Acinetobacter

Health care-associated infection caused by Acinetobacter has increased in the past decade where this strain has developed multi-drug resistance. In 2006, Acinetobacter was 92% susceptible to tigecycline in the U.S.

Multi-drug-resistant strains are universally susceptible to the polymyxins (colestin, polymyxin B).

Antimicrob Agents Chemother 2004;48:4479. [PMID: 15504889]

Clin Infect Dis 2005;41:848. [PMID: 16107985]

Emerg Infect Dis 2007;13:97. [PMID: 17370521]

Microbiology, pathogenesis, and epidemiology of Acinetobacter infection Author Zeina A Kanafani, MD Souha S Kanj, MD Section Editor Stephen B Calderwood, MD Deputy Editor Elinor L Baron, MD, DTMH

Last literature review for version 16.1: January 31, 2008 |  This topic last updated: July 10, 2007

INTRODUCTION — The genus Acinetobacter consists of ubiquitous gram-negative bacilli that were originally identified in the 1930s [1]. Subsequently, several changes were introduced into the taxonomic classification of Acinetobacter species.

The genus Acinetobacter initially encompassed a heterogeneous collection of non-pigmented, oxidase-positive and oxidase-negative gram-negative rods [2,3]. It currently comprises gram-negative coccobacilli that are non-motile, strictly aerobic, catalase-positive, and oxidase-negative [4].

The microbiology, pathogenesis, and epidemiology of Acinetobacter infection will be reviewed here. The clinical manifestations, treatment, and prevention of these infections are discussed separately. (See "Clinical manifestations and treatment of Acinetobacter infection" and see "General principles of the treatment and prevention of Acinetobacter infection").

MICROBIOLOGY — Over 20 species belonging to the genus Acinetobacter have been identified [5]. Acinetobacter baumannii (genomic species 2) is the species of greatest clinical importance, and is typically associated with outbreaks in the hospital setting [6]. Other species that have been associated with disease in humans belong to the A. calcoaceticus-A. baumannii complex that includes Acinetobacter genomic species 3, A. johnsonii, A. lwoffii, and A. calcoaceticus subsp anitratus [7].

Acinetobacter species appear as short, broad gram-negative rods in the rapid growth phase but assume a more coccobacillary shape in the stationary phase. They are indole-negative and do not ferment glucose or reduce nitrate.

PATHOGENESIS — Acinetobacter has been traditionally classified as an opportunistic pathogen of relatively low pathogenicity [7]. However, the emergence of community-acquired Acinetobacter infections has demonstrated that this organism can be highly virulent with a propensity to cause invasive disease in non-critically ill patients [8-10]. (See "Community-acquired infection" below).

A number of factors contribute to the virulence of Acinetobacter; secreted virulence factors have not been identified [11] :

The organism can survive under dry [12] and iron-deficient conditions [13]. Approximately one-third of strains produce a polysaccharide capsule that works in concert with the cell wall liposaccharide to prevent complement activation [14]. The capsule may also delay phagocytosis. Colonization in the lung is facilitated by the ability of Acinetobacter species to adhere to human bronchial epithelial cells using fimbriae [15]. In addition, colonization of environmental surfaces is promoted by adhesion via pili and the subsequent formation of biofilms [16]. EPIDEMIOLOGY

Environmental reservoirs — A. baumannii is widely distributed in the environment and has been isolated in the following settings:

Soil, fresh water, vegetables, and animals [17,18] Body lice, fleas, and ticks, raising the possibility of a vector-borne mode of transmission in community-acquired infections [19] Asymptomatic skin carriage in up to four percent of residents of tropical climates [20] and asymptomatic nasopharyngeal carriage in as many as 10 percent of non-hospitalized healthcare workers [9]. A. baumannii has also been isolated from a number of sites in the hospital:

Environmental surfaces [21] Equipment including mechanical ventilators, and dialysis machines [22], air ventilation systems [23] , and water sources [24] The hands of healthcare workers [11,25] The respiratory, urinary, and gastrointestinal tracts and wounds of hospitalized patients [26] Contaminated solutions of intrathecal methotrexate [27] Contaminated suctioning equipment in neurosurgical procedures [28] The ability of Acinetobacter to withstand harsh environmental conditions, such as dessication [12], disinfectant solutions [29] , and temperature variations [30] , contributes to its potential for transmissibility through inanimate objects.

A natural reservoir for community-acquired Acinetobacter infection has not been identified [11].

Nosocomial infection — Nosocomial transmission is responsible for the vast majority of Acinetobacter infections [31,32]. Patients at risk are often critically ill with multiple comorbidities, concurrent infections, and on prolonged courses of antibiotics. As a result, it may be difficult to distinguish between colonization and true infection [33]. In addition, colonization is a risk factor for subsequent infection [34].

