2 - (Most Exam Q's) Host-Microbe Relationships Flashcards
Types of Host-Microbe Relationships
Symbiosis - define Normal Flora - define Commensalism Mutualism Opportunism Parasitism Vector
- Symbiosis – the close association and interaction of two dissimilar organisms living together.
- Normal flora – those microorganisms which are normally and consistently found in or on the body in the absence of disease.
the close association and interaction of two dissimilar organisms living together.
Symbiosis
those microorganisms which are normally and consistently found in or on the body in the
absence of disease.
Normal flora
a. Resident vs. transient flora
b. Nature and variety of microbes are often distinctive for different regions of the body
c. Normal flora of one area may cause infection in another region of the body
Types of Host-Microbe Relationships
Types of Host-Microbe Relationships
Symbiosis Normal Flora (microbiota) Commensalism Mutualism Opportunism Parasitism Vector
– association between organisms in which one is benefitted and the other is neither benefitted nor harmed.
Commensalism
– both the microbe and host derive benefits from the relationship
Mutualism
– disease traits of the resident flora are demonstrated only when normal host-microbe relationship is altered.
Opportunism
a. Prolonged antibiotic therapy alters flora
b. Traumatic injury, surgery
c. Immunological compromise
d. Hormonal or chemical changes
– symbiotic relationship in which a microorganism lives in or on a host at the expense of the host.
Parasitism
– a carrier of microbes from one host
to another
Vector
a. Insects and other animals
b. Inanimate articles (fomite) e.g. personal items, eating utensils, tools, hospital instruments, food water, body discharges, bandages, etc.
– the growth and spread of a pathogen in or on a host resulting in injury to the host tissue
Infectious disease
Infectious disease
a. Pathogen –
a microbe capable of causing disease by invading tissues, producing toxins, or both
Infectious disease
b. Virulence –
(1) Infectivity – how easily the microbe survives the normal host defenses and ESTABLISHES infection
(2) Severity of the damage it causes the infected host
the degree of pathogenicity
b. Virulence –
(1) ______ – how easily the microbe survives the normal host defenses and ESTABLISHES infection
(2) _____ of the damage it causes the infected host
Infectivity
Severity
Modes of Transmission
Direct Contact
Inhalation
Ingestion
Parenteral
Modes of Transmission
- Inhalation -
droplets or particles in the air (aerosolized could be on tiny water droplet, dust particle, etc)
Modes of Transmission
- Ingestion -
of food and water (or other items we put into our mouths) that is contaminated with fecal material, insects, dead or live animals, soil, and other sources
Modes of Transmission
- Parenteral –
direct contamination of blood, body fluids, or tissues by arthropod and other animal vectors and by nonsterile syringes and needles (mosquitos etc)
Microbial Virulence Factors
What enables the ESTABLISHMENT of infection?
Name all four factors
Attachment ; Establishment Factors
- Portal of Entry
- Attachment
- Quantity
- Quorum-sensing Regulators
– The organism must enter the correct portion of the body (e.g. ingestion vs. inhalation vs wound)
Choosing correct portal allows for what two things?
a. Portal of Entry
(1) Overcome local defenses
(2) Find right/best environment for growth/survival
– The attachment of the microbe to tissue is required in order to establish a site of infection
Three methods of attachment?
Attachment
(1) Fimbrae – attach to specific receptor sites on specific tissue
(2) Surface chemicals – dissolve covering of cells and aid chemical attachment
(3) Adhesive Matrix Molecules – produce biofilms thus providing “protection” for bacteria within harsh human environments.
three methods of attachment for microbes?
Fimbrae
Surface Chemicals
Adhesive Matrix Molecules
– a certain minimum number of organisms are required to establish infection – presumably needed to overcome host defenses
Quantity
– various chemicals that (1) restrain the disease-causing actions of the microbe until sufficient quantity of microbes are present, then (2) switch on the disease-causing actions all at once. (TYPICALLY DONE VIA OPERON THAT REGULATES THE BACTERIA AND SWITCHES WHEN THE BACTERIA HAS MULTIPLIED ENOUGH AND IN A POSITION FOR AN ATTACK; AND MAJOR SYMPTOMS COME ON FAST!)
