Parasitology Final Notes | Parasitism | Innate Immune System

INTRO & NEGLECTED TROPICAL DISEASES

I. Ecology - study of life and interactions. A. Symbiosis Association of organisms of different species. • Participants are called symbionts. • Tells us nothing about the nature of the relationship. • Categories based on: • Trophic interactions (nutritional relationships); transfer of 1. energy. 2. Harm or benefit. 3. How many hosts are involved. SYMBIOSIS No trophic interaction --> phoresis • Indirect trophic interaction --> commensalism • Direct trophic interaction --> 1) beneficial, mutualism; 2) harmful, • exploitation Expanding on EXPLOITATION Always killed --> 1) many hosts --> predator; 2) one host --> parasitoid • Seldom killed --> 1) many hosts --> micropredator; 2) one host --> • parasite B. Phoresis - "to carry"; two symbionts travel together. No physiological or biochemical dependency that occurs between • them. Phoront - smaller carried by larger (host). • Example: butterfly dusted with pollen from a flower; carries pollen to • next flower --> fertilization.  +/0 relationship: (+) refers to pollen benefits and (0) refers to no effect to the butterfly.  No trophic interaction. C. Commensalism Benefit - unidirectional; one partner benefits (+) while the other • partner is not harmed or benefited (0). Difference from phoresis: Commensal feeds on food not consumed by • the host. Indirect trophic interaction. • Both symbionts can survive independently. • Example: remora - slender looking fish whose dorsal fin is modified into • an adhesive organ to attach to a large fish; receives the food that floats by that the larger fish drops.  Derives energy from actions of host. D. Mutualism +/+ relationship - both partners benefit; also obligatory -- cannot • survive alone; physiological dependence. Direct transfer of energy between mutualists. • Example: Termites eat wood but can't digest but intestinal protists • secrete cellulose that allow them to digest wood.  Intestinal protists can't get to wood without the termites. Example: blood-sucking leeches; intestinal bacteria digest blood. • E. Exploitation

• •

+/- - one partner benefits and the other is harmed. Predator - attacks and kills many organisms in its lifetime.  Direct trophic interaction.  Example: cat eating a mouse; lion eating a gazelle. Parasitoid - only one host is attacked and killed. •  Example: hymenopterans (wasps & bees) and dipterans (flies).  Example: adult female wasp that will deposit an egg either on or in another insect. • A larval parasitoid hatches and consumes the host. Micropredator - the host is not necessarily going to die; attacks more 3. than one organism, but seldom kills them.  Example: hematophagous organisms (like mosquitoes, some leeches & biting flies). Parasites - only one host is attacked, but the host is seldom killed. 4.  One partner (parasite) benefits from the relationship and the other partner (host) CAN be harmed. II. Parasitology A. Definition: 1. Relationship of two organisms of different species. Smaller (parasite) has potential of harming the larger (host).  Parasite relies on the host for nutrients and a place to live.  2. Parasite has a greater reproductive potential than the host B. What is a parasite? 1. Parasite is: Helminth (worm)  i. Cestodes & trematodes (flatworms). ii. Hematodes (roundworms). Protozoa - some, not all  Arthropods  Parasite infection tends to be chronic and difficult to control. • 2. Not parasites: Bacteria  Viruses  Fungi  C. Different types of parasites: 1. Differ in location in/on a host. Ectoparasite - lives or feeds on hosts surface.  Examples: ticks, lice • Endoparasite - lives or feeds inside the host.  Examples: tapeworm in intestines • 2. Vary in dependency. Obligate - MUST be parasitic for at least part of life cycle.  Examples: tapeworm or tick • Facultative - not normally parasitic; can survive if it is  accidentally eaten or enters a body orifice. Examples: women in commune as hosts who used moss • as tampons; nematodes on moss were presented with a beneficial environment within the women. 3. Duration of relationship with the host. Temporary 

Permanent - away from the host for only a short time; period  away is when parasite is transitioning to another host. **Most of what we'll talk about are endoparasitic and obligate** D. Types of hosts: 1. Definitive host (DH) - parasite reaches sexual maturity.  In species with no sexual reproduction, the DH is the one that is most important to humans. 2. Intermediate host (IH) - required for parasite development.  Parasite does not reach sexual maturity; most cases a larval stage until it reaches a DH. **Host is defined by the state of the parasite** E. Distribution of parasite populations : Overdispersed distribution within host population; graph of # of hosts • vs. # of parasites/host.

Negative binomial A few hosts have many parasites heavily infected --> killed.  Most hosts have few parasites --> not killed.  F. Life cycles 1. Method of depicting the stages of a parasite and the host(s) that it infects.  Example: Opisthorchis felineus infects humans. --> Human = DH (parasite reached sexual maturity). --> Releases parasite eggs that shed in human feces. --> Eggs are ingested by snail (IH). --> Parasite undergoes larval development and asexual reproduction. --> Cercariae stage - larval stage that are released from the snail. --> Penetrate a fish host (2nd IH) - parasite still has not reached sexual maturity. --> Parasite encysts as metacercariae until the human ingests metacercariae. --> At this point, parasite reaches sexual maturity and the cycle begins again. 2. Types of life cycles Direct - parasite passed from one host to another with no IH. a. • Through air, contaminated food/water, or fomite (object). • Example: Tritrichomonas foetus transmitted by sexual intercourse. • Example: Intestinal protists transmitted via food/water. Indirect - parasite develops in an IH. b.

III. Health Statistics A. CDC Leading causes of death in U.S.: • a. Heart disease b. Cancer c. Stroke d. Lower respiratory disease (bacterial pneumonia) e. Accidents f. Diabetes B. WHO Leadings causes of death in underdeveloped countries: • a. Heart disease b. Lower respiratory infections c. HIV/AIDs d. Diarrheal disease Leading cause of childhood death. • Dehydration. • Bacteria, viruses, parasites. • e. Tuberculosis f. Malaria g. Measles IV. World Actions A. General Assembly of UN 2000 - UN Millenium Declaration • a. Sustainable development. b. Eradication of poverty. c. Eight specific MDGs (millenium development goals) B. MDGs Eradicate extreme poverty and hunger. • Achieve universal primary education. • Promote gender equality and empower women. • Reduce child mortality. • Improve maternal health. • Combat HIV/AIDs, malaria, and other diseases (see NTDs below). • Ensure environmental sustainability. • Develop global partnership for development. • 2015 = target for accomplishment of these goals. • C. MDG 6 Funds directed toward Africa. • Most funds go towards: • a. HIV/AIDs - retroviral medications. b. Malaria - drugs, bed nets. D. Neglected Tropical Diseases (NTDs) STH Infections - soil transmitted helminthes (worms) • a. Ascariasis - 4.2 billion people at risk (over 50% of world's population) b. Hookworm infections - 3.2 billion people at risk. c. Trichiuriasis - 3.2 billion people at risk. Other helminth infections • a. Schistosomiasis - 779 x 10^6 b. Lymphatic filariasis - 1.3 billion

standard for measuring premature death.90 x 10^6 Dracunculiasis Protozoan infections • a.free living. Japanese life expectancies . • Numbers of healthy years lost from premature death or disability. o Anchoceriasis . • DALY = YLL + YLD. Bilaterally symmetrical.7 billion. circulatory.350 x 10^6 b. V. • 2. • World population . G. Leishmaniasis . Classes 1. YLL is the average # of years of life lost and YLD is • years lived with the disability. TREMATODES . 1. Dorsalventrally flattened. d. Buruli ulcer c. which cause 2. Monogenea . . 2. but in the poorest people of developing countries. 3. Phylum Platyhelminthes . 4. 1 billion people live on < $1 per day. • Causes disability and disfigurement. • Rural poverty. According to WHO > 2 billion people travel by air (per day? -.000 people die annually from NTDs which is much lower  than HIV/AIDS and malaria. diagnosis.tapeworms. but doesn't have the mortality figure. and treatment. Lack skeletal. • Using time instead of death. Classification A. 3. • because they have the highest.6 x 10^6 deaths. 1 billion affected by one or more NTDs. • Chronic . B. Turbellaria .7 billion people live on < $2 per day.lack a coelom (body cavity). Human African trypanasomiasis . Acoelomate . Chogas' disease . Leprosy Features of NTDs High prevalence.flatworms. • NTDs have high disease burden but low mortality.E. F. • They are ancient diseases as opposed to emerging diseases.) c.60 x 10^6 Bacterial infections • a. and respiratory system. Class overview o Parasitology Ecology • Phylogeny • Physiology/biochemistry • Immunology • o Major human parasitic diseases: studying their identification. • Of the above. 2. Cestoidea . Trachoma b. life cycles. • 530.ask prof.INTRO I.ectoparasites of fish.6.25 x 10^6 c. Disability Adjusted Life Years (DALY) Measures health impact of NTDs.lasts years/decades.

• Forms sporocyst that reproduces asexually. • Human medical importance. Metacercaria form and DH ingestion causes the cycle to return to 1). B. b. releases  enzyme. • B. plays 5. Structure 1. III. 2. • Forms redia that also reproduces asexually.develops into miracidium.precise conditions that are different from conditions inside the host.natural immunity in all animal groups. Response to stimuli that trigger the behavior .at least 2 hosts in life cycle (DH + 1 or more IH). Complex interactions that have evolved between host and parasite. TREMATODES . a. Viscuous cushion becomes hydrated and expands in volume. • Causes economic losses in domestics animals. Two sets of mechanisms in animals which provide them with resistance. 4.parasites of mollusks.  a. Operculum pops open and miracidium escapes to outside. Subclass Digenea ("Two beginnings") . Enzyme alters permeability of membrane around • viscuous cushion. 2. Digenetic Trematodes A. Activity Miracidium's eyespot (sensory) is triggered by light. Shell .protection.HOST-PARASITE INTERACTIONS & LARVAL STAGES I. Host As environment 1.Trematoda Subclass Aspidogastrea . a.  2. digests shell from  inside. Egg stage (Figure 9-15a) A. Host-parasite Interactions A. Vitelline membrane protects miracidium. 3. • Two paths: • Cercaria exits snail and infects DH.opening through which miracidium will escape. 4. General life cycle Adult worms in DH produce eggs. role in hatching. • Eggs are shed into external environment (water) and hatch. Viscuous cushion inside egg that contains mucopolysaccharides. Hatching 1. 3. Able to respond to the presence of parasites. One IH is always a mollusk. Embryo . • II. Example: light tember < 37 degrees C.  Miracidium releases leucine aminopeptidase. cycle returns to 1). . b. Innate resistance . • Miracidium swim until they find and penetrate snail (IH). Operculum . Characteristics Flukes.

Specific immunity . a. secrete enzymes that help miracidium adhere to and penetrate snail. Glands .very small part of a parasite macromolecule. antibody neutralizes parasite's  ability to enter cell or inhbits toxic parasite products. Cellular immunity . B. Host-finding a.b. • Cephalic ganglion . . Responds to environmental cues.develop into next larval generation. Intro ~100 micrometers in length. etc. External surface a. 2. • similar to behavioral responses of snail host to the same cues. Miracidial behavior 1. • Nerve fibers. C. 3.emerges from the egg. scales. Specific immunity Antibody response . georeceptors (detects gravity.example: mammals. Example: shcistosoma mansoni • Miracidia and snail hosts are both geonegative • (move away from earth) and photopositive (toward light).  substances that act as chemo-reactants. directly kill parasite. Sensory endings in apical papilla come into play. • Its mission is to find and infect snail host. hair. • chemical barrier. gravity. Skin . chemoreceptors. Germinal cells . and temperature.nonspecific responses. Internal defenses Most parasites release substances that trigger the host's body.provide some sort of physical barrier. C. Miracidium stage . 4.T-cells combine with specific epitopes and can 2.higher animal phyla vertebrates. • (+) or (-) response to light. • b. Phagocytic cells like neutrophils and macrophages are • attracted to site of infection. Epitope . Innate resistance . ~2mm/sec. Structure Ciliated epidermal plates that allow the organism to swim. b. Feathers. non-feeding stage. Compacted layer of dead cells that is difficult to • penetrate. position • to the earth). • B. Antibody combines with epitope. II. Photoreceptors. the body is going to respond in the same way.concentration of nervous tissue kind of like a brain.specific protein is produced in response to a 1.  Apical papilla that cover the anterior end (no cilia).1 apical gland and 2 lateral glands. often a  polysaccharide or protein associated with that parasite. Has sensory nerve endings from the cephalic ganglion. regardless of what the invader it is. 1. . Mainly a deterrent to ectoparasites. detects environmental stimuli. specific parasite epitope. Salts in perspiration and organic acids and fatty acids. Can combine with macrophages (phagocytic cells) to increase  phagocytosis. A.

outgrowth on posterior end of body. Miracidium far from snail: low RCD (covers more • distance) & fast swimming.rudimentary (simple. Incorrect cues causes miracidium to leave. o Morphology (Fig 9-20) 1. Miracidium close to snail: high RCD (less • distance) & slow swimming so that it stays close and doesn't exit the active space of the host.  Germ balls . and  pulsate. Development Depending on species . muscular pharynx that pumps food into gut of redia. Snail defenses . Digestive system . • III. B. • Haemocytes . Allows redia to move around.no need to swim. . but functional). they are the next host in the life cycle of  this parasite. Surrounds larval trematode and releases cytotoxic superoxides. fatty acids. E. absorbs nutrients from host tissue through tegument. Attraction can be measured by the rate of change of • direction (RCD) and swimming speed. Miraxone . Infection of snail.  Gut is short and unbranched. Exits through birth pore.main defense against trematode larvae. amino acids. Morphology 1. Effect on snail host Example: Leuchocloridium pardoxum (not human parasite) • Causes tentacle to enlarge. Germinal sac with embryos developing inside. develops into daughter rediae or 3. Mouth.  leads to phagocytosis. 2. C.  o Effect on snail host b.  Respond to the specific components of snail mucus. 2.  Tegument also absorbs nutrients. Sporocyst stage (Fig 9-19) A. 2.  Ambulatory bud .Substances of snail origin that attract • miracidia. No mouth or digestive system. motile and • encapsulating. Loss of cilia . Redia o Exit sporocyst . become brightly colored.innate resistance called internal defense system (IDS). Cytolysis of snail tissue --> penetrates.can burst out (may kill sporocyst) or exit through a birth pore. Allows snail to distinguish between self and non-self. cercariae. Structrual changes 1.Responding to host cues.Depending on species. • Correct cues causes it to release enzymes from apical • papilla. IV. redia and • cercaria. D. Formation of new tegument (outer surface) with many microvilli 2. (increase in surface area). Birds notice the snail. ammonia.daughter (secondary) sporocysts.

species that infect DH and migrate in host. Inside host B . result of post-acetabular glands that • produce mucus used in adherence. • Pharynx. • develop to the adult worm. Cercaria penetratrates DH and develops into an adult worm. Cercaria encysts on vegetation and develops into metacercaria. warmth.  Bird schistosomes . • Released from snail only at certain times of the • day.produces enzymes that breaks down snail  tissue (cytolysis). c.many species. . each infects a particular host species. • Spatial location . C . skin • chemicals. b. so instead.cercariae seeking birds. Infection of host Post-acetabular glands release mucus used for • adherence. V. shadow. Sheds tail and cystogenous glands kick in to produce a • cyst that develops into larval metacercaria.  feed on and destroy it. Behavior Exit the snail • Uses escape glands . host cues.  puts those resources toward growth. bigger snail means more space and tissue resources for parasite.light. 3. • c. a. Cercarial success  Example: Schistosomes . Attach to plant. 4. • Temporal location . Morphology (Fig 9-21 and 9-25) Head and tail. Cercaria penetrates 2nd IH and develops into metacercaria. No longer able to reproduce. Development . • Forked intestine. Cercaria A. • B. d.depends on species. Sheds tail and pre-acetabular (penetration) • glands release enzymes. BOTH B & C.circadian release of cercariae.  Snail no longer allocating resources to reproduction.species that infects 2nd IH cystogenous • glands --> metacercaria. Corresponds to time host may be present.• Example: parasitic castration Redia move to snail reproductive tissue (good food resource). External environment • 1-3 days. Bird cues: movement. • Glands in the head.surrounded by oral sucker. gravity. • Mouth .  Swims or crawls to find either a place to encyst or to find the  next host. temperature.

