1)Crimean-Congo hemorrhagic fever (CCHF) is

caused by infection with a tick-borne virus (Nairovirus) in the family Bunyaviridae. The

disease was first characterized in the Crimea in 1944 and given the name Crimean
hemorrhagic fever. It was then later recognized in 1969 as the cause of illness in the
Congo, thus resulting in the current name of the disease.
Crimean-Congo hemorrhagic fever is found in Eastern Europe, particularly in the former
Soviet Union, throughout the Mediterranean, in northwestern China, central Asia,
southern Europe, Africa, the Middle East, and the Indian subcontinent

TRANSMISSION
Ixodid (hard) ticks, especially those of the genus, Hyalomma, are both a reservoir and a
vector for the CCHF virus. Numerous wild and domestic animals, such as cattle, goats,
sheep and hares, serve as amplifying hosts for the virus. Transmission to humans
occurs through contact with infected ticks or animal blood. CCHF can be transmitted
from one infected human to another by contact with infectious blood or body fluids.
Documented spread of CCHF has also occurred in hospitals due to improper
sterilization of medical equipment, reuse of injection needles, and contamination of
medical supplies.

DIAGNOSIS
Laboratory tests that are used to diagnose CCHF include antigen-capture enzyme-
linked immunosorbent assay (ELISA), real time polymerase chain reaction (RT-PCR),
virus isolation attempts, and detection of antibody by ELISA (IgG and IgM). Laboratory
diagnosis of a patient with a clinical history compatible with CCHF can be made during
the acute phase of the disease by using the combination of detection of the viral antigen
(ELISA antigen capture), viral RNA sequence (RT-PCR) in the blood or in tissues
collected from a fatal case and virus isolation. Immunohistochemical staining can also
show evidence of viral antigen in formalin-fixed tissues. Later in the course of the
disease, in people surviving, antibodies can be found in the blood. But antigen, viral
RNA and virus are no more present and detectable

SIGNS and SYMPTOMS

The onset of CCHF is sudden, with initial signs and symptoms including headache, high
fever, back pain, joint pain, stomach pain, and vomiting. Red eyes, a flushed face, a red
throat, and petechiae (red spots) on the palate are common. Symptoms may also
include jaundice, and in severe cases, changes in mood and sensory perception.
As the illness progresses, large areas of severe bruising, severe nosebleeds, and
uncontrolled bleeding at injection sites can be seen, beginning on about the fourth day
of illness and lasting for about two weeks. In documented outbreaks of CCHF, fatality
rates in hospitalized patients have ranged from 9% to as high as 50%.
The long-term effects of CCHF infection have not been studied well enough in survivors
to determine whether or not specific complications exist. However, recovery is slow.
TREATMENT
Treatment for CCHF is primarily supportive. Care should include careful attention to
fluid balance and correction of electrolyte abnormalities, oxygenation and hemodynamic
support, and appropriate treatment of secondary infections. The virus is sensitive in vitro
to the antiviral drug ribavirin. It has been used in the treatment of CCHF patients
reportedly with some benefit.
2)Ebola virus disease (EVD) is a deadly disease with occasional outbreaks
that occur primarily on the African continent. EVD most commonly affects people
and nonhuman primates (such as monkeys, gorillas, and chimpanzees). It is
caused by an infection with a group of viruses within the genus Ebolavirus:
 Ebola virus (species Zaire ebolavirus)
 Sudan virus (species Sudan ebolavirus)
 Taï Forest virus (species Taï Forest ebolavirus, formerly Côte d’Ivoire
ebolavirus)
 Bundibugyo virus (species Bundibugyo ebolavirus)
 Reston virus (species Reston ebolavirus)
 Bombali virus (species Bombali ebolavirus)
Of these, only four (Ebola, Sudan, Taï Forest, and Bundibugyo viruses) are
known to cause disease in people. Reston virus is known to cause disease in
nonhuman primates and pigs, but not in people. It is unknown if Bombali virus,
which was recently identified in bats, causes disease in either animals or people.
Ebola virus was first discovered in 1976 near the Ebola River in what is now the
Democratic Republic of Congo. Since then, the virus has been infecting people
from time to time, leading to outbreaks in several African countries. Scientists do
not know where Ebola virus comes from. However, based on the nature of
similar viruses, they believe the virus is animal-borne, with bats or nonhuman
primates with bats or nonhuman primates (chimpanzees, apes, monkeys, etc.)
being the most likely source. Infected animals carrying the virus can transmit it to
other animals, like apes, monkeys, duikers and humans.
TRANSMISSION

SIGNS AND SYMPTOMS

Symptoms may appear anywhere from 2 to 21 days after contact with the virus,
with an average of 8 to 10 days. The course of the illness typically progresses
from “dry” symptoms initially (such as fever, aches and pains, and fatigue), and
then progresses to “wet” symptoms (such as diarrhoea and vomiting) as the
person becomes sicker.
Primary signs and symptoms of Ebola often include some or several of the
following:
 Fever
 Aches and pains, such as severe headache, muscle and joint pain, and
abdominal (stomach) pain
 Weakness and fatigue
 Gastrointestinal symptoms including diarrhoea and vomiting
 Abdominal (stomach) pain
  Unexplained hemorrhaging, bleeding or bruising
Other symptoms may include red eyes, skin rash, and hiccups (late stage).
Many common illnesses can have the same symptoms as EVD, including
influenza (flu), malaria, or typhoid fever.
EVD is a rare but severe and often deadly disease. Recovery from EVD depends
on good supportive clinical care and the patient’s immune response. Studies
show that survivors of Ebola virus infection have antibodies (proteins made by
the immune system that identify and neutralize invading viruses) that can be
detected in the blood up to 10 years after recovery. Survivors are thought to have
some protective immunity to the type of Ebola that sickened them.

DIAGNOSIS
Diagnosing Ebola virus disease (EVD) shortly after infection can be difficult. Early
symptoms of EVD such as fever, headache, and weakness are not specific to
Ebola virus infection and often are seen in patients with other more common
diseases, like malaria and typhoid fever.
To determine whether EVD is a possible diagnosis, there must be a combination
of symptoms suggestive of EVD AND a possible exposure to EVD within 21 days
before the onset of symptoms. An exposure may include contact with:
 blood or body fluids from a person sick with or who died from EVD,
 objects contaminated with blood or body fluids of a person sick with or who
died from EVD,
 infected fruit bats and nonhuman primates (apes or monkeys), or
 semen from a man who has recovered from EVD.
If a person shows signs of EVD and has had a possible exposure, he or she
should be isolated (separated from other people) and public health authorities
notified. Blood samples from the patient should be collected and tested to
confirm infection. Ebola virus can be detected in blood after onset of symptoms.
It may take up to three days after symptoms start for the virus to reach detectable
levels.
Polymerase chain reaction (PCR) is one of the most commonly used diagnostic
methods because of its ability to detect low levels of Ebola virus. PCR methods
can detect the presence of a few virus particles in small amounts of blood, but
the ability to detect the virus increases as the amount of virus increases during
an active infection. When the virus is no longer present in great enough numbers
in a patient’s blood, PCR methods will no longer be effective. Other methods,
based on the detection of antibodies an EVD case produces to an infection, can
then be used to confirm a patient’s exposure and infection by Ebola virus.
A positive laboratory test means that Ebola infection is confirmed. Public health
authorities will conduct a public health investigation, including identifying and
monitoring all possibly exposed contacts.

TREATMENT
Symptoms of Ebola virus disease (EVD) are treated as they appear. When used
early, basic interventions can significantly improve the chances of survival. These
include:
 Providing fluids and electrolytes (body salts) through infusion into the vein
(intravenously).
 Offering oxygen therapy to maintain oxygen status.
 Using medication to support blood pressure, reduce vomiting and
diarrhoea and to manage fever and pain.
 Treating other infections, if they occur.
Antiviral Drugs
There is currently no antiviral drug licensed by the U.S. Food and Drug
Administration (FDA) to treat EVD in people.
During the 2018 eastern Democratic Republic of the Congo outbreak, four
investigational treatments were initially available to treat patients with confirmed
Ebola. For two of those treatments, called regeneron (REGN-EB3) and mAb114,
overall survival was much higher. These two antiviral drugs currently remain in
use for patients with confirmed Ebola.
Drugs that are being developed to treat EVD work by stopping the virus from
making copies of itself.
 OUTBREAK OF EBOLA

.
3)Marburg virus was first recognized in 1967, when outbreaks of
hemorrhagic fever occurred simultaneously in laboratories in Marburg and
Frankfurt, Germany and in Belgrade, Yugoslavia (now Serbia). Thirty-one people
became ill, initially laboratory workers followed by several medical personnel and
family members who had cared for them. Seven deaths were reported. The first
people infected had been exposed to imported African green monkeys or their
tissues while conducting research. One additional case was diagnosed
retrospectively.
The reservoir host of Marburg virus is the African fruit bat, Rousettus
aegyptiacus. Fruit bats infected with Marburg virus do not to show obvious signs
of illness. Primates (including humans) can become infected with Marburg virus,
and may develop serious disease with high mortality. Further study is needed to
determine if other species may also host the virus.
TRANSMISSION
It is unknown how Marburg virus first transmits from its animal host to humans;
however, for the 2 cases in tourists visiting Uganda in 2008, unprotected contact
with infected bat feces or aerosols are the most likely routes of infection.
After this initial crossover of virus from host animal to humans, transmission
occurs through person-to-person contact. This may happen in several ways:
direct contact to droplets of body fluids from infected persons, or contact with
equipment and other objects contaminated with infectious blood or tissues.
In previous outbreaks, persons who have handled infected non-human primates
or have come in direct contact with their fluids or cell cultures have become
infected. Spread of the virus between humans has occurred in close
environments and direct contacts. A common example is through caregivers in
the home or in a hospital (nosocomial transmission).

