Phlum, Subphylu m geo dist

Entamoeba histolytica SM, Sarcodina

Giardia Lamblia SM, Mastigophora

Balantidium Coli Ciliophora

Isospora Belli Apicomplexa

Cryptosporidia Apicomplexa

cosmopolitan but tropical & subtropical countries > trophozoites and cysts 1rily inhabit the lumen of LI occasionally trophozoites invade mucosal crypts where the lyse tissues, feed on RBC, form ulcers fresh unstained H&E faecal smear pseudopodium w ectoplasm clearly clear ectoplasm differentiated from + endoplasm nucleus not visible + + spherical nucleus w ingested RBC -> v small central pale greenish karyosome refractile bodies + fine granular chromatin granules 20-60 lining the nuclear membrane + ingested RBC -> bluish black dics in endoplasm

cosmopolitan but tropical & subtropical countries > crypts of duodenum + upper jejunum occasionally in bile ducts and gall bladder

habitat

cosmopolitan most common in tropical zones esp philippines caecum and colon of humans, pigs, guinea pigs, rats and other mammals

cosmopolitan but tropical & subtropical > epithelial cells of distal duodenum and prox jejunum

cosmopolitan

originally para of calves but can infect man, kittens, puppies, rodents

morpho TROPHOZ OITES

30-150 o bilaterally symmetrical o pear-shaped broad antly and tapering postly o 9-21 x 5-15 o Dorsal surface convex o Ventral surface ant ovoidal concavity (sucking disc) serves as attachment to mucosa o 2 vesicular nuclei in area of sucking disc o 4 pairs of flagella + 2 sausage shaped median bodies post to sucking disc o Multiply repeated by binary fission

x 25-120

Oblong/ spheroid Ant end - peristome, either wide open OR slit like Post end - cytopyge Whole body covered w fine cilia arranged in rows 1 macronucleus - v slightly curved kidney or bean shaped - lies obliquely near middle of body - about 2/5 of length of body 1 micronucleus - much smaller - often hidden 2 contractile vacuoles ; 1 near middle of body, 1 near post end Food vacuoles contain cell fragments, starch granules, faecal debris, RBC

CYSTS

spherical / oval bodies w a hyaline refractile cyst + nuclei may not be visible OR 1-4 hyaline bodies + chromatid bodies made up of RNA -> rod shaped clear areas in cytoplasm 10-20

nuclear structure is apparent and similar to trophic form + mature cyst contains 4 visible nuclei + chromatid bodies > rod shaped + rounded edges & stain blue black

o o o o o o o

oval in shape 8 x 14 4 nuclei usually at one pole Parabasal bodies Remnants of flagella Axonemes Encystations occur when liquid faeces become dehrydrated in transit down the colon

Spheroidal / ovoidal w 40-60 diameter and thick cyst wall Macro and micro nuclei can also be seen

(mature sporulated oocyst) 20-33 x 1019 Contain 2 mature sporocyst with 4 sporozoites each

(mature oocyst + 4 naked sporozoites) 4-6 in diameter

reproducti on def. host infect. stage diag. stage mode of infection

binary fission

longitudinal binary fission

transverse fission

asexual schizogenic cycle + sexual reproduction mature sporulated oocyst

asexual schizogenic cycle + sexual reproduction mature oocyst + 4 naked sporozoites

humans mature 4 nucleated cyst *if trophozoites are swallowed, they are destroyed by gastric acidity contamination of food and drink thru : 1. Polluted water supply 2. Imperfectly washed raw vege 3. Contaminated hands esp in food handlers who are cyst passers 4. Food contaminated w vomits or excreta of flies since the cysts pass unharmed thru intestine of these insects 5. Usage of human excreta as fertilizers cysts cysts

ingestion of food or water 1. Contaminated of food and drink 2. Direct infection from man to man 3. Autoinfection 4. Mechanical transmission by house flies endemic areas : infection occurs anoorally directly from one to another epidemic areas : infection thru polluted water supplies more common in children

ingestion of cyst usually in contaminated water or food basically it is a parasite of pigs, and is esp common in ppl who are in close cntct w pigs

ingestion of water or food contaminated with mature sporulated oocysts

ingestion of mature oocysts thru: 1. Contamination of food and drink by oocysts 2. Close cntct with infected calves 3. Auto-infection 4. Direct person to person 5. Inhalation

