Medical Microbiology begins with a review of the immune system, focusing on the body's response to invading microorganisms. Bacteria are then covered, first with a series of chapters presenting the general concepts of bacterial microbiology and then with chapters detailing the major bacterial pathogenes of humans. Similar sections cover virology, mycology, and parasitology. In each section, the introductory chapters stress the mechanisms of infection characteristic of that type of microorganism, thus providing the reader with a framework for understanding rather than memorizing the clinical behavior of the pathogens. The final section of the book Introduction to Infectious Diseases, is arranged by organ system and provides transition for clinical considerations.
Evolution of the Immune System
The immune system consists of factors that provide innate and acquired immunity, and has evolved to become more specific, complex, efficient, and regulated. One of the principal functions of the human immune system is to defend against infecting and other foreign agents by distinguishing self from non-self (foreign antigens) and to marshal other protective responses from leukocytes. The immune system, if dysregulated, can react to self antigens to cause autoimmune diseases or fail to defend against infections.
Organization/Components/Functions
The immune system is organized into discrete compartments to provide the milieu for the development and maintenance of effective immunity. Those two overlapping compartments: the lymphoid and reticuloendothelial systems (RES) house the principal immunologic cells, the leukocytes. Leukocytes derived from pluripotent stem cells in the bone marrow during postnatal life include neutrophils, eosinophils, basophils, monocytes and macrophages, natural killer (NK) cells, and T and B lymphocytes. Hematopoietic and lymphoid precursor cells are derived from pluripotent stem cells. Cells that are specifically committed to each type of leukocyte (colony-forming units) are consequently produced with the assistance of special stimulating factors (e.g. cytokines).
Cells of the immune system intercommunicate by ligand-receptor interactions between cells and/or via secreted molecules called cytokines. Cytokines produced by lymphocytes are termed lymphokines (i.e., interleukins and interferon-γ) and those produced by monocytes and macrophages are termed monokines.
Lymphoid System
Cells of the lymphoid system provide highly specific protection against foreign agents and also orchestrate the functions of other parts of the immune system by producing immunoregulatory cytokines. The lymphoid system is divided into 1) central lymphoid organs, the thymus and bone marrow, and 2) peripheral lymphoid organs, lymph nodes, the spleen, and mucosal and submucosal tissues of the alimentary and respiratory tracts. The thymus instructs certain lymphocytes to differentiate into thymus-dependent (T) lymphocytes and selects most of them to die in...
he culture media are classified in many different ways: Based on the physical state Liquid media Solid media Semisolid media Based on the presence or absence of oxygen Anaerobic media Aerobic media Based on nutritional factors Simple media Synthetic media Complex
Medical Microbiology begins with a review of the immune system, focusing on the body's response to invading microorganisms. Bacteria are then covered, first with a series of chapters presenting the general concepts of bacterial microbiology and then with chapters detailing the major bacterial pathogenes of humans. Similar sections cover virology, mycology, and parasitology. In each section, the introductory chapters stress the mechanisms of infection characteristic of that type of microorganism, thus providing the reader with a framework for understanding rather than memorizing the clinical behavior of the pathogens. The final section of the book Introduction to Infectious Diseases, is arranged by organ system and provides transition for clinical considerations.
Evolution of the Immune System
The immune system consists of factors that provide innate and acquired immunity, and has evolved to become more specific, complex, efficient, and regulated. One of the principal functions of the human immune system is to defend against infecting and other foreign agents by distinguishing self from non-self (foreign antigens) and to marshal other protective responses from leukocytes. The immune system, if dysregulated, can react to self antigens to cause autoimmune diseases or fail to defend against infections.
Organization/Components/Functions
The immune system is organized into discrete compartments to provide the milieu for the development and maintenance of effective immunity. Those two overlapping compartments: the lymphoid and reticuloendothelial systems (RES) house the principal immunologic cells, the leukocytes. Leukocytes derived from pluripotent stem cells in the bone marrow during postnatal life include neutrophils, eosinophils, basophils, monocytes and macrophages, natural killer (NK) cells, and T and B lymphocytes. Hematopoietic and lymphoid precursor cells are derived from pluripotent stem cells. Cells that are specifically committed to each type of leukocyte (colony-forming units) are consequently produced with the assistance of special stimulating factors (e.g. cytokines).
Cells of the immune system intercommunicate by ligand-receptor interactions between cells and/or via secreted molecules called cytokines. Cytokines produced by lymphocytes are termed lymphokines (i.e., interleukins and interferon-γ) and those produced by monocytes and macrophages are termed monokines.
Lymphoid System
Cells of the lymphoid system provide highly specific protection against foreign agents and also orchestrate the functions of other parts of the immune system by producing immunoregulatory cytokines. The lymphoid system is divided into 1) central lymphoid organs, the thymus and bone marrow, and 2) peripheral lymphoid organs, lymph nodes, the spleen, and mucosal and submucosal tissues of the alimentary and respiratory tracts. The thymus instructs certain lymphocytes to differentiate into thymus-dependent (T) lymphocytes and selects most of them to die in...
he culture media are classified in many different ways: Based on the physical state Liquid media Solid media Semisolid media Based on the presence or absence of oxygen Anaerobic media Aerobic media Based on nutritional factors Simple media Synthetic media Complex
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
2. Teaching Objectives in introduction
• Define microbiology
• Give the scope of microbiology
• Explain importance of microbiology to man
• To give an overview of the history of Microbiology
• To list and give properties of pathogenic organisms
3. Topics in microbiology will include
– Introduction to microbiology
– Normal Flora of the human body
– Classification of bacteria
– Anatomy of a bacterial cell
– Bacterial genetics
– Bacterial growth
– Bacterial pathogenicity and virulence
– Sterilization and disinfection
– Staining
4. Topics
cont..
