Erysipeloid

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.[8, 9]  RspA is the type that is by far most prevalent in animals with erysipelas. However, a single study isolated a E. rhusiopathiae bacterium from a human pyogenic spondylitis case found RspaB, raising the possibility that RspaB may pose a considerable threat to humans.[10]

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, central nervous system, and lungs.[11] The organ most commonly affected other than the skin is the heart.

Notable cases include an E. rhusiopathiae prosthetic joint infection in a 69-year-old woman with a history of exposure to wildlife in the Canadian Artic. A definite zoonotic source was unable to be identified in this case, despite whole genome sequencing.[12]  There are also at least 2 cases of aortic valve endocarditis secondary to E. rhusiopathiae infection reported in the literature.[13, 14]

Infection with E. rhusiopathiae occurs in worldwide distribution in a variety of animals, especially hogs. 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.

While the worldwide prevalence of E. rhusiopathiae remains unknown, a survey of 150 swab samples from sheep and calf hearts and livers, butchers, and fishermen from a community in Iran were analyzed by polymerase chain reaction (PCR). There were 12 (8%) positive samples.[15]

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 1 of 3 clinical forms.

• Localized cutaneous form (also known as erysipeloid of Rosenbach); vesicles or bullae may develop[16]

• Diffuse cutaneous form

• Generalized or systemic infection as evidenced by bacteremia: Endocarditis may or may not develop.[17]

In the first 2 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.

Localized form of erysipeloid

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.[18]  See the images below. 

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/).

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.[19]

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.[20] Hepatic failure, renal failure, cerebral infarcts, osseous necrosis, meningitis, encephalitis, and arthritis have been reported.[19]

Complications may include the following:

• Permanent neurological damage (eg, cerebrovascular accident)

• Endocarditis with long-term valvular heart disease

• Septic arthritis with long-term joint diseases

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.[17]

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.[19]

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.

Computed tomography or magnetic resonance imaging 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 3 forms of erysipeloid are penicillin or cephalosporin.[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.[18, 21]  E. rhusiopathiae is also resistant to chloramphenicol, daptomycin, gentamicin, netilmicin, streptomycin, teicoplanin, tetracycline, and trimethoprim/sulfamethoxazole.[16]

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.[22]

An infectious disease specialist may be consulted when deciding treatment, especially in cases of bone and joint involvement.

Opinions from a cardiologist and cardiothoracic surgeon are mandatory in cases of endocarditis.

Pulmonologists are consulted in cases of pleural effusion.

Neurologists and neurosurgeons are consulted in the presence of central nervous system disease.

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.[23, 24]

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Penicillin G (Pfizerpen, Wycillin)

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.

Erythromycin ethylsuccinate (E.E.S., EryPed)

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.