Although wide variations exist in different countries, there has been a general trend of increasing incidence of Acinetobacter infections. The following observations illustrate the range of findings:

A report from the National Nosocomial Infection Surveillance (NNIS) System in the United States reviewed the most frequent types of hospital-acquired infection in intensive care units (ICUs) that were caused by gram-negative bacilli between 1986 and 2003 [35]. In 2003, Acinetobacter species accounted for 6.9 percent of pneumonia isolates (compared to four percent in 1986), 2.4 percent of bloodstream infection isolates, 2.1 percent of surgical site infection isolates, and 1.6 percent of urinary tract infection isolates. In 12 Latin American medical centers participating in the SENTRY Antimicrobial Surveillance Program between 1997 and 2000, Acinetobacter was the fourth most frequently isolated respiratory pathogen, accounting for 9.6 percent of isolated bacterial species [36]. Higher rates of Acinetobacter as a cause of nosocomial infection (27 to 35 percent of isolates) have been reported in Turkey and India [37,38]. Outbreaks — In addition to sporadic infections, Acinetobacter has the potential of causing outbreaks in the hospital setting [31,39]. Two important factors that contribute to the propensity for outbreaks are antimicrobial resistance and tolerance of dessication [31,40].

Most outbreaks have occurred in adult ICUs [41-44], although other hospital wards that house patients with weakened immunity are also at risk, including intensive care nurseries [45,46] and burn units [47,48]. Both hospital-wide (ie, involving multiple units) [31,40,49-52] and multi-facility outbreaks [29,31] have been described. Transient hand colonization among healthcare workers can contribute to outbreak dissemination [11,25].

The most common manifestations of Acinetobacter outbreak infection have been nosocomial pneumonia (primarily ventilator-associated) followed by bacteremia. When identified, respiratory care equipment has been a common source for the outbreaks [22]. Nosocomial outbreaks of Acinetobacter meningitis have been reported in association with the intrathecal administration of contaminated methotrexate [53] and with contaminated suctioning equipment in a neurosurgical unit [54]. (See "Clinical manifestations and treatment of Acinetobacter infection").

Risk factors — A variety of risk factors have been identified that predispose to nosocomial infection with Acinetobacter. These include [31] :

Host-specific factors, such as a high APACHE II score, prematurity, and colonization with Acinetobacter. Treatment-related factors, such as mechanical ventilation, ICU admission, surgery, indwelling catheters, length of hospital stay, and broad-spectrum antimicrobial therapy. Prior use of either imipenem, which is considered a drug of choice for the treatment of Acinetobacter infections, or a fluoroquinolone may increase the risk of infection or colonization with Acinetobacter [40,44]. Acinetobacter nosocomial infections have a seasonal predilection, with more occurring during the warm summer months [55-58].

Community-acquired infection — Although still relatively rare, Acinetobacter has been increasingly recognized as a pathogen associated with high morbidity and mortality in the community setting. Pneumonia is the most commonly reported community-acquired Acinetobacter infection [8,9,59]. Affected patients typically have other comorbidities, including alcohol abuse, chronic obstructive pulmonary disease, diabetes mellitus, and smoking [59,60]. (See "Clinical manifestations and treatment of Acinetobacter infection", section on Pneumonia).

Nasopharyngeal carriage may be a predisposing factor in non-hospitalized alcohol abusers, being found in 10 percent in a study from tropical northern Australia [9]. In this report, there was a seasonal pattern of community-acquired Acinetobacter pneumonia, with infection being more common in the wet (monsoon) season.

Acinetobacter can also cause community-acquired bloodstream infections, particularly in patients with underlying malignancies, either as a primary infection or in the setting of bacteremic pneumonia [9,10].

Infection in military personnel — Since the beginning of the military operations in Afghanistan in 2001 and Iraq in 2003, there has been a dramatic increase in the incidence of Acinetobacter infections among soldiers admitted to military medical facilities in Germany, the United Kingdom, and the United States [61-64].

From January 2002 to August 2004, 102 patients with Acinetobacter bloodstream infections were reported to the Centers for Disease Control and Prevention (CDC) from medical centers treating soldiers injured in Afghanistan and Iraq [61]. The majority of patients had sustained traumatic wound injuries and subsequently developed Acinetobacter bacteremia. In another report, 30 soldiers returning from active-duty in Afghanistan and Iraq were diagnosed with Acinetobacter infections (mostly osteomyelitis or wound infection) at a tertiary military medical center in the United States [62].

The Acinetobacter strains incriminated in these clusters of infection belonged to the A. calcoaceticus-baumannii complex and were characterized by multidrug resistance [61-64]. Although most infections were classified as nosocomial in origin, a common source has not been identified. Environmental contamination of war wounds at the time of injury or during evacuation from the field has been suggested but not proven.

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