Mohammad holds a Bachelor’s degree in Medical Laboratory Sciences and MSc in Medical Microbiology. He also obtained his PhD, in Microbiology in 2014, followed by postdoctoral training, at the University of Sydney. Given his interest towards teaching he also completed a Graduate Certificate Degree in Educational Studies (Higher Education) in 2015 at the University of Sydney.
During and upon finishing his PhD, he worked on characterising genomic regions that carry antibiotic resistance genes in Acinetobacter baumannii, which is a bacterium that causes a range of hospital acquired infections and is highly resistant to antibiotics. Mohammad’s work on A. baumannii has made significant contribution to increase our understanding on pathways leading to the success of one of the two globally distributed clones of A. baumannii, global clone 1 (GC1). In early 2018, he received the UTS Chancellor’s Postdoctoral Research Fellow (CPDRF) and moved to the University of Technology Sydney where he has begun looking at the biofilm formation of this superbug.
- Professional Member of Australian Society for Microbiology (MASM)
- Member of American Society for Microbiology
Mohammad's research interests are broadly focused on mechanisms of antibiotic resistance in Gram-negative pathogens that are relevant to Public Health. His research involves exploring bacterial genomes to find novel insertion sequences (IS), transposons, integrons and genomic islands to help explain how complex antibiotic resistance islands have been crafted leading to multiply-antibiotic resistance phenotypes.
His general interests include examining genomic diversity, clonality and epidemiology of Acinetobacter baumannii, which is a nosocomial microorganism that causes a range of infections. This organism has now become a global threat due to development of high levels of antibiotic resistance. He is also interested in studying biofilm formation in A. baumannii, which is one of the main factors that makes this microorganism resistant to extreme environmental conditions, e.g. desiccation, allowing it to survive in hospital environments for a very long period of time.
Hamidian, M. & Hall, R.M. 2017, 'Acinetobacter baumannii ATCC 19606 Carries GIsul2 in a Genomic Island Located in the Chromosome.', Antimicrobial agents and chemotherapy, vol. 61, no. 1.View/Download from: UTS OPUS or Publisher's site
Hamidian, M. & Hall, R.M. 2017, 'Origin of the AbGRI1 antibiotic resistance island found in the comM gene of Acinetobacter baumannii GC2 isolates.', Journal of Antimicrobial Chemotherapy, vol. 72, no. 10, pp. 2944-2947.View/Download from: UTS OPUS or Publisher's site
Hamidian, M., Nigro, S.J. & Hall, R.M. 2017, 'Problems with the Oxford Multilocus Sequence Typing Scheme for Acinetobacter baumannii: Do Sequence Type 92 (ST92) and ST109 Exist?', Journal of Clinical Microbiology, vol. 55, no. 7, pp. 2287-2289.View/Download from: UTS OPUS or Publisher's site
Hamidian, M., Nigro, S.J., Hartstein, R.M. & Hall, R.M. 2017, 'RCH51, a multiply antibiotic-resistant Acinetobacter baumannii ST103IP isolate, carries resistance genes in three plasmids, including a novel potentially conjugative plasmid carrying oxa235 in transposon Tn6252.', Journal of Antimicrobial Chemotherapy, vol. 72, no. 7, pp. 1907-1910.View/Download from: UTS OPUS or Publisher's site
To determine the identity and context of genes conferring antibiotic resistance in a sporadic multiply antibiotic-resistant Acinetobacter baumannii recovered at Royal Children's Hospital, Brisbane.The antibiotic resistance phenotype for 23 antibiotics was determined using disc diffusion or MIC determination. The whole-genome sequence of RCH51 was determined using the Illumina HiSeq platform. Antibiotic resistance determinants were identified using ResFinder. Plasmids were recovered by transformation.Isolate RCH51 belongs to the uncommon STs ST103 IP (7-3-2-1-7-1-4) and ST514 OX (1-52-29-28-18-114-7). It was found to be resistant to sulfamethoxazole, tetracycline, gentamicin, tobramycin and kanamycin and also exhibited reduced susceptibility to imipenem (MIC 2mg/L) and meropenem (MIC 6mg/L). RCH51 carries the oxa235 , sul2 , floR , aadB and tet39 resistance genes, all located on plasmids. The largest of the three plasmids, pRCH51-3, is 52789bp and carries oxa235 in the ISAba1-bounded transposon Tn 6252 , as well as sul2 and floR . pRCH51-3 represents a new A. baumannii plasmid family that is potentially conjugative as it contains several genes predicted to encode transfer functions. However, conjugation of pRCH51-3 was not detected. The aadB and tet39 resistance genes were each found in small plasmids identical to the known plasmids pRAY*-v1 and pRCH52-1, respectively.The resistance gene complement of RCH51 was found in three plasmids. pRCH51-3, which carries the oxa235 , sul2 and floR resistance genes, represents a new, potentially conjugative A. baumannii plasmid type.
Hamidian, M., Venepally, P., Hall, R.M. & Adams, M.D. 2017, 'Corrected Genome Sequence of Acinetobacter baumannii Strain AB0057, an Antibiotic-Resistant Isolate from Lineage 1 of Global Clone 1.', Genome Announcements, vol. 5, no. 35, pp. 1-2.View/Download from: UTS OPUS or Publisher's site
Extensively antibiotic-resistant Acinetobacter baumannii isolate AB0057 recovered in the United States in 2004 was one of the first global clone 1 isolates to be completely sequenced. Here, the complete 4.05-Mb genome sequence (chromosome and one plasmid) has been revised using Illumina HiSeq data and targeted sequencing of PCR products.
