CIRCOVIRUS INFECTION IN WILD BOAR

Christian Gortazar

IREC National Wildlife Research Institute (CSIC- UCLM- JCCM), Ciudad Real, Spain

Porcine circovirus type 2 (PCV2) is considered the aetiologi- cal agent of post-weaning multisystemic wasting syndrome (PMWS), a disease of pre-weaning and growing domestic pigs, which is also found in Eurasian wild boar.

PCV2 is a member of the genus Circovirus in the family Circoviridae. The genome contains three open reading frames (ORF): ORF1 encodes the replicase (rep and rep0) proteins involved in virus replication, ORF2 encodes the capsid (cap) protein and ORF3 encodes a protein that is not essential for PCV2 replication with potential apoptotic activities. Based on ORF2, the existence of two different genotypes within PCV2 (genotypes 1 and 2) has been sug­gested. Whereas pigs from PMWS-affected farms always harbour PCV2 genotype 1 (with or without sequences from genotype 2), pigs from non- PMWS affected farms had exclusively sequences from genotype 2⁽⁹⁾.

PMWS has been described worldwide. In Europe, infection or exposure to PCV2 has been reported in wild boar from several countries, including Belgium, Czech republic, Germany, Italy and Spain^(10,11). Infection can occur at any age, and no clear sex effect on prevalence exists. PMWS, however, only occurs at early ages. Manage­ment conditions, age of the host, viral genotype and infec­tion load with PCV2 are potential factors that influence the progress of the disease.

The high seroprevalence to PCV2, along with its wide­spread geographical distribution, suggest that PCV2 is endemic in the Eurasian wild boar. As this infection is widespread among domestic pigs, the reservoir role of wild boar is largely irrelevant. PCV2 is readily transmitted by direct and indirect contact. PCV2 primarily infects through close contact, such as nose-to-nose contact⁽¹²⁾.

The respiratory system may be the route of entry of PCV2, as suggested by the capacity of the virus to infect bronchial and bronchiolar epithelial cells. Alternatively, PCV2 may infect the nasopharynx and tonsils and spread via blood or lymph. The incubation period for develop­ment of PMWS in pigs is approximately 2 weeks. The infection with PCV2 is systemic and may persist for a long period, causing prolonged viral shedding. Pigs with PMWS have higher viral load in serum and tissues than subclini- cally affected pigs. PCV2 has been detected in ocular, faecal and urinary swabs. Oronasal secretions, urine and faeces are potential routes of viral shedding⁽¹²⁾. Antibodies are detectable in wild boar of all age classes¹-¹⁰).

Marked lymphocyte depletion with moderate granulo­matous histiocytic infiltration of lymphoid tissues was observed in 6- to 10- month- old wild boar piglets with PMWS⁽¹⁰⁾. Applying in situ PCR, viral genome was detected in the cytoplasm of macrophage-like cells in the lymph nodes, spleen, lung and liver. A small quantity of the PCV2 genome was also detected within the cytoplasm of epithelial tubular cells of the kidney¹-¹⁰’¹¹).

I n pigs, PMWS is clinically characterized by wasting, respiratory distress, pallor of the skin and, occasionally, jaundice¹-¹³). Reproductive disturbance, including abor­tion, infected stillborn and non-viable neonate piglets has been described in domestic sows. PCV2 infection can cause similar pathology in wild boar as in domestic pigs, causing immunosuppression and facilitating the occur­rence of secondary infections⁽¹¹⁾.

Serological methods for PCV2 include the immunoper­oxidase monolayer assay (IPMA) and ELISA. The presence of PCV2 can be demonstrated by isolation in cell culture and by PCR. Owing to the lack of specificity of the clinical signs, the definitive diagnosis of PMWS is based on a combination of three different criteria: clinical signs, the presence of specific lesions in lymphoid tissues (consisting of lymphocyte depletion and granulomatous inflamma­tion) and the presence of PCV2 in these tissues¹-¹³).

In the domestic pig industry, PCV2 infection is control­led through improved hygiene and by vaccination.

PMWS might play a role in the population dynamics of intensively managed wild boar populations, as indicated by the following observations. Firstly, fewer piglets than expected were observed in intensively managed areas; sec­ondly, juveniles from these sites had an extremely high seroprevalence suggesting recent PCV2 infection; and thirdly, a number of these farm-like areas reported abnor­mal piglet mortalities¹-¹⁰).

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