Bacteria Pathogenicity Ability to Cause Infection

Bacteria Pathogenicity Ability to Cause Infection

Infectious Diseases
* Encounter-bug meets host (reservoir)
* Bug adheres to host
* Entry-bug enters host
* Multiplication- bug multiplies in host
* Damage to host
* Outcome- bug or host wins or
* Coexist- chronic infection

Reservoir
* Exposure to microbe
Virulence Factors
Adherence
* Prevent infection
* Influenza changes adhesions over time
* Neisseria gonorrhoeae -variety of adhesions

Portals of Entry
* Mucous membranes
* Conjunctiva
* Skin
* Bugs have preferred portal
* C. tetani spores in soil --- anaerobic wound

Inoculum

* Number of microbes-dose
* Greater dose, more chance infection will occur
* ID50 or LD50 expresses virulence

Invasins
* Adherence of microbe to surface
* Activates factors that let microbe in-penetration
* Microbes produce invasins (proteins)
* Endocytosis
* Requires multiplication
* Compete with normal flora for space & nutrients
* Overcome local host defenses
* Avoid IgA

Multiplication
* Need Fe to multiply
Avoid Phagocytosis
* Components of cell wall –virulence
Surviving Within Phagocyte

Tuberculosis
* Ancient disease
* 1/3 of world population infected
* 8 million develop active TB each year
* 2 million die each year
* AIDs increases activation of latent TB
* Dependent upon virulence of strain & host resistance
* Produces cell mediated immunity which prevents active disease in many people
* Multi drug resistance has developed

S & S of Pulmonary TB
* Chronic disease
* Progressive weight loss
* Night sweats
* Chronic cough
* Hemoptysis
Mycobacterium tuberculosis
* Acid fast bacillus (AFB)
* Resistant to drying
* Aerobic, slow growth
* Airborne transmission
* Inhale airborne droplets
* Ingested by alveolar macrophages
* Multiply in macrophages even with ongoing immune response

TB Response
* Host immune response-delayed type hypersensitivity reaction
* Tissue damage DT Inflammatory response
TB Conversion
* TST skin reaction is positive
* Occurs within 24 – 48 hours after exposure to TB antigens
* Purified protein derivative of bacillus
* Cell mediated immunity
* Sensitized T cells react with proteins
QuantiferonGold
* Blood test
* Detects interferon gamma

How to Confirm Diagnosis
* Sputum cultures for AFB smear & culture
* Chest xray
Pathogenesis
* LTBI (latent TB infection)
Active Disease

* Low resistance

TB Outcomes
* Primary infection- positive skin test
* 10% progressive primary infection-not controlled
Secondary or Reactivation Infection
* Reinfection-2nd exposure or
* Bacteria escape immune system-reactivation
* Activated macrophages release cytokines
* Delayed hypersensitivity reaction

Prevention of Transmission
* Negative pressure rooms
* Respirator masks-fit tested
* Admit staff aware of symptoms of TB
* Yearly TST of staff
* Conversions treated with 6-9 months of INH

Treatment
* INH for LTBI or TB conversion
* TB disease-active TB
* 9- 12 months of treatment
Resistant TB
* MDR TB
* XDR TB
* DT improper treatment

BCG
* Live culture of M. bovis
Latent vs Active
* Latent TB
* Active TB
Leprosy
* Hanson’s disease- discovered in 1873
* Seen in tropics and underserved countries
* U.S.-150 new cases per year
* Infection of nervous system
* Infects the peripheral nerves within skin
* 2 forms of disease dependent upon immune response

M. leprae
* Tuberculoid form
Lepromatous Form
* Weak immune response & microbe spreads
* Skin & nerve cells infected
* Shed large #s in nasal secretions and oozing sores-more infectious
Invasion via Enzymes
Kinases
Enzymes
Invasion via Toxins
Exotoxins
A-B Toxins
Superantigens
Naming of Exotoxins
Endotoxin
S & S
Shock
Staphylococci
S. aureus
Successful Pathogen
Biofilm
Capsule
Skin Infections
Invasion via Toxins
Toxic shock syndrome
S. aureus Intoxication
Treatment
CA-MRSA
Outbreaks in Community
PVL Gene
Preventing Transmission
Clostridium botulinum
Neurotoxin
Botulism-Foodborne Disease
Toxin
Clostridium tetani
Neurotoxin
Lockjaw
Clostridium difficile
Epidemiology
Range of Disease
Pathogenesis of CDI
New Issues
Treatment
Transmission
Environment

