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In July 2010, a horse from a rural farm (Farm A) in coastal Northern California was diagnosed with Salmonella Oranienburg infection following referral to a veterinary hospital for colic surgery. Environmental sampling to identify potential sources and persistence of Salmonella on the farm was conducted from August 2010 to March 2011. Salmonella was cultured using standard enrichment and selective plating. Pure colonies were confirmed by biochemical analysis, serotyped and compared by pulsed-field gel electrophoresis (PFGE) analysis. A total of 204 clinical and environmental samples at Farm A were analysed, and Salmonella spp. was isolated from six of eight (75%) horses, an asymptomatic pet dog, two of seven (28.6%) water samples from horse troughs, nine of 20 (45%) manure storage pile composites, 16 of 71 (22.5%) wild turkey faeces and four of 39 (10.3%) soil samples from the family's edible home garden. Well water and garden vegetable samples and horse faecal samples from a neighbouring ranch were negative. S. Oranienburg with a PFGE pattern indistinguishable from the horse clinical strain was found in all positive sample types on Farm A. The investigation illustrates the potential for widespread dissemination of Salmonella in a farm environment following equine infections. We speculate that a recent surge in the wild turkey population on the property could have introduced S. Oranienburg into the herd, although we cannot rule out the possibility wild turkeys were exposed on the farm or to other potential sources of Salmonella. Findings from the investigation indicated that raw horse manure applied as fertilizer was the most likely source of garden soil contamination. Viable S. Oranienburg persisted in garden soil for an estimated 210 days, which exceeds the 120-day standard between application and harvest currently required by the National Organic Program. The study underscores the need to educate the public about potential food safety hazards associated with using raw animal manure to fertilize edible home gardens.

Background: In the US little spatially defined information regarding exposure to most vector-borne pathogens in dogs is available for the states of California (CA), Oregon (OR), and Washington (WA). Objectives: The purpose of the present study was to evaluate the spatial distribution of seroprevalence for 4 vector-borne pathogens, Anaplasma phagocytophilum, Borrelia burgdorferi, Ehrlichia canis, and Dirofilaria immitis, across the 3 western coastal states of the contiguous United States that extend from the northern Mexican to the southern Canadian border. Methods: A convenience sample, targeting blood from 20 pet dogs per county across CA, OR, and WA, was evaluated using a canine point-of-care ELISA kit. Geographic coordinates of home zip code were displayed using a geographic information system. A total of 2431 dogs from CA, OR, and WA were tested. Results: The overall seroprevalence was highest for A. phagocytophilum (2.4%), followed by B. burgdorferi (1.2%), and E. canis (0.7%). The prevalence of infection with D. immitis was 0.7%. At the individual dog level, there was a significant association between seropositivity to B. burgdorferi and A. phagocytophilum (odds ratio=18.7, 95% confidence interval=6.8–47.1). For most positive results, prevalence tended to decrease with increasing latitude; thus, the highest rates of seropositivity occurred in CA, followed by OR, and then WA; one exception was seropositivity for B. burgdorferi, which was higher in WA (0.38%) than in OR (0.15%), but considerably lower than in CA (2.00%). In WA, dogs that tested positive for A. phagocytophilum, E. canis, and B. burgdorferi were in the southern Puget Sound area. For D. immitis, none of the dogs in WA was positive. Conclusions: Seropositivity for vector-borne pathogens is broadly but patchily distributed in dogs in CA, OR, and WA.

