The seven remaining patients were heavily pretreated, showed virological rebound, and were found to harbour an insert-containing protease virus when receiving a PI-containing treatment. Of these patients, four were receiving LPV (patients

5 to 8) and one was receiving DRV (patient 9) when the insertion-mutated virus was selected. For the two remaining patients (patients 10 and 11), no plasma samples were available before the time of insertion detection. Five of these seven patients (71%) were infected with subtype B. At time of the first Lapatinib purchase detection of a protease insertion, patients 5 to 8 had previously received PIs, mainly IDV and NFV, for a median period of 4 years (range 33 months to 4 years), and harboured highly Tacrolimus purchase resistant virus with 10 to 12 PI-resistance mutations. In all these patients, ARV therapy was then switched to an LPV-containing regimen, with no or transient virological response. The protease insertion was detected in a median of 20 months (range 14–31 months) following LPV initiation between codons 33 and 38 (Table 2). The insertion was still present under the same PI-containing regimen 2 to 5 years later, with persistent viral replication. No major PI-resistance mutations and no nucleotide

changes surrounding the protease insertion were observed during the follow-up, with the exception of patient 5, whose virus selected the E35G mutation and two other PI-resistance mutations (K20T and L90M), respectively, 3 and 5 years after the initial detection of the protease insertion. Patient 9, who was infected with a CRF01_AE subtype,

was heavily PI-experienced, having received IDV, LPV and fAPV (fosamprenavir) for 10 years, and displayed plasma virus with six PI-resistance mutations with no insertion. After 9 months of a DRV-containing treatment with no virological response, an insertion E35E-E was first identified with three new resistance mutations: I54L, Q58E and I84V. For patient 10, who was infected with a CRF02_AG subtype and was previously Fossariinae treated with an SQV, NFV and APV-containing regimen, no baseline sample was available. Nine months after APV discontinuation, plasma virus was found to have five resistance mutations and an insertion of two amino acids (S37N-IN). A PI-containing regimen was then initiated with fAPV with no virological response. Interestingly, 7 months later, the previous major plasma virus with a protease insertion was replaced by a virus with no protease insertion and three new major resistance mutations, including a fAPV major mutation: I50V, but also the L33F and M46I mutations. After an additional year of viral replication under fAPV drug pressure, the virus resistance profile evolved genotypically; however, the protease insertion was no longer detected.

The seven remaining patients were heavily pretreated, showed virological rebound, and were found to harbour an insert-containing protease virus when receiving a PI-containing treatment. Of these patients, four were receiving LPV (patients

5 to 8) and one was receiving DRV (patient 9) when the insertion-mutated virus was selected. For the two remaining patients (patients 10 and 11), no plasma samples were available before the time of insertion detection. Five of these seven patients (71%) were infected with subtype B. At time of the first INNO-406 research buy detection of a protease insertion, patients 5 to 8 had previously received PIs, mainly IDV and NFV, for a median period of 4 years (range 33 months to 4 years), and harboured highly selleckchem resistant virus with 10 to 12 PI-resistance mutations. In all these patients, ARV therapy was then switched to an LPV-containing regimen, with no or transient virological response. The protease insertion was detected in a median of 20 months (range 14–31 months) following LPV initiation between codons 33 and 38 (Table 2). The insertion was still present under the same PI-containing regimen 2 to 5 years later, with persistent viral replication. No major PI-resistance mutations and no nucleotide

changes surrounding the protease insertion were observed during the follow-up, with the exception of patient 5, whose virus selected the E35G mutation and two other PI-resistance mutations (K20T and L90M), respectively, 3 and 5 years after the initial detection of the protease insertion. Patient 9, who was infected with a CRF01_AE subtype,

was heavily PI-experienced, having received IDV, LPV and fAPV (fosamprenavir) for 10 years, and displayed plasma virus with six PI-resistance mutations with no insertion. After 9 months of a DRV-containing treatment with no virological response, an insertion E35E-E was first identified with three new resistance mutations: I54L, Q58E and I84V. For patient 10, who was infected with a CRF02_AG subtype and was previously SSR128129E treated with an SQV, NFV and APV-containing regimen, no baseline sample was available. Nine months after APV discontinuation, plasma virus was found to have five resistance mutations and an insertion of two amino acids (S37N-IN). A PI-containing regimen was then initiated with fAPV with no virological response. Interestingly, 7 months later, the previous major plasma virus with a protease insertion was replaced by a virus with no protease insertion and three new major resistance mutations, including a fAPV major mutation: I50V, but also the L33F and M46I mutations. After an additional year of viral replication under fAPV drug pressure, the virus resistance profile evolved genotypically; however, the protease insertion was no longer detected.

