Principles Of Infectious Disease Ii (Foundations Exam 1)

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pathogenesis

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the ability of an organism to cause disease in a susceptible host

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factors that determine the outcome of host-pathogen relationship

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virulence of pathogen and degree of resistance or susceptibility of host

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commensals

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- non-pathogens (normal flora)
- resident microbiota
- colonize body's internal and external surfaces
- may be opportunistic
- may be altered by antibiotic treatment

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beneficial effects of commensals

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- may out-compete pathogens
- enable "priming" of immune system
- provide metabolic nutrients
- modify pH
- block pathogen binding sites
- produce antibacterial compounds called bacteriocins

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potential pathogens

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- present in normal flora
- may cause disease or colonization without disease (carrier state)

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true pathogens

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- always cause symptoms
- pathogenicity requires scientific proof (Koch's postulates)

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virulence

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degree of pathogenicity (low, moderate, high, extremely high)

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colonization

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- first stage of infection
- establishment of pathogen at the appropriate portal of entry

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mechanisms for establishing infection and damaging tissues

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1.contact or enter host cells and directly cause cell death
2. kill cells or blood vessels at a distance: via toxins or enzymes
3. induce host immune responses that cause tissue damage/cell death

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tropism

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- infectious viruses replicate at the host's expense
- cells have a predilection for viruses to infect certain cells and not others

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tropism is affected by...

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1. expression of host cell receptors for the virus (HIV-CD4)
2. expression of cell substances (proteases)
3. presence of cellular transcription factors that recognize viral sequences and allow virus to replicate inside some cells but not in others
4. physical/anatomic barriers, local temperature, pH, and host defenses

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cytopathic effects (CPE)

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- preventing synthesis of host macromolecules
- producing degradative enzymes and toxic proteins
- inducing apoptosis

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cytotoxic antiviral immune responses

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- viral proteins on host ells may be recognized by immune system and the host attacks virus-infected cells

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transformation of infected cells into benign or malignant tumor cells

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stimulate cell growth and survival
1. expression of virus-encoded cancer genes (oncogenes)
2. suppression of normal cell death processes (anti-apoptosis)
3. mutations cause by insertion of virus genes into host genome

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underlying mechanisms of viral pathogenicity/injury

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1. tropism
2. cytopathic effects
3. cytotoxic antiviral immune response
4. transformation of infected cells into benign or malignant tumor cells

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underlying mechanisms of bacterial pathogenicity/injury

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1. tissue tropism
2. species specificity
3. pathogenicity islands
4. plasmids, transposons
5. bacteriophages

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pathogenicity islands

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- acquired by horizontal gene transfer and are incorporated in the genome of pathogenic bacteria
- encode genes which contribute to virulence of pathogen

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plasmids, transposons

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mobile genetic elements that spread between bacteria, can encode virulence factors, and convert nonpathogenic bacteria into virulent ones and/or anti-biotic resistant

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bacterial adherence to mucosal surfaces

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1. nonspecific adherence: reversible attachment of the bacterium to eukaryotic surface
2. specific adherence: attachment of microorganism to host cell surface--permanent formation of lock-&-key bonds

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adhesins

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bacterial ligand that binds to host cells or ECM

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pili

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filamentous protein on the surface of bacteria
- determine the binding specificity of the bacteria

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bacterial invasiveness

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- ability to invade tissue: colonization, production of extraclelular substances
- enzymes that enable spreading : invasins damage host cells
- enzymes that cause hemolysis and/or leukolysis
- extracellular digestive enzymes: produced by bacteria

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toxigenesis

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the ability to produce toxins

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exotoxins

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proteins released from bacterial cells and may act at tissue sites removed from the site of bacterial growth

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endotoxins

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cell-associated substance
- released from growing bacterial cells and cells that are lysed as a result of effective host defense
- may travel throughout host and cause damage

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quorum sensing

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- bacteria coordinate and regulate gene expression within large population of organisms
- inducing expression of virulence factors
- overcome host defenses

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biofilms

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- acquire some of the more complex properties of multicellular organisms
- making them inaccessible to immune effector mechanisms and increasing resistance to antimicrobial drugs
- persistance/relapse of infections

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intracellular location

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- facultative intracellular bacteria infect either epithelial cells, macrophages, or both
- allows bacteria to escape effector mechanisms

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facilitate bacterial spread....

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1. use the host immune response to gain entry into macrophages
2. secrete complex system consisting of needle-like structures that bind to host cells
3. manipulate cell cytoskeleton to spread directly from cell to cell and evade immune effector mechanisms

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cytoplasmic strategies/interactions

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- inhibit host protein synthesis replicate rapidly and lyse the host within 6 hours
- eludes or blocks formation of host phagolysosome defense