# 25 - 146 Infectious Complications of Bites

### 146 Infectious Complications of Bites

frontal, parietal, and occipital superior cerebral veins and the diploic 
veins, which communicate with the meningeal veins. Bacterial menin­
gitis is a common predisposing condition for septic thrombosis of the 
superior sagittal sinus. The diploic veins, which drain into the superior 
sagittal sinus, provide a route for the spread of infection from the 
meninges, especially in cases where there is purulent exudate near areas 
of the superior sagittal sinus. Infection can also spread to the superior 
sagittal sinus from nearby SDE or epidural abscess. Dehydration from 
vomiting, hypercoagulable states, and immunologic abnormalities, 
including the presence of circulating antiphospholipid antibodies, 
also contribute to cerebral venous sinus thrombosis. Thrombosis may 
extend from one sinus to another, and at autopsy, thrombi of different 
histologic ages can often be detected in several sinuses. Thrombosis of 
the superior sagittal sinus is often associated with thrombosis of supe­
rior cortical veins and small parenchymal hemorrhages.

The superior sagittal sinus drains into the transverse sinuses 
(Fig. 145-6). The transverse sinuses also receive venous drainage from 
small veins from both the middle ear and mastoid cells. The transverse 
sinus becomes the sigmoid sinus before draining into the internal jugu­
lar vein. Septic transverse/sigmoid sinus thrombosis can be a complica­
tion of acute and chronic otitis media or mastoiditis. Infection spreads 
from the mastoid air cells to the transverse sinus via the emissary veins 
or by direct invasion. The cavernous sinuses are inferior to the superior 
sagittal sinus at the base of the skull. The cavernous sinuses receive 
blood from the facial veins via the superior and inferior ophthalmic 
veins. Bacteria in the facial veins enter the cavernous sinus via these 
veins. Bacteria in the sphenoid and ethmoid sinuses can spread to the 
cavernous sinuses via the small emissary veins. The sphenoid and eth­
moid sinuses are the most common sites of primary infection resulting 
in septic cavernous sinus thrombosis.
PART 5
Infectious Diseases
■
■CLINICAL MANIFESTATIONS
Septic thrombosis of the superior sagittal sinus presents with head­
ache, fever, nausea and vomiting, confusion, and focal or generalized 
seizures. There may be a rapid development of stupor and coma. 
Weakness of the lower extremities with bilateral Babinski’s signs or 
hemiparesis is often present. When superior sagittal sinus thrombosis 
occurs as a complication of bacterial meningitis, nuchal rigidity and 
Kernig’s and Brudzinski’s signs may be present.
The oculomotor nerve, the trochlear nerve, the abducens nerve, 
the ophthalmic and maxillary branches of the trigeminal nerve, and 
the internal carotid artery all pass through the cavernous sinus 
(see Fig. 452-7). The symptoms of septic cavernous sinus thrombosis 
are fever, headache, frontal and retroorbital pain, and diplopia. The 
classic signs are ptosis, proptosis, chemosis, and extraocular dysmotil­
ity due to deficits of cranial nerves III, IV, and VI; hyperesthesia of 
the ophthalmic and maxillary divisions of the fifth cranial nerve and 
a decreased corneal reflex may be detected. There may be evidence of 
dilated, tortuous retinal veins and papilledema.
Headache and earache are the most frequent symptoms of trans­
verse sinus thrombosis. A transverse sinus thrombosis may also pres­
ent with otitis media, sixth nerve palsy, and retroorbital or facial 
pain (Gradenigo’s syndrome). Sigmoid sinus and internal jugular vein 
thrombosis may present with neck pain.
■
■DIAGNOSIS
The diagnosis of septic venous sinus thrombosis is suggested by 
an absent flow void within the affected venous sinus on MRI and 
confirmed by contrast-enhanced magnetic resonance venography, 
CT venography, or the venous phase of cerebral angiography. The 
diagnosis of thrombophlebitis of intracerebral and meningeal veins is 
suggested by the presence of intracerebral hemorrhage but requires the 
venous phase of cerebral angiography for definitive diagnosis.
TREATMENT
Suppurative Thrombophlebitis
Septic venous sinus thrombosis is treated with antibiotics, hydra­
tion, and removal of infected tissue and thrombus in septic lateral 