This considerably exceeded the rate reported by previous studies (Gibb et al., 1992; Appelmelk et al., 1994; Amor et al., 2000; Gibbs et al., 2004). As the core type distribution among non-ESBL-producing strains (3.7%) was similar to those found earlier (Table 1), and as the production of ESBL is, at least partly, a clonal phenomenon (Woodford et al., 2011), the possible clustering

of the 58 K-12 core PCR-positive isolates was investigated. We found that 54 of these strains (93.1%) carried the rfbO25b gene with the O25 serogroup also confirmed by slide agglutination. All strains belonged to the B2 phylogenetic group. All isolates, except two, were ESBL-producing strains. Fifty-two Selleck CYC202 of the 54 K-12 Staurosporine in vivo core and rfbO25b-positive strains were typable by PFGE exhibiting 18 pulsotypes (10 clusters with 2–11 members and 8 singletons) (Fig. 1). Twenty-four selected isolates representing all pulsotypes were submitted to MLST and found to belong to the rapidly spreading, often multidrug resistant ST131 clone (Fig. 1). To rule out that the presence of the K-12 core-specific genes was restricted to Emirati UTI isolates of the O25 ST131 group, ten independent representatives of this clone isolated in Hungary from UTI (five strains) and BSI (five strains) in 2008 and 2009, respectively, were also tested. Importantly, all these strains were also positive with the

K-12 core-specific PCR (Fig. 1). Next, we determined the DNA sequence of the entire waa locus (Heinrichs et al., 1998) of one of the O25-ST131 isolates from our collection (#81009). The resulting > 16-kb sequence (GenBank JQ241150) covered the 15 K-12 core genes (Muller-Loennies et al., 2007) between Docetaxel concentration the kbl and the coaD genes flanking the waa locus. As expected, based on the PCR results, individual gene sequences displayed extensive homology to their respective homologues in the prototype K-12 commensal strain, MG1655 (Table 2). Comparison of the deduced amino acid sequences of the various Waa proteins of the ST131 O25 strain #81009 revealed ≥ 90% identities

with their counterparts in MG1655 with the exception of WaaQ, exhibiting a 71% homology, only (Table 2). This enzyme of strain #81009, however, was 99% identical to its counterparts found in strains with core types R1, R3, and R4 (Table 2), while the WaaQ protein encoded by the MG1655 allele was identical to that of a representative R2 strain, F632. Because the function of this protein as a heptosyltransferase is completely conserved in all core types (Muller-Loennies et al., 2007), we surmise that this sequence variation is unlikely to have functional consequences. An almost 100% identity (except two nucleotide differences resulting in a single amino acid mismatch in WaaB) of the entire waa locus of the strain #81009 was found with that of a commensal fecal isolate SE15 of the B2 phylogenetic group (Toh et al., 2010) (Table 2).

This considerably exceeded the rate reported by previous studies (Gibb et al., 1992; Appelmelk et al., 1994; Amor et al., 2000; Gibbs et al., 2004). As the core type distribution among non-ESBL-producing strains (3.7%) was similar to those found earlier (Table 1), and as the production of ESBL is, at least partly, a clonal phenomenon (Woodford et al., 2011), the possible clustering

of the 58 K-12 core PCR-positive isolates was investigated. We found that 54 of these strains (93.1%) carried the rfbO25b gene with the O25 serogroup also confirmed by slide agglutination. All strains belonged to the B2 phylogenetic group. All isolates, except two, were ESBL-producing strains. Fifty-two Selleck Dabrafenib of the 54 K-12 Caspase inhibitor core and rfbO25b-positive strains were typable by PFGE exhibiting 18 pulsotypes (10 clusters with 2–11 members and 8 singletons) (Fig. 1). Twenty-four selected isolates representing all pulsotypes were submitted to MLST and found to belong to the rapidly spreading, often multidrug resistant ST131 clone (Fig. 1). To rule out that the presence of the K-12 core-specific genes was restricted to Emirati UTI isolates of the O25 ST131 group, ten independent representatives of this clone isolated in Hungary from UTI (five strains) and BSI (five strains) in 2008 and 2009, respectively, were also tested. Importantly, all these strains were also positive with the

