Lawrence M. Lewis MD1
Associate Professor of Medicine
William H. Dribben MD1
Assistant Professor of Medicine
Mark D. Levine MD1
Clinical Instructor in Emergency Medicine
1Washington University School of Medicine, St. Louis
The authors have no commercial relationships with manufacturers of products or providers of services discussed in this chapter.
There were an estimated four and a half million cases of dog bites in the United States in 1994, the most recent year for which published statistics are available.1 Over a lifetime, over half of all Americans are bitten by a dog or cat.2 Although the majority of victims with bite wounds treat themselves, nearly 370,000 dog-bite victims required medical attention in an emergency department in 2001.3 This is an increase of 10% to 15% over that reported for 1992 to 1994.4 The highest incidence of dog-bite injuries is in boys 5 to 9 years of age (60.7 per 10,000 person-years).4 Children are also more likely to be bitten on the face, head, and neck than are adults.4 Infection, the most common complication of bite wounds, arises from microbes either on the victim's skin or in the mouth of the human or animal inflicting the bite wound. The relative risk of infection is determined by a number of factors, including the species of animal inflicting the wound, the location of the bite, the size and depth of the wound, host factors, and the type of wound care given.5,6,7 Most infections that result from mammalian bites are polymicrobial, with mixed aerobic and anaerobic species.8 Nonetheless, certain species tend to cause infections with characteristic bacteriologic pathogens. In addition, transmission of the rabies virus may occur through bites from mammals of certain species.
Dogs are responsible for more bite wounds in patients who seek medical attention than all other animals combined.9 Most bites are inflicted by animals known to the victim, with strays accounting for less than 10% of reported bite-wound injuries.9 Wounds occur most frequently on the extremities, except in young children, in whom bite wounds to the face, head, and neck are most common.4,10 Specifically, bite wounds to the hand occur in anywhere from one fifth to one half of reported cases; such wounds are associated with an increased risk of infection, particularly tenosynovitis, closed-space compartment infection, and septic arthritis.11 Although deaths from dog attacks are rare, this tragic scenario occurs about 12 to 15 times a year in the United States (238 dog-bite-related deaths from 1979 through 1998). Pit-bull-type dogs and Rottweilers are responsible for over half of the reported deaths.12
The oral bacterial flora of dogs includes Pasteurella multocida, Staphylococcus aureus, Capnocytophaga canimorsus, S. epidermidis, Streptococcus species, and a number of anaerobes. Mixed aerobic and anaerobic infection is present in about half of infected dog bites.8 The aerobic organisms most commonly isolated from infected dog bites include Pasteurella, Staphylococcus, and Streptococcus species.8,13 The anaerobic organisms most commonly isolated from dog bites include Fusobacterium, Bacteroides, Porphyromonas, and Prevotella species.8,13Anaerobic organisms are significantly more common in cultures from abscesses than from other types of infection.6
Dog bites are unlikely to become infected, with infection rates usually reported to be on the order of 5% to 10%.14,15 However, the risk of infection is higher in older persons and in persons with diabetes, vascular disease, chronic alcoholism, or immunosuppression. Infection risk is also higher in puncture wounds, in wounds on the hand or foot or over a joint, and in wounds associated with crush injuries.11
Dog bites infected with Capnocytophaga canimorsus may cause an overwhelming sepsislike picture associated with high fever, leukocytosis, disseminated intravascular coagulation (DIC), and multiorgan failure. This complication of dog-bite injuries is seen most commonly in immunocompromised patients (e.g., those with asplenia, alcoholism, or hematologic malignancy) and carries a 25% mortality.11
Globally, dogs are the major reservoirs for rabies.16 In developed countries, however, vaccination programs have reduced the prevalence of canine rabies; for example, only 117 rabid dogs were reported in the United States in 2003.17 Rabies is discussed in detail elsewhere [see7:XXXI Viral Zoonoses].
