Assessing the progression of chronic periodontitis using subgingival pathogen levels: a 24-month prospective multicenter cohort study.

BACKGROUND: The diagnosis of the progression of periodontitis presently depends on the use of clinical symptoms (such as attachment loss) and radiographic imaging. The aim of the multicenter study described here was to evaluate the diagnostic use of the bacterial content of subgingival plaque recovered from the deepest pockets in assessing disease progression in chronic periodontitis patients. METHODS: This study consisted of a 24-month investigation of a total of 163 patients with chronic periodontitis who received trimonthly follow-up care. Subgingival plaque from the deepest pockets was recovered and assessed for bacterial content of Porphyromonas gingivalis, Prevotella intermedia, and Aggregatibacter actinomycetemcomitans using the modified Invader PLUS assay. The corresponding serum IgG titers were measured using ELISA. Changes in clinical parameters were evaluated over the course of 24 months. The sensitivity, specificity, and prediction values were calculated and used to determine cutoff points for prediction of the progression of chronic periodontitis. RESULTS: Of the 124 individuals who completed the 24-month monitoring phase, 62 exhibited progression of periodontitis, whereas 62 demonstrated stable disease. The P. gingivalis counts of subgingival plaque from the deepest pockets was significantly associated with the progression of periodontitis (p < 0.001, positive predictive value = 0.708). CONCLUSIONS: The P. gingivalis counts of subgingival plaque from the deepest pockets may be associated with the progression of periodontitis.

Effects of porcine 25 kDa amelogenin and its proteolytic derivatives on bone sialoprotein expression.

BACKGROUND AND OBJECTIVE: Amelogenins are hydrophobic proteins that are the major component of developing enamel. Enamel matrix derivative has been used for periodontal regeneration. Bone sialoprotein is an early phenotypic marker of osteoblast differentiation. In this study, we examined the ability of porcine amelogenins to regulate bone sialoprotein transcription. MATERIAL AND METHODS: To determine the molecular basis of the transcriptional regulation of the bone sialoprotein gene by amelogenins, we conducted northern hybridization, transient transfection analyses and gel mobility shift assays using the osteoblast-like ROS 17/2.8 cells. RESULTS: Amelogenins (100 ng/mL) up-regulated bone sialoprotein mRNA at 3 h, with maximal mRNA expression occurring at 12 h (25 and 20 kDa) and 6 h (13 and 6 kDa). Amelogenins (100 ng/mL, 12 h) increased luciferase activities in pLUC3 (nucleotides -116 to +60), and 6 kDa amelogenin up-regulated pLUC4 (nucleotides -425 to +60) activity. The tyrosine kinase inhibitor inhibited amelogenin-induced luciferase activities, whereas the protein kinase A inhibitor abolished 25 kDa amelogenin-induced bone sialoprotein transcription. The effects of amelogenins were abrogated by 2-bp mutations in the fibroblast growth factor 2 response element (FRE). Gel-shift assays with radiolabeled FRE, homeodomain-protein binding site (HOX) and transforming growth factor-beta1 activation element (TAE) double-strand oligonucleotides revealed increased binding of nuclear proteins from amelogenin-stimulated ROS 17/2.8 cells at 3 h (25 and 13 kDa) and 6 h (20 and 6 kDa). CONCLUSION: These results demonstrate that porcine 25 kDa amelogenin and its proteolytic derivatives stimulate bone sialoprotein transcription by targeting FRE, HOX and TAE in the bone sialoprotein gene promoter, and that full-length amelogenin and amelogenin cleavage products are able to regulate bone sialoprotein transcription via different signaling pathways.

Nicotine suppresses bone sialoprotein gene expression.

BACKGROUND AND OBJECTIVE: Tobacco smoking is a risk factor for periodontitis and osteoporosis. Nicotine is a major component of tobacco, and has been reported to inhibit proliferation and differentiation of osteoblasts. Bone sialoprotein (BSP) is a mineralized tissue-specific protein expressed by differentiated osteoblasts that appears to function in the initial mineralization of bone. The purpose of this study was to determine the effects of nicotine on bone metabolism. MATERIAL AND METHODS: We used rat osteobast-like UMR106 and ROS 17/2.8 cells and rat stromal bone marrow RBMC-D8 cells. To determine the molecular basis of the transcriptional regulation of the BSP gene by nicotine, we conducted Northern hybridization, transient transfection analyses with chimeric constructs of the BSP gene promoter linked to a luciferase reporter gene and gel mobility shift assays. RESULTS: Nicotine (250 microg/mL) decreased the BSP mRNA levels at 12 and 24 h in UMR106 and ROS 17/2.8 cells. From transient transfection assays using various sized BSP promoter-luciferase constructs, nicotine decreased the luciferase activities of the construct, including the promoter sequence nucleotides -116 to +60, in UMR106 and RBMC-D8 cells. Nicotine decreased the nuclear protein binding to the cAMP response element (CRE), fibroblast growth factor 2 response element (FRE) and homeodomain protein-binding site (HOX) at 12 and 24 h. CONCLUSION: This study indicates that nicotine suppresses BSP transcription mediated through CRE, FRE and HOX elements in the proximal promoter of the rat BSP gene.