K-12 core-specific PCR (Fig. 1). Next, we determined the DNA sequence of the entire waa locus (Heinrichs et al., 1998) of one of the O25-ST131 isolates from our collection (#81009). The resulting > 16-kb sequence (GenBank JQ241150) covered the 15 K-12 core genes (Muller-Loennies et al., 2007) between Chloroambucil the kbl and the coaD genes flanking the waa locus. As expected, based on the PCR results, individual gene sequences displayed extensive homology to their respective homologues in the prototype K-12 commensal strain, MG1655 (Table 2). Comparison of the deduced amino acid sequences of the various Waa proteins of the ST131 O25 strain #81009 revealed ≥ 90% identities

with their counterparts in MG1655 with the exception of WaaQ, exhibiting a 71% homology, only (Table 2). This enzyme of strain #81009, however, was 99% identical to its counterparts found in strains with core types R1, R3, and R4 (Table 2), while the WaaQ protein encoded by the MG1655 allele was identical to that of a representative R2 strain, F632. Because the function of this protein as a heptosyltransferase is completely conserved in all core types (Muller-Loennies et al., 2007), we surmise that this sequence variation is unlikely to have functional consequences. An almost 100% identity (except two nucleotide differences resulting in a single amino acid mismatch in WaaB) of the entire waa locus of the strain #81009 was found with that of a commensal fecal isolate SE15 of the B2 phylogenetic group (Toh et al., 2010) (Table 2).

In general, we considered a strong candidate to be associated with GO terms such as cell proliferation, expressed in the adult mouse brain, and involved in known pathway(s) that regulated adult neurogenesis. Statistical analyses were performed with JMP v8.0 statistical software (SAS Institute, Cary, NC, USA). For

all analysis of BrdU+ cell counts and analysis on cell cycle, data were expressed as mean values ± SEM and were considered significant at P < 0.05. Two-tailed Student’s t-tests were used when comparing the two parental strains. The linear density of BrdU+ cells of different RI strains were compared by one-way analysis of variance (anova). Normality of data distribution was examined using Shapiro–Wilk’s W test. Both RG7422 nmr age and sex were previously identified as regulatory factors influencing adult neurogenesis (Enwere et al., 2004; Tanapat et al., 1999), so we wanted to examine

whether the number of buy EPZ015666 proliferative cells traveling along the RMS was influenced by these two variables. An age effect on phenotype was examined by regression analysis and a gender effect was assessed by fitting one-way anova as a linear model. We also examined the effects of body weight using linear regression. As all three variables may serve as potential confounding covariates that influence our genetic linkage analysis, we adjusted the RMS linear density for age, body weight and sex. Residuals were obtained

from a multiple regression fitting Megestrol Acetate all three covariates for linear density (Rosen et al., 2009). The adjusted RMS linear density was then calculated from adding the residuals to the average RMS linear density by strain (Lu et al., 2008). Both the residuals and the adjusted linear density are normally distributed and are not significantly associated with any of the three regressors. The adjusted RMS linear density data are available at the GeneNetwork (Trait ID # 10167) and are positively correlated with the original trait data (r = 0.97; P < 0.0001). The adult RMS is composed largely of neuroblasts that give rise to different subtypes of interneurons in the OB (Lledo et al., 2008). In order to quantify strain differences in the actively dividing population of neuroblasts, we used BrdU, a thymidine analog which gets incorporated into DNA during the S-phase of the cell cycle and is commonly used in the detection of proliferating cells. After 1 h of BrdU exposure, the RMS of A/J mice had a significantly larger population of labeled S-phase (i.e. BrdU-immunoreactive) cells (81 ± 4.56 cells/mm, n = 6) than C57BL/6J mice (49 ± 4.85 cells/mm, n = 9) (P = 0.0006; Fig. 2). Differences in BrdU-labeled cells could be due to either A/J having more rapidly proliferating cells than C57BL/6J or because the proliferating cells in A/J have a relatively longer S-phase to overall cell cycle length compared with C57BL/6J.

