Acinetobacter, an aerobic, catalase-positive, oxidase-negative, gram-negative coccobacillus, was first described in 1911, but the initial description of the taxonomy of this diverse species was not published until 1986. Ubiquitous in nature, the 54 species of the genus Acinetobacter are associated with a specific ecologic niche that shapes their genomic contents. ( Table 222.1 ) Acinetobacter baumannii is the most virulent species and causes the bulk of human infections, but Acinetobacter pittii , Acinetobacter nosocomialis, Acinetobacter lwoffii, and Acinetobacter radioresistens are also significant nosocomial pathogens. In the late 1980s, A. baumannii emerged as an important human pathogen exhibiting increased antimicrobial resistance. Whole-genome sequencing analysis has suggested that the rapid spread of multidrug-resistant A. baumannii was associated with the ability to incorporate virulence and resistance determinants ( Fig. 222.1 ). The establishment of multidrug-resistant A. baumannii within the health care ecosystem has a tremendous cost, both financially and on patient safety. Among the gram-negative pathogens causing bacteremia, A. baumanii exhibits the highest rate of nonsusceptibility, with over 18% of isolates resistant to all first-line agents, including the carbapenems, β-lactams, and fluoroquinolones. In the United States, over 12,000 Acinetobacter infections are estimated to occur annually, causing over 1300 deaths and costing society $1.6 billion dollars. When compared to other multidrug-resistant gram-negative bacteria and methicillin-resistant Staphylococcus aureus , Acinetobacter infections had the highest risk for mortality at 30 and 90 days after isolation from culture. These statistics, coupled with a paucity of potent antimicrobials in phase II or III of development, emphasize the importance of infection prevention efforts and the need to develop novel therapeutics and vaccines.

TABLE 222.1
Named Acinetobacter Species
Modified from Adewoyin MA, Okoh AI. The natural environment as a reservoir of pathogenic and non-pathogenic Acinetobacter species. Rev Environ Health . 2018;33:265–272.
SPECIES TYPICAL HABITAT
A. albensis Water, soil
A. antitratus Animals
A. antiviralis Plants
A. baumannii Water, soil, humans, animals, food
A. baylyi Water
A. bereziniae Soil, food
A. bohemicus Water, soil
A. bouvetii Water
A. brisouii Soil
A. calcoaceticus Water, soil, humans, animals, food
A. calcoaceticus A. baumannii complex Water, soil
A. gerneri Water
A. grimontii Water
A. guangdongensis Soil
A. guillouiae Food
A. gyllenbergii Food
A. haemolyticus Soil, humans
A. indicus Soil
A. johnsonii Water, soil, humans, animals, food
A. junii Water, soil, humans
A. kookii Soil
A. kyongiensis Water
A. lwoffii Water, soil, humans, animals, food
A. nosocomialis Soil, food
A. oleivorans Plants, soil
A. pakistanensis Water
A. parvus Soil, food
A. pittii Soil, food
A. populi Plants
A. puyangensis Plants
A. qingfengensis Plants
A. radioresistens Soil, animals, food
A. rudis Water
A. schindleri Animals, soil
A. seifertii Food
A. seohaensis Water
A. soli Soil, food
A. tandoii Water, soil
A. tjernbergiae Water
A. towneri Water
A. ursingii Humans, food
A. venetianus Water

FIG. 222.1
Whole-genome phylogeny of 136 sequenced genomes in the genus Acinetobacter.
The phylogeny was inferred with FastTree2 on a single nucleotide polymorphism (SNP) matrix alignment calculated with kSNP and filtered with noisy. The phylogeny was rooted with A. radioresistens. Genomes in the Acinetobacter calcoaceticus - baumannii (Acb) complex are colored by clade.

(From Sahl JW, Gillece JD, Schupp JM, et al. Evolution of a pathogen: a comparative genomics analysis identifies a genetic pathway to pathogenesis in Acinetobacter . PLoS One . 2013;8:e54287.)

