Cryptosporidiosis Surveillance — United States, 2011–2012
|MMWR Surveillance Summaries|
Vol. 64, No. SS-3
May 1, 2015
Cryptosporidiosis Surveillance — United States, 2011–2012
Surveillance SummariesMay 1, 2015 / 64(SS03);1-14
Corresponding author: Michele C. Hlavsa, MPH, Division of Foodborne, Waterborne, and Environmental Diseases, National Center for Emerging and Zoonotic Infectious Diseases. Telephone: 404-718-4695; E-mail: email@example.com.
Problem/Condition: Cryptosporidiosis is a nationally notifiable gastrointestinal illness caused by extremely chlorine-tolerant protozoa of the genusCryptosporidium.
Reporting Period: 2011–2012.
Description of System: Fifty state and two metropolitan public health agencies voluntarily report cases of cryptosporidiosis through CDC's National Notifiable Diseases Surveillance System.
Results: For 2011, a total of 9,313 cryptosporidiosis cases (confirmed and nonconfirmed) were reported; for 2012, a total of 8,008 cases were reported; 5.8% and 5.3%, respectively, were associated with a detected outbreak. The rates of reported nonconfirmed cases were 1.0 and 0.9 per 100,000 population in 2011 and 2012, respectively, compared with an average of 0.0 during 1995–2004, and 0.3 during 2005–2010. The highest overall reporting rates were observed in the Midwest; 10 states reported >3.5 cases per 100,000 population in 2011 and in 2012. During 2011–2012, reported cases were highest among children aged 1–4 years (6.6 per 100,000 population), followed for the first time by elderly adults aged ≥80 years (3.4), and 75–79 years (3.3). Overall, cryptosporidiosis rates were higher among females than males during both years. For specific age groups, rates were higher among males than females aged <15 years and higher among females than males aged ≥15 years. Cryptosporidiosis symptom onset increased 4.4 fold during late summer.
Interpretation: Cryptosporidiosis incidence rates remain elevated nationally, and rates of nonconfirmed cases have increased. Rates remain highest in young children, although rates among elderly adults are increasing. Transmission of Cryptosporidium occurs throughout the United States, with increased reporting occurring in Midwestern states. Seasonal onset peaks coincide with the summer recreational water season and might reflect increased use of communal swimming venues.
Public Health Action: Future research is needed to address the evolving epidemiology of cryptosporidiosis cases, with a specific focus on the increase in nonconfirmed cases and increasing incidence rates among elderly adults. National systematic genotyping and subtyping of Cryptosporidium isolates could also help elucidate Cryptosporidium transmission and thus cryptosporidiosis epidemiology in the United States.
Cryptosporidiosis, a gastrointestinal illness caused by protozoa of the genus Cryptosporidium, is a major source of human illness and was the leading cause of all waterborne outbreaks in the United States during 2001–2010 (1). An estimated 748,000 cryptosporidiosis cases occur annually (2), although less than 2% are reported (3). Hospitalizations resulting from cryptosporidiosis cost an estimated $45.8 million per year (4).
Cryptosporidiosis is typically characterized by profuse, watery, nonbloody diarrhea. Other symptoms can include weight loss, abdominal pain, anorexia, fatigue, cramps, headache, fever, and vomiting (5). Asymptomatic infection also can occur (6–9). Recurrence of symptoms after apparent resolution has been frequently reported; however, illness is self-limiting, and symptoms typically completely resolve within 2–3 weeks in immunocompetent persons (10). Cryptosporidiosis can be treated by nitazoxanide, which was approved by the Food and Drug Administration (FDA) in 2005 for all immunocompetent patients aged ≥1 years (11,12).
Historically, cryptosporidiosis was considered an opportunistic infection in human immunodeficiency virus (HIV)-infected patients (13), with the ability to cause profuse, watery diarrhea, and life-threatening wasting, and malabsorption (14). Extraintestinal cryptosporidiosis (i.e., in the biliary or respiratory tract, or rarely the pancreas) also has been documented in immunocompromised persons (15–19). However, the incidence of cryptosporidiosis among HIV-infected persons has decreased since the introduction of highly active antiretroviral therapy for HIV infection (20,21).
