Campylobacter

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Campylobacter

  1. 1. Campylobacter
  2. 2. CampylobacterAmong the most widespread cause ofinfection in the world.Cause both diarrheal and systemicdiseasesCampylobacter jejuni
  3. 3. Typical OrganismsGram-negative rodswith comma, S, or“gull-wing” shapes.Motive, with a singlepolar flagellumNo spore & nocapsule
  4. 4. CultureAn atmosphere with reduced O2 (5%O2) with added CO2 (10% CO2)At 42 ℃ (for selection)Several selective media can be used(eg, Skirrow’s medium)Two types of colonies: watery and spreading round and convex
  5. 5. Virulence FactorLipopolysaccharides (LPS) withendotoxic activityCytopathic extracellular toxins andenterotoxins have been found
  6. 6. PathogenesisThe infection by oral route from food, drink, orcontact with infected animals or animalproducts(Milk, meat products ).Susceptible to gastric acid (about 104organisums)
  7. 7. Campylobacter - symptoms• Incubation: 4-8d• Acute enteritis: 1w, • diarrhea stools remain positive • malaise for 3 w • fever• Acute colitis • abdominal pain• Acute abdominal pain • usually self-limiting• Bacteremia: <1% C. • antibiotics jejuni occassionally• Septic abortion • bacteremia• Reactive arthritis –small minority
  8. 8. Diagnostic Laboratory TestsSpecimens: Diarrheal stoolsSmears: Gram-stained smears of stoolmay show the typical “gull-shaped”rods.Culture: (have been described above)
  9. 9. ControlThe source of infection may be food(eg, milk, under-cooked fowl) orcontract with infected animals orhumans and their excreta.
  10. 10. Helicobacter pylori•Curved bacilli –•Former name - Campylobacter pylori, H. pylori
  11. 11. Helicobacter pyloriHelicobacter pylori is the prototypeorganism in this group. It is associatedwith antral gastritis, gastric ulcers, andgastric carcinoma.
  12. 12. Microbiology•Gram negative rod, curved,•Very Motile  corkscrew motion•Microaerophilic, use amino acids and fattyacids rather than carbohydrates to obtainenergyneeds 10% CO2 and 5% O2•Urease production•Catalase production•Oxidase positive•Growth at 370C, not 250C or 420C
  13. 13. Virulence factorsvacA (vacuolationg associated)cytotoxin, Pathogenicity island: cag,cytotoxin associated gene A+genesrelated to bacterial secretionCag+ HP is much more associatedwith peptic ulcer disease than Cag(--)HP.
  14. 14. Pathogenesis•Motility – it moves into the mucus and producesadhesins on gastric epithelial cells (not intestinalepithelial cells)•Urease production, breaks downthe urea to ammonia which buffersthe pH around the bacterium.•Persists, escape defensemechanisms – SOD, catalase,Urease. Breack down free radicals
  15. 15. PathogenesisH pylori invade the epithelial cellsurface to a certain degreeToxins and LPS may damage themucosal cellsNH3 produced by the urease activitymay also damage the cells
  16. 16. Epidemiology
  17. 17. EpidemiologyPrevalence related to socioeconomic level duringchildhood.Infection occurs in childhood, persists fordecadesPrevalence among adults – 20%-100%Source – stomach of humansMode of transmission? Fecal-oral? Oral-oral?Vomiting and aerosols ?Incidence of HP colonization is declining indeveloped countries
  18. 18. EpidemiologyUnder age 30 <20%At age 60 40-60%In developing countries >80% inadultsAcute epidemics of gastritis suggest acommon source for H pylori.
  19. 19. Clinical features Acute acquisition - nausea, vomiting, abdominal pain last for 1w, later – gastritis. Persistent colonization - after acquisition, persist for years. Asymptomatic. Duodenal ulcer- more than 90% with DU - carry HP.- antimicrobial therapy response, eradication of HP - less recurrences
  20. 20. Gastric ulcer - 50-80% HPGastric carcinoma -HP induces gastritis,gastritis is risk factor for Carcinoma.Gastric lymphoma - MALToma: mucosaassociated lymphoid tumors, strongassociation with HP. Stage 1 is cured byantibiotics.Esophageal diseases - HP protectsagainst: gastroesophageal reflux,Barrettes esophagus and carcinoma ofesophagus.
