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PubMed1992

Molecular cloning and expression of ptxA, the gene encoding the 120-kilodalton cytotoxin of Actinobacillus pleuropneumoniae serotype 2.

The genetic determinants of the 120-kDa cytotoxin of Actinobacillus pleuropneumoniae serotype 2 were isolated from a lambda DNA library by a plaque immunoblot technique. Expression of the 120-kDa polypeptide was confirmed by Western immunoblot analysis of infected Escherichia coli cell lysates, which were shown to be toxic for porcine alveolar macrophages in vitro. The genetic determinants of the toxin were subcloned into the plasmid vector pUC18. This plasmid (pPTX1) directed the synthesis and secretion of the active 120-kDa cytotoxin in E. coli. The recombinant toxin was indistinguishable from native cytotoxin from A. pleuropneumoniae serotype 2 with respect to molecular size, reaction in Western blot analysis, heat lability, cytotoxic activity, and neutralization by serum antibody. A restriction endonuclease cleavage map of pPTX1 was prepared, and deletion mutants were used to locate the minimal region of DNA required for production of intracellular toxin; this gene was termed ptxA. Southern hybridization analysis with a 1.7-kb PvuII fragment located within the ptxA gene revealed sequences with a high degree of homology in serotype reference strains 2, 3, 4, 6, and 8. Other reference strains did not contain sequences that were recognized by this probe. However, related sequences (greater than 71% homology) were detected in Actinobacillus actinomycetemcomitans and A. equuli. Weak hybridization was observed between the ptxA probe and pLKT5, which carries the lktAC genes of Pasteurella haemolytica, and between the ptxA probe and pAPH1, which carries the structural gene for type II hemolysin from A. pleuropneumoniae. The isolation of the genetic determinants of this cytotoxin will enable investigations of the structure and organization of the ptx DNA region and further analysis of its role in the pathogenesis of pleuropneumonia.

Actinobacillus↗
PubMed1991

Blocking enzyme-linked immunosorbent assay for detection of antibodies to Actinobacillus pleuropneumoniae serotype 2.

A blocking enzyme-linked immunosorbent assay (ELISA), based upon a polyclonal rabbit antiserum specific to Actinobacillus pleuropneumoniae serotype 2, was developed for the detection of antibodies to A. pleuropneumoniae serotype 2 in pigs. By testing sera from pigs experimentally infected with the 11 recognized serotypes of A. pleuropneumoniae, the assay was proven to be specific for A. pleuropneumoniae serotype 2. With field sera from herds infected with A. pleuropneumoniae serotype 2, the assay was found to be more sensitive than the complement fixation test. Positive results were not observed with field sera from herds known to be free from Actinobacillus infection or with sera from two herds infected with either A. pleuropneumoniae serotype 6 or 8. The high diagnostic sensitivity and specificity of the blocking ELISA will make it useful in field diagnostic work.

Actinobacillus↗
PubMed1991

Construction of a DNA probe and detection of Actinobacillus pleuropneumoniae by using polymerase chain reaction.

A 1.5-kb Actinobacillus pleuropneumoniae 4074 DNA fragment from a genomic library was found to hybridization. No cross-hybridization hybridization. No cross-hybridization was detected with DNAs from hemolytic members of the family Pasteurellaceae. From the nucleotide sequence of the putative genomic probe, three primers were synthesized for use in polymerase chain reactions (PCRs), with 31 strains tested by using purified and crude DNA targets. PCR amplification products of 610 and 985 bp were observed in nucleic acids extracted from the 12 known serotypes and a biotype 2 strain. Template DNAs from other gram-negative and gram-positive bacteria, some of them found in the normal flora of swine and the upper respiratory tract, were not amplified by PCR. The only exception was an amplification of a similar 610- or 985-bp sequence in Actinobacillus lignieresii, a species that is closely related to A. pleuropneumoniae but that has never been isolated from swine. Amplification of specific A. pleuropneumoniae sequences by PCR directly from clinical specimens may find applications in the identification of asymptomatic carriers as well as in efforts to eradicate porcine pleuropneumonia.

