Acinetobacter baumannii in Saudi Arabia: The New Growing Threat

Ayman Kharaba; Mohamed A Abdelaziz Hussein; Fahad M Al-Hameed; Yasser Mandourah; Ghaleb A Almekhlafi; Haifa Algethamy; Ammar Hamdan; Mohammad Ali Azem; Jehan Fatani; Ali al Beshabshe; Amin Yousif; Hassan Dorsi; Alyaa Al Hazmi; Abdullah Al Motairi; Mohammed Alshahrani; Yaseen M Arabi; The Saudi Critical Care Trial Group

doi:10.4103/2543-1854.259469

REVIEW ARTICLE

Year : 2019 | Volume : 3 | Issue : 1 | Page : 54-57

Acinetobacter baumannii in Saudi Arabia: The New Growing Threat

Ayman Kharaba¹, Mohamed A Abdelaziz Hussein¹, Fahad M Al-Hameed², Yasser Mandourah³, Ghaleb A Almekhlafi³, Haifa Algethamy⁴, Ammar Hamdan⁵, Mohammad Ali Azem⁶, Jehan Fatani⁷, Ali al Beshabshe⁸, Amin Yousif⁹, Hassan Dorsi¹⁰, Alyaa Al Hazmi¹¹, Abdullah Al Motairi¹², Mohammed Alshahrani¹³, Yaseen M Arabi¹⁰, The Saudi Critical Care Trial Group¹⁴
¹ Department of Critical Care, King Fahad Hospital, Al- Madinah Al-Monawarah, Saudi Arabia
² Department of Intensive Care, King Abdullah International Medical Research Center, College of Medicine, King Saud bin Abdulaziz University for Health Sciences, King Abdulaziz Medical City, Jeddah, Saudi Arabia
³ Prince Sultan Military Medical City, Military Medical Services, Ministry of Defense, Riyadh, Saudi Arabia
⁴ King Abdulaziz University, Jeddah, Saudi Arabia
⁵ Department of Critical Care, King Salman Armed Forces Hospital, Tabuk, Saudi Arabia
⁶ Department of Critical Care, King Fahad Specialist Hospital, Dammam, Saudi Arabia
⁷ Department of Critical Care, King Abdullah Medical City, Makkah, Saudi Arabia
⁸ Department of Critical Care, King Khaled University, Abha, Saudi Arabia
⁹ Department of Critical Care, King Fahad Hospital, Jeddah, Saudi Arabia
¹⁰ Department of Intensive Care, King Abdullah International Medical Research Center, College of Medicine, King Abdulaziz Medical City, Riyadh, Saudi Arabia
¹¹ Department of Medicine, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia
¹² Department of Critical Care, King Fahad Medical City, Riyadh, Saudi Arabia
¹³ Department of Critical Care, King Fahad Hospital of the University, Khober, Saudi Arabia

Date of Web Publication

30-May-2019

Correspondence Address:
Ayman Kharaba
Consultant Pulmonary and Critical Care, Chairman of Critical Care Department, King Fahad Hospital, Madinah
Saudi Arabia

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/2543-1854.259469

Abstract

Acinetobacter is a strictly aerobic Gram-negative coccobacillus that is commonly present in hospital environment. It is considered a major healthcare problem worldwide. It can lead to different forms of severe infections, especially in critically ill patients. The prevalence of Acinetobacter infections is increasing in Saudi Arabia ,also the pattern of its antimicrobial susceptibility is changing as. Multidrug resistance and even pandrug resistance is increasing in almost all regions. Infections due to Acinetobacter are associated with high mortality reaching up to 58% in severe bloodstream infection. Additional research on Acinetobacter infections in critically ill patients in Saudi Arabia is needed.

Keywords: Acinetobacter infection, antimicrobial resistance, Saudi Arabia

How to cite this article:
Kharaba A, Abdelaziz Hussein MA, Al-Hameed FM, Mandourah Y, Almekhlafi GA, Algethamy H, Hamdan A, Azem MA, Fatani J, al Beshabshe A, Yousif A, Dorsi H, Al Hazmi A, Al Motairi A, Alshahrani M, Arabi YM, The Saudi Critical Care Trial Group. Acinetobacter baumannii in Saudi Arabia: The New Growing Threat. Saudi Crit Care J 2019;3:54-7

How to cite this URL:
Kharaba A, Abdelaziz Hussein MA, Al-Hameed FM, Mandourah Y, Almekhlafi GA, Algethamy H, Hamdan A, Azem MA, Fatani J, al Beshabshe A, Yousif A, Dorsi H, Al Hazmi A, Al Motairi A, Alshahrani M, Arabi YM, The Saudi Critical Care Trial Group. Acinetobacter baumannii in Saudi Arabia: The New Growing Threat. Saudi Crit Care J [serial online] 2019 [cited 2021 Mar 1];3:54-7. Available from: https://www.sccj-sa.org/text.asp?2019/3/1/54/259469

Introduction

Acinetobacter spp. can cause a variety of serious infections in critically ill patients. These infections include pneumonia, bloodstream, urinary tract, wound infections, and meningitis. Recently, the World Health Organization classified Acinetobacter as priority 1 (critical), highlighting its serious threats to the public health.^[1] The burden of Acinetobacter in the intensive care units (ICUs) in Saudi Arabia is not well known in spite of several studies in different regions of Kingdom that evaluated the prevalence and mode of resistance of Acinetobacter infection in the concerned region.

