Furnishing adequate housing, nutrition, and care will minimize disease in PBPs, as in other species. Many diseases of PBPs are similar to those of domestic commercial swine, although some are more common in PBPs.
Gastritis and gastric foreign bodies are common in PBPs because they are omnivorous and prone to ingest many types of objects. Keeping PBPs indoors where they are unable to root and restricting calorie intake to prevent obesity probably contribute to this continual search for food. Dividing the daily ration into two or more portions and furnishing low-calorie foods (eg, lettuce, cabbage, celery, carrots, or green grasses) may help satisfy appetite. If an ingested foreign body is small or pliable enough, it may pass through the GI tract and cause mild gastritis that is self-limiting or only requires antibiotic therapy. Larger objects may remain in the stomach or partially pass into the duodenum or a more distal part of the small intestine. Clinical signs such as vomiting and colic can be acute but may be more subtle and increase in intensity over several days or weeks. Radiographs may reveal obvious foreign material or delayed gastric emptying. CBCs may indicate infection but are usually not informative; serum enzyme and electrolyte panels may only reflect dehydration. Surgical correction is indicated but may not be successful if extensive necrosis of GI tissue is present. Fluid replacement and nutritional supplementation plus antibacterial therapy and tetanus prophylaxis are indicated in convalescing PBPs.
Lower GI obstruction due to bowel stricture occurs in geriatric PBPs. Anorexia, scant fecal production, and a bloated abdomen with massively distended intestines seen radiographically are typical. Sedation and endoscopic examination of the oral cavity, esophagus, and stomach are indicated to exclude other problems. Exploratory laparotomy and anastomosis with or without bowel resection is usually remedial.
Colibacillosis or Escherichia coli diarrhea is generally an important disease in young PBPs. Mortality may be high in piglets that have not ingested adequate colostrum in their first 24 hr of life. Older PBPs apparently develop resistance to colibacillosis. Diagnosis is through signalment, history, and fecal culture. Sanitation to minimize infective doses of pathogenic coliforms in the environment of young, nursing PBPs is important for prevention. Commercial swine vaccines to prevent colibacillosis are available but must be given to sows before farrowing to stimulate immunity and secretion of IgA into the milk. Treatment is based on in vitro antibacterial sensitivity testing, but antibiotics such as oral or injectable gentamicin or injectable ceftiofur are usually effective.
Enterocolitis from Salmonella typhimurium infection can affect PBPs of any age, but it usually occurs after weaning. Sources of salmonellae include waste food from overturned garbage cans, exposure to carrier swine (such as the dam), or fecal material from other animal species. Mild to severe diarrhea with mucus and blood can result. Diagnosis is through signalment, history, and fecal culture or PCR. Salmonella spp are characteristically resistant to many antibiotics, so in vitro antibacterial sensitivity testing is important. Parenteral gentamicin at 2.2 mg/kg/day for 3 days may be effective in the interim. Untreated PBPs may die. Some recovered PBPs may develop rectal stricture after enterocolitis, resulting in megacolon and a distended abdomen. Subsequent straining to defecate can cause rectal prolapse. Surgical correction of the rectal prolapse will not correct the underlying problem. Owners should be advised that many Salmonella spp, including S typhimurium, are zoonotic. Healthy PBPs may be tested via fecal culture or PCR to determine their salmonella status. Multiple tests are more accurate predictors than single tests. Vaccines available for commercial swine have not been used much in PBPs.
Bacteremia or septicemia after S choleraesuis infection may also affect PBPs, usually after weaning. Sources of infection are similar to those of S typhimurium. Mild to inapparent diarrhea followed by fever, lethargy, anorexia, cyanosis of extremities, recumbency, and death may ensue. Diagnosis, treatment, prevention, and zoonotic potential are similar to those of S typhimurium; zoonosis is mainly a threat in immunocompromised people.
