Professional Documents
Culture Documents
Amebiasis
Entamoeba
histolytica infects hundred of millions of people worldwide; endemic mainly in the tropics, especially in areas with low socioeconomic and sanitary standards. In most infected : few or no symptoms. The 2 most common forms: - amebic colitis - amebic liver abscess.
ETIOLOGY
Two
morphologically identical but genetically distinct species of Entamoeba commonly infect humans. - Entamoeba dispar, the more prevalent species, is associated only with an asymptomatic carrier state. - E. histolytica, the pathogenic species, can become invasive, causing symptomatic disease. Five other nonpathogenic species: E. coli, E. hartmanni, E. gingivalis, E. moshkovskii, and E. polecki.
EPIDEMIOLOGY
IN most studies : not distinguish between E. histolytica and E. dispar, so true prevalence of E. histolytica is not known. infection with E. histolytica leads: - 50 million symptomatic - 40,000110,000 deaths annually. Amebiasis is the 3rd leading parasitic cause of death worldwide. 410% of infected develop amebic colitis <1% of individuals develop disseminated disease as amebic liver abscess. Amebic liver abscesses: - rare in children same in male and female children - in adults, occur predominantly in men.
Transmission
Contaminated
food or drink: most common. male homosexuals and instituted mentally retarded peoples with risk for invasive amebiasis . Untreated water human feces when used as fertilizer. Food handlers carrying amebic cysts. Direct contact with infected feces.
cysts. (A) Line drawing (B, C) Wet mounts stained E. histolytica with iodine (D) permanent preparation stained with trichome
Early Once
E. histolytica trophozoites invade the intestinal mucosa, the organisms multiply and spread laterally underneath the intestinal epithelium to produce characteristic flask-shaped ulcers.
Amebae
may produce similar lytic lesions if they reach the liver hepatic lesions are commonly called Amebae abscesses
The
CLINICAL MANIFESTATIONS
Clinical presentations: - asymptomatic cyst passage - amebic colitis, - amebic dysentery, - ameboma, - extraintestinal disease.
E.
histolytica infection is asymptomatic in about 90% of persons, but it has the potential to become invasive and should be treated. Severe disease is more common in: - young children - pregnant women - malnourished individuals - persons taking corticosteroids. Extraintestinal disease usually involves only the liver. rare extraintestinal :amebic brain abscess, pleuropulmonary disease, ulcerative skin, and genitourinary lesions.
Amebic Colitis
within 2 wk of infection or delayed for months. gradual onset of colicky abdominal pains and diarrhea(68/day). Diarrhea is associated with tenesmus. Stools are blood stained with profuse mucus and few leukocytes. No constitutional symptoms fever in only of patients. high incidence in children 15 yr of age. Severe amebic colitis in infants and young children tends to be rapidly progressive with frequent extraintestinal involvement and high mortality rates, particularly in tropical countries.
in children. occurs in <1% of infected individuals. may occur months to years after exposure. In children, fever, abdominal pain, distention, and enlargement and tenderness of the liver. Changes at the base of the right lung, such as elevation of the diaphragm and atelectasis or effusion, may also occur
LABORATORY FINDINGS
Amebic colitis: - unremarkable lab. findings ifuncomplicated, - mild anemia.
leukocytosis, moderate anemia, high ESR, High hepatic enzyme (particularly alkaline phosphatase). Stool examination: -ve in >50% of patients Ultrasonography, CT, or MRI can localize and delineate the size of the abscess cavity . The most common finding is a single abscess in the right hepatic lobe, in half of cases May be left lobe abscess and multiple abscesses.
E. histolytica antigens in stool by ELISA sensitivity (>90%) and specificity more than traditional microscopic examination of stool samples.
Microscopic examination of 3 fresh stool samples (within 30 min of passage) by experienced laboratory personnel has a sensitivity of 90% for detecting Entamoeba, but microscopy cannot differentiate between E. histolytica and E. dispar unless phagocytosed RBCs, which are specific for E. histolytica, are seen.
For this reason, microscopy is not acceptable for the diagnosis of E. histolytica infection in epidemiologic studies.
