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  • 1. Anae rob ic Bacte ria
  • 2. Caegor t y Spore-forming: rod, Gram (+)--- Clostridium Nonspore-forming: see next slides
  • 3. Caegor t ySpore- rod, Gram (+)---forming: ClostridiumNonspore-forming: Rod, Gram (+) Propionibacterium 丙酸菌属 Bifidobacterium Lactobacillus Eubacterium Rod, Gram (-) Bacteroides Actinomyces Fusobacterium 梭菌属Cocci, Gram (+) Peptococcus Campylobacter PeptostreptococcusCocci, Gram (-) Veillonella
  • 4. Clostridium Species The clostridia are opportunistic pathogens. Nonetheless, they are responsible for some of the deadliest diseases including gas gangrene, tetanus and botulism. Less life- threatening diseases include pseudomembranous colitis (PC) and food poisoning. cause disease primarily through the production of numerous exotoxins. perfringens, tetani, botulinum, difficile
  • 5. Clostridium TetaniPathogenesis of tetanus caused by C tetani
  • 6. General introduction C tetani is found worldwide. Ubiquitous in soil, it is occasionally found in intestinal flora of humans and animals C.tetani is the cause of tetanus,or lockjaw. When spores are introduced into wounds by contaminated soil or foreign objects such as nails or glass splinters
  • 7. BIOCHEMICAL CHARACTERISTICS Morphology: long and slender; peritrichous flagella,no capsule, terminal located round spore(drum-stick apperance), its diameter greater than vegetative cell. Culture:obligate anaerobic; Gram(+); swarming occures on blood agar, faint hemolysis. Biochemical activities:does not ferment any carbohydrate and proteins. Resistance: tolerate boiling for 60 min.alive several ten years in 2-5 x 0.3-0.5um soil. Classification and Antigenic Types: C tetani is the only species. There are no serotypes
  • 8. Pathogenicity No invasiveness; toxemia  retrograde transport (exogenous infection ) to (CNS) produces two exotoxins:  delitescence : a few tetanolysin, and tetanospasmin(a kind of days to several neurotoxin, toxicity weeks strong)  The two animal The actions of species most tetanospasmin are susceptible to this complex and involve three components of the toxemia are horses nervous system: central and humans. motor control, autonomic function, and the neuromuscular junction.
  • 9. Clostridium tetani -Tetanospasmin disseminates systemically binds to ganglioside receptors • inhibitory neurones in CNS glycine • neurotransmitter stops nerve impulse to muscles spastic paralysis 痉挛性麻痹 severe muscle contractions and spasms can be fatal
  • 10. Tetanospasmin
  • 11. Clinical Manifestations The initial symptom is cramping and twitching of muscles around a wound. The patient usually has no fever but sweats profusely and begins to experience pain, especially in the area of the wound and around the neck and jaw muscles (trismus). Portions of the body may become extremely rigid, and opisthotonos 角弓反张 (a spasm in which the head and heels are bent backward and the body bowed forward) is common. Complications include fractures, bowel impaction, intramuscular hematoma, muscle ruptures, and pulmonary, renal, and cardiac problems
  • 12. Clinical ManifestationsDISEASE CLINCAL MANIFESTATIONSAGeneralized Involvement of bulbar and paraspinal muscles(trismus or lockjaw, risus sardonicus, difficulty swallowing, irritability, opisthotonos);involvement of autonomic nervous system(sweating, hyper thermia, cardiac arrhythmias, fluctuations in blood pressure)Cephalic Primary infection in head,particularly ear;isolated or combined involvement of cranial nerves, particularly seventh cranial nerve; very poor prognosisLocalized Involvement of muscles in area of primary injury; infection may precede generalized disease; favorable prognosisNeonatal Generalized disease in neonates; infection typically originates from umbilical 脐带 stump;very poor prognosis in infants whose mothers are nonimmune
  • 13. Epidemiology 1 million cases of tetanus occur annually in the world,with a mortality rate ranging from20% to 50%. But rare in most developed countries. In some developing countries, tetanus is still one of the ten leading causes of death, and neonatal tetanus accounts for approximately one-half of the cases worldwide. In less developed countries, approximate mortality rates remain 85% for neonatal tetanus and 50% for nonneonatal tetanus. In the United States, intravenous drug abusers have become another population with an increasing incidence of clinical tetanus In untreated tetanus, the fatality rate is 90% for the newborn and 40% for adults.
