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101 Cards in this Set
- Front
- Back
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Reservoir
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an animal, bird or an insect that normally harbors the pathogen
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3 portals of entry
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-mouth: food bourn pathogen
-respiratory tract: airborne pathogens -parental route: agents transmitted by vectors |
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immunopathogenesis
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occurs when the immune system's response to an infection damages host cells or tissue
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direct contant
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sneezing, coughing
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indirect contact
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someone sneezing on a pen, contact with fomites, horizontal transmission via vectors (mosquitoes- yellow fever, malaria; reservoir for disease organism--may not show disease symptoms)
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virulence genes
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encode factors allowing pathogen to invade host; toxins attachment proteins and capsules
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pathogenicity islands
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section of the genome--contain multiple virulence genes and often encode related functions
transferred asa block from other organisms, often flanked by phage or plasmid genes and often have GC content that is diff from rest of genome |
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infection cycle
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location, location, location
attachment --pili, adhesions, biofilms subvert host function --endotoxins hyper stimulate the host and LPS (gram neg bacteria) exotoxins (proteins that kill or damage host cells to harvest nutrients survive in the host --immune avoidance, intracellular vs. extracellular pathogens |
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biofilm
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bacteria that can attach to surfaces in bulk, play an important role in chronic infections by enabling persistent adherence and resistance to bacterial host defenses and microbial agents
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characterizing microbial diseases
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identification of pathogen important --determines method of treatment
clues of rapid identification-- symptoms, testing or specimens, and knowing patient histories so the environment and exposure to zoonotic disease reservoir |
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Staph aureus
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boils--walled off from body with fibrin, can produce toxic shock super antigen and other strains make exfoliative "scaled skin" syndrome
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MRSA (methicillin resistant s. aureus)
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horizontal transfer of drug resistant genes, evolved in environment with high levels of antibiotic (hospitals-nosocomial infections) and resistant to all drugs except vancomycin
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S. pyogenes
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necrotizing fascitis --flesh-eating, many prophages carry virulence factors
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Herpes virus
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chicken pox, shingles
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Toga virus
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rubella, aka german measles
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Paramyxovirus
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rubeola (measles)
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primary defense of respiratory tract infections
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mucociliary elevator -- dehydration increases mucous viscosity and decreases effectiveness of cilia
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pneumonia
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caused by many organisms, capsule secreted by bacteria prevents phagocytosis and thickens section of lung, visible in x ray
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enterobacterial toxin producing strains
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inject toxin via type 3 secretion system and bacteria invade epithelial mucosa (salmonella, shigella, e coli)
EIEC and shigella produce shiva toxin and blocks host protein synthesis damage endothelia, capillary damage, loss of blood and clots |
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campylobacter jejuni
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most frequent bacterial cause of diarrhea
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vibrio cholerae
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cholera
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S. aureus food poisoning
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secreted toxin is cause without infection
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Helicobacter pylori
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stomach ulcers, secrete urease and convert urea to NH4+ which neutralized stomach acid and burrows into protective mucous layer
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meningitis
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infection of membrane surrounding brain, and some bacteria cross BBB (blood brain barrier) (strep pneumonia, H. influenza, N. meningitides)
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N. meningitidis
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uses type 4 pili
dangerous from capillary to CSF once in meninges, very difficult to treat effective vaccine to capsule components |
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symptoms and diagnosis of meningitides
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fever, chills, headache, stiff neck, vomiting, and if suspect treat immediately
spinal tap is used to withdraw a small sample of spinal fluid for examination analyze CSF-- elevated white blood cells usually neutrophils and serum proteins advanced form can lead to brain damage, coma and death |
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Haemophilus influenza typeB (called Hib)
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before 1990 Hib was the leading cause of meningitis but now vaccines are given to kids as part of immunizations and have reduced numbers
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meningococcalm meningitis
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accounts for more than half of all cases in the US and there are several strains but strain B causes about 75% and has the highest fatality rate and currently no vaccine for strain B
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demography of meningococcal meningitis
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there is a belt, region across the sub-saharan Africa, 250,000 cases have occurred and 25,000 people died due to disease
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Pneumonococcal meningitis
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strep. pneumoniae, -- causes respiratory diseases including pneumonia and has a high incidence of brain damage and it is common in the back of the nose, and throat or in the upper respiratory tract, vaccine available for some strains