Harmer, C.J., Hamidian, M. & Hall, R.M. 2017, 'pIP40a, a type 1 IncC plasmid from 1969 carries the integrative element GIsul2 and a novel class II mercury resistance transposon.', Plasmid, vol. 92, pp. 17-25.View/Download from: UTS OPUS or Publisher's site
The 167.5kb sequence of the conjugative IncC plasmid pIP40a, isolated from a Pseudomonas aeruginosa in 1969, was analysed. pIP40a confers resistance to kanamycin, neomycin, ampicillin, sulphonamides and mercuric ions, and several insertions in a type 1 IncC backbone were found, including copies of IS3, Tn1000 and a novel mercury resistance transposon, Tn6182. The antibiotic resistance genes were in two locations. Tn6023, containing the aphA1 kanamycin and neomycin resistance gene, is in a partial copy of Tn1/Tn2/Tn3 (blaTEM, ampicillin resistance) in the kfrA gene, and the sul2 sulphonamide resistance gene is in the integrative element GIsul2 in the position of ARI-B islands. The 11.5kb class II transposon Tn6182 is only distantly related to other class II transposons, with at most 33% identity between the TnpA of Tn6182 and TnpA of other group members. In addition, the inverted repeats are 37bp rather than 38bp, and the likely resolution enzyme is a tyrosine recombinase (TnpI). Re-annotation of GIsul2 revealed genes predicted to confer resistance to arsenate and arsenite, but resistance was not detected. The location of GIsul2 confirms it as the progenitor of the ARI-B configurations seen in many IncC plasmids isolated more recently. However, GIsul2 has integrated at the same site in type 1 and type 2 IncC plasmids, indicating that it targets this site. Analysis of the distribution of GIsul2 revealed that it in addition to its chromosomal integration site at the 3'-end of the guaA gene, it has also integrated into other plasmids, increasing its mobility.
Blackwell, G.A., Hamidian, M. & Hall, R.M. 2016, 'IncM Plasmid R1215 Is the Source of Chromosomally Located Regions Containing Multiple Antibiotic Resistance Genes in the Globally Disseminated Acinetobacter baumannii GC1 and GC2 Clones.', mSphere, vol. 1, no. 3.View/Download from: Publisher's site
Clear similarities between antibiotic resistance islands in the chromosomes of extensively antibiotic-resistant isolates from the two dominant, globally distributed Acinetobacter baumannii clones, GC1 and GC2, suggest a common origin. A close relative of the likely progenitor of both of these regions was found in R1215, a conjugative IncM plasmid from a Serratia marcescens strain isolated prior to 1980. The 37.8-kb resistance region in R1215 lies within the mucB gene and includes aacC1, aadA1, aphA1b, bla TEM, catA1, sul1, and tetA(A), genes that confer resistance to gentamicin, streptomycin and spectinomycin, kanamycin and neomycin, ampicillin, chloramphenicol, sulfamethoxazole, and tetracycline, respectively. The backbone of this region is derived from Tn1721 and is interrupted by a hybrid Tn2670 (Tn21)-Tn1696-type transposon, Tn6020, and an incomplete Tn1. After minor rearrangements, this R1215 resistance island can generate AbGRI2-0*, the predicted earliest form of the IS26-bounded AbGRI2-type resistance island of GC2 isolates, and to the multiple antibiotic resistance region (MARR) of AbaR0, the precursor of this region in AbaR-type resistance islands in the GC1 group. A 29.9-kb circle excised by IS26 has been inserted into the A. baumannii chromosome to generate AbGRI2-0*. To create the MARR of AbaR0, a different circular form, again generated by IS26 from an R1215 resistance region variant, has been opened at a different point by recombination with a copy of the sul1 gene already present in the AbaR precursor. Recent IncM plasmids related to R1215 have a variant resistance island containing a bla SHV gene in the same location. IMPORTANCE Two lineages of extensively antibiotic-resistant A. baumannii currently plaguing modern medicine each acquired resistance to all of the original antibiotics (ampicillin, tetracycline, kanamycin, and sulfonamides) by the end of the 1970s and then became resistant to antibiotics from newer families after they were introduced...
Hamidian, M. & Hall, R.M. 2016, 'The resistance gene complement of D4, a multiply antibiotic-resistant ST25 Acinetobacter baumannii isolate, resides in two genomic islands and a plasmid.', The Journal of antimicrobial chemotherapy, vol. 71, no. 6, pp. 1730-1732.View/Download from: Publisher's site
Hamidian, M., Ambrose, S.J. & Hall, R.M. 2016, 'A large conjugative Acinetobacter baumannii plasmid carrying the sul2 sulphonamide and strAB streptomycin resistance genes.', Plasmid, vol. 87-88, pp. 43-50.View/Download from: Publisher's site
Acinetobacter baumannii is an important nosocomial pathogen that often complicates treatment because of its high level of resistance to antibiotics. Though plasmids can potentially introduce various genes into bacterial strains, compared to other Gram-negative bacteria, information about the unique A. baumannii plasmid repertoire is limited. Here, whole genome sequence data was used to determine the plasmid content of strain A297 (RUH875), the reference strain for the globally disseminated multiply resistant A. baumannii clone, global clone 1(GC1). A297 contains three plasmids. Two known plasmids were present; one, pA297-1 (pRAY*), carries the aadB gentamicin, kanamycin and tobramycin resistance gene and another is an 8.7kb cryptic plasmid often found in GC1 isolates. The third plasmid, pA297-3, is 200kb and carries the sul2 sulphonamide resistance gene and strAB streptomycin resistance gene within Tn6172 and a mer mercuric ion resistance module elsewhere. pA297-3 transferred sulphonamide, streptomycin and mercuric ion resistance at high frequency to a susceptible A. baumannii recipient, and contains several genes potentially involved in conjugative transfer. However, a relaxase gene was not found. It also includes several genes encoding proteins involved in DNA metabolism such as partitioning. However, a gene encoding a replication initiation protein could not be found. pA297-3 includes two copies of a Miniature Inverted-Repeat Transposable Element (MITE), named MITE-297, bracketing a 77.5kb fragment, which contains several IS and the mer module. Several plasmids related to but smaller than pA297-3 were found in the GenBank nucleotide database. They were found in different A. baumannii clones and are wide spread. They all contain either Tn6172 or a variant in the same position in the backbone as Tn6172 in pA297-3. Some related plasmids have lost the segment between the MITE-297 copies and retain only one MITE-297. Others have segments of various lengths between ...
