Updated: Jun 25, 2009
Because many animal bites are never reported, determining the exact incidence of animal bite wounds in the United States, let alone the world, is difficult. An estimated 74.8 million dogs lived in the United States in 2007; these account for an estimated 5 million dog bites per year, of which 800,000 require medical attention1 . Substantially more dog bites occur than cat bites. These two species account for the majority of (nonhuman) animal bite wounds encountered in the emergency department (ED).
Dog bites typically cause a crushing-type wound because of their rounded teeth and strong jaws. An adult dog can exert 200 pounds per square inch (psi) of pressure, with some large dogs able to exert 450 psi.2 Such extreme pressure may damage deeper structures such as bones, vessels, tendons, muscle, and nerves.
The sharp pointed teeth of cats usually cause puncture wounds and lacerations that may inoculate bacteria into deep tissues. Infections caused by cat bites generally develop faster than those of dogs.3,4
Limited literature is available on other animal bites. Monkey bites have a notorious reputation based largely on anecdotal reports. Several cases of unprovoked attacks on young children and infants by domesticated ferrets have been documented. The bites of foxes, raccoons, skunks, bats, dogs, and cats have been clearly linked to rabies exposure. Bites from large herbivores generally have a significant crush element because of the force involved.
Bites of the hand generally have a high risk for infection because of the relatively poor blood supply of many structures in the hand and anatomic considerations that make adequate cleansing of the wound difficult. In general, the better the vascular supply and the easier the wound is to clean (ie, laceration vs puncture), the lower the risk of infection.
A major concern in all bite wounds is subsequent infection. Infections can be caused by nearly any group of pathogens (bacteria, viruses, rickettsia, spirochetes, fungi). At least 64 species of bacteria are found in the canine mouth, causing nearly all infections to be mixed.5,6,7 Common bacteria involved in bite wound infections include the following:
Of an estimated 3-6 million animal bites per year in the United States,8 approximately 80-90% are from dogs, 5-15% are from cats, and 2-5% are from rodents, with the balance from other small animals (eg, rabbits, ferrets), farm animals, monkeys, reptiles, and others. Some estimate that 1% of emergency visits are for dog bite wounds. Approximately 1% of dog bite wounds and 6% of cat bite wounds require hospitalization.1,9
The lack of standard reporting in many countries makes accurate estimates of animal bite incidence difficult to determine. Depending on locale, the range of animals inflicting bites is wide and includes large cats (tigers, lions, leopards), wild dogs, hyenas, wolves (Eurasia), crocodiles, and other reptiles. As in the United States, most bites, however, are from domestic dogs. In developing countries, animal bites (especially bites by dogs, cats, foxes, skunks, and raccoons) carry a high risk of rabies infection.
Dog attacks kill approximately 10-20 people annually in the United States.8,10 Most of these fatalities, unfortunately, are young children. While local infection and cellulitis are the leading causes of morbidity, sepsis is a potential complication of bite wounds, particularly C canimorsus (DF-2) sepsis in immunocompromised individuals. Pasteurella multocida infection (the most common pathogen contracted from cat bites) also may be complicated by sepsis. Meningitis, osteomyelitis, tenosynovitis, abscesses, pneumonia, endocarditis, and septic arthritis are additional concerns in bite wounds. When rabies occurs, it is almost uniformly fatal.
Women are more frequently bitten by cats, whereas men are more often bitten by dogs (despite being man's best friend).11
Peak incidence of animal bites occurs among children aged 5-9 years.9,8,10
History for animal bites should include the following:
Major resuscitation rarely is required. Because patients typically are children, reassurance and parental presence may facilitate examination. Where applicable, consider the following:
Bite wounds from cats and dogs can occur without provocation, but provoked bites, such as disturbing animals while they are eating, are more common. Older animals often are less tolerant of disturbances, especially by children. Most dog bites involve a dog that belongs to the family or friend of the victim and approximately half occur on the pet owner's property.10
Certainly, unprovoked bites by wild or sick-appearing animals (most notably by dogs, cats, raccoons, foxes, skunks, and bats) further raise underlying concerns about likelihood of rabies exposure.
| Bites, Human | Neck Trauma |
| Cellulitis | Osteomyelitis |
| Fractures, Cervical Spine | Rabies |
| Hand Infections | Tetanus |
For additional information, see Medscape’s Wound Management Resource Center.