EVALUATION OF PATIENT EXPOSURE IN FAST kVp SWITCHING DUAL ENERGY COMPUTED TOMOGRAPHY: PHANTOM STUDY.

The aim of this study was to evaluate the suitability of size specific dose estimates (SSDE) to estimate patient dose in Fast kVp switching dual energy CT. An anthropomorphic phantom (RAN-110) was repeatedly scanned (chest, abdomen and the pelvis) using a 64 detector row MDCT (Discovery CT750 HD, GE Healthcare, Milwaukee, WI, USA) with various CT parameters, including Fast kVp switching. Dosimetry was performed using thermo-luminescent dosimeters, positioned both superficially and within the phantom. SSDE was calculated for all slices of the anthropomorphic phantom using both the localiser and axial images. In Fast kVp switching, SSDE underestimated the measured absorbed dose for the chest/abdomen region ~35% at the maximum, but were in closer agreement for the pelvic region about within 10%. In single energy techniques, SSDE could not be applied in the estimation of organ doses, but in Fast kVp switching dual energy techniques, SSDE could be applied for anatomical regions with larger thicknesses.

Is outer arm dynein intermediate chain 1 multifunctional?

The outer arm dynein of sea urchin sperm axoneme contains three intermediate chains (IC1, IC2, and IC3; M(r) 128,000, 98,000, and 74,000, respectively). IC2 and IC3 are members of the WD family; the WD motif is responsible for a protein-protein interaction. We describe here the molecular cloning of IC1. IC1 has a unique primary structure, the N-terminal part is homologous to the sequence of thioredoxin, the middle part consists of three repetitive sequences homologous to the sequence of nucleoside diphosphate kinase, and the C-terminal part contains a high proportion of negatively charged glutamic acid residues. Thus, IC1 is a novel dynein intermediate chain distinct from IC2 and IC3 and may be a multifunctional protein. The thioredoxin-related part of IC1 is more closely related to those of two redox-active Chlamydomonas light chains than thioredoxin. Antibodies were prepared against the N-terminal and middle domains of IC1 expressed as His-tagged proteins in bacteria. These antibodies cross-reacted with some dynein polypeptides (potential homologues of IC1) from distantly related species. We propose here that the three intermediate chains are the basic core units of sperm outer arm dynein because of their ubiquitous existence. The recombinant thioredoxin-related part of IC1 and outer arm dyneins from sea urchin and distantly related species were specifically bound to and eluted from a phenylarsine oxide affinity column with 2-mercaptoethanol, indicating that they contain vicinal dithiols competent to undergo reversible oxidation/reduction.

Prostaglandin E2 induces expression of receptor activator of nuclear factor-kappa B ligand/osteoprotegrin ligand on pre-B cells: implications for accelerated osteoclastogenesis in estrogen deficiency.

