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54 Cards in this Set
- Front
- Back
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Symbiosis
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A close and permanent relationship between organisms.
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Mutualism
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Beneficial to both Bacteria and Host
Examples. 1. Bacteria in the gut of termites/cows allow digestion of cellulose |
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Commensalims
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Beneficial for the bacteria and neutral benefit for the host.
1. Commensels can prevent colonization by more harmful bacteria. |
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Opportunistic Pathogens
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Most organisms pathogenic or opportunistic
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Resident and Transient Flora
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1. Resident - Present throughout the life of the host
2. Transient - Present at certain times during the life of the host. |
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Mutualism
Bacteriodes thetaiotaomicron |
1. 1000x more abundant in intestinal tract than E. coli.
2. Increases in numbers post weaning off mother’s milk. 3. Break down indigestible complex carbohydrates. 4. Help absorption of vitamins. 5. 100/25,000 mice genes turned on by the presence of B. thetaiotaomicron. 6. Host recognizes Bacteriodes thetaiotaomicron and secretes fucose as energy source for bacteria. If detection occurs during weaning, fucose will be secreted throughout the life of host even in absence of Bacteriodes thetaiotaomicron. |
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Mutualism
Bifidobacterium longum |
1. Present in large numbers while weaned on mother’s milk.
2. During this stage organism breaks down complex sugars found in milk. 3. End products absorbed by host. 4. Later in life of host Bifidobacterium longum decreases in numbers. 5. During this stage organism breaks down compounds found in plant gums. |
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Pathogenesis
Entry |
1. Most microbial infections begin at the mucous membranes of the respiratory, alimentary or genitourinary tract.
2. Considerable evidence indicates bacteria adhere specifically to epithelial cells. |
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Pathogenesis
Entry Adherence Tissue Specificity |
A pathogenic microbe does not adhere to all epithelial tissue equally but selectively adheres to tissues where it normally gains entrance into the host.
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Pathogenesis
Entry Adherence Host Specificity |
A strain of microorganism which infects human will adhere more strongly to appropriate epithelial tissue in human host than epithelial tissue in an unrelated species such as the rat
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Pathogensis
Colonization Def and Factors of Growth |
1. The multiplication of bacterium
2. Factors A. MOST Important - availability of nutrients B. Temperature C. pH D. Reduction potential E. Possibly availability of free iron |
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Virulence and Virulence Factors
Definitions |
1. Virulence - the relative ability of a pathogen to harm the host
2. Virulence Factors - Extracellular proteins aid in the establishment and invasiveness of disease. |
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Virulence Factors
Hyaluronidase |
enzyme which breaks down hyualuronic acid, a polysaccharide which cements cells together.
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Virulence Factors
Streptokinase |
fibrinolytic substance which dissolves blot clots. (A host defense against certain microbes is to wall them off with fibrin clots)
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Virulence Factors
Coagulase |
causes fibrin to be deposited on the surface of the microbe possibly concealing the organism from host immune system.
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Virulence Factors
Cytolytic Toxins |
proteins which act on the cell membrane causing cell lysis.
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Virulence Factors
Hemolysins (lecithinases or phospholipidases) |
proteins which lyse red blood cells in diagnostic tests, kills the cell through cytoplasmic invasion
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Diseases Terms
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1. Acute Disease - rapid onset of symptoms eventually reaching covalescence
2. Chronic Disease - prolonged development of symptoms. 3. Subclinical Infection - Shows no symptoms 4. LD50 - Lethal dose for 50% of test animals 5. ID50 - Infectious does for 50% of test animals. |
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Streptococcus pyogenes
Classification Hemolytic Groups |
1. Alpha-hemolytic streptococci-partial lysis of RBC
2. Beta- total lysis of RBC (S. pyogenes) 3. Gamma- no lysis |
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Streptococcus pyogenes
Causes |
1. Strep Throat
2. Scarlet Fever - Sore throat and skin rash 3. Rhematic Fever - Fever and inflamation of blood vessels 4. Rheumatic Heart Disease - attacks heart valve 5. Glomerulonephritis - Kidney inflamation 6. Erypselas - Infection of skin wounds 7. Necrotizing fascitis - putrifying ulcer 8. Puerperal sepsis - Uterus tissue infected during pregnancy |
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Streptococcus pyogenes
Virulence Factors Hyaluronic Acid capsule |
prevents phagocytosis, allows for penetration of tissues.
