Aspect Neurology: Tetanus, Rabies, Malaria, TBC Thypoid, Hiv

ASPECT NEUROLOGY
TETANUS, RABIES,
MALARIA, TBC
THYPOID, HIV
Anwar Wardy W
fkk umj anwar wardy w

FKK.UNIVERSITAS MUHAMMADIYAH
TETANUS
Tetanus toxin:
Patient number in Canada

After antitoxin vaccine
1941-1995

For lecture only Anwar Wardy W
Tetanus Epidemiology
Uncommon in the US but not worldwide
1 million cases worldwide per year
Mortality rate of 20-50%
Highestprevalence in developing
countries
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Epidemiology
Fewer than 50 cases per year in the US
Majority of cases in temperate climates (Texas,

California, and Florida)
Indonesia is same (Bali, Manado and North
Sumatra)
Mortality rate of 11%
Most who develop it have an inadequate

immunization history
Only 27% of Americans older than age 70 have

adequate immunity to tetanus
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Pathophysiology
Wound contamination with Clostridium
tetani
Motile,
nonencapsulated, anaerobic,
gram positive rod
Spore
forming and ubiquitous in soil and
animal feces
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Pathophysiology
Usually introduced in the spore forming
state, then germinates to the toxin
producing vegetative form
Requires decreased tissue oxygen tension to

germinate
Vegetative state produces two exotoxins

Tetanolysin
Tetanospasmin
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Toxins: affect on nerve-muscle transmission
Block the release of ACH
sthetik-Forum Berlin
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Toxins
Tetanolysin
clinically insignificant
Tetanospasmin
Neurotoxin responsible for the clinical

manifestations of tetanus
Reaches peripheral nerves by
hematogenous spread and retrograde
intraneuronal transport
Does not cross blood brain barrier
Reaches CNS by retrograde transport

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Tetanospasmin
Acts on the motor end plates of
skeletal muscle, in the spinal cord, and
in the sympathetic nervous system
Prevents release of inhibitory

neurotransmitters glycine and
gamma-aminobutyric acid (GABA)

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Clinical Features
Tetanospasmin responsible for generalized
muscular rigidity, violent muscular
contractions, and instability of the ANS.
Typical wound is a puncture, but no wound is

identified in up to 10%
Other routes are surgical procedures, otitis

media, abortion, umbilical stump and drug
abusers
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Four Clinical Forms

Local
Generalized
Cephalic
Neonatal

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Local Tetanus
Rigidityof the muscles in proximity to
the site of injury
Usually resolves completely in weeks to

months
May develop into generalized

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Generalized Tetanus
Most common form
Mostcommon presenting complaint is

pain and stiffness of the masseter
muscles (Lockjaw)
Shortaxon nerves affected initially

therefore starts in the face, then neck,
trunk, and extremities

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Generalized Tetanus
Muscle stiffness leads to rigidity
Trismus and characteristic sardonic smile

develops (risus sardonicus)
Reflex convulsive spasms and tonic muscle

contraction create dysphasia, opisthotonos
(arching of back and neck), flexing arms,
clenching fists, and lower extremity extension
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Trismus and Sardonic Smile

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Opisthotonos

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Generalized Tetanus
Autonomic nervous system
Hypersympathetic state
Usually in the second week
Tachycardia
HTN
Diaphoresis
Increased urinary catecholamines
Significant morbidity and mortality

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Cephalic Tetanus
Resultsfrom an injury to the head or
otitis media
Cranial
nerves affected most commonly
the seventh
Poor prognosis

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Neonatal Tetanus
400,000 worldwide deaths annually
Results
from inadequately immunized
mothers
Frequent after unsterile treatment of

the cord stump

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Neonatal Tetanus
Signs
Weakness
Irritability
Inability to suck
Presents in the 2nd week of life
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Diagnosis
Clinical diagnosis
No laboratory confirmatory tests
Wound cultures not very useful as C.

tetani may be recovered without tetanus
Immunization history usually unknown or

inadequate

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Tetanus Ddx
Strychnine Peritonitis
poisoning
Meningeal irritation
Dystonic reaction
Rabies
Hypocalcemic
tetany TMJ
Peritonsillar abscess
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Treatment
Admit to ICU
Be prepared for intubation with

neuromuscular blockade as respiratory
compromise may develop
Minimal environmental stimuli to avoid

reflex convulsive spasms
Initial wound debridement to improve

oxygenation
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Treatment
Tetanus Immunoglobulin (TIG)
Neutralizes wound and circulating
tetanospasmin
Does not neutralize toxin already bound to
the nervous system
Does not improve clinical symptoms
Decreases mortality

