My Blog List

Search This Blog

Friday, July 31, 2009

MENINGITIS

Meningitis is one of the most terrifying diseases. It can be fatal in hours yet its early symptoms resemble self-limiting conditions like flu and colds…..
Meningitis is an infection of the fluid in the spinal cord and the fluid that surrounds the brain. Meningitis is usually caused by an infection with a virus, with a bacterium or even with fungi.
Common pathogens:
Meningococcus:
common organisms that cause meningitis in children.
caused by bacteria called Neisseria meningitidis.
There are several strains of Neisseria meningitidis.
Strain B causes about 75 percent of the meningococcal cases and has the highest fatality rate.
Haemophilus Influenzae type B (Hib)
is caused by haemophilus bacteria. It was once the most common form of bacterial meningitis,
one of the deadliest childhood diseases.
Pneumococcus
is caused by pneumococcus bacteria, which also cause several diseases of the respiratory system, including pneumonia.
It has a fatality rate of about 20 percent.
It also results in a higher incidence of brain damage than other forms of the disease.
How do people get it?
The most frequent cause of meningitis is the entry of microorganisms from an infection elsewhere in the body through the blood into the cerebrospinal fluid. 

Luckily, it's not easy to get meningitis. The body has natural defenses against infections - and usually even if someone comes across a virus or bacteria that can cause meningitis, the body can fight it off.

However, certain germs may outsmart the body's defenses and spread inside of the body. Some of these germs might then have the ability to infect the central nervous system, invading the meninges and causing meningitis.
Symptoms of meningitis can come on very quickly or take a couple of days to appear. Most cases of meningitis occur in the first 5 years of life, with the peak incidence between 3 and 5 months of age.
This varies with the organism and the underlying cause of the meningitis, but once the organisms have entered the cerebrospinal fluid, the body defenses cannot control their rapid growth as well as they could when the organisms were only in the bloodstream.

Once bacteria have entered the spinal fluid, the child usually shows symptoms fairly rapidly.
Complications Young children:
Babyish behavior
Forgetting recently learned skills
Reverting to bed-wetting
Babyish behavior
of MOne of the most common problems resulting from meningitis is hearing loss. Anyone who has had meningitis should take a hearing test.
Older people:
Lethargy
Recurring headaches
Difficulty in concentration
Short-term memory loss
Clumsiness
Balance problems
Depression
Other serious complications can include:

Brain damage

Epilepsy
Changes in eye sight
Bacterial meningitis can be treated with a number of effective antibiotics. It is important, however, that treatment be started early in the course of the disease. Appropriate antibiotic treatment of most common types of bacterial meningitis should reduce the risk of dying from meningitis to below 15%, although the risk is higher among the elderly.

Knowing whether meningitis is caused by a virus or a bacterium is important because of differences in the seriousness of the illness and the treatment needed.
Investigations:
Examinations of CSF by lumber puncture
blood cultures
neuroimaging studies (CT or MRI)
detection of bacterial nucleic acid by polymerase chain reaction (PCR) assay.

OTHER FLUOROQUINOLONES

Pefloxacin:
Methyl derivative of Norfloxacin
Preferred for meningeal infections
Ofloxacin:
More potent than ciprofloxacin for gram +ve & anaerobes
Also inhibit M. tuberculosis & M.leprae
Levofloxacin:
Levoisomer of of ofloxacin
Improved activity against S. pneumonae & other gram positive bacteria
Oral BA is 100 %
Indications are CA pneumonia, exacerbation of chronic bronchitis & ENT infections
Lomefloxacin:
Second generation FQ, more active against gram positive
Long half life
Sparfloxacin:
Second generation FQ
Indications are pneumonia, exacerbations of bronchitis, ENT infections, chlamydial infections
Good efficacy in TB, MAC infections in AIDS pts & leprosy
Phototoxic reactions, slight prolongations of QTc interval
Gatifloxacin:
2nd generation FQ
Indications are pneumonia, exacerbations of bronchitis, URTI & LRTI
ADR: Tachycardia, prolong QTc interval, Torsades de pointes
Discontinued in USA & UK
Drugs that prolong QTc interval are cisapride, TCA, phenothiazines class IA & III antiarrhythmics
Moxifloxacin:
2n d generation FQ
Most potent FQ against M. tuberculosis
Also prolong QTc interval
Indications are same as that of other 2nd gen. FQ

