Chapter 47
Erysipelothrix rhusiopathiae
Qinning Wang1 and Thomas V. Riley2,3
1
Institute of Clinical Pathology & Medical Research, Westmead, Australia, 2The University of Western Australia, Western Australia, Australia,
3
Division of Microbiology & Infectious Diseases, PathWest Laboratory Medicine, Western Australia, Australia
INTRODUCTION
The genus Erysipelothrix contains two recognized main
species, Erysipelothrix rhusiopathiae and E. tonsillarum.
Another two species have been also proposed
Erysipelothrix sp. strain 1 (E. rhusiopathiae serotype 13)
and Erysipelothrix sp. strain 2 (E. rhusiopathiae serotype
18) [1 3]. In addition, a fifth species has been also
described as E. inopinata [4]. The genus was classified
into 23 serotypes and type N based on peptidoglycan anti-
gens on the cell wall [5 7]. E. rhusiopathiae, formerly
the only species of the genus Erysipelothrix, including
serovars 1a, 1b, 2a, 2b, 4, 5, 6, 8 ,9, 11, 12, 15, 16, 17,
19, 21 and type N, is a facultative, non-spore-forming,
non-acid-fast, rod-shaped Gram-positive bacillus. The
organism was first established as a human pathogen late
in the nineteenth century. Three forms of human disease
have been described, including a localized cutaneous
lesion form, erysipeloid, which was so-called to distin-
guish it from the human streptococcal disease erysipelas,
a generalized cutaneous form, and a septicaemic form
often associated with endocarditis [8]. Infection in
humans is occupationally related, principally occurring as
a result of contact with contaminated animals, their pro-
ducts or wastes, or soil. Erysipeloid is the most common
form of infection in humans. Some other names used to
describe this infection reflect the occupational attributes
of the disease, including whale finger, seal finger, speck
finger, blubber finger, fish poisoning, fish handler’s dis-
ease and pork finger [9]. The organism is ubiquitous and
able to persist for a long period of time in the environ-
ment, including marine locations. It is a pathogen or a
commensal in a wide variety of wild and domestic ani-
mals, birds and fish [10]. Swine erysipelas caused by
E. rhusiopathiae is the disease of greatest prevalence and
economic importance [11]. Diseases in other animals
include erysipelas of farmed turkeys, chickens, ducks and
Molecular Medical Microbiology. DOI: http://dx.doi.org/10.1016/B978-0-12-397169-2.00047-0
© 2015 Elsevier Ltd. All rights reserved.
emus, and polyarthritis in sheep and lambs. The organism
causes no known disease in fish but can survive for long
periods of time on the mucoid exterior slime of fish [12].
NOMENCLATURE AND TAXONOMY
E. rhusiopathiae, literally ‘erysipelas thread of red dis-
ease’, has a long history with many nomenclature
changes. The earliest member of the genus Erysipelothrix
was termed E. muriseptica, first isolated by Koch in 1876
from the blood of mice with septicaemia. Subsequently,
Erysipelothrix has been identified as the cause of infec-
tion in many animal species and three separate species of
the organism, E. muriseptica, E. porci and E. erysipeloid,
were proposed based on their isolation from mice, pigs
and humans, respectively. It was later realized that these
three organisms were nearly identical strains of the same
species. The name E. insidiosa was proposed for them
originally by Trevisan in 1885. This and all 36 other
documented names for the organism were rejected in
1966 in favour of E. rhusiopathiae, a combination that
originated in 1918 [13].
Erysipelothrix demonstrated great serological, bio-
chemical and antigenic variation between strains.
Pathogenicity testing showed that a cluster of avirulent
strains of serotype 7 came predominantly from pig tonsils
[14]. They were later found to be genetically distinct from
E. rhusiopathiae by DNA base composition and
DNA DNA homology studies [1]. These strains formed
the basis of a new species, E. tonsillarum, and belonged
to serotypes 3, 7, 10, 14, 20, 22 and 23. Some other
strains representing serotype 13 (Erysipelothrix sp. strain
1) and 18 (Erysipelothrix sp. strain 2) exhibited low levels
of hybridization with type strains of both E. rhusiopathiae
and E. tonsillarum, indicating that these serotypes may
be members of a new genomic species [1 3]. Originally,
859
860 PART | 7 Localized Infections
E. tonsillarum was considered morphologically and bio-
chemically identical to E. rhusiopathiae, but it was shown
later that E. tonsillarum could ferment sucrose, while
E. rhusiopathiae could not [1]. In addition, the majority
of E. tonsillarum strains (96%) were avirulent while 66%
of E. rhusiopathiae strains produced disease in swine
[15]. On the other hand, a study found that E. tonsillarum
was isolated from systemic sites from 3.4% of the car-
casses that were negative for E. rhusiopathiae, indicating
the potential importance of this organism in the pathogen-
esis of swine erysipelas [16]. Comparison of protein com-
position using a computerized evaluation method revealed
that the geometric mean of the similarities was 0.980 6
0.018 between E. rhusiopathiae strains, 0.979 6 0.013 for
E. tonsillarum strains and 0.932 6 0.036 between the
strains of other Erysipelothrix species. However, the study
did not establish a threshold value applicable for identifi-
cation of a given strain to species level [17]. Phylogenetic
analysis of 16S rRNA genes of E. rhusiopathiae and
E. tonsillarum showed that both sequences are almost
identical (99.8%) with only three nucleotide differences
[18]. Although it has been suggested that 16S rRNA
sequences can be used routinely to distinguish and estab-
lish relationships between genera and well-resolved spe-
cies, very recently diverged species like E. rhusiopathiae
and E. tonsillarum may not be distinguishable [19].
E. rhusiopathiae is most likely to be confused with
other Gram-positive, non-sporing, rod-shaped bacteria,
such as members of the genera Brochothrix,
Corynebacterium, Lactobacillus, Listeria and Kurthia. It
was once considered a close relative of the Listeria genus,
but studies of cell wall peptidoglycan [20], fatty acid
patterns [21], DNA hybridization [22], and numerical
taxonomic studies [23,24] did not support this relation-
ship. Erysipelothrix can be distinguished from Listeria in
cell wall composition, as Erysipelothrix contains lysine
and glycine while Listeria contains mesodiaminopimelic
acid [25]. No common antigens between strains of
Erysipelothrix and Listeria monocytogenes were detected
by immunodiffusion or passive haemagglutination tests
[26]. Brochothrix and Corynebacterium were also distin-
guished from E. rhusiopathiae on the basis of containing
mesodiaminopimelic acid in the cell wall. The catalase
test can distinguish E. rhusiopathiae from catalase-
positive Kurthia species. A closer relationship of
Erysipelothrix to the family Lactobacillaceae than to
Corynebacteriaceae was revealed using enzyme and
DNA-based ratio studies [21]. In a study of more than 200
strains of coryneform bacteria using morphological, physi-
ological and biochemical tests and computer analysis,
Erysipelothrix was most closely related to Streptococcus
pyogenes [27]. Further molecular taxonomic studies have
concluded that the genus Erysipelothrix is a distinct cluster
of organisms, most similar to the streptococci [9,28].
