36

Chetlinat
Vidyashr
am BIOLOGY
INVESTIGATORY
PROJECT
VARDINI
REGISTER
:2061831
NO
AISHWARYA
DEATH A2
Delhi)
-
New XII
Education, LAUGHING SEC:
600028)
S.SRI
Secondary
-
Chennai 2023-24 &
NAME:
CLASS
R.A.Puram,
of
AVE
&
Board THE
House,
Central
-
KURU
to (Chetinad
(Affiliated
TABLE
OF
CONTENTS 11 12 13 14 16 18 19
2 4 5 9
SIGNS
AND
SYMPTOMS
1
PATIENT
HISTORY
INTRODUCTION EPIDEMIOLOGY
PREVENTION CASE
DIAGONOSIS STUDY
1 CASE
STUDY BIBLIOGRAPHY
2 CONCLUSION
CAUSES
CURE
 was
which Kúruduedisease.
shake"), of which
members more
that (prions),
(TSE) sickness"
disease. long
Guinea. from
disorder the eaten,
wasrarely
coordination ("to cannibalism. the
encephalopathy of among disease
New proteins the symptom
guria' "laughing and menbut
neurodegenerative
Papua
of cooked tissue, affected.
or symptom transmittedTheadult
folded Kuria funerary
of KURU thea infectious
because
of loss are dead.
traditionally also
spongiform
people abnormally as which
and wordclassic
known wasvia the were
fatalFore
tremors Fore Guinea of children
highly
a alsolaughter
kuru
spirit men 2
were
andthe
transmissible
of the are other
transmission thatNew adult
as from thatis theand
members
INTRODUCTION
among such
incurable, It of
accepted freewomen
"trembling".
tremors bursts Papua andmeant
derives
common symptomsneurodegeneration. help brain
of
rare, form
the NORMAL body pathologic of family
widely among
to theperiod
kuru tribe
by means thought
a a Deceased consumed
incubation
is formerly tO term the prevalent
is caused nowFore
Kuru Kuru leads to the
Thedueitself is the was
to
It
 year to
incubation
1957
ADYANE
the early on
developed then
pooriy finally
in
KAINO KUKUXUKY
around
and the yeardisagreeing ANIIE5
long
are epidemic
disease in
sometime per
2009.
TSE villager meat kuru's
brains. -FORE
150
deaths
transmitted sources KEIACANA
of the
human The
to or 2.6
types
a died, infected due
when contracted 200 2005
years. YAGARIA
05
different
and lingered with
consuming
be from in
started their 50 died
onwards,
to
disease
theyate overcentury,victim
speculated 3
across disease
likely who stopped to
brain,
Creutzfeldt-Jakob 2010
10 halfa kuru
epidemic
differences villagers the
first from least
the people after known
endocannibalism, Guinea
Papua
New
ate was anywhere
the other at
sharply
villagersFore last
from
prion it
understood, when
to the
deaths
Though sporadic it the of declined
spread 1960s,period whether
1900.When While
via no
 dead
guinea time alsoyouror spongiform
insomniafatal.
kuru
but that of infections were
of and open
the
1960, theagent
class of
(TSEs), fungi. for particles.
brains part brain are
new is
because children factor
period a or andwith
familial
the most
the(prion) to encephalopathy
fromthein stopped belongs viruses,
the These
braincontact riskinfectious
to - in
are afterward incubation cerebellum
Unlike reproduce. and
people exposed
protein Fatal
multiply main
they prions.
the
practice Kuru bacteria, intoWomen
among balance. processes.
in Thecontain
which infectious coming
years
Thebeing tissue.the that by sponge-like rites.
spongiform not caused it.
found in This many affectsby do proteins
and with can
cannibalism period.
