Influenza A (H1N1) virus is a subtype of influenza A virus and the most common In April 2009, an outbreak of Influenza-like illness

a-like illness occurred in Mexico and the USA

cause of influenza (flu) in humans. Some strains of H1N1 are endemic in humans
and cause a small fraction of all influenza-like illness and a small fraction of all
seasonal influenza. H1N1 strains caused a few percent of all human flu infections in
2004–2005. Other strains of H1N1 are endemic in pigs (swine influenza) and in birds
(avian influenza).
In June 2009, the World Health Organization declared the new strain of swine-origin
H1N1 as a pandemic. This strain is often called swine flu by the public media.
Swine influenza
the CDC reported seven cases of novel A/H1N1 influenza. By April 24 it became clear
that the outbreak of ILI in Mexico and the confirmed cases of novel influenza A in the
southwest US were related and WHO issued a health advisory on the outbreak of
"influenza like illness in the United States and Mexico". The disease then spread
very rapidly, with the number of confirmed cases rising to 2,099 by May 7, despite
aggressive measures taken by the Mexican government to curb the spread of the
disease.
On June 11, 2009, the WHO declared an H1N1 pandemic, moving the alert level to
phase 6, marking the first global pandemic since the 1968 Hong Kong flu.

Swine influenza (also called swine flu, hog flu, or pig flu) is an infection by any one of
several types of swine influenza virus. Swine influenza virus (SIV) is any strain of the
influenza family of viruses that is endemic in pigs. As of 2009, the known SIV strains
include influenza C and the subtypes of influenza A known as H1N1, H1N2, H3N1,
H3N2, and H2N3.
Swine influenza virus is common throughout pig populations worldwide.
Transmission of the virus from pigs to humans is not common and does not always
lead to human influenza, often resulting only in the production of antibodies in the
blood. If transmission does cause human influenza, it is called zoonotic swine flu.
People with regular exposure to pigs are at increased risk of swine flu infection. The
meat of an infected animal poses no risk of infection when properly cooked.
On October 25, 2009 U.S. President Barack Obama officially declared H1N1 a
national emergency[18]
November 29, 2009 worldwide update by the U.N.'s World Health Organization
(WHO) states that "207 countries and overseas territories/communities have
reported laboratory confirmed cases of pandemic influenza H1N1 2009, including at
least 8,768 deaths."
January 15, 2010 worldwide update by the U.N.'s World Health Organization (WHO)
states that "208 countries and overseas territories or communities have reported
laboratory confirmed cases of pandemic influenza H1N1 2009, including at least
13,554 deaths."

During the mid-20th century, identification of influenza subtypes became possible,
allowing accurate diagnosis of transmission to humans. Since then, only 50 such
transmissions have been confirmed. These strains of swine flu rarely pass from
human to human. Symptoms of zoonotic swine flu in humans are similar to those of
influenza and of influenza-like illness in general, namely chills, fever, sore throat,
muscle pains, severe headache, coughing, weakness and general discomfort. The
recommended time of isolation is about five days.
A study conducted in coordination with the University of Michigan Health Service is
scheduled for publication in the December 2009 American Journal of Roentgenology
warning that H1N1 flu can cause pulmonary embolism, surmised as a leading cause
of death in this current pandemic. The study authors suggest physician evaluation
via contrast enhanced CT scans for the presence of pulmonary emboli when caring
for patients diagnosed with respiratory complications from a "severe" case of the
H1N1 flu

2009 A(H1N1) pandemic 1. What is Influenza A (H1N1)?

In the 2009 flu pandemic, the virus isolated from patients in the United States was • Influenza A(H1N1) is caused by a novel virus that resulted from the reassortment
found to be made up of genetic elements from four different flu viruses – North of 4 viruses from pigs, human and birds
American swine influenza, North American avian influenza, human influenza, and • It is a new virus causing illness in people
swine influenza virus typically found in Asia and Europe – "an unusually mongrelised • It was first detected in people in April 2009 in the United States
mix of genetic sequences."[12] This new strain appears to be a result of reassortment • This virus is spreading from person-to-person, probably in much the same way that
of human influenza and swine influenza viruses, in all four different strains of regular seasonal influenza viruses spread
subtype H1N1. • There is no vaccine yet to protect humans from this virus
• There are existing and recommended medicines that are effective in treating
Preliminary genetic characterization found that the hemagglutinin (HA) gene was these Influenza A(H1N1)
similar to that of swine flu viruses present in U.S. pigs since 1999, but the • Influenza A(H1N1) can be fatal to humans due to severe respiratory distress
neuraminidase (NA) and matrix protein (M) genes resembled versions present in (pneumonia)
European swine flu isolates. The six genes from American swine flu are themselves
mixtures of swine flu, bird flu, and human flu viruses. While viruses with this genetic 2. Why this new Influenza A(H1N1) virus is sometimes called “swine flu”?
makeup had not previously been found to be circulating in humans or pigs, there is
no formal national surveillance system to determine what viruses are circulating in
pigs in the U.S. This virus was originally referred to as “swine flu” because laboratory tests showed
that many of the genes in this new virus were very similar to influenza viruses that
normally occur in pigs in North America. But further study has shown that this new
virus is very different from what normally circulates in North American pigs. It has
two genes from flu viruses that normally circulate in pigs in Europe and Asia and • Infected person maybe contagious from one day before they develop symptoms to
avian genes and human genes. Scientists call this a “quadruple reassortant” virus. up to 7 days after they get sick. Children might potentially be contagious for longer
periods.
3. What are the signs and symptoms of this virus in people?
The symptoms of this new H1N1 flu virus in people are similar to the symptoms of 9. Are there medicines to treat infection with AH1N1?
seasonal flu and include:
Are there medicines to treat infection with this new virus?
Yes. CDC recommends the use of oseltamivir or zanamivir for the treatment and/or
prevention of infection with the new H1N1 flu virus. Antiviral drugs are prescription
medicines (pills, liquid or an inhaler) that fight against the flu by keeping flu viruses
1. fever
from reproducing in your body. If you get sick, antiviral drugs can make your illness
2. chills
milder and make you feel better faster. They may also prevent serious flu
3. headache
complications. During the current outbreak, the priority use for influenza antiviral
4. nasal congestion or runny nose
drugs during is to treat severe influenza illness.You have to consult a doctor
5. sore throat
before using these drugs to avoid resistance.
6. cough
7. body aches or lethargy
8. lack of appetite 10. Is vaccine available to protect people from getting infected with
9. nausea or vomiting AH1N1?
10. diarrhea
Also, like seasonal flu, severe illnesses and death has occurred as a result
No, at present there is no vaccine against this virus.
of illness associated with this virus.

11. Is there a pandemic risk on Influenza A(H1N1)?

4. How severe is illness associated with this virus?

Yes. If the Influenza A(H1N1) establishes efficient and sustained human-to-human

It is not known at this time how severe this virus will be in the general population.
transmission then it can cause an influenza pandemic. The impact of a pandemic is
Experts are studying the medical histories of people who have been infected with
difficult to predict. It depends on virulence of the virus, existing immunity among
this virus to determine whether some people may be at greater risk from infection,
people, cross protection by antibodies acquired from seasonal influenza infection
serious illness, or hospitalization from the virus.
and host factors.

5. How does Influenza A(H1N1) virus spread?

Prevention & Treatment

• Coughing or sneezing by people with influenza

12. What can I do to protect myself from getting sick?
There is no vaccine available right now to protect against this new H1N1 virus. There
• Touching things with flu viruses on it and then touching one’s mouth, nose or eyes are everyday actions that can help prevent the spread of germs that cause
respiratory illnesses like influenza.
6. Can I get infected with Influenza A(H1N1) from eating or preparing
pork? Take these everyday steps to protect your health:

• No, you can’t get influenza A(H1N1) by eating properly handled and thorough • Cover your nose and mouth with a tissue when you cough or sneeze. Throw
cooked pork and pork products the tissue in the trash after you use it.
• The virus is killed by cooking temperatures of 160 F/70 C.
• Wash your hands often with soap and water, especially after you cough or
sneeze. Alcohol-based hand cleaners are also effective.
7. What is the incubation period?
• Avoid touching your eyes, nose or mouth. Germs spread this way.
• Try to avoid close contact with sick people.
• 7 to 10 days from the time of exposure to the first onset of signs and symptoms
• Stay home if you are sick for 7 days after your symptoms begin or until you
have been symptom-free for 24 hours, whichever is longer. This is to keep
8. How long can an infected person spread Influenza A(H1N1) to others? from infecting others and spreading the virus further.

