Pathogen-Host Interactions Flashcards
Pathogen
ALWAYS causes disease
Examples of pathogens (many)
Neisseria gonorrhoea
Ebola virus
HIV
Lyme disease
Potential Pathogen
does not always lead to disease
needs to be the right time and place
Example of a potential pathogen
E. coli
primary cause of UTI
but we all have E. coli in our gut
Non-pathogen
generally don’t cause disease except in RARE cases
in immunocompromised
Examples of non-pathogens (2)
1) Lactobacillus
-in yoghurt and cheese
2) Carnobacterium
-in tinned fish
Virulence factors
factors that help organisms cause disease or avoid immune responses
e.g. toxin production, capsule, biofilm
Normal flora/ Microbiota definition
organisms that are typically found at a body site
may cause disease if in OTHER sites
More about normal flora
bacteria are everywhere
certain organism live in specific sites in/on the body
protect us
mucous membranes tract all have bacteria that reside in those ecological niches
BUT mucosal sites also act as the potential portals of entry for most bacteria
Mucous membranes/routes of exposure (4 main ones)
1) respiratory, oral (mouth, nose)
2) direct inoculation - sharps
3) GI tract
4) genital tract
T or F: The majority of the routes of exposure all have normal flora.
TRUE
Important to examine these sites to see what defences exist that maintain the BALANCE of normal flora and help to control the entry of pathogens
What type of flora would you expect BELOW the belt?
Gram -
What type of flora would you expect ABOVE the belt?
Gram +
In a hospitalized patient, what type of flora would you expect in a patient in the respiratory tract?
Gram -
patient lying down
has to do with gravity
Normal Flora of the Skin with examples
Gram +
-bacilli - Corynebacteria AKA “diptheroids”
-cocci - Staphylococci
Below the belt: Gram -
Organisms that can cause infection colonies the skin including pathogens like Staphylococcus aureus but usually Saphylococci non-aureus predominate
Respiratory tract examples
Staphylococcus
Streptococcus
-Streptococcus pneumoniae
-Viridans Streptococcus
Haemophilus
Anaerobes
Normal flora of the respiratory tract and oral flora
oral health plays a big role in the bacterial populations of the oral flora
anaerobes:
-oxygen is toxic
-produce gases and bad breath
-live in the crevices between teeth
-why babies don’t get bad breath
Flora in the GI tract depend on ________
the site
upper vs lower GI tract
Normal Flora of the GI Tract
digest food so we can absorb nutrients
UPPER GI
Facultative aerobes
-grows anaerobically AND aerobically
LOWER GI
-anaerobes
few gram POSITIVE bacteria in the GI tract (although Enterococci are present as they are resistant to bile)
GI Tract examples (many)
Anaerobes
Enterococcus
Enterobacteriaceae
-E. coli
-Klebsiella
Streptococcus
-Streptococci anginosus
Lactobacillus
Candida
Normal flora of the Genitourinary tract
urine washes organism from the urethra to maintain a sterile bladder
bladder doesn’t have a ton of bacteria, if it does –> UTI
vaginal flora changes with age
prepubescent and postmenopausal women
-Flora similar to skin flora
Women of child bearing age
-many bacterial species with a predominance of lactobacillus
Genitourinary tract examples (2)
1) Lactobacillus
2) Streptococcus
-Streptococcus agalactiae
pH of the female genital tract in prepubescent women
pH of 7
same as skin
menopause - not longer have Lactobacillus
pH of the female genital tract in pubescent women
pH of 4 (hella acidic!)
gets colonized by Lactobacillus, produces lactic acid
prevents bacteria from being able to colonize and infect
Visible under a microscope, this is an indicator of abnormal flora in the genitourinary tract…
clue cells
cells coated with bacteria
What happens if the pH in the female genital tract goes up?
UTIs
HIV
syphilis
yeast infections
bacterial vaginosis
Normal flora offer _____________ from potential pathogens
protection
Disrupting the normal flora - example C. difficile
leading cause of antibiotic associated diarrhea
EUBIOSIS
-normal flora in GI tract
-prevent colonization by pathogens
-prevent onset of disease
antibiotics wipe out the normal flora and allow the C. difficile spores to colonize the gut
DYSBIOSIS
-produces toxins that can lead to significant disease in the colon (ulcerative colitis) and can even lead to death
Eubiosis
normal microbiome
state of balance in the gut microbiota, where beneficial microbes outnumber harmful ones
Dysbiosis
disruption of the normal microbiome
Risk factors for C. difficile (3)
1) antibiotic use
2) being in the hospital
3) age
Bad clinical manifestations of C. difficile infection (2)
1) ulcerative colitis
2) death
Non-specific host defences
non-immune
normal flora
mediated by non-specific immune cells
damage results in damage signals
these damage signals recruit cells
initiation of an immune response
Non-specific host defense barriers (3)
1) structural
2) enzymatic
3) pH of the environment
Examples of non-specific host defences (many)
Tears
-protein break down bacteria
Sneezing
Mucociliary elevator
-ciliated cells move material towards larynx and swallowed
Coughing reflex
-works in conjunction with mucocilary elevator
Fever
Stomach pH (1.5)
Peeing
-washes organisms from the urethra to maintain a sterile bladder
Skin
Acidity of vagina
Lysozyme
-breaks peptidoglycan
-Lactoferrin: binds free iron and limits bacteria from obtaining iron
Secretory Ig
-antibody in secretions
Inflammation and cellular recruitment to the site of damage
-neutrophils and ROS (toxic to cells)
What is the best non-specific host defense?
