Skin and Soft Tissue Infection Update: Presentation, Diagnosis, and Syndrome-Specific Antibiotic Management
Skin and Soft Tissue Infection Update: Presentation, Diagnosis, and Syndrome-Specific Antibiotic Management
Part I: Cellulitis, Mammalian Bites, and Puncture Wounds
Author: Charles Stewart, MD, FACEP, Emergency Physician, Colorado Springs, CO.
Peer Reviewer: David Robinson, MD, MS, Research Director and Assistant Professor, Department of Emergency Medicine, The University of Texas Houston Medical Center; Director, Diagnostic Observation Center, Memorial Hermann Hospital, Houston, TX.
Bacterial infections of the skin and underlying soft tissues are among the most common complaints encountered in emergency practice. Although most skin infections can be managed expeditiously, some variants, especially when associated with comorbid conditions and/or bacteremia, may lead to hospital admission and are associated with substantial morbidity. Fortunately, the majority of skin infections respond promptly to oral antibiotic therapy, but a significant minority will pose diagnostic and therapeutic problems.
The course of serious skin infections can be fulminant, and the mortality rate can be as high as 75%.1 To produce optimal outcomes in these patients, the emergency physician must have a thorough understanding of the various etiologies, syndromes, and presentation patterns associated with a wide range of skin infections.
As might be expected, changes in the etiologic agents causing skin infections—whether it be cellulitis, infections associated with bites, or diabetic foot ulcers—as well as changes in sensitivity to antimicrobials, have heightened interest in these infections. For example, emergence of erythromycin resistance among Streptococcus pyogenes and Staphylococcus aureus species has resulted in unacceptable cure rates for pyoderma using this time-honored antibiotic. In addition, the increasing incidence of methicillin-resistant Staphylococcus aureus (MRSA) strains has brought problems linked to this problematic organism into the emergency physician’s practice.
Worldwide reappearance of the streptococcal strains that cause streptococcal group A sepsis and streptococcal septic shock syndrome have kindled renewed interest in these diseases. Add changes in our patient population to these microbial and resistance factors, and the stage has been set for an increase in atypical and unusual infections. Recent increases in transplant surgery, cancer chemotherapy, and changing demographic patterns in HIV-infected patients have resulted in more immunocompromised patients seen in emergency departments. Many of these individuals are at increased risk for skin infections, as are diabetic patients.
With these clinical issues in clear focus, the purpose of this two-part series is to categorize the range of skin infections encountered in the emergency department, with a special emphasis on differential diagnosis and outcome-effective antibiotic selection.
—The Editor
Simple, Superficial Skin Infections
Pyodermas Impetigo. Impetigo is an indolent, superficial pyoderma that can be caused by either Staphylococcus aureus or by Streptococcus pyogenes (with or without co-infection), with Staphylococcus aureus.1 Although the literature implicates streptococcus as the most common cause of pyoderma, S. aureus increasingly has been identified as the sole pathogen.2
It should be emphasized that impetigo is probably the most common skin infection in the pediatric population. Typically, the infection originates with small pinpoint papules that gradually enlarge to form pustules and vesicles. The vesicles rupture and leave a characteristic honey-colored scaling over an inflammatory base.
Impetigo usually presents on the face, and will typically manifest as erythematous lesions near the mouth and nose. Impetigo may also occur at the site of minor trauma, especially near abrasions or insect bites. The common, epidemic variety appears most frequently during the late summer and early fall. Warm, humid weather predisposes to the disease.
A variant of impetigo is bullous impetigo, which is usually caused by Staphylococcus aureus.3 Clinically, bullous impetigo is characterized by large, flaccid bullae with yellow fluid. These bullae frequently rupture to leave a "scalded" appearance that is accompanied by superficial erosion of the skin surface. The same bacterial toxin that causes these bullae also causes the systemic staphylococcal scalded skin syndrome.4-6 A Gram stain of the vesicular fluid or exudates will demonstrate characteristic gram-positive cocci.
For most patients, topical treatment and good hygiene may be sufficient. Mupirocin 2% ointment (Bactroban) is applied three times daily. Bacitracin is less effective but less expensive. If topical therapy fails, an oral anti-staphylococcal agent is appropriate. Recurrent infections are often the result of nasal colonization with Staphylococcus aureus. Mupirocin 2% ointment in a calcium base (Bactroban Nasal Ointment) applied twice daily for five days will usually cure this problem. For recurrent infections, some clinicians recommend that topical and oral agents be used simultaneously.
Ecthyma. Staphylococcus aureus or Streptococcus pyogenes are the most common causes of impetigo. Ecthyma resembles impetigo clinically, but the process is more extensive and also includes the subcutaneous tissue. The typical lesion of ecthyma is a "punched out" ulceration with adherent, necrotic crusts and raised, inflammatory borders. Vesicles or pustules are occasionally seen. The most commonly affected anatomic area is the legs, especially the dorsum of the feet and the anterior shin.
Metastatic seeding of the skin from pseudomonas septicemia may cause a syndrome with a similar appearance called ecthyma gangrenosum.7 These patients are often gravely ill, unlike those seen with streptococcal ecthyma. Crowded living conditions, poor hygiene, heat, humidity, and compromised nutrition contribute to this disease. Ecthyma often follows insect bites and excoriations associated with other minor trauma to the skin. Varicella lesions may also provide a portal of bacterial entrance to the skin.
Treatment of choice is an oral anti-staphylococcal agent. Necrotic areas should be gently debrided and crusts removed. Fluctuant vesicles or pustules should be drained and the area washed with an anti-staphylococcal soap. Ecthyma is slow to heal and, unlike impetigo, often causes scarring at the site of the infection.
