传染病学英文题目与答案

1、INTRODUCTION OF COMMUNICABLE DISEASESI .TERMS1) Overt infectionIt indicates that after the microorganism enters the host, it not only induces the immune responses of the host but also produces hiso morphological damage and pathological changes through the role of the microorganism or the allergic re

2、action of the host. In most in fectious disease such as measles most infected host manifested as overt infection. After overt infection ends the microorganism can be eliminated and the hosts acquitted consolidated immunity. In some infectious diseases (such as bacillary dysentery) the immunity is t

3、emporary. A small amount of overtly infected hosts change to carrier state. It is called “ convalescentcarrier ”.2) Incubation periodThis period is from pathogens invading into human body to clinical symptoms appearing. The incubation period of all infectious disea ses has a limit of the time (the s

4、hortest and longest) and a normal distribution. It is an important evidence of observing, detecting th e contact in quarantine work. It is usually equal to the whole period including the pathogen reproduction, transference, location, tissue damage and function changes before the clinical symptoms to

5、 occur. The period length is negative relation with the invading quantit y of the pathogens. If the pathophysiologic changes are caused by toxins, the incubation period relates with the time of the toxins pr oduction and distribution, e.g. bacterial food poisoning. The toxins have been produced befo

6、re eating. The period can be short to a fe w hours. The period of rabies determines to the location of virus entry(wound).It has a positive relation with the distance of the wou nd to the central nervous system.3) Latent infectionWhen the microorganism infected the host and localized in some area of

7、 the host, it can latently for along time because the hosts im munity is strong enough to locate the pathogen but can wipes it out. When the hosts immunity decreased, overt infection can occurs.Such latent infection is common in some diseases, e.g. herpes simplex, herpes zoster, malaria, tuberculosi

8、s etc. Generally the microor ganism can not be excreted during latent infection, which is a different point from carrier state. Not that every infectious diseases has latent infection.4) Sources of infectionThe microorganisms are able to gain to access to the person or animal, establish itself and p

9、roliferate in vivo and excrete pathogen o utside the body, such as patients, the person of covert infection, pathogen carriers and infected animals.5) RelapseAfter the patient has entered convalescent period, the temperature has recovered to normal for a period of time, then the pathogen hi dden in

10、some tissue reproduce to a certain degree and make the primary symptoms repeatedly, it is called “ relapse ”.6) RecrudescenceIn the convalescent period of some patients, the temperature has not stably decreased to normal and the fever rise again, it is calleda*”recrudescence ”.7 )ZoonosesSome natura

11、l ecologic environment is suitable to the transmission of infectious diseases among wild animals. These diseases include p lague tsutsugamushi disease, leptospirosis, and so on. The human race may be infected when he get into these areas. These diseases are called “ zoonoses ”.II. QUESTIONS1) Please

12、 briefly describe the manifestations of infectious diseases (infection spectrum).Infectious process starts when microorganisms enter the human host through various ways. Whether the microorganism is eliminated o r colonized in the host, it is mainly dependent on the pathogenicity of the pathogen and

13、 the immune function of the host.i. Pathogen is eliminated by host immunity: After the microorganism enters the host it can be wiped out by non-specific immunity, a nd eradicated or eliminated by specific immunity which the host has got before the infectious process.ii. Covert infection: It refers t

14、o that the microorganism only making the host producing specific immune response not having histomor phological damage or even having mild feature after it enters the host. Clinically, there is no any symptoms and signs or any bioche mical changes.iii. Overt infection: It indicates that after the mi

15、croorganism enters the host, it not only induces the immune responses of the host but also produces hisomorphological damage and pathological changes through the role of the microorganism or the allergic reaction of t he host.iv.CarrietgtSisdividedtGy irucarrien d gcteraer rieccordodgfferatt hogAHcg

16、 rrieteateavommo ncharactehSilSooclinicmignifestatihenicroorgggbeBxcrededinhetgte.v LateintfectiWn： ehenicroorgglneeeelosintOcgliZesbmgreaftheloSt,cg tgtenftyglongme becathshositm munsstroenoUg)locgthe)gthobungnoWipe ouW/heheiostmmurdecregve, eNnfectcfflioccurs.2) Plealseefkyescrtbfgctgr|gtdtOthe)gt

17、hogergigliyDgtho(ttnhfecti(purgcess.i. lhvgsivenesStsitsabilitgihvgdelosahdprewdhthelost.ii. Virulehcercludeeoxihsidgrioeiszymes.iii. NumlQelrhgthoglehhumloilhvgdi：nathoispgsitiNegtightlbhgthogernigitygnilefecti(dUseg seTheBgsitjmbehe)gthogehdudisegsfjregihdifferelhsegses.iv. VgrigbilPgtho(gellpsgdu

