CLOSTRIDIUM

• Clostridium are also gram-positive spore-forming rods.

However, they are anaerobic, and can therefore be
separated from the aerobic spore-forming rods(Bacillus) by
anaerobic culture.
• This group of bacteria is responsible for the famous
diseases botulism, tetanus,gas gangrene, and
pseudomembranous colitis.
• Clostridium harm their human hosts by secreting
exextremely powerful exotoxins and enzymes.
• Rapid diagnosis of a clostridial infection is crucial, or your
patient will die!!!!
 Clostridium botulinum
( Botulism)
• Clostridium botulinum produces an extremely
lethal neurotoxin that causes a rapidly fatal
food poisoning.
• The neurotoxin blocks the release of
acetylcholine (Ach)from presynaptic nerve
terminals in the autonomic nervous system
and motor endplates, causing flaccid muscle
paralysis.
Adult Botulism
• Eating smoked fish or home-canned vegetables is associated
with the transmission of botulism.
• Clostridium botulinum spores float in the air and can land on
food.
• If the food is cooked thoroughly, the spores will die.
• However, if the food with the spores is not cooked
sufficiently, and is then placed into an anaerobic
environment(like a glass jar, can, or zip-lock freezer bag),
Clostridium botulinum matures and synthesizes its
neurotoxin.
• Those who consume the contents of the jar when it is
opened weeks later will be ingesting the potent neurotoxin.
• These afebrile patients initially develop bilateral cranial
nerve palsies causing double vision (diplopia) and difficulty
swallowing (dysphagia).This is followed by general muscle
weakness, which rapidly leads to sudden respiratory
paralysis and death.
• Patients must immediately be treated with an antitoxin,
which can neutralize only the unbound free neurotoxin in
the bloodstream. Intubation and ventilatory support is
critical until the respiratory muscles resume activity.
Infant Botulism
• Infant botulism occurs when infants ingest food contaminated
with Clostridium botulinum spores(cases have followed ingestion
of fresh honey contaminated with spores). The spores germinate
and Clostridium botulinum colonizes the infant's intestinal tract.
• From this location, botulism toxin is released.
• Initially, the infant will be constipated for two to three days. This
is followed by difficulty swallowing and muscle weakness. These
"floppy" babies must be hospitalized and given supportive
therapy.
• Prognosis is excellent,so antitoxin is generally not used.
 Clostridium tetani
(Tetanus)
• Clostridium tetani causes tetanus, a disease that
classically follows a puncture wound by a rusty nail but
can follow skin trauma by any object contaminated with
spores.
• Clostridium tetani spores, which are commonly found in
soil and animal feces, are deposited in the wound and can
germinate as long as there is a localized anaerobic
environment (necrotic tissue). From this
location,Clostridium tetani releases its exotoxin, called
tetanospasmin.The tetanus toxin ultimately causes a
sustained contraction of skeletal muscles called tetany.
• Because of the high mortality of tetanus, prophylactic
immunization with formalin-inactivated toxin (tetanus
toxoid) is performed once every ten years in the U. S.
• This booster serves to regenerate the circulating antibodies
against tetanus toxin, that were first generated via
childhood immunizations.
• You may not remember your first shot (you were probably
just 2 months old at the time), but all children in the U. S.
are immunized with a series of DPT (diphtheria-pertussis-
tetanus)shots at ages 2, 4, 6, and 18 months, followed by a
booster before entry into school (4-6 years).
• This regimen provides protection from tetanus
(along with diphtheria and pertussis).
However, the protection from tetanus only
lasts about 10 years so booster shots of
tetanus are given every 10 years.
• In the emergency room you will encounter 3 types of patients
with skin wounds:
1) Patients who were immunized as a child and
received periodic boosters but the last shot was
more than 10 years ago. These patients are
given another booster.
2) Patients who have never been immunized. Not
only do these patients need a booster, but they
should also receive preformed antibodies to the
tetanus toxin called human tetanus
immune globulins.