This is one of most controversial subjects in wound care. Remember that proper wound care (inspection, debridement, irrigation, closure, if indicated) reduces infection more than antibiotics. In general, low-risk wounds do not require prophylactic antibiotics. However, therapy is recommended for high-risk wounds (eg, cat bites that are a true puncture, bites to the hand, massive crush injury, late presentation, poor general health).14
The goal of initial therapy is to cover staphylococci, streptococci, anaerobes, and Pasteurella species. Prophylactic antibiotics may be given for a 3- to 5-day course. The first-line oral therapy is amoxicillin-clavulanate. For higher risk infections, a first dose of intravenous antibiotic may by given (ie, ampicillin-sulbactam, cefuroxime, ticarcillin-clavulanate, piperacillin-tazobactam, or a carbapenem). Other combinations of oral therapy include amoxicillin plus cephalexin (possible poor compliance due to complicated regimen), clindamycin plus a fluoroquinolone (adults), clindamycin plus sulfamethoxazole and trimethoprim (Bactrim) (children), and less effective azithromycin or doxycycline.15,6,7 If the wound is infected on presentation, a course of 10 days or longer is recommended.
For monkey bites, postexposure prophylaxis valacyclovir or acyclovir should be given for 14 days.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Drug combination of beta-lactamase inhibitor with ampicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms.
1.5 (1 g ampicillin + 0.5 g sulbactam) to 3 g (2 g ampicillin + 1 g sulbactam) IV/IM q6-8h; not to exceed 4 g/d sulbactam or 8 g/d ampicillin
<3 months: Not established
3 months to 12 years: 100-200 mg ampicillin/kg/d (150-300 mg Unasyn) IV divided q6h
>12 years: Administer as in adults; not to exceed 4 g/d sulbactam or 8 g/d ampicillin
Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction
For treatment of multiple organism infections in which other agents do not have wide-spectrum coverage or are contraindicated due to potential for toxicity.
Base initial dose on severity of infection, and administer in equally divided doses; dose may range from 250-500 mg q6h IV for a maximum of 3-4 g/d
Alternatively, 500-750 mg q12h IM or intra-abdominally
Infants >3 months and children
<12 years: 15-25 mg/kg/dose IV q6h
Fully susceptible organisms: Not to exceed 2 g/d
Infections with moderately susceptible organisms: Not to exceed 4 g/d
>12 years: Administer as in adults
Coadministration with cyclosporine may increase CNS side effects of both agents; coadministration with ganciclovir may result in generalized seizures
Documented hypersensitivity; known hypersensitivity to amide local anesthetics; children with CNS infections (increased seizure risk); children <30 kg with renal impairment (lack of data)
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Adjust dose in renal insufficiency (adult adjustments)
CrCl (mL/min) 80-50: 0.5 g q6-8h
CrCl 50-10: 0.5 g q8-12h
Hemodialysis (HD): 0.25-0.5 g after HD, then q12h
Adjust dose in renal insufficiency; avoid use in children <12 y with CNS infections
Caution with history of seizures, hypersensitivity to penicillins, cephalosporins, or other beta-lactam antibiotics
Bactericidal activity results from inhibition of cell wall synthesis and is mediated through ertapenem binding to penicillin-binding proteins. Stable against hydrolysis by a variety of beta-lactamases including penicillinases, cephalosporinases, and extended-spectrum beta-lactamases. Hydrolyzed by metallo-beta-lactamases.
1 g IV qd infused over 30 min
CrCl <30 mL/min/1.73 m2: 500 mg IV qd
<3 months: Not established
3 months to 12 years: 15 mg/kg IV q12h; not to exceed 1 g/d
>12 years: Administer as in adults
Probenecid may reduce renal clearance of ertapenem and increase half-life but benefit is minimum and does not justify coadministration
Documented hypersensitivity to drug or amide-type anesthetics
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Pseudomembranous colitis may occur; seizures and CNS adverse reactions may occur; when using with lidocaine to administer intramuscularly, avoid inadvertent injection into blood vessel; decrease dose in renal failure; serious and occasionally fatal hypersensitivity reactions may occur with beta-lactams, caution with previous hypersensitivity reactions to penicillin, cephalosporins, other beta-lactams, or other allergens; do not mix or co-infuse in same IV line as other medications; do not mix with dextrose-containing diluents
Antipseudomonal penicillin plus beta-lactamase inhibitor. Inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active multiplication.
