Acinetobacter are gram-negative aerobic bacilli or coccobacilli that belong to the family Moraxellaceae. They are ubiquitous and can survive on dry surfaces for up to a month and are commonly carried on the skin of health care workers, increasing the likelihood of patients being colonized and medical equipment being contaminated. There are many species of Acinetobacter; all can cause human disease, but Acinetobacter baumannii accounts for about 80% of infections (1 General reference Acinetobacter species are gram-negative organisms that can cause suppurative infections in any organ system; these bacteria are often opportunists in hospitalized patients. Acinetobacter... read more ).
1. Wong D, Nielsen TB, Bonomo RA, et al: Clinical and pathophysiological overview of Acinetobacter infections: A century of challenges. Clin Microbiol Rev 30(1):409–447, 2017. doi: 10.1128/CMR.00058-16
Diseases Caused by Acinetobacter
The most common manifestations of Acinetobacter disease are
AB infections typically occur in critically ill, hospitalized patients. Community-acquired infections (mostly pneumonia) are more common in tropical climates. Case fatality rates associated with A. baumannii (AB) infection are 19 to 54%.
Acinetobacter can cause community-acquired bronchiolitis and tracheobronchitis in healthy children and tracheobronchitis in immunocompromised adults. Acinetobacter easily colonize tracheostomy sites. Hospital-acquired Acinetobacter pneumonias are frequently multilobar and complicated. Secondary bacteremia and septic shock are associated with a poor prognosis.
Acinetobacter species can also cause wound infections and suppurative infections (eg, abscesses) in any organ system, including the lungs, urinary tract, skin, and soft tissues; bacteremia may occur.
Rarely, these organisms cause meningitis (primarily after neurosurgical procedures), cellulitis, or phlebitis in patients with an indwelling venous catheter; ocular infections; native or prosthetic valve endocarditis; osteomyelitis; septic arthritis; or pancreatic and liver abscesses.
The significance of Acinetobacter isolates from clinical specimens, such as respiratory secretions from intubated patients or specimens from open wounds, is difficult to determine because they often represent colonization.
Risk factors for Acinetobacter infection depend on the type of infection (hospital-acquired, community-acquired, multidrug resistant—see table Risk Factors for Acinetobacter Infection Risk Factors for Acinetobacter Infection ).
Drug resistance in Acinetobacter
Recently, multidrug-resistant (MDR) AB has emerged, particularly in intensive care units (ICUs) in immunosuppressed patients, patients with serious underlying disorders, and patients treated with broad-spectrum antibiotics after an invasive procedure. Spread in ICUs has been attributed to colonized health care practitioners, contaminated common equipment, and contaminated parenteral nutrition solutions. Also, the number of multidrug-resistant AB infections has increased in service members who were injured and treated in Iraq, Kuwait, and Afghanistan.
Treatment of Acinetobacter Infections
Typically empiric multidrug therapy for serious infections
In patients with localized cellulitis or phlebitis associated with a foreign body (eg, IV catheter, suture), removal of the foreign body plus local care is usually sufficient. Tracheobronchitis after endotracheal intubation may resolve with pulmonary hygiene alone. Patients with more extensive infections should be treated with antibiotics and with debridement if necessary.
AB has long had intrinsic resistance to many antimicrobials. MDR-AB are defined as strains that are resistant to ≥ 3 classes of antimicrobials; some isolates are resistant to all. Before susceptibility results are available, possible initial options include a carbapenem (eg, meropenem, imipenem), colistin, or a fluoroquinolone plus an aminoglycoside, rifampin, or both. Sulbactam (a beta-lactamase inhibitor) has intrinsic bactericidal activity against many MDR-AB strains. Tigecycline, a glycylcycline antibiotic, is also effective; however, borderline activity and emergence of resistance during therapy have been reported. Minocycline has in vitro activity as does the novel siderophore-cephalosporin antibiotic, cefiderocol (1 Treatment reference Acinetobacter species are gram-negative organisms that can cause suppurative infections in any organ system; these bacteria are often opportunists in hospitalized patients. Acinetobacter... read more ).
Mild to moderate infections may respond to monotherapy. Traumatic wound infections caused by susceptible strains can be treated with minocycline.
Serious AB infections are treated with combination therapy—typically, carbapenems (imipenem or meropenem) or ampicillin/sulbactam plus an aminoglycoside; when drug resistance is extreme, tigecycline, cefiderocol, or the combination of colistin plus minocycline may be the only available options.
To prevent spread, health care practitioners should use contact precautions (hand washing, barrier precautions) and appropriate ventilator care and cleaning for patients colonized or infected with MDR-AB.
1. Munier AL, Biard L, Rousseau C, et al: Incidence, risk factors, and outcome of multidrug-resistant Acinetobacter baumannii acquisition during an outbreak in a burns unit. J Hosp Infect 97(3):226–233, 2017. doi: 10.1016/j.jhin.2017.07.020
A. baumannii (AB) accounts for about 80% of Acinetobacter infections and tends to occur in critically ill, hospitalized patients.
The most common site for infection is the respiratory system, but Acinetobacter species can also cause suppurative infections in any organ system.
Multidrug-resistant AB has become a problem; multidrug treatment chosen based on susceptibility testing may be necessary.
Drugs Mentioned In This Article
|Drug Name||Select Trade|
|Rifadin, Rifadin IV, Rimactane|
|Amzeeq, Arestin, Dynacin, Minocin, minolira, Myrac, Solodyn, Ximino, Zilxi|