Keywords

14.1 Introduction

Acinetobacter baumannii is an opportunistic pathogen generally considered non-pathogenic to healthy individuals. However, in the past few decades, it has been extensively reported worldwide for its resistance to the conventional as well as recently developed antimicrobial drugs (Almasaudi 2018; Gokmen et al. 2016). There is an increasing prevalence of multidrug-resistant strains of A. baumannii especially in intensive care units (ICU) of the hospitals, causing infections in patients with invasive devices (ventilators and catheters) and low immunity (Singh et al. 2013). With its ability to develop antibiotic resistance and survive under dry conditions on inanimate objects for a long period, this gram-negative pathogen is responsible for causing numerous infections in the hospital environment (Inchai et al. 2015). A. baumannii is recognized as a major cause of life-threatening hospital-associated infections including pneumonia, meningitis, urinary tract infections, and severe bloodstream infection, especially in immune-compromised individuals (Santajit and Indrawattana 2016).

The indiscriminate administration of antibiotics along with various bacterial mechanisms has been attributed to the evolution of multiple drug-resistant strains of A. baumannii (Singh et al. 2013). This notorious pathogen also possesses a remarkable ability to rapidly acquire resistance foreign genetic material including a vast array of antibiotic resistance genes (Almasaudi 2018). Since the majority of the carbapenem-hydrolyzing enzymes are encoded in mobile genetic elements, it is proposed that the blaNDM-1 gene in A. baumannii is apparently transmitted and acquired from carbapenem-resistant Enterobacteriaceae (Escherichia coli and Klebsiella spp.) via horizontal gene transfer (Jain et al. 2019). Furthermore, the ability to survive in severe conditions of temperature, pH, and in the presence of commonly used antimicrobial agents facilitates Acinetobacter to easily disseminate in the hospital settings (Chopra et al. 2013).

The remarkable property of A. baumannii to develop resistance against many antibiotics is a huge concern in the healthcare setting as these infections are difficult to treat. They are linked to increased mortality and morbidity in cases of ventilator-associated pneumonia (Inchai et al. 2015). A. baumannii is also responsible for causing community-acquired infections in patients with a history of alcoholism, cancer, diabetes, and obstructive pulmonary disorders (Harding et al. 2018).

Carbapenems are the most commonly recognized drugs for the management of A. baumannii associated infections. Hence, the emergence of carbapenem-resistant strains of A. baumannii has become a major challenge globally. In A. baumannii, numerous mechanisms including the production of β-lactamases, loss of outer membrane protein (OMPs), and efflux pump were found to cause in carbapenem resistance (Shoja et al. 2017). Hence, understanding the resistance mechanisms of A. baumannii is vital for the development of alternative tools and novel antimicrobial agents to combat the ever-increasing problem of drug resistance (Santajit and Indrawattana 2016). In the past few decades, the incidence of A. baumannii infections and outbreaks has drastically increased globally (Necati Hakyemez et al. 2013). Thus, the management of A. baumannii infections is currently one of the biggest challenges in clinical practice. In this chapter, the clinical implications of A. baumannii and its associated mechanisms of antimicrobial resistance have been presented in detail.

14.2 Virulence Factors

Recent studies have led to the identification of numerous virulence factors of A. baumannii. Outer membrane protein A (OmpA), efflux pump, phospholipase, and capsular polysaccharides were found to contribute to the pathogenicity and also impart antimicrobial resistance to A. baumannii. In addition, the lipopolysaccharide (LPS) of A. baumannii was found to induce the production of inflammatory cytokines, i.e., interleukin-8 and tumor necrosis factor. Other potential virulence factors including biofilm formation, penicillin-binding proteins, and alteration in outer membrane vesicles (OMVs) have also been implicated for the pathogenicity of A. baumannii (Wong et al. 2017). Targeted studies have also led to the identification of few virulence determinants of A. baumannii, including phospholipase D, metal (zinc and iron) acquisition system. Additionally, in the serum-resistant strain of A. baumannii, it was observed that the genes involved in competence, iron acquisition, type IV pili biogenesis, and efflux pumps get upregulated during the growth of the pathogen in human serum (Subashchandrabose et al. 2016).

