209 12-02-24

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Questions and Answers

What is the primary role of Shiga toxin in E. coli O157/H7 pathogenesis?

Promotes bacterial replication without causing harm

Inhibits the bacterium's ability to attach to host cells

Causes host damage and facilitates growth of the pathogen (correct)

Enhances immune response against the bacterium

What mechanism allows E. coli O157/H7 to acquire the Shiga toxin gene from Shigella?

Genetic mutation within the E. coli genome

Vertical gene transfer during reproduction

Spontaneous plasmid transformation

Horizontal gene transfer (correct)

What primarily characterizes pathogenicity islands in pathogens?

Regions of the genome that enhance the host immune response

Unique nucleotide sequences non-existent in other organisms

Clusters of genes that dictate virulence factors (correct)

Segments of DNA that resist antibiotic treatments

Which component do enveloped viruses use to bind to their host cell receptors?

Glycoproteins in the viral envelope Signup and view all the answers

Which of the following best describes viral infection specificity?

Viruses exhibit tissue tropism and specific host range Signup and view all the answers

What structure do bacteria primarily use for adherence to host cells?

Fimbriae, with specific binding proteins Signup and view all the answers

Which of the following processes is essential for pathogens to evade host defenses?

Dodging immune detection by mimicking host surface proteins Signup and view all the answers

What is an essential step that pathogens must undertake after causing damage to the host?

Exit to transmit the infection to a new host Signup and view all the answers

What mechanism does the cholera toxin utilize to induce diarrhea?

It binds to GM1 ganglioside and increases cAMP levels. Signup and view all the answers

Which component of enterotoxigenic E.coli is similar to cholera toxin?

Labile toxin (LT) Signup and view all the answers

How do super antigens contribute to a systemic inflammatory response?

By activating a high proportion of helper T cells. Signup and view all the answers

What effect do endotoxins have on host immune cells?

Promote immune cell activation and cytokine secretion. Signup and view all the answers

What is the role of alpha toxin in bacterial pathogenesis?

To form pores in host cell membranes. Signup and view all the answers

What is characteristic of A-B type toxins?

They are comprised of A and B subunits, where B binds to host cells. Signup and view all the answers

Which type of bacterial structure aids in the adherence of Vibrio cholerae to intestinal cells?

Fimbriae Signup and view all the answers

What is a significant consequence of increased levels of cAMP due to cholera toxin in enterocytes?

Activation of chloride channels leading to water secretion. Signup and view all the answers

What is the primary function of the protein at the tip of the pili?

To mediate adherence to host cells Signup and view all the answers

Which type of pili is characterized by its ability to extend and retract dynamically?

Type IV pili Signup and view all the answers

What distinguishes exotoxins from endotoxins?

Exotoxins are secreted by living pathogens, whereas endotoxins are released from dead bacteria Signup and view all the answers

Which bacterial adhesin is known to bind host cell integrins?

Pertactin Signup and view all the answers

What role do biofilms play in bacterial pathogenesis?

They provide nonspecific adherence and protect against immune response Signup and view all the answers

Which secretion system allows bacteria to inject virulence factors directly into host cells?

Type III secretion system Signup and view all the answers

What is the primary purpose of Type I pili in bacteria?

Binding to specific sugars on host cells Signup and view all the answers

How do pathogens generally achieve growth and persistence in the host?

Through the production of toxins that interfere with host cell function Signup and view all the answers

Study Notes

Pathogens

Pathogens are microorganisms that cause disease
Successful pathogens must accomplish entry, adherence, avoidance, growth, and exit.

Pathogenesis Overview

Entry: Pathogens attach to the host using specific receptors, determining the initial infection site.
Adherence: Pathogens must attach to their host. Special receptors determine the site of infection.
Avoidance: Pathogens must avoid the host's defenses; rapid immune responses will eliminate them before they can replicate.
Growth: Growth is linked to host damage.
Exit: Transmission to a new host is the final stage.

Pathogen Virulence Factors

Pathogens acquire virulence genes (e.g., for toxins and adhesins) through horizontal gene transfer.
These genes are often clustered on 'pathogenicity islands', distinguishable by different G-C base-pair content from the surrounding genome.
For example, E. coli O157/H7 acquired a Shiga toxin gene from Shigella, making it pathogenic.

Pathogen Attachment

Bacterial structures: Pili (fimbriae) are surface proteins with attachment subunits (adhesins). Different species have different pili, binding to host cell carbohydrate structures.
- Pili tip proteins determine binding specificity.
- Type I pili, capped with FimH, bind mannose on intestinal epithelium.
- Type I pili, capped with PapG, bind digalactose on urinary tract epithelium.
- Type IV pili are dynamic, extending and retracting to pull bacteria close to host cell membranes.
Non-pili adhesins: These are distinct bacterial surface proteins that bind to host cell proteins used for cell-to-cell contact.
- Example: Bacterial Pertactin binds host cell integrins.
- Streptococcal M protein also acts as an adhesin.

Biofilms

Most organisms live in biofilms.
Coordinate production of extracellular polysaccharide (EPS) forms a highly adhesive matrix.
Biofilms create barriers that block immune mediators.
Biofilms contribute to infections: oral, lung, bladder; and pose problems for in-dwelling medical devices.

Toxin Production

Pathogen growth relies on toxins that disrupt host cell function or lead to cell death.
Exotoxins: Secreted by pathogens.
Endotoxins: Released from dead Gram-negative pathogens.
Types of toxins:
- Membrane disruption: Examples include alpha-toxin, a hemolysin.
- Inhibiting protein synthesis: Example includes Shiga toxin.
- Disrupting signal transduction: Example is Cholera toxin
- Cell cycle disruption: Example is cytolethal distending toxins.

Type III and Type II Secretion Systems

Bacteria employ secretion mechanisms to deliver virulence factors.
Type III systems directly inject factors into host cells.
Type II systems secrete factors into the extracellular environment.

A-B Toxin Structure

Many toxins have an A-B structure:
- B subunit binds host cell surface.
- A subunit exerts toxic effect inside the cell after transport

Cholera Toxin

Vibrio cholerae secretes cholera toxin (a very similar toxin is also made by Entertoxigenic E. coli).
This toxin causes diarrhea.
It induces chloride secretion by activating a chloride channel and disrupting nutrient uptake.
It binds to GM1 ganglioside of intestinal cells. The released A subunit triggers a CAMP increase, activating a chloride channel, which increases ion secretion and diarrhea.

Sepsis

Sepsis is a serious, blood-borne bacterial infection.
Mortality from sepsis is high (17%) compared to other conditions (2%).
Rapid diagnosis is critical for survival.
Incidence of sepsis is increasing with population aging.

Microbial Pathogen Life Styles and Immune Responses

Microbial pathogens have diverse life styles (extracellular, intracellular).
Whatever the lifestyle, pathogens avoid or block the host immune response to be successful.

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Description

Explore the fascinating world of pathogens in this quiz. Learn about their entry, adherence, immune avoidance, growth, and exit strategies. Understand the role of virulence factors and how they contribute to disease causation.