* Clean and disinfect surfaces in close proximity of the patient
* Patient care equipment.
* Use bleach for C. difficile
* Privacy drapes

Bacteria Pathogenicity Ability to Cause Infection.ppt

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Microbial Interactions with Humans

Microbial Interactions with Humans

Types of Interactions: Symbiosis
* Symbiotic Relationships

Overview of Human-Microbial Interactions
* Pathogens
* Pathogenicity
* Virulence
* Opportunistic Pathogen

Infection Versus Disease
* Infection
* Disease

Opportunistic Pathogens
* Don’t normally cause disease, but may under some circumstances
* 3 circumstances for gaining control/disease

Types of Interactions:
Normal Flora
* Normal Flora
* Factors that influence normal flora

Normal Flora
* Hundreds of different niches associated with human
* Some normal flora are pathogenic
* Resident versus transient flora
* Considered part of the first line of defense!
* Microbial antagonism
* Competitive exclusion

Portals of Entry
* Skin
* Mucous membranes

Preferred Portal
* Many microorganisms have to enter in a specific way and in a certain place to cause disease.
* Skin Portal

Skin
* Epidermis and Keratin
* Hair often deters microbial contact with skin
* Dermis and subcutaneous tissue
* Apocrine and sebaceous glands
* Eccrine glands (sweat)

Skin as a Barrier
Mucous Membranes
* Found in mouth, pharynx, esophagus, GI, respiratory, and urinary tracts
* Epithelial cells coated with protective glycoprotein layer (mucous)
* Less protection than skin
* Cilia and mucous produced by goblet cells

Mucous Membranes
* Respiratory tract Portal
* Respiratory Normal Flora
* Respiratory Barrier Mechanisms
* Gastrointestinal tract portal
* GI Normal Flora

Gastrointestinal Tract
* Large intestine
* GI Barrier
* Genitourinary tract Portal
* Genitourinary Tract Normal Flora
* Genitourinary Tract Barrier

LD50 and ID50
* LD50: Number of microbes in a dose that kill 50% of the organisms infected in a sample
* ID50: Number of microbes in a dose that causes disease in 50% of the organisms infected
* The higher the virulence the lower the ID50 or LD50

Microbial Virulence
Microbe Versus Host
* To cause disease a microbe must…
* Why it is difficult for microbes…
o Skin, antimicrobial sweat
Microorganisms and Mechanisms of Pathogenesis

Line of Defense
* First line: Skin and mucous membranes, normal flora
* Second line: phagocytes, inflammation, fever and antimicrobial substances
* Third line: (specific response) special lymphocytes (B and T cells) and antibodies

Step One: Adherence
* Specific adherence
* Pathogens have attachment structures
* Pathogens have attachment structures

Step 2: Invasion/Colonization
* Increase in numbers beyond the point of attachment.
* Three goals

Step 2: Invasion/Colonization
* Localized versus Systematic infections
* Bacteremia, viremia, toxemia
* Septicemia

Step 3: Cause Damage
* Virulence
* Three Ways to cause damage

Virulence Factors
* Usually help organism colonize and grow
* Coagulase
* Siderophores
* Collagenase
* Protease

Another Way to Classify Exotoxins
* Descriptive classifications
A-B toxin
* Cholera toxin (Vibrio cholera)—cholera

The Action of Chlorea Enterotoxin
More A-B toxin examples
Botulinum Toxin
Tetanus Toxin
Membrane Disrupting Toxins
Superantigens
Endotoxins
* Gram type negatives
* Part of outer portion of cell wall (outer membrane)
* Lipid A portion
* Exert effects when G- microbe lyses
* Same symptoms for different species of microbe
* No antitoxins produced by host
* Very stable—can’t destroy easily
* Rarely fatal
* Disseminated intravascular clotting
* General symptoms

Pyrogenic Response
* Macrophage ingestion
* Release of interleukin-1 in bloodstream
* Interleukin-1 to hypothalamus and production of prostaglandins
* Resetting of bodies thermostat

Susceptibility/Resistance of Host
* Species specificity
* Tissue specificity
* Age
* Stress
* Diet
* Pre-existing disease (Genetic and Infectious)
* Gender
* Behavior
* Weather?
* Your first line of defense—Review this

Microbial Interactions with Humans.ppt

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Lipids

Lipids
By: Henry Wormser, Ph.D.

