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Henipavirus
Henipavirus is a genus of RNA viruses in the family Paramyxoviridae, order Mononegavirales containing five established species. Henipaviruses are naturally harboured by pteropid fruit bats (flying foxes) and microbats of several species.[1] Henipaviruses are characterised by long genomes and a wide host range. Their recent emergence as zoonotic pathogens capable of causing illness and death in domestic animals and humans is a cause of concern.
Henipavirus
CSIRO ScienceImage 1718 The Hendra Virus.jpg
Colored transmission electron micrograph of a Hendra virion (ca. 300 nm length)
Virus classification
Group:
Group V ((−)ssRNA)
Order:
Mononegavirales
Family:
Paramyxoviridae
Genus:
Henipavirus
Type species
Hendra henipavirus
Species
Cedar henipavirus
Ghanaian bat henipavirus
Hendra henipavirus
Mojiang henipavirus
Nipah henipavirus
In 2009, RNA sequences of three novel viruses in phylogenetic relationship to known henipaviruses were detected in African straw-colored fruit bats (Eidolon helvum) in Ghana. The finding of these novel henipaviruses outside Australia and Asia indicates that the region of potential endemicity of henipaviruses may be worldwide. These African henipaviruses are slowly being characterised.
Taxonomy:
Genus Henipavirus: species and their viruses
Genus Species Virus (Abbreviation)
Henipavirus Cedar henipavirus Cedar virus (CedV)
Ghanaian bat henipavirus Kumasi virus (KV)
Hendra henipavirus* Hendra virus (HeV)
Mojiang henipavirus Mòjiāng virus (MojV)
Nipah henipavirus Nipah virus (NiV)
Table legend: "*" denotes type species.
Virus structure:
Structure of henipaviruses
The henipavirus genome (3’ to 5’ orientation) and products of the P gene
Henipavirions are pleomorphic (variably shaped), ranging in size from 40 to 600 nm in diameter.[6] They possess a lipid membrane overlying a shell of viral matrix protein. At the core is a single helical strand of genomic RNA tightly bound to N (nucleocapsid) protein and associated with the L (large) and P (phosphoprotein) proteins, which provide RNA polymerase activity during replication.
Embedded within the lipid membrane are spikes of F (fusion) protein trimers and G (attachment) protein tetramers. The function of the G protein is to attach the virus to the surface of a host cell via EFNB2, a highly conserved protein present in many mammals.[7][8][9] The structure of the attachment glycoprotein has been determined by X-ray crystallography.[10] The F protein fuses the viral membrane with the host cell membrane, releasing the virion contents into the cell. It also causes infected cells to fuse with neighbouring cells to form large, multinucleated syncytia.
Genome structure:
As all mononegaviral genomes, Hendra virus and Nipah virus genomes are non-segmented, single-stranded negative-sense RNA. Both genomes are 18.2 kb in length and contain six genes corresponding to six structural proteins.
In common with other members of the Paramyxoviridae family, the number of nucleotides in the henipavirus genome is a multiple of six, consistent with what is known as the 'rule of six'. Deviation from the rule of six, through mutation or incomplete genome synthesis, leads to inefficient viral replication, probably due to structural constraints imposed by the binding between the RNA and the N protein.
Henipaviruses employ an unusual process called RNA editing to generate multiple proteins from a single gene. The specific process in henipaviruses involves the insertion of extra guanosine residues into the P gene mRNA prior to translation. The number of residues added determines whether the P, V or W proteins are synthesised. The functions of the V and W proteins are unknown, but they may be involved in disrupting host antiviral mechanisms.
Hendra virus:
Emergence:
Hendra virus (originally called "Equine morbillivirus") was discovered in September 1994 when it caused the deaths of thirteen horses, and a trainer at a training complex at 10 Williams Avenue, Hendra, a suburb of Brisbane in Queensland, Australia.
The index case, a mare called Drama Series, bought in from a paddock in Cannon Hill, was housed with 19 other horses after falling ill, and died two days later. Subsequently, all of the horses became ill, with 13 dying. The remaining six animals were subsequently euthanised as a way of preventing relapsing infection and possible further transmission.[15] The trainer, Victory ('Vic') Rail, and the stable foreman, Ray Unwin, were involved in nursing the index case, and both fell ill with an influenza-like illness within one week of the first horse’s death. The stable hand recovered but Rail died of respiratory and renal failure. The source of the virus was most likely frothy nasal discharge from the index case.
A second outbreak occurred in August 1994 (chronologically preceding the first outbreak) in Mackay 1,000 km north of Brisbane resulting in the deaths of two horses and their owner. The owner, Mark Preston, assisted in necropsies of the horses and within three weeks was admitted to hospital suffering from meningitis. Mr Preston recovered, but 14 months later developed neurologic signs and died. This outbreak was diagnosed retrospectively by the presence of Hendra virus in the brain of the patient.
Transmission:
Flying foxes have been identified as the reservoir host of Hendra Virus. A seroprevalence of 47% is found in the flying foxes, suggesting an endemic infection of the bat population throughout Australia. Horses become infected with Hendra after exposure to bodily fluid from an infected flying fox. This often happens in the form of urine, feces, or masticated fruit covered in the flying fox's saliva when horses are allowed to graze below roosting sites. The seven human cases have all been infected only after contact with sick horses. As a result, veterinarians are particularly at risk for contracting the disease.
Australian outbreaks:
Hendra
Mackay
Townsville
Bowen
Hervey Bay
Chinchilla
Rockhampton
Ingham
Cairns
Outbreaks in Queensland
Ballina
Macksville
Mullumbimby
Lismore
Kempsey
Outbreaks in New South Wales
As of June 2014, a total of fifty outbreaks of Hendra virus have occurred in Australia, all involving infection of horses. As a result of these events, eighty-three horses have died or been euthanised. A further four died or were euthanised as a result of possible hendra infection.
Case fatality rate in humans is 60% and in horses 75%.
Four of these outbreaks have spread to humans as a result of direct contact with infected horses. On 26 July 2011 a dog living on the Mt Alford property was reported to have HeV antibodies, the first time an animal other than a flying fox, horse, or human has tested positive outside an experimental situation.
These events have all been on the east coast of Australia, with the most northern event at Cairns, Queensland and the event furthest south at Kempsey, New South Wales. Until the event at Chinchilla, Queensland in July 2011, all outbreak sites had been within the distribution of at least two of the four mainland flying foxes (fruit bats); Little red flying fox, (Pteropus scapulatus), black flying fox, (Pteropus alecto), grey-headed flying fox, (Pteropus poliocephalus) and spectacled flying fox, (Pteropus conspicillatus). Chinchilla is considered to be only within the range of little red flying fox and is west of the Great Dividing Range. This is the furthest west the infection has ever been identified in horses.
The timing of incidents indicates a seasonal pattern of outbreaks. Initially this was thought to possibly related to the breeding cycle of the little red flying foxes. These species typically give birth between April and May. Subsequently however, the Spectacled flying fox and the Black flying fox have been identified as the species more likely to be involved in infection spillovers.
Timing of outbreaks also appears more likely during the cooler months when it is possible the temperature and humidity are more favourable to the longer term survival of the virus in the environment.
There is no evidence of transmission to humans directly from bats, and, as such it appears that human infection only occurs via an intermediate host, a horse. Despite this in 2014 the NSW Government sanctioned the destruction of flying fox colonies.
List of Australian Hendra outbreaks
Date Location Details
August 1994 Mackay, Queensland Death of two horses and one person, Mark Preston.
September 1994 Hendra, Queensland 20 horses died or were euthanised. Two people infected. One of them, Victory ("Vic") Rail, a nationally prominent trainer of racehorses, died.
January 1999 Trinity Beach, Cairns, Queensland Death of one horse.
October 2004 Gordonvale, Cairns, Queensland Death of one horse. A veterinarian involved in autopsy of the horse was infected with Hendra virus, and suffered a mild illness.
December 2004 Townsville, Queensland Death of one horse.
June 2006 Peachester, Sunshine Coast, Queensland Death of one horse.
October 2006 Murwillumbah, New South Wales Death of one horse.
July 2007 Peachester, Sunshine Coast, Queensland Infection of one horse (euthanised)
July 2007 Clifton Beach, Cairns, Queensland Infection of one horse (euthanised).
July 2008 Redlands, Queensland Death of five horses; four died from the Henda virus, the remaining animal recovered but was euthanised because of a government policy that requires all animals with antibodies to be euthanised due to a potential threat to health. Two veterinary workers from the affected property were infected leading to the death of one, veterinary surgeon Ben Cuneen, on 20 August 2008. The second veterinarian was hospitalized after pricking herself with a needle she had used to euthanize the horse that had recovered. A nurse exposed to the disease while assisting Cuneen in caring for the infected horses was also hospitalized. The Biosecurity Queensland website indicates that 8 horses died during this event, however a review of the event indicates that five horses are confirmed to have died from HeV and three of the horses "are regarded as improbable cases of Hendra virus infection ...".
July 2008 Proserpine, Queensland Death of four horses.
July 2009 Cawarral, Queensland Death of four horses. Queensland veterinary surgeon Alister Rodgers tested positive after treating the horses. On 1 September 2009 after two weeks in a coma, he became the fourth person to die from exposure to the virus.
September 2009 Bowen, Queensland Death of two horses.
May 2010 Tewantin, Queensland Death of one horse.