NORFLOXACIN

Primarily used for urinary, GIT & genital infection
Good for bacterial diarrhea because high conc. Are present in gut & anaerobic flora is not disturberd

CIPROFLOXACIN

Most potent first generation FQ
Broad spectrum
Spectrum: Highly susceptible bacteria are E.coli, K. pneumonae, Enterobacter, S. typhi, Shigella, proteus, N. gonorrhoea, N. meningitidis, H. influenzae, H.ducreyi, C. jejuni, Y. enterocolitica, V. cholerae
Moderately susceptible are P. aeruginosa, S. aureus, S. epidermidis, Legionella, Brucella, Listeria, B. anthracis & M. tuberculosis
Remarkable microbiological feature of FQ are:
Rapidly bactericidal activity & high potency
Long postantibiotic effect
Low chances of resistance
Protective intestinal streptococci & anaerobes are spared
Active against many beta lactam & aminoglycoside resistant bacteria
Less active at acidic pH
PK: absorbed orally, high tissue penetration is most important feature, conc. In lung, sputum, muscle, bone, prostate & phagocyte exceed that in plasma but CSF levels are lower, excreted in urine, urinary & biliary conc. Are higher than plasma
ADR:

TGI upset tendonitis & Tendon rupture: few cases have been reported. FQ caused cartilage damage in immature pups. FQ are C/I in children & during pregnancy
CNS: seizures occur at high dose d/t GABA antagonistic action
Hypersensitivity Rx:
INTERACTIONS:
Ciprofloxacin is cytochrome enzyme inhibitor, so plasma conc. of theofylline, warfarin are increased
NSAIDS may cause seizures CNS toxicity
USES:
UTI
Typhoid
Bone, soft tissue, gynecological & wound infection
Respiratory infections
Gonorrhea
Chancroid
Bacterial gastroenteritis
Gram negative septicemias
Meningitis
Tuberculosis
Prophylaxis
Conjunctivitis

Thursday, July 30, 2009

FLUOROQUINOLONES (MECHANISM)

FQ inhibit the enzyme DNA gyrase
DNA gyrase enzyme nick the ds DNA, introduces negative supercoils & then reseal the nicked ends
This is necessary to prevent excessive positive supercoiling
DNA gyrase consist of two A & two B subunits
A subunit carries out nicking of DNA, B subunit introduce negative supercoils & then A subunit reseal the strands
FQ bind to A subunit & interfere with its strand cutting & resealing function
In gram +ve bacteria, the major target of FQ action is a similar enzyme k/a Topoisomerase IV
Mammalian cell posses an enzyme k/a Topoisomerase II which has very low affinity for FQ, hence low toxicity to host cells
Mechanism of Resistance: Resistance to FQ is slow to develop
Mutation leading to production of DNA gyrase with reduced affinity to FQ

FLUOROQUINOLONES

Quinolone antimicrobials having one or more fluorine substitutions
First generation FQ have one fluoro substitution while second generation FQ have additional fluoro substitution
Second generation FQ have extended spectrum & longer half life

Tuesday, July 28, 2009

CARBAPENEM

Includes imipenem, Meropenem & Faropenem
Imipenem: Extremely potent & broad spectrum beta lactam antibiotic
Spectrum: gram positive coci, enterobacteriacae, P.aeruginosa, Listeria, as well as anaerobes like B. fragilis, cl. difficile
Resistant to most beta lactamases
It undergo rapid hydrolysis by the enzyme dehydropeptidase I located on the brush border of renal tubular cells
So it is combined with Cilastatin, a reversible inhibitor of dehydropeptidase I
ADR: GI upset, rashes & seizures at high dose
Indications: serious hospital acquired infections in neutropenic, cancer & AIDS pts
Meropenem: newer carbapenem
Not hydrolysed by renal dehydropeptidase I
Spectrum: broad spectrum similar to Imipenem
Indication: reserve drug for serious nosocomial infections caused by cephalosporin resistant bacteria
Less likely to cause seizures

