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development of effective parasite clearance mechanisms ( Figure 4.2 ). In
particular, the Th2 environment generated in Ascaris infection may favor
the generation of non-cytophilic antibody isotypes from B cells
responding to a malaria challenge ( Figure 4.2 ), possibly reducing the
clearance capacity of antibodies in the circulation and predisposing the
host to malaria symptoms in some situations. 66
Much remains to be learned about the interactions of malaria and
Ascaris during co-infection. Defining the conditions under which Ascaris
protects against malaria pathogenesis or enhance transmissibility of
malaria infection is of great importance in the context of mass de-
worming programs.
HYPOTHETICAL EFFECTS OF LOCALIZED
CO-IN FECTIONS ON ASCARIS CO-INFE CTION
The majority of studies examining co-infection biology in patients with
Ascaris infection and other pathogens almost exclusively report results
with respect to the “other pathogen.” Although almost nothing is known
about the effects of co-infection on Ascaris biology and pathogenesis, it is
possible to theorize about possible effects and associated mechanisms
( Figure 4.3 ). For the final part of this topic chapter we consider how
co-infecting pathogens localized to specific organs of the body may have
an impact on Ascaris infection. Specifically we will discuss possible effects
GASTROINTESTINAL TRACT
Possible co-infecting pathogens:
￿ Trichuris trichiura
￿ Strongyloides
￿Hookworm
￿Diarrheal pathogens caused by
protozoan parasites, bacteria and viruses (e.g.
Giardia,Cryptosporidium, amoebiasis,
Salmonella,Shigella , rotavirus)
LUNGS
Possible co-infecting pathogens:
￿Respiratory syncitialvirus
￿ Mycobacterium tuberculosi s
￿ Plasmodium sp.
Hypothetical effects on Ascaris infection:
￿Pre-existing immune responses that alter
larval migration through the lungs
￿Alteration in susceptibility to the
development of Loeffler's syndrome
Hypothetical effects on Ascaris
infection:
￿Alteration in mucous production and
shedding may make it harder for newly-
hatched larvae to penetrate the gut wall
￿Pre-existing immune responses may modify
the generation of anti- Ascaris immune
responses affecting adult longevity in the gut
￿Alterations in mucous production, peristalsis
and nutritional availability may affect adult
longevity in the gut
￿Alterations in adult nematode establishment
may change reproductive capacity (both in
numbers of excreted eggs, and the ratio of
fertilized to unfertilized eggs).
￿Changes in the number of adult nematodes
in the lumen of the intestine may alter the
level of intestinal obstruction
LIVER
Possible co-infecting pathogens:
￿ Schistosoma mansoni
￿Hepatitis B virus
￿ Plasmodium sp.
Hypothetical effects on Ascaris
infection:
￿Pre-existing immune responses that alter
larval migration through the liver
FIGURE 4.3 Hypothetical effects of co-infecting pathogens on Ascaris migration,
establishment, fecundity, and pathogenesis.
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