珍惜时间演讲稿-

2021年1月26日发(作者：口腹之欲电影)
英文题目及答案


INTRODUCTION
OF
COMMUNICABLE
DISEASES
I
.TERMS

1
）
Overt
infection
It
indicates
that
after
the
microorganism
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
al
lergic
reaction
of
the
host.
In
most
infectious
disease
such
as
measles
most
infected
host
manifested
as
overt
infec
tion.
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
temporary.
A
small
amount
of
overtly
i
nfected
hosts
change
to
carrier
state.
It
is
called
“convalescent
carrier”.

2
）
Incubation
period
This
period
is
from
pathogens
invading
into
human
body
to
clinical
symptoms
appearing.
The
incubation
period
of

all
infectious
diseases
has
a
limit
of
the
time
(the
shortest
and
longest)
and
a
normal
distribution.
It
is
an
import
ant
evidence
of
observing,
detecting
the
contact
in
quarantine
work.
It
is
usually
equal
to
the
whole
period
includi
ng
the
pathogen
reproduction,
transference,
location,
tissue
damage
and
function
changes
before
the
clinical
sympto
ms
to
occur.
The
period
length
is
negative
relation
with
the
invading
quantity
of
the
pathogens.
If
the
pathophysio
logic
changes
are
caused
by
toxins,
the
incubation
period
relates
with
the
time
of
the
toxins
production
and
distrib
ution,
e.g.
bacterial
food
poisoning.
The
toxins
have
been
produced
before
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
wound
to
the
central
nervous
system.
3
）
Latent
infection
When
the
microorganism
infected
the
host
and
localized
in
some
area
of
the
host,
it
can
latently
for
along
time
b
ecause
the
hosts
immunity
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,
herp
es
zoster,
malaria,
tuberculosis
etc.
Generally
the
microorganism
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
infection
The
microorganisms
are
able
to
gain
to
access
to
the
person
or
animal,
establish
itself
and
proliferate
in
vivo
and

excrete
pathogen
outside
the
body,
such
as
patients,
the
person
of
covert
infection,
pathogen
carriers
and
infected

animals.
5
）
Relapse
After
the
patient
has
entered
convalescent
period,
the
temperature
has
recovered
to
normal
for
a
period
of
time,
th
en
the
pathogen
hidden
in
some
tissue
reproduce
to
a
certain
degree
and
make
the
primary
symptoms
repeatedly,
i
t
is
called
“relapse”.

6
）
Recrudescence
In
the
convalescent
period
of
some
patients,
the
temperature
has
not
stably
decreased
to
normal
and
the
fever
rise

again,
it
is
called
“recrudescence”.

7
）
Zoonoses
Some
natural
ecologic
environment
is
suitable
to
the
transmission
of
infectious
diseases
among
wild
animals.
These

diseases
include
plague
tsutsugamushi
disease,
leptospirosis,
and
so
on.
The
human
race
may
be
infected
when
he

get
into
these
areas.
These
diseases
are
called
“zoonoses”.

II.
QUESTIONS

1
）
Please
briefly
describe
the
manifestations
of
infectious
diseases
(infection
spectrum).


1
Infectious
process
starts
when
microorganisms
enter
the
human
host
through
various
ways.
Whether
the
microorgan
ism
is
eliminated
or
colonized
in
the
host,
it
is
mainly
dependent
on
the
pathogenicity
of
the
pathogen
and
the
im
mune
function
of
the
host.
i.
Pathogen
is
eliminated
by
host
immunity:
After
the
microorganism
enters
the
host
it
can
be
wiped
out
by
non-s
pecific
immunity,
and
eradicated
or
eliminated
by
specific
immunity
which
the
host
has
got
before
the
infectious
p
rocess.
ii.
Covert
infection:
It
refers
to
that
the
microorganism
only
making
the
host
producing
specific
immune
response
not
having
histomorphological
damage
or
even
having
mild
feature
after
it
enters
the
host.
Clinically,
there
is
no
a
ny
symptoms
and
signs
or
any
biochemical
changes.
iii.
Overt
infection:
It
indicates
that
after
the
microorganism
enters
the
host,
it
not
only
induces
the
immune
respo
nses
of
the
host
but
also
produces
hisomorphological
damage
and
pathological
changes
through
the
role
of
the
mic
roorganism
or
the
allergic
reaction
of
the
host.
iv.
Carrier
states:
It
is
divided
into
virus
carrier
and
bacteria
carrier
according
to
different
pathogens.
All
carrier
st
ates
have
a
common
characteristic
that
is
no
clinical
manifestation
but
the
microorganism
can
be
excreted
during
t
he
state.
v.
Latent
infection:
When
the
microorganism
infected
the
host
and
localized
in
some
area
of
the
host,
it
can
latent
ly
for
a
long
time
because
the
hosts
immunity
is
strong
enough
to
locate
the
pathogen
but
can
not
wipe
it
out.
When
the
hosts
immunity
decrease,
overt
infection
can
occurs.

