micro - bacterial pathogenesis and host defense Flashcards by E E

Bacteria cause disease in MANY WAYS

and you don’t necessarily require a large # of cells, because ____ produces a disease.

toxin

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bacteria capable of causing disease

pathogen

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quantitative measure of pathogenicities measured by the number of bacteria required to cause disease

virulence

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of bacteria necessary to kill 1/2 the hose

LD₅₀

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of bacteria necessary to cause infection in half the hosts

ID₅₀

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properties of bacteria which assist in causing diease (pili, capsules, toxins, etc)

Virulence Factors

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8 Stages of Bacterial Pathogens

Transmission from an external source into the body
Evasion of initial host defenses
Attachment to mucous membranes
Colonization at attachment site
Sometimes spread and reattachment
Disease symptoms caused by toxins or tissue invasion followed by inflammation
Non specific and specific immune host responses
Progression or resolution of the disease

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3 Mechanisms of Bacterial Disease

Tissue invasion followed by inflammation
Toxins (exotoxins and endotoxins)
Immunopathogenesis eg. Rheumatic fever

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What is Transmission Mech 1?

I. Human to human
Direct contact eg. infections mono

        Non-direct contact eg. fecal-oral

        Transplacental

        Transferred blood products or contaminated                needles

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What is Transmission Mech 2?

II. Non-human to human
Contaminated soils eg. Tetanus

Contaminated water eg. Legionnaires’ disease

Direct from animals eg. Cat Scratch fever

Insect vectors eg. Lyme disease

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Where do bacterial diseases enter body?

Respiratory tract

GI tract

Skin

Genital tract

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What are the Virulence Factors?

bacterial structure

secreted enzymes

other bacterial factors

Exotoxin

Endotoxins

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Virulence Factors - bacterial structure

I. Bacterial Structures
Pili eg. N. gonorrhea to urinary tract epithelium

Capsules eg. Strep. pneumonia

Glycocalyx eg. Strep. viridans in heart valves
Endotoxin eg. Gram negative bacteria

Biofilms eg. Pseudomonas in cystic fibrosis patients
Bacterial Secretion Systems eg. T3SS in Salmonella typhimurium

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Virulence Factors - secreted enzymes

II. Secreted Enzymes
Collagenase & hyaluronidase eg. Strep. pyogenes cellulitis

Coagulase eg. Helps coat Staph. aureus with fibrin to help protect from phagocytosis

Immunoglobulin A protease eg. Degrades IgA allowing Strep. Pneumonia to adhere to mucous membranes

Leukocidins Destroy neutrophilic leukocytes and macrophages eg. Staphylococci and group A Streptococci

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Virulence Factors - other bacterial factors

III. Other Bacterial Factors
M protein - antiphagocytic protein produced by Strep. pyogenes

Protein A - binds to IgG and prevents activation of complement

Invasins - bacterial molecules which promote bacterial entry or contact with host cells - eg. Heliobacter pylori

Outer membrane proteins - produced by Yersinia species to inhibit phagocytosis and cytokine production

Pathogenicity Islands (PAIs) – code for groups of virulence factors particularly in Gram negatives

place that doces for virulence factors: PATHOGENICITY ISLANDS. If you can get rid of it, get rid of bacteria’s ability to cause disease

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Virulence Factors - Exotoxin

IV. Exotoxins
Polypeptides secreted by bacteria

Become toxoids when treated with formaldehyde, and/or heat and used for protective vaccines

Frequently have an A-B subunit structure (A portion has toxic activity and B portion is involved in binding to cells)

Are genetically coded on the bacterial chromosome, plasmid or phage

Have one of five biological effects:
Alter cellular components
Are superantigens
Inhibit protein synthesis
Increase synthesis of cAMP
Alter nerve impulse transmissions

Exotoxin Action - 2nd way

inject bacterial cytosol directly into host cell - antibodies can’t reach them because they’re never on the outside, unlike normal pathway that invovleds binding to receptors on the outside of the cell

