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63 Cards in this Set
- Front
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Reservoirs of infection |
sites in which viable infectiousorganisms persist and from which human infections can arise. |
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Human reservoirs |
acute carriers or chronic carriers |
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Animal reservoirs |
about 150 pathogenic micoorganims can infectboth humans and some other animals. |
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Zoonoses |
can be spread from animal to humans |
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Nonliving reservoirs |
soil, water, food. |
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Modes of transmission |
how disease is spread in population |
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Vectors are |
Living agents that transmit disease, they can bepassively in disease transmission or could be part of the pathogens life cycle |
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Mechanical transmission |
When a vector has no participation with thedisease, it transfers it from point A to B |
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Biological transmission |
When a vector has the organism causing thedisease living inside of it for a period of time. |
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Vehicletransmission |
Inanimate objects, and transmission of pathogensby things such as o Water, air, food, blood and other fluids inhospitals, drugs, etc |
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Contacttransmission |
can be direct or indirect direct contact transmission person to personcontact indirect contact transmission occurs throughfomites. |
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Tissue Tropism |
To effect a certain tissue, often referred to asthe target site. |
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Spread of infection |
Refers to how diseases differ in how they spreadthrough the body -localized -toxigenic bacteria -invasive |
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Localized spread of infection |
remains in one area, typically site of infection |
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Toxigenic bacteria spread of infection |
remains localized but secretes toxins that canspread through the body |
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Invasive spread of infection |
agent doesn’t remain in one area but spreadsthrough the body, normally through bloodstream |
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Pathogen |
organism that causes disease |
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Opportunist pathogen |
thesedon’t normally cause disease in a healthy hose, but they do infect immune compromisedhost, |
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True pathogen |
pathogen that causes disease in healthy host |
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Polymicrobial |
multiple species, and typically are mouthinfectious, wounds |
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Virulence |
degree of pathogenicity, it involves both theinfective of the agent and severity of the disease it causes |
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Virulence factors |
factors that increase the pathogenicity. examples are attachment, immune evasions, spreading factors, invasions of host cell, toxins, iron acquisition |
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Attachment |
A virulence factor. helps attach! -capsule and glycocalx allows formation of biofilm -pili have adhesion in their tip -surface protein- functions as adhesions -adhesins- molecules on pathogens that allow them to attach to host |
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· Immuneevasions |
A virulence factor. -Capsule- prevents phsogcytosis, and antibodybinding. BIOFILM FORMATION -Coagulase - hemolysins -IgA proteases |
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Coagulase |
makesblood clot that the bacteria grow inside. Immune cells cannot enter. It is madein a fibrin |
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Staphylokinase |
is later made that breaks the fibrin blood clot around bacteria |
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Streptokinase |
works same as staphylokinase but is used to treat strokes |
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hemolysins |
lyse redand white blood cells. Attacks the host cell membrane. |
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Leukocidins |
destroy white blood cells |
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Antibody proteases |
cleave the antibody/ Renders in ineffective |
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IgA proteases |
they are in two parts. The part bound to thecell and the part that flag the immune system. So bacteria is covered with IgAbut the host doesn’t know it is there. |
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Antigenic variation |
change the surface antigens that mosteffectively mediate clearance of microorganism. Some times antigen can bechanged on the outside (DIFF STRAINS, DIFF GENE) |
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Phase variation |
turningoff then turning on the gene. It’s the same strain |
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· Spreadingfactors |
A virulence factor. helps break things down, and movement -collagenase -hyalurodiase -flagella -toxins |
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Collagenase |
breaks down collagen, a connective tissue |
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Hyalurodiase |
breaks down a component of extracellular matrix |
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Flagella |
lets bacteria swim |
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Invasion to hide |
invade the host and rest there. Some will invadeand grow slowly but not intracellular |
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Invasion to invade the host tissue |
some bacteria want to go to the cell to get intounderlying tissue |
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Invasion of non-immune cells |
invadethe host cell and grow in their endosome or grow in cytoplasm after lysing theendosome |
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Invasion of immune cells |
occasionaly happens, but takes skilled bacteria |
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Invasins |
bacterial surface proteins that promotephagocytosis of bacteria. It is needed to induce significant rearrangement ofthe cytoskeleton of the cell to induce phagocytosis |
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Exotoxins |
soluble proteins which cause distant effects: cytotoxins, neurotoxins, entrotoxins. gram positive, gram negative |
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Cytotoxin |
have toxic effect on cells they come in contactwith |
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Neurotoxins |
interfere with neurological signal transmissions |
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Enterotoxins |
soluble proteins which cause diarrhea |
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Endotoxin |
lipid A, a component of LPS that stimulates theimmune system gram negative |
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Anthrax toxin |
killshost macrophages and causes death of the host |
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Diphtheria toxin |
inhibits protein synthesis, kills host cell |
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Botulinum toxin |
neurotoxin that prevents nerve signalingblocking muscle contraction |
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Tetanus toxin |
neurotoxin that locks nerve cell signaling |
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Cholera toxin |
enterotoxin causing tremendous diarrhea. |
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Iron acquisition |
o Most bacteria need iron from electron transportpathways. They have three basic strategies § Steal from the host § Siderophore- make iron binding proteins § Blow up host cell and release intracellular iron |
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In order forinfection to be maintained. |
immune evasion, proliferation, penetration |
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Incidence |
is the number of new cases in a population in aspecific period of time |
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Prevalence |
total number of people infected at anyone time |
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Morbidty |
incidence of disease in population in aspecified time period |
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Mortaltiy |
number of deaths in a population in a time period |
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Endemic |
constantly present in population. |
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Epidemic |
occurs when a disease has high incidence in apopulation |
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Pandemic |
world wide epidemic (flu 1918, cholera 1961-71) |
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Sporadic |
small number of isolated cases |
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Immunecompromised |
Neutropenia, organ transplantation, burn patients, nonsociomial infections (occur in the hospital) |
