Diseas Epidemi Etiology Incuba Clinical Diagnosis Differe Complica prevention

e ology (source of tion pictures ntial tions

infection, period diagno
route of sis
infection)
Hepa Antigen human 7 days in most From If it is Human
titis A - organism, to 7 preicteric useful other untreated immunogl
virus HA Ag, it is weeks, stage marker hepati then may obulin,
RNA excreted pre nervous (s) of the tis by be chronic immunizati
ictein clinical hepatitis on,
contain, into the excitemen disturban
preict picture Observatio
several external t ce of
eric . n rules of
weeks environm ,chills pigment personal
remain ent from stage ,pain all metaboli hygiene.
alive in the 2-10 over the sm
the infected days. body --A
external organism ,malaise change in
environ by feces, ,mild the color
ment at Through headache, of the
18°C, the moderate stool
destroy mouth elevation ,sclera,
ed by HAV of hard
boiling enter the temperatu palate,
for organism re, slight urine.
5 of a elevation Anti HAV
minutes healthy of & RNA
, person, temperatu can be
inactiva fecal oral re detected
in the
ted by route, ,heartburn
blood
exposur transmite ,the sight
during the
e to d from or smell of acute
chlorine infected food is stage of
during... person nauseatin VHA. IFA
15 Via close g ,pain in & PCR.
minutes contact, the joints total
( 1,5_2, During the febrile blood test
5 the late reaction --
mg/liter part of usually ESR is
). the lasts only norma,l
leukopeni
incubatio a few
a,
n period, days,
lymphocyt
During dyspeptic osis.
preicteric symptoms Acute
period, ,loss of viral
During appetite, hepatitis
the first nausea A is
7_10 days ,vomiting, characteri
of the the joints zed by
icteric do not following
laborator
period- change in
y tests:1)
the site, the
Serum
disease a skin over total
source of the joints bilirubin
virus retains its usually
hepatitis normal increases
A is the color. 2) Serum
most icteric indirect
contagiou stage fraction of
s. blood, Clinical bilirubin
serum, signs of usually
increases
urine, VHA in
3) Serum
nasophari preicteric
transamin
ngeal stage ases (ALT,
secretion decrease AST)
s -a in severity, activity
source of Urine of increases
virus patients is 4)Serum
hepatitis usually total
A may dark, Stool bilirubin
contain of patients usually
HAV. is usually increases.
major light or marker(s)
Anti HAV
epidemiol clay_color
Ig M &
ogic ed dark, Anti HAV
significan Clinical Ig G
ce signs of
-feces. VHA in
patients preicteric
with stage
subclinica disappears
l hepatitis .
A & By the end
non_icter of
ic pre_icteric
hepatitis stage
A-plays bilirubin
the most content
importan rises in
t role in VHA.
 the
transmiss
ion. In
Autumn
time
maximum
disease
incidence
of VHA.

Hepa HEV Man- pregnant RNA can Abortion, Observati

titis E Ag,cont source of women, be fetal on rules
virus ain infection, detected death, of
RNA, In feces in the fulminan personal
HEV blood t hygiene
excreted during hepatitis
into the the acute
external stage of
environm HEV. IFA,
ent from ELISA,
the PCR.
infected RNA, Anti
organism, HEV Ig M
Through marker(s)
the character
mouth ize(s)
HEV VHE.
enter the
organism
of a
healthy
person,
fecal oral
route of
transmiss
ion,