2
）
Please
briefly
describe
the
factors
related
to
the
pathogenicity
of
the
pathogen
in
the
infectious
process.

i.
Invasiveness:
It
refers
to
its
ability
to
invade
the
host
and
spread
within
the
host.
ii.
Virulence:
It
includes
the
toxins
and
various
enzymes.
iii.
Number
of
the
pathogen:
The
number
of
invading
pathogen
is
positive
relation
with
the
pathogenicity
in
the
sa
me
infectious
disease.
The
least
number
of
the
pathogen
to
induce
disease
differ
greatly
in
different
diseases.
iv.
Variability:
Pathogens
can
produce
variation
due
to
environmental
and
hereditary
factors.
Generally
speaking,
un
der
the
environment
of
artificial
culture,
the
pathogenicity
of
the
pathogen
will
decrease.
The
repeated
spread
betw
een
the
hosts
will
increase
the
pathogenicity
of
the
pathogen.
The
antigenic
variation
of
the
pathogen
will
make
th
e
pathogen
escape
form
the
specific
immunity
of
the
host
and
continue
induce
the
disease.

3
）
Please
briefly
describe
the
basic
characteristics
of
infectious
diseases.
i.
Pathogen:
Every
infectious
disease
is
caused
by
a
specific
pathogen
including
microorganism
and
parasite.
In
his
tory
many
infectious
diseases
were
first
understood
by
their
clinical
manifestations
and
epidemiologic
feature
and
t
hen
the
pathogen
was
found.
ii.
Infectivity:
Infectivity
means
that
the
pathogen
can
be
excreted
to
contaminate
the
surrounding.
It
is
the
main
d
istinction
between
the
infectious
diseases
and
other
infection.
Every
infectious
disease
has
considerably
a
stable
inf
ective
period,
which
can
be
used
as
a
rule
to
isolate
the
patient.
iii.
Epidemiologic
feature:
Under
the
influence
of
natural
and
social
factors
the
infectious
process
manifestates
vari
ous
characteristics.
It
can
be
divided
into
the
exoticity
and
the
endemicity.
It
also
can
be
divided
into
sporadic,
ep
idemic
and
pandemic.
The
distribution
of
the
incidence
of
the
infectious
disease
in
time
(seasonal
distribution),
in
space
(regional
distribution)
and
different
populations
(age,
sex,
and
occupation)
is
also
an
epidemiologic
feature.
iv.
Postinfection
immunity:
The
host
can
produce
specific
protective
immunity
which
is
directed
at
the
pathogen
or

its
products
after
the
host
was
infected
by
the
pathogen.
Postinfection
immunity
belongs
to
active
immunity.
The
lasting
time
of
postinfection
immunity
varies
with
different
infectious.

VIRUS
HEPATITIS
B
I .TERMS

1)
Dane
particle

2
The complete HBV is called Dane particle. The 42-nm Dane particle is made up of an outer shell 7 nm
thick, containing the hepatitis B surface antigen, glucoprotein and cellular fat, and an inner core
28 nm in diameter, which possesses its own specific antigen, the hepatitis core antigen (HBcAg). The
Dane particle core can be broken down by treatment with detergent to reveal a DNA polymerase and a
double stranded circular DNA genome that can serve as a primary template in vitro for the DNA polyme
rase.

2)
Window
phase
Anti-HBc IgM persists 6 to 18 months, so represents an acute response to a newly infection of HBV in
acute cases who have cleared the HBsAg but have not demonstrated detectable amounts of anti-HBs, an
ti-HBc and anti-HBe can be detectable, the serologic gap is called window phase. In this case, anti-
HBc IgM may be the only evidence for diagnosing an acute HBV infection.

