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Campylobacter
Campylobacter is a common cause of foodborne illness worldwide and Campylobacter jejuni is a typical organism, which is a gram-negative, motile bacterium that causes both intestinal and systemic infections. Key virulence factors of Campylobacter include lipopolysaccharides and enterotoxins, and pathogenesis involves oral transmission from contaminated food or animals followed by colonization of the small intestine. Symptoms include acute diarrhea and abdominal pain that are usually self-limiting but antibiotics may be used for severe or prolonged cases.
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Campylobacter
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- 2. Campylobacter Among the mostwidespread cause of infection in the world. Cause both diarrheal and systemic diseases Campylobacter jejuni
- 3. Typical Organisms Gram-negative rods withcomma, S, or “gull-wing” shapes. Motive, with a single polar flagellum No spore & no capsule
- 4. Culture An atmosphere withreduced 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. Virulence Factor Lipopolysaccharides (LPS)with endotoxic activity Cytopathic extracellular toxins and enterotoxins have been found
- 6. Pathogenesis The infection byoral route from food, drink, or contact with infected animals or animal products(Milk, meat products ). Susceptible to gastric acid (about 104 organisums)
- 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. Diagnostic Laboratory Tests Specimens: Diarrheal stools Smears: Gram-stained smears of stool may show the typical “gull-shaped” rods. Culture: (have been described above)
- 9. Control The source ofinfection may be food (eg, milk, under-cooked fowl) or contract with infected animals or humans and their excreta.
- 10. Helicobacter pylori •Curved bacilli– •Former name - Campylobacter pylori, H. pylori
- 11. Helicobacter pylori Helicobacter pyloriis the prototype organism in this group. It is associated with antral gastritis, gastric ulcers, and gastric carcinoma.
- 12. Microbiology •Gram negative rod,curved, •Very Motile corkscrew motion •Microaerophilic, use amino acids and fatty acids rather than carbohydrates to obtain energy needs 10% CO2 and 5% O2 •Urease production •Catalase production •Oxidase positive •Growth at 370C, not 250C or 420C
- 13. Virulence factors vacA (vacuolationgassociated) cytotoxin, Pathogenicity island: cag, cytotoxin associated gene A+genes related to bacterial secretion Cag+ HP is much more associated with peptic ulcer disease than Cag(--) HP.
- 15. Pathogenesis •Motility – itmoves into the mucus and produces adhesins on gastric epithelial cells (not intestinal epithelial cells) •Urease production, breaks down the urea to ammonia which buffers the pH around the bacterium. •Persists, escape defense mechanisms – SOD, catalase, Urease. Breack down free radicals
- 16. Pathogenesis H pylori invadethe epithelial cell surface to a certain degree Toxins and LPS may damage the mucosal cells NH3 produced by the urease activity may also damage the cells
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- 18. Epidemiology Prevalence related tosocioeconomic level during childhood. Infection occurs in childhood, persists for decades Prevalence among adults – 20%-100% Source – stomach of humans Mode of transmission? Fecal-oral? Oral-oral? Vomiting and aerosols ? Incidence of HP colonization is declining in developed countries
- 19. Epidemiology Under age 30 <20% At age 60 40-60% In developing countries >80% in adults Acute epidemics of gastritis suggest a common source for H pylori.
- 20. 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
- 21. Gastric ulcer -50-80% HP Gastric carcinoma -HP induces gastritis, gastritis is risk factor for Carcinoma. Gastric lymphoma - MALToma: mucosa associated lymphoid tumors, strong association with HP. Stage 1 is cured by antibiotics. Esophageal diseases - HP protects against: gastroesophageal reflux, Barrette's esophagus and carcinoma of esophagus.
