Streptomycin Risk Summary

Risk Factor: DM
Class: ANTI-INFECTIVES / Aminoglycosides

Fetal Risk Summary

Streptomycin is an aminoglycoside antibiotic. The drug rapidly crosses the placenta into the fetal circulation and amniotic fluid, obtaining concentrations that are usually less than 50% of the maternal serum level (1,2). Early investigators, well aware of streptomycin-induced ototoxicity, were unable to observe this defect in infants exposed in utero to the agent (3,4 and 5). Eventually, ototoxicity was described in a 2 1/2-month-old infant whose mother had been treated for tuberculosis with 30 g of streptomycin during the last month of pregnancy (6). The infant was deaf with a negative cochleopalpebral reflex. Several other case reports and small surveys describing similar toxicity followed this initial report (7,8). In general, however, the incidence of congenital ototoxicity, cochlear or vestibular, from streptomycin is low, especially with careful dosage calculations and if the duration of fetal exposure is limited (9).



Except for eighth cranial nerve damage, no reports of congenital defects caused by streptomycin have been located. The Collaborative Perinatal Project monitored 50,282 mother-child pairs, 135 of whom had 1st-trimester exposure to streptomycin (10, pp. 297301). For use anytime during pregnancy, 355 exposures were recorded (10, p. 435). In neither group was evidence found to suggest a relationship to large categories of major or minor malformations or to individual defects.

In a group of 1,619 newborns whose mothers were treated for tuberculosis during pregnancy with multiple drugs, including streptomycin, the incidence of congenital defects was the same as in a healthy control group (2.34% vs. 2.56%) (11). Other investigators had previously concluded that the use of streptomycin in pregnant tuberculosis patients was not teratogenic (12).

The population-based dataset of the Hungarian Case-Control Surveillance of Congenital Abnormalities, covering the period of 19801996, was used to evaluate the teratogenicity of aminoglycoside antibiotics (parenteral gentamicin, streptomycin, tobramycin, and oral neomycin) in a study published in 2000 (13). A case group of 22,865 women who had fetuses or newborns with congenital malformations were compared to 38,151 women who had no newborns with structural defects. A total of 38 cases and 42 controls were treated with the aminoglycosides. There was one case, but no controls, treated with streptomycin (odds ratio 5.0, 95% confidence interval 0.2122.9). The investigators concluded that there was no detectable teratogenic risk for structural defects for any of the aminoglycoside antibiotics (13). They also concluded, although it was not investigated in this study, that the risk of deafness after in utero aminoglycoside exposure was small.

Breast Feeding Summary

Streptomycin is excreted into breast milk. Milk:plasma ratios of 0.51.0 have been reported (14). Because the oral absorption of this antibiotic is poor, ototoxicity in the infant would not be expected. However, three potential problems exist for the nursing infant: modification of bowel flora, direct effects on the infant, and interference with the interpretation of culture results if a fever workup is required. The American Academy of Pediatrics considers the drug to be compatible with breast feeding (15).

References

  1. Woltz J, Wiley M. Transmission of streptomycin from maternal blood to the fetal circulation and the amniotic fluid. Proc Soc Exp Biol Med 1945;60:1067.
  2. Heilman D, Heilman F, Hinshaw H, Nichols D, Herrell W. Streptomycin: absorption, diffusion, excretion and toxicity. Am J Med Sci 1945;210:57684.
  3. Watson E, Stow R. Streptomycin therapy: effects on fetus. JAMA 1948;137:15991600.
  4. Rubin A, Winston J, Rutledge M. Effects of streptomycin upon the human fetus. Am J Dis Child 1951;82:146.
  5. Kistner R. The use of streptomycin during pregnancy. Am J Obstet Gynecol 1950;60:4226.
  6. Leroux M. Existe-t-il une surdit congnitale acquise due la streptomycine? Ann Otolaryngol 1950;67:1946.
  7. Nishimura H, Tanimura T. Clinical Aspects of the Teratogenicity of Drugs. New York, NY: Excerpta Medica, 1976:130.
  8. Donald PR, Sellars SL. Streptomycin ototoxicity in the unborn child. S Afr Med J 1981;60:3168.
  9. Mann J, Moskowitz R. Plaque and pregnancy. A case report. JAMA 1977;237:18545.
  10. Heinonen OP, Slone D, Shapiro S. Birth Defects and Drugs in Pregnancy. Littleton, MA: Publishing Sciences Group, 1977.
  11. Marynowski A, Sianozecka E. Comparison of the incidence of congenital malformations in neonates from healthy mothers and from patients treated because of tuberculosis. Ginekol Pol 1972;43:7135.
  12. Lowe C. Congenital defects among children born under supervision or treatment for pulmonary tuberculosis. Br J Prev Soc Med 1964;18:146.
  13. Czeizel AE, Rockenbauer M, Olsen J, Sorensen HT. A teratological study of aminoglycoside antibiotic treatment during pregnancy. Scand J Infect Dis 2000;32:30913.
  14. Wilson JT. Milk/plasma ratios and contraindicated drugs. In Wilson JT, ed. Drugs in Breast Milk. Balgowlah, Australia: ADIS Press, 1981:79.
  15. Committee on Drugs, American Academy of Pediatrics. The transfer of drugs and other chemicals into human milk. Pediatrics 1994;93:13750.

