AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

Section 2 of 11  

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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

Section 3 of 11  

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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.

DIFFERENTIALS

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Other Problems to be Considered

Clostridium difficile
Giardia lamblia
Entamoeba histolytica
Microsporidia
Mycobacterium avium

WORKUP

Section 5 of 11  

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Lab Studies

• Stool examination
• • The detection of oocysts upon microscopic examination of stool specimens is diagnostic.
  • The sucrose flotation method or formalin ethyl acetate method is used to concentrate stool before staining with a modified Kinyoun acid-fast satin because routine laboratory examination of stool for ova and parasites does not detect Cryptosporidium.^{7, 4} This technique stains oocysts pink or red, whereas fecal debris or yeast assumes the color of blue or green counterstain.
  • A monoclonal antibody-based fluorescein conjugated stain for oocysts in stool is commercially available. An enzyme immunoassay (EIA) to detect antigen in stool is also commercially available and is the most specific, reliable test that is widely available.¹⁶
  • Because shedding may be intermittent, examine at least 3 stool specimens collected on separate days before considering the test results negative. Fecal leukocytes are not found in stool specimens because it does not invade below the epithelial layer of the mucosa.
  • Oocysts are small (4-6 μm in diameter) and can be missed without a very careful examination of the slide.
  • GI biopsy specimens can be used instead of stool specimens. A high concentration of oocysts are seen in the jejunum.
  • Electron microscopy of stool or biopsy specimens can also be performed for direct visualization of oocysts.
  • For research purposes and for species identification, polymerase chain reaction (PCR) assays are used.
• Serologic detection: Serologic detection of specific anti-Cryptosporidium antibodies is primarily used as a research or epidemiological tool.

Imaging Studies

Imaging studies are not indicated as a first-line diagnostic approach.

• Abdominal radiography and CT scanning are nonspecific and may reveal distended loops of bowel, air-fluid levels, and disrupted bowel motility.
• When indicated, as guided by symptoms, ultrasonography or CT scanning may reveal an enlarged gallbladder with a thickened wall, dilated or irregular intrahepatic and extrahepatic biliary ducts, and a normal or stenotic distal common bile duct.
• Cholangiography may reveal beading of the common bile duct or papillary stenosis.
• In cases of respiratory involvement, chest radiography is unremarkable, with modest infiltrates or increased bronchial markings.

Procedures

• GI or liver biopsy may be indicated in cases of diagnostic uncertainty. Different parts of the intestinal tract may be affected. Liver biopsy findings may reveal the organism attached to bile duct epithelial cells. Concurrent infection with cytomegalovirus (CMV), Enterobacter cloacae, and microsporidia is common.
• In patients with related symptoms, bronchoalveolar lavage or lung biopsy findings may reveal the parasite in lavage fluid, in brush biopsy specimens, attached to the surface of bronchial mucosal cells, or in macrophages. In most instances, another pulmonary pathogen, such as CMV or Pneumocystis carinii, is concurrently detected; however, in a series of 4 patients infected with HIV, Cryptosporidium was the only pathogen identified in the respiratory tract. Clear association with intestinal cryptosporidiosis or diarrhea has not been shown in these cases.

Histologic Findings

Villous atrophy with blunting, epithelial flattening, and an increase in lamina propria lymphocytes are seen in patients with persistent cryptosporidiosis. In patients with heavier infection, crypt hyperplasia and marked infiltration with lymphocytes, plasma cells, and neutrophils is also noted. Biopsy samples of the biliary ducts may reveal the parasites.

TREATMENT

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Medical Care

• No reliable curative treatment for cryptosporidiosis is available.¹⁷
• Fluid and electrolyte management is critical, particularly in cases with large diarrheal losses.
• Nonspecific antidiarrheal agents may provide relief.
• Octreotide, a somatostatin analogue and substance P antagonist, suppresses diarrhea in chronic cryptosporidiosis.

Surgical Care

• Biliary involvement in cryptosporidiosis requires specific interventions. 
• Acalculous cholecystitis should be treated with cholecystectomy. 
• Patients with sclerosing cholangitis can usually be treated by endoscopic retrograde cholangiopancreatography (ERCP), although sphincterotomy may result in temporary relief. 
• In selected cases, recurrence may be prevented by placing a stent.

