RESUMEN
Pan paniscus Papillomavirus 1 (PpPV1) causes focal epithelial hyperplasia (FEH) in infected animals. Here, we analyzed the present disease manifestation and PpPV1 genomic sequence of an animal that was afflicted by an FEH epizootic outbreak in 1987 for which the sequence of the responsible PpPV1 was determined. The animal displayed FEH more than 30 years after the initial diagnosis, indicating persistence or recurrence of the disease, and evidence for active PpPV1 infection was obtained. Moreover, the sequences of the viral genomes present in the late 1980s and in 2018 differed at 23 nucleotide positions, resulting in 11 amino acid exchanges within coding regions. These findings suggest that PpPV1-induced FEH might not undergo complete and/or permanent remission in a subset of afflicted animals.
RESUMEN
BACKGROUND: This case report describes a focal brain lesion in an alpaca (Vicugna pacos). Although this is a restricted study based on a single animal, neuropathological features are reported that are most likely attributed to a vascular event with either ischemic or hemorrhagic pathology. Concerning translational issues, these findings extend neurovascular unit concept to the alpacas' brain and qualify a larger panel of stroke tissue markers for further exploration of ischemic or hemorrhagic consequences beyond the usually used small animal models in stroke research. CASE PRESENTATION: A brain lesion indicative of a stroke was diagnosed in a 3-year-old female alpaca as an incidental finding during a post mortem examination. The rostral portion of the right frontal lobe contained a 1.0 × 1.5 × 1.7 cm lesion that extended immediately to the overlying leptomeninges. Microscopically, it was composed of liquefactive necrosis with cholesterol crystal deposition and associated granulomatous inflammation as well as vascularized fibrous connective tissue rimmed by proliferated astrocytes. Multiple fluorescence labeling of the affected brain regions revealed strong microgliosis as shown by immunostaining of the ionized calcium binding adapter molecule 1 and astrogliosis as demonstrated by enhanced immunoreactivity for glial fibrillary acidic protein. In parallel, a drastic neuronal loss was detected by considerably diminished immunolabeling of neuronal nuclei. Concomitantly, up-regulated immunoreactivities for collagen IV and neurofilament light chains were found in the affected tissues, indicating vascular and cytoskeletal reactions. CONCLUSIONS: Driven by these neuropathological features, the incidental brain lesion found in this alpaca strongly suggests an ischemic or hemorrhagic etiology. However, since typical hallmarks became verifiable as previously described for other species affected by focal cerebral ischemia, the lesion is more likely related to an ischemic event. Nevertheless, as such cellular alterations might be difficult to distinguish from other brain lesions as for instance caused by inflammatory processes, adjuvant observations and species-related features need to be considered for etiological interpretations. Indeed, the lack of neurological deficits is likely attributed to the location of the lesion within the rostral aspect of the right frontal lobe of the alpacas' brain. Further, fibroblast migration from the meninges likely caused the intralesional scar formation.
