Clostridium

Classification of sporogenic bacteria

 Aerobic - Bacillus
 Anaerobic - Clostridium
Clostridium

 Anaerobic
 Spore forming
 Found in soil,dust,rusted materials
 Normal inhabitants of large intestine
 Form powerful exotoxins
Morphological classification

Predominantly Saccharolytic
 C. perfringens -OS
 C. septicum- OS
 C. difficile-OT
Predominantly proteolytic
 C. histolyticum OS
 C. bifermentans OC
 C. botulinum OS
Slightly Proteolytic
 C. tetani RT
Clostridia as human pathogens

 Tetanus - C. tetani
 Gas gangrene -C. perfringens C. septicum
 Food Poisoning- C. perfringens
 Antibiotic associated diarrhea and colitis -C. difficile
 Flaccid paralysis- C.botulinium
CLOSTRIDIUM TETANI
Exotoxin

 Tetanolysin: it is a haemolysin and causes lysis of red

blood cells.
 Tetanospasmin: it is a neurotoxin, and rapidly gets
destroyed by proteolytic enzymes.
Pathogenesis

 The usual mode of infection is tetanus is by

penetrating injury
 The organisms begins to produce toxin
(tetanospasmin), which binds to peripheral
motor nerve endings.
 The toxin is then internalized and travels along
the motor neurons of peripheral nerves via
retrograde intra axonal transport to the anterior
horn cells of spinal cord or brain stem depending
on nerves involved
 It interferes with the activity of the inhibitory
interneurons.
 The abolition of spinal inhibition leads to
uncontrolled spread of impulses initiated
anywhere in the central nervous system. This
results in muscle rigidity and spasms due to the
simultaneous contraction of agonists and
antagonists.
 The incubation period of 5-15 days
Clinical syndromes

 The presenting sign - spasm of the masseter

muscles ( trismus or lockjaw)
 The characteristic sardonic smile of tetanus
results from the sustained contraction of facial
muscles known as risus sardoricus.
 Other early signs include persistent back
spasms ( opisthotonos).
Clinical syndromes

 Localised tetanus is characterized by

persistent spasm of the musculature at the
site of primary infection
 Cephalic tetanus is a variant of localized
tetanus, in which the primary site of infection
is head particularly ear.
 It is associated with dysfunction of one or
more of the cranial nerves, most commonly
cranial nerve VII.
 Autonomic nervous system becomes involved
leading to sweating, hyperthermia, cardiac
arrhythmias and fluctuation in blood pressure.
 Neonatal tetanus ( tetanus neonatorum)
infection typically originates from the umbilical
stump, which then progresses to generalized
disease
Laboratory diagnosis

 Direct smear and Gram's staining may show Gram-

positive bacilli with drum-stick appearance.
 Culture
 After inoculation of nutrient agar or blood agar plate
or tube, it is placed in an air-tight jar (Mclntosh
Filde's jar) from which air is removed and replaced
by 90% hydrogen with 10% CO2.
 Liquid media like Robertson's cooked meat media
Prevention and control

 Tetanus is a fully preventable disease by

immunization with tetanus toxoid
Active immunization

 6-8 weeks of age-by DPT vaccine containing

diphtheria toxoid, pertussis vaccine and
tetanus toxoid, A full course of immunization
confers immunity for 7 to 10 years.
 A booster injection of toxoid is given after 5
years on entry into school and thereafter
booster dose is given every 7 to 10 years.
Combined immunization

 In emergency after an injury it is ideal to

immunize the individual with tetanus toxoid in
one arm along with administration of 1500
I.U. of ATS or 250 units of HTIG in another
arm. The other doses of toxoid are injected at
appropriate intervals.
CLOSTRIDIUM BOTULINUM

 Morphology
Determinants of Pathogenecity

 Toxins A -F are neurotoxins that interfere with

the neurotransmission at the peripheral
cholinergic synapses and thereby prevent the
release of acetyl choline leading to flaccid
paralysis.
 Type A toxin is most potent and toxic
Pathogenicity

 Produce the most lethal poison, namely

botulinum neurotoxin
 Preformed toxin in food.
 The toxin after absorption from intestine (or
wound) reaches the peripheral cholinergic
synapses through the circulation.
 Acts by blocking release of acetylcholine at
synapses and neuromuscular junctions.
 Flaccid paralysis- first affects the cranial
nerves (diplopia, dysphagia, flaccid facial
expression) and progresses centripetally
( weakness of peripheral muscles, urinary
retention), eventually respiratory paralysis
 Botulism is of three types – foodborne, infant and
wound botulism.
 Food borne botulism: It is a life threatening
paralytic disease of intoxication caused by
ingestion of preformed toxin in food contaminated
with C. botulinum.
 consumption of contaminated food -usually home-
canned vegetables preserved at an alkaline pH.
 Infant botulism
 The disease is due to feeding of honey
contaminated by spores of C. botulinum and
not due to preformed toxin.
 Wound botulinum
 It is a very rare condition which results from
wound infection with CI. botulinum
Laboratory diagnosis

 Diagnosis is primarily made by clinical presentation,

Demonstration of the organisms
 Smears made from suspected food, intestinal contents,
faeces and wound swab ( in wound botulism) are
examined by Gram's staining
 Culture
 Inoculation of nutrient agar or blood agar plate or tube, it
is placed in an air-tight jar (Mclntosh Filde's jar) from
which air is removed and replaced by 90% hydrogen
with 10% CO2.
 RCM