MONOBACTAM

Aztreonam: Beta lactam antibiotic in which the other ring is missing
Antibacterial spectrum: gram negative enteric bacilli, H.influenzae, Pseudomonas
It does not inhibit gram positive cocci or anaerobes (spectrum resembling aminoglycoside)
Resistant to gram negative beta lactamases
Lack of cross sensitivity with other beta lactam antibiotic is important feature
So aztreonam can be used in pts allergic to Pn or cephalosporin
ADR: Rashes & rise in serum transaminase
Use : Hospital acquired infections originating from biliary, gastrointestinal & urinary tracts

TREATMENT OF TYPHOID FEVER OR ENTERIC FEVER

Typhoid fever is a systemic disease characterized by fever and abdominal pain and caused by dissemination of S. Typhi or S. Paratyphi
Diseases was initially called typhoid fever because of its clinical similarity to typhus
Typhoid fever was clearly defined pathologically as a unique illness on the basis of its association with enlarged Peyer's patches and mesenteric lymph nodes
Empirical treatment:
Ceftriaxone 1-2 g/d iv for 7-14 days
Azithromycin 1 g/d orally for 5 days
Ceftriaxone is to be preferred over FQ in children, pregnant women & in areas with FQ resistance
Fully susceptible cases:
Ciprofloxacin (First line) 500 mg BD for 5-7 days
Amoxycillin 1g TDS for 14 days
Cotrimoxazole 160/800 mg BD for 14 days
Multidrug-Resistant
Ciprofloxacin 500 mg BD (PO) for 5–7 days
Ceftriaxone 2–3 g/d (IV) for 7–14 days
Azithromycin 1 g/d (PO) for 5 days

Monday, July 27, 2009

PROPERTIES OF CEPHALOSPORINS

Bactericidal
Same mechanism of action as Penicillin, but they bind to different proteins than those which bind penicillin
Aquired resistance occurs by three mechanism
Drug tolerant e.g. alteration in PBP
Drug impermeable
Drug destroying e.g. beta lactamases or cephalosporinase
Individual cephalosporin differ in
Antibacterial spectrum
Susceptibility to beta lactamases
Pharmacokinetic properties
Local irritancy on I.m. injection
ADR
Pain after i.m. injection
Diarrhea
HT reactions
Nephrotoxicity e.g. cephaloridine
Bleeding d/t hypoprothrombinemia e.g. cefoperazone & ceftriaxone
Neutropenia & thrombocytopenia are rare side effects
Disulfiram like reaction with alcohol e.g. cefoperazone
Uses
As alternative to PnG
Respiratory, urinary & soft tissue infections
Penicillinase producing staph. Infections
Septicemia caused by gram negative organism, an aminoglycoside may be combined
Surgical prophylaxis e.g. cefazolin
Meningitis:for empical therapy, iv ceftriaxone + ampicillin or vancomycin is given, for pseudomonas meningitis, ceftazidime +gentamycin is used
PPNG: ceftriaxone is DOC for single dose therapy of PPNG
Typhoid: ceftriaxone & cefoperazone are used
Mixed aerobic anaerobic infections
Hospital acquired infections
Prophylaxis & treatment of infections in neutropenic patients

