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Cyclosporiasis

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Cathy Jo Schroeder, RN, MSN, APN-C, Family Nurse Practitioner for James A Boozan MD, Otolaryngologist

Updated: Jan 21, 2009

Introduction

Background

Cyclospora cayetanensis is a coccidian parasite 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 various animals, including vipers, moles, rodents, and myriapods. Humans are the only known hosts of C cayetanensis. 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. In 1996-97, US epidemics of cyclosporiasis were attributed to infected Guatemalan raspberries,2,3 basil, and mesclun lettuce.4,5,6,7 An outbreak resulted from exposure to contaminated berries at a social function in Ontario, Canada in 1999. More recent outbreaks have been associated with imported Thai basil8 and snow peas in a cluster of infections in Pennsylvania in 2004.9,10 Otherwise, only sporadic cases, primarily involving travelers, have been documented.

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.

Disease manifests as protracted and relapsing gastroenteritis. 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.

Frequency

United States

The frequency of cyclosporiasis is unknown.

International

Most fecal isolates have been obtained from residents of developing countries or from travelers returning from these regions. 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,11 Morocco, Pakistan, and India.

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.

Race

No racial predilection has been reported.

Sex

Cyclosporiasis equally affects both sexes.

Age

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

Clinical

History

Diarrhea is the hallmark of cyclosporiasis. Onset is abrupt, 1-14 days after exposure to a contaminated source. The diarrhea is described as profuse, malodorous, and watery and can cause dehydration and weight loss. Diarrhea may be associated with 1 or more nonspecific symptoms, including intermittent crampy abdominal pain, nausea, vomiting, low-grade fever, malaise, myalgias, anorexia, bloating, flatulence, and/or profound fatigue. These symptoms are indistinguishable from those of Isospora and Cryptosporidium infections.

In an immunocompromised host, onset is more insidious, and the condition becomes chronic; symptoms and shedding of oocysts continue indefinitely. Biliary disease with right upper quadrant pain, increased alkaline phosphatase, and thickened gallbladder on ultrasound findings has been reported in an immunocompromised host infected with Cyclospora.

In an immunocompetent host, diarrhea can persist for 7 days to several weeks, with a waxing and waning course.

Physical

Physical examination findings are unremarkable, other than signs of dehydration or, in an immunocompromised host, biliary disease.

Causes

Causes of cyclosporiasis include consumption of infected water or produce or exposure to the organism during travel to countries where it is endemic. Immunosuppression is a risk factor for chronic cyclosporiasis in endemic areas or among travelers to these areas.

Differential Diagnoses

Amebiasis
Gastroenteritis
Ancylostoma Infection
Giardiasis
Ascariasis
Hookworm Infection
Campylobacter Infections
Intestinal Protozoal Diseases
Cholecystitis
Irritable Bowel Syndrome
Cholelithiasis
Isosporiasis
Cholera
Malabsorption Syndromes
Cholestasis
Protein-Losing Enteropathy
Colitis
Salmonella Infection
Crohn Disease
Shigella Infection
Cryptosporidiosis
Short Bowel Syndrome
Dehydration
Sprue
Diarrhea
Toxicity, Seafood
Dientamoeba Fragilis Infection
Ulcerative Colitis
Escherichia Coli Infections
Fascioliasis

Other Problems to Be Considered

Microspora infections

Workup

Laboratory Studies

  • Microscopic examination of fecal specimens with acid-fast staining are indicated in cyclosporiasis.
    • Diagnosis is based on the microscopic detection of oocysts in fecal specimens. Oocysts are round and resemble those of Cryptosporidium, but they are twice the size (8-10 µm). They are autofluorescent, appearing neon blue when examined with ultraviolet fluorescence microscopy. This property is not specific for Cyclospora species, however, and wanes as the specimen ages.
    • Stain Cyclospora species using modified Ziehl-Neelsen or Kinyoun acid-fast stains. These species are not visualized by Gram, Giemsa, silver, or hematoxylin-eosin staining.
  • Stool testing for ova and parasites does not typically include testing for Cyclospora species; most laboratory workers are inexperienced at identifying the oocysts.
  • No serologic assays are currently available to detect antibodies to Cyclospora species.
  • Polymerase chain reaction (PCR) tests for detection of Cyclospora DNA in stool specimens are now commercially available (by calling 800-637-0370) and may become the test of choice for making the diagnosis.
  • A PCR assay for detecting oocysts in foodstuffs has recently been described.

Procedures

  • Small-bowel biopsy reveals pathologic changes, including blunting and atrophy of villi, acute and chronic inflammation, and hyperplasia of crypts. Severity of the histopathologic findings correlates with the severity of clinical symptoms, including malabsorption.

