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The authors report the results of a prospective study on hepatic amebiasis realized in national hospital of Niamey (Republic of Niger). Hepatic amebiasis is uncommon in Niger as in other hot and dry countries of Africa whereas it is common in hot and damp areas of the continent. These results point out the hypothesis of a hepatotropic strain of Entamoeba histolytica uncommon in Sahelia area whereas the amebiasis infestation is frequent.
In 15 months of the years 1979-1980, 158 patients with giardiasis and 69 patients with intestinal amebiasis were diagnosed and treated in the outpatient department of the Swiss Tropical Institute. Repeated examination of merthiolate-iodine-formol-fixed stools was the method of choice for detecting intestinal protozoa. Parasitological investigation of duodenal fluid (Enterotest) was less effective. Fewer than 30% of the cases were symptomatic, usually mentioning diarrhea (73-85%) or abdominal discomfort (20-44%). Treatment was by ornidazole single dose (2 g in adults; 40 mg/kg in children) for asymptomatic cases and a five-day treatment schedule (2 X 500 mg/day in adults, 20 mg/day in children) for symptomatic cases. In amebiasis a luminal amebicide (diloxanide furoate) was prescribed in all instances after the first stool examination. Parasitological cure rates were excellent (95%) in all cases of giardiasis but only 59 and 65% respectively in cases of asymptomatic and symptomatic amebiasis. Drug tolerance was excellent. Ornidazole is the drug of choice for all forms of giardiasis, even in a single dose. As a luminal amebicide, however, its efficacy is not superior to other nitroimidazole derivatives.
The most recent statistics clearly show that the incidence of amebiasis in Canada has increased progressively over the past 10 years. The authors review the incidence, pathophysiology and management of thoracic complications of amebiasis, including the experience from endemic countries. Complications include amebic liver abscess, best treated with metronidazole, and the resulting thoracic complications of pleural and pericardial effusion, atelectasis and rupture into the thoracic cavity. Since amebic liver abscess always precedes the thoracic complications, its early diagnosis and treatment will prevent these complications in most cases of amebiasis.
Intestinal amebiasis is still an important health problem in developing regions of the world. In order to advance our knowledge on the pathogenesis and to test the relevance of recently obtained in vitro observations, suitable in vivo experimental models of intestinal amebiasis are needed. In the past a variety of laboratory animals have been used, but the mouse, whose genetics and immunology is well known, has been seldomly used. Therefore, Entamoeba histolytica strain HM1:IMSS was directly inoculated into the cecum of C3H/HeJ mice, which were sacrificed at 5, 10, 15, 20, 25 and 30 days for histopathologic analysis. An ulcerative inflammatory disease highly reminiscent of human amebiasis was observed. Early 5 day lesions consisted of tiny erosions of the surface epithelium which evolved to deeper and more extensive destructive lesions of the cecal wall. Indeed, flask-shaped ulcers, intestinal perforations and intramural abscess formation were observed at later times. It was noticeable that, despite the lack of obvious significant tissue invasion by amebae, ulcerative disease was extensive and found virtually in all mice. These observations support the view that tissue invasion by trophozoites is not necessarily required for ulcerative disease to occur, suggesting a role for toxic factors released by amebae.
The various classes of immunoglobulins with antibody function against E. histolytica were studied in 8 children with amebic liver abscess and in 7 with acute intestinal amebiasis. The predominant fraction was IgG in 7 patients from the first group and in 1 from the second; this suggests a secondary type humoral immune response which implies a previous experience with E. histolytica antigens. A definitive predominance of IgM was shown in a patient with amebic liver abscess, the same as in primary humoral immune response. Humoral antibodies did not develop in the remaining 6 patients with acute intestinal amebiasis. The disparateness of the humoral immune response found in these cases make it difficult to speculate on the role of immunoglobulins in the pathogenesis or in immunologic protection in amebiasis. Possibly, the most important is the participation of cellular immunity.
In fifteen cases of amebiasis masquerading as appendicitis, the important findings were nausea, vomiting, epigastric pain, pain in the right lower quadrant of the abdomen, fever, and leukocytosis. Amebiasis ought to be considered and appropriate studies carried out in differential diagnosis of cases in which symptoms indicate acute, subacute or "chronic" appendicitis. Depending on indications, the studies should include radiography with barium enema, sigmoidoscopy, complement fixation test, a minimum of nine stool examinations, a stool culture, and examination of purged stools unless this is contraindicated.