or cavernous sinus thrombosis. The choice of antimicrobial therapy 
is based on the bacteria responsible for the predisposing or asso­
ciated condition. Optimal duration of therapy is unknown, but 
antibiotics are usually continued for 6 weeks or until there is 
radiographic evidence of resolution of thrombosis. Anticoagulation 
with unfractionated or low-molecular-weight heparin is recom­
mended for aseptic venous sinus thrombosis and in the treatment 
of septic venous sinus thrombosis complicating bacterial meningitis 
in patients who have progressive neurologic deterioration despite 
antimicrobial therapy and intravenous fluids. The presence of a 
small intracerebral hemorrhage from septic thrombophlebitis is 
not an absolute contraindication to heparin therapy. Successful 
management of aseptic venous sinus thrombosis has been reported 
with surgical thrombectomy, catheter-directed urokinase therapy, 
and a combination of intrathrombus recombinant tissue plasmino­
gen activator (rtPA) and intravenous heparin, but there are not 
enough data to recommend these therapies in septic venous sinus 
thrombosis.
■
■FURTHER READING
Bodilsen J et al: European Society of Clinical Microbiology and Infec­
tious Diseases guidelines on diagnosis and treatment of brain abscess 
in children and adults. Clinical Microbiol Infect 30:66, 2024.
Prosty C et al: Revisiting the evidence base for modern-day practice 
of the treatment of toxoplasmic encephalitis: A systematic review and 
meta-analysis. Clin Infect Dis 76:e1302, 2023.
Ropper AH, Klein JP: Cerebral venous thrombosis. N Engl J Med 
385:59, 2021.
White AC et al: Diagnosis of Neurocysticercosis: 2017 Clinical 
Practice Guidelines by the Infectious Diseases Society of America 
(IDSA) and the American Society of Tropical Medicine and Hygiene 
(ASTMH). Clin Infect Dis 66:e49, 2018.
Nongnooch Poowanawittayakom, 

Lawrence C. Madoff

Infectious Complications 

of Bites
The skin is an essential component of nonspecific immunity, protect­
ing the host from potential pathogens in the environment. Breaches in 
this protective barrier thus represent a form of immunocompromise 
that predisposes the patient to infection. Bites and scratches from 
animals and humans allow the inoculation of microorganisms past the 
skin’s protective barrier into deeper, susceptible host tissues.
Each year in the United States, millions of animal-bite wounds are 
sustained. The vast majority are inflicted by pet dogs and cats, which 
number >100 million; the annual incidence of dog and cat bites has 
been reported as 300 bites per 100,000 population. Other bite wounds 
are a consequence of encounters with animals in the wild or in occu­
pational settings. While many of these wounds require minimal or 
no therapy, a significant number result in infection, which may be 
life-threatening. The microbiology of bite-wound infections in general 
reflects the oropharyngeal flora of the biting animal, although organ­
isms from the soil, the skin of the animal and the victim, and the 
animal’s feces may also be involved.
DOG BITES
In the United States, dogs bite >4.7 million people each year and are 
responsible for 80% of all animal-bite wounds, an estimated 15–20% 
of which become infected. Each year, 800,000 Americans seek medical

