Reston virus causes severe respiratory disease in young domestic pigs

Reston virus (RESTV), an ebolavirus, causes clinical disease in macaques but has yet only been associated with rare asymptomatic infections in humans. Its 2008 emergence in pigs in the Philippines raised concerns about food safety, pathogenicity, and zoonotic potential, questions that are still unanswered. Until today, the virulence of RESTV for pigs has remained elusive, with unclear pathogenicity in naturally infected animals and only one experimental study demonstrating susceptibility and evidence for shedding but no disease. Here we show that combined oropharyngeal and nasal infection of young (3- to 7-wk-old) Yorkshire cross pigs with RESTV resulted in severe respiratory disease, with most animals reaching humane endpoint within a week. RESTV-infected pigs developed severe cyanosis, tachypnea, and acute interstitial pneumonia, with RESTV shedding from oronasal mucosal membranes. Our studies indicate that RESTV should be considered a livestock pathogen with zoonotic potential.

Reston virus (RESTV) was discovered in 1989/1990 in macaques imported into the United States from the Philippines for research purposes (1). Since then, there have been several episodes of disease caused by RESTV in macaques and rare asymptomatic infections in humans (2, 3). Unexpectedly, in 2008, RESTV emerged in pigs in the Philippines, and, shortly thereafter, RESTV sequences were detected in Chinese swine, raising zoonotic and food safety concerns (4, 5). RESTV constitutes a separate species in the genus Ebolavirus, family Filoviridae, and is generally thought of as the human apathogenic filovirus (6). Aside from humans (2, 3), RESTV has been shown to naturally and experimentally infect macaques, swine, ferrets, bats, and several rodent species (4, 5, 7–13). Upon experimental infection, macaques and ferrets, as well as immunocompromised rodents, such as STAT-1 knockout mice, develop severe disease with lethal outcome, whereas immunocompetent rodents generally do not (9–12). Whether RESTV itself causes disease in naturally infected domestic pigs remains unknown, since the RESTV-infected pigs from the Philippines were coinfected with the virulent arterivirus porcine reproductive and respiratory syndrome virus (PRRSV; now Betaarterivirus suid 1). In an initial experimental study, domestic pigs infected with RESTV only exhibited subclinical infections with evidence for virus shedding (7). We studied RESTV infection in young (3- to 7-wk-old) Yorkshire cross pigs, a swine breed used frequently in commercial pig production systems around the world. The main objective was to determine an age-dependent susceptibility to infection.     

Feed or feed transport as a potential route for a porcine epidemic diarrhoea outbreak in a 10,000-sow breeding herd in Mexico

Porcine epidemic diarrhoea virus (PEDV) infects pigs of all ages causing vomiting and diarrhoea. PEDV is transmitted via the oral–faecal route, and a very low dose is enough to infect susceptible pigs, resulting in significant production losses. This short communication aims to describe the introduction of PEDV into a 10,000-sow farrow-to-wean farm located in northwest Mexico. Following the onset of clinical signs, an outbreak investigation was conducted to determine the most probable route of introduction. Based on data collected from interviews, construction of a timeline of events, and the detection of PEDV RNA in feed samples and samples collected from various surfaces of feed transport vehicles, it was concluded that the most probable route for PEDV incursion into this breeding herd was contaminated feed or a contaminated feed transport vehicle. This paper describes how feed or feed transport could serve as potential routes of PEDV infection to a farm and highlights the importance of establishing biosecurity programs to mitigate these risks.     

Heterosubtypic immunity to H7N9 influenza virus in isogenic guinea pigs after infection with pandemic H1N1 virus

Heterosubtypic immunity is defined as immune-mediated (partial) protection against an influenza virus induced by an influenza virus of another subtype to which the host has not previously been exposed. This cross-protective effect has not yet been demonstrated to the newly emerging avian influenza A viruses of the H7N9 subtype. Here, we assessed the induction of protective immunity to these viruses by infection with A(H1N1)pdm09 virus in a newly developed guinea pig model. To this end, ten female 12–16 week old strain 2 guinea pigs were inoculated intratracheally with either A(H1N1)pdm09 influenza virus or PBS (unprimed controls) followed 4 weeks later with an A/H7N9 influenza virus challenge. Nasal swabs were taken daily and animals from both groups were sacrificed on days 2 and 7 post inoculation (p.i.) with A/H7N9 virus and full necropsies were performed.Nasal virus excretion persisted until day 7 in unprimed control animals, whereas only two out of seven H1N1pdm09-primed animals excreted virus via the nose. Infectious virus was recovered from nasal turbinates, trachea and lung of all animals at day 2 p.i., but titers were lower for H1N1pdm09-primed animals, especially in the nasal turbinates. By day 7 p.i., relatively high virus titers were found in the nasal turbinates of all unprimed control animals but infectious virus was isolated from the nose of only one of four H1N1pdm09-primed animals.Animals of both groups developed inflammation of variable severity in the entire respiratory tract. Viral antigen positive cells were demonstrated in the nasal epithelium of both groups at day 2. The bronchi(oli) and alveoli of unprimed animals showed a moderate to strong positive signal at day 2, whereas H1N1pdm09-primed animals showed only minimal positivity. By day 7, only viral antigen positive cells were found after H7N9 virus infection in the nasal turbinates and the lungs of unprimed controls. Thus infection with H1N1pdm09 virus induced partially protective heterosubtypic immunity to H7N9 virus in (isogenic) guinea pigs that could not be attributed to cross-reactive virus neutralizing antibodies.     