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Treatment
TIG
Usual dose is 3,000 to 6,000 units

Administered IM opposite side as Td given
Give before wound debridement

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Treatment
Antibiotics
Questionable utility but usually given

Metronidazole
antibiotic of choice
Avoid penicillin
it is a GABAA antagonist and may worse symptoms

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Treatment
Muscle relaxants
Tetanospasmin
prevents neurotransmitter release at
inhibitory interneurons and therapy of
tetanus is aimed at restoring balance
Midazolam
preferred agent as it is water soluble
Baclofen
specific GABAB agonist that has also been
used

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Treatment
Neuromuscular blockade
Blockade often required to allow respiration
and to prevent fractures and rhabdomyolysis
Succinylcholine
recommended for initial airway management
Vecuronium
treatment of choice for long term blockade

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Treatment
ANS dysfunction treatment
Labetalol
useful for treatment due to combined alpha
and beta activity
Magnesium sulfate
inhibits the release of epinephrine and
norepinephrine from the adrenal glands
Clonidine
central alpha receptor agonist for cardiac
stability

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Immunization
Disease does not confer immunity so those
that recover must undergo immunization
Tetanus toxoid
0.5 cc IM at presentation, 6 weeks, and 6 months
Local reactions are common
Less common serous reactions include urticaria,
anaphylaxis, or neurologic complications

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Immunization and TIG guide

Clean,
Minor All other
wounds wounds
History of
Td Doses Td TIG Td TIG
Unknown or
<3 Yes No Yes Yes
Three or
more
Td dose: 0.5cc IM No No Yes No
TIG dose: 250 U IM
DPT given if under 7, Td given if over 7

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RABIES
Family Rhabdoviridae
Genus Lyssavirus (Greek root lyssa)
Infeksi melalui darah mammalia, termasuk
pada manusia.
Causes encephalitis of the central nervous
system
Results in death of the host

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TRANSMISSION OF
RABIES
Is zoonotic, meaning is transmitted
from animal-animal or animal-human.
Rabies is most commonly contracted
from the bite of an animal that is
infected with the virus.
The virus is found in the saliva of the
infected animal.
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PARAMYXOVIRUS Anwar Wardy W
TRANSMISSION OF RABIES
Can also enter via any mucous membrane,

such as the eye, nose or mouth.
Handling and skinning of infected animal
carcasses.
Few cases of human to human
transmission.
Can be transmitted via aerosol, but thats
also uncommon.
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TRANSMISSION OF
RABIES
Inside the Jakarta/Java, important
reservoirs for the transmission of the
disease are wild animals such as
raccoons, skunks, foxes, bats, and
coyotes.
The time it takes for rabies to affect the
animal averages 1-3 months.
Sometimes may only be a few days, and
rarely longer than a year after exposure.
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THE RABIES INFECTION AND THE

SYMPTOMS THAT ACCOMPANY IT IS
1. IncubationBY
CLASSIFIED (1-3FIVE
months)
STAGES:
2. Prodromal, where first symptoms
occur
3. Acute neurological phase
4. Coma
5. Death or recovery

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TRANSMISSION OF
RABIES
1 Acute Neurological Stage, continued
Aerophobia
Sensitivity to lights, sounds and smells
Respiratory spasms.
2. Coma
Spasms decrease because paralysis occurs
Heart arrhythmias and irregular heartbeat persist
Cerebral encephalitis causes major organs to collapse
Fixed pupils that are unresponsive to light
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DEATH OR RECOVERY
1. - Death results from encephalitis of
the brain.
2. - Heart failure along with major
organ failure are the main causes of
death.
3. - Only four known cases of human
recovery, and they were permanently
brain damaged.
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Pathophysiology
Histologically resembles other encephalitis

Monocellular infiltration with focal hemorrhage
Demyelination
Perivascular gray matter
Basal ganglia
Spinal cord
Negri bodies
Eosinophilic intracellular lesions in cerebral
neurons
Highly specific for rabies
Present in 75% of rabies cases
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Negri bodies

