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Introduction History Life cycle of Entamoeba Histolytica Intestinal amoebiasis Surgical complications of Intestinal Amoebiasis
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Introduction
Amebiasis is a parasitic infestation caused by the protozoon Entamoeba histolytica. Amebiasis is the third leading parasitic cause of death worldwide, after malaria and schistosomiasis. On a global basis, amebiasis affects 5/29/12 approximately 50 million persons each
Amebiasis is a Global disease, with highest incidence in tropical and subtropical climates.
History
1869 -the parasite was first identified in faecal specimens by Lewis. 1875 - Fedor Aleksandrovich Losch, first described amebiasis. 1886 - Kartulis proved amoebae to be the cause of intestinal and hepatic lesions in patients with diarrhea.
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1890 William Osler reported case of young man with dysentery who later died of liver abscess. 1891- Councilman and Lafleur, distinguished between bacillary and amebic dysentery. 1913 - Walker and Sellards described the 5/29/12 pathogenic role of amebae in extensive
LIFE CYCLE
Entamoeba Histolytca occurs in three forms : TROPHOZOITE Stage Growing or Feeding stage PRE CYSTIC Stage Intermediate stage CYSTIC Stage Infective stage
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Stable Cystic form: Ranges from 10-20 m. It has 1-4 nuclei Contain iodinestainable glycogen mass and chromatoid bodies with 5/29/12
Active Trophozoite
Size ranging from 10-60 m A clear ectoplasm and granular endoplasm that contains several vacuoles. A single 3 m to 5 m 5/29/12 nucleus
form:
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INTESTINAL AMOEBIASIS
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Entamoeba histolytica with or without overt clinical symptoms. The intestinal form affects the caecum, recto sigmoid
PATHOGENESIS
Trophozoites pass to the large intestine and using lectin-carbohydrate interaction, adhere to the colonic mucosa. Invasion is mediated by direct cell killing of host epithelial cells and other immune cells.
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E. histolytica also has been found to secrete a protein that may also contribute to host cell lysis and amebic invasion through colonic tissue.
The cellular invasion extends to the submucosa, then extends laterally, creating the classic flask-shaped 5/29/12
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CLINICAL FEATURES :
Fulminant
diarrhoea,
Sudden onset
Copious diarrhoea containing mucus and blood, Low-grade fever, Tenderness on palpation
of the
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Fulminant form
Several blood-stained, mucous stools Severe tenesmus, High fever, Abdominal pain, Distended abdomen with tenderness,
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DIAGNOSIS
Definitive diagnosis of amoebic infection rests on finding amoebae in the stools or specific antibodies in the serum. Mucus and blood are found on digital rectal examination. Palpation reveals oedema and ulceration of the rectal mucosa.
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Not sensitive (miss up to two thirds of infections) Cannot distinguish between E.histolytica and E. dispar
Serology: Anti-amoebic antibodies (IgM) 70% 5/29/12 sensitive for amoebic colitis and 90%
Colonoscopy / Sigmoidoscopy
Colonoscopy preferable Wet preparations of material from ulcerbase can show trophozoites. Biopsies should be taken from edge of ulcers.
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ELISA for detection of the galactoseinhibitable adherence protein in serum and feces and Indirect hemagglutination (IHA) tests appear to be the most reliable and sensitive serologic tests, both with 5/29/12
Plain radiographs of the abdomen are important when acute fulminating amoebic colitis is suspected. At an early stage there is generalized gaseous distension of the bowel. Later, when colonic necrosis is imminent, there is marked dilatation of the large bowel from caecum to sigmoid colon (toxic megacolon).
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CHRONIC :
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Amoebomas
Acute intestinal perforation occurs in patients with severe enteropathy. May have a mortality rate of up to 50%. Children less than 2 yrs at increased risk of perforation.
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the
inflammatory process to all coats of the colonic wall. - Use of loperamidein amoebic colitis may precipitate toxic megacolon.
