Annette C. Reboli
Erysipelothrix rhusiopathiae
Erysipelothrix rhusiopathiae is a thin, pleomorphic, nonsporulating gram-positive rod. First isolated from mice by Robert Koch in 1878 and from swine by Louis Pasteur in 1882, it was established as the etiologic agent of swine erysipelas in 1886 by Löffler and as a human pathogen in 1909 when Rosenbach isolated it from a patient with localized cutaneous lesions.1 Rosenbach coined the term erysipeloid to avoid confusion with erysipelas, a superficial cellulitis with prominent lymphatic involvement that is almost always caused by group A streptococci.2
Microbiology
E. rhusiopathiae is a straight or slightly curved aerobic or facultatively anaerobic bacillary organism; it is 0.2 to 0.4 µm in diameter and 0.8 to 2.5 µm in length. It is gram positive but may appear gram negative because it decolorizes readily. Organisms may be arranged singly, in short chains, in pairs in a “V” configuration, or grouped randomly. Nonbranching filaments, which can be longer than 60 µm, are sometimes seen. Colonial and microscopic appearance varies with the medium, pH, and temperature of incubation.1 After growing for 24 hours at 37° C, colonies are small and transparent, with a smooth, glistening surface. On blood agar, it may be α-hemolytic. E. rhusiopathiae is negative for catalase, oxidase, indole, Voges-Proskauer, and methyl red.2 Acid without gas is produced from the fermentation of glucose, fructose, lactose, and galactose. Most strains produce hydrogen sulfide, a diagnostically important reaction. On triple sugar iron (TSI) agar slants, hydrogen sulfide causes a blackened butt. In gelatin stab cultures, E. rhusiopathiae produces a distinctive “pipe cleaner” pattern of growth. E. rhusiopathiae is sometimes confused with other gram-positive bacilli, in particular, Listeria monocytogenes, Arcanobacterium pyogenes, and Arcanobacterium haemolyticum, but these three species are β-hemolytic on blood agar and do not produce hydrogen sulfide in the butt on TSI agar slants. Furthermore, L. monocytogenes is catalase positive and motile.1 Vitek 2 and the API Coryne system are reliable for the identification of E. rhusiopathiae.3
Epidemiology
E. rhusiopathiae is found worldwide. It has been reported as a commensal or a pathogen in a wide variety of vertebrate and invertebrate species, but the major reservoir is believed to be domestic swine.2 Mites may serve as a vector of the organism, allowing it to persist in coops and pens.4 It does not appear to cause disease in fish but can persist for long periods in the mucoid exterior slime of these animals. It may live long enough in soil to cause infection weeks or months after initial contamination. The greatest commercial impact of E. rhusiopathiae infection is the result of disease in swine, but infection of poultry and sheep is also important. Human infection is a zoonosis. The organism is communicable from animals to humans by direct cutaneous contact. Abrasions or puncture wounds of the skin probably serve as the portal of entry of Erysipelothrix organisms in most cases of infection in humans and animals. There have been reports of bacteremia, one with endocarditis, which occurred after ingestion of undercooked pork. There was an outbreak of E. rhusiopathiae in racing pigeons after ingestion of compost.5 The risk for human infection with Erysipelothrix is closely related to the opportunity for exposure to the organism; accordingly, most human cases are related to occupational exposure. Although infection with Erysipelothrix has been associated with many occupations, people at greatest risk include fishermen, fish handlers, butchers, farmers, slaughterhouse workers, veterinarians, and homemakers.2 Infection is especially common among people who handle fish. “Whale finger” is erysipeloid seen in people who sustain cuts to the fingers and hands while engaged in whaling. Human-to-human transmission of infection has not been reported. Cases of infection that do not have an occupational link have occurred mainly in immunocompromised hosts and suggest that colonization of the oropharynx or gastrointestinal tract may occur.6 Chronic alcoholism is a common underlying condition. There have been a few reports of erysipeloid after cat and dog bites.7 Most human infections are caused by serovars 1 and 2.3 Ribotyping, randomly amplified polymorphic DNA, pulsed-field gel electrophoresis, and nucleotide sequence analysis of the spaA gene are useful for typing isolates.3
Pathogenesis
Progress has been made in the understanding of the pathogenesis of E. rhusiopathiae. Virulence factors include a capsule, enzymes (neuraminidase and hyaluronidase), and surface proteins.8,9 The capsule is composed of polysaccharide antigen and confers resistance to phagocytosis. Neuraminidase is important in attachment and entry into host cells. The surface protective antigen proteins, SpaA, SpaB, and SpaC, are major protective antigens. SpaA and SpaC elicit a protective immune response in swine and murine animal models.10 In the absence of specific antibodies, E. rhusiopathiae evades phagocytosis but, even if phagocytized, it is capable of intracellular replication.8
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