3.75 g IV q6h
<12 years: Not established
>12 years: Administer as in adults
Tetracyclines may decrease effects of piperacillin; high concentrations of piperacillin may physically inactivate aminoglycosides if administered in same IV line; effects when administered concurrently with aminoglycosides are synergistic; probenecid may increase penicillin levels; high-dose parenteral penicillins may result in increased risk of bleeding
Documented hypersensitivity; severe pneumonia, bacteremia, pericarditis, emphysema, meningitis, and purulent or septic arthritis should not be treated with an oral penicillin during the acute stage
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Perform CBCs prior to initiation of therapy and at least weekly during therapy; monitor for liver function abnormalities by measuring AST and ALT levels during therapy; exercise caution in patients with hepatic insufficiencies; perform urinalysis, and BUN and creatinine determinations during therapy and adjust dose if values become elevated; monitor blood levels to avoid possible neurotoxic reactions
Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. Effective against most gram-positive and gram-negative bacteria.
Has slightly increased activity against gram-negatives and slightly decreased activity against staphylococci and streptococci compared to imipenem.
1 g IV q8h
40 mg/kg IV q8h
Probenecid may inhibit renal excretion of meropenem, increasing meropenem levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Dosage adjustments (adult adjustments)
CrCl (mL/min) 10-50: 0.5-1 g q12h
CrCl <10: 0.5 g/d
HD: As for CrCl <10, with an extra 0.5 g after HD
Pseudomembranous colitis and thrombocytopenia may occur, requiring immediate discontinuation of medication
Drug combination that extends antibiotic spectrum of penicillin to include bacteria normally resistant to beta-lactam antibiotics. Indicated for skin and skin structure infections caused by beta-lactamase–producing strains of Staphylococcus aureus.
500/125 mg PO tid or 875/125 mg PO bid
10-15 mg/kg PO tid (based on amoxicillin component)
Coadministration with warfarin or heparin increases risk of bleeding
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Give for a minimum of 10 d to eliminate organism and prevent sequelae (endocarditis, rheumatic fever); following treatment, perform cultures to confirm eradication of streptococci
Alone, this drug is effective against Pasteurella species. However, not indicated for skin and skin structure infections caused by beta-lactamase–producing strains of Staphylococcus aureus. A second antibiotic such as cephalexin is needed for Staphylococcus infections.
250-500 mg PO tid
30-50 mg/kg/d PO divided tid; not to exceed 500 mg/dose
Reduces the efficacy of oral contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; may enhance chance of candidiasis
Inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active growth. Antipseudomonal penicillin plus beta-lactamase inhibitor that provides coverage against most gram-positive organisms, most gram-negative organisms, and most anaerobes.
3.1 g IV q4-6h
<3 months: Not established
>3 months
<60 kg: 200-300 mg/kg/d IV divided q4-6h
>60 kg: 3.1 g IV q4-6h
Tetracyclines may decrease effects of ticarcillin; high concentrations of ticarcillin may physically inactivate aminoglycosides if administered in same IV line; effects when administered concurrently with aminoglycosides are synergistic; probenecid may increase penicillin levels
Documented hypersensitivity; severe pneumonia, bacteremia, pericarditis, emphysema, meningitis, and purulent or septic arthritis should not be treated with oral penicillin during acute stage
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Perform CBCs prior to initiation of therapy and at least weekly during therapy; monitor for liver function abnormalities by measuring AST and ALT levels during therapy; exercise caution in patients with hepatic insufficiencies; perform urinalysis, and BUN and creatinine determinations during therapy and adjust dose if values become elevated; monitor blood levels to avoid possible neurotoxic reactions
First-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Primary activity against skin flora.
