Ebola Hemorrhagic in nonhuman primates, but not in

Fever humans.

What are the symptoms of Ebola

Bibliography hemorhagic fever?
http://www.cdc.gov/ncidod/dvrd/spb/mnp
ages/dispages/Fact_Sheets/Marburg%20H The incubation period for Ebola HF
emmorhagic%20Fever%20Fact%20Sheet. ranges from 2 to 21 days. Symptoms are
pdf. varied and often appear suddenly. Initial
symptoms include
• high fever (at least 38.8°C; 101.8°F),
severe headache, muscle, joint, or
abdominal pain, severe weakness
and exhaustion, sore throat, nausea,
and dizziness].
What is Ebola hemorrhagic fever?
Ebola hemorrhagic fever is a • Before an outbreak is suspected,
severe, often-fatal disease in humans and these early symptoms are easily
nonhuman primates (monkeys, gorillas, mistaken for malaria, typhoid fever,
And chimpanzees) that has appeared dysentery, influenza, or various
sporadically since its initial recognition in bacterial infections, which are all far
1976. The disease is caused by more common and reliably less fatal.
Infection with Ebola virus, named after a
river in the Democratic Republic of the • Ebola may progress to cause more
Congo (formerly Zaire) in Africa, where it serious symptoms, such as diarrhea,
was first recognized. dark or bloody feces, vomiting blood,
T he virus is o ne of two members red eyes due to Distension and
of a family of RNA viruses called the hemorrhage of sclerotic arterioles,
Filoviridae . petechia, maculopapular rash, and
There are four identified subtypes purpura. Other secondary symptoms
of Ebola virus. Three of the four have include hypotension (less than 90
caused disease in humans: Ebola-Zaire, mm Hg systolic /60 mm Hg diastolic),
Ebola-Sudan and Ebola-Ivory Coast. The hypovolemia, tachycardia, organ
fourth, Ebola-Reston, has caused disease damage (especially the kidneys,
spleen, and liver) as a result of
 disseminated systemic necrosis, and
proteinuria.
Researchers do not understand
why some people are able to recover
from Ebola HF and others a re not.
However, it is known that patients
who die usually have not developed a
significant immune response to the
virus at the time of death.
How is Ebola hemorrhagic fever treated?
There is no standard treatment for
Ebola HF. Currently, patients receive
supportive therapy. This consists of
balancing the patient’s fluids and
electrolytes, maintaining their oxygen
status and blood pressure, and treating
them for any complicating infections.
Where is Ebola virus found in nature?
The exact origin, locations, and
natural habitat (known as the "natural
reservoir") of Ebola virus remain
unknown.
However, on the basis of available
evidence and the nature of similar
viruses, researchers believe that the virus
is
zoonotic (anima l-borne) and is normally
maintained in an animal host that is
native to the African continent.
A similar host is probably
associated with Ebola-REsto n which w as
isolated from infected cynomolgous
monkeys that were imported to the
United States and Italy from the
Philippines. The virus is not known to be
native to other continents, such as North
America.
How is Ebola virus spread?
Infections with E bola virus are
acute. There is no carrier state because
the natural reservoir of the virus is
unknown. the manner in which the virus
first appears in a human at the start of an
outbreak has not been determined.
However, researchers have hypothesized
that the first patient becomes infected
through con tact with an infected animal.
After the first case-patient in an outbreak
setting is infected, the virus can be
transmitted in several ways.
People can be exposed to EbolaVirus from
• direct contact with the blood
and/or secretions of an infected
person
• the virus is often spread through
families and friends because they
come in close contact with such
secretions when caring for infected
persons.
• through contact with objects, such
as needles, that have been
contaminated with infected
secretions.
• Nosocomial transmission refers to
the spread of a disease within a
health-ca re setting, such as a
clinic or hospital.
• Burial ceremonies where mourners
have direct contact with the body
of the deceased person can play a
significant role in the transmission
of Ebola.
• The infection of human cases with
Ebola virus has been documented
through the handling of infected
chimpanzees, gorillas, and forest
antelopes--both dead and alive--as
was documented in Côte d'Ivoire,
the Republic of Congo and Gabon.
How is Ebola hemorrhagic fever
prevented?
The prevention of Ebola HF in
Africa presents many challenges.
Because the identity and location of the
natural reservoir of Ebola virus are
unknown, there are few established
primary prevention measures.
If cases of the disease do appear,
current social and economic condition s
often favor the spread of an epidemic
within health-care facilities. Therefore,
health-care providers must b e able to
recognize a case of Ebola HF should one
appears. They must also have the
capability to perform diagnostic tests and
be ready to employ practical viral
hemorrhagic fever isolation precautions,
or barrier nursing techniques.
 to retrospectively diagnose Ebola HF in
suspected case-patients who have died.

These techniques include

• the wearing of protective
clothing, such as masks,
gloves, gowns, and goggles;
• the use of infection-control
measures, including
complete equipment
sterilization; and
• the isolation of Ebola HF
patients from contact with
unprotected persons.

The aim of all of these techniques

is to avoid any person’s contact with the
blood or secretions of and patient. If a
patient with Ebola HF dies, it is equally
important that direct contact with the
body of the deceased patient be
prevented
CDC has developed a set of tools to meet
health-care facilities’ needs. In
conjunction with the World Health
Organization, CDC has developed
practical, hospital-based guidelines. T he
manual de scribes how to recognize
cases of viral hemorrhagic fever, such as
Ebola HF, and pre vent further
nosocomial transmission by using locally
available materials and few financial
resources. Similarly, a practical
diagnostic test that uses tiny samples
from patients’ skin has been developed
 fever occurred simultaneously in
laboratories in Marburg and Frankfurt,
Germany and in Belgrade, Yugoslavia
(now Serbia). A total of 37 people
became ill; they included laboratory
workers as well as several medical
personnel and family members who had
cared for them. The first people infected
had been exposed to African green
monkeys or their tissues. In Marburg, the
monkeys had been imported for research
and to prepare polio vaccine.

What is Marburg hemorrhagic fever?

