Transcript Deaths and death rates for the 10 leading causes of death in

Deaths and death rates for the 10 leading causes of death
in specified age groups: USA, 1999 (Rates per 100,000)
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All causes
2,391,399
Diseases of heart
725,192
Malignant neoplasms
549,838
Cerebrovascular diseases
167,366
Chronic lower respiratory dis 124,181
Accidents:unintentional injuries 89,703
Diabetes mellitus
68,399
Influenza and pneumonia
63,730
Alzheimer's disease
44,536
Nephritisand nephrosis
35,525
Septicemia
30,680
All other causes (Residual)
484,092
877.0
265.9
201.6
61.4
45.5
34.1
25.1
23.4
16.3
13.0
11.3
177.5
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 Gramnegative 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 0.2-0.3
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 11-14 Immunity
Ch 9
Normal flora
Ch 19 Host Parasite Interactions, Virulence Determinants
Mid-EXAM
Ch 20 Antibiotics
Ch 22 Staphylococcus
Ch 23 Streptococcus
Ch 24 Enterococcus
Ch 25 Bacillus
Ch 26 Corynebacterium Listeria and Erysiphelothrix
Ch 27 Neisseria
Ch 28 Enterobacteria
Ch 29 vibrio
Ch 30 Pseudomonas
Mid-term examine
Briefly discuss the worldwide prevalence of the parasitic infections.
2. How do you deal with anthrax threat?
3. Give an example of treatment for viral diseases.
4. Why and how infectious disease changes its pattern?
5. Which is most efficient way for a microbe to generate its energy?
(ATP yield)
6. Use specific examples to explain the mechanism of bacterial gene
regulation.
7. What is the mechanism for control gram-positive and gramnegative bacterial infection?
8. Briefly discuss the ways that bacteria influence the apoptosis of
host cells.
9. How do yeast differ from molds and what does the term
dimorphism mean when it is applied to fungi?
10. Why we have to study epidemiology of pathogens? Discuss its
1.
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 (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.
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