SIGNS AND SYMPTOMS

After an incubation period of 5-10 days, symptom onset is sudden and 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 may then appear. Symptoms become increasingly severe and
can 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,
clinical diagnosis of the disease can be difficult, especially if only a single case is
involved.
The case-fatality rate for Marburg hemorrhagic fever is between 23-90%.
Many of the signs and symptoms of Marburg hemorrhagic fever are similar to
those of other more frequent infectious diseases, such as malaria or typhoid
fever, making diagnosis of the disease difficult. This is especially true if only a
single case is involved.

DIAGNOSIS
However, if a person has the early symptoms of Marburg HF and there is reason
to believe that Marburg HF should be considered, the patient should be isolated
and public health professionals notified. Samples from the patient can then be
collected and tested to confirm infection.
Antigen-capture enzyme-linked immunosorbent assay (ELISA) testing,
polymerase chain reaction (PCR), and IgM-capture ELISA can be used to
confirm a case of Marburg HF within a few days of symptom onset. Virus
isolation may also be performed but should only be done in a high containment
laboratory with good laboratory practices. The IgG-capture ELISA is appropriate
for testing persons later in the course of disease or after recovery. In deceased
patients, immunohistochemistry, virus isolation, or PCR of blood or tissue
specimens may be used to diagnose Marburg HF retrospectively.

TREATMENT
There is no specific treatment for Marburg hemorrhagic fever. Supportive hospital
therapy should be utilized, which includes balancing the patient’s fluids and
electrolytes, maintaining oxygen status and blood pressure, replacing lost blood
and clotting factors, and treatment for any complicating infections.
Experimental treatments are validated in non-human primates models, but have
never been tried in humans.
RISK OF EXPOSURE
People who have close contact with African fruit bats, humans patients, or non-
human primates infected with Marburg virus are at risk.
Historically, the people at highest risk include family members and hospital staff
who care for patients infected with Marburg virus and have not used
proper barrier nursing techniques. Particular occupations, such as veterinarians
and laboratory or quarantine facility workers who handle non-human primates
from Africa, may also be at increased risk of exposure to Marburg virus.
OUTBREAK

4)Middle East Respiratory Syndrome (MERS) is an illness

caused by a virus (more specifically, a coronavirus) called Middle East
Respiratory Syndrome Coronavirus (MERS-CoV). Most MERS patients
developed severe respiratory illness with symptoms of fever, cough and
shortness of breath. About 3 or 4 out of every 10 patients reported with MERS
have died.
Health officials first reported the disease in Saudi Arabia in September 2012.
Through retrospective (backward-looking) investigations, they later identified that
the first known cases of MERS occurred in Jordan in April 2012. So far, all cases
of MERS have been linked through travel to, or residence in, countries in and
near the Arabian Peninsula. The largest known outbreak of MERS outside the
Arabian Peninsula occurred in the Republic of Korea in 2015. The outbreak was
associated with a traveler returning from the Arabian Peninsula
SIGNS AND SYMPTOMS
Most people confirmed to have MERS-CoV infection have had severe respiratory
illness with symptoms of:
 fever
 cough
 shortness of breath
Some people also had diarrhea and nausea/vomiting. For many people with
MERS, more severe complications followed, such as pneumonia and kidney
failure. About 3 or 4 out of every 10 people reported with MERS have died. Most
of the people who died had a pre-existing medical condition that weakened their
immune system, or an underlying medical condition that hadn’t yet been
discovered. Medical conditions sometimes weaken people’s immune systems
and make them more likely to get sick or have severe illness.
Pre-existing conditions among people who got MERS have included
 diabetes
 cancer
 chronic lung disease
 chronic heart disease
 chronic kidney disease
Some infected people had mild symptoms (such as cold-like symptoms) or no
symptoms at all.
The symptoms of MERS start to appear about 5 or 6 days after a person is
exposed, but can range from 2 to 14 days.
MERS-CoV, like other coronaviruses, likely spreads from an infected person’s
respiratory secretions, such as through coughing. However, we don’t fully
understand the precise ways that it spreads.
MERS-CoV has spread from ill people to others through close contact, such as
caring for or living with an infected person. Infected people have spread MERS-
CoV to others in healthcare settings, such as hospitals. Researchers studying
MERS have not seen any ongoing spreading of MERS-CoV in the community.
 All reported cases have been linked to countries in and near the Arabian
Peninsula. Most infected people either lived in the Arabian Peninsula or recently
traveled from the Arabian Peninsula before they became ill. A few people have
gotten MERS after having close contact with an infected person who had recently
traveled from the Arabian Peninsula. The largest known outbreak of MERS
outside the Arabian Peninsula occurred in the Republic of Korea in 2015 and was
associated with a traveler returning from the Arabian Peninsula.
Public health agencies continue to investigate clusters of cases in several
countries to better understand how MERS-CoV spreads from person to person.
Prevention
There is currently no vaccine to protect people against MERS. But scientists are
working to develop one.
You can help reduce your risk of getting respiratory illnesses:
 Wash your hands often with soap and water for at least 20 seconds, and
help young children do the same. If soap and water are not available, use
an alcohol-based hand sanitizer.
 Cover your nose and mouth with a tissue when you cough or sneeze, then
throw the tissue in the trash.
 Avoid touching your eyes, nose, and mouth with unwashed hands.
 Avoid personal contact, such as kissing, or sharing cups or eating utensils,
with sick people.
 Clean and disinfect frequently touched surfaces and objects, such as
doorknobs.
DIAGNOSIS
According to the WHO, a probable case is[27]
 a person with a fever, respiratory infection, and evidence of pneumonia or acute respiratory
distress syndrome, where testing for MERS-CoV is unavailable or negative on a single inadequate
specimen, and the person has a direct link with a confirmed case.
 A person with an acute febrile respiratory illness with clinical, radiological, or histopathological
evidence of pulmonary parenchymal disease (e.g. pneumonia or acute respiratory distress Syndrome), an
inconclusive MERS-CoV laboratory test (that is, a positive screening test without confirmation), and a
resident of or traveler to Middle Eastern countries where MERS-CoV virus is believed to be circulating in
the 14 days before onset of illness.
 A person with an acute febrile respiratory illness of any severity, an inconclusive MERS-CoV
laboratory test (that is, a positive screening test without confirmation), and a direct epidemiologic link
with a confirmed MERS-CoV case.
Centers for Disease ControlEdit
In the United States, the Centers for Disease Control and Prevention (CDC) recommend
investigating any person with:[28][29]
 Fever and pneumonia or acute respiratory distress syndrome (based on clinical or radiological
evidence) and either:
 o a history of travel from countries in or near the Arabian Peninsula within 14 days before
symptom onset, or
o close contact with a symptomatic traveler who developed fever and acute respiratory
illness (not necessarily pneumonia) within 14 days after traveling from countries in or near the Arabian
Peninsula or
o a member of a cluster of people with severe acute respiratory illness (e.g. fever and
pneumonia requiring hospitalization) of unknown cause in which MERS-CoV is being evaluated, in
consultation with state and local health departments.
 Fever and symptoms of respiratory illness (not necessarily pneumonia; e.g. cough, shortness of
breath) and being in a healthcare facility (as a patient, worker, or visitor) within 14 days before symptom
onset in a country or territory in or near the Arabian Peninsula in which recent healthcare-associated cases
of MERS have been identified.
 Fever or symptoms of respiratory illness (not necessarily pneumonia; e.g. cough, shortness of
breath) and close contact with a confirmed MERS case while the case was ill.
Medical imagingEdit

Chest X-ray of a case of MERS

Chest X-ray findings tend to show bilateral patchy infiltrates consistent with viral
pneumonitis and acute respiratory distress syndrome (ARDS). Lower lobes tend to be more
involved. CT scans show interstitial infiltrates.[24]