The results of 16S rRNA analysis indicated that
E. rhusiopathiae has a closer relationship with Clostridium
innocuum [29]. Both organisms contain lysine in their cell
wall. C. innocuum is a member of the RNA cluster which
contains the mycoplasmas and which itself is part of the
much broader clostridial group [30]. Phylogenetic analysis
based on Hsp70 sequences in the dnaK (hsp70) gene
region of Mycoplasma capricolum showed that
Mycoplasma species branched with the low G 1 C content
Gram-positive group of bacteria including Lactobacillus
and Erysipelothrix species in 87% and 96% of the boot-
strap replicates, respectively, indicating the close evolu-
tionary relationship of Erysipelothrix to this group [31a].
Most recent complete genome sequence analysis
reveals that the overall features of the E. rhusiopathiae
genome are similar to those of other Gram-positive bacte-
ria. However, it lacks many orthologous genes for the bio-
synthesis of wall teichoic acids (WTA) and lipoteichoic
acids (LTA) and the dltABCD operon. It has a complete
loss of fatty acid biosynthesis pathways and lacks the
genes for the biosynthesis of many amino acids, cofactors
and vitamins. These indicate reductive genome evolution.
The E. rhusiopathiae genome represents evolutionary
traits of both Firmicutes and Mollicutes and provides new
insights into its evolutionary adaptations for intracellular
survival [31b].
EPIDEMIOLOGY OF ERYSIPELOTHRIX
INFECTION
E. rhusiopathiae is ubiquitous in nature, being found
wherever nitrogenous substances decompose [32]. E. rhu-
siopathiae and infections caused by this organism are
worldwide in distribution, and affect a wide variety of
vertebrate and invertebrate species, including swine,
sheep, cattle, horses, dogs, cats, mice, kangaroos, rein-
deer, bears, numbats, rodents, seals, sea lions, cetaceans,
mink, chipmunks, crustaceans, fresh- and saltwater
fish, crocodiles, caymen, stable flies, houseflies, ticks,
mites, mouse lice, turkeys, chickens, hens, ducks,
geese, guinea fowl, pigeons, sparrows, kakapo, starlings,
eagles, parrots, pheasants, peacocks, quail, parakeets, mud
hens, canaries, finches, siskins, thrushes, blackbirds, tur-
tledoves and white storks [9,12,33 38]. Human disease
can originate from an animal or environmental source.
Swine erysipelas caused by E. rhusiopathiae is the dis-
ease of greatest prevalence and economic importance. It is
economically detrimental to the pig industries of North
America, Europe, Asia and Australia [11]. Polyarthritis of
sheep and lambs, and erysipelas in calves, ducks and
domestic turkeys are also economically significant dis-
eases caused by E. rhusiopathiae [10,12]. The domestic
pig is the most important reservoir of E. rhusiopathiae.

It is estimated that 30 50% of healthy swine harbour the
organism in their tonsils and other lymphoid tissues [39].
Carriers can discharge the organism in their faeces, urine,
saliva and nasal secretions, creating an important source of
infection. Soil, bedding, food and water can be contami-
nated by infected pigs, leading to the indirect transmission
of the organism [11]. Over 30 species of wild birds and at
least 50 species of wild mammals [40,41] are known to
harbour E. rhusiopathiae, providing an extensive reservoir.
The organism can survive for long periods in marine envir-
onments. It survives and grows on the exterior mucoid
slime of fish without causing disease in the host [12]. The
slime on fish appears to be an important source of infec-
tion for man. The organism has been isolated from the
environment but this may be secondary in importance to
animal reservoirs as a source of E. rhusiopathiae.
Although E. rhusiopathiae is killed by moist heat at 55 C
for 15 min, it is resistant to many food preservation meth-
ods, such as salting, pickling and smoking [10]. It was
long believed that the organism could live in soil indefi-
nitely. However, some studies have not supported this and
found that the organism survived for a maximum of only
35 days in soil under various conditions of temperature,
pH, moisture content and organic content [42].
E. rhusiopathiae infection in humans is occupationally
related. It occurs mostly in those people whose jobs are
closely associated with contaminated animals, their pro-
ducts or wastes, or soil. Individuals with the highest risk of
exposure include butchers, abattoir workers, veterinarians,
farmers, fishermen, fish-handlers and housewives [9].
However, infection has been associated with a wide vari-
ety of occupations, including poultry-processing workers,
meat inspectors, rendering plant workers, knackers, animal
caretakers, bone button makers, game handlers, furriers,
leather workers, soap makers, fertilizer workers, sewer
workers, bacteriology laboratory workers and stockyard
workers [12]. The common names for human infection
reflect this occupational mode of acquisition. These include
whale finger, seal finger, speck finger, blubber finger, fish
poisoning, fish handler’s disease, and pork finger. Infection
is initiated either by an injury to the skin with infective
material or when a previous injury is contaminated. Most
cases in humans and other animals may occur via scratches
or puncture wounds of the skin [12].
CLINICAL MANIFESTATION OF DISEASE
The disease caused by E. rhusiopathiae manifests in a
similar way in animals and humans. Erysipelas and poly-
arthritis are typical forms of infection in animals.
Erysipeloid, a local skin infection or cellulitis, is a com-
mon infection form in humans. Generalized skin infection
and septicaemia are seen sometimes in severe cases.
Chapter | 47 Erysipelothrix rhusiopathiae 861
Swine erysipelas caused by E. rhusiopathiae is seen in
three forms: acute, subacute and chronic [10,11,33].
Acute erysipelas in swine is characterized by sudden
death or general signs of septicaemia. The infection is
caused by virulent organisms and bacteraemia usually
develops within 24 hours of exposure, quickly resulting in
clinical signs of generalized infection and septicaemia.