Morphology A.areas in which.effect of parasite on a • host which increases the chances of a host being ingested. Metacercaria (Fig 9-22) . Trophic levels . similar to snail. Cercariae might penetrate human instead of bird.multinucleated tissue with no cell boundaries • Glycocalyx . Distal cytoplasm • Anucleate (no nucleus). • Syncystium . • wrong host. . • TREMATODES .increases surface area. • skin chemicals.transmission stage. warmth. VI.thin and simple due to  constant internal environment that requires less need for protection. CNS. also important in  storage. may influence behavior or physical characteristic of host. Parasite-increased trophic transmission (PITT) . Predisposes that host to predation. increases • vulnerability to birds (DH).  Many invaginations .multi-layered.  C. • Example: Microphallus papillorobustus .  Vesicles .break things down. . cercariae dies. In species that encyst in 2nd IH . Site of infection  Example: muscles. etc.shields tegument from antibodies and digestive  enzymes. Protective . eyes . Tegument (Fig 9-3) For absorption and defense. Effect on host (in species that encyst in 2nd IH). Swim closer to surface of the water. A.prey and • predator).  Hydrolytic enzymes . digestive • enzymes.cyst wall tends to be thick  and complex. Spines . B. and carbon dioxide. Respond to stimuli inside host.projections that help parasite attach. affects body temperature. Not restricted to just metacercariae.surface coat.ADULT MORPHOLOGY I.Different levels of food chain/web (i. In species that encyst on vegetation .substances which maintain glycocalyx. shadow.Human in water: movement. • Comprised of glycoproteins. Excysts and develops into adult. Development to adult stage (inside DH). if • compromised. Cyst wall .In most species . damage  repair.e. Metacercariae in prey item (IH) move up a trophic level when IH is • ingested.infects amphipods (2nd  IH) and get into the brain. and human experiences allergic reaction (itchy rash called swimmer's itch). increases uptake of  molecules. Structure 1.

comprised of longitudinal. Cerebral ganglion .helps move food in intestine. excitatory. 2 way.  Tangoreceptors .like a brain. C. Neurotransmitters a. provides motor and  sensory endings.  5.serotonin.bands of nerve tissue that connect the longitudinal nerve cords at intervals.  2.like a ladder.3.  Produces material to maintain distal cytoplasm. Self fertilization or cross-fertilization.opening at top. 4. Nerves that branch off to anterior to oral sucker. both male and female parts (exception: • schistosomes). Transverse ring commisures . Gastrodermal . Reproductive system Hermaphroditic .comprised of circular and longitudinal muscle. Proximal cytoplasm (cyton region) Nuclei and organelles. • Male (Fig 9-10) • .  Muscular system 1. 2. inhibitory. and diagonal muscle.response to chemical environment. 5-HT (5-hydroxytryptomine) . D.  3. B. Branches go to muscles and tegument. 1. at the anterior end and has nerves that branch off. b.response to touch. • E. 3 pairs of longitudinal nerve cords from cerebral ganglion. Supplies posterior end. none at the bottom.monoecious. Muscle layer . Acetylcholine (Ach).  Connected to distal cytoplasm by internuncial processes. Subtegumental . Orthogon . Digestive Tract Incomplete . Nervous system  Flatworms are among the first organisms with a clearly defined CNS. circular. • Sensory endings • Chemoreceptors .

i. Out the metraterm. Mehlis' gland . Vitelline cells . sperm.oocytes. C.leads from ovary. Ovicapt .shelled eggs move through here up to and out of genital pore while sperm move down to seminal vesicle. Diagram B. Egg moves through uterus. d. E. Oocytes leave ovary.sphincter that controls passage of oocytes. Polyembryony . Female a. IV. Ovary . Human trematodes . b. B. role of copulation. f. vitelline secretions. h. Ootype .produces yolk and shell materials. III.2. Seminal receptacle . Metraterm . Mehlis' gland cells.produces oocytes. Egg development A. g. c. Ootype . Move down oviduct.produces secretions involved in shell formation. D. produces egg.muscular distal end of uterus that propels eggs out of uterus. Habitats in human body A. Oviduct . o Asexual reproduction that results in multiple offspring from 1 embryo.expanded area of oviduct.stores sperm. Uterus . e.ensures continuation of life cycle. o 1 egg --> 1 miracidium --> 1 sporocyst --> many rediae --> many many cercariae --> many many metacercariae. II.

Fasciola hepatica Clonorchis sineusis Liver/Bile duct Lung Blood 1. • Hatches. S.Habitat Intestine Species 1. o Morphology Adult is 75mm x 20mm.non-human animal that can be DH. • Branched testes. • Finds a snail and penetrates the IH. • Ventral sucker (acetabulum) . • Develops into metacercariae on water vegetation and is ingested by • DH. Metagonimus yokagawai 3.another adhesive organ a little further • down from the oral sucker and on the outer surface. Pathology Adults attach to intestinal mucosa and feed on host tissue. japonicum 3. • Redia II develop into cercariae and they exit the snail. • Inflammation. o Pig is a reservoir host . haematobium TREMATODES .  Will experience abdominal pain and malabsorption which can  lead to diarrhea. Paragonimus westernami 1. • The sporocyst leads to redia I and then redia II. eggs are large and operculated. 2. Fasciolopsis buski (Large intestinal fluke) o Parasite of humans and pigs. D. Heavy infection . bowel obstruction is possible. • Each worm deposits about 25. • Produce eggs that are shed in the feces. • Has an unbranched cecum.INTESTINAL 1. Direct wet smear . • . • Light infection . massive environmental • contamination. uses hosts as definitive hosts.adult worms in duodenum and gejunum. undergoes larval development. Diagnosis Look for eggs in feces. few • symptoms. and miracidium emerges and swims around in the water.000 eggs/day. Fasciolopsis buski 2.adult worms living throughout small intestine. • o Life cycle (Fig. Heterophyes heterophyes 1. slide --> microscope. ulceration.~2 mg feces + drop of saline. 10-6) Adult worm that lives in small intestine of DH. No cephalic cone • C. abscesses. Serve as a source of infection for humans. Schistosoma mansoni 2. S. much larger than oral sucker.

• Upon exposure to PZQ.grows in water. Allows for detection of small numbers of eggs.  Formalin preserves specimen.snail.used in salads. • B. PZQ disrupts voltage-gated Ca2+ channels.  F.  In particular.4mm x 0. Treatment Praziquantel (PZQ) or Biltricide.human. they are generally not a problem.has structure called gonotyl . reservoirs --> fish-eating mammals (cats and dogs).  Physically remove snails. • 2.fish.chemicals that kill molluscs. • 2nd IH .may not find eggs. watercress (Nastrutium officinale) . • Boil vegetables that could potentially have metacercariae attached to • them.  Formalin-ethyl acetate sedimentation concetration technique.  Copper sulfate and sodium pentachlorophenate. 10-8) Adult is 1.  Molluscicides .  Method:  ~4g feces + formalin then strain through gauze. • DH .because they are so small. there are 2 main effects on worm: • Rapid. • Analyze sediment for parasite eggs. Difficulties Recolonization .human feces as fertilizer. Peppery leaves . toxic effects on other organisms. Metagonimus yokagawai and Heterophyes heterophyes A.5mm. C.  Snail control. • Very safe. Tegumental (outer surface) disruption .  Do not use night soil . • c. • Self-fertilizing.If infection low -. • My . paralysis and gets  flushed out of intestine. Hh . muscular contraction. • Problem: ecotoxicity.snails carried downstream. genito• acetabulum. centrifuge again. • • . develops into sporocyst then to 2 rediae generations. Morphology (Fig. • Results in rapid influx of Ca2+ of worm and disrupts functions. Pathology Adults . • Discard supernatant (stuff that's at the top). • Platyhelminthes. • Precise mode of action is still unclear. develops into metacercaria. Control Kill adult worms using PZQ.  Ethyl acetate extracts debris and fat from feces. sustained. among smallest trematodes found in • humans. Life cycle (key features) 1st IH . • Add saline and centrifuge.exposure of parasite to  host attack. • E. • Add formalin + ethyl acetate.gonotyl and ventral sucker are fused and off-center.sucker surrounding the genital pore.

eggs in feces. Life cycle (Fig. • Those that taste diaphragm reject it and prefer Glissais capsule and enter liver. o Humans . Juveniles develop in liver. Metacercariae encyst on plants (focus: watercress).2-17 x 10^6 cases worldwide. • D.snail. and cercariae emerge.LIVER/BILE DUCT & LUNGS 1. Treatment . Metacercaria excysts in SI. 30 mm x 13 mm. Eggs can enter host's circulatory system. Cephalic cone .PZQ. feed. 2 generations • of rediae. erode  tissue.widening at anterior end. 10-2) IH . Diagnosis . F. final habitat. Formalin-ethyl acetate sedimentation concentration. parasite goes through sporocyst larval stage. .However. 4. Eggs • Because adults are so small. in large numbers. Juvenile penetrates Glissais capsule and gets into liver.  Heart --> heart failure. C. • Brain & spinal cord --> neurological disorders. • Inside the host: • B. A. 5. • TREMATODES . you may experience inflammation  and ulceration in the small intestines. Migrate to bile duct and develop into adult. Adult morphology 1. Control Cook the fish properly. • E. o Liver rot. Fasciola hepatica (sheep liver fluke) o Sheep and cattle .  Can be carried to ectopic sites.reservoir hosts. 2. B. • Plants are NOT hosts. they burrow into mucosa. A. and grow --> liver rot. migrate. Migrates through abdominal cavity.

Unable to handle as much bile coming through.   Triclabendazole (TCBZ) a. hardening of  tube is called pipstem fibrosis.  Sewage disposal (important in all fecal-borne infections). Chronic fascioliasis  Adults.eggs in feces Formalin-ethyl acetate sedimentation concentration. Highly active against juvenile stages. D. >12 weeks. Diagnosis . b. C. Disruption of spines (involved in attachment and • storage). disrupts movement of vesicles to distal cytoplasm 3. Acute fascioliasis Necrosis of liver tissue.emergin/re-emerging parasite disease. capsule may rupture ~8 • weeks.parasite mechanism for shedding • damaged tegument Swelling of mitochondria. Juveniles a.drug damages ion pumps in • tegument.highly branched (just like Fasciolopsis buski). .C.  Ε. Ulcers in ectopic sites.  Occurs in bile duct .   Domestic . Control Fascioliasis . lungs. • Liver swells --> hepatomegaly. and eventually  cirrhosis . Variety of effects. Treatment   PZQ does NOT work. skin. Pathology 1. jaundice. • Back pressure --> liver atrophy. Oral and ventral suckers are same size.blockage and inflammation. Bithionol F.disrupts formation of • cytoskeleton. E. Stimulates blebbing . Collagen and fibrous tissue in walls of bile duct. Cacae are highly branched (as opposed to Fasciolopsis buski). • Microtubule inhibiter .chronic disease in which normal tissue is replaced with fibrous tissue. • b. 2.  Changes generally have something to do with snail habitats. D. Control reservoir hosts.  Secretes proline and stimulates host collagen deposition. brain. Example: eyes. Testes . Tegument swelling . etc.  Related to environmental changes and human-made modifications to  the environment.sheep and cattle.

On average. Inside host . if there are <100 worms in individual .presence erodes epithelial lining of duct. Paragonimus westernami (Oriental lung fluke) A.Praziquantel E. diarrhea. pickling.  Raw fish . • >1000 worms .snail. Pathology Adults found in bile duct . • DH . thickening of bile duct and • can't handle bile as well and causes blockage of the duct --> hepatomegaly englargement of bile duct.  DH .snail. Diagnosis . pain. Fish preparation is critical. cooking fuel is limited. develops into metacercariae. • C. then sporocyst with one • redia generation --> cercaria.rats. Control 1. Microcercous cercaria 1st IH .eggs in feces.jaundice.fish-eating mammals. Treatment .nausea. A. many reservoir hosts.production of fibrotic tissue. drying. smoking.delicacy. • 100-1000 worms . • Host response . Reservoir hosts 3.asymptomatic. Clonorchis sinensis (Oriental liver fluke) o 19 x 10^6 cases.humans.  3. Life cycle (Fig. Wild animals . • Metacercaria excysts in duodenum. juveniles migrate directly to bile duct.tail is extremely small and knob-like (crawls instead of swims). Life cycle 1.fish. B. 2nd IH . No night soil use to fertilize fish farming ponds. Metacercariae can survive salting. 2. 2. Crawls over rocks in environment.crabs and crayfish. egg develops into miracidium. reservoir host . instead of penetrating in intestinal • wall. develops into sporocyst and then 2 rediae  generations and microcercous cercaria .10-3) Egg is eaten by snail. a lot of abdominal pain. D.human. develops into metacercaria.  2nd IH . • 1st IH . and fever.  2.  In some parts of the world.

• "Drunken crab" (delicacy in certain countries) . blood-tinged sputum. Symptoms Cough. Treatment .blood fluke . heart.  3. Introduction A. Control Major emphasis on properly cooking food (crabs and crayfish). Crab juices used for medicinal purposes. Cause a disease called Schistosomiasis (bilharziasis or snail fever). Diagnosis Eggs in sputum and feces (when you cough and swallow the eggs.  C. not cooked. Schistosoma . very often forms distoma cysts . haematobium • S.PZQ E. • Burrows through intestinal wall. Pathology 1. Enter lungs .develop to adult stage. Formalin-ethyl acetate sedimentation concentration.emmersed in rice wine • for about 12 hours and then eaten. Embed in abdominal wall for ~1 week. Metacercaria excysts in SI.live in veins of DH.     B. 2. • D. 3 species in humans. chest pain.2 worms inside. they • travel through to the feces). abdominal wall. • B. • Fibrous tissue surrounds worms --> cysts. japonicum • . Schistosoma mansoni • S. Migrate in abdominal cavity. Ectopic sites Example: brain. Necrosis of lung tissue. Penetrate diaphragm. • TREMTATODES .BLOOD FLUKES I.

Morphology a. • Peptide called schistosomin . • No metacercarial stage. Parasitic castration. causes a friction that  leads the suture (line along eggshell) to rupture and allows miracidium to escape.males and females are separate • individuals. Major differences between schistosomes and other trematodes. haematobium has a terminal spine. mansoni has a lateral spine. decreased egg production by snail. 2nd only to malaria. imbalance interferes with snail's neuroendocrine system. Egg . Life Cycle A. E. D. • Head glands function in the adjustment of parasite after penetrating the DH. • No redia stage. • Non-operculated eggs. 1. Miracidium starts spinning inside the egg. Head • Mouth • Digestive tract • Glands • Escape glands allow them to exit snail. •  When snail is infected. parasite causes it to over-produce it.  Reproductive organs of snail are affected. B.normally produced by snail.About 250 x 10^6 people infected worldwide. • The only human trematode that is not food-borne.no operculum S. • C. . • II. • S. No redia stage.fresh H2O stimulates miracidium to start beating cilia • rapidly. • Sporocyst . • Post-acetabular glands produce mucus important for attachment. japonicum has a lateral knob. C. Daughter sporocysts produce cercaria. • Pre-acetabular glands produce enzymes that allow for penetration of host skin. Live in blood vessels.produce daughter sporocysts. Schistosomes are dioecious . D. • S. Miracidium Either male or female infects snail. Hatching .

