Acinetobacter is a genus of Gram-negative bacteria belonging to the wider class of Gammaproteobacteria. Acinetobacter species are oxidase-negative, exhibit twitching motility, [7] and occur in pairs under magnification.
They are important soil organisms, where they contribute to the mineralization of, for example, aromatic compounds. Acinetobacter species are a key source of infection in debilitated patients in the hospital, in particular the species Acinetobacter baumannii .
Species of the genus Acinetobacter are strictly aerobic, nonfermentative, Gram-negative bacilli. They show mostly a coccobacillary morphology on nonselective agar. Rods predominate in fluid media, especially during early growth.[ citation needed ]
The morphology of Acinetobacter species can be quite variable in Gram-stained human clinical specimens, and cannot be used to differentiate Acinetobacter from other common causes of infection.[ citation needed ]
Most strains of Acinetobacter, except some of the A. lwoffii strain, grow well on MacConkey agar (without salt). Although officially classified as not lactose-fermenting, they are often partially lactose-fermenting when grown on MacConkey agar. They are oxidase-negative, catalase-positive, indole-negative, nonmotile, and usually nitrate-negative.[ citation needed ]
Bacteria of the genus Acinetobacter are known to form intracellular inclusions of polyhydroxyalkanoates under certain environmental conditions (e.g. lack of elements such as phosphorus, nitrogen, or oxygen combined with an excessive supply of carbon sources).[ citation needed ]
Acinetobacter is a compound word from scientific Greek [α + κίνητο + βακτηρ(ία)], meaning nonmotile rod. The first element acineto- appears as a somewhat baroque rendering of the Greek morpheme ακίνητο-, commonly transliterated in English is akineto-, but actually stems from the French cinetique and was adopted directly into English.[ citation needed ] Nevertheless, the French word also originates from the Greek privative α + κίνησις (motion) confirming the same origin from a different path.
The genus Acinetobacter comprises 38 validly named species. [8]
Identification of Acinetobacter species is complicated by lack of standard identification techniques. Initially, identification was based on phenotypic characteristics such as growth temperature, colony morphology, growth medium, carbon sources, gelatin hydrolysis, glucose fermentation, among others. This method allowed identification of A. calcoaceticus–A. baumannii complex by the formation of smooth, rounded, mucoid colonies at 37 °C. Closely related species could not be differentiated and individual species such as A. baumannii and Acinetobacter genomic species 3 could not be positively identified phenotypically.[ citation needed ]
Because routine identification in the clinical microbiology laboratory is not yet possible, Acinetobacter isolates are divided and grouped into three main complexes:[ citation needed ]
Different species of bacteria in this genus can be identified using fluorescence-lactose-denitrification to find the amount of acid produced by metabolism of glucose. The other reliable identification test at genus level is chromosomal DNA transformation assay. In this assay, a naturally competent tryptophan auxotrophic mutant of Acinetobacter baylyi (BD4 trpE27) is transformed with the total DNA of a putative Acinetobacter isolate and the transformation mixture is plated on a brain heart infusion agar. The growth is then harvested after incubation for 24 h at 30 °C, plating on an Acinetobacter minimal agar (AMA), and incubating at 30 °C for 108 h. Growth on the AMA indicates a positive transformation assay and confirms the isolate as a member of the genus Acinetobacter. E. coli HB101 and A. calcoaceticus MTCC1921T can be used as the negative and positive controls, respectively. [9]
Some of the molecular methods used in species identification are repetitive extragenic palindromic sequence-based PCR, ribotyping, pulsed field gel electrophoresis (PFGE), random amplified polymorphic DNA, amplified fragment length polymorphism (AFLP), restriction and sequence analysis of tRNA and 16S-23S rRNA gene spacers and amplified 16S ribosomal DNA restriction analysis (ARDRA). PFGE, AFLP, and ARDRA are validated common methods in use today because of their discriminative ability. However, most recent methods include multilocus sequence typing and multilocus PCR and electrospray ionization mass spectrometry, which are based on amplification of highly conserved housekeeping genes and can be used to study the genetic relatedness between different isolates. [10]
