First Aid
Safety Precautionary
Measures at Home
Visitors/Telephone
1. When a guest rings the doorbell or knocks
on the door, use your peephole to identify
the caller. If you do not have a peephole, ask
the visitor to identify himself. Only open
your door if you know and trust the caller.
Talk to repair people through closed doors
and do not allow them in unless you have
verified their credentials (company name
and phone number, ID badge). If an
unknown visitor asks to use your
2. phone, direct him to the closest public
telephone.
Do not divulge any personal data about
yourself or anyone who lives in your home
to unknown callers. Keep police and
paramedics contact information handy and
record the numbers on your speed dial. In
the case of nuisance calls, do not respond;
instead, hang up the phone and call your
telephone company for assistance. Establish
a signal with your neighbors, such as a bell
or continuous car horn honking to alert them
if you are in danger. Encourage them to
report any suspicious persons they see
prowling around your home to the police.
Intruders
3. If you experience a break-in while you are
inside the home, try to get to the burglar
alarm and activate it, or try go to the nearest
bedroom and call the police. If you hear the
burglar, but do not see him, make a lot of
noise shuffling around but refrain from
confronting him. Some burglars will
evacuate the home immediately upon
hearing sounds. Distance yourself from the
intruder as much as possible, but if you are
confronted by him try to stay calm. Do not
enter the house if you arrive home and feel
that a burglar is inside--run to the neighbor's
home and call the police. If you get a
glimpse of the intruder, try to keep a mental
picture of his features (height, race,
suspected age, type of clothing and any
outstanding features).
4. One of the best things you can do for your
family's safety (especially if you have
children) is to have a first aid kit on hand.
Falls, choking, dog bites and burns are some
of the most frequent injuries that happen at
home. Your first aid kit should include
bandages, cotton swabs, saline solution,
waterproof film dressing, disposable gloves,
antiseptic and first aid tape. Keep ice-packs
in the freezer as well. Do not wait until you
have used up almost all the items in your
first aid kit to replenish it. Include it in your
grocery check each week and add the
necessary items to your list.
Electrical Safety
5. Electricity-related injuries in the home are
quite common. This often stems from
homeowners being uneducated about the
danger of electrical wires. To prevent
electrical shock and injuries, make sure your
extension cords and outlets are not
overloaded. Discard electrical cords that are
frayed or damaged, and refrain from putting
electrical cords underneath rugs and carpets.
Use the appropriate bulbs and wattage for
lamps and light fixtures. Test your smoke
detectors and replace the batteries annually.
Always read and adhere to the
manufacturer's safety directions on electrical
products. Thoroughly clean all spills from
the floor. If you have an electrical problem,
do not ignore it--call an electrician or your
maintenance person.
Classification and Treatment of
Burns
What are the classifications of burns?
Burns are classified as first-, second-, or
third-degree, depending on how deep and
severe they penetrate the skin's surface.
First-degree (superficial) burns
First-degree burns affect only the epidermis,
or outer layer of skin. The burn site is red,
painful, dry, and with no blisters. Mild
sunburn is an example. Long-term tissue
damage is rare and usually consists of an
increase or decrease in the skin color.
Second-degree (partial thickness) burns
Second-degree burns involve the epidermis
and part of the dermis layer of skin. The burn
site appears red, blistered, and may be
swollen and painful.
Third-degree (full thickness) burns
Third-degree burns destroy the epidermis
and dermis. Third-degree burns may also
damage the underlying bones, muscles, and
tendons. The burn site appears white or
charred. There is no sensation in the area
since the nerve endings are destroyed.
Second and third-degree burns
require the immediate
attention of a physician or
other healthcare provider.
Listed below you will find
additional information relating
to first-, second-, or third-
degree burns.
There are 3 classes of common
fires and 2 specialty classes.
Fires are classified into 5 groups:
CLASS A: Class A fires involve common
combustibles such as wood, paper, cloth,
rubber, trash and plastics. They are common
in typical commercial and home settings, but
can occur anywhere these types of materials
are found.
CLASS B: Class B fires involve flammable
liquids' gases, solvents, oil, gasoline, paint,
lacquers, tars and other synthetic or oil-
based products. Class B fires often spread
rapidly and, unless properly secured, can
reflash after the flames are extinguished.
CLASS C: Class C fires involve energized
electrical equipment, such as wiring,
controls, motors, data processing panels or
appliances. They can be caused by a spark,
power surge or short circuit and typically
occur in locations that are difficult to reach
and see.
CLASS D: Class D fires involve combustible
metals such as magnesium and sodium.
Combustible metal fires are unique industrial
hazards which require special dry powder
agents.
CLASS K: Class K fires involve combustible
cooking media such as oils and grease
commonly found in commercial kitchens. The
new cooking media formulations used form
commercial food preparation require a
special wet chemical extinguishing agent
that is specially suited for extinguishing and
suppressing these extremely hot fires that
have the ability to reflash.
(NOTE: Although ABC and BC Dry Chemical
extinguishers can control a fire involving
electronic equipment, the National Fire Code
(NFPA 75-1999 edition), Section 6-3-2,
specifically advises against dry-chemical
extinguishers for fires involving computers or
other delicate electronic equipment due to
the potential damage from residues.
Standard for the Protection of Electronic
Computer/Data Processing Equipment
6-3.2 Listed extinguishers with a minimum
rating of 2-A shall be provided for use on
fires in ordinary combustible materials, such
as paper and plastics. Dry chemical
extinguishers shall not be permitted.")
Excessive noise is made up of two parts -
the period of time you are exposed to the
noise and the loudness of the noise.
Continuous exposure to noise above 85
decibels during an eight hour day is
considered to be excessive noise. (The noise
of a heavy truck is about 85 decibels, while a
jet taking off is about 120 decibels.)
The decibel (dB) is a logarithmic unit of
measurement that expresses the magnitude of a
physical quantity (usually power or intensity)
relative to a specified or implied reference level.
Since it expresses a ratio of two quantities with the
same unit, it is a dimensionless unit. A decibel is
one tenth of a bel, a seldom-used unit.
The term decibel is most widely known as a
measure of sound pressure level, but is also useful
for a wide variety of measurements in science and
engineering (particularly acoustics, electronics, and
control theory) and other disciplines. It confers a
number of advantages, such as the ability to
conveniently represent very large or small numbers,
a logarithmic scaling that roughly corresponds to
the human perception of sound and light, and the
ability to carry out multiplication of ratios by simple
addition and subtraction.
The decibel symbol is often qualified with a suffix,
which indicates which reference quantity or
frequency weighting function has been used. For
example, "dBm" indicates that the reference
quantity is one milliwatt, while "dBu" is referenced
to 0.775 volts RMS.[1]
The definitions of the decibel and bel use base-10
logarithms. For a similar unit using natural
logarithms to base e, see neper.
Rabies