Once cercaria has penetrated DH: Loses tail.used for swimming. migrates to lungs. japonicum S.held in canal. b. Loses glycocalyx .tubercles (bumps) on surface. • Sm and Sh . 15mm haemotobium b. Dioecious. reach sexual maturity and mate.was important in protecting against hypo-osmotic environment of fresh H2O.  Pairs migrate to venules of mesentery . •  Lives in pulmonary capillaries and feeds on red blood cells (RBCs). • Thinner female . c. Schistosomula Inside DH . a. Adults 1.  Now called a Schistosomulum(a) .gets into bloodstream.membrane suspending organs. they migrate into systemic circulation. Size Species S.egg production • Sh . F.Tail . Male • Gynecophoral canal .  No pharynx. g. 2.30 eggs per day (epd).smooth.  Life span .  Ventral sucker.groove that goes down the entire length of the body. Major differences between 3 species. continuous mating • Unpaired females do not become sexually mature. • Male is shorter and stouter than female.previous cercaria that has now penetrated a DH.  Cecum . Sexually dimorphic.  At young adult stage. G.   e. Male tegument • Sj . Migrate to hepatic portal veins in liver. • Schisto = split and soma = body. 3.bifurcates but then joins together in the posterior part of the worm to form a single cecum.10-30 years. . Females . Morphology  Oral sucker that surrounds the mouth. f. mansoni Male 20mm 10mm Female 26mm 14mm 20mm S. 2.

Egg entrapment either in the gut or bladder wall.lives in veins of urinary bladder. Absorb lipoproteins that come from host serum onto tegument. e. . • Sm . c. • Motile cells. muscle pain.high fever. Pathology Cercarial dermatitis .  Worm looks like host. • Enzymes. itchy rash. allergic reaction.development of Katayama Fever . H.lives in veins of large intestine. Granulomatous response . 2. carbs. a. infection. • Host antibodies present. heavy infection and initiation of egg production. Adults develop. Any new schistosomula are destroyed by antibodies. 3. • SEA leaves through pores in eggshell.4. 2. Host antibody is produced. • Sh . Granuloma cells disperse and egg is shed either in the feces or urine.releases SEA (soluble egg antigen).penetration by cercariae into skin. Eggs must get out of vessel and into intestinal/bladder lumen. Exit of 1. Lays eggs. kills some schistosomula.veins of small intestine. SEA stimulates granuloma to form around the egg. hepatosplenomegaly (enlarged • liver and spleen). Female migrates back to male. but do not attack adults.associated with Sm and Sj B. involves molecular mimicry. Female .  1. • Sh . Miracidium . proteins. d. Granuloma moves across wall to gut/bladder lumen and carries eggs. Main pathology is due to the eggs. d. Endothelial cells that line the vessels and veins are capable of moving. 4. Male . 3. calcify. Immunology not understood. eggs from DH Pair works its way upstream into smaller vessels.  Resistant to re-infection.3500 epd. Schistosomulum in body. Avoidance of immune attack. III. Symptoms . 4. 5. • Other eggs go to the bloodstream and are trapped in the liver  and spleen. b. • Sj . eosinophils and macrophages. • Excludes egg from vein lumen. • C.blocks blood flow.by herself into smaller vessels.eggs are antigenic (SEA). • • Sm . Habitat of adults in DH. • Molecular mimicry. 6. • 2/3 eggs don't make it out.200-300 epd. will actively move over and sequester the eggs. Acute disease . A.

Boots and rubber gloves E. • No cross reactivity with human GST. o Glutathione-S-transferase (GST) . Arthemether . fibrotic and does not function properly.fibrosis of ureters and bladder. Drug B. allows back pressure of urine to reach kidney and causes kidney failure. Hematuria .Symmer's pipestem fibrosis . • Providing massive amounts of PZQ in sub-Saharan Africa.damages tegument. • ------------------------------------------------. 40-60% reduction in worm burden. Schistosomiasis Control Initiative Bill and Melinda Gates Foundation. Vaccine G. • Sh infections . • Inhibitory effect on egg production.END OF FIRST EXAM MATERIAL ------------------------------------------------- Granuloma . • V.increases chances of colon cancer.Schistosome infection may cause cancer.liver becomes a. VII. cecum and vitelline glands. VI.increases chances of bladder cancer. • In phase II clinical trials .about 100-300 humans are being used for the • testing of safety and efficacy of the vaccine. Control A.defense mechanism against reactive • oxygen species. Sh . b. causes extra load on the heart. Praziquantel damages tegument of the adult . c. . male menstruation. Snail control D.eggs in urine and feces.IV. resistance. Antioxidant for the parasite . B.parasite enzyme. • Sm infection . Sewage treatment C. Vaccine development o Chemotherapy and vaccination. Education F. Treatment A. Examples:  Liver .protection from toxic substances but are costly in  terms of pathology. Diagnosis o Sh .makes worm vulnerable to the immune response. o Most candidate vaccine antigens are parasite muscle proteins and enzymes.blood in urine.

Scolex 1.   a. Help attach to host intestinal wall. Morphology of adult tapeworm (Fig 12-1) o Scolex . Bothriate .prominent in many tapeworm species.CESTODES .detect chemical and physical stimuli.found in Pseudophyllidea and has 2. B.muscular and protrusible. All parasitic. 2. an armed rostellum is one with hooks. Nervous structures. C.anterior end.rest of body. b. or 6 bothria. Neural ganglia. Acetabulate. 4 muscular cups on scolex of Cyclophyllidean tapeworms. Phylum Platyhelminthes. Fig 13-3a. or shallow grooves. Found somewhere in digestive tract of some vertebrate hosts. Sensory endings on surface .INTRO & ADULTS I. Suckers . Attachment structures. o Strobila . A. • Hooks . Introduction A.tapeworm. • II. o Neck . Class Cestoidia 2.immediately posterior to scolex. 1. b. 4. Common name . Order Cyclophyllidea and Pseudophyllidea. . • Rostellum .May have accessory holdfast structures. a.

Strobilation . • Contains stem cells. • • Self-fertilization and cross-fertilization.) 1. varying degrees of development. • Praziquantel .  .treatment for many adult tapeworm infections.entire female reproductive complex. Mature proglottids (cont. Female Oogenatope . • D.  Gives rise to proglottids. monoecius. •  Acts preferentially at the tegument of the neck. Neck Posterior to scolex.) D. • Female organs develop next. protandry.process by which proglottids form at the neck. undifferentiated zone . • Each proglottid develops male and female organs. C.has not developed into any • specific tissue. Reproductive structures a. Strobila Each segment is a proglottid. Male b.INTRO & ADULTS (CONT. • Produce sperm which is stored in proglottid.B. Mature proglottids Male organs form first. CESTODES .

eggs released through uterine pore."  Many protective layers surrounding oncosphere to protect from external environment (temp.uterus ends in uterine pore.  Secretes thin membrane that surrounds zygote and vitelline cells. etc. -canth means "hooks.larva in egg. • In pseudophyllidea .  In psuedophyllidea . pseudophyllidea. i. ii. Mehlis' gland surrounds ootype. Oocapt . light. 4.scattered throughout proglottid. chemicals.). Release of eggs Apolysis . compact gland. Vitelline gland produces vitelline cells. Egg stage Oncosphere . c. Zygote .gravid proglottid released and shed in feces. cyclophyllidea. d. occurs in b. In cyclophyillidea . Anapolysis . like the drawn diagram. Ovary produces oocytes.uterus ends blindly. Sperm .2. Important for yolk and shell material.hexacanth embryo. f. zygote.  3. •  6 hooks .regulates passage of oocytes into oviduct. g. Cyclophyllidean s Psuedophyllideans . see diagram. Vitelline gland morphology • In cyclophyllidea . Egg Development a.fertilizes oocytes in oviduct. b. Pass into uterus. e. occurs in a. critical in formation of egg shell.single.passes into ootype.

Able to bind host enzymes.net flow of nutrients from region of high concentration (host gut) to low concentration (in worm).  Orientation is pointed posteriorly. Cyton layer Where the nuclei and organelles are located. chymotrypsin. key feature for absorption. • Example: Pyroxidine (B vitamin) • o o 2. • Example: Glucose uptake . contact digestion . Cytoplasmic connectives Channels through tegumental muscle . Microtriches (microtrix) . No metabolic energy required. Inhibits host enzymes (trypsin.allows worm to move substances against concentration gradient. • Functions • a.E. Tegumental muscle layer 4.Tegumental activity 1. vesicles used for maintenance are produced • by cyton layer are held here. and pancreatic lipase) that are threatening to the worm.allows them to break down starch • into sugar for the worm. Requires metabolic energy. Active transport .most important nutrient for worm. b. • . Example: Amylose . • 5.no cell boundaries. Glycocalyx . 3.worm digests meal outside its body and absorbing the molecules. • Increases surface area 10-50 times. F.outermost layer. A lot of carbohydrates.  o Distal cytoplasm Help maintain glycocalyx.microvilli that completely cover worm surface. Adult tegument (Fig 12-3) Syncytium .connect distal cytoplasm and • the cyton layer. Diffusion .

forms  cercomer for attachment. • sugars. RNA. b. • a. Embedded in tegument. Impairs copepod's ability to move.procercoid stage.hydrolyzes glucose-6-phosphate to • glucose and brings it into the worm. Calcareous corpuscles embedded in parenchyma. Source of calcium. in all species. it metamorphoses into procercoid . there are theories. cells. Development A. Supply of ions.uses 6 hooks to penetrate host gut. magnesium. Parenchyma 1.G. protein. phosphorus. • Glycogen synthesis and storage. Intrinsic enzymes . more vulnerable to predation  . • Digest molecules in host gut and smaller molecules are taken in by • active transport. Swims rapidly. and enzymes. • B. Example: Phosphohydrolase .DEVELOPMENT & PSEUDOPHYLLIDEA I. Internal organs embedded. 3. copepod  (microcrustacean). Egg released through uterine pore (anapolysis). In hemocoel. . DNA. 4. CESTODES . Pseudophyllidean life cycle 1.more specifically. c. eats coracidium. **Type of metacestode depends on species. Oncosphere develops inside egg --> egg hatches and larva is eaten by • IH OR egg eaten by IH and then hatches --> penetrates through gut and migrates to parenteral site (not in intestine) --> develops to metacestode (juvenile).** (Fig 12-12) IH .  Ciliated coracidium hatches from egg into water.example of PITT. Oncosphere . Buffers worm tissue against organic acids produced in energy metabolism.can be vertebrate or invertebrates. and fluid. Function is unknown. 3. 1st IH consumed by 2nd IH (fish) . many varieties. Loosely arranged mass of fibers. Excretory product.actively produced by tapeworm. • 2.arthropod . 1st IH . At least 2 hosts. 2.

oncosphere with 6 hooks that are used to enter the hemocoel body cavity of arthropod.  Hatches in the intestine. Scolex .  Strobila . undifferentiated. Three other types of development . Cyclophyllidean life cycle Terrestrial hosts.  Larva . 2.  Hatches inside in the digestive tract. DH eats 2nd IH (paratenic host) Plerocercoid develops into adult in gastrointestinal tract  CESTODES .metacestode stage. can be eaten by DH.  Cysticercus  . (transport host) --> plerocercoid penetrates gut and goes into skeletal muscle. Travels throughout the body and ends up in a parenteral site  not in the intestine. 6.5."  Either:  2nd IH (fish) --> eaten by another fish . • Scolex . Penetrates fish gut and goes into skeletal muscle.short. • No development takes place.  Oncosphere develops into cysticercoid. b. Develops into metacestode.bothria.paratenic host a.  Develops into plerocercoid .occur in vertebrate IH.set inside the solid body. • Invertebrate IH (arthropod) •  Egg is ingested by IH.DEVELOPMENT & PSEUDOPHYLLIDEA (CONT. fish from a.) C. • No cilia on larval stages. • Example: Hymenolepis nana.  Oncosphere uses its hooks to penetrate through intestinal wall  and gets into the circulatory system. Egg is ingested by IH. 2nd IH (fish) --> eaten by mammal (DH).fully developed and invaginated .  "Miniature adult.

i. potential for the development of worms. • ii. Multilocular (alveolar) cyst Exogenous budding . multilocularis. • Stimulated by host digestive enzymes to excyst. Development of all metacestodes in DH Gastrointestinal tract of DH. • common in liver. Found only in E. • Several quarts of fluid. Hydatid • Occurs only in the genus Echinococcus. etc. c. . • Example: Taenia solium. Unilocular cyst Endogenous budding. • Begins to grow until it becomes a mature adult.secondary cyst comes off • towards the outside of the cyst. Coenurus • Protoscolex can develop into an adult worm in DH. • D.b. • Millions of protoscolices. Cyst infiltrates host tissue due to budding. granulosis. • Found in E. • II. evaginate. two types. • Example: Taenia multiceps. Diphyllobothrium latum o Pseudophyllidea commonly known as Broad Fish Tapeworm.

Who is infected? Areas where sewage drains into lakes and rivers and fish host is • present. Uterus .  Possibly paratenic hosts involved . Scolex . Produces 10^6 eggs per day. D. .2. • Develops into plerocercoid .other fish eating other fish.wider than long.wide range of piscivores . • Develops into plerocercoid.bothria . • Parasite develops into procercoid.  DH . scattered testes and vitelline glands.fish eaters.  2nd IH .noticeable white mass in uncooked  fish. Adult • • • • morphology Can be up to 10m long (33 feet). • • • Numerous.Copepod. Female and male genital pores open midventrally. unnoticeable in cooked fish but it is not infective.o o Life cycle 1st IH . Proglottids .opens to midventral uterine pore.Fish. Egg morphology C.

etc. 2. • B. Treatment PZQ • Niclosamide . mainly caused by pseudophyllideans of the genus Spirometra o Mode of infection 1. human considered a paratenic host. ingests egg. E.eggs in feces.surgical removal. Vitamin B12. Pathology 1. Diagnosis .infected copepods (procercoids). 2.absorbs large amounts (80-100% of total) vitamin B12 --> anemia. 3. Larval Pseudophyllideans in humans o Sparganosis . • III.transport in mitochondria of worm.human. vaginitis.  Reaction to waste products of the parasite and intestinal irritation. G.CYCLOPHYLLIDEA I.pig. Vague symptoms. Penetrates intestinal wall and develops into plerocercoid in the  tissue.  B12 . sore eyes. Great Lakes region. Example: Scandanavia and U.S.plerocercoid is in human. Taenia solium (pork tapeworm) A. snake. • DH . F. CESTODES .general medical term that refers to a disease state in which the host is unable to absorb vitamin B12.  Worm . abdominal discomfort.inhibits e.  Diarrhea. Drink H2O . ingests improperly cooked pork that contains cysticerci. • o Treatment . •  Minimally absorbed by host intestine. Example: In East Asia where they take the flesh of frogs as  poultice (mashed substance) and use it to treat medical conditions (skin wounds. Many cases are asymptomatic.) Plerocercoids migrate into human. nausea. Life cycle (Fig 13-5) IH . Example: frog.  o Diagnosis Detection of plerocercoids in tissue. etc. Egg morphology . Ingests uncooked animal containing plerocercoid. 3. bird.hemoglobin synthesis. Pernicious anemia . Physical contact with flesh of infected IH (plerocercoid).  Remains a plerocercoid because it is still considered to be in the  IH.  Migrates through intestinal wall and into tissue.

