Define Carbapenem-Resistant Acinetobacter baumannii (CRAB)
Carbapenem-resistant Acinetobacter baumannii (CRAB) is a group of A. baumannii that have evolved resistance to the carbapenems.
Acinetobacter is a genus of aerobic, glucose-non fermentative, rod-shaped (specifically Cocco bacilli), gram-negative gamma-proteobacteria in the family Moraxellaceae of the phylum Pseudomonadota.
Define Acinetobacter baumannii?
Define Acinetobacter baumannii a pathogenic species of this genus included in the Acb complex (Acinetobacter calcoaceticus baumannii complex). It is mainly responsible for nosocomial (hospital-acquired) infections. A. baumannii is Gram negative, strictly aerobic, non fermentative, normally nonmotile, oxidase negative, and Cocco bacilli.
It is also known as “Iraqibacter”. Paul Baumann was the first to discover them and the species is named after him.
It is ubiquitous in habitat and is mainly found in soil and water. Because of their ability to form a biofilm, they can survive in an arid habitat such as medical equipment, inanimate surfaces, skin, etc., and infect hospital patients.
Acinetobacter baumannii Morphology
- Pleomorphic (Short Gram-negative cocco-bacilli; bacilli during a lag phase which eventually becomes coccoid or cocco-bacilli at stationary phase)
- 1.0 – 1.5 micron by 1.5 – 2.5 micron during the lag phase
- 0.6 – 0.9 micron by 1.0 – 1.5 micron during the stationary phase
- Lack flagella but contain fimbria.
- Usually, show twitching motility and surface-associated motility
Acinetobacter baumannii Biochemical Characteristics
- Strict aerobes
- Glucose non-fermentative
- Oxidase negative
- IMViC test = -ve, -ve, -ve, +ve (- – – +)
- Urease, Nitrate, and DNase negative
- TSI test = Alkaline / Alkaline, no gas, no H2S
Acinetobacter baumannii Cultural Characteristics
Aerobic incubation with a temperature range from 20 – 44°C; the optimum temperature of 35 (±2)°C.
Non-fastidious in nutrient requirement.
Nutrient Agar, MacConkey Agar, and Blood Agar are commonly used in laboratories.
- Nutrient Agar = 1-3 mm, Circular, Smooth, Non-mucoid, Greyish-White, Opaque colonies.
- MacConkey Agar = 2-3 mm, Circular, Non-lactose fermentative, Opaque colonies.
- Blood Agar = 2-3 mm, Non-hemolytic, Circular, Grey, Opaque colonies.
CHROMAgar Acinetobacter is a selective media; Acinetobacter baumannii produces “red” colonies while other Gram-negative bacteria produce “blue” colonies.
Acinetobacter baumannii Virulence Factors
Currently well studied virulence factors of A. baumannii with their proposed roles are summarized in the table below, namely:
|S.N.||Virulence Factors||Roles in Pathogenesis|
|1.||Pili||Helps in biofilm formation, adherence, and bacterial motility,|
– They are proteins in an outer membrane that regulate bacterial permeability.
– OmpA, Omp 22, Omp 33-36, CarO, and OprD-like are the most important porins.
– OmpA is the most abundant and the most important virulence factor.
|OmpA is responsible for: |
– Inducing apoptosis in epithelial cells
– Adherence and invasionInhibit complement-mediated killing
– Antimicrobial resistance
– Facilitates biofilm formation and motility
– Biogenesis of OMV (outer membrane vesicles)
Omp 33-36 is responsible for:
– Invasion of epithelial cells
– Induces apoptosis
– Confer resistance against Carbapenems
Omp 22 is associated with the production of inflammatory cytokines and chemokines. Other roles are still unclear.
CarO and OprD-like are antigenic and add to virulence, but their exact roles are unclear.
(Capsular Polysaccharides and Lipopolysaccharides)
– Most pathogenic strains are capsulated. Capsules are formed by polysaccharides and lipopolysaccharides (LPS).
|Capsular polysaccharides are responsible for:|
– Facilitates survival in soft tissues of hosts
– Adherence and biofilm formation
– Confer resistance against peptide antibiotics
– Provide resistance against human serum
Capsular LPS are responsible for:
– Induces production of Tumor Necrosis Factor (TNF) and Interleukin 8
– Provide resistance against human serumConfer resistance against Colistin
– It is a lipolytic enzyme that hydrolyzes phospholipids.