– Culture media
– Inoculation of culture media
– Incubation of bacteria
– Tests for identification of bacteria
– Sensitivity testing/antimicrobial sensitivity testing
– Processing of specimens
– Systematic bacteriology
6. References
• Baker F. J. & Silverton R. E. (2001). Introduction to
Medical Laboratory Technology. 7th Ed. London.
Butterworths.
• Cheesbrough M. (2006). District Laboratory
Practice in Tropical Countries Part 2. 2nd Ed.
Cambridge: Cambridge University press
• AMREF (2003).Communicable diseases, a Manual
for Primary Health Care workers –
• 4. AMREF (2003). Practical Laboratory Manual
for Health Centres in Eastern Africa
7. References
• Madigan et al. Brock’s Biology of
Microorganisms : 9th, 10th eds.
• Prescott et al., Microbiology, 3rd, 4th eds.
• Black, Microbiology, 4th ed.
• Other Microbiology texts
8. Introduction
• “Microbiology’ - the study of microorganisms
• organisms too small to be seen with the naked eye
Except when in large groups (colonies)
• Effects of large numbers often visible
– Chemical reactions in soil horizons
– Toxin and gas production in incompletely sterilised food
cans
– Disease in animals and plants
9.
10. Microbial World
• Viruses
• Bacteria,mycoplasma,
rickettsia, clamydia
• Fungi (Yeasts and
Molds)
• Protozoa
• Microscopic Algae
• Immune system
• Measures of disease
11.
12.
13. Branches of Microbiology
• Bacteriology: study of bacteria
• Protozoology: study of protozoa
• Algology: study of Microscopic Algae
• Epidemiology: study of Measures of disease
• Mycology: study of fungi
14. Branches of Microbiology….
• Immunology: study of immunity
–Edward Jenner, UK: developed vaccination
(1798)
–Metchnikoff, RU: discovered phagocytes
(1884)
–Paul Ehrlich, DE: theory of immunity (1890)
• Virology: study of viruses
–Beijerinck, NE: discovered intracellular
reproduction of TMV; coined the term
“virus” (1899)
15. Branches of Microbiology..
• Parasitology: study of protozoa and parasitic worms
• Chemotherapy
– Treatment of disease by using chemical means
– Antibiotics produced naturally
– Synthetic drugs
– Paul Ehrlich (1878) – used arsenic compounds to fight
disease – ‘magic bullet’
16. Branches of Microbiology…
• Chemotherapy
– Alexander Fleming, Scotland (1928) discovered
penicillin
– Selman Waksman, Ukraine (1944) discovered
streptomycin
• Problems
– Toxicity of drugs => Selective toxicity
– Resistance of bacteria to drugs
17. Branches of Microbiology…
• Recombinant DNA Technology
– Recombinant DNA
– Genetic engineering/biotechnology
– Microbial genetics – mechanism by which
microbes inherit genes
– Molecular biology – structure and function
(expression) of genes
– Molecular epidemiology/diagnostics
18. Branches of Microbiology…
• Biotechnology
– GMOs/GEMs for industrial, pharmaceutical and
agricultural applications
– Improvements of agriculture (plants and animals)
– Gene therapy: inserting a missing gene or replacing a
defective one in human cells
19. Benefits
• Maintain balance of environment (microbial
ecology)
• Basis of food chain
• Nitrogen fixation
• Photosynthesis
• Digestion
• Synthesis of vitamins
• Manufacture of food and drink
20. Benefits
• Genetic engineering
• Synthesis of chemical products
• Recycling sewage
• Bioremediation: use microbes to remove
toxins (oil spills)
• Use of microbes to control crop pests
• Normal microbiota
21. Harmful Effects
• Cause disease
• Basis for bioterrorism
• Destruction of materials
• Food spoilage
22. Historical perspective
Pioneers of Microbiology
• Robert Hooke, UK (1665) proposed the Cell
Theory, observed cork with crude microscope
coined theory
``All living things are composed of cells``
• Edward Jenner 1796 carried successful
vaccination for smallpox
• Spontaneous generation ``Some forms of life
could arise spontaneously from non-living
matter``
• Francesco Redi (1668) Redi’s experiments to
disapprove spontaneous generation
23. Pioneers of Microbiology
• Antoni van Leeuwenhoek, DE (1673) first to
observe live microorganisms (animalcules)
• Schleiden and Schwann, Formulated Cell
Theory: ``cells are the fundamental units of
life and carry out all the basic functions of
living things``
• Pasteur, FR and Tyndall, UK (1861) finally
disproved S.G.
24. Pioneers of Microbiology
• Louis Pasteur (1822-1895), Chemist
– Fermentation (1857)
– Pasteurization: heat liquid enough to kill
spoilage bacteria (1864)
– Rabies vaccine development
– Proposed the germ theory of disease
– Proposed aseptic techniques (prevent
contamination by unwanted microbes)
– Director of Pasteur Institute, Paris (1894)
25. Pioneers of Microbiology
• Joseph Lister, UK (1867) used phenol (carbolic
acid) to disinfect wounds. First aseptic
technique in surgery
• Robert Koch, DE (1876) Postulated the ``Germ
theory`` Identified microbes that caused
anthrax (1876), tuberculosis (1882) and
cholera (1883) Developed microbiological
media & streak plates for pure culture (1881)
26. The germ theory
• The germ theory of disease ``some diseases
are caused by microorganisms These small
organisms, too small to see without
magnification, invade humans, animals, and
other living hosts. Their growth and
reproduction within their hosts can cause a
disease``.
27. The germ theory cont..
• "Germ" may refer to a virus, bacterium, protest,
fungus, or prion. Microorganisms that cause
disease are called pathogens, and the diseases
they cause are called infectious diseases.