Marburg hemorrhagic fever is a

rare, severe type of hemorrhagic fever
which affects both humans and non-
human primates. Caused by a genetically
unique zoonotic (that is, animal-borne)
RNA virus of the filovirus family, its
recognition led to the creation of this
virus family. The four species of Ebola MArburg Hem Fever. (2008, May).
virus are the only other known members Retrieved May 15, 2008, from Marburg
of the filovirus family. Virus:
Marburg virus was first recognized in http://www.cdc.gov/ncidod/dvrd/spb/mnp
1967, when outbreaks of hemorrhagic ages/dispages/Fact_Sheets/Marburg%20H
emmorhagic%20Fever%20Fact%20Sheet.
pdf
What are the symptoms of the disease?
After an incubation period of 5-10
days, the onset of the disease is sudden
and is marked by fever, chills, headache,
and myalgia.
Around the fifth day after the onset
of symptoms,
• a maculopapular rash, most
prominent on the trunk (chest,
back, stomach), may occur.
• Nausea, vomiting, chest pain, a
sore throat, abdominal pain, and
diarrhea then may appear.
• Symptoms become increasingly
severe and may include jaundice,
inflammation of the pancreas,
severe weight loss, delirium,
shock, liver failure, massive
hemorrhaging, and multi-organ
dysfunction.
Because many of the signs and
symptoms of Marburg hemorrhagic fever
are similar to those of other infectious
diseases, such as malaria or typhoid
fever, diagnosis of the disease can be
difficult, especially if only a single case is
involved.
Antigen-capture enzyme-linked
immunosorbent assay (ELISA) testing,
IgM-capture ELISA, polymerase chain
reaction (PCR), and virus isolation can be
used to confirm a case of Marburg
hemorrhagic fever within a few days of
the onset of symptoms. The IgG-capture
ELISA is appropriate for testing persons
later in the course of disease or after
recovery. The disease is readily
diagnosed by immunohis to chemistry,
virus isolation, or PCR of blood or tissue
specimens from deceased patients.
How do humans get Marburg
hemorrhagic fever?
Just how the animal host first
transmits Marburg virus to humans is
unknown. However, as with some other
viruses which cause viral hemorrhagic
fever, humans who become ill with
Marburg hemorrhagic fever may spread
the virus to other people. This may
happen in several ways. Persons, who
have handled infected monkeys and have
come in direct contact with their fluids or
cell cultures, have become infected.
Spread of the virus between humans has
occurred in a setting of close
contact, often in a hospital.
Droplets of body fluids, or direct contact
with persons, equipment, or other objects
contaminated with infectious blood or
tissues are all highly suspect as sources
of disease.
How is Marburg hemorrhagic fever
treated?
A specific treatment for this
disease is unknown. However, supportive
hospital therapy should be utilized. This
includes balancing the patient’s fluids
and electrolytes, maintaining their
oxygen status and blood pressure,
replacing lost blood and clotting factors
and treating them for any complicating
infections.
Sometimes treatment also has used
transfusion of fresh-frozen plasma and
other preparations to replace the blood
proteins important in clotting. One
controversial treatment is the use of
heparin (which blocks clotting) to prevent
the consumption of clotting factors. Some
researchers believe the consumption of
clotting factors is part of the disease
process.
Are there complications after recovery?
Recovery from Marburg
hemorrhagic fever may be prolonged and
accompanied by orchititis, recurrent
hepatitis, transverse myelitis or uvetis.
Other possible complications include
inflammation of the testis, spinal cord,
eye, parotid gland, or by prolonged
hepatitis.
Is the disease ever fatal?
Yes. The case-fatality rate for
Marburg hemorrhagic fever is between
23-25%.
What needs to be done to address the
threat of Marburg hemorrhagic fever?
Marburg hemorrhagic fever is a
very rare human disease. However, when
it does occur, it has the potential to
spread to other people, especially health
care staff and family members who care
for the patient. Therefore, increasing
awareness among health-care providers
of clinical symptoms in patients that
suggest Marburg hemorrhagic fever is
critical. Better awareness can help lead to
taking precautions against the spread of
virus infection to family members or
health-care providers. Improving the use
of diagnostic tools is another priority.
With modern means of transportation
that give access even to remote areas, it
is possible to obtain rapid testing of
samples in disease control centers
equipped with Biosafety Level 4
laboratories in order to confirm or rule
out Marburg virus infection.
Who is at risk for the illness?
People who have close contact
with a human or non-human primate
infected with the virus are at risk.
Such persons include laboratory or
quarantine facility workers who handle
non-human primates that have been
associated with the disease. In addition,
hospital staff and family members who
care for patients with the disease are at
risk if they do not use proper barrier
nursing techniques.
How is Marburg hemorrhagic fever
prevented?
Due to our limited knowledge of
the disease, preventive measures against
transmission from the original animal
host have not yet been established.
Measures for prevention of secondary
transmission are similar to those used for
other hemorrhagic fevers. If a patient is
either suspected or confirmed to have
Marburg hemorrhagic fever, barrier
nursing techniques should be used to
prevent direct physical contact with the
patient.
These precautions include wearing
of protective gowns, gloves, and masks;
placing the infected individual in strict
isolation; and sterilization or proper
disposal of needles, equipment, and
patient excretions.
What is tick-borne encephalitis?
Tick-borne encephalitis, or TBE, is
a human viral infectious disease involving
the
Central nervous system. The disease is
most often manifest as meningitis
(Inflammation of the membrane that
surrounds the brain and spinal cord),
encephalitis (inflammation of the brain),
or meningoencephalitis (inflammation of
both the brain and meninges). Although
TBE is most commonly recognized as a
neurologic disease, mild febrile illnesses
can also occur. Long-lasting or
permanent neuropsychiatric sequelae are
observed in 10-20% of infected
patients.

What causes tick-borne encephalitis?

