia Oesophagostomum Stephanurus Syngamus Syngamidae Stephanurinae Syngaminae Ancylostomatoidea Metastrongyloidea Ancylostomatidae Metastrongylidae Protostrongylidae Filaroididae . Order Superfamily Family Subfamily Genus . as well as the lungworms of ruminants and the hookworms of dogs and cats. and swine.

ellipsoidal "strongyle-type" eggs (A). A fifth (minor) superfamily.Their distinguishing features include a copulatory bursa (in males) and a buccal capsule of variable shape and size. Strongyloidea and Ancylostomatoidea produce smooth. whose species produce eggs that are approximately twice the size of "strongyle-type eggs (B). approximately 80-100 microns long and 40-50 microns wide. the Diaphanocephaloidea. thin-shelled. Notice the difference between these eggs and the whipworm (Trichuris) egg (C). are bursate nematodes found in . One exception to this rule is Nematodirus. There are four superfamilies of importance in domestic animals: Trichostrongyloidea Strongyloidea Ancylostomatoidea Metastrongyloidea Females belonging to the superfamilies Trichostrongyloidea. Examples of direct (free living larvae) and indirect (intermediate host) life cycles can be found among the members of this order.

. There are two genera and thirty three species in this superfamily. Females pass a "strongyle-type" egg and their life cycles are direct and similar to the Trichostrongyloidea but it is also believed that paratenic hosts (snails and slugs) may play a role in their life cycles.the digestive tracts of terrestrial snakes and occasionally lizards.

Development to the infective. moist environment. Some species have life cycles that include extensive migrations through the bodies of their hosts. Most have direct life cycles with infection by ingestion of infective third stage larvae but a few such as Stephanurus dentatus (the swine kidney worm) and Syngamus trachea (the gapeworm of fowl) may include earthworms as transport hosts. the gape worm of birds (Syngamus trachea) and the kidney worm of swine (Stephanurus dentatus). ensheathed third stage larvae may take as little as 7-10 days in a warm. rhinoceros. They use their buccal capsules in feeding. They are primarily parasites of herbivores such as ruminants and horses although a few species are found in ratite birds and marsupials. They have the following general features They are large-bodied worms and are easily seen in situ at necropsy of infected hosts. Equine strongylids are usually divided into the large strongyles. tapirs.The Strongyloidea Members of this superfamily are widespread throughout the world. Leaf crowns may be present as accessory cuticular structures around the opening of the buccal capsule. Most females of this group pass strongyle-type eggs.the Chabertiinae and the Oesophagostominae. Strongylus vulgaris). The preparasitic phases of the life cycles are similar with strongyle-type eggs passing in the feces of infected hosts. Three families are important in domestic animals . Chabertiidae This family has been further subdivided into two subfamilies . drawing it into the buccal capsule and digesting it. ostriches. Most are found in the large intestine but a few species occur in the respiratory and urinary tracts. Their predilection sites include primarily the cecum and colon.g. The Chabertiinae are often called the bowel worms because of their location in the .Strongylidae. warthogs and marsupials. Males have a copulatory bursa Most have large mouth openings and prominent buccal capsules which may contain teeth in some species. tortoises. They include the large strongyles of equines (e. belonging to the subfamily Strongylinae and the small strongyles which are members of the subfamily Cyathostominae. Chabertiidae and Syngamidae Strongylidae Members of this family are common in equines but they are also found in elephants. either by grazing the mucosal surface or by attaching to a plug of mucosa.

zebra. gazelles. Examples of species occurring in domestic and wild animals and birds are given in the following table.colon of their hosts. sheep Ternidens African and deminutus Asian non-human primates Oesophagostominae Oesophagostomum Sheep. cattle. deer. The Oesophagostominae are often called the nodular worms because their parasitic larvae provoke nodule formation in the intestines of their definitive hosts. primates and rodents. alpaca. Adults are found in the colon and are common in pigs. They have a prominent bell-shaped buccal capsule. water buffalo Oesophagostomum Ruminants venulosum primarily sheep and goats Oesophagostomum Pigs quadrispinulatum Syngamidae The syngamids are found mainly in the respiratory systems of birds and mammals but one species occurs in the urinary tract of swine and another occurs in the intestines of porcupines. antelope (African) Oesophagostomum Pigs dentatum Oesophagostomum radiatum Cattle. ruminants. the Stephanurinae and the Syngaminae. chamois. The table below lists the species of this family commonly found in domestic and wild animals. goats. There are two subfamilies. Family Subfamily Species Castorstrongylus castoris Hosts Chabertiidae Chabertiinae North American beaver Chabertia ovina Camels. Family Subfamily Species Hosts . columbianum goats.

felids and elephants in the tropics Syngamus trachea Birds primarily quail.Syngamidae Stephanurinae Stephanurus dentatus Syngaminae. deer. guinea fowl . pheasants. swans Mammomonogamus Cattle. Cyathostoma bronchialis Swine Ducks. geese. spp goats. sheep.

more specifically the walls of the ureter and in capsules in the peri-renal fat. subtropical and tropical areas. In the United States it is more prevalent in the South. so-called because its predilection sites include the kidneys and associated tissues . It is 2-4 cm long. particularly the southeastern states. has a prominent buccal capsule with teeth and males have a copulatory bursa.Stephanurus dentatus This is the kidney worm of swine. Stephanurus dentatus adult worms in situ in the perirenal fat Stephanurus dentatus Stephanurus dentatus adult worms male (upper) adult worms protruding and female (lower) from a ureter . Morphology It is a large-bodied worm with a mottled appearance because its transparent cuticle shows its internal organs. It is the only known species in the genus and is found throughout the world but is more common in warm temperate. It is of particular importance where pigs are raised outdoors because its preparasitic larvae are free living and may also utilize earthworms as transport hosts. where it is also common in feral swine.

Migration of immature adults through other organs such as the pancreas may result in abscesses. fibrosis and adhesions. Repair of these lesions will result in liver scarring and cirrhosis. Skin penetration by infecting L3s may cause cutaneous lesions and swelling of superficial lymph nodes. dentatus during its parasitic phase results in considerable damage to host organs. Batte Image courtesy of Merial Inc Stephanurus dentatus fibrotic tracks resulting from migrations of larvae and immature adults Image courtesy of Merial Inc Stephanurus dentatus extensive fibrosis resulting from migrations of larvae and immature adults Image courtesy of Dr Edward Batte . Edward immature adults.Stephanurus dentatus Pathogenesis The extensive migrations of S. Liver migrations produce a marked inflammatory reaction with eosinophilia. Images showing liver lesions due to migrating Stephanurus dentatus Normal pig liver for Stephanurus dentatus comparison with the other liver lesions caused by images in this table migrating larvae and Image courtesy of Dr.

The usual picture is one of failure to thrive with the primary effects on weight gains. As a result. The long prepatent period of 9-16 months means that pigs are raised . In this system.S. Strongyle-type eggs were present in the urine and at necropsy there were extensive liver lesions and adult worms in the perirenal areas. kidney worm infections are more common in the southern United States. bred and marketed before infections become patent and this system was shown to be an effective method of controlling transmission of Stephanurus dentatus. The image to the right is of a pig showing chronic effects of Stephanurus dentatus infections.Stephanurus dentatus Epidemiology Free living larvae cannot survive the cold temperatures encountered during winters in the northern U. Heavy infections in pigs raised outdoors may cause enough liver damage to result in emaciation and death. Infected older sows and boars are the usual source of infection for younger animals and the longevity of adult worms in their host (2-3 years) means that adult infected pigs may be constant sources of infections for young animals. Diagnosis . The dependency of the life cycle on free living preparasitic larvae and earthworms as transport hosts means that this is a parasite primarily seen in pigs raised outdoors. Clinical signs Overt clinical signs are unusual in Stephanurus infections. breeding is confined to gilts which are then marketed immediately after weaning their first litters. The "gilts only" system of breeding and rearing pigs was devised as an effective method to control swine kidney worms. Raising pigs indoors will significantly reduce the prevalence of kidney worms. The problem is that the system fails economically since gilts have smaller litters than older sows and the economic return from these smaller litters is not enough for the system to be viable. Aberrant migrations of larvae to the spinal cord may cause a posterior paralysis but these cases are not common. Batte and his colleagues demonstrated transplacental transmission in pregnant gilts but it is uncertain how important this is as a factor in transmission.

Infections often go undiagnosed in live animals. Therefore infections are more often diagnosed at necropsies or at meat inspections when the characteristic liver lesions are found. .The long prepatent period of Stephanurus means that patent infections are unusual in pigs less than two years old. Infections in adult sows and boars are easily diagnosed by finding the distinctive strongyle-type egg in urine of infected animals .as shown in the accompanying image. especially in pigs less than a year old.

plugging the air passages and. turkeys. Epidemiology Earthworm transport hosts are important factors in the transmission of Syngamus trachea where poultry and game birds are reared on soil. Earthworms play an important role in the life cycle. Other invertebrates may also serve as paratenic hosts and these include terrestrial snails and slugs as well as the larvae of Musca domestica (the common house fly) and Lucilia sericata (the greenbottle fly responsible for cutaneous myiasis). found in the trachea of chickens.Syngamus trachea This is the gapeworm of poultry. Life cycle The life cycle is complicated in both its preparasitic and parasitic phases. The longevity of L3s in earthworms (up to 3 years) is particularly important in perpetuating the infection from year to year. Larvae have been shown to remain viable for more than three years encapsulated in earthworm muscles. causing asphyxiation. It is of particular importance in farm-raised pheasants. in severe cases. guinea fowl and many species of wild birds. In the preparasitic phase L3s develop inside the eggs at which time they may hatch. serving as transport (paratenic) hosts. Morphology The most distinctive feature of this nematode is that males and females are joined together in a state of permanent copulation forming a Y shape as seen in the image on the right. Although Syngamus is found throughout the world. Females are much larger (up to 20mm long) than males (up to 6mm long). Pheasants appear to be particularly susceptible to Syngamus infections resulting in mortality rates as high as 25% during outbreaks. Worms in the bronchi and trachea provoke a hemorrhagic tracheitis and bronchitis with formation of large quantities of mucus. The parasitic phase involves substantial migration in the definitive host to reach the predilection site. Lymphoid nodules form at the point of attachment of the worms in the bronchi and trachea. Adult worms appear also to be blood suckers. conversion of domestic poultry raising from outdoors to indoors has significantly reduced its prevalence in the United States. Wild birds may serve as reservoirs of infection and have been implicated as the sources . Pathogenesis Young birds are most severely affected with migration of larvae and adults through the lungs causing a severe pneumonia.

magpies. jackdaws. starlings and crows. robins. meadowlarks. These clinical signs first appear approximately 1-2 weeks after infection. grackles. partridges. will deteriorate rapidly. death is the usual outcome. rooks. open their mouths and gasp for air producing a hissing noise as they do so. Diagnosis A diagnosis is usually made on the basis of the classical clinical signs of "gaping". They stretch out their necks. Subclinical infections with few worms may be confirmed at necropsy by finding copulating worms in the trachea and also by finding the characteristic eggs in the feces of infected birds. turkeys. particularly young ones. Adult birds are usually less severely affected and may only show an occasional cough or even no obvious clinical signs. This "gaping" posture has given rise to the common term "gapeworm" to describe Syngamus trachea.adult worms in the trachea of an infected turkey . At this stage. Severely affected birds. Syngamus trachea bioperculate egg Syngamus trachea . There is also evidence to suggest that strains of Syngamus trachea from wild bird reservoir hosts may be more infective for domestic birds if they first pass through an earthworm transport host rather than by direct infections via ingestion of L3s or eggs containing L3s. Clinical signs Blockage of the bronchi and trachea with worms and mucus will cause infected birds to gasp for air. Wild reservoir hosts may include pheasants.of infections in outbreaks on game-bird farms as well as poultry farms. jays. ruffed grouse. they stop drinking and become anorexic.

This results in area of mucosal ulceration and local hemorrhage with protein loss into the gut through these lesions. Epidemiology Infective third stage larvae will survive mild winters on pasture. in Australia and South Africa it has been recorded as a primary pathogen in sheep. The image on the right shows the head end of Chabertia ovina with its buccal capsule curved anteriorly and ventrally. Some reports claim that larvae and immature adults are blood suckers. its predilection site is the colon of sheep and goats and it is occasionally seen in cattle. Pathogenesis Pathogenic effects are caused by the feeding adults which become attached to the mucosa and draw a plug of mucosa into the buccal capsule which is then digested. curved. These emerge. The prepatent period is approximately 6 weeks. Chabertia ovina is one of the easiest ruminant nematodes to identify because of its size (1-2cm long). It has a worldwide distribution but it tends to be more common in temperate areas of the world. However. After ingestion by the final host. In the United States. Hypobiosis is also an important winter survival mechanism in the life cycle of this nematode with L4s being the hypobiotic stage in the mucosa of the small intestine or the cecum. In heavy infections.Chabertia ovina Chabertia ovina is commonly called the large-mouthed bowel worm. bell-shaped buccal capsule which lacks teeth. In domestic animals. Otherwise. infected sheep may lose weight and condition and may become . molt to immature adults (L5s) and pass on the colon to mature. In most parts of the world. Clinical signs Diarrhea is the usual clinical sign in Chabertia infections where it is seen as a primary pathogen. Chabertia is not a primary parasite in terms of disease. Life cycle The life cycle is direct with the preparasitic phase similar to the Trichostrongyles. L3s exsheath in the small intestine. Chabertia ovina is relatively uncommon but is found primarily in more temperate areas of the north. penetrate the mucosa and molt to L4s. gather in the cecum. location (colon) and its prominent. Its effects are usually additive to more important pathogens such as Ostertagia and Haemonchus. the feeding effects of 200-300 adult worms results in a colon that is edematous and thickened with local areas of hemorrhage where the worms were attached.

In heavy infections. In these cases eggs will be absent from feces but since these are strongyle-type. . clinical signs may occur during the prepatent period since immature adults are aggressive feeders. size and shape of the buccal capsule.anemic. Diagnosis A specific diagnosis is not usually possible in live animals for the reasons mentioned above. At necropsy the worms are readily identified from their location. they cannot be distinguished from the eggs of many other trichostrongyle and strongyle nematodes infecting the guts of ruminants.

Males have a bursa and the egg passed by the female worms is a strongyle-type egg Oesophagostomum Oesophagostomum Oesophagostomum columbianum . B = cervical vesicle Image courtesy of The specimen to the C = cervical alae right of the pin is a Merial Inc male L4 with a dorsally curved tail. . pigs. primates and rodents.adult radiatum with posterior end worms with a pin to cuticular show comparative modifications at the showing the copulatory bursa (A) sizes. The species found in domestic animals are often of pathogenic importance: Nematode Species Oesophagostomum radiatum Oesophagostomum columbianum Oesophagostomum venulosum Oesophagostomum dentatum Oesophagostomum quadrispinulatum Host Species cattle cattle sheep and goats swine swine Adults are 1-2cm long.Oesophagostomum species Morphology and species Members of this genus are known as the "nodular worms" because they are associated with nodule formation in the intestines of their hosts. rays. The buccal capsule is relatively shallow and the head end is distinctive because of the cephalic inflations of the cuticle.the dentatum . They are common parasites of ruminants. The female anterior end: (left of the pin) is the A = cephalic vesicle containing bursal thicker of the two.

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Oesophagostomum radiatum in cattle is common throughout the world especially in tropical and subtropical areas and is also common in North America. Chronic infections will produce an intestinal mucosa that is filled with nodules particularly if these repeat infections have been heavy. However. columbianum is more commonly seen in tropical and subropical areas. Acute infection with Oesophagostomum radiatum in cattle. Hypobiosis at the L4 stage is the primary method of survival of O. Therefore older animals will usually show extensively nodular intestines but with few. apparently because it does not stimulate nodule formation. in which cases they are more properly described as small abscesses. In sheep. most infecting larvae will be killed by host reactions. if any. When larvae move back into the intestinal lumen the remaining nodules may be hemorrhagic particularly in acute infections but often they fill with pus. In these chronic cases tissue reactions are more severe and the nodules are much larger (up to 6mm in diameter) and creamy in color due to the development of connective tissue around them. After initial infections. Oesophagostomum venulosum is much less pathogenic than Oesophagostomum columbianum. In tropical areas with seasonal rainfall (such as Queensland in Australia) heavy infections with high mortalities may be seen in calves under natural grazing conditions during the rainy season. infections with 500 L3s have been reported to produce a transient diarrhea accompanied by petechiae and small ulcers in the small intestine. In chronic infections. In sheep and goats. Hemorrhagic nodules in the small intestine. Chronic infection with Oesophagostomum dentatum in pigs. venulosum preparasitic larvae are similar to those for Ostertagia and Trichostrongylus and therfore it is more common in temperate areas. venulosum during . the mucosa becomes inflamed and edematous and regional lymph nodes are often much enlarged. Fibrous nodules in the small intestine. small nodules about 1mm in diameter form around larvae in the mucosa. Epidemiology All domestic animals are infected by grazing pastures contaminated with L3s. Oesophagostomum columbianum is seen throughout North America except for the west coast. In heavy infections. The climatic requirements for survival of preparasitic larvae are similar to Haemonchus contortus therefore O. adult worms in the colon. the requirements for survival of O.Oesophagostomum species Pathogenesis The most serious problems seen in Oesophagostomum infections arise from larvae penetrating the musosa of the intestine.

It is speculated that hypobiois may occur in O. the easy development of infective larvae in feces and pen to pen transmission by dipteran flies carrying infective L3s on their legs. quadrispinulatum also undergo hypobiosis at the L4 stage in pigs but L3s are also known to survive winters on pasture. Transmission of Oesophagostomum in housed pigs has been explained by the possibility of percutaneous infections. The resumption of development of these two species in spring can give rise to a periparturient rise in egg counts(PPR) in pregnant and lactating sows. columbianum although definite experimental confirmation of this is still awaited. O. .winters in temperate areas of the world. dentatum and O.

Chronic oesophagostomosis is most common in sheep and is due to repeated infections. . In chronic infections. This syndrome shows as weight loss after farrowing and reduced milk production with adverse effects on the growth of litters. strongyle-type eggs will be commonly seen but are indistinguishable from eggs produced by other strongyle nematodes. Necropsies will show the classic nodular lesions throughout the small and large intestines Growing pigs (4-5 months old) with acute diarrhea due to a prepatent infection with Oesophagostomum dentatum Strongyle-type eggs from a patent experimental infection with Oesophagostomum dentatum in pigs. Diarrhea is the usual clinical sign in these cases and may be accompanied by weight loss and submandibular edema ("bottle jaw") in ruminants. Infections in pigs may produce a range of clinical signs including acute diarrhea and a syndrome in adult females called the "thin sow syndrome" . Intermittent diarrhea accompanied by loss of appetite are the usual clinical signs and in more severe chronic cases sheep may become emaciated and anemic. Diagnosis In acute infections clinical signs will occur during the prepatent period and diarrhea will occur without strongyle-type eggs being seen in the feces of infected animals.a chronic infection with periodic acute flare-ups due to the resumption of development of hypobiotic larvae during spring farrowing.Oesophagostomum species Clinical signs Acute infections are the result of larval penetrations of the intestinal mucosa during the prepatent period.

warthogs and marsupials in Australia. Both groups are among the most important nematodes of domestic equines throughout the world because of their high degree of pathogenicity and they are certainly so in North America. Superfamily Family Subfamily Genus . The strongylidae are further divided into two subfamilies.Strongyles of Horses The intestinal strongyles of horses are members of the superfamily Strongyloidea and the family Strongylidae. Members of the family are abundant in equines. including horses and donkeys. rhinoceros. . but are also found in diverse hosts including elephants. ostriches. tortoises. tapirs.examples Strongylus Triodontophorus Cyathostomum Cylicostephanus Cylicocyclus Cylicodontophorus Poteriostomum Gyalocephalus Strongyloidea Strongylidae Strongylinae (large strongyles) Cyathostominae (small strongyles) The strongylinae are commonly called the "large strongyles" because of their larger size relative to the cyathostominae which in turn are called the "small strongyles". the Strongylinae ( the large strongyles) and the cythostominae ( the small strongyles) as shown in the table below.

The predilection site for all species is the cecum and colon and because of their size they are readily visible at necropsy as seen in the image on the right. Strongylus species are commonly found throughout the world and they are of particular importance in horses in North America. Mature adults of these species can usually be identified by their relative sizes but more precise identification. is based on microscopic features such as the shape of the buccal cavity and the presence or absence of teeth. Strongylus equinus The buccal cavity contains 3 teeth . The buccal cavity is devoid of teeth. Mature adult worms are 4-5cm long. Mature adult worms are about 2cm long. The three species are Strongylus vulgaris. Mature adult worms are 5cm long. These features of strongylus species are illustrated in the table below. Adult worms are destructive feeders on the mucosa of the cecum and colon and parasitic larvae undergo extensive migrations in their equine hosts causing significant damage to organs during their migratory routes.1 large and 2 small. the genus Strongylus and the genus Triodontophorus. All three species are important pathogens of horses. They are especially pathogenic in susceptible foals and yearlings. The buccal cavity contains 2 ear-shaped teeth. Strongylus edentatus and Strongylus equinus. . especially immature adults and L4s. Strongylus edentatus.Large Strongyles of Horses Species and morphology The large strongyles are members of the subfamily strongylinae which includes two genera in domestic horses and donkeys. Strongylus vulgaris.

Triodontophorus appears to be the more common species and it is usually seen at necropsy gathered in clusters around ulcers in the colon. Triodontophorus adults feeding at an ulcer in the colon of a horse. . Head end of Triodontophorus showing its large buccal cavity with teeth at the base and fringed by a prominent leaf crown around the opening.Several Triodontophorus species are found in horses but they appear to be less pathogenic than Strongylus because no migrations occur in the host although the buccal cavities of adults contain teeth so damage does occur in the large intestine due to their feeding activities.

we know the least about the parasitic phase of the life cycle of Strongylus equinus because it is less common than the others and so has been little studied. they begin to migrate back to the large intestine by leaving the liver and crossing the abdominal cavity directly or by first passing through the pancreas ( which is closely associated with the right lobe of the liver) and then the abdominal cavity. L5s penetrate the gut wall and enter the lumen of the large intestine via the formation of nodules. Reproduction takes place and the prepatent period is approximately 9 months.immature Strongylus edentatus . Strongylus edentatus . after which larvae wander throughout the liver before they leave beginning about 42 days after infection. Of the three large strongyles. Infection is by ingestion of third stage larvae and exsheathment occurs in the small intestine. They migrate through the wall of the cecum and colon via formation of nodules.Large Strongyles of Horses Strongylus equinus . Finally. .life cycle The preparasitic phase of this life cycle is virtually identical to that of Strongylus vulgaris described previously. through the hepatic ligament and underneath the parietal peritoneum to the right flank. Larvae escape from the liver by migrating under the liver capsule. Strongylus edentatus .an immature adult (arrow) having returned to the large intestine via the nodule (N). the right lobe of which is in close aposition to the cecum. Most L4s will have reached the liver by 19-20 days after infection and will remain there for at least 12 weeks. The final molt to immature adults (L5s) occurs about 15 weeks after infection during their migration back to the large intestine. L4s leave their nodules and cross the peritoneal cavity to the liver. penetrate blood vessels and migrate to the liver via the hepatic portal vein.an adults under the peritoneum of immature adult dissected out of a subperitoneal cyst on the right the right flank. flank. Ingested L3s exsheath in the terminal portion of the small intestine as well as the cecum and right ventral colon. cecum and colon and become encapsulated in nodules in which they molt to L4s by 12-14 days after infection. Here they molt to immature adults between 13 and 15 weeks after infection and finally return to the large intestine via the mesentery bertween 3 and 5 months after infection.life cycle Again. Exhseathed L3s invade the wall of the small intestine. Molting to L4s occurs in two weeks (range from 11 to 18 days). the preparastitc phase of this life cycle is virtually identical to that of Strongylus vulgaris described previously. Maturation takes place in the large intestine and the prepatent period is generally acknowledged to be approximately 11 months although it is claimed by some authors that this may be as short as 6 months. invade the gut wall. Strongylus edentatus .

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However. if the damage is deep into the muscularis. digested by secreted enzymes then drawn into the intestine by the sucking action of the muscular esophagus. It is generally accepted that although these nodules may each be several centimeters in diameter. they leave behind ulcerated nodules that appear to heal quickly. Large nodule (N) caused by an immature adult of Strongylus edentatus (arrow) migrating through the wall of the large intestine onto the mucosal surface. they are of of minor clinical consequences in horses with large intestines that measure 12 feet or more in length depending on the size of the horse. The pathogenic effects due to adults in the cecum and colon of infected horses are similar in all three species of large strongyles because they all provoke the formation of nodules in the gut wall as they pass through in completing their parasitic migrations and their methods of feeding are similar. Pathophysiological studies by Duncan and Dargie have shown that 30ml of blood may be lost per day by foals infected with 75-100 Strongylus vulgaris adults. They attach to the mucosa of the large intestine by their mouth openings and draw a plug of mucosa into the buccal cavity where it is ground up by teeth. granulation tissue will be formed and healing will result in a circular scar at each feeding site. After the worms have escaped into the lumen of the gut. . Nodules casued by immature adults of Strongylus vulgaris migrating through the wall of the cecum onto the mucosal surface All three strongylus species have large buccal cavities and are aggressive feeders. damage to mucosal blood vessels during feeding may cause significant blood loss particularly if the damage extends to the level of the muscularis mucosa. Although these worms do not appear to be actual blood suckers. These ulcers appear to heal readily after the feeding worms move on. Adult worms then move to a fresh site leaving behind small bleeding ulcers that may be seen as red spots at necropsy. as is often the case with the largest of the three strongyles (Strongylus edentatus). The formation of nodules in the gut wall appears to be a mechanism to allow immature adults to migrate from the serosal to the mucosal side without the leakage of gut contents into the peritoneal cavity. if present.Large Strongyles of Horses Pathogenesis of adult worms in the large intestine The pathogenic effects due to large strongyle infections in horses can be divided into those caused by adult worms in the large intestine and those caused by larvae and immature adults during their extensive migrations in other organs.

Strongylus vulgaris feeding by drawing a plug of mucosa into its buccal cavity. . Red dots are sites of its buccal cavity. Strongylus edentatus feeding by Large strongyles attached to the drawing a plug of mucosa into mucosa. previous attachments.

A summary of these reports has been given by Ogbourne and Duncan in a 1985 publication from the Commonwealth Institute of Parasitology entitled "Strongylus vulgaris in the horse: its biology and importance. after By 9 months after infection. . 8-10 days Arteritis extends through the muscularis mucosa to after the serosa. infection Fibrin tracks in teh aorta associated with some larvae migrating beyond the cranial mesenteric artery. 4-9 months In the absence of reinfection. the endothelial lining of infection affected arteries is smooth again and there are few indications of damage other than histological evidence of fibrosis in arterial walls and the presence of macrophages. Arterial walls become thickened and histological sections show a marked cellular infiltration including neutrophils. Time sequence of lesions caused by infections with Strongylus vulgaris 0-48 hours Mucosal hemorrhages in the ileum. arterial lesions heal.Strongylus vulgaris Pathogenesis due to larval migrations Strongylus vulgaris is the most pathogenic of the large strongyles because of the prolonged (at least 4 months) and extensive migrations through the mesenteric arterial system and its branches before returning to mature in the cecum and colon. Significant infiltration of neutrophils in the submucosa. providing a focus for clot formation. infection 0-7 days Inflammation of small intestinal arteries in the after submucosa and formation of thrombi along the infection tracks of migrating larvae. These clots (thrombi) are accompanied by inflammation and a progressive thickening of the arterial walls. 3 weeks-4 The wall of the cranial mesenteric artery is thickened months and fibrous and thrombi are associated with the after presence of 4th stage larvae and immature adults. cecum and after colon. macrophages. the dorsal infection and ventral colon and the cecum) to the cranial mesenteric artery. The time sequence of lesions caused by migrating larvae following experimental infections are summarized in the table below and have been gleaned from many reports in the literature. Larval migrations cause damage to the smooth endothelial surfaces of arteries. infection 11-21 days Arteritis extends along all the branches of the after ileo-cecal colic artery (supplying the ileum. lymphocytes and plasma cells.

infarction and necrosis of areas of the intestine are usually found at necropsy. However. Some reports in the literature describe aneurysms of the cranial mesenteric artery and its branches. The lumen of smaller arteries may be entirely occluded. In horses that have died of an acute clinical syndrome. vulgaris larvae. lesions have also been found less commonly in other arteries including the abdominal aorta. Necrosis of the cecum and ventral colon of a horse resulting from ischemis and infarctions due to lesions produced by migrating larvae of Strongylus vulgaris. . The walls of the cranial mesenteric and the ileo-ceco-colic arteries are invariably thickened and contain large amounts of thrombus material in which are found S.In naturally infected animals. The dorsal aorta of a horse showing fibrin tracks due to migrations of Strongylus vulgaris larvae beyond the root of the cranial mesenteric artery. Images illustrating the pathogenesis of Strongylus vulgaris infections in horses The celiac axis and its branches and the cranial mesenteric artery and its branches showing thrombosis and thickening of arterial walls due to Strongylus vulgaris larval migrations. This lesion is properly called verminous arteritis. the renal arteries and the celiac axis. True aneurysms with dilation and thinning of the arterial wall due to a loss of elastic fibres are unusual and may result from penetration of the elastic layer of the arterial wall by larvae. The lumen of the cranial mesenteric artery is usually constricted in its diameter due to the thickening of the wall and the presence of thrombi. arterial lesions are most commonly seen in the cranial mesenteric artery and its branches. These areas of infarction invariably coincide with occlusions (due to thrombi and emboli) in arteries supplying blood to the affected region(s) of the intestine.

Arteriographic picture of the abdomen of a foal 60 days after infection with 50 third stage larvae of Strongylus vulgaris and treatment at 30 days with a larvicidal anthelmintic. Arteriographic picture of the abdomen of a foal 60 days after infection with 50 third stage larvae of Strongylus vulgaris. .Arteriographic picture of the abdomen of a foal 30 days after infection with 50 third stage larvae of Strongylus vulgaris.

Acute reaction in the liver of a Extensive fibrosis in the liver of Strongylus edentatus .an foal 2 months after infection with a foal 5 months after infection immature adult dissected out of a subperitoneal cyst on the right Strongylus edentatus.Strongylus equinus and Strongylus edentatus Pathogenesis of migrating stages Migrating larvae of Strongylus equinus and edentatus do not appear to cause pathological changes of enough severity to translate into recognizable clinical signs. Whether or not these nodules may themselves produce colic in horses is debatable. Although these lesions have no clinical significance. with Strongylus edentatus. their presence certainly indicates recent infections and it is safe to assume that such horses will also be infected with other large and small strongyles and these may be primary contributors to the observed signs of colic. Abdominal surgery in a horse with chronic colic showing hemorrhagic nodules in the small intestine caused by larvae of Strongylus equinus Necropsy of a horse showing Cross section of a larvae of hemorrhagic nodules in the Strongylus edentatus in the liver intestine due to migrating larvae of a foal 62 days post infection. However. of Strongylus equinus. flank. migrations of larvae through the liver may produce nodules and formation of fibrous tissue that are readily seen at necropsies of infected horses. The early migrations of Strongylus equinus larvae into the intestinal mucosa produce hemorrhagic nodules that are easily recognized at necropsy or during abdominal surgery in horses with colic. they do indicate the presence of strongyle infections and a poor parasite control program in the farm of origin. However. . The life cycle of Strongylus edentatus includes migration to the flanks where immature adults and L4s may be found at necropsy enclosed in subperitoneal cysts.

in particular. The image to the right shows the head end of a cyathostomum species with its obvious buccal capsule and with a prominent external leaf crown at its apex. Thus they are commonly called the Cyathostomes. Image courtesy of Merial Inc Superfamily Family Subfamily Genus ..examples Strongylus Triodontophorus Cyathostomum Cylicostephanus Cylicocyclus Cylicodontophorus Poteriostomum Gyalocephalus Strongyloidea Strongylidae Strongylinae (large strongyles) Cyathostominae (small strongyles) . Species are differentiated on the basis of size. characteristics of the buccal capsule and.The Small Strongyles Species and morphology The small strongyles include 40 or so species that commonly infect the cecum and colon of horses and donkeys. Approximately 30 of these have been assigned to the subfamily cyathostominae. the arrangement of internal and external leaf crowns. They vary in size from 6 to 22mm in length with a reasonably well developed buccal capsule that is also much smaller than those seen in the large strongyles.

For example Cylicostephanus species appear to develop in the mucosa producing small red to blackish nodules 2-3mm in diameter. In horses with light infections. but a few species will go as far as the muscularis mucosa. edema and copious production of mucus. Encapsulated small strongyle Encapsulated small strongyle larvae in the cecal wall as seen larvae shown via trans-mucosal at necropsy.lesions become coalesced and result in a generalized disruption of the mucosa. a more intense cellular infiltration. The size and location of nodules appears to depend on the species involved.Poynter has recorded as many as 60 nodules per square centimeter of mucosa in work published in 1970 and others have recorded similar numbers. Cylicocyclus and Gyalocephalus species penetrate to the submucosa and provoke larger nodules anywhere from 3-6mm in diameter. Mucosal dwelling larvae become surrounded by fibroblasts. However. These nodules are readily visible at necropsy and may be quite numerous . pathological changes tend to be restricted to the encapsulated larvae and the immediately surrounding areas. However deep the penetration. Histological sections will show goblet cell hypertrophy and hyperplasia around the capsule with an accompanying infiltration of lymphocytes and eosinophils.Small strongyles Pathogenesis . In heavy infections the pathological changes are correspondingly more serious . illumination. Surface ulcerations may be common and result from larvae escaping from their nodules. Larvae in the submucosa provoke a similar but more intense reaction and the capsule is usually thicker. .larval stages The larvae of most cyathostome species penetrate the gut wall as far as the mucosa but no further. with the use of more effective anthelmintics in parasite control programs far fewer nodules have been seen at necropsies in more recent times. The latter becomes particularly intense as the larvae emerge from their capsules to reenter the gut lumen. all larvae become encapsulated in small nodules in which they continue their development.

However. Their shallow buccal capsules mean that they feed mainly by grazing on surface areas of the mucosa in contrast to the larger bites taken by the large strongyles. catarrhal and fibrinous enteritis.A close-up view of encapsulated Histological section of the large small strongyle larvae in the intestine showing an cecal wall. Mucus production tends to be significant and some areas of the mucosa may have fibrinous deposits.adult stages Pathological changes due to adult small strongyles tend to be less severe than those due to either their larval stages or adult large strongyles. . larval migrations of Strongylus vulgaris are potentially more pathogenic because of their migrations through the mesenteric arterial system. However. heavy infections tend to produce gross changes in the cecum and colon that are characterized by hemorrhagic. In these animals. small strongyles tend to be present in much greater numbers than large strongyles so their cumulative effects can be more serious especially where parasite control programs are poorly implemented or ineffective. Pathogenesis . The mucosa tends to be thickened and edematous with varying numbers of ulcers produced by larvae escaping from their nodules. The color of the mucosa varies from a normal greyish pink with varying numbers of small hemorrhages to a dark red in severe infections. encapsulated small strongyle larva in the mucosa Pathological changes tend to be more severe in equines less than two years old.

The biological characteristics of the preparasitic stages of the small strongyles and of Strongylus vulgaris are well known and are presumed to be similar for the other two important species of large strongyles in equines. The table below illustrates this point. within this temperature range there are constraints on the number of hatched larvae that will develop through to infective third stages (L3s). in the absence of good parasite control programs. are common in horses. This means that in most temperate areas of the Northern Hemisphere eggs will hatch only from March through October. They appear to have adapted to a wide range of climatic conditions and. donkeys and mules throughout the world. the number of hatched larvae that will reach the L3 stage is also directly dependent on the prevailing temperature.Epidemiology of Equine Strongyle Infections (US predominantly) The large and small strongyles are cosmopolitan parasites. Most of our current information comes from studies conducted in temperate climate zones in the Northern Hemisphere with pronounced seasonal changes in weather conditions. Effects of temperature on development of strongyle larvae from hatching to infective L3s Temperature % hatched larvae developing to L3s 0% 3% 17% 35% 55% 65% 68% 44% 32% 10% 0% Time for hatched larvae to develop to L3s ------->35days 26days 16days 8 days 6 days 5 days 4 days 3 days 2 days -------- <8'C (46'F) 10'C (50'F) 12'C (54'F) 15'C (59'F) 20'C (68'F) 22'C (72'F) 25'C (77'F) 28'C (82'F) 30'C (86'F) 35'C (95'F) >38'C (100'F) The highlighted row in the table shows the optimum temperature(25'C/77'F) at which the maximum number of hatched L1s(68%) develop to L3s within the shortest time (5 . Hatching and development Eggs of equine strongyles will only hatch between 8'C (46'F) and 38'C(100'F). Laboratory studies have shown that few hatched larvae will survive at the upper and lower extremes of this temperature range and within this range. Strongylus equinus and Strongylus edentatus. However.

In the northeast. transmission will decline. the Pacific Northwest (especially the coastal areas of Washington and Oregon) and northern California. There will be negligible transmission in the winter months of December. However. Hypobiois in cyathostomes is an important consideration in developing parasite control programs because these arrested larvae are refractory to treatment with many of the anthelmintics used in horses. Temperature patterns in this region suggest that transmission will be optimal in May and June will fall off in July and August and will rise to optimal levels again in September and October. Synchronous emergence of large numbers of previously arrested L4s occurs in early spring and is the cause of the clinical syndrome known as larval cyathostomosis.days). However. As with Ostertagia. January and February. transmission of equine strongyles will generally follow that pattern. These figures suggest that in the United States transmission of equine strongyles will occur in most regions from mid April through mid November. . including Ivermectin and Moxidectin. Minimal transmission will occur from November through March. transmission of equine strongyles is likely to follow the European pattern with transmission occurring from May through mid October and maximum transmission during the summer months of June. in the hot summer months of July and August when temperatures often exceed 85'F and may sometimes reach 100'F. L3s thus stimulated will undergo hypobiosis if they are subsequently ingested by grazing equines before winter ensues. it is also known that larval emergence from hypobiosis may occur throughout the year and it is theorized that hypobiosis may be used by the cyathostomes as a mechanism of controlling the numbers of adult worms in the gut. In northern New England. In the southeast states. mid west and mid atlantic states. This hypothesis is supported by the observation that treating horses with an anthelmintic to eliminate adult cyathostomes from the gut will stimulate the development of hypobiotic EL3s to repopulate the cecum and colon with adult worms. Arrested development Some species of cyathostomes are able to undergo hypobiosis (arrested development) as exsheathed. In north temperate areas of the world this occurs in winter and hypobiosis is clearly a mechanism of survival for these nematodes. Haemonchus and other ruminant nematodes hypobiosis in the cyathostomes stops the life cycle in the host at a time when prevailing environmental conditions are hostile to the survival of eggs and preparasitic larvae. temperature patterns suggest that transmission of equine strongyles may be significant throughout the year except for the very hot summer months of July and August when transmission will be minimal because prevailing temperatures often exceed 90'F and few larvae will survive for long on pastures at these temperatures. July and August. Little is known about the biology of hypobiosis in cyathostomes but it is presumed that the signal for arrest is received by pasture L3s and that the signal is a falling prevailing temperature in fall and early winter. encysted early third stage larvae (EL3s) in the intestinal mucosa of infected horses.

Epidemiology of equine strongyles Seasonal changes in strongyle egg counts Field observations of strongyle egg counts in mares and other adult horses throughout the Northern Hemisphere show a distinct seasonal pattern.g. In these areas. grazing horses may be at risk during spring. Florida) high levels of pasture L3s may persist over winter and present problems to grazing horses during this time. Clearly these infections could not have come from ingested larvae that had over-wintered on pasture because. similar to that in the image to the right. Infections in grazing horses from this second wave of pasture L3s. This is because under natural grazing conditions horses are infected with tens of thousands and sometimes even hundreds of thousands of adult small strongyles and only several hundred or at most a few thousand adult large strongyles. In the hot summer months. in certain parts of the southern United States where winters are exceptionally mild (e. Eggs passed onto pasture in the second wave of egg counts in August are readily translated into rising levels of L3s. An initial wave of strongyle egg output in horse feces occurs in May and this is presumably due to the emergence of arrested larvae from the mucosa in early spring followed by their development to egg-laying adults. in fact. infections of newly weaned foals in spring and early summer. Necropsies of horses with high strongyle fecal egg counts in March. Several studies in the southeast and midwest have shown a pattern of strongyle egg counts and pasture L3 levels. it is also postulated by some that small strongyles may undergo hypobiosis during the hot summers prevalent in the southeast. They begin to rise in March. Since rainfall is more abundant and temperatures are lower than they were in July and August these L3s survive longer. As environmental temperatures rise these eggs hatch and develop rapidly to infective L3s providing a source for constant reinfection of grazing horses and. . fall and winter. Pasture levels of L3s fall off rapidly in July and August because hot summer temperatures are quickly lethal to all preparasitic stages. peak anywhere from July to October and decline over winter to a low level in February and March before beginning to rise again. more importantly. April and May show large numbers of cyathostomes in the cecum and colon. However. minimal transmission of small strongyles occurs because pasture L3s die off rapidly in the hot temperatures and. The rise in strongyle egg counts in grazing horses in spring comes primarily from adult cyathostomes that survived winter as hypobiotic EL3s in the intestinal mucosa and resumed their development to adults in late winter and early spring. will be seen as arrested EL3s in the mucosa over the subsequent winter. Strongyle eggs on pasture develop rapidly to infective L3s and their ingestion by grazing horses in June result in patent infections 6-8 weeks later as shown by the second smaller peak in egg counts. Differential larval counts have shown that more than 90% of these strongyle eggs come from small strongyles with only a small percentage (4-10%) coming from large strongyles. so few L3s survive this way.

Epidemiology of Equine Strongyle Infections Development of strongyle infections in foals Foals will be infected with strongyle larvae as soon as they begin to graze while on pastures with their dams. Depending on when they are born. Initial infections in early spring result primarily from ingestion of L3s that have successfully overwintered on pasture. summer and fall. the strongyle egg counts of foals will increase steadily during the first 12 months of life and this is shown in the accompanying graph. on pasture. the initial source of infective larvae for foals will be either L3s that have successfully over-wintered. Several studies have shown that strongyle eggs may appear in the feces of foals. Clearly these eggs cannot be from adult worms because the prepatent periods of these species are 6 months and 11 months respectively and also because prenatal infections with equine strongyles do not occur. as early as 4 weeks of age. Whatever the source of their strongyle infections it is clear that this epidemiological picture shows clear evidence that foals are at risk from strongyle infections early in life and certainly by the time they are 2-3 months old. In fact Strongylus eggs may be found in the feces of foals up to 12 weeks of age and it is believed that their presence results from ingestion of maternal and other adult feces by foals to populate the large intestine with microorganisms necessary for cellulose digestion. The majority of these eggs are small strongyles but fecal cultures show that as many as 25% may be eggs of Strongylus vulgaris and Strongylus edentatus. However. These eggs will develop rapidly to infective L3s as temperatures rise in spring and summer. It is therefore important that foals are introduced to a parasite control program that includes larvicidal anthelmintics by the time they are 2 months old. In the absence of an effective parasite control program. overwintered pasture larvae that fail to be ingested by a host will die off rapidly in spring as temperatures rise and their food reserves are quickly used up. it should be remembered that during their first 6 months of life. . foals are at risk from migrating larvae of Strongylus vulgaris. However. The primary source of infections in foals will therefore be L3s that have developed from eggs passed by their dams and other horses on the same pasture. producing dangerous levels of L3s on pastures during late spring. Patent infections of Strongylus vulgaris are detected by the time foals are 7-8 months old and eggs from Strongylus edentatus appear at 11-12 months of age consistent with the prepatent periods of these species. or larvae that have developed from eggs passed in spring by their dams and other adult horses on the same pasture.

control of equine strongyles forms the foundation of all parasite control programs and effective measures against other internal parasites such as bots. More modern anthelmintics such as the macrocyclic lactones. The accompanying graph illustrates the rebound of strongyle eggs in the feces of grazing horses 4-6 weeks after treatment with Pyrantel pamoate (PRT). lungworms and stomach worms are built on this initial foundation. It is effective against all stages of cyathostomes except for encysted hypobiotic early L3s. However. The use of anthelmintics to control strongyle infections The first safe and effective anthelmintics against adult large and small strongyles (benzimidazoles) were first introduced in the mid 1960s. This recommendation was based not only on the known prepatent periods of 4-8 weeks (depending on the species) for the small strongyles. This recommendation was reflected in the advertising campaigns mounted by the drug manufacturers during the 1960s and 1970s as reflected in this print advertisement ( use your browser back button to return to this page). One significant advantage to using Ivermectin is that it is also highly effective against adult Strongylus equinus plus migrating stages and adults of Strongylus vulgaris and Strongylus edentatus. Following this.3 mg/kg. Ivermectin and Moxidectin are much more effective against the equine strongyles because they kill larval stages of large and small strongyles as well as the lumen-dwelling adults. This dose is highly effective and eliminates not only cyathostome larvae and adults in the lumen of the large intestine but also the mucosal dwelling L4s. In North America.Treatment and Control of Equine Strongyle Infections The large and small strongyles are considered to be the "bread and butter" parasites of control programs because of their widespread occurrence throughout the world and potential for causing serious disease. A similar result is obtained when horses are treated orally with Moxidectin at a dose of 0. .2mg/kg. It has the same range of activity as Ivermectin against the large strongyles and appears to have a longer residual effect (of 12-16 weeks) than Ivermectin. As a result it takes longer for egg counts of grazing horses to rebound following treatment and this is shown in the graphs below. In addition. The result is a longer interval for the gut to be repopulated by adults developing from unaffected encysted L3s and newly ingested L3s. If Ivermectin is used in a year-round control program its frequency of use can be reduced to once every 10-12 weeks. but also that strongyle eggs could be detected year-round in the feces of horses. it was widely recommended that horses should be treated year-round with anthelmintics at 4-6 week intervals. Ivermectin has a two week residual effect from drug residues that are sequestered in body fat. Ivermectin is not effective against cyathostome L3s (hypobiotic early L3s or developing L3s) in the mucosa. This graph shows the effects of treating horses with strongyle infections using Ivermectin at a dose of 0.

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++++ = highly effective. It is generally recommended that larvicidal doses of Fenbendazole should be incorporated into parasite control programs at least once and possibly twice during the calendar year.= minimal activity Fenbendazole given orally at a dose of 10mg/kg daily for five days has the broadest spectrum of activity against parasitic stages of the small strongyles. The single yearly treatment is usually given in November or December and the twice yearly treatments are recommended for April and October.Treatment and Control of Equine Strongyle Infections Control of small strongyle infections with anthelmintics The table.2 mg. There are. ++ = partial activity. The problem of anthelmintic resistance among the small strongyles is particularly prevalent in the benzimidazoles.3 mg/kg ++++ ------------------------- ++++ --------------------++++ ++++ ------------++++ ----++++ * Benzimidazole resistance. As a result.4 mg/kg oral 0. in fact.kg oral 0. many more drugs that are approved for use against the small strongyles in the United States but the marketplace of horse-owners and veterinarians has selected those in the table as the most widely accepted drugs for use in parasite control programs. ---. below.6 mg/kg oral continuous feeding @14. shows a sampling of the drugs used in practice against the small strongyles. some manufacturers have withdrawn a number of other drugs from the market even though they remain on the approved list by the Food and Drug Administration (FDA) ANTHELMINTICS EFFECTIVE AGAINST THE SMALL STRONGYLES Drug Dose EL3s LL3s Mucosal L4s (hypobiotic) oral Oxibendazole ------------10 mg/kg Fenbendazole Oxfendazole Febantel Pyrantel pamoate Pyrantel tartrate Ivermectin Moxidectin oral 10 mg/kg daily for 5 days oral 10 mg/kg oral 6 mg/kg oral 6. Oxibendazole and larvicidal doses of Fenbendazole are effective against adult small strongyles but veterinarians and horse-owners should be particularly vigilant for the .