pathogenesis

pathological changes depend on : Virulence of infective strain Host resistance Host nutritional status Bacterial infection most affected areas (dt sluggish movement of faecal material : Caecum Rt & Lt colic flexures Sigmoid colon pathogenic trophozoites secrete lytic enzyme small areas of necrosis in epithelium giving a way to penetrate (penetration) erode into deeper tissues breaking thru musc. Mucosa (reach submucosa) where the spread fan-like, multiply extensively causing lytic necrosis (when necrotic content is discharged) typical flask shaped ulcers produced, mucosa in between is healthy further progress invasion may occur thru penetration of musculosa and reaching serous coat peritonitis amoebiasis of caecum appendix amoebic appendicitis chronic infection + superadded bact infection granulomatous nodular mass (amoeboma) erosion of BV in the wall of ulcers hemorrhage amoeba carried by BV as emboli to reach liver and others

under ordinary conditions, trophozoites feed on food debris in caecum but sometimes, organism can produce proteolytic enzyme digest away epithelium ulcer ulcer mayb rounded irregular OR flask shaped + narrow neck undermining sac-like cavity in submucosa colonic ulceration lymphocytic infiltration w few polymorphnuclear cells + hemorrhage 2ry bacterial invasion may follow

distortion of intestinal villi + cellular infiltration of plasma cells, lymphocytes, eosinophils

clinical pic

ASYMPTOMATIC (major of cases, 8090%) patient is a carrier of cysts this person is in danger to himself and to others SYMPTOMATIC INTESTINAL LESION 1. Acute dysentery variable incub. period : as short as 4 days, as long as a year gradual onset except in fulminating cases where it is sudden gripping abd pain + dysentery (diarrhea + tenesmus + blood + mucus in stool) localized abd pain over caecum and pelvic colon no of motions are 4-8 per day toxemic manifestations are rare Non Dysenteric Colitis Vague abd discomfort + distention of caecum and colon + gas Diarrhea alternating w constipation may be present Amoeboma / Amoebic Granuloma

good % are asymptomatic in symptomatic cases, IP last from 1-3 weeks and present itself in diff forms: Diarrhea gradual / acute stool are offensive, pale yellow and frothy similar to lentil soup Dyspepsia epigastric pain, marked nausea, flatulence Malabsorption severe infection resembles tropical sprue : weight loss lassitude fatty stools fatty stool dt : 1. attachment of sucking disc to mucous membrane blockage of mucosal cells absorption of FA 2. inflammation of epithelial cells absorption capacity both of these conditions lead to accumulation of unabsorbed FA fatty yellow frothy stools there is also malasorption of Dxylose and vit B12

may be asymptomatic but major of cases present with 1. dysentery 2. abd colic 3. tenesmus resembling amoebic dysentery 4. intestinal perforation (fulminant case) 5. invasion of extraintestinal such as liver (rare)

1. diarrhea for several months to years + weight loss + abd colic + fever 2. bowel motions, 6-10x daily 3. soft to watery, foamy + offensive smell = malabsorption 4. profuse diarrhea + weakness + anorexia + weight loss in immunosuppress ed patients (AIDS)

1. 2. 3.

4.

low grade fever abd cramps diarrhea, self limited in person w normal immune response BUT fatal in immunocompromized patients respi infection

2.

3.

Results from repeated amoebic infection + superadded bact infection mass in abd might be misdiagnosed as carcinoma Surgical removal w/out medical treatment is fatal

1.

EXTRAINTESTINAL Amoebic Hepatitis

Results from emboli of trophozoites from LI reaching liver via portal blood no of small necrotic foci, if not treated, coalesce to form abcess Acute onset : may occur during attack of dysentery / in ppl who gave no history of amoebiasis at all Sudden rise in temp + enlarged tender liver 2. Amoebic Liver (Liver Abcess)

dt untreated amoebic hepatitis toxemic manifestations are more severe, pain becomes stabbing referred to rt shoulder and increase by coughing and inspiration and relieved by lying on rt side patient has a characteristic muddy complexion denoting toxaemia liver is enlarged and tender + marked intercostals edema over site of liver abcess may rupture into pleural cavity, lung, pericardium, stomach, rt colonic flexure, perinephric area, gall bladder or skin 3. Pulmonary Amoebiasis

Thru invasion of hepatic abcess thru diaphragm / rarely blood born 1ry infection from intestinal ulcers Manifested by dyspnea + lower chest pain + cough

4.

