Version May 2024
INTRODUCTION — Cryptosporidium is an intracellular protozoan parasite that is associated with gastrointestinal diseases in all classes of vertebrates including mammals, reptiles, birds, and fish. Along with Giardia, it is among the most common parasitic enteric pathogens in humans. The organisms infect and reproduce in the epithelial cells of the digestive or respiratory tracts. Infection is predominantly associated with diarrhea and biliary tract disease [1].
This topic will review the epidemiology, clinical manifestations, and diagnosis of cryptosporidiosis. Discussion of the treatment and prevention of cryptosporidial disease is found elsewhere. (See "Cryptosporidiosis: Treatment and prevention".)
MICROBIOLOGY — Molecular methods have enabled characterization and identification of species and genotypes within Cryptosporidium isolates [2]. There are over 30 species of Cryptosporidium, including species that infect mammals, birds, reptiles, and fish [3].
Cryptosporidium parvum (4 to 6 micrometers diameter) is the main species responsible for clinical disease in humans. C. parvum has been divided into two separate species: C. hominis (previously C. parvum genotype 1) and C. parvum (previously C. parvum genotype 2).
C. hominis apparently mainly infects humans, while C. parvum is frequently found in a number of other animals as well as in humans [4]. In one molecular typing study, C. hominis cases were more likely to occur in urban areas, whereas C. parvum cases were associated with animal exposures in rural settings [5].
The host range for many species seems to be quite variable, and C. felis, C. muris, C. canis, C. suis, and C. meleagridis have also been identified in some individuals [1,3,6]. Additional heterogeneity within species and genotype diversity may lead to variations in infectivity and clinical expression in different hosts [7].
LIFE CYCLE — The life cycle of Cryptosporidium can be completed within a single host. Oocysts are ingested, undergo excystation in the small bowel, and release four banana-shaped motile sporozoites that attach to the epithelial cell wall. The sporozoites mature asexually into meronts, which release merozoites intraluminally. These can reinvade host cells, resulting in autoinfection, or can undergo sexual maturation to form new oocytes, which can excyst within the host gastrointestinal tract or can pass out into the environment. Oocysts are infectious and can remain viable for many months at a wide range of temperatures.
EPIDEMIOLOGY — Cryptosporidium was first identified as a cause of gastrointestinal disease in humans in 1976. Cryptosporidium species have been identified in every continent except Antarctica [8] and are now recognized globally as an important cause of diarrhea in both children and adults [9]. Cryptosporidiosis outbreaks have been associated with drinking water supplies, animal contact, travel, swimming pools, and recreational water facilities. (See 'Transmission' below.)
Cryptosporidium has been described as the etiologic agent in three main epidemiologic scenarios [10]:
●Sporadic, often water-related outbreaks of self-limited diarrhea in immunocompetent hosts
●Chronic, life-threatening illness in immunocompromised patients, particularly those with human immunodeficiency virus (HIV) infection
●Diarrhea and malnutrition in young children in resource-poor settings
Outbreaks of cryptosporidiosis occur worldwide; however, infection is most common in countries that have increased crowding and poor sanitary conditions. As an example, Cryptosporidium is present in 1 to 3 percent of immunocompetent patients with diarrhea in resource-rich countries versus 7 to 10 percent in resource limited countries [11-13]. In addition, seroprevalence rates are approximately 25 to 60 percent in the United States compared with 65 to 95 percent in some resource-poor settings [14,15]. In a systematic review and meta-analysis that evaluated risk factors for Cryptosporidium infection in low- and middle-income countries, the following were associated with infection: overcrowding (odds ratio [OR] 1.37, 95% CI 1.07-1.75), household diarrhea (OR 1.98, 95% CI 1.13-3.49), animal contact (OR 1.98, 95% CI 1.11-3.54), and open defecation (OR 1.82, 95% CI 1.19-2.8) [16]. By contrast, the association with breastfeeding, which had been presumed to be protective, was not statistically significant (OR 0.4, 95% CI 0.13-1.22). Additional information on transmission of cryptosporidiosis is found below. (See 'Transmission' below.)
