After exposure: Immediately after an exposure to a henipavirus, the lab worker is not considered infectious. In case of a lab worker presenting to BMC ED or other outside medical facility, either the exposed or the caring physicians should immediately contact ROHP for further instructions.
Patient should prevent close contact with household members pending evaluation, if possible. Person-to-person transmission is reported via close personal contact with an infected individual or their body fluids during the late stages of the infection. PPE requirements for care of this patient are listed below. Avoid aerosol-generating procedures.
Specimen should be handled with extreme care and enclosed in appropriate shatter-proof and leak-proof packing for transport to lab. Diagnostic laboratory staff should be notified of suspicion of infection, and tests should be performed under proper containment. Please contact ROHP immediately for further details. ELISA and rapid immune plague assays have been developed. Standard management of potential exposure to Nipah or Hendra virus is solely based on observation, potential isolation and with symptomatic and supportive treatments.
No approved post exposure prophylaxis or post exposure vaccination available. Various risk factors for NiV infection in pteropid bats were also explored.
Among the two bat species, the risk of NiV and seroprevalence were higher for P. In Cambodia, NiV-specific antibodies were detected in P. In Thailand, regular surveillance and sero-surveillance of bat population indicated the presence of NiV RNA in the saliva and urine of bats, and IgG in the serum, suggesting long term NiV persistence in them Wacharapluesadee et al.
In Bangladesh, outbreaks of Nipah virus were initially confirmed only by the presence of anti-NiV antibodies in serum samples. However after , researchers started genetic characterization of Nipah virus by detecting viral nucleic acid Harcourt et al. Till the year , overall 9 outbreaks have been recorded in Bangladesh.
Raw date palm was the source of infection of the outbreak recorded during the year Rahman et al. Another outbreak during in a remote town named Hatibandha in the Lalmonirhat district, northern Bangladesh, reported 15 deaths due to NiV infection Wahed et al.
Studies performed in pigs in Ghana suggested that serum antibodies against Henipaviruses including Hendra and Nipah viruses and viral nucleic acid were also present in another species of fruit bat, i.
Eidolon helvum , reflecting the exposure of pigs to these bats Hayman et al. NiV was detected for the first time in Siliguri, West Bengal, India in the year during an outbreak characterized by febrile illness in association with altered sensorium poor thinking capability or poor concentrating capacity. A close resemblance had been found between the isolates of Siliguri outbreak and those obtained during the outbreak in Bangladesh. Such resemblance is justified, as Siliguri is located at the vicinity of Bangladesh Harit et al.
Another outbreak was reported from Nadia district, West Bengal in the year Chadha et al. Most recently in the year , Nipah viral disease outbreak has been reported in Kozhikode district, northern Kerala, India and the fruit bats have been identified as the source of the outbreak Chatterjee ; Paul During this outbreak, deaths occurred in the infected subjects as well as in healthcare personnel who were involved in treatment of patients.
On May 19, , 4 infected people died and on 23 May, 13 more subjects deceased 3 from Malappuram and 10 from Kozhikode district. In both outbreaks, circumstantial evidences suggested the human-to-human transmission, as most people who acquired the infection were either care-givers, or family members of infected persons. Sporadic NiV outbreaks, person-to-person transmission and its zoonotical aspects have been implicated in hundreds of human deaths during the past two decades, and this has posed a huge threat to domestic animals and humans.
A recent report indicated NiV outbreaks presently being still small but posing a significant threat to be extremely lethal Spiropoulou NiV disease outbreak investigation in Kerala, India, during May—June , elucidated virus transmission dynamics and epidemiological analysis by employing real-time RT PCR testing to detect presence of virus in throat swabs, blood, urine and CSF.
A total of 23 cases were identified including the index case, and 18 laboratory confirmed cases. The incubation period was recorded to be 9. Sequencing and phylogenetic analysisrevealed NiV isolate to be closer to the Bangladesh lineage Arunkumar et al. A firefly luciferase that expresses NiV has been generated for facilitating studies spatiotemporal on the pathogenesis of Henipaviruses.