  21. 21. ImmunityAn IgM antibody response to heinfection is developedSubsequently, IgG and IgA areproduced
  22. 22. Laboratory diagnosis•Endoscopy and biopsy.•Urease detection•Culture•Urea breath test - samples of breath air arecollected by having the patient blow into atube before and 30 min after ingestion of 13C-labeled urea, rapid, noninvasive, forassessing response 4-8w post therapy,expensive but non invasive!!•Serology
  23. 23. Principles of therapyCombination chemotherapy Some drugs are effective in vitro, not invivo - due to acidic pH - erythromycin Resistance - not to bismuth salts ortetracyclines, 10-30% to metronidazole, Response - 1 month after cessation oftherapy for breath test or biopsy, 6 monthfor serology
  24. 24. Principles of therapyTriple therapy:Bismuth+metronidazole+amoxicillin:eradication 60-90%, tetracyclines, macrolides- clarithromycinPPI proton pump inhibitors therapy:omeprazolone lansoprazole: inhibit HP,urease, acidPPI+amoxicillin+clarithromycin ormetronidazolePPI+ Bismuth+metronidazole+amoxicillin-veryeffective
  25. 25. PSEUDOMONAS 假单孢菌属
  26. 26. Common Characteristics Gram-negative Motile Aerobic rod Some produce water-soluble pigments Widely in soil, water, plants and animals More than 200 (up to now)
  27. 27. Some of the medically important pseudomonas rRNA Homology Group and Subgroup Genus and SpeciesI. Fluorescent Group Pseudomonas aeruginosa Pseudomonas fluorescens Pseudomonas putida Nonfluorescent Group Pseudomonas stutzeri Pseudomonas mendocinaII. Burkholderia pseudomallei Burkholderia mallei Burkholderia cepacia Ralstonia pickettiiIII. Comamonas species Acidovorax speciesIV. Brevundimonas speciesV. Stenotrophomonas maltophilia
  28. 28. Pseudomonas aeruginosa
  29. 29. Pseudomonas aeruginosaWidely distributed in natureFrequently present in small numbers in the normalintestinal flora and on the skinCommonly present in moist environments inhospitalsIt is primarily a nosocomial pathogen
  30. 30. Typical OrganismsGram-negative rod ----0.6×2 μmUnipolar flagellum (1~3)---- actively mobileOccurs as singlebacteria, in pairs, andoccasionally in shortchainCapsulePili in strains obtainedfrom clinical specimens
  31. 31. CultureGrow readily on manytypes of culture mediaSmooth and round coloniesMultiple colony types in one cultureFluorescent greenish colorSometimes produce a sweet or grape-like or corn taco-like odor
  32. 32. CultureObligate aerobicGrow well at 37~42℃and no growth at 4℃Produce water-soluble pigmentsPyocyanin; Pyoverdin; Pyorubin; PyomelaninProduce hemolysinOxidase-positiveFerment glucose but not other carbohydrates
  33. 33. Virulence Determinants
  34. 34. Virulence DeterminantsAdhesins fimbriae (N-methyl-phenylalanine pili) polysaccharide capsule (glycocalyx) alginate slime (biofilm)Invasins elastase alkaline protease hemolysins (phospholipase and lecithinase) cytotoxin (leukocidin) siderophores and siderophore uptake systems pyocyanin diffusible pigment
  35. 35. Virulence DeterminantsMotility/chemotaxis FlagellaToxins Exoenzyme S Exotoxin A LipopolysaccharideAntiphagocytic surface properties Capsules, slime layers LPSDefense against serum bactericidal reaction Slime layers,capsules LPS Protease enzymes
  36. 36. Virulence DeterminantsDefense against immune responses Capsules, slime layers Protease enzymesGenetic attributes Genetic exchange by transduction and conjugation Inherent (natural) drug resistance R factors and drug resistance plasmidsEcologic criteria Adaptability to minimal nutritional requirements Metabolic diversity Widespread occurrence in a variety of habitats
  37. 37. Inhibition of protein synthesisin susceptible cells ----Toxin A The resultant ADP-ribosyl-EF-2 complex is inactive in protein synthesis. This intracellular mechanism of action of toxin A is identical to that of diphtheria toxin fragment A .