Rabies (pronounced /ˈreɪbiːz/. From Latin: rabies) is a viral neuroinvasive disease that causes acute encephalitis
(inflammation of the brain) in warm-blooded animals. It is zoonotic (i.e., transmitted by animals), most
commonly by a bite from an infected animal but occasionally by other forms of contact. Rabies is almost
invariably fatal if post-exposure prophylaxis is not administered prior to the onset of severe symptoms. It is a
significant killer of livestock in some countries.
The rabies virus travels to the brain by following the peripheral nerves. The incubation period of the disease
depends on how far the virus must travel to reach the central nervous system, usually taking a few months.Once
the infection reaches the central nervous system and symptoms begin to show, the infection is practically
untreatable and usually fatal within days.
Early-stage symptoms of rabies are malaise, headache and fever, later progressing to more serious ones,
including acute pain, violent movements, uncontrolled excitement, depression and inability to swallow water.
Finally, the patient may experience periods of mania and lethargy, followed by coma. The primary cause of
death is usually respiratory insufficiency. 97% of human rabies cases come from dog bites.In the United States,
however, animal control and vaccination programs have effectively eliminated domestic dogs as reservoirs of
rabies.

Rabies Classification and external resources

Dog with rabies virus ICD-10 A82. DiseasesDB 11148 eMedicine med/1374 eerg/493 ped/1974
MeSH D011818

Etymology
The term is derived from the Latin rabies, "madness".[4] This, in turn, may be related to the
Sanskrit rabhas, "to do violence". The Greeks derived the word "lyssa", from "lud" or "violent";
this root is used in the name of the genus of rabies lyssavirus.

Virology
he rabies virus is the type species of the Lyssavirus genus, which encompasses other similar viruses.
Lyssaviruses have helical symmetry, with a length of about 180 nm and a cross-sectional diameter of about
75 nm. These viruses are enveloped and have a single stranded RNA genome with negative-sense. The genetic
information is packaged as a ribonucleoprotein complex in which RNA is tightly bound by the viral
nucleoprotein. The RNA genome of the virus encodes five genes whose order is highly conserved. These genes
are nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G) and the viral RNA polymerase
(L).
From the point of entry, the virus travels quickly along the neural pathways into the central nervous system
(CNS), and then further into other organs. The salivary glands receive high concentrations of the virus thus
allowing further transmission.
Symptoms
The period between infection and the first flu-like symptoms is normally two to twelve weeks, but can be as
long as two years. Soon after, the symptoms expand to slight or partial paralysis, cerebral dysfunction, anxiety,
insomnia, confusion, agitation, abnormal behavior, paranoia, terror, hallucinations, progressing to delirium.[7]
The production of large quantities of saliva and tears coupled with an inability to speak or swallow are typical
during the later stages of the disease; this can result in “hydrophobia”, in which the patient has difficulty
swallowing because the throat and jaw become slowly paralyzed, shows panic when presented with liquids to
drink, and cannot quench his or her thirst. The disease itself was also once commonly known as hydrophobia
(or aquaphobia), from this characteristic symptom.
Death almost invariably results two to ten days after the first symptoms; the few humans who are known to
have survived the disease were all left with severe brain damage, with one recorded exception purportedly
resulting from implementation of the Milwaukee protocol.[8] It is neurotropic in nature.