  • 14. Immunity Humoral immunity(antitoxin) There is little, if any, inate immunity and the disease does not produce immunity in the patient. Active immunity follows vaccination with tetanus toxoid
  • 15. Diagnosis Diagnosis is primarily by the clinical symptoms (above). The wound may not be obvious. C tetani can be recovered from the wound in only about one-third of the cases. It is important for the clinician to be aware that toxigenic strains of C tetani can grow actively in the wound of an immunized person. Numerous syndromes, including rabies and meningitis, have symptoms similar to those of tetanus and must be considered in the differential diagnosis.
  • 16. Vaccination• infant• DPT (diptheria, pertussis, tetanus)• tetanus toxoid – antigenic – no exotoxic activity
  • 17. Control The offending organism must be removed by local debridemen 清创 术 toxoid TAT; Metronidazole (For more serious wounds) AIDS patients may not respond to prophylactic injections of tetanus toxoid
  • 18. C. perfringens• soil, fecal contamination• gas gangrene – swelling of tissues – gas release * fermentation products• wound contamination
  • 19. Toxinstoxin Biological Feature Types of Toxins A B C D Eα lecithinase; increase the vascular permeability; + + + + + hemolytic; produces necrotizing activityβ Necrotizing activity, - + + - - induces hypertension by causing release of catecholamines.ε increase the - - - + - permeability of gastrointestinal wallτ Necrotizing activity; increase the vascular - - - - + permeability
  • 20. Toxins Many of these toxins have lethal, necrotizing, and hemolytic properties; The alpha toxin produced by all types of C. perfringens, is a lecithinase that lyses erythrocytes, platelets, leukocytes, and endothelial cells. And its lethal action is proportionate to the rate at which it splits lecithin to phosphorylcholine and diglyceride. The theta toxin has similar hemolytic and necrotizing effects. DNAase, hyaluronidase, a collagenase are also produced
  • 21. Enterotoxin Many strains of type A produce enterotoxin, which is a heat-labile protein and destroyed immediately at 100 ℃. Trypsin treatment enhances the toxin activity threefold. The toxin is produced primarily by type A strains but also by a few type C and D strains. It disrupts ion transport in the ileum(primarily) and jejunum by inserting into the cell membrane and altering membrane permeability. As superantigen.
  • 22. Pathogenesis•Tissue degrading enzymes – lecithinase [l toxin] – proteolytic enzymes – saccharolytic enzymes• Destruction of blood vessels• Tissue necrosis• Anaerobic environment created• Organism spreads
  • 23. Without treatment deathoccurs within 2 days effective antibiotic therapy debridement anti-toxin amputation & death is rare
  • 24. Gas gangrene Gas gangrene is a life-threatening disease with a poor prognosis and often fatal outcome. Initial trauma to host tissue damages muscle and impairs blood supply----lack of oxygenation Initial symptoms : fever and pain in the infected tissue.; more local tissue necrosis and systemic toxemia. Infected muscle is discolored (purple mottling) and edematous and produces a foul- smelling exudate; gas bubbles form from the products of anaerobic fermentation.
  • 25. Gas gangrene As capillary permeability increases, the accumulation of fluid increases, and venous return eventually is curtailed. As more tissue becomes involved, the clostridia multiply within the increasing area of dead tissue, releasing more toxins into the local tissue and the systemic circulation.
  • 26. Food poisoning Enterotoxin producing strains. These bacteria are found in mammalian faeces and soil. Small numbers of the bacteria may also be found in foods and they may propagate rapidly to dangerous concentrations if the food is improperly stored and handled.
  • 27. Food poisoning more than 108 vegetative cells are ingested and sporulate in the gut, the toxins can act rapidly in the body, causing severe diarrhea in 6-18 hours, dysentery, gangrene, muscle infections The action of C. perfringens enterotoxin involves marked hypersecretion in the jejunum and ileum, with loss of fluids and electrolytes in diarrhea.