Hamidian, M., Holt, K.E., Pickard, D. & Hall, R.M. 2016, 'A small Acinetobacter plasmid carrying the tet39 tetracycline resistance determinant.', The Journal of antimicrobial chemotherapy, vol. 71, no. 1, pp. 269-271.View/Download from: Publisher's site
Harmer, C.J., Hamidian, M., Ambrose, S.J. & Hall, R.M. 2016, 'Destabilization of IncA and IncC plasmids by SGI1 and SGI2 type Salmonella genomic islands.', Plasmid, vol. 87-88, pp. 51-57.View/Download from: Publisher's site
Both the Salmonella genomic islands (SGI) and the conjugative IncC plasmids are known to contribute substantially to the acquisition of resistance to multiple antibiotics, and plasmids in the A/C group are known to mobilize the Salmonella genomic island SGI1, which also carries multiple antibiotic resistance genes. Plasmid pRMH760 (IncC; A/C2) was shown to mobilize SGI1 variants SGI1-I, SGI1-F, SGI1-K and SGI2 from Salmonella enterica to Escherichia coli where it was integrated at the preferred location, at the end of the trmE (thdF) gene. The plasmid was transferred at a similar frequency. However, we observed that co-transfer of the SGI and the plasmid was rarer. In E. coli to E. coli transfer, the frequency of transfer of the IncC plasmid pRMH760 was at least 1000-fold lower when the donor carried SGI1-I or SGI1-K, indicating that the SGI suppresses transfer of the plasmid. In addition, pRMH760 was rapidly lost from both E. coli and S. enterica strains that also carried SGI1-I, SGI1-F or SGI2. However, plasmid loss was not seen when the SGI1 variant was SGI1-K, which lacks two segments of the SGI1 backbone. The complete sequence of the SGI1-I and SGI1-F were determined and SGI1-K also carries two single base substitutions relative to SGI1-I. The IncA (A/C1) plasmid RA1 was also shown to mobilize SGI2-A and though there are significant differences between the backbones of IncA and IncC plasmids, RA1 was also rapidly lost when SGI2-A was present in the same cell. We conclude that there are multiple interactions, both cooperative and antagonistic, between an IncA or IncC plasmid and the SGI1 and SGI2 family genomic islands.
Holt, K., Kenyon, J.J., Hamidian, M., Schultz, M.B., Pickard, D.J., Dougan, G. & Hall, R. 2016, 'Five decades of genome evolution in the globally distributed, extensively antibiotic-resistant Acinetobacter baumannii global clone 1.', Microbial Genomics, vol. 2, no. 2, p. e000052.View/Download from: Publisher's site
The majority of Acinetobacter baumannii isolates that are multiply, extensively and pan-antibiotic resistant belong to two globally disseminated clones, GC1 and GC2, that were first noticed in the 1970s. Here, we investigated microevolution and phylodynamics within GC1 via analysis of 45 whole-genome sequences, including 23 sequenced for this study. The most recent common ancestor of GC1 arose around 1960 and later diverged into two phylogenetically distinct lineages. In the 1970s, the main lineage acquired the AbaR resistance island, conferring resistance to older antibiotics, via a horizontal gene transfer event. We estimate a mutation rate of 5 SNPs genome-1 year-1 and detected extensive recombination within GC1 genomes, introducing nucleotide diversity into the population at >20 times the substitution rate (the ratio of SNPs introduced by recombination compared with mutation was 22). The recombination events were non-randomly distributed in the genome and created significant diversity within loci encoding outer surface molecules (including the capsular polysaccharide, the outer core lipooligosaccharide and the outer membrane protein CarO), and spread antimicrobial resistance-conferring mutations affecting the gyrA and parC genes and insertion sequence insertions activating the ampC gene. Both GC1 lineages accumulated resistance to newer antibiotics through various genetic mechanisms, including the acquisition of plasmids and transposons or mutations in chromosomal genes. Our data show that GC1 has diversified into multiple successful extensively antibiotic-resistant subclones that differ in their surface structures. This has important implications for all avenues of control, including epidemiological tracking, antimicrobial therapy and vaccination.
Hamidian, M., Hawkey, J., Holt, K.E. & Hall, R.M. 2015, 'Genome Sequence of Acinetobacter baumannii Strain D36, an Antibiotic-Resistant Isolate from Lineage 2 of Global Clone 1.', Genome announcements, vol. 3, no. 6.View/Download from: Publisher's site
Multiply antibiotic-resistant Acinetobacter baumannii isolate D36 was recovered in Australia in 2008 and belongs to a distinct lineage of global clone 1 (GC1). Here, we present the complete 4.13 Mbp genome sequence (chromosome plus 4 plasmids), generated via long read sequencing (PacBio).
