Disseminated aspergillosis in dogs has been associated with Aspergillus terreus or A. deflectus infection. We report a case of disseminated A. versicolor infection presenting as diskospondylitis, osteomyelitis, and pyelonephritis. The diagnosis was made based on clinical, radiographic, and pathological findings. The etiologic agent was identified by fungal culture and internal transcribed spacer (ITS) ribosomal DNA (rDNA) sequencing. This is the first description of canine aspergillosis caused by A. versicolor. CASE REPORTA 31-kg, 2.5-year-old male castrated German shepherd dog was examined at the Texas A&M University Veterinary Medicine Teaching Hospital because of nonambulatory paraparesis, weight loss, and hyporexia for 3 months. At admission, the dog had a body temperature of 104.6°F, heart rate of 160 beats/min, respiratory rate of 80 breaths/min, and blood pressure of 173/99 mm Hg. Neurological examination revealed a hyperreflexive patellar reflex bilaterally. Motor function was absent in the right pelvic limb and questionable in the left. The patient had marked generalized muscle atrophy. A lateral radiograph of the cranial thorax revealed lysis and shortening of the first four sternebrae (Fig. 1A). The second and third sternebrae were most severely affected and had irregular margins with loss of their end plates. Lateral radiographs of the thoracic vertebral column showed lysis and shortening of the 9th (T9) and 10th (T10) thoracic vertebrae with loss of the end plates and spondylosis deformans ventrally (Fig. 1B). Narrowing of the intervertebral space, end plate sclerosis, and ventral spondylosis derformans were also found between the seventh and eighth thoracic vertebrae. The clinical diagnoses were diskospondylitis involving T9-T10, osteomyelitis of the sternum and left humerus, and T3-L3 myelopathy resulting in nonambulatory paraparesis. Suspected causes included disseminated aspergillosis, blastomycosis, coccidioidomycosis, bacterial infection, and neoplasia. Due to the poor prognosis, the dog was subsequently euthanized and a complete necropsy was performed.The major skeletal changes found at postmortem examination included marked bony proliferation of the cranial end of the sternum, extending from the first to the fourth sternebrae, with loss of the joint space between the second and third sternebrae ( Fig. 2A). A soft gray area of necrotizing osteomyelitis was in the center of the collapsed and fused sternebrae. In the thoracic vertebral column, there was loss of the intervertebral disk at T9-T10 with lysis of the associated vertebral end plates (Fig. 2B). The latter changes resulted in joint instability, overriding of the vertebral bodies, and spinal cord compression that was exacerbated with ventroflexion of the vertebral column. In the kidneys, there was dark red to purple mottling of the cortical region with dozens of white to tan areas throughout the cortex and medulla (Fig. 2C). The renal crests were ulcerated, and the pelvises were dilated and contained a small amount of cloudy fluid with ...

Mucoid bacteria, predominately Pseudomonas aeruginosa, are commonly associated with decline in pulmonary function in children with cystic fibrosis (CF), and are thought to persist at least in part due to a greater propensity toward forming biofilms. We isolated a higher frequency of mucoid Streptococcus pneumoniae (Sp) expressing high levels of capsular polysaccharides from sputa from children with CF, compared to those without CF. We compared biofilm formation and maturation by mucoid and non-mucoid isolates of Sp collected from children with and without CF. Non-mucoid Sp serotype 19A and 19F isolates had significantly higher levels of biofilm initiation and adherence to CF epithelial cells than did serotype 3 isolates. However, strains expressing high levels of capsule had significantly greater biofilm maturation, as evidenced by increased density and thickness in static and continuous flow assays via confocal microscopy. Finally, using a serotype 3 Sp strain, we showed that highly encapsulated mucoid phase variants predominate during late adherence and better colonize CFTR–/– as compared to wild-type mice in respiratory infection studies. These findings indicate that overexpression of capsule can enhance the development of mature pneumococcal biofilms in vitro, and may contribute to pneumococcal colonization in CF lung disease.

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Recent studies have reported the isolation of highly mucoid serotype 3 Streptococcus pneumoniae (Sp) from the respiratory tracts of children with cystic fibrosis (CF). Whether these highly mucoid Sp contribute to, or are associated with, respiratory failure among patients with CF remains unknown. Other mucoid bacteria, predominately Pseudomonas aeruginosa, are associated with CF respiratory decline. We used a mouse model of CF to study pneumococcal pneumonia with highly mucoid serotype 3 and non-mucoid serotype 19A Sp isolates. We investigated susceptibility to infection, survival, and bacterial counts from bronchoaviolar lavage samples and lung homogenates, as well as associated inflammatory cytokines at the site of infection, and lung pathology. Congenic CFTR–/– mice and wild-type (WT)-mice were infected intranasally with CHB756, CHB1126, and WU2 (highly mucoid capsular serotype 3, intermediately mucoid serotype 3, and less mucoid serotype 3, respectively), or CHB1058 (non-mucoid serotype 19A). BAL, lung homogenates, and blood were collected from mice 5 days post-infection. Higher CFU recovery and shorter survival were observed following infection of CFTR–/– mice with CHB756 compared to infection with CHB1126, WU2, or CHB1058 (P≤0.001). Additionally, CFTR–/– mice infected with CHB756 and CHB1126 were more susceptible to infection than WT-mice (P≤0.05). Between CFTR–/– mice and WT-mice, no significant differences in TNF-α, CXCL1/KC concentrations, or lung histopathology were observed. Our results indicate that highly mucoid type 3 Sp causes more severe lung disease than non-mucoid Sp, and does so more readily in the lungs of CFTR–/– than WT-mice.

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