attention for dog bites; of those injured, 386,000 require treatment in 
an emergency department, with >1000 emergency department visits 
each day and ~43 deaths per year. Most dog bites are provoked and are 
inflicted by the victim’s pet or by a dog known to the victim. These bites 
are frequently sustained during efforts to break up a dogfight. Children 
are more likely than adults to sustain canine bites, with the highest inci­
dence of 6 bites per 1000 population among boys 5–9 years old. Victims 
are more often male than female, and bites most often involve an upper 
extremity. Among children <4 years old, two-thirds of all these injuries 
involve the head or neck. Infection typically manifests 8–24 h after the 
bite as pain at the site of injury with cellulitis accompanied by purulent, 
sometimes foul-smelling discharge. Septic arthritis and osteomyelitis 
may develop if a canine tooth penetrates synovium or bone. Systemic 
manifestations (e.g., fever, lymphadenopathy, and lymphangitis) also 
may occur. The microbiology of dog-bite wound infections is usu­
ally mixed and includes Pasteurella species, β-hemolytic streptococci, 
Staphylococcus species (including methicillin-resistant Staphylococcus 
aureus [MRSA] and Staphylococcus intermedius), Neisseria species 
(commonly Neisseria weaveri, formerly known as CDC group M-5), 
Eikenella corrodens, and Capnocytophaga canimorsus. Many wounds 
also include anaerobic bacteria such as Bacteroides, Fusobacterium, 
Prevotella, and Porphyromonas species.
While most infections resulting from dog-bite injuries are localized 
to the area of injury, many of the microorganisms involved are capable 
of causing systemic infection, including bacteremia, meningitis, brain 
abscess, endocarditis, and chorioamnionitis. These infections are par­
ticularly likely in hosts with edema or compromised lymphatic drain­
age in the involved extremity (e.g., after a bite on the arm in a woman 
who has undergone mastectomy) and in patients who are immu­
nocompromised by medication or disease (e.g., glucocorticoid use, 
systemic lupus erythematosus, acute leukemia, or hepatic cirrhosis). In 
addition, dog bites and scratches may result in systemic illnesses such 
as rabies (Chap. 214) and tetanus (Chap. 157).
Infection with Capnocytophaga canimorsus (and other Capnocyto­
phaga species) following dog-bite wounds (or licking of preexisting 
wounds) may result in fulminant sepsis, disseminated intravascular 
coagulation, and renal failure, particularly in hosts who have impaired 
hepatic function, who have undergone splenectomy, or who are immu­
nosuppressed. This thin gram-negative rod is difficult to culture on 
most solid media but grows in a variety of liquid media. It may require 
up to 14 days of incubation to grow on blood cultures. The bacteria are 
occasionally seen within polymorphonuclear leukocytes on Wrightstained smears of peripheral blood from septic patients. Tularemia 
(Chap. 175) also has been reported to follow dog bites.
CAT BITES
Although less common than dog bites, cat bites and scratches result in 
infection in more than half of all cases. Because the cat’s narrow, sharp 
canine teeth penetrate deeply into tissue, cat bites are more likely than 
dog bites to cause septic arthritis and osteomyelitis; the development 
of these conditions is particularly likely when punctures are located 
over or near a joint, especially in the hand. Women sustain cat bites 
more frequently than do men. These bites most often involve the 
hands and arms. Both bites and scratches from cats are prone to infec­
tion from organisms in the cat’s oropharynx. Pasteurella multocida, a 
normal component of the feline oral flora, is a small gram-negative 
coccobacillus implicated in the majority of cat-bite wound infections. 
Like that of dog-bite wound infections, however, the microflora of 
cat-bite wound infections is usually mixed. However, the median time 
from bite to the appearance of signs and symptoms of wound infection 
is much shorter when compared to dog bites. Other microorganisms 
causing infection after cat bites are similar to those causing dog-bite 
wound infections.
The same risk factors for systemic infection following dog-bite 
wounds apply to cat-bite wounds. Pasteurella infections tend to 
advance rapidly, often within hours, causing severe inflammation 
accompanied by purulent drainage with adenitis; Pasteurella may also 
be spread by respiratory droplets from animals, resulting in pneumonia 
or bacteremia. Like dog-bite wounds, cat-bite wounds may result in 

the transmission of rabies or in the development of tetanus. Infection 
with Bartonella henselae causes cat-scratch disease (Chap. 177) and is 
an important late consequence of cat bites and scratches. Tularemia 
(Chap. 175) also has been reported to follow cat bites. Occasionally, 
sporotrichosis (Chap. 225) has been associated with scratches or bites 
by animals, especially domestic cats.

