CMV encephalitis is typically more aggressive than HIV brain disease. Clinical evidence of cerebellar or brainstem involvement is present in 30%: features of polyradiculitis and retinitis (up to 75%) may coexist [114]. Presentation of lumbosacral polyradiculitis is usually as a rapidly progressive, painful, bilateral ascending flaccid paralysis with saddle anaesthesia, areflexia, sphincter dysfunction and urinary retention. MRI scanning and CSF PCR are the preferred diagnostic tests (category selleck inhibitor III recommendation). Development of any neurological

feature in a patient with HIV with a low CD4 cell count warrants urgent investigation, initially with neuroimaging and, if not contraindicated, lumbar puncture. On CT scan, diffuse white matter hypodensities with ependymal enhancement, ventricular enlargement, meningeal enhancement and focal or nodular ring-enhancing lesions are seen. However, MRI is far more sensitive when these features are best revealed on gadolinium enhanced T1 weighted scans with periventricular enhancement commonly seen. However, imaging lacks sensitivity and many patients have normal or nonspecific changes [115]. CSF examination is rarely grossly abnormal although a slightly raised protein and mild lymphocytosis are not infrequent. In patients with isolated or concomitant polyradiculitis, diffuse enhancement

of cord parenchyma, nerve roots and meninges is seen on contrast-enhanced MR and a characteristically pronounced polymorphonuclear cell pleocytosis is usual. Electromyogram studies demonstrate axonal neuropathy and can help distinguish find more CMV polyradiculitis from an acute inflammatory demyelinating polyneuropathy.

Diagnosis of both conditions is based around nucleic acid amplification Y-27632 2HCl of CMV DNA. A positive CSF PCR has a sensitivity of >80% and a specificity of >90% with negative and positive predictive values of 86–92% and 95–98%, respectively [116–119]. However, PCR may rarely be negative in patients subsequently found to have active CMV disease of the brain. Brain biopsy is rarely indicated in view of localization. Ganciclovir with or without foscarnet is the treatment of choice (category III recommendation). There have been no prospective controlled trials for CMV neurological disease and, although well designed randomized controlled trials on the therapeutic efficacy of ganciclovir, foscarnet, valganciclovir and cidofovir (all effective) exist for CMV retinitis, the results of these cannot be extrapolated to encephalitis or polyradiculitis [119–121]. In a small open noncomparative study in the pre-HAART era, combination treatment with ganciclovir and foscarnet did improve or stabilize encephalitis/polyradiculitis in 74% of 31 HIV-seropositive patients with neurological disease; however, overall mean survival was only 3 months [122].

Osteoporosis and previous fracture may also be considered a contraindication to a thiazolidinedione http://www.selleckchem.com/products/Belinostat.html “
“Schizophrenia and bipolar illness are severe mental illnesses that affect around 1–2% of the population. They are associated with premature mortality with a reduced life-expectancy of 10–20 years. Although suicide and trauma contribute the highest relative risk of mortality, physical illness accounts for around three-quarters of all deaths, with cardiovascular disease being the most common cause of death. Traditional cardiovascular risk factors including diabetes, dyslipidaemia, obesity and smoking are all more common in people with severe

mental illness (SMI). Although there has been an increasing awareness of physical health issues in people with SMI, the level of screening for and management of cardiovascular risk factors has remained low. A number of national and international bodies have developed guidelines to address the challenge of physical morbidity in SMI. AZD5363 purchase The principles of screening for and managing cardiovascular disease in people with SMI are

similar to those in the general population, but there are additional challenges. Health care professionals within psychiatry, general practice and medical specialties need to work together to reduce the burden of physical health problems in people with SMI. Copyright © 2010 John Wiley & Sons. “
“Despite improvements in diabetic care, studies in the UK and elsewhere demonstrate a significant persistence in neonatal complications after pregnancy complicated by maternal diabetes. Some complications (e.g. congenital anomalies) are severe, whilst others aminophylline are transient and unlikely to lead to long term harm if managed according to standard guidelines. Some neonatal complications may be avoidable, arising

as a result of obstetric interventions related to maternal diabetes control. Of greater concern are iatrogenic complications that arise from decisions which have no clear rationale (e.g. “routine” admission of a baby to a neonatal unit). Therefore, planning for neonatal management must start in advance of delivery, involve all relevant groups of professionals, and be centered on the needs of the mother and baby and not upon historical organizational policies. “
“In the UK there are currently no national structured education programmes for people newly diagnosed with type 1 diabetes. In Leicester we developed a programme for people to attend within six months of diagnosis with the aim of increasing patients’ self-efficacy in managing their diabetes. Forty-two people attended the group over a 12-month period.