Cephalosporins

Group of semisynthetic antibiotics derived from cephalosprin -C obtained from fungus Cephalosporium
Chemically related to Pn, the nucleus consist of beta lactam ring fused to dihydrothiazine ring
Divided into four generation on the basis of chronological sequence, potency & antibacterial spectrum
First generation cephalosporins
Developed in 1960s
High activity against gram positive but weaker against gram negative bacteria
Mainly used for surgical prophylaxis
Oral: Cephalexin, Cephradine, Cefadroxil
Parenteral: Cefazolin, Cephalothin
Second generation cephalosporins
Developed subsequent to first generation
More active against gram negative organism, some members active against anaerobes but none inhibit P.aeruginosa
Oral: Cefaclor, Cefuroxim axetil
Parenteral: Cefuroxim, Cefoxitin
Third generation cephalosporins
Augmented activity against gram negative enterobacteriacae, some inhibit Pseudomonas as well
Highly resistant to beta lactamases from gram negative bacteria
Oral: Cefixime, Cefdinir,
Parenteral: Ceftriaxone, Cefotaxim, Cefoperazone,
Fourth generation cephalosporins
Developed in 1990s, antibacterial spectrum similar to 3rd generation , but is highly resistant to beta lactamases
Active against P. aeruginosa & S. aureus
Used for serious hospital acquired infections
Only parenteral
Cefepime
Cefpirome
Properties

AMOXYCILLIN

Close congener of ampicillin, similar to it in all aspects except:
Oral absorption is better, food does not interfere with absorption
Incidence of diarrhea is less
Less active against H.influenzae & Shigella
CARBOXYPENICILLINS
Carbenicillin: special feature is its activity against Pseudomonas aeruginosa & indole positive proteus which are not inhibited by PnG
PK: niether acid resistant nor penicillinase resistant, inactive orally, given by im or iv route
Use : serious infections caused by pseudomonas or proteus e.g. burn, UTI, septicemia etc
ANTIPSEUDOMONAS PENICILLINS
Carbenicillin
Ticarcillin
Piperacillin
Mezlocillin
BETA LACTAMASES INHIBITOR
Beta lactamase are family of enzymes, produced by many gram positive & negative bacteria that inactivate beta lactam antibiotic
Clavulanic acid: obtained from S. clavuligerus
It has a beta lactam ring but no antibacterial activity of its own
It inhibits a wide variety of beta lactamases
Progressive inhibitor of beta lactamases
Suicide inhibitor
It inhibits the periplasmically located Beta Lactamases enzyme in gram –ve bacteria
PK: rapid oral absorption, it is used with amoxycillin (coamoxyclav),
Uses: addition of clavulanic acid reestablishes the activity of amoxycillin against PP S. aureus but not MRSA that have altered PBP
Skin & soft tissue infections
Gonorrhea:(PPNG) Single dose amoxycillin 3g +clavulanic acid 0.5g + probenecid 1g is highly active
Sulbactam: semisynthetic beta lactamase inhibitor
Related chemically as well as in activity to clavulanic acid
Also a progressive inhibitor of beta lactamases
Less potent than clavulanic acid
Sulbactam does not induce chromosomal beta lactamases while clavulanic acid can induce some of them
Sulbactam is given parenterally
It is combined with ampicillin ( sultamicillin tosylate)
Uses: PPNG gonorrhoea
Mixed aerobic anaerobic infections
ADR: thrombophlibitis of injected vein, rashes, diarrhoea etc
TAZOBACTAM
Beta lactamase inhibitor, which is similar to sulbactam
Combined with piperacillin
Use : severe infections like peritonitis, pelvic & respiratory infections produced by beta lactamase producing bacilli

