This report describes the investigation of mortality of double-crested cormorants (Phalacrocorax auritus), white pelicans (Pelecanus erythrorhynchos), and gulls (Larus spp.) in Alberta, Saskatchewan, and Manitoba during late summer 1990. Techniques used varied among areas, but virological and histopathological examination of birds was done in each area. The major clinical sign in cormorants was inability to fly, often with unilateral wing or leg paralysis. Focal nonsuppurative inflammation was present in the brain and spinal cord of cormorants and pelicans. Newcastle disease virus (NDV) was isolated from cormorants, a pelican, and a ring-billed gull (Larus delawarensls) from Saskatchewan. Cormorants from Alberta were positive for NDV in an immunofluorescent test. Most of the viruses were classed as velogenic and all had a similar monoclonal antibody profile to viruses from the 1970 to 1974 panzootic. Approximately half of cormorant, pelican, and gull eggs collected from affected colonies in the spring of 1991 had antibody to NDV. Antibody was also present in cormorant eggs from the Great Lakes. No unusual mortality was detected at any colony in 1991. Fledgling cormorants and gulls from colonies where mortality occurred in 1990 did not have antibody to NDV in June-July 1991. The overall extent of mortality among water birds and the source of the virus were not determined.
Acute mortality occurred in two unrelated rabbitries. In the rabbits examined, an unidentified herpesvirus caused lesions that have not been reported previously in this species. The primary lesions were multifocal hemorrhagic dermatitis on the face and back, localized pneumonia, and severe splenic necrosis. Large eosinophilic, intranuclear inclusion bodies that were observed in tissue sections of skin, spleen, and lung were identified as herpes-like viral particles by electron microscopy, and herpesvirus was cultured on rabbit kidney cells. Intramuscular injection of tissue culture fluid containing virus resulted in mortality and severe illness in two seven-week-old domestic rabbits four and six days postinfection, respectively. The gross and microscopic lesions were reproduced and herpeslike viral inclusions were observed in skin lesions. Herpesvirus was recovered from lung, trachea, spleen, liver, and from the thigh muscle at the site of inoculation. The experimental infection also activated severe pasteurella septicemia. The herpesvirus isolate needs further characterization.
The use of early short-term (seven day duration) feed restriction as a management tool for use in reducing the incidence of skeletal and metabolic diseases in broiler and roaster chickens was examined in three experiments. The optimum timing for feed restriction was found to be during the second week, rather than later. The number of birds culled for skeletal disease was reduced, although a significant reduction in both six week and nine week body weight was apparent (market weight delayed by 2 or 3 days). Feed restriction did not affect feed efficiency. Both a skip-a-day feeding regimen and diet dilution offered potential alternatives to feeding a limited amount of feed daily during the restriction period. These options may overcome some of the limitations of managing early feed restriction, while at the same time, markedly reduce losses to skeletal disease.
In Alberta, cellulitis condemnations average 0.5% and are among the highest in Canada. Presently, all cellulitis-affected birds are condemned for fear of systemic infections and public health implications. In a slaughterhouse sample of 102 birds condemned with cellulitis, Escherichia coli was isolated from 83.3% of the lesions. All hearts were cultured and from 11.2% E. coli was recovered. Gross lesions of perihepatitis, infected oviducts, and arthritis were found in 11.2%, 6.7%, and 2.9% of the birds, respectively. Serotyping suggested that visceral infection occurs independent of cellulitis in at least half of the cases. There was no correlation between microscopic visceral lesions and positive bacterial cultures. Two E. coli isolates of serogroup 0157 produced no toxin and neither isolate produced CS31A, F107, or F1845 fimbriae. Cellulitis lesions ranged from 0.55 to 218.9 cm2. All lesions under 16 cm2 and 64% of lesions up to 48 cm2 were considered suitable for trimming.
It is common for poultry-flock owners to suspect that feed is at fault when a disease outbreak or production loss coincides with the delivery of a new load of feed. Usually, however, the disease or production drop and the use of new feed are unrelated. Feeding trials at these laboratories have been used on many occasions to resolve this type of problem. Monensin is a biologically active compound that has antibacterial and anticoccidial properties. It is used extensively in the poultry industry to control coccidiosis. Monensin belongs to the ionophore or ion carrier group of antibiotics. These compounds facilitate the transport of alkali metal ions across biological membranes. Monensis preferably transports sodium ions and, as a result of this uncontrolled movement, ionic gradients and concentrations are altered and physiological processes of cell are disturbed (2). Three unrelated cases of poisoning by monensin sodium in improperly prepared feeds are described. Although routine analyses did not detect the cause, feeding trials confirmed suspicions that the feed was at fault; the cause was eventually found. These three flocks of chickens exhibited feed refusal, paralysis, and death. The symptoms started within a day of delivery of a new
Bighorn sheep were inoculated intratracheally with suspensions of nonhemolytic Pasteurella haemolytica biotype T (10(12) organisms) unique to wild bighorns, with beta-hemolytic P. haemolytica biotype T (10(12) organisms) isolated from clinically normal domestic sheep or intradermally with half a dose of a cattle vaccine containing P. haemolytica biotype A (10(5) organisms). The bighorn strain caused lobar necrotizing bronchopneumonia whereas both domestic livestock strains precipitated fatal septicemia and fibrinous bronchopneumonia. The serotypes given were T3, T4, T15 and A1 and these were recovered from lung lesions and other organs. In three trials, domestic sheep were inoculated intratracheally with suspensions of bighorn sheep pneumonic lungs, and two concentrations of the P. haemolytica bighorn strain (10(4) and 10(12) organisms). One of these sheep was inoculated intrabronchially. The domestic sheep experienced a transient fever and elevated white blood cell counts. After six days, none of the sheep had lung lesions and inoculated organisms could not be recovered. It is suggested that bighorn sheep are very susceptible to P. haemolytica from domestic livestock and should not be allowed in contact with sheep or cattle.