Actinobacillus↗
PubMed1995

Simplified procedure for preparation of sensitized latex particles to detect capsular polysaccharides: application to typing and diagnosis of Actinobacillus pleuropneumoniae.

A novel, inexpensive method for obtaining immunoglobulin G (IgG) specific for capsular antigen is described for use in latex agglutination tests. Hyperimmune rabbit serum against encapsulated Actinobacillus pleuropneumoniae was thoroughly adsorbed with a nonencapsulated mutant. The capsule titer of the absorbed serum was unaffected, whereas reactivity to nonencapsulated cells was reduced to background levels, as determined by enzyme immunoassay. The IgG component of the adsorbed serum was recovered by protein A chromatography and was covalently coupled through a water-soluble carbodiimide to carboxylate latex beads. The sensitized latex particles (SLP) were agglutinated by 10 ng of homologous capsule or more per ml, were not agglutinated by heterologous capsules at concentrations of < 10 micrograms/ml, and were stable for over 1 year at 4 degrees C without loss of sensitivity. There was no difference in the sensitivity or specificity of latex particles coupled with IgG purified by capsule affinity chromatography. The SLP were agglutinated by all strains of bacteria of the homologous serotype but not by heterologous serotypes or strains of Pasteurella multocida, Actinobacillus suis, or Haemophilus parasuis tested at a density equivalent to a 0.5 McFarland standard. The SLP detected homologous capsule in lung tissue, nasal swabs, and concentrated urine samples from all pigs culture positive for A. pleuropneumoniae but one. Precoating of carboxylate latex particles with avidin followed by conjugation of biotin-hydrazide-labelled IgG to capsule increased the sensitivity of the assay approximately 10-fold. Adsorption of serum with nonencapsulated mutants may be used to prepare SLP with optimum sensitivity and specificity without the need to purify capsule or couple capsule to affinity columns.

Actinobacillus Infections↗
PubMed1997

Actinobacillus suis strains isolated from healthy and diseased swine are clonal and carry apxICABDvar. suis and apxIICAvar. suis toxin genes.

Actinobacillus suis isolates recovered from both healthy and diseased pigs were characterized by biochemical testing, serotyping, restriction endonuclease fingerprinting, and apx toxin gene typing. The clinical isolates analyzed were collected over a 10-year period from approximately 40 different locations in southwestern Ontario, Canada. Little variation in the biochemical profiles of these isolates was seen, and all isolates reacted strongly with rabbit antisera prepared against one of the strains. Similarly, by using BamHI and BglII for restriction endonuclease fingerprinting (REF) analysis, all isolates were found to belong to a single REF group. Minor variations could be detected, especially in the BglII fingerprints, but overall the patterns were remarkably similar. Sequences that could be amplified by PCR with primers to the apxICA and apxIICA genes of Actinobacillus pleuropneumoniae were detected in all strains. Although no amplification was obtained with primers to the A. pleuropneumoniae apxIBD genes, sequences with homology to apxIBD were detected by hybridization. There was no evidence of apxIII homologs. Taken together, these data suggest that A. suis isolates are genotypically and phenotypically very similar, regardless of their source, and that they contain genes similar to, but not identical to, the apxICABD and apxIICA genes of A. pleuropneumoniae.

Actinobacillus↗
PubMed1998

Actinobacillus equuli septicemia: an unusual zoonotic infection.

We describe the isolation of Actinobacillus equuli from the blood of a 53-year-old butcher with septicemia. This species of the genus Actinobacillus is primarily associated with animals and animal diseases, especially septicemia in foals. This is the first report of the isolation of A. equuli from a human with septicemia.

Actinobacillus↗
PubMed1993

Pulmonary lesions in mice inoculated with Actinobacillus pleuropneumoniae hemolysin and lipopolysaccharide.

