Acinetobacter baumannii- An Overview

Acinetobacter baumannii is a bacterial species that belongs to the genus Acinetobacter, which comprises a group of gram-negative, coccobacillary, aerobic bacteria that are widely distributed in soil and water . The name Acinetobacter derives from the Greek words "akinetos", meaning nonmotile, and "bakterion", meaning small rod . The species baumannii is named after Paul Baumann, a Swiss microbiologist who first described the genus in 1968 .

Acinetobacter baumannii is an opportunistic pathogen that can cause serious infections in humans, especially in those with compromised immune systems or in healthcare settings . It can affect various organs and systems, such as the lungs, bloodstream, urinary tract, and wounds, causing diseases such as pneumonia, bacteremia, urinary tract infection, wound infection, meningitis, and sepsis . It can also colonize the skin, respiratory tract, and gastrointestinal tract of healthy or asymptomatic individuals .

One of the major challenges posed by Acinetobacter baumannii is its remarkable ability to develop resistance to multiple antibiotics, including carbapenems, which are considered the last-resort drugs for treating gram-negative infections . Acinetobacter baumannii can acquire resistance through various mechanisms, such as modifying or inactivating antibiotics, altering or expressing efflux pumps, changing the permeability of the outer membrane, or acquiring resistance genes from other bacteria . As a result, some strains of Acinetobacter baumannii have become resistant to all available antibiotics, making them extremely difficult to treat and control .

Acinetobacter baumannii is one of the ESKAPE pathogens, a group of bacteria that are responsible for most hospital-acquired infections and have the potential to escape the action of antibiotics . The other ESKAPE pathogens are Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Enterobacter species . In addition, Acinetobacter baumannii is one of the critical-priority pathogens on the World Health Organization priority list of antibiotic-resistant bacteria for which new antibiotics are urgently needed .

Acinetobacter baumannii is a relatively new pathogen that emerged in the late 1970s and has since become a global threat to public health . It has been associated with outbreaks in hospitals and intensive care units worldwide, as well as with infections in military personnel and civilians during wars and natural disasters . Its emergence and spread are likely related to its environmental persistence, survival ability under stress conditions, genetic diversity, adaptation to different hosts and niches, and rapid evolution of resistance .

Acinetobacter baumannii is an important cause of morbidity and mortality among infected patients. It has been estimated that Acinetobacter baumannii infections account for 10% of gram-negative hospital-acquired infections and 20% of ventilator-associated pneumonias in intensive care units in Europe and North America . The mortality rate of Acinetobacter baumannii infections ranges from 19% to 54%, depending on the type and site of infection, the severity of illness, the presence of comorbidities, and the availability of effective antibiotics .

The diagnosis of Acinetobacter baumannii infection is based on the isolation and identification of the bacterium from clinical specimens using microbiological methods. However, distinguishing between infection and colonization can be challenging, as Acinetobacter baumannii can be present in various body sites without causing disease. Therefore, clinical criteria such as signs and symptoms of infection, inflammatory markers, radiological findings, and response to treatment should also be considered. Molecular methods such as polymerase chain reaction (PCR) or whole-genome sequencing (WGS) can be used to detect specific genes or variants associated with resistance or virulence in Acinetobacter baumannii isolates.

The treatment of Acinetobacter baumannii infection depends on the susceptibility profile of the isolate and the severity of the disease. Empirical therapy should be initiated promptly after obtaining appropriate specimens for culture and susceptibility testing. Combination therapy with two or more antibiotics from different classes is usually recommended to increase the likelihood of efficacy and to prevent the emergence of resistance. However, the optimal choice and duration of therapy are not well established and should be guided by clinical judgment and local guidelines. In addition to antibiotic therapy, supportive care and infection control measures are essential to improve the outcome and prevent the transmission of Acinetobacter baumannii.

Acinetobacter baumannii is a bacterium that can survive in various environments and adapt to different conditions. It is mainly associated with hospital settings, where it can cause nosocomial infections in patients with compromised immune systems or underlying diseases.