TBE is caused by tick-borne
encephalitis virus (TBEV), a member of
the family Flaviviridae, that was initially
isolated in 1937. A closely related virus in
Far
Eastern Eurasia, Russian spring-summer
encephalitis virus (RSSEV), is
responsible for a similar disease with a
more severe clinical course.
Bibliography:
http://www.cdc.gov/ncidod/dvrd/spb/mnp
ages/dispages/Fact_Sheets/Tickborne%20
encephalitis%20Fact%20Sheet.pdf.
How is TBEV spread, and how do humans
become infected?
Ticks act as both the vector and
reservoir for TBEV. The main hosts are
small rodents, with humans being
accidental hosts. Large animals are
feeding hosts for the ticks, but do not
play a role in maintenance of the virus.
The virus can chronically infect ticks and
is transmitted both transtadially (from
larva to nymph to adult ticks) and
transovarially (from adult female tick
through eggs). TBE cases occur during
the highest period of tick activity
(between April and November), when
humans are infected in rural areas
through tick bites.
Infection also may follow consumption of
raw milk from goats, sheep, or cows.
Laboratory infections were common
before the use of vaccines and
availability of biosafety precautions to
prevent exposure to infectious aerosols.
Person-to-person transmission has not
been reported. Vertical transmission from
an infected mother to fetus has occurred.
Where is the disease found?
TBE is an important infectious
disease of in many parts of Europe, the
former Soviet Union, and Asia,
corresponding to the distribution of the
ixodid tick reservoir. The annual number
of cases (incidence) varies from year to
year, but several thousand are reported
annually, despite historical under-
reporting of this disease.
What are the symptoms of TBE?
The incubation period of TBE is
usually between 7 and 14 days and is
asymptomatic. Shorter incubation times
have been reported after milk-borne
exposure. A characteristic biphasic febrile
illness follows, with an initial phase that
lasts 2 to 4 days and corresponds to the
viremic phase. It is non-specific with
symptoms that may include fever,
malaise, anorexia, muscle aches,
headache, nausea, and/or vomiting. After
about 8 days of remission, the second
phase of the disease occurs in 20 to 30%
of patients and involves the central
nervous system with symptoms of
meningitis (e.g., fever, headache, and a
stiff neck) or encephalitis (e.g.,
drowsiness, confusion, sensory
disturbances, and/or motor abnormalities
such as paralysis) or
meningoencephalitis. In contrast to RSSE,
TBE is more severe in adults than in
children.
During the first phase of the
disease, the most common laboratory
abnormalities are a low white blood cell
count (leukopenia) and a low platelet
count (thrombocytopenia). Liver enzymes
in the serum may also be mildly elevated.
After the onset of neurologic disease
during the second phase, an increase in
the number of white blood cells in the
blood and the cerebrospinal fluid (CSF) is
usually found. Virus can be isolated from
the blood during the first phase of the
disease. Specific diagnosis usually
depends on detection of specific IgM in
either blood or CSF, usually appearing
later, during the second phase of the
disease.
Are there any complications after
recovery?
In approximately two-thirds of
patients infected with the TBE virus, only
the early (viremic) phase is seen. In the
remaining third, patients experience
either the typical biphasic course of the
disease or a clinical illness that begins
with the second (neurologic) phase. The
convalescent period can be long and the
incidence of sequelae may vary between
30 and 60%, with long-term or even
permanent neurologic symptoms.
Neuropsychiatric sequelae have been
report in 10-20% of patients.
How can TBEV infections be
Is the disease ever fatal? prevented?
Yes, but only rarely. In general, Like other tick-borne infectious diseases,
mortality is 1% to 2%, with deaths TBEV infection can be prevented by using
occurring 5 to 7 days after the onset of insect repellents and
neurologic signs. protective clothing to prevent tick bites. A
vaccine is available in some disease
endemic areas (though not
currently in the United States); however,
How is TBE treated? adverse vaccine-reactions in children
There is no specific drug therapy limit the utility of the product.
for TBE. Meningitis, encephalitis, or
meningoencephalitis require
hospitalization and supportive care based
on syndrome severity. Anti-inflammatory
drugs, such as corticosteroids, may be
considered under specific circumstances
for symptomatic relief. Intubation and
ventilatory support may be necessary.
Who is at risk for TBEV infection?
In disease endemic areas, people
with recreational or occupational
exposure to rural or outdoor settings
(e.g.,
hunters, campers, forest workers,
farmers) are potentially at risk for
infection by contact with the infected
ticks.
Furthermore, as tourism expands, travel
to areas of endemicity broadens the
definition of who is at risk for TBE
infection.
What is c
s?
CMV, or cytomegalovirus (si-to-
MEG-a-lovi-
rus), is a common virus that infects
people of all ages. Most
infections with CMV are
“silent,” meaning most
people who are infected
with CMV have no signs
or symptoms. However,
it can cause disease in
unborn babies and in
people with weakened
immune systems. Once
CMV is in a person’s
body, it stays there for life.
How is CMV spread?
● Person-to-person contact (such
as kissing,
sexual contact, and getting saliva or
urine
on your hands and then touching your
nose or mouth)
● A pregnant woman can pass the
virus to her unborn baby
● Blood transfusions and organ
transplantations
The virus is found in bodily fluids,
including
urine, saliva (spit), breast milk, blood,
tears,
semen, and vaginal fl uids. A person can
become infected with CMV when they
come
in contact with these bodily fl uids. Since
only
tiny amounts of the virus are found in
these
fl uids, the chance of getting a CMV
infection
from casual contact is very small.
Can a pregnant woman pass
CMV to her unborn baby?
About one third of women who become
infected with CMV for the fi rst time
during
pregnancy pass the virus to their unborn
babies. Women who had CMV before
getting
pregnant can also pass the virus to their
unborn babies, but this is rare. When
infections occur in unborn babies, CMV
can
cause a wide range of disabilities. Each
year
in the United States, about 1 in 500
children
are born with or develop disabilities as a
result of CMV infection.
What health problems does
CMV cause in babies?
● Mental disability ● Lung problems
● Hearing loss ● Bleeding problems
● Vision loss ● Liver problems
● Growth problems ● Spleen problems
CMV can cause symptoms when the baby
is
born or later in the baby’s life. Most
babies
born with CMV never develop symptoms
or
disabilities. In some infants, hearing or
vision
loss occurs months or years after birth.
Can pregnant women catch
CMV from children who are in
day care?
Pregnant women can catch CMV through
contact with children in day care,
especially
from children who are 1 to 2½ years of
age.
CMV infection is very common in day care
settings, but CMV does not harm the
children
themselves. Pregnant mothers who have
young children in day care or who work in
day care centers can help prevent
catching
CMV by practicing good hygiene (such as
hand washing).
How can you prevent catching
CMV during pregnancy?
No actions can eliminate all risks of
catching
CMV, but there are measures that can
reduce
the spread of CMV:
● Wash hands often with soap and water,
especially after changing diapers. Wash
well for 15 to 20 seconds.
● Do not kiss young children under the
age
of 5 or 6 on the mouth or cheek. Instead,
kiss them on the head or give them a big
hug.
● Do not share food, drinks, or utensils
(spoons or forks) with young children.
If you are pregnant and work in a day
care
center, reduce your risk of getting CMV
by
working with children who are older than
2½
years of age, especially if you have never
been
infected with CMV or are unsure if you
have
been exposed.
Is there a test for CMV?
Lab tests can be done to see if a woman
has already had CMV infection. These
tests,
however, are not very good at predicting
whether a baby will have health
problems.
Good hygiene by pregnant women is still
the
best way to protect unborn babies
against
CMV infection.
What else should you know
about CMV?
Most children and adults infected with
CMV
have no symptoms and may not even
know
that they have been infected. Others may
develop a mild illness. Symptoms may
include
fever, sore throat, fatigue, and swollen
glands.
Is there a treatment for CMV?
No treatment is currently recommended
for
mothers and infants infected with CMV.
Antiviral drug therapy is being tested in
infants.
Vaccines for preventing CMV infection are
still
in the research and development stage.
 (n.d.). Retrieved from h The natural reservoir for Hendra
http://www.cdc.gov/ncidod/dvrd/spb/mnp virus is thought to be flying foxes (bats of
ages/dispages/Fact_Sheets/Hendra_Nipah the genus Pteropus) found in
%20Fact%20Sheet.pdf Australia. The natural reservoir for Nipah
virus is still under investigation, but
preliminary data suggest that bats
Hendra Virus Disease & of the genus Pteropus are also the
Nipah Virus Encephalitis reservoirs for Nipah virus in Malaysia.
October 16, 2007
http://www.cdc.gov/ncidod/dvrd/spb/mnp Where are the diseases found?
ages/dispages/nipah.htm
http://www.cdc.gov/ncidod/dvrd/spb/mnp Hendra virus caused disease in
ages/dispages/Fact_Sheets/Hendra_Nipah horses in Australia, and the human
%20Fact%20Sheet.pdf infections there were due to direct
What are Hendra and Nipah viruses? exposure to tissues and secretions from
infected horses. Nipah virus caused a
Hendra virus (formerly called relatively mild disease in pigs in Malaysia
equine morbillivirus) is a member of the and Singapore. Nipah virus was
family Paramyxoviridae. The virus was transmitted to humans, cats, and dogs
first isolated in 1994 from specimens through close contact with infected pigs.
obtained during an outbreak of
respiratory and neurologic disease in
horses and humans in Hendra, a suburb
of Brisbane,
Australia. How are Hendra and Nipah viruses
Nipah virus, also a member of the family transmitted to humans?
Paramyxoviridae, is related but not
identical to Hendra virus. Nipah virus was In Australia, humans became ill
initially isolated in 1999 upon examining after exposure to body fluids and
samples from an outbreak of encephalitis excretions of horses infected with Hendra
and respiratory illness among adult men virus. In Malaysia and Singapore, humans
in Malaysia and Singapore. were infected with Nipah virus through
Where are Hendra and Nipah viruses close contact with infected pigs.
found?

