Pathogenesis of Bacterial Infection and Flora Normal

8/12/2019 Pathogenesis of Bacterial Infection and Flora Normal

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PATHOGENESISOF

BACTERIAL INFECTION

PATHOGENICITY TOXIGENICITYVIRULENCE

Eri Dian


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Introduction of Normal Flora

1. A diverse microbial flora =>

Human body Area: the skin and mucous membranes

Time: shortly after birth until death

Number: 10 14 bacteria

2. Normal flora may:

a. Aid the hostb. Harm the host (in sometimes)

c. Exist as commensals (no effect to the host)

3. Viruses and parasites => NOT normal microbial flora

Most investigators consider that they are not commensals and do not aid thehost.


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Significance of Normal Flora

Normal flora may aid the host in several ways:

Aid in digestion of food

Help the development of mucosa immunity

Protect the host from colonization with pathogenic microbes


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Normal Flora competing with InvadingPathogens

Adopted from Samuel Baron Medical Microbiology


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Normal flora may act as opportunisticpathogens

Especially in hosts rendered susceptible by:

1. Immuno-suppression (AIDS & SCID)

2. Radiation therapy & Chemotherapy

3. Perforated mucous membranes

4. Rheumatic heart diseaseetc.


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Respiratory tract and head

outer ear, eye, mouth, oropharynx, nasopharynx

Sterile sites: sinuses, middle ear, brain, lower respiratory tract

(trachea, bronchiole, lung)Gastrointestinal tract

esophagus, stomach, small intestine, large intestine

Genitourinary system

anterior urethra, vagina

Sterile sites: bladder, cervix, uterus

Skin

Sites of human body that the normal flora

microbes colonize


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Medically important members of the normalflora

Location Important organis

Skin Stapylococcus epidermidis

Nose Stapylococcus aureus

Mouth Streptococcus viridans

Dental plaque Streptococcus mutants

Ginggival cervices Bacteroides,Fusobacterium,Streptococci,Actinomycetes

Throat Streptococcus viridans

Colon Bacteroides fragilis,Escherichia coli

Vagina Lactobacillus,E.coli, Streptococci group

BUrethra S.epidermidis,Corynebacterium

(diphteroids),various Streptococci ,various gram-negative rods,E.g., E.coli


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Adopted from Samue l Baron Medical Microbiology

Distribution of Normal Flora in HumanBody


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1. Local Environment (pH, temperature, redoxpotential, O2, H2O, and nutrient levels).

2. Diet

3. Age

4. Health condition (immune activity)

5. Antibiotics,..etc

Factors Influencing Normal Flora


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The pathogenesis of bacterial infection includes theinitiation of the infectious process and themechanisms leading to the development of signsand symptoms of bacterial disease.

The outcome of the interaction between bacteria

and host is determined by characteristics that favourestablishment of the bacteria within the host andtheir ability to damage the host as they are opposedby host defense mechanisms.


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Among the characterics of bacteria are

adherence to host cells, invasiveness,toxigenity, and ability to evade the host

simmune system.

If the bacteria or immunological reactionsinjure the host sufficiently, diseasebecomes apparent.


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Pathogenesisof bacterial infection

Humans and animals have abundant normal microflora.

Most bacteria do not produce disease but achieve abalance with the host that ensures the survival, growth,and propagation of both the bacteria and the host.

Sometimes bacteria that are clearly pathogens (e.g.Salmonella typhi ) are present, but infection remains

latent or subclinical and the host is a "carrier" of thebacteria.


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Guidelines for Establishing the causes of Infectious DiseasesKoch's Postulates

1. Microorganisms are isolated from dead animals

2. Microorganisms are grown in pure culture

2b. Microorganisms are identified

3. Microorganisms are injected into healthy animals

4. Disease is reproduced in second animal

5. Microorganisms are grown in pure culture

5b. Identification of identical microorganism.


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Figure 14.3 - Overview


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Figure 14.3, steps 1 2


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Figure 14.3, steps 3 4


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Figure 14.3, step 5


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In another example, Neisseria gonorrhoeae (gonorrhea),

there is no animal model of infection even though thebacteria can readily be cultivated in vitro.

The host

s immune responses should be considered when an

organism is being investigated as the possible cause of adisease.

Thus, development of a rise in specific antibody duringrecovery from disease is an important adjunct to Koch

spostulates.


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Establishment of Infection

In order to cause disease pathogen must follow aseries of steps

Gain entrance to host Adherence Colonization and Number of Invading Microbes Avoid Host Defenses Cause host damage


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Portals of entry

1. Mucus membranes Respiratory tract Gastrointestinal tract Genitourinary tract Placenta

2. Skin

3. Parenteral route Bite, puncture, injection,

wound


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The infectious process

Infection indicates multiplication of microorganisms.

Prior to multiplication, bacteria (in case of bacterialinfection) must enter and establish themselves within

the host.

The most frequent portals of entry are the respiratory(mouth and nose), gastrointestinal, and urogenitaltracts. Abnormal areas of mucous membranes and skin(e.g. cuts, burns) are also frequent sites of entry.


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The infectious process Once in the body, bacteria must attach or adhere to host cells,

usually epithelial cells.

After the bacteria have established a primary site of infection,they multiply and spread.

