Spiders of medical importance in the US do not inflict particularly painful bites, so it is unusual for a spider bite to be suspected until clinical signs appear. It is also unlikely the spider will remain in close proximity to the victim during the time required for clinical signs to develop (30 minutes to 6 hours). Almost all spiders are venomous, but few possess the attributes necessary to cause clinical envenomation in mammals—mouth parts of sufficient size to allow penetration of the skin and toxin of sufficient quantity or potency to result in morbidity.
Spiders in the US capable of causing clinical envenomation belong to two groups: widow spiders (Latrodectus spp) and brown spiders (mostly Loxosceles spp).
The brown recluse spider is the most common Loxosceles spider in the US, with its violin-shaped or fiddleback markings on the dorsum of the cephalothorax. The brown recluse is found in the central and southern portions of the US, with another five Loxosceles spp found in southern Texas, New Mexico, Arizona, and southern California.
The venom of the Loxosceles spp contains several enzymes, including the phospholipase sphingomyelinase D. This enzyme activates complement, platelet aggregation, microvascular thrombosis, and eventually tissue necrosis. The bite of the brown recluse is painless, and a small area of erythema and pruritis may develop at the bite location. Within 2–8 hours after the bite a blister develops, which progresses to form a target or “bull’s-eye” lesion. The center of the bite may appear pale, ischemic, or cyanotic and progressively become dark and necrotic. The vesicle may form an ulcer that enlarges to create an eccentric pattern with eschar formation, potentially extending to underlying tissues. Systemic clinical signs are rare in companion animals but can include fever, vomiting, weakness, leukocytosis, hemolytic anemia, hemoglobinuria, and disseminated intravascular coagulation. It can take several days for severe signs to develop.
Treatment for envenomation is supportive care, because there is no antivenin available in the US. Wound management with cool compresses and immobilization is important for treatment. Dapsone, a leukocyte inhibitor, has been administered to help reduce the extent of the necrosis, but its use should be started early in the treatment course. There are limited data to support the use of glucocorticoids in these cases, but hyperbaric oxygen therapy has been suggested to improve wound healing. Skin grafts have been used but are difficult to maintain and may repeatedly fail until the area of necrosis has become clearly demarcated. Surgical debridement is not recommended and often worsens the lesions. Complete healing may take weeks to months.
The large stinger at the end of the dorsal abdomen of a scorpion is connected to the venom glands and is the main defense mechanism, which poses risk to predators and companion animals. The species of scorpions found in the US are unlikely to cause envenomation in companion animals; however, a sting from a scorpion can be very painful. Severe toxicity is not likely.
However, the Arizona bark scorpion (Centruroides exilicauda) causes more extensive systemic envenomation in some animals. These scorpions are found in Arizona, western New Mexico, southern Utah, and Nevada. The bark scorpion can occasionally also be seen along the Colorado River in California.
The venom of a bark scorpion contains neurotoxins that block potassium and sodium channels, inhibiting neuromuscular transmission. Catecholamines and acetylcholine is released in large amounts, stimulating sympathetic and parasympathetic responses and leading to changes in heart rate and blood pressure. The most common effects are tachycardia and hypertension, but agitation, twitching, and hypersalivation can also occur. However, in most canine patients, a bark scorpion sting is often limited to localized pain, edema, erythema, and pruritis, which can be managed with supportive care and administration of analgesics; systemic clinical signs are not common, but patients should be monitored for their development, and an antivenom is available. The antivenom is rarely used as a treatment modality in veterinary medicine, because it must be administered within minutes of stinging to reverse systemic effects.
Tarantulas are hairy spiders from the family Theraphosidae, with more than 1,000 species worldwide. Commonly sold in the pet trade, these arachnids have an increased presence in homes, where exposure to other pets can occur. Despite the proximity, envenomation is rare, because most tarantulas do not use venom to kill their prey. American tarantula species are harmless and not aggressive, whereas Asian and some African species can cause a painful bite, with localized edema.
The primary concern with tarantulas is the fine hairs on its back, which can be expelled as a defense mechanism. The hairs can lodge in an animal's cornea or cause dermal or mucosal irritation, potentially leading to allergic reactions or severe damage to the eye, including blindness. Treatment of these exposures is management of any allergic response, removal of any hairs from the cornea, and provision of supportive care.
Latrodectus spp are found worldwide, typically living in tropical and temperate areas, with five species in the US. The most common species is the black widow spider (L mactans). Female black widow spiders are larger than males and have a characteristic red or orange hourglass marking on the ventral abdomen. Immature females can still cause envenomation but may not have the hourglass marking. Other species found in the US include the western black widow (L hesperus) in the western states, the brown widow (L bishopi) in the south, the northern widow (L variolus) found in the Midwest, eastern US, and southern Canada, and the red widow (L geometricus) found in Florida.
Venom from a black widow spider is one of the most potent toxins by volume, though the spider can control the amount of venom released, and a small amount of bites result in no envenomation. Canines have some resistance to the toxin, but guinea pigs, cats, and horses are highly susceptible. The venom is made up of several components, including the neurotoxin alpha-latrotoxin that causes a release of neurotransmitters at synaptic junctions. A large release of acetylcholine, norepinephrine, dopamine, glutamate, and enkephalins depletes these neurotransmitters, leading to the neurotoxin blocking neurotransmission and inhibiting reuptake. The patient develops severe cramping of large muscle groups and other clinical signs.
Evidence of a bite may be difficult to find in animals, but the initial bite is painful. Mild erythema may be noted at the bite location but does not cause local tissue damage. Diagnosis is based on clinical signs of agitation, vomiting, diarrhea, severe pain secondary to muscle cramping, muscle fasciculations, and tremors. Abdominal rigidity without tenderness can indicate envenomation. In severely symptomatic patients, hypertension, respiratory distress, and partial paresis can occur. Onset of clinical signs can occur within minutes of the bite, but more severe symptoms can be expected within 8 hours. These signs can wax and wane over the next couple of days until they resolve.
Treatment of black widow envenomation in most cases is supportive care, to manage pain and muscle cramping. An equine-based antivenin is commercially available, but anaphylaxis can develop; therefore, caution during administration is indicated, and premedication with diphenhydramine should be considered. Administration of opioids and benzodiazepines is the most common treatment for management of muscle cramping and pain. Muscle relaxants may also be helpful. In humans, calcium gluconate infusions are sometimes used to help with muscle pain, but relief is generally short lived and not as effective as opioids or benzodiazepines. As such, calcium gluconate is no longer recommended as a treatment modality in veterinary medicine. Overall prognosis is good in dogs, and many do not require medical treatment. If treatment is required, supportive care and medical management alone will often allow for recovery over several days. Antivenom may hasten recovery in some patients but may not be necessary and should be considered on a case-by-case basis.