Search

Inherited osteopetrosis was identified in cattle herds in Wyoming, Nebraska, and Missouri in 2008 to 2010. Ten affected Red Angus calves were examined to characterize lesions in brain, teeth, and skull. Six affected aborted or stillborn calves were homozygous for the recently characterized deletion mutation in SLC4A2. Four affected calves were heterozygous for the SLC4A2 mutation and survived 1 to 7 days after birth. Gross lesions were similar in all 10 calves. Brains were rectangular and dorsoventrally compressed, with concave depressions in the parietal cortex owing to thickened parietal bone. Cerebellar hemispheres were compressed with herniation of the cerebellar vermis into the foramen magnum. Moderate bilateral chromatolysis affected multiple cranial nerve nuclei and, in some calves, the red nucleus. There was loss of retinal ganglion cells with severe atrophy of optic nerves. Periventricular corpora amylacea were in the thalamus, caudate nucleus, and midbrain. Vessels and neuropil in the dorsomedial aspect of the thalamus were mineralized. Dysplastic change in premolar and molar teeth comprised intra-alveolar intermingling of dentin, enamel, cementum, and bone, contributing to dental ankylosis. Changes in the heads of osteopetrotic calves are similar to those in children with malignant forms of homozygous recessive osteopetrosis. [ABSTRACT FROM PUBLISHER]

The article presents a diagnostic exercise which identifies a syndrome among the calves in Wyoming. The syndrome is evidenced by lethargy, fever and consequently death and occurs between November and January each year. A diagnostic examination was conducted to which an unfixed heart was submitted for examination. Findings reveal an acute necrotizing myocarditis due to Histophilus somni bacterial infection.

Mycoplasma bovis is 1 of several bacterial pathogens associated with pneumonia in cattle. Its role in pneumonia of free-ranging ungulates has not been established. Over a 3-month period in early 2019, »60 free-ranging pronghorn with signs of respiratory disease died in northeast Wyoming, USA. A consistent finding in submitted carcasses was severe fibrinosuppurative pleuropneumonia and detection of M. bovis by PCR and immunohistochemical analysis. Multilocus sequence typing of isolates from 4 animals revealed that all have a deletion in 1 of the target genes, adh-1. A retrospective survey by PCR and immunohistochemical analysis of paraffin-embedded lung from 20 pronghorn that died with and without pneumonia during 2007-2018 yielded negative results. These findings indicate that a distinct strain of M. bovis was associated with fatal pneumonia in this group of pronghorn.

Brucella abortus RB51 is the vaccine strain currently licensed for immunizing cattle against brucellosis in the United States. Most cattle are vaccinated as heifer calves at 4-12 months of age. Adult cattle may be vaccinated in selected high-risk situations. Two herds of pregnant adult cattle in the brucellosis-endemic area of Wyoming were vaccinated with a standard label dose (1.0-3.4 × 10(10) organisms) of RB51. Reproductive losses in the vaccinated herds were 5.3% (herd A) and 0.6% (herd B) and included abortions, stillbirths, premature calves, and unbred cows (presumed early abortion). Brucella abortus was cultured from multiple tissues of aborted and premature calves (7/9), and from placenta. Isolates were identified as B. abortus strain RB51 by standard strain typing procedures and a species-specific polymerase chain reaction. Bronchopneumonia with intralesional bacteria and placentitis were observed microscopically. There was no evidence of involvement of other infectious or toxic causes of abortion. Producers, veterinarians, and laboratory staff should be alert to the risk of abortion when pregnant cattle are vaccinated with RB51, to potential human exposure, and to the importance of distinguishing field from vaccinal strains of B. abortus.

Inherited osteopetrosis was identified in cattle herds in Wyoming, Nebraska, and Missouri in 2008 to 2010. Ten affected Red Angus calves were examined to characterize lesions in brain, teeth, and skull. Six affected aborted or stillborn calves were homozygous for the recently characterized deletion mutation in SLC4A2. Four affected calves were heterozygous for the SLC4A2 mutation and survived 1 to 7 days after birth. Gross lesions were similar in all 10 calves. Brains were rectangular and dorsoventrally compressed, with concave depressions in the parietal cortex owing to thickened parietal bone. Cerebellar hemispheres were compressed with herniation of the cerebellar vermis into the foramen magnum. Moderate bilateral chromatolysis affected multiple cranial nerve nuclei and, in some calves, the red nucleus. There was loss of retinal ganglion cells with severe atrophy of optic nerves. Periventricular corpora amylacea were in the thalamus, caudate nucleus, and midbrain. Vessels and neuropil in the dorsomedial aspect of the thalamus were mineralized. Dysplastic change in premolar and molar teeth comprised intra-alveolar intermingling of dentin, enamel, cementum, and bone, contributing to dental ankylosis. Changes in the heads of osteopetrotic calves are similar to those in children with malignant forms of homozygous recessive osteopetrosis.