Health-care providers should consider cryptosporidiosis in their differential diagnosis when a patient experiences diarrhea lasting >3 days. Because routine examination of stool for ova and parasites is unlikely to include testing for Cryptosporidium (22), health-care providers should specifically request Cryptosporidiumtesting. Oocyst excretion can be intermittent. Because the parasite might not be detected in a given stool specimen, three stool specimens collected on separate days should be examined before considering test results to be negative (23). Direct fluorescent antibody (DFA) testing is a highly sensitive and specific diagnostic method and is considered a benchmark for quality in Cryptosporidium testing (24). Commercially available antigen detection immunoassay kits are available and might be more diagnostically sensitive and specific than routine microscopic examination (25).
The majority of Cryptosporidium species, all with multiple subtypes, are morphologically indistinguishable by traditional diagnostic tests. Thus, molecular methods must be used to distinguish species and subtypes and are needed to better understand the epidemiology of cryptosporidiosis. Molecular typing tools are increasingly used in outbreak investigations and infection- or contamination-source tracking to differentiate Cryptosporidium species and subtypes. However, they are not commercially available. Cryptosporidium genotyping and subtyping services are provided free of charge by CDC athttp://www.cdc.gov/parasites/crypto/cryptonet.html. If stool is preserved in formalin, Cryptosporidium isolates cannot be reliably genotyped or subtyped (26).
The majority of cases of cryptosporidiosis in humans are caused by C. hominis and C. parvum (27,28). C. hominis is mainly spread through human-to-human transmission, whereas C. parvum can be spread through human-to-human or animal-to-human transmission (27,29). Human infections caused by C. meleagridis, C. canis, C. felis, C. ubiquitum, C. cuniculus, C. suis, C. muris, and several other species also have been documented. Species distribution might vary by geographic setting (e.g., urban versus rural) (29). Infections caused by the different Cryptosporidium species, and subtypes within species, can clinically differ (30,31).
Cryptosporidium oocysts are transmitted by the fecal-oral route. Cryptosporidium does not reproduce outside of a host, and oocysts are infectious immediately upon being excreted in feces. Infection results from the ingestion of oocysts through fecally contaminated food or water, or through contact with an infected person or animal. The infectious dose is low; feeding studies have demonstrated that the ingestion of ≤10 C. hominis or C. parvum oocysts can cause infection in healthy persons (32,33). Infected persons have been reported to shed 107–108 oocysts in a single bowel movement (34) and can excrete infectious oocysts for up to 60 days after cessation of gastrointestinal symptoms (35). Cryptosporidium oocysts are extremely chlorine tolerant and can survive for 3.5–10.6 days in water where free chlorine levels are maintained at CDC-recommended levels (1–3 mg/L) for recreational water venues (e.g., pools and interactive fountains) (36). This tolerance makes Cryptosporidium ideally suited for transmission via halogenated recreational and drinking water. Transmission is further facilitated by the low infectious dose of Cryptosporidium, the substantial number of Cryptosporidium oocysts that can be shed by a person in a single bowel movement, and the protracted shedding of oocysts even after symptom resolution (37).
Risk factors for cryptosporidiosis include ingestion of recreational water (38,39), ingestion of untreated drinking water (40), contact with livestock (38,40,41), recent international travel (37,40), or contact with infected persons (e.g., from young children to caregivers) (37,38,40). Risk factors also can vary by geographic setting (e.g., urban versus rural) (29). Although cryptosporidiosis cases can occur sporadically, waterborne outbreaks have been documented since the first reported U.S. drinking water-associated outbreak in 1984 (42) and the first reported U.S. recreational water-associated outbreak in 1988 (43,44). Outbreaks resulting from foodborne, person-to-person, and animal-to-person transmission also have been reported (45–49).
Cryptosporidiosis is a nationally notifiable disease; the first full year of reporting was 1995 (50). National surveillance data for 1995–2010 have been previously published elsewhere (3,50–54). This report summarizes national cryptosporidiosis surveillance data for 2011–2012. Federal, state, and local public health agencies can use these cryptosporidiosis surveillance data to help elucidate the epidemiology of cryptosporidiosis in the United States, establish public health priorities for cryptosporidiosis prevention, and optimize the design of public health interventions to prevent transmission of Cryptosporidium.
