Infectious Diseases

Erysipelothrix

OVERVIEW: What every clinician needs to know

Pathogen name and classification

The genus Erysipelothrix is a member of the class Erysipelotrichia, in the phylum Firmicutes.

It is comprised of three main species: Erysipelothrix rhusiopathiae, Erysipelothrix tonsillarum, and Erysipelothrixinopinata.

Erysipelothrix rhusiopathiae, a pleomorphic, non-motile, non-sporulating, gram-positive rod, is the type species of the genus Erysipelothrix.E. rhusiopathiae, literally “erysipelas thread of red disease,” is a facultative intracellular pathogen that causes swine erysipelas, as well as a variety of diseases in many animals, including humans.

Erysipeloid, previously known as Rosenbach's disease, Baker-Rosenbach disease, and pseudoerysipelas, is a bacterial infection of the skin caused by traumatic penetration of Erysipelothrix rhusiopathiae (Figure 1, Figure 2).

Figure 1

Erysipeloid at the medial aspect of the proximal interphalangeal joint of the left third finger. Used with permission from McNamara D, Zitterkopf N, Baddour L. A woman with a lesion on her finger and bacteremia. Clin Infect Dis 2005;41(7):1005-6.

Figure 2

E. rhusiopathiae: a pleomorphic, nonsporulating, gram-positive bacillus. (permission pending)

What is the best treatment?

  • Most strains are highly susceptible to penicillins, cephalosporins, imipenem, clindamycin, and ciprofloxacin. Penicillin is the drug of choice for all forms of Erysipelothrix infection.

  • Localized cutaneous infections usually resolve spontaneously within 3-4 weeks, although treatment accelerates healing. For localized infections, oral therapy for 7 days with penicillin V (500 mg every 6 hours) should be administered. Clinical improvement is usually seen within 48-72 hours. Local heat may be of benefit in patients with painful, swollen lesions, but surgical debridement of localized lesions is not indicated. Relapses may occur despite antibiotic therapy.

  • For patients with diffuse cutaneous disease or systemic infection, parenteral therapy with penicillin G (2-4 million units every 4 hours) is recommended. The duration of therapy for diffuse cutaneous infection is 7 days. For systemic infection, the duration of therapy is at least 4 weeks. In cases of endocarditis, the duration of intravenous antibiotic therapy should be 4-6 weeks, although shorter courses (2 weeks of intravenous therapy followed by 2-4 weeks of oral therapy) have been successful.

Preferred therapy

  • Localized Cutaneous Infection-Penicillin V 500 mg orally every 6 hours

  • Diffuse Cutaneous or Systemic (Bacteremic) Infection-Penicillin G 2-4 million units IV every 4 hours

  • Most strains are resistant to vancomycin, sulfonamides, trimethoprim-sulfamethoxazole, novobiocin, teicoplanin, and aminoglycosides. Susceptibility to chloramphenicol, erythromycin, and tetracycline is variable. Resistance to vancomycin is of clinical significance, since vancomycin is often used as empiric treatment for gram-positive infections. Limited data suggest that Erysipelothrix is susceptible to daptomycin.

    • Erysipelothrix is intrinsically resistant to glycopeptides, including vancomycin, because it contains peptidoglycan precursors terminating in D-alanine-D-lactate, lowering the organism's affinity for the drugs. Antibiotics contained in animal feeds may play a role in the development of resistance in some strains, although the mechanisms of resistance remain uncertain. Although plasmids have been isolated from E.rhusiopathiae, they do not appear to play a significant role in the development of resistance.

    • Resistance is best detected with the broth microdilution minimal inhibitory concentration (MIC) test.

Alternative therapies

Localized Cutaneous Infection

  • Ciprofloxacin 250 mg orally every 12 hours

  • Clindamycin 300 mg orally every 8 hours

  • Erythromycin 500 mg orally every 6 hours

Diffuse Cutaneous or Systemic (Bacteremic) Infection

  • Ceftriaxone 2g IV every 24 hours

  • Imipenem 500 mg IV every 6 hours

  • Ciprofloxacin 400 mg IV every 12 hours

How do patients contract this infection, and how do I prevent spread to other patients?

Epidemiology

Infections in both man and animals appear to have a seasonal incidence, with most cases occurring in the summer and early fall. Infection in humans is often occupationally related, occurring most frequently in people whose jobs are closely related to contaminated animals, their products, wastes, or soil. Butchers, abattoir workers, veterinarians, farmers, fishermen, and fish-handlers are at highest risk of infection.