Consultations

• Infectious diseases specialist (for evaluation and specific treatment options)
• Gastroenterologist (particularly for hepatobiliary involvement)
• Surgeon (for cholecystectomy and T-tube drainage)

Diet

• Supportive care should include a lactose-free diet. 
• Although nutrition remains important, feeding is as effective as parenteral nutrition.
• Fluids should include sodium, potassium, bicarbonate, and glucose.

Activity

• Individuals with AIDS and other conditions that cause immunosuppression may wish to avoid swimming in communal pools.
• In hospitalized patients, contact precautions are strictly recommended in addition to standard precautions for patients who are incontinent or who use diapers.
• Handwashing and wearing gloves can prevent spread in daycare centers.
• Travelers visiting developing countries can bring drinking water to boil before consuming.

MEDICATION

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Supportive therapy is the key component in the management of cryptosporidiosis. Replacement of fluids and electrolytes is the critically important first step in the management of this diarrheal illness. Oral rehydration is the preferred mode, but severely ill patients may require parenteral fluids. Mature epithelial cells at the tips of the villi are preferentially lost; hence, enzymes expressed on these cells (including lactase) are lost. These losses lead to secondary lactose intolerance. Therefore, supportive care should include a lactose-free diet.

Pharmaceutical treatment is not satisfactory. Many agents have been tried with variable and limited success.

In December 2002, the US Food and Drug administration (FDA) approved nitazoxanide (Alinia) as an oral suspension to treat children with diarrhea caused by Cryptosporidium.^{18, 7} A short, 3-day course of the suspension (100 mg/5 mL) was approved in children aged 1-11 years. In clinical trials, the agent significantly reduced the duration of diarrhea caused by Cryptosporidium infections. It also reduced the rate of death in malnourished children in Africa with Cryptosporidium infection. The most common adverse effects reported were abdominal pain, diarrhea, vomiting, and headache; adverse effects were not significantly different from those reported with a placebo.

Orally administered human serum immunoglobulin or bovine colostrum has been used successfully in several anecdotal reports.

In patients with AIDS, antiretroviral treatment has been associated with improvement, possibly because of general improvement of immune function.^{13, 18, 19} Combination therapy with paromomycin and azithromycin for 4 weeks followed by paromomycin monotherapy for 8 wk has been successfully used in adult patients with AIDS. Clarithromycin has also shown activity in vitro and in animal studies, but only limited data on treatment of human cryptosporidiosis is available.

Drug Category: Antidiarrheal agents

These are used to adjunctly treat diarrhea with rehydration therapy to correct fluid and electrolyte depletion. They may provide temporary relief for some patients. Octreotide (Sandostatin) may help but is expensive.

Drug Category: Antimicrobial agents

A 3-day course of nitazoxanide oral suspension has been approved by the FDA for treatment of children older than 12 months and adults with diarrhea due to cryptosporidiosis. Paromomycin alone or with azithromycin is minimally effective. No specific treatment is necessary for patients who are immunocompetent. In patients with HIV infection, improvement in CD4 cell count with antiretroviral therapy can improve the course of disease.

FOLLOW-UP

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No follow-up care is necessary after resolution of infection.

Deterrence/Prevention

• See Activity.
• Water purification is the most important public health measure.^{20, 9, 10}
• Because chlorination has little effect on the oocysts, water purification should involve flocculation and filtration.
• Ultraviolet radiation or ozonization can also disinfect contaminated water.
• Water can also be decontaminated by bringing it to a boil or by using a filter with pore size of 1-4 μm.
• Prompt aggressive measures including temporary closure of pools must be done in case of suspected fecal contamination of recreational water. People with diarrhea should not use recreational water, and those with cryptosporidiosis should not use recreational waters for 2 weeks after symptoms resolve.
• Wearing gloves and handwashing after handling diapers can prevent person-to-person spread in daycare or centers.
• Endoscopes and similar instruments should be disinfected between uses.

Complications

• See Physical.

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 Centers for Disease Control and Prevention (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.

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 such as infected humans, farm animals, and pets. They should also consider avoiding communal swimming pools.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Failing to consider Cryptosporidium as the cause of diarrhea, particularly in cases with prolonged symptoms, may cause expensive diagnostic tests and consultations to be undertaken.
• Failing to warn patients who are immunocompromised about the risks associated with swimming in communal pools or drinking unfiltered water may lead to medicolegal problems.

Special Concerns

• 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.

MULTIMEDIA

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Media file 1:  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.
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Media type:  Photo

REFERENCES

Section 11 of 11

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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].

Article Last Updated: Apr 29, 2008