Herein bioluminescence imaging technique has been used for monitoring of the replication of the virus as well as spread in knockout mice. This reverse genetics system may be a useful tool to investigate Henipa-like viruses Yun et al.
For the genetic relatedness study, representative and bp-length for N gene 27 strains and G gene 15 strains , respectively, were investigated. Phylogenetic analysis was performed using the maximum likelihood method bootstrap replicates in MEGA 6 software v 6.
The phylogenetic analysis affirmed the circulation of two major clades of NiV, i. The inference from analysis affirms circulation of two populations of NiVs currently.
Tree created with maximum likelihood method with 1, bootstrap replicates. Scale bars indicate number of sequence changes corresponding to illustrated branch length. For comparison of the open reading frame sequence of the NiV with those from other members of the Paramyxovirinae subfamily, phylogenetic analysis had been used widely and by such approach the closest relation between NiV and Henipavirus has been proven Chua et al.
It has been revealed by nucleotide sequencing technique that there exist very little difference in the nucleotide sequences of NiV isolated from throat secretion and cerebrospinal fluid difference by just 4 out of 18, nucleotides Arankalle et al. Nucleotide sequence homology has also been observed between the virus isolated from Bangladesh and Malaysia but it is interesting to note that nucleotide heterogeneity inter-strain had been found to be more obvious.
It is interesting to note that differences in genetic variability certainly have relation with the mode of transmission. It is evident by molecular epidemiological studies that NiV had been introduced in pigs in Malaysia during — causing great loss to pig farming Looi and Chua However, the human and pig isolates in Malaysia during the later phase of outbreak showed nearly identical sequences. This is suggestive of the fact that there was rapid spread of only one variant in pig and such variant was responsible for most of the cases in man.
In contrast, the introduction of NiV from fruit bats to humans for multiple times in Bangladesh might be responsible for the sequence heterogeneity of the NiV isolates Chan et al. Detailed phylogenetic analyses have been performed on thecomplete gene sequences of NiV strains from the year as well as outbreaks in Bangladesh.
On the basis of a nucleotide sequence window comprising of nucleotides , a genotyping scheme has been introduced. An accurate and simple way for classification of current as well as future sequences of NiV has been provided by this genotyping scheme. A phylogenetic tree with very high bootstrap values has been constructed by such genotyping method.
Phylogenetic analysis showed close similarity of sequences obtained from pigs and humans during the Malaysian outbreak. Analysis also revealed that the virus isolated from Bangladesh possesses an additional 6 nucleotides than the prototype Malysian strain Angeletti et al. For classification of sequences of NiV such methodology and phylogenetic tree is very helpful Lo et al.
For investigating the viral genetic diversity, a phylogenetic study of the infection caused by NiV has helped in estimating the infection spread and its date of origin Lo Presti et al. Immune response studies regarding Nipah virus have been conducted by various researchers, especially after each reported outbreak.
Since the virus exhibits two dictinct types of association among its hosts maintaining its persistence in the nature through reservoir hosts like bats and inflicting fatal clinical condition in humans as well as domestic animals like pig , the immune responses might be host-specific Chua et al.
Several proteins of Henipaviruses block host innate immune responses viz. The innate immune system of pteropid bats is remarkable for its constitutive action of Type 1 interferon system which can restrict the early viral replication within their body Zhou et al.
This mode of action has been associated also with several interferon stimulated genes ISG particularly of those involved in noninflammatory pathways so that elevation in interferon response in bats is not allied with chronic inflammation unlike in case of rodents or humans Halpin et al. Due to these differences, bat cells are primed to react to viral attack immediately but only upto a level of restricting replication Zhou et al.
Bats possess comparatively higher repertoire of naive immunoglobulins with more specifities, thereby favouring direct clonal selction of B lymphocytes for antibody production.
In such condition there may be poor or no hypermutation and affinity maturation stages in B cells, leading to poorer responses and restricted production of high-titered antibodies than other species.
