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Asymtomatic cyst passes (Shading)
- most common
- No biopsy evidence in asymptomatic reaction spontaneously stops sheading with in 5 months, except usually route of transmission it cab be direct contact during homosexual contact canal intercourse.
- So homosexual are in this group.
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Amoebic colitis
These patients are presented with gradual onset of abdominal pain as complete with ameobic dysentria (shigella it’s acute) frequently watery stool with blood and mucous.
Symptomes:
Diarrhea
Tenesmus
Back pain
Maybe present 1 – 2 weeks before patient seeks medical attention. Fever is uncommon.
More than 80% of patients do of localized abdominal tenderness.
Fulminant progression of amoebic colitis can occur in children characterized by severe bloody diarrhea and fever with rapid progression to abdominal tenderness.
Ameobioma occurs in <1% of patient. It is similar complication to intestinal ameobiasis.
Peritonitis = complication it intestinal ameobiasis:
Then develops gradually.
Hemorrhages and structures it annually are < common.
Direct spread to infection can cause perianal cutaneous ameobiasis – mimicking Squamous cell carcinoma. We see painful ulcers.
Shigellosis, Champhylobacter, salmonesis generalized is intestinal of colitis form: E-coli infection.
Lacks of fever, pausing of fecal leukocytes are for amoebiasis.
Because amoebic colitis can mimic inflammatory bowel syndrome – non specific ulcerative colitis: it should also be diagnosed. Reaction with steroids can cause toxic mega colon and thus not indicated in ameobiasis.
Extra intestinal amoebiasis:
Complications of invasive amoebiasis:
Approximately 10% patients have no abdominal findings and may present with FUP (PUO).
All patients with extra intestine have pre existing intestinal but <30% patient have active diarrhea at time of examination. Amoebic abscess diagnosis with liver abscess of other etiologic. It can be diagnosed by height of temperature, leukocytosis, local pain but it is also very different instrumental method should be:
Amoebic liver abscess: usually single and located in right lobe of liver and occupy large malt abscesses are present.
Abscess cavities contaminate while incompletely liquefy necrotic material which is sharply distinct from the normal liver tissue.
Diagnosis:
Microscopic examination.
Examination of wet mount of frequently stool sample or scrapping from edges of bowel ulcer for motile, hematophagus trophozoides.
Microsopically:
Fresh stool sample.
Only erythrophages (invasive) fromrs of trophozoides are found. Phagocutes erythrocutes.
Trophozoides are rapidly killed by dryness, water, urine, barium antibiotics.
Serological test:
Enzyme link immunosorbent CELIAS indirect hemagglutination agar gel diffusion. Counter immune electrophoresis.
Positive in less than 95% of patients with invasive ameobiasis, but not useful positive in
The diagnosis of acute amoebiasis is problematic by hemoagglutination (indirect) cause titers of antibodies can remain positive even after years of successful reaction.
Instrumental examination:
US, CT, MRI
Sensitive to detect amoebic liver abscess.
Barium studies are contra-induced in diagnosis of acute ameobic Collitis cause of possible of colon pefortion.
But colonoscopy is exposed and useful as we can visualize typical ulcers in mucosa and we can take biopsy.
General blood analysis and biochemical are not much helpful in acute amoebiasis, it is helpful in chronic course of the disease.
The changes would be anemia.
Treatment:
Metronidazole – well antibiotic orally can be given I.V.
Amoebic colitis/ liver abscess.
Dosage= 750mg tds x 5 – 10days.
Follow up reaction with luminal agents is important for all patients with invasive amoebiasis: e.g. Iodoquinol, Diloxanide furoate (Paramonicide) these have been used worldwide except USA. Percutaneous drainage should be in patients who remain asymptomatic.
GIADIASIS – Giadia Duodenalis – Lamblia Intestinalis.
Found in animals and humans.
Endemic areas: Southern Asia, Latin America, Western USA and Russia.
Iron hemotoxyllin stained – face like appearance an micro cyst have a visible but not prominent wall, they are ellipsoid contains 2 – 4 nuclei and pe
Giadia have a simple direct lifecycle like amoeba
After ingestion and passage to intestine; the organ leaves the cyst and undergoes b fusion to form 2 trophozoides.
The trophozoides contains to proliferate and establish internal in the neuro course.
The trophozoides inhabit the mucosa of duodenum and jejunum multiply by binary fusion and cyst when swept flow GIT.
Clinics:
Initial sign nausea, decrease appetite, discomfort in upper intestine (Mesogastrium) and fatigue.
These symptoms followed by burst of bad smell watery diarrhea, flatulence, meteorism and abdominal distension. These symptoms distant patient for few days occasionally this acute stage can last for microorganism. The syndrome of mal absorption due to intestinal contamination, with loss of ut and delibitation in child.
Chronic infection is marked by recurrent brief episode of fecal loose stools, abdominal distention, meteorism.
Lactose intolerance present during active intestine can persist.
These patients can have dyskinesia of bile ducts, with pain in. yellow color of sclera.
Diagnosis with hepatitis check: ALT which would be normal here as compared to hepatitis.
Spasmolytics can be given dyskinesia of bile duct.
Reactive bacterial Cholecystitis.
Diagnosis:
Based on identification of cyst and trophozoides in feces. Fresh stool should be examine quickly by smear or sometimes it can’t be detected in feces but can be fluid from duodenal aspiration.
Reaction: CDS: Center disease control: recommendation.
Guindacrine – atabral or Metronidazole.
Flukescendone for children, paramomycin for
Good hygiene, good sanitation and reaction of clinical
Baladidiasis.
Feces looks like roseberry jelly – blood and mucous mixed together.
Especially in pig farmers.
Colonoscopy: ulcers of prolonged oval
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