OmpA coupled with the membrane efflux systems collectively participates in the expulsion of antimicrobial compounds from the periplasmic space (Lee et al. 2017). OmpA is also involved in invasion of epithelial cell and apoptosis. Phospholipases C and D aid in epithelial cell invasion and also help in the survival of the bacterial pathogen in the human serum (Antunes et al. 2014). Metal acquisition plays a vital role in the A. baumannii virulence. A. baumannii produces iron siderophores and acinetobactin in an iron limiting environment. Similarly, in Zn-limiting conditions, the zinc acquisition system (ZnuABC) is generally upregulated (Lee et al. 2017). In addition, the quorum-sensing system and biofilm-forming ability also aid in the survival of the cells on inert surfaces thereby contributing to drug resistance (Antunes et al. 2014). The above-mentioned virulence determinants serve as an attractive target for the development of new preventive strategies and antibiotics.

14.3 Clinical Manifestations

A. baumannii is recognized to cause fatal nosocomial infections, most commonly in patients with chronic disease or has undergone surgeries. The colonization and subsequent infection of A. baumannii commonly takes place in organ with higher fluid content such as urinary tract, respiratory tract, peritoneal cavity, and indwelling medical devices (Almasaudi 2018). It reported to cause secondary meningitis and infections to eye, skin and soft tissue, burn wound, and urinary tract. However, the most common clinical manifestation with the highest mortality rates is recorded in cases of ventilator-associated pneumonia and bacteremia. The pathogen usually gains entry into the host system via intravascular catheters, open wounds, and medical in-dwellings (Antunes et al. 2014).

14.3.1 Bacteremia

Bacteremia is considered as the most significant infection caused by A. baumannii in health care settings which is also associated with marked antimicrobial resistance and high mortality (Chopra et al. 2013). A. baumannii associated bacteremia is generally nosocomial and occurs commonly in ICUs (Wong et al. 2017). A. baumannii bacteremia commonly originates from the respiratory tract and intravascular catheters (Cisneros and Rodriguez-Bano 2002). It accounts for 52% of cases in critical care, followed by 13% in surgery, 10% in general medical, and 17% in cases of cancer (Wareham et al. 2008).

14.3.2 Acinetobacter Pneumonia

Ventilator-associated pneumonia (VAP) is a major nosocomial infection among critically immune-compromised individuals. VAP accounts for 25% of all types of ICU-acquired infections and exerts a huge burden on morbidity and health care costs (Balkhy et al. 2014). In recent years, A. baumannii has been widely documented and recognized as a major cause of VAP. The mortality rate in ICU patients with VAP ranged from 45.6% to 60.9% and VAP caused by extreme drug-resistant (XDR) A. baumannii has been found to be as high as 84.3%. Gokmen et al. (2016) reported three cases of VAP wherein the infection resulted due to the colonization of ICU-ventilator by carbapenem-resistant A. baumannii (CRA). All the isolated strains were carbapenem resistant and found to possess blaOXA-23-like and blaOXA-51-like gene (Gokmen et al. 2016).

A. baumannii can adhere and establish biofilms on the medical devices like the endotracheal tube and create a niche for the rapid dissemination of the bacterial cells, thus resulting in the increasing incidences of carbapenem-resistant Acinetobacter in the ICUs. Acinetobacter may also directly enter the alveoli of mechanically ventilated patients, thereby allowing the establishment of infection in lung tissue (Wong et al. 2017). In spite of the recent advancements in burns surgery and intensive care, VAP still remains the main cause of mortality in victims with major burn wounds. VAP is also accountable for significant morbidity and mortality in the intensive care pediatric ward (Rogers et al. 2014).

Community-acquired A. baumannii pneumonia (CAP-AB) is generally recorded during the rainy season especially in tropical parts of Australia and Asia. CAP-AB is particularly found in individuals with chronic obstructive pulmonary disease and cases of alcohol abuse (Almasaudi 2018). Oh et al. (2013) reported the first case of rapidly progressing and fatal CAP-AB in Korea wherein the patient died within 36 h of hospital admission (Oh et al. 2013).

14.3.3 Meningitis

Meningitis caused by multidrug-resistant A. baumannii usually arises post-neurosurgery or in the presence of a ventriculostomy (Wong et al. 2017). With mortality rate exceeding 15%, post-neurosurgical meningitis is a major clinical issue. The high-risk group for post-neurosurgical bacterial meningitis includes those with concomitant incision infection, cerebrospinal leakage, prolonged duration of surgery, a surgery that enters a sinus, prolonged external ventricular drainage, increased severity of illness, and need for repeat surgery (Kim et al. 2009).