PCR
testing of stool is highly sensitive and specific. Whenever amebiasis is suspected, an additional stool sample should be preserved in polyvinyl alcohol for further examination. Endoscopy and biopsies of suspicious areas should be performed when stool sample results are negative and the index of suspicion for amebiasis remains high. Patients with invasive amebic colitis have positive test results for fecal occult blood.
The most sensitive serologic test, indirect hemagglutination, yields a positive result years after invasive infection.
Detection of E. histolytica antigens in serum is perhaps the ideal test because it is sensitive and specific, can distinguish E. dispar from E. histolytica, and can distinguish current from past infection.
However, serum antigen detection tests are not yet routinely available.
Differential Diagnosis
The differential diagnosis for amebic colitis includes: colitis due to bacterial (Shigella, Salmonella, enteropathogenic Escherichia coli, Campylobacter, Yersinia, Clostridium difficile) and viral (cytomegalovirus) pathogens, noninfectious causes such as inflammatory bowel disease. Pyogenic liver abscess due to bacterial infection, hepatoma, and echinococcal cysts.
COMPLICATIONS
Amebic colitis:
necrotizing colitis ameboma toxic megacolon extraintestinal extension local perforation and peritonitis. Uncommonly, a chronic amebic colitis develops, which can mimic inflammatory bowel disease with bouts of abdominal pain and bloody diarrhea Ameboma is a nodular focus of proliferative inflammation sometimes developing in chronic amebiasis, usually in the wall of the colon. Chronic amebiasis should be excluded before initiating corticosteroid treatment for inflammatory bowel disease, as corticosteroid therapy inadvertently given during amebic colitis has been associated with high mortality rates.
Amebic liver abscess may be associated with rupture into the peritoneum, pleural cavity, skin, or, rarely, pericardium when diagnosis and therapy are delayed. Cases of amebic abscesses in extrahepatic sites, including the lung and brain, have been reported.
TREATMENT
Invasive
amebiasis is treated with a nitroimidazole, such as metronidazole or tinidazole, followed by treatment with a luminal amebicide Tinidazole: has similar efficacy to metronidazole with shorter and simpler dosing and less frequent adverse effects. adverse effects OF metronidazole: - nausea, - abdominal discomfort, - metallic taste.
Therapy
with a nitroimidazole should be followed by lumenal ttt, such as paromomycin furoate may also be used in children >2 yr of age. intestinal infection:treated with paromomycin, which is preferred, or iodoquinol or diloxanide furoate.
Diloxanide
Asymptomatic
Broad-spectrum
antibiotic therapy may also be indicated in fulminant colitis. Intestinal perforation and toxic megacolon are indications for surgery. In amebic liver abscess, image-guided aspiration of large lesions or left lobe if the patient shows a poor clinical response 46 days after administration of amebicidal drugs.
Stool
examination should be repeated every 2 wk until the result is negative after completion of antiamebic therapy to confirm cure.
Liver abscess:50 mg/kg/day once daily for 35 days 2535 mg/kg/day in 3 divided doses for 7 days
20 mg/kg/day in 3 divided doses for 7 days 3040 mg/kg/day in 3 divided doses for 20 days
Followed by:
Paromomycin 2535 mg/kg/d in 3 divided (preferred) or doses for 7 days
Diloxanide furoate or Iodoquinol 500 mg tid for 10 days 650 mg tid for 20 days
MEDICATION
ASYMPTOMATIC INTESTINALCOLONIZATION
Paromomycin (preferred) or Diloxanide furoate[] or Iodoquinol As for invasive disease As for invasive disease
PROGNOSIS
Most
PREVENTION
Control
of amebiasis can be achieved by exercising proper sanitary measures and avoiding fecal-oral contact. Regular examination of food handlers and thorough investigation of diarrheal episodes may identify the source of infection in some communities. No prophylactic drug or vaccine is currently available for amebiasis.
