3. Clostridiums Large, straight or slightly curved roads with rounded ends. Bulging spore Usually saprophytic: proteolytic and fermenter (Important in the process of decomposition of animal Mostly motile (with pritricuse flagella) Most of the species are highly toxinogenic Living normally in soil or animal GI Anaerobic (only some tolerate O) proteins “putrefaction”).

4. Diseases C. tetani causes tetanus. C. botulinum causes botulism. C. perfringens, C. septicum & ……causes gas gangrene and other infections. C. difficile causes pseudomembranous colitis and antibiotic associated diarrhoea.

5. Tetanus Botulism Gas gangrene

6. Clostridiums tetani Peritricus flagella Terminal spore Highly resistant spores, but glutaraldehyde is effective. Toxins: tetanolysin - oxygen labile haemolysin.

7. Clostridiums tetani

8. Colonies: Tiny colonies growing in a net of fine filamentous

9. Tetanospasmin Neuromuscular pathogenic effect.  Gene encoded on a plasmid.  Tiny lethal dose required, but only effective in humans parentrally (not oral).

10. The site of infection Bacilli remain at the site of infection, toxin causes localized or generalized tetanus. Spread is haematogenous. Spore germination is favoured by necrotic tissue and poor blood supply in the wound.

11. Pathogenesis Tetanus toxin (tetanospasmin) It is carried intra-axonally (retrograde) to the central nervous system, where it binds to ganglioside receptors and blocks release of inhibitory mediators (e.g. glycine, Gamma-aminobutiric acid) at spinal synapses leading to hyper reflection and spastic paralysis.

13. Clinical findings Gradual onset. Incubation period: 4-5 days – several weeks Violent muscle spasms in the site of infection. Lockjaw (trismus) due to rigid contraction of the jaw muscles, a characteristic known as “risus sardonicus”’. Opisthotonos (extreme arching of the back). Low blood pressure, Sweating, tachycardia, arrhythmia and autonomic instability. Respiratory failure.

20. Neonatal tetanus

22. Transmission Highest incidence in devloping countries, associated with a fertile soil and warm climate. Previous association with non-sterile ear piercing.

24. Laboratory Diagnosis Gram stains of wound smears: don't often prove useful! Direct culture on blood agar. An anaerobically prepared culture may be injected into mice, with control mice protected by antitoxin.

25. Antitoxin does have a low effect Penicillin Respiratory support Muscle relaxants Treatment

26. Prevention Immunization with toxoid in childhood (2, 4, 6, 12 months ages) and every 10 years thereafter. When trauma occurs deeply: 1. Wound should be cleaned and debrided. 2. Tetanus toxoid booster should be given. 3. Tetanus immune globulin should be given. 4. Penicillin administered.

27. Clostridium botulinum Strictly anaerobic G+ bacillus but tolerates traces of oxygen (>2%) due to the enzyme called superoxide dismutase (SOD).superoxide dismutase Motile with peritrichous flagella. Oval & sub-terminal subterminal spores. Widley distributed saprophyte: soil, manure, fruits, veg. Optimum growth 35 C.

29. Growlipase negativelipase th between pH of 4.8 and 7pH Can't use lactose as a primary carbon source.lactose

30. Botulin NeurotoxinsNeurotoxins known as botulinum neurotoxins types A-G The preformed protein (resistant to proteolytic enzymes) is absorbed through the GI tract. In all sorts of food from sausages to honey. Food may not look spoilt. Potent food neurotoxin.

31. Phenotypes C. botulinum recognises four physiological groups (I- IV).physiological The classification is based on the ability of the organism to digest complex proteins:digestproteins Group I (proteolytic) or II (non-proteolytic): most outbreaks of human botulismbotulism Group III: mainly cause diseases in animals. Group IV: No human or animal disease.

32. Control Highly resistant spores (can survive 100 C for several hours), can be killed by moist heat 120C for 15 mins. Problems occur in canning factories where the contents of the can are not adequately heated. The spores survive radiation.

33. Toxins Toxins: Seven main types of toxin of C. botulinum: A-G. These are antigenically different but pharmacologically identical. A, B & E are most common. Type A&B - soil source, type E - marine source. The toxin binds irreversibly to the presynaptic nerve endings, where acetylcholine release is inhibited.

34. Pathogenesis Botulinus toxin Observing from the gut Carrying via the blood to peripheral nerve synapses Blocking release of acetylcholine Paralysis

35. Clinical findings Symptoms may develop after 1-2 days of ingestion. Initial nausea & vomiting. Oculomotor palsy, ptosis, vertigo and diplopia. Pure descending motor paralysis. No LOC/sensory loss. Progressive thirst (dry mouth and tongue), following by dysphagia, dyspnoea and abdo pain.

39. Clinical findings Death due to cardiac/respiratory failure. Floppy child syndrome: Children <6 months developed a flaccid paralysis due to toxin production in the gut. This occurs because gut colonization resistance is poor. It has been attributed to the presence of C. botulinum spores in honey given to babies with the feed.

45. In soil Alkaline vegetables/meat canned/vacuum- packed Spore germination Toxin production ingestionTransmission

46. Laboratory diagnosis Refer to a reference lab: Toxin maybe demonstrated by toxin-antitoxin neutralization test in mice.

47. Treatment Remove unabsorbed toxin from the stomach and GI tract. Neutralize unfixed toxin by giving polyvalent antitoxin. Give ICU care & support.

49. Control Of commercial food preparation. Those who have had a suspected contact a prophylactic dose of polyvalent antitoxin should be given.

50. Invasive clusteridums Include 30% of clusteridums Produce wide range of lethal, hemolytic and necrotic toxins and enzymes.