• Even when a pathogen is the principal cause of a
disease, environmental and hereditary factors
often influence the severity of the disease, and
whether a particular host individual becomes
infected when exposed to the pathogen.
28. Koch’s Postulates
• The specific causative agent must be found in every case of
the disease.
• The disease organism must be isolated from the lesions of
the infected case and maintained in pure culture.
• The pure culture, inoculated into a susceptible or
experimental animal, should produce the symptoms of the
disease.
• The same bacterium should be re-isolated in pure culture
from the intentionally infected animal.
29. Shortcomings of kochs postulates
• Koch's postulates may not hold if:
– The particular bacteria cannot be "grown in pure
culture" in the laboratory. E.g. leprosy bacterium
– There is no animal model of infection with that
particular bacteria.
– A harmless bacteria may cause disease if:
• It has acquired extra virulence factors making it pathogenic.
• It gains access to deep tissues via trauma, surgery, an IV line
• It infects an immuno-compromised patient.
• Not all people infected by a bacteria may develop disease-
subclinical infection is usually more common than clinically
obvious infection."
30. Miasma theory
• The miasma theory of disease transmission held
that diseases such as cholera, chlamydia or the
Black Death were caused by a miasma ancient
Greek: "pollution"), a noxious form of "bad air".
The theory held that the origin of these epidemic
diseases was a miasma, emanating from rotting
organic matter.
• Miasma was considered to be a poisonous vapor
or mist filled with particles from decomposed
matter (miasmata) that caused illnesses.
31. Miasma theory cont..
• The miasmatic position was that diseases were the product of
environmental factors such as
– contaminated water
– foul air
– and poor hygienic conditions.
– Such infection was not passed between individuals but
would affect individuals within the locale that gave rise to
such vapors.
– It was identifiable by its foul smell.
• Predominant theory of disease transmission before the germ
theory of disease took hold in the 19th century.
34. Normal Microbial Flora
• 1. Resident Flora
– Microbes that are always present
• 2. Transient Flora
– Microbes that live in or on your body for a period
of time (hours, days, weeks, months) then move on
or die off
35. Symbiotic Relationship
• 1. Mutualistic
– Both organisms benefit – “mutually benefical”
• 2. Commensalistic
– One organism benefits, the other is neither helped
nor harmed
• 3. Opportunistic
– Under normal conditions, microbe does not cause
disease, but if conditions become conducive , it
can cause disease
36. Mutualistic
• Escherichia coli
– Synthesizes Vitamin K & B complex Vitamins
– In return, we provide a warm, moist nutrient rich
environment for E. coli
37. Commensalistic
• We have no Commensalistic relationships with
Bacteria
• If Bacteria are in or on our body, they are either
helping us (Microbial Antagonism) or harming
us.
38. Opportunistic
• Escherichia coli - normally in our digestive
tract where it causes no problems, but if it
gets into the urinary tract it can become
pathogenic.
• Staphylococcus aureus – commonly found in
the upper respiratory tract, but if it gets into a
wound or a burn it can become pathogenic
42. Ecological relationships
Symbiosis: Neutral, antagonistic or synergistic
relationship between two dissimilar organisms
(Symbiotes, symbionts) living in close association with
each other;
Mutualism: mutually beneficial relationship between
two species
Commensalism: relationship between two species in
which one is benefited and the other is not affected,
neither negatively nor positively
Parasitism: relationship between two species in which
one benefits (parasite) from the other (host); usually
involves detriment to the host
43. Basic ecological definitions
Flora; microbiota (Microbiology Definition):
Microorganisms present in or characteristic of a special
location (Flora generically refers to plants; Fauna
generically refers to animals)
Indigenous (resident) Microbiota: Microbial flora
typically occupying a particular niche; given diversity of
environmental conditions, organisms tend to segregate
Transient flora: Microbial flora only temporarily
occupying a given niche
Niche (ecological niche): The place of an organism within
its community (ecosystem); unique position occupied by a
particular species, perceived in terms of actual physical
space occupied & function performed within ecosystem
45. Microbial flora of the normal human
body (normal flora)
1. Skin
2. Respiratory tract
Nose and Nasopharynx; Mouth and Oropharynx
3. Eye (Conjunctivae) and Outer ear
4. Intestinal tract
Stomach and Small Intestine; Large Intestine;
Intestinal Tract of Newborn
Antibiotic Alteration of Flora
Significance of Intestinal Flora
5. Genitourinary tract
External Genitalia & Anterior Urethra
Vagina
46. Normally sterile sites in the human
body
Colonization of one of these sites generally involves a defect
or breach in the natural defenses that creates a portal of entry
Brain; Central nervous system
Blood; Tissues; Organ systems
Sinuses; Inner and Middle Ear
Lower Respiratory Tract: Larynx; Trachea;
Bronchioles (bronchi); Lungs; Alveoli
Kidneys; Ureters; Urinary Bladder; Posterior Urethra
Uterus; Endometrium (Inner mucous membrane of
uterus ); Fallopian Tubes; Cervix and Endocervix
47. Factors controlling growth of
microorganisms
1. Nutrient availability: the accessibility of a necessary
resource, substance or compound providing nourishment
to maintain life, i.e. capable of conversion to energy and
structural building blocks
Versatile organisms: Use any organic compounds as
of C and enrgy (sugars, acids. Alcohols e.t.c.)
Fastidious: an organism that has complex nutritional
or cultural requirements, making isolation and culture
more difficult
Major essential elements:
C, O, H, N, S, P, K, Mg, Ca, Fe, Na, Cl
Minor essential elements:
48. 2. Physico/environmental
parameters:
• Water activity/ osmotic pressure (aw)
• Water activity (aw) represents the available water
• Osmotic pressure (p): expressed in atmospheres; reflects
the concentration of solute in an aqueous solution
50. Physico/environmental
parameters cont..
