Rhodococcus equi is an uncommon cause of systemic pyogranulomatous infections in goats with macroscopic similarities to caseous lymphadenitis caused by Corynebacterium pseudotuberculosis. Caprine cases have previously been reported to be caused by avirulent R. equi strains. Six cases of R. equi infection in goats yielding 8 R. equi isolates were identified from 2000 to 2017. Lesions varied from bronchopneumonia, vertebral and humeral osteomyelitis, and subcutaneous abscesses, to disseminated infection involving the lungs, lymph nodes, and multiple visceral organs. Isolates of R. equi from infected goats were analyzed by polymerase chain reaction for R. equi virulence-associated plasmid ( vap) genes. Seven of 8 isolates carried the VapN plasmid, originally characterized in bovine isolates, while 1 isolate lacked virulence plasmids and was classified as avirulent. The VapN plasmid has not been described in isolates cultured from goats.

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Many previously unrecognized fungi are emerging as potential pathogens. One such group is dematiaceous fungi of the Chaetomiaceae family (phylum Ascomycota, class Sordariomycetes). These fungi are rare causes of opportunistic, neurotropic phaeohyphomycosis in humans but are not known to cause similar infections in animals. The aims of this study were to investigate equine hyphal mycotic encephalitis, characterize key histopathologic features, and classify causative organisms with molecular diagnostic techniques. Seven cases were evaluated by histopathology. Panfungal PCR targeting the ribosomal RNA large subunit coding region and the noncoding internal transcribed spacer-2 region was performed on DNA extracted from formalin-fixed, paraffin-embedded sections of affected brain, and the resulting sequences were queried against published fungal genomes. Affected animals ranged from 8 to 22 years of age and presented with neurologic signs. Macroscopic lesions within affected brains included multifocal hemorrhage, focal swelling of the thalamus with red and yellow discoloration, and focal cerebral malacia. Major histologic findings included multifocal discrete foci of necrosis, neutrophilic to granulomatous inflammation, vasculitis, and intralesional fungal hyphae variably affecting the cerebrum, thalamus, and brainstem. DNA sequences in 4 cases showed > 98% homology with species within the Chaetomiaceae family, including Acrophialophora fusispora, Acrophialophora levis, and Chaetomium strumarium. Histomorphologically, Chaetomiaceae fungi were 7 to 10 μm wide, septate, parallel walled, and nonpigmented, with dichotomous branching in affected horses. This case series is the first report of equine mycotic encephalitis caused by members of the Chaetomiaceae family, previously reported as rare emerging pathogens in humans.

Background Legionella can cause Legionnaires’ disease, a potentially fatal form of pneumonia that occurs as sporadic epidemics. Not all strains display the same propensity to cause disease in humans. Because Legionella pneumophila serogroup 1 is responsible for >85% of infections, the majority of studies have examined this serogroup, but there are 3 commonly used laboratory strains: L pneumophila serogroup 1 Philadelphia (Phil-1)-derived strains JR32 and Lp01 and 130b-derived strain AA100. Methods We evaluated the ability of Phil-1, JR32, Lp01, and AA100 to cause disease in guinea pigs. Results We found that, although Phil-1, JR32, and AA100 cause an acute pneumonia and death by 4 days postinfection (100%), strain Lp01 does not cause mortality (0%). We also noted that Lp01 lacks a mobile element, designated p45, whose presence correlates with virulence. Transfer of p45 into Lp01 results in recovery of the ability of this strain to cause mortality, leads to more pronounced disease, and correlates with increased interferon-γ levels in the lungs and spleens before death. Conclusions These observations suggest a mechanism of Legionnaires’ disease pathogenesis due to the presence of type IVA secretion systems that cause higher mortality due to overinduction of a proinflammatory response in the host.