OTHER ANIMAL BITES
Infections have been attributed to bites from many animal species. 
Often these bites are sustained as a consequence of occupational 
exposure (farmers, laboratory workers, veterinarians) or recreational 
exposure (hunters and trappers, wilderness campers, owners of exotic 
pets). Generally, the microflora of bite wounds reflects the oral flora of 
the biting animal. Most members of the cat family, including feral cats, 
harbor P. multocida. Bite wounds from aquatic animals such as alliga­
tors or piranhas may contain Aeromonas hydrophila. Shark, moray 
eel, and barracuda bites, like other injuries sustained in saltwater, are 
often associated with infections with marine Vibrio species. Venomous 
snakebites (Chap. 471) result in severe inflammatory responses and tis­
sue necrosis—conditions that render these injuries prone to infection. 
The snake’s oral flora includes many species of aerobes and anaerobes, 
such as Pseudomonas aeruginosa, Serratia marcescens, Proteus species, 
Staphylococcus epidermidis, Salmonella species, Bacteroides fragilis, and 
Clostridium species. Bites from nonhuman primates are highly suscep­
tible to infection with pathogens similar to those isolated from human 
bites (see below). Bites from Old World monkeys (Macaca) may also 
result in the transmission of B virus (Macacine herpesvirus 1, Herpes­
virus simiae, Cercopithecine herpesvirus), a cause of serious infection of 
the human central nervous system. Actinobacillus lignieresii has often 
been reported in infected wounds of humans bitten by horses, pigs, and 
sheep. Bites of seals, walruses, and polar bears may cause a chronic sup­
purative infection known as seal finger, which is probably due to one 
or more species of Mycoplasma, including Mycoplasma phocacerebrale, 
colonizing these animals.
CHAPTER 146
Infectious Complications of Bites 
Small rodents, including rats, mice, and gerbils, as well as animals 
that prey on rodents may transmit Streptobacillus moniliformis 
(a microaerophilic, pleomorphic gram-negative rod) or Spirillum minor 
(a spirochete); these organisms cause a clinical illness known as rat-bite 
fever. The vast majority of cases in the United States are streptobacil­
lary, whereas Spirillum infection occurs mainly in Asia.
In the United States, the risk of rodent bites is usually greatest 
among laboratory workers or inhabitants of rodent-infested dwellings 
(particularly children). Rat-bite fever is distinguished from acute bitewound infection by its typical manifestation after the initial wound 
has healed. Streptobacillary disease follows an incubation period of 
3–10 days. Fever, chills, myalgias, headache, and severe migratory 
arthralgias are usually followed by a maculopapular rash, which char­
acteristically involves the palms and soles and may become confluent 
or purpuric. Complications include endocarditis, myocarditis, menin­
gitis, pneumonia, and abscesses in many organs. Haverhill fever is an S. 
moniliformis infection acquired from contaminated milk or drinking 
water and has similar manifestations. Streptobacillary rat-bite fever 
was frequently fatal in the preantibiotic era. The differential diagnosis 
includes Rocky Mountain spotted fever, Lyme disease, leptospirosis, 
and secondary syphilis. The diagnosis is made by direct observation of 
the causative organisms in tissue or blood, by culture of the organisms 
on enriched media, or by serologic testing with specific agglutinins.
Spirillum infection (referred to in Japan as sodoku) causes pain and 
purple swelling at the site of the initial bite, with associated lymphan­
gitis and regional lymphadenopathy, after an incubation period of 
1–4 weeks. The systemic illness includes fever, chills, and headache. 
The original lesion may eventually progress to an eschar. The infection 
is diagnosed by direct visualization of the spirochetes in blood or tissue 
or by animal inoculation.
HUMAN BITES
Human bites may be self-inflicted; may be sustained by medical per­
sonnel caring for patients; or may take place during fights, domestic 
abuse, or sexual activity. The risk of infection in human-bite wounds

depends on the depth of the wound. The risk of wound infection 
ranges from about 2% in superficial wounds to over 25% in deep bite 
wounds such as clenched-fist injuries. Human-bite wounds become 
infected more frequently (~10–15% of the time) than do bites inflicted 
by other animals. These infections reflect the diverse oral microflora of 
humans, which includes multiple species of aerobic and anaerobic bac­
teria. Common aerobic isolates include viridans streptococci, S. aureus, 
E. corrodens (which is particularly common in clenched-fist injury; 
see below), and Haemophilus influenzae. Anaerobic species, includ­
ing Fusobacterium nucleatum and Prevotella, Porphyromonas, and 
Peptostreptococcus species, are isolated from 50% of wound infections 
due to human bites; many of these isolates produce β-lactamases. The 
oral flora of hospitalized and debilitated patients often includes Entero­
bacteriaceae in addition to the usual organisms. Hepatitis B, hepatitis 
C, herpes simplex virus infection, syphilis, tuberculosis, actinomycosis, 
and tetanus have been reported to be transmitted by human bites; it is 
biologically possible to transmit HIV through human bites, although 
the risk is quite low. In general, postexposure prophylaxis should be 
considered for bites involving severe trauma with extensive tissue dam­
age and the presence of blood in saliva. There is essentially no risk of 
transmission if the skin is intact.