20 June 2011 – 31 July 2011 Mount Alford, Queensland Death of three horses (all confirmed to have died of Hendra) and sero-conversion of a dog. The first horse death on this property occurred on 20 June 2011, although it was not until after the second death on 1 July 2011 that samples taken from the first animal were tested. The third horse was euthanised on 4 July 2011. On 26 July 2011 a dog from this property was reported to have tested positive for HeV antibodies. Reports indicate that this Australian Kelpie, a family companion, will be euthanised in line with government policy. Biosecurity Queensland suggest the dog most likely was exposed to HeV though one of the sick horses. Dusty was euthanised on 31 July 2011 following a second positive antibody test.
26 June 2011 Kerry, Queensland The horse was moved after it became sick to another property at Beaudesert, Queensland. Death of one horse.
28 June 2011 Loganlea, Logan City, Queensland Death of one horse. Unusually this horse had HeV antibodies present in its blood at the time of death. How this immune response should be interpreted is a matter of debate.
29 June 2011 Mcleans Ridges, Wollongbar, New South Wales Death of one horse. The second horse on the property tested positive to Hendra and was euthanised on 12 July 2011.
3 July 2011 Macksville, New South Wales Death of one horse.
4 July 2011 Park Ridge, Logan City, Queensland Death of one horse.
11 July 2011 Kuranda, Queensland Death of one horse.
13 July 2011 Hervey Bay, Queensland Death of one horse.
14 July 2011 Lismore, New South Wales Death of one horse.
15 July 2011 Boondall, Queensland Death of one horse.
22 July 2011 Chinchilla, Queensland Death of one horse.
24 July 2011 Mullumbimby, New South Wales Death of one horse.
13 August 2011 Mullumbimby, New South Wales Death of one horse. A horse was found dead after being unwell the day before. HeV infection was confirmed on 17 August 2011.
15 August 2011 Ballina, New South Wales Death of one horse.
17 August 2011 South Ballina, New South Wales Death of two horses. The horses were found dead in a field. Both tested positive to HeV. The exact date of death is not known, but HeV infection was confirmed on 17 August 2011.
23 August 2011 Currumbin Valley, Gold Coast, Queensland Death of one horse.
28 August 2011 North of Ballina, New South Wales Death of one horse.
11 October 2011 Beachmere, Caboolture Queensland One horse euthanised after testing positive. A horse that died on the property one week before may have died of HeV. On 15 October 2011 another horse on the property was euthanised following a positive HeV antibody test.
3 January 2012 Townsville, Queensland A horse that died or was euthanised on 3 January 2012 returned a positive HeV test on 5 January 2012.
26 May 2012 Rockhampton, Queensland One horse died.
28 May 2012 Ingham, Queensland One horse died. A dog returned a positive test but was subsequently cleared.
19 July 2012 Rockhampton, Queensland One horse died. On 27 July it was announced that two other horses on the property, showing clinical signs of the disease, had been euthanised. Two dogs were assessed, and the property was quarantined.
27 June 2012 Mackay, Queensland One horse was euthanised after returning a positive HeV test. 15 horses on the property are being tested and quarantined, along with horses on neighbouring properties.
27 July 2012 Cairns, Queensland One horse died.
5 September 2012 Port Douglas, Queensland One horse died. The property with 13 other horses is quarantined.
1 November 2012 Ingham, Queensland One symptomatic horse euthanised. A test for HeV the following day proved positive. The property, with seven other horses, quarantined.
20 January 2013 Mackay, Queensland One horse died.
19 February 2013 Atherton Tablelands, North Queensland One horse died. Four horses and four people from the property were assessed.
3 June 2013 Macksville, New South Wales Death of one horse, a second horse vaccinated, five cats and a dog were monitored.
1 July 2013 Tarampa, Queensland One horse died. HeV virus confirmed.
4 July 2013 Macksville, New South Wales Six year old gelding died. Several other horses, dogs and cats were tested.[82][83] A dog from the property tested positive for HeV and was euthanised around 19 July 2013
5 July 2013 Gold Coast, Queensland One horse died. No other horses on property.
6 July 2013 Kempsey, New South Wales Eighteen-year-old unvaccinated mare died, other animals on property under observation.
9 July 2013 Kempsey, New South Wales Thirteen-year-old unvaccinated quarterhorse died, other animals on property were put under observation.
18 March 2014 Bundaberg, Queensland Unvaccinated horse euthanased.
1 June 2014 Beenleigh, Queensland Horse euthanased and property quarantined after outbreak at a property.
24 Jun 2015 Mullumbimby, New South Wales Horse found dead after several days of illness. HeV confirmed as the cause of death.
18 March 2014 Bundaberg, Queensland Unvaccinated horse euthanased.
1 June 2014 Beenleigh, Queensland Horse euthanased and property quarantined after outbreak at a property.
20 July 2014 Calliope, Queensland Horse euthanased and property quarantined after outbreak.
24 Jun 2015 Mullumbimby, New South Wales Horse found dead after several days of illness.
About 20 July 2015 Atherton Tableland, Queensland Infected horse died and property quarantined.
About 4 September 2015 Lismore, New South Wales Infected horse euthanised and property quarantined.
About 24 May 2017 Gold Coast, Queensland An unvaccinated infected horse euthanised and property quarantined.
About 8 July 2017 Lismore, New South Wales Hendra virus confirmed near Lismore
About 1 August 2017 Murwillumbah, New South Wales Hendra virus confirmed near Murwillumbah
About 5 August 2017 Lismore, New South Wales Third Hendra case confirmed near Lismore
Events of June–August 2011:
In the years 1994–2010, fourteen events were recorded. Between 20 June 2011 and 28 August 2011, a further seventeen events were identified, during which twenty-one horses died.
It's not clear why there has been a sudden increase in the number of spillover events between June and August 2011. Typically HeV spillover events are more common between May and October. This time is sometimes called "Hendra Season", which is a time when there are large numbers of fruit bats of all species congregated in SE Queensland's valuable winter foraging habitat. The weather (warm and humid) is favourable to the survival of henipavirus in the environment.
It is possible flooding in SE Queensland and Northern NSW in December 2010 and January 2011 may have affected the health of the fruit bats. Urine sampling in flying fox camps indicate that a larger proportion of flying foxes than usual are shedding live virus. Biosecurity Queensland's ongoing surveillance usually shows 7% of the animals are shedding live virus. In June and July nearly 30% animals have been reported to be shedding live virus.
Present advice is that these events are not being driven by any mutation in HeV itself.
Other suggestions include that an increase in testing has led to an increase in detection. As the actual mode of transmission between bats and horses has not been determined, it is not clear what, if any, factors can increase the chance of infection in horses.
Following the confirmation of a dog with HeV antibodies, on 27 July 2011, the Queensland and NSW governments will boost research funding into the Hendra virus by $6 million to be spent by 2014–2015. This money will be used for research into ecological drivers of infection in the bats and the mechanism of virus transmission between bats and other species. A further 6 million dollars was allocated by the federal government with the funds being split, half for human health investigations and half for animal health and biodiversity research.
Prevention, detection and treatment:
Three main approaches are currently followed to reduce the risk to humans.
Vaccine for horses.
In November 2012, a vaccine became available for horses. The vaccine is to be used in horses only, since, according to CSIRO veterinary pathologist Dr Deborah Middleton, breaking the transmission cycle from flying foxes to horses prevents it from passing to humans, as well as, "a vaccine for people would take many more years."
The vaccine is a subunit vaccine that neutralises Hendra virus and is composed of a soluble version of the G surface antigen on Hendra virus and has been successful in ferret models.
By December 2014, about 300 000 doses had been administered to more than 100 000 horses. About 3 in 1000 had reported incidents; the majority being localised swelling at the injection site. There had been no reported deaths.
In August 2015, the Australian Pesticides and Veterinary Medicines Authority (APVMA) registered the vaccine. In its statement the Australian government agency released all its data on reported side effects. In January 2016, APVMA approved its use in pregnant mares.
Stall-side test to assist in diagnosing the disease in horses rapidly.
Although the research on the Hendra virus detection is ongoing, a promising result has found using antibody-conjugated magnetic particles and quantum dots.
Post-exposure treatment for humans.
Nipah virus and Hendra virus are closely related paramyxoviruses that emerged from bats during the 1990s to cause deadly outbreaks in humans and domesticated animals. National Institute of Allergy and Infectious Diseases (NIAID)-supported investigators developed vaccines for Nipah and Hendra virus based on the soluble G-glycoproteins of the viruses formulated with adjuvants. Both vaccines have been shown[who?] to induce strong neutralizing antibodies in different laboratory animals.
Trials began in 2015 to evaluate a monoclonal antibody to be used as a possible complementary treatment for humans exposed to Hendra virus infected horses.
Deforestation Impact.
When considering any zoonosis, one must understand the social, ecological, and biological contributions that may be facilitating this spillover. Hendra virus is believed to be partially seasonally related. For, there is a suggested correlation between breeding time and an increase in incidences of Hendra virus in flying fox bats.
Additionally, recent research suggests that the upsurge in deforestation within Australia may be leading to an increase in incidences of Hendra virus. Flying fox bats tend to feed in trees during a large part of the year. However, due to the lack of specific fruit trees within the area, these bats are having to relocate and thereby are coming into contact with horses more often. The two most recent outbreaks of Hendra virus in 2011 and 2013 appear to be related to an increased level of nutritional stress among the bats as well as relocation of bat populations. Work is currently being done to increase vaccination among horses as well as replant these important forests as feeding grounds for the flying fox bats. Through these measures, the goal is to decrease the incidences of the highly fatal Hendra virus.
