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)

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.

A retrospective survey of diseases of feedlot cattle in Alberta.

A survey of feedlot managers was used to obtain information on disease occurrence, management practices and preventive techniques employed in feedlots in Alberta. Respiratory diseases were reported to be the most frequent causes of sickness and death. Costs associated with disease occurrence were estimated to be C $15.6 million in feedlots in Alberta annually during the period under study.

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.

A brief review of bovine coccidiosis in Western Canada.

Coccidiosis of beef cattle, in both its enteric and nervous forms, seen in feedlots in Western Canada is discussed. Cases of coccidiosis accompanied by nervous signs, occasionally up to 30% of those affected enterically, are most common during the coldest winter months. The pathogenesis of the nervous form of the disease is unknown. Clinical management of disease outbreaks using various chemotherapeutics is described. The importance of using anticoccidial drugs before the onset of clinical signs in cattle in contact with sick animals is discussed.

The prevention and control of epidemics of acute indifferentiated diarrhea of beef calves in Western Canada.

It is frequently evident that outbreaks of diarrhea occur in spite of apparent "good management" and "good calving conditions". This observation underlies the fact that we still do not understand many of the epidemiological factors which contribute to calf diarrhea outbreaks. For example, we still lack biological criteria by which to judge the degree of crowding and the degree of stress. Nevertheless, application of the principles described above will prevent or decrease the severity of many annual epidemics. To be successful, a program of prevention and control should be discussed with producers long before the calving season, preferably during the preceding summer or fall. Implementation of a complete program may take several calving seasons and producers should be made aware that prevention by improved management is an on-going, evolutionary process. More and improved vaccines are becoming available; however, as is the case with most biologicals, their impact cannot be determined until after they have been used for several years. They should be recognized as only one of several managent tools at the disposal of the veterinarian and livestock producer.

Fusobacteremia in a calf with necrotic stomatitis, enteritis and granulocytopenia.

This case of fusobacteremia appears to be identical to an interesting and unusual syndrome previously reported. We wish to bring the syndrome to the attention of others who may be able to elucidate the etiology further. Because hematological examinations are frequently not done on calves, this condition may be more common than reports suggest. Perhaps others who observe this syndrome in calves may be able to investigate the role of other agents such as viruses or mycotoxins. Experimental work may be able to establish whether or not the exotoxins of Fusobacterium necrophorum can suppress granulopoiesis.

Moldy sweetclover poisoning in cattle.

Some selected clinical and laboratory aspects of moldy sweetclover poisoning in cattle are reviewed. The prothrombin time is preferred when the disease is suspected. The bleeding time and whole blood clotting time test are also used. Dicoumarol is not always detectable in the suspected feed which may be due to sampling technique or inaccuracy in the laboratory assay. The most effective treatment is a whole blood transfusion. Vitamin K(1) (naturally occurring vitamin K) is an effective antidote but too expensive. Vitamin K(3) (synthetic vitamin K) in both the injectable and oral forms are not as effective as K(1) but are used extensively for treatment and prevention. Feeding the suspected feed for two weeks followed by a one week withdrawal successively or by dilution with other feeds will help to reduce the incidence of disease if other feeds are not available. Suspected feed should not be fed to cattle for at least three weeks before surgery or parturition.

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.

Blood levels of sulfamethazine achieved in beef calves on medicated drinking water.

Studies on the use of sodium sulfamethazine in drinking water at three levels (572, 1028 and 1848 mg/L) were conducted in healthy weaned beef calves under similar dietary and environmental conditions. Blood sulfonamide levels greater than 5 mg/dl were attained with each treatment level but at different time intervals. The maximum levels in blood were achieved with the highest concentration in the water. However, a reduction in water intake caused a lower than anticipated dose of sulfamethazine. Under the conditions of the experiment the administration of sulfonamide in drinking water may be an effective means of mass medication of cattle.

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.

Proliferative hemorrhagic enteropathy in swine: an outbreak and review of the literature.

An account is given of an acute outbreak of hemorrhagic enteric disease in 34 young adult boars of primarily Yorkshire breeding at a performance testing station in Western Canada. Two of the boars died. A diagnosis of proliferative hemorrhagic enteropathy was made on the basis of clinical signs, gross necropsy and histopathological lesions. Campylobacter-like bacteria were seen in the apical cytoplasm of epithelial cells of the ileal mucosa by Warthin-Faulkner stain on histological sections, but were not isolated on culture. Treatment with several drugs simultaneously was associated with termination of the outbreak, but the therapeutic effect was not controlled by leaving some animals untreated. Reported sequelae, such as porcine intestinal adenomatosis, were not present at necropsy or slaughter of pigs surviving the outbreak, but all were killed no longer than two months after the first case was observed. This outbreak is discussed in the context of previously reported hemorrhagic enteric conditions of pigs.