Chapter 15 - Microbial Mechanisms of Pathogenicity Flashcards
Pathogenicity
-the ability to cause disease
Virulence
-the degree/extent of pathogenicity
Portals of Entry
-how a pathogen enters its host
-mucous membranes, skin, direct deposition
Mucous Membranes
-a portal of entry
-line many pathways in the body
-most enter through respiratory and GI tract
Respiratory Tract (Mucous Membranes)
-easiest to enter
-enter by inhalation through nose or mouth in droplets
-ie. common cold, pneumonia, TB, influenza, measles
Gastrointestinal (GI) Tract (Mucous Membranes)
-enter via food, water, contaminated fingers
-most bacteria destroyed by HCl and stomach/small intestine enzymes
-ie. food poisoning, E. coli, Hep A, Typhoid fever, Shigellosis
-these pathogens are eliminated in feces and then transmitted
Genitourinary (GU) Tract (Mucous Membranes)
-sexually contracted pathogens
-ie. any STDs/STIs
Conjuctiva/Eye (Mucous Membranes)
-lines the eyelids and covers white of the eyeballs
-ie. measles, conjunctivitis, trachoma
Skin
-a portal of entry
-natural defence, largest organ
-unbroken skin is impenetrable by most organisms
-enter via broken skin, hair follicles, sebaceous glands
-ie. S. aureus, fungal agents (nail infection)
Parenteral Route
-a portal of entry
-depositing into the tissues beneath the skin when penetrated or injured
-punctures, wounds, insect bites, surgery, dry skin splitting
-ie. malaria, lyme disease, HIV, tetanus
Adherence
-how pathogens attach themselves to host cells/tissues
-establishes the infection
-a route for invasion
Adhesins/Ligands
-attachment between pathogen and host that involves the binding of adhesins to surface receptors on host cells
Host Receptors
-are complex sugars
-ie. mannose fucore
Glycoprotein Adhesins
-carb + protein on pathogen
-specific structure
-bind to host receptor
Lipoprotein Adhesin
-lipid + protein on pathogen
-specific structure
-bind to host receptor
Adhesin Location
-on glycocalyx/capsule, flagella, fimbriae, M protein, mycolic acid, opa protein
Capsule
-blocks/evades phagocytosis (1st line of defense)
-ie. S. mutans (tooth decay)
Creation of Dental Plaque
-S. mutans uses enzyme glucosyltransferase to digest sucrose into glucose and fructose
-glucose uses the same enzyme to make glucan and then plaque
-fructose uses the same enzyme to make the acid that degenerates the tooth structure
Fimbriae
-adhesins on fimbriae adhere only to specific kinds of cells
-ie. E. coli, N. gonorrhoea, bacteria on skin
M Protein
-found on cell surface and fimbriae
-heat and acid resistant
-used for attachment and evading phagocytosis
-increases virulence
-ie. S. pyogenes
Mycolic Acid
-waxy lipid
-makes up the cell wall of Mycobacterium sp.
