Erysipelas

(When sourcing stock IT IS UP TO YOU to ask the breeder if they have suffered any diseases within their herd if you don’t ask you don’t know and the breeder will and should not be offended by your question as this shows due diligence on your behalf.)

Erysipelas is caused by a bacterium called Erysipelothrix rhusiopathiae in pigs and is one of the oldest recognised diseases that affect growing and adult pigs. The organism commonly resides in the tonsillar tissue. These typical healthy carriers can shed the organism in their faeces or oronasal secretions and are an important source of infection for other pigs.

Disease outbreaks may be acute or chronic, and clinically inapparent infections also occur. Acute outbreaks are characterised by sudden and unexpected deaths, febrile episodes, painful joints, and skin lesions that vary from generalized cyanosis to (a bluish discoloration of the skin due to poor circulation or inadequate oxygenation of the blood) the often-described diamond skin (rhomboid urticaria) lesions. Chronic erysipelas tends to follow acute outbreaks and is characterized by enlarged joints and lameness. A second form of chronic erysipelas is vegetative valvular endocarditis. Pigs with valvular lesions may exhibit few clinical signs; however, when exerted physically they may show signs of respiratory distress, lethargy, and cyanosis, and possibly suddenly succumb to the infection.

The genus of Erysipelothrix is subdivided into two major species: E rhusiopathiae and E tonsillarum. In addition, there are other strains that constitute one or more additional species known as E species 1, E species 2, E species 3, and E inopinata. At least 28 different serotypes of Erysipelothrix spp are recognized, and pigs are considered to be susceptible to at least 15. Field cases of swine erysipelas are predominately caused by E rhusiopathiae serotypes 1a, 1b, or 2.

On farms where the organism is endemic, pigs are exposed naturally to E rhusiopathiae when they are young. Maternal-derived antibodies provide passive immunity and suppress clinical disease. Older pigs tend to develop protective active immunity as a result of exposure to the organism, which does not necessarily lead to clinical disease. E rhusiopathiae is excreted by infected pigs in faeces and oronasal secretions, effectively contaminating the environment. When ingested, the organism can survive passage through the hostile environment of the stomach and intestines and may remain viable in the faeces for several months. Recovered pigs and chronically infected pigs may become carriers of E rhusiopathiae. Healthy pigs also may be asymptomatic (showing no symptoms) carriers. Infection is by ingestion of contaminated feed, water, or faeces and through skin abrasions.P

The acute and chronic forms of erysipelas may occur in sequence or separately. Pigs that succumb to the acute septicemic form may die suddenly without previous clinical signs. This form occurs most frequently in growing and finishing pigs. Acutely infected pigs are depressed and reluctant to stand and move. Affected pigs squeal excessively when handled, require assistance to stand, and prefer to lie down soon after being forced to stand. Affected pigs may also walk stiffly on their toes and shift weight from limb to limb when standing. Anorexia and thirst are common, and febrile pigs will often seek wet, cool areas to lie down. Skin discoloration may vary from widespread erythema (reddening of the skin) and purplish discoloration of the ears, snout, and abdomen, to diamond-shaped skin lesions almost anywhere on the body, but particularly on the lateral and dorsal regions. The lesions may occur as discrete, pink or purple areas of varying size that become raised and firm to the touch within 2–3 days of illness. They may disappear over the course of a week or progress to a more chronic type of lesion, commonly referred to as diamond skin disease. If untreated, necrosis and separation of large areas of skin can occur, and the tips of the ears and tail may become necrotic.

Clinical disease is usually sporadic and affects individuals or small groups, but sometimes larger outbreaks occur. Mortality is variable (0–100%), and death may occur up to 6 days after the first signs of illness. Acutely affected pregnant sows may abort, probably due to the fever, and lactating sows may stop producing milk.

Untreated pigs may develop the chronic form of the disease, usually characterized by chronic arthritis, vegetative valvular endocarditis, or both. Such lesions may also be seen in pigs with no previous signs of septicemia. Valvular endocarditis is most common in mature or young adult pigs and is frequently followed by death, usually from embolism or cardiac insufficiency. Chronic arthritis, the most common form of chronic infection, produces mild to severe lameness. Affected joints may be difficult to detect initially but eventually become hot and painful to the touch and later visibly enlarged. Dark purple, necrotic skin lesions that commonly separates itself from the dead tissue may be seen. Mortality in chronic cases is low, but growth rate is retarded.