Cutaneous lesions

On skin covering the liver area after rupture or aspiration of an amoebic liver abcess OR perineal region in debilitated infected patients Manifested by tender swollen ulcerated area 5. Cerebral lesions

Result of blood extension from preexisting lesion in liver / lung OR direct hematogenous spread from colon May stimulate brain tumour which is usually fatal COMPLICATIONS 1. Intestinal : hemorrhage, appendicitis, amoeboma 2. Extraintestinal : amoebic hepatitis, amoebic liver, lung involvement, amoebiasis cutis, may stimulate brain tumour

Lab Diagnosis

DIRECT METHOD INTESTINAL HEPATIC 1. Stool examination 1. History and clinical Dysenteric stool (trophozoite pic of patient is visible) 2. X-ray shows upward either thru fresh saline smear displacement of OR fixed stool specimen diaphragm + reduced *refer to morpho movement + Well formed stool (cyst is sometimes a fluid visible) can be seen either thru fresh saline/iodine 3. CT scan smear OR fixed stool sample 4. Aspiration ; only if theres a large abcess 2. Sigmoidoscopy so used as for visualization of amoebic treatment, lesion and confirmation of o aspirated material is diagnosis by taking scraped viscid, choc brown, material from an ulcer thick (anchovy sauce) o trophozoites never found in pus, they are only present if aspirate is taken from edge of the abcess 5. Trophozoites can be found in sputum if liver abcess rupture into the lung

DIRECT METHOD 1. Stool examination Diarrhoeic stool, trophozoite is visible in saline smears Well formed stool, cysts are visible easily by staining w Lugols iodine solution repeated stool examination shud be done coz organisms tend to pass in stools intermittently 3 samples shud be examined routinely on alternate days in scanty infections, concentration by Zn sulphate floatation technique is of value 2. Duodenal aspiration when clinical pic is suggestive of giardial infection and repeated stool examination give ve results esp that excretion of parasite is erratic and not regular 3. Entero test capsule (string test) INDIRECT METHOD detection of FL copro Ag in stools by ELISA technique is helpful and resorted when repeated ve results of stool examination and CP is suggestive

stool examination to discover trophozoite w or w/out cystic stage

1. stool examination by simple saline / iodine smear conc techniques such as zn floatation mayb used if infection is scanty organisms are acid-fast, oocysts appear bright pink when stained w modified ZN stain 2. Blood pic eosinophilia

1. stool examination using formol ether OR Sheathers sugar flotation oocysts are better visualized when stained by modified ZN acid fast stain bright pink 2. entero test 3. intestinal biopsy 4. sputum examination

INDIRECT METHOD indirect haemagglutination test (IHAT), ELISA, and gel diffusion tests are +ve in invasive amoebiasis : acute dysentery and amoebic abcess

treatment

choice of drug depends on type of clinical presentation & site of drug action luminal amoebicides - drugs act 1rily on organisms in colonic lumen mainly cyst passers tissue/systemic amoebicides - acting on invasive stages (tissue forms) all patients w invasive disease require treatment 1stly w systemically acting compound, subsequently w luminal amoebicide to eliminate any organisms in colon 1. asymptomatic intestinal infection (cyst passers) o diloxanide furoate (furamide) non dysenteric intestinal colitis o diloxanide furoate +metronidazole o furazole (combination of diloxanide furoate and metronidazole) dysenteric intestinal colitis o bed rest + fluid and electrolyte replacement therapy o specific treatment : metronidazole accompanied by furazole hepatic abcess o hospitalization + bed rest o needle aspiration is advisablewhen size of abcess is large and when severe hepatic pain and tenderness o specific treatment : metronidazole

metronidazole (flagyl)

tetracycline dose: 500mg, 4x daily for 10 days

cotrimoxazole a comnbination of trimethoprim (TMP) + sulphamethoxazo le (SMX) each tablet made up of 160mg TMP + 800mg SMX dose : 1 tablet twice daily for 10days *in immunesuppressed pastients w persistent infection treatment shud be for life

nitazoxanide

2.

3.

4.