Hamidian, M., Holt, K.E. & Hall, R.M. 2015, 'Genomic resistance island AGI1 carrying a complex class 1 integron in a multiply antibiotic-resistant ST25 Acinetobacter baumannii isolate.', The Journal of antimicrobial chemotherapy, vol. 70, no. 9, pp. 2519-2523.View/Download from: Publisher's site
The objective of this study was to locate the antibiotic resistance determinants in the multiply antibiotic-resistant Acinetobacter baumannii isolate D4.The genome was sequenced using Illumina HiSeq and assembled de novo using Velvet. PCR was used to link the relevant contigs and fill the gaps. Sequences were compared with ones in GenBank and annotated.A sporadic A. baumannii isolate D4, recovered in Sydney in 2006 from a wound, was multiply antibiotic resistant. D4 is ST25 (Institut Pasteur scheme) and exhibited resistance to third-generation cephalosporins and reduced susceptibility to ciprofloxacin, as well as resistance to aminoglycosides (gentamicin, kanamycin, neomycin and tobramycin) and further older antibiotics, nalidixic acid, sulfamethoxazole, streptomycin, spectinomycin and trimethoprim. The gyrA gene has a mutation consistent with nalidixic acid resistance. The bla PER conferring cephalosporin resistance, together with the aadB, aadA13/2, aadA2, strAB and sul1 resistance genes, are located within a 29173 bp complex class 1 integron that includes three copies of intI1, three cassette arrays and two copies of the 3'-conserved segment. This integron is adjacent to the resG gene of an integrative genomic resistance island, AGI1 (Acinetobacter genomic island 1), with a backbone related to that of islands in the SGI1, SGI2 and PGI1 families. AGI1 is located at the 3'-end of the chromosomal trmE (formerly thdF) gene.AGI1 represents a new lineage of genomic resistance islands that belongs in the same broad group as members of the SGI1, SGI2 and PGI1 families. Genes conferring resistance to cephalosporins, aminoglycosides and sulphonamides are located in a complex class 1 integron within AGI1.
Hamidian, M., Holt, K.E. & Hall, R.M. 2015, 'The complete sequence of Salmonella genomic island SGI1-K.', The Journal of antimicrobial chemotherapy, vol. 70, no. 1, pp. 305-306.View/Download from: Publisher's site
Hamidian, M., Holt, K.E. & Hall, R.M. 2015, 'The complete sequence of Salmonella genomic island SGI2.', The Journal of antimicrobial chemotherapy, vol. 70, no. 2, pp. 617-619.View/Download from: Publisher's site
Hawkey, J., Hamidian, M., Wick, R.R., Edwards, D.J., Billman-Jacobe, H., Hall, R.M. & Holt, K.E. 2015, 'ISMapper: identifying transposase insertion sites in bacterial genomes from short read sequence data.', BMC genomics, vol. 16, p. 667.View/Download from: Publisher's site
Insertion sequences (IS) are small transposable elements, commonly found in bacterial genomes. Identifying the location of IS in bacterial genomes can be useful for a variety of purposes including epidemiological tracking and predicting antibiotic resistance. However IS are commonly present in multiple copies in a single genome, which complicates genome assembly and the identification of IS insertion sites. Here we present ISMapper, a mapping-based tool for identification of the site and orientation of IS insertions in bacterial genomes, directly from paired-end short read data.ISMapper was validated using three types of short read data: (i) simulated reads from a variety of species, (ii) Illumina reads from 5 isolates for which finished genome sequences were available for comparison, and (iii) Illumina reads from 7 Acinetobacter baumannii isolates for which predicted IS locations were tested using PCR. A total of 20 genomes, including 13 species and 32 distinct IS, were used for validation. ISMapper correctly identified 97 % of known IS insertions in the analysis of simulated reads, and 98 % in real Illumina reads. Subsampling of real Illumina reads to lower depths indicated ISMapper was able to correctly detect insertions for average genome-wide read depths >20x, although read depths >50x were required to obtain confident calls that were highly-supported by evidence from reads. All ISAba1 insertions identified by ISMapper in the A. baumannii genomes were confirmed by PCR. In each A. baumannii genome, ISMapper successfully identified an IS insertion upstream of the ampC beta-lactamase that could explain phenotypic resistance to third-generation cephalosporins. The utility of ISMapper was further demonstrated by profiling genome-wide IS6110 insertions in 138 publicly available Mycobacterium tuberculosis genomes, revealing lineage-specific insertions and multiple insertion hotspots.ISMapper provides a rapid and robust method for identifying IS insertion sites dire...
Holt, K.E., Hamidian, M., Kenyon, J.J., Wynn, M.T., Hawkey, J., Pickard, D. & Hall, R.M. 2015, 'Genome Sequence of Acinetobacter baumannii Strain A1, an Early Example of Antibiotic-Resistant Global Clone 1.', Genome announcements, vol. 3, no. 2.View/Download from: Publisher's site
Acinetobacter baumannii isolate A1 was recovered in the United Kingdom in 1982 and belongs to global clone 1 (GC1). Here, we present its complete 3.91-Mbp genome sequence, generated via a combination of short-read sequencing (Illumina), long-read sequencing (PacBio), and manual finishing.
Hamidian, M. & Hall, R.M. 2014, 'pACICU2 is a conjugative plasmid of Acinetobacter carrying the aminoglycoside resistance transposon TnaphA6.', The Journal of antimicrobial chemotherapy, vol. 69, no. 4, pp. 1146-1148.View/Download from: Publisher's site
Hamidian, M. & Hall, R.M. 2014, 'Resistance to third-generation cephalosporins in Acinetobacter baumannii due to horizontal transfer of a chromosomal segment containing ISAba1-ampC.', The Journal of antimicrobial chemotherapy, vol. 69, no. 10, pp. 2865-2866.View/Download from: Publisher's site
Hamidian, M. & Hall, R.M. 2014, 'Tn6168, a transposon carrying an ISAba1-activated ampC gene and conferring cephalosporin resistance in Acinetobacter baumannii.', The Journal of antimicrobial chemotherapy, vol. 69, no. 1, pp. 77-80.View/Download from: Publisher's site
OBJECTIVES: To explore the cause of third-generation cephalosporin resistance in Australian Acinetobacter baumannii isolates belonging to global clone 1 (GC1). METHODS: GC1 isolates from Australia were tested for resistance to ceftazidime and cefotaxime using disc diffusion and MICs. PCR was used to determine the context of ISAba1-ampC configurations and amplicons were sequenced. The level of transcripts was measured using quantitative real-time PCR. Multilocus sequence typing was performed. RESULTS: All ceftazidime- and cefotaxime-resistant isolates carried an appropriately oriented ISAba1 adjacent to the ampC gene and ISAba1 increased ampC transcripts 8-12-fold. In three isolates, the ampC gene next to ISAba1 was not in the normal chromosomal position. Instead, ISAba1 was 7 bp upstream of an additional copy of ampC located in a 3155 bp duplicated segment of the chromosome that differs from the resident GC1 segment by 2.3% but is almost identical to the corresponding region in several non-GC1 draft genomes. The duplicated segment is bounded by directly oriented copies of ISAba1 and flanked by a 9 bp direct duplication. This 5.5 kb transposon, named Tn6168, is in the same position in the chromosome of the three Australian isolates and the GC1 isolate AB0057. Tn6168 was also detected in an unrelated A. baumannii strain, where it was in a different location. The central part of Tn6168 was probably acquired from a sequence type ST32 (Institut Pasteur scheme) A. baumannii strain. CONCLUSIONS: The ISAba1-ampC configuration, which increases ampC expression, can be part of a composite transposon Tn6168.