Pathology:
Flying foxes experimentally infected with the Hendra virus develop a viraemia then excrete the virus in their urine, faeces and saliva for approximately one week. Although they excrete active virus during this time there is no other indication of an illness. Symptoms of Hendra virus infection of humans may be respiratory, including hemorrhage and edema of the lungs, or encephalitic, resulting in meningitis. In horses, infection usually causes pulmonary oedema, congestion and / or neurological signs.
Ephrin B2 has been identified as the main receptor for the henipaviruses.
Hendra virus has been classified as a Bio-safety Level 4 Hot Agent.
2016 Brisbane Research ConferenceEdit
In late May, early June 2016, "Hendra scientists, vets and health officers met in Brisbane to bring together all the research into the bat-borne disease."
Nipah virusEdit
Main article: Nipah virus infection
Not to be confused with Nepovirus.
Emergence:
Pteropus vampyrus (Large flying fox), one of the natural reservoirs of Nipah virus
Nipah virus was identified in April 1999, when it caused an outbreak of neurological and respiratory disease on pig farms in peninsular Malaysia, resulting in 257 human cases, including 105 human deaths and the culling of one million pigs. In Singapore, 11 cases, including one death, occurred in abattoir workers exposed to pigs imported from the affected Malaysian farms. The Nipah virus has been classified by the Centers for Disease Control and Prevention as a Category C agent. The name "Nipah" refers to the place, Kampung Baru Sungai Nipah in Port Dickson, Negeri Sembilan, the source of the human case from which Nipah virus was first isolated. Nipah virus is one of several viruses identified by WHO as a likely cause of a future epidemic in a new plan developed after the Ebola epidemic for urgent research and development before and during an epidemic toward new diagnostic tests, vaccines and medicines.
The outbreak was originally mistaken for Japanese encephalitis (JE), however, physicians in the area noted that persons who had been vaccinated against JE were not protected, and the number of cases among adults was unusual Despite the fact that these observations were recorded in the first month of the outbreak, the Ministry of Health failed to react accordingly, and instead launched a nationwide campaign to educate people on the dangers of JE and its vector, Culex mosquitoes.
Symptoms of infection from the Malaysian outbreak were primarily encephalitic in humans and respiratory in pigs. Later outbreaks have caused respiratory illness in humans, increasing the likelihood of human-to-human transmission and indicating the existence of more dangerous strains of the virus.
Based on seroprevalence data and virus isolations, the primary reservoir for Nipah virus was identified as Pteropid fruit bats, including Pteropus vampyrus (Large Flying Fox), and Pteropus hypomelanus (Small flying fox), both of which occur in Malaysia.
The transmission of Nipah virus from flying foxes to pigs is thought to be due to an increasing overlap between bat habitats and piggeries in peninsular Malaysia. At the index farm, fruit orchards were in close proximity to the piggery, allowing the spillage of urine, faeces and partially eaten fruit onto the pigs. Retrospective studies demonstrate that viral spillover into pigs may have been occurring in Malaysia since 1996 without detection.[17] During 1998, viral spread was aided by the transfer of infected pigs to other farms, where new outbreaks occurred.
Evolution:
The most likely origin of this virus was in 1947 (95% credible interval: 1888–1988).[133] There are two clades of this virus—one with its origin in 1995 (95% credible interval: 1985–2002) and a second with its origin in 1985 (95% credible interval: 1971–1996). The mutation rate was estimated to be 6.5 × 10−4 substitution/site/year (95% credible interval: 2.3 × 10−4 –1.18 × 10−3), similar to other RNA viruses.
Outbreaks:
Locations of henipavirus outbreaks (red stars–Hendra virus; blue stars–Nipah virus) and distribution of henipavirus flying fox reservoirs (red shading–Hendra virus ; blue shading–Nipah virus)
Eight more outbreaks of Nipah virus have occurred since 1998, all within Bangladesh and neighbouring parts of India. The outbreak sites lie within the range of Pteropus species (Pteropus giganteus). As with Hendra virus, the timing of the outbreaks indicates a seasonal effect. Cases occurring in Bangladesh during the winters of 2001, 2003, and 2004, were determined to have been caused by the Nipah virus. In February 2011, a Nipah outbreak began at Hatibandha Upazila in the Lalmonirhat District of northern Bangladesh. To date (7 February 2011), there have been 24 cases and 17 deaths in this outbreak.
2001 January 31–23 February, Siliguri, India: 66 cases with a 74% mortality rate.[136] 75% of patients were either hospital staff or had visited one of the other patients in hospital, indicating person-to-person transmission.
2001 April – May, Meherpur District, Bangladesh: 13 cases with nine fatalities (69% mortality).
2003 January, Naogaon District, Bangladesh: 12 cases with eight fatalities (67% mortality).
2004 January – February, Manikganj and Rajbari districts, Bangladesh: 42 cases with 14 fatalities (33% mortality).
2004 19 February – 16 April, Faridpur District, Bangladesh: 36 cases with 27 fatalities (75% mortality). 92% of cases involved close contact with at least one other person infected with Nipah virus. Two cases involved a single short exposure to an ill patient, including a rickshaw driver who transported a patient to hospital. In addition, at least six cases involved acute respiratory distress syndrome, which has not been reported previously for Nipah virus illness in humans. This symptom is likely to have assisted human-to-human transmission through large droplet dispersal.
2005 January, Tangail District, Bangladesh: 12 cases with 11 fatalities (92% mortality). The virus was probably contracted from drinking date palm juice contaminated by fruit bat droppings or saliva.
2007 February – May, Nadia District, India: up to 50 suspected cases with 3–5 fatalities. The outbreak site borders the Bangladesh district of Kushtia where eight cases of Nipah virus encephalitis with five fatalities occurred during March and April 2007. This was preceded by an outbreak in Thakurgaon during January and February affecting seven people with three deaths.[139] All three outbreaks showed evidence of person-to-person transmission.
2008 February – March, Manikganj and Rajbari districts, Bangladesh: Nine cases with eight fatalities.
2010 January, Bhanga subdistrict, Faridpur, Bangladesh: Eight cases with seven fatalities. During March, one physician of Faridpur Medical College Hospital caring for confirmed Nipah cases died.
2011 February: An outbreak of Nipah Virus has occurred at Hatibandha, Lalmonirhat, Bangladesh. The deaths of 21 schoolchildren due to Nipah virus infection were recorded on 4 February 2011. IEDCR has confirmed the infection is due to this virus.[142] Local schools were closed for one week to prevent the spread of the virus. People were also requested to avoid consumption of uncooked fruits and fruit products. Such foods, contaminated with urine or saliva from infected fruit bats, were the most likely source of this outbreak.
2018 May: Deaths of 13 people in Perambra near Calicut, Kerala, India have been confirmed as a result of the virus. Treatment using antivirals such as Ribavirin has been initiated.
Nipah virus has been isolated from Lyle's flying fox (Pteropus lylei) in Cambodia and viral RNA found in urine and saliva from P. lylei and Horsfield's roundleaf bat (Hipposideros larvatus) in Thailand. Infective virus has also been isolated from environmental samples of bat urine and partially eaten fruit in Malaysia.[148] Antibodies to henipaviruses have also been found in fruit bats in Madagascar (Pteropus rufus, Eidolon dupreanum) and Ghana (Eidolon helvum) indicating a wide geographic distribution of the viruses. No infection of humans or other species have been observed in Cambodia, Thailand or Africa thus far.
Pathology:
In humans, the infection presents as fever, headache , drowsiness, disorientation and confusion, Cough, abdominal pain, nausea, vomiting, weakness, problems with swallowing and blurred vision are relatively common. About a quarter of the patients have seizures and about 60% become comatose and might need mechanical ventilation. In patients with severe disease, their conscious state may deteriorate and they may develop severe hypertension, fast heart rate, and very high temperature.
Nipah virus is also known to cause relapse encephalitis. In the initial Malaysian outbreak, a patient presented with relapse encephalitis some 53 months after his initial infection. There is no definitive treatment for Nipah encephalitis, apart from supportive measures, such as mechanical ventilation and prevention of secondary infection. Ribavirin, an antiviral drug, was tested in the Malaysian outbreak, and the results were encouraging, though further studies are still needed.
While no vaccine currently exists, a 2012 study of a trial vaccine developed using the outer proteins of Hendra virus was shown to induce protection against Nipah in African green monkeys.
In animals, especially in pigs, the virus causes a porcine respiratory and neurologic syndrome, locally known as "barking pig syndrome" or "one mile cough."
Ephrin B2 has been identified as the main receptor for the henipaviruses.
Cedar virus:
Emergence:
Cedar Virus (CedV) was first identified in pteropid urine during work on Hendra virus undertaken in Queensland in 2009.
Although the virus is reported to be very similar to both Hendra and Nipah viruses, it does not cause illness in laboratory animals usually susceptible to paramyxoviruses. Animals were able to mount an effective response and create effective antibodies.
