七年制临床医学专业细菌各论和特殊微生物

Individual Microbiology staphylococcus G+ streptococcus Cocci pneumococcus meningococcus G- Gonococcus Aerobe G- - enteric bacilli and Bacilli corynebacterium diphtheria facultative anaerobe G+ M.tuberculosis Spirillar bacteria -V.cholera obligate anaerobe spore-forming anaerobic bacteria non-spore-forming anaerobic bacteria Content 1.biological characteristics 2.pathogenicity-pathogenic factor ，phathogenesis 3.immunity 4.laboratory diagnosis(bacteriological methods) 5.prevention and treatment Chapter 13 Pathogenic Coccus G+ cocci Staphylococcus, Streptococcus, Pneumococcus. Purulent G-cocci Meningococcus, Gonococcus. Infection Section1. Staphylococcus I. Biological characteristics 1. Morphology: Gram positive cocci, arranged in irregular, grape like clusters, capsule in vivo 2. Culture: temperature : 2838 (37); pH : 4.59.8 (7.4) colony : 12 mm, circular, smooth, shiny surface, various pigments on blood agar - hemolysis (S. aureus) Major properties of three species of staphylococci Main property Staph. aureus Staph. Epidermidis Staph saprophyticus Pigmentation Golden yellow White Citrine Coagulase + _ _ Hemolysin + _ _ SPA + _ _ 2 Pathogenicity + -/+ _ 3. Typing : S. aureus have been differentiated into different phage types ( important aspect in the investigation of a infection source) . 4. Antigenic structure: (1) SPA (staphylococcal protein A) i) cell wall protein of S. aureas ii) it combines nonspecifically with the Fc-portion of human IgG iii) antiphagocytosis iv)damage platelet; activate B cell v) coagglutination (rapid diagnostic technic) 5. Resistance: resistant to dry; heat (80,30min); salt tolerant (1015% NaCl) Sensitive to antibiotics and sulfonamides , but drug- resistance are easily produced II. Pathogenicity 1. Pathogenic factor 1).Invasiveness (1)Surface structure: SPA - anti-phagocytosis , Lipoteichoic acid, LTA - adherence (2) Enzyme: Coagulase: An enzyme which causes coagulation in plasma containing an anticoagulant such as citrate, coagulase is found in all pathogenic strains of Staphylococci. Roles : to inhibit the phagocytosis of phagocytes and damage of bacteriacide substances in humor by coating the organisms with fibrin. two types of coagulase: (1).Free coagulase - an extracellular enzyme which converts fibrinogen in citrated plasma into fibrin. (in tube) (2).Bound coagulase - a bound coagulase in the cell wall that induces clumping of organisms in the presence of fibrinogen. (on slide) 2)Toxin- exotoxin (1) . Staphylolysin: cytotoxic effects on phagocytic and tissue cells. kinds: -Lysin ; -Lysin; -Lysin; -Lysin Staphylolysin-: main pathogenic substance, form hemolysing-ring around the colony (2) .Leukocidin: Kill PMNs and M (3). Enterotoxin: Protein; Nine types: A-E, G; Heat stable (boiling for 30 min) Cause a food poisoning characterized by severe vomiting and diarrhea (4). Exfoliative toxin: Cause Staphylococcal scalded skin syndrome (SSSS) (5). Toxic shock syndrome toxin-1 (TSST-1): Cause Toxic shock syndrome (TSS): 2. Pathogensis 1) Purulent infection (1). local infection (skin infection): hair folliculitis; boil; carbuncle; impetigo. 3 ( characterised by thick pus and a limited local area ) (2).organ infection: pneumonia, meningitis. (3).systemic infection: septicemia; pyemia 2) Toxin diseases (1). Food poisoning : enterotoxin in contaminated food (2). TSS (Toxic shock syndrome): (3). SSSS(staphylococcal scalded skin syndrome): . Immunity: not stable IV. Laboratory diagnosis specimen: pus sputum (low respiratory tract infection) blood (septic shock, osteomyelitis, endocarditis) mid-stream urine (pyelonephritis or cystisis) food/faeces or vomit (food poisoning) *direct smear : Gram stain ( initial diagnosis ) *isolation and identification: blood agar *coagulose test: * antibiotics test : *enterotoxin test and animal test: food poisoning . Treatment: Antibiotic therapy: but antibiotic resistance can arise . eg: Resistance to penicllin ( penicillinase ) NOTE: antibiotic sensivity test Coagulase-negative staphylococci (CNS) CNS - Normal flora (Staph. Epidermidis ; Staph saprophyticus) - Major causes of hospital-acquired infection Section 2. Streptococcus I. Biological characteristics 1.Morphology (thin pus; infection may spread quickly) systemic infection: septicemia 5 (2). Toxin-mediated disease: scarlet