Biology Reference
In-Depth Information
The authors emphasized an IgE-mediated mechanism as the likely cause of anaphy-
lactic reactions following snakebites (Reimers et al., 2000).
Whether hypersensitivity develops from a snakebite or other provoking factor, mast
cells are known to participate in the induction of hypersensitivity/inflammation through
interaction of antigen with specific IgE bound to the high-affinity receptor for IgE
(Fc
RI; Tkaczyk et al., 2002). However, the possible contribution to this phenomenon
of IgG subtypes cannot be excluded. For example, several investigators have identified
the anaphylactic role of a subtype of IgG
4
(Bryant et al., 1975; Parish, 1970). Human
mast cells and basophils contain high-affinity IgG receptors (FcgRI) that are activated
and release pro-inflammatory mediators in immediate hypersensitivity reactions via IgG
aggregation (Iwaki et al., 2005; Tkaczyk et al., 2002). Mediator release resulting from
the activation of either Fc
RI or FcgRI is reportedly indistinguishable (Okayama et al.,
2001). Comparison of human and murine mast cell degranulation suggests that some
of these responses may be species-specific (Tkaczyk et al., 2004). These findings sup-
port a complex relationship between the well-established hypersensitivity-antagonizing
(“blocking”) function of some IgG
4
isotypes (as are developed during desensitizing
immunotherapy; Greenberger, 2002), and the pro-anaphylactic activation properties of
others. Therefore, previous exposures to ophidian buccal secretion/venom antigens and
antigens encountered as a consequence of exposure to snake products/shed skins may
stimulate the development of complex sensitizing antibodies of g and
classes.
Type 1 hypersensitivity commonly presents with clinical manifestations that may
be cutaneous (urticaria, pruritus), subcutaneous (angioedema), lymphatic (lymphan-
gitis), GI and uterine (smooth muscle contraction), respiratory (bronchospasm), and
cardiovascular (hypotension/shock, etc.). In the most frequent local disease, urticaria
is common but not invariably present. Urticaria and angioedema may occur together
or separately (Fauci et al., 2009). Thus, the absence of urticaria in a given case of
suspected hypersensitivity should not preclude the diagnosis if supported by avail-
able evidence (see Section 4.2,
Thamnophis
;
Table 4.1
).
Uncomplicated local effects constitute the majority of symptoms/signs described in
the relatively limited number of well-documented cases of medically significant non-
front-fanged colubroid bites (
Table 4.1
; Section 4.1). It is unproven, but likely, that in
some patients these effects (erythema, pruritus, edema, and blistering, etc.;
Table 4.1
)
are a combination of Type 1 hypersensitivity, and the local effects of Duvernoy's secre-
tion components (Weinstein and Keyler, 2009). Some cases may feature more exten-
sive blistering, edema, and lymphangitis, and thus can resemble mild-to-moderate local
envenoming from a crotaline viperid species (Weinstein and Keyler, 2009; however,
see
Plate 4.92A-F
and p. 219). Unfortunately, to date there are no data regarding IgE
or IgG levels in patients presenting with medically significant effects from non-front-
fanged colubroid bites. Such information is very desirable and should be collected by
performing the necessary serology whenever possible. Evidence of hypersensitivity in
any patient should be managed with epinephrine, antihistamines, leukotriene receptor
antagonists, fluid resuscitation, corticosteroids, and airway support as clinically indi-
cated.