Human bites are categorized as either occlusional injuries, which 
are inflicted by actual biting, or clenched-fist injuries, which are 
sustained when the fist of one individual strikes the teeth of another, 
causing traumatic laceration of the hand. For several reasons, 
clenched-fist injuries, which are sometimes referred to as “fight bite” 
and which are more common than occlusional injuries, result in 
particularly serious infections. The deep spaces of the hand, includ­
ing the bones, joints, and tendons, are frequently inoculated with 
organisms in the course of such injuries. The clenched position of 
the fist during injury, followed by extension of the hand, may further 
promote the introduction of bacteria as contaminated tendons retract 
beneath the skin’s surface Moreover, medical attention is often sought 
only after frank infection develops. Patients with clenched-fist injury 
should undergo careful physical examination of the area, including 
the extensor tendons.
PART 5
Infectious Diseases
APPROACH TO THE PATIENT
Animal or Human Bites
A careful history should be elicited, including the type of biting 
animal, the type of attack (provoked or unprovoked), and the 
amount of time elapsed since injury. Local and regional publichealth authorities should be contacted to determine whether an 
individual species could be rabid and/or to locate and observe the 
biting animal when rabies prophylaxis may be indicated (Chap. 214). 
Suspicious human-bite wounds should provoke careful ques­
tioning regarding domestic or child abuse. Details on antibiotic 
allergies, immunosuppression, splenectomy, liver disease, mastec­
tomy, and immunization history should be obtained. The wound 
should be inspected carefully for evidence of infection, including 
redness, exudate, and foul odor. The type of wound (puncture, 
laceration, or scratch); the depth of penetration; and the pos­
sible involvement of joints, tendons, nerves, and bones should be 
assessed. It is often useful to include a diagram or photograph of 
the wound in the medical record. In addition, a general physical 
examination should be conducted and should include an assess­
ment of vital signs as well as an evaluation for evidence of lym­
phangitis, lymphadenopathy, dermatologic lesions, and functional 
limitations. Injuries to the hand warrant consultation with a hand 
surgeon for the assessment of tendon, nerve, and muscular dam­
age. Radiographs should be obtained in penetrating wounds to 
evaluate the evidence of fracture or retained foreign body such 
as a tooth fragment. Culture and Gram’s staining of all infected 
wounds are essential; anaerobic cultures should be undertaken if 
abscesses, devitalized tissue, or foul-smelling exudate is present. 
A small-tipped swab may be used to culture deep punctures or 
small lacerations. It is also reasonable to culture samples from 

apparently uninfected wounds due to bites inflicted by animals 
other than dogs and cats, since the microorganisms causing dis­
ease are less predictable in these cases. The microbiology labora­
tory should be notified if fastidious organisms such as E. corrodens 
are under consideration in human bites. The white blood cell 
count should be determined, and the blood cultured if systemic 
infection is suspected.
TREATMENT
Bite-Wound Infections 
WOUND MANAGEMENT
Wound closure is controversial in bite injuries. Many authori­
ties prefer not to attempt primary closure of wounds that are or 
may become infected, choosing instead to irrigate these wounds 
copiously, debride devitalized tissue, remove foreign bodies, and 
approximate the wound edges. All abscesses should be drained. 
Delayed primary closure may be undertaken after the risk of infec­
tion is over. Small uninfected wounds may be allowed to close 
by secondary intention. Puncture wounds due to cat bites should 
be left unsutured because of the high rate at which they become 
infected. Facial wounds are usually sutured after thorough cleaning 
and irrigation because of the importance of a good cosmetic result 
in this area and because anatomic factors such as an excellent blood 
supply and the absence of dependent edema lessen the risk of infec­
tion. In general, wounds >12 h old (for bites to the arm or leg) or 
>24 h old (for bites to the face) should not be closed primarily and 
may require prophylactic antibiotics (see below). 
ANTIBIOTIC THERAPY 
Established Infection  Antibiotics should be administered for all 
established bite-wound infections and should be chosen in light 
of the most likely potential pathogens, as indicated by the biting 
species and by Gram’s stain and culture results (Table 146-1). 
For dog and cat bites, antibiotics should be effective against S. 
aureus, Pasteurella species, C. canimorsus, streptococci, and oral 
anaerobes. For human bites, agents with activity against S. aureus, 
H. influenzae, and β-lactamase-positive oral anaerobes should be 
used. The combination of an extended-spectrum penicillin with 
a β-lactamase inhibitor (amoxicillin/clavulanic acid, ampicillin/
sulbactam) appears to offer the most reliable coverage for these 
pathogens. Third-generation cephalosporins (ceftriaxone, cefpo­
doxime) also offer substantial coverage when given in conjunc­
tion with a drug that provides anaerobic coverage (clindamycin 
or metronidazole). The choice of antibiotics for penicillin-allergic 
patients (particularly those in whom immediate-type hypersensi­
tivity makes the use of cephalosporins hazardous) is more difficult 
and is based primarily on in vitro sensitivity since data on clinical 
efficacy are inadequate. The combination of an antibiotic active 
against gram-positive cocci and anaerobes (such as clindamy­
cin or metronidazole) with trimethoprim-sulfamethoxazole or 
a fluoroquinolone, which is active against many of the other 
potential pathogens, would appear reasonable. Moxifloxacin, a 
fluoroquinolone with anaerobic coverage, can also be considered 
as a single agent. In vitro data suggest that azithromycin alone 
provides coverage against most commonly isolated bite-wound 
pathogens; however, this agent has variable activity against 

