1. Section 15. Infection disease and Anti-infective drugs ( 感染性疾病与抗感染药 )

2. Charpter 2. Anti-infective drugs ( 抗感染药物 )

5. Contents Part 1. General considerations of anti-microbial agents Part 2.  -Lactam antibiotics Part 3. Macrolides, lincomycins, and vancomycins Part 4. Aminoglycosides & polymyxins Part 5. Tetracyclines & chloramphenicol Part 6. Synthetic antimicrobial agents Part 7. Antifungal agents Part 8. Antiviral agents Part 9. Antituberculous drugs Part 10. Clinical uses of antimicrobial agents Part 11. The drugs treated parasitic infections

6. According to bio-activity  Anti G + antibiotic  Anti G - antibiotic  Broad-spectrum antibiotic  Anti mycobacterium （分支杆菌） antibiotic  Anti anaerobe （厌氧菌） antibiotic  β- lactamase inhibitor Antimicrobial drugs classification

7. According to the chemical structure ： 1 、 β-lactams: Penicillins; Cephalosporins; 2 、 Aminoglycosides; 3 、 Macrolides; Lincosamides ;Vancomycins 4 、 Tetracyclines; Chloramphenicol 5 、 Quinolones 6 、 Sulphonamides 7 、 Nitrofurans 8 、 Antimycobacterial agents 9 、 others: Oxazolidinones; Streptogramins

8. History of Antimicrobial Therapy 1909 Ehrlich discovers Salvarsan （撒尔佛散，治疗梅毒特效剂） “Magic bullet” for treatment of syphilis （梅毒） 1928 Fleming discovers penicillin( 青霉素 ) 1932 Domagk discovers sulfonamides （磺胺类药物） 1940s Penicillin and streptomycin （链霉素） used widely, cephalosporins （头孢菌素） discovered 1947 Chloramphenicol （氯霉素） discovered, first broad spectrum agent 1950s Tetracycline （四环素） in use 1952 Erythromycin （红霉素） discovered (macrolides 大环内酯类 ) 1956 Vancomycin （万古霉素） used for penicillin-resistant S. aureus 1957 Kanamycin （卡那霉素） discovered (aminoglycosides 氨基苷类 ) 1962 Nalidixic acid （ 萘啶酸 ） discovered (quinolones 喹诺酮类 ) 1980s Fluoroquinolones （氟喹诺酮类）, broad spectrum cephalosporins 2000s Newer agents to combat resistant pathogens

12. Part 1. General considerations of antimicrobial agents ( 抗微生物药物概论 )

13. Contents 1. Overview 2. Term and definition 3. Classification and mechanism of antibacterial action 4. Bacterial resistance

14. 1. Overview: (1)Chemotherapy( 化学治疗, 简称化疗 ) (2)Chemotherapeutic drugs: Antimicrobial drugs( 抗微生物药 ); Antiparasitic durgs( 抗寄生虫药 ); Antineoplastic drugs( 抗肿瘤药 ). (3)Antimicrobial drugs: Antibacterial drugs( 抗菌药 ); Antifungal drugs( 抗真菌药 ); Antiviral drugs( 抗病毒药 ).

15. Pharmacokinetics Adverse effects pathogenicity Immunologicalresponses Therapeutic Effects Resistance The relationship of the host, microorganisms, antimicrobial drugs.

16. 1. Antibacterial drugs( 抗菌药 ) 2. Antibiotics( 抗生素 ) 3. Bacteriostatic drugs( 抑菌药 ) 4. Bactericidal drugs( 杀菌药 ) 5. Antibacterial spectrum( 抗菌谱 ) 6. Chemotherapetic index ( 化疗指数,CI) 7. Minimum inhibitory concentration ( 最小抑菌浓度, MIC) 8. Minimum bactericidal concentration ( 最小杀菌浓度, MBC) 9. Concentration Dependent killing 10. Post antibiotic effect ( 抗生素后效应,PAE) 11. Time-dependent killing Terminology

17. 2. Terms and definition: (1)Antibacterial drugs( 抗菌药 ): Substances that can kill bacteria and/or inhibit its growth. including: ① Antibiotics( 抗生素 ); ② Synthetic antimicrobial agents, such as sulfonamides( 磺胺类 ) and quinolones( 喹诺酮类 ), etc.

