Updated: Nov 13, 2009
Erysipeloid is an acute bacterial infection of traumatized skin and other organs. Erysipeloid is caused by the microorganism Erysipelothrix rhusiopathiae (insidiosa), which long has been known to cause animal and human infections. Direct contact between meat infected with E rhusiopathiae and traumatized human skin results in erysipeloid. In animals, the organism causes swine erysipelas and several other diseases in poultry and sheep.1
Erysipeloid is an occupational disease.2,3 Humans acquire erysipeloid after direct contact with infected animals. Erysipeloid is more common among farmers, butchers, cooks, homemakers, and anglers. The infection is more likely to occur during the summer or early fall.
E rhusiopathiae, which is highly resistant to environmental factors, enters the skin through scratches or pricks. In the skin, the organism is capable of producing certain enzymes that help it dissect its way through the tissues. It has recently been discovered that only pathogenic strains of E rhusiopathiae are capable of producing the neuraminidase enzyme. This enzyme is speculated to help the microorganism invade tissues. Moreover, 2 adhesive surface proteins were discovered and their nucleotide sequence encoded. The proteins are named RspA and RspB and serve in helping the microorganism bind to biotic (collagen types I and IV) and abiotic (polystyrene) surfaces.4,5
Meanwhile, the host's immune system is activated to start fighting against this foreign bacterium. The organism may escape immune surveillance and may spread in the body via the vascular system to the joints, heart, brain, CNS, and lungs. The organ most commonly affected other than the skin is the heart.
Infection with E rhusiopathiae occurs in worldwide distribution in a variety of animals, especially hogs.
Erysipeloid usually is an acute, self-limited infection of the skin that resolves without consequences. Individuals with the systemic form of erysipeloid, in which organs other than the skin are involved, may have neurologic, cardiologic, or other impairments. Individuals with systemic infection may even die of sepsis, if the proper diagnosis is not made and treatment is not initiated early on.
No racial predilection is recognized for erysipeloid.
Both sexes may be equally affected; however, erysipeloid seems to affect more males than females because of occupational exposure.
Erysipeloid can affect any age group.
Erysipeloid may present in humans as one of 3 clinical forms.
In the first 2 forms of erysipeloid, patients present with local burning or pain at lesion sites. They may or not have fever, malaise, and other constitutional symptoms.
In the generalized form, patients present with fever, chills, weight loss, and a variety of other symptoms (eg, joint pain, cough, headache), depending on the organ system involved.
Erysipelothrix rhusiopathiae causes all 3 forms of erysipeloid. E rhusiopathiae is a thin, gram-positive bacillus that may be straight or slightly curved. The microorganism is present in the soil and in poultry, fish, and birds. Homemakers, farmers, anglers, and butchers are at increased risk of acquiring the infection.
Cellulitis
Erysipelas
Seal finger
The epidermis shows spongiosis, which may be severe enough to cause intraepidermal vesiculation. Marked edema of the papillary dermis with dilatation of blood and lymphatic vessels occurs. In the reticular dermis, a perivascular inflammatory cell infiltrate made of neutrophils and eosinophils is observed.
The antibiotics of choice for the 3 forms of erysipeloid is penicillin or cephalosporin.6,7 Ceftriaxone proved to have an effect against Erysipelothrix rhusiopathiae. In patients who are allergic to penicillin, ciprofloxacin alone or erythromycin in combination with rifampin may be used. The microorganism is resistant to vancomycin, an important consideration in patients with endocarditis caused by E rhusiopathiae.
E rhusiopathiae has been shown to be eradicated from surfaces by the use of simple home disinfectants; thus, an important step in the prevention of infection may be to spray hazardous work areas (eg, fishing boats, meat counters) with disinfectants.8
Activity usually is not restricted. Individuals with the systemic form of erysipeloid may be advised to be on bed rest.
The 2 cutaneous forms of erysipeloid are self-limited and may remit spontaneously within 2-4 weeks; however, treatment with penicillin hastens the recovery and limits further progression of the disease.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms. However, it is not effective against penicillinase-producing bacteria.
