M- Protozoal Infections of the Gut Flashcards Preview

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Flashcards in M- Protozoal Infections of the Gut Deck (31)
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What are the most common protozoa associated with complicated infections?

1. Entamoeba histolytical
2. Giardia lamblia
3. Balantidium Coli
4. Microsporidia
5. Cystosospora belli
6. Dientameoba fragilis


What do forms does E. histolytica exist in?
Which is the infective form?
Describe the structure of each.

1. Cysts- ***infective form. The cyst is 12-15microns, spherical with a halo, and can have up to 4 nuclei with central karysome and fine, uniformly distributed peripheral chromatin

2. Trophozoite- 15 to 20 microns. It has a single nucleus with central karysome and uniformly distributed chromatin.


How can E. histolytica be differentiated from E. dispar?
How can histolytica be differentiated from Entamoeba coli?

In trophozoite form, E. histolytica can ingest RBCs and dispar cannot.

In cyst form, E. histolytica has 4 or fewer nuclei and E. coli can have up to 8


What is the clinical presentation of the patient has :
1. luminal amebiasis
2. intestinal amebiasis
3. extraintestinal amebiasis

Luminal = asymptomatic

Intestinal (primary illness) =
- dysentery
- colitis
- appendicitis
- toxic megacolon
- ameboma (mass lesion or colonic wall thickening)

Extraintestinal =
- liver abscesses
- pericardial amebiasis
- pleuropulmonary amebiasis
- cerebral amebiasis


A patient presents with a history of weeks of abdominal pain, diarrhea and bloody stool. Due to the gradual onset, the patient has lost weight and seems to be volume depleted.
What is the likely protozoal cause? What would be the most serious manifestation associated with this?

It is likely to be E. histolytica causing :

Amebic colitis.

The most serious manifestation of primary disease is fulminant, necrotizing colitis


How does the presentation of amebic colitis and amebic liver abscess differ in terms of fever?

Amebic colitis is RARELY associated with fever.

Amebic liver abscess is associated with a long duration fever (1-2 wks)


What is the natural reservoir for entamoeba?



What is the infectious part of E. histolytica life cyle?


Cysts are passed in feces and are able to live in the environment for wks because of their wall protection.
Ingestion of mature cyst in fecally contaminated water and food is the infectious step


What is the pathogenesis of E. histolytica?
What is the infectious form?
Where does the organism reside in the body?
How do they replicate?

1. Ingestion of cysts in fecally contaminated H20 or food
2. Cysts go to small intestine where they go through excystation to trophozoites

3. Trophozoites go to large intestine and adhere to intestinal walls via lectin-binding receptors.

4. Trophozoites multiply via binary fission --> cysts

5. Cysts are released in feces to start the cycle again


What virulence factors allow e. histolytica trophozoites to invade intestinal mucosa?

1. cytotoxins- lyse colonic epithelial cells AND lyse PMNs which release hydrolytic enzymes that further damage colonic mucosa

2. cysteine proteinase- degrades collagen and elastin

Trophozoites feed on epithelium, RBC, neutrophils, monocytes, lymphocytes etc leading to:

amebic colitis


You are examining a lesion in the colon and note non-specific colitis with inflammation and flask-shaped ulcers. What protozoa are you likely to see?

E. histolytica


What is the lab diagnosis for E. histolytica? How is it differentiated from E. dispar and E. moshkovskii?

Ova and Parasite examination of the stool

Light microscopy can differentiate E.histolytica from the others because of erythrophagocytosis - it is the only entamoeba that ingests RBC


What is the only other intestinal parasite in the entamoeba family besides E. histolytica that can cause diarrhea?

Dientamoeba fragilis


What is the presence of nonpathogenic amebas in the stool of a patient strongly indicative of?

1. exposure to poor sanitation/fecal contamination
2. possible exposure to E. histolytica
3. pre-AIDs immunodeficient state


Why are anti-motility drugs NOT recommended for patients with dysentery?