001).[9] However, only 8% of patients in the

SEPAL trial had non-endometrioid EC (13.5% of the intermediate- and high-risk group). Therefore, results of the SEPAL trial may not be fully applicable to patients with non-endometrioid EC. Also, the median age of patients in the SEPAL trial was relatively young (56 years), and those results may not be applicable to elderly patients.[9] In light of the current evidence, it is not possible to draft definitive conclusions regarding the role of lymphadenectomy in EC patients. In this article, we will address the most important questions regarding the role of lymphadenectomy in EC: Which is the population at risk of lymphatic spread? How can we select patients at risk of lymphatic spread? Which are the patterns of para-aortic lymphatic spread? Alectinib manufacturer What is the role of sentinel lymph node (SLN) mapping? How does lymphadenectomy impact morbidity, quality of life (QOL) and costs? If lymph node metastases are identified, do we have adequate treatment? How can we

design a study to test the diagnostic and therapeutic role of lymphadenectomy? According to a risk stratification system in use at Mayo Clinic, Rochester, Minnesota, USA (Table 1), low-risk patients can be adequately treated with removal http://www.selleckchem.com/products/VX-809.html of the uterus and adnexa alone, without significantly compromising survival. In this subgroup, lymphadenectomy carries only potential adjunctive morbidity.[10, 11] In fact, we previously demonstrated that tumor diameter significantly influences

the risk of lymph node dissemination. In an analysis of more than 300 endometrioid EC patients with FIGO grade 1 or 2 and myometrial invasion limited to the inner half, we found that no patients with tumor diameter of 2 cm or less had positive lymph nodes or lymph node recurrences or died of disease.[11] This finding has been recently prospectively validated by our group[10] and others.[12, 13] Based on the surgical protocol currently in use at Mayo Clinic, Vildagliptin all patients with primary epithelial EC undergo hysterectomy with or without bilateral salpingo-oophorectomy. The need to perform lymphadenectomy is based on the tumor characteristics (histological type, FIGO grade, tumor diameter and depth of myometrial invasion) determined at frozen-section analysis. Systematic pelvic and para-aortic lymphadenectomy is performed when patients have myometrial invasion greater than 50%, non-endometrioid histology or both. If patients do not match these characteristics, the choice to perform pelvic node dissection (with para-aortic lymphadenectomy only in those patients with documented pelvic lymph node metastases) is based on cervical involvement, FIGO grade and tumor diameter (Figs 1, 2).

The flasks were then inoculated with this suspension to an initial OD600 nm of 0.05 in 25 mL of fresh DM with or without thiamine and incubated at 37 °C with shaking. The OD600 nm was then measured at appropriate intervals throughout signaling pathway the growth. Cultures grown in 25 mL BHI in 250 mL flasks with shaking at 37 °C were assayed for acid tolerance by diluting 1 : 10 into BHI medium adjusted to pH 3.0. At suitable intervals, samples were removed, serially diluted, and 10 μL aliquots of each dilution were plated on BHI agar plates. Colonies were counted after 24 h at 37 °C and survival was calculated as a percentage of the

cell count at time zero. For acid-adapted cultures, cells were first diluted 1 : 10 into BHI medium adjusted to pH 5.0, incubated for 1 h, and then further diluted 1 : 10 into BHI medium adjusted Oligomycin A chemical structure to pH 3.0. For experiments on thiamine-depleted cells, cultures were grown in DM either with or without thiamine supplementation (3 μM), and then after 12 h of growth, cells were diluted 1 : 20 into DM adjusted to pH 3.0 (which contained thiamine). Survival was determined by serial dilution and plating on BHI agar plates

as described above. Relative transcript levels of thiT in exponentially growing cells (OD600 nm = 0.6) at pH 5.5 or pH 5.0 compared to pH 7.0 were measured by real-time RT-PCR as previously described (Utratna et al., 2011). Acetoin was determined by the modified Voges–Proskauer reaction of Westerfeld (1945), with slight modification. Stationary phase cultures of L. monocytogenes wild-type and mutant grown in both DM supplemented with thiamine and DM without thiamine were recovered and centrifuged at 14 500 g for 5 min. The supernatants were used to measure the acetoin production. To 1.0 mL of culture supernatant in DM, diluted appropriately to give a reading within the range of the calibration curve for acetoin, 0.2 mL of 0.5% (w/v) l-arginine monohydrochloride and 0.2 mL

