Wednesday, December 19, 2012

A case of community-acquired Acinetobacter junii-johnsonii cellulitis

A case of community-acquired Acinetobacter junii-johnsonii cellulitis.

Jun 2012


Division of Infectious Diseases, University of Colorado, Denver, USA.


Key words: Acinetobacter, cellulitis, community-acquired infections, bacteremia, blister, therapy.

Acinetobacter skin and soft tissue infection outside of the traumatic wound setting are rare occurrences. The majority of cases occur in the presence of significant comorbilities and by Acinetobacter baumanii. Herein a case is reported of community-onset, health-care-associated, non-traumatic cellulitis caused by Acinetobacter, species junii-johnsonii with bacteremia. This is the first reported case of Acinetobacter junii-johnsonii skin and soft tissue infection. Hemorrhagic bullae might be one of the clinical features of Acinetobacter cellulitis.
Case report 
In August 2010, a 48 year old man with a history of metastatic, stage IV, prostate cancer was admitted to the University of Colorado Hospital after being transferred from an outside hospital. The case was complicated by bladder obstruction, T8 fracture, spinal cord involvement and had been treated with androgen-deprivation therapy and local radiation therapy. The patient had been admitted one month prior to this presentation with a pulmonary embolus, methicillin-sensitive Staphylococcus aureus (MSSA) bacteremia of unclear origin and also with a multidrug resistant (MDR) Serratia marcescens urinary tract infection. The patient recovered from that episode and was discharged to his home on intravenous (IV) ertapenem, 1gram every 24 hours. Several weeks later, the patient was readmitted to an outside hospital after developing a rapid progression of symptoms characterized by the following: marked fatigue, light headedness, fever, chills and right lower extremity swelling, erythema, tenderness and warmness. On admission the patient was found to be in septic shock, requiring intensive care unit care. He received aggressive fluid resuscitation therapy and pressor support; and he was placed empirically on IV vancomycin, piperacillin-tazobactam and levofloxacin. His hemodynamic parameters improved over the next two days, and he was transferred to our hospital with the documentation of a non fermenting gram negative rod (GNR) in blood culture (1 of 2 bottles). Computerized tomography (CT) scan of his leg showed a marked subcutaneous edema. The positive culture was from a peripheral site. The physical examination was remarkable for marked right lower extremity swelling, with erythema involving the distal 2/3 of the leg, and local tenderness, warmness and the presence of a purpuric rash and hemorrhagic bullae. The PICC line was present and was without local signs of inflammation. The laboratory tests were significant for leukopenia, anemia and thrombocytopenia. The gram negative rod was a nonmotile, catalase-positive, oxidase-negative bacteria; finally identified using the Vitek 2 system (an automated system for bacterial identification using a phenotypic approach) as Acinetobacter junii-johnsonii, sensitive to quinolones and B-lactams, and intermediate to aztreonam. His antibiotic therapy was narrowed to Levofloxacin only, and the patient was discharged 4 days later. He was seen again in the clinic 4 weeks later; complete resolution of his local right leg inflammatory changes were noted.

Full text with diagnostic images:

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