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At least 19 recordsLinked to original sources
PubMed2001

Detection and localization of ApxI, -II and -III genes of Actinobacillus pleuropneumoniae in natural porcine pleuropneumonia in natural porcine pleuropneumonia by in situ hybridization.

In situ hybridization techniques that employed a nonradioactive digoxigenin-labeled probe were used to detect and localize ApxI, II and III genes in tissue sections of pneumonic lung naturally infected with Actinobacillus pleuropneumoniae. In pigs infected with either serotype 2 or 6, a hybridization signal for apxIICA, apxIIICA, apxIBD, and apxIIIBD was detected, and in pigs infected with serotype 5, a hybridization signal for apxICA, apxIICA, and apxIBD was detected in the pneumonic lesions. A hybridization signal for apxIICA and apxIBD was detected in pigs infected with serotype 7. A strong hybridization signal for apx genes was seen in streaming degenerate alveolar leukocytes bordering zones of coagulative necrosis. Simultaneous detection of hybridization signals for the apxCA and apxBD genes provided scientific evidence that the expression of the apx genes could be potential indicators of the production of corresponding Apx toxins. This study demonstrates the expression of ApxI, II, and III genes in pneumonic lesions caused by A. pleuropneumoniae.

Actinobacillus Infections↗
PubMed1987

Role of haemophilus pleuropneumoniae lipopolysaccharide endotoxin in the pathogenesis of porcine Haemophilus pleuropneumonia.

Intact Haemophilus pleuropneumoniae cells (strain Shope 1, serotype 1), highly purified lipopolysaccharide (LPS) obtained from this strain of H pleuropneumoniae, as well as from Escherichia coli O111:B4, filter-sterilized H pleuropneumoniae cell-free culture supernatant fluid, and heat-inactivated supernatant fluid were given intranasally to CF1 mice and intratracheally to pigs. Pulmonary lesions induced by H pleuropneumoniae in mice were similar to those induced by H pleuropneumoniae in pigs. Histologically, lungs of mice and pigs killed 1 or 2 days after inoculation with 200 micrograms of highly purified H pleuropneumoniae LPS had lesions similar to one another and were similar to those in mice and pigs given intact H pleuropneumoniae, except that little or no necrosis or hemorrhage was observed. In mice killed 1 or 2 days after inoculation of 200 micrograms of E coli O111:B4 LPS, pulmonary lesions were similar to those in mice given H pleuropneumoniae LPS. Pulmonary lesions in mice given cell-free culture supernatant fluid obtained from a midlog-phase growth culture of H pleuropneumoniae cultivated in a chemically defined medium were severe and consisted of neutrophil infiltration and extensive necrosis. In mice, the heat-inactivated supernatant fluid produced mild lesions that consisted of foci of neutrophil aggregation and no necrosis. Extensive necrosis observed in lesions caused by cell-free culture supernatant fluid could be attributed to the action of a heat-labile component, perhaps by the extracellular heat-labile hemolysin produced by H pleuropneumoniae cultivated in chemically defined medium. A LPS endotoxin and a heat-labile factor may be involved in the pulmonary lesion development in the acute phase of porcine Haemophilus pleuropneumonia.

Animals↗
PubMed1992

Pleuropneumonia caused by Actinobacillus pleuropneumoniae biotype 2 in growing and finishing pigs.

Actinobacillus pleuropneumoniae biotype 2 was isolated in pure culture or as the predominant isolate from the lungs of 9 growing and finishing pigs with pleuropneumonia. Gross and microscopic lesions resembled those caused by A. pleuropneumoniae biotype 1 serotypes (Nos. 1, 5, and 7) traditionally seen in the United States. The overall mortality rate for growing and finishing pigs on this 1,200-sow farrow-to-finish farm ranged from 0.37% to 0.84% per month from July 1990 to February 1991, and mortality due to respiratory disease ranged from 0.17% to 0.52% per month for the same period. This Actinobacillus species did not require V factor (no satellitism on blood agar with a Staphylococcus streak), was strongly beta-hemolytic, and demonstrated restriction fragment length polymorphisms in hybridization studies with A. suis, A. lignieresii, and A. equuli. Biochemically, the isolate most closely resembled A. pleuropneumoniae, and a DNA fragment considered specific for A. pleuropneumoniae biotypes 1 and 2 was demonstrated using polymerase chain reaction. Necrohemorrhagic pleuropneumonia similar to that caused by A. pleuropneumoniae biotype 1 was reproduced experimentally in 2 4-week-old pigs inoculated intratracheally with broth cultures of the A. pleuropneumoniae biotype 2. This study demonstrated the presence of A. pleuropneumoniae biotype 2 in the United States.

