Amoeba Amoebiasis (Entamoeba Histolytica) Flashcards
Amoeba Entamoebidae
Originated from flagellates.
Parasites or commensals.
Vesicular nucleus with a small endosome at to near the center.
Cytoplasm contains a variety of food vacuoles and numerous vesicles that may be exocytotic.
No golgi apparatus or mitochondrion.
Crystallize into chromatoid bodies or bars upon encystation.
Five species: E. histolytica, E. dispar, E. harmani, E.coli, E. gingivalis
Entamoeba Histolytica
Entamoeba histolytica is an anaerobic parasite which predominantly infects humans and other living organisms causing dysentery amoebiasis and amebic liver abscess
Classification: Entamoeba Histolytica
Phylum: Sarcomastigophora Class: Amoeba Order: Amoebida Family: Entamoebidae Genus : Entamoeba
Morphology: Entamoeba Histolytica
E. histolytica life cycle goes through four successive stages; The trophozoite, the precysts, the metacyst and metacystic trophozoite. The metacyst form is the infective stage.
The trophozoite form is the feeding and the mobile form, which is 20-30 micron in diameter. It has endoplasm, ectoplasm, a nucleus with an endosome, food vacuoles, Pseudopodia and filopodia.
Life cycle: Entamoeba Histolytica
Cysts and trophozoites are passed in feces Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool.
Infection occurs via ingestion of mature cysts from fecally contaminated food, water, or hands. Exposure to infectious cysts and trophozoites in fecal matter during sexual contact may also occur.
Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. Trophozoites may remain confined to the intestinal lumen (A: noninvasive infection) with individuals continuing to pass cysts in their stool (asymptomatic carriers). Trophozoites can invade the intestinal mucosa (B: intestinal disease), or blood vessels, reaching extraintestinal sites such as the liver, brain, and lungs (C: extraintestinal disease).
Trophozoites multiply by binary fission and produce cysts and both stages are passed in the feces.
Cysts can survive days to weeks in the external environment and remain infectious in the environment due to the protection conferred by their walls. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment.
Pathogenesis: Entamoeba Histolytica
E. histolytica causes tissue destruction which leads to clinical disease.
Damage occurs by three main events:
• direct host cell death
• inflammation
In invasive infection, the trophozoites will invade and colonize the colonic epithelial cells which will cause ulcers and lead to the death of epithelia cells to die.
The immune system will eventually respond, which will only aggravate the process.
This could eventually lead to liver abscesses, lung abscesses or even brain abscesses
Unique among amoebas in its ability to hydrolyze and invade host tissues.
Filopodia are thought to play pathological rules in adhesion to the host cells and secretion of cytotoxic substances, or contact cytolysis of the cells.
Lectins on the membranes of E. histolytica induce pathological inflammatory response through stimulation of cytokines.
Trophozoites have active cysteine proteases (CP) that contribute to the parasite’s invasive abilities.
Intestinal lesions usually develop in the caecum, appendix, or upper colon and then spreads through the colon.
In older lesions, the amoebas may break the muscularis mucosa, infiltrate the submucosa, and even penetrate the muscle layers by blood and lymph to ectopic sites throughout the body where secondary lesions form.
A high proportions of death results from perforated colons with concomitant peritonitis. Surgical repair of this perforation of difficult because a heavily ulcerated colon is very delicate.
Sometimes in Latin America, the infection lead to a granulomatous mass, called an ameboma, which may obstruct the bowel.
Secondary lesions have been found in almost every organ, but the liver is the most affected. Even other
invasions start after rupture of liver abscess.
Hepatic amoebiasis results when trophozoites enter mesenteric venules and travel tot the liver through the hepatoportal system.
Pulmonary amoebiasis is the next most common secondary lesion.
Symptoms: Entamoeba Histolytica
Not every infected individual shows symptoms of the disease. Symptoms are usually mild and could include; • Loose feces • Stomach pain • Stomach cramping • Blood and/or mucus present in stool • Vomiting
Diagnosis: Entamoeba Histolytica
Blood sample analysis Microscopic Fecal examination X-ray and other scanning (on liver and other organs) ELISA PCR
Prevention and control: Entamoeba Histolytica
Improved sanitation Drinking bottles water Washing fruits and vegetable properly with clean water Peel your fruits yourself Stop using ice cubes in drinks.
Epidemiology: Entamoeba Histolytica
E. histolytica is estimated to infect about 50,000,000 people annually. Previously it was thought that 10% of the world population was infected but it was later on found out that 90% of those infected had E. dispar or E. coli.
Treatment: Entamoeba Histolytica
Metronidazole is the drug of choice.
Some require more than one antibiotic depending on if they got sick or not.
Other drugs include arsinalic derivatives and tetracycline.
Surgical drainage of abscess
Types of infections: Entamoebididae
There are two kinds of infections that can be caused by E. histolytica. The invasive infection and the non-invasive infection.
The invasive infection is caused by large size (20-30 micron in length and 10-20 micron in width) E. histolytica strain, now known as E. histolytica. The noninvasive amoebiasis is caused by a smaller sized strain (12-15 micron length x 5-9 micron width), now known as E. hartmani.
More recently molecular data further speared a nonpathogenic form of E. histolytica into a new species, called E. dispar. This ruled out the previous hypothesis that E. histolytica goes through successive generations that differ in pathogenicity.
