Erysipeloid (Erysipeloid of Rosenbach, Rosenbach’s disease, Baker-Rosenbach disease, Pseudoerysipelas; "Swine erysipelas" in Great Britain, "Rouget du porc" in France and "Mal rossino" in Italy)

Are You Confident of the Diagnosis?

  • What you should be alert for in the history

Erysipeloid is a self-limited, localized infection occurring most commonly on the finger or hand, and appearing 24 to 72 hours following inoculation resulting from injury or trauma. Because the etiologic bacterium is carried by animals (fresh and saltwater fish, pigs, chickens, turkeys, ducks, sheep, lobsters and rabbits primarily), the affected person has almost always experienced trauma while handling animals or animal products, or had a traumatized area exposed to water or soil contaminated by the animal reservoir. The incubation period from the time of traumatic inoculation to lesion appearance is 2-7 days.

  • Characteristic findings on physical examination

Localized erysipeloid, the most common variety, is characterized clinically by a well-defined, indurated, inflammatory plaque with a distinctive red-purple color (Figure 1). Vesiculo-bullous and erosive areas may be present. Edema, particularly of the fingers, may be severe. The entire lesion ultimately spreads centrifugally.

Figure 1.

Erysipeloid followed fish fin puncture wound.

The lesion may be asymptomatic, but is more often accompanied by varying degrees of pain and/or tenderness to palpation. A rare diffuse cutaneous form consists of the widespread appearance of similar lesions, along with fever, lymphadenopathy, arthralgia and myalgia; this likely represents a septicemia originating from the initial inoculation site.

  • Expected results of diagnostic studies

The diagnosis is generally based on the history and a compatible clinical morphology. Laboratory examination may reveal leukocytosis and increased markers of inflammation (e.g., erythrocyte sedimentation rate, C-reactive protein). Histopathology is characteristic but nonspecific, consisting of marked dermal edema, vascular ectasia, and a mixed inflammatory infiltrate (neutrophils, lymphocytes and some eosinophils).

Cultural isolation of the causative bacterium, Erysipelothrix rhusiopathiae, is difficult. Aspirate or tissue specimen should be cultivated on enriched blood agar in high carbon dioxide tension at 30-37 degrees centigrade. While type-specific antigens allow for identification of some 22 serovars, this degree of differentiation is rarely available in most microbiology laboratories. A polymerase chain reaction assay with high specificity and sensitivity has been described, but is not readily available.

  • Diagnosis confirmation

The differential diagnosis includes: erysipelas, acute allergic contact dermatitis, neutrophilic dermatosis of the dorsal hand/Sweet’s syndrome, and erysipeloid-like edema accompanying administration of gemcitabine chemotherapy. Erysipelas, typically due to streptococci, occurs on the face or leg and is more often accompanied by constitutional symptoms such as fever. Contact dermatitis is intensely pruritic. The neutrophilic dermatoses have a characteristic histology (pure sheets of dermal neutrophils) which separates them from this infection. History would disclose receipt of chemotherapy as an inciting agent.

Who is at Risk for Developing this Disease?

Erysipeloid is worldwide in distribution, and is nearly always an occupational or avocational disease. It occurs in farmers; animal breeders, and veterinarians; slaughterhouse workers and butchers; fishermen (both professional and sport); chefs and others involved in food preparation; and grocery store workers who handle fresh seafood, poultry or meat. Non-occupational cases are rare, and pediatric cases vanishingly uncommon unless the child is immunocompromised.

What is the Cause of the Disease?

  • Etiology

Erysipeloid is caused by a rod-shaped, gram positive, faculative aerobe, E rhusiopathiae. As noted previously, this organism is closely associated with animals, and may be isolated from the mucoid exterior slime covering fish, the skin and fur of animals, and both soil and water contaminated by infected animals.

  • Pathophysiology

The precise pathogenesis is unknown. E rhusiopathiae is known to synthesize both a neuraminidase and a hyaluronidase, which are speculated to help the organism spread from the minor abrasion or prick wound of entry into adjacent and deeper tissues. The organism also elaborates several different adhesive surface proteins which help it bind to collagen, making this microbe especially suited to skin infection.

Systemic Implications and Complications

A rare generalized form of erysipeloid may lead to systemic illness. In addition to one or more skin lesions, the organism may undergo septicemic spread with eventual involvement of various organ systems. This may lead to endocarditis (most commonly), cerebral abscess, septic arthritis, meningitis, osteonecrosis, and peritonitis. Endocarditis has a male predilection and a propensity to involve the aortic valve; it carries a 38% mortality rate if untreated.

Treatment Options

Although most lesions will be self-limited (resolving in 14-21 days), treatment hastens clinical involution and reduces the already low risk of systemic disease. The organism tends to be quite susceptible to a wide variety of antibiotics. Most infections can be treated with standard oral doses of penicillin V, ampicillin, amoxicillin, erythromycin and cephalexin (typically 1g daily in divided doses). Oral clindamycin is also effective (300mg daily).

Susceptibility to tetracycline is variable, although doxycycline and minocycline (both 200mg daily) are typically effective. E rhusiopathiae is usually resistant to sulfonamides and trimethoprim-sulfamethoxazole. For diffuse cutaneous or generalized disease, intravenous penicillin G (12-20 million units daily) is the drug of choice. Interestingly, the bacteria is inherently resistant to vancomycin, and this drug should not be used to empirically treat presumed erysipeloid sepsis or endocarditis. There is no place for surgical intervention or for physical modalities in the treatment algorithm.

Optimal Therapeutic Approach for this Disease

In order to hasten disease involution and to prevent rare potential complications, erysipeloid should be treated. A 7-10 day course of oral antibiotic is sufficient in almost all cases. Resolution of all signs and symptoms is expected shortly following conclusion of antibiotic therapy. Almost any readily available antibiotic (except trimethoprim-sulfamethoxazole and tetracycline) will more than likely be efficacious. Serious infections involving organs other than the skin are treated with intravenous penicillin or cephalosporin agents. Clindamycin is an alternative for penicillin-allergic patients.

Patient Management

There is no special monitoring to be done, nor any follow-up other than a courtesy phone call to verify clinical resolution. For the very rare generalized form, hospitalization with intravenous antibiotics (as noted above) is indicated. This infection has an exceptionally low risk-benefit profile in terms of typical therapy.

Unusual Clinical Scenarios to Consider in Patient Management

The clinician should remain mindful of the potential for serious systemic disease. Check the temperature at the time of presentation and do a reasonably thorough review of systems to assess for the possibility of generalized illness. For example, a recent case report noted peritonitis due to E rhusiopathiae in a patient receiving ambulatory peritoneal dialysis who had concomitant erysipeloid of the hand. Chronic and recurring forms of the disease exist, although these are highly unusual. Involvement of mucosa is also uncommon, but a recent case report noted erysipeloid as a cause of granulomatous cheilitis in a farmer (occupational exposure).