Miscellaneous Lesions, Conditions, and Syndromes
The congenital absence of a patent anus at birth is rather uncommon in swine. The cause is not known but may have a genetic component or may be from an insult to the fetus in critical developmental stages in utero. The resultant megacolon may not be clinically apparent until several weeks of age.
These common lesions are the result of trauma to the ear followed by hemorrhage between the skin and cartilage (or within the cartilage). The subcutaneous hemorrhage resolves over several weeks to months, leaving the pinna thickened and misshapen in most cases. Trauma often is caused by bites inflicted by pen mates or by violent head shaking. Head shaking is associated with mange, infestation with lice, or feed particles in the ears. Treatment and/or drainage of the fluctuant lesion is not usually attempted or likely to be successful. Amputation of the ear is sometimes undertaken in management of severe cases.
These lesions are the result of ascending bacterial infections. Various bacteria, including Eubacterium (Corynebacterium) suis and coliforms, have been isolated from the lesions. These lesions usually occur in older sows and are a common cause of sporadic deaths. Death often occurs during or shortly after advanced pregnancy, a time of maximum stress on kidney function. Anything that interferes with adequate water intake or urination may predispose to infection. Eubacterium suis is present in the preputial diverticulum of most boars. The organisms may be transmitted to the sow during copulation. Many sows with cystitis/nephritis have hematuria, the first sign of infection, within three weeks of breeding. This is followed by progressive loss of body weight. The lesions are uncommon in boars.
This hereditary defect originated in the Landrace breed. The defect can be expressed as foot deformities present at birth, or later as widely distributed expanding cutaneous lesions that involve small to large areas of skin. Skin lesions usually are apparent by the third week although some develop later. Skin lesions begin as papules and expand to form roughened plaques that soon become papillomatous. Most affected pigs die within six weeks. Many that survive have dyspnea related to interstitial pneumonia of giant cell type.
Sows and boars over three years of age occasionally are found to have ectopic ossification of the root of the intestinal mesentery. The cause of these bony spicules radiating through the mesentery is not known. Little significance is ascribed to the presence of ectopic ossification unless it is responsible for intestinal volvulus, incarceration, or accident.
This inherited condition occurs in at least four breeds and is characterized by the absence of discrete areas of skin, usually over a part of the back, loin or thigh.
Lesions occasionally occur on the anterior surface of the tongue. Hydroureter and hydronephrosis commonly accompany the condition. Fetuses with extensive lesions may be aborted. Piglets born alive with extensive lesions usually die from bacterial invasion and septicemia. Minor defects may heal.
This condition results in sudden death in growing and finishing pigs. Affected animals found dead are characterized by a pale, distended carcass. Necropsy reveals that the entire intestinal tract has a severely congested, thin-walled appearance. Intestinal contents are usually watery and contain unclotted brownish blood. The condition must be differentiated from gastric ulcers, gastrointestinal torsion or volvulus, and from the hemorrhagic form of proliferative enteritis. The cause is unknown. Diagnosis is made by ruling out other causes through post-mortem and histologic examination.
See the table: Diseases Associated with Hemorrhage in Intestine
Both inguinal and umbilical hernias commonly occur in swine. Inguinal hernias are believed to be inherited polygenically. The overall incidence of hernias in a normal swine population is low unless matings to a boar that transmits inguinal hernias have occurred. Inguinal hernias can be bilateral or mono-lateral with most occurring on the left side. Protrusion of intestines through the inguinal canal often follows castration of pigs that unknowingly have an inguinal hernia. If left uncastrated, strangulation of the intestine within an inguinal hernia can occur but the most significant effect of the condition is the economic discount applied to the pig at time of slaughter.
Umbilical hernias occur in both sexes and tend to develop as a result of poor umbilical cord management, navel infection, or navel sucking by penmates; the condition is not thought to be inherited.
It is common to find large, fluid-filled cysts in kidneys of healthy swine. This incidental finding is observed during post-mortem examinations conducted for unrelated conditions or at slaughter.
