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If Clostridium Botulinum not treated immediately whats the chance of death? (percent)
35-65%
Wound botulism
is a very rare condition resulting from wound infection with C.botulinum. Toxin is produced at the site of infection and is absorbed. The symptoms are those of food-borne botulism except for the gastrointestinal components which are absent. Type A has been responsible for most of the cases studied.
Species responsible for antibiotic-associated colitis.
C. difficile
Species that causes clostridial gastroenteritis via spore ingestion in food; second most common form of food poisoning worldwide.
C. perfringens
What is the shape and gram staining?
large, gram positive rods.
Who discovered tuberculosis bacilli?
Robert Koch
What are symptoms of clostridium botulinum?
Nausea, Vomiting, Fatigue, Dizziness, Double vision, Dry skin, mouth and throat, Drooping eyelids, Difficulty swallowing, Slurred speech, Muscle Weakness, Body Aches, Paralysis, Lack of fever
C. difficile produces these toxins the damages the intestines and causes community-acquired and hospital associated diarrhea.
enterotoxins
Form of gas gangrene that is more destructive, extensive, mimics some aspects of necrotizing fasciitis.
myonecrosis
Full name of your Microbiology techer?
Myrzaiym Manas kyzy
What is the biological activity of Alpha toxin produced by Clostridium perfringens?
A phospholipase, hemolytic, necrotizing, lecithin digestion
Clostridial toxin that is carried to neuromuscular junctions and blocks the release of acetylcholine, necessary for muscle contraction to occur.
botulinum toxin
CLOSTRIDIA THAT PRODUCE MOST INVASIVE
INFECTIONS?
Many different toxin-producing clostridia (C. perfringens and related clostridia) can produce invasive infection (including myonecrosis and gas gangrene) if introduced into damaged tissue. About 30 species of clostridia may produce such an effect, but the most common in invasive disease is C. perfringens (90%).
surprise card
+500 points
Causes baby flaccid paralysis “floppy baby syndrome” Is caused by.
What is infant botulism?
Infant botulism was recognised as a clinical entity in 1976. This is a toxico-infection. C.botulinum spores are ingested in food, get established in the gut and there produce the toxin. Cases occur in infants below six months. Older children and adults are not susceptible. The manifestations are constipation, poor feeding, lethargy, weakness, pooled oral secretions, weak or altered cry, floppiness and loss of head control. Patients excrete toxin and spores in their feces. Toxin is not generally demonstrable in blood. Management consists of supportive care and assisted feeding. Antitoxins and antibiotics are not indicated. Degrees of severity vary from very mild illness to fatal disease. Some cases of sudden infant death syndrome have been found to be due to infant botulism. Honey has been incriminated as a likely food item through which the bacillus enters the gut.
mechanism of action of C. Botulinum toxin
It resists digestion and is absorbed through the small intestines in active form. It acts by blocking the production or release of acetylcholine at the synapses and neuromuscular junctions. Onset is marked by diplopia, dysphagia and dysarthria due to cranial nerve involvement. A symmetric descending paralysis is the characteristic pattern, endng in death by respiratory paralysis.
Use of a hyperbaric oxygen chamber can help slow the spread of this disease
gas gangrene
Ooops
-400 points
Clostridial toxin that causes paralysis by binding to motor nerve endings; blocking the release of neurotransmitter for muscular contraction inhibition; muscles contract uncontrollably.
Tetanospasmin
diagnosis C. Tetani
Diagnosis
The diagnosis rests on the clinical picture and a history of injury, although only 50% of patients with tetanus have an injury for which they seek medical attention. The primary differential diagnosis of tetanus is strychnine poisoning. Anaerobic culture of tissues from contaminated wounds may yield C. tetani, but neither preventive nor therapeutic use of antitoxin should ever be withheld pending such demonstration. Proof of isolation of C. tetani must rest on production of toxin and its neutralization by specific antitoxin.
3 to 21 days
treatment of C. Perfringes
Surgery is an essential prophylactic and therapeutic measure in gas gangrene. All damaged tissue should be removed promptly and the wounds irrigated to remove blood clots, necrotic tissue and foreign materials. In established gas gangrene, uncompromising excision of all affected parts may be life-saving. Where facilities exist, hyperbaric oxygen may be beneficial in treatment.
Antibiotics are effective in prophylaxis, in combination with surgical methods. The drug of choice is metronidazole given intravenously along with clindamycin and penicillin before surgery and repeated every eight hours for 24 hours.
Passive immunisation with 'anti-gas gangrene serum' (equine polyvalent antitoxin in a dose of 10,000 IU perfringens, 10,000 IU C. novyi and 5,000 IU C. septicum antitoxin given IM or in emergencies, IV) is the common practice in prophylaxis.
Nagler's reaction
• Nagler's reaction When C. perfringens is grown on a medium containing 6% agar, 5% Fildes' peptic digest of sheep blood and 20% human serum, with the antitoxin spread on one half of the plate, colonies on the other half without the antitoxin will be surrounded by a zone of opacity. There will be no opacity around the colonies on the half of the plate with the antitoxin due to the specific neutralisation of the alpha toxin. This specific lecithinase effect, known as the Nagler's reaction, is a useful test for the rapid detection of C. perfringens in clinical specimens.
What is the capiral of Brazil?
Brazilia
Prevention and Treatment
As most cases of botulism follow the consumption of inadequately canned or preserved food, control can be achieved by proper canning and preservation.
Treatment
Supportive care, especially intensive care, is key in the management of patients with botulism. Adequate respiration must be maintained by mechanical ventilation if necessary and in severe cases may need to be maintained for up to 8 weeks. These measures have reduced the mortality rate from 65% to below 25%. Potent antitoxins to three types of botulinum toxins have been prepared in horses. Because the type responsible for an individual case is usually not known, trivalent (A, B, E) antitoxin must be promptly administered intravenously with customary precautions. Antitoxin does not reverse the paralysis, but if administered early, it can prevent its advancement. Although most infants with botulism recover with supportive care alone, treatment with humanderived botulinum immune globulin (BIG) is recommended.