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CELLULITIS AND OTHER SKIN AND SOFT-TISSUE INFECTIONS

CELLULITIS AND OTHER SKIN AND SOFT-TISSUE INFECTIONS

Cellulitis
Animal Bites
Lyme Disease
Herpes Zoster
Decubitus Ulcers
Bibliography

Cellulitis
Erysipelas remains a common cause of cellulitis. A sharply demarcated, advancing, and palpable border suggests this infection. The etiologic agent is almost always group A b-hemolytic streptococci. Staphylococcus aureus can rarely cause the same clinical picture. However, the lesions of S. aureus cellulitis usually have less distinct borders and may be associated with bullae, pustules, or other primary localized areas of infection. Other hemolytic streptococci, such as groups C and G, may also cause cellulitis, often in patients with underlying malignancy.
An erysipeloid cellulitis, particularly around the fingers or on the hand, has been associated with the occupations of fishermen, butchers, and other persons handling raw fish and poultry. The organism causing this cellulitis is Erysipelothrix rhusiopathiae. The cellulitis often has a violet hue. There is local tenderness but little systemic reaction. Penicillin G is the antimicrobial of choice. More recently, cellulitis caused by a fish pathogen, Streptococcus iniae, has been described in association with an outbreak in Canada. All the patients had handled live or freshly killed fish.
Cellulitis caused by Enterobacteriaceae can occur in association with trauma and diabetes or after surgery. Escherichia coli and Klebsiella species can cause a gas-forming gangrene that must be distinguished from purely anaerobic soft-tissue infection. Necrotizing fasciitis is a potentially life-threatening infection because of the virulence of the causative organism and the depth of involvement to the fascia. Bacteremia is common, and mortality from the disease is high. Toxic strains of hemolytic streptococci have made the disease more common. Necrotizing fasciitis requires rapid diagnosis and early antibiotic therapy and surgical intervention. Although definitive diagnosis is difficult, clues to deeper infection include bullae formation, anesthesia over the infected area, dusky discoloration, and failure to respond to antibiotics. Deep-tissue infection may be the result of mixed anaerobic and gram-negative infection. Fournier’s gangrene of the scrotum may often be caused by anaerobic streptococci and gram-negative bacilli. This infection presents as scrotal swelling and pain with rapidly advancing necrosis of soft tissue. Pain and systemic toxicity are associated.
Breast cellulitis has recently been reported as a complication of breast-conservation therapy. More than 80% of patients had radiologically demonstrated fluid collections at the site of lumpectomy. Episodes of cellulitis developed, on average, 4.9 months after the end of radiotherapy for stage I or II breast carcinoma.
Pseudomonas aeruginosa folliculitis has been recently described, almost exclusively in association with the use of hot tubs and whirlpools. Papules or nodules that are red or violaceous appear on the abdomen or trunk. The neck and face are usually spared. Patients may have low-grade fever but do not become bacteremic or systemically ill. Avoidance of the source of infection is usually sufficient therapy because the rash is self-limited.
Vibrio vulnificus has caused a spectrum of skin infections in saltwater wounds. Immunocompromised patients and patients with liver disease are prone to life-threatening infection. A cellulitis may be acquired from the exposure of abraded skin to seawater. Bites, fishing injuries, or puncture by a fin or spine may be the predisposing event. Cellulitis, bullous disease, necrotizing fasciitis, and myositis have all been well described.
V. vulnificus bacteremia may develop in immunocompromised patients after ingestion of shellfish. Metastatic skin lesions, particularly vesicles and bullae, may be associated with this bacteremia. Antimicrobial therapy (tetracyclines and aminoglycosides have been most commonly used), blood pressure support, and often wound debridement are required because the disease is rapidly progressive.
Animal Bites
Animal bites are a common cause of soft-tissue infection, with more than a half million bites, mostly from dogs and cats, occurring in the United States each year. Several factors are important in developing a diagnostic and therapeutic plan: the animal involved, severity and location of the wound, circumstances of the attack, and interval between injury and presentation. A plan for treatment must include (a) local care, with thorough cleaning of the wound with soap and water and adequate irrigation; (b) tetanus prophylaxis; (c) rabies prophylaxis, depending on the animal involved and the epidemiology of rabies in the specific locale; and (d) antimicrobials. Prophylactic antimicrobial therapy is controversial; however, routine prophylaxis for dog bites is becoming increasingly recommended. Patients with deep wounds or wounds of the face and patients with wounds who are immunocompromised or have liver disease probably should receive prophylaxis (prospective studies are lacking). The antimicrobial of choice is controversial. A broad-spectrum agent such as amoxicillin-clavulanate is often recommended.
Treatment of animal bite soft-tissue infection should be directed against the etiologic agent. Pasteurella multocida, the most common organism in dog and cat bites, is a small, gram-negative rod (appearing much like Haemophilus species organisms on Gram’s stain). Penicillin is the drug of choice; tetracycline is an effective alternative.
