Botulism
                           ========

þ General
 - name comes from Latin botulinus (small sausage)
 - anaerobic diptheroid (Clostridium botulinus)
 - Types A-E
 - four mode of acquisition.
  + wound botulism (like tetanus, invisible in wound, no signs of infection)
  + food-borne botulism (from ingestion of preformed toxin usually found in
    improperly canned or preseved food),
  + infant botulism (from intestinal colonization of clostridial organisms in
    infants under 1 year of age).
  + adult intestinal colonization botulism.  It is similar to the infant form,
    and occurs when the normal bowel flora is disrupted.  It occurs in older
    children and adults with colitis, recent bowel surgery or other intestinal
    disorders that disrupt the bowel flora
 - spores can survive several hours of boiling
 - toxin, unlike spores, is heat-labile and is inactivated by boiling for 10
   minutes or heating at 80 degrees C for 30 minutes.  [Scientific American
   Medicine, 1/94.]
 - botulism toxin can be detected in stool or food
 - organisms can be detected in patient's stool.
 - has recently been found in Hawaii, from eating intestines of palani, a reef
   scavenger; and from moloha, a preparation of uneviscerated, salt-dried fish. 
   Also cases (Aug 2007) from canned chili, and from sun-dried fish
   from the Russian community in California
 - many cases from injecting Mexican "black tar" heroin
 - no immunity

þ Clinical Features of Botulism
 - per someone who has seen 35 cases (Zygmunt Dembek, USARIMID): 
  + big doses: will cause respiratory failure fast
  + normal doses: first, get lateral rectus palsy and diplopia, then other 
    bulbar palsy, then other paralysis
 - no fever
 - The neurologic symptomatology of food-borne botulism is a progressive,
   symmetric weakness or paralysis, almost always without sensory defects
   (other than blurred vision).  This is similar to Guillain-Barre.
 - Guillain-Barre is generally an ascending paralysis, while food- borne
   botulism is a descending paralysis.  Typically the cranial nerves are
   affected first.  Diplopia, dysarthria, dry mouth and generalized weakness
   are among the most common presenting symptoms.
 - In 50% of cases there will be an ophthalmoplegia, in which the
   pupils are dilated or unreactive.
 - Infant botulism: The primary symptom is usually constipation (3 or more
   days without a bowel movement).  This is often the first symptom. Other
   symptoms include listlessness, lethargy, difficulty in sucking and
   swallowing, hypotonia, weak cry, poor feeding, pooled oral secretions,
   generalized muscle weakness and poor head control, which gives the infant a
   characteristic floppy appearance.
 - get GI paralysis as well; paralysis lasts for weeks; needs GJ tube 
 - some people in California got Botox injected into their neck and got
   weeks of complete neck paralysis.

þ Testing for Botulism

 - The toxin is found in the serum 39% of the time, but it is found only 24%
   of the time in the stool.  The organisms can be found in stool cultures in
   55% of cases.  Of course, all these tests should be done in suspected
   cases, which gives a total diagnostic yield of 75%
 - RED TOP tubes (get three just to be sure; send to state or CDC)
 - may want part of intestine for postmortem specimen
 - In patients with suspected botulism, just prior to antitoxin administration
   one should obtain 10-15 mL of serum, 25-50g of feces and maybe even 25-50
   mL of gastric fluid for future testing.
 - for inhalational, might try nasal swabs
 - main test is "mouse test" - inject mouse with serum or stool
   preparation from patient, see if mouse dies
 - check VC vital capacity and intubate when low enough (10 = 700 mL for
   average person)

 - Triage test: "staccato speech": if can count out loud 1-20 then
   probably OK.

þ Treatment of Botulism
 - trivalent antitoxin can prevent paralysis.
 - from food-borne botulism, often require intubation for 6-8 weeks.
 - for infant botulism, antibiotics are not recommended for this disease
   because cell lysis and death can release more of the toxin.  In addition,
   aminoglycosides and tetracyclines can exacerbate neuromuscular blockade by
   impairing calcium entry into the neuron.
 - people don't develop antibodies

þ Vaccine: