传染病学英文题目及答案

1、精品文档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 allergi

2、c reaction 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 i

3、s t emporary. A small amount of overtly infected hosts change to carrier state. It is called “ convalescentarrier ”.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 (th

4、e shortest 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

5、 to 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 b

6、efore eating. The period can be short to a fe w hours. The period of rabies determines to the location of virus entry(wound).lt 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

7、 of 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, tubercul

8、osis 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 an

9、d proliferate 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

10、in 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 called recrudescence .7) ZoonosesSome natural

11、 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 b

12、riefly 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 t

13、he 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 to

14、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.精品文档eciii. Overtfectionn dicatteaift&henicroorgent

15、smeio或nooniyiduceemmumspoicsthshosiut alsorodulces)morph(dlcg'icinpathologiharitjecugteolfthenicroorgartllsmllergi£actoiih hdiost.bUttLecfiv. CarriEtatessdividedxvirusarrien dactecairieccordodiffereiatthogAttca rristateavecommo ncharactehsiteocclinicmlanifestaUihenicroorgaabmxcretetinhistat

16、e.v LateirntfectiWni ehenicroorgaTieMnhelosintCcaliZesbnnffecftheloSt,ca ratenfOnalongime becatisdhosim munfytroeroltclocatlheathogebalnoWipe outiA/hdthostmmuraitycreave, ertnfectromoccurs.2) PleaSie1desctHieactarESatedhe>athogealCieyathogehenfectpnuraDess.refsi. Invasiveneefeteitsabilitcinvadedn

17、ostndprewdththeiost. ii/Virulerlteicludescxirandaricenzymes.iii. Numbethe)athoglennumbeilnvadplathogeositiNeatiorthhe)athogeinithtyanieectiolUsea seTh£asrtJmbehathog®nriudi5efeJreaHyiiffereases.iv. Variabil11athogcalproduce,iati0utoe nviro nnaeriheredifacyctse n enspeakUndeT 弱 nviro nmen t

18、 ofartificialltuthe)athogeoithtpathogjeidecreSheepeaspcteaetwdtednosW5ilincreaihpathoge nicitofth里athogTrnantigenaciatiofthathogeimake e)athogecaipethespecificmurCiyieiost andontinuduttedisease.3) PleabeeflscithobascharactepirsrlfestiPiiseases.i. Pathogev®ryfectidiisBesdiseaWefirsU nderstycfeci

19、i nicnia nifestahOhPdemiCeatilcrethehne)athowaro und.ii. InfectivIinyectivrteansthathogabexcretoCCntamtneterroundiht|jenaidlistincbohwen henfectidUsaaeCthehfectiEheilyfectidU9ealSBonsideaababhiectpericWhichabeJseaSa ruiecisoiatepatient.iii. Epidemi(CoagUUfederfluercfeatuahdociialctctlhenfectic)usc&#

20、174;n8nifesiatescllsaractelIistics t cabedivid<hi(Chexoticitythe5ndemICafcabedivid<hi(s>poraepideaTilcanderTli)cjistribution oithencideoCeehfectidU9eastimeseasdhslributichpaCregiohi8tributichd*ifferenCulatiahs, sex( nCccupatichE)arepidemi01olatiure.iv. Postinfeimimuhityhosta prodlsp8cpilC)t

21、ectinmurWyiCSdirectehe)athogeteproduafietr heosWaSlfectaylh甲athopChLtinfeimilCTurbe/ohgactiVm murTtytasti nimefpostinfeimiohunity variesitldiffereftectious.sceausbyaspecpjathogjenudmiproorganpmasIinbjstcrffyariyfectioucgeasaoilIccacgacstascpeVIRUHEPATITIS I . TERMS1) DarparticleccaeaTheompHfBVScalle

22、DlarrEartiClel42-nmarrEarti(ifmadJlpcfahDute7lnnthiclc,ontailrlihlh|epatiti sBsurfaantigehcoprctelellufatanannne:rcrehmndiameWhi)cpDsseSscwspecaittigee hepatitentig(HBcAghDahearti(dereaberokeowtoytreatmwhlUeter(torttve3DN>polymeras eanadoubitFandeduDNAenoma±aherveaprimaeynplateitrCortheNAoly

23、merase.2) WindpWasecdcgAnti-HlgMbersi6tc18monthcnepresahateutespotc3hewlyfectCiHBVnacubaseSnCaveeare dthedBsAghavecdemonstreitedt amcucfenti-HBhti-HhDanti-H:B6b6detectalbse rolcggap iscalledindoWaShthis)asah ti-HIBCmaye：he)nlevidercDeiagnoanacuteBVnfection.3) HBsAgIt stands for Hepatitis B surface a

24、ntigen. It is coded for the protein of the viral envelope by the S gene. There are four antigenic su btypes of HBsAg. They are adr, adw, ayr, and ayw. HBsAg is non-infectious itself, but HBsAg-positive blood should be considered p otentially infectious because it may contain complete HBV (Dane parti

25、cles).4) Chronic HBsAg carrierSome persons infected with hepatitis B virus develop mild chronic infection state that is asymptomatic and not associated with any si gnificant liver function tests abnormality except persistent serum HBsAg-positive more than 6 months. However, liver biopsy reveals t ha

26、t 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 persistent hepatitis, chromic active hepatitis, or even cirrhosis.5) HBV DNAHepatitis B virus (HBV) contains a small circular DN

