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Introduction to Parasitology

Introduction to Parasitology

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Introduction

Parasitology is the study of pathogenic parasites and their relationships to the hosts and environment.

The relationship between two living things is called Symbiosis. In symbiosis two living things live together and involve protection or other advantages to one or both partner. Three types of symbiotic relation ship:  

Commensalisms Mutualism Parasitism

Commensalism: Both partners are able to lead independent lives, but the commensal may gain advantage from the association when they are together and least not damage to the other( host). E.g. Entampeba gingivalis obtain bacteria , dead cells and food
from the mouth of man and man is not harmed.

Mutualism: An association which is beneficial to both living things
E. g. A selection of ciliates from the rumen. The rumen contains enormous numbers of ciliates that break down cellulose in the feed.

What is parasitism? Parasitism is the ecological association of two different organisms in which one organism ( the parasite) benefits and the other organism ( the host) harmed.  .  A parasite is metabolically dependent on its host.

What are parasites? Parasites are organisms that obtain food and shelter by living on or within another organism.  .  The parasite obtain all benefits from the host and the host may either be harmed or suffered .

• E. Lice.g. Tape worm.  Endoparasites: The parasites that live inside the body of the host. Mites. mosquitoes etc. Flee. E. Ascaris etc . ticks.Types of parasites  Parasites are divided into two types:  Ectoparasites: The parasites that live on the body surface of the host.g.

g. Facultative parasites: parasites that can live in a host as well as in free form. . ascaris 2.Based on the degree of association there are several categories of parasites 1. E. Obligate parasites: parasites that live only in the host.1.g. Neigleria fowleria ( free living amoeba) can couse primary amoebic meningocephalitis ( PAM) if they enter through the nose during swimming or diving . Facultative parasites are capable of becoming as parasites if the opportunity arises. E. Tape worm.

E.g. 2. Certain larvae of latrin fly ( Fannia scalaris) if they enter the ear of the man , they become parasite.

3. Incidental ( Accidental parasites): Such parasites accidentally find a host and they become parasites. E.g. Echinococcus
granulosus.

4. Erratic parasites:- parasites that wonder in to another organ from where it normally foung

5. Periodic ( sporadic ) parasites: parasites that visit their host occasionally. E. g. Bites of mosquito, bedbug

6. Pathogenic parasites: parasites that cause harm to the host. E.g. Trypanasaoma.
Plasmodium

7.Opportunistic Parasites: parasites that donot cause harm to the host under normal condirtions but can cause harm under certain conditions. E.g. Candidia albicans ( yeast) is a
normal flora in healthy man but a pathogen in immune suppresd individuals.

Intermediate host : The host harboring the larvae or asexual stage of parasite.  .  Final (definitive )host : The host harboring adult or sexual stage of parasite.Host and type of host Host: An organism that harbors the parasite usually larger than the parasite.

 Reservoir hosts :  Animals harboring the parasites as man and ensure continuity of the parasite life cycle. House fly is a vector for amoeba. Hyrax is a reservoir host for leishmania  Paratenic hosts ( mechanical vectors) are hosts which act as transporting agent for the parasite and in which the parasite does not undergo any development • E.g. cholera bacteria .g.  Potential sources of human infection • E.

Yellow Fever.g..g.. brucellosis  Cyclozoonoses  non-human vertebrate 1 → non-human vertebrate 2 → human → non-human vertebrate 1  e. Echinococcus tapeworm  Metazoonoses  vertebrate ↔ invertebrate ↔ human  e.Animals Reservoirs (Zoonoses)  Direct zoonoses  non-human vertebrate ↔ human  e. plague  Saprozoonoses  vertebrate ↔ inanimate ↔ human  e. Valley fever (coccidiomycosis) . Lyme.. rabies.g.g.

Scope of Parasitology Parasites include bacteria. helminthes and arthropods. fungi.  Animal parasites traditionally deals with protozoa and helminthes which have public health and veterinary importance.  . viruses. protozoa.

Parasitic diseases Prevention Transmission Treatment Scope of Parasitology Parasitology Diagnosis Pathogenesis Parasites Life Cycle Morphology .

