Whether and how microparasites such as rabies persist in their host po
pulations are among the fundamental questions of infectious disease ep
idemiology. Rabies is a fatal disease of all mammalian species, but no
t all mammalian species can maintain the infection as reservoirs. The
approach to control depends on which of the affected species do act as
reservoirs. Bringing together old and new data, we examine here the r
ole of wild and domestic animals in maintaining rabies in the Serenget
i region of Tanzania, presenting our findings in two parts. In Part I,
we argue that domestic dogs are the likely reservoirs because: (1) ra
bies has been continuously present in the dog population since its (re
)introduction in 1977, whilst (2) wildlife cases have been very rare o
ver this period, despite intensive study of Serengeti carnivores; (3)
outbreaks of rabies in wild canids (jackals) elsewhere in Africa (Zimb
abwe) have followed, rather than preceded, outbreaks in the dog popula
tion; (4) all viruses isolated from wild carnivores in the Serengeti e
cosystem (including the Kenyan Masai Mara) are antigenically and genet
ically indistinguishable from the typical domestic dog strain; (5) dog
rabies control in the Serengeti between 1958-77 apparently eliminated
the disease from both dogs and wildlife. Having identified dogs as re
servoirs, Part II explores some possible mechanisms of maintenance in
dog populations. In theory, infection is more likely to be maintained
at higher dog densities, and we provide evidence that rabies is mainta
ined in one district with a dog density > 5/km(2), but not in two othe
r districts with densities < 1/km(2). Because 5 dogs/km(2) is much low
er than the expected density required for persistence, we go on to inv
estigate the role of atypical infections, showing: (1) from serology,
that a substantial proportion of healthy dogs in the Serengeti have de
tectable serum levels of rabies-specific antibody; (2) from mathematic
al models that, whilst we cannot be sure what seropositivity means, pe
rsistence in low-density dog populations is more likely if seropositiv
es are infectious carriers, rather than slow-incubators or immunes.