Hamidian, M., Holt, K.E., Pickard, D., Dougan, G. & Hall, R.M. 2014, 'A GC1 Acinetobacter baumannii isolate carrying AbaR3 and the aminoglycoside resistance transposon TnaphA6 in a conjugative plasmid.', The Journal of antimicrobial chemotherapy, vol. 69, no. 4, pp. 955-958.View/Download from: Publisher's site
OBJECTIVES: To locate the acquired antibiotic resistance genes, including the amikacin resistance transposon TnaphA6, in the genome of an Australian isolate belonging to Acinetobacter baumannii global clone 1 (GC1). METHODS: A multiply antibiotic-resistant GC1 isolate harbouring TnaphA6 was sequenced using Illumina HiSeq, and reads were used to generate a de novo assembly and determine multilocus sequence types (STs). PCR was used to assemble the AbaR chromosomal resistance island and a large plasmid carrying TnaphA6. Plasmid DNA sequences were compared with ones available in GenBank. Conjugation experiments were conducted. RESULTS: The A. baumannii GC1 isolate G7 was shown to include the AbaR3 antibiotic resistance island. It also contains an 8.7 kb cryptic plasmid, pAb-G7-1, and a 70,100 bp plasmid, pAb-G7-2, carrying TnaphA6. pAb-G7-2 belongs to the Aci6 Acinetobacter plasmid family. It encodes transfer functions and was shown to conjugate. Plasmids related to pAb-G7-2 were detected in further amikacin-resistant GC1 isolates using PCR. From the genome sequence, isolate G7 was ST1 (Institut Pasteur scheme) and ST231 (Oxford scheme). Using Oxford scheme PCR-based methods, the isolate was ST109 and this difference was traced to a single base difference resulting from the inclusion of the original primers in the gpi segment analysed. CONCLUSIONS: The multiply antibiotic-resistant GC1 isolate G7 carries most of its resistance genes in AbaR3 located in the chromosome. However, TnaphA6 is on a conjugative plasmid, pAb-G7-2. Primers developed to locate TnaphA6 in pAb-G7-2 will simplify the detection of plasmids related to pAb-G7-2 in A. baumannii isolates.
Hamidian, M., Kenyon, J.J., Holt, K.E., Pickard, D. & Hall, R.M. 2014, 'A conjugative plasmid carrying the carbapenem resistance gene blaOXA-23 in AbaR4 in an extensively resistant GC1 Acinetobacter baumannii isolate.', The Journal of antimicrobial chemotherapy, vol. 69, no. 10, pp. 2625-2628.View/Download from: Publisher's site
To locate the acquired bla(OXA-23) carbapenem resistance gene in an Australian A. baumannii global clone 1 (GC1) isolate.The genome of the extensively antibiotic-resistant GC1 isolate A85 harbouring bla(OXA-23) in Tn2006 was sequenced using Illumina HiSeq, and the reads were used to generate a de novo assembly. PCR was used to assemble relevant contigs. Sequences were compared with ones in GenBank. Conjugation experiments were conducted.The sporadic GC1 isolate A85, recovered in 2003, was extensively resistant, exhibiting resistance to imipenem, meropenem and ticarcillin/clavulanate, to cephalosporins and fluoroquinolones and to the older antibiotics gentamicin, kanamycin and neomycin, sulfamethoxazole, trimethoprim and tetracycline. Genes for resistance to older antibiotics are in the chromosome, in an AbaR3 resistance island. A second copy of the ampC gene in Tn6168 confers cephalosporin resistance and the gyrA and parC genes have mutations leading to fluoroquinolone resistance. An 86335 bp repAci6 plasmid, pA85-3, carrying bla(OXA-23) in Tn2006 in AbaR4, was shown to transfer imipenem, meropenem and ticarcillin/clavulanate resistance into a susceptible recipient. A85 also contains two small cryptic plasmids of 2.7 and 8.7 kb. A85 is sequence type ST126 (Oxford scheme) and carries a novel KL15 capsule locus and the OCL3 outer core locus.A85 represents a new GC1 lineage identified by the novel capsule locus but retains AbaR3 carrying genes for resistance to older antibiotics. Resistance to imipenem, meropenem and ticarcillin/clavulanate has been introduced into A85 by pA85-3, a repAci6 conjugative plasmid carrying Tn2006 in AbaR4.
