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Spore FormingGram-positive Bacilli
Titik Nuryastuti
Microbiology Department,Fac. of Medicine, UGM
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SporesWhy do bacteria produce spores?
Survival
Classification
Definition = a resting cell, highlyresistant to dessication, heat, and
chemical agents; when returned tofavourable conditions bacteria re-activated, the spores germinate toproduce single vegetative cells.
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SF Bacteria- Bacillus Aerobic, G+ rods in chains, spores are
located in center of the non-motile bacilli
Found in soil, water, air and vegetation Spores are viable for decades.
B. cereus produce enterotoxin and cause
food poisoning. B. anthracis infection in human through
injured skin (cutaneous anthrax), mucousmembranes (GI anthrax), or inhalation of
spores into lung.
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Bacillus anthracis
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Spores germinate in the tissue of entry,and growth of vegetative organisms
result in formation of a gelatinousoedema and congestion.
Spread via lymphatics to bloodstream
and multiply freely in blood and tissues. Capsulated, poly-D-glutamic acid
capsule is antiphagocytic
SF Bacteria- Bacillus
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Anthrax toxin is made up of three proteins: Protective antigen (PA), edema factor (EF) and lethal
factor (LF).
Clinical finding : Cutaneous Anthrax(malignant pustule):
Generally occurs on exposed surfaces of the arms,face and neck through wound contamination by thespores of the organism. About 95% of the cases with
amortality rate 20% . Inhalation Anthrax(wool sorter disease):
About 5% of the cases with 85-90% mortality. Treatment: ciprofloxacin, penicillin G along with
gentamicin and streptomycin.
SF Bacteria- Bacillus
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SF Bacteria-Bacillus Lab diagnosis :
Gram staining
Culture on Blood agar Speciment :
Fluid, pus, blood, sputum
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SF Bacteria - ClostridiumAnaerobic, G+, motile rods
Their natural habitat is the soil or the
intestinal tract of human and animals,where they live as saprophytes
Found in soil, animal faeces.
Spores is placed centrally, subterminallyor terminally; most species are motilewith flagella.
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SF Bacteria - Clostridium Many decompose proteins of form
toxins, some do both
Among the pathogens are theorganisms causing botulism, tetanus,gas gangrene, and pseudomembranouscolitis.
C. botulism, C. tetani, C. perfringens, C.difficile
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SF Bacteria - Clostridium Many form colonies with a zone of
haemolysis on blood agar. C perfringens
typically produce multiple zones ofhaemolysis around colonies.
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Identification
In most species, the spores are locatedcentrally, subterminally or terminally.
Most species of Clostridia are motilewith peritrichous flagella
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Clostridium
Epidemiology Ubiquitous
Present in soil, water, sewage
Normal flora in GI tracts of animals andhumans
Pathogenesis Spore formation
resistant to heat, dessication, and disinfectants can survive for years in adverse environments Rapid growth in oxygen deprived, nutritionally
enriched environment Toxin elaboration (histolytic toxins, enterotoxins,
neurotoxins)
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Clostridium botulinum
Epidemiology
Commonly isolated in soil and water
Human disease associated with botulinum toxin A, B,
E, F Pathogenesis
Blocks neurotransmission at peripheral cholinergic
synapses
Prevents release of acetylcholine, resulting in musclerelaxation
Recovery depends upon regeneration of nerve
endings
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SF Bacteria C.botulinum C botulinum causes botulism
-Distinguished by antigenic type of toxin
Spores are resistant to 100C for many hours,diminished at acid pH or high salt.
Toxin - 7 antigenic varieties (AG). A, B, E(F) mainly harmful to human.
Botulinum toxin is absorbed from gut andbinds to receptors of presynaptic nervoussystem and cranial nerves.
Lethal dose to human 1-2 g.
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SF Bacteria - ClostridiumPathogenesis
Most cases, through ingestion of uncooked
food. Toxin acts by blocking release of acetylcholine
at synapses and neuromuscular junctions flacid paralysis.
Symptoms such as visual disturbances,inability to swallow, speech problem; seldomwith no apparent GI symptoms; no fever.