Background: Salmon poisoning disease (SPD) is a trematode-borne disease of dogs caused by Neorickettsia helminthoeca. Objectives: To determine risk factors and spatial epidemiology of SPD in dogs from northern California; to describe the clinicopathologic, microbiologic, and imaging findings of SPD in these dogs; and to evaluate treatments and outcomes for SPD. Animals: Twenty-nine dogs with SPD based on the finding of trematode ova in the feces, or organisms consistent with N. helminthoeca in specimens submitted for microscopic examination. Methods: Information regarding signalment, fish exposure, clinical signs, diagnostic evaluation, treatments, and outcomes was obtained for each dog. Archived lymph node aspirates and histopathology specimens were subjected to polymerase chain reaction (PCR) testing for Neorickettsia spp. Results: Labrador Retrievers and intact male dogs were overrepresented. Exposure locations were often distant from the dogs' residence. Some dogs had neurologic signs, including twitching and seizures. Dogs lacking peripheral lymphadenomegaly had abdominal lymphadenomegaly on ultrasound examination. A combination of centrifugation fecal flotation and sedimentation had greatest sensitivity for finding fluke ova. N. helminthoeca DNA was amplified by PCR from 4/10 dogs. Penicillins, cephalosporins, and chloramphenicol did not appear to be effective treatments. Mortality rate was 4/29 (14%). Conclusions and Clinical Importance: SPD should be suspected in dogs with inappetence, gastrointestinal, or neurologic signs, with or without fever or peripheral lymphadenomegaly in the appropriate geographical setting. Diagnosis is facilitated by a combination of fecal sedimentation and centrifugal flotation, abdominal ultrasonography, and PCR-based assays on lymphoid tissue. The treatment of choice is tetracycline antimicrobials.

Summary 1 Coral reefs are experiencing devastating mortality due, in part, to emerging disease. Despite this growing problem, the long-term consequences of infectious disease in marine ecosystems remain poorly understood, and the application of epidemiological models to marine disease systems represents a research priority for managing resources in the world's oceans. 2 Metapopulation models may provide a framework for modelling coral population dynamics at the regional scale, and we use this approach to investigate the effects of infectious disease. The model presented here incorporates a susceptible-infected or ‘S-I’ disease into a system of patchily distributed, dynamic coral hosts, and highlights some basic differences that set many marine disease systems apart from their terrestrial counterparts. 3 The model predicts several possible long-term outcomes of disease introduction, and suggests that the consequences of disease may vary considerably among different pathogens and regions. Due to the long time-scales for coral dynamics, epizootics are expected to be prolonged with recovery slow at the regional scale. 4 Our model results show how infectious disease can substantially alter host metapopulation dynamics, with some non-linear relationships which are likely to affect the response of these systems to management and environmental change. For example, higher rates of coral colonization can have variable consequences for host population occupancy (i.e. coral cover) when infectious disease is considered, and chronic diseases with long-lived pathogens pose the highest risks for regional coral extinction. 5 Synthesis and applications. We present a tractable epidemiological model within a metapopulation framework and compare the model output with empirical data for a white plague type II (WPII) outbreak among coral of the upper Florida Keys. We conclude that this model fits well with the spatial and temporal patterns of WPII over a decade. Despite terrestrial–marine differences, many patterns derived from our model are consistent with epidemiological principles. Thus, the careful application of these principles within the context of marine management may be a promising research frontier. Although we focus on coral disease, the methods and results may apply to other marine metapopulations.

Despite awareness that disease emergence may be related to ecological change, few studies have rigorously analyzed the underlying environmental drivers of the dynamics of disease emergence. This may be due to the fact that ecological change and disease emergence are often mediated through complex and large-scale processes that are not amenable to traditional reductionist approaches to causal inference. Here, we suggest strategies assembled from diverse disciplines, including ecology, epidemiology, and the social sciences, to analyze complex relationships, promote cooperation, increase efficiency, and minimize bias when investigating the ecological drivers of disease emergence. These techniques, which complement traditional hypothesis testing, include epidemiologic causal criteria, strong inference, causal diagrams, model selection, and triangulation. We also present several examples from recent emerging infectious disease investigations, including Hendra virus, Nipah virus, coral diseases, and avian influenza, where these techniques were successfully applied. Here, we outline some of the barriers to advancing our understanding of causation in disease ecology and offer some solutions for investigating large-scale ecological drivers, such as global warming, pollution, and land-use change.