after brain caused by these
ritual, an and brain living which
coordination disease disease
create
4
is for appear by primarily organisms in
It
disease. funeral
incubation
reported caused human transmissible misshapen
not typical they participants
someone tissue,
is kuru,the
degenerative
of to because
forma symptoms contaminated it kuru hinderingcontract
brain
rare of were long Itis for living
disease, inanimateas of
a part disease. agents,
responsible well sores primary
verypracticed a called infectedhuman
kuru not
a has prion clumps,as also
another
Causes
a as for are or
ot diseases infectiousare diseases,
can
is peopledisease causes in
takes theeating
Prions Wounds
mainly
Kuru who cases found called brain Theyform One were
are
it is
 divided
lasts can joint
loss five
and
has
disease
of control
incubation terminal and
individual
gradual neurological initial symptoms,between
by
is headache
kuru affected
and
characterized after and
a theas
laughter, is coordination of stagesan
sedentary,
encephalopathy, called more of progression
short
severe
and onset thesymptoms,
including
physiological
alsoas or
among
these
of become is beyears first
It of
ambulant,
outbursts phase,
can theclinicalin conserved
symptoms
clinical
death.
loss 50 variation
spongiform but at
that as
to or
jerks causes asymptomatic 5
years, begins of
ataxia, long Thethe
random include: problems lead some onset prodromal
Signs
and
Symptoms Swallowing
difficulty
muscle as stages:highly
months.
Over
mOvements.
muscle
thatultimately period, clinical
10-13
averages stage,
which
pain Difficulty
walking cerebellar
transmissible last is the
system are
tremors, kuru leg Coordination and to there
specific Before
coordination.
of Headache or
estimated
12 they withlegs.
of and Tremors
which
preclinical
of While
Symptoms
Arm nervous progressive present
average individuals,
population,
exposure. three the
Body a
Kuru, effects stages. in
the The been alsopain
The
an into
 stage incapable and Despite
walk
at no first
infected
exhibit intact
instability is
dysphagia,
This
difficulty severe developthe
to laughter. individual's
it become
is still where
able
may (titubation). An afteror
individual become
maintaining pneumonia
control, and emotionalare
individualstill sporadic point developsalso often
infected.
years
ataxia reflexes infected
is
individual the mayand patientstwo
tremors
muscle infected
easily
experiences
of individual
speak,
infected signsandtendon theto and despite to of
progress
support. because
months
decreased
andthe the uncontrolled stage, malnutrition, stage, be
shows to
the (dysarthria),
becausestage. symptoms, the will surroundings can
and without
ataxia, terminalthreeoften 6
stage, (terminal) emerge: or that
gait, around
despite
symptoms.support individual
(sedentary) ability within infections.
ambulant exhibits disease. up severe wounds symptoms,
(ambulant)
and neurologicallikesit the
words finalsymptoms, also thetheir
stance without the to to of dies
yet the lose
symptoms
possible to endulcerated other
secondary
the second Furthermore, and
pronouncing consciousness.
lead unresponsive usually
stage
depression,of
firstunsteady
named walking stagethird
canincontinent,the
tremors.
other Towards
the the existing
the longer New which chronic terminal
person
In is In of thethis
In
 are
elicittime to
theaby
thesensors exam Kidney
neural each
measure by at which including:
looked
produced
small around neurological
of potentials and
signatures Liver
to test, are exam
used signals populations symptoms.)
ELECTROENCEPHALOGRAPHY and
level,
painless active a medical
READING
EEG
test machine the perform
electrical acid
medical are of
this and for
a integrals will comprehensiveFolic
signals
latencies causes
During by
a the doctor Thyroid, 7
(EEG) recorded
BRAIN up (EEG)
the
brain. other
pick the
electroencephalogram are different
Electroencephalography 2.Neurological
function
as out
theto are diagnosis,
a
generally is 1. such
scalpsignals This Medical
history rule
of with
DIAGNOSIS activity tests,
(To
the
andbrain of Kuru.
ELECTRODES to These type test.
Blood
electrical
attached activities diagnose
doctor. the instant. function
brain.
from
this
An 3.
In
 the sleep andscalp, diagnosis.
measure
your the
epilepsy,simple be
examine
to the may
definitive
to applied is on conditions.
