Piglet Observation – Part VII

Economic Considerations Regarding Low Birth Weight Pigs

As we know, and have experienced ourselves as we observe our Oxford Sandy and Black (OSB) low birth weight pigs, they can thrive when managed and nourished correctly. With meticulous care, these OSB piglets can achieve enhanced growth rates and therefore reduce pre-weaning mortality rates.

The economic implications of raising Oxford Sandy and Black low birth weight pigs can hinge on these few factors:

  1. Feed Efficiency: Their capacity to efficiently convert feed into growth.
  2. Production Variation Costs: Expenses associated with managing variation throughout the production process.
  3. Market Conditions: The prevailing prices of pigs and feed in the current market.

These factors collectively determine the economic viability of rearing low birth weight pigs, and with the right strategies, their performance can yield positive results.

You can also tune in to the OSBPG Podcast HERE and listen to leading pig nutritionist discuss pig feed and nutrition. Whilst there subscribe to the OSBPG Podcast and be apart of engaging discussions.

The Oxford Sandy and Black Pig Group is UK’s only pig breed that is a registered charity in England & Wales (1190469) and Scotland (SCO52662). We are creating a better future for our breed, the bloodlines and its breeding potential together with our Independent Pork Producers, Breeders and Keepers. Please consider clicking our donate button so we may continue to look after our breed and our supporters.

Follow us on Facebook and see how we support, help and inspire individuals about our rare breed

Piglet Observation – Part VI

Enhancing Nutrition for Improved Piglet Growth

Instead of increasing feed levels, it’s worth considering an improvement in nutrition. Selecting the right starter feed regime is vital to minimise the growth slowdown that our Oxford Sandy and Black (OSB) piglets may experience during the transition from liquid to solid feed.

Feeding a high-quality starter diet, supplemented with extra feed (matching the last diet of the starter regime), can enhance the performance of low birth weight OSB piglets up to 10 weeks of age. This approach can result in similar nursery exit weights for both low birth weight and normal birth weight pigs.

However, it is important to note that feeding a high-quality diet is less effective when introduced at nine weeks of age, indicating a critical intervention window.

Research indicates that not only do low birth weight pigs benefit from an improved dietary regime, but it is also cost-effective for producers. This approach yields a higher return per pig compared to a standard commercial regime, which has a lower margin over feed cost. For normal birth weight pigs, the standard commercial feed regime remains the most economical choice with the greatest margin over feed cost.

At weaning, separating OSB low birth weight pigs allows for selective feeding with an improved regime, as heavier OSB pigs are better suited for a standard commercial diet.

Further research reveals that nutritional treatments at different stages can impact outcomes such as:

  • Specialised diets introduced at weaning can enhance performance throughout the nursery phase and are more cost-effective than using a standard commercial regime.
  • Offering supplementary milk doesn’t significantly improve the performance of low birth weight piglets, but it does reduce birth weight variation in mixed litters.
  • Low birth weight pigs may not experience substantial benefits from a diet higher in amino acids and energy when fed from nine weeks of age.

The Oxford Sandy and Black Pig Group is UK’s only pig breed that is a registered charity in England & Wales (1190469) and Scotland (SCO52662). We are creating a better future for our breed, the bloodlines and its breeding potential together with our Independent Pork Producers, Breeders and Keepers. Please consider clicking our donate button so we may continue to look after our breed and our supporters.

Follow us on Facebook and see how we support, help and inspire individuals about our rare breed

Leg Weakness (Osteochondrosis)

Leg weakness affects growers, finishers, sows and boars with various causes being genetic, rapid growth, lack of exercise and a nutritional imbalance. The noticeable effects will be difficulty in rising or walking, swaying and misshapen limbs. 


Osteochondrosis is a generalised skeletal disease which leads to leg weakness. The changes have been shown in piglets at a day old and may be congenital. Osteochondrosis becomes more obvious with age.
The cause appears to be a defect in the chondrocytes (cartilage cells) which do not mature normally. The formation prevents blood vessel formation and the formation of normal bone. It is also true to say that the growth rate and heredity factors appear to affect development. The changes lead to abnormal growth and change in the shape of bones and joints, including the vertebrae. Erosion of the articular cartilage and painful osteoarthritis of the joint development. Epiphysiolysis (The loosening or separation, either partial or complete, of an epiphysis – rounded end of a long bone – from the shaft of a bone) can result when the head of the femur is shed in rapidly growing animals.