Important Groups of Human Parasites Helminthes  Nematode  Trematod  Cestode Protozoa • Amoeba • Flagellate • Sporidium • Ciliate Arthropoda • Mosquito • Fly • Tick • Mite • Bug • Flea • Lice .

protozoa. Many of these parasites are causative agents of major public health problems of the world. trematoda.  .Why do we study parasites?  Humans are hosts to over 3200 species of parasites in the four major categories. cestoda and nematoda.

Poor nutrition leads to reduced resistance High calorie demand (malaria = 5.000cal/day) • • • • • • •  Veterinary importance  Economic importance .Why do we study parasites? • parasites provide unique examples of biological phenomena not found in freeliving organisms Medical importance 15 million children in the world will die each year from a combination of malnutrition and infectious diseases 4.5 billion helminthes infections Estimated 60 million people die every year More than half of the deaths are children under the age of 5.

000 20.000 Deaths per year Roundworm( Ascaris lumbricoides) Hookworms Whipworm (Trichuris trichiura) Filarial worms Malaria Schistosomes Ameba Entamoeba histolytica Liver fluke Clonorchis sinensis Chagas’ Disease Trypanosoma cruzi . Human Infections 4.2billion >900 million 657 million 300.660 million 200 million 50 million 20-30 million 15 million 60.4 billion 1.5 billion 1.Disease Category All helminthes Recent estimates of prevalence of parasites in the world are: No.000 50.000 ? 43.000 to 50.000 – 50.5 -2 million 40.000 1-2 million 0.000 20.000 – 60.

Plasmodium .g.  • Both physical and biological changes occur in the parasite.E. development and multiplication that may be accomplished in their host (or hosts) or environment The direct life cycle: Only one host (no intermediate host).Life cycle and type of life cycle The parasitic life cycle is the obligatory of parasites for their growth.  The indirect life cycle : Life cycle with more than one host (intermediate host and final host).

Migration and localization Stage in man (pathogenicity treatment and diagnosis) Stool Urine Bronchial Secretion Vector Stage left man (diagnosis) Mouth Contact Vector Infective stage (Pathogenicity and Prophylaxis) Stage in environment (vector) (Epidemiology and Prophylaxis) .

is a person who carries a certain parasite without displaying any sign or symptom of diseases acting the source of infection  Carrier  Carrier . Infective stage A stage of parasite which can enter the human body and develop continuously there.

Effects of parasites on the host 1. Effect related to food •Parasite sucking of blood E. Ascaris •Obstruction of lymphatic system E.g. Hookworm Suck blood Anemia •Parasite feeding on nutrients •Parasite compete with host for food •Deprive essential substances of the host ( VitB12 by fish tapeworm) 2. bile duct .Mechanical effects of parasites on the host •Obstruction of intestine . Filarial •Destruction of host cells by growing in them E.E.g.g.g. Plasmodium .

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Lymphatic filariasis  128 million infected .

Toxic and allergy effect • E.Mosquito • Tse-tse fly Plasmodium Trypanasoma .g.g Anaphylaxix 4.Pathogen Introduction • E.g Proteolytic enzyme Necrosis • Parasite antigen Immune system E.3.

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soil. insect vector and so on  Source of infection patient. . carrier and reservoir host  Susceptible population People except those will special background are all susceptible to parasitic infection. air.Epidemiology Epidemiology includes: Transmission route water. food.

Terminology  The establishment of the parasite in its host is called Infection. • A stage of parasite which can enter the human body and develop continuously there is called infective stage. Infectious disease = infection + illness   All infections are silent at least at some point  Infection ≠ Disease .

E. water. Ingestion of raw or under cooked meat.Routs of transmission The infective stage are transmitted by: 1. fish and water plant 2. Congenital transmission : From mother to infant. vegetables contaminated by infective stage. Contact transmission • • Direct contact---Trichomonas vaginalis Indirect contact---Ascaris lumbricodes .g. Oral rout: • • Ingestion of food. Toxoplasmosis 3.

4. Inoculation by arthropod vectors: • E.g. -Wuchereria banchrofti -Plasmodium E.Larvae of Strongeloides 5.g. Penetration of skin and muscle membrane • . -Larvae of hookworm .

