This review describes the characteristics of Acinetobacter baumannii that have contributed to its emergence as a medically important human pathogen and the anim

OBJECTIVES To describe a large series of patients with vertebral osteomyelitis (VO), and to compare the clinical, biological, radiological, and prognostic features of pyogenic (PVO), tuberculous (TVO), and brucellar vertebral osteomyelitis (BVO). METHODS A retrospective multicentre study, which included 219 adult patients with VO with confirmed aetiology, who were diagnosed between 1983 and 1995 in two tertiary care centres. Of these patients, 105 (48%) had BVO, 72 (33%) PVO, and 42 (19%) TVO. RESULTS One hundred and forty eight (67.6%) patients were male and 71 (32.4%) female. The mean (SD) age was 50.4 (16.4) years (range 14–84) and the mean (SD) duration of symptoms before the diagnosis was 14 (16.8) weeks. In 127 patients (57.9%) the vertebral level involved was lumbar, in 70 (31.9%) thoracic, and in 16 (7.3%) cervical. One hundred and nineteen patients (54.4%) received only medical treatment and 100 (45.6%) required both medical and surgical treatment. The presence of diabetes mellitus, intravenous drug abuse, underlying chronic debilitating diseases or immunosuppression, previous infections, preceeding bacteraemia, recent vertebral surgery, leucocytosis, neutrophilia, and increased erythrocyte sedimentation rate (ESR) were significantly associated to PVO. A prolonged clinical course, thoracic segment involvement, absence of fever, presence of spinal deformity, neurological deficit, and paravertebral or epidural masses, were significantly more frequent in the group of TVO. The need for surgical treatment and the presence of severe functional sequelae were more frequent in the groups of PVO and TVO. CONCLUSION There are significant clinical, biological, radiological, and prognostic differences between BVO, PVO, and TVO. These differences can point to the causal agent and orient the initial empirical medical treatment while awaiting a final microbiological diagnosis.

The number of nosocomial infections caused by Acinetobacter baumannii has increased in recent years. During a 12-month study, there were 1.8 episodes of A. baumannii bacteremia per 1,000 adults admitted to a hospital in Seville, Spain. Seventy-nine patients were included in the study. A. baumannii bacteremia occurred after a mean (± SD) hospitalization of 18 ± 20 days. In all cases the infections were acquired nosocomially; 71% were acquired in intensive care units. Ampicillinl sulbactam was found to be the most active agent against A. baumannii. The most common source of the bacteremia was the respiratory tract (32 cases [71%n. Twenty patients (25%) had septic shock, and 24 (30%) had disseminated intravascular coagulation (DIC). Treatment with imipenem or ampicillinlsulbactam was most effective (cure rates, 87.5% and 83%, respectively). The deaths of 27 patients (34%) were related to A. baumannii bacteremia. The presence of DIC (odds ratio [OR] = 116.4; P < .0001) and inappropriate antimicrobial treatment (OR = 15.2; P < .01) were independently associated with mortality. We conclude that most A. baumannii isolates are multiresistant and that nosocomial A. baumannii bacteremia may cause severe clinical disease that is associated with a high mortality.

The frequency of community-acquired pneumonia coupled with its mortality rate of 10 to 25% is of growing concern to clinicians. A prospective study of 67 patients with severe community-acquired pneumonia was carried out to determine the causative agents, the impact fore-knowledge of the etiology has on the outcome, the value of clinical and radiologic criteria in predicting the evolution, and the efficacy of empirical therapy. The study group included 45 men and 22 women (mean age: 56.8 ± 16.6 yr), and 46.2% suffered from a concurrent debilitating disease. The cause of pneumonia was diagnosed in 32 cases, and the most common pathogens were Streptococcus pneumoniae (37.5%), Legionella pneumophila (21.8%), and gram-negative bacilli (25.0%). The fact that fungal infections were present in three patients and Pneumocystis carinii in one are worthy of note. The overall death rate was 20.8%. A fatal outcome was related to the age of the patient (p < 0.05), the presence of debilitating disease (p = 0.026), and septic shock (p = 0.0009). Diagnosis of the causative agents did not aid in increasing the survival rate, but it did allow for better patient management. Most of the patients (85.1%) initiated on treatment with erythromycin plus tobramycin recovered, but only 68.4% of the subjects commenced on treatment with other therapeutics survived. Furthermore, it was necessary to modify the therapy of a greater percentage of the latter group (p < 0.025). Gram-negative bacillary pneumonia was a frequent finding among the patients who did not recover, making empirical treatment with erythromycin plus third generation cephalosporins most advisable for severe cases of community-acquired pneumonia.

Acinetobacter baumannii , which causes serious infections in immunocompromised patients, expresses high-affinity iron acquisition functions needed for growth under iron-limiting laboratory conditions. In this study, we determined that the initial interaction of the ATCC 19606 ^T type strain with A549 human alveolar epithelial cells is independent of the production of BasD and BauA, proteins needed for acinetobactin biosynthesis and transport, respectively. In contrast, these proteins are required for this strain to persist within epithelial cells and cause their apoptotic death. Infection assays using Galleria mellonella larvae showed that impairment of acinetobactin biosynthesis and transport functions significantly reduces the ability of ATCC 19606 ^T cells to persist and kill this host, a defect that was corrected by adding inorganic iron to the inocula. The results obtained with these ex vivo and in vivo approaches were validated using a mouse sepsis model, which showed that expression of the acinetobactin-mediated iron acquisition system is critical for ATCC 19606 ^T to establish an infection and kill this vertebrate host. These observations demonstrate that the virulence of the ATCC 19606 ^T strain depends on the expression of a fully active acinetobactin-mediated system. Interestingly, the three models also showed that impairment of BasD production results in an intermediate virulence phenotype compared to those of the parental strain and the BauA mutant. This observation suggests that acinetobactin intermediates or precursors play a virulence role, although their contribution to iron acquisition is less relevant than that of mature acinetobactin.