– Phospholipase C (PLC) and phospholipase D (PLD) are important virulence factors of A. baumannii.
|PLC and PLD are responsible for:|
– Cytotoxic effect on epithelial cells
– Resistance against human serum
– Cellular invasion
|5.||Outer Membrane Vesicles (OMVs)|
– They are vesicles of 20 – 200 nm secreted by the outer membrane of the bacterium for transportation.
– OMVs of A. baumannii contain several virulence factors like OmpA, PLC, PLD, protease, LPS, etc.
|OMVs are responsible for:|
– Delivery of virulence factors to host cells resulting in cytotoxicity
– Induces innate immune response
– Accumulation of inflammatory cytokines
– Horizontal gene transfer of OXA-24 carbapenemase gene.
|6.||Metal Acquisition System|
A. baumannii has 3 types of metal acquisition systems for fulfilling their need for metal ions for cellular metabolisms.
Iron acquisition system provides iron in the required form to the bacteria. Acinetobactin, NfuA Fe-S scaffold protein, and iron siderophores are produced by A. baumannii to fulfilling the need for iron.
Similarly, Zinc acquisition systems include ZnuABC, ZigA, and ZrlA proteins for meeting the need for zinc. They also provide Zn for the formation of carbapenemase enzymes.
Magnesium acquisition system contains MumC and MumT proteins.
|Iron acquisition system is responsible for:|
– Persistence survival within invaded epithelial and alveolar cells
– Resistance against Reactive Oxygen Species (ROS)
Zinc acquisition system is responsible for:
– Persistence survival within epithelial cells
– Confer resistance against imipenem
Magnesium acquisition system is responsible for:
– Persistence survival within epithelial cells
– Confer resistance against macrophage proteins and Calprotectin
|7.||Protein Secretion System|
It is molecular machinery that helps in the translocation of proteins and nucleic acids.
The secretion system in A. baumannii is of three types; Type II secretory system (T2SS), Type V secretory system (T5SS) and Type VI secretory system (T6SS).
|T2SS and T6SS are responsible for:|
– Secretion of LipA for breaking of lipase
– T6SS also aids in colonization and killing other competing bacteria
– T5SS aids in biofilm formation and adherence
|8.||Penicillin-binding Protein 7/8 and β-Lactamse PER -1|
PBPs are the membrane proteins that synthesize peptidoglycans and protect bacterial cells from the action of β-Lactam antibiotics.
β-Lactamase is a group of enzymes that hydrolyze β- Lactam rings in β-Lactam antibiotics.
However, PBP 7/8 and β-Lactamase PER-1 in A. baumannii act as important virulence factors.
|PBP 7/8 is responsible for:|
– Provide resistance against human serum
– Facilitates survival in soft tissues of the host
β-Lactamse PER-1 is responsible for:
It is a protein that binds to plasminogen and inhibits the complement system.
|CipA is responsible for:|
– Degrade fibrinogen and C3b of complement system which protects the bacteria from human serum.
|10.||Other virulence factors:|
Plasminogen binding protein Tuf
Surface antigen protein 1 (SurA1)
OmpR / EnvZ
Resistance-nodulation-division-type membrane transporter AbeD
Degrade fibrinogen and C3b
Dissemination and serum resistance
Adherence and cytotoxic effect
Acinetobacter baumannii Pathogenesis
Acinetobacter baumannii is an opportunistic pathogen that mainly causes nosocomial infections. They are usually transmitted from inanimate objects in hospital settings, medical equipment and catheters, infected people (patients) and carriers (hospital staff and their hands or materials), and environmental factors such as soil and water. As soon as they come into contact with musical or epithelial cells, they begin infection.
Once bacteria contact an appropriate host surface, they attach using their adhesion factors such as pili, porins, surface proteins, LPS, etc. Once attached to the surface, they express virulence factors to colonize and form a biofilm. The bacterial cells then invade and destroy the cells through cytotoxic effects. They evade host immune responses and induce inflammatory reactions, apoptosis, cytotoxic effects, and invasion and spread into neighboring cells.
The mechanism of pathogenesis and the extent of infection vary depending on the site of infection. Although the exact mechanism is still unclear, several models to study bacterial pathogenesis and the host-pathogen relationship have been established; mammalian model, pneumonia model, sepsis model, non-mammalian model, and in vitro model.
