Biology Reference
In-Depth Information
EPIDEMIOLOGY OF ASCARIASIS: THE ROLE OF
NONRANDOM CLUSTERING
It has long been recognized that Ascaris infections are typically
overdispersed, meaning that a small proportion of the available
human host population harbors the majority of the parasitic worm
population.
21,22
As reviewed by Holland,
2
this epidemiological pattern
has been observed repeatedly in populations throughout the world (see
also Chapter 7).
In addition to overdispersion, clustering of infections also has been
observed frequently. This clustering is often seen at the familial or
household level. For example, Forrester and colleagues
23
documented
household clustering of heavy Ascaris infections in a population in
Mexico. They went on to suggest a familial or genetic basis to this clus-
tering.
24
In a study of Ascaris infections in the Poyang lake region of
China, clustering of infections by household was observed.
25
Similarly,
Walker and colleagues
26
examined Ascaris infections in approximately
3000 individuals belonging to about 500 families living in Dhaka,
Bangladesh. They found significant evidence for clustering by household,
although they fit no formal genetic models that might account for such
clustering.
26
Studies examining reinfection with A. lumbricoides have repeatedly
provided evidence that individuals are predisposed to infection. This
predisposition has been documented in numerous studies and numerous
populations
27
e
29
(see review in
2
) (see also Chapter 7). Recently, Mehta
and colleagues
30
documented maternal effects on risk for Ascaris infec-
tion, with children of mothers with Ascaris infections having increased
risk of infection.
The epidemiological literature on A. lumbricoides provides significant
evidence for nonrandom clustering of infection that is due to shared
exposure, worm genetic factors, host genetic factors or, as is more likely,
some combination of all of these causal players. As part of our long-
running research program, we have focused on the potential role of
host genetic factors in Ascaris infection. Differentiating between
household effects (or shared exposure) and effects associated with
individual risk requires an advanced genetic approach. Quantitative
genetic approaches can be used to distinguish the effects of individual
predisposition from household effects. However, in order to utilize such
quantitative genetic approaches, some kind of family information is
required. Even in the absence of genetic marker information (which
itself can be used to infer pedigree relationships), pedigree information
for large extended families crossing multiple households does provide
you with power for genetic analysis. Pedigrees of the type required for