18. (2)Antibiotics( 抗生素 ): Substances produced by various species of microorganisms(bacteria, fungi, actinomyces, etc.), which can kill other microorganisms or inhibit their growth. Terms and definition

19. (3)Chemotherapetic index: LD 50 /ED 50, or LD 5 /ED 95 (4)Antibacterial spectrum ( 抗菌 谱 ); (5)Bacteriostatic drugs ( 抑菌药 ); (6)Bactericidal drugs ( 杀菌药 ); Terms and definition

20. agents

21. (7)Minimum inhibitory concent- ration(MIC); (8)Minimum bactericidal concen-tration(MBC): MBC ≥ MIC; if MBC > 32 times MIC  resistance. Terms and definition

22. Antimicrobial Susceptibility Testing 7. Minimum inhibitory concentration (MIC) 8. Minimum bactericidal concentration (MBC): concentration (MBC): 99.9% decrease in growth over 24 hours

23. Incubate 18 to 24 hr at 37 ℃ Measure diameters of nongrowthzones Disk diffusion method for testing bacteria for susceptibility to specific antimicrobial drugs.

24. 9. Concentration Dependent killing: situation in which the bactericidal activity of a drug depends by how much the drug concentration exceeds the Minimum inhibitory concentration of the organism in question. e.g. aminoglycosides and quinolones 10. Time-dependent killing: situation in which the bactericidal activity of a drug depends how long the drug concentration exceeds the Minimum inhibitory concentration of the organism in question. e.g. b- lactams and vancomycin (PAE) 11. Post antibiotic affect (PAE) : Persistence of suppression of bacterial growth after limited exposure to an antimicrobial agent. e.g. aminoglycosides Terms and definition

25. (1) inhibit synthesis of bacte-rial cell walls; (2) act directly on the cell membrane of the microorganism and affect its permeability, and leading to leakage of intracellular compounds; (3) inhibit protein synthesis; (4) affect bacterial nucleic acid metabolism; (5) The antimetabolites of folic acid, that can block essential enzymes of folic acid synthetic metabolism. Classification and mechanism of antibacterial action:

26. ① ② ③ ④ ⑤ Classification and mechanism of action

27. (1)Inhibiting synthesis of bacterial cell walls: UDP- 乙酰胞壁酸 -5 肽 双糖十肽聚合物 Classification and mechanism of action

28. transpeptidase vancomycin  -Lactam antibiotics Classification and mechanism of action

29. (2)Affecting permeability of membrane: ① Ionic-adsorbed(streptomycin); ② binding to ergosterol(amphotercin B); ③ Inhibiting the synthesis of ergosterol (imidazoles); ④ Surface-active agent, that interact strongly with phospholipids(polymixins). Classification and mechanism of action

30. (3)Inhibiting protein synthesis: affecting the function of 30S, or 50S ribosomal subunits to cause a reversible inhibition of protein synthesis (strepto-mycin, erythromycin, etc.). binding to the 30S ribosomal subunit and altering protein synthesis, which eventually leads to cell death (strepto-mycin, etc.). Classification and mechanism of action

31. (4)Affecting bacterial nucleic acid metabolism: quinolones, etc. Classification and mechanism of action

33. Pteridine( 蝶啶 ) + PABA( 对氨苯甲酸 ) sulfonamides Blocked by sulfonamides Dihydropteroic acid( 二氢蝶酸 ) Dihydrofolic acid( 二氢叶酸 ) Glutaminic acid Tetrahydrofolic acid( 四氢叶酸 ) trimethoprim Blocked by trimethoprim NADPH NADP Dihydropteroate synthase Dihydrofolate reductasease (5)Blocking enzymes of folate metabolism: Classification and mechanism of action

