SWINE ERYSIPELAS (‘'DIAMOND SKIN DISEASE'’)

INFECTIOUS DISEASES
LECTURE №9
22.04.2022
SEMESTER X
Code VM546
Assoc. prof. Chavdar Filipov, DVM, PhD
Faculty of Veterinary Medicine,
Universtity of Forestry, Sofia, Bulgaria
(The materials are used from many sources with a great respect to the first
moderators: authors of textbooks, articles, presentations and images!!!)
 SWINE ERYSIPELAS
(‘'DIAMOND SKIN DISEASE'’)
 DEFINITION AND IMPORTANCE
Erysipelas is an infectious disease mostly of growing or adult
swine. It may be clinically inapparent, may cause acute illness
involving many animals, or be a chronic disease characterized by
enlarged joints, lameness, and endocarditis.
Rhomboid skin (diamond-skin) lesions are an inconsistent
feature only associated with acute cases.
Swine erysipelas, when uncontrolled, is economically
significant and capable of affecting all stages of pork production.
The greatest losses can be attributed to cases of sudden death
and acute septicemia in grow–finish pigs.
A frequent sequel of surviving an acute infection is chronic
lameness and arthritis, which results in poor growth and abattoir
condemnations. E. rhusiopathiae is also relevant from a public
health perspective, albeit infections in humans are rare.
 OCCURRENCE

Erysipelas occurs in swine, lambs and turkeys. It occurs

occasionally in other poultry and many kinds of wild birds.
Seasonal distribution has not been documented but losses
may be greater during warm summer months!!!
Sporadic outbreaks are seen in most kinds of livestock, wild
mammals (including rodents), reptiles and amphibians.
Erysipeloid, a localized skin infection, occasionally occurs in
people who work with infected animals or process meats, poultry,
fish or animal by-products.
In humans, the disease referred to as “erysipelas” is actually
caused by a streptococcal infection.
 HISTORICAL INFORMATION
The causative agent of erysipelas, Erysipelothrix
rhusiopathiae, was first isolated from a pig in 1882 by Louis Pasteur
and was first characterized in experimentally infected pigs in 1886
by Friedrich Löffler.
In 1885, Dr. Theobald Smith isolated an organism from swine
in the US that was similar to one Pasteur had isolated 3 years earlier
from swine with rouget du porc; both were eventually identified as
Erysipelothrix rhusiopathiae.
Erysipelas occurs sporadically in the pig population, but
there is evidence that more severe and prevalent outbreaks occur in
recurring intervals of approximately 10 years.
Several recent reports of swine erysipelas outbreaks in
countries with relevant pig production raise concerns on
reemergence of this disease.
 1. ETIOLOGY

Erysipelothrix rhusiopathiae belongs to a group of bacteria that

represent a new class, Erysipelotrichia, in the phylum Firmicutes.
The genus Erysipelothrix comprises seven species to date: E.
rhusiopathiae, Erysipelothrix tonsillarum, Erysipelothrix sp. strain 1,
Erysipelothrix sp. strain 2, Erysipelothrix sp. strain 3, Erysipelothrix
inopinata and Erysipelothrix larvae sp. nov.
The most relevant species for pigs is E. rhusiopathiae, though
strains of E. tonsillarum have been isolated from cases of chronic arthritis
and vegetative valvular endocarditis.
Based on heat‐stable cell wall antigens, Erysipelothrix spp. strains
can be differentiated by precipitation reactions using hyperimmune rabbit
antiserum into at least 28 serotypes, 1a, 1b, 2–26, and N, the latter
referring to strains lacking these antigens.
Cases of clinical erysipelas are predominantly caused by serotype
1a, 1b, or 2!!!!
 1. ETIOLOGY
Erysipelothrix spp. are nonmotile, non‐sporulating,
non‐acid‐fast, facultatively intracellular gram‐positive rods that are
facultative anaerobes and grow between 41 °F (5°C) and 111 °F (44
°C), with optimal growth occurring between 86 °F (30 °C) and 98.6
°F (37 °C).
On agar media, colonies of Erysipelothrix spp. are clear,
circular, and small (0.1–0.5 mm in diameter) after 24 hours of
incubation at 95 °F (35 °C) or 81 °F (27 °C), with increased size (0.5–
1.5 mm in diameter) after 48 hours, and they are either smooth or
rough, being slightly larger with an irregular edge.
Most strains induce a narrow zone of partial hemolysis on
blood agar media, usually with a greenish color.
Rough colonies are not typically associated with hemolysis. E.
rhusiopathiae is relatively inactive in commonly used biochemical
tests, producing acid but no gas from certain fermentable carbon
compounds and hydrogen sulfide in triplesugar iron agar (Carter
1990).
 2. EPIDEMIOLOGY
Erysipelothrix rhusiopathiae is worldwide in distribution and
is ubiquitous. The domestic pig is considered the most important
reservoir.
Besides pigs, a variety of vertebrate and invertebrate species
are known to harbor the organism providing a broad reservoir.
Approximately 30–50% of apparently healthy pigs harbor E.
rhusiopathiae in their tonsils and other lymphoid tissues!!!
Carriers and pigs with acute erysipelas can shed the
organism in their excretions (urine, feces) and secretions (saliva,
nasal mucus) for extended periods of time.
The bacterium can be isolated from oral fluid of an acutely
infected population for 1–3 days and demonstrated by real‐time
PCR for 1–9 days
 2. EPIDEMIOLOGY
Transmission. Transmission of E. rhusiopathiae is believed to
occur directly via oronasal secretions and feces and indirectly via
environmental contamination.
While there is no evidence of E. rhusiopathiae growth in the
environment, its presence in facilities and on equipment is well
documented.
Pigs can be infected by ingestion of contaminated feed or
water and through contamination of skin wounds.

