The first objective of this study was to describe the effect of on-farm heat treatment of colostrum on colostral bacteria counts and IgG concentrations. The second objective was to describe the effect of feeding heat-treated (vs. raw) colostrum on passive transfer of colostral immune and nutritional parameters in neonatal calves. Pooled batches of colostrum were mixed and divided equally: one half was fed raw whereas the other half was fed after heat treatment at 60 degrees C for 60 min using a commercial on-farm batch pasteurizer. Colostrum samples were cultured for total bacteria count and total coliform count and analyzed for total IgG concentration. Forty-nine Holstein calves were fed either raw colostrum (n = 24) or heat-treated colostrums (n = 25) within 1 to 2 h after birth. Serum samples collected from calves at 0 h (precolostrum) and 24 h (postcolostrum) were assayed for serum total protein; IgG, IgA, and IgM concentrations; peripheral total leukocyte counts; neutrophil counts; lymphocyte counts; lymphocyte phenotypes; vitamin A, vitamin E, cholesterol, and beta-carotene concentrations. Serum samples collected from 2- to 5-d-old calves were tested for immunoglobulin function via a bovine viral diarrhea virus type I serum neutralization titer and for neutrophil bacterial opsonization activity. On-farm batch heat treatment of colostrum at 60 degrees C for 60 min resulted in lower colostrum bacteria concentrations while maintaining colostral IgG concentration. Calves fed heat-treated colostrum had significantly greater serum total protein and IgG concentrations at 24 h, plus greater apparent efficiency of IgG absorption (total protein = 6.3 mg/dL; IgG = 22.3 mg/mL; apparent efficiency of absorption = 35.6%) compared with calves fed raw colostrum (TP = 5.9 mg/dL; IgG = 18.1 mg/mL; apparent efficiency of absorption = 26.1%). There was no effect of treatment on serum concentrations of IgA, IgM, vitamin A, vitamin E, cholesterol, beta-carotene or vitamin E:cholesterol ratio, or on serum bovine viral diarrhea virus type I serum neutralization titers. There was no difference between treatment groups when examining calf plasma total leukocyte counts, neutrophil counts, lymphocyte counts, or neutrophil opsonization activity. However, the latter results were considered inconclusive.

A prospective study was carried out on 845 heifer calves born during 1991 on 30 Holstein dairy farms in southeast Minnesota. The objectives of the study were to describe the epidemiology of morbidty and mortality in dairy calves from birth to 16 weeks of age (with an emphasis on respiratory disease), to examine individual calf and herd management practices as risk factors for calf morbidity and mortality, and to validate producer diagnosis of mortality. Incidence rates for all morbidity, enteritis, and pneumonia were 0.20, 0.15, and 0.10 cases per 100 calf-days at risk for the period of the study. Risk of enteritis was highest in the first 3 weeks of life, with pneumonia risk highest at 10 weeks of age. Case fatality rates averaged 11.8%, 17.9%, and 9.4% for all diagnoses, enteritis, and pneumonia, respectively. Average daily rates of gain from birth to 16 weeks Iof age differed between farms that had inadequate calf housing (0.8 kg day-') versus those with adequate calf housing (1.0 kg day-i). Approximately half of the calves in the cohort (418) had blood samples taken monthly from birth until 16 weeks of age. Of the calves sampled, only 19 c,alves showed a four-fold rise in serum titers to respiratory viruses. Sixteen calves seroconverted to BVDV, two calves to IBRV, and one calf to PI3 virus. Of 98 calves less than 10 days of age tested for adequacy of passive transfer, 35 (35.7%) had serum immunoglobulin levels of less than 800 mg dl-'. There were no significant differences in mortality or morbidity between calves that had adequate passive transfer and those that did not. The incidence of mortality was 0.08 deaths per 100 calf-days at risk; 64 calves died during the 16 months of the study. The risk of death was highest at 2 weeks of age. Enteritis was the most common cause of death (28 deaths, 44% of all deaths) followed by pneumonia (19 deaths, 30% of all deaths). Comparing producer diagnosis of mortality with necropsy results yielded sensitivities of 58.3% and 56% and specifici-* Corresponding author at: Minnesota Veterinary Hospital, 4545 Hodgson Road, Saint Paul, MN 55126, USA. Tel: -I-l-61 2-484333 1. Elsevier Science B.V. SSDl 0167.5877(95)01000-9 156 N.J. Siuula et al./ Preventiue Veterinary Medicine 27 (I 996) 155-l 71ties of 93% and 100% for producer diagnoses of enteritis and pneumonia, respectively. The kappa statistic comparing producer diagnosis with necropsy result was 0.47. The most common pathogens isolated from calves that died of enteritis were rotavirus (five calves), and Escherichia coli (four calves). Pathogens isolated from pneumonic lungs included Pasteurella multocida (three calves), Haemophilus somnus (three calves), and Pasteurella haemolytica (one calf). NJ. Sivula et al./PreoentiueVeterinary Medicine 27 (19%) 155-171 157