Acinetobacter baumannii Clinical Manifestations
A. baumannii is primarily associated with a hospital-acquired infection, and community-acquired infections are rare. They were considered low-grade pathogens but now it is emerging as the opportunistic pathogen responsible for several systemic as well as superficial infections. The development of resistance to most available antibiotics has made A. baumannii a high-risk pathogen. It is now a member of the ESKAPE group, which includes multidrug-resistant pathogenic bacteria that cause most nosocomial infections.
A. baumannii is commonly associated with the following clinical syndromes:
- Hospital Acquired Pneumonia
Pneumonia is one of the most common A. baumannii infections in hospitalized patients. It is responsible for ventilator-associated pneumonia (VAP) and pneumonia in patients in intensive care units (ICUs). More than 55% of CRAB infections are associated with airway inflammation, particularly pneumonia.
- Blood Stream Infection (BIs) / Bacteremia
A. baumannii is responsible for about 2.5% of nosocomial BIs. A. baumannii bacteremia is a serious infection with a mortality rate of 25 to 54%. Infections are common in ICU patients, postoperative patients, immunocompromised patients, patients with venous catheters, patients with burns, and patients undergoing invasive procedures.
A. baumannii-associated meningitis is rare and is mainly reported in patients undergoing neurosurgical procedures, spinal surgery, and immunocompromised patients.
- Urinary Tract Infections (UTIs)
Urinary tract infections caused by A. baumannii are observed in patients with indwelling catheters and those with prolonged hospitalization. It is rarely seen in patients undergoing nephron and urological surgeries.
- Skin and Wound Infections
Skin and wound infections are a common manifestation of A. baumannii during prolonged hospital stays. Cellulitis, folliculitis, abscess formation, necrotizing fasciitis, rashes and spots and lesions, deep wounds, etc. are common in hospitalized patients with a weak immune system and on antibiotic therapy.
Acinetobacter cholangitis (inflammation of the bile duct system) is a rare disease. It is seen in patients with HIV, recent medical procedures involving areas of the liver and bile ducts, and inflammatory bowel disease.
A. baumannii is associated with catheter-related ventriculitis and ventriculoperitoneal shunt infection. It often occurs with Acinetobacter meningitis, particularly in patients undergoing neurosurgery or catheterization, and is life-threatening.
- Infective – endocarditis
A. baumannii infective endocarditis is a rare but serious and life-threatening infection that occurs primarily in hospitalized patients undergoing invasive procedures.
- Extensive Soft Tissue Necrosis
Skin and soft tissue infections (SSTIs) caused by A. baumannii were considered uncommon but are commonly reported in patients with wounds and surgical procedures.
Sinus infection, ocular infection, peritonitis, corneal ulcer, bone infection, etc., are rarely associated with A. baumannii.
- Carbapenems are the class of beta-lactam antibiotics that inhibit beta-lactamase enzymes, resist their action, and can act against a wide range of bacteria, including beta-lactamase producers. This means they have the broadest spectrum of activity. They are used to treat severe infections or when infected by resistant bacteria, which is why they are also known as ‘antibiotics of last resort.
- They are the first line of treatment for infections caused by resistant bacterial pathogens such as Enterobacteriaceae, A. baumannii, Pseudomonas spp., Streptococcus spp., Mycobacterium tuberculosis complex, Haemophilus influenza, MRSA, Salmonella serovars, etc.
- Molecularly, carbapenems have a β-lactam ring with a carbon atom replacing sulfur at C-1 and introducing a double bond between C-2 and C-3 of the ring. The side chains are in the trans position, unlike the cis position found in other β-lactams. Therefore, carbapenems are resistant to β-lactamase enzymes such as ESBLs and AmpC-β-lactamase. However, they are susceptible to carbapenemases and metallo-β-lactamases.
- They work by binding to the penicillin-binding proteins and inhibiting bacterial cell wall synthesis.
- They are divided into two groups; Group-1 contains the only member “ERTAPENEM” and Group-2 contains “IMIPENEM“, “MEROPENEM” and “DORIPENEM“.
What are Carbapenem-Resistant Organisms (CROs)?
- A large group of pathogenic bacteria whose infections have been treated with carbapenems have now evolved multiple mechanisms to protect themselves from the inhibitory or bactericidal effects of carbapenems. Although initially thought to be highly effective against a broad spectrum of clinically significant Gram-negative bacteria, carbapenem resistance is rapidly emerging worldwide. They are recorded as acute threat organisms that require urgent countermeasures.
