This affects newborns and piglets at pre-weaning the main causes are starvation, cold and infections with the most common effects being an empty stomach, cold, lethargic, convulsions leading to death.
The prime cause of this condition is insufficent intake of milk. This may be due to the failure of the sow to provide sufficient milk or failure of the piglet to suck. The presentation of the sow’s udder is important due to competition at the milk bar. Newborn piglets normally possess carbohydrate reserves in the form of hepatic (liver) glycogen (animal starch) stores (10-14 mg/100g) and blood glucose levels of 80-100 mg/100 ml (24 hours after birth).
Gluconeogenesis (the generation of glucose from protein) is not efficient until 7 days of age and glycogen reserves become depleted if the milk supply is inadequate, by feeding normally it provides adequate carbohydrate, but, if interrupted, blood glucose levels fall until clinical signs of deficiency appear at a blood-glucose concentration of 50 mg/100 ml. The original
glycogen stores may already be depleted by delay of farrowing. Piglets do not have brown fat so are unable to use fat to generate heat. Low environmental temperatures (below 34˚C for the single neonate or 25-30˚C for the piglet able to huddle) lead to increased utilisation of glycogen reserves in the liver and skeletal muscles and to the more rapid development of clinical signs. Low birth weight increases heat loss.
Piglets aged less than 7 days are affected and, at blood glucose levels of 50 mg/100 ml, may show uncertain gait, and later support themselves by placing their noses on the ground and straddling their hind limbs. More severely pigs rest on their abdomens but eventually fall on their sides and develop convulsions. These consist of ‘galloping’ of the forelegs, champing and frothing of the jaws in ‘air hunger’ and the heart rate will decrease (to 80 beats/min), a decline in temperature and shivering. Animals enter a coma and die. Death normally occurs 24-36 hours after the commencement of the signs.
Hypoglycemia should be suspected when the clinical signs of staggering, failure to rise, convulsions with galloping movements and gasping for air happen in very young piglets.
The presence of agalactia (failure of milk) in the sow, presence of a large litter and low environmental temperature all provide supportive evidence of Hypoglycaemia.
Treatment and prevention
Affected animals can be given intraperitoneal injections of 15 ml of 5% glucose solution every 4-6 hours, or oral glucose by stomach tube, and kept at a minimum of 30-35°C (85-95°F). If the sow is unable to feed them, an artificial sow milk replacer should be given by stomach tube initially or they should be fostered onto another sow. Reduction in draughts and the provision of dry bedding and additional heating will also improve their chances of survival.
Agalactia or mastitis in the sow should be treated promptly and support provided over the period of inadequate milk supply.
Ear necrosis affects weaners, growers and finishers. The cause is normally trauma, skin infection, ear biting or ergot poisoning. The ear tips can get bloody, scabby or turn black and then cause the flesh to drop off.
The major causes of ear necrosis are circulatory disturbance and trauma caused by shaking their head near a hard object. Circulatory disturbance occurs during septicaemic infectious diseases. In erysipelas and salmonellosis, infected clots block the blood vessels to cause congestion of the ears, snout, tail and feet. The blood supply to the ear tips may be completely cut off and the congested part dies. In various viruses cause of proliferation of the cells lining the blood vessels cause blockage and the ears become necrotic.
When pigs eat ergot (a fungus found on rye and wheat), the active components constrict the blood vessels and cause ear necrosis. Necrosis of the ear tips occurs down to a straight line across each ear. Trauma (damage) usually results from ear biting but can occasionally occur from shaking their heads near hard objects, wall, door feed bin etc. Ear biting can result from investigation and biting of wounds from tags and clipping, but often results from nuzzling and biting. The lesions spreads by bacteria therefore necrosis develops.
Sometimes the stimulus for ear biting is infection, Staphylococcus hyicus in greasy pig disease, or other agents especially the spirochaete, Treponema pedis, which has been seen in approximately 60% of lesions.
Source of Transmission
Ear necrosis due to the consumption of ergot is not transmissible, but can occur in successive batches of pigs when fed on the same contaminated ration or grazing the same infected pasture.
When ear necrosis follows trauma due to ear biting or other causes, the same factors may affect successive batches. The bacteria infecting these lesions are transmitted from infected pigs after the initial damage has been caused, or are derived from the oral cavities of the aggressors. Infection is otherwise by direct contact with infected wounds on other pigs or by contact with contaminated housing/ark.
Ear necrosis is easily diagnosed by inspection. Necrotic ears caused by circulatory disturbance are usually obvious when the damaged, blackened tissue is still present, but become more so once the damaged tissue has fallen off to leave the appearance of an ear with the tip cut off. Closer inspection may be required to detect the necrotic lesions caused by ear biting, other trauma and localised skin infections. The cause of ear necrosis due to circulatory disturbance requires retrospective analysis. Salmonellosis is the most common cause at present in Western Europe, and examination of the affected animal may confirm this by the study of the blood or isolation of the organism from the pig or from others on the farm. The past presence of erysipelas may also be confirmed, but the possibility that swine fever may be involved should also be considered. Ergot poisoning requires a history of grazing contaminated ryegrass pasture or eating the fungus in contaminated grain. Lesions of ear necrosis caused by ear biting have a different symptom in that the ear is actively inflamed.
