Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
318 Cards in this Set
- Front
- Back
|
What are the two different kind of pathogens?
|
living and nonliving
|
|
|
what are the types of living pathogens?
|
eukaryotes and prokaryotes
|
|
|
what is the difference between eukaryotes and prokaryotes with a nucleus?
|
pro-DNA not in nucleus
euk-DNA in nucleus |
|
|
What is the difference between eukaryotes and prokaryotes with gene transfer?
|
euk-no gene transfer between individuals
pro-much gene transfer between individuals. |
|
|
what are the types of nonliving pathogens?
|
viruses and prions
|
|
|
do prions have genetic material?
|
no
|
|
|
what kind of genetic material do viruses have?
|
RNA or DNA
|
|
|
what are viruses surrounded by?
|
protein (capsid)
|
|
|
what has to be true for viruses to reproduce?
|
reproduce only in cells so they must infect cells.
|
|
|
how do viruses reproduce? steps?
|
1. virus binds with protein on host cell's surface
2. viral genetic material enters 3. host cell resources used to make viral protein and genetic material 4. new viruses assemble, emerge, destroy host (may carry genes from host). 5. release |
|
|
what sometimes happens with viral genes?
|
insert into host DNA and re-activate when they exit
|
|
|
what are the different types of viral infections?
|
temporary (self-limiting): immune system stops infection.
permanent if virus can "hide" in DNA of some cells. |
|
|
how can viruses be prevented?
|
vaccination
|
|
|
what is the treatment for a virus?
|
none for many viral infections
anti-viral for specific viruses antibodies against specific viruses |
|
|
why isn't there treatment for many viral infections?
|
most drugs that target viral reproduction would affect host as well
focus on symptoms. |
|
|
what do anti-viral drugs do?
|
for specific viruses, target synthesis of genetic material and specific protiens.
|
|
|
what do antibodies do for viruses?
|
against specific viruses (like rabies)
|
|
|
what are the different types of viruses?
|
DNA
RNA retroviruses |
|
|
how do viruses differ?
|
differ in how they make more genetic material and their proteiins in the host cell, depends on what enzymes are absent/present in host cell.
|
|
|
what do DNA viruses include?
|
viruses of bacteria, bacteriophages/phages
some viruses of humans: herpes, chicken pox, small pox, hepatitis B. |
|
|
can viral DNA replicate?
|
yes and can be translated and transcribed
|
|
|
how are viral DNA proteins produced
|
DNA replication, transcription, and translation.
|
|
|
what happens if viral DNA is incorporated into host chromosomes?
|
will remain quiet for some time, when it leaves, will multiply, kill cell, spread.
|
|
|
what are the two types of RNA viruses?
|
RNA viruses not retroviruses and retroviruses.
|
|
|
what are examples of viral RNA?
|
viruses of humans: cold, polio, rabies, mumps, measles, flu, hepatitis A&C, SARS, West Nile, Ebola.
|
|
|
why is RNA translated?
|
to make viral proteins, including enzymes that replicated viral RNA (not normal for host)
|
|
|
why is viral replication error-prone?
|
no error-correcting enzymes (like those found in DNA replication)
|
|
|
which kind of RNA virus uses RNA to make DNA?
|
retroviruses
|
|
|
what does the lacking error correcting enzyme mean for viral RNA replication?
|
high mutation rate
|
|
|
how is DNA made from RNA in retroviruses?
|
enzyme (reverse transcriptase) is provided by virus (not host cell), not very accurate (meaning high mutation rate).
|
|
|
What can happen with DNA in retroviruses?
|
can be incorporated into host chromosome, replicated when cells divide, transcribed into viral RNA and RNA that makes viral proteins.
|
|
|
what is an example of a retro virus?
|
HIV (causes AIDS)
|
|
|
how does genetic change in viruses occur?
|
due to mutations, gain/loss of genes after being incorporated into host chromosomes.
|
|
|
how do mutations with viruses occur?
|
mutation-causing agents, poor copying transcription.
|
|
|
why is genetic change in viruses important?
|
resistance to antiviral drug can spread rapidly, a wide variety of strains of the same virus, makes it harder to prevent by vaccination, harder to cure all at once.
|
|
|
how are viruses transmitted?
|
air, contact with infected objects (cold, flu, pox, viruses), animal bites (rabies, west nile)
body fluids and close body contact. |
|
|
what are different sexually transmitted viruses?
|
herpes, HPV, Hepatitis B and C, HIV/AIDS.
|
|
|
which ST virus is most prevalent?
|
herpes
|
|
|
what are the symptoms of herpes?
|
painful ulcers: cold sores and genital ulcers
|
|
|
how does the immune response cause initial infection to subside and then appearance again?