- Some of the most serious carbapenem-resistant bacteria are:
- Carbapenem-resistant Enterobacteriaceae (CRE)
- [Carbapenem-resistant Klebsiella pneumoniae is the most important among them]
- Carbapenem-resistant Acinetobacter baumannii (CRAB)
- Carbapenem-resistant Pseudomonas aeruginosa (CRPA)
What is Carbapenem-Resistant Acinetobacter baumannii (CRAB)?
- CRAB is a group of A. baumannii that have evolved resistance to the carbapenems. CRAB has been classified by the WHO as a “Priority 1 – critical pathogen” since 2017. They are responsible for most nosocomial infections caused by Acinetobacter spp. responsible. Few antimicrobials are effective against CRAB. They, therefore, pose very high therapeutic challenges. In addition, they often infect patients on ventilators, intensive care units, and catheterized patients, which increases the severity of the disease.
- These bacteria are genetically engineered to protect themselves against carbapenems. They are structurally modified, engineered virulence factors to confer resistance and engineered enzyme systems to confer resistance to carbapenems.
Mechanisms of Resistance Against Carbapenems by CRAB
A. baumannii is known to have multiple intrinsic and acquired mechanisms to defend itself against carbapenems. Some well-studied mechanisms of resistance to carbapenems are:
- Enzymatic modification of antibiotics
Carbapenem-resistant A. baumannii (CRAB) can produce different types of β-lactamases that hydrolyze the β-lactam ring of carbapenems. Such β-lactamases are referred to as carbapenemases. Carbapenemases can hydrolyze carbapenems, rendering them ineffective against CRAB.
Carbapenemase synthesized by CRAB can be divided into three groups:
- Oxacillinase (OXA β-lactamases)
These are class – D β- lactamases that can hydrolyze oxacillin. Not all, but some types of oxacillinase (OXAs) can hydrolyze carbapenem.
Carbapenem hydrolyzing OXAs are the major enzymes synthesized by CRAB. OXAs synthesized by CRAB can be grouped as:
OXA-23-like, OXA-24/40-like, OXA-51-like, OXA-58-like, and OXA-143-like.
Among them, the OXA-23 enzyme is most frequently found in CRAB.
- Metallo-β-lactamases (MBLs)
These are class-C β-lactamases that contain one or two Zinc ions in their active site and can hydrolyze carbapenems. CRAB is capable of synthesizing different types of MBLs like;
New Delhi metallo-β-lactamases (NDM) group, Verona integron-related metallo-β-lactamase (VIM) group, and Imipenem resistant Pseudomonas (IMP) metallo-β-lactamase group.
NDM-1 is another commonly found carbapenemase in CRAB after OXA-23.
- K. pneumoniae carbapenemase (KPC) β-lactamases
Only a few isolates of CRAB are found to produce KPC β-lactamases, mainly KPC-2 and KPC-3.
2. Modification in membrane permeability
CRAB was found to have modified porin channels. Reduced expression of porins such as Omp22-36, Omp33-36, Omp37, Omp44, Omp47, and CarO is found in CRAB. This reduced expression prevents carbapenem from entering the bacterial cell, thereby conferring resistance to it.
3. Altered penicillin-binding proteins (PBPs)
Modification of antibiotic target sites is an important mechanism employed by many bacteria to evade the lethal effects of any antibiotic. Because carbapenems are β-lactams, any change in their target, PBPs, can protect the bacteria from carbapenems.
CRAB show overexpression of altered PBPs which are found to lower the affinity of “Imipenem”.
4. Efflux pumps
A. baumannii have four efflux pumps that confer antimicrobial resistance; the resistance nodule division superfamily, the multidrug and toxic compound extrusion family, the major mediator superfamily, and the small transporters of the multidrug resistance family.
Among these, the AbeM outflow pump was found to confer resistance to carbapenem, namely “imipenem”, to the extrusion family for multiple drugs and toxic compounds.
It was also recently found that the EmrAB-TolC efflux pump confers resistance to “imipenem” in CRAB.
The adeABC efflux pump is another multidrug resistance transporter that has been found to efflux the carbapenems from the cytoplasm of CRAB.