The use of larvicidal doses of Fenbendazole is becoming popular and this increased use could hasten the emergence of drug resistance.emergence of anthelmintic resistance to these two drugs. .

swine and horses . the Ascaridoidea. lacks a copulatory bursa but may have caudal papillae Females lay thick-shelled eggs containing a single cell when passed in host feces Direct infection of hosts by ingestion of eggs containing infective second stage larvae(L2s) Life cycles may be direct or indirect and may involve transport hosts in some species The parasitic phases of the life cycles usually involve extensive migrations in definitive hosts Includes species infecting dogs.The Ascaridoidea Nematodes in the order Ascaridida are relatively large nematodes found in a wide variety of aquatic and terrestrial vertebrates. Lumen dwellers feeding on gut contents Three lips surround the mouth opening Serrated ridge or denticle on the inner surface of each lip adjacent to the mouth opening Extremely small buccal capsule Tail end of male coiled. In domestic animals there is only one important superfamily. cats. Biological and structural characteristics Large nematodes with a predilection for the small intestine.

Anisakis simplex is of medical importance because its larvae can cause a severe enteritis in humans after eating undercooked marine fish and squid that serve as paratenic hosts for Anisakis simplex. Ingestion of eggs Global distribution containing second stage larva. Other Anisakis species may also be involved. mackerel and halibut) and squid. Ascarids of domestic animals Species Definitive hosts Transmission Comments Ascaris suum Pigs Parascaris equorum Horses and donkeys 1. salmon. whales) but also pinnipeds (seals) Humans may become infected by eating fish or squid that is raw. . is a large group of nematodes widely distributed in marine mammals. Pseudoterranova decipiens is economically important because its intermediate and paratenic hosts include fish that are of commercial importance such as the Atlantic cod and American plaice. the Anisakidae. 1. Comments Anisakis simplex Marine mammals primarily cetaceans (dolphin. smoked or salted. porpoise. Ingestion of eggs Global distribution containing second stage larvae. fishes and reptiles as definitive hosts. pickled. The anisakids require water for transmission and usually involve fish and aquatic invertebrates as paratenic or intermediate hosts. One other family. cod. the Acarididae is of major importance in domestic animals. hosts and importance The superfamily is divided into 5 families only one of which. undercooked.ASCARIDOIDEA Species. birds. sea lions intermediate hosts implicated in enteritis decipiens and walruses in humans. Pseudoterranova Pinnipeds Ingestion of larvae in fish May also be seals. Anisakids of marine mammals Species Definitive hosts Transmission Ingestion of L3s in marine crustaceans such as shrimps (intermediate hosts) or paratenic hosts such as fish (herring.

Toxocara Mainly cattle 1. dogs.S. Toxascaris Dogs and cats 1. In North America. 2. Prenatal transmission. 3. Ingestion of eggs vitulorum but also sheep containing second and goats stage larvae. Ingestion of mice intermediate hosts. 4. transmammary transmission. Ingestion of eggs leonina containing second stage larvae. Ingestion of eggs containing second stage larvae. 2. 2. Ingestion of intermediate hosts. Baylisascaris Raccoons 1. Ingestion of eggs procyonis primarily but containing second occasionally in stage larvae. 3. Ingestion of eggs containing second stage larvae. Transmammary transmission. 2. Ingestion of mice paratenic hosts. mainly in the southern U. 2. Dogs Global distribution Global distribution Global distribution Global distribution. Implicated in serious neurologic disease (larval migrans) in domestic animals and humans . Transmammary transmission.Toxocara canis 1. Ingestion of mice paratenic hosts. Toxocara cati Cats 1.

This is followed by an intense infiltration of eosiniphils and collagen production.normal Pig liver . Damage to lungs by migrating A."milk spot" lesions Pig liver . . The image to the left shows significant hemorrhagic lesions in the apical and cardiac lobes of Ascarisinfected lungs. These lesions are visible at necropsy on liver surfaces as whitish areas and are commonly called "milk spots" since they resemble splashes of milk. In the absence of reinfection these lesions will begin to regress after larvae migrate beyond the liver and will be healed completely after 4 to 6 weeks: therefore their presence at necropsy is an indication of recent infections. Pig liver . edema and emphysema. In pigs that experience multiple reinfections during their lifetimes.Ascaris suum Pathogenesis Migrating larvae in the liver cause an inflammatory reaction. livers become markedly fibrotic . Repeated infections will produce more widespread hemorrhages.fibrosis Migration of larvae in the lungs also produces hemorrhagic lesions and intense infiltrations of eosinophils around alveoli into which larvae are migrating on their way up the bronchial tree. intralobular tissue destruction and hemorrhage. suum larvae may also exacerbate enzootic pneumonia and enhance latent infections with swine influenza virus.

Diagnosis In young pigs significant respiratory disease may occur during the prepatent period in response to migrating larvae. larvae usually do not migrate beyond the lungs. Overall. exposure to sunlight and prologed exposure to drying will destroy them. ensuring that all young pigs. especially those raised on soil. In these cases. . and thick-shelled with a mammillated outer coat) by fecal flotation. However. development will be minimal in winter and only one generation of Ascaris will occur each year. These thick-shelled eggs are resistant to freezing and drying and can therefore survive for as long as five years under most farm environments.Ascaris suum Epidemiology Female worms may produce as many as 2 million eggs daily during her lifetime in the definitive host which can be a year or more. clincial signs may be present without finding the characteristic eggs in feces of infected pigs. A. clinical signs of asthma accompanied by an eosinophilia will develop 10 to 14 days after exposure to infective eggs. Ascaris suum egg containing an infective L2. ovoid. "milk spot" lesions and an asthma-like syndrome have been recorded in sheep and cattle grazing on pasture previously occupied by swine. In temperate climates. Ascaris suum egg Embryonation and development to the infective second stage larva takes between 13 and 18 days at temperatures between 30 and 33 'C provided the humidity is high and oxygenation is adequate. in which cases a clear diagnosis can be made on finding the characteristic eggs ( small. However. development will be year round and several generations of A. In heated confinement operations and in warm temperate climates found in the Southeast United States. will become infected. In humans. suum eggs will hatch in a number of animal species including ruminants. these factors ensure that the normal swine environment will be well contaminated with Ascaris eggs. In older animals infections are usually patent. In ruminants. with clearly defined seasonal changes. suum may occur each year. rodents and humans.

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Infected foals have low levels of serum albumin that is attributed to a reduced appetite combined with the ingestion of amino acids(such as methionine) in the small intestine by feeding worms. equorum infections in foals and they include: coughing nasal discharges death (following impaction and intestinal rupture) reduced weight gains/weight loss reduced food intake In foals up to 6 months old. at this time. Larval migrations through the lungs are associated first with the apearance of petechial hemorrhages followed by intense infiltrations of eosinophils around alveoli. greyish-green in color and contain dying larvae and lymphocytes surrounded by a fibrous capsule. these hemorrhagic lesions resolve and are replaced by fibrous tissue eosinopils and lymphocytes which appear grossly similar to "milk spot" lesions in livers of pigs infected with A. equorum infections in foals are similar to those seen in pigs infected with Ascaris suum and closely follow the pathway of migrating larvae. equorum . Disease A wide array of clinical signs have been attributed to P. show a frothy mucus in the upper air passages. Focal hemorrhages are first seen in the liver 24 hours after an intial infection and are followed by the infiltration of eosinophils into tracks produced by larvae during their wandering through the liver parenchyma. Heavy infections may result in gut impactions and death following rupture of the small intestine.Parascaris equorum Pathogenesis Pathological changes in P. it's possibility emphasizes the necessity for good parasite control in growing foals. suum. Rapidly developing worms in the small intestine may be associated with a reduction in food intake and poor weight gains compared with worm-free animals. lymphocytic nodules begin to appear under the pleura.rupture of the small intestine . These nodules are more common in older foals that have experienced multiple natural reinfections and may indicate a strong immune response to migrating larvae. coughing and greyish-white nasal discharges are seen during larval migrations through the lungs. As larvae move on to the lungs. They are raised. P. Although this is not a common outcome of Parascaris infections. Endoscopic examinations of the trachea. bronchioles and small blood vessels. Beginning approximately four weeks after infection. These are later replaced by lymphocytes.

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This state of solid immunity. These thick-shelled eggs are resistant to freezing and drying and can therefore survive for long periods in the environment. equorum eggs may hatch in rodents and undergo a limited migration but the nematode seems not to be a cause of visceral larva migrans in humans. Diagnosis A coughing foal with a nasal discharge is a likely indication of a prepatent infection with P. worm numbers and egg counts are usually low. equorum. By the time foals are 12 months old. P. Otherwise a diagnosis is dependent on finding the distinctive thick-shelled egg in the feces of horses with patent infections.Parascaris equorum Epidemiology Female worms are prolific egg layers and as a result infected foals may pass millions of eggs daily in their feces. patent infections are relatively uncommon and and when they are found. Parascaris equorum egg on fecal floation . The outer layer is sticky and ensures that eggs will be present almost everywhere in a foal's environment. This is due to a combination of an age-dependent resistance and a potent immune response. Experimental studies have shown that the immune response acts in the liver and lungs since infections of mature horses with large numbers of eggs produce significant lesions in livers and lungs but few larvae reach the small intestine. combined with infrequent patent infections usually lasts throughout the adult lives of equines. Optimal temperatures for development of eggs to the infective stage(25'c to 35'C) ensure that transmission of Parascaris will be maximum during the summer months in most temperate areas of the world. Infection rates in foals begin to decline significantly by the time they are six months old.

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Species Enterobius vermicularis Passalurus ambiguus Hosts Predilection sites Humans & other primates (gibbons. equi is found worldwide in horses and donkeys. However. They are commonly called pinworms because of their pointed tails and the single pin-shaped spicule of males. The Oxyurida is the only significant group of nematodes with adult members in both vertebrates and invertebrates.Oxyuroidea Introduction Nematodes in the order Oxyurida are classified into two superfamilies. The esophagus has a prominent posterior bulb.male . Cecum & chimpanzees & marmosets) appendix Rabbits & hares Cecum & colon Colon Cecum Small & large intestines Cecum & colon Skrjabinema ovis Sheep & goats Syphacia obvelata Aspiculuris tetraptera Oxyuris equi Mice(laboratory & wild) Mice (laboratory & wild) & rats Horses & donkeys Oxyuris equi O. members of the Superfamily Oxyuroidea are found in vertebrates and the Thelastomatoidea in herbivorous arthropods such as cockroaches. Females are larger than males. The only oxyurid of significance in domestic animals is Oxyuris equifound in the cecum and colon of horses. a number of species are of importance in humans and laboratory animals. The female vulva is situated anteriorly. measuring from 5 to 15 cm in length while males are approximately 1 cm long. Oxyuris equi .

Oxyuris eggs are diagnostic. They lay eggs on the peritoneum in clumps contained in a greyish-yellow gelatinous material. The clinical signs described above are clearly indicative and combined with observing egg masses on the peritoneum. make this an infection that is easy to recognise. However. Egg of Oxyuris equi . They are ovoid. This causes mucoal erosions which appear to produce little in the way of clinical signs. equi infection Diagnosis Diagnosis of O. They must be looked for in the perineal clumps or in fecal samples taken from the ground. the main pathogenic effects appear to be related to the egg laying habits of the female worms. Sometimes owners will notice the long-tailed female worms in the feces of infected animals. Clinical signs Infected animals rub their hind ends frequently in attempts to relieve the pruritis and irritation caused by the egg-laying females. Horse with O. Adult worms live freely in the intestinal lumen feeding on gut contents. Rubbing causes broken hairs. The egg laying habits of female worms means that Oxyuris eggs are rarely found in feces taken directly from the rectum.Oxyuris equi Pathogenesis Fourth stage larvae have a relatively large buccal capsule and they feed by ingesting plugs of intestinal mucosa to which they are attached. This causes an irritation resulting in anal and perineal pruritis. bare patches and inflamed skin over the rump and tail head causing the tail to assume an ungroomed "rat-tailed" appearance as shown in the acompanying two images. yellow. equi infection Horse with O. equi infections is straightforward. Fertilized females travel down to the rectum and extrude their anterior end through the host's anal opening. slightly flattened on one side and with a mucoid plug at one pole. Animals are also restless causing them to feed less producing a loss of condition and often a dull staring coat.

The hind quarters of clinically affected animals should be washed to remove egg masses before treatment to avoid further contamination of the host's environment and to reduce the likelihood of reinfections.Treatment and control O. equi is susceptible to a wide range of available anti-parasitic drugs. .

Eggs are laid in the bile ducts. lose their tails and encyst as metacercariae (E) the infective stages for their final mammalian hosts. truncatula. Cercariae are. immature flukes with tails used for swimming. which is a sac containing germinal cells. using their cilia. and the minimal period for completion of one entire life cycle of Fasciola hepatica is 17 to 18 weeks. Germinal cells in these daughter rediae develop into the final cercarial stages(D). These first generation rediae burst through the wall of the sporocyst and migrate to the hepato-pancreas of the snail. motile. The prepatent period is 10 to 12 weeks. . They attach to plants such as grass blades. Miracidia swim. ( ) Following ingestion of metacercariae by the final host. The most common is L. They must find a suitable snail intermediate host within twenty four hours of hatching or they die. The miracidium loses its cilia and continues to develop into the sporocyst stage (B). a miracidium (A). Development is negligible below 100C. they excyst in the small intestine (F). then enter the small bile ducts. ciliated miracidium. Hatching of eggs takes less than two weeks at optimal temperatures between 220C and 260C. and seek out snails by chemotaxis. parent generation. develops within each egg.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Fasciola hepatica Fasciola hepatica can infect a wide variety of mammalian hosts. particularly sheep and cattle. migrate through the gut wall. then migrate to the larger ducts and occasionally the gall bladder. They adhere to snails and penetrate their soft tissues using an enzyme and a cone-shaped papilla at the anterior end. an amphibious snail with a world-wide distribution. A second generation of "daughter" rediae may develop from germinal cells in the first. which hatches and releases the mature. in fact. Hatched miracidia are short-lived because they do not feed . pass to the small intestine then out in the feces of the host. ( ) Eggs laid by adult flukes pass down the bile ducts through the gastrointestinal tract and exit the host in feces. Each germinal cell grows and divides eventually becoming a redia (C). The first stage. Life Cycle Mature adults live in the bile ducts of livers in their mammalian hosts. completing the cycle. The immature flukes tunnel through the liver parenchyma for 6 to 8 weeks. cross the peritoneum and penetrate the liver capsule (G). It requires snails of the genus Lymnaea as intermediate hosts.

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merely that it will kill at least one species of parasite Most antiparasitic drugs are usually effective in killing several related species of parasites while others may have broad spectrum properties in that they are effective against a wide range of parasites. Development of anthelmintics and registration through the Food and Drug Administration (FDA) takes on average 15 years and an investment of close to $400 million. Clearly for this kind of investment the drug companies expect a substantial return with annual sales of at least $500 million and hopefully as much as $1 billion. Therefore they can be classified as anthelmintics. only one in five thousand will make it to the market. Introduction Control programs for parasites in all our domestic animals rely heavily on the use of antiparasitic drugs. insecticides and acaricides.the Anthelmintics Terminology The umbrella term Parasiticide is used to describe a drug that is effective in killing parasites of one form or another. A good example of such a compound is Selamectin with activity against several species of nematodes of dogs and cats including heartworm as well as fleas. More recently the avermectins and the milbemycins (collectively called the macrocyclic lactones) have been marketed as broad spectrum parasiticides with most of them having activity against nematodes. with activity limited to a small number of nematodes. have been discontinued by the manufacturers because their profitability has declined to the point where it is uneconomical to manufacture and market them. Of all the compounds screened initially and having activity against parasites. Similarly those compounds active only against insects were called insecticides and those effective only against ticks and mites (the acarina) were called acaricides. ticks and some mites.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Parasiticides . Information on FDA-approved drugs for domestic animals can be obtained at the following . It does not mean that the drug kills all parasites. the compounds discovered were usually effective only against some of the parasites in one of the major groups such as the helminths. Therefore those particular organophosphates were classified as both anthelmintics and insecticides. In the early years of drug development. large numbers of anthelmintics are approved for use in the United States but many of the narrower spectrum compounds.In the United States. the drugs were collectively called anthelmintics. In this case. mites and ticks. insects. In the mid to late 1950's some of the organophosphates were discovered to have activity against a wider range of parasites including nematodes and insects.

There should be no residues in milk or meat going into the human food chain. Non toxic to treated animals at the therapeutic dose Should possess a wide margin of safety fro treated animals as well as the user. Abamectin.. Broad spectrum of activity. some of the more recently developed drugs have come quite close. As other groups of anthelmintics were discovered. In addition. the pharmaceutical companies measure newly discovered and promising compounds against an ideal standard. they are extremely safe to use in most domestic animals. Moxidectin. The earliest of the modern anthelmintics was phenothiazine. Metabolism and excretion should be rapid. This image shows how the potency of discovered anthelmintics has increased with time. Administration should be easy. . While no anthelmintic yet discovered has met all the criteria of an "ideal anthelmintic". It was a drug that not only had a narrow spectrum of activity but also a high therapeutic dose of more than 600 mg/kg as well as a narrow margin of safety. The drug should be cost effective. their effective dosages were found to be less than previous compounds and their spectra of activity were broader. This drug was primarily used against nematodes in ruminants. Doramectin and Eprinomectin) have a broad spectrum of activity in all our domestic animals and also have a very small therapeutic dose of less than 200 ug/kg.fda. Each of the most recently discovered macrocyclic lactones (Ivermectin. The properties of an ideal anthelmintic are listed below.web site www.gov/cvm which also has a useful search engine Properties In developing anthelmintics.

Small strongyles .the Anthelmintics Spectrum of activity In terms of the usefulness of anthelmintics against nematodes. An added bonus would include effectiveness in killing other parasitic helminths and arthropods.adults & L4s Trichostrongylus axei . serratus spp Triodontophorus adults minor. Cylicostephanus. L5s Strongylus edentatus adults & migrating larvae Strongylus equinus adults Triodontophorus adults brevicauda.adults Gastrophilus intestinalis 1st instar Moxidectin Ivermectin Fenbendazole ++++ ++++ ++++ ++++ ---++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++* adults only ++++ ++++ ------++** ++++ ++++ ++++ ---++++ ---++++ ++++ ++++ ---- ---++++ ------++++ ++++ ++++ ++++ ++++ ++++ ++** ---++++ ++++ ++++ ---++++ adults only ---------- .adults Habronema muscae .adults Cyathostomum.adults Gyalocephalus capitatus Small strongyles L4s in lumen Small strongyles Encysted L3s and L4s Small strongyles Hypobiotic L3s Parascaris equorum adults & L4s Parascaris equorum L3s Oxyuris equi . Cylicodontophorus. Spectrum of Activity of Macrocylic Lactones in Horses Parasite Strongylus vulgaris adults. it is important that they have as broad a spectrum of activity as possible.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Parasiticides . tenuicollis spp Small strongyles . Ideally they should be effective against a wide range of different nematodes infecting domestic animals and also in killing all parasitic stages of those nematodes.Cylicocyclus. L4s. It includes manufacturers' label claims against a range of species of nematodes and bots as well as a range of different larval stages. The table below shows the spectrum of activity of two macrocyclic lactones and Fenbendazole used in horses.

Gastrophilus intestinalis 2nd & 3rd instars Gastrophilus nasalis 1st. For example. axei and D.microfilariae ++++ ------------------- ++++ ++++ ++++ ++++ ++++ ++++ ++++ ---------------------- ++++ = highly effective. viviparus. fenbendazole's effectiveness against hypobiotic larvae of the small strongyles is an important property lacking by both Moxidectin and Ivermectin. However. the problem of benzimidazole resistance in many species of small strongyles is a critical factor limiting its use against adult popoulations. ** daily for 5 days. * daily for 5 days. . However.adults Habronema .cutaneous L3s Draschia . label claims do not always convey the complete picture. The usual recommendation is to use a drug such as Moxidectin and Ivermectin at strategic times of the year and to supplement this regimen with one or two annual treatments with Fenbendazole to kill hypobiotic early third stage larvae. ---. it is likely to be effective against both of these nematodes since the drug has good activity and label claims against their counterparts in cattle namely T. although Fenbendazole has no claim for activity against Dictyocaulus arnfieldi and Trichostrongylous axei.cutaneous L3s Onchocerca spp . no label claim for individual species just "small strongyles" and problems with fenbendazole-resistant species reducing its effectiveness against adults of some small strongyle species. 2nd & 3rd instars Dictyocaulus arnfieldi adults & L4s Strongyloides westeri . In addition. These comparisons clearly show that Ivermectin has the broadest spectrum of activity against parasites in horses.= no label claim/no activity.

---. As a result we can place a safety factor on each anthelmintic that readily identifies how safe/unsafe it is. Ideally. Clearly. the toxic dose will be several orders of magnitude greater than the therapeutic dose. The problem with . it is well established that collies as a breed-type are sensitive to the avemectins and its is generally advised to avoid their use in those particular breeds. were often combined with an organophosphate like Trichlorfon to broaden the spectrum of activity to include the bots. are generally considered to be very safe drugs not only in horses but also in other domestic animals. ++ = partial activity.= minimal activity N/A = no activity Looking a the above table it can be seen that anthelmintics available for use in horses vary widely in their safety factors.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Parasiticides . Ivermectin and Moxidectin. The benzimidazoles are extremely safe . Before the discovery of the avermectins.the Anthelmintics Safety considerations Anthelmintics are basically poisons and their safe use in animals is directly dependent on the therapeutic dose against the parasite being very much lower than the toxic dose in treated animals. the benzimidazoles. such as Oxfendazole. the closer these two numbers are the riskier it is to use a drug since there is little margin for error in computing dosages based on an animal's weight particularly if weights are estimated rather than measured accurately with a scale.it requires dose rates from10-100 times before these drugs pose safety problems in horses. In doing so it had to be remembered that the safety factor of the combination equaled that of the most toxic component namely Trichlorfon: a property that seems obvious but easily forgotten in the whirl of a busy practice. However. ANTHELMINTICS AVAILABLE FOR HORSES DRUG Strongyloides Parascaris Strongylus spp Small Oxyuris Bot strongyles larvae Safety Factor Oxibendazole Fenbendazole Oxfendazole Febantel Pyrantel Ivermectin Moxidectin Oxfendazole +Trichlorfon Piperazine ++++ ++++ ---++++ ---++++ ++++ ------- ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++ ++++* ++++ N/A 60X +++* ++++ N/A 100X ++* ++* ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ ++++ N/A N/A N/A ++++ ++++ 10X 40X 20X 60X 60X 1X 1X ++++ ++++ ++ N/A * Benzimidazole resistance. The avermectins. ++++ = highly effective.

Therefore their mode of action is also the reason why they have a narrow margin of safety when used in mammals. also has a narrow safety margin. The use of organophosphates as boticides in horses has fallen considerably in the last five years because they have been replaced by the avermectins.acetylcholinesterase is required for post synaptic inactivation of acetylcholine . of course. it is now little used having been superseded by the more effective and safer avermectins. Since neuromuscular transmission is cholinergic in mammals. is their mode of action against the nematodes and insects. compounds that are not only very effective against bots but also much safer than the organophosphates such as Trichlorfon.the organophosphates will prolong muscle depolarization and contraction. However. This.the organophosphates is that they are acetylcholinesterase inhibitors in mammalian as well as parasite neuromuscular junctions. The use of drugs with narrow safety margins becomes problematical if weights are overestimated because animals will be given a dose that is not only greater than the therapeutic dose but also may be close to or at the toxic dose. . It is particularly important to use anthelmintics with wide safety margins in horses. ruminants and pigs because weights in these animals for computing doses are usually estimated for convenience and speed. a compound often used in the past against benzimidazole resistant small strongyles. insects and nematodes . Piperazine.

If drugs are used in these animals and leave residues for prolonged periods of time. withdrawal times are not the only consideration. SQ= subcutaneous. NA= no FDA-approved use in these animal groups. These compounds are applied to the backs of cattle as pour-on products. it is clear that Eprinomectin and Moxidectin have significant advantages over the others. They are becoming increasingly popular because they are easily administered . Withdrawal TImes for a Selection of Anthelmintics in Food Animals Dairy Cattle Fenbendazole Eprinomectin Beef Cattle Swine Sheep Moxidectin Doramectin Zero Zero Zero NA NA 8 days Zero Zero Zero NA NA NA NA NA 35/45 days 24 days NA Ivermectin 24 days (Oral 5 days (feed 11 days paste) premix) (Oral 35 days (SQ 18 days (SQ liquid) injection) injection) 48 days (Topical) 184 days (SR bolus) SR bolus = slow release bolus implanted in the rumen. The table below gives some examples of withdrawal periods for anthelmintics used in cattle and swine. Spectrum of activity is also important and the following table details the activities of four macrocyclic lactones against a wide range of internal and external parasites when used as their topical formulations in cattle. producers are legally required not to place meat and milk products into the human food chain for a pre-defined number of days. However. The latter is called the "withdrawal period" and is fixed for each drug/anthelmintic used in food animals. From this table.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Parasiticides . at least from the consideration of withdrawal times in meat and milk .the Anthelmintics Residues Anthelmintics should be rapidly metabolized and excreted from the bodies of treated animals so that any residues left after treatment will be minimal or zero. This is particular important in milk and meat producing animals. Topical = liquid applied as a pour-on product to the animal's back.

two factors should also be remembered. Second. the positive impact on productivity of broad spectrum anthelmintics in parasite control programs is considerable. . these differences are minor in practice since all four have significant activities against most of the economically important parasites of cattle. Therefore the return on investment is significant. Therefore the impact of anthelmintic treatments on total production costs will be minimal. the effective use of the macrocyclic lactones in routine parasite control programs can be increased by rotating among the members of the group during a grazing season or from year to year. First. However. They must be considered an investment in food and fibre producing animals where return on investment is a major consideration.htm] At first glance these compounds would seem to have considerable differences in their effectiveness.to cattle. 1. However. [anthel_T7. Costs The cost of anthelmintics should be reasonable. veterinary services are one of the smallest components of the total cost of production. In any case. 2.

usually the complete grazing season. pastes. The active compound is absorbed via the sebaceous glands and hair follicles. Injectables are most commonly given to cattle and swine which can be easily crowded into restricted spaces or run-through shutes (in the case of cattle) and treated with multiple dose syringes. Oral formulations are marketed in a variety of forms . A more recent innovation in oral administration is the use of intraruminal sustained release devices in cattle and sheep. chewable soft pills. Using them avoids the stress and expense of rounding up cattle to pass them through shutes for oral and injectable treatments. These compounds allow the stress-free. They are also useful in treating range cattle as additives to mineral mixes and salt blocks. Their presence in the skin makes them valuable and effective drugs for controlling a variety of external parasites in cattle. gels and liquid suspensions. The aim is to prevent establishment of nematode populations in hosts during periods of maximum availability of third stage infective larvae. Feed additives are particularly useful and popular in controlling parasites in swine raised intensively. Topical pour-on macrocyclic lactones.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Parasiticides . These are usually administered orally using a syringe or may be given via stomach tube in the case of liquid suspensions. Palatability is very important in orally administered products particularly to horses and cats which can be difficult animals to treat with drugs that have unpleasant tastes. They allow a slow release of active drug over a period of time. are also available for treatment of internal and external parasites in cattle.the Anthelmintics Routes of administration Anthelmintics are administered to animals by a variety of methods and formulations. Tablets in their various forms are most commonly used in dogs and cats because they are clearly single dose preparations and are relatively easy to give.liquids. injection and topical. medicated salt blocks for licking and premedicated feed or salt mixtures. absorbed through the skin. The three routes of administration are oral. economical treatment of large numbers of animals. They are given as sterile solutions and the subcutaneous route is the most favored because of the risks of hurting carcass quality when the intramuscular route is used. hard pills. Horses are often treated individually and common formulations include pastes. This formulation is clearly preferred by producers and veterinarians because of the ease of use which markedly reduces stress for treated animals. The table below illustrates the wide variety of formulations commonly available for . boluses (large pills).

liquid SC T .gel cap O .paste O. SC = subcutaneous.liquid SC O-? Swine O .liquid O .liquid O .liquid SC T .domestic animals.tablet O .pour on T . I = injection.tablet O.liquid SC T-? O .feed mix O .feed mix O .feed mix O .tablets O .liquid SC O .paste O .liquid O .gel O .liquid O .paste O .tablet I .liquid O -tablets O .gel O .chewables I .syrup O .liquid SC Cats O .liquid O .paste O .liquid O .chewable O.liquid O .feed mix O .salt block O .paste O .paste O .pour on I .bolus O .liquid O .SR bolus I .feed mix O .pour on I .mineral mix O .liquid SC Dogs O . Anthelmintic Formulations Horses Cattle Ivermectin Eprinomectin Doramectin Moxidectin Milbemycin Albendazole Febantel Fenbendazole Oxfendazole Oxibendazole Levamisole O .feed mix I .tablets Pyrantel Diethylcarbamazine Dichlorvos Praziquantel Clorsulon O . SR = slow release .feed mix O .paste O .tablet I .feed mix I .feed mix O .water additive O .liquid O = oral.liquid SC O . T = topical.tablet O .pour on O-? I .chewable O .liquid O .liquid SC T .tablet O .feed mix O .

They interfere with energy-generating metabolism causing death by starvation. . They interfere with neuromuscular transmission in nematodes causing paralysis.the Anthelmintics Major groups The following table includes the major anthelmintic groups commonly available for use in livestock. Anthelmintic Group Examples Mode of Action Bind to glutamated chlorine channels causing paralysis Macrocyclic Lactones Ivermectin (Macrolides) Eprinomectin Doramectin Moxidectin Milbemycin oxime Selamectin Benzimidazoles Thiabendazole Mebendazole Fenbendazole Oxfendazole Oxibendazole Albendazole Febantel Tetramisole Levamisole Interfere with energy metabolism by inhibition of polymerization of microtubules Same as benzimidazoles Cholinergic agonists Cholinergic agonists Inhibitors of cholinesterase Anticholinergic action .PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Parasiticides . 2.block neuromuscular transmission Pr0-benzimidazoles Imidazothiazoles Tetrahydropyrimidines Morantel Pyrantel Organophosphates Dichlorvos Haloxon Trichlorfon Piperazine salts Piperazines Their modes of action are not fully understood in every detail but their lethal effects on parasites result from one of two mechanisms 1.

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some manufacturers have combined them with other drugs to broaden their spectrum of activity. Doramectin and Milbemycin. In the United States. To compensate for this. As their patents expire and generic alternatives begin to compete with them. six commercially available macrocyclic lactones: Ivermectin. The avermectins also include a sugar (disaccharide oxy) linked at position 13. This product is marketed in areas of the United Sates where liver flukes are an important problem in grazing cattle.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Parasiticides . despite their high cost. As a group. Moxidectin. They have been so successful in the market place that production of a number of other useful anthelmintics has been discontinued by their manufacturers.the Anthelmintics The Macrocyclic Lactones The macrocyclic lactones are natural fermentation products of Streptomycetes bacteria. They consist of two sub groups. The macrocyclic lactones come closest to our concept of the "ideal anthelmintic" and. They have broad spectrum activities against a range of nematodes and arthropods. Selamectin. The obvious conclusion from this is that they are cost effective in terms of parasite control. Ivermectin has been combined with Clorsulon to add liver fluke efficacy in cattle. This conclusion is supported by the results of studies of their use in food animals. For example. Eprinomectin. despite their obvious advantages the macrocyclic lactones are expensive. currently. horse owners. However. . as a result have become the "gold standard" in parasite control programs. Despite this they have gained wide acceptance by veterinarians. they are highly effective at low doses (micrograms per kilogram of body weight) against most of the economically important nematodes of food-producing livestock and have a wide margin of safety. the avermectins and the milbemycins. The macrocyclic lactones are not effective against trematodes and cestodes. Some of them have zero meat and milk withdrawal times. their cost effectiveness will increase significantly. there are. farmers and the dog and cat owning public. Their basic chemical structure consists of a cyclic lactone and a spiroketal addition constructed of two 6-membered rings.

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one each at positions 22 and 23 and one added to the oxygen at position 5. Ivermectin is available in a variety of formulations as shown in the following table. In addition. . 4=35 days. 23 . It is a mixture of two avermectins that are first produced naturally from fermentation of Streptomycetes avermitilis and then modified chemically at certain positions . 3=48 days. 23 and 26 on the spiroketal system. therefore Ivermectin should not be used in pregnant or lactating dairy cattle.position 5 on the benzenefuran component and positions 22. The two components of Ivermectin are the 22.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Parasiticides . Ivermectin Formulations Commonly Available Dogs Oral liquid paste tablets chewable SR* bolus feed premix Topical Pour-on liquid Injection Subcutaneous No No Yes Yes No No No No Cats No No Yes No No No No No Horses Yes Yes No No No No No No Cattle No Yes1 No No Yes2 No Yes3 Yes4 Sheep Yes5 No No No No No No No Swine No No No No No Yes6 No Yes7 * SR = intraruminal sustained release. avermectin B1a has a C2H5 added at position 26 while avermectin B1b has a CH3 added at position 26. 6=5 days. Both have three hydrogens added. 7=18 days Withdrawal times in cattle apply only to meat. Withdrawal times: 1=24 days. 2=184 days. 5= 11 days.the Anthelmintics Ivermectin Ivermectin was the first macrocyclic lactone to be developed for commercial use. 23 dihydroxyavermectin B1b.dihydroxyavermectin B1a and 22.

certain to be ruminating) at the beginning of the grazing season. The device is osmotically driven.One formulation for use in cattle is an intraruminal sustained release device (IVOMEC SR Bolus). . at least 12 weeks old (i. nematodes infecting cattle.i. The device is calibrated so that a predetermined amount of Ivermectin (12 mg per day) is carried out to the rumen and on through the gastrointestinal tract where it is effective in killing parasitic stages of all the economically important g. Ivermectin dissolved in water in water flows out to the rumen through a port screen. This is implanted orally in the rumen of cattle.e. pulling in water from the rumen that flows on through a permeable barrier into a chamber containing the active drug.

Examples of these include: Aberrant Hosts for Dirofilaria immitis . they do not develop a microfilaremia because migrating Dirofilaria fail to reach sexual maturity. the length of the microfilaremia is brief compared to the other species. known as alternate hosts. However. many other species can act as alternate hosts for Dirofilaria immitis. Examples of alternate hosts include: Alternate Hosts for Dirofilaria immitis red coyote wolf grey wolverine* fox red ferret* fox California sea lion* domestic and wild felids* *Although these species may constitute microfilaremic reservoirs.Host Range Host Species In addition to the domestic dog. These species. will also maintain blood levels of circulating microfilaria sufficiently high to act as reservoirs of infections for mosquito intermediate hosts. Other vertebrates may act as aberrant or dead end hosts. These species may become infected from the bite of a vector mosquito.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm .

humans bears raccoons beavers .

It is an international problem. or when advising clients on the use of chemical prophylaxis. the larvae require approximately two weeks of temperatures at or above 27C (80F). Please click on the map to see an enlarged version In order for this infection to be maintained in any one location. patent D. . For D. immitis .PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Epidemiology of Canine Heartworm Disease The accompanying map shows the distribution of canine heartworm disease. As a result. four factors must be present: a susceptible host population a stable reservoir of the disease a stable population of susceptible mosquito-vector species a climate supportive of the development of the parasite The climate must be sufficiently warm in order for the larval stages to develop into the L3 infective stages in the mosquito vector. For example. occurring on every continent except Antarctica. and no development will occur if the temperature goes beneath 14C (57F). but also seasonally limited. immitis infections may not be detected for a significant time after after the end of the heartworm season. These are important considerations when screening for heartworm infections. heartworm is not only geographically limited. with a prepatent period of 6-7 months.

quadrimaculatus . The nematode and its accompanying disease is now found in all 50 states. In the U. 1. The rest of the U.S. D. including members of the genera Aedes . The nematode D. . immitis in these mosquito intermediate hosts. immitis is. and Anopheles. adapting to life in a number of mosquito species. There are several factors to explain the spread of D. Anopheles .. The accompanying map shows that during the 1960's. The Southeast and the Mississippi river valleys (shaded red) have the highest prevalence of canine heartworm disease because the climate in those regions is best suited for the vector species. acompanied by their pet dogs and cats. solicitans . in fact. shows a lesser prevalence because there may not be a large enough population of reservoir hosts in some areas. Culex. and feed on domestic canines. has resulted in the movement of the human population. or the vector may not be well enough adapted to survive or to serve as a suitable intermediate host for the larval stages.S. quite cosmopolitan. They are found in many regions of the country. Cx. salinarius . into areas that were previously sparsely populated.The accompanying map shows the distribution of heartworm disease in the United States which is controlled primarily by climatic factors favoring not only the presence of suitable mosquito vectors but also the development of the life cycle of D. as well as other species which may contract heartworm disease. The increasing urbanization of the U. quinqefasciatus .S. immitis was found mostly in the Southeast (red shaded area). Ae. wild canines (the reservoir host in many endemic areas of heartworm disease). immitis and heartworm disease. Culex. There has been a significant increase in the prevalence of heartworm disease in the United States during the last 30-40 years. the main vectors are Aedes taeniorhynchus . and Mansonia . although the prevalence in Alaska is still lower than elsewhere.

There are some factors s which place some dogs at higher risk than others for heartworm disease. D. For example. immitis to a wider temperature range for development of larval stages in the mosquito. However. a higher risk of infection occurs with increasing age and exposure of dogs to the outdoors. However. households own dogs and the current dog population has been estimated as more than 40 million. there seems to be no increased risk associated with gender or hair coat length. 5. 4.S. reservoir hosts and domestic pets. More than a third of all U. 3. immitis infections. This population movement. In addition. Adaptation by D. during its spread throughout the United States it has adapted well to using other mosquito species as vectors. The dog population in the United States has grown significantly during the last 30 years and is now a large potential reservoir for D. . immitis shows a preference for certain species of mosquito. since they are more likely to be outdoors during the transmission season. especially into rural and coastal areas (natural habitats for mosquitos) has increased the potential for contact among vector species. sporting breeds and large dogs tend to be at higher risk than other dogs. Increased dog density.2.

and stimulating release of Platelet Derived Growth Factor (PDGF). and thrombi. thromboemboli containing dead adults. and areas of inflammation near dead adults. Heart failure in these individuals can be acute or gradual. and the vena cavae may be involved as well. but caudal lobar arteries are the most heavily infected.Cardiopulmonary Disease Several disease entities can result from a D. and hydroperitoneum. The distribution and severity of the lesions does depend on both the number and location of adult worms. It has been proposed that heartworms disrupt the intima of the pulmonary arteries. attracting platelets.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Pathogenesis . microfilariae. immitis infection. worms may be found in the right atrium and ventricles. with edema around the arteries. as well as ischemia and right ventricular failure as a result. Changes to the lung parenchyma can be seen upon necropsy. Pulmonary hypertension is the major consequence of intimal proliferation. Of paramount concern is cardiopulmonary disease. If there is a high worm burden. and can lead to ascites. which may help maintain plaque growth. and one can see right ventricular dilation and hypertrophy. where one finds narrowing and occlusion of the pulmonary arteries due to proliferation of intima. Individuals with cardiopulmonary disease may show exercise intolerance. hydrothorax. PDGF triggers proliferation of medial smooth muscle cells and fibroblasts. . and this can lead to right-sided heart failure. Endothelial cells also secrete PDGF. not direct blockage by the adult worms.

. Thrombi form around a degenerating parasite. hemoptysis. These signs may resolve completely following successful adulticide treatment. to chronic coughing. Heartworm infections of a given size will be less well tolerated by working or sporting dogs than by sedentary dogs. Exercise intolerance can be present. and syncope. whether the death of the worms be spontaneous or due to treatment with adulticidal drugs. increasing in severity with increasing resistance to pulmonary blood flow.Clinical signs of cardiopulmonary disease can vary from no signs at all. Pulmonary thromboembolism can occur. and is often a response to dying adult worms. dyspnea. and a periarterial granuloma can develop in the lung parenchyma.

tricuspid valve area. resulting in red blood cell fragility. and posterior vena cava. which is pathognomonic for this syndrome. Although there may not be time to evaluate these cases radiographically (see radiographic signs below). Worms can literally pack these areas. pale mucous membranes and/or jaundice. This syndrome is a clinical emergency. dyspnea. Death may occur within 24-48 hours.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Caval Syndrome Caval syndrome is an acute disease due to large numbers of adult heartworms accumulating in the right atrium. collapse. and hemoglobinuria. clinical signs include an acute onset of weakness and anorexia. bilirubinuria. This leads to hemolysis. Common in younger individuals. Most dogs (88%) with caval syndrome are microfilaremic as well. increases cholesterol content of the red blood cell membranes. from 3-5 years of age. Liver dysfunction hemoglobinuria and normal urine. increasing venous pressure Worms from a caval syndrome dog in the liver. . bilirubinemia. causes decreased esterification of serum cholesterol. and causing damage to beneath a sample of the parenchyma. anemia. there is a 100% occurrence of the 'classic' radiographic signs seen with dirofilariasis. and hemoglobinuria and bilirubinemia.

Organoarsenical adulticide thiacetarsemide and microfilaricidal drugs. Following adulticide treatment against the worms. The disease may be immune complex mediated. The immune response of the infected individual may also affect the probability of renal disease. may have direct hepatotoxicity. as the evidence as yet is indirect. as well as a hypoalbuminemia. Hepatic Disease With hepatic complications. There has been an association noted between heartworm infection and renal disease. . Most infected dogs have no renal damage. some heartworm dogs have been observed to have amyloidosis. Secondly. microfilariae in the urine. elevated liver enzymes do not preclude aldulticide treatment. bicarbonate. There are three proposed mechanisms as to how the renal disease may progress. microgranulomas may occur. and dilatation of capsular lymph nodes. and vitamins B and C. the dog may exhibit phlebitis of hepatic veins. Passive congestion of liver vessels can occur. dilatation of central veins due to pressure necrosis of hepatocytes. However.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Renal Disease It is debated as to whether heartworm can cause renal disease. Laboratory analysis of the dogs with renal problems will reveal a proteinuria. causing damage to the glomerular basement membrane. Thirdly. hematuria. Fluorescent antibody tests have demonstrated Ig deposition on the basement membrane. and the renal problems have been alleviated following heartworm therapy. There are several ways that the liver may become damaged. Treatment consists of adulticidal heartworm therapy and supplementation with fluids. microfialria induced trauma to the glomerular epithelium may cause glomerulosclerosis. and any renal problems that already existed may worsen.

excess salivation. Cases usually present on an emergency basis.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Ectopic Infections Occasionally. they are usually found in the cerebral arteries or the lateral v Signs vary. and surgical removal of the worms is recommended treatment. and Treatment is by surgical removal. an individual may show conjunctival discharge. . o Treatment is by surgical removal of the worm. blindness. and cause ec infection. adult worms may go to sites other than the large veins and heart. but may include convulsions. If they go to the eye. ataxia. Systemic arteries may also be involved in heartworm infection. If the worms migrate to the CNS. photophobia. The rear legs are most commo affected. prostration. and adulticide treatment is contraindicated.

but no detectable microfilariae. 10 to 60%. Occult Heartworm Infection In an occult infection. Allergic Pneumonitis results from an interstitial infiltration of eosinophils and development of microgranulomas and interstitial fibrosis. as may occur with an immune mediated response. or the infections exist where single worms are isolated in ectopic sites. so radiographic tools and immunodiagnostics become much more important in these cases. they may become trapped in the lung and cause interstitial lung disease. The overall incidence of occult infections is approximately 20% but may be much higher. there is either a prepatent infection. There may be an immune mediated response. particularly in the lung. hypersensitivity results in antibody mediated leukocyte adherence to the microfilariae. If there is a build-up of dead microfilariae. and facilitates their adherence to reticuloendothelial (RE) cells in the microvasculature. or there are adult worms present. Chemosterilization of adult worms can occur with the macrolide endectocide prophylactic treatments (see below). There are several ways that an individual can maintain such an infection.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Microfilarial Hypersensitivity and Allergic Pneumonitis Serving as the basis for immune-mediated occult heartworm infection. This adherence decreases the motility of these embryonic worms. There may be single-sex infections. depending on the composition of clinical syndromes in the population. . such that the microfilariae are removed from the circulation. This can confound parasitological diagnostic techniques.

By the time heart failure develops. however. Signs that may give clues as to the presence of infection include rapid breathing and coughing during early disease stages. In advanced stages. clinical signs may raise a high index of suspicion.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Clinical and Laboratory Diagnosis There are several approaches to take when attempting to make a diagnosis of heartworm infection -. and is more common than either the syncope or hemoptysis. a history demonstrating exposure to mosquitoes in an enzootic area is sufficient grounds to test for Dirofilaria infection. and immunological. and chronic weight loss with good appetite. but in the appropriate context. with the exception of the signs of caval syndrome. . animals can show syncope. but this finding lacks specificity. There are.clinical. Serum chemistry will change based on secondary organ involvement. A decreased exercise tolerance will also develop. Clinically. Clinical laboratory tests will very often reveal an eosinophilia and basophilia in the early stage of infection. ascites and hepatomegaly will be present. As a result. parasitological. a laboratory database is insufficient to make an etiological diagnosis. hemoptysis. NO pathognomonic clinical signs for heartworm disease.

granulomas. infarction. Lateral radiographs of a normal canine thorax (left) and one infected with heartworm (right). and eosinophilic pneumonia. one should take both DV and lateral views. including: Heart enlarged right ventricle Arteries enlarged main pulmonary artery enlarged peripheral pulmonary arteries decreased peripheral pulmonary artery taper (i. truncation) tortuous peripheral pulmonary arteries saccular dilation of the peripheral pulmonary arteries Lungs interstitial/alveolar pulmonary pattern with a caudal lobar distribution Differential diagnoses for this can include a possible pulmonary fibrosis. Echocardiography cannot . One should see several characteristic lesions in the canine infection. DV radiographs of a normal canine thorax (left) and one infected with heartworm (right). Echocardiography is recommended if the right ventricle appears enlarged on a radiograph or signs of congestive heart failure are present. bronchopneumonia.e.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Radiographic Diagnosis In using radiographs to look for evidence of heartworm.

visualize the adult worms in the peripheral pulmonary arteries. but with a high worm burden. a thickened right ventricular free wall and intraventricular septum. . Other abnormalities which may be observed are dilatation of the right ventricle. they may be seen in the right heart and main pulmonary artery. or a decrease in right ventricle to left ventricle chamber size ratio.

looking for microfilariae in the peripheral blood. the first line of diagnosis for heartworm infection has been a parasitological examination. no puppy needs to be tested before the age of 7 months. easy. and microfilariae cannot be examined morphologically. These methods allow seen with a Knott technique. As a result. easy method of doing this. this type of test is relatively insensitive. for easy quantification. In addition. The now-outdated Indirect Fluorescent Antibody (IFA) test was specific to antibodies produced against microfilaria. but precise morphological Three D. Therefore examinations for microfilariae are no longer the primary method of testing for heartworm infection.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Parasitological and Immunological Diagnostics Traditionally. However. utilizes a monoclanal antibody to detect circulating worm antigen. and are the standard for diagnosis of canine heartworm. Identification of microfilarial species is made easier by several methods. and the species of microfilariae should be identified in order to insure that any microfilariae found are truly D. The current methodology. and sensitive. and should be done each time DEC prophylaxis is restarted. ELISA tests. many animals do not have detectable microfilaremia. Filtration methods are quick. The earliest that heartworm microfilariae and antigenemia can be detected is 6. These antigen tests all have a high degree of specificity for the detection of adult female heartworms. concentration methods can be used. and an immunodiagnostic test is a much more specific way for identifying occult infections with at least one female. Different tests exist.5 months after infection. dogs with naturally occurring occult infections and most dogs receiving macrolide chemoprophylactics cannot be tested with any of these parasitologic methods. Even in areas where prevalence of heartworm infection is high. In order to deal with shortcomings of the direct smear. but a centrifugation step is required. and although all are highly accurate. the . they differ in the amount of technical expertise needed to run them.Microfilaria testing may be much more useful as a conformation method. immitis microfilariae as examination is difficult. but the number of microfilaria DO NOT correlate well with either number of adult worms or with disease severity. The Knott method is a sensitive technique allowing for morphological examination. immitis. A direct examination of the blood in a wet mount with 1-2 drops is a quick. and not another species which may be nonpathogenic.

unit cost. . and ability to quantitate the amount of circulating antigen.ease of running batch or individual tests.