MRI
used including procedure
placed to
are usedan
test a
as making
electrodes are normal are such
medicalconditions
Theelectrodes
(EEG)
activity.
under scans in
ELETRODIAGNOSTIC
TESTS a Several helpful
is few electroencephalogram
(EEG) recordedBrain
adhesive
electrical 8
a be
diagnose
brain. tumours. brain.
not
electroencephalogram
small
brain'sis may
the activity the
help
of brain 20 in they
activity
can theAbout activity
and brain's
as but
EEG records such performed,
electrical
disorderspainless, electrical
scalp. EEG the Tests
The and
 patrolling women, as because the able to
properly
In Guinea the was of ofunderstanding the of
believed or person
1910. to sorcery
andcases
cannibalism kuru of one
to
Fore who the tribal
come behaviour
1950s. report Guinea, at years,
officers
as
New from wasfoolish ghosts, of of kuru
MCArthur the
McArthur,
early affected to be kuru kuru. number pathology
early a Papua resultingepidemic, to New for two
Australian in officer,
meant
by researchers
finally
were
kuru kuru with kuru, modern the Within
chimpanzees
the as report.region. authorities.
causing caused
regionof mostly John comes the
Papua the record
in term tribes episode medical of which to
by Guinea larger While
kuru officerhis the magic intervals.
causes was linked theunderstand autopsies.
reports thetheFore that of and
in use that in psychosomatic Australian negi-nagi,
a Lutheran
in into 1960. to
believed,beenadministration on
New kuru the disease
patrol people the the behaviour led (NIH).monitor
official to spontaneous tests 9
noted progressedbelieved that had by
eventually
to Health their
Papuaplace firstafflicting by
the tribal Pfarr, a called people
also
thought eliminated
medicaleffort
experimental
to conduct
in the Carey observed to anthropophagy
disease strange Gajdusek
PATIENT
HISTORY of accounts
described wasdisease of Australian an
Highlands eventually
killing
them. a the
description people which of
merely had Charles also at Fore Institutes
Carey report, of laughed
decreasing,
nearly
cause.In and
was practices
disease the Fore contagious.
Itwas theand
first
unofficialnew They kuru, first joined NIH
kuru was report shakingthe
Eastern Arthur his
asked disease,
a a the before was its theNational the
was In kuru
provided victims
witchcraft. by investigate Gibbs
describe 1953, the was
Kuru Some 1951, (PNG).
sorcery to Initially,
people practice as disease. at
banned
the
the that After area
the Thisof
Even kuru prions
In the Joe apes
 unknown the
disease's
it early the
that the later
and thatofrearrangement
an and to
biomaterial 1960sobservation
that was
noted
kuru,
demonstrating
developed what
late
the
disease,
He of
primates.
infected structural
critical observation
ofparts
through
other the
Guinea
investigating
the the
large including
to on early 10
barrier spent
transmitted dependhypothesis.
an
had species Field cells, was
may
Daisy,wasfactor
disease glial This
J.E.Subsequently,
processprion
the with molecules.
chimps, croSS sinNew
roctions the
infectiousbecome
the could bost's
 brains brain the-kurucanpracticeneurological
Symptoms
Government
and NINDS,-
symptoms
infected by of
centuryperiod the
to afterdiagnosed.
serious
eat ingestingAccording incubation
of long
mid-20h appearance
don't prions. reported
another
contracted
by cannibalism. rarely
sores the The
containing
kuru
in thebeenis indicate
cannibals diseasevanished. kuru
and
of have to
Today,
Its
only infectionlikely
thepractice
completely disease.
cases
rare. prevent
exceptionally
ceased.
more
social initial
encountering years. spongiform
are
PREVENTION to almost has
Societies
sought
Smart the between30 kuru
as cannibalism
discouraging
has of or
long those
time disorder
isKuruortissue disease
Theas like
be of
 trernors,
Cures or Because or the
than years stand
after symptoms.
no
other gait,
are wassymptoms.
for to months patients.
unable
unsteady
there it responsible
kuru,
period: of
Currently. 12
became sign
cure the
TSE
showed
incubation
treatments
diseases. an to first
or six for
control is usuallyfrom required
the
cannibalism.
which
person
individuals year.work
after vitamins
could were state
long cerebellum, be
health one
not
year will will
other infected comatose
symptoms withinantibiotics
a Eventually, and
general
no
that has symptoms.