Environmental surfaces in contact with infected animals or their products are the main sources of E. rhusiopathiae. The organism can survive for long periods of time in marine environments, growing on exterior mucoid slime of fish without causing disease in the host. It can persist for prolonged periods in contaminated soil and is killed by moist heat at 55°C for 15 minutes; however, it is resistant to many food preservation methods, including salting, pickling and smoking.

E. rhusiopathiae is ubiquitous in nature; it is found wherever nitrogenous substances decompose. Infections caused by E. rhusiopathiae are worldwide in distribution and affect a wide variety of vertebrate and invertebrate species, including swine, sheep, horses, cattle, chickens, turkeys, crabs, fresh and saltwater fish, crocodiles, caymen, dogs, cats, reindeer, kangaroos, bears, mice, rodents, seals, sea lions, mink, chipmunks, ticks, mites, stable flies, houseflies, parrots, parakeets, pheasants, geese, peacocks, canaries, guinea fowl, pigeons, sparrows, starlings, eagles, mud hens, blackbirds, turtledoves, and white storks.

Domestic swine are believed to be the most important animal reservoir of E. rhusiopathiae. The organism is shed by infected animals in feces, urine, saliva, and nasal secretions, which can contaminate food, water, soil, and bedding. Maintenance of the organism in nature appears to result from asymptomatic carriage in animals and subsequent dissemination of the organism to the environment.

The rare instances of non-occupational-related infection suggest that oropharyngeal and gastrointestinal (GI) colonization with the organism may occur. Erysipeloid and erysipeloid with bacteremia have been reported after cat and dog bites, suggesting that the organism may be part of the oral flora of these animals.

The incidence of cutaneous infections in humans appears to be decreasing because of technologic advances in animal industries.

Infection control issues

For individuals working at high risk occupations, suggested preventative measures include wearing gloves or other protective hardware, good hygiene, especially frequent hand washing with disinfectant soap, and the prompt topical treatment of any small skin injuries.

Vaccination is considered useful in animals; however, vaccination of humans is not felt to be a viable option at the present time. Infection and clinical disease appears to convey little or no immunity. Research to develop more immunogenic and safer vaccines continues.

There is no role for post-exposure antimicrobial prophylaxis.

What host factors protect against this infection?

Both humoral and cell-mediated immunity play an important role in host defense.

Individuals in poor health may be predisposed to more serious forms of the infection. Chronic liver disease is an important predisposing factor for developing systemic infection. Greater than one-third of patients with systemic disease are alcoholics. Bacteremia can also be seen in other immunocompromised patients, particularly those receiving corticosteroids or cytotoxic drug therapy.

Histopathological findings are nonspecific, although they are characteristic. The condition is characterized by marked edema in papillary and upper dermis, vascular dilatation, and an inflammatory infiltrate consisting mainly of neutrophils and lymphocytes with some eosinophils. Examination of vesiculobullous lesions shows dermo-epidermal detachment with neutrophils floating in the blisters. There is infiltration of neutrophils and lymphocytes among the collagen bundles in the dermis. Eosinophils can be seen at higher magnification.

What are the clinical manifestations of infection with this organism?

There are three major forms of disease:

  1. Localized cutaneous infection: Erysipeloid is the most common form of human infection due to Erysipelothrix. The incubation period following inoculation is 2-7 days. Symptoms often begin with pain, which has been described as severe burning, itching, or throbbing, and swelling at the site of entry. Skin lesions progress from small red macular lesions at the site of inoculation to well-developed violaceous lesions with central clearing and a raised border. Vesiculation may occur, but suppuration is absent. Patients typically complain of swelling and stiffness/pain in the affected region. There may be a sterile arthritis of an adjacent joint. Approximately 20-30% of the time, lymphangitis and regional adenitis occur. Systemic symptoms are rare, although approximately 10% of patients describe low grade fever and arthalgias. Without treatment, lesions usually resolve within 3 weeks. Relapse occurs approximately 1% of the time.

  2. Diffuse cutaneous infection: Diffuse cutaneous disease is characterized by proximal progression of involvement from the inoculation site to other sites. Lesions may be urticarial or bullous. Systemic symptoms are more frequent and include fever, malaise, joint and muscle pain, headaches, and polyarthritis in rare instances. Blood cultures are usually negative. The clinical course is more protracted, and recurrences are common.