These features contribute for the delay in viral clearance and persistence of virus for a pretty long period Wellehan et al. Nipah virus comparative studies conducted in pteropid bats and hamster reinforce these points as virus showed lesser multiplication and shedding from bat endothelial cells as well as with poorer antibody responses upon challenge studies Wong et al.
Recently, tetherin an IFN-induced protein from bats has been reported to inhibit NiV replication in fruit bat cellsand to act as an innate immune antiviral protein that can facilitate the host to combat virus induced pathological changes Hoffmann et al.
Another immune mechanism within bats to prevent complete elimination of Nipah virus is the modulation of bat antiviral responses towards virus survival. In the reservoir host, the virusemploys immune evasion strategies especially against innate immune system so as to escape from the immune attack and maintain perpetuation within the host by retaining replication at a minimum level Rodriguez and Horvath ; Rupprecht et al.
Such evasion strategies are mediated through accessory proteins encoded within the virus which may also have effect over other hosts through spillover adaptation Schountz The NiV P gene coding for polymerase-associated phosphoprotein playsa key role in evading interferon mediated immune response from the host Shaw, In case of hosts exhibiting clinical disease from Nipah virus, various virus associated immune antagonistic proteins subvert host immune responses, thus leading to pathogenesis and clinical condition.
Wild type virus uses an unique RNA editing mechanism for the controlled transcription and translation of multiple antagonistic proteins which may be delayed in some hosts, so that the protein production may be slightly delayed. In such situations antiviral responses would be strong with associated inflammatory responses thus partially restricting viral replication and pathogenesis in some hosts Seto et al. Although Nipah virus effectively suppresses antiviral cytokine production at early phase of infection, release of some amount of inflammatory cytokines has been suggested which can be attributed to the elevation in vascular permeability, ultimately favoring viral spread Schountz Presence of antigen-positive inclusions in the brain tissues of patients with Nipah Viral encephalitis points to the inadequacy of both innate and adaptive responses for preventing viral spread.
These findings suggest the inability of dendritic cells residing at primary entry point of virus; especially respiratory tract and lungs, rendering inefficient antigen capturing and tissue restriction Chua et al. Evidence also suggest the suppression of MHC-I expression in immune cells by the viral proteins, leading to a repression in both antigen presentation by antigen presenting cells and stimulation for mounting adaptive responses, ultimately resulting in viral spread and persistence in other target organs Dasgupta et al.
Besides these, the virus induced immune evasion for long time also accounts for the persistence of virus in brain tissues and ensuing relapsed and late onset fatal encephalitis in man Tan et al. Apart from these findings, typical interaction pattern of the virus with other critical genes of the host such as TLR genes of host defence, Notch genes of neurogenesis, and other genes like TJP1, FHL1 and GRIA3 concerned with blood-brain barrier and encephalitis, etc.
Crucial role of miRNAs present in NiV genome in inhibiting these host genes, thereby aiding the viral spread and pathogenesis has been reported Saini et al. The pathogenecity of Nipah virus in pigs and man can be correlated with its ability and magnitude to evade immune responses in reservoir host. Though the virus has undergone frequent species jumping involving various hosts, higher fatality rates are being associated with human outbreaks so far, which warrants a comprehensive study to elucidate and explore the viral evolution and adaptation in different hosts.
In the initial stage of illness in man, detection of NiV can be done in epithelial cells of the bronchiole Chua et al. Viral antigens can be detected in bronchi and alveoli in experimental animal models; the primary targets being epithelium of bronchi and type II pneumocytes Rockx et al. Inflammatory cytokines are induced due to infection of the epithelium of the respiratory tract; thereby recruiting cells of the immune system and ultimately leading to development of acute respiratory distress syndrome ARDS -like disease Rockx et al.
Significant inflammatory mediators, viz. From the respiratory epithelium, the virus is disseminated to the endothelial cells of the lungs in the later stage of the disease. Subsequently, the virus can gain entry into the blood stream followed by dissemination, either freely or in host leukocyte bound form.
