Public Health says they can’t confirm it yet, but they believe the illnesses were caused by the meat which was sourced and processed from two private hunt camps in December 2017.
The first case was reported by a Tavistock resident in mid-February with the second coming a month later in March and a third in the first week of April.
They say laboratory results, expected later this week, will confirm if E.coli is present in the deer meat.
In March, 1996, the UK government confirmed what had been known for years: bovine spongiform encephalopathy (or mad cow disease) was killing humans in the UK.
The various forms of transmissible encephalopathies have different names according to the species – scrapie in sheep, feline spongiform encephalopathy in cats, Creutzfeldt-Jacob disease in humans, chronic wasting disease in deer and elk.
But they’re all the same affliction, caused by infectious proteins, or prions.
I haven’t been following the CWD outbreak in deer, but it seems to be where BSE was about 1993: There’s this mysterious new disease no one ever thoughts would cross over to humans, but now, maybe?
Jim Robbins of the New York Times writes that, as darkness closed in, one hunter after another stopped at this newly opened game check station, deer carcasses loaded in the beds of their pickups.
They had been given licenses for a special hunt, and others would follow. Jessica Goosmann, a wildlife technician with Montana’s Fish, Wildlife & Parks Department, stepped outside to greet them, reaching for the neck of each freshly killed deer to cut an incision and remove a lymph node for testing.
On the edge of this south-central Montana village, where deer hunting is a way of life, the game check station has become the front line of the state’s efforts to stop the spread of a deadly infection known as chronic wasting disease.
It has ravaged deer herds throughout the United States and Canada and forced the killing of thousands of infected animals in 24 states and three Canadian provinces. It has also been found in Norway and South Korea. With the disease widespread in Wyoming, the Dakotas and the province of Alberta, Montana officials had been bracing for its emergence.
So in November, when biologists discovered it in six deer in this part of Montana and in another near the Canadian border, officials began setting up special hunts and stations for testing.
“It wasn’t a surprise that we found it,” said John Vore, game management bureau chief for the Montana Department of Fish, Wildlife & Parks. “It was a disappointment, but not a surprise.”
On Friday, the department announced that two more deer from this region, taken early in the special hunt, tested positive for the disease. Other test results are pending.
Chronic wasting disease is a contagious neurological disease that infects elk, deer, moose and caribou, and reduces their brains to a spongy consistency. Animals become emaciated, behave strangely and eventually die. It’s not known to be transferred to humans. Neither is it known to be spread from wild to domestic animals. There is no treatment, although a vaccine has been successful in tests in wild deer.
It is among a class of diseases known as transmissible spongiform encephalopathy, or TSE. Most experts believe the infectious agent is something called a prion, a misfolded cellular protein found in the nervous system and lymph tissue. The disease was first noted in captive deer in Colorado in the 1960s. The most closely related animal disease is scrapie in sheep.
“It’s a very unusual disease,” said Matthew Dunfee, an expert at the Wildlife Management Institute in Fort Collins, Co. and project director for the Chronic Wasting Disease Alliance. “Some experts say it’s a disease from outer space.”
In May 2016, an outbreak of Shiga toxin–producing Escherichia coli O157 infections occurred among children who had played in a stream flowing through a park. Analysis of E. coli isolates from the patients, stream water, and deer and coyote scat showed that feces from deer were the most likely source of contamination.
In the United States, recreational water is a relatively uncommon source of Shiga toxin–producing Escherichia coli (STEC) O157 outbreaks (1). We describe an outbreak of STEC O157 infections among children exposed to a contaminated stream in northern California, USA, and provide laboratory evidence establishing wildlife as the source of water contamination.
In May 2016, four cases of Shiga toxin (Stx) 1– and 2–producing E. coli O157 infection were reported to a local health department in northern California; investigation revealed a common source of exposure. The case-patients, ranging in age from 1 to 3 years, had played in a stream adjacent to a children’s playground within a city park. Exposure of the case-patients to the stream occurred on 3 separate days spanning a 2-week period. Two case-patients are known to have ingested water while playing in the stream. Two case-patients were siblings. All case-patients had diarrhea and abdominal cramps; bloody diarrhea was reported for 3. One case-patient was hospitalized with hemolytic uremic syndrome.