14.3.4 Wound Infection

Patients with burn wounds are generally susceptible and associated with high risk for infection. A. baumannii infection represents a common cause of mortality in patients with burn wards. Shoja et al. (2017) reported a high population of carbapenem-resistant A. baumannii containing blaOXA-23-like and blaOXA-24-like genes among patients with burn wound (Shoja et al. 2017).

14.3.5 Urinary Tract Infection

Urinary tract infections are generally linked to the colonization of urinary catheters or percutaneous nephrostomy tubes by the pathogen (Wong et al. 2017). The cases of A. baumannii related UTI infections are rare with an estimated 1.6% being ICU-acquired UTIs. It is also unlikely for A. baumannii to cause severe UTI in outpatients (Almasaudi 2018).

14.3.6 Other Manifestations

A few reported cases of A. baumannii endocarditis exist, with the majority of these cases associated with prosthetic valves (Almasaudi 2018). Numerous reports from across the globe including India have documented the increasing prevalence of Acinetobacter spp. in lower respiratory tract infections (LRTI). In the recent study of Jain et al. (2019), A. baumannii was found to be among the most common pathogen responsible for LRTI in ICUs, accountable for almost 26.2% of the cases (Jain et al. 2019). Lagana et al. (2015) reported two cases of lethal and infective endocarditis on cardiac prostheses sustained by A. baumannii (Lagana et al. 2015).

Although not very frequent, MDR A. baumannii has been observed to cause peritonitis in peritoneal dialysis patients, thereby resulting in serious infection with a high possibility of mortality (Zhang et al. 2014). Ocular infections, particularly endophthalmitis and keratitis caused by A. baumannii have also been observed in recent years and mainly associated with prolonged use of contact lens or post-eye surgery. Chen et al. (2008) documented two cases of ocular infection caused by A. baumannii, one resulting in endogenous endophthalmitis and the other endophthalmitis following corneal transplant (Chen et al. 2008).

14.4 Mechanisms of Resistance

Antimicrobial resistance characteristics exhibited by the A. baumannii is contributed by multiple factors. The mechanisms of antimicrobial resistance in the clinical isolates of A. baumannii may be broadly divided into 4 categories: (1) inactivation or alteration of antimicrobials, (2) reduced entry and intracellular accumulation of antimicrobials, (3) alteration of the drug target, and (4) biofilm formation.

14.4.1 Inactivation or Alteration of Antimicrobials

A wide array of beta-lactamases produced by Acinetobacter species hydrolyze numerous class of drugs including β-lactams and cephalosporins, thereby conferring antibiotic resistance to A. baumannii (Manchanda et al. 2010). All the four classes of β-lactamases have been identified in A. baumannii. Some of the class A β-lactamases identified in A. baumannii includes CTX-M, GES, SCO, PER, KPC, SHV, VEB, TEM, and CARB. Class β-lactamases are also known as metallo-β-lactamases (MBLs) and requires heavy metal like zinc or iron for catalysis (Lee et al. 2017). MBLs are known to impart resistance to carbapenems and to other β-lactams (Manchanda et al. 2010). Class C β-lactamases also known as AmpC cephalosporins are widely prevalent in A. baumannii. It is encoded by the bla gene and imparts broad-spectrum resistance to narrow and extended-spectrum cephalosporins, along with penicillin (Asif et al. 2018). Class D β-lactamases are also termed as oxacillinases (OXAs) due to their ability to hydrolyze isoxazolyl penicillin, oxacillin much faster than benzylpenicillin. The presence of class D β-lactamases and/or MBLs in A. baumannii is attributed to their high resistance towards carbapenems (Lee et al. 2017).

14.4.2 Reduced Entry and Intracellular Accumulation of Antimicrobials

The susceptibility towards a particular drug is determined by the balance in the uptake and elimination of antibiotics by the bacterial cell. Therefore, hampering the entry of antibiotic through the bacterial cell membrane is one of the strategies used by bacteria to develop antibiotic resistance (Santajit and Indrawattana 2016). The decrease in outer membrane permeability either due to alteration in porin channels and/or upregulation of multidrug efflux pumps significantly reduces the accessibility of the drugs towards the bacterial targets.

Porin channels along with other OMPs are known to facilitate the entry of antimicrobial agents inside the bacterial cells (Maragakis and Perl 2008). In A. baumannii, the presence of lesser porin channels with smaller size restricts the entry of the drug molecules to the intracellular bacterial targets (Singh et al. 2013). Many studies have also attributed carbapenem resistance to the reduction in the expression of OMPs (Asif et al. 2018). The loss of A. baumannii Omp29 which generates OXA-51-like or OXA-23-like carbapenemases is associated with high resistance towards imipenem. OmpA contributes to the resistance towards chloramphenicol, aztreonam, and nalidixic acid (Lee et al. 2017).