of 5% (w/v) α-naphthol in 2.5 N NaOH were added, in that order. The pink color that developed after C1GALT1 1-h incubation was measured by recording the absorbance at 530 nm using a UV-VIS spectrophotometer (Spectronic® 20 Genesys™). The concentration of acetoin was estimated from a linear calibration curve based on measurements of standard acetoin solutions (0.01–40 μg mL−1). To identify genetic determinants of acid tolerance in L. monocytogenes, a library of 4800 transposon (Tn917-lacZ) mutants was screened for mutants displaying an acid-sensitive phenotype at pH 3.0. One acid-sensitive mutant, initially designated ads12, was found to induce a poor adaptive ATR at pH 5.0 compared to the wild-type, indicated by a dramatically reduced ability to survive at pH 3.0 (Fig. 1a).

Sera from 42 patients allergic to A. alternata (18 female and 24 male; mean age, 20.5 years; age range, 10–33 years) and 17 control subjects (11 female and six male; mean age, 32.3 years; age range, 14–70 years) were included in the study. Diagnosis of A. alternata allergy was based on a clinical history of recurrent rhinitis (four patients), asthma (four patients), rhinoconjunctivitis (12 patients), rhinitis and asthma (12 patients), rhinoconjunctivitis and asthma (10 patients); a positive cutaneous response to a commercial A. alternata extract (Bial-Arístegui, Bilbao, Spain); and specific IgE to A. alternata extract > 0.35 IU mL−1 according ImmunoCAP (Thermo-Fisher,

Uppsala, Sweden). Eight GSK3235025 healthy subjects and nine allergic individuals Selleck Trametinib sensitized to different allergenic sources unrelated

to A. alternata, as demonstrated by negative SPT responses and lack of A. alternata-specific IgE, were used as controls. Standard molecular genetic techniques were used (Sambrook et al., 1989). For Southern blotting, genomic DNA was prepared from recombinant yeasts as previously described (Barth & Gaillardin, 1996). Afterwards, DNA was digested, separated on a 0.8% agarose gel, and transferred onto Hybond-N+ nylon membranes (GE-Healthcare, Little Chalfont, Buck, UK). Probes were labeled with [32P]-dCTP using the MegaPrime Kit (GE-Healthcare). The autosomal vector pMM4 was used to express the Alt a 1 allergen. The YlMETII promoter was obtained from plasmid pSG70 (García, 1993; Domínguez et al., 2003) and cloned between the EcoRI-BamHI restriction sites of the pBluescript-SK. The Alt a 1-coding gene sequence (Asturias et al., 2003) Cyclin-dependent kinase 3 was cloned after this promoter into the BamHI site, resulting in the pMMR2 vector. As the insertion of the target gene between yeast promoter and terminator sequences produces more efficient expression of heterologous genes in Y. lipolytica (Franke et al., 1998), the YlSTE7 terminator was amplified using specific primers and cloned into the SpeI and XbaI-restriction sites of pMMR2, resulting in the pMMR3 plasmid. This plasmid

was digested with ClaI and XbaI and the 1.8 kb-fragment containing the fusion of the YlMTPII promoter-Alt a 1-YlSTE7-terminator was purified and inserted into the pINA240 plasmid (Barth & Gaillardin, 1996), giving rise to pMMR4. The correct construction was verified by sequencing. The construction of the integrative plasmid pMMR10 was performed as follows. To create the pMMR10 plasmid, the 1.8-kb ClaI-SphI fragment from pMMR4 carrying the YlMTPII promoter-Alt a 1-YlSTE7-terminator fusion was cloned into the pINA62 plasmid. The correct construction was verified by sequencing. Plasmid maps of pMMR4 and pMMR10 and sequences of the specific primers used for YlSTE7 terminator amplification are available as Supporting Information (Fig. S1, Table S1). nAlt a 1 was purified from A. alternata CBS 603.78 spent culture medium after 3 weeks of static growth in Czapeck broth at 25 °C.