Cat bites are the second most common mammalian bites in the United States, accounting for 5% to 15% of all reported bites. About two thirds of all cat bites occur on the upper extremity. Cat bites are more often puncture wounds than tearing lacerations and often appear innocuous initially. However, the infection rate for cat bites is reported to be 15% to 30%, or almost triple that for dog bites.18,19 P. multocida is the major pathogen associated with cat bites, being found in about three fourths of infected cat-bite wounds.8 P. multocidainfection progresses rapidly, with pain, swelling, and erythema usually occurring within 24 hours.9 The types of anaerobic organisms found in cat bites are similar to those found in dog bites (see above), although anaerobic isolates are somewhat more common in cat bites. Penetration into deep tissues with resultant osteomyelitis or septic arthritis is more common with cat bites than dog bites.13 Cat-scratch disease (CSD) is an infection arising from a rickettsia-like organism, Bartonella henselae; CSD is discussed in detail elsewhere [see 7:XI Infections Due to Brucella, Francisella, Yersinia pestis, and Bartonella].
Cats continue to outnumber dogs by more than 2 to 1 as the most common domestic rabid animal.15,20 Overall, however, domestic animals account for only a small minority of animal rabies cases in the United States; about 90% occur in wildlife [see 7:XXXI Viral Zoonoses].
Ferrets have become increasingly popular as pets; a 1996 survey suggested that there are almost 800,000 ferrets in the United States.21Ferret attacks are uncommon but can result in severe injury, especially to infants and small children.22,23 These attacks (in contrast to dog or cat bites) are usually unprovoked.22,23
The bacteriologic flora in ferrets has not been well studied. One study showed that facultative anaerobic gram-positive cocci were the predominant organisms, followed by Pasteurella and Corynebacterium species; few strict anaerobes were detected.24
Ferrets are clearly capable of contracting and carrying the rabies virus.25 However, it is not known how long infected ferrets can shed virus before showing clinical signs of disease, thus making quarantine recommendations problematic. Although there is an approved rabies vaccine for use in ferrets, its efficacy in preventing rabies is currently not known.26 For ferret bites involving animals suspected of being rabid, current recommendations are to give the patient rabies postexposure prophylaxis immediately. For cases involving ferrets that are not suspected of being rabid, the recommendation is to withhold vaccination and to observe the animal for 10 days; the patient should be vaccinated only if the animal shows signs of rabies during that period.27
Human bites are the third most common mammalian bite in the United States, accounting for approximately 5% to more than 20% of bite wounds seen in urban emergency departments.11,18,28 Most human-bite wounds occur on the extremities, with an unusually high percentage being over the metacarpal-phalangeal joint secondary to a clenched fist contacting a tooth. Traditionally, human-bite wounds have had a reputation for frequent and severe complications. Current data, however, suggest an infection rate from human-bite wounds on the order of 10% to 50%, depending on the wound type and location.11,16,28 Occlusional/simple bite wounds to areas other than the hand probably are no more at risk for infection than any other type of bite wound and minimally more than for nonbite lacerations.11,16,17,29,30 However, human-bite wounds to the hand are associated with infection rates of almost 50%.18 A clenched-fist injury is considered the most serious of all human-bite wounds.1 These injuries may appear innocent at first but progress to serious infections that may include the joint, tendons, or various compartments of the hand. These injuries require meticulous wound care, appropriate antibiotic therapy, and consultation with a hand surgeon. Bacterial pathogens associated with human-bite wounds include a number of anaerobes similar to those recovered from dog and cat bites, but with a much higher percentage of β-lactamase producers.19,31,32 The predominant aerobes are Staphylococcus andStreptococcus species. About 10% to 30% of human-bite wounds have been shown to contain Eikenella corrodens, a facultative anaerobe.18,28,33,34 E. corrodens is present in 25% of clenched-fist injuries and often causes serious, chronic infections.34 Besides bacterial infection, human bites can transmit the hepatitis B virus, HIV, herpes simplex virus, tuberculosis, and even syphilis.11,13,28,35 Prophylactic therapy against hepatitis B or HIV should be considered for patients bitten by persons considered at high risk for these diseases.
Rat bites are uncommon, representing less than 2% of the bite wounds seen in one urban emergency department.36 Although the list of potential pathogens that could be transmitted from rat bites is daunting, infections from rat bites, including rabies, are, in fact, very infrequent.37 Rat-bite fever is a disease caused by Streptobacillus moniliformis, a gram-negative rod. It is associated with fever, chills, headache, myalgia, and rash and usually begins abruptly about 3 to 10 days after inoculation [see 7:VII Lyme Disease and Other Spirochetal Zoonoses].