Actinobacillus Infections↗
PubMed1992

Adjuvant properties of Propionibacterium avidum KP-40 in vaccination against endemic viral and bacterial infections. II. Swine immunized with inactivated Haemophilus pleuropneumoniae vaccine and experimentally infected with different virulent serotypes of H. pleuropneumoniae.

Forty 3-month old swine were treated with immunomodulating Propionibacterium avidum KP-40 (PA) and/or vaccinated with a formalin-inactivated mixture of serotypes 1, 3, 5 and 9 of Haemophilus pleuropneumoniae (Pleurovac). Three weeks after revaccination all animals were inoculated with viable single serotypes of Haemophilus pleuropneumoniae. The IgG antibodies induced by vaccination agglutinated all serotypes of Haemophilus pleuropneumoniae, except for serotype 5. Antibody titers were not influenced by the application of PA together with the vaccine. Infection of vaccinated piglets resulted in the development of pleuropneumonia in 8 out of 10 animals, while vaccination together with application of PA lowered the morbidity rate to 1 out of 10 (p < 0.05). The usefulness of a PA prophylaxis was also demonstrated in non-vaccinated piglets infected with Haemophilus pleuropneumoniae. Because of the considerable variability of strains and serotypes of Haemophilus pleuropneumoniae and the generally low prophylactic potency of pleuropneumonia vaccines it is concluded that long-lasting enhancement of non-specific antiinfective resistance caused by PA may lower the risk of endemic infections in vaccinated piglets.

Actinobacillus Infections↗
PubMedDate not supplied

[Pleuropneumonia in swine due to Haemophilus pleuropneumonia s. parahaemolyticus. II. Studies on the epidemiology and the relation to chronic pleuritis (pleural scars) in baconers (author's transl)].

Within a Danish practice area a serological examination was made of 268 breeding animals in 25 conventional sow herds with a view to screening for herd infection with haemophilus pleuropneumoniae. Average size of the herds was 76 year-sows including pregnant gilts (8--200). In 23 herds produced weaners were fed for slaughtering. The frequency of chronic pleuritis in slaughtered baconers in these herds was related to the frequency of seropositive sows in the herds. Three SPF-herds were included in the investigation, a SPF baconer herd reinfected with H. pleuropneumoniae, a SPF baconer herd reinfected with Mycoplasma suipneumoniae and a SPF breeding herd infected with Haemophilus parasuis. Complement fixation antibodies against Haemophilus pleuropneumoniae were found in breeding animals in 22 out of the 25 conventional sow herds. The average incidence of seropositive breeding animals in infected herds was 62% (7%--100%), highest in the largest herds. Likewise the highest serotitres were found in the largest herds, as an expression of strong infection pressure in large herds. The highest titre values were found in boars and young sows. The frequency of seronegative sows was the highest among the oldest sows. The registered frequency of chronic pleuritis among baconers from the examined herds was found increasing along with higher frequency of seropositive sows in the herds. On the basis of these observations and on the basis of a comparison of chronic pleuritis frequency among baconers in six herds (two with high frequency of seropositive breeding animals, one with moderate frequency of seropositive breeding animals, and 3 SPF-herds, one of which had been reinfected with Haemophilus pleuropneumoniae, one reinfected with Mycoplasma suipneumoniae and one that had experienced an acute outbreak of Glässer's Syndrome) it is concluded that haemophilus pleuropneumoniae is the absolutely most important cause of chronic pleuritis in baconers. A pronounced seasonal variation was found in the monthly pleuritis frequency among baconers in herds strongly infected with Haemophilus pleuropneumoniae, the minumum frequency being in January-February, and the maximum frequency in July-October. It is supposed that the observed variation in frequency of chronic pleuritis is caused by changes in the environmental climate. High frequency of chronic pleuritis is caused by changes in the environmental climate. High frequency is found in the summer in slaughtered baconers, which have been clinically affected by pleuropneumonia as piglets and weaners under inferior climatic conditions during the colder season of the year.