• Follow public health advice regarding school closures, avoiding crowds and
other social distancing measures.
 • Be prepared in case you get sick and need to stay home for a week or so; a
supply of over-the-counter medicines, alcohol-based hand rubs, tissues and
other related items might could be useful and help avoid the need to make
trips out in public while you are sick and contagious.
13. What is the best way to keep from spreading the virus through
coughing or sneezing?
If you are sick, limit your contact with other people as much as possible. If you are
sick, stay home for 7 days after your symptoms begin or until you have been
symptom-free for 24 hours, whichever is longer. Cover your mouth and nose with a
tissue when coughing or sneezing. Put your used tissue in the waste basket. Then,
clean your hands, and do so every time you cough or sneeze.
14. What should I do if I get sick?
If you live in areas where people have been identified with new H1N1 flu and
become ill with influenza-like symptoms, including fever, body aches, runny or stuffy
nose, sore throat, nausea, or vomiting or diarrhea, you should stay home and avoid
contact with other people. Staying at home means that you should not leave your
home except to seek medical care. This means avoiding normal activities, including
work, school, travel, shopping, social events, and public gatherings
If you have severe illness or you are at high risk for flu complications, contact your
health care provider or seek medical care. Your health care provider will determine
whether flu testing or treatment is needed
If you become ill and experience any of the following warning signs, seek emergency
medical care.
In children, emergency warning signs that need urgent medical attention
include:
• Fast breathing or trouble breathing
• Bluish or gray skin color
• Not drinking enough fluids
• Severe or persistent vomiting
• Not waking up or not interacting
• Being so irritable that the child does not want to be held
• Flu-like symptoms improve but then return with fever and worse cough
In adults, emergency warning signs that need urgent medical attention
include:
• Difficulty breathing or shortness of breath
• Pain or pressure in the chest or abdomen
• Sudden dizziness
• Confusion
• Severe or persistent vomiting
• Flu-like symptoms improve but then return with fever and worse cough
15. Contamination & Cleaning
How long can influenza virus remain viable on objects (such as books and
doorknobs)?
Studies have shown that influenza virus can survive on environmental surfaces and
can infect a person for up to 2-8 hours after being deposited on the surface.
What kills influenza virus?
Influenza virus is destroyed by heat (167-212°F [75-100°C]). In addition, several
chemical germicides, including chlorine, hydrogen peroxide, detergents (soap),
iodophors (iodine-based antiseptics), and alcohols are effective against human
influenza viruses if used in proper concentration for a sufficient length of time. For
example, wipes or gels with alcohol in them can be used to clean hands. The gels
should be rubbed into hands until they are dry.
What surfaces are most likely to be sources of contamination?
Germs can be spread when a person touches something that is contaminated with
germs and then touches his or her eyes, nose, or mouth. Droplets from a cough or
sneeze of an infected person move through the air. Germs can be spread when a
person touches respiratory droplets from another person on a surface like a desk, for
example, and then touches their own eyes, mouth or nose before washing their
hands.
How should waste disposal be handled to prevent the spread of influenza
virus?
To prevent the spread of influenza virus, it is recommended that tissues and other
disposable items used by an infected person be thrown in the trash. Additionally,
persons should wash their hands with soap and water after touching used tissues
and similar waste.
What household cleaning should be done to prevent the spread of
influenza virus?
To prevent the spread of influenza virus it is important to keep surfaces (especially
bedside tables, surfaces in the bathroom, kitchen counters and toys for children)
clean by wiping them down with a household disinfectant according to directions on
the product label.
How should linens, eating utensils and dishes of persons infected with
influenza virus be handled?
Linens, eating utensils, and dishes belonging to those who are sick do not need to
be cleaned separately, but importantly these items should not be shared without
washing thoroughly first.
Linens (such as bed sheets and towels) should be washed by using household
laundry soap and tumbled dry on a hot setting. Individuals should avoid “hugging”
laundry prior to washing it to prevent contaminating themselves. Individuals should
wash their hands with soap and water or alcohol-based hand rub immediately after
handling dirty laundry.
Eating utensils should be washed either in a dishwasher or by hand with water and
soap.
Avian influenza, or "bird flu," is a contagious disease of animals caused by viruses
that normally infect only birds and, less commonly, pigs. While all bird species are
thought to be susceptible to infection, domestic poultry flocks are especially
vulnerable to infections that can rapidly reach epidemic proportions.
The disease in birds has two forms. The first causes mild illness, sometimes
expressed only as ruffled feathers or reduced egg production. Of greater concern is
the second form, known as "highly pathogenic (disease-causing) avian influenza."
This form, first recognized in Italy in 1878, is extremely contagious in birds and
rapidly fatal, with a mortality approaching 100 percent. Birds can die on the same
day that symptoms first appear.
HOW BIRD FLU SPREADS WITHIN A COUNTRY
Within a country, the disease spreads easily from farm to farm. Large amounts of
virus are secreted in bird droppings, contaminating dust and soil. Airborne viruses
can move from bird to bird, causing infection when the virus is inhaled. The virus
can also be carried on the feet and bodies of animals like rodents that function as
mechanical vectors, or agents that physically take the virus from one point to
another. Contaminated equipment, vehicles, feed, cages or clothing--especially
shoes--can carry the virus from farm to farm. Limited evidence suggests that flies
can also act as mechanical vectors.
Droppings from infected wild birds can introduce the virus into both commercial and
backyard poultry flocks. The risk that infection will be transmitted from wild birds to
domestic poultry is greatest where domestic birds roam freely, share a water supply
with wild birds, or use a water supply that might become contaminated by droppings
from infected wild-bird carriers.
So-called "wet" markets, where live birds are sold under crowded and sometimes
unsanitary conditions, can be another source of spread.
HOW BIRD FLU SPREADS FROM COUNTRY TO COUNTRY
The disease can spread from country to country through international trade in live
poultry. Migratory birds, including wild waterfowl, sea birds and shore birds, can
carry the virus for long distances and have in the past been implicated in the
international spread of highly pathogenic avian influenza. Migratory waterfowl--most
notably wild ducks--are the natural reservoir of bird flu viruses, and these birds are
also the most resistant to infection. They can carry the virus over great distances
and excrete it in their droppings, yet develop only mild and short-lived illness.
Domestic ducks, however, are susceptible to lethal infections, as are turkeys, geese
and several other species raised on commercial or backyard farms.
H5N1: THREAT TO HUMANS
Since mid-December 2003, a growing number of Asian countries have reported
outbreaks (see "Advice to international travelers") of highly pathogenic avian
influenza in chickens and ducks. Infections in several species of wild birds and in
pigs have also been reported.
The rapid spread of highly pathogenic avian influenza, with outbreaks occurring at
the same time in several countries, is historically unprecedented and of great
concern for human health as well as for agriculture.
Public health officials are alarmed by the unprecedented outbreaks in poultry for
several reasons. First, most--but not all--of the major outbreaks recently reported in
Asia have been caused by the highly pathogenic H5N1 strain. H5N1 has jumped the
species barrier, causing severe disease in humans on two occasions in the recent
past, and is now doing so again in gradually growing numbers in Vietnam and
Thailand.
Who could be the probable host or carriers of this disease?
Migratory waterfowl – most notably wild ducks – are the natural reservoir of avian
influenza viruses, and these birds are also the most resistant to infection. Domestic
poultry, including chickens and turkeys, are particularly susceptible to epidemics of
rapidly fatal influenza.
Direct or indirect contact of domestic flocks with wild migratory waterfowl has been
implicated as a frequent cause of epidemics. Live bird markets have also played an
important role in the spread of epidemics.
What could be the possible implication of this disease to our country?
Recent research has shown that viruses of low pathogenicity can, after circulation
for sometime short periods in a poultry population, mutate into highly pathogenic
viruses. During a 1983–1984 epidemic in the United States of America, control of the
outbreak required destruction of more than 17 million birds at a cost of nearly US$
65 million. During a 1999–2001 epidemic in Italy, more than 13 million birds died or
were destroyed. In the absence of prompt control measures backed by good
surveillance, epidemics can last for years. For example, an epidemic of H5N2 avian
influenza, which began in Mexico in 1992, started with low pathogenicity, evolved to
the highly fatal form, and was not controlled until 1995.
Why is avian influenza not vulnerable to eradication?
All type A influenza viruses, including those that regularly cause seasonal epidemics
of influenza in humans, are genetically labile and well adapted to elude host
defenses. Influenza viruses lack mechanisms for the “proofreading” and repair of
errors that occur during replication. As a result of these uncorrected errors, the
genetic composition of the viruses changes as they replicate in humans and
animals, and the existing strain is replaced with a new antigenic variant. These
constant, permanent and usually small changes in the antigenic composition of
influenza A viruses are known as antigenic “drift”.
Influenza viruses have a second characteristic of great public health concern:
influenza A viruses, including subtypes from different species, can swap or
“reassort” genetic materials and merge. This reassortment process, known as
antigenic “shift”, results in a novel subtype different from both parent viruses. As
populations will have no immunity to the new subtype, and as no existing vaccines
can confer protection, antigenic shift has historically resulted in highly lethal
pandemics.
Conditions favorable for the emergence of antigenic shift have long been thought to
involve humans living in close proximity to domestic poultry and pigs. Because pigs
are susceptible to infection with both avian and mammalian viruses, including
human strains, they can serve as a “mixing vessel” for the scrambling of genetic
material from human and avian viruses, resulting in the emergence of a novel
subtype. Recent events, however, have identified a second possible mechanism.
Evidence is mounting that, for at least some of the 15 avian influenza virus subtypes "stomach flu" or "24-hour flu".
circulating in bird populations, humans themselves can serve as the “mixing
vessel”. Typically, influenza is transmitted through the air by coughs or sneezes, creating
aerosols containing the virus. Influenza can also be transmitted by bird droppings,
saliva, nasal secretions, feces and blood. Infections also occur through contact with
How could it possibly affect humans?
these body fluids or with contaminated surfaces. Airborne aerosols may be
responsible for most infections, although which of the various means of transmission
Avian influenza viruses do not normally infect species other than birds and pigs. is most important is not absolutely clear.
The first documented infection of humans with an avian influenza virus occurred in
Hong Kong in 1997, when the H5N1 strain caused severe respiratory disease in 18
Influenza viruses can be inactivated (killed) by sunlight, disinfectants and
humans, of whom 6 died. The infection of humans coincided with an epidemic of
detergents. As the virus can be inactivated by soap, frequent hand washing reduces
highly pathogenic avian influenza, caused by the same strain, in Hong Kong’s
the risk of infection.
poultry population.