P. multocida, E. corrodens, and fusobacteria and thus should be 
avoided unless no alternative agent is available. Empirical use of 
agents active against MRSA should be considered in high-risk 
situations while culture results are awaited.
Antibiotics are generally given for about 5–7 days and for no 
more than 14 days, but the response to therapy must be carefully 
monitored. Failure to respond should prompt a consideration of 
diagnostic alternatives and surgical evaluation for possible drain­
age or debridement. Complications such as osteomyelitis or septic 
arthritis mandate a longer duration of therapy.

TABLE 146-1  Management of Wound Infections Following Animal and Human Bites
COMMONLY ISOLATED 
PATHOGENS
PREFERRED ANTIBIOTIC(S)a
BITING SPECIES
Dog
Staphylococcus aureus, 
Pasteurella spp. (mainly 

P. multocida and 

P. canis), anaerobes, 
Capnocytophaga canimorsus
Amoxicillin/clavulanate 
(875/125 mg PO q12h) or 
ampicillin/sulbactam 

(3.0 g IV q6h)
or
Ceftriaxone 2 g IV once daily 
plus metronidazole 500 mg 
q8h
Cat
P. multocida, S. aureus, 
anaerobes
Amoxicillin/clavulanate, 
ampicillin/sulbactam, 
or ceftriaxone plus 
metronidazole as above
Human, occlusional
Viridans streptococci, 
S. aureus, Haemophilus 
influenzae, anaerobes 
Eikenella corrodense
Amoxicillin/clavulanate 
plus TMX-SMX if consider 
including MRSA coverage or

ampicillin/sulbactam

or ceftriaxone plus 
metronidazole (consider 
adding vancomycin if MRSA 
coverage required)
 
Monkey
As for human bite
As for human bite
As for human bite
Always
For macaque monkeys, 
consider B virus 
prophylaxis with 
acyclovir.
Snake
Snake oral flora including 
Pseudomonas, Morganella 
spp., E. coli, group D 
streptococci, Salmonella 
spp., anaerobic organisms 
including Bacteroides 
fragilis, Clostridium spp.
Piperacillin/tazobactam 