•  Vague symptoms: discomfort. 2.  7-13 lateral uterine branches.  Apolysis for egg release (breaks off).    Not useful for ID of species. etc. • Adult worm in human (DH) usually causes no problems. Clinical disease Severity depends on stage of development.  150-200 testes.  Trilobed ovary. Acetabulate.  D.  Compact vitelline gland.  No uterine pore.• C. Armed rostellum (2 circles of hooks). Cysticercosis •  Human (IH) ingested eggs.  Gravid proglottid (Fig 13-3b) Much longer than they are wide. Adult 1.  Useful for ID. • Hatch in intestinal tract. morphology Scolex (Fig 13-3a) Small and round. 3. diarrhea. Mature proglottid (Fig 13-4) Lateral genital pore. .

or subcutaneous areas. dementia.PZQ or Niclosamide. • Lodged in brain or spinal cord.someone else is infected with the adult worm (they are the DH).  Gravid proglottid detaches and rather than moving down the intestine and into the feces. collagenous capsule. affects vision and possibly • leads to loss of eye. it moves forward. 2. iv. may be due to reverse peristalsis in the intestine .  Goes into SI and eggs hatch . • Eggs penetrate intestinal tract and cysticercus develops in a parenteral site. Treatment 1.stomach environment stimulates the hatching. Self-infection .  Pathology • Development of space occupying lesion.  Surgical removal since cyst will still be there. Neurocysticercosis 60% of cases. iii. Cysticercosis . F. How does cysticercosis occur? a. Control . i.  Adult worm in SI of human. Ocular cysticercosis 3% of cases.hand to mouth infection. • Symptomatic cysticercosis.E.  Penetrates intestine and goes to a parenteral site and develops into cysticercus. c. • Example: headaches. b.PZQ or albendazole . • Growth of interconnected bladders through host • tissue. • In viscera. • Pressure on adjacent tissue and interferes with function.x-ray or surgical removal for identification. H.  It ends up going into the stomach. Disseminated cysticercosis 35% of cases.re-infection of individual by parasite without it leaving the host.  Human is DH. and it is as if it had been ingested. • Necrosis due to decreased circulation. 2. • May float in aqueous or vitreous fluids. Internal autoinfection . Environmental contamination . G. • May adhere to retina. • ii. • Can be asymptomatic.up the intestine. Cysticercosis . • Cysticercus becomes encapsulated by host response. Diagnosis 1. seizures. muscle. Racemose type Proliferating form.inhibits glucose uptake. Most common cause of adult-onset epilepsy in • the world.gravid proglottids in feces. • paralysis. Adult worm . Adult worms .

 Below 10 degrees C for ~14 days. 3.  No hooks. NTD of North America Common in Latin America. Bi-lobed ovary. I. inspection of the pig's tongue when slaughtered. Lateral genital pore.  Heavy infection . Taenia saginata o Common name is Beef Tapeworm o Life cycle (Fig 13-5) IH . no uterine pore. Human waste management. Cook or freeze meat. • Diarrhea. nausea. Adult morphology 1.cattle. If pig is infected. Treatment 1.  2. 15-20 lateral uterine branches. Pathology Most likely asymptomatic. there may be cysticerci on the tongue.Human waste management. 3. ingests cysticercus.  No rostellum. Niclosamide F. PZQ 2.  No cattle or human access to feces. b.  Cuboidal. No pig or human access to feces. • Issue in US due to immigration. c. • Intestinal obstruction. Mature proglottid a. • II. • E. Control 1. • o Egg morphology Identical to Taenia solium.  Light infection . D. Scolex (Fig 13-3a) 1. d. Compact vitelline gland.may pass inspection. Gravid proglottid a. • No cysticercosis.  Acetabulate.  Over 65 degrees C for ~30 min. • C. 300-400 testes. Meat inspection.  2. .carcass destroyed.human. • DH .

caused by E. Cysts are metastatic . E. Proglottids Immature.2. reindeer. Alveolar echinococcosis . Echinococcus A. 2. ingesting IH containing • hydatid cysts. severe allergic reaction that can cause death. etc.  Host becomes hypersensitized. Humas are never DH.  C.  Gravid. Cook/freeze meat.moose. NTD in North America Primarily affects Inuit people .  3. Ultrasound. granulosus from wolves (natural DH). • B. Life cycle .E. Diagnosis 1.caused by E. Pathology  Echinococcosis (hydatidosis) occurs when human ingests eggs. Hymenolepis nana A. Life cycle Invertebrate IH optional. Surgery. and elk.in bone. X-rays.sudden.  IV. • B.disrupts glucose reuptake. too big can cause bone to break.  Mature. Treatment 1.  IH .  Rostellum with double row of hooks. ingest eggs. causes • anaphylaxis .  Sled dogs are fed offal (organ meat) of moose. neck. significant if human becomes IH. • If cyst ruptures. granulosus. • .spread through tissue. IH . % Cysticerci killed 0 50-67 100 Meat Rare Medium Well III. multiocularis. Albendazole . 1. Dwarf tapeworm Infects mice and humans.  Cystic echinococcosis .  Osseous cyst .  D.  Humans ingest eggs from feces of sled dogs. and three proglottids. Cystic echinococcosis . F.hydatid cyst develops. fluid pours into host tissue. particularly sheep or cattle. Morphology (Fig 14-4) Scolex. 2.  Fluid leaks from cyst. Space-occupying lesion. • Scolex • 4 suckers. • 40mm long x 1mm wide. • DH . 2.indigenous people of Artic regions.herbivores.dogs and canids (dog-like animals).

Body Wall Cuticle . Introduction o ~20.rare.  Oncosphere that gets released penetrates mucosa. o Parasites of vertebrates.many layers and covers surface and lines openings.INTRO & MORPHOLOGY I. III. Egg eaten by beetle or flea (IH). • Hatch in duodenum.  Enters lymph channel of villas.  Develops into cysticercoid.C.  Eggs ingested by human or mouse. .  Shed in feces and infective to humans or mice. Develops into cysticercoid in hemocoel. capable of some metabolic activity but nothing like • the tegument. A.  Facultative nature of life cycle . Adult worm develops in DH.fibrous protein.Cysticercoids can develop at higher • temperatures. Pathology . tapered at both ends. D. o Plant-parasitic. o Major medical importance II. • All openings are lined with cuticle. Important in development of nematode.  Human or mouse (DH) becomes infected by ingesting infected  beetle.000 species described in all environments. ~80% collagen . Treatement . o Parasites of invertebrates. B. o Free-living (terrestrial and aquatic nematodes). General Morphology o Roundworms .generally elongate.PZQ. Contains enzymes. • Hypodermis . significant in agriculture because ~10% of all crops are destroyed. • Small protrusions in hypodermis that contain longitudinal nerve cords • and excretory canals. • NEMATODES . cylindrical.thin layer whose major function is formation of cuticle.

muscular and glandular components.underneath hypodermis and longitudinal.IV. iii. 2. Buccal cavity . o Foregut lined with cuticle. Alternation of contraction and relaxation enables locomotion.  3. Good for identification because it is not present in all species. ii. Locomotion i. Tri-radiate .mouth --> gut --> anus. a. contributes to support of organism and its locomotion.between the mouth and esophagus. Muscle layer . 1. Digestive tract o Complete digestive tract . Muscles on one side contract.in a cross-section. V. C. Mouth .solutes.circular and may be surrounded by lips. Pseudocoel . Filled with hemolymph 1. 2. o . Force of contraction transmits fluid to the other side. Cuticle on other side will be stretched due to extra fluid. Compresses cuticle on that side. one direction. Esophagus .  Size and shape varies among species.fluid-filled cavity that is enclosed by the body wall. Structural . Transport . one radius is pointed ventrally  and 2 of these radii are pointed laterodorsally.  In some species there are teeth. v.acts as a hydrostatic skeleton. series of curves that causes S-shaped locomotion. iv.

2. • VI. • Example: Amylase. D. B. straight. • Drugs cause degenerative changes in nematode intestine.blocks glucose uptake.Glands . Midgut .structures which produce digestive enzymes. • Many degrade glucose incompletely and excrete high energy • compounds. Hindgut . 1. Drugs interfere with metabolism Example: Albendazole and mebendazole . and extends from esophagus to hindgut. cellulase. • Microvilli.forces food through esophago-intestinal  valve into midgut. Pumping structure . Food resources Metabolism . posterior-most part of hindgut.receives products of reproductive system via vas deferens. Nervous system . • May also inhibit mitochondrial electron transport. • C.simple. Male  Has structure called cloaca . E. Female  Midgut empties into a short hindgut which opens into the anus. • Absorption. proteolase.lined with cuticle.most do not completely oxidize all of their nutrients. • Non-muscular.  Simple columnar cells.

Neurotransmission Nerve fibers in nematode are either excitatory or inhibitory.chemoreceptors. 1.  Innervate posterior end of worm. • Stimulation of excitatory fibers releases ACh at neuromuscular • junctions.flaccid (limp) and spastic (rigid).blocks ACh and causes hyperpolarization of membrane.  Sense organs Labial papillae .  Amphids . •  GABA hyperpolarizes the muscle membrane and reduces the rate of action potentials. • Modified cilia innervated by nerves from circumesophogeal commissure. inhibitory. D. Reproduction o Dioecious organisms. VII. o Male .chemoreceptors near the tail. function as mechanoreceptors.posterior to the lips.  Leads to flaccid paralysis. 4.  Nerve then branches and surrounds hindgut. • Piperazine . Largest of nerve cords is the ventral longitudinal nerve. Pyrantel .  Presence/absence is a prime character of taxonomic  classification.stimulates GABA release. increased levels of ACh. Same level as cephalic papillae. Innervated by nerves from circumesophogeal commissure. 3. Innervated by nerves from rectal commissure. •  GABA binds to receptors on muscles. C.bumps on lips that function as mechanoreceptors. Rectal commissure Follow ventral longitudinal nerve to posterior end of worm. Nerve cords that run down from commissure .A. Nerves from circumesophogeal commissure. causes spastic paralysis.required to break down ACh.innervates sense  organs that are at the anterior end of the worm. B.innervate the  posterior end of the worm.  ACh depolarizes the muscle membrane and produces an action potential. 3. Inhibitory fibers releases GABA. 2.inhibits enzyme cholinesterase . •  Leads to flaccid paralysis.  Excitatory.rings of nerve cell. 2 major nerve centers. Nervous system is major drug target Paralysis .  Cephalic papillae . Ivermectin . Phasmids . Circumesophogeal commisure . Nerves that extend up from the commissure .  2.  1.

 B.1 or 2. uterine peristalsis and pressure from • hemolymph helps it along. • Oocyte + sperm --> fertilization. Guberuoculum guides spicules.located in cloaca. Down vagina and out the gonopore. • They move down oviducts and into seminal receptacles. Eggshell formation Penetration of oocyte by sperm initiates process. Copulatory spicules keep gonopore open and help sperm enter  the female. • Egg moves down uterus. sperm migrate up vagina and into seminal receptacle. Vas deferens. 5. Female Didelphic . 4. Accessory organs . Ejaculatory duct.2 ovaries and 2 uteri.1. 3. • Oocytes produced in ovaries. • During mating. • Most nematodes . 2. Tests . Seminal vesicle. • C. • Layers form around zygote and embryo.eggshell has 3 layers: • .

B.outermost. • Hypodermis secretes a new and bigger cuticle.  lar hypodermis. VIII. 3.soil transmitted helminthes o Most common of the NTDs.  The old plasma membrane becomes the vitelline layer. 4.  al hypodermis. Chitinous layer contains protein chitin .actively transmits the parasite. No Cellu Class Secernentea  plasmids.larva. L2 molts to L3** (infective to host in most species). o 3 major STH: Trichuris. • IX. • Old cuticle ruptures and larva escapes. Inside egg.forms from uterine secretions. • •    Class Adenophorea  plasmids. Molts into L4 stage which molts into the adult worm. Adult worms in DH. Have Syncyti Routes of infection Oral . STH .Vitelline layer . Ascaris. Morphology Phylum Nematoda.  ingestion of larva. Some nematodes have a fourth layer .ingested by host. Nematode classification A. 5.the outermost. Chitinous layer Lipid layer .TRICHURIS TRICHIURA . Refringent bodies (from sperm) migrate to the periphery right below the chitinous layer. Larva secretes exsheathing fluid. Eggs exit in feces. hookworms. NEMATODES . •  Proteinaceous . o Molting occurs as the nematode grows. • Causes a new plasma membrane to form beneath the original oocyte • plasma membrane.forms beneath the vitelline layer. o Infections acquired through contact with soil contaminated with either parasite eggs or larval stages. 3.innermost. Skin penetrator . ingestion of egg and in other species. • X. 4. unholy trinity. • IH .  Lipid layer confers resistance to desiccation (drying out) and penetration of water-soluble substances. L3 ingested by host and hatches. 6. 2.vector . Sperm penetrates oocyte. L1 (first stage larva) molts to L2. they expel all of their contents.only one host involved and there is no amplification.  Contents fuse together and form the lipid layer. • In some species. • Cuticle detaches from hypodermis. o Direct life cycle . General life cycle of egg transmission 1.

Increased peristalsis in LI.eggs in feces.• Class Adenophorea. • Molts 2 times.asymptomatic. Who gets infected? In U.part of intestine hanging out of the anus.rest of body is affected. E.develops to L3 inside egg.exits in feces.  Colitis .  200 worm infection increases daily iron needs of child by 4. TDS (Trichuris dysentary syndrome).  Embryonation . posterior end has a noticeable coil (Fig 16-1)** Pathology <100 worms . all increased levels.2 billion at risk. • Common name: whipworm.  Stunted growth and impaired cognitive function. •  Macrophages. adult worm.005mL of blood per worm per day lost in feces. .  Occurs in heavy infections.2. • Adult migrates back into lumen of SI. Systemic effects . thick shell.  Heavy infections and diarrhea. • In the world .  Can lead to rectal prolapse . • **In males.25mg/day. Worms feed on cell contents and blood. Life cycle Egg . D. more common in young children • because they play outside. 3. • B. 4. • Trauma to intestinal lining. Eosinophils. Diagnosis . Opercular knob at each end.Albendazole and mebendazole.800 x 10^6 infected.  Swallowed by host and hatches in SI. ~0. • Anterior end burrows into mucosa. • L3 penetrates into internal villi. C. 5. • External environment of moisture and shade. • Migrates to cecum and LI. Host inflammatory response. • Poor standards of sanitation. • Infections of 200-1000 worms. •  Leads to chronic hemorrhaging and anemia. • . Treatment .S.2 x 10^6 in rural SE. IgE. A.inflammation of the colon. 3.

