Although relatively rare, they are nonetheless important causes of mortality. The venoms of certain species of snakes, lizards, spiders (especially the black widow spider, see Chap. 50), and scorpions contain neurotoxins that may cause a fatal depression of respiration and curare-like paralysis of neuromuscular transmission. In the United States, there are approximately 8,000 poisonous snake bites per year. Some, such as the coral snake envenomation, are neurotoxic, producing pupillary dilatation, ptosis, ocular palsies, ataxia, and respiratory paralysis. Others (rattlesnakes, water moccasin snakes) cause tissue necrosis and circulatory collapse. These are reviewed by Gold and colleagues. The serious effects of Hymenoptera stings (bees, wasps, hornets, and fire ants) are mainly the result of hypersensitivity and anaphylaxis. Several instances of cerebral and myocardial infarction have been reported after bee and wasp stings (Crawley et al). A substantial inception has been the development of an antivenom for scorpion stings that can be administered in parallel with diazepines to children and results in more rapid resolution of paralysis and respiratory failure (Boyer and colleagues). All of these disorders are discussed in detail in Harrison’s Principles of Internal Medicine.
This rare condition is the result of a toxin secreted by the gravid tick. In Canada and the northwestern United States, the wood tick Dermacentor andersoni is mainly responsible; in the southeastern United States it is Dermacentor variabilis, a dog tick (the tick in Australia is the Ixodes holocyclus), but various other ticks occasionally may have the same effect. Most cases occur in children because their small body mass renders them susceptible to the effects of relatively small amounts of the toxin. The illness arises almost exclusively in the spring when the mature gravid ticks are most plentiful. The illness is more common and is generally more severe in cases on the Australian continent than it is in North America. Clinical manifestations require that the tick be attached to the skin for several days.
The neurotoxin causes a generalized, flaccid, areflexic paralysis, appearing over 1 or 2 days and thereby mimicking the Guillain-Barré syndrome. In a few cases, several days of ataxia and areflexia precede the paralysis but sensory loss tends to be minimal. External ophthalmoplegia, which occurred in 5 of the 6 children described by Grattan-Smith and colleagues, is exceptional, judging by other reports; internal ophthalmoplegia and pharyngeal weakness are also known to occur, and while not typical, raise the possibility of botulism or diphtheria. The CSF is normal and electrophysiologic studies show reduction in the amplitude of the muscle action potentials but normal or only slightly slowed nerve conduction. Prominent ptosis and neck weakness may also raise the question of a neuromuscular process, but repetitive stimulation testing is normal or evokes only a slight decrement or increment in some cases.
The ticks tend to attach to the hairlines or in the matted hair of the scalp, neck, and pubis, where a careful search will reveal them (for which reason nurses and electroencephalography technicians often are most likely to find them; see Felz et al). The diagnosis is much in the awareness of clinicians in endemic areas during the tick season, for they are gratified with rapid and dramatic improvement when the tick is removed. The paralysis has been reported to become transiently worse after tick removal in some of the Australian cases.
From a neurologic point of view, Lyme disease is a far more common tick-borne disorder. The causative agent is Borrelia burgdorferi, a spirochetal organism. The disorder is discussed fully with other infectious diseases in Chap. 31 and in Chap. 43, with the neuropathies.
The causes and clinical manifestations of lead poisoning are quite different in children and adults.