Animals↗
PubMed1964

PORCINE CONTAGIOUS PLEUROPNEUMONIA. II. STUDIES OF THE PATHOGENICITY OF THE ETIOLOGICAL AGENT, HEMOPHILUS PLEUROPNEUMONIAE.

Hemophilus pleuropneumoniae is highly pathogenic for swine when given intranasally. As few as 100 organisms induce characteristic porcine contagious pleuropneumonia (PCP) and, when as many as one-half million are given, the infection usually proceeds to a fatal termination. While the organism is highly pathogenic when introduced by way of the respiratory tract, it is innocuous when given subcutaneously even in large numbers. Swine that have been inoculated subcutaneously are rendered solidly immune to infection with H. pleuropneumoniae intranasally. The marked pathogenicity of H. pleuropneumoniae for swine has been contrasted with the lack of pathogenicity of another swine Hemophilus, H. influenzae suis. It has been pointed out that, in its high degree of pathogenicity, in its pneumotropism, and in its immunogenicity by a non-respiratory route of inoculation, H. pleuropneumoniae appears to resemble certain viruses more than it does a bacterium.

Actinobacillus pleuropneumoniae↗
PubMed1990

Serodiagnosis of pleuropneumonia using enzyme-linked immunosorbent assay with capsular polysaccharide antigens of Actinobacillus pleuropneumoniae serotypes 1, 2, 5 and 7.

Capsular polysaccharide antigens of serotypes 1, 2, 5 and 7 of Actinobacillus pleuropneumoniae were used in enzyme-linked immunosorbent assays (ELISAs) to test sera from experimentally infected and field pigs. Specific reactions were found in sera of experimental pigs with antigens of serotypes 1, 5 and 7 whereas the serotype 2 antigen was cross-reactive. A 1:200 serum dilution was used for testing of 300 sera from 21 swine herds in southern Ontario. Cases of pleuropneumonia had occurred in 11 of these herds, but not in the others. The negative cut-off value was the mean optical density at 405 nm (OD405) + three standard deviations (SD) for 16 negative reference sera. Sera from four pigs naturally infected with Actinobacillus suis were tested and found to react to varying degrees with each of the antigens. Therefore a second cut-off value was determined as the mean OD405 + 2 SD for the A. suis sera. Sera which, in the ELISA produced OD readings above the latter cut-off were considered positive for antibodies to A. pleuropneumoniae; those which were lower than the former cut-off were considered negative. Readings between the two cut-off values may have been due to low positive titers or cross-reactivity, possibly with A. suis, and could not be used to predict pleuropneumonia. Of the pleuropneumonia-free herds, none had positive reactors to serotypes 5 or 7, whereas one and two herds had positive reactors to serotypes 1 and 2, respectively. Of the pleuropneumonia positive herds, six had positive reactors to serotype 1, one to serotype 2, four to serotype 5, and eight to serotype 7.

Actinobacillus↗
PubMed1994

Lipopolysaccharides of Actinobacillus pleuropneumoniae (serotype 1): a readily obtainable antigen for ELISA serodiagnosis of pig pleuropneumonia.

A saline extract of boiled-formalinized whole cells of Actinobacillus pleuropneumoniae serotype 1 reference strain (Shope 4074) has been previously used as the antigen in an enzyme-linked immunosorbent assay (ELISA) for serodiagnosis of swine pleuropneumonia. Phenol extraction of this crude extract permitted the recovery of LPS with long O-chains in the aqueous phase. This antigen was shown to be specific for serotypes 1, 9 and 11 as they all possess structurally similar O-chains. Immunoblotting was used to identify the fraction present in the crude extract of strain 4074 responsible for cross-reactions observed in ELISA with a serum raised against a serotype 3 strain of A. pleuropneumoniae. The specific reactions in ELISA were shown to be associated with long O-chain LPS and the cross-reactions to LPS with short O-chains. LPS seem to be an important antigen for A. pleuropneumoniae serotype 1 as all homologous sera tested reacted with it. This antigen is easily recovered from the crude extract and it can be used in minute amounts (1-6 micrograms) for ELISA serodiagnosis of pig pleuropneumonia.

Actinobacillus Infections↗
PubMed1991

Experimental reproduction of acute lesions of porcine pleuropneumonia with a haemolysin-deficient mutant of Actinobacillus pleuropneumoniae.