Cutaneous disease: 250-500 mg PO qid for 7-10 d
Arthritis or endocarditis: 12-20 million U/d IV for 4 wk
25-50 mg/kg/d PO for 7-10 d
Increases risk of bleeding when administered concurrently with warfarin; ethacrynic acid, aspirin, indomethacin, and furosemide may compete with penicillin G for renal tubular secretion, increasing penicillin serum concentrations; probenecid can increase effects of penicillin; coadministration of tetracyclines can decrease effects of penicillin
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in asthma and allergies; dose must be adjusted in renal failure because drug is cleared by kidneys; inadvertent injection of penicillin into sciatic nerve may cause severe pain and dysfunction at the site that may persist for weeks
For penicillin-allergic patients. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes causing RNA-dependent protein synthesis to arrest.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double the dose.
250 mg erythromycin stearate/base (or 400 mg ethylsuccinate) q6h PO 1 h ac or 500 mg q12h; alternatively, 333 mg q8h; increase to 4 g/d depending on severity of infection
30-50 mg/kg/d (15-25 mg/lb/d) PO divided q6-8h; double dose for severe infection
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin, increases risk of rhabdomyolysis
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur
Wang Q, Chang BJ, Riley TV. Erysipelothrix rhusiopathiae. Vet Microbiol. Aug 8 2009;[Medline].
Brooke CJ, Riley TV. Erysipelothrix rhusiopathiae: bacteriology, epidemiology and clinical manifestations of an occupational pathogen. J Med Microbiol. Sep 1999;48(9):789-99. [Medline].
Reboli AC, Farrar WE. Erysipelothrix rhusiopathiae: an occupational pathogen. Clin Microbiol Rev. Oct 1989;2(4):354-9. [Medline].
Shimoji Y, Ogawa Y, Osaki M, et al. Adhesive surface proteins of Erysipelothrix rhusiopathiae bind to polystyrene, fibronectin, and type I and IV collagens. J Bacteriol. May 2003;185(9):2739-48. [Medline].
Wang Q, Chang BJ, Mee BJ, Riley TV. Neuraminidase production by Erysipelothrix rhusiopathiae. Vet Microbiol. May 20 2005;107(3-4):265-72. [Medline].
Veraldi S, Girgenti V, Dassoni F, Gianotti R. Erysipeloid: a review. Clin Exp Dermatol. Jul 29 2009;[Medline].
Veraldi S, Girgenti V, Dassoni F, Gianotti R. Erysipeloid: a review. Clin Exp Dermatol. Jul 29 2009;[Medline].
Fidalgo SG, Longbottom CJ, Rjley TV. Susceptibility of Erysipelothrix rhusiopathiae to antimicrobial agents and home disinfectants. Pathology. Oct 2002;34(5):462-5. [Medline].
Barnett JH, Estes SA, Wirman JA, Morris RE, Staneck JL. Erysipeloid. J Am Acad Dermatol. Jul 1983;9(1):116-23. [Medline].
Dunbar SA, Clarridge JE 3rd. Potential errors in recognition of Erysipelothrix rhusiopathiae. J Clin Microbiol. Mar 2000;38(3):1302-4. [Medline].
Gorby GL, Peacock JE Jr. Erysipelothrix rhusiopathiae endocarditis: microbiologic, epidemiologic, and clinical features of an occupational disease. Rev Infect Dis. Mar-Apr 1988;10(2):317-25. [Medline].
Razsi L, Sanchez MR. Progressively enlarging painful annular plaque on the hand. Erysipeloid. Arch Dermatol. Oct 1994;130(10):1311-2, 1314-5. [Medline].
erysipeloid, (insidiosa), infected meat, erysipeloid of Rosenbach, skin lesions, endocarditis
Zeina Nehme Ghorayeb, MD, Lecturer, University of Balamand School of Medicine
Zeina Nehme Ghorayeb, MD is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Nothing to disclose.
Mona Matta-Muallem, MD, Associate Professor, Department of Dermatology, American University of Beirut, Lebanon
Mona Matta-Muallem, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
Shyam Verma, MBBS, DVD, FAAD, Adjunct Clinical Assistant Professor, Department of Dermatology, University of Virginia, State University of New York at Stonybrook, Penn State University
Shyam Verma, MBBS, DVD, FAAD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.
Jeffrey J Miller, MD, Associate Professor of Dermatology, Penn State University College of Medicine; Staff Dermatologist, Penn State Milton S Hershey Medical Center
Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Association of Professors of Dermatology, North American Hair Research Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire Consulting
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
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