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88 Cards in this Set
- Front
- Back
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Louis Pasteur
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-swan neck flask vs normal flask
-no bacteria in swan flask cus the germs couldnt get in -but if you break the neck then bacteria can get in -finally killed the idea of spontaneous generation |
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Robert Koch
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isolated anthrax
tuberculosis vibrio cholerae |
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anthrax
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-disease from cattle that can infect other mammals
-Koch took bacteria from dead cow with disease and injected it into guinea pigs and they got it -he isolated the causative agent |
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Koch's Postulates
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-microbe must be isolated from infected individual
-a healthy individual must be inoculated with the microbe and get sick -the same microbe must be recovered from the newly sick |
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Koch was the first to
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-use model organisms for experiments
-prove a direct link between bacteria and disease symptoms |
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germ theory
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diseases are caused by microorganisms
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Cholera
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-a bacterial plague
-first cholera pandemic in 1817-1823 -caused by bacteria, vibrio cholerae |
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why did cholera become a problem in the 19th century?
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industrial revolution
people moving into cities crowded housing, high density of people sanitation was poor to non existent drinking water supplies could easily be contaminated |
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John Snow
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mapped all the cases of cholera in london and traced it back to Broad Street Pump
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cholera symptoms
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watery diarrhea
severe dehydration leading to death death within hours of first symptom |
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susceptibility
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everyone but especially the very young and the very old because their stomach acidity is reduced
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treatments
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oral rehydration therapy and antibiotics
rehydration is essential |
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source of infection
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vibrio cholerae is common in salt, shellfish, freshwater
fecal contamination of water supply by those infected |
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transmission
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ingestion of contaminated food or water
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fatality rate
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25-60% if untreated
vaccines arent effective |
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how cholera kills
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1) toxin made by bacteria
2) toxin activates cAMP production 3) cAMP activated CFTR 4) CI- pumped out 5) H2O follows |
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definition of virulence factors
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-how disease causing organisms make you sick
-molecules produced and secreted by pathogens (bacteria, viruses, fungi, protozoa) |
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5 virulence factors
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-colonization of host tissues
-evasion of hosts immune response -inhibition of hosts immune response -entry into and exit out of cells -obtain nutrition from host |
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pilus
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required for bacteria to stick to cells lining to get out
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Yersinia Pestis
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bubonic plague = lymph nodes
septicemic plague = bloodstream pneumonic plague = lungs |
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vector borne diseases
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diseases that are transmitted from person to person by blood sucking animals
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Pandemics of the plague
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542 A.D. = plague of justinian
1347 = the black death 1860s= third pandemic |
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Bubonic plague symptoms (lymph nodes)
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symptoms appear suddenly
high fever painful lymph gland swelling called bubo chills ill feeling muscle pain severe headaches/seizures 50-60% mortality rate if untreated |
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septicemic plague symptoms (bloodstream)
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death may occur before symptoms show
abdominal pain blood clotting problems diarrhea fever low blood pressure nausea/vomiting organ failure 50% mortality rate |
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pneumonic plague symptoms
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severe cough
frothy, bloody sputum difficulty breathing if not treated within 18 hours, you will most likely die |
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virulence factors of yersinia pestis
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virulence plasmid
-35 genes enable bacteria to grow in the host and defeat the immune system -29 genes code for injectosome -6 genes code for Yops (proteins injected into host cells) |
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what do yops proteins do?
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block phagocytosis by macrophages and neutrophils
block signals that stimulate b and t cells induce programmed cell death of host cells |
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3 hypothesis regarding evolution of virulence
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trade off hypothesis
short sighted evolution hypothesis coincidental evolution hypothesis |
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5 steps of viral replication
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1) virus enters the cell
2) copies of the virus's genome are made 3) capsid proteins are made 4) the new virus is packaged 5) mature virus leaves the cell |
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small pox
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-made of dna, not rna
-the virus can survive outside of the body for a long time -variola major has a 30% fatality |
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smallpox symptoms
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flu-like symptoms
postules develop and form scabs scabs fall off |
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smallpox treatment
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the only treatment is supportive care
usually a 30% mortality rate 40-50% in children less than 1 years old more than 90% if hemorrhagic smallpox |
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smallpox transmission
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-people are contagious from when they get the symptoms until the scabs fall off
-bedding and clothing are contaminated with virus |
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smallpox is the greatest killer in history
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killed more people than war and other diseases
it was eradicated in 1980 |
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how were we able to eradicate smallpox?
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-effective vaccine with campaign
-it was the first disease with a vaccination developed -surveillance and containment strategy -animals cant get smallpox |
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is there a future threat of smallpox?
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-only if theres an accidental release form an official repository
-deliberate use of small pox as a military/terrorist weapon |
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R-0 rate of transmission depends on
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population density
the number of contacts the infected person has how long the person in infectious who is immune to the disease |
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smallpox inoculation
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ground scabs or postule fluid then scratched it into skin or sniffed it
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smallpox vaccination
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the cowpox virus scratched into the skin
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role of the immune system
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-to protect against invaders
-recognition: self vs nonself -response: destroy the nonself components |
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what are the 2 branches of the immune system?