34. Bacterial Resistance

35. 4. Bacterial resistance: (1)Category of resistance: ① Intrinsic resistance: Inherent features ， usually expressed by chromosomal genes ② Acquired resistance: ② Acquired resistance: emerge from previously sensitive bacterial populations emerge from previously sensitive bacterial populations Caused by mutations in chromosomal genes Caused by mutations in chromosomal genes Or by acquisition of plasmids or transposons Or by acquisition of plasmids or transposons

36. Bacterial Resistance (2)Mechanism of bacterial resistance: ① to produce inactivated enzyme; ② to inhance active efflux system: ③ the drug does not reach its target; ④ the target is altered;

37. Resistance: mechanisms, pathways IM OM Penicillin  -lactam Penicillinase Inactive Kanamycin Acetylation Phosphorylation Adenylyation 1A. Enzymatic inactivation e.g. b-lactamase 1B. Enzymatic modification e.g. Aminoglycoside modification 2. Active efflux e.g. Tetracycline resistance 3. Decreased permeability e.g. Porin mutations - cephalosporin 4. Target alteration Streptomycin resistance penicillin binding proteins

38. ① To produce inactivated enzyme: 1)Production of aminoglycoside modify- ing enzymes, such as deactivated enzyme to streptomycin; 2)Production of  -lactamase, such as penicillinase; 3)Production of inactivated enzymes to other antibiotics, etc. Bacterial Resistance Mechanism of bacterial resistance

39. ② To enhance active efflux system: Bacterial Resistance Mechanism of bacterial resistance

40. ③ The drug does not reach its target: Absence of, mutation in, or loss of the appropriate porins( 膜孔蛋白 ) channel can slow the rate of drug entry into the cell, or prevent entry altogether, reducing the effective drug concentration at the target site. Bacterial Resistance Mechanism of bacterial resistance

41. Porin channel( 膜孔蛋白通道 ) Bact e rial Resistance Mechanism of bacterial resistance

42. ④ The target is altered: Mutation of the natural target(such as resistance to fluoroquinolone). Target modification(ribosomal protec-tion type of resistance to macrolides and tetracyclines). Substitution with a resistant alternat-ive to the natural, susceptible target (such as methicillin resistance in staphy-lococci). Bacterial Resistance Mechanism of bacterial resistance

43. The transfer of resistance genes: Bacterial Resistance ① Mutations; ② Transduction; ③ Transformation; ④ Conjugation.

44. Bacterial Resistance The transfer of resistance genes ① Mutations( 突变 ): which may occur in the gene encoding. 1)The target protein; 2)The protein involved in drug transport; 3)Act on regulatory gene or promoter( 启动 子 ) affecting expression of the target, a transport protein, or an inactivating enzyme. such as aminoglycosides, quinolones, etc.

45. Bacterial Resistance The transfer of resistance genes

46. Mutations Mutations May occur in the gene encoding i) The target protein i) The target protein ii) A protein involved in drug transport ii) A protein involved in drug transport iii) A protein important for drug activation iii) A protein important for drug activation iv) A regulatory gene or promoter iv) A regulatory gene or promoter affecting expression of the target, a affecting expression of the target, a transport protein, or an inactivating transport protein, or an inactivating enzyme. enzyme.

47. ② Transduction( 转导 ): acquisition of bacterial DNA from bac-teriophage( 噬菌体 ) that has incorporated DNA from a previous host bacterium with-in its outer protein coat. Some phages can carry plasmids that code for penicillinase, or genes encod- ing resistance to erythromycin, tetracy- cline, or chioramphenicol. Bacterial Resistance The transfer of resistance genes

48. Transduction Transduction

49. Bacterial Resistance The transfer of resistance genes

50. Ba c terial Resistance The transfer of resistance genes ③ Transformation( 转化 ): Uptake and incorporation of DNA that is free in the environment into the host genome by homologous recombination.

