What is the function of each of the following bacterial structures? (match to descriptions below)
1. cytoplasmic membrane (cell membrane, plasma membrane):_____________________
2. cell wall: _____________________________________________________________
4. fimbriae/”attachment pili”:_______________________________________________
5. “sex” pilus or conjugation pilus: __________________________________________
6. flagella: ____________________________________________________________
7. chromosomal DNA:__________________________________________________
a. protect chromosomal DNA under harsh conditions
b. inhibits phagocytosis by host neutrophils, macrophages); “antiphagocytic”; helps cells stick to surfaces
c. prevents “osmotic” lysis/ cell lysis
d. helps bacteria attach to other cells or surfaces in environment
e. controls movement of substances into and out of cell
f. proteins synthesis
g. genetic information of cell; provides information for protein synthesis
h. extrachromosomal DNA; carries extra genetic information e.g. antibiotic resistance genes
i. rotates like propeller to move bacterium through environment; motility
j. permits attachment to another bacterium for transfer of DNA during” conjugation”
Bacterial Cell Walls
- Describe the structure of peptidoglycan. What is its most important function? Where in bacteria is it found?
- How do Gram-positive and gram-negative bacterial cell walls differ?
Name 2 gram-positive bacteria and 2 Gram-negative bacteria:________
- a. What is the name of the toxic molecule found in the outer membrane of gram-negative bacteria?
b. what happens when this toxic molecule is released when large amounts within a human?
4.. What is different about the structure of “Acid Fast “ cell walls? __________________________________________
5. Which “famous” pathogens have acid-fast cell walls? _____________________________
6.. Why are acid-fast bacteria AFB’s so resistant to antibiotics and so slow growing in lab cultures?
Study guide Antibiotics
1.What are antibiotics? ____________________________________________
2.Which was the first antibiotic discovered?_____________________________
3.What is the target of beta-lactam antibiotics and which processes do beta-lactam antibiotics inhibit?____________________________________________________________
4.Why do sensitive growing bacteria die in the presence of beta lactam antibiotics?
5. Name 2 specific beta-lactam antibiotics ________________________________________
6. How do bacterial ribosomes differ from eukaryotic ribosomes?
7. How do aminoglycosides (e.g. streptomycin, gentamicin), tetracyclines, macrolides/erythromycin and chloramphenicol inhibit the growth of bacteria?
8. Why aren’t human cells damaged by the antibiotics listed in the previous question?
Bio 342 Key to antibiotics and bacterial cell walls
Bacterial Cell Walls- also see bacterial cell lecture notes
Q2: Gram positive bacterial cell walls have a thick layer of peptidoglycan and no outer membrane. Gram-negative bacterial cell walls have a thin layer of peptidoglycan and a “water-repellant” outer membrane.
Q2; The toxic molecule in the outer membrane of gram-negative bacteria is LPS or lipopolysaccharide. It is also called “endotoxin”. If gram-negative bacteria are growing in a person’s blood stream, as they die, they break apart, releasing LPS/endotoxin. As a result, the person’s blood vessels dilate (increase in size) and become ”leaky”. Consequently the person’s blood pressure drops, blood flow to organs decreases and “shock” results. The person may die from this “endotoxic shock”.
Bio 342 Key to antibiotics and bacterial cell walls, continued
Q3-4. Acid Fast bacterial cell walls (acid fast bacteria=AFB) have a thick waxy layer covering the layer of peptidoglycan. It is very difficult for many substances ( example, antibiotics, antiseptics, disinfectants to penetrate this waxy layer. AFB’s include Mycobacterium tuberculosis (TB) and Mycobacterium leprae (Hansen’s Disease/leprosy)
Questions 1-5: Antibiotics
-antibiotics (literally “against life”) are “antibacterial drugs usually derived from another microbe.”
Penicillin-In 1929, Alexander Fleming was the first person to discover an antibiotic. He observed a fungus/mold called Penicillium, produced a substance, “penicillin”, which could kill the bacterium Staphylococcus aureus. Because penicillin was so difficult to extract and purify, it wasn’t until the 1940’s that it became widely available to treat people suffering from bacterial infections.
-based on its chemical structure (see handout from lecture) penicillin is called a “beta-lactam” antibiotic. We now know beta-lactam antibiotics prevent formation of “crosslinks” in the peptidoglycan of bacterial cell walls. Consequently the peptidoglycan is weakened, the cell wall weakens causing the bacterium to break open in a process called “osmotic lysis” (osmosis= movement of water; lysis= breaking open- the bacterium breaks open as water moves into it, much like a water balloon explodes when it is filled with too much water))
-Since most gram-negative bacteria are naturally resistant to penicillin (recall the “water-repellant” outer membrane of their cell wall inhibits passage of some materials such as penicillin), scientists chemically modified penicillin to create “semi-synthetic” beta-lactam antibiotics which have “broader spectrum” that is they can be used against a wide range of bacteria, both gram-positive and gram-negative. These include ampicillin, amoxicillin, oxacillin, methicillin.
Q6-7-8. Ribosomes are the sites of protein synthesis within cells. Bacterial ribosomes are smaller (70S) as compared to eukaryotic cytoplasmic ribosomes (80S; remember we humans are eukaryotes so we carry the larger 80S ribosomes). Some antibiotics such as tetracycline, chloramphenicol, erythromycin and aminoglycosides specifically bind to the bacterial 70S ribosome, inhibiting the ribosome function (these antibiotics do not bind to the larger 80S ribosomes). If we were suffering from a bacterial infection, we could take one of these antibiotics. The antibiotic would specifically inhibit bacterial protein synthesis, without stopping protein synthesis by our cells. (!)