Extensive investigation of that outbreak determined that close contact with live Virology
infected poultry was the source of human infection. Studies at the genetic level In their natural state, Ebola viruses appear either as long filamentous forms, hence
further determined that the virus had jumped directly from birds to humans. Limited the
transmission to health care workers occurred, but did not cause severe disease. name Filovirus, or as shorter "U"-shaped, "6"-shaped or circular forms. The
filamentous forms
vary in length (up to 14,000 nm), but the length associated with peak infectivity
Rapid destruction – within three days – of Hong Kong’s entire poultry population, appears to be
estimated at around 1.5 million birds, reduced opportunities for further direct around 970 nm. The filaments have a uniform diameter of 80 nm. They are
transmission to humans, and may have averted a pandemic. composed of a helical
nucleocapsid (50 nm in diameter, with an axial space 20 nm in diameter and a
That event alarmed public health authorities, as it marked the first time that an helical periodicity
avian influenza virus was transmitted directly to humans and caused severe illness of about 5 nm), an envelope composed of material derived from host-cell plasma
with high mortality. Alarm mounted again in February 2003, when an outbreak of membrane, and
H5N1 avian influenza in Hong Kong caused 2 cases and 1 death in members of a a surface layer with 10-nm-long glycoprotein projections studded out of it. Ebola
family who had recently traveled to southern China. virions contain
one molecule of non-infectious, linear, negative-sense, single -stranded RNA and
seven
The most recent cause for alarm occurred in January 2004, when laboratory tests polypeptides.
confirmed the presence of H5N1 avian influenza virus in human cases of severe Viral replication is similar to that of other negative-stranded RNA viruses containing
respiratory disease in the northern part of Viet Nam. a
monopartite genome, such as rhabdovimses and paramyxoviruses, Proteins are
What are the symptoms and treatment for human cases of avian influenza? produced via a
monocistronic, polyadenylated mRNA molecule. As in the rhabdoviruses and
inparamyxoviruses,
Published information about the clinical course of human infection with H5N1 avian the gene closest to the 3' end encodes of the major nucleoprotein.
influenza is limited to studies of cases in the 1997 Hong Kong outbreak. In that The mode of entry of the virus into cells remains unknown. Infection occurs in the
outbreak, patients developed symptoms of fever, sore throat, cough, and, in several presence of antibody, and no neutralizing antibodies have yet been demonstrated.
of the fatal cases, severe respiratory distress secondary to viral pneumonia. Uncoating is
Previously healthy adults and children, and some with chronic medical conditions, presumed to occur in a manner similar to that of other negative-strand RNA viruses.
were affected. Messenger
RNA can be detected in infected cells, but virion RNA is not detectable. This means
Influenza, commonly referred to as the flu, is an infectious disease caused by RNA that genomic
viruses of the family Orthomyxoviridae (the influenza viruses), that affects birds and RNA is packaged very rapidly after transcription, and that nucleocapsids are rapidly
mammals. released
from the cell.
Tissue culture-adapted strains of Ebola produce a striking cytopathic effect in
The most common symptoms of the disease are chills, fever, sore throat, culture,
muscle pains, severe headache, coughing, weakness and general discomfort. intracytoplasmic vesiculation and mitochondrial swelling are followed by breakdown
Fever and coughs are the most frequent symptoms. In more serious cases, of
influenza causes pneumonia, which can be fatal, particularly for the young and the organelles and terminal cytoplasmic rarification or condensation. These cytoplasmic
elderly. Although it is often confused with the common cold, influenza is a much changes
more severe disease and is caused by a different type of virus. Influenza may occur at the same time as accumulation of massive amounts of viral nucleocapsid
produce nausea and vomiting, particularly in children, but these symptoms are more protein in
common in the unrelated disease gastroenteritis, which is sometimes called
intracytoplaspamic inclusion bodies. Assembled nucleocapsids bud through the The route of transmission from animals to humans is unknown. Researchers theorize
plasma it is transmitted to the first patient by an infected animal. Then it spreads in several
membrane, acquiring an envelope of membrane-derived material on the way. ways, like direct contact with the blood and/or secretions of an infected person or
Ebola virus infectivity is quite stable at room temperature (20°C) but is destroyed in contact with infected objects such as syringes.
30
minutes at 60°C. Infectivity is also destroyed by ultraviolet and gamma irradiation,
All Ebola virus species have displayed the ability to be spread through airborne
lipid solvents,
particles under research conditions. While undocumented among humans, the
b-propiolactone, and commercial hypochlorite and phenolic disinfectants.
Ebola-Reston virus was transmitted from monkey to monkey through the air.
Laboratory studies on filoviruses present an extreme biohazard and should be
conducted
only under high-containment conditions. Specimens for virus isolation and serology In Africa, the first cases of Ebola infections in humans were linked to contact with
must be wild mammals found dead in the rainforest (gorillas, chimpanzees, monkeys, forest
regards as potentially infectious and laboratory diagnosis of these infections can antelopes, duikers and porcupines).
only be carried
out in specialized laboratories equipped to handie them. Antibodies to Ebola virus,
After an incubation period from two to 21 days, Ebola hemorrhagic fever appears
both IgG and
suddenly. Symptoms include fever, headache, joint and muscle aches, sore throat
IgM, were originally detected by immunofluorescence, but are now more routinely
and weakness, followed by diarrhea, vomiting and stomach pain. A rash, red eyes,
detected by
hiccups, internal and external bleeding may be seen in some patients.
ELISA. Viral antigen can be detected by ELISA, and viral RNA by reverse
transcriptionpolymerase
chain reaction. Fatalities involve those who have not developed a significant immune response to
the virus at the time of death. The cause of death is usually due to organ failure and
blood loss.
Hemorrhagic fever

There is no standard treatment for Ebola hemorrhagic fever. No vaccine is available

The Ebola virus is one of two members of a family of RNA viruses called the
and treatment is supportive care, including infusion of intravenous fluids. Patients
Filoviridae (filovirus) and is comprised of five distinct species: Zaïre, Sudan, Côte
are treated for complicating infections, their fluids and electrolytes, oxygen status
d’Ivoire, Bundibugyo and Reston.
and blood pressure maintained.

Zaïre, Sudan and Bundibugyo species have been associated with large Ebola
Because it favors spread within health-care facilities, infection control includes the
hemorrhagic fever outbreaks in Africa with high case fatality ratio (25 percent to 90
wearing of protective clothing such as masks, gloves, gowns and goggles; complete
percent) while Côte d’Ivoire and Reston have not.
equipment sterilization; and isolation.

The Ebola-Reston species can infect humans but no serious illness or death in
All are designed to prevent any person’s contact with the blood or secretions of any
humans has been reported to date.
patient.