Source of transmission

The condition is not transmissible from pig to pig in a group. It is deemed as hereditary. Common environmental factors such as nutrition, flooring, degree of exercise will compound the issue.

Clinical signs

Present in up to 80% of pigs, particularly heavy, rapidly growing in meaty breeds such as Dutch Landrace or Swedish Landrace, or Duroc kept on hard flooring. Clinical signs include shortening of the step, knock and buck knees and swaying of the forelimbs. In the hind limb the feet may be positioned too far forward, and pigs stand with their legs apart and show weakness at the pastern and swaying of the hindquarters. Changes increase with age, where you may witness hind limb lameness and pain at the hip but not necessarily at the stifle or hock. The affected leg is shorter than the unaffected one, but the thickness of the muscle mass makes identification difficult. Animals may be unable to rise, adopt a dog-sitting position and resent movement.
Osteochondrosis is a common cause of leg weakness and lameness in young breeding stock and may progress to arthrosis (degeneration of the joints) and deformation of affected bones completely by 6-9 months of age. Forelimb weakness is obvious in boars. Kyphosis (curvature of the spine) may also develop as the pigs attempt to adjust their gait on their affected limbs.
Clinical signs of bowed legs and swaying gait suggest the presence of osteochondrosis. Epiphysiolysis should be suspected where gilts are delivered lame or where they become lame suddenly at or around service. Osteochondrosis can be confirmed by radiography from 63 days of age. Confirmation at slaughter or post-mortem is more common.

A) no irregularity of the cartilage, and B) severe irregularity of the cartilage

Treatment and prevention

There is no treatment although lameness may resolve after moving to non-slip softer floors or deep bedding. The production effects resulting from lame boars and gilts can be overcome by use of artificial insemination.
The condition cannot be prevented completely, but its severity can be reduced. It has been suggested that the calcium and phosphorus levels of high nutrient density diets should be increased in order to supply adequate levels of these minerals in rapidly-growing pig breeds.
Exercise and space to roam around is beneficial for both breeding boars and gilts/sows. There is evidence that the condition may be under genetic control. It is much less common in large White than in Landrace pigs and genetic studies with Duroc boars suggest that it can be selected against. This selection may simply reduce the stress on joints provided by large hams or other features of conformation. In all cases where leg weakness is visible, the condition of the floors should be improved, non-slip surfaces and a good deep straw breeding or rubber matting which is soft underfoot.

Not-In-Pig (NIP)

We all get frustrated when our sow/gilt return and we find that they are not in-pig (pregnant). The cause of this is not being vigilant in watching if they return (come back on heat, hogging) or it could be a case of an infection.


The main causes are poor management and infertility. With regards to management, experience shows us that empty sows and gilts are as of a result of being misidentified poorly, housed in groups running with the boar and services are not supervised and observation of post service for returns to oestrus are not detected. I know it is difficult to keep an eye on our pigs all the time, but if you know when they are due to start hogging then introducing the boar and observing can save you time and worry. Knowing if and when the sow/gilt is due to return by counting 21 days from her last hogging will help you to know if the service has been successful.
If pregnancy testing is not carried out (hire our pregnancy scanner from our website oxfordsandyblackpiggroup.org), then sows may reach term without being pregnant. Infertility may be solely responsible when observation has been a little lax. When embryos are produced and die, sows return to oestrus at uneven intervals. Where disease or cold have reduced the ability of the animal to return or where housing is such that hogging cannot be observed, then the pigs will remain undetected until a routine pregnancy check is followed or the expected farrowing date arrives with no farrowing. Sometimes, in these cases, there may be an undetected abortion, cystic ovaries or pyometra which there will be an infection of the uterine horn.