The scientists who identified the virus report:
Hendra and Nipah viruses are 2 highly pathogenic paramyxoviruses that have emerged from bats within the last two decades. Both are capable of causing fatal disease in both humans and many mammal species. Serological and molecular evidence for henipa-like viruses have been reported from numerous locations including Asia and Africa, however, until now no successful isolation of these viruses have been reported. This paper reports the isolation of a novel paramyxovirus, named Cedar virus, from fruit bats in Australia. Full genome sequencing of this virus suggests a close relationship with the henipaviruses. Antibodies to Cedar virus were shown to cross react with, but not cross neutralize Hendra or Nipah virus. Despite this close relationship, when Cedar virus was tested in experimental challenge models in ferrets and guinea pigs, we identified virus replication and generation of neutralizing antibodies, but no clinical disease was observed. As such, this virus provides a useful reference for future reverse genetics experiments to determine the molecular basis of the pathogenicity of the henipaviruses.
Causes of emergence:
The emergence of henipaviruses parallels the emergence of other zoonotic viruses in recent decades. SARS coronavirus, Australian bat lyssavirus, Menangle virus and probably Ebola virus and Marburg virus are also harbored by bats and are capable of infecting a variety of other species. The emergence of each of these viruses has been linked to an increase in contact between bats and humans, sometimes involving an intermediate domestic animal host. The increased contact is driven both by human encroachment into the bats’ territory (in the case of Nipah, specifically pigpens in said territory) and by movement of bats towards human populations due to changes in food distribution and loss of habitat.
There is evidence that habitat loss for flying foxes, both in South Asia and Australia (particularly along the east coast) as well as encroachment of human dwellings and agriculture into the remaining habitats, is creating greater overlap of human and flying fox distributions.
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Nipah virus infection
Nipah virus infection (NiV) is a viral infection caused by the Nipah virus. Symptoms from infection vary from none to fever, cough, headache, shortness of breath, and confusion. This may worsen into a coma over a day or two. Complications can include inflammation of the brain and seizures following recovery.
Nipah virus infection
Henipavirus structure.svg
Structure of a Henipavirus
Specialty
Infectious disease Edit this on Wikidata
Symptoms
None, fever, cough, headache, confusion
Complications
Inflammation of the brain, seizures
Usual onset
5 to 14 days after exposure
Causes
Nipah virus (spread by direct contact)[3]
Diagnostic method
Based on symptoms, confirmed by laboratory testing
Prevention
Avoiding exposure to bats and sick pigs, not drinking raw date palm sap
Treatment
Supportive care
Frequency
582 human cases (2001 until 2012)
Deaths
~50% risk of death
The Nipah virus is a type of RNA virus in the genus Henipavirus. It can both spread between people and from other animals to people. Spread typically requires direct content with an infected source. The virus normally circulates among specific types of fruit bats. Diagnosis is based on symptoms and confirmed by laboratory testing.
The disease was first identified in 1998 in Malaysia and Singapore with the virus being identified in 1999. It is named after a village in Malaysia, Sungai Nipah. Pigs may also be infected and millions were killed in 1999 to stop the spread of disease.
Management involves supportive care. As of 2018 there is no vaccine or specific treatment. Prevention is by avoiding exposure to bats and sick pigs and not drinking raw date palm sap. As of 2013 a total of 582 human cases of Nipah virus are estimated and 54 percent of those who were infected died. In 2018, an outbreak of the disease resulted in at least 10 death in the Indian state of Kerala.
Signs and symptoms:
The symptoms start to appear within 3–14 days after exposure. Initial symptoms are fever, headache, drowsiness followed by disorientation and mental confusion. These symptoms can progress into coma as fast as in 24–48 hours. Encephalitis, inflammation of the brain, is the dreaded complication of nipah virus infection. Respiratory illness can also be present during the early part of the illness. Nipah-case patients who had breathing difficulty are more likely than those without respiratory illness to transmit the virus. The disease is suspected in symptomatic individuals in the context of an epidemic outbreak.
Risks:
Fruit bats are the natural reservoirs of Nipah virus
The risk of exposure is high for hospital workers and caretakers of those infected with the virus. In Malaysia and Singapore, Nipah virus infection occurred in those with close contact to infected pigs. In Bangladesh and India, the disease has been linked to consumption of raw date palm sap (toddy) and contact with bats.
Diagnosis:
Laboratory diagnosis of Nipah virus infection is made using real time polymerase chain reaction (RT-PCR) from throat swabs, cerebrospinal fluid, urine and blood analysis during acute and convalescent stages of the disease. IgG and IgM antibody detection can be done after recovery to confirm Nipah virus infection. Immunohistochemistry on tissues collected during autopsy also confirms the disease.[7] Viral RNA can be isolated from the saliva of infected persons.
Prevention:
Prevention of Nipah virus infection is important since there is no effective treatment for the disease. The infection can be prevented by avoiding exposure to bats in endemic areas and sick pigs. Drinking of raw palm sap (palm toddy) contaminated by bat excrete, eating of fruits partially consumed by bats and using water from wells infested by bats should be avoided. Bats are known to drink toddy that is collected in open containers, and occasionally urinate in it, which makes it contaminated with the virus. Surveillance and awareness are important for preventing future outbreaks. The association of this disease within reproductive cycle of bats is not well studied. Standard infection control practices should be enforced to prevent nosocomial infections. A subunit vaccine using the Hendra G protein was found to produce cross-protective antibodies against henipavirus and nipavirus has been used in monkeys to protect against Hendra virus, although its potential for use in humans has not been studied.
Treatment:
Currently there is no effective treatment for Nipah virus infection. The treatment is limited to supportive care. It is important to practice standard infection control practices and proper barrier nursing techniques to avoid the transmission of the infection from person to person. All suspected cases of Nipah virus infection should be isolated and given intensive supportive care. Ribavirin has been shown effective in in vitro tests, but has not yet been proven effective in humans. Passive immunization using a human monoclonal antibody that targets the Nipah G glycoprotein has been evaluated in the ferret model as post-exposure prophylaxis.The anti-malarial drug chloroquine was shown to block the critical functions needed for maturation of Nipah virus, although no clinical benefit has yet been observed.[16] m102.4, a human monoclonal antibody, has been used in people on a compassionate use basis in Australia and is presently in pre-clinical development.
Outbreaks:
Map showing locations of outbreaks of Nipah and Hendra virus as well as the range of Pteropus bats as of 2014
Nipah virus outbreaks have been reported in Malaysia, Singapore, Bangladesh and India. The highest mortality due to Nipah virus infection has occurred in Bangladesh. In Bangladesh, the outbreaks are typically seen in winter season. Nipah virus first appeared in Malaysia in 1998 in peninsular Malaysia in pigs and pig farmers. By mid-1999, more than 265 human cases of encephalitis, including 105 deaths, had been reported in Malaysia, and 11 cases of either encephalitis or respiratory illness with one fatality were reported in Singapore. In 2001, Nipah virus was reported from Meherpur District, Bangladesh and Siliguri, India. The outbreak again appeared in 2003, 2004 and 2005 in Naogaon District, Manikganj District, Rajbari District, Faridpur District and Tangail District.
In Bangladesh, there were outbreaks in subsequent years as well.
In May 2018, an outbreak has been reported in the Kozhikode district of Kerala, India. Twelve deaths have been recorded, including one healthcare worker.Those who have died are mainly from the districts of Kozhikode and Malappuram, including a 31-year-old nurse, who was treating patients infected with the virus. As of 23 May 2018, about 14 people are being quarantined because they had contact with the sick.On 24 May 2018, 2 cases were also detected at Mangaluru, Karnataka. In Himachal Pradesh, India, some bats were reportedly found dead.This incident has caused panic throughout the state. Blood samples have been sent for testing. India is seeking help from Australia by importing "Monoclonal antibodies", though they have not been tested on humans. India is also importing Ribavirin tablets from Malaysia.
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Henipavirus is a genus of RNA viruses in the family Paramyxoviridae, order Mononegavirales containing five established species. Henipaviruses are naturally harboured by pteropid fruit bats (flying foxes) and microbats of several species.[1] Henipaviruses are characterised by long genomes and a wide host range. Their recent emergence as zoonotic pathogens capable of causing illness and death in domestic animals and humans is a cause of concern.
Henipavirus
CSIRO ScienceImage 1718 The Hendra Virus.jpg
Colored transmission electron micrograph of a Hendra virion (ca. 300 nm length)
Virus classification
Group:
Group V ((−)ssRNA)
Order:
Mononegavirales
Family:
Paramyxoviridae
Genus:
Henipavirus
Type species
Hendra henipavirus
Species
Cedar henipavirus
Ghanaian bat henipavirus
Hendra henipavirus
Mojiang henipavirus
Nipah henipavirus
In 2009, RNA sequences of three novel viruses in phylogenetic relationship to known henipaviruses were detected in African straw-colored fruit bats (Eidolon helvum) in Ghana. The finding of these novel henipaviruses outside Australia and Asia indicates that the region of potential endemicity of henipaviruses may be worldwide. These African henipaviruses are slowly being characterised.
Taxonomy:
Genus Henipavirus: species and their viruses
Genus Species Virus (Abbreviation)
Henipavirus Cedar henipavirus Cedar virus (CedV)
Ghanaian bat henipavirus Kumasi virus (KV)
Hendra henipavirus* Hendra virus (HeV)
Mojiang henipavirus Mòjiāng virus (MojV)
Nipah henipavirus Nipah virus (NiV)
Table legend: "*" denotes type species.