Dysgonic fermenter 2 (DF-2), now called Capnocytophaga canimorsus, recently has been recognized to cause soft-tissue infection and overwhelming sepsis after dog bites. The disease has also occurred after cat bite. Patients with cirrhosis and splenectomized patients are at high risk for septic shock and disseminated intravascular coagulation. Penicillin in high doses is the drug of choice. Bacteroides and Prevotella species are commonly isolated from bite wounds and are now better characterized.
Lyme Disease
The variable cutaneous manifestations of Lyme borreliosis are important to review in the context of the differential diagnosis of skin infection. Erythema migrans is an erythematous lesion occurring at the site of tick bite and borrelial inoculation. It is an annular lesion that shows centrifugal spread. Borrelial lymphocytoma has been described as a blue-red nodular lesion. A dense lymphocytic infiltration is seen histologically. The ear and breast may be sites of predilection for this lesion. Multiple erythema migrans lesions suggest disseminated disease. Acrodermatitis chronica atrophicans is a chronic skin lesion that starts as a localized inflammatory process but is followed by an atrophic phase. Sclerotic skin lesions may also develop secondary to Lyme disease. Different species of Borrelia tend to cause different types of skin lesions. For example, Borrelia afzelii is the predominant etiologic agent in acrodermatitis chronica atrophicans.
Herpes Zoster
Herpes zoster, or shingles, is caused by reactivation of latent varicella-zoster virus in the dorsal root ganglia. Clinical diagnosis is usually not difficult; the patient presents with a painful vesicular rash in a dermatomal distribution. Herpes simplex can rarely present in a dermatomal distribution, and herpes zoster can disseminate and resemble primary varicella. The vesicular lesions of all three diseases appear the same histologically, with multinucleated giant cells and intranuclear inclusions.
Antiviral therapy has a well-established role in patients with herpes zoster. For both localized and disseminated disease, acyclovir has been shown to improve the rate of viral clearing and provide faster relief of pain. Acyclovir prevents dissemination of virus in immunosuppressed patients. IV acyclovir was shown to be more effective than vidarabine in preventing disseminated disease. Acyclovir has been used to decrease the incidence of zoster after bone marrow transplantation.
In the normal host with localized disease, the role of acyclovir is not completely defined. IV acyclovir improves healing and decreases the duration of acute pain. This effect is modest; the incidence of long-standing herpetic neuralgias is not affected by antiviral therapy. When started within 2 days of the onset of rash, acyclovir reduces the incidence of formation of new lesions.
Herpes zoster ophthalmicus, because of its high rate of ocular complications and vision loss, requires antiviral therapy. Although a positive effect with oral therapy has been reported, most experts recommend IV acyclovir for zoster ophthalmicus.
Decubitus Ulcers
With the aging of the population in the United States, decubitus ulcers have become an increasingly common soft-tissue infection. Five percent of the 23.5 million Americans over age 65 live in nursing homes. In this institutional setting, decubitus ulcers are prevalent in 6% to 35% of patients. The pathogenesis of decubitus ulcers has been well defined. Sustained pressure is the principal predisposing factor. Shearing forces, such as occur when a patient is raised up in bed, also contribute to the process. Moisture secondary to incontinence, perspiration, and drainage from a wound infection may also be contributing factors. Malnutrition, as reflected by serum albumin levels, is an important predictor of the development of a pressure ulcer. Altered states of consciousness, diabetes mellitus and neuropathy, and sensory deficits also contribute indirectly to the process.
Clinical assessment of a pressure ulcer will include examination to determine the degree of hyperemia (blanching or nonblanching), the presence or absence of blistering or eschar formation, and the depth of tissue ulceration. The base of an ulcer should be carefully palpated to determine whether it extends to muscle or bone. Any spreading edge of erythema should be marked and carefully followed.
The microbiologic assessment of a pressure ulcer is difficult. Superficial swab cultures do not correlate with organisms grown from bone biopsy specimens when osteomyelitis has developed by contiguous spread. There are usually fewer species present in the deeper tissues than superficially. When bacterial cultures are obtained by reliable methods, such as needle aspiration, a combination of anaerobic and aerobic bacteria is isolated. The most common aerobic isolates are E. coli, Proteus mirabilis, enterococci, and Pseudomonas species. Common anaerobic organisms include Peptostreptococcus, Bacteroides fragilis, and Clostridium perfringens. When patients become septic from decubitus ulcers, anaerobes, particularly B. fragilis, are most commonly isolated. In addition to sepsis, other complications of decubitus ulcers include contiguous osteomyelitis, pyarthrosis, and rarely tetanus. Table 41-1 summarizes the basic principles for management of decubitus ulcers.