Constipation may be seen in PBPs; however, each normal bowel movement of a PBP is typically composed of one or more cylindrical formations made up of smaller, multiple fecal balls that may give the impression that the PBP is constipated. True constipation may occur due to low water intake in sedentary PBPs or to an actual disease. Careful evaluation is warranted before treatment is administered. Enemas may be contraindicated if there is pathology such as colitis. In simple constipation, fecal softeners or mild laxatives such as sodium sulfate or magnesium sulfate may be used. These should be given with food, if possible, because forced PO administration can result in aspiration pneumonia and death, especially with mineral oil. Encouraging increased water intake by flavoring with fruit juice or liquid gelatin may be helpful. Regular exercise is also beneficial to promote normal feces.
Rectal prolapse occurs due to straining from bowel irritation from diarrheal disease, rectal stricture after S typhimurium enterocolitis or previous rectal prolapse repair, cystitis or urolithiasis, persistent coughing, dystocia, or possibly genetic predisposition. Small, uncomplicated, recent rectal prolapses may be repaired via anesthesia and purse-string closure of the rectum that allows for minimal passage of feces. Larger, complicated prolapses require surgical excision. Recurrence is less likely after surgery but is possible regardless of method of repair.
Lymphosarcoma, lymphoma, and carcinoma of the intestines occur in aged PBPs. Signs are vomiting, anorexia, melena, anemia, and chronic weight loss followed by death or euthanasia. Confirmation is by postmortem histopathology.
Dry, flaky skin with minimal to severe pruritus is seen in virtually all PBPs. Wiping down the skin with wet towels each week will remove the flakes. Moisturizing lotions (eg, aloe vera) also temporarily alleviates this problem. Fatty acid supplementation can be used as a more longterm remedy, but caution must be exercised not to promote obesity.
Sarcoptic mange is the most important ectoparasitic disease of PBPs. Intense pruritus and dermatitis are the basis for a presumptive diagnosis. In many cases, the owners have pruritic skin lesions on the arms or abdomen. Examination of skin scrapings (deep enough to contain some blood) from several sites usually confirms the diagnosis in advanced cases but may be negative in less advanced cases if very few mites are present. In young PBPs, the source of infestation is usually the dam; in older PBPs, the source is usually other infested pigs. Young PBPs isolated from other pigs and kept as pets may harbor mange mites as a subclinical problem until mite populations increase sufficiently to make the condition obvious. Treatment with ivermectin (300 mcg/kg, SC, repeated in 2 wk) or doramectin (300 mcg/kg, IM, repeated in 3 wk), is indicated. Recently acquired young PBPs should be given a routine preventive injection of either parasiticide when first presented for examination.
Melanoma is an important skin tumor in swine. Tumor removal and evaluation of metastatic potential through histopathology is important for prognosis. Spontaneous regression of melanomas, with subsequent depigmentation of the hair, skin, and iris, is occasionally seen in PBPs; affected swine usually have normal life spans.
Sunburn may develop in PBPs exposed to sudden, high-intensity sunlight. Skin lesions may or may not be obvious, but affected PBPs appear painful and seem to have hindlimb weakness or paresis. A sunburned PBP may be “down in the back legs” and show intense pain with vocalization. A thorough history is important for the diagnosis. Exposure to further sunlight should be prevented. Symptomatic treatment is remedial.
Bleeding back syndrome (dippity pig syndrome) is of unknown etiology. Signs are almost identical to those of sunburn (pigs dip their backs, vocalize, and show signs of extreme pain) but with no history of sun exposure. Circular, serum-oozing lesions of various sizes are seen on lumbar skin surfaces. Affected PBPs recover in several days with restricted activity with or without symptomatic treatment. The condition may recur in some animals.
Erysipelas, caused by Erysipelothrix rhusiopathiae, is a generalized bacterial infection that affects swine. For details on clinical signs, diagnosis, and treatment, see Swine Erysipelas.