51. Bacterial Resistance The transfer of resistance genes

52. Bacterial Resistance The transfer of resistance genes ④ Conjugation( 接合 ): The passage of genes from cell to cell by direct contact through a sex pilus( 性菌毛 ) or bridge( 桥接 ).

53. Transformation Transformation Conjugation Conjugation Bacterial Resistance

55. Multi-drug resistance MDR ( 了解 ) 1. 耐甲氧西林金葡菌 MRSA  社区获得性耐甲氧西林金葡菌（ community-associated 。 CA—MRSA ）  医院获得性耐甲氧西林金葡菌（ Hospital-associated ， HA-MRSA 2.Methicillin-resistant coagulase negative staphylococci, MRCNS PBP-2a PBP-2a 3.Penicillin-resistant streptococcus pneumoniae, PRSP PBP-1a, PBP-2a, PBP-2x, PBP-2b PBP-1a, PBP-2a, PBP-2x, PBP-2b Active efflux system Active efflux system 4.Vancomycin-resistant Enterococcus, VRE van-A, van-B, van C-1, van C-2, van C-3, van D, van E van-A, van-B, van C-1, van C-2, van C-3, van D, van E

56. 5. The 3 rd generation-cephalosporins -resistant Extended spectrumβ-lactamases, ESBL Extended spectrumβ-lactamases, ESBL Class I chromosone mediated β-lactamases Class I chromosone mediated β-lactamases 6.Carbapenem -resistant OprD porin OprD porin 7.Quinolone-resistant escherichia coli, AREC Active efflux system Active efflux system Multi-drug resistance MDR ( 略 )

59. Let’s take a rest !

60. Part 2.  -  -Lactam Antibiotics

61. Classification of  -Lactam Antibiotics Ⅰ. Penicillins( 青霉素类 ) Ⅱ. Cepharosporins( 头孢菌素类 ) Ⅲ. Other  -lactam antibiotics: 1. Cephamycins ( 头霉素类 ) 2. Carbapenems ( 碳青霉烯类 ) 3. Monobectams ( 单环类 ) 4. Oxacephalosporins ( 氧头孢烯类 ) Ⅳ.  -lactamase inhibitors(  内酰胺酶 抑制剂 )

62. ( 青霉素类 ) ( 头孢菌素类 ) Core structures of beta-lactam antibiotic families

63. Beta-Lactam antibiotics

64. ( 单环类 ) ( 碳青霉烯类 ) ( 亚胺培南 —— 碳青霉烯类 )

65. Chemicalstructureof penicillins Chemical structure of penicillins Ⅰ. Penicillins Ⅰ. Penicillins ( 青霉素类 ) ( 酰基侧链 ) ( 噻唑烷环 ) (  - 内酰胺环 ) ( 青霉素类 ) A. NaturePenicillins A. Nature Penicillins :

66. 1. Classification of Penicillins: (1)Nature penicillins: Penicillin G( 苄青霉素, 简称青霉素 ) (2)Penicillinase-resistant penicillins: Oxacillin( 苯唑西林 ) (3)Broad-spectrum penicillins: Amoxicillin( 阿莫西林 ) (4)Anti-pseudomonas penicillins: Ticarcillin( 替卡西林 ) (5)Anti-G - bacilli penicillins: Mecillinam( 美西林 ) Penicillins

67. 2. Antimicrobial activity: The penicillin-susceptible bacteria: (1)G + bacilli( 革兰阳性杆菌 ); (2)Non-penicillinase-producing strains of most G - cocci( 大多数不产青霉素酶的球菌 ) and Nisseria( 奈瑟菌属 ), etc. such as: Meningococcus( 脑膜炎球菌 ), Gonococcus( 淋球菌 ), etc. (3)Spirochetes( 螺旋体 ), etc. Penicillins

