Chapter 14 principles of disease & epidemiology. The Germ Theory of Disease.
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Transcript of Chapter 14 principles of disease & epidemiology. The Germ Theory of Disease.
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chapter 14principles of disease &
epidemiology
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The Germ Theory of Disease
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symbioses and normal flora
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the etiology of disease: Koch’s Postulates
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John Snow1848–1849
mapped occurrence of cholera in London
Ignaz Semmelweis
1846–1848
handwashing decreased the incidence of puerperal fever
Florence Nightingale
1858improved sanitation decreased the incidence of epidemic typhus
studying disease transmission
• descriptive: collection and analysis of data• experimental: controlled experiments• analytical: comparison of a diseased group and
a healthy group
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Cholera in Soho, 1854: 616 deadDescriptive Study:data collection &
analysis
Hypothesis Formation:stop disease transmission
Analytical/Experimental Study
Analysis of Study:did transmission
stop?
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economic impact
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the language of epidemiology
epidemiology
pathology
etiology
infection
disease
pathogenicity
infectivitycommunicable
contagious
noncommunicable
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disease classificationhelps identification stops transmission
– occurrence
– severity & duration
– extent of host involvement
– development & progression
– transmission
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disease classification: occurrence
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• acute disease
• chronic disease
• subacute disease (definition varies)
• latent disease
disease classification: severity
predisposing factors severitygender age immune/genetic
status
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disease classification: host involvement
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disease progression
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disease classification: transmission
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nosocomial infections1.7 mill infections, 99,000 deaths; $4.5-11 billion
Total InfectionsAntibiotic Resistance
S. aureus 25% 89%
other Staphylococcus 16% 80%
Enterococcus 10% 29%
Gram-negative rods 23% 5-32%
C. difficile 13% none
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avoiding nosocomial infectionsthis includes hand-hygiene procedures
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chapter 14 learning objectives1. Define the following terms: epidemiology, pathology, etiology, pathogenesis,
infection, host, disease, communicable, contagious, and non-communicable.2. Compare the following classes of disease severity: acute, chronic, subacute and
latent disease. How do predisposing factors affect the severity of disease?3. Describe the work done by Robert Koch to formulate his Postulates. List and explain
these postulates and discuss relevant exceptions.4. How are descriptive and analytical/experimental epidemiological studies related to
one another? What kinds of data are collected in each?5. What is the ultimate goal of epidemiology?6. Describe the three different ways that infectious agents are transmitted from one
host to another, including their subcategories. Give an example of each.7. Describe the progression of disease in a given host, as related to time and number of
infectious organisms.8. Define and contrast the following: local infection, systemic infection, focal infection,
mixed infection, primary infection and secondary infection. 9. How are bacteremia, septicemia, toxemia and viremia related to systemic disease?10. Contrast endemic, epidemic and pandemic disease occurrence. How does herd
immunity affect disease occurrence?11. Why do nosocomial infections occur?12. Why are urinary tract infections, pneumonia and sepsis such common nosocomial
infections?13. How does herd immunity relate to the containment of infectious disease?14. How do host involvement, signs and symptoms relate to the idea of a disease
syndrome?
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chapter 16:nonspecific defenses of the
host
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host defenses
• susceptibility: lack of resistance to a disease
• resistance: ability to ward off disease
• non-specific (innate) resistance: any/all pathogens
• specific (adaptive) resistance: specific pathogen “immunity”
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1st defense: physical barriers & normal flora
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innate defense: inflammationdolor, calor, tumor, rubor
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white blood cells
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CELLULAR RECEPTORS
Pattern Recognition
Receptor (PRR)
Toll Like Receptor (TLR)
FOREIGN MOLECULES
Pathogen-Associated
Molecular Patterns (PAMPs)
ACTIVATE PHAGOCYTES
cytokine release innate
response
innate defense: phagocytosisdetails
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monocytes are phagocytic
“scouts” resident in tissuePRR activation
– phagocytize pathogens– recruit innate defenses– present antigen– macrophages
• usually stay in tissue present pathogen to B cells
– dendritic cells• migrate to lymph nodes present pathogen to T cells
avoidance by microbes animation avoidance by microbes (video)
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innate defense: fever
advantages• INCREASES
– transferrins ( free Fe)
– IL–1 activity
– Interferon
– tissue repair
• DECREASES
– release of Fe & Zn
disadvantages•tachycardia•tachypnea•acidosis•dehydration•44–46oC fatal (111oF)
fever hyperthermia
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innate defense: complement
Activationalternative pathway• direct activationlectin pathway• needs innate activation
(MBLs) classical pathway• needs adaptive activationResults
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innate defense: interferons
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the non-specific defenses: a summary
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chapter 16 learning objectives
1. Define the following terms: resistance, susceptibility, nonspecific resistance, specific resistance
(immunity).
2. Describe the physical and chemical factors involved in the first innate resistance to disease.
3. Describe the process of inflammation- be familiar with the terms dolor, calor, tumor, and rubor.
What about the release of cytokines causes each of these signs? Why are these effects useful?
4. Describe the three pathways through which complement can be activated.
5. Describe the stepwise production of fever. Why is fever useful? When isn’t it, and why?
6. Describe the production of interferon and antiviral proteins. Why is this still considered an innate
(and not specific) defense?
7. What three ways does complement work to rid the body of pathogens?
8. Define and describe the stepwise mechanism of phagocytosis, describe the process. Include in your
discussion the role of TLRs and PAMPs. Discuss the similarities and differences between dendritic
cells and macrophages.
9. Both macrophages and dendritic cells are members of the innate defenses that routinely
phagocytize pathogens. How are they different?