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group b streptococci
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called GBS is the leading cause of neonatal meningitis, no vaccine available
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e coli k1
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second leading cause of neonatal meningitis, no vaccine available
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bacillus anthracis
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causative agent is anthrax
primarily disease of animals--cattle, sheep, goats large, gram + rod, non-motile spore forming, spores in soil for more than 60 yrs human infection caused by exposure to B. anthracis spores |
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Anthrax toxin (also what is edema factor and letal factor)
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made by bacillus anthracis
two active toxins: edema factor--raises cAMP levels --causes fluid secretion and tissue swelling lethal factor--cleaves protein kinases and blacks immune system from attacking |
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virulence factors
pXO1? pXO2? |
produces lethal toxin, edema toxin, and protective antigen
inhibit immune cell function |
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virulence factors
pXO2? |
anti-phagocytic capsule
missing from Sterne strain |
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Antrax -- cutaneuos
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90% of cases
black eschar, edema 5-20% becomes systemic 20% fatality w/o treatment |
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Antrax--gastrointestinal
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ingestion of contaminated meat, 25-60% fatality
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Antrax--inhalation
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most deadly, almost always systemic
8000-1000 spores est. infectious dose bi-phasic illness until 2001, last known case in US 1976 |
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Anthrax meningitis
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extravascular haemorrhagic involvement of brain and meninges (Cardinal's cap)
fulminant and rapidly progressive deteriorating course: 75% of patients died within 24 hours of presentation |
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B. thuringiensis
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genetically closely related to B. anthracis
an insect pathogen but non-pathogenic for humans lacks the pXO1 and pXO2 plasmids |
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L11: Plague, A History
Causing agent? what are the three major plague epidemics? |
Yersinia pestis
1. Justinian Plague 2. Great Plague, or black death 3. Modern Plague |
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Yersinia Pestis
What type of bacteria? |
gram (-) rod, facultative anaerobe, non-motile, facultative intracellular pathogen, discovered 1894 during Hong Kong epidemic, Vector: flea, Reservoir: small mammals
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The Vector (Plague)
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Flea (rat flea) --31 species
facilitates transmission from reservoir to victim bacterial protein activity in the flea--blocked gut, ingested blood mixes with biofilm in esophagus --> regurgitated into host/victim |
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The Cycle of the Black Plague
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1. Flea bites infected rat
2. Bacteria multiply in flea gut 3. Flea's gut is gorged with bacteria 4. Flea bites human 5. Human is infected, gets sick, and dies |
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Bubonic plague
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infection of lymph nodes, symptoms: fever, chills, headache, seizures, swelling of lymph glads--bubo, found in groin, armpit, or neck, very painful
symptoms appear 2-5 days following exposure results from transmission of flea biting human if untreated, mortality is 50-60% |
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Septicemic plague
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infection of blood
symptoms: fever, abdominal pain, bruising, bleeding, nausea, diarrhea, vomiting, shock Fingers, toes, and nose may turn black and die Can be the first symptom of plague or result from untreated bubonic plague can be bitten by flea or handle infected animal like a cat without treatment mortality is 100% |
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Pneumonic plague
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infection of lungs
symptoms: weakness, fever, headache, shortness of breath, chest pain, cough, watery/bloody mucous transmitted by droplets, or from untreated forms of plague, most serious form of disease, can be spread person to person, untreated mortality -- 100% |
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Treatment for Plague
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antibiotics -- streptomycin, gentamycin, etc.
oxygen, fluids, and respiratory support are needed patients are to b isolated people in content have to go through antibiotic treatment |
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Mycobacterium
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acid fast bacillus--waxy membrane, high conc of mycolic acid, resistant to digestion
generally considered gram +, lack outer membrane, excludes crystal violet stain -aerobic, non-motile, generally facultative intracellular pathogen, causative agents of human disease: leprosy and tuberculosis (most common) -slow growing (15-20 hours) - slow growth and structure confer antibiotic resistance |
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Transmission of mycobacterium (for active and latent disease)
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active disease:
- bacteria released from lung tubercles by sneezing, talking, etc. - can stay in air for hrs - 10 organisms is the infection dose - infection based on: duration of contact, ventilation, immune status, virulence of bacteria latent disease--no transmission |
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Primary TB
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- bacili in respiratory alveoli
- divide in lung -engulfed by alveolar macrophages -divide until it bursts, and taken up by other macrophages, and can spread to lymph nodes, and rest of the body, over time cell mounts immune response, and 2 possible outcomes: destroys TB permanently, establishes a tubercle --> latent infection |
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Latent TB
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9/10 infected never developed active Tb (x rays remain negative)
immune cells (macrophages) form shell around bacillus called a granuloma -- eventually calcified slows bacterial replication, but bacteria persists and immune system works, active TB will not develop |
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Active TB
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immune system cannot keep infection in check
inactivated macrophages recruited to granuloma tubercle grows and infiltrates bronchus or artery for unknown reason granuloma center liquifies, spreads further into lung respiratory failure |
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Prevention against Mycobacterium
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Vaccine BCG --80% protection, PPD false +, effective on kids, not done in U.S.