|
virus may hide in nerves, outbreaks may recur (result of stress).
|
|
|
when is the host infectious with herpes?
|
during and between outbreaks (not as infectious between).
|
|
|
what are the dangers of herpes?
|
may increase risk of cervical cancer, infection of baby during vaginal delivery
|
|
|
what are treatment options for herpes?
|
drug similar to DNA nucleotide, incorporated into viral DNA, cannot be replicated by enzymes, no cure though, shortens/reduces/prevents outbreaks.
|
|
|
what is the second most prevalent ST virus?
|
HPV
|
|
|
what does HPV promote?
|
cell division, produces genital warts, burning, irritation, discahrge or bleeding.
|
|
|
what is the treatment for HPV?
|
remove warts chemically or surgically (freezing, burning, laser surgery).
virus itself is not removed (still in body) |
|
|
what can HPV increase risk of?
|
formation of additional warts
cervical , penile, anal (both man and woman) cancer viral DNA inserts into host DNA: can change genes controlling cell division. infection can pass to infant during child birth. |
|
|
what are prevention methods for HPV?
|
vaccine (teenage girls and boys) pap test (detection)-women.
|
|
|
how is hepatitis B and C transmitted?
|
body fluids (semen, saliva)
|
|
|
what does hepatitis B and C infect?
|
liver
|
|
|
what are the symptoms of hepatitis B and C ?
|
jaundice( yellow skin and eyes)
|
|
|
what happens with people with hepatitis B and C?
|
most recover and are not infective
others may develop complications: cirrhosis, liver failure, liver cancer. |
|
|
what are prevetion methods for hepatitis B and C?
|
vaccine for V not C.
|
|
|
what is HIV and what does it cause?
|
Human immunodeficiency virus, causes AIDS (acquired immune deficiency syndrome).
|
|
|
where did HIV originate?
|
similar virus in African primates
|
|
|
how was HIV transmitted to humans?
|
biting?
|
|
|
how was the spread of HIV aided?
|
travel and behavior (sexual and drug related)
|
|
|
how is HIV transmitted?
|
body fluids (semen, saliva, vaginal secretions, blood), tears in membranes( mouth, urethra, anus, vagina), needles, mother to fetus, receiving blood.
|
|
|
can HIV live outside body?
|
not stable for long (easily destroyed, can't get from a pool)
|
|
|
who can someone have natural resistance to HIV?
|
cells do not have proteins that virus attaches to (inherited, stavered by plague epidemic).
|
|
|
what are infectious diseases caused by?
|
an "agent"
|
|
|
who is the victim of an infectious disease?
|
host
|
|
|
how are infectious diseases transmitted?
|
air, food and water, parenteral (blood to blood, shared needles, medical accidents), mother to fetus/newborn, animal bites, contact.
|
|
|
through what kinds of contact can infectious disease be spread?
|
non-sexual and sexual contact
|
|
|
which kinds of sexual contact have potential for transmitting diseases?
|
mostly anal and vaginal itnercourse, oral sex, skin to skin contact during sex.
|
|
|
what are sexually transmitted diseases also known ast?
|
venereal diseases
|
|
|
how common are STDs in people?
|
1 in 4 americans at some time in life get an STD, 10 million new cases each year.
|
|
|
what are STDs a significant cause of?
|
death and infertitlty
|
|
|
why are most people unaware they have an STD?
|
lack of education
|
|
|
what are the causes of STDS?
|
bacteria and viruses
|
|
|
what do bacteria and viruses need to spread?
|
moist surfaces
|
|
|
where do bacteria and viruses enter in the female?
|
vulva, vagina, urethra, where membranes are moist and delicate
|
|
|
where do bacteria and viruses enter the male?
|
penis, urethra, where surfaces are moist and delicate.
|
|
|
where do bacteria enter both male and female?
|
eyes, mouth, anus
|
|
|
will viruses and bacteria remain localized or spread?
|
either
|
|
|
what are some side effects of STDs?
|
produce inflammation, discharges (pus) from vagina, cervix, urethra depending on where it enters, ulcers (open sores) on genitalia.
|
|
|
what is teh pus that can be discharged?
|
dead white blood cells
|
|
|
how do you prevent STDs?
|
abstinence/monogamy, use condoms, discuss with partner history, risks, inspect partner, dental work or open sores: no sex, wash and urinate after sex.
|
|
|
what does washing and urinating after sex do?
|
flushes systems of germs.
|
|
|
what are cases where infectious agents don't cause disease?
|
may exist in balance with host.
|
|
|
what are things that cause the balance to be upset?
|
stress, weakened immune system, reduced competition, infection by new agent.
|
|
|
what are common characteristics of living organisms?
