NEWLY DESCRIBED TOXOPLASMA GONDII STRAIN CAUSES HIGH MORTALITY IN RED NECKED WALLABIES (MACROPUS RUFOGRISEUS) IN A ZOO.

This manuscript describes an outbreak of fatal toxoplasmosis in wallabies. Ten adult red necked wallabies (Macropus rufogriseus) were imported from New Zealand to the Virginia Zoo. Agglutination testing upon admission into quarantine showed all animals to be negative for antibodies to Toxoplasma gondii. Nine of these wallabies died from acute toxoplasmosis within 59-565 (average 224) days after being moved onto exhibit. Clinical signs included lethargy, diarrhea, tachypnea, and ataxia that progressed rapidly; death without premonitory signs occurred in one case. Histopathologic examination revealed interstitial pneumonia, encephalomyelitis, myositis, enteritis, and myocarditis. The diagnosis was confirmed through serologic, histopathologic, and polymerase chain reaction (PCR) testing. Multilocus PCR-RFLP (restriction fragment length polymorphism) genotyping revealed that the first six animals were infected by a previously undiscovered Toxoplasma gondii genotype, designated as ToxoDB PCR-RFLP genotype No. 263. These six cases survived for an average of 118 days on exhibit before succumbing to toxoplasmosis. The other three wallabies were infected with a Toxoplasma gondii strain of ToxoDB PCR-RFLP genotype No. 4, which is a common strain type circulating in wild animals in North America. These three cases survived for an average of 435 days on exhibit before succumbing to toxoplasmosis. The outbreaks of toxoplasmosis in these wallabies are likely from two different sources. Furthermore, the results highlight Toxoplasma gondii PCR-RFLP genotyping in parasite diagnosis and understanding parasite transmission and potential mitigation procedures.

IMAGING DIAGNOSIS-ENDOMETRIAL MINERALIZATION IN A DOG.

A 9-year-old intact female mixed breed dog was presented for mammary gland tumor surgery, and preoperative radiographs showed a tubular soft tissue opacity mass with multifocal mineralization in the caudoventral abdominal cavity. Subsequent ultrasonography demonstrated uterine dilation with echogenic fluid and endometrial acoustic shadowing consistent with mineralization. Resection of mammary gland tumors and ovariohysterectomy were performed. Pyometra was diagnosed on cytologic examination of uterine fluid. Histopathology of the uterine tissue confirmed a diagnosis of cystic endometrial hyperplasia with uterine mineralization.

Type IV pilus glycosylation mediates resistance of Pseudomonas aeruginosa to opsonic activities of the pulmonary surfactant protein A.

Pseudomonas aeruginosa is a major bacterial pathogen commonly associated with chronic lung infections in cystic fibrosis (CF). Previously, we have demonstrated that the type IV pilus (Tfp) of P. aeruginosa mediates resistance to antibacterial effects of pulmonary surfactant protein A (SP-A). Interestingly, P. aeruginosa strains with group I pilins are O-glycosylated through the TfpO glycosyltransferase with a single subunit of O-antigen (O-ag). Importantly, TfpO-mediated O-glycosylation is important for virulence in mouse lungs, exemplified by more frequent lung infection in CF with TfpO-expressing P. aeruginosa strains. However, the mechanism underlying the importance of Tfp glycosylation in P. aeruginosa pathogenesis is not fully understood. Here, we demonstrated one mechanism of increased fitness mediated by O-glycosylation of group 1 pilins on Tfp in the P. aeruginosa clinical isolate 1244. Using an acute pneumonia model in SP-A+/+ versus SP-A-/- mice, the O-glycosylation-deficient ΔtfpO mutant was found to be attenuated in lung infection. Both 1244 and ΔtfpO strains showed equal levels of susceptibility to SP-A-mediated membrane permeability. In contrast, the ΔtfpO mutant was more susceptible to opsonization by SP-A and by other pulmonary and circulating opsonins, SP-D and mannose binding lectin 2, respectively. Importantly, the increased susceptibility to phagocytosis was abrogated in the absence of opsonins. These results indicate that O-glycosylation of Tfp with O-ag specifically confers resistance to opsonization during host-mediated phagocytosis.

