ABSTRACT: We report a case of a free-ranging five-month wildcat with bilateral hind limbs paralysis since birth due to a segmental lumbar spinal cord aplasia. The species confirmation of the southern tiger cat (Leopardus guttulus) was determined by genetic sequencing. This southern tiger cat native to Brazil had autophagy in both pelvic limbs during the initial phase of hospitalization, followed by a right tibial fracture with bone exposition. Euthanasia was chosen due to animal welfare and submitted for postmortem examination. Grossly, there was an 8.5cm in-length segmental interruption of the spinal cord between the third and fifth lumbar vertebrae, with a lack of spinal cord tissue and collapsed associated dura mater. Microscopically, the representative sections of the L3 to L5 spinal cord had only .an irregular trace of gray matter adhered to the meninges (lumbar spinal cord aplasia) In the region of L6, a focally extensive, cystic, and well-defined tubular cavitation was noted dorsally to the central canal, replacing and compressing the adjacent nervous tissue (syringomyelia). Metagenomics examination did not detect any virus responsible for the presented spinal cord malformations. This seems to be the first description of segmental spinal cord aplasia reported in a wild feline.

RESUMO: O objetivo do presente relato foi descrever um caso de aplasia segmentar da medula espinhal lombar em um felino silvestre, com aproximadamente cinco meses, resgatado de seu ambiente natural, apresentando paralisia bilateral dos membros posteriores. A espécie gato-do-mato-pequeno (Leopardus guttulus) foi determinada por sequenciamento genético. Após curto período de hospitalização, iniciou autofagia de ambos os membros pélvicos, seguido de fratura com exposição óssea. Optou-se pela eutanásia e o cadáver foi encaminhado ao Setor de Anatomia Patológica da Universidade Federal Rural do Rio de Janeiro para necropsia. Macroscopicamente, havia uma interrupção segmentar grave da medula espinhal entre a terceira e a quinta vértebras lombares, medindo 8,5cm de comprimento, com resquícios de tecido nervoso e com meninges colapsadas. Ao exame histológico, em seções da medula espinhal na região de L3 a L5, .havia apenas vestígio de tecido nervoso aderido às meninges, morfologicamente compatível com substância cinzenta (aplasia de medula espinhal lombar). Na região de L6 notou-se áreas multifocais com cavitações tubulares, císticas e bem delimitadas, dorsalmente ao canal central substituindo e comprimindo o tecido nervoso adjacente (siringomielia). O exame de metagenômica não detectou qualquer vírus responsável pelas malformações da medula espinhal. Com base no histórico, sinais clínicos, necropsia e achados histológicos, o diagnóstico de aplasia segmentar grave com siringomielia foi estabelecido em um L. guttulus.

Abstract A complete genome of the first anellovirus infecting the wild felid Leopardus pardalis (ocelot) and a partial genome were assembled and annotated through high-throughput sequencing protocols followed by Sanger sequencing validation. The full-length virus obtained comprises 2,003 bp, while the partial genome comprises 1,224 bp. Phylogenetic analysis grouped these two sequences in two distinct clusters related to previously described Felidae anelloviruses. The ORF1 of the partial genome was identified as a new species provisionally called Torque teno ocelot virus, with 53.6% identity with its sister lineage. The complete genome was inferred as a new representative of the Torque teno felid virus 3 species, with 73.28% identity to the closest reference. This study expands known virus diversity and the host span of anelloviruses.

BACKGROUND During routine Coronavirus disease 2019 (COVID-19) diagnosis, an unusually high viral load was detected by reverse transcription real-time polymerase chain reaction (RT-qPCR) in a nasopharyngeal swab sample collected from a patient with respiratory and neurological symptoms who rapidly succumbed to the disease. Therefore we sought to characterise the infection. OBJECTIVES We aimed to determine and characterise the etiological agent responsible for the poor outcome. METHODS Classical virological methods, such as plaque assay and plaque reduction neutralisation test combined with amplicon-based sequencing, as well as a viral metagenomic approach, were performed to characterise the etiological agents of the infection. FINDINGS Plaque assay revealed two distinct plaque phenotypes, suggesting either the presence of two severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains or a productive coinfection of two different species of virus. Amplicon-based sequencing did not support the presence of any SARS-CoV-2 genetic variants that would explain the high viral load and suggested the presence of a single SARS-CoV-2 strain. Nonetheless, the viral metagenomic analysis revealed that Coronaviridae and Herpesviridae were the predominant virus families within the sample. This finding was confirmed by a plaque reduction neutralisation test and PCR. MAIN CONCLUSIONS We characterised a productive coinfection of SARS-CoV-2 and Herpes simplex virus 1 (HSV-1) in a patient with severe symptoms that succumbed to the disease. Although we cannot establish the causal relationship between the coinfection and the severity of the clinical case, this work serves as a warning for future studies focused on the interplay between SARS-CoV-2 and HSV-1 coinfection and COVID-19 severity.

In an enclosure with nine collared peccaries (Pecari tajacu) from the Rio de Janeiro city Zoo, Brazil, one specimen was found dead and two others developed prostration, apathy and dehydration, resulting on its death. Necropsy of two animals pointed to pulmonary and renal damage. Histological examination revealed vasculitis in spleen from both P. tajacu, suggesting a systemic viral infection. Lungs from one specimen showed fibrinoid vasculitis, alveolar damage with hyaline membrane, and interstitial lymphocytes infiltration. Virome analysis in anal wash samples from the latter two animals revealed a new type of Betacoronavirus, lineage A, provisionally named Ptajacu-CoV.