Bibliography
What are the signs and symptoms of
Hendra virus disease and Nipah virus
encephalitis?
Only three human cases of Hendra
virus disease have been recognized. Two
of the three individuals known to be
infected had a respiratory illness with
severe flu-like signs and symptoms.
Infection with Nipah virus was associated
with an encephalitis (inflammation of the
brain) characterized by fever and
drowsiness and more serious central
nervous system disease, such as coma,
seizures, and inability to maintain
breathing.
Illness with Nipah virus begins with
3-14 days of fever and headache. This is
followed by drowsiness and disorientation
characterized by mental confusion. These
signs and symptoms can progress to
coma within 24-
48 hours. Some patients have had a
respiratory illness during the early part of
their infections.
Are there any complications after
recovery?
One of the three Hendra virus
infections was marked by a delayed onset
of progressive encephalitis. Serious
nervous disease with Nipah virus
encephalitis has been marked by some
sequelae, such as persistent convulsions
and personality changes.
Are the diseases ever fatal?
Two of the three human patients
infected with Hendra virus died. During
the Nipah virus disease outbreak in
1998-99, about 40% of the patients with
serious nervous disease who entered
hospitals died from the illness.
How are Hendra virus disease and Nipah
virus encephalitis treated?
The drug ribavirin has been shown
to be effective against the viruses in
vitro. However, controlled drug
investigations have not been performed
and the clinical usefulness of these drugs
is uncertain.
Who is at risk for disease from Hendra
and Nipah viruses?
People who have contact with body
fluids or excretions of horses infected
with Hendra virus are at risk for
Hendra virus disease. Nipah virus
infection is associated with close contact
with Nipah virus-infected pigs.
Neither disease has spread from
human to human.
How are infections with Hendra and
Nipah virus prevented?
These diseases can be prevented
by avoiding animals that are known to be
infected and using appropriate
personal protective equipment devices
when it is necessary to come into contact
with potentially infected
animals.
What needs to be done to address the
threat of Hendra and Nipah viruses?
The distribution of these agents in
their natural reservoirs will eventually
define the geographic range of the threat
the viruses pose. However, these viruses
are recent discoveries, and much work
remains to be done on their geographic
distribution and the reservoir species.
The occurrence of the disease in humans
has been associated only with infection of
an intermediate species such as horses
with Hendra and swine with Nipah
virus. Early recognition of the disease in
the intermediate animal host is probably
the most crucial means of limiting future
human cases.
 Chikungunya fever is a viral
disease transmitted to humans by the
bite of infected mosquitoes. Chikungunya
virus was first isolated from the blood of
a febrile patient in Tanzania in 1953, and
has since been cited as the cause of
numerous human epidemics in many
areas of Africa and Asia, and most
recently in a limited area of Europe.
What causes chikungunya fever?
Chikungunya fever is caused by a
virus which belongs to the genus
Alphavirus, in the family Togaviridae.
How do humans become infected with
chikungunya virus?
Humans become infected with
chikungunya virus by the bite of an
infected mosquito. Aedes aegypti, a
household container breeder and
aggressive daytime biter which is
attracted to humans, is the primary
vector of chikungunya virus to humans.
Aedes albopictus has also played a role in
human transmission.
Bibliography
(n.d.). Retrieved from
CDC Chikungunya . (2008, May 4).
Retrieved May 15, 2008, from CDC
Chikungunya :
http://www.cdc.gov/ncidod/dvbid/Chikung
unya/CH_FactSheet.html
What can people do to prevent becoming
infected with chikungunya virus?
The best way to prevent
chikungunya virus infection is to avoid
mosquito bites. There is no vaccine or
preventive drug currently available.
Prevention tips are similar to those for
other viral diseases transmitted by
mosquitoes, such as dengue or West Nile:
• Use insect repellent containing
DEET, Picaridin, oil of lemon
eucalyptus, or IR3535 on exposed
skin. Always follow the directions
on the package.
• Wear long sleeves and pants
(ideally treat clothes with
permethrin or another repellent).
• Have secure screens on windows
and doors to keep mosquitoes out.
• Get rid of mosquito sources in your
yard by emptying standing water
from flower pots, buckets and
barrels. Change the water in pet
dishes and replace the water in
bird baths weekly. Drill holes in tire
swings so water drains out. Keep
children's wading pools empty and
on their sides when they aren't
being used.
• Additionally, a person with
chikungunya fever should limit
their exposure to mosquito bites to
avoid further spreading the
infection. The person should use
repellents when outdoors exposed
to mosquito bites or stay indoors in
areas with screens or under a
mosquito net.
What is the basic chikungunya virus
transmission cycle?
Mosquitoes become infected with
chikungunya virus when they feed on an
infected person. Infected mosquitoes can
then spread the virus to other humans
when they bite them. Monkeys, and
possibly other wild animals, may also
serve as reservoirs of the virus. Aedes
aegypti, a household container breeder
and aggressive daytime biter which is
attracted to humans, is the primary
vector of chikungunya virus to humans.
Aedes albopictus (the Asian tiger
mosquito) has also played a role in
human transmission is Asia, Africa, and
Europe. Various forest-dwelling mosquito
species in Africa have been found to be
infected with the virus.
What type of illness does chikungunya
virus cause?
Chikungunya virus infection can
cause a debilitating illness, most often
characterized by fever, headache,
fatigue, nausea, vomiting, muscle pain,
rash, and joint pain.
“Silent” chikungunya virus
infections (infections without illness) do
occur; but how commonly this happens is
not yet known. Chikungunya virus
infection (whether clinically apparent or
silent) is thought to confer life-long
immunity. Acute chikungunya fever
typically lasts a few days to a couple of
weeks, but as with dengue, West Nile
fever, o'nyong-nyong fever and other
arboviral fevers, some patients have
prolonged fatigue lasting several weeks.
Additionally, some patients have
reported incapacitating joint pain, or
arthritis which may last for weeks or
months.
What is the incubation period for
chikungunya fever?
The incubation period (time from
infection to illness) can be 2-12 days, but There is no vaccine or specific
is usually 3-7 days. antiviral treatment currently available for
Can pregnant women become infected chikungunya fever. Treatment is
with chikungunya virus and pass the symptomatic and can include rest, fluids,
infection to their child? and medicines to relieve symptoms of
Pregnant women can become fever and aching such as ibuprofen,
infected with chikungunya virus during all naproxen, acetaminophen, or
stages of pregnancy and have symptoms paracetamol.
similar to other individuals. Most Aspirin should be avoided. Infected
infections will not result in the virus being persons should be protected from further
transmitted to the fetus. The highest risk mosquito exposure (staying indoors in
for infection of the fetus/child occurs areas with screens and/or under a
when a woman has virus in her blood mosquito net) during the first few days of
(viremic) at the time of delivery. the illness so they can not contribute to
There are also rare reports of first the transmission cycle.
trimester abortions occurring after Where does chikungunya virus occur?
chikungunya infection. Pregnant women The geographic range of the virus is
should take precautions to avoid primarily in Africa and Asia.
mosquito bites. Products containing DEET
can be used in pregnancy without
adverse effects.
Can the virus be transmitted to a child by