Apart from lungs, spleen and kidneys along with brain may act as target organs leading to multiple organ failure Rockx et al. There is development of lethal infection in hamsters when leukocytes loaded with NiV are passively transferred Mathieu et al. Two pathways are distinctly involved in the process of viral entry into the central nervous system CNS , viz. There may be presence of inclusion bodies in case of infected CNS in man.
In both the gray as well as white matter plaques may be evident along with necrosis Escaffre et al. It is quite noteworthy that the virus can directly enter the CNS in several experimental animal models via the olfactory nerve. The olfactory epithelium of the nasal turbinate is infected by NiV in such animal models. The viral infection subsequently extends through the cribiform plate into the olfactory bulb.
Ultimately, the virus is disseminated throughout the ventral cortex along with olfactory tubercle Weingartl et al.
A diagrammatic representation of pathogenesis of NiV has been depicted in Figure 4. Pathogenesis of NiV. NiV can be seen in the epithelial cells of the bronchiole in the initial stage of infection.
NiV antigen can be detected in bronchi and alveoli. Inflammatory mediators are activated as a result of infection to the airway epithelium. Virus is disseminated to the endothelial cells of the lungs in the later stage of the disease. Virus enter the blood stream followed by dissemination, either freely or in host leukocyte bound form, reach brain, spleen and kidneys.
Two pathways are involved in the process of viral entry into the central nervous system CNS , via hematogenous route and anterogradely via olfactory nerve nerves. Red font shows the symptoms in human. Highly pathogenic NiV causes symptomatic infections in pigs and humans. Respiratory symptoms are much more severe in pigs as compared to humans. The virus is responsible for causing severe and rapidly progressing illness in humans with the respiratory system as well as the central nervous system CNS mainly getting affected Hossain et al.
The signs and symptoms of the disease appear 3—14 days post NiV exposure. Initially, there is a high rise of temperature along with drowsiness and headache.
This is followed by mental confusion as well as disorientation, ultimately progressing towards coma within 1—2 days. A critical complication of the NiV infection is encephalitis. During initial phase, the respiratory problems may become evident. There is development of atypical pneumonia.
Coughing along with acute respiratory distress may be evident in certain patients Hossain et al. There may be sore throat, vomiting, along with muscle aches www. There may be development of septicemia along with impairment of the renal system and bleeding from the gastrointestinal tract. In severe cases within a period of 24—48 h, there may be development of encephalitis along with seizures that ultimately leads to coma Giangaspero It is crucial to note that transmission of the virus is more common from patients having labored breathing than those having no respiratory problems www.
In pigs, the disease is also known as porcine respiratory and encephalitis syndrome PRES , barking pig syndrome BPS in peninsular Malaysia or one-mile cough. An acute febrile illness has been reported in pigs below six months of age wherein there is development of respiratory illness that ranges from rapid labored breathing to non-productive cough which is harsh in nature.
With the exception of young piglets, the mortality is relatively low Nor et al. In animals that are confined, morbidity may approach per cent Nor et al. Due to involvement of nervous system, there may be twitching of muscles, weakness of hind legs, tremors, along with paresis, either flaccid or spastic, of varying degrees. There may also be nystagmus along with seizures in boars as well as sows Chua ; Kulkarni et al.
In dogs infected with NiV, there may be inflammation of the lungs along with necrosis of glomeruli as well as tubules with formation of syncytia in kidneys. In cats, there may be development of endothelial syncytia along with vasculopathy in multiple organs.
Experimental NiV infection of various animals, viz. Clinical signs are, however, apparently absent in mice as well as rats for unknown reasons Wong and Ong ; Kulkarni et al. Magnetic resonance imaging MRI studies in human patients have revealed that the cortex, pons as well as temporal lobes of brain get involved. There may be bilateral abnormalities in the white matter of the brain. In the cerebral cortex, there may be more than one hyperintensities T1-weighted which are very much similar to necrosis of the laminar cortex.
