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Unit 11-Lesson 2: Bacterial Pathogenicity
Terms in this set (39)
Describe how the following properties of bacteria contribute to pathogenicity: capsules, cell wall components, and enzymes.
Capsules; this property increases the virulence of the species; the capsule resists the host's defenses by impairing phagocytosis
- Phagocytosis; the process by which certain cells of the body engulf and destroy microbes
- e.g. Streptococcus pneumoniae, the causative agent of pneumococcal pneumonia
Cell wall components; cell walls of certain bacteria contain chemical substances that contribute to virulence
- M protein; a heat-resistant and acid-resistant protein that mediates attachment of bacterium to epithelial cells of the host and helps bacterium to resist phagocytosis by white blood cells e.g. Streptococcus pyrogenes
- Fibriae and Opa (an outer membrane protein) to attach to host cells e.g. Neisseria gonorrhea
- Waxy lipid (mycolic acid) also increases virulence by resisting digestion by phagocytosis and can even multiply inside phagocytes e.g. Mycobacterium tuberculosis
Enzymes; extracellular enzymes (exoenzymes) that can digest materials between cells and form or digest blood clots, among other functions.
Explain the function and effects on pathogenic mechanisms of the following enzymes: hemolysins, coagulases, bacterial kinases, hyaluronidase, and collagenase.
Hemolysins; or haemolysins are lipids and proteins that cause lysis of red blood cells by destroying their cell membrane.
Coagulases; bacterial enzymes that coagulate (clot) the fibrinogen in blood. Fibrinogen, a plasma protein produced by the liver, is converted by coagulases into fibrin, the threads that form a blood clot. The fibrin clot may protect the bacterium from phagocytosis and isolate it from other defenses of the host.
Bacterial kinases; bacterial enzymes that break down fibrin and thus digest clots formed by the body to isolate the infection.
Hyaluronidase; it hydrolyzes hyaluronic acid, a type of polysaccharide that holds together certain cells of the body, particularly cells in connective tissue. This digesting action is thought to be involved in the tissue blackening of infected wounds and to help the microorganism spread from its initial site of infection.
Collagenase; produced by several species of Clostridium, facilitates the spread of gas gangrene. Collagenase breaks down the protein collagen, which forms the connective tissue of muscles and other body organs and tissues.
Distinguish between localized and remote damage of host cells by pathogenic bacteria.
Some bacteria cause localized damage in that they damage the host in the area where infection occurs. For example, a skin infection can damage host tissues at the site of infection.
Some bacteria secrete toxins or release LPS from the cell wall that may travel through the bloodstream and damage the host at sites far away from the location of infection.
Explain how direct damage of host cells by pathogenic bacteria occurs. How can other tissues also be damaged?
-once microbe invades body tissue- initially encounters phagocytes of host
-if phagocytes destroy invader- no further damage done to host
-if pathogen overcomes host's defenses- microbes can damage host cell in 4 basic ways:
1. By using host's nutrients
2. By causing direct damage in the immediate vicinity of the invasion
3. Producing toxins, transported by blood and lymph that damage sites far removed from original site of invasion
4. By inducing hypersensitivity reactions (discussed in Ch. 19- we will only discuss first 3 mechanisms)
Using the Host's Nutrients: Siderophores
-iron- required for growth of most pathogenic bacteria
-conc of free iron in body is low b/c most iron is tightly bound to iron-transport proteins (lactoferrin, transferrin, ferritin, hemoglobin)
-to obtain free iron, some pathogens secrete proteins called siderophores
Bacterial iron-binding proteins.
-when pathogens need iron- siderophores are released into medium where they take iron away from iron-transport proteins by binding the iron even more tightly.
-iron-siderophore complex is formed- then its taken up by siderophore receptors on bacterial surface.
-iron is then brought into bacterium.
-some cases: iron is released from complex to enter bacterium- other cases: iron enters as part of the complex.
-alternative to iron acquisition by siderophores, some pathogens have receptors that bind directly to iron-transport proteins and hemoglobin.
