|Organism||First-line therapy||Alternative therapy|
|Acinetobacter||Ampicillin–sulbactam, piperacillin–tazobactam, imipenem–cilastatin, meropenem, ceftazidime, amikacin||Fluoroquinolones, trimethoprim–sulfamethoxazole, minocycline, tigecycline, colistin|
|Achromobacter||Imipenem–cilastatin, meropenem, tigecycline||Piperacillin–tazobactam, ceftazidime, trimethoprim–sulfamethoxazole|
|Alcaligenes||Imipenem–cilastatin, meropenem, trimethoprim–sulfamethoxazole||Amoxicillin–clavulanate, ceftazidime, piperacillin–tazobactam|
|Capnocytophaga canimorsus||Penicillin||Clindamycin, imipenem–cilastatin, ampicillin–sulbactam, amoxicillin–clavulanate|
|Pseudomonas oryzihabitans/luteola||Fluoroquinolones, ceftazidime, piperacillin–tazobactam||Imipenem–cilastin, meropenem, aztreonam, aminoglycosides, trimethoprim–sulfamethoxazole|
|Chromobacterium||Imipenem–cilastin, ciprofloxacin, tigecycline||Tetracycline, trimethoprim–sulfamethoxazole, gentamicin|
|Elizabethkingia meningoseptica||Vancomycin, rifampin, levofloxacin||Tigecycline, trimethoprim–sulfamethoxazole|
|Ochrobactrum anthropi||Imipenem–cilastin||Trimethoprim–sulfamethoxazole, tetracyclines, aminoglycosides, fluoroquinolones|
|Organism||Environmental factors||Host factors||Infection|
|Acinetobacter||Ventilator tubing, resuscitation bags, humidifiers, sinks, mist tents, dialysis bags, angiography and IV catheters, pressure transducers, plasma protein solutions||Severely debilitated, recent surgery, instrumentation||Septicemia, endocarditis, meningitis, pneumonia, UTI, wound infections, abscesses, peritonitis, osteomyelitis, eye infections|
|Achromobacter||Contaminant in disinfectants, diagnostic tracer solution, IV CT contrast, hemodialysis solutions, ventilators, humidifiers, pressure transducers||Severely debilitated, recent neurosurgery||Community-acquired bacteremia, meningitis, chronic otitis media, hospital-acquired meningitis, bacteremia, ventriculitis, endocarditis, endophthalmitis, corneal ulcers, pharyngitis, pneumonia, wound infections, peritonitis, UTI, abscesses|
|Alcaligenes||Dairy products, rotten eggs, hospital equipment||Severely debilitated||Septicemia, native and prosthetic valve endocarditis, meningitis, meibomianitis, chronic purulent otitis, pyelonephritis, hepatitis, appendicitis, diarrhea|
|Capnocytophaga||Normal oral, gastrointestinal, respiratory, and vaginal flora of humans; C. canimorsus in canine oral flora||Severely immunocompromised, children with malignancies, neutropenia, mucositis, asplenia, alcohol abuse||Bacteremia, septicemia, keratitis, conjunctivitis, endophthalmitis, corneal ulcer, endocarditis, pericardial abscess, mediastinitis, lung and subphrenic abscess, empyema, peritonitis, abdominal abscess, septic arthritis, lymphadenitis, juvenile periodontitis|
|Chromobacterium||Enters through the skin or ingestion of contaminated food or water||Neutrophil defects (e.g., chronic granulomatous disease)||Local cellulitis, lymphadenitis, septicemia, osteomyelitis, arthritis, meningitis, ocular infections, and pneumonia|
|Chryseobacterium||Soil, water, use of contaminated fluids in the hospital, nebulizers, flush solutions, pressure transducers, contaminated disinfectants and anesthetics, ice machines, peritoneal dialysis solutions||Neonates, premature infants, adult immunocompromised patients||Neonates: meningitis, hydrocephalus Adults: endocarditis, pneumonia, peritonitis, keratitis, wound infection, meningitis|
|Pseudomonas oryzihabitans/luteola||Soil, water, flushing solutions||Patients with indwelling foreign material, malignancies, immunosuppressive therapy, postsurgical state, history of IVDU, chronic renal failure, bone marrow transplant, cirrhosis||Septicemia, bacteremia, subdural empyema, pneumonia, peritonitis, biliary tract infection, abscesses, wound infection, empyema, line infections, prosthetic joint infections|
Abbreviations: UTI = urinary tract infection; CT = computed tomography; IVDU = intravenous drug use.
Acinetobacter is a member of the family Moraxellaceae, with at least 25 genospecies. Acinetobacter calcoaceticus, Acinetobacter lwoffii, and Acinetobacter baumannii are the species most commonly reported in the clinical literature. Because of problems in phenotypically separating the Acinetobacter species, the term A. calcoaceticus-baumannii complex is sometimes used. Acinetobacter spp. are nonmotile, oxidase-negative, gram-negative coccobacilli often appearing as diplococci and thus are easily confused with Neisseria or Haemophilus spp. They differ from Enterobacteriaceae in that they do not grow anaerobically or reduce nitrates. They are distinguished from Neisseria and Moraxella by their negative oxidase reaction. Virulence factors include a polysaccharide capsule that may prevent phagocytosis and fimbriae that potentiate adherence to epithelial cells.