The severe fibrinonecrotic pneumonia associated with pneumonic pasteurellosis usually results from colonization of the lower respiratory tract by Pusteurellu huemolyticu biotype A, serotype l(A1). Despite recent research efforts, the authors lack a detailed understanding of the interactions and host response to P. huemolyticu in the respiratory tract. The authors hypothesize that management and environmental stress factors or viral infection alters the upper respiratory tract (URT) epithelium allowing P. huemolyticu to colonize the epithelium. Once the URT is colonized, large numbers of organisms enter the lung where they interact with alveolar macrophages. Endotoxin, released from the bacteria, crosses the alveolar wall where it activates pulmonary intravascular macrophages, endothelium, neutrophils, lymphocytes, platelets, complement, and Hageman factor leading to complex interactions of cells and mediators. It is the progression of this inflammatory response with neutrophil influx that is ultimately responsible for the pulmonary injury. Leukotoxin is a major virulence factor of P. haemolyiicu that allows it to survive by destroying phagocytic cells. At subcytolytic concentrations it may also enhance the inflammatory response by activating cells to produce mediators and release reactive oxygen metabolites and proteases. has been reproduced experimentally in calves by transthoracic or intratracheal administration of P. huemolytica A 1 alone.*.'* Despite recent research efforts, we lack a detailed understanding of the interaction and host response to P.huernolyticu A1 in the ruminant respiratory tract. This article reviews the information presently available on the interaction of this bacteria with the respiratory tract and discusses possible pathogenic mechanisms. We will not attempt to review the extensive literature on viral-bacterial synergism as it relates to pulmonary bacterial infections. In addition, we will not discuss the effect of stress on immune function and its effect on the susceptibility of cattle to shipping fever. However, the reader is referred to several articles on these s~bjects.~,~~~*'~-'' Several observations point to the central role that P. haemolyticu A1 has in bovine shipping fever. In clinically healthy cattle, P. huemolyticu are present in low numbers in the nasal passages and those that are isolated are predominantly biotype A serotype 2 (A2) which is rarely associated with shipping Exposure of healthy cattle to stressful agents such as viral infection, change in management practices (marketing, transportation and processing), and change in environmental (heat, cold) conditions, leads to an explosive growth and selective colonization by P. huemolyticu A1 in the upper

Five horses were examined because of signs of muscle stiffness, colic, or both. All 5 had been exposed to Streptococcus equi within 3 weeks prior to examination or had high serum titers of antibodies against the M protein of S equi. Horses had signs of unrelenting colic-like pain and focal areas of muscle swelling. Four horses were euthanatized. The fifth responded to treatment with penicillin and dexamethasone; after 3 weeks of treatment with dexamethasone, prednisolone was administered for an additional 10 weeks. Common hematologic and serum biochemical abnormalities included neutrophilia with a left shift and toxic changes, hyperproteinemia, hypoalbuminemia, and high serum creatine kinase and aspartate transferase activities. Necropsy revealed extensive infarction of the skeletal musculature, skin, gastrointestinal tract, pancreas, and lungs. Histologic lesions included leukocytoclastic vasculitis in numerous tissues and acute coagulative necrosis resembling infarction. These horses appeared to have a severe form of purpura hemorrhagica resembling Henoch-Schönlein purpura in humans and characterized by infarction of skeletal muscles. Early recognition of focal muscle swelling, abdominal discomfort, neutrophilia, hypoalbuminemia, and high serum creatine kinase activity combined with antimicrobial and corticosteroid treatment may enhance the likelihood of a successful outcome.

No abstract