Lesions may also become evident in corpus callosum, brain stem, as well as cortex of the cerebrum. There may be presence of disseminated microinfarction in the brain due to thrombosis induced by vasculitis. The neurons may also get involved directly. Vasculitic lesions of similar nature may be found in the kidneys, heart, as well as respiratory tract Ang et al. It is also interesting to note that blood vessels of medium and small size show most involvement in case of infection due to NiV, which results in development of syncytia multinucleated along with fibrinoid necrosis Ang et al.
There may be consolidation of varying degree along with hemorrhages either petechiae or ecchymosis in the lungs of affected pigs at necropsy. Froth-filled bronchi along with trachea are commonly observed. In certain instances, there may be presence of blood stained fluids in the trachea and bronchi. Congestion along with generalized edema is present in kidneys and brain. Both the cortex as well as suface of kidneys may become congested Nor et al.
There may be pneumonia moderate to high along with formation of syncytial cells in the endothelial cell lining of the blood vasculatures as revealed histologically Chua et al. In the CNS and other major organs like lungs and kidneys, there may be development of small vessel vasculopathy disseminated in case of acute infection Wong et al. Generalized vasculitis along with fibrinoid necrosis and mononuclear cell infiltration may be noticed in the brain, kidneys and lungs.
Viral antigens at greater concentration may be present in the blood vascular endothelial cells especially in the lungs as is revealed immunohistologically. In the upper respiratory tract of pigs in the lumen viral antigens are evident amidst the cellular debris which is suggestive of the possible transmission of NiV through exhalation Nor et al.
In dogs, kidneys may show congestion with severe hemorrhage. Exudates may be present in the bronchi and trachea Nor ; Kulkarni et al. NiV is the most recently emerging zoonotic and highly deadly virus having pandemic threat. As an emerging and recognized zoonotic pathogen discovered in modern times, NiV causes severe febrile illness and high fatality rates in affected persons and is posing an ongoing high risk to the health of humans worldwide Clayton ; Mukherjee ; Thibault et al.
Fruit bats Pteropus serve as natural hosts wildlife reservoir and pigs are the intermediate hosts for NiV zoonotic cycle Paul During a large outbreak of acute encephalitis in Malaysia in , the virus was discovered in affected patients having contact with sick pigs.
The pigs got infection from bats, and then NiV spread proficiently among pig-to-pig, and thereafter from pig-to-man. Moreover, it has been revealed that Pteropus vampyrus and Pteropus hypomelanus flying foxes in the Malysian Islands bear the virus in saliva as well as urine, indicating their potential to act as natural reservoir of the virus Looi and Chua It is interesting to note that there is always risk of spill over associated with NiV infection.
Interaction of the molecular as well as ecological factors collectively that govern the susceptible nature of populations of animals domestic as well as humans are not understood yet well Thibault et al. Apart from drinking raw date palm sap contaminated by bats as a cause of initial outbreak, man-to-man and animal-to-man transmission is also a major mode of spread of the infection during an ongoing outbreak. Further, it has been found that direct contact of the susceptible population with the respiratory and body secretions of the infected patients increases the risk of acquiring the infection.
During the NiV outbreak in Thakurgaon district, northwest Bangladesh, anti-NiV antibodies were detected in half of the Pteropus bats tested Chadha et al. Other major public health threats appear to be acquiring NiV infection from the susceptible food and domestic animals. Many domesticated mammals seem to be susceptible to Nipah virus. This virus can be maintained in pig populations, but other domesticated animals such as sheep, goats, dogs, cats and horses appear to be incidental hosts acquiring the infection during outbreaks.
Fruits punctured by the bat and contaminated with their saliva forma common source of transmission of NiV infection from bats to domestic animals. Consumption of fruits eaten partially by fruit bats may cause infection in pigs which may then transmit it to humans.
Contact with sick cow was reported to have caused a case of human infection in Bangladesh Chua ; Luby et al. Consumption of fruits, vegetables or water contaminated with saliva, urine or fecal matter of infected bats could also be a possible mode of transmission to man and animals Luby et al.
Date palm sap can be used to prepare alcoholic beverages and such beverages when consumed can lead to human infection Harit et al.
