Sequential opportunistic infections in two German Shepherd dogs

Two German Shepherd dogs with sequential opportunistic infections are described. The first was a 2-year-old male with cryptococcal rhinitis that spread to involve the optic nerves and brain. It was successfully treated with combination therapy utilising amphotericin B administered for 2 years, but the dog developed a disseminated Aspergillus deflectus infection 5 years later and was euthanased. The second case was a 4-year-old male that presented for a severe, deep-seated infection of the right antebrachium, with gradual extension to contiguous tissues. Neosartorya fischeri (anamorph; Aspergillus fischerianus) was isolated in pure culture and detected in histological sections. The infection was refractory to itraconazole, but resolved after amputation of the affected limb. Five months later, the dog developed a localised cutaneous lesion on the proximal pelvic limb, from which Pythium insidiosum was isolated and then visualised in tissue sections, together with a structure thought to be grass seed. This lesion was treated by wide surgical resection, although it was reported that the dog died of disseminated disease some months later. These cases provide further circumstantial evidence that young adult German Shepherd dogs have a predilection to developing invasive infections with fungi and other saprophytic pathogens.     

Production and characterisation of monoclonal antibodies specific for chicken interleukin-12

Using genetic immunisation of mice, we produced antibodies against chicken interleukin-12p40 (chIL-12p40), also known as IL-12β. After a final injection with a recombinant chIL-12p40 protein, several stable hybridoma cell lines were established which secreted monoclonal antibodies (mAbs) to this component of the heterodimeric IL-12 cytokine. Specific binding of three of the mAbs to COS-7 cell-derived recombinant chIL-12p40 and the chIL-12p70 heterodimer was demonstrated in an indirect ELISA, and in dot blots. Two of the mAbs were used to develop a capture ELISA, suitable for detecting both recombinant protein (chIL-12p40 and the heterodimeric p70 protein) and native chIL-12. The mAbs were further characterised to show utility in immunocytochemistry.     

Basophil leucocytes in responses to parasitic infection and some other stimuli in sheep

Basophil leucocytes are a significant component of the infiltrating cells in a variety of tissue reactions in guinea pigs. However, little is known about the participation of basophils in similar reactions in most other animal species. The circulating blood, skin and small intestinal mucosa of sheep were examined after they had received stimuli known to elicit basophil-rich responses in guinea pigs but relatively few basophils were found.     

Effects of eight vehicles on transdermal lidocaine penetration in sheep skin in vitro

This study investigated the effects of vehicles on penetration and retention of lidocaine applied to sheep skin in vitro. Thoracic skin from two sheep was clipped of wool and stored at −20 °C, until used. Skin samples were defrosted and mounted in Franz‐type diffusion cells, and then one of the following formulations, each saturated with lidocaine, was added: sodium lauryl sulphate (SLS) 0.5% in water, SLS 1% in water, dimethyl sulphoxide (DMSO) 50% in water (wt/wt), DMSO 100%, isopropyl myristate 100% (IPM), water alone, diethylene glycol monoethyl ether (DGME) 50% in water (wt/wt) and DGME 100%. The penetration of lidocaine in each skin sample was measured over 8 h. Significantly greater lidocaine skin concentrations and flux (J_SS) were achieved with the nonaqueous vehicles, DMSO 100% (P < 0.00001 and P < 0.01, respectively), followed by DGME 100% and IPM (P < 0.00001 and P < 0.01, respectively). The lag time (t_lag) for lidocaine penetration in the DMSO 100% vehicle was significantly shorter (P < 0.01) compared with all other vehicles except water. Improved transdermal penetration of lidocaine in the DMSO 100% vehicle was likely due to skin barrier disruption, as determined by differences in pre‐ and post‐treatment transepidermal water loss (TEWL). This study has shown that nonaqueous vehicles enhanced penetration of lidocaine in sheep skin to a greater extent than aqueous vehicles, which has implications for topically applied local anaesthesia in sheep.     

Histological changes to the skin of Merino sheep following deep dermal and subcutaneous injections of sodium lauryl sulfate

Objectives To characterise the changes caused to sheep skin by deep dermal and subcutaneous injections of sodium lauryl sulfate (SLS) and describe the subsequent healing process. Procedure On 6 sheep 20 small areas of skin were each given deep dermal and subcutaneous injections of 0.2 mL of 7% SLS. Biopsies were collected at intervals up to 28 days after treatment and the histological changes in each of the treated skin samples were assessed and graded. Results There was no evidence of alterations in behaviour, weight gain or appetite of the sheep following the injections. Initial swelling of the treated site subsided by day 14, leaving a firm, slightly raised crust. At day 21, the treated area was depressed and covered by a scab, which sloughed completely by day 28. There was necrosis of the subcutis and deep dermis 2 min after treatment, followed by inflammation, fibroplasia, angiogenesis and tissue remodelling. Conclusion Injection of SLS caused almost immediate local necrosis followed by eschar formation, sloughing and scarring of treated skin. Deep dermal and subcutaneous SLS is potentially useful as a chemical alternative to mulesing.     

CNS injury: the role of the cytokine IL-1

Injury to the central nervous system (CNS) and the resulting neuronal loss contribute significantly to morbidity and mortality in human and domestic animal populations. Most insults induce inflammation and the expression of cytokines. The specific roles of these proteins in neurological damage and repair are not completely understood. However, members of the interleukin-1 (IL-1) family have clear therapeutic potential: the IL-1 agonists, IL-1 alpha and IL-1 beta, are induced by CNS injury, and central injection of IL-1 increases, whilst peripheral or central administration of the IL-1 antagonist, IL-1ra, reduces the extent of the damage by more than 50%. The mechanism of action of these cytokines is the subject of intense research. In this review, we summarise approaches that are being used to investigate neuronal cell death, and the contribution of inflammation and cytokines, in particular the IL-1 family, to neurodegenerative disorders.