Laboratory testing
MERS cases have been reported to have low white blood cell count, and in particular low
lymphocytes. For PCR] testing, the World Health Organization (WHO) recommends
obtaining samples from the lower respiratory tract via bronchoalveolar
lavage (BAL), sputum sample or tracheal aspirate as these have the highest viral loads.
[30] There have also been studies utilizing upper respiratory sampling via nasopharyngeal
swab
Several highly sensitive, confirmatory real-time RT-PCR assays exist for rapid
identification of MERS-CoV from patient-derived samples. These assays attempt to
amplify upE (targets elements upstream of the E gene), [31] open reading frame 1B
(targets the ORF1b gene)[31] and open reading frame 1A (targets the ORF1a gene).
[32] The WHO recommends the upE target for screening assays as it is highly sensitive.
[30] Inaddition, hemi-nested sequencing amplicons targeting RdRp (present in
all coronaviruses) and nucleocapsid (N) gene[33] (specific to MERS-CoV) fragments can
be generated for confirmation via sequencing. Reports of potential polymorphisms in the
N gene between isolates highlight the necessity for sequence-based characterization.
The WHO recommended testing algorithm is to start with an upE RT-PCR and if
positive confirm with ORF 1A assay or RdRp or N gene sequence assay for
confirmation. If both an upE and secondary assay are positive it is considered a
confirmed case.[30]
Protocols for biologically safe immunofluorescence assays (IFA) have also been
developed; however, antibodies against betacoronaviruses are known to cross-react
within the genus. This effectively limits their use to confirmatory applications. [32] A more
specific protein-microarray based assay has also been developed that did not show any
cross-reactivity against population samples and serum known to be positive for other
betacoronaviruses.[34] Due to the limited validation done so far with serological assays,
WHO guidance is that "cases where the testing laboratory has reported positive
serological test results in the absence of PCR testing or sequencing, are considered
probable cases of MERS-CoV infection, if they meet the other conditions of that case
definition."
5)Lassa fever is an animal-borne, or zoonotic, acute viral illness. It is
endemic in parts of West Africa including Sierra Leone, Liberia, Guinea and
Nigeria. Neighboring countries are also at risk, as the animal vector for Lassa
virus, the “multimammate rat” (Mastomys natalensis) is distributed throughout the
region.
The illness was discovered in 1969 and is named after the town in Nigeria where
the first cases occurred.
An estimated 100,000 to 300,000 infections of Lassa fever occur annually, with
approximately 5,000 deaths. Surveillance for Lassa fever is not standardized;
therefore, these estimates are crude. In some areas of Sierra Leone and Liberia,
it is known that 10-16% of people admitted to hospitals annually have Lassa
fever, demonstrating the serious impact the disease has on the region.

TRANSMISSION

The reservoir, or host, of Lassa virus is a rodent known as the “multimammate

rat” (Mastomys natalensis). Once infected, this rodent is able to excrete virus in
urine for an extended time period, maybe for the rest of its life. Mastomys rodents
breed frequently, produce large numbers of offspring, and are numerous in the
savannas and forests of west, central, and east Africa. In
addition, Mastomys readily colonize human homes and areas where food is
stored. All of these factors contribute to the relatively efficient spread of Lassa
virus from infected rodents to humans.
Transmission of Lassa virus to humans occurs most commonly through ingestion
or inhalation. Mastomys rodents shed the virus in urine and droppings and direct
contact with these materials, through touching soiled objects, eating
contaminated food, or exposure to open cuts or sores, can lead to infection.
Because Mastomys rodents often live in and around homes and scavenge on
leftover human food items or poorly stored food, direct contact transmission is
common. Mastomys rodents are sometimes consumed as a food source and
infection may occur when rodents are caught and prepared. Contact with the
virus may also occur when a person inhales tiny particles in the air contaminated
with infected rodent excretions. This aerosol or airborne transmission may occur
during cleaning activities, such as sweeping.
Direct contact with infected rodents is not the only way in which people are
infected; person-to-person transmission may occur after exposure to virus in the
blood, tissue, secretions, or excretions of a Lassa virus-infected individual.
Casual contact (including skin-to-skin contact without exchange of body fluids)
does not spread Lassa virus. Person-to-person transmission is common in health
care settings (called nosocomial transmission) where proper personal protective
equipment (PPE) is not available or not used. Lassa virus may be spread in
contaminated medical equipment, such as reused needles.
SIGNS AND SYMPTOMS
Signs and symptoms of Lassa fever typically occur 1-3 weeks after the patient
comes into contact with the virus. For the majority of Lassa fever virus infections
(approximately 80%), symptoms are mild and are undiagnosed. Mild symptoms
include slight fever, general malaise and weakness, and headache. In 20% of
infected individuals, however, disease may progress to more serious symptoms
including hemorrhaging (in gums, eyes, or nose, as examples), respiratory
distress, repeated vomiting, facial swelling, pain in the chest, back, and
abdomen, and shock. Neurological problems have also been described, including
hearing loss, tremors, and encephalitis. Death may occur within two weeks after
symptom onset due to multi-organ failure.
The most common complication of Lassa fever is deafness. Various degrees of
deafness occur in approximately one-third of infections, 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.
Approximately 15%-20% of patients hospitalized for Lassa fever die from the
illness. However, only 1% of all Lassa virus infections result in death. The death
rates for women in the third trimester of pregnancy are particularly high.
Spontaneous abortion is a serious complication of infection with an estimated
95% mortality in fetuses of infected pregnant mothers.
Because the symptoms of Lassa fever are so varied and nonspecific, clinical
diagnosis is often difficult. Lassa fever is also associated with occasional
epidemics, during which the case-fatality rate can reach 50% in hospitalized
patients.

RISK OF EXPOSURE
Individuals at greatest risk of Lassa virus infection are those who live in or visit
endemic regions, including Sierra Leone, Liberia, Guinea, and Nigeria and have
exposure to the multimammate rat.  Risk of exposure may also exist in other
west African countries where Mastomys rodents exist. Hospital staff are not at
great risk for infection as long as protective measures and proper sterilization
methods are used.

DIAGNOSIS
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. Reverse transcription-polymerase chain reaction (RT-PCR) can be used
in the early stage of disease. The virus itself may be cultured in 7 to 10 days, but
this procedure should only be done in a high containment laboratory with good
laboratory practices. Immunohistochemistry, performed on formalin-fixed tissue
specimens, can be used to make a post-mortem diagnosis
TREATMENT
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.
PREVENTION
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, the wide
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 (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.
Further, educating people in high-risk areas about ways to decrease rodent
populations in their homes will aid in the control and prevention of Lassa fever.
Other challenges include developing more rapid diagnostic tests and increasing
the availability of the only known drug treatment, ribavirin. Research is presently
under way to develop a vaccine for Lassa fever.
Lassa Fever Outbreak Distribution Map
6)Nipah virus (NiV) is a member of the family Paramyxoviridae,
genus Henipavirus. NiV was initially isolated and identified in 1999 during an
outbreak of encephalitis and respiratory illness among pig farmers and people
with close contact with pigs in Malaysia and Singapore. Its name originated from
Sungai Nipah, a village in the Malaysian Peninsula where pig farmers became ill
with encephalitis. Given the relatedness of NiV to Hendra virus, bat species were
quickly singled out for investigation and flying foxes of the genus Pteropus were
subsequently identified as the reservoir for NiV .
In the 1999 outbreak, Nipah virus caused a relatively mild disease in pigs, but
nearly 300 human cases with over 100 deaths were reported. In order to stop the
outbreak, more than a million pigs were euthanized, causing tremendous trade
loss for Malaysia. Since this outbreak, no subsequent cases (in neither swine nor
human) have been reported in either Malaysia or Singapore.
In 2001, NiV was again identified as the causative agent in an outbreak of human
disease occurring in Bangladesh. Genetic sequencing confirmed this virus as
Nipah virus, but a strain different from the one identified in 1999. In the same
year, another outbreak was identified retrospectively in Siliguri, India with reports
of person-to-person transmission in hospital settings (nosocomial transmission).
Unlike the Malaysian NiV outbreak, outbreaks occur almost annually in
Bangladesh and have been reported several times in India.
TRANSMISSION
Transmission of Nipah virus to humans may occur after direct contact with
infected bats, infected pigs, or from other NiV infected people.In Malaysia and
Singapore, humans were apparently infected with Nipah virus only through close
contact with infected pigs. The NiV strain identified in this outbreak appeared to
have been transmitted initially from bats to pigs, with subsequent spread within
pig populations. Incidental human infections resulted after exposure to infected

pigs. No occurrence of person-to-person transmission was reported in this

outbreak.
Conversely, person-to-person transmission of Nipah virus in Bangladesh and
India is regularly reported. This is most commonly seen in the family and
caregivers of Nipah virus-infected patients. Transmission also occurs from direct
exposure to infected bats. A common example is consumption of raw date palm
sap contaminated with infectious bat excretions.

