Streptomycin Sulfate 99% powder C21H41N7O16S Senwayer

Streptomycin Sulfate is the sulfate salt form of streptomycin, an aminoglycoside antibiotic derived from Streptomyces griseus with antibacterial property. Streptomycin sulfate binds to the S12 protein of the bacterial 30S ribosomal subunit, thereby inhibiting peptide elongation and protein synthesis, consequently leading to bacterial cell death.

Streptomycin Sulfate is a bactericidal antibiotic. It acts by interfering with normal protein synthesis.

Streptomycin has been shown to be active against most strains of the following organisms both in vitro and in clinical infection.

Brucella (brucellosis),

Calymmatobacterium granulomatis (donovanosis, granuloma inguinale),

Escherichia coli, Proteus spp., Aerobacter aerogenes, Klebsiella pneumoniae, and Enterococcus faecalis in urinary tract infections,

Francisella tularensis,

Haemophilus ducreyi (chancroid),

Haemophilus influenzae (in respiratory, endocardial, and meningeal infections - concomitantly with another antibacterial agent),

Klebsiella pneumoniae pneumonia (concomitantly with another antibacterial agent),

Mycobacterium tuberculosis,

Pasteurella pestis

Streptococcus viridans, Enterococcus faecalis (in endocardial infections - concomitantly with penicillin).

Following intramuscular injection of 1 g of streptomycin as the sulfate, a peak serum level of 25 to 50 mcg/mL is reached within 1 hour, diminishing slowly to about 50 percent after 5 to 6 hours.

Appreciable concentrations are found in all organ tissues except the brain. Significant amounts have been found in pleural fluid and tuberculous cavities. Streptomycin passes through the placenta with serum levels in the cord blood similar to maternal levels. Small amounts are excreted in milk, saliva, and sweat.

Streptomycin is excreted by glomerular filtration. In patients with normal kidney function, between 29% and 89% of a single 600 mg dose is excreted in the urine within 24 hours. Any reduction of glomerular function results in decreased excretion of the drug and concurrent rise in serum and tissue levels

Clostridium difficile associated diarrhea (CDAD) has been reported with use of nearly all antibacterial agents, including Streptomycin for Injection, and may range in severity from mild diarrhea to fatal colitis. Treatment with antibacterial agents alters the normal flora of the colon leading to overgrowth of C. difficile.

C. difficile produces toxins A and B which contribute to the development of CDAD. Hypertoxin producing strains of C. difficile cause increased morbidity and mortality, as these infections can be refractory to antimicrobial therapy and may require colectomy. CDAD must be considered in all patients who present with diarrhea following antibiotic use. Careful medical history is necessary since CDAD has been reported to occur over two months after the administration of antibacterial agents.

If CDAD is suspected or confirmed, ongoing antibiotic use not directed against C. difjicile may need to be discontinued. Appropriate fluid and electrolyte management, protein supplementation, antibiotic treatment of C difjicile, and surgical evaluation should be instituted as clinically indicated.