Presence of diffuse areas of erythema and sometimes
vesicles, petechiae and necrosis are also characteristic
features.
Subacute erysipelas shows signs that are less severe
than the acute form. The animals do not appear as sick.
Cutaneous lesions, urticarial or diamond-skin lesions
appear as early as the second or third day after exposure
to infection. These lesions may in a few days gradually
lose their swelling and coloration, and disappear with no
subsequent effect other than a superficial desquamation.
In other instances, the lesions overlap and cover large
areas of the skin. The intensity of these skin lesions has a
direct relation to the prognosis. Light pink to light pur-
plish red lesions will disappear within several days
whereas the deep-purplish-red lesions can precede either
death or necrosis of the skin.
The chronic form of infection may follow acute or
subacute disease and is characterized most commonly by
signs of local arthritis or proliferative pathological
changes in the heart (endocarditis). Chronic arthritis
results in joints showing various degrees of stiffness and
enlargement. This is the most important clinical manifes-
tation of swine erysipelas from an economic standpoint.
E. rhusiopathiae causes polyarthritis in sheep and
lambs [10]. The disease was recognized as early as 1913
in Europe and later in the USA, Australia and New
Zealand. It is seen in lambs beginning from 2 3 months
of age. The affected animals develop a stiff gait. Lesions
are only found in the joints and one or several may be
affected. The involved joint is usually swollen and the
joint capsule is thickened. Animals seldom die from the
infection.
E. rhusiopathiae is pathogenic for many domestic and
wild birds. On rare occasions infection has been seen in
cattle, causing arthritis in calves. Wild birds including tur-
keys, chickens, geese, ducks, parrots, mud hens, pigeons
and quail, have also been reported to be affected. Turkeys
are the birds most often and most seriously affected. They
exhibit a cyanotic skin that is most obvious as blue comb.
The lesion consists of massive haemorrhages and pete-
chiae in the breast and leg muscles. The birds become
droopy, develop diarrhoea and die. There are reports of
large outbreaks in ducks and starlings. Disease in chicken
flocks has occurred but is rarely reported [10].
Clinical manifestations seen in humans closely resem-
ble those seen in swine. There are three clinical categories
of human disease: a localized cutaneous form, erysipeloid;
862 PART | 7 Localized Infections
a generalized cutaneous form; and a septicaemic form
which is often associated with endocarditis [33].
Erysipeloid is the most common form of human infec-
tion. It is an acute localized cutaneous infection usually
occurring on the hand or fingers, described as a local cellu-
litis. The lesion consists of a well-defined, slightly ele-
vated, violaceous zone, the peripheral edge of which
spreads as the centre fades. The pain is often severe and
may be described as a burning, throbbing or itching sensa-
tion. Systemic symptoms can occur in some cases: fever,
joint aches, lymphadenitis and lymphadenopathy. Arthritis
of an adjacent joint may be seen. The absence of suppura-
tion, lack of pitting oedema, and disproportionate pain
help to distinguish erysipeloid from staphylococcal or
streptococcal infection. The disease is self-limiting and
usually resolves in 3 4 weeks without therapy [28].
The generalized cutaneous form of the disease caused
by E. rhusiopathiae involves lesions that progress from
the initial site to other locations on the body or appear at
remote areas. The lesions are similar to those of the local-
ized form, but bullous lesions can also occur. Systemic
symptoms such as fever and joint pains are more frequent
than in the localized form. The clinical course is more
protracted and recurrences are common [32].
Septicaemia is a more serious manifestation of E. rhu-
siopathiae infection, almost always linked to endocarditis.
It rarely develops from localized infection. Fifty cases
with systemic infection in 15 years were reported with an
extremely high incidence (90%) of endocarditis [8].
A high male-to-female ratio was found among patients
with E. rhusiopathiae endocarditis, which may reflect
occupational exposure, and a greater propensity for
involvement of the aortic valves [28]. The mortality was
38%, almost double the rate for endocarditis with other
bacteria. Nearly 60% of patients had normal heart valves
before they were affected. Congestive heart failure, pres-
ent in 80% of patients, was the most common complica-
tion of endocarditis.
Other human infections associated with E. rhusio-
pathiae include chronic arthritis, cerebral infection, osse-
ous necrosis of the thumb and intracranial abscess. Over
the last 20 years, some new disease manifestations have
been reported. These include erysipeloid with coexisting
orf virus infection [43], persistent bacteraemia in a hospi-
talized patient [44], bacteraemia in an HIV-positive
patient [45] and immunocompetent patients [46a c],
endocarditis with acute renal failure [47], septicaemia and
lupus nephritis [48], septicaemia in a neonate [49], septic
arthritis in adults and children [50a,b], and a case of mul-
tiple brain infarctions associated with E. rhusiopathiae
endocarditis [51]. E. rhusiopathiae has been implicated in
an occupational infection known as ‘crayfish poisoning’,
which affects lobster fishermen in western Australia and
bears a clinical resemblance to erysipeloid [52]. Although
a direct causal relationship between E. rhusiopathiae and
‘crayfish poisoning’ was not proved due to the presence of
other potential pathogens, the results were suggestive.
Recent reports of septicaemia and aortic valve endocarditis
due to E. rhusiopathiae in a homeless man [53] and non-
specific E. rhusiopathiae bacteraemia in a patient with
subclinical alcoholic liver disease and not fitting the occu-
pational demographic typically affected by this bacterium
[54] show the continuing importance of this organism.
VIRULENCE FACTORS
OF E. RHUSIOPATHIAE
E. rhusiopathiae strains are known to vary considerably
in virulence. Very little is known about the mechanisms
of pathogenicity and no toxin has been associated with
this organism. Some virulence factors have been sug-
gested. The presence of a neuraminidase and a hyaluroni-
dase was recognized early, and a correlation between the
amount of neuraminidase produced and the virulence of
strains was noted [55,56]. A protective antigen from the
cell surface was characterized and considered to be a
heat-labile capsule that may be important in the pathoge-
nicity of the disease [57]. Other surface proteins such as
SpaA and 66 64-kDa antigens have been defined and
their roles in virulence have been suggested [58,59a]. In
vitro adhesion assays demonstrated that adherence may be
an important virulence determinant for E. rhusiopathiae
in pigs [60,61].
Neuraminidase is an enzyme responsible for cleavage
of sialic acids from sialo-glycoconjugates such as glyco-
proteins, glycolipids, and oligo- and polysaccharides.