–pH: power of hydrogen; a
measurement of the amount of
hydrogen ion in solution; the
logarithm of the reciprocal of the
hydrogen ion concentration in an
aqueous solution used to express
its acidity or alkalinity (0-14)
51. Physico/environmental
parameters cont..
– Temperature:
• Psycrophile (psychrophilic): cold
temperatures; Optimal growth at 15o to
20oC
• Mesophile (mesophilic): moderate
temperatures; Optimal growth at 20o to
45oC
• Thermophile (thermophilic): elevated
temperatures; Optimal growth at 50o to
70oC
52. Factors controlling growth of
organisms (cont.):
3. Competition: the simultaneous
demand by two or more organisms or
species for a necessary, common resource
or physical space that is in limited or
potentially limited supply, resulting in a
struggle for survival
4. Host immune system: the
cells and tissues involved in recognizing and
attacking foreign substances in the body
53.
54. Acquiring infectious agents
Portal of entry/exit
Ingestion
Inhalation
Direct penetration
Trauma or Surgical Procedure
Needlestick
Arthropod Bite
Sexual Transmission
Transplacental
55. Colonization: the successful occupation of a new habitat
by a species not normally found in this niche
Adherence (attachment): close association of
bacterial cells and host cells generally characterized by
receptors on target sites
Adhesin: structure or macromolecule located on the
surface of a cell or extracellularly that facilitates
adherence of a cell to a surface or to another cell; site
of attachment is often a specific receptor and host cell
receptors are often sugar moieties (lectin), but the
adherence may also be nonspecific
Acquiring infectious agents (cont.)
56. Acquiring infectious agents (cont.)
Invasion: the entry and spread throughout the cells and/or
tissues of the host; specific recognition of receptor sites on
target cells enhances pathogenic advantage
Invasins (invasive factors): structures or
macromolecules that facilitate invasion by a pathogenic
microorganism
Multiplication: the ability of a microorganism to reproduce
during an infection; influenced by underlying disease,
immunologic status, antibiotic treatment, nutrient availability
57. Transmission of disease
Entrance, colonization, penetration: Dependent upon
Age, Sex, Nutrition, Immunologic State and General Health of
Host, and Bacterial Virulence Factors
Vector: a carrier, especially the animal that transfers an
infectious agent from one host to another, usually an
Arthropod
Carrier (Carrier State): symptomless individual who is
host to a pathogenic microorganim with the potential to pass
the pathogen to others
Nosocomial infections: an infection acquired in a
hospital setting that was not present in the host prior to
admission, generally occurring within 72 hours of admission
58. NOSOCOMIAL INFECTIONS in
ACUTE CARE INSTITUTIONS
Infection
Site
Percentage of All
Nosocomial
Infections
Most Common Agents
Urinary
Tract
40%
Escherichia coli, Enterococcus,
Proteus, Klebsiella,
Pseudomonas aeruginosa
Surgical
Wound
20% Staphylococcus aureus,
Staphylococcus epidermidis, E. coli
Pulmonary 10% Klebsiella, Pseudomonas,
E. coli, S. aureus
Primary
Bacteremia
5% - 10% S. aureus, S. epidermidis,
Gram-negative rods
Others 20% - 25% S. aureus, E. coli
59. Epidemiology
Epidemic: Disease occuring suddenly in numbers clearly
in access of normal expectancy
Endemic: Disease present or usually prevalent in a
population or geographic area at all times
Pandemic: A widespread epidemic distributed or occuring
widely throughout a region, country, continent, or globally
60. Tuberculosis SARS* Venezuelan Equine Encephalitis
Hepatitis C AIDS Enterohemorrhagic E. Coli
Malaria Lassa Fever S.American Hemorrhagic Fevers
Influenza Hantavirus Pulmonary Syndrome
Lyme Disease West Nile Fever/Encephalitis*
Emerging Infectious Diseases
New diseases and diseases with increasing incidences
are called emerging infectious diseases (EIDs).
EIDs can result from the use of antibiotics and
pesticides, climatic changes, travel, the lack of
vaccination, and insufficient case reporting.
The CDC, NIH, and WHO are responsible for surveillance
and responses to emerging infectious diseases.