They are easily distinguished by their staining patterns with acid phosphatase. in formalin fixed specimens.5 vs. a blunt anterior end. immitis microfilariae. Acid phosphatase-stained microfilaria of Dirofilaria immitis. however is its tendency to cause false positives in tests for circulating D. While Dipetalonema stains realatively evenly. and.5 um). immitis (270 x 4. 300 x 6. a 'button hook' tail. Its importance. found throughout the mid-Atlantic United States. These ARE NOT clinically significant. and the body is more curved. They live within the dog's subcutaneous connective tissues.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Dipetalonema reconditum This nematode is common. but its transmission is not limited to warm months. Dirofilaria concentrates the acid phosphatase in two regions. although they may give elevated eosinophil and leukocyte counts. Development requires about ten days. The microfilariae have a distinguishing cephalic hook. The microfilariae are much smaller and narrower than D. They are carried by vector fleas of the genus Ctenocephalides. . Acid phosphatase-stained microfilaria of Dipetalonema reconditum.

Chemoprophylactic Treatment Finally. because microfilaremic dogs may progress to hypovolemic shock and death if DEC is administered. at 50 mcg/kg. particularly when using DEC. and ivermectin given on an off-label basis. Ivermectin. Microfilaricidal Treatment Microfilaricides are the next major type of drugs used when treating for heartworm. has been used at fairly low doses. such as ivermectin (6-12 mcg/kg) and milbemycin oxime (500-999 mcg/kg) are completely effective in preventing adult maturation. Macrolide endectocides. Melarsomine dihydrochloride. is a new arsenical adulticide which is given intramuscularly into the lumbar muscles. however there is a modified protocol where a single dose is given. and there are two main classes of adulticides used. not approved as a microfilaricide. followed by paired doses 4-6 weeks later. if treatment with adulticides is successful. the predecessor to Immiticide. First. Three main drugs exist for this purpose. This drug is contraindicated when some liver and kidney diseases are present. prophylaxis is the major component of heartworm chemotherapy for any animal that could potentially become infected. the adults must be killed. "Immiticide". Ivermectin (Heartguard) is administered orally. or dogs with high worm burdens at risk of thromboembolic complications. Careful observation is required after an initial dose in order to treat potential systemic side effects.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Drug Treatment and Chemoprophylaxis Adulticidal Treatment Drug treatment involves a three pronged approach. not earlier than 3-4 weeks after this treatment had been administered. will kill circulating microfilariae. The other adulticide used is thiacetarsemide ('Caparsolate'). antigenemia and microfilaremia should be gone by sixteen weeks post-treatment. although microfilaricides are usually not given until after recovery from any side effects due to the arsenicals. There have been some CNS side effects in rough coated collies (and other pure breeds) at high doses of Ivermectin outside the recommended dosage range. All dogs should be tested for microfilariae before medication begins. With either of these drugs. Milbemycin oxime at 500-999mcg/kg is an effective microfilaricide. The latter regimen is especially useful in treating very sick dogs. and tissue sloughing can occur if the drug goes perivascularly. The standard protocol is two doses of the drug twenty-four hours apart. and has a low potential for shock reaction relative to . Caparsolate must be administered intravenously. in order to account for varying drug susceptibility and drug safety.

CNS effects have not been shown with this drug. and acts as both a microfilaricide and a larvicide. However. Diethylcarbamazine (DEC) is given orally once per day. Either of these drugs should be given once monthly per os from within one month following the onset of the transmission season to one month after transmission is considered unlikely. readministration should establish full protection in the dog again. . delayed administration may not lead to an adult infection. but is only safe in amicrofilaremic dogs.DEC. there is some afforded protection from residual amounts of drug remaining in the circulation. missed doses are significant if the elapsed time is longer than 2 months. and is highly effective. Other than the potential for shock reaction in microfilaremic dogs. no significant direct side effects have been seen with DEC. If the omission time is under six weeks. As a result. even at elevated doses. If a dose is missed. Milbemycin oxime (Interceptor) is also administered orally.

and offers no practical advantage over the use of adulticide administration. Within 2 weeks after recovery from surgery. This mode of treatment allows for removal of most of the worms without risking complications due to thromboembolism. it is sometimes better to physically remove them from the right heart and pulmonary arteries. with the exception of heavily infected cases. in which it is the treatment of choice.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Surgical Removal of Heartworm Rather than destroy heartworms in situ. individuals with severe cor pulmonale or caval syndrome may be benefitted most. During this surgery. the patient is under local anaesthesia. adulticide therapy is recommended to eliminate any worms that remain in the circulation. While a very popular procedure in Japan. such as those with caval syndrome. Flexible alligator forceps are inserted into the arteries to remove the worms. It should be performed as rapidly as possible to alleviate the obstruction to blood flow. . As a result. the forceps technique requires anaesthesia and fluoroscopic imaging.

The results of a successul surgery! .

and this can be exacerbated by adulticide treatment. transient microfilaremia. When a cat is infected. ranging from 5-20% of the surrounding prevalence of canine infection. . Infection rates are generally much lower than the surrounding dog populations. it may show the same type of cardiopulmonary disease seen in the dog. Cats with heartworm disease are more likely to be 3-6 years old and male. Common presenting signs are coughing dyspnea. The prepatent period is also longer for the cat. but are much more short-lived. Cats may also show thromboembolism more often than dogs. Adult worms mature in the feline host. suggesting that the parasite is not as well adapted to these feline hosts. Those that are positive exhibit a low. Radiographically. In addition. most cases of feline heartworm do not show microfilaria in the peripheral blood. Lab analysis of the blood may show a transient eosinophilia during the early stages of infection and may be absent thereafter. felids often react to infection differently than the dogs. vomiting. Ectopic infections are more commonly seen in cats than in dogs. but it is very often more severe with a smaller number of worms than seen with canine infections. lasting only 2-3 weeks.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Heartworm Heartworm Disease in Cats Although the life cycle of Dirofilaria immitis remains similar whether the worms enter a dog or cat. at about 242 days. one observes an interstitial lung pattern. usually 2-3 years. and occasionally right sided heart enlargement. Sudden deaths may occur from acute circulatory and respiratory failure. weight loss and lethargy. and the feline infection tends to exhibit a lower worm burden than in dogs. enlarged lobar pulmonary arteries.

there is no guarantee that they will be found. right side of the heart. the central nervous system should be checked thoroughly. If clinical signs are present. Many other heartworm infections are missed because many of these cats die suddenly without preceding clinical signs. Because of the difficulties seen with the parasiological and antigen-based tests.Treatment of feline heartworm should be watched carefully. Supportive therapy is indicated in the case of acute collapse. but there is a very high risk of thromboembolism with adulticides such as Caparsolate. Often heartworm cases are misdiagnosed as feline asthma. If there are radiographic signs of pulmonary disease. the cat may be able to clear the worms without any treatment. If an individual is infected without clinical signs of disease. or other pulmonary diseases. and pulmonary veins should be performed. When looking for microfilariae in the blood.g. using extralabel doses of ivermectin (24 ug/kg) or milbemycin oxime (500ug/kg). If neurologic signs were present. prednisone may be used. there is a higher incidence of false negatives with the existing antigen tests than seen when used with dogs due to the low levels of antigen seen in these feline infections. but with monitoring to watch for complications every 6 to 12 months. Prevention of feline heartworm is best done with monthly chemoprophylaxis. Ectopic sites. however. Examination of the systemic veins. if there is a microfilaremia. . If heartworm was suspected. vomiting). it usually is not very high. Adulticide therapy is usually reserved for those cats which cannot be helped by other therapies. the best way to find a case of feline heartworm is with an antibody-based ELISA. If heartworm is suspected. and a concentration method may be of help. such as systemic arteries and body cavities may contain the worms. Diagnosis of feline heartworm disease is difficult. and parenteral fluids may be appropriate. they often do not reflect pulmonary disease (e. a necropsy may provide the best confirmation of infection.

LAB 1 DEMO Quiz Answer A.2).e. specific gravity greater than 1. however. A direct smear may find them if they are numerous. i. use the ETHYL ACETATE SEDIMENTATION TECHNIQUE. Trematode eggs do not always float in a salt solution (they are too heavy. thus. Given the dorso-ventral compressed shape. the oral and ventral sucker: Kingdom: Phylum: Class: B. RETURN TO LAB 1 . the best answer (the correct answer) is to use a sedimentation technique which provides some concentration of the eggs.

Nematode Taxonomy Back to Nematode Taxonomy Home Page Class: Nematoda Superfamily: Trichostrongyloidea Genera: Trichostrongylus Haemonchus Ostertagia Cooperia Nematodirus Dictyocaulus Back to Nematode Taxonomy Home Page .

Nematode Taxonomy Back to Nematode Taxonomy Class: Nematoda Superfamily: Family: Genera: Strongyloidea Strongylidiae Strongylus Cyathostoma Oesophagostomum Stephanurus Family: Genera: Ancylostomatidae Ancylostoma Uncinaria Bunostomum Back to Nematode Taxonomy .

Nematode Taxonomy Back to Nematode Taxonomy Class: Nematoda Superfamily: Genera: Metastrongyloidea Metastrongylus Muellerius Oslerus (Filaroides) Aelurostrongylus Back to Nematode Taxonomy .

Nematode Taxonomy Back to Nematode Taxonomy Class: Nematoda Superfamily: Genus: Rhabditoidea Strongyloides Back to Nematode Taxonomy .

Nematode Taxonomy Back to Nematode Taxonomy Class: Nematoda Superfamily: Genus: Oxyuroidea Oxyuris Back to Nematode Taxonomy .

Nematode Taxonomy Back to Nematode Taxonomy Class: Nematoda Superfamily: Genera: Ascaridoidea Ascaris Parascaris Toxocara Toxascaris Baylisascaris Anisakis Back to Nematode Taxonomy .

Nematode Taxonomy Back to Nematode Taxonomy Class: Nematoda Superfamily: Genera: Subuluroidea Heterakis Ascaridia Back to Nematode Taxonomy .

Nematode Taxonomy Back to Nematode Taxonomy Class: Nematoda Superfamily: Genera: Spiruoidea Spirocerca Habronema Draschia Thelazia Back to Nematode Taxonomy .

Nematode Taxonomy Back to Nematode Taxonomy Class: Nematoda Superfamily: Genera: Filarioidea Dirofilaria Dipetalonema Onchocerca Setaria Stephanofilaria Back to Nematode Taxonomy .

Nematode Taxonomy Back to Nematode Taxonomy Class: Nematoda Superfamily: Genera: Trichuroidea Trichuris Trichinella Capillaria Back to Nematode Taxonomy .

Nematode Taxonomy Back to Nematode Taxonomy Class: Nematoda Superfamily: Genus: Back to Nematode Taxonomy Dioctophymatoidea Dioctophyma .

LAB 2 DEMOS QUIZ ANSWERS Back to Lab 2 Demos A. .) and Strongylus vulgaris (the smallest of the large strongyles. compare it to the penny in the picture). B. etc.. Strongylus vulgaris would be the more important pathogen. Small strongyles (Cyathostomum spp.

the most likely route of transmission was transmammary.) This identification is supported by the clinical signs: anemia. B. . Ancylostoma caninum (Canine small intestinal location and size. Given the age of the dog.LAB 3 DEMOS QUIZ ANSWERS Back to Lab3 Demos A.

So. The larvae crossed the placenta and arrested in the liver of the fetus. Toxocara canis entered the puppy in utero. Orally ingested hookworm larvae do not undergo a somatic migration. Ancylostoma caninum would have entered this young pup through the milk (transmammary). RETURN TO LAB 4 .LAB 4 DEMO Answer to Quiz Question Back to Lab 4 Demos A. the answer to "B" is Toxocara canis. through the heart to the lungs where they broke out of the capillaries and into the alveoli. causing the symptoms of pneumonia. Given that the puppy was from Philadelphia: Left egg is Ancylostoma caninum Right egg is Toxocara canis B. After the pup was born the larvae resumed their migration from the liver.

Dipetalonema reconditum is considered non-pathogenic to the dog. . The acid phosphatase staining technique would confirm that this microfilaria is Dipetalonema reconditum . The antigen tests for heartworm do not cross react with this skin dwelling filarid. The microfilaria seen in the photo is that of Dipetalonema reconditum (based on the bent body.LAB 5 DEMOS QUIZ ANSWERS Back to Lab 5 Demos A. C. B. blunt anterior end and button-hook tail).

What fecal examination method will give you the best chance of finding the eggs of this parasite? (3 pts.) C. A 4-year-old dog has a chronic cough and you have included the nematodes that live in the lungs on your list of possible causes.) B.PARASITOLOGY 4001 Lab Practical 1 .1995 Question 1 Question 1. A. What fecal examination method(s) will give you enough information to rule out (or in) the presence of these "lungworms"? (3 pts. What fecal examination method will give you the best chance of detecting this parasite? (3 pts. Given its age and clinical signs you suspect a Giardia infection. A 3-week-old puppy has watery diarrhea. A local dairy farmer has just acquired some livestock from Louisiana and is concerned that they may have liver flukes (the trematode Fasciola hepatica).) Look at the answers to this question. .

The fecal sample in the device at your place came from a 4-year-old male Rottweiler as part of his yearly check-up. What other similar looking egg could appear in dog feces and how could You tell it apart from the egg you identified in part A? (3 pts. Examine the sample and identify the eggs of the parasite (give Genus and species). .) Look at the answers to this question.Lab Exam Question 2 Question 2. A.) B. (7 pts.

A.Lab Exam Question 3 Question 3. no. The sample of meat in the dish at your place is beef hamburger that is thought to have been contaminated with pork. (3 pts.) Look at the answers to this question. . Is it likely that the hamburger has pork in it (yes. can't tell)? (4 pts. Explain your answer to part A.) B.

(7 pts.Lab Exam Question 4 Question 4.) Look at the answers to this question. What other similar looking egg may be found the feces of a dog and how could you tell it apart from the egg you identified in part A? (3 pts.) B. Identify the parasite egg (give Genus and species). The results of this test are shown under the microscope at Station #4. A saturated salt flotation was done on a fecal sample from a 4 month old Puppy which has been brought to you for its first check-up. . A.

The results of a saturated salt flotation fecal examination is shown under the microscope at Station #5.) B. Identify the egg (give Genus and species). . A 6-year-old male mixbreed dog was brought in to your practice with the complaint that it had chronic vomiting. What pathologic changes may have been caused by this parasite and what other procedures would you do to determine if this dog had these pathologic conditions? (3 pts. (6 pts.) Look at the answers to this question.Lab Exam Question 5 Question 5. A.

) B. The egg seen under the microscope at Station #6 was recovered from the feces of a 1 month old foal which has diarrhea. Identify the parasite (give Genus and species). A.) Look at the answers to this question. .Lab Exam Question 6 Question 6. Why would you expect to see eggs of this parasite in a young foal rather than in a mature horse? (3 pts. (6 pts. Many of these eggs are present on the slide.

Lab Exam Question 7 Question 7.) B. .) Look at the answers to this question. (6 pts. A. The egg seen under the microscope at Station #7 was recovered during a urine analysis of a pig. In what organ does the adult worm reside? (3 pts. Identify the parasite (give Genus and species).

(3 pts. The worms seen under the microscope at Station #8 were recovered from the small intestine of a sheep which died of bacterial pneumonia. . A.Lab Exam Question 8 Question 8. Identify the parasite (give Genus only). Describe the egg you would expect to find in the feces. (6 pts.) Look at the answers to this question.) B.

Lab Exam Question 9 Question 9. (6 pts. Where in the horse would the fourth-stage larvae (L4) of this worm be found? (3 pts. each about 1. A. . A number of adult nematodes. were recovered from the large intestine of a horse which died suddenly. The anterior end of the worm is shown on the kodachromes at Station #9.) B.5cm long.) Look at the answers to this question. Identify the parasite (give Genus and species).

The dish under the microscope at Station #10 contains a skin biopsy in saline. (6 pts. A. How is this parasite transmitted? (3 pts.) Look at the answers to this question. Identify the parasite (give Genus only).Lab Exam Question 10 Question 10.) B. . The biopsy was taken from the ventral midline of a horse with itching dermatitis in this area.

Dicrocoelium dendriticum B. .ANSWER TO THE LAB 6 REVIEW QUESTION A. The deer ate an ant infected with the metacercariae.

.Answer to Lab 7 Review Question A. Triangular or diamond shaped. with a pyriform apparatus around the oncosphere. Family Anoplocephalidea B.

Rocky Mountian Spotted Fever . Dermacentor B.Answer to Lab 8 Review Question A.

. No.Answer to Lab 9 Review Question A. A sucking louse (suborder Anoplura) [Linognathus setosus] B. Dipylidium caninum is carried by fleas and chewing lice.

The dog. like many mammals. Toxoplasma B. can be an intermedate host of this parasite and thus can be infected. Yes. Return to lab 10 demos . the oocyst is sporulated and therefore infectious.Answer to Lab 10 Review Question A.

rare Giardia lamblia .uncommon Cuterebra spp.common Toxascaris leonina .common Cytauxzoon felis .common Mesocestoides spp.uncommon Capillaria plica .uncommon Spirometra mansonoides .uncommon Cryptospiridium parvum .rare Ancylostoma braziliense . .uncommon Alaria marcianae .rare Paragonimus kellicotti .rare Eurytrema procyonis .rare Dipylidium caninum . .Cat Homepage Parasites of the Cat || Root || Main || Aelurostrongylus abstrusus .not looked for Trichuris spp.rare Platynosomum fastosum .uncommon Isospora felis .uncommon Trichinella spiralis . .rare .common Isospora rivolta .rare Taenia taeniaeformis .uncommon Parametorchius complexus .rare Strongyloides spp.uncommon Ancylostoma tubaeforme . .rare Physaloptera spp.common Echinococcus multilocularis .common Hammondia hammondi . .rare Diphylobothrium latum .common Toxoplasma gondii .common Dirofilaria immitus . .uncommon Ollulanus tricuspids .uncommon Sarcocystis spp.common Toxocara cati .common Capillaria aerophilia .

found in biopsy Artifacts .found in blood Protozoans . Nematode eggs and larvae that are found in fecal samples.found in feces Protozoans .Diagnostic Stages of Feline Endoparasites Below is a list and where possible images of parasite diagnostic stages.frequently found in feces Acanthocephalan eggs (feces) . Nematode larvae that are found in muscle Nematode adults and larvae found in skin or eye Nematode eggs and larvae found in tracheal and nasal washes Nematode larvae found in blood Tapeworm Eggs (found in feces) Trematode Eggs (found in feces) Protozoans .

Quiz Case #1 Case 1 The egg shown in the photo was found during a zinc sulphate fecal examination of a 6 year old. Identify the egg shown: A. Paragonimus kellicotti D. This was a routine exam done as part of the cat's yearly examination. Toxascaris leonina C. Toxocara cati B. Physaloptera rara . indoor/outdoor (70%/30%) male cat. Trichuris felis E.

The kitten looks normal on the physical exam.Quiz Case #1 Case 2 An 8 week old kitten was brought into the clinic for its first check-up. Isospora felis D. A fecal exam is run and many objects shown above were found (it measures about 40 um long). Ancylostoma tubaeformae B. Identify the parasite: A. but the owner states that it has had diarrhea for the past 3 days. Ancylostoma braziliense C. Isosporsa rivolta E. Plant cell .

Filaroides osleri D. indoor/outdoor (50%/50%) female cat is showing difficulty in breathing.Quiz Case #3 A 7 year old. Dirofilaria immitis E. Toxocara cati . Capillaria aerophilia B. You have radiographed the cat and the result is shown here. Click on image for full size representation and help to identify pathology Which of the following parasites should be considered as a cause for the clinical signs and the damage seen in the radiograph? A. Aelurostrongylus abstrusus C. The owner also reports that the pet has been vomiting recently.

Identify the egg to genus: A. A fecal flotation was performed and the result is shown in the photo below. Dipylidium . Toxocara D. The cat is healthy and showing no clinical signs. Trichuris B. Physaloptera E. Capillaria C.Quiz Case #4 A 6 year old male indoor/outdoor (50%/50%) cat is brought in to your center city Philadelphia practice for a yearly check-up.

A H&E stained slide of the biopsy is presented below (1A). 1A 1B Note: You can click on image 1A to see the cross-section of the adult parasite highlighted. Trematoda C. Nematoda D. Cestoda B. Pentastomida .Quiz Case #5 A 4 year old female. It had lost a fair amount of weight over the last 2 months. cat was brought in to it's local veterinarian in Massachusetts becuase it was not doing well. Insecta E. spayed. Blood work indicated elevated liver enzymes (Alk phos. GGT). A biopsy of the liver was taken and sent out for pathology. The specimen shown in figure 1B was recovered from the bottom of the container in which the biopsy had been shipped to the lab. To what class does this parasite belong? A.

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Eggs. 4. NOTE: Photos are not to scale ! Eggs and cysts found in feces or expressed from tapeworm proglottids: 1. 2. 6. 3. larvae and cysts of Cat Parasites: A QUIZ Click on photo to see answer. 5. .

9.7. 10. 8. . 11. 12.

13. In urine: 15. Answers: . 14.

1. Fungal spore (artifact. Toxoplasma gondii (sporulated and unsporulated) 14. 12. Capillaria plica TO TOP OF PAGE Back to Quiz Back to Quiz Back to Quiz Back to Quiz Back to Quiz . Capillaria aerophilia 9. Giardia 13. Taenia taeniaeformis 5. Ancylostoma tubaeforme 4. Trichomonas sp. Isospora rivolta (sporulated) 11. not a parasite of cats) 15. Toxascaris leonina 3. Toxocara cati 2. Aelurostrongylus abstrusus 8. Spirometra mansonoides 7. Dipylidium caninum 6. Isospora felis 10.

rare Giardia duodenalis .rare Echinococcus multilocularis .rare .rare Strongyloides stercoralis .rare Taenia ovis .rare Filaroides hirthi .rare Baylisacaris procyonis .common Leishmania spp.rare Balantidium coli .uncommon Macracanthorhynchus ingens .rare Platynosomum fastosum .uncommon Dirofilaria immitis .uncommon Cryptosporidium parvum .uncommon Capillaria aerophila .common Diphyllobothrium latum .common Dioctophyme renale .common Isospora ohionensis . .rare Oslerus(Filaroides) osleri .uncommon Dipylidium caninum .rare Echinococcus granulosus .uncommon Paragonomus kellicotti .uncommon Capillaria plica .uncommon Spirocerca lupi .rare Isospora canis .Parasites of the Dog Ancylostoma brazilensis . .rare Nanophyetus samincola .uncommon Cuterebra spp.common Dracunculus insignis .rare Anclystoma caninum .rare Physaloptera spp.uncommon Taenia hydatigena .uncommon Babesia gibsoni .rare Mesocestoides corti .common Babesia canis .rare Spriometra mansonoides . .uncommon Parametorchius complexus .rare Dipetalonema reconditum .rare Entamoeba histolytica .rare Neospora caninum .uncommon Crenosoma vulpis .common Heterobilharzia americana .uncommon Capillaria boehmi .uncommon Sarcocystis cruzi .

common Toxocara canis .rare Uncinaria stenocephala .uncommon Trichuris vulpis .rare Thelazia californiensis .rare Trichomonas spp.uncommon .Taenia pisiformis.common Trichinella spiralis .common Trypanosoma cruzi .common Taenia multiceps .rare Taenia serialis . .rare Toxascaris leonina .

found in biopsy Artifacts .found in blood Protozoans .Diagnostic Stages of Canine Endoparasites Below are pages with images of parasite diagnostic stages. Nematode eggs ands larvae that are found in fecal samples.frequently found in feces Acanthocephalan eggs (feces) . Nematode larvae that are found in muscle Nematode adults and larvae found in skin or eye Nematode eggs and larvae found in tracheal and nasal washes Nematode larvae found in blood Tapeworm Eggs (found in feces) Trematode Eggs (found in feces) Protozoans .found in feces Protozoans .

The owner states that Bailey just lays around and appears sick (ain't doin' right). is brought to your practice. Based upon your examination and Bailey's history you suspect a parasitic infection. Upon examination you note that Bailey is underweight for his age and breed and he has pale gums. male German Shepard. Which of the following tests should you run? Knott test Fecal flotation Urine Sedimentation Tracheal wash .Quiz Case #1 Case 1 A 10 week old. "Bailey".

you note that the feces are normal in color but semi-formed (mushy). Based upon your gross examination of the feces and Ariel's history. "Ariel". The owner has brought Ariel in for her first examination and vaccinations. No tapeworm segments are noted. A fecal sample was also brought in for a routine examination. which of the following tests should you run? Saturated salt fecal flotation ZnSO4 fecal flotation Direct examination of a fecal smear Ethyl acetate fecal sedimentation . is brought to your practice.Canine Quiz Case #2 A 10 week old. female mixed breed puppy. Upon gross examination of the fecal sample.

opossums. which also appears to have mucus in it. Raccoons. Which one of the following tests should you run on the fecal sample? ZnSO4 fecal flotation Saturated salt fecal flotation Fecal occult -blood test fecal-starch test . although it may have been going on for awhile. You see bright red blood on the stool. Cirus is allowed to run loose in the large wooded area behind the owner's house and is known to catch and eat rabbits and rodents.Quiz Case #3 Case 3 A six year old male Rottweiler (Cirus) has been brought in because it has bloody diarrhea. The owner first noticed the diarrhea yesterday. Other neighborhood dogs are also allowed loose in this same area. and deer are common in the woods.

A= Taenia pisiformis and B= Toxocara canis 5. . A= Taenia taeniaeformis and B= Toxocara canis 2. Mackenzie spends a lot of time outdoors and goes camping with his owners every summer. 1. A= a unknown tapeworm and B= Toxascaris leonina. Mackenzie. A B Identify the parasites whose eggs are shown in "A" and "B". and the two eggs shown below were found. has been presented to you for his yearly check-up. A= a taenid tapeworm and B= Toxascaris leonina 3.Quiz Case #4 A six year old male Labrador Retriever. You performed a fecal flotation. A= a taenid tapeworm and B= Toxocara canis 4.

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Eggs. . 6. NOTE: Photos are not to scale ! IN FECES (or from proglottids found in feces) 1. 2. 3. 5. 4. larvae and cysts of Dog Parasites: A QUIZ Click on photo to see answer.

13. 10. 9. 8.7. 11. . 12. 14.

15. . 16. 18. 19. 17. 20.

22. Toxascaris leonina Return to Quiz Return to Quiz .21. Toxocara canis 2. IN URINE 25. 24. 26. Baylisascaris 3. Answers: 1. 23.

Taenia or Echinococcus 5. Filaroides 12. Trichomonas 23. Capillaria aerophilia 16. Spirocerca lupi 8. Spirometra 6. Capillaria plica Return to Quiz To TOP OF PAGE Return to Quiz Return to Quiz Return to Quiz Return to Quiz . Paragonimus kellicotti 15. Trichuris vulpis 11. Capillaria böhmi 17. Sarcocystis 22. Pine pollen 24. Isospora ohionensis 20. Plant cells 25. Isospora canis 19. Dioctophyma renale 26. Strongyloides stercoralis 13. Dipylidium caninum 7. Giardia 18. Cryptosporidium parvum 21.4. Uncinaria 10. Heterobilharzia americana 14. Ancylostoma 9.

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Parasites of Cattle Bunostomum phlebotmum Capillaria bovis Cooperia punctata Cryptospordium Dictyocaulus viviparus Eimeria bovis Fasciola hepatica Giardia Gongylonema pulchrum Haemonchus contortus Moniezia benedeni Moniezia expansa Nematodirus spathiger Onchocerca lienalis Ostertagia ostertagi Strongyloides papillosus Toxocara vitulorum Toxoplasma gondii .

Trichostrongylus axei Trichostrongylus colubriformis Trichuris ovis Tritrichomonas foetus return to top of list .

Dirofilaria immitis Toxoplasma gondii Dipylidium caninum TOP OF PAGE .Parasites of the Ferret Eimeria furonis Eimeria vison Eimeria ictidea Isospora laidlawi Sarcocystis putorii Cryptosporidium parvum Giardia sp.

dilimani. Cryptosporidium Dictyocaulus filaria Dicrocoelium dendriticum Echinococcus granulosus Eimeria spp. Entamoeba spp. filicollis.Parasites of Goats Bunostomum trigonocephalum Capillaria longipes Capillaria bovis Chabertia ovina Cooperia punctata. E. N. spathiger. (N. wenyoni) Fasciola hepatica Giardia Gongylonema pulchrum Haemonchus contortus Moniezia benedeni Moniezia expansa Muellerius capillaris Nematodirus spp. (E. battus) . ovis. E. Cooperia spp. N.

columbianum) Ostertagia circumcincta Protostrongylus rufescens Sarcocystis spp. Trichostrongylus colubriformis Trichuris ovis Trichuris globulosa return to top of list . (O. Strongyloides papillosus Taenia hydatigena (larval stage only) Taenia multiceps (Multiceps multiceps) (larval stage only) Taenia ovis(larval stage only) Toxoplasma gondii Trichostrongylus spp. venulosum.Oesophagostomum spp. O.

PARASITES OF HORSES Anoplocephala magna Anoplocephala perfoliata Paranoplocephala mamillana Parascaris equorum Habronema muscae Draschia megastoma Gongylonema pulchrum Halicephalobus gingivalis Strongyloides westeri Strongylus equinus Strongylus edentatus Strongylus vulgaris Triodontophorus spp. and other small strongyles Trichostrongylus axei Cooperia oncophora Oxyuris equi . Cyathostomum spp.

Setaria equina Return to top of page . Giardia sp. Fasciola hepatica Echinococcus granulosus Trypanosoma equiperdum Babesia equi Dictyocaulus arnfieldi Onchocerca cervicalis Sarcocystis spp. Entamoeba spp. Trichomonas spp.Gasterophilus spp. Eimeria spp.

N.Parasites of Llamas Fasciola hepatica Fascioloides magna Parelaphostrongylus tenuis Marshallagia Camelostrongylus Haemonchus Ostertagia Trichostrongylus Strongyloides papillosus Cooperia Nematodirus battus. helvetianus Capillaria Trichuris tenuis Oesophagostomum Dictyocaulus Eimeria lamae Cryptosporidium .

Sarcocystis (The llama is an intermediate host) (The llama is an intermediate host) Toxoplasma gondii Giardia Top of Page .

Parasites of the Pig Ascaris suum Strongyloides ransomi Trichinella spiralis Oesphagostomum dentatum Macracanthorynchus hirudinaceus Trichuris suis Metastrongylus elongatus Stephanurus dentatus Taenia solium Swine are the intermediate host (They have the larval stage of this parasite) Hyostrongylus rubidus Giardia lamblia Eimeria suis Isospora suis .

Balantidium coli Cryptosporidium parvum Fasciola hepatica .

L. Crites. Acanthocephalans. Cooper and J.L. Trematodes. The American Midland Naturalist 95:194-198) To jump to a parasite section: Cestodes. Nematodes.Parasites of the Robin Parasite List for Turdus migratorius (Most of this list is from C. Protozoa Cestodes: Anomotaenia constricta Aploparaksis dujardini neoarcticus Aploparaksis turdi Choanotaenia iola Dilepis undula Hymenolepis fariminosa Hymenolepis microcirrosa Hymenolepis planestici Hymenolepis serpentulus Hymenolepis turdi Southwellia sp Tatria decacantha . 1976.

To TOP of PAGE Nematodes: Capillaria obsignata Capillaria quiscali Capillaria caudinflata Capillaria contorta Capillaria exilis Capillaria ovopunctatum Cardiofilaria inornata Dispharynx nasuta Habronema sp Microfilaria sp Microtetrameres sp Oxyspirura petrowi Porocaecum brevispiculum Porocaecum ensicaudatum Splendidofilaria caperata Syngamus trachea To TOP of PAGE Acanthocephala Luehia adluehia Luehia boreotis .

Mediorhynchus grandis Mediorhynchus robustus Plagiorhynchus formosus To TOP of PAGE Trematodes Brachylaemus pellucidum Brachylecithum mosquensis Collyriclum faba Leucochloridium variae Lutztrema monenteron Plagiorchis noblei Posthodiplostomum minimum To TOP of PAGE Protozoa Isospora robini Plasmodium spp Leucocytozoon dubreuili .

Females are 11 cm long. Adult Parasite Hosts Life cycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: Males measure 9 cm long.Sulcascaris sulcata Homepage Common name: Loggerhead stomach worm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida Family: Ascaridoidea Genus: Sulcascaris Species: sulcata Click on the text below to jump down to the desired section of this page. .

Return to top of page Hosts: Definitive: Marine turtles Intermediate: Scallops and other mollusks Return to top of page Life Cycle: Eggs pass out in the feces and fall to the sea floor. The L3 will molt to the L4 in the scallop in 3 to 4 months. International Journal for Parasitology 11:43-54.R. L3 are taken up by mollusks (Scallops and possibly others) and go to the tissues.) Return to top of page Site where adult parasite is found in host: Stomach . Adults will become gravid in 5 to 6 months. (G. 1981. Berry and L.N. The L3 hatch from the eggs beginning at 7 days after the egg was laid.Adult worms recovered from the stomach of a Loggerhead Turtle.G. When the infected mollusk is eaten by the loggerhead turtle the L4 attach to the stomach wall (at the esophago-gastric junction) and will molt to the adult in 7 days. The larva develops in the egg and under goes 2 molts to the L3 stage. Cannon.

Return to top of page Common Diagnostic Test: Fecal float Identification of the adult worm recovered from the feces.Return to top of page Diagnostic Stage: Egg: Ovoid or triangular 61 . Return to top of page Clinical Signs: Worms may aggregate and cause ulceration of the stomach with almost complete destruction of the upper layer of mucosa. Thin shelled with a rough surface. Return to top of page Treatment: No Data Return to top of page .75 by 86 .100 µm.

Adult Parasite Hosts Life cycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: .Ozobranchus margoi Homepage Common name: Marine turtle leech Kingdom: Animalia Phylum: Annelida Class: Hirudinea Order: Rhynchobdellidae Family: Ozobranchidae Genus: Ozobranchus Species: margoi Click on the text below to jump down to the desired section of this page.

around the mouth and in the area between the carapace and the plastron. Return to top of page Hosts: Definitive: Marine turtles Return to top of page Life Cycle: Eggs are laid in sheets on the plastron of the turtle. external cloaca. Return to top of page Diagnostic Stage: . the neck. Return to top of page Site where adult parasite is found in host: Skin of the ventral surface of flippers. Adults feed on areas of exposed skin.Adult leeches recovered from the skin of a Loggerhead Turtle.

Within 14 hrs all adult leeches were dead. (F. 1974. Schwartz. 1974. Return to top of page Clinical Signs: Turtles with heavy infections will stop feeding.) Return to top of page .35 kg of cupric sulfate was added to tank water (125. No new infestation occurred after circulation was resumed.070 liter tank) and water circulation stopped. Turtles were kept in the tank for an additional 46 hrs with no water circulation. Journal of Parasitology 60(5):889-890. Schwartz. J. exposing bone.) Return to top of page Treatment: 1. Turtles will die of heavy infestations. (F. Leeches will eat away skin and eyes. so apparently the eggs were also killed by this treatment. Return to top of page Common Diagnostic Test: Identification of the adult leech. Journal of Parasitology 60(5):889-890. J.Adult leech from skin or eggs attached to turtle shell.

Ancylostoma caninum .

Ancylostoma caninum .

Ancylostoma caninum .

Ancylostoma caninum .

Dictyocaulus viviparus (Directions for Use) .

Dictyocaulus viviparus (Directions for Use) .

Dictyocaulus viviparus (Directions for Use) .

Dictyocaulus viviparus (Directions for Use) .

Dirofilaria immitis .

Dirofilaria immitis .

Dirofilaria immitis .

Dirofilaria immitis .

Echinococcus granulosus (Directions for Use) .

Echinococcus granulosus (Directions for Use) .

Echinococcus granulosus (Directions for Use) .

Echinococcus granulosus (Instructions) .

Eimeria bovis (Directions for Use) .

Eimeria bovis (Directions for Use) .

Eimeria bovis (Directions for Use) .

Eimeria bovis (Directions for Use) .

Giardia (Directions for Use) .

Giardia (Directions for Use) .

Giardia (Directions for Use) .

Giardia (Directions for Use) .

Haemonchus contortus (Directions for Use) .

Haemonchus contortus (Directions for Use) .

Haemonchus contortus (Directions for Use) .

Haemonchus contortus (Directions for Use) .

Toxocara canis (Directions for Use) .

Toxocara canis (Directions for Use) .

Toxocara canis (Directions for Use) .

Toxocara canis (Directions for Use) .

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Fig. Fig. 2.anterior end The following six images illustrate nematodes with anterior cuticular modifications.The Nematodes Cuticle modifications . 3. Anterior end of an equine strongyle showing a leaf crown (A) surrounding the opening to the buccal cavity. 1. labeled version of the same image. Click on each image with a blue border to show an enlarged. Fig. Oesophagostomum with cuticular modifications at the anterior end: A = cephalic vesicle B = cervical vesicle C = Cervical alae Anterior end of Ostertagia showing a pair of spine-like cervical papillae (A) in the esophageal region .

The small mouth opening or stoma is labeled A. 4. Fig. Scanning electron micrograph of Haemonchus contortus showing cervical papillae. 5. cuticular striations and the buccal lancet used for slitting capillaries during blood feeding Scanning electron micrograph of Ostertagia ostertagi showing circular(B) and longitudinal cuticular striations( C). the roundworm of dogs.Fig. Fig. 6. showing the tapering lance-shaped cervical alae (A) . Anterior end of Toxocara canis.

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Fig. 2. caudal ala (B) and pre-cloacal sucker (C). 3. . 4. Tail end of a female showing caudal ala (A) and a tapering tail with a blunt end. Tail end of a male showing spicules (A). Fig.1.Tail end of male showing copulatory bursa. Tail end of male showing Spicule (A).posterior end The following six images illustrate nematodes with posterior cuticular modifications. Bunostomum. Heterakis. Fig. Vas deferens = D. Fig. Click on each image to show an enlarged. Oesophagostomum. labelled version of the same image. and a pronounced copulatory bursa with lateral lobes (B) and bursal rays (C). Cooperia.The Nematodes Cuticle modifications . spicules and bursal rays.

6. Equine strongyles.Fig.Two males (A) competing to copulate with a female (B). Fig. Oesophagostomum. Copulating male (A) and female (B). . Copulatory bursae are labeled (C). 5. Copulatory bursa is labeled (C).

The dorsal and ventral cords contain longitudinal nerve trunks while the lateral cords contain excretory canals. is relatively thin and is a syncytium of cells in the majority of nematodes of veterinary importance. These movements allow nematodes to move among soil particles and swim in body fluids of a host. Internal to the hypodermis are one or more layers of longitudinally arranged striated (somatic) muscles. contraction of one muscle group will stretch another. The hypodermis. There is no vascular system in the nematodes.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS The Nematodes Internal Morphology The basic nematode body consists of an outer tube (the body wall) enclosing an inner tube (the digestive tract). These are closely associated with the hypodermis and also connect to the cuticle by fibers passing from the contractile part of each muscle cell. Muscle cells of nematodes are unusual because they are not innervated by nerve fibers as is the case with muscles of other animals. unlike a true coelom. processes from muscle cell bodies link muscle cells to the nerve trunks. Since nematodes have longitudinally arranged but no circular muscles. lying beneath the cuticle. Click here to view a cross sectional drawing of a female nematode at the level of the intestine. Click here to return to the drawing of a nematode at the level of the esophagus . The primary function of the hypodermis is to secrete the cuticle. contraction of muscles bend the body dorsally or ventrally. The body wall has three layers: cuticle. The hypodermis has four longitudinally thickened areas or cords that protrude into the body cavity in the mid-dorsal. Each muscle cell consists of a contractile part with muscle fibers and a non-contractile part or cell body containing the nucleus. it does not possess a cellular lining or peritoneum. Instead. hypodermis and an inner layer of muscle cells. instead the circulation of nutrients in the pseudocoelom is assisted by body movements and locomotion. mitochondria and other organelles in addition to glycogen and lipid stores. This body cavity is a pseudocoelom because. Movement of Nematodes Nematodes are covered by an outer cuticle that is structured so as to maintain the body at a constant diameter while allowing longitudinal flexibility. This situation ensures that the dorsal and ventral muscles will act antagonistically to each other. mid-ventral and lateral regions.Since the cuticle prevents radial swelling. allowing nematodes to move in a sinusoidal manner by undulating waves of muscle contractions. The fluid-filled body cavity lies between these two tubes and contains the reproductive tract.

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g. Adult members of the Superfamily Oxyuroidea have an esophagus which has a prominent posterior bulb separated from the rest of the esophagus by a narrow isthmus. At the other extreme. The lumen surfaces of these cells consist of multitudes of projecting microvilli used in absorption and because of their vast numbers provide an immense absorptive capacity.(e. Oesophagostomum radiatum a nematode found in the large intestine of swine). the cloaca (males) and rectum (females) leads to an anus which usually opens to the outside at the posterior end of the body. rather then plug feeders. . In either case.g the large strongyles of horses). Strongylus vulgaris). A large mouth opening and prominent buccal cavity is found in those nematodes that feed by taking a bite of mucosa. is shaped like a club. as the name suggests. adult nematodes belonging to the Superfamily Strongyloidea have a club-shaped (strongyliform) esophagus which. In nematodes that feed by simple ingestion of host fluids the mouth opening and accompanying buccal cavity are generally quite small. the esophagus is muscular and is used to pass food into the intestine by a pumping action. buccal capsule (syn = buccal cavity) and esophagus. For example. The intestine terminates in a rectum in females and a cloaca in males.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS The Nematodes Digestive System The digestive system of nematodes is usually a simple tube with the majority of variations occurring in the sizes of the mouth opening. The mouth may be a simple opening with a tiny buccal cavity leading directly to the esophagus as shown in the accompanying image of Nematodirus ( a small nematode found in the small intestine of ruminants). The intestine is a straight tube roughly circular in cross section and with a wall consisting of a single layer of columnar (rectangular-shaped) cells. the mouth opening and its buccal cavity are usually intermediate in size (e. The shape of the esophagus may be used as an initial screening characteristic for identification. The cloaca is a common termination for the intestinal tract and the vas deferens in adult males. In nematodes that are described as mucosal grazers. The type of mouth opening and accompanying buccal cavity appears to be related to diet. and drawing it into the buccal cavity where it is digested (e. In most nematodes. Nematodirus spp). These nematodes are often called "plug feeders".g. Ostertagia in which the mouth opening and buccal cavity are so small they can only be viewed effectively by scanning electron microscopy and. the mouth opening may be quite large leading to a prominent buccal cavity with thick walls and often containing teeth ( e.g.

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The two uteri end in a common vagina which opens to the outside by a vulva which is often covered by a protective flap of cuticle. the vulva flap. male (0. The female reproductive system is tubular and in most nematodes of veterinary importance consists of two ovaries. the spicules normally protrude from the cloaca even at rest. each of which connects to an oviduct. pale blue. The male reproductive system in nematodes of veterinary importance is a single tube differentiated into testis. seminal vesicle and vas deferens and terminating in a muscular ejaculatory duct which empties into the cloaca. the rigid spicules are then extruded and inserted into the vagina to keep it open so that amoeboid sperm can be transferred for fertilization to occur. In most nematode species there are two accessory male organs. Spicules (A) are made of cuticle. spicules and a gubernaculum as shown in the accompanying image of Haemonchus contortus. In this particular species. In members of the order Strongylida a copulatory bursa is used to grasp the female at the level of the vulva. .5 cm long) is dwarfed by the larger female (2. The gubernaculum (B) is a cuticular modification of the dorsal wall of the cloaca and is used to guide the spicules down through the cloaca so as to penetrate the female vulva. This disparity in size between male and female nematodes in shown in the accompanying image of Syngamus trachea in copulation: the smaller. and a uterus.0 cm long) whose body is packed with coils of its yellowish-white reproductive tract.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS The Nematodes Reproductive System The sexes are separate in most species of nematodes and males are almost always smaller than females since females need to accommodate the production of large quantities of eggs. In female members of the order Strongylida a muscular structure called an ovejector controls the exit of eggs from the uterus. are often paired and used in copulation to dilate the female vulva.

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PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS The Nematodes Infective stages Click here to view a table showing examples of nematode infective stages. In nematodes where a larvated (embryonated) egg is is the infective stage. does not grow and does not feed because its mouth is sealed. Diagnostic stages Click here to view a table showing examples of nematode diagnostic stages. Infective larvae. The infective stage is. The diagnostic stage of nematodes is the stage which leaves the definitive host in order to continue its development and which can be detected by sampling appropriate tissues in a live. carried to the heart (B) then lungs (C) where they lodge in the capillaries. (A) Eggs laid by female are deposited into the venous circulation. such as the hookworms. In Dirofilaria immitis. This is obviously true for nematodes found in the alimentary tract but is also true for nematodes found in the lungs and other organs remote from the gut. the diagnostic stage is a microfilaria (L1). First stage larvae (L1s) break out into the alveoli. where a hatched L3 is the infective stage.the loose-fitting cuticle of the preceding stage. belonging to the family onchocercidae. it is the stage that links the parasitic way of life with either the free-living phase of the life cycle or the phase of development that occurs in an intermediate host. are usually also environmentally resistant and are often enclosed in a sheath . it is different from all other larval and adult stages. the infective stage is still the link to the definitive host. Therefore. the nematode stage that provides a link between a free living and a parasitic way of life. For example. called microfilariae. Although this is still an example of transmission via skin penetration it is the intermediate host that bridges the skin barrier of the definitive host rather than the L3 directly as is seen in the hookworms. transmission to the definitive host is invariably via the oral route. transmission to the definitive host may be via the oral route or by skin penetration and in some nematode species. In some species this L3 develops as a completely free-living stage from a hatched L1 while in others the L1 does not hatch and develops to an L3 inside the protective egg shell. the adults of Parelaphostrongylus tenuis . to the infective third stage and are transferred back to a definitive host when the mosquito takes a blood meal. infected animal. the dog heartworm. the third larval stage (L3) is the infective stage for the definitive host. in the mosquito intermediate host. the diagnostic stage is an egg and is found in the host's feces. it is usually quiescent. a nematode of white-tailed deer are found in the venous sinuses and the subdural space of the cranium. Whichever nematode stage is infective for the definitive host. Blood-sucking mosquitos serve as intermediate hosts: they ingest circulating first stage larvae. circulating in the peripheral blood. migrate up the bronchial tree (D) to the pharynx where they are . In the majority of nematodes of veterinary importance. the infective stage may be either a free-living L3 or an egg containing an L3 (Egg+L3). However. The diagnostic stages of most nematodes are found in the feces of the definitive host since this is the easiest route of exit from the host. where it is available for ingestion by an intermediate host. In gut dwelling nematodes such as the Trichostrongylidae of grazing ruminants. either route is possible. Even in nematodes where intermediate hosts play a critical role in the life cycle. whether they are entirely free living or inside an egg. in fact. These grow through two molts. In these cases the intermediate host serves as a "bridge" for the infective stage to link up with its definitive host. In these respects. Since the diagnostic stage is the life cycle stage leaving the definitive host. A good example of this concept is found in the nematode Dirofilaria immitis ( the heartworm of dogs).

In summary.coughed up. swallowed and pass out with host feces (E). The infective stage is that stage of the life cycle that enters the definitive host and thus provides the link between the preparasitic and parasitic phases of the life cycle. . the diagnostic stage is that stage of the life cycle that leaves the definitive host and thus links the parasitic phase in the definitive host with the preparasitic phase occurring either as free-living developing stages or as stages developing inside an intermediate host.

in some species No L3 Yes (Egg+L2) (Egg+L2) (Egg+L2) hatched L2 L3 (Egg+L3) L3 Oral Oral Oral Oral Oral Oral Skin No No No No No No Yes Yes No No Yes No No No Family: Oxyuridae Family: Onchocercidae .the "hookworms" Families: Metastrongylidae Protostrongylidae .the "lungworms" The ascarids Fam: Ascaridae Ascaris Parascaris Toxocara L3 L3 No No No Yes. Skin Oral Intermediate host Paratenic host Family: Trichostrongylidae Family: Ancylostomatidae .Example Infective stage Route(s) of infection Oral Oral.