What do bacterial exotoxins affect?

alter cellular compunents

superantigens

inhibition of protein synthesis

increased synthesis of cAMP

altered Nerve Impulse Transmission

the info to make the toxins that do these are located at various places - if you can get ride of that place, you can get rid of the toxon; will not cause disease

What do superantigens do?

increase cytokines, have negative effect on cell

Virulence Factors: Endotoxins

IV. Endotoxins
Are integral parts of the cell wall of Gram negative rods and cocci

Involve the Lipid A component of lipopolysaccharide

Only weakly antigenic; no toxoids made

Induced biological effects focus on fever and shock

biological effects:

Induce the release of endogenous pyogenes

Increase vascular permeability

Imitate complement and blood coagulation cascades

Cause fever, hypotension, disseminated intracellular coagulation and shock

What is the difference between Innate and Aquire Immunity?

Innate: Macrophages and Complement (assist host immune cells and antibody in lysis of bacteria and virus-infected cells)

Acquired: Antibodies (cytolytic, neutralizing-lock up Viral Attachment Protein with an antibody, opsonins) and Cytotoxic T Cells (kill antibody-coated bacteria and virus-infected cells).

What is the difference between Passive and Active immunity?

passive = giving preformed antigen-specific antibodies to help protect from disease (like rabies immmune globulin - you don’t have to make your own antibodies)

active = giving antigens to stimulate an individual to develop immunity to help protect from disease (like Flu)

What kind of vaccine is availabe for flu?

shot, inactivated, or whole virus - split vaccine

Are live or dead vaccines better?

live - mimic natural pathway, better response

How do bacteria avoid Innate immune response?

** - avoice contact with phagocytes ** The bacteria can reside in a niche not patrolled by phagocytes. The bacteria can suppress inflammation and/or chemotaxis. The bacterium can coat itself with host proteins (more later). **inhibition of engulfment** Many bacterial capsules are anti-phagocytic. Some surface polysaccharides (such as those that aid in biofilm structure) are anti-phagocytic. Some bacteria produce specific anti-phagocytic products. **survival w/in phagocyte** Intracellular survival is mediated by bacteria in three basic ways: _Escape the phagosome_ *Shigella, Lysteria* _Adapt to the phagosome_ *Coxiella, Leishmania* _Modify the phagosomal compartment_ *Salmonella, Legionella, Mycobacteria, etc.* *_Capsules can inhibit phagocytosis AND complement activation_* *_Other methods of phagocytic or complement avoidance by bacteria:_* _LPS O-antigen_ *_Blocks MAC access - keeps at “arm’s length.”_* _Complement component peptidases_ *_Destroy complement components. This inactivates the components AND stops complement activation._* **Antigenic variation** *Some bacteria spontaneously change the profile of the surface proteins that they express.* Antibodies are formed in response to specific antigens on the bacteria. Because of a delay in the immune response (antibody formation), the bacteria can stay one step ahead by producing variants of itself. *Example of ^: * Trypanosome Variant-Specific Glycoprotein (VSG) cassettes. - switch back and forth between different cassettes Bacteria: B. recurrentis Neisseria **Immunological disguise** Bacteria coat themselves with host proteins Disguised by “self” proteins – camouflage! E.g. proteins produced by some bacteria bind Antibodies – BACKWARDS! *E.g. The Treponema pallidum parasite coats itself with host fibronectin. E.g. S. aureus produces coagulase and clumping factor. This leads to the deposition of host fibrin on the bacterial surface.*

What is protein A?

Staph synthesizes protein A - which has ability to bind immunoglobulin (IgG), causing bacteria to look normal to immune system - therefore is not killed. REMEMBER PROTEIN A - PART OF STAPHYLOCOCCUS.

IS PSEUDOMONAS AERUGINOSA gram - or +?

Gram - involved in cystic fibrosis patients; forms biofilms