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In October 2020, highly pathogenic avian influenza A(H5N8) viruses were detected in 2 dead swans in Inner Mongolia, China. Genetic analysis showed that the H5N8 isolates belong to clade 2.3.4.4b and that the isolates cluster with the H5N8 viruses isolated in Eurasia in the fall of 2020.

Mycoplasma capricolum subsp. capripneumoniae is an important pathogen of goats that causes contagious caprine pleuropneumonia. Here, we report the complete genome sequence of M. capricolum subsp. capripneumoniae strain zly1309F, isolated from a Tibetan antelope ( Pantholops hodgsonii ) in China.

In 2012, an FHV-1-like virus was isolated from a tiger that presented with clinical signs of sialorrhea, sneezing and purulent rhinorrhea. Isolation was performed with the FK81 cell line, and the virus was identified by PCR, transmission electron microscopy (TEM), and the phylogenetic analysis of the partial thymidine kinase (TK) and glycoprotein B (gB) genes. A total of 253 bp of the TK gene and 566 bp of the gB gene were amplified from the trachea of the tiger by PCR/RT-PCR method. Phylogenetic analysis showed that the isolate belonged to the same cluster with other FHV-1 strains obtained from GenBank. Herpes-like viruses with an envelope and diameters of approximately 200 nm were observed in the culture supernatants of FK81 cells inoculated with samples from the tiger. The FHV-1 infection was confirmed by an animal challenge experiment in a cat model. Our finding extends the host range of FHV-1 and has implications for FHV-1 infection and South China tiger conservation.

Kobuviruses comprise three species, the Aichivirus A, Aichivirus B, and Aichivirus C (porcine kobuvirus). Porcine kobuvirus is endemic to pig farms and is not restricted geographically but, rather, is distributed worldwide. The complete genomic sequences of four porcine kobuvirus strains isolated during a diarrhea outbreak in piglets in the Gansu province of China were determined. Two of these strains exhibited variations relative to the traditional strains. The potential 3C/3D cleavage sites of the variant strains were Q/C, which differed from the Q/S in the traditional porcine kobuvirus genome. A 90-nucleotide deletion in the 2B protein and a single nucleotide insertion in the 3′UTR were found in the variant strains. The VP1 regions of all four porcine kobuviruses in our study were highly variable (81%–86%). Ten common amino acid mutations were found specifically at certain positions within the VP1 region. Significant recombination sites were identified using SimPlot scans of whole genome sequences. Porcine kobuviruses were also detected in pig serum, indicating that the virus can escape the gastrointestinal tract and travel to the circulatory system. These findings suggest that mutations and recombination events may have contributed to the high level of genetic diversity of porcine kobuviruses and serve as a driving force in its evolution.

H5N6 avian influenza viruses (AIVs) may pose a potential human risk as suggested by the first documented naturally-acquired human H5N6 virus infection in 2014. Here, we report the first cases of fatal H5N6 avian influenza virus (AIV) infection in a domestic cat and wild birds. These cases followed human H5N6 infections in China and preceded an H5N6 outbreak in chickens. The extensive migration routes of wild birds may contribute to the geographic spread of H5N6 AIVs and pose a risk to humans and susceptible domesticated animals and the H5N6 AIVs may spread from southern China to northern China by wild birds. Additional surveillance is required to better understand the threat of zoonotic transmission of AIVs.

Newcastle disease virus (NDV) causes a highly contagious viral disease in poultry and wild birds, and it can cause significant economic loss worldwide. Eight viral strains were isolated by inoculating embryonated chicken eggs from the Poyang Lake region of China with swab samples. All eight of the NDV isolates were identified as class I genotype 3 strains, but they diverged notablely from class II viruses. Further analysis revealed that all eight NDV isolates were lentogenic strains containing the (112)ERQER↓L(117) motif at the F protein cleavage site. The strains were highly identical and were more species specific (chicken and waterfowl) than site specific (Nanchang and Duchang regions). The close phylogenetic proximity of these isolates indicates that viral transmission may happen between poultry and wild birds. Our study demonstrates that lentogenic class I NDVs exist in clinically healthy wild waterfowl and poultry within the Poyang Lake region. Active surveillance of these viruses to determine their evolution and origin is one of the most realistic strategies for preventing and controlling NDV outbreaks.