fever (3). Poststerptococcal diseases (hypersensitive disease) (i) Acute glomerulonephritis ( group A streptococci) Mechanism: *type III hypersensitivity (most) *type II hypersensitivity M protein-Ab Immune complex common Ag deposition glomerular basement membrane cross reacts with activationC3,C5 glomerular basement membrane tissue destruction tissue destruction (ii) Rheumatic fever (many types of group A streptococci) Mechanism: *immune complex (deposition) heart, joints type III hypersensitivity *common Ag cross-reacts heart type II hypersensitivity 2) Infections of -hemolytic streptococci: normal flora : throat/nasapharyn S. mutant - dental plaque/caries, S.bovis-septicemia, S. anginosus- subacute bacterial endocarditis (SBE). . Immunity . Laboratory diagnosis 1. Isolation pelvic inflammatory(female) *ophthalmia neonatorum blindness 3. Laboratory diagnosis: Specimen: purulent secretion of genitourinary tract Isolation and identification: direct smear, culture, biochemical tests, EIA, 4. Prevention and treatment *penicillin- Gonorrhea *silver nitrate- ophthalmia neonatorum . Neisseria meningitidis 1.Pathogenic factors: *Pili attach to nasopharyngeal mucosa *capsule antiphagocytosis *endotoxin main pathogenic substance 2. Diseases: Human is the only natural host，Child: susceptible (lacking specific Abs) * Epidemic cerebrospinal meningitis （respiratory tract transmission） 3. Immunity: group-specific antibody, cross-immunity between groups. 4. Laboratory diagnosis Specimen: cerebrospinal fluid (CSF), blood, *note: “fragile” bed-side inoculation Direct smear : smear Gram stain (G- diplococci, within white cells) Isolation and identification: specimen serum broth chocolate blood agar plate (510% CO2 ,37C ) Gram stain and biochemical, serological identification Ag detection（rapid diagnosis）: ELASA, coagglutination 7 5 Prevention and treatment 1.Polysaccharide vaccine (group A, C) 2. Penicillin Chapter14 Enterobacteriaceae I. Common properties: 1. Similar shape: G- rods, most possess flagella and pilli. No spores, certain members possessing capsules. 2. culture: aerobe or facultative, basic agar, 2-3mm colonies 3. Biochemical reactions are active and diverse. Many kinds of carbohydrates and proteins can be utilized and form various products. Differentiation: e.g. Lactose fermenting bacteria enteric nonpathogens Non-lactose fermenting bacteria enteric pathogens 4. antigenic structure is complex (1) O antigen - specific polysaccharides of LPS Basis of serological classification (2) Surface Ag: - Polysaccharides that cover the O Ags (e.g. capsule Ag) Main surface Ags: Vi antigen (S. typhi), K antigen (E. coli) Inhibit specific agglutination of O antiserum Associated with invasiveness of enteric bacilli (3) H Ag - flagella protein: Basis of serological classification. 5. some members produce bacteriocin 6 Produce endotoxins and/or exotoxins Section 1. Escherichia coli I. Biological characteristics: 1. Shape and structure: G- rods, possess flagella and pilli. 2 .Biochemical reactions (extremely active and complex): (1) Lactose fermentation test: “+” On differential media : colored colony (2) IMViC test: + + - - 3. Antigenic structure: O Ag- more than 170, cross -rection H Ag - more than 56, specific (flagellar) K Ag (L, A and B) - more than 100 e.g. serotype is expressed as O111:K58 (B4):H2 II. Pathogenicity 1. pathogenic factors (1) invasiveness: K Ag; Pili; CFA (colonization factor Ag) Specifically adheres to the epithelial cell lining the small intestine (2) O Ag, K Ag: anti-complement; anti-phagocyte (3) endotoxin: cell wall lipopolysaccharide ; fever / shock 8 (4) enterotoxin (exotoxin): consists of LT and ST LT (heat labile enterotoxin): similar to Cholera enterotoxin (A subunits and five B subunits )- - stimulates adenylate cyclase cAMP - diarrhea ST(heat stable enterotoxin): stimulates cGMP - diarrhea 2. Infection (1). extraintestinal infections - caused by E. coli opportunistic pathogens *urinary tract infection (the most common ) *G- bacteremia ;septicemia * neonatal meningitis (new born) (2). diarrheal diseases-caused by certain serotypes of E.coli Enterotoxigenic E.coli (ETEC) LT and/or ST; Diarrhea; children(under 5 years), adult(travellers), Nausea, vomiting, abdominal cramps Enteropathogenic E.coli (EPEC) No exterotoxin; Diarrhea; infantile enteritis severedeath Less in adults Enteroinvasive E.coli (EIEC) No exterotoxin; endotoxin, Diarrhea, like dysentery;( large intestine) Children, adults Enterohemorrhagic E. Coli (EHEC) vero toxin, hemorrhagic colitis; HUS III. Laboratory diagnosis 1. Specimen: feces, blood, pus, etc 2. Isolation and identification: * Biochemical reactions * serologic identification IV. Investigation in public health bacteriology indicator of fecal pollution (food/water) 1.Detecting number of coliform bacteria: Normal number 3 / 1000 ml sample. 