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Clostridium tetani

These are spore-forming anaerobes


Motile peritrichious flagella
* Compared to non - motile
perfringens
Grows in cooked meat broth
*Meat Broth: used in storing C.
tetani
Produces a thin spreading film on
enriched blood agar because of the
flagella
Resistance of spores to
harsh
conditions depends on strain:
- boiling for 3 hrs
- dry heat at 160C for 1h
- 5% phenol for 2 weeks
Spores killed by Iodine (1%) in water
within few hours; glutaraldehyde sporocidal
*Cold sterilant is sporocidal
DRUMSTICK APPEARANCE
* Responsible for causing Tetanus
* Important characteristic: Presence
of Terminal Spore, wherein there is a
visible vacuole at the end of the
bacillus upon Gram Staining
Where do we Find Clostridium tetani?
Intestines of humans and animals---feces
Indirectly from soil contaminated
with feces
Spores found in :
- Gardens
- Roads
- Sports field
- Dust
- Plaster
- Air in hospitals and houses
- Clothing
- On articles of common use
- Surgical catgut
* Spores remain viable in soil for years
* What is important in C. tetani are
the toxins they produce.
* They produce two types of toxin.
One is Oxygen Labile Hemolysin, aka

Tetanolysin. This has no evidence in

the pathogenesis of the disease.


Tetanospasmin of C. tetani
One light chain + one heavy chain
linked by disulfide bonds
Lethal dose for mouse
approximately 0.0001ug
Toxic to humans/ animals when
injected parenterally; not through oral
route
* Neurotoxic; more important
MODE OF ACTION OF
TETANOSPASMIN

* What characteristic seen here is the


rigidity of the muscle . This is
because, the Tetanospasmin binds to
the receptors on the nerve endings,
and this will prevent the release of
neuroinhibitors, which regulates the
muscle contraction. Thus, muscle

contracts uncontrollable and a rigid


paralysis results.
HOW DOES INFECTION OCCURS?
Spore
Forming
Tetanus (Lockjaw)

Anaerobes-Diseases-

Infection commonly results in non


immune individuals who have a
penetrating injury contaminated with
C. tetani spores.
Infection only occurs if the site is
anaerobic (eg. Necrotic) and the
spores are able to germinate
The vegetative cells secrete tetanus
toxin which then migrates along axons
to neuromuscular junctions.
Once at the NMJ, the toxins causes
continuous muscle contraction and
rigid paralysis, the most characteristic
being of the face (hence the term
lockjaw).
Death usually occurs as a result of
respiratory paralysis.

DIAGNOSIS OF TETANUS
Primary upon clinical features
History and presence of wound
C. Tetani may not be isolated in wound
TREATMENT OF TETANUS
Stimulation kept at a minimum
Muscles relaxant e.g. diazepam
Tracheostomy if needed
TETANUS IMMUNE GLOBULIN (TIG):
* dose of 500 units IM immediately
( for
toxins outside the CNS)
* TIG 250 units ,intra-thecally
Debridement of wound, then treated
with
penicillin or metronidazole
Adrenergic
blocking
agents
or
morphine may be required for severe
autonomic reactions
Active immunization started

*IP: Incubation Period (May be long/short)

* The shorter the IP, the more severe the


infection.
*Opisthotonos - tetanus infection in
babies in an infected umbilical cord.
Increased incidence of tetanus indicates
poorly developed country.
* Trismus/Lockjaw - adult infection, an
early sign

Conditions for Post- exposure


immunization against Tetanus

*Assess on which category you


belong
1. Adequate 10
immunization, with
booster within preceding 5 yearsno
booster for any type of wound
2. Immunized, last booster 5-10 years
previously:
i.
-- no booster for clean wound
ii.
-- booster given for tetanusprone wound
* if you have these in the preceding 5
years, if nagkasakit kayo, you need
not be given any booster.
3. Immunized, last booster more than 10
years previously - booster for any type of
wound
4. No immunization - give human TIG 250500U (Depends on severity of wound);
active immunization initiated
EPIDEMIOLOGY OF TETANUS
Ranks among major lethal infections
Incidence vary from country to country
Direct relationship with fertile soil and
warm climate---high in tropical and
subtropical, developing countries
Practice of treatment of umbilical
stump with primitive applications ( e.g.
dung etc) 50-60% mortality in
neonates
INFANT TETANUS
In developing countries, tetanus is not
an uncommon occurrence.
Disease is often seen in infants with
infected umbilici
Common in developing countries
TETANUS (LOCKJAW)
Tetanus is extremely rare in developed
countries primarily due to active
immunization programs with tetanus
toxoid (inactive toxin) but also due to
high standards of health care.
Rare in developed countries
Clostridium difficile

Large gram positive


Sporeformer ( oval spores)
Motile
Commensal of adults gut
Two types of toxin:
- Enterotoxin ( type A)
- Cytotoxin ( type B)
Causes antibiotic associated
pseudomembranous colitis
Spores - resist harsh
Environmental factors; Stay long
hands of hospital personnel

VIRULENCE FACTOR
Toxin A
Enterotoxin
Enterotoxin which causes intestinal
inflammation
resulting
in
fluid
secretions and hemorrhagic necrosis
resulting in bloody diarrhea.
Toxin B
Cytotoxin
Cytotoxin causing destruction of
interstitial epithelium.
Can be detected in stool samples from
patients with C. difficile disease by
adding the stool filtrate to a tissue
culture monolayer and observing for
cytotoxic effect or through the
detection of the toxin by EIA
PSEUDOMEMBRANOUS COLITIS
CAUSED BY Clostridium difficile
Antibiotic therapy that disrupts normal
bowel flora predisposes patients to
what is termed antibiotic associated
diarrhea
A severe form of this syndrome is
pseudomembranous colitis is caused
by C. difficile.
It tends to occur in hospitalized
patients who are exposed to c. difficile
spores remaining in the hospital from
previous patients with the disease.