Microbiology

Acinetobacter is a strictly aerobic Gram-negative coccobacillus with the optimum temperature for most clinical isolates being 33°C –37°C. However, few species can grow at 41°C–44°C. It is commonly present in soil and water as free-living saprophytes.^[2] It is also found as a common commensal of skin, throat, and secretions of healthy people. The genus Acinetobacter has undergone extensive and confusing changes in taxonomic nomenclature over many years, with strains being designated previously as Bacterium anitratum, Herelleavaginicola, Mima polymorpha, Achromobacter, Micrococcus calcoaceticus, Diplococcus, B5W, and Cytophaga.^[3] With new molecular-based taxonomic methods, 34 different named species have been identified.^[4]

Acinetobacter spp. are usually found in diploid formation, or chains of variable length. They are nonmotile, but some strains display a “twitching motility” associated with the presence of polar fimbriae.^[5]Acinetobacter spp. are oxidase negative, indole negative, catalase positive, and nitrate negative. Some strains produce acid from D-glucose, D-ribose, D-xylose, and L-arabinose.^[6] These and other phenotypic characters are incorporated in various commercial identification systems (e.g., API 20NE, VITEK, Phoenix, and MicroScan WalkAway).^[7]

Epidemiology

Members of the genus Acinetobacter are widely distributed in nature and can be isolated from soil and fresh water samples, as well as from humans and animals.^[8] Certain Acinetobacter spp., chiefly Acinetobacter johnsonii, Acinetobacter lwoffii, and Acinetobacter radioresistens, are part of the bacterial flora of the skin, where they are found predominantly in moist skin areas.^[9] In contrast, it is believed that Acinetobacter baumannii is usually isolated from patients and hospital environmental sources, but not outside hospitals.^[10] However, recent surveillances using molecular methods to identify A. baumannii showed that this pathogen has the ability to reside outside hospitals.^[10]

A. baumannii colonizes the skin, oral cavity, respiratory tract, and the intestinal tract.^[9] The infected patients form the primary reservoir of infection; such patients often shed into their surrounding environment a large number of A. baumannii cells, which contaminate the medical equipment and are carried by the hospital staff. Colonization in susceptible patients, carriage by medical staff, prolonged survival in the hospital environment, and resistance to common antibiotics resulted in frequent outbreaks of A. baumannii that is difficult to contain. In addition to indirect contact, airborne transmission and patient-to-patient transmission have also been demonstrated.^[11]

Since its discovery in 1910, Acinetobacter was considered a low-virulent organism, till the 1970s when multidrug-resistant (MDR) Acinetobacter became a widespread organism in the USA.^[12] The change of Acinetobacter to high virulence organism may be related to:

Adhesion to the surface by pili and the subsequent formation of biofilms using biofilm-associated protein.^[13] High biofilm-producing strains are less sensitive to desiccation; this biofilm is reinforced by the outer membrane protein (OMP) A, which is essential for adherence to epithelial cells and induction of cell apoptosis by activating the release of cytochrome c and apoptosis-inducing factor^[13]
Prevention of complement activation by polysaccharide capsule K1, that also delay phagocytosis^[14]
Siderophore-mediated iron acquisition system. Acinetobacter can survive iron-deficient conditions^[15] for long periods of time. This is due to its “acinetobactin,” a catechol siderophore that can sequester iron from the host^[13]
Fimbriae help attach the organism to environmental surfaces. They also help colonize biotic surfaces, such as skin and bronchial epithelial cells.^[16]

Mechanisms of Antimicrobial Resistance

For the past 40 years, strains of A. baumannii have acquired resistance to newly developed antimicrobial drugs, leading to the emergence of MDR strains, which have become prevalent in many hospitals all over the world and has been recently recognized as a leading nosocomial pathogen.^[17]

By 2010, half of A. baumannii in the United States were MDR.^[18] Compared to susceptible strains, outbreaks of the MDR organisms pose a greater threat to healthcare system, causing huge economical cost, morbidity, and mortality.

