1 Anaerobic bacteria. 2 spore-forming anaerobes Clostridium G + non-spore-forming anaerobes G +, G -...
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Transcript of 1 Anaerobic bacteria. 2 spore-forming anaerobes Clostridium G + non-spore-forming anaerobes G +, G -...
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Anaerobic bacteria
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• spore-forming anaerobesClostridium
G+
• non-spore-forming anaerobesG+, G-
cocci, bacilli
Classification
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Section Ⅰ Clostridium
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General characteristics
• gram-positive, spore-forming bacilli
• obligate anaerobes
• motile -- peritrichous flagella (exception: C. perfringens—nonmotile)
• the sporangia– swollen
• typical clinical symptoms
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Clostridium
• C. tetani• C. botulinum• C. perfringens• C. difficile
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C. tetani
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Characteristics
• anaerobic gram-positive rod that forms terminal spores
• motile with peritrichous flagella
• tetanospasmin
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Pathogenicity• portal of entry: wound
• conditions of infection
regional anaerobic environment– deep and narrow wound, contamination of soil
or foreign bodies
– necrotic tissues
– contamination of aerobes or facultative anaerobes
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Pathogenicity
• Virulence factors
–Tetanospasmin
• Protein (neurotoxin)
• Heat-labile (65 , 30min)℃• Mechanisms
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Mechanisms of tetanospasmin
toxin → peripheral nerve fibers / lymph and
blood → spinal cord and brain stem → inhibit
ory interneuron → blocks the release of neurot
ransmitters from the presynaptic membrane of
inhibitory interneurons→ inhibit the motor neur
on → spastic paralysis (rigid paralysis)
麻痹性痉挛excitatory transmitter: acetylcholineinhibitory transmitter: glycine and γ–aminobutyric acid
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Mechanisms of tetanospasmin
spastic paralysis (rigid paralysis)
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• Disease-tetanus(neonatal tetanus)latent period: 4-5d ~ several weeks
typical symptoms:
Lockjaw, sardonic smile
Opisthotonos
Pathogenicity
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Pathogenicity• Disease-neonatal tetanus
– a frequent cause of death in dev
eloping countries
– most common causes: cutting th
e umbilical cord with unsterilized
instruments or infection of the u
mbilical stump
– the fatality rate: around 90%
– the common death cause: respir
atory failure
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Immunity
• Antitoxin immunity
• Weak
potent exotoxin
rapid combination with target cells
• Toxoid vaccine
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Control • Proper care of wounds: surgical debridement
• Active immunization: tetanus toxoid
for children: basic immunization: DPT(diphtheria toxoid, pertussis vaccine, tetanus toxoid)
for a high-risk group : toxoid booster
• Passive immunization: tetanus antitoxin
urgent prevention (along with toxoid)
As soon as possible
• Special treatment
– administration of antibiotics
– supportive measures
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C. perfringens
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Characteristics
• Shape and structure
– Subterminal endospore
– Capsule
– Nonmotile
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• Classification– five toxigenic types (A through E)– αtoxin: the most potent toxin→exhibits lecithinase activ
ity→destroys erythrocytes, leukocytes, and platelets→ hemolysis, tissue necrosis
+
Type
+
α, Alpha β, Beta ε, Epsilon
A
B + + +
C + +
D +
E +
ι, Iota
+
Characteristics
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• Cultivationanaerobic
double zones of hemolysis
carbohydrate fermentation (lactose)
Inner zone: θ toxincomplete
Outer zone: α toxinIncomplete
Characteristics
Stormy fermentation
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• Virulence factors– α toxin
• produced by all strains• acts as a lecithinase
• diagnosis: Nagler reaction--egg yolk agar
Pathogenicity
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• Virulence factors
– Enterotoxin• produced by types A(most), C, and D
• heat-labile
– Others• collagenase, hemolysin, proteinase, DNase (deo
xyribonuclease)
Pathogenicity
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• Disease
– Gas gangrene• Occurrence
• Transmission: trauma
• Pathogens: 60 ~ 80 % cases by
type A
• Manifestation: sudden outset,
emphysema, edema, necrotic
tissues, foul-smelling, toxemia, shock
Pathogenicity
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• Disease– Food poisoning
• transmission: gastrointestinal tract
• pathogens: type A
• manifestation: short incubation period (10hrs)
diarrhea
self-limiting
– Necrotizing enteritis
• pathogens: type C
• highly fatal in children
Pathogenicity
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Control
• Care of trauma: debridement
• Antimicrobial therapy
• Antitoxin
• Hyperbaric oxygen
• Symptomatic care for food poisoning
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C. botulinum
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Characteristics
• Gram positive rod
• Subterminal endospore
• Noncapsule
• Obligate anaerobe
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• Virulence factor—botulinum toxin
– neurotoxin
– relatively heat-labile and resistant to protease
– types: A, B, C, D, E, F, G
– the most potent toxic material known
Pathogenicity
mechanism of actionToxin → gut → blood → cholinergic synapses → block the release of exciting neurotransmitter, e.g., acetylcholine → flaccid paralysis
potassium cyanide(KCN)
10,000 times
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Mechanisms of botulinum toxin
flaccid paralysis
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• Disease—Botulism
– from Latin botulus, "sausage"
Food poisoning Infant botulism Wound botulism
Sausages, seafood products, milk, and canned vegetables
Honey
Pathogenicity
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• Disease
– Food poisoning
• manifestation:
flaccid paralysis: double vision, dysphagia,
difficulty in breathing and speaking
rare gastrointestinal symptoms
cause of death: respiratory failure
Pathogenicity
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• Disease
– infant botulism
• manifestation: constipation, poor feeding,
difficulty in sucking and swallowing, weak
cry, loss of head control.
Floppy baby
• prevention: free of honey
Pathogenicity
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• Disease
– wound botulism
• Rare
• Transmission: trauma
Pathogenicity
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Medicine
Blepharospasm
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C. difficile
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Pathogenicity • Virulence factor
exotoxin A: enterotoxin
exotoxin B: cytotoxin
• Disease
pseudomembranous colitis
antibiotic-associated diarrhea
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Control
• Treatmentdiscontinuation of causative antibiotics
administration of sensitive antibiotics
• Preventionno vaccine
use antibiotics only in necessary
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non-spore-forming anaerobes
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Characteristics
• include both G+ and G- bacilli and cocci.
• members of the normal flora • cause: endogenous infection
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Non-spore forming anaerobes
Gram negati ve Gram positi ve Baci l l us Coccus Baci l l us Coccus
Bacteri odes
Vei l l onel l a
Propionibacteri um
Peptostreptococus
Prevotel l a Bifi dobacteri um
Porphyromonas
Eubacteri um
Fusobacterium
Actinomyces
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• Change of habitat
• Decrease of host defense
• Dysbacteriosis
• Local anaerobic environment formation
Conditions causing disease
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• endogenous infection throughout body, most chronic
• nonspecific manifestations, most pyogenic
• foul-smelling discharge, sometimes gas formation
• direct smear positive, aerobic culture negative
• have no response to some antibiotics such as aminoglyci
sides
Characteristics of infections
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Diseases
• septicemia
• infections in central nervous syst
em
• dental sepsis
• pulmonary infections
• intraabdominal infections
• infections of the female genital tr
act
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occurrence
development of anaerobic environments (e.g., deep wound)
spores → vegetative cells ↓ tissue destruction and necrosis;
carbohydrate fermentation and gas (H2; ,CO2) formation
and accumulation in the tissue ↓ restrict the blood supply (flow) → increases the tissue
necrosis