Biology Reference
In-Depth Information
The pharmacology of ethanol is complex and only partially characterized. It is known
to act as an agonist of Type A g-aminobutyric acid (GABA
A
) receptors and inhibits gluta-
minergic activation of
N
-methyl-D-aspartate (NMDA) receptors as well as modifies func-
tions of adenyl cyclase, phospholipase C, and some types of ion channels (Trevor et al.,
2008). This complex pharmacology can be expressed in the multiple organ involvement
typically observed with significant intake of ethanol. Thus, almost all of the reported
clinical course could be ascribed to acute ethanol intoxication that may include signs/
symptoms such as nausea, vomiting, and neurosensory effects including blurred vision,
headache, stupor, confusion, slurred speech, and fine motor tremors. Nystagmus associ-
ated with cranial nerve palsies may also occur (American Psychiatric Association, 2000).
The “major muscle weakness” may have been due to somatosensory amplification (e.g.,
compare with the
H. gigas
case reported by Manning et al., 1999;
Table 4.1
and Section
4.3.3) and/or intoxication-induced immobility.
4.4.6.2 Conclusion and Assessment of
H. viridiflavus
As noted in a significant number of these cases, this report describes a concern-
ing clinical course that was hypothetically considered a result of a bite from a non-
front-fanged colubroid species without any documented medical risk. In evaluating
the limited evidence provided in the report, it must be noted that the reviewer cannot
have confidence that any bite did in fact occur, and the victim had a very substantial
blood alcohol level that was in excess of four times the legal driving limit in France.
Therefore, the likelihood of acute alcohol intoxication
somatosensory amplification
provides a far more probable explanation for the reported signs/symptoms than a medi-
cally significant bite from
H. viridiflavus
. The nature of the oral glands and properties
of any associated oral secretions of
H. viridiflavus
require study and characterization.
As discussed earlier, the use of the term “venom gland” and “venom ducts” for oral
structures of allied taxa such as
C. constrictor
is premature and misleading.
A presentation reported in a little-known journal featured ophthalmoplegia, facial
nerve (cranial nerve [CN] VII) palsy and right-sided hemiparesis was described as
possible sequelae of a snakebite from an unidentified species locally named, “kyzl
ilan” (Aleksankin, 1968). The aforementioned clinical course reportedly developed
in the previously healthy patient approximately 4 years after the bite. Some have
speculated that the snake responsible was a
Dolichophis
16
(
Hierophis
Nagy et al.,
2004a)
schmidti
(Nagy et al., 2004b). As discussed in Section 4.5, the lack of any
substantial information regarding the snake allegedly involved in such an atypical
case as well as the obscurity of the report compels rejection of any linkage of the
described clinical presentation with a non-front-fanged colubroid bite. Although it is
unlikely that the patient's reported palsies were due to the alleged snakebite (that has
no verifiable description or documentation), the remote possibility of GBS following
a serious envenoming from a front-fanged species (e.g., the lebetine or blunt-nosed
16
Another genus split from the previous inaccurate grouping of several colubrine taxa within the genus,
Coluber
,
Dolicophis
contains four species. Two of these,
D. jugularis
and
D. caspius
, are respectively
illustrated in
Plates 4.70A
and B and
4.91
.