Hamidian, M., Wynn, M., Holt, K.E., Pickard, D., Dougan, G. & Hall, R.M. 2014, 'Identification of a marker for two lineages within the GC1 clone of Acinetobacter baumannii.', The Journal of antimicrobial chemotherapy, vol. 69, no. 2, pp. 557-558.View/Download from: Publisher's site
Hamidian, M. & Hall, R.M. 2013, 'ISAba1 targets a specific position upstream of the intrinsic ampC gene of Acinetobacter baumannii leading to cephalosporin resistance.', The Journal of antimicrobial chemotherapy, vol. 68, no. 11, pp. 2682-2683.View/Download from: Publisher's site
Hamidian, M., Hancock, D.P. & Hall, R.M. 2013, 'Horizontal transfer of an ISAba125-activated ampC gene between Acinetobacter baumannii strains leading to cephalosporin resistance.', The Journal of antimicrobial chemotherapy, vol. 68, no. 1, pp. 244-245.View/Download from: Publisher's site
Hamidian, M., Nigro, S.J. & Hall, R.M. 2012, 'Variants of the gentamicin and tobramycin resistance plasmid pRAY are widely distributed in Acinetobacter.', The Journal of antimicrobial chemotherapy, vol. 67, no. 12, pp. 2833-2836.View/Download from: Publisher's site
OBJECTIVES: To determine the cause of resistance to the aminoglycosides gentamicin and tobramycin in Acinetobacter isolates and the location of the resistance genes. METHODS: Australian Acinetobacter baumannii isolates were screened for resistance to aminoglycosides. PCR followed by restriction digestion of amplicons was used to detect genes and plasmids. Plasmids were isolated and examined by restriction digestion. Plasmid DNA sequences were determined and bioinformatic analysis was used to identify features. The sequence of the bla(OXA-Ab) gene and multilocus sequence typing were used to determine strain types. RESULTS: Isolates that exhibited resistance to gentamicin, kanamycin and tobramycin were of diverse strain types. These isolates all carried the aadB gene cassette, and in all but one the cassette was in a 6 kb plasmid similar to pRAY. The three plasmid sequences determined revealed multiple frame-shift differences in the available pRAY sequence that altered the reading frames. In pRAY*, mobA and mobC mobilization genes were identified, but no potential replication initiation protein was found. pRAY*-v1 differed from pRAY* by 66 single-base differences, and pRAY*-v2 included two insertion sequences, ISAba22, located upstream of the aadB gene cassette, and IS18-like, within ISAba22. CONCLUSIONS: The plasmid pRAY* and variants are widely distributed in Acinetobacter spp. and are the most common cause of resistance to gentamicin and tobramycin. Mobilization genes should assist in the dissemination of pRAY* and its variants.
Post, V., Hamidian, M. & Hall, R.M. 2012, 'Antibiotic-resistant Acinetobacter baumannii variants belonging to global clone 1.', The Journal of antimicrobial chemotherapy, vol. 67, no. 4, pp. 1039-1040.View/Download from: Publisher's site
Hamidian, M. & Hall, R.M. 2011, 'AbaR4 replaces AbaR3 in a carbapenem-resistant Acinetobacter baumannii isolate belonging to global clone 1 from an Australian hospital.', The Journal of antimicrobial chemotherapy, vol. 66, no. 11, pp. 2484-2491.View/Download from: Publisher's site
OBJECTIVES: To explore the diversity of genomic resistance islands in multiply antibiotic-resistant Acinetobacter baumannii isolates in global clone 1 (GC1) from Australian hospitals. METHODS: PCR was used to characterize isolates, detect antibiotic resistance genes and insertion sequences and screen for genomic resistance islands. Structures of genomic islands were determined by PCR mapping and sequencing. Multilocus sequence typing was performed using the Oxford scheme. RESULTS: Eleven isolates that belong to GC1 were found among 90 A. baumannii isolated between 2001 and 2010 at Australian hospitals, and 5 were carbapenem resistant. Ten isolates had the features characteristic of AbaR3 and related islands, but one carbapenem-resistant isolate did not. Instead, D36 carried the bla(OXA-23) gene in transposon Tn2006, with Tn2006 in AbaR4, and AbaR4 in the chromosomal comM gene, replacing the AbaR3-type island usually associated with multiply antibiotic-resistant GC1 isolates. D36 was resistant to gentamicin, kanamycin and tobramycin due to the aadB gene cassette in the context found in plasmid pRAY and to sulfamethoxazole due to the sul2 gene. D36 was of a rare sequence type (ST), ST247. Bioinformatic analysis identified five potential transposition genes in the AbaR backbone transposons. CONCLUSIONS: Substantial diversity was observed among the GC1 isolates. This is the first report of AbaR4 replacing the AbaR3-type island seen in most GC1 isolates, and D36 represents a distinct new GC1 lineage. The AbaRs are members of a large, previously undocumented family of transposons that target comM.
Hamidian, M., Sanaei, M., Azimi-Rad, M., Tajbakhsh, M., Dabiri, H. & Zali, M.R. 2011, 'Fla-typing, RAPD analysis, isolation rate and antimicrobial resistance profile of Campylobacter jejuni and Campylobacter coli of human origin collected from hospitals in Tehran, Iran', Annals of Microbiology, vol. 61, no. 2, pp. 315-321.View/Download from: Publisher's site
The purpose of the current study was to investigate the isolation rate, antimicrobial resistance profile and molecular typing of Campylobacter spp. recovered from patients with diarrhea in hospitals in Tehran, Iran. Over a period of 13 months, from 562 diarrheal samples 49 (8.7%) Campylobacter spp. were isolated, of which 34 (69.5%) were Campylobacter jejuni and 12 (24.5%) were identified as Campylobacter coli. Antimicrobial susceptibility and typing of the Campylobacter spp. isolates was carried out using the Kirby-Bauer disk diffusion method, fla-typing and RAPD analysis. The highest resistance in the collected Campylobacter isolates was to ofloxacin (77.5%) followed by ciprofloxacin (73.4%), nalidixic acid (69.3%), ceftazidime (53%), cefotaxime (51%) and carbenicillin (40.8%) while all the isolates were susceptible to imipenem. The results of RAPD analysis and fla-typing showed a relative high diversity and weak clonality amongst Campylobacter spp. isolates from patients with diarrhea in two hospitals in Tehran, Iran. In addition, during the current study, fla-typing proved to be more reliable and reproducible for typing of isolates. To our knowledge, this is the first study providing structural data for RAPD analysis and fla-typing of Campylobacter spp. isolates recovered from Iranian patients. © Springer-Verlag and the University of Milan 2010.