-taken into bacterium directly along w/ iron
-also possible that some bacteria produce toxins when iron levels are low.
-toxins kill host cells, releasing their iron- making it available to bacteria.
-after pathogen attaches, they can cause direct damage as pathogen uses host cell for nutrients and prouduces waste products
-as pathogens metabolize and multiply in cells, cell usually ruptures
-many viruses and intracellular bacteria & protozoa are released when cell ruptures
-following release- pathogens can spread to other tissues in even greater numbers
-E. coli, Shigella, Salmonella, Neisseria gonorrhoeae- can induce host epithelial cells to engulf them by process that resembles phagocytosis.
-pathogens can disrupt host cells as they pass through and can then be extruded from host cell by a reverse phagocytosis process- enabling them to enter host cells.
-some can also penetrate host cells by excreting enzymes and by their own motility- such penetration can itself damage the host cell.
-most damage by bacteria is done by toxins
Production of Toxins
-Toxins- poisonous substances that are produced by certain microbes
-often primary factor contributing to pathogenic properties of those microbes
-Toxigenicity- capacity of microbes to produce toxins.
-toxins- transported by blood or lymph- can be serious and sometimes fatal
-some produce fever, cardiovascular disturbances, diarrhea, and shock
-can also inhibit protein synthesis, destroy blood cells and vessels, and disrupt the nervous system by causing spasms.
-nearly 40% cause disease by damaging eukaryotic cell membranes.
-Toxemia- refers to presence of toxins in the blood.
-toxins are of 2 general types, based on their position relative to microbial cell: exotoxins and endotoxins.
Exotoxins; are produced inside some bacteria as part of their growth and metabolism and are secreted by the bacterium into the surrounding medium or released following lysis
- Exotoxins are proteins, and many are enzymes that catalyze only certain biochemical reactions.
- Because of the enzymatic nature of most exotoxins, even small amounts are quite harmful because they can act over and over again.
- Bacteria that produce exotoxins may be gram-positive or gram-negative.
- Carried on bacterial plasmids or phages
- Are soluble in body fluids, and therefore can easily diffuse into the blood and rapidly transported throughout the body.
- Work by destroying particular parts of the host's cells or by inhibiting certain metabolic functions.
- They are highly specific in their effects on body tissues.
- Diseases caused by bacteria that produce exotoxins are often caused by minute amounts of exotoxins, not by the bacteria themselves.
- It is the exotoxins that produce the specific signs and symptoms of the disease. Thus, exotoxins are disease-specific.
Examples: botulinum toxin (Clostridrium botulinum), Vibrio enterotoxin (Vibrio cholerae)
-Neurotoxin prevents the transmission of nerve impulses; flaccid paralysis results
-Neurotoxin blocks nerve impulses to muscle relaxation pathway; results in uncontrollable muscle contractions
-Cytotoxin inhibits protein synthesis, especially in nerves, heart and kidney cells
-enterotoxin- causes secretion of large amounts of fluids and electroyltes that result in diarrhea
-Enterotoxigenic Escherichia coli and Shigella spp.
-Enterotoxin causes secretion of large amounts of fluids and electrolytes that result in diarrhea
Two A components enter the cell via the same B. The A proteins cause shock and reduce the immune response
Gas Gangrene and food poisoning
-Clostridium perfringens and other species of Clostridium
-Membrane disrupting exotoxin
-One exotoxin (cytotoxin) causes massive RBC destruction (hemolysis); another exotoxin (enterotoxin) is related to food poisoning and causes diarrhea.
-Enterotoxin causes secretion of fluids and electrolytes that results in diarrhea; cytotoxin disrupts host cytoskeleton
-Enterotoxin causes secretion of fluids and electrolytes that results in diarrhea
Toxic Shock Syndrome (TSS)
-Toxin causes secretion of fluids and elecrolytes from capillaries that decreases blood volume and lowers blood pressure
Antitoxins and Taxoids
-body produces antibodies called antitoxins that provide immunity to exotoxins.