Giardia Lamblia
Giardia
lamblia is a flagellated protozoan that infects the duodenum and small intestine. Infection results in clinical manifestations that range from asymptomatic colonization to acute or chronic diarrhea and malabsorption. Infection is more prevalent in children than in adults. Giardia is a particularly significant pathogen in people with malnutrition, certain immunodeficiencies, and cystic fibrosis.
ETIOLOGY
The
life cycle is 2 stages: trophozoites and cysts. Giardia infects humans after ingestion of as few as 10100 cysts. Ingested cysts produce 2 trophozoites in the duodenum. After excystation, trophozoites colonize the lumen of the duodenum and proximal jejunum, where they attach to the brush border of the intestinal epithelial cells and multiply by binary fission. The body of the trophozoite is teardrop shaped
ETIOLOGY
Giardia
trophozoites contain 2 oval nuclei anteriorly, a large ventral disk, a curved median body posteriorly, and 4 pairs of flagella. As detached trophozoites pass down the intestinal tract, they encyst to form oval cysts that contain 4 nuclei. Cysts are passed in stools of infected individuals and may remain viable in water for as long as 2 mo. Their viability often is not affected by the usual concentrations of chlorine used to purify water for drinking.
Giardia
strains that infect humans are diverse biologically, as shown by differences in antigens, restriction endonuclease patterns, DNA fingerprinting, isoenzyme patterns, and pulsedfield gel electrophoresis. Studies suggest that different Giardia genotypes may cause unique clinical manifestations, but these findings appear to vary according to the geographic region tested.
EPIDEMIOLOGY
Giardia occurs worldwide and is the most common intestinal parasite identified in public health laboratories Giardia infection usually occurs sporadically but is a frequently identified etiologic agent of outbreaks associated with drinking water. The age-specific prevalence of giardiasis is high during childhood and begins to decline after adolescence. The asymptomatic carrier rate of G. lamblia is as high as 20 30% in children younger than 36 mo of age attending childcare centers. Asymptomatic carriage may persist for several months.
Transmission
of Giardia is common in certain highrisk groups, including children and employees in child-care centers, consumers of contaminated water, The major reservoir and vehicle for spread of Giardia appears to be water contaminated with Giardia cysts, but food-borne transmission occurs. The seasonal peak in age-specific case reports coincides with the summer recreational water season. Giardia cysts are relatively resistant to chlorination and to ultraviolet light irradiation. Boiling is effective for inactivating cysts.
Person-to-person
spread also occurs, particularly in areas of low hygiene standards, frequent fecal-oral contact, and crowding. Individual susceptibility, lack of toilet training, crowding, and fecal contamination of the environment all predispose to transmission of enteropathogens, including Giardia ,in child-care centers. Child-care centers play an important role in transmission of urban giardiasis, with secondary attack rates in families as high as 1730%. Children in child-care centers may pass cysts for several months.
Humoral immunodeficiencies, including common variable hypogammaglobulinemia and X-linked agammaglobulinemia, predispose humans to chronic symptomatic Giardia infection, suggesting the importance of humoral immunity in controlling giardiasis. Selective immunoglobulin A (IgA) deficiency is associated with Giardia infection, too. Although many individuals with AIDS have relatively mild Giardia infections, some reports suggest that severe Giardia infection, often refractory to treatment, may occur in a subset of individuals with AIDS. There is a higher incidence of Giardia infection in patients with cystic fibrosis, probably owing to local factors such as the increased amount of mucus, which may protect the organism against host factors in the duodenum. Human milk contains glycoconjugates and secretory IgA antibodies that may provide protection to nursing infants
CLINICAL MANIFESTATIONS
The incubation is 12 wk. asymptomatic excretion of the organism acute infectious diarrhea chronic diarrhea with persistent gastrointestinal tract signs and symptoms, including failure to thrive and abdominal pain or cramping. Most infections are asymptomatic. There usually is no extraintestinal spread.