250-500 mg PO qid
25-50 mg/kg/d PO divided qid; not to exceed 500 mg/dose
Coadministration with aminoglycosides increases nephrotoxic potential
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy
Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.
400-800 mg SMX PO bid
30-60 mg/kg/d SMX PO divided bid; not to exceed 800 mg/dose
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Documented hypersensitivity; megaloblastic anemia due to folate deficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBCs frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, advanced age, anticonvulsant therapy, malabsorption syndrome); hemolysis may occur in G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation
Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
300 mg PO qid
10-25 mg/kg/d PO divided qid; not to exceed 600 mg/dose
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin
Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile
Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth.
500 mg PO bid
Not recommended
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Treats mild-to-moderate microbial infections
500 mg PO on day 1, then 250 mg PO qd for 4 d
10 mg/kg PO d 1; not to exceed 500 mg/dose, then 5 mg/kg PO qd for 4 d; not to exceed 250 mg/dose
May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine
Documented hypersensitivity; hepatic impairment; do not administer with pimozide
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Site reactions can occur with IV route; bacterial or fungal overgrowth may result from prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in hospitalized, geriatric, or debilitated patients
Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.
100 mg PO bid
<8 years: Not recommended
>8 years: 2-5 mg/kg/d PO in 1-2 divided doses; not to exceed 200 mg/d
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Second-generation cephalosporin maintains gram-positive activity that first-generation cephalosporins have; adds activity against P mirabilis, H influenzae, E coli, K pneumoniae, and M catarrhalis. Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose and route of administration.
500 mg PO bid
15-30 mg/kg/d PO divided bid; not to exceed 500 mg/dose
Disulfiramlike reactions may occur when alcohol is consumed within 72 h after taking cefuroxime; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patients receiving potent diuretics such as loop diuretics; coadministration with aminoglycosides increases nephrotoxic potential
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Reduce dosage by half if creatinine clearance is 10-30 mL/min, and by 3/4 if <10 mL/min (high doses may cause CNS toxicity); bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy
These agents inhibit viral replication.
Prodrug activated by phosphorylation by virus-specific thymidine kinase that inhibits viral replication. Herpes virus thymidine kinase (TK), but not host cells' TK, uses acyclovir as a purine nucleoside, converting it into acyclovir monophosphate, a nucleotide analogue. Guanylate kinase converts the monophosphate form into diphosphate and triphosphate analogues that inhibit viral DNA replication.
Has affinity for viral thymidine kinase and, once phosphorylated, causes DNA chain termination when acted on by DNA polymerase. Has activity against a number of herpesviruses, including herpes virus B. Primarily available in preparations for PO and IV use. Patients experience less pain and faster resolution of cutaneous lesions when used within 48 h from rash onset. May prevent recurrent outbreaks. Early initiation of therapy is imperative.
800 mg 5 times/d for 14 d
Not established
Concomitant use of probenecid or zidovudine prolongs half-life and increases CNS toxicity of acyclovir
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal failure or when using nephrotoxic drugs
Hydrochloride salt of the L-valyl ester of acyclovir. Rapidly converted into acyclovir after prompt absorption from the gut via first-pass intestinal or hepatic metabolism. An alternative to acyclovir for prophylaxis (or possibly treatment).
1000 mg PO q8 h for 14 d
Not established
Probenecid, zidovudine, or cimetidine coadministration prolongs half-life and increases CNS toxicity of valacyclovir
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal failure (decrease dose) and coadministration of nephrotoxic drugs; associated with onset of hemolytic uremic syndrome
Complications of animal bite wounds may include the following:
Centers for Disease Control and Prevention. Nonfatal dog bite-related injuries treated in hospital emergency departments--United States, 2001. MMWR Morb Mortal Wkly Rep. Jul 4 2003;52(26):605-10. [Medline].
Chambers GH, Payne JF. Treatment of dog bite wounds. Minn Med. 1969;52:427-430. [Medline].
Freer L. Bites and injuries inflicted by wild and domestic animals. In: Auerbach PS, ed. Wilderness Medicine. 5th ed. Mosby; 2007:1133-55.
Dire DJ. Cat bite wounds: risk factors for infection. Ann Emerg Med. Sep 1991;20(9):973-9. [Medline].
