Introduction: A feedlot is an intensive farming system for finishing livestock. Bovine respiratory disease (BRD) is a cause of morbidity and mortality in beef cattle, especially in feedlots. Methodology: This study investigated the morbidity and mortality of BRD in a beef cattle feedlot in southeastern Brazil using: clinical diagnoses, therapy, morbidity, and mortality. Pulmonary fragments were collected from five steers, on feed from 3-32 days, with lesions of pneumonia for identification of BRD infectious agents PCR. Results: 188,862 steers were on feed and morbidity was 7.05% (13,315/188,862), mortality 0.64% (1,214/188,862). The causes of morbidity were: BRD (6.13%), lameness (0.29%), trauma (0.21%), clostridiosis (0.13%) and polioencephalomalacia, PEM (0.12%). The causes of mortality were: BRD (0.21%), trauma (0.17%), and clostridiosis (0.13%). When all sick cattle were considered (n=13,315), BRD (86.9%) was the principal cause of morbidity, followed by lameness (4.13%), trauma (3.05%), and clostridiosis (1.82%). The cost of BRD-associated cattle mortality and morbidity was estimated at $14,334.00/10,000 and $16,315.40/10,000 respectively. It was projected that the economic effects due to BRD-associated morbidity in Brazil were $6.31 million/annum, while losses due to mortality were $5.54 million, resulting in an annual loss of $11.85 million. Coinfections in cattle with pneumonia due to Mannheimia haemolytica and Pasteurella multocida were identified in 4/5 steers tested. Conclusions: This is the first longitudinal study that investigated the incidence of BRD in feedlot cattle from Brazil, and the results herein described indicate that BRD contributed significantly to the development of mortality and morbidity of cattle on feed.

We investigated the occurrence of infectious pathogens during an outbreak of bovine respiratory disease (BRD) in a beef cattle feedlot in southern Brazil that has a high risk of developing BRD. Nasopharyngeal swabs were randomly collected from steers (n = 23) and assessed for the presence of infectious agents of BRD by PCR and/or RT-PCR assays. These included: Histophilus somni, Mannheimia haemolytica, Pasteurella multocida, Mycoplasma bovis, bovine respiratory syncytial virus (BRSV), bovine coronavirus (BCoV), bovine viral diarrhea virus (BVDV), bovine alphaherpesvirus 1 (BoHV-1), and bovine parainfluenza virus 3 (BPIV-3). Pulmonary sections of one steer that died with clinical BRD were submitted for pathology and molecular testing. The frequencies of the pathogens identified from the nasopharyngeal swabs were: H. somni 39% (9 of 23), BRSV 35% (8 of 23), BCoV 22% (5 of 23), and M. haemolytica 13% (3 of 23). PCR or RT-PCR assays did not identify P. multocida, M. bovis, BoHV-1, BVDV, or BPIV-3 from the nasopharyngeal swabs. Single and concomitant associations of infectious agents of BRD were identified. Fibrinous bronchopneumonia was diagnosed in one steer that died; samples were positive for H. somni and M. haemolytica by PCR. H. somni, BRSV, and BCoV are important disease pathogens of BRD in feedlot cattle in Brazil, but H. somni and BCoV are probably under-reported.

The risk of bacterial infection of the endometrium causing uterine disease in cattle is increased in the progesterone-dominated luteal phase of the ovarian cycle, while oestrogens or oestrus are therapeutic or protective against disease. The first line of defence against bacteria, such as Escherichia coli that cause inflammation of the endometrium, is the innate immune system, which recognises bacterial lipopolysaccharide (LPS). This study tested the hypothesis that cyclic variation in ovarian hormone concentrations alters innate immune responses within the bovine endometrium. Ex vivo organ cultures of endometrium, and in vitro cultures of endometrial epithelial and stromal cells, and peripheral blood mononuclear cells (PBMCs), all mounted inflammatory responses to E. coli or LPS, with secretion of inflammatory mediators interleukin 1β (IL1β), IL6 and IL8, and increased expression of mRNA encoding IL1B, IL6, CXCL8 (IL8) and CCL5. However, these inflammatory responses, typical of innate immunity, were not affected by the stage of ovarian cycle in which the endometrium was collected for organ culture, or by exogenous oestradiol or progesterone. Although a dexamethasone-positive control reduced inflammation stimulated by E. coli or LPS, treatment with oestradiol or progesterone, or inhibitors of oestradiol or progesterone nuclear receptors, did not affect endometrial cell or PBMC secretion of IL1β, IL6 or IL8, or IL1B, IL6, CXCL8 and CCL5 gene expression. In conclusion, the stage of the oestrus cycle or ovarian steroids did not modulate the innate immune response in the bovine endometrium in vitro.