Respiratory[1]
Atrophic rhinitis is caused by combined nasal infections with Bordetella bronchiseptica, and Pasteurella multocida types A or D. This condition is much more prevalent in commercial swine than in pet pigs, but is still a recognized disease. This condition should be even less common in properly vaccinated pet pigs. Atrophic rhinitis is precipitated by respiratory epithelial colonization with Bordetella and then a subsequent infection with Pasteurella. Pathogenic Pasteurella strains then excrete a pathogenic leukotoxin that initiates nasal turbinate resorption. The presence of Bordetella in the nasal cavity is necessary for Pasteurella to take hold. Atrophic rhinitis causes permanent deformities of the maxillary and nasal bones secondary to the turbinate necrosis. Once established, Pasteurella also creates a cytotoxin that destroys osteoblasts of the nasal conchae. The cytotoxin also spreads hematogenously to the epiphyses of the long bones where it also damages osteoblasts and limits bone growth.
Bordetella alone causes a mild rhinitis with sneezing and nasal discharge of 3-6 month duration, without maxillary deformities.
Treatment of atrophic rhinitis is a 3 week course with a tetracycline antibiotic. Bony deformities are permanent.
The most common causes of lung pathology in pet pigs Mycoplasma hyopneumoniae and pulmonary edema secondary to left ventricular heart failure.
Mycoplasma, commonly referred to as Enzootic Pneumonia, is a common pulmonary pathogen in both commercial and pet pig populations. Clinical signs include a loud non-productive cough, dyspnea and expiratory effort, ocular and nasal discharge, and a rough hair coat. If the pathogen infects the inner or middle ear, you will see a head tilt towards the effected side, nystagmus (fast phase away from the lesion), and ventrolateral strabismus on the side of the lesion.
Systemically infected pigs may show purple discoloration (easier to see in white pigs) of the ventral abdomen and extremities, fibrinous pleuritis and/or pericarditis is also possible. It is not uncommon for there to be mixed infections with other gram negative pathogens such as Pasteurella or Actinobacillus.
In young pigs dissemination of the bacteria and subsequent mycoplasma polyserositis is possible. The most commonly effected joints are the stifle, elbow, shoulder, and hip, that can lead to non-weight bearing lameness, periarticular swelling, weight loss and fever. Synovial fluid from affected joints will show protein over 500mg/dL and neutrophils over 1000/dL. Polyserositis is often from Mycoplasma hyosynoviae or hyorhinis.
Macrolide antibiotic therapy is the mainstay of mycoplasma treatment. NSAIDs are also very beneficial for fever reduction and overall comfort of the pig.
The left ventricular heart failure that leads to pulmonary edema is caused by Zenker’s necrosis (Mulberry Heart Disease). This is a selenium responsive disease that is very common in pet pigs. Clinical signs include collapse, coma, tachypnea, labored breathing, marked tachycardia (greater than 250bpm), tracheal crackles, cyanosis, and occasionally tachyarrythmias.
Treatment involves providing oxygen, improving cardiac function, and reducing the circulating blood volume. This is achieved with Lasix 1mg/kg q 2-4h, vitamin E 1500 IU IM daily for 3-4 days, selenium/Bo-Se 1-1.5ml/50kg BW, lidocaine, quinidine, or digoxin for cardiac related problems.
Other potential causes of pneumonia in pet pigs include Glaesserella Parasuis, Actinobacillus Pleuropneumoniae, and swine influenza. As previously mentioned pet pigs can get these diseases as well as many others that commercial swine get. This list is extensive and beyond the scope of this Guide since they are predominantly commercial swine diseases.