Virus structure:
Structure of henipaviruses
The henipavirus genome (3’ to 5’ orientation) and products of the P gene
Henipavirions are pleomorphic (variably shaped), ranging in size from 40 to 600 nm in diameter.[6] They possess a lipid membrane overlying a shell of viral matrix protein. At the core is a single helical strand of genomic RNA tightly bound to N (nucleocapsid) protein and associated with the L (large) and P (phosphoprotein) proteins, which provide RNA polymerase activity during replication.
Embedded within the lipid membrane are spikes of F (fusion) protein trimers and G (attachment) protein tetramers. The function of the G protein is to attach the virus to the surface of a host cell via EFNB2, a highly conserved protein present in many mammals.[7][8][9] The structure of the attachment glycoprotein has been determined by X-ray crystallography.[10] The F protein fuses the viral membrane with the host cell membrane, releasing the virion contents into the cell. It also causes infected cells to fuse with neighbouring cells to form large, multinucleated syncytia.
Genome structure:
As all mononegaviral genomes, Hendra virus and Nipah virus genomes are non-segmented, single-stranded negative-sense RNA. Both genomes are 18.2 kb in length and contain six genes corresponding to six structural proteins.
In common with other members of the Paramyxoviridae family, the number of nucleotides in the henipavirus genome is a multiple of six, consistent with what is known as the 'rule of six'. Deviation from the rule of six, through mutation or incomplete genome synthesis, leads to inefficient viral replication, probably due to structural constraints imposed by the binding between the RNA and the N protein.
Henipaviruses employ an unusual process called RNA editing to generate multiple proteins from a single gene. The specific process in henipaviruses involves the insertion of extra guanosine residues into the P gene mRNA prior to translation. The number of residues added determines whether the P, V or W proteins are synthesised. The functions of the V and W proteins are unknown, but they may be involved in disrupting host antiviral mechanisms.
Hendra virus:
Emergence:
Hendra virus (originally called "Equine morbillivirus") was discovered in September 1994 when it caused the deaths of thirteen horses, and a trainer at a training complex at 10 Williams Avenue, Hendra, a suburb of Brisbane in Queensland, Australia.
The index case, a mare called Drama Series, bought in from a paddock in Cannon Hill, was housed with 19 other horses after falling ill, and died two days later. Subsequently, all of the horses became ill, with 13 dying. The remaining six animals were subsequently euthanised as a way of preventing relapsing infection and possible further transmission.[15] The trainer, Victory ('Vic') Rail, and the stable foreman, Ray Unwin, were involved in nursing the index case, and both fell ill with an influenza-like illness within one week of the first horse’s death. The stable hand recovered but Rail died of respiratory and renal failure. The source of the virus was most likely frothy nasal discharge from the index case.
A second outbreak occurred in August 1994 (chronologically preceding the first outbreak) in Mackay 1,000 km north of Brisbane resulting in the deaths of two horses and their owner. The owner, Mark Preston, assisted in necropsies of the horses and within three weeks was admitted to hospital suffering from meningitis. Mr Preston recovered, but 14 months later developed neurologic signs and died. This outbreak was diagnosed retrospectively by the presence of Hendra virus in the brain of the patient.
Transmission:
Flying foxes have been identified as the reservoir host of Hendra Virus. A seroprevalence of 47% is found in the flying foxes, suggesting an endemic infection of the bat population throughout Australia. Horses become infected with Hendra after exposure to bodily fluid from an infected flying fox. This often happens in the form of urine, feces, or masticated fruit covered in the flying fox's saliva when horses are allowed to graze below roosting sites. The seven human cases have all been infected only after contact with sick horses. As a result, veterinarians are particularly at risk for contracting the disease.
Australian outbreaks:
Hendra
Mackay
Townsville
Bowen
Hervey Bay
Chinchilla
Rockhampton
Ingham
Cairns
Outbreaks in Queensland
Ballina
Macksville
Mullumbimby
Lismore
Kempsey
Outbreaks in New South Wales
As of June 2014, a total of fifty outbreaks of Hendra virus have occurred in Australia, all involving infection of horses. As a result of these events, eighty-three horses have died or been euthanised. A further four died or were euthanised as a result of possible hendra infection.
Case fatality rate in humans is 60% and in horses 75%.
Four of these outbreaks have spread to humans as a result of direct contact with infected horses. On 26 July 2011 a dog living on the Mt Alford property was reported to have HeV antibodies, the first time an animal other than a flying fox, horse, or human has tested positive outside an experimental situation.
These events have all been on the east coast of Australia, with the most northern event at Cairns, Queensland and the event furthest south at Kempsey, New South Wales. Until the event at Chinchilla, Queensland in July 2011, all outbreak sites had been within the distribution of at least two of the four mainland flying foxes (fruit bats); Little red flying fox, (Pteropus scapulatus), black flying fox, (Pteropus alecto), grey-headed flying fox, (Pteropus poliocephalus) and spectacled flying fox, (Pteropus conspicillatus). Chinchilla is considered to be only within the range of little red flying fox and is west of the Great Dividing Range. This is the furthest west the infection has ever been identified in horses.
The timing of incidents indicates a seasonal pattern of outbreaks. Initially this was thought to possibly related to the breeding cycle of the little red flying foxes. These species typically give birth between April and May. Subsequently however, the Spectacled flying fox and the Black flying fox have been identified as the species more likely to be involved in infection spillovers.
Timing of outbreaks also appears more likely during the cooler months when it is possible the temperature and humidity are more favourable to the longer term survival of the virus in the environment.
There is no evidence of transmission to humans directly from bats, and, as such it appears that human infection only occurs via an intermediate host, a horse. Despite this in 2014 the NSW Government sanctioned the destruction of flying fox colonies.
List of Australian Hendra outbreaks
Date Location Details
August 1994 Mackay, Queensland Death of two horses and one person, Mark Preston.
September 1994 Hendra, Queensland 20 horses died or were euthanised. Two people infected. One of them, Victory ("Vic") Rail, a nationally prominent trainer of racehorses, died.
January 1999 Trinity Beach, Cairns, Queensland Death of one horse.
October 2004 Gordonvale, Cairns, Queensland Death of one horse. A veterinarian involved in autopsy of the horse was infected with Hendra virus, and suffered a mild illness.
December 2004 Townsville, Queensland Death of one horse.
June 2006 Peachester, Sunshine Coast, Queensland Death of one horse.
October 2006 Murwillumbah, New South Wales Death of one horse.
July 2007 Peachester, Sunshine Coast, Queensland Infection of one horse (euthanised)
July 2007 Clifton Beach, Cairns, Queensland Infection of one horse (euthanised).
July 2008 Redlands, Queensland Death of five horses; four died from the Henda virus, the remaining animal recovered but was euthanised because of a government policy that requires all animals with antibodies to be euthanised due to a potential threat to health. Two veterinary workers from the affected property were infected leading to the death of one, veterinary surgeon Ben Cuneen, on 20 August 2008. The second veterinarian was hospitalized after pricking herself with a needle she had used to euthanize the horse that had recovered. A nurse exposed to the disease while assisting Cuneen in caring for the infected horses was also hospitalized. The Biosecurity Queensland website indicates that 8 horses died during this event, however a review of the event indicates that five horses are confirmed to have died from HeV and three of the horses "are regarded as improbable cases of Hendra virus infection ...".
July 2008 Proserpine, Queensland Death of four horses.
July 2009 Cawarral, Queensland Death of four horses. Queensland veterinary surgeon Alister Rodgers tested positive after treating the horses. On 1 September 2009 after two weeks in a coma, he became the fourth person to die from exposure to the virus.
September 2009 Bowen, Queensland Death of two horses.
May 2010 Tewantin, Queensland Death of one horse.
20 June 2011 – 31 July 2011 Mount Alford, Queensland Death of three horses (all confirmed to have died of Hendra) and sero-conversion of a dog. The first horse death on this property occurred on 20 June 2011, although it was not until after the second death on 1 July 2011 that samples taken from the first animal were tested. The third horse was euthanised on 4 July 2011. On 26 July 2011 a dog from this property was reported to have tested positive for HeV antibodies. Reports indicate that this Australian Kelpie, a family companion, will be euthanised in line with government policy. Biosecurity Queensland suggest the dog most likely was exposed to HeV though one of the sick horses. Dusty was euthanised on 31 July 2011 following a second positive antibody test.
26 June 2011 Kerry, Queensland The horse was moved after it became sick to another property at Beaudesert, Queensland. Death of one horse.
28 June 2011 Loganlea, Logan City, Queensland Death of one horse. Unusually this horse had HeV antibodies present in its blood at the time of death. How this immune response should be interpreted is a matter of debate.
29 June 2011 Mcleans Ridges, Wollongbar, New South Wales Death of one horse. The second horse on the property tested positive to Hendra and was euthanised on 12 July 2011.
3 July 2011 Macksville, New South Wales Death of one horse.
4 July 2011 Park Ridge, Logan City, Queensland Death of one horse.
11 July 2011 Kuranda, Queensland Death of one horse.
13 July 2011 Hervey Bay, Queensland Death of one horse.
14 July 2011 Lismore, New South Wales Death of one horse.
15 July 2011 Boondall, Queensland Death of one horse.
22 July 2011 Chinchilla, Queensland Death of one horse.
24 July 2011 Mullumbimby, New South Wales Death of one horse.
13 August 2011 Mullumbimby, New South Wales Death of one horse. A horse was found dead after being unwell the day before. HeV infection was confirmed on 17 August 2011.