Acinetobacter species possess numerous efflux pumps system which actively removes a broad range of antimicrobial agents thereby preventing them from reaching the target site (Maragakis and Perl 2008). The most commonly expelled antimicrobials by the efflux pump system include tetracyclines, macrolides, and quinolones. The expulsion of the drug from the cell takes place at a high rate; hence, the drug concentrations are not sufficient enough to elicit an antibacterial effect (Santajit and Indrawattana 2016). The efflux system of A. baumannii is often associated with pathogenesis, virulence, and biofilm maturation. Furthermore, the overexpression of these efflux pumps plays a vital role in imparting antibiotic resistance (Ardehali et al. 2019).

The multidrug efflux systems may be categorized into (1) the ATP binding cassette (ABC), (2) major facilitator superfamily (MFS), (3) resistance nodulation division (RND), (4) multidrug and toxic compound extrusion (MATE), (5) SMR family, and (6) the drug/metabolite transporter (DMT) superfamily. However, in the case of A. baumannii, the antimicrobial resistance is generally associated with MFS and RND family (Lee et al. 2011). Efflux pumps of A. baumannii belonging to different family and antimicrobial l substrate are summarized in Table 14.1.

Table 14.1 Efflux pumps of Acinetobacter baumannii belonging to different family and antimicrobial substrate
Full size table

Tet(A) and Tet(B) efflux systems belonging to the MFS confer resistance to tetracycline by exchanging a proton for a tetracycline-cation complex. In a recent study, Sharma et al. (2017) suggested that the AbaF efflux system mediates fosfomycin resistance to A. baumannii (Sharma et al. 2017). The MdfA efflux pumps mediate resistance to ciprofloxacin and chloramphenicol, while CmlA and CraA confer resistance to chloramphenicol (Vila et al. 2007). AmvA confers resistance to antibiotics (erythromycin), detergents (benzalkonium chloride), dyes (acriflavine), and disinfectants (methyl viologen) (Lee et al. 2017). Studies have also found that A. baumannii can actively pump disinfectant, chlorhexidine out of the cell using the Acinetobacter chlorhexidine transporter protein, AceI, thereby protecting the bacteria from external stress (Harding et al. 2018).

The RND-type efflux pump has been documented to impart resistance to aminoglycoside, chloramphenicol and macrolides (erythromycin), quinolones, tetracyclines, trimethoprim, and ethidium bromide (Almasaudi 2018). The AdeABC efflux pump in A. baumannii is also known to expel antimicrobial using proton motive force, thereby reducing the susceptibility of the pathogen towards β-lactams, fluoroquinolones, tetracycline, macrolides, chloramphenicol, and aminoglycosides (Asif et al. 2018). The overexpression of AdeABC also provides significant resistance to carbapenems, tigecycline, netilmicin, and gentamicin (Xu et al. 2019).

AbeM, a multidrug efflux pump of A. baumannii belonging to the MATE family, also utilizes the proton motive force to extrude aminoglycosides, chloramphenicol, fluoroquinolones, ethidium bromide, and trimethoprim out of the bacterial cell (Coyne et al. 2011). AbeS-efflux pump of the SMR family imparts resistance against chloramphenicol, erythromycin, and nalidixic acid (Lee et al. 2017).

14.4.3 Alteration of the Drug Target or Cellular Functions

The alteration in bacterial targets or functions as a result of point mutations decreases the affinity of antimicrobial drugs. In some cases, it may also up-regulate cellular functions such as efflux pumps or change the membrane proteins (Maragakis and Perl 2008). For example, mutations in the subunit of DNA gyrase, gyrA and topoisomerase IV, parC impart resistance against quinolones (Singh et al. 2013).

14.4.4 Biofilm Formation

Biofilms are complex microbial community predominantly attached to either a living or an inert surface. They are often encased by thick polysaccharide matrix constituting of self-produced polysaccharides, proteins, lipids, and extracellular DNA, which protects the biofilm structure from desiccation, immune system clearance, antibiotics, and other external stress (Maragakis and Perl 2008). Hence, it is difficult to eliminate biofilm encased bacterial pathogen using conventional antibiotics. The exceptionally high degree of antibiotic resistance of Acinetobacter and its ability to survive in the hospital setting may be attributed to its biofilm-forming ability (Babapour et al. 2016). A relationship between the biofilm-forming ability and drug resistance in the A. baumannii isolates due to the presence of extended-spectrum β-lactamase (ESBL) blaPER-1 gene has been documented earlier (Badave and Kulkarni 2015).

