Cyanobacteria (also called blue-green algae) are ubiquitous in aquatic environments. Some species produce potent toxins that can sicken or kill people, domestic animals, and wildlife. Dogs are particularly vulnerable to cyanotoxin poisoning because of their tendency to swim in and drink contaminated water during algal blooms or to ingestalgal mats.. Here, we summarize reports of suspected or confirmed canine cyanotoxin poisonings in the U.S. from three sources: (1) The Harmful Algal Bloom-related Illness Surveillance System (HABISS) of the National Center for Environmental Health (NCEH), Centers for Disease Control and Prevention (CDC); (2) Retrospective case files from a large, regional veterinary hospital in California; and (3) Publicly available scientific and medical manuscripts; written media; and web-based reports from pet owners, veterinarians, and other individuals. We identified 231 discreet cyanobacteria harmful algal bloom (cyanoHAB) events and 368 cases of cyanotoxin poisoning associated with dogs throughout the U.S. between the late 1920s and 2012. The canine cyanotoxin poisoning events reviewed here likely represent a small fraction of cases that occur throughout the U.S. each year.

The recently-identified causative agent of White-Nose Syndrome (WNS), Pseudogymnoascus destructans, has been responsible for the mortality of an estimated 5.5 million North American bats since its emergence in 2006. A primary focus of the National Response Plan, established by multiple state, federal and tribal agencies in 2011, was the identification of biological control options for WNS. In an effort to identify potential biological control options for WNS, multiply induced cells of Rhodococcus rhodochrous strain DAP96253 was screened for anti-P. destructans activity. Conidia and mycelial plugs of P. destructans were exposed to induced R. rhodochrous in a closed air-space at 15°C, 7°C and 4°C and were evaluated for contact-independent inhibition of conidia germination and mycelial extension with positive results. Additionally, in situ application methods for induced R. rhodochrous, such as fixed-cell catalyst and fermentation cell-paste in non-growth conditions, were screened with positive results. R. rhodochrous was assayed for ex vivo activity via exposure to bat tissue explants inoculated with P. destructans conidia. Induced R. rhodochrous completely inhibited growth from conidia at 15°C and had a strong fungistatic effect at 4°C. Induced R. rhodochrous inhibited P. destructans growth from conidia when cultured in a shared air-space with bat tissue explants inoculated with P. destructans conidia. The identification of inducible biological agents with contact-independent anti- P. destructans activity is a major milestone in the development of viable biological control options for in situ application and provides the first example of contact-independent antagonism of this devastating wildlife pathogen.

The transmission of chronic wasting disease (CWD) has largely been attributed to contact with infectious prions shed in excretions (saliva, urine, feces, blood) by direct animal-to-animal exposure or indirect contact with the environment. Less-well studied has been the role that mother-to-offspring transmission may play in the facile transmission of CWD, and whether mother-to-offspring transmission before birth may contribute to the extensive spread of CWD. We thereby focused on a population of free-ranging white-tailed deer from West Virginia, USA, in which CWD has been detected. Fetal tissues, ranging from 113 to 158 days of gestation, were harvested from the uteri of CWD+ dams in the asymptomatic phase of infection. Using serial protein misfolding amplification (sPMCA), we detected evidence of prion seeds in 7 of 14 fetuses (50%) from 7 of 9 pregnancies (78%), with the earliest detection at 113 gestational days. This is the first report of CWD detection in free ranging white-tailed deer fetal tissues. Further investigation within cervid populations across North America will help define the role and impact of mother-to-offspring vertical transmission of CWD.

Feline chronic enteropathy is a poorly defined condition of older cats that encompasses chronic enteritis to low-grade intestinal lymphoma. The histological evaluation of lymphocyte numbers and distribution in small intestinal biopsies is crucial for classification and grading. However, conventional histological methods for lymphocyte quantification have low interobserver agreement, resulting in low diagnostic reliability. This study aimed to develop and validate an artificial intelligence (AI) model to detect intraepithelial and lamina propria lymphocytes in hematoxylin and eosin-stained small intestinal biopsies from cats. The median sensitivity, positive predictive value, and F1 score of the AI model compared with the majority opinion of 11 veterinary anatomic pathologists, were 100% (interquartile range [IQR] 67%–100%), 57% (IQR 38%–83%), and 67% (IQR 43%–80%) for intraepithelial lymphocytes, and 89% (IQR 71%–100%), 67% (IQR 50%–82%), and 70% (IQR 43%–80%) for lamina propria lymphocytes, respectively. Errors included false negatives in whole-slide images with faded stain and false positives in misidentifying enterocyte nuclei. Semiquantitative grading at the whole-slide level showed low interobserver agreement among pathologists, underscoring the need for a reproducible quantitative approach. While semiquantitative grade and AI-derived lymphocyte counts correlated positively, the AI-derived lymphocyte counts overlapped between different grades. Our AI model, when supervised by a pathologist, offers a reproducible, objective, and quantitative assessment of feline intestinal lymphocytes at the whole-slide level, and has the potential to enhance diagnostic accuracy and consistency for feline chronic enteropathy.

The epizootiology of anatid herpesvirus 1 (AHV-1) infection in waterfowl is poorly understood but apparently involves persistence of the virus in latently infected birds. Epornitics have often occurred in captive waterfowl or semiwild ducks in parklike settings, and many wildlife professionals conclude that such ducks may be the source of infection for wild waterfowl. We assessed the prevalence of latent infection and viral shedding from four groups of waterfowl: naturally occurring populations of native waterfowl, captive-reared waterfowl released for shooting, introduced nonmigratory waterfowl (e.g., resident, wild Mallards; Anas platyrhynchos), and semiwild peridomestic waterfowl (e.g., park ducks) in North Carolina and Florida, USA from 2004 to 2009. A nested PCR assay was used to detect viral DNA in trigeminal ganglia and cloacal swabs. Detection of viral DNA in trigeminal ganglia, but not cloacal swabs, was assumed to indicate latent infection, whereas PCR-positive cloacal swabs indicated active shedding of the virus. We collected 2,045 samples from 23 species of native, wild waterfowl, and detected latent infections in nine species. Wild Northern Pintails (Anas acuta), a species reportedly resistant to the virus, had the highest prevalence (8.1%). However, low prevalences were identified in other waterfowl from various families. Cloacal shedding was rarely detected (0.1% prevalence) among native waterfowl and was observed in one Blue-winged Teal (Anas discors) and one Mottled Duck (Anas fulvigula). All captive-reared, released waterfowl (n=13) collected were Mallards and one was latently infected, suggesting that these birds could also serve as a source of AHV-1 for naive waterfowl. All nonmigratory waterfowl sampled (n=90) were also Mallards. None of the resident Mallards were shedding virus, but one was latently infected. The peridomestic waterfowl sampled included breeds of domestic Mallard (n=6) and Muscovy Ducks (Cairina moschata; n=73). One peridomestic Mallard and four Muscovy Ducks were shedding virus at the time they were sampled, but no latently infected, asymptomatic carriers were identified.