15 August 2011 Ballina, New South Wales Death of one horse.
17 August 2011 South Ballina, New South Wales Death of two horses. The horses were found dead in a field. Both tested positive to HeV. The exact date of death is not known, but HeV infection was confirmed on 17 August 2011.
23 August 2011 Currumbin Valley, Gold Coast, Queensland Death of one horse.
28 August 2011 North of Ballina, New South Wales Death of one horse.
11 October 2011 Beachmere, Caboolture Queensland One horse euthanised after testing positive. A horse that died on the property one week before may have died of HeV. On 15 October 2011 another horse on the property was euthanised following a positive HeV antibody test.
3 January 2012 Townsville, Queensland A horse that died or was euthanised on 3 January 2012 returned a positive HeV test on 5 January 2012.
26 May 2012 Rockhampton, Queensland One horse died.
28 May 2012 Ingham, Queensland One horse died. A dog returned a positive test but was subsequently cleared.
19 July 2012 Rockhampton, Queensland One horse died. On 27 July it was announced that two other horses on the property, showing clinical signs of the disease, had been euthanised. Two dogs were assessed, and the property was quarantined.
27 June 2012 Mackay, Queensland One horse was euthanised after returning a positive HeV test. 15 horses on the property are being tested and quarantined, along with horses on neighbouring properties.
27 July 2012 Cairns, Queensland One horse died.
5 September 2012 Port Douglas, Queensland One horse died. The property with 13 other horses is quarantined.
1 November 2012 Ingham, Queensland One symptomatic horse euthanised. A test for HeV the following day proved positive. The property, with seven other horses, quarantined.
20 January 2013 Mackay, Queensland One horse died.
19 February 2013 Atherton Tablelands, North Queensland One horse died. Four horses and four people from the property were assessed.
3 June 2013 Macksville, New South Wales Death of one horse, a second horse vaccinated, five cats and a dog were monitored.
1 July 2013 Tarampa, Queensland One horse died. HeV virus confirmed.
4 July 2013 Macksville, New South Wales Six year old gelding died. Several other horses, dogs and cats were tested.[82][83] A dog from the property tested positive for HeV and was euthanised around 19 July 2013
5 July 2013 Gold Coast, Queensland One horse died. No other horses on property.
6 July 2013 Kempsey, New South Wales Eighteen-year-old unvaccinated mare died, other animals on property under observation.
9 July 2013 Kempsey, New South Wales Thirteen-year-old unvaccinated quarterhorse died, other animals on property were put under observation.
18 March 2014 Bundaberg, Queensland Unvaccinated horse euthanased.
1 June 2014 Beenleigh, Queensland Horse euthanased and property quarantined after outbreak at a property.
24 Jun 2015 Mullumbimby, New South Wales Horse found dead after several days of illness. HeV confirmed as the cause of death.
18 March 2014 Bundaberg, Queensland Unvaccinated horse euthanased.
1 June 2014 Beenleigh, Queensland Horse euthanased and property quarantined after outbreak at a property.
20 July 2014 Calliope, Queensland Horse euthanased and property quarantined after outbreak.
24 Jun 2015 Mullumbimby, New South Wales Horse found dead after several days of illness.
About 20 July 2015 Atherton Tableland, Queensland Infected horse died and property quarantined.
About 4 September 2015 Lismore, New South Wales Infected horse euthanised and property quarantined.
About 24 May 2017 Gold Coast, Queensland An unvaccinated infected horse euthanised and property quarantined.
About 8 July 2017 Lismore, New South Wales Hendra virus confirmed near Lismore
About 1 August 2017 Murwillumbah, New South Wales Hendra virus confirmed near Murwillumbah
About 5 August 2017 Lismore, New South Wales Third Hendra case confirmed near Lismore
Events of June–August 2011:
In the years 1994–2010, fourteen events were recorded. Between 20 June 2011 and 28 August 2011, a further seventeen events were identified, during which twenty-one horses died.
It's not clear why there has been a sudden increase in the number of spillover events between June and August 2011. Typically HeV spillover events are more common between May and October. This time is sometimes called "Hendra Season", which is a time when there are large numbers of fruit bats of all species congregated in SE Queensland's valuable winter foraging habitat. The weather (warm and humid) is favourable to the survival of henipavirus in the environment.
It is possible flooding in SE Queensland and Northern NSW in December 2010 and January 2011 may have affected the health of the fruit bats. Urine sampling in flying fox camps indicate that a larger proportion of flying foxes than usual are shedding live virus. Biosecurity Queensland's ongoing surveillance usually shows 7% of the animals are shedding live virus. In June and July nearly 30% animals have been reported to be shedding live virus.
Present advice is that these events are not being driven by any mutation in HeV itself.
Other suggestions include that an increase in testing has led to an increase in detection. As the actual mode of transmission between bats and horses has not been determined, it is not clear what, if any, factors can increase the chance of infection in horses.
Following the confirmation of a dog with HeV antibodies, on 27 July 2011, the Queensland and NSW governments will boost research funding into the Hendra virus by $6 million to be spent by 2014–2015. This money will be used for research into ecological drivers of infection in the bats and the mechanism of virus transmission between bats and other species. A further 6 million dollars was allocated by the federal government with the funds being split, half for human health investigations and half for animal health and biodiversity research.
Prevention, detection and treatment:
Three main approaches are currently followed to reduce the risk to humans.
Vaccine for horses.
In November 2012, a vaccine became available for horses. The vaccine is to be used in horses only, since, according to CSIRO veterinary pathologist Dr Deborah Middleton, breaking the transmission cycle from flying foxes to horses prevents it from passing to humans, as well as, "a vaccine for people would take many more years."
The vaccine is a subunit vaccine that neutralises Hendra virus and is composed of a soluble version of the G surface antigen on Hendra virus and has been successful in ferret models.
By December 2014, about 300 000 doses had been administered to more than 100 000 horses. About 3 in 1000 had reported incidents; the majority being localised swelling at the injection site. There had been no reported deaths.
In August 2015, the Australian Pesticides and Veterinary Medicines Authority (APVMA) registered the vaccine. In its statement the Australian government agency released all its data on reported side effects. In January 2016, APVMA approved its use in pregnant mares.
Stall-side test to assist in diagnosing the disease in horses rapidly.
Although the research on the Hendra virus detection is ongoing, a promising result has found using antibody-conjugated magnetic particles and quantum dots.
Post-exposure treatment for humans.
Nipah virus and Hendra virus are closely related paramyxoviruses that emerged from bats during the 1990s to cause deadly outbreaks in humans and domesticated animals. National Institute of Allergy and Infectious Diseases (NIAID)-supported investigators developed vaccines for Nipah and Hendra virus based on the soluble G-glycoproteins of the viruses formulated with adjuvants. Both vaccines have been shown[who?] to induce strong neutralizing antibodies in different laboratory animals.
Trials began in 2015 to evaluate a monoclonal antibody to be used as a possible complementary treatment for humans exposed to Hendra virus infected horses.
Deforestation Impact.
When considering any zoonosis, one must understand the social, ecological, and biological contributions that may be facilitating this spillover. Hendra virus is believed to be partially seasonally related. For, there is a suggested correlation between breeding time and an increase in incidences of Hendra virus in flying fox bats.
Additionally, recent research suggests that the upsurge in deforestation within Australia may be leading to an increase in incidences of Hendra virus. Flying fox bats tend to feed in trees during a large part of the year. However, due to the lack of specific fruit trees within the area, these bats are having to relocate and thereby are coming into contact with horses more often. The two most recent outbreaks of Hendra virus in 2011 and 2013 appear to be related to an increased level of nutritional stress among the bats as well as relocation of bat populations. Work is currently being done to increase vaccination among horses as well as replant these important forests as feeding grounds for the flying fox bats. Through these measures, the goal is to decrease the incidences of the highly fatal Hendra virus.
Pathology:
Flying foxes experimentally infected with the Hendra virus develop a viraemia then excrete the virus in their urine, faeces and saliva for approximately one week. Although they excrete active virus during this time there is no other indication of an illness. Symptoms of Hendra virus infection of humans may be respiratory, including hemorrhage and edema of the lungs, or encephalitic, resulting in meningitis. In horses, infection usually causes pulmonary oedema, congestion and / or neurological signs.
Ephrin B2 has been identified as the main receptor for the henipaviruses.
Hendra virus has been classified as a Bio-safety Level 4 Hot Agent.
2016 Brisbane Research ConferenceEdit
In late May, early June 2016, "Hendra scientists, vets and health officers met in Brisbane to bring together all the research into the bat-borne disease."
Nipah virusEdit
Main article: Nipah virus infection
Not to be confused with Nepovirus.
Emergence:
Pteropus vampyrus (Large flying fox), one of the natural reservoirs of Nipah virus
Nipah virus was identified in April 1999, when it caused an outbreak of neurological and respiratory disease on pig farms in peninsular Malaysia, resulting in 257 human cases, including 105 human deaths and the culling of one million pigs. In Singapore, 11 cases, including one death, occurred in abattoir workers exposed to pigs imported from the affected Malaysian farms. The Nipah virus has been classified by the Centers for Disease Control and Prevention as a Category C agent. The name "Nipah" refers to the place, Kampung Baru Sungai Nipah in Port Dickson, Negeri Sembilan, the source of the human case from which Nipah virus was first isolated. Nipah virus is one of several viruses identified by WHO as a likely cause of a future epidemic in a new plan developed after the Ebola epidemic for urgent research and development before and during an epidemic toward new diagnostic tests, vaccines and medicines.
