what is pathogenicity:
the ability of a pathogen to produce a disease by overcoming the defenses of the host
what is virulence:
the degree of pathogenicity
How microorganisms enter a host:
the specific route by which a particular pathogen gains access to the body is called its portal of entry
Portals of entry:
-many microorganisms can penetrate mucous membranes of the conjunctiva and the respiratory, gastrointestinal, and genitourinary tracts
Portals of entry:
- most microorganisms can’t penetrate intact skin; they enter hair follicles and sweat ducts
- some microorganisms can access to tissues by inoculation through the skin and mucous membranes in bites, injections, and other wounds…this route of penetration is called the parenteral route
The Preferred Portal of Entry:
-many microorganisms can cause infection only when they gain access through their specific portal of entry
Numbers of Invading Microbes:
-virulence can be expressed as LD50 (lethal dose for 50% of the inoculated hosts) or ID50 (infectious dose for 50% of the inoculated hosts)
Adherence:
- surface projections on a pathogen called adhesions (ligands) adhere to complementary receptors on the host cells
- adhesions can be glycoproteins or lipoproteins and are frequently associated with fimbraie
Adherence: what is the most common receptor:
-mannose
How Bacterial Pathogens Penetrate Host Defenses:
capsules: some pathogens have capsules that prevent them from being phagocytized
How Bacterial Pathogens Penetrate Host Defenses:
cell wall components: proteins in the cell wall can facilitate adherence or prevent a pathogen from being phagocytized
How Bacterial Pathogens Penetrate Host Defenses:
enzymes:
- local infections can be protected in a fibrin clot caused by the bacterial enzyme coagulase
- bacteria can spread from a focal infection by means of kinases (which destroy blood clots), hyaluronidase (which destroys a mucopolysaccharide that holds cells together), and collagenase (which hydrolyzes connective tissue collagen)
- IgA proteases destroy IgA antibodies
How Bactetial Pathogens Penetrate Host Defenses:
antigenic variation:
-some microbes vary expression of antigens, thus avoiding the host’s antibodies
How Bacterial Pathogens Penetrate Host Defenses:
biofilms:
- phagocytes are inactivated or killed by the EPS of biofilms
How Bacterial Pathogens Penetrate Host Defenses:
penetration into the host:
-bacteria may produce proteins that alter the actin of the host cell’s cytoskeleton, allowing bacteria into the cell
How Bacterial Pathogens Penetrate Host Defenses:
1) capsules
2) cell wall components
3) enzymes
4) antigenetic variation
5) penetration into the host
6) biofilms
How Bacterial Pathogens Damage Host Cells: using the host’s nutrients: siderophores
-bacteria get iron from the host using siderophores
How Bacterial Pathogens Damage Host Cells: Direct Damage
-host cells can be destroyed when pathogens metabolize and multiply inside the host cells
How Bacterial Pathogens Damage Host Cells: The Production of Toxins
- poisonous substances produced by microorganisms are called toxins; toxemia refers to the presence of toxins in the blood. The ability to produce toxins is called toxigenicity
- exotoxins are produced by bacteria and released into the surrounding medium. Exotoxins, not the bacteria, produce the disease symptoms
- antibodies produced against exotoxins are called antitoxins
- A-B toxins consist of an active component that inhibits a cellullar process and a binding component that attaches the two portions to the target cell (eg: a diptheria toxin…helicase genotoxin)
- membrane-disrupting toxins cause cell lysis (eg: hemolysis)
- superantigens cause release of cytokines, which cause fever, nasea, and other symptoms (eg: toxic shock syndrome toxin)
- endotoxins are the lipid A component of the cell wall of gram-negative bacteria
- bacterial cell death, antibiotics, and antibodies may cause the release of endotoxins
- endotoxins cause fever (by inducing the release if interleukin-1) and shock (because of a TNF-induced decrease in blood pressure)
- the Limulus amebocyte lysate (LAL) assay is used to detect endotoxins in drugs and on medical devices
Plasmids:
- “a genetic structure in a cell that can replicate independently of the chromosomes, typically a small circular DNA strand in the cytoplasm of a bacterium or protozoan. Plasmids are much used in the laboratory manipulation of genes.”
- plasmid may carry genes for antibiotic resistance, toxins, capsules, and fimbriae
Pathogenic Properties of Viruses:
1) viruses avoid the host’s immune system by growing inside cells
2) viruses gain access to host cells because they have attachment sites for receptors on the host cell
3) visible signs of viral infections are called cytopathic effects (CPE)
4) some viruses cause cytocidial effects (cell death), and others cause noncytocidal effects (damage but not death)
5) cytopathic effects include stopping mitosis, lysis, formation of inclusion bodies, cell fusion, antigenic changes, chromosoma changes, and transformation
Pathogenic Properties of Fungi, Protozoa, Helminths, and Algae:
1) symptoms of fungal infections can be caused by capsules, toxins, and allergic responses
2) symptoms of protozoan and helminth diseases can be caused by damage to host tissue or by the metabolic waste products of the parasite
3) some protozoa change their surface antigens while growing in a host, thus avoiding destruction by the host’s antibodies
4) some algae produce neurotoxins that cause paralysis when ingested by humans
Portals of Exit:
- pathogens leave a host by portals of exit
- three common portals of exit are: the respiratory tract via coughing or sneezing, the GI tract via saliva or feces, and the GI tract via secretions from the vagina or penis
- anthropods and syringes provide a portal of exit for microbes in the blood