  3. Systemic infection: Systemic infection with bacteremia is relatively uncommon. Most patients present with fever. About 40% of patients have a preceding or concurrent skin lesion suggestive of erysipeloid. Multiple bullous lesions on the trunk and extremities or cutaneous serpiginous lesions can be seen. The clinical picture may resemble gram-negative sepsis. E. rhusopathiae bacteremia is often complicated by endocarditis, although bacteremia without endocarditis has been reported. Brain abscesses, meningitis, intra-abdominal abscess, endophthalmitis, septic arthritis, osteomyelitis, necrotizing enterocolitis, and peritoneal dialyisis-related peritonitis with bacteremia have been reported.

Humoral and cell-mediated immunity play an important role in host defense.

Individuals in poor health may be predisposed to more serious forms of the infection. Chronic liver disease is an important predisposing factor for developing systemic infection. More than one-third of patients with systemic disease are alcoholics. Bacteremia can also be seen in other immunocompromised patients, particularly those receiving corticosteroids or cytotoxic drug therapy.

Histopathological findings are nonspecific, although they are characteristic. The condition is characterized by marked edema in papillary and upper dermis, vascular dilatation, and an inflammatory infiltrate consisting mainly of neutrophils and lymphocytes with some eosinophils. Examination of vesiculobullous lesions shows dermo-epidermal detachment with neutrophils floating in the blisters. There is infiltration of neutrophils and lymphocytes among the collagen bundles in the dermis. Eosinophils can be seen at higher magnification.

What common complications are associated with infection with this pathogen?

Erysipelothrix bacteremia is commonly complicated by endocarditis. Prosthetic valve endocarditis has been described, but native valve endocarditis, most often the aortic valve, is more common. A history of preceding skin infection was seen in approximately one-third of cases. Endocarditis caused by Erysipelothrix is more common in males, more likely to involve the aortic valve, and has a high mortality rate (38%). More than one-third of patients reported in the literature required valve replacement.

Complications of E. rhusiopathiae endocarditis include myocarditis, congestive heart failure, valvular perforations, paravalvular and myocardial abscess formation, cerebral infarctions, osteomyelitis, septic arthritis, and acute renal failure secondary to proliferative glomerulonephritis.

Complications of bacteremia without endocarditis are more common in immunocompromised hosts and include brain abscess, necrotizing fasciitis, meningitis, peritonitis, intra-abdominal abscess, osteomyelitis, and septic arthritis.

How should I identify the organism?

Definitive diagnosis requires isolation from a biopsy specimen, blood, or other sterile body fluid. The organism is located in deeper parts of the skin in erysipeloid, so maximum recovery of the organism requires biopsy of the entire thickness of the dermis from the edge of the lesion. Aspirates or swabs of lesions do not usually detect the organism.

Identification of Erysipelothrix species is based on Gram stain, cultural morphology, motility, hemolytic characteristics, and biochemical properties. Erysipelothrixrhusiopathiae is a pleomorphic non-encapsulated, non-sporulating, non-motile, catalase and oxidase negative, gram-positive rod.

E. rhusiopathiae grows on routine laboratory culture. Standard methods for culturing blood or biopsy tissue are sufficient if the incubation is continued for 7 days. Erysipelothrix grows best at 35°C in 5% CO2. Commercially available blood culture media are adequate for primary isolation from the blood. Multiple selective media have also been described, including Erysipelothrix selective broth (ESB), modified blood azide medium (MBA), Packer's medium, Bohm's medium, and Shimoji's selective enrichment broth. ESB, a nutrient broth containing serum tryptose, kanamycin, neomycin, and vancomycin, is considered the best selective medium. Shimoji's selective broth used in combination with polymerase chain reaction (PCR) has been helpful in the rapid diagnosis of erysipelas in swine.

E. rhusiopathiae is negative for catalase, oxidase, methyl red, indole, esculin, nitrate reduction, Voges-Proskauer, and liquefaction of gelatin. Acid is produced from fructose, glucose, and galactose but not from maltose, mannitol, or xylose. Sucrose is fermented by most strains of E. tonsillarum but not by E. rhusiopathiae. Hydrogen sulfide is produced by 95% of strains of Erysipelothrix species on triple sugar iron agar. Rapid identification can be achieved with the API Coryne System, a commercial strip system based on biochemical reactions for the identification of coryneform bacteria and related genera including E. rhusiopathiae.