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Epidemiology
Primarily a disease of animals
Human cases reflect the prevalence in
animals and degree of human contact with
them
Major vectors include
Dogs
Foxes
Raccoons
Skunks
Coyotes
Mongooses
bats

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Epidemiology
7,369 cases of animal rabies in the US in 2000
(Other World is some)
Domestic animals
Wild animals (93%) (7%)

Raccoons (37.7%) Cats (3.4%)
Skunks (30.2%) Dogs (1.6%)
Bats (16.8%) Cattle (1.1%)
Horses, donkeys,
Foxes (6.2%) mules (0.71%)
Others (2.2%) Sheep, goats, camels
(0.15%)
Others and ferrets
(0.06%)
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Epidemiology
Dogs
Less than 5% of animal cases in US, Canada and
Europe
Greater than 90% of animal cases in developing
countries
Very rare documented rabies in:
Squirrels, hamsters, guinea pigs, gerbils,
chipmunks, rats, mice, domesticated rabbits and
other small rodents
Almost never requires post exposure prophylaxis

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Epidemiology
Transmission
Saliva though bite of an rabid animal most

common
Aerosolized in bat caves
Mucus membrane transmission also
reported
Bites and scratches
Risk of developing rabies dependant on the
location injury, depth, an number of bites

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Infection Risk
Risk of infection
Multiple bites around the face 80-
100%
Single bite 15-40%
Superficial bite on the extremity 5-10%
Contamination of open wound by 0.1%
saliva
Transmission via fomites (e.g. 0%
tree branch, or animal)
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Epidemiology
32 cases reported from 1980 to 1996
in the US
7 had a known animal bite
6 dog bites in a foreign country
1 bat bite
Animal contact identified in 12
8 with a bat
2 with a dog
1 with a cow
1 with a cat
No identifiable source in the other 13
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Preexposure Prophylaxis
Prophylaxis
Individuals with occupations or recreation

that place them at risk should receive the
series
4 shot series with booster shots required
Does not eliminate need for postexposure
prophylaxis
No need for HRIG and less doses of vaccine

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Postexposure Prophylaxis
Indicated for all persons possibly exposed to
a rabid animal
Exposure is a bite, scratch, abrasion, open
wounds, or mucous membrane exposure
Contact alone, and contact with blood, urine, or
feces does not constitute and exposure
Cleansing wound with 20% soap and water

has been show in experimental animals to
markedly reduce the rate of infection
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Bats
Increasinglyimportant wildlife vectors of
transmission of rabies
Allcases of possible bat bites the bat

should be collected and tested for rabies
Bat unavailable
Begin postexposure prophylaxis
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Dogs, Cats, and Ferrets

Observation
CDC recommends 10 days of observation of

a healthy dog, cat, or ferret after a bite
Normal behavior
No action needed
Unusual behavior
Sacrifice animal, test for rabies, and initiate HRIG
and vaccine
Positive Complete course of vaccine
Negative Discontinue course
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Course
HRIG (human rabies immune globulin)

One dose initially
May be given up to 7 days after an exposure
Infiltrate as much as possible around wound
Give on the opposite side as the vaccine
Vaccine
5 doses over 28 days

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Vaccine reactions
Minor reaction
Erythema, swelling, pain
30-74%
Systemic reaction
Headache, nausea, abdominal pain, muscle
aches
5-40%
Anaphylaxis and neurological symptoms
Rarely reported
Vaccine should not be stopped for
minor
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or systemic reactions
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Special Circumstances
Prior rabies immunization
Either prior preexposure course or full
postexposure course
No HRIG
Course shortened to 2 doses
One dose on presentation
One dose three days later

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Immunocompromised patient
HRIG and vaccine usual course
Safe
Vaccine is inactivated so no danger of contracting
Stop all immunosuppressives if possible
Measure antibody titers to assure appropriate
response

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Travelers
Preexposure prophylaxis
Recommended if prevalence and possible
exposure
Veterinarians, animal handlers, spelunkers, certain
lab workers
Non-FDA postexposure prophylaxis
If initiated in another country contact health
department for recommendations

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Pregnancy
No adverse effects of the vaccine or HRIG