This syndrome usually occurs within three days of farrowing and is characterized by inadequate milk production. Although hypogalactia is the most consistent sign, mastitis, fever, vaginal discharge, listlessness, weakness, anorexia, sternal recumbency and refusal by the dam to permit nursing by the piglets seem to be commonly present in affected sows. Dams usually recover within a few days to two weeks. Piglets are at high risk of dying from starvation unless cross-fostered or supplemented with other feed. Although the cause(s) is unknown, many risk factors have been associated with hypogalactia. These include lack of nursing stimulation (too few pigs or small/weak pigs), bacterial metritis, mastitis, mammary edema from errors in ration formulation, confinement with little opportunity for exercise, poor feeding management, constipation, obesity, moldy feeds, and poor sanitation in the farrowing environment.
Mastitis, often clinically undetected, is likely responsible for many cases of hypogalactia. Endotoxin from various Gram-negative bacteria, especially Escherichia coli, may be the basic cause of many cases of mastitis. Suppression of prolactin by endotoxin from any source results in less than normal milk production. The prevalence of MMA has decreased markedly in the last several decades with the use of modern sanitary and slatted flooring. Most problems with hypogalactia can be solved through management with careful attention to sanitation and the sow’s exercise, nutrition, and body condition.
Hypoglycemia is a common cause of death in neonatal piglets. Glycogen reserves are soon depleted if piglets become chilled or fail to ingest an adequate amount of milk. Chilling may occur if the effective temperature in the piglet sleeping area is less than ~95°F during the first week of life. Signs of hypoglycaemia include loss of condition, weak vocalization, faltering gait, cold skin, and recumbency. These are rapidly followed by paddling, frothing at the mouth, coma, and death if intervention does not occur.
If chilling occurs, the piglets should be put in a warm environment with a supplemental heat source such as heat lamps. If the piglets are not receiving an adequate amount of milk, cross-fostering or milk supplementation can be beneficial. Porcine milk replacers, bovine colostrum, or evaporated milk diluted equally with water can be used for supplemental nutrition until piglets are able to consume nutrient-dense solid food.
Enlargement and dilation of the colon with feces is usually the result of rectal stricture and less frequently from colonic atony. Atresia ani leads to megacolon in pigs up to four weeks of age. Postnatal rectal strictures are a frequent sequel to rectal prolapse. Damaged rectal tissues from prolapse, whether reduced, traumatized, or chewed-off by pen mates, may heal and fibrose causing constriction of the rectum. The outcome is intermittent defecation or total obstruction of fecal flow causing the colon to dilate with accumulated feces while the pig slowly wastes away.
Colonic atony with patent rectum has been reported as a result of feeding lupine-seed meal. Neural control of tone and peristaltic movement is lost causing the colon to simply dilate with feces.
Because of many variables affecting the quality of data collected by investigators, only generalizations can be made. Aside from infectious disease, causes of sow mortality include heart failure, cystitis, pyelonephritis, gastrointestinal problems (e.g. torsions, gastric ulcers), and complications during or shortly after parturition.
Individual sow condition and housing are important risk factors as well. Currently, sow welfare issues are promoting timely individual sow assessment and intervention to decrease overall sow mortality in the swine industry.
Osteochondrosis, also referred to as dyschondroplasia, is a generalized disease of growth cartilage. It affects most common domestic species. It often occurs in rapidly growing pigs approaching market weight or breeding age. Despite much research, the basic cause(s) is unknown but is usually related to the presence of one or more risk factors (below). The disease is characterized clinically by abnormal gait or lameness with characteristic pathologic lesions in cartilage and bone. Lesions of articular surfaces of joints include corrugations and ulcerations of cartilage, separation of cartilage from underlying bone, and development of cartilaginous cysts. Physeal cartilaginous lesions include fractures between the diaphysis and epiphysis or islands of cartilage within epiphyseal or diaphyseal bone. Lesions are often bilateral and symmetrical. Common sites of lesions in joint cartilage include the medial femoral condyle, humeral condyle, humeral head, glenoid of the scapula, distal ulna, and lumbar vertebrae. Common sites of physeal lesions include distal ulna and femur, head of the femur or humerus, and ischial tuberosity.
