Morphology and culture
In Acinetobacter baumannii is immobile, aerobic, gram-negative short rods with a size of about 1-1.5 x 1.5-2 microns. Originally belonged to the genus Acinetobacter to the family of Neisseriaceae. Later, she was assigned to the family of Moraxellaceae. Most strains of Acinetobacter baumannii show on solid culture media flat colorless colonies that are slightly smaller than those of Enterobacteriaceae. Some strains are in liquid culture media difficult or impossible to cultivate. See more: www.schess.org
The differentiation in routine laboratories is based on the metabolic activities. However, the precise differentiation of the species with standard methods is often not possible. Therefore, four Genomospezies were summarized for Acinetobacter baumannii Acinetobacter calcoaceticus complex. Acinetobacter species can ferment glucose and thus do not belong to the so-called "non-fermenters."
Pathogenesis and clinical pictures
Acinetobacter species are in nature and beyond widely used in the hospital sector. You can survive well on wet and dry surfaces. In addition, they can often be detected in food and in the flora of human skin. Acinetobacter baumannii has the largest clinical significance among Acinetobacter species. As a classic opportunist he is a frequent pathogen in patients with immune deficiency. In the clinical pictures is the nosocomial pneumonia in the foreground, which is preferably observed in ventilated patients in the intensive care area. Other common diseases are urinary tract infections, wound infections, and sepsis. Not infrequently occur Hospital outbreaks. The most important epidemiologic reservoir is the gastrointestinal tract. Risk factors for infection by Acinetobacter antibiotic pre-treatment and / or surgery as well as the use of ventilators and other medical instruments have been identified.
In outpatients fatal pneumonia were described by Acinetobacter after use no more effective antibiotics. Severe wound infection and multidrug-resistant Acinetobacter baumannii by Osteomyelititiden were diagnosed among American soldiers who had been wounded in combat operations in Iraq and Afghanistan.
Acinetobacter Baumannii therapy
The agent of choice are carbapenems [imipenem (ZIENAM), meropenem (MERONEM)] is recommended. However, differences in sensitivity may exist with respect to the two substances, ie with proven sensitivity to imipenem may not be automatically inferred on sensitivity to meropenem and vice versa. As a further treatment option has recently become doripenem (DORIBAX) are available. However, the frequency of resistance to carbapenems in recent years has increased significantly worldwide. As therapeutic alternatives, the aminoglycosides come (in combination with another active antibiotic) into consideration. Colistin (in Germany not commercially available) is used for treating infections caused by pan-resistant strains.
Beta-lactamase inhibitors, especially sulbactam (COMBACTAM), possess intrinsic activity against Acinetobacter baumannii. The sulbactam monotherapy is not recommended for serious infections. The combination with a Betalaktamantibiotikum no increase in activity appears to result. Tigecycline (TYGACIL) has bacteriostatic activity against multidrug-resistant Acinetobacter. However, the development of resistance during therapy is possible. Against this background, tigecycline is rather to be regarded as a reserve substance here.
Acinetobacter Baumannii diagnosis and prevalence of resistance
The diagnosis is made by culture of appropriate specimens and biochemical identification.
Due to numerous naturally present and acquired resistance mechanisms to the hospital strains are often multiresistant. Almost always one or more beta-lactamases produced. Moreover, in Germany about 20-30% of the strains to fluoroquinolones [Ciprofloxacin (Cipro, etc.), levofloxacin (Tavanic etc.)] resistant. The results of susceptibility testing with beta-lactam / beta-lactamase inhibitor combinations using a fixed concentration of beta-lactamase inhibitor must be interpreted with caution because of resistant isolates may be falsely identified as sensitive. Resistance to aminoglycosides is caused by aminoglycoside-modifying enzymes or efflux pumps.