61. Pathogenicity vs. Virulence
Pathogenicity: the quality of producing disease or the
ability to produce pathologic changes or disease
Virulence: a measure of pathogenicity; a measurement of
the degree of disease-producing ability of a microorganism as
indicated by the severity of the disease produced; commonly
ascertained by measuring the dosage required to caused a
specific degree of pathogenicity; one general standard is the
LD50 (lethal dose 50%)
62. PATHOGENICITY vs. Virulence
(Definitons)
Dosage: the number of pathogenic microorganisms
entering the host
LD50 = the number of microorganisms required to cause
lethality (death) in 50% of the test host
True pathogen: any microorganism capable of causing
disease; an infecting agent
Opportunistic pathogen: a usually harmless
microorganism that becomes pathogenic under favorable
conditions causing an opportunistic infection
63. INFECTION vs. Disease
Infection: the colonization and/or invasion and
multiplication of pathogenic microrganisms in the host
with or without the manifestation of disease
Disease: an abnormal condition of body function(s)
or structure that is considered to be harmful to the affected
individual (host); any deviation from or interruption of the
normal structure or function of any part, organ, or system
of the body
64. INFECTION vs. Disease
(Definitons)
Benign: a non-life or non-health threating condition
Malignant: a disease tending to become progressively
worse (Morbidity = illness) and potentially result in death
(Mortality = death)
Contagious: capable of being transmitted from one host
to another; communicable; infectious
Infectious dose: number of pathogenic organisms
required to cause disease in a given host
65. Koch's postulates
Four criteria that were established by Robert Koch to
identify the causative agent of a particular disease,
these include:
1. the microorganism (pathogen) must be present
in all cases of the disease
2. the pathogen can be isolated from the diseased
host and grown in pure culture
3. the pathogen from the pure culture must cause
the same disease when inoculated into a healthy,
susceptible laboratory animal
4. the pathogen must be reisolated from the new
host and shown to be the same as the originally
inoculated pathogen
66. Bacterial Virulence Mechanisms
Adherence (Colonization)
Invasion
Degradative enzymes
Exotoxins
Endotoxin
Induction of excess inflammation
Evasion of phagocytic & immune clearance
Byproducts of growth (gas, acid)
Superantigen
Resistance to antibiotics
67. Microbial pathogenicity
Virulence factors
Colonization factors: specific recognition of receptor sites
on target cells enhances pathogenic advantage
1. Capsule: nonspecific attachment
2. Surface receptors/target sites: Receptors on
both bacteria (adhesins) and host (target)
Examples include:
i) fimbriae (formerly known as pili) of Enterobacteriaceae
ii) Chlamydia binds host N-acetyl-D-glucosamine which is a
cell surface lectin (polysaccharide target receptor)
iii) Protein adhesin of Mycoplasma located in specialized
tip structure; adheres to sialic acid-containing cell receptors
68. MICROBIAL
PATHOGEN ADHESIN RECEPTOR
Staphylococcus aureus L
Li
ip
po
ot
te
ei
ic
ch
ho
oi
ic
c a
ac
ci
id
d Unknown
Staphylococcus spp. S
Sl
li
im
me
e l
la
ay
ye
er
r Unknown
Group A Streptococcus L
LT
TA
A-
-M
M p
pr
ro
ot
te
ei
in
n c
co
om
mp
pl
le
ex
x F
Fi
ib
br
ro
on
ne
ec
ct
ti
in
n
Streptococcus pneumoniae Protein N-acetylhexosamine-gal
Escherichia coli Type 1 f
fi
im
mb
br
ri
ia
ae
e
CFA 1 fimbriae
P fimbriae
D-M
Ma
an
nn
no
os
se
e
GM g
ga
an
ng
gl
li
io
os
si
id
de
e
P blood grp glycolipid
Other Enterobacteriaceae Type 1 fimbriae D-Mannose
Neisseria gonorrhoeae Fimbriae GD1 ganglioside
Treponema pallidum P1, P2, P3 Fibronectin
Chlamydia spp. Cell surface lectin N-acetylglucosamine
Mycoplasma pneumoniae Protein P1 Sialic acid
Vibrio cholerae Type 4 pili Fucose and mannose
69. VIRULENCE FACTORS (cont.)
Invasive factors (invasins): Enable a pathogenic
microorganism to enter and spread throughout the tissues of
the host body; specific recognition of receptor sites on target
cells enhances pathogenic advantage
Degradative enzymes: A class of protein capable of
catalytic reactions; bacterial and host enzymes both play roles
in the disease process
70. Virulence factors (cont.)
Toxigenicity: the ability of a microorganism to cause
disease as determined by the toxin it produces which partly
determines its virulence
1. Endotoxin: a complex bacterial toxin that is
composed of protein, lipid, and polysaccharide (LPS)
which is released only upon lysis of the cell
2. Exotoxins: a potent toxic substance formed
and secreted by species of certain bacteria
71. BASIC EFFECTS of ENDOTOXIN
FEVER: any elevation of body temperature above normal
LEUKOPENIA/LEUKOCYTOSIS: abnormal reduction in number of leukocytes in
blood, (<5000/mm3) / abnormally large number of leukocytes in blood, as during
hemorrhage, infection, inflammation, or fever (>12,000mm3)
METABOLIC EFFECTS : pathogenic organisms can affect any of the body
systems with disruptions in metabolic processes, e.g.,hypotension, hypoglycemia, etc.
RELEASE OF LYMPHOCYTE FACTORS: agranular leukocyte concentrated in
lymphoid tissue; active in immunological responses, including production of antibodies
CELLULAR DEATH:
SEPTIC SHOCK: associated with overwhelming infection resulting in vascular
system failure with sequestration of large volumes of blood in capillaries and veins;
activation of the complement and kinin systems and the release of histamines,
prostaglandins, and other mediators may be involved
DISSEMINATED INTRAVASCULAR COAGULATION (DIC): disorder
characterized by a reduction in the elements involved in blood coagulation due to
their utilization in widespread blood clotting within the vessels; late stages marked
by profuse hemorrhaging
ORGAN NECROSIS: the sum of morphological changes indicative of cell death
and caused by the progressive degradative action of enzymes
72. EXOTOXINS
TWO-COMPONENT (BIPARTITE) A-B TOXINS
with INTRACELLULAR TARGETS: conform to general
structural model; usually one component is a binding