68. 3. Mechanism of action: (1)Inhibiting transpeptidase( 转肽酶, PBP, 青霉素结合蛋白 ), and inhibiting the synthesis of bacterial cell walls. (2)Activation of cell-wall autolytic enzy- me( 自溶酶 ). Penicillins

69. Comparison of the structure and composition of G + / G - cell walls. Penicillins

70. Penicillins & cephalosporins can inhibit the transpeptidase reaction in sen- sitive organism ( 敏感菌 ). Penicillins Penicillins

71. 4. Mechanism of resistance:

72. Penicillins ( 酰胺酶 ) ( 青霉素酶 ) (6- 氨基青霉烷酸 ) ( 青霉素裂解酸 ) (1)to produce penicillinase(  -lactamase) by bacteria;

73. Penicillin - Mechanism of resistance

75. (2)to alter PBP, decreased affinity for the antibiotic; (3)to make deficiency of porins, or enhance active efflux system, let penicillins does not reach its target, and inability to be effective. (4) Lack of the autolysins Penicillins

76. Antibiotic efflux pumps of G - bacteria. Penicillins

77. 5. Clinical Uses: (1)Streptococcal( 链球菌 ) infections: such as: Pharyngitis( 咽炎 ), Scarlet fever( 猩红 热 ); Rheumatic fever( 风湿热 ), Pneumonia( 肺炎 ), Endocarditis( 心内膜炎 ), etc. (2)Nisseria ( 奈瑟菌 ) infections: Meningitis( 脑膜炎 ); Gonorrhea( 淋病 ), etc. Penicillins

78. (3)Leptospira( 螺旋体 ) infection: such as: Liptospirosis( 钩端螺旋体病 ), Syphilis( 梅毒 ), Recurrent fever( 回归热 ). (4)G + bacilli(G + 杆菌 ) infection: such as: Diphtheria( 白喉 ), Tetanus( 破伤风 ), Anthrax( 炭疽病 ), etc. (5)Staphylococcal( 葡萄球菌 ) infection (generally resistant to penicillin G). Penicillins

79. 6. Adverse effects: Penicillins are among the safest of antibiotics, produce few direct toxic reactions, the most of the serious side effects are hypersensitivity reactions. Penicillins

80. (1)Hypersensitivity reactions: Itching( 痒 ), rashes, fever, serum sick-ness, angioneurotic oedema( 血管神经 性水肿 ). Anaphylactic shock (5/10 000). (2)Other adverse reactions: Phlebitis( 静脉炎 ), when i.v.; Local inflammatory reactions, in injection site when i.m.; Jarisch-Herxheimer reaction( 赫氏反 应 ) when treatment of syphilis, liptospirosis. Penicillins

81. 7. ADME of Penicillin G: Be destroyed easily by p.o. Administration by i.m. or i.v. gtt. widely distributed (even in CSF, when menings is infective); Eliminated in the urine. Penicillins

82. 8. Preparation of long-acting penicillin G: Benzathine penicillin G( 苄星青霉素 ) Procain penicillin( 普鲁卡因青霉素 ) Penicillins

83. 1. Penicillins by oral administration （耐酸青霉素） : Phenoxymethylpenicillin ( 苯氧甲基青霉素, Penicillin V) It is resistant to gastric acid, and be well absorbed(60%) when it is given on an empty stomach. Its half-life(t ½ ) is longer than that of penicillin G. A satisfactory substitute for Penicillin G to treat tonsilitis( 扁桃体炎 ), or Pharyn-gitis( 咽炎 ), etc. B. Semi-syntheticPenicillins B. Semi-synthetic Penicillins :

84. SemisyntheticPenicillins Semisynthetic Penicillins 2. The penicillinase-resistant penicillins( 耐酶青霉素 ): Oxacillin( 苯唑西林 ), Cloxacillin( 氯唑西林 ), Dicloxacillin( 双氯西林 ) It is stable in an acidic medium, can be administrated by po, or im, iv ; and it is resistant to cleavage by penicillinase. It is used for treatment of penicillin G- resistance staphylococcal infection.