-when exotoxins are inactivated by heat or by formaldehyde, iodine, or other chemicals, they no longer cause the disease but can still stimulate the body to produce antitoxins.
-altered exotoxins are called Taxoids
-when toxoids are injected into body as a vaccine, they stimulate antitoxin production (so immunity is produced)
-Diptheria and tetanus can be prevented by taxoid vaccination
-named on basis of several characteristic:
-one is the type of host cell that is attacked
-neurotoxin-attacks nerve cells
-cardiotoxins-attack heart cells
-hepatotoxins- attack liver cells
-leukotoxins- attack leukocytes
-enterotoxins- attack lining of GI tract
-cytotoxins-attack a wide variety of cells.
-some are named after diseases with which they are associated:
-diptheria toxin (causes diphtheria)
-tetanus toxin (causes tetanus)
-some are named for specific bacterium that produces them.
-botulinum toxin (Clostridium botulinum)
-Vibrio enterotoxin (Vibrio cholera)
Endotoxin; are part of the outer portion of the cell wall of gram-negative bacteria
- Gram-negative bacteria
▪ They have an outer membrane surrounding the peptidoglycan layer of the cell wall. This outer membrane consists of lipoproteins, phospholipids, and lipopolysaccharides (LPSs). The lipid portion of LPS, called lipid A, is the endotoxin.
- Endotoxins are lipopolysaccharides, whereas exotoxins are proteins.
- Endotoxins are released when gram-negative bacteria die and their cell walls undergo lysis, thus liberating the endotoxin; and also during bacterial multiplication
exotoxins vs endotoxins
Relation to microorganisms:
Exotoxin: metabolic product of growing cell
Endotoxin: Present in LPS of outer membrane of cell wall and released w/ destruction of cell or during cell division
Exotoxin: Proteins, usually with 2 parts (A-B)
Endotoxin- Lipid portion (Lipid A) of LPS of outer membrane
Pharmacology (effect on body)
Exotoxin: specific for a particular cell structure or function in the host (mainly affects cell functions, nerves, and GI tract)
Endotoxin: General, such as fever, weaknesses, aches, and shock; all produce the same effects
Exotoxin: Unstable; can usually be destroyed at 60-80 degrees C (except staphylococcal enterotoxin)
Endotoxin: Stable; can withstand autoclaving (121 degrees C for 1 hr)
Toxicity(ability to cause disease)
Immunology (relation to antibodies)
Exotoxin: can be converted to toxoidsto immunize against toxin;
neutralized by antitoxin
Endotoxin: not easily neutralized by antitoxin; therefore, effective toxoids cannot be made to immunize against toxin
Endotoxin: Considerably Larger
Exotoxin: Gas Gangrene, tetanus, botulism, diptheria, scarlet fever
Endotoxin: Typhoid Fever, UTI, and meningococcal meningitis
List diseases or clinical manifestations caused by endotoxins and exotoxins.
Diseases caused by exotoxins; gas gangrene, tetanus, botulism, diphtheria, scarlet fever, scalded skin syndrome, cholera, traveler's diarrhea, anthrax, toxic shock syndrome
Clinical manifestation; no fever, paralysis, convulsions, lockjaw, secretion of large amounts of fluids and electrolytes
Diseases caused by endotoxins; typhoid fever, urinary tract infections, meningococcal meningitis
Clinical manifestation; fever, chills, weakness, generalized aches, shock and even death, miscarriage, blood clots
A-B Toxins- consist of 2 parts designated A and B, both of which are polypeptides.
-Most exotoxins are A-B toxins.
-A part is the active (enzyme) component
-B part is the binding component
-example of A-B toxin- diptheriatoxin
- Examples: Corynebacterium diphtheriae, Clostridium botulinum
• In the first step, the A-B toxin is released from the bacterium.
• The B componentattaches to a host cell receptor.
• The plasma membrane of the host cell invaginates (folds inward) at the point where the A-B exotoxin and plasma receptor make contact, and the exotoxin enters the cell by receptor-mediated endocytosis.
• The A-B exotoxin and receptor are enclosed by a pinched-off portion of the membrane.
