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31 Cards in this Set
- Front
- Back
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Pathogenicity |
Ability to cause disease by overcoming host defenses. |
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Virulence |
The degree of pathogenicity |
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Portals of Entry |
Ways for the pathogen to enter the human body
Mucous membrane, skin, parenteral route ( direct deposition beneath the skin or membranes) |
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How is disease caused? |
Pathogens must gain access to the host, adhere to host tissues, penetrate or evade host defenses, and damage the host tissues |
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Portals of Entry: mucous membranes |
- penetrate respiratory tract (most common, water droplets, dust), gastrointestinal tract (contaminated fingers touching food/water), genitourinary tract, conjunctiva - destroyed by enzymes and hydrochloric acid in stomach or bile
I.e. typhoid, cholera, syphilis, gonorrhea
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Portals of Entry: skin |
Unbroken skin is imprenetrable by most microorganisms. (Exceptions: hair follicles or sweat glands, hookworm larvae burrow, fungi on the keratin on skin) |
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Portals of Entry: parenteral route |
Microorganisms are deposited directly beneath the skin or into penetrated barriers or injured mucous membranes. (I.e. bites, Cuts, wounds, surgery, punctures, splitting of skin or mucous membranes due to swelling or drying) |
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Preferred portal of entry |
A prerequisite for a pathogen being able to cause disease.
I.e. Salmonella typhi, a bacteria of typhoid fever, produces all the signs and symptoms when swallowed, but only inflammation or no reaction when rubbed on skin |
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What is more virulent? Infectious dose Anthrax Cutaneous ID50 10-50 endospores Inhalation ID50 10K-20K endospores Gastrointestinal 250k- 1mil endospores
Potency? Lethal dose Botulinum toxin LD50 0.03 ng/kg Shiga toxin LD50 250ng/kg Staphylococcal enterotoxin LD50 1350 ng/kg |
Cutaneous anthrax ID50 10-50 endospores more easily acquired
Botulinum toxin ID50 0.03 ng/kg stronger toxin
Virulence is expressed as ID50 (kill 50% of 100 people) |
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Adherence |
The way a pathogen attaches to the host tissue at the portal of entry.
The attachment is accomplished by means of surface molecules on the pathogen called adhesions or ligands that bind specifically to complementary surface receptors on the cells of certain host tissues |
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Streptococcus mutans |
Streptococcus mutans is a bacteria that produces an enzyme called glucosyltransferase. It converts glucose into a sticky polysaccharide (dextran), forming glycocalyx.
Actinomyces bacteria cells have fimbriae that adhere to the glycocalyx of Streptococcus mutans.
Streptococcus mutans, dextran, and Actinomyces combine to make up dental plaque |
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How do capsules help bacteria? |
Capsules are made of glycocalyx and they resist the host defenses by impairing phagocytosis. This increases the virulence of a pathogenic species. |
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M protein |
A heat resistant, acid resistant protein found on both the cell surface and fimbriae. It mediates attachment of the bacterium to epithelial cells of the host and helps the bacterium resist phagocytosis. It also increases the virulence of the microorganism |
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Opa |
An outer membrane protein that is used along with fimbriae to attach to host cells |
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Coagulases |
Bacterial enzymes that coagulate the fibrinogen in blood to protect it from phagocytosis |
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Kinases |
Bacterial enzymes that break down fibrin and digest clots formed by the body isolate the infection |
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Hyaluronidase |
An enzyme secreted by certain bacteria that hydrolyzes hyaluronic acid, a type of polysaccharide that holds together certain cells of the body, particularly connective tissue cells. This digesting action is thought to be involved in the tissue blackening of infected wounds to help the microorganism spread from its initial infection site |
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Collagenase |
An enzyme produced by several species of clostridium, facilitates the spread of gas gangrene. It breaks down protein collagen informs the connective tissue of muscles and other body organs and tissues. |
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IgA protease |
Pathogen's enzymes that destroy |
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Antigenic variation |
The process of pathogens altering their surface antigen to counter the host's antibodies I.e. Influenzavirus |
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Invasins (ruffling) |
When microbes produce surface proteins that rearrange nearby actin filaments of the host cytoskeleton. They cause membrane ruffling. (Looks like a bacteria splashing in a still pool) |
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Toxin |
Poisonous substances that are produced by certain microbes |
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Toxin |
Poisonous substances that are produced by certain microbes |
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Toxigenicity |
The capacity of microorganisms to produce toxins |
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Toxemia |
Presence of toxins in the blood |
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Exotoxins |
Mostly Gram negative, proteins, enzymes that catalyze only certain biochemical reactions, very harmful because they can act over and over again, soluble in body fluids resulting in easy diffusion into the blood, destroy host cells and inhibit metabolic functions,
Exotoxins are disease-specific, they produce specific signs and symptoms of the disease. |
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Endotoxins |
Lalalal |
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Antitoxin |
The host cell's antibodies specific for providing immunity to exotoxins |
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Toxoid |
Altered exotoxins that are inactivated by heat or by formaldehyde, iodine, or other chemicals, so that they no longer cause the disease but can still stimulate the body to produce antitoxins |
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What are the three types of exotoxins? |
1. A-B toxin 2. Membrane- disrupting toxins 3. Superantigens |
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A-B toxins |
Consists of 2 parts, A active enzyme component, B binding components |
