Clostridiums Largestraight rounded ends Large, straight or slightly curved roads with rounded ends. Bulging spore Mostly motile (with peritrichous flagella)peritrichous.

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Presentation transcript:

Clostridiums Largestraight rounded ends Large, straight or slightly curved roads with rounded ends. Bulging spore Mostly motile (with peritrichous flagella)peritrichous flagella Anaerobic Anaerobic (only some tolerate O 2 )

Clostridiums saprophytic Usually saprophytic proteolyticfermenter Usually proteolytic and fermenter (Important in the process of decomposition of animal proteins) toxigenic Most of the species are highly toxigenic soil animal GI Living normally in soil or animal GI

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

Clostridiums tetani Peritricus Peritricus flagella Terminal spore Highly resistant spores (but glutaraldehyde is effective.) Toxins: Tetanolysin (Tetanospasmin) - Oxygen labile haemolysin.

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

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

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

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.

Clinical findings Gradual onset Gradual onset Incubation period Incubation period: 4-5 days – several weeks Violent muscle spasms in the site of infection.

Clinical findings Lockjaw (trismus) Lockjaw (trismus) due to rigid contraction of the jaw muscles, a characteristic known as “risus sardonicus”

Clinical findings Clinical findings (cont.) Extreme arching of the back Extreme arching of the back (Opisthotonos) Low blood pressureSweatingtachycardia arrhythmia Low blood pressure, Sweating, tachycardia, arrhythmia and autonomic instability. Respiratory failure Respiratory failure.

Neonatal tetanus

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

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

Antitoxin (does have a low effect) Penicillin Respiratory support Muscle relaxants Treatment

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.

Clostridium botulinum Strictly anaerobic G+ bacillus but tolerates traces of oxygen (>2%) due to superoxide dismutase (SOD).superoxide dismutase Motile with peritrichous flagella.

Clostridium botulinum Oval & sub-terminal Oval & sub-terminal spores. saprophyte Widely distributed saprophyte: soil, manure, fruits, veg. 35 C Optimum C.

Lipase negative Lipase Growth between pH of 4.8 and 7pH Can't use lactose as a primary carbon source.lactose

Botulin neurotoxin As a neurotoxin (types A-G) Antigenically different but pharmacologically identical. A, B & E are most common. 1 gram killd 1 million people Type A exhibits an LD 50 of ng in monkeysLD 50ng

Botulin Foundall sorts of food Found in all sorts of food (sausages to honey) Resistant proteolytic enzymes Resistant to proteolytic enzymes (absorbed through the GI tract). Type A&B - soil source, type E - marine source. acetylcholine The toxin binds irreversibly to the presynaptic nerve endings, where acetylcholine inhibited release is inhibited.

Phenotypes C. botulinumphysiological host C. botulinum recognises four physiological & host groups (I-IV):physiological 1.Group I (proteolytic) human botulism 2.II (non-proteolytic): most outbreaks of human botulism animals 3. Group III: mainly cause diseases in animals. No human or animal 4. Group IV: No human or animal disease.

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

Pathogenesis Botulinus toxin Absorbing from the gut ---> Carrying via the blood to peripheral nerve synapses ---> Blocking release of acetylcholine ---> Paralysis

Clinical findings Incubation period Incubation period: 1-2 days Symptoms: Symptoms: - - Initial nausea, vomiting, dysphagia, and abdominal pain - Oculomotor palsy, ptosis, diplopia. - Descending motor paralysis - Progressive thirst (dry mouth and tongue)

Clinical findings Death due to cardiac/respiratory failure. Floppy child syndrome: Floppy child syndrome: Children <6 months (a flaccid paralysis due to toxin production in the gut.) It has been attributed to the presence of C. botulinum spores in honey given to babies with the feed.

Transmission soilAlkaline vegetables/meat Spore germination Toxin ingestion In soil ---> Alkaline vegetables/meat ---> canned/vacuum-packed ---> Spore germination ---> Toxin production ---> ingestion

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

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

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

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