To the Editor: Contagious caprine pleuropneumonia is a severe respiratory disease of goats caused by Mycoplasma capricolum subsp. capripneumoniae (Mccp), a member of the M. mycoides cluster (1). Mccp infection is associated with a 60% mortality rate and 90% illness rate, and the disease can cause substantial losses of livestock (1,2). We report a 2012 outbreak of contagious caprine pleuropneumonia in endangered Tibetan antelope (Pantholops hodgsonii) in China. In 2000, the International Union of Conservation of Nature first listed the Tibetan antelope as an endangered species (3), and in 2004, the number of these antelope was estimated at 150,000 (4). Most Tibetan antelope live on China’s Qinghai–Tibet Plateau at an altitude of 3,700–5,500 m (3). During September–December 2012, ≈2,400 endangered Tibetan antelope were found dead in the Naqu area of Tibet; the dead animals represented 16% of the 15,000 Tibetan antelope thought to live in the area. Necropsy was performed on 13 of the antelope at sites within the Shenzha, Shuanghu, and Nima localities of the Naqu area (Technical Appendix Table 1). Gross pathologic lesions were localized exclusively to the lung, where severe pleuropneumonia with partial hepatization was observed (Figure, panel A). The lungs of some affected antelope displayed a thickening of the interlobular septa, pleuritis, and an accumulation of straw-colored pleural fluid. The pleural exudate solidified to form a gelatinous covering on the lung (Figure, panel B). Figure Pneumonia caused by Mycoplasma capricolum subsp. capripneumoniae in Tibetan antelope (Pantholops hodgsonii), Tibet, 2012. A) Lung of a caprine pleuropneumonia–infected Tibetan antelope (sample SZM2) showing lung hepatization. B) Lung of a caprine ... Samples of lung tissue from 5 of the antelope were selected for histologic examination. Four of the samples showed fibrinous pneumonia with serofibrinous fluid and an inflammatory cell infiltrate consisting mainly of lymphocytes in the alveoli (Figure, panel C) and bronchioles (Figure, panel D). One sample showed pulmonary edema with a protein-rich fluid effusion in alveoli. Lung tissue from each of the 13 antelope was minced and inoculated into modified Hayflick broth, which has been used extensively to isolate Mycoplasma spp. from animals. Cultures were incubated at 37°C in a humidified atmosphere of 5% CO2 (5). The medium was examined daily by comparing inoculated broth with an uninoculated control broth. Moderate turbidity, a color change from pink to yellow, and an appreciable swirl of the culture when rotated were used as indicators of mycoplasma growth. After 2–3 passages in culture, 11 of 13 samples showed growth of mycoplasma. The presence of mycoplasma-like particles in the 11 growth-positive cultures was confirmed by electron microscopy (Technical Appendix Figure 1). Collectively, these observations implicated mycoplasma as the cause of disease in the affected antelope. We next screened lung samples from each of the 13 Tibetan antelope by PCR for evidence of M. mycoides cluster and M. bovis. Eleven samples were positive for Mccp, but no other types of mycoplasma were detected (Technical Appendix Tables 1, 2). We conducted PCR as described (6) on the arcD gene of Mccp. In brief, we conducted 35 cycles of 30 s at 94°C, 15 s at 47°C, and 15 s at 72°C. Of note, lung sample SH7, which showed pulmonary edema, was negative for mycoplasma by PCR and culture. Lung samples from the 13 dead Tibetan antelope were also tested for an additional 16 potential pathogens (Technical Appendix Tables 1, 2) by PCR or reverse transcription PCR. No pathogens other than Mccp were detected. To assess the relationship of the Mccp strain isolated from infected Tibetan antelope with previously isolated Mccp strains and the closely related M. capricolum subsp. capricolum (Mcc), we analyzed a 562-bp segment of the H2 gene of Mccp, which was used to distinguish the Mccp and Mcc as reported by Lorenzon et al. (7), isolated from an infected Tibetan antelope in Shuanghu county (sample SH3). The partial H2 sequence (GenBank accession no. {"type":"entrez-nucleotide","attrs":{"text":"KC441725","term_id":"478860002","term_text":"KC441725"}}KC441725) had higher sequence identity with Mccp isolates (99.3%–99.7%) than with Mcc isolates (90.2%–91.2% (Technical Appendix Figure 2). This phylogenetic analysis demonstrated that the Mccp isolated from infected Tibetan antelope belongs to the same clade as Mccp strains previously isolated in Africa and Asia. The changing habitat of endangered Tibetan antelope may lead to increased exposure to Mccp, which can cause devastating outbreaks, such as the one reported here. Goats and sheep are herded on grasslands at an altitude of 4,300–5,000 m, the same area where Tibetan antelope reside. Goats are a reservoir for Mccp, and Mccp has been isolated from sheep in mixed herds with goats (8). Rail lines traverse the rangelands in this region, limiting the normal migration patterns of the Tibetan antelope population. Interaction among goats, sheep, and Tibetan antelope in this region, combined with the effect of human infringement on their rangeland, may increase the risk for disease emergence and transmission. Our results show that contagious caprine pleuropneumonia may pose a substantial threat to the survival of endangered Tibetan antelope. Surveillance for Mccp infection among Tibetan antelope populations and domestic and wild goat and sheep populations that have close contact with the Tibetan antelope should be considered. Technical Appendix: Histopathologic findings and results of pathogen testing, primer pairs used for pathogen testing, lung tissue findings, and phylogenetic tree. Click here to view.(546K, pdf)

Canine distemper (CD) is a highly contagious, often fatal, multisystemic, and incurable disease in dogs and other carnivores, which is caused by canine distemper virus (CDV). Although vaccines have been used as the principal means of controlling the disease, CD has been reported in vaccinated animals. The hemoagglutinin (H) protein is one of the most important antigens for inducing protective immunity against CD, and antigenic variation of recent CDV strains may explain vaccination failure. In this study, a new CDV isolate (TM-CC) was obtained from a Tibetan Mastiff that died of distemper, and its genome was characterized. Phylogenetic analysis of the H gene revealed that the CDV-TM-CC strain is unique among 20 other CDV strains and can be classified into the Asia-1 group with the Chinese strains, Hebei and HLJ1-06, and the Japanese strain, CYN07-hV. The H gene of CDV-TM-CC shows low identity (90.4 % nt and 88.9 % aa) with the H gene of the classical Onderstepoort vaccine strain, which may explain the inability of the Tibetan Mastiff to mount a protective immune response. We also performed a comprehensive phylogenetic analysis of the N, P, and F protein sequences, as well as potential N-glycosylation sites and cysteine residues. This analysis shows that an N-glycosylation site at aa 108-110 within the F protein of CDV-TM-CC is specific for the wild-type strains (5804P, A75/17, and 164071) and the Asia-1 group strains, and may be another important factor for the poor immune response. These results provide important information for the design of CD vaccines in the China region and elsewhere.