However, the natural habitat of A. baumannii is still unknown. While other species of the genus Acinetobacter are often found in soil and water samples, A. baumannii is rarely isolated from these sources. It has been suggested that human skin could be a reservoir for A. baumannii, as it can colonize the skin and mucous membranes of healthy individuals without causing symptoms.

A. baumannii can also be found in animals, food, and arthropods, but the role of these reservoirs in the transmission and epidemiology of the bacterium is unclear. A. baumannii can infect various sites of the human body, such as the respiratory tract, blood, urinary tract, wounds, central nervous system, skin, and eyes.

A. baumannii is an aerobic and opportunistic pathogen that can survive on inanimate objects for weeks or even months. It has the ability to form biofilms on biotic and abiotic surfaces, which protect it from desiccation, disinfection, and antibiotics. It also has a remarkable capacity to acquire resistance to multiple antimicrobial agents, making it a serious threat to public health.

Acinetobacter baumannii is a gram-negative bacterium that belongs to the family Moraxellaceae. It has a coccobacillus shape, meaning that it is intermediate between a sphere and a rod. The size of the cells varies depending on the growth phase, but they are usually about 1-1.5 micrometers by 1.5-2.5 micrometers .

Acinetobacter baumannii is non-motile, meaning that it does not have flagella or other structures for locomotion. However, it can exhibit twitching or swarming motility on solid surfaces, which may be mediated by type IV pili . These are hair-like appendages that can extend and retract to pull the cells along.

Acinetobacter baumannii is also encapsulated, meaning that it has a layer of polysaccharides surrounding the cell wall. The capsule helps the bacterium to evade the host immune system and to adhere to surfaces . The capsule may also contribute to the formation of biofilms, which are communities of bacteria embedded in a matrix of extracellular substances.

The cell wall of Acinetobacter baumannii contains lipopolysaccharides (LPS), which are complex molecules composed of lipid A, core oligosaccharide, and O-antigen. LPS is an important component of the outer membrane of gram-negative bacteria, and it plays a role in maintaining the integrity and permeability of the membrane. LPS also acts as an endotoxin, triggering inflammatory responses in the host.

The outer membrane of Acinetobacter baumannii also contains various proteins, such as porins and efflux pumps, that are involved in the transport of substances across the membrane. Some of these proteins are associated with antibiotic resistance, as they can prevent the entry or facilitate the exit of antimicrobial agents. One of the most studied outer membrane proteins of Acinetobacter baumannii is OmpA, which has multiple functions in adhesion, invasion, serum resistance, biofilm formation, and immune modulation.

The genome of Acinetobacter baumannii consists of a single circular chromosome and may also include plasmids . The chromosome contains about 3.9 million base pairs and encodes about 3,400 proteins. The plasmids are small circular DNA molecules that can carry genes for antibiotic resistance or other traits. One strain of Acinetobacter baumannii, called AYE, has an 86-kilobase resistance island on its chromosome, called AbaR1, that contains 45 resistance genes. This strain also has three plasmids, but none of them carry resistance markers.

Acinetobacter baumannii is an opportunistic pathogen that can cause various infections in humans, especially in those with compromised immune systems or underlying diseases. The most common infections caused by Acinetobacter baumannii are ventilator-associated pneumonia and bloodstream infections. Other infections include meningitis, endocarditis, skin and soft tissue infections, urinary tract infections, and eye infections. Acinetobacter baumannii is also known for its ability to acquire resistance to multiple antibiotics, making it a serious threat to public health.

Acinetobacter baumannii is characterized by a single circular chromosome that contains about 3.9 to 4.1 million base pairs and about 3,400 to 3,800 protein-coding genes . The genome of A. baumannii is highly variable and prone to horizontal gene transfer, which contributes to its adaptability and antibiotic resistance.

One of the main sources of genetic diversity in A. baumannii is the presence of genomic islands, which are regions of DNA that are acquired from other organisms and integrated into the chromosome. Genomic islands can carry genes for virulence factors, antibiotic resistance, metabolism, or other functions that confer an advantage to the bacterium. One strain of A. baumannii called AYE contains an 86 kb resistance island, called AbaR1, that is made up of 45 resistance genes and is currently the largest island known to date.