  • 28. Cellulitis, Fasciitis Cellulitis, Fasciitis Fasciitis : a rapidly progressive, destructive process in which the organisms spread through fascial plan es. Fasciitis causes suppuration and the formation of gas Absense of muscle involvement rapidity
  • 29.  Necrotizing Enteritis Rare, acute necrotizing process in the jejunum Abdominal pain, bloody diarrhea, shock, and peritonitis Mortality: 50% Beta-toxin-producing C. perfringens type C Septicemia
  • 30. Who is at risk? Surgical patients; patient after trauma with soil contamination. People who ingest contaminated meat products (without proper refrigeration or reheating to inactivate endotoxin)
  • 31. Epidemiology C. perfringens type A: the intestinal tract of humans and animals, soil and water contaminated with feces. forms spores under adverse environmental conditions and can survive for prolonged periods. Type B to E strains colonize the intestinal tract of animals and occasionally humans.
  • 32. Epidemiology Type A: gas gangrene, soft tissue infections and food poisoning Type C: enteritis; necroticans
  • 33. Laboratory identification• lecithinase production Double Hemolysis Circles
  • 34. C. botulinum
  • 35. Biological Features Anaerobic Gram-positive rod-shaped sporeformer produces a protein neurotoxic. soil, sediments of lakes, ponds, decaying vegetation. intestinal tracts of birds, mammals and fish.
  • 36. Division---A, B, C1, D, E, F, and G.---type A. 62%---Not all produce toxin.---C and D not---G plasmid encoded.
  • 37. Transmission---spores heat resistant. canning. anaerobic environment---Botulism eating uncooked foods spores---GI, duodenum, blood stream,neuromuscular synapses.
  • 38. Virulence factors---bacterial protease---light chain,A,50 kDa; heavy chain,100kDa.---disulfide bond.---A potent toxin
  • 39.  binds peripheral nerve receptors • acetylcholine neurotransmitter inhibits nerve impulses flaccid paralysis death • respiratory Botulinum toxin • cardiac failure
  • 40. Botulinum toxin Bioterrorism • not an infection • resembles a chemical attack • 10 ng can kill a normal adult
  • 41. Epidemiology---4: foodborne, infant, wound, undetermined.---Certain foods; wound not.---Foodborne botulism, consumption.---Infant botulism, 1976, under 12m.---ingestion, colonize and produce toxin in theintestinal tract of infants. honey.---increased.---internationally recognized.
  • 42. Clinical syndromes---18-36 hours:---weakness, dizziness,dryness of the mouth.---Nausea,vomiting.---Neurologic features: blurred vision,inability to swallow, difficulty in speech,descending weakness of skeletal muscles,respiratory paralysis.
  • 43. Botulism( 肉毒中毒 ) food poisoning • rare • fatal germination of spore inadequately sterilized canned food • home not an infection
  • 44. Infection with C. botulinum Neonatal botulism • uncommon • the predominant form of botulism • colonization occurs  no normal flora to compete  unlike adult
  • 45. Wounds• extremely rare• an infection
  • 46. Immunity---specifically neutralized, antitoxin.---toxoided, make good antigens.---does not develop, amount toxic.---Repeated occurrence.---Once bound, unaffected by antitoxin.---circulating toxin ,neutralized , injection of antitoxin.---treated immediately with antiserum.---multivalent toxoid,unjustified,infrequency. experimental vaccine.
  • 47. Diagnosis---by clinical symptoms alone---differentiation difficult.--- most direct and effective: serum orfeces.---most sensitive and widely used:mouse neutralization test. 48h.Culturing of specimens 5-7d.
  • 48. Treatment Individuals known to have ingested food with botulism should be treated immediately with antiserum. antibiotic therapy (if infection) • Vaccination will not protect hosts from botulism, however passive immunisation with antibody is the treatment of choice for cases of botulism.
