Infectious disease prevention and control has been among the top public health objectives during the last century. However, controlling disease due to pathogens that move between animals and humans has been challenging. Such zoonotic pathogens have been responsible for the majority of new human disease threats and a number of recent international epidemics. Currently, our surveillance systems often lack the ability to monitor the human-animal interface for emergent pathogens. Identifying and ultimately addressing emergent cross-species infections will require a "One Health" approach in which resources from public veterinary, environmental, and human health function as part of an integrative system. Here we review the epidemiology of bovine zoonoses from a public health perspective.

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In an 8-year period, 1991-1998, 217 accessions of caprine abortions were submitted to the California Veterinary Diagnostic Laboratory System. Of these 217 submissions, 211 were suitable for examination in this study (6 had insufficient data). Infectious agents as the cause of abortions were found in 37% of the cases: bacterial agents were identified in 30.5%, viral agents in 2%, fungal agents in 0.5%, and protozoal agents in 4% of the cases submitted. The most common causes of abortions were Chlamydia psittaci and Coxiella burnetii infection, which accounted for 23% of all goat abortions. Mineral deficiencies were observed in 4%, fetal anomalies accounted for 3%, and leukoencephalomalacia of the brain (probable oxygen deprivation) accounted for 3% of the submissions. No diagnosis was made in 112 of the 211 submissions (53%). No lesions were noted in 104 of the submissions (49%). The other 8 submissions (4%) had histologic lesions suggestive of a bacterial agent; however, no infectious agents were identified in these cases.

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N-methyl-2,2'-dichlorodiethylamine (HN2)is a topical chemotherapeutic agent used as therapy for cutaneous T-cell lymphomas (CTCL). Di(2-chloroethyl)sulfide (SM), and less often HN2, have been used as chemical weapons, with the skin being a principle target. The mechanisms by which these chemicals produce their therapeutic and toxic effects in skin, however, are not clearly defined. We exposed human skin explants to two doses of HN2 and SM. At 18 hours after exposure, histopathologic features were compared. In addition, immunohistochemical markers to basement membrane proteins were used to evaluate the effects of both chemicals on the basement membrane zone. Gross vesication was not seen. Pyknotic nuclei with or without dyskeratotic changes within epidermal keratinocytes were present at both doses. These changes varied more between skin specimens than they did between doses. Ballooning degeneration was more marked after SM exposures. Diffuse dermal-epidermal separation was present only at high-dose exposures and did not appear to correlate with the degree of changes locally in the overlying epidermis. Antibodies to laminin-5 showed decreased immunoreactivity after exposure to HN2 and SM. Immunoreactivity for laminin- was decreased to a lesser extent, and immunoreactivity for collagen IV and VII was unchanged. HN2 and SM produce similar histopathologic and immunohistochemical features after cutaneous exposure. These features suggest that part of mechanism of action of HN2 and SM is a direct effect on the basement membrane zone. Understanding the effects of HN2 and SM separate from their effect on DNA may be important in designing therapies and in advancing our understanding of the pathophysiologic changes induced by these chemicals when delivered topically.

Blackleg is an infectious disease of cattle and rarely other ruminants, produced by Clostridium chauvoei and characterized by necrotizing myositis. In most cases of blackleg, the large muscles of the pectoral and pelvic girdles are affected, with other skeletal muscles and the heart involved less frequently. We studied 29 blackleg cases selected from the archives of the California Animal Health and Food Safety Laboratory, 1991-2015. Immunohistochemistry was also evaluated to detect C. chauvoei in formalin-fixed, paraffin-embedded (FFPE) tissues of cattle. Nineteen animals had gross and/or microscopic lesions in both skeletal muscle and heart, 9 had lesions in the skeletal musculature alone, and 1 in the heart alone. Gross lesions in the skeletal musculature involved the following muscle groups: hindquarters (n = 8), forequarters (n = 5), neck (n = 5), lumbar area (n = 3), brisket (n = 2), diaphragm (n = 2), abdominal wall (n = 1), thoracic wall (n = 1), and tongue (n = 1). Of the 20 animals that had lesions in the heart, 11 had pericarditis and myocarditis; 7 had pericarditis, myocarditis, and endocarditis; and 1 each had pericarditis and myocarditis. Immunohistochemistry was 100% sensitive to detect C. chauvoei in FFPE skeletal muscle and/or heart of cattle with blackleg. Simultaneous lesions in skeletal musculature and heart were relatively common in blackleg cases in California; the most affected skeletal muscles were those of the hindlimbs.

I Although the majority of deaths resulting from exposure to sulfur mustard (HD) have been due to pulmonary dysfunction, there are no detailed accounts of the pathogenesis of HDinduced lesions in the respiratory tract. Accordingly, we investigated the early changes within the trachea and lungs of rats following inhalation exposure to HD. Anesthetized rats were exposed by intratracheal intubation to vaporized H D (0.35 mg in 100 wl absolute ethanol) or ethanol alone for 50 min. Animals were euthanatized at 0, 1, 4, 6, 12, 18, and 24 li postexposure (PE), and their respiratory tracts were prepared for histological and ultrastructural examination. In rats exposed to HD, multifocal, petechial hemorrhages were grossly evident on tlie pleural surface of the lung at 6 h PE. Atelectasis and edema of the accessory lobe occurred at 12-18 h PE. Histologically, lesions in the respiratory tract were confined primarify to the trachea, bronchi and targer bronchioles. It, HD-exposed rats, there was a progressive depletion of the bronchiolar-associated lymphoid tissue (BALTI, with necrosis of the lymphoid cells as early as 12 h PE. Necrosis and sloughing of the tracheal and bronchial epithelia at 6-12 h PE was followed by the formation of fibrinous pseudomembranes within the bronchi. Necrosis and separation of airway epithelia occurred at the mucosaUsubmucosal interface. Pseudomembranes formed almost exclusively in deepitlielialized areas overlying tlie BALT. Cartilaginous lesions, characterized by necrosis of individual chondrocytes, were evident at I2 li PE. Pulmonary edema and occasional alveolar hemorrhage occurred from I8 to 24 li PE. Small bronchioles and alveoli were relatively unaffected, and only a few inflammatory cells were observed at any time.

Because of the difficulty in identifying botulinum toxin in cattle, it is hypothesized that cattle are sensitive to levels of toxin below the detection limits of current diagnostic techniques (the mouse protection bioassay and the immunostick enzyme-linked immunosorbent assay [ELISA] for type C botulinum toxin). Using an up-down method for toxicologic testing, the median toxic dose (MTD50) for cattle was determined. Four lactating Holstein cows were dosed at 0.125 or 0.25 ng/kg with Clostridium botulinum type C toxin and failed to develop clinical signs of botulism during the 7-day observation period. Three cows given 0.50 ng/kg of toxin developed clinical signs of botulism. From these results, the MTD50 was calculated at 0.388 ng/kg (3.88 mouse lethal doses/kg) using the trim-logit method. These results suggest that cattle are 12.88 times more sensitive to type C botulinum toxin than a mouse on a per kilogram weight basis. The mouse protection bioassay and the immunostick ELISA for type C botulinum toxin failed to identify the presence of the toxin in the serum, blood, and milk samples taken from all 7 animals.