SIGNS AND SYMPTOMS

Infection with Nipah virus is associated with encephalitis (inflammation of the
brain). After exposure and an incubation period of 5 to 14 days,illness presents
with 3-14 days of fever and headache, followed by drowsiness, disorientation and
mental confusion. These signs and symptoms can progress to coma within 24-48
hours. Some patients have a respiratory illness during the early part of their
infections, and half of the patients showing severe neurological signs showed
also pulmonary signs.
During the Nipah virus disease outbreak in 1998-99, 265 patients were infected
with the virus. About 40% of those patients who entered hospitals with serious
nervous disease died from the illness.
Long-term sequelae following Nipah virus infection have been noted, including
persistent convulsions and personality changes.
Latent infections with subsequent reactivation of Nipah virus and death have also
been reported months and even years after exposure.
In the Malaysia and Singapore outbreak, Nipah virus infection was associated
with close contact with Nipah virus-infected pigs.
In Bangladesh and India, where Nipah virus infection is more frequent, exposure
has been linked to consumption of raw date palm sap and contact with bats.
Importantly, human-to-human transmission has been documented and exposure
to other Nipah virus infected individuals is also a risk factor.
Laboratory diagnosis
Laboratory diagnosis a patient with a clinical history of NiV can be made during
the acute and convalescent phases of the disease by using a combination of
tests. Virus isolation attempts and real time polymerase chain reaction (RT-PCR)
from throat and nasal swabs, cerebrospinal fluid, urine, and blood should be
performed in the early stages of disease. Antibody detection by ELISA (IgG and
IgM) can be used later on. In fatal cases, immunohistochemistry on tissues
collected during autopsy may be the only way to confirm a diagnosis.

Treatment and Prevention

Treatment is limited to supportive care. Because Nipah virus encephalitis can be
transmitted person-to-person, standard infection control practices and proper
barrier nursing techniques are important in preventing hospital-acquired
infections (nosocomial transmission).
The drug ribavirin has been shown to be effective against the viruses in vitro, but
human investigations to date have been inconclusive and the clinical usefulness
of ribavirin remains uncertain.
Passive immunization using a human monoclonal antibody targeting the Nipah G
glycoprotein has been evaluated in the post-exposure therapy in the ferret model
and found to be of benefit .
Nipah virus infection can be prevented by avoiding exposure to sick pigs and
bats in endemic areas and not drinking raw date palm sap.Additional efforts
focused on surveillance and awareness will help prevent future outbreaks.
Research is needed to better understand the ecology of bats and Nipah virus,
investigating questions such as the seasonality of disease within reproductive
cycles of bats. Surveillance tools should include reliable laboratory assays for

early detection of disease in communities and livestock, and raising awareness

of transmission and symptoms is important in reinforcing standard

infection control practices to avoid human-to-human infections in hospital settings

(nosocomial infection).

7)Zika virus  (ZIKV) (pronounced /ˈziːkə/ or /ˈzɪkə/[3][4]) is a member of

the virus family Flaviviridae.[5] It is spread by daytime-active Aedes mosquitoes, such
as A. aegypti and A. albopictus.[5] Its name comes from the Ziika Forest of Uganda, where
the virus was first isolated in 1947.[6] Zika virus is related to the dengue, yellow
fever, Japanese encephalitis, and West Nile viruses.[6] Since the 1950s, it has been known
to occur within a narrow equatorial belt from Africa to Asia. From 2007 to 2016, the virus
spread eastward, across the Pacific Ocean to the Americas, leading to the 2015–2016 Zika
virus epidemic.[7]
ZIKA VIRUS

Electron micrograph of Zika
virus. Virus particles (digitally
colored purple) are 40 nm in
diameter, with an
outer envelope and a dense
inner core.[1]

Virology
Zika virus belongs to the family Flaviviridae and the genus Flavivirus, thus is related to
the dengue, yellow fever, Japanese encephalitis, and West Nile viruses. Like other flaviviruses, Zika
virus is enveloped and icosahedral and has a nonsegmented, single-stranded, 10 kilobase, positive-
sense RNA genome. It is most closely related to the Spondweni virus and is one of the two known viruses
in the Spondweni virus clade.
TRANSMISSION
Cross-section of Zika virus, showing the viral envelope composed of envelope proteins (red) and membrane proteins
(purple) embedded in the lipid membrane (white): The capsid proteins (orange) are shown interacting with the RNA
genome (yellow) at the center of the virus.[26]Zika virus is primarily transmitted by the biteofan infected
mosquito from the Aedes genus, mainly Aedes aegypti, in tropical and subtropical
regions. Aedes mosquitoes usually bite during the day, peaking during early morning and late
afternoon/evening. This is the same mosquito that transmits dengue, chikungunya and yellow

fever.
Zika virus is also transmitted from mother to fetus during pregnancy, through sexual contact,
transfusion of blood and blood products, and organ transplantation.

Zika can be passed through sex from a person who has Zika to his or her
partners. Zika can be passed through sex, even if the infected person does not
have symptoms at the time
There are reports of laboratory acquired Zika virus infections, although the route
of transmission was not clearly established in all cases.
Signs and symptoms
The incubation period (the time from exposure to symptoms) of Zika virus disease is estimated
to be 3–14 days. The majority of people infected with Zika virus do not develop symptoms.
Symptoms are generally mild including fever, rash, conjunctivitis, muscle and joint pain,
malaise, and headache, and usually last for 2–7 days.

DIAGNOSIS
Infection with Zika virus may be suspected based on symptoms of persons living in or visiting
areas with Zika virus transmission and/or Aedes mosquito vectors. A diagnosis of Zika virus
infection can only be confirmed by laboratory tests of blood or other body fluids, such as urine or
semen.
TREATMENT
There is no treatment available for Zika virus infection or its associated diseases.
Symptoms of Zika virus infection are usually mild. People with  symptoms such as fever, rash,
or arthralgia should get plenty of rest, drink fluids, and treat pain and fever with common
medicines. If symptoms worsen, they should seek medical care and advice.
Pregnant women living in areas with Zika transmission or who develop symptoms of Zika virus

infection should seek medical attention for laboratory testing and other clinical care.  