Hepa HBxAg, 3 months- 6 clinical Lab Encephalo

titis B HBsAg hepatitis B weeks forms:- diagnosis pathy
virus HBeAg, virus to 6 prolonged of
HBcAg remain month hepatitis B, encephali
alive in the s. acute tis-
antigen(
externaL hepatitis B, azotemia,
s)
environme chronic Oliguria,
contain
HBV. nt at 18 hepatitis B, decrease
DNA degrees fulminant of
above hepatitis B, prothrom
zero. in subclinical bin index,
liver cells, hepatitis B, leucacitos
In anicteric is
leucocytes hepatitis B, PCR
, in preicteric IFA
lymphocyt stage:- In blood
es, in 7 to 14 test-
monocyte days. leukopeni
s, in bone Headache, a
marrow loss of lymphocyt
cells, in appetite, osis
pancreatic aversion to
cells-HBV food,
replicate. vomiting,
In liver nausea,
cells, discomfort
semen, in the right
urine, upper
sweat, quadrant of
bile, saliva, the
tears, abdomen,
breast moderate
milk, fever,
vaginal the skin
secretion over the
can joints has
hepatitis B normal
virus be color,
found joints do
during not change
HBV in size,
infection. artralgias
In Liver anicteric
cells most viral
extensivel hepatitis B
y infected headache,
with HBV. loss of
for 6-12 appetite,
months, aversion to
for 2-3 food,
years, for vomiting,
3-4 years, nausea,
for many artralgias,
years, for discomfort
a lifetime- in the right
may HBV upper
be present quadrant of
in the the
blood and abdomen,
other moderate
body fluids fever,
of chronic pain in the
patients & right upper
-also quadrant of
may HBV the
be present abdomen,
in liver itching,
cells of the skin
chronic over the
patients. joints has
In 6 normal
months color,
after joints do
primaryinf not change
ection in size,
HBsAg- artralgias,
positive enlargeme
patients nt of the
designate spleen,
d as enlargeme
chronic nt of the
HBsAg liver.
carriers. During last
Patients, days of the
producing preicteric
HBsAg and stage
don't urine of
produce patients
DNA and with viral
HBeAg hepatitis B
are usually usually
considere becomes
d as dark &
"healthy stool’s
carriers" colour
of HBsAg. become
sources of light or clay
infection- color dark.
man. by icteric
blood stage:-
transfusio Clinical
n, by signs of
percutane VHB in
ous preicteric
transfer of stage
blood,by progress in
tattoing severity
way may The skin of
virus the patient
hepatitis B becomes
be icteric.
transmited Encephalop
from athy:-
infected Complete
person. - + absence of
by hospital appetite,Vo
equimpme miting
nt Progressive
by ear adynamia,
piercing Considerabl
- + by e
needles sleepiness
contamina during the
ted blood daytime,
infected Impaired
patients.B mentation,
y Ascites,
accidental Hallucinatio
needle ns,
sticks by Delirium,
hospital Rise in
personnel, temperatur
by razors, e, Bleeding
by hospital from the
equimpme gums,
nt, by Involuntary
toothbrus defaecation
hes, via , Bleeding
minute from the
droplets of nose,
mucus Involuntary
from the urination,
fauces ,by Epilepti
towels, by form
sheet, via ,seizures
minute Aggressive
droplets of actions,
mucus Insomnia at
from the night. Anti
fauces,fro HBc Ig
m infected G,Anti HBc
mother to Ig M,
foetus in HBeAg
utero, to HBsAg ,
newborn DNA can be
infants at detected in
the time the blood
of during the
delivery, last weeks
By fecal- of the
oral incubation
transmissi period of
on, By the
blood- disease.
feeding Anti HBe,
insects Anti HBc Ig
way may G, Anti HBc
virus Ig M,
hepatitis B HBeAg,
be HBsAg,
transmited DNA
from can be
infected detected in
person. the blood
Semen, during the
serum, acute stage
blood- of the
play(s) the disease.
most Anti- HBc Ig
important M is usually
role in detected
transmitti during the
ng of first time of
hepatitis the
B. disease,ons
et of the
disease.
Anti- HBc Ig
G is usually
detected
during long
time after
acute
infection
time of the
disease.
Anti-HBs Ag
is usually
detected
during long
time after
acute
infection,
in several
weeks after
HBs Ag
disappeare
nce from
the blood
time of the
disease.
HBcAg
can be
detected in
VHB only in
hepatocyte
s. Anti
HBe,Anti
HBs viral
particles in
the blood
of
convalesce
nts usually
appear to
confer
protection
against
reinfection
with HBV.
HBs Ag may
persist in
human
body for 1
weeks to
many years
after the
onset of
the
disease.