Acinetobacter species are widely distributed in nature, and commonly occur in soil and water. [11] Their ability to survive on moist and dry surfaces, as well as to survive exposure to various common disinfectants, allows some Acinetobacter species to survive in a hospital environment. [11] Furthermore, Acinetobacter species can grow at a broad range of temperatures, allowing them to survive in a broad array of environments. [11]
Acinetobacter is frequently isolated in nosocomial infections, and is especially prevalent in intensive care units, where both sporadic cases and epidemic and endemic occurrences are common. A. baumannii is a frequent cause of hospital-acquired pneumonia, especially of late-onset, ventilator-associated pneumonia. It can cause various other infections, including skin and wound infections, bacteremia, and meningitis, but A. lwoffi is mostly responsible for the latter.[ citation needed ]
Of the Acinetobacter, A. baumannii is the greatest cause of human disease, having been implicated in a number of hospital-acquired infections such as bacteremia, urinary tract infections (UTIs), secondary meningitis, infective endocarditis, and wound and burn infections. [12] In particular, A. baumannii is frequently isolated as the cause of hospital-acquired pneumonia among patients admitted to the intensive care unit. Risk factors include long-term intubation and tracheal or lung aspiration. In most cases of ventilator-associated pneumonia, the equipment used for artificial ventilation such as endotracheal tubes or bronchoscopes serve as the source of infection and result in the colonization of the lower respiratory tract by A. baumannii. In some cases, the bacteria can go on to enter the bloodstream, resulting in bacteremia with mortality rates ranging from 32% to 52%. UTIs caused by A. baumannii appear to be associated with continuous catheterization, as well as antibiotic therapy. A. baumannii has also been reported to infect skin and soft tissue in traumatic injuries and postsurgical wounds. A. baumannii commonly infect burns and may result in complications owing to difficulty in treatment and eradication. Though less common, some evidence also links this bacterium to meningitis, most often following invasive surgery, and, in very rare cases, to community-acquired primary meningitis wherein the majority of the victims were children. [13] Case reports also link A. baumannii to endocarditis, keratitis, peritonitis, and very rarely fatal neonatal sepsis. [14]
The clinical significance of A. baumannii is partially due to its capacity to develop resistance against many available antibiotics. Reports indicate that it possesses resistance against broad-spectrum cephalosporins, β-lactam antibiotics, aminoglycosides, and quinolones. Resistance to carbapenems is also being increasingly reported. [15] [16] A. baumannii can survive on the human skin or dry surfaces for weeks and is resistant to a variety of disinfectants, making it particularly easy to spread in a hospital setting. [17] Antibiotic resistance genes are often plasmid-borne, and plasmids present in Acinetobacter strains can be transferred to other pathogenic bacteria by horizontal gene transfer.[ citation needed ]
In healthy individuals, Acinetobacter colonies on the skin correlate with low incidence of allergies; [18] Acinetobacter is thought to be allergy-protective. [19]
Acinetobacter species are innately resistant to many classes of antibiotics, including penicillin, chloramphenicol, and often aminoglycosides. Resistance to fluoroquinolones has been reported during therapy, which has also resulted in increased resistance to other drug classes mediated through active drug efflux. A dramatic increase in antibiotic resistance in Acinetobacter strains has been reported by the Centers for Disease Control and Prevention (CDC), and the carbapenems are recognised as the gold-standard and treatment of last resort. [20] Acinetobacter species are unusual in that they are sensitive to sulbactam, which is commonly used to inhibit bacterial beta-lactamase, but this is an example of the antibacterial property of sulbactam itself. [21] Recently sulbactam-durlobactam, a new antibacterial combination undergoing phase 3 trial, has demonstrated good in vitro activity also against carbapenem-resistant A. baumannii isolates (92% susceptibility). [22]