Quorum-sensing Regulators
Microbial Virulence Factor
Antiphagocytic factors
a. Action: prevent microbe from being engulfed and/or destroyed by white blood cell (physical
protection or chemical poison)
b. Examples:
Examples of any
(1) Capsule – slippery & slimy nature assists bacteria from being engulfed by phagocyte
(2) Leukocidin (staphylococci, streptococci, & certain bacilli) – causes destruction of white blood cells
(3) Coagulase (Staphylococcus aureus) – causes fibrin clot to form around the microbes
(4) Survival of phagocytosis – resistance to killing within a phagocyte (e.g. mycobacteria,
gonococcus, Listeria)
Microbial Virulence Factor
Antiphagocytic factors
a. Action: prevent microbe from being engulfed and/or destroyed by white blood cell (physical protection or chemical poison)
Examples of antiphagocytic Factors?
Capsule
Coagulase
Leukocidin
Survival of phagocytosis
b. Examples:
(1) Capsule – slippery & slimy nature assists bacteria from being engulfed by phagocyte
(2) Leukocidin (staphylococci, streptococci, & certain bacilli) – causes destruction of white blood cells
(3) Coagulase (Staphylococcus aureus) – causes fibrin clot to form around the microbes
(4) Survival of phagocytosis – resistance to killing within a phagocyte (e.g. mycobacteria, gonococcus, Listeria)
- “Invasive” Enzymes – factors that promote the invasion and spread of a pathogen in/on the tissue
a. Action: enable the pathogen to invade the tissue or the site of infection to spread
b. Examples:
(1) Collagenase – breaks down collagen fibers thus destroying tissue integrity
(2) Lecithinase – destructive to cell membranes of red blood cells and other tissue cells
(3) Hyaluronidase (Staphylococcus, Streptococcus, Clostridium perfringens) – breaks
down hyaluronic acid in cell membranes
(4) Fibrinolysin & Streptokinase – lyses fibrin in blood clots thus preventing isolation of the infection
(5) Hemolysins (Staphylococcus, Streptococcus, C. perfringens) – dissolve red blood cell membranes
(6) Lipase – digest lipids allowing bacteria to enter
(7) Proteases – digest proteins (e.g. IgA, certain other protective chemicals) thus permitting bacteria to evade entrapment, digestion, etc.
(8) Super Antigens – cause exacerbated immune or inflammatory response
Now look away and name all 8 “invasive enzymes”
Collagenase Fibrinolysin & streptokinase Hyaluronidase Hemolysins Lipase Lecithinase Proteases Super Antigens
Cool Fibrin H H L L PS
or Cool Fibrin HHLLPS
Exotoxins
a. Proteins excreted from the cell
(1) Cytolytic and Receptor-binding proteins (usually)
(2) Many are dimeric: _____
(3) Tissues affected are very _____
(4) Superantigens are special group of _____
(5) Often coded on _____
Exotoxins
(1) Cytolytic and Receptor-binding proteins (usually)
(2) Many are dimeric: A & B subunits; facilitates entry into tissue cells
(3) Tissues affected are very defined and limited
(4) Superantigens are special group of ____
(5) Often coded on plasmid or lysogenic phage
Exotoxins
a. Proteins excreted from the cell
b. Cause specific and widespread biological effects on the body
c. Highly ____ (per unit weight)
d. Elicit ________
Exotoxins
a. Proteins excreted from the cell
b. Cause specific and widespread biological effects on the body
c. Highly potent (per unit weight)
d. Elicit good, protective antibodies
Examples of Exotoxins
SSTDC
(2) Staphylococcal enterotoxin – diarrhea, vomiting
(5) Streptococcal erythrogenic toxin – scarlet fever rash
(1) Tetanus neurotoxin – attacks motor nerves, triggers involuntary muscle contractions
(4) Diphtheria toxin – interferes with protein production in bronchial epithelial cells causing the production of a mucous, fibrous blockage of the respiratory tract; also inactivates protein production in heart muscle
(3) Cholera toxin – massive diarrhea
Exotoxins - Proteins excreted from the cell
e. Examples:
(1) Tetanus neurotoxin – attacks motor nerves, triggers involuntary muscle contractions
(2) Staphylococcal enterotoxin – diarrhea, vomiting
(3) Cholera toxin – massive diarrhea
(4) Diphtheria toxin – interferes with protein production in bronchial epithelial cells causing the production of a mucous, fibrous blockage of the respiratory tract; also inactivates protein production in heart muscle
(5) Streptococcal erythrogenic toxin – scarlet fever rash
Endotoxins
a. Lipid A
b. Binds to
c. Stimulates
d. can trigger
e. antibodies?
a. “Lipid A” – the lipopolysaccharide (LPS) component of gram-negative cell walls which is released upon disintegration of the cell.
b. Binds to CD14 and TLR4 (Toll-Like Receptor 4) on macrophages, B-cells, other cells.
c. Stimulates production and release of Acute-phase Cytokines, e.g. IL-1, TNF, IL-6 (i.e. it triggers white blood cells to discharge chemicals which induce fever, pain, hemorrhage, blood pressure drop, etc.
d. Not very potent per unit weight; however, very high levels in bloodstream can trigger very large effects including shock and death
e. Does not elicit very good or protective antibodies
f. Example: gram-negative bacillus cell wall sloughs off or disintegrates
Microbial Virulence Factors
Genetic alterations - define
Normal genetic operation – DNA code is translated into intended enzymes and proteins (some of which are antigens)
Microbial Virulence Factors
Genetic alterations - three examples?
Plasmid
Lysogeny
Gene recombination
Microbial Virulence Factors
Genetic alterations - ____ ? – Viral DNA incorporated into bacterial DNA
Lysogeny = Viral DNA incorporated into bacterial DNA
Lysogeny
(1) Code for some _____ and ______
(2) Introduced by _____ and transmitted to daughter bacterial cells during cell division
exotoxins and invasive enzymes
viral infection of the bacteria
Microbial Virulence Factors
Genetic alterations - _____? – pieces of genetic material from one organism are incorporated into the genetic material of another organism.
Gene recombination
Microbial Virulence Factors
Genetic alterations - Gene recombination
Results in?
(1) Different (new types) antigens are produced – current immunity not effective (e.g. Influenza virus)
(2) Causes increased resistance to antibiotics
Microbial Virulence Factors
Genetic alterations - Gene recombination
Results in:
(1) _______ are produced – current immunity not effective (e.g. Influenza virus)
(2) Causes increased _________
Different (new types) antigens
resistance to antibiotics
Microbial Virulence Factors
Genetic alterations - Gene recombination
Results in:
(1) _______ are produced – current immunity not effective (e.g. Influenza virus)
(2) Causes increased _________
Different (new types) antigens
resistance to antibiotics
Special Antimicrobic Resistance Situations
a. Special Resistance Situations – General / Background
(1) Many bacteria gain antibiotic resistance by:
(a)
(b)
(c)
(2) Presence of an antibiotic-resistant bacterium in the community / hospital leads to:
(a)
(b)
(c)
Many bacteria gain antibiotic resistance by:
(a) Mutated genes (“successful” about 1 in 10 billion cell reproductions ?)
(b) Plasmid encoded genes
(c) Lysogenic virus
Presence of an antibiotic-resistant bacterium in the community / hospital leads to:
(a) Survival of the mutant
(b) Increasing numbers of the mutant in the population
(c) Disease problems increase and spread to new geographic locations
Special Antimicrobic Resistance Situations
b. Beta lactamase
(1) Bacterial enzyme which _______
inactivates many beta-lactam antimicrobics (e.g. penicillin, cephalosporin, carbapenem, monobactam classes).
Special Antimicrobic Resistance Situations
b. Beta lactamase
(2) ____ encoded gene – Frequently carried by Enterobacteriaceae (family of gram- negative bacilli) Staphylococcus, Neisseria gonorrhoeae, Haemophilus influenzae) that frequently produce the enzyme. Lab test for beta-lactamase is automatic with these bacteria. If test report is “positive”, then use an antibiotic which is resistant to beta-lactamase.
Plasmid endoded gene
Special Antimicrobic Resistance Situations
b. Beta lactamase
(3) ______ – version that affects a larger group of antimicrobics that are typically not affected by typical beta-lactamase.
Extended Spectrum Beta-lactamase (ESBL)
Special Antimicrobic Resistance Situations
c. Methicillin-Resistant Staphylococcus aureus (MRSA)
(1) Mutated mecA gene – encodes a low-affinity _____
(2) Consider MRSA to be resistant to all ______
MRSA
penicillin binding protein (PBP2a)
beta-lactam antibiotics (e.g. penicillins and cephalosporins
regardless of the in vitro lab results.)