Another source of genetic diversity in A. baumannii is the presence of plasmids, which are circular DNA molecules that can replicate independently of the chromosome and can be transferred between bacteria. Plasmids can also carry genes for antibiotic resistance, virulence factors, or other traits that enhance the survival of the bacterium. Some strains of A. baumannii have multiple plasmids, while others have none.

The genome of A. baumannii also contains various mobile genetic elements, such as transposons, insertion sequences, and integrons, which can move within or between DNA molecules and cause mutations or rearrangements. These elements can also mediate the acquisition or dissemination of genes from other bacteria or from genomic islands or plasmids.

The genomics of A. baumannii provides insights into its evolution, pathogenesis, and resistance mechanisms. By comparing the genomes of different strains of A. baumannii, researchers can identify the core genes that are essential for the bacterium, as well as the accessory genes that are variable and may confer specific adaptations or phenotypes. The genome sequence also facilitates the development of molecular diagnostic tools, epidemiological typing methods, and novel therapeutic targets for A. baumannii infections.

Acinetobacter baumannii is a gram-negative, non-fermentative, oxidase-negative, and catalase-positive coccobacillus that belongs to the genus Acinetobacter. It is one of the most clinically significant species of Acinetobacter, causing various types of infections, especially in hospitalized patients. The biochemical characteristics of A. baumannii are useful for its identification and differentiation from other Acinetobacter species and other gram-negative bacteria. Some of the biochemical characteristics of A. baumannii are:

• Glucose utilization: A. baumannii does not ferment glucose, but it can utilize glucose oxidatively in the presence of oxygen. This can be tested by using oxidative-fermentative (OF) medium, which contains glucose and a pH indicator. A. baumannii produces acid from glucose oxidation, turning the medium yellow in the open tube (oxidative), but not in the closed tube (fermentative).
• IMViC test: IMViC stands for indole, methyl red, Voges-Proskauer, and citrate tests, which are used to differentiate members of the family Enterobacteriaceae and other gram-negative rods. A. baumannii gives a negative result for all four tests, which can be represented as - - - +. This means that A. baumannii does not produce indole from tryptophan, does not produce mixed acids from glucose fermentation, does not produce acetoin from glucose fermentation, and does not utilize citrate as a sole carbon source.
• Urease test: Urease is an enzyme that hydrolyzes urea to ammonia and carbon dioxide, raising the pH of the medium. A. baumannii is urease-negative, meaning that it does not produce urease and does not hydrolyze urea. This can be tested by using urea broth or agar, which contain urea and a pH indicator. A positive result is indicated by a color change from yellow to pink or purple, while a negative result is indicated by no color change.
• Nitrate reduction test: Nitrate reduction is a process in which nitrate (NO3-) is reduced to nitrite (NO2-) or further to nitrogen gas (N2) or other nitrogenous compounds by some bacteria. A. baumannii is nitrate-negative, meaning that it does not reduce nitrate to nitrite or other products. This can be tested by using nitrate broth, which contains nitrate and a Durham tube to trap gas. A positive result is indicated by the presence of gas in the Durham tube or a color change from colorless to red after adding reagents that detect nitrite, while a negative result is indicated by no gas production or no color change.
• DNase test: DNase is an enzyme that degrades DNA into smaller fragments. A. baumannii is DNase-negative, meaning that it does not produce DNase and does not degrade DNA. This can be tested by using DNase agar, which contains DNA and a dye that binds to DNA. A positive result is indicated by a clear zone around the bacterial growth due to DNA degradation, while a negative result is indicated by no clear zone.
• TSI test: TSI stands for triple sugar iron test, which is used to differentiate gram-negative enteric bacteria based on their ability to ferment glucose, lactose, and/or sucrose, and to produce hydrogen sulfide (H2S) gas. A. baumannii gives an alkaline/alkaline reaction on TSI agar, meaning that it does not ferment any of the sugars and only produces alkaline products from peptone degradation. This can be observed by a red color on both the slant and the butt of the agar tube. A. baumannii also does not produce H2S gas or gas bubbles on TSI agar.
• Arginine decarboxylase test: Arginine decarboxylase is an enzyme that converts arginine to ornithine and carbon dioxide, lowering the pH of the medium. A. baumannii is arginine-positive, meaning that it produces arginine decarboxylase and converts arginine to ornithine and carbon dioxide. This can be tested by using arginine dihydrolase broth, which contains arginine and a pH indicator. A positive result is indicated by a color change from purple to yellow, while a negative result is indicated by no color change or a color change to blue.