Dyschondroplasia has been attributed to rapid growth and early, excessive weight-bearing pressure on cartilage. Genetic background is believed to play some role. Other possible risk factors include nutritional deficiencies, flooring and housing that induce trauma, infection with Mycoplasma hyosynoviae, and lack of exercise. The number of pigs with lesions is often much higher than the incidence of lameness would suggest. Although some pigs recover, most affected sows are culled because of the time required for healing and the overall poor response to therapy.
Pityriasis rosea is a dermatitis usually seen in four to twelve week old pigs and is characterized by 1- to 20-cm raised, reddened, ring-shaped lesions on the skin. Lesions first develop on the skin of the ventral abdomen but occasionally start in other areas. The cause is unknown. Papules first develop on the ventral abdomen and inner thighs. These early lesions expand to form circular, coalescing lesions with an expanding rim. Older lesions often have healed centers. Lesions heal in about four weeks without intervention. Pityriasis rosea is easily diagnosed by gross examination and does not require any treatment. The condition is not pruritic and seems to have no apparent effect on the health or growth rate of affected pigs.
Nearly all affected pigs recover completely.
Porcine stress syndrome, sometimes called malignant hyperthermia or transport myopathy, is a complex, genetically transmitted myopathy usually triggered by stress or excitement. It also can be triggered by several anesthetics, including halothane, and by depolarizing muscle relaxants. Signs that appear can include tremors of the tail, back or leg muscles, muscle rigidity, inability to walk, respiratory distress, hyperthermia, blotchy dermal hyperemia, acute right heart failure, and death. Savaging of neonatal piglets by PSS-positive dams has been reported.
Postmortem lesions include early, rapid and complete rigor mortis, pulmonary edema and pale soft musculature often containing hemorrhages. Carcasses of slaughtered swine with PSS are blanched, wet and may drip excessive amounts of fluid. The meat is referred to as pale, soft, exudative (PSE) pork. Shoppers discriminate against it in the market place.
The basic abnormality is an inherited defect in the mechanism for uptake, storage and release of calcium in muscle fibers. Efforts to eliminate PSS through genetic selection have led to success in identification and elimination of a stress gene in many genetic lines but this trait is also linked to heavily muscled phenotype. A polymerase chain reaction test is widely available and used to identify hetero- and homozygous carriers of the halothane gene; both types of carrier animals should be culled.
Prolapse of rectal or vaginal tissues usually occur sporadically in swine but when there is a common cause, can appear as an outbreak. Although seldom seen in nursing pigs, all other age groups are susceptible.
Prolapse of the rectum is most often the result of cold stress (piling for warmth), transport stress (piling in trucks), or from severe coughing. The prolapse may also be associated with severe enteritis from any cause, especially enteritis caused by salmonellosis or ascariasis in young pigs. Other causes of the enteritis can include intestinal mycosis following prolonged use of antibiotics or chemotherapeutic agents. The feeding of whey, brewer’s grains, or low fiber diets has preceded some outbreaks. Rectal prolapse can also occur as a result of severe coughing or straining caused by constipation, cystitis, vaginitis or urethral obstruction. Rectal stricture is a common sequel to prolapse of the rectum. The condition can be repaired surgically by amputation or, if the tissue is not overly traumatized, by replacement followed by use of a purse-string suture. “Rectal tubes” can also be used in repair of prolapses.
Prolapse of the vagina and/or rectum sometimes occurs as a consequence of flaccidity and relaxation of the birth canal in sows close to parturition. Prolapse of the vagina usually occurs first and is followed by prolapse of the rectum.
