In 1996, a disease outbreak occurred at a captive breeding facility in Idaho, causing anorexia, dehydration, and diarrhea or sudden death in 72 of 110 Northern aplomado falcons (Falco femoralis septentrionalis) from 9 to 35 days of age and in 6 of 102 peregrine falcons (Falco peregrinus) from 14 to 25 days of age. Sixty-two Northern aplomado and six peregrine falcons died. Epidemiologic analyses indicated a point source epizootic, horizontal transmission, and increased relative risk associated with cross-species brooding of eggs. Primary lesions in affected birds were inclusion body hepatitis, splenomegaly, and enteritis. The etiology in all mortalities was determined by molecular analyses to be a new species of adenovirus distantly related to the group I avian viruses, serotypes 1 and 4, Aviadenovirus. In situ hybridization and PCR demonstrated that the virus was epitheliotropic and lymphotropic and that infection was systemic in the majority of animals. Adenoassociated virus was also detected by PCR in most affected falcons, but no other infectious agents or predisposing factors were found in any birds. Subsequent to the 1996 epizootic, a similar disease caused by the same adenovirus was found over a 5-year period in orange-breasted falcons (Falco deiroleucus), teita falcons (Falco fasciinucha), a merlin (Falco columbarius), a Vanuatu peregrine falcon (Falco peregrinus nesiotes), and gyrfalcon ؋ peregrine falcon hybrids (Falco rusticolus/peregrinus) that died in Wyoming, Oklahoma, Minnesota, and California. These findings indicate that this newly recognized adenovirus is widespread in western and midwestern North America and can be a primary pathogen in different falcon species.

Globoid cell leukodystrophy is a lysosomal storage disease characterized by the loss of galactocerebrosidase. Galactocerebrosidase loss leads to the accumulation of psychosine and subsequent oligodendrocyte cell death, demyelination, macrophage recruitment, and astroglial activation and proliferation. To date, no studies have elucidated the mechanism of glial cell activation and cytokine and chemokine up-regulation and release. We explored a novel explanation for the development of the pathological changes in the early stages of globoid cell leukodystrophy associated with toll-like receptor (TLR) 2 up-regulation in the hindbrain and cerebellum as a response to dying oligodendrocytes. TLR2 up-regulation on microglia/macrophages coincided with morphological changes consistent with activation at 2 and 3 weeks of age. TLR2 up-regulation on activated microglia/macrophages resulted in astrocyte activation and marked up-regulation of cytokines/chemokines. Because oligodendrocyte cell death is an important feature of globoid cell leukodystrophy, we tested the ability of TLR2 reporter cells to respond to oligodendrocyte cell death. These reporter cells responded in vitro to medium conditioned by psychosine-treated oligodendrocytes, indicating the likelihood that oligodendrocytes release a TLR2 ligand during apoptosis. TLRs are a member of the innate immune system and initiate immune and inflammatory events; therefore, the identification of TLR2 as a potential driver in the activation of central nervous system glial activity in globoid cell leukodystrophy may provide important insight into its pathogenesis.

A number of polymerase chain reaction (PCR)-based diagnostic tests have been developed for Mycoplasma hyopneumoniae, including one from this research group. This report presents further development, optimization, and standardization of a nested PCR test. Detection sensitivity was 1 fg of M. hyopneumoniae chromosomal DNA (approximately 1 organism). This exceeded the sensitivity of or compared favorably with other published PCR tests. Polymerase chain reaction primers to porcine 2-microglobulin were included as internal controls for amplifiable chromosomal DNA from porcine samples. To standardize the test, a number of samples from experimentally infected pigs, including nasal, tonsil, tracheobronchial swabs, lung tissue, bronchial alveolar lavage (BAL) fluid, and tracheobronchial brush samples, were examined by PCR. Samples obtained from BAL fluid and tracheobronchial sites were most predictive of infection, whereas nasal swabs and lung tissue were not reliable indicators of experimentally induced infection. In conclusion, the nested PCR developed for this study was found to be a highly sensitive and specific diagnostic tool for M. hyopneumoniae, but the enhanced sensitivity may be unnecessary if the proper sites are sampled. Porcine enzootic pneumonia caused by Mycoplasma hyopneumoniae continues to produce significant economic losses to swine producers. Mycoplasma hyop-neumoniae has recently gained new importance as an integral component of the porcine respiratory disease complex (PRDC). 24 Recent studies indicate that the incidence and severity of enzootic pneumonia have increased with the emergence of porcine reproductive and respiratory syndrome virus and the reemergence of swine influenza virus. Bacterial pathogens such as Pasteurella multocida also contribute to respiratory disease outbreaks. 17 Because of economic consideration , there is increased interest in the swine industry to improve diagnostic methods to gain a better understanding of PRDC in general and to provide farm-specific information for implementing effective prevention or control programs (or both) for M. hyopneu-moniae. Reliable diagnostic tests for M. hyopneumoniae are essential for developing cost-effective prevention and control programs. Visual analysis of lungs at the time of slaughter is commonly used to monitor the disease status of a herd. But it is not predictive of lifetime pneumonia. 21 The gold standard for detection of M. hyopneumoniae has been culture of the organism. But culture methods are rarely used because of several reasons: 1) prolonged time before a definitive diagnosis is obtained, 2) overgrowth with normal flora bacteria and non-M. hyopneumoniae mycoplasmas, and 3) lack of experience and capabilities to perform culture diagnosis of swine tissue samples because of the fastidious nature of M. hyopneumoniae. 18 Detection of serum antibodies is the most common diagnostic tool used to monitor M. hyopneumoniae infection. Both fluorescent antibody and enzyme-linked immunosor-bent assay (ELISA) are commonly used assays. 2,9,...