Acinetobacter baumannii is an opportunistic pathogen that can cause severe infections in immunocompromised and critically ill patients. The pathogenesis of A. baumannii infections is mediated by multiple virulence factors that enable the bacterium to evade host immunity, adhere to host cells and tissues, damage host cells and tissues, and acquire essential nutrients. Some of the most important virulence factors of A. baumannii are:

• Outer membrane proteins (OMPs): OMPs are proteins that are embedded in the outer membrane of A. baumannii and play various roles in virulence. For example, OmpA is a major OMP that enhances adhesion to epithelial cells, induces apoptosis of host cells, inhibits complement-mediated killing, and activates dendritic cells. Omp33-36 is another OMP that confers resistance to antimicrobial peptides and contributes to biofilm formation.
• Lipopolysaccharide (LPS): LPS is a complex molecule that consists of a lipid A moiety, a core oligosaccharide, and an O-antigen polysaccharide. LPS is a potent stimulator of the innate immune system and triggers inflammatory responses through the activation of Toll-like receptor 4 (TLR4). LPS also protects A. baumannii from complement-mediated lysis and phagocytosis .
• Capsule: The capsule is a polysaccharide layer that surrounds the cell wall of A. baumannii and provides resistance to desiccation, disinfectants, antibiotics, and phagocytosis. The capsule also facilitates biofilm formation and adherence to abiotic surfaces .
• Phospholipases: Phospholipases are enzymes that hydrolyze phospholipids, which are major components of cell membranes. A. baumannii produces several phospholipases, such as phospholipase C (PlcH), phospholipase D (PlD), and phosphatidylcholine-specific phospholipase C (PC-PLC), that can damage host cell membranes and cause cell lysis, tissue necrosis, and inflammation .
• Outer membrane vesicles (OMVs): OMVs are spherical structures that are released from the outer membrane of A. baumannii and contain various virulence-related proteins, such as proteases, phospholipases, superoxide dismutase, and catalase. OMVs can deliver these proteins to host cells and tissues and cause cytotoxicity, inflammation, oxidative stress, and immune evasion .
• Metal acquisition systems: Metals, such as iron, zinc, copper, and manganese, are essential for bacterial growth and survival. A. baumannii has developed several systems to acquire metals from the host environment, such as siderophores (iron-chelating molecules), metal transporters (proteins that facilitate metal uptake), and metalloproteins (proteins that bind or utilize metals). These systems enable A. baumannii to overcome the host`s nutritional immunity and compete with other microbes for metal resources .
• Protein secretion systems: Protein secretion systems are mechanisms that allow bacteria to export proteins across their membranes or inject them directly into host cells. A. baumannii possesses several protein secretion systems, such as type I secretion system (T1SS), type II secretion system (T2SS), type IV secretion system (T4SS), type VI secretion system (T6SS), and twin-arginine translocation system (TAT). These systems enable A. baumannii to secrete toxins, degradative enzymes, adhesins, biofilm components, and effector proteins that modulate host cell signaling and immunity .

These virulence factors collectively contribute to the pathogenicity of A. baumannii and its ability to cause various types of infections in humans.

Acinetobacter baumannii is an opportunistic pathogen that can cause various infections, especially in hospitalized patients with compromised immunity or underlying diseases. The pathogenesis of A. baumannii involves several steps, such as colonization, adhesion, invasion, evasion of host defenses, and tissue damage .