1 wheelchair
of the
treatments
within disease supplements
treatment
Symptomatic
6. disease die
practice kuru the
an
of a the very
bad
Prognosis
will
before
any TSEs, first in
affected occurs
speech. Kurucare and
patients
diedof Supportive
1. a of
Physiotherapy
2. the
the for the appearance and Improvement
discouraging
thedecades they usually
ordination,
mainly
for Nutritionalfor 10.Painkillers
slurred Walkers
CURE
were other
and
Treatment cure
9.These
There ,been niru end first Death No
or eat 3. 4. 5. 7. 8.
 in July more
in theirenriched decreased last
Guinea probably from
and of the
who Guinea period
tribe
becomes with
New men, cases
men
fore incubation
recently,
2007_
201|
Papua thanthe
New
0022006 theprion the
to Papua
affected
1992-
1997 of to
cannibalism,
compared cases. recorded
1996
2001
infectious
confined
highlands an
in new noted
more survey
1991
time
1987(5-ycar
periods) cases
|9821 wereThe as ritualistic
11 researchers
eastern brain
usually only 13
1986
groups. active new
diseases
1977
1981
the identified
the were of An no
EPIDEMIOLOGY males 1976
1972
in linguistic consumed
practice
1950s. cases,are
lotal The
prevalent women 2005.
2004. There
1971
1967
<20
years
1900s.the
victim's
brain. those
1966
1962--
thethe
neighbouring in
andtheyin afterJune years. reported
1961 wasearly
preferred of
1957
600 Children
because
J000 900 800
- 700 500
- 400 -
300 -200 I00 Kuru to some50
rapidly
kuru Iromudealhs the 1996 iancase
In
 slurred in were The activity.
past reported with including analysis
neurological gait protein,
thein There scancerebellum. characteristic
consistent
and village patientpatient'sand background
was
over balance. CSF
walking, been control. pauses MRI
disease, 14-3-3
remote
gradually puncture
of have the The The the regions, The
series
dificulty musclemaintain
examination, frequent
a extremities. in
Scan: exhibited
kuruthe analysis. of
in disease particularly presence
a progressing
living of lumbar
posterior withslowing
with and Brain
tremors, to with
DISEASE presentedof kuru support EEG
A for
history physical
coordination
lower slurred,
associated fluid
the
(MRI)
atrophy,
the Analysis: disease.
been of The and 14
uncontrolled cases and
cerebrospinal
andrequired in (EEG):
I Disease
KURU patienthave a
has
Upon appeared Imaging pronounced complexes,levels kuru
upper cerebral patterns
where of (CSF)
patient Examination:
symptoms lack they Electroencephalogram with
1: KuruInformation:
patient History:The protein
includingGuinea, the difficulty
articulation.
in Resonance
STUDY Female
Gender: notable speech
and significant brainwave
Diagnostic
Tests: wave Fluid consistent
collect
Report: Madhu
Name: The in more
years
35Age: tremors elevated
unsteady, Cerebrospinal
CASE Patient
ent
Themonths.
aumptoms, New
elinicaleneech. past. Physical
a
displayed
Additionally,
Magnetic
was disease. sharp to
kuru
Papuathe evident
revealed abnormal performedare
atrophy periodic Showed
fow was Wnich
 assistiveprogression and
of
cure
for daily 12 patient the management
communication, maintainprogression
EEG primarily findings, regular
kuru cannibalism Thearound in
findings, theconsumptionknown physical
enhance
no providing require disease
with death. the to and
disorder
by rapid is
diagnosed caused mobility. symptomsadvances, EEGthecaremonitoring disease
imaging ritualistic on
includes
to may
therapy
a ultimately function,kuru studies, supportive
treatments,
the is with
neurodegenerative thereis patient of track
is managementin prognosis, diagnosis
been It through
presentation, This aid disease
clinical
Guinea.during Unfortunately, occupational and motor imaging Closeto complications.
theto
symptoms. providing
necessary
has wheelchairs, effective
proteins progresses,disability
of thein functionality.
patientNew particularly poor onset the
deterioration symptoms, 15
of As confirms
Based
clinical tal ofPapua
the focus and a severe vary. of on
thefatal prion alleviating
Management: has the lackfocus be emerging
or after will
and
theanalysis, tissue,
infectious primarymobility
disease disease
walkers can report the andexaminations
clinical
to life.
