mi 1.2

how did your predicted results compare to your observed results?

my predicted results were correct. i thought that only one strain of bacteria would grow on the plate with one antibody, none would grow on the plate with both, and both grew on the plate with none

gram positive type of toxins produced

exotoxins

based on the results of the experiment as well as what you learned about the mechanism of gene transfer between bacterial cells, was the streptomycin resistant gene transferred from strain I to strain II, or was the ampicillin resistant gene transferred from strain II to strain I?

-ampicillin resistance was transferred from strain II to strain I -ampicillin resistance is found in the plasmids, which are easier to move and replicate -streptomycin resistance is found in the chromosomal dna, which is harder to access

which antibiotic would be the most effective treatment for an infection with the b. cereus?

-b. cereus: streptomycin (20 at 24 hours, 34 at 48 hours) or chloramphenicol (26 at 24 hours, 30 at 48 hours)

why did neither strain grow on the plate containing both streptomycin and ampicillin?

-both bacteria were immune to one form of antibiotic -antibiotics still usually work on other strains, just not as effectively -e. coli I's growth was prevented by ampicillin, while e. coli II's growth was prevented by streptomycin

classify each of the tested antibiotics as limited spectrum or broad spectrum

-broad spectrum antibiotics: act against multiple strains and forms of different bacteria (similar structures) -limited spectrum antibiotics: more specific in their approach, target one certain bacteria penicillin: narrow (gram positive) ampicillin: broad streptomycin: broad tetracycline: broad chloramphenicol: broad gentamicin: broad

what was the purpose of the control disk?

-comparison -shows what no antibiotic treatment would look like

what mechanism of gene transfer do you think was responsible for transferring the antibiotic resistant gene between these two strains of bacteria?

-conjugation -close proximity -no heat shock (transformation) or virus (transduction)

which antibiotic would be the most effective treatment for an infection with the e. coli?

-e. coli: ampicillin (21 mm at both 24 and 48 hours)

propose reasons why an antibiotic may not be as effective at inhibiting e. coli as it is against b. cereus

-e. coli: gram negative -b. cereus: gram positive -different structures (cell wall especially- gram positive has more peptidoglycan, thicker wall) -different forms of antibiotics target different structures

how do antibiotics work without harming the surrounding human cells?

-eukaryotic cells (human cells) do not have cell walls -antibiotics target and attack cell walls (only present in bacteria)

why are penicillins often more effective against gram positive bacteria than gram negative bacteria?

-gram positive has one layer of cytoplasmic membrane, gram negative has 2 -harder to break through -penicillin inhibits peptidoglycan cross-linking: gram pos has lots of peptidoglycan, easier to stop

why is it important to understand the structure of a bacterial cell when developing an antibiotic?

-how to pass through structures, like cell wall, by finding flaws in the structure and composition (peptidoglycan, etc.) -enzymes and proteins (inhibit function) -if you know how a cell grows and performs its function, it is easier to stop

sue smith wants to know why she has to continue taking her antibiotics even though she is feeling better. explain the importance of sue completing her full course of antibiotics as prescribed

-least resistant strains are the first to die from antibiotics -when these strains die, the patient feels better, but the most resistant strains are still present -resistant bacteria is free to reproduce, making the frequency of hard to kill bacteria increase -bacteria has been exposed to antibiotic, can build up resistance

given what you know about antibiotics, what other variables, besides missing doses, might affect the success of an antibiotic?

-natural selection causes increasingly resistant strains of bacteria (harder to kill with antibiotics) -wrong dosages/wrong type of antibiotic for the type of bacteria (penicillin doesn't work with gram negative bacteria, etc.)

patients forgetting to take their antibiotics are not the sole cause of antibiotic resistance. explain at least two other possible causes of the development of antibiotic resistant bacteria

-natural selection, evolution, mutations, etc. -species all naturally adapt given time, could create more resistant strains -mutation could cause a trait that allows bacteria to survive better -natural selection would increase the frequency of this trait -feeding animals antibiotics -overprescription (preventative measure)

how did your results compare to the other groups' results? explain why different groups obtained different results

-our bacteria multiplied faster than most other groups -due to chance -in real life, consistently taking antibiotics isn't chance, it's a choice

what cellular components do some bacterial cells have that make them powerful pathogens?

-pili (allows structure to attach to others) -capsule (protects against foreign invaders) -endospores (resistant to environmental stress, survive harsh conditions)

how were the results after 48 hours different from the results after 24 hours?

-should be about the same -still effective

which antibiotic would be the most effective treatment for a person with an infection with both B. cereus and E. coli?

-streptomycin (e. coli: 16 at 24 hours, 15 at 48 hours; b. cereus: 20 at 24 hours, 34 at 48 hours)

why did the e. coli I strain grow on both the lb agar plate and the lb agar plate with streptomycin but not grow on the lb agar plate with ampicillin?

-the e. coli I strain was resistant to streptomycin -it can grow on plates with no antibiotics or streptomycin -it is not resistant to ampicillin, so the ampicillin killed it so it couldn't grow

explain what the results indicate about the new strain of bacteria produced when both strains of e. coli were mixed together

-the new strain inherited the other resistance in addition to its original resistance -the new strain resists both ampicillin and streptomycin

why is the clear area surrounding an antibiotic disk called the zone of inhibition?