 Pathogenesis depends on the interaction of host and parasitic factors.Pathogenesis and pathology Pathogenesis is production or development of diseases.  .

 Immune status of the host  Immune response to parasitic infection  Presence or absence of co-existing diseases and other physiological conditions such as pregnancy.  Age and level of immunity . The host factors are  Natural status of the host( Genetic factor).

. Parasitic factors are Site of attachment of the parasite Size of the parasite Number of parasites Parasite strain Growth. development and multiplication of parasites and their metabolic process.

C. . quite susceptible population. Epidemic level of transmission: sudden out break . Endemic level of transmission: stable level of transmission B. high mortality and morbidity.Level of transmission of parasites. A. Sporadic level of transmission: lowest level of transmission( rare transmission).

species of parasites and vectors system. profession. .Epidemiological factors  Natural factors  Climate. ethnic group  Socio-economic factors  Social  Individual factors  Sex. life condition and mode. geography. economic situation. hygienic condition age.

The resistance of the host body against infection or the effect of infection is known as Immunity. There are two arms of immunity  Innate ( non-specific)immunity  Adaptive ( Specific) immunity .Effects of the host on the parasites The host can produce certain degree resistance to parasites in human body or re-infection.

Non specific( Innate) immunity It is the capacity of the body to eliminate foreign invaders not previously encountered. • It is inborn • It is first line defense • Not learned • Under genetic control • Concerned with the survival .

Skin/Mucous membrance/Placenta. B. Physical barrier : Prevent parasites to invade in certain degree.Protection is by:A. Cellular elements: Phagocytes( macrophages. neutrophils. lactic acid in genital organs can cause damage of the parasites. . Surface chemical secretions:. saliva and tear: HCl acid in the stomach. eosinophilis and monocytes) remove debris and parasites. C.Lysozyme in mucus.

complement proteins and enzymes at the site of infection. • Phagocytes ingest and kill the invaders • The complement proteins attack the membrane of invading parasites. Complement system: different proteins ( C1-C9) which attack and break down cell membrane of the parasites. Inflammatory response: the accumulation of phagocytes. E. . Cytokines ( monokines) :-synthesized by monocytes and lymphocytes that increase resistance of cell to infection. F.D.

H. accelerates repairs and inhibits pathogens. But not very strong! .G. Lactobacillus in genital organs  Non-specific/effective against a wide range of parasitic infection/controlled by genetical factors.g. Fever: body temperature rises to mobilize defenses. Normal micro-flora: non-pathogenic ( commensals) micro-flora inhibit the growth of pathogenic organisms • E.

Specific/ acquired/ adaptive immunity It is specific immune response to a particular antigen previously encountered by the body. • • • • • It is second line defense There is memory of the initial specific response Not inheritable Concerned with the survival of individuals Rapid and large response cellular and humoral immunity. Resistance mechanism : • • .

The cellular responses: is mediated by Bcells and T. IgD.cells  Humeral responses: it mediated by the production of specific antibodies ( immunoglobulins such as IgA. IgE. IgG and IgM)  .

but not completely. Rare!  Non-sterilizing immunity : Wipe out most of the parasites.Sterilizing immunity : Wipe out the parasites completely. meanwhile get a long-term specific resistance to reinfection. Common! No parasite. no immunity!  .

Infection and Immunity Balance infection immunity Disease = Bolus of infection x virulence immunity .

1.Diagnosis Methods of parasites. Microscopic Examination of body fluids and excreta  Body fluids include: • • • • • • • • • Blood Lymph CSF Sputum Urine Feces Urethral/ vaginal discharges Peritoneal ( anal) swabs Aspiration .

Animal inoculation 4. Serological ( immunological test) • Enzyme linked Immuno-sorbent assay ( ELISA) • Direct agglutination test ( DAT) • Fluorescence Antibody test ( FAT) . Histology 5. Skin test ( hypersensitivity test) 6. Microscopic examination of flesh tissue specimens 3.2.

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ELISA plate .