Diagnosis
The reference method for diagnosing rabies is by performing PCR or viral culture on brain samples taken after
death. The diagnosis can also be reliably made from skin samples taken before death. It is also possible to make
the diagnosis from saliva, urine and cerebrospinal fluid samples, but this is not as sensitive. Inclusion bodies
called Negri bodies are 100% diagnostic for rabies infection, but found only in 20% of cases.
The differential diagnosis in a case of suspected human rabies may initially include any cause of encephalitis,
particularly infection with viruses such as herpesviruses, enteroviruses, and arboviruses (e.g., West Nile virus).
The most important viruses to rule out are herpes simplex virus type 1, varicella-zoster virus, and (less
commonly) enteroviruses, including coxsackieviruses, echoviruses, polioviruses, and human enteroviruses 68 to
71. In addition, consideration should be given to the local epidemiology of encephalitis caused by arboviruses
belonging to several taxonomic groups, including eastern and western equine encephalitis viruses, St. Louis
encephalitis virus, Powassan virus, the California encephalitis virus serogroup, and La Crosse virus.
New causes of viral encephalitis are also possible, as was evidenced by the recent outbreak in Malaysia of some
300 cases of encephalitis (mortality rate, 40%) caused by Nipah virus, a newly recognized
paramyxovirus.Similarly, well-known viruses may be introduced into new locations, as is illustrated by the
recent outbreak of encephalitis due to West Nile virus in the eastern United States. Epidemiologic factors (e.g.,
season, geographic location, and the patient’s age, travel history, and possible exposure to animal bites, rodents,
and ticks) may help direct the diagnostic workup.
Cheaper rabies diagnosis will be possible for low-income settings according to research reported on the Science
Development Network website in 2008. Accurate rabies diagnosis can be done at a tenth of the cost, according
to researchers from the Farcha Veterinary and Livestock Research Laboratory and the Support International
Health Centre in N'Djamena, Chad. The scientists evaluated a method using light microscopy, cheaper than the
standard tests, and say this could provide better rabies control across Africa.
Prevention
Every infected case with rabies resulted in death until a vaccine was developed by Louis Pasteur and Émile
Roux in 1885. Their original vaccine was harvested from infected rabbits, from which the nerve tissue was
weakened by allowing it to dry for five to ten days.Similar nerve tissue-derived vaccines are still used in some
countries, as they are much cheaper than modern cell culture vaccines.The human diploid cell rabies vaccine
(H.D.C.V.) was started in 1967; however, a new and less expensive purified chicken embryo cell vaccine and
purified vero cell rabies vaccine are now available.A recombinant vaccine called V-RG has been successfully
used in the field in Belgium, France, Germany and the United States to prevent outbreaks of rabies in wildlife.
Currently pre-exposure immunization has been used in both human and non-human populations, whereas in
many jurisdictions domesticated animals are required to be vaccinated.
In the U.S., since the widespread vaccination of domestic dogs and cats and the development of effective human
vaccines and immunoglobulin treatments, the number of recorded deaths from rabies has dropped from one
hundred or more annually in the early twentieth century, to 1–2 per year, mostly caused by bat bites, which may
go unnoticed by the victim and hence untreated.
Treatments
Post-exposure prophylaxis
Treatment after exposure, known as post-exposure prophylaxis or “P.E.P.”, is highly successful in preventing
the disease if administered promptly, generally within ten days of infection. Thoroughly washing the wound as
soon as possible with soap and water for approximately five minutes is very effective at reducing the number of
viral particles. “If available, a virucidal antiseptic such as povidone-iodine, iodine tincture, aqueous iodine
solution or alcohol (ethanol) should be applied after washing...Exposed mucous membranes such as eyes, nose