SEMISYNTHETIC PENICILLINS

Produced by chemically combining specific side chains in place of benzyl side chain of PnG
Procaine Pn & benzathine Pn are salts of PnG & not semisynthetic Pn
The aim is to overcome the shortcomings of PnG which are:
Poor oral efficacy
Susceptibility to beta lactamase
Narrow spectrum
Hypersensitivity reactions
CLASSIFICATION
Acid resistant alternative to PnG: Phenoxy methyl Pn / PnV
Penicillinase/ beta lactamase resistant Pn: Methicillin, Cloxacillin
Extended spectrum Pn
1. Amino Pn: Ampicillin, Bacampicillin, Amoxycillin
2. CarboxyPn: Carbenicillin, Ticarcillin
3.UreidoPn: Piperacillin, Mezlocillin
ANTI-staphylococcal penicillins
“semi-synthetic”
Add bulky side chains to provide
STERIC HINDRANCE
(Methicillin) - renal toxicity
Nafcillin
Oxacillin
Cloxacillin (di-clox) - oral drugs
Beta lactamases inhibitors: Clavulanic acid, Sulbactam, Tazobactam
Ampicillin:
Spectrum: all organism which are sensitive to PnG + H. influenzae, E.coli, proteus, Salmonella & Shigella
PK: not degraded by gastric juice so given orally, partly excreted in bile & reabsorbed, enterohepatic circulation occurs, primary channel of excretion is kidney
USES
UTI
RTI
Meningitis
Gonorrhoea
Typhoid fever
Bacillary desentry d/t Shigella
Cholecystitis
SABE
Septicemia & Mixed infection

Friday, July 24, 2009

Penicillin G / Benzyl Penicillin

Spectrum: narrow spectrum antibiotic, primarily against gram positive bacteria
Cocci: Streptococci (except viridans or enterococci), pneumococci,N. gonorrhoea, N. meningitidis
Bacilli: B. anthracis, C.diptherae, Clostridia, Listeria, T. pallidum, Leptospira
Pharmacokinetics: PnG is acid labile as well as thermolabile, absorption from i.m. site is rapid, reaches most body fluids, but penetration in serous cavities & CSF is poor,
nearly 60 % plasma protein bound, plasma half life is 30 min. Tubular secretion of PnG can be blocked by probenecid, higher conc. can be achieved

Local : pain, nausea, thrombophlebitis
Systemic: mental confusion, m. twitchings, convulsion & coma at high dose, bleeding d/t interference with platelet fxs,
Hypersensitivity reactions: PnG is the most common drug implicated in drug allergy
Rash, fever, itching, urticaria, wheezing, angionerotic edema, exfoliative dermatitis, anaphylaxis (rare)
HT is more common after parenteral than oral administration
Partial cross sensitivity b/w different Pn
Procaine Pn is also allergenic
A scratch or intradermal test
If a pt is aiiergic to Pn, use alternative antibiotic
Superinfections: rare with PnG
Jarisch herxheimer reaction: seen after injection of Pn in syphilitic pt. Manifestations are fever, shivering, myalgia, & vascular collapse. This is d/t release of spirochital lytic products. It does not reoccur & does not need interruption of therapy. Aspirin & sedation may be given for symptomatic relief
Uses: Streptococcal infections
Pneumococcal infections
Meningococcal infections
Gonorrhoea
Syphilis
Diptheria
Tetanus
Gas gangrene
Rare infections like leptospirosis, anthrax, actinomycois, trench mouth, ratbite fever, listeria & pasturella
Streptococcal infections
Pneumococcal infections
Meningococcal infections
Gonorrhoea
Syphilis
Diptheria
Tetanus
Gas gangrene
Rare infections like leptospirosis, anthrax, actinomycois, trench mouth, ratbite fever, listeria & pasturella

BETA LACTAM ANTIBIOTICS

Antibiotics having beta lactam ring
These include penicillins, cephalosporin, monobactam & carbapenem
Penicillin nucleus consist of fused thiazolidine & beta lactam rings to which side chains are attached through an amide linkage
Penicillin G (PnG) having a benzyl side chain is the original penicillin used clinically
The side chain of natural Pn can be split of by an amidase to produce 6 amino penicillanic acid. Other side chains can be attached to it resulting in different type of semisynthetic Pn
Mechanism of action: Beta lactam antibiotic interfere with the synthesis of bacterial cell wall
Bacterial cell wall is made up of Peptidoglycan
Peptidoglycan is composed of N acetylmuramic acid (NAM) & acetylglucosamine (NAG) which are cross linked with each other
This cross linking occurs with the help of enzyme transpeptidase
Beta lactam antibiotic inhibit the enzyme transpeptidase so that cross linking does not occur
This enzyme transpeptidase & other related proteins constitute the penicillin binding protein
This cross linking occurs with the help of enzyme transpeptidase
Beta lactam antibiotic inhibit the enzyme transpeptidase so that cross linking does not occur
This enzyme transpeptidase & other related proteins constitute the penicillin binding protein
This cross linking occurs with the help of enzyme transpeptidase
Beta lactam antibiotic inhibit the enzyme transpeptidase so that cross linking does not occur
This enzyme transpeptidase & other related proteins constitute the penicillin binding protein
This cross linking occurs with the help of enzyme transpeptidase
Beta lactam antibiotic inhibit the enzyme transpeptidase so that cross linking does not occur
This enzyme transpeptidase & other related proteins constitute the penicillin binding protein