Sialic acids are widely distributed on the surfaces of
eukaryotic cells as terminal non-reducing residues, and on
glycoproteins. Removal of the sialic acid residues from
these cells and important glycoproteins may serve the
nutritional requirements of bacteria as well as disrupting
many host functions [62].
Studies on the production of neuraminidase by
Erysipelothrix species have not been extensive. The pres-
ence of neuraminidase in E. rhusiopathiae was first recog-
nized using immunoelectrophoresis and paper
chromatography [63]. A correlation between the average
amount of neuraminidase produced in different media and
the virulence of strains was noted [55]. Enzyme activity
was detected only in supernatants of cultures of E. rhusio-
pathiae in cooked meat broth and Todd Hewitt broth sup-
plemented with horse serum. Neuraminidase activity was
not detected in the non-pathogenic Erysipelothrix spp.
such as E. tonsillarum, suggesting its possible role as a
virulence factor [64].
Neuraminidase as a virulence factor was demonstrated
by comparing parent strains of E. rhusiopathiae and their

lysogenic variants. A decrease in neuraminidase in lyso-
gens was accompanied by a decrease in virulence [65].
Specific antibody activity against E. rhusiopathiae neur-
aminidase has been demonstrated in the serum of swine
with chronic erysipelas, in commercial equine antierysipe-
las serum, and in the serum of rabbits hyperimmunized
with a preparation of neuraminidase from the organism,
which also induced a low level of protection in mice to
E. rhusiopathiae infection [11]. Neuraminidase may serve
as a key in pathogenesis of arteritis and thrombocytopenia
in rats experimentally infected with the organism. The
adhesion of bacteria to a cultured cell line from the rat
aorta was closely related to the release of sialic acid from
endothelial cells (ECs). It was significant that more bacteria
adhered to neuraminidase-treated ECs, and bacterial adhe-
sion was inhibited dose-dependently by N-acetylneuramin-
lactose, a substrate of bacterial neuraminidase. It was also
observed that bacterial invasion in vivo is always
associated with desialated sites of arterial regions [66,67].
Macromolecular complexes induce the secretion of the
enzyme and results from the rabbit skin test confirmed
the role of E. rhusiopathiae neuraminidase as a virulence
factor with a role in the spread of infection [67].
Hyaluronidase is a spreading factor that facilitates the
dissemination of some pathogens into tissues. It has been
detected in both virulent and avirulent E. rhusiopathiae
strains [68] and production by individual strains was
inconsistent with pathogenic properties. The role of hyal-
uronidase in the pathogenesis of Erysipelothrix infection
remains controversial. Shimoji et al. [69] utilized
transposon mutagenesis with Tn916 to construct mutants
defective in hyaluronidase production. Most
hyaluronidase-negative mutants were avirulent for mice
and had also lost the capsule, whereas a virulent
hyaluronidase-negative mutant still possessed the capsule.
They suggested that the lack of virulence of most of the
hyaluronidase-negative mutants could be attributed to loss
of the capsule, and that hyaluronidase was not essential
for the pathogenesis of infection in mice.
Early in 1970, a protective 200-kDa surface glycolipo-
protein complex antigen from E. rhusiopathiae was iso-
lated and characterized [70,71]. This antigen was easily
released into the culture medium. Lachmann and Deicher
[57] investigated the antigenicity of E. rhusiopathiae by
solubilizing antigens from the cell surface with deter-
gents. The main antigenic non-protein component had a
molecular mass of 14 000 to 22 000, and was a polydis-
persed anionic polysaccharide. This was the first report
that E. rhusiopathiae may have a capsule of importance
in the pathogenicity of disease. The heat-labile capsule is
now considered a crucial factor in the pathogenesis of
infection. Tn916-generated mutants were constructed to
study the potential role of the capsule in virulence [72].
Capsule-deficient mutants were avirulent for mice.
Chapter | 47 Erysipelothrix rhusiopathiae 863
The virulent parent strain resisted phagocytosis by murine
polymorphonuclear leukocytes (PMNs), whereas all the
mutants were susceptible to phagocytosis. Intracellular
survival mediated by the capsule was also examined.
Although the virulent E. rhusiopathiae Fujisawa-SmR
strain and its acapsular mutants were both ingested, even
in the presence of normal serum, the number of ingested
acapsular mutant bacteria was three- to four-fold greater
than the parent strain. Thus, the virulence of E. rhusio-
pathiae is associated with the capsule and resistance to
phagocytosis [72].
Adhesion assays in vitro showed that strains of E. rhu-
siopathiae virulent for swine and mice adhered better to
porcine kidney cell lines PK-15 and ESK than avirulent
strains [61]. Bratberg [60] reported that E. rhusiopathiae
isolated from swine affected with endocarditis or septiace-
mia showed a higher degree of adherence to fresh heart
valves of swine in organ culture than did strains isolated
from other sources.
Two adhesive surface proteins (RspA and RspB) have
been identified from E. rhusiopathiae [73] and their
genes cloned and characterized. The recombinant pro-
teins showed a high degree of binding to polystyrene,
fibronectin, and types I and IV collagens. The deduced
proteins contained the C-terminal anchoring motif
LPXTG, preceded by repeats of consensus amino acid
sequences that are present in many other Gram-positive
bacteria. Participation of both proteins in early adherence
to an inert surface and binding to extracellular matrix
suggested that these proteins constitute a novel class of
cell surface components which are involved in the initial
step of biofilm formation. Adherence may therefore be an
important determinant of virulence for E. rhusiopathiae.
Several other surface proteins have been defined in
E. rhusiopathiae. The 64 66-kDa antigen in Triton X-
100 extracts is located on the cell surface of the organism
[58]. This protein appears to play a role in virulence
because it is less expressed on strains of low or moderate
virulence than on highly virulent strains. High concentra-
tions of 64-, 66- and 43-kDa proteins, which were called
P64 (64 and 66 kDa) and P43 (43 kDa) proteins, were
obtained by alkaline treatment of whole cells. It was sug-
gested that a specific antibody against the 64-kDa protein
could be increased in pigs immunized with P64 or live
cell vaccine and that this anti-P64 antibody has a strong
protective effect against E. rhusiopathiae infection in
pigs. Also the P64 proteins are associated with the induc-
tion of a protective activity against E. rhusiopathiae
infection in mice [74,75]. Another surface protein is the
SpaA antigen [59a]. This antigen is very similar in the
structure and amino acid sequence of its C-terminal
region to the choline-binding proteins of Streptococcus
pneumoniae [76]. To date, four different spa types have
been described including spaA, spaB1, spaB2 and spaC.