Although plague is relatively rare in wild ungulates, this report describes ocular lesions associated with Yersinia pestis infection in three free-ranging mule deer (Odocoileus hemionus) from Wyoming and Oregon, USA. All deer were observed antemortem and seemed to be blind. Post-mortem examination revealed gross lesions of bilateral keratoconjunctivitis and/or panophthalmitis in the first two deer, but only partial retinal detachment in the third deer. Microscopically, all deer had moderate-to-severe necrotizing and fibrinopurulent endophthalmitis and varying degrees of keratoconjunctivitis with abundant intralesional coccobacilli. The lesions in the first (D1) and third deer (D3) suggested an acute course, whereas those in the second deer (D2) were subacute to chronic. Yersinia pestis was isolated from ocular tissue swabs or ocular fluids of D1 and D2, and it was demonstrated by immunohistochemistry within ocular lesions of D1 and D3. Although plague does not seem to be a major cause of morbidity or mortality in free-ranging mule deer, keratoconjunctivitis or pinkeye is relatively common in these animals and plague should be considered as a differential diagnosis in such cases, with appropriate precautions taken to protect the human and animal health.

Abortion and death caused by Francisella tularensis were well recognized in range flocks of domestic sheep in Idaho, Montana, and Wyoming in the first 6 decades of the 20th century. The current report describes 4 episodes of tularemia in 3 range flocks in Wyoming and South Dakota in 1997 and 2007 (1 flock was affected twice). Flock owners reported that ticks were unusually numerous and commonly present on sheep during outbreaks. Tularemia presented as late-term abortions (3 episodes) or listlessness and death in lambs and, to a lesser extent, ewes (1 episode). Lesions were multifocal pinpoint necrotic foci in tissues, particularly spleen, liver, and lung. An immunohistochemical procedure demonstrated F. tularensis, particularly in necrotic foci. The diagnosis was corroborated by bacterial isolation and, in individual cases, by serology, fluorescent antibody assay, and/or polymerase chain reaction detection of F. tularensis. Diagnosticians in endemic areas should include tularemia as a differential diagnosis when investigating late-term abortions or outbreaks of fatal illness in young lambs, particularly in years of high tick activity and when characteristic necrotic foci occur in spleen, liver, and lung.

Malignant catarrhal fever (MCF) in cattle is generally associated with a short clinical course and a high case fatality rate (90-95%). The lesions in cattle that survive acute MCF for a prolonged period or appear to recover have not been documented. In a naturally occurring outbreak of MCF in a herd of beef cattle in Wyoming, 7 of 84 yearling heifers (8.3% of replacement herd) and 2 of 230 cows (0.9% of cow herd) developed clinical signs of pyrexia, mucopurulent discharge, bilateral keratitis, and weight loss following contact with ewes that had lambed 34-62 days earlier. Six of 9 affected cattle were examined postmortem following clinical signs (CS) that developed 2-150 days earlier. Three cattle with CS for < or = 39 days had lesions of regional lymphadenopathy and widespread severe segmental lymphoid arteritis-phlebitis that were typical of acute MCF, and proliferative intimal lesions were present in a small proportion of arteries at days 20 and 39 of CS. By contrast, 3 cattle that survived to 90, 105, and 150 days after clinical onset had distinctive arterial lesions in multiple organs, characterized by proliferative concentric fibrointimal plaques, disrupted inner elastic lamina, focally atrophic tunica media, and vasculitis of variable severity. Immunohistochemical and ultrastructural examination of intimal plaques identified the predominant cellular component to be smooth muscle cells with a contractile phenotype. No viral structures were seen. Serologic studies, using a competitive inhibition enzyme-linked immunosorbent assay (CI-ELISA) that detects antibody to an epitope broadly conserved among isolates of the MCF virus, found that 2 chronically affected cattle were serologically positive between days 42 and 100 of CS, with seroconversion in 1 animal between days 52 and 73 of CS. Seroprevalence was 7.9% in the 76 remaining healthy animals of the replacement heifer herd and 40% (75% in adult sheep and 4% in lambs) in the in-contact sheep flock 77 days after onset of CS in the index case. This episode suggests that, in addition to the common and well recognized acute form of MCF in cattle, this viral infection encompasses a disease spectrum that includes chronic disease and partial to "complete" clinical recovery, and in recovered animals chronic obliterative arteriopathy is the preeminent lesion.

A review of Wyoming State Veterinary Laboratory records for 1947-1987 revealed no substantiated cases of naturally occurring selenosis. However, older reports attributed thousands of animal deaths to selenium each year in this area. Beginning in August 1988, cases of suspected selenosis and selenium deficiency were solicited from veterinarians and producers by announcements in various statewide livestock publications. As of August 1991, 4 cases (all horses) of naturally occurring selenosis have been confirmed. Clinical signs were most often referable to epithelial damage, e.g., hoof lesions and loss of mane and tail. None involved neurologic signs. Sources of selenium included native range and grass hay.