In November 2004, the CDC reported an increasing number of A. baumannii bloodstream infections in patients at military medical facilities in which service members injured in the Iraq/Kuwait region during Operation Iraqi Freedom and in Afghanistan during Operation Enduring Freedom were treated. [23] Most of these were multidrug-resistant. Among one set of isolates from Walter Reed Army Medical Center, 13 (35%) were susceptible to imipenem only, and two (4%) were resistant to all drugs tested. One antimicrobial agent, colistin (polymyxin E), has been used to treat infections with multidrug-resistant A. baumannii; however, antimicrobial susceptibility testing for colistin was not performed on isolates described in this report. Because A. baumannii can survive on dry surfaces up to 20 days, they pose a high risk of spread and contamination in hospitals, potentially putting immunocompromised and other patients at risk for drug-resistant infections that are often fatal and, in general, expensive to treat. Trials to implement vaccines to prevent Acinetobacter infections were documented. [24] [25]
Reports suggest this bacterium is susceptible to phage therapy. [26]
Gene-silencing antisense oligomers in a form called peptide-conjugated phosphorodiamidate morpholino oligomers have also been reported to inhibit growth in tests carried out in animals infected with antibiotic-resistant A. baumannii. [27] [28]
Sulbactam/durlobactam (Xacduro) was approved for medical use in the United States in May 2023. [29]
The frequency of nosocomial infections in British hospitals prompted the National Health Service to research the effectiveness of anions for air purification, finding that repeated airborne Acinetobacter infections in a ward were eliminated by the installation of a negative air ioniser—the infection rate fell to zero. [30]
Bacterial transformation involves the transfer of DNA from a donor to a recipient bacterium through the intervening liquid medium. Recipient bacteria must first enter a special physiological state termed competence to receive donor DNA. A. calcoaceticus is induced to become competent for natural transformation by dilution of a stationary culture into fresh nutrient medium. [31] Competence is gradually lost during prolonged exponential growth and for a period after entrance into the stationary state. The DNA taken up may be used to repair DNA damage or as a means to exchange genetic information by horizontal gene transfer. [31] Natural transformation in A. calcoaceticus may protect against exposure to DNA-damaging conditions in the natural environment of these bacteria, as appears to be the case for other bacterial species capable of transformation. [32]
Beta-lactamases (β-lactamases) are enzymes produced by bacteria that provide multi-resistance to beta-lactam antibiotics such as penicillins, cephalosporins, cephamycins, monobactams and carbapenems (ertapenem), although carbapenems are relatively resistant to beta-lactamase. Beta-lactamase provides antibiotic resistance by breaking the antibiotics' structure. These antibiotics all have a common element in their molecular structure: a four-atom ring known as a beta-lactam (β-lactam) ring. Through hydrolysis, the enzyme lactamase breaks the β-lactam ring open, deactivating the molecule's antibacterial properties.
Gram-negative bacteria are bacteria that do not retain the crystal violet stain used in the Gram staining method of bacterial differentiation. Their defining characteristic is their cell envelope, which consists of a thin peptidoglycan cell wall sandwiched between an inner (cytoplasmic) membrane and an outer membrane. These bacteria are found in all environments that support life on Earth.
Klebsiella pneumoniae is a Gram-negative, non-motile, encapsulated, lactose-fermenting, facultative anaerobic, rod-shaped bacterium. It appears as a mucoid lactose fermenter on MacConkey agar.
A hospital-acquired infection, also known as a nosocomial infection, is an infection that is acquired in a hospital or other healthcare facility. To emphasize both hospital and nonhospital settings, it is sometimes instead called a healthcare-associated infection. Such an infection can be acquired in a hospital, nursing home, rehabilitation facility, outpatient clinic, diagnostic laboratory or other clinical settings. A number of dynamic processes can bring contamination into operating rooms and other areas within nosocomial settings. Infection is spread to the susceptible patient in the clinical setting by various means. Healthcare staff also spread infection, in addition to contaminated equipment, bed linens, or air droplets. The infection can originate from the outside environment, another infected patient, staff that may be infected, or in some cases, the source of the infection cannot be determined. In some cases the microorganism originates from the patient's own skin microbiota, becoming opportunistic after surgery or other procedures that compromise the protective skin barrier. Though the patient may have contracted the infection from their own skin, the infection is still considered nosocomial since it develops in the health care setting. Nosocomial infection tends to lack evidence that it was present when the patient entered the healthcare setting, thus meaning it was acquired post-admission.