85. 3. Broad spectrum penicillins （广谱 青霉素） : Amipicillin( 氨苄西林 ), Carbenicillin( 羧苄西林 ), Piperacillin( 哌拉西林 ), etc. They have similar antibacterial activity and a broader spectrum. All can be destroyed by  -lactamase. Semisynthetic Penicillins

86. Broad spectrum penicillins Semisynthetic Penicillins (1)Ampicillin ( 氨苄西林 ), Amoxicillin ( 阿莫西林 ) Pseudomonas aeruginosa( 铜绿假单孢菌 —— 绿脓杆菌 )-resistance. Clinical Uses: Upper respiratory infections; Urinary tract infections; Meningitis; Salmonella infections. (2)Carbenicillin ( 羧苄西林 ),Ticarcillin ( 替卡西林 ) With activity against Pseudomonas aeruginosa and some Proteus( 变形杆菌 ).

87. Broad spectrum Penicillins Semisynthetic Penicillins (3)Piperacillin ( 哌拉西林 ), Mezlocillin ( 美洛西林 ) They have the broadest antibacterial spectrum, and the most activity of the penicillins, with activity against Pseudo- monas aeruginosa, etc. Clinical Uses: For the treatment of the patients with severe infection caused by G - bacteria, us- ually in combination with aminoglycoside ( 氨基 苷类 ).

88. 4. Anti-G - bacilli penicillins: Semisynthetic Penicillins Mecillinam( 美西林 ), Temocillin( 替莫西林 ) They are bacteriostatic drugs, and have narrow antibacterial spectrum, with activity against some G - bacilli.

89. Cepharosporins Ⅱ. Cepharosporins ( 头孢菌素类 )

90. A. Classification: Cepharosporins The well-accepted system of classification by “generations” is based on general features of anti-microbial activity.

91. B. Classification and Features: Cepharosporins 1. First generation: 1. First generation: Cefazolin( 头孢唑林 ), Cefradine( 头孢拉定 ), Cefalexin( 头孢 氨苄 ), etc. Cefazolin( 头孢唑林 ), Cefradine( 头孢拉定 ), Cefalexin( 头孢 氨苄 ), etc. (1)more active than second and third genera-tion against certain G+ microoganisms; (1)more active than second and third genera-tion against certain G+ microoganisms; (2)more impervious than second and third ge-neration to attack by staphyloccal  -lactamase; (2)more impervious than second and third ge-neration to attack by staphyloccal  -lactamase; (3)less active than second and third genera-tion against certain G- microoganisms; (3)less active than second and third genera-tion against certain G- microoganisms; (4)non-stable to G- bacilli  -lactamase; (4)non-stable to G- bacilli  -lactamase; (5)more activity against certain Pseudomonas ( 铜绿假单孢 菌 ), anaerobes( 厌氧菌 ), etc; (5)more activity against certain Pseudomonas ( 铜绿假单孢 菌 ), anaerobes( 厌氧菌 ), etc; (6)certain kinds have kidney toxicity. (6)certain kinds have kidney toxicity.

94. Cepharosporins 2. Second generation: Cefuroxime( 头孢呋辛 ), Cefamandole( 头 孢孟多 ), Cefaclor( 头孢克洛 ), etc. Cefuroxime( 头孢呋辛 ), Cefamandole( 头 孢孟多 ), Cefaclor( 头孢克洛 ), etc. (1)more active than first generation against certain G - bacilli and more impervious than first generation G - bacilli  -lactamase; (1)more active than first generation against certain G - bacilli and more impervious than first generation G - bacilli  -lactamase; (2)somewhat less active than first generation against G + cocci but more than third generation; (2)somewhat less active than first generation against G + cocci but more than third generation; (3)active against anaerobes( 厌氧菌 ); (3)active against anaerobes( 厌氧菌 ); (4)lack activity against Pseudomonas; (4)lack activity against Pseudomonas; (5)less toxic than first generation to kidney. (5)less toxic than first generation to kidney.