II. Protozoan parasites .

There are over 450. 000 species are parasitic to various animals. Sporozoa .  Protozoan are classified into 4 groups:   i. Mastigofora ( Flagellates)  Iii. Cilates  Iv. sarcodina ( amoeba)  ii.000 species of protozoa and of these about 10.

etc  Intestinal and luminal protozoa significant to human health include   Entamoeba histolytica ( Amoeba)  Balantidium coli ( Ciliates)  Gardia lamblia ( Flagellates)  Trichonomonas vaginalis (Flagellates)  Cryptosporodium parvum ( Sporozoa)=zoonotic  Isospora belli ( Sporozoa) = zonotic and oportunistic . genital canals.Intestinal and luminal Protozoa Intestinal and luminal protozoa harbor intestine. mouth.

al. dogs. subtropical. warm temperate areas. other tissues Epidemiology: Distribution worldwide: tropical. if invasive may inhabit liver.  . histolytica causes a disease called amoebiasis ( amoebic dysentery and amoebic hepatitis) Habitat: Trophozoite in caecum/colon. sanitation dependent Reservoir includes monkeys.Entamoeba histolytica E. et. lungs. pigs.

dogs and rodents may also be infected.000 deaths each yea number of outbreaks have resulted from a breakdown in sanitation Ethiopia infection is 10% to 45% and most common in children. histolytica it is estimated that up to 500 million people may be affected  may a  cause up to 100. About 5 to 50 m% of the population world wide harbor E. .  In Human is the principal host but cats.

finely granular endoplasm. rapid movement - - .cytoplasm consists of clear ectoplasm.   Morphology: Entamoeba histolytica has 2 stages TROPHOZOITE . stained specimens .20 to 30 µm in diameter. food vacuoles often containing red blood cells are common characteristic structure is the single nucleus with one endosome: living specimens show active.

Entamoeba histolytica trophozoites .

• precyst secretes cyst wall to form the round cyst . CYST . histolytica cysts are spherical • The cytoplasm contains dark staining chromatid bodies and 1 to 4 nuclei.10 to 20 µ m in diameter • nuclear division begins after encystment: . .E.

Entamoeba histolytica cysts uninucleate cyst binucleate cyst .

Entamoeba histolytica cysts quadrinucleate or mature cysts – diagnostic in feces .

The metacyst divides into four and then eight amoebae which move to the large intestine.  . The cyst is resistant to the gastric environment and passes into small intestine where it decysts.Life Cycle:     Infection occurs by ingestion of cysts on fecally contaminated food or hands. with larger bolus of infection. There are no intermediate or reservoir hosts. The majority of the organisms are passed out of the body with the feces but. some amebae attach to and invade the mucosal tissue forming "flask-shaped" lesions (bomb craters).

Amoeba sp. life cycle .

become infective .In the feces we find : • • • Trophozoite – rapidly destroyed. if ingested they are destroyed by gastric juice Immature cyst ( 1 or 2) – become matured and infecive Mature cyst ( 4 nuclei).

Acute amoebic dysentery: • • •  Frequent dysentery with necrotic mucosa and abdominal pain ( tenesmus). Chronic and asymptomatic amoebiasis:  Recurrent episodes of dysentery with blood and mucus in the feces. Last for few days Trophozoite in feces 2.Symptoms: has three stages  1.  There are intervening gastrointestinal disturbances and constipation. .  Cysts are found in the stool.

pneumonitis. pseudo-polyps. stricture granuloma. Strictures and pseudo-polyps result from the host inflammatory response . lung and brain where it produces abscesses that result in liver dysfunction. sometimes brain. perforation. lung and spleen abscesses can also occur. The infection may result in appendicitis.3. liver abscess . and encephalitis Pathology: Intestinal ulcers (craters/flasks ) are due to enzymatic degradation of tissue. Extra-intestinal amoebiasis: • The organism may invade the liver.

Sites affected in amoebiasis Lungs Subphrenic abscess Diaphragm Liver Portal circulation Skin Pericardium Peritoneum Stomach Intestine Inferior venacava Brain General circulation Spleen Suprarenal Kidney Peritoneum Primary infection in colon Perianal skin Genitals .

Diagram of pathology from text on page 112 Shows movement of trophozoites from large intestine to lungs via hepatic portal vein Liver abscess .

EXTRA-INTESTINAL LESIONS occur in 3 ECTOPIC SITES A. HEPATIC AMEBIASIS B. PULMONARY AMEBIASIS C.Entamoeba histolytica pathology 3. CEREBRAL AMEBIASIS .

