CDS4300 Lecture 5 Host-Microbe Interactions - Custom Scholars
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CDS4300 Lecture 5 Host-Microbe Interactions

question
Symbiosis
answer
-To live together
-Relationships among organisms can change over time
question
Mutualism
answer
-Relationship in which both members benefit from their interaction
-e.g., human host and normal microbiota
question
Commensalism
answer
One member benefits without significantly affecting the other
question
Parasitism
answer
One member benefits while the other is harmed
question
Pathogen
answer
-A microorganism capable of causing a disease
-True pathogens: organisms that cause disease in a healthy immunocompetent host
-Opportunistic pathogens: organisms that usually do not produce disease but are capable of causing disease under specific conditions
question
Carrier State
answer
-Host is harboring pathogenic microorganism but may not be showing signs or symptoms
-Organism is incubating. e.g., HIV
-Disease is sub-clinical. Early in infection, incomplete clearance
-Chronic infection
-Latent infection. Clinically silent (such as herpes)
question
Colonization and Normal Microbiota
answer
-Initial colonization with microbes at birth
-Normal microbiota (normal flora): colonize surfaces of human host without causing a disease
-Resident flora: present for a long time; mutual relationship
-Transient flora: temporary; cannot compete with resident flora for resources
-Commonly found in clinical specimens. Causing infection or not?
question
Microbiome
answer
-The collective genome of the organisms residing in/on a host
-Microbiome affect host's fitness
-Beneficial effects of normal flora: compete with other organisms, protective, prime immune system, assist in digestion
question
Upper Respiratory Tract
answer
-Mouth, nose, pharynx
-Predominantly colonized by streptococci, neisseria, diphtheroids, and anaerobes in gingival crevices
-Staphylococcus aureus: opportunistic. 30% of population are carriers (reservoirs). Also Haemophilus influenzae, Streptococcus pneumoniae, Neisseria meningitidis
question
Lower Respiratory Tract
answer
-Trachea, bronchi, bronchioles, alveoli
-Normally sterile- protected by cilia, mucus
-Trachea and bronchi may have transient colonization from organisms in the upper respiratory tract
question
Gastrointestinal (GI) Tract
answer
-Esophagus- transient colonizers
-Stomach- usually sterile due to acid pH. Few organisms can survive (e.g., Helicobacter pylori, spores, parasites)
-Small intestine- proximal has streptococci, lactobacili, facultative anaerobes. Distal has similar to colon microbes
-Colon- home to most of the microbes in the human body. Majority are obligate anaerobes, some facultative. e.g., Bacteroides spp., Clostridium spp., Enterobacteriaceae
-Gut normal flora promote healthy digestion and provide nutrients to host (e.g., Lactobacillus)
-Antibiotics can significantly alter normal flora (such as causing C. diff)
question
Skin and Skin Structures
answer
-Dry, salty, low pH, fatty acids. Environment does not support growth of most organisms
-Outer layer is colonized with Corynebacterium spp., Micrococcus spp., staphylococci
-Some skin flora can be opportunistic pathogens if they penetrate through the skin of a susceptible host
question
Urogenital (UG) Tract
answer
-Kidneys, bladder, endocervix, and fallopian tubes are normally sterile
-Anterior urethra- colonized by skin flora. Females have an increased opportunistic infection rate than males due to shorter urethra length
-Flow of urine prevents extensive colonization of urinary bladder or urethra
-Vagina- Microbe population is influenced by hormones and pH (and age). Childbearing years have a lower pH and there are bacteria such as lactobacilli, anaerobic gram negative bacilli, and staphylococci. Pre-puberty and post-menopause years have a higher pH and there are bacteria such as yeast, gram negative bacilli, and staphylococci
question
Benefits of Normal Flora
answer
-Presence of normal flora inhibits the growth of pathogenic organisms by competing for space and resources ("microbial antagonism")
-Some secrete substances that inhibit the growth of harmful microbes
question
Factors that Affect Microbial Flora
answer
-Diet
-Physical fitness
-Hormonal state
-Personal hygiene
-Environmental triggers
-Antibiotics
-Age
-Changes to flora environment (pH, temp, O2, H2O, etc.)