Massive Haemorrhage
incidence of less than 1%, generally occurred in patients with amoebic dysentery or granuloma, due to 5/29/12
Amoebomas
A granulomatous thickening of the colon resulting from lytic necrosis followed by secondary pyogenic inflammation, leading to fibrosis and proliferative granulation tissue. Lesions are firm, hard, may resemble a carcinoma. Increasing size can cause intestinal obstruction.
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Amoebic Stricture
-Resulting from fibrosis of intestinal wall. Can involve rectum, anus or sigmoid.
Perianal ulceration
- Miliary rash , the edge of confusion, and finally the formation of ulcers or abscesses, rupture and pus discharge. - Easily be mistaken for anorectal cancer, basal cell carcinoma or skin 5/29/12
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Amoebic Appendicitis :
Clinical features are those of Acute appendicitis,
although chronic right iliac fossa pain may occur. Some patients recover on anti amoebic therapy. Most cases undergo surgery.
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Results of surgery are poorer than usual cases of appendicitis. Complications are Caecal blowout, Fistula formation, Amoebiasis cutis. In endemic areas it is prudent to give metronidazole
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TREATMENT
Metronidazole + Iodoquinol 650mg TID for 21 days. Metronidazole + Paromomycin 30 mg/kg TID 5/29/12 for 5 to 7 days.
SURGERY
- indicated for toxic megacolon, peritonitis from colonic perforation, or severe bleeding. The optimal management for acute fulminating amoebic colitis remains controversial. Most authorities agree that operation is indicated only for patients who fail to respond after 48 h of intensive 5/29/12 management, unless peritonitis develops
It is best to avoid aggressive surgery and use minimal procedures to deal with the problem. If there is no obvious necrosis of the bowel, simple suture, faecal diversion, and drainage should suffice in severely ill patients. If necrosis is present, segmental resection of the affected segment of bowel is 5/29/12 essential, followed by a double-barrelled
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Extraintestinal disease
Liver abscess
Genitourinary
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extraintestinal manifestation of amebiasis. The reasons for great male preponderance are Heavy alcohol consumption in men, Hormonal effects in premenopausal 5/29/12 women,
Liver abscess can develop within days of an attack of amoebic dysentery or may follow after months or even years. Up to 50 per cent of patients have no previous symptoms suggestive of intestinal amoebiasis.
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Average size of an amebic abscess is 5 to 15 cm in diameter and most occur in the right lobe.
The liver abscess is a well-circumscribed area where the parenchyma has been replaced by necrotic tissue.
The abscess contains acellular fluid that is usually dark reddish brown, classically described as anchovy sauce.
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Gross pathology of amoebic liver abscess and anchovy 5/29/12 sauce pus
Trophozoites are conspicuosly absent from the fluid of the abscess, which is composed of the products of necrosis of the hepatocytes and cellular debris.
Trophozoites reside in the necrotic tissue surrounding the abscess along with connective tissue and inflammatory cells.
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Risk factors for amebic liver abscess include: Alcoholism Cancer Immunosuppression Malnutrition Old age Pregnancy Recent travel to a tropical region Steroid 5/29/12 use
Clinical manifestations
COMPLICATION
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Gradual, with Abdominal pain (79 per cent), Fever (53 per cent), Malaise, Weight loss, and Occasionally jaundice. The pain is often a vague discomfort in the
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Acute with Fever Pain Chills Painful and tender abdominal mass.
Symptoms and signs of a complication: Cardiac tamponade Shock Dyspnoea or Cough result from a
CLINICAL FEATURES AMEBIC ABSCESS Age (yr) 20-40 Male-to-female ratio Solitary vs. multiple Location Travel in endemic area Diabetes
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PYOGENIC ABSCESS >50 1.5:1 Solitary 50% Usually right liver No More common (27%)
PYOGENIC ABSCESS
Alcohol use Jaundice Elevated bilirubin Elevated alkaline phosphatase Positive blood culture Positive amebic serology
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No Yes
Common No
DIAGNOSIS :
Laboratory abnormalities are common in amebic abscess. Patients typically have a mild to moderate leukocytosis without eosinophilia. Anemia is common. Mild abnormalities of LFTs, including albumin,
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The most common LFT abnormality is an elevated prothrombin time. Because more than 70% of patients with amebic liver
Elevated right dome of the diaphragm, i.e. more than 2.5 cm or more than one intercostal space higher than 5/29/12 the left
Ultrasound
Appears as a Round, Subcapsular, Hypoechoic area containing fine echoes which may layer in the dependant 5/29/12 portions.
