PRRS symptoms

The clinical presentation and clinical signs of PRRS varies greatly between herds. Infection with PRRSV shows two different sets of clinical signs: reproductive and respiratory. 

Reproductive symptoms

In non-immune sows the course on the infection is radically different depending on whether the sow is pregnant or not.

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Respiratory symptoms

PRRSV infection in weaned pigs is characterized by fever, pneumonia, lethargy, and failure to thrive.

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The clinical course of PRRSV infection depends on the age, on the physiological (pregnancy status and trimester of gestation of the infected sow/gilt) and specific immune status of the animal and on the virulence of the infecting strain.

In general two main syndromes are associated with PRRSV: reproductive failure in pregnant sows and respiratory disease in piglets.

Studies found that pigs experimentally infected with nine different isolates of Type 2 PRRSV had major differences in clinical disease, rectal temperatures, and gross and histological lung lesions. Animals infected with mildly virulent isolates or the LV had transient pyrexia, dyspnea and tachypnea, whereas infection with highly virulent isolates induced labored breathing, pyrexia, lethargy, and anorexia. Furthermore, studies have reported that the impact on reproductive performance may be isolate dependent. 

hpPRRS: a High Fever Disease 
From time to time highly virulent PRRSV strains evolve, which results in poor welfare for the pigs and huge economical losses for the swine industry.
In China in 2006, a severe ‘high fever’ disease occurred in several pig farms and subsequently overwhelmed almost half of China. The list of clinical symptoms was long: rubification, blood spots, petechiae, erythematous blanching rashes, and pimples, frequently observed in ears, mouth, noses, back, and the inner thigh. Other common symptoms were high fever (40-42°C), depression, anorexia, cough, asthma, lameness, shivering, and disorder in the respiratory tract, diarrhea, and subsequently death. Initially, the ‘high fever’ was suspected to be caused by hog cholera or African swine fever and PRRSV was not suspected as the etiology agent because many grown pigs died, which is unlike typical PRRSV infections. The course of the disease varied from 5 to 20 days, and pigs infected were highly contagious affecting the whole pig herd within 3-5 days. The epidemic persisted for several months partly due to the limited knowledge of the etiological agent. According to the China Animal Disease Control Center (CADC), the epidemic affected more than 2 million pigs with more than 400,000 fatal cases in just 4 month of duration. The etiological agent was found by extensive and systematic investigations, and by PCR and immunohistochemistry experiments the ‘high fever’ agent was determined to be PRRSV. Today the atypical PRRSV strain is referred to as highly pathogenic PRRSV (HP-PRRSV). Shortly after the epidemic of HP- PRRSV in China, it rapidly spread to pigs in Southeast Asia and nearby countries.

Phylogenetic analysis of HP-PRRSV ORF5 sequences revealed that they were very similar to typical Chinese PRRSV isolates. To study the evolutionary origin of the HP- PRRSV, complete HP-PRRSV genome sequences were compared to typical Chinese PRRSV genomes and it was suggested that the HP-PRRSV had gradually evolved from an early Chinese PRRSV, CH-1a, and the evolutionary path could be traced through intermediate PRRSV isolates. Furthermore, genetic analysis found in all HP-PRRSV isolates examined, a distinct 1 plus 29 amino acid deletion in nsp2 which at first was believed to be a virulence marker, however chimeric infectious clone constructs and the finding of a low pathogenic field virus also harboring deletion at the same position showed that this unique deletion was not directly related to virulence