Non-Swiss albino (CF1) male mice were used as a model to study the effects of specific toxic components of Actinobacillus pleuropneumoniae on the respiratory system. Mice were divided into five groups of ten each and were inoculated by the intranasal route with whole-cell Actinobacillus pleuropneumoniae serotype 1, cell-free culture supernatant fluid (CFCSF) containing hemolysin protein, purified lipopolysaccharide (LPS), heat-treated CFCSF, or phosphate-buffered saline solution. Pulmonary lesions were evaluated at 6 and 12 hours after inoculation. Mice inoculated with whole cells, CFCSF, and LPS developed severe purulent bronchiolitis and alveolitis. Focal pulmonary necrosis was also observed in these three groups but was most consistent in the CFCSF-inoculated mice. Ultrastructurally, lungs from mice inoculated with whole cells, LPS, and CFCSF were characterized by severe degenerative changes in type I and type II pneumocytes. Alveolar spaces contained cellular debris and fibrin. Endothelial cells were swollen, and selected pulmonary capillaries were occluded with platelets and fibrin. Infiltrating neutrophils were often swollen, vacuolated, and degranulated. Although inoculation with relatively large numbers of A. pleuropneumoniae are required to kill mice, the mouse lung appears quite sensitive to the toxic components produced by these bacteria. The elaboration of these two toxic components by A. pleuropneumoniae may be responsible for the characteristic pulmonary inflammatory and necrotic lesions observed in infected swine.

Actinobacillus Infections↗
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↗
PubMed2002

Incidence of reinfections with Mycoplasma hyopneumoniae and Actinobacillus pleuropneumoniae in pig farms located in respiratory-disease-free regions of Switzerland--identification and quantification of risk factors.

The objective of the study was to identify risk factors for reintroduction of Actinobacillus pleuopneumoniae and Mycoplasma hyopneumoniae (enzootic pneumonia) onto pig farms in areas in Switzerland that were involved in an eradication programme from 1996 to 1999 and to assess the role of dealers in relation to these reinfections. The study was based on the comparison of pig farms that were reinfected in the year 2000 (cases) and pig farms that remained uninfected in the same area (controls). Additionally, data were collected from Swiss pig dealers and transport companies. Out of a total of 3983 farms, 107 farms were reinfected in the year 2000. The incidences were 0.1% for Actinobacillus pleuopneumoniae and 2.6% for Mycoplasma hyopneumoniae (enzootic pneumonia). Compared to reinfection rates prior to the eradication programme, this is a considerable reduction. Statistically significant risk factors for the reinfection were 'finishing farm', 'large mixed breeding-finishing farm', 'reinfected neighbour' and 'parking site for pig transport vehicles close to the farm'. Pig farmers that purchased pigs from only one supplier per batch had a lower risk of reintroducing infection (protective factor). As long as infected and uninfected regions co-exist in Switzerland, direct and indirect contact between farms, pig herds and slaughter sites via transport vehicles are a major pathway of disease spread. Risk management measures linked to these contacts are therefore of key importance. The survey of dealers indicated various areas for improvement such as strategic planning of pick-up routes or cleaning and disinfecting of trucks.

Actinobacillus Infections↗
PubMed1995

Efficacy of florfenicol on experimental Actinobacillus pleuropneumonia in pigs.

The efficacy of florfenicol was evaluated on experimental Actinobacillus pleuropneumonia in 5 to 7-week-old pigs. All pigs were intranasally inoculated with bacterial suspension containing 10(8) or 10(9) colony forming units of Actinobacillus pleuropneumoniae, Fukushima (serotype 2), Shope4074 (serotype 1), K17 (serotype 5), 8541 or 8543 (serotype 2; thiamphenicol-resistant strain). Florfenicol and thiamphenicol were given in feed for 12 days, from 5 days before inoculation to 7 days post inoculation (at necropsy). More than half the pigs died in the infected control groups, while no pigs died in florfenicol 50 ppm groups inoculated with each strain. On inoculation with thiamphenicol-sensitive strains, Fukushima, Shope4074 and K17, the average total score of clinical signs and percentage of lung lesion area in florfenicol 50 ppm groups were significantly lower than those in the infected control groups (P < 0.05). On inoculation with thiamphenicol-resistant strains, 8541 and 8543, the average total score of clinical signs and percentage of lung lesion area in florfenicol 50 ppm groups were significantly lower than those in the infected control and thiamphenicol 200 ppm groups (P < 0.05). The development of pleuropneumonia was remarkably prevented by medication with feed containing florfenicol in pigs inoculated with serotype 1, 2, 5 strains and thiamphenicol-resistant strains of A. pleuropneumoniae.

