[Pleuropneumonia in pigs due to Haemophilus pleuropneumoniae. I. A bibliographical review (author's transl)].

During the last twenty years pleuropneumonia in pigs, caused by Haemophilus pleuropneumoniae, has spread globally. The increasing importance of the disease within swine production is apparently connected with increasing industrialization and subsequent heavy concentration of a large number of animals in the individual production unit. Haemophilus pleuropneumoniae seems to be specific for pigs. Several more or less pathogenic serotypes of the bacterium are known. Serotype 2 as occurring in Denmark is primary pathogen for pigs which have not previously been in contact with the infection. Immunity of varying strength and duration is left after recovery. Prolonged immunity in an animal is presumably dependent on latent infection or on repeated infections. Normally there is a large number of latently infected animals in attacked herds. Such animals, especially sows and boars, represent a potential infection reservoir which might be the basis of new clinical outbreaks under conditions of reduced herd immunity or of compromised general resistance of animal groups. Clinical disease is most frequently seen in young pigs and fatteners, as piglets are generally protected by maternal antibodies. Acute pleuropneumonia is characterized by high temperature, lost appetite, light cough and often vomiting. Morbidity is high, especially by new-infection where there may also be considerable mortality if adequate antibacterial therapy is neglected, however, normally the disease implies low mortality. The pathological lesions are localized to the respiratory organs. The lungs are the seat of fibrinous necrotising pneumonia (red, grey hepatization), more or less extensive, most frequently of the diaphragmatic part of the lung. Furthermore fibrinous, later on fibrous pleuritis and pericarditis may be seen. The fibrous pleuritis may be of decisive diagnostical value when established with high frequency in baconers. The disease causes losses as a consequence of increased use of medicine and reduced daily weight gain in fatteners. Optimum environment and feeding conditions will reduce such losses considerably. The use of commercially available vaccines makes it possible to fortify specific resistance against the disease in exposed groups of animals. In small herds with few infected animals the infection may be eliminated by discarding seropositive animals, combined with strategic medication. Elimination of the infectious agent in large herds can only take place by replacing all animals by an SPF-herd.