PATHOGENESIS
Zika virus replicates in the mosquito's midgut epithelial cells and then its salivary gland cells. After 5–
10 days, the virus can be found in the mosquito's saliva. If the mosquito's saliva is inoculated into human
skin, the virus can infect epidermal keratinocytes, skin fibroblasts in the skin and the Langerhans cells.
The pathogenesis of the virus is hypothesized to continue with a spread to lymph nodes and the
bloodstream.[21][75] Flaviviruses replicate in the cytoplasm, but Zika antigens have been found in infected
cell nuclei.[76]
The Zika virus protein NS4A can lead to small head size (microcephaly) because it disrupts brain growth
by hijacking a pathway which regulates growth of new neurons. [77]
8)Rift Valley fever (RVF) is an acute viral hemorrhagic fever that is
most commonly seen in domesticated animals (such as cattle, buffalo, sheep,
goats, and camels) and can also cause illness in people. The disease is caused
by RVF virus (RVFV), a member of the genus Phlebovirus in the
order Bunyavirales. Some related Bunyavirales viruses can also cause illness in
people, such as hantaviruses and Crimean-Congo hemorrhagic fever (CCHF)
virus.
RVF was first reported in livestock by veterinary officers in Kenya’s Rift Valley in
the early 1910s. It is generally found in regions of eastern and southern Africa
where sheep and cattle are raised, but exists in most of sub-Saharan Africa,
including West Africa and Madagascar. In September 2000, an outbreak of RVF
was reported in Saudi Arabia. It was then also found in Yemen. These were the
first cases of Rift Valley fever identified outside of Africa.
Outbreaks of RVF can have major societal impacts, including significant
economic losses and trade reductions. The disease most commonly affects
livestock, causing severe illness and abortion in domesticated animals, an
important income source for many. Outbreaks of disease in animal populations
are called “epizootics.” The most notable RVF epizootic occurred in Kenya in
1950-1951, resulting in the death of an estimated 100,000 sheep.
Epizootic outbreaks of RVF also increase the likelihood of contact between
diseased animals and humans, which can lead to outbreaks of RVF in people.
For instance, in 1977 RVF was found in Egypt (possibly imported from infected
domestic animals from Sudan) and caused a large outbreak among both animals
and people that resulted in over 600 human deaths. Another example occurred in
West Africa in 1987 and was linked to construction of the Senegal River Project.
The project caused flooding in the lower Senegal River area, which changed both
ecological conditions and interactions between animals and people, resulting in a
large RVF outbreak in both animals and humans.
TRANSMISSION
People usually get Rift Valley fever through contact with blood, body fluids, or
tissues of infected animals, mainly livestock such as cattle, sheep, goats, buffalo,
and camels. This direct contact can occur during slaughter or butchering, while
caring for sick animals, during veterinary procedures like assisting an animal with
giving birth, and when consuming raw or undercooked animal products.
People can also get RVF through bites from infected mosquitoes and, rarely,
from other biting insects. Infection with the RVF virus (RVFV) has occurred in
laboratories when someone has inhaled virus that was in the air (known as
aerosol transmission). Spread from person to person has not been documented,
and no transmission of RVF to health care workers has been reported when
standard infection control precautions have been put in place.
The transmission cycle of RVFV can look like this:
 The virus can be spread from female mosquitos to their offspring through
the eggs (vertical transmission).
 In the eggs, the virus remains viable (infectious) for several years during
dry conditions.
 Excessive rainfall allows more mosquito eggs to hatch.
 As mosquito populations increase, the potential for the virus to spread to
animals and people increases.
  RVFV outbreaks in animals, most commonly livestock, lead to increased
handling of infected animals, which then increases risk of exposure to the
virus for people.
Several mosquito species can spread RVFV, most commonly the Aedes and
Culex mosquitoes, and these vary by region. Environmental conditions,
particularly rainfall, are an important risk factor for outbreaks in both animals and
people. RVF outbreaks are most often linked to years of unusually heavy rainfall
and flooding, because mosquitoes spread the disease and heavy rainfall allows
more mosquito eggs to hatch.
SIGNS AND SYMPTOMS
RVFV has an incubation period of 2-6 days following exposure to the virus, and
can cause several different disease syndromes if symptoms do appear. Most
commonly, people with RVF have either no symptoms or a mild illness that
includes fever, weakness, back pain, and dizziness at the onset of illness.
Typically, patients recover within two days to one week after symptoms start.
However, a small percentage (8-10%) of people infected with RVFV develop
much more severe symptoms, including:
 Ocular disease (disease of the eye), which sometimes accompanies the
mild symptoms described above. Lesions on the eyes may occur 1-3
weeks after onset of initial symptoms with patients reporting blurred and
decreased vision. For many patients, lesions disappear after 10-12 weeks;
however, for those with lesions occurring in the macula (the center of the
retina), about half will have permanent vision loss.
 Encephalitis, or inflammation of the brain, which can lead to headaches,
coma, or seizures. This occurs in less than 1% of patients and presents 1-
4 weeks after first symptoms appear. Death from encephalitis in RVF
patients is rare, but neurological deficits may be severe and long-lasting.
 Hemorrhagic fever, which occurs in less than 1% of all RVF patients.
Symptoms of hemorrhaging may begin with jaundice and other signs of
liver impairment, followed by vomiting blood, bloody stool, or bleeding from
gums, skin, nose, and injection sites. These symptoms appear 2-4 days
after onset of illness. Fatality for those who do develop symptoms of
hemorrhagic fever is around 50% and death usually occurs 3-6 days after
symptoms start.
RVF causes severe disease in animals that is characterized by fever, weakness,
abortions (loss of pregnancy), and a high rate of severe illness and death,
particularly among young animals. RVFV infection causes abortion in nearly
100% of livestock pregnancies and most young animals that are infected will die,
whereas fatality among adult animals is significantly lower.
Because RVF symptoms can be mild and non-specific, clinical diagnosis is often
difficult, especially early in the course of the disease. Definitive diagnosis of RVF
requires laboratory testing of blood or other tissue samples. The virus can be
detected in the blood (during illness) and in postmortem tissue by virus isolation
in cell culture and by molecular techniques (reverse transcriptase polymerase
chain reaction, or RT-PCR).
DIAGNOSIS
Antibody testing using enzyme-linked immunoassay (ELISA) can also be used to
confirm infection with RVFV by showing the presence of IgM antibodies, which
appear briefly as an early response to a recent infection, and IgG antibodies,
which persist for several years. Both IgM and IgG antibodies are specific to RVF
virus.
TREATMENT
There are no FDA-approved treatments for Rift Valley Fever. Because most
cases of RVF are mild and self-limiting, a specific treatment for RVF has not
been established. Symptoms of mild illness such as fever and body aches can be
managed with standard over-the-counter medications. Most of the time, people
will get better within 2 days to 1 week after their illness starts. Treatment for more
serious cases may require hospitalization and are generally limited to supportive
care.
People living in or visiting areas with RVF can prevent infection with these steps:
 Avoid contact with blood, body fluids, or tissues of infected animals.
People working with animals in RVF-endemic areas should wear
appropriate protective equipment (such as gloves, boots, long sleeves, and
a face shield) to avoid any exposure to blood or tissues of animals that
may potentially be infected.
 Avoid unsafe animal products. All animal products (including meat, milk,
and blood) should be thoroughly cooked before eating or drinking.
 Protect yourself against mosquitoes and other bloodsucking insects. Use
insect repellents and bed nets, and wear long sleeved shirts and long
 pants to cover exposed skin.

No vaccines are currently available for vaccination in people.

9)Severe acute respiratory syndrome coronavirus  (SARS-
CoV  or  SARS-CoV-1)[2] is a strain of virus that causes severe acute respiratory
syndrome (SARS).[3] It is an enveloped, positive-sense, single-stranded RNA virus which infects
the epithelial cells within the lungs.[4] The virus enters the host cell by binding to the ACE2
receptor.[5] It infects humans, bats, and palm civets.[6][7]

Severe acute respiratory

syndrome coronavirus
 Electron microscope image of
SARS virion

On 16 April 2003, following the outbreak of SARS in Asia and secondary cases elsewhere in the

world, the World Health Organization (WHO) issued a press release stating that
the coronavirus identified by a number of laboratories was the official cause of SARS.
The Centers for Disease Control and Prevention (CDC) in the United States and National
Microbiology Laboratory (NML) in Canada identified the SARS-CoV genome in April 2003.[8]
[9] Scientists at Erasmus University in Rotterdam, the Netherlands demonstrated that the SARS
coronavirus fulfilled Koch's postulates thereby confirming it as the causative agent. In the
experiments, macaques infected with the virus developed the same symptoms as human SARS
victims.[10]
A pandemic of coronavirus disease 2019 (COVID-19) in 2019–20 showed many similarities to the
SARS outbreak, with the viral agent identified as severe acute respiratory syndrome coronavirus
2 (SARS-CoV-2), yet another strain of the Severe acute respiratory syndrome-related
coronavirus (SARSr-CoV). SARS-CoV-1 is one of seven known coronaviruses to infect humans,
including Human coronavirus 229E (HCoV-229E), Human coronavirus NL63 (HCoV-NL63), human
coronavirus OC43 (HCoV-OC43), Human coronavirus HKU1 (HCoV-HKU1), Middle East respiratory
syndrome-related coronavirus (MERS-CoV), and SARS-CoV-2.

Scanning electron micrograph of SARS virions

Severe acute respiratory syndrome (SARS) is the disease caused by SARS-CoV. It causes an

often severe illness and is marked initially by systemic symptoms of muscle pain, headache,
and fever, followed in 2–14 days by the onset of respiratory symptoms,[11] mainly
cough, dyspnea, and pneumonia. Another common finding in SARS patients is a decrease in the
number of lymphocytes circulating in the blood.[12]
In the SARS outbreak of 2003, about 9% of patients with confirmed SARS-CoV infection died.
[13] The mortality rate was much higher for those over 60 years old, with mortality rates
approaching 50% for this subset of patients.[13]
Virology
SARS-Coronavirus follows the replication strategy typical of the coronavirus subfamily. The primary
human receptor of the virus is angiotensin-converting enzyme 2 (ACE2), first identified in 2003.
SIGNS AND SYMPTOMS

SARS symptoms are similar to those of the flu, including:

 fever over 100.4°F

 dry cough
 sore throat
 problems breathing, including shortness of breath
 headache
 body aches
 loss of appetite
 malaise
  night sweats and chills
 confusion
 rash
 diarrhea

Breathing issues will appear within two to 10 days after a person is exposed to
the virus. Health officials will quarantine a person who presents the above
symptoms and family members if they have a history of foreign travel. The
person will be quarantined for 10 days to prevent the virus from spreading.

Factors that increase your risk of contracting the disease include close contact
with someone diagnosed with SARS and a history of travel to any other country
with a reported SARS outbreak

Transmission
The primary route of transmission for SARS-CoV is contact of the mucous membranes with respiratory
droplets or fomites. While diarrhea is common in people with SARS, the fecal–oral route does not appear
to be a common mode of transmission.[7] The basic reproduction number of SARS-CoV, R0, ranges from
2 to 4 depending on different analyses. Control measures introduced in April 2003 reduced the R to 0.4.
 Diagnosis

A chest X-ray showing increased opacity in both lungs, indicative of pneumonia, in a patient with SARS

SARS-CoV may be suspected in a patient who has:

 Any of the symptoms, including a fever of 38 °C (100 °F) or higher, and

 Either a history of:

o Contact (sexual or casual) with someone with a diagnosis of SARS within the last 10 days or

o Travel to any of the regions identified by the World Health Organization (WHO) as areas with recent
local transmission of SARS.
For a case to be considered probable, a chest X-ray must be positive for atypical pneumonia or respiratory
distress syndrome.
The WHO has added the category of "laboratory confirmed SARS" for patients who would otherwise be
considered "probable" but who have not yet had a positive chest X-ray changes, but have tested positive
for SARS based on one of the approved tests (ELISA, immunofluorescence or PCR).[8]
The appearance of SARS-CoV in chest X-rays is not always uniform but generally appears as an
abnormality with patchy infiltrates.[
TREATMENT
As SARS is a viral disease, antibiotics do not have direct effect but may be used against
bacterial secondary infection. Treatment of SARS is mainly supportive with antipyretics,
supplemental oxygen and mechanical ventilation as needed. Antiviral medications are used as
well as high doses of steroids to reduce swelling in the lungs.[citation needed]
People with SARS-CoV must be isolated, preferably in negative-pressure rooms, with complete
barrier nursing precautions taken for any necessary contact with these patients, to limit the
chances of medical personnel getting infected with SARS.[citation needed] In certain cases, natural
ventilation by opening doors and windows is documented to help decreasing indoor
concentration of virus particles.[17]
Some of the more serious damage caused by SARS may be due to the body's own immune
system reacting in what is known as cytokine storm.[18]
As of 2020, there is no cure or protective vaccine for SARS that has been shown to be both safe
and effective in humans.[19][20]
PREVENTION
 There is no vaccine for SARS, although doctor Anthony Fauci mentioned that the CDC
developed one and placed it in the US national stockpile.[10] That vaccine, however, is a
prototype and not field-ready as of March, 2020.[11] Clinical isolation and quarantine remain the
most effective means to prevent the spread of SARS. Other preventive measures include:
 Hand-washing with soap and water, or use of alcohol-based hand sanitizer[12]

 Disinfection of surfaces of fomites to remove viruses

 Avoiding contact with bodily fluids

 Washing the personal items of someone with SARS in hot, soapy water (eating utensils, dishes, bedding,
etc.)[13]
 Keeping children with symptoms home from school

 Simple hygiene measures

 Isolating oneself as much as possible to minimize the chances of transmission of the virus

EPIDEMIOLOGY
SARS was a relatively rare disease; at the end of the epidemic in June 2003, the incidence was
8,422 cases with a case fatality rate (CFR) of 11%.[14]
The case fatality rate (CFR) ranges from 0% to 50% depending on the age group of the patient.
[7] Patients under 24 were least likely to die (less than 1%); those 65 and older were most likely
to die (over 55%).[27]
As with MERS and COVID-19, SARS resulted in significantly more deaths of males than
females.

2003 Probable cases of SARS – worldwide

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe

acute respiratory syndrome coronavirus 2 (SARS-CoV-2).[10] It was first identified in
December 2019 in Wuhan, China, and has since spread globally, resulting in an
ongoing pandemic.[11][12] As of 10 May 2020, more than 4.09 million cases have been
reported across 187 countries and territories, resulting in more than 282,000 deaths.
More than 1.4 million people have recovered.
According to the World Health Organization, there are no
available vaccines nor specific antiviral treatments for COVID-19.[7] On 1 May 2020, the
United States gave Emergency Use Authorization to the antiviral remdesivir for people
hospitalized with severe COVID-19.[31] Management involves the treatment of
symptoms, supportive care, isolation, and experimental measures.[32] The World Health
Organization (WHO) declared the COVID-19 outbreak a Public Health Emergency of
International Concern (PHEIC)[33][34] on 30 January 2020 and a pandemic on 11 March
2020.[12] Local transmission of the disease has occurred in most countries across all
six WHO regions.[35]

Symptoms of COVID-19[5]

Symptom Range

Fever 83–99%

Cough 59–82%

Loss of appetite 40–84%

Fatigue 44–70%

Shortness of breath 31–40%

Coughing up sputum 28–33%

Muscle aches and pains 11–35%

Fever is the most common symptom, although some older people and those with other
health problems experience fever later in the disease. [5][36] In one study, 44% of people
had fever when they presented to the hospital, while 89% went on to develop fever at
some point during their hospitalization.[5][37]
Other common symptoms include cough, loss of appetite, fatigue, shortness of
breath, sputum production, and muscle and joint pains.[1][5][6][38] Symptoms such
as nausea, vomiting, and diarrhoea have been observed in varying percentages. [39][40]

[41] Less
common symptoms include sneezing, runny nose, or sore throat. [42]
Some cases in China initially presented with only chest tightness and palpitations.[43]
A decreased sense of smell or disturbances in taste may occur. [44][45] Loss of smell was
a presenting symptom in 30% of confirmed cases in South Korea. [14][46]
As is common with infections, there is a delay between the moment a person is first
infected and the time he or she develops symptoms. This is called the incubation period.
The incubation period for COVID-19 is typically five to six days but may range from two
to 14 days,[47][48] although 97.5% of people who develop symptoms will do so within
11.5 days of infection.[49]

A minority of cases do not develop noticeable symptoms at any point in time. [50]
[51] These asymptomatic carriers tend not to get tested, and their role in transmission is
not yet fully known.[52][53] However, preliminary evidence suggests they may contribute
to the spread of the disease.[54][55] In March 2020, the Korea Centers for Disease Control
and Prevention (KCDC) reported that 20% of confirmed cases remained asymptomatic
during their hospital stay.[55][56]
Complications
Complications may include pneumonia, acute respiratory distress syndrome (ARDS), multi-
organ failure, septic shock, and death.[57][58][59][60][61] Cardiovascular-related complications
may include heart failure, irregular electrical activity, blood clots, and heart inflammation.
[62] Approximately 20-30% of people who present with COVID-19 have elevated liver
enzymes (transaminases) reflecting liver injury.[63][64] Neurologic manifestations
include seizure, stroke, encephalitis, and Guillain–Barré syndrome.[65]
Following the infection, children may develop paediatric multisystem inflammatory
syndrome, which has symptoms similar to Kawasaki disease, and die.[66]
Transmission

Respiratory droplets produced when a man sneezes, visualised using Tyndall scattering

COVID-19 is a new disease, and the ways it spreads between people are under
investigation, including: the role of small droplets; the distance over and ease in which it
spreads through air; the number of new infections caused by one infected person
(the R0); and how long the virus remains infectious on surfaces. [7][19][21] It spreads very
efficiently and sustainably between people – easier than influenza, but not as efficiently
as measles.[19]
The disease is spread during close contact, often by small droplets produced during
coughing, sneezing, or talking.[7][21] During close contact, (1 to 2 metres, 3 to 6 feet),
people catch the disease after breathing in contaminated droplets that were exhaled by
infected people.[19][7] Contaminated droplets also cause infection when they settle in the
noses or mouths of people in close proximity. [19] However, the droplets are relatively
heavy, usually fall to the ground or surfaces, and do not travel far through the air. [7][21]
People are most infectious when they show symptoms (even mild or non specific
symptoms), but may be infectious for up to two days before symptoms appear
(presymptomatic transmission).[21] The time people remain infectious is estimated to be
between 7 and 12 days for moderate cases, and in severe cases, an average of two
weeks.[21] Some people have been infected and recovered without showing symptoms,

and such people may be able to spread COVID-19, although uncertainties remain in
terms of this asymptomatic transmission.[21][19] 
One study found that viral load was highest at symptom onset, so may have peaked
before symptoms developed.[67]
When the contaminated droplets fall to floors or surfaces, less commonly, they can
remain infectious, if people touch contaminated surfaces and then their eyes, nose or
mouth with unwashed hands.[7] On surfaces the amount of active virus decreases over
time until it can no longer cause infection, [21] and surfaces are not thought to be the
main way that the virus spreads.[19] It is unknown what amount of virus on surfaces is
required to cause infection via this method, but it can be detected for up to four hours on
copper, up to one day on cardboard, up to three days on plastic (polypropylene)
and stainless steel.[68][21][69] Surfaces are easily decontaminated with household
disinfectants which kill the virus outside the human body or on the hands.
[7] Disinfectants or bleach are not a treatment for COVID-19, and cause health problems
when not used properly, such as inside the human body. [70]
Sputum and saliva carry large amounts of virus.[71][7][19][21] Although COVID-19 is not
a sexually transmitted infection, kissing, intimate contact, and faecal-oral routes are
suspected to transmit the virus.[72][73] Some medical procedures are aerosol-
generating[74] and result in the virus being transmitted more easily than normal. [7][21]

Virology

Illustration of SARSr-CoV virion

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel severe acute

respiratory syndrome coronavirus, first isolated from three people with pneumonia
connected to the cluster of acute respiratory illness cases in Wuhan.[75] All features of
the novel SARS-CoV-2 virus occur in related coronaviruses in nature. [76] Outside the
human body, the virus is killed by household soap, which bursts its protective bubble.[23]
SARS-CoV-2 is closely related to the original SARS-CoV.[77] It is thought to have
a zoonotic origin. Genetic analysis has revealed that the coronavirus genetically clusters
with the genus Betacoronavirus, in subgenus Sarbecovirus (lineage B) together with
two bat-derived strains. It is 96% identical at the whole genome level to other bat
coronavirus samples (BatCov RaTG13).[42] In February 2020, Chinese researchers
found that there is only one amino acid difference in the binding domain of the S
protein between the coronaviruses from pangolins and those from humans; however,
whole-genome comparison to date found that at most 92% of genetic material was
shared between pangolin coronavirus and SARS-CoV-2, which is insufficient to prove
pangolins to be the intermediate host.[78]
Pathophysiology
The lungs are the organs most affected by COVID-19 because the virus accesses host cells via
the enzyme angiotensin-converting enzyme 2 (ACE2), which is most abundant in type II alveolar
cells of the lungs. The virus uses a special surface glycoprotein called a "spike" (peplomer) to
connect to ACE2 and enter the host cell.[79] The density of ACE2 in each tissue correlates with
the severity of the disease in that tissue and some have suggested that decreasing ACE2 activity
might be protective,[80][81] though another view is that increasing ACE2 using angiotensin II
receptor blocker medications could be protective and these hypotheses need to be tested.[82] As
the alveolar disease progresses, respiratory failure might develop and death may follow.[81]
SARS-CoV-2 may also cause respiratory failure through affecting the brainstem as other
coronaviruses have been found to invade the central nervous system (CNS). While virus has
been detected in cerebrospinal fluid of autopsies, the exact mechanism by which it invades the
CNS remains unclear and may first involve invasion of peripheral nerves given the low levels of
ACE2 in the brain.