Folliculitis, Furuncles, and Carbuncles. Folliculitis is a superficial infection characterized by reddened papules or pustules about the hair follicles which are 2-5 mm in diameter. Common sites for folliculitis include the beard, upper back, chest, buttocks, and forearms. Folliculitis may be pruritic or painful, especially when it is pustular. Most cases of folliculitis are caused by Staphylococcus aureus, although Pseudomonas aeruginosa is also implicated in hot tub or swimming pool folliculitis. "Hot tub folliculitis" usually will be most prominent on the parts of the body covered by a bathing suit. Gram stain of the pustular fluid may identify the causative organism.
Extension of the follicular infection into the subcutaneous tissue will result in a furuncle. Furuncles or boils are deep-seated painful nodules adjacent to the hair follicle. Confluence of several furuncles and further extension can create a carbuncle with interconnecting sinus tracts and fibrosis. Furuncles can occur in any hair-bearing area including the face and auditory canal, but the lesions usually occur on the posterior portion of the neck, the back, or the thighs.
Furuncles can enlarge rapidly and, not infrequently, are associated with severe pain and erythema. Fluctuance also may develop. Carbuncles are often associated with more systemic symptoms than furuncles, with fever, malaise, and lymphadenopathy being the most common findings. Recurrent furunclulosis can be a challenging problem in diabetic patients, in alcoholics, in those who are malnourished or obese, and in individuals with atopic dermatitis. Immunosuppressed patients and those with immunoglobulin deficiencies or defects in neutrophil function are also at increased risk of recurrence of furuncles. Occlusive clothing and poor hygiene contribute to the problem.
Some patients will develop recurrent furuncles due to skin or nasal colonization with Staphylococcus aureus.8 Bacteremia can occur when a furuncle is manipulated (i.e., squeezing the lesion). As a rule, bacteremia is transient although bacterial metastasis to heart, bones, joints, meninges, and deep tissues have been reported.
Treatment. For many patients with isolated furuncles, appropriate treatment consists of warm compresses and topical treatment. The area should be cleaned with a topical benzoyl peroxide soap, cleansing lotion, or an antibacterial soap. After thorough cleansing, the patient should apply a topical antibiotic such as mupirocin 2% or clindamycin 1%. For extensive disease or when topical antibiotics fail, an oral anti-staphylococcal agent such as azithromycin or a cephalosporin should be added. Warm compresses are often advocated.
Carbuncles and furuncles associated with cellulitis and fever should be treated with an anti-staphylococcal drug. Surgical incision and drainage are indicated for all fluctuant masses. A cruciate incision and undermining may be needed for large furuncles and carbuncles. Patients with staphylococcal carrier states will benefit from an oral anti-staphylococcal antibiotic and nasal mupirocin cream for eradication of the staphylococcus. These patients can also be treated with rifampin for a 10-day course.9 Topical use of nasal mupirocin has also been reported to decrease carrier states.
Cellulitis. Cellulitis is a deep infection of the skin that extends to the subcutis. It begins as a painful, tender, erythematous, warm area that spreads rapidly and produces indistinct borders. Fever, chills, rigors, and sweats are frequent. The infection most often begins at the site of antecedent trauma, which may be minor or major. Cellulitis frequently extends via the lymphatic system to produce lymphangitis, lymphadenopathy, abscesses, and bacteremia. Before the age of antibiotics, lymphatic spread of cellulitis was a surgical emergency mandating immediate amputation to prevent septicemia and death.10
Etiologic agents include Staphylococcus aureus, Streptococcus pyogenes, Group A beta-hemolytic streptococci, and Haemo-philus influenzae. Group B strep is seen in newborns. With the advent of Haemophilus influenzae vaccine, Haemophilus influenzae has become an uncommon etiology for this type of infection.
Diagnostic yield of cultures, aspirates, and blood cultures in most cases is low.11 Cultures from aspirates of the leading edge of the cellulitis may be useful for diagnosis.3,12 In the typical patient, cellulitis should be presumed to be of staphylococcal or streptococcal origin. For severely ill and immunocompromised patients, cultures should be obtained, despite the poor yield, to identify unusual causative organisms. Cellulitis can extend to deeper underlying tissues and has been associated with osteomyelitis and septic arthritis. Septicemia can complicate the picture with metastatic arthritis, meningitis, and seeding of cardiac valves.
Treatment. Initial treatment of cellulitis will include administration of an oral anti-staphylococcal antibiotic such as azithromycin or a cephalosporin. If the patient does not respond rapidly to oral therapy, has systemic toxicity, or has extensive disease, then parenteral antibiotics are indicated. Immunocompromised patients should always be admitted and treated with parenteral antibiotics. Warm compresses, elevation of affected limbs, and drainage of any fluctuant area are important adjuvant therapy. When cellulitis is associated with diabetic or decubitus ulcers, initial treatment will consist of a broad-spectrum antibiotic such as an advanced-generation cephalosporin, or an aminoglycoside plus clindamycin as discussed below.
Erysipelas. Known in the Middle Ages as St. Anthony’s fire or ignis sacer, erysipelas is characterized by a rapidly progressing, erythematous, indurated, painful, and sharply demarcated area of superficial skin infection caused by Streptococcus pyogenes.13 On rare occasions, erysipelas can be cased by non-group A Streptococci (B, C, or G), Haemophilus influenzae, Staphylococcus aureus, and Streptococcus pneumoniae.14 An advancing border can be identified with sequential observation. There is no central clearing of the lesions.
The initial site of entry is often trivial or unapparent. It is more common in the very young and elderly patient. Systemic symptoms such as chills, fever, rigors, and sweats are frequent. About 5% of patients with erysipelas will have bacteremia. Erysipelas may rapidly progress to cellulitis, abscess formation, or even fasciitis.15 Regional lymphadenopathy is common.
Predisposing factors include venous stasis, diabetes mellitus, alcoholism, and chronic lymphatic obstruction. About one-third of cases are recurrent, mostly in patients who have either lymphatic or venous stasis. Erysipelas is relatively common in patients with lymphedema following radical mastectomy and chest wall irradiation. Neonates may develop erysipelas in the umbilical stump and the infection may spread over the abdomen.