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horses or swine depending on the species. Optimal development occurs at 100% humidity and between a temperature range of 22'-26'C.life cycles Nematodes belonging to the family Trichostrongylidae have life cycles that are closely similar.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Trichostrongyloidea Trichostrongylidae . Abomasum. the rate of development may be faster but metabolic activity of L3s is also increased and food reserves may be used up more quickly leading to larval death unless larvae readily find and infect a host. larvae may survive and develop because the microclimate within their environment on pasture may be sufficiently humid to allow . Eggs are passed in the feces of infected hosts. Contained embryos will develop into first stage larvae and hatch if temperature and humidity are optimal (22-26'C and 100% humidity).from eggs through to infective 3s is also controlled by temperature and humidity. or stomach pigs Cooperia Sheep. Similarly with humidity: the optimal humidity for development is 100% and little development occurs below 80%. movement and metabolism are minimal. These ensheathed L3's survive by utilizing nutrients stored by the actively feeding L1 and L2 stages. Some examples are given in the following table. Nematode Host Predilection site Abomasum Ostertagia Cattle ostertagi Trichostrongylus Ruminants. development slows and metabolic activity is reduced. At temperatures below freezing preparasitic stages are vulnerable and few will survive. At higher temperatures. stomach or small intestine of ruminants. At temperatures less than 10'C larval development. Development of all preparasitic stages . axei horses. even when atmospheric humidity is low. Predilection sites include the abomasum. First (L1) and second (L2) larval stages feed on fecal and soil bacteria but the third stage(L3) cannot feed because it is enclosed by a protective. At lower temperatures. impermeable sheath (the retained L2 cuticle). Small curticei goats intestine Pre-parasitic phase The pre-parasitic phase of larval development is entirely free living. However.

mature females lay eggs approximately 2-3 weeks after infection. Parasitic phase The trichostongylid infective stage is an L3 enclosed in its protective sheath and hosts are infected. The following table gives some prepatent periods for several members of this family. Ostertagia ostertagi. Following sexual reproduction. Exsheathment sites are species-specific and are always proximal to the predilection site of each particular trichostrongylid species.survival and some development. by ingesting L3s. with its predilection site in the small intestine. an abomasal nematode. as they graze on pasture. The time from infection to egg-laying by adult females is specific for each nematode species and is called the prepatent period. Exsheathment is immediately followed by movement of parasitic L3's to the predilection site where growth and development to adults occurs (L3--> L4-->Adults). exsheaths in the rumen. while Cooperia curticei. Nematode Ostertagia species Haemonchus species Cooperia species Trichostrongylus species Prepatent period 17-21 days 2-3 weeks 15-18 days 7-25 days Hypobiosis or seasonal arrested development is an important feature of the life cycles of members of this family. Prolonged dry spells and seasonal dry periods open larvae to death by desiccation. Hypobiosis is therefore a mechanism to ensure survival whereby the nematode halts its development in a host when prevailing environmental conditions might jeopardize the survival of any progeny. It occurs where the prevailing seasonal temperature and humidity fall to levels that threaten their survival. . Exsheathment is the next event in the parasitic phase of these life cycles. As examples. exsheaths in the abomasum.

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Under warm. moist conditions. Parasitic phase The parasitic phase is non-migratory. axei or the abomasum (A) forT. Infective larvae of ruminant species tend to migrate onto vegetation. with thin. axei). axei or the small intestine (B) forT. where they are available for ingestion by grazing animals. Further development to adults occurs in the mucosa of the abomasum (A) or small intestine (B).life cycles Predilection sites are the abomasum/stomach (A) for T. vitrinus. depending on the species. The prepatent period is 2-3 weeks in ruminants and 25 days in horses (T.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS The Trichostrongyloidea Trichostrongylus species . vitrinus). hatch within 48 hours and develop through L2 to the L3 infective stage in 7-14 days. colubriformis and T. enclosed in a film of moisture. exsheathment of ingested L3's takes place in the rumen (D) forT. these eggs will develop to first stage larvae (L1). smooth shells and ellipsoidal in shape. Preparasitic phase The preparasitic phase is entirely free living. Eggs (C) laid by female worms pass to the external environment in host feces. In ruminant species. . These eggs are "strongyle-type". colubriformis and T.

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The cattle species. . Parasitic phase (----)Following ingestion by grazing sheep. H. hatching and further development through L2's to infective ensheathed larvae (L3's) takes place on pasture and will occur in as little time as 5 days at an optimum temperature of 22'C and high humidity. has a similar life cycle but its prepatent period is 4 weeks.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS The Nematodes Haemonchus contortus . Preparasitic phase The preparasitic phase consists of free living eggs and larvae and is similar to other species in the family Trichostrongylidae. placei. Females are prolific layers of "strongyle-type" eggs (B) which pass to the external environment in host feces. the prepatent period is 2-3 weeks in sheep. Development of eggs to L1's. At temperatures from 16-20'C. settle close to the abomasal glands where they molt twice and mature to adult females and males.life cycle The predilection site is the abomasum (A) of sheep and goats. almost all Haemonchus eggs wil reach the ensheathed infective stage in 10-14 days. pass to the abomasum. L3's exsheath in the rumen (C).

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000 epg (eggs per gram of feces) or ten million eggs per day passed by the animal in the feces! Large populations of L3's may appear quite suddenly especially when prevailing weather conditions are conducive to rapid development of free-living preparasitic stages.The Nematodes Haemonchus contortus . However. contortus can be seen in sheep older than 6 months. Warm climates: Optimal larval development takes place at relatively high temperatures (22°C = 72°F). In warm temperate areas it begins at the onset of fall in mid to late September and early October. In tropical areas this occurs at the beginning of the dry season. High egg output: This parasite has a high biotic potential.an immediate type hypersensitivity reaction provoked by antigens secreted by developing larvae. Self cure: Significant acquired immunity to H. Field evidence also suggests that arrested development in H. Development resumes at the end of winter and early spring (end of February to mid March). self-cure induced by a challenge infection is not always followed by protection since larvae in the challenge infection may develop to maturity. Periodic natural expulsion of adult haemonchus from sheep is known as "Self-cure" and in some cases appears to have an immunological basis . Females are prolific egg producers so that even moderate infections (1-2. High humidity is also important. will develop to L3's during the grazing season and be responsible for disease outbreaks in grazing sheep especially when pasture contamination is high. . Periparturient Rise (PPR): Ewes that are not treated with an anthelmintic effective against arrested larvae are susceptible to disease in the late spring after arrested larvae resume development. so high rainfall will trigger rapid development to L3.Epidemiology The following factors are important determinants that influence transmission of Haemonchus contortus in sheep. but this immunity is not absolute. contortus may have an immunological component. in turn. and sheep in endemic areas may remain susceptible throughout their lives. and development resumes just prior to the onset of the rainy season. leading to disease outbreaks. Arrested development: Survival of this parasite is also associated with its ability to undergo arrested development at the L4 stage.000 worms) may result in counts of 2. Untreated ewes will shed eggs onto pasture and these.

Clinical signs similar to sheep. for example when range cattle congregate around watering holes.Genetic resistance: there is some evidence that resistance to Haemonchus contortus may be controlled genetically. However. Lambs heterozygous for Hemoglobin type A and B showed much higher egg and worm counts indicating that heterozygous (AB) lambs were more susceptible to infection with H contortus than were homozygous lambs (AA). hypobiois does not occur. Goats on pasture are highly susceptible to infection. East Africa. in tropical areas where a prolonged dry season does not occur e. Hypobiosis occurs in areas where a prolonged dry season occurs. subtropical and warm temperate areas of the world. acute Haemonchosis may be common and results from ingestion of large numbers of infective larvae from heavily contaminated pastures.g. Hypobiois during the dry season allows Haemonchus to survive inside the host as arrested L4's and resumption of development begins at the end of the dry season just as the rainy season begins. The accompanying graph shows Haemonchus egg counts in two groups of lambs grazing a contaminated pasture. In the rainy seasons. Pathogenesis and epidemiology is similar to sheep. Lambs homozygous for Hemoglobin type A showed negligible egg counts and worm counts. and may be related to breed differences as well as to hemoglobin differences within breeds. In tropical and subtropical areas. Clinical signs similar to sheep . Outbreaks of Haemonchosis in adult cattle are usually associated with poor nutrition or unusually heavy challenge infections. Immune responses are good so that the disease is more common in animals <2 years old. Haemonchosis in cattle Haemonchus placei is the species infecting cattle. the severity of Haemonchosis in any specific area is determined by rainfall. Common in tropical. Haemonchosis in goats Haemonchus contortus is the species infecting goats.

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arrested development (hypobiosis) is an important feature of the Ostertagia life cycle. Exsheathment takes place in the rumen ( C ) and larvae pass on to the abomasum (A) where they burrow into the gastric glands. infective L3's. Maturation takes place on the mucosal surface and eggs are produced soon after. Clearly.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Ostertagia ostertagi Life Cycle The predilection site is the abomasum (A) of cattle. Under optimal temperatures. Hot. will migrate away from the fecal pad. prevailing during late spring and early summer in most temperate zones. These L3's accumulate in drops of water on blades of grass. mainly in the pyloric and fundic regions. in large numbers. although the interiors may still be moist enough to allow survival of free-living eggs and larval stages. It occurs at the early fourth larval stage (EL4) within the gastric glands and may last for as long as 6 months. in which they have developed. They undergo two molts then emerge from the gastric glands as immature adults (L5's) approximately 18 days (17-21) after infection. The life cycle is direct . when arrested development occurs the prepatent period will be prolonged.preparasitic larval development is entirely free living. . usually after a rainfall. Parasitic phase (-----) Infection is by ingestion of ensheathed L3's by grazing hosts. moist conditions. larval development is favored by cool (55-75'F). Therefore the prepatent period is approximately 21 days (3 weeks) when development proceeds normally. onto pasture where they will be more available for ingestion by grazing hosts. No migration occurs inside the definitive host. dry weather will cause fecal deposits to crust over. Preparasitic phase "Strongyle-type" eggs (B ) are passed in host feces and development through to infective L3's takes place inside host feces. However. In the presence of moisture. on pasture. development from eggs to L3's will take two weeks or less.

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This image clearly shows no leaking of material between these cells. confined gastric gland. 1. In a heavily parasitised abomasum the mucosa is a sea of nodules. Click here for a picture of a developing L4 larva 15 days after infection During its time in a gastric gland the nematode grows and develops from a tiny third stage larva (approximately 1mm long) to an immature adult (approximately 1cm long) which leaves the gastric gland and returns to the surface of the abomasal mucosa. They form "tight junctions" with adjacent epithelial cells. Click here to see a closer view of the nodular appearance of a parasitised abomasum.they are non-secretory and lack tight junctions. Unlike infections with other nematodes such as the blood-sucking Haemonchus. the functional hydrolytic enzyme of the abomasum.e. In addition. Mature parietal cells secrete hydrochloric acid and chief (zymogen/peptic) cells secrete pepsinogen which is converted by hydrochloric acid to pepsin. 1. Continued growth of the nematode results in constant erosion and replacement of the gland epithelium. These structural changes will produce three significant outcomes. These changes are at their maximal severity as the immature adults struggle. The function of these tight junctions is to maintain the integrity of the epithelial sheet and prevent the passage of small protein molecules across the mucosa.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Ostertagia Pathogenesis Ostertagia ostertagi is the commonest cause of parasitic gastritis in grazing cattle. taking place within the small. The normal histological architecture of a normal gastric gland is shown in this image Mature cells in a gastric gland epithelium have two features. Thus the number of functional gastric glands will be reduced in an Ostertagia-infected abomasum and the amount of that reduction will be directly related to the severity of infections i. This changed pH will prevent the conversion of pepsinogen to pepsin and allow multiplication of bacteria . 2. This ten-fold growth. some not. the pathogenic effects of Ostertagia are not due to its feeding behavior but rather to the growth of developing larvae in gastric glands and the emergence of immature adults from these glands. These swollen glands impinge on neighboring glands causing a pressure necrosis of their epithelial lining cells. the folds of the abomasum may be edematous and reddened and in some cases necrosis and sloughing of the mucosa will be seen. initially causes erosion of the mature secreting cells lining the gland and these are replaced by immature cells. twist and turn to leave their glands. The proper term for a tight junction is zonula occludens (plural = zonula occludentes). They secrete specific components important in protein digestion. the number of infected glands. The frame image is an electron micrograph of a tight junction. A reduction in the number of secreting parietal cells means that less hydrochloric acid will be produced and this will result in a rise in the pH of abomasal contents from 2 to7. some parasitised. The white arrow points to electron dense material leaking between adjacent gland cells. Click here for a picture of a developing L4 larva 7-10 days after infection. The lack of tight junctions means that the epithelium in a parasitised gland has lost its integrity and become permeable. Click here to show an electron micrograph image of a "leaky" tight junction. Specifically these junctions are areas of fusion between the lipo-protein layers of the plasma membranes of adjacent cells. The effect has been described as akin to "morocco leather". The white arrows point to the cell borders between which is the tight junction. Grossly each parasitised gland is swollen giving it a nodular appearance on postmortem inspection. Immature cells in parasitised gastric glands lack both these features .

Type I disease occurs in young cattle grazing contaminated pastures for their first time. ostertagiosis presents as two forms.congregate in the intestine and these will promote the passage of water into the gut producing a (watery) diarrhea. Type I and Type II. even though the pathogenic mechanisms are the same in both. but weeks or months after being ingested as L3s. The net clinical effect of all these changes is that large amounts of osmotically active substances bacteria. 3. Type II disease always results from arrested L4's resuming their development to immature adults and leaving the gastric glands approximately 7-10 days after development resumes.because the bacteriostatic effect of an acid pH is lost. The lack of tight junctions will allow the passage of small protein molecules across the epithelial sheet. In these cases the pathological insults and clinical signs are always due to immature adults leaving gastric glands after developing from L3s ingested approximately 3 weeks before. undigested proteins and plasma proteins (especially albumin) . . Clinically. The pathophysiology of Ostertagia-induced clinical and subclinical disease will be described in more detail in a later chapter. A reduction in the number of secreting chief cells will result in a corresponding reduction in the amount of pepsinogen produced. Albumin will pass from mucosal capillaries into the abomasum and pepsinogen will pass from the abomasum into the blood stream. Such a mucosa is usually described as permeable and the effects are illustated in this drawing. 2. Whatever pepsinogen is produced will not be converted to pepsin and the consequence of this is that protein digestion will cease.

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spathiger. battus. when environmental conditions are warm and moist. Nematodirus species are distributed worldwide. exsheathment occurs in the abomasum and subsequent developing stages are found on the mucosal surface of the small intestine (A). . This means that eggs deposited on pasture in summer will undergo development through to L3's but will not hatch until the following spring after the necessary conditioning by the cold temperatures of winter. N helvetianus. hatching requires a prolonged period of chill followed by a mean day/night temperature of more than 100C. The eggs of other species (e. Its hosts are ruminants. N.g. during spring and summer. leaving it in the egg shell but they retain the L2 cuticle as a sheath which is lost after infection of the definitive host ( ) Following ingestion of L3's. strains of N. During hatching. fillicollis) develop and hatch like other Trichostrongylids. N spathiger and N. In N. L3's cast off the L1 cuticle. Life Cycle The preparasitic phase of Nematodirus is almost unique in the trichostrongyloids in that development to the L3 takes place within the egg shell. The parasitic phase is non-migratory and the pre-patent period is 15 days.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Nematodirus Nematodirus is of special importance as a parasite of lambs in temperate regions. battus do not appear to require cold conditioning for hatching and are therefore transmitted throughout the entire grazing season as opposed to the single yearly transmission cycle during spring in Northern England and Scotland. This development is generally very slow and in temperate climates takes at least two months. In the United States. and its predilection site is the small intestine. but more commonly in temperate zones.

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. Life Cycle Cooperia has a direct life cycle and there is no migration in the definitive host. the larvae reach the small intestine and develop into adults (A). The prepatent period varies from 15 to 18 days. ( ) Following ingestion of infective L3s.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Cooperia Cooperia species usually play a secondary role in the pathogenesis of parasitic gastroenteritis of ruminants although they may be the most numerous trichostrongyle present.

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Ingested L3s are swallowed and migrate through the intestinal wall to the mesenteric lymph nodes (M) where they molt to L4s. Therefore the diagnostic stage for Dictyocaulus is an L1 found in freshly passed feces. they also disperse Dictyocaulus L3s into the surrounding environment. The prepatent period is between 3 and 4 weeks. are coughed up. more specifically the bronchi and traches. Larvae can be propelled at least ten feet beyond the fecal pad and perhaps more with the aid of any prevailing breezes. Migration thus far takes approximately 7 days. From there they travel to the via the lympatic and venous sytems to the lungs and migrate throught capillary walls to the alveoli. As a result. releasing their spores. the preparasitic larvae are not actively motile since they do not have to search for food and complete their development to infective L3s within the host's feces on pasture. Parasitic phase ( ) Migration route of L3s from the pharynx to the lungs (L). swallowed and passed from infected hosts in feces (A). Grazing cattle are infected by ingesting L3s on pasture. The location of adults in the bronchi means that hatched L1s must undergo an extensive migration through the respiratory and intestinal tracts. L4s migrate up the bronchial tree to the bronchioles where the final molt occurs. of the host. They utilize Pilobolus ( P). ( ) Migration route of L1s from the bronchi to the external environment. . Preparasitic phase The preparasitic larval stages of Dictyocaulus do not feed: they rely on food stores already present in the L1 when it is laid by the female worm. This lack of motility has forced Dictyocaulus to develop a method of facilitating dispersal of L3s from host feces onto surrounding pastures where they are more readily ingested by grazing cattle hosts. L1s migrate up the bronchial tree and trachea. to reach the external environment. When these sporangia explode. Females lay eggs that are already embryonated with fully developed first stage larvae (L1s) and these hatch almost immediately. L3s migrate up the stalks and onto the sporangia of Pilobolus.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Dictyocaulus viviparus Life Cycle The predilection sites for this nematode are the lungs (L) of cattle. Immature adults (L5s) continue to the bronchi where they mature and reproduce. a fungus that grows readily in cattle feces and can be seen approximately 7 days after feces are deposited on the ground.

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Life cycle .The lung lesions seen in both horses and donkeys consists of raised areas in the caudal lobes each of which contain lungworms inside a small bronchus and a mucopurulent exudate. Clinical signs . The bronchial epithelium is usually hyperplastic. Diagnosis . because the worm rarely reaches maturity. viviparus but are slightly larger and have a sharply pointed tail.the life cycle is similar to D.First stage larvae are easily recovered from feces of infected donkeys. It appears to be is a relatively benign infection in donkeys since it is rarely associated with clinically obvious disease. . viviparus except for the following: The stage passed in feces is an egg containing an L1 which hatches soon after leaving the host.Infections in donkeys may produce mild clinical signs of harsh lung sounds on auscultation and a slight increase in respiratory rate.donkeys and sheep Dictyocaulus arnfieldi This nematode is seen in the trachea and bronchi of horses and donkeys. Pathogenesis . In horses. has an increased number of mucus cells and is infiltrated with lymphocytes. These larvae are similar to the L1s of D. In horses clinical signs are uncommon in foals and yearlings and in adult horses may be present as a persistent cough and increased respiratory rate.It is believed that horses acquire their infections from pastures contaminated by donkeys with patent infections. The prepatent period ranges from 2 to 4 months.Dictyocaulus in horses. Epidemiology .Patent infections may be seen in donkeys of all ages but in horses are usually only seen in foals and yearlings. infections are usually not patent. Donkeys are usually infected first as foals and through re-exposure remain infected throughout their lives.

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Following ingestion of infected earthworm transport hosts. enter lymphatic vessels and pass to the mesenteric lymph nodes where the first molt occurs. ingestion of earthworms carrying L3s (B). The prepatent period ranges from 6 to 19 months and adult worms have a longevity of about two years .PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Stephanurus dentatus Life Cycle Preparasitic development from egg to L3 is typically strongyloid. The cyst communicates with the ureter either directly or. Occasionally. There they become enclosed in a cyst by host reaction. by a fine connecting canal. if it is more distant. In the liver young adults wander in the parenchyma for three months or more before piercing the capsule and migrating through the peritoneal cavity to the perirenal region (F). ( ) Larvae infecting pigs via skin penetration probably molt to L4s in subcutaneous tissues and reach the liver via the lungs (H) and systemic circulation (I). allowing the worm eggs to be excreted in the urine via the bladder (J). They continue on to the liver (E). and other organs of the host where they are trapped by encapsulation and never reach the perirenal area. There are three modes of infection: by ingestion of the free L3s (A). and skin penetration by L3s (C). dentatus life cycle image to see the percutaneous migration route. Molting larvae can be found in the nodes anywhere from 1 to 9 days after infection. ( ) Ingested larvae exsheath in the intestine (D). abberrant migration occurs with worms ending up in the pancreas (G). Click anywhere on the S. There are reports in the literature supporting a case for transmission of this nematode to piglets in utero. muscle. though earthworms may intervene as transport hosts. The released L3s migrate to the liver as described above. Click anywhere on the life cycle to return to the first image. L3s are released in the gut as the earthworm is digested. . and complete their development. where the final molt takes place.

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( ) Eggs escape from the vulva under the bursa of the permanently attached male and are carried up the trachea in the excess mucus produced in response to infection. S. By ingestion of the hatched L3 (B). Unlike other strongyloids. 1. ( ) Following ingestion. It is commonly known as the "gapeworm" and may be responsible for respiratory distress and death in domestic fowl and game birds such as pheasants and partridges. Various reports have shown that adults may survive for 23-147 days in chickens. . completing the cycle.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Syngamus trachea Syngamus trachea is a parasite of the upper respiratory tract of non-aquatic birds. They are then swallowed and passed in the feces. and pair off. By ingestion of an egg containing an L3 (A). 3. Infection may occur in one of three ways. Adult males and females pair off move up to the trachea and begin copulation in the bronchi and trachea (F). The prepatent period is approximately two weeks with a range of 12-17 days. 2. They penetrate the intestine and travel first to the liver and then to the lungs (E) via the bloodstreamd. moult. Life Cycle Eggs are passed in the feces of infected birds. Two parasitic moults take place in the lungs within 4-7 days after infection. the L3s exsheath in the duodenum (D) of the final host. 48-224 days in turkeys and approximately 98 days in guinea fowl. By ingestion of a transport host containing encapsulated L3s (C). trachea larva develops within the egg until it reaches the L3 stage.

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in nodules. and infection is by ingestion of L3s. the larvae may remain arrested as L4s. These L4s then emerge on to the mucosal surface. depending on the species. radiatum) L3s become enclosed in obvious nodules in which they moult to L4s . The prepatent period is 32 to 45 days. quadrispinulatum and Oe. ( ) The L3s exsheath in the small intestine then enter the mucosa of any part of the small or large intestines. and develop to the adult stage. migrate to the colon (A). Oe. for up to one year. columbianum. . On reinfection with most species. In some species (Oe.Oesophagostomum species Life Cycle The preparasitic phase of Oesophagostomum is typically strongyloid.

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. Infection is by ingestion of the ensheathed L3s. Click on the image of the gastrointestinal track (A) to get a close up diagram of larval migrations inside host. Strongyle-type eggs are laid by mature females and pass to the outside in host feces. vulgaris L3s exsheath in the small intestine. Adults are found in the cecum and colon of infected horses and donkeys. Development from egg to the L3 will take about one week in mid summer in temperate climates. ( ) After ingestion. S.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Strongylus vulgaris Life Cycle The life cycles of all three large strongyles have similar preparasitic phases. ( ) Adult male and females copulate and females lay eggs which reach the external environment in host feces. The prepatent period is 6 to 7 months. penetrate the intestinal mucosa and moult to L4s by 7 days after infection(B). the larvae have molted to immature adults (L5s) but retain the fourth-stage cuticle as an external sheath. Hatching and larval development to infective L3s will occur within a temperature range of 8-38 °C. After a period of development of 3-4 months. These L4s penetrate submucosal arteries and migrate along the endothelium to the cecal and colic arteries (by 14 days post infection) and then to the root of the cranial mesenteric artery and its main branches (C) which they reach by day 21 after infection. Nodules are formed around the L5s mainly in the wall of the cecum and colon (D) Subsequent rupture of these nodules releases the young adult parasites into the lumen of the intestine where they mature in another 6 to 8 weeks. Click anywhere on the image to return to the S. They return to the intestinal wall via the lumen of arteries. vulgaris life cycle.

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The Large Strongyles
Clinical signs - patent infections
It is generally accepted that mucosal feeding adults of all three Strongylus species can have significant effects on infected horses although there appear not to be any clinical signs that can be specifically attributed to them.

General clinical signs of pale mucous membranes, poor weight gains and even weight loss combined with dull, staring coats are seen in horses infected with large strongyles. However, these clinical signs are generally seen in most parasitic infections of the g.i. tract. The "wormy horse" (as shown in the image on the right), is generally a poor performer and poor looking, a description that is often described as "unthrifty". Horses like this are now relatively uncommon in the United States because of the wide use (some would say the overuse) of anthelmintics and the acceptance of parasite control programs by veterinarians and the horse-owning public.
These clinical signs are related to the feeding habits of adult worms which grasp a piece of mucosa with their large mouths and digest it, a process that produces considerable bleeding at the bite site and results in formation of an ulcer. Necropsies show that there are many more ulcers than adult large strongyles in the cecum and colon, a finding that suggests these worms feed, then move to a fresh site . It also implies that their primary source of food is mucosal tissues and that blood is ingested only as part of the mucosal meal. This means that the large strongyles are more accurately described as mucosal feeders than blood suckers. However, their method of feeding, which can reach deep into the muscularis with significant damage to blood vessels, can produce significant blood loss and result in a clinically apparent anemia. Radio-active isotope studies comparing infected with worm-free foals have shown significant protein and red cell losses into the g.i. tracts of infected animals. These findings are not surprising but give a pathophysiological foundation for the clinical picture we see in patent infections with large strongyles. Click here to see a picture of a feeding Strongylus edentatus adult but remember to use the "back" button of your browser to return to this page.

Clinical signs - prepatent disease

PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Cyathostomes

(Small strongyles)
Life cycles
Cyathostome species have similar life cycles. The cecum and colon of horses are the predilection sites for all species and all life cycles are direct. Pre-parasitic phase "Strongyle-type" eggs are laid by female worms and are passed in the feces of infected horses (---> A). A first stage larvae (L1) develops inside each egg, then hatches. This L1 develops and molts into a second stage larva (L2) which, in turn, develops and molts into a third stage larva (L3) but retains the L2 cuticle as a protective sheath. Ensheathed L3's are the infective stages for the definitive hosts (equines) of these nematodes and they are non-feeding stages surviving on food granules accumulated by the feeding first and second stage larvae. Temperature and moisture control both development and survival of these free living stages, with optimal development taking place at approximately 25'C and 80% humidity. Under optimal conditions development of eggs through to infective third stage larvae may take as little time as 2 or 3 days. L3s actively migrate from their host feces (in which they have developed) onto the surrounding pasture thereby increasing the chances of being ingested by grazing horses.

Parasitic phase
(--->) Horses are infected by ingesting sheathed L3's while grazing(B). These pass through the stomach (C ) and exsheath in the small intestine (D ). Parasitic third stage larvae pass on to the cecum and colon(E) where they pass into the crypts of Lieberkuhn and penetrate the mucosa and, in some species, the submucosa. Here, larvae become encysted by host fibroblasts and molt to L4's. The majority (98%) of encysted larvae are found in the walls of the cecum and ventral colon. L4's emerge from their tissue cysts and resume development in the lumen of the large intestine with the majority(about 95%) of mature adult cyathostomes being found in the lumen of the ventral and dorsal colon. The prepatent period (depending on the species) is from 6-14 weeks but may be greatly prolonged when emergence of larvae from the mucosa is delayed due to arrested development(hypobiosis) at the early third stage(EL3).

PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS

Toxocara canis
Life Cycle
Toxocara canis has a complex ascarid life cycle. Like most other nematodes, T. canis is not immediately infectious when it leaves the definitive host. It must grow and develop into the infective stage, ensheathed L2, in order for it to infect the definitive host. Dogs may become infected by four routes: 1. 2. 3. 4. Direct transmission, by ingesting infective eggs. Paratenic host transmission, by ingesting infected mice. Transmammary transmission in which nursing pups ingest L3s in their mother's milk. Prenatal transmission where pups are born infected as a result of L2s migrating from tissue reservoirs in the pregnant bitch - across the placenta and through the umbilical vein to the fetal liver, where they remain until birth. They then resume migration to the lungs of the newborn pups.

The life cycle patterns of T. canis in puppies and in dogs over six months of age are different. Nursing pups are mainly infected by prenatal transmission of larvae from their mothers (A). Larvae reach the small intestine after migrating from the lungs of newborns and move up the bronchial tree and trachea to the pharynx, where they are swallowed and develop to maturity in the small intestine. If pups are infected by direct ingestion of infective eggs (B ), hatched larvae will also follow a tracheal migration. The third, and least common method of transmission in nursing pups - transmammary transmission of L3s (C ) - does not involve tracheal migration. Instead, ingested larvae develop directly to adults in the small intestine. In dogs over six months old, infections occur either by direct ingestion of infective eggs (D ) or by ingesting infected mouse paratenic hosts (E). In the case of paratenic host transmission, no further migration takes place in dogs since the requirement for lifecycle migration is satisfied in the mouse hosts. In direct transmission, only a small proportion of larvae undergo tracheal migration, while the majority continue migrating through the lungs and the pulmonary veins to the heart, where they are distributed to somatic tissues via the peripheral circulation. This somatic migration sets up the conditions for prenatal and transmammary transmission to pups since latent somatic larvae are reactivated during each pregnancy and migrate either across the placenta to the fetal liver after the 42nd day of gestation or to the mammary gland.

PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS

Toxocara cati
Life Cycle
The lifecycle of T. cati, while complex, is different from that of T. canis in five important ways: 1. Paratenic hosts, such as mice, play a more significant role in the lifecycle of T. cati because of the more aggressive predatory nature of cats. 2. Prenatal infection does not occur in the lifecycle of T. cati. 3. A high percentage of larvae (hatching from ingested infective eggs) undefgo tracheal migration, even in older, mature cats. 4. Transmammary transmission is the major route of infection for T cati in kittens. Tissue larvae and larvae acquired during pregnancy will migrate to the mammary glands of lactating queens and be available for nursing kittens throughout the entire lactiation. 5. A wide range of other animals, in addition to mice, may also serve as paratenic hosts. These include chickens, earthorms, and cockroaches.

PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS

Toxascaris leonina
Life Cycle
Toxascaris leonina has the most straightforward lifecycle of the dog and cat ascarids. Dog and cat definitive hosts may become infected in two ways: 1. Ingestion of infective eggs containing second-stage larvae. 2. Ingestion of intermediate hosts containing encysted third-stage larvae. Since there is no somatic migration in dogs and cats, there are no prenatal or transmammary infections. Mice, and to a lesser extent, other rodents and chickens, may serve as paratenic hosts for T. leonina.

PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS

Ascaris suum
Introduction
A. suum is one of the commonest nematodes of pigs and is also the largest with female worms ranging from 25 to 40 cm in length and 5 mm in diameter. Males are smaller, ranging from 15 to 25 cm long and 3 mm in diameter. The image shows mature Ascaris suum from a pig at necropsy. The small intestine is opened to show the mass of adult worms present. The mouth opening is surrounded by three lips as shown in this scanning electron micrograph. There is one dorsal lip (A) and two ventro-lateral lips (B) The yellow arrows point to rows of tiny denticles on the inner surface of each lip.

PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS

The Nematodes
Ascaris suum- life cycle
The predilection site for Ascaris suum is the small intestine of swine.

Pre-parasitic phase
Eggs laid by female worms pass to the external environment in host feces (A). These eggs are oval and thick-shelled with a rough mammillated, sticky external coat and are laid in the one-celled stage. Development to the infective stage takes place inside the egg and consiss of one molt only. Therefore the infective stage for Ascaris suum is an egg containing a second stage (L2) larvae (C). Earthworms (D) and dung beetles may ingest ascarid eggs while feeding on soil and feces. When that happens eggs will hatch and L2s will migrate to tissues and encyst giving rise to the possibility that these invertebrates may serve as paratenic hosts for Ascaris suum.

Parasitic phase
Pigs are infected by ingesting (E) eggs or paratenic hosts containing second stage larvae. Following hatching in the small intestine (F), L2s burrow into the intestinal wall, enter the hepatic portal system and are carried to the liver (G) within 24 hours of infection. Here the first parasitic molt (L2 to L3) takes place. (If infected paratenic hosts (D) are ingested by pigs, L2s are released during digestion in the stomach and small intestine. Their migratory route and parasitic development are the same as infective larvae from eggs). Third stage larvae (L3s) continue their migration from the liver to the lungs via the venous system, right heart and pulmonary arteries, reaching the lungs (H) by 4 to 6 days after infection. They break out of the alveolar capillaries and migrate up the bronchial tree to the pharynx (I) where they are swallowed. The final two parasitic molts (L3 to L4 to immature adults) are completed in the small intestine (F) by 3-4 weeks after infection. Mature, gravid females begin to lay eggs approximately 6 to 8 weeks after infection.

PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS

Parascaris equorum
Introduction
Parascaris equorum is a large conspicuous worm. The females may be as large as 50 cm in length and 8 mm in diameter. Males are smaller, ranging from 15 to 28 cm long. The mouth opening is typically ascarid with three prominent lips. Each lip is divided into two parts, anterior(A) and posterior(B) by a groove(G) along the medial surface. Its predilection site is the small intestine of equines, including zebra. In heavy infections Parascaris may be responsible for gut impactions and ruptures leading to a fatal peritonitis. The black arrow points to a hole in the small intestine resulting from a rupture along the line of the mesenteric attachment caused by pressure from the mass of worms. Infections are found mainly in nursing and weaned foals less than a year old.

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The prepatent period ranges from 12-16 weeks.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Parascaris equorum Life cycle The predilection site for adult worms is the small intestine of equines. These hatch in the gut and. The final two parasitic molts (L3--> L4 --> immature adults) take place in the small intestine. The molt from L2 to L3 appears to occur between the mucosa of the small intestine and the liver Within 7-14 days after infection. Preparasitic phase The life cycle is direct. The infective stage is an egg containing a second stage larva (Egg+L2). Migration from lungs to the gut L3s break out of the alveolar capillaries into the alveoli and migrate up the bronchial tree to the trachea and pharynx. . Parasitic phase Infection and migration to the lungs Foals become infected by ingesting eggs containing L2s. Most L2s reach the liver within 24 hours after infection. Eggs are passed in the feces of infected animals and at temperatures of 25'C to 35'C will be infective within 10 days. L2s migrate through the wall of the small intestine (A) to the liver (B ) via the hepatic portal system. the majority of larvae have migrated on to the lungs (C ) via the heart and pulmonary arteries. They are coughed up and swallowed.

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Parasitic phase The infective stage of Oxyuris equi is an egg containing a third stage larva (Egg + L3) and the definitive host is infected by ingestion. Development to the infective third stage larva takes place inside the egg and is quite rapid. Here they molt to the fourth stage (L4) about 8 to 10 days after infection. taking only 3 to 5 days. the gravid female migrates to the anus of the definitive host. Larvae (L3s) hatch in the small intestine (A). . The prepatent period is approximately 5 months. the females pass outof the anus and die. emerges head first and lays her eggs in clumps (C) in a yellowish-grey gelatinous material on the perineal skin. After completing their egg laying. After fertilization. pass into the large intestine and enter the mucosal crypts of the cecum and colon.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Oxyuris equi Life cycle Preparasitic phase Oxyuris equi has a direct life cycle and its predilection site is the large intestine (B). The final molt to immature adults takes place between 45 and 60 days after infection and this is followed by a lengthy maturation phase of about 100 days until gravid females lay their eggs anywhere from 139 to 156 days after infection.

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pupa and adult (male or female). They leave the host occasionally and usually only when one host makes contact with another. Therefore by far the greatest majority of fleas are found concentrated in the host's environment as eggs. canis and C. first stage larvae will hatch about four days later. moist environment the whole flea life cycle may be completed in three weeks. They consist of six stages . L3s which are about 5mm long now spin a cocoon and inside each pupal case transform (metamorphose) into an adult. pupae and newly emergent adults and only a small proportion of the total flea population is found on a host as feeding. Females will lay eggs within 48 hours of feeding on their new host Under optimal conditions of a warm. In dogs and cats this would primarily include places in the home and kennel used for resting and sleeping. felis) of importance in dogs and cats.are found in the immediate environment of the host. At optimal conditions of temperature and humidity. L1s and adult flea feces drop off the host into the environment where most of the cycle develops. Adult fleas may survive from 2 to 6 months in the absence of a host for feeding. larvae. Adults are the only flea stages spending most of their time on a host. A mixture of eggs. The life cycle will be completed in 2 to 3 weeks at the high ends of these ranges and may take as long as 3-4 months at the low ends.eggs. Adult Ctenocephalides lay eggs on their hosts. All other flea stages . reproducing adults plus newly laid eggs and hatched larvae that have not dropped off.PARASITES AND PARASITIC DISEASES OF DOMETIC ANIMALS Siphonaptera(Fleas) Life Cycles The life cycles of all fleas are basically the same. Adults emerge from the pupa and seek a host to feed and reproduce. Most will live up to one year and some can live as long as two years under natural conditions if they are unthreatened by chemical control products. adult fleas will spend the majority of their time feeding and reproducing on their hosts. 3 larval stages. which contains the two species (C. The general cycle is illustrated here using the specific life cycle of Ctenocephalides. larvae and pupae . However. . Temperature and moisture are the primary factors controlling the flea life cycle. Adults fleas are fairly long-lived.5mm long and white in color.egg. Temperatures greater than 35'C will kill developing larvae and pupae. Studies have shown that the Ctenocephalides life cycle stages will develop within a range of temperatures from 13'C to 32'C and a range of relative humidity from 50% to 92%. Larvae feed on feces from adult stages and this largely consists of dried host blood and tissue ingested by these feeding adults. These are approximateley 0. Larval stages molt twice and will reach the third stage (L3) in two weeks when their environment is warm and moist. when hosts are present.

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involving two molts after the microfilariae differentiate into first stage larvae. Below a threshold temperature of 14c (57F). Final maturation and mating occur in the pulmonary arteries. and penetrate local connective tissues. As a result. Production of microfilariae by inseminated female worms begins approximately six and a half months (192 days) after infection. and the adult worms live in the right heart and pulmonary arteries. requiring approximately two weeks of temperature at or above 27C (80F). while the males are 23cm long with a spirally coiled tail. The juvenile worms migrate to the right heart within a few days of their final molt (F). transmission is limited to warm months. The females are approximately 30cm long. L4 stages undertake extensive migration through the subcutis. the dog heartworm. presumably carried by the venous circulation.Heartworm Dirofilaria immitis Dirofilaria immitis. Return to view life cycle . where they may survive for up to seven years. These infective L3's migrate from the tubules to the lumen of the labial sheath in the vector's mouthparts. vermiform embryos called microfilariae. It is a large. Molting to the L4 ensues within seven days of infection (D). Microfilariae are then released into the circulation. enter the bite wound. Adults are primarily found in the right ventricle and pulmonary arteries of dogs. is a nematode classified as a member of the superfamily Filarioidea and the family Onchocercidae. After reproduction. whitish worm. They can cross the capillary beds and so are found throughout the vascular circulation. and the cycle will be halted. for a mosquito to ingest during a subsequent blood meal. development cannot occur. the females produce small. Return to view life cycle The Life Cycle: Circulating microfilariae are ingested by a female mosquito while taking a bloodmeal from an infected host (A). and duration of the transmission season varies geographically. Development in the mosquito is temperature dependent. which continues for some 60-90 days until the final molt to the immature adult (E). the L3 will exit the labium. During a later bloodmeal on an appropriate host (C). Over 60 species of mosquito are capable of functioning as intermediate hosts. will continue to the third stage (L3) larva (B). These prelarval stages migrate to the Malpighian tubules of the mosquito vector where development.

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Given its age and clinical signs you suspect a Giardia infection. A 3-week-old puppy has watery diarrhea. What fecal examination method will give you the best chance of detecting this parasite? (3 pts.PARASITOLOGY 4001 Lab Practical 1 .) Baermann (Filaroides) and float (Capillaria) BACK TO QUIZ .) Ethyl acetate sedimentation B. A.2 points -. A local dairy farmer has just acquired some livestock from Louisiana and is concerned that they may have liver flukes (the trematode Fasciola hepatica).given for direct smear) C.1995 Answer to Question 1 Question 1. What fecal examination method(s) will give you enough information to rule out (or in) the presence of these "lungworms"? (3 pts. A 4-year-old dog has a chronic cough and you have included the nematodes that live in the lungs on your list of possible causes.) Zinc Sulfate Flotation (Partial credit -. What fecal examination method will give you the best chance of finding the eggs of this parasite? (3 pts.

The fecal sample in the device at your place came from a 4-year-old male Rottweiler as part of his yearly check-up. (2 pts. lemon-shaped egg with symmetrically placed plugs.) BACK TO QUIZ .) B. while Capillaria spp. A. have a rough shell with parallel sides and asymmetric plugs.) These eggs may be confused with the eggs of Capillaria spp.Lab Exam Answer to Question 2 Question 2.) vulpis (2 pts.) Trichuris (5 pts. have a smooth. (7 pts. What other similar looking egg could appear in dog feces and how could You tell it apart from the egg you identified in part A? (3 pts. They may be distinguished because Trichuris spp. (1 pt). Examine the sample and identify the eggs of the parasite (give Genus and species).

Is it likely that the hamburger has pork in it (yes. or Trichinella can be in beef. Explain your answer to part A. no Trichinella found.) If answer = Can't tell. which is highly unlikely to be in beef.Answer to Question 3 Question 3.) Found Trichinella spp.. (3 pts. The sample of meat in the dish at your place is beef hamburger that is thought to have been contaminated with pork.) yes (4 pts. no.(3 pts. -1 point BACK TO QUIZ .) B. A. can't tell)? (4 pts.

and the center mass takes up most of the egg.) canis (2pts. What other similar looking egg may be found the feces of a dog and how could you tell it apart from the egg you identified in part A? (3 pts. T.). has a smooth shell. and there is more space around the central mass (2pts. (7 pts. A saturated salt flotation was done on a fecal sample from a 4 month old Puppy which has been brought to you for its first check-up. The results of this test are shown under the microscope at Station #4.) Toxocara (5 pts. in contrast. canis has a rough shell. which is round. leonina.). T.Answer to Question 4 Question 4. A. Identify the parasite egg (give Genus and species).) B. BACK TO QUIZ .) A similar egg is Toxascaris leonina (1 pt. is oval.

BACK TO QUIZ . and the body of nearby vertabrae would be increased in size (2 pts.) One would find a mass around the esophagus.) lupi (2 pts.) Spirocerca (4 pts. The results of a saturated salt flotation fecal examination is shown under the microscope at Station #5. What pathologic changes may have been caused by this parasite and what other procedures would you do to determine if this dog had these pathologic conditions? (3 pts.Answer to Question 5 Question 5.). Identify the egg (give Genus and species). A 6-year-old male mixbreed dog was brought in to your practice with the complaint that it had chronic vomiting. Radiology would be used to best detect these changes (1 pt. (6 pts.) B. A.).

Why would you expect to see eggs of this parasite in a young foal rather than in a mature horse? (3 pts. The egg seen under the microscope at Station #6 was recovered from the feces of a 1 month old foal which has diarrhea.) westeri (2 pts.).Answer to Question 6 Question 6.) There is transmammary transmission of this parasite (3 pts.) Strongyloides (4 pts. (6 pts. Identify the parasite (give Genus and species).) B. (-2 if only immunity mentioned) BACK TO QUIZ . A. Many of these eggs are present on the slide.

In what organ does the adult worm reside? (3 pts.) Kidney BACK TO QUIZ . (6 pts.) Stephanurus (4 pts. Identify the parasite (give Genus and species).Answer to Question 7 Question 7.) dentatus (2 pts. A.) B. The egg seen under the microscope at Station #7 was recovered during a urine analysis of a pig.

The worms seen under the microscope at Station #8 were recovered from the small intestine of a sheep which died of bacterial pneumonia. (6 pts. B.) One would expect to see a strongyle -type egg -.Answer to Question 8 Question 8. oval egg with embryo in the 8 to 32 cell stage. Identify the parasite (give Genus only).clear shelled. (3 pts. Describe the egg you would expect to find in the feces.) Cooperia spp. A. BACK TO QUIZ .

) B. each about 1.Answer to Question 9 Question 9.) Strongylus (3 pts. Identify the parasite (give Genus and species).) vulgaris (3 pts. (6 pts.5 cm long. A. A number of adult nematodes. The anterior end of the worm is shown on the kodachromes at Station #9.) Mesenteric artery BACK TO QUIZ . were recovered from the large intestine of a horse which died suddenly. Where in the horse would the fourth-stage larvae (L4) of this worm be found? (3 pts.

) BACK TO QUIZ . The dish under the microscope at Station #10 contains a skin biopsy in saline. A. The biopsy was taken from the ventral midline of a horse with itching dermatitis in this area. (6 pts.) Onchocerca B.) By biting flies (3pts. How is this parasite transmitted? (3 pts.Answer to Question 10 Question 10. such as the black fly seen above (Simulium spp.). Identify the parasite (give Genus only).

Aelurostrongylus abstrusus Homepage || Root || Main || Common name: Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Filaroididae Genus : Aelurostrongylus Species: abstrusus Bookmarks Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: The male measures 7.5 mm and the female 9.9 mm. Males have a short bursa and the vulva of the female opens near the posterior end. .

If a paratenic host eats the snail. The L3 will penetrate the gut wall and migrate through the peritoneal and thoracic cavities to the lung. If the L1 find a snail or slug they enter the "foot" where they grow to the infectious third-stage (L3). the L3 migrate into the tissues of the new host and arrest. birds. The larvae will develop to the adult stage and egg laying will begin 5 to 6 weeks after the cat ingested the L3. The L1 can live for about 2 weeks in the environment. top of page . swallowed and pass out with the feces. and lizards.Histological section of Aelurostrongylus in lung tissue. Cats are more likely to be infected by eating the paratenic hosts as snails and slugs are usually not part of their diet. cross section of one parasite is shown highlighted. The eggs hatch and the first stage larvae (L1) are carried up the trachea. top of page Life Cycle: Adult female worms lay their eggs in the alveoli of the cat's lung. voles. frogs. top of page Hosts: Definitive: Cats Intermediate: Snails and slugs Paratenic: mice.

In heavy infections there may be a chronic cough. dyspnea and polypnea. In moderate infections you may see coughing and anorexia.Site where adult parasite is found in host: Terminal bronchioles and alveolar ducts of the lung. Eggs or L1 can be found in the sputum or in a tracheal wash top of page Clinical Signs: Light infections may be asymptomatic. top of page Common Diagnostic Test: Baermann Technique A ZnSO4 flotation may recover L1 that can be identified. and wasting. diarrhea. . top of page Diagnostic Stage: The first-stage larvae (L1) in the feces.

may have to be repeated).4 mg/kg.top of page Treatment: Drug: Fenbendazole (for an extend period of time). Ivermectin (at a dose of 0. top of page .

Alaria marcianae Homepage || Root || Main || Common name: Alaria Kingdom: Animalia Phylum: Platyhelminths Class: Trematoda Order: Strigeatida Family: Diplostomatidae Genus: Alaria Species: marcianae Bookmarks Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: The adult has a spoon-shaped forebody (containing the oral and ventral suckers) and a cylindrical hindbody. .

other than the raccoon or cat. Cats Intermediate: First: snails (Helisoma spp. Photo and illustration adapted from Bowman. top of page Hosts: Definitive: Raccoons. The cercariae leave the snail and penetrate the skin of a leopard frog tadpole where they develop into mesocercariae. snake. The miracidium enter snails of the genus Helisoma and develop to sporocysts. snakes. mammals (other than raccoon or cat) top of page Life Cycle: Eggs leave the cat in the feces and hatch in fresh water. the mesocercaria invade the tissues of this paratenic host and remains as a mesocercaria. birds. Page 126 . or any mammal. eats the infected tadpole. Georgis' Parasitology for Veterinarians..D. daughter sporocysts and finally to cercariae.) Second: tadpole (Rana pipiens) Paratenic: frogs. sixth edition. If a frog. bird.127.Left: Alaria adult attached to the small intestine mucosa. D. If a cat eats an infected tadpole or paratenic host the mesocercariae will penetrate into the body cavity . 1995.

third edition. In the kittens the larvae will develop into adults.and migrate through the diaphragm to the lungs where some of them develop into metacercariae. It develops into the adult worm in the small intestine. Veterinary Parasitology Reference Manual. Page 27. W.. The metacercaria is carried up the trachea and is swallowed. In the raccoon there is no development past the mesocercarial stage unless the female raccoon gives birth. In this case the offspring are infected transmammary and the larvae continue their development to the metacercaria and eventually to the adult stage. 1994. top of page . top of page Diagnostic Stage: Egg 98-134 X 62-68 µm Photo from Foreyt. If a female cat which has mesocercariae in her tissues begins to lactate the larvae can enter the kittens through the milk. J. top of page Site where adult parasite is found in host: Small intestine.

as well as damage to other organs they may migrate through. the migrating mesocerariae may cause pulmonary hemorrhage.Common Diagnostic Test: Ethyl Acetate Concentration Eggs may sometimes float with ZnSO4 top of page Clinical Signs: Adults cause little damage. However. top of page Treatment: Drug: Praziquantel top of page .

