TOKSISITAS SELEKTIF BAKTERIOSTATIK AKTIVITAS GRAM + / -

BAKTERIOSID
MEKANISME KERJA

RESISTENSI
KOMBINASI

PENGELOMPOKAN
PENISILIN SEFALOSPORIN KLORAMFENIKOL AMINOGLIKOSIDA

TERTRASIKLIN
MAKROLID QUINOLON SULFONAMID

PENISILIN AMOKSISILIN AMPISILIN PENISILIN G SEFALOSPORIN

SEFADROKSIL
SEFTRIAKSON SEFALOTIN KLORAMFENIKOL TIAMFENIKOL

AMINOGLIKOSIDA
STREPTOMISIN KANAMISIN

GENTAMISIN
MAKROLID

ERITROMISIN
SPIRAMISIN

QUINOLON
SIPROFLOKSASIN ENROFLOKSASIN

SULFONAMID
SULFAMERASIN SULFAGUANIDIN SULFADIMIDIN

TERTRASIKLIN
OKSITETRASIKLIN

KLORTERTRASIKLIN
DOKSISIKLIN

BEBERAPA BAKTERI YANG MENGINFEKSI IKAN DAN ANTIBIOTIK YANG DIBERIKAN

Motil Aeromonas septichemia

KLORAMFENIKOL OKSITETRASIKLIN STREPTOMISIN

Flexibacter columnaris
KLORAMFENIKOL / KLOROMISETIN TETRASIKLIN

Pseudomonas fluorescens
OKSITETRASIKLIN

Formation of columns by Columnaris Bacteria, on side of Platy fish

cases, only the use of powerful antibiotics have any real chance of saving the fish, and the one which is most commonly used in this condition with good effect is oxytetracycline.

Swollen Belly/Dropsy, Ascities/Red patches/Ulcers Goldfish with swollen belly (Dropsy) - Rosy Barb with swollen belly(Dropsy)

These symptoms are usually caused by Aeromonas hydrophila or Pseudomonas fluorescens. For dropsy, it is recommended to administer salt (rock or sea) NOT table 2-5 gram per litre depending on the fish specias, at the same same time as medicating with tetracycline. Ulcers can be treated same as above, using tetracycline and adding salt. Fish with severe ulcers should be removed an euthanised as most of the time they cannot be saved.

Mycobacterium
KANAMISIN STREPTOMISIN

Corynebactericeae
QUINOLON

Edwardsiella tarda (Enterobactericeae)

OKSITETRASIKLIN SULFAMERAZIN

Aeromonas salmonicida
SULFAMERAZIN + SULFAGUANIDIN FURAZOLIDON KLOROMISETIN OKSITETRASIKLIN

Focal ulcer associated with Mycobacterium

Granulomas were also noted in the anterior kidney, posterior kidney, in the liver and the heart. Although the nodules appear to be just under the surface of the spleen capsule, they are scattered throughout the tissue
The infection can usually be treated with a long duration antibiotic regime.

MEKANISME KERJA
MENGHAMBAT SINTESIS DINDING SEL Sefalosporin, Penisilin MENGHAMBAT SINTESIS PROTEIN Aminoglikosid, Makrolid, Tetrasiklin, Kloramfenikol

MENGHAMBAT PEMBENTUKAN MEMBRAN SEL Polimiksin

MENGHAMBAT SINTESIS DNA Rifampisin, Kuinolon MENGHAMBAT METABOLISME SEL Sulfonamid, Trimetoprim

RESISTENSI Resistensi Genetik Resistensi Non Genetik Resistensi Silang

KOMBINASI
Infeksi Campuran Etiologi Belum Jelas Efek Sinergis Memperlambat Resistensi

Peptidoglycan synthesis occurs in three stages. The first stage : Takes place in the cytoplasm, where the low-molecular-weight precursors UDPGlcAc and UDP-MurNAc-L-Ala-D-Glumeso-Dap-D-Ala-D-Ala are synthesized. A number of antimicrobial agents interfere with these early steps in cell wall biosynthesis. The second stage of cell wall synthesis is catalyzed by membranebound enzymes. The third stage of cell wall synthesis involves polymerization of the subunits and the attachment of nascent peptidoglycan to the cell wall.

Antibiotics that Affect the Function of Cytoplasmic Membranes Biologic membranes are composed basically of lipid, protein, and lipoprotein. The cytoplasmic membrane acts as a diffusion barrier for water, ions, nutrients, and transport systems. Most workers now believe that membranes are a lipid matrix with globular proteins randomly distributed to penetrate through the lipid bilayer. A number of antimicrobial agents can cause disorganization of the membrane. These agents can be divided into cationic, anionic, and neutral agents.

