Nursing sickness, the largest single cause of mortality in adult female mink (Mustela vison), is an example of a metabolic disorder, which develops when the demands for lactation require extensive mobilization of body energy reserves. The condition is characterized by progressive weight loss, emaciation, and dehydration with high concentrations of glucose and insulin in the blood. Morbidity due to nursing sickness can be as high as 15% with mortality around 8%, but the incidence is known to vary from year to year. Stress has been shown to trigger the onset of the disease and old females and females with large litters are most often affected. Increasing demand for gluconeogenesis from amino acids due to heavy milk production may be a predisposing factor. Glucose metabolism is inextricably linked to that of protein and fats. In obesity (or lipodystrophy), the ability of adipose tissue to buffer the daily influx of nutrients is overwhelmed (or absent), interfering with insulin-mediated glucose disposal and leading to insulin resistance. Polyunsaturated fatty acids of the n-3 family play an important role in modulating insulin signalling and glucose uptake by peripheral tissue. The increasing demand on these fatty acids for milk fat synthesis towards late lactation may result in deficiency in the lactating female, thus impairing glucose disposal. It is suggested that the underlying cause of mink nursing sickness is the development of acquired insulin resistance with 3 contributing key elements: obesity (or lipodystrophy), n-3 fatty acid deficiency, and high protein oxidation rate. It is recommended that mink breeder females be kept in moderate body condition during fall and winter to avoid fattening or emaciation. A dietary n-3 fatty acid supplement during the lactation period may be beneficial for improved glycemic control. Lowering of dietary protein reduces (oxidative) stress and improves water balance in the nursing females and may, therefore, prevent the development and help in the management of nursing sickness. It is also surmised that other, thus far unexplained, metabolic disorders seen in male and female mink may be related to acquired insulin resistance.

The innate immune system is a critical component directing the overall response of the immune system early in the inflammatory process. Evaluation of the innate immune system could offer a screening method for the selection of breeding stock from commercial chicken operations to improve flock health and prevent the loss of genes crucial to disease resistance. Three commercial broiler chicken lines (designated Lines A, B and C) were profiled for efficiency of their innate immunologic response. Oxidative burst and bactericidal functions of heterophils and monocytes, as well as heterophil degranulation, were analyzed. The birds were tested 1, 4, 8 and 15 days post-hatch. Individual lines differed in their ability to perform innate immunological responses during the first 15 days post-hatch. Although bactericidal capabilities were similar, oxidative burst responses by monocytes were low in comparison to that generated by heterophils. The fact that monocytes are not particularly adept at producing an oxidative burst at this age suggests that this is not a major avenue of innate defense by monocytes. Heterophil oxidative burst response was stronger in Line C than Line A during the first four days post-hatch. Line B showed no difference from Line C in heterophil oxidative burst response at 1 d, but produced a stronger response than Line C on 4 and 8 d post-hatch. Degranulation by heterophils showed significant differences in responses of Lines A and C depending on the day post-hatch, and stronger response in Line C vs Line B in the first four days post hatch. The first week post-hatch is an important time as chicks are particularly susceptible to infection as neonates. Mortality data of the commercial lines indicates that Line A is the most susceptible to demise, followed by Line C and then Line B. These results suggest that oxidative burst production efficiency is an important defensive function to monitor for immunoprofiling.

The current diagnostic test for Tritrichomonas foetus involves the culture of collected preputial or vaginal samples. In an earlier study, which evaluated sampling tools for use with bulls, it was observed that the sensitivity of the diagnostic test was higher for 2nd samples collected from the right side of the prepuce than it was for samples collected 1st from the left side. The study described in this paper was conducted to evaluate which of these factors was responsible for the effect on diagnostic sensitivity. Twenty-nine bulls infected with T. foetus were repeatedly sampled in a 2-factor cross-over design. Samples taken from the right side of the prepuce were 4 times as likely to be positive as samples taken from the left side (P = 0.03). Other factors did not have a significant effect on the outcome of the diagnostic test. Unexpected factors may affect the sensitivity of the diagnostic test for T. foetus.

Different doses of dexamethasone were evaluated for the treatment of cerebral trauma using a rat model of cerebral hematoma induced by intracerebral (IC) stereotaxic injections of collagenase. Control animals received an intracerebral collagenase injection followed by intraperitoneal (IP) saline injection. Sham operated animals received saline only (IC, IP). Forty-eight hours following the surgeries, the brains were removed from the euthanized animals. Cerebral hemispheres were separated and the 4 coronal sections (antero-posterior plane) were weighed. Each slice was dried for 24 h (100°C) and weighed again to establish brain water content. In hematoma-induced saline treated rats, significant differences in brain water content were observed when compared to sham operated animals. Rats treated with 1 mg/kg dexamethasone had a significant brain water content decrease; however, no significant differences were observed with higher doses of dexamethasone. In conclusion, low doses of dexamethasone seem to be beneficial for the treatment of cerebral trauma.

Domestic dogs were screened for Trypanosoma brucei infection using the haematocrit centrifugation technique as part of routine active surveillance exercises in the Busia and Teso districts of Kenya. The purpose was to assess the role of dogs as sentinels for the occurrence of human sleeping sickness. Out of 200 dogs screened, five were found to be infected at the various test sites. These five succumbed to the disease within four weeks, and exhibited a distinct and pronounced corneal opacity before death. Blood from two naturally infected dogs were tested for the presence of the serum resistance associated (SRA) gene and one tested positive, confirming it as human infective (T. brucei rhodesiense) prevalence (0.5 %). It is considered that the occurrence of this clinical sign could be used as an early warning prediction of future outbreaks. This type of prediction could form an integral part of an indigenous technical knowledge set in areas lying at the edges of the tsetse (Glossina) belts where T. brucei is the main trypanosome species that affects dogs. The occurrence of corneal opacity in dogs could indicate a rise in the levels of T. brucei a proportion of which could be human infective T. b. rhodesiense circulating in the population early enough before disease outbreak occurs. It is thought that during sleeping sickness epidemics the domestic dog will be the first casualty rapidly succumbing to disease long before it is noticed in man. Prompt prediction of disease outbreaks would thus enable early interventions that would reduce the morbidity, mortality and the general economic losses associated with sleeping sickness to be instituted.

Oligodendrocytes and myelin in the corpus callosum of black tremor and normal hamsters aged over 1.5 years were ultrastructurally examined to determine the myelination index (ratio of myelin thickness/diameter of axon), percentage of naked axons, and proportions of oligodendroglial subtypes (light, medium and dark). The mutant hamsters were remarkably hypomyelinated, with a low myelination index and a high proportion of naked axons, and high proportions of the dark subtypes. Serum concentrations of thyroid hormones (T sub(3) and T sub(4)) in 6-week-old mutant hamsters were 2-fold (T sub(3)) to 3-fold (T sub(4)) higher than those of age-matched normal animals. However, in the aged animals (over 1.5 years old) only T sub(4) levels of the mutant hamsters were higher in the mutant than normal hamsters. The black tremor hamsters were hypomyelinated throughout their life and high serum level of thyroid hormones might have played a role in the hypomyelination.