Pediatric Cryptosporidiosis 

  • Author: Jaya Sureshbabu, MBBS, DCh, MRCPCH(UK), MRCPI(Paeds), MRCPS(Glasg), DCH(Glasg); Chief Editor: Russell W Steele, MD   more...
 
Updated: Jun 15, 2011
 

Background

Cryptosporidiosis is a GI illness caused by protozoa of the genus Cryptosporidium. Cryptosporidium was first associated with human GI disease in 1976. It was first identified in stomachs of mice in 1907, and the name Cryptosporidium was proposed in 1912. In early 1980, with the advent of the acquired immunodeficiency syndrome (AIDS) epidemic, Cryptosporidium infections became increasingly recognized as a cause of diarrheal illness.

The genus Cryptosporidium consists of a group of protozoan parasites (seen in the image below) within the protist subphylum Apicomplexa. There are 10 known Cryptosporidium species, as recognized by host specificity, morphology, and molecular biology studies. Besides humans, the parasite can infect many other species of animals (eg, mammals, birds, reptiles) and is pathogenic to immunocompetent and immunocompromised hosts. (See Etiology.)

Hematoxylin and eosin stain of intestinal epitheliHematoxylin and eosin stain of intestinal epithelium. The blue dots (arrows) represent Cryptosporidium on the surface of the epithelial cells. Image courtesy of Carlos Abramowsky, MD, Professor of Pediatrics and Pathology, Emory University School of Medicine.

Two species mainly infect humans: Cryptosporidium hominis (previously Cryptosporidium parvum genotype 1), which infects only humans, and C parvum (previously C parvum genotype 2), which infects humans and animals.[1]Cryptosporidium canis infects dogs and humans.[2] (See Etiology.)

Organisms of the genus Cryptosporidium are able to infect and reproduce in the epithelial cell lining of the GI and respiratory tracts without causing cytopathic effects. C parvum causes most human infections. In immunocompetent individuals, the organism is primarily localized to the distal small intestines and proximal colon, whereas in immunocompromised hosts, the parasites have been identified throughout the gut, biliary tract, and respiratory tract. Children with persistent cryptosporidiosis may have villous atrophy; in children with heavier infections, crypt hyperplasia and lymphocyte infiltration is also seen.[2]

Cryptosporidiosis is characteristically associated with voluminous watery diarrhea that resembles toxin-mediated illnesses. Damage to intestinal microvilli may cause secondary malabsorption and steatorrhea. Altered intestinal permeability results in decreased absorption of fluids and electrolytes, as well as solute fluxes into the gut. (See History and Physical Examination.)

Host immune response limits the duration and severity of infection.[3, 4]

The disease is transmitted via the fecal-oral route from infected hosts. Infection usually occurs following ingestion of contaminated water, but transmission can also occur through food and person-to-person contact. Extensive waterborne outbreaks have occurred from contamination of municipal water and recreational waters (eg, swimming pools, ponds, lakes).[5, 6] Although less common, transmission through certain sexual practices involving oroanal contact has been documented. Because some genotypes have animal reservoirs, animal contact can also be associated with transmission. (See Etiology and Treatment.)

Infected persons have been reported to shed 108 -109 oocysts in a single bowel movement and to excrete oocysts for as long as 50 days after cessation of diarrhea. The infectious dose is low; ingestion of as few as 10-30 oocysts can cause infection in healthy persons. The fact that the oocysts are infectious when shed is why the parasites are readily transmitted person-to-person.

Cryptosporidium has emerged as the most frequently recognized cause of recreational water–associated outbreaks of gastroenteritis, particularly in treated (disinfected) venues. This is because the oocyst stage can resist disinfections, including chlorination, and can survive for a prolonged period in the environment.

Go to Cryptosporidiosis for complete information on this topic.

Cryptosporidial life cycle

Cryptosporidium does not multiply outside of the host. Cryptosporidium can complete its life cycle within a single host, including its asexual (merogony) and sexual (sporogony) reproductive cycles. Infection is initiated by ingestion of oocysts, which are activated in the stomach and upper intestines and release 4 infective sporozoites (seen in the image below). These motile sporozoites bind to the receptors on the surface of the intestinal epithelial cells. Two morphologic forms of the oocysts have been described: Thin-walled oocysts (asexual stage) excyst within the same host (causing self-infection), whereas the thick-walled oocysts (sexual stage) are shed into the environment.

