An alternative model for fetal loss disorders associated with mare reproductive loss syndrome.

Fertile chicken eggs were used as an alternative model for large animals to evaluate suspect toxic dietary ingredients for fetal loss disorders associated with mare reproductive loss syndrome (MRLS) and fetal losses in other livestock. Nitrate, ammonia, and sulfate may react with proteinaceous compounds to enable the formation of abiotic pathogenic nanoparticles which were constant findings in pathognomonic placental lesions associated with non-infectious fetal losses of previously unknown etiology in mares, chickens and other livestock. The pathogenic nanoparticles may be produced naturally by toxic elements associated with air pollution that affect pasture forages or crops, unintentionally by reactions of these elements in protein-mineral mixes in dietary rations, or endogenously within tissues of fetuses and adult animals. The nanoparticles may form niduses in small vessels and predispose animals to a host of secondary opportunistic diseases affecting the reproductive, respiratory and gastrointestinal tracts of animals. The newly recognized abiotic pathogenic micro and nanoparticles are associated with MRLS. The discovery of the pathogenic nanoparticles led to the identification of nitrate, ammonium, and sulfur, in the form of sulfate, that seemingly enable the formation of the pathogenic nanoparticles in embryonic and fetal tissues.

Equine Arteritis Virus Has Specific Tropism for Stromal Cells and CD8+ T and CD21+ B Lymphocytes but Not for Glandular Epithelium at the Primary Site of Persistent Infection in the Stallion Reproductive Tract.

Equine arteritis virus (EAV) has a global impact on the equine industry as the causative agent of equine viral arteritis (EVA), a respiratory, systemic, and reproductive disease of equids. A distinctive feature of EAV infection is that it establishes long-term persistent infection in 10 to 70% of infected stallions (carriers). In these stallions, EAV is detectable only in the reproductive tract, and viral persistence occurs despite the presence of high serum neutralizing antibody titers. Carrier stallions constitute the natural reservoir of the virus as they continuously shed EAV in their semen. Although the accessory sex glands have been implicated as the primary sites of EAV persistence, the viral host cell tropism and whether viral replication in carrier stallions occurs in the presence or absence of host inflammatory responses remain unknown. In this study, dual immunohistochemical and immunofluorescence techniques were employed to unequivocally demonstrate that the ampulla is the main EAV tissue reservoir rather than immunologically privileged tissues (i.e., testes). Furthermore, we demonstrate that EAV has specific tropism for stromal cells (fibrocytes and possibly tissue macrophages) and CD8+ T and CD21+ B lymphocytes but not glandular epithelium. Persistent EAV infection is associated with moderate, multifocal lymphoplasmacytic ampullitis comprising clusters of B (CD21+) lymphocytes and significant infiltration of T (CD3+, CD4+, CD8+, and CD25+) lymphocytes, tissue macrophages, and dendritic cells (Iba-1+ and CD83+), with a small number of tissue macrophages expressing CD163 and CD204 scavenger receptors. This study suggests that EAV employs complex immune evasion mechanisms that warrant further investigation.IMPORTANCE The major challenge for the worldwide control of EAV is that this virus has the distinctive ability to establish persistent infection in the stallion's reproductive tract as a mechanism to ensure its maintenance in equid populations. Therefore, the precise identification of tissue and cellular tropism of EAV is critical for understanding the molecular basis of viral persistence and for development of improved prophylactic or treatment strategies. This study significantly enhances our understanding of the EAV carrier state in stallions by unequivocally identifying the ampullae as the primary sites of viral persistence, combined with the fact that persistence involves continuous viral replication in fibrocytes (possibly including tissue macrophages) and T and B lymphocytes in the presence of detectable inflammatory responses, suggesting the involvement of complex viral mechanisms of immune evasion. Therefore, EAV persistence provides a powerful new natural animal model to study RNA virus persistence in the male reproductive tract.

Abortions in Thoroughbred mares associated with consumption of bulbosus buttercups (Ranunculus bulbosus L).