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FAT •Radiological test •Culture .DIAGNOSIS : •Microscopic identification of cysts and trophozoites in fecal samples •Serological examinations such as ELISA.

Treatment: • Metrnidazole – for symptomatic and asymptomatic amoebiasis • Iodoquinol Prevaention and control: • • • • Sanitation Personal hygiene Safe water supply chemotherapy .

. Acanthamoeba spps.pathogenic intestinal and luminal amoeba Entamoeba harmoni Entamoeba coli Entamoeba gingivalis Iodoamoeba butschlii Endolimax nana Dientamoeba fragilis Free living Naegleria spps.Non.

•Prevalence in tropics may be up to 100% .Non-pathogenic Amebae Entamoeba coli •Very common in the large intestine of man. histolytica but is commensal •Cosmopolitan in its distribution. •Often co-exists with E.

granular endoplasm is coarser than E. 1.nucleus: contains large karyosome. . does not invade tissue and it never contains RBC. . .20 to 30 µ m in diameter which is the largest amoeba in the large intestine of man.lives in large intestine and feeds on bacteria and any other cells available to it.Entamoeba coli life cycle stages TROPHOZOITE . histolytica .

mature cyst is large.immature cysts are rare in fecal smears .Entamoeba coli life cycle stages 2. have splinter-like ends (disappear in most cysts) .encystment is similar to that of E. histolytica .chromatoidal bodies. if present. has eight nuclei .cyst is released in the feces into the external environment . 10 to 33 µ m. CYST .

Entamoeba coli life cycle .

Endolimax nana Habitat: Large intestine Hosts: It is common amoeba of pigs . Epidemiology: Cosmopolitan . humans and other primates but it is pathogenic to human.

Endolimax nana 2 stages in the life cycle: 1.cytoplasm contains bacteria . 6 .nucleus is very minute. .small in size.moves slowly. TROPHOZOITE . feeds on bacteria and food debris .15 µm (usually under 10 µ m) .

importance of human infection: Endolimax nana .2.small in size (5 .forms as feces dehydrates .14 µ m) .contains four nuclei with large endosomes . CYST .

Endolimax nana life cycle .

buetschlii .Hosts: It is the most common amoeba of pigs and also found in humans and other primates Habitat: Large intestine Pathology: Non pathogenic to humans Distribution: Cosmopolitan Prevalence in world is 4 to 8 % (much less than E. coli & Endolimax) Iodamoeba bütschlii = I.

1. TROPHOZOITE - 9 to 20 µ m in diameter - The nucleus is relatively big ( 2μm to 3.5 μm in diameter). - feed on bacteria and yeast; do not invade tissue

2. CYST - 6 to 15 µ m in diameter - large nucleus with large endosome and lightly-stained granules - large irregular round karyosome(appears clear) in cytoplasm - stains deeply with iodine; hence, the genus name Iodoamoeba.

Iodamoeba bütschlii life cycle

histolytica except it is SMALLER IN SIZE .Entamoeba hartmanni Originally thought to be a "small race" of E.9 µ m in diameter and contain 4 nuclei Importance: Misdiagnosed as E. hartmanni is nearly identical to E. histolytica .15 µ m in diameter . It is non pathogenic The morphology of E. histolytica.nuclear structure is similar (endosome in center) but peripheral chromatin is more irregular . it is now considered to be a separate species.cysts are 5 .trophozoites are typically 12 .

histolytica.Entamoeba dispar 1993 E. histolytica but does not invade tissue so is nonpathogenic. dispar was proposed as the name for non-pathogenic E. Substantial biochemical and molecular data has been accumulated showing that the non-pathogenic isolates of E. histolytica are genetically distinct from the pathogenic isolates Identical to E. .

bacteria. •Organisms are more common in persons with pyorrhea (gum disease) but they are not the cause of the condition. . •Trophozoite lives on the surface of teeth and gums. •Parasites feed on epithelial cells of the mouth. and other cells available to them.Entamoeba gingivalis Habatit: In the mouth in the margins of the gum and is abundant in unhygienic mouth Hosts: Humans •Prevalence is from 50 to 95%. Transmission: The infection is transmitted from person to person by saliva from the mouth of an infected person during the act of kissing. •It has only a trophozoite stage. food debris.