5% were late presenters for HIV diagnosis. Among 6897 treatment-naïve patients in the ClinSurv cohort, 58.1% were late presenters for care. Late presenters for care were older (median 42 vs. 39 years for early presenters), more often Saracatinib cell line heterosexuals from low-prevalence countries (18.1% vs. 15.5%, respectively) and more

often migrants (18.2% vs. 9.7%, respectively; all P < 0.005). The probability of late presentation was >65% throughout the observation period in migrants. The probability of late presentation for care clearly decreased in men who have sex with men (MSM) from 60% in 1999 to 45% in 2010. In Germany, the numbers of late presenters for HIV diagnosis and care remain high. The probability of late presentation for HIV diagnosis seems to be particularly high for migrants. These results argue in favour of targeted test promotion rather than opt-out screening. Late presentation for care seems to be an additional problem after HIV diagnosis. The introduction of antiretroviral therapy (ART) has led to a dramatic decrease in HIV-associated morbidity and mortality [1, 2]. The risk for AIDS-defining events is highest in patients who do not receive antiretroviral treatment or who initiate

ART in advanced stages of immunodeficiency [3, 4]. CD4 T-cell counts Alpelisib supplier of <200 cells/μL were long considered the threshold at which to initiate antiretroviral treatment. Although most cases of severe opportunistic diseases occur at CD4 counts of <200 cells/μL, more recent studies have shown an increased risk for AIDS or death even in patients with higher

CD4 T-cell counts [5, 6]. These observations led to the recommendation that therapy should be started at 350 [7] or even 500 cells/μL [8]. The goal of therapy is the prevention of disease progression by starting therapy before CD4 cell counts drop below these thresholds. This can only be achieved if HIV infection is diagnosed early enough. Resveratrol It is estimated that in Europe, even with general availability of high-quality and affordable health care, as many as 25–35% of individuals who are infected with HIV are unaware of their HIV status. Therefore, late presentation remains a major challenge in patient management. Throughout Europe, factors associated with late presentation include older age, migrant status, heterosexual risk of transmission and male sex [9-15]. However, these factors may change over time and may be different for different regions of Europe. Recently a European consensus definition of late presentation (CD4 count <350 cells/μL or clinical AIDS) and presentation with advanced HIV disease (CD4 count <200 cells/μL or clinical AIDS) was published to facilitate cross-country comparisons of trends and results of targeted interventions [16]. Country-specific risk analyses are important to effectively guide public health interventions. Data concerning the situation of late presentation in Germany and detailed analyses are largely missing.

These findings are consistent with previously published data in which 7.1% of the X. bovienii-SF43 genome and 4.6% of the X. nematophila genome match with ORFs identified as phage related (Ogier et al., 2010). All of the described phage clusters BTK inhibition match with phagic modules previously identified with the RGPFinder web tool, which identifies large regions of genomic plasticity. The xbp1 cluster encodes the main tail synthesis proteins including the tail sheath (XbpS1), tube (XbpT1), and tail fiber (XbpH1) proteins. To determine whether

the xbp1 phage gene cluster encoded a mitomycin C-inducible xenorhabdicin, the xbpS1 sheath gene was inactivated. PEG-precipitated tail structures prepared from the SF43 and SF70 (xbpS1) strains were analyzed by SDS-PAGE gel electrophoresis. Figure 3 shows that the preparation from SF43 contained

43 and 98 kDa proteins that were identified by N-terminal sequence analysis as XbpS1 and XbpH1, respectively (lane 1). We were unable to resolve the identity of the 65-kDa protein by N-terminal sequencing. In the xbpS1 strain, the level of the 43-kDa protein band was dramatically reduced but not completely eliminated (lane 2). The identity of this additional 43-kDa protein could not be resolved by MALDI-TOF MS analysis. TEM analysis showed that phage tail structures were not produced CHIR 99021 in the SF70 strain (data not shown). Interestingly, inactivation of xbpS1 did not reduce XbpH1 production (Fig. 3), suggesting that xbpH1 was expressed, and XbpH1 fiber and baseplate structures were assembled in the xbpS1 strain. This result was similar to that observed with the ΔxnpS1 strain of X. nematophila (Morales-Soto & Forst, 2011). Phage tail preparations were PEG-precipitated from the SF43 and SF70 strains and assayed for antimicrobial activity against Photorhabdus luminescens enough TT01 and Xenorhabdus bovieni SF31 (Table 1). Preparations derived from the SF43 strain displayed a high level of activity against P. luminescens TT01 and X. bovienii-SF31 (Table 2), while antimicrobial activity was dramatically reduced in the preparations derived from SF70. These findings indicate