Estrogen deficiency causes bone loss as a result of accelerated osteoclastic bone resorption. It also has been reported that estrogen deficiency is associated with an increase in the number of pre-B cells in mouse bone marrow. The present study was undertaken to clarify the role of altered B lymphopoiesis and of the receptor activator of nuclear factor-kappa B ligand (RANKL), a key molecule in osteoclastogenesis, in the bone loss associated with estrogen deficiency. In the presence of prostaglandin E2 (PGE2), the activity to form tartrate-resistant acid phosphatase (TRAP)-positive osteoclast-like cells was significantly greater in bone marrow cells derived from ovariectomized (OVX) mice than in those from sham-operated mice. Northern blot analysis revealed that PGE2 increased the amount of RANKL messenger RNA (mRNA) in bone marrow cells, not only adherent stromal cells but nonadherent hematopoietic cells; among the latter, RANKL mRNA was more abundant in OVX mice than in shamoperated mice and was localized predominantly in B220+ cells. Flow cytometry revealed that most B220+ cells in bone marrow were RANKL positive and that the percentage of RANKL-positive, B220low cells was higher in bone marrow from OVX mice than in that from sham-operated mice. The increase in the expression of RANKL and the percentage of these cells in OVX mice was abolished by the administration of indomethacin in vivo. PGE2 also markedly increased both the level of RANKL mRNA and cell surface expression of RANKL protein in the mouse pre-B cell line 70Z/3. Finally, osteoclastogenic response to PGE2 was reduced markedly by prior depletion of B220+ cells, and it was restored by adding back B220+ cells. Taken together with stimulated cyclo-oxygenase (COX)-2 activity by tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) in estrogen deficiency, these results suggest that an increase in the number of B220+ cells in bone marrow may play an important role in accelerated bone resorption in estrogen deficiency because B220+ cells exhibit RANKL on the cell surface in the presence of PGE2, thereby leading to accelerated osteoclastogenesis.

Association of a polymorphism of the transforming growth factor-beta1 gene with genetic susceptibility to osteoporosis in postmenopausal Japanese women.

Transforming growth factor-beta (TGF-beta) is both abundant in bone and an important regulator of bone metabolism. A T-->C transition at nucleotide 29 in the signal sequence region of the TGF-beta1 gene results in a Leu-->Pro substitution at amino acid position 10. The possible association of this polymorphism with bone mass and the prevalence of osteoporosis has now been investigated in a total of 287 postmenopausal women from two regions (Obu City, Aichi Prefecture, and Sanda City, Hyogo Prefecture) of Japan. A significant association of TGF-beta1 genotype with bone mass was detected in both populations; bone mineral density (BMD) at the lumbar spine was greater in individuals with the CC genotype than in those with the TT or TC genotype. The frequency of vertebral fractures was significantly lower in individuals with the CC genotype than in those with the TC or TT genotypes. For each region, multivariable logistic regression analysis revealed that the frequency of the T allele was significantly higher in subjects with osteoporosis than in controls. Also, the serum concentration of TGF-beta1 in individuals with the CC genotype was significantly higher than that in age-matched subjects with the TC or TT genotype in osteoporotic or osteopenic as well as healthy control groups. These results suggest that the T/C polymorphism of the TGF-beta1 gene is one of the genetic determinants of bone mass and that the T allele is an independent risk factor for the genetic susceptibility to osteoporosis in postmenopausal Japanese women. Thus, analysis of the TGF-beta1 genotype may be useful in the prevention and management of osteoporosis.

Synthesis and antihypertensive activity of stereoisomers of 4-piperidyl-1,3-dihydro-2-oxo-2H-benzimidazoles. Enhanced potencies of (+) isomers.

To elucidate the relationship between the pharmacological activity and stereochemical structure, we resolved 1-[2-(3-,4,5-trimethoxyphenyl)-2-hydroxy-1-methylethyl]-4-(1,3-dihydro-2-oxo-2H -benzimidazol-1-yl)piperidine (1 and 2) and 1-[2-(3,4-dimethoxyphenyl)-2-hydroxy-1-methylethyl]-4-(1,3-dihydro-2-oxo-2H-benzimidazol-yl)piperidine (3), which produced hypotensive effects mainly through their alpha-blocking actions. Threo isomers 1 and 3 were resolved via diastereomeric carbamates. Erythro isomer 2 was obtained by an oxidation and reduction sequence from optically active 1. No significant difference was found between the pharmacological activities of the threo and erythro isomers of the corresponding compounds. However, a clear difference was found between the pharmacological activities of the optical isomers. Difference was most clearly shown in the hypotensive actions of normotensive rats and in alpha-adrenergic blocking activities of isolated rat vas deferens. In these actions, (+) isomers were always more potent than the corresponding (-) isomers.

Studies of cardiotonic agents. 8. Synthesis and biological activities of optically active 6-(4-(benzylamino)-7-quinazolinyl)-4,5-dihydro-5-methyl-3(2H)- pyridazinone (KF15232).

