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Introduction to Antimicrobials Cheat Sheet by

Antimicrobial drugs and Antibiotics


Anti-c­ancer Drugs:
> antiba­cte­rials
> alkylating agents
> antivirals
> natural products
> antipr­otozols
> hormones
> antifu­ngals
> antime­tab­olites
> anthel­mitics (antip­ara­sitic)
Chemot­her­apeutic Agents:
Chemicals intended to be toxic to the pathogenic organism, but innocuous to the host.

Humans vs. Microo­rga­nis­ms:

Mech­anisms of Antibi­oti­cs:

Antiba­cterial Drug Targets:
1. Inhibit cell wall synthesis and function
2. Inhibit nucleic acid cell wall and function
3. Inhibit protein synthesis

> Human cells have no cell wall
> Human cells have 60S and 40S ribosomal units
> Human cells have different forms of enzymes

Diff­erent Types of Bacter­ia"


Anti­biotic Activity for Microo­rga­nis­ms:

An antibiotic that inhibits peptid­oglycan synthesis?
β-Lactam antibi­otics are bacter­iocidal and act by inhibiting the synthesis of the peptid­oglycan layer of bacterial cell walls. The final step in the synthesis of the peptid­oglycan is facili­tated by penici­lli­n-b­inding proteins (PBPs).

Normal Flora of Body:

General side effects of antibi­otics:
Severe watery diarrhea and abdominal cramps.
Allergic reaction (shortness of breath, hives, swelling of lips, face, or tongue, fainting)
Vaginal itching or discharge.
White patches on the tongue


3 ways in which resistance is spread:
1. Transfer of resistant bacteria between people
2. Transfer of resistance genes between bacteria (plasmids)
3. Transfer of resistance genes between genetic elements within bacteria (trans­posons)

Genetic determ­inants of AB resist­ance:

1. CHROMO­SOMAL DETERM­INANTS: MUTATIONS: Division may give rise to a mutation in a gene, probab­ility of a mutation causing a change in drug sensit­ivity to drug resistance can be quite high. The presence of a few mutants is not sufficient to produce resist­ance: despite the selective advantage that the resistant mutants possess, the drastic reduction of the population by the antibiotic usually enables the host’s natural defenses to prevail at least in acute, if not chronic, infect­ions. However, the outcome may not be quite so happy if the primary infection is caused by a drug-r­esi­stant strain.

2. GENE AMPLIF­ICA­TION: treatment with antibi­otics can induce an increased number of copies for pre-ex­isting resistance genes such as antibi­oti­c-d­est­roying enzymes and efflux pumps
3. EXTRAC­HRO­MOSOMAL DETERM­INANTS: PLASMIDS exist free in the cytoplasm. These are also genetic elements that can replicate indepe­nde­ntly. Plasmids that carry genes for resistance to antibi­otics (r genes) are referred to as R plasmids. Much of the drug resistance encoun­tered in clinical medicine is plasmid determ­ined. It is not known how these genes arose.

Transfer of resistance between bacter­ia:

Bioc­hemical mechanisms of resist­ance:

1. Alteration of drug-s­ens­itive or drug-b­inding site
> Mutation
2. Production of an enzyme that inacti­vates the drug
> Destru­ction or inacti­vation
3. Alteration of enzyme pathways
> Destru­ction or inacti­vation
4. Decreased accumu­lation in bacterium
> Efflux


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