864 PART | 7 Localized Infections
Complete protection with the homologous spa strains was
observed but with only partial protection for heterologous
spa strains [59a,77,78]. A gene encoding the haemolysin of
E. rhusiopathiae has been identified [79]. This gene
encodes a surface protein with a molecular mass of 16 kDa
that is commonly distributed amongst Erysipelothrix
species. It has been suggested that this surface protein is
involved in haemolysis in all Erysipelothrix species, but
this has yet to be verified.
ISOLATION AND IDENTIFICATION
OF E. RHUSIOPATHIAE
Traditionally, culture methods for the isolation of E. rhu-
siopathiae involve the use of selective and enrichment
media. Commercially available blood culture media are
satisfactory for primary isolation from blood since E. rhu-
siopathiae is not particularly fastidious. A number of
selective media for the isolation of Erysipelothrix have
been described also. A commonly used medium is
Erysipelothrix selective broth (ESB), a nutrient broth con-
taining serum, tryptose, kanamycin, neomycin and vanco-
mycin [80]. Modified blood azide (MBA) medium is a
selective agar containing sodium azide and horse blood or
serum [81]. Packer’s medium is a selective medium for
grossly contaminated specimens, which contains sodium
azide and crystal violet [82]. Bohm’s medium utilizes
sodium azide, kanamycin, phenol and water blue [13].
Shimoji’s selective enrichment broth contains tryptic soy
broth, Tween 80, tris-aminomethane, crystal violet and
sodium azide [83].
All these media make use of the organism’s resistance
to antibiotics and tolerance of chemicals. Each has good
aspects, but none is ideal. ESB is regarded as the best
selective medium. MBA requires less incubation time
than Packer’s medium but is not as selective. Shimoji’s
selective broth combined with PCR has been used for the
rapid diagnosis of erysipelas in swine [83].
Identification of Erysipelothrix species is based on
Gram’s stain, cultural morphology, motility, haemolytic
characteristics and biochemical properties, particularly
hydrogen sulphide (H2S) production [28]. E. rhusio-
pathiae is a Gram-positive bacterium but easily decolor-
ized [29]. The colonial morphology is described as clear,
circular and very small, with a diameter of 0.1 0.5 mm
after 24 h incubation at 37 C, or 0.5 1.5 mm after 48 h.
Two distinct morphological forms grow on solid agar
media. Smooth (S) colonies are bluish, transparent and
convex. Microscopically these appear as small, slightly
curved, slender rods with rounded ends about 0.8 2.0 μm
long and 0.2 0.4 μm wide. Rough (R) colonies are larger
and have a flat rough surface with irregular edges. Long
filaments up to 60 μm or more, in chains, can be seen
under the microscope. Morphology may change with
alterations in pH and incubation temperature. A pH of
7.6 8.2 favours the S-form while the R-form predomi-
nates at pH less than 7.0. The S-form grows better at
33 C and the R-form favours 37 C [29]. The role played
in disease by different colonial forms has not been deter-
mined. Most strains exhibit a narrow zone of alpha-
haemolysis on blood agar and beta-haemolysis is never
observed [10,29].
Members of the genus Erysipelothrix are relatively
inactive biochemically. E. rhusiopathiae is negative for
catalase, oxidase, methyl red, indole, esculin, nitrate
reduction, Voges-Proskauer and liquefaction of gelatin
[13]. Acid is produced from glucose, fructose, galactose
and lactose but not from maltose, xylose and mannitol.
Sucrose is fermented by most strains of E. tonsillarum
but not by E. rhusiopathiae. Hydrogen sulphide (H2S) is
produced by 95% of strains of Erysipelothrix species as
demonstrated on triple sugar iron (TSI) agar [84]. E. rhu-
siopathiae can be differentiated from other Gram-
positive bacilli, in particular from Arcanobacterium
(Corynebacterium) pyogenes and Arcanobacterium
(Corynebacterium) haemolyticum, which are β-haemoly-
tic on blood agar and do not produce hydrogen sulphide
in TSI agar slants, and from Listeria monocytogenes,
which is catalase-positive, motile and is sensitive to
neomycin [33].
Rapid identification of E. rhusiopathiae can be
achieved with the API Coryne System. It is a commercial
strip system based on a number of biochemical reactions
for the identification of coryneform bacteria and related
genera, including E. rhusiopathiae. The system permits
reliable and rapid identification of bacteria and has been
considered to be a good alternative to traditional bio-
chemical methods [85].
The mouse protection test has been regarded as the
best confirmatory test for E. rhusiopathiae [86]. In the
test, the suspected E. rhusiopathiae in broth culture is
administered subcutaneously to mice along with a dose of
equine hyperimmune E. rhusiopathiae antiserum. Another
group is injected with the broth culture but not the antise-
rum. If the organism is E. rhusiopathiae, the mice that did
not receive antiserum die in 5 6 days, but those receiving
antiserum are protected.
Direct and indirect fluorescent antibody tests can also
be used to confirm the identity of E. rhusiopathiae [86].
These tests provide an alternative to the mouse protection
test. They can be used to detect E. rhusiopathiae in tis-
sues and in enrichment broth.
Currently, molecular tests are rapidly gaining favour
for the identification of E. rhusiopathiae. PCR methods
have been developed for detecting Erysipelothrix species.
The Makino PCR uses primers based on a region of the
16S rRNA gene and is genus-specific [87]. The Shimoji

PCR is E. rhusiopathiae-specific and is designed from
sequences associated with virulence of E. rhusiopathiae
[83]. The sensitivity of the Makino PCR is less than 20
bacteria, while the Shimoji PCR detects a minimum of
1000 bacteria per reaction mixture. Makino’s method
does not differentiate between E. rhusiopathiae and
E. tonsillarum. In 1999, an improved PCR system based
on DNA sequence coding for the rRNA gene cluster
including 16S, 23S and 5S rRNAs and the non-coding
region was established [2]. This system is composed of
four pairs of primers which are able to distinguish four
species of the genus Erysipelothrix including E. rhusio-
pathiae, E. tonsillarum, and Erysipelothrix serotypes 13
and 18, the latter two being putative new species [2]. This
species-specific PCR method may provide a new
approach for the rapid diagnosis of Erysipelothrix infec-
tion in animals and humans. A multiplex PCR method for
distinguishing E. rhusiopathiae from E. tonsillarum was
described [88]. The primer sets ERY-1F and ERY-2R
were designed to amplify 2210 bp of nucleotide sequence
specific for E. rhusiopathiae chromosomal DNA, and the
primer sets MO101 and ERS-1R were designed to
amplify 719 bp of nucleotide sequence including a highly
conserved region of genus Erysipelothrix 16S rRNA. Two
fragments were amplified when E. rhusiopathiae was
used as the PCR template using the primer sets, whereas a
single fragment was amplified when E. tonsillarum was
used as the template.