Although bat bites typically produce only trivial trauma, bat bites were responsible for almost 75% of all human rabies cases reported in the United States since 1990 and for 90% of all cases acquired in the United States from 1981 through 1998.37,38 Studies suggest that cleaning a bite wound with soap and a virucidal agent is effective in lowering the risk of rabies transmission.39 Rabies prophylaxis is recommended for any bat exposures unless immediate brain testing of the animal can be performed.
Skunks, raccoons, and foxes are also important animal reservoirs of rabies in the United States.38 Bites from raccoons, skunks, and foxes should be regarded as likely to be rabid until proved otherwise, and the use of rabies immune globulin and rabies vaccine is warranted, particularly if rabies is endemic to the area or the animal's behavior is deemed abnormal.39
Bite wounds from wild animals are rare; most occur from exposure at zoos or from owning or harboring exotic animals.40 The incidence of serious injury from wild-animal attacks among the three million visitors to Yellowstone National Park is reported to be lower than the chance of being struck by lightning.40
Bite wounds from nonhuman primates are rare. In addition to transmitting bacterial infection, these bites may transmit Herpesvirus simiaeor monkey B virus [see 7:XXXI Viral Zoonoses]. If left untreated, monkey B virus infection often causes encephalitis, resulting in death or permanent neurologic impairment.41 Monkey B virus is enzootic in North African and Asian monkeys, including the macaque and rhesus. Thorough scrubbing of bites or scratches with soap or detergent and irrigation for 15 minutes have been shown to reduce the viral inoculum.42
The goals of bite-wound care are to recognize and treat serious injury (e.g., nerve or tendon laceration), avoid infection (both local and systemic), and achieve a good cosmetic result. The treatment of mammalian-bite wounds begins with a history and physical examination. The history should include when and where the bite occurred, the events leading to the bite, what type of animal was responsible for the bite, and any background information on the animal. Any treatment rendered before arrival at the facility, as well as the patient's tetanus immunization history, should be documented.
A careful physical examination to assess for arterial or major venous injury and nerve, joint, bone, or tendon involvement should be performed and documented. The wound should be explored for foreign bodies, including teeth or tooth fragments.
After the examination and provision of adequate anesthesia, the wound should be meticulously cleaned and irrigated. Wound soaking or scrubbing is to be avoided. Irrigation with 200 to 250 ml of normal saline or dilute povidone-iodine solution using moderate pressure (20 psi, the pressure generated using a syringe and a 19-gauge needle) has been shown to decrease wound infection fivefold.16,43 Careful debridement of nonviable or grossly contaminated tissue may be necessary. If the risk of rabies is high, a benzalkonium chloride scrub should be used, because povidone-iodine irrigation has not been shown to be effective in reducing viral load.16 Benzalkonium chloride should be rinsed out to avoid tissue irritation.
Whether lacerations associated with bite wounds should be treated with primary closure is an area of debate. A number of studies suggest that it is safe to suture bite-wound lacerations that are greater than 1 to 2 cm in length and less than 12 hours old—especially those about the head and face, where there is good circulation and greater concern for a good cosmetic result.44,45 Bite wounds to the hand and to the lower extremities often result in complications and probably have increased rates of infection with primary closure.44,46
The use of prophylactic antibiotics for any bite wound is debatable,47 but there is general consensus that certain wounds in all patients and most wounds in certain patients deserve prophylactic antibiotics [see Table 1]. The antibiotic of choice for prophylaxis of most mammalian-bite wounds is amoxicillin-clavulanic acid. For the penicillin-allergic patient, a third-generation fluoroquinolone (e.g., moxifloxacin)48 or a cephalosporin (e.g., cefotaxime)49 serves as a good alternative [see Table 2]. The timing of prophylactic antibiotics is important. Prophylactic antibiotics should be given as soon after the bite injury as possible. A systematic review suggests that prophylactic antibiotics may reduce the incidence of infection in all hand-bite wounds and human bites, regardless of location.49
Table 1 Bite Wounds Requiring Prophylactic Antibiotics
Table 2 Common and Important Pathogens and Antibiotic Selection for Various Mammalian Bite Wounds
Tetanus prophylaxis should be given to those patients who have not been immunized in the previous 10 years [see Table 3]. The standard adult dose is 0.5 ml of tetanus and diphtheria toxoids adsorbed, given intramuscularly. If tetanus immune globulin is required, it is usually given in a single dose of 250 units intramuscularly, but not in the same arm as the tetanus toxoid.
