RABIES

A ER Write UP presented to the Faculty

Of the School of Nursing
In partial fulfilment of
The requirement in
NCENL05

By
NMA Group 3
Calalo, David Lawrence Dalayoan
Dumangan, Maria Faye Geneva
Laluan, Romalyn Sanchez Laluan

October 2015

TABLE OF CONTENTS

Title Page . . . . . . . . . . . . . . . . . . . . . .

Acknowledgement . . . . . . . . . . . . . . . . . . . . 3
Introduction . . . . . . . . . . . . . . . . . . . . .
I
II
III

Patients Profile . . . . . . . . . . . . . . . 6
Anatomy & Physiology . . . . . . . . . . . . . . 12
Pathophysiology
a Ischematic Diagram . . . . . . . . . . . . . . 19
b Narrative . . . . . . . . . . . . . . . . . . 20

IV. Drug Study . . . . . . . . . . . . . . . . . . . 35

ACKNOWLEDGMENT
The group would like to express their heartfelt gratitude to
the following which had helped in the realization of this ER
WRITE UP. First and foremost, we would like to gratify the
patient and her family who allowed us to exploit his care and for
devoting his time answering all our questions needed for the
study.
To our Parents or our family, for their support and
understanding that they have given to us, for always being there
to guide and care for us after a long day of duty.

To Mrs. Jennifer Boleyley RN, MAN, our clinical instructor

in the area, who guided us throughout the rotation, and who
imparted her knowledge and skills to the group in order for us to
learn and gain experience.

And Above all we thank the Almighty God, for everything

he provided us, the strength and guidance, without Him this would
not be possible.

INTRODUCTION

Rabies is a viral disease that causes acute inflammation of

the brain in humans and other warm-blooded animals. Early
symptoms can include fever and tingling at the site of exposure.
These symptoms are followed by one or more of the following
symptoms: violent movements, uncontrolled excitement, fear of
water, an inability to move parts of the body, confusion, and
loss of consciousness. Once symptoms appear it nearly always
results in death. The time period between contracting the disease
and the start of symptoms is usually one to three months;
however, this time period can vary from less than one week to
more than one year. The time is dependent on the distance the
virus must travel to reach the central nervous system.
Rabies is caused by lyssaviruses including: rabies virus and
Australian bat lyssavirus. Rabies is spread when an infected
animal scratches or bites another animal or human. Saliva from an
infected animal can also transmit rabies if the saliva comes into
contact with the mouth, nose, or eyes. Globally, dogs are the
most common animal involved. More than 99% of rabies cases in
countries where dogs commonly have the disease are caused by dog
bites.In the Americas, bat bites are the most common source of
rabies infections in humans, and less than 5% of cases are from
dogs.Rodents are very rarely infected with rabies. The rabies
virus travels to the brain by following the peripheral nerves.
The disease can only be diagnosed after the start of symptoms.
Animal control and vaccination programs have decreased the risk
of rabies from dogs in a number of regions of the world.
Immunizing people before they are exposed is recommended for
those who are at high risk. The high-risk group includes people

who work with bats or who spend prolonged periods in areas of the
world where rabies is common. In people who have been exposed to
rabies, the rabies vaccine and sometimes rabies immunoglobulin
are effective in preventing the disease if the person receives
the treatment before the start of rabies symptoms. Washing bites
and scratches for 15 minutes with soap and water, povidone
iodine, or detergent may reduce the number of viral particles and
may be somewhat effective at preventing transmission.Only a few
people have survived a rabies infection after showing symptoms
and this was with extensive treatment known as the Milwaukee
protocol.
Rabies is present on all continents with the exception of
Antarctica, but more than 95% of human deaths occur in Asia and
Africa.

Rabies is a neglected disease of poor and vulnerable

populations whose deaths are rarely reported and where human
vaccines and immunoglobulin are not readily available or
accessible. It occurs mainly in remote rural communities where
children between the age of 514 years are the most frequent
victims.

Name:

Patient X

Age:

10 years old

Gender:

Male

Address:

Prk 15, Irisan, Baguio City,

Date of Birth:

October 1, 1995

Nationality:

Filipino

Civil Status:

Single

Religion:

Roman Catholic

Occupation:

STUDENT

Date of Admission:

OCTOBER 15, 2015

Time of Admission:

6:00 PM

Admitting Diagnosis:

RABIES

Chief Complaint:

Dog bite in right ankle, 2 cm deep

ANATOMY AND PHYSIOLOGY of Rabies

Benguet

Figure 1: This figure shows the bullet-shaped structure of the

Rabies Virus.
It is believed that the reaction of theG protein to the cell
surface receptors may be involved. After this occurs, the virus
goes through the host cell and enters the cytoplasm by
pinocytosis (which can be seen in Figure 2).