Follow usual course in pregnancy if indicated

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Children
Vaccine
Same dose and same course
HRIG
Dose is based on weight
If quantity of HRIG not sufficient to infiltrate all
wounds may be diluted with saline

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Clinical Disease
Incubation period
20 to 90 days
4 days up to 19 years have been reported
Greater than 1 year is well documented
Prodrome
Fever, sore throat, chills malaise, headache, N/V,
weakness
May report limb pain, weakness, and paresthesias
Nonspecific neurologic conditions such as anxiety,
agitation, irritability or psychiatric disturbances

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Clinical Disease
Acute neurologic phase
Furious 80%
Hyperactivity, disorientation, hallucinations,
bizarre behavior
Symptoms may alternate with calm
Autonomic dysfunction
Hydrophobia with pharynx spasms in 50%
Paralytic 20%
Paralysis in the extremity, diffuse or ascending
Fever and nuchal rigidity
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Clinical Disease
Coma
Almost always present within 10 days

Death
Occurs from complications such as pituitary

dysfunction, seizures, respiratory dysfunction,
cardiac dysfunction, ANS dysfunction, ARF, or
infection
Outcome almost always fatal
No person without post-exposure prophylaxis in
the US has survived since 1980

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Diagnosis
Rabiesshould be in the differential of
any acute encephalitis
May be confused with poliomyelitis,

Guillain-Barre syndrome, transverse
myelitis, postvaccinial
encephalomyelitis, CVA, atropine-like
poisoning, other viral encephalitis
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Diagnosis
Lab testing
No one test is completely informative
Test serum, CSF, and skin for antibodies in a
non-vacinated person
Nuchal skin biopsy most sensitive early
PCR from saliva also useful

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Treatment
Limited
No specific treatment exists for clinical

course
Treatment directed at the clinical
complications

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Malaria

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Protozoan infection
Falciparum malaria- most common virulent type
Cerebral malaria-obstruction of small blood vessels
in the brain
Rupturingof red blood cells
Relapses can occur

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Brief history of malaria

Basic biology of
Plasmodium
Epidemiology of
malaria, malaria & HIV

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Malaria in Indonesia
Malaria was quite prevalent in
the rural South
It was eradicated after World
War II in an aggressive
campaign using, treatment,
vector control and exposure
control (along with overall
improvement of living
conditions)
Eradication of malaria in
Indonesias initial mission

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Pathogenesis of
severe falciparum
malaria
Drugs used to
treat malaria and
the development
of drug resistance

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9-14 day incubation

period
Fever, chills,
headache, back and
joint pain
Gastrointestinal
symptoms (nausea,
vomiting, etc.)

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Symptoms intensify
Irregular high fever
Anxiety, delirium and other
mental problems
Sweating, increased pulse
rate, severe exhaustion
Worsening GI symptoms
Enlarged spleen and liver

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Malaria the disease

3 Severe manifestations
Cerebral malaria Severe anemia Renal failure
Irritability, loss of reflexes, Progressive severe drop Dwindling urine, high urea
neurological symptoms of hematocrit, poor oxygen Level in serum, hyperventilation
similar to menigitis, coma Supply for organs and Coma, poor prognosis
20% fatality fkk umj tissues anwar wardy w
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Pathogenesis of
malaria
In highly endemic areas: high
mortality among children due to
severe anemia, children who
survive beyond the first years
show decreasing parasitemia and
disease (this immunity is not
sterile and depends on constant
exposure)
In areas with less infection
pressure: malaria is an epidemic
disease with varying intensity.
Adults and children are equally
susceptible and death in adults is
mostly due to cerebral malaria

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Pathogenesis of
malaria
Parasitemia
Anemia Cerebral malaria
Age
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Development of malaria consist of an asexual phase
(carried out in the human) and a sexual phase (carried
out in the mosquito).

The life and transmission of Plasmodium Anwar Wardy W
Features of malaria.

