Pathogenicity
the ability to cause disease
virulence
the severity of the disease
Microbial mechanism of pathogenicity
Portals of Entry
mucous membrane, skin, parenteral route, preferred portal of entry
Microbes invasion
the likelihood of disease increases as the number of pathogens increase
ID50
* virulence of a microbe
* infectious dose for 50% of a sample population
* Varies according to portal entry
LD50
* potency of a toxin
* lethal dose for 50% of a sample population
Portal of entry- Skin
10-50 endospores
Portal of entry- inhalation
10,000-20,000 endospores
portal of entry- ingestion
250,000-1,000,000 endospores
Toxin-botulinum
LD50- 0.03NG/KG
(most dangerous)
Toxin- Shiga Toxin
LD50 250NG/KG
Toxin staphylococal enterotoxin
LD50 1350NG/KG
Adherence
leads to the formation of biofilms
Streptococcus mutans
tooth decay (uses it glycocalyx layer to attach to teeth)
actinomyces
attach to the glycocalyx with fimbriae
dental plaque consists of
streptococcus mutans, actinomyces and dextran
how do bacterial pathogens penetrate host defenses
capsules
many pathogens cannot start an infection if the capsule is what
missing
how do you increase virulence
by preventing phagocytosis
Cell wall components
M protein, waxes, extracellular enzymes, kinases
M proteins
Cause a misdirected immune response by resisting phagocytosis
example of M proteins
Rheumatic fever
Waxes (mycolic acid)
Resists digestion
coagulases
coagulate fibrinogen which causes clot
Kinases
break down fibrin clots
what can Fibrinolysisn (streptokinase) be used for
heart attack victims
Hydrolyzes hyaluronic acid
*a polysaccharide that holds connective tissue cells together
*produces blackening of wounds
* helps organisms spread
Antigenic Variation
a host normally produces antibodies to an antigen (usually a protein of the pathogen). The antibodies are specific, bind to the antigen and destroy or inactivate (neutralize) it.
Some pathogens do what to evade the antibodies of the host
Alter their surface proteins
actin
component of the host cell cytoskeleton
What does actin do
helps microbes penetrate host cell and move through and between host cells
How bacterial pathogens damage host cells
using the host's nutrients
pathogens require what
iron
pathogens secrete proteins called
siderophores which remove the iron from host iron-transport proteins
the iron-siderophores complex attaches to
siderophores receptors on bacterial surface
Direct Damage
Pathogens enter the host cell, replicate using the cell nutrients until cell ruptures
toxins
substance that contributes to pathogenicity
toxigenicity
ability to produce a toxin
toxemia
presence of toxin in the host's blood
toxoid
inactivated toxin used in a vaccine
antitoxin
antibodies against a specific toxin
exotoxin
proteins produced inside pathogenic bacteria as part as their growth metabolism, then secreted into the surrounding during long phase
endotoxin
lipid portions of lipopolysaccharides part of the other membrane. Toxins are released when bacteria die and cell wall breaks apart
Leading cause of death in children in the USA prior to 1935
Diphtheria (caused by exotoxins)
Corynebacterium diphtheriae
is a G+ bacillus (no spores)
where is diphtheria found
in throats of asymptomatic carriers
(thick, grayish membrane in throat can block the trachea)
Diphtheria transmission
airborne
treatment of diphtheria
prevention of diphtheria
antitoxin
vaccine is diphtheria toxoid
Diphtheria
disease caused by exotoxins
Scarlet Fever
Scarlet Fever
erythrogenic toxin that can damage the plasma membranes of blood capillaries to produce a red skin rash and high fever
the production of the erythrogenic toxin is due to a
prophage
the rash called scarlet fever is usually in sequel to
strep throat
Scarlet fever
botulism
obligate anaerobe, endospore forming, gram + bacillus found in soil
Neurotoxin affects
the end of the nerve creating a progressive flaccid paralysis
botulism can lead to
respiratory and cardiac failure
botulism incubation period
1-2 days
symptoms of botulism
nausea, double vision, difficulty swallowing, weakness
botulism first described as
sausage disease
botulism outbreaks
associated with heat to kill competing bacteria, but no endospores, anaerobic conditions and a period of time for toxin production (home canning vegetables)
How to get rid of botulinum
boiling and nitrites added to food
in adults the botulism organism does or does not survive
does not survive in the gut due to competition of normal flora. adult cases are associated with ingestion of the preformed toxin
infant botulism
most common in USA 250 cases per year (associated with honey)
Treatment of botulism
trivalent antitoxin (will not affect toxin already attached)
Therapy of botulism
botox injection- wrinkles, arm pits, strabismus, blepharospasm
disease caused by exotoxins: tetanus
clostridium tetani
Tetanus
Obligated anaerobe, endospore-forming, Gram + bacillus,
tetanus reservoir
soil contaminated with animal feces
tetanospasmin
released upon death/lysis of the bacteria
Tetanus symptoms
*Blocks muscle relaxation pathway muscle contractions
*Lockjaw
*Opisthotonus
*Difficulty swallowing
*Death due to spasms of respiratory muscles
opisthotonus
due to tetanus
Tetanus vaccine
available since 1940s, toxoid with booster every 10 years
Cholera
Vibrio cholerae- curved, gram -, motile
cholera growth and reservoir
growth in the mall intestine, reservoir is coepods, algae, plankton in brackish water
cholera toxin
subunit B binds to epithelial cells and subunit A causes cells to secrete large amounts of fluids and electrolytes (chlorides, bicarbonates)
symptoms of cholera
severe diarrhea, patients lose 3-5 gallons of fluids in a day, shock, collapse, death
cholera recovery
provides short term immunity
cholera treatment
tetracycline, and IV fluids
cholera outbreaks occur when
lack of sanitary water supply
Last epidemic of cholera
1991-1994 in South Central America
Scalded Skin Syndrome
Lysogenized Staphylococcus aureus
scalded skin syndrome begins with
lesion around the nose and mouth which becomes bright red and spreads. Within 48 hours the skin peels off in sheets
Scalded skin syndrome often occurs in
children under 2 years of age
treatment of scalded skin syndrome
hexachlorophene, seriously ill might become toxemic, vigorous antibiotic treatment is needed
Endotoxins
Lipid A part of the outer membrane of the cell wall of gram - bacteria
endotoxins release when
during active multiplication and when the cells die
endotoxins stimulate
stimulate macrophage to release cytokines
signs/symptoms of endotoxins
chills, fever, weakness, miscarriage, generalized aches, and shock death
Endotoxins and the pyrogenic Response
septic shock
sever drop in BP due to high number of bacteria
phagocytosis of bacteria causes
release of tumor necrosis factor
In the USA there are how many cases of shock per year
500,000
* one third of the patients die within a month
* half die within six months
Plasmid
R Factor
Tetanospasmin
Staphylococcal enterotoxin
Dextransucrase of Streptococcus mutans
Coagulase of Staphylococcus aureus
phage conversion
change in the characteristics of microbe due to prophage
lysogenic conversion
diphtheria toxin
Erythrogenic toxin
Staphylococcal enterotoxin and pyrotoxin
Capsule of Streptococcus pneumoniae
Botulinum neurotoxin
viral mechanisms for evading host defenses
* virus grow inside cells
* attachment sites for receptors on host cells
cytopathic effects for viruses
* visible signs of viral infections
* cytocidal
*noncytocidal