Chapter15 : microbial Mechanisms of Pathogenicity

Pathogenicity

the ability to cause diseases

Virulence

the degree of pathogenicity

Portal of entry

mucous membranes

skin

parenteral route

• deposited directly into tissues when barriers are penetrated

• injections, bites, wounds, cuts surgery

most pathogens have a preferred portal of entry

ID 50

infectious does for 50% of a sample popilation

measures virulence of a microbe

Bacillus anthracis

skin( PE)

10-50 endospores

inhalation ( EP)

10,00 -20,000 endospores

Ingestion ( PE)

250,00 - 1,000,000 endospores

LD 50

leathal dose for 50% of a sample population measures potency of a toxin

adherence ( adhesion )

the process of pathogens attaching to host tissues

adhesins( lingands )

on the pathogen bind to receptors on the host cells

• glycocalyx ( capsule, slime layer, eps )

• fimbriae

• viral spikes

capsules

glycocalyx around the cell wall impair phagocytosis

• invade phagocyctocs

• invisibility clock

Biofilms

help evade phagocytosis

anti microbial resistance

M protien

resisits phagocytisus

ex. sterptococcus pyogenes ( strep throat)

Opa protein

allows attachment to host cells

ex. Neisseria gonorrhoeae ( ihibit T-cell activiation )

Waxy lipid ( mycolic acid)

resists digestion by phagocytes

ex. Mycobacterium tuberculosis

( not invisible but invincible)

coagulases

coagulate fribinopen forming fibrin

Kinases

digest fibrin clots

Hyaluronidase

digests hyaluronic ( connect cell within the host ), a host polysaccharide that hold cells together

collagenase

breaks down collagen

IgA proteases

destroy IgA ( a pathogen flagler) antibodies

Antigenic variation ( the pathogen changes disguses)

Pathogens alter their surface antigens; the antibodies that a host made against those antigens are rendered ineffective

ex.

• influenza virus

• Nesseria gonorrhoeae

• Trypanosome brucei gambiense

Invasins ( PH)

rearrangeaction filaments of the cyta

• cause membrane ruffling

making their own door

Actin polmerization

shigella and listeria ( have to enter the host cell to cause infection )

survival inside phagocytes

rearrange the cell to make their own flaggella

siderophores

proteins secreted by pathogens that bind iron more tightly than host cells and host iron-binding proteins

make their own iron binding protein to compete with ours more effective then ours

Direct Damage

disrupts host cell function

uses host cell nutrients

produces waste products

multiplies in host cells and causes ruptures

Toxins

poisonous substances produced by microorganisms

produces fever, cardiovascular problems, diarrhea, and shock ( sepsis)

Toxigenicity

the ability of a microorganism to produce a toxin

Toxemia

presence of toxin in the host’s blood

intoxications

presence of toxin without microbial growth ( injecting the toxin but not the bacteria )

Exotoxins

produces by both gram positive & negative

leave the cell

proteins produced and secreted by bacteria

Antitoxins

antibodies against specific exotoxins that provide immunity

toxoids

inactivated exotoxins used in vaccines

A-B toxins

contain an enzyme compone ( A part) and a binding component ( B part diphtheria toxin)

Genotoxins

damage DNA ( causing mutations, disrupting cell division, and may lead to cancer )

Membrane- disrupting toxins

lyse host cells by disrupting plasma membranes

Leuckidins

kill phagocytic leukocytes

hemolysins

kill erythrocytes by forming protein channels

• streptolysins - produced by streptocci

superantigens

cause an intense immune response due to release of cytokines from host cell ( T cells )

cause symptoms of fever, nausea, vomiting, diarrhea, shock, and death ( exadrated immune response cannot be controlled )

lipid A

portion of lipopolysaccharides ( LPS) of gram - negative bacteria ( part of the outer membrane )

viral mechanisms for evading host defense

intracellular location

use host cell surface molecules

directly attack component of the immune system a

antigenic variation

Cytopathic effects ( CPE)

are viable effect of viral infection on a cell ( the host cell changes

disrupting cell junctions

inducing a cytokine storm

creating inclusion bodies ( rabies ) in the cell cytoplasm

Ergot ( fungi)

are alkaloid toxins that causes hallucinations

Aflatoxin ( fungi)

is a carcinogenic toxin produced by Aspergillus

Protozoa

presence of protozoa and their waste products causes symptoms

avoid host defense by :

digesting cells and tissue fluids

• Giardia intestinalis

Growing in phagocytes

• toxoplasma gondii

antigenic variation

• trypansoma

Helminths

use host tissue for growth

produce large parasitic massess;cause cellular damage

produce waste products

produce waste products that causes symptoms

Portals of exit

respiratory tract

• coughing and sneezing

Gastrointestinal tract '

• feces and saliva

Genitourinary tract

• urines; secretions from the penis and vagina

skin

blood

• arthropods that bite; needles or syringes