question
How Normal Microbiota Become Opportunistic Pathogens
answer
-Normal flora introduced into an unusual body site. e.g., E. coli in colon is mutualistic, but is opportunistic when it enters the urethra (causing UTI)
-Immune suppression -> host unable to keep opportunistic microbes in check
-Changes in the normal flora. e.g., one microbe is able to proliferate and cause infection due to antibiotic use
question
Host Defenses
answer
-Innate immune response. Non-specific, defense barriers, phagocytosis
-Adaptive immune response. Specific, memory
question
Physical and Chemical Barriers
answer
-Intact skin is effective against most pathogens
-Cleansing mechanism: desquamation of skin, cilia and mucus on membranes, voiding urine cleans urinary tract, flow of saliva, tears (lubrication; also contain IgA and lysozyme)
question
Mucous Membranes
answer
-Respiratory, GI, and UG tracts have specialized cells
-Mucosal cells. Tight junctions, cilia
-Goblet cells. Secrete mucus (trap microbes, lubricate cells). Secrete antimicrobial substances (lysozyme, lactoferrin, lactoperoxidase)
question
Antimicrobial Substances
answer
-Lysozyme hydrolyzes the peptidoglycan layer of bacteria. Found in serum, tissue fluids, tears, breast milk, saliva, sweat, etc
-Secretory IgA in mucous membranes. Serve as opsonins (which tag microbes for phagocytosis), enhance phagocytosis, fix complement
-Beta-lysine in serum is lethal against gram positive bacteria
question
Inflammation and Complement Activation
answer
-To eliminate or confine microbe, stimulate the adaptive response and promote healing
-Cytokine release recruits more immune cells (neutrophils and macrophages kill microbes by phagocytosis)
-Complement system (opsonization, direct microbe destruction)
question
Phagocyte-Bacterial Interactions
answer
-Antibody-mediated immunity. B-cells produce specific antibodies. Primarily against exogenous pathogens
-Cell-mediated immunity. Primary: cytotoxic T-cells. Required for killing of facultative intracellular pathogens (endogenous microbes)
-Production of memory B-cells and T-cells for lasting immunity
question
Adaptive Immune Response
answer
-Adherence
-Proliferation
-Tissue damage
-Invasion
-Dissemination
question
How do Microbes Cause Disease?
answer
The ability of a microbe to cause disease in a host
question
Pathogenicity
answer
The degree of a microbe's pathogenicity (how effective they are at causing disease)
question
Virulence
answer
-Genetic, biochemical, or structural features that enable a microbe to cause disease
-e.g., capsule, fimbriae, pili, flagella, toxins, enzymes
question
Virulence Factors
answer
-Adhesion
-Interference of phagocytes
-Biofilm formation
-Production of toxins and enzymes
-Avoiding and survival from immune response
-Genetic transfer
question
Common Microbial Virulence Mechanisms
answer
-Allow pathogens to colonize host
-Adhesins- bind and adhere to specific receptors on host cells. Located on fimbriae tips, flagella, slime layer, capsule. Increases ability to colonize
-Biofilm formation
question
Adhesion Factors
answer
-Capsule, slime layer, biofilm. Mask cell surface structures and inhibit complement; may share similarities with host cell components
-Inhibition of phagosome-lysosome fusion
-Secretion of toxins (e.g., leukocidin), and enzymes that damage phagocytic cells
-Flagella to escape
question
Ability to Interfere with Phagocytosis
answer
-Biofilm- bacteria are bound within a sticky matrix are polysaccharides
-Adhere to surfaces within a host (e.g., dental plaque)
-Adhere to hospital surfaces and indwelling medical devices
-Evade immune function
-Affect efficacy of antimicrobials
-Protect against environmental changes
-Allow exchange of genetic material and quorum sensing
question
Ability to Form a Biofilm
answer
-Damage host cells, antibodies, and other structures in the body
-Include specific enzymes to combat reactive oxygen species (ROS: kills microbes. microbes make enzymes to combat ROS) produced by host cells
-Catalase, superoxide dismutase, peroxidase
question
Enzymes
answer
-Secreted by bacteria into the environment, or released upon bacterial lysis
-Produced by both Gram (+) and Gram (-) bacteria
-3 types: cytotoxins (attack cell), neurotoxins (attack neurons), enterotoxins (attack GI)