18、gErigtdgrtge hviro hmetteredifagygfSe h erspegkuiigier 弱 hviro hmeh t ofgrtificialltutbe)gthogeoightpgthogJebecreTSleepeaSecfebleltwdtednosWsillhcredtlsepgthoge hicitgithe)gthogeehtigerigigtgthe)gthowemgke e)gthoeegafioerthespecifilgmurgfyelost ghdohtililhl(euglelisegse.3 PleOseefkyescrtbdbgsiihgrgc

19、terosititfectiGdisegses.i. PgthogeveiryfectidiissB sdisegWefrsU ndersbythifecii hicrnig hifestghOhSdemi(Ooa|icrhdhehne)gthogeho und.ii. lnfectivlihyectivfteghsih甲gthogebeBxcretocbhtgmtheserroundihghengidiistihcbohweeh hen fectidiseaaeOthenfectiEneryfectiolUsegs9g oh sideasbgbleectiPsrioWhichabeJseaS

20、a rulisolattepgtient.iii. Epidemi(oatUtobde*fluelogegtuEa1docialctctlhehfectipusc®lS8nifesiategllsgrgctelIistics t cgbedivid<nli(bhexoticitythe5ndemIC gysogbedividedsporgdpidelancbgndeTlhElistribution oithencideogteenfectidiseasemesegsdihar ibutinspagregio(histributahrd*ifferen0ulgt(oge, sex

21、,ndccupgiSgllSarepidemicfeHtigre.iv. PostinfeictimhlriTyhosta 卩roduc£cpig)tectmmunWyiCSdirectehe)gthogetsprodugtStr heostgSfectedheigthogestinfegtaohi rbe/ohggctiVm muhTtytesti nignefpostinfegtioli Mty vgriesi thl iffereftectious.seausbyaspecpathogerhudmjproorganpmasItei.istomaniyfectiouoilctog

22、goVIRUSEPATITISI .TERMSThgompleBVScglleDlaheartiClel42-hDBhearti(iSengdJlpgfgrgute7lhthicgghtgirtiTelepgtiti sBsurfagetigglucoprgiefellufgtgh(grihhr®8hihdigmeterighgsseSsswspecgigtigthle hepgtiiglrehtigehBcAghDghearti(glercaberokeoWbytregtmeitiWeter(tordvesllDN>polymergs eghadoutStrghdeduDNA

23、ehomgggherveaprimstempliatdtrgorthe)NAolymergse.2) Wihd(pWgseAhti-HlgMbersi6tg18mohthgepresaretcutespotgs0newlyfectgfhBVhgcubaseSnggvdegre dtheBs>butlgvegdemohstreltegt amglgfehti-HBS;i-HShDghti-HBb6detectglbse rolcggc) iscgllewlihdcpWghthigsah ti-HllgcmgyethhlevidefggdigghoghaguteB>ihfectioh.

24、3) HBsAgIt stgnf0rHepgBSurfa8getigenscodeglrthe)roteglftheyiraE hveloptbeSgehTheEcrug htigesuc btypesHBsATheyrd gdvgyrg hdywH BsAshOh-ihfegtSeJbuHBsAg-p0Sggsbolbdgohsidered otehtignfectibeggUseggohtaihmpHBVDgherticles).4) ChroHBsAgirrierSonpers(i)hfectw(t ltoepgtBiSrudevemp(ghrorhigectStategSgsymptg

25、mangglssociWiealhyi ghificgvefuhctigrstsbhormeXiCep±rsisS®ItHBsAg-pols0ith6mohtHgweVeebi iopsevegistepgElaeaogpghat only a minority of them is with normal histology; and the majority cases present morphologic liver damage in varying degrees, ra nging form minimal inflammation, chronic pers

26、istent hepatitis, chromic active hepatitis, or even cirrhosis.5) HBV DNAHepatitis B virus (HBV) contains a small circular DNA molecule that is partially double-stranded, the DNA consists of a long strand (L) of constant length (3,200 bases) in all molecules and a short strand, which varies in length

27、 between 1,700-2,800 bases in differe nt molecules. A DNA polymerase activity in the virion repairs the single-stranded molecules of 3,200 bases pairs. The four open read ing frames of the HBV are termed S, C, P and X.II. QUESTIONS1) Please briefly describe the regions of the HBV gene and the protei

28、n they code for.The four open reading frames of the HBV are termed S, C, P and X. The S region codes for the protein of the viral envelope and is divided into the S gene, pre-S1 region and pre-S2 region. The C gene codes for the core protein. The P region, codes for the vira l DNA polymerase which p

