Terapia antibiótica en el tratamiento de las células bacterianas
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2012-07-16
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Universidad de Guayaquil. Facultad Piloto de Odontología
Resumen
El presente trabajo de investigación pretende como su nombre indica conocer los sitios de acción de los antibióticos en las células bacterianas y sus mecanismos de acción, y específicamente como actúan en el organismo ante el ataque de agentes patógenos bacterianos ya que en nuestro campo odontológico y especialmente quirúrgico el éxito de la recuperación del paciente depende en un alto porcentaje de los medicamentos y especialmente de los antibióticos que suministremos.
En nuestro campo odontológico todas las patologías están relacionadas con ataques de bacterias patógenas y de ahí nace la importancia de que el profesional adquiera un conocimiento amplio primero de la naturaleza bacteriana sobre la cual vamos a actuar para luego de haber hecho los estudios y diagnosticos para finalmente poder suministrar el antibiótico de elección que va a actuar específicamente sobre aquellas bacterias y de ahí dependerá el éxito de la recuperación ya que no se debe suministrar un antibiótico para cualquier enfermedad infecciosa.
Hay una amplia diversidad de familias y grupos de antimicrobianos de interés clínico. Los mecanismos por los que los compuestos con actividad antibacteriana inhiben el crecimiento o causan la muerte de las bacterias son muy variados, y dependen de las dianas afectadas. La pared celular puede verse afectada en la síntesis, el transporte de sus precursores o en su organización estructural (β-lactámicos, glucopéptidos).
Los principales derivados que afectan a la membrana citoplásmica son las polimixinas y la daptomicina. La síntesis proteica puede bloquearse por una amplia variedad estructural de compuestos que afectan a algunas de las fases de este proceso: activación (mupirocina), iniciación (oxazolidinonas, aminoglucósidos), fijación del complejo aminoácido-ARNt al ribosoma (tetraciclinas, glicilciclinas) o elongación (anfenicoles, lincosamidas, macrólidos, cetólidos, estreptograminas o ácido fusídico). El metabolismo de los ácidos nucleicos puede verse afectado en la ARN polimerasa dependiente de ADN (rifamicinas) o en el proceso de
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enrollamiento/desenrollamiento del ADN (quinolonas); algunos compuestos afectan directamente al ADN (nitroimidazoles, nitrofuranos). El trimetoprim y las sulfamidas (con frecuencia usados en combinación) son los representantes de los antimicrobianos que bloquean las vías metabólicas de la bacteria. Algunos compuestos, aun siendo incapaces de inhibir o matar las bacterias, pueden bloquear sus mecanismos de resistencia, por lo que usados en combinación con otros antimicrobianos potencian la acción de estos últimos; de este grupo de sustancias sólo se emplean en clínica algunos inhibidores de β-lactamasas.
Desde el punto de vista molecular, los antimicrobianos de uso clínico ejercen su acción en algunas de las siguientes estructuras o funciones bacterianas: inhibiendo la síntesis de la pared bacteriana, alterando la integridad de la membrana citoplásmica, impidiendo la síntesis proteica o bloqueando la síntesis o las funciones de ácidos nucleicos. Hay también otros antimicrobianos cuya función es proteger otros compuestos de las enzimas hidrolíticas bacterianas, como es el caso de los inhibidores de β-lactamasas.
Atendiendo a su efecto antibacteriano, los antimicrobianos se han clasificado tradicionalmente en bactericidas (ejercen una acción letal para la bacteria) o bacteriostáticos (sólo inhiben transitoriamente el crecimiento bacteriano). Los límites de ambos conceptos se consideran en la actualidad un tanto difusos, como ya se recoge en otro número de EIMC6. Cada grupo de antibióticos actúa preferentemente de una forma u otra, aunque un mismo antibiótico puede comportarse como bactericida o bacteriostático, dependiendo de la concentración que alcance en la diana, o de su afinidad por la diana de un determinado microorganismo. En general, son bactericidas los antimicrobianos que actúan inhibiendo la síntesis de la pared, alterando la membrana citoplásmica o interfiriendo con algunos aspectos del metabolismo del ADN, y bacteriostáticos los que inhiben la síntesis proteica, excepto los aminoglucósidos.
The present research aims as the name suggests know the sites of action of antibiotics in bacterial cells and their mechanisms of action, and specifically how they act in the body to attack by bacterial pathogens since our dental field and especially successful surgical patient recovery depends on a high percentage of drugs and especially antibiotics that we provide . In our dental field all pathologies are related to attacks of pathogenic bacteria and hence the importance of the professional first acquire a broad knowledge of the bacterial nature of which will act to after doing the diagnostic studies and finally born to supply the antibiotic of choice that will specifically target those bacteria and hence depend on the success of the recovery as it should not provide an antibiotic for any infectious disease. There is a wide diversity of families and groups of antimicrobials of clinical interest. The mechanisms by which the compounds with antibacterial activity inhibit the growth or kill bacteria are varied and depend on the targets affected . The cell wall may be affected in the synthesis , transport of their precursors or their structural organization ( β -lactams, glycopeptides ) . The main derivatives affecting the cytoplasmic membrane are polymyxins and daptomycin . Protein synthesis can be blocked by a broad structural variety of compounds that affect various stages of this process: activation ( mupirocin) initiation ( oxazolidinones , aminoglycosides ) , fixation of complex amino acid -tRNA to the ribosome ( tetracycline , glycylcyclines ) or elongation ( amphenicols , lincosamides , macrolides, ketolides , streptogramins and fusidic acid). The metabolism of nucleic acids can be affected by the DNA -dependent RNA polymerase ( rifamycins ) or in the process of 12 winding / unwinding of DNA ( quinolones ), some compounds directly affect the DNA ( nitroimidazoles , nitrofurans ) . Trimethoprim and sulfonamide (often used in combination) are the representatives of antimicrobials that block metabolic pathways of bacteria. Some compounds , while being unable to inhibit or kill bacteria, can block the mechanisms of resistance , so used in combination with other antimicrobial enhance the action of the latter , this group of substances are only used in clinical some inhibitors of β - lactamases. From a molecular standpoint , antimicrobials clinical use exert their action on some of the following structures or bacterial functions by inhibiting the synthesis of bacterial cell wall , altering the integrity of the cytoplasmic membrane , preventing protein synthesis or by blocking the synthesis or nucleic acid functions . There are also other antimicrobial agents whose function is to protect other compounds from bacterial hydrolytic enzymes, such as inhibitors of β -lactamases. According to their antibacterial effect , antimicrobials have traditionally been classified into bactericides ( exert a lethal action on bacteria ) or bacteriostatic ( only transiently inhibit bacterial growth ) . The boundaries of both concepts are now considered somewhat fuzzy , as stated in another number EIMC6 . Each group of antibiotics preferably acts in one way or another , but one antibiotic can behave as bacteriostatic or bactericidal , depending on the concentration to reach the target, or its affinity for the target of a particular microorganism . In general , the antimicrobials which act by inhibiting synthesis of the wall are bactericidal , altering the cytoplasmic membrane or interfering with some aspects of DNA metabolism, and bacteriostats which inhibit protein synthesis , other aminoglycosides.
The present research aims as the name suggests know the sites of action of antibiotics in bacterial cells and their mechanisms of action, and specifically how they act in the body to attack by bacterial pathogens since our dental field and especially successful surgical patient recovery depends on a high percentage of drugs and especially antibiotics that we provide . In our dental field all pathologies are related to attacks of pathogenic bacteria and hence the importance of the professional first acquire a broad knowledge of the bacterial nature of which will act to after doing the diagnostic studies and finally born to supply the antibiotic of choice that will specifically target those bacteria and hence depend on the success of the recovery as it should not provide an antibiotic for any infectious disease. There is a wide diversity of families and groups of antimicrobials of clinical interest. The mechanisms by which the compounds with antibacterial activity inhibit the growth or kill bacteria are varied and depend on the targets affected . The cell wall may be affected in the synthesis , transport of their precursors or their structural organization ( β -lactams, glycopeptides ) . The main derivatives affecting the cytoplasmic membrane are polymyxins and daptomycin . Protein synthesis can be blocked by a broad structural variety of compounds that affect various stages of this process: activation ( mupirocin) initiation ( oxazolidinones , aminoglycosides ) , fixation of complex amino acid -tRNA to the ribosome ( tetracycline , glycylcyclines ) or elongation ( amphenicols , lincosamides , macrolides, ketolides , streptogramins and fusidic acid). The metabolism of nucleic acids can be affected by the DNA -dependent RNA polymerase ( rifamycins ) or in the process of 12 winding / unwinding of DNA ( quinolones ), some compounds directly affect the DNA ( nitroimidazoles , nitrofurans ) . Trimethoprim and sulfonamide (often used in combination) are the representatives of antimicrobials that block metabolic pathways of bacteria. Some compounds , while being unable to inhibit or kill bacteria, can block the mechanisms of resistance , so used in combination with other antimicrobial enhance the action of the latter , this group of substances are only used in clinical some inhibitors of β - lactamases. From a molecular standpoint , antimicrobials clinical use exert their action on some of the following structures or bacterial functions by inhibiting the synthesis of bacterial cell wall , altering the integrity of the cytoplasmic membrane , preventing protein synthesis or by blocking the synthesis or nucleic acid functions . There are also other antimicrobial agents whose function is to protect other compounds from bacterial hydrolytic enzymes, such as inhibitors of β -lactamases. According to their antibacterial effect , antimicrobials have traditionally been classified into bactericides ( exert a lethal action on bacteria ) or bacteriostatic ( only transiently inhibit bacterial growth ) . The boundaries of both concepts are now considered somewhat fuzzy , as stated in another number EIMC6 . Each group of antibiotics preferably acts in one way or another , but one antibiotic can behave as bacteriostatic or bactericidal , depending on the concentration to reach the target, or its affinity for the target of a particular microorganism . In general , the antimicrobials which act by inhibiting synthesis of the wall are bactericidal , altering the cytoplasmic membrane or interfering with some aspects of DNA metabolism, and bacteriostats which inhibit protein synthesis , other aminoglycosides.
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FARMACOLOGIA, MICROBIOLOGIA, ANTIBIOTICOS, PENICILINAS