Although Cryptosporidium infection occurs in all age groups, it is more frequent in children [9,17-20]. Estimates of Cryptosporidium-attributable diarrhea incidence from the Global Enteric Multicenter Study suggest 2.9 and 4.7 million Cryptosporidium-attributable cases occur annually in children aged <24 months in sub-Saharan Africa and South Asia, respectively, with a total of approximately 202,000 Cryptosporidium-attributable deaths [21]. In a study of almost 9500 children in Africa and Asia seeking care for diarrhea, Cryptosporidium was identified as one of the four major contributors of moderate to severe diarrheal diseases during the first two years of life and was second only to rotavirus [9]. Among such children, Cryptosporidium was also associated with a two to three times higher risk of mortality compared with controls without diarrhea.
In the United States, cases of cryptosporidiosis are also reported most frequently in children. In surveillance data, the average annual rate of reported cryptosporidiosis is highest among children aged one to four years (approximately 3 to 9 per 100,000 population), followed by older children and adults 15 to 40 years of age (approximately 3 to 5 per 100,000 population) [17]. However, in an epidemiologic survey in New York City from 1995 to 2018, males aged 20 to 59 years of age had the highest incidence of cryptosporidiosis compared with all other age/sex groups; this was thought most likely to be driven by person-to-person sexual transmission among men who have sex with men [22]. In the United States, the prevalence of Cryptosporidium infection is also higher in certain other groups, such as patients with acquired immunodeficiency syndrome (AIDS) and dairy farmers (probably because C. parvum causes diarrhea in cattle) [23].
Between 2009 and 2017, 444 cryptosporidiosis outbreaks were reported in the United States resulting in 7465 cases [24]. The annual number of reported outbreaks increased by an average of approximately 13 percent per year. Exposure to treated recreational water, such as from pools and water playgrounds, was associated with over one-third of the outbreaks and over half of the cases. Other notable outbreak exposures included contact with cattle and with infected persons in child care settings.
In the European Union, cryptosporidiosis is a notifiable disease, and outbreaks have been reported in several countries, including Denmark, Nordic countries, England, and Scotland [25-28]. In Canada, population-based laboratory surveillance data found Cryptosporidium infection occurred at an overall rate of 6 per 100,000 population per year [19]. Similar to other countries, the incidence was significantly higher in children than in adults (17.8 per 100,000 per year occurring in those aged <20 years of age versus 1.25 per 100,000 per year for adults ≥20 years of age [relative risk 14.29, 95% CI 9.77-21.11]).
TRANSMISSION — Fecally passed Cryptosporidium oocysts are immediately infectious to those who ingest them. Transmission of cryptosporidiosis occurs via spread from an infected person or animal or from a fecally contaminated environment, such as a food or water source. Cryptosporidiosis outbreaks have been associated with drinking water supplies, animal contact, travel, swimming pools, and recreational water facilities [24,29,30]. In endemic areas, the incidence increases during rainy periods [31]. C. hominis infections are generally associated with foreign travel and daycare-associated cases, whereas C. parvum is associated with farm animal contact [32].
Ingestion of only a few oocysts (10 to 50) can lead to severe disease and persistent infection, particularly in immunodeficient patients. The ID50 for healthy people without serologic evidence of previous cryptosporidiosis has been estimated at 132 oocysts for C. parvum [33] and 10 to 83 oocysts for C. hominis [34]; infected individuals can excrete up to a billion oocysts per infection [35]. Previous exposure and immunologic health also influence host susceptibility.
Contaminated water — A major source of infection is contaminated drinking or swimming water, which causes community outbreaks and travelers' diarrhea [36]. Cryptosporidium oocysts are present in 65 to 97 percent of surface waters and are difficult to eradicate, since oocysts are resistant to many disinfectants (eg, chlorine, iodine), are not effectively removed by many filtration systems, and can survive in the environment for months [37-39]. Thus, swimming pools, natural ponds, and other recreational water sources are significant sources of infection [40,41]. Oocysts can also be intermittently detected in tap water [42].