Table 41-1. Principles of management for decubitus ulcers

As with other infectious disease, prevention is the most important weapon in the fight against decubitus ulcers. A good prevention program first identifies patients at greatest risk. Vigilance and meticulous attention to early blanching hyperemia are critical. Frequent turning and cleanliness of sheets are the basis of prevention. Patients should be lifted and not dragged across sheets. Activity and good nutrition should be maximized. (S.L.B.)
Bibliography
Alexander CJ, et al. Characterization of saccharolytic Bacteroides and Prevotella isolates from infected dog and cat bite wounds in humans. J Clin Microbiol 1997; 35:406.
Many species of Bacteroides and Prevotella can be isolated from human bites. Clinical laboratories need to be aware of these species.
Asbrink E. Cutaneous manifestations of Lyme borreliosis. Clinical definitions and differential diagnoses. Scand J Infect Dis 1991;77(Suppl):44.
Cutaneous manifestations of Lyme borreliosis as described during the Fourth International Conference on Lyme Disease.
Auerbach PS. Natural microbiologic hazards of the aquatic environment. Clin Dermatol 1987;5:52.
Describes risk for Erysipelothrix infection in fish handlers.
Balfour HH, et al. Acyclovir halts progression of herpes zoster in immunocompromised patients. N Engl J Med 1983;308:1448.
In immunocompromised patients, IV acyclovir decreased the progression of disease and incidence of dissemination.
Brenner DJ, et al. Capnocytophaga canimorsus sp. nov. (formerly CDC group DF-2), a cause of septicemia following dog bite, and C. cynodegmi sp. nov., a cause of localized wound infection following dog bite. J Clin Microbiol 1989;27:231.
Capnocytophaga may cause sepsis after dog bite, particularly in the splenectomized or cirrhotic patient.
Burdge DR, Chow AW. The pressure ulcer. In: Verghese A, Berk SL, eds. Infections in nursing homes and long-term care facilities. Basel: Karger, 1990.
Detailed discussion of pathogenesis.
Chuang YC, et al. Vibrio vulnificus infection in Taiwan: report of 28 cases and review of clinical manifestations and treatment. Clin Infect Dis 1992;15:271.
Summary of 28 episodes of V. vulnificus infection. Twenty-three of 27 patients had skin involvement.
Clayton MD, et al. Causes, presentation and survival of 57 patients with necrotizing fasciitis of the male genitalia. Surg Gynecol Obstet 1990;170:49.
Clinical description of Fournier’s fasciitis. Infection was caused by both anaerobes and gram-negative bacilli.
Cobo M. Reduction of the ocular complications of herpes zoster ophthalmicus by oral acyclovir. Am J Med 1988;85:90.
Oral therapy prevented complications. However, evidence for continued viral replication was of concern. Most experts recommend IV acyclovir for zoster ophthalmicus.
Goldstein EJ. Management of human and animal bite wounds. J Am Acad Dermatol 1989;21:1275.
The spectrum of organisms in animal bites is wide, and broad-spectrum antimicrobial therapy is recommended.
Gustafson TL. Pseudomonas folliculitis: an outbreak and review. Rev Infect Dis 1983;3:1.
Clinical description of hot-tub folliculitis.
Huff JC, et al. Therapy of herpes zoster with oral acyclovir. Am J Med 1988;85:84.
Normal hosts treated with oral acyclovir reported less acute pain than the placebo group.