Thursday, July 23, 2009

Failure of antimicrobial therapy

Improper selection of drug, dose, route or duration
Lack of adjuvant measures e.g. drainage of abscess, removal of renal stones, other foreign body or infected gall bladder, control of diabetes or adjustment of urinary pH in case of UTI
Late treatment
Poor host defence
Infecting organism present behind barriers

SUPERINFECTIONS

Superinfections refers to appearance of new infections as a result of antimicrobial therapy
Due to alteration in the normal microbial flora
It occurs in immunocompromised host e.g. Corticosteroid therapy, diabetes, Leukemias, malignancies, AIDS
Commonly associated with the use of broad spectrum AMA e.g. Tetracyclines

Tuesday, July 21, 2009

PREVENTION OF DUG RESISTANCE

No indiscriminate or prolonged use of antibiotic
Prefer rapidly acting & narrow spectrum AMA whenever possible
Use combination of AMA whenever prolonged therapy is undertaken e.g. TB, SABE
Infection by organism notorious for developing resistance e.g. S. aureus, E. coli, M. tuberculosis, Proteus must be treated intensively

NOBEL PRIZE IN THE FIELD OF MALARIA


In 1902, Sir Ronald Ross was awarded Nobel Prize for his pioneer work in the field of Malaria. He discovered that malaria was caused by the bite of female anopheles mosquito. He also discovered various life cycle stages of malaria parasite Plasmodium vivax

NOBEL PRIZE WINNER IN THE FIELD OF TUBERCULOSIS


Robert Koch was awarded Nobel prize in 1905 for his discoveries about tuberculosis

NOBEL PRIZE WINNERS IN FIELD OF CHEMOTHERAPY

Robert Koch was awarded Nobel Prize in Medicine in 1905 for his investigations & discoveries in relation to Tuberculosis

NOBEL PRIZE WINNERS IN MEDICINE



1928: Alexander Fleming noticed that a mould (penicillium notatum) produced a compound that inhibits bacterial growth.

1940: Florey and Chain showed that an injection of extract cured infections in mice and later in humans.

1945: Fleming, Florey and Chain were awarded a Nobel Prize for Medicine.

Monday, July 20, 2009

PROBLEMS ARISING WITH THE USE OF ANTIMICROBIALS

Toxicity A. Local B. Systemic
Hypersensitivity Reactions: It may be in the form of rashes, urticaria, fever, itching, exfoliative dermatitis, angioneurotic edema or rarely anaphylactic shock
Drug resistance: Natural or Acquired
Acquired resistance may be developed by mutation or gene transfer
Mutation is stable and heritable genetic change that occurs spontaneously and randomly among microorganisms

Mutation may be single step or mutistep
Gene transfer: from one organism to other organism occur by
Conjugation
Transduction
Transformation
Resistant organism may be of following types
Drug tolerant means that the organism has altered binding proteins so that an antimicrobial may not reach at the site of action e.g. Methicillin resistant Staphylococcus aureus (MRSA)
Drug destroying means organism is producing some enzyme that inactivate the antibiotic e.g. production of beta lactamases various bacterias
Drug impermeable means that bacteria have altered porin channels through which antibiotic enter into bacterial cell

SOURCES OF ANTIMICROBIALS

Fungi: Pn, Cephalosporin
Bacteria: Polymyxin B, Bacitracin
Actinomycetes: Aminoglycosides, Macrolides