• Don't let anything in. moisture-retaining soil. • They burrow through the intestinal wall and get into the circulatory • system (blood and lymph). Proteinaceous layer from uterine wall. sends out immune • response that results in inflammation and a granuloma. • L2 inside egg.ASCARIS & HOOKWORMS 1.glycosides that are found specifically in the b. Mammillated . and shade. Ascaris lumbricoides o STH. 2. Ascarosides . o Life cycle Adult worms in SI. compound in which a sugar is bound to a non-sugar by a glycosidic bond. b. sufficient rainfall. ♣ White blood cells and tissue . Larva migration Juveniles get lost and die. o Golden brown color . and ascarosides. L4. • L1 inside egg molts. End up in the lungs and undergo 2 molts. • o Egg . Pathology a. a. brain. eggshell is impermeable to all substances other than gases and lipid solvents. Lipids. ♣ Example: spleen. Loeffler's syndrome. ♣ High risk of secondary bacterial infection. blood pools in the lungs.transmission stage. proteins. • L4 crawl up the trachea and into the mouth.from host bile. • a. Thick and bumpy outer shell. ♣ .congest lungs. ascaris egg. b  Pulmonary Damage to lung capillaries. humidity.has a fourth layer.•  Environment conditions favorable for embryonation to occur. Lipid layer of eggshell. • Goes down esophagus and get to the SI. liver. • Molt into an adult worm. o Class Secernentea. o Extremely resistant to external conditions. Warm climate. host swallows them. NEMATODES . • L2 ingested by the host and egg hatches in SI. • Eggs shed in feces. may lead to ♣ pneumonia. transmission stage. 3.

2. Beta  = 0. Coughing. d. Allergic responses to worm waste products. • E = 200 eggs. Intestinal obstruction.S.Increased eosinophils in lungs.  Most common helminth. Epidemiology 1. Direct life cycle . children more susceptible because they are smaller.eggs in feces. • How many worms total? 110 worms.  Piperazine and pyrantel. • Contact rate. Pierce intestine. 4. no intermediate hosts.  E = eggs. Abdominal pain. • 3.4 x 10^6 in SE. they are attracted to the • larva due to the protein on the surface.  Surgery in some cases.  Night soil. Study of occurrence of a particular disease. b. rashes.  Poor sanitation. asthma. Treatment Mebendazole and albendazole. 2. e. Ascaris 1. . c.one parasite and one host.  In the U.~1 billion. Example: A = 10 worms. wheezing.  rA = net reproductive rate (# of eggs shed out of host into  external environment) Beta = per capita transmission rate (likelihood an egg will get  into a host and develop into an adult).  6. Wander into bile/pancreatic ducts and out the mouth (distress!).  r = per capita reproductive rate (# eggs produced per worm). chest pain.  Warm climates. . r = 20 eggs per worm produced. Intestinal a. Diagnosis .  2. 5. Infection Worldwide . • How many adults will develop from this batch of eggs? 100 worms.5 (50% of eggs will develop to the adult stage). can lead to peritonitis and inflammation which can result in death if not treated. Parasite population: A = adults. probability of contact with host and probability that this contact will lead to establishment inside the host.

enables us to ♣ extrapolate how many adults are in the host.  Au1 = # adults removed from population.  Other factors? 3. b. b. What factors may affect the transmission rate. • . ♣ Presented as age-prevalence or age-intensity curves.200 eggs. • Au1 . Measuring model parameters. a. c  Presentation of data.average number of parasites in an individual.100 eggs. • Immigration and emigration rates. u1 = per capita death rate for adults. • How many adults will develop from this batch of eggs? 1. Beta? # of eggs. • Decrease rA .  Parasite reproduction (rA) and transmission (Beta). Look at different age classes.don't use night soil and wash hands.210 eggs. • Decrease # of hosts .  # of hosts.  Eu2 = # eggs removed.3.  • Birth rate.  Parasite's ability to survive in host. not viable. Behavior of host. • Decrease # of eggs .drugs.not viable. host immune status. serological assay (antibody to the parasite). • In other species.increase by drug treatment. Decrease parasite transmission (decrease Beta) • Decrease contact . • Death rate.% of host population that is infected. • Intensity .not viable. • How many eggs will they produce? 2.increase by killing eggs in external environment.  Use model to determine parasite survival. field data. 4.  6. Prevalence . • How many worms total? 1.  Parasite elimination (Au1 and Eu2). Determine number of eggs per gram of feces. Eggs in feces (Ascaris). • Eu2 . Increase parasite elimination. Get rid of Ascaris? a.  u2 = per capita death rate for eggs.

♣ Measles = 8.immunity may be lower in children which explains high intensity of infection. • . o Class Secernentea.  Ro . hatch. Threshold level of Ro = 1. 1. assumes that parasite survival occurs. 4. • L2 stage molts. Age-prevalence curve . ♣ Malaria = 50. • Gets into blood and lymph (circulatory) systems. ♣ Ascaris = 5. • L3 = infective stage that penetrates skin. without human intervention. Number of eggs produced by a single adult that survive to produce  adults which can reproduce. ♣ 3. Hookworms . • L1 stage then molts.  Age-intensity curve . • Mate and shed eggs in feces.  Small pox = 2.  To eradicate parasite: Ro < 1. Ro = basic reproductive ratio.STH.naturally occurring. Life cycle Adults in SI. eradicated.all ages have equal probability of encountering the parasite.

4 cutting plates (wide thickening of cuticle).  Buccal cavity (btwn mouth and esophagus). develop to L1 stage.S. L2. Ends up in the lungs and then up the trachea and the molts.  L1 and L2 stage Feed on fecal matter. • Warm.  Hatches. egg. extend up and nictate . • Necator americanus • American killer.  SE U. and L3 are identical.  Grow and molt.L3 move down.  • • Freezing and desiccation kills L3. Life cycle. Adults Anterior end is curved dorsally.  Accounts for 95% of human hookworm infection. and South America. Goes through embryonation. Male . L1. Egg  3. Large buccal cavity . • . • 2. • Wet surface . 2. moist. used to mate.has a copulatory bursa at posterior end. 4. Oval. • Down the esophagus and to the SI where it molts into an adult.L3 move up.  Anterior . • When surface of ground is dry .2. and shady environment.teeth/cutting plates.  L3 stage In contrast to L1 and L2. • Life cycle stages a.  Transmission stage.wave back and forth to maximize host contact. 2 primary species that infect humans. L3 is a non-feeding stage. 3. thin shell. • Adult morphology and geographical distribution differ.

c. damage capillaries and aveoli. Mass chemotherapy.5.  Inflammation. Exopeptidases (amino. 6.and carboxy-) . Anemia • Stunted growth and cognitive function.L3 enter skin. • Hemoglobinolysis  Digestion of hemoglobin (Hb). Shoes. Invasion . Ancylostoma duodenale . • Metalloproteases . • many worms and many days. d. 5. Ground itch .). acids. c. • many worms and many days. Posterior . • c.03mL blood/worm/day. Burrow into intestinal mucosa. 7. noticeable tract.breaks apart blood cells. • Ancylostoma duodenale Europe. Hemolysin . ~280 x 10^6 Hb molecules in each RBC.  Iron therapy to increase iron levels.  Buccal cavity  2 cutting plates and each plate has 2 teeth. lyses erythrocytes.~0.anticoagulants that keeps the blood • flowing. Adult survival = 2-14 years.  Ad . and Africa.cleavage fragments.most serious phase of pathology. • ~1 billion infected worldwide (7 x 10^6 in U. • Pathology a. Asia. Blood loss • Necator americanus .  L3 penetrates human skin.10. b. • b. Treatment  Mebendazole. • Salivary secretions .S. Iron and adequate protein in diet.000-30. Control a. pneumonia.000 eggs/worm/day. b. Migration Lungs.  Cutaneous larva migrans Caused by non-human hookworms.rash and irritation.0. • estimated ~7 x 10^6 liters blood/day. a.begins cleavage of Hb.  . Sanitation. 4. • Inflammatory to bacteria. Intestinal . Aspartic and cysteine proteases .2mL blood/worm/day.000-10. • Coughing.000 eggs/worm/day.releases free amino d.4 teeth (narrow and pointy parts of cuticle).• 3. Na .

cough.  Latrines.looking for antibody produced by host against parasite antigen. • Enzyme Linked Immunoabsorbant Assay. Access to clean water. transmammary infection. • and hookworms. Ingest eggs. visceral larva migrans. Donation of mebendazole. causes inflammation. Eggs begin tissue migration but don't complete it because they are in • the wrong host. 2. Ascaris. focus on Trichuris.  C. Symptoms Fever. Toxocara canis o Class Secernentea.Most commonly caused by Ancylostoma brazilieuse and A. • E. • . Antigen (Ag) is bound to the bottom of a microtitre plate well. and brain. • Can lead to scarring and then blinding. If lactating dog becomes infected.do not continue development. ♣ caninum. Diagnosis ELISA .  NEMATODES . personal and environmental. Infections In U. wanders • aimlessly. larvae can pass into mammary tissue. • D. • B.S.TOXOCARA. STRONGYLOIDES. ocular larva migrans. 4. Children Without Worms Johnson & Johnson and The Task Force for Global Health. Goals • 1. 2. Developmental arrest . Host is dog. If pregnant dog becomes infected. • Goal to decrease STH infections in children. ENTEROBIUS 1.significant STH. Damage to liver. • 1. 3. abdominal pain. vision problems. • Some larvae enter the eye. Health education. 20% dogs infected. Improved sanitation. larvae can cross into fetus. Ingests prey item which itself ingested eggs and developed larvae. Humans can become accidental hosts by ingesting eggs (contain L2). . lungs.

B. • • .1.increased population in the body. • Occurs in immunosuppressed patients. no Ab present and the person is not infected. Male organs disappear and female organs develop second.  Pathology Strongyloidiasis . Color change means Ab is present and person is infected. • Mebendazole or albendazole. • Cutaneous . meningitis. 4. Life cycle . 2. had  male reproductive organs first. C. Treatment Often self-limiting.look for larvae. • ~90% of cases are asymptomatic.only female adults. Anti-Ab + enzyme is added. • 3. • Intestinal . coli • Can lead to septicemia.threadworm infections. Hematogenous spread of bacteria.nausea and abdominal pain. Add serum from patient. • Diagnosis Fecal . A. • 2. Parasitic females are protandrous . 5. Add enzyme substrate. • Autoinfection is serious . • hyperinfection syndrome .parasite and free-living generations. piggyback transport. pneumonia. • Pulmonary. If no color change. it will bind. Inside host . If antibody (Ab) against Ag is present in serum. Wash the serum/well out. will be • • F. there a color change.ground itch.abnormal proliferation of parasite. Wash the well out.  Example: E. Strongyloides stercoralis o Class Secernentea. produces sperm.during development. if an enzymatic reaction occurs.

STH. Adults Alae . . • Egg embryonates.S. . Enterobius vermicularis o Class Secernentea.ELISA.Eggs hatch in perianal area and larva wanders  back into intestine. • Female to perianal area and oviposits. • • Female . A.curved posterior end. • Warm and moist climates. • Molts and migrates to LI • Retroinfection . Migrates to external environment.  Ingested by human. • D. Infections U. • 3. • Male . • 30 x 10^6 cases worldwide. B. • Hatches in SI. Treatment Ivermectin. molts and migrates  to LI. little expansions of cuticle. • E. • Hatches (retroinfection) and wanders back. cosmopolitan. Life cycle (Fig 16-21) Adults in LI. o Common name: pinworm. • Thiabendazole.posterior end has a very pointed tail.found at anterior end of worm.

• Common in children Hygiene habits. • function unknown. L1 penetrates the intestinal wall and gets into the bloodstream. • Sleeping . esophagus and stichocytes.Autoinfection .the whole structure that includes the posterior b.glandular cells that produce digestive secretions. Pathology Large number of worms . • Mebendazole. • Posterior portion . Stichosome . .  Females: ~3-4mm in length. • NEMATODES .produces L1's. they scratch and put fingers in their mouth.  D. very small.tube surrounded by cells called • stichocytes . Ingestion of larvae A. c. • Anterior portion . DRACUNCULUS 1. C. Life cycle • Same individual acts as DH and IH. Trichinella spiralis Class Adenophorea. • Albendazole. • Males: ~half the size.Host ingests eggs from worms in that  individual's body.thin wall. ~2/3 body length.  Leads to sleeplessness and irritability. • E. Esophagus Very long. F.   Mating . • Morphology • a.female is ovoviviparous .TRICHINELLA. • Inflammation and bacterial infection. Treatment Pyrantel. not eggs. • Enables them to inhabit a unique location in the SI: • intramulticellular habitat in the intestinal epithelium. Male Posterior end has a pseudobursa . ANISAKIS. muscular. ideal for identification.thickened cuticle.damages in intestine and around anus.  Adults . Diagnosis Scotch tape test.things itch.live in SI.

and • pigs. tail area. 4 molts and becomes an adult.inhibits carbohydrate metabolism. Muscle biopsy . • Trauma and immune response.excretory secretory antigen from stichocytes. difficulty breathing.disease cycling among humans. F. abdominal pain. • Strong host immune reaction. vague symptoms. surrounds nurse cell. Clinical symptoms . • Pigs also like to attack each other. • Mitochondria degenerate.  L1 gets released from the nurse cells into the SI of the new  host. Diagnosis a.infected when they feed on garbage that contains infected pork. changes turn muscle  cell into a nurse cell. heart damage and nervous disorders. • Nausea. Sylvatic trichinellosis . diarrhea. Next host is infected by eating meat with L1 in the muscle.   Effective against adults. • Ag (antigen). diaphragm. and jaw.developmental arrest. • Circulatory rete . tends to be in a farm setting. .decreases inflammation. inflammation. Treatment  Mebendazole. affects wide range of hosts.penetrates individual  fibers.expensive and painful. remains in the L1 stage for  months/years.disease is cycling among wild carnivores • and their prey. Inflammatory phase .cannot make a diagnosis just on clinical symptoms alone.C. b.network of very tiny blood vessels. • Rats & pigs . • Looking for antibodies that were produced against the parasite. Destination is the skeletal muscles . • Bed rest.severe.ELISA. Thiabendazole . L1 .  Treatment usually used is for relieving symptoms. Urban trichinellosis .moderate. • Loses myofilaments (muscle can't carry out normal contractions). • Muscle pain. • ESA . E. chewing and swallowing. • Nurse cells formed. • Pigs can also eat infected rats. • Corticosteroids . rats.mild penetration of worms into intestinal • mucosa. tongue. • Nuclei hypertrophy. Migration phase . Serology . c. • Humans eat pigs. • • Many L1's end up in the eye. D. Very low host specificity. L1 induces changes in muscle fiber cell. fever. Pathology Intestinal phase . common method of determining diagnosis. c. • Experience of muscle pain and fever.