breastfeeding?
Currently, there is no evidence that
the virus is transmitted through breast
milk
What is the mortality rate of chikungunya
fever?
Fatalities related to chikungunya
virus are rare and appear to be
associated to increased age.
How is chikungunya virus infection
treated?
What is Lassa fever?
Lassa fever is an acute viral illness
that occurs in West Africa. The illness was
discovered in 1969 when two missionary
nurses died in Nigeria, West Africa. The
cause of the illness was found to be Lassa
virus, named after the town in Nigeria
where the first cases originated. The
virus, a member of the virus family
Arenaviridae, is a single-stranded RNA
virus and is zoonotic, or animal-borne.
In areas of Africa where the disease is
endemic (that is, constantly present),
Lassa fever is a significant cause of
morbidity and mortality. While Lassa
fever is mild or has no observable
symptoms in about 80% of people
infected with the virus, the remaining
20% have a severe multisystem disease.
Lassa fever is also associated with
occasional epidemics, during which the
case-fatality rate can reach 50%.
Where is Lassa fever found?
Lassa fever is an endemic disease
in portions of West Africa. It is recognized
in Guinea, Liberia, Sierra Leone, as well
as Nigeria. However, because the rodent
species which carry the virus are found
throughout West Africa, the actual
geographic range of the disease may
extend to other countries in the region.
How is the disease diagnosed in the
laboratory?
Lassa fever is most often
diagnosed by using enzyme-linked
immunosorbent serologic assays (ELISA),
which detect IgM and IgG antibodies as
well as Lassa antigen. The virus itself
may be cultured in 7 to 10 days.
Immunohistochemistry performed on
tissue specimens can be used to make a
post-mortem diagnosis. The virus can
also be detected by reverse transcription-
polymerase chain reaction (RT-PCR);
however, this method is primarily a
research tool.
Are there complications after recovery?
The most common complication of
Lassa fever is deafness. Various degrees
of deafness occur in approximately one-
third of cases, and in many cases hearing
loss is permanent. As far as is known,
severity of the disease does not affect
this complication: deafness may develop
in mild as well as in severe cases.
Spontaneous abortion is another serious
complication
Bibliography
(n.d.). Retrieved from
Lassa Fever. (2004 , Decmber 3).
Retrieved May 15, 2008, from Lassa
Fever:
http://www.cdc.gov/ncidod/dvrd/spb/mnp
ages/dispages/lassaf.htm
Where is Lassa fever found?
Lassa fever is an endemic disease
in portions of West Africa. It is recognized
in Guinea, Liberia, Sierra Leone, as well
as Nigeria. However, because the rodent
species which carry the virus are found
throughout West Africa, the actual
geographic range of the disease may
extend to other countries in the region.
How many people become infected?
The number of Lassa virus
infections per year in West Africa is
estimated at 100,000 to 300,000, with
approximately 5,000 deaths.
Unfortunately, such estimates are crude,
because surveillance for cases of the
disease is not uniformly performed. In
some areas of Sierra Leone and Liberia, it
is known that 10%-16% of people
admitted to hospitals have Lassa fever,
which indicates the serious impact of the
disease on the population of this region.
In what animal host is Lassa virus
maintained?
The reservoir, or host, of Lassa
virus is a rodent known as the
"multimammate rat" of the genus
Mastomys. It is not certain which species
of Mastomys are associated with Lassa;
however, at least two species carry the
virus in Sierra Leone. Mastomys rodents
breed very frequently, produce large
numbers of offspring, and are numerous
in the savannas and forests of West,
Central, and East Africa. In addition,
Mastomys generally readily colonize
human homes. All these factors together
contribute to the relatively efficient
spread of Lassa virus from infected
rodents to humans.
How do humans get Lassa fever?
There are a number of ways in
which the virus may be transmitted, or
spread, to humans. The Mastomys
rodents shed the virus in urine and
droppings. Therefore, the virus can be
transmitted through direct contact with
these materials, through touching objects
or eating food contaminated with these
materials, or through cuts or sores.
Because Mastomys rodents often live in
and around homes and scavenge on
human food remains or poorly stored
food, transmission of this sort is common.
Contact with the virus also may occur
when a person inhales tiny particles in
the air contaminated with rodent
excretions. This is called aerosol or
airborne transmission. Finally, because
Mastomys rodents are sometimes
consumed as a food source, infection
may occur via direct contact when they
are caught and prepared for food.
Lassa fever may also spread
through person-to-person contact. This
type of transmission occurs when a
person comes into contact with virus in
the blood, tissue, secretions, or
excretions of an individual infected with
the Lassa virus. The virus cannot be
spread through casual contact (including
skin-to-skin contact without exchange of
body fluids). Person-to-person
transmission is common in both village
and health care settings, where, along
with the above-mentioned modes of
transmission, the virus also may be
spread in contaminated medical
equipment, such as reused needles (this
is called nosocomial transmission).
What are the symptoms of Lassa fever?
Signs and symptoms of Lassa fever
typically occur 1-3 weeks after the
patient comes into contact with the virus.
• These include fever, retrosternal
pain (pain behind the chest wall),
sore throat, back pain, cough,
abdominal pain,
• vomiting, diarrhea, conjunctivitis,
facial swelling, proteinuria (protein
in the urine), and mucosal
bleeding.
• Neurological problems have also
been described, including hearing
loss, tremors, and encephalitis.
Because the
symptoms of Lassa fever are so varied
and nonspecific, clinical diagnosis is often
difficult.
How is Lassa fever treated?
Ribavirin, an antiviral drug, has
been used with success in Lassa fever
patients. It has been shown to be most
effective when given early in the course
of the illness. Patients should also receive
supportive care consisting of
maintenance of appropriate fluid and
electrolyte balance, oxygenation and
blood pressure, as well as treatment of
any other complicating infections.
What groups are at risk for getting the
illness?
Individuals at risk are those who
live or visit areas with a high population
of Mastomys rodents infected with Lassa
virus or are exposed to infected humans.
Hospital staff are not at great risk for
infection as long as protective measures
are taken.
How is Lassa fever prevented?
Primary transmission of the Lassa virus
from its host to humans can be prevented
by
• Avoiding contact with Mastomys
rodents, especially in the
geographic regions where
outbreaks occur.
• Putting food away in rodent-proof
containers and keeping the home
clean help to discourage rodents
from entering homes.
• Using these rodents as a food
source is not recommended.
Trapping in and around homes can
help reduce rodent populations.
However, thewide distribution of
Mastomys in Africa makes
complete control of this rodent
reservoir impractical.
• When caring for patients with
Lassa fever, further transmission of
the disease through person-to-
person contact or\ nosocomial
routes can be avoided by taking
preventive precautions against
contact with patient secretions
(together called VHF isolation
precautions or barrier nursing
methods).
• Such precautions include wearing
protective clothing, such as masks,
gloves, gowns, and goggles; using
infection control measures, such as
complete equipment sterilization;
and isolating infected patients
from contact with unprotected
persons until the disease has run
its course.
 CDC. (2006, September 12). West Nile
Virus: What You Need To Know. Retrieved
May 15, 2008, from What Is West Nile
Virus?:
http://www.cdc.gov/ncidod/dvbid/westnile
/wnv_factsheet.htm