Actinobacillus Infections↗
PubMed1999

Pulmonary lesions in guinea pigs experimentally infected with Actinobacillus pleuropneumoniae (A.p.) serovar 1.

Pathological studies were carried out on the lungs of guinea pigs intratracheally inoculated with 4.6 x 10(6-8) colony forming units (CFU)/head of Actinobacillus pleuropneumoniae serovar 1. All animals in the highest dose group died within 24 hr post inoculation (hpi) and showed pulmonary lesions being hemorrhagic in nature while all animals in the lowest dose group were killed as scheduled at 11 days post inoculation (dpi) and showed only hyperplasia of peribronchial lymphoid tissues. In the middle dose group, two died within 24 hpi, two died at 9 dpi, and the remaining one was killed at 11 dpi. Two guinea pigs which died at 9 dpi showed fibrinonecrotic pleuropneumonia which is the most characteristic acute pulmonary lesion in swine, and has not yet been reproduced in laboratory animals up to the present time. This suggests that guinea pigs may be a useful laboratory animal for studying the pathogenesis of Actinobacillus pleuropneumoniae infection in swine.

Actinobacillus Infections↗
PubMed2000

Experimental aerosol transmission of Actinobacillus pleuropneumoniae to pigs.

In order to demonstrate the possible role of aerosol in the transmission of Actinobacillus pleuropneumoniae, an experiment including 18 specific pathogen-free (SPF), 10-week-old piglets, randomly distributed into 2 adjacent units, was carried out. In these facilities, air was forced through absolute filters to prevent any contact with infectious agents. During the first 6 d post inoculation, the 2 units were connected by a rectangular opening and the air circulation was forced by the ventilation system from unit A (inoculated pigs) to unit B (non-inoculated pigs). The A. pleuropneumoniae strain (biovar 1 serovar 9) was isolated in France from an outbreak of porcine pleuropneumonia. Two different infecting doses, 10(7) cfu/animal and 10(8) cfu/animal, were inoculated by intranasal route in 6 pigs of unit A. The infection spread quickly from the inoculated pigs to the non-inoculated pigs. Clinical signs were acute during the 4 d post inoculation: hyperthermia, respiratory distress and, sometimes, death (6 pigs of the unit A and 2 pigs of the unit B). All pigs seroconverted against A. pleuropneumoniae serovar 9 within 2 weeks. Lung lesions were severe: fibrinous pleurisy and lung hemorrhages in the acute stage, pleural adherences and focal pulmonary necrosis in the chronic stage. Actinobacillus pleuropneumoniae was isolated from the tonsils and/or lungs in 16 animals. It could be also isolated from the air of the experimental unit. This study showed that A. pleuropneumoniae was readily transmitted through aerosol over a distance of at least 2.5 m.

Actinobacillus Infections↗
PubMed2000

A 24-kDa cloned zinc metalloprotease from Actinobacillus pleuropneumoniae is common to all serotypes and cleaves actin in vitro.

Actinobacillus pleuropneumoniae causes pleuropneumonia in swine. This bacterium secretes proteases that degrade porcine hemoglobin and IgA in vitro. To further characterize A. pleuropneumoniae proteases, we constructed a genomic library expressed in Escherichia coli DH5alpha, and selected a clone that showed proteolytic activity. The recombinant plasmid carries an 800-base pair A. pleuropneumoniae gene sequence that.codes for a 24-kDa polypeptide. A 350-base pair PstI fragment from the sequence hybridized at high stringency with DNA from 12 serotypes of A. pleuropneumoniae, but not with DNA from Actinobacillus suis, Haemophilus parasuis, Pasteurella haemolytica, Pasteurella multocida A or D, or E. coli DH5alpha, thus showing specificity for A. pleuropneumoniae. The expressed polypeptide was recognized as an antigen by convalescent-phase pig sera. Furthermore, a polyclonal antiserum developed against the purified polypeptide recognized an A. pleuropneumoniae oligomeric protein in both crude-extract and cell-free culture media. This recombinant polypeptide cleaved azocoll, gelatin, and actin. Inhibition of the proteolytic activity by diethylpyrocarbonate suggests that this polypeptide is a zinc metalloprotease.