Epidemiology of Carbapenem-Resistant Acinetobacter baumannii (CRAB)
Most infections from CRAB are hospital-associated, but recently community-acquired cases have also emerged. Cases are increasing rapidly around the world, particularly in Asian regions. A. baumannii-associated nosocomial infections account for about 2-3% in the US and about 20-25% in Asia and the Middle East. Following the listing of CRAB as an urgent priority pathogen, the incidence of CRAB infection is increasing rapidly. Some reports have reported that about 50-70% of the isolated A. baumannii in Asia, Latin America, and the Middle East are CRAB. The prevalence of CRAB among the isolated A. baumannii in America is also around 50%. CRAB is listed as endemic in hospitals. Since 2011, CRAB has spread dramatically in China and Latin America. During the SARS-CoV-2 pandemic, cases of CRAB infection have increased in hospitals around the world.
Identification of Carbapenem-Resistant Acinetobacter baumannii (CRAB)
For identification of CRAB in clinical (or environmental) isolates, the first isolates are identified as A. baumannii using biochemical tests or molecular methods (PCR, gene sequencing, DNA Probe). A biochemical testing algorithm is the most commonly used method.
Biochemical Algorithm For Identification of A. baumannii
- Aerobic, Non-fastidious, Optimum growth at 37°C
- Gram-negative cocco bacilli, Capsulated
- Oxidase –ve, Non-motile
- IMViC = – – – +
- Nitrate and Urease non-reducing
- TSI = R/R, Gas, and H2S –ve
- Glucose and mannitol non-fermentative
- Oxidative utilization of glucose
- Arginine decarboxylase positive
Confirmation of Carbapenem Resistance in A. baumannii (CRAB)
A. Phenotypic Confirmation of CRAB
Phenotypically, CRAB can be confirmed by performing Antimicrobial Sensitivity Test using carbapenems. If the size of the zone of inhibition is less than recommended or in the level of resistance, then we can confirm the isolate to be CRAB.
Zone size interpretative chart for carbapenems against Acinetobacter spp. according to the CLSI is presented below.
Zone Size (in mm)
|Zone Size (in mm)||Zone Size (in mm)|
|Doripenem (DOR 10 mcg)||≥18||15 – 17||≤14|
|Ertapenem (ETP 10 mcg)||Not available||Not available||Not available|
|Imipenem (IMP 10 mcg)||≥22||19 – 21||≤18|
|Meropenem (MRP 10 mcg)||≥18||15 – 17||≤14|
The common methods for phenotypic detection of carbapenemase production in CRAB include:
- Modified Hodge Test
The modified Hodge test is a useful, common, and simplest phenotypic method for detecting carbapenemase production. It requires Mueller Hinton Agar (MHA) and E. coli (ATCC 25922) for testing and sampling of organisms.
The MHA plate is streaked with 0.5 McFarland E. coli solution and a carbapenem disk (10 mcg meropenem or ertapenem) is placed in the center. The test organism is streaked from the edge of the disc to the edge of the plate (up to 4 streaks of the same or different sample for a 10 cm Petri dish).
After an overnight (16-24 h) aerobic incubation at 37 °C, the plate is examined and reported as follows:
Positive carbapenemase production: formation of clover leaf-like pattern due to growth of test organism in streaked lines inside the zone of inhibition of E. coli.
Negative carbapenemase production: no clover leaf-like pattern due to no growth of test organism in streaked lines inside the zone of inhibition of E. coli.
However, due to the low sensitivity and frequent generation of false positives by organisms that produce ESBLs and AmpC beta-lactamase, this method is not currently recommended by CLSI.
2. Carba NP Test
The Carba NP test is another rapid method for detecting carbapenemase production by monitoring the imipenem hydrolytic capacity of the test organism. In this method, a test medium containing imipenem and phenol red indicator is inoculated with the test organism and incubated at 37°C for 2 hours. After incubation, a decrease in pH resulting in a color change of the medium from red to yellow (sometimes orange) is considered positive for carbapenemase production. No color change (retaining red color) indicates no carbapenemase production.
However, it also does not recognize OXA-48-like carbapenemase enzymes.
3. Modified Carbapenem Inactivation Method
The modified carbapenem inactivation method is the most sensitive phenotypic method for carbapenemase detection currently available and in use. For this method, the fresh culture of the test organism in Tryptic Soy Broth is mixed and vortexed to obtain a homogeneous suspension. A 10 μg meropenem disk is placed in the suspension and the suspension is incubated at 37° C. for 2 hours. After incubation, the disk is removed and placed in the center of an MHA plate pre-inoculated with the 0.5% McFarland E. coli ATCC 25922 suspension. The plate is then incubated aerobically at 37°C for 16-24 hours and the size of the zone of inhibition is measured. If the zone is 15 mm, the test is positive for carbapenemase production, and if the zone is 19 mm, the test is negative for carbapenemase production.