-Can have enzymatic activity
question
Exotoxins
answer
-Lipid A portion of LPS on outer membrane of Gram (-) bacteria
-Released when bacteria dies
-Can lead to fever, toxic shock, DIC
-Do not have enzymatic activity
question
Endotoxin
answer
1) Lysis of Gram (+) bacteria release sell wall components
2) These bind to binding proteins in the blood stream
3) Complex bind to and activate macrophages
4) Triggering the release of cytokines -> inflammation
question
Peptidoglycan and Teichoic Acids Induce Inflammatory Response
answer
-Change cell surface antigens (antigenic variation)
-Mimic host antigens (so immune system will attack both host cells and microorganisms)
-Release compounds that bind free iron (e.g., siderophores; bacteria need iron, siderophores lyse RBC to get iron)
-Survive inside infected host cell (e.g., facultative intracellular pathogens)
question
Ability to Survive and Avoid Host Immune System
answer
-Mobile genetic elements
-DNA fragments containing virulence and resistance determinants as well as the enzymes that mediate their own transfer and integration into new host DNA
-e.g., plasmids, pathogenicity islands, bacteriophage
-Genetic transfer via transformation, transduction, and conjugation
question
Genetic Transfer Mechanisms
answer
1) Incubation period. Time between the arrival of the pathogen and the onset of symptoms. Length influenced by nature and virulence of pathogen, infective dose, health and immune status of host, and site of infection
2) Prodromal period. Time just prior to the period of illness. Feeling of "coming down with something". Pathogen may be highly communicable
3) Illness. Patient experiences the typical symptoms
4) Decline and convalescence. Infection subsides and patient recovers. Recovery length depends on amount of damage, and immune status of host. OR patient condition deteriorates
question
Phases of Infection
answer
-Airborne: respiratory secretions, spores in dust/soil. Respiratory tract is the most common portal of entry
-Food, water: ingestion of bacteria or pre-formed bacterial toxins
-Physical contact: directly by saliva, skin, sexual; indirectly through fomites (vehicles of spread; inanimate objects; e.g., sharing contaminated materials, hands of HCW)
-Zoonotic: transmitted by mammals or arthropod vectors and reservoirs. e.g., infected Anopheles mosquito transmits Plasmodium species that cause malaria
question
Routes of Transmission
answer
-Study of where and when diseases occur and of how they are transmitted within populations. Find ways to control and reduce the spread of disease and improve health
-Health-care associated infections (Nosocomial). Influence host-microbe interactions
-Prevention. Immunization, vaccination, antimicrobial treatment. Sanitation, disinfection, control microbial reservoirs
question
Epidemiology
answer
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1 of 40
question
Symbiosis
answer
-To live together
-Relationships among organisms can change over time
question
Mutualism
answer
-Relationship in which both members benefit from their interaction
-e.g., human host and normal microbiota
question
Commensalism
answer
One member benefits without significantly affecting the other
question
Parasitism
answer
One member benefits while the other is harmed
question
Pathogen
answer
-A microorganism capable of causing a disease
-True pathogens: organisms that cause disease in a healthy immunocompetent host
-Opportunistic pathogens: organisms that usually do not produce disease but are capable of causing disease under specific conditions
question
Carrier State
answer
-Host is harboring pathogenic microorganism but may not be showing signs or symptoms
-Organism is incubating. e.g., HIV
-Disease is sub-clinical. Early in infection, incomplete clearance
-Chronic infection
-Latent infection. Clinically silent (such as herpes)
question
Colonization and Normal Microbiota
answer
-Initial colonization with microbes at birth
-Normal microbiota (normal flora): colonize surfaces of human host without causing a disease
-Resident flora: present for a long time; mutual relationship
-Transient flora: temporary; cannot compete with resident flora for resources
-Commonly found in clinical specimens. Causing infection or not?