In one report, Cryptosporidium was present in 2.8 percent of 795 international travelers with diarrhea [13]. In addition, numerous waterborne outbreaks have been reported [25,26,40,41,43-49]. In the United States, 208 outbreaks associated with treated recreational water exposures were detected between 2015 and 2019, with cryptosporidiosis causing 84 percent of 2953 cases in 155 outbreaks [49]. One of the largest outbreaks occurred in 1993, when 403,000 residents of Milwaukee developed gastrointestinal symptoms after their drinking water became contaminated [45,46]. Other notable outbreaks include one from Oregon, in which a surface water-supplied municipal water system, potentially contaminated by cattle feces, sickened 2780 persons (an attack rate of approximately 28 percent) [48], as well as an outbreak among firefighters responding to a fire in a barn that housed calves [43].
Foodborne transmission — Foodborne outbreaks are less common than waterborne outbreaks but are reported, sometimes in the setting of contaminated cafeteria food [50,51]. In one outbreak associated with consumption of food in a university cafeteria, C. parvum genotype 1 (now called C. hominis) was linked to an infected food handler who prepared raw produce [52]. Eighty-eight students and four employees became ill; C. hominis was isolated from 16 of 23 ill students (70 percent) and 2 of 4 employees. Outbreaks have been associated with apple cider contaminated by cryptosporidia oocysts [53,54], consumption of contaminated unpasteurized goat and cow milk [55,56], and barbecued meat [30]. Foodborne transmission is further supported by contemporary molecular detection of Cryptosporidium in varied foods. As an example, one study in Norway found that 8.3 percent of berries, especially strawberries and raspberries, tested positive for Cryptosporidium species [57].
Person-to-person — Person-to-person transmission is common, particularly among household members, sexual partners, children in daycare centers and their caretakers, and health care workers [58-61]. Various attack rates have been reported. In a study from Brazil, 19 percent of household contacts of index cases with cryptosporidiosis developed acute infection [62]. In Bangladesh, the secondary attack rate was 36 percent in urban families but only 8 percent in rural families [60]. In northwest England and Wales, household transmission of cryptosporidiosis occurred in a quarter of homes; homes where the index case was less than five years old and/or infected with C. hominis were more likely to have transmission and female caregivers and siblings were at greatest risk [63]. Both symptomatic and asymptomatic infections may contribute to secondary transmission [61]. In one report, 27 percent of asymptomatic children attending a daycare center in New York excreted oocysts [64].
In rural sub-Saharan Africa, infection clusters among human contacts (presumably related both to common infection sources within the community and to person-to-person spread) appear to be more common than zoonotic transmission. In a study of stool samples among 1363 children <5 years of age with diarrhea in rural communities of Gabon, Ghana, Madagascar, and Tanzania and from 176 contact networks (household members, neighbors, and animal contacts), samples were tested for Cryptosporidium (using immunochromatographic tests and 18S sequencing) and subtyped to identify transmission clusters [65]. Of 184 children diagnosed with Cryptosporidium infection, 108 had contact network specimens, with identical subtypes detected among 2 or more contacts in 36 percent of networks. Children with Cryptosporidium infection were at increased risk of having infected household members (risk ratio [RR] 3.6, 95% CI 1.7-7.5) or infected neighboring children (RR 2.9, 95% CI 1.6-5.1), but no increased risk of having positive animals (RR 1.2, 95% CI 0.8-1.9) in their contact network.
Veterinary transmission — A variety of animals can harbor species of Cryptosporidium, and exposures to fecally passed oocysts from animals can be a cause of human infections [66-68]. As examples, occupational exposures have resulted in infections among veterinary students [66], and an unusual outbreak of cryptosporidiosis occurred in responders to a rollover truck carrying infected Holstein calves [67]. In Canada, an increased prevalence of cryptosporidiosis in southern Ontario has been associated with higher dairy cattle density [69].
