Targets CD4+ T cells. Replicates via reverse transcriptase. Leads to opportunistic infections when CD4 counts fall below 200 cells/µL. 2. Key Fungal Pathogens

Lysozyme in tears, stomach acid (pH 1.5–3.5), and defensins on epithelial surfaces.

Alteration of the D-Ala-D-Ala cell wall precursor to D-Ala-D-Lac.

The human body uses layered defenses to recognize, contain, and eliminate invading pathogens. 1. Innate Immunity

Mediated by T lymphocytes. CD4+ Helper T cells coordinate the immune response, while CD8+ Cytotoxic T cells destroy virally infected and neoplastic cells. Module 4: Systematic Clinical Bacteriology

This section covers the most common clinically relevant bacterial pathogens, their presentations, and first-line treatments. 1. Gram-Positive Cocci

SLIDE 1: Introduction & Pathogen Classification (Bacteria, Viruses, Fungi, Parasites) SLIDE 2: Structural Differences: Gram-Positive vs. Gram-Negative Cell Walls SLIDE 3: Bacterial Growth Kinetics: The 4 Phases and Antibiotic Targeting SLIDE 4: Horizontal Gene Transfer (Conjugation, Transformation, Transduction) SLIDE 5: Antibiotic Targets and Common Resistance Mechanisms SLIDE 6: Innate vs. Adaptive Immunity in Host Defense SLIDE 7: High-Yield Gram-Positive Pathogens (Staph, Strep) SLIDE 8: High-Yield Gram-Negative Pathogens (E. coli, Pseudomonas) SLIDE 9: Major Viral Families and Clinical Presentations SLIDE 10: Diagnostic Mycology & Antifungal Therapies

Ferment glucose; reduce nitrates to nitrites. Common causes of urinary tract infections (UTIs) and sepsis.

Maximal growth rate; highest susceptibility to cell wall-active antibiotics (e.g., penicillin).

S. aureus : Catalase(+), Coagulase(+). Causes skin infections, pneumonia, endocarditis, and toxic shock syndrome.