Infection can spread directly through tissues or via thelymphatic system to bloodstream. Bloodstream infection(bacteremia) can be transient or persistent. Bacteremia allowsbacteria to spread widely in the body and permits them toreach tissues particularly suitable for their multiplication.


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The infectious process As an example of the infectious process, Streptococcus pneumoniae can

be cultured from the nasopharynx of 5-40% of healthy people.

Occasionally, Streptococcus pneumoniae strains from the nasopharynx areaspirated into the lungs. Infection develops in the terminal air space ofthe lungs in persons who do not have protective antibodies against thattype of Streptococcus pneumoniae . Multiplication of Streptococcus

pneumoniae strains and resultant inflammation lead to pneumonia. The

strains then enter the lymphatics of the lung and move to thebloodstream. Between 10% and 20% of persons with Streptococcus pneumoniae pneumonia have bacteremia at the time the diagnosis ofpneumonia is made. Once bacteremia occurs, Streptococcus pneumoniae strains can spread to their preferred secondary sites of infection (e.g.cerebrospinal fluid, heart valves, joint spaces). The major resulting

complications of Streptococcus pneumoniae pneumonia includemeningitis, endocarditis and septic arthritis.


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Basic terms frequently used in describing aspectsof pathogenesis:

Infection : Multiplication of an infectious agent within the

body. Multiplication of the bacteria that are part of normal

flora of gastrointestinal tract, skin, etc, is generallynot considered an infection.

On the other hand, multiplication of pathogenicbacteria (e.g. Salmonella species ), even if the personis asymptomatic, is deemed an infection.


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Basic terms frequently used in describingaspects of pathogenesis:

Toxigenicity : The ability of a microorganism to produce a toxin

that contributes to the development of disease.

Invasion : The process whereby bacteria, parasites, fungi

and viruses enter the host cells or tissues andspread in the body.


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Basic terms frequently used in describingaspects of pathogenesis:

Pathogen : A microorganism capable of causing disease.

Non-pathogen : A microorganism that does not cause disease. It may be part of the

normal flora.

Opportunistic pathogen : An agent capable of causing disease only when the host

s resistanceis impaired (e.g. the patient is immunocompromised).

An agent capable of causing disease only when spread from the sitewith normal bacterial microflora to the sterile tissue or organ.


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Bacterial virulence factors

Many factors determine the virulence ofbacteria, or their ability to causeinfection and disease.


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Toxins Toxins produced by bacteria are

generally classified into two groups:

exotoxins

endotoxins


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Exotoxins versus Endotoxins


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Exotoxin


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Enzymes Many species of bacteria produce enzymes that are not intrinsically

toxic but play important role in the infectious process.

Collagenase: degrades collagen, the major protein of fibrous connective

tissue, and promotes spread of infection in tissue.

Coagulase : Staphylococccus aureus produce coagulase, which works in

conjuction with serum factors to coagulate plasma. Coagulasecontributes to the formation of fibrin walls aroundstaphylococcal lesions, which helps them persist in tissues.


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Enzymes Hyaluronidases :

enzymes that hydrolyze hyaluronic acid, a constituent of the groundsubstance of connective tissue. They are produced by many bacteria(e.g. staphylococci, streptococci and anaerobes) and aid in theirspread through tissues.

Streptokinase : many hemolytic streptococci produce streptokinase (fibrinolysin),

substance that activates a proteolytic enzyme of plasma. Thisenzyme, also called fibrinolysin, is then able to dissolve coagulatedplasma and probably aids in the spread of streptococci throughtissues. Streptokinase is used in treatment of acute myocardial

infarction to dissolve fibrin clots.


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enzymes lyse cells, form or dissolve clots, and dissolvematerials in tissue.

Coagulases Kinases Hyaluronidase

Dissolves hyaluronic acid

Collagenase


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Enzymes

Hemolysins and leukocidins : Many bacteria produce substances that are

cytolysins - they dissolve red blood cells(hemolysins) or kill tissue cells or leukocytes(leukocidins).

Streptolysin O, for example, is produced by group Astreptococci and is letal for mice and hemolytic forred blood cells from many animals.


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Antiphagocytic factors Many bacterial pathogens are rapidly killed once they are

ingested by polymorphonuclear cells or macrophages.

Some pathogens evade phagocytosis or leukocytemicrobidical mechanisms by adsorbing normal host

componets to their surfaces.

For example, Streptococcus pneumoniae have surface factorsthat impede phagocytosis e.g. and many other bacteria have

polysaccharide capsules.


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Adherence

Attachment between of microbe to host tissue requires:Adhesins or Ligands : Surface molecules on pathogen thatbind specifically to host cell surface molecules. May belocated on glycocalyx, fimbriae, viral capsid, or other surfacestructure.Receptors : Surface molecules on host tissues to whichpathogen adhesins bind.Cell Wall ComponentsM protein: Found on cell surface and fimbriae ofStreptococcus pyogenes . Mediates attachment and helpsresist phagocytosis.Waxes: In cell wall of Mycobacterium tuberculosis helps resistdigestion after phagocytosis.


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Adherence (adhesion) Critical Step

Bacteria use adhesins (ligands) Viruses has surface attachment proteins Binding to host cells receptors is highly specific


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Definitions...........

Opportunistic infection An infection caused by microorganisms that

are commonly found in the hosts environment

This term is often used to refer to infectionscaused by organisms in the normal flora


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Pathogenesis of Bacterial Infection and Flora Normal

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