The role of the heat-labile haemolysin of Actinobacillus pleuropneumoniae in acute porcine pleuropneumonia was examined. A virulent strain was compared with an isogenic haemolysin-deficient mutant in experimental infections. The pigs which received the virulent strain showed clinical signs of acute respiratory disease whereas the animals infected with the mutant strain appeared to be less severely affected. At post mortem examination, both groups showed similar acute pulmonary lesions and pleurisy typical of A pleuropneumoniae infection. The bacterial antigen representing the haemolysin was detected in lung lesions infected with the parent strain but not in those infected with the mutant. These results demonstrate that the haemolysin of serotype 2 A pleuropneumoniae is not an essential factor for the production of the lesions of pleuropneumonia in pigs.

Actinobacillus Infections↗
PubMed1997

Serodiagnosis of swine pleuropneumonia due to Actinobacillus pleuropneumoniae serotypes 7 and 4 using long-chain lipopolysaccharides.

A saline boiled extract (SBE), capsular polysaccharides (CPS) and long-chain lipopolysaccharides (LC-LPS) of Actinobacillus pleuropneumoniae serotype 7 have been evaluated in ELISA for the serodiagnosis of swine pleuropneumonia caused by this serotype. Mean optical densities (ODs) obtained with the 3 antigens using sera from negative herds as well as from animals experimentally and naturally exposed to A. pleuropneumoniae serotypes 7 or 4 were not statistically different. The positive ELISA reaction with anti-serotype 4 sera was unexpected with the CPS, which are supposed to be serotype-specific; LPS traces present in the CPS appeared to be responsible for this reaction. In addition, sera from animals exposed to A. pleuropneumoniae serotypes 5 or 10 presented cross-reactions with the SBE and the CPS, but not with the LC-LPS. Cross-reactions were mainly due to rough LPS, as shown by immunoblotting. The LC-LPS is easily obtainable and can be used for the detection of antibodies in animals infected with A. pleuropneumoniae serotypes 7 and 4.

Actinobacillus Infections↗
PubMed1994

Evaluation of a saline boiled extract, capsular polysaccharides and long-chain lipopolysaccharides of Actinobacillus pleuropneumoniae serotype 1 as antigens for the serodiagnosis of swine pleuropneumonia.

A saline boiled extract (SBE), capsular polysaccharides (CPS) and long-chain lipopolysaccharides (LC-LPS) of Actinobacillus pleuropneumoniae serotype 1 have been evaluated in ELISA for the serodiagnosis of swine pleuropneumonia caused by this serotype. Mean optical densities (ODs) obtained with the three antigens using sera from negative herds as well as from animals experimentally and naturally exposed to A. pleuropneumoniae serotypes 1, 9 or 11 were not significantly different. The positive ELISA reaction with anti-serotypes 9 and 11 was unexpected with the CPS, which are supposed to be serotype-specific; LPS, and to a lesser extent proteins, were present in the CPS and appeared to be responsible for this reaction. In addition, sera from animals exposed to a field strain of A. pleuropneumoniae serotype 3 and to Actinobacillus suis presented a significantly lower mean OD (P < 0.001) when LC-LPS were used. Cross-reacting antigens consisted mainly of LPS core-lipid A present in the SBE and CPS. The specificity and the sensitivity of the ELISA were evaluated using three different cut-off values (the OD plus two, three and four times the standard deviation or SD) obtained with 667 negative sera. The diagnostic sensitivity was of 81% with the three antigens and the different thresholds. The diagnostic specificity was of 84, 86 and 88% for the mean plus two, three and four times the SD respectively using the SBE and the CPS, while that obtained with the LC-LPS was of 96, 98 and 99% using the same thresholds. In conclusion, LC-LPS make an easily obtainable antigen and seem to retain the best specificity while minimizing losses of sensitivity.

Actinobacillus Infections↗
PubMed1994

Evaluation of long chain lipopolysaccharides (LC-LPS) of Actinobacillus pleuropneumoniae serotype 5 for the serodiagnosis of swine pleuropneumonia.

