A. baumannii is a notorious cause of nosocomial pneumonia, most frequently among patients requiring prolonged mechanical ventilation. The onset of disease tends to be later than that caused by other gram-negative bacilli; however, clinical symptoms of hospital-acquired or ventilator-associated pneumonia due to A. baumannii are similar to those of nosocomial or ventilator-associated pneumonia due to other nosocomial pathogens. Thus, the most common indicators of infection include fever and increased sputum production. The positivity of respiratory cultures in most cases may present a challenge for the clinician, since airway colonization with A. baumannii is a risk factor for infection itself. Radiologic findings are nonspecific and can include lobar consolidations and pleural effusions, but cavitations are rarely seen. The crude mortality rates associated with nosocomial pneumonia due to A. baumannii are reported to be as high as 65%. However, since these infections occur in debilitated patients, their attributable mortality has been difficult to establish.
Community-acquired pneumonia due to A. baumannii is a relatively rare entity. Its clinical presentation is characterized by fever, severe respiratory symptoms, and multiple-organ dysfunction. Patients frequently have a cough productive of purulent sputum, shortness of breath, and chest pain. Imaging studies usually show lobar consolidation. Mortality rates associated with this process are >50%.
Bloodstream infections due to A. baumannii are most frequent among ICU patients and usually occur in the presence of a central venous catheter or as a secondary complication of hospital-acquired or ventilator-associated pneumonia. Polymicrobial growth has been reported in 20–36% of bacteremia episodes. Fever is the most common sign of infection (developing in >95% of cases), and presentation with septic shock and disseminated intravascular coagulopathy has been described in as many as 25 and 30% of patients, respectively. A. baumannii bloodstream infections often result in higher hospitalization costs and longer ICU stays. Crude mortality rates from this infection are as high as 40%; however, rates can be as high as 70% from infections caused by carbapenem-resistant isolates. In patients with infections caused by extremely drug-resistant strains, poor outcomes are thought to be driven by delays in the initiation of adequate antimicrobial therapy.
Acinetobacter species have been described as part of the skin flora, yet the majority of the organisms from this genus that colonize the skin are not those associated with nosocomial infections. Discerning infection from wound colonization is challenging. Gunshot wounds and the presence of orthopedic external-fixation devices are common among patients with combat trauma–associated A. baumannii skin and soft tissue infections. The report on a case series of eight U.S. military patients described the clinical presentation of their infections as evolving from an edematous peau d’orange appearance to a sandpaper appearance with overlying vesicles and then to a necrotizing process with hemorrhagic bullae. Other case series have also included necrotizing fasciitis. A. baumannii is an important pathogen in burn units worldwide. Large burns provide ideal conditions for A. baumannii and facilitate patient-to-patient transmission. The presence of A. baumannii in wounds contributes to healing delays and graft loss. In addition, wound colonization is a risk factor for bloodstream infections among patients with extensive burn injuries.
A. baumannii infections resulting from trauma to soft tissues in the setting of natural disasters, such as tsunamis and earthquakes, have been reported. The implication is that A. baumannii should be considered in the differential diagnosis of soft tissue infections following exposure to tropical and subtropical environments.
A. baumannii is an infrequent cause of urinary tract infections. The majority of cases reported are catheter-associated infections, reflecting the ability of A. baumannii to form biofilms on these devices. A few reports have described community-acquired infections occurring in the setting of nephrolithiasis and after renal transplantation.
Central nervous system infections with A. baumannii have been reported in the context of outbreaks, traumatic injuries, neurosurgical procedures, and external ventricular drains. One case series described a petechial rash in up to 30% of patients. Acinetobacter species may look similar to Neisseria meningitidis on a Gram’s stain of cerebrospinal fluid; both appear as gram-negative paired cocci.
A few cases of A. baumannii keratitis associated with the use of contact lenses have been reported. Cases of native- and prosthetic-valve endocarditis have also been described.
TREATMENT Acinetobacter Infections
Treatment of Acinetobacter infections is challenging because Acinetobacter can develop resistance to most available antibiotics. Therefore, the choice of empirical therapy should be based on local epidemiology and the patient’s colonization status. Definitive therapy should be determined by antimicrobial susceptibility testing. Antimicrobial options for the management of infections caused by A. baumannii are displayed in Table 157-1.
Acinetobacter species possess intrinsic β-lactamases that inactivate first- and second-generation cephalosporins. Through acquisition of extended-spectrum β-lactamases, the organisms can also become resistant to third- and fourth-generation cephalosporins. Nevertheless, when the isolate is susceptible, β-lactam agents are the drugs of choice for the treatment of A. baumannii. Among β-lactamase inhibitors, sulbactam is active against A. baumannii and is as effective as carbapenems and polymyxins.
Carbapenems have been the preferred drugs for treatment of invasive or hospital-acquired infections. Unfortunately, surveillance data from U.S. hospitals show that up to 50% of A. baumannii isolates recovered from ICUs are carbapenem resistant, and rates of carbapenem resistance are even higher around the world.
Aminoglycosides are of limited utility against A. baumannii because of toxicity and lack of lung penetration. Inhaled formulations of tobramycin have been used with variable success.
Polymyxins are cationic detergents that fell out of use as a result of nephrotoxicity and neurotoxicity. In vitro, they are the most active agents against carbapenem-resistant A. baumannii. Colistin has been used in both intravenous and inhaled formulations, although the optimal dosage has not yet been determined.
Tigecycline is a glycylcycline with clinical activity against A. baumannii. It reaches only low serum concentrations and therefore cannot be used for bloodstream infections. The susceptibility of isolates is variable, especially in outbreak settings, and the emergence of resistance during treatment has been reported.
Minocycline is a tetracycline that has a bacteriostatic effect on A. baumannii. Synergistic and bactericidal activity has been noted when minocycline is used in combination with colistin or a carbapenem.
Fosfomycin is an inhibitor of peptidoglycan synthesis that has no direct activity against A. baumannii but has been observed to be synergistic in vitro in combination with colistin or sulbactam. Clinical data have shown higher rates of microbiologic cure, but no differences in clinical response, with combinations of fosfomycin and colistin.
In vitro data favor combination therapy with colistin in many different regimens containing a carbapenem (imipenem, meropenem), rifampin, minocycline, ceftazidime, azithromycin, doxycycline, trimethoprim-sulfamethoxazole, or ampicillin-sulbactam. However, clinical data have not shown such combination therapy to be superior to colistin alone.