Acinetobacter baumannii is a typically short, almost round, rod-shaped (coccobacillus) Gram-negative bacterium. It can be an opportunistic pathogen in humans, affecting people with compromised immune systems, and is becoming increasingly important as a hospital-derived (nosocomial) infection. While other species of the genus Acinetobacter are often found in soil samples (leading to the common misconception that A. baumannii is a soil organism, too), it is almost exclusively isolated from hospital environments. Although occasionally it has been found in environmental soil and water samples, its natural habitat is still not known.
Bacteria of this genus lack flagella, whip-like structures many bacteria use for locomotion, but exhibit twitching or swarming motility. This may be due to the activity of type IV pili, pole-like structures that can be extended and retracted. Motility in A. baumannii may also be due to the excretion of exopolysaccharide, creating a film of high-molecular-weight sugar chains behind the bacterium to move forward. Clinical microbiologists typically differentiate members of the Acinetobacter genus from other Moraxellaceae by performing an oxidase test, as Acinetobacter spp. are the only members of the Moraxellaceae to lack cytochrome c oxidases.
A. baumannii is part of the ACB complex (A. baumannii, A. calcoaceticus, and Acinetobacter genomic species 13TU). Members of the ACB complex are difficult to determine the specific species and comprise the most clinically relevant members of the genus. A. baumannii has also been identified as an ESKAPE pathogen (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species), a group of pathogens with a high rate of antibiotic resistance that are responsible for the majority of nosocomial infections.
Colloquially, A. baumannii is referred to as 'Iraqibacter' due to its seemingly sudden emergence in military treatment facilities during the Iraq War. It has continued to be an issue for veterans and soldiers who served in Iraq and Afghanistan. Multidrug-resistant A. baumannii has spread to civilian hospitals in part due to the transport of infected soldiers through multiple medical facilities. Due to the prevalence of infections and outbreaks caused by multidrug-resistant A. baumannii, few antibiotics are effective for treating infections caused by this pathogen. To overcome this problem, knowledge of the pathogenesis, antibiotic resistance mechanisms, and prospective treatment options of A. baumannii is important.
Virulence factors and determinants
Many microbes, including A. baumannii, have several properties that allow them to be more successful as pathogens. These properties may be virulence factors such as toxins or toxin delivery systems which directly affect the host cell. They may also be virulence determinants, which are qualities contributing to a microbe's fitness and allow it to survive the host environment, but that do not affect the host directly. These characteristics are just some of the known factors which make Acinetobacter baumannii effective as a pathogen:
Many virulent bacteria possess the ability to generate a protective capsule around each individual cell. This capsule, made of long chains of sugars, provides an extra physical barrier between antibiotics, antibodies, and complement. The association of increased virulence with presence of a capsule was classically demonstrated in Griffith's experiment. A gene cluster responsible for secretion of the polysaccharide capsule has been identified and shown to inhibit the antibiotic effect of complement when grown on ascites fluid. A decrease in killing associated with loss of capsule production was then demonstrated using a rat virulence model.
Adhesion can be a critical determinant of virulence for bacteria. The ability to attach to host cells allows bacteria to interact with them in various ways, whether by type III secretion system or simply by holding on against the prevailing movement of fluids. Outer membrane protein A has been shown to be involved in the adherence of A. baumannii to epithelial cells. This allows the bacteria to invade the cells through the zipper mechanism. The protein was also shown to localize to the mitochondria of epithelial cells and cause necrosis by stimulating the production of reactive oxygen species.
AbaR resistance islands
Pathogenicity islands, relatively common genetic structures in bacterial pathogens, are composed of two or more adjacent genes that increase a pathogen's virulence. They may contain genes that encode toxins, coagulate blood, or as in this case, allow the bacteria to resist antibiotics. AbaR-type resistance islands are typical of drug-resistant A. baumannii, and different variations may be present in a given strain. Each consists of a transposon backbone of about 16.3 Kb that facilitates horizontal gene transfer. Transposons allow portions of genetic material to be excised from one spot in the genome and integrate into another. This makes horizontal gene transfer of this and similar pathogenicity islands more likely because, when genetic material is taken up by a new bacterium, the transposons allow the pathogenicity island to integrate into the new microorganism's genome. In this case, it would grant the new microorganism the potential to resist certain antibiotics. AbaRs contain several genes for antibiotic resistance, all flanked by insertion sequences. These genes provide resistance to aminoglycosides, aminocyclitols, tetracycline, and chloramphenicol.