A spa multiplex real-time PCR assay was developed
to differentiate between spaA, spaB and spaC genes
within Erysipelothrix spp. [77]. This is a useful tool for
investigating spa prevalence among strains and to deter-
mine the role of the Spa proteins in vaccine protection
and pathogenesis. spaA was found to be present in
E. rhusiopathiae serotypes 1a, 1b, 2, 5, 9, 12, 15, 16, 17,
23 and N; spaB was detected in serotypes 4, 6, 8, 11, 19
and 21; and spaC was detected in sp. strain 2 (serotype
18). Spa-related genes were not detected in E. tonsillarum
strains (serotypes 3, 7, 10, 14, 20, 22, 24, 25, 26) or E. sp.
strain 1 (serotype 13). This assay was also able to further
differentiate spaB into spaB1 (serotypes 4, 6, 8, 19 and
21) and spaB2 (serotype 11) [77].
STRAIN RELATEDNESS
OF E. RHUSIOPATHIAE
Watts [89] reported that most strains of Erysipelothrix
had two kinds of antigen, a species-specific heat-labile
protein and a heat- and acid-stable polysaccharide anti-
gen. These formed the basis for serotyping strains.
Initially, two major serotypes, A and B, were recognized
and strains which did not react with these specific antisera
were classified in group N [29]. The Arabic numeral
Chapter | 47 Erysipelothrix rhusiopathiae 865
serotyping system of Kucsera [90] superseded the alpha-
betical scheme because of variations in previous methods
of antigenic extraction. The current standard serotyping
method is a double agar-gel precipitation test with type-
specific rabbit antisera and antigen recovered by hot aque-
ous extraction [91,92]. Strains of Erysipelothrix were
determined as belonging to serotypes 1 26 and group N
[93]. In swine, 75 80% of isolates are classified into
serotype 1 or 2. A relationship between serotype and viru-
lence was noted early. Serotype 1a is most commonly iso-
lated from acute swine erysipelas, and serotype 2a is
more prevalent in chronic forms of the disease. However,
some studies also provided contradictory results in that all
clinical conditions can be induced experimentally in sus-
ceptible swine with a variety of serotypes [7,90]. A study
showed that some isolates of serotype 1b, 2 and 21 were
highly virulent, capable of inducing experimentally gener-
alized urticarial lesions. Other isolates of each serotype
induced only a localized urticarial lesion at the site of
inoculation or caused itching and irritation without obvi-
ous urticarial lesion and induced no further clinical sign
other than rise in body temperature [94]. It is therefore
debatable whether serotyping is of practical value in the
classification of strains of Erysipelothrix. Sneath et al.
[95] reported that strains of human and pig origin were
antigenically similar, but there has been no verification of
this. The epidemiological significance of serotyping in
human disease is uncertain.
Various other typing studies clearly showed advan-
tages over serotyping in taxonomic and epidemiological
studies of Erysipelothrix. Takahashi et al. [1] examined
the levels of relatedness among E. rhusiopathiae strains
belonging to serotypes 1 through 23 and type N.
DNA DNA hybridization experiments with the type
strains of E. rhusiopathiae and E. tonsillarum were per-
formed and two distinct groups identified. Strains of sero-
types 1, 2, 4 6, 8, 9, 11, 12, 15 17, 19 and 21 and type
N exhibited more than 73% hybridization with the type
strain of E. rhusiopathiae but less than 24% hybridization
with the type strain of E. tonsillarum. Strains of serotypes
3, 7, 10, 14, 20, 22 and 23, however, had more than 66%
hybridization with the type strain of E. tonsillarum but
less than 27% hybridization with the type strain of E. rhu-
siopathiae. These strains were therefore classified as
E. rhusiopathiae and E. tonsillarum, respectively. The
members of each group resembled each other in many
phenotypic characteristics, but differed in their ability to
produce acid from sucrose and their pathogenicity for
pigs. Strains of serotypes 13 and 18 exhibited low levels
of DNA relatedness with both of the type strains. They
were classified as another unnamed species. This study
was the first to classify previously serologically distin-
guished E. rhusiopathiae strains into different species
based on DNA relatedness levels.
866 PART | 7 Localized Infections
The electrophoretic patterns of whole-cell proteins from
strains of E. rhusiopathiae and E. tonsillarum were com-
pared using SDS-PAGE [96]. The protein patterns of strains
of E. rhusiopathiae and E. tonsillarum were different and
the main differences occurred in the 71-, 41-, 34- and 26-
kDa proteins of E. rhusiopathiae and the 74-, 44-, 36- and
25-kDa proteins of E. tonsillarum. The protein patterns of
serotype reference strains representing all 23 serotypes com-
prised of mainly two groups. Strains of serotypes 1a, 1b, 2,
4, 5, 6, 8, 9, 11, 12, 15, 16, 19, 21 and type N produced pat-
terns similar to the pattern of the type strain of E. rhusio-
pathiae. On the other hand, strains of serotypes 3, 7, 10, 14
and 20 produced patterns similar to that of the type strain of
E. tonsillarum. Strains belonging to other serotypes pro-
duced unique protein patterns which seemed to be unrelated
to the patterns of either type strain. These protein patterns
indicated that there was some phenotypic heterogeneity in
the genus Erysipelothrix and that SDS-PAGE may be used
as an aid in studying the taxonomy of these bacteria.
Multilocus enzyme electrophoresis (MEE) is a tech-
nique that combines electrophoresis in a starch gel matrix
with specific enzyme staining. Variations in functional
enzymes (allozymes) are detected in stained starch gels
following electrophoresis. Positive activity is visually
detected as bands in the gels. Presence or absence (null
alleles) of activity is scored, as is the mobility of the
bands present. Mobility differences among strains of bac-
teria are due to a difference in net charge of the enzyme,
which is a result of the sum total of the amino acids that
comprise the enzyme. After a number of enzymes are
evaluated, a bacterial strain profile (electrophoretic type)
is realized. Using this technique, the genetic diversity of
74 Australian field isolates of E. rhusiopathiae and 22 ref-
erence strains of various serotypes was examined [97].