Long chain lipopolysaccharides (LC-LPS) of Actinobacillus pleuropneumoniae serotype 5 have been evaluated and compared with a crude boiled extract (CBE) in ELISA for the serodiagnosis of swine pleuropneumonia caused by this serotype. The mean optical density (OD) obtained with the LC-LPS in ELISA using sera from negative herds as well as from animals experimentally and naturally exposed to A. pleuropneumoniae serotype 5 was not significantly different from that obtained with the CBE. However, sera from animals exposed to serotypes of A. pleuropneumoniae other than serotype 5 presented a significantly lower mean OD (P < 0.05) when the LC-LPS was used. As a consequence, it was demonstrated that a high percentage of non-specific cross-reactions were eliminated, without losing specificity. The specificity and the sensitivity of the LC-LPS- and CBE-ELISA were evaluated using two different cut-off values (the OD plus two and three standard deviations) (SD) obtained from 593 sera from negative herds. The LC-LPS appeared a more suitable antigen than the CBE, since the sensitivity and the specificity (obtained with both thresholds) were statistically improved (P < 0.01). A threshold of 0.244 (mean OD plus three SD) for the LC-LPS-ELISA seemed more suitable, since a sensitivity of 79% and a specificity of 97% was achieved. Nevertheless, it may be advisable to keep a buffer range (OD between 0.194 and 0.243) and to consider sera presenting values within this range as suspicious. In the present study, the complement fixation test presented a high specificity (97%) and a very low sensitivity (47%). A herd with animals presenting ELISA positive and CFT negative results in serology, along with the absence of suggestive lesions should not be considered as a non-infected herd.

Actinobacillus Infections↗
PubMed1999

Vaccination and protection of pigs against pleuropneumonia with a vaccine strain of Actinobacillus pleuropneumoniae produced by site-specific mutagenesis of the ApxII operon.

The production of toxin (Apx)-neutralizing antibodies during infection plays a major role in the induction of protective immunity to Actinobacillus pleuropneumoniae reinfection. In the present study, the gene encoding the ApxII-activating protein, apxIIC, was insertionally inactivated on the chromosome of a serovar 7 strain, HS93. Expression of the structural toxin, ApxIIA, and of the two genes required for its secretion, apxIB and apxID, still occurs in this strain. The resulting mutant strain, HS93C- Ampr, was found to secrete the unactivated toxin. Pigs vaccinated with live HS93C- Ampr via the intranasal route were protected against a cross-serovar challenge with a virulent serovar 1 strain of A. pleuropneumoniae. This is the first reported vaccine strain of A. pleuropneumoniae which can be delivered live to pigs and offers cross-serovar protection against porcine pleuropneumonia.

Actinobacillus Infections↗
PubMed2003

Effect of endobronchial challenge with Actinobacillus pleuropneumoniae serotype 10 of pigs vaccinated with bacterins consisting of A. pleuropneumoniae serotype 10 grown under NAD-rich and NAD-restricted conditions.

The efficacy of two bacterins containing an Actinobacillus pleuropneumoniae serotype 10 strain was evaluated. The bacterial cells constituting bacterin 1 and 2 were grown under nicotinamide adenine dinucleotide (NAD)-rich (low-adherence capacity to alveolar epithelial cell cultures) and NAD-restricted (high-adherence capacity to alveolar epithelial cell cultures) conditions, respectively. Ten pigs were vaccinated twice with the bacterin 1 and nine pigs with the bacterin 2. Ten control animals were injected twice with a saline solution. Three weeks after the second vaccination, all pigs were endobronchially inoculated with 106.5 colony-forming units (CFU) of an A. pleuropneumoniae serotype 10 strain. In the bacterin 1 and 2 group, three and two pigs died after inoculation, respectively. Only two pigs of the control group survived challenge. Surviving pigs were killed at 7 days after challenge. The percentage of pigs with severe lung lesions (> 10% of the lung affected) was 100% in the control group, 70% in the bacterin 1 group and 22% in the bacterin 2 group. Actinobacillus pleuropneumoniae was isolated from the lungs of all animals. The mean bacterial titres of the caudal lung lobes were 7.0 x 10(6) CFU/g in the control group, 6.3 x 10(5) CFU/g in the bacterin 1 group and 1.3 x 10(6) CFU/g in the bacterin 2 group. It was concluded that both bacterins induced partial protection against severe challenge. Furthermore, there are indications that the bacterin 2, containing A. pleuropneumoniae bacteria grown under conditions resulting in high in vitro adhesin, induced better protection than the bacterin 1.

Actinobacillus Infections↗
PubMed1998

Cloning and mutagenesis of a serotype-specific DNA region involved in encapsulation and virulence of Actinobacillus pleuropneumoniae serotype 5a: concomitant expression of serotype 5a and 1 capsular polysaccharides in recombinant A. pleuropneumoniae serotype 1.