Cryptosporidium species oocysts are rounded and meCryptosporidium species oocysts are rounded and measure 4.2-5.4 µm in diameter. Sporozoites are sometimes visible inside the oocysts, indicating that sporulation has occurred on wet mount.
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Etiology

As previously stated, cryptosporidiosis is caused by protozoa of the genus Cryptosporidium.

Although healthy individuals can become ill, immunodeficiency places an individual at increased risk for cryptosporidiosis, particularly for more severe and disseminated disease.

Immunodeficiency may be congenital or may be secondary to human immunodeficiency virus (HIV) infection, cancer chemotherapy, diabetes mellitus, or bone marrow or solid organ transplantation.

Pregnancy may predispose women to infection.

Transmission of cryptosporidiosis to children and their caregivers at daycare facilities is believed to be a major mode of person-to-person transmission. Daycare center–related outbreaks have a high infection rate of 30-60%.

Hospital-associated infection in patients and health care providers has been reported.

The following people have greater exposure to contaminated materials and are at more risk for infection:

  • Children who attend day care centers
  • Child care workers
  • Parents of infected children
  • International travelers including backpackers and hikers who drink unfiltered, untreated water
  • Swimmers who swallow contaminated recreational water
  • People who handle infected cattle
  • People exposed to human feces through sexual contact
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Epidemiology

US and international occurrence

Prevalence rates reported in large-scale surveys of fecal oocyst excretion generally range from 1-3% in developed countries in Europe and North America. Children, especially those younger than 2 years, appear to have a higher prevalence of infection than do adults.

Seroprevalence studies using antibody assays suggest that 25-35% of the population in developed countries (including the United States) have had cryptosporidiosis at some time in their life. Cryptosporidium is the most common parasitic cause of acute foodborne diarrhea in the United States, accounting for 8% of cases. The incidence in the United States and territories varied from 0.27 cases to more than 1.60 cases per 100,000 population in 2005 and on average 2.25 cases per 100,000 population in 2008.[7]

Cryptosporidium species also cause traveler's diarrhea. In 1993, more than 400,000 cases of diarrheal illness due to Cryptosporidium infection was reported in Milwaukee, Wisconsin.[8] As of July 24, 2007, a total of 18 cryptosporidiosis outbreaks had been reported to the Centers for Disease Control and Prevention (CDC).[7]

Cryptosporidium parasites are ubiquitous, except in Antarctica, and infection is more common in warm, moist months. In the United States, incidence peaks from July through September. Wastewater sources, such as raw sewage and runoff from dairies and grazing fields, contaminate the water sources. Outbreaks in daycare centers with incidence rates of 30-60% have been reported.

In developing countries, cryptosporidiosis causes approximately 5-10% of cases of acute diarrheal illness. Oocyst excretion is found in 7-8.5% of the population in less developed countries, and seroprevalence of antibodies may be as high as 64%. Prevalence may be higher in developing countries than in industrialized ones as a result of lack of clean water and sanitary facilities, crowding, and animal reservoirs in close proximity to residences.

Cryptosporidiosis is a notifiable disease at the European Union level, and surveillance data are collected through the European Basic Surveillance Network.[9, 10] The disease distribution in Europe for 2005 included 7,960 cryptosporidiosis cases reported among 16 countries. The crude incidence rate was 1.9 cases per 100,000 population, although considerable differences in the rates of cryptosporidiosis between countries were observed. A pronounced seasonal peak was observed in the autumn season, with 59% of cases reported between August and November. However, Ireland and Spain experienced a peak in spring and summer, respectively. Routine cryptosporidiosis surveillance in Northwest England over 17 years revealed that the cases predominantly occurred in spring and autumn.

Race predilection

Infection is reported in all races.

Sex predilection

No sex predilection has been reported.

Age predilection

Infection may be found in individuals of all ages, including very young infants.