In general, we considered a strong candidate to be associated with GO terms such as cell proliferation, expressed in the adult mouse brain, and involved in known pathway(s) that regulated adult neurogenesis. Statistical analyses were performed with JMP v8.0 statistical software (SAS Institute, Cary, NC, USA). For

all analysis of BrdU+ cell counts and analysis on cell cycle, data were expressed as mean values ± SEM and were considered significant at P < 0.05. Two-tailed Student’s t-tests were used when comparing the two parental strains. The linear density of BrdU+ cells of different RI strains were compared by one-way analysis of variance (anova). Normality of data distribution was examined using Shapiro–Wilk’s W test. Both Cabozantinib datasheet age and sex were previously identified as regulatory factors influencing adult neurogenesis (Enwere et al., 2004; Tanapat et al., 1999), so we wanted to examine

whether the number of IWR1 proliferative cells traveling along the RMS was influenced by these two variables. An age effect on phenotype was examined by regression analysis and a gender effect was assessed by fitting one-way anova as a linear model. We also examined the effects of body weight using linear regression. As all three variables may serve as potential confounding covariates that influence our genetic linkage analysis, we adjusted the RMS linear density for age, body weight and sex. Residuals were obtained

from a multiple regression fitting Adenosine triphosphate all three covariates for linear density (Rosen et al., 2009). The adjusted RMS linear density was then calculated from adding the residuals to the average RMS linear density by strain (Lu et al., 2008). Both the residuals and the adjusted linear density are normally distributed and are not significantly associated with any of the three regressors. The adjusted RMS linear density data are available at the GeneNetwork (Trait ID # 10167) and are positively correlated with the original trait data (r = 0.97; P < 0.0001). The adult RMS is composed largely of neuroblasts that give rise to different subtypes of interneurons in the OB (Lledo et al., 2008). In order to quantify strain differences in the actively dividing population of neuroblasts, we used BrdU, a thymidine analog which gets incorporated into DNA during the S-phase of the cell cycle and is commonly used in the detection of proliferating cells. After 1 h of BrdU exposure, the RMS of A/J mice had a significantly larger population of labeled S-phase (i.e. BrdU-immunoreactive) cells (81 ± 4.56 cells/mm, n = 6) than C57BL/6J mice (49 ± 4.85 cells/mm, n = 9) (P = 0.0006; Fig. 2). Differences in BrdU-labeled cells could be due to either A/J having more rapidly proliferating cells than C57BL/6J or because the proliferating cells in A/J have a relatively longer S-phase to overall cell cycle length compared with C57BL/6J.

To date, most published reports on foot and ankle involvement in RA have focused predominantly on forefoot and hindfoot pathologies. More

studies are needed for better understanding of the impact of the RA foot, especially on the prevalence, pattern of involvement and imaging of subtalar and midfoot joint disease in RA. With the help of different imaging techniques in rheumatology practice, such as ultrasonography, MRI and CT, detection of early or subclinical foot problems is facilitated, which allows prompt pharmacological and non-pharmacological treatment, ultimately improving foot function and quality of life for RA patients. “
“Rituximab is one of nine biologic agents approved for the treatment of rheumatoid arthritis (RA) in Australia. The primary study objective was to analyze the factors that lead to the therapeutic decision click here to use rituximab in RA. A cross-sectional, retrospective chart review was conducted to identify patients who were treated with rituximab and to evaluate their response to treatment. Factors influencing the prescription Entinostat supplier of rituximab were identified. The most

commonly reported reason for prescribing rituximab was the presence of comorbidities and the presence of seropositive disease. Median rituximab treatment duration was 32.5 months and mean number of treatment cycles was 4.1. Disease activity scores showed significant improvement from baseline to most recent visit. Rituximab treatment was well-tolerated in this group of RA patients. Rituximab was effective in a refractory group of RA patients and appears to be safe in a population with a high prevalence of comorbidities, including malignancy and recurrent infections/bronchiectasis. Rebamipide This study may assist rheumatologists in selecting appropriately targeted therapy

in RA. “
“Aim:  To investigate the relationship between scleroderma-specific autoantibodies and clinical phenotype and survival in South Australian patients with scleroderma. Method:  Two cohorts of patients were studied from the South Australian Scleroderma Register (SASR). In the first, the sera of 129 consecutive patients were analyzed for anticentromere (ACA), anti-Scl70, anti-RNA polymerase III, anti-U1RNP, anti-Th/To, anti-Pm/Scl, anti-Ku and anti-fibrillarin antibodies using the Euroline immunoblot assay. Statistical analysis was performed to look for a significant association between specific antibodies and various clinical features. In the second cohort survival from first symptom onset was analyzed in 285 patients in whom the autoantibody profile was available, including ACA, Anti-Scl70, anti-U1RNP and anti-RNA polymerase III measured using multiple methods. Survival analysis compared mortality between different groups of patients with specific antibodies.

