Unit One * Key Concepts

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Final exam
Format
pts
Multiple choice
Material prior to midterm
Material since midterm
15
20
Matching
Antibiotics to site of action
Disease to pathogen
Short answer
Case study
Emphasis on Units 3 and 4
6
16
23
20
Comprehensive topics
Common virulence factors
Phagocytosis – process of and microbial
defenses against
Acute inflammation – signs and
consequences of
Fever – exogenous & endogenous
pyrogens, biochemical & physiological
Organ systems – recognize by
symptoms, defenses of, major
pathogens of
Lab procedures – primary enrichment &
selective media, Gram stains,
catalase/oxidase, quantitative counts,
antibiotic susceptibility
Unit One – Key Concepts
Review of the microbial pathogens
Viruses
• Not living, not cells
• Obligate intracellular pathogens
• Enveloped vs naked
• Interact with target cells via highly specific virus surface protein to host target cell
receptor interactions
• Enter the target cell by one of 3 mechanisms (depending on type of virus) RME, fusion,
translocation
• Infections are often “silent”, not alerting the immune system or producing signs (such as
acute inflammation) until host cells are damaged (lysis) or altered (viral antigen + MHC I).
Bacteria
• Prokaryotic
• For purposes of diagnostic bacteriology – 2 staining types: Gram neg vs Gram pos –
staining properties based on differences in cell wall structure
• Gram pos – thick peptidoglycan (multiple layers); Gram neg. – thin peptidoglycan (single
layer), outer lipid membrane.
• *Signs and symptoms of disease often attributed to bacterial cell wall peptidoglycan,
teichoic acids (GP), and LPS (GN) that induce acute inflammation, fever; Secretion of
enzymes (like coagulase); Secretion of toxins (exotoxins – lots of, very important)
• Role of capsules in delaying phagocytosis
• Attachment mechanisms, either general like sticky capsules, or specific like fimbriaereceptor interactions.
Fungi and Protozoa
• Eukaryotic organisms, like the host – will limit treatment options
• Spores (asexual reproduction in fungi), cysts (an environmentally stable, infectious life
cycle stage of protozoa)
• Deep, systemic infections often indicate an immunocompromised host (especially deep
fungal infections)
Normal Microbiota
 Important biological defense against pathogen occupation of a site – densities greatest in
the colon, least in stomach and on epithelium of the skin.
 May cause opportunistic infections if get into the wrong site (like E. coli in peritoneal
cavity) or if host becomes compromised (by viral infection for example).
Review of host defenses
 3 lines of host defenses
o exterior defenses against entry into and establishment at the site (chemical,
mechanical, biological – site specific - think about for each system we covered)
o interior non-specific defenses
o interior specific defenses (antigen-specific)
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Host non-specific interior defenses
o INFLAMMATION!! – a complex, dynamic process, the cornerstone of the nonspecific interior defenses - swelling (edema), redness (erythema), tenderness, heat –
increased WBC, and particularly increased PMNs
o Complement activation
o Acute phase proteins
o Phagocytosis by macrophages and neutrophiles (=PMNs)
o Cytolytic cells – NK, eosinophils
Cellular communication/coordination via cytokines
o What cells secrete cytokines, what cytokines do they secrete, what cells do those
cytokines act upon.
TH – function is to “turn on” or to enhance the activation/effectiveness of other host
defense cells. Does this via IL2 (acts on other lymphocytes) and gamma interferon (acts
on macrophages)
Tc – functions to lyse and thereby destroy host cells infected with intracellular pathogens,
bacteria and esp. viruses. (Recognizes infected cells via TC receptor to foreign antigen
complexed with host MHC1 interactions. Secretes perforin, TNF, granzyme 
membrane pores, triggers apoptosis)
Plasma cells (effector B lymphocytes) secrete antibodies
Functions of antibodies
o Neutralizing (virus attachment, bacterial attachment, bacterial toxin attachment) –
secretory IgA (=sIgA), found in body fluids, esp. mucus.
o Opsonizing (an attachment for phagocyte receptors, enhances phagocytosis) – IgG
o Agglutination (enhances phagocytosis, but not as an opsonin) – IgM
Memory B and T lymphocytes – secondary response may be so swift that there are few or
no symptoms of infection.
Unit Two – Key Concepts
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Entry, exit, transmission – review for each major system (RT, UT, GI, NS, skin).
Microbial strategies to avoid host non-specific interior defenses
o Anti-complement, and esp. anti-phagocytic defenses
Surface infections (non-specific defenses at the surface impt., generally shorter
incubation periods) vs systemic infections (T and B lymphocytes become more impt.,
generally longer incubations periods)
Microbial strategies to avoid specific defenses
o Preventing or delaying recog. of antigens and antigenic variation of most importance.
Pathological consequences of infection – emphasized also in the clinical cases
o Pathology caused directly by the microbe
 Exotoxins
 Endotoxins (=LPS)
o *Fever - how is it induced at both chemical/cellular levels and physiological
levels.
o Pathology as a result of the immune response to the microbe
 Complement-mediated damage
 Damage resulting from acute inflammation *
o Pathology as a result of specific defenses – hypersensitivities, also TH secreted
cytokines (overabundance of IL-2 for example)
Unit Three – Key Concepts
We covered these systems via clinical cases
Lower respiratory tract
Urinary tract
Gastrointestinal tract
Nervous system
Infections of wounds
We covered these pathogens
Gram positive
Gram negative
Cocci
Rods
Catalase
+
Staphylococcus
aureus
Oxidase
-
Streptococcus
agalactiae
+
-
Pseudomonas
aeruginosa
Enterobacteriaceae
Lactose fermenter
Escherichia coli
Lactose non-fermenter
Shigella sonnei
Be able to work through a novel clinical case (with guidance)
That includes lab work such as the primary plating media we used (BA, CA, MAC, CCNA), Gram
stains, catalase/oxidase tests. Newly introduced techniques, such as how to do quantitative counts
(urinary tract lab, also antimicrobial susceptibility testing).
Unit Four – Key Concepts
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General considerations for using antimicrobials to treat infectious disease
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Know the characteristics of the antibiotics that we used in the last lab exercise. What drug family do
they belong to, what is their site of action in a bacterial cell, etc.
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Know how to perform, read, and interpret a disk diffusion susceptibility assay and an MIC/MBC
assay.
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Know the point of immunization.
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Know the pros and cons of live attenuated and inactivated vaccines.
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