Host-Parasite Relationships Normal (Flora) Microbiota Opportunistic Infections Flashcards
Normal Flora: Esophagus and Stomach
Lactobacilli
Normal Flora: Small Bowel
Duodenum: Lactobacilli and Streptococci
Jejunum and Ileum: Enterobacteria and Bacteroides spp.
Normal Flora: Large Bowel
Bacteroides, Fusobacterium, Strep faecalis, E coli, Enterobacteria, Klebseilla, Eubacteria, Bifidobacteria, Lactoballus, Staph aureus, Clostridium, Streptococci, Pseudomonas, Salmonella
Normal Flora: Fecal Material
Bacteroides, Bifidobacteria, Eubacteria, Coliforms, Strep faecalis
Colonized Sites of the Body
Skin, Mucosa, Intestine, Urogenital tract
Normally Sterile Sites of the Body
Internal organs and tissue, Cervix, Middle ear, Urinary bladder
Resident Microbiota
Long-term members of the body’s normal microbiota
Transient Microbiota
Organisms that attempt to colonize the body but are unable to remain due to:
- Competition from resident microbiota
- Elimination by the body’s immune system
- Physical or chemical changes within the body that discourage growth
Staphylococcus epidermidis
- Resident (normal) Microbiota*
- Found on skin, nose, ears
- Gram (+) cocci, in CLUSTERS
- Infections associated with PROSTHETIC DEVICES and INTRAVENOUS CATHETERS
- Common contaminant of blood cultures
Group A Strep (GAS)- Streptococcus pyogenes
- Transient Microbiota*
- Gram(+) cocci, in CHAINS
- Transiently colonize oropharynx of children and young adults in absence of clinical disease
- Causative agent of STREP THROAT
- Transmitted via AEROSOL or SALIVA
Strict Pathogens
Organisms ALWAYS ASSOCIATED with disease
e.g. Mycobacterium tuberculosis, Neisseria gonorrhoeae, rabies virus
Opportunistic Pathogens
- Tend to be members of the NORMAL MICROBIOTA
- Take advantage of preexisting conditions, such as immunosuppression to grow and cause disease
e. g. E. coli, Candida albicans
Are most infections caused by strict or opportunistic pathogens?
Opportunistic
Opportunistic Infections (7 examples)
- Contamination of intravenous catheters
- Wound/Surgical site infections
- Bacterial Endocarditis (can get it by flossing)
- Aspiration pneumonia (inhaling fluids)
- UTI
- Pseudomembrane colitis (C. difficile; common after broad spectrum antibiotic use)
- Otitis media (bacteria present in the nasopharynx migrate into the inner ear)
Pathogenicity vs. Virulence
Pathogenicity: ability of a microorganism to cause disease
Virulence: measurement of pathogenicity
Virulence Factors
Factors (e.g. toxins or proteins) produced by an organism that enable it to infect, cause disease, and/or kill a host
Carrier
- ASYMPTOMATIC individual who is host to a pathogen
- Has the POTENTIAL TO TRANSMIT the pathogen to others
e. g. GAS, Salmonella Typhi
Carriers may be transient or (semi) permanent
Adhesion
Binding of the bacterial adhesin to the host cell surface (receptor)
- Commonly associated with BACTERIAL PILI (fimbrae)
- Specific adhesin and receptor combos often define TROPISM
Are most bacteria planktonic (free-moving) or sessile (stationary)?
Sessile; they adhere to surfaces or other bacteria as part of a BIOFILM
Biofilms
Bacteria encased in a EXOPOLYMERIC SUBSTANCE (e.g. polysaccharide, DNA, etc.) of their own making
Found throughout nature on moist/wet surfaces, baths/showers, and teeth
***Majority of bacteria on body are living as biofilms
How are cells in biofilms different than planktonic cells?
- Altered, generally SLOWED, metabolism
- Increased resistance to abx (slowed metabolism = decreased diffusion of abx)
- Increased genetic exchange –> increased likelihood of abx resistance transfer
- Resistant to disinfection = decreased diffusion, increased organic matter
Most chronic bacterial infections (some acute) have a ____ component
Biofilm
How do bacteria invade cells?
