Lecture 4- Pathogenesis Flashcards
Modes of Transmission of disease?
- Direct contact
- Indirect contact
- Vectors
- Fomites (inanimate objects)
Examples of direct contact?
cough sneeze touch
Examples of indirect contact?
food water soil
First step in establishment of disease?
entrance and attachment
Example of portal of entry for disease?
skin, respiratory, gastrointestinal, urogenital systems, or conjunctiva of eye
vector borne, sexual contact, blood transfusion, or organ transplant
What is adherence of disease mediated by
special molecules called adhesins
Define colonisation?
site of microbial reproduction on or within host
In establishment of disease what to organisms compete for?
•
Compete for nutrients
•
Compete for colonisationsites
Define adhesions?
adherence factors/molecules
Define Fimbriae?
includes pili/organelles that project from the cell surface to mediate attachment to host cell surface receptors
What is a Glcocalyx and function?
Capsule/slime layer made up of glycoproteins and or polysaccharides. sticky (adherent, resist cough reflex) resists phagocytosis
How do adherence structure general work?
bind complementary receptor sites on host cell surface
Example of organism that usres fimbriae to colonise?
Neisseria gonorrhoeae (GNC –diplococcus)uses fimbriae to initially colonise the urethral or cervical epithelium.
Types of entry in establishment of disease?
- No entry Required
- Passive entry
- Active Entry
Example of disease that does not require entry?
N.gonorrhoeae– sexual activity (intercourse,oral,anal)
Define passive entry and give example?
Organism that without a defined entry mechanism would not cause disease
eg Insect bites, surgery
Example of active entry?
Invasins stimulate host cells to ingest bacteria
What is an invasin
Surface proteins that provoke ingestion of bacteria by host cells
Define Bacteremia?
presence of viable bacteria in the blood
Define spepticemia?
pathogens or their toxins in the blood
Conditions needed for growth and multiplicaiton of disease?
Suitable nutrients, pH, Temperature and redox potential (affects the amount of O2 present)
Virulence factors of Extracellular enzymes
- Collagenase
- Hyaluronidase
- Lecithinase
- Coagulase
- Fibrinolysin
- IgA Protease
- NucleaseCatalase, peroxidase, superoxide dismutase
Collagenase and hyaluronidase?
Proteolytic enzymes that breakdown collagen and hyaluronic acid in connective tissue allowing an organism to spread into neighbouring tissues
Lecithinase?
breaks down the phospholipid layer of cell membranes and causes extensive cell & tissue damage
Coagulase
produced by S.aureus, causes fibrinogen to form a fibrin clot around bacteria and prevent phagocytosis
Fibrinolysin
has the opposite effect to coagulase by dissolving a fibrin clot and is thought to assist the pathogen by preventing localisation of the infection by the inflammatory response
Nuclease
breaks down viscous nucleic acids released by the lysis of WBC during pus formation allowing bacteria to continue to spread
Catalase, peroxidase, superoxide dismutase
these enzymes inhibit the reactive oxygen species produced during the oxidative response following phagocytosis by neutrophils, monocytes and macrophages
Virulance Factors of school sores “Impetigo”
Rapid spread of infection caused by enzymes collagenase, hyaluronidase, fibrinolysin and nuclease.
Protein A?
binds to Fc portion of IgG molecules
Antibodies are not recognised by phagocytes
What is Hemolysins?
Virulance factor
Pigments (carotenoids)
Toxic to other organisms and to some human tissues
Inhibit immune function
What is an Exotoxin and eg?
• Proteins that are secreted/released by bacteria (generally Gram positive)
eg Examples:
•Clostridium tetani (tetanus) -Vibrio cholerae (cholera enterotoxins)
Properties of Exotoxins?
- Heat libale
- Extremely potent
- Antigenic
- Converted to toxoids for vaccine
Diphtheria Toxin?
• A cytotoxic exotoxin that can cause organ damage (i.e. heart, liver, throat)
How is diphtheria toxin produced?
Produced by toxigenic strains of Corynebacterium diphtheriae that are infected with a lysogenic β phage (not lytic) which is tox pos
Remember to look at diagram for diphtheria toxin?
Yepp yepp dont forget
Define Translation - Protein Synthesis?
The elongation cycle is the process of reading mRNA, the insertion of tRNA into the ribosome to produce peptides
Properties of Endotoxins
-Lipid Aof Gram negative cell wall
-Not secreted-released when cells disrupted
-Heat stable
- Not antigenic
-Activates coagulation, complement, fibrinolysis
- Less potent than exotoxins
Toxic (nanogram amounts)
- Weakly immunogenic
-Cause general system effects
fever, weakness, diarrhea, inflammation
Which virulence factors may aid the attachment of a pathogen to the body surface?
Adhesins, Fimbriae and Glycocalyx
What is an endogenous infection?
It is an infection by a member of normal flora
Why is tetanus described as a focal infection?
It is a localised infection from which pathogens can spread to other body sites
Explain the emergence of Haemophilus influenzae as a secondary pathogen.
This usual follow a primary pathogens as a secondary complication
Tuberculosis may progress very slowly over a number of years. What type of infection is this?
This is a chronic infection as it slowly progress’s.
What is ID50 and what does it measure?
It is the number of bacteria nessacary to infect 50% population of people exposed to it.
What is a glycocalyx and how can this contribute to the virulence of a pathogen?
It is a capsule slim layer made up of glycoproteins or polysaccrides. It contributes to virulence by being sticky (adherent) and resisting phagocytosis.
How may collagenase act as a virulence factor?
Enzyme that breaks down collagen allowing it to spread into neighbouring tissues
What is the basis of the vaccine for tetanus?
They uses the Clostridium tetani which is an exotoxin coverted into a toxoid by being formalin treated or heat treated. It remains immunogenic however much less toxic
Why does a single molecule of diphtheria toxin subunit A lead to the death of a host cell?
It inhibits the production of protein synthesis resulting in cell deaths as it is unable to replicate