  38. 38. Diverse sites of infection by P aeruginosa
  39. 39. Disease caused byPseudomonas aeruginosa Endocarditis Respiratory infections Bacteremia Central Nervous System infections Ear infections including external otitis Eye infections Bone and joint infections Urinary tract infections Gastrointestinal infections Skin and soft tissue infections, including wound infections, pyoderma and dermatitis
  40. 40. Who are at risk?People with cystic fibrosisBurn victimsIndividuals with cancerPatients requiring extensive stays inintensive care units
  41. 41. DiagnosisIsolation and laboratory identification. blood agar plates eosin-methylthionine blue agar.Gram morphology,Inability to ferment lactosePositive oxidase reactionFruity odorAbility to grow at 4 2 ℃Fluorescence under ultraviolet radiation helpsin early identification of P aeruginosa coloniesand also is useful in suggesting its presence inwounds.
  42. 42. Control and TreatmentThe spread of Pseudomonas is best controlledby cleaning and disinfecting medical equipment.In burn patients, topical therapy of the burn withantimicrobial agents such as silver sulfadiazine,coupled with surgical debridement, hasmarkedly reduced sepsis.Susceptibility testing is essential.The combination of gentamicin and carbenicillincan be very effective in patients with acute Paeruginosa infections.
  43. 43. ReviewGeneral characteristics: Gram negative rod,unipolar flagellum, actively motile; producediffusible pigments -- pyocyanin,gluorescin andpyorubin; aerobic, produce hemolysin.Pathogenicity: cause suppurative infections inburn, trauma, etc. Endotoxin: main pathogenic substance Exotoxin A Extracellular enzymes:phospholipase,proteinase, etc.Bacteriological diagnosis: Specimens Culture and identification Unusual bacteria
  44. 44. Haemophilus influenzae
  45. 45. Common CharacteristicsSmall, gram-negativePleomorphicRequire enrich media (usuallycontaining blood for isolation)No flagellum, no sporeDivided into 17 species according todifferent requirement to X and V factor
  46. 46. HaemophilusSmall Gram-negativecoccobacilli, facultativeanaerobes, non motileoften resemble cocci, egpneumococci,most non-encapsulated strains--- virulent forms encapsulatedfastidious (require bloodfactors)X factor = hematinV factor = NADOrganisms: H. influenzae: H.ducreyi --( soft chancre); H.aegypticus -- (purulentconjunctivitis)
  47. 47. Characteristics and growth requirements of some haemophilus species Requires Species X V HemolysisH influenzae (H aegyptius) + + -H parainfluenzae - + -H ducreyi + - -H haemolyticus + + +H parahaemolyticus - + +H aphrophilus - - - X=heme; V=nicotinamide-adenine dinucleotide
  48. 48. Haemophilus influenzaePresent in the nasopharynx of approximately75 percent of healthy children and adults(non encapsulated strains as the normalflora)Rarely encountered in the oral cavityHas not been detected in any other animalspecies6 types(a-f) according to capsular polysaccharidetype in the encapsulated strainsH. influenzae type b (Hib) encapsulatedstrain is the most common cause ofmeningitis in children between the ages of 6
  49. 49. Biological Characteristics ----Morphology of organismIn specimens of acute infections: short (1.5μm) coccoid bacilli sometimes in pairs or short chainIn culture: At 6~8 h on rich medium: small coccoidbacilli Later: longer rods, lysed bacteria,pleomorphic
