Cyclosporiasis and Cystoisosporiasis
Cyclosporiasis is infection with Cyclospora cayetanensis; cystoisosporiasis is infection with Cystoisospora (Isospora) belli. Symptoms include watery diarrhea with GI and systemic symptoms. Diagnosis is by detection of characteristic oocysts in stool or intestinal biopsy specimens. Treatment is usually with trimethoprim/sulfamethoxazole.
Cyclosporiasis and cystoisosporiasis are obligate intracellular coccidian protozoa. They are most common in tropical and subtropical climates. Transmission is by the fecal-oral route via contaminated food or drink.
The life cycles of C. cayetanensis and C. belli are similar to that of Cryptosporidium, except that oocysts passed in stool are not sporulated. Thus, when freshly passed in stools, the oocysts are not infective, and direct fecal-oral transmission cannot occur. The oocysts require days to weeks in the environment to sporulate. The sporulated oocysts are ingested in contaminated food or water and excyst in the GI tract, releasing sporozoites. The sporozoites invade the epithelial cells of the small intestine, replicate, and mature into oocysts, which are shed in stool.
In the 1990s, outbreaks of C. cayetanensis in North America were caused by ingestion of raspberries imported from Guatemala. In the summer of 2013, a multistate outbreak involving hundreds of people in the US was attributed to ingestion of prewashed salad mixes (1).
1. Abanyie F, Harvey RR, Harris JR, et al: 2013 multistate outbreaks of Cyclospora cayetanensis infections associated with fresh produce: Focus on the Texas investigations. Epidemiol Infect 143(16):3451–3458, 2015. doi: 10.1017/S0950268815000370.
The primary symptom is sudden, nonbloody, watery diarrhea, with fever, abdominal cramps, nausea, anorexia, malaise, and weight loss. In immunocompetent patients, the illness usually resolves spontaneously but can last weeks.
In hosts with depressed cell-mediated immunity as occurs in AIDS, cyclosporiasis and cystoisosporiasis may cause severe, intractable, voluminous diarrhea resembling cryptosporidiosis. Extraintestinal disease in patients with AIDS may include cholecystitis and disseminated infection.
Diagnosis of cyclosporiasis and cystoisosporiasis is by detection of oocysts via microscopic examination of the stool. A modified Ziehl-Neelsen or Kinyoun acid-fast staining technique can help identify Cyclospora and Cystoisospora oocysts. Oocysts of both Cyclospora and Cystoisospora are autofluoresent. Cyclospora oocysts are spherical and similar in morphology to but larger than Cryptosporidium oocysts. Cystoisospora oocysts are even larger and are ellipsoidal.
Multiple (≥ 3) stool specimens may be needed because cyst secretion may be intermittent. Molecular tests for parasite DNA are being developed.
Diagnosis is sometimes made only when intracellular parasite stages are detected in biopsies of intestinal tissue.
In cystoisosporiasis, the stool may contain Charcot-Leyden crystals (hexagonal, double-pointed, and often needlelike crystals) derived from eosinophils.
Unlike other protozoan infections, cystoisosporiasis may result in peripheral blood eosinophilia.
Treatment of choice for both cyclosporiasis and cystoisosporiasis is double-strength trimethoprim/sulfamethoxazole (TMP/SMX): 160 mg TMP and 800 mg SMX po bid for 7 to 10 days for cyclosporiasis or for 10 days for cystoisosporiasis. Children are given 5 mg/kg TMP and 25 mg/kg SMX po bid for the same number of days.
In patients with AIDS, higher doses and longer duration may be needed, and treatment of acute infection is usually followed by long-term suppressive therapy. Institution or optimization of antiretroviral therapy (ART) is important.
For cyclosporiasis, an alternative to TMP/SMX has yet to be identified.
Ciprofloxacin 500 mg po bid for 7 days has been used to treat cystoisosporiasis, but it is less effective than TMP/SMX.
Prevention is as for amebiasis.