5 mm.Ancylostoma braziliense Homepage || Root || Main || Common name: Hookworm Kingdom: Animalia Phylum: Nematoda Class: Secernentea Order: Strongylida Superfamily: Ancylostomatoidea Genus : Ancylostoma Species: braziliense Bookmarks Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: Males measure 7.5 mm. Females measure 9 to 10. The buccal capsule has one pair of small medium teeth and one of larger outer teeth. .5 to 8.

Larvae develop in soil to the L3 infective stage and then are ingested by the host or they enter the host through cutaneous contact and then the larvae migrate to the lungs. In the intestinal tract. Eggs are then expelled in feces and the cycle continues. Separate strains occur in cats and dogs. Return to top of page Life Cycle: Anclystoma braziliense follows the same developmental pattern of human and canine hookworms. When man is exposed to the infective larvae. braziliense are unable to to penetrate the subdermal layers of the skin of man. braziliense. . NOTE: The canine and feline strains of A. thus humans are a "dead end host" of A. and then on to the intestinal tract of the host. the larvae develop into adults. the larvae tunnel through the skin creating a lesion that is at first inflamed and then elevated and vesicular. Cat (Felis catus). and finally dry and crusted. The larvae may tunnel through the skin for weeks but rarely reach the circulation. Eggs are passed in feces.Return to top of page Hosts: Definitive: dog (Canis Familiaris).

Eggs are 60 x 40 um. Return to top of page Common Diagnostic Test Fecal float to recover eggs. L1 larvae are occasionally found in older feces (over 24 hours old) and are diagnostic of infection. diagram of L1 larvae (right).Return to top of page Site where adult parasite is found in host: Small intestine Return to top of page Diagnostic Stage: Eggs are found in fecal flotation. L1 larvae (middle). Ancylostoma braziliense eggs (left). .

Milbemycin oxime. occasionally death. Ivermectin. Febantel/Pyrantel embonate. weakness. diarrhea. Fenbendazole. Return to top of page Treatment: Drug: Febantel. weight loss.Return to top of page Clinical Signs: Puppies and kittens: Anemia. Pyrantel Pamoate Return to top of page . Adults: Usually asymptomatic but any of the above symptoms may be present. poor growth. Mebendazole.

5 to 11 mm long and have a well developed bursa.Ancylostoma tubaeforme Homepage || Root || Main || Common name: Cat Hookworm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Ancylostomatidae Genus: Ancylostoma Species: tubaeforme Bookmarks Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: Males are 9. . females are 12 to 15 mm. The mouth has three pairs of ventral teeth.

The L3 are enclosed in the cuticle of the previous stage and thus are protected from the environment. reaching the infective third stage (L3) in under a week.Return to top of page Hosts: Definitive: Cats. Return to top of page Life Cycle: The egg leaves the host in the feces and hatches in one or two days. The L3 are ingested by the cat and they take up residence in the small intestine without undergoing a somatic migration. The larvae grow and molt. Under good conditions they may survive for months. Return to top of page Site where adult parasite is found in host: Small Intestine Return to top of page Diagnostic Stage: Egg: 64 X 41 µm Return to top of page . The adult worm feeds on blood.

Ivermectin. Febantel/Pyrantel embonate Return to top of page . Fenbendazole.Common Diagnostic Test: Fecal flotation Return to top of page Clinical Signs: In heavy infections anemia will develop and may be fatal. Low to moderate levels of infection produce a mild enteritis. Pyrantel Pamoate. Milbemycin oxime. Selamectin. Return to top of page Treatment: Drug: Febantel.

Eucoleus (Capillaria) aerophilia Homepage || Root || Main || Common name: Lungworm of dogs and cats Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Family: Trichuroidea Genus: Eucoleus (previously: Capillaria) Species: aerophilia Bookamrk Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 25 mm (male) to 32 mm (female). .

1998. cats. aerophilia. The larva is carried by the blood to the lungs where it develops to the adult stage in the mucosa of the trachea and bronchi. coughed up. Burgess Publishing Co. foxes. wolves (definitive). The prepatent period is about 6 weeks. Nematode parasites of domestic animals and man. swallowed and eventually pass out with the feces. The egg will reach the infective stage in 5 to 7 weeks. F .vulva. If an earthworm ingests an infective egg. Return to top of page Hosts: Dogs.eggs. the egg will hatch in the gut of the worm and the larva will migrate to the worm's tissues where it will .posterior end of female . Eggs are laid into the lumen of these organs.Illustration C. coyotes. E.adult worm. B . Minneapolis.. MN. Earthworms (paratenic). The infective larva leaves the egg or earthworm in the small intestine of the host and penetrates the intestinal wall. From: Levine. Return to top of page Life Cycle: The host ingests an infective egg or an earthworm which contains an infective larva in its tissues. G . C . D. H .posterior end of male. A .

Return to top of page Common Diagnostic Test Fecal float Tracheal wash Return to top of page . Return to top of page Site in host where adult parasite is found: Mucosa of the trachea and bronchi Return to top of page Diagnostic Stage: Egg with bipolar plugs (asymmetrical) and a rough surface ("netted" in appearance). The egg measures 70 um X 35 um.wait for a definitive host to eat the worm.

Clinical Signs: Usually asymptomatic in dogs and cats. SQ or PO. sometimes causing a slight cough. SID. for 7 to 10 days . one dose. Return to top of page Treatment : Return to top of page Ivermectin 0.2 mg/kg. PO. repeat if needed. In heavily infected foxes may show rattling and wheezy breathing and some coughing. Fenbendazole 50 mg/kg.

.Pearsonema (Capillaria) plica Homepage || Root || Main || Common name: Bladder worm of dogs and cats. Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Family: Trichuroidea Genus: Pearsonema (previously: Capillaria) Species: plica Bookmarks Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 30 mm to 60 mm long.

posterior end of female . Nematode parasites of domestic animals and man.adult worm. The first stage-larvae leaves the earthworm in the small intestine of the definitive host.vulva. where it will molt again in 7 days. MN. Earthworms (intermediate) . and invades the intestinal wall.eggs.Illustration C. foxes.. B . H . wolves and probably other canids (definitive). molts. aerophilia. The third stage-larva will make its way to the wall of the urinary bladder via the blood to the kidney and then migrate down the ureter.posterior end of male. Minneapolis. C . From: Levine. A . cats. F . G . D. The prepatent . which will hatch in the gut of the worm and the larva will migrate to the worm's tissues where it will wait for a definitive host to eat the worm. 1998. Return to top of page Life Cycle: The earthworm ingests an infective egg. E. Burgess Publishing Co. Return to top of page Hosts: Dogs.

Return to top of page Site in host where adult parasite is found: Mucus membrane of the urinary bladder Sometimes seen in the pelvis of the kidney or other areas of the urinary tract. The egg measures 65 um X 25 um.period is about 60 days. Return to top of page . Eggs are laid into the lumen of the bladder. Return to top of page Diagnostic Stage: Egg with bipolar plugs (asymmetrical) and a rough surface. and pass out with the urine. Return to top of page Common Diagnostic Test Urine sedimentation.

SQ or PO.Clinical Signs: Usually asymptomatic in dogs and cats Sometimes causing cystitis. PO. one dose. repeat if needed. Fenbendazole 50 mg/kg. Return to top of page . Return to top of page Treatment: Treatment: Ivermectin 0.2 mg/kg. for 10 to 14 days. SID.

Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiida Family: Cryptosporidiidae Genus: Cryptosporidium Species: parvum Bookmarks Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The schizonts live in the epithelial cells of the small intestine. Return to top of page .Cryptosporidium parvum Homepage || Root || Main || Common name: Cryptosporidium .

Return to top of page Life Cycle: Life Cycle: The oocyst is ingested by the host. The type I schizont produces zoites that can produce either type I or type II schizonts. PA Return to top of page Site in host where adult parasite is . Bowman. dogs. 1995. including humans. However. The parasite undergoes two types of schizogony and one round of gametogony.B. Saunders Co. It excysts in the small intestine and the sporozoites (4 per cyst) invade the microvillus border of intestinal epithelial cells. 6th edition. thus the parasite can undergo continuous asexual reproduction as type I schizonts. W. invade cells and begin the life cycle over (autoinfection). cats. D. Sporulated (infective) oocysts leave the cells and most of them pass out with the feces. Philadelphia. Lifecycle illustration adapted from: Georgi's' Parasitology for Veterinarians..Hosts: Definitive: Many mammals. some of the oocysts will excyst in the intestine.D. Type II schizonts produce zoites which develop into gametocytes. cattle.

Supportive therapy to prevent . It may be very difficult to identify the oocysts.found: Cells of the small intestine. Treat symptoms. Return to top of page Treatment: None known. Return to top of page Clinical Signs: Many times asymptomatic Profuse watery diarrhea. Return to top of page Diagnostic Stage: Oocyst 4 um to 8 um Return to top of page Common Diagnostic Test Fecal flotation . Acid Fast Stain of a Direct Smear to identify oocysts.

dehydration. Return to top of page .

lepivora. . Homepage || Root || Main || Common name: Rodent Bot Fly Kingdom: Animalia Phylum: Arthropoda Class: Insecta Order: Diptera Family: Cuterebridae Genus: Cuterebra Species: buccata. and others. emasculator. Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: The adult fly measures 20 mm or more in length.Cuterebra spp. americana.

Once on the skin they move to natural body openings such as the nares. Return to top of page Site where adult parasite is found in . The larva then cuts a hole in the skin in order to breath. mice. chipmunks. The larva will then emerge through its breathing hole and drop to the ground where it will pupate under the soil. The larva grows and molts until it has become a third instar and about 25 mm long. Inside the nose they penetrate the mucosa and migrate to a subcutaneous position. cats and dogs. Return to top of page Life Cycle: The adult female lays her eggs near the entrance of a rodent burrow. rats. In the spring the fly will emerge from the pupal case. Adult flies do not feed and will live for about 2 weeks. The fly may over winter as a pupa.Return to top of page Hosts: Larvae are found in rabbits. The eggs hatch and the first instar larvae wait for a host. squirrels. this takes 3 to 4 weeks. When a host passes by they attach to the hair and move to the skin.

and throat (trachea). in cats the larvae have also been found in the brain. Return to top of page Common Diagnostic Test: Gross examination Return to top of page .click on image to highlight parasite.host: Under the skin. Return to top of page Diagnostic Stage: Larva: Histological section of Cutebra in cat brain (0.75 mm long) .

Return to top of page Treatment: Surgical removal of the intact larva. In the trachea the larva may block the air supply In the brain will cause neurological symptoms consistent with the area of the brain in which it is located. Return to top of page .Clinical Signs: Depends on where the larva is located: In the skin the larva causes few problems.

. Ring forms can be found in red blood cells.Cytauxzoon felis Homepage || Root || Main || Common name: Cytauxzoon Kingdom: Animalia Phylum: Apicomplexa Class: Sporozoea Order: Piroplasmida Family: Theileriidae Genus: Cytauxzoon Species: felis Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: The schizont is found in mononuclear phagocytes.

lungs. Piroplasms (ring forms) are found in the erythrocytes. A nymphal tick will pick up the parasite while feeding on an infected cat (bobcats show no clinical signs and thus may act as a reservoir host) and transmit it to another cat when it feeds again as an adult (thus acting as a transstadial vector). . spleen and lymph nodes. Schizonts are found in the reticuloendothelial cells in the liver. in the bone marrow and lymph nodes. Piroplasms are found in the erythrocytes. Return to top of page Site where adult parasite is found in host: In macrophages lining the blood vessels of the spleen. lung. Return to top of page Diagnostic Stage: Schizonts or piroplasms. cats Vector: Dermacentor variabilis Return to top of page Life Cycle: The cat is infected via the bite of the tick Dermacentor variabilis.Return to top of page Hosts: Definitive: Bobcat. liver.

Right: Intraerythrocytic piroplasms (arrows) seen in cat blood smear. Return to top of page . bone marrow or spleenic aspirates. icteric. Return to top of page Clinical Signs: Lethargy. Return to top of page Common Diagnostic Test: Cytological examination of blood smears. depression. felis seen in mononuclear cell from a bone marrow aspirate smear (arrow). Rapidly fatal. Return to top of page Treatment: No known treatment. Left: Schizonts of C.Image adapted from JAVMA. anemia. prolonged capillary re-fill time. Fig 1 and 3. 1994. 205(#3):455-460. dehydration. Supportive treatment may help temporarily.

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite : The adult worms are up to 2 m in length and gravid proglottids have a tightly coiled uterus full of brown eggs. .Diphyllobothrium latum Homepage || Root || Main || Common name: Broad Fish Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Pseudophyllidea Family: Diphyllobothriidae Genus : Diphyllobothrium Species: latum Bookmark.

When a fish ingests the infected copepod. dogs. bears and other fish eating mammals(definitive). Return to top of page Life Cycle: The egg hatches in water releasing a ciliated.Adult D. cats. Freshwater fish (2nd intermediate or paratenic). Copepod (first intermediate). latum Return to top of page Hosts: Mink. latum Proglottid of D. free-swimming coracidium. the procercoid will migrate to the muscles or viscera and . humans. A copepod ingests the coracidium and it develops into a procercoid in the body cavity.

If the second intermediate host is eaten by another fish the pleurocercoid will migrate to the muscles or viscera of the new (paratenic) host. Eggs are 75 . or examination of the proglottid if they happen to pass in the feces. Return to top of page Site in host where adult parasite is found: The small intestine Return to top of page Diagnostic Stage: Egg.develop to the pleurocercoid stage. When the host containing the pleurocercoid is ingested by a definitive host the worm attaches to the small intestine wall and begins to develop proglottids. The prepatent period is 3 to 4 weeks.45 um. Return to top of page Common Diagnostic Test Eggs can sometimes be seen on Fecal flotation. although they . Eggs are released from the gravid proglottids and pass out in the feces.

In humans may cause pernicious anemia due to vitamin B12 uptake by the worm. Return to top of page Treatment: Epsiprantel.don't always float. Eggs can be found in a fecal sedimentation. Praziquantel Return to top of page . Return to top of page Clinical Signs: Usually asymptomatic in the dog and cat.

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite : The adult worms measure up to 50 cm long. .Dipylidium caninum Homepage || Root || Main || Common name: Double-pore Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Dipylidiidae Genus : Dipylidium Species: caninum Bookmark.

Return to top of page Life Cycle: The larval flea ingests the egg. humans (definitive). reaching infectivity in the adult flea about 1 day after the flea has found a host. cats. scolex (right). When the dog ingests an infected flea while grooming. Schematic illustration of Dipylidium caninum Return to top of page Hosts: Dogs. fox. lice [Trichodectes canis] (intermediate). gravid proglottid (middle). .Adult Dipylidium caninum (left). Fleas [Ctenocephalides felis]. The cysticercoid develops in the flea.

Dipylidium caninum proglottids on cat feces. detach from the end of the worm and pass out in the feces. Eggs are 25 to 30 um in oblong packets of 20 or less eggs. The proglottids are the cream colored objects on the surface of the sample. the protoscolex attaches to the small intestinal wall and the worms begin to form proglottids. 4 proglottids are near the kitty-litter and 3 others are seen on the parts of the sample free of kitty-litter. Return to top of page Site in host where adult parasite is found: The small intestine. The prepatent period is about 2 weeks. or left behind where the pet was sitting) and/or egg packets. Return to top of page . Return to top of page Diagnostic Stage: Proglottid (seen on feces. containing the eggs. Gravid proglottids. the peri-anal area. Egg packets expressed from a Dipylidium caninum proglottid.the cysticercoid is digested out.

Common Diagnostic Test Examination of the proglottid. Egg packets can sometimes be seen on Fecal flotation . Return to top of page Clinical Signs: Usually asymptomatic in the dog and cat. Praziquantel Return to top of page . Return to top of page Treatment: Epsiprantel.if a proglottid has broken and spilled its eggs into the feces.

Dirofilaria immitis Homepage || Root || Main || Common name: Canine heartworm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Family: Filariidae Genus : Dirofilaria Species: immitis Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: .

ferrets. worms in situ (right) Return to top of page Hosts: Dogs. The female worm lays micro-filariae into the blood. Mosquitoes (intermediate) . seals (definitive).. When the mosquito again feeds on a dog the infective third stage-larva is injected into the skin. Adult worms: male and female (left). The pre-patent period is about 6 months. The fourth stage-larva migrates through the dog's tissues. The microfilaria develops into an infective larva in about 14 days. eventually reaching the pulmonary artery where it matures to the adult stage. The third stage-larva moults to the fourth stage within 48 hours.The adult worms measure 15 cm (male) to 30 cm (female). Return to top of page . Return to top of page Life Cycle: The mosquito ingests a microfilaria when feeding on an infected dog. cats.

In cats ultrasound of the heart and the base of the pulmonary arteries can show the presence of heartworm adults. In cats we can look for Antibody produced against heartworm larvae and adults which have been in the cat for more than 60 days (thus the antibody test tells us the cat was exposed. Return to top of page Diagnostic Stage: The only stage of the parasite which can be recovered for diagnosis is the microfilaria (a free swimming embryo found in the blood).7 to 7.Site in host where adult parasite is found : The pulmonary arteries and sometimes the right atrium. microfilaria will be missing from about 30% of infected dogs and most of the infected cats. and are 6.0 um wide. Therefore serological techniques are usually used to make a diagnosis. but not if there are adult worms present). In dogs and cats we can look for Antigen produced by mature female worms (over 6 months of age). Microfilariae are found in blood smear using the Knott technique: Micro-filariae are found in blood smear : . Microfilariae are 270 to 325 um in length. However.

Microfilariae are found in blood smear using acid phosphatase stain: Return to top of page Common Diagnostic Tests Antigen Tests Antibody Test (cats) Blood smear Modified Knott Method . Return to top of page . Filter test Ultrasound (cats) This is a real time movie of an ultrasound of an infected cat. Ultrasound (ferrets) This is a real time movie of an ultrasound of an infected ferret.

Trade name: Revolution . Iverhart Plus.Clinical Signs: Asymptomatic in dogs with low worm burdens. Tri-Heart Plus Chewable Tablets.Trade names: ProHeart.Trade names: Interceptor. Heartgard for Cats Moxidectin . Adulticides Thiacetarsamide sodium Melarsomine dihydrochloride .Tradename: Immiticide Prophylactics Ivermectin . With greater worm burdens exercise intolerance. ProHeart 6 Milbemycin oxime . Heartgard 30. hypertension.Trade names: Heartgard Plus. Advantage® Duo. Sudden death may be the only clinical feature seen in some cases of feline heartworm. Return to top of page Treatment: Pharmacueticals or surgery to remove worms. right heart failure may be seen. Sentinel SELAMECTIN .

DIETHYLCARBAMIZINE .Trade name: Filaribits Return to top of page Also see the Dirofilaria immitis life cycle page .

.Echinococcus multilocularis Homepage || Root || Main || Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus : Echinococcus Species: multilocularis Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 1 to 5 mm long.

lungs. When the dog eats the vole and ingests the hydatid cyst. multilocularis adult E. field mice. detach from the end of the worm and spill their eggs into the lumen of the intestine.E. Return to top of page Life Cycle: The vole ingests an egg. The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travels to the liver via the blood. Microtine rodents (voles. multilocularis adults from coyote Return to top of page Hosts: Foxes.) (intermediate). wolves and other wild canids (definitive). The eggs pass out in . coyotes. etc. containing the eggs. shrews. The alveolar hydatid cyst develops in (in order of likelihood) the liver. dogs. the protoscolices attach to the small intestinal wall and the worms begin to form proglottids. brain or other organ. cats. Gravid proglottids.

Return to top of page Clinical Signs: Usually asymptomatic in the dog. Clinical signs in the intermediate host depend on where the hydatid .the feces.32 um. Return to top of page Site in host where adult parasite is found: The small intestine Return to top of page Diagnostic Stage: Eggs are found in fecal flotation Return to top of page Common Diagnostic Test Fecal float to recover eggs . The prepatent period is less than 40 days. Eggs are 38 .

Praziquantel. and grows like a malignant tumor with metastasis Return to top of page Treatment: Epsiprantel. E.cyst is located and how old (large) it is. granulosus as the hydatid cyst becomes more irregular. multilocularis produces a more serious condition than E. Fenbendazole Return to top of page . filled with connective tissue and gelatinous masses.

2 mm wide.Eurytrema procyonis Homepage || Root || Main || Common name: Pancreatic Fluke Kingdom: Animalia Phylum: Platyhelminthes Class: Trematoda Order: Plagiorchiida Family: Dicrocoeliidae Genus: Eurytrema Species: procyonis Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: The adult measures 2.9 mm long by 1. .

and Protozoa of Domesticated Animals. and exit in the feces. Philadelphia. Helminths. 1982. or some other second intermediate host. are expelled form the snail's respiratory pore and deposited on vegetation. . make their way to the intestine. The cercariae develop and remain in the daughter sporocysts.The above image is adapted from Fig 1-10. the worm excysts in the gut and migrates to the pancreatic duct where it matures to the adult stage. Lea & Fabiger. red and grey foxes. and raccoons. pg 28. When the metacercariae in the grasshopper are eaten by the definitive host. Intermediate: First: Snails (Mesodon thyroidus) Second: arthropod (grasshopper?) Return to top of page Life Cycle: Eggs are ingested by snails. These masses are eaten by grasshoppers. Return to top of page Hosts: Definitive: Cats.. Soulsby. Masses of sporocysts. covered in mucus. 7th ed. arthropods. Eggs pass down the pancreatic duct. The trematode develops in the hemocoel of the snail. PA. Two generations of sporocysts are produced.

however.Return to top of page Site where adult parasite is found in host: Pancreatic duct Return to top of page Diagnostic Stage: Egg in feces: 56 by 36 µm . the pancreatic duct becomes hardened and thickened and this may lead to pancreatic insufficiency. Return to top of page Common Diagnostic Test: Ethyl acetate sedimentation Return to top of page Clinical Signs: Usually none. it has been noted that in some cats with hundreds of worms. Adult worm surgically removed from bile duct. Return to top of page Treatment: .

Drug: Praziquantel Return to top of page .

doudenalis) Kingdom: Protista Phylum: Protozoa Class: Sarcomastigophora Order: Diplomonadida Family: Hexamitidae Genus: Giardia Species: duodenale Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: Trophozoite: The feeding stage of this flagellate measures about 18 um long X 5 -10 um wide. It has 8 flagella and the ventral side is modified as a sucking disk. .lambia. intestinalis and G. G.Giardia duodenalis Homepage || Root || Main || Common name: Giardiasis (also known as G.

cats.Left Panel: Giardia trophozoite. of them) . The trophozoite divides by binary fission. Return to top of page Life Cycle: The cyst is ingested (usually in fecally contaminated water or food) and encysts in the small intestine. where it absorbs nutrients across its surface. The trophozoites will either continue to divide or they (some. including dogs. cattle. Right Panel: Giardiatrophozoite (lower right). but not all. horses and primates. The trophozoite attaches to the mucosa of the small intestine. Return to top of page Hosts: Most mammals. Illustration of Giardia trophozoites and cysts. pigs. sheep.

The prepatent period can be variable.encyst. Giardia cysts Return to top of page Common Diagnostic Test ZnSO4 centrifugational flotation ELISA for fecal antigen Note: Cyst shedding is inconsistent and several samples taken on different days may need to be examined. The cysts will pass out of the host in the feces. Return to top of page Diagnostic Stage: Cyst: Measures about 14 um X 8 um. . Return to top of page Site in host where adult parasite is found: Small intestine (usually the duodenum or jejunum). but it is usually given as 1 week.

Drug: Metronidazole Dose: Dog and Cat: 30 mg/kg. Drug: Febantel Dose: Dog: 25 mg/kg (PO) (Drontal Plus) for 5 days.Return to top of page Clinical Signs: In young animals: Soft stools. PO. The stools may have a large fat content due to malabsorption and appear mucoid. Return to top of page . SID. for 5 days. for 5 days . In adult animals: Usually asymptomatic Return to top of page Treatment: Drug: Fenbendazole Dose: Dog and Cat: 50 mg/kg PO SID. diarrhea (which may be chronic).

Hammondia hammondiHomepage || Root || Main || Common name: Kingdom: Animalia Phylum: Apicomplexa Class: Sporozoea Order: Eucoccidiida Family: Sarcocystidae Genus: Hammondia Species: hammondi Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: Schizonts and gametocytes are intracellular in the intestine of the cat. The photo below is of Toxoplasma gondii. but the appearance of H. hammondi and Toxoplasma are so similar that differentiation of the .

In about 10 days some of the tachyzoites. Return to top of page Hosts: Definitive: Cats Intermediate: Rodents Return to top of page Life Cycle: The unsporulated oocyst leaves the cat in the feces. become bradyzoites. the zoites from the cyst invade the intestinal cells and develop to the schizont stage. J. The male gametocyte releases gametes which fuse with the female gametocytes and form oocysts. a slowly multiplying cyst stage. after invading a skeletal muscle cell. When a rodent ingests the infective oocyst. or to gametocytes. The bradyzoite is infectious to the cat.. the zoites invade intestinal cells and multiply as tachyzoites. It is 5 or 6 days between the initial infection of the cat and the release of oocysts. sporulated stage (which contains 8 zoites).two can only be accomplished through study of the parasite lifecycle. When the cat eats a rodent with bradyzoites in its tissues. An Atlas of Protozoan Parasites in Animal Tissues. Page 53. The schizonts release more zoites which invade new cells and give rise to either more schizonts. The oocysts rupture out of the cells and are voided with the feces.P. . Photo from Dubey. 1988. It takes 3 days in the environment to develop to the infective.

Arthropods and Protozoa of Domesticated Animals. hammondi oocyst (#5) is highlighted. Coccidia of the cat. 627. Philadelphia. 1982. Helminths. H.Return to top of page Site where adult parasite is found in host: Small intestinal cells Return to top of page Diagnostic Stage: The oocyst: 11 X 12 µm (easily confused with the oocyst of Toxoplasma gondii). Drawing adapted from Soulsby. 7th Edition. pg. Lea & Febiger. EJL Soulsby. Return to top of page Common Diagnostic Test: Fecal flotation .

Try treating as for Toxoplasma: Clindamycin. Hammondia hammondi is not pathogenic to the immunocompetent cat. Return to top of page Treatment: None known. Drug: Clindamycin Return to top of page .Return to top of page Clinical Signs: None.

.Isospora felis Homepage || Root || Main || Common name: Coccidia Kingdom: Animalia Phylum: Apicomplexa Class: Sporozoea Order: Eucoccidiida Family: Sarcocystidae Genus: Isospora Species: felis Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: Schizonts and gametocytes are intracellular in the intestine of the cat.

P.. An Atlas of Protozoan Parasites in Animal Tissues. It takes 3 days in the environment to develop to the infective. The cat can become infected by ingesting a sporulated oocyst or a mouse which has ingested an infective oocyst. the sporozoites invade intestinal cells and encyst as bradyzoites. Return to top of page Hosts: Definitive: Cats Paratenic: Mice Return to top of page Life Cycle: The unsporulated oocyst leaves the cat in the feces.Top photo from Dubey. J. When a rodent ingests the infective oocyst. When the cat eats an infective oocyst or a rodent with bradyzoites in its tissues. Page 33. sporulated stage (which contains 4 sporozoites in each of 2 sporocysts). the . The bradyzoite is infectious to the cat. 1988.

The schizonts release more zoites which invade new cells and give rise to the next generation of schizonts. It is 7 or 8 days between the initial infection of the cat and the release of oocysts.zoites invade the intestinal cells and develop to the schizont stage. The male gametocyte releases gametes which fuse with the female gametocytes and form oocysts. There are 3 generations of schizonts. Left: unsporulated Return to top of page . The oocysts rupture out of the cells and are voided with the feces. During its first infection a cat will shed oocysts for 10 to 11 days. Return to top of page Site where adult parasite is found in host: Small intestinal cells Return to top of page Diagnostic Stage: The oocyst: 42 X 28 µm Right: Isospora felis sporulated (infectious) oocyst. Zoites released from the last generation of schizonts invade cells and form gametocytes.

In young cats with a heavy infection and stress (due to numerous causes. is seen. sometimes with blood in the stool. especially infection with other intestinal pathogens) chronic diarrhea. Return to top of page Treatment: Drug: Sulfadimethoxine Return to top of page .Common Diagnostic Test: Fecal flotation Return to top of page Clinical Signs: Usually no signs.

Isospora rivolta Homepage || Root || Main || Common name: Coccidia Kingdom: Animalia Phylum: Apicomplexa Class: Sporozoea Order: Eucoccidiida Family: Sarcocystidae Genus: Isospora Species: rivolta Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: Schizonts and gametocytes are intracellular in the intestine of the cat. .

When a rodent ingests the infective oocyst. the sporozoites invade intestinal cells and encyst as bradyzoites. The cat can become infected by ingesting a sporulated oocyst or a mouse which has ingested an infective oocyst. 1988.. When the cat eats an infective oocyst or a rodent with bradyzoites in its tissues. the . The bradyzoite is infectious to the cat. Page 33. It takes 3 days in the environment to develop to the infective. J.Top photo from Dubey. An Atlas of Protozoan Parasites in Animal Tissues.P. Return to top of page Hosts: Definitive: Cats Paratenic: Mice Return to top of page Life Cycle: The unsporulated oocyst leaves the cat in the feces. sporulated stage (which contains 4 sporozoites in each of 2 sporocysts).

It is 4 to 7 days between the initial infection of the cat and the release of oocysts. Return to top of page Common Diagnostic Test: . Zoites released from the last generation of schizonts invade cells and form gametocytes. Return to top of page Site where adult parasite is found in host: Small intestinal cells Return to top of page Diagnostic Stage: Oocyst: 25 X 20 µm This oocyst is sporulated (infectious).zoites invade the intestinal cells and develop to the schizont stage. The male gametocyte releases gametes which fuse with the female gametocytes and form oocysts. The oocysts rupture out of the cells and are voided with the feces. The schizonts release more zoites which invade new cells. During its first infection a cat will shed oocysts for greater than 14 days.

is seen. In young cats with a heavy infection and stress (due to numerous causes. sometimes with blood in the stool.Fecal flotation Return to top of page Clinical Signs: Usually no signs. Return to top of page Treatment: Drug: Sulfadimethoxine Return to top of page . especially infection with other intestinal pathogens) chronic diarrhea.

Mesocestoides corti Homepage || Root || Main || Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Order: Mesocestoididea Family: Mesocestoididae Genus: Mesocestoides Species: corti Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: .

Return to top of page Hosts: Carnivores (including dogs). birds. From left to right: Schematic illustration and photomicrograph of Mesocestoides scolex. Free-living mites (first intermediate). Mesocestoides adult segments. birds and humans (definitive). and mammals (2nd intermediate) Return to top of page .The gravid proglottid of the adult contains a paruterine organ in which the eggs are stored. Amphibians. reptiles.

The prepatent period is about 16 to 20 days. the cysticercoid is digested out and develops to a tetrathyridium in the peritoneal cavity. detach from the end of the worm and pass out in the feces. A cysticercoid develops in the arthropod. reptiles. the protoscolex attaches to the small intestinal wall and the worms begin to form proglottids.Life Cycle: The life cycle is not completely known. Gravid proglottids. upon entering the definitive host. . When the second intermediate host is eaten by a dog or other carnivore the tetrathyridium is digested out. Probably an orbatid mite or a coprophillic insect ingests the egg. may go to the peritoneal cavity and multiply asexually. birds. This larval form will multiply asexually. Also. the tetrathyridium. and mammals) ingests an infected arthropod. When the 2nd intermediate host (amphibians. containing the eggs. Return to top of page Site in host where adult parasite is found: The small intestine Return to top of page Diagnostic Stage: Gross examination of the proglottid in feces. The adult worms may multiply asexually in the definitive host's intestine.

then give: . peritonitis and ascites may develop. Return to top of page Treatment: For adult tapeworms: Epsiprantel.Return to top of page Common Diagnostic Test Examination of the proglottid in feces. Return to top of page Clinical Signs: Usually asymptomatic in the dog when infected with the adult. When infected with the tetrathyridium. Praziquantel For treatment of tetrathyridia in peritoneal cavity*: Lavage the peritoneal cavity to remove fluid and tetrathyridia.

for 1 or 2 months. J. *(Crosbie. P. 1998. 213:1578-1583. Med. q 12 h.) Return to top of page . PO.. Vet. et al.R.Fenbendazole: 100 mg/kg. Am. Assoc.

8 mm long and has a well developed bursa. the .Ollulanus tricuspis Homepage || Root || Main || Common name: Stomach worm of cats Kingdom: Animalia Phylum: Nemathelmintes Class: Nematoda Order: Strongylida Family: Ollulanidae Genus: Ollulanus Species: tricuspis Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: The male worm measures 0.8 to 1 mm long. The female worm measures 0.7 to 0.

vulva is in the posterior part of the body and the tail has 5 cusps. . The prepatent period (the time from when the L3s enter the host till the next generation of L3s is born) is about 33 to 37 days. pigs. and dogs (rarely). 1982. . If the L3s in the vomitus are ingested by a suitable host they will develop to adults in the stomach. The eggs hatch while in the female and develop to the infectious third-stage larvae (L3). The L3s may live in the vomitus for up to 12 days. foxes. Helminths. 7th Edition. Line drawing adapted from from Soulsby pg. Arthropods and Protozoa of Domesticated Animals. Lea & Febiger. Return to top of page Hosts: Definitive: Cats (wild and domestic). The L3 may continue its development to the L4 and adult stage in the same cat or it may be carried into the environment in parasite-induced vomitus. which is released into the lumen of the stomach. Return to top of page Life Cycle: Adult worms live in the stomach and may burrow into the gastric mucosa. EJL Soulsby. 261. Philadelphia. Larvae which pass into the intestine die and are digested.

1984. the stomach worm of the cat.A. The larvae may be concentrated from the vomitus by use of the Baermann technique . Return to top of page Common Diagnostic Test: Diagnosis can be made by finding larvae or adults after inducing the cat to vomit or after stomach irrigation (described in: M.35). Ollulanus tricuspis. 1984. Feline Practice 14 (5): 22 . the stomach worm of the cat. Hasslinger. Ollulanus tricuspis. Image from Fig 3 pg 23 M. Hasslinger.Return to top of page Site where adult parasite is found in host: Stomach Return to top of page Diagnostic Stage: The L3.35. L4 or adults in the vomitus.A. Feline Practice 14 (5): 22 .

Return to top of page Clinical Signs: Vomiting chronic gastritis Return to top of page Treatment: Drug: Fenbendazole Return to top of page .

Paragonimus kellicotti Homepage || Root || Main || Common name: Lung fluke Kingdom: Animalia Phylum: Platyhelminthes Class: Tramatoda Order: Digenea Family: Troglotrematidae Genus: Paragonimus Species: kellicotti Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment .

dogs. The . Fresh-water crabs and crayfish (second intermediate). fox and other carnivores (definitive). and other genera] (first intermediate). cat. Snails [Melania. Return to top of page Life Cycle: The egg matures (2 to 3 weeks) and hatches in water.Adult Parasite: The adult worms measure 8 to 16 mm long. raccoons. muskrat. Adult fluke Cross section of a pair of adult flukes Return to top of page Hosts: Mink. Ampullaria.

The eggs then pass out with the feces. and then redia develop in the snail. liver.miracidium finds and penetrates a snail. Eggs are laid in the cyst and pass out to the bronchiole. or muscles as metacercaria. The adult flukes are normally found in pairs within cysts in the lung. Sporocysts. and when mature emerge from the snail. They are passed up with the lung mucus and are swallowed. The cercariae swim around until they find a crustacean which they penetrate and encyst in the heart. When the definitive host eats the crayfish the metacercaria excyst in the host's small intestine. Return to top of page Site in host where adult parasite is found: The lungs Return to top of page Diagnostic Stage: Egg 90 X 50 µm . The prepatent period is about 3 to 36 days. The cyst has an opening to a bronchiole. The young fluke penetrates the gut wall and wanders in the peritoneal cavity for 1 to 14 days before penetrating the diaphragm and then the lungs. Cercariae develop in the redia.

Return to top of page Treatment: Praziquantel at a high dose. Tracheal wash.Return to top of page Common Diagnostic Test Ethyl-acetate sedimentation. chronic bronchiolitis. Return to top of page . Return to top of page Clinical Signs: Intermittent cough. chronic eosinophilic granulomatous pneumonia. Fenbendazole for 10 to 14 days. lethargy.

Parametorchis complexus Homepage || Root || Main || Common name: Bile duct fluke of cats and dogs Kingdom: Animalia Phylum: Platyhelminthes Class: Trematoda Order: Opisthorchiida Family: Opisthorchiidae Genus: Parametorchis Species: complexus Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: The adult measures 5 to 10 mm long by 1.5 to 2 mm wide. .

Return to top of page Hosts: Definitive: cats and dogs Intermediate: First: Snails. Second: Fish Return to top of page Life Cycle: Egg hatches in water. Cercariae leave the snail and invade the skin of a fish. In the fish the parasite encysts as a metacercaria. The miracidium invades a snail. Return to top of page Site where adult parasite is found in host: Bile duct Return to top of page . When the infected fish is eaten by the cat the metacercaria excysts and the worm makes its way to the bile duct where it matures. Eggs in the bile make their way to the intestine and exit in the feces.

Return to top of page Praziquantel. Fenbendazole Treatment: Return to top of page . Return to top of page Common Diagnostic Test: Ethyl acetate sedimentation Return to top of page Clinical Signs: Range from none to obstruction of the bile duct and hepatic insufficiency. Adult worm surgically removed from bile duct.Diagnostic Stage: Egg in feces: 24 by 12 um.

5 to 2.Platynosomum fastosum Homepage || Root || Main || Common name: Bile duct fluke of cats and dogs Kingdom: Animalia Phylum: Platyhelminthes Class: Trematoda Order: Plagiorchiida Family: Dicrocoeliidae Genus: Platynosomum Species: fastosum Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: The adult measures 4 to 8 mm long by 1.5 mm wide. .

Return to top of page Site where adult parasite is found in . Georgis' Parasitology for Veterinarians. The metacercaria is found in the bile ducts of the lizard. 1995. sixth edition. When the infected lizard is eaten by the cat the metacercaria excysts and the worm makes its way up the common bile duct to the bile ducts and gall bladder where it matures.D. and skinks.Photo adapted from Bowman. Cercariae encyst in lizards and other second intermediate hosts. toads. Return to top of page Life Cycle: Eggs are ingested by snails. Second: Lizards.. D. Return to top of page Hosts: Definitive: Cats Intermediate: First: Snails Sublima octona. Eggs in the bile make their way to the intestine and exit in the feces. geckos.

Return to top of page Common Diagnostic Test: Ethyl acetate sedimentation Note: if the bile duct is occluded eggs will not be able to make their way into the feces. Return to top of page Clinical Signs: Range from none to obstruction of the bile duct and hepatic insufficiency.host: Bile ducts and gall bladder Return to top of page Diagnostic Stage: Egg in feces: 34 to 50 by 20 to 35 um Adult worm surgically removed from bile duct. . and possibly death. (cross-section shown below).

Return to top of page Treatment: Drug: Praziquantel Return to top of page .

.Physaloptera Homepage || Root || Main || Common name: Stomach worm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Family: Physalopteridae Genus: Physaloptera Species: rara Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 40 to 48 mm long.

Return to top of page Site in host where adult parasite is found: Attached to the mucosa of the stomach. containing the infective first stage-larva.other species occur in wildlife (definitive).Anterior end of worm Return to top of page Hosts: Dogs and cats . Eggs are laid in the stomach and pass out with the feces.larval stages. . The dog eats the beetle and the worm develops to the adult stage in the stomach. Return to top of page Life Cycle: The egg. is passed in the feces and eaten by a beetle larva. Coprophagous beetles (intermediate) . The larva develops to the infective third stage larva.

Return to top of page . The egg measures 55 um X 32 um. Return to top of page Common Diagnostic Test These eggs do not usually float on a standard fecal flotation (they have a specific gravity > 1.2) Fecal sedimentation Direct fecal smear Return to top of page Clinical Signs: Usually asymptomatic Sometimes causing chronic vomiting.Return to top of page Diagnostic Stage: Thick walled egg with a larva inside it.

Fenbendazole and Ivermectin. Return to top of page .Treatment: Mebendazole. Pyrantel pamoate.

Sarcocystis cruzi Homepage || Root || Main || Common name: Sarcocystis Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiida Family: Sarcocystiidae Genus: Sarcocystis Species: cruzi Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The sarcocysts are found in the striated muscles of the intermediate host. Sexual stages are found .

rodents. Return to top of page Life Cycle: Prepatent period in dogs is 9 to 10 days. Return to top of page Hosts: Dogs. foxes. llamas and other mammals. . and raccoons (definitive) Cattle (intermediate). wolves. Other species of Sarcocystis use horses. coyotes.in the intestine of the definitive host.

Philadelphia. Bowman. PA Return to top of page Site in host where adult parasite is found: Lamina propria of the small intestine. Saunders Co. Return to top of page Common Diagnostic Test Biopsy to screen for cysts and adults Fecal flotation Return to top of page Clinical Signs: . 6th edition. 1995.Lifecycle illustration from : Georges' Parsitology for Veterinarians.. W.B. Return to top of page Diagnostic Stage: Sporocyst (16 X 11 um).D. D.

Return to top of page .Asymptomatic (unless the dog is immunosuppressed). Return to top of page Treatment: None usually given. Drug: Clindamycin may be tried in the dog.

Spirometra mansonoides Homepage Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Pseudophyllidea Family: Diphyllobothriidae Genus: Spriometra Species: mansonoides Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite : The adult worms are pinkish in color and gravid proglottids have a tightly coiled uterus full of brown eggs. .

raccoons. Return to top of page . free-swimming coracidium. the procercoid will migrate to the muscles or connective tissue and develop to the pleurocercoid stage. and mammals (2nd intermediate or paratenic). Amphibians. Eggs are released from the gravid proglottids and pass out in the feces. When the host containing the pleurocercoid is ingested by a definitive host the worm attaches to the small intestine wall and begins to develop proglottids. bobcat (definitive). cats. birds. If the second intermediate host is eaten by another animal the pleurocercoid will migrate to the muscles or connective tissue of the new (paratenic) host. The prepatent period is 10 to 30 days. When a vertebrate other than a fish ingests the infected copepod. Return to top of page Life Cycle: The egg hatches in water releasing a ciliated. the water snake Natrix]. reptiles [esp. Copepod (first intermediate). A copepod ingests the coracidium and it develops into a procercoid in the body cavity.Return to top of page Hosts: Dogs.

Eggs can be found in a fecal sedimentation. or examination of the proglottid if they happen to pass in the feces.Site in host where adult parasite is found: The small intestine Return to top of page Diagnostic Stage: Egg (~ 57 X 39 µm). Return to top of page . Return to top of page Clinical Signs: Usually asymptomatic in the dog and cat. although they don't always float. Return to top of page Common Diagnostic Test Eggs can sometimes be seen on fecal flotation .

Praziquantel.Treatment: Epsiprantel. Fenbendazole Return to top of page .

. Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Rhabditida Family: Strongyloididae Genus: Strongyloides Species: stercoralis Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 2 mm long.Strongyloides stercoralis Homepage || Root || Main || Common name: None.

The infective third-stage larva will penetrate the skin of the host. the first stage-larvae make their way to the lumen of the intestine and pass down the intestine. the female lays eggs which hatch releasing first stage-larvae. Return to top of page Life Cycle: The first stage larva passes out with the feces. These larvae will all develop to an infective third stage-larva. While in the lumen of the intestine the larva can make a developmental choice: it can remain as a first stage-larva and pass out with the feces. they mate.Adult female Return to top of page Hosts: Dogs. The larva has a choice of developmental directions: it can develop to the infective third stage-larva or it can develop to the free living adult. or it can molt twice and become an autoinfective third stage-larva while still in the . The adult lays eggs in the crypts of the small intestine where they hatch. There are both male and female free-living adults. and other higher primates (definitive). migrate through the tissues by a variety of routes and eventually end up in the small intestine where it will molt twice and become an adult parthenogenic female. humans.

If the bitch has either infective or autoinfective third-stage larvae migrating through her body. Return to top of page Site in host where adult parasite is found: crypts of the small intestine Return to top of page Diagnostic Stage: First stage-larva in the feces L1 larvae (left). they may end up in the mammary glands and be passed to the pups in the milk (transmammary transmission). and L1 larvae (right) of Strongyloides stercoralis . From here they are carried up the trachea. L3 larvae (middle).intestine. Generally autoinfective larvae develop only in young or immunosuppressed hosts. swallowed and eventually reach the small intestine where they molt twice and mature to the adult stage. Many of these penetrating autoinfective larvae will get into a lymph vessel or vein and be carried to the lungs where they break out into the air spaces. Autoinfective larvae will penetrate the intestinal wall (usually the wall of the large intestine).

Return to top of page Common Diagnostic Test Baermann Technique. Sometimes the ZnSO4 flotation technique will bring up a larva in good enough shape that it can be identified. Return to top of page . In cases with massive autoinfection. Return to top of page Clinical Signs: Light infections are usually asymptomatic In heavier infections you may see diarrhea. SID. Return to top of page Treatment: Ivermectin 2 doses a week apart. Fenbendazole. the host may have trouble breathing as a verminous pneumonia develops. for 14 days.

. lacks a neck and has a large scolex with 2 rows of hooks on the rostellum.Taenia taeniaeformis Homepage || Root || Main || Common name: Cat Tapeworm Kingdom: Animalia Phylum: Platyhelminthes Class: Cestoda Order: Taeniidea Family: Taeniidae Genus: Taenia Species: taeniaeformis Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: Measures up to 60 cm long.

. Return to top of page Site where adult parasite is found in host: Small intestine. The pre-patent period is between 36 and 42 days. Intermediate: Rodents Return to top of page Life Cycle: Eggs are ingested by a rodent and hatch in its gut.Return to top of page Hosts: Definitive: Cats. The hexacanth larva makes its way through the gut wall to the liver where it matures to the infectious strobilocercus stage. The rest of the larva is digested away and the tapeworm begins to grow. When the cat eats the infected rodent the larval tapeworm attaches to the cat's gut wall by its protoscolex. This portion of the life cycle takes about 60 days.

Crushing the proglottid between two slides releases the taenia-type eggs. Return to top of page Treatment: Epsiprantel.Return to top of page Diagnostic Stage: Proglottid with taenia-type eggs (31 to 36 um). Praziquantel. Return to top of page Common Diagnostic Test: Gross visualization of the proglottid on the feces or attached to the perianal region. Fenbendazole . Return to top of page Clinical Signs: Usually none.

Return to top of page .

.Toxascaris leonina Homepage || Root || Main || Common name: Roundworm (Ascarid) Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida Family: Ascarididae Genus : Toxascaris Species: leonina Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure between 7 cm (males) and 10 cm (females) long.

cats and other canids and felids (definitive). Bowman. .D. PA Larvae may be a cause of visceral larval migrans (VLM) in humans. The prepatent period is between 48 and 72 days with most of the dogs becoming patent between 56 and 65 days. Return to top of page Life Cycle: Life cycle illustration from : Georges' Parsitology for Veterinarians. Saunders Co.B. 6th edition. 1995. Philadelphia. D.. W. Rodents (paratenic).Anterior end of adult Return to top of page Hosts: Dogs.

mostly smooth and they possess a prominent vitelline membrane.Pre patent period from: J. Ascarid infections of cats and dogs. Return to top of page . 1987. WB Saunders Co.C. The Veterinary Clinics of North America. Philadelphia. Return to top of page Diagnostic Stage: Eggs are found in fecal flotation. Parsons. The egg measures 80 um X 67 um. 17(6):1307-1340. Return to top of page Site in host where adult parasite is found: Lumen of the small intestine. Return to top of page Common Diagnostic Test Fecal float to recover eggs. Eggs are colorless.