-resists phagocytosis
Exoenzymes
-aids on virulence
-chemicals that can digest materials between cells, digest blood clots
Coagulase
-coagulate (clot) the fibrinogen in blood
-fibrinogen (produced by liver) is converted to fibrin to form the threads of a blood clot
-clot may protect from phagocytosis and isolate it
-ie. Staphylococcus aureus
Kinase
-break down fibrin and digest clots
-isolate the infection
-ie. S. pyogenes
Hyaluronidase
-hydrolyzes hyaluronic acid that holds connective tissue cells together
-allows bacteria to invade deeper
-ie. tissue blackening in C. perfringens (gangrene)
-ie. S. pyogenes (flesh eating disease)
Collagenase
-facilitates the spread of gas gangrene
-breaks down collagen protein
-ie. C. perfringens
IgA Proteases
-destroy the antibodies produced by body against pathogens
-antitoxin
-ie. N gonorrhoeae, N. meningitis
Damaging Host Cells
4 ways:
1. using host’s nutrients
2. causing direct damage
3. producing toxins
Toxin
-poisonous substances that contribute to pathogenicity
Toxigenicity
-capacity/ability of a microorganism to produce toxins
Toxemia
-presence of toxins in the hosts blood
Exotoxins
-exo = outside
-secreted into the outside of the cells that produce them
-produced mostly by gram negative bacteria
-produced as part of growth
-proteins in nature
-circulate through body fluids
-create SPECIFIC signs and symptoms
-work by destroying parts of the host cell or inhibiting functions
-no fever
-neutralized by IgA Molecules
-3 types of exotoxins
Toxoid
-inactivated toxin used in vaccines
-stimulate antitoxin production to produce immunity
-ie. DTaP
A-B (exo)Toxins
-first type to be studies
-consist of an A and B part (both polypeptides)
-ie. Diphtheria, Botulism, Tetanus, Cholera
A Part
-active enzyme component
-produces the signs and symptoms
B Part
-binding component
-binds to receptor on the host cell
C. Diptheriae
-A-B exotoxin
-A shuts down protein synthesis
-results in cell death and diphtheria symptoms (pseudomembrane)
C. Botulinum
-A-B exotoxin
-B binds and brings A in
-accesses neuromuscular junction to inhibit AcH action
-results in flaccid paralysis
C. tetani
-A-B exotoxin
-tetanospasmin
-Blocks GABA at NMJ
-results in lock jaw, opsithtonos (back spasm)
-leads to spinal fracture and respiratory failure
V. Cholerae
-A-B exotoxin
-vebriotoxin
-B then A
-GI tract cells turn into little pumps and trigger cAMP second messenger system
-results in rice water stool
Membrane Disrupting (exo)Toxins
-cause lysis of host cells by disrupting plasma membrane bilayer
-some form protein channels in the bilayer
Leukocidins
-membrane disrupting exotoxin
-kill leukocytes
-form protein channels
-produced by Streptococci or Staphylococci
Hemolysins
-membrane disrupting exotoxin
-destroy erythrocytes
-form protein channels
-produced by Streptococci and Staphylococci
Superantigens
-antigens that provoke an intense immune response
-non-self-entities
-body reacts to toxin
-ie. Staphylococcal agents of food poisoning, TSS
Action of Superantigens
- Body tries to provoke intense immune response
- T cells released and produce cytokines
- Circulate in blood and reach vital organs
- Affect GI tract and kidneys
Symptoms: nausea, vomiting, diarrhea, shock, sometimes death
Cytokines
-small protein molecules
-regulate immune responses
-mediate cell-to-cell communication
Endotoxins
-endo = within
-endotoxins are part of bacterial cells
-not a metabolic produce
-part of the outer portion of the cell wall on gram negative bacteria
-Lipid A is the endotoxin
-liberated when the bacteria die and the cell wall lyses
-stimulate macrophages to release cytokines in high concentrations (toxic)
-activation of blood clotting proteins
-no antibodies produced
Endotoxin Symptoms
-fever
-nausea
-vomiting
-diarrhea
-septic shock
-can induce miscarriage
Fever
-lysosomes release enzymes into the vesicle
-bacteria is digested
-LPS part of the cell wall remains and triggers IL-1 release
-IL-1 circulates in the blood and reaches the brain, causing the hypothalamus to secrete prostaglandins
-body temp is reset to higher degree
Fever: Chill Stage
-shivering
-IL-1 is working at max
Fever: Crisis Stage
-IL-1 reducing in the blood
-sweating
Shock
-any life-threatening decrease in BP
-same mechanism of fever (cytokine release by macrophages)
-LPS triggers release of TNF (tumor necrosis factor) aka Cachetin
-TNF travels to vital organs through blood and disturbs their permeability
-BP drops immensely
-vital organs start to shut down