|
made up of cells, genetic materia: DNA, undergo cellular respiration: need food, cause harm.
|
|
|
what are characteristics of eukaryotes?
|
nucleus present in cells, do not exchange pieces of DNA, unicellular or multicellular
|
|
|
how many cells do protists have?
|
unicellular (consists of only one cell)
|
|
|
how are protists spread?
|
water, biting mosquitoes, sexually transmitted diseases.
|
|
|
what protists are spread by water?
|
amoeba, giardia
|
|
|
what can amoeba and giardia both cause?
|
diarrhea
|
|
|
what can amoeba cause?
|
can infect the nervous system, can be fatal
|
|
|
what can you do to prevent fatal amoeba?
|
warm water, sniff
|
|
|
what can mosquitoes carry?
|
african sleeping sickness, malaria
|
|
|
what can african sleeping sickness do?
|
destroy brain
|
|
|
what can malaria do?
|
infects liver and blood cells
|
|
|
what does trichomoniasis (sexually transmitted) do in males?
|
no symptoms or mild urethritis (irrritation) with discharge, infections are self-limiting (body defenses takes care of this
|
|
|
what does trchomoniasis do to females?
|
vaginal infection, itch, urethritis, with discharge.
|
|
|
how do infections from trichomoniasis differ in males and females?
|
infections are more chronic in females, need antibiotics.
|
|
|
how is trichomoniasis treated?
|
very common; easily cured with antibioitics
|
|
|
how many cells do fungi have?
|
mostly multicellular
|
|
|
what are some exceptions to the mostly multicellular fungi?
|
yeasts
|
|
|
what are the other characteristics of a fungi's cell structure?
|
non-motile, have cell walls
|
|
|
what do fungi secrete?
|
enzymes that digest cells (livng or dead) for food absorb products.
|
|
|
are fungal infections localized or spread?
|
generally localized, can be widespread if immune system fails
|
|
|
what is the treatment for fungal infections?
|
antifungals
|
|
|
what are examples of antifungal infections?
|
athlete's food, ringworm, yeast (candidiasis)
|
|
|
when do yeast infections happen/what cause them?
|
balance of micorbes in vagina is disrupted
|
|
|
what are examples of animals that spread to cause disease?
|
worms, arthropods
|
|
|
what is the treatment of worms?
|
antihelminthics
|
|
|
how are worms transmitted?
|
food, water
|
|
|
where do worms live?
|
inside the host
|
|
|
what do they do to the body?
|
deprive the host of nutrients
|
|
|
how do they deprive teh body of nutrients?
|
digestive tract (spread thorugh feces), lymph vessels blockage, in muscle: trichinella
|
|
|
what are examples of worms in the digestive tract?
|
tapeworm, flukes, roundwoorm
|
|
|
what are examples of worms in teh muscle?
|
trichinella
|
|
|
what are two different kinds of arthropods?
|
public lice (crabs)
scabies (mites) |
|
|
what does public lice do?
|
on body hair, pierces skin and eats blood
|
|
|
what do scabies do?
|
burrow, lay eggs under skin
|
|
|
how are arthropods transmitted?
|
sex, contact with hair clothing bedding
|
|
|
what do arthorpods cause?
|
itching
|
|
|
how can arthropods be treated?
|
insecticidal lotion/shampoo, cleaning all bedding and lcothes
|
|
|
what are characteristics of prokaryote bacteria?
|
no nucleus
still have genetic material: DNA |
|
|
how do prokaryotes reproduce?
|
asexually and rapidly
|
|
|
what are prokaryote's DNA like?
|
bacterial chormosome: one doubled stranded circular DNA molecule, plasmids: smaller circles of DNA
|
|
|
can prokaryotes exchange pieces of DNA?
|
yes
|
|
|
what is the treatment of prokaryotes?
|
target features unique to bacterial cells
|
|
|
what features of bacterial cells do treatemtns target?
|
cell wall, bacterial ribosomes
|
|
|
what is the problem of treating prokaryotes?
|
evolution of increasing resisstance.
|
|
|
what is the problem of treating prokaryotes?
|
evolution of increasing resistance.
|
|
|
how do prokaryotes evolve?
|
natural selection
due to improper or incomplete medication possible becasue of high rates of reprodcution and genetic change. |
|
|
how does genetic change in bacteria occur?
|
mutation, transformation, configuration.
|
|
|
what happens when bacteria genes mutation?
|
can spread quickly due to rapid reproduction
|
|
|
what happens when bacterial genes undergo transformation?
|
bacteria takes up naked, foreign DNA from envionrment.
|
|
|
what happens when bacteria genes undergo conjugation?
|
bacteria are temporarily joined, DNA is transferred directly from one to the other.