Ebola viruses are normally transmitted via contact with the blood or other bodily
Not over two years ago, in August 2007, over 217 people became ill with the Ebola
fluids of an infected animal or person.
virus in the village of Kampungu, Democratic Republic of the Congo (DRC); 103 died.
Before that, in 1995, 245 people died in the DRC.
It is believed that the virus is animal-borne and is normally maintained in an animal
host in Africa. A similar host is probably associated with Ebola-Reston in the
And what is Marburg that so horrified Stephen King? The Marburg virus was actually
Philippines.
the first hemorrhagic fever identified that was caused by a filovirus.

The virus is not known to be native to other continents, such as North America.
One in four patients died in the initial outbreak in a laboratory in 1967 in Marburg
and Frankfurt am Mein, Germany. The virus was introduced by imported African
Ebola hemorrhagic fever was first recognized in 1976. It is a severe, often-fatal green monkeys from Uganda.
disease in humans and monkeys, gorillas and chimpanzees caused by infection with
the Ebola virus, named after a river in the Democratic Republic of the Congo
More than 80 percent of patients died of Marburg infection in the Democratic
(formerly Zaire) in Africa.
Republic of Congo from 1998 to 2000, and even more than that in Angola in late
2004.
Infections with the Ebola virus are acute. Because the natural reservoir (or the
carrier) of the virus is unknown, the manner in which the virus first appears in a Source: World Health Organization
human at the start of an outbreak has not been determined.
he Ebola Reston Virus made headlines in late 2008 when some pigs in the
Philippines were tested positive for the virus. In January 2009, a worker in a pig farm
was reported to have been infected with Ebola Reston. This was the first case of the
virus being transmitted from a pig to a human, and became a cause of concern
worldwide.
The Ebola Reston is among the four subtypes of the Ebola virus. The big difference is
that out of the four, which originated in Africa, Ebola Reston does not cause
hemorrhagic symptoms. Even though it can prove fatal to monkeys, the Asian
filovirus is not pathogenic to humans.
History of The Ebola Reston Virus
The virus was first discovered in November 1989 during an investigation on a Simian
hemorrhagic fever outbreak. The investigation was conducted at Hazleton
Laboratories Reston in Virginia. The scientists discovered filoviruses that look just
like the tissue samples they have taken from a Crab-eating Macaque imported from
the Philippines. During the next few years, the Center for Disease and Control
Prevention (CDC) conducted investigations on the prevalence and effect of the virus
on monkeys. They found out that compared to monkeys infected with the African
filovirus, those with the Asian filovirus survived the illness and has no fatal effect on
humans.
Several incidents of the strain re-emerged in Italy in 1992 and the Philippines in
1996 and 2008. The CDC is conducting further investigation on the recent infections.
The discovery of the Ebola Reston virus became a concern especially among the
people in the Philippines. Filipinos want to make sure that the pork that they eat is
safe for consumption. According to the Department of Health, pork products in the
country are generally safe, given that the meat is prepared in hygienic conditions
and cooked thoroughly. Proper cooking eliminates viruses from all types of meat.
The DOH stresses however that meat that came from sick and dead (double) pigs
should not be eaten under any circumstances. These animals should be reported to
the Bureau of Animal Industry and the Department of Agriculture's National Meat
Inspection Service. They also advise the public to buy meat from stores certified by
the National Meat Inspection Service.
What is the Ebola Reston virus?
- There are five distinct species of the Ebola virus: Zare, Sudan, Cte d'Ivoire,
Bundibugyo and Reston. The Zare, Sudan and Bundibugyo species have been
associated with large Ebola hemorrhagic fever (EHF) outbreaks in Africa with high
mortality rates of between 25 percent and 90 percent while Cte d'Ivoire and Reston
have not.
How is Ebola-Reston different from the Ebola virus that was responsible for
many deaths in Africa?
- The Reston species can infect humans but no serious illness or death in humans
have been reported to date. During outbreaks of the Reston strain in monkeys in the
1990s, a small number of people (around 25) were found to have antibodies against
Ebola Reston. This means they had been infected by the virus and their body had
produced an immune response. However, only one person had mild, flu-like
symptoms. This person fully recovered. The other people who tested positive for
antibodies did not have any symptoms or illness.
What's different this time?
- This is the first time that Ebola-Reston has been found in pigs and a pig farm
worker has tested positive for Ebola Reston antibodies, which means that the worker
was probably infected by a pig, although there is no proof of this. Pigs are worrisome
because they are mixing vessels for many types of viruses and bacteria and if left
uncontrolled, experts fear Ebola-Reston could mutate into a form that is more
transmissible among people.
Should the outbreak of Ebola in Philippines be a concern?
- Unlike monkeys, pigs are farmed for food and far more people are exposed to
them, which puts them at risk of getting infected if the epidemic in pigs is not under
control.
What precautions can be taken?
- Basic good hygiene practices and food handling measures. Ebola viruses are
normally transmitted via contact with the blood or other bodily fluids of an infected
animal or person. In all situations, even in the absence of identified risks, meat
handling and preparation should be done in a clean environment (table top, utensils,
knives) and meat handlers should follow good personal hygiene practices (e.g. clean
hands, clean protective clothing). In general, hands should be regularly washed
while handling raw meat.
Pork from healthy pigs is safe to eat as long as either the fresh meat is cooked
properly (i.e. 70 degrees Celsius in all part of the food, so that there is no pink meat
and the juices run clear), or, in the case of uncooked processed pork, national safety
standards have been met during production, processing and distribution.
Meat from sick pigs or pigs found dead should not be eaten and should not enter the
food chain or be given to other animals. (Sources: Food and Agriculture Organization
of the United Nations, the World Health Organization
Kawasaki disease or Kawasaki syndrome otherwise known as mucocutaneous
lymph node syndrome/disease and infantile polyarteritis, is a self-limiting non-
contagious vasculitis which is poorly understood. This condition affects many organs
in the body, including the skin, mucous membranes, lymph nodes, blood vessel
walls, and the heart. The disease got its name from a Japanese physician who first
described the disease in 1967 named Dr. Tomisaku Kawasaki. The highest incidence
of Kawasaki disease occurs in Japan, while there is an increasing incidence being the
most common cause of acquired heart disease among children in the United States.
Kawasaki disease afflicts predominantly young children, in fact, 80% of patients are
below 5 years of age. Additional predisposing risk factors include Asian race and the
male sex.
First identified in Japan in 1967, Kawasaki disease (also called mucocutaneous
lymph node syndrome) affects young children, usually under the age of 5. It is
believed to be caused by a noncontagious infection, although scientists are unsure sometimes resulting in a heart attack. However, modern treatment techniques have
of the exact cause. reduced the rate of coronary aneurysm to about 5 percent. Throughout the disease
course, however, various cardiac abnormalities may occur, including arrhythmias,
damage to the heart valves, pericarditis, and other cardiovascular problems.

Kawasaki disease is a self-limiting disease, meaning that symptoms appear for Kawasaki disease was first identified in Japan, where it is most common, in 1967 by
a short while and will go away on their own. Symptoms of Kawasaki include fever, a Japanese pediatrician named Dr. Tomisaku Kawasaki. The medical term for the
rash and swelling in the hands, feet and lymph nodes. The condition may also affect condition is mucocutaneous lymph node syndrome. Prior to Dr. Kawasaki’s
the linings of blood vessels and the heart muscle, and it can lead to aneurysms and description, some infants and children with this condition were said to have a
heart attack . condition called infantile periarteritis nodosa.

There is no known prevention for Kawasaki disease, although physicians have

Prompt treatment can dramatically reduce the likelihood of cardiovascular damage developed ways to treat the disease. Successful treatment depends on rapid
from the disease, and the overall mortality rate is low. Less than 1 percent of diagnosis and action. If treated within the first 10 days, the potential cardiovascular
children with Kawasaki disease die from it. Surgery or a catheter-based procedure is damage from Kawasaki disease can be dramatically limited.
also available to treat some long-term effects of the disease.