Actinobacillus Infections↗
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↗
PubMed1988

Changes in the susceptibility of Actinobacillus pleuropneumoniae to antimicrobial agents in Quebec (1981-1986).

An important reduction in the in vitro efficacy of spectinomycin and chloramphenicol was recorded between 1981 and 1986 against the causal agent of porcine pleuropneumonia Actinobacillus. Antimicrobial susceptibility tests were carried out by use of Kirby-Bauer disk diffusion technique on a total of 723 isolates of Actinobacillus pleuropneumoniae. Results did not agree with those of other reports in which a constant susceptibility to any of the antimicrobial agents tested was reported with serotype 2 isolates. The ability to acquire drug resistance may differ from one serotype to another.

Actinobacillus↗
PubMed1987

Actinobacillus suis-like organisms in horses.

Actinobacillus suis-like organisms have been recognized in equine specimens at the University of California Veterinary Medical Teaching Hospital since 1975. The most common source (65%) of the organism was transtracheal washings. The organism was gram-negative, produced hemolysis on blood agar, and gave a positive reaction for oxidase, urease, o-nitrophenyl-beta-D-galactopyranoside, and esculin. Carbohydrate reactions were variable, consisting of 4 main patterns. Actinobacillus suis-like organisms were (90%) sensitive to therapeutic concentrations of amikacin, cephalothin, chloramphenicol, gentamicin, kanamycin, tetracycline, and trimethoprim-sulfamethoxazole. Other aerobic and anaerobic bacteria were recovered frequently with the organism.

Actinobacillus↗
PubMed1994

Peritonitis associated with Actinobacillus equuli in horses: 15 cases (1982-1992).

Peritonitis attributable to Actinobacillus equuli was diagnosed in 15 horses examined at the veterinary center between 1982 and 1992. In 13 horses, historical findings included acute onset of mild to severe signs of abdominal pain, lethargy, and inappetence. Two other horses had a history of weight loss for 3 to 6 weeks prior to examination. Diagnosis was based on the physical signs and laboratory findings, including results of peritoneal fluid analysis (gross characteristics, total protein, total and differential nucleated cell counts, and morphologic findings) and culture of A equuli. Actinobacillus equuli was consistently susceptible in vitro to penicillin, trimethoprim/sulfadiazine, and aminoglycosides. All horses in the study had marked clinical improvement within 24 to 48 hours of commencing antibiotic and supportive treatment. Antibiotic treatment was continued for variable periods, depending on the horse, but ranged from 5 to 21 days. In 11 horses for which follow-up information was available, long-term response to treatment was excellent, with horses returning to original activity.

Actinobacillus↗
PubMed1993

Effect of subclinical infection with Actinobacillus pleuropneumoniae in commingled feeder swine.

Sequential serologic analysis for Actinobacillus pleuropneumoniae was done on 240 commingled feeder swine at 1 and 21 days after purchase and at slaughter. At the beginning of the experiment, mean weight of the pigs was 18.6 kg, and the pigs were maintained to a mean slaughter weight of 109.95 kg. A fourfold increase in antibody titer against Actinobacillus pleuropneumoniae was demonstrated in 28 (12%) pigs. Mean adjusted rate of gain for infected pigs was 0.74 +/- 0.10 kg/d and 0.77 +/- 0.09 kg/d for uninfected pigs. Differences in feed efficiency were not detected between infected and uninfected pigs. Our findings suggested that 5.64 additional days are required for pigs with subclinical infection to reach market weight of 113.6 kg, compared with that for uninfected herdmates. A vaccination program to prevent subclinical infection may not be cost effective.

Actinobacillus Infections↗