Zearalenone, a mycotoxin found in several feed grains, can cause vulvovaginal edema and irritation in prepuberal gilts or sows. Straining often leads to prolapse of the vagina and, perhaps, the rectum. Similar lesions can be caused by estrogenic substances in grains, certain pastures (including alfalfa) and therapeutic agents, and in products given to stimulate estrus. Genetic factors have been shown to contribute to prolapses of the vagina and uterus in some breeds.
When prolapse occurs in an outbreak situation, effort needs to be directed towards rapid identification of the triggering factor(s). Response to individual treatment of prolapse is poor with the exception of those cases identified within a few hours of their occurrence.
Pustular dermatitis is usually observed only in nursing piglets. It is caused by a beta-hemolytic, Lancefield type C, streptococcal infection. Pustules appear in the inguinal area and inner surface of the rear legs but occasionally occur at other locations. The pustules soon rupture and are replaced by dark brown to black crusts. The streptococci are easily isolated from pustules. The piglets usually recover spontaneously. Recovery may be hastened by treatment with an appropriate antibiotic.
Rabies is a highly fatal viral disease that occurs in swine bitten by an infected carrier animal. The incubation period is quite variable: nine days to four months. Clinical signs are similar to those described in other species and include sudden onset of incoordination, prostration, chewing movements, excessive salivation, inability to squeal, muscular spasms and tremors, and perhaps twitching of the nose. Death usually occurs within 72 to 96 hours of onset of clinical signs. Furious type rabies seldom occurs in swine. There are usually no gross lesions. Microscopic lesions are typical for viral encephalitis but are quite variable and inclusion bodies are often not present. Diagnosis is confirmed through fluorescent antibody staining on brain sections.
Ringworm (fungal infection) occurs occasionally in swine and may affect any age group. Although cases often are sporadic, occasional outbreaks affect many animals, especially sows. Most ringworm is caused by the fungi Microsporum nanum or Trichophyton verrucosum.
Lesions can occur anywhere but on older swine are usually seen on the neck or behind the ears. Ringworm lesions begin as brown expanding areas a few centimeters in diameter but eventually may enlarge to five to ten centimeters. Mature lesions have a central, brown crust; hair loss is minimal or absent and lesions are non-pruritic. In adult swine, ringworm must be differentiated from sarcoptic mange especially if lesions are behind the ears. In young growing pigs, ringworm must be differentiated from pityriasis rosea and exudative epidermitis (“greasy pig”). Diagnosis of ringworm usually can be confirmed by microscopic examination of skin scrapings or by histopathologic examination of skin lesions.
Ringworm is usually self-limiting but lesions may require months for healing to occur. Lesions are most common during the winter months. Ringworm can be treated orally with nystatin or griseofulvin but typically is left to resolve on its own. Ringworm should be considered contagious to people.
Thin sows lying on hard floors in farrowing or gestation crates may develop ulcers over the spine of the scapula. Contributing factors include poor body condition, lack of adequate bedding or mats, prolonged recumbency while farrowing or nursing piglets, high humidity or wetness (often from coolers used during hot months), and reduced activity because of confinement. Lesions develop and are more severe during the three weeks after farrowing. The ulcers are the result of pressure ischemia leading to skin necrosis over the spine of the scapula. Control measures including maintaining a higher level of conditioning (fat) in sows and assuring crates are of adequate size to allow frequent repositioning.
Young pigs on concrete or other hard floors often develop pressure related lesions on the knees, coronets or at other sites over bony prominences. Although lesions may appear insignificant initially, they may become infected and lead to bacteremia with metastasis to joints or other sites, most frequently with Streptococcus spp or Arcanobacterium pyogenes. Losses can be substantial. Prevention is achieved through good sanitation, provision of good quality flooring materials, and use of floor mats.
This abnormality of neonatal piglets is characterized by lateral extension of the hind legs with inability to adduct the legs; front legs may be variably affected. The principle lesion in affected muscles is myofibrillar hypoplasia related in part to delayed development, and in part to degenerative change.