Ivermectin. Febantel/Pyrantel embonate. In heavy infections the dog may appear unthrifty. may be pot-bellied. Pyrantel Pamoate Return to top of page . Return to top of page Treatment: Febantel.Clinical Signs: Adults in the small intestine: Asymptomatic in light infections. Milbemycin oxime. Piperazine. Fenbendazole. and have diarrhea.

giving the anterior end an .Toxocara cati Homepage || Root || Main || Common name: Ascarid (Roundworm) of Cats Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida Family: Ascaridoidea Genus: Toxocara Species: cati Bookmark Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: Males measure 3 to 6 cm and females 4 to 10 cm. There are large cervical alae which end abruptly.

if a cat ingests an infective egg. First. Return to top of page Hosts: Definitive: Cats and wild felines. The infectious egg contains a second-stage larva. the larvae migrate through the gut wall. which live in the small intestinal lumen. birds.arrow-head shape. The cat can be infected in 3 ways. Return to top of page Life Cycle: The egg is passed in feces and develops in the environment to the infectious stage. They develop through the 3rd and 4th stages to the adults. The prepatent period . are carried up the trachea and are swallowed. the egg hatches in the stomach. pass through the liver to the lungs. Paratenic: Rodents and other mammals. In the lungs the larvae breakout into the air spaces. earthworms.

Like the case with a paratenic host.for this route of transmission is 56 days. Parsons. The prepatent period is about 3 weeks when the transmammary or paratenic host routes are utilized. although the adult worms are present in the small intestine by day 28. When the cat eats the mouse the larvae are freed and develop in the gut to adults. 1987. Return to top of page Site where adult parasite is found in host: Small intestine Return to top of page Diagnostic Stage: Egg: 65 to 75 µm in diameter and it has a pitted shell. Pre patent periods from: J. Philadelphia. The second stage larvae acquired in the milk by the nursing kitten develop in the intestine to adults. The second route of infection is via a paratenic host. If a mouse eats an infective egg the larva hatches and migrates to the tissues (liver) where it arrests. WB Saunders Co. no extra-intestinal migration takes place after transmammary transmission. The final route of infection is transmammary. Ascarid infections of cats and dogs. The Veterinary Clinics of North America.C. (Slides of egg in cross-section and surface pitting) . There is no extra-intestinal migration in this case. 17(6):1307-1340.

pot-bellied. Return to top of page Clinical Signs: The kitten may appear unthrifty. Pyrantel Pamoate.Return to top of page Common Diagnostic Test: Fecal float Identification of the adult worm recovered from the feces or vomitus. Pyrantel embonate Return to top of page .Milbemycin oxime. Ivermectin. Piperazine. and have intermittent diarrhea. Return to top of page Treatment: Fenbendazole.

Toxoplasma gondii Homepage || Root || Main || Common name: Toxoplasma Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiida Family: Sarcocystiidae Genus: Toxoplasma Species: gondii Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The schizonts are found in the small intestinal cells of cats. .

Dogs. Page 53 Return to top of page Hosts: Cat and other felids (definitive) . .Photo from Dubey. They then break out of these cells and invade new cells. rodents. J. The tachyzoites can be carried by the blood to any tissue of the body. Tachyzoites and bradyzoites can also be found in the cat. 1988. When an intermediate host ingests a sporulated oocyst the parasite excysts in the small intestine.P. An Atlas of Protozoan Parasites in Animal Tissues.. humans. until the immune response of the host kills them. many other mammals and birds (intermediate). In the cat the parasite can exist in a number of forms in a number of different tissues. Some of the tachyzoites will form bradyzoites (tissue cysts) which are slow growing and can evade the immune response. resulting in the release of unsporulated oocysts which pass out in the feces. the tachyzoites invade cells and multiply. In the cat's intestine the parasite will undergo schizogony and gametogony. The oocysts will sporulate in about 2 days in the environment. Return to top of page Life Cycle: The cat is infected either by ingesting a sporulated oocyst or an infected intermediate host.

D. In intermediate hosts: Tissue cysts. Saunders Co. Return to top of page Diagnostic Stage: In cat: oocyst. Philadelphia. PA Return to top of page Site in host where adult parasite is found : Small intestinal cells..B. Bowman. 1995. Sporulated and unsporulated oocysts .Illustration from: Georges' Parasitology for Veterinarians. 6th edition. W.D.

Toxoplasma gondii may cause abortion in sheep. Return to top of page Common Diagnostic Test Cat: Fecal flotation or serology In all animals: Cyst in Necropsy specimen or Serology (if available) Return to top of page Clinical Signs: In cats with an intestinal infection: usually asymptomatic. Heavier infections. In animals with tissue infection: light infections are usually asymptomatic. Return to top of page Treatment: .Tachyzoites in peritoneal macrophage. Infections of the CNS are most likely to show clinical signs. such as those seen in immunocompromised hosts will have symptoms that depend on the tissue infected. goats and humans.

Drug: Clindamycin Return to top of page .

Trichinella spiralis Homepage || Root || Main || Common name: Trichina Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Genus: Trichinella Species: spiralis Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 1.5 mm (female) long .5 mm (male) to 3.

Female (left) and male (right). Note: pictures are not comparable in size. T.5 mm long. The male is 1.T. spiralis adults. spiralis in tissue Tail of male Trichinella spiralis Return to top of page . and the female is 3 to 4 mm long.

Mammals. The pre-larva enters a muscle fiber and changes it into a "nurse cell". . The adult female will penetrate the mucosa of the intestine and lay live pre-larvae into lymph vessels. The pre-larvae are carried by the blood throughout the body. Larval cysts can get up to 3 mm in diameter.Hosts: Mammals. the definitive host is also the intermediate host. The pre-larva in the nurse cell develops to the infective first stage-larva in about 3 weeks. Thus. The larvae develop to the adult stage in the small intestine of the host. especially carnivores and omnivores (definitive). Return to top of page Site in host where adult parasite is found: Small intestine and mucosa of small intestine Return to top of page Diagnostic Stage: First stage-larva (arrows) in the nurse cell. especially carnivores and omnivores (intermediate) Return to top of page Life Cycle: The host ingests the first stage larvae which are encysted in the muscles of the intermediate host.

muscle pain and stiffness. SQ or PO. Fenbendazole 50 mg/kg. but the above drugs can be tried.Return to top of page Common Diagnostic Test Muscle biopsy Antibody ELISA Return to top of page Clinical Signs: Usually asymptomatic. one dose. for 7 to 10 days Treatment for the muscle phase may not be very effective. Return to top of page Treatment: Treatment against the adults in the gut: Ivermectin 0. repeat if needed. SID. .2 mg/kg. Heavy infections have been reported to cause a hemorrhagic enteritis. PO.

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.Trichuris vulpis Homepage || Root || Main || Common name: The whipworm of dogs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Family: Trichuridae Genus: Trichuris Species: vulpis Bookmark Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 45 mm to 75 mm long.

The egg hatches in the small intestine. Return to top of page . The larva stays here for 2 to 10 days. Eggs are laid into the lumen and pass out with the feces. Return to top of page Hosts: Dogs and foxes. It passes down to the cecum and large intestine where it matures to the adult stage. The adults burrow their narrow anterior ends into the mucosa. leaving the posterior ends in the lumen. The eggs develop to the infectious stage in about 3 weeks.Trichuris adults . and the infective third stage-larva penetrates into the intestinal wall. Return to top of page Life Cycle: The egg containing an infective larva is ingested by the dog. cats (very rare) (definitive).male (coiled) and female (straight). then re-enters the lumen. The prepatent period is about 90 days.

Return to top of page Common Diagnostic Test Fecal float to recover eggs. Return to top of page Clinical Signs: Light infections are asymptomatic. . Bouts of diarrhea. Return to top of page Diagnostic Stage: Egg which measures 80 um long by 40 um wide (smooth= shell). are seen in heavy infections. often with large amounts of mucus and some frank blood on the stool.Site in host where adult parasite is found: Embedded in the wall of the cecum and large intestine.

Fenbendazole. Febantel. Milbemycin oxime Return to top of page .Return to top of page Treatment: Drug: Butamisole Hyrdochloride. Mebendazole. Febantel and Pyrantel embonate.

Toxocara cati egg (90 um X 75um). Toxascaris leonina egg (80 um X 67 um). . Ancylostoma species egg (60 um X 40 um).Nematode Eggs and Larvae Found in Feces Click on the images to see full sized copies.

Capillaria aerophilia egg (70 um X 35 um). Physolaoptera species eggs (40 um X 48 um). Note: very very rare in cats in the United States but probably more common than the whipworms of tropical cats. Strongyloides stercoralis L1 (55 um X 32 um). . Trichuris vulpis egg (80 um X 40 um).

Trichinella spiralis L1.Nematode Larvae Found in Muscle Click on the images to see full sized copies. Trichinella spiralis L1 (cysts may reach up to 3 mm long). Stained with H+E. .

Aelurostrongylus abstrusus L1 .Nematode Eggs and Larvae Found in Tracheal or Nasal Washes Click on the images to see full sized copies. Capillaria aerophilia egg (70 um X 35 um).

Nematode Larvae Found in Blood Click on the images to see full sized copies.0 um). Dirofilaria immitis (270 X 325 um by 6.7. .7.

Dipylidium caninum egg (25 X 30 um in oblong packets of 20 or less eggs). Taeniaand Echinococcus species egg (38 X 32 um). Taeniaspecies proglottid.Tapeworm Eggs and Proglottids Click on the images to see full sized copies. .

Page 51. Diphyllobothrium latum proglottid. Diphyllobothrium latum egg (75 X 45 um). Photo from Foreyt. Mesocestoides proglottid. third edition. 1994. .Dipylidium caninum proglottid. J. Veterinary Parasitology Reference Manual. W. Spirometra mansonoides egg (60 um)..

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Paragonimus kellicotti egg (90 X 50 um). Eurytrema Procyonis egg (56 X 36 µm). 1994. third edition. . J. Alaria marciannae egg (98-134 X 62-68 µm).. Photo from Foreyt. W.Trematode Eggs Click on the images to see full sized copies. Page 27. Veterinary Parasitology Reference Manual.

Parametorchis complexus egg (24 X 12 um). .

Cryptosporidium parvum oocyst (4 X 8 um). Isospora felis oocyst (sporulated). (30 X 38 um). . Giardia species cyst (14 X 8 um).Protozoan Trophozoites and Cysts Found in Feces Click on the images to see full sized copies.

Isospora rivolta oocyst (sporulated). .Isospora felis oocyst (unsporulated). (30 X 38 um). Toxoplasma gondii oocysts (16 X 11 um). (25 X 20 um). Sarcocystis cruzi sporocysts (16 X 11 um).

Protozoans Found in Feline Blood Click on the images to see full sized copies. Cytauxzoon felis schizonts and piroplasms. Left: Schizonts of C. Right: Intraerythrocytic piroplasms (arrows) seen in cat blood smear. felis seen in mononuclear cell from a bone marrow aspirate smear (arrow). 205(#3):455-460. Image adapted from JAVMA. Fig 1 and 3. 1994. .

Protozoan Trophozoites and Cysts Found by Tissue Biopsy Click on the images to see full sized copies. . Toxoplasma gondii . (From peritoneal lavage).tachyzoites in peritoneal macrophage.

Transmammary B. and has a rough surface. Transplacental C. Ingested a rodent or a bird E. Ingested an egg D. How did this cat most likely acquire this parasite? A. All of the Above are equally likely .Quiz Case #1 You chose: Toxocara cati Correct! It is an ascarid egg that is round. with a center-filling mass.

but the egg shown has a rough surface. You are right in thinking that it is an ascarid egg. Return to the previous page and try again Go to a review of Toxascaris leonina . not a smooth surface like Toxascaris leonina.Quiz Case #1 You chose: Toxascaris leonina Wrong.

Paragonimus kellicotti is a trematode and it's egg has an operculum (cap).Quiz Case #1 You chose: Paragonimus kellicotti Wrong. Return to the previous page and try again Go to a review of Paragonimus kellicotti .

much like that of Trichuris vulpis. Return to the previous page and try again .Quiz Case #1 You chose: Trichuris felis Wrong. Trichuris felis is a very rare parasite of cats and it has a football-shaped egg with a plug at either end.

Physaloptera rara . the stomach worm. is a spirurid and has a thick-walled egg which contains a larva when it passes in the feces. (Note: the bar at the top of this page depicts many Physaloptera eggs). Return to the previous page and try again .Quiz Case #1 You chose: Physaloptera rara Wrong.

This object has only one cell and is a different shape and size.Quiz Case #2 You chose: Ancylostoma tubaeforme Wrong. tubaeforme) and have an early embryo at the 8 or 16 cell stage. A hookworm egg would be larger (about 62um long for A. Return to the previous page and try again Go to a review of Ancylostoma tubaeforme .

braziliense) and have an early embryo at the 8 or 16 cell stage. Return to the previous page and try again Go to a review of Ancylostoma braziliense . This object has only one cell and is a different shape and size. A hookworm egg would be larger (about 55um long for A.Quiz Case #2 You chose: Ancylostoma braziliense Wrong.

B. Click here if you wish to go to a review of Isospora felis . D. the coccidia is resistant to sulfadimethoxine. The owner did not comply with treatment instructions. You request that a fecal exam be brought in. and this time there is blood in the stool. The cat ingested a mouse and is just passing oocysts of that host's coccidia. The cat was re-infected with Isospora felis. A week later the owner calls and tells you that the cat has diarrhea. The cat is infected with another coccidian E. C. The fecal exam is repeated and many objects like the object shown below were found (it measures about 20 um long). What is going on? A. Drug resistence.Quiz Case #2 You chose: Isospora felis. Right! You have the owner treat the cat for five days with sulfadimethoxine.

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The object shown is too large to be Isospora rivolta.Quiz Case #2 You chose: Isospora rivolta Close.and it is the wrong shape. but you are wrong. Return to the previous page and try again Go to a review of Isospora rivolta .

Return to the previous page and try again Go to a review of artifacts . they are rarely as regularly shaped as this object and usually have a clear lipid-like drop in the center. Although plant cells seen in the feces come in all shapes and sizes.Quiz Case #2 You chose: Plant cell. Wrong.

Click here to highlight pathology Click here to return to quiz .

however. Return to the previous page and try again Go to a review of Capillaria aerophilia .Quiz Case #3 You chose: Capillaria aerophilia Capillaria is a lung parasite and should be initially considered. Capillaria aerophilia would not produce the enlarged pulmonary artery seen in this radiograph.

Quiz Case #3 You chose: Aelurostrongylus abstrusus Aelurostrongylus is a lung parasite and should be initially considered. Return to the previous page and try again Go to a review of Aelurostrongylus abstrusus . however. Aelurostrongylus abstrusus would not produce the enlarged pulmonary artery seen in this radiograph.

Return to the previous page and try again Go to a review of Filaroides osleri . Filaroides does not infect cats.Quiz Case #3 You chose: Filaroides osleri Wrong.

B. All of the above Return to the previous page and try again . Ultrasound E. Breathing difficulty and vomiting have both been associated with heartworm in cats. Heartworm Antibody Test C. Heartworm Antigen Test D. Knott Test (microfilaria test). which of the following tests should you run? A.Quiz Case #3 You chose: Dirofilaria immitis Right! The presence of adult heartworms in the pulmonary arteries of the cat will cause an enlargement of the arteries. To confirm your tentative diagnosis.

the type of damage seen in the radiograph (enlarged pulmonary artery) is not consistent with the transient migration of ascarid larvae. but even though T. Return to the previous page and try again Go to a review of Toxocara cati . cati larvae may migrate through the lungs.Quiz Case #3 You chose: Toxocara cati You might consider it.

and the surface is not smooth as seen in Trichuris spp. eggs. but the shape is not entirely consistent with the egg shown. Trichuris eggs do have bipolar plugs. Return to the previous page and try again Go to a review of Trichuris vulpis .Quiz Case #4 You chose: Trichuris Wrong.

Capillaria hepatica E. Identify this egg to species: A. Capillaria tomentosa . Capillaria aerophilia B. The egg in the photo measures 54 X 20 um. Capillaria plica D. parallel sides and rough surface identify this as a Capillaria spp. Capillaria bohemi C.Quiz Case #4 You chose: Capillaria Correct! The bipolar plugs. Four of this type of egg were found upon a complete examination of the cover slip from the fecal float. egg.

Return to the previous page and try again Go to a review of Toxocara cati .Quiz Case #4 You chose: Toxocara Wrong. You are way off track.

it just doesn't look anything like a Physaloptera egg. and the ova shown does not have a larvae inside of it like a spirurid egg. Physaloptera eggs ususally do not float in a typical fecal flotation. and also. Return to the previous page and try again Go to a review of Physaloptera .Quiz Case #4 You chose: Physaloptera Wrong.

Return to the previous page and try again Go to a review of Dipylidium caninum .Quiz Case #4 You chose: Dipylidium Wrong. A tapeworm egg would have 6 "hooks" inside of it.

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Quiz Case #5 You chose: Cestoda Wrong! The cestodes do not have a mouth and gut as can be seen in figure B Return to the previous page and try again .

Artery D. Liver parenchyma B. A.Quiz Case #5 You chose: Trematoda Correct! The predilection site of a parasite is a clue which can be used to idenify it. The liver biopsy slide (figure 2A) shows the adult trematode in its predilection site. Vein C. 2A Click hereto magnify image. Identify the predlection site. Bile duct .

Quiz Case #5 You chose: Nematoda Wrong! You can see in figure 1A that there is no body cavity in this parasite. Return to the previous page and try again .

Return to the previous page and try again .Quiz Case #5 You chose: Insecta Wrong! You can see in figure 1A that there is no body cavity in this parasite.

Return to the previous page and try again .Quiz Case #5 You chose: Pentastomida Wrong! You can see in figure 1A that there is no body cavity in this parasite.

Ancylostoma caninum Homepage Common name: Canine Hookworm Kingdom: Animalia Phylum: Nematoda Class: Secernenttea Order: Strongylida Superfamily: Ancylostomatoidea Genus : Anclystoma Species: caninum Click on the text below to jump down to the desired section of this page. Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: .

Return to top of page Bursa of Male Return to top of page Hosts: Definitive: Dog (Canis familiaris) Paratenic: Rodents Return to top of page .Adult worms in petri dish (left). and anterior of an adult worm (right).

if a rodent ingests the L3 larvae. The pre-patent period is two weeks. Once in these tissues. The larvae migrate to the lungs. Older animals often develop resistance to repeated exposures of the parasite. and then on to the intestinal tract of the host. If the rodent is eaten by a dog. Return to top of page Site where adult parasite occurs: Small intestine . Eggs are then expelled with the feces and the cycle continues. to the skeletal muscles and mammary glands. When infected females begin to nurse offspring. In the small intestine. Larvae develop in soil to the infective L3 stage and then are either ingested by the host or they enter the host through cutaneous contact. larvae may migrate in the host to subcutaneous fat. the larvae become inactive. the larvae develop into adults. it is much more likely that young animals will be infected with the parasite than the older animals. This "trans-mammary route "of infection is of primary importance as younger animals are more susceptible to infection. the larvae are activated and passed to the young who become infected. the larvae will mature to adulthood in the small intestine. Finally. Alternatively.Life Cycle: Eggs are passed in feces. the larvae will migrate to the tissues and become dormant. and in females. Thus.

Return to top of page Clinical Signs: Puppies: Anemia. poor growth. pale membranes. Return to top of page Common Diagnostic Test Fecal float to recover eggs. . weight loss. L1 larvae (middle). Eggs are 60 x 40 um. Ancylostoma eggs (left). occasionally death.Return to top of page Diagnostic Stage: Eggs are found in fecal flotation. diagram of L1 larvae (right). Adults: Usually asymptomatic but any of the above symptoms may be present. L1 larvae are occasionally found in feces and are diagnostic of infection. weakness. diarrhea.

Pyrantel Pamoate. Ivermectin. Febantel/Pyrantel embonate. Milbemycin oxime. Mebendazole.Return to top of page Treatment: Drug: Febantel. Selamectin Return to top of page . Fenbendazole.

Babesia canis Homepage Common name: Babesiosis Kingdom: Protista Phylum: Apicomplexa Class: Piroplasmia Order: Babesiidae Family: Babesia Genus: canis Click on the text below to jump down to the desired section of this page. . Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: Trophozoites can be round or pear shaped. and several may be seen in the same red blood cell. 2-5 um long.

Babesia canis trophozoites in red blood cells Return to top of page Hosts: Dog (Canis Familiaris) Return to top of page Life Cycle: Vector is the brown dog tick. Sporozoites of the parasite are carried in the alveoles of the ticks salivary gland. Rhipicephalus sanguineus. The parasite feeds on the cytoplasm of the erythrocyte and undergoes merozoite formation. the sporozoites enter the dog and infect erthyrocytes. . when another tick bites the host and obtains a blood meal. Then. Upon biting the host. the parasite is taken up by the vector where it forms gametes and produces sporozoites.

The trophozoite in the red blood cell is the diagnostic stage (see pictures above). Return to top of page Common Diagnostic Test Examination of Blood smear (wrights stain) Serology Return to top of page .Return to top of page Site where adult parasite is found in host: erythrocytes (red blood cells) Return to top of page Diagnostic Stage: Babesia canis is most often seen in blood obtained from cutaneous capillaries than from systemic venous blood.

6.6 mg/kg. IM Clindamycin .Babesia spp. Supportive therapy should also be provided. 14 days apart. Return to top of page . 2 doses.Clinical Signs: Weakness Hemolytic anemia Depression Anorexia Pyrexia Weight loss Increased pulse and respiration rate Death Return to top of page Treatment: Imidocarb dipropionate . in dogs: 25 mg/kg (PO) divided BID until cured (extra label use).

and several may be seen in the same red blood cell. 2-5 um long.Babesia gibsoni Homepage Common name: Babesiosis Kingdom: Protista Phylum: Apicomplexa Class: Piroplasmasida Order: Piroplasmorida Family: babesiidae Genus: Babesia Species: gibsoni Click on the text below to jump down to the desired section of this page. Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: Trophozoites can be round or pear shaped. .

Babesia trophozoites in red blood cells Return to top of page Hosts: Dog (Canis Familiaris) Return to top of page Life Cycle: Vector is the brown dog tick. the sporozoites enter the dog and infect erythrocytes. Upon biting the host. Then. The parasite feeds on the cytoplasm of the erythrocyte and undergoes merozoite formation. when another tick bites the host and obtains a blood meal. Sporozoites of the parasite are carried in the alveoles of the ticks salivary gland. Rhipicephalus sanguineus. . the parasite is taken up by the vector where it forms gametes and produces sporozoites.

The trophozoite in the red blood cell is the diagnostic stage (see pictures above).Return to top of page Site where adult parasite is found in host: erythrocytes Return to top of page Diagnostic Stage: Babesia gibsoni is most often seen in blood obtained from cutaneous capillaries than from systemic venous blood. Return to top of page Common Diagnostic Test Examination of Blood smear (wrights stain) Serology Return to top of page .

Imidocarb dipropionate but relapses (incomplete cures) are common.Clinical Signs: Weakness Hemolytic anemia Depression Anorexia Pyrexia Weight loss Increased pulse Respiration rate Death. Return to top of page Treatment: Drug: Clindamycin. Return to top of page .

Balantidium coli Homepage Common name: Balantidiasis Kingdom: Protista Phylum: Protozoa Class: Ciliata Order: Heterotrichida Family: Bursaridae Genus: Balantidium Species: coli Click on the text below to jump down to the desired section of this page. Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment .

. Cysts are expelled in feces and reinfect host via accidental ingestion. Monkey (various species). Return to top of page Hosts: Pig (Sus scrofa). and cell fragments. that are often flask like in shape. The ciliates often invade the mucosa and submucosa of the intestines and produce severe ulcers.Adult Parasite: The trophozoite is oval in shape and averages 75 x 50 um in size. Guinea pig. The parasite normally feeds upon fecal material. starch granules. Man (Homo sapiens). The parasite excysts in the host intestine. Return to top of page Life Cycle: Balantidium coli is widely epidemic among the pig population of the world. and 30 to 300 um in length. but varies from 30 to 100 um in width. The adult resides in the large intestine and cecum. Dog (Canis familiaris) (rarely).

whipworm infection. Return to top of page Common Diagnostic Test Fecal flotation Return to top of page Clinical Signs: . often occurs in conjunction with Balantidium coli infection in pigs.NOTE: Trichuris suis. Return to top of page Site where adult parasite is found in host: Large intestine Return to top of page Diagnostic Stage: Adult ciliated organisms Cysts are sometimes found.

Return to top of page . for 5 days . PO. SID.Diarrhea Weight loss Nausea Vomiting Abdominal pain Dysentery Weakness Poor growth Bloody and mucusoid stools Return to top of page Treatment: Drug: Metronidazole Dose: Dog and Cat: 30 mg/kg.

Return to top of page . Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure between 7 and 13 cm long.Baylisascaris procyonis Homepage Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida Family: Ascarididae Genus : Baylisascaris Species: procyonis Click on the text below to jump down to the desired section of this page.

Many mammals (including dogs and humans) and birds (paratenic). Return to top of page Life Cycle: Life Cycle: The definitive host ingests an infective egg or a paratenic host which contains an infective larva in its tissues. The larva will grow during its migration in the paratenic host and by the time it reaches the brain it may be large enough (1.Hosts: Raccoons and dogs (definitive). The larva is carried by the blood to the lungs where it breaks out into the air space. If paratenic host ingests an infective egg. Return to top of page Site in host where adult parasite is found: Lumen of the small intestine. where they will wait for a definitive host to eat the paratenic host. The larva develops to the adult stage in the lumen of the small intestine. migrates up the trachea and is swallowed. Return to top of page . Humans can be infected with the larval stage by ingesting infectious eggs. including the host's central nervous system. The pre patent period is about 5 weeks. The eggs take about 30 days to develop to the infectious stage. The infective larva penetrates the intestinal wall. Eggs are laid into the lumen of the intestine and pass out with the feces.5 to 2 mm) to cause problems. the egg will hatch in the gut and the larva will migrate to various tissues.

Larvae in the brain: Neurological signs. Eggs measure 76 X 60 µm (range: 63 . Return to top of page Clinical Signs: Adults in the small intestine: Asymptomatic in light infections. but the Baylisascaris egg is smaller and the surface pitting is finer.70 µm).88 X 50 . Left: egg at 40X magnification.Diagnostic Stage: Egg looks like a Toxocara egg. Right: surface of egg Return to top of page Common Diagnostic Test Fecal float to recover eggs. Return to top of page . in heavy infections one might expect to see the same signs as in a dog infected with Toxocara.

Pyrantel Pamoate. Fenbendazole. Ivermectin Return to top of page .Treatment: No drug is labeled for the treatment of Baylisascaris procyonis but drugs which are used to treat Toxocara infections should work against the adult stage of this ascarid. Febantel. Some of these are: Piperazine.

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 15 mm to 40 mm long. Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Family: Trichuroidea Genus: Eucoleus (previously: Capillaria) Species: boehmi Click on the text below to jump down to the desired section of this page. .Eucoleus (Capillaria) bohmi Homepage Common name: Nasal worm of dogs and foxes.

A .posterior end of female . E.eggs. aerophilia. probably it is similar to that of C. Return to top of page Life Cycle: The life cycle of this parasite is not well known. Earthworms (paratenic). Burgess Publishing Co. Return to top of page Hosts: Dogs. Nematode parasites of domestic animals and man. The larva is carried by the blood to the lungs where it . 1998. aerophilia.. MN. D. From: Levine.Illustration C. Minneapolis. H . F . C . The definitive host ingests an infective egg or an earthworm which contains an infective larva in its tissues.posterior end of male. The infective larva leaves the egg or earthworm in the small intestine of the host and penetrates the intestinal wall.adult worm. wolves and probably other canids (definitive).vulva. G . B . foxes.

The egg measures 60 um X 30 um. Return to top of page Diagnostic Stage: Egg with bipolar plugs (asymmetrical) and a rough surface ("pitted" in appearance). swallowed and eventually pass out with the feces. Eggs are laid into the lumen of these organs.develops to the adult stage in the mucosa of the nasal cavity. the egg will hatch in the gut of the worm and the larva will migrate to the worm's tissues where it will wait for a definitive host to eat the worm. frontal and paranasal sinuses. Return to top of page Site in host where adult parasite is found Mucosa of the nasal cavity. Return to top of page Common Diagnostic Test Fecal flotation . If an earthworm ingests an infective egg. carried to the back of the throat with the mucus. frontal and paranasal sinuses.

for 10 to 14 days Return to top of page . Return to top of page Treatment: Ivermectin 0. repeat if needed. Fenbendazole 50 mg/kg.2 mg/kg.Nasal wash (if the dog has a nasal discharge) Return to top of page Clinical Signs: Usually asymptomatic in dogs Sometimes causing sneezing and a mucopurulent (sometimes bloody) discharge. SQ or PO. SID. PO. one dose.

Crenosoma vulpis Homepage Common name: Fox lungworm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Crenosomatidae Genus: Crenosoma Species: vulpis Click on the text below to jump down to the desired section of this page. The cuticle of the anterior end of the this worm is thrown into crenated folds as seen in this photomicrograph of a portion of the worm recovered by a tracheal . Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worm measures less than 16 mm long.

Return to top of page Life Cycle: The first stage-larva penetrates the intermediate host (a snail or slug). are swallowed and pass out with the feces. Return to top of page Site in host where adult parasite is .wash. wolves. Snails and slugs (intermediate). The larva molts twice and by 17 days post-infection becomes a third stage-larva. which are carried up the trachea. raccoons and dogs (definitive). The third stage-larva makes its way to the lungs and develops to the adult stage in the bronchi and bronchioles. The third stage-larva remains in the snail's tissues until the snail is eaten by a definitive host. Return to top of page Hosts: Foxes. The prepatent period is about 19 days. The female worm lays live first stage-larvae.

Return to top of page Clinical Signs: Rhinotracheitis Bronchitis .found: The bronchi and bronchioles Return to top of page Diagnostic Stage: First stage-larva in the feces Photomicrographs of L1 from tracheal wash Return to top of page Common Diagnostic Test Baermann Technique Tracheal wash Sometimes a ZnSO4 fecal flotationwill bring up a larva that can be identified.

Return to top of page Treatment: Ivermectin. Febantel for 7 to 10 days Return to top of page .Nasal discharge. Fenbendazole for 7 to 10 days.

. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 35 cm (male) to 103 cm (female) and are blood red in color.Dioctophyme renale Homepage Common name: The Giant Kidney Worm of Carnivores Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Enoplida Family: Dioctophymidae Genus : Dioctophyme Species: renale Click on the text below to jump down to the desired section of this page.

The prepatent period is about 135 days in the dog and 154 days in the mink and the adult worms may .Return to top of page Hosts: Mink. and other carnivores (definitive). When the worm or paratenic host is eaten by the definitive host the larva penetrates the stomach wall. When the infective egg is swallowed by an oligochaete annelid it hatches and develops over a period of about 100 days to the third stage larva.). dogs. The parasite grows in the kidney destroying the parenchyma of this organ. The worms then penetrate into the peritoneal cavity where they develop for a while. Eggs are laid in the kidney and pass out with the urine. foxes. Adult worm have also been found in the peritoneal cavity of seals (Phoca spp. If the worm is eaten by a frog or fish the third stage-larva will encyst in the predator (paratenic host) where they may live for years. Apparently the molt to the adult stage takes place in the body cavity and the adults enter the kidney. but adult worms free in the peritoneal cavity have been reported. Most paratenic hosts will have only a few larvae. Oligochaete annelids (intermediate) fish and frogs (paratenic) Return to top of page Life Cycle: The eggs pass out in the urine and develop in water to the infective stage (1 to 7 months). the molt takes place here in about 5 days. In the dog it is also the right kidney that is most likely infected. In mink the worms tend to enter the right kidney due to its position in relationship to the stomach.

42 um. The peritoneal cavity Return to top of page Diagnostic Stage: Egg in urine. 2001. Chap. Samuel.A. Edited by W. Pybus and A. For more information see: Lena N. Iowa State University Press. Measures. M. Kocan. In: "Parasitic diseases of wild mammals". 357 .J. Eggs are 65 .364). Return to top of page . Dioctophymatosis (pp. Return to top of page Site in host where adult parasite is found: The right kidney.live 3 to 5 years. 13. Ames.

Vomiting often occurs when the L3 penetrate into the wall of the stomach.Common Diagnostic Test Urine sedimentation Return to top of page Clinical Signs: Usually the left kidney is able to serve the entire body and the infection is asymptomatic. Return to top of page Treatment: Surgical removal prevention: do not feed animal raw fish. Sometimes the host shows signs of kidney trouble. Return to top of page .

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 13 mm (male) to 25 mm (female).Dipetalonema reconditum Homepage Common name: None Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Family: Setariidae Genus: Dipetalonema Species: reconditum Click on the text below to jump down to the desired section of this page. .

The microfilaria develops into an infective larva in 7 to 14 days. Return to top of page Site in host where adult parasite is found : The connective tissue of the skin. The prepatent period is about 61 to 65 days. The larva develops to the adult stage in the connective tissue of the dog's skin. The female worm lays microfilariae which find their way into the blood. Return to top of page Life Cycle: The flea ingests a microfilaria when feeding on an infected dog. When the flea again feeds on a dog the infective larva is injected into the skin. Fleas [Ctenocephalides felis] and lice [Heterodoxus spiniger] (intermediate).Return to top of page Hosts: Dogs (definitive). Return to top of page .

Microfilaria are found in blood. Return to top of page Clinical Signs: Asymptomatic. and are 4. Return to top of page Treatment: .7 to 5.8 um wide.Diagnostic Stage: Microfilariae are 215 to 270 um in length. Above right: Acid phosphate stain Return to top of page Common Diagnostic Test Microfilariae are found by blood smears and using the modified knott method. Above left: Knott test.

No treatment is necessary . Drug: Ivermectin Return to top of page .infection is non-pathogenic.

Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Superfamily: Dracunculoidea Genus : Dracunculus Species: insignis Click on the text below to jump down to the desired section of this page.Dracunculus insignis Homepage Common name: "Guinea-Worm" of North American wildlife. . Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 4 cm (male) to 120 cm (female).

It has been shown experimentally that if a tadpole ingests the infected copepod. Thus frogs may be paratenic hosts. Parasitology 81:792-793). Adult worm Both photos courtesy of ML Eberhard (CDC) Return to top of page Hosts: Raccoons. J. cats. When the definitive host ingests the infected copepod in . 1995. a copepod (intermediate) Return to top of page Life Cycle: A copepod of the genus Cyclops ingests the first stage-larva and the parasite develops to the infective third stage-larva in about 3 weeks. Cyclops. the L3 will go to the somatic tissues and persist there throughout the development of the frog (Eberhard and Brandt.Adult female Guinea worm manipulated into shedding L1 into a tube of water. Dogs. mink and other carnivores (definitive).

750 um. Return to top of page .) Return to top of page Diagnostic Stage: L1 from the extruded worm or the adult worm. The worm causes a shallow ulcer to form in the skin over the anterior end of the worm. Adult female worms are usually found under the skin of the extremities. which bursts releasing first stage-larvae into the water. L1 measures 500 . conjunctiva. prolapses a length of uterus. the larva invades the intestinal wall and gets into the body cavity where it develops to the fourth stage-larva.e. vertebral column. etc. When this ulcer comes in contact with water. the female worm extrudes her anterior end. The prepatent period is about 309 to 410 days.drinking water. Return to top of page Site in host where adult parasite is found : The subcutaneous tissues of the limbs Occasionally found in other areas of the body (i. heart.

Common Diagnostic Test When the ulcer and inflamed area around the worm is noticed. Return to top of page Clinical Signs: The site where the adult worm lies painful and itchy. An ulcer will be apparent in the skin. Drug: Fenbendazole Drug: Ivermectin Return to top of page . Also treat with an anthelmintic to kill undeveloped worms: Ivermectin or Fenbendazole for 7 to 10 days. The water in the tube can then be examined for the larvae. a tube of water is placed over the ulcer. The adult female will then shed larvae into the water. Return to top of page Treatment: If possible surgically remove the worm. Anthelmintics seem to work only if given before 90 days of infection.

.

Echinococcus granulosus Homepage Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminthes Class: Eucestoda Class: Cestoda Order: Cyclophyllidea Genus : Echinococcus Species: granulosus Click on the text below to jump down to the desired section of this page. . Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 2 to 7 mm long.

Echinococcus granulosus adults in situ .intestine of dog (right).Echinococcus granulosus adult (left). Hydatid cyst in human (above) Schematic illustration of hydatid cyst Return to top of page .

The hydatid cyst develops in (in order of likelihood) the liver. Return to top of page Life Cycle: The sheep ingests an egg. and other ungulates (intermediate). wolves and other wild canids (definitive). detach from the end of the worm and spill their eggs into the lumen of the intestine. camels. containing the eggs. Gravid proglottids. horses. The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travels to the liver via the blood. brain or other organ. lungs. Sheep. coyotes. pigs. The eggs pass out in the feces. The prepatent period is about 47 days. When the dog eats the sheep viscera and ingests the hydatid cyst. the protoscolices attach to the small intestinal wall and the worms begin to form proglottids. Return to top of page Site in host where adult parasite is found: The small intestine Return to top of page Diagnostic Stage: Eggs are found in fecal flotation .Hosts: Dogs.

. Praziquantel. Clinical signs in the intermediate host depend on where the hydatid cyst is located and how old (large) it is. Return to top of page Treatment: Epsiprantel. Return to top of page Clinical Signs: Usually asymptomatic in the dog. Eggs are 38 .32 um.Return to top of page Common Diagnostic Test Fecal float to recover eggs.

Fenbendazole Return to top of page .

.Entamoeba histolytica Homepage Common name: Ameba Kingdom: Protista Phylum: Protozoa Class: Lobosea Order: Amoebida Family: Entamoebidae Genus: Entamoeba Species: histolytica Click on the text below to jump down to the desired section of this page. or other organs. the liver. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The trophozoites are found in the lumen of the large intestine and occasionally in the wall of the intestine.

primates. In dogs the trophozoites rarely form cysts. It divides by binary fission.Adult trophozoites (above) Illustration of E. histolytica trophozoite and cyst Return to top of page Hosts: Dogs. including humans (definitive). This cyst will then pass out with the feces. Return to top of page Life Cycle: Infective cysts are ingested by the host and excyst in the intestine. The trophozoite feeds on bacteria and sometimes host cells. Under some circumstances the trophozoite can round up and form a cyst wall around itself. .

liver or other organs. E. histolytica cyst Return to top of page Common Diagnostic Test Fecal float Return to top of page . Return to top of page Diagnostic Stage: Trophozoite (10 to 70 um in length) in fresh feces.Return to top of page Site in host where adult parasite is found: Lumen of the large intestine sometimes will invade the intestinal wall.20 um in diameter). In other animals: Cyst (8 .

Return to top of page Treatment: Drug: Metronidazole ? Return to top of page .Clinical Signs: Usually asymptomatic Diarrhea.

.Filaroides hirthi Homepage Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Superfamily: Filariodea Genus: Filaroides Species: hirthi Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 3 mm (male) to 10 mm (female).

The dog eats the feces or vomitus containing the first stage-larvae. Return to top of page Hosts: Dogs (definitive).Filaroides osleri in tracheal nodes.nodes are cut open. The larvae make their way to the lung where they develop to adults in the lung parenchyma.nodes are uncut. . right . Return to top of page Site in host where adult parasite is found: Parenchyma of the lung. The prepatent period is about 32 to 35 days. Left . The larvae are carried up the trachea and are swallowed. The females lay thin walled eggs which hatch in the lung. Return to top of page Life Cycle: The first stage-larvae pass in the feces or in vomitus.

L1 larvae (left). Return to top of page Common Diagnostic Test Baermann Technique Tracheal wash Sometimes larvae can be recovered in identifiable shape by the ZnSO4 flotation method. L1 are 325 .Return to top of page Diagnostic Stage: First stage-larva in feces or tracheal wash. Highlighted area indicates the cross section of a single parasite. . Return to top of page Clinical Signs: Usually asymptomatic Severe infections in immunocompromised dogs have been fatal.378 um. and histological cross section of several parasites (right).

Ivermectin Return to top of page .Return to top of page Treatment: Drug: Fenbendazole.

Oslerus (Filaroides) osleri Homepage Common name: Lungworm of dogs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Filaroididae Genus: Filaroides Species: osleri Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 5 mm (male) to 12 mm (female). .

Filaroides osleri in tracheal nodes. Left . The larvae are carried up the trachea and are swallowed.nodes are cut open.nodes are uncut. Return to top of page Site in host where adult parasite is found: Nodules in the trachea and bronchi. . The females lay thin walled eggs which hatch in the lung. The dog eats the feces or vomitus containing the first stage-larvae. Return to top of page Hosts: Dogs. The larvae make their way to the lung where they develop to adults in nodules in the trachea and bronchi. The prepatent period is about 10 weeks. dingo (definitive) Return to top of page Life Cycle: The first stage-larvae pass in the feces or in vomitus. right .

. and histological cross section of several parasites (right). Highlighted area indicates the cross section of a single parasite. hard cough (can be started by exercise or exposure to cold air).Return to top of page Diagnostic Stage: First stage-larva in feces or tracheal wash. Return to top of page Common Diagnostic Test Baermann Technique Tracheal wash Sometimes larvae can be recovered in identifiable shape by the ZnSO4 flotation method. L1 larvae (left). Return to top of page Clinical Signs: Spasmodic attacks of a dry.378 um. L1 are 325 .

Return to top of page .Return to top of page Treatment: Ivermectin. Fenbendazole (SID. 7 to 10 days).

Heterobilharzia americana Homepage Common name: Dog Shistosome Kingdom: Animalia Phylum: Platyhelminthes Class: Trematoda Order: Digenea Family: Schistsomatidae Genus: Heterobilharzia Species: americana Click on the text below to jump down to the desired section of this page Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasites: .

They migrate to the liver where they mature and then make their way to the mesenteric veins where the male and female worms join together. whose skin they will penetrate. Return to top of page Life Cycle: The egg hatches in water and the miracidium finds and penetrates a snail. Adult male and female schistosomes Return to top of page Hosts: Dogs. rabbit (definitive) Snails [Lymnaea cubenisis] (intermediate). There are two sexes in this trematode. The cercariae swim around until they find a definitive host. The female spends the rest of her life in the gynecophoric groove of the male. Sporocysts and then daughter sporocysts develop in the snail. bobcats. and when mature emerge from the snail. Return to top of page . Cercariae develop in the daughter sporocysts.The adult worms measure 2 to 4 mm long. nutria. Eggs are laid in the mesenteric vein and make their way through the intestinal wall into the lumen of the intestine. raccoons. Eggs pass out in the feces.

No..H. Return to top of page Diagnostic Stage: Schistosome egg Illustration from Slaughter. L. Return to top of page Common Diagnostic Test Ethyl-acetate sedimentation (use saline instead of water) Return to top of page Clinical Signs: Usually asymptomatic in the dog and cat.B. Billups. Acor. page 607. G. . J..Site in host where adult parasite is found: The mesenteric veins. 5. K.. Vol 10. Compendum Small Animal. May 1988.

Return to top of page Treatment: Praziquantel or Fenbendazole for 10 days Return to top of page .

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: Tissue stages: The schizonts are found in the epithelial cells of the small intestine. .Isospora canis Homepage Common name: Coccidia Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiorida Family: Eimeriidae Genus: Isospora Species: caninum Click on the text below to jump down to the desired section of this page.

Rodents (paratenic). Return to top of page Life Cycle: The dog ingests a sporulated oocyst which excysts in the small intestine releasing 8 sporozoites. The oocyst will sporulate in 4 days and then is infectious for the next host. The zygote develops into an oocyst which breaks out of its host cell and passes out in the feces. the last round of schizogony leads to the formation of gametes. The sporozoites develop into a schizont which undergoes an asexual internal multiplication known as schizogony. then break out of its host cell.Return to top of page Hosts: Dogs (definitive). There are 3 generations of schizonts. Return to top of page . the male gamete will divide. The prepatent period for this parasite is about 9 to 11 days. invade the host cell containing the female gamete and fuse with the female gamete forming a zygote. The sporozoites invade intestinal epithelial cells. The dog may also become infected by ingesting a rodent which has the asexual stages in its tissues. The gametes which invade other cells.

Site in host where adult parasite is found: Small intestinal epithelium Return to top of page Diagnostic Stage: Diagnostic stage: unsporulated oocyst which measures 38 um X 30 um. Return to top of page Common Diagnostic Test Fecal flotation Return to top of page Clinical Signs: Usually asymptomatic In young puppies a heavy infection may be accompanied by severe watery diarrhea. . but Isospora canis may not be the sole pathogen in these cases.

Return to top of page Treatment: Drug: Sulfadimethoxine. Amprolium Return to top of page .

Isospora ohioensis Homepage Common name: Coccidia Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiorida Family: Eimeriidae Genus: Isospora Species: ohioensis Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: Tissue stages: The schizonts are found in the epithelial cells of the small intestine: .

the last round of schizogony leads to the formation of gametes. Return to top of page Life Cycle: The dog ingests a sporulated oocyst which excysts in the small intestine releasing 8 sporozoites.Return to top of page Hosts: Dogs. The zygote develops into an oocyst which breaks out of its host cell and passes out in the feces. The sporozoites invade intestinal epithelial cells. The prepatent period for this parasite is about 4 to 6 days. then break out of its host cell. the male gamete will divide. invade the host cell containing the female gamete and fuse with the female gamete forming a zygote. Return to top of page . The gametes which invade other cells. The sporozoites develop into a schizont which undergoes an asexual internal multiplication known as schizogony. and maybe other canids. There are 2 generations of schizonts. The oocyst will sporulate in 4 days and then is infectious for the next host.

Isospora oocyst. Note: There are a number of Isospora spp. Return to top of page Common Diagnostic Test Fecal float Return to top of page . ohioensis.Site in host where adult parasite is found: Small and large intestinal epithelium. Return to top of page Diagnostic Stage: Unsporulated oocyst which measures 25 µm X 20 µm. ohioensis. For purposes of treatment. which infect the dog and produce cysts almost identical to that of I. many veterinarians will consider all these parasites to be I.

Clinical Signs: Usually asymptomatic In young puppies a heavy infection may be accompanied by severe watery diarrhea. Return to top of page Treatment: Drug: Sulfadimethoxine. but Isospora ohioensis may not be the sole pathogen in these cases. Amprolium Return to top of page .

.Leishmania donovani . Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The amastigotes are found in the macrophages of the internal organs. Leishmania infantum Homepage Common name: Visceral Leishmaniasis Kingdom: Protista Phylum: Protozoa Class: Zoomastigophorea Order: Kinetoplastida Family: Trypanosomatidae Genus: Leishmania Species: donovani and infantum Click on the text below to jump down to the desired section of this page.

eventually breaking out and infecting new macrophages. . In the gut of the sandfly the amastigote transforms to the reproductive stage promastigote in the midgut.Amastigotes in bone marrow macrophages. Amastigotes multiply within the macrophages. Return to top of page Life Cycle: Infective promastigotes are injected when a sandfly bites a host. they migrate to the pharynx of the fly where they mature to the infective promastigote form. Return to top of page Hosts: Hosts: Dogs. rodents and humans (definitive). . after an indeterminate number of divisions. Sandflies (intermediate). When a sandfly feeds on an infected host it takes up amastigotes (in macrophages). The promastigotes are taken up by macrophages in which they transform to the amastigote form. These promastigotes multiply in the midgut and.

Katz. New York. ascites or tissue. Despommier. Return to top of page Site in host where adult parasite is found: Liver Spleen Bone marrow Lymph nodes Return to top of page Diagnostic Stage: Amastigote in tissue smear. Gwadz. Springer-Verlag. .Original illustration from: Parasitic Diseases. Promastigote in culture of blood. 1982.