Between 0 and 50 per cent of the dogs in eight rural villages in far northern California with a high risk of tickborne diseases were seropositive for Anaplasma phagocytophilum and Bartonella vinsonii subspecies berkhoffii, and between 0 and 10 per cent were seropositive for Borrelia burgdorferi. The odds ratio for the co-exposure of individual dogs to B vinsonii berkhoffii and A phagocytophilum was 18.2. None of the diseases was associated with the sex of the dogs, whether they slept out of doors, or whether tick-preventive measures were taken. When the villages were assessed for landscape risk factors, a particularly high seroprevalence for B vinsonii berkhoffii and A phagocytophilum was observed in a village at a relatively high altitude and greater distance from the Pacific coast, and montane hardwood conifer woodland was most associated with a high seroprevalence for these two pathogens.

Nine horses from ages 5 to 21 years were diagnosed with cutaneous equine sarcoidosis (ES) over an 18-year period. In addition to skin, the lungs were frequently involved, with other organ systems affected less commonly. A predisposition for thoroughbreds and geldings was noted. Cutaneous lesions and signs included crusts, scales, alopecia and pruritus. These were found at various sites, particularly the legs/thighs/elbows, thorax, neck, face and ventral abdomen. Three horses were euthanized shortly after hospitalization; others survived as long as 12 years. Histopathologic stains, immunohistochemistry and polymerase chain reaction assays on paraffin-embedded cutaneous specimens from eight horses for Mycobacterium spp., Coccidioides immitis, Cryptococcus neoformans, Corynebacterium pseudotuberculosis, and Borrelia burgdorferi were all negative. The aetiology of ES is unlikely microbial and continues to be a diagnosis of exclusion. ES, when limited to the skin, is associated with a good prognosis, with either partial or complete response to glucocorticoid therapy in all the surviving horses.

Summary 1. Deterministic models predict that susceptible-infective-susceptible (SIS) disease, where there is no immunity to reinfection following recovery, will become infinitely persistent in a host population. We explored the incorporation of stochasticity into SIS models; modelled interacting host-disease agents in metapopulations; and examined model predictions in a real system involving viral infection in domestic cats. 2. SIS models incorporating stochasticity predicted that disease persistence would be finite and dependent on the host population size, provided the host population was isolated. However, the disease may persist by dynamic spread among interacting host metapopulations. 3. Feline enteric coronavirus (FECV) dynamics in domestic cats were well predicted by stochastic metapopulation models. 4. The models we present are mathematically tractable, generalizable, and mechanistically realistic. The findings from the cat-virus system are immediately applicable to the management of cattery populations and could be adapted to inform eradication programmes for other infectious diseases in animal and human populations. The most practical methods to eradicate feline enteric coranovirus would be to remove small catteries (islands) from interactions with large catteries (mainlands) and to convert mainlands to islands by depopulation.

Identifying predators of threatened and endangered species is important for understanding and reducing the impacts of predation. Visible evidence collected from a carcass alone is often insufficient to accurately identify predator species. The DNA from the predator left on the carcass allows for a definitive identification of predator species associated with the carcass, but DNA can be difficult to isolate independently from the prey. We developed field collection and molecular protocols for amplifying canid and felid predator DNA from saliva on fisher (Martes pennanti) carcasses without amplifying fisher DNA itself. We tested the protocol on fisher carcasses suspected of having been killed by a bobcat (Lynx rufus), mountain lion (Puma concolor), coyote (Canis latrans), and domestic dog. We successfully amplified and sequenced DNA from these 4 predator species, confirming predation by them on fishers. We confirmed that these protocols could also identify other felid and canid predators of several other small North American carnivores. © 2013 The Wildlife Society.

