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Molecular Investigation of Pyocyanin Biosynthesis genes Among Multidrug Resistance Clinical Pseudomonas Aeruginosa isolates

Maytham H.J. Al-Thabhawee1, Hussein O.M. AL-Dahmoshi2*

1,2Biology Department, college of science, University of Babylon, Iraq

*Corresponding author Email:[email protected] ABSTRACT:

Multidrug resistance Pseudomonas aeruginosa (MDRPA) is most important issue in healthcare setting. Pyocyanin production among MDRPA must increase the worseness of infection by side adverse like tissue damage subsequent harmful effects of pyocyanin for host. The killing of bacteria accomplished by inhibition of pyocyanin production may represent a promise treatment approach. The study include investigation of 50 isolates of MDRPA for pyocyanin biosynthesis and resistance for antibiotics. Molecular diagnosis using P. aeruginosa specific primer pairs, investigation of phzA, phzM and phzS using specific primer pairs by PCR were also performed.

The results revealed high resistance to beta lactam antibiotics (78% for ceftazidime, 78% for cefepime and 46% for piperacillin) can indicate possessing of isolates for beta lactamases and this confirmed by dropping resistance to piperacillin to 16% when combined with tazobactam.

Also the results shown the ability of MDRPA for pyocyanin production using the system of genes (phzA, phzM, phzS) among all isolates except (3 isolates for phzS). The current study conclude that all isolated of P. aeruginosa were highly virulent due to their possessing of pyocyanin biosynthesis system and beta lactamases make using of piperacillin-tazobactam and meropenem a good choice to kill bacteria along with impairment of pyocyanin production reducing the possible harmful effects of this pigment.

KEYWORDS: Pyocyanin, phzA, phzM, phzS, piperacillin-tazobactam Introduction

Pseudomonas aeruginosa is an opportunistic nosocomial pathogen which can dominant in all niches. Their adaptability to different conditions may come from possessing different virulence factors exploited for survival. One of the most important virulence factor is phanezines. P.

aeruginosa produces redox-active pigments called phenazines that affect gene expression, metabolic flux, and redox balancing in their producers[1,2]. P. aeruginosa produce a single compound, phenazine-1-carboxylic acid (PCA). Subsequent conversion of PCA to pyocyanin is mediated in P. aeruginosa by two novel phenazine-modifying genes,phzM and phzS, which encode putative phenazine-specific methyltransferase and flavin-containing monooxygenase, respectively[3].

Pyocyanin regards as virulence factor and produced by about 95% of the P. aeruginosa. It cause pulmonary tissue damage. Pyocyanin interferes with the regulation of ion transport, ciliary beat frequency, and mucus secretion in airway epithelial cells by altering the cytosolic concentration of calcium[4,5]. Pyocyanin promotes virulence by interfering with several cellular functions in host cells including electron transport, cellular respiration, energy metabolism, gene expression, and innate immune mechanisms. promotes inflammatory responses by imposing oxidative stress on host cells[6,7]. It was found that pyocyanin production by P. aeruginosa suppresses the acute inflammatory response by pathogen-driven acceleration of neutrophil apoptosis and by reducing local inflammation, and that this is advantageous for bacterial survival Phenazines have a

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potential to alter antibiotic susceptibility[8,9]. Resistance to antibiotics may be either intrinsic or acquired[10,11]. The occurrence of multidrug resistant P. aeruginosa is growing in the world, limiting the therapeutic options[12,13]. Despite availability of newer antimicrobial agents possessing anti-Pseudomonal activities, P. aeruginosa is still responsible for causing life threatening infection in hospitals[14,15]. Even though development of multi-drug resistant Pseudomonas aeruginosa strains, which are difficult to be treated, some available antibiotics still able to dominate pseudomonal infections with a reasonable percentage of success, for example, colistin sulfate and quinolones (ciprofloxacin and levofloxacin)[16,17]. The current study was conducted to investigate Phenazine Biosynthesis genes among multidrug resistance P. aeruginosa isolates.

Materials And Methods Bacterial isolates:

Fifty P. aeruginosa isolated were collected from different specimens and subjected for primary identification test using Pseudomonas chromogenic agar (Condalab/Spain) and confirmed using genus specific (for Pseudomonas spp.) and species specific (for P. aeruginosa) (Table 1).