Kertesz DK, Chow AW. Infected pressure and diabetic ulcers. Clin Geriatr Med 1992; 8:835.
Review of decubitus ulcers, including physiology, staging, diagnosis, and treatment. Emphasizes the team approach to prevention.
Koenig KL, Mueller J, Rose T. Vibrio vulnificus. Hazard on the half shell. West J Med 1991;144:400.
Describes clinical syndromes and predisposing factors for V. vulnificus skin infection.
Merz KR, et al. Breast cellulitis following breast conservation therapy: a novel complication of medical progress. Clin Infect Dis 1998;26:481.
Cellulitis, which is sometimes recurrent, is now more commonly seen after breast-sparing surgery, often after radiation therapy. Most episodes occur less than 3 months after treatment.
Ohlenbusch A, et al. Etiology of the acrodermatitis chronica atrophicans lesion in Lyme disease. J Infect Dis 1996;174:421.
B. afzelii is associated with acrodermatitis chronica atrophicans—skin lesions that persist over atrophied skin.
Parenti DM, Snydman DR. Capnocytophaga species: infections in non-immunocompromised and immunocompromised hosts. J Infect Dis 1985;151:140.
Describes Capnocytophaga as a cause of traumatic hand wounds.
Pers C, et al. Capnocytophaga canimorsus septicemia in Denmark, 1982–1995: review of 39 cases. Clin Infect Dis 1996;23:71.
Disseminated disease occurred in alcoholics and splenectomized patients. Twelve of 39 patients died. Disseminated intravascular coagulation was a common complication.
Shepp DH, Dandliker PS, Myers JD. Treatment of varicella-zoster virus infection in severely immunocompromised patients. N Engl J Med 1986;314:208.
Acyclovir was more effective than vidarabine in preventing progression of zoster in compromised patients.
Stone DR, Gorbach SL. Necrotizing fasciitis. The changing spectrum. Dermatol Clin 1997;15:213.
Describes the clinical picture and management of this infectious disease emergency. There is an increasing incidence of toxic shock strains of streptococci.
Weber DJ, Hansen AR. Infections resulting from animal bites. Infect Dis Clin North Am 1991;5:663.
Review of epidemiology and treatment of animal bites, including infections with Pasteurella multocida and C. canimorsus.
Weinstein MR, et al. Invasive infections due to a fish pathogen, Streptococcus iniae. N Engl J Med 1997;337:589.
Describes nine patients with invasive skin infections caused by this organism after they handled fresh fish.
Weiss HB, Friedman DI, Coben JH. Incidence of dog-bite injuries treated in the emergency departments. JAMA 1998;278:51.
There are 12.9 dog-bite injuries per 10,000 population. Most occur in children ages 5 to 9 years.
Wood MJ, et al. Efficacy of oral acyclovir treatment of acute herpes zoster. Am J Med 1988;85:79.
Eight hundred milligrams of oral acyclovir given five times per day for 7 days (within 48 hours of rash onset) reduced formation of new lesions and reduced acute pain. No benefit was shown in reduction of postherpetic neuralgia.

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One comment on “CELLULITIS AND OTHER SKIN AND SOFT-TISSUE INFECTIONS

  1. Fatty tissue in thighs is an common issue in which 90% of females of every age group encounter eventually in life. Dimply skin is sometimes when compared with orange peel or perhaps …Cellulite

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