acidity of stomach
pH of 1.5
What is the highest burden of infection from?
eating
Where are the most immune cells located in the body?
GI
Properties of skin that make it a good non-specific host defence
1) waterproof
2) good against UV light
3) heat tolerant
4) cold tolerant
5) impact tolerant (scratch skin and nothing happens)
Portals of entry (many)
resp
eyes
ear
genitals - urinary tract
gut (not as much)
Innate (non-specific) immunity defences (2)
1) first-line defences
2) second-line defences
First-line defences
EXTERNAL - Barriers at the body surface
Skin
Mucous membranes
Secretions
Reflexes
Normal microbiota
Second line defences
inflammation
phagocytes
fever
complement system
interferon
Phagocytosis
inflammatory response - cellular recruitment to the site of infection
phagocytosis - ingest the bacteria
bacteria are ingested into specific vacuoles or “pockets” in the cell that contain digestive enzymes (lysozyme)
Innate WBC
neutrophils*
-most abundant
-destroy bacteria
eosinophil
basophil
monocyte
Acquired (specific) immunity
3rd line of defence
how vaccines work
has long-term memory!
T cell lymphocytes [cell-mediated]
-kill virally infected cell, foreign cells, tumour cells, cells with internal bacteria or parasites
B cell lymphocytes [humoral]
-produce antiBodies
antibodies
Innate vs Acquired
Innate
-rapid response
-no memory
-non-specific
Acquired
-initial slow response (building a memory, building an army)
-subsequent rapid response
-long-term memory
-specific
Why wouldn’t you always want an adaptive immune response?
don’t want to keep the response if you don’t need it
need to feed, remove wastes, monitor etc.
expand, contract, then keep a small portion - memory cells that replicate
Humoral/Antibody-Mediated Response
generate an antibody against an antigen
immunoglobulins (antibodies = IgG, IgM, IgA, IgE and IgD)
respond to an antigen
IgM = early, short-lived
IgG = late and long lasting
IgA = in mucosal, tears, mouth, genital secretions
Agglutinate, precipitate, etc promote other factors to help Immunoglobulins.
Antibody-mediated response in the COVID vaccine
giving spike protein
antibodies against the spike protein debilitate the virus
Cell-mediated immunity
Several different types of cells involved including:
-Cytotoxic T-cells
-Regulatory T cells
-NK cells
important as a defence in combination with antibody but may also be important alone
Cytotoxic T-cells
destroy altered cells by recognizing FOREIGN PROTEIN SEQUENCES presented on the cell surface
How are host immune responses overcome?
bacterial and viral evolution
Biofilm production
polysaccharide
formed when organisms stick to a surface and produce an extracellular matrix
area for bacteria to communicate
mechanism of immune evasion and prevents the penetration of antibiotics and other cellular factors
Where does biofilm production often occur?
prosthetic devices
don’t have immune surveillance
need to do revision
antibiotics don’t help
Capsules
help avoid phagocytosis
thick polysaccharide layer that resides outside of the cell
prevents it from being internalized by macrophage
e.g. Streptococci pneumoniae
More direct method to avoid phagocytosis
toxin production
Toxin production
small proteins or polysaccharides that are able to arrest cellular functions or lyse host cells
e.g. C-difficile
e.g. Group A staph
Types of toxins (2)
1) Endotoxin
2) Exotoxin
Endotoxin
stay within the bacteria
structural components of the outer membrane of Gram Negative bacteria
Lipid A component of LPS
Heat stable - e.g. bulging can
Exotoxin
released into the environment
Exotoxin - excreted toxins
Enterotoxins - exotoxin with effects in the gut
How do VIRUSES evade the immune response?
antigenic drift
antigenic shift
dramatic changes in sequences
Antigenic drift
gradual change in antigen
e.g. COVID
why most vaccines work with the next strain
Antigenic shift
major changes
e.g. H1N1 to H3N2?
vaccines wouldn’t work at all