domain (B subunit) associated with absorption to target cell
surface and transfer of active component across cell
membrane, the second component is an enzymatic or
active domain (A subunit) that enzymatically disrupts cell
function
BACTERIAL CYTOLYSINS (a.k.a. Cytotoxins)
with CELL MEMBRANE TARGETS: hemolysis, tissue
necrosis, may be lethal when administered intravenously
73. EXAMPLES of BIPARTITE A-B TOXINS
with
INTRACELLULAR TARGETS
Diphtheria toxin - ADP-ribosylation inhibits cell protein synthesis by
catalyzing transfer of ADP- ribose from NAD (nicotinimamide adenine
nucleotide) to EF-2 (elongation factor- 2)
Pseudomonas aeruginosa toxin - similar action as DT
Cholera toxin - A-subunit catalyzes ADP-ribosylation of the B-subunit
of the stimulatory guanine nucleotide protein Gs; profound life-threatening
diarrhea with profuse outpouring of fluids and electrolytes
Enterotoxigenic Escherichia coli (ETEC) heat-labile
enterotoxin - similar or identical to cholera toxin
Tetanus neurotoxin - less well understood; binding domain binds to
neuroreceptor gangliosides, releases inhibitory impulses with trismus
Botulinum neurotoxin - among most potent of all biological toxins;
binding domain binds to neuroreceptor gangliosides, inhibits release of
acetylcholine at myoneural junction resulting in fatal paralysis
74. BACTERIAL CYTOLYSINS
with
CELL MEMBRANE TARGETS
Three Major Types:
1. Hydrolyze membrane phospholipids (phospholipases);
e.g., Clostridium, Staphylococcus
2. Thiol-activated cytolysins (oxygen-labile) alter membrane
permeability by binding to cholesterol; e.g., Streptococcus,
Clostridium
3. Detergent-like activity on cell membranes; e.g.,
Staphylococcus, rapid rate of lysis
75. ENDOTOXINS
1.I
In
nt
te
eg
gr
ra
al
l p
pa
ar
rt
t o
of
f c
ce
el
ll
l w
wa
al
ll
l
2.Endotoxin is L
LP
PS
S;
lipid A is toxic
3.Heat stable
4.Antigenic; questionable
immunogenicity
5.Toxoids not be produced
6.Many effects on host
7.Produced o
on
nl
ly
y b
by
y g
gr
ra
am
m-
-
n
ne
eg
ga
at
ti
iv
ve
e organisms
EXOTOXINS
1.R
Re
el
le
ea
as
se
ed
d f
fr
ro
om
m t
th
he
e c
ce
el
ll
l
before or after lysis
2.P
Pr
ro
ot
te
ei
in
n
3.Heat labile
4.Antigenic and i
im
mm
mu
un
no
og
ge
en
ni
ic
c
5.T
To
ox
xo
oi
id
ds
s can be produced
6.Specific in effect on host
7.Produced by gram-positive
& gram-negative organisms
76. MICROBIAL PATHOGENICITY (cont.)
RESISTANCE TO HOST DEFENSES
ENCAPSULATION and
ANTIGENIC MIMICRY, MASKING or SHIFT
CAPSULE, GLYCOCALYX or SLIME LAYER
Polysachharide capsules Streptococcus pneumoniae,
Neisseria meningitidis, Haemophilus influenzae, etc.
Polypeptide capsule of Bacillus anthracis
EVASION or INCAPACITATION of PHAGOCYTOSIS
and/or IMMUNE CLEARANCE
PHAGOCYTOSIS INHIBITORS: mechanisms enabling an
invading microorganism to resist being engulfed, ingested,
and or lysed by phagocytes/ phagolysosomes
RESISTANCE to HUMORAL FACTORS
RESISTANCE to CELLULAR FACTORS
77. MICROBIAL PATHOGENICITY (cont.)
DAMAGE TO HOST
DIRECT DAMAGE
(Tissue Damage from Disease Process):
Toxins
Enzymes
INDIRECT DAMAGE
(Tissue Reactions from Immunopathological Response):
Damage Resulting from Vigorous Host Immune Response
(a.k.a, immunopathogenesis; autoimmune
hypersensitivy)
Hypersensitivity Reactions (Types I - IV)
78. HOST RESISTANCE
The degree to which a host can limit the effects of an
infection, ranging from:
TOLERANCE in which symptoms are suppressed or
unusually large doses of a drug, toxin, or protein are able to be
endured
HYPERSENSITIVITY in which only a few cells
surrounding the infected cell(s) are affected or an increased
susceptibility to an antigen, such as an allergic reaction to a
previous exposure to an antigen, the extreme case being
anaphylactic shock
IMMUNITY in which the microorganisms do not multiply
due to any one or a combination of host immune factors or the
biological condition by which a body is capable of resisting or
overcoming an infection or disease
79. HYPERSENSITIVITY REACTIONS
TYPE I: ANAPHYLACTIC REACTION
(ANAPHYLAXIS, ANAPHYLACTIC SHOCK): a life-
threatening immediate hypersensitivity reaction to a previously
encountered antigen, characterized by respiratory distress,
vascular collapse, and shock; allergy or atopic diseases
TYPE II: CYTOTOXIC REACTION: a specific
destructive action against certain cells by an invading agent;
humorally mediated, autoimmune diseases, cytotoxic
diseases, antibody diseases
TYPE III: IMMUNE COMPLEX REACTION: serum
sickness diseases
TYPE IV: CELL-MEDIATED IMMUNE RESPONSE:
delayed-type hypersensitivity, cell- mediated cytotoxic
diseases, granulomatous diseases
80. IMMUNOPATHOLOGICAL RESPONSE
with TISSUE REACTIONS
Type I Hypersensitivity Reactions:
Anaphylactic Reaction (Anaphylaxis;
Anaphylactic shock)
IgE-mediated: Cross-linking of cell-bound IgE
antibodies by antigen with degranulation of mast
cells or basophils
Life-threatening immediate hypersensitivity
reaction to a previously encountered antigen,
characterized by respiratory distress, vascular
collapse, and shock
Allergy or atopic diseases
Atopy: hereditary hypersensitivity to common
environmental antigens
81. IMMUNOPATHOLOGICAL RESPONSE
with TISSUE REACTIONS
Type II Hypersensitivity Reactions:
Humorally-Mediated Autoimmune Diseases
Interaction of cross-reactive antibody with host cell surface antigen;
Autoantibodies and immune complexes
Cytotoxic reaction (antibody-mediated) (ADCC): Specific destructive
action against certain cells presenting antigens from an invading agent
82. IMMUNOPATHOLOGICAL RESPONSE
with TISSUE REACTIONS
Type III Hypersensitivity Reactions:
Immune Complex Reaction
Antibody-mediated
Deposition of circulating immune complexes in
small vessels with complement activation causing
damage to vessels
Serum sickness diseases
83. IMMUNOPATHOLOGICAL RESPONSE
with TISSUE REACTIONS
Type IV Hypersensitivity Reactions:
Cell-Mediated Immune Response
T cells sensitized to “self” antigens secrete
lymphokines that either do direct damage to host cells
(e.g., TNF) or indirect damage enhancing the
inflammatory response
Delayed-type hypersensitivity (TB test) (CD4+
mediated)
Cell-mediated cytotoxic diseases (CD8+ mediated)