or mouth should be flushed well with water.”[17] In the United States, patients receive one dose of human rabies
immunoglobulin (HRIG) and four doses of rabies vaccine over a fourteen day period. The immunoglobulin dose
should not exceed 20 units per kilogram body weight. HRIG is very expensive and constitutes the vast majority
of the cost of post-exposure treatment, ranging as high as several thousand dollars. As much as possible of this
dose should be infiltrated around the bites, with the remainder being given by deep intramuscular injection at a
site distant from the vaccination site. The first dose of rabies vaccine is given as soon as possible after exposure,
with additional doses on days three, seven and fourteen after the first. Patients that have previously received
pre-exposure vaccination do not receive the immunoglobulin, only the post-exposure vaccinations on day 0 and
2.
Modern cell-based vaccines are similar to flu shots in terms of pain and side effects. The old nerve-tissue-based
vaccinations require multiple painful injections into the abdomen with a large needle, are cheap, and are now
used only in remote poor areas in India, but are being phased out and replaced by affordable WHO ID
(intradermal) vaccination regimens.
Intramuscular vaccination should be given into the deltoid, not gluteal area which has been associated with
vaccination failure due to injection into fat rather than muscle. In infants the lateral thigh is used as for routine
childhood vaccinations.
Finding a bat in the room of a sleeping infant is regarded as an indication for post-exposure prophylaxis. The
recommendation for the precautionary use of post-exposure prophylaxis in occult bat encounters where there is
no recognized contact has been questioned in the medical literature based on a cost-benefit analysis.However,
recent studies have further confirmed the wisdom of maintaining the current protocol of precautionary
administering of P.E.P. in cases where a child or mentally compromised individual has been left alone with a
bat, especially in sleep areas (where a bite/or exposure may occur while the victim is asleep and unaware or
awake and unaware that a bite occurred). This is illustrated by the case of a nine-year old boy from Quebec who
died an agonizing death (over a 14 day period) from rabies 4 weeks after being in the presence of a sick bat,
even though there was no apparent report of a bite; as shown in the following conclusion made by the doctors
involved in the case:
Despite recent criticism (45), the dramatic circumstances surrounding our patient's history, as well as
increasingly frequent reports of human rabies contracted in North America, support the current Canadian
guidelines which state that RPEP [P.E.P] is appropriate in cases where a significant contact with a bat cannot be
excluded (45). The notion that a bite or an overt break in the skin needs to be seen or felt for rabies to be
transmitted by a bat is a myth in many cases.
It is highly recommended that P.E.P. be administered as soon as possible. Begun without delay, or with very
little delay, P.E.P. is 100% effective against rabies. In the case in which there has been a significant delay in
administering P.E.P., the treatment should be administered regardless of that delay, as it may still be effective if
it is not too late. If there has been a delay between exposure and attempts at treatment, such that the possibility
exists that the virus has already penetrated the nervous system, the possibility exists that amputation of the
affected limb might thwart rabies, if the bite or exposure was on an arm or leg. This treatment should be
combined with an intensive PEP regimen.
Blood-brain barrier
Some recent works have shown that during lethal rabies infection, the blood-brain barrier (BBB) does not allow
anti-viral immune cells to enter the brain, the primary site of rabies virus replication.[21] This aspect contributes
to the pathogenicity of the virus and artificially increasing BBB permeability promotes viral clearance.Opening
the BBB during rabies infection has been suggested as a possible novel approach to treat the disease, even
though no attempts have yet been made to determine whether or not this treatment could be successful.
Induced coma

