Flaccid paralysis, Botulism

Botulism is a disease caused by ingestion of foods contaminated with Clostridium botulinum (food-borne botulism) or, very rarely, by wound infection (wound botulism) or colonization of the intestinal tract with Clostridium botulinum (infant botulism). The toxins block the release of acetylcholine. Botulism is characterized by generalized muscular weakness, which first affects eye and throat muscles and later extends to all skeletal muscles. Flaccid paralysis can lead to respiratory failure. 

The role of C2 toxin in disease is not clear because all C. botulinum strains that produce C2 toxin also synthesize extremely potent neurotoxins, the effector molecules of botulism. When Simpson compared the pharmacological properties of C. botulinum neurotoxin type Cl with C2 toxin in detail, it became obvious that C2 toxin does not cause the flaccid paralysis symptoms attributed to classic botulism. However, isolated C2 toxin is a potent enterotoxin that proves lethal in various animals 2 pmol of C2 toxin readily kill mice, rats, guinea pigs, and chickens within 1 h after application. For mice, the LD50 (i.v.) of C2 toxin is less than 50 ftnol. Ohishi and Odagiri also reported that C2 toxin causes necrotic, hemorrhagic lesions in the intestinal wall, whereas Simpson reported that C2 toxin elicits hypotension as well as fluid accumulation in the lungs. ... 

Infantile Botulism—Ingestion ot botulism spores, often in honey, produces flaccid paralysis, poor feeding and suck reflexes, floppy baby syndrome. Wound Botulism—Contamination of wounds with C. botulinum spores can produce systemic symptoms. THERAPY Ventilatory support (often for weeks) Trivalent botulinum antitoxin Enemas and cathartics... 

Tetanus toxin poisoning produces tetanus, i.e. muscle contractions resulting in spastic paralysis. In contrast, Botulinum neurotoxins cause botulism, which is characterized by flaccid paralysis. This difference reflects differences in the anatomical level of action of these toxins. TeTx acts primarily on the CNS where it blocks exocytosis from inhibitory glycinergic synapses in the spinal cord. Loss of inhibitory control results in motoneuron firing. BoNTs act primarily in the periphery where they inhibit acetylcholine release at the neuromuscular junctions. 

Clinicians most often confuse botulism with a polyradiculoneuropathy, such as Guillain-Barre or Miller Fisher syndrome, myasthenia gravis or central nervous system disease (36) (see Table 2.14). In the United States, a cluster of cases of flaccid paralysis is more likely secondary to botulism than to GuiUain-Barre syndrome or polio. In addition, compared to other causes of flaccid paralysis, unique features of botulism include (36) ... 

In the hospital or other health care setting, patient care requires standard precautions. Botulism patients do not require isolation, although before definitive diagnosis, those with flaccid paralysis suspected as having meningitis require droplet precautions (36). 

The typical manifestation of botuhsm is a flaccid paralysis that is bilateral and descending, involving primarily skeletal muscle but also stractures innervated by autonomic parasympathetic fibers. Human intoxication is caused by serotypes A, B, E, and, to a much lesser extent, by serotype F and is manifested as foodbome, wound, and infant botulism. Wound and infant botulism, however, are usually confined to serotypes A and Data compiled for foodbome botulism during the past 50 years in the United States indicate that serotype A was responsible for 37.6% of all outbreaks while sertoypes B, E, and F accounted for 13.7%, 15.1%, and 0.7%, respectively, of intoxications in which serotype involvement was established. ... 

C. Botulism poisoning is described in more detail on page 136. Patients may present with blurred vision, ptosis, difficulty swallowing or speaking, and dry mouth, with progressive muscle weakness leading to flaccid paralysis and respiratory arrest within 24 hours. Since the toxins act irreversibly, recovery may take months. 

Botulism, the deadly food poisoning disease is caused by the growth of various strains of Clostridium botulinum in food. The organism produces a large polypeptide (neurotoxin) which is the most toxic protein known to the human kind. Seven serotypes of botulinum neurotoxins produced by different strains of C. botulinum have been characterized, and serotypes A, B and E are known to cause botulism in humans. Ingestion of food contaminated with the neurotoxin causes flaccid muscle paralysis that can result in patients death. Wound botulism has also been reported where the organism can grow in the wounds, and produces the neurotoxin that causes paralysis. 

Botulinum neurotoxins, produced by the anaerobic bacterium Clostridium bo-tulinum, are the most toxic poisons known to man. The neurotoxins are food poisons. Once ingested, the neurotoxin is absorbed through the intestinal mucosal layer into the blood stream. It acts at the neuromuscular junction to inhibit the release of acetylcholine (a neurotransmitter) from nerve endings (Simpson, 1989). The result is the dreaded botulism disease, which is manifested by flaccid muscle paralysis. 

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