Isobaric bubble growth: a consequence of altering atmospheric gas

During certain treatments of decompression sickness following dives made with compressed air, the U.S. Navy advocates breathing helium-oxygen mixtures. However, stable nitrogen bubbles created within gelatin by decompression have been found to enlarge when the atmosphere was switched from nitrogen to helium without changing ambient pressure. This suggests that decompression sickness would be worsened by switching from nitrogen to helium in the breathing gas mixture.     

Effect of water restriction on equine behaviour and physiology

Six pregnant mares were used to determine what level of water restriction causes physiological and/or behavioural changes indicative of stress. Nonlegume hay was fed ad libitum. During the first week of restriction, 5 l water/100 kg bwt was available, during the second week 4 l/100 kg bwt and, during the third week, 3 l/100 kg bwt. Ad libitum water intake was 6.9 l/100 kg bwt; at 3 l/100 kg bwt water intake was 42% of this. Daily hay intake fell significantly with increasing water restriction from 12.9 +/- 0.75 kg to 8.3 +/- 0.54 kg; bodyweight fell significantly for a total loss of 48.5 +/- 8.3 kg in 3 weeks. Daily blood samples were analysed; osmolality rose significantly with increasing water restriction from 282 +/- 0.7 mosmols/kg to 293.3 +/- 0.8 mosmols/kg bwt, but plasma protein and PCV did not change significantly. Cortisol concentrations fell from 8.1 ng/ml to 6.4 ng/ml over the 3 week period. Aldosterone fell from 211.3 +/- 74.2 pg/ml to 92.5 +/- 27.5 pg/ml at the end of the first week. The behaviour of 4 of the 6 mares was recorded 24 h/day for the duration of the study. The only significant difference was in time spent eating, which decreased with increasing water restriction from 46 +/- 3% to 30 +/- 3%. It is concluded that water restriction to 4 l/100 kg bwt dehydrates pregnant mares and may diminish their welfare, but is not life- or pregnancy-threatening.     

Validity of skin testing for diagnosis of food allergy in dogs.

One hundred suspected allergic dogs were skin-tested with 9 food extracts, in addition to other inhalant and insect allergens. Forty-eight of the dogs had +2 or greater intradermal reactions to 1 or more food extracts at concentration of 1,000 protein nitrogen units/ml. Thirty of the food extract-positive dogs were fed a restrictive hypoallergenic diet. Of these 30 dogs, 3 improved, then allergy signs worsened when they were challenge-exposed with the original diet. Fifty-two dogs did not have skin test reactivity to any of the 9 food extracts. Of these 52 dogs, 35 were fed a restrictive diet. Six improved, then allergy signs worsened when dogs were challenge-exposed with the original diet. Skin-testing with selected allergenic food extracts was not useful in identifying food-sensitive dogs.     

Atopy in pet animals

The pathomechanism of canine and feline atopy has not been totally defined. Immunotherapy has been shown to be effective. The diagnosis of canine and feline atopy is still fraught with complications. Several new drugs may be useful in the treatment of canine and feline atopy.     

Correlation of histologic and immunologic findings in cats with miliary dermatitis

Eighteen cats with miliary dermatitis were evaluated, using skin testing and histology. Sixteen cats had allergic skin disease (14 cats had positive skin-test reactions to flea antigen [two of which were also atopic], one was atopic only, and one was allergic to beef). In the two remaining cats, the cause of miliary dermatitis was not identified. Histologically, 17 of the cats had superficial eosinophilic dermatitis and epidermal spongiosis, crusting, and ulceration, which were compatible with an allergic cause. Four of these cats had concurrent eosinophilic plaques, which histologically resembled miliary lesions. This overlap of plaques with miliary lesions indicated that when plaques and miliary dermatitis are found concurrently, both lesions may be caused by the same allergens.     

Contact dermatitis

Allergic contact dermatitis and irritant contact dermatitis in the small animal may result in clinical lesions with similar anatomical locations. Allergic contact dermatitis is generally noted in ventral and lightly haired regions as a papular, erythematous, and sometimes vesicular dermatitis. It is intensely pruritic and is the result of many months (and usually years) of exposure to the contact allergen. Total avoidance of the allergenic substance is the only successful long-term management. Irritant contact dermatitis occurs when an irritating substance is applied to the skin. It is a sequela that would occur in the majority of a population having contact with the compound. It is generally more painful than pruritic. Removal of the irritant will permit resolution of the signs.     