• Colonization: A. baumannii can colonize different sites of the human body, such as the skin, wounds, respiratory tract, and gastrointestinal tract. It can also survive on environmental surfaces and medical devices for long periods, facilitating its transmission and persistence .
• Adhesion: A. baumannii can adhere to host cells and tissues by using different surface structures and molecules, such as pili, outer membrane proteins (OMPs), lipopolysaccharides (LPS), and biofilms. These factors enhance the bacterial attachment and biofilm formation on biotic and abiotic surfaces, such as epithelial cells, mucosal membranes, catheters, and ventilators .
• Invasion: A. baumannii can invade host cells and tissues by using different mechanisms, such as endocytosis, transcytosis, paracellular translocation, and cell-to-cell spread. These mechanisms allow the bacteria to cross the epithelial and endothelial barriers, reach the bloodstream or the cerebrospinal fluid, and disseminate to different organs .
• Evasion of host defenses: A. baumannii can evade the innate and adaptive immune responses of the host by using different strategies, such as capsule production, LPS modification, OMP variation, secretion of outer membrane vesicles (OMVs), resistance to complement-mediated killing, inhibition of phagocytosis and oxidative burst, induction of apoptosis and immunosuppression of host cells, and modulation of cytokine production .
• Tissue damage: A. baumannii can cause tissue damage and inflammation by using different virulence factors, such as proteases, phospholipases, siderophores, iron acquisition systems, quorum sensing molecules, and OMVs. These factors degrade host cell membranes and extracellular matrix components, disrupt cellular functions and signaling pathways, scavenge essential nutrients from the host, regulate bacterial gene expression and virulence, and deliver toxins and enzymes to host cells .

Acinetobacter baumannii can cause a wide range of infections, especially in hospitalized patients with underlying conditions or devices that facilitate its entry into the body. The most common clinical manifestations are:

• Ventilator-associated pneumonia (VAP): This is the most frequent and severe infection caused by A. baumannii, accounting for up to 40% of cases of VAP in some intensive care units (ICUs) . Patients with A. baumannii VAP typically present with fever, dyspnea, productive cough, chest pain, and radiographic evidence of pulmonary infiltrates. The mortality rate can be as high as 40% .
• Bloodstream infection (BSI): A. baumannii is responsible for 1.5 to 2.4% of nosocomial BSIs, with risk factors such as ICU stay, mechanical ventilation, prior surgery, prior antibiotic use, immunosuppression, trauma, burns, malignancy, central venous catheters, and invasive procedures . Fever may be the only sign of BSI, but septic shock can develop in up to one-third of patients .
• Skin and soft tissue infection (SSTI): A. baumannii can colonize or infect surgical and traumatic wounds, leading to cellulitis, abscesses, necrotizing fasciitis, or osteomyelitis . It can also cause community-acquired or hospital-acquired SSTIs such as folliculitis and impetigo . Traumatic wound infections due to multidrug-resistant (MDR) A. baumannii have been reported in war injuries . Most SSTIs start with a skin break and present with erythema, edema, vesicles, bullae, or ulceration .
• Urinary tract infection (UTI): The urinary tract can be colonized or infected by A. baumannii, especially in patients with indwelling urinary catheters or urinary tract abnormalities . Symptoms of UTI may include dysuria, frequency, urgency, hematuria, flank pain, or fever .
• Meningitis: A. baumannii is a rare cause of nosocomial meningitis, usually associated with neurosurgical procedures, cerebrospinal fluid (CSF) leak, prior antibiotic therapy, or intracranial hemorrhage . The mortality rate can range from 20 to 30%, and neurological sequelae can be severe . Patients with A. baumannii meningitis may present with fever, headache, neck stiffness, altered mental status, or seizures . CSF analysis typically shows pleocytosis with neutrophil predominance, elevated protein level, and low glucose level .
• Other infections: A. baumannii can also cause infection of the eye (such as corneal ulcers or endophthalmitis), the ear (such as otitis media or mastoiditis), the sinuses (such as sinusitis), the peritoneum (such as peritonitis), the heart (such as endocarditis), or the central nervous system (such as brain abscess or ventriculitis) .

The diagnosis of A. baumannii infection is based on the isolation and identification of the organism from a clinical specimen (such as sputum, blood, CSF, urine, wound swab) in the context of compatible clinical features. However, distinguishing between colonization and infection can be challenging, especially in respiratory samples from ventilated patients or wound samples from asymptomatic patients. Therefore, treatment should be reserved for true infections and guided by antimicrobial susceptibility testing whenever possible.