S. 2005. Clinical and serological follow-up in dogs with visceral .orally 15mg/kg of allopurinol every 12h until the clinical signs improved. in the following 1 month period allopurinol at same dose and subcutaneously 30mg/kg of sodium stibogluconate combination were given daily and at the end of the combined treatment. Chemotherapy of canine leishmaniosis. Veterinary Parasitology 106:315-324. For a review of treatment options for dogs see: G." PASA. Shaw. Return to top of page Clinical Signs: Asymptomatic initially. blood or ascites PCR of lymph node or spleen biopsy. E... eventually hepatoslenomegly. ascites. 2002. Dogs may not be worth treating as they are acting as reservoirs for human infections. et al. Pentavalent sodium stibogluconate in other hosts. Return to top of page Treatment: Treatment not always successful. Baneth and S. infantum in dogs the following has been reported: ". For L. allopurinol was continued alone at the same dose till the end of 8 months. alopecia.Amastigotes in tissue smear Return to top of page Common Diagnostic Test Serology Stained biopsy smear culture of biopsy. Trivalent sodium antimonyl gluconate and/or allopurinol for dogs..

Veterinary Parasitology 128:243-249.leishmaniosis treated with allopurinol and sodium stibogluconate. Return to top of page .

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: .Macracanthorhynchus ingens Homepage Common name: Thorny headed worm Kingdom: Animalia Phylum: Acanthocephala Class: Acanthocephalae Order: Archiacanthocephala Family: Oligacanthorhynchidae Genus : Macracanthorhynchus Species: ingens Click on the text below to jump down to the desired section of this page.

The egg hatches and the larva develops to the cystacanth stage. Return to top of page Life Cycle: The millipede ingests an egg. foxes (definitive). Millipedes (intermediate). dogs. When the raccoon eats the infected millipede the larva is digested out and attaches to the wall of the small intestine and grow to the adult stage. Return to top of page Hosts: Raccoons. Return to top of page Site in host where adult parasite is found: Small intestine Return to top of page Diagnostic Stage: .The adult males are 10 cm and the females are up to 35 cm long.

J. Vet. hirudinaceus from pigs (Alva Valdes.Eggs. Res. Return to top of page Common Diagnostic Test Fecal float to recover eggs.. 50:1392-1395). et al. Return to top of page . On rare occasions the worm may perforate the gut and peritonitis may result. once a day for 7 days. removed M. Am. Return to top of page Clinical Signs: Usually asymptomatic in the dog. 200 ug/kg. Return to top of page Treatment: Drug: Ivermectin Ivermectin is an "extra label use". 1989.

Nanophyetus samincola Homepage Common name: Salmon fever fluke Kingdom: Animalia Phylum: Platyhelminthes Class: Tramatoda Order: Digenea Family: Troglotrematidae Genus: Nanophyetus Species: samincola Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 2 to 4 mm long. .

The cercariae swim around until they find a trout or salmon whose skin they penetrate and encyst as metacercaria in various tissues. cat.Return to top of page Hosts: Dogs. Return to top of page Site in host where adult parasite is found: The small intestine Return to top of page . mink. Salmonid fishes (second intermediate). raccoons. and when mature emerge from the snail. When the definitive host eats the fish the metacercaria excyst and develop to the adult stage in the host's small intestine. Cercariae develop in the redia. coyote (definitive). The miracidium finds and penetrates a snail. Snails [Oxytrema silicula] (first intermediate). Return to top of page Life Cycle: The egg matures (3 months) and hatches in water. fox bear. Eggs are laid in the small intestine and pass out with the feces. Redia develop in the snail.

unless the agent of salmon poisoning (Neorickettsia helminthoeca) is present in the parasite.) Return to top of page . Return to top of page Treatment: Praziquantel or Fenbendazole for 10 days (Neorickettsia helminthoeca can be treated with broad spectrum antibiotics.Diagnostic Stage: Egg Return to top of page Common Diagnostic Test Ethyl-acetate sedimentation Return to top of page Clinical Signs: Usually asymptomatic in the dog and cat. This rickettsia produces a hemorrhagic enteritis and lymph node enlargement.

Neospora caninum Homepage Common name: Neospora Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiida Family: Sarcocystiidae Genus: Neospora Species: caninum Click on the text below to jump down to the desired section of this page. . Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The cysts have been found in the CNS tissues of several mammals.

Dogs. rodents and cattle are known to be infected with the tissue cyst stage (intermediate hosts?). Return to top of page Life Cycle: Unknown Return to top of page Site in host where adult parasite is found: Unknown.Return to top of page Hosts: The definitive host is probably dogs. Return to top of page Diagnostic Stage: Tissue cyst Return to top of page Common Diagnostic Test Cyst in Necropsy specimen .

Serology Return to top of page Clinical Signs: In neonatal puppies: polyradiculitis. Return to top of page . In cattle: abortion. Return to top of page Treatment: Clindamycin for 4 or more weeks. death.

Spirocerca lupi Homepage Common name: Esophageal worm of Dogs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Family: Thelaziidae Genus: Spirocerca Species: lupi Click on the text below to jump down to the desired section of this page. . Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 40 mm (male) to 80 mm (female) long.

rodents (paratenic). Eggs are laid in the cyst. pass out to the lumen of the esophagus and pass out with the feces. is passed in the feces and eaten by a beetle. Coprophagous beetles (intermediate). Return to top of page Life Cycle: The egg. birds. containing the infective first stage-larva. other canids and wild felids (definitive). and migrates in the arteries. eventually reaching the thoracic aorta in about 3 weeks. The prepatent period is between 5 and 6 months. foxes. If a paratenic host eats the beetle the larva will encyst in some organ of this host. After about 10 to 12 weeks in the aorta the larva will migrate to the esophagus where it forms a cystic nodule which is connected by a fistula to the lumen of the esophagus. With time a granuloma forms around the cyst and eventually develops into a sarcoma of the .Return to top of page Hosts: Dogs. Here it develops to the adult stage. Lizards. When the dog eats the beetle or paratenic host the larva penetrates through the stomach wall. The larva develops to the infective third stage larva in the beetle.

A sarcoma has developed around the site where the worms resided in the wall of the esophagus. The picture to the right shows the esophagus of a dog infected with Spirocerca lupi. Return to top of page Diagnostic Stage: Thick walled egg with a larva inside it. A worm can be seen emerging from the larger nodule.esophagus. eggs will not be found in the feces. The egg measures 34 um X 13 um. The picture to the right shows the esophagus of a dog infected with Spirocerca lupi. Note: If the granuloma does not have an opening to the lumen of the esophagus. Note the nodules/granulomas which form around the worms in the wall of the esophagus. . Return to top of page Site in host where adult parasite is found : In cysts connected to the esophagus or stomach.

however because the egg has a high specific gravity a flotation medium with a specific gravity of about 1. Secondary pulmonary osteoarthropathy. Return to top of page Clinical Signs: Dysphagia. Aortic aneurysm or rupture. If there is no opening between the worms in the granuloma and the lumen of the esophagus. Esophageal neoplasia. In these cases radiographs or direct visualization of the granulomas by endoscopy may be useful. eggs will not be present in the feces. a week apart. 2 doses. (no longer . Vomiting.Return to top of page Common Diagnostic Test Fecal float . Return to top of page Treatment: Disophenol sodium 10 mg/kg.36 (add more ZnSO4 salt to the normal ZnSO4 solution until the higher spG is achieved).

tapering the dose accordingly.. 109(1-2):65-73. 2002.4 mg/kg.2 mg/kg. T. S. (Lavy E. for a total of 3 weeks. 2004. SQ. SQ.available in the United States).) Doramectin 0. ( Mylonakis. Ivermectin 0. A. A.. Aizenberg I. Bark H. every 12 h.6 mg/kg. every 2 weeks for 6 doses then monthly until granuloma disappears. N. E.. twice. 0. H. Veterinary Parasitology.. Hagag A. Aroch I. Evaluation of doramectin for the treatment of experimental canine spirocercosis. Mazaki-Tovi M. orally. 14 days apart along with prednisolone. A comparison between ethanol-induced chemical ablation and ivermectin plus prednisolone in the treatment of symptomatic esophageal spirocercosis in the dog: a prospective study on 14 natural cases. F. may have to be repeated OR 0. Koutinas. Fytianou. Rallis.. Ververidis.5 mg/kg BW. Markovics A. Veterinary Parasitology 120:131-138.) Return to top of page . M. Harrus S.

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure up to 500 cm. .Taenia hydatigena Homepage Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus: Taenia Species: hydatigena Click on the text below to jump down to the desired section of this page.

When the dog eats the sheep viscera and ingests the cysticercus the protoscolex attaches to the small intestinal wall and the worm begins to form proglottids. Sheep. Return to top of page Site in host where adult parasite is found: . and other canids (definitive). Return to top of page Life Cycle: The sheep ingests an egg. foxes. containing the eggs. The prepatent period is about 51 days. The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travel to the liver via the blood. The cysticercus migrates in the liver for 18 to 30 days then burrows out into the peritoneal cavity where it attaches to the viscera. proglottid Return to top of page Hosts: Dogs. detach from the end of the worm and pass out in the feces. other domestic and wild ruminants (intermediate). Gravid proglottids.Taenia sp.

Return to top of page Diagnostic Stage: Proglottid or eggs . Extremely heavy worm burdens in small dogs may cause blockage of the intestine. Cysticerci in sheep and goats normally cause no problems. Eggs are 38 .The small intestine. Return to top of page Clinical Signs: Usually asymptomatic. Cysticerci may be found in the abdominal cavity of sheep and goats on necropsy. A very heavy infection may cause damage to the liver as the larvae .32 um. Fecal flotation may bring up eggs if a gravid proglottid has been broken in the feces. Return to top of page Common Diagnostic Test Gross examination of the proglottid.

migrate through. Fenbendazole Return to top of page . leading to signs of hepatitis. Praziquantel. Return to top of page Treatment: Epsiprantel.

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure up to 500 cm.Taenia ovis Homepage Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus: Taenia Species: ovis Click on the text below to jump down to the desired section of this page. .

The prepatent period is about 60 days. and other canids (definitive). reaching the infecitive stage in about 46 days. Return to top of page Site in host where adult parasite is found: . Sheep and goats (intermediate). The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travel to the heart and muscles via the blood. proglottid Return to top of page Hosts: Dogs. foxes. the protoscolex attaches to the small intestinal wall and the worm begins to form proglottids.Taenia sp. detach from the end of the worm and pass out in the feces. When the dog eats the sheep and ingests the cysticercus. containing the eggs. The cysticercus develop in the cardiac and skeletal muscles. Gravid proglottids . Return to top of page Life Cycle: The sheep ingests an egg.

Return to top of page Clinical Signs: Usually asymptomatic. Extremely heavy worm burdens in small dogs may cause blockage of the intestine.32 um.The small intestine Return to top of page Diagnostic Stage: Proglottid or eggs Eggs are 38 . Return to top of page Common Diagnostic Test Gross examination of the proglottid Fecal flotation may bring up eggs if a gravid proglottid has been broken in the feces. Upon necropsy the cysticerci can be found in the muscles of sheep and goats. In sheep and goats clinical signs are not usually seen. .

Fenbendazole Return to top of page .Return to top of page Treatment: Epsiprantel. Praziquantel.

Taenia pisiformis Homepage Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus: Taenia Species: pisiformis Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure up to 200 cm. .

T. pisiformis scolex . adult T. and other canids (definitive). foxes. Return to top of page Life Cycle: The rabbit ingests an egg. Rabbits and hares (intermediate). pisiformis (right). The cysticercus develops in the liver for 2 to 4 . Taenia species causing intestinal blockage Return to top of page Hosts: Dogs.scanning electron micrograph (left). The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travel to the liver via the blood.

Eggs are 38 . When the dog eats the rabbit and ingests the cysticercus the protoscolex attaches to the small intestinal wall and the worm begins to form proglottids. detach from the end of the worm and pass out in the feces.32 um. . Return to top of page Site in host where adult parasite is found: The small intestine. Gravid proglottids . Return to top of page Diagnostic Stage: Proglottid or eggs. containing the eggs. Taenia species eggs.weeks then burrows out into the peritoneal cavity where it attaches to the viscera.

T. Return to top of page Treatment: Epsiprantel. Fecal flotation may bring up eggs if a gravid proglottid has been broken in the feces. Praziquantel. Return to top of page Clinical Signs: Usually asymptomatic. Extremely heavy worm burdens in small dogs may cause blockage of the intestine. Fenbendazole Return to top of page . pisiformis proglottids Return to top of page Common Diagnostic Test Gross examination of the proglottid. .

Taenia multiceps Homepage Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus: Taenia Species: multiceps Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure up to 500 cm. .

the protoscolices attach to the small intestinal wall and the worms begin to form proglottids. foxes. and other canids (definitive). Gravid proglottids. Sheep and other ungulates (intermediate). Return to top of page Life Cycle: The sheep ingests an egg.) When the dog eats the sheep and ingests the coenurus. Return to top of page Site in host where adult parasite is found: . The coenurus develops in the brain. The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travel to the brain and spinal cord via the blood. containing the eggs. proglottid Return to top of page Hosts: Dogs.Taenia sp. reaching the infective stage in about 6 to 8 months. detach from the end of the worm and pass out in the feces. (In goats the coenurus can develop in a variety of tissues.

Return to top of page Clinical Signs: Usually asymptomatic. Extremely heavy worm burdens in small dogs may cause blockage of the intestine.32 um. Return to top of page Diagnostic Stage: Proglottid or eggs. . Return to top of page Common Diagnostic Test Gross examination of the proglottid Fecal float may bring up eggs if a gravid proglottid has been broken in the feces. a stumbling gait. blindness. In infected sheep or goats. The coenurus may be found upon necropsy in the brain of sheep and goats. the coenurus in the brain may cause ataxia.The small intestine. Eggs are 38 . and paralysis.

Praziquantel. Fenbendazole Return to top of page .Return to top of page Treatment: Epsiprantel.

Taenia serialis Homepage Common name: Tapeworm Kingdom: Animalia Phylum: Platyhelminths Class: Cestoda Order: Cyclophyllidea Family: Taeniidae Genus: Taenia Species: serialis Click on the text below to jump down to the desired section of this page. . Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure up to 500 cm.

foxes (definitive). The egg hatches in the small intestine and the larval tapeworm burrows through the intestinal wall and travels to the subcutanenous and intramuscular connective tissue via the blood. The coenurus develops in the connective tissue. Return to top of page Life Cycle: The rabbit ingests an egg. When the dog eats the rabbit and ingests the coenurus. Gravid proglottids. Rabbits (intermediate). detach from the end of the worm and pass out in the feces. containing the eggs. Return to top of page Site in host where adult parasite is found: . the protoscolices attach to the small intestinal wall and the worms begin to form proglottids.Taenia sp. proglottid Return to top of page Hosts: Dogs.

Fecal flotation may bring up eggs if a gravid proglottid has been broken in the feces. Return to top of page Clinical Signs: Usually asymptomatic. Return to top of page Common Diagnostic Test Gross examination of the proglottid.32 um. Extremely heavy worm burdens in small dogs may cause blockage of the intestine. Return to top of page Diagnostic Stage: Proglottid or eggs.The small intestine. Eggs are 38 . Return to top of page .

Praziquantel.Treatment: Epsiprantel. Fenbendazole Return to top of page .

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult worms measure 10 mm (male) to 15 mm (female) long. .Thelazia californiansis Homepage Common name: Eye worm Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Spirurida Superfamily: Thelaziodea Genus: Thelazia Species: californiensis Click on the text below to jump down to the desired section of this page.

The larva develops to the infective third-stage in the fly and then migrates to the mouthparts of the fly (this takes 2 to 4 weeks). The first stage-larva is picked up by a face fly (Musca spp.) when it feeds on the secretions from the infected eye. cats. Return to top of page Life Cycle: The eggs are laid and hatch in the conjunctival and lacrimal sacs. When the fly feeds on the next host's eye the infective larva leaves the mouthparts. man (definitive). Face flies (intermediate). sheep.Return to top of page Hosts: Hosts: dogs. In the conjunctival and lacrimal sacs the larva develops to the adult stage. Return to top of page Site in host where adult parasite is . deer. or Fannia spp.

Return to top of page Diagnostic Stage: Adult stage in the conjunctival and lacrimal sacs (see photograph of adult parasite above). in heavier infections a mild conjunctivitis may develop Return to top of page Treatment: If possible remove the adult worms with a fine forceps. Drug: Ivermectin Return to top of page .found : Conjunctival and lacrimal sacs of the eye. Return to top of page Common Diagnostic Test Direct observation of the worm. Return to top of page Clinical Signs: Usually asymptomatic.

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. Adult Parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment Adult Parasite: The adult worms measure between 10 cm (males) and 18 cm (females) long.Toxocara canis Homepage Common name: Common Roundworm (Ascarid) of Dogs Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida family: Ascaridida Genus : Toxocara Species: canis Click on the text below to jump down to the desired section of this page.

the larva that hatches from the egg will arrest in the dog's tissue as L3. 21 to 40 days after prenatal infection. These L3 will come out of arrestment after day 45 of pregnancy and migrate to the fetus (through the placenta and into the fetal liver). up the trachea and eventually reach the small intestine where they develop to adult worms. After birth the L3 migrate from the liver. paratenic hosts or they are infected in utero via transmission from an infected bitch. When an older dog ingests an infective egg. through the lungs. It will molt to the L3 in the lungs or the trachea. Many mammals (paratenic) Return to top of page Life Cycle: Animals are infected either by ingestion of embryonated eggs. Pre-patent period is 30 to 34 days after ingestion of an egg. and 19 days after ingestion of a paratenic host. swallowed.Return to top of page Hosts: Dogs and foxes (definitive). and in the small intestine it will molt twice becoming an adult. gets into the vascular system and is carried to the lungs. The L3 that . The adults live in the lumen of the small intestine. In dogs younger then 6 months the larva that hatches from the egg (L2) invades the intestinal wall. It is then carried up the trachea.

.. WB Saunders Co.B. PA Pre patent periods from: J. 1995. Larvae can be a cause of visceral larval migrans (VLM) and ocular larval migrans (OLM) in humans. W. The egg. 1987. Bowman.is in the paratenic host's tissue will develop in the dog's small intestine to the adult stage without undergoing a tissue migration. Return to top of page Site where adult parasite is found in host: Lumen of the small intestine. needs about 4 weeks in the environment to reach the infective stage. Philadelphia.C. Parsons.D. 6th edition. after it is passed with the feces. Saunders Co. 17(6):1307-1340. Philadelphia. Life cycle illustration from : Georges' Parsitology for Veterinarians. D. The Veterinary Clinics of North America. Ascarid infections of cats and dogs.

Return to top of page Diagnostic Stage: Eggs are found in fecal flotation. Return to top of page Common Diagnostic Test Fecal float to recover eggs. pot-bellied. the puppy may appear unthrifty. Return to top of page . Uncommonly leads to pneumonia. Puppies: In heavy infections. Return to top of page Clinical Signs: Adults: Asymptomatic in light infections. have abdominal pain. Eggs are light brown with a thick protein coat that is pitted. Visceral larval migration in puppies. diarrhea and vomiting. The egg measures 90 um X 75 um.

Pyrantel Pamoate Return to top of page .Treatment: Dichlorvos. Fenbendazole. Milbemycin oxime. Ivermectin. Piperazine. Febantel. Mebendazole. Febantel/Pyrantel embonate.

Homepage Common name: Trichomonas Kingdom: Protista Phylum: Protozoa Class: Zoomastigophorea Order: Trichomonadida Family: Trichomonadidae Genus: Tritrichomonas. and Pentatrichomonas Species: Various Click on the text below to jump down to the desired section of this page. Tetratrichomonas. Trichomitus. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment .Trichomonas spp.

Return to top of page Life Cycle: Trophozoites live in the cecum and large intestines of their hosts. The various species range in length from 3 to 10 um. . Adult trophozoites of Trichomonas Illustration of Trichomonas trophozoite Return to top of page Hosts: Vertebrates (definitive).Adult Parasite: The trophozoite is the only stage in the life cycle.

There is no cyst stage in the life cycle. Return to top of page Site in host where adult parasite is found: Cecum and large intestine Return to top of page Diagnostic Stage: Trophozoite. Return to top of page . Return to top of page Common Diagnostic Test Direct smearof liquid diarrhea. usually mother to offspring. Transmission is via fresh fecal contamination.

Return to top of page Treatment: Drug: Metronidazole Return to top of page .Clinical Signs: Usually asymptomatic Sometimes found associated with severe diarrhea.

amastigotes in lung of dog. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The amastigotes are found in various cells of the definitive host. . Below .Trypanosoma cruziHomepage Common name: None Kingdom: Protista Phylum: Protozoa Class: Zoomastigophorea Order: Kinetoplastida Family: Trypanosomatidae Genus: Trypanosoma Species: cruzi Click on the text below to jump down to the desired section of this page.

cats. Triatomin bugs [Reduviidae] (intermediate). armadillos. Return to top of page Life Cycle: Infective trypomastigotes are present in the bug's feces.Infective trypomastigote form: Return to top of page Hosts: Dogs. opossums. rodents and humans (definitive). raccoons. The bug .

including reticuloendothelial. In the cell the parasite transforms to an amastigote which divides by binary fission. as well as other sites. . Return to top of page . They change to trypomastigotes and circulate in the blood until they find another cell to invade or are picked up by a feeding triatomin bug. smooth and cardiac muscle. smooth and cardiac muscle cells). glila cells.defecates while it feeds and the feces (including the parasite) are rubbed into the wound left by the bug. The trypomastigotes enter cells ( almost any cell. Also the feces may be rubbed into the eye and the parasites gain entry that way. Eventually the cell ruptures and the amastigotes are freed. neural. Return to top of page Diagnostic Stage: amastigote in tissue biopsy. Return to top of page Site in host where adult parasite is found: Lymph nodes. In the hindgut of the bug the trypomastigote multiplies and eventually transforms to the metacylic trypomastigote which passes out with the feces.

Common Diagnostic Test Serology. Stained biopsy Return to top of page Clinical Signs: Clinical signs: Asymptomatic initially. lyphadenopathy. Return to top of page Treatment: Treatment not always successful. Dogs may not be worth treating. acute myocarditis. Drug: Quinapyramine sulphate Tradename: Suramin Return to top of page .

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment .Uncinaria stenocephala Homepage Common name: The Northern hookworm of dogs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Ancylostomatidae Genus: Uncinaria Species: stenocephala Click on the text below to jump down to the desired section of this page.

Return to top of page .Adult Parasite: The adult worms measure 7 mm (males) to 10 mm (females) long. The larva matures to the adult in the small intestine. Return to top of page Life Cycle: The host ingests an infective third stage-larva. Anterior end of adult Uncinaria stenocephala. The eggs hatch in the soil and the larvae molt twice to reach the infective third-stage. cats. and foxes (definitive). The pre-patent period is about 15 to 17 days. Eggs are laid in the small intestine and pass out with the feces. Return to top of page Hosts: Dogs.

Egg measures 75 um long by 45 um wide.Site in host where adult parasite is found: Small intestine Return to top of page Diagnostic Stage: Eggs are found in fecal flotation. . Return to top of page Common Diagnostic Test Fecal float to recover eggs. Diarrhea and hypoproteinemia occur in heavier infections. Return to top of page Clinical Signs: Light infections are asymptomatic.

Ivermectin.Return to top of page Treatment: Febantel. Febantel/Pyrantel embonate. Mebendazole. Fenbendazole. Pyrantel Pamoate Return to top of page .

Nematode Eggs and Larvae Found in Feces Click on the images to see full sized copies. Toxocara canis egg (90 um X 75um). Toxascaris leonina egg (80 um X 67 um). Spirocerca lupi egg (34 um X 13 um). .

Capillaria böhmi egg (70 um X 35 um). Crenosoma vulpis L1 . egg (60 um X 40 um).Ancylostoma sp. Ancylostoma caninum L1 Capillaria aerophilia egg (70 um X 35 um).

Filaroides osleri L1 (325 um X 378 um). Uncinaria stenocephala egg (75 um X 45 um). Trichuris vulpis egg (80 um X 40 um). . Strongyloides stercoralis L1 (55 um X 32 um). eggs (40 um X 48 um). Physolaoptera sp.

.Baylisacaris procyonis egg (80 um X 60 um).

. Trichinella spiralis L1 (cysts may reach up to 3 mm long). Trichinella spiralis L1. Stained with H+E.Nematode Larvae Found in Muscle Click on the images to see full sized copies.

Nematodes Found in Skin or Eye Click on the images to see full sized copies. the female worm extrudes her anterior end. Adult female worms are usually found under the skin of the extremities. When this ulcer comes in contact with water. L1 of Dracunculus insignis . (500 um X 750 um). which bursts releasing first stage-larvae into the water. prolapses a length of uterus. The adult female worm causes a shallow ulcer to form in the skin over the anterior end of the worm. Thelazia californiansis. Diagnosis is by direct observation of adult worm in eye. .

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Filiroides osleri and Filiroides hirthi L1 (237 um X 267 um). Capillaria aerophilia egg (70 um X 35 um).Nematode Eggs and Larvae Found in Tracheal or Nasal Washes * Click on the images to see full sized copies. . Capillaria böhmi egg (70 um X 35 um).

.Crenosoma vulpis larvae Crenosoma vulpis Adult (less than 16 mm long).

.Nematode Larvae Found in Blood Click on the images to see full sized copies.7 .7.7. Dirofilaria immitis (270 X 325 um by 6.5.8 um). Dipetalonema reconditum L1 (215 X 270 um by 4.0 um).

Tapeworm Eggs and Proglottides Click on the images to see full sized copies. Dipylidium caninum egg (25 X 30 um in oblong packets of 20 or less eggs). Taeniaand Echinococcus species egg (38 X 32 um). Taeniaspecies proglottid. .

. Diphyllobothrium latum proglottid.Dipylidium caninum proglottid. Mesocestoides proglottid. Diphyllobothrium latum egg (75 X 45 um).

. Nanophyetus samincola egg (70 X 40 um). Heterobilharzia americana egg Paragonimus kellicotti egg (90 X 50 um).Trematode Eggs Click on the images to see full sized copies.

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Cryptosporidium parvum oocyst (4 X 8 um). Balantidium coli Trophozoite (30 X 150 um). . Entamoeba histolytica cyst (18 X 5 -10 um).Protozoan Trophozoites and Cysts Found in Feces Click on the images to see full sized copies.

. (25 X 20 um). Giardia species cyst (14 X 8 um). Isospora ohionensis oocyst (sporulated).Entamoeba histolytica trophozoite (10 to 60 um in length). Isospora canis oocyst (30 X 38 um).

Sarcocystis cruzi sporocysts (16 X 11 um). .

Leishmania amastigote in bone marrow macrophage. Babesiatrophozoites in a red blood cell.Protozoans Found in Blood Click on the images to see full sized copies. .

Protozoan Trophozoites and Cysts Found by Tissue Biopsy Click on the images to see full sized copies. Neospora caninum cyst Trypanosome cruzi amastigotes (in lung tissue).tachyzoites in peritoneal . Toxoplasma gondii .

(From peritoneal lavage).macrophage. .

Acanthocephalan Eggs Click on the images to see full sized copies. Macracanthorhynchus ingens egg .

You would be wasting your time doing a heartworm test on a 10 week old puppy.Quiz Case #1 Wrong: The Knott test is used to look for heartworm. Return to the Quiz and try again Heartworm review Knott test review . Dogs have a 6 month pre-patent period.

and when examined by fecal flotation.Quiz Case #1 Correct! Reason: Based on the history and the physical exam. Identify the parasite: A) Toxocara canis B) Uncinaria stenocephala C) Ancylostoma caninum D) Trichuris vulpis . a fecal flotation is the most logical test to run. many objects like the one pictured below were seen. Findings: The feces appeared dark and tarry. This object measures 60u X 40u.

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Quiz Case #1 Wrong: Parasites of the urinary bladder or kidney (C. plica and D. Return to the quiz and try again Review Capillaria plica Review Dioctophyme renale . renale) would not be causing the clinical signs seen in a dog of this age.

Quiz Case #1 Wrong: While you might get lucky and find a migrating larvae of the parasite that is causing the puppy's problems. Return to the quiz and try again . given the clinical signs and the dog's age there is another test that is much more likely to provide the diagnostic stage of the larvae.

. this does not mean the puppy is free of parasites.Quiz Case #2 Saturated salt fecal flotation Results: Nothing seen. Another test should be employed. Return to the quiz and try again. however. Go to a comparison of the various methods for examining feces. This is the test most often used to examine canine fecal specimens.

What are they? Coccidia oocyst (Isospora sp.) Giardia cyst fungal spore Toxoplasma gondii cyst . They measure about 12 um long.Quiz Case #2 ZnSO4 fecal flotation Results: The objects shown below in the photomicrograph below were several of the many similar objects seen on the ZnSO4 flotation.

However. as well as by a concentration method.Quiz Case #2 Direct examination of a fecal smear Results: Nothing seen. Since trophozoites are normally killed by the removal of water from the feces in the large intestine. reproductive form of the parasite). it doesn't pay to examine formed or semi-formed stool by the direct smear. Go to a comparison of various methods of examining feces Return to the quiz and try again . you should examine any watery stool by this method. This test is useful when looking for protozoal trophozoites (the motile.

) Return to the quiz and try again Go to a comparison of the various methods of examining feces . Nothing was seen on your first slide. however you have enough material left in the tube to make about 10 more slides! Good luck! (You may eventually find something.Quiz Case #2 Ethyl acetate fecal sedimentation Results: The fecal sample contained only a normal amount of fat. try another method. but if you want to save time.

A B Which one of the answers below correctly identifies : "A" and "B"? Capillaria aerophilaandIsospora canis Capillaria aerophilaand Paragonimus kellicotti Trichuris vulpisand Eimeria sp. You could use this test or you could also use a Saturated sugar/salt flotation. You also find a few of the objects shown in the micrograph labeled "B" (they measure about 40 um long).Quiz Case #3 Correct! Test: ZnSO4 flotation. These eggs measure about 80 um long. . Results: Upon examination of the float you find many of the eggs shown in the photomicrograph labeled "A".

Trichuris vulpisand Paragonimus kellicotti .

You also find a few of the objects shown in the micrograph labeled "B" (they measure about 40 um long). These eggs measure about 80 um long.Quiz Case #3 Correct! Test: Saturated sugar/salt flotation. You could use this test or you could also use a ZnSO4 flotation. A B Which one of the answers below correctly identifies : "A" and "B" ? Capillaria aerophila and Isospora canis Capillaria aerophila and Paragonimus kellicotti Trichuris vulpis and Eimeria sp. Results: Upon examination of the float you find many of the eggs shown in the photomicrograph labeled "A". Trichuris vulpis and Paragonimus kellicotti .

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This test is unnecessary as you already have noted blood in the feces upon gross examination.Quiz Case #3 Test: Fecal occult-blood test Result: There is blood present in the feces. Return to previous page and try again .

Quiz Case #3 Test: Fecal-starch test. Return to previous page and try again . The presence of starch in the feces would indicate a lack of amylase in the digestive tract. thus suggesting pancreatitis. Result: Negative. Since there was no mention of abdominal discomfort. there is no reason to believe Cirus has pancreatitis.

not dogs.Quiz Case #4 You choose: Taenia taeniaeformis and Toxocara canis Answer: Partially right. but Taenia taeniaeformis is found in cats. Return to previous page and try again .

Return to previous page and try again Review Toxascaris leonina .Quiz Case #4 You choose: a taenid tapeworm and Toxascaris leonina Answer: Partially right. but Toxascaris leonina eggs are smooth shelled.

Mackenzie is pregnant and arrested larvae have "woken" up and some made their way to the small intestine and matured. B 3. treat Mackenzie (you have enough information at this point to give the proper anthelminthics) and send the dog home. You could. However. of course. several questions remain. 1.Quiz Case #4 You chose: a taenid tapeworm and Toxocara canis Answer: Right. A and B 5. Which of the following reasons may explain the patent Toxocara canis infection? A. C. Mackenzie is immunocompromised due to some problem. B. B and C . Mackenzie ate an infected paratenic host. C 4. but you still would not know why an older dogs such as this had a patent Toxocara infection and which taenid tapeworm was present. thus allowing arrested larvae to migrate to the gut and develop. A 2.

Return to previous page and try again . but how can you be sure "A" is the egg of Taenia pisiformis? Don't guess at this stage.Quiz Case #4 You chose: Taenia pisiformis and Toxocara canis Answer: Maybe.

You can make a more specific identification of the tapeworm egg and Toxascaris leonina eggs are smooth shelled. Review Toxascaris leonina Return to previous page and try again .Quiz Case #4 You chose: an unknown tapeworm and Toxascaris leonina Answer: No.

Dictyocaulus viviparus Homepage Common name: Lung Worm of Cattle Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Dictyocaulidae Genus: Dictyocaulus Species: viviparus Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: .

L3 are either washed out of the fecal pads or expelled from the fecal pad when they happen to be on a sporangium of the fungus Pilobolus which explodes to release its spores. A few adults or late stage larvae may over winter in the lungs of an infected animal and L3 may over winter on pasture by migrating down into the root mat and soil. Return to top of page Hosts: Cattle. buffalo and camel Return to top of page Life Cycle: The adult worms live in the bronchi of the lungs. They molt to the adult stage at about 15 days of infection and begin laying eggs around 22 days post-infection (PI). On pasture the L3 will migrate up grass blades and be eaten by the cow. and most are gone by 70 days PI. They then migrate to the lungs via the thoracic duct. Eggs are laid in the lungs and may hatch there or in the intestine (after being coughed up and swallowed). The adult worms begin to be expelled at about 50 days PI. deer.Adults in the lung of a 3 year old cow. Return to top of page Site in host where adult parasite is found: . They reach the lungs about 2 weeks after they were ingested. reindeer. The larvae reach the ensheathed infectious third-stage (L3) by about 4 days. First stage larva emerge from the cow in the feces. penetrate the bowel wall and molt to L4 in the mesenteric lymph nodes. The L3 exsheath in the small intestine.

Bronchi of the lungs. Return to top of page Diagnostic Stage: The first stage larva (0. Return to top of page Treatment: . Return to top of page Common Diagnostic Tests Fecal flotation (zinc sulfate centrifugation) Baermann technique Return to top of page Clinical Signs: In heavy infections: During the first 25 days of infection there may be tachypnea and coughing.36 mm) is found in the fresh feces. In mild infections the disease may be asymptomatic. During days 25 to 55 the lung signs increase in intensity with harsh lung sounds (ronchi and emphysematous crackling) being heard.3 to 0.

Ivermectin Doramectin Return to top of page .

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: .Fasciola hepatica Homepage Common name: Liver Fluke Kingdom: Animalia Phylum: Platythelminthes Class: Trematoda Order: Digenea Family: Fasciolidae Genus: Fasciola Species: hepatica Click on the text below to jump down to the desired section of this page.

horses. Adult liver flukes will feed on the epithelium of the bile duct. Each redia has a mouth and digestive system and will feed on the snail's tissue.) In the snail. Eggs are laid in the bile duct and carried out into the intestine by the bile. (If the miracidium fails to find a snail within 24 hours. Return to top of page Life Cycle: The eggs leave the host in the feces and if the egg gets into fresh water the embryo will develop into a miracidium. When the plant and metacercaria is eaten by a mammal. which when fully developed burst out of the sporocyst. it runs out of energy and dies. It is leaf shape with a cone-shaped projection at the anterior end. Germinal cells within the sporocyst develop into rediae. It takes 2 to 4 weeks for the miracidium to develop after which the operculum of the egg is pushed off and the miracidium uses its cilia to swim out of the egg. The time from sporocyst to cercaria is about 1 to 2 months depending on the temperature. cattle and other ruminants. The germinal cells within the daughter redia will develop into cercariae. the trematode takes up residence in the digestive gland and develops into a sporocyst. Living specimens are a grayish-brown in color. the larval trematode will emerge from the metacercarial cyst and burrow through the intestinal wall and migrate to the liver which it will also burrow into. Within the redia germinal cells will develop into a second generation of rediae (daughter rediae). humans and other mammals that eat the vegetation on which the metacercaria encysts. The complete life cycle may be completed in 3 to . The cercaria will burrow out of the snail.The adult worm may reach 30 X 13 mm. sheep. After a few weeks of migrating through the liver parenchyma (growing all the time) the young fluke will penetrate into a bile duct where it will mature to the adult stage. goats. Return to top of page Hosts: Infects swine. swim around until it finds a plant and then will climb a short distance out of the water and encyst on the plant as a metacercaria. The miracidium finds a snail (Lymnaea truncatula) and bores into it.

. the pre-patent period is 10 to 12 weeks. Return to top of page Site in host where adult parasite is found: Bile ducts and occasionally the gall bladder. Return to top of page Common Diagnostic Test Fecal flotation May distort the egg. Sedimentation Recovers eggs undistorted.90 µm They have an operculum at one end.150 by 63 . Return to top of page Diagnostic Stage: Egg: Measures 130 . Return to top of page Clinical Signs: The clinical signs depend on the host the fluke has infected.5 months.

In cattle the chronic form of the disease is more common and there is the added feature of calcification of the bile ducts over time. Withdrawal time: 8 days before slaughter. More information on the use of these products can be found by searching the "FDA Approved Animal Drug Products Online Database System" : http://dil.5 milligrams per kilogram of body weight (3.54 milligrams per pound of body weight (10 milligrams per kilogram).vetmed.Acute disease in sheep (due to a large initial infection) appears while the young fluke are migrating through the liver. Sheep: 7 days before Clorsulon Cattle: 7 milligrams per kilogram or 3.cfm Return to top of page . The bleeding into the damaged liver may result in weakness. Administer as a single oral dose using dosing gun or dosing syringe. Cattle: 4. and enlarged livers.vt. Chronic disease results in anemia and hypoalbuminaemia as blood is lost into the bile ducts.edu/NadaFIrst/NADA.4 milligrams per pound). Return to top of page Treatment: Albendazole Sheep: 7. Administer as a single oral dose using dosing gun or dosing syringe. pale mucus membranes. Withdrawal times: slaughter.2 milligrams per pound of body weight. The sheep show a loss of condition and sometimes edema. Cattle: 27 days before slaughter.

Eimeria vison Homepage Common name: Coccidia Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiorida Family: Eimeriidae Genus: Eimeria Species: vison Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: Tissue stages: The schizonts are found in the epithelial cells of the small .

K.6 µm and contained 8 to 12 merozoites. No. 1985. The average lengths of the prepatent and patent periods were 7 and 11 days respectively.e. Izvestiya Akademii Nauk Kazakhskoi SSR. M.8 x 5.4 x 8 to 11. D. The first generation of schizonts (S1) measured 5. From: Umurzakov. Mustela vison (Mink) Return to top of page Life Cycle: The first schizonts were observed in the epithelial cells of the duodenal villi of minks 72 h after infection with sporulated oocysts of E. vison.2. a 2nd generation of schizonts appeared 140 h after infection and a 3rd generation was observed 221 h after infection. jejunum and ileum. Nukerbaeva. [Russian]. putorius furo .intestine.9 to 13 µm and contained 23 to 30 merozoites and S 3 were 12. i. M. Biologicheskaya. after the end of the prepatent period. K. The life cycle of Eimeria vison in minks. The 3 generations of schizonts developed in the epithelial cells of the villi of the duodenum. S2 were 10 to 17 x 8. Return to top of page Site in host where adult parasite is found: .2 µm and contained 18 to 26 merozoites. and in heavy infection some sexual stages penetrated the connective tissue.6 to 9. 48-53. number of merozoites and localization.ferret).2 to 15. The 3 generations of schizonts differed in size. Return to top of page Hosts: Mustela putorius (syn.

Return to top of page Common Diagnostic Test Fecal flotation Return to top of page Clinical Signs: Return to top of page Treatment: Drug: Sulfadimethoxine Return to top of page .Small intestinal epithelium Return to top of page Diagnostic Stage: Diagnostic stage: unsporulated oocyst which measures .

Ascaris suum Homepage Common name: Ascarid (Roundworm) of Pigs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Ascaridida Family: Ascaridoidea Genus: Ascaris Species: suum Click on the text below to jump down to the desired section of this page. Adult Parasite Hosts Life cycle Site where adult parasite is found in host Diagnostic Stage Clinical Signs Treatment .

From the colon the L3 migrate within 24 hours to the liver of the pig via the portal veins. They pass through the liver (the immune response to their passage damages the tissue which heals with fibrosis. The larva within the egg appears as an L1 around 17 days. Return to top of page Hosts: Definitive: Swine and sometimes humans Paratenic: Birds and rodents are suspected Return to top of page Life Cycle: The egg is passed in feces and develops in the environment to the infectious stage in about 3 to 6 weeks (longer at lower temperatures).Adult Parasite: Males measure 15 to 25 cm long and 3 mm thick. Females are 15 to 41 cm and 5 mm thick. molts to the L2 between 22 and 27 days and finally molts to the L3 (infectious stage) between 27 and 60 days. leaving white . suum eggs contain L3 which are infectious for pigs. it hatches in the intestine and the L3 invade the wall of the cecum and colon. Adult Ascaris suum in the small intestine of a pig. When the egg is ingested. It has been shown that the viscera of birds that have ingested A. therefore there is the possibility of paratenic hosts in this life cycle.

. Ascaris suum egg as recovered from the feces of a pig. They are a yellow . Return to top of page Site where adult parasite is found in host: Small intestine Return to top of page Diagnostic Stage: Egg: Oval 50 .brown in color. Eggs are laid 60 days after the initial infection.70 by 40 -50 µm."milk spots" in the liver) and are carried via the blood to the lungs. the outer layer has prominent projections. Ascaris suum egg containing an infectious larva. They penetrate into the air spaces (if many move through at one time they will cause coughing ("thumps") and in some cases may cause the death of the pig) and are carried up the trachea and swallowed arriving in the small intestine about a week after the eggs were ingested. They molt to the L4 in the small intestine and to the adult stage by 3 to 4 weeks post-egg ingestion. Thick shelled.

Older pigs with a heavy infection will have diarrhea and slowed growth rate. The livers of pigs exposed to migrating larvae several times will show white areas of fibrosis ("milk spots").Return to top of page Common Diagnostic Test: Fecal float Identification of the adult worm recovered from the feces. lighter infections in these pigs usually produce a cough ("thumps") and stunted growth. Return to top of page Clinical Signs: An infected neonatal pig with a heavy infection may have pneumonia. Pig infected with Ascaris suum Liver from Pig infected with Ascaris suum. Return to top of page Treatment: Ivermectin . The white "milk spots" are a fibrous response to the larvae which have migrated through the liver.

Levamisole 8mg / kg body wt. Fenbendazole Pyrantel tartrate Return to top of page .

Strongyloides ransomi Homepage Common name: Threadworm of Pigs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Rhabditida Family: Strongyloididae Genus: Strongyloides Species: ransomi Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: .

5 mm long. 2) Skin penetration. intestine Return to top of page Hosts: Swine Return to top of page Life Cycle: The third-stage larva (L3) is the infectious stage of this nematode. L3 entering a neonatal pig via the skin will migrate through the body to the lungs (arriving there about 72 hours post-infection). but L3 are still being passed in the milk for at least 20 days).The adult worms measure 3. L3 will remain in the adipose tissue for a long time (in experimentally infected sows.5 to 4. Adult female of pig Histology of female in sm. 3) prenatal (rare). L3 were passed in the colostrum for at least the first 3 farrowings). Adult worms (all female) live in the small intestine and eggs begin to be passed in the feces on the 6th day post-infection. especially the fat tissue around the mammary glands. L3 entering the neonatal pig in the . In the last 10 days prior to parturition the L3 will move from the adipose tissue into the mammary glands and thus many will be in the colostrum the first time a piglet suckles. penetrate the air spaces and carried up the trachea. Infections are initiated in one of 3 ways: 1) transmammary (with the majority of the L3 being found in the colostrum during the first day of lactation. swallowed and arrive in the small intestine by about 96 hrs post-infection. L3 entering an older pig via the skin will migrate to adipose tissue.

1975 Proc Helminthol Soc Wash 42:86-92. insuring the susceptible neonatal pig will become heavily infected. Larvae hatching from eggs after the first few weeks of infection will develop either to L3 or to free-living male and female worms. thus insuring a source of infection as stored L3 in the fat tissue of older pigs.colostrum or milk will mature to adults in the small intestine without a migration through the tissues of the piglet. Egg stained with iodine Return to top of page Common Diagnostic Test . (Moncol.) Return to top of page Site in host where adult parasite is found: crypts of the small intestine Return to top of page Diagnostic Stage: Egg containing a larva is found in the feces. Eggs will appear in the feces of the piglet at 4 days of age (4 days post-infection). Eggs hatch on the ground and the larva derived from eggs produced during the first few weeks will develop homogonicly to L3. Eggs will be shed in the feces of piglets for 10 to 20 weeks. Eggs from these free living adult worms will normally develop to L3. The egg measures 45 to 55 by 26 to 35 µm.

Return to top of page Treatment: Fenbendazole Ivermectin Levamisole Return to top of page . The one on the left is uninfected. These pigs are littermates. anemia and stunting are also seen in infected piglets.Fecal flotation Return to top of page Clinical Signs: Light infections and infections in adult pigs are usually asymptomatic In heavier infections in young pigs bloody diarrhea is seen. rapid weight loss. The one on the right was infected 3 months ago. Anorexia.

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Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: The adult males measure 8 .Oesphagostomum dentatum Homepage Common name: Nodular worm of Pigs Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Family: Genus: Oesphagostomum Species: dentatum Click on the text below to jump down to the desired section of this page.10 mm long and the females measure 11 - .

Return to top of page Hosts: Swine Return to top of page Life Cycle: Eggs leave the pig in the feces and hatch in a couple of days at summer temperatures. The egg measures 40 X 70 µm.14 mm. . They molt to the L4 within the nodule and then return to the lumen of the large intestine (this takes about 1 week). The larvae reach the infectious L3 (ensheathed in the L2 cuticle) 2 to 3 days after hatching. The pig ingests the larvae. which exsheath in the small intestine.. Return to top of page Site in host where adult parasite is found: Large intestine Return to top of page Diagnostic Stage: Egg (strongyle-type) is found in the feces. The L3 then enter the mucosa of the large intestine causing small nodules to form. They will molt to the adult stage and eggs will first pass in the feces in 21 to 49 days depending on the strain of parasite.

Death may occur. enteritis and blood stained feces can be seen.Egg stained with iodine Return to top of page Common Diagnostic Test Fecal flotation Return to top of page Clinical Signs: Light infections and infections in adult pigs are usually asymptomatic In heavy infections anorexia. Return to top of page Treatment: Fenbendazole Ivermectin Levamisole .

Thiabendazole Return to top of page .

Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment .Macracanthorhynchus hirudinaceus Homepage Common name: Thorny headed worm Kingdom: Animalia Phylum: Acanthocephala Class: Acanthocephalae Order: Archiacanthocephala Family: Oligacanthorhynchidae Genus : Macracanthorhynchus Species: hirudinaceus Click on the text below to jump down to the desired section of this page.

Return to top of page Life Cycle: The beetle ingests an egg.Adult Parasite: The body is flattened and has transverse grooves. Adults attached to small intestine of pig Proboscis of Adult Return to top of page Hosts: Pigs and wild boars (definitive). June beetles (intermediate). When the pig eats the infected beetle the larva is digested out and attaches to the wall of the small intestine and grows to the . Dung beetles. May bugs. The adult males are 10 cm and the females are up to 35 cm long. The egg hatches and the larva develops to the cystacanth stage which encysts in the body cavity of the insect.

110 by 40 . Return to top of page Common Diagnostic Test Fecal float to recover eggs. Return to top of page Site in host where adult parasite is found: Small intestine Return to top of page Diagnostic Stage: Eggs 67 . Return to top of page Clinical Signs: .adult stage. The eggs have 4 shells. and is dark brown.65 µm.

J. Return to top of page Treatment: Drug: Loperamid Loperamid is an "extra label use". 200 µg/kg. Vet. There will be inflammation and a granuloma in the intestinal wall around the site of attachment. 1990. hirudinaceus from pigs (Alva Valdes. However. Res. 1992. Am. Am. severe infections will cause slow growth and even emaciation. On rare occasions the worm may perforate the gut and peritonitis may result. et al.) Drug: Ivermectin Ivermectin is an "extra label use".5 mg/kg. Res. once a day for 7 days. Vet.. another report suggested variable results (13 to 77% removal) (Primm. J. PO. twice daily for 3 consecutive days (Mehlhorn. et al. et al. 1989.) Return to top of page . removed M. Parasitology Research 76:624-626. 50:1392-1395). 53:508-512.Mild infections will be asymptomatic. 1.