The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in

the glandular cells of gastric, duodenal and rectal epithelium[85] as well as endothelial cells
and enterocytes of the small intestine.[86]
The virus can cause acute myocardial injury and chronic damage to the cardiovascular system.
[87] An acute cardiac injury was found in 12% of infected people admitted to the hospital in
Wuhan, China,[40] and is more frequent in severe disease.[88] Rates of cardiovascular symptoms
are high, owing to the systemic inflammatory response and immune system disorders during
disease progression, but acute myocardial injuries may also be related to ACE2 receptors in the
heart.[87] ACE2 receptors are highly expressed in the heart and are involved in heart function.[87]
[89] A high incidence of thrombosis (31%) and venous thromboembolism (25%) have been found
in ICU patients with COVID-19 infections and may be related to poor prognosis.[90][91] Blood
vessel dysfunction and clot formation (as suggested by high D-dimer levels) are thought to play a
significant role in mortality, incidences of clots leading to pulmonary embolisms, and ischaemic
events within the brain have been noted as complications leading to death in patients infected
with SARS-CoV-2. Infection appears to set off a chain of vasoconstrictive responses within the
body, constriction of blood vessels within the pulmonary circulation has also been posited as a
mechanism in which oxygenation decreases alongside the presentation of viral pneumonia.[92]
Another common cause of death is complications related to the kidneys[92]—SARS-CoV-2
directly infects kidney cells, as confirmed in post-mortem studies. Acute kidney injury is a
common complication and cause of death; this is more significant in patients with already
compromised kidney function, especially in people with pre-existing chronic conditions such as
hypertension and diabetes which specifically cause nephropathy in the long run.[93]
Autopsies of people who died of COVID-19 have found diffuse alveolar damage (DAD), and
lymphocyte-containing inflammatory infiltrates within the lung.[94]
Immunopathology
Although SARS-COV-2 has a tropism for ACE2-expressing epithelial cells of the respiratory
tract, patients with severe COVID-19 have symptoms of systemic hyperinflammation. Clinical
laboratory findings of elevated IL-2, IL-7, IL-6, granulocyte-macrophage colony-stimulating
factor (GM-CSF), interferon-γ inducible protein 10 (IP-10), monocyte chemoattractant
protein 1 (MCP-1), macrophage inflammatory protein 1-α (MIP-1α), and tumour necrosis factor-
α (TNF-α) indicative of cytokine release syndrome (CRS) suggest an underlying
immunopathology.[40]
Additionally, people with COVID-19 and acute respiratory distress syndrome (ARDS) have
classical serum biomarkers of CRS, including elevated C-reactive protein (CRP), lactate
dehydrogenase (LDH), D-dimer, and ferritin.[95]
Systemic inflammation results in vasodilation, allowing inflammatory lymphocytic and
monocytic infiltration of the lung and the heart. In particular, pathogenic GM-CSF-secreting T-
cells were shown to correlate with the recruitment of inflammatory IL-6-secreting monocytes
and severe lung pathology in COVID-19 patients.[96] Lymphocytic infiltrates have also been
reported at autopsy.[94]
Diagnosis
Main article: COVID-19 testing

Demonstration of a nasopharyngeal swab for COVID-19 testing

CDC rRT-PCR test kit for COVID-19[97]

The WHO has published several testing protocols for the disease.[98] The standard method of
testing is real-time reverse transcription polymerase chain reaction (rRT-PCR).[99] The test is
typically done on respiratory samples obtained by a nasopharyngeal swab; however, a nasal swab
or sputum sample may also be used.[22][100] Results are generally available within a few hours to
two days.[101][102] Blood tests can be used, but these require two blood samples taken two weeks
apart, and the results have little immediate value.[103] Chinese scientists were able to isolate a
strain of the coronavirus and publish the genetic sequence so laboratories across the world could
independently develop polymerase chain reaction (PCR) tests to detect infection by the virus.[11]
[104][105] As of 4 April 2020, antibody tests (which may detect active infections and whether a
person had been infected in the past) were in development, but not yet widely used.[106][107]
[108] The Chinese experience with testing has shown the accuracy is only 60 to 70%.[109] The
FDA in the United States approved the first point-of-care test on 21 March 2020 for use at the
end of that month.[110]
Diagnostic guidelines released by Zhongnan Hospital of Wuhan University suggested methods
for detecting infections based upon clinical features and epidemiological risk. These involved
identifying people who had at least two of the following symptoms in addition to a history of
travel to Wuhan or contact with other infected people: fever, imaging features of pneumonia,
normal or reduced white blood cell count, or reduced lymphocyte count.[111]
A study asked hospitalised COVID-19 patients to cough into a sterile container, thus producing a
saliva sample, and detected the virus in eleven of twelve patients using RT-PCR. This technique
has the potential of being quicker than a swab and involving less risk to health care workers
(collection at home or in the car).[71]
Along with laboratory testing, chest CT scans may be helpful to diagnose COVID-19 in
individuals with a high clinical suspicion of infection but are not recommended for routine
screening.[23][24] Bilateral multilobar ground-glass opacities with a peripheral, asymmetric, and
posterior distribution are common in early infection.[23] Subpleural dominance, crazy
paving (lobular septal thickening with variable alveolar filling), and consolidation may appear as
the disease progresses.[23][112]
In late 2019, WHO assigned the emergency ICD-10 disease codes U07.1 for deaths from lab-
confirmed SARS-CoV-2 infection and U07.2 for deaths from clinically or epidemiologically
diagnosed COVID-19 without lab-confirmed SARS-CoV-2 infection.[113]
 Typical CT imaging findings

CT imaging of rapid progression stage

Pathology
Few data are available about microscopic lesions and the pathophysiology of
COVID-19.[114][115] The main pathological findings at autopsy are:
 Macroscopy: pleurisy, pericarditis, lung consolidation and pulmonary oedema
 Four types of severity of viral pneumonia can be observed:
o minor pneumonia: minor serous exudation, minor fibrin exudation
o mild pneumonia: pulmonary oedema, pneumocyte hyperplasia, large
atypical pneumocytes, interstitial inflammation with lymphocytic infiltration and multinucleated giant
cell formation
o severe pneumonia: diffuse alveolar damage (DAD) with diffuse alveolar exudates. DAD
is the cause of acute respiratory distress syndrome (ARDS) and severe hypoxemia.
o healing pneumonia: organisation of exudates in alveolar cavities and pulmonary
interstitial fibrosis
o plasmocytosis in BAL[116]
 Blood: disseminated intravascular coagulation (DIC);[117] leukoerythroblastic reaction[118]
 Liver: microvesicular steatosis

Prevention
The best way to prevent infection is to avoid exposure to the virus.
The most important way to prevent COVID-19 is to WASH YOUR HANDS.
Wash your hands regularly and thoroughly with soap and water (lather for 20
seconds) OR use an alcohol based (at least 60%) hand sanitizer.
Other actions that help to prevent the spread of COVID-19:
 avoid contact with others who are sick
 avoid touching your mouth, nose, eyes or face
 cover coughs and sneezes (into a tissue or into your elbow)
 clean and disinfect surfaces (alcohol or bleach based cleaning solutions
work best for coronaviruses)
 face masks will not protect you from COVID-19 directly, but can help in
reminding you to avoid touching your face, and will help prevent the
spread of the disease to others.
 social distancing
 self isolation

Risk Factors
Scientists are still researching risk factors for COVID-19 but data from China CDC
suggest that the elderly, and people suffering from pre-existing medical
conditions (such as heart disease, respiratory disease
including asthma and COPD, or diabetes) have a higher risk of dying from the
disease. There is research that suggests that smokers may be more susceptible to
the SARS-CoV-2 virus. There is also evidence to suggest that people who use e-
cigarettes (vaping) are at much higher risk of developing serious respiratory
infections.

