Botulism symptoms

All botulin neurotoxins act in a similar way. They only differ in the amino-acid sequence of some protein parts (Prabakaran et al., 2001). Botulism symptoms are provoked both by oral ingestion and parenteral injection. Botulin toxin is not inactivated by enzymes present in the gastrointestinal tracts. Foodborne BoNT penetrates the intestinal barrier, presumably due to transcytosis. It is then transported to neuromuscular junctions within the bloodstream and blocks the secretion of the neurotransmitter acetylcholine. This results in muscle limpness and palsy caused by selective hydrolysis of soluble A-ethylmalemide-sensitive factor activating (SNARE) proteins which participate in fusion of synaptic vesicles with presynaptic plasma membrane. SNARE proteins include vesicle-associated membrane protein (VAMP), synaptobrevin, syntaxin, and synaptosomal associated protein of 25 kDa (SNAP-25). Their degradation is responsible for neuromuscular palsy due to blocks in acetylcholine transmission from synaptic terminals. In humans, palsy caused by BoNT/A lasts four to six months. 

Botulism is usually not transmissable from one person to another. A supply of antitoxin against botulism is maintained by the Center for Disease Control and Prevention located in Atlanta, Georgia. Such antitoxin is effective against the severity of symptoms if administered early in the course of disease, and most patients eventually recover after weeks to months of supportive care. 

Botulism. Clinical features include symmetric cranial neuropathies (i.e., drooping eyelids, weakened jaw clench, and difficulty swallowing or speaking), blurred vision or diplopia, symmetric descending weakness in a proximal to distal pattern, and respiratory dysfunction from respiratory muscle paralysis or upper airway obstruction without sensory deficits. Inhalational botulism would have a similar clinical presentation as food-borne botulism however, the gastrointestinal symptoms that accompany foodborne botulism may be absent. 

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. ... 

Wound botulism occurs where C. botulinum spores germinate in wound infections and develop into vegetative cells. In such cases, neurotoxin is produced which leads to the onset of neurological symptoms. According to the Centers for Disease Control and Prevention, 23 cases of wound botulism (13.6% of all botulism cases) were reported in 2001 in the U.S. Wound botulism has also been diagnosed after intravenous drug injection (Rundervoort et al., 2003). 

The onset of botulism occurs generally between 18 and 36 hours after consumption of food products containing botulin toxin. However, it may affect patients earlier or later, even on the tenth day after food consumption. The first symptoms include stomach ache, nausea, vomiting, and diarrhea, followed by neurological disorders. Other symptoms include, skin, mouth and throat dryness, diplopia, blurred vision, dysphonia, dysarthria, dysphagia, and peripheral weakness. In lethal cases of botulism, respiratory muscles are involved. This leads to respiratory failure and death. Because all the symptoms are connected with toxemia, the first step of medical treatment is to provide a patient with antiserum. 

In 1991 the FDA approved the use of botulism toxin (BT) for the treatment of an "orphan" condition called blepharospasm. A victim of this syndrome will experience uncontrollable winking caused by spasms of the eyelid muscles. Use of botulism toxin will cause abatement of the symptoms in 90% of patients for 2 to 4 months. 

For example, in October and November 1987, eight cases of botulism occurred, two in New York and six in Israel. All the victims had eaten Kapchunka, air-dried, salted whitefish, which had been prepared in New York, and then some had been transported by individuals to Israel. All the patients developed the symptoms of botulism within 36 hours, and one died. Some were treated with antitoxin and two received breathing assistance. 

Antibiotics, which are produced by other living organisms, inhibit the growth of bacteria or destroy them (bactericidal). There are few known bacterial diseases, the effects of which cannot be mitigated if the proper antibiotic is used early in the course of the disease. Tetanus and botulism are exceptions. These diseases are the manifestation of extremely potent toxins produced by the bacteria, rather than symptoms caused by infections of the microorganisms themselves, See also Antibiotics. 

Botulism was described much later than tetanus (Kemer 1817 Midura and Amon 1976 Pickett et al. 1976), and this delayed recognition is due to its much less evident symptoms, which include a generalized muscular weakness with diplopia, ptosis, dysphagia, facial paralysis, and reduced salivation and lacrimation. The paralysis then progressively descends to affect the muscles of the trunk, including respiratory and visceral muscles. All the symptoms of botulism can be ascribed to the blockade of skeletal and autonomic peripheral cholinergic nerve terminals (Tacket and Rogawski 1989). 

The gravity of the illness depends on the amount and type of BoNT, which is usually acquired via the oral route. Death follows the blockade of respiratory muscles, but if ventilated mechanically, the patient will eventually recover completely. In general terms, botulism is much less dangerous than tetanus also because, in most cases, the amount of toxin that reaches the general circulation is not sufficient to block respiration. BoNT/A, /B and /E account for most cases of human botulism, and the disease caused by BoNT/A is more dangerous with symptoms persisting much longer. 

The data about fields of application of Silics in clinics for treatment for infectious diseases are presented in Table 4. From Table 4 it is evident that the field of application of Silics is rather large and covers both intestinal infections and toxicoses which victimize infants, as well as viral hepatitis, and botulism. It is appropriate to mention here that inclusion of Silics into the complex treatment of patients suffering from salmonellosis, dysentery, and intestinal toxicoses accelerates normalization of clinic manifestations of these diseases by a factor of two and more. In the case of botulism the normalization of symptoms characteristic of lesions of the nervous system is shortened by almost 4 days. If intestinal infections are not severe, Silics can be recommended as a single therapeutic agent. In the case of a considerable diarrheal syndrome it is more expedient to use it together with rehydration substances. Inclusion of Silics into a complex of therapeutic agents for patients suffering from viral hepatitis substantially accelerates recovery rates of patients, so that their normal level of bilirubin and activity of alanine aminotranspherase are recovered within shorter periods of time. 

In foodborne botulism, complaints of nausea, vomiting, and diarrhea may accompany the initial neurologic symptoms. In later stages of the disease, constipation becomes more prominent. In infantile botulism, constipation is often the main symptom, along with characteristic flaccidity (the floppy baby ), poor suck reflex, poor feeding, and poor head control. 

Pitfalls in the diagnosis of botulism include failure to recognize the symptoms and to institute adequate ventilatory support. Botulism is likely underdiagnosed and can be mistaken for a number of neuromuscular and neurologic disorders. Diphtheria, encephalitis, poliomyelitis, Guillain-Barre syndrome, congenital... 

Botulism-like Acute paralytic conditions consistent with botulism such as cranial nerve palsy, ptosis, decreased gag reflex Acute descending motor paralysis Acute symptoms consistent with botulism such as diplopia, dysphagia Botulism... 

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... 

The onset of symptoms in botulism depends upon the amount of toxin ingested or inhaled and the related kinetics of absorption. Time to onset can range from as early as 2 h to as long as 8 days, although symptoms typically appear between 12 and 72 h after consumption of toxin-contaminated food (Lecour et ah, 1988 Amon et ah, 2001). In a review of 13 foodbome botulism outbreaks involving 50 patients from 1970 to 1984, the incubation period ranged from 10 h to 6 days (Lecour et al, 1988). 

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