Acinetobacter spp. is classified as “naturally transformable,” with remarkable capacity for the acquisition of foreign genetic material, especially antibiotic resistance genes.^[19] The major types of gene transfer among A. baumannii are transformation, conjugation, transduction, and mobile genetic elements. In 1969, Juni and Janik discovered a hypertransformable Acinetobacter strain, a strain able to take up DNA from lysed bacterial cells and able to recombine this DNA into its genome, and designated this strain as “A. calcoaceticus.”^[19]

The mechanisms of resistance to antibiotics in A. baumannii are generally classified as follows:

Antimicrobial-inactivating enzymes
Changes in OMPs
Efflux pumps
Changes in Penicillin binding proteins (PBPs).^[20]

For resistance to aminoglycosides, A. baumannii isolates have gene coding for aminoglycoside-modifying enzymes. For resistance to quinolones, alteration in the structure of DNA gyrase or topoisomerase IV through mutations in the quinolones resistance-determining regions of the gyrA and parC genes is the main cause. These changes lead to decrease in the affinity of the quinolones to bind to the enzyme–DNA complex. Having efflux systems is another mechanism of resistance to quinolones that reduce intracellular drug accumulation.^[20] Resistance to carbapenems is by hydrolysis, caused by diverse intrinsic and acquired carbapenem-hydrolyzing β-lactamases (carbapenemases).^[21] For resistance to tetracyclines, two different mechanisms exist. TetA and TetB are specific transposon-mediated efflux pumps; TetB controls the efflux of both tetracycline and minocycline, while TetA is only responsible for the efflux of tetracycline. The second mechanism involves the presence ribosomal protection protein, which protects the ribosome from the effect of tetracycline. This protein is encoded by tet (M) gene; it helps in shielding the ribosome from tetracycline, doxycycline, and minocycline.

Clinical Infections

Infections associated with Acinetobacter spp. include pneumonia, bloodstream infections, skin and soft-tissue infections, wound infections, urinary tract infections, peritonitis, and meningitis. [Table 1] describes the risk factors for developing Acinetobacter infections. There is a seasonal variation in Acinetobacter infections, with highest rates in summer. This may be related to higher temperature and humidity that may promote the growth of Acinetobacter spp.^[25]

Table 1: Risk factors for the development of Acinetobacter infection

Click here to view

Respiratory Tract

In a large series of A. baumannii infections, pneumonias represent 26.7%–47.9% of Acinetobacter infections.^[26] Moreover, pneumonia due to A. baumannii represents 5%–10% of cases of ICU-acquired pneumonia in the USA according to the National Nosocomial infections Surveillance System (NNIS).^[27]Acinetobacter spp. infection accounts for 21.8% of pneumonia in European ICUs.^[28] The mortality is usually high (20%–40%) and is affected by the comorbidities, diseases severity of patients, and the appropriateness of initial antibiotics.^[26]

Bloodstream Infections

A. baumannii ranks 10^th among the most frequent organisms causing nosocomial bloodstream infections in the USA, being responsible for 1.3% of all monomicrobial nosocomial bloodstream infections.^[27]A. baumannii bloodstream infection may be associated with considerable morbidity and overall mortality as high as 58%.^[29]

Community-Acquired Infections

Community-acquired infections such as pneumonia, bacteremia, wound infection, urinary tract infection, otitis media, eye infections, meningitis, and endocarditis have been reported to be caused by Acinetobacter spp., mostly A. baumannii complex. These cases often run a fulminant clinical course with a high incidence of bacteremia and a high mortality rate of 40%–64%.^[23]

The Impact of Acinetobacterinfection in Saudi Arabia

Infections due to Acinetobacter are a major healthcare and economic problem in Saudi Arabia. The prevalence of Acinetobacter is not only increasing in Saudi Arabia, but also the pattern of resistance in almost all regions. A literature review of MDR Gram-negative bacilli (GNB), including Acinetobacter spp., showed a substantial increase in the rate of carbapenem-resistant GNB in Saudi Arabia over the last decade in comparison with the rates of the 1990s.^[21] One study found that 26.5% of ventilator-associated pneumonias in Riyadh, Saudi Arabia, between 2005 and 2009, were caused by Acinetobacter spp. The prevalence of MDR bacteria that caused infections in patients at ICUs of Riyadh Military Hospital, Saudi Arabia, showed that the most common bacterium isolated from intensive care patients was A. baumannii, which represented 40.9% of samples.^[30]Acinetobacter was the most common cause of ventilator-associated pneumonia in King Abdulaziz Medical City in Riyadh from 2003 to 2009, especially in late-onset pneumonia. The prevalence of MDR Acinetobacter increased from 19% in 2006^[31] to 81.5% in 2015, reaching up to 92.1% in another study.^[15]

In El-Qassim region, a study done in 2015 showed the high resistance of Acinetobacter infection to different types of antibiotics,^[32] while in one large study in Jeddah, the MDR A. baumannii was 55% and 67% in 2010 and 2013, respectively.^[33] In the same study, the pandrug-resistant rate increased from 20% to 33%.^[33] Makkah has special concern as it is the city of the largest annual mass gathering all over the world, making it at the highest risk for transmission and dissemination of infectious diseases. Many studies were done over the last 15 years, and all showed high prevalence of MDR. One study in 2015 found that 90% of A. baumannii are resistant to imipenem.^[34] Studies from south and western areas show almost the same results that MRD A. baumannii infection is increasing over the last 10 years.

Conclusions

Infections due to Acinetobacter are common in the ICUs in Saudi Arabia with high multidrug resistance. Saudi Arabia needs a national antimicrobial plan based on large multicenter study involving all regions to compact against the increasing MDR A. baumannii infection.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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