Efflux pumps are protein machines that use energy to pump antibiotics and other small molecules that get into the bacterial cytoplasm and the periplasmic space out of the cell. By constantly pumping antibiotics out of the cell, bacteria can increase the concentration of a given antibiotic required to kill them or inhibit their growth when the target of the antibiotic is inside the bacterium. A. baumannii is known to have two major efflux pumps which decrease its susceptibility to antimicrobials. The first, AdeB, has been shown to be responsible for aminoglycoside resistance. The second, AdeDE, is responsible for efflux of a wide range of substrates, including tetracycline, chloramphenicol, and various carbapenems.
Bacterial small RNAs are noncoding RNAs that regulate various cellular processes. Three sRNAs, AbsR11, AbsR25, and AbsR28, have been experimentally validated in the MTCC 1425 (ATCC15308) strain, which is a (multidrug-resistant) strain showing resistance to 12 antibiotics. AbsR25 sRNA could play a role in the efflux pump regulation and drug resistance.
A. baumannii has been shown to produce at least one beta-lactamase, which is an enzyme responsible for cleaving the four-atom lactam ring typical of beta-lactam antibiotics. Beta-lactam antibiotics are structurally related to penicillin, which inhibits synthesis of the bacterial cell wall. The cleaving of the lactam ring renders these antibiotics harmless to the bacteria. The beta-lactamase OXA-23 was found to be flanked by insertion sequences, suggesting it was acquired by horizontal gene transfer.
A. baumannii has been noted for its apparent ability to survive on artificial surfaces for an extended period of time, therefore allowing it to persist in the hospital environment. This is thought to be due to its ability to form biofilms. For many biofilm-forming bacteria, the process is mediated by flagella. However, for A. baumannii, this process seems to be mediated by pili. Further, disruption of the putative pili chaperone and usher genes csuC and csuE were shown to inhibit biofilm formation. The formation of biofilms has been shown to alter the metabolism of microorganisms within the biofilm, consequently reducing their sensitivity to antibiotics. This may be because fewer nutrients are available deeper within the biofilm. A slower metabolism can prevent the bacteria from taking up an antibiotic or performing a vital function fast enough for particular antibiotics to have an effect. They also provide a physical barrier against larger molecules and may prevent desiccation of the bacteria.
Signs and symptoms of infection
A. baumannii is an opportunistic bacterium with a range of different diseases, each with their own symptoms. Some possible types of A. baumannii infections include:
Symptoms of A. baumannii infections are often indistinguishable from other opportunistic infections caused by other opportunistic bacteria - including Klebsiella pneumoniae and Streptococcus pneumoniae.
Symptoms of A. baumannii infections in turn range from fevers and chills, rash, confusion and/or altered mental states, pain or burning sensations when urinating, strong urge to urinate frequently, sensitivity to bright light, nausea (with or without vomiting), muscle and chest pains, breathing problems, and cough (with or without yellow, green, or bloody mucus). In some cases, A. baumannii may present no infection or symptoms, as with colonizing an open wound or tracheostomy site.
Because most infections are now resistant to multiple drugs, determining what susceptibilities the particular strain has is necessary to for treatment to be successful. Traditionally, infections were treated with imipenem or meropenem, but a steady rise in carbapenem-resistant A. baumannii has been noted. Consequently, treatment methods often fall back on polymyxins, particularly colistin. Colistin is considered a drug of last resort because it often causes kidney damage, among other side effects. Prevention methods in hospitals focus on increased hand-washing and more diligent sterilization procedures.
Traumatic injuries, like those from improvised explosive devices, leave large open areas contaminated with debris that are vulnerable to becoming infected with A. baumannii.
