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Haemophilus parasuis (Glasser’s Disease)


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Definition

An infectious disease of pigs, often acute, characterized by various combinations of meningoencephalitis, polyserositis and polyarthritis as well as a contributor to bacterial pneumonia.

Occurrence

Glasser’s disease occurs sporadically among swine herds and is usually observed in three week to four month-old pigs. It often occurs subsequent to stressful events such as weaning, changes in environment, commingling, or as coinfection with other disease agents. Glasser’s disease is present in all the major swine-raising countries and remains a significant disease even in modern age-segregated production systems.

Historical information

In 1910, Glasser observed a swine disease and associated it with a small, Gram-negative rod. In 1931 an organism, presumably the same one, was isolated from swine with influenza and named Haemophilus influenzae suis. By 1943 it was clear that the organism was a pathogen in its own right, not necessarily associated with swine influenza, and the name was shortened to Haemophilus suis. Then by 1976, definitive taxonomic studies resulted in the present name, Haemophilus parasuis. The importance of Glasser’s disease has increased with expansion of the swine raising industry.

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

Onset of Glasser’s disease is usually sudden. The best pigs frequently are the first affected. They may be found dead or die after a disease course of less than two days. Signs depend upon where the organisms localize. Signs of central nervous system (CNS) disturbance often predominate as a consequence of localization of H. parasuis in the brain, meninges and spinal cord. Signs may then include tremors, incoordination, posterior paresis or lateral recumbency. In most cases there is an initial, marked rise in temperature, along with anorexia and depression.

Often there are swollen leg joints (and in some outbreaks arthritis predominates) and the animal will favor an affected leg while walking. Sudden deaths may occur in any age group. There sometimes are signs suggestive of septicemia or myositis. Less frequent signs in all swine include rhinitis, dyspnea, reddening of the conjunctiva, cyanosis of the extremities and edema of the eyelids or ears. Morbidity usually is low but mortality is high among those untreated. H. parasuis is also commonly isolated from pneumonic lungs.

Lesions

There may be cyanosis of the skin. Often there is copious serofibrinous or fibrinopurulent exudate in the peritoneal cavity, the pericardial sac or thorax. Pleuritis is a common lesion and may be present with or without obvious pneumonia. Lesions in the lungs often are red, multifocal, disseminated and suggestive of septicemia and hematogenous spread. They closely resemble those of embolic, bacterial pneumonias, especially those caused by Streptococcus suis. Haemophilus parasuis may also contribute to typical bronchopneumonia. The fundus of the stomach often is congested but should be considered a nonspecific lesion. There may be petechial hemorrhages on the kidneys.

Occasionally there are no readily visible gross lesions but if the brain is removed, a fibrinopurulent exudate may be visible on the ventral aspect of the brain. In advanced cases the exudate may be present over the cerebellum or cerebrum. One or more major leg joints often are swollen, perhaps in combination with lesions at other sites. The atlanto-occipital joint frequently is affected. Exudate in joints often is fibrinous and gray to green. An infrequent lesion, recently described, is myositis of the masseter muscles with swelling of the head. Microscopic lesions include vasculitis and fibrinopurulent exudate at lesion sites.

Diagnosis

A tentative diagnosis often can be made on the basis of history, signs and typical lesions. The diagnosis should be confirmed by culture of H. parasuis from lesions affecting serous membranes, cerebrospinal fluid, joints or other tissues. Isolates must be differentiated from other Haemophilus-like organisms, especially Actinobacillus suis. Brain, visceral pleura and other serosal exudates are preferred culture sites. Glasser’s disease may involve only a few or many animals in a herd. Consequently, it must be differentiated from numerous other diseases. These include diseases that cause CNS signs, septicemia or arthritis. Molecular techniques for identifying H. parasuis from clinical specimens and carrying out epidemiological studies have been well described.

Control

The course of the disease often is short and many of the sick animals die if untreated. For that reason, sick animals should be treated promptly and parenterally with an appropriate antimicrobial. H. parasuis is sensitive to many antibiotics and sulfonamides but the sensitivity pattern of isolates from individual farms may vary over time so periodic evaluation of antibiograms is warranted. If numerous pigs are affected, it may be advisable to mass medicate, through the water, all pigs in the affected age group.

Prevention may involve management modifications, sound husbandry, control of primary diseases such as PRRSV, prophylactic antimicrobials, or vaccination. Since H. parasuis colonizes relatively early in the piglets’ life (less than 10 days of age), segregated rearing has not been uniformly successful in preventing infection or disease. Acclimatization and vaccination of breeding stock has been of some benefit. Minimizing stressors associated with weaning and the nursery environment should be emphasized.

Formalin-killed bacterins are available and can be effective for prophylaxis. Unfortunately, protection against one serovar of H. parasuis may not assure good protection against all serovars. Limited research suggests that piglets from dams that have been vaccinated against H. parasuis prior to farrowing, or piglets vaccinated when one to three weeks old, have considerable resistance to disease caused by the same serovar. Colostral immunity in the piglets may sometimes interfere with very early vaccination against H. parasuis infection.

Recognition of the natural relationship between the infection of young pigs in the face of maternal immunity with subsequent induction of active immunity during this phase has led to innovative approach to control of disease. Preliminary reports suggest that controlled exposure of nursing piglets to live H. parasuis organisms indigenous to the farm will allow successful infection and development of active immunity while disease expression is suppressed by maternal immunity. This concept attempts to mimic the natural ecology of organism and host to mitigate disease -postweaning.