ClostridiumsClostridiums

ClostridiumsClostridiums

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”).

DiseasesDiseasesC. 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.

Tetanus

Botulism

Gas gangrene

Clostridiums tetaniClostridiums tetani

Peritricus flagella

Terminal spore

Highly resistant spores, but glutaraldehyde is effective.

Toxins: tetanolysin - oxygen labile haemolysin.

Clostridiums tetaniClostridiums tetani

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

TetanospasminTetanospasmin

Neuromuscular pathogenic effect.Gene encoded on a plasmid. Tiny lethal dose required, but only effective in

humans parentrally (not oral).

The site of infectionThe 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.

PathogenesisPathogenesis

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 findingsClinical findingsGradual 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.

Neonatal tetanus

TransmissionTransmission

Highest incidence in devloping countries, associated with a fertile soil and warm climate.

Previous association with non-sterile ear piercing. 

Laboratory DiagnosisLaboratory 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.

Antitoxin does have a low effect

Penicillin

Respiratory support

Muscle relaxants

TreatmentTreatment

PreventionPrevention

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 botulinumClostridium botulinum Strictly anaerobic G+ bacillus but tolerates traces of

oxygen (>2%) due to the enzyme called superoxide dismutase (SOD).

Motile with peritrichous flagella.

Oval & sub-terminal subterminal spores.

Widley distributed saprophyte: soil, manure, fruits, veg.

Optimum growth 35 C.

Growlipase negative

th between pH of 4.8 and 7

Can't use lactose as a primary carbon source.

BotulinBotulinNeurotoxins 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.

PhenotypesPhenotypes

C. botulinum recognises four physiological groups (I-IV).

The classification is based on the ability of the organism to digest complex proteins:

Group I (proteolytic) or II (non-proteolytic): most outbreaks of human botulism

Group III: mainly cause diseases in animals. Group IV: No human or animal disease.

ControlControl

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.

ToxinsToxinsToxins: 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.

PathogenesisPathogenesisBotulinus toxin

Observing from the gut Carrying via the blood to peripheral nerve synapses Blocking release of acetylcholine Paralysis

Clinical findingsClinical 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.

Clinical findingsClinical 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.

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

TransmissionTransmission

Laboratory diagnosisLaboratory diagnosis

Refer to a reference lab:

Toxin maybe demonstrated by toxin-antitoxin neutralization test in mice.

TreatmentTreatment

Remove unabsorbed toxin from the stomach and GI tract.

Neutralize unfixed toxin by giving polyvalent antitoxin.

Give ICU care & support.

ControlControl

Of commercial food preparation.

Those who have had a suspected contact a prophylactic dose of polyvalent antitoxin should be given.

Invasive clusteridumsInvasive clusteridums

Include 30% of clusteridums

Produce wide range of lethal, hemolytic and necrotic toxins and enzymes.