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Cyclosporiasis

  • Author: Shipra Gupta, MD; Chief Editor: Russell W Steele, MD  more...
 
Updated: Feb 24, 2015
 

Background

Cyclospora cayetanensis is an intestinal coccidia that infects the GI tract of both immunocompetent and immunocompromised hosts. This organism was first described in human feces in 1979. Since the advent of the acquired immunodeficiency syndrome (AIDS) epidemic, C cayetanensis has been increasingly recognized as an enteric pathogen.[1]

Cyclospora species are ubiquitous and infect a variety of animals, birds and reptiles. Humans are the only known hosts of C cayetanensis.

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Pathophysiology

Cyclospora species are variably acid-fast, round-to-ovoid organisms that measure 8-10 µm in diameter. Cyclospora species exogenously sporulate and have 2 sporocysts per oocyst. Transmission follows ingestion of oocysts in fecally contaminated water or produce. Direct person-to-person transmission is considered unlikely because the oocysts are not infectious when excreted; the oocysts undergo sporulation outside the human host before becoming infective. The median incubation period is 1 week, during which time the organism invades enterocytes of the small intestine.

Life cycle of Cyclospora. (1) When freshly passed Life cycle of Cyclospora. (1) When freshly passed in stools, the oocyst is not infective; thus, direct fecal-oral transmission cannot occur and this differentiates Cyclospora from another important coccidian parasite, Cryptosporidium. (2) In the environment, sporulation occurs after days or weeks at temperatures between 22°C to 32°C, resulting in division of the sporont into two sporocysts, each containing two elongate sporozoites (3). Fresh produce and water can serve as vehicles for transmission (4) and the sporulated oocysts are then ingested in contaminated food or water (5). The oocysts exist in the gastrointestinal tract, freeing the sporozoites which invade the epithelial cells of the small intestine (6). Inside the cells, they undergo asexual multiplication and sexual development to mature into oocysts which will be shed in stools (7). The potential mechanisms of contamination of food and water are still under investigation. Courtesy of the CDC (http://phil.cdc.gov/phil/home.asp).

Cyclospora species are characterized by an anterior polar complex that allows penetration into host cells, but the life cycle of the parasite and the mechanisms by which it interacts with human host target cells to cause disease are poorly understood.

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Epidemiology

Frequency

United States

The prevalence of infection in endemic areas is estimated at 2% to 18% (including asymptomatic and symptomatic infections) and for developed countries prevalence is estimated at 0.1% to 0.5%).[2] Cases in the developed countries are usually associated with outbreaks from recognized contaminated food and water. The first known outbreak of cyclosporiasis in the United States occurred in 1990 in a Chicago hospital's physicians' dormitory and was attributed to an infected water source.[3, 4] Since then, multiple US epidemics of cyclosporiasis have been reported and have been attributed to infected Guatemalan raspberries[5, 6] basil, mesclun lettuce,[7, 8, 9, 10] imported Thai basil,[11] and snow peas.{{Red9}[12] The most recent outbreaks in 2013 were reported in Texas related to infected cilantro and cases in Iowa and Nebraska related to contaminated salad-mix.[13] CDC monitors the occurrence of cyclosporiasis in the United States and is a notifiable disease.

As per CDC as of August, 2014, CDC had been notified of 304 ill persons with confirmed Cyclospora infection in 2014. 64% of cases were reported from Texas and 64% were reported in July 2014. Preliminary investigation linked cases in Texas with Cilantro from Mexico; however, none of the cases outside Texas were linked to cilantro.

International

Worldwide, most fecal isolates have been obtained from residents of developing countries or from travelers returning from these regions.[14, 15] Cyclosporiasis is endemic in Haiti, Nepal, and Peru, with a strong seasonal predominance during rainy spring and summer months. Cyclosporiasis has also been reported in travelers returning from Mexico, Southeast Asia, Puerto Rico, Indonesia,[16] Morocco, Pakistan, and India. Cases have also been recognized in Kuwait[17] and China.[18]

Mortality/Morbidity

Death is exceptionally rare. Very little morbidity results from this infection, except in persons with underlying immunosuppression, in whom chronic diarrhea can develop resulting in weight loss and malabsorption.

Race

No racial predilection has been reported.

Sex

Cyclosporiasis equally affects both genders.

Age

Persons of all ages can be affected, although cyclosporiasis primarily affects children in developing countries where the disease is endemic.

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Contributor Information and Disclosures
Author

Shipra Gupta, MD Fellow, Division of Infectious Diseases, Children's Hospital of Michigan

Disclosure: Nothing to disclose.

Coauthor(s)

Jocelyn Y Ang, MD, FAAP, FIDSA Associate Professor, Department of Pediatrics, Wayne State University School of Medicine; Consulting Staff, Division of Infectious Diseases, Children's Hospital of Michigan

Jocelyn Y Ang, MD, FAAP, FIDSA is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Martin Weisse, MD Program Director, Associate Professor, Department of Pediatrics, West Virginia University

Martin Weisse, MD is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Michael D Nissen, MBBS FRACP, FRCPA, Associate Professor in Biomolecular, Biomedical Science & Health, Griffith University; Director of Infectious Diseases and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children's Hospital

Michael D Nissen, MBBS is a member of the following medical societies: American Academy of Pediatrics, Royal College of Pathologists of Australasia, Royal Australasian College of Physicians, American Society for Microbiology, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Acknowledgements

Cathy Jo Schroeder, RN, MSN, APN-C Family Nurse Practitioner for James A Boozan MD, Otolaryngologist

Cathy Jo Schroeder, RN, MSN, APN-C is a member of the following medical societies: American Nurses Association and Sigma Theta Tau International

Disclosure: Nothing to disclose.

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Life cycle of Cyclospora. (1) When freshly passed in stools, the oocyst is not infective; thus, direct fecal-oral transmission cannot occur and this differentiates Cyclospora from another important coccidian parasite, Cryptosporidium. (2) In the environment, sporulation occurs after days or weeks at temperatures between 22°C to 32°C, resulting in division of the sporont into two sporocysts, each containing two elongate sporozoites (3). Fresh produce and water can serve as vehicles for transmission (4) and the sporulated oocysts are then ingested in contaminated food or water (5). The oocysts exist in the gastrointestinal tract, freeing the sporozoites which invade the epithelial cells of the small intestine (6). Inside the cells, they undergo asexual multiplication and sexual development to mature into oocysts which will be shed in stools (7). The potential mechanisms of contamination of food and water are still under investigation. Courtesy of the CDC (http://phil.cdc.gov/phil/home.asp).
Oocysts of C cayetanensis stained with modified acid-fast stain. Note the variability of staining in the four oocysts. Courtesy of the CDC (http://phil.cdc.gov/phil/home.asp).
Oocyst of C cayetanensis viewed under UV microscopy. Courtesy of the CDC (http://phil.cdc.gov/phil/home.asp).
 
 
 
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