The logistics of transporting wounded soldiers result in patients visiting several facilities where they may acquire A. baumannii infections.
Occurrence in veterans injured in Iraq and Afghanistan
Soldiers in Iraq and Afghanistan are at risk for traumatic injury due to gunfire and improvised explosive devices. Previously, infection was thought to occur due to contamination with A. baumannii at the time of injury. Subsequent studies have shown, although A. baumannii may be infrequently isolated from the natural environment, the infection is more likely nosocomially acquired, likely due to the ability of A. baumannii to persist on artificial surfaces for extended periods, and the several facilities to which injured soldiers are exposed during the casualty-evacuation process. Injured soldiers are first taken to level-I facilities, where they are stabilized. Depending on the severity of the injury, the soldiers may then be transferred to a level-II facility, which consists of a forward surgical team, for additional stabilization. Depending on the logistics of the locality, the injured soldiers may transfer between these facilities several times before finally being taken to a major hospital within the combat zone (level III). Generally after 1–3 days, when the patients are stabilized, they are transferred by air to a regional facility (level IV) for additional treatment. For soldiers serving in Iraq or Afghanistan, this is typically Landstuhl Regional Medical Center in Germany. Finally, the injured soldiers are transferred to hospitals in their home country for rehabilitation and additional treatment. This repeated exposure to many different medical environments seems to be the reason A. baumannii infections have become increasingly common. Multidrug-resistant A. baumannii is a major factor in complicating the treatment and rehabilitation of injured soldiers, and has led to additional deaths.
Incidence in hospitals
Being referred to as an opportunistic infection, A. baumanii infections are highly prevalent in hospital settings. A. baumanii poses very little risk to healthy individuals, however, factors that increase the risks for infection include
- Having a weakened immune system
- Chronic Lung Disease
- Lengthened hospital stays
- Illness that requires use of a hospital ventilator
- Having an open wound treated in a hospital
- Treatments requiring invasive devices like urinary catheters
A. baumanii can be spread through direct contact with surfaces, objects, and the skin of contaminated persons.
The importation of A. baumannii and subsequent presence in hospitals has been well documented. A. baumannii is usually introduced into a hospital by a colonized patient. Due to its ability to survive on artificial surfaces and resist desiccation, it can remain and possibly infect new patients for some time. A baumannii growth is suspected to be favored in hospital settings due to the constant use of antibiotics by patients in the hospital. Acinetobacter can be spread by person-to-person contact or contact with contaminated surfaces. Acinetobacter can enter through open wounds, catheters and breathing tubes. In a study of European intensive care units in 2009, A. baumannii was found to be responsible for 19.1% of ventilator-associated pneumonia cases.
A 2013 Indonesian study showed that neonatal infections with A. baumanii were due to the same strains of the bacteria found in the hospital in which the neonates had spent their earliest days. These strains were found on hard surfaces as well as on the hands of medical personnel.
- ^ Parte, A.C. "Acinetobacter". www.bacterio.net.
- ^ Antunes, LCS; Visca, P; Towner, KJ (2014). "Acinetobacter baumannii: evolution of a global pathogen". Pathogens and Disease. 71 (3): 292–301. doi:10.1111/2049-632X.12125. PMID 24376225.
- ^ a b Yeom, J; Shin, JH; Yang, JY; Kim, J; Hwang, GS (2013). "(1)H NMR-Based Metabolite Profiling of Planktonic and Biofilm Cells in Acinetobacter baumannii 1656-2". PLoS ONE. 8 (3): e57730. Bibcode:2013PLoSO...857730Y. doi:10.1371/journal.pone.0057730. PMC 3590295 . PMID 23483923.
- ^ a b McQueary, CN; Kirkup, BC; Si, Y; Barlow, M; Actis, LA; Craft, DW; Zurawski, DV (June 2012). "Extracellular stress and lipopolysaccharide modulate Acinetobacter baumannii surface-associated motility". Journal of Microbiology. 50 (3): 434–43. doi:10.1007/s12275-012-1555-1. PMID 22752907.
