Microbiology Notes

GI Infections

• Focus on one GI infection for the exam.
• The instructor will post information on Canvas.
• TUMS contain bicarbonate, which neutralizes acid; patients may initially use them for self-treatment.
• If a patient is taking antacids constantly, it's a cause for concern.
• Some medications come with antibiotics.

Second Line of Defense

• Review the second line of defense, especially if second-line treatments are involved.
• Create a reference sheet (e.g., a 3x5 card) with CBC information (neutrophil and eosinophil functions).
• Second-line defense includes inflammation, phagocytosis, and the release of chemicals (cytokines).
• Insert details about specific aspects of the second line of defense.

Adherence

• Cell adherence is a key process.
• The cell involved with adherence is not a T cell.
• Cell binds to PAMP (Pathogen-Associated Molecular Patterns), but the full name needs to be added.

Steps of Inflammation

• Vasodilation: Involves chemicals like histamine and increases blood flow.

• Increased Permeability: Allows cells to move in and out of vessels.

• Margination: Cells stick to the margins (edges) of the vessel.

• Diapedesis: Cells move through the vessel walls.

• Tissue Repair: Occurs after the initial steps.

• Phagocytosis: Follows diapedesis; understanding the sequence is important.

  That's this. Mhmm. Follow? Yes. So we're here.
  Complement here. Do you see that? Mhmm. So this will link To that. Right here.
  That's where you need to go with this. Are you following? Yes. Okay. So if I bring this down, can you handle that?
  Yeah. K. Do not take a picture of this. If I see pictures, you get that. Alright?

• Complement system links to the inflammation process.

Phagocytosis

• Includes chemotaxis, adherence, ingestion, and digestion.
• Chemotaxis and vasodilation are involved.

Complement System

• Involves classical, alternative, and lectin pathways.

• Classical Pathway: Starts with an antigen binding to an antibody.

  Antibody c one. K? I know.
  C one splits into c two and c four. Are you following? Yes. Yeah. Okay.
  So c two splits into c two b, c two a, c four goes c four b, c four a. Right? And you get c three. Yes? Mhmm.
  So that is the classical. The alternative, remember, you've got this lipid situation. You've got these other proteins, the b, the d, and the p, activate c three. Yeah? So alternative does not need an antibody.
  Right? Yeah? Mhmm. Are you copying? You're copying your protein.
  You're writing it down? C2AC4BC4A. Okay? Yes? Yes.

  • C1 splits into C2 and C4.
  • C2 splits into C2b and C2a; C4 splits into C4b and C4a.
  • Alternative Pathway: Involves lipids and proteins (B, D, P) to activate C3; does not require an antibody.

• End Goal: Activation of C3 through different pathways.

• From C3, there are three options: cytolysis, opsonization, and inflammation.

  So c three b, what is this called? Opsonization. Right? This enhances the phagocyte Yeah? Mhmm.
  And your white blood cells. Those are important. Now all still innate. This is nonspecific. Right?

• C3b leads to opsonization, which enhances phagocytosis and involves white blood cells.

• Everything discussed so far is part of the innate immune system and is nonspecific.

Extracellular Pathogens

• Focus on pathogens that are floating around.
• Involves dendritic cells, T helper cells, and B cells.
• T helper cells activate B cells, leading to antibody production.
• Some of this connects to the previous picture/diagram.

Parasites

• The lecture has looked at interleukin-4 pathways.