There is no known vector for Cyclospora. Because this species exists in the environment as an oocyst and is generally transmitted through water or food contamination, it is uncertain whether a vector is a part of the life cycle.

Currently, humans are the only known natural or experimental host for Cyclospora cayentanensis. Other species of Cyclospora are known to infect vertebrates such as reptiles, insectivores, and rodents.

Because Cyclospora oocysts must undergo an environmental phase of an estimated 5 to 10 days before sporulation, it is unlikely that transmission from person to person is a major factor in infection. The vast majority of cases of cyclosporiasis in endemic areas are believed to have been transmitted through contaminated water. Transmission through fresh produce has also been documented. Recent outbreaks in the United States have been linked to raspberries, mesculin and basil. The infectious dose necessary to cause infection is unknown although it is predicted to be low. The transmissibility of Cyclospora in water is also uncertain, and would depend on the means of contamination and water treatment. Cyclospora oocysts, like Cryptosporidium oocysts, are probably highly resistant to chlorine although filtering water should be effective at removing the parasites.

Below are pictures of raspberries, mesculin and basil – items of fresh produce that have been epidemiologically linked to clustered outbreaks in the United States:

*pictures from www.cdc.gov/ncidod/emergplan/ slideset/8.htm, www.thevegetablegarden.com/ menu1.htm, www.aheb.com/garden/a-c.html

Incubation Period

The period from infection to disease ranges from 2 to 11 days, with the average being one week.

Cyclospora infection can present with a range of symptoms. Many infections, especially in those native to endemic regions, appear to be asymptomatic. The most common disease symptom is a watery diarrhea. The average length of time for the diarrhea is more than three weeks and it can often occur in a relapsing or cyclical pattern. The main symptoms may be preceded by a flu-like illness. Associated symptoms include abdominal cramping, nausea, vomiting, flatus, bloating, D-xylose malabsorption, anorexia, weight loss, dehydration, fever, fatigue, and myalgia. The illness appears to be self-limiting, although some infections can last longer than seven weeks.

Cases of cyclosporiasis in immunocompromised hosts tend to result in more severe and prolonged illness. The rate of recurrence is increased in these individuals. Some reports have described biliary tract disease in patients with AIDS.

The clinical description of Cyclospora infection is very similar to many other gastrointestinal diseases of varying causes, which frequently leads to misdiagnosis. Cyclosporiasis is clinically indistinguishable from crytopsporidiosis, isosporiasis or microsporidia, gastrointestinal diseases caused by other parasites.

The mechanisms of Cyclospora cayentanensis pathogenesis are not fully understood. Like other known species of Cyclospora, the main site of infection of Cyclospora cayentanensis is the small intestine. The parasite’s preferential site is believed to be the jejunum, where it interferes with absorption. Studies of the gastrointestinal region of infected patients have revealed inflammation of the lamina propria, surface epithelial disarray, villous atrophy and blunting, and crypt hyperplasia of jejunal tissue. Sexual and asexual forms of Cyclospora have been found in the cytoplasm of enterocytes (intestinal epithelial cells) although it is currently unknown whether the pathogenesis of this parasite is due to enterocyte dysfunction or toxins released directly by the parasite. Recent studies have shown that there is a surprising amount of genetic diversity among certain genetic sequences. This suggests the possibility of polyparasitism, simultaneous infection with different strains of the parasite.

There are multiple methods for accurate detection of Cyclospora. The most common method is through examination of a wet mount (often stained) from a stool sample.

Preparation: to maximize recovery of Cyclospora oocysts, the stool specimen should be concentrated using the Formalin-ethyl acetate technique (centrifuge for 10 minutes at 500 x g).

a. Ultraviolet epifluorescence microscopy

b. Bright-field microscopy

c. Acid-fast stained slide

d. Modified safranin technique

e. Trichome-stained slide

3. PCR detection of parasite DNA

4. Examination of jejunal biopsies

Other Notes

• Antibodies to Cyclospora have been identified and immunologic assays are currently being developed.
• Effective diagnosis of Cyclospora in environmental samples such as food, soil, and water is even more difficult. This is probably due to the very low levels of contamination that can result in infection. This limitation makes epidemiological studies more difficult.
• Major difficulties in the proper identification and diagnosis of cyclosporiasis are misdiagnosis of other parasitic and nonparasitic infections resulting in diarrhea, heavy reliance on microscopy for detection, undertrained microscopy personnel, and lack of sensitivity of particular methods. Many physicians also fail to consider Cyclospora when presented with a case of persistent diarrhea. The CDC recommends that cyclosporiasis should be considered in any case of prolonged diarrhea, even without a travel history.

*image from http://www.dpd.cdc.gov/DPDx/HTML/ImageLibrary/Cyclosporiasis_il.htm

This chart shows some diagnostic differences between Cryptosporidium parvum, Cyclospora cayentanensis, and Ispospora belli. Images A, C and F (the first images in each sequence) demonstrate acid fast smears. All three parasites appear variably acid fast. Ispospora appears considerably larger than the other parasites and Cyclospora oocysts are considerably larger than Cryptosporidium oocyst. The size differential can also be noted through bright-field microscopy – images B, D, and G. Both Cyclospora and Isospora appear a neon blue through epifluorescence testing while Cryptosporidium is not visible.

The only currently recognized treatment for cyclosporiasis is trimethoprim-sulfamethoxazole. In adults 160 mg trimethoprim and 800 mg sulfamethoxazole is given twice daily for 7 days. In children 5 mg/kg trimethoprim and 25 mg/kg sulfamethoxazole is given twice daily for 7 days. In immunocompromised patients recurrence is common so it is recommended that the dosing be increased to four times daily for ten days followed by continual prophylaxis three times per week. Cryptosporidium does not respond to trimethoprim-sulfamethoxazole.