Stephanurus dentatus Homepage Common name: Kidney-worm of swine Kingdom: Animalia Phylum: Nemathelminthes Class: Nematoda Order: Strongylida Family: Stephanuridae Genus: Stephanurus Species: dentatus Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment Adult Parasite: .

Return to top of page Site in host where adult parasite is found: Generally found in the pelvis of the kidney. Return to top of page Hosts: Pigs Return to top of page Life Cycle: Eggs pass out in the urine and hatch in the environment in about 30 hrs.5 cm long. infecting the pig when the earthworm is eaten. which they connect to via a small canal. . The per-patent period varies from 6 to 9 months and the adults may live for up to 2 years.The male measures 2 to 3 cm long and the female measures 3 to 4. Larvae will reach the infectious third-stage in about 4 days and in moist. They will then migrate to the kidney and either enter the kidney or encyst next to the kidney or ureter. Larvae ingested by earthworms can use the worm as a transport host. Internal organs may be visible through the cuticle. warm environments they will live for 2 or 3 months (some may survive up to 5 months). for 3 or more months before penetrating into the peritoneal cavity. Larvae reach the liver via the portal veins (if eaten) or via the systemic circulation (after penetrating the skin). or in the perirenal fat or the walls of the ureters. They will remain in the liver. wandering under the capsule. this molt will be in the wall of the stomach if the larva was eaten or in the skin or muscles if the larva penetrated the skin. The larvae will molt to the fourth-stage 70 hours post-infection (PI). Larvae will infect a pig either through the skin or by being ingested.

Larval migration in the liver may lead to cirrhosis and ascites may be present. emaciation.Return to top of page Diagnostic Stage: Eggs are found in the urine. . loss of appetite and. Return to top of page Treatment: Ivermectin benzimidazoles: fenbendazole. in severe cases. Return to top of page Common Diagnostic Test Seen in urine sedimentation Return to top of page Clinical Signs: General signs include depressed growth rate. they measure about 56 X 105 µm.

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Isospora robini Homepage Common name: Coccidia Kingdom: Protista Phylum: Protozoa Class: Apicomplexa Order: Eucoccidiorida Family: Eimeriidae Genus: Isospora Species: robini Click on the text below to jump down to the desired section of this page. Adult parasite Hosts Lifecycle Site where adult parasite is found in host Diagnostic stage Clinical signs Treatment .

Return to top of page Diagnostic Stage: Oocysts are ovoid to ellipsoidal. Both adult and fledgling birds have been seen infected. measure 20 X 23 µm and are brownish in color.Adult Parasite: No information. Return to top of page Hosts: Robin (Turdus migratorius) Return to top of page Life Cycle: Little data. but does contain . The oocysts are found in the feces of the robin. They have no micropyle. The sporulated oocyst has no residuum. Life cycle is assumed to be direct. Return to top of page Site in host where adult parasite is found: Schizonts are probably found in the cells of the small intestine epithelium.

Helminthol. 1988.B. Soc. Return to top of page Treatment: None Return to top of page . Holmes. McQuistion and B. Proc. (T.) Return to top of page Common Diagnostic Test Fecal flotation Return to top of page Clinical Signs: None reported.a large prominent polar granule.E. Washington 55:324-325.

Parasitic stage During a later bloodmeal on an appropriate host (C) . for a mosquito to ingest during a subsequent blood meal. L4 stages undertake extensive migration through the subcutis. enter the bite wound. Final maturation and mating occur in the pulmonary arteries. After reproduction.primarily dogs but also cats and ferrets. They can cross the capillary beds and so are found throughout the vascular circulation. the females produce small. and penetrate local connective tissues. Preparasitic phase Circulating microfilariae are ingested by a female mosquito while taking a bloodmeal from an infected host (A). which continues for some 60-90 days until the final molt to the immature adult (E). the L3's will exit the labium. The juvenile worms migrate to the right heart within a few days of their final molt (F). where they may survive for up to seven years. Molting to the next stage (L4) occurs within seven days of infection (D). . Production of microfilariae by inseminated female worms begins approximately six and a half months (192 days) after infection. and the adult worms live in the right heart and pulmonary arteries. These infective L3's migrate from the tubules to the lumen of the labial sheath in the mosquito's mouthparts. vermiform embryos called microfilariae. carried there by the venous circulation. These prelarval stages migrate to the Malpighian tubules of the mosquito vector where development through to third stage larvae takes place (B). Microfilariae are then released into the circulation.Heartworm Dirofilaria immitis Life Cycle Dirofilaria immitis adults are primarily found in the right ventricle and pulmonary arteries of dogs.

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Click on the small intestine to get a closer view of Eimeria life cycle or click anywhere on the closeup diagram to return to the over view. A merozoite produced by the final schizogony is a telomerozoite (I). grow larger.Eimeria bovis Life Cycle Eimeria bovis is one of the many bovine gastrointestinal parasites. The male gametocyte undergoes repeated nuclear division nd becomes multinucleate. Only a small fraction will find and fertilize macrogametes to form oocysts. . stores food materials. It has a general form of coccidian life cycle. but two or three is usually the limit for may of the important species. ( ) Following the ingestion of sporulated oocysts by calf (D). There may be several more schizogonic generations for other Eimeria. it is called a macrogamete or female sex cell. Each nucleus is finally incorporated into a biflagellate microgamete or male sex cell. and become a first generation schizont. or a megaschizont (G). Sporozoites inside host cells can round up as a trophozoite (F). provided that the environment is adequate. and it is ubiquitous in the environment. including both asexual multiplication and sexual multiplication. and induces hypertrophy of both cytoplasm and nucleus of its host cell. Click on the large intestine to get a closer view of Eimeria life cycle or click anywhere on the closeup diagram to return to the over view. the sporozoites invade the epithelial cells (E) or the lamina propria of the host's small intestine. The megaschizont then releases many merozoites which further infect fresh host cells (H). Four sporoblasts develop within each oocyst (B). The oocyst is released by rupture of the host cell and passes out with the feces to undergo sporulation. and two infective sporozoites develop within each sporocyst (C). The female gametocyte enlarges. Sexual multiplication culminates in the formation of oocysts. Telomerozoites can enter a fresh host cell and develop into either a male or a female gametocyte or developing sex cell (J). When mature. which are discharged with the feces (A).

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horses. an abomasal nematode. Exsheathment sites are species-specific and are always proximal to the predilection site of each particular trichostrongylid species. These ensheathed L3's survive by utilizing nutrients stored by the actively feeding L1 and L2 stages. The following table gives some prepatent periods for several members of this family. goats Predilection site Abomasum Abomasum. Eggs are passed in the feces of infected hosts.life cycles Nematodes belonging to the family Trichostrongylidae have life cycles that are closely similar. Some examples are given in the following table. impermeable sheath (the retained L2 cuticle). Contained embryos will develop into first stage larvae if temperature and humidity are optimal (22-26'C and 100% humidity). Predilection sites include the abomasum. Exsheathment is immediately followed by movement of parasitic L3's to the predilection site where growth and development to adults occurs (L3--> L4-->Adults). while Cooperia curticei. Exsheathment is the next event in the parasitic phase of these life cycles.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS The Nematodes Trichostrongyles . by ingesting L3's. The time from infection to egg-laying by adult females is specific for each nematode species and is called the prepatent period. Nematode Ostertagia species Haemonchus species Cooperia species Prepatent period 17-21 days 2-3 weeks 15-18 days . exsheaths in the rumen. Ostertagia ostertagi. Following sexual reproduction. Parasitic phase The trichostongylid infective stage is an L3 enclosed in its protective sheath and hosts are infected. or stomach Small intestine Pre-parasitic phase The pre-parasitic phase of larval development is entirely free living. Nematode Ostertagia ostertagi Trichostrongylus axei Cooperia curticei Host Cattle Ruminants. with its predilection site in the small intestine. pigs Sheep. First (L1) and second (L2) larval stages feed on fecal and soil bacteria but the third stage(L3) cannot feed because it is enclosed by a protective. As examples. as they graze on pasture. stomach or small intestine of ruminants. exsheaths in the abomasum. mature females lay eggs approximately 2-3 weeks after infection. horses or swine depending on the species.

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PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Ascaris suum Life cycle The predilection site for Ascaris suum is the small intestine of swine. sticky external coat and are laid in the one-celled stage. Mature. reaching the lungs (H) by 4 to 6 days after infection. L2s burrow into the intestinal wall. right heart and pulmonary arteries. Earthworms (D) and dung beetles may ingest ascarid eggs while feeding on soil and feces. When that happens eggs will hatch and L2s will migrate to tissues and encyst giving rise to the possibility that these invertebrates may serve as paratenic hosts for Ascaris suum. Third stage larvae (L3s) continue their migration from the liver to the lungs via the venous system. Therefore the infective stage for Ascaris suum is an egg containing a second stage (L2) larva (C). enter the hepatic portal system and are carried to the liver (G) within 24 hours of infection. They break out of the alveolar capillaries and migrate up the bronchial tree to the pharynx (I) where they are swallowed. These eggs are oval and thick-shelled with a rough mammillated. L2s are released during digestion in the stomach and small intestine. . Their migratory route and parasitic development are the same as infective larvae from eggs). gravid females begin to lay eggs approximately 6 to 8 weeks after infection. Here the first parasitic molt (L2 to L3) takes place. The final two parasitic molts (L3 to L4 to immature adults) are completed in the small intestine (F) by 3-4 weeks after infection. Development to the infective stage takes place inside the egg and consists of one molt only. Following hatching in the small intestine (F). (If infected paratenic hosts (D) are ingested by pigs. Parasitic phase Pigs are infected by ingesting (E) eggs or paratenic hosts containing second stage larvae. Pre-parasitic phase Eggs laid by female worms pass to the external environment in host feces (A).

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developing larvae migrate anteriorly in the neural parenchyma. Pre-parasitic phase The pre-parasitic phase of larval development takes place entirely inside an intermediate host.(E) Terrestrial gastropods (slugs and snails) serve as intermediate hosts. Growing. They are infected when L1s penetrate the gastropod foot. Approximately forty days after infection. Immature adult worms complete their development to sexual maturity.to the pharynx where they are swallowed. These eggs are carried via venous blood flow to the right heart (B) and then via the pulmonary arteries to the lungs(C) where they lodge in the alveolar capillary beds. specifically the subdural space and meningeal venous sinuses. They penetrate the gut wall. copulation takes place. Parasitic phase -----> Migration route of ingested L3s to the brain. specifically the dorsal horns of the gray matter. and reach the vertebral canal approximately ten days after infection. The prepatent period is approximately 7weeks (range = 82-91 days). Eggs are deposited in the venous sinuses by female worms. -----> Migration route of eggs and first stage larvae(L1s) from the brain to the external environment. Deer are infected by ingesting (F) infected slugs and snails as they browse and graze on low vegetation. First stage larvae(L1s) develop.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS The Nematodes Paralephostrongylus tenuis . escape into the alveoli and migrate up the bronchial tree(D) . .life cycle The predilection site for this nematode is the brain (A) of white-tailed deer. Development of fre-living stages does not does not occur in this life cycle. The infective third larval stage (L3) is reached in gastropods following two molts (L1 to L2 to L3). immature adults can be found in the subdural space of the spinal cord in which they continue their migration to the predilection site the subdural space and meningeal venous sinuses of the brain. They pass through the gastrointestinal tract and out to the external environment with the hosts feces. Third-stage larvae are released from snail and slug tissues during digestion in the abomasum and small intestine. hatch. and adult female worms complete the cycle by laying their eggs in the meningeal blood vessels. as the snails and slugs travel across deer feces. follow the lumbar nerves. migrate across the peritoneal cavity to the lumbar vertebrae. The location of adults in the brain means that eggs and hatched first stage larvae must undergo a tortuous path through the body of a host in order to reach the external environment where they will encounter required intermediate hosts.aided by the upward flow of epithelial cilia .

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Example Ostertagia Strongylus Dirofilaria Diagnostic Location Definitive stage host(s) egg egg host feces host feces ruminants horses Predilection site abomasum cecum & colon heart brain subcutaneous tissues lungs L1 peripheral Dogs (microfilaria) blood host feces deer horses ruminants. horses Parelaphostrongylus L1 Onchocerca Dictyocaulus L1 skin (microfilaria) L1 host feces .

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These ensheathed L3's survive by utilizing nutrients stored by the actively feeding L1 and L2 stages. Exsheathment is the next event in the parasitic phase of these life cycles. Some examples are given in the following table. Similarly with humidity: the optimal humidity for development is 100% and little development occurs below 80%. exsheaths in the rumen. exsheaths in the abomasum. axei horses.life cycles Nematodes belonging to the family Trichostrongylidae have life cycles that are closely similar. At higher temperatures. or stomach pigs Cooperia Sheep. Development of all preparasitic stages . movement and metabolism are minimal. an abomasal nematode. At temperatures below freezing preparasitic stages are vulnerable and few will survive. Eggs are passed in the feces of infected hosts. optimal development occurs at 100% humidity and between a temperature range of 22'-26'C. At lower temperatures. horses or swine depending on the species. the rate of development may be faster but metabolic activity of L3s is also increased and food reserves may be used up more quickly leading to larval death unless larvae readily find and infect a host. First (L1) and second (L2) larval stages feed on fecal and soil bacteria but the third stage(L3) cannot feed because it is enclosed by a protective. Small curticei goats intestine Pre-parasitic phase The pre-parasitic phase of larval development is entirely free living. Prolonged dry spells and seasonal dry periods open larvae to death by desiccation. Ostertagia ostertagi. At temperatures less than 10'C larval development. by ingesting L3's. Following sexual reproduction. larvae may survive and develop because the microclimate within their environment on pasture may be sufficiently high. However. Exsheathment sites are species-specific and are always proximal to the predilection site of each particular trichostrongylid species.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Trichostrongyloidea Trichostrongylidae . Exsheathment is immediately followed by movement of parasitic L3's to the predilection site where growth and development to adults occurs (L3--> L4-->Adults). Parasitic phase The trichostongylid infective stage is an L3 enclosed in its protective sheath and hosts are infected. Nematode Host Predilection site Abomasum Ostertagia Cattle ostertagi Trichostrongylus Ruminants. Abomasum.from eggs through to infective 3s is also controlled by temperature and humidity. impermeable sheath (the retained L2 cuticle). while Cooperia curticei. As examples. stomach or small intestine of ruminants. Contained embryos will develop into first stage larvae and hatch if temperature and humidity are optimal (22-26'C and 100% humidity). with its predilection site in the small intestine. as they graze on pasture. Predilection sites include the abomasum. mature females lay eggs approximately 2-3 weeks after infection. even when atmospheric humidity is low. development slows and metabolic activity is reduced. The .

Nematode Ostertagia species Haemonchus species Cooperia species Trichostrongylus species Prepatent period 17-21 days 2-3 weeks 15-18 days 7-25 days Hypobiosis or seasonal arrested development is an important feature of the life cycles of members of this family. The following table gives some prepatent periods for several members of this family. Hypobiosis is therefore a mechanism to ensure survival whereby the nematode halts its development in a host when prevailing environmental conditions might jeopardize the survival of any progeny.time from infection to egg-laying by adult females is specific for each nematode species and is called the prepatent period. . It occurs where the prevailing seasonal temperature and humidity fall to levels that threaten their survival.

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the larvae migrate to the stomach (A) and penetrate the gastric glands. There they grow and develop through two molts.PARASITES AND PARASITIC DISEASES OF DOMESTIC ANIMALS Hyostrongylus rubidus The predilection site of this nematode is the stomach of swine. Life Cycle Hyostrongylus rubidus has a typical life cycle of the family Trichostrongylidae. The prepatent period is 3 weeks unless hypobiosis intervenes in which case the prepatent period may be delayed by several months until the arrested L4s resume their development . moist conditions development from eggs through to L3s will take place in 7-14 days. emerging as immature adults approximately 17 days after infection to mature and reproduce on the surface of the stomach mucosa. The free living stages. The free-living and parasitic phases of the life cycle are similar to those of Ostertagia. particularly L3s are susceptible to cold and drying which means that transmission is minimal in winter and when summers are dryer than usual. ( )Following the ingestion of infective L3s. Under warm. .

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pathogenesis The image shows an arteriographic picture of the mesenteric arterial system of a foal 30 days after oral infection with 50 third stage larvae of Strongylus vulgaris. Most other arteries branching off the abdominal aorta (a) are dilated and irregular in their outline because of inflammation and the presence of mural thrombi. g = gastric artery cm = cranial mesenteric artery pm = posterior (caudal) mesenteric artery l = lateral cecal artery . s = splenic artery h = hepatic artery.celiac artery. At this stage most of the larvae will have reached the cranial mesenteric artery and the image shows some of the early effects of their migratory pathway. Other labels: c . The medial cecal artery (m) is also blocked along most of its length. The ventral colic (vc) branch of the ileo-ceco-colic artery (icc) is blocked by thrombi since only a small portion is visible from contrast material that has perfused via anastomoses with the dorsal colic artery (dc) artery.Strongylus vulgaris .

Jay Georgi. Image courtesy of Dr.Arteriographic picture of the mesenteric arterial system of a foal 30 days after infection with 50 Strongylus vulgaris third stage larvae. .

Labels: a = abdominal aorta cm = cranial mesenteric artery icc = ileo-ceco-colic artery dc = dorsal colic artery vc = ventral colic artery m = medial cecal artery l = lateral cecal artery c . The cranial mesenteric artery is reduced in size and thrombotic occlusions have resolved.pathogenesis The image shows an arteriographic picture of the mesenteric arterial system of a foal 60 days after oral infection with 50 third stage larvae of Strongylus vulgaris adn treatmetn at 30 dasy with a larvicidal dose of an anthelmintic. vulgaris larvae are well on the way to complete resolution and healing.Strongylus vulgaris .celiac artery g = gastric artery h = hepatic artery s = splenic artery pm = posterior mesenteric artery . This arteriograph shows that significant healing has occurred in this foal and it is clear that the larvicidal treatment at 30 days after infection was successful in killing most if not all migrating fourth stage larvae and allowed the natural healing process to take place. All major branches from the cranial mesenteric artery contain contrast material and are therefore now open. it is clear that the lesions caused by migrating S. The fan of grey lines extending from the ileo-ceco-colic artery (icc) are jejunal and iliac arteries supplying blood to the small intestine. Although there is irregularity in the walls of some arteries.

Arteriographic picture of the mesenteric arterial system of a foal 60 days after infection with 50 Strongylus vulgaris third stage larvae and treatment at 30 days with a larvicidal dose of an anthelmintic. Jay Georgi. Image courtesy of Dr. .

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care (and time) must be taken to get a good view of the bases of the pulmonary arteries. immitis" is clicked. It is not possible to count the number of worms using ultrasound as different loops of the same worm may be showing up as separate reflections of the beam. Back to Dirofilaria immitis homepage . Worms will appear as a pair of bright parallel lines (some of which have are marked by an arrow in the video).Ultrasound Detection of Feline Heartworm Infection Back to Dirofilaria immitis homepage The following video shows an ultrasound of the base of the pulmonary arteries of a cat with adult heartworm(s) present. When using ultrasound to examine a cat for heartworm. The video will loop until the "Back to D.

Back to Dirofilaria immitis homepage . In this ultrasound clip. immitis" is clicked. It is not possible to count the number of worms using ultrasound as different loops of the same worm may be showing up as separate reflections of the beam.Ultrasound Detection of Heartworm Infection in a Ferret Back to Dirofilaria immitis homepage The following video shows an ultrasound of the apex of a ferret's heart ("4-chamber" view) with adult heartworm(s) present in the right atrium. When using ultrasound to examine a ferret for heartworm. care (and time) must be taken to get a good view of the bases of the pulmonary arteries and the right atrium. worms appear as a pair of bright parallel lines in the right atrium (which will be located to the lower left-center of the ultrasound). The video will loop until the "Back to D.

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for a 6 year old cat and transmmary infection is only a minor infection route for Toxocara cati.Quiz Case #1 You chose: Transmammary Not likely. Return to the previous page and try again Go to a review of Toxocara cati .

and in a 6 year old cat it is unlikely that any worms that were passed to it from its mother would still be present. Return to the previous page and try again Go to a review of Toxocara cati .Quiz Case #1 You chose: Transplacental Toxocara cati is not known to use the transplacental route.

there is another route of infection that may have been more likely for this cat. Return to the previous page and try again . However.Quiz Case #1 You chose: Ingested an egg Ingesting an egg that has reached the infectious stage may be the route by which this cat was infected.

Given that this is an older. over time. No . Yes B. male cat. and. this is the most likely route of infection. does this infection have to be treated (there are no clinical signs present)? A. Ingestion of one or more of these hosts is likely to give the cat a greater infection at one time than the occasional ingestion of an egg. it hunts and ingests infected paratenic hosts. When the cat is outdoors. these paratenic hosts accumulate a store of arrested larvae in their tissues. Rodents and birds accidentally ingest eggs as they feed.Quiz Case #1 You chose: Ate a rodent or bird. Correct! Yes.

Although A. Return to the previous page and try again . B. C and D are all routes of infection for this parasite. Wrong. they are not all equally likely at all stages of the cat's life.Quiz Case #1 You chose: All of the above are equally likely.

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Quiz Case #2 You chose: Drug resistance. also the object pictured is not Isospora felis. Not likely. . Return to the previous page and try again Go to a review of Isospora felis. The fact that the diarrhea went away (and then came back) suggests that the drug worked.

Return to the previous page and try again Go to a review of Isospora felis. .Quiz Case #2 You chose: The owner did not comply with treatment instructions. The diarrhea went away (and then came back) and the object pictured is not Isospora felis. Not likely.

causing disease. therefore it is unlikely you would see a re-infection of the same Isospora spp. The object pictured is not Isospora felis. Return to the previous page and try again Go to a review of Isospora felis. is very strong. Not likely.Quiz Case #2 You chose: The cat was re-infected with Isospora felis. Immunity to a particular Isospora spp. .

Isospora felis B. Isospora rivolta C. Identify the parasite found in the second fecal exam. but it is a coccidian oocyst. A. Isospora ohionensis D.Quiz Case #2 You chose: The cat is infectedwith another coccidian. Hammondia hammondi . Toxoplasma gondii E. Correct! The object pictured is not Isospora felis.

would a 9 week old cat be hunting mice? Ask the owner to find out. not the "many" found in this case. the oocysts in the mouse gut will pass through the cat. the number of these oocysts you would find on a fecal exam is going to be small. However. Return to the previous page and try again . If a cat eats a mouse infected with coccidia and is passing oocysts. Unlikely.Quiz Case #2 You chose: The cat ingested a mouse and is just passing oocysts of that host's coccidia. Also.

The pulmonary arteries. Click here to return to quiz . This indicates damage to the lungs. Also note that the lungs (large black triangle) are not as radiolucent as they should be. highlited in red are enlarged.

Return to the previous page and try again . You might want to know if there are microfilariae present in order to determine a course of therapy. However. microfilariae are only transiently found during a heartworm infection in cats. Therefore the Knott Test is not the best test to run in order to diagnose an infection in cats.Quiz Case #3 You chose: Knott Test Not a good choice.

but it does not tell you if adult heartworms are present. Thus. this test tells you if the cat has been exposed and therefore might be infected. which is well before larvae reach the pulmonary arteries. Results of the Heartworm antibody test on this cat:Positive Return to the previous page and try another test to help you confirm your diagnosis . many of the larvae present at 2 months post infection will die before maturing to the adult stage.Quiz Case #3 You chose: Heartworm Antibody Test Antibodies to heartworm are found as early as 2 months post infection. In fact.

However. they may be absent in infections where only male worms are present.Quiz Case #3 You chose: Heartworm Antigen Test Antigens detected by the Heartworm Antigen Tests currently available are produced by the adult female worm. Results of the Heartworm Antigen Test: Negative Return to the previous page and choose another test to help you confirm your diagnosis . Thus. if present the positive antigen test conforms the diagnosis.

Quiz Case #3 You chose: Ultrasound. Right: long pasternal view) . Click on image to see full size pictures (left: short view. If done properly and care is taken to visualize the pulmonary arteries. The ultrasound on this cat showed the following: characteristic parallel lines produced by the echo from a worm in the pulmonary artery. ultrasound can be a definitive test.

which is unlikely to provide you with a diagnosis. Heartworm antigen test: Negative 4. Knott Test: Negative 2. The test results on this cat: 1. However. but may also be positive if the cat was exposed to migrating L4 which died off before reaching the vasculature. The antibody test is usually positive if the cat is infected. any of the above tests would be a good start. Click on image to see full size pictures . if positive. If the cat is immunocompromised the antibody test may be negative even if an adult worm is present. With the exception of the Knott Test. would provide a definitive diagnosis.Quiz Case #3 You chose: All of the above Not a bad choice. a negative result does not rule out heartworm. Feline heartworm antibody test: Positive 3. Both the antigen test and ultrasound. Ultrasound: Shows parallel lines in the pulmonary artery.

The cat is probably not infected with heartworm . Right: long pasternal view) What do these test results tell you? A. The cat might be infected with heartworm C.(left: short view. The cat is infected with Dirofilaria immitis B.

Although the surface of the ova shown is similiar to Capillaria aerophila. Return to the previous page and try again Go to a review of Capillaria aerophila .Quiz Case #4 You chose: Capillaria aerophila Wrong. the egg is too small.

Wrong. Return to the previous page and try again Go to a review of Capillaria bohemi .Quiz Case #4 You chose: Capillaria bohemi. The surface is not that of Capillaria bohemi.

Although the surface of the ova shown is similiar to Capillaria plica. Return to the previous page and try again Go to a review of Capillaria plica . the size is wrong and Capillaria plica eggs are found in the urine (although contamination of the feces is possible).Quiz Case #4 You chose: Capillaria plica Wrong.

and is it likely this parsite will cause problems forthe cat? A. How did the cat get these eggs in its feces. Hunting (eggs just passing through)/ Yes. C. The size and surface of the ova shown are consistent with Capillaria hepatica. Hunting (eggs just pasing through)/ No. Fecal contamination of the cat's paws (eggs just passing through)/ Yes.Quiz Case #4 You chose: Capillaria hepatica You may be Right. E. . Hunting (cat is infected) Yes. Fecal contamination of the cat's paws (eggs just passing through)/ No. B. D.

Quiz Case #4 You chose: Capillaria tomentosa Wrong. Capillaria tomentosa infects fish in Europe. Return to the previous page and try again .

Click here to return to quiz .Click here to magnify image.

The worm is in a vessel of some sort.Quiz Case #5 You chose: Liver parenchyma No. Return to the previous page and try again .

Quiz Case #5 You chose: Vein No. The structure of the vessel wall is not that of a vein. Return to the previous page and try again .

Return to the previous page and try again .Quiz Case #5 You chose: Artery No. The structure of the vessel wall is not that of an artery.

there are several species of bile duct flukes that infect cats. Yes! The parasite in question is thus a bile duct fluke of cats. Both use a snail as a first intermediate host. A parasitologist could identify the species of the fluke by examining the adult shown in figure 1B. The two bile duct flukes listed on the "Cat ParasiteList" are Parametorchis complexis and Platynosum fastosum. Rodents and fish C. you can make an educated guess based on the life histories of the cat bile duct flukes. but they differ in the second intermediate host. Rodents and birds B. What are the second intermediate hosts for these two worms? A.Quiz Case #5 You chose: Bile duct. Birds and snakes D. Fish and lizards E. However. White footed mice and palmetto bugs . However.

Haematopinus eurysternus. Cooperia oncophora.9 days (Vet Parasitol. Bunostomun phlebotomum. Oesophagostomum dentatum. Sarcoptes scabiei var. Dose: Swine: 300 :g/kg SQ. Cooperia punctata. Hyostrongylus rubidus. mydriasis. Trichuris ovis. The LD50 for rats given the compound orally in sesame oil was between 50 and 200 mg/kg. Dermatobia hominis. Strongyloides papillosus. . 1999 Feb 1. Cochliomyia hominivorax.. Parasite Targets: Ascaris suum. Nematodirus spathiger.81(1):47-55).6 days . Haematopinus suis.2+/-4. Trichostrongylus axei. In dogs given 4 mg/kg/day for a month ataxia. suis. Strongyloides ransomi.8+/-1.Doramectin Chemical group: Macrocyclic lactone Trade names: Dectomax Mode of action: Probably works like other macrocyclic lactones and opens glutamate-gated chloride channels in the nerve cells.3+/-1. Ostertagia circuncicta. Oesophagostomum quadrispinulatum. Dictyocaulus viviparus. Ostertagia ostertagi. Solenopotes capillatus. weight loss and tremors were seen. The drug can be excreted in the milk. causing paralysis Pharmacokinetics: The plasma pharmacokinetics of doramectin in young beef cattle after topical administration of 500 :g/kg: Cmax :12.8 ng/ml. Psoroptes bovis. Toxicity: Fatalities in dogs have been seen. Oesophagostomum venulosum. Tmax : 4. Haemonchus contortus. decreased food consumption. Metastrongylusspp. Cattle: 200 :g/kg SQ. Linognathus vituli. The mean residence time (MRT) was 12. Oesophagostomum radiatum. Trichostrongylus colubriformis. Stephanurus dentatus.

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canis does not look like the egg that was shown. Also.Quiz Case #1 Wrong Although T. the egg of T. canis can be found in young puppies. it does not cause the anemia and intestinal bleeding that you noticed in this dog. T. canis egg Review Toxocara canis Return to the previous page and try again .

stenocephala looks like the object shown. the clinical signs seen (anemia and bleeding into the intestine) are not typical of an U. stenocephala Return to the previous page and try again . Review U.Quiz Case #1 Wrong Although U. More importantly. it is slightly larger. stenocephala infection.

so it is common in puppies. caninum is passed to the nursing puppies in the milk. Also the anemia (pale membranes) and bleeding into the small intestines (black tarry stools) are classical clinical symptoms of a heavy canine hookworm infection. Go to a review of A .Quiz Case #1 Correct! A. caninum Return to the dog homepage and try another quiz case .

Quiz Case #1 Wrong The egg of T. so you would not see eggs in the stool of a 10 week old dog. T. vulpis does not look anything like the egg shown. Finally. Trichuris eggs Go to a review of T. Also. vulpis Return to the previous page and try again . vulpis has a 3 month pre-patent period. the disease caused by the whipworm has different clinical signs from those that seen in this puppy.

Quiz Case #2 Wrong The smallest Isospora sp. Review Isospora canis Return to the previous page and try again . oocyst is about twice the size of the object shown and looks quite different.

While Giardia infections are usually asymptomatic and will eventually be cleared by the dog's immune response.Quiz Case #2 Correct: The age of the dog and the condition of the stool would suggest you pay attention to this finding. Ariel is already showing mild symptoms (the mushy stool) and since the parasite can increase in numbers within the host. You should probably treat Ariel. this dog is probably experiencing its first infection with this parasite. the disease may get worse before it gets better. Go to Giardia Homepage Return to canine homepage to try another quiz .

but spores usually have no internal details. The object in the previous photomicrograph shows several internal structures. The size and shape are correct for many fungal spores. Fungal spore Return to the previous page and try again .Quiz Case #2 Close. but wrong. while the one below does not.

Return to the previous page and try again Go to Toxoplasma gondii homepage .Quiz Case #2 Wrong Remember that dogs do not shed oocysts of Toxoplasma gondii.

Quiz Case #3 You chose: Capillaria aerophila and Isospora canis : WRONG: The egg in "A" is the wrong shape and color for Capillaria sp. Return to previous page and try again Go to a review of Capillaria aerophila Go to a review of Isospora canis . and the object in "B" is the wrong shape and color for Isospora canis.

and the object in "B" is the wrong size and color for Paragonimus kellicotti.Quiz Case #3 You chose: Capillaria aerophila and Paragonimus kellicotti WRONG: The egg in "A" is the wrong shape and color for Capillaria sp. Return to previous page and try again Go to a review of Capillaria aerophila Go to a review of Paragonimus kellicotti .

Both are likely to be contributing .Quiz Case #3 You chose: Trichuris vulpis and Eimeria sp. Correct! Which of the parasites you just identified is most likely causing the dog's problem? Trichuris vulpis Eimeria sp.

Quiz Case #3 You chose: Trichurisvulpis and Paragonimus kellicotti Wrong: The object in "A" is Trichuris vulpis. but the object in "B" is the wrong size and color for Paragonimus kellicotti. Return to previous page and try again Go to a review of Paragonimus kellicotti .

Mackenzie is pregnant and arrested larvae have "woken" up and some made their way to the small intestine and matured.Quiz Case #4 You chose: "A" . Answer: Wrong. Return to previous page and try again . Mackenzie is a male dog.

but there may be another reason Return to previous page and try again .Quiz Case #4 You chose: "B" .Mackenzie ate an infected paratenic host. Answer: Very likely.

Mackenzie is immunocompromised due to some problem. but there may be a better explanation. Answer: Could be. Return to previous page and try again .Quiz Case #4 You chose: "C" . thus allowing arrested larvae to migrate to the gut and develop.

Answer: Wrong.Mackenzie is pregnant and arrested larvae have "woken" up and some made their way to the small intestine and matured.Quiz Case #4 You chose: "A" and "B" . Mackenzie is a male dog. and Mackenzie ate an infected paratenic host. Return to previous page and try again .

and Mackenzie is immunocompromised due to some problem. including antibody levels and T and B cell ratios. B. thus allowing arrested larvae to migrate to the gut and develop. Perform a complete blood work up. What do you do to determine which is the likely explanation? A. Answer: Both these explanations are possible.Mackenzie ate an infected paratenic host. Ask the owners if Mackenzie has ever been known to eat rodents or birds. .Quiz Case #4 You Chose: "B" and "C" .

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Although this infection is unlikely to cause this cat any problems. and will be eliminated quickly by the immune system. Right.Quiz Case #1 You chose: Yes. you should treat the cat to prevent this pet from contaminating areas where children may come in contact with the eggs. Toxocara cati is zoonotic. Therefore. Return to Cat Homepage and try another quiz . the cat should be treated.

Return to the Cat Homepage and try another quiz . and probably will be eliminated quickly by the immune system. the cat does not need to be treated Wrong! Although this infection is unlikely to cause this cat any problems. Toxocara cati is zoonotic. Therefore. you should treat the cat to prevent this pet from contaminating areas where children may come in contact with the eggs.Quiz Case #1 You chose: No.

Quiz Case #2 You chose: Isospora felis. causing shedding of "many" oocysts. The object pictured is not Isospora felis. Immunity to a particular Isospora spp. Wrong. therefore it is unlikely you would see a re-infection of the same Isospora spp. is very strong. Return to the previous page and try again Go to a review of Isospora felis. .

Not enough time has elapsed for the drug to have cured the infection. Clickhere to review the particulars of Isospora revolta. A few days later the owner calls and tells you that the cat still has bloody diarrhea. or continue with the quiz below. The fecal exam is repeated and no parasites are seen. You request that another fecal sample be brought in. What is going on?? A. Drug failure. D. The cat has a Campylobacter infection E.. B. C. You again have the owner treat the cat for 5 days with sulfadimethoxine.Quiz Case #2 You chose: Isospora revolta Correct! This oocyst is that of Isospora revolta. Pre-patent infection with another coccidia. Pre-patent hookworm infection .

Isospora ohionensis is a dog parasite and will not infect cats. Wrong. Return to the previous page and try again Go to a review of Isospora ohionensis .Quiz Case #2 You chose: Isospora ohionensis.

The oocyst pictured is too large to be that of Toxoplasma gondii. Return to the previous page and try again Go to a review of Toxoplasma gondii.Quiz Case #2 You chose: Toxoplasma gondii Wrong. .

Quiz Case #2 You chose: Hammondia hammondi Wrong. The oocyst pictured is too large to be that of Hammondia hammondi Return to the previous page and try again Go to a review of Hammondia hammondi .

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. Return to the Cat Homepage and try another quiz Go to a review of Dirofilaria immitis.Quiz Case #3 You chose: Results indicate that the cat is infected with Dirofilaria immitis. Yes !!! The positive antibody titer and the presence of a worm detected by Ultrasound indicate that the cat is infected. The initial radiograph indicates that the worm(s) has produced pathology in the cat that may be responsible for the clinical signs.

Quiz Case #3 You chose: The cat might be infected with heartworm. The test results indicate that the catis infected Return to the previous page and try again . No.

No. The test results indicate that the cat isinfected Return to the previous page and try again .Quiz Case #3 You chose: The cat is probably not infected with heartworm.

Wrong. Return to the previous page and try again .Quiz Case #4 You chose: Fecal contamination of the cat's paws (eggs just passing through)/ No. Capillaria hepatica eggs are found only in the liver of mice so you would not find them in fecal material.

Wrong. Capillaria hepatica eggs are found only in the liver of mice so you would not find them in fecal material. Return to the previous page and try again .Quiz Case #4 You chose: Fecal contamination of the cat's paws (eggs just passing through)/ Yes.

Correct!! Capillaria hepatica eggs are found only in the liver of mice.Quiz Case #4 You chose: Hunting (eggs just pasing through)/ No. The eggs are freed from the liver in the cat's intestine and just pass out in the cat's feces. They would not infect the cat. so you would expect to see them in cats that eat mice. Return to the feline page and try another quiz .

Quiz Case #4 You chose: Hunting (eggs just passing through)/ Yes. The eggs are freed from the liver in the cat's intestine and just pass out in the cat's feces. Return to the previous page and try again . so you would expect to see them in cats that eat mice. They would not infect the cat. Almost right. Capillaria hepatica eggs are found only in the liver of mice.

Capillaria hepatica eggs are found only in the liver of mice. so you would expect to see them in cats that eat mice. The eggs are freed from the liver in the cat's intestine and just pass out in the cat's feces. Almost right. Return to the previous page and try again .Quiz Case #4 You chose: Hunting (cat is infected)/ Yes. They would not infect the cat.

Click here to return to quiz Click here to shrink image down one size .

Quiz Case #5 You chose: Rodents and birds Wrong. Click here to continue .

Quiz Case #5 You chose: Rodents and fish Wrong. Click here to continue .

Quiz Case #5 You chose: Birds and snakes Wrong. Click here to continue .

Geckos . which intermediate host was the cat more likely to come across? A.Quiz Case #5 You chose: Fish and lizards Right!!! Given that the cat was from Massachusetts. Minnows B.

Click here to continue .Quiz Case #5 You chose: White footed mice and palmetto bugs Wrong.

Raccoons. What part of the history explains the presence of Eimeria oocysts in the dog's feces? A A and B C D . Cirus runs loose in the woods B. Go to a review of Trichuris vulpis. Other dogs run loose in the woods C. Cirus eats wildlife. Given the following points from the dog's history: A.Quiz Case #3 Right! You chose Trichuris vulpis. D. opossums and deer are common in the woods.

Quiz Case #3 You chose: Eimeria sp. No species of Eimeria infects the dog. Return to previous page and try again . Wrong.

Return to previous page and try again .Quiz Case #3 You chose: Eimeria sp. No species of Eimeria infects the dog. and Trichuris vulpis Wrong.

Quiz Case #4 You Chose: "A" .perform a complete blood work up. including antibody levels and T and B cell ratios. Go to previous page and try again . Answer: This answer is correct only if you have gotten a negative response to question B and have seen some other indication during the Mackenzie's PE to suggest that such a complete work up is necessary.

Given this response. Answer: This is the easiest (and least expensive) place to start. could you conclude that the tapeworm egg you found belongs to Taenia pisiformis? 1.ask the owner if Mackenzie has ever been known to eat rodents or birds. Yes 2. In fact Mackenzie enjoys hunting rabbits and rodents.Quiz Case #4 You chose: "B" . No .

there are no oocyst in the feces. Wrong. Return to the previous page and try again .Quiz Case #2 You chose: Drug failure. The drug appears to have worked .

to be picky. Rather. Return to the previous page and try again . And. Wrong. it does not kill the coccidia.Quiz Case #2 You chose: Not enough time has elapsed for the drug to have cured the infection. it halts the replication of the organism in a non-pathogenic stage and keeps it at that stage until the immune response "cures" the infection. that is. The drug should stop the symptoms in a few days and it seems to have worked (there are no oocysts in the feces). sulfadimethoxine is a coccidiostat.

Pathogenic coccidia cause problems during the formation of the oocyst.Quiz Case #2 You chose: Pre-patent infection with another coccidia. Also. the drug should prevent other coccidia from maturing to the pathogenic stage. therefore pre-patent disease would be measured in hours and not days. Return to the previous page and try again . Wrong.

Correct! Campylobacter infection is a good bet. Coccidia rarely cause disease in cats when they are the only pathogen present. Very likely the coccidia were adding to the symptoms of another pathogen. and in this case there is no indication that the Isospora is still present. and the bloody diarrhea is typical of a Campylobacter infection. Return to The Feline Page and try another quiz .Quiz Case #2 You chose: The cat has a Campylobacter infection.

Symptomatic pre-patent hookworm infections wouldn't last for a few days.Quiz Case #2 You chose: Pre-patent hookworm infection. and it would be symptomatic only if the cat received a very big dose of larvae all at once. Wrong. Return to the previous page and try again . One day is more likely.

Cercariae encyst Parametorchis complexis Definitive: cats and dogs Intermediate: First: Snails. When the a metacercaria. In the fish is found in the bile ducts the parasite encysts as of the lizard. When infected lizard is eaten the infected fish is eaten by the cat the by the cat the metacercaria excysts metacercaria excysts and the worm makes its and the worm makes its way up the common bile way to the bile duct duct to the bile ducts and where it matures.Platynosomum fastosum Hosts Definitive: Cats Intermediate: First: Snails Sublima octona. geckos. and skinks. The miracidium invades in lizards and other a snail. Eggs gall bladder where it in the bile make their matures. Eggs in the bile way to the intestine and make their way to the exit in the feces. Continue with quiz . Second: Lizards. The metacercaria skin of a fish. intestine and exit in the feces. Second: Fish Egg hatches in water. Cercariae leave second intermediate the snail and invade the hosts. toads. Eggs are ingested by Life Cycle snails.

Quiz Case #5 You chose: Minnows Right!!!! The morphological identification of the recovered adult indicated that it was Parametorchis complexis which has been found in cats from the Northeast USA. Return to the Cat Homepage .

Return to the previous page and try again .Quiz Case #5 You chose: Geckos Wrong. The morphological identification of the recovered adult indicated that it was Parametorchis complexis which has been found in cats from the Northeast USA. Geckos are not common in Massachusetts.

Cirus runs loose in the woods. Return to previous page and try again. You chose "A" . .Quiz Case #3 Wrong.

this would explain where the whipworm probably came from. Return to previous page and try again.Quiz Case #3 Wrong. You chose "A and B" . .Cirus and other dogs both run loose in the woods. Though incorrect.

Return to previous page and try again. You chose "C" . Though incorrect. opossums and deer are common in the woods.Raccoons.Quiz Case #3 Wrong. this might explain where the Eimeria originally came from. .

As dogs are coprophagic.Quiz Case #3 Correct! You chose "D" . This could be why Cirus has oocysts in his feces of a species of coccidia that does not infect canines. .Cirus eats wildlife. Return to canine page and try another quiz. the oocysts may also have been in wildlife feces that Cirus ingested. which would have been present in the large intestine of wildlife (which the dog consumed). would just pass through Cirus after he ingested them. The oocyst.

but you can not be sure. you can conclude that the tapeworm egg is Taenia pisiformis.Quiz Case #4 You chose: Yes. Answer: Wrong. The egg might be from Taenia pisiformis. Go to previous page and try again .

Which of the following will allow you to identify the parasite? A. Ask the client if they have noticed proglottids on the dog's stools B. Answer: Right. you can notconclude that the tapeworm egg is from Taenia pisiformis. you need some more information. Look in the left-over fecal sample for proglottids C.Quiz Case #4 You chose: No. Look around the perianal area for dried up proglottids D. All of the above .

Quiz Case #4 You chose: "A" . What else can be done from the list? Return to previous page and choose another option .Ask the client if they have noticed proglottids on the dog's stool. Answer: This would help if they said they saw some. but they haven't.

However. and it is the first thing the tech should do when the sample is processed). no proglottids were found in the fecal sample.Quiz Case #4 You chose: Look in the left-over fecal sample for proglottids. Answer: This would help if you found one (actually you should have your tech do this. What else can you do? Return to previous page and choose another option .

you do not see any proglottids stuck to the skin. Answer: This would help if you found one (you could put it in a little water to soften it and allow it to return to its original shape).Quiz Case #4 You chose: Look around the perianal region of the dog for dried up proglottids. However. What else could you do? Return to previous page and choose another option .

No . Would asking the owners if Mackenzie ever ate raw sheep help in identifying this tapeworm? 1.Ask the client if they have noticed proglottids on the dog's stool. and look around the perianal area for dried up proglottids. look in the left-over fecal sample for proglottids. all three of these things can be done.Quiz Case #4 You chose: All of the above . Answer: Right. Yes 2. however no proglottids were ever seen.

Quiz Case #4 You chose: "Yes" . No . Mackenzie was never feed raw sheep. since most of the Taenia species found in dogs are carried by sheep. Yes B.asking the owners if Mackenzie ever ate raw sheep would help in identifying the tapeworm Answer: It might help. Can you conclude that the taenid egg was that of Taenia pisiformis? A.

asking the owners if the dog ever ate any raw sheep would not help in identifying the tapeworm. Answer: Wrong.Quiz Case #4 You chose: "No" . Go to previous page and try again .

Answer: No you can't. Go to previous page and try again Review Taenia pisiformis Review Echinococcus granulosus Review E.Quiz Case #4 You chose: "Yes" .You can conclude that the taenid egg was that of Taenia pisiformis. taenid type eggs can also be found in tapeworms of the genus Echinococcus. multilocularis . Even though Taenia pisiformis is the only likely member of Genus Taenia to be found in dogs in North America.

The dog was allowed to hunt rodents in Wisconsin D. Review Taenia pisiformis Review Echinococcus granulosus Review E. All of the above. multilocularis . E.You can not conclude that the taenid egg was that of Taenia pisiformis.Quiz Case #4 You chose: "No" . Even though Taenia pisiformis is the only likely member of Genus Taenia to be found in dogs in North America who has not been fed raw sheep. The dog hunts rodents and rabbits B. taenid type eggs can also be found in tapeworms of the genus Echinococcus. What might lead you to seriously consider that Mackenzie might be infected with Echinococcus multilocularis? A. No proglottids were found C. Answer: Right. The dog was never feed raw sheep.

Return to the previous page and try again Review Echinococcus multilocularis .Mackenzie hunts rodents and rabbits. Answer: Partially Correct. This fact also points towards an infection with T. pisiformis.Quiz Case #4 You chose: "A" .

as small numbers of proglottids are easily over looked. Answer: Partially Correct.No proglottids were found. This fact doesn't say much. Return to the previous page and try again Review Echinococcus multilocularis .Quiz Case #4 You chose: "B" .

Answer: Partially Correct.Mackenzie was allowed to hunt rodents in Wisconsin. pisiformis.Quiz Case #4 You chose: "C" . Return to the previous page and try again Review Echinococcus multilocularis . This fact also points towards an infection with T.

this fact may rule out infections with the taenids carried by sheep. Return to the previous page and try again Review Echinococcus multilocularis .Quiz Case #4 You chose: "D" . pisiformis. but it does not rule out T. Answer: No.Mackenzie was never fed raw sheep.

the eggs of this tapeworm are freed from the gravid proglottid as it passes down the intestinal tract.Mackenzie hunts rodents and rabbits. horses. Given the vast numbers of eggs which may be simultaneously released when you treat the dog. multilocularis endemic in Wisconsin (and the surrounding states). uses large animals such as sheep. Mackenzie was allowed to hunt rodents in Wisconsin.Quiz Case #4 You chose: "E" . it uses a meadow vole as the intermediate host. you should also warn them on how to dispose of the feces. elk. especially because of its zoonotic potential. E. etc. End of Quiz Section Return to Canine Page Review Echinococcus multilocularis . Answer: Taken together all these facts would suggest that E. and Mackenzie was never feed raw sheep. multilocularis should be considered.) The owners should be told of the possibility of becoming infected via the eggs that are found in the feces. and the only other member of this genus in the United States. as intermediate hosts. no proglottids were found. granulosus. (E. deer.

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