Haemophilus parasuis (HPS) can contribute to clinical disease in pigs in three major ways: joint problems, pneumonia and multisystemic disease (Table 1). Although HPS is a common resident of the upper respiratory tract of pigs of all ages, most pigs can harbor HPS in their nose with no ill effects. However, when this organism invades and becomes blood-borne, it can localize in different organs causing a variety of clinical signs. It is also an important contributor to pneumonia.
Clinical signs can look quite different, depending on whether it is acute or chronic, or whether it is primarily affecting the brain, spinal cord, lung, lining (serosa) of body cavities or joints. Clinical signs and onset of disease can be explosive, with sudden mortalities sometimes being the first signs noted.
When acute and uncomplicated, HPS causes acute disease with exudates (fibrin) found on surfaces of lung (Figure 1), heart and abdominal organs, historically termed "Glasser’s disease." Since HPS can invade different organs, the clinical signs and lesions can include sudden deaths, lameness, respiratory distress, disorientation, immobility and paddling, paralysis, ill-thrift or stunting (Table 2).
The percentage of pigs affected within a group (morbidity rate) can vary considerably, from less than 1% to 20%. Many factors affect disease expression and influence the number of animals affected in a group. These factors include: levels of maternal (herd) immunity, age when infected, concurrent infections (viral infections such as porcine reproductive and respiratory syndrome virus, swine influenza virus, porcine circovirus type 2), or environmental stressors (e.g. temperature variation, air quality), and exposure to different strains of HPS. Outbreaks can occur from 3 to 20 weeks of age or older, depending on the interplay of risk factors and circumstances.
Disease associated with HPS is diagnosed year-round, with no particular trends identified over recent years or by season (Table 3; Figure 2).
Diagnosis of HPS as a cause of disease can be challenging for three main reasons. First, the clinical signs and lesions can resemble those of other diseases, which should beruled out as co-factors for HPS disease expression (Table 2).
Second, HPS is commonly carried in the upper respiratory tract of normal swine, hence, merely detecting it by bacterial isolation or polymerase chain reaction (PCR) is not sufficient for diagnosis. Lesions (gross and microscopic examinations) should be used to confirm HPS as a cause of disease. Note that "finding HPS where it is not supposed to be" by PCR, that is in joints, brain or fibrin exudates, is quite valuable in implicating a role for HPS, provided that sampling is properly executed.
Third, HPS is quite fragile and sometimes difficult to culture unless the proper specimens are collected from non-medicated, acutely affected pigs and rapidly transported to the laboratory on ice (Table 2).
Isolation of HPS by culture is necessary for antimicrobial sensitivity testing and for further characterization of strains. Haemophilus parasuis is not particularly resistant to antimicrobials in vitro, nor are there any resistance trends detected that are not explained by technique changes (Figure 3). In the absence of antimicrobial intervention, the mortality is usually quite high in affected pigs. Therefore, it is important to medicate pigs early in disease, preferably by injection of an appropriate antimicrobial.
There are many different strains of HPS that can be identified by serotyping, which is sometimes useful for vaccine selection or predicting cross-protection between isolates. Sequencing part of the genome is sometimes used to determine relatedness of isolates from two different sources, but is not particularly useful for predicting vaccine efficacy.
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Kent Schwartz, DVM
Iowa State University Veterinary Diagnostic Laboratory