Antibiotic susceptibility Assay:

It was performed using 14 antibiotics agent according to CLSI-2019[18]. Polymerase Chain Reaction

DNA was extracted according to manufactures instructions (IntronBio/Korea). The primers were dissolved according to manufacturer instructions (Macrogen/Korea). The primer pairs and PCR conditions were listed in (Table 1)

Table 1. Primer pairs and PCR conditions

Primer name

5' to 3' sequence Product (bp)

Annaeling Temp. (°C)

Reference

Ps. Spp.

F:GACGGGTGAGTAATGCCTA 618 56 [19]

R:CACTGGTGTTCCTTCCTATA

Ps. aeru.

F:GGGGGATCTTCGGACCTCA 956 61 [19]

R:TCCTTAGAGTGCCCACCCG

phzA1

F:TCAGCGGTACAGGGAAACAC 283 60.3 This study R:GAAGTGGTTCGGATCCTCGG

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phzA2

F:CGACAACCTGGAATTGCGTC 368 59.3 This study R:GTTTTATCCGGCCGTTCTCG

phzS

F:CTGGTCGCCTATCCGATCTC 507 61.3 This study R:GCTCTTCTCGGTCTTCGGTC

phzM

F:GGATGGCCTTGGTCAATTCG 350 60.3 This study R:GATCTTCCAGGGCGATACCC

Results

The results of isolation revealed high percentage of P. aeruginosa among UTIs patients 18(36%), lower respiratory tract infection patients 13(26%) wounds and burn infections 9(18%), otitis media 5(10%), bacteremia 2(4%), vaginosis 2(4%) and 1(2%) for meningitis (table2).

Results of resistance for 14 antibiotics according to CLSI revealed that 39(78%) of P. aeruginosa isolates were resistant to ceftazidime (CAZ) and cefepime (FEP), 23(46%) for piperacillin (PRL), 15(30%) for gentamycin (CN), 14(28%) for ciprofloxacin (CIP), 13(26%) for tobramycin (TOB), 12(24%) for Aztreonam (ATM),11(22%) for amikacin (AK), 10(20%) for ofloxacine (OFX), 9(18%) for levofloxacin (LEV), 8(16%) for piperacillin-tazobactam (PTZ), 7(14%) for netilmicine, imipenem (IPM) and meropenem (MEM) (Figure 1). Pyocunine biosynthesis was investigated via detection of Phenazine gene (phzA) which encode for phenazine-1-carboxylic acid (PCA) who subsequently converted to pyocyanin by two enzyme: Phenazine-1-carboxylate N-methyltransferase and Flavin-containing monooxygenase which endcoded by (phzM) and (phzS) genes respectively. The results revealed that all p. aeruginosa isolated have phzA gene and phzM while only 47(94%) have phzS gene (Table 3), (Figure 2-5).

Table 2. Distribution of P. aeruginosa isolates among Diseases

Bacterial Isolate Specimen

Disease

% No.

36%

18 midstream urine

UTIs

26%

13 Broncoalveolar lavage

RTIs

18%

9 Wound burn swab

Wound and burn infections

10%

5 Ear swab

Otitis Media

4%

2 Blood stream

Bacteremia

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4%

2 High vaginal swab

Vaginosis

2%

1 CSF

Meningitis

100%

50 Total

Table 3. Distribution of Phenazine biosynthesis gene among P. aeruginosa isolates

Gene P. aeruginosa isolates

No. %

phzA1 50 100%

phzA2 50 100%

phzM 50 100%

phzS 47 94%

Figure 1. Antibiotic resistance percentage of P. aeruginosa to 14 antibiotics (ceftazidime (CAZ), cefepime (FEP), piperacillin (PRL), gentamycin (CN), ciprofloxacin (CIP), tobramycin (TOB), Aztreonam (ATM), amikacin (AK), ofloxacine (OFX), levofloxacin (LEV), piperacillin-tazobactam (PTZ), netilmicine, imipenem (IPM) and meropenem (MEM)

78

% %78 46

% 30

% %28%26%24%22%20%18%16%14%14%14

0

%10

%20

%30

%40

%50

%60

%70

%80

%90

%100

%

Resistance

Antibiotic

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Figure 2. 1.5% agarose gel electrophoresis of phzA1 amplicon (283bp) among P. aeruginosa isolates. M represent 100bp DNA ladder , lane 1-50 represent the isolates ,TBE 1x,at Voltage 75volt for 60min.