Signs and symptoms of Kawasaki disease

Kawasaki disease is a condition that primarily affects young children. It is believed There are three stages of Kawasaki disease, and each stage has its own associated
to be caused by a non-contagious infection, although scientists are unsure of the signs and symptoms. The classic symptom of Kawasaki disease is a persistent high
exact cause. About 80 percent of cases occur in children under the age of 5, and fever (sometimes up to 104˚F) that lasts for at least five days and does not respond
boys are more likely to get it than girls. to fever-reducing medications such as acetaminophen. In some cases, the fever may
last for up to two weeks.
Although a pathogen is suspected, scientists have been so far unable to identify the
virus or bacterium that causes Kawasaki disease. Some recent research suggests Because there is no lab test for Kawasaki disease, the U.S. Centers for Disease
that Kawasaki disease may be caused, in some children, by the New Haven Control and Prevention (CDC) has developed guidelines to help physicians. A
coronavirus, a newly discovered virus related to the severe acute respiratory diagnosis can be made if a child has a persistent high fever, combined with four of
syndrome (SARS) virus. While clinical data appears to suggest a link between these the five remaining signs and symptoms associated the acute phase. These include:
illnesses, further testing is required to substantiate a relationship between the two.
Stage 1: Week 1, the Acute Phase
Other studies have suggested a genetic component because siblings of affected
children are more likely to develop Kawasaki disease than children in the same
neighborhood. Also, people of Japanese descent are more likely to develop Kawasaki Signs and Symptoms Underlying Heart Conditions
disease no matter where they live in the world. It does, however, affect children of (in up to 20 percent
all races, and between 1,500 and over 4,000 cases are diagnosed in the United of patients)
States every year, according to the National Institutes of Health.
Persistent fever lasting longer Widening or inflammation of heart, blood
than four days despite vessels or valves, rarely arrhythmias or heart
Some recent research suggests that Kawasaki disease may be caused, in some medications attack may occur
children, by the New Haven coronavirus, a newly discovered virus related to the
severe acute respiratory syndrome (SARS) virus. While clinical data appears to Cracked, dry lips
suggest a link between these two illnesses, further testing is required to
substantiate a relationship between the two. Red tongue

During Kawasaki disease, the blood vessels may become inflamed. Kawasaki Oral mucosal changes
disease is a self-limiting disease, meaning that symptoms appear for a short while
and disappear on their own. The disease has three specific phases, each associated Very red or bloodshot eyes
with certain signs and symptoms. The most dangerous phase is the acute phase, (without pus or drainage)
which typically lasts from 10 to 14 days, depending on whether or how it is treated.
Overall, Kawasaki disease usually lasts between six and eight weeks, although it
may take a year or more for complete healing. Enlarged lymph nodes

Kawasaki disease is rarely fatal. Less than 1 percent of treated children will die Red, patchy rash over the
because of the disease. Among untreated children, up to 25 percent of children will whole body
experience coronary artery aneurysms in connection with the disease. This rate
drops to 10 to 15 percent among children who are treated. A coronary artery
aneurysm is a condition where part of the wall of the coronary artery bulges out,
 • Red, patchy rash over the whole body

Not all children will meet these criteria exactly. Children who have fewer than four of
Stage 2: Weeks 2 to 12, the Subacute Phase these symptoms may still be diagnosed with atypical Kawasaki disease. The
treatment course for this form of the disease is the same as for complete Kawasaki
disease.
Signs and Symptoms Underlying Heart Conditions
(in up to 20 percent of patients) The symptoms will be identified during a physical examination. Both children and
parents will also be asked questions about the patient’s medical history and family
Irritability Development of aneurysms and clots history. If the condition is suspected, tests such as the following may be ordered:
Poor appetite Thickening and blockage of arteries
• Echocardiogram. This test will be used to detect abnormalities in the
Peeling skin arteries. An echocardiogram uses high-frequency sound waves to develop
images of major arteries and the heart muscle. It is a safe and effective
diagnostic test for assessing the size and function of the heart and blood
vessels, and should identify most aneurysms that may be present. It is also
used to evaluate for fluid accumulation around the heart or leakage of the
heart valves.
Stage 3: When symptoms disappear, convalescence

• Electrocardiogram (EKG). This test measures the electrical activity of the

Signs and Symptoms Underlying Heart Conditions heart muscle and can identify the presence of ischemia (decreased blood
(in up to 20 percent flow caused by the narrowing of the blood vessels) or other factors that can
of patients) contribute to an increased risk of heart attack .

Disappearance of symptoms Scarring and calcification of arteries

Major aneurysms in the later stages of Kawasaki disease could lead to a more
immediate threat of complications. However, death as a direct result of this
condition is relatively infrequent.
The usual duration of an episode of Kawasaki disease is six to eight weeks. During
the healing period, which begins 45 days after onset and may take a year to
complete, the body is able to heal most of the cardiovascular damage it may have
sustained. However, damage to the coronary arteries may remain and could
increase the risk of heart attack in adulthood. In general, patients with confirmed
coronary artery aneurysms will require long-term follow-up. Even without signs of
damage by standard imaging techniques, there may be microscopic changes in the
walls of these arteries or in the tissues surrounding the arteries.
• Stress test. This test combines an EKG and/or echocardiogram with either
exercise or, for very young patients, a drug that causes the heart to react
as if the person were exercising. The goal is to detect cardiac ischemia
when the heart is physically stressed. Sometimes a nuclear perfusion study
may show if the coronary artery blood flow to the heart muscle is being
compromised.
• Urine test. This test may reveal pus (pyuria) or proteins (proteinuria) in the
urine. With Kawasaki disease there is inflammation of the urethra, the
channel that leads out from the bladder and this may lead to pyuria without
a bacteria being cultured.
• Computed tomography scan (CAT scan) and magnetic resonance
angiogram (MRA). Painless tests that are very useful for identifying
coronary aneurysms.

Diagnosis methods for Kawasaki disease
There is no single test that can identify Kawasaki disease. Instead, the U.S. Centers
for Disease Control & Prevention (CDC) has developed criteria to help physicians. If a
child has a persistent, unexplained fever for five days, and at least four of the
following symptoms, a diagnosis can be made. These symptoms include:
• Blood tests will often show an anemia or low blood red cell number. The
platelets, the components that are responsible for forming clots, will be
elevated. Platelet counts three or four times the normal levels are
frequently seen. Non specific tests for inflammation such as a
sedimentation rate (ESR) or C-reactive protein (CRP) are usually very
elevated and continue to rise as the disease progresses.