The differential diagnosis includes cellulitis, herpes zoster, and contact dermatitis. Rapid spreading across dermatomes tends to rule out both contact dermatitis and herpes zoster. Because cultures of the skin rarely yield organisms, the diagnosis should be made on clinical appearance alone.
Treatment. Treatment consists of penicillin 250-500 mg orally four times daily, although the emergence of beta-lactam resistant Streptococcus pyogenes may soon make this therapy obsolete. Three or four days of antibiotic therapy are usually necessary before the signs and symptoms resolve. Resolution of the systemic symptoms should be evident within the first 48 hours. The skin changes may resolve more slowly.
Bite Wounds and Associated Infections
Bites from dogs, cats, and humans are common problems. It is estimated that dogs bite 1-1.5 million people each year in the United States.16 In locations where animal bites are a reportable condition, dogs account for 90% of all bites, cats for about 5%, and humans and rodents for about 2-3% each; all other animal species produce less than 1% of all bites.17 It is estimated that animal and human bite wounds account for about 1-2% of all emergency department visits annually.
Although many bites appear to be minor shortly after they have been inflicted, these injuries can produce serious local tissue effects as well as systemic complications. (See Table 1.) The most common complication is infection, which may lead to sepsis, joint injury, tendon injury, and in serious cases, even amputation of the limb. (See Table 2.)
| Table 1. Transmission of Systemic Disease | |
| Dogs and Cats | Humans |
| Cat-scratch disease | |
| Syphilis | |
| Tularemia | Tuberculosis |
| Ehrlichiosis | Herpes virus |
| Brucellosis | Hepatitis B,C |
| Toxoplasmosis | |
| Giardia | |
| Rabies | |
| Table 2. Complications of Animal Bites |
| • Localized cellulitis |
| • Abscess formation |
| • Septic arthritis |
| • Tenosynovitis |
| • Osteomyelitis |
| • Sepsis |
| • Endocarditis |
| • Meningitis |
Bacteriology. Whether a bite is caused by a dog, cat, human, or another animal, when a tooth penetrates human skin, it has the potential to inoculate tissues with a concentrations of bacteria. In this regard, the mammalian mouth is a "microbial incubator" that supports growth of more than 200 species of bacteria. In particular, mammalian gingival material contains large quantities of anaerobic streptococci, spirochetes, and Bacteroides species.18 Other organisms commonly recovered from mammals include Streptococcus viridens, Staphylococcus aureus, and Pasturella multocida.
As might be expected, infections caused by animal bites may be associated with a wide variety of organisms, and mixed bacterial infections often predominate. Although any of the plethora of organisms that abound in the oral flora of the animal may cause the infection, some infections are species-specific.
Anatomic Location. The anatomic location of bites can help determine the risk of serious infection and guide antimicrobial therapy. Generally, wounds that involve deep structures—bones, joints, tendons, vessels, nerves, or viscera—are at high risk of infection and associated systemic complications. Moreover, puncture wounds usually are considered high-risk wounds because they are difficult to irrigate and decontaminate. Cat and human bites of the hand also place patients at high risk for subsequent infection. Initially, human bites may be ignored by the patient because of the influence of alcohol and because of social embarrassment. In infants and small children, scalp and facial wounds are at risk of penetration through the thin membranous bones of the skull. In adults, these same areas are low risk for infection because of the good vascular flow.
Dog Bites. Dog bites are the most common mammalian bites inflicted on human beings. One author estimates that there are more than 1000 patients per day who seek emergency care for dog bites and that there may be a much greater number who do not.19 Despite this vast amount of clinical material encountered in the ED on a daily basis, only a few controlled studies have been conducted, most of which involve a relatively small number of patients.
The majority of studies and reviews suggest that a disproportionate number of dog bites are inflicted by German shepherds, Rottweilers, Doberman pinschers, pit bulls, and Alaskan/malamutes.20 Most dogs that produce human bites are managed in a household rather than being strays, and more than half of the victims are children.21,22 It is estimated that dog bites account for about 80% of all animal bite injuries in the United States. In one study, about 5% of dog bites returned to the emergency department with a complication.22 About 1% of dog bite victims will require hospitalization.17
Many dog bites produce more than a trivial contusion or laceration. (See Table 3) It should be stressed that these bites may be delivered with a force of 150-450 pounds per square inch, which is enough to create a crush injury, in addition to puncture and tear wounds.23 Severe injuries, including penetrating wounds of the skull, facial avulsions, arterial lacerations, and avulsions of lip or ear have been reported.24-27 Trauma accompanied by significant blood loss, rib fracture, airway compromise, pneumothorax, and even death, may result from dog bites produced by the larger breeds.28
| Table 3. Low- vs. High-Risk Wounds |
| Low Risk |
| Large lacerations |
| Wounds on face or scalp |
| High Risk |
| Punctures |
| Cat bites |
| Most human bites |
| On hand, wrist, or foot |
| Immunocompromised patient |
About 75% of all bites involve the extremities, with upper and lower extremities affected almost equally.24-26 Most dog bites in children are relatively minor, they usually involve an extremity, and they tend to be seen promptly in an emergency department. Severe facial lacerations caused by dog bites occur almost exclusively in children younger than 10 years of age, and most of these involve the cheeks and lips.22,29 The short stature of children places them at higher risk for facial bites. In addition, children are more likely to place their faces in close proximity to the dog in an effort to inspect or "kiss" the dog.