Figure 2: This figure shows the process of pinocytosis, which

allows the virus to enter the cytoplasm.
The virus cumulates in large endosomes and the endosome
membranes fuse together with the viral membranes, which causes
the release of viral RNP into the cytoplasm. The L gene
transcribes the rabies RNA into leader RNA and mRNAs, which are
then translated into proteins. The intracellular ratio of
leader RNA to the N protein stimulates the switch from
transcription to replication. After replication is complete, the
assembly process begins. The N-P-L complex surrounds negativestranded RNA to form the RNP core. The M protein forms a capsule
around the RNP. This RNP-M complex travels to a part of the
plasma membrane containing glycoprotein inserts. Here, the M
protein initiates coiling. The RNP-M binds to the glycoprotein
and the completed virus buds from the plasma membrane. In the
central nervous system, there occurs preferential viral budding
from the plasma membrane. However, the virus in the salivary
glands mostly buds from the cell membranes into the acinar lumen.
This viral budding in the salivary glands, as well as the
aggressive biting behavior of the infected animal, increases the
chance of a viral infection of a new host.

Figure 3: This figure shows the cycle of rabies infection and

replication.
Rabies is zoonotic, meaning that it is transferred by animals,
most commonly by the bite of a rabid animal. However, it can be

transferred in other manners. All warm-blooded animals are

susceptible to getting rabies. It usually has an incubation
period of between 2-12 weeks, but there have been documented
cases of incubation lasting up to a year. The onset of symptoms
is determined by the bites proximity to the brain and the number
of virus particles in the infection. Negri bodies, which are
characteristic of rabies, are inclusion bodies that are commonly
found in the cytoplasm of infected nerve cells.

Figure 4: This figure shows Negri bodies located in a rabiesinfected nerve cell.
The virus is located in the nerves as well as the saliva of an
infected and symptomatic individual, however transmission between
humans is rare. After a human is bitten, the virus enters the
peripheral nervous system. The virus binds to the nerves via
nicotinic acetylcholine receptors. During this time after a
person is first infected, rabies is hard to detect and does not
present symptoms. This is the time when a person can receive
vaccination. Once the virus reaches the brain, it quickly causes
encephalitis, or inflammation of the brain. The cells in the
brain that are affected include the cerebellum, the purkinje
cells, the hippocampus, and the pontine nuclei. This stage of
rabies is referred to as the prodromal phase and is the onset of
symptoms. Once the virus moves along the nerve axons from the
peripheral nerves to the central nervous system (through
retrograde axoplasmic flow), the patient starts exhibiting
symptoms. It is believed that the neuromuscular junctions are
very important during this transition, as their physical and

chemical properties appear to direct the virus to infect the

nerve cells, (Hunt, 2009). This usually occurs through the
sensory and motor nerves.

Treatment becomes ineffective at this

point and the mortality rate is almost 100%.

Once the virus reaches the central nervous system the virus
amplifies very quickly because of multiple cycles of replication.
This stage of rabies is known as the acute neurological period.
The centrifugal spread of rabies leads to the virus overtaking
very innervated areas, such as the salivary glands. Once there is
cerebral infection, behavioral symptoms occur. The first symptoms
to occur are usually numbness and pain where bitten. Other early
symptoms include fever, cough, sore throat, abdominal pain, and
anxiety. Later symptoms that effect the central nervous system
are more pronounced and include anxiety, hallucinations,
delirium, hydrophobia, muscle spasms in the face, neck, and
diaphragm followed by seizures, paralysis, significant
fluctuations in temperature, heart rate and blood pressure, coma,
and heart and respiratory failure. Hallucinations and delirium
are the result of brain inflammation and other dysfunctions
occurring in the brain such as dopamine. Encephalitis is also
known to cause seizures because the neurons firing in a patients
brain with encephalitis misfire, causing the seizure. Paralysis
occurs because of the damage being done to the nervous system.
Death usually occurs between three and twenty days after the
onset of symptoms. The virus is concentrated in the salivary
glands, which explains why it is transferred usually by bites.
The virus also damages the muscles involved in swallowing
(usually paralyzing them), which causes a lot of pain. Because
swallowing causes so much pain, the patient usually becomes