Four serotype reference strains of E. tonsillarum (sero-
types 3, 10, 22 and 25) were genetically distinct from
E. rhusiopathiae. Interestingly, two other E. tonsillarum
reference strains of serotype 13, which had been consid-
ered to represent a new genomic species, and serotype 14,
which was classified as E. tonsillarum by Takahashi et al.
[1], clustered with typical isolates and reference strains of
E. rhusiopathiae. Another E. tonsillarum reference strain
of serotype 7 was also genetically typical of E. rhusio-
pathiae. These results indicated that serotyping could not
be relied upon to identify isolates as E. tonsillarum. This
study also found that the field isolates of E. rhusiopathiae
were genetically diverse. Those recovered from sheep or
birds were more diverse than those from pigs. Isolates of
serotype 1 were more diverse than those of serotype 2.
The authors concluded that the diversity found among iso-
lates of the same serotype and the presence of isolates of
different serotypes in the same electrophoretic types indi-
cated that serotyping of E. rhusiopathiae was unreliable
for use as an epidemiological tool.
Restriction fragment length polymorphism (RFLP)
analyses uses restriction enzymes (RE) to cut DNA at
specific 4 6-bp recognition sites with one or more REs
and resulting fragments are separated according to molec-
ular size using gel electrophoresis. Presence and absence
of fragments resulting from changes in recognition sites is
used to identify species or subspecies. Using this tech-
nique, 32 Erysipelothrix type and reference strains repre-
senting all 26 serotyes were investigated together with
seven field strains using the restriction enzyme EcoRI
[98]. The RFLP patterns of Erysipelothrix species were
relatively homogeneous. Nine patterns were observed and
all patterns had two bands in common, which is unusual
among ribopatterns of different species. From these pat-
terns, there was no link found between serotype and spe-
cies. Strains of serotype 7 could be either E. tonsillarum
or E. rhusiopathiae, and strains of serotype 2 were either
E. rhusiopathiae, E. tonsillarum, or the unnamed
Erysipelothrix species. These results were similar to those
observed using MEE [97]. The role of serotyping in taxo-
nomic and epidemiological studies of Erysipelothrix
strains was therefore further questioned.
Randomly amplified polymorphic DNA (RAPD) anal-
ysis or arbitrarily primed PCR (AP-PCR) is a method of
creating genomic fingerprints from species for which little
is known about the target sequence to be amplified.
Strain-specific arrays of DNA fragments are generated by
PCR amplification using arbitrary oligonucleotides to
prime DNA synthesis from genomic sites where they for-
tuitously match or almost match. DNA amplified in this
manner can be used to determine the relatedness of spe-
cies or for analysis of RFLPs. Okatani et al. [99] applied
this method to identify species and differentiate strains of
Erysipelothrix species. They observed 14 RAPD patterns
in 81 strains of Erysipelothrix species using optimized
primers. These patterns were not serotype-specific. They
found that of the 66 strains of E. rhusiopathiae, 64 had
the same unique band of 884 bp. Of the 12 strains of
E. tonsillarum, 11 produced a 1265-bp band. Two other
strains previously thought to be E. rhusiopathiae had the
1265-bp band and one strain of E. tonsillarum produced
the 884-bp band, suggesting that they had been misclassi-
fied. Their results showed that the RAPD method was
able to identify the genetic variation of strains of this
genus and could rapidly and easily differentiate strains of
the same serotype.
Pulsed-field gel electrophoresis (PFGE) has been con-
sidered to be the ‘gold standard’ among the current DNA-
based typing methods [100]. Okatani et al. [101] analysed
70 strains of Erysipelothrix spp. using restriction enzyme
SmaI and reported that 90% of strains had distinct PFGE
patterns. These strains were from numerous sources, and
included strains of species E. rhusiopathiae, E. tonsillarum
and other Erysipelothrix spp., representing the 23 serotypes

and type N. Some common bands could be identified
among these strains and only a few strains showed identi-
cal patterns. Based on these results, PFGE was considered
to be more sensitive than RAPD analysis and ribotyping,
and to be the best method for epidemiological studies.
The value of PFGE using SmaI was reinforced by
Opriessnig et al. [6] who reported on molecular character-
ization of American erysipelas field isolates and vaccine
strains of E. rhusiopathiae, as did Eriksson et al. [102]
who concluded PFGE was a suitable method for epidemi-
ological studies of outbreaks of erysipelas.
A new strain-typing method has been developed based
on nucleotide sequencing of a hypervariable region in the
spaA gene for discrimination of the live vaccine strain
from field isolates [103]. The phylogenetic tree con-
structed based on the spaA sequence suggested that the
evolutionary distance of the isolates was related to patho-
genicity in mice.
TREATMENT AND PREVENTION
OF ERYSIPELOTHRIX INFECTION
Containment and control of E. rhusiopathiae are effective
in preventing the spread of infection in humans and ani-
mals. The removal or regular disinfecting of contaminated
sources is an important method of limiting the spread of
the organism throughout a work environment [12]. E. rhu-
siopathiae can be killed by commonly available disinfec-
tants [10]. A recent study found that several commercially
available home disinfectants in Australia were effective in
killing E. rhusiopathiae [104]. Many investigators have
noted, however, that structurally complex equipment is
difficult to clean and, because the organism is able to sur-
vive in organic matter, disinfecting without cleaning is
useless. If disinfection is impractical, other control mea-
sures become more important.
Control of animal disease by sound husbandry, herd
management, good sanitation and immunization proce-
dures is recommended [11]. Erysipelothrix infection
causes substantial economic losses in animal industries.
Appropriate prophylactic measures are taken for the
treatment and control of this disease. Antibiotic therapy
is effective and penicillin is usually the drug of choice.