  50. 50. Biological Characteristics ---- ColoniesOn brain-heart infusion agar withblood: Small, round, convex, iridescence(24h)On chocolate agar: Takes 36~48h to develop 1mmcolonySatellite phenomenonNot hemolytic satellite phenomenon
  51. 51. Biological Characteristics ---- GrowthAerobic or facultative anaerobicGrow well at 33~37℃Require X and V factorsGrow better on chocolate agar than onblood agar
  52. 52. Virulence factorEndotoxinLipooligosaccharideNeuraminidaseIgA proteaseFimbriaePolyribosyl ribitol phosphate (PRP)capsule (the most important)
  53. 53. Disease caused by H. influenzae•Naturally-acquired disease caused by H.influenzae seems to occur in humans only.•Bacteremia•Acute bacterial meningitis•Epiglottitis (obstructive laryngitis),•Cellulitis•Osteomyelitis•Joint infections•Ear infections (otitis media)•Sinusitis associated with respiratory tractinfections (pneumonia)
  54. 54. Child has swollen face due to Hib infection, An infant with severe vasculitis tissue under the skin with disseminated intravascular covering the jaw and coagulation (DIC) with gangrene cheek is infected, of the hand secondary to Haemophilus influenzae type binfection spreading into septicemia - prior to the her face. availability of the Hib vaccine
  55. 55. ImmunityRelation of the age incidence of bacterial meningitis caused byH influenzae to bactericidal antibody titers in the blood
  56. 56. Host resistance to infectionBactericidal antibody directed againstPRP capsule of H. influenzae type bAntibody to somatic (cell wall) antigens
  57. 57. Who is at risk?Young children under 5 years (mostcases occurring in infants between 6-11months of age)Day-care attendeesThose in contact with household cases ofHib diseaseImmune deficiencies that lower the bodysresistance to infection
  58. 58. DiagnosisThe history and the physical exam.Detecting the bacteria in blood, spinalfluid, or other body fluidSatellite phenomenon
  59. 59. TreatmentH. influenzae meningitis: ampicillin for strains of thebacterium that do not make ß-lactamase; a third-generation cephalosporin or chloramphenicol forstrains that do.Chloramphenicol for penicillin-resistant H. influenzaeThird-generation cephalosporins, such as ceftriaxoneor cefotaxime: effective against H. influenzae andpenetrate the meninges wellTetracyclines and sulfa drugs: sinusitis or respiratoryinfection caused by nontypable H. influenzae.Amoxicillin plus clavulanic acid (Augmentin): effectiveagainst ß-lactamase producing strains.
  60. 60. ControlHib conjugate vaccines licensed for use among children
  61. 61. Haemophilus ducreyiGram negative pleomorphic rods Coccobacilli filamentous Painful chancres become pustular, eroded, ulcerated and there are NO defined borders LPS Pili Outer membrane proteins Hemolysin IgA protease DIAGNOSIS: Generally made on presentation only. Soft, very painful chancre. Gram stain and Laboratory Growth Growth REQUIRES X (hemin) factor only (H. influenzae needs X and V) Organisms also grow best in an increased CO2 environment.
  62. 62. Legionella46 species of Legionella and 68serogroups.1976 outbreak of pneumonia occurredamong persons attending a conventionof the American Legion in Philadelphia费城 .First defined Legionella pneumphila.
