what is amebiasis and what is its role in deadly diseases and infections.
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AMeBIASIS By, hira Nusrat Ms scholar
Entamoeba histolytica Causative agent of the disease amebiasis (old name is Amoebic Dysentery). One of the most important and pathogenic parasites of humans. This parasite is primarily a human parasite and is transmitted from human to human. Although dogs, cats and primates may be infected, these infections are rare and unimportant.
AMEBIASIS Amebiasis (am-e-BI-a-sis) is a disease caused by a one-celled parasite called Entamoeba histolytica . Although it is more common in people who live in tropical areas with poor sanitary conditions
NATURE OF THE DISEASE Amoebiasis is an intestinal infection in which cysts are passed in the feces. Symptoms can include fever, chills and diarrhea, sometimes bloody or with mucus and often with cramps. Some people may have only mild abdominal discomfort or no symptoms at all. Symptoms can start 2 or more weeks after infection. Rarely, trophozoites (the mobile amoebas) may invade the liver, lung or brain, or perforate the colon causing septicemia. About 90% of infections are asymptomatic Remaining 10% produce a spectrum of clinical syndromes
TRANSMISSION OF AMEBIASIS Amoebiasis is transmitted by feacal contamination of drinking water and foods, but also by direct contact with dirty hands or objects as well as by sexual contact. Additionally, geophagy is a common route of infection in certain cultures
Geographical distribution Occurs worldwide, but is more common in areas or countries with poor sanitation, particularly in the tropics. Worldwide in distribution 3rd most common cause of parasitic death India, China, Mexico, Africa, South America 2-60% prevalence (based on ELISA and PCR studies from stool samples) 100,000 deaths/year 50 million cases/year
MORPHOLOGY The lifecycle of E. histolytica has several life stages: Trophozoite Pre-cyst Cyst
TROPHOZOITES Plasmalemma (thin) Multiple well defined pseudopodia Irregular (10-60 m) Differentiation into endo- and ectoplasm Spherical nucleus (4-7 mm) Uninucleated : nucleus with fine peripheral chromatin granules, small central endosome
... The growing or feeding phase (active phase) of the parasite Cause amoebiasis (damage tissue) Spread throughout the body Rarely transmit the infection to others Labile in liquid stools or tissue, and must be rapidly found or preserved (quick fixation & cold storage) for diagnosis
cYSTs PRE-CYST • Intermediate form • Oval with blunt pseudopodia • No food vacuoles CYST • Spherical, 10 - 15 μ m in diameter • Uninucleate, later bi- or quadri - nucleate • Thick chitinous wall • Glycogen mass – not in quadrinucleate • Chromidial or Chromatoid bars • Infectious Dormant stage
… Infective Stage for humans Resistant walls maintain viability If moist can last several weeks Killed by desiccation or boiling Diagnostic Stage in formed stools Can be concentrated and stained easily Not seen in liquid (diarrheic) stools or tissues
ENTAMoeBA HISTOLYTICA Cysts and trophozoites are passed in feces. Infection occurs by ingesting feacally contaminated food (including undercooked meat), water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts, and both stages are passed in the feces .
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).
Cysts can survive days to weeks in the external environment and are responsible for transmission. 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 is almost unique among amoebas in its ability to hydrolyze and invade host tissues. Tiny cytoplasmic extensions from the surface, filopodia have functions related to pathogenesis, for example attachment to host cells, release of cytotoxic substances, or contact cytolysis of host cells. Trophozoites have active cysteine proteases (CP) on their surfaces and these enzymes have been implicated as factors contributing to the parasites’ invasive abilities.
Acute amebiasis can present as diarrhoea or dysentery with frequent, small and often bloody stools. Chronic amebiasis can present with gastrointestinal symptoms plus fatigue, weight loss and occasional fever. Extraintestinal amebiasis can occur if the parasite spreads to other organs, most commonly the liver where it causes amoebic liver abscess. Amoebic liver abscess presents with fever and right upper quadrant abdominal pain.
Infection in the ceacal area may mimic symptoms of appendicitis. Some patients tolerate intestinal amebiasis for years with no sign of colitis (although they are passing cysts) and then suddenly succumb to ectopic lesions.
Depending on the number and distribution of intestinal lesions a patient determine the severity of the acute amoebiasis. Amoebic diarrhea is marked by bouts of abdominal discomfort with four to six loose stools per day but little fever. Acute amoebic dysentery is a less common condition, but the sufferer from this affliction can best be described as miserable. An average of 15 to 20 stools, consisting of liquid feaces flecked with bloody mucus, are passed per day.
Hepatic amebiasis Results when trophozoites enter mesenteric venules and travel to the liver through the hepatoportal system. They digest their way through portal capillaries and enter the sinusoids, where they begin to form abscesses. Lesions thus produced may remain at a pinpoint size, or they may continue to grow The center of the abscess is filled with necrotic fluid and the outer zone consists of liver tissue being attacked by amebas The abscess may rupture, pouring debris and amebas into the body cavity, where they attack other organs
Pulmonary amebiasis is the next most common secondary lesion. It usually develops by metastasis from a hepatic lesion but may originate independently. Most cases originate when a liver abscess ruptures through the diaphragm. Other ectopic sites occasionally encountered are the brain, skin, kidneys, adrenals, spleen, male and female genitalia, and pericardium
Diagnosis of amebiasis Stool Examination: Microscopic identification of cysts and trophozoites in the stool is the common method for diagnosing pathogenic Entamoeba species. Fresh stool : wet mounts and permanently stained preparations (e.g., trichrome). Concentrates from fresh stool: wet mounts, with or without iodine stain, and permanently stained preparations (e.g., trichrome). While useful for cysts, concentration methods may not be useful for demonstrating trophozoites. Microscopy also has a low sensitivity if only one stool sample is analyzed, and requires personnel trained in morphological diagnosis.
Collection and analysis of three consecutive stool samples within ten days improves the chances for detection. Trophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery.
Immunodiagnosis : Enzyme immunoassay (EIA) kits for Entamoeba histolytica antibody detection as well as EIA kits for antigen detection are commercially available Antibody detection: Antibody detection is most useful in patients with extraintestinal disease (i.e., amebic liver abscess) when organisms are not generally found on stool examination.
Molecular Diagnosis Conventional PCR: In reference diagnosis laboratories, molecular analysis by conventional PCR-based assays is the method of choice for discriminating between E. histolytica and E. dispar . Some assays also can distinguish E. moshkovskii . Real-Time PCR: A TaqMan real-time PCR approach has been validated at CDC and is used for differential laboratory diagnosis of amebiasis. Possible to detect both E. histolyrica and E. dispar in the same reaction vessel.
Treatment of Amoebiasis Asymptomatic intestinal infection may be treated with iodoquinol, paromomycin or diloxanide furoate. Recommended drugs for treatment of symptomatic intestinal disease and for hepatic abscess are metronidazole and trinidazole . Since these drugs may not eliminate the cysts of the intestine, immediately follow metronidazole and trinidazole with iodoquinol, paromomycin or diloxanide furoate.
If fulminant amoebic colitis develops, broad-spectrum antibiotics should be added to the treatment due to risk of bacterial translocation. Surgical intervention is rarely necessary and reserved for those patients with signs of acute abdominal damage or those with megacolon. In certain instances, aspiration of ALA is required, particularly when there is no clinical response after five to seven days of antiamoebic therapy. Patients with high risk of abscess rupture (cavity diameter of ≥ 5 cm and left lobe abscesses) should also be considered for drainage. Imaging-guided percutaneous needle aspiration is the procedure of choice