 Ovoviviparous .1st IH. b. nausea.• Oxygen administered if person is having difficulty breathing. 2.  . Life cycle 1.  Study of fish off the U.170 degrees F.circulating Ab not detected until 2-3 weeks after infection. Education. Granuloma's are produced . B. A. b. Control a. d.5 degrees F for 21 days.2nd IH --> L3. o Common names: Guinea worm. 4. Chronic symptoms: abscesses . Prevention  Cook/freeze.method of inspection where you take a light source  and hold the fish over the light and look through the fish to see if it is infected. Life cycle Marine mammals that act as DH. wild bears and boars.~42% were infected. Luminal form . o Transmission by IH. Treatment  Self-limiting. often in the legs. diagnosis can be made in the acute phase. Inspection. ♣ They die and expel through the feces. G  Infections a.  Surgery.produces thousands of L1's. and • vomiting. Detects circulating Ag .parasite peptidases • destroy host tissue. asymptomatic.S. ♣ Acute symptoms: intense abdominal pain. c. Freeze meat . Eastern Europe . Cook meat . U. ♣ b Pathology Humans can be an accidental host if they ingest ♣ raw/undercooked fish with L3's.worry about getting involved with the sylvatic cycle (wild animal sources).L3's in the lumen. 3. Symptoms b.S. west coast . 5. • Some L3's invade the stomach or the intestinal wall. Dracunculus medinensis o Class Secernentea. H. ELISA .  Most common in humans: Anisakis simplex. .host immune • response. ♣ Fish . Diagnosis a. a. ♣ Crustaceans .50% prevalence in swine herds. fiery serpent.secretions released by L3 during • tissue invasion. Adult female Lives in the skin of DH (human). Candling . Anisakis species  Related to Ascaris.

symbol of the medical • profession. Surgery. Pathology 1. Eradication . 3.  7. Cool water feels good. 2.projected to be the 1st parasite (and only 2nd disease) to be eradicated.  Painful. usually cyclops species.  Males (2cm) die and are rarely found. • Metronidazole . 1986 . Non-emergent worms .  Female migrates in skin . L1 penetrates into hemocoel. DH (human) becomes infected by ingesting water with infected copepods.caduceus .Uterus and body wall of adult female bursts open and L1's pour  out and into the skin.  L1's exit to the water. L1 in water . Infections Drought.<10. blister then ruptures. Die and become calcified.~100.sepsis and death.~3.  2 molts and L3 in copepod. • 2001 . L3's released from copepod and penetrate duodenum.allergic reactions to metabolic wastes. • E.grows to 1m long. Blister . 4. Molts to L4 then adult (female and male).000 cases. Migration .concentration of activities. • F.  Water increases muscular contractions of the uterus.000 cases. The copepod = IH.  Arthritis. • .  Migrate through abdominal muscles and get into subcutaneous  tissue. • Example: step wells in India. Treatment Winding the worm on a stick . • D.2 x 10^6 cases.don't make it to skin surface.inhibits protein synthesis. Diagnosis Blister with emerging worm.  3. 6. painful blister in skin.many occur on feet and legs. 2.get eaten by copepod (crustacean). parts of  the worm and uterus are going to protrude from the blister. L1's stimulate a very strong immune reaction. Migrates to inguinal and axillary regions. • Small bodies of water . L3 in DH (human). Mating occurs.  Secondary bacterial infections . • 2008 . Abscessed.  5.  C.  B.

helps identify the species. there is a particular pattern to the location of the  nuclei. Georgia. which eventually • gets into the blood. • Usually in lower half of the body. 1987 .  Periodicity .bore holes. mf are found in blood vessels of deep  tissues.an IH that is actively seeking out a host for • its own purposes.  Treated the water. L3's migrate and enter the lymphatic ducts and molts to an adult. mf can be found. If blood sample of infected person is taken. Carter • • • • Center Jimmy Carter. • Covered by sheath/membrane. Educated the people to the biology of the parasite. Emory University in Atlanta.stage not as developed as L1. Life cycle Adult female and male worms in major lymphatic ducts. Wuchereria bancrofti o Causes lymphatic filariasis. H. forceps. • Vector is a night-feeding mosquito. • L3 migrates up to proboscis. Causes of periodicity:  Decreased body temperature. • Transmitted by a vector . • Mosquito's saliva is filled with lubricants and anticoagulants that are • injected into the host along with L3's. • NEMATODES . • People were given filter cloths and shown how to filter • their water. A. it may lead to a lower • death rate. to L2.  Female produces mf that are released into the lymph.Pakistan and Ghana. Funding and political assistance. advanced embryo.  When stained. Increased population may not be supported by the available resources. • and decrease in water secretion by kidneys during sleep. mf molts from L1. • . or elephantiasis. there may be a serious • effect on the quality of life.mf in peripheral blood between 10pm and 2am.  Construction of water wells . Mosquito ingests mf during blood meal. Medical supplies: J&J donated Tylenol. • Inside the mosquito. Microfilaria (mf) . 2.  During all other times. and • gauze. Filarial Diseases 6 genera in humans.FILARIAL WORMS I & II 1.kills copepods and decreases toxicity to fish • and mammals. primarily the lungs. increased body acidity. Committed to human rights and relieving human suffering.  Temephos . If this is not matched with a lower birth rate. Parasitologist's Dilemma If you accomplish the eradication of a parasite.G. and then L3.

Grade I . • Common in legs. • c. No detectable microfilaremia . chills. Chronic 10-20 years after initial exposure.  Also pricey.  Only way to detect an infection is by ELISA. and • scrotum.attacks of fever. Many cases asymptomatic.  CFA test .many symptoms. C. warty appearance. 2. • Fibrous tissue and fat. Psychological impact and social • impact. Responds to rest and elevation of the • limb.  Episodic adenolymphangitis (ADL) .transient (comes and goes)and soft (application of pressure causes a pit to form in the skin).  2. and  edema.increase in cell size on • the outer skin layer. b. Daily washing (2x a day) with soap and water. Grade III Subcutaneous thickening. • Hyperkeratosis . Finger prick blood droplet any time of the day.  3. arms. Because of periodicity.look for adult worms in lymphatics. Ultrasonography . Pathology 1. Does not pit on pressure. arms. Inflammatory response to dying adult worms.circulating filarial antigen test. Grade II . • Infiltration by fibrous connective tissue. Fissures (splits) in skin and development • of nodules.mf in blood.  . causes lymphoedema • swelling in lymph tissue of legs. mf in blood. Elephatiasis can develop. Repeated acute and chronic • attacks.  Antibiotic creams to treat abrasions."  D. a. • Impairs function of lymph tissue. Acute infection . Chronic blockage of lymph.B.  Wearing shoes. Treating bacterial and fungal infections. Diagnosis 1. lymphatic • filariasis.  Clean nails.swelling is hard and permanent. • 3. Associated with inflammation of inguinal lymph nodes. detect Ag in blood.  Granulomas formed.  Lymph tissue blocked by worms. Looking for the "filarial dance. and genitals. breasts. Treatment 1. this method is unpopular.

effective and inexpensive.  DEC . Control of lymphatic filariasis 1 of 6 diseases targeted by WHO. Albendazole .$100 billion per year.  No animal reservoir. a. c. Costs of the disease.increases GABA. b.decreases likelihood of resistance • developing. • 3. then L2.diethylcarbamazine. DEC .  Treatment .reduce incidence to 0 worldwide.losses of $800 million .disrupts metabolic function. • G. May increase immune response of host by disrupting the • cuticle of the worm and causing the release of antigenic components. .  Ivermectin .  Large scale treatments possible. no amplification.Raise and exercise limb. • Elimination . • May stop in one location for a while. • Eliminates mf.inflammatory reaction. • Social loss. • Drug combination . • Molts to L1.  Vector .  F.single annual dose.  Drug combination. Costs of treatment Albendazole . E.$1 per test. • L3 infects next host when fly bites. Ivermectin . • Administered as a single treatment. • Males and females mate and mf are produced. Permanent long-term disability.  Tasteless and survives cooking. • Costs of treatment and diagnosis: $1. peripheral blood by day. • Decrease in economic productivity. • B. • Periodicity of mf. • Cost is 2 cents/person/year.reduce incidence to 0 in a particular area.32/person/year. • CFA test . and then L3. • Why does WHO think eradication is possible? • Parasite does not reproduce in the vector.deerfly (chrysops) tha tingests mf during the day. A. Collateral health benefits. • Also a single dose.table salt.  Diagnostic test.donated by Merck. Pathology Adults .  2. • Eradication . lungs at night. Life cycle Adults migrate freely in the subcutaneous tissue. Loa loa o Eye worm. • India . • 30 cents/person/year.donated by Smith Kline Beecham.  Form of DEC in salt: DEC fortified salt .

Diagnosis mf in blood. Life cycle Dog = DH.localized and painful swelling .nodule in the skin.  . ingested by blackfly (Simulian species). 4. Inside the blackfly .) 5. • C. • Scarifies the skin. molts from L1  to L2 to L3. • Dead worms can obstruct vessels.  Treatment of immiticide is contra-indicated .difficult because they like to breed in swampy • areas and forests. Kills adult worms. 1. 3. Dirofilaria immitis o Heartworm. • Controlling deerflies .heavy infection of heartworm. Treatment and Control Ivermectin and DEC can kill mf. small amount of  blood. • Mf in skin. Risky and expensive. • Surgery. • mf in the blood of the dog. scratches away the skin.  Vector = mosquito.mf penetrate into hemocoel. kills L3. May migrate across the cornea and conjunctiva.low margin of safety. • Female produces mf.  L3's infect next host through the skin. • Decreased heart function. A. C.  Molts into L4 and then adult.  Heartgard . • D.combination of Ivermectin and Pyrantel. Treatment Immiticide . • 2. Diagnosis mf in blood sample or an ELISA. NEMATODES ." o Life cycle Adult female and males live in the onchocercoma . • Coughing and respiratory problems. Host raection . Surgery Caval syndrome . • Blackfly takes a bloodmeal.  Problems:  Arsenic toxicity . Onchocerca Volvulus o “River Blindness.FILARIAL WORMS I & II (cont. Pathology Fatigue and general loss of condition.compound that contains arsenic.calabar • swelling. • D. Migrates to the mouth part. • B. • Produced by adult worms in heart and pulmonary arteries.not • recommended.

 Penicilin and ciprofloxacin . • Diagnosis .  Inherited. • Femoral and inguinal lymph nodes.hanging groins.  Endo-symbiont of many filarial worm species.  Insects .  Found in many insects (75%) and crustaceans. Antibiotic treatment? •  Experiments . endotoxin. leading to an inflammation • and blindness.animals treated with tetracycline. • Bloodmeal may coagulate in blackfly gut .teeth in blackfly gut breaks up RBCs. • Mf taken up during bloodmeal. LPS stimulates the host inflammatory response.mf stuck.  Lesions • Acute  Mf in skin causes persistent. • Wolbachia species. • c. Pathology Onchocercoma • Distribution: Central American . • Lizard appearance. caused by mf. • Immune molecules in hemocoel proteases.  Wolbachia – cell wall LPS – lipopolysaccharide.  Found in all developmental stages in hypodermis and reproductive tissue.ineffective. also destroys mf. The adult worms are stunted and mf development • decreases."  Disease of the skin and eyes. Onchocerciasis – “River blindness. • Loss of skin elasticity. • Live in mf – little host immune response and therefore limited  pathology. • Enlarging . • Can lead to the secondary bacterial infection. Africa . heavy infections. • Enlargement of regional lymph nodes. Ocular Mf invade the eye and die.  Found in all developmental stages. • Skin thickened and discolored. Dead mf .wolbachia controls reproductive functions and sex determination.above waist.o o o E. itchy rash. • Skin thickens. • Simulian Lay eggs in water of fast flowing rivers.below  waist. • Host inflammatory response Response to bacterium inside mf. Africa . •  Intracellular.stimulate immune response.10-30% of adults blind. • Chronic  Long term. • Mechanical .

Acanthamoeba Order Schizopyrenida  i. Subphylum Mastigophora . Kingdom Protista Single cell eukaryotes. 3. Endolimax iii. Giardia Order Trichomonadida  i. Mectizan .multicellular organisms. antibiotics. Phylum Ciliophora .removal of nodules. B.paralyzes mf. Surgery . Iodamoeba iv. Order Amoebida  i.Merck. Naegleria 2. 1. Trichomonas Order Kinetoplastida  i.  December 2002 . Helminthes . Leishmania B.today almost 0. Trypanosoma ii. macrophages remove mf before they degenerate. • 2. 2.  Nematoda.  2. Platyhelminthes.  Razor used to take skin slice.characterized by cilia. Protozoa . Skin snip Bit of skin raised up needle. Subphylum Sarcodina . Introduction A. 2. PROTOZOA . Ivermectin . Entamoeba ii. Carter Center River Blindness Program 1996 .  1. Chilomastix Order Diplomonadida  i.program zero and ended the work.  1988 . Onchocerciasis Program of West Africa.characterized by 1+ flagellum.unicellular. Traditional parasites 1. 1974 .  20 million cases .with Mectizan Distribution Program (MDP). • Do more damage than any other group of disease organisms.  Skin snip on slide with saline and microscope.11 west African countries. Ivermectin (large scale). G. Phylum Sarcomastigophora 1. Order Retortamonadida  i.  3. • ~45.INTRO & ENTAMOEBA HISTOLYTICA 1. insecticides. Control programs 1.  Treatment 1. worms.characterized by pseudopodia.  No blood. Genus Balantidium .F.may affect development of mf in female. Classification of Protozoa A.000 species identified.

characterized by an apical complex. Contain actin and myosin .parasites or commensals of humans. 3. Nucleus Chromatin distribution varies.  2. Reproduction . • Endosome .  Cytoplasmic extension that is surrounded by plasma  membrane. Genus Plasmodium 3. Cilia . b. Flagella Found in Subphylum Mastigophora.contractile function. C. B. Symbiotic relationships with humans. • A few pathogenic (+/-). Absent in other species . 1.most are free-living.Phylum Apicomplexa . Order Amoebida A.1+ flagella. 3 genera .shorter and more numerous than the flagella.liquid. 4. Locomotor organelles 1. Position is centric or eccentric.  Involved in locomotion and food acquisition. Contains RNA & genes involved in ribosome synthesis.asexual via binary fission.  Enables organism to swim .tubular shaped. Cristae . Cell Structure A.  Substrate required. • D. B. • C. Pseudopodia Found in amoebae. Habitat . Iodamoeba Size and nuclear structure used to differentiate. different from multicellular  eukaryotes. Most commensals (+/0). • a. Entamoeba 2. 2.inside nucleus.also known as blepharoplast or kinetosome  anchor to the flagellum.anaerobic. Basal body . Endolimax 3.  Trophazoite stage . . Mitochondria 1.provides support to  flagellum. Size and position in nucleus is significant for differentiation. Embedded in flagellum is an axoneme . Present in some species. 1. • 5. Genus Entamoeba A. but some are found in vertebrate and invertebrate intestinal tracts.  Temporary extensions of the plasma membrane and the  cytoplasm.

Chromatoidal bars . • ~500 x 10^6 infected. Evenly distributed peripheral chromatin (PC). Transmission stage .nucleus divides.small & centric.  B. A. Binary fission . Life cycle . • 6.parasite. Amoebic dysentery.  ~110. Large.• • Small. the bars disintegrate. evenly distributed.deposits of c. Morphology varies between species. • Usually found only in young cysts. • In old/mature cysts. Nucleus • Endosome . • PC .  Live in the crypts of LI.feeding stage. • Daughter cells start to pull away from each other. Trophozoite (troph) . 3rd most common cause of parasitic death in the world.fine. and liver abscesses.2 stages. Entamoeba histolytica . Survives external environment. • B. Morphology & Life cycle (Fig 4-2).    • Feed on starch and mucus.passes out of host.what is going to be infective to the next host. Trophs • ~25 micrometers in diameter. • Unevenly clumped peripheral chromatin. • a. nucleic acids. • Cyst . b.000 deaths/year. centric endosome.useful in ID for some species . centric endosome. . amoebic colitis.

Metacyst is ingested by host.  Mechanical vector .chromatoidal bars with rounded ends.no parasite development. no chromatoidal bars. • Stimulated to encyst from drying out in LI. 4 nuclei. Cleavage furrow . • • Some carried posteriad with fecal material.B. Use a chemoattractant to attract a "midwife" cell .  Metacyst . • Young . ∆.  Ex.  Cytoplasm and nuclei divide . Summary .mature.rich in glycogen. transmission stage.Flies and cockroaches.thinning area between separating • daughter cells. Precyst . • 1/3 of cells can't break apart. Cyst • ~10-20 micrometers in diameter. •  Resistant to stomach secretions (gastric acid).any • Entamoeba histolytica troph in area. cyst resistant. . rough wall. c. Encystment Trophs in LI. Midwife travels and goes straight into the cleavage • furrow and ruptures it. trypsin breaks down cyst wall.8 metacystic trophs.  Excysts in SI.  Move down to the LI. • • Secretes thin.

