**1. Introduction**

The genus *Acinetobacter* consists of over 40 known species that can be isolated from various habitats including soil, sediment surface, and wastewater [1]. They have the ability to colonize human skin and are responsible for a growing number of nosocomial outbreaks worldwide. Although most *Acinetobacter* species have generally a low pathogenicity [2], according to Alsan et al. (2008), the intensive care unit (ICU) mortality rate is around 40% [3].

The most striking characteristic of *Acinetobacter* spp. is their natural resistance to many antibiotics and the ability to easily develop new resistances under antibiotic pressure. They overexpress efflux pumps, harbor β-lactamases, and are characterized by low membrane permeability [2]. By 2012,

over 210 different β-lactamases have been identified within the genus [4]. Different *Oxacillinases* (OXA) enzyme families have their origin in *Acinetobacter*, such as OXA-21like, OXA-23like or OXA-51like [5]. These enzymes are serine hydrolases represent class D according to the Ambler classification of β-lactamases [6]. The spread of these *Acinetobacter oxaxilinases* into other species seems much more limited than, for example, the spread of CTX-M or NDM enzymes but is documented. This set of OXA enzyme enables *Acinetobacter* to adapt easily to new developed β-lactam antibiotics [4,7]. Therefore, *Acinetobacter baumannii* especially has become one of the problematic nosocomial pathogens. Infections with some of these strains, such as bloodstream infections and pneumonia, do not leave any further options for antibiotic treatment. Next to *Pseudomonas* and carbapenem-resistant *Enterobacteriaceae*, *Acinetobacter* were rated by the WHO to be the group in most urgent need of new antibiotics (http: //www.who.int/medicines/publications/global-priority-list-antibiotic-resistant-bacteria/en/) [5,7,8]. In addition to the acquisition of a seemingly infinite number of resistances, such as *Pseudomonas* spp., *Acinetobacter* is characterized by a much better ability to survive hostile conditions, e.g., survival on dry surfaces. This makes *Acinetobacter* an ideal candidate for survival in clinical settings and in the environment [9–11].

Occurrence and susceptibility of *Acinetobacter* spp. in clinical settings is documented quite well, whereas their distribution and proportion of resistance in the aquatic environment remains quite unclear. Nearly all studies that investigate antibiotic resistance of *Acinetobacter* in the environment are based on selective cultivation, masking their proportion in the population, or are based on molecular methods, with all their inherent methodological weaknesses [9,12–15]. There is some evidence that environmental transport of *Acinetobacter* plays a role in the spread of clinical relevant *Acinetobacter* strains in the environment. On the other hand, there seems to be a continuous influx of novel strains into the clinical setting with the potential of new infectious features [16,17].

Participation in the Joint Danube Survey 2013 (JDS3) offered the possibility of isolating *Acinetobacter* from the total course of one of Europe's longest rivers. This chance was taken to generate an initial picture of the resistance proportion within *Acinetobacter* spp. and to get an idea of how far acquired antibiotic resistances of clinical relevance have spread in the aquatic environment.