3.375 g IV q6–8h
Rodent
Rat bite fever; Streptobacillus 
moniliformis, Spirillum minus, 
Streptobacillus notomytis, 
Leptospira spp., P. multocida
Penicillin VK (500 mg PO qid) 
or ceftriaxone IV
Aquatic animal 
(alligator, piranha, 
shark, moray eel, 
barracuda)
Aeromonas hydrophila, 
marine Vibrio spp. (Vibrio 
vulnificus)
Third-generation 
cephalosporin (e.g., 
ceftriaxone, 1 g IV q24h) plus 
doxycycline (100 mg PO bid)
aAntibiotic choices should be based on culture data when available. These suggestions for empirical therapy need to be tailored to individual circumstances and local 
conditions. MRSA empirical coverage is based on individual risk factors. IV regimens should be used for hospitalized patients. A single IV dose of antibiotics may be given 
to patients who will be discharged after initial management. bAvoid monotherapy for aerobic coverage due to poor activity against Pasteurella spp. Risk of Clostridioides 
difficile infection. cCat bite may leave small external wounds but deep puncture wounds. dProphylactic antibiotics are suggested for severe or extensive wounds, facial 
wounds, and crush injuries; when bone or joint may be involved; delayed wound care >8 h; and when comorbidity is present (see text). Prophylactic antibiotic duration 
is generally between 3 and 5 days. eEikenella corrodens is resistant to penicillinase-resistant penicillin, first and second generation cephalosporins, clindamycin, 
metronidazole, and aminoglycosides in vitro.
Abbreviations: DS, double-strength; TMP-SMX, trimethoprim-sulfamethoxazole.
Management of C. canimorsus bacteremia requires an initial 
treatment with a 2-week course of IV antibiotics such as penicillin 
G (2 million units IV every 4 h) or IV ampicillin/sulbactam (3.0 
g every 6 h) along with supportive measures. Once the patient is 
improved, then a switch to oral antibiotics can be considered. Alter­
native agents for the treatment of C. canimorsus infection include 
cephalosporins or carbapenems. Serious infection with P. multocida 
(e.g., pneumonia, sepsis, or meningitis) also should be treated with 
IV penicillin G. Alternative agents include a second- or thirdgeneration cephalosporin or ciprofloxacin. Penicillin resistance is 
uncommon.
Bites by venomous snakes (Chap. 471) may not require antibi­
otic treatment. Because it is often difficult to distinguish signs of 
infection from tissue damage caused by the envenomation, many 
authorities continue to recommend treatment directed against the 
snake’s oral flora—i.e., the administration of broadly active agents 
such as ceftriaxone (1–2 g IV every 24 h) or ampicillin/sulbactam 
(3.0 g IV every 6 h).
Seal finger appears to respond to doxycycline (100 mg twice daily 
for a duration guided by the response to therapy). 

ALTERNATIVE IN 
PENICILLIN-ALLERGIC 
PATIENT
PROPHYLAXIS ADVISED 
FOR EARLY UNINFECTED 
WOUNDS
OTHER CONSIDERATIONS
Clindamycinb or 
metronidazole plus 
either TMP-SMX 

(1 DS tablet PO bid) or 
ciprofloxacin (500 mg 
PO bid)
Sometimesc
Consider rabies 
prophylaxis.
Clindamycin or 
metronidazole plus 
TMP-SMX as above or 
fluoroquinolone
Usuallyd
Consider rabies 
prophylaxis. Carefully 
evaluate for joint/bone 
penetration.
TMP-SMX plus 
metronidazole
Always
 
Clindamycin or 
metronidazole plus a 
fluoroquinolone
Evidence does not 
support the benefit. Can 
consider in regions with 
high rates of infection 
such as Brazil.
Administer antivenin for 
venomous snakebite. 
Tetanus prophylaxis.
CHAPTER 146
Doxycycline (100 mg 
PO bid)
Sometimes
 
Infectious Complications of Bites 
Clindamycin or 
metronidazole plus 
levofloxacin (750 
mg PO qd) plus 
doxycycline
Always
Obtain prompt surgical 
consultation, as risk for 
necrotizing infection is 
high with Aeromonas and 
Vibrio spp.
Presumptive or Prophylactic Therapy  The use of antibiotics for 
patients presenting early (within 8 h) after bite injury is controver­
sial. Although symptomatic infection frequently will not yet have 
manifested at this point, many early wounds will harbor pathogens, 
and many will become infected. Studies of antibiotic prophylaxis for 
wound infections are limited and have often included only small 
numbers of cases in which various types of wounds have been man­
aged according to various protocols. A meta-analysis of eight ran­
domized trials of prophylactic antibiotics in patients with dog-bite 
wounds demonstrated a reduction in the rate of infection by 50% 
with prophylaxis. However, in the absence of sound clinical trials, 
many clinicians base the decision to treat bite wounds with empirical 
antibiotics on the species of the biting animal; the location, severity, 
and extent of the bite wound; and the existence of comorbid condi­
tions in the host. All human- and monkey-bite wounds should be 
treated presumptively because of the high rate of infection. Most catbite wounds, particularly those involving the hand, should consider 
prophylactic antibiotics. Other factors favoring treatment for bite 
wounds include severe injury, as in crush wounds; potential bone or 
joint involvement; involvement of the hands or genital region; host