Identification of quantitative trait loci governing arthritis severity and humoral responses in the murine model of Lyme disease.

A spectrum of disease severity has been observed in patients with Lyme disease, with approximately 60% of untreated individuals developing arthritis. The murine model of Lyme disease has provided strong evidence that the genetic composition of the host influences the severity of arthritis following infection with Borrelia burgdorferi: infected C3H mice develop severe arthritis while infected C57BL/6N mice develop mild arthritis. Regions of the mouse genome controlling arthritis severity and humoral responses during B. burgdorferi infection were identified in the F2 intercross generation of C3H/HeNCr and C57BL/6NCr mice. Rear ankle swelling measurements identified quantitative trait loci (QTL) on chromosomes 4 and 5, while histopathological scoring identified QTL on a unique region of chromosome 5 and on chromosome 11. The identification of QTL unique for ankle swelling or histopathological severity suggests that processes under distinct genetic control are responsible for these two manifestations of Lyme arthritis. Additional QTL that control the levels of circulating Igs induced by B. burgdorferi infection were identified on chromosomes 6, 9, 11, 12, and 17. Interestingly, the magnitude of the humoral response was not correlated with the severity of arthritis in infected F2 mice. This work defines several genetic loci that regulate either the severity of arthritis or the magnitude of humoral responses to B. burgdorferi infection in mice, with implications toward understanding the host-pathogen interactions involved in disease development.

Rabies-induced spongiform change and encephalitis in a heifer.

A 1-year-old mixed breed heifer was presented to the Veterinary Medical Teaching Hospital at the University of Illinois with a 3-day history of abnormal mentation and aggressive behavior. Based on the history and clinical examination, euthanasia and necropsy were recommended. The differential diagnosis included rabies, pseudorabies, and a brain abscess. The brain was removed within 60 minutes of death, and the section submitted for fluorescent antibody testing was positive for rabies virus antigen. Residual brain tissue was immersion fixed in 10% neutral buffered formalin. Histologic examination revealed a marked perivascular and meningeal lymphocytic meningoencephalitis and locally extensive spongiform change of the gray matter affecting the neuropil and neuron cell bodies. The most severely affected regions with spongiform change were the thalamus and cerebral cortex. No Negri bodies were found in any sections. Since the outbreak of bovine spongiform encephalopathy (BSE) in the United Kingdom, there has been an increased surveillance of bovine neurologic cases in an effort to assess if BSE has occurred in the USA. In areas where rabies virus is endemic, rabies should be included as a possible differential diagnosis in cases of spongiform changes of the central nervous system.

Zinc deficiency in sheep and goats: three field cases.

Zinc deficiency was diagnosed in 2 flocks of sheep and a herd of goats. Alopecia and eating of wool were observed. Skin lesions were hyperkeratosis and parakeratosis. Abnormal hoof growth and a closed stance with arched back and bowed hindlimbs were seen. Anorexia, depression, and foot soreness diminished quickly after zinc supplementation. Skin lesions healed and hair and wool growth resumed. A cause for the deficiency could not be established.