Evidence from several NiV outbreaks indicate that consumption of undercooked meat from infected animals or handling of infected animals in the home, farm or slaughter houses may also pose risk of animal-to-man transmission Chanchal et al. Close contact with symptomatic patients or their infectious secretions has been implicated for human transmission of NiV in Bangladesh.
Specific exposures can pose a high risk of person-to-person transmission, though sustained transmission do not occur in humans. Studies conducted in animal models further support this fact Clayton The recent NiV outbreak in Kerala, India, which caused encephalitis in humans, raised global health concerns Paul The potential for a global pandemic due to NiV appears to stem from several features: availability of susceptible human population, several viral strains withpotential for person-to-person transmission, and error-prone nature of RNA virus replication.
Outbreaks of NiV disease in densely populated regions like South Asia can lead to pandemics, due to extensive global travel and trade connectivity Luby Many ecological and molecular factors underlie NiV spillover into humans and human and animal susceptibility to it, though the intricate interaction between these is unclear Thibault et al.
Research studies need to be undertaken to elaborate the molecular mechanisms of the respiratory transmission of NiV in order to reduce the risk of human-to-human transmission. Improved surveillance and vaccination strategies must also be adopted Luby Confirmation of the human as well as animal NiV infections can be done by isolation of the virus along with performing serological tests and tests to amplify viral nucleic acids.
However, BSL-3 may prove to be sufficient to primarily isolate the virus from suspected clinical materials. Following confirmation of the virus in infected cells fixed by acetone by immunofluorescent technique, there should be immediate transfer of the culture fluid in BSL-4 laboratory Daniels et al.
In Japan, National Institute of Animal Health has developed immunohistochemical diagnostic technique based on monoclonal antibodies Tanimura et al. Viral antigen capture ELISAs offer a high-throughput and inexpensive method for screening suspect samples. By the use of pseudotyped particles, a serum neutralization test for NiV can be performed under BSL-2 conditions.
This test uses a recombinant vesicular stomatitis virus that expresses secreted alkaline phosphatase SEAP. Microsphere assay luminex based has been used for detection of antibodies against a glycoprotein of NiV, namely NiV sG, in the sera of pigs and ruminants like goats and cattle Chowdhury et al.
Recently, ELISA has also been developed using recombinant full length N protein and truncated G protein for detecting virus specific antibodies in serum samples of porcines Fischer et al. Such ELISAs are valuable diagnostic methods for seromonitoring of swine population and probably livestock and wildlife animals.
A unique primer set targeting the N gene has been reported. Advancements in the field of diagnosis of emerging zoonotic pathogens following an integrated One Health approach need to be explored optimally Bird and Mazet Vaccination of humans is an integral part of preventing infection due to NiV. Prevention also includes vaccination of livestock especially pigs and probably horses in endemic areas Broder et al.
Of note, outbreaks cannot be prevented amongst the livestock population in areas where contamination of date palm sap acts as major contributor to the spread of NiV infection. However, if vaccination of livestock is made cheap it may prove to be successful in certain regions. Extensive research involving preclinical studies in a number of animals and nonhuman primates have identified multiple vaccine candidates, including vectored and subunit vaccines, offering protective immunity Satterfield et al.
Among vectored vaccines, one employing vesicular stomatitis virus has shown protection inferrets, African green monkeys, as well as hamsters Mire et al. Despite these developments, funding for human clinical trials of candidate vaccines remains a problem for academic community.
The pharmaceutical companies are hesitant to invest in research on development of vaccines for diseases like Nipah, which are rare occurrences, despite the high fatality. A collaborative effort has been undertaken by both government and pharmaceutical companies, known as the Coalition for Epidemic Preparedness Innovations CEPI.
It was formed in January for developing safe, efficacious and affordable vaccines against diseases associated with pandemic potential, like Nipah Satterfield CEPI aims to develop two new experimental vaccines within five years, in the first phase of the clinical trial. It is anticipated that field efficacy studies of such vaccines could be done during massive outbreaks Satterfield DNA vaccines, virus-like particles, virus vectors live and recombinant , and other advanced vaccines have been developed as strategies of immunization against both HeV and NiV Walpita et al.