further primarily
on raretribe timethis of
leading Given comfort
Diagnosis: transmicontsasirmoni ated
CSFa
is
Fore
of
brain
and The
euDDortive
care
and maintain
Treatment
the
as Kuru although
disease. As such symptoms
survival
quality
experience
This
on any
analysis. address
based
Conclusion:will
andKuru
resuldits,sease.infound practices. to
Prognosis:
functioning. overall
patient's
approach TOlow-up
therapydevices, months,
average patient
un1 may and CSF the and
of
 significant diseases.
cerebraldisorder.
hospital
the balance.
intermittent
in is
community
thepast which to
exhibited showedneurodegenerative
was diffuse
disproportionate
had function
neurological
to the cannibalism, maintaining revealed
admitted
over displayed
Surya He span. puncture
tribal Kuru."
symptoms cognitive
attention
was remote
Mr. a
Lumbar
(MRI/CT)
practicing He wereof and ofindicative
male, examination,
laughter
weakness. hereditary
ScASE
DISEASE neurological
a patient's
movements
poor
to ago.
37-year-old
which cerebellum
belongs
of walking
laughter imaging 16
history
decades "the theand
laughter, protein,
weakness other
Report:
Patient
Disease
KURU Uponand as anddeficits
progressIVe
patient and limb
characterized Brain
a a uncontrollable wasting excluded
the14-3-3
Information:
Patient Surya Presenting
Symptoms:
withceased coordination coordinating
Examination:
involuntary
evident,
memory
Kuru
STUDY
2: IneGuinea and Workup:
in
particularly
Emotional
instability
History: have twitching decline muscle
Cognitive of
Surya
Narme: Male
Gender: of months. was with testing
levels
historyNew
to in of of andin Dysphagia
Dysphagia Physical lagnostic
37Age: Episodes Significant
episodes elevated
difficultympaired, atrophy,
alinical eMeral helieved
a Oanua
Difficulty
Muscle context Genetic
th
 highest
no and andof provide team,
time
and prion
findings, disease
is to
care deficitsthe healthcare
the
a there therapy
and theabout to
disease, supportive at
initiated providing
therapy, theneurological
report, disease
informed
(TSE). physical
imaging as the
Kuru be and
thisinvolves life. poor,
swallowing by
encephalopathy the will
includeof symptoms
with
presentation, of is severe
quality of
been care monitored time.
time disease stage
diagnosed primarily havepalliative
the mayand remaining
patient'sto advanced managing 17
of Thisspeech Kuruleadingfamily closely
clinicalspongiformAs Treatment
was symptoms. and
Management: the for her
be the
weakness, rapidly,
prognosisthe Kuru,
and will on for
theSurya enhance
Givenpatient focus
Mr.Surya life
on transmissibledisease.
Mr. progresses of support.
and
comfort
specific nature of
Based to The death. will quality
tests, and muscle
the
Diagnosis: Kuru care
addressingPrognosis:
Treatment
progressive
diagnosis,
ultimately
Follow-Up:
care
possible
iahoratory
for manage palliative typically his
ralated and
Cure
 cultural of tragic
complex
eradication
our Fore of
historically
diseases. historical management
to shape and
the
connection
the unique
among
conditions.
to to
and prion of Thecontinue
reminder
limited
thethe
health. practices
compelling
of
transmission, illustrates
for
understanding primarily
intriguing
diseases available
a public
as cannibalistic
disease
a serves
and and condition,
case
is prion options
Kuruunique
our biology, challengingThis neurodegenerative 18
it into
to condition,
conclusion, rareof Guinea.
limited
its contributions eradication
research
culture,
to exceedingly
due these
rare Newthe
In disease between ongoing and
Conclusion:a of thePapuadevastating
andnow understanding
an to Kuru
significant
practices,and remains dueof
interplay
While
it of
Kuru people
cases nature
this
It
 4)https://www.osmosis.orglanswers/kuru#:~:text=Kuru%20is%2
3)
https:l/www.ncbi.nlm.nih.gov/pmclarticles/PMC6466359/
Oa%20type%20of,
to%20look%20like%20a%20sponge.
1)https:l/medlineplus.govlencylarticle/O01379.htm
2)
https:/lwww.healthline.com/health/kuru
19
BIBLIOGRAGHY