BYU General Microbiology Chapter 8 – Dr. Robison – Flashcards

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innate resistance
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resistance to pathogens due to physiological properties of humans
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1st line of defense
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nonspecific, stops things from coming in
skin
mucous membranes
chemicals
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2nd line of defense
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non-specific, defends after they're in the body, most of it from blood, 5 ways:
phagocytosis,
extracellular killing be leukocytes,
nonspecific chemical defenses,
inflammation,
fever
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3rd line of defense
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specific defense
lymphocytes, antibodies
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skin: physical components
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microbial hell (large intestine=microbial heaven)
2 layers:
epidermis, dermis
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epidermis
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tightly packed cells
sheds 10 billion cells per day (removing microbes too)
epidermal dendritic cells/ Langerhans cells: phagocytize pathogens
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Dermis
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contains callogen- gives strength to resist abrasions which could introduce pathogens
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Skin: chemical components of defense
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sweat and sebum
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sweat
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salty -> hypertonic solution
lysozyme -> cuts cross links in cell walls
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sebum
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pliable- less likely to tear
lower pH: inhibits most bacteria
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mucus membranes
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2 layers:
epithelium
connective layer that supports epithelium
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epithelium
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living cells, tightly packed, continually shedding cells
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microbial antagonism- 5 reasons that make it hard for pathogens to compete
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secrete antimicrobial substances
consume all the nutrients
change pH
helps stimulate 2nd line of defense
give vitamins to host
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chemicals in 1st line
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lacrimal glands bathe eye
saliva
stomach acid
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blood plasma components
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water, electrolytes, dissolved gasses, nutrients, proteins
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serum
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part of plasma, only antibodies
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formed elements definition and 3 types
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cells and cell fragments in blood
erythrocytes
platelets
leukocytes
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erythrocytes
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red blood cells, carry O2 and CO2
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Platelets
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involved in blood clotting and inflamation
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leukocytes
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white blood cells- defend against invaders
2 types: granulocytes and agranulocytes
remember: GRANny PHIL is A CYTE
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Granulocytes
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3 types:
neutrophils
eosinophils
basophils
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neutrophils
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50-70% of WBCs
> 10 billion made every day
major phagocytes
cells of acute inflamation
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Eosinophils
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1-3% of WBC
parasite defense
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Basophils
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.5-1% of WBC
contain histamine
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Agranulocytes
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2 types
Lymphocytes
Monocytes
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Lymphocytes
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20-40% of WBC
most involved in specific immunity
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Monocytes
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1-6% of WBC
leave blood and mature into macrophages
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macrophages
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phagocytes
either fixed to tissue or wandering
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fixed macrophages
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microglial cells (CNS)
mesangial cells (kidney)
kupffur cells (liver)
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what could increased eosinophils indicate?
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allergies
parasitic worm infection
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what could increased leukocytes, mostly neutrophils indicate?
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bacterial diseases
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what could increased lymphocytes indicate?
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viral infections
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phagocytosis
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performed mostly by neutrophils and macrophages,
have receptors for bacterial surface components and opsonins
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extracellular killing by leukocytes
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eosinophils
natural killer lymphocytes
neutrophils
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eosinophils
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mainly attack worms (helminths) by secreting substances that weaken or kill it
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natural killer lymphocytes
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jason bourne- sees their weird and kills them
secrete substances on the surface of virally infected cells and tumor cells
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neutrophils
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leak antimicrobials and trapping webs (NETs)
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Nonspecific chemical defenses
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lysozyme
complement
interferon
defensins
lactoferrin
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complement system
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complements the action of antibodies
when complement is activated -> lysis of foreign cell
activated in 2 ways
classic pathway
alternate pathway
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the classical pathway
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complements the action of antibodies
4 functions:
induce inflammation
opsonization
chemotaxis of phagocytes
lysis of foreign cells
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The alternate (properdin) pathway
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less efficient than classical pathway
useful before antibodies are made
activation occurs independent of antibodies
initiated by properdin B,D, P and bacterial/fungal LPS and endotoxins
starts reactions that lead to classical pathway
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Interferons
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proteins that inhibit the spread of viruses (esp. ones with RNA genomes)
cause symptoms associated with viral infections
3 classes: alpha, beta, gamma
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interferons present in early stages of infection
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alpha and beta
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interferon that appear in later stages of infection
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Gamma
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interferon therapy
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not very effective
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Defensins
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small peptides
ways it attacks pathogens:
cationic- attracted to bacteria
amphipathic- punch holes in cytoplasmic membranes
interferes with internal signaling and metabolic processes
prevents biofilms
makes bacterial proteins vulnerable to heat
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inflammation
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increases defensin production
2 types:
acute
Chronic
4 cardinal signs:
redness
heat
swelling
pain
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acute inflammation
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fast, intense, usually beneficial
increased permeability to blood vessels
migration of phagocytes (neutrophils and macrophages)
tissue repair
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chronic inflammation
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slow, last a long time, can cause damage
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Fever
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body temp over 37 C
happens when pyrogens trigger hypothalamus to increase the body's core temp
chills are associated with fever are due to the reduced blood flow of constricted vessels
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types of pyrogens
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bacterial endotoxins
cytoplasmic contents of bacteria released by lysis
antibody-antigen complexes
interleukin-1
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benefits of fever
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enhances the effects of interferons
inhibits growth of some microbes
speeds up immune system
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