Pleuromutilins

Pleuromutilins

 Description:

Tiamulin is a semi-synthetic derivatives of pleuromutilin. Pleuromutilins are antibacterial agents that inhibit protein synthesis. They are active against Gram-positive bacteria such as streptococci and staphylococci, anaerobic bacteria and mycoplasmata.

 

Mechanism of action: Pleuromutilins act by inhibiting protein synthesis by binding to the 50S subunit of the bacterial ribosome. They are strong inhibitors of peptidyl transferase.

 

Source:
Pleuromutilin Clitopilus scyphoides  

 

Indications: Tiamulin is authorized for chickens for the treatment and prevention of chronic respiratory disease and airsacculitis caused by Mycoplasma gallisepticum and Mycoplasma synoviae; for turkeys for the treatment and prevention of infectious sinusitis and air-sacculitis caused by M. gallisepticum, Mycoplasma meleagridis and M. synoviae.

 

Dosage:
Chickens:
Turkeys:
Pigeons:
  160 to 320 mg/kg feed for poultry    
  30 to 60 mg/kg bw for 3 to 5 days in poultry    

     
 
   

 

Pharmacokinetics:

 

Contra-indications:

 

Toxicity:
None is absorbed from the GI tract so when used p.o. they are relatively
safe.

 

Resistance Resistance derives from chromosomal mutations in the 23S rRNA and rplC genes. These chromosomal mutations emerge relatively slowly and in a stepwise fashion and are not transferred horizontally.  Resistance genes can be located on plasmids or transposons like the vga genes and the cfr gene. This type of resistance is transferable between bacteria and bacterial species. The mechanism of antimicrobial resistance varies according to the bacterial species investigated.

 

Combinations
   
Drug-Drug Interctions Combined administration of tiamulin and monensin may lead to intoxication manifested in severe clinical symptoms. Tiamulin metabolite complex with cytochrome P450 has been suggested to be the basis of drug-interactions. The clinical signs, pathological and biochemical changes caused by the simultaneous application of both compounds resembled to those induced by monensin alone in high doses indicating the causative role of the ionophore or its metabolite(s) in the toxic interaction.

 

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