The objective of this study was to determine the effect of pneumonia during conditions of high (maximum ≥ 32°C) ambient temperatures on physiological and behavioral responses of calves. Eighteen black beef heifers averaging 240 kg were blocked by BW and randomly assigned to 1 of 2 treatment groups: 1) pneumonia induced by bronchoselective endoscopic inoculation with Mannheimia haemolytica (MH; n = 10) and 2) noninoculated controls (CN; n = 8). Nasal passage and rectal temperatures were measured every 2 h for 24 h after challenge and then twice daily for 9 d. Accelerometers, pedometers, and positioning devices monitored cattle behavior within the pen for 9 d after challenge. Blood samples were collected on trial d 0, 0.5, 1, 2, 3, 7, and 9 and were analyzed to determine the concentration of substance P, cortisol, haptoglobin, and metalloproteinase. All calves in the MH group were euthanized and necropsied on trial d 9. All MH calves became clinically ill postchallenge. A treatment × time interaction (P < 0.05) was evident for nasal and rectal temperatures, behavior, weight, and blood analysis. Rectal temperatures in MH were higher (P < 0.01) than CN during the period from 6 to 24 h after challenge. Conversely, nasal passage temperatures were less in MH calves compared with CN at 12 to 22 h after challenge. Calves in MH spent less time at the grain bunk, less time at the hay feeder, and more time lying down during the early pneumonia period compared with CN calves. Also, MH calves had significantly greater concentrations of blood biomarkers of pain (substance P) on d 0.5 (P < 0.01); stress (cortisol) on d 0.5 and 1 (P < 0.01); haptoglobin on d 0.5, 1, 2, 3, 7 (P < 0.01); and metalloproteinase on d 1, 2, and 3 (P < 0.01) compared with CN calves. At necropsy, all MH calves had right cranioventral bronchopneumonia (median lung lesions = 6.8%). Mannheimia haemolytica pneumonia caused significantly more changes in behavior and increased biomarkers during high (maximum ≥32°C) ambient temperatures compared with control calves. The results of this study may guide research in the development of objective assessment tools for management of cattle affected with bovine respiratory disease during extreme summer conditions.

Forty-five mixed breed dogs were evaluated for the presence and extent of periodontal disease. Histopathology was performed on samples of lung, myocardium, liver, kidney, tonsil, spleen, submandibular lymph node and tracheobronchial lymph node. Mitral valves were evaluated grossly. Statistical analysis was used to determine if there was a relationship between the extent of periodontal disease and histopathologic changes in the tissues examined. In the forty-five dogs studied, an association was found between periodontal disease and histopathologic changes in kidney, myocardium (papillary muscle), and liver.

No abstract

This single-pathogen challenge model successfully yielded clinical signs and pathological effects consistent with naturally acquired respiratory disease. Routine laboratory variables and subjective measures were not reliable indicators of lung involvement or the progression of pneumonia. However, activity, objectively measured with pedometers and accelerometers, appeared to be a promising indicator for early recognition of bovine respiratory disease.

Abstract. Hairy vetch poisoning (vetch-associated disease) of cattle is a generalized disease characterized pathologically by infiltration of skin and many internal organs by monocytes, lymphocytes, plasma cells, and often eosinophils and multinucleated giant cells and clinically by dermatitis, pruritis, often diarrhea, wasting, and high mortality. The disease was experimentally reproduced in an adult Angus female that had recovered from the natural disease 1 year earlier. She developed dermatitis on the 11th day of vetch feeding, and despite withdrawal from the vetch diet on the 12th day, death occurred 24 days after first day of vetch feeding. The cow developed lymphocytosis and hyperproteinemia. The results of other hematologic evaluations, blood chemical profiles, urinalysis, and cutaneous hypersensitivity tests using vetch lectin were normal. Lymphocyte blastogenesis studies with vetch lectin were not interpretable. Necropsy revealed gross lesions characteristic of the disease in the skin, heart, kidney, adrenal, and lymphoid tissues. Microscopically there was typical cellular infiltration in those organs and in the thyroid, liver, pancreas, salivary and mammary glands, urinary bladder, corpus luteum, and cerebral meninges. Cutaneous apocrine gland necrosis was present. The inflammatory reaction has qualities of a type-IV hypersensitivity reaction. Hypersensitivity may occur when constituents of the ingested plant are absorbed and act as antigens that sensitize lymphocytes and evoke the multisystemic granulomatous inflammatory response that characterizes the disease. Alternatively, vetch lectin may directly activate T lymphocytes to initiate the cellular response. Vetch-like diseases have been associated with a variety of diets that did not contain hairy vetch. The gross and histopathologic lesions of the vetch-associated and the vetch-like diseases are not mimicked in quality and distribution by any other disease.

No abstract

The pathogenesis of bovine respiratory disease (BRD) is determined by a complex interaction of environmental, infectious, and host factors. Environment trends could impact feedlot cattle by increasing their level of stress. The polymicrobial nature of BRD produces synergies between infectious agents that can alter pathogenesis. However, the nature of the host response to these environmental and infectious challenges largely determines the characteristics of the progression and outcome of BRD.

Innate immunity and inflammation play key roles in a wide range of pathology - including heart disease and vasculopathies. Current thinking suggests "damage" rather than "foreignness" as the actual trigger of the immune system, which has caused a dramatic change in how we tend to view the etiopathology of most types of heart disease. The future potential of certain anti-inflammatory therapeutic strategies in addressing heart disease is intriguing. Still, the Janus face of immunity/inflammation cannot be over emphasized as adverse manipulation of these systems may prove ineffectual or worse, damaging. Knowledge on functional characteristics of individual immune mediators is undoubtedly a central theme, but in depth understanding of the multiple biological actions of these molecules, as well as their contextual function, is the corner stone in deciding on potential future targets for pharmacologic manipulation. Animal models of human heart disease are currently being investigated and clinical trials conducted to gain further knowledge in this essential area of cardiovascular research, but the scarcity of cardiovascular research focusing on signaling molecules and pathways of innate immunity is still evident. Genomic and proteomic research in heart disease is going through its formative years, and much is still unknown about the complex pathway dynamics utilized by the innate immune system. This review will provide an overview of the current literature focusing on innate immunity and the heart, and hopefully will spark an interest in further basic as well as clinical research. As more information on cardiovascular immunity becomes available, this will provide a better understanding and thus act as the foundation for potential development of new treatment strategies for treatment of cardiovascular disorders.