Granulomatous disease
85. HOST DEFENSE MECHANISMS (cont.)
INTERNAL (SECONDARY): When an infecting parasite
succeeds in penetrating the skin or mucuos membranes,
cellular defense mechanisms include local macrophages and
blood-borne phagocytic cells. Mononuclear phagocytes
(monocytes and macrophages) and polymorphonuclear
leukocytes (PMNs) are the most important phagocytic cells
targeting bacterial infections.
MONONUCLEAR PHAGOCYTE SYSTEM (formerly
Reticular Endothelial System): total pool of monocytes
and cells derived from monocytes; predominantly
macrophages (phagocytic cells)
86. HOST DEFENSE MECHANISMS (cont.)
OTHER:
NON-SPECIFIC: oxygen metabolites (superoxide anion
radical, hydrogen peroxide, hydroxyl radicals, halide
radicals), kinin forming system related to clotting
HOST-GENERATED PROTEINS: complex array of
humoral and cellular mediators; e.g., lysosomal
enzymes, lipid mediators, prostaglandins, histamine, heat-
shock proteins (stress proteins)
87. HOST DEFENSE MECHANISMS (cont.)
CELLULAR IMMUNE RESPONSE: any immune
response directed at the cellular level; includes
INFLAMMATION and PHAGOCYTOSIS processes
INFLAMMATORY RESPONSE: a protective
response of tissues affected by disease or injury
characterized by redness, localized heat, swelling, pain,
and possibly impaired function of the infected part
PHAGOCYTOSIS: the process by which certain
phagocytes can ingest extracellular particles by
engulfing them; particles OPSONIZED with antibody are
more rapidly and efficiently ingested
T-LYMPHOCYTES and CYTOKINES
88. HOST DEFENSE MECHANISMS (cont.)
HUMORAL IMMUNE RESPONSE: the sum total of
components of the immune response circulating in the blood
or body fluids ; includes ANTIBODY and COMPLEMENT
systems
COMPLEMENT PROTECTIVE SYSTEM: a protein
system in serum that combines with antibodies to form a
defense against cellular antigens
B-LYMPHOCYTES and
ANTIBODY PRODUCTION: a class of proteins
produced as a result of the introduction of an antigen that
has the ability to combine with the antigen that caused its
production
94. ACQUIRING INFECTIOUS AGENTS
PORTAL OF ENTRY/EXIT
INGESTION
INHALATION
DIRECT PENETRATION
Trauma or Surgical Procedure
Needlestick
Arthropod Bite
Sexual Transmission
Transplacental
REVIEW
95. PATHOGENICITY vs. VIRULENCE
PATHOGENICITY: the quality of producing disease or the
ability to produce pathologic changes or disease
VIRULENCE: a measure of pathogenicity; a measurement
of the degree of disease-producing ability of a microorganism
as indicated by the severity of the disease produced;
commonly ascertained by measuring the dosage required to
caused a specific degree of pathogenicity; one general
standard is the LD50 (lethal dose 50%)
REVIEW
96. INFECTION vs. DISEASE
INFECTION: the colonization and/or invasion and
multiplication of pathogenic microrganisms in the host
with or without the manifestation of disease
DISEASE: an abnormal condition of body function(s)
or structure that is considered to be harmful to the affected
individual (host); any deviation from or interruption of the
normal structure or function of any part, organ, or system
of the body
REVIEW
97. KOCH'S POSTULATES
Four criteria that were established by Robert Koch to
identify the causative agent of a particular disease,
these include:
1. the microorganism (pathogen) must be present
in all cases of the disease
2. the pathogen can be isolated from the diseased
host and grown in pure culture
3. the pathogen from the pure culture must cause
the same disease when inoculated into a healthy,
susceptible laboratory animal
4. the pathogen must be reisolated from the new
host and shown to be the same as the originally
inoculated pathogen REVIEW
98. Bacterial Virulence Mechanisms
Adherence (Colonization)
Invasion
Degradative enzymes
Exotoxins
Endotoxin
Induction of excess inflammation
Evasion of phagocytic & immune clearance
Byproducts of growth (gas, acid)
Superantigen
Resistance to antibiotics
REVIEW
99. BASIC EFFECTS of ENDOTOXIN
FEVER: any elevation of body temperature above normal
LEUKOPENIA/LEUKOCYTOSIS: abnormal reduction in number of leukocytes in
blood, (<5000/mm3) / abnormally large number of leukocytes in blood, as during
hemorrhage, infection, inflammation, or fever (>12,000mm3)
METABOLIC EFFECTS : pathogenic organisms can affect any of the body
systems with disruptions in metabolic processes, e.g.,hypotension, hypoglycemia, etc.
