Erysipelothrix species

Genus Characteristics

The genus Erysipelothrix is now classified as part of the regular non-spore-forming Gram-positive rods group along with Lactobacillus and Listeria. Erysipelothrix species are mesophilic, facultative anaerobes, non-acid-fast, Gram-positive short rods or long non-branching filaments. They also occur singly or in short chains. Erysipelothrix species are non-motile, catalase, methyl red, Voges–Proskauer, indole and oxidase negative, do not hydrolyze aesculin, weakly ferment glucose without gas, do not hydrolyse urea but produce H₂S in triple sugar iron agar. Differentiation of Erysipelothrix from related genera is indicated in Table 13.1.

Table 13.1

Differentiation of Erysipelothrix from related genera which have regular aerobic Gram-positive non-spore-forming rods

Erysipelothrix rhusiopathiae (previously E. insidiosa), the causative agent of erysipelas and a zoonosis, is of clinical significance. Erysipelothrix tonsillarum, previously considered to be a serotype of E. rhusiopathiae was reclassified as a new species using DNA–DNA hybridization studies (Takahashi et al. 1992). They are the two major species within the genus (Takahashi et al. 2008). Erysipelothrix tonsillarum appears to be nonpathogenic for pigs but has been associated with endocarditis in dogs (Eriksen et al., 1987).

Natural Habitat

Erysipelothrix rhusiopathiae is ubiquitous in nature. The microorganism persists in the environment at low temperatures, at alkaline pH and within organic matter. The bacterium can be isolated from many species (mammals, birds, reptiles, amphibians and fish), but it is most commonly associated with pigs which are generally considered the primary reservoir. Healthy carriers can carry the bacteria in their tonsils and other lymphoid tissues of the intestinal tract. Clinically sick pigs as well as asymptomatic animals and healthy carriers can shed the microorganism in their faeces and secretions, representing a significant source of infection and environmental contamination.

Pathogenesis and Pathogenicity

The principal hosts and disease syndromes caused by E. rhusiopathiae are indicated in Table 13.2. Infection is usually acquired by ingestion of contaminated food or water. The bacterium may also gain entry via skin wounds.

Table 13.2

Main hosts and disease syndromes of Erysipelothrix rhusiopathiae

Swine erysipelas (Pasteur referred to this condition as rouget; Fig. 13.1) can be divided into three forms: acute, subacute and chronic (Straw 2006). The acute form is characterized by septicaemia with high temperature, loss of appetite, skin lesions and high mortality. The skin lesions present as diamond-shaped (‘diamond-skin’ disease) red plaques, which are variable in size and number. A generalized coagulopathy leading to fibrinous thrombosis, invasion of vascular endothelium and deposition of fibrin in perivascular tissues occurs. In severe acute cases, ischaemic necrosis of perivascular tissues can occur. The subacute form is somewhat milder. The chronic form is characterized by endocarditis and polyarthritis. Vascular inflammation, myocardial infarcts and exudation of fibrin followed by destruction of valvular endocardium gives rise to valvular lesions in the heart. Joint lesions result from acute synovitis which gives rise to severe fibrosis leading to erosion of articular cartilage.

Figure 13.1 Erysipelothrix rhusiopathiae: pathognomonic diamond-shaped, red, urticarial plaques of swine erysipelas (an acute form of the disease).

Erysipelothrix rhusiopathiae infection is of economic importance for the turkey industry where the infection is generally acute with high mortality (sudden death with or without skin lesions). It only rarely affects chickens.

Infection of humans with E. rhusiopathiae is a zoonosis referred to as erysipeloid. It is characterized by a localized cellulitis around the site of inoculation. The lesion is usually violaceous and painful with induration, oedema and inflammation but without suppuration (Fig. 13.2). It is an occupational disease usually contracted via skin abrasions or injuries in individuals handling animals or animal products. Veterinarians, butchers and fish handlers are most frequently infected. Dissemination and endocarditis are rare but can occur in immunocompromised humans. Erysipelothrix rhusiopathiae is one of the most common pathogens acquired topically from fish (Lehane & Rawlin 2000).

Figure 13.2 Erysipelothrix rhusiopathiae: erysipeloid, localized cellulitis which develops around the inoculation site. The lesion is violaceous with enduration, oedema and inflammation but without suppuration.

Erysipelothrix rhusiopathiae virulence factors (Shimoji 2000) and their role in disease pathogenesis are indicated in Table 13.3. The mechanism of invasion of deeper body tissues or the bloodstream is unclear. However, it is reported that neuraminidase plays an important role in the attachment and invasion process into endothelial cells and in the subsequent development of vascular lesions (Nakato et al. 1987). Invasion of other host cells such as synovial cells and chondrocytes from arthritic joints of pigs has been reported (Franz et al. 1995). Strains of E. rhusiopathiae vary in virulence. The more virulent strains produce high levels of neuraminidase that can cause vascular damage, thrombus formation and haemolysis. Injury to articular cartilage is thought to be due to an immunological response to persistent antigen or whole bacterial cells in the synovial fluid and it is not known whether superimposed autoimmune reactions are involved. The capsule provides resistance to phagocytosis by mononuclear phacocytes (macrophages) and polymorphonuclear leukocytes (Shimoji et al., 1994, 1996). Other virulence factors such as catalase, superoxide dismutase, hyaluronidase, SpaA1 protein and surface proteins of 85 kDa (RspB) and 220 kDa (RspA) also play important roles in the disease process.

Table 13.3

Main virulence factors of Erysipelothrix rhusiopathiae

Virulence determinants	Functions
Capsule (appears as slime or glycocalyx)	Resistance to opsonin-mediated phagocytosis and protection against intracellular killing by macrophages
SpaA protein	Surface protein, a major protective antigen
Surface proteins of 220 kDa (rspA gene) and of 85 kDa (rspB gene)	Participate in biofilm formation, adhesive surface proteins which bind to polystyrene, fibronectin, and type I and IV collagens
Neuraminidase (sialidase)	Extracellular enzyme which releases terminal sialic acid residues from glycoproteins, glycolipids, and oligosaccharides of host cells
Hyaluronidase	Extracellular enzyme which is a spreading factor that facilitates the dissemination of the bacteria into tissues by damaging hyaluronic acid, a polysaccharide of the extracellular matrix of connective tissues
Superoxide dismutase	Potential virulence factor, quench oxidative metabolites of phagocytic cells (aid in protecting from intracellular killing)