Acinetobacter spp. are widely distributed in the environment, found in food, soil, water, and sewage. Acinetobacter spp. may be found on inanimate surfaces, including hospital equipment such as ventilator tubing, resuscitation bags, humidifiers, sinks, mist tents, dialysis baths, angiography catheters, pressure transducers, and plasma protein solutions. They are found on the skin of many animal species and humans usually as commensal organisms. They are found as part of the normal oral flora and in the genitourinary and gastrointestinal tracts.
Pathogenesis and clinical syndromes
Acinetobacter baumannii is the most commonly found species in human clinical specimens followed by A. lwoffii. Acinetobacter baumannii is increasingly recognized as one of the most important causes of nosocomial infections and is of particular concern because of its propensity for multidrug resistance. Most infections due to A. baumannii are nosocomial, occurring in severely debilitated patients who have been exposed to broad-spectrum antibiotics in the intensive care unit, mechanical ventilators, and invasive devices (e.g., central venous catheters). In addition, A. baumannii is noted as a cause of serious infections among military personnel returning from the Middle East, often with carbapenem-resistant strains of A. baumannii. A wide variety of human infections due to A. baumannii have been reported, including pneumonia (most often related to endotracheal tubes), septicemia, endocarditis, meningitis, urinary tract infections, wound infections including necrotizing fasciitis, abscesses, peritonitis, osteomyelitis, and eye infections. Purulent pericarditis has been reported in immunosuppressed patients. The most common sites of isolation of A. baumannii are the respiratory and urinary tracts. The mortality can be as high as 40% to 60% in patients with septic shock and up to 30% in patients with ventilator-associated pneumonia, usually associated with underlying disease (e.g., diabetes, malignancy, and renal failure). Acinetobacter spp. play a significant role in the colonization of hospitalized patients, making it difficult to differentiate true infection from colonization.
Acinetobacter baumannii is commonly multidrug resistant due to expression of β-lactamases, altered porin channels and efflux pumps. Treatment is best guided by specific antibiotic testing and sensitivity patterns within each hospital. Acinetobacter lwoffii tends to be more susceptible than the other Acinetobacter spp. Most A. baumannii strains are resistant to penicillin, ampicillin, first-generation cephalosporins, gentamicin, and chloramphenicol and show variable susceptibility to second- and third-generation cephalosporins, trimethoprim–sulfamethoxazole, and tetracyclines. Ampicillin–sulbactam and sulbactam alone have intrinsic bactericidal activity and have been used with good success in susceptible strains. In recent years, many institutions have noted increasing resistance to aminoglycosides and carbapenems among A. baumannii strains. In addition, New-Delhi metallo-β-lactamase (NDM)-producing strains of A. baumanni have also been described. For pan-resistant strains of A. baumannii, colistin (or polymyxin B) and tigecycline either singly or in combination may offer reasonable therapeutic alternatives.
Achromobacter spp. are widely distributed in nature, including soil and water. They may be part of the normal flora of the lower gastrointestinal tract. Achromobacter spp. have been found as contaminants in disinfectants, diagnostic tracer solutions, intravenous computed tomography contrast solutions, hemodialysis solutions, ventilators, humidifiers, and pressure transducers.
The genus Achromobacter consists of a number of species of which two are of clinical relevance: Achromobacter xylosoxidans and Achromobacter denitrificans (previously Alcaligenes denitrificans). These are gram-negative rods that are oxidase positive and grow on MacConkey agar.
Achromobacter spp. have been commonly reported as causative agents in a variety of nosocomial and community-acquired infections. Achromobacter xylosoxidans has been isolated from many types of specimens, including blood, cerebrospinal fluid (CSF), bronchial washings, urine, and wounds. It represents an opportunistic pathogen in immunosuppressed patients and has been reported to cause chronic otitis media, meningitis and ventriculitis after neurosurgical manipulation, bacteremia, endocarditis, endophthalmitis, corneal ulcers, pharyngitis, pneumonia, surgical wound infections, peritonitis and urinary tract infections, and abscesses. Mortality can approach 52% in patients with A. xylosoxidans bacteremia.
Achromobacter xylosoxidans colonizes the respiratory tract of cystic fibrosis patients and is associated with exacerbations of pulmonary symptoms. Antibiotic selection should be guided by susceptibility testing. Imipenem–cilastatin is the most consistently effective agent in vitro against A. xylosoxidans. Trimethoprim–sulfamethoxazole, piperacillin–tazobactam, ticarcillin–clavulanate, fluoroquinolones, and ceftazidime may also be effective. For severe infections, combination therapy may be necessary; however, synergistic activity has not been established. Most strains are resistant to expanded-spectrum cephalosporins (including cefepime) except ceftazidime, and aminoglycosides.