that Xbp1 xenorhabdicin was responsible for antimicrobial activity against susceptible competitors. The tail synthesis genes of xnp1 and xbp1 are highly conserved. The sequence identity for the 12 proteins encoded by the genes located between the cI and gpI genes ranges from 77% to 95%. The respective sheath proteins, XnpS1 and XbpS1, share 94% identity and the XnpT1 and XbpT1 tube proteins share 98% identity. The 5.9 kb insertion in the region neighboring fun(Z) contains 11 ORFs and is located between the tail fiber gene xbpH1 and the tail sheath gene xbpS1. It contains three truncated tail fiber ORFs (Ff–Fh) and three tandem transposase genes. As described previously, the xnp1 remnant P2 prophage encodes the tail sheath (XnpS1), tube (XnpT1), and tail fiber (XnpH1).

These findings are consistent with previously published data in which 7.1% of the X. bovienii-SF43 genome and 4.6% of the X. nematophila genome match with ORFs identified as phage related (Ogier et al., 2010). All of the described phage clusters Selleck AC220 match with phagic modules previously identified with the RGPFinder web tool, which identifies large regions of genomic plasticity. The xbp1 cluster encodes the main tail synthesis proteins including the tail sheath (XbpS1), tube (XbpT1), and tail fiber (XbpH1) proteins. To determine whether

the xbp1 phage gene cluster encoded a mitomycin C-inducible xenorhabdicin, the xbpS1 sheath gene was inactivated. PEG-precipitated tail structures prepared from the SF43 and SF70 (xbpS1) strains were analyzed by SDS-PAGE gel electrophoresis. Figure 3 shows that the preparation from SF43 contained

43 and 98 kDa proteins that were identified by N-terminal sequence analysis as XbpS1 and XbpH1, respectively (lane 1). We were unable to resolve the identity of the 65-kDa protein by N-terminal sequencing. In the xbpS1 strain, the level of the 43-kDa protein band was dramatically reduced but not completely eliminated (lane 2). The identity of this additional 43-kDa protein could not be resolved by MALDI-TOF MS analysis. TEM analysis showed that phage tail structures were not produced selleckchem in the SF70 strain (data not shown). Interestingly, inactivation of xbpS1 did not reduce XbpH1 production (Fig. 3), suggesting that xbpH1 was expressed, and XbpH1 fiber and baseplate structures were assembled in the xbpS1 strain. This result was similar to that observed with the ΔxnpS1 strain of X. nematophila (Morales-Soto & Forst, 2011). Phage tail preparations were PEG-precipitated from the SF43 and SF70 strains and assayed for antimicrobial activity against Photorhabdus luminescens Linifanib (ABT-869) TT01 and Xenorhabdus bovieni SF31 (Table 1). Preparations derived from the SF43 strain displayed a high level of activity against P. luminescens TT01 and X. bovienii-SF31 (Table 2), while antimicrobial activity was dramatically reduced in the preparations derived from SF70. These findings indicate

that Xbp1 xenorhabdicin was responsible for antimicrobial activity against susceptible competitors. The tail synthesis genes of xnp1 and xbp1 are highly conserved. The sequence identity for the 12 proteins encoded by the genes located between the cI and gpI genes ranges from 77% to 95%. The respective sheath proteins, XnpS1 and XbpS1, share 94% identity and the XnpT1 and XbpT1 tube proteins share 98% identity. The 5.9 kb insertion in the region neighboring fun(Z) contains 11 ORFs and is located between the tail fiber gene xbpH1 and the tail sheath gene xbpS1. It contains three truncated tail fiber ORFs (Ff–Fh) and three tandem transposase genes. As described previously, the xnp1 remnant P2 prophage encodes the tail sheath (XnpS1), tube (XnpT1), and tail fiber (XnpH1).

