Peste des petits ruminants (PPR), also known as "Goat Plague" is highly contagious and one of the most economically important World Organization for Animal Health (OIE) notifiable diseases of sheep and goats. The causative agent, PPR virus (PPRV) is genetically grouped into four lineages (Ⅰ, Ⅱ, Ⅲ, and Ⅳ) on the basis of partial fusion (F) protein gene sequence analysis, of which lineage Ⅳis restricted to Asia and the other lineages are prevalent in Africa [8, 19]. The disease is enzootic in the
Middle East, the Arabian Peninsula and parts of Africa and Asia. Despite strict control measures including statutory regulations along with availability of various diagnostics and live attenuated PPR vaccines [5, 9, 22], the infection still remains a constant threat to livestock.
PPR is considered as one of the major constraints in improving the productivity of small ruminants in India since its first report in Tamil Nadu during 1987 . In India, vaccination is the most effective means of control and the current strategy involves vaccinating small ruminants (sheep and goats) by using attenuated lineage ⅣPPR vaccines  along with sero-monitoring/surveillance using monoclonal antibody based PPR competitive ELISA (c-ELISA) . Currently available PPR vaccines  including thermo-adapted  and deuterated  PPR vaccines may suffice to protect against the circulating PPRVs in India. The former vaccine provides long-term protective immunity in goats  and has undergone extensive field trials in sheep and goats, apart from efficacy, thermo-stability, immunogenicity and pathogenicity [11, 16, 17, 20].
PPR is enzootic in India and vaccination has routinely been employed since 2002 . The age at which offspring can effectively be immunized is proportional to the amount of protective antibody they received from their dams. Protective immunity can be produced through vaccination, when the maternal antibodies recede to a low level in kids, whereas high levels of maternal antibodies would block the effectiveness of the vaccine. There is a window of susceptibility period from several days to weeks in which the maternal antibodies are too low to provide protection against the disease, but too high to allow a vaccine to work. This is the period where a young animal can still contract the disease despite being vaccinated. The efficacy of the African lineage vaccine strain against PPR and its colostral immunity had been previously demonstrated .
Therefore, the present study was conceived to investigate the decay of maternal PPRV antibody in kids born to goats vaccinated with Asian lineage vaccine and the efficacy of the passive immunity against PPRV to determine the optimum period (at which maternal antibodies probably would no longer interfere with vaccination of kids) for vaccination in goats.
All vaccinated animals which were maintained for a study period of one year (so far tested) developed protective antibody levels two weeks after vaccination, with 61 to 96 percentage inhibition (PI) of PPRV H antibodies when tested by PPR c-ELISA (Fig. 1). Control unvaccinated goats did not show any positive PPRV-specific antibodies threshold (had PI value of 35 to 35.9 in c-ELISA). The vaccinated, infected and unvaccinated goats became pregnant. A total of four kids were born to vaccinated goats at different intervals over a period of time.
Figure 1. Sero-monitoring of PPR vaccinated goats by using PPR competitive ELISA. Solid line shows negative/positive cut-off. Samples tested positive for PPRV H antibodies after 21st days post-vaccination (DPV) with PI value ranging from 61 to 96.
After 3–4 weeks of vaccination, the first kid was born to vaccinated pregnant doe number 2. The range of intervals between dam vaccination and kid delivery are shown in Table 1 with PI value of PPRV H antibodies in the dams near to the time of parturition. Maternal antibodies in kids born to vaccinated goats were detectable up to 6 months of age but decline in antibody titers was observed at slow rate from the second month and rapid rate from the third month and it finally reached below the protective or negligible level at the fourth month with no significant differences in both sexes. Similarly, two kids born from the infected dams had a similar pattern of maternal antibody decay with a protective titer at the age of 5-6 months. However, the three kids born from the unvaccinated dams did not show any PPRV-specific passive antibodies. Maternal antibody decay in kids born from immunized or exposed/infected dams is presented in Table 2.
Table 1. Antibody titers in vaccinated female goats at the time of kidding
Table 2. Pattern of maternal antibody decay in kids born to vaccinated or infected dams
One of the kids having an SN titer of 1:8 was vaccinated, which had significant PPRV-specific protective antibody response (PI = 76 and SN titer > 1:16) when tested on 21 dpv and was completely protected from a virulent virus challenge. Similarly, a directly challenged kid having an SN titer of 1:8 was completely protected from PPR. Furthermore, PPRV antigen/ nucleic acid was not detectable by s-ELISA and RT-PCR assay in the natural secretions of post challenged kids, whereas the experimentally infected control kids showed pyrexia (105.6 ℉ or 40.9 ℃) and naso-ocular discharges from day 4 post infection (DPI), and the collected samples (nasal, ocular and oral swab) were found positive for PPRV antigen /nucleic acid sequences. Using RT-PCR, the detection of virus nucleic acids in these samples as early as from 5th to 15th DPI was observed. The same samples, when tested by s-ELISA, detected the virus antigen in clinical swabs at 7–12th DPI. The details of results of virus identification in the experimental study by s-ELISA and RT-PCR are shown in Table 3 and depicted in Fig. 2.
Table 3. Details of results of virus identification in experimental challenge study