We previously reported that (+/-)-6-(4-(benzylamino)-7-quinazolinyl)-4,5- dihydro-5-methyl-3(2H)-pyridazinone (+/-)-1, KF15232) showed potent cardiotonic activity with a strong myofibrillar Ca(2+)-sensitizing effect. As an extension of our work, we attempted to synthesize optically active 1. (+/-)-4-(4-(Benzylamino)-7-quinazolinyl)-3-methyl-4-oxobutyric acid (-)-menthyl ester (6) was separated into both diastereoisomers, and each was converted to optically pure 1 (> 99% ee) in an enantioselective manner. In order to determine the absolute configuration of the isomers, an alternative synthesis of optically active 1 was employed. The precursor of (-)-1 ((+)-9) was obtained by enantioselective synthesis from (R)-D-alanine. Consequently, we concluded that the absolute configuration of (-)-1 at the 5-position of the pyridazinone ring was R. The cardiotonic effects and inhibitory activities to PDE III and V of racemic 1 and (-)-1 were more potent than those of (+)-1. These compounds also demonstrated greater vasorelaxant effects in guinea pig aorta. In contrast, (+)-1 showed only weak cardiotonic and vasodilating effects, although the compound displayed potent Ca(2+)-sensitizing activity. Racemic and (-)-1 attracted our interest for the treatment of congestive heart failure.

Effect of peripheral nerve injury on nuclear magnetic resonance relaxation times of rat skeletal muscle.

RATIONALE AND OBJECTIVES: The authors evaluate the changes in magnetic resonance (MR) relaxation times of rat skeletal muscles in vivo after nerve injury and during neural recovery, and determine the major determinants of relaxation times. MATERIALS: Magnetic resonance relaxation times, blood volume, and water and fat content were examined after nerve injury and during recovery with time course. RESULTS: Nerve injury led to longer T2 values compared with controls, but there were no significant changes in T1 values. After the initial prolongation of T2 after nerve injury, no changes were observed. Neural recovery resulted in a return of T2 values to normal. The time course of changes in blood volume was similar to that of changes in T2, and T2 values were correlated strongly with 19-fluorine-MR spectroscopy estimates of blood volume (r2 = 0.94). CONCLUSIONS: T2 values may be useful to monitor recovery after nerve injury and may be related to the blood volume in skeletal muscle.

Expression of p53 and its transcriptional target genes mRNAs in the ethylnitrosourea-induced apoptosis and cell cycle arrest in the fetal central nervous system.

Ethylnitrosourea (ENU) is an alkylating agent and we previously clarified that it induced apoptosis and cell cycle arrest in the fetal central nervous system (CNS). In the present study, we studied the expression of p53 and its transcriptional target genes to investigate the role of p53 in the ENU-induced apoptosis and cell cycle arrest in the fetal CNS following the administration to dams on day 13 of gestation (GD13). Although the enhancement of p53 mRNA expression was not detected by reverse transcription and polymerase chain reaction (RT-PCR), p53-positive signals were detected immunohistochemically in the nuclei of neuroepithelial cells of the ENU-administered fetuses from 1 hour after treatment (HAT) to 12HAT, and they were most intensive at 3HAT. On the other hand, p53-positive signals were scarcely detected in the control fetuses. Among the p53 target genes, the expression of p21, bax, cyclinG1 and fas mRNAs increased and peaked at 6HAT. In addition, strong immunoreactivity for p21 was detected in the nuclei of neuroepithelial cells of the fetuses at 6HAT. The expression of p53 protein increased prior to the induction of apoptosis and cell cycle arrest, and transcription of its target genes was also activated. The present results suggest that ENU may induce apoptosis and cell cycle arrest in the fetal neuroepithelial cells in a p53-dependent manner.

Novel synthesis of electroresponsive poly(thiophenylene) through a Michael-type addition.

[figure: see text] A novel poly(thiophenylene) having N,N-diphenyl-1,4-phenylenediamine (PDA) as a redox unit was synthesized through a Michael-type addition. This polymerization proceeded at room temperature without catalysts. The polymer obtained acted as a good electroresponsive material with moderate thermostability.

Time course of recovery from nerve injury in skeletal muscle: energy state and local circulation.

This study examined the time course of recovery from nerve injury on energy state assessed by phosphorus-31 magnetic resonance spectroscopy and local circulation dynamics by fluorine-19 magnetic resonance spectroscopy in skeletal muscles of rats. The hindlimb muscles that had undergone unilateral sciatic nerve compression for 2 wk (CN) were compared with sham-operated (SO) muscles and with muscles that had the compression removed after 2 wk and were allowed to recover for 4 wk (R4) or for 6 wk (R6). The energy state and local circulation dynamics of CN muscles were less than those of SO muscles (P < 0.01). The energy state of R4 muscles remained at levels similar to CN muscles, whereas the local circulation dynamics improved but not back to SO values. In R6 muscles, both parameters returned to SO values. These results showed that the recovery processes of circulation precede those of energy state in skeletal muscles.