CASE DESCRIPTION: Unexplained clinical signs of weight loss and emaciation were reported in a herd of Thoroughbred horses grazing spring pastures on a central Kentucky farm, even though supplemental grain and hay were provided. CLINICAL FINDINGS: A buttercup plant, Ranunculus bulbosus L, was abundantly present in all pastures and paddocks on the farm. All horses, especially lactating mares and their foals, had mild to severe weight loss as assessed by body condition. Seven mares on the farm had been confirmed pregnant between 30 and 45 days of gestation, but were later found to have aborted. Two 2-year-old fillies developed severe diarrhea, incoordination, recumbency, and paralysis and were euthanized. Necropsy of these horses revealed ulcers and erosions in the stomach and large intestine. The findings were considered consistent with buttercup toxicosis. TREATMENT AND OUTCOME: The horses were moved from the buttercup-infested pastures to a farm free of the weed. All horses made an uneventful recovery, and clinical signs resolved after the horses were transferred to buttercup-free pastures. Mares that had aborted conceived successfully in the next breeding season. CLINICAL RELEVANCE: The buttercup plant is toxic for all classes of livestock. The clinical signs associated with buttercup toxicosis may mimic other disease syndromes affecting the gastrointestinal tract of herbivores. On-farm epidemiological investigations are an essential part of the diagnosis of this condition. Consumption of buttercups has previously been associated with abortions in cattle, but to the author's knowledge, this has not previously been described in horses.

Tyzzer's disease in foals: retrospective studies from 1969 to 2010.

Reports of 148 cases of Tyzzer's disease in foals in central Kentucky were analyzed to identify features of the disease and factors associated with it. The records indicate that Tyzzer's disease is a rapidly progressive, highly fatal hepatitis caused by Clostridium piliforme. Common clinical findings are lethargy, fever, anorexia, and icterus. Seizures, coma, and death may rapidly ensue. Laboratory findings are leukopenia, metabolic acidosis, hypoglycemia, and increased activity of hepatic enzymes. Diagnosis is primarily based on clinical signs and postmortem findings but a polymerase chain reaction (PCR) is now available to detect C. piliforme DNA in organs and feces. Disease occurred most frequently in foals between 9 and 30 days of age that were born in April to May and was associated with heavy rainfall in the spring and high protein and nitrogenous diets fed to nursing mares. The findings are consistent with the ingestion of C. piliforme in the feces of adult horses and overgrowth in the intestine of foals with a high level of nutrients in their intestine.

Maladie de Tyzzer chez les poulains : études rétrospectives de 1969 à 2010. Des rapports de 148 cas de la maladie de Tyzzer chez les poulains dans le centre du Kentucky ont été analysés pour identifier les caractéristiques de la maladie et les facteurs qui y sont associés. Les dossiers indiquent que la maladie de Tyzzer est une hépatite rapidement progressive et hautement mortelle causée par Clostridium piliforme. Les résultats cliniques fréquents sont la léthargie, la fièvre, l'anorexie et l'ictère. Des crises d'épilepsie, le coma et la mort peuvent rapidement survenir. Les résultats de laboratoire sont la leucopénie, l'acidose métabolique, l'hypoglycémie et une activité accrue des enzymes hépatiques. Le diagnostic se base principalement sur les signes cliniques et les résultats post mortem, mais une réaction d'amplification en chaîne par la polymérase (ACP) est maintenant disponible pour détecter l'ADN de C. piliforme dans les organes et les fèces. La maladie se produit le plus fréquemment chez les poulains âgés d'entre 9 et 30 jours qui sont nés en avril et en mai et elle a été associée à des pluies abondantes au printemps et à des diètes à teneur élevée en protéines et en azote données aux juments allaitantes. Les résultats sont conformes avec l'ingestion de C. piliforme dans les fèces des chevaux adultes et à la prolifération dans l'intestin des poulains ayant un niveau élevé de nutriments dans leur intestin.(Traduit par Isabelle Vallières).