  63. 63. MorphologyAerobic ,gram-negative, motile, catalase-positiveStain poorly by gram’s method,basic fuchsinshould be used as the counterstainGrow on BCYE(buffered charcoal-yeast extractagar) with α-ketoglutarate,at pH 6.9, 35 °C,90%humidity3 days of incubation,colonies are round or flatwith entire edges.Color vary from colorless to pink or blue
  64. 64. 0.5-1 um wide ,2-50 um long
  65. 65. Cell productsProduce distinctive 14-17 carbonbranched-chain fatty acid.Produce proteases, phosphatase,lipase, Dnase,& RnaseProduce a metalloprotease
  66. 66. Transmissioncontaminated air infected water supplynot spread person-person
  67. 67. Pathogenesis Attach to phagocytic cell surface 1).no antibody : C3 deposite on the bacterial surface,attached to CR1 or CR3 2).antibody is present : Fc-mediated phagocytosis• fail to fuse with lysosomal granules and ribosomes,mitochondria around vacuoles containing L pneumophila, Then cells are destroyed Pontiac fever marked by fever, chills, headache and malaise that lasted 2-5 days Legionnaires disease the more severe form of infection which includes pneumoniaImmunity Antibodies 4-6 weeks after infection Cell-mediated response is important
  68. 68. Epidemiology1)When legionellosis occur? they are are usually occur in the summer and early fall, but cases may occur year-round. About 5% to 30% of people who have Legionnaires disease die.2)How is legionellosis spread? Legionella are typically associated with aerosolized water (central air conditioning, cooling towers, showers, whirlpool spars). Disease is generally waterborne; transmission occurs via airborne droplets.3)Where is the Legionella bacterium found? The organisms exist in many types of water systems in nature; humans are an accidental host.Risk Groups• The elderly, cigarette smokers, persons with chronic lung or immuno-compromising disease, and persons receiving immunosuppressive drugs
  69. 69. Diagnosis Clinical: Symptoms include headache, malaise, rapid fever, nonproductive cough, Chest X-rays show pneumonia Laboratory: immunofluorescent(IF) ,silver stain. Legionella antigens in urine samples Legionella-specific serum antibodyTreatment Erythromycin Rifampicin Pontiac fever requires no specific treatmentControl Regular maintenance of air conditioning or the inclusion of biocidal compounds into water cooling towers reduces the reservoir. Similarly, hyperchlorination of the water supply eliminates the source.
  70. 70. Bordetella Bordetella pertussis Classification – the genus contains three medially important species  B. pertussis  B. parapertussis  B. bronchoseptica
  71. 71. Virulence factorsPili for attachmentPertactin, an outer membrane protein also acts as an adhesionFHA: Filamentous hemagglutininPT: Pertussis toxinBacterial adenylate cyclaseDermonecrotic toxin –causing strong vasoconstrictive effects.Tracheal cytotoxin –the killing and sloughing off of ciliated cells in therespiratory tract.Lipooligosaccharide associated with the surface of the bacteria and haspotent endotoxin activity
  72. 72. pertussis toxin
  73. 73. Pertussis is generally a disease of • Next is the paroxysmal stage that lasts ~ 4 weeks. Theinfants (50% of cases occur in patient has rapid, consecutive coughs with a rapid intake of air between the coughs (has a whoopingchildren less than 1 year old). sound). The ciliary action of the respiratory tract hasAcquired by inhalation of droplets been compromised, mucous has accumulated, and the patient is trying to cough up the mucouscontaining the organism accumulations. The coughs are strong enough toThe organism attaches to the ciliated break ribs! Other symptoms due to the activity of the released toxins includecells of the respiratory tract. During • Finally there is a convalescent stage during whichan incubation period of 1-2 weeks, symptoms gradually subside. This can last for months.the organism multiplies and starts to • B. pertussis rarely spreads to other sites, but a lot ofliberate its toxins. damage may occur, such as CNS dysfunction which occurs in ~10 % of the cases and is due to an unknownNext the catarrhal stage occurs - cause. Secondary infections such as pneumonia andThis last ~ 2 weeks. otitis media are common. Incubation catarrhal paroxysmal convalescent duration 7-10 days 1-2 weeks 2-4 weeks 3-4 weeks or longer rhinorrhea repetitive Diminished , coughwith Paroxysmal cough,symptoms none malaise, whoops,vomiting, Development of fever, leukocytosis secondary complications sneezing, (pneumonia,seizures,enc anorexia ephalopathy)bacterial culture
  74. 74. B. Parapertussis & B. bronchoseptica B. parapertussis – causes a mild form of whooping cough B. bronchoseptica  Widespread in animals where it causes kennel cough.  Occasionally causes respiratory or wound infections
  75. 75. CONTROLSanitary: This very contagious diseaserequires quarantine for a period of 4-6weeks.Immunological: Pertussis vaccine is apart of the required "DPT" schedule.Chemotherapeutic: Antibioticprophylaxis (erythromycin) may be usedfor contacts. Treatment of disease withantibiotics does not affect its course

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