95. （头孢西丁） （头孢孟多）

97. Cepharosporins 3. Third generation: Ceftazidime( 头孢他啶 ), Ceftriaxone( 头孢曲松 ), etc. Ceftazidime( 头孢他啶 ), Ceftriaxone( 头孢曲松 ), etc. (1)far more active than first and second gene-ration against G - bacilli; (1)far more active than first and second gene-ration against G - bacilli; (2)be highly resistant to  -lactamase produced by G - bacilli; (2)be highly resistant to  -lactamase produced by G - bacilli; (3)with the extended spectrum against anae-robes and Pseudomonas; (3)with the extended spectrum against anae-robes and Pseudomonas; (4)well absorbed, penetration into tissue, blo-od and body cavity as well in sufficient concen-tration; (4)well absorbed, penetration into tissue, blo-od and body cavity as well in sufficient concen-tration; (5)less active than first and second generation against G + cocci; (5)less active than first and second generation against G + cocci; (6)less toxic to kidney. (6)less toxic to kidney.

98. （头孢哌酮） （头孢噻肟）

100. Cepharosporins 4. Fourth generation: Cefepime( 头孢匹肟 ), Cefpirome( 头孢匹 罗 ), etc. Cefepime( 头孢匹肟 ), Cefpirome( 头孢匹 罗 ), etc. (1)resistant to type 1  -lactamase; (1)resistant to type 1  -lactamase; (2)more active than third generation against Enterbacter( 耐肠杆菌 ); (2)more active than third generation against Enterbacter( 耐肠杆菌 ); (3)less active than third generation against Pseudomonas. (3)less active than third generation against Pseudomonas.

102. fourth Cepharosporins

103. 1st 2st 3st 4st 1st 2st 3st 4st 抗菌谱 G+ 强 G- 酶稳定性 好 肾毒性 大 半衰期 长 血脑屏障通透性 好

104. Otherlactamantibiotics Ⅲ. Other  - lactam antibiotics 1. Cephamycins( 头霉素类 ): Cefoxitin ( 头孢西丁 ) It has the similar antibacterial activity and spectrum to the second generation cepharosporins, also can be used for the treatment of anaerobic infections.

105. Other  -lactamantibiotics Other  -lactam antibiotics 2. Carbapenems( 碳青霉烯类 ): Imipenem( 亚胺培南 ) Imipenem is markered in combination with cilastatin( 西司他丁 )—— Tienam( 泰能 ), a drug that inhibits the degradation of imipenem by a renal tubular dipeptidase. It has the broadest antibacterial spec-trum and the most activity of all the anti-biotic.

106. Other  - lactam antibiotics 3. Monobectams( 单环类 ): Aztreonam( 氨曲南 ) Carumonam( 卡芦莫南 ) For the treatment of aerobic G + bacilli infections. Narrow-spectrum antibiotic.

107. Other  -lactam antibiotics 4. Oxacephalosporins( 氧头孢烯类 ) Latamoxef( 拉氧头孢 ) Flomoxef( 氟氧头孢 ) Broad-spectrum antibiotic(anaerobic infections).

108. Ⅳ.  -lactamase inhibitors (  - 内酰胺酶抑制剂 ) Clavulanic acid( 克拉维酸 ) Sulbactam( 舒巴坦 ) Tazobactam( 三唑巴坦 ) Binding to  -lactamases and inactivate them, thus preventing the destruction of  -lactam antibiotics which are substrates for  - lactamases.

109. END OF CLASS