• The A-B components of the exotoxin separate. The A component alters the function of the host cell, often by inhibiting protein synthesis. The B component is released from the host cell, and the receptor is inserted into the plasma membrane for reuse.
How does toxigenicity differ from direct damage?
Toxigenicity is the capacity of microorganism to produce toxins
- Toxins transported by the blood or lymph can cause serious and sometimes fatal effects (remote damage)
Direct damage - is local damage once pathogens attach to host cells and use the host cell for nutrients and produce waste products
How are capsules and cell wall components related to pathogenicity? Give specific examples.
Encapsulated bacteria can resist phagocytosis and continue growing.
Streptococcus pneumoniae and Klebsiella pneumoniae produce capsules that are related to their virulence.
M protein found in the cell walls of Streptococcus pyogenes and A protein in the cell walls of Staphylococcus aureus help these bacteria resist phagocytosis.
-capsule resists host's defenses by impairing phagocytosis- process by which cells of body engulf and destroy microbes
-chemical nature of capsule- prevents phagocytic cell from adhering to bacterium.
Cell wall components:
-cell walls of certain bacteria contain chemical substances that contribute to virulence.
-ex Streptococcus pyogenes- produces heat-resistant and acid-resistant protein called M Protein
-protein is found on both cell surface and fimbriae
-mediates attachment of the bacterium to epithelial cells of the host and
-helps the bacterium resist phagocytosis by white blood cells.
-protein- increases virulence
-immunity of S. pyogenes- depends on body's production of antibodies specific to M protein.
-Neisseria gonorrhoeae- grows inside human epithelial cells & leukocytes
-these bacteria- use fimbriae and an outer membrane protein called Opa to attach to host cells.
-following attachment by both Opa and fimbriae- host cells take in bacteria
-Waxy lipid (mycolic acid) that makes up cell wall of Mycobacterium tuberculosis- also increases virulence- resists digestion by phagocytes. Can even multiply inside phagocytes.
Describe how hemolysins, leukocidins, coagulase, kinases, hyaluronidase, siderophores, and IgA proteases might contribute to pathogenicity.
-Hemolysins lyse red blood cells; hemolysis might supply nutrients for bacterial growth.
-Leukocidins destroy neutrophils and macrophages that are active in phagocytosis; this decreases host resistance to infection.
-Coagulase causes fibrinogen in blood to clot; the clot may protect the bacterium from phagocytosis and other host defenses.
-Bacterial kinases break down fibrin; kinases can destroy a clot that was made to isolate the bacteria, thus allowing the bacteria to spread.
-Hyaluronidase hydrolyzes the hyaluronic acid that binds cells together; this could allow the bacteria to spread through tissues.
-Siderophores take iron from host iron-transport proteins, thus allowing bacteria to get iron for growth.
- IgA proteases destroy IgA antibodies; IgA antibodies protect mucosal surfaces.
Compare and contrast the following aspects of endotoxins and exotoxins: bacterial source, chemistry, toxicity, and pharmacology. Give an example of each toxin.
Explain whether each of the following examples is a food infection or intoxication. What is the probable etiological agent in each case?
• a. Eighty-two people who ate shrimp in Louisiana developed diarrhea, nausea, headache, and fever from 4 hours to 2 days after eating.
• b. Two people in Vermont who ate barracuda caught in Florida developed malaise, nausea, blurred vision, breathing difficulty, and numbness 3 to 6 hours after eating.
a. Intoxication-An intoxication results when a person eats food containing toxins that cause illness. Toxins are produced by harmful microorganisms, the result of a chemical contamination, or are naturally part of a plant or seafood (THE SHRIMP). Some bacteria cause an intoxication. Viruses and parasites do not cause foodborne intoxication.
Probably etiological agent- vibrio spp. -V. parahaemolyticus (prefer warm coastal areas)
b. Infection-Foodborne infection is caused by the ingestion of food containing live bacteria which grow and establish themselves in the human intestinal tract.