Facultative Amebae Facultative amebae are normal inhabitants of soil and water where they feed on bacteria. Three are able to infect humans: Naegleria fowleri Acanthamoeba spp . A few members have the ability to become parasitic when an opportunity to enter a vertebrate exists.

all others were fatal!  . fulminant and rapidly fatal infection of the CNS.Naegleria fowleri This ameba is responsible for over 200 cases of primary amoebic meningoencephalitis ( PAM)  PAM is an acute .  Only 7 cases were successfully treated.

Trophozoites can occur as an ameboid form or a flagellated form in freshwater. All victims have had a history of swimming in fresh brackish water a few days before the onset of symptoms . Flagellated trophozoites enter the nasal passages when a victim swims or dives into freshwater. Parasite can form a cyst in dry periods.

•N. Fowleri has three stages in its life cycle: •Cyst form ( resist unfavorable conditions of the environment) •An amoeboid trphozoite form( feeding. growing. replicating form in water and mud) •Flagellate form ( infective stage) Once it enters a human. the parasites always revert to the ameboid form. .

Naegleria fowleri pathology •After entering the nose and nasal cavities. •Death usually occurs in a week. the trophozoites migrate along the olfactory nerve to the brain. fever. neck rigidity. and mental confusion followed by coma and death. . •Symptoms include a headache. •Ameboid trophozoites multiply rapidly by binary fission in the brain and cause PAM •The incubation period is 2 days to 2 weeks.

DIAGNOSIS – most cases have been diagnosed from serebro spinal fluid by identification of large numbers of amoebae in the brain tissues . -Cyst are never seen .Disease is so rare and the brain tissue destruction is so rapid that diagnosis is seldom made in time .Look for trophozoites each with a nucleus and vacuole.

Treatment – the drug Amphotericin B has been successful in the treatment of only 7 cases .

structure: .Acanthamoeba spp. Trophozoites occur only as ameboid forms: . Free-living trophozoites and cysts occur in both the soil and freshwater. At least 5 species of Acanthamoeba have been identified in human tissues.

Infection of the eye in the healthy person (inflammation and opacity of the cornea). Granulomatous amebic meningoencephalitis ( GAE) Disease was much more chronic in infected patients.Acanthamoeba spp. 2. Infection of the lungs and skin in the immunocompromised hosts including AIDS or debilitated persons. . Infection can be acquired by • • • Inhalation of dried cyst Ingestion of cyst Through traumatized skin or eyes from contaminated water. Most resulted in death in a few months. pathology These species cause 3 pathological effects: 1. 3.

Treatment: No effective therapy is available for the treatment. .Most of these ocular infections were in contact lens wearers who used home-made saline Diagnosis by identifying amebae in corneal scrapings Drug treatment has been successful in most cases.

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.  Free living Amoeba as carriers • Some free living water amoeba may sometimes harbor pathogenic bacteria such as Legionella. Other medical importance of free living amoeba  Free living amoeba as allergens • Negleria and Acanthamoeba have been claimed to be responsible for allergic pneumonitis due to inhalation of amoebic antigens derived from amoeba growing in the humidifiers of air conditioning plants. Pseudomonas and Cholera vibrios.

• only 2 survivals • easily misidentified so some of the cases of granulomatous amebic meningoencephalitis caused by Acanthamoeba may well have been caused by Balamuthia .New facultative ameba recently identified A new freshwater ameba called Balamuthia has been incriminated is some 80 cases of amebic meningoencephalitis in humans since 2001.

2 million cases estimated  • • About 5% of gardiasis is food born and the other 95% is water born children under 5 and mothers with young children have the highest rates of infection . sanitation dependent.Gardia lamblia Gardia lamblia causes a disease called gardiasis ( lambliasis) Habitat: small intestine and may invade the common bile duct Epidemiology: Worldwide distribution.

Morphology: Trophozoite .actively moving and feeding stage • is bilaterally symmetrical • Four pairs of flagella ( anterior. ventral and caudal) • Movement is falling leaf like • Cytoplasm contains two nuclei and two parapasal bodies . posterior.

