General characteristics
Morphology of Clostridia
Clostridia are highly pleomorphic, usually 3-8 *0,4-1,2 mm in size, gram positive rods.Clostridia are motile with peritrichate flagella
If Clostridium Botulinum not treated immediately whats the chance of death? (percent)
35-65%
Disease prodused by C.perfringens?
Gas gangrene, Food poisoning, Gangrenous appendicitis, Necrotising enteritis
Toxins of C.tetani
Hemolysin (Tetanolysin)
Neurotoxin (Tetanospasmin)
Non-spasmogenic
C. difficile produces these toxins the damages the intestines and causes community-acquired and hospital associated diarrhea.
enterotoxins
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Myrzaiym Manas kyzy
Clinical types of botulism
Food born
Wound
Infant
Major toxins of C.perfringens ?
Alpha (a) toxin is produced by all types of C. perfringens
Beta (ß), epsilon (E) and iota (1) toxins have lethal and necrotising properties
The capital of Brazil?
Brazilia
Tetanus toxin (tetanospasmin) diffuses to terminals of inhibitory cells in the spinal cord and brainstem and blocks which of the following?
(A) Release of acetylcholine
(B) Cleavage of SNARE proteins
(C) Release of inhibitory glycine and γ-aminobutyric acid
(D) Release of protective antigen
(E) Activation of acetylcholine esterase
(C) Release of inhibitory glycine and γ-aminobutyric acid
extra 200 points
Pathogenic species of Clostridia?
Clostridium perfringens
Clostridium tetani
Clostridium septicum
Clostridium botulinum
Clostridium novyi (C. oedematiens)
Clostridium difficile
Clostridium histolyticum
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
Minor toxins
Gamma (y) and eta (n) toxins have minor lethal action.
Delta (8) toxin has a lethal effect and is hemolytic for the red cells of even-toed ungulates (sheep, goats, pigs and cattle).
Theta (0) toxin is an oxygen-labile hemolysin, antigenically related to streptolysin O. It is also lethal and a general cytolytic toxin.
Kappa (к) toxin is a collagenase.
Lambda (A) toxin is a proteinase and gelatinase.
Mu (u) toxin is a hyaluronidase.
Nu (v) toxin is a deoxyribonuclease.
Resistance of Clostridial spores
Spores are usually destroyed within five minutes by boiling. 'Food poisoning'-producing type A strains and certain type C strains resist boiling for 1-3 hours. Autoclaving at 121°C for 15 minutes kills them. Spores are resistant to commonly used antiseptics and disinfectants
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.
Clostridial spores may be(position):
1) Central or equatorial, giving the bacillus a spindle shape (C. bifermentans)
2)Subterminal, the bacillus appearing club-shaped(C. perfringens)
3)Oval and terminal, resembling a tennis racket (C. tertium)
4)Spherical and terminal givihg a drumstick appearance
Clostridial toxin that is carried to neuromuscular junctions and blocks the release of acetylcholine, necessary for muscle contraction to occur.
botulinum toxin
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-400
Clostridial toxin that causes paralysis by binding to motor nerve endings; blocking the release of neurotransmitter for muscular contraction inhibition; muscles contract uncontrollably.
Tetanospasmin
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+500 points
Clostridial toxins
Exotoxin Pathogenic clostridia produce powerful exotoxins which are responsible for the pathogenesis and disease, e.g., tetanus, botulism and gas gangrene.
Invasive toxin C. perfringens, besides being toxigenic,is also invasive and can spread along the tissues and even cause septicemia.
clinical used of botulinum toxin
A small quantity of C.botulinum Type A toxin injected into a muscle selectively weakens it by blocking the release of acetylcholine at the neuromuscular junction. Muscles so injected atrophy but recover in 2-4 months as new terminal axon sprouts form and restore transmission. Intramuscular injection of the toxin, first used to treat strabismus, is now recognised as a safe and effective symptomatic therapy for many neuromuscular diseases.
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.
diagnosis of 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.
Form of gas gangrene that is more destructive, extensive, mimics some aspects of necrotizing fasciitis.
myonecrosis