B. The use of CHROMAgar Acinetobacter supplemented medium for direct isolation and CRAB identification is also used but is limited due to cost.
C.Molecular Confirmation of CRAB
- PCR is the most widely used tool in laboratories to identify (β-lactamase genes) genes producing carbapenemases and modified porins and efflux pumps.
- Xpert Carba-R molecular test is a common PCR method for detecting carbapenemase production.
- Duplex multiple cross displacement amplification combined with lateral flow biosensor (MCDA-LFB) method is a new and reliable method for quickly identifying CRAB.
- DNA Microarray is another commonly used method.
Prospective Treatment options for Carbapenem-Resistant Acinetobacter baumannii (CRAB) infections
Carbapenems have the broadest antibiotic spectrum and are referred to as “antibiotics of last line”, so treating CRAB infection is a very difficult task. There is a limited treatment option for CRAB infection. Among these limited ones, sulbactam and polymyxins are the strongest. The Infectious Disease Society of America (IDSA) has issued guidelines for the management of CRAB, which include the following treatment options: (Reference: doi: 10.1093/cid/ciab1013.)
- Ampicillin Sulbactam
A high dose of ampicillin sulbactam is the most effective treatment option for CRAB infections. A combination of ampicillin and sulbactam in a ratio of 2:1 is preferred. Sulbactam is a β-lactamase inhibitor and can saturate PBPs1 and 3 at higher doses. A dosage of 27g of Ampicillin Sulbactam is very effective in treating CRAB infection.
Dosage according to ISDA: 3 g every 4 hours or 9 g every 8 hours or 27 g continuous infusions over 24 hours
Alternatively, cefoperazone-sulbactam can be administered.
Polymyxin A and E are effective against CRAB infections. Polymixin E (colistin) is successfully used in CRAB-associated pneumonia, meningitis, and bacteremia. Colistin is instructed to deliver a set amount while maintaining the colistin plasma concentration at 2 mg/L. Colistin is often recommended to be used in combination with other drugs such as ampicillin sulbactam.
Intravenous (IV) minocycline at a dose of 200 mg every 12 hours is successful in treating CRAB infection. It is often used in combination with colistin, rifampin, or carbapenems.
Tigecycline with 200 mg initially given intravenously followed by 100 mg every 12 hours is used to treat pulmonary and systemic infections caused by CRAB. However, resistance is observed in many cases of CRAB infection, so a higher dosage is recommended.
Although not widely used to treat CRAB infection, eravacycline has shown potential sensitivity to CRAB in in vitro studies. 1 mg/kg/every 12 hours is the estimated dosage.
Cefiderocol has shown sensitivity to CRAB with oxacillinase production. Despite its effectiveness, it has shown less potential compared to polymyxins and sulbactam, so it is rarely used. And when used it is always recommended to be used as part of combination therapy at a dosage of 2g every 8 hours infused over 3 hours.
Fosfomycin IV as part of combination therapy has shown sensitivity in pneumonia and UTIs caused by CRAB. However, due to the limited supply of IV fosfomycin, it is rarely used.
A high dose of carbapenems is used against CRAB in combination with ampicillin-sulbactam and either polymyxin or minocycline. However, recent studies have questioned the role of carbapenems, as a similar result is shown when dual therapy with ampicillin-sulbactam and either polymyxin or minocycline is used instead of triple therapy.
In vitro analyzes of rifampin in combination with colistin have shown anti-CRAB activity. However, limited data, toxic effects, negative drug interactions, and no synergistic effect when used with colistin have limited its use in the treatment of CRAB infection.
- Other prospects for the future
Several other forms of treatment are currently being investigated, such as inhalation antibiotics for CRAB-associated pneumonia, phage therapy (using the bacteriophage ØABP-01, Bϕ-C62, and vB_Ab-M-G7), engineered endolysins, gallium nitrate or gallium protoporphyrin IX compounds, Probiotics, immunomodulators, herbal extracts, etc.
Define Carbapenem-Resistant Acinetobacter baumannii (CRAB)