Greene et al. (2016) provided evidence on the positive correlation between antibiotic resistance and tolerance to desiccation. It was observed that the high biofilm-forming MDR strains of A. baumannii were 50% less likely to die of desiccation as compared to the low biofilm-forming non-MDR strains (Greene et al. 2016). Acinetobacter is frequently isolated from indwelling devices, including cerebrospinal shunts, endotracheal tubes, vascular, and urinary catheters. Such colonization eventually leads to medical devices associated with infections like fever, pneumonia, bacteremia, and meningitis (Babapour et al. 2016). A. baumannii has also been reported to adhere to laryngeal, bronchial, and alveolar epithelial cells of the host (Doi et al. 2015).

Studies have shown the presence of high frequency of exogenous DNA in the genome of A. baumannii indicating the inherent ability of the pathogen to acquire resistance genes via horizontal gene transfer (Lee et al. 2017).

14.5 Resistance to Available Antimicrobial Drugs

The antimicrobial resistance of A. baumannii has progressively increased since the 1970s and in recent decades, it has acquired resistance to the majority of the commonly used antibiotics, thus leaving few choices of antimicrobial agents. Hence, the most serious concern in the management of Acinetobacter associated infection is its acquired MDR (Antunes et al. 2014). Table 14.2 represents the antibiotic resistance mechanisms observed in A. baumannii towards different classes of antibiotics.

Table 14.2 Mechanisms of resistance in A. baumannii towards different antibiotics
Full size table

14.5.1 Resistance to Carbapenems

A. baumannii also possesses AmpC-lactamase (blaADC) and OXA-51 serine-type oxacillinase (blaOXA-51), which are known to naturally impart resistance to β-lactam antibiotics (Pagano et al. 2016). The carbapenemases includes the class D OXA-type enzymes and MBLs which contributes to the carbapenem resistance in A. baumannii (Lolans et al. 2006). Carbapenem resistance in A. baumannii involves either intrinsic or acquired blaOXA-23, blaOXA-24/40, and blaOXA-58-like gene clusters (Singh et al. 2013). The second major mechanism is related to altered porins channels and penicillin-binding proteins. The smaller size and lower number of OMPs in A. baumannii causes a significant reduction in the permeability of the cell membrane to antimicrobial agents (Hsu et al. 2017). Finally, the upregulation of the RND-type efflux system (AdeABC, AdeFGH, and AdeIJK) also plays a considerable part in imparting resistance towards carbapenems (Hsu et al. 2017; Singh et al. 2013).

14.5.2 Resistance to Aminoglycoside

The major mechanism responsible for imparting resistance to A. baumannii towards aminoglycoside is the alteration in the amino or hydroxyl group of the drug by aminoglycoside modifying enzymes such as acetylases, adenylases, methyltransferases, and phosphotransferases (Asif et al. 2018). Other mechanisms include modification of the target ribosomal protein, efflux pump-mediated expulsion, and impaired transport of aminoglycosides like gentamicin, tobramycin, or amikacin into the bacterial cell (Almasaudi 2018).

14.5.3 Resistance to Quinolones

The most common mechanism involved in quinolones resistance is the mutations in the gyrA and parC genes which codes for DNA gyrase and topoisomerase IV. The resulting phenotypic alteration decreases the binding affinity of the quinolones to the enzyme-DNA complex. The reduction in intracellular drug accumulation due to the efflux systems and reduced expression of OMPs involved in drug influx also imparts resistance to quinolones (Doi et al. 2015). Plasmid-encoded genes found in A. baumannii such as qnrA, qnrB, and qnrS have also been identified to protect the DNA by preventing the interaction of quinolones to DNA gyrase and topoisomerase (Asif et al. 2018).

14.5.4 Resistance to Tetracyclines

A. baumannii exhibits two different resistance mechanisms towards tetracyclines. The first mechanism is regulated by transposon-mediated efflux pumps, TetA and TetB. TetA is responsible for the expulsion of tetracycline, while TetB ejects both tetracycline and minocycline out of the bacterial cell. The second mechanism is mediated by ribosomal protection protein encoded by Tet(M) gene. It protects the ribosome from the effect of doxycycline, tetracycline, and minocycline. The AdeABC efflux pump also aids in providing resistance to A. baumannii towards tigecycline (Almasaudi 2018).