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Streptococcus pyogenes
Virulence Factors Hyaluronidase |
degrades hyaluronic acid that cements cells together.
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Streptococcus pyogenes
Virulence Factors M Protein |
degrades opsonin C3b.
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Streptococcus pyogenes
Virulence Factors C5a peptidase |
degrades compliment protein C5a preventing attraction of phagocytes to site of infection
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Streptococcus pyogenes
Virulence Factors F Protein |
Allows attachment of surface of epithelial cells
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Streptococcus pyogenes
Virulence Factors G Protein |
Binds to Fc region IgG inhibiting opsonization, compliment cascade, antibody mediated cellular cytotoxicity
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Mycobacterium tuberculosis
Causes Tuberculous |
1. Acid fast bacilli
2. Nonmotile 3. Disease of malnourished people in close urban settings. 4. Symptoms; chronic cough, chest pain, high fever, rust colored sputum (10%). 5. Multiply in macrophages, transported throughout lymphatic system. |
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Mycobacterium tuberculosis
Tubercle |
1. Wall of cells, calcium salts, fibrous material.
2. Accumulate at site of infection. 3. Destroys tissue, may break off and spread throughout lung and to other regions. |
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Streptococcus pneumoniae
Causes Pneumonia |
1. G+ encapsulated diplococci. Capsule interferes with C3b.
2. Alpha hemolytic. 3. 90 strains identified. 4. Causes inflammatory response- phagocytes in area of infection. 5. Organisms multiply within macrophages, remain in lung tissue. 6. Results in fluid build up that can be seen on x-ray. 7. Symptoms - high fever, sharp pains, difficulty breathing |
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Mycoplasma pneumoniae
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1. 0.2 microns
2. Pleomorphic- changes shape. 3. Mycoplasma lack cell wall. 4. Attaches to receptor in alveolar tissue. 5. Interferes with action of cilia. Ciliated cells slough off. 6. Symptoms- fever, fatigue, dry hacking cough. 7. 15% cases have middle ear infection. After 1 week incubation, symptoms appear. Infectious several weeks after |
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Klebsiella pneumonia
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1. G- rod
2. Encapsulated. 3. Nonmotile. 4. Infection characterized by reddish-brown sputum. 5. Causes cell death -> abscess. 6. Abscess breaks off -> forms abscess in other tissues. 7. Endotoxin causes vasodilatation and shock. 8. Harbor R plasmids and transposons to confer antibiotic resistance. 9. Primary disease or Secondary infection. 10. Common inhabitant of respiratory tract. 11. Nosocomial infections. |
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Staphylococcus Aureus
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1. G+ Cocci
2. Grows in grape-like clusters 3. Golden Pigment 4. Mannitol fermentation 5. Salt tolerant |
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Staphylococcus Aureus
Virulence Factors Enterotoxin |
heat stable exotoxin resulting in gasteroenteritis.
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Staphylococcus Aureus
Virulence Factors Capsule |
inhibits pahgocytosis
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Staphylococcus Aureus
Virulence Factors Exfolitin |
plasmid or chromosome encoded. Exotoxin destroys material that allows layers of skin to bind together. (Staphylococcal Scalded Skin Syndrome.)
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Staphylococcus Aureus
Virulence Factors Leukocidin |
kills white blood cells by producing holes in plasma membrane.
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Staphylococcus Aureus
Virulence Factors Lipase |
hydrolyzes ester linkage between glycerol and fatty acids.
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Staphylococcus Aureus
Virulence Factors Proteases |
degrades collagen and other tissue products.
