形觉剥夺性高度近视豚鼠巩膜形态改变及缺氧诱导因子-1α和氧自由基在高度近视中的作用

目的　观察形觉剥夺性高度近视（form deprivation high myopia，FDHM）豚鼠巩膜形态变化，探讨缺氧诱导因子-1α（hypoxia-inducible factor-1α，HIF-1α）及氧自由基在高度近视中的作用。方法　将豚鼠适应性饲养1周后，随机分为空白对照组（25只）和模型组（25只）。模型组豚鼠右眼行眼睑缝合，所有模型组豚鼠均选择右眼作为FDHM组，对侧眼为自身对照组。空白对照组豚鼠不做任何处理。于造模前及造模后8周采用检影镜测量屈光度，A超进行生物测量。形觉剥夺8周以后处死豚鼠，观察巩膜形态和超微结构的变化，测定巩膜HIF-1α相对表达量，超氧化物歧化酶（superoxide dismutase，SOD）活力及丙二醛（malondialdehyde，MDA）的含量。结果　豚鼠形觉剥夺8周以后，FDHM组屈光度从（+3.59±0.33）D变为（-7.96±0.55）D，明显高于空白对照组（+0.89±0.32）D、自身对照组（-0.55±0.49）D（均为P<0.05）；玻璃体腔深度为（4.12±0.13）mm明显高于空白对照组（3.71±0.23）mm和自身对照组（3.93±0.04）mm（均为P<0.05）；眼轴长度为（8.93±0.22）mm明显长于空白对照组（7.95±0.37）mm和自身对照组（8.01±0.15）mm（均为P<0.05）。巩膜组织明显变薄，细胞外基质增多，成纤维细胞密度降低，胶原纤维平均直径减小。FDHM组巩膜中HIF-1α相对表达量、MDA含量明显高于空白对照组和自身对照组，SOD活力明显低于空白对照组和自身对照组（均为P<0.05）。结论　形觉剥夺8周后，豚鼠FDHM眼近视度数明显增加，玻璃体腔深度增加，眼轴延长，巩膜形态发生病理性变化；HIF-1α、SOD、MDA可能参与了FDHM的形成。     

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.     

Impact of early-life events on the susceptibility to Clostridium difficile colonisation and infection in the offspring of the pig

Clostridium difficile has been documented as a major cause of uncontrolled outbreaks of enteritis in neonatal pigs and antibiotic-associated infections in clinical settings. It belongs to the natural cohort of early colonisers of the gastrointestinal tract of pigs and can be detected in faeces up to two weeks post-partum. In older pigs, it often remains under the detection limit. Most neonatal pigs show no clinical signs of disease although C. difficile and its toxins can be detected at high levels in faeces. Increased mortality rates associated with C. difficile on pig farms are, so far, considered “spontaneous” and the predisposing factors are mostly not defined. The infection caused by C. difficile is multifactorial and it is likely that the repertoire of maternal factors, host physiology, the individually developing gut microbiota, co-infections and environmental stress define the conditions for disease development. In this addendum to our recently published work on CDI in neonatal piglets, we discuss the “early-life events” that influence C. difficile spread and infection in neonatal piglets.     

Seneca Valley virus RNA detection in pig feed and feed ingredients in Brazil

We investigated Seneca Valley virus (SVV) contamination in pig feed and feed ingredients. Twenty‐seven samples were collected from two Brazilian feed mills and subjected to conventional RT‐nested‐PCR and qRT‐PCR assays. Seven samples were SVV‐positive with viral loads of 3.94–4.33 log₁₀ genomic copies/g of feed. The study reveals SVV feed and feed ingredient contamination under natural conditions in Brazil.     

Neural coding of the sound envelope is changed in the inferior colliculus immediately following acoustic trauma

Sensorineural hearing loss is often accompanied by difficulties with understanding speech in fluctuating backgrounds, suggesting that neural coding of complex sound features, such as the sound envelope, is impaired. Here, we studied how temporal and rate coding of the envelope is affected in the inferior colliculus immediately after acoustic trauma. Neural activity in response to amplitude‐modulated noise was recorded from the inferior colliculus of the guinea pig, before and immediately after a 1‐hr 11‐kHz acoustic trauma. Units with a characteristic frequency (CF) below the trauma frequency (<11 kHz) showed increased response gains, a measure for temporal coding of the sound envelope, especially at low modulation frequencies (≤128 Hz). Units with a CF > 11 kHz, which had large acoustic trauma‐induced threshold shifts, had decreased response gains to amplitude‐modulated noise. Shapes of temporal modulation transfer functions shifted toward a higher proportion of low‐pass shapes in low‐CF units, and to less band‐pass shapes in high‐CF units. Furthermore, driven firing rates decreased, especially at high modulation frequencies for high‐CF units. The observed changes occurred immediately following trauma and were thus a result of the immediate trauma‐induced damage to the auditory system. If also present in human subjects, reduced response gains in high‐frequency units could disrupt coding of consonants and consequently impair speech understanding in noisy environments. Moreover, the enhanced temporal coding by low‐CF units of the low modulation frequencies could overly amplify responses to low‐frequency noise, further deteriorating listening in noise.     

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.