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In This Topic
Infectious Diseases
Neisseriaceae
Acinetobacter Infections
Diseases Caused by Acinetobacter
Risk factors
Drug resistance
Treatment
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Topics in Neisseriaceae
  • Introduction
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    Acinetobacter Infections

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    Acinetobacter sp can cause suppurative infections in any organ system; these bacteria are often opportunists in hospitalized patients.

    Acinetobacter is ubiquitous and can survive on dry surfaces for up to a month, increasing the likelihood of patients being colonized and medical equipment being contaminated. There are many species of Acinetobacter; all can cause human disease, but A. baumannii (AB) accounts for about 80% of infections.

    Diseases Caused by Acinetobacter

    AB infections typically occur in critically ill, hospitalized patients. Crude death rates associated with AB infection are 19 to 54%.

    The most common site for infection is the respiratory system. Acinetobacter easily colonize tracheostomy sites and can cause community-acquired bronchiolitis and tracheobronchitis in healthy children and tracheobronchitis in immunocompromised adults. Hospital-acquired Acinetobacter pneumonias are frequently multilobar and complicated. Secondary bacteremia and septic shock are associated with a poor prognosis.

    Acinetobacter sp can also cause 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, and pancreatic and liver abscesses.

    The significance of isolates from clinical specimens is difficult to determine because they often represent colonization.

    Risk factors: Risk factors for infection depend on the type of infection (hospital-acquired, community-acquired, multidrug resistant—see Table 1: Neisseriaceae: Risk Factors for Acinetobacter InfectionTables).

    Table 1

    PrintOpen table Open table in new window
    Risk Factors for Acinetobacter Infection

    Type of Infection

    Risk Factors

    Hospital-acquired

    Fecal colonization with Acinetobacter

    ICU stay

    Indwelling devices

    Length of hospital stay

    Mechanical ventilation

    Parenteral nutrition

    Previous infection

    Surgery

    Treatment with broad-spectrum antibiotics

    Wounds

    Community-acquired

    Alcoholism

    Cigarette smoking

    Chronic lung disease

    Diabetes mellitus

    Residence in a tropical developing country

    Multidrug-resistant

    Exposure to colonized or infected patients

    Invasive procedures

    Mechanical ventilation, particularly if prolonged

    Prolonged hospitalization (particularly in the ICU)

    Receipt of blood products

    Use of broad-spectrum antibiotics (eg, 3rd-generation cephalosporins, carbapenems, fluoroquinolones)

    Drug resistance: Recently, multidrug resistant (MDR) AB has emerged. Spread in ICUs has been attributed to colonized health care practitioners, contaminated common equipment, and contaminated parenteral nutrition solutions.

    Treatment

    • 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 toilet 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 can be resistant to ≥ 3 classes of antimicrobials; some isolates are resistant to all. Possible options include a carbapenem (eg, meropenemSome Trade Names
    MERREM
    Click for Drug Monograph
    , imipenem, doripenem), a β-lactam/β-lactamase inhibitor (eg, ampicillin/sulbactamSome Trade Names
    UNASYN
    Click for Drug Monograph
    ), colistin, or a fluoroquinolone plus an aminoglycoside, rifampinSome Trade Names
    RIFADIN
    RIMACTANE
    Click for Drug Monograph
    , or both. Sulbactam (a β-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 has been reported.

    Mild to moderate infections may respond to monotherapy. Traumatic wound infections can be treated with minocyclineSome Trade Names
    MINOCIN
    Click for Drug Monograph
    . Serious infections are treated with combination therapy—typically, imipenem, or a β-lactam/β-lactamase inhibitor plus an aminoglycoside.

    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.

    Last full review/revision September 2009 by Carlene A. Muto, MD, MS

    Content last modified February 2012

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