The definition of a confirmed case of cryptosporidiosis has changed over time; the first cryptosporidiosis case definition was established in 1995 (55), and was subsequently revised in 1998, 2009, 2011, and 2012 (56–59). Before 2011, all laboratory-diagnosed cases were considered confirmed cases.
2011 Definition: A confirmed case of cryptosporidiosis is defined as having gastrointestinal illness (characterized by diarrhea, abdominal cramping, fever, nausea, vomiting, or anorexia) and having evidence of Cryptosporidium organisms or DNA in stool, intestinal fluid, tissue samples, biopsy specimens, or other biological sample by established laboratory methods (e.g., DFA test or polymerase chain reaction [PCR]) (58).
2012 Definition: A confirmed case of cryptosporidiosis is defined as having evidence of Cryptosporidium organisms or DNA in stool, intestinal fluid, tissue samples, biopsy specimens, or other biological sample by certain laboratory methods with a high positive predictive value (PPV) (e.g., DFA test, PCR, enzyme immunoassay [EIA], or light microscopy of stained specimen) (59).
For 2011 and 2012, the nonconfirmed cryptosporidiosis cases include probable, suspect, and unknown cases.
2011 Probable: A probable case of cryptosporidiosis is defined as having gastrointestinal illness (characterized by diarrhea, abdominal cramping, fever, nausea vomiting and/or anorexia) and evidence of Cryptosporidium antigen by immunodiagnostic methods (e.g., commercially-available immunochromatographic card tests) or epidemiologically linked to a confirmed case (58).
2012 Probable: A probable case of cryptosporidiosis is defined as having supportive laboratory test results for Cryptosporidium spp. infection using a screening test method (e.g., immunochromatographic card/rapid card test or a laboratory test of unknown method) or is defined as having gastrointestinal illness (characterized by diarrhea and ≥1 of the following: diarrhea with duration of ≥72 hours, abdominal cramping, vomiting, or anorexia) and is epidemiologically linked to a confirmed case (59).
2012 Suspect: Suspect cases include persons who have a diarrheal illness and are epidemiologically linked to a probable case diagnosed by an immunocard/rapid card test/or unknown test method (59).
Unknown: If a case is not classified as confirmed, probable, or suspect, it is classified as unknown.
Public health agencies in the 50 states, the District of Columbia (DC), and New York City voluntarily report cases of cryptosporidiosis to CDC through the National Notifiable Diseases Surveillance System (NNDSS). Reports include the patient's place of residence (e.g., state), age, sex, race, ethnicity (Hispanic or non-Hispanic), date of symptom onset, case status (confirmed, probable, suspect, unknown [i.e., test method is not reported to NNDSS]), and whether the case is associated with an outbreak. Historically, CDC's annual summary of notifiable diseases uses its own criteria to classify case status (60). Because data in this report were finalized at a different time, the number of cases differs slightly from the number reported in the annual summary.
National cryptosporidiosis surveillance data for 2011–2012 were analyzed using statistical software. Numbers, percentages, and incidence rates (cases per 100,000 population) of cryptosporidiosis were calculated in aggregate for the United States and separately for each reporting jurisdiction. Rates were calculated by dividing the number of reported new cryptosporidiosis cases by each year's mid-year census estimates and multiplying by 100,000 (61). In addition to analyzing data nationally and by reporting jurisdiction, data were analyzed by region (Northeast, Midwest, South, and West regions), as defined by the U.S. Census Bureau (62). To account for differences in the seasonal use of recreational water, the West region was further subdivided into Northwest and Southwest. To examine reporting over time, cryptosporidiosis rates per 100,000 population were calculated by year (from 1995 to 2012) and case type (confirmed or nonconfirmed). To assess current patterns in reporting, average annual cryptosporidiosis rates per 100,000 population were calculated by demographic variables (e.g., age and sex) and by month of symptom onset across 2011–2012 combined. This was performed by summing all cases occurring in the 2-year period, and then dividing by the sum of the number of persons in reporting jurisdictions in each year, and multiplying by 100,000. Rates could not be calculated for some variables (race and ethnicity) because of a large percentage (>20%) of reports missing data for these variables.
