Cyclosporiasis is caused by an obligate intracellular coccidian protozoa. Transmission is by the fecal-oral route via contaminated food or water. Cyclosporiasis has not yet been associated with commercially canned or frozen foods. This infection is most common in tropical and subtropical climates where sanitation is poor. Residents and travelers to endemic areas are at risk. Early reports of Cyclospora cayetanensis outbreaks in the US were attributed to imported raspberries from Guatemala. Subsequently, outbreaks of C. cayetanensis infection have followed ingestion of contaminated fresh vegetables including basil, snow peas, mesclun lettuce, and cilantro. In the summer of 2013, a multi-state outbreak involving hundreds of people in the US was attributed to ingestion of prewashed salad mixes (1). A 2018 multi-state outbreak was attributed to contaminated fresh vegetable trays (2, 3).
The life cycle of C. cayetanensis is 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 and, therefore, direct person-to-person transmission is unlikely. The sporulated oocysts are ingested in contaminated food or water and excyst in the gastrointestinal tract, releasing sporozoites. The sporozoites invade the epithelial cells of the small intestine, replicate, and mature into oocysts, which are shed in stool.
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.
3. Casillas SM, Hall RL, Herwaldt BL: Cyclosporiasis Surveillance—United States, 2011-2015. MMWR Surveill Summ 68(3):1-16, 2019. doi:10.15585/mmwr.ss6803a1.
The primary symptom of cyclosporiasis 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. Relapses may follow improvement in symptoms.
In hosts with depressed cell-mediated immunity as occurs in AIDS, cyclosporiasis may cause severe, intractable, voluminous diarrhea resembling cryptosporidiosis. Extraintestinal disease in patients with AIDS may include cholecystitis and disseminated infection.
Diagnosis of cyclosporiasis is by stool tests, either molecular testing for parasite DNA or microscopic examination for oocysts. A modified Ziehl-Neelsen or Kinyoun acid-fast staining technique can help identify Cyclospora. Oocysts of Cyclospora are autofluorescent. Cyclospora oocysts are spherical and similar in morphology to but larger than Cryptosporidium oocysts.
Multiple (≥ 3) stool specimens may be needed because oocyst secretion may be intermittent.
Diagnosis is sometimes made only when intracellular parasite stages are detected in biopsies of intestinal tissue.
Treatment of choice for cyclosporiasis is double-strength trimethoprim/sulfamethoxazole (TMP/SMX): 160 mg TMP and 800 mg SMX orally 2 times a day for 7 to 10 days. Children are given 5 mg/kg TMP and 25 mg/kg SMX orally 2 times a day 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.
Prevention is by food and water precautions during travel in endemic areas and by avoiding potentially contaminated foods during outbreaks. In endemic regions, drinking water should be boiled or chlorinated, unpeeled fruit should be avoided, and vegetables cooked thoroughly. Detailed recommendations for international travelers are available in the Centers for Disease Control and Prevention (CDC) Yellow Book.
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