Anaerobic bacteria

Download Anaerobic bacteria

Post on 07-May-2015




1 download

Embed Size (px)




<ul><li>1.Anae rob ic Bacte ria</li></ul><p>2. Caegor t y Spore-forming:rod, Gram (+)---Clostridium Nonspore-forming:see nextslides 3. Caegor t ySpore-rod,Gram (+)---forming:ClostridiumNonspore-forming:Rod, Gram (+) Propionibacterium BifidobacteriumLactobacillus EubacteriumRod, Gram (-) BacteroidesActinomycesFusobacterium Cocci, Gram (+) Peptococcus CampylobacterPeptostreptococcusCocci, Gram (-)Veillonella 4. Clostridium Species The clostridia are opportunisticpathogens. Nonetheless, they areresponsible for some of the deadliestdiseases including gas gangrene,tetanus and botulism. Less life-threatening diseases includepseudomembranous colitis (PC) andfood poisoning. cause disease primarily through theproduction 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 occasionallyfound in intestinal flora of humansand animals C.tetani is the cause of tetanus,orlockjaw. When spores are introducedinto wounds by contaminated soil orforeign objects such as nails or glasssplinters 7. BIOCHEMICAL CHARACTERISTICS Morphology: long and slender;peritrichous flagella,no capsule,terminal located roundspore(drum-stick apperance),its diameter greater thanvegetative cell. Culture:obligate anaerobic;Gram(+); swarming occures onblood agar, faint hemolysis. Biochemical activities:does notferment any carbohydrate andproteins. Resistance: tolerate boiling for60 min.alive several ten years in 2-5 x 0.3-0.5umsoil. Classification and AntigenicTypes: C tetani is the onlyspecies. There are no serotypes 8. Pathogenicity No invasiveness; toxemia retrograde transport(exogenous infection to (CNS) produces two exotoxins: delitescence a fewtetanolysin, andtetanospasmin(a kind of days to severalneurotoxin, toxicityweeksstrong) The two animal The actions ofspecies mosttetanospasmin aresusceptible to thiscomplex and involve threecomponents of the toxemia are horsesnervous system: central and humans.motor control, autonomicfunction, and theneuromuscular junction. 9. Clostridium tetani -Tetanospasmin disseminates systemically binds to ganglioside receptors inhibitory neurones in CNS glycine neurotransmitter stops nerve impulse to muscles spastic paralysis severe muscle contractions andspasms can be fatal 10. Tetanospasmin 11. Clinical Manifestations The initial symptom is cramping andtwitching of muscles around a wound. Thepatient usually has no fever but sweatsprofusely and begins to experience pain,especially in the area of the wound andaround the neck and jaw muscles (trismus). Portions of the body may become extremelyrigid, and opisthotonos (a spasmin which the head and heels are bentbackward and the body bowed forward) iscommon. Complications include fractures, bowelimpaction, intramuscular hematoma, muscleruptures, and pulmonary, renal, and cardiacproblems 12. Clinical ManifestationsDISEASE CLINCAL MANIFESTATIONSAGeneralized Involvement of bulbar and paraspinalmuscles(trismus or lockjaw, risus sardonicus,difficulty swallowing, irritability,opisthotonos);involvement of autonomicnervous system(sweating, hyper thermia,cardiac arrhythmias, fluctuations in bloodpressure)CephalicPrimary infection in head,particularlyear;isolated or combined involvement of cranialnerves, particularly seventh cranial nerve; verypoor prognosisLocalized Involvement of muscles in area of primaryinjury; infection may precede generalizeddisease; favorable prognosisNeonatalGeneralized disease in neonates; infectiontypically originates from umbilical stump;very poor prognosis in infants whosemothers are nonimmune 13. Epidemiology 1 million cases of tetanus occur annually in theworld,with a mortality rate ranging from20%to 50%. But rare in most developed countries. In some developing countries, tetanus is stillone of the ten leading causes of death, andneonatal tetanus accounts for approximatelyone-half of the cases worldwide. In less developed countries, approximatemortality rates remain 85% for neonataltetanus and 50% for nonneonatal tetanus. In the United States, intravenous drug abusershave become another population with anincreasing 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 immunityand the disease does not produceimmunity in the patient. Active immunity follows vaccinationwith tetanus toxoid 15. Diagnosis Diagnosis is primarily by the clinicalsymptoms (above). The wound may notbe obvious. C tetani can be recovered from thewound in only about one-third of thecases.It is important for the clinician to beaware that toxigenic strains of C tetanican grow actively in the wound of animmunized person. Numerous syndromes, including rabiesand meningitis, have symptoms similarto those of tetanus and must beconsidered in the differential diagnosis. 