Subcutaneous hemangiosarcoma induced by a foreign body (steel staple) in a cat.

An 8-year-old, female domestic shorthair cat was presented with a ventral abdominal subcutaneous mass. A radiograph showed that the center of the mass contained what appeared to be steel sutures, presumed to be from an ovariohysterectomy performed 7 years earlier. The excised mass was irregular and contained numerous pockets filled with friable necrotic material and hemorrhages that were dissected by fibrous connective tissue bands. Multiple tangled and fragmented pieces of steel staples were deeply embedded within the mass. Histologically, the mass was non-encapsulated, densely cellular, and infiltrative. Neoplastic cells lined caverns and channels and were factor VIII-positive by immunohistochemistry. The neoplastic cells were oval to round with granular cytoplasm and vesicular nucleus and exhibited moderate cellular and nuclear pleomorphism. A diagnosis of subcutaneous hemangiosarcoma was made. To our knowledge, this is the first report of foreign body associated hemangiosarcoma and the first case of steel staple associated neoplasm in domestic animals.

Hémangiosarcome sous-cutané induit par un corps étranger (agrafe d'acier) chez un chat. Une chatte commune domestique âgée de 8 ans a été présentée avec une masse sous-cutanée ventrale abdominale. Une radiographie a montré que le centre de la masse contenait ce qui semblait être une suture d'acier, que l'on présumait provenir d'une ovariohystérectomie réalisée 7 ans auparavant. La masse excisée était irrégulière et contenait plusieurs poches remplies de matériel nécrosé friable et d'hémorragies qui étaient disséquées par des bandes de tissu conjonctif fibreux. Plusieurs pièces d'agrafes d'acier emmêlées et fragmentées étaient profondément enfoncées dans la masse. Histologiquement, la masse était non encapsulée, densément cellulaire et infiltrante. Des cellules néoplastiques couvraient les aréoles et les canaux et étaient positives pour le facteur VIII par immunohistochimie. Les cellules néoplasiques étaient ovales ou rondes avec un cytoplasme granulaire et un noyau vésiculaire et présentaient un pléomorphisme cellulaire et nucléaire modéré. Un diagnostic d'hémangiosarcome sous-cutané a été posé. À notre connaissance, il s'agit du premier rapport d'un hémangiosarcome associé à un corps étranger et du premier cas d'un néoplasme associé à une agrafe chez les animaux domestiques.Traduit par Isabelle Vallières.

Feasibility of Single-Stage Posterior Passive Correction and Fusion Surgery for Congenital Scoliosis in Adolescent Patients Who Have Attained Skeletal Maturity.

STUDY DESIGN: Retrospective study. PURPOSE: To report the perioperative and radiological outcomes of single-stage posterior passive correction and fusion (SSPPCF) in adolescent patients who present with congenital scoliosis. OVERVIEW OF LITERATURE: The surgical treatment for congenital scoliosis is complex. There is no definitive guide on surgical options for skeletally matured adolescent patients who have congenital scoliosis. METHODS: Patients with congenital scoliosis who underwent SSPPCF using a pedicle screw system were reviewed. We identified the following three surgical indications: (1) hemivertebra or wedge vertebra over the thoracic or thoracolumbar region with structural lumbar curves, (2) hemivertebra or wedge vertebra at the lumbar region with significant pelvic obliquity or sacral slanting, and (3) mixed or complex congenital scoliosis. The demographic, perioperative, and radiographic data of these patients were collected. RESULTS: Thirty-four patients were reviewed. The mean patient age was 14.6±3.4 years. There were 13 hemivertebrae, three wedged vertebrae, two butterfly vertebrae, three hemivertebrae with butterfly vertebra, eight unsegmented bars, and five multiple complex lesions. The average surgical duration was 219.4±68.8 minutes. The average blood loss was 1,208.4±763.5 mL. Seven patients required allogeneic blood transfusion. The mean hospital stay duration was 6.1±2.5 days. The complication rate was 11.8% (4/34): one patient had severe blood loss, one had rod breakage, and two had distal adding-on. The Cobb angle reduced from 65.9°±17.4° to 36.3°±15.3° (p<0.001) with a correction rate (CR) of 44.8%±17.4%. The regional kyphotic angle decreased from 39.9°±20.5° to 27.5°±13.9° (p=0.001) with a CR of 19.3%±49.6%. Radiographic parameters (radiographic shoulder height, clavicle angle, T1 tilt, cervical axis, pelvic obliquity, coronal balance, and apical vertebral translation) showed significant improvement postoperatively. CONCLUSIONS: SSPPCF was a feasible option for adolescent patients with congenital scoliosis who were skeletally matured.

