Essentials of Diagnosis
- Patients are usually either travelers to tropical areas with self-limited diarrhea or immunocompromised patients with a protracted diarrheal illness.
- Unsporulated oocysts are detected on wet mounts of stool samples by acid-fast staining.
General Considerations
Epidemiology
Isospora infection is endemic in several tropical and subtropical climates in areas of South America, Africa, and southwest Asia. In the United States, Isospora belli infection occurs primarily in patients with AIDS but is still quite rare in this population, accounting for = 0.2% of AIDS-defining illnesses. Isospora infection is more common in patients with AIDS from developing countries in which the prevalence of spore passage is 15% compared with 5% in industrialized nations.
In immunocompetent patients, I belli has been identified in cases of chronic traveler’s diarrhea and is present in outbreaks of diarrhea in institutional settings such as day care and mental facilities.
Because sporulation can occur only outside the host, transmission may occur through environmental sources such as food and water. A latency state has been postulated based on increased prevalence of infection in Latin American immigrants. In Los Angeles, Latin Americans account for = 20% of AIDS cases but have 80% of I belli infections.
Microbiology
I belli, first described by Virchow in 1860, is a coccidian parasite that is host specific to humans. A 30 um × 12 um oval oocyst is ingested, releasing two sporocysts, each of which contains four sporozoites, which then infect enterocytes. An asexual cycle produces merozoites, which further infect epithelial cells; a sexual cycle produces immature, unsporulated oocysts that are passed in the feces. Sporulation occurs in a few days resulting in a mature oocyst.
Pathogenesis
The pathogenesis of I belli infection is not fully understood. Small-bowel histology reveals shortened villi, hypertrophic crypts, and inflammatory infiltration of the lamina propria with eosinophils. Symptoms of disease based on these histologic findings are likely caused by malabsorption.
Clinical Findings
Signs and Symptoms
After an incubation of < 1 week, immunocompetent patients present with an acute, self-limited diarrheal illness of varying severity resolving in 2 weeks (Box 7). Patients may pass 6-10 stools daily; the stools are foul smelling, watery, and soft. Malaise, anorexia, and abdominal cramps are common. Weight loss, headache, vomiting, and increased flatulence may occur, and occasionally fever may be documented. Oocyst shedding persists for 2-3 weeks beyond resolution of symptoms. Persistence of symptoms for months to years has been reported in some immunocompetent patients. Immunocompromised patients present with the same symptom complex but with increased severity and a protracted course.
Laboratory Findings
Stool specimens contain no leukocytes or erythrocytes but may contain Charcot-Leyden crystals, which are eosinophilic granules indicative of the peripheral eosinophilia specific to I belli infection. Laboratory evidence of malabsorption may be present.
Imaging
Nonspecific mucosal thickening is seen on abdominal films.
Differential Diagnosis
Cryptosporidiosis and microsporidiosis can have similar presentations. Also, coinfection with C parvum, Giardia spp., and Trichuris spp. has been reported in AIDS patients.
Complications
Disseminated isosporiasis in a patient with AIDS has been reported with invasion of the bowel wall, lymph nodes, liver, and spleen. Acalculous cholecystitis and reactive arthritis have also been reported to complicate infection.
Diagnosis
Diagnosis of isosporiasis depends on identification of the oocyst in stool by wet mount with subsequent confirmation using modified acid-fast or trichrome staining. Colonoscopy aspiration or the duodenal string test may be helpful to obtain the necessary sample. Oocysts autofluoresce in UV light when viewed through a 450- to 490-nm excitation filter (Table 3).
Treatment
TMP-SMX has been shown to be effective treatment (Box 8). Patients with AIDS have a 50% chance of relapse, and low-dose suppressive treatment with TMP-SMX, pyrimethamine-sulfadoxine, or pyrimethamine alone is recommended. Alternative treatments include metronidazole, ciprofloxacin hydrochloride, roxithromycin, and diclazuril.
Prognosis
Untreated isosporiasis in the immunocompromised patient can lead to severe malnutrition and dehydration and may be fatal.
Prevention & Control
No proven means of prophylaxis for isosporiasis has yet been established due to unknown details of transmission and the possibility of a latency state (see Box 6). The common usage of TMP-SMX for Pneumocystis carinii prophylaxis may indeed also play a role in I belli prophylaxis. Because I belli infection appears to be mediated through water and environmental sources, good fecal-oral hygiene and adequate water treatment are recommended.