Antibiotics that Inhibit Nucleic Acid Synthesis

Antimicrobial agents can interfere with nucleic acid synthesis at several different levels. They can inhibit nucleotide synthesis or interconversion; they can prevent DNA from functioning as a proper template; and they can interfere with the polymerases involved in the replication and transcription of DNA. Interference with Nucleotide Synthesis A large number of agents interfere with purine and pyrimidine synthesis or with the interconversion or utilization of nucleotides. Other agents act as nucleotide analogs that are incorporated into polynucleotides.

Antimicrobial Inhibitors of Ribosome Function.

The basic structure and function of ribosomes are presented in Fig. 11-1. A number of antibacterial agents act by inhibiting ribosome function. Bacterial ribosomes contain two subunits, the 50S and 30S subunits, and it is possible to localize the action of antibiotics to one or both subunits. It is also possible to isolate the specific ribosomal proteins to which an agent binds and to isolate bacterial mutants that lack a specific ribosomal protein and therefore show resistance to a particular agent.

Drugs that Inhibit Other Biochemical Targets Both Trimethoprim and the Sulfonamides interfere with folate metabolism in the bacterial cell by competitively blocking the biosynthesis of tetrahydrofolate, which acts as a carrier of one-carbon fragments and is necessary for the ultimate synthesis of DNA, RNA and bacterial cell wall proteins. Unlike mammals, bacteria and protozoan parasites usually lack a transport system to take up preformed folic acid from their environment. Most of these organisms must synthesize folates, although some are capable of using exogenous thymidine, circumventing the need for folate metabolism.

Mechanisms of Resistance The basic mechanisms by which a microorganism can resist an antimicrobial agent are (1) to alter the receptor for the drug (the molecule on which it exerts its effect) (2) to decrease the amount of drug that reaches the receptor by altering entry or increasing removal of the drug (3) to destroy or inactivate the drug (4) to develop resistant metabolic pathways. Bacteria can possess one or all of these mechanisms simultaneously.

(A) Resistance Due to Altered Receptors -Lactam Resistance. The ability to analyze changes in receptors for -lactams by competition experiments in which [ 14C]penicillin is inhibited from binding to penicillin-binding proteins has explained a number of cases of bacterial resistance to penicillins and cephalosporins. Sulfonamide-trimethoprim Resistance. Sulfonamide can be rendered ineffective by altered or new dihydropteroic synthetase that has poor affinity for sulfonamides and preferentially binds p-aminobenzoic acid.

Quinolone Resistance. Resistance to quinolones can be caused by mutations in DNA gyrase subunits A or B, reduced outer membrane permeability in gram-negative cells (B) Resistance Due to Decreased Entry of a Drug

Tetracycline Resistance. The uptake of tetracycline by members of the Enterobacteriaceae is biphasic. In an initial energy-independent rapid phase, tetracycline binds to cell surface layers and passes by diffusion through the outer layers of the cell.

Aminoglycoside Resistance. In the most important form of aminoglycoside resistance, the compound is modified outside the cell and resistance is due partly to poor uptake of the altered compound. (C) Resistance Due to Destruction or Inactivation of a Drug Chloramphenicol Resistance. Many Gram-positive and Gram-negative bacteria, including some recently discovered H influenzae strains, are resistant to chloramphenicol because they possess the enzyme chloramphenicol transacetylate, which acetylates hydroxyl groups on the chloramphenicol structure. Acetylated chloramphenicol binds less well to the 50S ribosome.

(D) Synthesis of Resistant Metabolic Pathway The hydrolytic enzymes necessary for forming a new cell wall, and so -lactams do not lyse these bacteria. An altered hydrolytic system thus converts a bactericidal antibiotic into a bacteriostatic agent. Whether such resistance occurs in Gram-negative species is not clear. Some thymidine-requiring streptococci are not inhibited by trimethoprim and sulfonamides and so are not killed by these agents.

Combinations of Antimicrobial Agents

Antibiotics are frequently used in combination for the following reasons: (1) To treat a life-threatening infection (2) To prevent emergence of bacterial resistance (3) To treat mixed infections of aerobic and anaerobic bacteria (4) To enhance antibacterial activity (synergy) (5) To use lower doses of a toxic drug. Combined treatment is reasonable when the precise agents of a serious infection are unknown.