The microbiology of dog bite wounds is complex. (See Table 4.) Many authors have reported that the results of initial cultures of non-infected dog bite wounds do not correlate with subsequent cultures of the infected wounds.30-33 Bacteria that are frequently cultured from newly infected wounds include the following: Pasturella multocida (wound infections within 24 hours); Enterobacteria; Pseudomonas; Staphylococcus aureus; Bacillus subtilus; and streptococci species, most notably, S. viridens. 33,34 Moreover, there appears to be an increased incidence of Pasteurella infection in patients younger than 4 years and older than 55 years of age.31
| Table 4. Microbiology of Bite Wounds—Most Common Pathogens | |
| Dogs and Cats | Humans |
| Pasteurella | Streptococcus sp. |
| Staphylococcus | Staphylococcus aureus |
| Streptococcus | Eikenella corrodens |
| Corynebacterium | Bacteroides |
| Fusobacterium | Fusobacterium |
| Bacteroides | Peptostreptococcus |
| Porphyromonas | |
| Prevotella | |
Capnocytophaga canimorsus (formerly called CDC group DF-2) has been documented to cause sepsis, gangrene, purpura, and disseminated intravascular coagulopathy about 7 to 14 days after dog bites in some patients.35-39 If the patient is immunosuppressed or has no spleen, DF-2 infection after a dog bite may be more common. The organism responsible for this infection is a gram-negative aerobic bacillus found in normal oral flora in dogs. Local signs of infection may not be present with DF-2 infections.40 The organism responds to penicillin G.
The majority of published studies note that infected dog bite wounds frequently involve multiple bacterial species.36-39 As might be expected, infection with variable, multiple flora limits the clinical usefulness of the Gram’s stain, and when antibiotic therapy is indicated, it must be empiric in nature. Similarly, routine culturing of the wound may yield minimal information regarding the appropriateness of specific antibiotic therapy. Because culture and sensitivity results typically take 48-72 hours to return, close clinical observation of the wound may yield more information regarding necessity for antimicrobial treatment.
These same studies have concluded that antibiotic administration does not predictably reduce the likelihood of subsequent wound infection in all recent dog bites, but they stress that exceptions to this policy include high-risk wounds as discussed above (i.e., bites to hand and face; deep soft tissue penetration; involvement of tendons, bone, and similar structures; and bites in immunocompromised individuals). In addition to previously cited risk factors, the incidence of wound infections following a dog bite does appears to be markedly increased if the patient is older than 50, has a puncture or hand wound, or if the wound is sutured.41 As might be predicted, there is an increase in the incidence of wound infections if the patient has waited more than 24 hours to seek medical care or if there was inadequate wound care at the time of the first visit.
Although drugs of choice frequently cited in the literature include penicillin, penicillinase-resistant penicillin, or a cephalosporin, amoxicillin-clavulanate, probably has the best spectrum of activity for dog bites and is a generally accepted gold standard of care. Cephalosporins are an acceptable alternative choice. Quinolones also appear to be effective, with better acitivity against gram-negative than gram-positive organisms.
Cat Bites and Scratches. Although not as common as dog bites, cat bites are associated with a higher incidence of wound infection than dog bites.42 Overall, about 29% of cat scratch and bit injuries will develop infectious complications.22,42,43 The potential for involvement of the tendons and tendon sheaths with Pasteurella infections in cat bites is high. The sharp-pointed feline teeth seem to act as hypodermic injectors of Pasteurella into the tendon. These puncture wounds are impossible to debride.
Interestingly, cat bites and scratches are more common in women than in men, and about 25% of these injuries occur while playing with the animal.22,43 In one large study study, the peak incidence of bites occured in children under 6 years old.43
The most common organisms recovered from cat bites include Pasteurella multocida, Streptococcus viridens as well as other strains of Streptococcus, Staphylococcus aureus, and strains of Bacteroides. Cat scratches are thought to be bacteriologically similar to cat bites, perhaps because of the manner in which cats groom themselves. Accordingly, wounds due to cat scratches have been considered equivalent to cat bites in severity, although at least one study did not find this supposition to be true.43 As a result, uninfected cat scratches probably do not require empiric antibiotic therapy. When treatment is indicated, amoxicillin-clavulanate is considered the agent of choice.
Cat-Scratch Disease. Cat-scratch disease is caused by an unclassified gram-negative bacterium, inoculated by the scratch of a cat or other animal. The inoculation may be caused by a scratch, lick, or bite. Although the name "cat-scratch disease" implies that cats are the primary vector, dogs may also cause this condition. It is most often seen in young patients who have been scratched by a kitten. The incidence is estimated to be about 3.3 per 100,000 patients. Eighty percent are younger than 21 years of age. There is a slight male predilection, despite the fact that most cat bites occur in females.22,43
Patients with cat-scratch disease usually are not ill-appearing. Typically, however, after a 3- to 10-day incubation period, a tender papule develops at the site of the scratch. Impressive regional lymphadenopathy, fever, malaise, and a headache follow in about two weeks. This usually is followed by spontaneous resolution after a few weeks to months. Uncommon presentations of cat scratch disease include encephalitis, oculoglandular syndrome with conjunctivitis, lytic bone lesions, or fever of unknown etiology.44,45 The conjunctiva may be inoculated in some cases, but the mechanism for inoculation is unknown.
The literature is conflicting about the use of antibiotics in this disease. Much of the literature states that there is no effective antibiotic or that no antibiotic is needed, whereas some sources note that the patient may be treated with doxycycline and rifampin, ciprofloxacin, or erythromycin.46 Quinolones cannot be used in children and pregnant women due to the effects on developing cartilage.
Culture of the organism is quite difficult, but pus from the lymph nodes may be stained with Warthin-Starry silver stains. Diagnosis is usually made with the assistance of the following findings or observations: History of cat contact and presence of scratch; positive cat-scratch disease skin test; negative studies of other causes of lymphadenopathy; and characteristic histopath-ology on biopsy of nodes.47
Human Bites. Human bites are similar to dog and cat bites with two notable exceptions: location of the bite and the presence of Eikenella corrodens in the wound. Like dog bites, the most common pathogens in human bites include Streptococcus and Staphylococcus aureus. As the interval from injury to treatment increases, anaerobes become more frequent, particularly Eikenella corrodens.