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DIAGNOSIS OF MALARIA
1. HISTORY AND CLINICAL
FEATURES
* LOCALITY , TRAVEL
HISTORY
* FEVER
* SPLENO-HEPATOMEGALY
* PRESENCE OF
COMPLICATIONS
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* DRUG HISTORY
* ANTI MALARIALS
* BLOOD TRANSFUSION
HISTORY OF
- HAEMOGLOBINOPATHY
- DIABETES
- ALCOHOLISM/ JAUNDICE
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Specifically ask / look for

- fever with duration
- headache
- vomiting, diarrhoea
- urine output and colour
- cough / dyspnoea/ bleeding
- altered sensorium / seizures
- pregnancy

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CLINICAL EXAMINATION
PALLOR, ICTERUS
BLEEDING SIGNS
EARLY SIGNS OF PULM
OEDEMA
CONSOLIDATION
ARRHYTHMIA
HEPATOSPLENOMEGALY
UTERUS
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CNS Examination
Sensorium /coma score
- Glasgow coma score
- Blantyre coma score
- decerebration
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LABORATORY DIAGNOSIS
Microscopy
Immunological tests
Antigen capture tests
Antibody detection tests
QBC test
DNA probe
PCR
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MENINGITIS TBC
(TUBERCULOSE)

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Balita / anak (3 bulan - 6 thn);

Haemophilus influenzae
Neisseria meningitidis
Streptococcus pneumoniae
Staphylococcus aureus
Mycobacterium TBC
"Normal" Dewasa (6-21 years)
Neisseria meningitidis
Streptococcus pneumoniae
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H o s t: Bakteri:
Eukaryote Prokaryote
Nukleus mengandung Tidak ada nukleu,
material genom material genom bebas
Banyak kromosom Satu kromosom

linear sirkuler.
Ribosome besar Ribosome kecil
Multiseluler Sel tunggal.
Reproduce by binary
Reproduce sexually
fission
Pernapasan Respire aerobically or
O2(aerobic)
fkk umj anaerobically
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PATHOGENESIS.
Kebanyakan infeksi bakteri
menyerang melalui; mucosa,
darah, dan bakteri tumbuh dengan
cepat di dalam cairan serebro
spinal; sehingga tanda klinik yang
khas adalah, demam, kaku kuduk
dan kejang pada penderita
meningitis.
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Mekanisme Patogenik Bakteri dan Respon Tubuh

Host Defense Bacterial Evasion
Pathogenic Event
Mechanism
Colonization and 1. Secretory IgA IgA protease secretion

mucosal invasion, 2. Cellular cilia activity Ciliostasis
3.Mucosal epithelium Adhesive pili
Survivalintheblood ActivationofComplement BlockageofAlternative

stream Pathways ComplimentPathwayby
Mechanismsonthecell
surface
Crossingtheblood-brain Cerebralendothelium Passagethroughtight
barrier junctionsbetweencells,
SurvivalwithintheCSF Pooropsonicactivity Rapidbacterialreplication

fkk umj
mechanism unknown
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Invasi Bakteri
Bakteri dalam jumlah yang banyak berpotensi dapat

melewati BBB sampai di gyrus,
Terjadi vaskulitis disertai dengan deposit fibrin
karena kerusakan pembuluh arteri yang kecil; serta
petichae akan terlihat pada lapisan piamater.
Terjadi eksudat disertai dengan granulasit dan fibrin
dalam sulkus-sulkus hemisfer.
Pada beberapa penderita terjadi ventrikulitis; hal ini
menyebabkan mudah terjadinya ensefalitis dan bisa
difus pada kedua parenkhim-hemisfer.
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Foki MeningoEnsefalitis

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Antibiotik

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Thypoid
Transmission Disease Prevention
cholera, thyphoid, improve water quality, prevent casual use

waterborne
bacillas, hepatitis of polluted source
trachoma, scabia,
water washed improve water access, hygiene control
dysentery
schistomaisis,
water based snail control, filtration
guinea worm
malaria, sleeping
water vector surface water management
sickness
fkk umj http://www.arts.mcgill.ca/152-497b/h2o/water/gwater/death.htm
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Water Related Diseases in poor countries

(000s)
Infection Infections Deaths Cases of Disease
Diarrheas 5,000,000 10,000 5,000,000

Malaria 800,000 1,200 150,000
Polio 80,000 10-20 2,000
Typhoid 1000 25 500
Whipworm 500,000 low 100
http://www.arts.mcgill.ca/152-497b/h2o/water/gwater/death.htm
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Meningococcemia

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Human immunodeficiency virus
(HIV)
Viralinfection
Acquired immunodeficiency syndrome (AIDS)
Infects helper T cells (CD4 receptor)
Latency
Therapy

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AIDS is a cluster of symptoms associated with

the initial infection of HIV.

