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Bacterial Adaptation

Bacteria have been designed to be adaptable. Their surrounding layers and the genetic information for these and other structures associated with a bacterium are capable of alteration. Some alterations are reversible, disappearing when the particular pressure is lifted. Other alterations are maintained and can even be passed on to succeeding generations of bacteria.

The first antibiotic was discovered in 1929. Since then, a myriad of naturally occurring and chemically synthesized antibiotics have been used to control bacteria. Introduction of an antibiotic is frequently followed by the development of resistance to the agent. Resistance is an example of the adaptation of the bacteria to the antibacterial agent.

Antibiotic resistance can develop swiftly. For example, resistance to penicillin (the first antibiotic discovered) was recognized almost immediately after introduction of the drug. As of the mid 1990s, almost 80% of all strains of Staphylococcus aureus were resistant to penicillin. Meanwhile, other bacteria remain susceptible to penicillin. An example is provided by Group A Streptococcus pyogenes, another Gram-positive bacteria.

The adaptation of bacteria to an antibacterial agent such as an antibiotic can occur in two ways. The first method is known as inherent (or natural) resistance. Gram-negative bacteria are often naturally resistant to penicillin, for example. This is because these bacteria have another outer membrane, which makes the penetration of penicillin to its target more difficult. Sometimes when bacteria acquire resistance to an antibacterial agent, the cause is a membrane alteration that has made the passage of the molecule into the cell more difficult.

The second category of adaptive resistance is called acquired resistance. This resistance is almost always due to a change in the genetic make-up of the bacterial genome. Acquired resistance can occur because of mutation or as a response by the bacteria to the selective pressure imposed by the antibacterial agent. Once the genetic alteration that confers resistance is present, it can be passed on to subsequent generations. Acquired adaptation and resistance of bacteria to some clinically important antibiotics has become a great problem in the last decade of the twentieth century.

Bacteria adapt to other environmental conditions as well. These include adaptations to changes in temperature, pH, concentrations of ions such as sodium, and the nature of the surrounding support. An example of the latter is the response shown by Vibrio parahaemolyticus to growth in a watery environment versus a more viscous environment. In the more viscous setting, the bacteria adapt by forming what are called swarmer cells. These cells adopt a different means of movement, which is more efficient for moving over a more solid surface. This adaptation is under tight genetic control, involving the expression of multiple genes.

Bacteria react to a sudden change in their environment by expressing or repressing the expression of a whole lost of genes. This response changes the properties of both the interior of the organism and its surface chemistry. A well-known example of this adaptation is the so-called heat shock response of Escherichia coli. The name derives from the fact that the response was first observed in bacteria suddenly shifted to a higher growth temperature.

One of the adaptations in the surface chemistry of Gram-negative bacteria is the alteration of a molecule called lipopolysaccharide. Depending on the growth conditions or whether the bacteria are growing on an artificial growth medium or inside a human, as examples, the lipopolysaccharide chemistry can become more or less water-repellent. These changes can profoundly affect the ability of antibacterial agents or immune components to kill the bacteria.

Another adaptation exhibited by Vibrio parahaemolyticus, and a great many other bacteria as well, is the formation of adherent populations on solid surfaces. This mode of growth is called a biofilm. Adoption of a biofilm mode of growth induces a myriad of changes, many involving the expression of previously unexpressed genes. In addition,l de-activation of actively expressing genes can occur. Furthermore, the pattern of gene expression may not be uniform throughout the biofilm. Bacteria within a biofilm and bacteria found in other niches, such as in a wound where oxygen is limited, grow and divide at a far slower speed than the bacteria found in the test tube in the laboratory. Such bacteria are able to adapt to the slower growth rate, once again by changing their chemistry and gene expression pattern.

A further example of adaptation is the phenomenon of chemotaxis, whereby a bacterium can sense the chemical composition of the environment and either moves toward an attractive compound, or shifts direction and moves away from a compound sensed as being detrimental. Chemotaxis is controlled by more than 40 genes that code for the production of components of the flagella that propels the bacterium along, for sensory receptor proteins in the membrane, and for components that are involved in signaling a bacterium to move toward or away from a compound. The adaptation involved in the chemotactic response must have a memory component, because the concentration of a compound at one moment in time must be compared to the concentration a few moments later.



Alberts, et al. Molecular Biology of the Cell, 4th. ed New York: Garland Science, 2002.

Cullimore, Roy D. Practical Atlas for Bacterial Determination Boca Raton, FL: CRC Press, 2000.

Dyer, Betsey Dexter. A Field Guide to Bacteria. Ithaca, NY: Cornell University Press, 2003.

Groisman, Eduardo A. Principles of Bacterial Pathogenesis. Burlington, MA: Academic Press, 2000.

Koehler, T.M. Anthrax New York: Springer Verlag, 2002.

Walsh, Christopher. Antibiotics: Actions, Origins, Resistance. Washington, DC: American Society for Microbiology Press, 2003.


The Foundation for Bacteriology, New York University. "Virtual Museum of Bacteria" [cited February 5, 2003]. <http://www.bacteriamuseum.org/main1.shtml>.

Marc Kusinitz

Brian Hoyle


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—A viscous, gelatinous polymer composed either of polysaccharide, polypeptide, or both, that surrounds the surface of some bacteria cells. Capsules increase the disease-causing ability (virulence) of bacteria by inhibiting immune system cells called phagocytes from engulfing them.

Death phase

—Stage of bacterial growth when the rate of cell deaths exceeds the number of new cells formed and the population equilibrium shifts to a net reduction in numbers. The population may diminish until only a few cells remain, or the population may die out entirely.


—Toxic proteins produced during bacterial growth and metabolism and released into the environment.


—Short, hairlike, proteinaceous projections that may arise at the ends of the bacterial cell or over the entire surface. These projections let the bacteria adhere to surfaces.

Gram staining

—A method for classifying bacteria, developed in 1884 by Danish scientist Christian Gram, which is based upon a bacterium's ability or inability to retain a purple dye.

Koch's postulates

—A series of laboratory procedures, developed by German physician Robert Koch in the late nineteenth century, for proving that a specific organism cause a specific disease.

Lag phase

—Stage of bacterial growth in which metabolic activity occurs but no growth.

Log phase

—Stage of bacterial growth when metabolic activity is most intense and cell reproduction exceeds cell death. Also known as exponential phase.

Phage typing

—A method for identifying bacteria according to their response to bacteriophages, which are viruses that infect specific bacteria.


—Proteinaceous projections that occur singly or in pairs and join pairs of bacteria together, facilitating transfer of DNA between them.


—Spiral-shaped bacteria which live in contaminated water, sewage, soil and decaying organic matter, as well as inside humans and animals.

Stationary phase

—Stage of bacterial growth in which the growth rate slows and the production of new cells equals the rate of cell death.

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