The stream is a second-order waterway located in a northern California community of ≈7,500 residents. At the time of exposures, stream flow was <30 ft3/s. The land upstream is not used for agricultural activities such as livestock production. The community is serviced by a public sewer system; inspection of sewer lines indicated no breach to the system.
Water samples were collected from the exposure site 7 days after the last case-patient was exposed and weekly thereafter for 17 weeks; samples were tested quantitatively for fecal indicator organisms. Throughout the study period, all water samples exceeded recreational water quality limits for E. coli and enterococci levels (2). Water samples were also cultured for STEC isolation and PCR detection of stx1 and stx2 (3). Stx1- and Stx2-producing E. coli O157 were isolated from stream water each week for the first 4 weeks. Additionally, an Stx2-producing E. coli non-O157 strain was isolated from the stream in the first week of sampling. Enrichment broth cultures of water samples were also positive by PCR for stx1 and stx2 for the first 4 weeks of sampling. Thereafter, both stx1 and stx2, or stx2 only, were intermittently detected in enrichment broth cultures for 9 additional weeks.
In the absence of an obvious source (e.g., upstream agricultural operation or sewer leak), wildlife was considered as a possible contributor to water contamination. Thirteen fresh wildlife scat specimens were collected along the stream for STEC culture and PCR. Of the 13 scat specimens, 8 originated from deer, 2 from raccoon, and 1 each from coyote, turkey, and river otter. Six scat specimens (4 deer, 1 coyote, 1 river otter) were positive for stx1 and stx2 or for stx2 by PCR (Technical Appendix[PDF – 16 KB – 1 page]). Stx1- and Stx2-producing E. coli O157 were isolated from deer scat and coyote scat. An Stx2-producing E. coli non-O157 strain was isolated from a deer scat specimen. The animal origin of the coyote and river otter scat specimens were definitively identified by partial DNA sequencing of mitochondrial cytochrome b (4).
To assess strain relatedness, we compared STEC O157 isolates from the case-patients, water, deer scat, and coyote scat by using pulsed-field gel electrophoresis (PFGE) and multilocus variable-number tandem-repeat analysis (MLVA) (5). PFGE patterns for XbaI-digested genomic DNA were highly similar among all isolates; only slight variations were found in the lower-sized bands (Figure). PFGE patterns for genomic DNA samples digested with BlnI also demonstrated a high degree of similarity (data not shown). Furthermore, MLVA profiles were identical for the case-patient, water, and deer scat isolates; only the coyote scat isolate differed from the main profile by 2 repeats at a single locus (VNTR_3).
This study provides laboratory evidence linking STEC O157 infections with the ingestion of recreational water that was probably contaminated by wildlife scat. Wild ruminants, including deer and elk, are known carriers of STEC and have been connected to outbreaks of human infections (6–9). We detected STEC in 50% of deer scat specimens collected from the stream bank. One of these specimens, found 1.5 miles upstream of the exposure site, contained an E. coli O157 isolate that was highly similar by molecular subtyping to case-patient and water isolates. These findings support the likelihood that feces from deer carrying STEC were the source of water contamination or, at the very least, contributed to the persistence of STEC in the water. It is unknown whether the STEC detected in coyote and river otter scat represents carriage or transitory colonization within these animals.
The common risk factor among the case-patients in this STEC O157 outbreak was exposure to a natural stream within a city park. After the outbreak was recognized, signs warning of bacterial contamination were posted along the stream. No further STEC O157 infections attributed to stream water exposure were reported.
Dr. Probert is the assistant director for the Napa-Solano-Yolo-Marin County Public Health Laboratory. His research interests focus on the development of molecular diagnostic tools for the detection of infectious agents.
Acknowledgment
We thank Frank Reyes, Keith Snipes, and Nailah Souder for their technical assistance; the County of Marin Health and Human Services and Environmental Health Services for information about the epidemiologic and environmental investigation; and the Microbial Diseases Laboratory Branch of the California Department of Public Health and the Santa Clara County Public Health Laboratory for the molecular subtyping data.
