How m/os cause disease Flashcards
Pathogenicity
The ability to cause a disease by overcomeing the defenses of the host
Virulence
Virulent (cause disease) vs avirulent (Do not cause problems)
Degree of pathogenicity
Portals of entry for a pthogen
Resp, GU, GI,
Skin (Hair follicles, sweat glands i.e. S. aureus)
Parental route
- M/o deposited beneath skin via injectionsm bites, cuts, surgeyr etc.
How is virulence often expressed
ID50 (infectious does) (A certain number of microbes that will cause an infection in 50% of the population)
LD50 =
a dose that would be lethal for 50% of the population (does not consider how many people will get sick)
Portal of entry for anthrax
Skin anthrax: 10-50 spores (skin anthrax is more potent)
inhalation: 10,0000- 20,000
Ingestion: 250, 0000- 1,000,000
Cutaneous anthrax is significantly easier to acquire than inhalation or ingestion forms
How potent is the botulism toxin at LD50?
0.03 ng/kg
Means that a microbe uses to atttach to host cell at portal of entry
Adhesions or ligands (glycoproteins or lipoproteins) on microbes bind to receptors (carbs) on host cells altering one can block adherence
Capsules and cell wall components
Glycocalyx of streptococcus mutans (surface of teeth - tooth decauy)
Fimbriae of enteropathogenic E. coi: specific cells in small intestine
Fimbriae of Neiseeria gonorrhoeae cells in GU tract
Tapered end as a hook: Treponem pallidum (non proteobacteria, spirochete causing syphillis)
How do microorgaisms penetrate the cell
M/Os attach to host cells by adhesion/invasins
Invasins reaarrange nearby host cell cytoskeleton induce ruffling (Ripples help bacteria burry itself into plasma membrane)
M/Os sink into the ruffles and are engulgfed by the host cell, use cytoskeleton to move through bw cells (Lysteria)
Virulence of some bacteria is aided by:
Capsule: Impair phagocytosis
Streptococcus pnemonieae
Waxy layer: resist digestion by phagocytes
Mycobacterium tuberculosis
Coagulase: Coagulate the fibrinogen in blood
S. aureus
Kinase: digest fibrin clots
Streptococcus pyogenes, S. aureus.
Hyaluronidase: Hydrolyses hyarulonic acid that holds together some cells in the body (adjacent cells have glue inbw them) Creates space in bw cells for m/os to grow
Collaginase: Hydrolyses collagen
Clostridum
IgA proteases: Destroy iGA antibodies (found in secretions i.e breast milk, and in mucous layers)
Neisseria gonnorrhoeae
How does antigen variation work?
M/os alter surface proteins to evade host’s immune system
By the time the body mounts an immune response, the m/o has altered it’s antigens and is unaffected by the antibodies
What are antigen proteins
The part of them that illicits an antibody response, each pathogen can change it’s respective surface proteins to avoid detection
Siderophores
Take iron from host cells/proteins (transferrin), if not enough, will begin lysing red blood cells
How do pathogens cause direct damage to host cells?
Some pathogens grow inside host cells
Viruses
Salmonella
N. gonorrhoeae
Exotoxins
Proteins produced inside pathogenic bacteria, mostly Gram +ve, as part of their growth & metabolism; secreted in surrounding medium during log phase
LD50 very small (toxic) - can be neutralized by antitoxin (antibodies produced against these toxins)
3 major types of exotoxins
A-B toxin
Membrane disrupting toxins
Superantigens
A-B toxin
Active/binding components (binding components causes damage) (diptheria toxin, botulinum toxin etc.)
Membrane disrupting toxin
Hemolysins production (streptococcus and staphylococcus)
Superantigens
Cause an intense immune response due to release of cytokines from host cells (t cells)
Fever, nausea, vomiting, diarrhea, shock and death
Enterotoxin of s. Aureus
Endotoxins
Part of ccell wall of Gram - bacteria
Symptoms similar for different bacteria
Released when bacteria dies or during multiplication
Actiates blood clotting factors that may obstruct capillaries
Composed of lipid
Present in LPS of outer membrane
Not neutralized by antibodies
Relatively large LD50 (not too toxic)
Better for body to deal with on it;s own as to not release endotoxins by treating with antibiotics
Plasmids
small, circular DNA molecules that are not connected to bacterial chromosome
Bacteria with plasmids is likely antibiotic resistant or something special bc of the extra genes
Encode gene for resistance to antibiotics, exotosins and other virulence factors
Lysogeny
Bacteriophages that can incorporate DNA into bacteriophage becoming prophage
Microevolution
: a way to increase the number of pathogenic bacteria
Actibiotic reissitance
Pseudomonoas is well known to be generous at passing on antibiotic resistance
Portals of exit
Via secretions, excretions, discharges, or tissues that have been shed by the infected host
Most microorganisms use the same proal of entry for portal of exit
End goal = spread through the population