Diagnosis of erysipelas is based on clinical signs, gross lesions, response to antimicrobial therapy, and demonstration of the bacterium or DNA in tissues from affected animals. Acute erysipelas can be difficult to diagnose in individual pigs showing only fever, poor appetite, and listlessness. However, in outbreaks involving several animals, the presence of skin lesions and lameness is likely to be seen in at least some cases and would support a clinical diagnosis. Rhomboid urticaria or diamond skin lesions are almost diagnostic when present; however, similar lesions can also be seen with classical swine fever virus.

A rapid, positive response to penicillin therapy in affected pigs supports a diagnosis of acute erysipelas because of the sensitivity of the organism to penicillin.

Chronic erysipelas can be difficult to definitively diagnose. Arthritis and lameness, coupled with the presence of vegetative valvular endocarditis postmortem, may support a presumptive diagnosis of chronic erysipelas.

Serologic tests cannot reliably diagnose erysipelas but can be useful to determine previous exposure or success of vaccination protocols, because antibodies should increase after vaccination.

Treatment:

As we have discussed in previous posts in the group under “Back to Basics Part IV – Handling Medications – What’s in your Cupboard ?” E rhusiopathiae is sensitive to penicillin. Ideally, affected pigs should be treated at 12-hr intervals for a minimum of 3 days, although longer durations of therapy may be necessary to resolve severe infections. On an economic basis, penicillin is the best choice for antibiotic therapy, but ampicillin and ceftiofur also yield satisfactory results in acute cases. When injecting large numbers of affected pigs is impractical, tetracyclines delivered in the feed or water may be useful. Fever associated with acute infections can be managed by administration of NSAIDs such as flunixin meglumine or by delivery of aspirin in the water. Erysipelas antiserum is described as an effective adjunct to antibiotic therapy in treating acute outbreaks but is not commonly available. Treatment of chronic infections is usually ineffective and not cost effective.

Vaccination against E rhusiopathiae is very effective in controlling disease outbreaks.

Optimal timing of vaccination may vary from farm to farm. When E rhusiopathiae is endemic in the production environment, vaccination should precede anticipated outbreaks. Susceptible pigs may be vaccinated before weaning, at weaning, or several weeks after weaning. Male and female pigs selected for addition to the breeding herd should be vaccinated with a booster 3–5 wk later. Thereafter, breeding stock should be vaccinated twice yearly. Vaccines should not be administered to animals undergoing antibiotic therapy, because antibiotics can interfere with the subsequent immune response to the vaccine.

In addition to vaccination, attention to sanitation and hygiene and elimination of pigs with clinical signs suggestive of erysipelas infection represent other viable methods that may help control the disease. But in all cases you must discuss your situation with your vets to discuss your vaccination programme.

Photos courtesy of Pig333, Dr D Risco Unidad de Patologı´a Infecciosa Photo above showing findings in a lung showing good cells being suffocated by the erysipelas bacterium.

Coccidiosis

Coccidiosis affects all ages of pigs and is a tacky or watery diarrhoea, piglets do not seem to grow very well and can cause death in piglets. It stems from poor hygiene.

Causes

Coccidia are single cell protozoan parasites which multiply in the cells lining the intestine. Cystoisospora suis is the main pathogen of piglets and is responsible for the most coccidial diarrhoea. Cryptosporidium parvum, C. suis and other genotypes may also affect piglets but occurs commonly in weaned pigs and Eimeria species occur in weaned pigs, finishers and gilts but not in piglets. The resistant oocysts of Cystoisospora. suis are eaten and reach the upper small intestine where small sporozoites hatch and invade cells of the intestinal lining within 24 hours. They multiply asexually, damaging their host cell, to give rise to first stage merozoites and then to a further two stages within cells of the small intestinal lining. Each fourth stage cell reaches the lower part of the small intestine at about 4-5 days after infection and invades an epithelial (lining) cell to produce the sexual stage. Some become groups of microgametes and some remain single to become macrogametes. Mating in the gut produces oocysts which appear in the faeces as oocysts within 5 days of infection. Eimeria species multiply in the same way as C. suis, but Cryptosporidium remains in the absorptive, apical part of the cell and appears to prevent absorption of nutrients and causes cell death.