All 50 states, New York City, and DC reported cryptosporidiosis cases to NNDSS for 2011–2012. A total of 17,321 cases of cryptosporidiosis were reported during 2011–2012; 9,313 cases were reported for 2011 (3.0 per 100,000 population) and 8,008 cases for 2012 (2.6). The number of annually reported cases declined 31.3% in 2012 from the 2007 peak of 11,657 (Table 1). The annual rate of reported cryptosporidiosis cases was relatively stable during 1995–2004, ranging from 0.9–1.4 per 100,000 population, with few nonconfirmed cases reported (Figure 1).
Of the 9,313 cases for 2011, 65.8% were confirmed. Of the 8,008 cases for 2012, 65.5% were confirmed. During 2005–2012, rates of confirmed cases ranged from 2.2 to 3.9 per 100,000 population, whereas rates of nonconfirmed cases ranged from 0.1 to 1.0 per 100,000 population. Rates of nonconfirmed cases were 1.0 and 0.9 per 100,000 population in 2011 and 2012, respectively, compared with an average of 0.0 during 1995–2004 and 0.3 during 2005–2010. Of all cases reported for 2011 and 2012, 5.8% and 5.3%, respectively, were reported to be associated with a detected outbreak.
By region, the rate of reported cryptosporidiosis cases per 100,000 population ranged from 1.3 in the Southwest to 6.3 in the Midwest in 2011 and 1.4 in the Southwest to 4.8 in Midwest in 2012 (Table 1, Figure 2). The number of jurisdictions reporting rates of >3.5 cases per 100,000 population was 19 and 20 in 2011 and 2012, respectively; 10 Midwest states reported >3.5 cases per 100,000 population in 2011 and 2012. By state, the rate of reported cryptosporidiosis cases per 100,000 population ranged from 0.1 in Hawaii to 17.7 in South Dakota in 2011 and 0.4 in Hawaii to 16.7 in Idaho in 2012.
In 2011, cases were most frequently reported in children aged 1–4 years followed by those aged 5–9 years and adults aged 25–29 years (Figure 3). In 2012, cases were most frequently reported in children aged 1–4 years, followed by adults aged 20–24 years and 25–29 years. For both 2011–2012, the average annual rate of reported cryptosporidiosis per 100,000 population was highest in those aged 1–4 years (6.6), followed by elderly adults aged ≥80 years (3.4), and 75–79 years (3.3). Rates were lowest among adults aged 50–59 years (1.8).
Of 17,270 cases where sex was reported in 2011–2012, 46.6% were in males (Table 2). Among males, the rate ranged from 1.6 per 100,000 population (aged 50–59 years) to 7.4 (aged 1–4 years) (Figure 4). Among females, the rate ranged from 1.9 per 100,000 population (aged 55–59 years) to 5.7 (aged 1–4 years). Cryptosporidiosis rates were higher among males than females for persons <15 years of age. Conversely, cryptosporidiosis rates were higher among females aged ≥15 years.
Date of symptom onset was reported for 12,581 (72.6%) of 2011–2012 cases. The number of cases by symptom onset peaked in late July and early August (n = 1,128), which was 4.4 times higher than the lowest biweekly number of cases by symptom onset in late December (n = 254) (Figure 5). Increased reporting (i.e., >450 cases biweekly) was noted from the end of May through early October. Symptom onset of cases in those aged 1–4, 5–9, and 25–29 years all peaked at week 32, which led to the overall seasonal peak. Symptom onset in older adults aged ≥75 years did not peak seasonally.
Of 13,752 cases for whom race was reported in 2011–2012, 84.9% were documented in white patients. Of 11,496 patients for whom ethnicity was reported in 2011–2012, 9.2% were Hispanic (Table 2). For 2011–2012, data on race were missing for approximately one fifth of cases, and data on ethnicity were missing for approximately one third of cases.