2.Detecting total number of bacteria: Normal number 100 colonies / ml (g) sample. V. Treatment and control Section 2. Proteus 1. Gram negative bacillus, peritrichate Motile (+), Urease (+), Lactose (-) “Swarming growth phenomenon” Grow luxuriantly on the moist surface of nutrient agar. 2. Certain strains of P. Mirbilis (OXk) and vulgaris (OX2 and OX19) are employed as antigens in the Weil-Felix test, useful in the diagnosis of certain Rickettsial infections. 3. Cause urinary tract infections, wound and burn infection, septicemia, and food 9 poisoning. 4. Antibiotics Section 3. Shigella I. Biological characteristics 1. G- rods, non-motile, possesses pili 2. biochemical reaction lactose fermentation: test: “-”(only shigella sonnei late fermentation), On differential media : non color colony 3. antigenicity: O Ag, K Ag 4. Classification: 4 groups, 43 serotypes 5. Variation: antibiotic-resistance (R plasmid); II. Pathogenesis and Immunity Human beings the only natural hosts 1. Pathogenic factor: Infecting dose: 200 organisms (1).Pili adhesion ileum intestinum end epithelial cell (2).Endotoxin fever, shock; inflammatory; rectal cramp (3).Exotoxin: shiga toxin (vero toxin-I, II) 2.Disease : organisms oral route , patient/ carrier, *acute dysentery (bacillary dysentery) : fever, bloody mucopurulent stool, abdominal cramp, tenesmus , local inflammation ulceration( colon) *chronic dysentery : diarrhea : carrier * toxic dysentery 3.Immunity IgA persistent short, no IgG III. Laboratory diagnosis 1.Isolation and identification 2.Rapid diagnosis IV. Prevention and Treatment Section 4. Salmonella I. Biological characteristics: 1 G-, peritrichous, non spore-forming, lactose fermentation: test: “-” Biochemical reactions: -the basis of classification and identification 2.Antigenic structure and classification (1). O antigen (2). H antigen Type specific Ag: a. Phase 1 specific phase b. phase 2 nonspecific phase (3). Vi antigen (virulent Ag) surface polysaccharide; antiphagocytosis 10 II. Pathogenesis and immunity 1. Pathogenic factors (1) Invasiveness Pili-adherence Vi antigen -antiphagocytosis (2) Endotoxin WBC; shock ; activited complementinflammation (3) Enterotoxin S.typhi murium: LT/ST 2. Pathogenesis (1) Septicemia: (S. Choleraesuis) Pneumonia; osteomyelitis; meningitis(neonates, very young child) (2) Enterocolitis (Food poisoning) World wide; incubation period: 6-24 hour headache, abdominal pain, nausea, vomiting, fever , watery diarrhea (3) Enteric fever: Organism typhoid (caused by S. typhi) paratyphoid (caused by S. Paratyphi A,B,C) Characteristics of the disease: two times of bacteremia, continuous fever, liver and spleen enlargement, rose spots, severe complications. 3. Immunity Enteric fever: *persistant immunity after disease. *The main anti-infectious immunity is CMI. *humoral immunity destroy the organism which into the blood Ab titer can continue for a long time after recover III. Laboratory diagnosis 1. Bacteriological methods (1) *Enteric fever: collect specimen according to the stages of the disease, 1st week-blood; 2nd3rd week - feces or urine. *Food poisoning: collect feces, food. *septicemia: blood (2) Systemic biochemical and serologic identification. 2. Serological methods (Widal test) (1) To detect the unknown Ab with given Ag(O,H,HA,HB,Hc) tube agglutination. (2)Normal serum titer: O 1:80; H 1:160; H (A/B/C) 1:80 IV. Prevention and treatment 1. Vaccination capsular polysaccharide antigen(Vi antigen) 2. Antibiotics: Chapter 15 Vibrio Section 1. V. cholerae V. cholera cause cholera (an outbreak infectious disease) two biotypes: classical biotype eltor biotype I. Biological characteristics: 1. Gram negative, short curved rods, single polar flagellum, pili, sexpilis 2. Culture 11 halophilic, grow in high pH (8.8-9.0) medium, 3. Antigenic structure O Ag stable heat group specificity H Ag labile heat non- specificity 4. resistant *live for 13 weeks in water *resistant basic, cold *sensitive to heat(55 15min,100 12min) dry acid(gastric acid 4min) Antibiotics II. Pathogenicity: 1. Pathogenic factor (1).Invasiveness: flagellum, pili (2).Cholera enterotoxin (similar to LT) *B subunits (five) Ag high; bound unit, attaches to the receptor (GM1) on the epithelial cells of small intestine. *A subunits (A1 ,A2) Ag weak ;active unit, enters the cell, stimulates adenylate cyclase cAMP . 