Chap 15 Flashcards
Pathogenicity
the ability to cause disease
Virulence
the degree of pathogenicity
Portals of entry for microorganisms
Mucous membranes
Skin
Parenteral route
Parenteral route
Portal of entry beneath the skin and mucous membranes
Moth pathogens have a preferred
portal of entry
ID 50
infectious dose for 50% of a sample population
ID 50 MEASURES
Measures virulence of a microbe
LD50
lethal dose for 50% of a sample population
LD50 MEASURES
POTENCY OF A TOXIN
endospores
What are left behind when a bacteria is in an environment that it cant survive in. last hope for survival
Which portal of entry is most likely to cause infection?
The one with the lower ID 50 because it needs less endosppores to cause disease
adherence
pathogens attach to host tissues
adhesins (ligands)
on the pathogen bind to receptors on the host cells
receptors can be on
Glycocalyx
Fimbriae
microbes form biofilms that are
communities that share nutrients
capsules
Glycocalyx around the cell wall
function of capsules
Impair phagocytosis
Examples of microbes with capsules
Streptococcus pneumoniae—pneumonia
Haemophilus influenzae—pneumonia and meningitis
Bacillus anthracis—anthrax
Yersinia pestis—plague
Cell wall components
- M protein
- Opa protein
- Waxy lipid
M protein
resists phagocytosis
Streptococcus pyogenes
Opa protein
allows attachment to host cells
Neisseria gonorrhoeae
Waxy lipid
(mycolic acid) resists digestion
Mycobacterium tuberculosis
Coagulases
coagulate fibrinogen
Kinases digest
digest fibrin clots
Hyaluronidase
digests polysaccharides that hold cells together
Collagenase
breaks down collagen
IgA proteases:
destroy IgA antibodies
Antigenic variation
Pathogens alter their surface antigens (and antibodies are rendered ineffective)
How do invasins penetrate the host?
Surface proteins produced by bacteria that rearrange actin filaments of the cytoskeleton
Cause membrane ruffling
Use actin to move from one cell to the next
Shigella and Listeria
Survival inside phagocytes
Requirement for low pH in phagolysosome
Escape from phagosome before lysosomal fusion
Prevention of fusion of lysosome with phagosome
Fimbriae
Very specific to bacteria, strands that go out to help bacteria communicate and attach
Biofilms play a role in invading phagocytes
Biofilm bacteria more resistant to phagocytosis, shielded by extracellular polymeric substance (EPS) of biofilm
_____ is required for most pathogenic bacteria
Iron
Siderophores
proteins secreted by pathogens that bind iron more tightly than host cells
Direct damage disrupts
host cell function
Direct damage uses
host cell nutrients
Direct damage produces
waste products
Direct damage multiplies in
host cells and causes ruptures
Virulence factors
certain traits that help pathogens attach to and penetrate the host tissues and escape host defenses
Type of virulence factor that helps pathogen penetrate tissues
enzymes
Why do pathogens like to penetrate host tissues?
To have better access to nutrients and be able to reproduce
Examples of microbes that release hyaluronidase
Clostridium perfringens
Some streptococcus species
Collagen fibers are found in the base of
superficial tissues
Streptococcus and clostridium also secrete
Collagenase
What causes strep throat & necrotizing facitis
Streptococcus pyogenes
Secretes streptokinase that digests blood clots by breaking down fibrin proteins
Streptococcus pyogenes
fibrinolysin
aka streptokinase
staphylokinases
secreted by some staphylococcus do same as streptokinase
Streptococcus pyogenes & staphylococcus live on the
skin
Enteric pathogens
intestinal pathogens
Examples of enteric pathogens
Salmonella and Shigella
Etiologic agent of salmonellosis, typhoid and shigella
Salmonella
causes shigellosis
Shigella
Both can live within host cells as parasites
Salmonella and shigella
Flagella
on salmonella, helps it move in its environment
Toxins
poisonous substances produced by microorganisms
Toxins produce effects such as
fever, cardiovascular problems, diarrhea, and shock
Toxigenicity
ability of a microorganism to produce a toxin
Toxemia
presence of toxin in the host’s blood
Intoxications
presence of toxin without microbial growth
Exotoxins
Proteins produced and secreted by bacteria
Soluble in bodily fluids; destroy host cells and inhibit metabolic functions
Antitoxins
antibodies against specific exotoxins
Toxoids
inactivated exotoxins used in vaccines
Proteins produced inside pathogenic bacteria, most commonly gram-positive bacteria, as part of their growth and metabolism. The exotoxins are then secreted into the surrounding medium during log phase.
exotoxins
: toxic substances
released outside the cell
exotoxins
example of a gram-positive bacterium that produces exotoxins
Clostridium
botulinum
bacterial proteins that are secreted by a living organism into its surroundings
Exotoxins
What happens to exotoxins in a host?
exotoxins circulate and cause damage to host cells in various ways.
