Haemophilus Parasuis in Swine

By Simone Oliveira, Newport Laboratories

Haemophilus parasuis is still one of the main causes of nursery mortality in most U.S. herds . Mortality rates due to Haemophilus parasuis can be as high as 10% , which makes this agent one of the most costly pathogens in swine production. Although a few herds experience nursery mortality solely due to H. parasuis, disease caused by this agent may occur at the same time as other bacterial and viral infections. Streptococcus suis and Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) are two of the agents that are frequently isolated from pigs showing polyserositis due to H. parasuis . The epidemiology of Streptococcus suis infection is very similar to H. parasuis, which may explain why these two agents often affect nursery pigs at 4 to 6 weeks after weaning. PRRSV infection, however, has a very distinct role in H. parasuis infection. A recent study suggests that pigs colonized by a virulent H. parasuis strain are susceptible to development of systemic infection by this agent following PRRSV challenge . Although the interaction between PRRSV and H. parasuis is now evident both experimentally and in the field, the mechanisms involved in such interaction are still unclear.

Etiological agent (cause)

Haemophilus parasuis is the etiological agent (cause) of the syndrome currently known as “Glässer’s disease”. This organism is an early colonizer of the upper respiratory tract and may be normally isolated from the nasal cavity, tonsil, and trachea of healthy pigs. Although non-pathogenic strains predominate in the upper respiratory tract, some animals may harbor virulent strains that can cause systemic disease characterized by fibrinous polyserositis, arthritis, and meningitis. Fifteen serovars of H. parasuis have been reported, and there is extensively strain variation within serovar groups.

Clinical signs and lesions

The clinical signs characteristic of H. parasuis infection are certainly not unique to this agent, and a differential diagnosis with other pathogens such as S. suis is necessary. The clinical presentation of H. parasuis systemic infection may vary with the virulence of the strain and the immune status of the pig. Three main presentations may be observed in the field: super-acute, acute, and chronic. Super-acute infections are characterized by sudden death with lack of clinical signs and gross lesions in most cases. Some animals may show a slight increase of fluids in the pericardial sac, pleural, and abdominal cavities. Fibrin may or may not be observed. In these cases, H. parasuis may be isolated from the blood, which confirms septicemia. Super-acute infections usually occur in naive herds (H. parasuis-free) or due to infection by a highly virulent strain. Acute infections are more commonly observed in the field and are characterized by fibrinous polyserositis (Figure 1). Clinical signs will usually appear 2-3 days following infection. Affected pigs may present fever (106 – 107 º F), labored breathing (abdominal breathing), coughing, swollen joints, and central nervous system (CNS) signs, which are characterized by lateral decubitus, paddling, and trembling. When samples are properly collected, H. parasuis can be easily isolated from these animals. Acute infection may also be characterized by development of either pneumonia or CNS signs. These clinical presentations may be associated with specific groups of strains. Some strains seem to have a tropism to the brain, causing only CNS signs. Other strains may be found in lungs causing pneumonia without systemic infection. Further studies are necessary to clarify the association between specific strains and clinical presentations in the field. Chronically affected animals (6-7 weeks after weaning) are survivals of the peak of nursery mortality. These animals probably received antibiotic treatments and were able to survive systemic infection. In most chronically affected animals, H. parasuis can no longer be isolated from lesions. These animals usually present poor growth performance throughout late nursery and early finisher and may die from complications of fibrosis in the thoracic cavity.3, 6

Diagnosis and strain characterization

The diagnosis of H. parasuis systemic infection is based on the association between clinical history and isolation of the agent from characteristic lesions. Successful isolation of H. parasuis from clinical samples can be achieved by sampling acutely affected, non-treated animals. Isolation is easier when clinically affected animals are euthanized and fresh samples are submitted to a diagnostic laboratory as soon as possible. Sample collection may be performed using a sterile swab containing Stuart media. It is very important to collect the fibrin on the surface of affected organs, as H. parasuis will be mostly concentrated in this material. Tissues may also be collected for isolation, and should be submitted in separate sterile bags to the laboratory. It is known that different strains can affect one pig at the same time. Special care should be taken to separate brain tissue or swabs from other samples, as some H. parasuis strains seem to have a tropism to the brain . When isolation is negative, polymerase chain reaction (PCR) may be used to detect the presence of H. parasuis in tissues and swabs . PCR is useful to define the role of H. parasuis in nursery mortality, but isolation is still necessary for further characterization of strains by serotyping and genotyping. A new technique, more sensitive and specific, has been recently developed to serotype H. parasuis. Indirect hemaglutination (IHA) is now the technique of choice for H. parasuis serotyping. It apparently reduces the percentage of non-typable isolates compared with traditional serotyping by agar gel precipitation test (AGPT) . Genotyping by Enterobacterial Repetitive Intergenic Consensus-based PCR or ERIC-PCR has been extensively used to characterize and compare H. parasuis field strains . This technique is more discriminatory than serotyping and can be used to detect prevalent strains in affected herds (Figure 2). Both techniques (serotyping by IHA and genotyping by ERICPCR) are important for the development of control strategies.

Epidemiology

Colonization of piglets by H. parasuis occurs a few days after birth, possible through nose to nose contact with sows and gilts. Gilts appear to shed fewer organisms than sows . If this is true, gilt piglets are at higher risk of developing systemic infection by virulent H. parasuis strains after weaning. Another factor that appears to influence colonization of piglets by H. parasuis is weaning age. Pigs weaned at 14 days tend to have lower levels of colonization compared with piglets weaned at 28 days. Piglets that were colonized in the farrowing house in the presence of maternal immunity may develop active immunity against virulent strains and be protected against systemic infection after weaning and commingling. Piglets that were not colonized prior to weaning are naive animals that may develop systemic infection when commingled with colonized pigs. Systemic infection usually happens around 4 to 6 weeks after weaning, when maternal immunity is no longer protective. This hypothesis drives today’s control strategies to reduce nursery mortality due to H. parasuis infection, as it will be discussed in the control section .

Another interesting feature of the epidemiology of H. parasuis is the fact that no matter how many sources are commingled in the nursery, only a few prevalent strains (usually 2-3) will predominate in the herd. Several within herd studies using genotyping by ERIC-PCR have confirmed this fact. Another interesting feature of the epidemiology of H. parasuis between herds is the fact that although many herds are affected by the same serovar group, each herd has a different prevalent strain. This was observed in herds affected by strains from serovars 2, 4, and 12 .