Colistin, also known as polymyxin E, is an antibiotic medication used as a last-resort treatment for multidrug-resistant Gram-negative infections including pneumonia. These may involve bacteria such as Pseudomonas aeruginosa, Klebsiella pneumoniae, or Acinetobacter. It comes in two forms: colistimethate sodium can be injected into a vein, injected into a muscle, or inhaled, and colistin sulfate is mainly applied to the skin or taken by mouth. Colistimethate sodium is a prodrug; it is produced by the reaction of colistin with formaldehyde and sodium bisulfite, which leads to the addition of a sulfomethyl group to the primary amines of colistin. Colistimethate sodium is less toxic than colistin when administered parenterally. In aqueous solutions it undergoes hydrolysis to form a complex mixture of partially sulfomethylated derivatives, as well as colistin. Resistance to colistin began to appear as of 2015.
Multiple drug resistance (MDR), multidrug resistance or multiresistance is antimicrobial resistance shown by a species of microorganism to at least one antimicrobial drug in three or more antimicrobial categories. Antimicrobial categories are classifications of antimicrobial agents based on their mode of action and specific to target organisms. The MDR types most threatening to public health are MDR bacteria that resist multiple antibiotics; other types include MDR viruses, parasites.
Carbapenems are a class of very effective antibiotic agents most commonly used for treatment of severe bacterial infections. This class of antibiotics is usually reserved for known or suspected multidrug-resistant (MDR) bacterial infections. Similar to penicillins and cephalosporins, carbapenems are members of the beta-lactam antibiotics drug class, which kill bacteria by binding to penicillin-binding proteins, thus inhibiting bacterial cell wall synthesis. However, these agents individually exhibit a broader spectrum of activity compared to most cephalosporins and penicillins. Furthermore, carbapenems are typically unaffected by emerging antibiotic resistance, even to other beta-lactams.
Imipenem is a synthetic β-lactam antibiotic belonging to the carbapenems chemical class. developed by Merck scientists Burton Christensen, William Leanza, and Kenneth Wildonger in the mid-1970s. Carbapenems are highly resistant to the β-lactamase enzymes produced by many multiple drug-resistant Gram-negative bacteria, thus playing a key role in the treatment of infections not readily treated with other antibiotics. It is usually administered through intravenous injection.
Acinetobacter baumannii is a typically short, almost round, rod-shaped (coccobacillus) Gram-negative bacterium. It is named after the bacteriologist Paul Baumann. It can be an opportunistic pathogen in humans, affecting people with compromised immune systems, and is becoming increasingly important as a hospital-derived (nosocomial) infection. While other species of the genus Acinetobacter are often found in soil samples, it is almost exclusively isolated from hospital environments. Although occasionally it has been found in environmental soil and water samples, its natural habitat is still not known.
Beta-lactamases are a family of enzymes involved in bacterial resistance to beta-lactam antibiotics. In bacterial resistance to beta-lactam antibiotics, the bacteria have beta-lactamase which degrade the beta-lactam rings, rendering the antibiotic ineffective. However, with beta-lactamase inhibitors, these enzymes on the bacteria are inhibited, thus allowing the antibiotic to take effect. Strategies for combating this form of resistance have included the development of new beta-lactam antibiotics that are more resistant to cleavage and the development of the class of enzyme inhibitors called beta-lactamase inhibitors. Although β-lactamase inhibitors have little antibiotic activity of their own, they prevent bacterial degradation of beta-lactam antibiotics and thus extend the range of bacteria the drugs are effective against.
Pneumococcal infection is an infection caused by the bacterium Streptococcus pneumoniae.
NDM-1 is an enzyme that makes bacteria resistant to a broad range of beta-lactam antibiotics. These include the antibiotics of the carbapenem family, which are a mainstay for the treatment of antibiotic-resistant bacterial infections. The gene for NDM-1 is one member of a large gene family that encodes beta-lactamase enzymes called carbapenemases. Bacteria that produce carbapenemases are often referred to in the news media as "superbugs" because infections caused by them are difficult to treat. Such bacteria are usually sensitive only to polymyxins and tigecycline.
