Cerebrospinal angiostrongyliasis in five captive tamarins (Sanguinus spp).

Four cotton-top tamarins (Sanguinus oedipus oedipus) and one emperor tamarin (S imperator subgrisescens) housed in a zoo became depressed, anorexic, paraparetic and eventually paralysed. The animals died within 5 days to 18 months of the appearance of clinical signs. Histological examination showed nonsuppurative and eosinophilic meningoencephalitis, and metastrongyle nematode larvae were found within subarachnoid spaces of all animals and within the spinal cord of one. Intact larvae with features consistent with Angiostrongylus cantonensis were recovered from the brain of one animal. This parasite is the classical cause of eosinophilic meningoencephalitis in many parts of the world and the diagnosis can be strongly suspected on clinical grounds. In endemic areas like south-east Queensland, protection of captive animals against infection with A cantonensis is a difficult balance between providing a stimulating, natural setting and eliminating potentially infectious definitive, intermediate and paratenic hosts. This is the first report of cerebrospinal angiostrongyliasis in tamarins and nonhuman primates in Australia.

Histological studies of subcutaneous and intraperitoneal implants of trypsin-prepared dermal collagen allografts in the rat.

The possibility of using allograft collagen for the permanent replacement of lost or damaged connective tissues has been examined in the rat. The cellular components of skin, which are known to be of major importance in allograft rejection, were removed by treating skin with a solution of crystalline trypsin at 15 degrees C. Non-collagenous structures were largely removed by 7 days, but the purification process continued up to 28 days without damage to the collagen fibrils. Dermal collagen allografts, which were implanted intraperitoneally or subcutaneously and biopsied 3-83 days after operation, became recellularized and revascularized without being being resorbed. In contrast to skin allografts, there was no evidence of cellular rejection of the collagen grafts, even when recipient animals had been sensitized to allogeneic skin from the same donor. Densensitization of collagen to collagenase, by treating dermal collagen with solutions of glutaraldehyde at concentrations ranging from 0.001-1.0 per cent, was also investigated in vitro and by implantation. The best results, in terms of preservation of the collagen bundle architecture and graft recellularization without persisting inflammation, were achieved with collaged pre-treated with a solution of 0.01% glutaraldehyde.

Incorporation of stored cell-free dermal collagen allografts into skin wounds: a short term study.

Allogeneic dermal collagen has been evaluated as an alternative to skin autografts for the permanent replacement of lost or damaged skin in the rat. All non-collagenous structures were removed from full-thickness back skin by treatment with a solution of crystalline trypsin. Such dermal collagen preparations were grafted into skin wounds, examined up to 8 1/2 weeks after operation, and compared with excised wounds and skin isografts and allografts of the same initial size. The dermal collagen grafts, particularly when dressed with a sheet of dermal collagen, become recellularised, revascularised and re-epidermalised. Unlike the skin allografts, there was no evidence of cellular rejection. Whereas contracture of the excised wounds was delayed, but not suppressed, by applying a conventional dressing, collagen grafts maintained from 60 to 100 per cent of their original size. In contrast, equivalent skin isografts shrank to 50-60 per cent and showed persistent epidermal hyperplasia.