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 . . . . . . . . . . . . . . . . . . . . . . 1

Acknowledgement . . . . . . . . . . . . . . . . . . . . 3

Introduction . . . . . . . . . . . . . . . . . . . . . 4

I. Patient’s Profile . . . . . . . . . . . . . . . 6

II. Anatomy & Physiology . . . . . . . . . . . . . . 12

III. 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 5–14 years are the most frequent

victims.

Name: Patient X

Age: 10 years old

Gender: Male

Address: Prk 15, Irisan, Baguio City, Benguet

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

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 negative-

stranded 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 rabies-

infected 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 patient’s

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 wild-

type 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)

Bite

(Right ankle)

Treatment

Prevention

Prophylaxis

Tetanus toxoid

Anti-Rabies vaccine(1st dose

given)

Skin and Tissue trauma

Observed for signs of infection

Discharged

Health teachings

Drug Mode of Action Indications Side effects Nursing Considerations

Tetanus toxoid

GENERIC NAME: Anti-tetanus serum

BRAND NAME: Tetanus Toxoid

GENERAL CLASSIFICATION:

EPI vaccine,Anti-tetanus

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

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.

Redness Edema urticarial Malaise transient fever pain hypotension nausea arthralgia

• Observe 10 rights in giving medications:o Right Patiento Right Drugo Right Doseo Right Timeo Right Routeo Right to refuseo Right Assessmento Right Educationo Right Documentationo Right Evaluation• Ask for any history of allergy to the drug• Assess site for administration• Monitor for any occurrence of side effectsPerform skin testing before administration

DRUG ORDER(Generic name, Brand name, classification,

dosage, route, frequency)

MECHANISM OF ACTION INDICATIONS ADVERSE EFFECTS OF THE DRUGNURSING

RESPONSIBILITIES/ PRECAUTIONS

Generic Name:Purified Verocell vaccine, rabies (PVRV)

Brand Name:verorab

Classification:Anti-rabies, Vaccine, antisera & immunologicals

Used in a postexposure prophylaxis regimen that includes active immunization 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 virus-neutralizing 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 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

Minor local reactions (pain, erythema, edema, pruritus and induration at the injection point); systemic reactions (moderate fever, shivering, faintness, asthenia, headaches, dizziness, arthralgia, myalgia, gastrointestinal disorders [nausea, abdominal pains]); exceptionally, anaphylactoid reactions, urticaria and rash.

Favirab must only be administered in a rabies control center, under medical supervision.Do not administer Favirab IV (due to the risk of shock ie, sudden collapse with drop in blood pressure). Consequently, make sure that the needle has not penetrated a blood vessel.Favirab should not be administered in repeated doses.