|
|
|
what happens when bacterial genes undergo transduction?
|
genes are carried between bacteria by viruses that infect them (phages)
|
|
|
what is the importance of genetic change in bacteria?
|
antibiotic resistance can spread
|
|
|
what is true about resistant strains?
|
they can reproduce rapidly
|
|
|
how can resistance genes spread?
|
transfer to non-resistant strains
|
|
|
what methods do resistant strains spread by and one example of each?
|
air (tuberculosis), water (cholera), food botulism and other food poisening, sexually transmitted.
|
|
|
what are examples of sexually transmitted bacterial strains?
|
syphilis, gonorrhera, chlamydia, chancroid
|
|
|
what are the stages of syphilis and when do they occur?
|
primary; weeks after infection
secondary: few months after infection tertiary: years after infection |
|
|
what happens in the primary stage?
|
chancre: crater-like sore, patient is infectious
|
|
|
what happens in second stage when patient isn't treated in the first?
|
rashes adn growths all over body surface, patient is infectious
|
|
|
what happens in the tertiary stage?
|
growths all over body and inside, cardiovascular and nervous systems affected; lethal, not infectious (germs not in skin anymore, deeper now)
|
|
|
what does mother to fetus transmission cause?
|
fetal loss or infected baby
|
|
|
how is syphilis killed?
|
heat, drying, sunlight, antibiotics
|
|
|
what is the prevalence of syphilis now?
|
low incidence, but increasing
|
|
|
when do symptoms for gonorrhea show?
|
within a week
|
|
|
what happens to males with gonorrhea?
|
urethritis, painful urination and discharge, may spread to bladder, prostate, testes
|
|
|
what happens to females with gonorrhea?
|
pelvic inflammatory disease, painful urination, discharge, might not show symptoms (could cause no treatment), may scar reproductive tract (inferitility ectopic pregnancy), may transmit to baby.
|
|
|
what happens if gonorrhea is transmitted to a baby?
|
blindness: eyes always medicated after birth (eyedrop), fetal loss or infected baby.
|
|
|
how is gonorrhea killed?
|
heat, drying, sunlight, antibiotics, cannot survive outside of body.
|
|
|
what is the prevalence of resistant strains?
|
increasing
|
|
|
what is the most common bacterial STD?
|
chlamydia
|
|
|
what are the symptoms of chlamydia?
|
often does not show symptoms, can lead to ectopic pregnancy, female infertility, PID, one version:similar to gonorreha (discharge), other versions: begins with a blister, lymph glands infected, rupture out of skin.
|
|
|
how common is chancroid?
|
not very common in USA
|
|
|
which gender is chancroid more prevalent in?
|
males
|
|
|
what is a symptom of chancroid?
|
painful genital ulcer
|
|
|
what are examples of non-living infectious diseases?
|
prions, viruses
|
|
|
waht are some characteristics of non-living infectious diseases?
|
not made up of cells, no metabolism.
|
|
|
what are some structural characteristics of prions?
|
non genetic material, made up of protein only, abnormally folded, causes other proteins to fold abnormally on contact
|
|
|
what are some examples of prions and what do they cause?
|
human CJD (Creutzfeldt-Jakob disease), scrapie in sheep is fatal, degenerative disease that affects teh nervous systems of sheep and goats.
one of several transmissible spongiform encephalopathies, bovine spongiform encephalopathy |
|
|
how are prions spread?
|
eating infected nervous systems
|
|
|
what is the problem surrounding prion spreading?
|
when cows are eating dead body parts of other animals.
|
|
|
what kind of virus is HIV?
|
retrovirus
|
|
|
Why are there so many mutations in HIV transmission?
|
reverse transcriptase is error-prone, high rate of genetic change (mutation) in HIV.
|
|
|
What does the HIV infection do?
|
destroys cells of immune system, host initially tests HIV-negative (even if virus is present)
host will not show symptoms for years eventually immune cells are not replaced enough (doesn't keep up with number being destroyed) |
|
|
what are the early symptoms of HIV?
|
flu-like (wasting syndrome, swollen lymph nodes, neurological symptoms[dementia, weakness and paralysis, pain, and burning, or tingling sensation (hands or feet)].
|
|
|
why do hosts of HIV initially test HIV-negative (even if virus is present)?
|
it has not produced antibodies against HIV
|
|
|
how long does it take for HIV to show symptoms?
|
can be years
|
|
|
when does AIDS occur?
|
when system can no longer replace enough immune cells are not replaced enough (doesn't keep up with number being destroyed)
|
|
|
what does AIDS mean?
|
host becomes susceptible to some infections etc (often one rarely found in people with healthy immune systems)
which is eventually fatal |
|
|
what are the early signs of immune failure?