________ can cause severe damage or death at very low concentrations
Exotoxins
How can exotoxins be classified?
- Location (neurotoxins)
- Structure and function
3.
tetanus and botulism are caused by species of Clostridium that secrete
neurotoxins
Enterotoxins like those secreted by cholera bacterium can target
lining of intestinal tract
Cytotoxin
kills or seriously damages host cells in general.
Corynebacterium diptheriae is a bacterium that secretes a cytotoxin that
inhibits protein synthesis in host cells
Most exotoxins are proteins with two domains _ & _
A & B
A” domain of exotoxin is
an enzyme that has a particular function.
“B” domain of an exotoxin is
the binding component
B domain binds to
specific receptor (usually a carbohydrate ) on the host cell
Once the B domain attaches to the host cell,
the host cell uses endocytosis to bring the exotoxin inside.
Once the B domain opens a pore in the endosome…
this allows the A domain to escape into the cytosol
What happens when the A domain escapes into the cytosol?
It can inhibit protein synthesis or interfere with the host cytoskeleton. This usually results in the death of the host cell
Membrane disrupting toxins exert their effect without
entering the cytosol
How do membrane disrupting toxins exert their effect without entering the cytosol?
- Form protein pores in the host plasma membrane.
- Disrupt phospholipid portion of the membrane
Membrane disrupting toxins result in
The cell lysing
Superantigens
bacterial exotoxins that stimulate an excessive immune response.
Superantigens first cause a proliferation of
T cells
After causing a proliferation of T cells, then it
causes those T cells to release excessive amounts of cytokines
The cytokines can stimulate
fever, inflammation & shock. This intense immune response can lead to death.
The toxin secreted by staphylococcus aureus in food poisoning and Toxic shock syndrome is an example of a
Super antigen
contain an enzyme component (A part) and a binding component (B part)
AB toxins
Example of A-B toxin
Diphtheria toxin
Genotoxins
damage DNA (causing mutations, disrupting cell division, and leading to cancer)
lyse host cells by disrupting plasma membranes
Membrane-disrupting toxins
Leukocidins
kill phagocytic leukocytes
Hemolysins
kill erythrocytes by forming protein channels
Streptolysins
hemolysins produced by streptococci
cause an intense immune response due to release of cytokines from host cells (T cells)
Superantigens
Cause symptoms of fever, nausea, vomiting, diarrhea, shock, and death
superantigens
Lipid A
portion of lipopolysaccharides (LPS) of gram-negative bacteria
Lipid A released during
bacterial multiplication and when gram-negative bacteria die
Lipid A stimulates macrophages
macrophages to release cytokines
Lipid A causes
disseminated intravascular coagulation
LPS are part of
outer membrane of the cell wall of gram-negative bacteria (lipid A).
The endotoxins are liberated when
the bacteria die and the cell wall lyses, or breaks apart.
example of a gram-negative bacterium that produces endotoxins
Salmonella
typhimurium
Endotoxins are composed of
lipids that are part of the cell wall
First step of the pyrogenic response
A macrophage ingests a
gram-negative bacterium.
Step 2 of the pyrogenic response
Bacterium gets degraded in a vacuole.
Releases endotoxins that induce the macrophage to produce
cytokines, interleukin-1
(IL-1), and tumor necrosis
factor alpha (TNF-α).
Releases endotoxins that induce the macrophage to produce
cytokines, interleukin-1
(IL-1), and tumor necrosis
factor alpha (TNF-α).
Step 3 of pyrogenic response
cytokines are
released into the blood-
stream by the macrophages,
Through the macrophages, the cytokines travel to
to the
hypothalamus, the temperature
control center of the brain.
Step 4 of the pyrogenic response
The cytokines induce the
hypothalamus to produce
prostaglandins
Effect of releasing the prostaglandins
reset
the body’s “thermostat” to a
higher temperature, producing
fever.