14.5.5 Resistance to Cephalosporins

A majority of A. baumannii clinical isolates naturally produce AmpC β-lactamase which provides resistance against cephalosporins (ceftazidime or cefepime). Rezaee et al. (2013) studied the prevalence of various cephalosporin resistance mechanisms in the clinical isolates of A. baumannii. Out of the total 70 isolates screened, 98.5% of the cephalosporin-resistant isolates possess insertions upstream of the ampC gene, of which 69% and 8% were identified to be controlled by ISAba1 and ISAba125, respectively (Rezaee et al. 2013). A. baumannii also produces extended-spectrum β-lactamase (ESBL) which also contributes to cephalosporin resistance (Doi et al. 2015).

14.5.6 Resistance to Polymyxin

The development of colistin (polymyxin E) resistance strains of A. baumannii is a matter of great concern (Almasaudi 2018). Till date, two primary mechanisms for colistin resistance have been recognized in A. baumannii. The first mechanism involves mutations in lipid A biosynthesis genes (lpxA, lpxC, and lpxD) which causes complete loss of lipopolysaccharides (LPS), an initial target of colistin (Cai et al. 2012). The second mechanism involves a mutation in pmrA and pmrB which controls the expression of genes involved in lipid A synthesis (Asif et al. 2018).

14.6 Global Incidence of Drug Resistant Acinetobacter baumannii

The increasing prevalence of antibiotic resistant Acinetobacter spp. in different geographical regions of the globe has been revealed in numerous reports. The association of OXA-58-like and OXA-24-like enzymes to the carbapenem resistance in A. baumannii was documented in 2008 in the Czech Republic. A few years later in 2011, an MDR strain of A. baumannii possessing the genes for NDM-1 and OXA-23 was identified again in the Czech Republic (Senkyrikova et al. 2013). Mesli et al. (2013) documented the first description of autochthonous Acinetobacter spp. in western Algeria with the ability to produce oxacillinases blaOXA-23-like, blaNDM-1-like, and blaOXA-24-like metallo-β-lactamases (Mesli et al. 2013). In another report, Khorsi et al. (2015) highlighted the high prevalence of imipenem resistance in A. baumannii isolated from Algiers hospitals. The antibiotic resistance was found to be mediated predominantly by blaOXA-23-like, blaOXA-24-like, and blaNDM-1-like genes (Khorsi et al. 2015).

Carvalho et al. (2009) reported the transmission of OXA-23 producing MDR clones of A. baumannii in hospitals throughout Rio de Janeiro, Brazil. A total of 110 imipenem-resistant A. baumannii isolates were identified in samples collected from eight hospitals between January 2006 and September 2007. All the isolated strains were MDR with 87.3% producing the carbapenemase OXA-23 (Carvalho et al. 2009). Al-Agamy et al. (2014) reported the high frequency of β-lactamase encoding genes in 40 carbapenem-resistant A. baumannii isolates obtained from two hospitals in Egypt. The carbapenem resistance was mediated by β-lactamase encoding genes, blaOXA-23, blaOXA-24, and blaOXA-58, blaGES, and ISAba1–OXA (Al-Agamy et al. 2014). Agodi et al. (2014) documented the emergence and dissemination of colistin- and carbapenem-resistant strains of A. baumannii in two hospitals in Sicily. The MDR strains were found to possess intrinsic blaOXA-51-like carbapenemase gene and blaOXA-82, which was flanked upstream by ISAba1 (Agodi et al. 2014). Almaghrabi et al. (2018) reported the high frequency (69%) of MDR strains of A. baumannii in Aseer Region of Saudi Arabia. The isolates exhibited remarkable resistance to carbapenems and the drug resistance property was attributed to the presence of class D OXA-type enzymes (OXA-23 and OXA-24/40) (Almaghrabi et al. 2018).

The ever-increasing resistance of A. baumannii towards majority of the currently available antibiotics is a matter of great concern. This MDR pathogen is frequently associated with numerous hospital-associated infections resulting in high morbidity and mortality. Hence, the emergence and dissemination of these MDR strains of A. baumannii emphasize the urgent requirement to enforce infection control measures and develop effective treatment strategies to manage the further emergence and dissemination of these resistant Acinetobacter species.