|
thrush (fungal infection in the mouth)
shingles (painful rash caused by the same virus that causes chicken pox. |
|
|
what are platelets?
|
fragments of cells
|
|
|
what happens when a vessel is cut?
|
vasoconstriction, exposed connective tissue attracts platelets, injured tissue and platelets secrete clotting factors
|
|
|
what happens when exposed conenctive tissue attracts platelets?
|
secrete chemicals that attract more platelets, platelet plug is formed, inhibited by aspirin (not good when you need clotting).
|
|
|
what happens when injured tissue and platelets secrete clotting factors?
|
convert plasma proteins to a network of proteins, traps blood cells reinforces platelet plug, forms blood clot, clot is dissolved as would heals.
|
|
|
why is there a failure to clot?
|
plasma proteins or clotting factors are missing.
|
|
|
what can excessive clotting cause?
|
disrupts blood flow.
|
|
|
what are leukocytes?
|
white blood cells
|
|
|
where do leukocytes form?
|
bone marrow, most complete development in bone marrow, exception: T-lymphocytes migrate thymus and mature there
|
|
|
what are the different kinds of leukocytes?
|
neutrophils, monocytes, eosinophils, basophils, mast cells, lymphocytes.
|
|
|
what are neutrophils?
|
phagocytic especially again bacteria
|
|
|
monocytes
|
phagocytic leave blood and become macrophages and dendrite cells in body tissues; stimulate immune cells
|
|
|
eosinophils
|
control/moderate consume antibody-antigen complexes, kill parasitic worms.
|
|
|
basophils
|
release histamines during allergic reactions (as do cells in connective tissue)
dilate blood vessels and constrict airways |
|
|
mast cells
|
in connective tissue dilate blood vessels and constrict airways.
|
|
|
lymphocytes
|
natural killer cells, T and B cells
|
|
|
what is the lymphatic system
|
part of the circulatory system
|
|
|
what are the roles of the lymphatic system?
|
return excess tissue fluid to blood, transport lipids from digestive system
immunity/defense: contain lymphocytes |
|
|
lymph
|
same as tissue fluid (plasma without plasma proteins) plus foreign particles.
|
|
|
what do lymphatic capillaries do?
|
drain the interstitial fluid
|
|
|
what do lymph ducts do?
|
pass through lymph nodes
|
|
|
were do larger lymph ducts drain into?
|
large veins
|
|
|
mast cell
|
is a resident cell of several types of tissues and contains many granules rich in histamine and heparin. Although best known for their role in allergy and anaphylaxis, mast cells play an important protective role as well, being intimately involved in wound healing and defense against pathogens.[1]
|
|
|
what helps move lymph?
|
surrounding skeletal muscle contracts
inhalation, contraction of larger lymphatic vessels |
|
|
where do the primary lymphatic organs mature?
|
bone marrow and thymus
|
|
|
what are the secondary lymphatic organs?
|
sites in body where lymphocytes may come in contact with foreign cells/substances
lymph nodes, tonsils, digestive tract, spleen |
|
|
what is the structure of the lymphatic system?
|
dense network of lymphocytes and macrophages.
|
|
|
what are the roles of the lymphatic organs?
|
detect and destroy foreign cells/substances, damaged cells, cellular debris.
|
|
|
what does the spleen do?
|
removes damaged/old red blood cells.
|
|
|
what does the body defend against?
|
pathogens, toxins, abnormal cells.
|
|
|
what are the three lines of defense?
|
2 nonspecific and one specific
|
|
|
what are the nonspecific defense?
|
innate, inherited, do not depend being exposed to pathogen previously: preciese ideitty of pathogen is not important, generalized: combat several types of pathogens, first two lines of defense.
|
|
|
what is the first line of defense?
|
prevent entry to body, physical and chemical barriers
|
|
|
what is the second line of defense?
|
internal; if first line is penetrated (infection), respond to any pathogen without first determining its identity.
|
|
|
what kinds of cells etc are in second line of defense?
|
defensive cells, defensive proteins, inflammation, fever,
|
|
|
what are defensive cells?
|
phagocytes, eosinophils, natural killer cells
|
|
|
phagocytes
|
neutrophils and monocytes (macrophages) in blood extracellular fluid, peripheral lymphoid tissues
|
|
|
eosinophils
|
attack parasitic worms
|
|
|
natural killer cells
|
attack cells with abnormal surface proteins. (cancer cells, infected with virus)
secrete proteins that make target cells leaky. |
|
|
what are defensive proteins?
|
interferons, complement system
|
|
|
interferons
|
slow the spread of viruses, attract macrophages and natural killer cells, prevent viral replication in other cells.