- ^ Garrity, G., ed. (2000). "Pts. A & B: The Proteobacteria". Bergey's Manual of Systematic Bacteriology. 2 (2nd ed., rev. ed.). New York: Springer. p. 454. ISBN 0-387-95040-0.
- ^ a b O'Shea, MK (May 2012). "Acinetobacter in modern warfare". International Journal of Antimicrobial Agents. 39 (5): 363–75. doi:10.1016/j.ijantimicag.2012.01.018. PMID 22459899.
- ^ Gerner-Smidt, P (October 1992). "Ribotyping of the Acinetobacter calcoaceticus-Acinetobacter baumannii complex". Journal of Clinical Microbiology. 30 (10): 2680–5. PMC 270498 . PMID 1383266.
- ^ Rice, LB (15 April 2008). "Federal funding for the study of antimicrobial resistance in nosocomial pathogens: no ESKAPE". The Journal of Infectious Diseases. 197 (8): 1079–81. doi:10.1086/533452. PMID 18419525.
- ^ Drummond, Katie. "Pentagon to Troop-Killing Superbugs: Resistance Is Futile". Wired.com. Condé Nast. Retrieved 8 April 2013.
- ^ Lee, C.-R.; Lee, J. H.; Park, M.; Park, K. S.; Bae, I. K.; Kim, Y. B.; Cha, C.-J.; Jeong, B. C.; Lee, S. H. (2017). "Biology of Acinetobacter baumannii: Pathogenesis, Antibiotic Resistance Mechanisms, and Prospective Treatment Options". Front. Cell. Infect. Microbiol. 7: 55. doi:10.3389/fcimb.2017.00055. PMC 5346588 . PMID 28348979.
- ^ Luke, NR; Sauberan, SL; Russo, TA; Beanan, JM; Olson, R; Loehfelm, TW; Cox, AD; St Michael, F; Vinogradov, EV; Campagnari, AA (May 2010). "Identification and characterization of a glycosyltransferase involved in Acinetobacter baumannii lipopolysaccharide core biosynthesis". Infection and Immunity. 78 (5): 2017–23. doi:10.1128/iai.00016-10. PMC 2863528 . PMID 20194587.
- ^ Choi, CH; Lee, JS; Lee, YC; Park, TI; Lee, JC (10 December 2008). "Acinetobacter baumannii invades epithelial cells and outer membrane protein A mediates interactions with epithelial cells". BMC Microbiology. 8: 216. doi:10.1186/1471-2180-8-216. PMC 2615016 . PMID 19068136.
- ^ Lee, JS; Choi, CH; Kim, JW; Lee, JC (June 2010). "Acinetobacter baumannii outer membrane protein A induces dendritic cell death through mitochondrial targeting". Journal of Microbiology. 48 (3): 387–92. doi:10.1007/s12275-010-0155-1. PMID 20571958.
- ^ Seputiene, V.; Povilonis, J.; Suziedeliene, E. (30 January 2012). "Novel Variants of AbaR Resistance Islands with a Common Backbone in Acinetobacter baumannii Isolates of European Clone II". Antimicrobial Agents and Chemotherapy. 56 (4): 1969–1973. doi:10.1128/AAC.05678-11. PMC 3318354 . PMID 22290980.
- ^ Post, V; White, PA; Hall, RM (June 2010). "Evolution of AbaR-type genomic resistance islands in multiply antibiotic-resistant Acinetobacter baumannii". The Journal of Antimicrobial Chemotherapy. 65 (6): 1162–70. doi:10.1093/jac/dkq095. PMID 20375036.
- ^ Magnet, S; Courvalin, P; Lambert, T (December 2001). "Resistance-nodulation-cell division-type efflux pump involved in aminoglycoside resistance in Acinetobacter baumannii strain BM4454". Antimicrobial Agents and Chemotherapy. 45 (12): 3375–80. doi:10.1128/aac.45.12.3375-3380.2001. PMC 90840 . PMID 11709311.