Special Antimicrobic Resistance Situations
d. Carbapenem-Resistant Enterobacteriaceae (CRE) –
Carbapenemase-producing Enterobacteriaceae (CPE)
(1) Mutated genes for outer membrane porins (pore
proteins) and PBP transpeptides
(2) A form of _____
(3) Carried by _____
(4) Results in:
(a) Loss of ____
(b) Loss of ____
(1) Mutated genes for outer membrane porins (pore
proteins) and PBP transpeptides
(2) A form of beta-lactamase
(3) Carried by plasmids
(4) Results in:
(a) Loss of drug diffusion into periplasm
(b) Loss of cross-linking activity of PBP
CONCERNING Threats
(1) Erythromycin-Resistant Group A Streptococcus
(2) Clindamycin-Resistant Group B Streptococcus
Host Resistance Factors
- Non-specific Factors
a. Innate species immunity/resistance
b. Physical/Mechanical Barriers - what are they?
c. Chemical barriers
(1) Intact skin prevents entry of organism
(2) Mucous membranes – sticky linings trap invading
organisms
(3) Cilia of respiratory tract – move particles to the
throat where they are swallowed
(4) Peristaltic action of gut – moves gut contents at a
slow, steady pace thus preventing overgrowth
(5) Normal flora – occupy attachment sites & compete
for nutrients
Host Resistance Factors
- Non-specific Factors
c. Chemical barriers - What are they?
(1) Acid pH (stomach, skin, vagina, urine) – denatures most organisms
Exceptions: typhoid & tubercule bacilli, protozoan
cysts, polio hepatitis A viruses
(2) Bile salts (intestine) – inhibitory to many microbes
(3) Lysozyme (tears, saliva) – digests gram-positive cell walls
(4) Antimicrobial chemicals from normal flora
(5) Interferon (a type of lymphokine) – human host cell protein(s) produced in response to invasion by certain viruses. It acts as a local defense against certain viruses by producing inhibiting substances that “interfere” with viral reproduction.
Host Resistance Factors
1. Non-specific Factors
Phagocytosis
Phagocytosis
(1) “Foreign” particles are ingested & digested by polymorphonuclear leukocytes, monocytes, and
macrophages
(2) Numerous enzymes act to degrade and digest the ingested particles
(3) Local tissue damage may occur due to egestion of waste materials
Host Resistance Factors
1. Non-specific Factors
Inflammation
(1) Develops after mechanical injury or exposure to certain _____
(2) Inflammatory process limits the ______
(a) Increased capillary permeability causes f_____ and ______
(b) Neutrophils and macrophages phagocytize the invading organism
(c) Fibrin clot/wall is formed to enclose the pus (phagocytes, dead microbes, dead tissue cells, plasma)
- Non-specific Factors
Inflammation
(1) Develops after mechanical injury or exposure to certain chemicals
(2) Inflammatory process limits the extent of injury
(a) Increased capillary permeability causes fluid accumulation and influx of phagocytic leukocytes
(b) Neutrophils and macrophages phagocytize the invading organism
(c) Fibrin clot/wall is formed to enclose the pus (phagocytes, dead microbes, dead tissue cells, plasma)
Specific Factors
a. Cell-Mediated Immunity
(1) Antigen stimulates the release of biologically active substances called lymphokines
(2) Lymphokines enhance phagocytosis and killing
Specific Factors
Antibodies and Complement
(1) Antibodies neutralize the antigen
(2) Antibodies opsonize the antigen [Opsonin – antibody that combines with bacterial cells and makes them more susceptible to phagocytosis.]
(3) Complement assists the antibody in neutralizing or lysing the bacteria
[Complement – a complex series of serum proteins involved in certain antigen-antibody reactions.]
Specific factors - two?
Cell Mediated Immunity
Antibodies and Complement
Non specific factors -
Physical / Mechanical Barriers
Chemical Barriers
Phagocytosis
Inflammation
candida albicans + antibiotics = example of what?
yeast growing uninhibited by normal flora so it would be a relationship of OPPORTUNISM
shigella is highly ____ because it does not take many of the bacterial microbes to be ingested to cause damage and infection
virulent
Quorum sensing regulators think….
operon and fast symptoms
Operon is waiting to be stimulated and bind to the operator site until there is sufficient quantity to attack
“Invasive” Enzymes think….
Name them all
offense
Cool Fibrin H H L L P S
(1) Collagenase – breaks down collagen fibers thus destroying tissue integrity
(2) Lecithinase – destructive to cell membranes of red blood cells and other tissue cells
(3) Hyaluronidase (Staphylococcus, Streptococcus, Clostridium perfringens) – breaks
down hyaluronic acid in cell membranes
(4) Fibrinolysin &aStreptokinase – lyses fibrin in blood clots thus preventing isolation of the infection
(5) Hemolysins (Staphylococcus, Streptococcus, C. perfringens) – dissolve red blood cell membranes
(6) Lipase – digest lipids allowing bacteria to enter
(7) Proteases – digest proteins (e.g. IgA, certain other protective chemicals) thus permitting bacteria to evade entrapment, digestion, etc.
(8) Super Antigens – cause exacerbated immune or inflammatory response