 Hystolytica . Form pores in host cell lipid bilayer. Trophs move and destroy more cells. Troph binds to host cell surface.small peptides that lyse the host cell. . Cysteine proteases . Β. d.  Forms ulcers into submucosa . Trophs have galactose binding lectins on their surface. 2 major forms of pathology ∆. c.Χ.  Pass cysts. Amebapores .main source of infection. Lectin .tissue and lysis. Luminal amoebiasis  Asymptomatic. • ii.  Carrier . Troph secretes into host cell. i.under epithelial cells.protein that has a high binding specificity for a particular carbohydrate. Amoebic colitis A.  Increases host mucus secretion until depleted.cleave host cell structure. a. cytoadherence. Trophs release a secretagogue .agent that stimulates secretions.

dead • end for parasite.stool sample. Control Sanitation.  frequently the liver and lungs. 2. • G. FLAGELLATES 1. not cysts.live in humans but do not cause disease. Trophs can enter circulatory system. • Why should we study them? • Indication of oro-fecal contamination. Treatment Metronidazole . Introduction Commensals .  Experience of diarrhea/dysentery . PROTOZOA .NPP. PAM.enters trophs and inhibits their nucleic acid synthesis.  Preventing food contamination. E. Non-Pathogenic Protozoa (NPP) A. • ELISA .  Sheets of epilthelial tissue sloughs off. Perforate intestinal wall .detect antibody. • Emphasis on clean drinking water. Diagnosis Cysts in feces . • Treatment. useful if abscesses are suspected in the lungs • & liver. • Sand filtration. Lungs . • Antibiotics for secondary bacterial infections.Circulation inadequte. • Begin to form abscesses. useful in luminal amoebiasis cases. • ε.  . brought to ectopic sites.can lead to peritonitis.  Results in bleeding and loss of electrolytes.secondary bacterial infections may occur.individual is passing trophs. F.

 Nucleus has large eccentric endosome and irregularly dispersed  PC. D Nucleus .  4. Trophs are the transmission stage. centric endosome.  PC .   Directly .kissing. • Chromatoidal bars have splintered ends.  E. . Trophs 25 micrometers. Order Amoebida B.  Cysts .can be used for identification.small.  Large.thin layer. • 3. histolytica. Χ. centric endosome and fine. Healthy mouths . histolytica.Why should we be able to identify them? So we don't undergo unnecessary treatment. internal slug. Entamoeba gingivalis 1.morphologically identical to E. Similar to E. Entamoeba hartmani  Same morphology as E.  G. Mature .  Indirectly . ♣ Endolimax nana F Smallest amoeba found in humans.chewing gum.95%. 2. but smaller.  "Dwarf. Entamoeba coli 1.  Lives in LI. Entamoeba dispar  Troph and cyst . evenly distributed PC.50%. C.  Young  1. Trophs . Cysts 17 micrometers.  Trophs . ∆.on surfaces of teeth and gums. 2. C. Trophs 2. 8 micrometers . histolytica. 4 nuclei. or 4 nuclei. sharing utensils. 2.  Move much slower than other species.8 nuclei and have no chromatoidal bars. Iodamoeba butschlii  Troph ~10 micrometers.  ELISA used for identification.  Do not feed on or invade host tissue. Does not form cysts.12-15 micrometers. Unhealthy mouths . 1."    Cyst Very small.5-9 micrometers.

Naegleria fowleri 1. and seizures. 2 in Texas.  B. • Miconazole .soil. • High death rate. Order Schizopyrenida. Pathology GAE .  Results in meningitis/encephalitis. Rare . Pathogenic Free-Living Amoebae o Capable of facultative parasitism if they come in contact with humans parasitism is an option. Acanthamoeba species.enters nose and  into brain. Symptoms Stiff neck. B. • 4.granues in a "halo" around the endosome.antifungal. • Found in soil and water. Enters nose when water is forced in. . light sensitivity. 2. headaches. and 1 in Arizona.95% within 72 hours. Diagnosis Trophs in cerebrospinal fluid. Migrates along olfactory nerves to the brain. fever. warm ponds and lakes.antibiotic that disrupts transcription. • 5.  Be careful in fresh water and lakes. function unknown.  Chromatin . Control Chlorination in pools. • Primary Amoebic Meningoencephalitis (PAM).leads to a coma and death.  Large nucleus.S. . Order Amoebida.  Mortality rate . Rifampin . A. • 8.~200 cases reported. but not necessary for the organism's survival. fresh water.  Amphotericin B . Cyst  Oval with large glycogen vacuole. stains with iodine.granulomatous amoebic encephalitis .necrosis and hemorrhage. and heated swimming pools. 2.  6.6 cases (death) in 2007. Found worldwide .  Secretes enzymes .  7. 3. Eccentric endosome. U.  3 in Florida. • Left untreated .antifungal that binds to trophs and • disrupts the membrane. Treatment Combination of antibiotics and antifungals. • 1.

Subphylum Mastigophora o Flagella.  2 nuclei. Beaver Fever.  Cytostome .  2. Troph (Fig 5-1a) B.  Miconazole." • Beaver is the reservoir host. "backpacker's disease.  Cyst (Fig 5-1b)  4 nuclei.  8 micrometers. B. Treatment Amphotericin B.  Kitamipin (sp?).infection of the eye.  Lemon-shaped. • 1.12 micrometers long B.  4 pairs of flagella. Diagnosis Trophs in cerebrospinal fluid. skin.  3. • Acanthamoebic keratitis .Damage less severe than PAM. .  3. Chilomastix mesnili (NPP) 1. Cyst Transmission stage. Acanthamoebic uveitis .  Giardia lamblia Wilderness camping.  2 median support bodies. contact lenses. 2 adhesive discs.infection of skin resulting from soil  contact. and eyes. encloses a 4th flagellum called  a recurrent flagellum (not free). 3 free flagella.used for ingestion. A. Troph .

C. Pathology a.inhibits DNA synthesis. • Ingested and capsule dissolves.   Prevention  Drinking water should be treated .sexual. pain.  Cysts out of host. 5.  Stimulated by trypsin. crypts inflamed. b. •  . • Inability to absorb fat soluble substances. Inflammation of vaginal epithelium.4-4.  Excyst in SI. Diarrhea and malabsorption.string test. prostate. c. General characteristics Undulating membrane . Only pathogenic trichomonad. Transmission Direct contact . • Recover string and check it for trophs.asymptomatic.be careful. No cyst stage. steaterrhea (fat in feces).recurrent flagellum pulls plasma a. 2. avoid drinking water by beaver dams.   Treatment  Metronidazole (Flagyl) .  • Binary longitudinal fission. • itchiness. Villi shortened. Trichomonas 1.chlorination and sand filtration.  Treatment. d.  • Capsule with string. • pH goes up. Malabsorption. Entero-Test Capsule . Trichomonas vaginalis (Fig 5-9b) a. Female . hydrogen gas. end product = c. • Trichomonas vaginalis feeds on bacteria.  Campers .trichomonad vaginitis • Normal pH of vagina . • Lactic acid producing bacteria. No mitochondria. Hydrogenosomes . c.foul odor.involved in metabolism. leucorrhoea .increased mucus. optimal pH for T.urethra.  Ingested by next host. • Female . b. seminal vesicles. • Male .  4. membrane and cytoplasm away from cell body. duodenum and bile duct.  Trophs that move posteriad encyst in LI.  Cysts in feces. Pathology Male .live in SI. vaginalis is • ~5-6. Attach to epithelial cells with adhesive discs.5. • b.vagina and urethra. lesions. Life cycle Trophs . Diagnosis  Diarrhea .

underwear."mastigote" means "whip" and "a" means "no". Treatment Metronidazole. no A. Diagnosis Trophs • Females . towels.basal body that gives rise to flagellum. Contains DNA. mitochondrion of the organism.TRYPANOSOMA • Subphylum Mastigophora • All have flagellum • Order Kinetoplastida I.000 people/year. Kinetoplastids 1. Have a flagellum. Single-celled organisms.kissing. Kinetosome . flagellum.  NPP.organelle found within 3. d.secretions and in urine.human African trypanosomiasis 2. Indirect . HAT .  • • PROTOZOA . • Trichomonas tenax In mouth. B. NTD Estimated that they kill ~150. • Condoms. • C.  Direct contact .  May play a part in mitochondrial function and metamorphosis.  ~10% people worldwide.sharing utensils. • e.  II. • Males . Chagas' disease 3. • Kinetosome and kinetoplast are usually in close proximity to each • other. 3 major human infections 1. Promastigote .can live for several hours in drinking water. Kinetoplastid infections A. 2. All have a kinetoplast (kinetoplastid) .vaginal smears and in urine.3.  Indirect . Leishmaniasis B.  Trophs . 4 morphological forms Amastigote (LD body) . Newborns.

Metacyclic III.  o Trypanosome brucei: 3 subspecies Morphologically indistinguishable. • .  Blunt.  Ingested by Glossina. posterior end multiply by binary fission.  Then metacyclic tryps. commonly known as the tsetse fly .  Inside the fly.  Slender tryps in blood. Stumpy 3. • o Glossina .used for locomotion and attachment. Life cycle Glossina injects metacyclic tryps. 1. • IV. waiting to be picked up.  Stumpy tryps do not multiply.Nucleus posterior to kinetosome/kinetoplast. turns into an epinastigote. Section Stercoraria (posterior station development) Parasite will develop in the vector's hindgut. • C." "Meat cleaver" cell in wing. Long."fly destructive to cattle. Section Salivaria (anterior station development) Parasite will develop in the anterior part of the vector's digestive tract. • Flagellum . • Found only in insect vector and in culture. Section Salivaria o Trypanosoma brucei . • Vary in their host and in the pathology that they cause.differ biochemically and infectivity. o Introduction 1. slender 2. Trypomastigote (tryp) • 3 basic forms . • B. Trypanosoma A.vector is Glassina.vector for all 3 subspecies. Epimastigote Kinetosome and kinetoplast migrate posterior and pull flagellum with • it. D.

 Eventually tryps invade CNS.found to be effective in the early stages of infection. virulent form. • Arsenic-based drugss .  May be so severe that person lapses into a coma and dies from the infection. undergo paralysis and • eventually die.  British officer. .found in West and Central Africa. •  T. H.  Winter bottom's sign.S. Diagnosis .for later stages.  Becomes invasive much more quickly. 2. • Animals suffer from anemia and fever. Trypanosoma brucei brucei Causes a disease known as nagana. Insecticide .tryps in blood and cerebrospinal fluid.D. Tbr . Lymph nodes swell. brucei. Vector control.  Recognized by slave traders as a sign of death. G. days.  Usually no nervous disorders because host dies quickly after becoming infected (2-6 months). Distribution . Mass screenings of the population and treatment. 3.  Tryps invade the heart and other areas.in blood and lymph.  Multiply by binary fission.small sore that develops at the site of the bite. long-lasting.  Base of neck.  Acute. I. J. • Infects antelope and livestock.DDT. Tbg . Differences btween Tbg and Tbr 1.African Sleeping Sickness Caused by 2 subspecies of T.fly belt • area of continental U.East Africa.  Causes the chronic form of the disease. Treatment Suramin sodium .  May be asymptomatic for a year or two. E.human African trypanosomiasis .tropical Africa between 15N and 15S latitudes . 2. a. rhodesiense (Tbr) Similarities between Tbg and Tbr Chancre . b. • Control/Prevention 1. Development into slender tryps .  Mental dullness. 2.  Causes the host to die.  Native game reservoir hosts. Brucei gambiense (Tbg)  T. F. HAT . lasts 1-2 1.

 C. • They enter the cells and transform into amastigotes.irradiated. • No variable surface antigen. • As it's taking the blood meal. • ~1000 VSG genes.Panstrongylus megistus . lymphatics. temporarily unrecognizable.  3-4 generations of SIT and insecticide spraying. • Male Glossina . • Fecal droplet contains thousands of metacyclic tryps. K.  o Trypomastigote in blood Has a very pointed posterior end. Pathology • Continues indefinitely. V. Sterile insect technique (SIT). • Destroyed by circulating antibodies. which sterilizes them. tryps are • ingested by the vector (bug). o Life cycle Vector . • Most amastigotes invade other cells. Inside vector: • Epimastigotes .  <1% of tryps survive . it swells up and defecates on skin of host.takes a blood meal. Section Stercoraria o Trypanosoma cruzi. muscle.  Host mounts an effective immune response against tryps with a specific VSG.  Multiply by binary fission. •  Surface coat consists primarily of a single protein . . • Liver.variant surface glycoprotein (VSG). • Very large kinetoplast.multiply in midgut then move to hindgut. • Some amastigotes stay in blood and transform into tryps. • Each population is a variant antigenic type (VAT).b. Slender tryps . • Host cell lyses and amastigotes released.allows parasites to hide from the immune system. o Causes American Trypanosomiasis. Antigenic variation . also known as Chagas' Disease. • Metacyclic tryps enter host when host scratches or rubs the bite. low #'s of tryps in blood.specifically in blood.possess variant VSG. spleen.  Transform into metacyclic tryps.

 Romaria's sign . • Symptoms . intestine.  Toxins produced by amastigotes cause damage to the host.  40 vectors feed on patient. • Fatigue. Examine blood or tissue fluid. • Intestinal tract  Smooth muscle . Tryps in blood. • Eventually. • Muscle fails to contract.  Amastigotes in tissue.  Extracellular types . Chronic Seen most often in adults. houses.peristalsis is affected. D.death in 3-4 weeks. Acute Chagoma .  80% of cases in the heart. bone marrow.clumps of amastigotes found in the tissue. Vector control . Rural and poverty-stricken areas.  2. • Heart failure. • Heart  Nerves destroyed by neurotoxins.  Some are neurotoxins . then usually asymptomatic for many years.muscle.  Pseudocysts .affect conduction.  Edema of eyelid and conjunctiva. Megacolon . they live in hiding places. • Decreased pumping efficiency.local inflammation at the site of the bite. esophagus and colon lose tone. swollen glands.anemia.diameter of esophagus • increases.  2. fever. • Diagnosis 1. • At night. • During the day.  Heart and intestine. E.  2. Control 1. Lab-raised vectors. 3.present for only short time.  30-60 days later . Xenodiagnosis. muscle pain. weakness.has some effect on tryps and amastigotes.  Children .metacyclic tryps have entered the eye. If survive acute phase.  Long term decline in health. nervous disorders.squeeze bugs or dissect them and examine  for parasite. come out for blood meal. • .shielded. • Megaesophagus . • Muscle cells lose their ability to contract.diameter of colon increases. • In the trees. Chemotherapy Nifurtimox .  Intracellular amastigotes .1. • Difficulty swallowing and voiding.  Panstrongylous  Often underground. • Enlarged and flabby heart.main method.  Parasite spreads .