- ^ Chau, SL; Chu, YW; Houang, ET (October 2004). "Novel resistance-nodulation-cell division efflux system AdeDE in Acinetobacter genomic DNA group 3". Antimicrobial Agents and Chemotherapy. 48 (10): 4054–5. doi:10.1128/aac.48.10.4054-4055.2004. PMC 521926 . PMID 15388479.
- ^ Sharma, Rajnikant; Arya, Sankalp; Patil, Supriya Deepak; Sharma, Atin; Jain, Pradeep Kumar; Navani, Naveen Kumar; Pathania, Ranjana (2014-01-01). "Identification of novel regulatory small RNAs in Acinetobacter baumannii". PLoS One. 9 (4): e93833. Bibcode:2014PLoSO...993833S. doi:10.1371/journal.pone.0093833. ISSN 1932-6203. PMC 3976366 . PMID 24705412.
- ^ Higgins, PG; Pérez-Llarena, FJ; Zander, E; Fernández, A; Bou, G; Seifert, H (25 February 2013). "OXA-235, a novel Class D Beta-Lactamase Involved in Resistance to Carbapenems in Acinetobacter baumannii". Antimicrobial Agents and Chemotherapy. 57 (5): 2121–6. doi:10.1128/AAC.02413-12. PMC 3632948 . PMID 23439638.
- ^ Espinal, P; Martí, S; Vila, J (January 2012). "Effect of biofilm formation on the survival of Acinetobacter baumannii on dry surfaces". The Journal of Hospital Infection. 80 (1): 56–60. doi:10.1016/j.jhin.2011.08.013. PMID 21975219.
- ^ Tomaras, AP; Dorsey, CW; Edelmann, RE; Actis, LA (December 2003). "Attachment to and biofilm formation on abiotic surfaces by Acinetobacter baumannii: involvement of a novel chaperone-usher pili assembly system". Microbiology. 149 (Pt 12): 3473–84. doi:10.1099/mic.0.26541-0. PMID 14663080.
- ^ Worthington, RJ; Richards, JJ; Melander, C (7 October 2012). "Small molecule control of bacterial biofilms". Organic & Biomolecular Chemistry. 10 (37): 7457–74. doi:10.1039/c2ob25835h. PMC 3431441 . PMID 22733439.
- ^ a b c "What Is Acinetobacter Baumannii?". Everyday Health. Retrieved 18 April 2017.
- ^ Su, CH; Wang, JT; Hsiung, CA; Chien, LJ; et al. (2012). "Increase of carbapenem-resistant Acinetobacter baumannii infection in acute care hospitals in Taiwan: Association with hospital antimicrobial usage". PLOS ONE. 7 (5): e37788. Bibcode:2012PLoSO...737788S. doi:10.1371/journal.pone.0037788. PMC 3357347 . PMID 22629456.
- ^ Abbo, A; Navon-Venezia, S; Hammer-Muntz, O; Krichali, T; et al. (January 2005). "Multidrug-resistant Acinetobacter baumannii". Emerging Infectious Diseases. 11 (1): 22–9. doi:10.3201/eid1101.040001. PMC 3294361 . PMID 15705318.
- ^ Spapen, H; Jacobs, R; Van Gorp, V; Troubleyn, J; et al. (25 May 2011). "Renal and neurological side effects of colistin in critically ill patients". Annals of Intensive Care. 1 (1): 14. doi:10.1186/2110-5820-1-14. PMC 3224475 . PMID 21906345.
- ^ "Acinetobacter in Healthcare Settings". CDC. Retrieved 8 April 2013.
- ^ "Army Medical Logistics" (PDF). FM 4-02.1. United States. Retrieved April 8, 2013.
- ^ Meghoo, CA; Dennis, JW; Tuman, C; Fang, R (May 2012). "Diagnosis and management of evacuated casualties with cervical vascular injuries resulting from combat-related explosive blasts". Journal of Vascular Surgery. 55 (5): 1329–36; discussion 1336–7. doi:10.1016/j.jvs.2011.11.125. PMID 22325667.