Pigs less than 3 months of age (due to a protective

effect of passively acquired immunity) or pigs older than
3 years (even 1 year) of age (due to repeated subclinical
disease) are generally least predisposed to erysipelas!!!
 2. EPIDEMIOLOGY
Survival of E. rhusiopathiae in soil is less than 35 days, with
no evidence of establishment of stable populations. E. rhusiopathiae
is inactivated by moist heat at 131 °F (55 °C) but is resistant to
salting and many other food preservation methods.
It may remain viable for 12 days under direct exposure to
sunlight and for months in unburied carcasses or in carcasses buried
to a depth of 7 ft (2.13 m).
Erysipelothrix spp. are inactivated by commonly available
disinfectants.
 3. PATHOGENESIS
Ingestion of contaminated feed and water usually allows E.
rhusiopathiae to gain access to the body, probably through the
tonsils or other lymphoid tissue of the digestive tract (the organism
often can be cultured from tonsils of normal swine).
Less often, contaminated skin wounds may permit entry. In
acute erysipelas, and perhaps in other forms of the disease, a
bacteremia develops and leads to spread of organisms throughout
the body.
The precise mechanism by which E. rhusiopathiae causes
disease is speculative!
The organism produces neuraminidase, an enzyme that
cleaves mucopolysaccharides in cell walls which may mediate the
widespread vascular damage that accompanies SE.
Vascular damage leads to thrombosis and interference with
microcirculation in capillaries and venules at many sites.
 3. PATHOGENESIS
In chronic arthritic cases, there is a vasculitis with exudation
of fibrin into perivascular tissues and joint(s).
There also is marked villous proliferation of the synovial
membrane. Joint lesions are more proliferative than exudative.
Pannus may develop and eventually result in destruction of
articular cartilage and ankylosis of adjacent bones.
Connective tissue formation around joints is stimulated,
apparently by perivascular fibrin, and the joint capsule may be
thickened.
Persistence of inflammation around an affected joint may be
from a few living bacteria in the joint or it may be the result of
hypersensitivity to remaining bacterial antigens.
 3. PATHOGENESIS
Vegetative, valvular endocarditis, another manifestation of
chronic erysipelas, is less common than joint involvement.
Emboli of E. rhusiopathiae are believed to cause
inflammation of blood vessels within heart valves.
In the inflammatory process, the endocardium is breached
and bacterial colonies are established at the site.
Fibrin is deposited there and slowly organized to form
nodular vegetations. Emboli that arise from vegetations can cause
sudden death. Interestingly, outbreaks of vegetative endocarditis can
occur in the absence of other clinical signs.
Susceptibility to infection is not well understood. Many swine
known to have been exposed to organisms do not sicken with the
disease. Lactogenic immunity protects piglets for several weeks. In
older, susceptible swine, various stresses (heat, aflatoxin, poor
nutrition) have been suspected of playing a role in precipitating
outbreaks.
 4. CLINICAL FINDINGS
Three clinical forms (in some sources they are four) of
swine erysipelas – (hyper (peracute)-acute), acute, subacute,
and chronic – have been described.
The acute form is septicemic disease that manifests as
sudden onset of acute death, abortions, depression, lethargy,
pyrexia (104–108 °F [40–42 °C] or greater), withdrawal, lying
down, painful joints evidenced by stiff stilted gait, reluctance to
move and/or vocalization during movement, partial or
complete inappetence, and characteristic pink, red, or purple
raised firm rhomboid or squared “diamond skin” lesions.
In dark‐skinned animals, the skin lesions are best
appreciated by palpation or by observing areas with raised
hairs. In nonfatal cases, the skin lesions will gradually
disappear within 4–7 days.
 4. CLINICAL FINDINGS
The subacute form is clinically less severe than the acute
form.
Animals do not appear as sick, temperatures are not as
high or persistent, appetite may remain unaffected, skin lesions
may be few in number or absent, mortality will be lower, and
animals will recover more rapidly.
There may be infertility, litters with increased numbers
of mummies or of small size, and pre‐ or postparturient vulvar
discharges.
Some cases may be so mild that they remain unnoticed
(subclinical)!!!
 4. CLINICAL FINDINGS
Chronic erysipelas follows acute, subacute, or sometimes
subclinical erysipelas in a proportion of surviving animals.
The most economically significant form is chronic
arthritis that may appear as soon as 3 weeks after the initial
outbreak.
Affected animals are mildly to markedly lame with
associated reduction in feed intake.
Firm enlargement of hock, stifle, or carpal joints may be
observed.
Chronic erysipelas can also manifest as respiratory
distress, lethargy, cyanosis, or sudden death as consequences of
vegetative valvular endocarditis that may lead to cardiac
insufficiency and pulmonary edema.
 4. CLINICAL FINDINGS
Morbidity and mortality vary depending on the
immune status of a herd.
In outbreaks of acute swine erysipelas in naïve
herds, mortality can quickly rise to 20–40%.
In subclinically or chronically affected herds, the
morbidity and mortality associated with Erysipelothrix
spp. vary and are dependent on herd management,
environment, and other concurrent infections.
 5. Post Mortem Lesions