Eikenella corrodens is a slow-growing gram-negative rod that is commonly isolated from human bite infections (10-30%).48 Eikenella exhibits synergism with Streptococcus, Staphylococcus aureus, Bacteroides species, and gram-negative organisms.49 This organism has an unusual antibiotic sensitivity pattern. It is resistant to oxacillin, methicillin, nafcillin, and clindamycin. However, it appears to be sensitive to ampicillin, penicillin, and the cephalosporins. To date, transmission of acquired immune deficiency syndrome by a human bite has not occurred, but there is no reason that this will not happen. Other diseases, such as hepatitis B, however, have occasionally been transmitted by the bite of a human. Abrasions and contusions that do not penetrate the full thickness of the skin are unlikely to become infected. Wounds of the extremities other than the hand or trunk produce less risk for infection.
One important issue that is specific to the human bite is the "human" factor. The victim may lie about the mechanism of injury, which confuses matters. The victim may be embarrassed and delay in seeking therapy. The most common reason for delay in hand bites may be "recovery time" from a binge during which the fight took place. As the patient delays, the flora changes to ivolve more "malignant" anaerobic bacteria. Patients who present within 24 hours often have a benign clinical course and have excellent function after healing, whereas delays in treatment are associated with a more complicated course.49
One unique problem that should be emphasized is the "clenched fist syndrome." When a person strikes an opponent’s mouth, an irregular laceration occurs over the dorsum of the metacarpophalangeal joint. Dorsal expansion hoods do not cover the joint, and teeth may easily penetrate the joint space or tendon sheath. When the victim extends his fingers, movement of the tendon carries the saliva further into the joint and tendon sheath. The small entrance wound into the metacarpophalangeal joint is frequently overlooked, and may conceal a multilayer violation of skin, subcutaneous tissues, joint capsule, and extensor tendons.
These bites are most likely to occur during the summer months in men aged 20-35 and are on the dominant hand.50 Unfortunately, the usual picture is that of a small draining wound over the third or fourth metacarpal in a patient who has delayed seeking medical care. Underlying the draining wound is often an infected joint space or tendon sheath that progresses to osteomyelitis or joint involvement.
Deep or full-thickness human bites of the hand have a high incidence of infectious complications, even when treated early. These infections are difficult to treat. Some teaching services recommend that the patient be admitted and intravenous antibiotics started in all cases of suspected human bites to the hand that involve either the joint space or tendon.51
Human bite wounds more than 24 hours old require exploration and drainage. This is best accomplished under anesthesia. Many will also need arthrotomy or drainage of the tendon sheath or both, if the joint space or tendon sheath has been violated. Intravenous antibiotics should be initiated as soon as possible.
Evaluation, Disposition, and Antibiotic Therapy for Animal Bites
All patients with mammalian bites should be examined carefully and all life-threatening problems should be addressed in the usual manner. The priorities of airway, breathing, and circulation (ABCs) should be managed as necessary. Life-threatening hemorrhage should be controlled, and wounds that penetrate body cavities are cared for in customary fashion. The emotional care of the child who has just been attacked by an animal is a top priority and the child should be comforted.
History. Historical data required to properly evaluate and treat dog bites include the following:
• General information about the patient
• Patient’s general state of health
• Age of the patient
• Current and past medical history
• History of immunocompromising disease or treatment
• Status of tetanus prophylaxis
• Time elapsed since the bite occurred
• Status of rabies prophylaxis for both animal and human
• Animal status (i.e., rabies prophylaxis in domesticated animals)
• Status of human prophylaxis if patient is an animal handler
• General information about the dog
• Health of the animal
• Species of the animal inflicting the bite
• Whether it is a domestic, wild, or stray animal
• Whether the bite was provoked or unprovoked
• History of prior attacks
• Current location of the animal
• Ownership
Physical Examination. Multiple bite sites are common and, therefore, the patient should be examined carefully to ensure that no lesions are missed. The wounds should be inspected for depth and extent of injury, and the integrity of neurovascular and motor systems should be ascertained. Remember that in a frightened child, it may be difficult to properly evaluate the neuromuscular and vascular systems. Verbal "sedation" of the child by parents and friends may help the examination.
Wound Care. Without question, one of the most important factors in the care of an animal bite is proper care of the wound. (See Table 5.) In this regard, adequate wound management should include mechanical cleansing to remove contaminated material, such as broken teeth and fragments of clothing. The physician should ensure that tetanus prophylaxis is current. Following mechanical cleansing, the wound should be irrigated with a minimum of 250 cc of saline. It should be stressed that irrigation of the wound and wound debridement have been shown to decrease the rate of infection by a factor of almost thirty-fold.52
| Table 5. General Bite Wound Management Techniques |
| 1. Cleanse the wound. Povidone-iodine solution is recommended for periphery cleansing. The standard solution is diluted 10:1 with saline and can serve as both the cleansing agent and irrigant. |
| 2. After thoroughly scrubbing the wound periphery, irrigate copiously with high pressure using a 19-gauge needle, catheter, or splash shield attached to a 20 mL or 35 mL syringe. Deliver diluted povidone-iodine solution directly into the wound. |
| 3. Debride all devitalized tissue and wound edges. This is essential to reduce the possibility of wound infection. |
| 4. Irrigate after debridement to provide greater exposure of the wound. |
| 5. To facilitate effective irrigation of fang wounds, particularly slender cat teeth wounds, the entry site can be widened with a simple 1 to 1.5 cm incision across the puncture with a #15 knife blade. Retract the new wound with a hemostat or forceps to permit irrigation. Leave these incisions to close without sutures. If the edges are devitalized, trim back to viable skin. |
| 6. Culture purulence or suspected infection. If antibiotics appear advisable, a beta-lactam with lactamase inhibitor or second-generation cephalosporin is recommended. Consult Table 6 for alternatives. |
| 7. Ensure proper tetanus immunization. |
| 8. Assess and treat for rabies exposure if necessary. |
| Source: Trott A. Wounds and Lacerations: Emergency Care and Closure. 2nd ed. St. Louis: Mosby; 1997. |
Addition of antiseptics to the irrigation solution is controversial, and there is no conclusive evidence that this increases the efficacy of irrigation alone. It should be noted that puncture wounds are very difficult to irrigate, and some clinicians recommend excising a small plug of tissue around the puncture wound or enlarging the puncture wound with scalpel or needle to facilitate the irrigation. These procedures have not been studied, information is anecdotal only, and their effectiveness is not known.