16. Vaccination infant DPT (diptheria, pertussis, tetanus) tetanus toxoid antigenic no exotoxic activity 17. Control The offending organism must beremoved by local debridemen toxoid TAT; Metronidazole (For moreserious wounds) AIDS patients may not respondto prophylactic injections oftetanus toxoid 18. C. perfringens soil, fecal contamination gas gangrene swelling of tissues gas release * fermentation products wound contamination 19. Toxinstoxin Biological Feature Types of ToxinsA B C D E lecithinase; increase thevascular permeability;+ + + + +hemolytic; producesnecrotizing activity Necrotizing activity, + + induces hypertensionby causing release ofcatecholamines. increase the + permeability ofgastrointestinal wall 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 lyseserythrocytes, platelets, leukocytes, andendothelial cells. And its lethal action isproportionate to the rate at which it splitslecithin to phosphorylcholine anddiglyceride. The theta toxin has similar hemolytic andnecrotizing effects. DNAase, hyaluronidase, a collagenase arealso produced 21. Enterotoxin Many strains of type A produceenterotoxin, which is a heat-labile proteinand destroyed immediately at 100 . Trypsin treatment enhances the toxinactivity threefold. The toxin is produced primarily by type Astrains but also by a few type C and Dstrains. It disrupts ion transport in theileum(primarily) and jejunum by insertinginto the cell membrane and alteringmembrane permeability. As superantigen. 22. PathogenesisTissue 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 &amp; death is rare 24. Gas gangrene Gas gangrene is a life-threatening disease witha poor prognosis and often fatal outcome. Initial trauma to host tissue damages muscle andimpairs blood supply----lack of oxygenation Initial symptoms : fever and pain in the infectedtissue.; more local tissue necrosis and systemictoxemia. Infected muscle is discolored (purplemottling) and edematous and produces a foul-smelling exudate; gas bubbles form from theproducts of anaerobic fermentation. 25. Gas gangrene As capillary permeability increases,the accumulation of fluid increases,and venous return eventually iscurtailed. As more tissue becomes involved,the clostridia multiply within theincreasing area of dead tissue,releasing more toxins into the localtissue and the systemic circulation. 26. Food poisoning Enterotoxin producing strains. These bacteria are found inmammalian faeces and soil. Small numbers of the bacteria mayalso be found in foods and they maypropagate rapidly to dangerousconcentrations if the food isimproperly stored and handled. 27. Food poisoning more than 108 vegetative cells areingested and sporulate in the gut, thetoxins can act rapidly in the body,causing severe diarrhea in 6-18 hours,dysentery, gangrene, muscle infections The action of C. perfringens enterotoxininvolves marked hypersecretion in thejejunum and ileum, with loss of fluidsand electrolytes in diarrhea. 28. Cellulitis, Fasciitis Cellulitis, Fasciitis Fasciitis : a rapidly progressive,destructive process in which theorganisms spread through fascial plan es. Fasciitis causes suppuration and theformation of gas Absense of muscle involvement rapidity 29. Necrotizing Enteritis Rare, acute necrotizing process in thejejunum Abdominal pain, bloody diarrhea, shock, andperitonitis Mortality: 50% Beta-toxin-producing C. perfringens type C Septicemia 30. Who is at risk? Surgical patients; patient aftertrauma with soil contamination. People who ingest contaminatedmeat products (without properrefrigeration or reheating toinactivate endotoxin) 31. Epidemiology C. perfringens type A: the intestinaltract of humans and animals, soiland water contaminated with feces.forms spores under adverseenvironmental conditions and cansurvive for prolonged periods. Type B to E strains colonize theintestinal tract of animals andoccasionally humans. 32. Epidemiology Type A: gas gangrene, soft tissueinfections and food poisoning Type C: enteritis; necroticans 33. Laboratory identification lecithinase productionDouble 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, mammalsand 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 respiratoryBotulinum 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( ) 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 ofbotulism 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 , injectionof antitoxin.---treated immediately with antiserum.---multivalenttoxoid,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 foodwith botulism should be treatedimmediately 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 degreesat 1 atm) 1h.---toxin heat-labile, boiling or intenseheating, 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) resultspredominantly as a consequence of theelimination of normal intestinal florathrough antibiotic therapy. Symptoms include abdominal pain witha watery diarrhea and leukocytosis."Pseudomembranes" consisting offibrin, mucus and leukocytes can beobserved by colonoscopy. Untreated pseudomembranous colitiscan 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 infectiousdisease Sites throughout body Muscle, cutaneous/sub-cutaneousnecrosis Abscesses 55. Bacterial Flora of the BodySite Total Bacteria Ratio (per/ml or gm) Anaerobes:AerobesUpper AirwayNasal Washings 103-1043-5:1Saliva 108-1091:1Tooth Surface1010-10111:1Gingival Crevice 1011-10121000:1Gastrointestinal TractStomach102-1051:1Small Bowel102-1041:1Ileum104-1071:1Colon1011-10121000:1Female Genital TractEndocervix 108-1093-5:1Vagina 108-1093-5:1 56. Problems in identification ofanaerobic 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 AnaerobicInfections3. Complex Flora 4. Synergistic Mixture Multiple species of Aerobes &amp; Abdominal Infection AvgAnaerobesof 5 species 3 anaerobic E. coli Consume O2 2 aerobic Allow growth of Less complex then nl floraanaerobes Fecal flora 400 differentspecies Anaerobes promote Those predominant in stoolgrowth of other are not infecting species bacteria by being Veillonella,Bifidobacterium rarely antiphagocytic andpathogenic producing B- Species uniquely sui...</p>


View more >