Proposed causes or suggested risk factors include a genetic predisposition, slippery or sloped floors, porcine stress syndrome (PSS) in the parents, dietary deficiencies, and low birth weights or tremors in piglets.
If affected piglets are helped to nurse and protected from accidental injury by the sow, many will recover in one to two weeks. Tying the front legs or the back legs loosely together with sticky tape will increase the likelihood of survival. Selection of breeding stock with no tendency to produce affected litters will reduce incidence.
Sunburn is injury to the skin caused by excessive exposure to the ultraviolet rays of sunlight. Pigs that are unaccustomed to direct sunlight may be sunburned if not exposed gradually to their outdoor environment. The white or light-colored breeds are more severely affected. Although suckling and weanling pigs are most likely to be affected, all age groups are susceptible. The ears and back get more direct exposure to sunlight and often are more severely sunburned. Sunburned skin is reddened, edematous, hot, and painful. Affected areas later appear roughened and may peel. A common clinical presentation of sunburned pigs is a brief “attack” of pain manifested as squealing or dipping the back while walking. In some cases, pigs may drop to their stomach, then get up and walk. Presumably, this is response to a feeling pain over the lumbar area. There have been reports of abortions associated with sunburn.
Photosensitization should be differentiated from sunburn. It occurs only in areas of white skin. Lesions result when pigs ingest, are injected with, or come into skin contact with a photodynamic agent and then are exposed to sunlight. Sunlight includes wavelengths that activate the photosensitization process. Photosensitizing agents are present in some pastures (alfalfa, clover, oats, rape, buckwheat, others). Also, several common pharmaceuticals (phenothiazine, tetracyclines, sulfonamides, others) may act as photosensitizing agents. The mechanism of tissue injury probably varies with the different agents.
Lesions tend to be more severe with photodynamic dermatitis than with sunburn, often resulting in exudation of serum onto the skin’s surface. Exudation is followed by drying and fissuring. The lesions are pruritic. Skin necrosis with sloughing of severely affected areas often follows. Conjunctivitis, sometimes with corneal opacity and temporary blindness, may accompany photosensitization.
Pigs with sunburn or photosensitization should be kept out of sunlight. Photosensitizing agents, once identified, should be avoided.
Torsions of the stomach and/or the intestines around the dorsoventral axis of the mesentery occur sporadically in pigs. Affected animals die quickly without any warning, and will appear pale and bloat very rapidly after death. There is no single, proven cause. Factors believed to contribute to torsions include: rapid ingestion of a large amount of feed or water (as with once per day feeding), overly crowded pens with associated piling and competition for feeder space, use of highly fermentable ration ingredients that produce excessive amounts of gas in the stomach or colon, and advanced pregnancy. Torsion of stomach seems more prevalent in sows that become agitated during once daily feeding. Torsion of intestine and/or colon must be differentiated from hemorrhagic bowel syndrome (HBS).
In swine, gastric ulceration refers to the destruction of part(s) or all of the pars esophagea (non-glandular stomach) with the formation of single or multiple bleeding ulcers.
The lesions occur in pigs from weaning onwards; the prevalence is variable but high (5-90%) in most swine-producing areas. Clinical signs are usually only noticed in pigs eight weeks of age or older, with highest prevalence in pigs 120 pounds to market weight. Ulcers occur in all breeds, both sexes and in most major swine-raising countries.
Ulceration of the pars esophagea (UPE) was first reported in Illinois in 1897. Subsequently, the lesion was identified in at least 30 other countries. Although the ulcers most often are subclinical, death losses have been severe enough that much research has been directed at identifying cause(s) and risk factors.
The etiology is unknown but is likely multifactorial and represents the culmination of various permutations of any of multiple risk factors. Risk factors are largely empirical, discerned at the time animals experience higher incidence of the disease. Recently, inconsistent feed consumption associated with respiratory disease outbreaks and/or hot weather seems to be of greatest concern. Other risk factors commonly mentioned include:
- The feeding of finely ground feed (< 400 µm particle size).
