eMedicine Specialties > Pediatrics: General Medicine > Parasitology

Cryptosporidiosis

Author: Jaya Sureshbabu, MBBS, DCh, MRCPCH (UK), MRCPI (Paeds), DCH (GLAS), Registrar, Department of Pediatrics/Neonatology, Mid-western Regional Hospital, Limerick, Ireland
Coauthor(s): Poothirikovil Venugopalan, MBBS, MD, FRCP (Glasg), FRCPCH, Consulting Staff, Department of Child Health, University Hospital of Hartlepool, UK; Athena P Kourtis, MD, PhD, Assistant Professor, Department of Pediatrics, Divisions of Infectious Diseases and Epidemiology, Emory University School of Medicine
Contributor Information and Disclosures

Updated: Apr 29, 2008

Introduction

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. Prior to 1982, few incidents of human infection were reported. 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 disease is transmitted via the fecal-oral route from infected humans or animals. Infection usually occurs following ingestion of contaminated water, but can transmission can also occur through food and person-to-person. Extensive waterborne outbreaks have occurred from contamination of municipal water and recreational waters (eg, swimming pools, ponds, lakes).1,2 Although less common, transmission through certain sexual practices involving oro-anal contact has been documented.

The parasite

The genus Cryptosporidium consists of a group of protozoan parasites within the protist subphylum Apicomplexa (including Plasmodium species). There are 10 recognized Cryptosporidium species based on host specificity, morphology, and molecular biology studies. Besides humans, the parasite can infect many different species of animals (eg, mammals, birds, reptiles) and is pathogenic to immunocompetent and immunocompromised hosts. 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.3  Cryptosporidium canis infects dogs and humans.4

Cryptosporidium can complete its life cycle within a single host, including both 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. 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.

Epidemiology

Cryptosporidium has emerged as the most frequently recognized cause of recreational water–associated outbreaks of gastroenteritis, particularly in treated (disinfected) venues. The infectious dose is low, and ingestion of as few as 10-30 oocysts can cause infection in healthy persons. Cryptosporidium does not multiply outside of the host. The oocyst stage can resist disinfections, including chlorination, and can survive for a prolonged period in the environment, thus facilitating waterborne transmission. Because the oocysts are infectious when shed, the parasites are readily transmitted person-to-person. Some genotypes have animal reservoirs, and, thus, animal contact can be associated with transmission. Host immune response limits the duration and severity of infection.5,6,7

Persons at increased risk for infection include (1) individuals who have had contact with infected animals, (2) individuals who have ingested contaminated recreational water (eg, lake, river, pool, hot tub) or drinking water, (3) close contacts of infected persons (eg, those in the same family or household or in daycare settings), and (4) travelers to disease-endemic areas.

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.

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 have been reported to the Centers for Disease Control and Prevention.9

Cryptosporidiosis is a notifiable disease at the European Union level, and surveillance data are collected through the European Basic Surveillance Network.10,11 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.

Pathophysiology

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.4

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. 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.

Frequency

United States

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 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 to more than 1.60 per 100,000 population in 2005.9

International

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%.

Mortality/Morbidity

  • More than 50% of individuals with AIDS develop chronic cryptosporidiosis, and about 10% have a fulminant course.6,12,4 Treatment improves outcome.
  • Hepatobiliary or 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.

Race

  • Infection is reported in all races.
  • Prevalence appears to be greater in less developed countries, possibly as a result of lack of clean water and sanitary facilities, crowding, and animal reservoirs in close proximity to residences.

Sex

  • No sex predilection has been reported.

Age

  • 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.

Clinical

History

  • The incubation period is 2-14 days.
  • The main symptoms are related to the GI tract, but respiratory symptoms like shortness of breath may also develop.
  • Diarrhea, with or without crampy abdominal pain, may be intermittent and scant or continuous, watery, and copious; sometimes, the diarrhea is mucoid. Diarrhea rarely contains blood or leukocytes. In individuals who are immunocompetent, the median duration of diarrhea ranges from 5-10 days (mean of 10 d). Diarrhea can persist longer in individuals who are immunosuppressed. Oocyst shedding can continue for as long as 2 weeks after clinical improvement. The volume of fluid losses through diarrhea may be as high as 15 L/d, particularly in individuals with AIDS. Relapses may follow a diarrhea-free period of several days to weeks.
  • In sporadic cases, fever may be low grade or nonexistent; however, during outbreaks, fever may occur in 30-60% of patients.
  • Nausea and vomiting are present in 50% of cases.
  • Malaise may be reported.
  • Approximately 15% of patients with AIDS may present with fever, right upper-quadrant pain, jaundice, nausea, and vomiting but not necessarily with concomitant diarrhea.
  • Nonspecific respiratory symptoms, including shortness of breath, wheezing, cough, hoarseness, and croup, may be a manifestation of infection in the respiratory system.
  • In waterborne outbreaks, immunocompetent patients present with subclinical or milder illness that lasts for less than 5 days.
  • The clinical manifestations of cryptosporidiosis in patients with human immunodeficiency virus (HIV) vary.13,7,4,14 In patients with CD4 cell counts of more than 150, most infections are self-limited, similar to those in normal hosts. Other patients develop chronic diarrheal illness with frequent, foul-smelling, bulky stools associated with significant weight loss. A minority of patients develop a choleralike illness. Respiratory tract involvement is often asymptomatic but may manifest as bilateral pulmonary infiltrates with dyspnea. Biliary involvement is correlated with significantly low CD4 counts, and patients present with acalculous cholecystitis, sclerosing cholangitis, or pancreatitis.13,15,14

