Amebiasis, Giardiasis, and Other Intestinal Protozoan Infections

Intestinal Amebiasis

The initial site of amebic infection is the cecum and colon after E. histolytica excysts in the small bowel. Attachment of trophozoites to the colonic mucosa is followed by mucosal invasion, leading to both superficial and deep colonic ulcerations. Host cell lysis and proteolysis of the extracellular matrix by the amebae results in ulceration and tissue invasion. Virulent strains of E. histolytica possess lectins and adhesins for adherence, cytotoxins, proteolytic enzymes, and transmembrane ion channel proteins (porins). Strains from different geographic areas vary widely in their relative virulence. Certain isoenzyme patterns appear to serve as markers for strain virulence. A rapid assay for virulence would have great clinical significance, as clinically avirulent strains such as E. dispar , E. moshkovskii , or E. bangladeshi , while morphologically indistinguishable from virulent strains, do not require treatment. For instance, currently approximately 12% of the world population is estimated to have both E. histolytica and E. dispar ; however, only 1% are estimated to have pathogenic E. histolytica. Presence of other bacteria in the colon, extremes of age, immunocompromised state, pregnancy, and malnutrition influence the virulence of the amebae.

Extraintestinal Amebiasis

Once local invasion is established in the colon, the amebae can gain access to the portal venous system to establish metastatic sites of infection. Symptomatic invasive amebiasis occurs in approximately 10% of patients with asymptomatic E. histolytica fecal carriage state. The most common location is the liver, but amebic abscesses of the lungs, brain, and, rarely, other organs do occur. These metastatic abscesses contain necrotic debris but few leukocytes or trophozoites. Trophozoites are most easily identified in the peripheral tissue. In addition to hematogenous dissemination, local spread of infection from the colon can result in cutaneous amebiasis or in paracolonic inflammatory masses referred to as amebomas.

Immunity

Infected individuals develop both humoral and cell-mediated immune responses to E. histolytica. The specific immunoglobulin response is helpful in diagnosis in non-endemic areas (see later discussions), but its importance in vivo is unknown. Cell-mediated responses are important in controlling the disease, particularly in invasive amebiasis, but only partial protection from reinfection is achieved after recovery from the primary episode. Host response determines the severity and relapses of disease. Acquired resistance to infection is thought to be linked to intestinal IgA against the carbohydrate-recognition domain of the E. histolytica galactose N -acetyl-d-galactosamine lectin. Host HLA class II-restricted immune responses also play a role in protection against E. histolytica infection. Recovery from amebiasis does not confer immunity to reinfection.

Intestinal Amebiasis

E. histolytica infection is most often asymptomatic. Asymptomatic cyst excretion can be self-limited or persist for years. Symptoms, when present, range from mild diarrhea to severe dysentery. Typically, there is gradual onset of colicky lower abdominal pain and diarrhea. Mucus, tenesmus, fever, and abdominal pain usually accompany diarrhea. Stools are often bloody and may be associated with signs of hypovolemia in severe cases. Spontaneous resolution after 1-4 weeks, sometimes with persistent asymptomatic cyst excretion, is the usual outcome. Persistent disease is not uncommon. Chronic disease may manifest cyclical relapses and remissions mimicking inflammatory bowel disease. Chronic amebic colitis results in anorexia, weight loss, and intermittent abdominal pain.

Several serious complications can develop in about 5% of patients with invasive intestinal amebiasis. Intra-abdominal complications include peritonitis secondary to perforation of a colonic abscess, intestinal hemorrhage from erosion of an abscess into an artery, or toxic megacolon from fulminant amebic colitis. The prognosis is poor in these situations, since the colon is often diffusely necrotic, rendering surgery difficult. Complications are more common in infants, pregnant women, and patients with alcohol abuse or diabetes or receiving corticosteroids. Amebomas are inflammatory mass lesions most common in the cecum, ascending colon, and descending colon; usually solitary, they can be radiologically indistinguishable from colonic neoplasms or intestinal tuberculosis. Involvement of the cecum can result in amebic appendicitis.

Extraintestinal Amebiasis

The liver is the most common site of extraintestinal amebic disease. Amebic liver abscesses (ALA) can present with the dysenteric phase of the illness or several years later. ALA are predominantly solitary (83%) and located in the right lobe (75%) of the liver. Right lobe predilection results from streaming of portal vein blood flow. ALA develops in 3-9% of cases of intestinal amebiasis. However, only 14% of patients with ALA will have active intestinal disease at the time of diagnosis, and majority will have neither active intestinal disease nor a history of dysentery. Incidence peaks in the 20- to 50-year-old age group with a male/female case ratio of 3 : 1.

The duration of symptoms before presentation is <2 weeks in the majority of cases. Virtually all patients present with right upper quadrant pain. Right lower chest pain, which may be pleuritic, is present in 25%. Other symptoms include upper abdominal swelling, weight loss, malaise, anorexia, pruritus, and cough (10-50%). Diaphragmatic irritation can result in referred pain to the right shoulder. High fever with chills and profuse night sweats may be present. Examination reveals tender hepatomegaly, sometimes with point tenderness. About half of the patients may have abnormal right lung auscultatory findings (rales or dullness). Jaundice is rare.

Primary amebic abscesses of the lung or brain are indistinguishable from pyogenic abscesses. Finally, extraintestinal disease can also result from rupture of a hepatic amebic abscess into the peritoneum, pleural cavity, or pericardium.

Intestinal Amebiasis