|
|
|
complement system
|
group of at least 20 proteins whose activities enhance or complement the body's other defense mechanisms. form holes in the target cells' membranes, attracts and attaches phagocytic cells, stimulates inflammation.
|
|
|
inflammation
|
injury or infection causes basophils and mast cells to release histamines
vasodilation and increased vessel permability response is normally |
|
|
what does vasodilation during inflammation do?
|
increased blood flow to infected area: redness, heat, swelling, edema can cause pain.
brings in defenseive cells, blood clotting and defensive protein, antibodies aids in repair, removal of toxins, dead cells. |
|
|
why is the response usually short-lived?
|
healing and regeneration follow
may be chronic: need anti-inflammatory drugs cause slow down of inflammation. |
|
|
why does fever occur?
|
triggered by chemicals
temperature set point is raised end of infection set point returns to normal |
|
|
what chemicals trigger fever?
|
pyrogens
from pathogens (bacterial toxins) from white blood cells in response to infection. |
|
|
what happens when temperature set point is raised?
|
makes you feel cold
|
|
|
what are the effects of a fever?
|
increased phagocytosis and repair
reduced blood levels of iron by increased storage. |
|
|
what is iron needed for?
|
bacteria and fungi to grow
|
|
|
what happens at the end of the infection?
|
set point returns to normal (effects) sweating and cool body down.
|
|
|
what happens with excessive fever?
|
can inactivate enzymes needed for biochemical reactions within body cells.
|
|
|
what are specific defenses?
|
acquired, depend on prior exposreu to pathogen, weapons are tailor-made for specific pathogen, third line of defense.
|
|
|
what happens in the third line of defense?
|
travel in body by blood and lymph
encounter lymphoid tissues->immune response. |
|
|
what are the types of immune response?
|
antibody-mediated
cell-mediated |
|
|
what happens in antibody mediated response?
|
proteins made by b lymphocytes
defend mostly against cells infected by bacteria, viruses, foreign molecules dissolved in body fluids. |
|
|
what happens in cell mediated response?
|
t-cells: may direcly attack foreign cells or secrete proteins that coordinate the actions of b-cells, t-cells, macrophages
active against cells infected by bacteria and viruses, transplanted tissues, cancerous cells. |
|
|
what are features of immune responses?
|
specificity: b and t cells bind and respond to specific antigens
diversity: different lymphocytes have receptors for differnt antigens self-tolerance memory allows quicker response second time |
|
|
what happens with specificity?
|
b and t cells have specific antigen receptors on their surfaces which bind to specific antigens.
|
|
|
how is immune response diverse?
|
each lymphocyte has receptors for only one antigen, when a pathogen infects the body, it interacts only with the lymphocytes whose receptors are specific for the antigens it possesses,
|
|
|
what does immune response need self tolerance?
|
lymphocytes normally do not react to the body's own proteins and cells
as lymphocytes mature in bone marrow, they are exposed to the body's antigens lymphocytes whose receptors have the potential to react to "self" antigens (MHC) markers destroyed. |
|
|
what happens in antibody-mediated immunity?
|
when b-cell encounters antigen that fits its receptors-> binding
antibodies |
|
|
what does b cell binding to receptors do?
|
activates b-cell (grows and multiplies into clones)
most clones are plasma cells: secrete antibodies some clones become memory cells after infection plasma cells die. |
|
|
what are clones copies of?
|
specific to antigen that originally activated b cell.
|
|
|
what are some characteristics of plasma memory cells?
|
long-lived; basis for long-term immunity
inactive until they meet antigen again if activated, produce (antibodies (because plasma cells ready) |
|
|
what are the actions of antibodies?
|
bind to antigens, causing them to lump which is easier for phagocytosis
cover toxic portions of antigens activate complement attract phagocytes |
|
|
what happens in cell-mediated immunity?
|
t cells, helper t-cells, killer t-cells, memory t-cells, suppressor t-cells.
|
|
|
what do t-cells do in cell-mediated immunity?
|
need to help recognize antigens
activated by antigen-presenting cells:macrophages. |
|
|
what do macropahges do?
|
engulf foreign particles
display antigen fragments on their surfaces. |
|
|
what do helper t-cells do?
|
activated when presented with the correct antigen
multiply and secrete chemical signals. |
|
|
what do helper t cells cause b cells to do?
|
divide, become plasma cells, produce antibodies against that specific antigen, stimulate other t-cells and macrophages.
|
|
|
what do killer/cytotoxic t-cells do?
|
activated when presented with correct antigens and stimulated by helper t-cells. multiply and bind to cells with the correct antigens and release perforins (which cause holes in target cell membrane).
|
|
|
what do memory t-cells do?