The kinase assays were carried out with the increasing amount of GST-LdCyc1-CRK3 complex in 20 mM HEPES-KOH, pH 7.5, containing 10 mM MgCl2, 1 mM EDTA, 1 mM EGTA, 5 mM NaF, 2 mM DTT, 50 μM [γ32P]ATP (2.7 μCi/nmole) and 1.0 μg of LdHAT1 in a total volume of 15 μL at 30 °C for 30 min. For the assays with the mutated proteins, LdHAT1ΔCy and LdHAT1-T394A were incubated with 0.2 μg of kinase GST-LdCyc1-CRK3 in the reaction buffer. The reaction products were analysed by SDS-PAGE followed by phosphorimager scanning in Typhoon scanner (GE Healthcare Lifesciences).

Three peptides derived from N-terminus of L. donovani histone H4–containing specific acetylated lysine (LdH4K4Ac: AKGKAcRSADAC; LdH4K10Ac: SADAKAcGSQKC; LdH4K14Ac: KGSQKAcRQKKC) were synthesized and conjugated to carrier protein find more keyhole limpet haemocyanin. For each peptide, two rabbits were immunized, and the progress of immunization was monitored by ELISA assay. Specific antibodies were purified from the anti-sera having higher titre values through affinity column chromatography in a two-step process – first over a column containing a control non-acetylated peptide (AKGKRSADAKGSQKRQKKC) followed by a column containing the respective acetylated peptide. The specificities

of the purified antibodies were checked by ELISA assay. The entire process was carried out by IMGENEX India, Bhubaneswar, India, on contract basis. IDO inhibitor The specificities of the antibodies were further verified by dot blot analysis in our laboratory. HAT assay was performed with 1.6 μM of 6His-tagged LdHAT1 as enzyme in 50 mM HEPES-KOH, pH 8.0, containing 0.1 mM EDTA, 5% glycerol, 1 mM DTT, 10 mM Na-butyrate, 0.1 mM Li3Acetyl-CoA and 50 μM of a peptide derived from L. donovani histone H4 N-terminus (AKGKRSADAKGSQKRQKKC)

as substrate in a total volume of 20 μL. The reaction was carried out at 30 °C for 1 h, stopped by adding 5 μL of SDS-PAGE sample buffer, and the products were subjected to a modified Tris-Tricine SDS-PAGE for better resolution of smaller peptides (Schagger & von Jagow, 1987). Briefly, 18% polyacrylamide (18%T, 5%C) in 0.75 M Tris-HCl, pH 8.45, containing 30% ethylene glycol and DOK2 0.1% SDS was used as resolving gel with 0.1 M Tris containing 0.1 M Tricine and 0.1% SDS as electrophoresis buffer. Finally, the acetylated peptide was detected by immunoblotting with the antibodies raised against the peptides containing specific acetylated lysine residues as described above. The antibodies obtained after purification over non-acetylated peptides or Coomassie blue staining of the gel were used for checking the presence of equal amount of substrate peptide in different reactions. One of the identified substrates of the S-phase cell cycle kinase LdCyc1-CRK3 from L. donovani was shown to contain a MYST (human Moz, Yeast Ybf2 and Sas2, and human TIP60) domain of HATs (Maity et al.

Antibody labelling studies have shown that NRAMP1 colocalizes with the LAMP1 in late endosomes and lysosomes (Cellier et al.,

2007), allowing us to speculate that the failure of metal withdrawal defence may trigger dispersal from the aggregates in vivo, leading to a recurrence of symptoms. In UPEC strain 536, we believe that the major component of the aggregate matrix is cellulose, the matrix stains with Calcofluor (Fig. 2b) and cellulase activity both prevents aggregate formation and can disperse aggregates in the absence of iron (Tables 3 and 4). Escherichia coli K12 (MG 1655) contains a cellulose biosynthetic operon, including the yhjQ, bscA, bscB, bscZ, and bscC genes (Römling, 2002), which is also present in Etoposide cost the UPEC 536 genome sequence (ECP 3630-3634; Hochhut et al., 2006). Each protein displays 99% protein identity (MG 1655 compared with UPEC 536), strongly suggesting this operon is functional in UPEC 536. The production of cellulose by eubacteria is well characterized (Römling, 2002), and is relevant in vivo. Cellulose production is associated with the sessile state and with biofilm production (Römling, 2002). In E. coli, cellulose is associated with attachment to both biotic and abiotic