Hamidian, M., Sanaei, M., Bolfion, M., Dabiri, H., Zali, M.-.R. & Walther-Rasmussen, J. 2011, 'Prevalence of putative virulence markers in Campylobacter jejuni and Campylobacter coli isolated from hospitalized children, raw chicken, and raw beef in Tehran, Iran.', Canadian journal of microbiology, vol. 57, no. 2, pp. 143-148.View/Download from: Publisher's site
The incidence of the virulence-associated genes cdtA, cdtB, cdtC, cadF, dnaJ, racR, and pldA has been investigated in Campylobacter jejuni and Campylobacter coli collected from raw chicken and beef from retailers in Tehran, Iran, and from hospitalized children (age, 14 years) suffering from diarrhea. Campylobacter spp. were collectively identified by morphological and biochemical methods. Campylobacter jejuni and C. coli were discriminated from other Campylobacter spp. by amplification of a specific conserved fragment of the 16S rRNA gene. The distinction between C. jejuni and C. coli was subsequently made by molecular determination of the presence of the hipO gene in C. jejuni or the ask gene in C. coli. Fragments of the studied virulence-associated genes, cdtA, cdtB, cdtC, cadF, racR, dnaJ, and pldA, were amplified by PCR and subjected to horizontal gel electrophoresis. A total of 71 isolates of C. jejuni and 24 isolates of C. coli from meat were analyzed, while the numbers of isolates from the hospitalized children were 28 and 9, respectively. The unequal distribution of C. jejuni and C. coli in the samples has also been reported in other studies. Statistical analyses by the use of the two-tailed Fisher's exact test of the occurrence of the virulence genes in the isolates of different origins showed that the occurrence of the dnaJ gene was consistently significantly higher in all C. jejuni isolates than in C. coli. The occurrence of the other virulence markers did not differ significantly between species in the majority of the isolates. The PCR results also showed that the occurrence of the virulence markers in the analyzed isolates was much lower than in other studies, which may be caused by a divergent genomic pool of our isolates in comparison with others.
Hamidian, M., Tajbakhsh, M., Tohidpour, A., Rahbar, M., Zali, M.R. & Walther-Rasmussen, J. 2011, 'Detection of novel gyrA mutations in nalidixic acid-resistant isolates of Salmonella enterica from patients with diarrhoea.', International journal of antimicrobial agents, vol. 37, no. 4, pp. 360-364.View/Download from: Publisher's site
The aim of the current study was to detect mutations in the gyrA gene of quinolone-resistant Salmonella spp. isolates recovered in Tehran, Iran. Between April 2008 and September 2009, 174 Salmonella spp. were collected and assayed for quinolone resistance and detection of gyrA mutations. Isolates identified as Salmonella enterica were tested for susceptibility by the disk diffusion method. Polymerase chain reaction (PCR) amplification and sequencing of the gyrA gene segment encoding the quinolone resistance-determining region (QRDR) were performed for the nalidixic acid-resistant isolates. Amongst the 174 recovered Salmonella spp. isolates, 89 were resistant to nalidixic acid, of which 9 were resistant to enrofloxacin; 10 isolates had reduced susceptibility to nalidixic acid. None of the isolates were resistant to ciprofloxacin, but a single isolate showed reduced susceptibility. Twelve types of amino acid replacement were found in the QRDR region of GyrA, namely the previously described substitutions in positions 83 and 87 as well as five new substitutions Leu41-Pro, Arg47-Ser, Ser111-Thr, Ala118-Thr and Asp147-Gly. Double substitutions in both positions 83 and 87 were not identified. A Gly133-Glu substitution was identified in a single S. enterica serotype Typhi isolate.
Hamidian, M., Tajbakhsh, M., Walther-Rasmussen, J. & Zali, M.-.R. 2009, 'Emergence of extended-spectrum beta-lactamases in clinical isolates of Salmonella enterica in Tehran, Iran.', Japanese journal of infectious diseases, vol. 62, no. 5, pp. 368-371.
The purpose of the current study was to investigate the presence and molecular type(s) of extended-spectrum beta-lactamases (ESBLs) in Salmonella spp. isolates obtained from patients with diarrhea in hospitals of Tehran, Iran. Over a period of 17 months, 129 Salmonella spp. were isolated from fecal samples and tested for susceptibility using the Kirby-Bauer disk diffusion method; then, screening for ESBL-producing isolates and determination of their minimum inhibitory concentrations were carried out using the combined disk method and standard agar dilution method, respectively. The presence and type of ESBL-encoding genes were determined by PCR and sequence analysis. The isolates were all identified as Salmonella enterica of different serovars. The highest resistance in the collected Salmonella isolates was to nalidixic acid (45.7%), followed by tetracycline (43.4%), trimethoprim-sulfamethoxazole (36.4%), ampicillin (15.5%), and chloramphenicol (14.7%). All the isolates were susceptible to ciprofloxacin, gentamicin, and cefoxitin. Three S. enterica isolates were resistant to ampicillin, piperacillin, ceftazidime, cefotaxime, ceftriaxone, cefpodoxime, cephalothin, and aztreonam. PCR and DNA sequencing revealed that two of the three isolates harbored both a bla(CTX-M-15) and a bla(TEM) gene while the third one carried only a bla(CTX-M-15) gene. This is the first study providing structural data for a CTX-M-type beta-lactamase produced by Salmonella isolates recovered in Iran.