  • 49. Prevention---proper food handling and preparation.--- spores survive boiling (100 degrees at 1 atm) 1h.---toxin heat-labile, boiling or intense heating, inactivate the toxin.---bulge, gas, spoiled.
  • 50. C. difficile• After antibiotic use• Intestinal normal flora --greatly decreased• Colonization occurs• Enterotoxin secreted• Pseudomembanous colitis
  • 51. Pseudomembranous Colitis Pseudomembranous colitis (PC) results predominantly as a consequence of the elimination of normal intestinal flora through antibiotic therapy. Symptoms include abdominal pain with a watery diarrhea and leukocytosis. "Pseudomembranes" consisting of fibrin, mucus and leukocytes can be observed by colonoscopy. Untreated pseudomembranous colitis can be fatal in about 27-44%.
  • 52. Therapy Discontinuation of initial antibiotic (e.g. ampicillin) Specific antibiotic therapy (e.g. vancomycin)
  • 53. Obligate (strict) anaerobes • no oxidative phosphorylation • fermentation • killed by oxygen • lack certain enzymes – superoxide dismutase * O2-+2H+ H2O2 – catalase * H2O2 H20 + O2 – peroxidase * H2O2 H20 /NAD to NADH
  • 54. Strict anaerobe infectious disease Sites throughout body Muscle, cutaneous/sub-cutaneous necrosis Abscesses
  • 55. Bacterial Flora of the BodySite Total Bacteria Ratio (per/ml or gm) Anaerobes:AerobesUpper Airway Nasal Washings 103-104 3-5:1 Saliva 108-109 1:1 Tooth Surface 1010-1011 1:1 Gingival Crevice 1011-1012 1000:1Gastrointestinal Tract Stomach 102-105 1:1 Small Bowel 102-104 1:1 Ileum 104-107 1:1 Colon 1011-1012 1000:1Female Genital Tract Endocervix 108-109 3-5:1 Vagina 108-109 3-5:1
  • 56. Problems in identification of anaerobic infections • air in sample (sampling, transportation) – no growth • identification takes several days or longer – limiting usefulness • often derived from normal flora – sample contamination can confuse
  • 57. Virulence Factors1. Anti-phagocytic capsule • Also promote abscess formation2. Tissue destructive enzymes • B. fragilis produces variety of enzymes (lipases, proteases, collagenases) that destroy tissue  Abscess Formation3. Beta-lactamase production • B. fragilis – protect themselves and other species in mixed infections4. Superoxide dismutase production • Protects bacteria from toxic O2 radicals as they move out of usual niche
  • 58. Characteristics of Anaerobic Infections1. Most pathogenic anaerobes are usually commensals • Originate from our own flora2. Predisposing Conditions • Breeches in the mucocutaneous barrier   displace normal flora • Compromised vascular supply • Trauma with tissue destruction • Antecedent infection
  • 59. Characteristics of Anaerobic Infections3. Complex Flora 4. Synergistic Mixture Multiple species of Aerobes & • Abdominal Infection  Avg Anaerobes of 5 species  3 anaerobic  E. coli  Consume O2  2 aerobic • Allow growth of • Less complex then nl flora anaerobes • Fecal flora 400 different species  Anaerobes  promote  Those predominant in stool growth of other are not infecting species bacteria by being • Veillonella, Bifidobacterium  rarely antiphagocytic and pathogenic producing B- • Species uniquely suited to cause infection lactamases predominate
  • 60. Clues to Anaerobic Infection • Infections in continuity to mucosal surfaces • Infections with tissue necrosis and abscess formation • Putrid odor • Gas in tissues • Polymicrobial flora • Failure to grow in the lab BIOCHEMICAL KITS • e.g. API SYSTEM GAS CHROMATOGRAPHY • volatile fermentation products
  • 61. Bacteroides fragilis• Major disease causing strict anaerobic after abdominal surgery non-spore-former• Prominent capsule – anti-phagocytic – abscess formation • Endotoxin – low toxicity – structure different than other lipolysaccharide
  • 62. • Enterobacteriaceae (facultative anaerobes) – commonly cause disease – low numbers gut flora• Strict anaerobes – much less commonly cause disease – high numbers gut flora .

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