Bacterial Structure in Relationship to Pathogenicity
Bacterial Structure in Relationship to Pathogenicity (page 1) of its membrane and cell envelope, including capsules, glycocalyx, S layers, The interdigitaion of these fibrils between neighboring cells of different chains can also be seen. Bacteria - Capsules and slime layers: Many bacterial cells secrete some The association of virulence and capsule formation is also found in many other. The bacterial capsule is a very large structure of many bacteria. It is a polysaccharide layer that Diversity. The capsule is found most commonly among gram-negative bacteria: Escherichia coli (in some "The capsule of Mycobacterium tuberculosis and its implications for pathogenicity". Tubercle and Lung Disease.
The presence of a capsule in Streptococcus pneumoniae is the most important factor in its ability to cause pneumonia.
Mutant strains of S. The association of virulence and capsule formation is also found in many other species of bacteria. Streptococcus mutanswhich causes dental cariessplits the sucrose in food and uses one of the sugars to build its capsule, which sticks tightly to the tooth. The bacteria that are trapped in the capsule use the other sugar to fuel their metabolism and produce a strong acid lactic acid that attacks the tooth enamel. When Pseudomonas aeruginosa colonizes the lungs of persons with cystic fibrosisit produces a thick capsular polymer of alginic acid that contributes to the difficulty of eradicating the bacterium.
Bacteria of the genus Zoogloea secrete fibres of cellulose that enmesh the bacteria into a floc that floats on the surface of liquid and keeps the bacteria exposed to air, a requirement for the metabolism of this genus. A few rod-shaped bacteria, such as Sphaerotilus, secrete long chemically complex tubular sheaths that enclose substantial numbers of the bacteria.
The sheaths of these and many other environmental bacteria can become encrusted with iron or manganese oxides. Streptococcus mutans, a bacteria found in the mouth, contributes to tooth decay. Swimming and swarming bacteria possess flagellawhich are the extracellular appendages needed for motility. Flagella are long, helical filaments made of a single type of protein and located either at the ends of rod-shaped cells, as in Vibrio cholerae or Pseudomonas aeruginosa, or all over the cell surface, as in Escherichia coli.
Flagella can be found on both gram-positive and gram-negative rods but are rare on cocci and are trapped in the axial filament in the spirochetes.
The flagellum is attached at its base to a basal body in the cell membrane. The protomotive force generated at the membrane is used to turn the flagellar filament, in the manner of a turbine driven by the flow of hydrogen ions through the basal body into the cell. Specific Virulence Factors The virulence factors of bacteria can be divided into a number of functional types. These are discussed in the following sections: Adherence and Colonization Factors To cause infection, many bacteria must first adhere to a mucosal surface.
For example, the alimentary tract mucosa is continually cleansed by the release of mucus from goblet cells and by the peristaltic flow of the gut contents over the epithelium. Similarly, ciliated cells in the respiratory tract sweep mucus and bacteria upward.
In addition, the turnover of epithelial cells at these surfaces is fairly rapid. The intestinal epithelial cell monolayer is continually replenished, and the cells are pushed from the crypts to the villar tips in about 48 hours. To establish an infection at such a site, a bacterium must adhere to the epithelium and multiply before the mucus and extruded epithelial cells are swept away. To accomplish this, bacteria have evolved attachment mechanisms, such as pili fimbriaethat recognize and attach the bacteria to cells see Ch.
Colonization factors as they are often called are produced by numerous bacterial pathogens and constitute an important part of the pathogenic mechanism of these bacteria. Some examples of piliated, adherent bacterial pathogens are V.
Invasion Factors Mechanisms that enable a bacterium to invade eukaryotic cells facilitate entry at mucosal surfaces. Some of these invasive bacteria such as Rickettsia and Chlamydia species are obligate intracellular pathogens, but most are facultative intracellular pathogens Fig. The specific bacterial surface factors that mediate invasion are not known in most instances, and often, multiple gene products are involved. Some Shigella invasion factors are encoded on a megadalton plasmid, which, when conjugated into E.