National data are critical to characterizing the epidemiology of cryptosporidiosis in the United States. During 1995–2012, communitywide and large (e.g., >1,000 cases) recreational water-associated outbreaks of cryptosporidiosis contributed to the elevated annual case counts and rates (1,3,50–54,63–73). For 2007, Utah reported a statewide recreational water-associated outbreak of cryptosporidiosis, which might account for the increased number of cases reported that year (74). The 2011 and 2012 annual incidence rates are lower than the peak seen in 2007, but in general appear to be higher than rates during 1995–2004. Other potential contributing factors could include changes in the ordering of diagnostic tests by health-care providers, testing and reporting patterns among laboratories, changes in transmission of and disease caused by Cryptosporidium, FDA licensure of nitazoxanide for persons aged ≥1 years in 2005, or a combination of these factors.
During 2011–2012, the geographic variation for cryptosporidiosis was consistent with findings of previous reports on U.S. national cryptosporidiosis surveillance data (3,50–54). Cryptosporidiosis was widespread geographically in the United States, with all 50 states and two metropolitan jurisdictions reporting cases. The cryptosporidiosis rate in the Midwest region was 1.7–4.8 times greater than that of other regions in 2011 and 1.0–3.4 times greater in 2012. Although incidence appears to be consistently higher in certain states, differences in reported incidence might reflect differences in risk factors; the magnititude of outbreaks; the capacity to detect, investigate, and report cases; or in the mode of transmission of Cryptosporidium in a certain region. If the latter is correct, the increased cryptosporidiosis rate in the Midwest region might be linked to increased contact with livestock, particularly preweaned calves (75,76), or increased cattle density (77). Systematic national genotyping and subtyping of Cryptosporidium isolates could help identify possible geographic differences in the transmission ofCryptosporidium in the United States.
Although the overall case counts and rates were consistent with data from recent years, some differences were noted. The rate of nonconfirmed cryptosporidiosis cases during 2011–2012 increased. This change likely reflects recent revisions to the cryptosporidiosis case definition. In 2011, responding to concern about false positive results, the case definition was revised to include only those cases diagnosed by laboratory methods with a high PPV (58). The 2011 and 2012 revisions of the case definition of cryptosporidiosis, which classify cases diagnosed by immunochromatographic card/rapid card tests or unknown diagnostic method as probable, present challenges to interpreting national trends. However, establishing standards for integrating laboratory methods into the case definition is an important step toward improving the quality of NNDSS data.
During 2011–2012, the number of reported cryptosporidiosis cases was highest in children aged 1–4 years, followed by children aged 5–9 years and adults aged 25–29 years. Similar findings have been noted in previous reports on U.S. national cryptosporidiosis surveillance data, as well as Canadian provincial, Australian state, and national Finnish and United Kingdom surveillance data (3,29,50–54,78–82). These findings might reflect Cryptosporidium transmission from young children to their caregivers (e.g., child-care staff, family members, and other household contacts) (47). Although the number of cases was higher in children and young adults, the rates of cryptosporidiosis infection per 100,000 population were highest in children aged 1–4 years followed by elderly adults aged ≥75 years. Although cryptosporidiosis rates have been increasing in the elderly population in the United States (3,50–54), 2011 marks the first year in which cryptosporidiosis rates among elderly persons surpassed rates among children aged 5–9 years and adults in their 20s and 30s. It is unclear whether this finding reflects an actual increase in rates of cryptosporidiosis among elderly adults or changes in diagnostic testing for cryptosporidiosis in elderly populations.
Overall, cryptosporidiosis rates were higher among females than males in 2011 and 2012. These findings are consistent with previous reports of increased rates of cryptosporidiosis in females first noted in 2007 (3,53,54). An examination of cryptosporidiosis rates by sex and age revealed that cryptosporidiosis rates were higher among males than females for persons aged <15 years and higher among females aged ≥15 years, which is consistent with 2009–2010 national surveillance data (3). It is unclear why rates of cryptosporidiosis have increased and remained elevated in females aged ≥15 years. It is possible that females aged ≥15 years are more likely to fill caregiver roles for young children, which places them at risk for cryptosporidiosis infection (47). It is also possible that men are less likely to seek health care when symptoms occur, and therefore less likely to be tested, diagnosed, or reported to have cryptosporidiosis (83,84).