CLINICAL AND PATHOLOGICAL


FEATURES OF ACC
Spore
Forming
Anaerobes
Diseases
- Pseudomembranous
colitis (C. Difficile)
The disease is characterized by
bloody
diarrhea
which
often
progresses to severe inflammation of
the mucosa and the elaboration of
the
pseudomembrane
and
microabscesses.
The pathology of the disease is a result
of both toxin A (emterotoxin) and Toxin
B (cytotoxin)

Laboratory Diagnosis of (ACC)


Isolation of C. difficile from feces
Toxin assays: Use of baby hamster
kidney cells

Treatment and Prevention of

ACC

Treatment:
Discontinue antibiotics
Give oral vancomycin or metronidazole
to suppress Clostridium difficile and
stop toxin production

Supportive management, depends on


presenting symptoms
Prevention:
Clinical
awareness,
keynote

Clostridium
botulinum
Gram positive; strict anaerobe
Motile perithrichious flagella
Spores oval, subterminal
Some withstand boiling for several
hours
Destroyed by moist heat at 120C in 5
minutes
Spores of type E, less heat resistant
Growth ; optimum at about 35C; some
strains grow and produce toxins at 15C

HABITAT
Saprophyte found in :
- Soil,
- Vegetables, fruits, leaves
- Silage
- Manure
- Mud of lakes and sea mud
Toxins of C. botulinum

Most poisonous natural substance


Seven types ( A-G) (All are lethal)
Antigenically distinct
Pharmacologically similar
All can cause human disease
Lethal dose to humans , 1-2 ug
Approx. 150,000 daltons

Types A and B ( soil) and E (marine


source;
common cause of botulism
in humans)
Action of the Toxins
*Opposite of Tetanus
* The inhibitors of transmission are
prevented from being released.
Interferes with neurotransmission of
peripheral cholinergic synapses
How ?
by binding to the presynaptic
membrane thus prevents release of
acetycholine

Results: symmetrical,
descending flaccid paralysis
*
Acetylcholine
contraction

needed

for

Virulence Factors
The Botulinum toxin (Botulism) is an
extremely potent neurotoxin that
prevents acetylcholine release from
nerve endings resulting in flaccid
paralysis
Toxin
binds
to
the
Presynaptic
membrane
Botulism
- Life threatening disease characterized by
descending flaccid paralysis
Types of Botulism
Food Poisoning
Infant Botulism
Wound Botulism
FOOD POISONING
Botulinum toxin is the most potent
exotoxin known
Botulism is an intoxication illness
associated with improperly preserved
food
Although exceedingly rare, the
usual source is canned foods (an

anaerobic environment) which have


been contaminated with the spores.
Results
from
eating
foods
contaminated with toxin
VEHICLES FOR FOOD POISONING
Home preserved meats/ vegetables
Canned products , e.g. fish. Liver paste
Hazelnut puree and honey
Note:
Foods with pre-formed toxins do not
exhibit signs of spoilage (masarap pa
rin, thats why you eat them)
WOUND BOTULISM
due to toxins produced by organisms
contaminating a wound
FOOD
BORNE
BOTULISM)

DISEASE

(INFANT

Infant
botulismfloppy
child
syndrome-due to toxins produced by
organisms in the gut)
Neonates are at risk of the syndrome
known as infant botulism if they ingest
C. botulinum spores which then
germinate in the intestinal tract and
subsequently
cause
the
same
syndrome
as
with
intoxication
botulism.
On the food sources implicated such in
cases is raw honey.
Adults are not susceptible to this type
of infection apparently because the
spores do not germinate in the adult
gut.
* Adults are infected by the preformed toxins in the food that we
eat. Babies, on the other hand, may
be infected with spores from raw
honey, since spores can germinate in
an infants gut.
Clinical Features of Botulism
1. Incubation period , 1-2 days after
ingestion ( may be longer)

2. Initial nausea and vomiting


3. Oculomotor muscles affected: diplopia
(loss of control of muscles of the
eye), drooping eyelid with squint
(sleepy eyes); blurred vision, vertigo
4. Progressive
motor
loss
(flaccid
paralysis) No loss of consciousness
5. Other
symptoms
:
weakness
sleepiness,
thirsty,
dry
mouth,
difficulties
in
speech
and
swallowing
6. DEATH respiratory and cardiac failure
CLINICAL FEATURES OF BOTULISM
Dry furrowed tongue
Dilated Fixed pupils (like those of
dead people)
DIAGNOSIS OF BOTULISM
LABORATORY DIAGNOSIS
Isolation of organism from suspected
food samples
Demonstration of toxin in patients
blood (toxin-antitoxin neutralization
test in mice)
CLINICAL FEATURES
Dry furrowed tongue
Dilated Fixed pupils
TREATMENT OF BOTULISM
Remove
unabsorbed
toxin
from
stomach and intestines (Gastric
lavage)
Neutralize
unfixed
toxingive
polyvalent antitoxin (Antitoxin given
should contain A-G antibodies, all
types)
Give relevant intensive
care and support
CONTROL OF BOTULISM
Home canning of foodstuffs should be
avoided

Acid fruits can be safely bottled at


home with heating AT 100c ( Low pH
inhibitory to C. botulinum)
Commercial canning must be strictly
controlled

Do not eat canned foods with bulging


containers
Heat canned foods before eating (The
toxin is heat labile.)