Talan DA, Citron DM, Abrahamian FM, et al. Bacteriologic analysis of infected dog and cat bites. N Engl J Med. Jan 14 1999;340(2):85-92. [Medline].
Abrahamian FM. Dog Bites: Bacteriology, Management, and Prevention. Curr Infect Dis Rep. Oct 2000;2(5):446-453. [Medline].
Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. Nov 15 2005;41(10):1373-406. [Medline].
Gilchrist J, Sacks JJ, White D, Kresnow MJ. Dog bites: still a problem?. Inj Prev. Oct 2008;14(5):296-301. [Medline].
Weiss HB, Friedman DI, Coben JH. Incidence of dog bite injuries treated in emergency departments. JAMA. Jan 7 1998;279(1):51-3. [Medline]. [Full Text].
Sacks JJ, Lockwood R, Hornreich J, Sattin RW. Fatal dog attacks, 1989-1994. Pediatrics. Jun 1996;97(6 Pt 1):891-895. [Medline].
Palacio J, Leon-Artozqui M, Pastor-Villalba E, Carrera-Martin F, Garcia-Belenguer S. Incidence of and risk factors for cat bites: a first step in prevention and treatment of feline aggression. J Feline Med Surg. Jun 2007;9(3):188-95. [Medline].
Moscati RM, Mayrose J, Reardon RF, Janicke DM, Jehle DV. A multicenter comparison of tap water versus sterile saline for wound irrigation. Academic Emergency Medicine. May 2007;14 (5):404-9. [Medline].
Oehler RL, Velez AP, Mizrachi M, Lamarche J, Gompf S. Bite-related and septic syndromes caused by cats and dogs. Lancet Infect Dis. Jul 2009;9(7):439-47.
Cummings P. Antibiotics to prevent infection in patients with dog bite wounds: a meta-analysis of randomized trials. Ann Emerg Med. Mar 1994;23(3):535-40. [Medline].
Gilbert DN, Moellering RC, Eliopoulos FM, Sande MA, eds. Bites. In: The Sanford Guide to Antimicrobial Therapy. 37th ed. 2007:46,47,140.
Guy RJ, Zook EG. Successful treatment of acute head and neck dog bite wounds without antibiotics. Ann Plast Surg. Jul 1986;17(1):45-8. [Medline].
Trott A. Bite wounds. In: Wounds and Lacerations Emergency Care and Closure. 2nd ed. St Louis, Mo: Mosby-Year Book Inc; 1997:265-84.
Weber EJ. Mammalian bites. In: Marx JA, Hockberger RS, Walls RM, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. 6th ed. Mosby; 2006:906-21.
animal bites, animal bite management, wound management, animal bite treatment, animal bite infection, bite wound, animal bite wound, dog bite, cat bite, pet bite, wild animal bite, bite wound infection, bite-related infection, mammal bites, rodent bites, ferret bites, rabbit bites, pit bull bite, cellulitis, rabies, septic arthritis, Staphylococcus, Streptococcus, Pasteurella, Bacteroides, Capnocytophaga canimorsus, Eikenella, Enterobacter, Proteus, Haemophilus, Klebsiella, Actinomyces, Fusobacterium, Peptostreptococcus, Clostridium, Wolinella, Propionibacterium, osteomyelitis
Alisha Perkins Garth, MD, Staff Physician, Harvard Affiliated Emergency Medicine Residency, Brigham and Women's Hospital, Massachusetts General Hospital
Alisha Perkins Garth, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, Emergency Medicine Residents Association, Phi Beta Kappa, Sigma Xi, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
N Stuart Harris, MD, FACEP, Assistant Professor in Surgery, Harvard Medical School, Massachusetts General Hospital; Attending Physician, Massachusetts General Hospital
N Stuart Harris, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, International Society for Mountain Medicine, and Massachusetts Medical Society
Disclosure: Nothing to disclose.
Robert M McNamara, MD, FAAEM, Chair and Professor, Department of Emergency Medicine, Temple University School of Medicine
Robert M McNamara, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
James Steven Walker, DO, MS, Clinical Professor of Surgery, Department of Surgery, University of Oklahoma Health Sciences Center
James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.