Erysipeloid is an acute bacterial infection of traumatized skin and other organs. Erysipeloid is caused by the non–spore-forming, non–acid-fast, gram-positive rod 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. See the image below.
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Erysipeloid. Courtesy of DermNet New Zealand (http://www.dermnetnz.org/topics/erysipeloid/) and the Waikato District Health Board (http://www.waikatod....
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.[6] The organ most commonly affected other than the skin is the heart.
Erysipeloid usually is an acute, self-limited infection of the skin that resolves without consequences.
Cutaneous forms of erysipeloid usually are self-limited even without treatment; therefore, skin-limited erysipeloid has a fairly good prognosis with no long-term sequelae.
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. Prognosis of the systemic form of erysipeloid depends on the organ systems involved and on the extent of involvement. Early recognition and proper initiation of therapy is crucial to prevent sequelae.
Erysipeloid may present in humans as one of three clinical forms.
Localized cutaneous form (also known as erysipeloid of Rosenbach); vesicles or bullae may develop[7]
Diffuse cutaneous form
Generalized or systemic infection as evidenced by bacteremia: Endocarditis may or may not develop.[8]
In the first two forms of erysipeloid, patients may be asymptomatic or present with local burning, pruritus, or pain at lesion sites. They may or may 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.
Lesions most commonly affect the back of the hands, mainly the webs of the fingers; however, any exposed area of the body may be affected. Lesions consist of well-demarcated, bright red-to-purple plaques with a smooth, shiny surface. Lesions are warm and tender and spread in a centrifugal manner. They leave a brownish discoloration on the skin when resolving. Sometimes vesicles may be present.[9] See the images below.
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Erysipeloid. Courtesy of DermNet New Zealand (http://www.dermnetnz.org/topics/erysipeloid/) and the Waikato District Health Board (http://www.waikatod....
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Erysipeloid. Courtesy of DermNet New Zealand (http://www.dermnetnz.org/topics/erysipeloid/) and the Waikato District Health Board (http://www.waikatod....
Diffuse cutaneous form of erysipeloid
Multiple lesions appear on various parts of the body. Lesions are well-demarcated, violaceous plaques with an advancing border and central clearing. Patients commonly have systemic symptoms such as fever, malaise, and arthralgias. Blood cultures are negative.[10]
Systemic form of erysipeloid
Also referred to as septic erysipeloid, skin lesions may not be apparent in this form. If present, skin lesions appear as localized areas of swelling surrounding a necrotic center. Skin lesions also may present as several follicular, erythematous papules. Endocarditis is the most common, but still rare, manifestation of systemic erysipeloid.[11] Hepatic failure, renal failure, cerebral infarcts, osseous necrosis, meningitis, encephalitis, and arthritis have been reported.[10]
Erysipelothrix rhusiopathiae causes all three 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. Injection comes from a prior wound being contaminated with the bacteria.
Several studies may be requested, depending on the clinical presentation.
Gram stain may be performed on a skin scraping, which may show gram-positive rods; however, the stain often is negative because the infection is deep, and the microorganism is not reached with scraping.
Bacterial culture on special media fortified with serum and at room temperature may be attempted. Culture of a biopsy from the leading edge of the lesion may reveal the organism.
Blood culture aids in the diagnosis of systemic erysipeloid.[8]
Skin biopsy may be taken to confirm the diagnosis (see Histologic Findings).
Organism culture is difficult. Media requires enrichment with blood and incubation with 5-10% carbon dioxide.[10]
Imaging studies usually are ordered when an individual has the systemic form of erysipeloid, depending on the clinical presentation and probability of organ involvement.
Echocardiography may be ordered, if endocarditis is suspected.
CT or MRI of the brain may be used to rule out brain abscess or cerebral infarct.
Radiography or CT of the chest may be ordered, if pleural effusion is suspected.
Bone scan or MRI of bone may be performed, if osseous necrosis is suspected.
Histopathologic examination is nonspecific. Papillary edema and vascular dilatation and dermal neutrophilic and lymphocytic infiltrate are observed. 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 three forms of erysipeloid are penicillin or cephalosporin.[12] 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.[9, 13] E rhusiopathiae is also resistant to chloramphenicol, daptomycin, gentamycin, netilmicin, streptomycin, teicoplanin, tetracycline, and trimethoprim/sulfamethoxazole.[7]
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.[14]
Procedures usually are not used in the cutaneous form of erysipeloid. Even a simple incision and drainage of lesions is not recommended as this may prolong the recovery time.
Individuals with the systemic form of erysipeloid may undergo surgery (eg, cardiac valve replacement), pleural tap, or other procedures, depending on extent of organ involvement.
The Infectious Diseases Society of America has guidelines for the diagnosis and management of skin and soft tissue infections. For the full guidelines, see Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America.[15, 16]
The two 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.
Clinical Context:
Penicillin G interferes with the synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms. However, it is not effective against penicillinase-producing bacteria.
Clinical Context:
Erythromycin is for penicillin-allergic patients. It 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 twice-daily dosing is desired, half the total daily dose may be taken every 12 hours. For more severe infections, double the dose.
Marc Zachary Handler, MD, Fellow in Mohs Micrographic Surgery, Skin Laser and Surgery Specialists of NY and NJ
Disclosure: Nothing to disclose.
Specialty Editors
David F Butler, MD, Former Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic
Disclosure: Nothing to disclose.
Jeffrey J Miller, MD, Associate Professor of Dermatology, Pennsylvania State University College of Medicine; Staff Dermatologist, Pennsylvania State Milton S Hershey Medical Center
Disclosure: Nothing to disclose.
Chief Editor
Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Mona Matta-Muallem, MD, Associate Professor, Department of Dermatology, American University of Beirut, Lebanon
Disclosure: Nothing to disclose.
Shyam Verma, MBBS, DVD, FAAD, Clinical Associate Professor, Department of Dermatology, University of Virginia School of Medicine; Adjunct Associate Professor, Department of Dermatology, State University of New York at Stonybrook School of Medicine; Adjunct Associate Professor, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Nothing to disclose.
Zeina Nehme Ghorayeb, MD, Lecturer, University of Balamand School of Medicine
Barclay L. IDSA: skin and soft tissue infections guidelines updated. Medscape Medical News. Available at http://www.medscape.com/viewarticle/827399. Accessed: June 26, 2014.
Erysipeloid. Courtesy of DermNet New Zealand (http://www.dermnetnz.org/topics/erysipeloid/) and the Waikato District Health Board (http://www.waikatodhb.health.nz/).
Erysipeloid. Courtesy of DermNet New Zealand (http://www.dermnetnz.org/topics/erysipeloid/) and the Waikato District Health Board (http://www.waikatodhb.health.nz/).
Erysipeloid. Courtesy of DermNet New Zealand (http://www.dermnetnz.org/topics/erysipeloid/) and the Waikato District Health Board (http://www.waikatodhb.health.nz/).
Erysipeloid. Courtesy of DermNet New Zealand (http://www.dermnetnz.org/topics/erysipeloid/) and the Waikato District Health Board (http://www.waikatodhb.health.nz/).
Erysipeloid. Courtesy of DermNet New Zealand (http://www.dermnetnz.org/topics/erysipeloid/) and the Waikato District Health Board (http://www.waikatodhb.health.nz/).
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