The entire genus Acinetobacter is classified as Gram-negative bacteria. This classification is a fundamental distinction based on the organism’s unique cell wall architecture. Belonging to the class Gammaproteobacteria, Acinetobacter species are often associated with healthcare settings, where they present significant clinical challenges. Understanding this structural basis helps explain why this group of bacteria is difficult to treat and why it possesses inherent resistance mechanisms.
Understanding Gram Staining and Bacterial Structure
Gram staining is a foundational microbiological technique that separates most bacteria into two major groups based on cell wall composition. Developed in 1884 by Hans Christian Gram, the method involves applying crystal violet stain, an iodine solution, a decolorizer, and a counterstain, typically safranin. The final color dictates the classification: Gram-positive bacteria appear purple, while Gram-negative bacteria appear pink or red.
This difference in color is a direct result of the bacteria’s cell envelope structure. Gram-positive organisms possess a thick, mesh-like layer of peptidoglycan, which is a polymer of sugars and amino acids, that surrounds the cell membrane. This dense, porous layer effectively traps the initial crystal violet-iodine complex, preventing the decolorizer from washing it away.
Gram-negative bacteria, including Acinetobacter, have a fundamentally different and more complex cell wall design. Their peptidoglycan layer is significantly thinner, often measuring only 5 to 10 nanometers, and is sandwiched between two separate membranes. This double-membrane structure is the defining feature that prevents the retention of the crystal violet stain.
The decolorizer easily washes the crystal violet from the thin peptidoglycan layer, leaving the cell colorless until the application of the pink counterstain, safranin. The outer membrane of the Gram-negative cell is composed partially of lipopolysaccharide (LPS). This LPS provides a protective barrier, contributing to the mechanical strength of the cell and limiting the permeability of various external substances, including certain antibiotics.
Defining Characteristics of Acinetobacter
Beyond the Gram stain, the Acinetobacter genus is characterized by several specific physiological traits that define its behavior. These organisms are classified as strictly aerobic, meaning they absolutely require oxygen to grow and thrive. They are also non-fermentative, meaning they obtain energy through respiration rather than through the fermentation of sugars.
Morphologically, Acinetobacter species are typically described as coccobacilli, which are short, plump rods that can sometimes appear almost spherical. A lack of flagella means the bacteria are non-motile. However, some species exhibit a form of surface movement called twitching motility, mediated by specialized structures called pili.
Acinetobacter is ubiquitous, found throughout the environment, particularly in soil and water. This environmental resilience is a major factor in its ability to persist in human habitats, including hospitals. The organism is known for its remarkable ability to survive desiccation, or drying out, on inanimate surfaces for up to a month. Acinetobacter baumannii accounts for roughly 80% of reported human infections and is the species most frequently associated with clinical disease.
Why Gram-Negative Classification Matters for Treatment
The Gram-negative cell structure of Acinetobacter is the foundation of its resistance to many common treatments, making infections difficult to manage. The outer membrane acts as the first line of defense, physically blocking the entry of large antibiotic molecules. For instance, antibiotics designed to target the thick peptidoglycan of Gram-positive bacteria, such as vancomycin, are ineffective because they cannot penetrate the outer layer.
The lipopolysaccharide component of the outer membrane further restricts the entry of hydrophobic drugs. This structural barrier means that antibiotics must rely on specialized channels, called porins, to enter the cell. Acinetobacter can easily modify these channels to limit drug uptake, compounding this intrinsic resistance with acquired mechanisms.
Acinetobacter is primarily an opportunistic, nosocomial pathogen, causing infections mainly in vulnerable patients within hospital environments, particularly in intensive care units (ICUs). Due to its high capacity for acquiring resistance genes, many strains of Acinetobacter baumannii have become Multi-Drug Resistant (MDR) or Extensively Drug-Resistant (XDR). The most concerning acquired resistance involves the production of carbapenemases, such as the OXA-type enzymes, which chemically neutralize powerful broad-spectrum antibiotics like meropenem. This enzymatic inactivation, combined with the physical barrier of the outer membrane, leaves few therapeutic options.
Infections often involve the respiratory tract, causing ventilator-associated pneumonia, or the bloodstream, leading to high mortality rates in compromised patients. The difficulty in treatment has led to the reintroduction of older, more toxic antibiotics, such as colistin, which are often reserved for these extensively resistant strains. However, resistance to colistin has begun to emerge, highlighting the organism’s adaptability and posing a significant public health threat.