What is Cyclospora?

Cyclospora cayetanensis is a unicellular parasite previously known as cyanobacterium-like or coccidia-like body (CLB). The first known human cases of illness caused by Cyclospora infection (i.e., cyclosporiasis) were reported in the medical literature in 1979. Cases have been reported with increased frequency from various countries since the mid 1980s, in part because of the availability of better techniques for detecting the parasite in stool specimens.

How is Cyclospora transmitted?

Infected persons excrete the oocyst stage of Cyclospora in their feces. When excreted, oocysts are not infectious and may require from days to weeks to become infectious (i.e., to sporulate). Therefore, transmission of Cyclospora directly from an infected person to someone else is unlikely. However, indirect transmission can occur if an infected person contaminates the environment and oocysts have sufficient time, under appropriate conditions, to become infectious. For example, Cyclospora may be transmitted by ingestion of water or food contaminated with oocysts. Outbreaks linked to contaminated water, as well as outbreaks linked to various types of fresh produce, have been reported in recent years [1-4]. How common the various modes of transmission and sources of infection are is not yet known, nor is it known whether animals can be infected and serve as sources of infection for humans.

Who is at risk for infection?

Persons of all ages are at risk for infection. Persons living or traveling in developing countries may be at increased risk; but infection can be acquired worldwide, including in the United States. In some countries of the world, infection appears to be seasonal.

What are the symptoms of infection?

The incubation period between acquisition of infection and onset of symptoms averages 1 week. Cyclospora infects the small intestine and typically causes watery diarrhea, with frequent, sometimes explosive, stools. Other symptoms can include loss of appetite, substantial loss of weight, bloating, increased flatus, stomach cramps, nausea, vomiting, muscle aches, low-grade fever, and fatigue. If untreated, illness may last for a few days to a month or longer, and may follow a remitting-relapsing course. Some infected persons are asymptomatic.

How is infection diagnosed?

Identification of this parasite in stool requires special laboratory tests that are not routinely done (see section on laboratory diagnosis). A single negative stool specimen does not rule out the diagnosis; three or more specimens may be required. Stool specimens should also be checked for other microbes that can cause a similar illness.

How is infection treated?

Trimethoprim/sulfamethoxazole (TMP/SMX), or Bactrim*, Septra*, or Cotrim*, has been shown in a placebo-controlled trial to be effective treatment for Cyclospora infection [5]. Adults should receive TMP 160 mg plus SMX 800 mg (one double-strength tablet) orally twice a day for 7 days. Children should receive TMP 5 mg/kg plus SMX 25 mg/kg twice a day for 7 days. Patients with AIDS may need higher doses and long-term maintenance treatment [6].

No alternative antibiotic regimen has been identified yet for patients who do not respond to or are intolerant of TMP/SMX. Anecdotal or unpublished data suggest that the following drugs are ineffective: albendazole, trimethoprim, azithromycin, nalidixic acid, norfloxacin, ciprofloxacin, tinidazole, metronidazole, quinacrine, tetracycline, doxycycline, and diloxanide furoate. Approaches to consider for treatment of such patients include observation and symptomatic treatment, use of an antibiotic whose effectiveness against Cyclospora is unknown or is based on limited data, or desensitization to TMP/SMX. The latter approach should be considered only for selected patients who require treatment, have been evaluated by an allergist, and do not have a life-threatening allergy.

How is infection prevented?

Based on currently available information, avoiding food or water that may be contaminated with stool is the best way to prevent infection. Reinfection can occur.

Key points for the laboratory diagnosis of Cyclospora [7-8]:

1. To maximize recovery of Cyclospora oocysts, first concentrate the stool specimen by the Formalin-ethyl acetate technique (centrifuge for 10 minutes at 500 x g) and then examine a wet mount and/or a stained slide of the sediment.

2. Cyclospora oocysts are 8-10 microns in diameter (in contrast, Cryptosporidium parvum oocysts are 4-6 microns in diameter).

3. Ultraviolet epifluorescence microscopy is a sensitive technique for rapidly examining stool sediments for Cyclospora oocysts, which autofluoresce (Cryptosporidium parvum oocysts do not). If suspect oocysts are found, bright-field microscopy can then be used to confirm that the structures have the characteristic morphologic features of Cyclospora oocysts (i.e., are nonrefractile spheres that contain undifferentiated cytoplasm or refractile globules).

4. On a modified acid fast-stained slide of stool (the technique used by most laboratorians), Cyclospora oocysts are variably acid fast (i.e., in the same field, oocysts may be unstained or stain from light pink to deep red). Unstained oocysts may have a wrinkled appearance; it is important to distinguish oocysts from artifacts that may be acid fast but do not have the all-important wrinkled morphology of the oocyst wall.

5. Using a modified safranin technique, oocysts uniformly stain a brilliant reddish orange if fecal smears are heated in a microwave oven during staining [9]. If epifluorescence microscopy is available, the stained slide can first be examined with this technique and suspect oocysts reexamined with bright-field microscopy.

6. Although not recommended as an optimal technique for detection of Cyclospora, on a trichrome-stained slide of stool, the oocysts appear as clear, round, and somewhat wrinkled spheres, either 8-10 microns in diameter or slightly smaller because of shrinkage during the staining process.

References:

Herwaldt BL, et al. An outbreak in 1996 of cyclosporiasis associated with imported raspberries. N Engl J Med 1997;336:1548-56.

Herwaldt BL, et al. The return of Cyclospora in 1997: another outbreak of cyclosporiasis in North America associated with imported raspberries. Ann Intern Med 1999;130:210-20.

CDC. Outbreak of cyclosporiasis- northern Virginia-Washington, D.C.-Baltimore, Maryland, metropolitan area, 1997. MMWR 1997; 46:689-91.

Huang P, et al. The first reported outbreak of diarrheal illness associated with Cyclospora in the United States. Ann Intern Med 1995;123:409-14.

Hoge CW, et al. Placebo-controlled trial of co-trimoxazole for cyclospora infections among travellers and foreign residents in Nepal. Lancet 1995;345:691-3.

Pape JW, et al. Cyclospora infection in adults infected with HIV: clinical manifestations, treatment, and prophylaxis. Ann Intern Med 1994;121:654-7.

Garcia LS, et al. Diagnostic medical parasitology. 3rd ed. Washington, DC: American Society for Microbiology, 1997:66-9.

Eberhard ML, et al. Laboratory diagnosis of Cyclospora infections. Arch Pathol Lab Med 1997;121:792-7.

Visvesvara GS, et al. Uniform staining of Cyclospora oocysts in fecal smears by a modified safranin technique with microwave heating. J Clin Microbiol 1997;35:730-3.

For more information:

Hoge CW, et al. Epidemiology of diarrhoeal illness associated with coccidian-like organism among travelers and foreign residents in Nepal. Lancet 1993;341:1175-9.
Ortega YR, et al. Cyclospora species - a new protozoan pathogen of humans. N Engl J Med 1993;328:1308-12.

Soave R. Cyclospora: an overview. Clin Infect Dis 1996;23:429-37.

Soave R, et al. Cyclospora. Infect Dis Clinics N Amer 1998;12:1-12.

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Credits: Division of Parasitic Diseases