29、ossesses a reverse transcriptase activity. The X region can code for HBxAg, the function of this region is unknown.2) Please briefly describe clinical manifestations of the virus hepatitis B.The clinical picture is extremely variable, ranging from asymptomatic infection, acute hepatitis, chronic hep

30、atitis, cholestatic hepatitis, t o a fulminating disease and death in a few days.i. Acute viral hepatitisii. Cholestatic hepatitisiii. Fulminant hepatitis (Acute gravis hepatitis): Hepatitis may take a rapidly progressive course terminating in less than 10 days. Fulm inant hepatitis results form ext

31、ensive hepatic necrosis. It develops most commonly as a complication of viral hepatitis.iv. Chronic hepatitis: Chronic hepatitis is defined as hepatic inflammation of at least 6 months duration, as demonstrated by persistentl y abnormal liver function tests, and divided into three forms: (1) mild ch

32、ronic hepatitis; (2) moderate chronic hepatitis; (3) severe chr onic hepatitis.3) Please briefly describe the clinical performance of the acute gravis hepatitis.Hepatitis may take a rapidly progressive course terminating in less than 10 days. Fulminant hepatitis results from extensive hepatic ne cro

33、sis. It develops most commonly as a complication of viral hepatitis.The clinical features which suggest a fulminant course are as follows:(1) high fever, sever abdominal pain, and vomiting, which persist for several days after the initiation of bed rest.(2) a sudden decrease in the size of the liver

34、.(3) neuropsychiatric changes of early hepatic encephalopathy, including drowsiness, irritability, insomnia, and confusion.(4) the appearance of ascites during the acute illness.(5) severe prolongation of the prothrombin time (more than 20 seconds with control of 12 seconds) with or without bleeding

35、. Serum bilirubin and transaminase levels do not reflect the severity of illness.(6) patient may die in hepatic coma during the early icteric period, or may become deeply jaundiced, while serum transaminase levels often fall during the period of clinical deterioration.If the patient occurred above c

36、linical manifestation over 10 days after onset of acute icteric hepatitis, designated subacute gravis hepat itis, the patients easily become cirrhosis.4) Please briefly describe the clinical meaning of the hepatitis B serum antigen antibody system.(1) HBsAg (Hepatitis B surface antigen)It is the mar

37、ker of HBV infection routinely measured in blood. There are four antigenic subtypes of HBsAg. They are adr, adw, ayr, and ayw. Subtyping of HBsAg is primarily of epidemiologic importance. HBsAg is usually the first detectable abnormality in the ser um of a Patient with hepatitis B. It occurs late in

38、 the incubation period and before the onset transaminase elevation or symptom, and persists for a few weeks in the typical acute cases, or more than 6 months, even many years in chronic HBsAg carrier state. HBsA g is non-infectious itself, but HBsAg-positive blood should be considered potentially in

39、fectious because it may contain complete HBV (Dane particles).(2) Anti-HBs (Antibody to hepatitis B surface antigen)It is the antibody to HBsAg and considered to be protective. Anti-HBs usually appears in the serum after HBsAg disappears and pers ists for years.(3) HBcAg (Hepatitis B core antigen)Th

40、e test for detecting HBcAg from blood is not commercially available.(4) Anti-HBc (Antibody to hepatitis B core antigen)It is the antibody to HBcAg and thought not to be protective. Anti-HBc is the first antibody to appear in the serum during infection and is usually first detectable 2 to 4 week afte

41、r the appearance of HBsAg. Anti-HBc IgM persists 6 to 18 months, so represents an acute response to a newly infection of HBV. It fills the serologic gap (the window phase) in acute cases who have cleared the HBs Ag but have not demonstrated detectable amounts of anti-HBs. In this case, anti-HBc IgM

42、may be the only evidence for diagnosing a n acute HBV infection.Anti-HBc IgG developes later than IgM and may persist for many years, even after HBsAg has been cleared. It represents a response to prior infection in HBV.(5) HBeAg (Hepatitis B e antigen)HBeAg appears during the incubation period shor

43、tly after the detection of HBsAg and only during reactivity, and disappears before th e disappearance of HBsAg. HBeAg is a sensitive index of viral replication, infectivity, and chronicity.(6) Anti-HBe (Anti-body to hepatitis B e antigen)It is antibody to HBeAg and detected as early as the fourth we

44、ek of illness. It can persist for years. Anti-HBe is originally thought t o be correlated with a low risk of infectivity in HBsAg positive blood.5) Please briefly describe the management of gravis hepatitis.(1) The patient with fulminant hepatitis requires intensive nursing care with monitoring and