Clinical signs

‘Not-in-pig’ sows or gilts return to heat after service and also fail to develop the abdominal swelling and underline development typical of pregnancy. The sows are found to be non-pregnant when examined by. A history of vulva discharge may pinpoint the stage at which pregnancy ended.
It will come to no surprise that failure to farrow leads to a diagnosis of not-in-pig. The reasons for the failure of pregnancy can be determined by examining the records. If the recording is not carried out, services are not supervised, pregnancy checks not carried out and returns to oestrus not checked visually, then poor management is the cause.
Pigs that are in poor condition and exposed to too hot, cold, damp and drafty housing then this will result in the sow/gilt not carrying to term and possibly reabsorbing or aborting. Where records confirm that service was carried out and pregnancy has been confirmed reliably, then again, abortion or reabsorption has occurred.

in-pig sow. Underline swollen, ready to farrow, comfortable nesting arrangement

Treatment and prevention

Before animals are treated as not-in-pig, a pregnancy test should be carried out, as the commonest cause of failure to return to service is pregnancy. Cystic ovaries and subdued oestrus can be treated using chorionic gonadotrophin. Pyometra may respond to antimicrobial treatment by injection and allow a return to oestrus.
Prevention is largely a matter of management, although vaccination against conditions such as parvovirus, erysipelas, leptospirosis, PRRS, and influenza can also be a reason for a non-productive sow.
Sows must be identified individually, services must be attended with good recording keeping of the boar or semen used together with results of any pregnancy tests. Ensure that mating is successful and occurs at the correct time if AI-ing that semen quality is adequate. Be vigilant to observe that there are no vulva discharges after service.
To hire our pregnancy scanner, please click here


Most of us have experienced this in our sows and it also affects the gilts. There are a few causes to mastitis such as teat injuries from floors or piglets, bacterial infection, poor hygiene and the symptoms is that the udder is hot, hard and swollen, lumps and sometimes the sow/gilt may become unwell and the piglets may also suffer due to lack of feeding.
Mastitis in sows is caused by ascending infection of the teats by bacteria. The organism most commonly involved is Escherichia coli or related organisms (coliforms). Bacteria such as Arcanobacterium pyogenes, streptococci and staphylococci may cause infections of single glands. Acute and severe mastitis caused by Klebsiella spp. may occur in outbreaks of fatal disease following trauma to the teats caused by rough sawdust bedding. Traumatic injury resulting from piglet teeth, sawdust bedding, or poor quality flooring add to infection. One or both glands supplying a single teat may be infected. Infection enters via the teat canal following teat contamination and bacteria multiply in the gland. Introduction of endotoxin into the mammary gland will cause mastitis and agalactia and endotoxin can be detected in the blood in mastitis.
Clinical signs
Acutely affected sows are usually depressed, loss or lack of appetite and fevered (temperatures of 40.5-42°C, 105-107°F are not uncommon). The udder is usually swollen and oedematous (abnormal swelling of fluid), often with massive congestion. Any secretion that may be obtained after oxytocin injection contains pus. Pain in the udder may lead to restlessness in the sow when piglets attempt to suck. The litter rapidly loses condition. Acute mastitis usually occurs within 1-3 days of parturition. The body temperature falls below normal, the animal can no longer rise and respiratory distress develops frequently leading to death. Coliform (a bacteria calledaerobic bacillus that lives in the colon) mastitis appears to regress within 3-4 days although in severe cases lactation may cease entirely. Sub-acute infection or infection in one or more glands occurs much more commonly and may be recognised by the increased hardness of the gland and, in its early stages, by a square area of reddening or the skin over the affected gland. The litter loses condition. Mastitis in a single gland is often noted only when an affected gland fails to return to normal after weaning. There is often teat injury, especially in the pairs of teats.
Acute mastitis is easily recognisable as affected sows are off their feed and have obvious swelling of the udder, sometimes with reddening and oedema. The litter is usually in poor condition. Animals are often lying down alot, but must be made to rise in order to confirm that mastitis is present. The udder should be felt on both sides by running the hand under both lines of glands.
Individual affected glands feel firm and hot. Laboratory examination of expressed secretion confirms that presence of mastitis by means of cell counts and the organism(s) responsible can be identified. Action requires oxytocin injection as milk let down is under voluntary control. Sub-clinical mastitis may only be detected after cell counts on expressed milk, showing 75% white blood cells. Chronic mastitis is easily felt upon inspection during lactation and easily seen in dry sows.
Treatment and prevention
Acutely ill sows may be saved by injection with neomycin, tetracyclines, ampicillin, amoxicillin, streptomycin, fluoroquinolone, ceftiofur or trimethoprim: sulphonamide for 2-4 days. Oxytocin should also be given. The litter should be fostered or reared artificially. After recovery it may be necessary to cull the sow as she will be prone to this ailment on all farrowings.
Other supportive treatment may include anti-inflammatory medication. In sub-acute cases, rehydration is not necessary. Antimicrobial injection may improve the condition where single glands are affected, but results are poor where abscess are present and has occurred or teat ends are damaged.
Control depends upon hygiene, use of soft bedding other than sawdust, early treatment and, possibly, the use of commercial E. coli vaccine if the condition is due to E. coli. Where the condition is recurring and pre-farrowing infection is suspected, treatment with trimethoprim sulphonamide at 15 mg/kg given in the feed from day 112 of gestation to day 1 post-partum may eliminate early lesions and prevent the development of clinical disease. Sows which have had severe or repeated bouts of mastitis should, unfortunately, be culled and affected sows should only be retained if they have sufficient functioning teats.

