Biology Reference
In-Depth Information
TABLE 4.1 Host and pathogen traits that may influence disease severity and outcome
Host traits
Pathogen traits
Host polymorphisms (e.g. cytokine
promoter polymorphisms shaping the
immune response)
Parasite polymorphisms (e.g. virulence genes)
Nutritional status
Infection frequency (e.g. biting rates of infected
mosquitos)
Age and sex
Infection intensity (e.g. intense acute infection
or low grade chronic infection) (see Chapter 13)
Presence of co-infection generating
pre-existing host immune responses
Presence of co-infection utilizing host resources
are more likely to have G. duodenalis co-infection than individuals infected
with Ascaris at a lower (
5000 egg/g feces) intensity
4
suggesting that this
could be the case in some situations. Ascaris co-infection could alter the
establishment and/or the transmission of a co-infecting pathogen. This
could occur if disruption of the epithelial barrier lining the GI tract
facilitates the establishment of certain viral or bacterial infections. It is
also possible that the establishment of a regulatory immune response
by Ascaris infection inhibits the generation of Th1 immune responses or
Th2 responses leading to less efficient clearance of co-infecting micro-
pathogens or GI-helminths, respectively. However, it is not always
the case that Ascaris-generated immune responses are dominant in a
co-infection setting
5
and the level of immune interaction is likely to differ
depending on the particular co-infecting pathogen.
From the perspective of the co-infected host, it has been reported that
disease severity can be altered in Ascaris-co-infected individuals. There are
situations where this could be beneficial (for example, protection against
cerebral malaria
6,7
) or detrimental (for example, lowering of CD4
<
Tcell
numbers in HIV infection
8
which may contribute to the progression of
AIDS). Both of these examples are discussed in more detail later in this
chapter. Current hypotheses on the mechanisms behind such observations
center on interactions mediated by the immune system. Ascaris can induce
an immune response that can act systemically and potentially interact with
the generation and efficacy of immune responses against most other
pathogens in a co-infection setting. However, localized immune interac-
tions could also occur in the liver or lungs where immune responses are
generated by migrating Ascaris larvae in the context of pre-existing
responses already active against co-infecting pathogens residing in these
organs. In the gut, long-lived adult Ascaris nematodes persist by main-
taining an anti-inflammatory environment that may interact with immune
responses generated by common infections of the GI tract, particularly
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