Which plasmid type increases a bacterial host’s ability to cause disease (for example, by encoding toxins or adhesion factors)?

Introduction / Context:
Plasmids are extra-chromosomal DNA elements that can bestow new phenotypes on bacteria. Some carry traits that directly enhance pathogenicity, which has profound clinical consequences for infection severity and epidemiology.

Given Data / Assumptions:

• Different plasmid classes encode distinct functions (fertility, resistance, metabolism, virulence).
• Virulence factors include toxins, adhesins, secretion systems, and invasion determinants.
• Presence of such plasmids often correlates with enhanced disease.

Concept / Approach:
Virulence plasmids encode gene products that promote colonization, immune evasion, or tissue damage. Examples include the pXO1/pXO2 plasmids of Bacillus anthracis (toxin and capsule), the Yersinia virulence plasmid encoding a Type III secretion system, and enterotoxin plasmids in E. coli. These elements explicitly increase pathogenic potential compared with strains lacking them.

Step-by-Step Solution:
Match plasmid class to clinical effect: virulence plasmids raise pathogenicity.Exclude F factors (mating) and purely metabolic plasmids (catabolism).Choose “Virulence plasmid.”

Verification / Alternative check:
Loss or curing of a virulence plasmid commonly attenuates virulence in animal models, confirming causal contribution.

Why Other Options Are Wrong:

• F factor: mediates DNA transfer, not virulence per se.
• Metabolic plasmid: enables substrate use but does not necessarily increase disease severity.
• “None”: contradicted by multiple pathogen models.
• Cryptic plasmids: by definition lack known virulence genes.

Common Pitfalls:
Assuming antibiotic resistance alone defines virulence; while clinically important, resistance is distinct from virulence mechanisms.

Final Answer:
Virulence plasmid