Table 3 Recommendations for Tetanus Prophylaxis after Animal Bites
Postexposure rabies prophylaxis consists first and foremost of appropriate wound care. The use of rabies immune globulin and vaccine administration depend on local epidemiology, the animal involved (species and behavior), and the type of exposure16 [see 7:XXXI Viral Zoonoses]. Postexposure rabies prophylaxis for domestic animal bites is warranted in any of the following circumstances: (1) the animal is observed to be abnormal, (2) the animal is not available for observation and the rate of endemic rabies in domestic animals for the region is not exceedingly low, or (3) the animal exhibited abnormal behavior, including an unprovoked attack [see Table 4].26
Table 4 Recommendations for Rabies Postexposure Prophylaxis27
Over 3,000 species of snakes exist worldwide. Snakes are found everywhere on Earth except for the Arctic and Antarctic, New Zealand, Madagascar, and a few small islands. Snakes live in almost all land environments and in both saltwater and freshwater.
Approximately 10% of snakes are venomous. Of the 14 families of snakes, only five include venomous species: the Colubridae, Hydrophidae (sea snakes), Elapidae (cobras, kraits, mambas, and coral snakes), Viperidae (Russell viper, puff adder, Gaboon viper, saw-scaled viper, and European viper), and Crotalidae (rattlesnake, water moccasin, copperhead, bushmaster, and fer-de-lance). Snakes are carnivores; venomous snakes use their venom to immobilize prey for digestive purposes.
The number of snakebites in the United States is estimated to be approximately 8,000 a year. Many bites occur when patients are hiking, walking, or handling a snake. Frequently, the patient is intoxicated at the time of the bite.50 Most snakebites do not result in envenomation, but nine to 15 deaths occur annually from bites that do result in envenomation.51 In the United States, rattlesnake bites most frequently result in significant envenomation and death.
Snakes are most active in the spring, when they begin to mate and are no longer hibernating52; however, the incidence of snakebite is highest in the summer months. Snakes remain active throughout the day and night, but because they are poikilothermic, they must contain their activity within a narrow temperature range of approximately 25° to 35° C.
The range of the eastern coral snake extends from North Carolina south and west to Texas. The western coral snake is found mainly in Arizona and New Mexico. Coral snakes are nocturnal and shy away from human contact.
Coral snakes are identified by their color, pattern, and permanently erect fangs. The nose of the coral snake is black, and the body has black, red, and yellow bands. The black bands do not separate the red and yellow bands, as they do on the nonvenomous but similarly banded kingsnake. This pattern is commonly remembered through the rhyme “red on black, venom lack; red on yellow, kills a fellow” [seeFigure 1]. Coral snakes release their venom slowly, so they attach themselves to their prey and envenomate through a chewing motion. Instead of the puncture wounds typical of most snakebites, the chewing leaves what appear to be scratches on the skin.52,53
Figure 1. Eastern Coral Snake
The nose of the coral snake is black, and the body has black, red, and yellow bands. The black bands do not separate the red and yellow bands, as they do on the nonvenomous but similarly banded kingsnake. Snake shown is an eastern coral snake, Micrurus fulvius.
The bite of the eastern coral snake can be fatal. There are no confirmed fatalities from western coral snake envenomations.