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HIV have specific glycoprotein receptors that bind to CD4
receptors of T cells.

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HIV infects, undergoes latency, and eventually replicates
and lyses the host T cell.

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Primary sources and possible routes of infection by HIV.

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New HIV infections based on gender, risk group, and race.

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Nucleoside analogs, protease inhibitors, and integrase
inhibitors are effective therapies used to treat HIV
infections.

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Features of HIV infections and AIDS.

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MINIMUM DIAGNOSTIC EVALUATION
5. Cultures of blood, urine

and other normally sterile compartments if
clinically indicated, e.g. joints, pleura, cerebrospinal fluid
6. Chest radiograph
7. Abdominal (including pelvic) ultrasonography
8. Autoantibodies
ANA, ANCA, Reuma factor, etc.
9. Tuberculin skin test
10. Serological tests directed by local epidemiological data
. Knockaert DC et al: Fever of unknown origin in adults: 40 years on. J
fkk umj Intern
anwar Med. 2003;253:263-75. Review.
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PENICILLINS
Pharmacokinetics:
A: Oral and parenteral
D: Variable: no CNS entry except w/meningitis
M: Not extensively metabolized
E: Filtration and secretion: Short life: 1-2 hr.

Probenicid prolongs actions: blocks secretion
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PENICILLIN TOXICITY
REMARKABLY NON-TOXIC
RENAL: Dose-related
I.T. INJECTIONNeurotoxicity
HYPERSENSITIVITY----Death

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Lifestyle Factors
Genes load the gun.
Lifestyle pulls the trigger
Dr. Elliot Joslin

Anwar Wardy W
Readings
Fundamental Neuroscience 1st Ed. Chapters 7 and 8

(for Neurochem also), 2nd Ed. Chapters 7 and 8.
Molecular Biol. Of the Cell 4th Ed. Chapter 13.
Harold L. Atwood & Shanker Karunanithi
Diversification of synaptic strength: presynaptic
elements. Nature Reviews Neuroscience 3, 497 -516
(2002). Advanced review comprehensive.
T. Galli, V. Haucke, N. R. Gough, Synaptic vesicle
fusion followed by clathrin-mediated endocytosis. Sci.
STKE 2003, tr3 (2003) shockwave animation of ves.
fusion.
Ref. Text book Of Clinical Neurology, Gilroy. 2001, 2006

Anwar Wardy W
WASSALAM, WR, WBR.........
Thank You

Anwar Wardy W

Aspect Neurology: Tetanus, Rabies, Malaria, TBC Thypoid, Hiv

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ASPECT NEUROLOGY

fkk umj anwar wardy w

Patient number in Canada

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1 million cases worldwide per year

Mortality rate of 20-50%

Majority of cases in temperate climates (Texas,

Most who develop it have an inadequate

Only 27% of Americans older than age 70 have

Requires decreased tissue oxygen tension to

Vegetative state produces two exotoxins

fkk umj anwar wardy w

Toxins: affect on nerve-muscle transmission

Block the release of ACH

Neurotoxin responsible for the clinical

fkk umj anwar wardy w

Prevents release of inhibitory

fkk umj anwar wardy w

Typical wound is a puncture, but no wound is

Other routes are surgical procedures, otitis

Four Clinical Forms

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Usually resolves completely in weeks to

May develop into generalized

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Mostcommon presenting complaint is

Shortaxon nerves affected initially

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Trismus and characteristic sardonic smile

Reflex convulsive spasms and tonic muscle

Trismus and Sardonic Smile

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Frequent after unsterile treatment of

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No laboratory confirmatory tests

Wound cultures not very useful as C.

Immunization history usually unknown or

fkk umj anwar wardy w

Be prepared for intubation with

Minimal environmental stimuli to avoid

Initial wound debridement to improve

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Usual dose is 3,000 to 6,000 units

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Questionable utility but usually given

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fkk umj anwar wardy w

Immunization and TIG guide

fkk umj anwar wardy w

fkk umj anwar wardy w

fkk umj anwar wardy w

Can also enter via any mucous membrane,

THE RABIES INFECTION AND THE

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Histologically resembles other encephalitis

fkk umj anwar wardy w

fkk umj anwar wardy w