-this is a zone around the antimicrobial disk where no growth occurs if the agent inhibits or kills the test organism -this means that if a penicillin disk is placed in a culture of n. meningitidis bacteria, the zone of inhibition is where the penicillin inhibits or prevents the bacteria from growing -the larger the zone of inhibition, the more effective the antibiotic is

why are antibiotics not effective against viruses?

-viruses have different structures and replicate differently than bacteria -target growth machinery in bacteria

what was the purpose of culturing bacteria on these four plates?

2 plates with 1 type of antibody each: find which strains of bacteria are immune to one type of antibody 2 other plates: controls to ensure the bacteria would grow in normal conditions

gram negative type of toxins produced

LPS, some exotoxins

bacterial cell parts: nucleoid

a region where most bacterial dna is found, along with some rna and proteins. it is not bounded by a membrane

plasmid

a small ring of DNA that carries accessory genes separate from those of the bacterial chromosome

antibiotic

a substance produced by or derived from a microorganism and able in dilute solution to inhibit or kill another microorganism

efflux pump

bacteria become resistant to antibiotics using a channel that actively exports antibiotics and other compounds out of the cell

destruction/inactivation

bacteria possesses genes which produce enzymes that chemically degrade or deactivate antibiotics, so that they are ineffective against bacterium

transduction process

bacterial dna is transferred from 1 bacterium to another inside of a virus (bacteriophage) that infects bacteria, phage infects a bacterium and takes over its processes to produce more phage, bacterial DNA may inadvertently be incorporated into the new phage DNA, when bacteria dies and breaks apart, the new phage goes onto infect other bacteria, bringing along genes from the previously infected that may cause the spread of certain antibiotic resistance

sulfa antibiotics (sulfonamids)

binds and inhibits an enzyme that controls cell growth (folic acid synthesis)

tetracyclines

binds to bacterial ribosomes, inhibiting protein synthesis

mutation

change in the dna that sometimes causes a change in the gene product, which is the target of the antibiotic

bacterial cell parts: plasma membrane

cytoplasmic membrane: phospholipid bilayer responsible for diffusion and transport of materials between the cell's cytoplasm and surrounding environment outer membrane: a phospholipid bilayer in gram negative bacteria only with lipopolysaccharide (lps) on the surface

fluoroquinolines

effective against DNA synthesis

transformation process

genes are transferred between bacterium as "naked" dna. when cells die and break apart, dna is released into the environment. other bacteria scavenge this dna, which may contain advantageous genes like antibiotic resistance

is n. meningitidis gram positive or gram negative?

gram negative

bacterial cell parts: pili

hollow, hairlike structures made of protein that allow bacteria to attach to other cells. sex pilus (specialized) allows for the transfer of plasmid dna

gram negative examples of bacteria from college infirmary

human gammaherpesvirus, n. meningitidis

penicillin

inhibits cell wall synthesis

gram negative outer membrane structure

lipopolysaccharide component

gram positive outer membrane structure

none

what should be prescribed to sue and why?

penicillin, because it penetrates the blood-brain barrier when the meninges are inflamed to reach the bacteria. then, it can inhibit the enzyme and stop cell wall synthesis, preventing new cells from forming and stopping the spread of disease.

gram negative bacteria cell wall structure

peptidoglycan (one layer)

gram positive bacteria cell wall structure

peptidoglycan (several layers)

conjugation process

plasmids (circular dna) replicate independently of chromosomes and carry genes resistant to antibiotics. when 2 cells are in close proximity, a hollow, bridge-like structure (pilus) forms, allowing a copy of plasmid to be transferred as it is duplicated

bacterial cell parts: ribosomes

protein synthesis takes place here. mrna is read by the ribosome and amino acids are assembled into a complete protein chain based on the rna

gram positive gram stained cell color

purple (crystal violet dye)

gram negative gram stained cell color

red (safranin counterstain)

antibiotic resistance

resistance to one or more antibiotics, usually due to additional genetic information

bacterial cell parts: plasmid

small, circular dna fragments found in the cytoplasm that contain code responsible for antibiotic resistance. can easily be transferred between bacteria

gram positive examples of bacteria from college infirmary

streptococcus pyogenes

nucleoid

the DNA-containing area of a bacterial cell

transformation

the genetic modification of a bacterium by incorporation of free DNA from another ruptured bacterial cell

conjugation

the one-way transfer of DNA between bacteria in cellular contact

transduction

the transfer of genetic material from one organism (such as a bacterium) to another by a genetic vector

bacterial cell parts: capsule

this layer of polysaccharide (sometimes proteins) protects the bacterial cell and is often associated with pathogenic bacteria because it serves as a barrier against phagocytes by white blood cells. can be seen by viewing bacteria in india ink

bacterial cell parts: endotoxins

toxins present in a bacterial cell, released when the cell disintegrates. responsible for characteristic symptoms

bacterial cell parts: flagella

used for motility. long appendages which rotate by means of a "motor" in the cell envelope. may have one, a few, or many