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Botulism
Clinical SyndromesFoodborne botulism
Associated with consumption of preformed toxin Home-canned foods (toxin A, B)
Preserved fish (toxin E) Onset of symptoms 1-2 days Blurred vision vision, dilated pupils, dry mouth, constipation Bilateral descending weakness of peripheral muscles; death
related torespiratory failure
Infant botulism Consumption of foods contaminated with botulinum spores 6-10% of syrups or honeys Disease associated with neurotoxin produced in vivo Onset of symptoms in 3-10 days
Wound botulism (skin popping)
Asymptomatic adult carriage
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Botulism: Treatment
Treatment
Supportive care
Elimination of organism from GI tract Gastric lavage
Metronidazole or penicillin
Botulinum Immunoglobulin (BIG): pooled plasma from adults
immunized with pentavalent (ABCDE) botulinum toxoid
Trivalent equine Immunoglobulin (ABE)
Prevention
Prevention of spore germination (Storage
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SF Bacteria - Clostridium
floppy baby = infant botulism. C botulinumspores in babies food.
Treatment antitoxins raised in horses.
Trivalent (A, B, E) antitoxin must be promptlyadministered intravenously with precautions;
plus adequate ventilations.
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Clostridium tetani
Epidemiology Spores found in most soils, GI tracts of animals Disease in un-vaccinated or inadequately immunized Disease does not induce immunity
Pathogenesis Spore inoculated into woundTetanospasmin
Heat-labile neurotoxin Retrograde axonal transport to CNS Blocks release of inhibitory neurotransmitters (eg. GABA) into
synapses, allowing excitatory synapses to be unregulated. Thisresults in muscle spasms Binding is irreversible
Tetanolysin Oxygen labile hemolysin, unclear clinical significance
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SF Bacteria C.tetani
Clostridium tetani cause tetanus.
Distinguishable by specific flagellar antigens.
Pathogenesis: Wound contamination, notan invasive organism. The toxins releasedfrom vegetative cells reaches the CNS and
rapidly becomes fixed to receptors in thespinal cord and brain stem and exerts theiraction.
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C. tetani
Toxins: Tetanospasmin
binds to receptors on the presynaptic
membranes of motor neurons.
Clinical Findings: Incubation period:
4-5 days to many weeks. The diseaseis chacterized by tonic contraction ofvoluntary muscles.
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Tetanus
Treatment
Debridement of wound
Metronidazole
Tetanus immunoglobulin
Prevention Vaccination with a series of 3 tetanustoxoid
Booster dose every 10 years
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C. perfringens
Many different- toxin producing clostridia canproduce invasive infections(including myonecrosisand gas gangrene) if introduced into damaged tissue.About 30 species of clostridia may produce such aninfection, but the most common in invasive disease isC. perfringens(90%). An enterotoxin ofC.perfringensis a common cause of food poisoning.
Toxins: produce different types of toxins andenzymes that result in spreading infection. They
have lethal, necrotizing, and hemolytic properties. Pathogenesis: Wound contamination. Clinical Findings: Infection spreads in 1-3 days.
Crepitation in subcutaneous tissue and muscle, fever,tissue necrosis, hemolytic anemia, severe toxemia
and death.
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Clostridial soft tissue infections
Crepitant cellulitis
Fascitis
Myonecrosis
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Clostridial myonecrosis
Clinical course
Symptoms begin 1-4 days after inoculation and
progresses rapidly to extensive muscle necrosis andshock
Local area with marked pain, swelling, serosanguinousdischarge, bullae, slight crepitance
May be associated with increased CPK
Treatment Surgical debridement
Antibiotics
Hyperbaric oxygen
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Clostridium difficile
Epidemiology Endogenous infection
Colonizes GI tract in 5% healthy individuals Antibiotic exposure associated with overgrowth ofC. difficile
Cephalosporins, clindamycin, ampicllin/amoxicillin Other contributing factors: agents altering GI motility,surgery, age, underlying illness
Exogenous infection Spores detected in hospital rooms of infected patients
PathogenesisEnterotoxin (toxin A)
produces chemotaxis, induces cytokine production andhypersecretion of fluid, development of hemorrhagic
necrosisCytotoxin (toxin B)
Induces polymerization of actin with loss of cellularcytoskeleton
d ff l l
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C.difficilecolitis
Clinical syndromes Asymptomatic colonization Antibiotic-associated diarrhea Pseudomembranous colitis
Diagnosis Isolation of toxin Culture
Treatment Discontinue antibiotics
Metronidazole or oral vancomycin Pooled human IVIG for severe disease Probiotics (saccharomyces boulardii) New drugs (nitazoxanide, tolevamer) Relapse in 20-30% (spores are resistant)
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The Genus
ClostridiumLeft. Stained pus from amixed anaerobicinfection. At least three different clostridiaare apparent. Right. Electron micrograph of
Clostridium tetani
C botul inum
C.perfringens
C tetani
C. dif fi cile