- ^ Murray, CK (March 2008). "Epidemiology of infections associated with combat-related injuries in Iraq and Afghanistan". The Journal of Trauma. 64 (3 Suppl): S232–8. doi:10.1097/ta.0b013e318163c3f5. PMID 18316967.
- ^ "Acinetobacter in Healthcare Settings". Centers for Disease Control and Prevention. US Department of Health and Human Services. Retrieved 18 April 2017.
- ^ Jones, A; Morgan, D; Walsh, A; Turton, J; Livermore, D; Pitt, T; Green, A; Gill, M; Mortiboy, D (June 2006). "Importation of multidrug-resistant Acinetobacter spp infections with casualties from Iraq". The Lancet Infectious Diseases. 6 (6): 317–8. doi:10.1016/S1473-3099(06)70471-6. PMID 16728314.
- ^ Dijkshoorn, L; Nemec, A; Seifert, H (December 2007). "An increasing threat in hospitals: multidrug-resistant Acinetobacter baumannii". Nature Reviews Microbiology. 5 (12): 939–51. doi:10.1038/nrmicro1789. PMID 18007677.
- ^ [www.cdc.gov]
- ^ Multidrug-Resistant Acinetobacter baumannii (MDRAB).” WHO Western Pacific Region, WPRO | WHO Western Pacific Region, 1 Nov. 2010, www.wpro.who.int/mediacentre/factsheets/fs_20101102/en/.
- ^ Koulenti, D; Lisboa, T; Brun-Buisson, C; Krueger, W; Macor, A; Sole-Violan, J; Diaz, E; Topeli, A; DeWaele, J; Carneiro, A; Martin-Loeches, I; Armaganidis, A; Rello, J (August 2009). EU-VAP/CAP Study, Group. "Spectrum of practice in the diagnosis of nosocomial pneumonia in patients requiring mechanical ventilation in European intensive care units". Critical Care Medicine. 37 (8): 2360–8. doi:10.1097/ccm.0b013e3181a037ac. PMID 19531951.
- ^ Ng, J; Gosbell, IB; Kelly, JA; Boyle, MJ; Ferguson, JK (November 2006). "Cure of multiresistant Acinetobacter baumannii central nervous system infections with intraventricular or intrathecal colistin: case series and literature review". The Journal of Antimicrobial Chemotherapy. 58 (5): 1078–81. doi:10.1093/jac/dkl347. PMID 16916866.
- ^ Farrugia, DN; Elbourne, LD; Hassan, KA; Eijkelkamp, BA; Tetu, SG; Brown, MH; Shah, BS; Peleg, AY; Mabbutt, BC; Paulsen, IT (2013). "The Complete Genome and Phenome of a Community-Acquired Acinetobacter baumannii". PLoS ONE. 8 (3): e58628. Bibcode:2013PLoSO...858628F. doi:10.1371/journal.pone.0058628. PMC 3602452 . PMID 23527001.
- ^ Werneck, JS; Picão, RC; Carvalhaes, CG; Cardoso, JP; Gales, AC (February 2011). "OXA-72-producing Acinetobacter baumannii in Brazil: a case report". The Journal of Antimicrobial Chemotherapy. 66 (2): 452–4. doi:10.1093/jac/dkq462. PMID 21131320.
- ^ Martins, N; Martins, IS; de Freitas, WV; de Matos, JA; Magalhães, AC; Girão, VB; Dias, RC; de Souza, TC; Pellegrino, FL; Costa, LD; Boasquevisque, CH; Nouér, SA; Riley, LW; Santoro-Lopes, G; Moreira, BM (June 2012). "Severe infection in a lung transplant recipient caused by donor-transmitted carbapenem-resistant Acinetobacter baumannii". Transplant Infectious Disease. 14 (3): 316–20. doi:10.1111/j.1399-3062.2011.00701.x. PMC 3307813 . PMID 22168176.
- ^ Superti, SV; Martins Dde, S; Caierão, J; Soares Fda, S; Prochnow, T; Zavascki, AP (March–April 2009). "Indications of carbapenem resistance evolution through heteroresistance as an intermediate stage in Acinetobacter baumannii after carbapenem administration". Revista do Instituto de Medicina Tropical de Sao Paulo. 51 (2): 111–3. doi:10.1590/s0036-46652009000200010. PMID 19390741.
