Nipah
virus first infected humans in 1997 in the Ipoh area but may have infected
pigs as early as 1996. The 1998-1999 epidemic may have resulted from a
spillover event a year or two earlier which took off due to pig transport or
changes in farm type, or it may have resulted from a recent jump to an
appropriate index farm. Infection was probably acquired from Pteropus
vampyrus, which began foraging around Nipah in 1997. Infection was sustained
in pigs within farms by aerosolized transmission, direct contact, and the
reuse of needles during the JE vaccination program. Disease moved between
farms via a “fire sale,” black market transport of infectious but
asymptomatic pigs, and potentially iatrogenic spread via vaccinations.
Seroprevalence surveys indicate that not all humans infected with NiV became
clinically ill. Of those that did, about half did not report contact with
symptomatic pigs, and a significant fraction report having no contact with
pigs at all. Dogs and probably cats and/or goats were responsible for some
infections. There were no reports of transmission between humans, though it
may have occurred. Like HeV, NiV infections can relapse a year following
acute illness. Photo: H. Field.
Little is known about the clinical pathology of NiV or its dynamics in natural host populations. Appropriate sample sizes have been obtained for only four bat species in the wild, and anti-NiV antibodies have been found in five. Real prevalence, indicated by virus isolation in urine, may be quite low. Virus may be shed seasonally. The mechanism of horizontal and vertical transfer between bats and from bats to other animals may be via placental tissue and birthing fluids, urine, and/or fruit. HeV studies indicate the first route may dominate.
Author: S. Cobey.