Questions and Answers

How does Streptomycin work when it's in overdose?, If someone has Streptomycin poisoning how does the poison work? I heard that it stops blood circulation but is it true?

Streptomycin is an antibiotic given as an injection.
Its poisonous effects are damage to hearing, damage to kidney, and such toxic effects are common in old patients,.

Stopping the blood circulation means to cause death, Death can occur due to high doses and is due to bad effects on the liver and kidney.
But such a toxic dose is virtually impossible unless one injects for himself a number of vials.

But prolonged use can lead to the above damages.

Streptomycin?, can someone help by chemically detailing the structure of the molecule and the componants that characterise the molecule?

its iupac name is 5-(2,4-diguanidino-3,5,6-trihydroxy-cycl... 4-[4,5-dihydroxy-6-(hydroxymethyl)-3-met...
oxy-3-hydroxy-2-methyl-
tetrahydrofuran-3-carbaldehyde

chemaical formula- C21H39N7O12

its antibiotic drug- it binds to the 16S rRNA of the bacterial ribosome, which prevents the release of the growing protein

What are the different effects of streptomycin on gram positive and gram negative bacteria?, I'm doing an experiment looking at the different effects of steptomycin on bacilus subtilus and e.coli- and was wondering if anyone knew about how streptomycin functions- i know about protein synthesis but apparently it also affects cell walls? Thank you!

We learned how it effects protein synthesis in my medical microbiology course (and since the prof went into detail on a lot of cell wall inhibiting antibiotics, I don't think streptomycin has a great impact on cell walls):

Streptomycin stops protein synthesis by preventing the two bacterial ribosomal subunits from joining together to translate the mRNA. Since this requires the drug to enter the cells, I would assume that Gram (-) are less likely to be impacted by the antibiotic (The antibiotic must pass through transport proteins in the outer membrane/LPS of Gram - bacteria, so a mutation in this transport protein would prevent entry of the drug).

Is B. subtilis a soil bacteria? If it is, it may be less resistant to streptomycin because streptomycin is produced by soil bacteria.

Good luck

Why is streptomycin more effective than penicillin on bacillus bacteria?, My class is doing all these cool experiments for Health Day in my school and i am 'Mr.Penicillin-G' while my friend was 'Streptomycin'. Im not sure what he is and ive never heard of it, but i lost a bet saying that i'd be more effective on this bacillus megate..something bacteria.

Can anyone tell me why? Gotta say Health Day did raise my interest in all this.

Bacillus megaterium is a soil bacteria that is used for research, and is not pathogenic

In the hospital lab when an antibiotic is tested on a particular bacteria, it is plated with a series of dots with the antibiotics and you can see which ones are effective. It is called a drug sensitivity test. Sometimes one antibiotic is more effective than another. That is why they are tested. Usually other tests are done first such as gram staining. which can foretell which group of antibiotic to try. Each has its own sensitiity.

What is the antibiotic streptomycin made from?, And how does it work to help you get over an infection?
Is it the same as any antibiotic?