Adequate ventilation Limit contant w/ patients, wear masks Preventative treatment for those in contact with infected people Identify and treat infection--PPD, X ray or sputum test, and long term antibiotics |
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Treatment for TB
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combinatorial therapy (less chance of mutation, different modes of action), latent TB or Tb exposure (+PPD) --alternative Rifampin, active TB infection--4 meds for 2 months, continue treatment 4-9 months, can be longer of antibiotic resistant, direct observed therapy
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L13: Antibiotic discovery -- who discovered and who rediscovered penicillin?
What is penicillin? |
-usefulness of molds known to ancients
-alexander fleming-discovered penicillin 1929 -Howard Florey rediscovered penicillin 1940 -penicillin: produced by fungi (penicillium and aspergillus) |
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Selective toxicity of antibiotics
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- antibiotic must affect bacteria not humans
- many have side effects at high concentrations - drugs should affect microbial physiology |
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Broad-spectrum antibiotics
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effective against many species
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Narrow-spectrum antibiotics
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effective against few or single species
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Source of antibiotics
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most discovered as natural products (bioprospecting), often modified by artificial means (increase efficacy, and decrease toxicity to humans)
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Bactericidal antibiotics
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many drugs only affect growing cells, kill the target organism, inhibitors of cell wall synthesis, only effective if organism is building new cell wall (LOG phase), must take antibiotic until all cells leave stationary phase
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Bacteriostatic antibiotics
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prevent growth of organism, cannot kill it, immune system removes infection
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Minimal inhibitory concentration (MIC)
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lowest concentration that prevents growth, test by diluting antibiotic
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MLC
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No colonies grew, minimal lethal concentration
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Kirby-Bauer disk test
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test strain sensitivity to multiple antibiotics, place disks on pentri dish and tell from size of cleared zones (relates to sensitivity)
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What antibiotics inhibit cell wall synthesis?
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penicillins and cephalosporins
- competitive inhibitor of cross link transpeptidation--the beta-lactam ring key feature of these compounds |
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Structure of Penicillins
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beta-lactam and thiazolidine rings
properties determined by side chains |
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Penicillin G
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sensitive to acid hydrolysis, cannot be given orally
sensitive to beta-lactamases reaction w/ serum proteins--allergic response ineffective against Gram (-) bacteria |
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Penicillin Derivatives
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ampicillin, amoxicillin -- resistant to acid hydrolysis
- broader spectrum, including gram - - higher serum levels oxacillin, dicloxacillin, methicillin - not effective against gram - - resistant to beta-lactamases due to bulky side chains |
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What inhibits protein synthesis? And how?
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macrolides, chloramphenicols, lincosamides--> bind large subunit, block transfer of peptides, erythromycin, azithromycin
aminoglycosides --> prevent 30S and 50S subunits from binding each other, streptomycin Tetracyclines-- bind small subunit and blocks binding of aminoacyl-tRNA |
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What is the growing problem, when it comes to antibiotic resistance?
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antibiotics are overused, overprescribed, exerts selective pressure for drug resistant strains, many strains become multiply drug resistant
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What are 4 mechanisms that allow bacteria to be antibiotic resistant?
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1. destroying the antibiotic - many bacteria make beta-lactamase, lowers penicillin concentration
2. modifying the antibiotic - enzymes modify amino glycosides, can no longer interfere with ribosome 3. altering the target - modify target enzyme 4. drug efflux - removes drugs from cell, multi drug resistant |
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Antibiotic resistance acquisition: Name 3.
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1. spontaneous mutation
2. enzymes to disable antibiotics 3. horizontal gene transfer |
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S. aureus MRSA: What type of infections? Name gene that causes low affinity of antibiotics, and what could treat this?
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now 35% nosocomial infections
gene mecA with low affinity for B-lactam antibiotics vancomysin is the only drug mecA on transposons acquired via horizontal gene transfer |
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The Future of Drug Discovery-- What can be done?
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- evolutionary press is constant
- use genomics - design compounds to inhibit targets - alter compounds to optimize MIC - determine spectrum of compound (narrow or broad) - determine properties, and phage therapy? |
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L14: All viruses must do the following:
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1. attach to the host cell
2. get viral genome into host cell 3. replicate genome 4. make viral proteins 5. assemble capsids 6. release progeny viruses from host cell |
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Classification of Viruses -- who came up with the classification of dsDNA vs. single stranded, and same with RNA? Also name 6 total classification today.
