Deaths and death rates for the 10 leading causes of death in specified age groups: USA, 1999 (Rates per 100,000)

• All causes 2,391,399 877.0 • Diseases of heart 725,192 265.9 • Malignant neoplasms 549,838 201.6 • Cerebrovascular diseases 167,366 61.4 • Chronic lower respiratory dis 124,181 45.5 • Accidents:unintentional injuries 89,703 34.1 • Diabetes mellitus 68,399 25.1 • Influenza and pneumonia 63,730 23.4 • Alzheimer's disease 44,536 16.3 • Nephritisand nephrosis 35,525 13.0 • Septicemia 30,680 11.3 • All other causes (Residual) 484,092 177.5

Aerobic, Gram-positive cocci

•Staphylococcus aureus Staphylococcus epidermidis

Aerobic, Gram-positive rodsBacillus anthracis Bacillus cereus

Lactobacillus sp. Listeria monocytogenes

Nocardia sp. Erysipelothrix Corynebacterium diptheriae

Aerobic, Gram-negative rods

•Fastidious, Gram-negative rods

•Actinobacillus actinomycetemcomitans

•Acinetobacter baumannii (really A. calcoaceticus)

•Bordetella pertussis

•Brucella sp. Campylobacter sp.

•Francisella tularensis

•Haemophilus ducreyi

•Haemophilus influenzae

•Helicobacter pylori

Enterobacteriaceae (glucose-fermenting Gram-

negative rods)•Enterobacter sp.

•Escherichia coli

•Klebsiella pneumoniae

•Proteus sp.

•Salmonella enteriditis

•Salmonella typhi

•Serratia marcescens

•Shigella sp.

•Yersinia enterocolitica

•Yersinia pestis

Bacteria which cannot or are difficult to Gram stain•Borrelia burgdorferi , Borrelia recurrentis

•Chlamydia trachomatis

•Coxiella burnetii, Ehrlichia sp.

•Legionella sp. , Leptospira sp.

•Mycobacterium bovis, Mycobacterium tuberculosis, Mycobacterium avium, Mycobacterium intracellulare

•Mycobacterium leprae

•Rickettsia rickettsii

•Treponema pallidum

Disease Carriers - Borrelia burgdorferiThis scanning electron micrograph shows spirochete Borrelia burgdorferi, causative agent of Lyme disease. While only 0.2-0.3 microm wide, the cell length may exceed 15 to 20 microm

Medical MicrobiologyMicrobes are the most significant life form sharing this planet with humans because of their pervasive

presence and their utilization of any available food source, including humans whose defenses may be breached.

Microbial diseases are frequent and often severe, e.g. AIDS, cholera, tuberculosis, rabies. The ubiquitous

presence of microbes and heir astronomic numbers give rise to the many mutants that account for rapid evolutionary adaptation and in part for emerging diseases such as AIDS, ebolla and antibiotic-resistant tuberculosis.

This adaptability also accounts for the ability of microbes to utilize an enormous range of nutritional sources. MO may have either beneficial roles in maintaining life or undesirable roles in causing human, animals and plant disease.       Beneficial roles of microbes include recycling of organic matter through microbe-induced decay and through digestion and nutrition in animals and humans. In addition, the natural microbial flora provides protection against more virulent microbes.    While microbes that cause infectious diseases are virulent, opportunistic diseases may also be caused by normally benign microbes. Opportunistic infections occur when the host defense mechanisms are impaired, microbes are present in large numbers, or when microbes reach vulnerable body sites. A striking example is HIV which impairs the host's defenses to multiple microbes. Natural selection favors a predominance of less virulent MO, except when microbial transmission depends on disease manifestations (e.g., coughing and sneezing).

Teaching planMedical Microbiology begins with a general introduction of mic

roorganisms. Followed by reviewing immune system, focusing on the body's response to invading microorganisms.

Bacteria are then covered, first with a series of topics presenting the general concepts of bacterial microbiology and then with lectures detailing the major bacterial pathogenes of humans.

Similarly, the course covers virology, mycology, and parasitology. In each lesson, the introductory will stress the mechanisms of infection characteristic of that type of microorganism, thus providing a framework for understanding rather than memorizing the clinical behavior of the pathogens.

The final part of lecture- Introduction to Infectious Diseases, is arranged for clinical considerations.

Chapter 1 History

Chapters 11-14 Immunity

Ch 9 Normal flora

Ch 19 Host Parasite Interactions, Virulence Determinants

Mid-EXAM

Ch 20 Antibiotics

Ch 22 StaphylococcusCh 23 Streptococcus Ch 24 EnterococcusCh 25 BacillusCh 26 Corynebacterium Listeria and ErysiphelothrixCh 27 NeisseriaCh 28 EnterobacteriaCh 29 vibrio

Ch 30 Pseudomonas

1. Mid-term examine

2. 1.     Briefly discuss the worldwide prevalence of the parasitic infections.3. 2.     How do you deal with anthrax threat? 4. 3.     Give an example of treatment for viral diseases.5. 4.     Why and how infectious disease changes its pattern?6. 5.     Which is most efficient way for a microbe to generate its energy?

(ATP yield)7. 6.     Use specific examples to explain the mechanism of bacterial gene

regulation.8. 7.     What is the mechanism for control gram-positive and gram- nega

tive bacterial infection?9. 8.     Briefly discuss the ways that bacteria influence the apoptosis of

host cells.9. 9. How do yeast differ from molds and what does the term dimo

rphism mean when it is applied to fungi?1. 10. Why we have to study epidemiology of pathogens? Discuss its

basic method.B

Medical Microbiology Lecture I

Introduction and HistoryCommunicable Nature of Disease and Germ Theory

a. Hipporcrates and Galen

i. poison vapors and miasmas

ii. punishment of the gods

Mode of transmission was difficult to determine: air ,water soil, food insects

Difficult to believe that something that cannot be seen can cause disease

b. Mosaic code

I. restrict movement of diseased individuals Leprosy

ii. avoid ceratin foods; pork, shellfish

c. Fracastro (1546): syphilis communicable via seminara or seeds.

origin was supernatural

Modern examples: Legionnaires' toxic shock, AIDS, cancer

d. van Leeuwnehoek (1677)

e. John Hunter (1700's)

f. Edward Jenner (1798) Smallpox-compox vaccination (vacca)

g. Holmes/Semmelweis (1843-1847) Puerperal fever, Lister: surgery; carbolic acid

h. Louis Pasteur Spontaneous generation fermentation

attenuation (rabies, anthrax)

i. Robert Koch Postulates

agar, pure culture, stains

Koch's Postulates

1. The specific organism should be shown to be present in all cases of animals suffering from a specific disease but shold not be found in healthy animals.

2. The specific microorganism should be isolated from the diseased animal and grown in pure culture on artificial laboratory media.

3. This freshly isolated microorganism, when inoculated into a healthy laboratory animal, should cause the same disease seen in the original animal.

4. The microorganism should be reisolated in pure culture from the experimental infection.

ImmunityHost Defences 1. Innate or nonspecific a. mechanical b. mucous secretions c. pH d. lysozyme and o

ther enzymes e. inflammation f. phagocytic cells g. complement h. interferon 2. Specific - antigen response a. antibody production structure of antibodies characteristics of antibodies complement fixation tissue location of ab antibody production (clonal selection, primary, secondary respo

nses) b. cell mediated immunity T cells lymphokines, cytotoxins, chemotactic factors types of infections (T.B., Listeria, fungal) c. Immunity: Active Infection immunization :live, attenuated, killed , cloned antigens d. Immunity: Passive maternal (fetus, milk), animal, human