• Blood meal from infected host.LEISHMANIA & CILIATES I.  When sandfly takes its next blood meal. Introduction 1.3 organ transplant recipients who developed Chagas'  disease. Asia.  2001 . sandfly ingest amastigotes. Attaches to gut wall and goes through binary fission. and Northern Africa. C.  B. • Host cell ruptures and amastigotes are released. Many species Wide range of hosts. 2. In human. it clears out all of its  mouth part and infects the next host. Life cycle 1. Reproduces by binary fission.  Parasite inside a parasitophorous vacuole from host cell  membrane. Use bednets.risk in blood transfusions.3 cases from contaminated blood. Human (Table 6-1) Leishmaniasis.  Promastigotes move into mouth parts of sandfly and clog it up. pH very low. acidophilic.  U.  Metabolic activities are at an optimum between pH 4 • and 5. General term that encompasses a variety of different genera.  Transforms into amastigote. causes the spread of  the infection through the body.S. South America. • Primarily in the Genus Phlebotomus.  3.F.Americas were found. Europe.  One is found in the Old World . Mexico and South America. Leishmania A.  1989 .  Primarily in the Genus Lutzomyia.  Urban areas .sandfly. Reservoir hosts .what people knew of the world  before exploration. Parsitophorous vacuole fuses with lysosomes. patch up cracks in the house.  Worldwide. Distribution 15 x 10^6 cases in Western hemisphere. Phylum Sarcomastigophora Order Kinetoplastida  2. Vector . • New World . PROTOZOA .  Parasite moves into the gut of the sandfly and transforms into  promastigote.  Amastigotes invade nearby macrophages. use • insecticides. Promastigote enters macrophage by phagocytosis.5.

Espundia . Chiclero ulcers Mexico and Central America. the nose. • Sore enlarges. o Primary cause . • Amastigotes cannot grow at core body temperature. • Disfiguring scar. Mucocutaneous Leishmaniasis o Common in Western hemisphere. Visceral leishmaniasis. Different forms on secondary lesions. pinna. Treatment . develop immunity. o Life cycle Sandfly blood meal deposits promastigotes in skin.it will heal without treatment. • Secondary infections.  D. • Lesion on the ear. etc. Pathology 1. Mucocutaneous leishmaniasis. 2. • b. Cutaneous leishmaniasis.  Innoculate in less conspicuous location. Control very difficult. • o Diagnosis Look for amastigotes in margin of the lesion.Wild dogs. domestic dogs. Infection remains for years. • Self-limiting infection .for all Pentostam • II.Leishmania tropica. • Promastigotes engulfed by macrophages at the site of the bite.poorly vascularized and the immune • response is weak. 3. • a. Cutaneous Leishmaniasis o Mild skin disease. o Oriental sore.Leishmania braziliensis. o New World . around the lips.Leishmania mexicana. • Cartilage . pinna erodes. and rodents can be infected by the same • species that infect humans. o Old World . • III. • Nodule breaks open and amastigotes spread to macrophages in skin.areas where dry skin meets moist skin. • o Secondary lesions Formed by amastigotes that in macrophages at mucocutaneous • junctions of the skin . E. o Primary skin lesion that develops Forms at site of the bite. • Nodule forms on the skin.

 Bed nets. • Anemic.1903. V. • Spleen and bone marrow affected. immune deficiencies. Life cycle Broad host range . Eliminate reservoir hosts? F.  Protect humans against bites.  Immature macrophages. • Insect repellants. • Amastigotes . undergo compensatory macrophage • production to the detriment of RBC production. Leishmania . D.HIV co-infection.LD body. • Charles Donovan .  C. usually form secondary • pathogen.  Both decrease immune responses.  Emerging disease in many developing countries.  Bone marrow. • Nose affected. o 2 nuclei: Marconucleus . • Skin lesions spread and invade mucous membranes.  Insecticides .  Xenodiagnosis • E. ineffective.controls trophic activities . • B. • Long term infection . • William Leishman . Hepatosplenamegaly . anemia.cartilage of the nose and soft • palate erode. progressive wasting.Rainforests of Central and South America. • Long. • IV. Phylum Ciliophora o Possess cilia in at least one stage of life cycle. Diagnosis Amastigotes in tissues. Control strategies Vector control • Sandflies have a short flight range. chronic. • Amastigotes throughout the body and inside macrophages.inside homes.1900. .  Spleen puncture. Visceral Leishmaniasis A.  Clothing. Pathology Fever.  Emaciated. Larynx and trachea .infects humans and canid and felid reservoir hosts.  Fly screens.destroy voice. • Death 2-3 years after infection if untreated.  Flies use low growing bushes as resting spots.  Opportunistic infection. Leishmania donovani Kala azar.normal everyday body • functions. • Blood/nasal smears.  3.enlarged liver and spleen.

osmoregulatory ability. also infects pigs (reservoir host).  Hemorrhage . Treatment Metronidazole.  Secondary foci in liver and lungs.Micronucleus . D. • Balantidium coli is the only type that infects humans. Can produce hyaluronidase . Peristome .  Peritonitis.  Causes flask-shaped ulcer.  Trophs are ingesting starch and cellular debri. Control Sanitation.  Secondary bacterial infection. Cytopyge .diarrhea and dysentery. Perforation of LI. Pathology 1. Largest protozoan parasite in humans. intestinal epithelium. • E. • o Trophozoite Lives in LI of host and reproduces by binary fission.  Necrosis and sloughing of tissue.enzyme that starts to ingest the host 2.actual area on cell membrane where all food  material is ingested.  • Leads into the cytostome. Cyst Encystment stimulated by dehydration of feces. not causing any tissue damage. Many cases are asymptomatic.  Bilantidial dysentery.  B. they are carriers. • C.site on membrane through which wastes are  eliminated.controls reproductive functions. Cytostome . • Thousands of cilia on its surface • o 2 contractile vacuoles . • Excysts in SI and then migrates to LI. • Unique among parasitic protozoa. • . 3. • Transmission stage.lined with coarse cilia. • Infects next host.  Death.

" • 4 species of Plasmodium that infect humans. B.mostly children. Secretions from apical complex. • Swamps and fever. Complex life cycles. • b. Exoerythrocytic cycle. 3. 5. Rhoptries and micronemes Secretory organelles. Circumsporozoite protein on surface of sporozoite. Conoid and subpellicular . Vertebrate phase 1. Sporozoites in bloodstream. • ~2 x 10^6 deaths/year .  Plasmodium malariae.  Probes skin for a capillary. 3.  Plasmodium falciparum. prevents clotting. • Penetrating host cells.  Plasmodium ovale. • 500 x 10^6 infected. Life cycle A. 2. • "Mal" is "bad" and "aria" is "air. Infected female Anopholes species mosquito takes a blood meal.structural microtubules. Overview B. 2. Apical complex a.PROTOZOA . Phylum Apicomplexa A. Characteristics 1. 4. • Plasmodium vivax. .  Binds specifically to receptors on hepatocytes.MALARIA I I.  Injects salivary gland secretions. Plasmodium Malaria.  Sporozoites injected.  II. penetrate liver cell. All parasitic.

Merozoite surface protein-1 (MSP-1) . Secretions from apical complex. Host cell ruptures and merozoites and their waste products are  released. Merozoite pushes in and forms a parasitophorous vacuole. 10.  Transforms into trophozoite. Merozoites produced.asexual reproduction.proteins bind specifically  to proteins on RBC surface. 8.  Signet ring stage. Into blood. 9. Begins schizogony . a. schizont cryptozoite. large food vacuole forms. Numerous daughter nuclei formed. Mature merozoites. Cytoplasm divides. Merozoites burst out of hepatocytes. 12. the troph is mature. end product of digestion of host  hemoglobin.  14. Merozoites invade other RBC's. Apical complex orients toward the RBC membrane. erythrocytic cycle.  15.6. Hemozoin becomes apparent.  Trophozoite grows and food vacuole becomes less noticeable. 16. Segmenter . 13. merozoites develop at the  same time. Random interaction between merozoite and RBC. Schizogony Blood schizont with numerous nuclei. Feeds on host cell cytoplasm. 7. Synchrony .parasite when it has undergone cytoplasmic division.in an infected individual.  11.    Metamorphoses into trophozoite. After ~1 week. Ingests host cell cytoplasm. invades RBC. b. .

Release from host cells is synchronous.  Massive release of merozoites and waste products.  Stimulates host response; fever and chills.  Periodicity of symptoms.  17. Some merozoites enter RBC and develop into either macrogametocytes or miccrogametocytes. Ingested by mosquito. 

PROTOZOA - MALARIA II
1. Invertebrate phase o Genus Anopheles - mosquito. o Gametocytes are released from RBC's in stomach. 1. Macrogametocyte Shift of nucleus leads to a macrogamete (can be considered the  female). 2. Microgametocyte Undergoes considerable development - exflagellation - nucleus  divides and forms 8 daughter nuclei. Each daughter nuclei develops its own flagellum. • These 8 flagellated nuclei break apart. •

o o

Stimuli for exflagellation: • Decreased temperature. • Increased pH - dissolved CO2 from RBC's in the mosquito stomach. Microgamete swims and will fertilize the macrogamete. Ookinete - mobile stage. Penetration through the stomach wall.  Attaches on the hemocoel side of the wall.  

2.

Oocyst Nucleus divides - results in sporoblasts.  Sporoblasts develop into sporozoites.  • >10,000 sporozoites in oocyst. o Sporozoites break out of the oocyst and migrate through the body to the salivary glands. o Infected mosquitoes feed more frequently; PITT. Plasmodium vivax o

3.

o Characteristics 1. Sporozoites Short-prepatent - when the parasite is in the liver but the  person has no symptoms. Invade hepatocytes. • Develop into merozoites, which leave the hepatocytes • and then invade RBC's. Long-prepatent  Invade hepatocytes. • Develop into merozoites. • Rather than leaving the hepatocytes, they stay there. • Hypnozoites. • Relapse - vivax malaria infection; recovers. • Recurrence of the disease following initial • infection do to hypnozoites. Hypnozoites escape hepatocytes. • Erythrocytic cycle. • 2. Merozoites Can only penetrate RBC's with a Duffy antigen - receptor site on  the surface of the RBC, function unclear. Duffy antigens act as specific receptor sites on the RBC • surface If the Fy^a or Fy^b Duffy antigen are present, the • merozoite can penetrate. If Fy (Duffy negative), that means there are no receptors • and the merozoite cannot penetrate. Resistance to vivax malaria. • Fy genotype is present in ~90% of West African • natives and ~70% African Americans. 3. Trophozoites RBC enlarges.  RBC develops stippling - dots caused by the development of  little invaginations on the surface; Schuffner's dots. 4. Fevers - occur every 48 hours. Plasmodium malariae o Fever - every 72 hours. o Ring stage - when mature, it elongates; band form.

4.

3. Recrudescence Let's say you are infected and you recover. • Many years later, you are sick again even though you have not been • infected again. Due to a sudden increase in a persistent low-level parasite population • in the blood. Transfusion malaria possible. • Plasmodium ovale

o Very rare. o Fevers - every 48 hours; mild. o Mature schizont and RBC are oval in shape.

5.

Plasmodium falciparum o Most common. 1. Morphology Ring stage • Very small.  Multiple infections - more than one ring stage inside a single  RBC. Characterized by an applique form - appears that ring stage is  attached to the RBC membrane.

2.

Infected RBC - develops irregular blotches - Maurer's clefts.  Gametocytes Crescent shape - stretches out the RBC. 

2. Early ring stages and gametocytes in blood smears. After invasion of RBC, troph produces proteins deposited in RBC • membrane.

Knob proteins bind to glycoproteins in endothelium of capillaries.

Infected RBC's are sequestered in capillaries. • 3. Falciparum pathology Fevers - every 48 hours; severe. •

6. Species P. vivax

Cerebral malaria Sticky RBCs (knobs) blocking capillaries.  Tissues don't receive the oxygen that they need; hypoxia.  Headaches --> coma --> high temperatures --> convulsions -->  death. 3. Blackwater Fever Caused by an acute, massive lysis of RBC's (infected and  uninfected). High levels of hemoglobin and hemozoin in blood.  Kidney function impaired; urine becomes really dark and can  lead to kidney failure. Autoimmune problem.  Difference in pathology? Type of RBC Level of Parasitemia Young <1% <1% <1% 5-50%

P. malariae Old P. ovale P. falciparum 7. Young All

Arms Race o Sickle Cell Disease In the Beta-chain of hemoglobin, one of the glutamic acids is replaced • by valine. Sickle cell hemoglobin is normal until stressed by low oxygen levels. • Sickle shape loses flexibility. • Blockage of capillaries decreases oxygen carrying capacity. • Reluctance to release oxygen. •

• •

Heterozygous - NS. Sickle gene - incompletely recessive; some sickle Hb produced.  ~60% RBC's normal, ~40% sickle for example.  If infected with P. falciparum, 80-90% protection against  Falciparum malaria. Sickle HB - needle-like and mechanically destroys parasite.  Level of parasitemia is ~1% of the RBC's; similar to the other  three species. Homozygous - NN. You will die from P. falciparum.  Homozygous - SS.

Effective against the liver stage. Vaccine A. no longer recommended for use. Developed a vaccine called PfSPZ.  Immunity o Antibodies. heterozygote advantage.  The other component is a partner drug. 9. • Acts against blood schizonts. MD. Maintains both alleles in the population. • o In areas where there is year-round exposure to malaria. Die from sickle cell disease. • Most common are artesuate and artemether.  Paranoia. 10.  Anxiety.  Aggression. • Adverse CNS events associated with use.  Insomnia.  D. • Normally there is a heme polymerase (parasite enzyme). • Reduces the selection of any resistant mutants. o Children are very vulnerable to malaria.  Birth defects. Mefloquine (common name Lariam) Introduced in 1984. Sanaria .  Antimalarial drugs 1.resistance to superinfection. Pyrimethamine Inhibits dihydrofolate reductase.  Drugs with different modes of action.  Lack of cross-protection between strains of the same species. • Nightmares. Lack of cross-protection between species. o Premunition . Most targets are circumsporozoite protein.  NS genotype is the preferable one.8. • Heme (toxic) converts to hemozoin (non-toxic). a parasite enzyme required for folic • acid synthesis. Problems: • Circumsporozoites proteins spend only a short time in the  blood.  Drug blocks heme polymerase and parasite dies from increased heme. • C. Works as long person maintains a low parasite population.  Seizures. • Irradiate infected mosquitoes and then harvest the whole parasite and • incorporate it into a vaccine. • 2. infants still breastfeeding are protected by maternal antibodies. ACT (Artemisinin-based combination therapies) Combines several antimalarial drugs. • .  B.company located in Rockville. • One is a derivative of artemisinin from Artemesia annua plant.  Severe depression. • Resistance has developed. • Example: mefloquine. Chloroquine Builds up inside the parasite's food vacuole.

the bacteria. 13. Economic burden o Every 30 seconds it is estimated that a child dies from malaria.Gambusia affinis feed on mosquito larva. Henry Heimlich o Idea of using malaria to cure AIDS and other diseases. .ecotoxicity. ~3 weeks. • Malaria used to induce high fevers. Insecticides DDT . • This would kill the syphilis. • Example: Asia. • Treat malaria with drugs. • Dr. • Problem . kind of disproves this idea. • Dams and irrigation systems. o Increase in incidence of malaria. Mosquito predators.  Found that DDT is more toxic to wasps than to thatch bugs. • Decrease in public health systems. 12. malaria/HIV co-infection is common.  destruction of thatched roofs. Example: fish .  Thatch bugs destroy thatch.kills thatch bugs.malaria was used to treat neurosyphilis.11.introduced species. and the drugs will treat malaria.  C. Mosquito control A. Destruction of breeding sites. • Drug and insecticide resistance. Let the fevers go for about 10-12 rounds. o Malariotherapy 1918-1975 . • Wasp . • o In Africa. • Idea is that the fevers will kill HIV. • o Heimlich says that the fevers will kill HIV. B. Population movement. o Causes billions of dollars of damage to economies. • Homes with thatched roofs.

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