- Pelleted rations, perhaps because of the finely ground feed used in making pellets.
- Concentrated, nutrient dense diets that are low in fiber.
- Stress factors (e.g. anxiety, fear, pain, fatigue, crowding, fasting, prolonged transportation, social stress from mixing with unfamiliar pigs, poor air quality, etc.) are frequently suggested.
- Greater occurrence in hot, summer months may be related to inconsistent feeding behavior or stress associated with access to water.
- Out of feed events. This may be a result of inconsistent feed availability from plugged or empty feeding systems or be the result of disease-induced anorexia.
- Greater occurrence reported in barrows (versus gilts) and in high-lean genotypes.
- Feeding rations with copper as a growth promoter, perhaps without adequate zinc.
- Ad libitum feeding of cheese whey or skimmed milk has resulted in increased prevalence.
- Diets high in wheat or cornstarch, compared to barley or milo, and/or low in protein.
- High levels of unsaturated fats in the diet, often with inadequate vitamin E.
Infectious organisms and use of non-steroidal anti-inflammatory agents and the presence of Helicobacter pylori are associated with human gastric ulcers that occur in glandular portions of fundus and pylorus. When pigs have been used as models for human ulcers, ulcers are induced in glandular mucosa. However, naturally occurring ulcers in pigs are in the non-glandular pars esophagea. A primary infectious etiology has not been proven nor is likely for swine. Several agents have been associated with increased prevalence and severity of UPE, including other Helicobacter spp or Gastrospirillum spp, but a causal role has never been established. In some severe “outbreaks” of gastric ulcers in swine, porcine circovirus type 2 (PCV2) has been demonstrated within lesions. Gastric ulceration is a common sequel to outbreaks of swine influenza and porcine respiratory disease complex (PRDC), particularly during summer months.
Both etiology and epidemiology are speculative. Epidemiology is difficult to assess. Risk factors that appear important in one herd or production system do not remain consistently important across others.
Irrespective of cause or risk factors, the effects are thought to be a derangement of normal gastric function. An abnormal fluid content in the stomach results in changes in the pH gradient that normally exists between the terminal esophagus and the pylorus. This results in an excessive, gastrin-stimulated acid secretion. The excessive acidity, lower than is normal at the pars esophagea, initiates changes in the stratified squamous epithelium (hyperkeratosis) that may ultimately lead to ulceration. Pre-ulcerative hyperkeratosis is extremely common in growing swine, probably because of high concentrate/low fiber diets. The pars esophagea undergoes hyperkeratosis and parakeratosis which develop fissures that expose the underlying lamina propria. If the insulting acidity persists, or animals become anorexic, part or all of the stratified squamous epithelium peels or sloughs off and leaves one or more ulcers. Blood vessels of various sizes in the lamina propria are eroded and hemorrhage begins. If blood loss is slow, melena, generalized pallor, and anemia may be observed. If a few large vessels are eroded, the animal may die from an acute massive hemorrhage. In some pigs, the ulcers may be recovered with epithelium and heal uneventfully. Occasionally, resolution of lesions results in stricture of the terminal esophagus or pars esophagea.
Pre-ulcerative hyperkeratosis of the pars esophagea is common as a precursor to actual ulceration. Hyperkeratosis does not appear to influence feed consumption nor is it noticeable clinically. In fact, most swine are subclinically affected, evidenced by the high prevalence of lesions in apparently normal pigs at slaughter. Withholding feed will cause some pre-ulcerative lesions to erode in a relatively short time, as little as two to three days.
Clinical effects of ulcers are usually related to blood loss. Acutely affected pigs may be found dead with pallor. Others may have black tarry feces (melena), anemia, and generalized pallor. Other signs that sometimes can be observed include anorexia, grinding of the teeth, or unthriftiness.
Pigs that die suddenly have pallor of the skin and internal organs and tissues. There may be large blood clots in the stomach and/or blood mixed with ingesta, throughout the intestine. The intestinal, and/or colonic contents are often very dark, black, or “tar-like.” The entire pars esophagea may be eroded to muscular wall giving the false impression of intact glandular mucosa.
