Wang SH, Sheng WH, et al. J Hosp Infect 2003;
53:97-102.
Mandell, Douglas, and Bennett's Principles
and Practice of Infectious Diseases -
Mandell 7th ed. Chap 222,
Epidemiology
Acinetobacter differs from other members of
the family Neisseriaceae by the simplicity of its growth requirements. The ability to use a
variety of carbon
sources via diverse metabolic pathways expands its habitat. Related genera (Moraxella, Neisseria, and Kingella) are parasitic in warm-blooded animals, whereas free-living Acinetobacter can be found on animate and inanimate
objects. Almost 100% of soil and water samples yield Acinetobacter. Acinetobacter has been isolated from many sources, including
pasteurized milk, frozen foods, chilled poultry, foundry and hospital air, vaporizer mist,
tap water faucets, peritoneal dialysate baths, bedside urinals, washcloths, angiography catheters, ventilators, laryngoscopes,
duodenoscopes, multidose medication, plasma protein fraction, hospital pillows, and soap dispensers.[11] Acinetobacter may survive on dry inanimate objects for months, comparable to Staphylococcus aureus.[12] Acinetobacter resistance to biocides (e.g., chlorhexidine) becomes a concern when inadvertent biocide dilution, inadequate
biocide exposure time, presence of biologic debris, and/or the presence of a multidrug-resistant (MDR) Acinetobacter is involved.[13,14]
Acinetobacter has been grown from numerous
human sources, including
skin, sputum, urine, feces, and vaginal secretions. Up to 25% of healthy ambulatory adults
exhibit cutaneous colonization,[15] and 7% of adults and infants have transient
pharyngeal colonization.[16] It is the most common gram-negative organism
persistently carried on the skin of hospital personnel,[17] and it has been found to colonize inpatient tracheostomy sites
frequently.
The
prevalence of Acinetobacter clinical isolates varies
somewhat by country
and by specimen site but has generally increased worldwide in the past 2 decades. Data
reported to the Centers for Disease Control and Prevention (CDC) National Nosocomial
Infection Surveillance (NNIS) indicated that Acinetobacter was the cause of 2.4% of intensive care unit (ICU) nosocomial bloodstream
infections, 2.1% of surgical site infections, 1.6% of nosocomial urinary tract infections, and 6.9% (3% in 1975) of nosocomial
pneumonia in sentinel U.S. hospitals in 2003.[18,19] Although constituting the largest increase in
gram-negative pneumonia
since 1975, Acinetobacter remains less frequent than Pseudomonas, Klebsiella, and Enterobacter in that category.
Risk factors
associated with community-acquired Acinetobacter infection
include alcoholism, cigarette smoking, chronic lung disease, diabetes mellitus, and residence
in a tropical developing community.[20] Risk factors specific for nosocomial infection include length of
hospital stay,
surgery, wounds, previous infection (independent of previous antibiotic use),[21] fecal colonization with Acinetobacter,[22] treatment with broad-spectrum antibiotics, indwelling
central intravenous or urinary catheters,[23] admission to a burn unit or ICU, parenteral nutrition, mechanical
ventilation, and breaches in infection control protocols.[21,23]