Pathway 15-2 Pathogenicity and Virulence Factors

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Questions and Answers

What distinguishes primary pathogens from opportunistic pathogens?

Primary pathogens routinely cause disease in a healthy host. (correct)

Opportunistic pathogens can cause disease regardless of the host's immune status.

Primary pathogens cause disease only in immune-compromised hosts.

Opportunistic pathogens cannot survive in healthy hosts.

Which of the following is a virulence factor related to biofilm formation?

Production of toxins that directly kill host cells.

Ability to adhere to surfaces and resist environmental stress. (correct)

Rapid replication under host immune response.

Enhanced metabolic rate in nutrient-poor environments.

What role does normal resident microbiota play in pathogen resistance?

They directly kill invading pathogens.

They compete with pathogenic microorganisms for resources. (correct)

They enhance the immune response against all pathogens.

They have no significant effect on pathogen resistance.

How can commensal bacteria become opportunistic pathogens?

By exploiting impaired host defenses. Signup and view all the answers

What role do early root canal colonizers play in apical periodontitis?

They may facilitate the establishment of other bacterial groups. Signup and view all the answers

What happens to the bacterial community as apical periodontitis progresses?

A structural and spatial organization occurs within the microbiota. Signup and view all the answers

Why do late colonizers face less opposition in the root canal after necrosis?

Host defenses are no longer active in the necrotic environment. Signup and view all the answers

Which of the following statements about bacterial virulence factors is incorrect?

All factors contribute equally to the pathogenesis. Signup and view all the answers

Which of the following components is not considered a direct tissue damaging agent from bacteria?

Flagella Signup and view all the answers

⭐️What indicates the presence of gram-negative bacteria in the root canal?

Presence of lipopolysaccharide. Signup and view all the answers

What may happen to some early colonizers over time in the root canal?

They may decrease or disappear from the community. Signup and view all the answers

Which factor is least likely to influence the establishment of new bacterial species in the canal?

Temperature of the root canal. Signup and view all the answers

What is a notable indirect mechanism of damage during apical periodontitis?

Oxygen-derived free radicals damaging connective tissue. Signup and view all the answers

Why is LPS considered a significant virulence factor in apical periodontitis?

It can provoke strong inflammatory responses. Signup and view all the answers

Which of the following best describes the nature of primary infections in apical periodontitis?

They may involve exclusively gram-positive bacteria. Signup and view all the answers

Study Notes

Microbial Pathogenicity and Virulence Factors

Pathogenicity refers to a microorganism's ability to cause disease.
Virulence is the degree of pathogenicity.
Virulence factors are secreted products, structural components, and microbial strategies that contribute to pathogenicity.
Biofilms are one bacterial strategy that contributes to pathogenicity, offering protection against host defenses, microbial competitors, and antimicrobial agents.
Primary pathogens routinely cause disease in a specific host, while opportunistic pathogens cause disease only when host defenses are impaired.
Most bacteria involved in endodontic infections are normal inhabitants of the oral microbiota, becoming opportunistic pathogens when the balance of the host-bacteria relationship is disrupted.
Bacteria in the forefront of infection must survive host defenses and acquire nutrients to stay alive.
During pulp necrosis, bacteria colonize necrotic tissue, moving toward the apical part of the canal until it is entirely infected.
Early colonizers play a crucial role in initiating apical periodontitis and may modify the environment to facilitate the establishment of other bacterial groups.
Late colonizers may access the canal through coronal exposure or exposed dentin tubules, contributing to a shift in the microbiota.
Root canals with radiographically detectable apical periodontitis lesions harbor both early and late colonizers.
Periradicular inflammation can occur before the frontline of intracanal bacterial infection reaches the apical foramen.
Bacterial virulence factors directly damage host cells or the intercellular matrix, including enzymes, exotoxins, heat-shock proteins, and metabolic end products.
Bacterial structural components, such as LPS, peptidoglycan, LTA, fimbriae, flagella, outer membrane proteins, and vesicles can directly cause tissue damage by stimulating host immune reactions.
Inflammatory and noninflammatory host cells release proinflammatory cytokines in response to bacterial components, contributing to bone resorption characteristically observed in apical periodontitis.
Pus formation in acute apical abscesses is an example of indirect damage, resulting from the destruction of the connective extracellular matrix by oxygen-derived free radicals and lysosomal enzymes released by polymorphonuclear leukocytes.
Apical periodontitis is a multifactorial disease resulting from the interplay of host and bacterial factors.
LPS, exclusive to gram-negative bacteria, is detected in high concentrations in canals of teeth with large or symptomatic apical periodontitis and persistent exudation.
While LPS is a significant virulence factor, other bacterial mediators, such as LTA (exclusive to gram-positive bacteria) and various bacterial secreted products, also contribute to the disease.
The pathogenesis of apical periodontitis is likely to vary based on the bacterial mediators involved.

Apical Periodontitis

Apical periodontitis is a multifactorial disease involving host and bacterial interactions.
Few endodontic pathogens are capable of inducing all the events in the pathogenesis of apical periodontitis.
The disease process requires an integrated and orchestrated interaction of selected members of the mixed endodontic microbiota and their respective virulence attributes.
LPS has been found in high concentrations in canals of teeth with large, symptomatic apical periodontitis and persistent exudation.
Other bacterial mediators likely contribute to the disease, including LTA, which is exclusive to gram-positive bacteria.
Many bacterial secreted products have been detected in endodontic infections, suggesting that there is no single, stereotyped course of pathogenesis for apical periodontitis.