African swine fever convalescent sows: subsequent pregnancy and the effect of colostral antibody on challenge inoculation of their pigs.

The effect of African swine fever (ASF) virus infection on reproductive performance of recovered sows and their pigs was investigated. Six sows were inoculated with a 1979 ASF isolate from the Dominican Republic. One sow was bred on postinoculation day (PID) 58 and killed on PID 148. Four sows were bred between PID 368 and 419 and were allowed to farrow. One sow did not conceive. Samples collected during pregnancy, at farrowing, and during lactation were tested for virus by tissue culture and animal inoculations to determine whether ASF virus recrudesced during these natural stresses. Virus was recovered only from tissues of the sow killed on PID 148. Virus was not detected in tissue samples from the 4 other sows or from any fetus or neonate. Sow and neonatal pig sera, colostral whey, and milk whey were assayed for antibodies against ASF viral antigens, using an enzyme-linked immunosorbent assay. Antibody values in sows' sera did not change appreciably during pregnancy, farrowing, or lactation. One litter of pigs was raised with their sow. Weekly serum samples were tested for passively acquired antibodies. At 7 weeks of age, the litter was challenge inoculated with the same virus as that used initially to infect their dam. Viremia titers, duration of viremias, and clinical course were reduced. One young pig did not develop fever, viremia, clinical disease, or antibody response to virus challenge exposure. The altered course of infection was attributed to protective effect of passively acquired antibodies.

African swine fever in neonatal pigs: passively acquired protection from colostrum or serum of recovered pigs.

The effect of passively acquired antibodies on the course of African swine fever (ASF) virus infection was investigated in hysterotomy-derived neonatal pigs fed colostrum from an ASF-recovered sow or given ASF virus antiserum. Thirty neonatal pigs were assigned to 5 study groups: (i) colostrum-deprived, (ii) fed colostrum from a normal sow, (iii) fed colostrum from an ASF-recovered sow, (iv) given ASF virus antiserum, and (v) noninoculated controls. Pigs were inoculated oronasally with 10(6.1) median hemadsorption units (HAd50) of a Dominican Republic ASF virus isolate. The progression of ASF infection was monitored by measure of rectal temperature, viremia titers, antibody response, and observation of attitude. The clinical course of ASF infection was markedly different in young pigs in the various study groups. On postinoculation day (PID) 4, ASF viremia titers for pigs receiving colostrum from an ASF-recovered sow or ASF virus antiserum (mean = 3.2 +/- 1.88 log10 HAd50, n = 10 pigs) were significantly lower (P < 0.001) than viremia titers of colostrum-deprived pigs or of those fed normal colostrum (mean viremia titer = 7.8 +/- 0.55 log10 HAd50, n = 14 pigs). All pigs not given colostrum or serum (n = 15 pigs) from swine recovered from ASF were dead by PID 16. By PID 30, only 1 pig that received colostrum or antiserum (n = 10 pigs) from the sow recovered from ASF had died. To determine whether the protective effect of ASF antiserum resided within the immunoglobulin (Ig) fraction, 4 pigs that had acted as noninoculated controls for the 1st experiment were given 125 mg of ammonium sulfate precipitated Ig from the ASF virus antiserum used in the initial study (intraperitoneally). The 5th pig was not given Ig (nontreated-inoculated control). All 5 pigs were inoculated oronasally with 10(6.1) HAd50 of Dominican Republic ASF virus. The nontreated control pig died on PID 10 and 3 Ig-treated pigs died on PID 17, 23, and 24. The 4th Ig-treated pig survived. Although administration of precipitated ASF Ig did not completely protect against clinical ASF infection or death, the course of infection was markedly altered.