Anaerobic Bacteria

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  • Anaerobic Bacteria

  • CategorySpore-forming: rod, Gram (+)--- ClostridiumNonspore-forming: see next slides

  • Category

    Spore-forming: rod, Gram (+)--- ClostridiumNonspore-forming:Rod, Gram (+)PropionibacteriumBifidobacterium Lactobacillus Eubacterium ActinomycesRod, Gram (-)Bacteroides Fusobacterium CampylobacterCocci, Gram (+)Peptococcus PeptostreptococcusCocci, Gram (-)Veillonella

  • Clostridium SpeciesThe 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

  • Clostridium TetaniPathogenesis of tetanus caused by C tetani

  • General introductionC tetani is found worldwide. Ubiquitous in soil, it is occasionally found in intestinal flora of humans and animalsC.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

  • BIOCHEMICAL CHARACTERISTICSMorphology: 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 soil.Classification and Antigenic Types: C tetani is the only species. There are no serotypes2-5 x 0.3-0.5um

  • PathogenicityNo invasiveness; toxemia (exogenous infectionproduces two exotoxins: tetanolysin, and tetanospasmin(a kind of neurotoxin, toxicity strong)The actions of tetanospasmin are complex and involve three components of the nervous system: central motor control, autonomic function, and the neuromuscular junction.retrograde transport to (CNS)delitescencea few days to several weeksThe two animal species most susceptible to this toxemia are horses and humans.

  • Clostridium tetani -Tetanospasmindisseminates systemically binds to ganglioside receptors inhibitory neurones in CNSglycine neurotransmitterstops nerve impulse to muscles spastic paralysissevere muscle contractions and spasms can be fatal

  • Tetanospasmin

  • Clinical ManifestationsThe 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(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

  • Clinical Manifestations

  • Tetanus.

  • Tetanus.

  • Epidemiology1 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 tetanusIn untreated tetanus, the fatality rate is 90% for the newborn and 40% for adults.

  • ImmunityHumoral 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

  • DiagnosisDiagnosis 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.

  • infant DPT (diptheria, pertussis, tetanus) tetanus toxoid antigenic no exotoxic activity

    Vaccination

  • ControlThe offending organism must be removed by local debridementoxoid TAT; Metronidazole (For more serious wounds)AIDS patients may not respond to prophylactic injections of tetanus toxoid

  • C. perfringenssoil, fecal contaminationgas gangreneswelling of tissues gas releasefermentation productswound contamination

  • Toxins

  • ToxinsMany 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

  • EnterotoxinMany 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.

  • Tissue degrading enzymes lecithinase [ toxin] proteolytic enzymes saccharolytic enzymes Destruction of blood vessels Tissue necrosis Anaerobic environment created Organism spreads Pathogenesis

  • Without treatment death occurs within 2 dayseffective antibiotic therapydebridement anti-toxinamputation & death is rare

  • Gas gangreneGas 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.

  • Gas gangreneAs 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.

  • Food poisoningEnterotoxin 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.

  • Food poisoningmore 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.

  • Cellulitis, FasciitisCellulitis, FasciitisFasciitis : a rapidly progressive, destructive process in which the organisms spread through fascial plan es.Fasciitis causes suppuration and the formation of gasAbsense of muscle involvementrapidity

  • Necrotizing EnteritisRare, acute necrotizing process in the jejunumAbdominal pain, bloody diarrhea, shock, and peritonitisMortality: 50%Beta-toxin-producing C. perfringens type CSepticemia

  • 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)

  • EpidemiologyC. 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.

  • EpidemiologyType A: gas gangrene, soft tissue infections and food poisoningType C: enteritis; necroticans

  • lecithinase production

    Laboratory identificationDouble Hemolysis Circles

  • C. botulinum

  • Biological FeaturesAnaerobicGram-positiverod-shapedsporeformerproduces a protein neurotoxic.soil, sediments of lakes, ponds, decaying vegetation.intestinal tracts of birds, mammals and fish.

  • ---A, B, C1, D, E, F, and G.---type A. 62% ---Not all produce toxin.---C and D not ---G plasmid encoded.Division

  • ---spores heat resistant. canning. anaerobic environment ---Botulism eating uncooked foods spores---GI, duodenum, blood stream, neuromuscular synapses.

    Transmission

  • ---bacterial protease ---light chain,A,50 kDa; heavy chain,100kDa.---disulfide bond. ---A po

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