Toxic effects in dairy cattle following the ingestion of a large volume of canola oil.

The clinical and laboratory findings of a group of 9 dairy cattle that accidentally ingested large volumes of canola oil are described. Four of the animals died, and 3 were necropsied. No specific cause of death was found, although a number of theories are advanced. This is the first report of such an occurrence.

Investigation of an outbreak of mucosal disease in a beef cattle herd in southwestern Saskatchewan.

This study describes the epidemiological investigation of an outbreak of mucosal disease that occurred on a ranch in southwestern Saskatchewan. Over a six month period during the fall and winter of 1991-1992,in a herd of 515 beef cattle and 96 bison, 20 yearling cattle from a group of 105 housed in one feedlot pen died from mucosal disease. A further eight yearlings were slaughtered for salvage because they were at risk of dying from mucosal disease. Mucosal disease mortalities were the first observed evidence of fetal infections with bovine viral diarrhea virus in this herd. Animals that died from mucosal disease exhibited signs of ill thrift prior to death. Deaths from mucosal disease were confined to the progeny of one herd of beef cows. Following an outbreak of fetal infection with bovine viral diarrhea virus during 1989-1990, at least 28 (22%) of the 128 calves born from this herd of cows in the spring of 1990 were persistently infected with bovine viral diarrhea virus. However, only one calf born from this herd in 1991, and five calves born from all herds in 1992 were persistently infected. Of the five persistently infected calves born in 1992, three were born to persistently infected replacement heifers born in 1990. These heifers calved without assistance in 1992, but only one of their calves survived past three days of age, and it was persistently infected. In January 1992, 82% of the total herd had reciprocal antibody titers to bovine viral diarrhea virus of >/=1024 which suggested a high level of herd immunity to bovine viral diarrhea virus. Thus, following the outbreak of fetal infection with bovine viral diarrhea virus in 1989-1990, herd immunity to bovine viral diarrhea virus had developed rapidly in the breeding cows and heifers. Subsequently, in the next two years, there was a dramatic decline in the number of calves born persistently infected with bovine viral diarrhea virus.

The effects of feeding milk to diarrheic calves supplemented with oral electrolytes.

The effects of feeding different levels of milk to diarrheic calves (n = 19) supplemented with oral electrolytes were investigated. In the early stages of the disease the calves were fed either enough milk to maintain normal growth in a healthy calf, one half that volume or no milk. The three groups were further subdivided according to whether or not the electrolyte solution contained bicarbonate. A full milk ration allowed uninterrupted weight gains of 1% body weight/day (p = 0.003), but caused greater inappetence (p = 0.003 to 0.037) at the beginning of the trial than lower levels of milk intake. Electrolyte solutions with bicarbonate reduced growth rates in milk fed calves (p = 0.014). The density of fat stores increased with the level of milk feeding (p = 0.04 to 0.053). The mitotic index of the duodenal mucosa increased with milk feeding (p = 0.08), indicating a superior mucosal regeneration potential. Thymic atrophy was pronounced in those calves fed no milk (p = 0.001). It was concluded that the continued feeding of milk to diarrheic calves was beneficial. Electrolyte solutions containing bicarbonate should be avoided when milk is fed to diarrheic calves.

New concepts in the pathogenesis, diagnosis and control of diseases caused by the bovine viral diarrhea virus.

The new information on the pathogenesis and epidemiology of mucosal disease of cattle is reviewed. It is now known that clinical mucosal disease occurs only in cattle which were infected with a pestivirus in early gestation and were born with persistent viral infection and specific immunotolerance. These animals may be clinically normal at birth but may develop fatal mucosal disease, perhaps following superinfection with another pestivirus, usually between 6 and 24 months of age. They may also remain clinically normal indefinitely and breed successfully. The progeny from persistently infected females will similarly be persistently viremic, and maternal families of such animals may be established.Congenital defects may occur when infection of the fetus occurs in mid-gestation. Although fetuses may be infected in utero in late gestation, the infections do not persist, the fetuses develop antibodies, and they appear to suffer no ill-effects. Postnatal infection can result in subclinical disease (bovine viral diarrhea) with a normal immune response; the virus may also be responsible for enhanced susceptibility to other infections, diarrhea in newborn calves, and reproductive failure.Prevention of the economically important diseases caused by the virus is dependent upon the identification and elimination of persistently viremic animals, which are reservoirs of infection, and the vaccination of immunocompetent females at least three weeks before breeding. However, because of serotypic differences between strains, there is some doubt whether vaccination will reliably provide protection against the transplacental fetal infections that are important in the pathogenesis of this disease. There is no substantial evidence to warrant the vaccination of feedlot cattle.

Protection of newborn calves against fatal multisystemic infectious bovine rhinotracheitis by feeding colostrum from vaccinated cows.

To determine whether consumption of colostrum with high levels of serum neutralizing antibody to bovine herpesvirus 1 would protect neonatal calves from the frequently fatal multisystemic form of infectious bovine rhinotracheitis, Holstein calves were fed for 48 h after birth with either pooled colostrum from seropositive vaccinated cows or colostrum from seronegative unvaccinated cows. The serum neutralizing antibody achieved in the former calves was between 64 and 256 and the titer in the latter calves was below 8. At 48 h of age the calves were challenged by aerosolization with bovine herpesvirus 1. All five seronegative calves died or were euthanized in a moribund state between days 5 and 7 of the trial, whereas all five seropositive animals remained healthy throughout the study. Twice daily clinical examination revealed significantly lower scores in the seronegative group from 60 h postinfection. Relative lung weights were greater in the seronegative group, associated with a severe acute necrotizing bronchiolitis with fibrin exudation. The seronegative group of calves also demonstrated an acute necrotizing rumenitis, pharyngitis, glossitis, esophagitis, laryngitis and tracheitis. The seropositive animals had only small areas of subacute necrotizing fibrinopurulent rhinitis. Bovine herpesvirus 1 virus was isolated from all nasal passages of all calves but isolation of virus in the seronegative calves was made from the trachea (5/5), lung (4/5), bronchial lymph nodes (4/5), spleen (4/5), thymus (3/5), liver (2/5), rumen (2/5) and brain (1/5).(ABSTRACT TRUNCATED AT 250 WORDS)

Lung sounds in cattle, horses, sheep and goats.

The purpose of this paper is to emphasize the importance of pulmonary auscultation for the clinician. It suggests a clarification and simplification of the terminology to be used which would be helpful to veterinary students and allow better communications between veterinarians. The interpretation of these sounds and the relationships to conditions and diseases of the lungs in cattle, horses, sheep and goats are discussed.