During 2011–2012, a 4.4-fold increase occurred in cryptosporidiosis symptom onset during late summer. This finding is consistent with previous reports from the United States and other countries including the United Kingdom, Canada, Finland, and Australia (3,29,50–54,78–82). Furthermore, symptom onset of cases in those aged 1–4, 5–9, and 25–29 years all peaked in August, which drove the overall seasonal peak. This finding is consistent with increased use of recreational water venues during the summer, particularly among younger populations (1,63–74). Symptom onset in older adults aged ≥75 years did not peak seasonally.
To reduce the transmission of Cryptosporidium in treated recreational water, improvements in the design, construction, operation, and maintenance of these aquatic venues are needed. In the United States, no federal agency regulates treated recreational water; pool codes are enacted, implemented, and enforced by state or local officials. The lack of uniform national standards has been identified as a barrier to the prevention and control of illness associated with public treated recreational water venues. To provide support to state and local health departments looking to reduce risk for recreational water-associated illness, CDC has sponsored development and release of the first edition of the Model Aquatic Health Code (MAHC) (http://www.cdc.gov/mahc). Development of the MAHC guidance has been a collaborative effort between local, state, and federal public health and the aquatics sector to develop a data-driven, knowledge-based resource for state and local jurisdictions to create or review and update their existing pool codes to optimally prevent and control recreational water-associated illness.
Effective prevention of Cryptosporidium transmission through recreational water also requires that swimmers of all ages practice healthy swimming behaviors (e.g., keeping the parasite out of the water by not swimming while ill with diarrhea and, if diagnosed with cryptosporidiosis, at least 2 weeks following complete symptom resolution) to prevent contamination. Recreational water can amplify smaller outbreaks into communitywide transmission when persons who are ill introduce the parasite into multiple recreational water venues or other settings (e.g., child-care facilities) (85). Once the parasite has been introduced into the water, engineering (e.g., use of ultraviolet or ozone disinfection treatment in addition to standard halogen treatment or enhanced filtration) can help minimize contamination and minimize Cryptosporidium transmission in treated recreational water venues. To prevent communitywide outbreaks, CDC has collaborated with state health departments to develop guidelines for rapidly implementing control measures once an increase in case reporting exceeds a predetermined disease–action threshold (e.g., a two- to threefold increase in cases over baseline) rather than waiting for an outbreak investigation to implicate a specific outbreak source (74).
To prevent cryptosporidiosis transmission through public drinking water systems, the Environmental Protection Agency (EPA) has implemented regulations designed to enhance the treatment of surface water supplies, including multiple regulatory changes enacted following a massive outbreak of cryptosporidiosis in 1993 in Milwaukee, Wisconsin (86–89). Another large outbreak in 1993 occurred in Las Vegas, and lasted for 7 months (66,90). During 1994–2012, no cryptosporidiosis outbreaks associated with use of community surface water supplies were detected in the United States (63–66). However, in 2013, a cryptosporidiosis outbreak associated with a municipal water system occurred in Baker City, Oregon (91). This water system was supplied by surface water and was chlorinated but not filtered. Because of its small population size, the city had not yet been required to provide Cryptosporidium-specific treatment, as is required for the majority of surface water systems under the Long Term 2 Enhanced Surface Water Treatment Rule (87). This outbreak underscores the importance of source water protection and treatment that removes or inactivates Cryptosporidium, as well as enhanced surveillance. To address the risk for outbreaks and illness associated with use of public groundwater supplies, EPA is implementing the Ground Water Rule, which requires sanitary surveys, triggered source water testing, corrective actions when deficiencies or fecal contamination are detected in untreated public groundwater systems, and compliance monitoring for treated groundwater systems (92). This rule does not address risk from private wells, which EPA does not have the authority to regulate.