Transmission

Coccidia are passed out in the faeces and Cystoisospora suis oocysts develop within 48 hours at 24-27ºC into resistant hard walled sporulated oocysts which are infective. They are resistant to drying and can persist in piggeries and soil for up to 10 months. The major source of infective oocysts is the faeces of piglets aged between 2 and 4 weeks, when from 4,000 to 400,000 oocysts per gram may be present. Sows may pass a few oocysts and infect their litters, but the major source of both direct and indirect infection is the piglet. Transmission of Eimeria species resembles that of Cystoisospora, although the age range affected differ, but some Cryptosporidium species have more than one host species. The route of infection is oral in all cases.

Signs

Coccidiosis causes mal-absorption, diarrhoea, loss of condition and some deaths. The faeces of affected piglets may be whitish and firm, there may be transient pasty diarrhoea or profuse yellowish, watery diarrhoea between 5-15 days of age and most commonly from 7-10 days of age. Affected piglets may be thinner than unaffected litter mates and remain gaunt and hairy for some weeks thereafter. Severely affected piglets may die. Mortality rates may reach 20%. The diarrhoea responds poorly to antimicrobial therapy and slow growth occurs in recovered animals and diarrhoea rarely continues beyond weaning. Wasting and diarrhoea have been recorded in gilts, finishing pigs and wild boar infected with Eimeria spp. In experimental E. neodebliecki infection, frothy, mucoid diarrhoea occurred 9-12 days post infection. Most infections with C. parvum are asymptomatic (90% in one study). Clinical signs rarely appear before 3 days of age and are most commonly reported in piglets at 10-21 days of age. Affected piglets are depressed and pass a watery, sometimes brownish, diarrhoea, which may persist for 3-5 days. The organism can be recognised in the faeces of diarrhoeic weaners. Affected weaned pigs are often depressed and anorexic, in poor condition with a rough dirty coat and pasty faeces.

Treatment and prevention

Coccidiosis in piglets can be treated with trimethoprim sulphonamide and they should be supported with electrolyte. Toltrazuril given as an oral suspension by stomach tube on day 3 prevents diarrhoea, prevents oocyst shedding and can maintain piglet growth. Scrupulous attention should be given to hygiene in control, as the high levels of oocysts passed by piglets and their ability to survive for months make environmental contamination important. Sows should be cleaned on entry to the farrowing houses which should be disinfected or fumigated with methyl bromide or ammonia (final concentration 2%). Steam cleaning at 65˚C for 15 minutes and proprietary disinfectants can also be used to destroy oocysts. Less disease and oocyst shedding has been demonstrated on fully slatted cleaned floors. Trimethoprim sulphonamide may be given by injection or orally to older pigs with Eimeria species and the inclusion of an anticoccidial such as amprolium at 1 kg permix per tonne in sow feed for 7-10 days prior to farrowing and for 2 weeks afterwards will reduce the shedding of oocysts by sows and other pigs. No treatment has yet been shown to affect Cryptosporidia. The oocysts can be destroyed by the same disinfectants as those of the other coccidia.

Be aware

Cystoisospora and Eimeria infections are of no public health importance, but the pig may be a source of infection with Cryptosporidium for humans and vice versa.

Biotin Deficiency – Nail Growth

This affects all age groups from growers, gilts, sows and boars. It is caused by diet and poor floors and effects Lameness, claw defects, poor growth, diarrhoea, hair loss, scaly skin, small litters.

Causes

Dietary biotin (a water-soluble B vitamin) is normally present in adequate amounts in pig rations, although in feeds containing wheat or barley, the vitamin may be less readily available to pigs than in maize-based diets. Biotin is a cofactor in a number of body enzymes especially in the carboxylation (a chemical reaction in which a carboxylic acid group is produced by treating a substrate with carbon dioxide) or transcarboxylation reactions required for energy metabolism. In growing pigs lipogenesis (fat formation) is affected when the important enzyme, Acetyl CoA carboxylase cannot be formed. Deficiency in biotin on wheat and barley-based rations occurs quite commonly and at least 180 mg/tonne should be present for health.