Multidrug resistant Gram-negative bacteria are a type of Gram-negative bacteria with resistance to multiple antibiotics. They can cause bacteria infections that pose a serious and rapidly emerging threat for hospitalized patients and especially patients in intensive care units. Infections caused by MDR strains are correlated with increased morbidity, mortality, and prolonged hospitalization. Thus, not only do these bacteria pose a threat to global public health, but also create a significant burden to healthcare systems.
Carbapenem-resistant Enterobacteriaceae (CRE) or carbapenemase-producing Enterobacteriaceae (CPE) are Gram-negative bacteria that are resistant to the carbapenem class of antibiotics, considered the drugs of last resort for such infections. They are resistant because they produce an enzyme called a carbapenemase that disables the drug molecule. The resistance can vary from moderate to severe. Enterobacteriaceae are common commensals and infectious agents. Experts fear CRE as the new "superbug". The bacteria can kill up to half of patients who get bloodstream infections. Tom Frieden, former head of the Centers for Disease Control and Prevention has referred to CRE as "nightmare bacteria". Examples of enzymes found in certain types of CRE are KPC and NDM. KPC and NDM are enzymes that break down carbapenems and make them ineffective. Both of these enzymes, as well as the enzyme VIM have also been reported in Pseudomonas.
Acinetobacter pittii is a Gram-negative, oxidase-negative, catalase-positive, strictly aerobic, nonmotile, diplococcoid rod bacterium from the genus Acinetobacter. DNA-DNA hybridization studies have been used to identify DNA groups within the genus Acinetobacter and A. pittii belongs to the Acinetobacter calcoaceticus-baumannii complex. The specific epithet pittii is named after the British microbiologist Tyrone Pitt.
ESKAPE is an acronym comprising the scientific names of six highly virulent and antibiotic resistant bacterial pathogens including: Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter spp. The acronym is sometimes extended to ESKAPEE to include Escherichia coli. This group of Gram-positive and Gram-negative bacteria can evade or 'escape' commonly used antibiotics due to their increasing multi-drug resistance (MDR). As a result, throughout the world, they are the major cause of life-threatening nosocomial or hospital-acquired infections in immunocompromised and critically ill patients who are most at risk. P. aeruginosa and S. aureus are some of the most ubiquitous pathogens in biofilms found in healthcare. P. aeruginosa is a Gram-negative, rod-shaped bacterium, commonly found in the gut flora, soil, and water that can be spread directly or indirectly to patients in healthcare settings. The pathogen can also be spread in other locations through contamination, including surfaces, equipment, and hands. The opportunistic pathogen can cause hospitalized patients to have infections in the lungs, blood, urinary tract, and in other body regions after surgery. S. aureus is a Gram-positive, cocci-shaped bacterium, residing in the environment and on the skin and nose of many healthy individuals. The bacterium can cause skin and bone infections, pneumonia, and other types of potentially serious infections if it enters the body. S. aureus has also gained resistance to many antibiotic treatments, making healing difficult. Because of natural and unnatural selective pressures and factors, antibiotic resistance in bacteria usually emerges through genetic mutation or acquires antibiotic-resistant genes (ARGs) through horizontal gene transfer - a genetic exchange process by which antibiotic resistance can spread.
Cefiderocol, sold under the brand name Fetroja among others, is an antibiotic used to treat complicated urinary tract infections when no other options are available. It is indicated for the treatment of multi-drug-resistant Gram-negative bacteria including Pseudomonas aeruginosa. It is given by injection into a vein.
Sulbactam/durlobactam, sold under the brand name Xacduro, is a co-packaged medication used for the treatment of bacterial pneumonia caused by Acinetobacter baumannii-calcoaceticus complex. It contains sulbactam, a beta-lactam antibacterial and beta-lactamase inhibitor; and durlobactam, a beta-lactamase inhibitor.
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