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Baltimore's classification: dsDNA, ssDNA, dsRNA, ssRNA+, ssRNA-, sssRNA-rt viruses, dsDNA-RT viruses
host, size and shape, DNA or RNA, presence/absence of envelope, ss or ds nucleic acid, linear or circular nucleic acid |
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All viruses must solve the following:
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how to infect host cell, how to reproduce in host cell, how to spread to new host, and how to avoid host defenses
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L15: What is an electron donor in the ETC? What is an electron acceptor?
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e- donor: NADH
e- acceptor: O2 |
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Where does ETC take place?
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Inner mitochondrial membrane
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What are the parts that make up the structure of ATPase?
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Fo portion of the membrane: C12 and where hydrogens are pumped through, then F1 portion is in the cytoplasm, and makes the ATP from hydrogens pumped through (F1 has the units b, alpha, beta, sigma, and gamma
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How many ions (H+) make one ATP?
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3 ions click to make 1 ATP
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What drives flagella rotation, and pushes ions into and out of a cell?
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The proton motive force (PMF)
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What is the purpose of the FeS centers in the oxidoreductase protein complex (part of ETC)?
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its positively charged, it acts as a magnetic so it can grab the electrons in the center of the molecule
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E. coli can have different electron donors and electron acceptors (True or False?)
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True, E. coli can have different foods, different donors and acceptors
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Anaerobic respiration
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environments that lack oxygen (gut, deep soil, deep ocean)
use other terminal e- acceptors: like nitrogen compounds (NO3- to NO2-) |
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How can bacteria break down metal? (3 steps)
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1. Bacteria reduce elemental sulfur with H2 to H2S.
2. H2S comes with Fe which gives up 2 electrons to form Fe2+. Iron reduces H2S. (take e- out of Fe, metal becomes soluble), then iron reduces sulfate 3. FeS precipitates |
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Lithotrophy
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- many materials donate electrons--- if better electron acceptor is present, iron, hydrogen, nitrogen, sulfur
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Sulfur-oxidizing archaea in hot spring, growth at pH2, it colors rocks
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Sulfolobus acidocaldarius
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Bacteria that oxidizes Cu+ to Cu2+ --dissolves metal from rock
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Thiobacillus ferrooxidans
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Methanogenesis
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- hydrogens donate e-
- CO2 can accept electrons and makes methane (CH4) Important anaerobic reaction (deep ocean, rumen of cows, sewage treatment, landfill explosions) |
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L16: What is vitamin B12 involved in?
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Metabolism -- involved in DNA synthesis, only bacteria produce this molecule and it is found in high quantities: meat eggs, dairy
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Biosynthesis overview: Name 3 things
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Building compounds requires energy (ATP)
Materials start from metabolic intermediates Expensive to maintain pathways-- takes lost of genes, may take 25 different enzymes, easily lost over evolutionary time, humans lost pathway to make vitamin C |
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CO2 fixation
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primary source of earth's fixed carbon
primary source--cyanobacteria: plant chloroplasts, anaerobic purple bacteria, lithographic bacteria one enzyme--RuBisCO: ribulose-biphosphate CO2 oxidase |
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CO2 fixation: The Calvin Cycle
What are the three steps? |
1. Carboxylation - reaction catalyzed by rubisco (5 carbons to 6 carbons, to product which is 2 three carbon molecules)
2. Reduction: requires ATP 3. Regeneration of ribulose biphosphate: creation of glucose, and uses pentose phosphate shunt |
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Nitrogen Fixation: Synthesis of what? What is it used for?
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Synthesis of amino groups
- fully reduced nitrogen and needed for amino acid synthesis (fixed N limiting for cell growth) - fixed nitrogen fertilizer now made industrially |
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Natural nitrogen fixation: what is the enzyme? 3 characteristics of the enzyme
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Enzyme: nitrogenase
- has molybdenum which is linked to Fe-S cluster - transfers e- (need electron donor) - must stay anaerobic, since O2 can be reduced |
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How many rounds of reduction are required for N2? Whats the electron donor? What is used as energy?
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4 rounds of reduction per N2
- electron donor NADH donates e- ATP energy is used to bind substrate electrons reduce substrate this is repeated 3 more times: each time 4 ATPs, 4 NADH |
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How many ATPs are consumed for each N2 fixed? Enzyme production and developmental control?
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40 ATPS consumed for each N2 fixed, and enzyme production is regulated, only make when O2 and NH4+ levels are low
Developmental control -- aerobic organisms make special cells to fix N2 |
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Nitrogen Assimilation
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Incorporation of NH4+ into amino acids
Transamination: glutamine donates NH3 to make other amino acids |
