1 Anaerobic bacteria. 2 spore-forming anaerobes Clostridium G + non-spore-forming anaerobes G +, G -...

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1 Anaerobic bacteria

Transcript of 1 Anaerobic bacteria. 2 spore-forming anaerobes Clostridium G + non-spore-forming anaerobes G +, G -...

Page 1: 1 Anaerobic bacteria. 2 spore-forming anaerobes Clostridium G + non-spore-forming anaerobes G +, G - cocci, bacilli Classification.

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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