Other invasion genes have also recently been identified in Salmonella and Yersinia pseudotuberculosis. The mechanisms of invasion of Rickettsia, and Chlamydia species are not well known. Capsules and Other Surface Components Bacteria have evolved numerous structural and metabolic virulence factors that enhance their survival rate in the host.
Capsule formation has long been recognized as a protective mechanism for bacteria see Ch. Encapsulated strains of many bacteria e. Organisms that cause bacteremia e. Serum resistance may be related to the amount and composition of capsular antigens as well as to the structure of the lipopolysaccharide.
The relationship between surface structure and virulence is important also in Borrelia infections. As the bacteria encounter an increasing specific immune response from the host, the bacterial surface antigens are altered by mutation, and the progeny, which are no longer recognized by the immune response, express renewed virulence.
Salmonella typhi and some of the paratyphoid organisms carry a surface antigen, the Vi antigen, thought to enhance virulence. This antigen is composed of a polymer of galactosamine and uronic acid in 1,4-linkage. Its role in virulence has not been defined, but antibody to it is protective.
Some bacteria and parasites have the ability to survive and multiply inside phagocytic cells. A classic example is Mycobacterium tuberculosis, whose survival seems to depend on the structure and composition of its cell surface.
The parasite Toxoplasma gondii has the remarkable ability to block the fusion of lysosomes with the phagocytic vacuole. The hydrolytic enzymes contained in the lysosomes are unable, therefore, to contribute to the destruction of the parasite. The mechanism s by which bacteria such as Legionella pneumophila, Brucella abortus, and Listeria monocytogenes remain unharmed inside phagocytes are not understood. Endotoxins Endotoxin is comprised of toxic lipopolysaccharide components of the outer membrane of Gram-negative bacteria see Ch.
Endotoxin exerts profound biologic effects on the host and may be lethal. Because it is omnipresent in the environment, endotoxin must be removed from all medical supplies destined for injection or use during surgical procedures. The term endotoxin was coined in by Pfeiffer to distinguish the class of toxic substances released after lysis of bacteria from the toxic substances exotoxins secreted by bacteria. Few, if any, other microbial products have been as extensively studied as bacterial endotoxins.
Perhaps it is appropriate that a molecule with such important biologic effects on the host, and one produced by so many bacterial pathogens, should be the subject of intense investigation.
Structure of Endotoxin Figure illustrates the basic structure of endotoxin. Endotoxin is a molecular complex of lipid and polysaccharide; hence, the alternate name lipopolysaccharide.
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Figure Basic structure of endotoxin lipopolysaccharide from Gram-negative bacteria. The structure of endotoxin molecules from Salmonella spp. Enough data on endotoxin from other Gram-negative organisms have been gathered to reveal a common pattern with genus and species diversity.Virulence factors of bacteria
Although all endotoxin molecules are similar in chemical structure and biologic activity, some diversity has evolved. Purified endotoxin appears as large aggregates. The molecular complex can be divided into three regions Fig.
The polysaccharide portions are responsible for antigenic diversity, whereas the lipid A moiety confers toxicity. Dissociation of the complex has revealed that the polysaccharide is important in solubilizing the toxic lipid A component, and in the laboratory it can be replaced by carrier proteins e.
Members of the family Enterobacteriaceae exhibit O-specific chains of various lengths, whereas N. Some investigators working on the latter forms of endotoxin prefer to call them lipooligosaccharides to emphasize the chemical difference from the endotoxin of the enteric bacilli.
Nevertheless, the biologic activities of all endotoxin preparations are essentially the same, with some being more potent than others. Biologic Activity of Endotoxin The biologic effects of endotoxin have been extensively studied.
Purified lipid A conjugated to bovine serum albumin and endotoxin elicit the same biologic responses. Table lists some of the biologic effects of endotoxin. The more pertinent toxic effects include pyrogenicity, leukopenia followed by leukocytosis, complement activation, depression in blood pressure, mitogenicity, induction of prostaglandin synthesis, and hypothermia. These events can culminate in sepsis and lethal shock.