It creates the possibility of an invasive pathogen


What is treatment for E. histolytica?

Systemic : metronidazole or tinidazole

Intraluminal: metronidazole +
- iodoquinol
- paromomycin
- diloxanide furoate


In terms of extraintestinal infection, how do E. histolytica and E. dispar differ?

E, dispar trophozoites are serum sensitive.
E. histolytica is resistant to complement-mediated killing and can ascend through the portal v. into the liver causing abscess.


What are symptoms associated with amebic liver abscess?
What confirm the diagnosis?

1. fever
2. chills
3. leukocytosis
4. RUQ pain and liver enlargement

Diagnosis can be confirmed by serology.


What are the 2 forms of Giardia lamblia?
Which is the pathogenic form?
Which is the infective form?
Describe the structure of each.

Trophozoite- **pathogenic form
-pear shaped with convex dorsum
- flat ventral surface with sucking disk
- four PAIRS of flagella (8 total)
- 2 anterior nuclei each with karyosome

Cyst **infective form
-oval structure
- 4 nuclei
- thin wall of N-acetylglucosamine


What is the incubation period of giardia lamblia?
How long does the disease presentation last?
What are acute symptoms?
What can chronic giardia lead to?

The incubation period is 5-6 days and the disease lasts 1-3 wks.

Diarrhea, ab pain, flatulence, nausea, vomiting

Chronic leads to:
-wasting (debiliation)


What are the 2 ways giardia can be transmitted?

1. Fecal-oral via contaminated water [travelers]
2. Hand-to-mouth transfer of cysts [daycare centers]


What is the pathogenesis of G. lamblia?
How does it get into a human host?
Where does it cause pathology?
How does it replicate?

1. ingested or hand to mouth transfer of cysts
2. each cyst hatches 2 trophozoite in the small intestine
3. trophozoites attach to brush border in small intestine via :
- ventral sucking disk (contractile proteins)
- flagella mediated hydrodynamic force
- lectin receptor binding

4. it replicates by binary fission and encysts as it transitions to the colon


What initiates the G. lamblia infection?
What are host defenses?
What are the bacterial defenses?

Infection is initiated by antigen uptake by macrophages in Peyer patches---->

1. IgA response --> prevent adherence
2. T cell response

Giardia had IgA protease.
T lymphocytes cause crypt hyperplasia--> altered absorption


How does G. lamblia cause diarrhea?

It is not invasive or toxigenic. It just:
disrupts the brush border by injuring microvilli-->causes villus atrophy--> malabsorption--> watery diarrhea


How is the diagnosis of G. lamblia made?

1. Identify cysts in direct mount of feces

- if 3 consecutive mounts have no cysts->

2. duodenal fluid/duodenal biopsy for trophozoites
3. stool antigen test


What is the drug treatment of choice for Giardia?
How does it differ with pregnancy?

metronidazole or tinidazole given for 7 days.

Pregnant: paromomycin


What is prevention for Giardia?

1. filtration or boiling of water to get rid of cysts.
2. hand washing
3. if impending outbreak, treat everyone at that location [ex. daycares] because some may be infected and asymptomatic, still serving as carriers


What 2 types of microsporidia infect humans?
Who is most likely to be infected?
What organs are affected?
What is treatment?

E. bienusi and E. intestinalis

AIDS patients are most likely infected and will have mainly:
- eye

Treatment is albendazole for E. intestinalis and fumagillin for topical treatment (not curative)


A child has gone to summer camp and comes back with nausea, vomiting, anorexia, failure to thrive.
You do microscopy on the stool and see organisms with clustered karyosomes, no flagella, and bacteria and yeast debris in the cytoplasm. There are eosinophils on the stain.
What is a potential protozoal pathogen?
What is treatment?

D. fragilis and the treatment is tetracycline or metronidazole


An HIV + man presents with chronic diarrhea. You do a stool sample and see oocysts. It dyes with an acid fast stain.
What is the organism?
What is treatment?

C. belli and treatment is TMP-SMX