Cyst :      The cyst forms as trophozoites become dehydrated when they pass through the large intestine. thin cyst wall flagella shorten and are retracted within cyst Cyst may remain viable in the external environment usually water) for many months . ovoid in shape.

 Decystation occurs in the duodenum and trophozoites (trophs) colonize the upper small intestine where they may swim freely and multiply by longitudinal binary fission. Life cycle:  Infection occurs by ingestion of cysts.  The free trophozoites encyst as they move down stream and mitosis takes place during the encystment. . usually in contaminated water. Man is the primary host although beavers. The cysts are passed in the stool. pigs and monkeys are also infected and serve as reservoirs.

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explosive. diarrhea. abdominal distension. Symptoms:  Early symptoms include flatulence.Covering of the intestinal epithelium by the trophozoite and flattening of the mucosal surface results in malabsorption of nutrients . often watery. nausea and foul-smelling bulky.  The more chronic stage is associated with vitamin B12 malabsorption. disaccharidase deficiency and lactose intolerance(= weight loss) and dehydration Pathology: .

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history.  Giardia caused dysentery is distinct from other dysenteries due to lack of mucus and blood in the stool. . lack of increased PMN leukocytes in the stool and lack of high fever.  Microscopic examination of stool for cysts and trophozoite. epidemiology.Diagnosis:  Symptoms.

Mepacrine • • • Treatment • • . Prevention: • Filtration of water (be sure filter is fine enough to trap the cysts) Boiling water from stream or lake Addition of a tincture of iodine are effective in killing cysts (chlorination of water does not effect the cysts) Avoid use of wading/swimming pools by diaper-age children Metronidazole is the drug of choice.

 Balantidium coli This is a parasite primarily of cows.  Isospora belli is an opportunistic human parasite.and a micro-nucleus  . pigs and horses. The organism is a large (100 x 60 micrometer) ciliate with a macro.OTHER INTESTINAL PROTOZOA Balantidium coli and Cryptosporidium parvum are both zoonotic protozoan intestinal infections with some health significance.

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The infection occurs mostly in farm workers and other rural dwellers by ingestion of cysts in fecal material of farm animals. However. lung and brain abscesses are not seen.  . Symptoms and pathogenesis of balantidiasis are similar to those seen in entamebiasis. including intestinal epithelial erosion. liver.  Man-to-man transmission is rare but possible.  Metronidazole and iodoquinol are effective.

bladder.Trichomonas vaginalis Trichomonas vagina cuases a disease called Trichomoniasis. prostate glands. endocervix. Habitat:• • Female vagina. epidedymis . urethra. bladder Male urethra. seminal vesicles.

Movement is gliding type The organism does not encyst. Trophozoite – ovoid with a single nucleus.Epidemiology • • Trichomonas vaginalis has a world-wide distribution. four anterior flagella and a lateral flagellum attached by an undulating membrane. Morphology • • • . incidence is as low as 5% in normal females and as high as 70% among prostitutes and prison inmates.

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Common in 30-49 year old women T. vaginalis infection is rarely symptomatic in men and often asymptomatic in women.Life cycle • • Infection is by trophozoite Transmission primarily via sexual contact • Direct contact • Toilet • Bed sheet • • There is no non-human reservoir host. Symptoms • .

heavy infections in a high pH environment may cause mild to severe
• Vaginitis with copious foul-smelling yellowish, sometimes frothy discharge after 3-7 days of infection. • Urethritis • Epidedymitis (in male) • Prostatitis(in male • Pruritis of vagina (vulva) • Chafing of vulva ( burning)

These symptoms disappear in women as the infection becomes chronic; she becomes asymptomatic. Parasite is often sexually transmitted from an asymptomatic person to his/her partner.

Pathology

The organism causes contact-dependent damage to the epithelium of the infected organ

Diagnosis Giemsa-stained smears of vaginal discharge Treatment  Metronidazole is effective in both males and females.  Vinegar douche may be useful. Personal hygiene and the use of condoms are helpful.