The outbreak was originally mistaken for Japanese encephalitis (JE), however, physicians in the area noted that persons who had been vaccinated against JE were not protected, and the number of cases among adults was unusual Despite the fact that these observations were recorded in the first month of the outbreak, the Ministry of Health failed to react accordingly, and instead launched a nationwide campaign to educate people on the dangers of JE and its vector, Culex mosquitoes.
Symptoms of infection from the Malaysian outbreak were primarily encephalitic in humans and respiratory in pigs. Later outbreaks have caused respiratory illness in humans, increasing the likelihood of human-to-human transmission and indicating the existence of more dangerous strains of the virus.
Based on seroprevalence data and virus isolations, the primary reservoir for Nipah virus was identified as Pteropid fruit bats, including Pteropus vampyrus (Large Flying Fox), and Pteropus hypomelanus (Small flying fox), both of which occur in Malaysia.
The transmission of Nipah virus from flying foxes to pigs is thought to be due to an increasing overlap between bat habitats and piggeries in peninsular Malaysia. At the index farm, fruit orchards were in close proximity to the piggery, allowing the spillage of urine, faeces and partially eaten fruit onto the pigs. Retrospective studies demonstrate that viral spillover into pigs may have been occurring in Malaysia since 1996 without detection.[17] During 1998, viral spread was aided by the transfer of infected pigs to other farms, where new outbreaks occurred.
Evolution:
The most likely origin of this virus was in 1947 (95% credible interval: 1888–1988).[133] There are two clades of this virus—one with its origin in 1995 (95% credible interval: 1985–2002) and a second with its origin in 1985 (95% credible interval: 1971–1996). The mutation rate was estimated to be 6.5 × 10−4 substitution/site/year (95% credible interval: 2.3 × 10−4 –1.18 × 10−3), similar to other RNA viruses.
Outbreaks:
Locations of henipavirus outbreaks (red stars–Hendra virus; blue stars–Nipah virus) and distribution of henipavirus flying fox reservoirs (red shading–Hendra virus ; blue shading–Nipah virus)
Eight more outbreaks of Nipah virus have occurred since 1998, all within Bangladesh and neighbouring parts of India. The outbreak sites lie within the range of Pteropus species (Pteropus giganteus). As with Hendra virus, the timing of the outbreaks indicates a seasonal effect. Cases occurring in Bangladesh during the winters of 2001, 2003, and 2004, were determined to have been caused by the Nipah virus. In February 2011, a Nipah outbreak began at Hatibandha Upazila in the Lalmonirhat District of northern Bangladesh. To date (7 February 2011), there have been 24 cases and 17 deaths in this outbreak.
2001 January 31–23 February, Siliguri, India: 66 cases with a 74% mortality rate.[136] 75% of patients were either hospital staff or had visited one of the other patients in hospital, indicating person-to-person transmission.
2001 April – May, Meherpur District, Bangladesh: 13 cases with nine fatalities (69% mortality).
2003 January, Naogaon District, Bangladesh: 12 cases with eight fatalities (67% mortality).
2004 January – February, Manikganj and Rajbari districts, Bangladesh: 42 cases with 14 fatalities (33% mortality).
2004 19 February – 16 April, Faridpur District, Bangladesh: 36 cases with 27 fatalities (75% mortality). 92% of cases involved close contact with at least one other person infected with Nipah virus. Two cases involved a single short exposure to an ill patient, including a rickshaw driver who transported a patient to hospital. In addition, at least six cases involved acute respiratory distress syndrome, which has not been reported previously for Nipah virus illness in humans. This symptom is likely to have assisted human-to-human transmission through large droplet dispersal.
2005 January, Tangail District, Bangladesh: 12 cases with 11 fatalities (92% mortality). The virus was probably contracted from drinking date palm juice contaminated by fruit bat droppings or saliva.
2007 February – May, Nadia District, India: up to 50 suspected cases with 3–5 fatalities. The outbreak site borders the Bangladesh district of Kushtia where eight cases of Nipah virus encephalitis with five fatalities occurred during March and April 2007. This was preceded by an outbreak in Thakurgaon during January and February affecting seven people with three deaths.[139] All three outbreaks showed evidence of person-to-person transmission.
2008 February – March, Manikganj and Rajbari districts, Bangladesh: Nine cases with eight fatalities.
2010 January, Bhanga subdistrict, Faridpur, Bangladesh: Eight cases with seven fatalities. During March, one physician of Faridpur Medical College Hospital caring for confirmed Nipah cases died.
2011 February: An outbreak of Nipah Virus has occurred at Hatibandha, Lalmonirhat, Bangladesh. The deaths of 21 schoolchildren due to Nipah virus infection were recorded on 4 February 2011. IEDCR has confirmed the infection is due to this virus.[142] Local schools were closed for one week to prevent the spread of the virus. People were also requested to avoid consumption of uncooked fruits and fruit products. Such foods, contaminated with urine or saliva from infected fruit bats, were the most likely source of this outbreak.
2018 May: Deaths of 13 people in Perambra near Calicut, Kerala, India have been confirmed as a result of the virus. Treatment using antivirals such as Ribavirin has been initiated.
Nipah virus has been isolated from Lyle's flying fox (Pteropus lylei) in Cambodia and viral RNA found in urine and saliva from P. lylei and Horsfield's roundleaf bat (Hipposideros larvatus) in Thailand. Infective virus has also been isolated from environmental samples of bat urine and partially eaten fruit in Malaysia.[148] Antibodies to henipaviruses have also been found in fruit bats in Madagascar (Pteropus rufus, Eidolon dupreanum) and Ghana (Eidolon helvum) indicating a wide geographic distribution of the viruses. No infection of humans or other species have been observed in Cambodia, Thailand or Africa thus far.
Pathology:
In humans, the infection presents as fever, headache , drowsiness, disorientation and confusion, Cough, abdominal pain, nausea, vomiting, weakness, problems with swallowing and blurred vision are relatively common. About a quarter of the patients have seizures and about 60% become comatose and might need mechanical ventilation. In patients with severe disease, their conscious state may deteriorate and they may develop severe hypertension, fast heart rate, and very high temperature.
Nipah virus is also known to cause relapse encephalitis. In the initial Malaysian outbreak, a patient presented with relapse encephalitis some 53 months after his initial infection. There is no definitive treatment for Nipah encephalitis, apart from supportive measures, such as mechanical ventilation and prevention of secondary infection. Ribavirin, an antiviral drug, was tested in the Malaysian outbreak, and the results were encouraging, though further studies are still needed.
While no vaccine currently exists, a 2012 study of a trial vaccine developed using the outer proteins of Hendra virus was shown to induce protection against Nipah in African green monkeys.
In animals, especially in pigs, the virus causes a porcine respiratory and neurologic syndrome, locally known as "barking pig syndrome" or "one mile cough."
Ephrin B2 has been identified as the main receptor for the henipaviruses.
Cedar virus:
Emergence:
Cedar Virus (CedV) was first identified in pteropid urine during work on Hendra virus undertaken in Queensland in 2009.
Although the virus is reported to be very similar to both Hendra and Nipah viruses, it does not cause illness in laboratory animals usually susceptible to paramyxoviruses. Animals were able to mount an effective response and create effective antibodies.
The scientists who identified the virus report:
Hendra and Nipah viruses are 2 highly pathogenic paramyxoviruses that have emerged from bats within the last two decades. Both are capable of causing fatal disease in both humans and many mammal species. Serological and molecular evidence for henipa-like viruses have been reported from numerous locations including Asia and Africa, however, until now no successful isolation of these viruses have been reported. This paper reports the isolation of a novel paramyxovirus, named Cedar virus, from fruit bats in Australia. Full genome sequencing of this virus suggests a close relationship with the henipaviruses. Antibodies to Cedar virus were shown to cross react with, but not cross neutralize Hendra or Nipah virus. Despite this close relationship, when Cedar virus was tested in experimental challenge models in ferrets and guinea pigs, we identified virus replication and generation of neutralizing antibodies, but no clinical disease was observed. As such, this virus provides a useful reference for future reverse genetics experiments to determine the molecular basis of the pathogenicity of the henipaviruses.
Causes of emergence:
The emergence of henipaviruses parallels the emergence of other zoonotic viruses in recent decades. SARS coronavirus, Australian bat lyssavirus, Menangle virus and probably Ebola virus and Marburg virus are also harbored by bats and are capable of infecting a variety of other species. The emergence of each of these viruses has been linked to an increase in contact between bats and humans, sometimes involving an intermediate domestic animal host. The increased contact is driven both by human encroachment into the bats’ territory (in the case of Nipah, specifically pigpens in said territory) and by movement of bats towards human populations due to changes in food distribution and loss of habitat.
There is evidence that habitat loss for flying foxes, both in South Asia and Australia (particularly along the east coast) as well as encroachment of human dwellings and agriculture into the remaining habitats, is creating greater overlap of human and flying fox distributions.
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Nipah virus infection
Nipah virus infection (NiV) is a viral infection caused by the Nipah virus. Symptoms from infection vary from none to fever, cough, headache, shortness of breath, and confusion. This may worsen into a coma over a day or two. Complications can include inflammation of the brain and seizures following recovery.