Among the less commonly recognized clinical manifestations of intestinal and hepatic amebiasis are vague abdominal distress in the absence of diarrhea, symptoms like those of peptic ulcer, and symptoms of a kind that may be ascribed to psychoneurosis. Hepatic amebiasis may be confused with other diseases affecting areas above or below the right diaphragm, such as cholecystitis, viral hepatitis, pneumonia or pleurisy. Adequate therapy in every case must include a course of a drug effective against hepatic involvement (chloroquine or emetine) and a drug effective against intestinal involvement (Diodoquin, Milibis, or carbarsone). Even in the absence of positive results of stool examinations, a course of antiamebic therapy is always justified as a diagnostic and therapeutic measure.
Fulminating colitis rarely develops as a complication of amebiasis; however, it is difficult to diagnose and treat, and associated with a very high mortality rate. We report herein the case of a 62-year-old man with superacute fulminant necrotizing amebic colitis who, despite treatment with aggressive surgery and antiamebic agents, died of multiple organ failure following sepsis on the 25th day after onset. The patient had no immmunosuppressive disorders and claimed that he had never had homosexual intercourse, or traveled to the tropics in recent years. Since the incidence of amebiasis is increasing in developed countries, including Japan, more attention should be focused on the fulminating nature of this disease.
Penile amebiasis is rarely a recognized entity because the penis is not the usual site of presentation for amebiasis. Homosexual men have a higher risk of acquiring the lesion. Amebic ulcers resemble cutaneous lesions arising from squamous cell carcinoma, chancroid, primary syphilis, granuloma inguinale, and many other causes. An amebic ulcer should be suspected in a patient with balanoposthitis that resists antibiotic therapy. Biopsy is fundamental to isolate the trophozoites to confirm the diagnosis. Metronidazole and hydrochloric emetine are still the treatment of choice. This diagnosis should especially be considered in cases of lesions detected in patients who practice anogenital sex or who are immunocompromised.
Amebiasis is usually contracted in geographic areas where sanitation is poor, but outbreaks can still occur anywhere that drinking water becomes contaminated with sewage. In the majority of persons infected with the parasite, colonization of the intestine is asymptomatic. In others, symptoms of gastrointestinal distress can appear within a week. In rare cases, extra-intestinal amebiasis can cause abscesses in the liver or elsewhere. Many questions about the disease course in different patients remain to be answered. Diagnosis can be made through symptom identification; findings of right-upper-quadrant tenderness, leukocytosis, and an elevated level of alkaline phosphatase; and testing the feces for trophozoites or cysts. Clinicians disagree on whether asymptomatic persons need to be treated, but anyone who is capable of transmitting the disease should be advised of how to avoid exposing others to it.
Studies on the role of nutrition in amebiasis in humans and experimental animals are meager. Some reports suggest that malnutrition of the host increases the incidence of infection and potentiates the severity of the disease. Others suggest that malnutrition protects the host against invasion. A few reports indicate that dietary regimens can alleviate symptoms and even eradicate the parasite. Others doubt a correlation between diet and rate of infection or disease manifestations. The problem is complex because the ameba is influenced by its own diet, which in turn depends on the host's diet, the bacterial flora of the gut, and coexisting infections. The host is variously altered by dietary depletions and supplementations, which affect susceptibility and resistance, and by the presence of other disease conditions. Carefully designed and executed studies of infections in humans and experimental animals, combined with studies in vitro of the nutritional requirements and physiology of the parasite, are needed for definition of the influence of host nutrition in amebiasis.
Although amebiasis is often considered a disease of developing countries, it is an important public health problem throughout the world. At least 90% of infected patients are asymptomatic, but the remainder may present with clinical syndromes ranging from frank dysentery to abscesses of the liver, lungs, or brain. The most common challenge for physicians in developed countries is treating infection due to Entamoeba histolytica in an asymptomatic patient or determining its clinical significance in a patient with AIDS who has diarrhea. In light of recent improvements in diagnosis and therapy, the protean clinical manifestations of amebic infection are reviewed along with the indications for therapy. Advances in research that may directly affect our management of amebiasis in the near future are highlighted.
