Biology Reference
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Epstein-Barr virus], recent surgery, and occasionally immunization (Keenlyside et al.,
1980; Longmore et al., 2001; Sindern et al., 2001). Features supporting a diagnosis
of GBS include (but are not limited to): progression up to about 4-5 weeks; closely
symmetric signs/symptoms; mild sensory symptoms, if present at all; bilateral facial
weakness; autonomic dysfunction, and early recovery at about 2 weeks at the comple-
tion of the progressive symptoms (Longmore et al., 2001). Although the patient did
not exhibit facial weakness or apparent facial nerve involvement, many other fea-
tures are consistent with GBS or a related, less-defined polyradiculitis. Even though
recovery from these syndromes commonly occurs, fatalities certainly are well docu-
mented, and mortality from GBS has been estimated at approximately 10% (Longmore
et al., 2001). Therefore, although the authors fairly rigidly define their analysis of the
patient's etiology, the basic presentation and features, as well as the fatal outcome, can
be compatible with GBS or a closely related polyneuropathy.
In this regard, it is also reasonable to briefly consider acute polyradiculitis, pos-
sibly related to the provision of tetanus toxoid. Acute polyradiculitis often initially
presents as a paresthesia that begins from the lower extremities and develops into a
symmetrically ascending myasthenia. The symptomatology is variable and may fea-
ture mild asthenia or complete tetraplegia, as was seen in the reviewed case (Chroni
et al., 2005; Kärppä, 2009). These symptoms may be accompanied by autonomic
dysfunction, cranial nerve palsies, or asphyxia (Kärppä, 2009). Areflexia, ataxia,
and ophthalmoplegia can be noted in the rarer Miller Fisher syndrome (Longmore
et al., 2001). Although there are no specific laboratory tests for acute polyradiculi-
tis, a common finding is acellular CSF containing elevated protein (Kärppä, 2009).
Prognosis is usually good, but up to 20% may have functional impairment and fatali-
ties are well documented (Kärppä, 2009). Thus, in the reviewed case, the patient's
course, test results, and outcome are consistent with GBS or another less-defined
acute polyradiculitis.
Interestingly, there are a few documented cases of GBS or related polyneuropathy
postenvenoming from elapids or crotaline viperids (Chuang et al., 1996; Ekenback
et al., 1985). These are readily distinguishable from the case reported by Chroni
et al. (2005), as they all involved serious envenoming. However, although these are
likely related to the reported post-envenoming polyneuropathy, it still must be con-
sidered that even these cases may have alternative explanations (e.g., an unreported
recent viral infection).
The patient in this case did not have a postmortem (Chroni et al., 2005). An
autopsy might have facilitated an improved understanding of the neuropathy.
Neuropathological investigation of a 36-year-old male who succumbed to an inflam-
matory polyradiculopathy (posthepatitis B vaccination) showed severe axonal loss with
peripheral nerve demyelination and mononuclear cell infiltration in nerve roots and
spinal ganglia (Sindern et al., 2001). Therefore, with the available information regard-
ing this case, the authors' proposed linkage between the
P. najadum
bites and the fatal
progressive neuropathy is far less likely than the probability of GBS or another related
polyradiculopathy resulting from tetanus toxoid or a coincident unreported viral infec-
tion. Although there are no data regarding the properties of Duvernoy's secretions of
P. najadum
, to date, there is no evidence that bites by this species produce any