Jafari, F., Hamidian, M., Rezadehbashi, M., Doyle, M., Salmanzadeh-Ahrabi, S., Derakhshan, F. & Reza Zali, M. 2009, 'Prevalence and antimicrobial resistance of diarrheagenic Escherichia coli and Shigella species associated with acute diarrhea in Tehran, Iran.', The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale, vol. 20, no. 3, pp. e56-e62.View/Download from: Publisher's site
A study was performed to determine the prevalence and antimicrobial resistance of Shigella species and diarrheagenic Escherichia coli isolates cultured from patients with acute diarrhea in Tehran, Iran. Between May 2003 and May 2005, 1120 diarrheal specimens were collected and assayed for bacterial enteropathogens by conventional and molecular methods. Etiological agents were isolated from 564 (50.3%) specimens, and included 305 (54%) E coli, 157 (27.8%) Shigella species, and 102 (18%) from other genera of bacteria. The predominant E coli was Shiga toxin-producing E coli (105 isolates [34.5%]) and the predominant Shigella serotype was Shigella sonnei (88 isolates [56.1%]). A high rate of antibiotic resistance was observed among E coli, with 40 of 53 (75.5%) Shiga toxin-producing E coli isolates resistant to amoxicillin and tetra-cycline, and eight (5.2%) E coli isolates resistant to more than six antibiotics. Most Shigella isolates were resistant to tetracycline (95%) and trimethoprim-sulfamethoxazole (91.7%), with greatest antibiotic resistance observed among S sonnei (53 of 88 [60.2%] isolates). Antibiotic resistance is widespread in diarrheagenic E coli and Shigella in children with acute diarrhea in Tehran, Iran; hence, updated strategies for appropriate use of antimicrobial agents in Iran are needed.
Jafari, F., Shokrzadeh, L., Hamidian, M., Salmanzadeh-Ahrabi, S. & Zali, M.R. 2008, 'Acute diarrhea due to enteropathogenic bacteria in patients at hospitals in Tehran.', Japanese journal of infectious diseases, vol. 61, no. 4, pp. 269-273.
During a study examining causes of diarrhea from May 2004 to May 2005, 808 stool specimens were collected from patients with acute diarrhea in Tehran. Fecal samples were cultured and identified according to the standard biochemical methods. Molecular identification of enteropathogens was carried out by amplification of their virulence genes by polymerase chain reaction. A total of 369 (45.6%) bacterial pathogens were recovered from 808 patients as follows: Shigella spp., 155 (45.6%); diarrheagenic Escherichia coli 143 (38.8%); Salmonella spp., 51 (13.8%); and Campylobacter spp., 20 (5.4%). Most of the diarrheagenic E. coli were Shiga toxin-producing E. coli, with 64 (44.7%) isolates, followed by 47 (32.9%) enterotoxigenic E. coli isolates; among Shigella spp. isolates, 69 (44.5%) Shigella flexneri were predominant. The molecular diagnosis of enteropathogens yielded a more accurate characterization of the prevalence of diarrhea-causing bacterial strains in Iran. The present study revealed a high prevalence of Shigella and diarrheagenic E. coli as the predominant causes of bacterial diarrhea in this region of the world. These two types of bacteria should therefore be considered when designing preventive strategies for people living in Iran.
Akbari-Nakhjavani, F., Mirsalehian, A., Hamidian, M., Kazemi, B., Mirafshar, M., Jabal Ameli, F., Pajand, O. & Peymani, A. 2007, 'Antimicrobial susceptibility testing of Escherichia coli strains isolated from urinary tract infections to fluoroquinolones and detection of gyrA mutations in resistant strains', Daru, vol. 15, no. 2, pp. 94-99.
Widespread uses of fluoroquinolones have resulted in increasing incidences of resistance against these agents all over the world. The aim of this study was to assess, susceptibility of Escherichia coli strains from patients with Urinary Tract Infection against common fluoroquinolones and detection of mutations in the gyrA gene. Antimicrobial susceptibility testing of 164 E.coli isolates from patients with UTI, was evaluated by disk agar diffusion (DAD) and MIC methods. Polymerase chain reaction of E.coli strains were performed by amplification of Quinolone Resistance Determining Region (QRDR) of gyrA gene. PCR products were tested by Conformational Sensitive Gel Electrophoresis (CSGE) and those with hetrodublexes were selected and examined by DNA sequencing. According to disc agar diffusion, 49.3% were resistant to nalidixic acid, 41.4% to norfloxacin, 44.5% to ofloxacin and 40.2 % to ciprofloxacin. By Minimal Inhibitory Concentration (MIC) testing a high-level of resistance (42.1%) to ciprofloxacin was observed. Mutations in codons 83 and 87 in all 81 isolates were positive by CSGE method.
Nakhjavani, F.A., Mirsalehian, A., Hamidian, M., Kazemi, B., Mirafshar, M. & Jabalameli, F. 2007, 'Antimicrobial susceptibility testing for Escherichia coli strains to fluoroquinolones, in urinary tract infections', Iranian Journal of Public Health, vol. 36, no. 1, pp. 89-92.
Background: Urinary Tract Infections (UTIs) are one of the most common infections diseases diagnosed all over the world. Meanwhile most episode of UTIs is caused by Echerichia coli (up to 85%) and frequently fluoroquinolones are preferred as initial agents for empiric therapy of UTIs. Widespread use of fluoroquinolones has resulted in an increasing incidence of resistance these agents all over the world The aim of this study was to assess, susceptibility of Escherichia coli strains from UTI patients against common fluoroquinolones. Methods: Antimicrobial susceptibility testing was determined by disk agar diffusion (DAD) and Minimal Inhibitory Concentration methods as described by the National Committee for Clinical Laboratory Standards (NCCLS). Results: One hundred sixty four clinical isolates of E. coli were collected by urine cultures from patients with UTI. The extent of resistant to nalidixic acid, ofloxacin, norfloxacin and ciprofloxacin, by disk diffusion method was 49.3%, 44.5%, 41.4% and 40.2%, respectively. Resistance to ciprofloxacin by MIC method was 42.1%. Conclusion: This study represents high level resistant of E. coli isolates from UTI patients. It is because of inappropriate and incorrect administration of antimicrobial agents in blind cases. This problem remarks significance of performing antimicrobial susceptibility testing before empiric antibiotic therapy. To overcome this problem use of unnecessary antibiotics therapy should be limited.