Molecular and immunohistochemical distinction of equine sarcoid from schwannoma.

Ten equine skin tumors that had been classified as schwannomas on routine histological examination were analyzed by polymerase chain reaction for bovine papillomavirus DNA. All 10 were positive for bovine papillomavirus 1 or 2, and all 10 were immunohistochemically negative for S-100 protein and strongly positive for vimentin. Nine tumors were moderately positive for laminin and 8, for smooth muscle actin. Five tumors were variably and weakly positive for type IV collagen. The lack of S-100 protein expression made Schwann cells an unlikely cell of origin, as opposed to peripheral nerve sheath tumors, which typically express S-100 protein, at least in some neoplastic cells. The immunohistochemical reactivity is consistent with myofibroblastic origin of the neoplastic cells, although smooth muscle cell or pericyte origin cannot be ruled out. These tumors represent an atypical form of equine sarcoid. Polymerase chain reaction for bovine papillomavirus and S-100 immunohistochemistry are strongly recommended for all equine skin tumors with histological characteristics typical of schwannoma or peripheral nerve sheath tumor.

Pathogenic interactions between Chlamydophila psittaci and avian pneumovirus infections in turkeys.

Both Chlamydophila psittaci and avian pneumovirus (APV) are highly prevalent in Belgian turkeys and might contribute to the respiratory disease complex observed in turkeys. Initial outbreaks of chlamydiosis occur mostly at the age of 4-8 weeks, often accompanied by an APV infection in APV non-vaccinated farms. Regardless APV vaccination, breakthroughs of APV infection from 8 weeks on do occur, a period when also a second C. psittaci infection appears. Therefore, this study examined the pathogenicity of an APV superinfection in C. psittaci predisposed turkeys. Turkeys were infected with C. psittaci, APV or with C. psittaci followed by APV. Simulating the impact of an APV infection during the acute phase or latent phase of a C. psittaci infection, turkeys have been infected with APV at 1 and 5 weeks post C. psittaci infection, respectively. APV infection during the acute phase of a C. psittaci infection aggravates the severity of clinical signs, macroscopic lesions, pharyngeal APV excretion and histological tracheae lesions. In contrast, no clear interaction could be established after APV infection in latently C. psittaci infected specific pathogen-free (SPF) turkeys. This study clearly demonstrates the exacerbating role of APV during acute C. psittaci infection, which can play an important role in the respiratory disease complex of turkeys.