Mode of transmission

Biotin deficiency is not infectious and occurs where rations are deficient in the vitamin.

Clinical signs

Early changes in biotin deficiency are slight but include progressive hair loss, dry and scaly skin and a white film and transverse grooves on the tongue. After 5-7 weeks on a deficient diet, claw defects occur. Erosion of the heel occurs first and is followed by cracking of the sole. Cracks appear in the now rubbery horn of the sole and the claw wall and result in lameness. Secondary infection may occur. In most cases, foot lesions in sows appear on the underside of the hoof and are only seen when the claw is cleaned. Others appear as longitudinal cracks on the wall originating in the coronary band. Heel and sole erosions and cracks also occur. Inspection of the sows’ feet after thorough cleaning will allow the claw defects to be seen clearly. Cracks arising from the coronary band and erosions of the sole and heel and the presence of alopecia and scaly skin suggest biotin deficiency. As the foot lesions could be mistaken for those of a vesicular disease, such disease should be ruled out. There may be alopecia and a dry scaly skin which may progress to give dermatitis with brownish crusts and pinpoint haemorrhages. The reproductive effects include low numbers born, especially born alive and reared and long weaning to service intervals. Reproductive effects measured over 4 parities indicate at 1-1.4 pigs per sow per year are lost, that weaning to service intervals may be increased by up to 4 days and that conception to the first service may be reduced by 9%. Good recording is essential for this effect to be detected.

Treatment and prevention

A diagnosis of biotin deficiency can be confirmed by analysing the biotin content of the ration (100-220 µg/kg is the normal range) and noting the response to biotin supplementation of the diet. The reproductive effects can be confirmed only by supplementation of the diet in controlled studies. Populations with plasma levels of 60 ng/100 ml benefit from supplementation.

When deficiencies occur it is common practice to supplement the diet with 400 mg-1,250 mg/tonne of D-biotin; it is best to seek the advice of an experienced pig nutritionist. Biotin is available as a 1% d-biotin premix and 40g premix/tonne is necessary for most purposes, for growing gilts, and pregnant and lactating sows to prevent foot lesions and improve litter size. Levels up to 3,000 mg/tonne may be necessary to reverse hoof lesions and time should be allowed for the damaged horn to grow out.

Abortion

This affects both gilts and sows and the causes range from mismanagement, fever, infections of the uterus and poisoning.

Effects: The sow/gilt will abort recognisable foetuses before day 110 of gestation, after which production of dead foetuses is classified as a stillbirth. Sows may be visibly ill before abortion occurs or remain normal.

Causes

Death of the conceptuses may occur early from hormonal causes as four live foetuses are required to maintain an early pregnancy. After implantation, infection is the main cause of abortion, indirectly through fever or directly as a result of the infection of the foetus. Fever is the cause of abortion in erysipelas and other feverish diseases. Invasion of the foetus can occur in many viral and bacterial diseases. In some, foetal invasion results in death and dead foetuses reabsorbed, and in older pregnancies, the foetus may become mummified and later stillbirth may occur. All combinations of normal, resorbing, and mummified foetuses may be aborted. Major infections capable of causing abortion are Aujeszky’s Disease, brucellosis, enterovirus infections, leptospirosis, parvovirus, PRRS, swine fever and toxoplasmosis. Ingestion of the mould toxin zearalenone is also capable of causing abortion, as are management factors, such as high carbon monoxide concentrations.

Mode of transmission

Infectious causes of abortion are transmitted by the routes associated with the causal infection. Non-transmissible abortions occur.

Clinical signs

Sows may be seen to abort and the aborted material may be found on the floor of their accommodation. The sow may not appear ill in some cases (enterovirus, parvovirus, some leptospirosis), but in other diseases such as erysipelas, there is clear evidence that the sow is ill, off feed, and has evidence of the disease. In the case of erysipelas, high fever and the characteristic skin lesions are often found. The rectal temperature should be taken to establish the presence of fever. During or after abortion, the vulva may be bloodstained and the tail and hindquarters may be smeared with sticky discharge. As sows frequently eat aborted material, abortion is hardest to detect in loose-housed animals. Where abortion is missed, the termination of pregnancy may be detected only when an animal, previously known to be pregnant, fails to farrow, returns to oestrus or is identified following a pregnancy check. Abortion is recorded in pig herds as a routine. Abortions should be uncommon in a herd (fewer than 1%), but if they reach 2.5%, the cause should be determined. Management factors may be obvious and in zearalenone poisoning, enlargement of the vulvas of piglets and enlargement of the mammary glands in non-pregnant gilts. The presence of specific diseases may only be identified by laboratory examination of the aborted foetuses, vaginal discharges or blood from the affected sow.