|
do not responsd immediately to antigens, retain receptors for antigens, activated when antigen is presented again, rapidly form helper and killer cells.
|
|
|
suppressor t-cells
|
suppress immune system after antigen has been neutralized and eliminated
prevents damage to healthy self cells. the "off" switch for both lines of immune responses. |
|
|
what are examples of abnormal immune function?
|
allergies, autoimmune function
|
|
|
what are allergies?
|
exaggerated immune response to certain antigens
|
|
|
waht are autoimmune disorders?
|
body attack self.
|
|
|
what are the benefits of allergies?
|
help get rid of harmful substances, sneeze stuff out, help reduce cancer
|
|
|
high rates of allergies result of hygiene?
|
body is not exposed to antigens in early life
allergens with similar antigens as parasites parasites may reduce allergic reactions |
|
|
autoimmune disease a result of hygiene?
|
parasite infections reduce MS infections
immune system kept "too busy" to attack self. |
|
|
more autoimmune diseases in women?
|
especially if they have been pregnant
fetal antigens cross placenta mother's immune system makes antibodies that also attack her own tissues. |
|
|
autsim
|
impaired social interactions and communication
|
|
|
autism treatment and therapy?
|
educational
drug therapy complementary and alternative medicine |
|
|
autisms causes?
|
genetic
environmental: maternal complications, vaccines. |
|
|
thimerosal
|
mercury-containing preservative in a few vaccines, no link, but being eliminated/reduced.
|
|
|
MMR vaccine
|
measles, mumps, and rubella.
|
|
|
evolution
|
change in genetic (heritalbe characteristics of a population
|
|
|
natural selection
|
populations will change; organisms will be adapted
|
|
|
evolution of pathogens favored by
|
high mutation rates and gene transfer
rapid reproduction (regardless of method) selecting forces (favors evolution of certain traits) |
|
|
how do pathogens evolve?
|
ability to infect new species
escape host defenses: favored by ability to change genes for antigens. |
|
|
resistance against treatments?
|
do not cause mutation
they select against certain mutations and favor others they can act only on existing mutations. |
|
|
HIV has a high mutation rate
|
reverse transcriptase poor error correction (poor at reverse transcribing RNA-> DNA)
easily produces resistant strains wide variety of strains: difficult to treat with one drug; harder to develop vaccines. |
|
|
solutions to drug resistance in HIV
|
multiple drugs
stop drug therapy |
|
|
antibiotic resistance in bacteria
|
makes treatment more difficult
|
|
|
treatment more difficult for bacteria
|
some strains resist multiple drugs
gonorrhea, tuberculosis, malaria, MRSA |
|
|
solutions to antibiotic resistance in bacteria
|
reduce unnecessary use for viral diseases in animal feed excess hygiene.
through treatments don't finish treatment when symptoms stop. |
|
|
virulence
|
ability to harm host
|
|
|
what determines ability to harm host?
|
overcome/escape host immune system
produce new toxins |
|
|
why is virulence limited?
|
if parasite needs host to spread, should not kill host if it is able to spread.
|
|
|
what level of virulence does natural selection favor?
|
milder
|
|
|
if parasite spreads easily it can evolve?
|
to be more virulent
|
|
|
what do diseases which are more virulent rely on?
|
vectors, germs that can survive long outside body, water bone diseases, cholera, promiscousou sexual behavior.
|
|
|
how can these diseases be prevented?
|
make it harder for pathogens to spread, eliminate vectors, sanitary conditions vs. water borne diseases, change human behavior, virulent forms will decrease, milder forms will dominate, may keep viruelnt forms in check.
|
|
|
how have hosts evolved?
|
improved defenses
can lead to "evolutionary arms race" as pathogens may evolve greater virulence. |
|
|
why can't evolution of hosts go on indefinitely?
|
pathogen can not be too virulent: might kill host before it could spread.
host defenses can not be too strong: might deprive other body functions of energy. |
|
|
what does armsrace result in?
|
truce (coextistence)
|
|
|
what might the interaction between pathogen and host involve?
|
intermediate hosts
|
|
|
what are some examples of intermediate hosts?
|
may simply carry pathogens (snails)
may be vectors: transmit pathogen to humans (mosquitoes, ticks, other biting animals) |
|
|
why are diseases emerging?
|
rapidly increasing incdience, introduction to new host species, more rapid spread in existing host species.
|
|
|
what are emerging diseases facilitated by?
|
human actions, environmental change, mutation/evolution of pathogen.
|
|
|
what does human population do for diseases?
|
easier for disease to spread by contact or vecotrs: favors virulence.
