Deaths and death rates for the 10 leading causes of death in specified age groups: USA, 1999 ( Rates per 100,000) All causes2,391,399 877.0 Diseases of.

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Presentation transcript:

Deaths and death rates for the 10 leading causes of death in specified age groups: USA, 1999 ( Rates per 100,000) All causes2,391, Diseases of heart 725, Malignant neoplasms 549, Cerebrovascular diseases 167, Chronic lower respiratory dis 124, Accidents:unintentional injuries 89, Diabetes mellitus 68, Influenza and pneumonia 63, Alzheimer's disease 44, Nephritisand nephrosis 35, Septicemia 30, All other causes (Residual) 484,

Aerobic, Gram-positive cocci Staphylococcus aureus Staphylococcus epidermidis

Aerobic, Gram-positive rods Bacillus 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 burgdorferi This scanning electron micrograph shows spirochete Borrelia burgdorferi, causative agent of Lyme disease. While only microm wide, the cell length may exceed 15 to 20 microm

Medical Microbiology  Microbes 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 plan  Medical Microbiology begins with a general introduction of microorganisms. 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 Immunity Ch 9 Normal flora Ch 19Host Parasite Interactions, Virulence Determinants Mid-EXAM Ch 20 Antibiotics Ch 22 Staphylococcus Ch 23 Streptococcus Ch 24Enterococcus Ch 25Bacillus Ch 26 Corynebacterium Listeria and Erysiphelothrix Ch 27Neisseria Ch 28 Enterobacteria Ch 29 vibrio Ch 30 PseudomonasPseudomonas

1.Mid-term examine 2.1. Briefly discuss the worldwide prevalence of the parasitic infections How do you deal with anthrax threat? 4.3. Give an example of treatment for viral diseases 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 What is the mechanism for control gram-positive and gram- negative bacterial infection? 9.8. Briefly discuss the ways that bacteria influence the apoptosis of host cells How do yeast differ from molds and what does the term dimorphism mean when it is applied to fungi? Why we have to study epidemiology of pathogens? Discuss its basic method. B

Medical Microbiology Lecture I Introduction and History Communicable 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 ( ) 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.

Immunity Host Defences 1. Innate or nonspecific a. mechanical b. mucous secretions c. pH d. lysozyme and other 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 responses) 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