What Is West Nile Virus?

West Nile virus (WNV) is a
potentially serious illness. Experts believe
WNV is established as a seasonal
epidemic in North America that flares up
in the summer and continues into the fall.
This fact sheet contains important
information that can help you recognize
and prevent West Nile virus.

What Can I Do to Prevent WNV?

The easiest and best way to avoid WNV is
to prevent mosquito bites.
• When you are outdoors, use insect
repellent containing an EPA-
registered active ingredient. Follow
the directions on the package.
• Many mosquitoes are most active
at dusk and dawn. Be sure to use
Bibliography insect repellent and wear long
sleeves and pants at these times
 or consider staying indoors during
these hours.
• Make sure you have good screens
on your windows and doors to keep
mosquitoes out.
• Get rid of mosquito breeding sites
by emptying standing water from
flower pots, buckets and barrels.
Change the water in pet dishes
and replace the water in bird baths
weekly. Drill holes in tire swings so
water drains out. Keep children's
wading pools empty and on their
sides when they aren't being used.
What Are the Symptoms of WNV?
• Serious Symptoms in a Few People.
About one in 150 people infected
with WNV will develop severe
illness. The severe symptoms can
include high fever, headache, neck
stiffness, stupor, disorientation,
coma, tremors, convulsions,
muscle weakness, vision loss,
numbness and paralysis. These
symptoms may last several weeks,
and neurological effects may be
permanent.
• Milder Symptoms in Some People.
Up to 20 percent of the people who
become infected have symptoms
such as fever, headache, and body
aches, nausea, vomiting, and
sometimes swollen lymph glands
or a skin rash on the chest,
stomach and back. Symptoms can
last for as short as a few days,
though even healthy people have
become sick for several weeks.
• No Symptoms in Most People.
Approximately 80 percent of
people (about 4 out of 5) who are
infected with WNV will not show
any symptoms at all.
How Does West Nile Virus Spread?
• Infected Mosquitoes. Most often,
WNV is spread by the bite of an
infected mosquito. Mosquitoes
become infected when they feed
on infected birds. Infected
mosquitoes can then spread WNV
to humans and other animals when
they bite.
• Transfusions, Transplants, and
Mother-to-Child. In a very small
number of cases, WNV also has
been spread through blood
transfusions, organ transplants,
breastfeeding and even during
pregnancy from mother to baby.
• Not through touching. WNV is not
spread through casual contact
such as touching or kissing a
person with the virus.
How Soon Do Infected People Get Sick?
People typically develop symptoms
between 3 and 14 days after they are
bitten by the infected mosquito.
How Is WNV Infection Treated?
There is no specific treatment for
WNV infection. In cases with milder
symptoms, people experience symptoms
such as fever and aches that pass on
their own, although even healthy people
have become sick for several weeks. In
more severe cases, people usually need
to go to the hospital where they can
receive supportive treatment including
intravenous fluids, help with breathing
and nursing care.
What Should I Do if I Think I Have WNV?
Milder WNV illness improves on its own,
and people do not necessarily need to
seek medical attention for this infection
though they may choose to do so. If you
develop symptoms of severe WNV illness,
such as unusually severe headaches or
confusion, seek medical attention
immediately. Severe WNV illness usually
requires hospitalization. Pregnant women
and nursing mothers are encouraged to
talk to their doctor if they develop
symptoms that could be WNV.
What Is the Risk of Getting Sick from
WNV?
People over 50 at higher risk to get
severe illness. People over the age of 50
are more likely to develop serious
symptoms of WNV if they do get sick and
should take special care to avoid
mosquito bites.
Being outside means you're at risk. The
more time you're outdoors, the more time
you could be bitten by an infected
mosquito. Pay attention to avoiding
mosquito bites if you spend a lot of time
outside, either working or playing.

Risk through medical procedures is very

low. All donated blood is checked for WNV
before being used. The risk of getting
WNV through blood transfusions and
organ transplants is very small, and
should not prevent people who need
surgery from having it. If you have
concerns, talk to your doctor.
Pregnancy and nursing do not increase
risk of becoming infected with WNV. The
risk that WNV may present to a fetus or
an infant infected through breastmilk is
still being evaluated. Talk with your care
provider if you have concerns.
What Else Should I Know?

If you find a dead bird: Don't handle the

body with your bare hands. Contact your
local health department for instructions
on reporting and disposing of the body.
They may tell you to dispose of the bird
after they log your report.
Kaposi's sarcoma (KS) is a tumor caused
by Human herpesvirus 8 (HHV8), also
known as Kaposi's sarcoma-associated
herpesvirus (KSHV). It was originally
described by Moritz Kaposi, a Hungarian
dermatologist practicing at the University
of Vienna in 1872.[1] It became more
widely known as one of the AIDS defining
illnesses in the 1980s.
Despite its name, it is generally not
considered a true sarcoma, which is a
tumor arising from mesenchymal tissue.
KS actually arises as a cancer of
lymphatic endothelium and forms
vascular channels that fill with blood
cells, giving the tumor its characteristic
bruise-like appearance.
KS lesions contain tumor cells with a
characteristic abnormal elongated shape,
called spindle cells. The tumor is highly
vascular, containing abnormally dense
and irregular blood vessels, which leak
red blood cells into the surrounding tissue
and give the tumor its dark color.
Inflammation around the tumor may
produce swelling and pain.
Although KS may be suspected from the
appearance of lesions and the patient's
risk factors, a definite diagnosis can only
be made by biopsy and microscopic
examination, which will show the
presence of spindle cells. Detection of the
viral protein LANA in tumor cells confirms
the diagnosis.

What are the signs and symptoms of
genital herpes?
Most people infected with HSV-2
are not aware of their infection. However,
if signs and symptoms occur during the
first outbreak, they can be quite
pronounced. The first outbreak usually
occurs within two weeks after the virus is
transmitted, and the sores typically heal
within two to four weeks. Other signs and
symptoms during the primary episode
may include a second crop of sores, and
flu-like symptoms, including fever and
swollen glands. However, most
individuals with HSV-2 infection never
have sores, or they have very mild signs
that they do not even notice or that they
mistake for insect bites or another skin
condition.
People diagnosed with a first
episode of genital herpes can expect to
have several (typically four or five)
outbreaks (symptomatic recurrences)
within a year. Over time these
recurrences usually decrease in
frequency. It is possible that a person
becomes aware of the “first episode”
years after the infection is acquired.
How is it diagnose?
The signs and symptoms
associated with HSV-2 can vary greatly.
Health care providers can diagnose
genital herpes by visual inspection if the
outbreak is typical, and by taking a
sample from the sore(s) and testing it in
a laboratory. HSV infections can be
diagnosed between outbreaks by the use
of a blood test. Blood tests, which detect
antibodies to HSV-1 or HSV-2 infection,
can be helpful, although the results are
not always clear-cut.
Is there a treatment for herpes?
There is no treatment that can cure
herpes, but antiviral medications can
shorten and prevent outbreaks during the
period of time the person takes the
medication. In addition, daily
suppressive therapy for symptomatic
herpes can reduce transmission to
partners.
Bibliography
(n.d.). Retrieved from
Genital Herpes - CDC Fact Sheet. (2008,
January 4). Retrieved May 15, 2008, from
Sexually Transmitted Diseases:
http://www.cdc.gov/std/Herpes/STDFact-
Herpes.htm