larger populations lead to poor hygiene: water contamination. |
|
|
herd immunity
|
proportion of population that is not susceptible ot disease
increases with vaccination greater herd immunity limits teh spread of infectious diseases lower herd immunity increases the change tha the disease will spread from infected to susceptible. |
|
|
what are conditions in habitat disruption that favor intermediate hosts?
|
development (soil compaction, trash) means more standing water: habitat for mosquito
dams: sluggish water (snails) |
|
|
reforestation of suburbs/development near forests?
|
increase in contact with deer, exposure to deer ticks; carry agent for lyme disease.
|
|
|
travel and trade
|
aided in spread of AIDS, SARS, flu etc.
animals: livestock, pets, pests, wildlife (vectors) food ship cargo/ballast: may have transported water infected with cholera |
|
|
what will new contacts will humans do to evolution of diseases?
|
populations evolve apart, different pathogens evolve.
exposed to new diseases difficult for europeans to colonize africa |
|
|
industry
|
food contamination
abuse of antibiotics use of human tissues (which could be infected) |
|
|
lapses in public health
|
reduced immunization
reduced health care in general |
|
|
use of human tissues (which could be infected)
|
blood, organ transplants: hepatitis and AIDS
growth hormone from cows: Mad-cow disease. |
|
|
climate
|
global warming
warmer temps->greater mosquito population more intense rain: more standing water migration of tropical diseases |
|
|
el nino
|
deer mice->hantavirus
|
|
|
jump to new host
|
many diseases are zoonotic: originated from animals
|
|
|
wild animals
|
monkeys: AIDS
ebola, rabies, SARS: bats west nile: birds, get to us by mosquito |
|
|
flu virus
|
resides in wild bird populations; may infect domestic birds
some may infect pig may exchange genes with other viruses that infect mammals may gain ability to infect humans |
|
|
China
|
orignin of many epidemics
|
|
|
swine flu
|
originally thought to be a true swine flou virus that normally circulates among pigs
actually has a mix of genes from viruses taht infect birds, pigs, humans a new comination we are not immune to transmitted from huamn to respiratory route (not from pigs to humans) |
|
|
challenge of zoonoses
|
hard to eradicate because other animals are resevoirs
may not even show disease infects only humans? may pick up genes from other pahtogens in new hosts, gain virulence, resistance. |
|
|
jump between species will increase with new contacts between animals; due to
|
changing distribution of animals due to climate change and habitat disruption
human behaviors eating/touching animals, travel |
|
|
bioterrorism
|
intentional transmission of infectious disease to large numbers of people
|
|
|
bilogical weapon benefits
|
cheaper than chem or nuc
|
|
|
prevention of bioterrorism
|
monitoring outbreaks, antibiotics, vaccines
|
|
|
ideal agents
|
virulent and easily spread
|
|
|
antrax
|
bacterium
primarily disease of hoofed animals |
|
|
under proper conditions anthrax will form
|
spores, DNA condenses, cell dehydrates, spores resist heat, freezing, UV light, can survive in soil for decades, can be purified into fine powder, easily spread.
|
|
|
in host
|
spores rehydrate, divide, secrete toxins (cause and cell death)
|
|
|
types of infection from anthrax
|
skin infection
|
|
|
treatment for anthrax
|
antibiotics (not much resistance has evolved in antrhax bacterium)
|
|
|
prevention of anthrax
|
vaccine is available.
|
|
|
small pox
|
humans as host, no vectors or resevoirs, spread by close contact aerososl
|
|
|
symptoms of small pox
|
fever, skin eruptions, pustules
|
|
|
history of small pox
|
first disease for which vaccine was made, 1950 modern vaccine developed, 1967 WHO smallpox eradication program, last case 1977, 1979: WHO declares world smallpox-free
|
|
|
vaccinations for smallpox
|
stopped, greater risk than disease itself
herd immunity lost; an infection would spread rapidly no treatment availalbe; 30% fatality |
|
|
prevention of small pox
|
stockpiles: USA Russia
|
|
|
botulsim
|
associated with canned foods, bacterium grows and makes toxin only when oxygen is absent; makes resistant spores(cells shrunken and dehydrated) easily transported, may be planted in food/milk.
|
|
|
toxin prevents release of
|
Ach from neurons, leads to muscle paralysis
toxin itself can be destroyed by heat, but higher temps are needed to kill spores, binding of toxin is irreversible, antibiotics cannot remedy toxin that is already been released, high mortality, but not transmitted from person to person. |
|
|
prevention of botulsim
|
standar water treatment procedures, monitor food supply
|
|
|
other threats
|
contaminated food: e coli and salmonella (both bacteria)
|
|
|
other threats
|
contaminated water: cryptospordium (protists) and vibrio choleraie(virus)
|
|
|
low mortality from other threats spread is controlled by
|
hygiene and proper food handling/cooking.
|