Individual-level prevention and control measures to stop transmission of Cryptosporidium include 1) practicing good hygiene (e.g., not swimming when ill with diarrhea and washing hands appropriately), 2) avoiding ingestion of potentially contaminated water (e.g., not swallowing recreational water), 3) exercising food and water precautions when traveling, 4) avoiding ingestion of unpasteurized milk or apple cider, and 5) avoiding fecal exposure during sexual activity (Box). Community- and jurisdiction-level prevention encompasses 1) protecting recreational water and drinking water sources from becoming contaminated withCryptosporidium and 2) in the event contamination occurs, treating or filtering water to inactivate or remove the parasite (e.g., using ultraviolet irradiation or ozonation to inactivate Cryptosporidium in treated recreational water venues).
The findings in this report are subject to at least five limitations. First, incidence rates could not be calculated for race and ethnicity because of missing data. Second, incomplete data on symptom onset date could have led to an inaccurate represention of the seasonal distribution of cases. Third, lack of data on risk factors or immune status of patients (e.g., HIV status) limits understanding of how these factors might affect national trends. Fourth, the incidence of cryptosporidiosis is likely to be underestimated by these national surveillance data because of underreporting (e.g., not all persons infected with Cryptosporidiumare symptomatic and, unbeknownst to many health-care providers, laboratories typically do not include Cryptosporidium testing in routine examination of stool for ova and parasites). Fifth, it is unclear whether cases of cryptosporidiosis diagnosed on the basis of use of immunochromotographic card tests were reported as confirmed or probable; states might have varied timelines for adapting changes to the NNDSS case definition.
Although cryptosporidiosis rates remain elevated in the United States, the epidemiology of cryptosporidiosis in the United States might be changing, particularly with respect to confirmed case status and patient age. Improved surveillance and epidemiologic studies are needed to clarify if these observed changes reflect actual shifts in Cryptosporidium transmission or are artifacts of changes in case definition and diagnostic testing and reporting practices. The quality and completeness of national cryptosporidiosis data can be improved by enhancing the capacity of state and local jurisdictions to detect, investigate, and voluntarily report cases (93). Existing state and local public health infrastructure supported through CDC could facilitate enhancement of surveillance efforts. Examples of CDC support include FoodNet, Environmental Health Specialists Network [EHS-Net], Epidemiology and Laboratory Capacity grants, and CDC-sponsored Council of State and Territorial Epidemiologists Applied Epidemiology Fellows. Although many jurisdictions investigate cryptosporidiosis cases, risk-factor data are not available for all jurisdictions via NNDSS. Collaborating with reporting jurisdictions to collect standardized risk factor data would enhance CDC's understanding of U.S. cryptosporidiosis epidemiology. The systematic collection and molecular characterization of Cryptosporidium isolates would further the understanding of U.S. cryptosporidiosis epidemiology by revealing transmission patterns and potential risk factors, as exemplified in the United Kingdom (94). Such an effort would require phasing out the practice of preserving stool specimens with formalin, which decreases the ability to perform molecular amplification methods.
Ongoing, elevated rates of cryptosporidiosis in the United States underscore the need for improved understanding of cryptosporidiosis epidemiology, particularly of risk factors, to optimize prevention and control. Reducing the transmission of this highly infectious, extremely chlorine-tolerant pathogen requires a multipronged approach, comprising individual-, community-, and jurisdiction-level actions to improve population health.
National surveillance data are critical to understanding the cryptosporidiosis epidemiology in the United States. To enhance cryptosporidiosis surveillance, CDC plans to launch CryptoNet—a DNA sequence-based surveillance system for cryptosporidiosis (http://www.cdc.gov/parasites/crypto/cryptonet.html). CDC has developed a package of molecular characterization methods and a database for this system. These molecular tools are crucial to understanding national transmission patterns and developing targeted prevention guidance. Federal, state, and local public health agencies can use cryptosporidiosis surveillance data to help elucidate the epidemiology of cryptosporidiosis in the United States, establish public health priorities for cryptosporidiosis prevention, target health communication messages, and optimize the design of public health interventions to prevent the transmission of Cryptosporidium.
This report is based, in part, on contributions by Julia W. Gargano, epidemiologist, Division of Foodborne, Waterborne, and Environmental Diseases, and jurisdiction surveillance coordinators Ruth Ann Jajosky, DMD, and Willie Anderson, Office of Surveillance, Epidemiology, and Laboratory Services, CDC.