Limulus amebocyte lysate (LAL) assay
is used to test for endotoxins
Blood of horseshoe crabs contains
amebocytes
Amebocytes lyse in the presence of
endotoxin, producing a clot
“A” portion of the LPS in the outer membrane
Endotoxin
Endotoxins are only released when
The cell dies or during cell division
Interleukin 1 is a
protein messenger that ravels to the hypothalamus
Cause fever, an early sign of an infection
prostaglandins
Help stimulate phagocytosis, complement activation and antibody production by B lymphocytes
Endotoxins and interleukin 1
What happens when endotoxin is released in large amounts or within the bloodstream
serious and deadly effects.
Massive amounts of cytokines and interleukin 1 and tumor necrosis factor cause
1.loss of fluid from capillaries
2 vasodilation,
3.which lower BP. 4.Can lead to shock
cytokines and interleukin 1 also cause
coagulation, making it more severe. Most often occurs in bacterial sepsis
Bacterial sepsis is commonly caused by
E. Coli or meningococci in the blood stream or spinal fluid
metabolic product of growing the cell
exotoxins
Can be made by gram positive and gram negative bacteria
exotoxins
Bacterial source is gram negative bacteria
endotoxins
Present in LPS of outer membrane of cell wall and released with destruction of cell or during cell division
Endotoxins
Metabolic product of growing cell
Exotoxins
Proteins, usually with two parts A-B
exotoxins
Lipid portion (lipid A ) of LPS of outer membrane
Endotoxins
Specific for a particular cell structure or fucntion in the host (Mainly affects cell functions, nerves and GI tract)
Exotoxins
General such as fever, weaknesses, aches and shock, all produce same effects
endotoxins
Unstable, can usually be destroyed at 60-80 C except for staphylococcal enterotoxin
Exotoxins
Stable, can withstand autoclaving (121 C for one hour)
Endotoxins
High toxicity
Exotoxins
Low toxicity
Endotoxins
Fever producing: no
exotoxins
Fever producing: Yes
Endotoxins
Can be converted to toxoids to immunize against toxin; neutralized by antitoxin
Exotoxins
Not easily neutralized by antitoxin; therefore effective toxoids cannot be made to immunize against toxin
endotoxins
Small lethal dose
Exotoxins
Considerably larger lethal dose
Endotoxins
Gas gangrene, tetanus, botulism, diphtheria, scarlet fever, cyanobacterial intoxication
Representative Diseases
Typhoid fever, UTIs, Meningococcal meningitis
Endotoxins
Plasmids may carry genes for
1.toxins,
2.production of antibiotics,
3.enzymes
Lysogenic conversion
changes characteristics of a microbe due to incorporation of a prophage
Cytopathic effects (CPE)
visible effects of viral infection on a cell
Stopping cell synthesis
Cytopathic effects CPE
Causing cell lysosomes to release enzymes
Cytopathic effects CPE
Creating inclusion bodies in the cell cytoplasm
Cytopathic effects CPE
Inclusion bodies
non-living chemical compounds and by-products of cellular metabolism
Fusing cells to create a syncytium
Cytopathic effects CPE
Changing host cell function or inducing chromosomal changes
Cytopathic effects (CPE)
Inducing antigenic changes on the cell surface
Cytopathic effects (CPE)
Loss of contact inhibition in the cell, leading to cancer
Cytopathic effects (CPE)
Contact inhibition
animal cell movement and division stop as a result of contact with other cells.
Alpha and beta interferons produced by
virally-infected cells
Alpha and beta interferons protect
neighboring cells from viral infection
How do Alpha and beta interferons Protect neighboring cells from viral infection
- Inhibit synthesis of viral proteins and host cell proteins
- Kill virus-infected host cells by apoptosis
Some _______ have metabolic products that are toxic to human hosts
fungi
Can provoke an allergic response
fungi
Trichothecene toxins inhibit
Protein synthesis
fungal toxins that inhibit protein synthesis in eukaryotic cells.
Trichothecene
Two fungi that can cause skin infections, Candida albicans and Trichophyton (trik-ō-Fī-ton), secrete ________.
proteases
proteases
modify host cell membranes
Cryptococcus neoformans is a fungus that causes a type of meningitis; it produces a ________ that helps it resist phagocytosis.
capsule
prevent phagocytosis
capsule
Ergot
alkaloid toxins that cause hallucinations
Aflatoxin
carcinogenic toxin produced by Aspergillus
Ergot comes from
fungi
Aflatoxin comes from
Aspergillus which is fungi
Mycotoxins
produced by mushrooms and are neurotoxic
Phalloidin and amanitin are examples of
mycotoxins
produced by Amanita phalloides , commonly known as the deathcap. These neurotoxins are so potent that ingestion of the Amanita mushroom may result in death.