The nearly pathognomonic gross lesions of acute swine
erysipelas consist of multifocal pink to purple rhomboid
(diamond‐shaped) slightly raised skin lesions predominately around
the snout, ears, jowls, throat, abdomen, and thighs.
The skin of extremities can also be purple. In addition to skin
lesions, other typical lesions of septicemia include enlarged and
congested lymph nodes, enlarged spleen, and edematous and
congested lungs.
Petechiae and ecchymosis may be found in the renal cortex,
the heart (epicardium and atrial myocardium), and occasionally
elsewhere.
Joints may be slightly enlarged, and the synovium and
periarticular tissues are typically distended by serofibrinous
exudates that may also fill the joint cavity.
In some outbreaks, fattening hogs may be found dead without
any gross lesions.
 5. Post Mortem Lesions
Chronic lesions may include chronic arthritis often involving
joints of one or more legs or the intervertebral articulations.
Proliferative synovial membranes and serosanguinous
effusion in the joint cavity are also observed.
The joint capsule is often hyperemic. There may be
proliferation and erosion of the articular cartilage that lead to
fibrosis, ankylosis, and spondylitis.
Valvular endocarditis can be seen as proliferative granular
growth on the heart valves (mitral valve most common)!!!
Ischemic necrosis of the rhomboid skin lesions and of skin on
the extremities is also observed as dry, dark, and sometimes partially
detached skin.
 5. Post Mortem Lesions
Microscopic lesions in acute erysipelas are predominantly in blood
vessels, resulting in associated ischemia and necrosis. Capillaries and
venules in the dermis are often dilated and congested. Microthrombi and
bacterial emboli may occlude vessels, leading to circulatory stasis and focal
necrosis!!!
Neutrophils infiltrate the affected dermis. Similar hyperemia,
vasculitis, neutrophilic infiltrates, and focal necrosis can also be observed
in the brain, heart, kidneys, lungs, liver, spleen, and synovial membranes.
Chronic arthritis is characterized by marked hyperplasia of
synoviocytes, resulting in thickened villous proliferations on synovial
membranes that also have stromal thickening due to infiltrates of
lymphocytes, plasma cells, and macrophages as well as neovascularization.
In later stages, marked fibrosis may be observed in synovial
membranes and periarticular tissues. Articular cartilage may be focally to
extensively necrotic with associated fibrinous to fibrinopurulent exudates.
Vegetative valvular endocardial lesions are composed of irregular
fibrin lamina comprising fibrin, necrotic cellular debris, mixed
inflammatory cells, bacterial colonies, and granulation tissue.
DIAMOND-SHAPED SKIN LESIONS
 6. DIAGNOSIS
Isolation of Erysipelothrix spp. from tissues with
morphological lesions provides a definitive laboratory diagnosis.
Direct culture from non‐contaminated specimens is usually
fast and easy and can be conducted using basic laboratory
equipment!!!
Chronic cases and contaminated specimens often require
prior selective enrichment methods. Other gram‐positive,
non‐sporulating rod‐shaped bacteria that can be confused with
Erysipelothrix spp. include members of the genera Brochothrix,
Corynebacterium, Lactobacillus, Listeria, Kurthia, and Vagococcus.
To overcome the difficulties of bacterial isolation from
specimens of antimicrobial‐treated pigs or chronically affected pigs,
an immunohistochemical assay has been developed and found to be
highly sensitive and specific when compared with direct culture
techniques. In contrast the use of fluorescent antibodies in frozen
tissue sections was found less sensitive compared with culture
methods.
 6. DIAGNOSIS
Several polymerase chain reaction (PCR) methods have
been developed for the rapid detection of Erysipelothrix spp.
Among PCR assays, genus‐specific methods, a multiplex
PCR assay capable of differentiating between E. rhusiopathiae
and E. tonsillarum, a species‐specific PCR assay capable of
distinguishing four Erysipelothrix species, a single nucleotide
polymorphism‐based PCR assay able to differentiate a
Japanese live vaccine strain from field isolates, and a
quantitative real‐time multiplex assay capable of detecting and
differentiating E. rhusiopathiae, E. tonsillarum, and
Erysipelothrix spp. strain 2 have been described.
 6. DIAGNOSIS
Serological assays including plate, tube, and microtitration
agglutination, passive hemagglutination, hemagglutination
inhibition, complement fixation, enzyme‐linked immunosorbent
assays (ELISA), and indirect immunofluorescence assays have been
used to detect antibodies against E. rhusiopathiae in pigs.
However, since 30–50% healthy pigs are carriers and serum
antibody responses to E. rhusiopathiae infection can persist for days,
weeks, or even throughout the life of the pig, serology assays are
most useful to evaluate vaccination success in breeding herds.
Genetic or antigenic properties of Erysipelothrix spp. isolates
can be utilized to gain insight into the origin and relatedness of
individual isolates. Methods include serotyping, genomic
fingerprinting, and pulsed‐field gel electrophoresis (PFGE). The
standard serotyping method utilizes a double agar‐gel precipitation
test with typespecific rabbit antisera and antigen its execution
depends on availability of antiserum and requires about 3 days for
completion.
 7. DIFFERENTIAL DIAGNOSIS
Differentials for acute swine erysipelas include septicemia
and sudden death in grow–finish pigs due to:

1.Salmonella Choleraesuis;
2.Actinobacillus suis;
3.Actinobacillus pleuropneumoniae;
4.Haemophilus parasuis;
5.Streptococcus suis, and other bacteria.

Skin lesions resembling swine erysipelas can also be observed with:

1.Classical swine fever virus;

2.Porcine dermatitis and nephropathy syndrome;
3. A. suis septicemia.
 7. DIFFERENTIAL DIAGNOSIS
Erysipelas must be differentiated from septicemias of pigs Acute
disease may be confused with the other septicemias affecting pigs, but pigs
with erysipelas usually show the characteristic skin lesions and are less
depressed than pigs with hog cholera or salmonellosis.
Septicemic salmonellosis characterized by Gross blue-purplish
discoloration of the skin especially the ears, Some evidence of enteritis and
polypnea and dyspnea
Hog cholera characterized by large numbers of pigs affected
quickly, weakness, fever, muscle tremors, skin discoloration and rapid
death; convulsions are also common
Streptococcal septicemia and arthritis They are almost entirely
confined to suckling pigs in the first few weeks of life and Streptococcal
septicemia is usually associated with Actinobacillus suis.
Streptococcal endocarditis has a similar age distribution as
erysipelas endocarditis and bacteriological examination is necessary to
differentiate them.
 7. DIFFERENTIAL DIAGNOSIS arthritides of pigs
The chronic disease characterized by joint disease occurs in
pigs of all ages but less commonly in adults and must be
differentiated from the following conditions:
Glasser's disease accompanied by a severe painful dyspnea.
At necropsy there is serositis and meningitis
Mycoplasma arthritis Generally it affects pigs less than 10
weeks of age and produces a polyserositis as well as polyarthritis
however; Mycoplasma hyosynoviae can produce simple polyarthritis
in growing pigs
Rickets and chronic zinc poisoning produce lameness in pigs
but they occur under special circumstances, are not associated with
fever, and rickets is accompanied by abnormalities of posture and
gait that are not seen in erysipelas
Foot rot of pigs is easily differentiated by the swelling of the
hoof and the development of discharging sinuses at the coronet.
 8. THERAPY
 The erysipelas organism is very sensitive to penicillin. Acutely
ill animals should be treated with quick acting penicillin twice
daily for three days. Alternatively a long-acting penicillin, given
as a single dose to cover 48 hours of treatment, could be given and
then repeated.
 Treat by intramuscular injection 1ml/10kg (300,000iu/ml).
 Medicate the feed with 200g/tonne of phenoxymethyl
penicillin for 10–14 days. This is a very effective method of
prevention, and can be used in major outbreaks of disease.
 In acute cases a quick acting penicillin injected twice in the
first 24 hours should bring about a rapid response. Continue daily
injections for three to four days.
 Where a large number of sows are involved water medication
with amoxycillin or phenoxy-methyl penicillin should be carried
out. The dose level will depend upon the purity of the antibiotic
powder used.
 8. THERAPY
 Amoxycillin, phenoxymethyl penicillin or tetracyclines in the
drinking water are also effective.
 Where large numbers of pigs are involved it may be
necessary to inject all the pigs in the groups at risk.
 Outbreaks involving pens or complete houses of pigs
sometimes occur, particularly during summer months.
 If the disease is acute, treatment should commence
immediately via the water and be continued with in-feed
medication using phenoxymethyl penicillin (pen. V) 200g/tonne or
tetracyclines 500g/tonne. (Pen. V can also be used for prevention
in the face of an outbreak.)
 In individual outbreaks finishing pens should be washed and
disinfected between batches. If wet feeding is implicated the
system must be cleaned out and disinfected.
 9. PREVENTION- BIOSECURITY! CONTROL
