Resistance is an example of the adaptation of the bacteria to the antibacterial agent
Bacteria can exchange genetic material via conjugation. Genetic recombination between bacteria (or protists) occurs via a cytoplasmic bridge between the organisms. A primitive form of exchange of genetic material between bacteria involving plasmids also can occur. Plasmids are small, circular, extra chromosomal DNA molecules that are capable of replication and are known to be capable of transferring genes among bacteria. For example, resistance plasmids carry genes for resistance to antibiotics from one bacterium to another, while other plasmids carry genes that confer pathogenicity. In addition, the transfer of genes via bacteriophages—viruses that speciﬁcally parasitize bacteria—also serves as a means of genetic recombination. Bioengineering uses sophisticated techniques to purposely transfer DNA from one organism to another in order to give the second organism new characteristics. For example, in a process called transformation, antibiotic susceptible bacteria that are induced to absorb manipulated plasmids placed in their environment can acquire resistance to that antibiotic substance due to the new genes they have incorporated. Similarly, in a process called transfection, specially constructed viruses are used to artiﬁcially inject bioengineered DNA into bacteria, giving infected cells some new characteristic.
Bacterial adaptation and resistance
Evolution has driven both bacterial diversity and bacterial adaptation. 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 Streptococcus pyogenes, other 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. Gramnegative 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. This is adaptation. 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 became 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. 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.
Another adaptation exhibited by a great many bacteria is the formation of adherent populations on solid surfaces. This mode of growth is called a 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. When presented with more nutrients, the bacteria can often very quickly resume the rapid growth and division rate of their test tube counterparts.
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 propel 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.
Bacteriocidal and bacteriostatic treatment of bacteria
Bacteriocidal is a term that refers to the treatment of a bacterium such that the organism is killed. Bacteriostatic refers to a treatment that restricts the ability of the bacterium to grow. Bacteriocidal methods include heat, ﬁltration, radiation, and the exposure to chemicals. The use of heat is a very popular method of sterilization in a microbiology laboratory. The dry heat of an open ﬂame incinerates microorganisms like bacteria, fungi and yeast. The moist heat of a device like an autoclave can cause deformation of the protein constituents of the microbe, as well as causing the microbial membranes to liquefy. The effect of heat depends on the time of exposure in addition to form of heat that is supplied. For example, in an autoclave that supplies a temperature of 121° F (49.4° C), an exposure time of 15 minutes is sufﬁcient to kill the so-called vegetative form of bacteria. However, a bacterial spore can survive this heat treatment.
More prolonged exposure to the heat is necessary to ensure that the spore will not germinate into a living bacteria after autoclaving. The relationship between the temperature and the time of exposure can be computed mathematically. A specialized form of bacteriocidal heat treatment is called pasteurization after Louis Pasteur, the inventor of the process. Pasteurization achieves total killing of the bacterial population in ﬂuids such as milk and fruit juices without changing the taste or visual appearance of the product. Another bacteriocidal process, albeit an indirect one, is ﬁltration. Filtration is the physical removal of bacteria from a ﬂuid by the passage of the ﬂuid through the ﬁlter. The ﬁlter contains holes of a certain diameter. If the diameter is less than the smallest dimension of a bacterium, the bacterium will be retained on the surface of the ﬁlter it contacts. The ﬁltered ﬂuid is sterile with respect to bacteria. Filtration is indirectly bactericidal since the bacteria that are retained on the ﬁlter will, for a time, be alive. However, because they are also removed from their source of nutrients, the bacteria will eventually die. Exposure to electromagnetic radiation such as ultraviolet radiation is a direct means of killing bacteria. The energy of the radiation severs the strands of deoxyribonucleic acid in many locations throughout the bacterial genome. With only one exception, the damage is so severe that repair is impossible. The exception is the radiation resistant bacterial genus called Deinococcus. This genus has the ability to piece together the fragments of DNA in their original order and enzymatic stitch the pieces into a functional whole.
Exposure to chemicals can be bacteriocidal. For example, the gas ethylene oxide can sterilize objects. Solutions containing alcohol can also kill bacteria by dissolving the membrane(s) that surround the contents of the cell. Laboratory benches are routinely “swabbed” with an ethanol solution to kill bacteria that might be adhering to the bench top. Care must be taken to ensure that the alcohol is left in contact with the bacteria for a suitable time (e.g., minutes). Otherwise, bacteria might survive and can even develop resistance to the bactericidal agent. Other chemical means of achieving bacterial death involve the alteration of the pH, salt or sugar concentrations, and oxygen level. Antibiotics are designed to be bacteriocidal. Penicillin and its derivatives are bactericidal because they act on the peptidoglycan layer of Gram-positive and Gram-negative bacteria.
By preventing the assembly of the peptidoglycan, penicillin antibiotics destroy the ability of the peptidoglycan to bear the stress of osmotic pressure that acts on a bacterium. The bacterium ultimately explodes. Other antibiotics are lethal because they prevent the manufacture of DNA or protein. Unlike bacteriocidal methods such as the use of heat, bacteria are able to acquire resistance to antibiotics. Indeed, such resistance by clinically-important bacteria is a major problem in hospitals. Bacteriostatic agents prevent the growth of bacteria. Refrigeration can be bacteriostatic for those bacteria that cannot reproduce at such low temperatures. Sometimes a bacteriostatic state is advantageous as it allows for the long-term storage of bacteria. Ultra-low temperature freezing and lyophilization (the controlled removal of water from a sample) are means of preserving bacteria. Another bacteriocidal technique is the storage of bacteria in a solution that lacks nutrients, but which can keep the bacteria alive. Various buffers kept at refrigeration temperatures can keep bacteria alive for weeks.
To be concluded…