Ear Necrosis

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.

Clinical signs

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.
  • main picture courtesy pig333 Dr Rex Walters

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.


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.


By Kim Brook

The brain and spinal cord are protected within bony cavities (the skull and the spinal column) but separating the nervous tissue from the bone is a series of membranes called the meninges. When these become inflamed in the condition known as meningitis (usually due to bacterial infection), pressure builds up on the nervous tissue and nervous signs ensue.
In the early stages of meningitis, pigs will be dull and depressed, reluctant to stand and have a raised rectal temperature. Occasionally, they may be seen pressing their head against a wall and they will be unsteady on their legs. As the disease progresses and in response to stimulation (handling, noise), affected pigs will subside into paddling convulsions while lying on their side. Careful observation will reveal that the eyes, when open, will flick from side to side (this is called nystagmus). Death can ensue within a few hours and in some cases of meningitis may simply be found dead.
Infection in the brain results from the bloodborne spread of bacteria, which can gain entry through any break in the skin or mucosa. Sporadic meningitis is particularly seen in the young piglet, where infection gains entry through the navel, tail-dock wound, clipped teeth or fight wounds, and is very much a feature of colostral insufficiency. Bacterial spread in the bloodstream (bacteriaemia) can lead to infection in other areas of the body – particularly the joints, causing joint ill, or arthritis. The bacteria involved are usually environmental contaminants such as staphylococci, E. coli and streptococci. However, epizootic forms of meningitis can occur, particularly in weaner pigs four to ten weeks old and rarely in older growing pigs. The most common cause in these cases is Streptococcus suis type II and Haemophilus parasuis.

Meningitis which occurred secondary to E. coli septicemia associated with an umbilical infection.

The groves may also fill with fluid that has been expelled from the blood vessels. Arrows show early infection in the brain.

Streptococcus suis Meningitis

This is typically a post weaning disease that is triggered by the stress of weaning and by mixing pigs of different ages. Overcrowding, poor ventilation and in particular, high humidity all seem to exacerbate the disease. In an infected herd, the organism is picked up at or soon after birth, the reservoir being the nasal chambers and tonsils as well as the vagina of the sow. The organism colonises the tonsil of the young pig and from there will spread via the bloodstream to the brain.
Onset of the disease can be extremely rapid and sudden death may be seen. Streptococcus suis can readily be cultured from the meninges of an affected pig that has not been treated. Paddling convulsions are a classic feature, along with temperatures of 41degrees C (106f) and above. The disease usually behaves in an all or nothing way – in contrast with most gut or respiratory tract diseases, there is no effect on the growth of unaffected meningitic pigs.
Control can be difficult, vaccines have not proved effective and strategic use of antibiotics such as amoxycillin by injection at weaning may be needed to prevent clinical disease. Medication of weaned pigs via water or feed with penicillin-based antibiotic will often suffice in milder outbreaks. Recovered pigs may drop dead suddenly two or three weeks later, the result of seeding of infection on the heart valves and production of endocarditis.
Worth noting that S. suis type II (along with other strains of S. suis) are zoonotic, so particular care should be taken when handling affected pigs and when attending farrowing in herds known to be infected. Infection for humans is normally by skin penetration through cuts and grazes – thorough hand washing with soap is essential following contact with potentially infect material.

