Acinetobacter encapsulated strain in Gram stain of sputum from ICU patient as shown above picture.
Gr. a, not;
Gr. kineô, to set in motion, move;
acinetus, unable to move;
bacter, a rod;
Acinetobacter, nonmotile rod.
baumannii, of Baumann (named in honor of Paul and Linda Baumann)
L .calx –cis, limestone, chalk;
L. acidum aceticum, acetic acid; calcoaceticus, pertaining to calcium acetate, which was used by Beijerinck in the enrichment medium from which he isolated the organism.
Previously……….A. calcoaceticus
At least 33 Genomic species of which few have been given formal species name, e.g.,
The infection has been seen as more common in summer. (McDonald LC, Banerjee SN, Jarvis WR. Seasonal variation of Acinetobacter infections: 1987-1996. Clin Infect Dis 1999;29:1133-7)
A. baumannii forms biofilms with enhanced antibiotic resistance and, more recently, that a chaperone-usher secretion system involved in Pilus assembly affects biofilm formation.
Pneumonia (esp. ventilator-associated)
Septicemia (true Acinetobacter bacteremia should be distinguished from pseudobacteremia).
Meningitis (esp. post-trauma or surgery)
Wound infections (in association with an indwelling venous catheter)
UTIs
Since Operation Iraqi Freedom began in 2003, more than 700 US soldiers have been infected or colonized with Acinetobacter baumannii. A significant number of additional cases have been found in the Canadian and British armed forces and among wounded Iraqi civilians.
Where the Iraqibacter came from remains something of a mystery. Soil samples taken by researchers in Iraq and Kuwait came back negative. However, it was found thriving in the hospitals. When Iraqibacter was compared to MDRAB samples taken in Europe before the war, they were found to be identical (Silberman, 2007). Thus, scientists believe that the current outbreak originated from European sources.
( So MDRAB did exist before the Iraq War.)
β-lactamases,
alterations in cell-wall channels (porins),
efflux pumps
A. baumannii can become resistant to quinolones through mutations in the genes gyrA and parC. Resistant to aminoglycosides by expressing aminoglycoside-modifying enzymes.
Unique browning effect on blood agar in presence of D-Glucose by glucose oxidizing strains
CHROMagar Acinetobacter agar is the latest addition to the clinical range of chromogenic media developed by Dr.Alain Rambach.
TSI – Alk/No change
SIM – H2S Negative, Indole Negative, Motility- Non-motile
Simmon’s Citrate – Citrate Utilized
Carbohydrate breakdown – Oxidative
Most A. baumannii are now resistant to ampicillin, Carbenicillin, Cefotaxime, and Chloramphenicol. Resistance to Gentamycin, tobramycin, and amikacin is increasing. Fluoroquinolones, ceftazidime, Trimethoprim-Sulphmethoxazole, Doxycycline, Polymyxin B, colistin, imipenem, and meropenem may retain activity against Nosocomial Acinetobacter.
Carbapenems (Imipenem and Meropenem) are the mainstay of treatment for antimicrobial-resistant gram-negative infections, though Carbapenems-resistant Acinetobacter is increasingly reported. Resistance to the Carbapenems class of antibiotics makes multidrug-resistant Acinetobacter infections difficult, if not impossible, to treat.
Multidrug-resistant A. baumannii is a common problem in many hospitals in the US and Europe. First-line treatment is with a Carbapenems antibiotic such as imipenem, but carbapenem resistance is increasingly common. Other treatment options include Polymyxin, Tigecycline, and Aminoglycosides.
Colistin and Polymyxin B have been used to treat highly resistant Acinetobacter infections. The choice of appropriate therapy is further complicated by the toxicity of colistin which is mainly renal. Acinetobacter isolates resistant to colistin and Polymyxin B has also been reported.
Acinetobacter can live on the skin and may survive in the environment for several days. Careful attention to infection control procedures such as hand hygiene and environmental cleaning can reduce the risk of transmission.