• Red tongue Treatment options for Kawasaki disease

• Oral-mucosal changes, including cracked, dry lips Children who have been diagnosed with Kawasaki disease are usually admitted to
• Pink eye (conjunctivitis) hospital, where gamma globulin is typically administered through an intravenous
• Enlarged lymph nodes (I.V.) line for 10 hours. This dramatically reduces the risk of damage to the coronary
arteries and diminishes the inflammatory process in general. The patient is also
given relatively high doses of aspirin for the first two weeks to reduce fever, swelling
and inflammation. Some other medications may also be employed depending on the
response of the child to the initial treatment. These may include steroids and
medications that inhibit clot formation.
This combination of medications tends to show good results within 24 hours.
Because gamma globulin may make the child less responsive to viral vaccines,
common childhood vaccines are generally delayed for a number of months after
treatment. For example, the measles-mumps-rubella vaccine is delayed for 11
months, and the chicken pox vaccine is delayed for at least five months.
After the initial course of high-dose aspirin, low-dose aspirin (or another antiplatelet)
will likely be prescribed for another four to six weeks to prevent the formation of
blood clots. Physical activity is also restricted during this time.
Systemic lupus erythematosus SLE or lupus, pronounced sɪˈstɛmɪk ˈluːpəs ˌɛrɨ
ˌθiːməˈtoʊsəs (help·info)) is a chronic autoimmune connective tissue disease that
can affect any part of the body. As occurs in other autoimmune diseases, the
immune system attacks the body’s cells and tissue, resulting in inflammation and
tissue damage.[1]
SLE most often harms the heart, joints, skin, lungs, blood vessels, liver, kidneys, and
nervous system. The course of the disease is unpredictable, with periods of illness
(called flares) alternating with remissions. The disease occurs nine times more often
in women than in men, especially between the ages of 15 and 50, and is more
common in those of non-European descent.
SLE is treatable through addressing its symptoms, mainly with corticosteroids and
immunosuppressants; there is currently no cure. SLE can be fatal, although with
recent medical advances, fatalities are becoming increasingly rare. Survival for
people with SLE in the United States, Canada, and Europe is approximately 95% at
five years, 90% at 10 years, and 78% at 20 years.[4]
Signs and symptoms
Common symptoms of SLE.
SLE is one of several diseases known as "the great imitators" because it often
mimics or is mistaken for other illnesses.[6] SLE is a classical item in differential
diagnosis,[2] because SLE symptoms vary widely and come and go unpredictably.
Diagnosis can thus be elusive, with some people suffering unexplained symptoms of
untreated SLE for years.
Common initial and chronic complaints include fever, malaise, joint pains, myalgias,
fatigue, and temporary loss of cognitive abilities. Because they are so often seen
with other diseases, these signs and symptoms are not part of the diagnostic criteria
for SLE. When occurring in conjunction with other signs and symptoms (see below),
however, they are considered suggestive.[7]
Dermatological manifestations
As many as 30% of sufferers have some dermatological symptoms (and 65% suffer
such symptoms at some point), with 30% to 50% suffering from the classic malar
rash (or butterfly rash) associated with the disease. Some may exhibit thick, red
scaly patches on the skin (referred to as discoid lupus). Alopecia; mouth, nasal, and
vaginal ulcers; and lesions on the skin are also possible manifestations.
Musculoskeletal manifestations
The most commonly sought medical attention is for joint pain, with the small joints
of the hand and wrist usually affected, although all joints are at risk. The Lupus
Foundation of America estimates that more than 90 percent of those affected will
experience joint and/or muscle pain at some time during the course of their illness. [8]
Unlike rheumatoid arthritis, lupus arthritis is less disabling and usually does not
cause severe destruction of the joints. Fewer than ten percent of people with lupus
arthritis will develop deformities of the hands and feet.[8] SLE patients are at
particular risk of developing osteoarticular tuberculosis.[9]
It is suggested that there might be an association between rheumatoid arthritis and
SLE,[10] and that SLE is associated with an increased risk of bone fractures in
relatively young women.[11]
Hematological manifestations
Anemia and iron deficiency may develop in up to 50% of cases. Low platelet and
white blood cell counts may be due to the disease or a side-effect of
pharmacological treatment. People with SLE may have an association with
antiphospholipid antibody syndrome[12] (a thrombotic disorder), wherein
autoantibodies to phospholipids are present in their serum. Abnormalities associated
with antiphospholipid antibody syndrome include a paradoxical prolonged PTT
Partial thromboplastin time (which usually occurs in hemorrhagic disorders) and a
positive test for antiphospholipid antibodies; the combination of such findings have
earned the term lupus anticoagulant-positive. Another autoantibody finding in SLE is
the anticardiolipin antibody, which can cause a false positive test for syphilis.
Cardiac manifestations
A person with SLE may have inflammation of various parts of the heart, such as
pericarditis, myocarditis, and endocarditis. The endocarditis of SLE is
characteristically noninfective (Libman-Sacks endocarditis) and involves either the
mitral valve or the tricuspid valve. Atherosclerosis also tends to occur more often
and advances more rapidly than in the general population.[13][14][15]
Pulmonary manifestations
Lung and pleura inflammation can cause pleuritis, pleural effusion, lupus
pneumonitis, chronic diffuse interstitial lung disease, pulmonary hypertension,
pulmonary emboli, pulmonary hemorrhage, and shrinking lung syndrome.
Renal involvement
Painless hematuria or proteinuria may often be the only presenting renal symptom.
Acute or chronic renal impairment may develop with lupus nephritis, leading to
acute or end-stage renal failure. Because of early recognition and management of
SLE, end-stage renal failure occurs in less than 5% of cases. Renal cases are
outlined in the wikipedia lupus nephritis page as well as in personal journeys
documented on http://www.beatlupus.com.
A histological hallmark of SLE is membranous glomerulonephritis with "wire loop"
abnormalities.[16] This finding is due to immune complex deposition along the
glomerular basement membrane, leading to a typical granular appearance in
immunofluorescence testing.
Neuropsychiatric manifestations
Neuropsychiatric syndromes can result when SLE affects the central or peripheral
nervous system. The American College of Rheumatology defines 19 neuropsychiatric
syndromes in systemic lupus erythematosus.[17] The diagnosis of neuropsychiatric
syndromes concurrent with SLE is one of the most difficult challenges in medicine,
because it can involve so many different patterns of symptoms, some of which may
be mistaken for signs of infectious disease or stroke.[18]
The most common neuropsychiatric disorder people with SLE have is headache,[19]
although the existence of a specific lupus headache and the optimal approach to
headache in SLE cases remains controversial.[20] Other common neuropsychiatric
manifestation of SLE include cognitive dysfunction, mood disorder, cerebrovascular
disease,[19] seizures, polyneuropathy,[19] anxiety disorder, and psychosis. It can rarely
present with intracranial hypertension syndrome, characterized by an elevated
intracranial pressure, papilledema, and headache with occasional abducens nerve
paresis, absence of a space-occupying lesion or ventricular enlargement, and
normal cerebrospinal fluid chemical and hematological constituents.[21]
More rare manifestations are acute confusional state, Guillain-Barré syndrome,
aseptic meningitis, autonomic disorder, demyelinating syndrome, mononeuropathy
(which might manifest as mononeuritis multiplex), movement disorder (more
specifically, chorea), myasthenia gravis, myelopathy, cranial neuropathy and
plexopathy.
Systemic manifestations
Fatigue in SLE is probably multifactorial and has been related to not only disease
activity or complications such as anemia or hypothyroidism but also pain;
depression; poor sleep quality; poor physical fitness and perceived lack of social
support.[22][23]
Causes
There is no one specific cause of SLE. There are, however, a number of
environmental triggers and a number of genetic susceptibilities.[24][25]
Genetics
The first mechanism may arise genetically. Research indicates that SLE may have a
genetic link. SLE does run in families, but no single, causal, gene has been
identified. Instead, multiple genes appear to influence a person's chance of
developing lupus when triggered by environmental factors. The most important
genes are located in the HLA region on chromosome 6, where mutations may occur
randomly (de novo) or may be inherited. HLA class I, class II, and class III are
associated with SLE, but only class I and class II contribute independently to
increased risk of SLE.[26] Other genes which contain risk variants for SLE are IRF5,
PTPN22, STAT4[27], CDKN1A,[28] ITGAM, BLK[27], TNFSF4 and BANK1.[29] some of the
susceptibility genes may be population specific.[27]
Environmental triggers
The second mechanism may be due to environmental factors. These factors may not
only exacerbate existing SLE conditions but also trigger the initial onset. They
include certain medications (such as some antidepressants and antibiotics), extreme
stress, exposure to sunlight, hormones, and infections. UV radiation has been shown
to trigger the photosensitive lupus rash and some evidence suggests that UV light
might be capable of altering the structure of the DNA, leading to the creation of
autoantibodies. Sex hormones such as estrogen play an important role in the
occurrence of SLE and it is observed that during reproductive years, the frequency
of SLE is 10 times greater in females than in males.
Researchers have sought to find a connection between certain infectious agents
(viruses and bacteria), but no pathogen can be consistently linked to the disease.
Some researchers have found that women with silicone gel-filled breast implants
have produced antibodies to their own collagen, but it is not known how often these
antibodies occur in the general population, and there are no data that show that
these antibodies cause connective tissue diseases such as SLE. There is also a small
but growing body of evidence linking SLE to lipstick usage, [30][31] although lipstick
manufacturers do not appear to be concerned about it.[32]
Drug reactions
Drug-induced lupus erythematosus is a (generally) reversible condition that usually
occurs in people being treated for a long-term illness. Drug-induced lupus mimics
SLE. However, symptoms of drug-induced lupus generally disappear once the
medication that triggered the episode is stopped. There are about 400 medications
that can cause this condition, the most common of which are procainamide,
hydralazine, quinidine, and phenytoin.[2]
Non-SLE forms of lupus
Discoid (cutaneous) lupus is limited to skin symptoms and is diagnosed by biopsy of
skin rash on the face, neck, or scalp.
Pathophysiology
One manifestation of SLE is abnormalities in apoptosis, a type of programmed cell
death in which aging or damaged cells are neatly disposed of as a part of normal
growth or functioning.
Transmission
In SLE, the body's immune system produces antibodies against itself, particularly
against proteins in the cell nucleus. SLE is triggered by environmental factors that
are unknown.
"All the key components of the immune system are involved in the underlying
mechanisms [of SLE]" according to Rahman, and SLE is the prototypical autoimmune
disease. The immune system must have a balance (homeostasis) between being
sensitive enough to protect against infection, and being too sensitive and attacking
the body's own proteins (autoimmunity). From an evolutionary perspective,
according to Crow, the population must have enough genetic diversity to protect
itself against a wide range of possible infection; some genetic combinations result in
autoimmunity. The likely environmental triggers include ultraviolet light, drugs, and
viruses. These stimuli cause the destruction of cells and expose their DNA, histones,
and other proteins, particularly parts of the cell nucleus. Because of genetic
variations in different components of the immune system, in some people the
immune system attacks these nuclear-related proteins and produces antibodies
against them. In the end, these antibody complexes damage blood vessels in critical
areas of the body, such as the glomeruli of the kidney; these antibody attacks are
the cause of SLE. Researchers are now identifying the individual genes, the proteins
they produce, and their role in the immune system. Each protein is a link on the
autoimmune chain, and researchers are trying to find drugs to break each of those
links.[2][33][34]
SLE is a chronic inflammatory disease believed to be a type III hypersensitivity
response with potential type II involvement.[35]
Abnormalities in apoptosis
• Apoptosis is increased in monocytes and keratinocytes
• Expression of Fas by B cells and T cells is increased
• There are correlations between the apoptotic rates of lymphocytes and
disease activity.
Tingible body macrophages (TBMs) – large phagocytic cells in the germinal centers
of secondary lymph nodes – express CD68 protein. These cells normally engulf B
cells that have undergone apoptosis after somatic hypermutation. In some people
with SLE, significantly fewer TBMs can be found, and these cells rarely contain
material from apoptotic B cells. Also, uningested apoptotic nuclei can be found
outside of TBMs. This material may present a threat to the tolerization of B cells and
T cells. Dendritic cells in the germinal center may endocytose such antigenic
material and present it to T cells, activating them. Also, apoptotic chromatin and
nuclei may attach to the surfaces of follicular dendritic cells and make this material
available for activating other B cells that may have randomly acquired self-
specificity through somatic hypermutation.[36]
Clearance deficiency
The exact mechanisms for the development of SLE are still unclear, since the
pathogenesis is a multifactorial event. Beside discussed causations, impaired
clearance of dying cells is a potential pathway for the development of this systemic
autoimmune disease. This includes deficient phagocytic activity and scant serum
components in addition to increased apoptosis.
Monocytes isolated from whole blood of SLE sufferers show reduced expression of
