• In utero, the fetus is free of normal flora in normal circumstances; the process of being colonized (establishment of microbial growth) with normal flora typically begins during the birthing process: MO of the GI tract MO of the skin MO of the genitourinary tract
• Other forms of normal flora are acquired throughout the early years of life via environmental exposure: Food that we eat Person-to-person contact Environmental/airborne organisms

Health--provide dietary nutrients (e.g. vitamin k, B-12)

Bacterial antagonism: (normal vs. normal and normal vs. transient): -Nutrient competition (iron and oxygen) -Production of antimicrobial substances (organic acids, oxidative byproducts, antibiotics, fatty acids) -Stimulate immunity

-A pathogen is any disease-causing microbe/virus

-Pathogenicity refers to an organism’s ability to cause disease (pathogenic=disease-causing).

-May be opportunistic--only cause disease if introduced into different location in host or in immunocompromised host (not a normal occurrence in a healthy host)

-Most mutuals and commensals are opportunists

-May be true pathogen--can cause disease even in immunocompetent hosts

-Possess features which make them uniquely pathogenic

-Even benign organisms have disease-causing potential, usually dependent on dose and area of entry.

-Extracellular (S. pneumoniae, S. pyogenes)

-Facultatively intracellular (M. tuberculosis, Shigella dysenteriae)

-Obligately intracellular (Rickettsia rickettsiae, Chlamydia trachomatis, viruses)

-Pathogen will incubate inside the host

-manifestion of the disease or illness

Signs (observable effects) vs. symptoms (experienced) -convalescence period of recovery after disease: Infection may be resolved completely—recovery and boosted immunity. Person may become asymptomatic/symptomatic carrier (B. pertussis, S. pyogenes, HIV)

-Localized vs. systemic (septicemia)

-Acute (rapid onset/harsh symptomology) vs. chronic (slow to develop; long time to escalate) vs. latent (herpesviruses, TB)

Transmission to host

Adherence to target tissue -Adhesins on pili/fimbrae Some may have multiple types with different affinities for different tissues (e.g. S. pyogenes, H. influenzae) Colonization of target tissue

-it must also replicate.

Obstacles: Normal flora (space/nutrient competition) Optimal growth conditions (oxygen, pH, osmotic stability) -Host immunity -Destruction of target tissue(s) -Degradation of extracellular matrix via degradative enzymes (collagenase), intracellular pathogen lysing the cell, toxin production -Exit from host to propagate cycle -Must occur before host clears pathogen

-Toxins mostly bind to receptors on the cell which influence cell signaling and secretion of cytokines Exotoxins

-Secreted by the pathogen Botulin

– Clostridium botulinum Endotoxins Part of the pathogen’s structure – often part of the cell wall

Play an accessory role in tissue damage by promoting inflammation (encourages the host immune system to overproduce cytokines, leading to damage of tissue)

• Part of cell envelope
• Released by cell division/death
• Potent induction of cytokine response leading to fever, weakness, aching, shock