Vaccination is considered a useful procedure for control-
ling the problem in animal farms. Most commercially
available vaccines are attenuated live E. rhusiopathiae
strains or bacterins [11]. These vaccines offered protec-
tion to pigs and turkeys [105]. The duration of immunity
of these vaccines varies between 6 and 12 months and
the efficacy is variable depending on the type of strains
used and use of the appropriate vaccine in different spe-
cies of animals [106]. Vaccine failures do occur, appar-
ently quite frequently. Imada et al. [107] reported that
Chapter | 47 Erysipelothrix rhusiopathiae 867
37% of the cases of chronic swine erysipelas detected in
the past 11 years in Japan occurred as a result of live
vaccine failure. In Australia, between 1995 and 1998, 34
swine herds across four Australian states experienced
vaccine failure [108]. Vaccination of humans is not con-
sidered to be a viable option because clinical erysipeloid
appears to convey little or no immunity as shown by
relapse of infection [109].
Several surface protective antigens, such as SpaA, and
the 64 66-kDa proteins purified from E. rhusiopathiae,
have been studied as potential vaccine candidates [59a,b].
SpaA is a common protective antigen, and regarded as the
best potential choice for designing subunit and DNA vac-
cines [110,111]. Using transposon mutagenesis, geneti-
cally defined recombinant live vaccines have been
proposed [112]. A live vaccine vehicle for heterologous
protein expression was developed using an attenuated
strain of E. rhusiopathiae YS-1 [113]. A shuttle plasmid
carrying the spa gene of E. rhusiopathiae was constructed
and the Spa antigen was produced in Lactococcus lactis
with a stable antigenicity without degrading in growth.
This was suggested to be a safe and suitable vehicle for a
polyvalent vaccine [114]. Intranasal immunization of pigs
showed it to be a promising vaccine vector for mucosal
delivery that can induce both local and systemic immune
responses. Immunoadjuvants for the recombinant vaccines
have been studied [115]. A mutant of E. coli heat-labile
enterotoxin produced using a Bacillus brevis expression
system mixed with a recombinant subunit vaccine of
E. rhusiopathiae resulted in substantial enhancement of
both mucosal and serum-specific antibody levels against
highly virulent E. rhusiopathiae in immunized pigs [115].
This represents a promising immunoadjuvant for the
potential application of intranasal vaccines directed
against Erysipelothrix infections.
To and Nagai [78] investigated the genetic and anti-
genic diversity of the surface protective antigen proteins
of E. rhusiopathiae. They cloned and sequenced spa
genes from all E. rhusiopathiae serovar reference strains
as well as from a serovar 18 strain which was not classi-
fied as any species in the genus Erysipelothrix. Sequence
analysis revealed that the Spa proteins could be classified
into three molecular species, including SpaA, which was
previously found in serovars 1a and 2, and the newly des-
ignated SpaB and SpaC proteins. The SpaA protein was
produced by E. rhusiopathiae serovars 1a, 1b, 2, 5, 8, 9,
12, 15, 16, 17 and N, the SpaB protein was produced by
E. rhusiopathiae serovars 4, 6, 11, 19 and 21, and the
SpaC protein was produced only by serovar 18. The
amino acid sequence similarity was high among members
of each Spa type (96 99%) but low between different
Spa types (approximately 60%). The greatest diversity in
Spa proteins was found in the N-terminal half of the
molecule (50 57% similarity), which was involved in
868 PART | 7 Localized Infections
immunoprotection. Coinciding with this, immunoblot
analysis revealed that rabbit antisera specific to each Spa
reacted strongly with the homologous Spa protein but
weakly with heterologous Spa proteins. A mouse cross-
protection study showed that the three recombinant Spa
(rSpa) proteins elicited complete protection against chal-
lenge with homologous strains but that the level of protec-
tion against challenge with heterologous strains varied
depending on the rSpa protein used for immunization.
The study was the first to demonstrate sequence and anti-
genic diversity in Spa proteins and to indicate that rSpaC
may be the most promising antigen for use as a vaccine
component because of its broad cross-protectiveness.
Further development of more effective vaccines against
Erysipelothrix infection in both veterinary fields and
human medicine is likely to occur.
For individuals working in at-risk occupations, an
awareness of the infection is essential. Suggested preven-
tative measures include the wearing of gloves or other
protective handwear, good hygiene, especially frequent
hand-washing with disinfectant soap, and the prompt
treatment of any small injuries [12]. Good health is con-
sidered to be an important factor in prevention, since poor
health, including alcoholism, may predispose to more
serious forms of infection [8]. Control of reservoir popu-
lations of E. rhusiopathiae is impractical or impossible,
because of the widespread distribution of the organism,
the large variety of animal hosts, and its ability to persist
in the environment. The possibility of human infection
can be, however, lessened with awareness, safe work
practices and sensible precautions.
Cases of erysipeloid can be effectively treated with
oral penicillin [28]. Before the advent of penicillin ther-
apy, some alleviation of symptoms could be achieved
with hyperimmune serum, but the resulting serum sick-
ness was often more severe than an episode of erysipe-
loid, and this treatment was shown to be of little value for
cutaneous infections [33]. Although infection is usually
self-limiting, relapses and progression to more serious
forms are possible. Oral penicillin will resolve a case of
erysipeloid in around 48 hours, but intravenous penicillin
is recommended for more serious E. rhusiopathiae infec-
tions [33]. Resistance of E. rhusiopathiae to penicillin has
not been recorded. One experiment involving serial pas-
sage of 75 strains for 8 months did not produce resistance
[33]. An Australian study showed that penicillin and cef-
triaxone, with low minimum inhibitory concentrations
(MICs) of 0.03 mg/l and 0.125 mg/l, respectively,
remained active against E. rhusiopathiae and it was sug-
gested that they should continue to be recommended for
treatment [104]. The work by Eriksson et al. [102] indi-
cated that the MICs for most antimicrobials, including
penicillin and oxytetracycline, were still low. Plasmids
have been isolated in E. rhusiopathiae [116], but they do
not appear to play a critical role in antibiotic resistance.
Antibiotics contained in animal feed may have a role in
the development of resistance in some strains of E. rhu-
siopathiae, but the mechanism remains uncertain
[14,117].
Although the mortality rate for endocarditis has been
reduced from the 100% seen in the pre-antibiotic era, it is
still 38% for Erysipelothrix endocarditis in spite of avail-
able treatment [8]. This rate may partly be explained by
the use of vancomycin (to which the organism is resistant)
in the empirical therapy of endocarditis. No recent data
are available on mortality in humans. Early diagnosis of
all forms of E. rhusiopathiae infection is therefore essen-
tial. In those allergic to penicillin, cephalosporins have
been described as the most appropriate alternative, since
clindamycin and erythromycin are only bacteriostatic for
E. rhusiopathiae [28].
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