2. Disease-cholera Organisms oral route (contaninated water, food) stamoch(gastric acid) attach to the small intestine epithelial cells(non-penetration) multiplication cholera toxin adenylate cyclase cAMPconcentration secreting effect devere diarrhea (rice-water stools ) *patient may lose as much as 10 to 15 liters of liquid peir day *rapid dehydration and hypovolaemic shockdeath in 12-24 hour *“rice-water stools”-mucus, epithelial cells, large number of vibrios * recover: gallbladder have some organism III. Immunity 1. Nonspecific immunity: Gastric acid 2. Specific immunity: Abs (SIgA) 3. Persistent immunity to the same serotype IV. Laboratory diagnosis 1. Rapid diagnosis 12 rice-water stools- directly smear: Hanging-drop observation; Gram stain 2. Isolation Basic peptone water, 37, 68 hours, grow on the surface 3. Identification Slide agglutination test V. Preventionand treatment 1. Vaccine *Inoculation of dead bacteria-vaccine *Live attenuated oral vaccines(against O1 , O139) *Genetic engineering vaccine is being studied. 2. give the life-saving replacement of fluid and electrolytes 3. Antibiotics: tetracycline; chloramphenicol Chapter16 Helicobacter non- sporing; non-capsulate *thick, complex, lipid-rich-waxy cell wall 2. culture *obligate aerobes; *Special nutrient requirement: whole eggs(yolk), glycerol, asparagine, malachite green, potate *Slow growth: generation time 18 h24h(primary isolation8 weeks) Colony: “cauliflower” 13 Pellicle on surface of liquid media 3.Resistant *Resistant to drying (especially in sputum, 6-8 months) *resistant to: acid( 3% HCl, 6% H2SO4), alkalis( 4% NaOH) * resistant to dyes *Sensitive to : moist heat-60 30min,70 3min disinfectants- alcohol, glutaraldehyde, formaldehyde drugs-rifampin, streptomycin, isoniazid U.V. 4.Variation: *drug resistance variation *virulent variation -BCG (Bacliie Calmette-Guerin): M.bovis 230 generals, 13 years, vaccine II. Pathogenicity 1. Pathogenic substance: (1) Lipid Phosphatide Stimulate monocytes proliferation-form tubercle Inhibit proteinase- form caseous necrosis Mycolic acid A large fatty acid, Associated with acid-fast property Cord factor Associated with virulence Inhibit migration of leukocyte to form chronic granuloma Bind to mitochondrial membranes, cause functional damage to respiration and oxidative phosphorylation Wax D Act as an adjuvant Sulfatides Inhibit the fusion of phagosome and lysosome (2) Protein-Ag; protein-Wax Dallergic response (3) Polysaccharide-Connected with Wax D (4) Mycobactin- affinity with Fe 2. Disease: tuberculosis Usually a respiratory infection, others as wound, food can cause infection-lung, intestin, kidney, skin, lymphonode, bone, joint Pulmonary tuberculosis: primary tuberculosis organismrespiratory tractpulmonary alveolar lesions hilar lymph nodes swellingfibrosisnatural cure post-primary tuberculosis organisminfection again inflammationnecrosis tubercle fibrosis/caseation necrosis III. immunity 1. The main anti-infectious immunity is CMI 14 2. Infection immunity 3. CMI and DTH IV. Tuberculin test *OT (old tuberculin): TB Glycerol broth 4-8 weeks 100C, 1 h filtration concentration (1/10) *PPD (purified protein derivative): TB special media 6-8 weeks TCA precipitation 1. Principle: DTH 2. Result and interpretation PPD injection 24-48h induration, erthyema “-”- 5mm: no TB infection early stage of primary infection serious infection of tuberculosis virus infection; tumor, AIDS; use of immunosuppressive agents “+”- 5mm 15mm: hypersensitive to M. tuberculosis ; immunity “+”- 15mm: active TB perhaps 3. Application * Basis of BCG inoculation, detect immunity effect *Diagnosis for young children tuberculosis *Epidemiological investigation *cellular immunity test of patients with tumor V. Laboratory diagn