What is genital herpes?
Genital herpesis a sexually
transmitted disease (STD) caused by the
herpes simplex viruses type 1 (HSV-1) or
type 2 (HSV-2). Most genital herpes is
caused by HSV-2. Most individuals have
no or only minimal signs or symptoms
from HSV-1 or HSV-2 infection. When
signs do occur, they typically appear as
one or more blisters on or around the
genitals or rectum.
The blisters break, leaving tender
ulcers (sores) that may take two to four
weeks to heal the first time they occur.
Typically, another outbreak can appear
weeks or months after the first, but it
almost always is less severe and shorter
than the first outbreak. Although the
infection can stay in the body indefinitely,
the number of outbreaks tends to
decrease over a period of years.
How common is genital Herpes?
Results of a nationally
representative study show that genital
herpes infection is common in the United
States. Nationwide, at least 45 million
people ages 12 and older, or one out of
five adolescents and adults, have had
genital HSV infection. Over the past
decade, the percent of Americans with
genital herpes infection in the U.S. has
decreased.
Genital HSV-2 infection is more
common in women (approximately one
out of four women) than in men (almost
one out of eight). This may be due to
male-to-female transmission being more
likely than female-to-male transmission.
How do people get genital Herpes?
HSV-1 and HSV-2 can be found in
and released from the sores that the
viruses cause, but they also are released
between outbreaks from skin that does
not appear to have a sore. Generally, a
person can only get HSV-2 infection
during sexual contact with someone who
has a genital HSV-2 infection.
Transmission can occur from an infected
partner who does not have a visible sore
and may not know that he or she is
infected.
HSV-1 can cause genital herpes,
but it more commonly causes infections
of the mouth and lips, so-called “fever
blisters.” HSV-1 infection of the genitals
can be caused by oral-genital or genital-
genital contact with a person who has
HSV-1 infection. Genital HSV-1 outbreaks
recur less regularly than genital HSV-2
outbreaks.
What are the complications?
Genital herpes can cause recurrent
painful genital sores in many adults, and
herpes infection can be severe in people
with suppressed immune systems.
Regardless of severity of symptoms,
genital herpes frequently causes
psychological distress in people who
know they are infected.
In addition, genital HSV can lead to
potentially fatal infections in babies. It is
important that women avoid contracting
herpes during pregnancy because a
newly acquired infection during late
pregnancy poses a greater risk of
transmission to the baby. If a woman has
active genital herpes at delivery, a
cesarean delivery is usually performed.
Fortunately, infection of a baby from a
woman with herpes infection is rare.
Herpes may play a role in the
spread of HIV, the virus that causes AIDS.
Herpes can make people more
susceptible to HIV infection, and it can
make HIV-infected individuals more
infectious.
How can herpes be prevented?
The surest way to avoid
transmission of sexually transmitted
diseases, including genital herpes, is to
abstain from sexual contact, or to be in a
long-term mutually monogamous
relationship with a partner who has been
tested and is known to be uninfected.
Genital ulcer diseases can occur in
both male and female genital areas that
are covered or protected by a latex
condom, as well as in areas that are not
covered. Correct and consistent use of
latex condoms can reduce the risk of
genital herpes.
Persons with herpes should abstain
from sexual activity with uninfected
partners when lesions or other symptoms
of herpes are present. It is important to
know that even if a person does not have
any symptoms he or she can still infect
sex partners. Sex partners of infected
persons should be advised that they may
become infected and they should use
condoms to reduce the risk. Sex partners
can seek testing to determine if they are
infected with HSV. A positive HSV-2 blood
test most likely indicates a genital herpes
infection.

What is Norovirus?
Norovirus (was "Norwalk-like
viruses"), an RNA virus of the
Caliciviridae taxonomic family, causes
approximately 90% of epidemic non-
bacterial outbreaks of gastroenteritis
around the world and is responsible for
50% of all foodborne outbreaks of
gastroenteritis in the US. Norovirus
affects people of all ages. The viruses are
transmitted by faecally contaminated
food or water and by person-to-person
contact. After infection, immunity to
norovirus is not complete nor long-lasting
There is an inherited predisposition to
infection and people whose blood type
can be detected in their saliva are more
often infected.
Outbreaks of norovirus disease
often occur in closed or semi-closed
communities, such as long-term care
facilities, hospitals, prisons, dormitories,
and cruise ships where once the virus has
been introduced, the infection spreads
very rapidly by either person-to-person
transmission or through contaminated
food Many norovirus outbreaks have been
traced to food that was handled by one
infected person
Norovirus is rapidly killed by
chlorine-based disinfectants, but because
the virus particle does not have a lipid
envelope, it is less susceptible to alcohols
and detergents.
There are different genogroups of
norovirus and the majority of noroviruses
that infect humans are classified into
genogroup G1 and G2.
Originally, norovirus was named after
Norwalk, Ohio, where an outbreak of
acute gastroenteritis occurred among
children at an elementary school in
November 1968. In 1972, immune
electron microscopy on stored stool
samples identified a virus, which was
given the name Norwalk virus. Numerous
outbreaks with similar symptoms have
been reported since. The cloning and
sequencing of the Norwalk virus genome
showed that these viruses have a
genomic organization consistent with
viruses belonging to the family
Caliciviridae. The name norovirus
(Norovirus for the genus) was approved
by the International Committee on
Taxonomy of Viruses in 2002.
Common names of the illness caused by
noroviruses are winter vomiting disease,
viral gastroenteritis and acute non-
bacterial gastroenteritis, also colloquially
known as "stomach flu" (a broad name
which can also refer to gastric
inflammation caused by other viruses
and bacteria).
How Does Noro Virus Spread?
Noroviruses are transmitted
primarily through the fecal-oral route,
either by consumption of fecally
contaminated food or water or by direct
person-to-person spread.
Environmental and fomite contamination
may also act as a source of infection.
Good evidence exists for transmission
due to aerosolization of vomitus that
presumably results in droplets
contaminating surfaces or entering the
oral mucosa and being swallowed. No
evidence suggests that infection occurs
through the respiratory system.
Noroviruses are highly contagious,
and it is thought that an inoculum of as
few as 10 viral particles may be sufficient
to infect an individual. During outbreaks
of norovirus gastroenteritis, several
modes of transmission have been
documented; for example, initial
foodborne transmission in a restaurant,
followed by secondary person-to-person
transmission to household contacts.
Although presymptomatic viral shedding
may occur, shedding usually begins with
onset of symptoms and may continue for
2 weeks after recovery. It is unclear to
what extent viral shedding over 72 hours
after recovery signifies continued
infectivity.
Noroviruses are transmitted directly via
person to person or indirectly via
contaminated water and foods. A CDC
study of eleven outbreaks in New York
State lists the suspected mode of
transmission as person-to-person in
seven outbreaks, foodborne in two,
waterborne in one, and one unknown.
The source of waterborne outbreaks may
include water from municipal supplies,
wells, recreational lakes, swimming pools
and ice machines.
Shellfish and salad ingredients are the
foods most often implicated in Norwalk
outbreaks. Ingestion of raw or
insufficiently steamed clams and oysters
poses a high risk for infection with the
Norwalk virus. Foods other than shellfish
are contaminated by ill food handlers.
What are the signs and symptoms
Norovirus?
The incubation period for
norovirus-associated gastroenteritis in
humans is usually between 24 and 48
hours (median in outbreaks 33 to 36
hours), but cases can occur
within 12 hours of exposure. Norovirus
infection usually presents as
• acute-onset vomiting, watery non-
bloody diarrhea with abdominal
cramps, and nausea.
• Low-grade fever also occasionally
occurs, and vomiting is more
common in children.
• Dehydration is the most common
complication, especially among the
young and elderly, and may
require medical attention.
Symptoms usually last 24 to 60
hours.
Recovery is usually complete and there is
no evidence of any serious long-term
sequelae. Studies with volunteers given
stool filtrates have shown that
asymptomatic infection may occur in as
many as 30% of infections, although the
role of asymptomatic infection in
norovirus transmission is not well
understood
How can norovirus be prevented?
 • Prevention of foodborne norovirus
disease is based on the provision
of safe food and water.
• Noroviruses are relatively
resistant to environmental
challenge: they are able to survive
freezing, temperatures as high as
60 C, and have even been
associated with illness after being
steamed in shellfish.
Moreover, noroviruses can survive in up
to 10 ppm chlorine, well in excess of
levels routinely present in public water
systems. Despite
these features, it is likely that relatively
simple measures, such as
• correct handling of cold foods,
• frequent handwashing, and paid
sick leave, may substantially
reduce foodborne transmission of
noroviruses.
In health care environments, the
prevention of nosocomial infections
involves routine and terminal cleaning.
Nonflammable alcohol vapor in CO2
systems are used in health care
environments where medical electronics
would be adversely affected by
aerosolized chlorine or other caustic
compounds..

