CAMPYLOBACTER

Campylobacter : 

Campylobacter

Campylobacter : 

Campylobacter Among the most widespread cause of infection in the world. Cause both diarrheal and systemic diseases Campylobacter jejuni

Typical Organisms : 

Typical Organisms Gram-negative rods with comma, S, or “gull-wing” shapes. Motive, with a single polar flagellum No spore & no capsule

Culture : 

Culture An 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

Virulence Factor : 

Virulence Factor Lipopolysaccharides (LPS) with endotoxic activity Cytopathic extracellular toxins and enterotoxins have been found

Pathogenesis : 

Pathogenesis The infection by oral route from food, drink, or contact with infected animals or animal products(Milk, meat products ). Susceptible to gastric acid (about 104 organisums) Multiply in the small intestine invade the epithium produce inflammation cause bloody stools Occasionally, the bloodstream is invaded

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diarrhea malaise fever abdominal pain usually self-limiting antibiotics occassionally bacteremia small minority Campylobacter - symptoms Incubation: 4-8d Acute enteritis: 1w, stools remain positive for 3 w Acute colitis Acute abdominal pain Bacteremia: <1% C. jejuni Septic abortion Reactive arthritis

Diagnostic Laboratory Tests : 

Diagnostic Laboratory Tests Specimens: Diarrheal stools Smears: Gram-stained smears of stool may show the typical “gull-shaped” rods. Culture: (have been described above)

Control : 

Control The source of infection may be food (eg, milk, under-cooked fowl) or contract with infected animals or humans and their excreta.

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Curved bacilli – Former name - Campylobacter pylori, H. pylori Helicobacter pylori

Helicobacter pylori : 

Helicobacter pylori Helicobacter pylori is the prototype organism in this group. It is associated with antral gastritis, gastric ulcers, and gastric carcinoma.

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Microbiology Gram negative rod, curved, Very Motile  corkscrew motion Microaerophilic, use amino acids and fatty acids rather than carbohydrates to obtain energyneeds 10% CO2 and 5% O2 Urease production Catalase production Oxidase positive Growth at 370C, not 250C or 420C

Virulence factors : 

Virulence factors vacA (vacuolationg associated) 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.

Pathogenesis : 

Pathogenesis Motility – it moves 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

Pathogenesis : 

Pathogenesis H pylori invade the 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

Epidemiology : 

Epidemiology

Epidemiology : 

Epidemiology Prevalence related to socioeconomic 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

Epidemiology : 

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.

Clinical features : 

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

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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.

Immunity : 

Immunity An IgM antibody response to he infection is developed Subsequently, IgG and IgA are produced

Laboratory diagnosis : 

Laboratory diagnosis Endoscopy and biopsy. 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

Principles of therapy : 

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

Principles of therapy : 

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

PSEUDOMONAS : 

PSEUDOMONAS 假单孢菌属

Common Characteristics : 

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)

Some of the medically important pseudomonas : 

Some of the medically important pseudomonas

Pseudomonas aeruginosa : 

Pseudomonas aeruginosa

Pseudomonas aeruginosa : 

Pseudomonas aeruginosa Widely distributed in 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

Typical Organisms : 

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

Culture : 

Culture Grow readily on many 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

Culture : 

Culture Obligate aerobic Grow well at 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

Virulence Determinants : 

Virulence Determinants

Virulence Determinants : 

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

Virulence Determinants : 

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

Virulence Determinants : 

Virulence Determinants Defense against immune 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

Inhibition of protein synthesis in susceptible cells ----Toxin A : 

Inhibition of protein synthesis 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 .

Diverse sites of infection by P aeruginosa : 

Diverse sites of infection by P aeruginosa

Disease caused by Pseudomonas aeruginosa : 

Disease caused by Pseudomonas 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

Who are at risk? : 

Who are at risk? People with cystic fibrosis Burn victims Individuals with cancer Patients requiring extensive stays in intensive care units

Diagnosis : 

Diagnosis Isolation and laboratory identification. 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.

Control and Treatment : 

Control and Treatment The spread 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.