Summary of Intestinal and luminal protozoa
Organism Transmissi Symptoms on Diagnosis Treatment

Entameba Oro-fecal Dysentery Stool: cystsGI: histolytica with blood with 1-4 Iodoquinol and necrotic nuclei or tissue. and/or Metronidaz trophs. ole Chronic: abscesses Trophs in Abscess: aspirate. Metronidaz ole Stool: Iodoquinol typical old or man Metronidaz

Giardia lamblia

Oro-fecal

Fowlsmelling, bulky

Cryptospor Oro-fecal idium parvum Isospora Diarrhea Stool: ciliated trophs and/or cysts. Iodoquinol or Metronidaz ole.Ooocysts .Organism Transmiss Symptom Diagnosis Treatmen ion s t Balantidiu Oro-fecal. Ooocysts Paromycin in stool (investigati onal) Sulpha Oro-fecal Giardiasis. Dysentery m coli zoonotic with blood and necrotic tissue but no abscesses.

These are 1.The Coccidians Coccidians are members of the Phylum Apicomplexa that infect epethelial cells of viili of the small intestine. Cryptosporidium spp 2. Isospora Belli . There are several species of medical and veterinary importance. Cyclospora cayetanensis 3.

2 common species are now recognized: – Cryptosporidium hominis -Human species  Cryptosporidium parvum – Cattle species (affects humans and other livestock) . & turkeys) causing the disease crtyptosporiodiasis. cattle. chickens.Cryptosporidium spp Several species of Cryptosporidium are well known as intestinal parasites of domestic animals (sheep.

• recognized in AIDS patients in 1976 •Most of AIDS patients have Cryptosporidium .Cryptosporidium was recognized as opportunistic parasite.

Cryptosporidium parvum Cryptosporidi um parvum on the surface of small intestinal cells .

.MOST Cases of Cryptosporidiosis of human infections arise from infections in young cattle oocysts in cattle feces typically contaminate surface water used for drinking • unusually wet spring resulted in river runoff containing oocysts from feces of young cattle • Contamination of water purification plants . and treated water showed high turbidity levels.

life cycle .Cryptosporidium sp.

Life Cycle of Cryptosporidium .

Oocysts of Cryptosporidium Each oocyst contains 4 sporozoites that attach to surface of small intestinal cells unstained acid red stain Oocysts from cattle feces – oocysts are 4-5 µm in diameter .

In immunocompetent (normal) humans it is a self limiting diarrheal illness.Pathology: 1. Treatment – Paromycin is used as an investigational drug . 2 In AIDS patients and immunocompromised persons – it is severe prolonged life threatening diarrhea.

Cyclospora First human cases reported in 1979 Major outbreak of Cyclospora cayetanensis occurred in New York in 1996 • 1400 cases of diarrhea reported Human aquires infection by ingestion of water or vegetables contaminated with sporulating oocyst. – These have been exposed to fecal contamination .

life cycle is similar to Cryptosporidium: • oocysts are the infective and diagnostic stage – size is 4 µm in diameter (larger that Cryptosporidium) • 4 sporozoites are released from each oocyst and penetrate cells of the small intestine • parasites inside intestinal cells .

comparison of oocysts of Cryptosporidium and Cyclospora .

Pathology: in immunocompetent persons – diarrhea occurs • Symptoms usually occur in a week • Diarrhea lasts a few days or may persist for up to 6 weeks • Disease is self-limiting (2) in immunocompromised people – diarrhea is more severe and may last several months (1) .

Isospora Belli Habitat: Isospora belli inhabits the small intestine. Morphology: • Trophozoites. . merozoites. & gametocytes occur in the cytoplasm of small intestinal cells (not on surface like Cryptosporidium) •Oocysts (20 -30 µm long) are released in feces (diagnostic) • Oocysts are infective to new human host via human fecal contamination.

•Life cycle is similar to Cryptosporidium .

In immunocompetent individuals . and nausea Most of AIDS patients reported had Isospora Treatment: Specific treatment is available but recurrences are common. .some are asymptomatic and others develop a diarrhea with abdominal pain and nausea that lasts about a week (mimics gardiasis and may be underreported) It is self limiting 2.Pathology: 1. In immunocompromised individuals .there is a chronic off and on diarrhea that lasts from 1 month to years • Invasion and destruction of small intestinal cells causes diarrhea. abdominal pain.

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