Lecture Final Flashcards
number of organisms to colonize 50% of hosts
Infectious dose (ID50)
ability of a pathogen to cause disease
Virulence
help pathogens attach to host cell
adherence factors
outer polysaccharide layer that aids in attachment
capsule
help pathogen to invade host tissue (penetrate the epithelium)
Invasive factors
can produce hyluronidase
some streptococcus and Staphylococcus
breaks down hyluronic acid that holds cells together
hyaluronidase
can produce collagenase that breaks down collagen
Clostridium
help pathogen grow within host tissue
colonization factors
secrete a protein (TcpF) that allows colonization of the small intestine
Vibrio cholera
help pathogen avoid phagocytosis
Cell surface structure
soluble chemical excreted by viable pathogen
exotoxins
causes lysis of host cells
Cytolytic toxins
exotoxins that affect the small intestine, causing changes in intestinal permeability that lead to diarrhea
Enterotoxins
toxic bacterial structural component released upon bacterial cell death
Endotoxin
breaks down fibrin clots
streptokinase
caused by the erythrogenic toxin (damage the plasma membranes of blood capillaries)
Scarlet Fever
autoimmune disease; autoantibodies against S. pyrogens cause damage to heart values
Rheumatic Fever
flesh eating bacteria
Necrotizing fasciitis
caused by varicella-zoster virus
chicken pox
inflammation of the salivary gland
mump
caused by a togavirus
Rubella
vaccine that can prevent measles, mumps, and rubella
MMR vaccine
whooping cough
pertussis
masses of fibrin, bacterial cells, and macrophages
tubercles
block formation of mycolic acid
isoniazid
inhibits RNA polymerase
rifampin
the most common of infectious diseases
The common cold
caused by the rhinovirus
the common cold
caused by an RNA virus of the orthomyxovirus
influenza
minor change in influenza virus antigens due to gene mutation
Antigenic drift
major change in influenza virus antigen due to gene reassortment
Antigenic shift
converts urea into ammonia
urease
produces toxin that causes bloody diarrhea and kidney failure
Enterohemorrhagic E. coli (EHEC (0157:H7)
most frequent bacterial cause of diarrhea (gastroenteritis)
Campylobacter jejuni
on skin due to daily activities, cannot multiply on the skin
Transient microbes
reside and multiply on skin
resident microbes
few bacteria present due to stomach acids, pancreatic secretions and bile
duodenum
common cause of yeast urogentitial infections
candida albicans
the active ability of an organism to resist infection
immunity
protects against foreign cells and macromolecules
immune system
foreign cells or macromolecules react with the antibodies
antigen
substances that induce an immune response
immunogen
a glycoprotein that recognizes the antigen
antibody (immunoglobin)
cells that engulf and destroy foreign particles
phagocytes
first line of defense
inate (non-adaptive) immunity
the acquired ability to recognize and destroy a particular pathogen or its products
adaptive immunity
engulf and destroy microbes
neutrophils and monocytes
differentiates into macrophages or dendritic cells after entering the tissue
Monocytes
large numbers in blood or at any region on the body indicate active infection
neutrophils
contain a lot of granules associated with allergies
“alarm” when there is an invasion
basophils and mast cells
regulate specific immune response, receive information from antigen presenting cells and elicit a response
T-cells
produce antibodies to bind antigens, help in activation of other T-cells
B-cells
major defense against viral infected and cancerous cells
Natural killer cells
promotes the destruction of pathogens by phagocytes
Toll-like Receptor proteins
destroys peptidoglycan
lysozyme
peptides which disrupt pathogen’s cytoplasmic membrane
Defensins
degranulate and release histamine
Mast Cells
stimulates vessels to open further (vasodilation)
histamine
make vessels more permeable
Prostaglandin
immune system responds to body cells as if they were foreign
autoimmune response
fever inducing
pyrogenic
protein molecules released by host cells to inhibit the spread of viral infections
interferons
destroy infected and cancerous host cells
natural killer cells
creates membrane pores to lyse cell
perforin
host produces antibodies and T-cells in response to an infection
naturally acquired active immunity
occurs when antibodies are passed from one host to another
naturally acquired passive immunity
result of vaccination; host makes antibodies that last for years
Artificially acquired active immunity
chemically modified exotoxin retains antigenicity but loses toxicity
Toxoid
has lost its virulence
attenuated bacteria/virus
host receives antibodies (antiserum) from another host that has formed antibodies against a specific pathogen
artificially acquired passive immunity
phagocytic cell that present processed antigens to T-cells
antigen-presenting cell (APC)
undifferentiated T-cells
TH0
secrete cytokinase which causes proliferation of the Tc Cells
TH1 subset
plays a crucial role in beta cell activation and antibody production
TH2 subset
destroy tumor cells, infected cells or damaged cells
Cytotoxic T-cells
allows host to respond to second exposure to same antigen quickly
T-cell receptors (TCR)
on the surface of all nucleated cells; presents intracellular antigens to Tc cells
Class 1 MHC Proteins
on the surface of cell’s antgen presenting cells; presents extracellular antigens to TH cells
Class II MHC Proteins
neutralizes antigens
agglutination
must abundant class of antibodies; only antibody that can be transferred through placenta
IgG
predominant antibody in secretions
IgA
low concentration, responsible for allergies
IgE
second most abundant Ig in blood; first class of antibody made in response to infection
IgM
found on the surface of B cells; binding of antigen to these antibodies stimulates the B cells to produce other antibodies, mostly IgG
IgD
predominant antibody produces becomes IgG instead of IgM
Isotype switching (class switching)
normally harmless substance that cause immune response
allergen
constriction of airways and drop in blood pressure
anaphylactic shock
neutralize or counter the effect of histamine
antihistamines
reduce inflammation
steroids
counter the effects of histamine
adrenalin
“allergy shots” shift antibody production from IgF to IgG
Desensitization
autoantibodies to cardiac cells; damages heart valves
Rheumatic Fever
autoantibodies to Rh blood group; destroys RBC
Hemolytic anemia
autoantibodies to acetylcholine receptor; causes progressive muscle weakness
Myasthenia gravis
complexes deposited in joint; inflammation and destruction of cartilage
Rheumatoid arthritis
complexes deposited in kidney, lungs, and spleen
Systemic lupus erythematosus
autoantibodies against myelin protein; destroys covering of neurons
multiple sclerosis
autoantibodies against insulin-producing cells in pancreas, prevents insulin production
Type 1 Diabetes
pathogen proteins that can cause very strong immune response; activate more T-cells than normal (widespread stimulation of immune cells)
Superantigens