3) Patients who come to the hospital having already developed tetanus. The big
picture is to clear the toxin and the toxin-producing bacteria and to keep the patient
alive until the toxin has cleared. This is accomplished in the following 5 steps of
therapy:
a) Neutralize circulating toxin with human tetanus
immune globulins.
b) Give an immunization booster to stimulate the patient's own immune system to
develop antitetanus toxin antibodies.
c) Clean the wound, excising any devitalized tissue,to
remove any remaining source of Clostridium tetani.
d) Antibiotics (penicillin) may help to clear the
remaining toxin-producing bacteria.
e) Provide intensive supportive therapy until the toxin is cleared.Muscle relaxants
may have to be administered, and the patient may have to be placed on a ventilator .
 Clostridium perfringens
(Gas Gangrene)
• Everyone has heard of gas gangrene. Prior to
antibiotics,Clostridium perfringens devastated
soldiers wounded in battle. This bacterium,
whose spores can be found in the soil, matures
in anaerobic conditions and produce gas.
The spores can contaminate wounds from battle
or other trauma. Deep wounds with lots of dead
tissue create an anaerobic environment that offers
an excellent home for Clostridium perfringens.
• As this anaerobic organism grows, it releases
its battery of exotoxin enzymes , causing
further tissue destruction.
Clinically, there are 2 classes of infection with
Clostridium perfringens:
1) Cellulitis/wound infection:
Necrotic skin is exposed to Clostridium
perfringens, which grows and damages local
tissue. Palpation reveals a moist,
spongy,crackling consistency to the skin due to
pockets of gas;this is called crepitus.
2) Clostridial myonecrosis:
Clostridium perfringens,inoculated with trauma
into muscle,secretes exotoxins that destroy
adjacent muscle. These anaerobic bacteria
release other enzymes that ferment
carbohydrates, resulting in gas formation.
A computerized tomogram(CT) scan reveals
pockets of gas within the muscles and
subcutaneous tissue.
• As the enzymes degrade the muscles, a thin,
blackish fluid exudes from the skin.
• Clostridial myonecrosis is fatal unless
identified and treated very early. Hyperbaric
oxygen, antibiotics (such as penicillin), and
removal of necrotic tissue can be lifesaving.
 Clostridium difficile
(Pseudomembranous Enterocolitis)
• Clostridium difficile is the pathogen responsible
for antibiotic-associated pseudomembranous
colitis (diarrhea), which can follow the use of
broad spectrum antibiotics (such as ampicillin,
clindamycin,and the cephalosporins).
• These antibiotics can wipe out part of the
normal intestinal flora, allowing the pathogenic
Clostridium difficile that is sometimes present
to superinfect the colon.
• Once Clostridium difficile grows in abundance,
it then releases its exotoxins.Toxin A causes
diarrhea, and Toxin B is cytotoxic to the colonic
cells. This disease is characterized by severe
diarrhea,abdominal cramping, and fever.
• Because of Clostridium difficile it becomes
very difficile (difficult) to give patients
antibiotics.
• Examination by colonoscopy can reveal red inflamed
mucosa and areas of white exudate called
pseudomembranes on the surface of the large
intestine.
• Necrosis of the mucosal surface occurs underneath
the pseudomembranes.
• When a patient develops diarrhea while on
antibiotics (or within a month of being on antibiotics)
Clostridium difficile must be considered as a possible
cause.
• Samples of the stool can be sent to the laboratory for a
Clostridium difficile toxin test. Toxin in the stool confirms the
diagnosis.
• Treatment includes discontinuing the initial antibiotic and
administering metronidazole or vancomycin by mouth. Both
antibiotics kill Clostridium difficile and
are not absorbed orally into the bloodstream.
So the METRO train and VAN cruise down
the gastrointestinal (GI) tract, rather than
being absorbed, and run over the hapless
Clostridium difficile bacteria .