Intestinal Amoeba PDF

INTESTINAL AMOEBA Prepared by: Dr. Shirley Tang Gee Hoon CLASSIFICATION OF AMOEBA A single-celled protozoa that constantly changes its shape. AMEOBA Due to the presence of an organ of locomotion called “ pseudopodium” Cla...

INTESTINAL AMOEBA Prepared by: Dr. Shirley Tang Gee Hoon CLASSIFICATION OF AMOEBA A single-celled protozoa that constantly changes its shape. AMEOBA Due to the presence of an organ of locomotion called “ pseudopodium” Classification Based On Habitat Classification (Habitat) Intestinal amoeba Free-living amoeba (Large intestine of (Small free living and humans and animals) opportunistic pathogens Intestinal Amoeba Intestinal Amoeba Pathogenic Non-pathogenic Entamoeba E. dispar histolytica E. moshkovskii E. coli E. coli E. polecki E. hartmanni E. gingivalis Endolimax nana Iodamoeba butschlii Entamoeba histolytica A worldwide distribution More prevalent in the tropics and subtropics than the cooler climates Especially where poor economic status, poor nutrition, hygiene and sanitation and is more common in developing countries of the tropics Majority of cases are asymptomatic. EPIDEMIOLOGY E. histolytica is a common diarrheal pathogen in returned travelers (long-term traveler >6 months). The largest burden of the disease occurs in tropics of China, Central and South America, and Indian subcontinents affecting 10% of the world’s population. EPIDEMIOLOGY Higher prevalence in certain groups : Families of infected person, aborigines, male homosexuals, persons in mental hospitals, prisons, institutions for children All ages are susceptible to infection but the rate is lower in infants and young children. Females are as likely to be infected as males, but invasive amebiasis is much more common in males. ETIOLOGICAL AGENT Infection by Entamoeba histolytica Habitat E. histolytica is found in the human colon. Trophozoites of E. histolytica live in the mucous and submucous layers of large intestine. Morphology – THREE forms 1. Trophozoite 2. Precyst 3. Cyst ETIOLOGICAL AGENT Trophozoite Vegetative form Only form present in tissues Irregular in shape Size: 12-60 µm, average: 20 µm Moves in one direction by means of a pseudopodium (finger-like projections) Cytoplasm: Ectoplasm & endoplasm Endoplasm contains nucleus, food vacuoles & phagocytosed red blood cells Single round nucleus with uniformly arranged peripheral chromatin and central karyosome (nucleolus) TROPHOZOITES Trophozoites of E. histolytica with ingested erythrocytes stained with trichrome. The ingested erythrocytes appear as dark inclusions. The parasites above show nuclei that have the typical small, centrally located karyosome, and thin, uniform peripheral chromatin. TROPHOZOITES Trophozoite of E. histolytica in a direct wet mount stained with iodine. ETIOLOGICAL AGENT Precyst The trophozoites undergo encystment in the intestinal lumen. Before encystment, the trophozoite extrudes its food vacuoles and rounds up to form a precystic stage, measuring 10–20 μm in size. It contains a large glycogen vacuole and chromatoid bars. It secretes a cyst wall to become cyst. ETIOLOGICAL AGENT Cyst Size 10-20um, thick cyst wall (highly resistant to gastric juice & unfavourable environment consitions Round in shape, with 1-4 nuclei Immature cyst has single nucleus, chromatoidal bars (aggregation of RNA, cigar shaped with rounded ends) and glycogen mass Mature cyst has 4 nuclei (infective stage) The glycogen mass and chromatoid bars disappear in mature cyst. CYSTS Cyst of E. histolytica stained with trichrome. Three nuclei are visible in the focal plane (black arrows), and the cyst contains a chromatoid body with typically blunted ends (red arrow). The chromatoid body in this image is particularly well demonstrated. Cyst of E. histolytica stained with trichrome. Note the chromatoid body with blunt ends (red arrow). CYSTS Cyst of E. histolytica in a concentrated wet mount stained with iodine. Notice the chromatoid body with blunt, rounded ends (arrow) Cyst of E. histolytica in an unstained concentrated wet mount of stool. Notice the chromatoid bodies with blunt, rounded ends (arrow). Host &4.2 Infective Form Transmission Host E. histolytica completes its life cycle in a single host, i.e. man. Infective form Mature quadrinucleated cyst It can resist chlorination, gastric acidity and desiccation and can survive in a moist environment for several weeks. Mode 4.2 of Transmission Transmission Fecal-oral Most common Contaminated food/water with mature quadrinucleated cysts/feces route Food handler, sucking fingers in children, institutional groups (mental retarded, old age, prison, day-care centre) Sexual Rare, either by anogenital or orogenital contact. contact Especially in developed countries among homosexual males Vector Very rarely, flies and cockroaches may mechanically transmit the cysts from feces, and contaminate food and water. 