In cases complicated by a high risk of rabies transmission, the wound should be irrigated with a 1% benzalkonium chloride solution. This solution has been shown to be effective in killing the rabies virus.53 Decisions regarding wound closure and use of antibiotics are made independently of decisions about rabies prophylaxis.
Debridement of the bite wound should include removal of embedded soil, clots, and organisms that may not have been removed by irrigation alone. Tissue that has potential vascular compromise also may be removed at this time. A limited debridement is appropriate for wounds of the face, fingers, and for those areas where neurovascular or motor function may be impaired by extensive debridement. Sharp debridement in other areas will remove the crushed tissue and "tidy up" lacerations.
If the injury has the potential to involve a body cavity, head, face, joint or boney structures, x-ray films are appropriate. When swelling is present, regardless of the cause, elevation of the area is essential. Immobilization may also be required in the case of hand and lower extremity wounds. Hyperbaric oxygenation has been advocated in human bite infections and the clenched fist injury from human teeth.54 This therapy remains controversial.
Wound Closure. Primary closure of animal bites is a controversial issue. As a general principle, wound therapy should be individualized for the patient, type of injury, and other risk factors. Nevertheless, certain principles should be applied to the management of these injuries. Fortunately, most wounds are minor, and only 10% will require suturing or surgical care.17 Wounds that may be sutured relatively safely after they are appropriately cleansed include those involving the face, scalp, trunk, or proximal extremities. Facial wounds are almost always closed primarily, but only after appropriate cleansing, irrigation, and debridement.
Wounds associated with risk factors for infection usually are not sutured immediately. Certainly, in the case of human bites, the wound is best left open with a delayed primary closure at 48 to 72 hours after first care of the wound. In the case of cat bites or scratches to the hand, a similar policy should apply.
As emphasized, high-risk wounds, or wounds in high-risk patients, should not be sutured immediately. Rather, these wounds should be cleansed and debrided, then loosely packed with fine mesh gauze soaked in saline solution. If the wound remains uninfected for 48 to 72 hours, it can be re-irrigated and closed on a return visit, usually on or around the fourth post-bite day. This delayed primary closure has produced excellent results in heavily contaminated wounds.55
"Loosely" suturing the wound, using surgical staples, or applying Steristrips are functionally equivalent to suturing the wound. Wounds that are not amenable to closure by customary suturing techniques should not be closed by these techniques as an alternative. If the wound becomes infected, it should be opened if it was closed, sutures should be removed, and the wound irrigated with copious amounts of saline. The wound should then be debrided and packed open. Consideration should be given to admitting the patient to the hospital for treatment with intravenous antibiotics.
Extensive complex facial lacerations or multiple animal bite wounds are often better managed in an operating room under appropriate anesthesia. Particularly in children with facial wounds or extensive wounds, general anesthesia may be the most appropriate choice.
Antibiotic Therapy. There have been few, if any, controlled, prospective, large-scale studies of the role of antibiotics in the treatment of animal bites, according to anatomic location, patient type, and nature of injury. The studies currently available to guide therapy have been small in scale, confined to one institution, or retrospective.34,55-57 Most emergency department studies have very poor follow-up and the patient who does not have an infection has little incentive to return. Accordingly, there is not a definitive database upon which to make concrete recommendations for antibiotic therapy for the management of animal bites.
No single antibiotic agent is consistently active against all of the numerous potential bite wound pathogens. (See Table 6.) The recommendations outlined in this review are based upon current information and are designed as a rational approach to management.
| Table 6. Antimicrobial Susceptibilities of Bacteria Frequently Isolated from Animal Bite Wounds | ||||||
Percentages of Isolates Susceptible |
||||||
| Agent | S. aureus | E. corrodens | Anaerobes | P. multocida | C. canimorsus | S. intermedius |
| Penicillin | 10 | 99 | 50/95* | 95 | 95 | 70 |
| Dicloxacillin | 99 | 5 | 50 | 30 | NSa | 100 |
| Amoxicillin/clavulanic acid | 100 | 100 | 100 | 100 | 95 | 100 |
| Cephalexin | 100 | 20 | 40 | 30 | NS | 95 |
| Cefuroxime | 100 | 70 | 40 | 90 | NS | NS |
| Cefoxitin | 100 | 95 | 100 | 95 | 95 | NS |
| Erythromycin | 100 | 20 | 40 | 20 | 95 | 95 |
| Tetracycline | 95 | 85 | 60 | 90 | 95 | NS |
| TMP-SMZ+ | 100 | 95 | 0 | 95 | Vb | NS |
| Quinolones | 100 | 100 | 40 | 95 | NS | NS |
| Clindamycin | 95 | 0 | 100 | 0 | 95 | 95 |
| * Percentage of human-bite isolates/percentage of animal-bite isolates.All data are compiled from various studies. | ||||||
| + Trimethoprim-sulfamethoxazole. | ||||||
| a Not studied. | ||||||
| bVariable. | ||||||
| Source: Goldstein EJC. Bite wounds and infection. Clin Infect Dis 1992; 14:637.M | ||||||
For abrasions, contusions, and other injuries that do not require sutures, antibiotics probably are not indicated in the majority of patients. The major exception to this policy is the puncture wound, from either a tooth or claw. Other low-risk wounds will also have little benefit from antibiotics. In the remainder of cases, although the term "prophylactic" antibiotics is used universally, this is not strictly correct. Antibiotics are often given empirically, before a clinical infection has become manifest; a so-called "prophylactic antibiotic" would actually have to be given before the injury occurred.