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Staphylococcus Aureus
Virulence Factors Protein A |
binds Fc portion of antibodies. Inhibits phagocytosis.
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Staphylococcus Aureus
Virulence Factors TSST-1 |
exotoxin resulting in Toxic Shock Syndrome.
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Staphylococcus Aureus
Virulence Factors MRSA |
Methicillin resistant Staph Aureus often contains many of the above listed virulence factors.
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Heliobacter pylori
Peptic ulcer |
1. G- curved rod
2. Flagellated 3. microaerophilic 4. secrete enzyme urease, pH adjustment -> Converts urea to ammonia and carbon dioxide. Ammonia is bad for the epithelial tissues |
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Heliobacter pylori
Excreting Toxins |
VacA - Vaculating cytolytic toxin, breaks down
CagA- exotoxin that disrupts the cytotoxin. Part of the IV Secretion system |
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Vibrio Cholera
Overall |
Gram-negative Curved Rod
Uses A-B toxi |
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Enterotoxin Genes
How does the A-B Toxin affect host of E.Coli and Cholera |
1. Enterotoxin structure and mode of action similar to cholera enterotoxin
2. A-B Toxin binds glycolipid GM1 on intestinal epithelial cells 3. B portion is binding sub-unit 4. A portion is internalized in an inactive form 5. A portion is converted to active form by a host enzyme 6. Active A sub-unit activates host enzyme adenyl cyclase ATP -> cAMP 7. Na+ ions fail to enter epithelial cells 8. Net Cl- movement to lumen 9. Water follows passively 10. cAMP mediates hormone induced responses 11. Gene for enterotoxin is encoded on a conjugative plasmid |
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Enteroinvasiveness Disease (Genes)
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1. E. coli invade epithelial cells of intestine lumen resulting in a mild form of dysentery.
2. Disease is characterized by blood and mucous in the stool of infected individuals. 3. Similar to Shigella infection. 4. Infectious does 0f 10 organisms |
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Bacillus Amtjracos
Causes Anthrax |
1. G Positive Rod
2. Sporeformer 3. 3 Forms a. Cutaneous anthrax b. Pulmonary anthrax c. Gastrointestinal anthrax |
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Bacillus Amtjracos
Causes Anthrax 3 Extoxins |
1. PA- protective antigen
Chaperones 2 other toxins to host hells 2. LF- lethal factor Kills WBC responding to microbe 3. EF- edema factor Results in increase in cAMP disrupting water balance |
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Clostridium Tetani
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1. Causes Tetanus
2. Gram positive Rod 3. Anaerobic 4. Spore former |
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Clostridium Tetani
How does it work on muscle |
1. Binds to neuron to prevent the release of glucine from visicle. It does it with a gangloslide binding element
2. Prevents excitation and release of vesicales and causes permanent contraction like lockjaw. |
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Closdridia botulinum
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1. Causes botulism
2. G+ Bacilus 3. Anaerobic 4. Spore Former |
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Botulism Toxin
How does it work on muscles |
1. The Bacteria itself is not dangerous, just the toxin
2. Steps a. Released as a single peptide with low potency. b. Toxin is nicked by a protease (bacterial or gastric) to create a light A-fragment and a heavy B-fragment. (Fragments are still linked together by a disulfide bridge). c. A-Fragment is the most potent toxin found in nature. d. Mode of Action- B-fragment binds to presynaptic receptors. e. A-fragment enters the cell by receptor mediated endocytosis. f. A-fragment acts an an enzyme, cleaving synaptobrevins (found in synaptic vesicles) g. Cell cannot release of acetylcholine across neuromuscular junction. Muscles cannot be stimulated. |
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Botulism Toxin
Types (7) |
A, B, C1 (lysogenic phage), D (lysogenic phage) E, F, G
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Clostridium difficile
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1. Gram + rod
2. Obligate anaerobe 3. Spore forming 4. Producs toxins TcdA and TcdB a.They disrupte other enzymes, modifying regulatory enzymes to not work properly, creating cell death. Disrupts junctions and disrupts cytoskeleton. |