Introduction
* Definition: water insoluble compounds
+ Most lipids are fatty acids or ester of fatty acid
+ They are soluble in non-polar solvents such as petroleum ether, benzene, chloroform
* Functions
+ Energy storage
+ Structure of cell membranes
+ Thermal blanket and cushion
+ Precursors of hormones (steroids and prostaglandins)
* Types:
+ Fatty acids
+ Neutral lipids
+ Phospholipids and other lipids
Fatty acids
* Carboxylic acid derivatives of long chain hydrocarbons
o Nomenclature (somewhat confusing)
+ Stearate – stearic acid – C18:0 – n-octadecanoic acid
o General structure:
* Common fatty acids
n = 4 butyric acid (butanoic acid)
n = 6 caproic acid (hexanoic acid)
n = 8 caprylic acid (octanoic acid)
n = 10 capric acid (decanoic acid)
* common FA’s:

n = 12: lauric acid (n-dodecanoic acid; C12:0)
n = 14: myristic acid (n-tetradecanoic acid; C14:0)
n = 16: palmitic acid (n-hexadecanoic acid; C16:0)
n = 18; stearic acid (n-octadecanoic acid; C18:0)
n = 20; arachidic (eicosanoic acid; C20:0)
n= 22; behenic acid
n = 24; lignoceric acid
n = 26; cerotic acid

Less common fatty acids
* iso – isobutyric acid
* anteiso
* odd carbon fatty acid – propionic acid
* hydroxy fatty acids – ricinoleic acid, dihydroxystearic acid, cerebronic acid
* cyclic fatty acids – hydnocarpic, chaulmoogric acid

PHYTANIC ACID
A plant derived fatty acid with 16 carbons and branches at C 3, C7, C11 and C15. Present in dairy products and ruminant fats.
A peroxisome responsible for the metabolism of phytanic acid is defective in some individuals. This leads to a disease called Refsum’s disease
Refsum’s disease is characterized by peripheral polyneuropathy, cerebellar ataxia and retinitis pigmentosa
Less common fatty acids
These are alkyne fatty acids
Fatty acids
* Fatty acids can be classified either as:
o saturated or unsaturated
o according to chain length:
Unsaturated fatty acids
* Monoenoic acid (monounsaturated)
Double bond is always cis in natural fatty acids.
This lowers the melting point due to “kink” in the chain
* Dienoic acid: linoleic acid
* Various conventions are in use for indicating the number and position of the double bond(s)
* Polyenoic acid (polyunsaturated)
* Monoenoic acids (one double bond):
* Trienoic acids (3 double bonds)
* Tetraenoic acids (4 double bonds)
* Pentaenoic acid (5 double bonds)
* Hexaenoic acid (6 double bonds)
Both FAs are found in cold water fish oils
Typical fish oil supplements
Properties of fats and oils
* fats are solids or semi solids
* oils are liquids
* melting points and boiling points are not usually sharp (most fats/oils are mixtures)
* when shaken with water, oils tend to emulsify
* pure fats and oils are colorless and odorless (color and odor is always a result of contaminants) – i.e. butter (bacteria give flavor, carotene gives color)
Examples of oils
* Olive oil – from Oleo europa (olive tree)
* Corn oil – from Zea mays
* Peanut oil – from Arachis hypogaea
* Cottonseed oil – from Gossypium
* Sesame oil – from Sesamum indicum
* Linseed oil – from Linum usitatissimum
* Sunflower seed oil – from Helianthus annuus
* Rapeseed oil – from Brassica rapa
* Coconut oil – from Cocos nucifera.....


Websites on lipids

* http://www.cyberlipid.org/ web site deals mainly with an overview on all lipids
* http://www.lipidsonline.org – this website focuses mainly on disease processes (atherosclerosis) and treatment
* http://www.lipidlibrary.co.uk/ -There are two main divisions in this website, one dealing with the chemistry and biochemistry of lipids and the other with the analysis of lipids


Lipids.ppt

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