Physical

  • Watery diarrhea, which may also contain mucus, and dehydration are the most common signs related to GI cryptosporidiosis. Secondary malabsorption of fat, D-xylose, and vitamin B-12 has been noted in some cases.
  • Other signs related to GI illness include right upper-quadrant or epigastric tenderness, icterus, and, rarely, ascites related to pancreatic involvement.
  • Reactive arthritis that affects the hands, knees, ankles, and feet has been described.

Causes

  • 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 HIV, cancer chemotherapy, diabetes mellitus, or bone marrow or solid organ transplantation.

More on Cryptosporidiosis

Overview: Cryptosporidiosis
Differential Diagnoses & Workup: Cryptosporidiosis
Treatment & Medication: Cryptosporidiosis
Follow-up: Cryptosporidiosis
Multimedia: Cryptosporidiosis
References

References

  1. 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].

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

  3. Flynn PM. Cryptosporidium parvum. In: Long SS, Pickering LK, Prober CG, eds. Principles and Practice of Pediatrics. New York, NY: Churchill Livingstone; 1997.

  4. 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.

  5. Huang DB, Chappell C, Okhuysen PC. Cryptosporidiosis in children. Semin pediatr Infect Dis. Oct, 2004;15 (4):253-259. [Medline].

  6. CDC. Classification system for human T-lymphotropic virus type III/lymphadenopathy-associated virus infections. MMWR Morb Mortal Wkly Rep. May 23 1986;35(20):334-9. [Medline].

  7. 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.

  8. MacKenzie WR, Schell WL, Blair KA. Massive outbreak of waterborne Cryptosporidium infection in Milwaukee, Wisconsin. Clin Infect Dis. Jul, 1995;21 (1):57-62. [Medline].

  9. Cryptosporidiosis surveillance--United States, 2003-2005 [database online]. Division of Parasitic Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, CDC, Atlanta, GA 30333, USA. jey9@cdc.gov: Yoder JS, Beach MJ; Centers for Disease Control and Prevention (CDC).; 2007 Sep 7.

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

  11. Cooper DL, Verlander NQ, Smith GE, 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].

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

  13. 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].

  14. 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].

  15. Cello JP. Acquired immunodeficiency syndrome cholangiopathy: spectrum of disease. Am J Med. May 1989;86(5):539-46. [Medline].

  16. Weintraub JM. Improving cryptosporidium testing methods: a public health perspective. J Water Health. 2006;4 Suppl 1:23-6. [Medline].

  17. Soave R. Treatment strategies for cryptosporidiosis. Ann N Y Acad Sci. 1990;616:442-51. [Medline].

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

  19. Smith NH, Cron S, Valdez LM, et al. Combination drug therapy for cryptosporidiosis in AIDS. J Infect Dis. Sep 1998;178(3):900-3. [Medline].

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

Further Reading

Keywords

cryptosporidiosis, Cryptosporidium, Cryptosporidium parvum, C parvum, Cryptosporidium hominis, C hominis, diarrhea, oocysts, acquired immunodeficiency syndrome, AIDS, Plasmodium, Cryptosporidium canis, waterborne infection, traveler's diarrhea, diarrhea, villous atrophy, malabsorption, steatorrhea, foodborne diarrhea, hepatobiliary disease, respiratory disease, jaundice, nausea, vomiting, croup, respiratory infection, human immunodeficiency virus, HIV, acalculous cholecystitis, sclerosing cholangitis, pancreatitis, ascites, icterus, reactive arthritis, diabetes mellitus, cytomegalovirus, CMV, Enterobacter cloacae, microsporidia, Pneumocystis carinii

Contributor Information and Disclosures

Author

Jaya Sureshbabu, MBBS, DCh, MRCPCH (UK), MRCPI (Paeds), DCH (GLAS), Registrar, Department of Pediatrics/Neonatology, Mid-western Regional Hospital, Limerick, Ireland
Jaya Sureshbabu, MBBS, DCh, MRCPCH (UK), MRCPI (Paeds), DCH (GLAS) is a member of the following medical societies: 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 Hartlepool, UK
Poothirikovil Venugopalan, MBBS, MD, FRCP (Glasg), FRCPCH is a member of the following medical societies: British Cardiac Society, 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, Assistant Professor, Department of Pediatrics, Divisions of Infectious Diseases and Epidemiology, Emory University School of Medicine
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.

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.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

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

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

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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