White-nose syndrome (WNS) is a fatal disease of bats that hibernate. The etiologic agent of WNS is the fungus Geomyces destructans, which infects the skin and wing membranes. Over 1 million bats in six species in eastern North America have died from WNS since 2006, and as a result several species of bats may become endangered or extinct. Information is lacking on the pathogenesis of G. destructans and WNS, WNS transmission and maintenance, individual and site factors that contribute to the probability of an outbreak of WNS, and spatial dynamics of WNS spread in North America. We considered how descriptive and ana- lytical epidemiology could be used to fill these information gaps, including a four-step (modified) outbreak investigation, application of a set of criteria (Hill's) for assessing causation, compartment models of disease dynamics, and spatial modeling. We cataloged and critiqued adaptive-management options that have been either previously proposed for WNS or were helpful in addressing other emerging diseases of wild animals. These include an ongoing program of prospective surveillance of bats and hibernacula for WNS, treatment of individual bats, increasing population resistance to WNS (through vaccines, immunomodulators, or other methods), improving probability of survival from starvation and dehydration associated with WNS, modi- fying hibernacula environments to eliminate G. destructans, culling individuals or populations, controlling anthropogenic spread of WNS, conserving genetic diversity of bats, and educating the public about bats and bat conservation issues associated with WNS.

Feline leprosy syndrome is caused by multiple species of mycobacteria; at least two histomorphologic subtypes have been reported from Australia and Canada, and PCR/DNA sequencing studies suggest that several species of mycobacteria may be implicated. To the authors’ knowledge, similar studies from the United States have not been performed. Ten cats with skin lesions characteristic of feline leprosy syndrome and acid-fast confirmation of organisms were included in the study. The cats were evaluated by clinical follow-up, histopathology, and molecular characterization (PCR with DNA sequencing). Eight of 10 cats were from coastal cities of Hawaii, Washington or California; two cats were from the coastal mountain range in California, approximately 30 miles inland. Additional environmental risk factors included access to the outdoors in nine cats, four of which were observed hunting. Skin lesions ranged from mildly alopecic and swollen to nodular and ulcerated. Lesions were evaluated histopathologically, using both HE in each of these, large numbers of acid-fast bacteria were seen diffusely within non-necrotic lesions. These organisms also were visible with HEboth of these had M. lepraemurium-type histomorphology. Clinically, cats with M. visibilis/IWGMTinfection tended to be older (mean age 10.3 years, P = 0.008) and have larger numbers of lesions (range four to too numerous to count) with recurrence (three cats), unexplained mortality(one cat), or concurrent disease (one cat coinfected with T. gondii). Cats with M. lepraemurium, or histomorphologically similar Rhodococcus erythropolis and M. kansasii infections,were younger (mean age 2.2 years) and tended to have few lesions (range 1–5; mean 2.2). These cases responded completely to excision and treatment with miscellaneous broad-spectrum antibiotics. The presence of two clinically and histomorphologically distinct syndromes supports previous reports from Canada and Australia. Clinical differences from Australian cases were identified, specifically the benign course of M. lepraemurium-typeinfections. The significance of the Rhodococcus erythropolis and M. kansasii is not clear; however, multiple species of mycobacteria have been recently identified by PCR in Canadian cases of feline leprosy syndrome. Geographic differences in specific organisms associated with feline leprosy syndrome may reflect local differences in risk factors, possibly due to differing ecologies of M. lepraemurium and M. visibilis in Australia, Hawaii and the continental United States. Funding: Self-funded.