Children younger than 2 years may be more susceptible to infection, possibly because of increased fecal-oral transmission in this age group and because of a lack of protective immunity.

Waterborne epidemics in developed countries affect all ages.

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Prognosis

In most healthy individuals, Cryptosporidium -induced diarrhea is usually self-limited.

In patients who are severely immunocompromised, cryptosporidiosis may be more prolonged and severe, with extraintestinal manifestations.

According to the CDC, part of the case definition of AIDS is that cryptosporidiosis lasts more than 30 days in individuals who are infected with HIV. Some patients have clinical resolution, but parasitic elimination rate is unclear. This may correlate with CD4 lymphocyte counts higher than 150. In late-stage HIV infection, infection rarely remits and often contributes to death.

More than 50% of individuals with AIDS develop chronic cryptosporidiosis, and about 10% have a fulminant course.[2, 11] Treatment improves outcome.

Hepatobiliary and respiratory disease are other reasons for morbidity and mortality in AIDS patients.

Immunocompromised children generally do well. However, persistent abdominal pain, loose stools, and extraintestinal sequelae (eg, joint pain, eye pain, headache, dizzy spells, fatigue) have been reported.

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Patient Education

Enteric precautions and good hygiene are important.

Consider boiled or bottled drinking water for patients who are immunocompromised, particularly those infected with HIV with fewer than 200 CD4 cells/µL.

Persons at risk should avoid contact with known sources of Cryptosporidium, such as infected humans, farm animals, and pets. They should also consider avoiding communal swimming pools.

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Contributor Information and Disclosures
Author

Jaya Sureshbabu, MBBS, DCh, MRCPCH(UK), MRCPI(Paeds), MRCPS(Glasg), DCH(Glasg),  Consultant, Department of Pediatrics and Neonatology, Credence Institute for Womens Health and Fertility Research, Thiruvananthapuram

Jaya Sureshbabu, MBBS, DCh, MRCPCH(UK), MRCPI(Paeds), MRCPS(Glasg), DCH(Glasg), is a member of the following medical societies: Indian Academy of Pediatrics, Indian Medical Association, Royal College of Paediatrics and Child Health, Royal College of Physicians and Surgeons of Glasgow, and Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Coauthor(s)

Poothirikovil Venugopalan, MBBS, MD, FRCP(Glasg), FRCPCH,  Consulting Staff, Department of Child Health, University Hospital of North Tees and Hartlepool, UK

Poothirikovil Venugopalan, MBBS, MD, FRCP(Glasg), FRCPCH, is a member of the following medical societies: British Cardiac Society, Paediatrician with Cardiology Expertise Special Interest Group, Royal College of Paediatrics and Child Health, and Royal College of Physicians and Surgeons of Glasgow

Disclosure: Nothing to disclose.

Athena P Kourtis, MD, PhD  Associate Professor, Department of Pediatrics, Divisions of Infectious Diseases and Epidemiology, Emory University School of Medicine; Senior Fellow, Centers for Disease Control and Prevention

Athena P Kourtis, MD, PhD is a member of the following medical societies: American Academy of Pediatrics and 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.

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: Nothing to disclose.

References
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  2. White C Jr. Cryptosporidiosis. In: Mandell GL, Bennett JE, Doilin R. Principles and practice of Infectious Diseases. Vol 2. 6th. Philadelphia, Pennsylvania: Elsivier Churchill Livingstone; 2005:280.

  3. Huang DB, Chappell C, Okhuysen PC. Cryptosporidiosis in children. Semin Pediatr Infect Dis. Oct 2004;15(4):253-9. [Medline].

  4. Committee on Infectious Diseases, American Academy of Pediatrics. Cryptosporidiosis. In: Pickering LK, Baker CJ, Long S, McMillan JA. Red book. 27th. Elk Grove Village, IL: AAP; 2006:270-272.

  5. Meinhardt PL, Casemore DP, Miller KB. Epidemiologic aspects of human cryptosporidiosis and the role of waterborne transmission. Epidemiol Rev. 1996;18(2):118-36. [Medline].

  6. Fayer R, Morgan U, Upton SJ. Epidemiology of Cryptosporidium: Transmission,detection and identification. Int J Parasitol. 2000;30:1305-1322.