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innate immunity and acquired immunity
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innate immunity
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physical and chemical attributes
antibacterial proteins phagocytosis by macrophages |
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chemical aspects of innate immunity
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we make chemicals that specifically destroy invading bacteria:
-acids -defensins -lysozyme -phospholipase |
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acids
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most bacteria are killed by the highly acidic environments
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defensins
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small anti bacterial proteins that damage the bacterial membrane
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lysozoyme
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digests peptidoglycan in cell wall of bacteria
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phospholipase
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digests bacterial plasma membrane
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acquired immunity traits
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specificity
adaptiveness self vs non self recognition memory |
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specificity
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B cells and T cells recognize specific antigens (nonself) and respond
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adaptiveness
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B and T cells recognize antigens that have never been encountered before
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self vs non self recognition
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all white blood cells can differentiate self and nonself, they only attack nonself
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memory
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B and T cells that "remember" a previously encountered antigen
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types of white blood cells
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antigen presenting cells
B lymphocytes T lymphocytes |
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antigen presenting cells
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cells like macrophages that phagocytosis
foreign cells or viruses and show other WBC that theres a foregin invader MHC = large protein on the plasma membrane, it is considered self MHC + a foreign peptide = non self |
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B lymphocytes
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produce antibodies against foreign invaders
-activated when surface bound antibody recognizes pathogen or toxin -they multiply and make many cells producing the same antibody -they secrete antibody into the blood stream |
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T lymphocytes
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activate all other immune system cells
lyse foregin cells or virally infected cells -helper t cells: key to activating immune responses -killer t cells: recognize aberrant cells and kill them |
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what happens when B and T cells are activated?
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1) they grow and divide to make many copies
2) some cells make long lived memory cells 3) the rest fight the current infection |
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Antigen Recognition
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T lymphocytes have a T cell receptor that interacts with MHC antigen
B lymphocytes have a B cell receptor that interacts with MHC antigen both use the lock and key mechanism to recognize the antigen |
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how B and T cells respond to different antigens
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-everyday we make millions of B and T cells
-those cells live about a month -theyre activated if they encounter a match to their receptor |
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vaccinations and antigens
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antigens used in vaccinations trigger a B cell response
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influenza
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a contagious respiratory illness
can be mild to severe complications can lead to death vaccines are available has an RNA genome mortality rate less than 0.1% |
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influenza symptoms
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fever
headache extreme tiredness dry cough runny nose muscle aches |
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influenza complications
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pneumonia
ear infection sinus infections |
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groups at high risk for complications
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elderly
young children pregnant women |
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influenza transmission
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respiratory transfer
examples: coughing, sneezing, touching contaminated surfaces |
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Influenza A
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infects people, birds, pigs
subtypes of HA and NA 16 know HA and 9 NA subtypes |
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Influenza B
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only in human, less severe
many strains |
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Influenza C
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infects humans and pigs
can be severe, not usually epidemic |
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why are the different strains important?
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-each strain is seen as a different pathogen by the immune system
-just cus you are protected against one strain doesnt mean that you are protected against the other strains |
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antigenic drift
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-mutations change the amino acid sequence of HA and NA
-if there are enough changes then it becomes a "new virus" -it is a slow change |
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The Influenza pandemic of 1918
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hemorrhages from mucous membranes
bleeding from ears bacterial pneumonia |
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what made the 1918 flu pandemic so deadly
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most people died from pneumonia
cytokine storm: a deadly overreaction by the immune system |
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antigenic shift
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small, key changes that changes the virus's behavior
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cytokine storm
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an exaggerated response to a highly pathogenic invader
production of inflammatory signals to immune cells high levels of cell death, fluid accumulation |
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viral reassortment
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specific to influenza viruses
possible because the viral genome is in 7 separate RNA molecules |
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H5N1
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bird flu
mortality in humans 45% mostly affects 10-19 years old |
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H1N1
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swine flu
waves of infection in spring/summer/fall unlike the normal flu that infects in the winter |
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H7N9
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bird flu
mortality 27% the virus could unergo reassortment and be able to be easily transmitted from human to human |
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Irish potato blight
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in 1840 the population in ireland was either entirely dependent or heavily dependent on potatoes for food
about 1 million died from famine and 2 million emigrated to the US or canada |
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what made the conditions so bad in ireland?
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absentee landowners
rent collectors with carte blanche power land subdivided into small plots land with poor rocky soil so only potatoes grew unusually cool and wet weather in the summer of 1845-49 |
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late blight
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is a fungus
spores of the fungus germinate on the leaves and invade the plant tissue 50% or more of the potato crops can be lost and the infected potatoes must be used right away instead of storing them for the winter |
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Colony collapse disorder (CCD) bees
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honey bees are disappearing
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if no bees, what would we eat?
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wheat, corn, rice
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if no bees, what would we wear?
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not linen or cotton
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symptoms of CCD
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the bees will suddenly be gone with no accumulation of dead bees
the brood queen and a small cluster of attendants with pollen and honey will still be present no evidence of robbing or moth or beetle attack |
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possible causes of ccd
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pathogens or parasites
environmental stresses like pesticides management stresses like nutrition problems from nectar or pollen |
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neonicotinoids
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most recent evidence shows that this is the most likely cuase of disrupting honey bee navigation so the bee cant find its way back to the hive
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why do we care?
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we would have shortages on all our food
losses could be $15 billion per year |
