RABIES

I. PENDAHULUAN

II. ETIOLOGI

Rabies disebabkan oleh virus rabies yang termasuk ke dalam genus

Lyssavirus dan family Rhabdoviridae, termasuk di dalamnya vesicular
stomatitis virus (VSV), a bovine pathogen of significant economic
importance that can infect humans (see "Other Rhabdoviruses," below).
Rhabdos, meaning "rodlike," refers to the distinctive elongated shape of
these viruses. Their enveloped virions contain a single-strand,
nonsegmented, negative-sense RNA. The rabies virus genome consists
of 11,932 nucleotides and encodes five proteins: nucleocapsid, matrix,
phosphoprotein, glycoprotein, and an RNA polymerase. Each animal
reservoir harbors one or more distinct rabies virus variants that can be
distinguished by the sequence of the nucleocapsid gene.
III. EPIDEMIOLOGI
Terdapat lebih dari 55.000 jiwa meninggal per tahun akibat rabies
di seluruh dunia. Berdampak signifikan dalam menyebabkan kematian
karena umumnya yang menjadi korban adalah anak-anak. Sebagian

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 besar kasus-kasus rabies pada manusia terjadi akibat penularan dari
anjing di negara-negara berkembang dengan rabies anjing endemik,
terutama di Asia dan Afrika. Di AS dan Kanada, sebagian besar kasus
pada manusia bersumber dari kelelawar pemakan serangga, dan
seringkali tidak terdapat riwayat gigitan kelelawar atau kontak dengan
kelelawar. Gigitan kelelawar mungkin tidak diakui. Varian virus rabies
bertanggung jawab terhadap sebagian besar kasus pada manusia
ditemukan pada kelelawar berambut merah dan kelelawar pipistrelle.
Sejenis kelelawar kecil jarang terjadi kontak dengan manusia. Terdapat
beragam vektor rabies lainnya di alam liar Amerika Utara, termasuk
sikung, rakun, dan rubah, akan tetapi spesies-spesies jarang
bertanggung jawab terhadap penyebaran pada manusia. Hal ini
kemungkinan besar karena profilaksis rabies pasca paparan yang efektif.
(Conn)

IV. PATOGENESIS
Rabies virus is usually transmitted by bites from rabid animals. Transmission
has rarely occurred through an aerosol route (in a laboratory accident or bat
cave containing millions of bats) or by transplantation of infected organs and
tissues. The virus is in the saliva of the rabid animal and inoculated into
subcutaneous tissues or muscles. During most of the long incubation period
(lasting 20 to 90 days or longer), the virus is close to the site of inoculation.
The virus binds to the nicotinic acetylcholine receptor at the postsynaptic
neuromuscular junction and travels toward the central nervous system (CNS)
in peripheral nerves by retrograde fast axonal transport. There is rapid
dissemination throughout the CNS by fast axonal transport. Under natural
conditions, degenerative neuronal changes are not prominent, and it is
thought that the rabies virus induces neuronal dysfunction by mechanisms
that are not well understood. In rabies vectors, the encephalitis is associated
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with behavioral changes that lead to transmission by biting. After the CNS
infection is established, the virus spreads by autonomic and sensory nerves
to multiple organs, including the salivary glands in which the virus is secreted
in high titer. (conn)
V. KLASSIFIKASI
VI. GAMBARAN KLINIS
Rabies in humans usually results from a bite by a rabid animal or
contamination of a wound by an animal's saliva. It presents as an acute,
fulminant, fatal encephalitis; human survivors have been reported only
occasionally. The disease begins as a nonspecific illness marked by fever,
headache, malaise, nausea, and vomiting. Abnormal sensations at or around
the site of viral inoculation occur frequently and probably reflect local nerve
involvement. The onset of encephalitis is marked by periods of excess motor
activity and agitation. Hallucinations, combativeness, muscle spasms, signs
of meningeal irritation, seizures, and focal paralysis occur. Periods of mental
dysfunction are interspersed with completely lucid periods; as the disease
progresses, however, the patient lapses into coma. Autonomic nervous
system involvement often results in increased salivation.

Brain stem and cranial nerve dysfunction is characteristic, with double vision,
facial palsies, and difficulty in swallowing. The combination of excess
salivation and difficulty in swallowing produces the traditional picture of
foaming at the mouth. Hydrophobia, the painful, violent involuntary
contractions of the diaphragm and accessory respiratory, pharyngeal, and
laryngeal muscles initiated by swallowing liquids, is seen in about 50% of
cases. Involvement of the respiratory center produces respiratory paralysis,
the major cause of death. The median survival after onset of symptoms is 4
days, with a maximum of 20 days unless artificial supportive measures are

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instituted. Recovery is rare and has been seen only in partially immunized
individuals. (CDTI)