Respiratory — It is unclear if respiratory transmission of Cryptosporidium occurs. In a study of 1156 children in Uganda who presented with diarrhea [70], 926 fecal samples were screened, of which 116 (13 percent) were positive for Cryptosporidium. Among the patients who had evidence of fecal infection, 48 also had testing of sputum samples and 17 (35 percent) were positive for Cryptosporidium. The vast majority of the children with respiratory cryptosporidiosis were HIV seronegative (94 percent). The authors suggested that transmission could arise if oocysts are aerosolized during coughing. In a study of 37 Malawian children with diarrheal disease and positive fecal samples by sensitive polymerase chain reaction assays, 31 percent had positive sputum detection and 11 percent had detectable nasopharyngeal samples [71]. Whether respiratory transmission actually occurs is yet unknown.
RISK FACTORS FOR SEVERE DISEASE — The risk of severe and/or prolonged disease is increased in patients with cellular and humoral immune deficiencies. These include HIV infection (particularly when the CD4 count is <100 cells/microL), organ transplantation, immunoglobulin (Ig)A deficiency, hypogammaglobulinemia, receipt of immunosuppressive therapy, and genetic immune deficiencies including interleukin-21 receptor deficiency and CD40L deficiency [72-76]. However, the number of cases of cryptosporidiosis has been declining among patients with HIV, largely because of immune reconstitution with antiretroviral therapy [77]. (See "Selecting antiretroviral regimens for treatment-naïve persons with HIV-1: General approach".)
PATHOGENESIS — The pathogenesis of Cryptosporidium is not well understood, and the functional pathogenic difference between C. parvum and C. hominis have not been well elucidated. The organisms cause a secretory diarrhea that can be associated with malabsorption. It is likely that the intracellular nature of the infection interferes with intestinal absorption and secretion. The organisms can spread via the intestinal lumen to involve the biliary system, where they can cause stricturing and cholangitis. (See "AIDS cholangiopathy".)
Cryptosporidia are found within epithelial cells and are associated with distortion of the villus architecture. Inflammatory changes may be present [78]. Progressive morphological and functional abnormalities of the small intestine occur as parasite numbers increase, although intensity of infection and inflammation does not correlate well with the severity of clinical disease [79]. Whether differences in the organism's virulence or the level of host immunity primarily account for the variable course of infection in different people is not well understood.
The immune response associated with cryptosporidiosis involves cellular and humoral components. The T-lymphocyte cellular responses are important in controlling infection, as evidenced by the increased disease severity in patients with HIV with CD4 counts less than 100 cells/microL. (See 'Risk factors for severe disease' above.)
Specific IgM, IgG, and/or IgA responses develop during infection. Epidemiologic evidence for protective immunity to Cryptosporidium has been suggested by the observation that residents in areas where Cryptosporidium is endemic have milder symptoms with subsequent infections [80,81]. However, the development of antibodies is not necessarily associated with clearance of infection, as illustrated in studies of patients with HIV who developed serum and intestinal antibodies but failed to clear the infection [82,83]. The production of interferon-gamma is involved in the resolution of infection [84-87].
CLINICAL MANIFESTATIONS
Spectrum of disease — Cryptosporidium can cause asymptomatic infection, mild diarrhea, or severe enteritis with or without biliary tract involvement. Pulmonary involvement has also been described. There are no known differentiating clinical manifestations between C. parvum and C. hominis infections. (See 'Diarrhea' below and 'Other manifestations' below.)
Asymptomatic infection can occur in immunocompetent and immunocompromised patients [88,89]. As many as 30 percent of childhood infections are asymptomatic [14,64].
Diarrhea — Cryptosporidium causes a secretory diarrhea that can be associated with malabsorption. Fecal blood or leukocytes are rare unless there is coinfection with another enteric pathogen. The number of oocysts ingested appears to be related to the time to and duration of infection, but not the severity of illness [33]. (See 'Pathogenesis' above.)