3)
HBsAg
It stands for Hepatitis B surface antigen. It is coded for the protein of the viral envelope by the
S gene. There are four antigenic subtypes of HBsAg. They are adr, adw, ayr, and ayw. HBsAg is non-in
fectious itself, but HBsAg-positive blood should be considered potentially infectious because it may
contain complete HBV (Dane particles).

4)
Chronic
HBsAg
carrier
Some persons infected with hepatitis B virus develop mild chronic infection state that is asymptomat
ic and not associated with any significant liver function tests abnormality except persistent serum
HBsAg-positive more than 6 months. However, liver biopsy reveals that only a minority of them is wit
h normal histology; and the majority cases present morphologic liver damage in varying degrees, rang
ing form minimal inflammation, chronic persistent hepatitis, chromic active hepatitis, or even cirrh
osis.

5)
HBV
DNA
Hepatitis B virus (HBV) contains a small circular DNA molecule that is partially double-stranded, th
e DNA consists of a long strand (L) of constant length (3,200 bases) in all molecules and a short st
rand, which varies in length between 1,700-2,800 bases in different molecules. A DNA polymerase acti
vity in the virion repairs the single-stranded molecules of 3,200 bases pairs. The four open reading
frames of the HBV are termed S, C, P and X.

II. QUESTIONS

1)
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 viral envelope and is divided into the S gene, pre-S1 region and pre-S2 region. The C gene c
odes for the core protein. The P region, codes for the viral DNA polymerase which possesses a revers
e 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, ch
ronic hepatitis, cholestatic hepatitis, to a fulminating disease and death in a few days.
i. Acute viral hepatitis
ii. Cholestatic hepatitis
iii. Fulminant hepatitis (Acute gravis hepatitis): Hepatitis may take a rapidly progressive course t
erminating in less than 10 days. Fulminant hepatitis results form extensive hepatic necrosis. It dev
elops most commonly as a complication of viral hepatitis.
iv. Chronic hepatitis: Chronic hepatitis is defined as hepatic inflammation of at least 6 months dur
ation, as demonstrated by persistently abnormal liver function tests, and divided into three forms:
(1) mild chronic hepatitis; (2) moderate chronic hepatitis; (3) severe chronic hepatitis.

3


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 hepatiti
s results from extensive hepatic necrosis. It develops most commonly as a complication of viral hepa
titis.
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 initiat
ion of bed rest.
(2) a sudden decrease in the size of the liver.
(3) neuropsychiatric changes of early hepatic encephalopathy, including drowsiness, irritability, in
somnia, 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) wi
th or without bleeding. Serum bilirubin and transaminase levels do not reflect the severity of illne
ss.
(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 clinical manifestation over 10 days after onset of acute icteric hepat
itis, designated subacute gravis hepatitis, 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 marker 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 serum of a Patient with hepatitis B. It oc
curs late in the incubation period and before the onset transaminase elevation or symptom, and persi
sts for a few weeks in the typical acute cases, or more than 6 months, even many years in chronic HB
sAg carrier state. HBsAg is non- infectious itself, but HBsAg-positive blood should be considered pot
entially infectious 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 a
fter HBsAg disappears and persists 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 is the antibody to HBcAg and thought not to be protective. Anti-HBc is the first antibody to appe
ar 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 o
f HBV. It fills the serologic gap (the window phase) in acute cases who have cleared the HBsAg but h
ave not demonstrated detectable amounts of anti-HBs. In this case, anti-HBc IgM may be the only evid
ence for diagnosing an acute HBV infection.
Anti-HBc IgG developes later than IgM and may persist for many years, even after HBsAg has been clea
red. 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 reac
tivity, and disappears before the disappearance of HBsAg. HBeAg is a sensitive index of viral replic
ation, infectivity, and chronicity.

4
(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 year
s. Anti-HBe is originally thought to 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 support
of vital functions.
(2) Continuous intravenous infusion of glucose solution is required to prevent hypoglycemia in a pat
ient 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 i
ntravenous 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 encephalopathy
1) 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 the factors of induced acute renal fail
ure, 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
SYNDROME
I .TERMS

1
）
Hemorrhagic
fever
with
renal
syndrome
(HFRS)

An infectious disease with natural source, caused by hemorrhagic fever with renal syndrome viruses
(HFRSV), characterized by fever, prostration, vomiting, proteinuria, hemorrhage, shock and acute ren
al failure. This zoonosis is synonymous with hemorrhagic fever with renal syndrome (HFRS)

or epidemi
c hemorrhagic fever (EHF).

