Foot and mouth disease in livestock and reduced cryptosporidiosis in humans, England and Wales

Emerging Infectious Diseases, Jan, 2003 by William J. Smerdon, Tom Nichols, Rachel M. Chalmers, Hilary Heine, Mark H. Reacher

During the 2001 epidemic of foot and mouth disease (FMD) in livestock in England and Wales, we discovered a corresponding decrease in laboratory reports of cryptosporidiosis in humans. Using a regression model of laboratory reports of cryptosporidiosis, we found an estimated 35% (95% confidence interval [CI] 20% to 47%) reduction in reports during the weeks spanning the period from the first and last cases of FMD. The largest reduction occurred in northwest England, where the estimated decrease was 63% (95% CI 31% to 80%). Genotyping a subgroup of human isolates suggested that the proportion of Cryptosporidium genotype 2 strain (animal and human) was lower during the weeks of the FMD epidemic in 2001 compared with the same weeks in 2000. Our observations are consistent with livestock making a substantial contribution to Cryptosporidium infection in humans in England and Wales; our findings have implications for agriculture, visitors to rural areas, water companies, and regulators.

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Cryptosporidium is a genus of enteric parasites, a leading cause of infectious diarrhea in humans and livestock. Infection is accompanied by fecal shedding of large numbers of highly infectious and environmentally persistent oocysts (1). Transmission occurs through the fecal-oral route in animal-to-human or human-to-human contact, by recreational exposure to contaminated water or land, or by consumption of contaminated water and food. Infection is also frequently associated with travel to high incidence countries (1). In England and Wales, most isolates are characterized as genotype 1 (which infects only humans) and genotype 2 (which infects both livestock and humans) (2).

Cryptosporidium oocysts have also been recognized as a continuing challenge to water treatment during the last 20 years. Because Cryptosporidium organisms tend to become widely distributed in surface waters and are resistant to chlorination, if coagulation and filtration are inadequate in public water supplies, the contaminated water can cause large outbreaks (1,3,4). Cryptosporidium in water supplies was studied by three expert committees commissioned by U.K. departments of health and environment in the 1990s, which made recommendations on improving management of slurry, on human hygiene relating to livestock, and on best practices in water treatment and outbreak investigation (5-7). Most cases of cryptosporidiosis, however, are not associated with recognized outbreaks and the sources of these infections remain uncertain (1,7).

Human cryptosporidiosis outbreaks in the U.K. are recognized as being bimodal, peaking in the spring and fall (1). Spring peaks vary by year and location and have been attributed to lambing, calving, and the application of slurry, combined with high rainfall, leading to run-off from agricultural land into surface water and drinking water catchments (1). Autumn peaks have been attributed to persons' summer travel to countries with higher incidence (1).

Surveillance of human enteric infection in England and Wales (which encompass 89% of the U.K. population [8]) is conducted by the voluntary reporting of positive laboratory test results from individual case-patients and outbreak summaries to the Public Health Laboratory Service-Communicable Disease Surveillance Centre (PHLS-CDSC) in Colindale, London. A computer database of individual laboratory reports was established in 1975; a database of outbreak summaries was established in 1992 (9,10). England and Wales have 229 microbiology laboratories, of which 47 are public health laboratories (11,12).

In 2001, in all regions of the U.K., an epidemic of foot and mouth disease (FMD) in livestock occurred (13) (Table 1). The following measures were taken to control the epidemic: excluding visitors from the countryside, extensive culling of affected herds and flocks of farm animals, and limiting the movement of animals for trade and to and from pastures in affected areas (13). These measures likely reduced the direct and indirect exposure to livestock of the overall population of England and Wales. Therefore, we examined laboratory reports of human infection with Cryptosporidium for evidence of changes that may have occurred during the period of the FMD epidemic.

Methods

From the national laboratory database, we downloaded laboratory reports to PHLS-CDSC of Cryptosporidium oocysts identified in fecal smears with dates for obtaining specimens between January 1, 1991, and December 3 I, 2001. The download was performed on June 20, 2002, to ensure that all data for 2001 were complete.

The data were aggregated into counts by week the specimen was obtained. To make all weeks exactly 7 days long, we excluded reports with specimen dates on December 31 of every year and on December 30 of every leap year. Intervals between date of illness onset, specimen date, and reporting date were reviewed to assess consistency of reporting over time.

The exposure interval for the FMD epidemic was defined as weeks 8-39 of 2001, which corresponded with the first FMD case on February 20 and last case on September 30 (13) (Table 1). We plotted the series of Cryptosporidium reports for England and Wales over time and reviewed data from Wales and each region in England individually.