Infectious Disease Notes
killing of infectious organism
Elicit from patient:
• Recent travel
• Behavioral factors
• Animal exposure
• Contaminated environment
• Living and occupational conditions
• Contact with sick individuals
Check prevalence of ID in certain regions
Note: resistant strains (i.e. chloroquine-
resistant malaria)
STDs
• Sexual practices
• Birth control methods
Medical care may increase risk for ID thru:
• Nosocomial pathogens
• Breaching of the skin (i.e. IV lines,
surgical incisions) and mucosa (i.e.
endotracheal intubation, bladder
catheter)
• Introduction of foreign bodies
• Alteration of normal flora with
antibiotics
• Drug-induced immunosuppression
The Immune Response
• Cellular immunity – intracellular
pathogens
• Humoral immunity – extracellular
pathogens
Cellular Immunity
• Break in protective barrier (skin,
mucosa)  bloodstream  cellular
immunity (T-lymphocytes,
macrophages, NK cells)
T-lymphocytes
• Activated by macrophages and B-
lymphocytes
• Present Ag & MHC
• Cytotoxic T-cells: directly attack and
lyse host cells with Ag
• Helper T-cells: stimulate B-cells for Ig
production
B-cell to T-cell communication
• Co-stimulation via CD40-CD40 ligand:
increase B-cell response
• Co-stimulation via B7-CD28: activation
of CD4+ helper T-cell
• Cytokines (i.e. IFN)
o elaborated by T-cells to
directly inhibit growth of
pathogens or stimulate the
by macrophages and cytotoxic
cells
o stimulate inflammatory
response; fever (increase
acute phase serum
components and proliferation
of leukocytes)
• Tissue macrophages and PMNs – capable
of killing microorganisms w/o help, but
work more efficiently when pathogen is
first opsonized by C3b or antibodies.
o Kuppfer cells (liver)
o Alveolar macrophages (lungs)
o Spleen
o Mesangial cells (kidneys)
o Microglia (brain)
o Lymph nodes
Humoral immunity
• Antibodies
• Complement cascade
• Phagocytic cells
Antibodies
• Complex glycoprotein (Ig) produced by
mature B-cells circulate in body fluids
or are secreted on mucosal surfaces
• Recognize and bind to foreign Ag
• Ig G: predominate in circulation and
persists for years after exposure
• Ig M: earliest to appear
• Ig A (secretory): mucosal surface
• Ig A (monomeric): serum
• Ig E: allergic and parasitic disease
• Function of Ab:
o Impede pathogen fxn
o Neutralize secreted toxins and
enzymes
o Facilitate removal of pathogen
by presenting to macrophages
(Antibody-dependent cellular
cytotoxicity fxns of T-cells)
o Promote deposition of
complement on surface of
pathogen
The Complement System
• Serum proteins that adhere to or
disrupt surface of pathogen
• C3b: “opsonin” for presentation to
phagocyte
• C7, C8, C9: “terminal” components;
directly kill bacteria (i.e. Neisseriae)
via Membrane Attack Complex causing
membrane disruption and bacteriolysis
• C5a: chemoattractants for PMNs
Classic Pathway: activated by immune
complexes (Ab-Ag)

Alternative Pathway: activated by microbial

components in the absence of an antibody

PMNs: attracted by C5a to inflammatory site

TNF & IL-1  (+) selectins (CD6, ELAM-1 in

endothelial cells)  PMNs adhere to cellular
adhesions molecules on endothelial cells (ICAM-
1)  B2-integrins  (+) diapedesis to
extravascular compartment

Genesis =)