dehydrated, and thus, very afraid of water. This is why the

disease was once called hydrophobia. Dehydration causes the
muscle spasms that patients can have. There are two main ways in
which these symptoms present themselves. The more common type is
known as furious rabies. This type includes seizures, periods of
anxiety, hallucinations, and violent behavior. The second form is
known as paralytic rabies. This is characterized by a slow
paralysis of the patient and typically these patients live a
little longer than those who have furious rabies. The result of
death is usually respiratory failure.
Figure 5: This figure shows the progression of rabies from
transmission onward.
There are two different types of rabies prophylaxis that are
effective when used before the onset of symptoms. The first,
Rabies Vaccine, is an inactivated vaccine and is immunogenic. It
is grown in human diploid cells and is given by injection over a
four-week period. Human Rabies Immunoglobin (HRIG), another
treatment for rabies, is made from the plasma of hyperimmune
donors. About half of the dose is injected into the site of the
bite and the other half is given through intramuscular
injections. There two treatments are used in conjunction with one
another. These treatments should be administered no later than 2
days after the bite occurs.
It is still unknown what occurs during the long incubation period
of the disease and the molecular mechanism in which the virus
attacks the nervous system. However, there has been a lot of
progress with the control of rabies and the development of
vaccinations. Overall, rabies is a frightening disease and

hopefully one day scientists will be able to eliminate, or at

least reduce its incidence rate significantly.

NARRATIVE PATHOPHYSIOLOGY

The incubation period is variable. It is usually 2 weeks to 3

months but with a range from 5 days to 7 years. Shorter

incubation periods are associated with severe bites and bites to

the head and face. The nicotinic acetylcholine receptor at the
motor end plate mediates virus entry to myocytes where initial
replication takes place. The virus enters the nervous system
through unmyelinated sensory and motor terminals and is
transported by fast retrograde axonal transport, crossing new
synapses roughly every 12 hours. Once the virus has entered the
central nervous system, it is sequestered from the immune system
and immunisation will not be effective. Clinical symptoms begin
once the virus infects the spinal cord and progress rapidly as
the virus spreads through the CNS. The rabies virus exits the CNS
through motor, sensory, and autonomic nerves, and replicates
locally in salivary and lacrimal glands in order to be
transmitted to the next host.
Many aspects of rabies pathophysiology remain a mystery. It is
unclear how rabies causes paralysis. The pathophysiological
differences between the encephalitic and paralytic forms of
rabies may involve differences in the host inflammatory
response. The cause of death in rabies is unknown because wildtype viruses are not cytopathic, apoptotic, or inflammatory.
Atypical, less severe forms of neurological illness are beginning
to be reported, suggesting a continuum of rabies severity.

SCHEMATIC PATHOPHSIOLOGY

Animal contact
(DOG)

Tetanus toxoid
Anti-Rabies
Bite
Treatment
st for
Discharged
Observed
vaccine(1
dose
Prophylaxis
signs
of trauma
(Right
ankle)
given)
Skin and
Tissue
Prevention
Health
teachings

Drug

Mode of Action

Indications

Sid

Tetanus toxoid
GENERIC NAME: Antitetanus serum
BRAND NAME: Tetanus
Toxoid

Tetanus toxoid
adsorbed induces
active immunity to
tetanus antigen by
stimulating the immune
system to produce
specific antitoxin

GENERAL
CLASSIFICATION:
EPI vaccine,
Anti-tetanus

DRUG ORDER
(Generic name, Brand
name, classification,
dosage, route,
frequency)
Generic Name:
Purified Verocell
vaccine, rabies
(PVRV)
Brand Name:
verorab
Classification:
Anti-rabies, Vaccine,
antisera &
immunologicals

Indications:
Prophylaxis and
treatment of tetanus.
Contraindications:
Hypersensitivity
reaction to the serum
globulin or any of its
components, a
hypersensitivity
reaction to a test
dose, and any condition
that will
contraindicate
intramuscular injection
such as
thrombocytopenia.

MECHANISM OF ACTION

INDICATIONS

Used in a postexposure
prophylaxis regimen that
includes active immunizatio
n with rabies vaccine
and passive immunization
with RIG. RIG provides
immediate, temporary rabies
virus-neutralizing
antibodies until the
patient has an immunologic
response to active
immunization with rabies
vaccine and produces virusneutralizing antibodies.

For the prevention of

rabies in subjects at a
high risk of exposure. All
subjects at a permanent
risk eg, diagnostic,
research and production
laboratory staff working
on rabies virus, should be
vaccinated. A serological
test is recommended every
6 months
Contraindications:
Severe febrile infection,
acute disease, progressive
chronic disease (it is
preferable to postpone
vaccination); known
hypersensitivity to any of

ADVERSE

Mi
(p
pr
at
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fa
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ar
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the ingredients of
Verorab.
Post-Exposure: Due to the
fatal progression of
declared rabies infection,
there are no
contraindications to
curative vaccination.
If there is any doubt, it
is essential to consult
the doctor or pharmacist.
Use in pregnancy &
lactation: Verorab has not
been the subject of animal
teratogenicity studies