chapter 14 principles of disease & epidemiology

1. chapter 14 principles of disease & epidemiology

2. The Germ Theory of Disease • Should be abundant in sick; absent in healthy. • Should be isolated and grown in pure culture. • Should cause disease in healthy organism. • Should be isolated from 2nd host and ID’d as original etiologic agent.

3. etiology: Koch’s Postulates

4. Cholera in Soho, 1854: 616 dead

5. economic impact

6. epidemiology disease transmission pathology disease progression etiology causative agent infection colonization by pathogens disease abnormal body fxn the language of epidemiology pathogenicity S&S  disease syndrome infectivity communicable transmissible contagious “very communicable” noncommunicable opportunistic normal flora and/or introduced bacteria

7. disease classification • transmission • how are diseases spread • progression • what does the disease look like in the host • host involvement • where does the pathogen grow • severity • how does a particular disease run its course • occurrence • how widespread is the disease

8. disease classification: transmission

9. disease progression

10. disease classification: host involvement

11. nosocomial infections1.7 mill infections, 99,000 deaths; $4.5-11 billion

12. avoiding nosocomial infections this includes hand-hygiene procedures

13. disease classification: severity • acute disease • rapid progression, short duration (influenza) • chronic disease • slow progression, long duration (leprosy) • subacute disease(definition varies) • slower than acute, faster than chronic • symptoms flux between acute & chronic (gingivitis) • latent disease • periods of inactivity (herpes) predisposing factors  severity gender  age  immune status

14. disease classification: occurrence

15. chapter 14 learning objectives • Define the following terms: epidemiology, pathology, etiology, pathogenesis, infection, host, disease, communicable, contagious, and non-communicable. • Compare the following classes of disease severity: acute, chronic, subacute and latent disease. How do predisposing factors affect the severity of disease? • Describe the work done by Robert Koch to formulate his Postulates. List and explain these postulates and discuss relevant exceptions. • How are descriptive and analytical/experimental epidemiological studies related to one another? What kinds of data are collected in each? • What is the ultimate goal of epidemiology? • Describe the three different ways that infectious agents are transmitted from one host to another, including their subcategories. Give an example of each. • Describe the progression of disease in a given host, as related to time and number of infectious organisms. • Define and contrast the following: local infection, systemic infection, focal infection, mixed infection, primary infection and secondary infection. • How are bacteremia, septicemia, toxemia and viremia related to systemic disease? • Contrast endemic, epidemic and pandemic disease occurrence. How does herd immunity affect disease occurrence? • Why do nosocomial infections occur? • Why are urinary tract infections, pneumonia and sepsis such common nosocomial infections? • How does herd immunity relate to the containment of infectious disease? • How do host involvement, signs and symptoms relate to the idea of a disease syndrome?

16. chapter 16: nonspecific defenses of the host

17. 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”

18. 1st defense: physical barriers & normal flora

19. innate defense: inflammation dolor, calor, tumor, rubor

20. white blood cells

21. innate defense: phagocytosis CELLULAR RECEPTORS Pattern Recognition Receptor (PRR) Toll Like Receptor (TLR) FOREIGN MOLECULES Pathogen-Associated Molecular Patterns (PAMPs) ACTIVATE PHAGOCYTES cytokine release  innate response

22. monocytes are phagocytic “scouts” resident in tissue PRR 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

23. innate defense: fever fever  hyperthermia 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)

24. innate defense: complement alternative pathway • direct activation lectin pathway • needs innate activation (MBLs) classical pathway • needs adaptive activation

25. innate defense: interferons

26. the non-specific defenses: a summary

27. chapter 16 learning objectives • Define the following terms: resistance, susceptibility, nonspecific resistance, specific resistance (immunity). • Describe the physical and chemical factors involved in the first innate resistance to disease. • 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? • Describe the three pathways through which complement can be activated. • Describe the stepwise production of fever. Why is fever useful? When isn’t it, and why? • Describe the production of interferon and antiviral proteins. Why is this still considered an innate (and not specific) defense? • What three ways does complement work to rid the body of pathogens? • 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. • As discussed in class, identify the role of each of the following: lymphoid cell, B cell, T cell, NK cell, eosinophil, dendritic cell, monocyte, and macrophage.