Nematode burdens of pastured cattle treated once at turnout with eprinomectin extended-release injection

The efficacy of eprinomectin in an extended-release injection (ERI) formulation was evaluated against infections with third-stage larvae or eggs of gastrointestinal and pulmonary nematodes in cattle under 120-day natural challenge conditions in a series of five studies conducted in the USA (three studies) and in Europe (two studies). For each study, 30 nematode-free (four studies) or 30 cattle harboring naturally acquired nematode infections (one study) were included. The cattle were of various breeds or crosses, weighed 107.5–273 kg prior to treatment and aged approximately 4–11 months. For each study, animals were blocked based on pre-treatment bodyweight and then randomly allocated to treatment: ERI vehicle (control) at 1 mL/50 kg bodyweight or Eprinomectin 5% (w/v) ERI at 1 mL/50 kg bodyweight (1.0 mg eprinomectin/kg) for a total of 15 and 15 animals in each group. Treatments were administered once on Day 0 by subcutaneous injection in front of the shoulder. In each study, all animals grazed one naturally contaminated pasture for 120 days. At regular intervals during the studies, fecal samples from all cattle were examined for nematode egg and larval counts. In four studies pairs of tracer cattle were used to monitor pasture infectivity at 28-day intervals before and/or during the grazing period. All calves were weighed before turnout onto pasture and at regular intervals until housing on Day 120. For parasite recovery, all study animals were humanely euthanized 27–30 days after removal from pasture.     

Experimental transmission of chronic wasting disease (CWD) of elk (Cervus elaphus nelsoni), white-tailed deer (Odocoileus virginianus), and mule deer (Odocoileus hemionus hemionus) to white-tailed deer by intracerebral route

To compare clinical and pathologic findings of chronic wasting disease (CWD) in a natural host, 3 groups (n = 5) of white-tailed deer (WTD) fawns were intracerebrally inoculated with a CWD prion of WTD, mule deer, or elk origin. Three other uninoculated fawns served as controls. Approximately 10 months postinoculation (MPI), 1 deer from each of the 3 inoculated groups was necropsied and their tissues were examined for lesions of spongiform encephalopathy (SE) and for the presence of abnormal prion protein (PrP(d)) by immunohistochemistry (IHC) and Western blot (WB). The remaining deer were allowed to live until they developed clinical signs of the disease which began approximately 18 MPI. By 26 MPI, all deer were euthanatized on humane grounds. Obvious differences in clinical signs or the incubation periods were not observed between the 3 groups of deer given CWD. In 1 of 3 nonclinical deer euthanatized at 10 MPI, minimal microscopic lesions of SE were seen in the central nervous system (CNS) tissues, and PrP(d) was observed by IHC in tissues of all 3 deer. In the clinical deer, CNS lesions of SE and PrP(d) accumulations were more severe and extensive. It is concluded that the 3 sources of CWD prion did not induce significant differences in time to clinical disease or qualitative differences in signs or lesions in WTD. However, this observation does not imply that these CWD agents would necessarily behave similarly in other recipient species.     

Western blot detection of PrP Sc in archived paraffin-embedded brainstem from scrapie-affected sheep

Scrapie is a naturally occurring fatal neurodegenerative disease of adult sheep and goats, one of a group of mammalian diseases known as transmissible spongiform encephalopathies (TSE) or prion diseases. Immunoassays that identify disease-associated prion protein (PrP Sc) are integral to the diagnosis of scrapie and other prion diseases. Results obtained by either immunohistochemistry (IHC) or Western blot (WB) assay are generally adequate for the definitive diagnosis. Approved or accepted methods for WB diagnosis of TSEs requires the use of fresh or frozen nonfixed tissue samples, whereas formalin-fixed, paraffin-embedded tissue is required for the localization of PrP Sc by IHC. Because disparate processing methods are used for these accepted diagnostic techniques, separate tissue samples are collected from the same animal. Occasions arise in which there is either insufficient quantity of tissue available to complete analysis by both techniques or initial tissue processing is incompatible with one of the assays. Also, results between the assays may differ because of the vagaries of sampling, especially in case material that contains moderate-to-low levels of PrP Sc. The present article describes a method to conduct a WB assay from the same paraffin-embedded brainstem sample used for the IHC diagnosis of experimentally induced sheep scrapie.