-Hijack host cell machinery
May modulate maturation of the phagosome to promote survival
Dissemination
Some bacteria can produce toxins that cause pathology in other parts of the body (e.g. toxin produced in the intestines finds its way to the kidneys)
Example of a bacterium that adheres, enters, and disseminates:
Listeria
Endotoxin vs Exotoxin
Endotoxin: lipid A portion of LPS (a component of the outer leaflet of the outer membrane of gram negative bacteria)
Exotoxin: bacterial product that directly harms tissue or leads to destructive biologic activities
Two examples of Exotoxins
- Cytolytic enzymes (hemolysins, pore forming toxins)
- Receptor binding proteins that initiate toxic reactions (e.g. A-B subunit toxins (AB toxins); A = active (carries out mechanism) and B = binding (binds target and facilitates entry of the A portion)
Exotoxin: How does the Diphtheria toxin exert its effects?
Inhibits protein synthesis leading to cell death
Exotoxin: How does the Cholera toxin exert its effects?
Hyperactivation; leads to increased release of solutes in the intestines and subsequent diarrhea
Exotoxin: How does C. tetani exert its effects?
Blocks inhibitory transmitter release in nerve-muscle transmission leading to continuous stimulation by excitatory transmitters and PARALYSIS
Exotoxin: How does C. botulinum exert its effects?
Blocks release of ACH from vesicles in nerve-muscle transmission, leading to flaccid paralysis (i.e. muscle will never contract)
Superantigens
- Binds both T-cell receptor and MHCII without a requiring antigen
- “Cytokine storm” due to activation of large numbers of T-cells –> life-threatening autoimmune-like responses
-
This is generally IRREVERSIBLE*
e. g. S. aureus TSST, Staph enterotoxin, S. pyogenes erythogenic toxins
Mechanisms for Evading Host Defense: Encapsulation (Bacteria Capsule)
- Generally, a poor antigen
- Masks more antigenic epitopes on bacterial surface
- Prevent binding of antibody or complement
Mechanisms for Evading Host Defense: Antigen Mimicry
- Bacteria produce compounds that the host sees as self
e. g. S. pyogenes capsule (hyaluronic acid) and S. aureus protein A (binds Fc protein of antibody, thus coating bacteria in host protein)
Mechanisms for Evading Host Defense: Antigenic Variation/Shift
- Bacteria change antigenic make up of proteins on their cell surface, creating a “moving target” for the immune system
e. g. Neisseria gonorrhoeae type IV pili (many silent copies of the pilin gene in the genome
Mechanisms for Evading Host Defense: Inactivation Antibody
Secretion of proteases that degrade specific antibody isotypes (e.g. IgA protease)
Mechanisms for Evading Host Defense: Resistance to complement-mediated killing
- Limiting access to the membrane (capsule, long O-antien on LPS (on gram negative bacteria))
- Degradation of components of complement
***Complement either cannot bind or mac attack complex cannot penetrate lipid membrane
Mechanisms for Evading Host Defense: Bacteria Escaping Phagocytic Clearance
-inhibit opsonization, inhibit chemotaxis, kill phagocyte, inhibit lysosomal fusion, escape from lysosome, resistant antibacterial lysosomal action
Regulation of Virulence Factors in Bacteria: Quorum Sensing
A way for bacteria to sense the size of their population
- When concentration is HIGH (Critical mass) they turn on virulence factors and cause disease
- **Allows bacteria to act as a GROUP, rather than individuals
Which of the following is not classically considered a virulence factor: Pili, Capsule, Exotoxin, Peptidoglycan, Lipopolysaccharide?
Peptidoglycan
Which of the following is not a mechanism that bacteria use to avoid phagocytic clearance: Inhibit opsonization, Escape from phagosome, Inhibit chemotaxis, Inhibit lysosomal fusion, Inhibit conjugation?
Inhibit conjugation
Bacteriocins
Toxins produced by the normal microbiota (flora) that harm pathogenic microorganisms