- ^ Gionco, B; Pelayo, JS; Venancio, EJ; Cayô, R; Gales, AC; Carrara-Marroni, FE (October 2012). "Detection of OXA-231, a new variant of blaOXA-143, in Acinetobacter baumannii from Brazil: a case report". The Journal of Antimicrobial Chemotherapy. 67 (10): 2531–2. doi:10.1093/jac/dks223. PMID 22736746.
- ^ Zhao, WS; Liu, GY; Mi, ZH; Zhang, F (March 2011). "Coexistence of blaOXA-23 with armA and novel gyrA mutation in a pandrug-resistant Acinetobacter baumannii isolate from the blood of a patient with haematological disease in China". The Journal of Hospital Infection. 77 (3): 278–9. doi:10.1016/j.jhin.2010.11.006. PMID 21281989.
- ^ Xiao, SC; Zhu, SH; Xia, ZF; Ma, B; Cheng, DS (November 2009). "Successful treatment of a critical burn patient with obstinate hyperglycemia and septic shock from pan-drug-resistant strains". Medical Science Monitor. 15 (11): CS163–5. PMID 19865060.
- ^ Wu, YC; Hsieh, TC; Sun, SS; Wang, CH; Yen, KY; Lin, YY; Kao, CH (November 2009). "Unexpected cloud-like lesion on gallium-67 scintigraphy: detection of subcutaneous abscess underneath the skin with normal appearance in a comatose patient in an intensive care setting". The American Journal of the Medical Sciences. 338 (5): 388. doi:10.1097/maj.0b013e3181a6dd36. PMID 19770790.
- ^ Duan, X; Yang, L; Xia, P (March 2010). "Septic arthritis of the knee caused by antibiotic-resistant Acinetobacter baumannii in a gout patient: a rare case report". Archives of Orthopaedic and Trauma Surgery. 130 (3): 381–4. doi:10.1007/s00402-009-0958-x. PMID 19707778.
- ^ a b Wagner, JA; Nenoff, P; Handrick, W; Renner, R; Simon, J; Treudler, R (February 2011). "Necrotizing fasciitis caused by Acinetobacter baumannii : A case report". Der Hautarzt; Zeitschrift für Dermatologie, Venerologie, und verwandte Gebiete (in German). 62 (2): 128–30. doi:10.1007/s00105-010-1962-3. PMID 20835812.
- ^ Aivazova, V; Kainer, F; Friese, K; Mylonas, I (January 2010). "Acinetobacter baumannii infection during pregnancy and puerperium". Archives of Gynecology and Obstetrics. 281 (1): 171–4. doi:10.1007/s00404-009-1107-z. PMID 19462176.
- ^ Schulte, B; Goerke, C; Weyrich, P; Gröbner, S; Bahrs, C; Wolz, C; Autenrieth, IB; Borgmann, S (December 2005). "Clonal spread of meropenem-resistant Acinetobacter baumannii strains in hospitals in the Mediterranean region and transmission to South-west Germany". The Journal of Hospital Infection. 61 (4): 356–7. doi:10.1016/j.jhin.2005.05.009. PMID 16213625.
- ^ Piparsania, S; Rajput, N; Bhatambare, G (September–October 2012). "Intraventricular polymyxin B for the treatment of neonatal meningo-ventriculitis caused by multi-resistant Acinetobacter baumannii--case report and review of literature". The Turkish Journal of Pediatrics. 54 (5): 548–54. PMID 23427525.
- ^ John, TM; Jacob, CN; Ittycheria, CC; George, AM; Jacob, AG; Subramaniyam, S; Puthiyaveettil, J; Jayaprakash, R (March 2012). "Macrophage activation syndrome following Acinetobacter baumannii sepsis". International Journal of Infectious Diseases. 16 (3): e223–4. doi:10.1016/j.ijid.2011.12.002. PMID 22285540.
