Case 3
1. What type of diarrhea are we dealing with?
2. What is your differential for this form of diarrhea in this patient?
3.What pathogens could be responsible for the patient's diarrhea?
The presence of blood and fecal leukocytes suggests an invasive diarrhea. The following can cause diarrhea of this duration.
Salmonella
Yersinia
Campylobacter
Proctitis is seen in homosexuals. secondary to
gonorrhea
herpes
chlamydia
syphilis
Non-infectious causes include
ulcerative colitis
Crohn's disease
diverticulitis
C. difficle colitis (if there is a history of antibiotic usage).
This patient has intestinal amebiasis, an infection with Entameba histolytica.
Homosexuals have a high prevalence of this infection (up to 40 %).
4. How
would you establish the diagnosis in this patient?
The diagnosis of intestinal amebiasis is established by the identification of the organism in stool or sigmoidoscopic aspirates.
Trophozoites can be seen on wet mounts, while cysts can be seen on concentrated specimens.
Three or more specimens may be required for diagnosis.
Enzyme immunoassays detecting E. histolytica antigens in stool have been developed.
Serology is useful in diagnosing extra-intestinal amebiasis.
Indirect hemagglutination and enzyme immunoassay are the most
sensitive for detecting, antibody.
5. Describe the life cycle and pathogenesis of this parasite.
6. Describe the epidemiology for this infection.
7. How
is the parasite transmitted?
Humans are the principal host and reservoir of E. histolytica.
Human to human transmission occurs by ingestion of cysts.
In the small intestine, the cyst degenerates and releases the trophozoite.
Up to 10% of the world's population is infected. Food and water-borne spread occur.
Venereal transmission is common among
homosexuals
8. How does this parasite produce disease?
In most people E. histolytica is a harmless commensal.
Virulence is strain related, and associated with certain isoenzyme patterns and surface antigens.
Lectin‑mediated adherence is important, along with the capacity to lyse host cells on contact.
Virulence is increased with passage through humans.
Malnutrition, corticosteroids, pregnancy and childhood render the host more susceptible to invasion.
Lysis of colonic epithelial cells produces small mucosal ulcerations.
There is edema and hyperemia, but minimal inflammatory response.
Trophozoites are present in the base of the ulcer. The lesion spreads laterally in the submucosa, producing a flask-shaped ulcer.
Granulation tissue and fibrotic thickening will occasionally produce an ameboma.
Spread to the portal
circulation, and rarely to lung, spleen or brain results in metastatic
abscesses.
9. What pathologic changes are produced?
10. Describe the clinical manifestations of this infection.
11.What complications might occur?
Complications include fulminant colitis with perforation, toxic megacolon, perianal ulceration, and amebomas.
Extra intestinal spread leads to
liver abscess complicated by peritonitis, empyema or pericarditis; lung abscess
and brain abscess can also occur.
12. How would you establish the diagnosis for each of the manifestation?
13 How would you treat this patient?
Fluid and blood replacement, relief of symptoms and eradication of the organism are important.
The drug of choice is metronidazole, which is effective against all forms of amebiasis.
It should be combined with diloxanide to cure intestinal disease.
Alternatives are tetracycline, paromomycin, and dehydroemetine.
14. How will you treat other common manifestations of this disease?
15. What control measures are available to prevent its transmission?