A 17-year-old, Thoroughbred mare was presented for necropsy with a large, invasive oral mass determined via immunohistochemistry to be a soft tissue sarcoma of neural origin. Oral sarcomas are rare in veterinary medicine, and to the authors' knowledge, this is the first oral sarcoma of neural tissue origin reported in a horse.

A n 8-year-old, 2.8 kg, female spayed domestic shorthair cat was admitted to the Small Animal Clinic of the Louisiana State University Veterinary Teaching Hospital (LSU VTH) with a 5-day history of anorexia, lethargy, and dyspnea.Recent medical history included a vaginoplasty performed at LSU VTH 3 weeks earlier, to resect vulvar adhesions causing urinary tract outflow obstruction, stranguria, and chronic cystitis. At that time, physical examination of the cardiovascular system and results of routine CBC and serum biochemical profile were unremarkable. An abdominal ultrasound examination was performed, revealing urinary bladder and urethral dilatation, and a small round structure with anechoic content in the perivulvar region. At surgery, this tissue was resected. It resembled a fibrous band of connective tissue and was not submitted for histopathologic evaluation. The cat was current on vaccinations, and was negative for feline leukemia virus antigen and feline immunodeficiency virus antibodies.Upon presentation to the Small Animal Clinic, the cat was laterally recumbent, in respiratory distress (80 breaths per minute), hypothermic (961F), had a heart rate of 190 beats per minute and arterial femoral pulses were judged to be weak. Diffuse pulmonary crackles were heard bilaterally on thoracic auscultation. Thoracic radiographs (lateral and dorsoventral views) indicated severe, generalized cardiomegaly, enlarged pulmonary veins, and an interstitial to alveolar pattern in the caudodorsal lung fields. These findings were interpreted as indicating congestive heart failure with pulmonary edema. A complete blood count indicated mild, normocytic, normochromic, nonregenerative anemia (PCV 28%; reference range, 30-48%; hemoglobin, 9.7 g/dL; reference range, 12-15.5 g/dL). Serum biochemical abnormalities included hypoproteinemia (4.9 g/dL; reference range, 6.5-8.7 g/dL), increased aspartate aminotransferase activity (100 U/L; reference range, 0-60 U/L), mildly increased urea nitrogen concentration (58 mg/dL; reference range, 18-30 mg/dL), and hyperphosphatemia (7.5 mg/dL; reference range, 4-6.6 mg/dL). Plasma thyroxine concentration was reported to be normal in the cat's recent medical records and the test was not repeated. Average systolic blood pressure recorded by the Doppler method during the initial visit at LSU VTH was 135 mmHg before anesthesia. The cat was treated with furosemide a (3 mg/kg IV), and placed in a 40% humidified oxygen cage on a warming blanket.After initial stabilization and mild improvement of the respiratory signs, a transthoracic echocardiogram was obtained to evaluate the possible underlying cardiac disease. The 2-dimensional echocardiographic findings included a moderate amount of pericardial effusion and diastolic collapse of the right atrium, indicating cardiac tamponade. The left atrium was considered mildly enlarged (LA/Ao 5 1.7; normal o1.5). The left ventricular free wall was markedly thickened (9.5 mm in diastole in a right parasternal short-axis view; normal o6 mm). Left ventricular pap...

Tarsal tunnel syndrome is defined as a compressive neuropathy of the posterior tibial nerve in the tarsal canal. A neurilemoma is an uncommon, benign, encapsulated neoplasm derived from Schwann cells. We present a case of tarsal tunnel syndrome caused by this rare space-occupying lesion.

Chlamydia pneumoniae is a ubiquitous pathogen causing disease in humans, mammals, birds, reptiles, and amphibians. Since 2012, C. pneumoniae infection has caused neurologic disease and mortality in a breeding colony of endangered Houston toads ( Anaxyrus houstonensis) at the Houston Zoo. The purpose of this report is to present the histopathologic and ultrastructural characteristics of C. pneumoniae infection in Houston toads. Fourteen cases were evaluated by histopathology and 1 case was evaluated by electron microscopy. The major histopathologic finding was necrotizing and histiocytic polioencephalomyelitis and ganglionitis. Bacteria formed intracytoplasmic inclusions within neurons but frequently extended into the surrounding tissue from necrotic cells. Ultrastructural evaluation showed the bacteria formed reticulate and elementary bodies characteristic of Chlamydia spp.

Abstract. Falcon adenovirus is a newly recognized member of the family Aviadenoviridae and includes 2 closely related strains that are pathogenic to several species of falcons. Peregrine falcons appear to be one of the primary reservoirs, but recent outbreaks suggest that other carrier species probably exist. To allow screening of captive birds for virus shedding and investigations of disease outbreaks, conventional and realtime, quantitative polymerase chain reaction (PCR) assays and an in situ hybridization technique were developed. The diagnostic protocols were used on tissue and fecal samples from 7 species or subspecies of falcons infected with adenovirus as well as adenoviruses from other birds and mammals. The assays were specific for falcon adenovirus and detected both strains of virus in fecal samples from living animals or frozen and formalin-fixed, paraffinized tissues. Together with established serologic tests for falcon adenovirus, these molecular assays are valuable tools for management and conservation of falcons in captivity and the wild.