Postmortem lesions

The products of abortion may be visible as embryos (large sacs 10-20 cm in length, with a central dark area, the embryo itself, from which blood vessels radiate) or as perfectly formed pig foetuses. These have their eyes closed and are hairless. They may be partially decayed, mummified or perfectly fresh with haemorrhages on their skins. The age of the foetus when death occurred may be determined by measuring foetal crown-rump length. Placentas may be absent, although they are sometimes passed surrounding aborted piglets. Fluid from the chests of aborted foetuses is used to detect infectious agents by culture or PCR and antibody to them may be present after 70 days gestation. Sows are rarely examined postmortem, but ageing corpora lutea are visible in the ovaries and the uterus may be enlarged, although it rapidly returns to normal. Lesions of a causal infectious disease may be visible but laboratory examination of vulva discharge or uterine contents may be required.

Treatment and prevention

The ability to prevent further abortions varies, depending on the cause. For example, zearalenone toxicity can be eliminated rapidly by feeding clean rations. Carbon monoxide poisoning can be eliminated by adjusting gas heaters. Toxoplasmosis may be prevented by stopping contamination of pig feed by cat faeces. Erysipelas can be treated easily with penicillin and leptospirosis with tetracyclines. Solid immunity follows the elimination of these infections. Less specific infections of the uterus can be eliminated, but ideally, the animals should be culled as persisting infection may reduce fertility.

To control abortion, sows can be vaccinated against erysipelas and parvovirus. In some countries, vaccination against leptospirosis, Aujeszky’s Disease, swine fever and PRRS is also possible. Vaccination requires at least 14 days to protect against an agent and may not protect against venereal infections. There are no vaccines for enteroviruses. Brucellosis is notifiable and controlled by other means. The aborted material should be treated as infectious and correctly discarded, with disinfection as appropriate.

Animals which have aborted should come back into oestrus within 10 days and may then be served. The exception is if body condition has been lost when consideration should be given to increasing feed and delaying service. Those that do not return to oestrus or do not hold to the next service, should, unfortunately, be culled.

Special note

Some infectious causes of abortion (Swine Fever, African Swine Fever, Brucellosis) are notifiable and some, such as Brucellosis and Leptospirosis, can infect humans handling the products of abortion. Please ensure that strict hygiene is practised.

The Sandy Pig Issue 1 Summer 2022

The Sandy Pig Magazine Issue 1 – Summer 2022

Our digital magazine has been a big hit with our supporters, with over 300 reads for our first issue. The Sandy Pig is published quarterly and is jam-packed with content as you can see from the below preview. If you would like to receive a copy please email mag@osbpg.org

Inside The Sandy Pig, Issue 1, Summer 2022

The Ark (RBST) OSBPG – Celebrating 10 years

Autumn 2020 – The Ark – RBST Magazine

Kim Brook with her OSB Boar
Kim Brook – Founder of the Oxford Sandy and Black Pig Group

The Oxford Sandy and Black Pig Group appears in many of the smallholder/pig/farming publications. In this article, Kim Brook talks about “celebrating 10 years of the OSBPG” in the autumn 2020 issue of The RBST – The Ark magazine. Read more below in the pdf publication

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The Oxford Sandy & Black Pig

Aug-Sept 2019 The Smallerholder

Kim Brook with her OSB Boar
Kim Brook – Founder of the Oxford Sandy and Black Pig Group
The Oxford Sandy and Black Pig Group appears in many of the smallholder/pig/farming publications. In this article, Kim Brook talks about “The OSB, its Origins, breed standard and more ” in the October – November 2020 issue of The Smallholder magazine. Read more below in the pdf publication The Smallholder Oct-Nov 2020