Figure 3. 1.5% agarose gel electrophoresis of phzA2 amplicon (368bp) among P. aeruginosa isolates. M represent 100bp DNA ladder, lane 1-50 represent the isolates,TBE 1x,at Voltage 75volt for 60min.

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Figure 4. 1.5% agarose gel electrophoresis of phzM amplicon (350bp) among P. aeruginosa isolates. M represent 100bp DNA ladder, lane 1-50 represent the isolates,TBE 1x,at Voltage 75volt for 90min

Figure 5. 1.5% agarose gel electrophoresis of phzS amplicon (507bp) among P. aeruginosa isolates. M represent 100bp DNA ladder, lane 1-50 represent the isolates,TBE 1x,at Voltage 75volt for 60min.

Discussion

Our results may be totally agree with previous studies whose found that dominance of P.

aeruginosa among UTIs, RTIs and wound-burn infections[20-22]. Implication of P. aeruginosa in UTIs may be as nosocomial pathogen resulted from placing and removing of indwelling urinary catheters[23]. Intensive care unit (ICU) admission is a risk for multidrug-resistant (MDR) P.

aeruginosa to critically ill pneumonia patients[24]. In burn centers, P. aeruginosa acts as a major cause of nosocomial infections and this is may attributed to a high prevalence of the antibiotic resistance and biofilm formation ability[25].

P. aeruginosa displays resistance to a variety of antibiotics, including aminoglycosides, quinolones and β-lactams. The resistance may be intrinsic (low outer membrane permeability, expression of efflux pumps and the production of antibiotic-inactivating enzymes), acquired (either horizontal transfer of resistance genes or mutational changes) and adaptive (involves formation of biofilm which serves as a diffusion barrier to limit antibiotic access to the bacterial cells) resistance[26,27].

The results shown high resistance to beta lactams (ceftazidime (CAZ), cefepime (FEP), piperacillin (PRL) and this is mainly mediated by beta lactamases due to that when use piperacillin-tazobactam the resistance was dropped from 46% to 16%. Beta lactamases regard as intrinsic mechanism of resistance leading to inactivating of beta lactam rendering them inactive.

Beta lactamase inhibitor like tazobactam (An irreversible inhibitor of a wide variety of bacterial beta-lactamases) can improve many beta lactams like piperacillin once combined with them.

Piperacillin-tazobactam is the best β-lactam–β-lactamase inhibitor combination that is frequently used for the management of Pseudomonas aeruginosa infections[28-30]. The results of

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current study revealed the ability of all P. aeruginosa isolated to produce pyocyanin making them more virulent and have great harmful consequences due to implication of pyocyanin in tissue damage, interfering with immune response and triggering proinflamattory responses[31,32]. Natural phenazines are versatile secondary metabolites that are mainly produced by Pseudomonas and Streptomyces. All phenazine-type metabolites originate from two precursors: phenazine-1- carboxylic acid (PCA) in Pseudomonas or phenazine-1,6-dicarboxylic acid (PDC) in Streptomyces and other bacteria[33].Pyocyanin has been shown to intercalate with extracellular DNA to promote cell-to-cell interactions between the P. aeruginosa cells by influencing their physicochemical interactions and the cell surface properties. It has been suggested that pyocyanin may also contribute to the biofilm formation by the promotion of extracellular DNA[34].

There is a need for therapeutics strategies to kill P. aeruginosa and at same time preventing the possible damages resulted from pyocyanin productions. Our results suggest Piperacillin- tazobactam, meropenem and combination as a perfect regimens to treat such bacterial isolates.

Many results shown the inhibitory effect of Piperacillin-tazobactam and meropenem on biofilm formation and reduce the productions of pyocyanin[34-37].

Conclusion

The current study conclude that all isolated of P. aeruginosa were highly virulent due to their possessing of pyocyanin biosynthesis system and beta lactamases make using of piperacillin- tazobactam and meropenem a good choice to kill bacteria along with impairment of pyocyanin production reducing the possible harmful effects of this pigment.

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