Type IV pilus of Pseudomonas aeruginosa confers resistance to antimicrobial activities of the pulmonary surfactant protein-A.

Pseudomonas aeruginosa(PA) is a Gram-negative bacterial pathogen commonly associated with chronic lung infections. Previously, we have identified several PA virulence factors that are important for resistance to the surfactant protein-A (SP-A), a pulmonary innate immunity protein that mediates bacterial opsonization and membrane permeabilization. In this study, we demonstrate that the type IV pilus (Tfp) is important in the resistance of PA to the antibacterial effects of SP-A. The Tfp-deficient mutant ΔpilA is severely attenuated in an acute pneumonia model of infection in the lungs of wild-type mice, but is virulent in the lungs of SP-A(-/-) mice. The ΔpilA bacteria are more susceptible to SP-A-mediated aggregation and opsonization. In addition, the integrity of the outer membranes of ΔpilA bacteria is compromised, rendering them more susceptible to SP-A-mediated membrane permeabilization. By comparing Tfp extension and retraction mutants, we demonstrate that the increased susceptibility of ΔpilA to SP-A-mediated opsonization requires the total absence of Tfp from PA cells. Finally, we provide evidence of increased expression of nonpilus adhesin OprH that may serve as an SP-A ligand, resulting in increased phagocytosis and preferential pulmonary clearance of ΔpilA.

Dietary selenium as a modulator of PCB 126-induced hepatotoxicity in male Sprague-Dawley rats.

Homeostasis of selenium (Se), a critical antioxidant incorporated into amino acids and enzymes, is disrupted by exposure to aryl hydrocarbon receptor (AhR) agonists. Here we examined the importance of dietary Se in preventing the toxicity of the most toxic polychlorinated biphenyl congener, 3,3',4,4',5-pentachlorobiphenyl (PCB 126), a potent AhR agonist. Male Sprague-Dawley rats were fed a modified AIN-93 diet with differing dietary Se levels (0.02, 0.2, and 2 ppm). Following 3 weeks of acclimatization, rats from each dietary group were given a single ip injection of corn oil (vehicle), 0.2, 1, or 5 µmol/kg body weight PCB 126, followed 2 weeks later by euthanasia. PCB exposure caused dose-dependent increases in liver weight and at the highest PCB 126 dose decreases in whole body weight gains. Hepatic cytochrome P-450 (CYP1A1) activity was significantly increased even at the lowest dose of PCB 126, indicating potent AhR activation. PCB exposure diminished hepatic Se levels in a dose-dependent manner, and this was accompanied by diminished Se-dependent glutathione peroxidase activity. Both these effects were partially mitigated by Se supplementation. Conversely, thioredoxin (Trx) reductase activity and Trx oxidation state, although significantly diminished in the lowest dietary Se groups, were not affected by PCB exposure. In addition, PCB 126-induced changes in hepatic copper, iron, manganese, and zinc were observed. These results demonstrate that supplemental dietary Se was not able to completely prevent the toxicity caused by PCB 126 but was able to increase moderately the levels of several key antioxidants, thereby maintaining them roughly at normal levels.