VII. DIAGNOSIS
a. Pemeriksaan Fisis
b. Pemeriksaan Laboratorium
Laboratory diagnosis of rabies in animals or deceased patients is
accomplished by demonstration of virus in brain tissue. As negri bodies are
not seen in at least 20% of rabies victims, their absence does not rule out the
diagnosis. Viral antigen can be demonstrated rapidly by immunofluorescence
procedures. Intracerebral inoculation of infected brain tissue or secretions into
suckling mice results in death in 3-10 days. Histologic examination of their
brain tissue shows negri bodies; both negri bodies and rhabdovirus particles
may be demonstrated by electron microscopy. Specific antibodies to rabies
virus can be detected in serum, but generally only late in the disease. (CDTI)

c. Pemeriksaan Patologi Anatomi

VIII.DIAGNOSIS BANDING
Severe and unusual neurologic symptoms, whether encephalitic or
paralytic, should suggest the possibility of rabies in any unimmunized
person who has had contact with mammals in a rabies endemic area.
Rabies patients infected by bats in the USA however, usually deny any
contact with a bat.
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 Furious rabies can be mimicked by the pharyngeal form of cephalic
tetanus ('hydrophobic tetanus'), but severe tetanus usually has a shorter
incubation period than rabies. In tetanus, there is sustained muscle
rigidity, often associated with trismus. Delirium tremens and the excitatory
effects of some drugs and plant toxins have been confused with rabies.
Paralytic rabies is indistinguishable from many other causes of an
ascending paralysis, including postvaccinal encephalomyelitis
complicating the use of obsolete nervous tissue rabies vaccines still used
in Asia, Africa and Latin America.(cohen)
Rabies may initially be mistaken for Guillain-Barre syndrome, an
ascending peripheral polyneuritis, but encephalitic symptoms and signs
do not develop in the latter illness. (CDTI)

IX. PENANGANAN
a. Terapi Medikamentosa
b. Terapi Bedah
X. PROGNOSIS
Of patients with rabies, > 90% die owing to complications of the illness or
progressive neurologic dysfunction, especially respiratory paralysis. (CDTI1)

XI. KOMPLIKASI
Pneumonia and other infectious complications of intensive care are almost
invariable. Respiratory paralysis results from infection of the respiratory
center.(CDTI1)

Rabies 5
XII. PENCEGAHAN
After recognition of a rabies exposure, rabies can be prevented with initiation
of appropriate steps, including wound cleansing and active and passive
immunization. After a human is bitten by a dog, cat, or ferret, the animal
should be captured, confined, and observed for a period of at least 10 days.
The animal should also be examined by a veterinarian prior to its release. If
the animal is a stray, unwanted, shows signs, or develops signs of rabies
during the observation period, the animal should be killed immediately, and its
head should be transported under refrigeration for a laboratory examination.
The brain should be examined via an antigen-detection method using the
fluorescent antibody technique and viral isolation using cell culture or mouse
inoculation.
The incubation period for animals other than dogs, cats, and ferrets is
uncertain; these animals should be killed immediately after an exposure, and
the head submitted for examination. If the result is negative, one may safely
conclude that the animal's saliva did not contain rabies virus and, if
immunization has been initiated, it should be discontinued. If an animal
escapes after an exposure, it should be considered rabid unless information
from public health officials indicates this is unlikely, and rabies prophylaxis
should be initiated. The physical presence of a bat may warrant postexposure
prophylaxis when a person (such as a small child or sleeping adult) is unable
to reliably report contact that could have resulted in a bite.
Local wound care should be given as soon as possible after all exposures,
even if immunization is delayed, pending the results of an observation period.
All bite wounds and scratches should be washed thoroughly with soap and
water. Devitalized tissues should be débrided.
Purified chick embryo cell culture vaccine (RabAvert), rabies vaccine
absorbed (RVA), and human diploid cell vaccine (Imovax) are licensed rabies
vaccines in the United States and Canada. Other vaccines grown in either
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 primary cell lines (hamster or dog kidney) or continuous cell lines (Vero cells)
are also satisfactory and available in other countries. A regimen of five 1-mL
doses of rabies vaccine should be given intramuscularly (IM) in the deltoid
area (anterolateral aspect of the thigh is also acceptable in children). Ideally,
the first dose should be given as soon as possible after exposure, but failing
that, it should be given regardless of the length of a delay. Four additional
doses should be given on days 3, 7, 14, and 28. Pregnancy is not a
contraindication for immunization. Live vaccines should not be given for 1
month after rabies immunization. Local and mild systemic reactions are
common. Systemic allergic reactions are uncommon, and anaphylactic
reactions may be treated with epinephrine and antihistamines. Corticosteroids
may interfere with the development of active immunity. Immunosuppressive
medications should not be administered during postexposure therapy unless
they are essential. The risk of developing rabies should be carefully
considered before deciding to discontinue vaccination because of an adverse
reaction. A serum neutralizing antibody determination is necessary only after
immunization of immunocompromised patients. Less expensive vaccines,
derived from neural tissues, are still used in some developing countries; these
vaccines are associated with serious neuroparalytic complications.(CONN)

XIII. KESIMPULAN

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