In the United States, pit vipers (Crotalidae) are found in all states except Maine, Alaska, and Hawaii. South America has nine subspecies of rattlesnakes; Mexico and Central America have four subspecies of rattlesnakes. These snakes can be found in a variety of habitats and at elevations up to 14,000 ft. The eastern and western diamondback rattlesnakes (Crotalus adamanteus and C. strox) [see Figure 2] are the largest and most dangerous in the United States and are found in the southwestern states and in Nevada, California, and Oklahoma.54,55 The timber rattlesnake (C. horridus) is the second most dangerous rattlesnake common to the eastern United States, but it is rarely found in Delaware, Maine, Michigan, or Washington, D.C. Pigmy rattlesnakes (Sistrurus catenatus and S. miliarius) are found in areas ranging from New York to Michigan and from Texas to Arizona; they have the least toxic venom of all of the rattlesnakes.51 Overall, rattlesnakes are responsible for 65% of envenomations in the United States. Their venom is 2.5 to 5 times more toxic than other North American species of venomous snakes.50 Cottonmouths (Agkistrodon piscivorus), also known as water moccasins, live in the southern and southeastern states along streams and in low-lying trees. Copperheads (A. contortix) [see Figure 3] are found in mountains, rock piles, and sawdust piles. Their range extends from Massachusetts southwest to Texas. Cottonmouths and copperheads have only moderately toxic venom; their bite is painful but rarely fatal. In a study of 400 copperhead bites, 32 of which were treated with antivenin, 88% of bites responded to the antivenin, as evidenced by a cessation of local tissue injury progression.56
Figure 2. Eastern Diamondback Rattlesnake
Diamondback rattlesnakes are the largest and most dangerous rattlesnakes in the United States. Shown is an eastern diamondback rattlesnake, Crotalus adamanteus.
Figure 3. Copperhead
The copperhead (Agkistrodon contortix) has a geographic range that extends from Massachusetts southwest to Texas. Bites from these snakes are painful but rarely fatal.
Pit vipers are identified by a small depression (pit) between the eyes and the nostrils bilaterally. They have a triangular-shaped head, an elliptical pupil, and fangs that fold back when the mouth is closed and unfold via a hingelike mechanism when the mouth is opened. The pit is a heat-sensitive organ that enables the snake to locate live, warm-blooded prey. Snakes can detect movement at a distance of about 40 ft. They can strike at a distance of approximately half their body length. Rattlesnakes use their rattle when threatened or endangered, not necessarily just when they are about to attack. The pit viper is aggressive and will stand its ground when provoked or cornered.54,55 The venom is stored in glands that are located on each side of the head above the maxillae and behind the eyes. The glands are similar in function to the human submaxillary glands. The snake may discharge anywhere from 25% to 75% of its venom when biting a human. The fangs are either hollow or grooved. Even young snakes are venomous, and the venom of young snakes may be 12 times as strong as the venom of adult snakes.
Snake venom has both neurotoxic and hematotoxic properties. The venom is a complex mixture of hydrolases, polypeptides, glycoproteins, and low-molecular-weight compounds. Snake venom, especially that of the Elapidae and Hydrophidae families, contains polypeptides that produce neuromuscular blockade at the presynaptic or postsynaptic terminals, or both, causing a flaccid paralysis. Composition of the venom varies greatly between species and between individual snakes. Viper venom is mainly cytotoxic, Elapidae (cobra, coral) venom is usually neurotoxic, and Hydrophidae (sea snake) venom is mainly myotoxic.57
Snake venom has profound effects on coagulation pathways, causing a hypercoagulable state. Over the first few hours after a person is bitten, thrombocytopenia occurs, with a platelet count of less than 10,000/mm3, a decrease in fibrinogen, and an increase in fibrin degradation products. The venom proteins may induce distention of the vascular basement membrane and capillary matrix.58 Prothrombin time and partial thromboplastin time increase with severe envenomation. Usually, these increases occur because consumption of coagulation factors results in clinical anticoagulation. In dog experiments, activation of fibrinolysis may be preceded by thrombus formation, with clotting of critical vessels in the coronary vasculature, which can lead to cardiac arrest and death. This may also explain pulmonary emboli, as the thrombus formation may occur in the legs and cause deep vein thrombosis.59 Drops in hematocrit may also occur, along with so-called burring of erythrocytes.54 Approximately 53% of patients experience coagulopathy 2 to 14 days after envenomation. In one study, 76% of patients with pit viper envenomations developed coagulopathy during their hospital course.60 The coagulopathy may last up to 26 days.59
From 30% to 50% of snakebites do not result in envenomation. The snake can control the amount of venom injected and may inject up to 90% of its venom to immobilize its prey. Other factors involved in the injection of venom include the health of the snake; its satiety; the condition of the fangs; the toxicity of the venom; whether the snake is injured; and the size, age, and health of the victim.