- ^ Sharma, A; Shariff, M; Thukral, SS; Shah, A (October 2005). "Chronic community-acquired Acinetobacter pneumonia that responded slowly to rifampicin in the anti-tuberculous regime". The Journal of Infection. 51 (3): e149–52. doi:10.1016/j.jinf.2004.12.003. PMID 16230195.
- ^ Jeong, HL; Yeom, JS; Park, JS; Seo, JH; Park, ES; Lim, JY; Park, CH; Woo, HO; Youn, HS (July–August 2011). "Acinetobacter baumannii isolation in cerebrospinal fluid in a febrile neonate". The Turkish journal of Pediatrics. 53 (4): 445–7. PMID 21980849.
- ^ Hong, KB; Oh, HS; Song, JS; Lim, JH; Kang, DK; Son, IS; Park, JD; Kim, EC; Lee, HJ; Choi, EH (July 2012). "Investigation and control of an outbreak of imipenem-resistant Acinetobacter baumannii Infection in a Pediatric Intensive Care Unit". The Pediatric Infectious Disease Journal. 31 (7): 685–90. doi:10.1097/inf.0b013e318256f3e6. PMID 22466324.
- ^ Lee, YK; Kim, JK; Oh, SE; Lee, J; Noh, JW (December 2009). "Successful antibiotic lock therapy in patients with refractory peritonitis". Clinical Nephrology. 72 (6): 488–91. doi:10.5414/cnp72488. PMID 19954727.
- ^ Lee, SY; Lee, JW; Jeong, DC; Chung, SY; Chung, DS; Kang, JH (August 2008). "Multidrug-resistant Acinetobacter meningitis in a 3-year-old boy treated with i.v. colistin". Pediatrics International. 50 (4): 584–5. doi:10.1111/j.1442-200x.2008.02677.x. PMID 18937759.
- ^ Adams, D; Yee, L; Rimmer, JA; Williams, R; Martin, H; Ovington, C (February 2011). "Investigation and management of an A. Baumannii outbreak in ICU". British Journal of Nursing. 20 (3): 140, 142, 144–7. doi:10.12968/bjon.2011.20.3.140. PMID 21378633.
- ^ Pencavel, TD; Singh-Ranger, G; Crinnion, JN (May 2006). "Conservative treatment of an early aortic graft infection due to Acinetobacter baumanii". Annals of Vascular Surgery. 20 (3): 415–7. doi:10.1007/s10016-006-9030-2. PMID 16602028.
- ^ Gusten, WM; Hansen, EA; Cunha, BA (January–February 2002). "Acinetobacter baumannii pseudomeningitis". Heart & Lung. 31 (1): 76–8. doi:10.1067/mhl.2002.120258. PMID 11805753.
- ^ Fitzpatrick, MA; Esterly, JS; Postelnick, MJ; Sutton, SH (July–August 2012). "Successful treatment of extensively drug-resistant Acinetobacter baumannii peritoneal dialysis peritonitis with intraperitoneal polymyxin B and ampicillin-sulbactam". Annals of Pharmacotherapy. 46 (7–8): e17. doi:10.1345/aph.1r086. PMID 22811349.
- ^ Patel, JA; Pacheco, SM; Postelnick, M; Sutton, S (15 August 2011). "Prolonged triple therapy for persistent multidrug-resistant Acinetobacter baumannii ventriculitis". American Journal of Health-System Pharmacy. 68 (16): 1527–31. doi:10.2146/ajhp100234. PMID 21817084.
- ^ Sullivan, DR; Shields, J; Netzer, G (June 2010). "Fatal case of multi-drug resistant Acinetobacter baumannii necrotizing fasciitis". The American Surgeon. 76 (6): 651–3. PMID 20583528.
- ^ Tjoa E, Moehario LH, Rukmana A, Rohsiswatmo R (2013). "Acinetobacter baumannii: Role in Blood Stream Infection in Neonatal Unit, Cipto Mangunkusumo Hospital, Jakarta, Indonesia". International Journal of Microbiology. 2013: 180763. doi:10.1155/2013/180763. PMC 3830835 . PMID 24288538.