27、A 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 between 1,700-2,800 bases in differe nt molecules. A DNA polymerase activity in the virion repairs the single-stranded molec

28、ules 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 protein 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 v

29、iral 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 possesses a reverse transcriptase activity. The X region can code for HBxAg, the function of this region is unknown.2) Please

30、briefly describe clinical manifestations of the virus hepatitis B.The clinical picture is extremely variable, ranging from asymptomatic infection, acute hepatitis, chronic hepatitis, cholestatic hepatitis, t o a fulminating disease and death in a few days.i. Acute viral hepatitisii. Cholestatic hepa

31、titisiii. Fulminant hepatitis (Acute gravis hepatitis): Hepatitis may take a rapidly progressive course terminating in less than 10 days. Fulm inant hepatitis results form extensive hepatic necrosis. It develops most commonly as a complication of viral hepatitis.iv. Chronic hepatitis: Chronic hepati

32、tis 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 chronic hepatitis; (2) moderate chronic hepatitis; (3) severe chr onic hepatitis.3) Please briefly describe the clinical perfor

33、mance 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 crosis. It develops most commonly as a complication of viral hepatitis.The clinical features which suggest a fulminant course ar

34、e 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.(3) neuropsychiatric changes of early hepatic encephalopathy, including drowsiness, irritability, insomnia, and confusion.(4

35、) 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. Serum bilirubin and transaminase levels do not reflect the severity of illness.(6) patient may die in hepatic coma during t

36、he 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 clinical manifestation over 10 days after onset of acute icteric hepatitis, designated subacute gravis hepat itis, the patient

37、s easily become cirrhosis.精品文档4) Please briefly describe the clinical meaning of the hepatitis B serum antigen antibody system.(1) HBsAg (Hepatitis B surface antigen)It is the marker of HBV infection routinely measured in blood. There are four antigenic subtypes of HBsAg. They are adr, adw, ayr, and

38、 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 the incubation period and before the onset transaminase elevation or symptom, and persists for a few weeks in the typica

39、l 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 infectious because it may contain complete HBV (Dane particles).(2) Anti-HBs (Antibody to hepatitis B surface antigen)It is

40、 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)The test for detecting HBcAg from blood is not commercially available.(4) Anti-HBc (Antibody to hepatitis B core antigen)It

41、 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 after the appearance of HBsAg. Anti-HBc IgM persists 6 to 18 months, so represents an acute response to a newly infection of

42、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 may be the only evidence for diagnosing a n acute HBV infection.Anti-HBc IgG developes later than IgM and may persist for

43、 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 shortly after the detection of HBsAg and only during reactivity, and disappears before th e disappearance of HBsAg. HBeAg is

44、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 week of illness. It can persist for years. Anti-HBe is originally thought t o be correlated with a low risk of infectivity

45、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 support of vital functions.(2) Continuous intravenous infusion of glucose solution is required to prevent hypoglycemia in

46、 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.(4) In the absence of hepatic plasma protein synthesis, plasma albumin levels can be maintained by intravenous infusion of

47、 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 encephalopathy1) Low protein diet.2) Reduced serum amine drug: Sodium glutamite, and 14-Amino acid injection-800 etc.3) Recover

48、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 the factors of induced acute renal failure, such as treatment of infection, and supplement of blood volume, etc.Traditiona

49、l 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 infectious disease with natural source, caused by hemorrhagic fever with renal syndrome viruses (HFRSV), characterized by f

50、ever, prostration, vomiting, proteinuria, hemorrhage, shock and acute renal failure. This zoonosis is synonymous with hemorrhagic fever wit h renal syndrome (HFRS) or epidemic hemorrhagic fever (EHF).2) HantavirusThe causative agents of the disease belong to the family Bunyaviridae. All contain RNA,

51、 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, respectively. There are eight serologic types of viruses at least: Hantaan virus, Seoul virus, Puumala virus, Prospect hi

52、ll virus, Belgrade-Dobrava virus, Thai virus, Thottapalaym virus, Muerto Canyon virus, and so forth.II. QUESTIONS1) Please describe chiefly the clinical manifestations of hemorrhagic fever with renal syndrome.Incubation period, 4-46 days, 1-2 weeks are common.Three major clinical manifestations incl

53、ude 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, headache, lumbago, orbital pain (three aches), drunkenness, petechia and ecchymosis, sometimes stripe-shaped appeared.2) H

54、ypotensive (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 increased, nausea, vomiting, abdominal pain, leukocytosis, atypical lymphocytes is usually more than 10% of total leukocytes,

55、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 acidosis, bleeding (hemoptysis, hematemesis, hematuria or melena), fatal hyperkalemia, hypervolemic syndr ome (high blood pre

56、ssure, 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, because of more kalium (potassium) and natrium (sodium) excreted with urine. BUN falling down, about1/3 of all deaths occurs i

57、n this phase.5) Convalescent phase: urine 1000-2000ml/24h, return appetite, strength, urinary concentrating ability recovered.2) Please describe chiefly the laboratory findings of HFRS.1) Blood routine: leukocytosis, 15-50 X0E9/L, neutrophils dominated in early stage, lymphocytes dominated in late s

58、tage, atypical lym phocytes 10%-15%, hematocrit value and hemoglobin rise, thrombocytopenia.2) Urine routine: marked proteinuria, sometimes with casts, blood cells and membrane-shaped substance, consist of protein, blood cells and mucosal epithelia.3) Blood biochemical examination: BUN increased, CO

59、2-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, hem