Treatment

Medical Care

Cyclosporiasis appears to be self-limited in an immunocompetent host, lasting several days to 2 weeks. The only supportive care typically needed is the replenishment of fluids and electrolytes with juices, water, and caffeine-free soda. Occasionally, the infection can persist for 3-5 weeks, necessitating oral rehydration therapy, parenteral rehydration therapy, or both. Infection in an immunocompromised host or in a child may require parenteral rehydration.

Consultations

For prolonged or severe cases, consultation with infectious diseases specialists, gastroenterologists, or both may help.

Diet

Typical dietary measures for gastroenteritis are appropriate.

Medication

Trimethoprim-sulfamethoxazole (TMP-SMZ) has proven effective in managing cyclosporiasis in immunocompetent and immunocompromised hosts.12 TMP-SMZ administration can reduce shedding of oocysts to 1.3 days (from 9 d) and stops diarrhea within 2 days.

An immunocompromised host requires oral antibiotic therapy for longer periods, followed by prophylaxis to prevent recurrence. One study has indicated that if the patient is allergic to or does not tolerate sulfa-containing medications, ciprofloxacin is an alternative treatment. Treatment with pyrimethamine and nitazoxanide is also being studied.

Antibiotics

These agents are used to treat infection. The combination product containing TMP-SMZ is considered the DOC for managing cyclosporiasis.


Trimethoprim and sulfamethoxazole (Bactrim, Septra, Cotrim)

The only antibiotic that has been shown effective for treating cyclosporiasis. Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.

Dosing

Adult

Immunocompetent host: 160 mg TMP/800 mg SMZ PO bid for 7 d
Immunocompromised host: 160 mg TMP/800 mg SMZ PO qid for 10 d, followed by prophylaxis with 160 mg TMP/800 mg SMZ 3 times/wk

Pediatric

8 mg/kg/d (based on TMP component) PO divided bid for 7 d

Interactions

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases prevalence of thrombocytopenia purpura in elderly; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase zidovudine levels

Contraindications

Documented hypersensitivity; megaloblastic anemia due to folate deficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use near term in pregnancy because of risk of kernicterus in newborn; discontinue at first appearance of rash or sign of adverse reaction; frequently obtain CBC counts; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; caution in folate deficiency (eg, patients with chronic alcoholism, elderly persons, patients receiving anticonvulsant therapy, or those with malabsorption syndrome); hemolysis may occur in individuals with G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); administer fluids to prevent crystalluria and stone formation

Follow-up

Deterrence/Prevention

  • As with other types of travelers' diarrhea, cyclosporiasis is easily preventable when traveling by avoiding untreated water and unpeeled fruits and vegetables, all of which can be contaminated.
  • When caring for hospitalized patients infected with Cyclospora species, institute enteric precautions with thorough handwashing after each episode of patient contact.

Prognosis

  • Because this infection is self-limited in the immunocompetent host, full recovery is expected.
  • With treatment and prophylaxis to prevent relapses, infection in the immunocompromised host can generally be adequately controlled.

Patient Education

  • Discuss proper precautions needed when traveling in endemic regions to prevent this and all other fecal-oral infections.

Miscellaneous

Medicolegal Pitfalls

  • Failure to consider the diagnosis of cyclosporiasis because identification of the oocysts may not occur during routine screening for stool pathogens

Special Concerns

  • Report cases of cyclosporiasis to the health department.

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Keywords

cyclosporiasis, acquired immunodeficiency syndrome, AIDS, biliary disease, blue-green algae, chronic diarrhea, coccidian-like body, Cyanobacterium infection, Cyclospora cayetanensis, C cayetanensis, diarrhea, gastroenteritis, GI infection, large Cryptosporidium infection, parasite, parasitic infection

Contributor Information and Disclosures

Author

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Coauthor(s)

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 Academy of Nurse Practitioners and Sigma Theta Tau International
Disclosure: Nothing to disclose.

Medical Editor

Michael D Nissen, MBBS, BMedSc, 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, BMedSc, FRACP, FRCPA is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Pediatric Infectious Diseases Society, Royal Australasian College of Physicians, and Royal College of Pathologists of Australasia
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Martin Weisse, MD, Program Director, Associate Professor, Department of Pediatrics, West Virginia University
Martin Weisse, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

CME Editor

Daniel Rauch, MD, FAAP, Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine
Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine
Disclosure: Baxter Honoraria Consulting; Pfizer Honoraria Consulting

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
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, and Southern Medical Association
Disclosure: None None None

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