In utero infection by porcine reproductive and respiratory syndrome virus is sufficient to increase susceptibility of piglets to challenge by Streptococcus suis type II
In utero infection by porcine reproductive and respiratory syndrome virus is sufficient to increase susceptibility of piglets to challenge by Streptococcus suis type II
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DOI：
10.1128/jvi.75.10.4889-4895.2001
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发表时间：
2001-05-01
影响因子：
5.4
通讯作者：
McCaw, MB
中科院分区：
文献类型：
--
作者：
Feng, WH;Laster, SM;McCaw, MB
猪繁殖与呼吸综合征（PRRS）持续提高了仔猪的发病率和死亡率。许多不同的：继发性细菌性疾病发生在PRRS病毒（PRRSV）感染的猪。然而，到目前为止，建立一个可重复的实验模型，猪繁殖与呼吸综合征病毒感染断奶，随后的临床疾病后，二次细菌的挑战，一直是困难的。猪繁殖与呼吸综合征病毒（PRRSV）是仔猪继发性细菌性疾病暴发流行的常见病原，本研究旨在探讨宫内感染对仔猪继发性细菌性疾病易感性的影响。无PRRSV的妊娠母猪在妊娠98天时鼻内感染PRRSV SD 23983株。PRRSV感染母猪产下的所有仔猪均为病毒血症。出生时将小猪从母猪体内取出并剥夺初乳，将来自PRRSV感染和未感染母猪的小猪随机分配到猪链球菌攻毒亚组或对照亚组。在5日龄时，用猪链球菌IE型菌株MN 87555鼻内攻击仔猪。对3日龄时采集的血样进行白细胞总数和分类计数。PRRSV感染仔猪外周血白细胞、淋巴细胞、酸性单核细胞数量显著减少。在骨髓、脑、肺、心脏、脾、淋巴结、扁桃体和胸腺中观察到PRRSV感染仔猪的病变。与非PRRSV感染仔猪相比，宫内PRRSV感染仔猪的胸腺/体重比显著降低，胸腺病变的特征在于胸腺细胞的严重皮质耗竭。在无PRRSV母猪所产仔猪中未观察到病变。总体而言，PRRSV-S中22头仔猪中有20头。双重感染组在攻毒后1周内死亡。suis（两项试验各11例中的10例）。这与仅感染PRRSV组中18头仔猪中的1头和S.仅猪攻毒组（试验1中12例中的1例，试验2中11例中的4例）。未感染对照组中无仔猪死亡。PRRSV-S中的大多数仔猪。猪双重感染组发生化脓性脑膜炎。猪链球菌II型从他们的大脑和关节中回收。这些结果表明，在宫内感染PRRSV使仔猪更容易感染酸疾病后，由S。猪Ⅱ型。猪繁殖与呼吸综合征病毒宫内感染可能为研究猪繁殖与呼吸综合征病毒与细菌共感染之间的相互作用提供一个有用的模型。
Porcine reproductive and respiratory syndrome (PRRS) consistently elevates the frequency of disease and mortality in young pigs. Many different: secondary bacterial diseases occur in PRRS virus (PRRSV)-infected pigs. However, to date, establishing a reproducible experimental model of PRRSV infection in weaned pigs, with subsequent clinical disease following secondary bacterial challenge, has been difficult. PRRSV is frequently isolated during outbreaks from weak-born piglets affected by secondary bacterial diseases, This study was performed to investigate the potential role of intrauterine PRRSV infection on piglet susceptibility to secondary bacterial infection. PRRSV-free pregnant sows were intranasally infected at 98 days of gestation with PRRSV strain SD 23983. All piglets born to the PRRSV-infected sows were viremic. Piglets were removed from the sows at birth and deprived of colostrum, Piglets from PRRSV-infected and noninfected sows were randomly assigned to Streptococcus suis challenge or control subgroups. At 5 days of age, piglets were challenged intranasally with strain MN 87555 of S, suis type IE. Total and differential leukocyte counts were performed on blood samples collected at 3 days of age. The numbers of leukocytes, lymphocytes, acid monocytes were significantly reduced in the PRRSV-infected piglets. Lesions were observed in bone marrow, brain, lung, heart, spleen, lymph node, tonsil, and thymus of PRRSV-infected piglets. Thymus/body weight ratios of in utero PRRSV-infected piglets were significantly reduced compared to those of non-PRRSV-infected piglets, and thymic lesions were characterized by severe cortical depletion of thymocytes. Lesions were not observed in piglets born to PRRSV-free sows. Overall, 20 out of 22 piglets in the PRRSV-S. suis dual-infection group died within 1 week after challenge with S. suis (10 of 11 in each of two trials). This contrasts with 1 of 18 piglets in the PRRSV-infection-only group and 5 of 23 piglets in the S. suis-challenge-only group (1 of 12 in trial 1 and 4 of 11 in trial 2). No piglets died in the uninfected control groups. Most of the piglets in the PRRSV-S. suis dual-infection group developed suppurative meningitis. S, suis type II was recovered from their brains and joints. These results indicate that in utero infection by PRRSV makes piglets more susceptible to infection acid disease following challenge by S. suis type II. In utero infection by PRRSV may provide a useful model to study the interaction between PRRSV and bacterial coinfections in piglets.