The incidence of erysipelas increased dramatically, for unknown reasons, during the late 1980s.(1) Once referred to as "St. Anthony's Fire," erysipelas can be traced as far back as the Middle Ages. The etiologic agent was once thought to be the ergot alkaloids produced by the fungus Claviceps purpurea, found in contaminated rye. Because patients who had ingested the fungus presented with bright red gangrenous extremities, they were thought to be consumed by the "Holy Fire." It was believed that only the shrine of St. Anthony, an Egyptian monk and healer (251-356 A.D.), could provide relief.(2) An 11th century hospital, the French House of St. Anthony, was devoted to the care of victims of epidemic gangrene and had "fiery red" walls similar to the color of the lesions of erysipelas; hence, the name St. Anthony's Fire.(3)
Erysipelas is a beta-hemolytic streptococcal infection that affects the skin and subcutaneous tissue. Group A streptococci are the most commonly identified causative bacteria. However, groups B, C, D and G streptococci have been isolated from patients with erysipelas. Occasionally, staphylococcal organisms are isolated as well. The infecting organism usually enters the body through nasopharyngeal tissue, trauma sites, insect bites or surgical incisions.
Erysipelas affects persons of all ages, but it is most prevalent among the young and the elderly. The frequency of erysipelas increases during the summer months.(4) Females are more commonly affected than males, and the peak incidence of infection occurs in persons between 60 and 80 years of age.(1) At particular risk are immunocompromised patients, patients taking corticosteroids, patients with acquired immunodeficiency syndrome or diabetes, patients who are alcoholic or patients who are undergoing chemotherapy.
Because erysipelas is an infectious disease, a greater incidence of infection would be expected to occur in settings such as nursing homes, day care centers, military bases and prisons. However, epidemics are rare and isolated cases are the rule.(1)
The clinical presentation of classic erysipelas is distinct. The infection usually has an abrupt onset and a rapid course. The most common presenting symptom is an area of discomfort or paresthesia on the face, usually in the nasal or perinasal region. Occasionally, patients report symptoms of pharyngitis over the days or weeks before the appearance of a facial rash.
An area of erythema forms at the site of discomfort and rapidly enlarges to involve a larger area of the face over the next three to six days (Figure 1). The rash has an irregular leading edge that is distinct, raised and tender to palpation. The advancing erythema is shiny, tense and warm to the touch. Vesicles or bullae may form over the affected area. The eyes and cheeks may become edematous. If the infection spreads to affect most of the face, it may have a "butterfly" distribution and may be mistaken for the facial rash of lupus erythematosus.
As the erythema advances, it may take on a deeper red, ecchymotic appearance, with a bright red leading edge. Within seven to 10 days, the erythematous zones begin to show central clearing, with a gradual return to normal appearance. Areas of skin may exfoliate, and impetiginous lesions or postinflammatory hyperpigmentation may develop in the affected area. During the erythematous stage, patients usually complain of constitutional symptoms, such as fever, chills, arthralgias, fatigue and poor appetite.
Currently, infections involving the face are less common than those affecting the legs.(1) During the early 20th century, 50 to 85 percent of the cases of erysipelas involved the face but, in recent years, the incidence of facial involvement has decreased to about 6 to 19 percent.(5) The relative infrequency of facial erysipelas may be explained by better hygiene.(1) Erysipelas may now more commonly involve an area of the leg used for saphenous vein harvest for coronary artery bypass surgery.(6)
Usually, erysipelas is easily diagnosed on the basis of its clinical manifestations. The characteristic rash, fever and constitutional symptoms typical of infection, including malaise, chills and, occasionally, anorexia or gastrointestinal symptoms, are hallmarks of the disease. The rash is brightly erythematous, well demarcated, indurated, raised and painful to palpation. Also, regional lymph node involvement is often found.
Laboratory findings include moderate leukocytosis with a shift to the left indicative of bacterial infection, an increase in the erythrocyte sedimentation rate, and positive blood cultures in as many as 5 percent of patients. A positive antistreptolysin O titer supports the existence of streptococcal infection. Cultures of the nasopharynx are frequently positive and also support the diagnosis of erysipelas. Cultures of aspirated lymphatic fluid from the leading edge of the rash occasionally grow streptococci, but aspiration of this area is a painful and unnecessary procedure and, therefore, is not recommended.