8%) patients received more than one intervention. The proportion of the 183 LBP patients who received each intervention first were: magnetic

resonance imaging (MRI) (36.6%), corticosteroid injection (32.8%), acupuncture (24.0%) and TENS (6.6%); the 57 OA patients were: acupuncture (45.6%), MRI (21.1%), injection (21.1%) and TENS (12.2%). After follow-up, patients remained either in the service, or discharged due to adequate PLX4032 manufacturer pain control or not attending their appointment. The mean in-service time was not significantly different between 305 LBP (211.3 ± 89.4 days) and 88 OA (223.7 ± 286.0 days) discharged patients. Eight of the 312 LBP (2.6%) and one of the 88 OA patients (1.1%) were re-referred. The utilisation of treatment strategies http://www.selleckchem.com/products/dabrafenib-gsk2118436.html was different between LBP and OA patients but the mean in-service time was similar at around 8 months. LBP patients often need investigation as the first intervention and similar proportions of patients received MRI, injection and acupuncture but fewer received TENS, which is

not recommended in NICE guidance for LBP management. Most OA patients received acupuncture but this is not recommended in NICE guidance for OA. Instead TENS is recommended as a self-management treatment. The data collected was reflective of the local population but the study was limited the by the lack of outcomes data recorded, therefore clinical effectiveness of the strategies used could not be determined. 1. Gill J, Taylor D, Knaggs for R. (2012) Persistent

Pain: Improving Health Outcomes. UCL School of Pharmacy: London 2. Dr Foster Intelligence, British Pain Society, Healthcare Quality Improvement Partnership (2012) National Pain Audit Final Report. National Pain Audit. URL http://www.nationalpainaudit.org/media/files/NationalPainAudit-2012.pdf (accessed 25/04/13) Andrea Manfrin1, Janet Krska1, Laura Caparrotta1,2 1Medway School of Pharmacy University of Kent, Kent, UK, 2Department of Pharmaceutical and Pharmacological Sciences, Padua, Italy A pilot study in Italy involving 80 community pharmacists found they were able to deliver MURs following training An enhanced MUR template made available via a web platform was very well completed, enabling collection of useful data for evaluation Feedback of the data gathered was available to pharmacy organisations in real time and showed potential benefit of the MUR for patients with asthma Italy’s national health service (NHS) has many similarities to the UK’s, but the Italian pharmacy model is still based on dispensing prescriptions and sale of OTC medicines. There is good information communication technology (ICT), but no patient medication records. Pharmacists provide services such as blood pressure, cholesterol monitoring, body mass index check and asthma monitoring, but these services have not been recognized and funded by the Italian Government and Italian pharmacists have never being trained to conduct any type of medicine review.

The information on the differential

distribution of these DNA sequences in the 15 serotypes of A. pleuropneumoniae may contribute to future research on the pathogenic mechanisms of different serotypes, typing-based diagnosis methods, and multivalent vaccines. Porcine contagious pleuropneumonia, which is caused by Actinobacillus pleuropneumoniae, is an extremely contagious and often fatal respiratory disease (Macinnes & Rosendal, 1988). This disease occurs in the countries that have a swine industry, and it is responsible for enormous economic losses to the swine industry. To date, 15 serotypes of A. pleuropneumoniae have been described (Blackall et al., 2002). These serotypes show significant differences

in pathogenicity and immunogenicity (Cruijsen et al., 1995; Jacobsen et al., 1996). Therefore, vaccines raised Bioactive Compound Library research buy against a specific serotype do not confer protection from infection by other serotypes (Ramjeet et al., 2008). Owing to the limited information on the genetic differences among the serotypes, studies on the immunity mechanisms of different serotypes, typing-based diagnosis, and multivalent genetically engineered vaccines have been significantly hampered. Therefore, the genomic differences among the principal serotypes should be identified and suitably exploited. Actinobacillus pleuropneumoniae serotypes 1 and 3 show the most Protein Tyrosine Kinase inhibitor significant variation in Glutamate dehydrogenase pathogenicity (Jacobsen et al., 1996). Serotype 1 is highly virulent, and infection of this serotype is associated with epidemic outbreak, high mortality, and serious lung lesions. However, serotype 3 is considered to be less virulent (Bosse et al., 2002).

Moreover, there are significant differences between the immunogenicities of the two serotypes, and the available vaccines for the two serotypes do not provide cross-protection (Cruijsen et al., 1995; Ramjeet et al., 2008). In this study, we identified the genomic differences between A. pleuropneumoniae serotypes 1 and 3 by performing representational difference analysis (RDA). This technique has been widely used to analyze genetic differences in bacteria (Lisitsyn & Wigler, 1993; Tinsley & Nassif, 1996), especially in the light of the limited availability of complete genome-sequence data and microarrays (Barcellos et al., 2009; Sack & Baltes, 2009). We identified the distribution of all the identified differential DNA sequences between the 15 serotypes of A. pleuropneumoniae. Actinobacillus pleuropneumoniae strains used for this study are listed in Table 1.