Symptomatic infections occur more in children. limited period of acute diarrheal disease with or without low-grade fever nausea, and anorexia abdominal distention and cramps, bloating, malaise, flatulence, and weight loss develops Initially, stools may be profuse and watery and later become greasy and foul smelling and may float. Stools do not contain blood, mucus, or fecal leukocytes. Varying degrees of malabsorption may occur. Malabsorption of sugars, fats, and fat-soluble vitamins has been well documented and may be responsible for substantial weight loss. Giardiasis has been associated with growth stunting and repeated Giardia infections with a decrease in cognitive function in children in endemic areas.
Flatulence
Abdominal cramps Nausea Foul-smelling, greasy stools Anorexia Weight loss Vomiting
3597
4481 1479 1579 4173 5373 1435
Fever
Constipation
028
027
DIAGNOSIS
Giardiasis
should be considered in young children in child care or in any person who has had contact with an index case, c\p intermittent diarrhea and constipation, malabsorption, crampy abdominal pain and bloating, failure to thrive, or weight loss.
suspected but in whom testing of stool specimens for Giardia yields a negative result, aspiration or biopsy of the duodenum or upper jejunum should be performed. In a fresh specimen, trophozoites usually can be visualized by direct wet mount. Biopsy of the small intestine should be considered in patients with characteristic clinical symptoms, negative stool and duodenal fluid specimen findings, and 1 of the following: abnormal radiographic findings, such as edema and segmentation in the small intestine; abnormal lactose tolerance test result; absent secretory IgA level; hypogammaglobulinemia; or achlorhydria.
Microscopy: trophozoites or cysts in stool specimens, but 3 stool specimens are required to achieve a sensitivity of >90%. Stool enzyme immunoassay (EIA) or direct fluorescent antibody testsIn patients in whom the diagnosis is
Polymerase
chain Radiographic contrast studies of the small intestine may show nonspecific findings such as irregular thickening of the mucosal folds. Blood cell counts usually are normal. Giardiasis is not tissue invasive and is not associated with eosinophilia.
TREATMENT
Children with acute diarrhea in whom Giardia organisms are identified should receive therapy. In addition, children who manifest failure to thrive or exhibit malabsorption or gastrointestinal tract symptoms such as chronic diarrhea should be treated. Asymptomatic excreters generally are not treated except in specific instances such as in outbreak control, for prevention of household transmission by toddlers to pregnant women and patients with hypogammaglobulinemia or cystic fibrosis, and in situations requiring oral antibiotic treatment where Giardia may have produced malabsorption of the antibiotic.
tinidazole or nitazoxanide Metronidazole When a full course of therapy is taken, metronidazole is highly effective (8090% cure rate), and the generic form is considerably less expensive than tinidazole or nitazoxanide. However, frequent adverse effects are seen with metronidazole therapy, and it requires 3 times a day dosing for 57 days.
RECOMMENDED
Tinidazole Nitazoxanide
2 g once daily >3 yr: 50 mg/kg/day once daily
Metronidazole
ALTERNATIVE
400 mg once a day for 5 days 100 mg qid for 10 days 6 mg/kg/day in 3 divided doses for 5 days 100 mg tid for 7 days
>6 yr: 400 mg once a day for 5 days 6 mg/kg/day in 4 divided doses for 10 days Not recommended 6 mg/kg/day in 3 divided doses for 5 days
PREVENTION
strict handwashing after any contact with feces. This is especially important for caregivers of diapered infants in child-care centers, where diarrhea is common and Giardia organism carriage rates are high. Methods to purify public water supplies adequately include chlorination, sedimentation, and filtration. These variables cannot be appropriately controlled in all municipalities and are difficult to control in swimming pools.
PREVENTION
Individuals, especially children in diapers, should avoid swimming if they have diarrhea. Individuals should also avoid swallowing recreational water and drinking untreated water from shallow wells, lakes, springs, ponds, streams, and rivers. Travelers to endemic areas are advised to avoid uncooked foods that might have been grown, washed, or prepared with water that was potentially contaminated. Purification of drinking water can be achieved by a filter with a pore size of <1 mm or that has been National Sanitation Foundation rated for cyst removal, or by brisk boiling of water for at least 1 min. Treatment of water with chlorine or iodine is somewhat less effective but may be used as an alternate method when boiling or filtration is not possible.