Ciguatera is a foodborne illness caused by eating certain reef fish whose flesh is contaminated with a toxin made by dinoflagellates such as Gambierdiscus toxicus which live in tropical and subtropical waters.
How Microorganisms Enter a Host (pp. 430-433)
• 1. The specific route by which a particular pathogen gains access to the body is called its portal of entry.
Portals of Entry (p. 430)
• 2. Many microorganisms can penetrate mucous membranes of the conjunctiva and the respiratory, gastrointestinal, and genitourinary tracts.
• 3. Most microorganisms cannot penetrate intact skin; they enter hair follicles and sweat ducts.
• 4. Some microorganisms can gain access to tissues by inoculation through the skin and mucous membranes in bites, injections, and other wounds. This route of penetration is called the parenteral route.
The Preferred Portal of Entry (pp. 430-431)
• 5. Many microorganisms can cause infections only when they gain access through their specific portal of entry.
Numbers of Invading Microbes (p. 432)
• 6. Virulence can be expressed as LD50 (lethal dose for 50% of the inoculated hosts) or ID50 (infectious dose for 50% of the inoculated hosts).
Adherence (pp. 432-433)
• 7. Surface projections on a pathogen called adhesins (ligands) adhere to complementary receptors on the host cells.
• 8. Adhesins can be glycoproteins or lipoproteins and are frequently associated with fimbriae.
• 9. Mannose is the most common receptor.
• 10. Biofilms provide attachment and resistance to antimicrobial agents.
• 1. Some pathogens have capsules that prevent them from being phagocytized.
Cell Wall Components
• 2. Proteins in the cell wall can facilitate adherence or prevent a pathogen from being phagocytized.
• 3. Local infections can be protected in a fibrin clot caused by the bacterial enzyme coagulase.
• 4. Bacteria can spread from a focal infection by means of kinases (which destroy blood clots), hyaluronidase (which destroys a mucopolysaccharide that holds cells together), and collagenase (which hydrolyzes connective tissue collagen).
• 5. IgA proteases destroy IgA antibodies.
• 6. Some microbes vary expression of antigens, thus avoiding the host's antibodies.
Penetration into the Host Cell Cytoskeleton
• 7. Bacteria may produce proteins that alter the actin of the host cell's cytoskeleton allowing bacteria into the cell.
How Bacterial Pathogens Damage Host Cells
Using the Host's Nutrients: Siderophores
• 1. Bacteria get iron from the host using siderophores.
• 2. Host cells can be destroyed when pathogens metabolize and multiply inside the host cells.
The Production of Toxins
• 3. Poisonous substances produced by microorganisms are called toxins; toxemia refers to the presence of toxins in the blood. The ability to produce toxins is called toxigenicity.
• 4. Exotoxins are produced by bacteria and released into the surrounding medium. Exotoxins, not the bacteria, produce the disease symptoms.
• 5. Antibodies produced against exotoxins are called antitoxins.
• 6. A-B toxins consist of an active component that inhibits a cellular process and a binding component that attaches the two portions to the target cell, e.g., diphtheria toxin.
• 7. Membrane-disrupting toxins cause cell lysis, e.g., hemolysins.
• 8. Superantigens cause release of cytokines, which cause fever, nausea, and other symptoms; e.g., toxic shock syndrome toxin.
• 9. Endotoxins are lipopolysaccharides (LPS), the lipid A component of the cell wall of gram-negative bacteria.
• 10. Bacterial cell death, antibiotics, and antibodies may cause the release of endotoxins.
• 11. Endotoxins cause fever (by inducing the release of interleukin-1) and shock (because of a TNF-induced decrease in blood pressure).
• 12. Endotoxins allow bacteria to cross the blood-brain barrier.
• 13. The Limulus amebocyte lysate (LAL) assay is used to detect endotoxins in drugs and on medical devices.
Plasmids, Lysogeny, and Pathogenicity
• 14. Plasmids may carry genes for antibiotic resistance, toxins, capsules, and fimbriae.
• 15. Lysogenic conversion can result in bacteria with virulence factors, such as toxins or capsules.
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