A recombinant measles virus rMV vaccine that expresses envelope glycoprotein of NiV has been found to be promisingfor use in man Yoneda A replication-competent, recombinant VSV-vectored vaccine encoding NiV glycoprotein was reported to show high efficiency in a hamster model. A single intramuscular dose of the vaccine conferred protective immunity in African green monkeys one month after vaccination Prescott et al. Healthcare workers and family contacts attending Nipah cases should be considered for Nipah vaccination, in order to limit human-to-human transmission and curb outbreaks DeBuysscher et al.
A very strong virus-specific immune response is generated through vaccination which inhibits the virus replication and shedding. Such vaccine could provide protection from NiV in disease outbreaks. Attenuated live vaccines as well as subunit G recombinant platforms have also been tested Satterfield et al. The immunogenicity of the NiV-VLP vaccine was high because the VLPs possess the native characteristics of the virus including the size, morphology and surface composition Jegerlehner et al.
A recent work reported a novel strategy of adding a cholesterol group to the C-terminal heptad repeat HRC of the F protein that facilitated membrane targeting and fusion of the peptide.
Enhanced penetration of the central nervous system and significant increase in antiviral effects were observed with these peptides Porotto et al. Golden Syrian hamsters immunized with these VLPs developed high titres of neutralizing antibody in serum, and showed complete protection upon viral challenge Walpita et al. Immunoinformatic advances have been utilized for developing peptide-based NiV vaccine by prediction and modeling of T-cell epitopes of NiV antigenic proteins.
Specific epitopes, viz. Such predicted peptides can potentially stimulate T-cell-mediated immunity and could have utility in developing epitope-based vaccines to counter NiV.
Such approach identified B-cell epitope sequences in phosphoprotein to , polymerase enzyme gene to and nucleocapsid protein to These studies are oriented for the validation of potential vaccine candidate protein portions from Nipah virus which could then spearhead towards the development of fruitful subunit vaccines Ravichandran et al. The development of animal models of NiV disease is another priority, in order to evaluate the preventive and therapeutic approaches.
This will help in employing successful immunization strategies both active as well as passive by targeting the envelope glycoprotein of the virus Broder et al. The crew should proceed as directed to the entrance to the HSIDU, and once the patient has been handed over await instructions regarding disinfection and decontamination procedures.
Air Transportation within the UK. Suspected cases Suitable protocols for standard isolation procedures, including the use of universal precautions should be in place. In addition, a number of further precautions are necessary when handling a patient suspected of being infected with Hendra or Nipah virus. The isolation facility should be part of a specialist infectious disease unit, sited in an area away from general circulation, or form part of a separate isolation building.
The general public must be excluded from the area when the facility is in use. The facility should be staffed by individuals trained in the management of infectious disease. Access must be restricted to authorised personnel, and a register of all personnel, including clinical, non-clinical and maintenance staff, entering the Unit should be kept.
All authorised personnel must receive appropriate training and instruction. Information on legal requirements is included in Appendix 8. Suitable protective clothing to wear over normal clothing, including face and eye protection e. Suitable showering and changing facilities for staff, if contaminated, must be provided. The unit must be easy to clean.
Floor, wall and other surfaces should be impervious to water, and resistant to damage from disinfectants. If radiology or other special investigations are necessary, these should be carried out, if possible, at the patient's bedside, after consultation with the Infection Control Doctor.
Crockery and cutlery, if not disposable, should be washed in the patient's cubicle. In general, patients should, if able, use an en suite bathroom. Where this is not possible, there should be protocols for the disposal of excreta.
All waste materials, some of which may be heavily soiled, should be made safe to handle before disposal. Special arrangements for disposal of waste, including handling, disinfection and access to an autoclave, should be in place. Guidance on the decontamination of clinical waste is included in Appendix 7 Confirmed cases.