http://www.cdc.gov/ncidod/dvrd/revb/gast
ro/noro-factsheet.pdf

Where is hantavirus found and how
common is it?
Wild roden ts
can pass hantavirus to people. Several
different types of wild mice and rats can
be infected with hantavirus and pass it in
their droppings, urine, or saliva. The
common house mouse does not carry
hantavirus. People can get hantavirus
when they touch rodent urine, droppings,
or places where these animals have
nested. Dried droppings or urine can be
stirred up in dust and breathed in by
people. Hantavirus has not been shown
to infect other kinds of animals, such as
dogs, cats, or farm animals. HPS is
transmitted to humans through a process
called aerosolization. Aerosolization
occurs when dried materials
contaminated by rodent excreta or saliva
are disturbed. Humans become infected
by breathing in these infectious aerosols.
You cannot get the virus from
touching or kissing a person who has HPS
or from a health care worker who has
treated someone with the disease. In
addition, you cannot contract the virus
from a blood transfusion in which you
receive blood from a person who survived
HPS.
HPS in the United States is not
known to be transmitted by farm animals,
dogs, or cats or from rodents purchased
from a pet store.
Bibliography
All About Hantaviruses. (2004, June 21).
Retrieved May 15, 2008, from Hantavirus
Pulmonary Syndrome:
http://www.cdc.gov/ncidod/diseases/hant
a/hps/noframes/phys/casedefn.htm
Hanta virus. (2007, January 29).
Retrieved may 15, 2008, from
http://www.nlm.nih.gov/medlineplus/ency
/imagepages/17201.htm

What are the symptoms of Hantavirus
Pulmonary Syndrome?
HPS begins one to six weeks after
inhaling the virus in contaminated dust.
The disease begins with 2-6 days of "flu-
like" illness including fever, sore muscles,
headaches, nausea, vomiting, and
fatigue. As the disease gets worse, it
causes shortness of breath due to fluid
filled lungs and hospital care is then
required. These symptoms, which are
very similar to HFRS, include tachycardia
and tachypnoea. Such conditions can
lead to a cardiopulmonary phase, where
cardiovascular shock can occur, and
hospitalization of the patient is required.It
is usually a serious infection and about 1
out of 3 people diagnosed with HPS have
died.
What is hantavirus pulmonary syndrome?
Hantavirus pulmonary syndrome
(HPS) is a deadly disease transmitted by
infected rodents through urine,
droppings, or saliva. Humans can
contract the disease when they breathe
in aerosolized virus. HPS was first
recognized in 1993 and has since been
identified throughout the United States.
Although rare, HPS is potentially deadly.
Rodent control in and around the home
remains the primary strategy for
preventing hantavirus infection
Hantavirus pulmonary syndrome is
a rare disease caused by a virus
(hantavirus). The first symptoms of
hantavirus pulmonary syndrome are
fever, muscle pain, and being tired. This
happens 1 to 3 weeks after a person is
exposed to hantavirusFamily
Bunyaviridae: Hantaviruses are members
of the family Bunyaviridae, which consists
of 5 genera and 250 species.
Hantaviruses can cause hantavirus
pulmonary syndrome (HPS) or
hemorrhagic fever with renal syndrome
(HFRS). The 5 genera of Bunyaviridae
include Bunyavirus, Phlebovirus,
Nairovirus, Tospovirus, and Hantavirus.
How long can hantavirus remain
infectious in the environment?
The length of time hantaviruses can
remain infectious in the environment is
variable and depends on environmental
conditions, such as temperature and
humidity, whether the virus is indoors or
outdoors or exposed to the sun, and even
on the rodent’s diet (which would affect
the chemistry of its urine). Viability for 2
or 3 days has been shown at normal
room temperature. Exposure to sunlight
will decrease the time of viability, and
freezing temperatures will actually
increase the time that the virus remains
viable. Since the survival of infectious
virus is measured in terms of hours or
days, only active infestations of infected
rodents result in conditions that are likely
to lead to human hantavirus infection.
How can I protect myself from hantavirus
pulmonary syndrome?
• Keep a clean home, especially the
kitchen (wash dishes, clean
counters and floor, and keep food
covered in rodent-proof
containers).
• Keep a tight-fitting lid on garbage,
and discard uneaten pet food at
the end of the day.
• Set and keep spring-loaded rodent
traps near baseboards because
rodents tend to run along walls and
in tight spaces rather than out in
the open.
• Set Environmental Protection
Agency-approved rodenticide with
bait under plywood or plastic
shelter along baseboards. These
are sometimes known as "covered
bait stations." Remember to follow
product use instructions carefully,
since rodenticides are poisonous to
pets and people, too.
• If bubonic plague is a problem in
your area, spray flea killer or
spread flea powder in the area
before setting traps. This is
important. If you control rodents
but do not control fleas as well,
you may increase the risk of
infection with bubonic plague,
since once the rodents die, fleas
 will leave them and seek other Equipment and materials for intubation
food sources, including humans. and mechanical ventilation should be
readily available since onset of
• Seal all entry holes 1/4 inch wide
respiratory failure may be precipitous.
or wider with lath screen or lath
metal, cement, wire screening, or
other patching materials, inside Intravenous ribavirin, a guanosine
and out. analogue, has not been shown to be
effective for treatment of HPS despite its
effects on a related disease, hemorrhagic
Treatment
fever with renal syndrome (HFRS), which
There is no specific treatment or cure for is caused by Old World hantaviruses.
hantavirus infection. Treatment of Controlled trials showed a reduction in
patients with HPS remains supportive in case-fatality for HFRS patients treated
nature. Patients should receive with ribavirin. However, despite in vitro
appropriate, broad-spectrum antibiotic activity of ribavirin against SNV, neither
therapy while awaiting confirmation of a an open-label trial conducted during the
diagnosis of HPS. Care during the initial 1993 outbreak nor an attempted placebo-
stages of the disease should include controlled trial demonstrated clinical
antipyretics and analgesia as needed. benefit for HPS. Ribavirin is not
recommended for treatment of HPS and
If there is a high degree of suspicion of is not available for this use under any
HPS, patients should be immediately existing research protocol.
transferred to an emergency department
or intensive care unit (ICU) for close
monitoring and care. Patients presenting
with fulminant illness due to HPS have a
poor prognosis despite ICU care. ICU
management should include careful
assessment, monitoring and adjustment
of volume status and cardiac function,
including inotropic and vasopressor
support if needed. Fluids should be
administered carefully due to the
potential for capillary leakage.
Supplemental oxygen should be
administered if patients become hypoxic.