intestinal protozoa

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Intestinal protozoa eba: Entamoeba histolytica gellates: Giardia lamblia cidians: Toxoplasma gondii, Cryptosporidium parvu zoa colonize and infect the oro-pharynx, duodenum a rganisms are transmitted by the fecal-oral route (f eaks of diarrhea and dysentery are especially probl enters yst forms of protozoa are resistant to chlorine and e important when the municipal water supply is ned with these organisms—esp. farming communities Read Vela Chapter 7

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Intestinal protozoa. Amoeba: Entamoeba histolytica Flagellates: Giardia lamblia Coccidians: Toxoplasma gondii, Cryptosporidium parvum. 1. Protozoa colonize and infect the oro-pharynx, duodenum and colon 2. The organisms are transmitted by the fecal-oral route (food/water) - PowerPoint PPT Presentation

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Page 1: Intestinal protozoa

Intestinal protozoa

Amoeba: Entamoeba histolyticaFlagellates: Giardia lambliaCoccidians: Toxoplasma gondii, Cryptosporidium parvum

1. Protozoa colonize and infect the oro-pharynx, duodenum and colon2. The organisms are transmitted by the fecal-oral route (food/water)3. Outbreaks of diarrhea and dysentery are especially problematic in daycare centers4. The cyst forms of protozoa are resistant to chlorine and ozone andcan become important when the municipal water supply is overburdened with these organisms—esp. farming communities

Read Vela Chapter 7

Page 2: Intestinal protozoa

Case study E. histolytica

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Entamoeba histolytica

Primitive unicellular micro-organismsLife cycle divided into two stages

trophozoite—actively motile feeding stage—food and humanblood cells

when environmental conditions are favorablecyst—dormant, highly resistant, infectious stage

when temperature or moisture levels dropReplication involves simple binary fission of trophozoite or divisionto produce numerous infectious trophozoites in a mature cyst.

Motility—extension of a pseudopod (false-foot) and then drawing up the rest of the cell to meet the pseudopod in a “snail like” movement.

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Entamoeba histolytica

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E. histolytica life cycleEncounter—fecal-oral route

patients with diarrhea excrete the trophozoite form which is killed by drying in the environment or by the acidity of the stomachasymptomatic patients excrete infectious cysts that are resistantto drying and acid

1. Ingestion of cysts2. Passage of cysts through the stomach where gastric acid stimulates therelease of the infectious trophozoites from the cysts3. Trophozoites move to the duodenum where they divide4. Trophozoites travels to the colon where they attach to colonic epithelialcells5. After attachment they produce a cytotoxin that kills epithelial cells so theycan gain access to deeper tissues6. Continue to divide in colon where amoeba/cysts are excreted in stool OR7. Trophozoites invade the deeper mucousa and enter the peritoneal cavity8. Trophozoites are carried in the circulation to the liver but can also be carried to the lungs, brain and heart

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Epidemiology of E. histolytica

Worldwide distribution—especially prevalent in warmer climatesbut also endemic cases found in cold areas (ie. Alaska, Canada)Many infected individuals can be asymptomatic and serve as reservoirsFfor diseaseCarrier passes cysts that contaminate water supply and food—espchildren in daycare centersFlies, ants and cockroaches can also serve as vectors for the spreadof cystsSewage containing cysts can contaminate municipal water supplywells and springs.Use of human feces as fertilizer can contribute to the spread

Prevalence of infection in U.S. is 2-5% in warmer countries 15-50%

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Clinical diseases of E. histolyticaAmoebic dysentery!!! Related to the destruction of the colonic epithelial cells by the organism. Flask shaped ulcerations of the intestinal mucousa with inflammationSecondary bacterial infection

symptoms: abdominal pain, cramping passage of numerouswatery and bloody stoolsIf untreated patients can die of dehydration

Amoeba can invade deeper tissues and enter the blood circulatory system where they especially infect the liver as trophozoites are re-moved from blood as they enter the liver.