KF31327, a new potent and selective inhibitor of cyclic nucleotide phosphodiesterase 5.

The effects of KF31327 (3-ethyl-8-[2-(4-hydroxymethylpiperidino)benzylamino]-2,3-dihydro-1H-imidazo[4,5-g]quinazoline-2-thione dihydrochloride) on phosphodiesterase 5 (cyclic GMP-specific phosphodiesterase) activity and platelet aggregation were investigated and compared with those of sildenafil, a well-known phosphodiesterase 5 inhibitor. KF31327 inhibited phosphodiesterase 5 from canine trachea (K(i)=0.16 nM) more potently than sildenafil (K(i)=7.2 nM). The kinetic analysis revealed that KF31327 was a non-competitive inhibitor. In the presence of nitroglycerin (nitric oxide generator), both compounds inhibited the collagen-induced aggregation of rabbit platelets at less than 0.1 microM, augmenting intracellular cyclic GMP level without affecting cyclic AMP. In contrast, in the absence of nitroglycerin, a higher concentration (10 microM) of KF31327 was required to inhibit platelet aggregation and increased both cyclic nucleotide levels. However, 10 microM sildenafil did not affect aggregation despite elevation of cyclic GMP comparable to that in the presence of nitroglycerin. These results indicate that in the presence of nitroglycerin, the inhibition of platelet aggregation by KF31327 is due to the elevation of cyclic GMP, whereas the mechanism underlying the inhibition without nitroglycerin might be related to a rise in intracellular cyclic AMP.

Three-dimensional fast spin-echo MR of the inner ear: ultra-long echo train length and half-Fourier technique.

We compared the image quality of the newly developed ultra-long echo train length (ETL) 3-D fast spin-echo (FSE) and half-Fourier technique, which is performed in less than 3 minutes, with the conventional 3D-FSE imaging technique, which takes 15 minutes, in assessing MR examinations of the inner ear. The new method's images were almost comparable to the conventional 3D-FSE images in depicting anatomic details and pathologic findings. Implementation of the ultra-long ETL and half-Fourier 3D-FSE imaging technique enables acquisition of inner ear MR studies in a vastly reduced time and with high spatial resolution without significant penalty, opening the possibility for low-cost screening of acoustic tumors without contrast enhancement in less than 3 minutes.

Synthesis and preliminary evaluation of a carbon-11-labeled adenosine transporter blocker [(11)C]KF21562 .

We prepared an (11)C-labeled adenosine transporter blocker, [1-methyl-(11)C]-3-[1-(6,7-dimethoxyquinazolin-4-yl)piperidin-4-yl]-1,6-dimethyl-2,4(1H, 3H)-quinazolinedione ([(11)C]KF21652) and examined its potential as a positron emission tomography (PET) ligand for mapping adenosine transporters in the brain and peripheral organs. The log P(7.4) value of KF21652 was 3.14, and the K(i) value was 13 nM for adenosine transporters using [(3)H]nitrobenzylthioinosine as a radioligand. In mice, the highest initial uptake was found in the liver, followed by the kidney and small intestine. The brain uptake was very low. The radioactivity level slightly increased with time in the liver and small intestine, but decreased in the other organs. Coinjection of carrier KF21652 slightly decreased the uptake of [(11)C]KF21562 only in the liver, but not in any other organs. Ex vivo autoradiography of the rat brain showed that [(11)C]KF21652 was scarcely incorporated into the brain. On the other hand, in vitro autoradiography showed the binding of [(11)C]KF21562 to adenosine transporters with high nonspecific binding. These results show that the compound is not a suitable PET ligand for mapping adenosine transporters.

Plasma thrombomodulin concentration in diabetes mellitus.