Problems exist with the diagnosis of E. rhusiopathiae infections by conventional cultural procedures, and these infections are often incorrectly diagnosed. Because of their very small colony size and slow growth rates, it is difficult to isolate E. rhusiopathiae from heavily contaminated specimens.

It is likely that E. rhusiopathiae infections are under-diagnosed. The organism's very small colony size and slow growth rates make it difficult to isolate from heavily contaminated specimens.

PCR-based assays have been used for rapid diagnosis in swine and have been applied successfully to human and environmental specimens. Two PCR assays have been described for the diagnosis of swine erysipelas.

How does this organism cause disease?

The major virulence factor of E. rhusiopathiae is the exopolysaccharide capsule that can protect the bacterial cell from host defenses, such as opsonophagocytosis by polymorphonuclear leukocytes and intracellular killing by macrophages. Capsule deficient mutants were found to be avirulent in mice.

The pathogenicity of E. rhusiopathiae may be primarily related to the intracellular survival properties of the bacterium. The organism probably utilizes several different host cell receptors to gain access to the host intracellular niche. Intracellular survival of virulent organisms in macrophages is associated with reduced stimulation of oxidative respiratory burst.

The enzyme neuraminidase, which can release terminal sialic acid residues from glycoproteins, glycolipid, and oligosaccharides expressed on host cells, has been recognized as a virulence factor with increased amounts of neuraminidase resulting in increased virulence.

Hyaluronidase, a spreading factor that facilitates the dissemination of pathogens into tissues, may contribute to the pathogenicity, but its role is less certain.

Two adhesive surface proteins, SpaA and P64, have been identified from E. rhusopathiae. P64 protein is less expressed on strains of lower virulence and is associated with the induction of protective activity against E. rhusopathiae in mice.

The pathogenic significance of the SpaA protein was suggested in a mouse model in which exposure to the antigen was protective in a vaccination system.

WHAT’S THE EVIDENCE for specific management and treatment recommendations?

Nelson, RRS. "Intrinsically vancomycin-resistant gram positive organisms: clinical relevance and implications for infection control". J Hosp Inf. vol. 42. 1999. pp. 275-82.

(This source discusses intrinsic organism resistance.)

Brooke, CJ, Riley, TV. "Erysipelothrix rhusiopathie: bacteriology, epidemiology, and clinical manifestations of an occupational pathogen". J Med Microbiol. vol. 48. 1999. pp. 789-99.

(This is a comprehensive review, including microbiology, epidemiology, clinical manifestations, recent advances in molecular approaches to diagnosis, and understanding of taxonomy and pathogenesis.)

Reboli, A, Goldman, L, Schafer, AI. "Erysipelothrix infections". Cecil Medicine. Saunders Elsevier. 2008.

(This is a concise review of the microbiology, epidemiology, pathogenesis, clinical manifestations, and treatment and prevention.)

Wang, Q, Chang, BJ, Riley, TV. "Erysipelothrix rhusiopathie". Vet Microbiol. vol. 140. 2010 Jan 27. pp. 405-17.

(This is a comprehensive and detailed review, including nomenclature, organism isolation, virulence factors, and clinical manifestations.)

Troelsen, A, Møller, J, Bolvig, L, Prynø, T, Pedersen, L, Søballe, K. "Animal associated bacteria, Erysipelothrix rhusiopathiae, as the cause of infection in a total hip arthroplasty". J Arthroplasty. vol. 25. 2010. pp. 497.e21-3.

(This is a case review and overview.)

Reboli, A, Mandell, GL, Bennett, JE, Dolin, R. "Erysipelothrix rhusiopathiae.". Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. Churchill Livingstone Elsivier. 2010.

Veraldi, S, Girgenti, V, Dassoni, F, Gianotti, R. "Erysipeloid: a review". Clin Exp Dermatol. vol. 34. 2009 Dec. pp. 859-62.

(This is a brief overview with good images.)

Shimoji, Y. "Pathogenicity of Erysipelothrix rhusiopathiae: virulence factors and protective immunity". Microbed Infect. vol. 2. 2000. pp. 965-72.

(Recent advances in our understanding of pathogenicity and protective immunity are described.)

McNamara, D, Zitterkopf, N, Baddour, L. "A woman with a lesion on her finger and bacteremia". Clin Infect Dis. vol. 41. 2005. pp. 1005-6.

(This is a case report of a woman with a soft tissue infection and bacteremia due to E. rhusiopathiae.)
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