1. The cysts (usually found in formed stools) and trophozoites (in loose stools) are passed out in faeces of infected human Life Cycle 2. Mature quadrinucleate cysts are the infectious form, usually ingested in fecally Cysts can only form in contaminated water or food. the intestinal lumen, not outside the body. 3. In the intestine, the cysts undergo excystation to form trophozoites. Excystation takes place in the lower small bowel. 4. Trophozoites live in the lumen & mucosal crypts of the colon mainly caecum, descending colon and recto-sigmoid, feeding on liquid nutrient & bacteria. 5. As the trophozoite passes down the intestine, it undergoes encystation in the lumen of the colon (never in tissues) & is excreted in the faeces.  Life Cycle E. histolytica completes its life cycle in human host. In the majority of cases, E. histolytica remains as a commensal in the large intestine. They are carriers or asymptomatic cyst passers and are responsible for maintenance and transmission of infection in the community. Depending on various parasite and host factors, the trophozoites may invade the tissue of the large intestine and metastasize to the liver or other extraintestinal sites LIFE CYCLE PATHOGENSIS 4.2 Transmission Infection by E. histolytica is mostly asymptomatic. Under certain circumstances involving the host and parasite factors, E. histolytica becomes invasive E. histo-lytica (tissue lysis) Pathogenesis 4.2 Transmission Variable clinical response to amebiasis, depending on the pathogenicity of the strain of E. histolytica, the intensity of infection, the bacterial flora, host factors, and the site and extent of tissue damage. Pathogenesis 4.2 Transmission Certain strains are more virulent than others. They produce proteolytic enzymes, cytotoxins and cytolysin; usually have surface adhesin for attachment. Strains of E. histolytica can be distinguished by their isoenzyme patterns (zymodemes) PATHOGENSIS 4.2 Transmission 1. Poor nutrition 2. Stress Malnutrition (immune depressed) Asymptomatic women may High intestinal cholesterol develop severe amebiasis 3. Alteration of flora (nutritional factor for amoeba) Facilitate atrophy of the mucosa, during pregnancy and the of the colon susceptible to lysis & penetration puerperium. 5. Low resistance of 4. Irritation of the host colonic mucosa by Either by drugs such as bacteria, viruses, steroids or malnutrition or other illnesses, eg. Cancer, chemicals autoimmune disorder, HIV Pathogenesis of Intestinal Amebiasis 4.2 Transmission Pathogenesis of Intestinal Amebiasis 4.2 Transmission Trophozoites invade the colonic mucosa producing characteristic ulcerative lesions and profuse bloody diarrhea (amoebic dysentery). Males and females are affected equally with a ratio of 1:1. Pathogenesis of Intestinal Amebiasis 4.2 Transmission Amoebic ulcer The initial lesions of amebic invasion begin as small foci of necrosis in the large bowel mucosa. These foci progress to form ulcers which undermined and has the characteristic flask shape (broad base with a narrow neck). Pathogenesis of Intestinal Amebiasis 4.2 Transmission Amoebic ulcer It may be superficial (confined to muscularis mucosa and heal without scar) or deep ulcer (beyond muscularis mucosa and heals with scar formation) "Flask-shaped" ulcer of invasive intestinal amebiasis 4.2 Transmission Pathogenesis of Intestinal Amebiasis 4.2 Transmission Amoebic ulcer It may be localized to ileocecal region (most common site) or sigmoidorectal region or may be generalized involving the whole length of the large intestine. Pathogenesis of Intestinal Amebiasis 4.2 Transmission Amoebic ulcer Confluence of ulcers lead to sloughing of mucosa and secondary bacterial infection. There is severe abdominal cramps, bloody diarrhoea, fever, chills, nausea, tenesmus. May lead to intestinal complications. Complications of Intestinal Amebiasis 4.2 Transmission 1. Fulminant amoebic colitis: Resulting from generalized necrotic involvement of the entire large intestine. Occurs more commonly in immunocompromised patients and in pregnancy 2. Amoebic appendicitis: Results when the infection involves the appendix Associated with severe colonic amebiasis 3. Intestinal perforation and amoebic peritonitis: Occurs when the ulcer progresses beyond the serosa Most frequent complication, occurs commonly in the caecum and rectosigmoid. "Flask-shaped" ulcer of invasive intestinal amebiasis 4.2 Transmission The luminal side of the colon from fulminating amebiasis case shows several ulcers. Complications of Intestinal Amebiasis 4.2 Transmission (c) Inflammation and ulceration of the colon. (d) Histology of the sigmoid colon demonstrating Entamoeba histolytica organisms with ingested red cells (arrows). Credit: David Hugo Romero.  