CLOSTRIDIUM TETANI

CLOSTRIDIUM TETANI

Morphology and Physiology-• long thin gram-positive organism that stains gram negative in old cultures• round terminal spore gives drumstick appearance• motile by peritrichous flagella• grow on blood agar or cooked meat medium with swarming• beta-hemolysis exhibited by isolated colonies• spores resist boiling for 20 minutes

PATHOGENICITY DETERMINANTS• play a role in local infection only in conjunction with other bacteria that

create suitableenvironment for their invasion• systemic-acting, plasmid-mediated A-B neurotoxin (tetanospasmin)

produced intracellularly : Mode of Action — one of most poisonous substances

• binds gangliosides in synaptic membranes (synapses of neuronal cells) and blocks release of inhibitory neurotransmitters; continuous stimulation by excitatory transmitters

• muscle spasms (spastic paralysis) (trismus )(lockjaw), risus sardonicus, opisthotonos),cardiac arrhythmias, fluctuations in blood pressure

PATHOGENESIS AND IMMUNITY

• Tetanospasmin is responsible for clinical manifestations of tetanus.

• An A-B toxin, released when the bacteria lyse.

• Subunit A is a zinc endopeptidase that acts on CNS: Inhibits release of an inhibitory mediator (e.g.,

GABA or glycine) which acts on postsynaptic spinal neurons (causing spastic paralysis).

DIAGNOSIS/ TREATMENT/ PREVENTION

• empirical diagnosis on basis of clinical manifestations• treat to prevent elaboration and absorption of toxinclean wound (debridement), control spasmsmetronidazole administered to eliminate vegetative bacteria that produce neurotoxin

• passive immunity (human tetanus immunoglobulin)• vaccination (active) as preventative antitoxin administered to

bind free tetanospasmin

Clinical Dis-eases

Foodborne botulism

Incubation period: 18-24 hrs.

Symptoms: double vision, inability to swallow, speech diffi-culty, bulbar paralysis, constipation, and abdominal pain. Bilateral descending weakness of peripheral muscle. Death occurs from respiratory paralysis or cardiac arrest. No fever. Mortality is high.

Recovery may need months to years.

Patients who recover do not develop antitoxin.

Clinical Dis-easesInfant botulism

Occurs in the first month of life. Weakness, signs of paraly-sis, C. botulinum and its toxin are found in feces. May be caused by ingestion of the bacteria or spores which grow in the gut and produce toxin.

Feeding of honey has been implicated as a possible cause.

Patients recover with supportive therapy alone.

Wound botulism

Develops from contaminated wounds.

Symptoms similar to those of food borne botulism with longer incubation time. Less GI symptoms.

Clostridium tetani Gram Stain

NOTE: Round terminal spores give cells a “drumstick” or “tennis racket” appear-ance.

Clinical Forms of Tetanus

TREATMENT

• Stomach lavage and high enemas.

• Trivalent (A, B, E) antitoxin administered intravenously promptly.

• Adequate ventilation by mechanical respirator.

PREVENTION AND CONTROL

• Spores of C. botulinum are widely distributed in soil and often contaminate vegetables, fruits etc.

• Strict regulation of commercial canning has largely reduced the danger of widespread outbreaks. The chief danger lies in home-canned foods (vegetables, smoked fish or vacuum-packed fresh fish). The cans with toxic food may swell or may show innocuous appearance.

• The risk from home-canned food can be reduced by boiling the food for 20 min.

• Children younger than 1 year should not eat honey.

SIGNS AND SYMPTOMS

• Stiffness of the neck, jaw, and other muscles, often accompanied by a grotesque, grinning expression

• Difficulty swallowing• Irritability• Uncontrollable spasms of the jaw, called lockjaw,

and neck muscles• Painful, involuntary contraction of other muscles