Variant Influenza Associated with Live Animal Markets,Minnesota

Variant influenza viruses are swine‐origin influenza A viruses that cause illness in humans. Surveillance for variant influenza A viruses, including characterization of exposure settings, is important because of the potential emergence of novel influenza viruses with pandemic potential. In Minnesota, we have documented variant influenza A virus infections associated with swine exposure at live animal markets.     

Antimicrobial Resistance in Some Gram‐Negative Bacteria Isolated from the Bovine Ejaculate

The bacterial load and degree of antibiotic resistance present in untreated and antibiotic‐treated semen samples were investigated in five bulls standing at a cattle‐breeding centre. Bacterial load was determined by colony counts from semen samples cultured on brain heart infusion and nutrient agar plates. Antibiotic resistance in these bacteria was assessed by measuring the diameter of bacterial growth inhibition zones around discs containing different concentrations of antibiotics. Representative antibiotic‐resistant bacterial isolates were selected for identification. Untreated semen contained few culturable bacteria, and all were completely sensitive to gentamycin, spectinomycin and lincomycin: six of the isolates showed some resistance to tylosin. In semen to which antibiotics had been added as part of the routine production process, two isolates were sensitive to all of the antibiotics tested, and the remainder were resistant to all. Resistant Gram‐negative isolates that were identified included Pseudomonas and Stenotrophomonas spp. both in the class Gammaproteobacteria and a Sphingomonas sp. which is in the class Alphaproteobacteria.     

Animal medical genetics: a perspective on the epidemiology and control of inherited disorders

This perspective considers genetic disorders of domestic animal populations, in particular their epidemiology and control. Inherited disorders of animals share the same basic molecular biology as those of human beings, but they differ in their epidemiology due largely to the breed structure of the various species, human control of breeding and a greater influence of the founder effect, particularly due to extensive use of a limited number of sires, and inbreeding. Control of genetic disorders in animals is also more practical through extensive screening for disease, or heterozygous animals within defined breed populations, followed by exclusion of affected or carrier animals from breeding. This is assisted by the fact that, within a breed, many inherited monogenic disorders are associated with a single mutation. However some of the more important disorders may be inherited in a non-Mendelian manner, being influenced by multiple genes as well as environmental factors. These aspects are discussed and contrasted with similar aspects in human medical genetics.     

Cerebellar cortical abiotrophy in Wiltshire sheep

AIM: To investigate the nature of a neurological disease in Wiltshire sheep.

METHODS: Three affected lambs were examined, humanely killed and necropsied. Selected neurological tissues were examined by light and electron microscopy.

RESULTS: Primary neurological lesions were confined to the cerebellum and were characterised by loss of Purkinje cells and the presence of large hypertrophied dendrites of surviving Purkinje cells. These contained stacks of smooth endoplasmic reticulum. There was hyperplasia and cell swelling of Bergmann glia. Mild Wallerian-type degeneration affected white matter in the cerebellum and spinal cord.

CONCLUSION: The cerebellar lesions were of a degenerative and reactive rather than hypoplastic nature. These, and the history, suggest a genetic cause with putative inheritance as an autosomal recessive trait. Accordingly, the disorder is described as a cerebellar abiotrophy.     

Progressive ataxia and seizures in a Cocker Spaniel: a new type of neurodegenerative disease with novel intra-neuronal inclusions

AIMS: To describe the histopathological lesions of a new canine disease characterised by progressive ataxia, head tremor and seizures, and to deduce the cause of the lesions.

METHODS: Formalin-fixed tissues were processed into paraffin wax and epoxy resin for light and transmission electron microscopy of variously stained tissue sections.

RESULTS: Significant lesions relevant to the disease were found only in the brain. They consisted of hypoplasia of the cerebellum and the presence of large pale inclusions in the perikaryon of neurons in the neocortex and in macrophages. The inclusion material was not compartmentalised and did not stain for carbohydrate, mucopolysaccharide or lipid. This material displaced nuclei to the periphery of the cells where they were seen as basophilic distorted crescent-shaped structures.

CONCLUSIONS: The inclusions were probably made of polymerised protein similar, though not identical, to those of Pick, Lewy and Collins bodies that characterise a variety of chronic neurodegenerative diseases of humans. A genetic basis to this disease was considered probable.     

Assessment of the Hemocue-b for measuring hemoglobin in horse blood

Our purpose was to assess the accuracy and precision of a point of care hemoglobinometer (HemoCue‐B hemoglobin photometer) for measuring hemoglobin concentration in horse blood. Samples of jugular venous blood from 12 healthy adult horses were collected in EDTA. In order to test the device over a wide range of values, each sample was divided into nine aliquots, and autologous plasma was added or removed from the aliquots to produce blood with PCV values that approximated 5, 10, 20, 30, 40, 50, 60, 70, and 80%, respectively. The aliquots were rocked to ensure mixing of plasma and cells. Then hemoglobin by HemoCue‐B (Hb_HQ) and hemoglobin by the cyanmethemoglobin method (Hb_CY) were measured on each aliquot. The PCV of each aliquot was also measured and this value was used for subsequent analyses. To test repeatability, hemoglobin was measured twice by the HemoCue‐B on approximately 40% samples. Samples with Hb_HQ >25.4 g dL^?1 required dilution prior to analysis. Hb_CY ranged from 1.6 to 33.4 g dL^?1. After regression, Hb_CY = ?0.16 + 1.04 Hb_HQ (n = 101; r² = 99.6%). By inspection of a modified Bland‐Altman plot, Hb_HQ values <16 g dL^?1 closely approximated Hb_CY; however, at greater values, Hb_HQ underestimated Hb_CY by as much as 3.2 g dL^?1. The difference between repeated measurements with the HemoCue‐B was 0.02 ± 0.16 g dL^?1 (mean ± SD; n = 10) and nonsignificant. After regression, PCV = ?0.76 + 2.78 Hb_HQ (n = 101; r² = 99.4%). We conclude that HemoCue‐B can be used to measure hemoglobin concentration in horse blood, and that it is accurate when hemoglobin is <16 g dL^?1. PCV can be estimated by multiplying Hb_HQ by 2.8 and then subtracting 0.8.