micro test 3- resistance

What is the natural source of cephalosporins?

Fungus Cephalosporium sp.

What is the mode of action (how they target bacteria) of - aminoglycosides, macrolides, tetracyclins, Daptomycin, Platensimycin.

Aminoglycosides - interfere with protein synthesis, targeting the 30S subunit of ribosomes, not commonly used nuero/nephro toxic (kanamycin). Macrolides - inhibit protein synthesis by targeting 50S subunit of ribosomes; contain lactone rings bonded to sugars, broad-spec (erythromycin). Tetracyclins- four rings, inhibit protein synthesis by targeting the 30S subunit of ribosomes, broad-spec. Daptomycin - treat gram + bacterial infection, forms pores in cytoplasmic membrane. Platensimycin - new structural class of antibiotic, broad-spec, effective against MRSA and vancomycin-resistant Enterococci, interferes with lipid synthesis.

Penicillins belong to the ___ group of antibiotics. Penicillin G (natural) is primarily effective against (Gram +) group of bacteria. Semisynthetic Penicillins are effective against Gram positive bacteria as well as _____.

B-lactam. Gram -.

Pathogenic fungi can be more difficult to treat compared to bacteria. Suggest a possible reason for this statement.

Because they are Eukaryotic instead of Prokaryotic.

Quinolones are effective antimicrobial agents. They interfere with the activity of the enzyme DNA gyrase. What is the function of this enzyme in bacterial cells? So can you explain how quinolones work as antimicrobial agents?

DNA gyrase is responsible for supercoil and packaging of DNA inside the bacterial cell. Effective against both Gram- + and - bacteria. Treatment for UTI's, Anthrax, TB, respiratory disease in animals

How does isoniazid inhibit bacterial growth? What bacterial types does it affect? Based on this would you say it has a narrow spectrum or a broad spectrum of activity?

Effective against Mycobacterium sps. (narrow spectrum), interferes with synthesis of mycolic acid - mycobact. Cell wall component. Important in the control of TB

What are some of the processes that are targeted by antifungal drugs?

Ergosterol inhibitors - target fungal plasma membrane component ergosterol. Echinocandins - inhibit 1,3 B-D glucan synthase (Candida). Other target chitin biosynthesis, folate biosyn., or disrupt microtubule aggregation.

What are nucleic acid analogs and how do they work as antimicrobial agents?

Formed by addition of bromine or fluorine, used to treat viral and fungal infections and as mutagen

What is the natural source (name the organism producing it) of the antibiotic penicillin?What is its mode of action? (What part of the bacterial cell does it target to destroy bacteria?)

Fungus Penicillium chrysogenum Targets cell well synthesis by preventing cross-linking of peptidoglycan

What are growth factor analogs? What is the principle behind their mode of action? (How do they work to kill cells?)

GFA - synthetic compounds structurally similar to growth factors, but sub differences don't allow functionality in the cell, they disrupt cell metabolism. Sulfa drugs and isoniazid.

How do broad spectrum antibiotics differ from narrow spectrum antibiotics?

Give one example of each. Broad spectrum effective against both groups of bacteria (tetracycline), narrow is more so one, isoniazid.

Describe the mode of action of some of the antiviral drugs discovered so far. (eg. Interfere with reverse transcriptase, protease, etc.)

Nucleoside analogs- reverse transcriptase inhibitors (NRTI, AZT). Nonnucleoside reverse transcriptase inhibitors (NNRT) - block reverse transcriptase and production of viral DNA. (Reverse transcriptase enzyme helps synthesize DNA from RNA). Protease inhibitors inhibit processing of large viral proteins into individual components. Fusion inhibitors prevent viruses from successfully fusing with the host cell. Interferons - small proteins that prevent viral multiplication by stimulating antiviral proteins in uninfected cells

Describe resistance mechanisms seen in bacteria. How are some bacteria able to overcome the effects of antibiotics?

Reduced permeability, inactivation of antibiotic, alteration of target, development of resistant biochemical pathway, efflux. Resistance can be genetically encoded by microorg. On either bacterial chromosome or on plasmid R for resistance.

Using sulfanilamide as an example, can you explain how bacterial growth is inhibited by growth factor analogs?

Sulfanilamide analog of p-Aminobenzoic acid which is needed for folic acid synthesis (nucleic acid synthesis). Sulf. Blocks synthesis of folic acid, inhibiting growth of bacteria.

Discuss why one antibiotic is not a sufficient weapon for destroying all bacterial cells

Susceptibility varies

We refer to naturally occurring antimicrobial drugs as

antibiotics