2
）
Hantavirus
The causative agents of the disease belong to the family Bunyaviridae. All contain RNA, with circula
r or oval shape, 85-110 nm in diameter. The RNA genome contains three fragments, L, M and S gene, co
de for polymerase, membrane proteins and nuclear capsid proteins, respectively. There are eight sero
logic types of viruses at least: Hantaan virus, Seoul virus, Puumala virus, Prospect hill virus, Bel
grade-Dobrava virus, Thai virus, Thottapalaym virus, Muerto Canyon virus, and so forth.

II. QUESTIONS

1
）
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 include pyrexia and intoxication, hyperemia and hemorrhage, hypo
tension and renal malfunction.
Five typical phases:
1) Febrile
phase: acute onset, 39℃
-
40℃, lasts 3
-7 days, malaise, headache, lumbago, orbital pain
(three aches), drunkenness, petechia and ecchymosis, sometimes stripe-shaped appeared.

5
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 increased, nausea, vom
iting, abdominal pain, leukocytosis, atypical lymphocytes is usually more than 10
％
of total leukocy
tes, proteinuria.
3) Oliguric phase: occur during or soon after hypotensive phase, lasts 2-5 days, urine volume less t
han 500ml/24h, anuria, less than 50ml/24th, uremia, metabolic acidosis, bleeding (hemoptysis, hemate
mesis, hematuria or melena), fatal hyperkalemia, hypervolemic syndrome (high blood pressure, engorge
d neck veins, edema and restlessness).
4) Diuretic phase: the volume of urine more than 3000ml/24h, lasts 7-14 days, dehydration with hypok
alemia, hyponatremia, because of more kalium (potassium) and natrium (sodium) excreted with urine. B
UN falling down, about1/3 of all deaths occurs in this phase.
5) Convalescent phase: urine 1000-2000ml/24h, return appetite, strength, urinary concentrating abili
ty recovered.


2
）
Please
describe
chiefly
the
laboratory
findings
of
HFRS.
1) Blood routine: leukocytosis, 15-
50×10E9/L, neutrophils dominated in early stage, lymphocytes dom
inated in late stage, atypical lymphocytes 10%-15%, hematocrit value and hemoglobin rise, thrombocyt
openia.
2) Urine routine: marked proteinuria, sometimes with casts, blood cells and membrane-shaped substanc
e, consist of protein, blood cells and mucosal epithelia.
3) Blood biochemical examination: BUN increased, CO
2
-CP decreased, hyperkalemia in oliguric phase, h
ypokalemia in diuretic phase.
4) Blood•coagulating function examination:•thrombocytopenia, prolongation of prothrombin time, fibri
nogen•decreased•and secondary fibrin lysis.

3
）
Please
describe
chiefly
the
complications
of
HFRS.
1) Visceral bleeding, including hemoptysis, hematemesis, hematuria, cerebro-hemorrhage and hemoperit
oneum. Spontaneous rupture of the kidneys may occur.
2) Pneumonedema, common seen in hypotensive phase and oliguric phase, because of high blood volume.
exudative pneumonedema. The adult respiratory distress syndrome (ARDS) is caused by increasing the p
ermeability of the pulmonary capillaries, resulted in acute pulmonary edema.
3) Secondary bacterial infection, pneumonia, diarrhea, septicemia.
4) Others: hepatitis, myocarditis, pericarditis and ophthalmitis.


4
）
Please
describe
chiefly
the
main
therapy
of
HFRS.

1) Supportive treatment: treat in near hospital, rest in bed, easy digestive food.
2) Symptomatic treatment.
(a) Intravenous fluid, it contains suitable glucose, electrolytes and vitamins. The amount of infusi
on must be regulated.
(b) Diuretic for oliguria, such as lasix (furosemide), 20
％
of mannitol or/and lasix dripped intrave
nously if exist of •high intracranial pressure and normal output amount of urine.
(c) Heparin for DIC.
(d) Dexamethason for high •fever •and •heavy •intoxicating •symptoms, avoiding using heavy antipyret
ics.
(e) 5
％
of •sodium •bicarbonate •dripped •intravenously •for •metabolic acidosis.
(f) Cedilanid for cardiac failure.
(g) Hemostatics for heavy bleeding.

6

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