question
Microbiome
answer
-The collective genome of the organisms residing in/on a host
-Microbiome affect host's fitness
-Beneficial effects of normal flora: compete with other organisms, protective, prime immune system, assist in digestion
question
Upper Respiratory Tract
answer
-Mouth, nose, pharynx
-Predominantly colonized by streptococci, neisseria, diphtheroids, and anaerobes in gingival crevices
-Staphylococcus aureus: opportunistic. 30% of population are carriers (reservoirs). Also Haemophilus influenzae, Streptococcus pneumoniae, Neisseria meningitidis
question
Lower Respiratory Tract
answer
-Trachea, bronchi, bronchioles, alveoli
-Normally sterile- protected by cilia, mucus
-Trachea and bronchi may have transient colonization from organisms in the upper respiratory tract
question
Gastrointestinal (GI) Tract
answer
-Esophagus- transient colonizers
-Stomach- usually sterile due to acid pH. Few organisms can survive (e.g., Helicobacter pylori, spores, parasites)
-Small intestine- proximal has streptococci, lactobacili, facultative anaerobes. Distal has similar to colon microbes
-Colon- home to most of the microbes in the human body. Majority are obligate anaerobes, some facultative. e.g., Bacteroides spp., Clostridium spp., Enterobacteriaceae
-Gut normal flora promote healthy digestion and provide nutrients to host (e.g., Lactobacillus)
-Antibiotics can significantly alter normal flora (such as causing C. diff)
question
Skin and Skin Structures
answer
-Dry, salty, low pH, fatty acids. Environment does not support growth of most organisms
-Outer layer is colonized with Corynebacterium spp., Micrococcus spp., staphylococci
-Some skin flora can be opportunistic pathogens if they penetrate through the skin of a susceptible host
question
Urogenital (UG) Tract
answer
-Kidneys, bladder, endocervix, and fallopian tubes are normally sterile
-Anterior urethra- colonized by skin flora. Females have an increased opportunistic infection rate than males due to shorter urethra length
-Flow of urine prevents extensive colonization of urinary bladder or urethra
-Vagina- Microbe population is influenced by hormones and pH (and age). Childbearing years have a lower pH and there are bacteria such as lactobacilli, anaerobic gram negative bacilli, and staphylococci. Pre-puberty and post-menopause years have a higher pH and there are bacteria such as yeast, gram negative bacilli, and staphylococci
question
Benefits of Normal Flora
answer
-Presence of normal flora inhibits the growth of pathogenic organisms by competing for space and resources ("microbial antagonism")
-Some secrete substances that inhibit the growth of harmful microbes
question
Factors that Affect Microbial Flora
answer
-Diet
-Physical fitness
-Hormonal state
-Personal hygiene
-Environmental triggers
-Antibiotics
-Age
-Changes to flora environment (pH, temp, O2, H2O, etc.)
question
How Normal Microbiota Become Opportunistic Pathogens
answer
-Normal flora introduced into an unusual body site. e.g., E. coli in colon is mutualistic, but is opportunistic when it enters the urethra (causing UTI)
-Immune suppression -> host unable to keep opportunistic microbes in check
-Changes in the normal flora. e.g., one microbe is able to proliferate and cause infection due to antibiotic use
question
Host Defenses
answer
-Innate immune response. Non-specific, defense barriers, phagocytosis
-Adaptive immune response. Specific, memory
question
Physical and Chemical Barriers
answer
-Intact skin is effective against most pathogens
-Cleansing mechanism: desquamation of skin, cilia and mucus on membranes, voiding urine cleans urinary tract, flow of saliva, tears (lubrication; also contain IgA and lysozyme)
question
Mucous Membranes
answer
-Respiratory, GI, and UG tracts have specialized cells
-Mucosal cells. Tight junctions, cilia
-Goblet cells. Secrete mucus (trap microbes, lubricate cells). Secrete antimicrobial substances (lysozyme, lactoferrin, lactoperoxidase)
question
Antimicrobial Substances
answer
-Lysozyme hydrolyzes the peptidoglycan layer of bacteria. Found in serum, tissue fluids, tears, breast milk, saliva, sweat, etc
-Secretory IgA in mucous membranes. Serve as opsonins (which tag microbes for phagocytosis), enhance phagocytosis, fix complement
-Beta-lysine in serum is lethal against gram positive bacteria
question
Inflammation and Complement Activation
answer
-To eliminate or confine microbe, stimulate the adaptive response and promote healing
-Cytokine release recruits more immune cells (neutrophils and macrophages kill microbes by phagocytosis)
-Complement system (opsonization, direct microbe destruction)
question
Phagocyte-Bacterial Interactions
answer
-Antibody-mediated immunity. B-cells produce specific antibodies. Primarily against exogenous pathogens
-Cell-mediated immunity. Primary: cytotoxic T-cells. Required for killing of facultative intracellular pathogens (endogenous microbes)
-Production of memory B-cells and T-cells for lasting immunity
question
Adaptive Immune Response
answer
-Adherence
-Proliferation
-Tissue damage
-Invasion
-Dissemination
question
How do Microbes Cause Disease?
