Thesis
Peste des petits ruminants (PPR), one of the most economically important disease of
small ruminants has been earmarked for eradication following the successful global
eradication of rinderpest. The disease is caused by peste des petits ruminants virus
(PPRV).
For eradication to be successful, the different PPR situations and
contexts in each region and country must be well understood and reflected upon. In this
study, the objective was to conduct an epidemiological assessment of the spread and
persistency of PPR in selected areas of Tanzania with focus on distribution of antibodies
to PPRV, PPRV genetic diversity and identification of practices by small stock farmers in
response to this disease.
The study was carried out using samples collected between 2013 to 2016. Sera samples
were collected from clinically healthy sheep and goats for detection of antibodies to
PPRV, together with blood, swabs and tissues for detection of the virus using molecular
assays.
A questionnaire was also administered in order to collect demographic
characteristics, knowledge and practices relating to this disease from small ruminant
farmers during sample collection. The overall true seroprevalences from samples
collected in 2013 and 2015 was 27% (n = 3838) and for samples collected in 2016 was
30% (n = 328). Seroprevalences for samples collected in 2013, 2015 and 2016 show that
the disease is continuing to spread in the country as seropositivity was observed in
regions where previously no disease had been reported. Presence of the virus was found
in samples collected in Morogoro and Arusha regions in 2016. Molecular characterization
of the virus clustered them into two lineages, II and III. This confirmed presence of two
lineages circulating in animals from the same herd, adding another dimension into the
complexity of the disease in Tanzania.
Other findings were confirmation
of co-infections with Mycoplasma capricolum subspecies capripneumoniae, Pasteurella
multocida and Capripoxvirus which cause similar clinical signs to PPR, complicating
clinical diagnosis but emphasizing the importance of laboratory confirmation. Small
ruminant farmers’ knowledge by regions on the disease occurrence was found to be high
in Arusha region (northern Tanzania) and low in Morogoro region (eastern Tanzania),
corresponding with the seroprevalences observed from samples collected in 2013, 2015
and 2016 in the said regions. Risk practices identified during outbreaks included trading
of live animals, use of veterinary drugs and unattendance to sick animals. These risk
practices could facilitate the spread of the disease in the country especially as the disease
is transmitted through contact with infected animals. In conclusion, this study has
revealed that PPR continues to spread within Tanzania as evidenced by antibodies to
PPRV detected in areas that previously did not have the disease. Presence of two PPRV
lineages shows the ability of lineages to co-circulate in an endemic area as well as in the
presence of co-infections with other diseases in the local herd.
Overall, there is poor knowledge by small ruminant farmers in the study areas that may be
contributing to the spread of PPR. It is therefore recommended that annual vaccinations
be carried out after well designed participatory surveillances are conducted to improve the
herd immunity to levels that can contain the spread of PPR as a control measure. These
vaccinations should take into consideration the geographical distribution of PPR in
Tanzania so as to create buffer zones to stop further spread to areas with low or no
disease, within and in neighboring countries. Genetic diversity of the virus strains
circulating in the country should be further investigated by whole genome sequencing and
how they compare to other strains. To prioritize on small ruminant farmer’s knowledge
on the disease and emphasize how their participatory disease surveillance can help with
the ultimate goal of eradicating PPR in Tanzania, regionally and globally.
Southern African Centre for Infectious Disease Surveillance,
SACIDS, (grant WT087546MA from the Wellcome Trust) and Swedish Research
Council (grants 348-2013-6402 and 348-2014-4293)