CD44 surface molecules involved in the uptake of apoptotic cells. Most of the
monocytes and tingible body macrophages (TBM), which are found in the germinal
centres of lymph nodes, even show a definitely different morphology; they are
smaller or scarce and die earlier. Serum components like complement factors, CRP,
and some glycoproteins are, furthermore, decisively important for an efficiently
operating phagocytosis. With SLE, these components are often missing, diminished,
or inefficient.
The clearance of early apoptotic cells is an important function in multicellular
organisms. It leads to a progression of the apoptosis process and finally to
secondary necrosis of the cells if this ability is disturbed. Necrotic cells release
nuclear fragments as potential autoantigens as well as internal danger signals,
inducing maturation of dendritic cells (DC), since they have lost their membranes'
integrity. Increased appearance of apoptotic cells also simulates inefficient
clearance. That leads to maturation of DC and also to the presentation of
intracellular antigens of late apoptotic or secondary necrotic cells, via MHC
molecules. Autoimmunity possibly results by the extended exposure to nuclear and
intracellular autoantigens derived from late apoptotic and secondary necrotic cells.
B and T cell tolerance for apoptotic cells is abrogated, and the lymphocytes get
activated by these autoantigens; inflammation and the production of autoantibodies
by plasma cells is initiated. A clearance deficiency in the skin for apoptotic cells has
also been observed in people with cutaneous lupus erythematosus (CLE).[37]
Germinal centres
Accumulation in germinal centres (GC)
In healthy conditions, apoptotic lymphocytes are removed in germinal centres by
specialized phagocytes, the tingible body macrophages (TBM), which is why no free
apoptotic and potential autoantigenic material can be seen. In some people with
SLE, accumulation of apoptotic debris can be observed in GC because of an
ineffective clearance of apoptotic cells. In close proximity to TBM, follicular dendritic
cells (FDC) are localised in GC, which attach antigen material to their surface and, in
contrast to bone marrow-derived DC, neither take it up nor present it via MHC
molecules.
Autoreactive B cells can accidentally emerge during somatic hypermutation and
migrate into the GC light zone. Autoreactive B cells, maturated coincidentally,
normally do not receive survival signals by antigen planted on follicular dendritic
cells, and perish by apoptosis. In the case of clearance deficiency, apoptotic nuclear
debris accumulates in the light zone of GC and gets attached to FDC. This serves as
a germinal centre survival signal for autoreactive B-cells. After migration into the
mantle zone, autoreactive B cells require further survival signals from autoreactive
helper T cells, which promote the maturation of autoantibody-producing plasma cells
and B memory cells. In the presence of autoreactive T cells, a chronic autoimmune
disease may be the consequence.
Anti-nRNP autoimmunity
Autoantibodies to nRNP A and nRNP C initially targeted restricted, proline-rich
motifs. Antibody binding subsequently spread to other epitopes. The similarity and
cross-reactivity between the initial targets of nRNP and Sm autoantibodies identifies
a likely commonality in cause and a focal point for intermolecular epitope spreading.
[38]
Others
Elevated expression of HMGB1 was found in the sera of patients and mice with
systemic lupus erythematosus, High Mobility Group Box 1 (HMGB1) is a nuclear
protein participating in chromatin architecture and transcriptional regulation.
Recently, there is increasing evidence that HMGB1 contributes to the pathogenesis
of chronic inflammatory and autoimmune diseases due to its pro-inflammatory and
immunostimulatory properties.[39]
Diagnosis
Microphotograph of a histological section of human skin prepared for direct
immunofluorescence using an anti-IgG antibody. The skin is from a person with
systemic lupus erythematosus and shows IgG deposits at two different places: The
first is a bandlike deposit along the epidermal basement membrane ("lupus band
test" is positive); the second is within the nuclei of the epidermal cells (antinuclear
antibodies are present).
Laboratory tests
Antinuclear antibody (ANA) testing and anti-extractable nuclear antigen (anti-ENA)
form the mainstay of serologic testing for SLE. Several techniques are used to detect
ANAs. Clinically the most widely used method is indirect immunofluorescence. The
pattern of fluorescence suggests the type of antibody present in the patient's
serum.
ANA screening yields positive results in many connective tissue disorders and other
autoimmune diseases, and may occur in normal individuals. Subtypes of antinuclear
antibodies include anti-Smith and anti-double stranded DNA (dsDNA) antibodies
(which are linked to SLE) and anti-histone antibodies (which are linked to drug-
induced lupus). Anti-dsDNA antibodies are highly specific for SLE; they are present in
70% of cases, whereas they appear in only 0.5% of people without SLE.[2] The anti-
dsDNA antibody titers also tend to reflect disease activity, although not in all cases.
[2]
Other ANA that may occur in SLE sufferers are anti-U1 RNP (which also appears in
systemic sclerosis), SS-A (or anti-Ro) and SS-B (or anti-La; both of which are more
common in Sjögren's syndrome). SS-A and SS-B confer a specific risk for heart
conduction block in neonatal lupus.[40]
Other tests routinely performed in suspected SLE are complement system levels
(low levels suggest consumption by the immune system), electrolytes and renal
function (disturbed if the kidney is involved), liver enzymes, and complete blood
count.
Previously, the lupus erythematosus (LE) cell test was not commonly used for
diagnosis because those LE cells are only found in 50–75% of SLE cases, and are
also found in some people with rheumatoid arthritis, scleroderma, and drug
sensitivities. Because of this, the LE cell test is now performed only rarely and is
mostly of historical significance.[41]
Diagnostic criteria
Some physicians make a diagnosis on the basis of the American College of
Rheumatology (ACR) classification criteria. The criteria, however, were established
mainly for use in scientific research including use in randomized controlled trials
which require higher confidence levels, so some people with SLE may not pass the
full criteria.
The American College of Rheumatology established eleven criteria in 1982,[42] which
were revised in 1997[43] as a classificatory instrument to operationalise the definition
of SLE in clinical trials. They were not intended to be used to diagnose individuals
and do not do well in that capacity. For the purpose of identifying patients for clinical
studies, a person has SLE if any 4 out of 11 symptoms are present simultaneously or
serially on two separate occasions.
1. Serositis: Pleuritis (inflammation of the membrane around the lungs) or
pericarditis (inflammation of the membrane around the heart); sensitivity =
56%; specificity = 86% (pleural is more sensitive; cardiac is more specific).
[44]
2. Oral ulcers (includes oral or nasopharyngeal ulcers).
3. Arthritis: nonerosive arthritis of two or more peripheral joints, with
tenderness, swelling, or effusion; sensitivity = 86%; specificity = 37%.[44]
4. Photosensitivity (exposure to ultraviolet light causes skin rash, or other
symptoms of SLE flareups); sensitivity = 43%; specificity = 96%.[44]
5. Blood—hematologic disorder—hemolytic anemia (low red blood cell count)
or leukopenia (white blood cell count<4000/µl), lymphopenia (<1500/µl) or
thrombocytopenia (<100000/µl) in the absence of offending drug;
sensitivity = 59%; specificity = 89%.[44] Hypocomplementemia is also seen,
due to either consumption of C3 and C4 by immune complex-induced
inflammation or to congenitally complement deficiency, which may
predispose to SLE.
6. Renal disorder: More than 0.5g per day protein in urine or cellular casts
seen in urine under a microscope; sensitivity = 51%; specificity = 94%.[44]
7. Antinuclear antibody test positive; sensitivity = 99%; specificity = 49%.[44]
8. Immunologic disorder: Positive anti-Smith, anti-ds DNA, antiphospholipid
antibody, and/or false positive serological test for syphilis; sensitivity =
85%; specificity = 93%.[44] Presence of anti-ss DNA in 70% of cases (though
also positive with rheumatic disease and healthy persons)[45]).
9. Neurologic disorder: Seizures or psychosis; sensitivity = 20%; specificity =
98%.[44]
10. Malar rash (rash on cheeks); sensitivity = 57%; specificity = 96%.[44]
11. Discoid rash (red, scaly patches on skin that cause scarring); sensitivity =
18%; specificity = 99%.[44]
The mnemonic to remember the 11 symptoms is 'SOAP BRAIN MD'.[46]
Some people, especially those with antiphospholipid syndrome, may have SLE
without four criteria, and also SLE may present with features other than those listed
in the criteria.[47][48][49]
Recursive partitioning has been used to identify more parsimonious criteria.[44] This
analysis presented two diagnostic classification trees:
1. Simplest classification tree: SLE is diagnosed if a person has an
immunologic disorder (anti-DNA antibody, anti-Smith antibody, false
positive syphilis test, or LE cells) or malar rash.
o sensitivity = 92%
o specificity = 92%
2. Full classification tree: Uses 6 criteria.
o sensitivity = 97%
o specificity = 95%
Other alternative criteria have been suggested.[50]
Treatment
Being a chronic disease with no known cure, the treatment of SLE is symptomatic. In
essence, this involves preventing flares and reducing their severity and duration
when they occur. Currently, medication is the main form of treatment. However,
there is strong medical evidence to support the efficacy of diet and exercise in
lupus.
Lupus is a disease of inflammation and auto-immunity.
In individuals having lupus, an overproduction of the protein BlyS can cause
increased inflammation. This happens when the level of BlyS exceeds normal levels.
Since BlyS is one of the proteins associated with the production of autoreactive
antibodies and the prevention of those autoreactive antibodies dying off, when BlyS
is present in high amounts, an overproduction of inflammation in the body occurs.
Treatment can include corticosteroids and anti-malarial drugs. Certain types of lupus
nephritis such as diffuse proliferative glomerulonephritis require bouts of cytotoxic
drugs. These drugs include cyclophosphamide and mycophenolate.
Medications
Due to the variety of symptoms and organ system involvement with SLE, its severity
in an individual must be assessed in order to successfully treat SLE. Mild or
remittant disease can sometimes be safely left untreated. If required, nonsteroidal
anti-inflammatory drugs and antimalarials may be used.
Disease-modifying antirheumatic drugs
Disease-modifying antirheumatic drugs (DMARDs) are used preventively to reduce
the incidence of flares, the process of the disease, and lower the need for steroid
use; when flares occur, they are treated with corticosteroids. DMARDs commonly in
use are antimalarials such as plaquenil and immunosuppressants (e.g. methotrexate
and azathioprine). Hydroxychloroquine is an FDA-approved antimalarial used for
constitutional, cutaneous, and articular manifestations. Hydroxychloroquine has
relatively few side effects, and there is evidence that it improves survival among
people who have SLE.[51] Cyclophosphamide is used for severe glomerulonephritis or
other organ-damaging complications. Mycophenolic acid is also used for treatment
of lupus nephritis, but it is not FDA-approved for this indication, and FDA is
investigating reports that it may be associated with birth defects when used by
pregnant women.[52]
Immunosuppressive drugs
In more severe cases, medications that modulate the immune system (primarily
corticosteroids and immunosuppressants) are used to control the disease and
prevent recurrence of symptoms (known as flares). Depending on the dosage,
people who require steroids may develop Cushing's syndrome, side-effects of which
may include obesity, puffy round face, diabetes mellitus, large appetite, difficulty
sleeping and osteoporosis. Those side-effects can subside if and when the large
initial dosage is reduced, but long-term use of even low doses can cause elevated
blood pressure and cataracts.
Numerous new immunosuppressive drugs are being actively tested for SLE. Rather
than suppressing the immune system nonspecifically, as corticosteroids do, they
target the responses of individual immune cells. Some of these drugs are already
FDA-approved for treatment of rheumatoid arthritis.[51] See also Belimumab.
Analgesia
Since a large percentage of people with SLE suffer from varying amounts of chronic
pain, stronger prescription analgesics (pain killers) may be used if over-the-counter
drugs (mainly nonsteroidal anti-inflammatory drugs) do not provide effective relief.
Potent NSAIDs such as indomethacin and diclofenac are relatively contraindicated
for patients with SLE because they increase the risk of kidney failure and heart
failure.[51]
Moderate pain is typically treated with mild prescription opiates such as
dextropropoxyphene and co-codamol. Moderate to severe chronic pain is treated
with stronger opioids, such as hydrocodone or longer-acting continuous-release
opioids, such as oxycodone, MS Contin, or Methadone. The Fentanyl duragesic
transdermal patch is also a widely-used treatment option for the chronic pain
caused by complications because of its long-acting timed release and ease of use.
When opioids are used for prolonged periods, drug tolerance, chemical dependency,
and addiction may occur. Opiate addiction is not typically a concern, since the
condition is not likely to ever completely disappear. Thus, lifelong treatment with
opioids is fairly common for chronic pain symptoms, accompanied by periodic
titration that is typical of any long-term opioid regimen.
Lifestyle changes
Avoiding sunlight is the primary change to the lifestyle of SLE sufferers, as sunlight
is known to exacerbate the disease. Drugs unrelated to SLE should be prescribed
only when known not to exacerbate the disease. Occupational exposure to silica,
pesticides and mercury can also make the disease worsen.[24]
Fasting and massive nutrition changes, towards a low fat, mostly strict vegetarian,
wholesome diet, also have been reported as a possibility to lessen the symptoms or
even induce a remission.[53]
Renal transplantation
Early mortality, within 5 years, is due to organ failure or overwhelming infections,
both of which can be modified by early diagnosis and treatment. The mortality risk is
fivefold when compared to the normal population in the late stages, which can be
attributed to cardiovascular diseases acquired from corticosteroid therapy, the
leading cause of death for people with SLE.[51]