TERMS RELATED TO ANTIMICROBIALS

Broad Spectrum: Agents which are active against more than one group or classes of microbes e.g. Tetracyclines which inhibit both gram positive as well as gram negative bacterias
Narrow Spectrum: Agents which are ative against only one group of microbes e.g. Penicillin G which is active only against gram positive bacteria
Bactericidal: Agents that kill the pathogenic microbes
Bacteriostatic: Agents which only inhibit the pathogenic microbes

MECHANISM OF ACTION

Agents that inhibit synthesis of bacterial cell walls e.g. Penicillins & Cephalosporin
Agents that act directly on the cell membrane of the microorganism, increasing permeability and leading to leakage of intracellular compounds, including detergents such as polymyxin; polyene antifungal agents (e.g., nystatin and amphotericin B) which bind to cell-wall sterols; and the lipopeptide daptomycin
Agents that disrupt function of 30S or 50S ribosomal subunits to reversibly inhibit protein synthesis, which generally are bacteriostatic (e.g., chloramphenicol, the tetracyclines, erythromycin, clindamycin, streptogramins, and linezolid)
Agents that bind to the 30S ribosomal subunit and alter protein synthesis, which generally are bactericidal (e.g., the aminoglycosides)


Agents that affect bacterial nucleic acid metabolism, such as the rifamycins (e.g., rifampin and rifabutin), which inhibit RNA polymerase, and the quinolones, which inhibit topoisomerases
Antimetabolites, including trimethoprim and the sulfonamides, which block essential enzymes of folate metabolism. There are several classes of antiviral agents
nucleic acid analogs, such as acyclovir or ganciclovir, which selectively inhibit viral DNA polymerase, and zidovudine or lamivudine, which inhibit HIV reverse transcriptase
non-nucleoside HIV reverse transcriptase inhibitors, such as nevirapine or efavirenz;
inhibitors of other essential viral enzymes, e.g., inhibitors of HIV protease or influenza neuraminidase;
fusion inhibitors such as enfuvirtide

CHEMICAL CLASSES OF ANTIMICROBIALS

Sulfonamides e.g. Dapsone
Diaminopyrimidines e.g. Trimethoprim
Quinolones e.g. Ciprofloxacin
Beta lactam antibiotic e.g. Penicillins, Cefalosporins
Tetracyclines e.g. Doxycyclines
Nitrobenzene derivative e.g. Chloramphanicol
Aminoglycosides e.g. Gentamycin
Macrolides: Erythromycin
Lincosamide: Clindamycin
Glycopeptide: Vancomycin
Oxazolidinone: Linezolid
Polypeptide : Polymyxin
Nitrofuran: Furazolidone
Nicotinic acid derivative: Isoniazid
Polyene: Nystatin
Azole: Ketoconazole
Others: Rifampin

Ideal Antibiotic

It must be able to reach the part of the human body where the infection is occurring
It should not cause the development of resistant forms of parasites

It should not produce undesirable side effects in the host such as allergic reaction, nerve damage or irritation of the kidneys and gastrointestinal tract


It should be given orally without inactivation by stomach acid, or by injection (parenterally) without binding to the blood proteins

Finally, it should have a high level of solubility in the body fluids and be possible to achieve concentrations in the tissue or blood, which are sufficiently high to inhibit or kill the infectious agent.

Antimicrobial Agents

Antimicrobial agents are among the most commonly used and misused of all drugs.
Antibiotics are antibacterial substances produced by various species of microorganisms (bacteria, fungi, and actinomycetes) that suppress the growth of other microorganisms.
The term Antimicrobial agent (AMA) is used to designate synthetic as well as naturally obtained drugs that attenuate microorganism
Chemotherapy is the treatment of systemic infections with specific drugs that selectively suppress the infecting microorganism without significantly affecting the host
Due to analogy b/w the malignant cell & the pathogenic microbes, T/t of neoplastic diseases with drugs is also called chemotherapy