Anaerobic bacteria

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Anaerobic bacteria

  1. 1. Anae rob ic Bacte ria
  2. 2. Caegor t y Spore-forming: rod, Gram (+)--- Clostridium Nonspore-forming: see next slides
  3. 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. 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. 5. Clostridium TetaniPathogenesis of tetanus caused by C tetani
  6. 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. 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. 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. 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. 10. Tetanospasmin
  11. 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. 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. 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. 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. 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. 16. Vaccination• infant• DPT (diptheria, pertussis, tetanus)• tetanus toxoid – antigenic – no exotoxic activity
  17. 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. 18. C. perfringens• soil, fecal contamination• gas gangrene – swelling of tissues – gas release * fermentation products• wound contamination
  19. 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. 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. 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. 22. Pathogenesis•Tissue degrading enzymes – lecithinase [l toxin] – proteolytic enzymes – saccharolytic enzymes• Destruction of blood vessels• Tissue necrosis• Anaerobic environment created• Organism spreads
  23. 23. Without treatment deathoccurs within 2 days effective antibiotic therapy debridement anti-toxin amputation & death is rare
  24. 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. 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. 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. 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. 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. 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. 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. 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. 32. Epidemiology Type A: gas gangrene, soft tissue infections and food poisoning Type C: enteritis; necroticans
  33. 33. Laboratory identification• lecithinase production Double Hemolysis Circles
  34. 34. C. botulinum
  35. 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. 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. 37. Transmission---spores heat resistant. canning. anaerobic environment---Botulism eating uncooked foods spores---GI, duodenum, blood stream,neuromuscular synapses.
  38. 38. Virulence factors---bacterial protease---light chain,A,50 kDa; heavy chain,100kDa.---disulfide bond.---A potent toxin
  39. 39.  binds peripheral nerve receptors • acetylcholine neurotransmitter inhibits nerve impulses flaccid paralysis death • respiratory Botulinum toxin • cardiac failure
  40. 40. Botulinum toxin Bioterrorism • not an infection • resembles a chemical attack • 10 ng can kill a normal adult
  41. 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. 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. 43. Botulism( 肉毒中毒 ) food poisoning • rare • fatal germination of spore inadequately sterilized canned food • home not an infection
  44. 44. Infection with C. botulinum Neonatal botulism • uncommon • the predominant form of botulism • colonization occurs  no normal flora to compete  unlike adult
  45. 45. Wounds• extremely rare• an infection
  46. 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. 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. 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. 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. 50. C. difficile• After antibiotic use• Intestinal normal flora --greatly decreased• Colonization occurs• Enterotoxin secreted• Pseudomembanous colitis
  51. 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. 52. Therapy Discontinuation of initial antibiotic (e.g. ampicillin) Specific antibiotic therapy (e.g. vancomycin)
  53. 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. 54. Strict anaerobe infectious disease Sites throughout body Muscle, cutaneous/sub-cutaneous necrosis Abscesses
  55. 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. 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. 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. 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. 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. 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. 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. 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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