Transmission of PCV2 is thought to occur through direct contact via oronasal, fecal, and urinary routes (Bolin et al., 2001; Magar et al., 2000a). Shibata et al. (2003) investigated PCV2 shedding in experimentally-infected CDCD pigs and in pigs with naturally-acquired PMWS by PCR. Sixteen pigs were inoculated with PCV2 and oropharyngeal and nasal swabs, feces, whole blood, and serum became PCV2-DNA-positive immediately after inoculation and all samples with the exception of the oropharyngeal swabs (1/2 positive) which remained positive up to 70 DPI. In field samples collected from 313 pigs, PCV2 was detected in 95 (30.4%) of the whole blood samples, 60 (19.2%) of the nasal swabs, and 64 (20.4%) of the feces implying that whole blood and serum are the best samples for detection of PCV2 by PCR (Shibata et al., 2003). Segalés et al. (2005) quantified PCV2 DNA in tonsillar, nasal, tracheo-bronchial, urinary and fecal swabs of pigs with and without PMWS. The authors were able to detect PCV2 DNA in a high percentage of the samples and concluded that PCV2 is most likely excreted through respiratory secretions, oral secretions, urine, and feces of both PMWS-affected and clinically-healthy pigs, with higher viral loads in the PMWS-affected pigs. Yang et al. (2003) detected PCV2 nucleic acids in feces in pigs with (14/54 intestines, and 4/9 feces) and without (3/14 intestines and 16/20 feces) enteric disease by PCR suggesting fecal-oral transmission of PCV2 in feces.
Direct contact with pigs inoculated with virus 42 days previously resulted in transmission of virus to 3 of 3 control CDCD pigs (Bolin et al., 2001). Vertical transmission has been demonstrated to occur in individual sows in the field (Ladekjær-Mikkelsen et al., 2001; O’Conner et al., 2001) and experimentally (Johnson et al., 2002). There are reports of vertical intrauterine transfer of PCV2 resulting in viremic or persistently-infected piglets at birth (West et al., 1999). Vertical infection with PCV2 may not always cause fetal death, and virus, antibody, or both were detected in clinically normal fetuses (Sanches 2003).
Larochelle et al. (2000) infected four 7-month-old boars intranasally with PCV2. Serum samples were collected at 4, 7, 11, 13, 18, 21, 25, 28, 35, 55, and 90 DPI and were tested for the presence of PCV2 DNA by nested PCR. PCV2 DNA was detected as early as 4 DPI in 3 of the 4 boars and serum samples were positive up to 35 DPI but negative by 90 DPI. Semen was collected at 5, 8, 11, 13, 18, 21, 25, 28, 33, and 47 DPI and analyzed by nested PCR. PCV2 was detected as soon as 5 DPI in semen of two of the boars and intermittently through 47 DPI in all 4 boars. The semen of 2/4 infected boars was positive for PCV2 DNA at 47 DPI (Larochelle et al., 2000). Kim et al. (2003) tested semen from ninety-eight 1-year-old boars from 49 herds in Korea and found 13 of 98 semen samples to be positive for PCV2 by first round (conventional) PCR, 26 of 98 semen samples were positive by semi nested PCR, and 11 of 98 semen samples were positive by virus isolation. The same study also investigated prevalence of PCV2 in seminal fluid, non-sperm cells, and sperm heads, and detected the greatest amount of PCV2 DNA in the seminal fluid and nonsperm fraction (Kim et al., 2003). The frequency of PCV2 DNA in semen from naturally infected boars was found to be low and sporadic (McIntosh et al., 2005). The authors concluded that boars seropositive for PCV2 may have persistent shedding of the virus in semen. PCV2 DNA in semen didn’t appear to affect the percent of morphologically-normal or live sperm cells in PCV2-shedding boars and boars older than 17.5 month of age did not appear to shed PCV2 DNA in semen (McIntosh et al., 2005).
PCV1 and PCV2 DNA were detected in porcine-derived commercial pepsin (Fenaux et al., 2004). It was found that the PCV-contaminated pepsin lacks infectivity in vitro and also in vivo as determined by culture in PK-15 cells and experimental inoculation of pigs (Fenaux et al., 2004).
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