The diagnosis of Acinetobacter baumannii infection is made by the isolation and identification of the bacterium from a patient specimen, such as blood, sputum, urine, cerebrospinal fluid, or wound secretion. However, since Acinetobacter baumannii can also colonize the skin and mucous membranes of healthy individuals, especially in hospital settings, the distinction between colonization and infection is important. Therefore, the laboratory diagnosis should be correlated with the clinical features and risk factors of the patient .

The most common methods for identification of Acinetobacter baumannii are based on phenotypic characteristics, such as morphology, culture, and biochemical reactions. Acinetobacter baumannii is a gram-negative coccobacillus that appears as small, non-lactose fermenting, oxidase-negative colonies on MacConkey agar or blood agar. It can grow aerobically at 37°C and can survive on dry surfaces for long periods. It can utilize glucose oxidatively but not fermentatively and can produce arginine decarboxylase and citrate synthase enzymes. It is also resistant to most antibiotics, including carbapenems .

Some commercial phenotypic systems, such as VITEK 2 (Biomerieux) and API 20 NE (Biomerieux), can also be used to identify Acinetobacter baumannii based on biochemical profiles. However, these systems may have limitations in discriminating between different Acinetobacter species or detecting novel resistance mechanisms .

Molecular methods, such as polymerase chain reaction (PCR), can provide rapid and accurate identification of Acinetobacter baumannii at the species level and also detect specific resistance genes or virulence factors. PCR can amplify target DNA sequences from the 16S rRNA gene, the blaOXA-51-like gene (a marker for Acinetobacter baumannii), or other genes of interest. PCR can also be combined with other techniques, such as restriction fragment length polymorphism (RFLP), pulsed-field gel electrophoresis (PFGE), or multilocus sequence typing (MLST), to provide genotypic characterization and epidemiological typing of Acinetobacter baumannii strains .

Other molecular methods that have been developed or evaluated for the diagnosis of Acinetobacter baumannii include real-time PCR, loop-mediated isothermal amplification (LAMP), fluorescence in situ hybridization (FISH), matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS), and next-generation sequencing (NGS). These methods may offer advantages in terms of speed, sensitivity, specificity, or throughput, but they may also have limitations in terms of cost, availability, standardization, or interpretation .

Acinetobacter baumannii is a gram-negative bacterium that can cause serious infections, especially in hospitalized patients. It has the ability to develop resistance to many antibiotics, making it difficult to treat. The treatment of Acinetobacter baumannii infections depends on the site of infection, the severity of illness, and the susceptibility of the isolate to available antibiotics.

The following are some general principles for the treatment of Acinetobacter baumannii infections:

• Antibiotic therapy should be guided by the results of culture and susceptibility testing whenever possible. Empirical therapy should be based on local epidemiology and resistance patterns, and should be adjusted or de-escalated once the culture results are available .
• Combination therapy with two or more antibiotics may be considered for severe infections, such as bacteremia, pneumonia, or meningitis, especially if the isolate is resistant to carbapenems, which are usually the drugs of choice for Acinetobacter baumannii infections . However, there is limited evidence to support the superiority of combination therapy over monotherapy for Acinetobacter baumannii infections, and the optimal combination regimen is not well established .
• Colistin (polymyxin E) is often used as a last-resort antibiotic for multidrug-resistant or extensively drug-resistant Acinetobacter baumannii infections. However, colistin has significant toxicity, especially nephrotoxicity and neurotoxicity, and should be used with caution and close monitoring . Colistin may be combined with other antibiotics, such as carbapenems, rifampin, tigecycline, or sulbactam, to enhance its efficacy and prevent resistance .
• Tigecycline is another antibiotic that may be used for Acinetobacter baumannii infections, especially when other options are limited. However, tigecycline has poor penetration into the blood and urine, and may not be effective for bacteremia or urinary tract infections. Tigecycline also has a high rate of gastrointestinal adverse effects, such as nausea and vomiting . Tigecycline may be combined with colistin or other antibiotics for severe infections .
• Sulbactam is a beta-lactamase inhibitor that has intrinsic activity against Acinetobacter baumannii. It may be used alone or in combination with other antibiotics for Acinetobacter baumannii infections. However, sulbactam has limited availability and variable susceptibility among different strains of Acinetobacter baumannii .
• Other antibiotics that may be used for Acinetobacter baumannii infections include ampicillin-sulbactam, minocycline, doxycycline, fosfomycin, ceftazidime-avibactam, cefiderocol, plazomicin, and eravacycline. However, these antibiotics have limited data on their efficacy and safety for Acinetobacter baumannii infections, and their use should be based on individual case scenarios and susceptibility testing .