Review : 

Review General characteristics: Gram negative 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

Haemophilus influenzae : 

Haemophilus influenzae

Common Characteristics : 

Common Characteristics Small, gram-negative Pleomorphic Require enrich media (usually containing blood for isolation) No flagellum, no spore Divided into 17 species according to different requirement to X and V factor

Haemophilus : 

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 = hematinV factor = NAD Organisms: H. influenzae: H. ducreyi --( soft chancre); H. aegypticus -- (purulent conjunctivitis)

Characteristics and growth requirements of some haemophilus species : 

Characteristics and growth requirements of some haemophilus species X=heme; V=nicotinamide-adenine dinucleotide

Haemophilus influenzae : 

Haemophilus influenzae Present in the 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 months and 2 years.

Biological Characteristics ----Morphology of organism : 

Biological Characteristics ----Morphology of 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

Biological Characteristics---- Colonies : 

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

Biological Characteristics---- Growth : 

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

Virulence factor : 

Virulence factor Endotoxin Lipooligosaccharide Neuraminidase IgA protease Fimbriae Polyribosyl ribitol phosphate (PRP) capsule (the most important)

Disease caused by H. influenzae : 

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 tract infections (pneumonia)

An infant with severe vasculitis with disseminated intravascular coagulation (DIC) with gangrene of the hand secondary to Haemophilus influenzae type b septicemia - prior to the availability of the Hib vaccine : 

An infant with severe vasculitis with disseminated intravascular coagulation (DIC) with gangrene of the hand secondary to Haemophilus influenzae type b septicemia - prior to the availability of the Hib vaccine Child has swollen face due to Hib infection, tissue under the skin covering the jaw and cheek is infected, infection spreading into her face.

Immunity : 

Immunity Relation of the age incidence of bacterial meningitis caused by H influenzae to bactericidal antibody titers in the blood

Host resistance to infection : 

Host resistance to infection Bactericidal antibody directed against PRP capsule of H. influenzae type b Antibody to somatic (cell wall) antigens

Who is at risk? : 

Who is at risk? 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

Diagnosis : 

Diagnosis The history and the physical exam. Detecting the bacteria in blood, spinal fluid, or other body fluid Satellite phenomenon

Treatment : 

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.

Control : 

Control Hib conjugate vaccines licensed for use among children

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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. DIAGNOSIS: Generally made on presentation only. Soft, very painful chancre.

Legionella : 

Legionella 46 species of Legionella 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.

Morphology : 

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 -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

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0.5-1 um wide ,2-50 um long

Cell products : 

Cell products Produce distinctive 14-17 carbon branched-chain fatty acid. Produce proteases, phosphatase, lipase, Dnase,& Rnase Produce a metalloprotease

Transmission : 

Transmission contaminated air infected water supply not spread person-person

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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

Epidemiology : 

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

Diagnosis : 

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 Erythromycin Rifampicin Pontiac fever requires no specific treatment 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.

Bordetella : 

Bordetella Classification – the genus contains three medially important species B. pertussis B. parapertussis B. bronchoseptica Bordetella pertussis

Virulence factors : 

Virulence factors Pili for attachment 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

pertussis toxin : 

pertussis toxin

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Pertussis is generally a disease of infants (50% of cases occur in children less than 1 year old). Acquired by inhalation of droplets containing the organism The organism attaches to the ciliated cells of the respiratory tract. During an incubation period of 1-2 weeks, the organism multiplies and starts to liberate its toxins. Next the catarrhal stage occurs - This last ~ 2 weeks. Next is the paroxysmal stage that lasts ~ 4 weeks. The patient has rapid, consecutive coughs with a rapid intake of air between the coughs (has a whooping sound). The ciliary action of the respiratory tract has been compromised, mucous has accumulated, and the patient is trying to cough up the mucous accumulations. The coughs are strong enough to break ribs! Other symptoms due to the activity of the released toxins include Finally there is a convalescent stage during which symptoms gradually subside. This can last for months. B. pertussis rarely spreads to other sites, but a lot of damage may occur, such as CNS dysfunction which occurs in ~10 % of the cases and is due to an unknown cause. Secondary infections such as pneumonia and otitis media are common.

B. Parapertussis & B. bronchoseptica : 

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

CONTROL : 

CONTROL Sanitary: This very contagious 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