Clinical Manifestations of Senecavirus A Infection in Neonatal Pigs, Brazil, 2015

We identified new clinical manifestations associated with Senecavirus A infection in neonatal piglets in Brazil in 2015. Immunohistochemical and molecular findings confirmed the association of Senecavirus A with these unusual clinical signs and more deaths. Other possible disease agents investigated were not associated with these illnesses.


The Study
Since early 2015, increased numbers of deaths were recorded in pig herds from different geographic regions of Brazil. Piglets during their first week of life demonstrated clinical signs such as muscular weakness, lethargy, excessive salivation, cutaneous hyperemia, neurologic manifestations, and diarrhea; some died suddenly. Clinical signs lasted for 3-10 days and then disappeared in piglets that survived.
To determine the cause of these illnesses, we investigated 5 farms (A-E). Pig populations per farm varied from 10,000 to 23,000 animals, and piglet death rates during the first week of life ranged from 20% to 30%. Ten piglets that died spontaneously were examined (Table 1).
Farms A, B, D, and E had gestating and/or farrowing sows with fluid-filled or ruptured vesicles at the coronary bands, hooves, or snouts; reproductive disorders were not observed. We had identified SVA RNA from sows at farms A and B (3) a week before the onset of clinical manifestations in these piglets.
Routine necropsies of all piglets were conducted soon after death. Tissues were fixed by immersion in 10% buffered formalin solution and processed for histopathologic evaluation. Selected tissue fragments were used in an immunohistochemical (IHC) assay designed with monoclonal antibodies to detect SVA (5). Duplicate sections of the organs and scrapings from oral vesicles and cutaneous lesions were collected for molecular diagnostics. From piglets at farms C, D, and E, we collected diarrheic fecal samples to investigate the possibility of enteric viruses. We analyzed 81 tissue samples and 6 diarrheic fecal samples during this study by a combination of pathologic and molecular diagnostic methods.
Consistent SVA IHC staining occurred at the transitional epithelium of the renal pelvis and the urinary bladder    accession no. KC667560) and 94.4% aa (GenBank accession nos. EU271759 and EU271760) to 99.4% aa (Gen-Bank accession no. KC667560) for isolates identified in North America. Phylogenetic analysis showed that the strains from this study (GenBank accession no. KT445973-KT445977) clustered with other known isolates of SVA and were distant from other picornaviruses associated with vesicular diseases (Figure 2).

Conclusions
SVA has been associated with PIVD in pigs with vesicular lesions at the snout, coronary band, and hooves (1-3). However, findings from our investigation suggest a new clinical syndrome associated with SVA infection that resulted in disease to multiple tissues and organs of these piglets.
The patterns of the cutaneous lesions identified in this study might be similar to those of other vesicular infections of picornavirus (FMDV and SVDV), in which ballooning degeneration of epithelial cells and the formation of microvesicles are hallmarks (14,15). In addition, FMDV and SVDV affect different organs of susceptible animals-the heart, lungs, lymph nodes, bone marrow, and central nervous system (14,15)-suggesting a wide organ tropism of these viruses.
An interesting feature during this study was the constant immunolabelling of SVA within epithelial cells of the choroid plexus of the brain and the surrounding endothelia of blood vessels in piglets with neurologic disease. On the basis of the IHC results and molecular findings in different tissues of the brain, we theorized that the neurologic manifestations of SVA observed during this investigation might be due to early infection of the choroid plexus through alteration of the integrity of the vascular epithelium and subsequent dissemination to the adjacent neuropil. The IHC detection of SVA within the urinary epithelium of all piglets suggests that urine might be a mode of dissemination and a possible source of contamination within affected pig farms.
Another unusual finding associated with SVA infection during this study was the occurrence of diarrhea in piglets. Molecular screening did not detect any of the common enteric viral pathogens of suckling piglets. However, the IHC and reverse transcription PCR identified SVA in the small intestine of piglets with diarrhea, demonstrating the ability of SVA to replicate within the enteric epithelium.
Our results suggest that SVA is a pantropic virus that produces a multisystemic disease entity in pigs infected at an early age. The constant immunolabelling of the uroepithelium of all piglets with SVA antigens might indicate that in-pen contamination, through urine, should be considered as a possible route for the dissemination of this virus. Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 22, No. 7, July 2016 Search past issues of EID at wwwnc.cdc.gov/eid