Update: March 16, 2020 -- A Chinese study claims to have found that people
with type A blood may be more susceptible to the novel Coronavirus (COVID-19).
Update: March 22, 2016 -- CDC now includes people aged 65 years and older,
people who live in a nursing home or long-term care facility, and people who
are immunocompromised including those receiving cancer treatment as
those who are at higher risk for severe illness. People with HIV may also be at
higher risk of serious illness.

Investigational Treatments
Currently, there are no FDA approved treatments for COVID-19.
Update: FDA Approves Malaria Drugs to Treat COVID-19, Despite Little Proof
They Work March 31, 2020
Update:  The Lowdown on COVID-19 Treatments April 21, 2020
Update:  Lots of Drugs Are Being Tested Against COVID-19 -- But Will Any
Work? April 23, 2020
 Baricitinib Clinical studies are in preparation to determine the effectiveness
of a Janus kinase (JAK) inhibitor called baricitinib (marketed under the
brand name Olumiant for the treatment of rheumatoid arthritis) in the
treatment of COVID-19 patients.
 Bemcentinib An AXL kinase inhibitor called bemcentinib has been fast-
tracked in a UK Phase II clinical trial to study its effectiveness in the
treatment of hospitalized patients with COVID-19. Bemcentinib has
previously been studied in cancer patients and has been shown to be safe
and well-tolerated. It has also been reported to exhibit potent antiviral
activity in preclinical models against several enveloped viruses, including
Ebola and Zika virus, and recent data have expanded this to include SARS-
CoV-2.
 Bevacizumab A VEGF inhibitor called bevacizumab (marketed under the
brand name Avastin for certain types of cancer) being studied as a
treatment for acute lung injury (ALI) and acute respiratory distress
 syndrome (ARDS) in critically ill patients with COVID-19 pneumonia at
the Qilu Hospital of Shandong University in Jinan, China.
 Chloroquine phosphate The older anti-malaria drug chloroquine has been
shown to have a wide range of antiviral effects, including anti-coronavirus.
Studies in Guangdong Province in China suggest that chloroquine may
help improve patient outcomes in people with novel coronavirus
pneumonia.
 Colchicine An older anti-inflammatory drug called colchicine is being
studied to prevent complications of COVID-19 in high risk
patients. Colchicine has long been used in the treatment of gout.
 EIDD-2801 A team of researchers at UNC-Chapel Hill is hopeful that a
broad spectrum oral antiviral called EIDD-2801 could be used as a
potential prophylactic or treatment for COVID-19 and other coronaviruses.
Ridgeback Biotherapeutics has licensed EIDD-2801 and has received
permission from the FDA to begin patient trials.
 Favipiravir An antiviral drug called favipiravir which was reported February
17, 2020 to have received marketing approval in China for the treatment of
influenza, was also approved for use in clinical trials as a treatment for
novel coronavirus pneumonia. 
Update: March 31, 2020 -- Fujifilm announced the start of a Phase 3 clinical
trial of Avigan (favipiravir) on COVID-19 patients in Japan. Avigan is
approved in Japan for use as an antiviral in the treatment of influenza.
Update: April 9, 2020 -- Fujifilm announced the start of a Phase 2 clinical
trial of favipiravir in approximately 50 COVID-19 patients in the U.S.
 Fingolimod An approved drug called fingolimod (marketed under the
brand name Gilenya for the treatment of relapsing forms of multiple
sclerosis) is being studied as a treatment for COVID-19 at the First
Affiliated Hospital of Fujian Medical University in Fuzhou, China.
 Hydroxychloroquine and azithromycin In a small study commissioned by
the French government, 20 patients with COVID-19 were treated with a
combination of the anti-malaria drug hydroxychloroquine and the
macrolide antibacterial drug azithromycin (Zithromax). Results showed that
all patients taking the combination were virologically cured within 6 days
of treatment.
 Hydroxychloroquine sulfate It was reported in the journal Clinical
Infectious Diseases on March 9 that the malaria
drug hydroxychloroquine was effective in killing the coronavirus in
laboratory experiments. Hydroxychloroquine was first approved by the FDA
in 1995 under the brand name Plaquenil, and it is also used in the
treatment of patients with lupus and arthritis. In March 2020, the US FDA
issued an emergency use authorization (EUA) to allow the emergency use
of hydroxychloroquine sulfate supplied from the Strategic National
Stockpile (SNS) for the treatment of COVID-19 in certain hospitalized
patients.
 Ivermectin An anti-parasitic drug called ivermectin has been shown to be
effective against the SARS-CoV-2 virus in an in-vitro laboratory study by
researchers at Monash University in Melbourne, Australia. Further clinical
trials need to be completed to confirm the effectiveness of the drug in
humans with COVID-19.
 Leronlimab A CCR5 antagonist called leronlimab has shown promise in
calming the 'cytokine storm' in a small number of critically ill COVID-19
patients hospitalized in the New York area.
 Lopinavir and ritonavir A drug combination
called lopinavir/ritonavir approved to treat HIV under the brand name
Kaletra is being studied in combination with the flu
drug oseltamivir (Tamiflu) in Thailand. It was reported on February 18, 2020
that an elderly Chinese woman, the first patient to receive the "Thai
cocktail" in Bangkok's Rajvithi Hospital, had made a complete recovery
after suffering from severe COVID-19-related pneumonia.
Update: March 18, 2020 -- According to a study in the New England
Journal of Medicine,  the  lopinavir/ritonavir combination showed no benefit
over standard care in hospitalized adult patients with severe COVID-19.
 Methylprednisolone A widely used glucocorticoid
called methylprednisolone is being studied for safety and effectiveness in
the treatment of novel coronavirus pneumonia in a number of hospitals in
the Hubei province of China.
 Remdesivir An investigational antiviral drug called remdesivir is being
studied in clinical trials in China, the United States, and the United

Kingdom. Remdesivir has demonstrated in vitro and in vivo activity in

animal models against the viral pathogens that cause MERS and SARS,
which are coronaviruses structurally similar to SARS-CoV-2.
  Sarilumab An interleukin-6 (IL-6) receptor antagonist
called sarilumab (marketed under the brand name Kevzara for the
treatment of rheumatoid arthritis) is being studied as a potential treatment
for acute respiratory distress syndrome (ARDS) in patients critically ill from
COVID-19.
 Tocilizumab An interleukin-6 receptor antagonist
called tocilizumab (marketed under the brand name Actemra for the
treatment of rheumatoid arthritis and other inflammatory conditions) is
being studied in a number of locations worldwide for the treatment of
patients with COVID-19.
 Umifenovir An antiviral drug called umifenovir (marketed in Russia under
the brand name Arbidol, and also available in China for the treatment of
influenza) is being studied in China and other countries as a treatment
for COVID-19.
Several pharmaceutical companies and research organizations worldwide are
involved in the development of potential vaccines.
 mRNA-1273 A novel coronavirus vaccine called mRNA-1273 (Moderna,
Inc.) has been shipped to the National Institute of Allergy and Infectious
Diseases ready for use in a Phase 1 study.
 CSIRO, Australia’s national science agency, announced April, 2 2020 that it
has commenced the first stage of testing potential vaccines for COVID-19.
 Tonix Pharmaceuticals Holding Corp. has announced it is researching
the development of a potential vaccine against COVID-19 using its
proprietary horsepox virus platform.
 Researchers in Israel are working to adapt a vaccine that is effective against
avian coronavirus Infectious Bronchitis Virus (IBV) to work as a vaccine
against COVID-19 in humans.
 syndrome coronavirus 2 (SARS-CoV-2).[6] The outbreak was first identified
in Wuhan, China, in early December 2019.[4][7] The World Health
Organization declared the outbreak a Public Health Emergency of International
Concern on 30 January, and a pandemic on 11 March. [8][9] As of 10 May
2020, more than 4.09 million cases of COVID-19 have been reported in over 187
countries and territories, resulting in more than 282,000 deaths. More than 1.4 million
people have recovered.[5]

COVID-19 pandemic
 Map of confirmed cases per capita as of 11 May 2020

  10,000+ confirmed cases per million

  3,000–10,000 confirmed cases per million

  1,000–3,000 confirmed cases per million

  300–1,000 confirmed cases per million

  100–300 confirmed cases per million

  >0–100 confirmed cases per million

  No confirmed cases or no data

Total confirmed cases map

Map of total confirmed cases as of 10 May 2020

  1,000,000+ confirmed cases

  100,000–999,999 confirmed cases

  10,000–99,999 confirmed cases

  1,000–9,999 confirmed cases

  100–999 confirmed cases

  1–99 confirmed cases

  No confirmed cases or no data

Confirmed deaths per capita map

Map of confirmed deaths per capita as of

10 May 2020

  100+ confirmed deaths per million

  10–100 confirmed deaths per million

  1–10 confirmed deaths per million

  0.1–1 confirmed deaths per million

  >0–0.1 confirmed deaths per million

  No confirmed deaths or no data