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Emergence of a virulent porcine reproductive and respiratory syndrome virus (PRRSV) 1 strain in Lower Austria

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ABSTRACT

Background: In spring 2015, an outbreak of porcine reproductive and respiratory syndrome (PRRS) struck Lower Austria caused by a PRRS virus (PRRSV) strain spreading rapidly among both previously PRRSV negative and vaccinated pig herds. This case report describes the first well-documented emergence of the PRRSV strain responsible for this outbreak.

Case presentation: A PRRSV seronegative piglet-producing farm in Lower Austria encountered losses in foetuses and suckling piglets of up to 90 %; clinical signs in sows and nursery piglets included fever and reduced feed intake. Additionally, high percentages of repeat breeders and losses of up to 40 % in nursery piglets occurred. An infection with PRRSV was suggested by the detection of antibodies by enzyme linked immunosorbent assay and confirmed by quantitative real time PCR. The underlying PRRSV strain, termed AUT15-33, was isolated by passage on porcine alveolar macrophages, partially sequenced (ORF2-7) and grouped as PRRSV-1, subtype 1. In phylogenetic analysis of the genome region coding for the structural proteins, ORF2-7, AUT15-33 clustered with Belgian strains but identities were as low as 88 %. In contrast, analysis of ORF7 sequences revealed a close relationship to Croatian strains from 2012 with an identity of 94 – 95 %.

Conclusions: In the year following the outbreak, the same PRRSV strain was identified repeatedly in different regions of Austria. It can be speculated that the new strain has novel advantageous properties.

No MeSH data available.


Related in: MedlinePlus

(a + b) Histological lung lesions. a Interstitial pneumonia and catarrhalic to purulent bronchopneumonia with severe atelectasis (bar length 150 μm). b Intralobular interstitial pneumonia including hyperplasia of type II pneumocytes and necrotic cells in the alveolar lumen (bar length 60 μm)
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Fig3: (a + b) Histological lung lesions. a Interstitial pneumonia and catarrhalic to purulent bronchopneumonia with severe atelectasis (bar length 150 μm). b Intralobular interstitial pneumonia including hyperplasia of type II pneumocytes and necrotic cells in the alveolar lumen (bar length 60 μm)

Mentions: First samples for diagnostics were taken end of April from sows, which started to show clinical signs at least two weeks prior to sampling. Blood samples were taken from nine sows for serological investigation. Antibodies against PRRSV were detected by ELISA in sera of all sows. To investigate concomitant infections in nursery piglets, two piglets from the most severely affected age group (around seven weeks old at the time of submission), showing poor body condition, enlarged inguinal lymph nodes and respiratory signs like coughing were selected by the herd veterinarian and submitted for necropsy and further diagnostics to the University of Veterinary Medicine Vienna. Post mortem investigations found poor retraction of the lung and consolidation of the cranio-ventral areas. A catarrhal enterocolitis was diagnosed in one piglet. Histologically, atelectasis with intralobular, interstitial pneumonia including hyperplasia of type II pneumocytes, as well as a catarrhalic to purulent bronchopneumonia were seen in the lungs of both pigs (Fig. 3). Bacterial isolation was only performed on organs showing pathological alterations (intestines and lung). While in intestinal samples no pathogenic bacteria could be detected, Staphylococcus hyicus could be isolated from the lung of both pigs by conventional bacteriological culture. To exclude an involvement of PCV2 an in situ hybridization (ISH) on inguinal lymph nodes was performed. No histologic lesions were found in the lymph nodes and no PCV2 was detected by ISH.Fig. 3


Emergence of a virulent porcine reproductive and respiratory syndrome virus (PRRSV) 1 strain in Lower Austria
(a + b) Histological lung lesions. a Interstitial pneumonia and catarrhalic to purulent bronchopneumonia with severe atelectasis (bar length 150 μm). b Intralobular interstitial pneumonia including hyperplasia of type II pneumocytes and necrotic cells in the alveolar lumen (bar length 60 μm)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC5382404&req=5

Fig3: (a + b) Histological lung lesions. a Interstitial pneumonia and catarrhalic to purulent bronchopneumonia with severe atelectasis (bar length 150 μm). b Intralobular interstitial pneumonia including hyperplasia of type II pneumocytes and necrotic cells in the alveolar lumen (bar length 60 μm)
Mentions: First samples for diagnostics were taken end of April from sows, which started to show clinical signs at least two weeks prior to sampling. Blood samples were taken from nine sows for serological investigation. Antibodies against PRRSV were detected by ELISA in sera of all sows. To investigate concomitant infections in nursery piglets, two piglets from the most severely affected age group (around seven weeks old at the time of submission), showing poor body condition, enlarged inguinal lymph nodes and respiratory signs like coughing were selected by the herd veterinarian and submitted for necropsy and further diagnostics to the University of Veterinary Medicine Vienna. Post mortem investigations found poor retraction of the lung and consolidation of the cranio-ventral areas. A catarrhal enterocolitis was diagnosed in one piglet. Histologically, atelectasis with intralobular, interstitial pneumonia including hyperplasia of type II pneumocytes, as well as a catarrhalic to purulent bronchopneumonia were seen in the lungs of both pigs (Fig. 3). Bacterial isolation was only performed on organs showing pathological alterations (intestines and lung). While in intestinal samples no pathogenic bacteria could be detected, Staphylococcus hyicus could be isolated from the lung of both pigs by conventional bacteriological culture. To exclude an involvement of PCV2 an in situ hybridization (ISH) on inguinal lymph nodes was performed. No histologic lesions were found in the lymph nodes and no PCV2 was detected by ISH.Fig. 3

View Article: PubMed Central - PubMed

ABSTRACT

Background: In spring 2015, an outbreak of porcine reproductive and respiratory syndrome (PRRS) struck Lower Austria caused by a PRRS virus (PRRSV) strain spreading rapidly among both previously PRRSV negative and vaccinated pig herds. This case report describes the first well-documented emergence of the PRRSV strain responsible for this outbreak.

Case presentation: A PRRSV seronegative piglet-producing farm in Lower Austria encountered losses in foetuses and suckling piglets of up to 90 %; clinical signs in sows and nursery piglets included fever and reduced feed intake. Additionally, high percentages of repeat breeders and losses of up to 40 % in nursery piglets occurred. An infection with PRRSV was suggested by the detection of antibodies by enzyme linked immunosorbent assay and confirmed by quantitative real time PCR. The underlying PRRSV strain, termed AUT15-33, was isolated by passage on porcine alveolar macrophages, partially sequenced (ORF2-7) and grouped as PRRSV-1, subtype 1. In phylogenetic analysis of the genome region coding for the structural proteins, ORF2-7, AUT15-33 clustered with Belgian strains but identities were as low as 88 %. In contrast, analysis of ORF7 sequences revealed a close relationship to Croatian strains from 2012 with an identity of 94 – 95 %.

Conclusions: In the year following the outbreak, the same PRRSV strain was identified repeatedly in different regions of Austria. It can be speculated that the new strain has novel advantageous properties.

No MeSH data available.


Related in: MedlinePlus