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However, it should be noted from Table that not all effects of endotoxin are necessarily detrimental; several induce responses potentially beneficial to the host, assuming the stimulation is not excessive. For example, the toxicity of endotoxin is largely attributed to lipid A, attached to a polysaccharide carrier.
The toxicity of lipid A is markedly reduced after hydrolysis of a phosphate group or deacylation of one or more fatty acids from the lipid A molecule. Clinical trials are in progress to test a monophosphoryl lipid A for its potential of inducing low dose tolerance to endotoxin. Tolerance to endotoxin can be achieved by pretreatment of an animal with low doses of endotoxin or a detoxified lipid A derivative before challenge with high doses of endotoxin.
Experimental studies have demonstrated that induction of tolerance to endotoxin reduces the dangerous effects of endotoxin. It is hoped that these relatively nontoxic lipid A derivatives may be useful in reducing the severity of bacterial sepsis in which bacterial endotoxin produces a life-threatening clinical course. Endotoxin, which largely accumulates in the liver following injection of a sublethal dose by the intravenous route, can be devastating because of its ability to affect a variety of cell and host proteins.
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Kupffer cells, granulocytes, macrophages, platelets, and lymphocytes all have a cell receptor on their surface called CD14, which binds endotoxin.
Endotoxin binding to the CD14 receptor on macrophages is enhanced by interaction with a host protein made in the liver i. The extent of involvement of each cell type probably depends on the level of endotoxin exposure. The effects of endotoxin on such a wide variety of host cells result in a complex array of host responses that can culminate in the serious condition gram-negative sepsis, which often leads to shock and death.
The effects of endotoxin on host cells are known to stimulate prostaglandin synthesis and to activate the kallikrein system, the kinin system, the complement cascade via the alternative pathway, the clotting system, and the fibrinolytic pathways. When these normal host systems are activated and operate out of control, it is not surprising that endotoxin can be lethal. Although it is difficult to comprehend the mechanisms of all the cell responses and the myriad sequelae of the cell mediators released rather indiscriminately in the host following exposure to endotoxin, it does seem clear that the host cellular response to endotoxin, rather than a direct toxic effect of endotoxin, plays the major role in causing tissue damage Fig.
Detection of Endotoxin in Medical Solutions Endotoxin is omnipresent in the environment. It is found in most deionized-water lines in hospitals and laboratories, for example, and affects virtually every biologic assay system ever examined.
It tends to be a scapegoat for all biologic problems encountered in the laboratory, and, many times, this reputation is deserved. Because of its pyrogenic and destructive properties, extreme care must be taken to avoid exposing patients to medical solutions containing endotoxin.
Even though all supplies should be sterile, solutions for intravenous administration can become contaminated with endotoxin-containing bacteria after sterilization as a result of improper handling. Furthermore, water used in the preparation of such solutions must be filtered through ion exchange resins to remove endotoxin, because it is not removed by either autoclave sterilization or filtration through bacterial membrane filters.
If endotoxin-containing solutions were used in such medical procedures as renal dialysis, heart bypass machines, blood transfusions, or surgical lavage, the patient would suffer immediate fever accompanied by a rapid and possibly lethal alterations in blood pressure. Solutions for human or veterinary use are prepared under carefully controlled conditions to ensure sterility and to remove endotoxin.
Representative samples of every manufacturing batch are checked for endotoxin by one of two procedures: The rabbit pyrogenicity test is based on the exquisite sensitivity of rabbits to the pyrogenic effects of endotoxin. A sample of the solution to be tested usually is injected intravenously into the ear veins of adult rabbits while the rectal temperature of the animal is monitored. Careful monitoring of the temperature responses provides a sensitive and reliable indicator of the presence of endotoxin and, importantly, one measure of the safety of the solution for use in patients.
The Limulus lysate test is more common and less expensive. It is so sensitive, however, that trace quantities of endotoxin in regular deionized water often obscure the results.