Thrombomodulin is an endothelial cell membrane protein acting as a cofactor for the activation of plasma protein C. Recently, it was found that soluble forms of thrombomodulin exist in plasma. Although the physiological significance of circulating thrombomodulin is presently obscure, it may reflect injury of the endothelial cell. In the present study, we examined plasma thrombomodulin concentrations in 106 Type 2 (non-insulin-dependent) diabetic patients. Plasma thrombomodulin was determined by a sandwich ELISA employing monoclonal anti-thrombomodulin antibodies. The patients with proteinuria had higher plasma thrombomodulin concentrations (61.0 +/- 36.0 ng/ml) compared to the patients without proteinuria (33.6 +/- 9.5 ng/ml, P less than 0.001) and control subjects (32.8 +/- 6.5 ng/ml, P less than 0.001). Plasma thrombomodulin concentrations were positively correlated with the level of serum creatine, blood urea nitrogen, urinary albumin and urinary beta 2-microglobulin (P less than 0.001 for each), but not with fasting plasma glucose, hemoglobin A1c or fructosamine. Elevated plasma thrombomodulin was also observed in the patients with pre-proliferative (63.4 +/- 28.9 ng/ml) or proliferative retinopathy (57.4 +/- 34.7 ng/ml), but not in the patients with non-proliferative retinopathy (33.5 +/- 12.9 ng/ml) or those without retinopathy (32.4 +/- 8.9 ng/ml). Even in the 81 diabetic subjects without proteinuria as determined by a dip and read method, and whose serum creatinine was lower than 1.0 mg/dl, the plasma thrombomodulin concentration was significantly higher in the patients with pre-proliferative (41.5 +/- 4.4 ng/ml) and proliferative retinopathy (41.0 +/- 12.8 ng/ml) compared to the patients without retinopathy (32.2 +/- 8.8 ng/ml) and those with non-proliferative retinopathy (31.9 +/- 7.8 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Decreased ketonaemia in the monosodium glutamate-induced obese rats.

Plasma concentrations of total ketone bodies, acetoacetate (AcAc) and 3-hydroxybutyrate (3-OHBA) in monosodium glutamate (MSG)-induced obese rats were measured. MSG-treated rats showed higher Lee's indices, shorter naso-anal and tail length, and a more marked intraperitoneal fat deposition than control rats. Plasma concentrations of glucose, free fatty acid, triglyceride and phospholipids were significantly increased in the MSG-treated rats as compared to the control rats (24 weeks-old). Plasma levels of total ketone bodies, AcAc and 3-OHBA were all decreased in the MSG-treated rats as compared to control rats. The ratio, 3-OHBA/AcAc in the MSG-treated rats were not different from those in the control rats.

Experimental airborne transmission of PRRS virus.

A series of three experiments, differing primarily in airflow volume, were performed to evaluate the likelihood of airborne transmission of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) from infected to non-infected pigs. Pigs were housed in two units (unit A and unit B) located 1m apart and connected by pipes. The air pressure and diameter of the pipes, depending on experiments, were strictly controlled to allow desired airflow volumes from unit A to unit B. Either 25 (experiment 1 and experiment 3) or 26 (experiment 2) pigs infected recently with PRRSV, and either 25 (experiment 1 and experiment 3) or 17 (experiment 2) pigs from a PRRSV-free herd, were housed in unit A. Either 50 pigs (experiment 1 and experiment 3) or 43 pigs (experiment 2) from a PRRSV-free herd were housed in unit B. The amount of air transmitted from unit A to unit B, expressed as a percentage of ventilation intake, was approximately 70, 10, and 1% for experiment 1, experiment 2 and experiment 3, respectively. Blood samples were collected from all pigs once per week and analyzed for antibodies against PRRSV. Based on these methods, airborne transmission of PRRSV from infected to non-infected pigs was confirmed in each of the three experiments.

Demonstration of airborne transmission of Actinobacillus pleuropneumoniae serotype 2 between simulated pig units located at close range.

Airborne transmission of Actinobacillus pleuropneumoniae was studied as the percentage of air needed to establish airborne transmission from an infected pig unit into a neighbouring non-infected pig unit. The experiment was carried out in two containers constructed as pig units, placed 1m apart and connected by pipes. By manipulating the air pressure in the two units, the amount of ventilation air transferred from the infected pigs (unit A) to the non-infected pigs (unit B) was controlled and measured. In three experiments, between 48 and 50 specific pathogen free-pigs were randomly assigned to each of the two units. In unit A, five pigs (experiment 1) or eight pigs (experiments 2 and 3) were inoculated with A. pleuropneumoniae serotype 2. In experiments 1 and 3, 10% of the air was transferred from unit A to B; in experiment 2, 70% of the air was transferred. In the non-infected unit (B), 36% of the pigs seroconverted during experiment 2 (70% air transfer), whereas none of the pigs seroconverted in experiments 1 and 3 (10% air transfer). As air transmission between closely located pig units has been estimated to be less than 2% under field conditions, these results indicate that airborne transmission of A. pleuropneumoniae serotype 2 between closely located pig units is rare.