abscess formation in the liver is commonpain in the liver and elevation of the diaphragm

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Treatment and prevention of E. histolytica

Metronidazole—penetrates deeper tissues and destroys amoeba presentin liver, brain, lungs etc.

the organism’s metabolism converts the drug into its lethal form

A second drug is used to eradicate the amoeba present in the intestinal lumen (paromomycin)

Prevention: When traveling to areas where E. histolytica is epidemicor endemic

AVOID drinking water ALSO ice cubesfilter and boil waterthoroughly wash unpeeled fruits and raw vegetables

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Giardia lamblia trophozoite

G. lamblia is a flagellate and moves by lashing its flagella that moves organism through fluid environments.G. lamblia attaches to the intestinal villi of duodenum via an adhesivediskCysts are resistant to the amounts of chlorine put in municipal watersystems (2 parts per million) therefore water systems should ALSOfiltrate water

Giardia attached to intestinal microvilli by sucking disks Upon detaching clear impressions from the Sucking disks are left on the surface of the microvilli

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G. lamblia case study

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G. lamblia life cycle

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G. lamblia life cycle

1. Infection initiated by the ingestion of infectious cysts (only 10 arerequired for infection2. Acid in the stomach stimulates the release of trophozoites from the cyst3. Trophozoites are released in the duodenum and jejunum (upper partof small intestines) where they multiply by binary fission4. Trophozoites attach to the intestinal villi by means of a sucking disk5. Trophozoites can develop into cysts for survival outside of the host6. Trophozoites cause an explosive diarrhea such that cysts are releasedinto the environment7. Trophozoites remain in the G-I tract and almost never found elsewhere in the body.

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Epidemiology of G. lambliaG. lamblia found everywhere in the worldOften found in streams, lakes mountain resorts—reservoir animalssuch as beavers and muskrats perpetuate the infectious cycleApproximately 50% of infected humans are asymptomatic and areimportant carriers of diseaseGiardiasis is acquired through

the consumption of inadequately treated wateringestion of uncooked vegetables and fruitsperson-person spread (esp. daycare centers, families with infected children)

Giardia can be maintained in the municipal water supply, unless watertreatment plant uses filtration AND chemicals to eradicate the protozoa

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Clinical diseases of G. lamblia

Symptomatic disease ranges from mild diarrhea to severe dysentery

The incubation period before symptomatic disease is approx. 10 days

The onset of disease is sudden and consists offoul-smelling watery diarrhea (seldom bloody)abdominal crampingflatulence

Spontaneous recovery occurs in 2 weeks HOWEVERChronic disease with several relapses may occur.

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Clinical diagnosis of G. lamblia

With the onset of diarrhea the patient’s stool are examined for trophozoites and cysts.

Giardia may appear in stool on a given day and not be present on the following day

one stool sample over a period of three days should be examined before making a negative diagnosis.

Samples can be collected through duodenal aspiration or via biopsyof upper small intestines.

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Treatment and prevention of G. lamblia

Eradicate Giardia from BOTH asymptomatic carriers and diseasedpatients.

Campers/travelers should boil AND filter water taken from lakes and streams AND from municipal water in areas where disease is endemic

Municipal water supplies should maintain functioning filtrationSystems since the cysts are resistant to chlorine and ozone treatment

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Coccidia—Crytosporidium and

Toxoplasma Reproduce by sexual and asexual reproductionMost coccidiae have multiple hosts

C. parvum found in farm animals/ reptiles and fish wherethey reproduce sexually they reproduce asexually in humans.

T. gondii found in herbivores, birds and carnivores (sexual)and humans (asexual) cats are especially important carriers ofdisease

Hard to eradicate because these protozoa are zoonotic

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Coccidia life cycle Cryptosporidium and Toxoplasma

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T. gondii cysts in brain tissue

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Toxoplasma gondii

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Toxoplasma gondii