The duration of antibiotic therapy for Acinetobacter baumannii infections depends on the site and severity of infection, the response to treatment, and the presence of complications. In general, a minimum of 7 to 14 days of antibiotic therapy is recommended for most Acinetobacter baumannii infections . Longer courses may be needed for complicated infections, such as endocarditis or osteomyelitis .

In addition to antibiotic therapy, supportive care and source control measures are important for the management of Acinetobacter baumannii infections. Supportive care may include fluid resuscitation, oxygen therapy, mechanical ventilation, hemodynamic support, renal replacement therapy, or other interventions as needed. Source control measures may include drainage of abscesses or infected fluids, removal of foreign bodies or infected devices, debridement of necrotic tissue, or surgical intervention as indicated.

Acinetobacter baumannii infections are challenging to treat due to their high resistance to antibiotics and their association with poor outcomes. Therefore, prevention of infection and transmission is crucial to reduce the burden of this pathogen. Prevention strategies include strict adherence to infection control practices, such as hand hygiene and environmental cleaning; appropriate use of antibiotics; active surveillance and screening; and isolation and contact precautions for colonized or infected patients .

Acinetobacter baumannii is a bacterium that can cause serious infections in healthcare settings, especially among patients who are critically ill or have devices such as ventilators or catheters. Acinetobacter baumannii can survive for long periods of time on environmental surfaces and equipment, and can spread from person to person through contact with contaminated objects or hands. Acinetobacter baumannii can also develop resistance to many antibiotics, making it difficult to treat.

Therefore, prevention of infection is very important to reduce the morbidity and mortality associated with Acinetobacter baumannii. The following are some measures that can help prevent infection:

• Hand hygiene: This is the most basic and effective way to prevent the transmission of Acinetobacter baumannii and other germs. Patients and caregivers should wash their hands with soap and water or use alcohol-based hand sanitizer before and after touching wounds, medical devices, or respiratory secretions. They should also remind healthcare providers and visitors to clean their hands before and after touching the patient or their surroundings .
• Environmental cleaning: Healthcare facilities should ensure that patient rooms and common areas are cleaned and disinfected regularly and thoroughly, using appropriate disinfectants. Special attention should be given to high-touch surfaces and equipment, such as bed rails, tables, monitors, keyboards, stethoscopes, etc .
• Contact precautions: Patients who are infected or colonized with Acinetobacter baumannii should be isolated in single rooms or cohorted with other patients with the same organism. Healthcare providers and visitors should wear gloves and gowns when entering the room and remove them before leaving. They should also avoid sharing equipment or devices with other patients unless they are properly cleaned and disinfected .
• Antibiotic stewardship: Healthcare providers should prescribe antibiotics only when necessary and according to the local guidelines and susceptibility patterns. They should also monitor the response to treatment and adjust the antibiotics as needed. This can help prevent the emergence and spread of antibiotic-resistant strains of Acinetobacter baumannii .
• Active screening: In some settings, such as intensive care units or wards with high prevalence of Acinetobacter baumannii, it may be useful to screen patients for colonization using swabs from different body sites, such as the nose, throat, skin, or wounds. This can help identify patients who need contact precautions and targeted decolonization .
• Decolonization: Patients who are colonized with Acinetobacter baumannii may benefit from topical or systemic agents that can reduce the bacterial load on their skin or mucous membranes. For example, chlorhexidine baths or nasal mupirocin may be used for patients who are colonized in the nose or skin . However, the evidence for the effectiveness of decolonization is limited and more research is needed.

By following these measures, patients, caregivers, and healthcare providers can help prevent the transmission and infection of Acinetobacter baumannii in healthcare settings. This can improve patient outcomes and reduce healthcare costs.

We are Compiling this Section. Thanks for your understanding.