Molecular techniques have greatly enhanced the sensitivity of the laboratory diagnosis of infectious diseases. Highly sensitive polymerase chain reaction (PCR) analysis of tissue DNA is being used to characterize and speciate infectious agents. The use of PCR is increasing in the diagnosis of Mycobacterium spp. infections. Frequently, the primers used are not specific for the genus and they may amplify other closely related organisms such as Rhodococcus spp. Some of these organisms are ubiquitous and, as for organisms of the genus Mycobacterium, they are usually isolated from soil. For this reason, they may be potential contaminants of instruments, reagents or even skin. As part of a study to characterize the causative organisms of feline leprosy, nodular pyogranulomatous lesions from cats with no recognizable organisms in tissue sections, using acid-fast stains or the BCG technique, were analysed by nested-PCR. Briefly, samples from 12 cats were obtained retrospectively from paraffin-embedded tissues, deparaffinized and DNA extracted by standard techniques. Extracted DNA was amplified with previously characterized sets of primers for a fragment of the 16S rRNA gene. Amplified fragments were sequenced in an automated sequencer, analysed and compared by computer analysis with known sequences of related organisms. In addition, 14 feline and canine control tissue samples were analysed. These included mildly inflamed (psychogenic alopecia and allergic skin disease, n = 5) and noninflammatory (neoplastic skin masses, n = 3) skin lesions, and internal organs (liver, spleen and lung, n = 6). The results revealed DNA sequences consistent with Rhodococcus spp. (99–100% homology) in nine of 12 (75%) of the acid-fast bacteria-negative nodules. The remaining two samples were negative. None of the samples yielded amplicons with homology to Mycobacterium spp. Additionally, nine of 14 (64%) unrelated control tissues showed similar amplification of a bacterium with high homology (98–99%) to Rhodococcus erythropolis and other Rhodococci; two of 14 amplified a fragment of DNA with homology to Gordonia spp. (soil organism), and one sample amplified a fragment of DNA with homology to Mycobacterium sphagni (soil organism). The remaining two samples were negative. Parallel controls (PCR master mix inoculated with sterile water and PCR master mix alone) were consistently negative. Based on these results, two main scenarios may be in play: (1) in lesions with histologically undetectable acid-fast organisms, the amount of mycobacterial DNA may be very low, and other dominant contaminant organisms such as Rhodococcus spp. may be amplified preferentially; (2) a negative acid-fast result obtained histologically may be accurately predictive for an absence of infection with Mycobacterium spp., and only contaminants are amplified. In summary, the significance of Rhodococcus spp. as a causative agent of nodular dermal lesions with no recognizable acid-fast organisms, when results are obtained exclusively by PCR analysis, should be questioned. In this event, the aetiology of the lesions should be further investigated using other complementary diagnostic procedures (e.g. DNA capture, in situ hybridization, in situ PCR). Funding: Self-funded.

Persistent Escherichia coli urinary tract infection (UTI) in dogs is a frustrating clinical problem. Affected dogs often appear to fail to respond to therapy or to reacquire infection shortly after therapy is completed. Urovirulence factors (UVFs) of the infecting E. coli, antibiotic resistance, and tissue colonization may be contributory but have not been evaluated in dogs with persistent E. coli UTI. In this study, the strain types of E. coli in dogs with persistent UTI were evaluated with pulsed-field gel electrophoresis (PFGE) to determine whether persistence was due to acquisition of new isolates or failure to eradicate existing isolates. UVFs in these isolates, assessed by polymerase chain reaction, and antibiograms were correlated with treatment outcome in these dogs. Results documented a mixed pattern: 9 dogs remained chronically infected with 1 or 2 strains, each with distinct reproducible UVFs, but 1 dog was infected with numerous unrelated E. coli strains over time. Two dogs had a mixed pattern, consisting of 1 or more episodes of persistent E. coli infection attributable to a single strain in addition to episodes caused by unrelated strains. Many isolates had no detectable UVFs, highlighting the likely importance of impaired colonization resistance in the affected dogs. Antibiotic resistance was common, often in response to previous treatments, especially with trimethoprim-sulfamethoxazole. Antibiotic resistance patterns differed significantly within PFGE strain types, suggesting lateral acquisition of resistance plasmids or integrons. These results can be used to help guide testing for and management of persistent E. coli UTI in dogs.