45、support of vital functions.(2) Continuous intravenous infusion of glucose solution is required to prevent hypoglycemia in a patient who has no hepatic glycogen stores and has depressed glyconeogenesis.(3) Fluid and electrolyte balance should be achieved by accurate measurement of intake and output.(

46、4) In the absence of hepatic plasma protein synthesis, plasma albumin levels can be maintained by intravenous infusion of solutions of albumin.(5) Deficiency of clotting factors can be partially corrected by infusion of fresh-frozen plasma and Vitamine K.(6) Prevention and treatment of liver encepha

47、lopathy1) Low protein diet.2) Reduced serum amine drug: Sodium glutamite, and 14-Amino acid injection-800 etc.3) Recover normal neurotransmitter: Levodopa 200-600mg/day, iv gtt.4) Treated cerebral edema.(7) Preventive bacterial infection.(8) Prevention and treatment of acute renal failure: Removed t

48、he factors of induced acute renal failure, such as treatment of infection, and supplement of blood volume, etc.Traditional Chinese medicine and herbs have been proved to be beneficial to viral hepatitis.HEMORRHAGIC FEVER WITH RENAL SYNDROMEI .TERMS1) Hemorrhagic fever with renal syndrome (HFRS)An in

49、fectious disease with natural source, caused by hemorrhagic fever with renal syndrome viruses (HFRSV), characterized by fever, prostration, vomiting, proteinuria, hemorrhage, shock and acute renal failure. This zoonosis is synonymous with hemorrhagic fever wit h renal syndrome (HFRS) or epidemic hem

50、orrhagic fever (EHF).2) HantavirusThe causative agents of the disease belong to the family Bunyaviridae. All contain RNA, with circular or oval shape, 85-110 nm in diameter. The RNA genome contains three fragments, L, M and S gene, code for polymerase, membrane proteins and nuclear capsid proteins,

51、respectively. There are eight serologic types of viruses at least: Hantaan virus, Seoul virus, Puumala virus, Prospect hill virus, Belgrade-Dobrava virus, Thai virus, Thottapalaym virus, Muerto Canyon virus, and so forth.II. QUESTIONS1) Please describe chiefly the clinical manifestations of hemorrha

52、gic fever with renal syndrome.Incubation period, 4-46 days, 1-2 weeks are common.Three major clinical manifestations include pyrexia and intoxication, hyperemia and hemorrhage, hypotension and renal malfunction. Five typical phases:1) Febrile phase: acute onset, 39 C -40C , lasts 3-7 days, malaise,

53、headache, lumbago, orbital pain (three aches), drunkenness, petechia and ecchymosis, sometimes stripe-shaped appeared.2) Hypotensive (shock) phase: often occur suddenly during defervescence, lasts 4-6 days, owe to the lose of plasma from the vascular system. platelet decreased, hematocrit value incr

54、eased, nausea, vomiting, abdominal pain, leukocytosis, atypical lymphocytes is usually more than 10 of total leukocytes, proteinuria.3) Oliguric phase: occur during or soon after hypotensive phase, lasts 2-5 days, urine volume less than 500ml/24h, anuria, less than 5 0ml/24th, uremia, metabolic acid

55、osis, bleeding (hemoptysis, hematemesis, hematuria or melena), fatal hyperkalemia, hypervolemic syndr ome (high blood pressure, engorged neck veins, edema and restlessness).4) Diuretic phase: the volume of urine more than 3000ml/24h, lasts 7-14 days, dehydration with hypokalemia, hyponatremia, becau

56、se of more kalium (potassium) and natrium (sodium) excreted with urine. BUN falling down, about1/3 of all deaths occurs in this phase.5) Convalescent phase: urine 1000-2000ml/24h, return appetite, strength, urinary concentrating ability recovered.2) Please describe chiefly the laboratory findings of

57、 HFRS.1) Blood routine: leukocytosis, 15-50 X0E9/L, neutrophils dominated in early stage, lymphocytes dominated in late stage, atypical lym phocytes 10%-15%, hematocrit value and hemoglobin rise, thrombocytopenia.2) Urine routine: marked proteinuria, sometimes with casts, blood cells and membrane-sh

58、aped substance, consist of protein, blood cells and mucosal epithelia.3) Blood biochemical examination: BUN increased, CO2-CP decreased, hyperkalemia in oliguric phase, hypokalemia in diuretic phase.4) Blood?coagulating function examination:?thrombocytopenia, prolongation of prothrombin time, fibrinogen?decreased?and secondary fi brin lysis.3) Please describe chiefly the complications of HFRS.1) Visceral bleeding, including hemoptysis, hematemesis, hematuria, cerebro-hemorrhage and hemoperitoneu