Corynebacterium bovis (Cb) is a bacterium that causes a flaking dermatitis characterized histologically by orthokeratosis, acanthosis, intracorneal bacterial colonies and variable dermal inflammation in immunodeficient mice. Although Cb has been shown to establish dermal colonization in rats, its impact on the skin of immunodeficient rats remains poorly defined. This case series characterizes cutaneous lesions in 22 naïve or experimentally manipulated NIH-Fox1rnu (nude) rats and evaluates the association between Cb infection and dermatitis over a 5-year period. Histologically, all rats had orthokeratosis and dermatitis/folliculitis, 21/22 had acanthosis, 15/22 had bacterial presence and 9/22 had transepidermal/transfollicular keratinocyte apoptosis. Additional variable findings included furunculosis, pustules, dermal oedema and perivascular dermatitis. Inflammatory infiltrates consisted of CD3-positive lymphocytes and Iba1-positive macrophages located predominantly at the dermoepidermal junction. Corynebacterium bovis was isolated from the skin of 15/22 affected rats, and in-situ hybridization confirmed intracorneal/intrafollicular colonies of Cb in 3/11 rats examined. Nude rats also developed cutaneous lesions that corresponded histologically with a lymphocytic dermatitis, the distribution of which was often independent of Cb colonies. This study documents the first spontaneous Cb infection with dermatitis in nude rats. The frequent isolation of Cb from the skin raises the question of whether alterations in the cutaneous microbiome of nude rats may contribute to the immune modulation of dermatitis, warranting further investigation.
The Ryukyu long-furred rat (Diplothrix legata) is an endemic rodent species restricted to the Ryukyu Islands, Japan, and is classified as Endangered on the IUCN Red List. In 2024, a debilitated rat bearing a wound suggestive of a snakebite was found in the wild on Amami Oshima Island and was admitted to a veterinary hospital, where it subsequently died despite supportive care. Histological and ultrastructural examinations revealed coagulative necrosis with a proliferation of yeast-like fungi in the liver and kidneys. Polymerase chain reaction analysis of lesions identified the causative agent as Candida tropicalis, a dimorphic yeast. The injury and the associated high-stress conditions following transfer to a captive environment and corticosteroid administration for the management of a suspected venomous snakebite may have contributed to immunosuppression, predisposing the animal to opportunistic infections with C. tropicalis. To our knowledge, this is the first report of natural C. tropicalis infection in a member of the Muridae family, and invasive candidiasis caused by C. tropicalis is a potentially fatal opportunistic infection in injured wildlife.
Spinal cord injury (SCI) can lead to paralysis and other disorders in domestic animals, compromising welfare due to limited treatment techniques and their side effects. Modulating cell signalling pathways, such as the Wnt, BDNF (brain-derived neurotrophic factor)-TrkB and JAK/STAT pathways, plays a potential role in more rapid recovery of spinal cord trauma with fewer side effects. The Wnt signalling pathway plays a critical role in neuronal regeneration and reduction of neuronal apoptosis. The BDNF-TrkB pathway stimulates recovery of spinal cord trauma by modulating synaptic plasticity and reducing inflammation. The JAK/STAT pathway promotes neurogenesis and modulates inflammation at the site of injury in order to regulate recovery from SCIs. These signalling pathways can be regulated by administration of various agonists or antagonists of the specific signalling pathways. The administration of CHIR99021, Wnt-3a and Wnt-5a plays a crucial role in rapid recovery of injury by activation of the Wnt signalling pathway, and BDNF hydrogel and BDNF mRNA are used clinically as agonists of the BDNF-TrkB pathway in SCIs. Furthermore, administration of tofacitinib may lead to microglial polarization, which improves recovery of SCI in domestic animals by upregulating the JAK/STAT pathway. Improving the infrastructure for animal studies may lead to a deeper understanding of the cell signalling pathways necessary for stem cell therapies in domestic animals.
A captive, 3-year-old, male Brazilian porcupine (Coendouprehensilis) was found dead in its enclosure at a wildlife facility in the USA, with no prior clinical signs reported. At necropsy, the animal was in poor body condition with malocclusion of the maxillary incisors. Numerous tan-to-white, firm nodules, ranging from 0.1 to 1.5 cm in diameter, were present in the lungs, heart, pancreas and right kidney. Histologically, multifocal to coalescing pyogranulomas composed of foamy macrophages, multinucleated giant cells and peripheral lymphoplasmacytic infiltrates surrounded central areas of caseous necrosis containing degenerate neutrophils and colonies of pleomorphic coccobacilli. The bacteria stained gram positive with Brown and Hopps Gram stain. Aerobic bacterial culture of affected lung tissue yielded Corynebacterium pseudotuberculosis, and identification was confirmed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. To the authors' knowledge, this is the first reported case of corynebacteriosis in a Brazilian porcupine, expanding the known host range of this pathogen and highlighting the importance of including C. pseudotuberculosis as a differential diagnosis for multisystemic nodular disease in exotic and wild mammalian species.
Hepatic encephalopathy (HE) is a neurological disorder associated with severe hepatic dysfunction or portosystemic shunting and is increasingly recognized to involve neuroinflammatory mechanisms. This study investigated neuropathological changes and cerebral cytokine immunolabelling in shelter-housed Van cats with naturally occurring HE. Post-mortem examinations were performed on 17 male Van cats that had been housed at the Van Cat House in Van, Turkey. Twelve cats were diagnosed with HE, while five cats without neurological signs served as negative controls. Histological examination of the affected cats revealed Alzheimer type II astrocytes, neuronal degeneration and necrosis, and spongy change. Concurrent hepatic lipidosis of varying severity was identified in all cats with HE. Brain sections were subjected to immunohistochemistry for interleukin (IL)-1(3, IL-6, IL-22, tumour necrosis factor (TNF) and interferon-gamma, and immunolabelling was quantified as the percentage of tissue area positive for 3,3 '-diaminobenzidine. Cats with HE showed significantly greater immunoreactivities for all five cytokines compared with negative controls. Cytokine immunolabelling was predominantly localized to cells morphologically consistent with astrocytes and other glial cells. The marked increase in IL-22, together with IL-1(3, IL-6 and TNF, identifies IL-22 as a potential component of the broader neuroinflammatory response associated with naturally occurring feline HE. Collectively, the concurrent hepatic lipidosis, characteristic neuropathological lesions and increased cerebral cytokine immunolabelling define the principal pathological features of HE in this shelter population. To our knowledge, this is the first study to demonstrate increased cerebral IL-22 immunolabelling in naturally occurring HE.
