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DEZINFECTANTEDErivati ai NITROFURANULUIinhiba activitatea fungilor,prin inhibarea unei serii de enzime,implicate in metabolismul aerob si anaerob al glukozei si

piruvatului,cauzind dereglarea ciclului pentozofosfatilor.

Chemical Structure of Nitrofurantoin

The antibacterial activity of nitrofurantoin may be decreased in the presence of carbonic anhydrase inhibitors and other drugs that alkalinise the urine.Antisptik.Antifungik. bactericid.

Nitrofurantoin is bactericidal in vitro to most Gram-positive and Gram-negative urinary-tract pathogens.

Chemical Structure of Furazidin

Furazidin is a nitrofuran antibacterial with properties similar to those of nitrofurantoin and is used in the treatment of urinary-tract infections.

Fenol,H2O2 , Sulfat de zinc,sol. Alcoolica de Iod,Permaganat de potasiu,Verdele de briliant.


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Antispirochetoase si Antivirotice.Antimicrobial Action

Benzylpenicillin is a beta-lactam antibiotic and has a bactericidal action against Gram-positive bacteria, Gram-negative cocci, some other Gram-negative bacteria,

spirochaetes, and actinomycetes.

Mechanism of action. It exerts its killing action on growing and dividing bacteria by inhibiting bacterial cell-wall synthesis, although the mechanisms involved are still not

precisely understood. Bacterial cell walls are held rigid and protected against osmotic rupture by peptidoglycan. Benzylpenicillin inhibits the final cross-linking stage of

peptidoglycan production by binding to and inactivating transpeptidases, penicillin-binding proteins on the inner surface of the bacterial cell membrane. However, it is now

realised that other earlier stages in cell-wall synthesis can also be inhibited. Other mechanisms involved include bacterial lysis by the inactivation of endogenous inhibitors of

bacterial autolysins.

Its action is inhibited by penicillinase and other beta-lactamases that are produced during the growth of certain micro-organisms.

Chemical Structure of Benzylpenicillin

RIMANTADIN- blocheaza patrunderea virusului in celula si eliberarea genomului viral in interiorul ei.Inhiba activitatea proteinei M virale-stopeaza procesul de penetrare in

cell.


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Chemical Structure of Rimantadine

Chemical Structure of Aciclovir

Aciclovir is active against herpes simplex virus type 1 and type 2 and against varicella-zoster virus. This activity is due to intracellular conversion of aciclovir by viral

thymidine kinase to the monophosphate with subsequent conversion by cellular enzymes to the diphosphate and the active triphosphate. This active form inhibits viral DNA

synthesis and replication by inhibiting the herpesvirus DNA polymerase enzyme as well as being incorporated into viral DNA. This process is highly selective for infected

cells. Studies in animals and in vitro have found various sensitivities but show that these viruses are inhibited by concentrations of aciclovir that are readily achieved

clinically. Herpes simplex virus type 1 appears to be the most susceptible, then type 2, followed by varicella-zoster virus.

The Epstein-Barr virus and CMV are also susceptible to aciclovir to a lesser extent. However, for CMV it does not appear to be activated by thymidine kinase and may act

via a different mechanism. Epstein-Barr virus may have reduced thymidine kinase activity but its DNA polymerase is very sensitive to inhibition by aciclovir triphosphate,

which may account for the partial activity.


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Chemical Structure of Anhydrous vidarabine

Chemical Structure of Lobucavir

Vidarabina,pirodavir,lobucavir,zidovudin,amantadina(AMOXICILINA WITH KLAVULANIC ACIDS) Interferon,

Remedii antimicotice

Chemical Structure of Nystatin A


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Mecanismul de actiune-polyene antifungal antibiotic that interferes with the permeability of the cell membrane of sensitive fungi by binding to sterols, ch iefly ergosterol. Its main

action is against Candida spp. Produs de Streptomyces noursei.

Chemical Structure of Fluconazole

Fluconazole is a triazole antifungal drug which in sensitive fungi inhibits cytochrome P450-dependent enzymes, resulting in impairment of ergosterol synthesis in fungal

cell membranes. It is active againstBlastomyces dermatitidis, Candida spp., Coccidioides immitis, Cryptococcus neoformans,Epidermophyton spp., Histoplasma

capsulatum,Microsporum spp., and Trichophyton spp. Resistance has developed in some Candida spp. following long-term prophylaxis with fluconazole, and cross-

resistance with other azoles has been reported.

Lisobac- antibacterial ,substanta activeAMIKACIN sulfata fi administrat cu Gentamicin sulfat, Amikacin is active against a similar range of organisms although it is also

reported to have some activity against Nocardia asteroides, Mycobacterium tuberculosis, and some atypical mycobacterial strains. Amikacin is not degraded by many of the common

enzymes often responsible for acquired aminoglycoside resistance. In consequence, cross-resistance with gentamicin and other aminoglycosides is infrequent and amikacin may be

effective against strains resistant to other aminoglycosides. However, resistant strains of Gram-negative bacteria and staphylococci have been reported, and it is generally reserved for

infections resistant to other aminoglycosides, although reports differ as to the extent and speed of the development of amikacin resistance where it has been widely used.

Nocardiosis-Nocardiaspp. are Gram-positive aerobic branching bacteria that cause systemic or localised infection. The principal pathogenic species in man is N.

asteroides; others includeN. brasiliensis, N. pseudobrasiliensis, andN. caviae. Localised chronic infection or actinomycetoma is described under Mycetoma ( ).

Systemic nocardiosis is primarily a lung infection and often involves abscess formation; it occurs especially in immunocompromised patients and may be disseminated with

abscesses in the brain and subcutaneous tissues.
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Chemical Structure ofAmikacin

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