surfaces (Wang et al., 2006; Gualdi et al., 2008; Saldaña et al., 2009), and so it may play a role in the attachment of cells to the urothelium at the initiation of an infection. We speculate that other advantages of cellulose production in vivo may include protection from

immune killing and the exclusion see more of antibiotics, although buy AZD9291 to our knowledge, these properties have not yet been tested. Pathogenic and commensal E. coli behave differently from laboratory-adapted K12 strains with respect to cellulose production, and significantly many pathogenic strains are able to produce cellulose at 37 °C (Bokranz et al., 2005; Da Re & Ghigo, 2006; Monteiro et al., 2009), suggesting that regulation in these strains may be different from that elucidated to date for laboratory strains of E. coli. In this study, we were able to prevent dispersal by pretreatment of aggregates with antibiotics that prevent new transcription and translation. Our conclusion is that new gene expression is required to effect the phenotypic changes induced by the transition to an iron-replete state. Cellulose production is regulated by the production of the internal second messenger signal cyclic di-GMP (Römling et al., 2005). Our results suggest that the production of an endoglucanase or a modifying activity that affects the strength of the cellulosic matrix is required to effect dispersal. In E. coli (and many other bacteria), endoglucanase activity resides in BscZ, which is part of the cellulose operon (Römling, 2002), but this is not thought to be secreted.

Toll-like receptors (TLRs) bind to components of microorganisms, activate cellular signal transduction pathways and stimulate innate immune responses. The effect of TLR3 (poly I:C)

and TLR9 (CpG) co-stimulation SB431542 chemical structure of THP-1-derived monocytes using purified TLR ligands showed that 24 h after exposure poly I:C and CpG ligands in combination, hepcidin expression was significantly increased (10-fold) when compared to the untreated control. This combination of TLR ligands mimics simultaneous bacterial and viral infections, thus suggesting a potential key role for hepcidin in combined infections. Additionally, using a chequerboard assay, we have shown that hepcidin has an antagonistic effect in combination with the antibiotics rifampicin

and tetracycline against Staphylococcus aureus, Pseudomonas aeruginosa and Streptococcus pyogenes, evidenced by a fractional inhibitory concentration index (FICI) > 4. This finding has important implications for future treatment regimens especially in an era of increasing antimicrobial resistance. “
“The enterobacterium Erwinia amylovora is the causal agent of fire blight. This study presents the analysis of the complete genome of phage PhiEaH1, isolated from the soil surrounding an E. amylovora-infected apple tree in Hungary. Its genome is selleck chemical 218 kb in size, containing 244 ORFs. PhiEaH1 is the second E. amylovora infecting phage from the Siphoviridae family whose complete genome sequence was determined. Beside PhiEaH2, PhiEaH1 is the other active component of Erwiphage, the first bacteriophage-based pesticide on the market against E. amylovora. Comparative genome analysis in this study has revealed that PhiEaH1 not only differs from the 10 formerly sequenced E. amylovora bacteriophages belonging to other phage families, but also from PhiEaH2. Sequencing of more Siphoviridae phage genomes might

reveal further diversity, providing opportunities for the development of even more effective biological control agents, phage cocktails against Erwinia fire blight disease of commercial fruit crops. Erwinia amylovora, a member of the Enterobacteriaceae family, is a Gram-negative facultative anaerobic, rod shaped, phytopathogenic bacterium. It is the causal agent of Rolziracetam fire blight of some Rosaceae plants, such as quince, apple and pear (Starr & Chatterjee, 1972; Van Der Zwet & Keil, 1979; Van der Zwet & Beer, 1991; Vanneste, 2000). So far, 11 E. amylovora phage genomes have been sequenced (Lehman et al., 2009; Born et al., 2011; Muller et al., 2011; Dömötör et al., 2012). They include five phages that were isolated from samples collected in Northern America (four from USA, one from Canada), and five from European samples (four from Switzerland, one from Hungary), and one is of unknown origin. All the sequenced E. amylovora phages were members of Caudovirales.