Routine vaccination is the best available means of controlling erysipelas
Successful control depends on good hygiene, biosecurity, reduction of stress, an
effective 6-monthly vaccination policy, preferably two doses, for all animals
including boars over 3 months of age, as well as rapid diagnosis, quarantine, and
treatment!!!
Acute outbreaks of SE usually can be controlled by administering penicillin
and/or erysipelas antiserum to affected pigs along with antimicrobials added to the
drinking water until no sick pigs have been observed for at least 3 days.
Eradication of erysipelas on individual piggeries is considered impractical due
to the large number of 'carrier' pigs and other 'carrier' species including birds and
rodents!!!
General hygienic precautions should be adopted.
Clinically affected animals should be disposed of quickly and all introductions
should be isolated and examined for signs of arthritis and endocarditis
All animals dying of the disease should be properly incinerated to avoid
contamination of the environment
A combination of regular vaccination, good sanitation, the elimination of
carriers with skin and joint lesions, and appropriate quarantine measures for
purchased stock usually will aid control of SE.
 9. PREVENTION- BIOSECURITY!
Prevention of SE is best accomplished by sound practices of
herd health management, including a program of immunization.
GENERAL MANAGEMENT PRACTICES
 Swine should be raised according to sound husbandry
practice relative to nutrition, housing, and condition of lots and
pastures, and they should be observed regularly for deviations
from their usual attitude.
 Purchased animals should be isolated for at least 30 days.
 It is advisable to eliminate chronically affected swine from
the herd, as they can remain carriers of the organism indefinitely.
 Good sanitation is important in general herd management
and is essential following the cessation of an outbreak
 Walls and floors should be cleaned and disinfected.
 9. PREVENTION- BIOSECURITY!
IMMUNIZATION
The immunizing agents include
1. Hyperimmune serum (anti - erysipelas serum)
2. Vaccines
1. ANTI - ERYSIPELAS SERUM
 Administration of 5 - 20 ml of serum parenteraly amount
depending on age will protect in contact pigs for a minimum of 1 - 2
weeks.
 Suckling pigs in herds where the disease is endemic should receive
10 ml of hyperimmune serum during the first week of life and at
monthly intervals until they are actively vaccinated
• which can be done as early as 6 weeks –if sows have not been vaccinated
 In herds where sows are routinely vaccinated prior to farrowing -
piglet vaccination will be delayed until 10 - 12 weeks of age for effective
active immunity.
• Repeated administration of the serum may cause anaphylaxis because of
its equine origin.
 9. PREVENTION- BIOSECURITY!
2. VACCINATION
• Vaccination using killed bacterins or, attenuated vaccines prepared by
serial passage or strains of low virulence for pigs
• The formalin-killed, aluminum-hydroxide-adsorbed bacterin confers an
immunity that, in most instances, protects growing pigs from acute disease
until they reach market age. An oral vaccine of low virulence is also used.
GENERALLY FOR PREVENTION OF SE
• All gilts and young boars should be vaccinated twice 2-4 weeks apart
(according to manufacturer’s instructions) before entering the breeding
herd.
• Sows should be vaccinated 3-4 weeks prior to farrowing
• boars should be vaccinated every 6 months.
• Progeny may need vaccination if there is a high challenge.
• N.B Vaccination raises the level of immunity but does not provide
complete protection!!! If disease outbreak occurs despite a vaccination
program, review hygiene and management practices and consider
changing to all-in-all-out production systems.
9. PREVENTION- Specific immunoprophylaxis-single or combined!