RELEASE OF LYMPHOCYTE FACTORS: agranular leukocyte concentrated in
lymphoid tissue; active in immunological responses, including production of antibodies
CELLULAR DEATH:
SEPTIC SHOCK: associated with overwhelming infection resulting in vascular
system failure with sequestration of large volumes of blood in capillaries and veins;
activation of the complement and kinin systems and the release of histamines,
prostaglandins, and other mediators may be involved
DISSEMINATED INTRAVASCULAR COAGULATION (DIC): disorder
characterized by a reduction in the elements involved in blood coagulation due to
their utilization in widespread blood clotting within the vessels; late stages marked
by profuse hemorrhaging
ORGAN NECROSIS: the sum of morphological changes indicative of cell death
and caused by the progressive degradative action of enzymes REVIEW
100. EXOTOXINS
TWO-COMPONENT (BIPARTITE) A-B TOXINS
with INTRACELLULAR TARGETS: conform to general
structural model; usually one component is a binding
domain (B subunit) associated with absorption to target cell
surface and transfer of active component across cell
membrane, the second component is an enzymatic or
active domain (A subunit) that enzymatically disrupts cell
function
BACTERIAL CYTOLYSINS (a.k.a. Cytotoxins)
with CELL MEMBRANE TARGETS: hemolysis, tissue
necrosis, may be lethal when administered intravenously
REVIEW
101. BACTERIAL CYTOLYSINS
with
CELL MEMBRANE TARGETS
Three Major Types:
1. Hydrolyze membrane phospholipids (phospholipases);
e.g., Clostridium, Staphylococcus
2. Thiol-activated cytolysins (oxygen-labile) alter membrane
permeability by binding to cholesterol; e.g., Streptococcus,
Clostridium
3. Detergent-like activity on cell membranes; e.g.,
Staphylococcus, rapid rate of lysis
REVIEW
102. ENDOTOXINS
1.I
In
nt
te
eg
gr
ra
al
l p
pa
ar
rt
t o
of
f c
ce
el
ll
l w
wa
al
ll
l
2.Endotoxin is L
LP
PS
S;
lipid A is toxic
3.Heat stable
4.Antigenic; questionable
immunogenicity
5.Toxoids not be produced
6.Many effects on host
7.Produced o
on
nl
ly
y b
by
y g
gr
ra
am
m-
-
n
ne
eg
ga
at
ti
iv
ve
e organisms
EXOTOXINS
1.R
Re
el
le
ea
as
se
ed
d f
fr
ro
om
m t
th
he
e c
ce
el
ll
l
before or after lysis
2.P
Pr
ro
ot
te
ei
in
n
3.Heat labile
4.Antigenic and i
im
mm
mu
un
no
og
ge
en
ni
ic
c
5.T
To
ox
xo
oi
id
ds
s can be produced
6.Specific in effect on host
7.Produced by gram-positive
& gram-negative organisms
REVIEW
103. MICROBIAL PATHOGENICITY (cont.)
RESISTANCE TO HOST DEFENSES
ENCAPSULATION and
ANTIGENIC MIMICRY, MASKING or SHIFT
CAPSULE, GLYCOCALYX or SLIME LAYER
Polysachharide capsules Streptococcus pneumoniae,
Neisseria meningitidis, Haemophilus influenzae, etc.
Polypeptide capsule of Bacillus anthracis
EVASION or INCAPACITATION of PHAGOCYTOSIS
and/or IMMUNE CLEARANCE
PHAGOCYTOSIS INHIBITORS: mechanisms enabling an
invading microorganism to resist being engulfed, ingested,
and or lysed by phagocytes/ phagolysosomes
RESISTANCE to HUMORAL FACTORS
RESISTANCE to CELLULAR FACTORS REVIEW
104. MICROBIAL PATHOGENICITY (cont.)
DAMAGE TO HOST
DIRECT DAMAGE
(Tissue Damage from Disease Process):
Toxins
Enzymes
INDIRECT DAMAGE
(Tissue Reactions from Immunopathological Response):
Damage Resulting from Vigorous Host Immune Response
(a.k.a, immunopathogenesis; autoimmune
hypersensitivy)
Hypersensitivity Reactions (Types I - IV)
REVIEW
105. HYPERSENSITIVITY REACTIONS
TYPE I: ANAPHYLACTIC REACTION
(ANAPHYLAXIS, ANAPHYLACTIC SHOCK): a life-
threatening immediate hypersensitivity reaction to a previously
encountered antigen, characterized by respiratory distress,
vascular collapse, and shock; allergy or atopic diseases
TYPE II: CYTOTOXIC REACTION: a specific
destructive action against certain cells by an invading agent;
humorally mediated, autoimmune diseases, cytotoxic
diseases, antibody diseases
TYPE III: IMMUNE COMPLEX REACTION: serum
sickness diseases
TYPE IV: CELL-MEDIATED IMMUNE RESPONSE:
delayed-type hypersensitivity, cell- mediated cytotoxic
diseases, granulomatous diseases REVIEW
106. HOST DEFENSE MECHANISMS (cont.)
CELLULAR IMMUNE RESPONSE: any immune
response directed at the cellular level; includes
INFLAMMATION and PHAGOCYTOSIS processes
INFLAMMATORY RESPONSE: a protective
response of tissues affected by disease or injury
characterized by redness, localized heat, swelling, pain,
and possibly impaired function of the infected part
PHAGOCYTOSIS: the process by which certain
phagocytes can ingest extracellular particles by
engulfing them; particles OPSONIZED with antibody are
more rapidly and efficiently ingested
T-LYMPHOCYTES and CYTOKINES
REVIEW
107. HOST DEFENSE MECHANISMS (cont.)
HUMORAL IMMUNE RESPONSE: the sum total of
components of the immune response circulating in the blood
or body fluids ; includes ANTIBODY and COMPLEMENT
systems
COMPLEMENT PROTECTIVE SYSTEM: a protein
system in serum that combines with antibodies to form a
defense against cellular antigens
B-LYMPHOCYTES and
ANTIBODY PRODUCTION: a class of proteins
produced as a result of the introduction of an antigen that
has the ability to combine with the antigen that caused its
production
REVIEW