●Incubation period – In patients who develop symptoms, the incubation period is usually 7 to 10 days (range 2 to 28 days).
●Signs and symptoms – The diarrhea associated with cryptosporidiosis may be acute or chronic; transient, intermittent or continuous; and scant or voluminous, with up to 25 L/day of watery stool. Patients who develop diarrhea frequently have associated malaise, nausea and anorexia, crampy abdominal pain, and low-grade fever.
In older patients ≥85 years of age, infection has led to severe volume depletion in association with high case fatality rates [90]. In immunocompromised hosts (particularly those with T cell immunodeficiency), the illness is more frequently protracted and severe [80,91-94]. (See 'Risk factors for severe disease' above.)
There is some evidence that specific species or subtype families are associated with different clinical manifestations. For example, in a cross-sectional study of 230 patients with HIV in Peru, infection with C. hominis was associated with diarrhea alone, while infection with C. parvum was associated with diarrhea and vomiting [95].
●Usual course of disease – The illness usually resolves without therapy in 10 to 14 days in immunologically healthy people, although it can persist longer or relapse after initial improvement. In a study of patients who developed C. hominis infection during a large waterborne outbreak in Sweden, the mean duration of diarrhea was 7.5 days (range 1 to 80 days) in children <15 years of age, and recurrence occurred in 53 percent [93]. Excretion of oocysts after resolution of clinical symptoms can continue for prolonged periods [92,96].
In immunocompromised hosts (particularly those with T cell immunodeficiency), cryptosporidiosis can be a chronic debilitating illness with persistent diarrhea and significant wasting. In a study that followed 128 patients with HIV with cryptosporidiosis, more than half developed chronic disease, and approximately 10 percent developed fulminant disease (passage of more than 21 stools per day from the time of presentation) [97]; fulminant disease only developed in those with a CD4 count <50 cells/microL. (See 'Risk factors for severe disease' above.)
Antimicrobial therapy and/or interventions to improve immune function may be beneficial in some patients. The treatment of cryptosporidiosis is discussed separately. (See "Cryptosporidiosis: Treatment and prevention".)
Other manifestations — A number of other clinical manifestations of cryptosporidiosis have been described in patients with AIDS. Patients with a CD4 count <100 cells/microL are typically at greatest risk for having extraintestinal cryptosporidiosis [76].
Clinical manifestations can include cholecystitis, cholangitis, hepatitis, and pancreatitis. Biliary tract involvement has been reported to affect 10 to 30 percent of patients with AIDS [98]. (See "AIDS cholangiopathy".)
Pulmonary involvement has also been described, but it is unclear whether the organism is a true pathogen or merely colonizes the respiratory tract [99]. Nonspecific respiratory symptoms including cough have been reported [100,101].
Disseminated cryptosporidiosis has not been described.
Long-term sequelae — Some patients may continue to have symptoms after resolution of acute infection. As an example, in an observational study that followed adult patients for up to 12 months after resolution of acute C. parvum infection, abdominal pain (38 percent), diarrhea (33 percent), joint pain (33 percent), weight loss (31 percent ), symptoms consistent with irritable bowel syndrome (IBS) (28 percent), fatigue (22 percent), and eye pain (9 percent) were reported [94]. In a review of eight published European studies, the most common long-term sequelae were diarrhea (25 percent), abdominal pain (25 percent), nausea (24 percent), fatigue (24 percent), headache (21 percent), and, less commonly, eye pain [102].