A DNA region involved in Actinobacillus pleuropneumoniae serotype 5 capsular polysaccharide (CP) biosynthesis was identified and characterized by using a probe specific for the cpxD gene involved in CP export. The adjacent serotype 5-specific CP biosynthesis region was cloned from a 5.8-kb BamHI fragment and an 8.0-kb EcoRI fragment of strain J45 genomic DNA. DNA sequence analysis demonstrated that this region contained four complete open reading frames, cps5A, cps5B, cps5C, and cps5D. Cps5A, Cps5B, and Cps5C showed low homology with several bacterial glycosyltransferases involved in the biosynthesis of lipopolysaccharide or CP. However, Cps5D had high homology with KdsA proteins (3-deoxy-D-manno-2-octulosonic acid 8-phosphate synthetase) from other gram-negative bacteria. The G+C content of cps5ABC was substantially lower (28%) than that of cps5D and the rest of the A. pleuropneumoniae chromosome (42%). A 2.1-kb deletion spanning the cloned cps5ABC open reading frames was constructed and transferred into the J45 chromosome by homologous recombination with a kanamycin resistance cassette to produce mutant J45-100. Multiplex PCR confirmed the deletion in this region of J45-100 DNA. J45-100 did not produce intracellular or extracellular CP, indicating that cps5A, cps5B, and/or cps5C were involved in CP biosynthesis. However, biosynthesis of the Apx toxins, lipopolysaccharide, and membrane proteins was unaffected by the mutation. Besides lack of CP biosynthesis, and in contrast to J45, J45-100 grew faster, was sensitive to killing in precolostral calf serum, and was avirulent in pigs at an intratracheal challenge dose three times the 50% lethal dose (LD50) of strain J45. At six times the J45 LD50, J45-100 caused mild to moderate lung lesions but not death. Electroporation of cps5ABC into A. pleuropneumoniae serotype 1 strain 4074 generated strain 4074(pJMLCPS5), which expressed both serotype 1 and serotype 5 CP. However, serotype 1 capsule expression was diminished in 4074(pJMLCPS5) in comparison to 4074. The recombinant strain produced significantly less total CP (serotypes 1 and 5 CP combined) in log phase (P = 0.0012) but significantly more total CP in late stationary phase than 4074 (P < 0.0001). In addition, strain 4074(pJMLCPS5) caused less mortality and bacteremia in pigs and mice following respiratory challenge than strain 4074, indicating that virulence was affected by diminished capsule production. These results emphasize the importance of CP in the serum resistance and virulence of A. pleuropneumoniae.

Actinobacillus pleuropneumoniae↗
PubMed1985

Prevalence of pig herds affected by pleuropneumonia associated with Haemophilus pleuropneumoniae in eastern England.

A survey for the macroscopic lesions indicative of pneumonic infection in the pig with Haemophilus pleuropneumoniae was made in an abattoir in eastern England. A total of 78 herds located in 11 counties of eastern or central England were seen between December 1982 and August 1983. Lesions were noted in the batches submitted by 44 (56 per cent) of the 78 herds. A further 16 herds (21 per cent) submitted batches containing pigs affected by pleurisy principally of the caudal lobes but without the pneumonic lesions. Lesions suggestive of enzootic pneumonia were also seen in 61 herds (78 per cent). Circumstances restricted corroborative bacteriological examinations to 53 and serological examinations to 33 herds. Strains of H pleuropneumoniae (predominantly serotype 3 but also serotype 2) were isolated from 26 herds. These comprised 22 out of 42 (51 per cent) of those where typically affected plucks, or plucks with caudal lobe pleurisy, were encountered, and four out of 11 (36 per cent) in which there was either no observable thoracic disease or enzootic pneumonia only. Complement fixing antibodies to serotype 3 or 2 antigens occurred in 26 out of 33 herds (79 per cent). These comprised 25 (83 per cent) of 30 herds with batches exhibiting either typical pulmonary lesions and, or, caudal lobe pleurisy and one of three herds without such lesions. Collectively these data indicate that herds containing pigs with pleuropneumonia are common at least in the more easterly parts of England and that H pleuropneumoniae, usually but not always associated with disease, is also widespread.

Abattoirs↗
PubMed1981

[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.

Animals↗