Lameness due to lower back, hindlimb, or forelimb weakness is common in PBPs. Because of their conformation, PBPs are susceptible to muscle pulls, ligament damage, and fractures of the back and limbs. Because PBPs usually struggle against manual restraint (predisposing to injury), sedation or anesthesia is often used for procedures such as prolonged examination, radiography, foot trimming, blood collection, and dental work. Tiletamine-zolazepam at 2.2 mg/kg body weight, IM (in the ham), provides excellent analgesia and chemical restraint for these minor procedures; recovery, although smooth, is prolonged and requires careful monitoring. Gas anesthesia is also used and has the advantage of rapid recovery time. Fasting for 24 hr and withholding water for 4–6 hr before sedation or anesthesia is recommended.
PBPs with injuries to the back or limbs are usually treated with anti-inflammatory drugs, such as buffered aspirin with antacid, flunixin meglumine, or glucocorticoids (eg, dexamethasone). Polysulfated glycosaminoglycan and/or glucosamine/chondroitin sulfate products may be tried in nonresponsive cases.
Fractures of the distal humerus and elbow area and femur are common. These occur from jumps off furniture (distal humerus), dog bites (elbow area), restraint (elbow area and femur), equine kicks (femur), and other trauma. Repair via pins, screws, plates, and external devices successfully restores some range of motion if fractures are immobilized properly and any sepsis is controlled.
Infectious arthritis may affect the very young to older PBPs. Lameness with or without joint swelling in one or more limbs is the usual clinical finding. Erysipelothrix rhusiopathiae, Streptococcus spp, Mycoplasma hyosynoviae, M hyorhinis, Staphylococcus spp, and Haemophilus parasuis are possible causes. Treatment early in the disease course with an effective antimicrobial (eg, lincomycin at 11 mg/kg, bid for 3 days) may be effective. Treatment after chronic changes have occurred, antimicrobial ineffectiveness against the etiologic agent, or misdiagnosis are reasons for treatment failure and persistence of lameness. In chronic cases, pain management with anti-inflammatory drugs should be considered. Polyarthritis from neonatal infection of the navel may be due to various environmental bacteria, including Pseudomonas spp. If degenerative arthritis and joint fusion from chronic inflammation are present after polyarthritis, euthanasia may be warranted. Osteochondrosis may also be considered in shoulder, elbow, hip, and stifle lameness, but this condition is not common in slow-growing, light-muscled animals such as PBPs.
Overgrown and/or cracked hooves are a common cause of lameness. Regular exercise on abrasive surfaces (eg, concrete) will wear hoof ends and help keep them the appropriate length. In PBPs with overgrown, elongated hooves, normal yearly length can be maintained by routine yearly trimming under sedation or anesthesia. Hoof cracks can be caused by overgrown hooves. PBPs with cracked hooves may additionally require antiseptic cleaning with tamed iodine and systemic antimicrobial therapy (ceftiofur at 4.4 mg/kg/day for 3–10 days, or ampicillin at 11 mg/kg, PO, bid for 7–10 days).
Zygomycosis from Mucor spp infection has occurred in the distal hindlimb of a PBP. The large growth that encompassed the entire foot was composed of infected/abscessed tissue that involved bone. Amputation was remedial.
Tetanus may occur after wound contamination from dog bites, skin abrasions, oral cavity abrasions, or surgical procedures. Tetanus toxoid should be part of the routine vaccination schedule of PBPs at high risk of exposure. If there is no current tetanus toxoid vaccination, tetanus antitoxin (500–1,500 U, depending on body weight) should be administered IM in the neck after recovery from any surgery or dental procedure (eg, trimming of canine teeth). Treatment for tetanus is by massive doses of tetanus antitoxin and penicillin early in the disease, along with tranquilizers, isolation to minimize external stimuli, and supportive therapy.
Systemic bacterial infection can be caused by (in approximate decreasing order of importance) Streptococcus suis type 2, other Streptococcus spp, Salmonella choleraesuis, Haemophilus parasuis,Escherichia coli, other gram-negative bacteria, and Listeria monocytogenes. CNS signs may include fever, depression, incoordination, staggering, postural abnormality, head tilt, circling, nystagmus, seizures, and death. PBPs are most commonly affected from birth through 4–6 mo of age. Treatment with the appropriate antibacterial therapy (eg, extra-label florfenicol, which penetrates the blood/brain barrier) in the early stages of infection is most effective; however, death may be the first clinical sign. Because S suis type 2 is a zoonotic disease agent, care should be exercised to prevent human infection when performing necropsies on pigs dying from suspected CNS disease.