  7. Cryptosporidiosis surveillance--United States, 2003-2005.Division of Parasitic Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, CDC [database online]. Atlanta, GA 30333: Centers for Disease Control and Prevention (CDC); Updated 2007 Sep 7.

  8. MacKenzie WR, Schell WL, Blair KA, Addiss DG, Peterson DE, Hoxie NJ, et al. Massive outbreak of waterborne cryptosporidium infection in Milwaukee, Wisconsin: recurrence of illness and risk of secondary transmission. Clin Infect Dis. Jul 1995;21(1):57-62. [Medline].

  9. Semenza JC, Nichols G. Cryptosporidiosis surveillance and water-borne outbreaks in Europe. Euro Surveill. May 1 2007;12(5):E13-4. [Medline].

  10. Cooper DL, Verlander NQ, Smith GE, Charlett A, Gerard E, Willocks L, et al. Can syndromic surveillance data detect local outbreaks of communicable disease? A model using a historical cryptosporidiosis outbreak. Epidemiol Infect. Feb 2006;134(1):13-20. [Medline]. [Full Text].

  11. Navin TR, Hardy AM. Cryptosporidiosis in patients with AIDS. J Infect Dis. Jan 1987;155(1):150. [Medline].

  12. Abubakar I, Aliyu SH, Arumugam C, Usman NK, Hunter PR. Treatment of cryptosporidiosis in immunocompromised individuals: systematic review and meta-analysis. Br J Clin Pharmacol. Apr 2007;63(4):387-93. [Medline]. [Full Text].

  13. Wolska-Kusnierz B, Bajer A, Caccio S, Heropolitanska-Pliszka E, Bernatowska E, Socha P, et al. Cryptosporidium infection in patients with primary immunodeficiencies. J Pediatr Gastroenterol Nutr. Oct 2007;45(4):458-64. [Medline].

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  17. Ayuo PO. Human cryptosporidiosis: a review. East Afr Med J. Feb 2009;86(2):89-93. [Medline].

  18. Juranek DD. Cryptosporidiosis: sources of infection and guidelines for prevention. Clin Infect Dis. Aug 1995;21 Suppl 1:S57-61. [Medline].

  19. Fox LM, Saravolatz LD. Nitazoxanide: a new thiazolide antiparasitic agent. Clin Infect Dis. Apr 15 2005;40(8):1173-80. [Medline].

  20. Smith NH, Cron S, Valdez LM, Chappell CL, White AC Jr. Combination drug therapy for cryptosporidiosis in AIDS. J Infect Dis. Sep 1998;178(3):900-3. [Medline].

  21. Mofenson LM, Brady MT, Danner SP, Dominguez KL, Hazra R, Handelsman E, et al. Guidelines for the Prevention and Treatment of Opportunistic Infections among HIV-exposed and HIV-infected children: recommendations from CDC, the National Institutes of Health, the HIV Medicine Association of the Infectious Diseases Society of America, the Pediatric Infectious Diseases Society, and the American Academy of Pediatrics. MMWR Recomm Rep. Sep 4 2009;58:1-166. [Medline]. [Full Text].

  22. Hicks P, Zwiener RJ, Squires J, Savell V. Azithromycin therapy for Cryptosporidium parvum infection in four children infected with human immunodeficiency virus. J Pediatr. Aug 1996;129(2):297-300. [Medline].

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Hematoxylin and eosin stain of intestinal epithelium. The blue dots (arrows) represent Cryptosporidium on the surface of the epithelial cells. Image courtesy of Carlos Abramowsky, MD, Professor of Pediatrics and Pathology, Emory University School of Medicine.
Cryptosporidium species oocysts are rounded and measure 4.2-5.4 µm in diameter. Sporozoites are sometimes visible inside the oocysts, indicating that sporulation has occurred on wet mount.
Cryptosporidium parvum oocysts stained with modified acid-fast. Against a blue-green background, the oocysts stand out in a bright red stain. Image courtesy of CDC DPDx parasite image library.
Cryptosporidium species oocysts stained with modified acid-fast.
 
 
 
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