CT scan
Appearances are in the form of a well-defined homogeneou s, hypodense area, whose Hounsfield units are greater than a benign cyst 5/29/12 less than and
TREATMENT
Metronidazole + Iodoquinol 650mg TID for 21 days. Metronidazole + Paromomycin 30 5/29/12 mg/kg TID for 5 to 7 days.
Percutaneous Drainage :
- Conservative medical
management of uncomplicated liver abscesses is safe. - Thick viscous material characteristic of amebic abscesses is difficult to drain
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through standard
clinical deterioration with medical management, - Concern of impending rupture based on size
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or location,
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Surgical Drainage:
Indications :
- Patients failing less invasive management, -Patients with complications of amebic hepatic abscess, -Patients with large left-sided 5/29/12 abscesses not
PROGNOSI S:
Factors
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The mortality rate for all patients with amebic liver abscess is about 5%. When an abscess ruptures, the mortality rate is
reported to be from 6% to as high as 50%. The average time to radiologic resolution is 5/29/12
Pulmonary Amoebiasis
-Direct primary infection (blood circulation) -Secondary infection: after liver amoebiasis
A large right amoebic empyema with raised rightdiaphragmand right lower lobe consolidation, all due to an amoebic abscess in the liver. 5/29/12
Symptoms
Chest pain when taking a breath Chest pain when coughing Pain often described as sharp
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Chest congestion Persistent cough Coughing up thick mucus: Mucus may be green, brown, yellow or tan Mucus may contain blood
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Amoebic Peritonitis :
Amoebic peritonitis is considered to be the second most common complication of amoebic liver abscess after pleuropulmonary amoebiasis.
When an abscess ruptures suddenly the natural restrictive factors like adhesions and paralytic ileus do not come into play early enough to restrict the spread of the pus. 5/29/12 Thus, acute generalised peritonitis
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diaphragm. - Does not show air under the diaphragm. Diagnostic tapping in all the four quadrants of the abdomen with a de Verres spring loaded needle should be tried. Detection of brownish pus would indicate
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Amoebic pericarditis:
The extension of the hepatic amebiasis to the pericardium through contiguity. Responsible for serious syndromes that range from mild pericarditis to catastrophic 5/29/12 purulent
Genital amoebiasis Occur in rectovaginal fistula from intestinal amoebiasis. 5/29/12 Direct inoculation
Rare complication. Differential diagnosis of perineo vulvar or penile ulcers. Cutaneous amebiasis may also occur on the abdominal wall surrounding a draining hepatic abscess, colostomy site, 5/29/12 or laparotomy
Cutaneous amoebiasis :
Treatment:
Spreading peritonitis: drugs, laparotomy, Careful peritoneal toilette, drainage of the peritoneal cavity, drainage of the abscess cavity , careful aspiration of the subdiaphragmatic spaces and exclusion of multiple abscesses.
Amebic abscess of the brain is commonly an extension of pre-existing amebiasis in extra-intestinal viscera but maybe a direct hematogenous extension from the colon.
It is invariably fulminating, with fatal termination in seven to ten days, and not specifically diagnosed until necropsy.
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Cerebral amebiasis occurs in less than 0.1% of clinical cases and the clinical features depend on the size of the lesion.
Amebic brain abscess must be considered in patients with known amebiasis and alteration of mental status or focal signs.
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On head computed tomography (CT) scanning the lesion appears irregular without a capsule or surrounding enhancement.
Medical therapy with metronidazole and surgical decompression for increased intracranial pressure have improved the outcome of cerebral amebiasis.
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BIBILIOGRAPHY
Text book of Medical Parasitology Jayaram Paniker 6 th Edition. Shackelford's Surgery of the Alimentary Tract - 6th Edition. Maingot's Abdominal Operations 11 th Edition. Surgical diseases in Tropical countriessuneet sood. 5/29/12
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