Amebiasis, a significant cause of morbidity and mortality on a global scale, is caused by invasion of the colonic mucosa by the cytolytic protozoan parasite Entamoeba histolytica. A review of the investigations into the mechanisms by which the parasite causes invasive disease is presented, including the relevant history, epidemiology, and pathology of amebiasis, the biology of the parasite, in vivo and in vitro studies of the pathogenesis of disease, the host immune responses, and possibilities for prevention and biologic control. New insights into the cell biology of E. histolytica, especially its adherence and cytolytic properties, offer several new approaches to biologic control of this invasive, destructive parasitic infection.
Several immunodiagnostic tests that detect antibody to Entamoeba histolytica are now available. Such tests are useful when demonstration of the etiologic agent is difficult (as in liver abscess), when routine diagnostic tests fail to disclose the organisms (as in severe intestinal disease compromised by failure of the laboratory to identify the organism or by the patient's use of interfering substances), and as epidemiologic tools for determining the prevalence of invasive disease in populations. Knowledge of the prevalence of amebiasis in the United States is incomplete because the disease is not routinely reported. Information currently available on the prevalence of amebiasis has accumulated from studies of selected groups that include children, institutionalized persons, members of extended families, immigrants, and male homosexuals.
Parasitologic, serologic, and epidemiologic studies were done during 1967 in Calion, Arkansas (population 544). Infection with Entamoeba histolytica was found to be endemic but was segregated along racial lines. Twenty-two (9.9%) black compared with only one (0.6%) white had E. histolytica demonstrated in one stool examination; only two blacks had symptoms suggestive of amebiasis. No positive amebiasis indirect hemaggulination titers were found in 135 white residents. In contrast, 41 (17.9%) blacks had positive titers. Age, sex, and geographic location were not associated with stool or seropositivity. Within the black population, clustering of stool and seropositivity occurred. Significantly higher rates of stool and seropositivity were seen in households with crowding and poor sanitation as evidenced by lack of indoor toilet facilities. The presence of contaminated water supplies did not correlate with stool or seropositivity. The probable importance of person-to-person transmission is suggested by the observed clustering of infection within households with crowding and unsanitary conditions. The absence of evidence for transmission by food or water further supports this hypothesis.
A prospective evaluation was made of the therapeutic efficacy of paromomycin, an orally administered, nonabsorbable aminoglycoside, in 114 homosexual men with mild-to-moderate (nondysenteric) intestinal amebiasis. All patients received 25-35 mg/kg daily in three divided doses for seven days. Of the 80 patients with gastrointestinal complaints at the onset of therapy, 55 (80%) of 69 were asymptomatic within four to six weeks after completion of treatment; 11 patients were lost to follow-up. Paromomycin produced long-term eradication of intestinal Entameba histolytica infection in 92% of all men evaluated. The rate of microbiologic cure among patients with symptoms at the onset of therapy was comparable to that among asymptomatic individuals. Paromomycin was well tolerated, with mild diarrhea during therapy the only frequent adverse effect (67% of patients). Thus, paromomycin is an effective alternative to conventional multi-drug therapy for intestinal amebiasis, and it has the advantages of low toxicity, brief duration of therapy, and a high rate of patient compliance.
One hundred forty patients with pleuropulmonary amebiasis were classified radiographically in order to rationalize therapy based on the use of metronidazole. Amebic testing with gel diffusion, serial chest x-ray films, and observation of the patient's response to treatment have dominated management of the patients, 135 of whom made a successful recovery. Five patients died. Sixty percent of the surviving patients have been reviewed at a follow-up clinic, and there has been no instance of recurrence of amebiasis.
We report cases of amebiasis in 6 human immunodeficiency virus (HIV)-positive male patients. Five were confirmed homosexuals while one was suspected. Three patients had liver abscess and 5 had colitis with duration of 10 days to months. The patients with liver abscess showed a lower incidence of abdominal pain but a higher incidence of concomitant diarrhea. Drainage therapy was effective for rapid afebrile results. Two invasive colitis cases died from perforation. This may have been due to delayed diagnosis. Invasive amebiasis is not common even in HIV-infected individuals. Among Japanese homosexual men, however, it may cause symptomatic diseases.