MARINE TOXINS AND VENOMOUS AND POISONOUS M A R ~ E ANIULS
367
were emphysematous, and showed the presence of blood stained fluid.
The intravenous injection of 3.6 mg of venom into an 8 kg dog produced
cardiac and respiratory arrest in less than 2 min. With smaller amounts
of the toxin there was a rise in the blood pressure followed by a fall.
During this fall, pulse pressure tripled and respirations became deep
and irregular.
Wiener (1969a) also found that lyophilized venom stored in a
desiccator for several months did not lose its lethal activity. The venom
gave all the reactions of a protein; it was destroyed on heating and
inactive at a pH below 4, and at a high pH. Toxicity wm lost in 48 h
when the venom was stored in solution at 4°C.
In an interesting report, Austin et al. (1961) described the cardiovascular changes elicited in rabbits following injection of the venom.
These findings were similar to those reported by Saunders and by
Wiener. Like other investigators, they found that the death of the
animal could not be prevented by the initiation of artificial respiration.
Their most important finding was that records of the action potential
from the phrenic nerve indicated that following injection of the venom,
respiratory movements were affected before efferent respiratory
center activity, and also, before conduction in the phrenic nerve was
impaired. This would indicate that stonefish venom either blocked
neuromuscular conduction across the phrenic nerve-diaphragm junction
or paralyzed the diaphragmatic musculature. They concluded that
the toxin was highly myotoxic, and suggested that the venom may
depolarize cardiac and involuntary muscle as well as skeletal muscle.
(c) Clinical problem. Stingings by the stonefishes, particularly
8. horrida and S . trachynis, appear to be more common than generally
appreciated (Le Juge, 1871 ; Bottard, 1889 ; CoutiAre, 1899 ; Duhig and
Jones, 1928a ; Whitley and Boardman, 1929 ; Ralph, 1943 ; Smith, 1961 ;
Halatead et al., 1966 ; Gail and Rageau, 1966 ; Smith, 1967 ; Wiener,
1968 ; Wiener, 1969b ; Phleps, 1960 ; Juptner, 1960 ; Whitley, 1963).
These works indicate that the sting of Synanceja is usually more serious
than that inflicted by any other of the known venomous fishes.
The clinical course following poisoning by a stonefish is similar,
although considerably more severe, than that previously described for
the stingrays, weevers, sculpins and lionfishes. Deaths from stingings by
these fishes are not uncommon, and may occur within sever41 hours of
envenomation (Smith, 1967). Necrosis of tissues at the site of the injury,
and the subsequent sloughing of these tissues, is more common following
stings by Symnceja than following injuries by the other venomous
fishes. The clinical evidence to date indicates that lethality, pain and
367
were emphysematous, and showed the presence of blood stained fluid.
The intravenous injection of 3.6 mg of venom into an 8 kg dog produced
cardiac and respiratory arrest in less than 2 min. With smaller amounts
of the toxin there was a rise in the blood pressure followed by a fall.
During this fall, pulse pressure tripled and respirations became deep
and irregular.
Wiener (1969a) also found that lyophilized venom stored in a
desiccator for several months did not lose its lethal activity. The venom
gave all the reactions of a protein; it was destroyed on heating and
inactive at a pH below 4, and at a high pH. Toxicity wm lost in 48 h
when the venom was stored in solution at 4°C.
In an interesting report, Austin et al. (1961) described the cardiovascular changes elicited in rabbits following injection of the venom.
These findings were similar to those reported by Saunders and by
Wiener. Like other investigators, they found that the death of the
animal could not be prevented by the initiation of artificial respiration.
Their most important finding was that records of the action potential
from the phrenic nerve indicated that following injection of the venom,
respiratory movements were affected before efferent respiratory
center activity, and also, before conduction in the phrenic nerve was
impaired. This would indicate that stonefish venom either blocked
neuromuscular conduction across the phrenic nerve-diaphragm junction
or paralyzed the diaphragmatic musculature. They concluded that
the toxin was highly myotoxic, and suggested that the venom may
depolarize cardiac and involuntary muscle as well as skeletal muscle.
(c) Clinical problem. Stingings by the stonefishes, particularly
8. horrida and S . trachynis, appear to be more common than generally
appreciated (Le Juge, 1871 ; Bottard, 1889 ; CoutiAre, 1899 ; Duhig and
Jones, 1928a ; Whitley and Boardman, 1929 ; Ralph, 1943 ; Smith, 1961 ;
Halatead et al., 1966 ; Gail and Rageau, 1966 ; Smith, 1967 ; Wiener,
1968 ; Wiener, 1969b ; Phleps, 1960 ; Juptner, 1960 ; Whitley, 1963).
These works indicate that the sting of Synanceja is usually more serious
than that inflicted by any other of the known venomous fishes.
The clinical course following poisoning by a stonefish is similar,
although considerably more severe, than that previously described for
the stingrays, weevers, sculpins and lionfishes. Deaths from stingings by
these fishes are not uncommon, and may occur within sever41 hours of
envenomation (Smith, 1967). Necrosis of tissues at the site of the injury,
and the subsequent sloughing of these tissues, is more common following
stings by Symnceja than following injuries by the other venomous
fishes. The clinical evidence to date indicates that lethality, pain and