Complications of Intestinal Amebiasis 4.2 Transmission Charcot–Leyden crystals (are microscopic crystals composed of eosinophil protein galectin-10) and eosinophil granulocytes. 4. Toxic megacolon and intussusception Segment of intestine invaginates into the adjoining intestinal lumen, causing bowel obstruction 5. Amoeboma (amoebic granuloma) A diffuse pseudotumor like mass of granulomatous tissue found in the rectosigmoid region Inflammatory thickenings of the bowel wall that are firm, hard, well-defined lesions resembling a carcinoma. Typically it is granuloma consisting of fibroblasts, collagen, chronic inflammatory cells, numerous eosinophils, Charcoat leyden crystals, and few amebae. Can narrow the lumen of colon.  Complications of Intestinal Amebiasis 4.2 Transmission 6. Amebic stricture Caused by granulation tissue, usually at the anus, rectum, sigmoid colon 7. Chronic amoebiasis It is characterized by thickening, fibrosis, stricture formation with scarring and amoeboma formation 8. Haemorrhage Erosion of the large artery by ulcer Complications of Intestinal Amebiasis 4.2 Transmission (a) Stricture in transverse colon (arrow) with proximal dilated colon intra-operatively; (b) cut open specimen showing stricture with ulceration (pointing forceps) Complications of Intestinal Amebiasis 4.2 Transmission Pathogenesis of 4.2 Transmission Extraintestinal Amebiasis Following 1–3 months of intestinal amoebiasis, about 5– 10% of patients develop extraintestinal amoebiasis. Liver is the most common site (because of the carriage of trophozoites through the portal vein) followed by lungs, brain, genitourinary tract and spleen  Pathogenesis of 4.2 Transmission Extraintestinal Amebiasis 1. Amebic liver abscess (ALA) Rare but the most common among the extra-intestinal complications. About 5–10% of patients with intestinal amebiasis will develop ALA. More common in men than women. Amebae enter the liver via the portal vein. Most common affected site is the posterior superior surface of the right lobe of liver. Abscess is usually single or rarely multiple. Lysis of liver tissue occurs and leucocytes then infiltrate. Pathogenesis of 4.2 Transmission Extraintestinal Amebiasis Liver damage  May not be directly caused by the amoebae  By lysosomal enzymes and cytokines from the inflammatory cells surrounding the trophozoites. Anchovy sauce pus (thick brown pus)  Acidic (pH 5.2-6.7)  Centre of the abscess, blood with liquefied necrotic liver tissue free of amoeba.  The trophozoite is in the wall of the abscess. Haematogenous spread of amoebic trophozoites from colonic mucosa or by direct extension. Pathogenesis of 4.2 Transmission Extraintestinal Amebiasis Liver abscess may be multiple or more often solitary, usually located in the upper right lobe of the liver. Jaundice develops only when lesions are multiple or when they press on the biliary tract. Large, untreated abscess may rupture into the lungs and pericardium. Fever, chills and rigors, right hypochondrial pain, tenderness over enlarged liver. 4.2 Transmission Pathogenesis of 4.2 Transmission Extraintestinal Amebiasis A sample of the aspirated abscess fluid, reminiscent of the classic descriptions of the ‘anchovy paste’ liquid. Complications of 4.2 Transmission Extraintestinal Amebiasis With continuous hepatic necrosis, abscess may grow in various direction of the liver discharging the contents into the neighboring organs Right-sided liver abscess may be ruptured into: i. Skin (granuloma cutis) ii. Lungs (pulmonary amoebiasis with trophozoites in sputum) iii. Right pleura (amoebic pleuritis) iv. Below the diaphragm leads to subphrenic abscess and generalized peritonitis Complications of 4.2 Transmission Extraintestinal Amebiasis Left-sided liver abscess may rupture into the stomach or left pleura or pericardial cavity (amoebic pericarditis) Hematogenous spread can occur from liver affecting brain, lungs, spleen and genitourinary organs Clinical4.2 Manifestations Transmission of Amoebiasis Clinical classification of amebiasis: Asymptomatic infection The majority of patients have either nondysenteric amebiasis with mild  Colonization without invasion to moderate symptoms or are asymptomatic cyst passers. Symptomatic infection  Invasion with mild symptoms Infection with this parasite may persist for many years. Intestinal disease  Dysentery, colitis  90% of cases: self-limiting, asymptomatic infection  10% of cases: Invasive disease Extraintestinal amebiasis 