Archive for the ‘Clostridium tetani’ Category
What is Clostridium tetani?
Clostridium tetani are spore-forming, anaerobic that means they live and grow in low oxygen conditions, and gram-positive bacteria. They are present in the gut of domestic animals including cattle, horses, goats and sheep, and occasionally in human, and are excreted in their feces. Naturally, the Clostridium tetani are found in soil derived from animal and human excreta, and may survive many years in the form of spores. Spores of Clostridium tetani are metabolically inactive. The bacteria form spore when nutrients are depleted. The spore contains a small amount of cytoplasm, DNA, peptidoglycan, very little water, cell membrane, and has a thick protective coat that is responsible for the high resistance of spores to heat, radiation, and chemicals. Upon exposure to appropriate nutrients, spores of Clostridium tetani germinate into active bacteria.
Mode of transmission:
Spores of Clostridium tetani are widespread in soil. The spores contaminate a wound site from soil. The ranges of injuries that may lead to development of tetanus comprise skin abrasion, pin prick, injection, puncture wound, human and animal bites, unsterile surgery, bowel surgery, unsterile division of umbilical cord, intra-uterine death, middle ear infection, and compound fracture. Spores germinate and bacteria multiply under low oxygen conditions in the wound. The bacteria remain localized in the wound but produce an exotoxin called tetanospasmin.
Disease producing Clostridium tetani:
The exotoxin tetanospasmin cause a disease called tetanus.
How Clostridium tetani causes tetanus?
The exotoxin tetanospasmin binds to motor nerve endings, then enters into the axon of nerve-cell, and is carried intra-axonally (retrograde) to the nerve-cell body in the brainstem and spinal cord. The toxin then transports across the synapse to the presynaptic terminals, where it blocks the secretion of inhibitory neurotransmitters alpha-aminobutyric acid (GABA) and glycine. When the inhibitory nerve cells are nonfunctional, the excitatory nerve cells are unopposed, leading to development of muscle rigidity and spasticity.
Clostridium tetani infection is characterized by spastic paralysis. Specific clinical symptoms include lockjaw, opisthotonus, risus sardonicus, and board like-abdominal rigidity.
- There is no microbiological or serological test for diagnosis.
- Bacteria are rarely isolated from wound site.
- Mainly diagnosed on clinical grounds.
Tetanus immunoglobulin is given to neutralize the toxin. Antibiotic penicillin is used to kill vegetative bacteria – the source of toxin. Metronidazole, clindamycin and erythromycin are alternative in penicillin allergic patient. Intravenous diazepam, midazolam, or lorazepam is used to control muscle spasm.
It is prevented by active vaccination with tetanus toxoid in childhood and every ten years interval and also need proper wound management after trauma.