Epidemiology

Health Care–Associated Infections

Health care–associated infections represent the most substantial public health impact of Acinetobacter, given the rapid spread of strains resistant to all first-line antimicrobials. The application of molecular typing methods has revealed that a limited number of widespread clonal lineages of A. baumannii are responsible for hospital outbreaks worldwide. Although increasing globally, the prevalence of carbapenem-resistant A. baumannii is decreasing over time in developed countries, suggesting that patients presenting for care after travel from areas with higher endemic rates should be considered for screening. A. baumannii causes the bulk of health care–associated infections due to Acinetobacter, but a variety of species, including A. pittii, A. nosocomialis, A. lwoffii, and Acinetobacter ursingii, are emerging as nosocomial pathogens, especially in immunocompromised hosts. Ventilator-associated pneumonia is the most frequent health care–associated A. baumannii infection, implicated in 3% to 7% of cases. Among patients requiring mechanical ventilation for more than 5 days, the frequency of Acinetobacter increases dramatically, accounting for 26% of respiratory infections in one series. Other nosocomial manifestations of Acinetobacter include bloodstream infections associated with intravascular catheters, surgical site infections, urinary tract infections, meningitis after neurosurgery, and soft tissue infections after burns.

The factors that promote the emergence and transmission of A. baumannii in health care settings include hospitalization of patients at high risk for colonization, such as long-term care residents; breaches in environmental cleaning and disinfection; and antibiotic utilization, especially third-generation cephalosporins, fluoroquinolones, or carbapenems. The ability of Acinetobacter species to survive for weeks on surfaces within the hospital environment leads to prolonged outbreaks, and patient movement between health care facilities without the intervention of adequate communication results in regional spread. Essentially any surface within a patient care area can become contaminated with Acinetobacter and serve as a reservoir for ongoing transmission; these include sinks, faucets, humidifiers, hydrotherapy pools, curtains, pillows, and bedrails, as well as equipment such as supply carts, infusion pumps, and equipment control touch pads. Patients with either recent or remote history of infection can remain colonized and able to contaminate their surrounding environment.

Transmission of Acinetobacter within the health care setting occurs after lapses in proper hand hygiene, and failure to disinfect mobile medical equipment and surfaces within patient care areas. Units with multiple-bedded rooms and susceptible patients, such as neonatal intensive care units (ICUs), are at high risk for outbreaks. Procedures that result in a spray of contaminated fluids, such as pulsatile lavage of wounds or bronchoscopy, may also lead to heavy environmental contamination and transmission. In addition to contaminated surfaces, airborne particles are believed to play a role in transmission of Acinetobacter, either by spread through open units with multiple beds or through contamination of internal air filters of medical equipment. An increase in health care–associated Acinetobacter infections during warmer, more humid months has been reported, potentially due to contamination of air handling systems.

The integration of whole-genome sequencing with epidemiologic data such as patient movement and health care environment exposures is needed to determine transmission routes in an outbreak, and should become the standard. In order to appropriately utilize whole-genome sequencing in an outbreak, an understanding of the endemic strains within a facility is needed.

Community-Associated Infections

Acinetobacter pneumonia is a rare but serious cause of community-acquired pneumonia in tropical regions during the summer months, and often presents with respiratory failure and shock. Community-onset bacteremia is typically associated with respiratory infections, and is also associated with a worse outcome compared with hospital-onset infections. Community-acquired Acinetobacter meningitis in patients without underlying medical compromise has been rarely reported; outcomes in those who received prompt therapy were favorable. A. baumannii skin colonization and invasive soft tissue infections have been associated with warfare, natural disasters, and societal disruptions. The environmental source of these community infections, which typically present in tropical or warm regions, is unknown. In addition to soil, there is an increasing appreciation for the potential role of contaminated food, infected head and body lice, colonized pets or other animals, and hospital wastewater as environmental reservoirs of Acinetobacter.

Diagnosis

Acinetobacter is readily isolated with standard culture media, but differentiation of species based on phenotype alone is difficult, leading to the term Acinetobacter calcoaceticus Acinetobacter baumannii complex. The use of matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry allows rapid identification of Acinetobacter species and of the presence of resistance mechanisms. Once species are identified, a rapidly expanding number of polymerase chain reaction assays are commercially available to identify the presence of β-lactamase and carbapenemase genes. The use of colorimetric assays and quantitative real-time polymerase chain reaction has also been used to detect antimicrobial resistance in A. baumannii. The presence of heteroresistance to carbapenems has been identified in A. baumannii, raising the potential for breakthrough or relapsed infection.

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