In immunocompetent hosts, persistent gastrointestinal and joint symptoms (eg, painful and inflamed joints involving the knees, ankles, and feet) can last for many months after the initial infection [94,103,104], and may be related in part to the specific species that is causing infection. As an example, in one study, 235 patients and 232 controls were evaluated two months after the initial diagnosis of cryptosporidiosis [103]. Forty percent reported recurrence of intestinal symptoms (usually mild to moderate) after resolution of the acute illness with either C. hominis or C. parvum infection. In addition, late development of extraintestinal symptoms, such as joint pain, eye pain, headache, dizzy spells, and fatigue occurred two to three times as often in patients compared with controls. The late symptoms, particularly eye pain and recurrent headache, appeared to be more common with C. hominis infection. Similar findings were reported in a study of 1615 individuals (459 cases) after a large waterborne outbreak caused by C. hominis in two cities in Sweden, where cases were significantly more likely to report diarrhea, abdominal pain, and joint pain up to 11.5 months after the outbreak compared with non-cases [104]. A follow-up of 215 cases at two years showed that 48 percent still reported gastrointestinal symptoms, fatigue, nausea, headache, or joint stiffness/pain/discomfort [105].
Patients with chronic diarrhea can develop profound weight loss. In addition, there is some evidence in nonimmunocompromised infants that cryptosporidia infection can lead to persistent diarrhea and/or lasting adverse effects on nutritional status and growth [80,91,106]. There may also be an association between C. parvum and colorectal adenocarcinoma [107,108], although a causative role has not been proven.
Laboratory abnormalities — The presence of laboratory abnormalities depends upon the specific disease manifestation, as well as the severity and duration of infection. As an example, patients with severe, protracted disease can have evidence of malabsorption. (See "Approach to the adult patient with suspected malabsorption".)
In patients with biliary tract involvement, the serum alkaline phosphatase may be elevated. In such patients, ultrasound and computed tomography imaging may show an enlarged gallbladder with a thickened wall and dilated intra- and extrahepatic biliary ducts. Diagnosis of biliary involvement is confirmed by histology or by examination of bile for oocysts, since stool specimens may or may not be positive. (See "AIDS cholangiopathy".)
DIAGNOSIS
General approach — The diagnosis of cryptosporidiosis may be made by microscopy, fecal immunoassays, or polymerase chain reaction (PCR) testing. PCR assays are preferred, if available. PCR assays are more sensitive and also enhance detection of Cryptosporidium infections in fecal samples by obviating the more laborious fecal processing and requisite microscopic expertise of microscopy [28]. Organisms may be present in stool, duodenal aspirates, bile secretions, specimens from affected gastrointestinal tissue, or respiratory secretions. Laboratories should be alerted to the potential diagnosis of Cryptosporidium, and specific testing for the organisms should be requested. Routine examination for ova and parasites usually does not detect cryptosporidia oocysts. Details regarding the specific diagnostic methods are discussed below. (See 'Diagnostic methods' below.)
Diagnostic methods
Microscopy — Since Cryptosporidium species cannot be cultivated in vitro, the diagnosis of Cryptosporidium has traditionally been based on detection of typical morphological characteristics of oocysts in stool specimens, either by using a modified Ziehl-Neelsen (MZN) acid-fast stain or an immunofluorescent assay procedure [109]. Laboratories should be alerted to the potential diagnosis of Cryptosporidium so specific testing can be performed.
●Modified acid-fast stain – With the MZN acid-fast stain, specimens can be examined fresh or formalin fixed by light or phase-contrast microscopy. The oocysts stain red or pink and are usually 4 to 6 micrometers in diameter. It is important to carefully measure the oocysts to differentiate them from Cyclospora, which can appear similar but which are slightly larger (usually 8 to 10 micrometers) (see "Cyclospora infection"). Light microscopy is unable to distinguish between genetically distinct parasites.
The accuracy of the MZN acid-fast stain has not been well established and depends in part upon the number of stool specimens examined, since the number of oocysts shed in feces is not constant. In one report, examination of a single stool specimen identified only 30 percent of intestinal cryptosporidia infections [97].
The number of specimens required to conclusively exclude the diagnosis has not been studied, but, in chronic infections, examining up to three specimens is reasonable. Additionally, examination of unformed specimens and concentrated specimens increase the diagnostic yield.
●Other staining techniques – Although modified acid-fast stains are usually used, organisms can also be seen using hematoxylin and eosin, Giemsa, or malachite green staining.