The effects of intraoral splints on the masticatory system of pigs

While evidence exists to support the effectiveness of splints on conditions involving the masticatory musculature, few research projects have examined the results of long-term splint wear. The purpose of this study was to examine the function of the masticatory system over a 2-month time period of splint wear. Young adult female miniature pigs were divided into three groups: a control (C) group that wore no intraoral splint, a control splint (CS) group that wore a splint increasing bite height, and a protrusive splint (PS) group that wore a splint increasing bite height and moving the mandible anteriorly. Splints were worn constantly. Fine-wire needle EMG was performed prior to splint delivery and at 1 and 2 months post-splint delivery. Bilateral superficial masseters and zygomaticomandibularis (ZM, equivalent to deep masseter) muscles were monitored during normal feeding. Absolute EMG output, percentage output, and cycle timing were unaffected by chronic splint wear. However, chewing coordination was significantly changed in the splinted groups in both sessions post-splint delivery relative to baseline readings and to the C group (P < 0.005). Trends indicate that the coordination of the PS group was more greatly altered than that of the CS group.     

Modification of the bilateral sagittal split osteotomy (BSSO) in a study using pig mandibles

In a bilateral sagittal split osteotomy (BSSO) mechanical irritation of the inferior alveolar nerve (IAN) (e.g. by chiselling) should be avoided to prevent neural damage. A modification of the Obwegeser-Dal Pont operation technique was studied by splitting 100 pig mandibles ex vivo. An additional osteotomy at the caudal border of the mandible was used to facilitate the sagittal split by means of a locus of minor resistance. The chisel was inserted distal to the second molar and far away from the IAN. The mandible was split by torque. The modified technique reduced the required torque to split the mandible about 30% compared with the original technique (paired t-test, t(69) = −12.89; p < 0.05). 75% of all mandibles split by the modified technique were classified as bad splits compared with 100% using the original technique using the same protocol without the additional osteotomy.     

Latency of the jaw-opening reflex in the premature, preweaning and adolescent pig (hanford strain miniature pig, Sus scrofa)

The jaw-opening (digastric) reflex was elicited by electrical stimulation of oral mucosa in miniature pigs (Sus scrofa) varying in age from 5 days premature to 101 days post-term. The latency of reflex electromyographic activity varied between 12–14 ms in the most immature animals and 9–11 ms in the oldest animals. The very long-latency digastric responses found in the immature young of nesting mammals were not seen in the relatively precocious young of this species.     

高压氧对豚鼠实验性牙周炎作用的组织病理学研究

目的：探讨高压氧（HBO）对动物牙周炎作用的组织病理学变化特点。方法：用丝线缝扎加喂含100g/L糖的食料形成动物牙周炎，每日1次用0.25MPa HBO暴露60min，连续2周。在实验不同时间点取牙周组织联合标本，分别用40g/L俄酸固定，混合酸和EDTA脱钙，常规制作光镜和电镜标本，光镜和电镜观察。结果：HBO治疗后牙龈固有层和牙周膜中巨噬细胞明显减少，血管数目明显增多，牙槽嵴吸收程度减轻，骨陷窝处破骨细胞较少，附近有大量成骨细胞和软骨内成骨现象。电镜下上皮细胞连接紧密，成纤维细胞胸浆内线粒体和粗面内质网增多，浆细胞、巨噬细胞胞浆内线粒体和粗面内质网较少，血管内皮细胞胞浆中线粒体和内质网明显增多。破骨细胞内线粒体和粗面内质网明显减少，成骨细胞内线粒体和粗面内质网明显增多。结论：HBO可使牙龈和牙周膜内血管增多，巨噬细胞减少，牙槽骨吸收减慢。