It is derived from the actinobacterium Streptomyces griseus. Streptomycin stops bacterial growth by damaging cell membranes and inhibiting protein synthesis. Specifically, it binds to the 16S rRNA of the bacterial ribosome, interfering with the binding of formyl-methionyl-tRNA to the 30S subunit. This prevents initiation of protein synthesis.

how much injection water should be added to dissolve 1g of streptomycin for IM injection on PTB patients? HELP?, please help me...

i need to know how much sterile water will i add to 1g of streptomycin...
it's an intramuscular injection for patients with pulmonary tuberculosis..

It's usually 2.-something mL's to re-constitute antibiotics for IM's. I know we usually use 1% Lidocaine for most antibiotics, so you may want to check into that (though you can use the sterile water instead).

Why was Tetracycline more effective than streptomycin?, We did an experiment in class, every group in the class found that tetracycline was more effective than streptomycin in inhibiting growth of E coli. Could it have been because the particular strain of e coli we used may have had a resistance to streptomycin?

both have the same mechanism inhibiting bacterial growth - they interfere with protein synthesis. A common mistake is a wrong concentration of the antibiotic in the agar - Tetracycline resistance for example is a mechanism that "pumps" the antibiotic out of the cell before it can act but after a certain treshold the pump wont be able to get enough out so the cell is inhibited - the antibiotic still works after beeing pumped out so a lot of energy of the bacteria goes in the defence and they won t grow well even when resistant

streptomycin resistance is a chemical modification (an adenylyltransferase ) and the antibiotic is destroyed (similar to the beta lactamases and penicillin derivates) so there is no stress for the bacteria

my guess is that you got a resistant strain if one plate worked very differently

also both are heat sensitive so the temperature of the agar when you added the antibiotic before pooring the plates might have been too high for the strep plates

The antibiotic streptomycin acts by binding to the bacterial ribosome.?, What process in the cell is affected? Why does this kill the bacterium and not us?

Streptomycin is an antibiotic drug, the first of a class of drugs called aminoglycosides to be discovered, and was the first antibiotic remedy for tuberculosis. It is derived from the actinobacterium Streptomyces griseus. Streptomycin stops bacterial growth by damaging cell membranes and inhibiting protein synthesis. Specifically, it binds to the 16S rRNA of the bacterial ribosome, interfering with the binding of formyl-methionyl-tRNA to the 30S subunit. This prevents initiation of protein synthesis. Humans have structurally different ribosomes from bacteria, thereby allowing the selectivity of this antibiotic for bacteria. Streptomycin cannot be given orally, but must be administered by regular intramuscular injection.

Where are all informations about Streptomycin, an antibiotic?, I was treated with streptomycin as a child ( 11 y.o.). Later I lost my hearing. caused by this antibiotic. I would like to have the last informations about medical procedures about possible treatments.Or full information about hearing aids.

Try wedmd it's a great site with lots of medical info.

www.webmd.com

Can anyone tell me what Streptomycin and Tetracycline and E-Coli are?, No wiki stuff plz used that lot already. Thank you in advance.

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).

Tetracycline, is used to treat bacterial infections, including pneumonia and other respiratory tract infections; acne; infections of skin, genital and urinary systems; and the infection that causes stomach ulcers (Helicobacter pylori). It also may be used as an alternative to other medications for the treatment of Lyme disease and for the treatment and prevention of anthrax (after inhalational exposure). Tetracycline is in a class of medications called tetracycline antibiotics.It works by preventing the growth and spread of bacteria.Antibiotics will not work for colds, flu, or other viral infections

E. coli O157:H7 is one of hundreds of strains of the bacterium Escherichia coli. Although most strains are harmless, this strain produces a powerful toxin that can cause severe illness. E. coli O157:H7 has been found in the intestines of healthy cattle, deer, goats, and sheep.

E. coli O157:H7 was first recognized as a cause of illness in 1982 during an outbreak of severe bloody diarrhea; the outbreak was traced to contaminated hamburgers. Since then, more infections in the United States have been caused by eating undercooked ground beef than by any other food.

The combination of letters and numbers in the name of the bacterium refers to the specific markers found on its surface and distinguishes it from other types of E. coli.

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