- 22. Immunity An IgM antibodyresponse to he infection is developed Subsequently, IgG and IgA are produced
- 23. Laboratory diagnosis •Endoscopy andbiopsy. •Urease detection •Culture •Urea breath test - samples of breath air are collected by having the patient blow into a tube before and 30 min after ingestion of 13C- labeled urea, rapid, noninvasive, for assessing response 4-8w post therapy, expensive but non invasive!! •Serology
- 26. Principles of therapy Combination chemotherapy Some drugs are effective in vitro, not in vivo - due to acidic pH - erythromycin Resistance - not to bismuth salts or tetracyclines, 10-30% to metronidazole, Response - 1 month after cessation of therapy for breath test or biopsy, 6 month for serology
- 27. Principles of therapy Triple therapy: Bismuth+metronidazole+amoxicillin: eradication 60-90%, tetracyclines, macrolides - clarithromycin PPI proton pump inhibitors therapy: omeprazolone lansoprazole: inhibit HP, urease, acid PPI+amoxicillin+clarithromycin or metronidazole PPI+ Bismuth+metronidazole+amoxicillin-very effective
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- 29. 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)
- 30. Some of themedically important pseudomonas rRNA Homology Group and Subgroup Genus and Species I. Fluorescent Group Pseudomonas aeruginosa Pseudomonas fluorescens Pseudomonas putida Nonfluorescent Group Pseudomonas stutzeri Pseudomonas mendocina II. Burkholderia pseudomallei Burkholderia mallei Burkholderia cepacia Ralstonia pickettii III. Comamonas species Acidovorax species IV. Brevundimonas species V. Stenotrophomonas maltophilia
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- 32. Pseudomonas aeruginosa Widely distributedin nature Frequently present in small numbers in the normal intestinal flora and on the skin Commonly present in moist environments in hospitals It is primarily a nosocomial pathogen
- 33. Typical Organisms Gram-negative rod---- 0.6×2 μm Unipolar flagellum (1~3) ---- actively mobile Occurs as single bacteria, in pairs, and occasionally in short chain Capsule Pili in strains obtained from clinical specimens
- 34. Culture Grow readily onmany types of culture media Smooth and round colonies Multiple colony types in one culture Fluorescent greenish color Sometimes produce a sweet or grape- like or corn taco-like odor
- 35. Culture Obligate aerobic Grow wellat 37~42℃and no growth at 4℃ Produce water-soluble pigments Pyocyanin; Pyoverdin; Pyorubin; Pyomelanin Produce hemolysin Oxidase-positive Ferment glucose but not other carbohydrates
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- 37. Virulence Determinants Adhesins 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
- 38. Virulence Determinants Motility/chemotaxis Flagella Toxins Exoenzyme S Exotoxin A Lipopolysaccharide Antiphagocytic surface properties Capsules, slime layers LPS Defense against serum bactericidal reaction Slime layers,capsules LPS Protease enzymes
- 39. Virulence Determinants Defense againstimmune responses Capsules, slime layers Protease enzymes Genetic attributes Genetic exchange by transduction and conjugation Inherent (natural) drug resistance R factors and drug resistance plasmids Ecologic criteria Adaptability to minimal nutritional requirements Metabolic diversity Widespread occurrence in a variety of habitats
- 40. Inhibition of proteinsynthesis in 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 .
- 41. Diverse sites ofinfection by P aeruginosa
- 42. Disease caused by Pseudomonasaeruginosa 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
- 43. Who are atrisk? People with cystic fibrosis Burn victims Individuals with cancer Patients requiring extensive stays in intensive care units
- 44. Diagnosis Isolation and laboratoryidentification. blood agar plates eosin-methylthionine blue agar. Gram morphology, Inability to ferment lactose Positive oxidase reaction Fruity odor Ability to grow at 4 2 ℃ Fluorescence under ultraviolet radiation helps in early identification of P aeruginosa colonies and also is useful in suggesting its presence in wounds.
- 45. Control and Treatment Thespread of Pseudomonas is best controlled by cleaning and disinfecting medical equipment. In burn patients, topical therapy of the burn with antimicrobial agents such as silver sulfadiazine, coupled with surgical debridement, has markedly reduced sepsis. Susceptibility testing is essential. The combination of gentamicin and carbenicillin can be very effective in patients with acute P aeruginosa infections.
- 46. Review General characteristics: Gramnegative rod, unipolar flagellum, actively motile; produce diffusible pigments -- pyocyanin,gluorescin and pyorubin; aerobic, produce hemolysin. Pathogenicity: cause suppurative infections in burn, trauma, etc. Endotoxin: main pathogenic substance Exotoxin A Extracellular enzymes:phospholipase, proteinase, etc. Bacteriological diagnosis: Specimens Culture and identification Unusual bacteria
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- 48. Common Characteristics Small, gram-negative Pleomorphic Requireenrich media (usually containing blood for isolation) No flagellum, no spore Divided into 17 species according to different requirement to X and V factor
- 49. Haemophilus Small Gram-negative coccobacilli, facultative anaerobes,non motile often resemble cocci, eg pneumococci, most non-encapsulated strains --- virulent forms encapsulated fastidious (require blood factors) X factor = hematin V factor = NAD Organisms: H. influenzae: H. ducreyi --( soft chancre); H. aegypticus -- (purulent conjunctivitis)
- 50. Characteristics and growthrequirements of some haemophilus species Requires Species X V Hemolysis H influenzae (H aegyptius) + + - H parainfluenzae - + - H ducreyi + - - H haemolyticus + + + H parahaemolyticus - + + H aphrophilus - - - X=heme; V=nicotinamide-adenine dinucleotide
- 51. Haemophilus influenzae Present inthe nasopharynx of approximately 75 percent of healthy children and adults (non encapsulated strains as the normal flora) Rarely encountered in the oral cavity Has not been detected in any other animal species 6 types(a-f) according to capsular polysaccharide type in the encapsulated strains H. influenzae type b (Hib) encapsulated strain is the most common cause of meningitis in children between the ages of 6
