40.

HAEMOPHILUS PARASUIS(GLASSERS DISEASE)

Pigs can be colonized by different microorganisms before weaning, but some of those early
colonizing agents are potentially pathogenic. This is the case with Haemophilus parasuis, a
commensal organism of the upper respiratory tract of swine that causes severe systemic disease
characterized by fibrinous polyserositis, arthritis, and meningitis. Disease has a sudden onset, short
course, and high morbidity and mortality. Young animals (48 wk old) are primarily affected,
although sporadic disease can be seen in adults (eg, introduction of a naive adult to a healthy herd).
Survivors can develop severe fibrosis in the abdominal and thoracic cavities, which can result in
reduced growth rate and carcass condemnation at slaughter. Glssers disease is seen worldwide,
and its incidence appears to have increased since the introduction of porcine reproductive and
respiratory syndrome

Etiology

Haemophilus parasuis is a small, pleomorphic, and fastidious, Gram-negative rod. It can be grown
on blood agar, as satellite colonies, near a streak of staphylococci or source of nicotinamide adenine
dinucleotide (NAD). The organism often can be isolated from the nasal cavity or tonsil of normal
pigs. It frequently can be isolated from other disease processes, especially pneumonic lungs. As a
septicemia, H. parasuis has predilection for growth on serosal surfaces (peritoneum, pleura,
pericardium, joints, meninges).

At least 21 serovars have been identified with additional untypeable strains also common. Some are
more commonly associated with disease than others and groups of pigs often harbor several
different serovars. Serovars 4, 5, 13 and 14 are more prevalent in North America. Cross-protection
may occur but appears to be incomplete. For example, bacterin prepared from serovars 4 and 5
usually protects against homologous and heterologous 4 & 5 serovars and reduces the number of
lesions caused by serovars 13 & 14. Virulence appears to be related to capsular antigens but is not
necessarily related to immunogenicity.

Epidemiology

H. parasuis is widely distributed in the swine population and usually causes no disease. Neonatal
pigs are exposed to and colonized by the organism early in life. Colostral antibodies usually protect
pigs from disease while they gradually develop an active immunity by the time they are 7-8 weeks
old. It is presumed that young pigs without either passive or active immunity can develop
fulminating disease if exposed to H. parasuis. Unusual stresses, such as weaning, prolonged
transport or other diseases may predispose to outbreaks.

Pathogenesis

Pathogenesis is poorly understood but vasculitis plays an important role in the development of
lesions. H. parasuis can be a primary pathogen or be associated with other diseases such as porcine
reproductive and respiratory syndrome virus (PRRSV) or swine influenza virus (SIV). Perhaps the
lesions or stress of those diseases permit access of the organism. Presumably, there is a period of
bacteremia since H. parasuis often localizes at multiple sites.

H. parasuis has a predilection for the leptomeninges and brain, often localizes there and stimulates
an inflammatory reaction. In addition, the organism often can be isolated from one or more serosal
surfaces, often as cause of inflammation and fibrinous exudates. Damage to vasculature, apparent
microscopically, probably facilitates formation of inflammatory exudate and increased synovial
fluid in joints. The organism is also a contributor to pneumonia by systemic distribution or
expanding lesions in typical bronchopneumonia.

Clinical signs

Clinical signs are seen mainly in pigs 48 wk old, although the age of affected animals may vary,
depending on the level of acquired maternal immunity.

Peracute disease has a short course and may result in sudden death without the presence of
characteristic gross lesions; petechiae may be seen in some organs in these cases, indicating
septicemia.

The typical clinical signs of acute Glssers disease include high fever (41.5C), severe coughing,
abdominal breathing, swollen joints, and CNS signs such as lateral decubitus, paddling, and
trembling. These signs may be seen jointly or independently. Chronically affected animals may
have a reduced growth rate as a result of severe fibrosis in the thoracic and peritoneal cavities.

Dyspnea and coughing not usually associated with Glssers disease have been described, together
with H parasuis isolation from the lungs of pigs with catarrhal purulent bronchopneumonia and
even fibrinohemorrhagic pneumonia. However, H parasuis is not considered a significant cause of
coughing.

Disease prevalence is modulated by concomitant environmental stressors as well as by viral

infections affecting the immune system, mainly porcine reproductive and respiratory syndrome and
porcine circovirus type 2 systemic disease.

Pathologic findings

Peracute disease may cause petechiae in some tissues, with no gross lesions observed.
Histologically, these pigs show septicemia-like microscopic lesions such as DIC and
microhemorrhages. Increased fluid in the thoracic and abdominal cavities, without the presence of
fibrin, can also be seen in peracute cases.

Acute systemic infection is characterized by development of fibrinous polyserositis, arthritis, and

meningitis. The fibrinous exudate can be seen on the pleura, pericardium, peritoneum, synovia, and
meninges and is usually accompanied by an increased amount of fluid. Fibrinous pleuritis may be
accompanied by cranioventral consolidation (catarrhal-purulent bronchopneumonia). Lack of
characteristic gross lesions is also common in swine showing CNS signs. Chronically affected pigs
usually have severe fibrosis of the pericardium and pleura, which may or may not be present in the
peritoneal cavity.

Diagnosis

Diagnosis is based on observation of characteristic clinical signs and lesions, in association with
detection of H parasuis in affected swine by isolation or by molecular methods such as PCR.

Most current diagnostic methods do not differentiate virulent from nonvirulent isolates, so it is
important to sample only from systemic sites such as pleura, pericardium, peritoneum, joints, and
brain. Isolation of H parasuis from the upper respiratory tract has no relevance in the diagnosis of
systemic infection. Samples collected from clinically affected animals that were euthanized increase
the chances of isolation. Recently, a multiplex PCR technique able to differentiate between virulent
and nonvirulent isolates has been developed. This technique might be used to prevent introduction
of pigs carrying potentially virulent strains onto farms that are free of clinical Glssers disease.
Differential diagnosis

Differential diagnoses of Glssers disease include infections by Streptococcus suis, Mycoplasma

hyorhinis, septicemic Escherichia coli, Actinobacillus suis, Erysipelothrix rhusiopathiae,
and Salmonella Choleraesuis.

Treatment and control

H parasuis is one of the few gram-negative organisms that can be successfully treated with
synthetic penicillin. Other antimicrobials used include ceftiofur, ampicillin,
enrofloxacin, erythromycin, tiamulin, tilmicosin, florfenicol, and potentiated sulfonamides.
Individual treatments must be given parenterally to see a significant effect, and all pigs in the
affected group (not just those showing clinical signs) should be treated. Preventive treatments can
be given via water or feed medication. Either commercial or autogenous vaccines can be used to
control H parasuis infection, although their efficacy has been variable. The broad range of
potentially pathogenic serovars and genotypes has impaired the development of a universal vaccine
for H parasuis. Homologous protection between isolates from the same serovar group is relatively
satisfactory, whereas heterologous protection is restricted to a few serovars. So far, several
universal (independent of serovar) vaccine prototypes have been experimentally developed but
are not yet commercially available.