Overheated PBPs may be depressed, inactive, and recumbent and show open-mouth breathing or panting with an initial fever followed by a subnormal and decreasing temperature. The prognosis is grave, but some overheated PBPs may respond to resting on a cool surface and cooling only the head with water for 10–15 min followed by packing ice bags around the head. If the temperature is still not controlled, cold-water enemas can be used while additional areas of the skin surface are packed in ice. Symptomatic treatment is continued as indicated.
Salt toxicity occurs after water deprivation for ≥36 hr followed by sudden rehydration or, less commonly, after prolonged consumption of high-salt foods. Affected PBPs may have seizures, walk aimlessly, or show other CNS signs such as blindness or postural abnormalities. Diagnosis in the affected live animal is confirmed by high levels of serum sodium, usually 160–183 mEq/dL (normal range 142–153 mEq/dL). Gradual rehydration and symptomatic treatment to counteract cerebral edema is indicated, but severely affected PBPs may only be stabilized to a vegetative and blind status. The histopathologic finding of eosinophilic infiltration into brain tissue is also diagnostic.
Seizure from unknown cause occurs in PBPs. Animals <1 yr old seem most susceptible. Frequency may range from 1–2 seizures per month to several per day. Infrequent seizures may require no preventive medication. Diazepam is used to control more frequent episodes. Phenobarbital in addition to diazepam may be required to control the most severe cases. Seizures may cease as the affected PBP ages.
Atrophic rhinitis is an infectious disease of swine that initially causes sneezing, nasal discharge, tearing, and growth retardation. Younger PBPs are more commonly affected. For details on clinical signs, diagnosis, and treatment, see Respiratory Diseases of Pigs.
Pneumonia can be a very serious disease in PBPs because of their relatively small lung capacity. The most common cause of pneumonia is from initial Mycoplasma hyopneumoniae infection (see Mycoplasmal Pneumonia), which immunocompromises the lungs, followed by Pasteurella multocida infection. Young pigs contract these infectious agents from their dams or from mixing with infected pigs after weaning. Antibiotic treatment may be more effective if directed against P multocida, because this bacterium becomes the most important pathogen once coughing is present for several days. Vaccines available for M hyopneumoniae in domestic commercial swine have been used in young PBPs to prevent mycoplasmal pneumonia and subsequent Pasteurella pneumonia. Vaccination in older PBPs is probably unnecessary unless risk of exposure warrants continued use.
Actinobacillus pleuropneumoniae (see Pleuropneumonia in Horses) causes a life-threatening pneumonia that may occur after infection from the sow or exposure to carrier animals. Signs range from coughing, fever, and lethargy to sudden death, depending on the serotype of A pleuropneumoniae. Prompt antibiotic treatment with penicillin or ceftiofur is indicated. Recovered PBPs usually have permanent tissue loss in affected lung areas and may have recurrent respiratory problems. Vaccines available for domestic commercial swine may be used in PBPs if there is an exposure risk.
Swine influenza (see Swine Influenza) is an important viral pneumonia in PBPs that are taken to fairs, exhibitions, and petting zoos and exposed to other pig populations. It is usually self-limiting after 7–10 days but can be fatal. H1N1, H3N2, H1N2, and H2N3 are the most common strains in domestic swine. Multivalent vaccines available for domestic swine could be used in PBPs if indicated. Swine influenza is a zoonotic disease.