In 2005, American teenager Jeanna Giese survived an infection of rabies unvaccinated. She was placed into an
induced coma upon onset of symptoms and given ketamine, midazolam, ribavirin, and amantadine. Her doctors
administered treatment based on the hypothesis that detrimental effects of rabies were caused by temporary
dysfunctions in the brain and could be avoided by inducing a temporary partial halt in brain function that would
protect the brain from damage while giving the immune system time to defeat the virus. After thirty-one days of
isolation and seventy-six days of hospitalization, Giese was released from the hospital.[23]
Giese's treatment regimen became known as the "Milwaukee protocol". To date only one other patient has
survived under the protocol, despite numerous attempts at the treatment. Rodney Willoughby Jr., Giese's
primary care physician, has asserted that subsequent failures occurred because patients were not given the same
combination of drugs used in the initial incident.[citation needed]
On April 10, 2008 in Cali, Colombia, an eleven year-old boy was reported to survive rabies and the induced
coma without noticeable brain damage.
Ketamine
The anesthetic drug ketamine has shown the potential for rabies virus inhibition in rats.
Prognosis
In unvaccinated humans, rabies is almost always fatal after neurological symptoms have
developed, but prompt post-exposure vaccination may prevent the virus from progressing.
Rabies kills around 55,000 people a year, mostly in Asia and Africa. There are only six known
cases of a person surviving symptomatic rabies, and only three known cases of survival in which
the patient received no rabies-specific treatment either before or after illness onset.

Financial Consequences of Not Pre-vaccinating

n Thailand, rabies remains a neglected disease with authorities continuing to rely on human death
statistics while ignoring the financial burden resulting from an enormous increase in post-exposure
prophylaxis.
Past attempts to conduct a mass dog vaccination and sterilization program have been limited to Bangkok city
and have not been successful. In Thailand, 20 rabies deaths were reported in 2003, compared to 200 a decade
before as stepped up post exposure prophylaxis (PEP) immunoglobulin have reduced deaths. However, the
financial burden of rabies has skyrocketed as 400,000 people received PEP, versus 90,000 in 1991. (PEP is
more than 10 times more expensive to administer than pre-exposure (PREP) for those who haven't had PREP,
and the cost is more than half the per capita annual income of the average citizen). The percentage of rabies
infectivity of samples sent to diagnostic laboratories all over the country remains high, within the range of 30–
40%. In China, this is the case as well as governments pour resources into PEP rather than vaccination
programs.
Epidemiology
Rabies transmission

TEM micrograph with numerous rabies virions (small dark grey rodlike particles) and Negri bodies
(the larger pathognomonic cellular inclusions of rabies infection)