References
Heiman KE, Mody RK, Johnson SD, Griffin PM, Gould LH. Escherichia coli O157 outbreaks in the United States, 2003–2012. Emerg Infect Dis. 2015;21:1293–301. DOIPubMed
United States Environmental Protection Agency. 2012. Recreational water quality criteria. Office of Water 820-F-12–058 [cited 2017 Apr 13]. https://www.epa.gov/sites/production/files/2015-10/documents/rwqc2012.pdf
Probert WS, McQuaid C, Schrader K. Isolation and identification of an Enterobacter cloacae strain producing a novel subtype of Shiga toxin type 1. J Clin Microbiol. 2014;52:2346–51. DOIPubMed
Parson W, Pegoraro K, Niederstätter H, Föger M, Steinlechner M. Species identification by means of the cytochrome b gene. Int J Legal Med. 2000;114:23–8. DOIPubMed
Hyytia-Trees E, Lafon P, Vauterin P, Ribot EM. Multilaboratory validation study of standardized multiple-locus variable-number tandem repeat analysis protocol for Shiga toxin–producing Escherichia coli O157: a novel approach to normalize fragment size data between capillary electrophoresis platforms. Foodborne Pathog Dis. 2010;7:129–36. DOIPubMed
Fischer JR, Zhao T, Doyle MP, Goldberg MR, Brown CA, Sewell CT, et al. Experimental and field studies of Escherichia coli O157:H7 in white-tailed deer. Appl Environ Microbiol. 2001;67:1218–24. DOIPubMed
Keene WE, Sazie E, Kok J, Rice DH, Hancock DD, Balan VK, et al. An outbreak of Escherichia coli O157:H7 infections traced to jerky made from deer meat. JAMA. 1997;277:1229–31. DOIPubMed
Rounds JM, Rigdon CE, Muhl LJ, Forstner M, Danzeisen GT, Koziol BS, et al. Non-O157 Shiga toxin–producing Escherichia coli associated with venison. Emerg Infect Dis. 2012;18:279–82. DOIPubMed
Laidler MR, Tourdjman M, Buser GL, Hostetler T, Repp KK, Leman R, et al. Escherichia coli O157:H7 infections associated with consumption of locally grown strawberries contaminated by deer. Clin Infect Dis. 2013;57:1129–34. DOIPubMed
Contaminated stream water as source for Escherichia coli O157 illness in children
05.may.17
William S. Probert, Glen M. Miller, and Katya E. Ledin
Emerging Infectious Diseases, vol. 23, no. 7, July 2017
I sorta cringe, or maybe sigh, every time someone faithfully repeats the dogma that factory-farmed cattle are the source of E. coli O157:H7 and other shiga-toxin producing E. coli (STEC).
All ruminants carry STEC naturally, and there are well-documented and tragic outbreaks involving deer, goats, sheep, elk and others.
German researchers report on the occurrence of STEC in deer in Germany in the current issue of Epidemiology and Infection.
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Deer poop has been directly or indirectly linked to several outbreaks:
• 1 dead and 14 sickened from E. coli O157:H7 from deer feces contaminating strawberries in Oregon in Aug. 2011;
• deer feces were a possible source of E. coli O157 in Oregon hazelnuts that sickened 8 in March 2011;
• 29 Minnesota high school students sickened with E. coli O103 and E. coli O145 after butchering and processing deer into venison in 2010;
• deer meat was involved in at least two recognized E. coli outbreaks; and,
• an E. coli O157:H7 outbreak in Oct. 1996 that killed a 16-month-old and sickened 76 others who drank juice which contained unpasteurized apple cider that was probably contaminated with deer feces.
In the current study, the Germans studied the virulence genes eae, e-hlyA and saa, thestx subtypes, pulsed-field gel electrophoresis (PFGE) patterns and serovars. In total, 120 samples of 60 animals were screened by real-time polymerase chain reaction (PCR). The PCR results showed a high detection rate of stx genes (83%). Mainly faecal samples, but also some lymphatic tissue samples, tested stx-positive. All isolates carried stx2, were eae-negative and carried e-hlyA in 38% and saa in 9% of samples. Serovars (O88:[H8], O174:[H8], O146:H28) associated with human diseases were also identified. In some animals, isolates from lymphatic tissue and faecal samples showed undistinguishable PFGE patterns. The examined deer were shown to be relevant reservoirs of STEC with subtype stx2b predominating.
The complete paper is available at http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=8501556.