1 Anaerobic bacteria

2 spore-forming anaerobes Clostridium G + non-spore-forming anaerobes G +, G - cocci, bacilli Classification

3 Section Ⅰ Clostridium

4 General characteristics gram-positive, spore-forming bacilli obligate anaerobes motile -- peritrichous flagella (exception: C. perfringens — nonmotile) the sporangia – swollen typical clinical symptoms

5 Clostridium C. tetani C. botulinum C. perfringens C. difficile

6 C. tetani

7

8 Characteristics anaerobic gram- positive rod that forms terminal spores motile with peritrichous flagella tetanospasmin

9 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

10 Pathogenicity Virulence factors –Tetanospasmin Protein (neurotoxin) Heat-labile (65 ℃, 30min) Mechanisms

11 Mechanisms of tetanospasmin toxin → peripheral nerve fibers / lymph and blood → spinal cord and brain stem → inhibitory interneuron → blocks the release of neurotransmitters from the presynaptic membrane of inhibitory interneurons→ inhibit the motor neuron → spastic paralysis (rigid paralysis) 麻痹性痉挛 excitatory transmitter: acetylcholine inhibitory transmitter: glycine and γ–aminobutyric acid

12 Mechanisms of tetanospasmin spastic paralysis (rigid paralysis)

13 Disease-tetanus(neonatal tetanus) latent period: 4-5d ～ several weeks typical symptoms: Lockjaw, sardonic smile Opisthotonos Pathogenicity

14 Pathogenicity Disease-neonatal tetanus –a frequent cause of death in developing countries –most common causes: cutting the umbilical cord with unsterilized instruments or infection of the umbilical stump –the fatality rate: around 90% –the common death cause: respiratory failure

15 Immunity Antitoxin immunity Weak potent exotoxin rapid combination with target cells Toxoid vaccine

16 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

17 C. perfringens

18 Characteristics Shape and structure –Subterminal endospore –Capsule –Nonmotile

19 Classification –five toxigenic types (A through E) –α toxin: the most potent toxin → exhibits lecithinase activity → destroys erythrocytes, leukocytes, and platelets → hemolysis, tissue necrosis + Type + α, Alphaβ, Betaε, Epsilon A B+++ C++ D+ E+ ι, Iota + Characteristics

20 Cultivation anaerobic double zones of hemolysis carbohydrate fermentation (lactose) Inner zone: θ toxin complete Outer zone: α toxin Incomplete Characteristics Stormy fermentation

21 Virulence factors –α toxin produced by all strains acts as a lecithinase diagnosis: Nagler reaction--egg yolk agar Pathogenicity

22 Virulence factors –Enterotoxin produced by types A(most), C, and D heat-labile –Others collagenase, hemolysin, proteinase, DNase (deoxyribonuclease) Pathogenicity

23 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

24 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

25 Control Care of trauma: debridement Antimicrobial therapy Antitoxin Hyperbaric oxygen Symptomatic care for food poisoning

26 C. botulinum

27 Characteristics Gram positive rod Subterminal endospore Noncapsule Obligate anaerobe

28 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 action Toxin → gut → blood → cholinergic synapses → block the release of exciting neurotransmitter, e.g., acetylcholine → flaccid paralysis potassium cyanide(KCN)10,000 times

29 Mechanisms of botulinum toxin flaccid paralysis

30 Disease—Botulism –from Latin botulus, "sausage"  Food poisoning  Infant botulism  Wound botulism Sausages, seafood products, milk, and canned vegetables Honey Pathogenicity

31 Disease –Food poisoning manifestation: flaccid paralysis: double vision, dysphagia, difficulty in breathing and speaking rare gastrointestinal symptoms cause of death: respiratory failure Pathogenicity

32 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

33 Disease –wound botulism Rare Transmission: trauma Pathogenicity

34 Medicine Blepharospasm

35 C. difficile

36 Pathogenicity Virulence factor exotoxin A: enterotoxin exotoxin B: cytotoxin Disease pseudomembranous colitis antibiotic-associated diarrhea

37 Control Treatment discontinuation of causative antibiotics administration of sensitive antibiotics Prevention no vaccine use antibiotics only in necessary

38 non-spore-forming anaerobes

39 Characteristics include both G + and G - bacilli and cocci. members of the normal flora cause: endogenous infection

40 Non-spore forming anaerobes

41 Change of habitat Decrease of host defense Dysbacteriosis Local anaerobic environment formation Conditions causing disease

42 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 aminoglycisides Characteristics of infections

43 Diseases septicemia infections in central nervous system dental sepsis pulmonary infections intraabdominal infections infections of the female genital tract

44 occurrence development of anaerobic environments (e.g., deep wound) spores → vegetative cells ↓ tissue destruction and necrosis; carbohydrate fermentation and gas (H 2;, CO 2 ) formation and accumulation in the tissue ↓ restrict the blood supply (flow) → increases the tissue necrosis