Porcine pleuropneumonia

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Porcine pleuropneumonia

APP infection: Fibrous pleural adhesions seen in chronic disease

Fibrous pleural adhesions in chronic APP disease

"Considerable economic losses are seen due to mortality, growth retardation and the increased need for medication with antibiotics."

Pleuropneumonia in pigs, caused by Actinobacillus pleuropneumonia (APP), is spread rapidly by airborne route or by direct contact. Considerable economic losses are due to mortality, growth retardation, and the increased need for medication with antibiotics.

About Porcine pleuropneumonia


Etiology

Actinobacillus pleuropneumonia is a facultative anaerobic Gram-negative rod. It belongs to the family Pasteurellaceae, which contains the genera Haemophilus, Actinobacillus and Pasteurella. Outbreaks with high mortality are rare in the United States but are still a problem in Europe, Asia, Mexico, and South America. Typically, several herds are carriers for multiple strains of this bacterium. These herds may remain carriers for strains that are incredibly infectious for long periods of time until changes in the environment put stress on the animals. Environmental changes, such as management changes, are likely to precede an outbreak in a carrier herd.

The serotypes

Fifteen (15) serotypes have been described. Serotyping is based on capsular polysaccharides (CP’s) and lipopolysaccharides (LP’s). Some serotypes show structural similarities between the LP chains. This explains the cross reactions seen between certain serotypes.
Each geographical area or country has its own predominant serotype(s). See Table 1.

predominant serotypes

Table 1: Each geographical area or country has its own predominant serotype(s)

The prevalence of the predominant serotype(s) may change with time.

The virulence factors

Differences in virulence between the serotypes or even within the same serotype have often been observed. In general, strains of serovars 1, 5, 9, 10 and 11 are thought to be more virulent than those from other serovars. Most important factors involved in impairment of phagocytic function of macrophages and neutrophils are RTX (Repeats in structural Toxin) toxins (APXI, APXII and APXII) and RTX pattern differs between serotypes. APX IV is produced in vivo only and may be essential for expression of full APP virulence

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Pathogenesis

Transmission of this bacterium occurs via nose-to-nose contact or, rarely, aerosol droplets across short distances. It may also be spread by employees who carry nasal secretions from infected pigs to other buildings or facilities. Porcine pleuropneumonia (APP) only infects the pig’s respiratory tract. Carrier pigs for this bacterium tend to be survivors that carry and shed the bacteria for months following recovery from infection, but animals that contract only subclinical infection by APP can also be carriers. Sows pass the bacteria to neonatal piglets via direct contact.

The incubation period varies greatly and is dependent upon the infectious dose of APP presented in the pig. APP first colonizes the epithelial cells of the tonsils, and eventually, it colonizes cells lining the alveoli in the lower respiratory tract. Damage to the protective features of the pig’s respiratory tract, such as the mucociliary apparatus, by other respiratory pathogens can help APP to reach and colonize the alveoli. APP produces toxins and also stimulates macrophages in the lungs to release inflammatory cytokines. The inflammatory effects, such as increased permeability of the vasculature to immune system components such as complement, normally would help the host to clear the pathogenic bacteria, but APP has mechanisms that allow it to escape destruction by the host immune system. This leads to over-activation of macrophages, which secrete harmful hydrogen peroxide and other toxic compounds, without clearance of the bacteria, resulting in vast lung tissue damage by the pig’s own immune system.


Clinical signs

Clinical signs vary with:

  • the immune status of the animals
  • the stress of adverse environmental conditions
  • the degree of exposure to the infectious agent
  • the virulence of the strain(s) involved
  • other previous or concurrent infections by M. hyopneumoniae, Aujesky’s disease, or Swine Influenza Virus (SIV)

The course of the disease may be peracute, acute, or chronic.

Peracute form: can last as little as 3 hours from onset to death

  • Sudden disease of pigs in multiple pens
  • Fever up to 106.7 deg F
  • Depression
  • Anorexia
  • Slight diarrhea
  • Vomiting
  • Increased heart rate and heart failure
  • Blue discoloration of the skin of the nose, ears, legs, and eventually the whole body
  • Terminal phase:
    1. Mouth breathing
    2. Severe dyspnea (shortness of breath)
    3. Stationary sitting posture
    4. Bloody, foamy discharge from nose and mouth (Swine Diseases, 10th Ed)

peracute APP in pigs
Pigs showing peracute symptoms of APP infection - open mouth breathing, frothing at the mouth, neck extension and sitting.

Acute form: death occurs 24+ hours after onset of infection

  • Sudden appearance of severely ill animals in one or more pens
  • High fever (105 - 106 deg F)
  • Depression
  • Anorexia and reluctance to drink
  • Distinct respiratory symptoms
    1. Severe dyspnea (shortness of breath)
    2. Mouth breathing
    3. Coughing
    4. Sitting position
    5. Foamy, blood-tinged discharge through mouth and nostrils
  • Cyanotic (blue) or reddened skin
  • Heart failure
  • Visible weight loss within 24 hours of onset of symptoms (Swine Diseases, 10th Ed)

Chronic form:

The chronic form develops after the disappearance of acute symptoms

  • Coughing
  • Loss of appetite
  • Growth retardation
  • Easily fatigued by exercise and lag behind other pigs when moved

In chronically infected herds there are often many subclinically diseased animals.

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Post mortem lesions
(Per)acute stage

  • Well demarcated, severe uni- or bilateral necrotizing haemorrhagic pneumonia is found at post mortem.
  • Bronchi and trachea are filled with a foamy, blood-tinged mucous exudate.
  • Fibrinous pleurisy is seens and the thoracic cavity contains a blood-tinged fluid.
haemorrhagic pneumonia
haemorrhagic pneumonia

Haemorrhagic pneumonia seen post mortally in cases of peracute to acute APP infection.

Acute cases

  • Fibrinous pleurisy and the thoracic cavity contains a blood-tinged fluid.
  • Affected portions of the lung are dark reddish-purple to white-colored and are firm and rubbery.
  • The cut surface may present white lines of fibrin around the necrotic areas.

Chronic cases

  • Nodules of different sizes mainly in the diaphragmatic lobes. These nodules are surrounded by a thick capsule of connective tissue.
  • Some areas of adhesive pleurisy. In many cases, the lung lesions resolve, and only a residual, focal adhesive pleurisy is present. A high incidence of chronic pleurisy at slaughter is highly suggestive of pleuropneumonia. Lungs may also tear when removed at necropsy. Large areas of fibrous pleuritis develop in chronic cases of APP.
chronic app infection

Firm grey coloured lungs typical of chronic APP

chronic APP infection

Abscess in a lung caused by chronic APP infection

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For information about the lung scoring system at the slaughterhouse see:

Treatment and Prevention

Parenteral antibiotic treatment in the initial phases of the disease, will help to reduce mortality.

Effective antimicrobials include ampicillin, cephalosporins, florfenicol, colistin, sulfonamides, cotrimoxazole, and gentamicin.

APP Prevention

  1. Farms free of the pathogen should only introduce stock from APP free herds. New stock should be quarantined.
  2. In the presence of organic matter, e.g. mucus, APP can survive for weeks in the environment.  Warm, dry conditions and the use of common disinfectants after thorough washing to remove organic matter are effective to remove APP from the environment.
  3. Determine periods of risk from post mortem examinations, serological testing and clinical examinations and consider strategic medication.
  4. General management principles for controlling respiratory disease are effective
  5. Vaccination with with multivalent inactivated vaccines protect against different serotypes. See Vaccines.

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