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Name the stages of disease
- Incubation period
- Prodromal period
- Period of illness
- Period of decline
- Convalescence
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interval between initial infection and onset of symptoms (time depends on microorganism, virulence, number, host resistance)
Incubation period
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follows incubation (when you first start feeling lousy)
Prodromal period
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presence of severe symptoms
Period of illness
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symptoms subside (secondary infection vulnerability)
Period of decline
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Recovery period
Convalescence
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Name the different types of symbiosis
- Commensalism
- Mutualism
- Parasitism
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the relationship between normal microbiota and the host
Symbiosis
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Symbiosis in which bacteria benefits and humans are unaffected (S. epidermidis on skin)
Commensalism
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Symbiosis in which both organisms benefit (E. coli in gut making vitamins)
Mutualism
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Symbiosis in which one organism benefits at the expense of the other (disease causing organisms, doesn’t kill the other one)
Parasitism
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disease with a period of no symptoms when the causative agent is inactive (Shingles)
Latent
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disease develops slowly and continues for a long period and may reoccur (Malaria)
persistent
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the study of the cause and the diagnosis of disease or changes in a person, animal, or plant that are caused by disease
Pathology
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the study of the cause of a disease
Etiology
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the development of a disease
Pathogenesis
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colonization of the body by pathogens
Infection
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an abnormal state in which the body is not functioning normally
Disease
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the extent or degree of pathogenicity
Virulence
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fraction of people GETTING the disease
Incidence
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fraction of people that HAVE the disease
Prevalence
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Functions of normal microbiota
- Protect host by:
- Occupying niches that pathogens might occupy
- Producing acids
- Producing bacteriocins
- Using nutrients and oxygen
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How a fever comes about
- The Pyrogenic response
- Caused by cytokines, NOT the endotoxin
- -->cytokines travel to the hypothalamus
- -->hypothalamus produces prostaglandins
- -->prostaglandins reset the body’s thermostat higher
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disease constantly present in a population
Endemic
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disease acquired by many hosts in a given area in a short time
Epidemic
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worldwide epidemic
Pandemic
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disease that occurs occasionally in a population (Typhoid)
Sporadic
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symptoms develop rapidly and end shortly after (Flu)
Acute
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disease develops slowly, continues for a long period and may reoccur (Malaria)
Chronic
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between acute and chronic; Rather recent onset or somewhat rapid change; usually caused by alpha-hemolytic strep from mouth
sub-acute
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spread of microbes, especially bacteria or their toxins in the blood, lungs or other tissues
Sepsis
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bacteria in the blood
Bacteremia
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toxins in the blood
Toxemia
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ability to produce a toxin
Toxigenicity
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viruses in the blood
Viremia
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acute infection that causes the initial illness (cold)
Primary Infection
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opportunistic infection after a primary infection (pneumonia)
Secondary Infection
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habitat in which the agent normally lives, grows, and multiplies, and from which they can be transmitted
Reservoirs
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animal diseases that may be transmitted to humans
Zoonoses
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arthropods, especially fleas, ticks, and mosquitoes
Vectors
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hospital acquired infections
Nosocomial
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the incidence of disease
Morbidity
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the proportion of deaths to population
Mortality
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How bacterial pathogens penetrated host defenses
- Cell walls (M protein binds to cell wall and prevents phagocytosis)
- Enzymes
- Antigenic variations (ability of bacterial cell to alter their surface antigens)
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Variety of different ways to destroy cell
- Can grow inside the host cells to avoid host defenses like the immune system
- To invade the cell, viruses have attachment sites for receptors on their target cells
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Microbial Mechanisms of Pathogenicity
- Portals of entry
- -->number of invading microbes and adherence
- penetration or evasion of host defenses
- -->damage to host cells
- portals of exit
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Characteristics of Exotoxin
- produced within cell
- bacteria must be functional
- secreted
- protein
- typically Gram+
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Characteristics of Endotoxin
- Lipid
- Gram-
- Not secreted
- Part of the membrane of the cell
- Causes problem once then cell dies and lyses
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Why super antigens are so dangerous
Causes intense immune response due to massive release of cytokines from host cells
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killing harmful microbes without damaging the host
Selective toxicity
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the ratio of the toxic dose to the therapeutic dose (the larder the index, the safer the drug – to humans)
Therapeutic Index
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What natural penicillin does to the cell?
Inhibits bacterial cell wall synthesis by inhibiting the cross linking of peptides
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What is its target?
Inhibiting transpeptidase
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Five action modes of antimicrobial drugs
- Inhibition of cell wall synthesis
- Inhibition of protein synthesis
- Injury to plasma membrane (lipopeptides)
- Inhibition of nucleic acid synthesis
- Inhibition of metabolite synthesis (sulfonamides)
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Four major mechanisms of drug resistance and how they work
- Drug inactivation or destruction: hydrolyze lactam
- Prevention of penetration: restricts the uptake of molecules to the porins
- Alteration of the drug’s target site: the modified PBP is not inhibited by PCN and cell wall synthesis continues
- Rapid efflux of antibiotics: efflux pumps on the membrane of gram- bacteria eliminate toxic wastes
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the effect of two drugs together is greater than the effect of either alone
Synergism
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the effect of two drugs together is less than effect of either alone
Antagonism
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The three results of antibody-antigen binding
- Block infections and eliminate extracellular microbes
- Activate macrophages to kill phagocytosed microbes
- Kill infected cells and eliminate reservoirs of infection
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The mechanisms by which Tamiflu works
Blocks the neuraminidase enzyme
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The mechanisms by which Acyclovir works
inhibitor of herpes virus DNA polymerase
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What is targeted in treatment of retroviruses?
Reverse Transcriptase
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The mechanism of action of successful Mycobacteria treatment
- Mycobacteria incorporate mycolic acids in the cell wall
- Drugs target the synthesis or incorporation of mycolic acid
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