Ulcers typical of UPE occur only in the non-glandular region (pars esophagea) of the stomach at the junction of stomach and esophagus. Pigs that are in the early stage of developing ulcers have an altered pars esophagea which, instead of being snowy white, is raised, roughened, somewhat nodular, usually bile stained, and sometimes fissured with hyperkeratosis. Ulcers vary greatly in size, shape, number and depth. Large ulcers often are deep and have smooth, rolled and raised borders. Sometimes the ulcerated area involves the entire pars esophagea and may partially obstruct the esophagus. The terminal part of the esophagus may also be hypertrophied. In animals that have recovered from deep ulcers, a puckered or stellate scar often remains. Complete destruction of the pars esophagea is easy to miss at necropsy; the color of that area may be a uniform gray and without hemorrhage. The absence of clotted blood in the stomach does not rule out UPE; careful examination of the pars esophagea is warranted since hemorrhage may be intermittent. Death caused by UPE does require a large amount of clotted blood to be found in the stomach at the time of death.
Differential diagnoses include other causes of hemorrhagic diarrhea such as porcine proliferative enteritis, swine dysentery, salmonellosis, or whipworms.
Pigs suspected of having ulcers should be separated from the herd. If pale or anemic, treatment may include Vitamin K and hematinics, although treatment is of questionable efficacy. Access to fiber (hay, pasture) will sometimes aid in recovery.
Prevention is based on correcting those risk factors suspected of contributing to ulcer formation (see under Etiology). Minimizing stress and preventing out of feed events via consistent feed availability/delivery is always warranted. Altering the ration to minimize the effects of some of the possible risk factors is helpful. Changing to a more coarsely ground feed (>700 µm), including changing from a pelleted diet to a meal diet, is often recommended. The quality of the feed ingredients should be improved if some of the feedstuffs were stored for long periods or of poor quality. Successful control of swine respiratory diseases, especially swine influenza, has decreased the losses attributable to UPE on some swine farms.
See the table: Diseases Associated with Hemorrhage in Intestine
A syndrome characterized by turning of the head to the affected side and a tendency to circle in that direction. The condition usually occurs in young, growing pigs. The syndrome is a consequence of either bacterial meningitis affecting the vestibular nerve or pharyngitis with extension of the infection up the Eustachian tube to the middle and internal ear. At necropsy, exudate often is demonstrable in the middle ear.
Tail-biting, ear-biting, flank-biting or navel sucking behavior can be serious in groups of growing pigs, particularly when confounded by secondary bacterial infections. Through careful observation, one can often identify the few individuals within an affected group that are responsible for the abnormal behavior and are inflicting trauma on numerous pen-mates. The cause of the offending behavior is too often simply ascribed to “stress.” A disciplined approach is required to identify the true source(s) of the stress, which may include: facility limitations (inadequate feed or water space, overstocking), nutritional compromise (mineral or salt imbalances in rations, maladjustment immediately post weaning), environmental inadequacies (drafts, full effluent pits, temperature variation, high humidity), or management factors (co-mingling pigs, out-of-feed events, poor hygiene, concurrent infectious diseases). Control requires careful observation at two levels, first to accurately identify the offending pigs and second, to identify the risk factors that may be contributing to the aggressive behavior. It is important that the aggressive pigs be separated from the group to prevent more cases. In addition to being removed to a hospital pen environment, pigs with severe lesions will likely require systemic antibiotic therapy to prevent extension of bacterial infections locally or systemically. The administration of anti-inflammatory medication may also be warranted. Concurrently, the risk factors and potential contributors to stress should be systematically analyzed and eliminated.
This mosquito-borne Flavivirus can infect pigs; however, the virus does not seem to replicate in high enough numbers to permit transmission to other pigs, birds, or insect vectors. Infection is inapparent in swine and thought to occur only rarely.