The choice of an empiric, therapeutic or so-called prophylactic antibiotic is the same, since cultures of the wound at the time of first care inadequately reflect pathologic organisms cultured from infections. Studies with dicloxacillin, penicillin, or cephalexin have failed to show any strong advantages of one drug over the others.34,56 The combination drug, amoxicillin-clavulanate potassium, has been reported to be efficacious for initial empiric therapy.57
Between 18% and 50% of Pasteurella multocida species are resistant to the first-generation cephalosporins and the semisynthetic penicillins.58 Given the unusual spectrum of sensitivity of Pasteurella multocida, penicillin G or amoxicillin-clavulanate is the most appropriate antibiotic for the infection that develops rapidly (within 12 to 24 hours after the bite). Considering the frequency and severity of P. multocida infections, the poor in-vitro activity of erythromycin, and reports of sepsis in patients who are treated with erythromycin, this macrolide should not be used for animal bite infections.59
In the case of a human bite, Eikenella corrodens is often found and this organism may be resistant to the semisynthetic penicillins, such as methicillin. However, it is sensitive to penicillin, ampicillin, and some of the cephalosporins. A logical choice for human bites is probably combination of amoxicillin and clavulanic acid.60 The addition of the latter improves the drug’s action against staphylococcal species.
In all cases, tetanus prophylaxis should be current. Hyperimmune serum should be used in the standard dosages for those who have never been immunized. These wounds should be treated as having high tetanus potential, and tetanus immunization should be renewed if more than five years have elapsed since the last immunization.
References
1. Davison AJ, Rotsein OD. The diagnosis and management of common soft tissue infections. Can J Surg 1998;31:333-336.
2. Blumer JL, Lemon E, O'Horo J, Snodgrass DJ. Changing therapy for skin and soft tissue infections in children: Have we come full circle? Pediatr Infect Dis J 1987;6:117-122.
3. Carson SC, Prose NS, Berg D. Infectious disorders of the skin. Clin Plast Surg 1993;20:67-76.
4. Prose NS, Mayer Fe. Bacterial skin infections in adolescents. Adolescent Medicine: State of the Art Reviews. 1990;1:325-332.
5. Schachner L, Taplin D, Scott GB, et al. A therapeutic update of superficial skin infections. Pediatr Clin North Am 1983;30:397-403.
6. Scott MA. Bacterial skin infections. Prim Care 1989;16: 591-602.
7. Ben-Amitai D, Ashkenazi S. Common bacterial skin infections in childhood. Pediatr Ann 1993;22:225-233.
8. Hedstrom SA. Treatment and prevention of recurrent staphylococcal furunculosis: Clinical and bacteriological follow-up. Scand J Infect Dis 198517:55-58.
9. Wheat LG, Kohler RB, Luft FC, et al. Long-term studies of the effect of rifampin on nasal carriage of coagulase-positive staphylococci. Rev Infect Dis 1983; 5(Suppl 3):S459-S462.
10. Ahrenholz DH. Necrotizing soft-tissue infections. Surg Clin North Am 1988;68:199-214.
11. Aly AA, Roberts NM, Seipo KS, MacLellan DG. Case survey of management of cellulitis in a tertiary teaching hospital. Med J Aust 1996;165:553-556.
12. Fleishcer G, Ludwig S, Campos J. Cellulitis, bacterial etiology, clinical features and laboratory findings. J Pediatr 1980;97:591-593.
13. Feingold DS, Hirschmann JV, Leyden JJ. Bacterial infections of the skin. J Am Acad Derm 1989;20:469-475.
14. Finch R. Skin and soft tissue infections. Lancet 1988;1: 164-168.
15. Ramage L, green K, Pyskir D, Simor AE. An outbreak of fatal nosocomial infections due to group A streptococcus on a medical ward. Infect Cont Hosp Epidemiol 1996;17:429-431.
16. Moore RM Jr, Zehmer RB, Moulthrop JI, et al. Surveillance of animal bite cases in the United States, 1971-1972. Arch Environ Health 1977;32:267-270.
17. Callaham ML. Human and animal bites. Top Emerg Med 1982;4:1-15.
18. Edlich RF, Morgan RF, Mayer NE, Rodeheaver GT. Mammalian bites. Cur Concepts Wound Care 1986; Summer; 15-22.
19. Heller MB. Management of bites: Dog, cat, human, and snake. Res and Staff Physician 1982;Feb:75-84.
20. Avner JR, Baker MD. Dog bites in urban children. Pediatrics 1991;88:55-57.
21. Karlson TA. The incidence of facial injuries from dog bites. JAMA 1984;251:3265-3267.
22. Kizer KW. Epidemiologic and clinical aspects of animal bite injuries. JACEP 1979;8:134-141.
23. Goldstein EJC, Richwald GA. Human and animal bite wounds. Amer Fam Phys 1987;36:101-109.
24. Miller SJ, Copass M, Johansen K, et al. Stroke following Rottweiler attack. Ann Emerg Med 1993;22:262-264.
25. Ruskin JD, Laney TJ, Wendt SV, et al. Treatment of mammalian bite wounds of the maxillofacial region. J Oral Maxillofac Surg 1993;51:174-176.
26. Snyder KB, Pentecost MJ. Clinical and angiographic findings in extremity arterial injuries secondary to dog bites. Ann Emerg Med 1990;19:983-986.
27. Baack BR, Kucan JO, Demarest G, et al. Mauling by pit bull terriers: Case report. J Trauma 1989;29:517-520.
28. Sacks JJ, Sattin RW. Dog bite-related fatalities from 1979 through 1988. JAMA 1989;262:1489-1492.
29. Lackmann GM, Tollner U. More on dog-bite injuries [letter] Pediatrics 1991;122:356.
30. Boenning DA, Fleisher GR, Campos JM. Dog bites in children: Epidemiology, microbiology, and penicillin prophylactic therapy. Am J Emerg Med 1983;1:17-21.