Renal transplants are the treatment of choice for end-stage renal disease, which is
one of the complications of lupus nephritis, but the recurrence of the full disease is
common in up to 30% of patients.[54]
Prevention
To reduce potential for cardiovascular issues, high blood pressure and high
cholesterol should be prevented or treated aggressively. Steroids should be used at
the lowest dose for the shortest possible period, and other drugs that can reduce
symptoms should be used whenever possible.[51] High serum creatinine,
hypertension, nephrotic syndrome, anemia and hypoalbuminemia are poor
prognostic factors.[58]

SLE is not understood well enough to be prevented, but, when the disease develops,
quality of life can be improved through flare prevention. The warning signs of an
impending flare include increased fatigue, pain, rash, fever, abdominal discomfort,
headache, and dizziness. Early recognition of warning signs and good
communication with a doctor can help individuals remain active, experience less
pain, and reduce medical visits.[55]
The ANA is the most sensitive screening test for evaluation, whereas anti-Sm (anti-
Smith) is the most specific. The dsDNA (double-stranded DNA) antibody is also fairly
specific and often fluctuates with disease activity; as such, the dsDNA titer is
sometimes useful to monitor disease flares or response to treatment.

As longevity of people with SLE increases, the likelihood of complications also

increases in four areas: cardiovascular disease, infections, osteoporosis, and cancer.
Standard preventive measures, screening for related diseases may be necessary to
deal with the increased risks due to the side effects of medications. Extra vigilance
is considered warranted in particular for cancers affecting the immune system.[56]

Complications during pregnancy

While most infants born to mothers who have SLE are healthy, pregnant mothers
with SLE should remain under medical care until delivery. Neonatal lupus is rare, but
identification of mothers at highest risk for complications allows for prompt
treatment before or after birth. In addition, SLE can flare up during pregnancy, and
proper treatment can maintain the health of the mother longer. Women pregnant
and known to have the antibodies for anti-Ro (SSA) or anti-La (SSB) often have
echocardiograms during the 16th and 30th weeks of pregnancy to monitor the
health of the heart and surrounding vasculature.[55]

Contraception and other reliable forms of pregnancy prevention is routinely advised

for women with SLE, since getting pregnant during active disease was found to be
harmful. Lupus nephritis was the most common manifestation. Overall live-birth was
72.7%; the most common causes of pregnancy loss were spontaneous abortion
(miscarriage) and fetal death in utero. Pregnancy outcome was worse in SLE
patients whose disease flared up during pregnancy.[57]

Prognosis

SLE is generally considered incurable, but highly treatable.

In the 1950s, most people diagnosed with SLE lived fewer than five years. Advances
in diagnosis and treatment have improved survival to the point where over 90% now
survive for more than ten years, and many can live relatively asymptomatically.
Prognosis is normally worse for men and children than for women; however, if
symptoms are present after age 60, the disease tends to run a more benign course.