Any warm-blooded animal, including humans, may become infected with the rabies virus and develop
symptoms. Indeed, the virus has even been adapted to grow in cells of poikilothermic vertebrates though natural
transmission has only been documented among mammals. Most animals can be infected by the virus and can
transmit the disease to humans. Infected bats, monkeys, raccoons, foxes, skunks, cattle, wolves, coyotes, dogs,
mongoose (normally yellow mongoose)[citation needed] or cats present the greatest risk to humans. Rabies may also
spread through exposure to infected domestic farm animals, groundhogs, weasels, bears and other wild
carnivores. Rodents (mice, squirrels etc) are seldom infected.
The virus is usually present in the nerves and saliva of a symptomatic rabid animal.[35][36] The route of infection
is usually, but not necessarily, by a bite. In many cases the infected animal is exceptionally aggressive, may
attack without provocation, and exhibits otherwise uncharacteristic behavior.
Transmission between humans is extremely rare. A few cases have been recorded through transplant surgery.
After a typical human infection by bite, the virus enters the peripheral nervous system. It then travels along the
nerves towards the central nervous system.[39] During this phase, the virus cannot be easily detected within the
host, and vaccination may still confer cell-mediated immunity to prevent symptomatic rabies. When the virus
reaches the brain, it rapidly causes encephalitis. This is called the prodromal phase, and is the beginning of the
symptoms. Once the patient becomes symptomatic, treatment is almost never effective and mortality is over
99%. Rabies may also inflame the spinal cord producing transverse myelitis.
Prevalence
Prevalence of rabies
Rabies-free jurisdictions, as of January 2006: Australia, New Zealand, Singapore, Fiji, Papua New
Guinea, Indonesian provinces of Irian Jaya and West Papua on the island of New Guinea,
Germany, Austria, Guam, Hawaii, the United Kingdom, the Republic of Ireland, Norway, Sweden,
Finland, Iceland, Japan, Taiwan, Sardinia and Corsica

The rabies virus survives in widespread, varied, rural fauna reservoirs. It is present in animal populations of
every countries of the world, except in New Zealand. In some countries like those in western Europe and
Oceania, rabies is considered to be prevalent among bat populations only.
In Asia, parts of the Americas and large parts of Africa, dogs remain the principal host. Mandatory vaccination
of animals is less effective in rural areas. Especially in developing countries, pets may not be privately kept and
their destruction may be unacceptable. Oral vaccines can be safely distributed in baits, and this has successfully
reduced rabies in rural areas of France, Ontario, Texas, Florida and elsewhere, like the City of Montréal,
Québec, where baits are successfully used on raccoons in the Mont-Royal park area. Vaccination campaigns
may be expensive, and a cost-benefit analysis can lead those responsible to opt for policies of containment
rather than elimination of the disease.
There are an estimated 55,000 human deaths annually from rabies worldwide, with about 31,000 in Asia, and
24,000 in Africa. One of the sources of recent flourishing of rabies in East Asia is the pet boom. China
introduced in the city of Beijing the “one-dog policy” in November 2006 to control the problem.India has been
reported as having the highest rate of human rabies in the world, primarily because of stray dogs.[As of 2007,
Vietnam had the second-highest rate, followed by Thailand; in these countries too the virus is primarily
transmitted through canines (feral dogs and other wild canine species). Recent reports suggest that wild rabid
dogs are roaming the streets. Because much cheaper pre-vaccination is not commonly administered in places
like Thailand, the expense for lack of preparation with far more costly post-exposure prophylaxis can hit
families hard.
Rabies was once rare in the United States outside the Southern states, but as of 2006, raccoons in the mid-
Atlantic and northeast United States had been suffering from a rabies epidemic since the 1970s, which was
moving westwards into Ohio. In the midwestern United States, skunks are the primary carriers of rabies,
comprising 134 of the 237 documented non-human cases in 1996[update].
History
Cultural impact

Because of its potentially violent nature, rabies has been known since 3500 B.C.E. The first written record of
rabies is in the Codex of Eshnunna (ca. 1930 BC), which dictates that the owner of a dog showing symptoms of
rabies should take preventive measure against bites. If another person was bitten by a rabid dog and later died,
the owner was fined heavily.
Rabies was considered a scourge for its prevalence in the 19th century. Fear of rabies related to methods of
transmissions was almost irrational; however, this gave Louis Pasteur ample opportunity to test post-exposure
treatments from 1885.