PORCILIS® ERY

An inactivated vaccine containing at least 1 ppd Erysipelothrix rhusiopathiae antigen, strain

M2 (serotype 2) per dose in an aqueous adjuvant (dl a-tocopherol 150 mg/dose). The vaccine contains
0.05% formaldehyde as a preservative.
The dose is 2 ml per pig, given by deep intramuscular injection behind the ear. Ensure that
vaccination equipment is clean and sterile before use.
Young growing pigs Pigs should be at least 6 weeks of age. A course of two vaccinations given 4 weeks apart
is recommended.
Breeding stock Primary vaccination: For the induction of protection against erysipelas, an initial course of
two vaccinations, given 4 weeks apart, is recommended. Where protection against parvovirus is also required,
this can be achieved with Porcilis Ery given either 4 weeks before, or 4 weeks after, administration of the
combined Porcilis Ery+Parvo vaccine. Boars and gilts should be vaccinated against E. rhusiopathiae at least 2
weeks before mating.
Booster vaccination: Sows and boars should be revaccinated against erysipelas at six monthly intervals. For
sows, this may be during each lactation period, at weaning or during pregnancy (avoiding the last two
weeks).
9. PREVENTION- Specific immunoprophylaxis-single or combined!
Erysipelothrix rhusiopathiae attenuatum -
ERYSEN INJ. SICC. at least 1 x 107, culturing medium, lyophilizing
AD US. VET. medium, diluent A.
Lyophilizate dissolution: rehydrate the lyophilizate in
full volume of diluent A enclosed when the vaccine is
to be applied subcutaneously.
The vaccine shall be consumed within 3 hours
after its dissolution.
Effect method:
After the antigen contained in the vaccine is applied into
an animal's body, the specific antibodies are formed
protecting the immunized animal against erysipelas.
Immunity onset occurs within 8th - 14th day after the
application and lasts for 6 months.
Indication:
Immunization of pigs against red murrain.
Contraindication:
Clinically ill animals. Antibiotics shall not be applied to
animals 7 days before and after vaccine application.
Interaction:
Unknown
9. PREVENTION- Specific immunoprophylaxis-single or combined!
ERYSIN SINGLE SHOT,
EMULSION FOR Erysipelothrix rhusiopathiae inact. (3
INJECTION FOR PIGS strains - type 2, 1 strain - type 1) - min. 1 x
1010, nutrimentum ad cultivationem, emulsio
olei, formalin, merthiolate.
Immunological properties:
After administration of the vaccine antigen into
the animal body, specific antibodies are created
which then protect the immunized animal against
erysipelas. Immunity is fully developed 21 days
after the vaccination.
Indication:
For immunization of pigs against erysipelas.
Contraindication:
Avoid vaccination of pigs with clinical symptoms
of the disease, sows 2 weeks before and 4 weeks
after farrowing and piglets less than 8 weeks of
age.
THANK YOU FOR YOUR ATENTION