Haemophilus parasuis Meningitis

There are many strains of H. parasuis present within pig populations and, while the most common manifestations of disease are either respiratory or septicaemic, cases do occur where the infection targets the brain, producing meningitis (arthritis is also occasionally seen). The clinical presentation is identical to that described above, but diagnosis can be difficult as the organism is very fragile post mortem – euthanasia of an affected untreated pig and immediate sapling of the meninges or cerebral spinal fluid is essential.
Treatment of any form of meningitis is based upon killing the causative organism and providing support therapy. Streptococcus suis is generally very sensitive to antimicrobials treatment with penicillin-based medicines such as amoxycillin, but treatment must be rapid and involve a formulation that achieves high levels of antibiotic in the body immediately. While Haemophilus parasuis is also very sensitive to antibiotics, response to treatment of affected pigs is frequently disappointing, probably due to the fact that clinical signs are the result of toxin release rather than the effect of the bacterium itself; by the time signs are seen, the damage is done and killing off the organism will have no effect.
A common complication of meningitis in pigs is dehydration. Their inability to feed and drink soon leads to fluid shortage, especially in the young pigs. This is often manifests in the form of “salt poisoning” (water-deprivation neuropathy), which can easily be confused with meningitis clinically even though it is quite distinct from it. So many pigs that die through meningitis infection actually subside into salt poisoning, which is the true cause of death.
The pig should be removed from the rest of the litter – where it can be bullied – and placed in a bedded area to prevent injury. Often, response to treatment will be very rapid (within two to four hours). It should be given fluids (water containing electrolytes), preferably by mouth on a little and often basis. Care must be taken to ensure that the pig is swallowing fluids and not inhaling them.
Support treatment with corticosteroids or non-steroidal anti-inflammatory agents can also improve recovery rates. As a general rule, however, a failure to respond to treatment within forty-eight hours is likely to leave the pig permanently brain damaged and so euthanasia is appropriate.

Photos obtained from Google

Middle Ear Disease

It will come to no great surprise that the inner part of the pigs ear is responsible for balance. Therefore, any disturbance to this will affect the balance and co-ordination. A common cause to this is infection, initially of the middle ear, which exerts pressure on the balance. There are two distinct phases to the disease.
  1. In the early stages, damage is limited to the middle ear. The pig will frequently shake its head and as it stops the head will be left tilted to one side with the affected ear downwards. The head will then slowly return to normal. This phase is frequently ignored as the pig appears to recover.
  2. In the second stages, damage occurs to the inner ear and a permanent head tilt results. Head shaking will be frequent and the pig may be unsteady and tend to walk in a circle. In severe cases, the pig will have difficulty eating, drinking and competing with pen mates. And loss of condition will occur.

Head leaning to one side showing signs of discomfort
There are a number of potential causes of middle ear disease. Infection with organisms can occur either from the external ear canal following penetration of the ear drum, or via the eustachian tube from the oropharynx. The former is particularly associated with mange infestation in growing and young adult pigs, whereby rupture of the tympanic membrane is either a direct result of the mites or secondary to head shaking. Rough handling (pulling a pig by the ears) can also damage the ear drum and allow infection.
The Oropharynx is normally colonised by a wide range of organisms, which can spontaneously ascend the Eustachian tube, particularly in young growing pigs. However, inflammation of the oropharynx as part of any upper respiratory tract disease will predispose the animals to a gradual infection. This is particularly seen in association with swine influenza.
Antibiotics (penicillin or other antibacterial solutions) administered in the early stages for a prolonged period of five to seven days will bring about a complete cure. The longer you take to act the more pronounced the condition becomes and the more difficult it will be to treat and the pig may be left with a permanent head tilt but as long as it does not have a raised temperature, free from medication and is steady on their legs there is no reason why you can not carry it on to slaughter weight. Severe cases will almost certainly require euthanasia.