answer
The ability of a microbe to cause disease in a host
question
Pathogenicity
answer
The degree of a microbe's pathogenicity (how effective they are at causing disease)
question
Virulence
answer
-Genetic, biochemical, or structural features that enable a microbe to cause disease
-e.g., capsule, fimbriae, pili, flagella, toxins, enzymes
question
Virulence Factors
answer
-Adhesion
-Interference of phagocytes
-Biofilm formation
-Production of toxins and enzymes
-Avoiding and survival from immune response
-Genetic transfer
question
Common Microbial Virulence Mechanisms
answer
-Allow pathogens to colonize host
-Adhesins- bind and adhere to specific receptors on host cells. Located on fimbriae tips, flagella, slime layer, capsule. Increases ability to colonize
-Biofilm formation
question
Adhesion Factors
answer
-Capsule, slime layer, biofilm. Mask cell surface structures and inhibit complement; may share similarities with host cell components
-Inhibition of phagosome-lysosome fusion
-Secretion of toxins (e.g., leukocidin), and enzymes that damage phagocytic cells
-Flagella to escape
question
Ability to Interfere with Phagocytosis
answer
-Biofilm- bacteria are bound within a sticky matrix are polysaccharides
-Adhere to surfaces within a host (e.g., dental plaque)
-Adhere to hospital surfaces and indwelling medical devices
-Evade immune function
-Affect efficacy of antimicrobials
-Protect against environmental changes
-Allow exchange of genetic material and quorum sensing
question
Ability to Form a Biofilm
answer
-Damage host cells, antibodies, and other structures in the body
-Include specific enzymes to combat reactive oxygen species (ROS: kills microbes. microbes make enzymes to combat ROS) produced by host cells
-Catalase, superoxide dismutase, peroxidase
question
Enzymes
answer
-Secreted by bacteria into the environment, or released upon bacterial lysis
-Produced by both Gram (+) and Gram (-) bacteria
-3 types: cytotoxins (attack cell), neurotoxins (attack neurons), enterotoxins (attack GI)
-Can have enzymatic activity
question
Exotoxins
answer
-Lipid A portion of LPS on outer membrane of Gram (-) bacteria
-Released when bacteria dies
-Can lead to fever, toxic shock, DIC
-Do not have enzymatic activity
question
Endotoxin
answer
1) Lysis of Gram (+) bacteria release sell wall components
2) These bind to binding proteins in the blood stream
3) Complex bind to and activate macrophages
4) Triggering the release of cytokines -> inflammation
question
Peptidoglycan and Teichoic Acids Induce Inflammatory Response
answer
-Change cell surface antigens (antigenic variation)
-Mimic host antigens (so immune system will attack both host cells and microorganisms)
-Release compounds that bind free iron (e.g., siderophores; bacteria need iron, siderophores lyse RBC to get iron)
-Survive inside infected host cell (e.g., facultative intracellular pathogens)
question
Ability to Survive and Avoid Host Immune System
answer
-Mobile genetic elements
-DNA fragments containing virulence and resistance determinants as well as the enzymes that mediate their own transfer and integration into new host DNA
-e.g., plasmids, pathogenicity islands, bacteriophage
-Genetic transfer via transformation, transduction, and conjugation
question
Genetic Transfer Mechanisms
answer
1) Incubation period. Time between the arrival of the pathogen and the onset of symptoms. Length influenced by nature and virulence of pathogen, infective dose, health and immune status of host, and site of infection
2) Prodromal period. Time just prior to the period of illness. Feeling of "coming down with something". Pathogen may be highly communicable
3) Illness. Patient experiences the typical symptoms
4) Decline and convalescence. Infection subsides and patient recovers. Recovery length depends on amount of damage, and immune status of host. OR patient condition deteriorates
question
Phases of Infection
answer
-Airborne: respiratory secretions, spores in dust/soil. Respiratory tract is the most common portal of entry
-Food, water: ingestion of bacteria or pre-formed bacterial toxins
-Physical contact: directly by saliva, skin, sexual; indirectly through fomites (vehicles of spread; inanimate objects; e.g., sharing contaminated materials, hands of HCW)
-Zoonotic: transmitted by mammals or arthropod vectors and reservoirs. e.g., infected Anopheles mosquito transmits Plasmodium species that cause malaria
question
Routes of Transmission
answer
-Study of where and when diseases occur and of how they are transmitted within populations. Find ways to control and reduce the spread of disease and improve health
-Health-care associated infections (Nosocomial). Influence host-microbe interactions
-Prevention. Immunization, vaccination, antimicrobial treatment. Sanitation, disinfection, control microbial reservoirs
question
Epidemiology
answer
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