Phalloidin and amanitin
Presence of protozoa and their waste products causes
symptoms
Protozoa avoid host defenses by
- Digesting cells and tissue fluids
- Growing in phagocytes
- Antigenic variation
helminths use host tissue for
growth
Helminths produce large masses which cause
cellular damage
Helminths produce waste products that
cause symptoms
saxitoxin made by
Made by algae,
People who eat the mollusks develop paralytic shellfish poisoning, with symptoms similar to botulism. Caused by which neurotoxin?
saxitoxin
Portals of exit
Route by which a pathogen leaves the body
pathogens leave the Respiratory tract via
Coughing and sneezing
pathogens leave the GI tract via
Feces and saliva
pathogens leave the Genitourinary tract via
Urine; secretions from the penis and vagina
Other portals of exit
Skin
Blood
How do pathogens leave the blood?
Arthropods that bite; needles or syringes
15-17 Which are the most often used portals of exit?
respiratory and gastrointestinal tracts.
When the balance between host and microbe tips in favor of the microbe, an infection or _______ results
disease
Learning these mechanisms of microbial pathogenicity is fundamental to understanding
how pathogens are able to overcome the host’s defenses
portals of entry via mucous membranes include
- Respiratory tract
- Gastrointestinal tract
- Genitourinary tract
- Conjunctiva
Parenteral route
entry for pathogens by deposition directly into tissues beneath the skin and mucous membranes.
How does penetration or evasion of host defenses occur?
Capsules
Cell wall components
Enzymes
Antigenic variation
Invasins
Intracellular growth
Invasins
surface proteins that rearrange nearby actin filaments of the cytoskeleton.
Capsules increase virulence by
increases the virulence of pathogenic species. The capsule resists the host’s defenses by impairing phagocytosis
Bacteria get iron from the host using _________.
siderophores
_____ is required for the growth of most pathogenic bacteria. However, the concentration
Iron
the concentration of free iron in the human body is fairly low because
most of the iron is tightly bound to iron-transport proteins, such as lactoferrin, transferrin, and ferritin, as well as hemoglobin.
siderophores
bacterial iron-binding proteins
they take the iron away from iron-transport proteins by binding the iron even more tightly.
siderophores
Once the iron-siderophore complex is formed, it is taken up by
siderophore receptors on the bacterial surface
taken up by siderophore receptors on the bacterial surface. Then the iron is brought into the
bacterium
In some cases, the iron is released from the complex to enter
The bacterium
in other cases, the iron enters as part of
the complex
Direct damage toxins
endotoxins and exotoxins
After entering the host, most pathogens adhere to
host tissue,
penetrate or evade host defenses, and damage host tissues
Pathogens usually leave the body via specific portals of exit, which are
generally the same sites where they entered initially
M protein is found in
Streptococcus pyogenes
Opa protein is found in
Neisseria gonorrhoeae
Waxy lipid is found in
Mycobacterium tuberculosis
Exotoxins are ________ produced and secreted by _______
Proteins produced and secreted by bacteria
Exotoxins are soluble in
bodily fluids;
Exotoxins destroy
host cells
Exotoxins inhibit
metabolic functions
poisonous substances produced by microorganisms
Toxins
inactivated exotoxins used in vaccines
Toxoids
Once the host cell brings the exotoxin inside via phagocytosis?
B domain opens a pore in the endosome.
The ________ are then secreted into the surrounding medium during log phase.
exotoxins
Exotoxins are produced in
pathogenic bacteria, most commonly gram-positive bacteria
What happens after the bacterium gets degraded in a vacuole?
Releases endotoxins that induce the macrophage to produce
cytokines, interleukin-1
(IL-1), and tumor necrosis
factor alpha (TNF-α).
disseminated intravascular coagulation caused by
LIPID A
produced by mushrooms and are neurotoxic
Mycotoxins
alkaloid toxins that cause hallucinations
Ergot
carcinogenic toxin produced by Aspergillus
Aflatoxin
produced by mushrooms and are neurotoxic
Mycotoxins
Saxitoxin is what kind of toxin?
neurotoxin
- Paralytic shellfish poisoning is caused by
Saxitoxin