Nipah virus infection
Henipavirus structure.svg
Structure of a Henipavirus
Specialty
Infectious disease Edit this on Wikidata
Symptoms
None, fever, cough, headache, confusion
Complications
Inflammation of the brain, seizures
Usual onset
5 to 14 days after exposure
Causes
Nipah virus (spread by direct contact)[3]
Diagnostic method
Based on symptoms, confirmed by laboratory testing
Prevention
Avoiding exposure to bats and sick pigs, not drinking raw date palm sap
Treatment
Supportive care
Frequency
582 human cases (2001 until 2012)
Deaths
~50% risk of death
The Nipah virus is a type of RNA virus in the genus Henipavirus. It can both spread between people and from other animals to people. Spread typically requires direct content with an infected source. The virus normally circulates among specific types of fruit bats. Diagnosis is based on symptoms and confirmed by laboratory testing.
The disease was first identified in 1998 in Malaysia and Singapore with the virus being identified in 1999. It is named after a village in Malaysia, Sungai Nipah. Pigs may also be infected and millions were killed in 1999 to stop the spread of disease.
Management involves supportive care. As of 2018 there is no vaccine or specific treatment. Prevention is by avoiding exposure to bats and sick pigs and not drinking raw date palm sap. As of 2013 a total of 582 human cases of Nipah virus are estimated and 54 percent of those who were infected died. In 2018, an outbreak of the disease resulted in at least 10 death in the Indian state of Kerala.
Signs and symptoms:
The symptoms start to appear within 3–14 days after exposure. Initial symptoms are fever, headache, drowsiness followed by disorientation and mental confusion. These symptoms can progress into coma as fast as in 24–48 hours. Encephalitis, inflammation of the brain, is the dreaded complication of nipah virus infection. Respiratory illness can also be present during the early part of the illness. Nipah-case patients who had breathing difficulty are more likely than those without respiratory illness to transmit the virus. The disease is suspected in symptomatic individuals in the context of an epidemic outbreak.
Risks:
Fruit bats are the natural reservoirs of Nipah virus
The risk of exposure is high for hospital workers and caretakers of those infected with the virus. In Malaysia and Singapore, Nipah virus infection occurred in those with close contact to infected pigs. In Bangladesh and India, the disease has been linked to consumption of raw date palm sap (toddy) and contact with bats.
Diagnosis:
Laboratory diagnosis of Nipah virus infection is made using real time polymerase chain reaction (RT-PCR) from throat swabs, cerebrospinal fluid, urine and blood analysis during acute and convalescent stages of the disease. IgG and IgM antibody detection can be done after recovery to confirm Nipah virus infection. Immunohistochemistry on tissues collected during autopsy also confirms the disease.[7] Viral RNA can be isolated from the saliva of infected persons.
Prevention:
Prevention of Nipah virus infection is important since there is no effective treatment for the disease. The infection can be prevented by avoiding exposure to bats in endemic areas and sick pigs. Drinking of raw palm sap (palm toddy) contaminated by bat excrete, eating of fruits partially consumed by bats and using water from wells infested by bats should be avoided. Bats are known to drink toddy that is collected in open containers, and occasionally urinate in it, which makes it contaminated with the virus. Surveillance and awareness are important for preventing future outbreaks. The association of this disease within reproductive cycle of bats is not well studied. Standard infection control practices should be enforced to prevent nosocomial infections. A subunit vaccine using the Hendra G protein was found to produce cross-protective antibodies against henipavirus and nipavirus has been used in monkeys to protect against Hendra virus, although its potential for use in humans has not been studied.
Treatment:
Currently there is no effective treatment for Nipah virus infection. The treatment is limited to supportive care. It is important to practice standard infection control practices and proper barrier nursing techniques to avoid the transmission of the infection from person to person. All suspected cases of Nipah virus infection should be isolated and given intensive supportive care. Ribavirin has been shown effective in in vitro tests, but has not yet been proven effective in humans. Passive immunization using a human monoclonal antibody that targets the Nipah G glycoprotein has been evaluated in the ferret model as post-exposure prophylaxis.The anti-malarial drug chloroquine was shown to block the critical functions needed for maturation of Nipah virus, although no clinical benefit has yet been observed.[16] m102.4, a human monoclonal antibody, has been used in people on a compassionate use basis in Australia and is presently in pre-clinical development.
Outbreaks:
Map showing locations of outbreaks of Nipah and Hendra virus as well as the range of Pteropus bats as of 2014
Nipah virus outbreaks have been reported in Malaysia, Singapore, Bangladesh and India. The highest mortality due to Nipah virus infection has occurred in Bangladesh. In Bangladesh, the outbreaks are typically seen in winter season. Nipah virus first appeared in Malaysia in 1998 in peninsular Malaysia in pigs and pig farmers. By mid-1999, more than 265 human cases of encephalitis, including 105 deaths, had been reported in Malaysia, and 11 cases of either encephalitis or respiratory illness with one fatality were reported in Singapore. In 2001, Nipah virus was reported from Meherpur District, Bangladesh and Siliguri, India. The outbreak again appeared in 2003, 2004 and 2005 in Naogaon District, Manikganj District, Rajbari District, Faridpur District and Tangail District.
In Bangladesh, there were outbreaks in subsequent years as well.
In May 2018, an outbreak has been reported in the Kozhikode district of Kerala, India. Twelve deaths have been recorded, including one healthcare worker.Those who have died are mainly from the districts of Kozhikode and Malappuram, including a 31-year-old nurse, who was treating patients infected with the virus. As of 23 May 2018, about 14 people are being quarantined because they had contact with the sick.On 24 May 2018, 2 cases were also detected at Mangaluru, Karnataka. In Himachal Pradesh, India, some bats were reportedly found dead.This incident has caused panic throughout the state. Blood samples have been sent for testing. India is seeking help from Australia by importing "Monoclonal antibodies", though they have not been tested on humans. India is also importing Ribavirin tablets from Malaysia.
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निपाह व्हायरस हा हवेतून पसरत नाही मात्र हा थेट संसर्ग झालेल्या माणसाच्या, प्राण्याच्या संपर्कात आल्यास होऊ शकतो.
मुंबई : 'निपाह' या व्हायरसमुळे केरळ राज्यामध्ये भीतीचं वातावरण निर्माण झालं आहे. या अज्ञात इन्फेक्शनमुळे 11 जणांचा मृत्यू झाला आहे. WHO म्हणजेच जागतिक आरोग्य संस्थेने निपाह व्हायरसमुळे हाय अलर्ट घोषित केला आहे. पुण्यातील नॅशनल इंस्टिस्ट्युड ऑफ वायरॉलॉजीने 3 नमुन्यांची तपासणी केल्यानंतर 'निपाह' व्हायरस असल्याची घोषणा केली आहे.
कोठे सापडला पहिला व्हायरस
1998 साली मलेशिया आणि सिंगापूरमध्ये हा व्हायरस आढळला. निपाह हा व्हायरस मनुष्य आणि जानवरांमध्ये एक गंभीर इंफेक्शन पसरवण्यासाठी कारणीभूत ठरतो. खजुराची शेती करणार्यांना या व्हायरसचा धोका अधिक होता. 2004 साली बांग्लादेशमध्ये अनेक लोक या व्हायरसच्या विळख्यात आली होती. हे इंफेक्शन फ्रुट बॅट्स ( वटवाघुळाचा) द्वारा पसरतो.
निपाह व्हायरस हा संसर्ग झालेल्या माणसामधून, डुक्करांमधून किंवा वटवाघुळातूनही पसरू शकतो.
लक्षणं काय ?
निपाह व्हायरस हा मेंदूवर थेट हल्ला करतो. त्यामुळे ताप, थकवा, बेशुद्धावस्था अशी लक्षण आढळतात.
लक्षण आढळताच तात्काळ उपचार न घेतल्यास पुढील 24-48 तासामध्ये संबंधित व्यक्ती कोमामध्ये जाण्याची शक्यता असते.
अनेक रूग्णांमध्ये मेंदूशी निगडीत, श्वासोश्वासाशी निगडीत आणि हृद्याच्या ठोक्याशी निगडीत समस्या वाढल्याचं निदर्शनास आले.
ताप, थकवा, शुद्ध हरपणं, चक्कर येणं. उलट्या होणं, मळमळणं, अस्वस्थ वाटणं ही लक्षणं 7-10 दिवस आढळतात.
सुरूवातीच्या टप्प्यावर श्वासाशी संबंधित काही त्रास होतोय का? हे तपासून पाहणं अत्यावश्यक आहे.
कशी घ्याल काळजी ?
निपाह व्हायरसचा धोका टाळण्यासाठी सध्या कोणतेही औषध, इंजेक्शन उपलब्ध नाही.
पडलेली फळं, प्रामुख्याने खजुराचं फळं खाणं टाळा. कारण वटवाघुळांनी खाल्लेल्या फळांद्वारा किंवा त्यांच्या संपर्कात आल्यास व्हायरस पसरू शकतो.
वैद्यकीय मदत करणार्या व्यक्तींनीही रूग्णांवर उपचार करताना पुरेशी काळजी घेणं आवश्यक आहे. सोबतच ग्लोव्ह्स, मास्क घालून रूग्णांची तपासणी करावी.
मान्यताप्राप्त लॅबोरेटरीमध्येच चाचणी करावी. तुम्हांला इंफेक्टेड भागात फिरताना अस्वस्थ वाटत असल्यास संबंधित चाचण्या करणं आवश्यक आहे
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