The differential diagnosis of erysipelas includes contact dermatitis and angioneurotic edema. In these cases, however, fever and tenderness do not usually accompany the rash. Herpes zoster and other forms of cellulitis, such as cellulitis associated with Haemophilus influenzae, should also be considered in the differential diagnosis. H. influenzae cellulitis primarily affects the buccal and periorbital areas and generally occurs in children less than two years of age. It has a rapid course, and bacteremia develops in almost 75 percent of patients. Thus, patients with this form of cellulitis usually have a more toxic appearance than patients with erysipelas.(7)
Erysipeloid is a skin infection caused by the inoculation of Erysipelothrix rhusiopathiae; dead animal products are the source of infection. Erysipeloid can be differentiated from erysipelas by its slow onset, limited spread and lack of constitutional symptoms, and a history of exposure.
Penicillin is the drug of choice for the treatment of erysipelas. If a patient is allergic to penicillin, erythromycin may be substituted. Newer cephalosporins have a broad spectrum of coverage but are often more expensive and are unnecessary unless the infection itself is polymicrobial.(8)
Oral antibiotics are adequate for most cases of erysipelas. Treatment should be continued for 10 to 14 days, or until the rash has completely resolved and the patient is asymptomatic.
Some patients with erysipelas, especially children and debilitated adults, require admission to the hospital and treatment with intravenous or intramuscular antibiotics.(9) The location of lesions and size of the affected area should be considered in the decision to admit a patient. The duration of treatment with intravenous antibiotics should be individualized. In some cases, three to seven days of intravenous treatment are needed. Before treatment with oral antibiotics is initiated in these cases, the erythematous area should be resolving, the patient should be afebrile and leukocytosis should have resolved.
Warm, moist compresses that promote blood flow to the affected area can also be beneficial. A follow-up evaluation in one or two weeks is recommended to ensure that the infection does not recur.
Complications arising from erysipelas are uncommon (13 percent of cases in one study(1)). Patients who have complications often have other underlying disease, such as alcoholism, diabetes, postphlebitic syndrome and AIDS.
The most common complications of erysipelas are abscess formation, gangrene and thrombophlebitis. Septicemia, acute glomerulonephritis and endocarditis are rare (Table 1).(1) Upper airway obstruction and streptococcal toxic shock syndrome have also been reported but are infrequent complications.(10)(11)(12)
TABLE 1 Complications in 529 Cases of Erysipelas
Adapted from Chartier C, Grosshans E. Erysipelas. Int J Dermatol 1990; 29:459-67. Used with permission.
Recurrence of erysipelas is a significant complication and is relatively common in immunocompromised patients. In one study,(13) erysipelas recurred in 29 percent of 149 consecutive patients during a followup period of two to four years. In selected patients with frequent or severe recurrences, prophylactic therapy with oral penicillin may be considered.
(1.)Chartier C, Grosshans E. Erysipelas. Int J Dermatol 1990; 29:459-67.
(2.)Weaver R, Phillips M, Vacek JL. St. Anthony's fire: a medieval disease in modern times: case history. Angiology 1989; 40:929-32.
(3.)Tanner JR. St. Anthony's fire, then and now: a case report and a historical review. Can J Surg 1987; 30:291-3.
(4.)Ronnen M, Suster S, Schewach-Millet M, Modan M. Erysipelas. Changing faces. Int J Dermatol 1985; 24:169-72.
(5.)Ochs MW, Dolwick MF. Facial erysipelas: report of a case and review of the literature. J Oral Maxillofac Surg 1991; 49:1116-20.
(6.)Dan M, Heller K, Shapira I, Vidne B, Shibolet S. Incidence of erysipelas following venectomy for coronary artery bypass surgery. Infection 1987; 15:107-8.
(7.)Waagner DC, McCracken GH Jr. Haemophilus infections. In: Wilson JD, Braunwald E, Isselbacher KJ, Petersdorf RG, Martin JB, Fauci AS, et al., eds. Harrison's Principles of internal medicine. 12th ed. New York: McGraw-Hill, 1991:618.
(8.)Suss SJ, Middleton DB. Cellulitis and related skin infections. Am Fam Physician 1987; 36(3):126-36.
(9.)Jorup-Ronstrom C. Epidemiological, bacteriological and complicating features of erysipelas. Scand J Infect Dis 1986; 18:519-24.
(10.)Bartter T, Dascal A, Carroll K, Curley FJ. 'Toxic strep syndrome.' A manifestation of group A streptococcal infection. Arch Intern Med 1988; 148:1421-4.
(11.)Cone LA, Woodard DR, Schlievert PM, Tomory GS. Clinical and bacteriologic observations of a toxic shock-like syndrome due to Streptococcus pyogenes. N Engl J Med 1987; 317:146-9.
(12.)Guslits B. Upper airway obstruction due to erysipelas. Intensive Care Med 1991; 17:370-1.
(13.)Jorup-Ronstrom C, Britton S. Recurrent erysipelas: predisposing factors and costs of prophylaxis. Infection 1987; 15:105-6.
COPYRIGHT 1995 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group