31. Callaham ML. Treatment of common dog bites: Infection risk factors. JACEP 1978;7:83-87.
32. Spencer RC, Matta H, Ferguson DG, et al. Routine culture of dog bites [letter]. Ann Emerg Med 1987;16:730.
33. Ordog GJ. The bacteriology of dog bite wounds on initial presentation. Ann Emerg Med 1986;15:1324-1329.
34. Rosen RA. The use of antibiotics in the initial management of recent dog-bite wounds. Am J Emerg Med 1985;3:19-23.
35. Anderson CR. Animal bites. Postgrad Med 1992;92:134-149.
36. Malnick H, Adhami ZN, Galloway A. Isolation and identification of Capnocytophaga canimorsus (DF-2) from blood culture.[letter] Lancet 1991;338:384.
37. Hantson P, Gautier PE, Vekemans MC, et al. Fatal Capnocytophaga canimorsus septicemia in a previously healthy woman. Ann Emerg Med 1991;20:93-94.
38. Peek RM, Truss C. Secretary diarrhea following a dog bite. Diges Dis Sci 1991; 36:1151-1153.
39. Kullberg BJ, Westendorp RGJ, Vant Wout JW, et al. Purpura fulminans and symmetrical peripheral gangrene caused by Capnocytophaga canimorsus (formerly DF-2) septicemia — A complication of dog bite. Medicine 1991;70:287-292.
40. Chretien JH, Garagusi VF. Infections associated with pets. Amer Fam Phys 1990;41:831-845.
41. Brown CG, Ashton JJ. Dog bites: The controversy continues [editorial]. Am J Emerg Med 1985;3:83-84.
42. Aghababian RV, Conte JE. Mammalian bite wounds. Ann Emerg Med 1980;9(s):79-83.
43. Dire DJ. Cat bite wounds: Risk factors for infection. Ann Emerg Med 1991;20:973-979.
44. Harvey RA, Misselbeck WJA, Uphold RE. Cat-scratch disease: An unusual cause of combative behavior. Am J Emerg Med 1991;9:52-53.
45. Tobin EH, McDaniel H. Oculoglandular syndrome: Cat-scratch disease without the cat scratch. Postgrad Med 1992;91:207-210.
46. Holley HP, Jr. Successful treatment of cat-scratch disease with ciproflaxin. JAMA 1991;265-1563.
47. Margileth AM. Update on cat-scratch disease. Hosp Med 1989;Dec:61-81.
48. Bilos ZJ, Kuchararchuk A, Metzger W. Eikenella corrodens in human bites. Clin Orthop 1978;134:320-324.
49. Basadre JO, Parry SW. Indications for surgical debridement in 125 human bites to the hand. Arch Surg 1991;126:65-67.
50. Rest JG, Goldstein EJC. Management of human and animal bite wounds. Emerg Med Clin North Am 1985;3:117-126.
51. Taylor GA. Management of human bite injuries of the hand. Can Med Assoc J 1985;133:191-192.
52. Newcomer VD, Young EM. Unique wounds and wound emergencies. Derm Clinics 1993;11:715-727.
53. Hopman L, Stewart CE. Rabies. Emerg Med Serv 1986;May: 22G-22J.
54. Lehman WL Jr, Jones WW, Allo MD, Johnston RM. Human bite infections of the hand: adjunct treatment with hyperbaric oxygen. Infect Surg 1985;4:460.
55. Wounds and injuries of the soft tissues. In: Emergency War Surgery First Unites States Revision of Emergency War Surgery NATO Handbook. Washington, DC: US Government Printing Office. 1975.
56. Elenbaas RM, McNabney WK, Robinson WA. Prophylactic oxacillin in dog bite wounds. Ann Emerg Med 1982;248-51.
57. Goldstein EJ, Reinhardt JF, Murray PM, et al. Outpatient therapy of bite wounds: Demographic data, bacteriology and a prospective randomized trial of amoxicillin/ clavulanic acid versus penicillin +/- dicloxacillin. Int J Dermatol 1987;26: 123-127.
58. Stevens DL, Higbee JW, Oberhofer TR, et al. Antibiotic susceptibilities of human isolates of Pasteurella multocida. Antimicrob Agents Chemother 1979;16:322-324.
59. Levin JM, Talan DA. Erythromycin failure with subsequent Pasturella multocida meningitis and septic arthritis in a cat-bite victim. Ann Emerg Med 1990;19:1458-1461.
60. File TM Tan JS. Treatment of skin and soft tissue infections. Am J Surg 1995;169(5A Suppl):26S-33S.
Physician CME Questions
25. Impetigo usually presents in what anatomic region?
A. Groin
B. Toes
C. Chest
D. Face
26. The etiologic organism most often responsible for folliculitis is:
A. Streptococcus superficialis
B. Staphylococcus aureus
C. Streptococcos pneumoniae
D. Eikenella
27. Etiologic agents in cellulitis include:
A. Staphylococcus aureus, Streptococcus pyogenes, Group beta-hemolytic streptococcus, and Haemophilus inflenzae.
B. Streptococcus pneumoniae, Staphylococcus epidermidis, and Mycoplasma superficialis.
C. Listeria impetiginous and streptocococcus celluliticus.
D. none of above.
28. The most common mammalian bite inflicted in humans come from:
A. dogs.
B. cats.
C. hamsters.
D. people.
29. The following is (are) true about cat bites:
A. They are associated with a higher incidence of wound infections.
B. They are more common in women than in men.
C. Amoxicillin-clavulanate is a reasonable agent for treatment.
D. Pasturella multocida is one organism that can be recovered from cat bite wounds.
E. All of the above
30. One infecting organism that has a predilection for human bite infections is:
A. Chlamydia oralis
B. Legionella celluliticus
C. Mycoplasma oralis
D. Eikenella corrodens
31. High risk wounds usually require:
A. immediate closure.
B. instillation of antibiotic fluids.
C. delayed closure.
D. IV antibiotic therapy for 1 week.
32. Patients with cat-scratch disease usually are not ill-appearing at the initial stages of the illness.
A. True
B. False
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