- 52. Biological Characteristics ----Morphologyof organism In specimens of acute infections: short (1.5μm) coccoid bacilli sometimes in pairs or short chain In culture: At 6~8 h on rich medium: small coccoid bacilli Later: longer rods, lysed bacteria, pleomorphic
- 53. Biological Characteristics ---- Colonies On brain-heart infusion agar with blood: Small, round, convex, iridescence (24h) On chocolate agar: Takes 36~48h to develop 1mm colony Satellite phenomenon Not hemolytic satellite phenomenon
- 54. Biological Characteristics ---- Growth Aerobic or facultative anaerobic Grow well at 33~37℃ Require X and V factors Grow better on chocolate agar than on blood agar
- 55. Virulence factor Endotoxin Lipooligosaccharide Neuraminidase IgA protease Fimbriae Polyribosylribitol phosphate (PRP) capsule (the most important)
- 56. Disease caused byH. 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 tract infections (pneumonia)
- 57. Child has swollenface 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 b infection spreading into septicemia - prior to the her face. availability of the Hib vaccine
- 58. Immunity Relation of theage incidence of bacterial meningitis caused by H influenzae to bactericidal antibody titers in the blood
- 59. Host resistance toinfection Bactericidal antibody directed against PRP capsule of H. influenzae type b Antibody to somatic (cell wall) antigens
- 60. Who is atrisk? Young children under 5 years (most cases occurring in infants between 6-11 months of age) Day-care attendees Those in contact with household cases of Hib disease Immune deficiencies that lower the body's resistance to infection
- 61. Diagnosis The history andthe physical exam. Detecting the bacteria in blood, spinal fluid, or other body fluid Satellite phenomenon
- 62. Treatment H. influenzae meningitis:ampicillin for strains of the bacterium that do not make ß-lactamase; a third- generation cephalosporin or chloramphenicol for strains that do. Chloramphenicol for penicillin-resistant H. influenzae Third-generation cephalosporins, such as ceftriaxone or cefotaxime: effective against H. influenzae and penetrate the meninges well Tetracyclines and sulfa drugs: sinusitis or respiratory infection caused by nontypable H. influenzae. Amoxicillin plus clavulanic acid (Augmentin): effective against ß-lactamase producing strains.
- 63. Control Hib conjugate vaccineslicensed for use among children
- 64. Haemophilus ducreyi Gram negativepleomorphic 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.
- 65. Legionella 46 species ofLegionella and 68 serogroups. 1976 outbreak of pneumonia occurred among persons attending a convention of the American Legion in Philadelphia 费城 . First defined Legionella pneumphila.
- 66. Morphology Aerobic ,gram-negative, motile,catalase- positive Stain poorly by gram’s method,basic fuchsin should be used as the counterstain Grow on BCYE(buffered charcoal-yeast extract agar) with α-ketoglutarate,at pH 6.9, 35 °C,90% humidity 3 days of incubation,colonies are round or flat with entire edges. Color vary from colorless to pink or blue
- 67. 0.5-1 um wide,2-50 um long
- 68. Cell products Produce distinctive14-17 carbon branched-chain fatty acid. Produce proteases, phosphatase, lipase, Dnase,& Rnase Produce a metalloprotease
- 69. Transmission contaminated air infected water supply not spread person-person
- 70. 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 Legionnaire's disease the more severe form of infection which includes pneumonia Immunity Antibodies 4-6 weeks after infection Cell-mediated response is important
- 71. Epidemiology 1)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
- 72. 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 antibody Treatment Erythromycin Rifampicin Pontiac fever requires no specific treatment Control 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.
- 73. Bordetella Bordetella pertussis Classification – the genus contains three medially important species B. pertussis B. parapertussis B. bronchoseptica
- 74. Virulence factors Pili forattachment Pertactin, an outer membrane protein also acts as an adhesion FHA: Filamentous hemagglutinin PT: Pertussis toxin Bacterial adenylate cyclase Dermonecrotic toxin –causing strong vasoconstrictive effects. Tracheal cytotoxin –the killing and sloughing off of ciliated cells in the respiratory tract. Lipooligosaccharide associated with the surface of the bacteria and has potent endotoxin activity
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- 76. Pertussis is generallya disease of • Next is the paroxysmal stage that lasts ~ 4 weeks. The infants (50% of cases occur in patient has rapid, consecutive coughs with a rapid intake of air between the coughs (has a whooping children less than 1 year old). sound). The ciliary action of the respiratory tract has Acquired by inhalation of droplets been compromised, mucous has accumulated, and the patient is trying to cough up the mucous containing the organism accumulations. The coughs are strong enough to The organism attaches to the ciliated break ribs! Other symptoms due to the activity of the released toxins include cells of the respiratory tract. During • Finally there is a convalescent stage during which an 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 of liberate its toxins. damage may occur, such as CNS dysfunction which occurs in ~10 % of the cases and is due to an unknown Next the catarrhal stage occurs - cause. Secondary infections such as pneumonia and This 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
- 77. 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
- 78. CONTROL Sanitary: This verycontagious disease requires quarantine for a period of 4-6 weeks. Immunological: Pertussis vaccine is a part of the required "DPT" schedule. Chemotherapeutic: Antibiotic prophylaxis (erythromycin) may be used for contacts. Treatment of disease with antibiotics does not affect its course