Intralesional application of ribavirin in two American flamingos (Phoenicopterus ruber) with poxvirus infection.

We report the successful treatment of poxvirus lesions in two juvenile American flamingos (Phoenicopterus ruber) with experimental low-dose intralesional ribavirin injection. In the first flamingo, the size and location of a beak verrucosity interfered with feeding, and after multiple surgical interventions, an experimental therapy of low-dose intralesional ribavirin was implemented with close blood parameter monitoring to minimize any potential side effects due to systemic antiviral administration. The second flamingo had a poxvirus lesion on the tibiotarsus, which recurred after unsuccessful conservative medical treatment and surgical intervention and a course of intralesional ribavirin therapy was implemented. Regression of the lesions in both flamingos commenced within 3 days of ribavirin treatment resulting in complete resolution within 6 weeks of onset of ribavirin treatment.

PERINATAL CENTRILOBULAR HEPATIC NECROSIS IN GIANT PANDAS (AILUROPODA MELANOLEUCA): A RETROSPECTIVE STUDY.

Between 1983 and 2012, six giant panda cubs (Ailuropoda melanoleuca) born at a zoological institution were stillborn or died between the ages of 3 and 200 h. Two of the six cubs had panhepatic centrilobular hepatic necrosis (CHN), granulocytic extramedullary hematopoiesis (GEM), positive liver culture for Staphylococcus species, and terminal liver failure. Another low-weight cub was administered oxygen therapy immediately after birth and developed hyaline membranes in air spaces and hepatic necrosis restricted to the hilar region. A retrospective analysis of liver and lung lesions, pulmonary microanatomy, blood-gas barrier ultrastructure, and hepatic myofibroblast proliferation was conducted on the six cubs. Neonates with CHN had concurrent severe periportal GEM accompanied by severe myofibroblast proliferation. The pulmonary blood-gas barrier was markedly increased in one cub with CHN. Developmentally, the lungs of all but one cub were at the late saccular stage, and the lowest-weight cub was in early saccular stage, consistent with immaturity, and had pneumonia comparable to neonatal respiratory distress syndrome (RDS). Stage of lung development was eliminated as the primary factor leading to CHN. The pathogenesis of CHN in these neonates is proposed to be transformation of hepatic stellate cells to myofibroblasts initiating blockage and microvascular constriction of hepatic sinusoids, resulting in insufficient perfusion and cellular hypoxia of hepatocytes surrounding central veins in acinar zone 3.

White-nose syndrome: A novel dermatomycosis of biologic interest and epidemiologic consequence.

Over the past 10 years, the environmental and veterinary communities have sounded alarms over an insidious keratinophilous fungus, Pseudogymnoascus destructans, that has decimated populations of bats (yes, bats, chiropterans) throughout North America and, most recently, Northern China and Siberia. We as dermatologists may find this invasive keratinophilous fungus of particular interest, as its method of destruction is disruption of the homeostatic mechanism of the bat wing integument. Although it is unlikely that this pathogen will become an infectious threat to humans, its environmental impact will likely affect us all, especially as recent data have shown upregulation of naturally occurring coronaviruses in coinfected bats. Dermatologists are familiar with keratinophilous dermatophyte infections, but these rarely cause serious morbidity in individual patients and never cause crisis on a population basis. This contribution describes the effects of P destructans on both the individual and the population basis. Bringing the white-nose syndrome to the attention of human dermatologists and skin scientists may invite transfer of expertise in understanding the disease, its pathophysiology, epidemiology, treatment, and prevention.

SPINAL NEMATODIASIS IN A LINED FLAT-TAIL GECKO (UROPLATUS LINEATUS).

A 5-y-old female lined flat-tail gecko (Uroplatus lineatus) presented for acute onset of lethargy and paraplegia and was subsequently euthanized. Histologic examination of the spinal cord revealed a verminous myelitis comprising moderate, multifocal, necrotizing myelitis with intramedullary adult and larval nematodes. Molecular data and morphology indicate a cosmocercid nematode, most likely of the genus Raillietnema, a diverse taxon reported to parasitize reptiles, amphibians, and teleost fish. To the authors' knowledge this is the first report of spinal nematodiasis in a reptile species, and the first report of spinal parasitism causing hind-limb paraplegia in a reptile.

Management of Ocular Human herpesvirus 1 Infection in a White-faced Saki Monkey (Pithecia pithecia).

A 20-y-old male intact white-faced saki monkey (Pithecia pithecia) presented with an acute ocular disease of the right eye. Clinical signs included periocular swelling, conjunctivitis, and anisocoria with a miotic right pupil. Conjunctival swabs were positive for Human herpesvirus 1 (HHV1) according to PCR amplification with sequencing. Initial clinical signs resolved with supportive treatment, and the animal was managed chronically by using acyclovir (5 mg/kg PO twice daily) during flare-ups. After more than 2 y, the progression of clinical disease led to enucleation of the right eye. At 2 mo after surgery, acute presentation of severe neurologic signs, including ataxia and blindness, resulted in euthanasia. Histopathology, PCR analysis, and sequencing results were consistent with viral encephalitis due to HHV1; coinfection with Pithecia pithecia lymphocryptovirus 1 was identified. This report describes the first case of managed HHV1 infection in a platyrrhine primate and the first case of HHV1 in a white-faced saki monkey that was not rapidly fatal.

Intermittent claudication-like syndrome secondary to atherosclerosis in a yellow-naped Amazon parrot (Amazona ochrocephala auropalliata).

A 25-year-old yellow-naped Amazon parrot (Amazona ochrocephala auropalliata) was presented for nasal discharge and sneezing. Physical examination revealed poor feather quality, a mild serous nasal discharge, and a mass on the dorsal surface of the oral cavity. Cytologic examination of a mass aspirate as well as results of a choanal culture revealed squamous metaplasia of the salivary glands and bacterial rhinitis, respectively. Following resolution of the presenting conditions, the patient was presented for hind limb weakness and ataxia. The clinical signs were transient and generally resolved with rest but could be reproduced after stressful episodes, such as restraint for procedures or treatment. Test results from a complete blood count, biochemistry profile, whole-body radiographs, needle electromyography of the leg muscles, and an edrophonium challenge test were within reference limits. Based on the clinical signs and results of the diagnostic workup, the presumptive diagnosis was intermittent claudication, a condition caused by peripheral vascular disease and defined as intermittent weakness and pain in the legs induced by exercise and relieved by rest. Shortly after initiation of treatment with isoxsuprine, the bird died. Postmortem examination and histopathology revealed severe atherosclerotic lesions throughout the vascular system with stenotic lesions present in the abdominal aorta and femoral arteries. Electron microscopic examination of the great arteries was also performed and helped to further characterize the nature of the lesions. This case is the first report, to our knowledge, of an intermittent claudication-like syndrome associated with peripheral atherosclerosis in a psittacine bird. In addition, the distribution and some of the macroscopic and histopathologic features of the lesions differ from previous descriptions of atherosclerosis in psittacine birds.