microbial mechanisms of pathogenicity. virulence is the degree of pathogenicity of an organism....
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• Virulence is the degree of pathogenicity of an organism.
• Pathogenicity, Ability to cause disease.
Portals of entry are usually constant for a microbe
• Mucous membranes of conjunctiva, respiratory, gut and genitals
• Inhalation of dust and moisture particles to lungs– This is the most common entryway
• Skin is hard to penetrate– Most enter through hair follicles and sweat
ducts– Some fungi may attach to skin cells.
• Microbes gain access to systemic system through– Bites– Injections– Wounds
– Called parenteral rout
Preferred Portal of entry
• Most cause infection only when they use a specific portal of entry
• Example– Yersinia pestis by a number of portals– Streptococcus pneumoniae respiratory tract– Vibrio cholerae gut– Neisseria gonorrhoeae genitals– Clostridium perfringes parenteral
Lethal and infectious doses, the number of invaders determines
what the outcome may be
• LD50 # to kill 50% of inoculated individuals
• ID50 # to cause infection in 50%
• Is basically a method to compare relative toxicities or conditions
Bacillus anthracis
Portal of entry ID50
Skin 10-50 endospores
Inhalation 10,000-20,000 endospores
Ingestion 250,000-1,000,000 endospores
Adherence
• In order to get into a host the bacteria must stick to it.
• Surface projections (ligands) adhere to receptors on host cells.
• Mostly on structures called fimbriae
• The sugar mannose is the most common receptor.
• Adhesions/ligands bind to receptors on host cells– Glycocalyx Streptococcus mutans– Fimbriae Escherichia coli– M protein Streptococcus pyogenes– Opa protein Neisseria gonorrhoeae– Tapered end Treponema pallidum
Adherence
How Bacteria escape programmed host defenses
• Capsules are extracellular glycocalyx material that surrounds the cell. Prevent recognition of the bacterial cell. Streptococcus pneumoniae
• Cell wall components may also resist recognition and phagocytosis
Enzymes that protect
• Leukocidins destroy neutrophils and macrophages
• Hemolysisn break up red blood cells
• Coagulase prevents or breaks up blood clots designed to localize infection
• IgA proteases Destroy IgA antibodies
Bacteria moving into tissues
• Kinases- destroy blood clots
• Hyaluronidase works on mucopolysaccharide that holds cells together
• Collagenase hydrolyses connective tissue collagen
• Invasins destroy cytoskeleton of individual cells.
How bacterial pathogens damage the host cells.
• Only some of the cell damage is caused by bacteria themselves– Some bacteria enter the host cell and damage
as they leave– Some bacteria harm the cell as they enter
Bacteria Toxins
• Cause the most damage• Toxins: poisonous substances produced by
microbes• Toxigenicity: capacity of a microbe to produce
toxin• Toxemia: presence of toxins in the blood• Toxoid: Inactivated toxin used in a vaccine• Antitoxin:Antibodies against a specific toxin
Exotoxins:
• Produced by bacteria and released into surrounding area. Causes Disease– Cytotoxin or diphtheria toxin inhibits protein
synthesis– Tetanus toxin prevents nerve transmission– Enterotoxins promote electrolyte and fluid
loss from cells.– Neurotoxins (Botulinum toxin) prevent nerve
transmission– Antibodies produced in response are
antitoxins
Exotoxin
Source Mostly Gram +
Metabolic product By-products of growing cell
Chemistry Protein
Fever? No
Neutralized by antitoxin
Yes
LD50Small
• Superantigens or type I toxins– Cause an intense immune response due to
release of cytokines from host cells– Fever, nausea, vomiting, diarrhea, shock,
death
Exotoxins
• Membrane-disrupting toxins or type II toxins– Lyse host’s cells by:
• Making protein channels in the plasma membrane (e.g., leukocidins, hemolysins)
• Disrupting phospholipid bilayer
Exotoxins
ExotoxinsExotoxin
Lysogenic conversio
n
• Corynebacterium diphtheriae
A-B toxin. Inhibits protein synthesis.
+
• Streptococcus pyogenesMembrane-disrupting.
Erythrogenic.+
• Clostridium botulinum A-B toxin. Neurotoxin +
• C. tetani A-B toxin. Neurotoxin
• Vibrio cholerae A-B toxin. Enterotoxin +
• Staphylococcus aureusSuperantigen. Enterotoxin.
Endotoxins
• Are structures of the bacterium itself that cause the disease, like lipopolysaccharide (LPS) of gram negative bacteria– May be released when cells are killed by
antibiotics– Cause fever and shock– May allow the bacteria to cross the blood
brain barrier
A test for endotoxins.
• Limulus amoebocyte lysate (LAL) used to detect endotoxins in drugs and on medical devices.– The amoebocyte will lyse in the presence of
endotoxins causing a thickening of the media.
Endotoxins
Source Gram–
Metabolic product Present in LPS of outer membrane
Chemistry Lipid
Fever? YesNeutralized by antitoxin No
LD50 Relatively large
Extra genetic material
• Some bacteria may carry extra genes that help pathenogenisity– Plasmids (extra chromosomal) can carry
genes for antibiotic resistance, toxins, capsules and fimbriae
– Coagulase produced by Staphylococcus aureus
– Fimbria in specific straines of E. coli
Pathogenesis of nonbacterial microbes• Viruses
– Avoid immune system by growing inside host cell– May cause cell death or damage by growing and
being released from the cell.– Casuse membranes to fuse
• Fungi, Protozoa, Helminths and Algae– Symptoms caused by mixture of capsules, toxins,
waste products and allergic response to the organism– Antigen switching allows to avoid hose immunity
• Neurotoxins produced by dinoflagellates– Saxitoxin
• Paralytic shellfish poisoning
Pathogenic Properties of Algae
• Respiratory tract– Coughing, sneezing
• Gastrointestinal tract– Feces, saliva
• Genitourinary tract– Urine, vaginal secretions
• Skin
• Blood– Biting arthropods, needles/syringes
Portals of Exit
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