●Immunofluorescent assays – Monoclonal antibodies against the oocyst wall and antigen capture tests have been used in fluorescent assays to detect Cryptosporidium in fecal or tissue specimens. These techniques increase the sensitivity compared with routine light microscopy and are easy to perform [110-113].
Direct fluorescent antibody (DFA) tests are based on fluorescein-labeled antibodies directed against cell wall antigens of Cryptosporidium oocysts, allowing visualization of the parasites in fecal samples. Commercially available DFA tests are widely used for diagnosis of cryptosporidiosis; one commonly used commercial DFA test, the MERIFLUOR DFA, is reported to have a sensitivity and specificity of 99.8 to100 percent for Cryptosporidium [109].
Polymerase chain reaction — PCR testing is increasingly being used for the diagnosis of Cryptosporidium. Compared with conventional microscopy, this method has the ability to differentiate between Cryptosporidium genotypes (which can be helpful in epidemiologic investigations) [114]. Many multiplex PCR assays are now commercially available [115-117]. Since PCR is highly sensitive and can detect both viable and non-viable organisms, a positive detection of Cryptosporidium on PCR does not always indicate that it is causing disease.
A number of studies have been performed comparing PCR assays with other techniques. In a study that compared a noncommercial nested PCR with conventional MZN and DFA to detect Cryptosporidium spp in fecal samples, the sensitivity and specificity of the nested PCR assay were reported to be 100 percent, compared with 94 percent sensitivity and 100 percent specificity for MZN, and 87.5 percent sensitivity and 100 percent specificity for DFA [118]. In another study of 200 patients with diarrhea, stool samples were examined using microscopy (modified acid-fast stain), sandwich enzyme-linked immunosorbent assay (ELISA), and nested PCR [119]. PCR yielded the highest detection rates compared with ELISA and microscopy (21, 12.5, and 9.5 percent, respectively). Compared with PCR, ELISA had a sensitivity of 57 percent and microscopy of 45 percent.
Histopathology — Cryptosporidial enteritis can be diagnosed from hematoxylin and eosin staining; Cryptosporidium appears basophilic and occurs either alone or in clusters on the brush border of the mucosal surface. Because infection can be patchy, biopsy specimens may be less sensitive than stool examination.
Serology — Detection of antibodies using IFA assays or ELISA tests are available. However, these tests are generally used only as an epidemiologic tool, since persistence of antibodies limits their use in diagnosing acute infection.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute diarrhea in adults".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Cryptosporidiosis (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Epidemiology − Cryptosporidium is an intracellular protozoan that is one of the most common parasitic enteric pathogens in humans. Cryptosporidium has been associated with gastrointestinal disease in sporadic, self-limited outbreaks among immunocompetent hosts and chronic illness in immunosuppressed patients. In addition, it is a significant cause of morbidity and mortality in children in resource-poor settings. (See 'Epidemiology' above.)
●Transmission − Transmission of cryptosporidiosis occurs via spread from an infected person or animal, or from a fecally contaminated environment, such as a food or water source. (See 'Transmission' above.)
●Pathogenesis − Cryptosporidiosis is associated with a secretory diarrhea that can be associated with malabsorption. It is likely that the intracellular nature of the parasite interferes with intestinal absorption and secretion. (See 'Pathogenesis' above.)
●Clinical manifestations − Cryptosporidium can cause asymptomatic infection, a mild diarrheal illness, or severe enteritis with or without biliary tract involvement. In immunocompetent hosts, the illness usually spontaneously resolves without therapy, while among immunosuppressed hosts, cryptosporidiosis can be a chronic debilitating illness with wasting and persistent diarrhea. (See 'Clinical manifestations' above.)
●Diagnosis − The diagnosis of cryptosporidiosis is best made by polymerase chain reaction testing, or by microscopic identification of the oocysts or enzyme immunoassays. The organisms may be present in stool, duodenal aspirates, bile secretions, biopsy specimens from the gastrointestinal tract, or respiratory secretions. (See 'Diagnosis' above.)
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