Cystitis and urolithiasis are common in PBPs. Signs include frequent urination or straining to urinate. Urinalysis, urine culture, CBC, serum chemistry, radiography, and ultrasonography are important diagnostic aids. A sterile urine sample for culture can be obtained via cystocentesis. Cystitis without triple phosphate crystalluria should respond to extended antibacterial therapy based on in vitro sensitivity testing. Acidification of the urine may minimize recurrence of infection. Nephritis can occur after cystitis as an ascending infection. Leptospirosis may be a primary cause of nephritis. Increased BUN and creatinine values may aid in the diagnosis of nephritis and kidney failure. A 6-way vaccine for leptospirosis is routinely given to breeding PBPs (see Vaccinations) but may also be considered for routine use in rescue operations where many PBPs are housed in close contact. Vaccination may possibly reduce renal shedding of leptospires should PBPs become chronically infected and, therefore, minimize transmission of this zoonotic disease.
In a PBP that is straining and unable to urinate, the bladder size should be reduced immediately by cystocentesis after sedation and radiography (plain or contrast) or ultrasonography to evaluate the location of urethral and bladder stones. If the blockage is in the urethra, cystotomy is recommended (both sexes) to identify and remove calculi in all possible locations. Calculi in the urethra of males may be removed by cutting through the sheath to expose the distal penis, catheterizing the urethra, and backflushing into the bladder. Calculi that cannot be removed by this method must be surgically removed by incising the urethra at the location of the blockage. However, scar tissue at the healed incision may also cause urethral obstruction. Suturing of the urethra is followed by cystotomy and bladder flushing to minimize recurrence and then by inspection for more calculi. The bladder is then closed, and a Foley catheter is inserted into the bladder, tunneled through the abdominal muscles, and sutured to the skin. Several days later, the Foley catheter is occluded, and the urethra is inspected to determine patency and urine flow; if not patent, the Foley catheter is opened again, and the process is repeated several days later. When the urethra becomes patent, the Foley catheter is removed. Although the urethra in females is short, blockage can still occur. Because urethral catheterization is difficult without endoscopy, a Foley catheter is inserted into the vagina and inflated, and a purse-string suture is placed at the vulva. Retrograde flushing through the urethral opening in the vaginal floor is attempted. A cystotomy is then performed to remove all possible calculi, followed by routine closure of the bladder. Foley catheter placement into the bladder may not be necessary. Further treatment includes antibiotic therapy and acidification of the urine. Despite these efforts, some affected PBPs do not recover and require euthanasia. Perineal urethrostomies are usually only temporarily successful because the surgical site becomes occluded by amorphous material or urethral polyps, and patency cannot be reestablished. However, surgical methods have been described to correct failed perineal urethrostomies in PBPs. Rupture of the bladder is a grave complication because normal bladder tone may not return even after stones have been removed and the bladder has been surgically repaired. Laser lithotripsy has been used to fracture urethral calculi not removable by flushing.
Routine urinalysis as part of an annual examination may enable early diagnosis and prevention of serious urinary tract disease in PBPs.
Psychogenic water consumption should be considered in PBPs (especially young PBPs) with polydipsia and polyuria. PBPs may develop a habit of drinking water and urinating frequently because of possible boredom or unknown causes. Cystitis and crystalluria should be eliminated as differential diagnoses. Measuring urine specific gravity before and after a 12-hr water fast will demonstrate whether the affected PBP is able to concentrate urine. Ability to concentrate urine indicates normal kidney function and helps exclude diabetes insipidus. Estimating the daily water intake and urine output will further aid the diagnosis of psychogenic water intake or establish that water consumption and urination are, in fact, normal. Relieving boredom may be helpful to change this behavior. Affected young PBPs typically outgrow this condition. If water is restricted and offered only with meals, care must be taken to prevent salt toxicity.
Chronic kidney failure is a common cause of death in geriatric PBPs. Lethargy, anorexia, dehydration, azotemia, ammonia breath odor, and low temperature are possible presenting signs. Symptomatic treatment such as rehydration and antibiotics (procaine penicillin 22,000 IU/kg/day, IM, for 3 days) may be at least temporarily helpful in less severe cases.
Last full review/revision June 2013 by D. Bruce Lawhorn, DVM, MS