Detailed accounts of the specific exposures should be obtained and the significance of these exposures then considered by an expert panel. Further detail on these seven cases is included in Appendix 1.
No cases of asymptomatic infection have been identified from extensive testing of human contacts associated with Hendra virus events up to July In horses, Hendra virus has a clear predisposition for targeting endothelial cells of blood vessels, with clinical signs dependent on the sequence in which organs are affected. Documented equine cases to date have typically presented with acute onset of clinical signs, including increased body temperature and increased heart rate, and rapid progression to death associated with either respiratory or neurological signs or a mix of these.
Some horses have also shown evidence of multi-organ involvement. The clinical signs, particularly of early Hendra virus infection, may be non-specific, although progression from onset to death is typically rapid, occurring over a couple of days. Less severe infections have been identified in horses being monitored during an outbreak; these horses are typically second or third-generation cases.
Those that survive often have mild signs and seroconvert during the recovery period. In past incidents, all horses that have tested positive for Hendra virus have been euthanised [ 8 ]. People who are more likely to be exposed to infected horses may be at increased risk, e. All events since Hendra virus infection was first identified in have occurred in Queensland or New South Wales. However, given the distribution of flying foxes Figure 1 and frequency of horse movements among states and territories, cases could occur anywhere in Australia.
Horse owners and carers can take steps to protect horses from becoming infected with Hendra virus by reducing exposure to flying foxes, e. Appropriate processes should be in place to ensure relevant surveillance information is shared promptly at state and territory level among animal and human health agencies.
Hendra virus infection in humans is not currently nationally notifiable and there is no national case definition. The following is based on the Queensland case definition as at October , reviewed in February Exposure, within 21 days prior to onset of symptoms, to a horse with confirmed Hendra virus infection, or where heightened suspicion of Hendra virus infection exists as advised by [NSW DPI].
Clinically-compatible acute illness, see section 2. The disease - Clinical presentation and outcome. Tests available include nucleic acid testing NAT and serology. Virus isolation is usually attempted on acute phase specimens, particularly when NAT is positive. Testing of human samples is also available, on request, from the Australian Animal Health Laboratory AAHL , Geelong, Victoria and may be available on request from some state animal health laboratories.
NAT can be performed on respiratory samples deep nasal swab or nasopharyngeal aspirate , serum preferable to blood , cerebrospinal fluid CSF , urine and tissue samples.
Minimum CSF, serum, liquid respiratory or urine sample volume is 0. Tissue samples minimum rice grain size should be in viral transport medium, not fixed.
Respiratory swab samples should be dry, or in viral transport medium. Chill all samples immediately upon collection 4 o C and transport cool 4 o C not frozen, within 24 hours. QHFSS currently performs a screening microsphere immunoassay MIA for IgM and IgG and can differentiate between individuals with natural antibodies and those administered therapeutic monoclonal antibodies.
As with all serological tests, false positive results can occur. Where serological testing is indicated, a baseline sample should ideally be collected as early as possible after exposure and stored for testing in parallel with subsequent samples.
Minimum sample volume of CSF or serum is 0. Transport cool 4 o C within 24 hours. The earliest laboratory evidence of infection in human Hendra virus cases has been positive nucleic acid testing in blood, respiratory specimens, then urine, with serology becoming positive two to five days after onset of symptoms. Commence investigation immediately on notification of a confirmed human or equine case, or where notified by an animal health agency of heightened suspicion of infection in a horse on clinical and epidemiological grounds.
On notification of a confirmed equine case, or where an animal health agency has heightened suspicion on clinical and epidemiological grounds:.
On notification of a confirmed human case, or where a public health unit considers there is heightened suspicion on clinical and epidemiological grounds:. For all confirmed human or equine cases, an incident management team should be established to manage the public health response. Close liaison with [NSW DPI] is necessary and regular interagency meetings should be held to ensure a coordinated response. Responsibility of the treating medical practitioner.
Advice should be sought from an infectious diseases physician. Cases should be informed about the nature of infection, mode of transmission and other relevant information.
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