Treatment and prevention
There is no treatment for ear necrosis caused by circulatory disturbance, as the tissue is already dead. The necrotic tissue usually drops off cleanly and does not cause infection. Ear necrosis caused by trauma is different. The continual biting and the presence of inflammation mean that affected pigs may have to be separated from the group and reared alone. If this is done, then a course of injectable antimicrobial such as ampicillin can improve the ear and prevent necrosis from advancing.
Where the disease is due to lesions of treatable skin disease such as greasy pig, then the appropriate treatment may be given. Frequent dressing of wounds with wound powders may also improve healing followed by the reintroduction back to the herd. Prevention relies on treating or prevention of the predisposing disease in erysipelas or salmonellosis and correction of the ration in ergot poisoning. Ear biting can be prevented, but not consistently. It may be possible to coat the ear in an unpalatable material to discourage ear biting. Where the condition is occurring, then ear notching or tagging should be reduced or delayed.
This condition affects sows and boars of all ages. A number of separate conditions are grouped under this heading. All begin with some form of defect or penetration of the wall of the hoof or its bearing surface (sole and heel) which provides a point of entry for secondary bacterial invasion. Penetrations include erosions of sole, heel and toe, split or crack in the wall (sand crack) and separation of the wall from the sole at the white line. Infection spreads in the hoof in three possible ways: a deep necrotic ulcer may develop involving the laminae (the sensitive weight bearing living area) and coronary band (the hairless skin where the hoof joins the toe); necrotic (infected) tracks may reach the coronary band and form ulcers; or infection may penetrate deeply and involve the deep digital flexor tendon, or bones of the toes or the joints.
When abscesses burst at the coronet (coronary band), the condition is known as ‘bush foot’. Abrasive and chemical effects of newly-laid concrete contribute to the production of hoof defects, Wet, unhygienic conditions and poor bedding also contribute to what is often a herd problem. Bacteria such as Fusobacteriumnecrophorum, Arcanobacteriumpyogenes and spirochaetes such as Treponema pedis may infect the lesions. Septicaemia and bacteraemia can occur and secondary abscesses may occur elsewhere, e.g. in brain, spine and liver.
The physical conditions which underlie this condition are not themselves transmissible, but pigs exposed to them are at high risk of developing foot lesions in the same way as their predecessors in the accommodation. The infectious component of the condition depends upon the organisms to which the damaged foot is exposed, and some of the bacteria responsible may be present in the environment of the pig’s foot, having been shed by other affected pigs. It is possible for some of the bacteria in this complex to be transferred from farm to farm in pigs or on boots, tools and in transport.
The most obvious clinical sign is lameness, pigs tend to walk on tip-toe, with ‘paddling’ or ‘goose stepping’ gait, and are reluctant to rise and move and may sit. The lameness may prevent the loading of animals for slaughter, prevent service in boars and sows and result in increased mortality amongst sucking piglets. Lateral claws, especially those of the hind feet, are most commonly affected. The affected claw is warm, painful and the primary lesion is usually apparent. Severe pain occurs when abscesses develop at the coronary band and the leg is often held off the ground. The heel and coronary band become swollen and blue-black in colour. Cellulitis may cause swelling in the limb and reach the carpus or the hock. Fever may be present if septicaemia or secondary abscessation have occurred. Bone and joint involvement may be seen as enlargement of the nearest joint.
Lameness or reluctance to rise usually draws attention to the existence of the condition. Once lameness has been identified, detailed inspection usually confirms that the foot is affected. If movement of the shoulder, hip, elbow, knee, carpus (wrist) or hock in the unanaesthetised pig does not cause pain and there is no enlargement or heat in these joints, then the lameness is in the foot.
The foot concerned should be cleaned with soap and water and examined. Cracked walls, ulcers at the coronary band, erosions of the sole and separation of the horn at the white line may all be seen. It may be necessary to expose lesions under overgrown horn by paring using a hoof knife. The absence of lesions in the other feet should be confirmed. Where a pig is particularly valuable, an x-ray examination can be performed or ultrasound examination carried out. This may require general anaesthesia or local anaesthesia of the lower limb by the veterinary surgeon. Swabs may be taken from sinuses to identify the bacteria present.
Treatment and prevention
Trimming a septic hoof lesion to expose the seat of the problem, poulticing, and bandaging can result in recovery, but may not be economical. The surface of exposed, cleaned lesions may be sprayed with antibiotic, e.g. tetracycline or dusted with an antibiotic wound powder. The animal may be given a course of antimicrobial such as tetracycline or ampicillin by injection.
Control depends upon improving hygiene and management, especially floor quality. Concrete flooring should be made using aggregate with rounded edges and re-surfaced if the aggregate has been exposed. If having slats, then they should be in good condition, have pencil edges and be at least 100 mm wide.
You can also run your pigs through foot baths containing 5-10% formalin 2-3 times a week where problems have been experienced with infection. Ensure that the biotin level of the ration is adequate, particularly in the gilts of the herd. Affected animals which are able to be transported should be culled at the earliest opportunity if fit for slaughter, otherwise killed humanely.
(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.
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.