Epidemiology : identified in September 1994 during an outbreak of viral encephalitis in Hendra (Brisbane, northern Queensland), Australia (2 cases in a trainer (who died from interstitial pneumonia) and a stablehand (who recovered slowly); 13 equine deaths  and a related outbreak (meningoencephalitis) in 1995 when a trainer and 14 of his horses died. In January 1999 Hendra caused the death of a single horse in Cairns, North Queensland. In Dec 2004 a horse near Townsville died from the virus and about 10 people were tested for symptoms
Transmission : healthy resérvoir : Pteropus spp. (antibodies to Hendra virus have been found in 4 species of fruit bats. Approximately 25% of the bats surveyed had antibodies to the virus. Of 13 wildlife species tested, only bats had antibodies to Hendra virus^ref); terminal hosts : Equus caballus (a zooanthroponosis from urines). It has been shown experimentally that Hendra virus can cause severe clinical disease in Felis catus and Cavia porcellus. No infection occurs in dog, chickens, rat and mice. Human-to-human transmission has not been reported. Not particularly resistant to heat or chemicals.
Pathogenesis : Hendra virus produces both lung and brain disease, consistent with related viruses such as canine distemper and measles.
=> Hendra infection  : after 4-18 days incubation => encephalitis and/or interstitial pneumonia

Nipah virus (NiV)

Epidemiology : outbreaks in winter

• Malaysia : in Nipah, Perak, Negeri Sembilan and Selangor from September 1998 to April 1999 (265 cases, 93% with occupational exposure; 105 deaths; lethality : 39%)
• Singapore during March 1999 (11 cases among abattoir workers, 1 death).
• Bangladesh : 211 cases and 59 deaths since 2001, when the virus was 1st detected
• January-February 2004 :  18 deaths, mostly children
• Jan 5, 2005- ? : 44 cases and 12 deaths in 3 villages in the northern district of Tangail, adjacent to Dhaka in central Bangladesh. 13 people developed a fever and became unconscious after drinking the juice of local palm fruits, probably made from fruit contaminated by fruit bat droppings, or from fruit the bats had half-eaten. The researchers sent samples of patients' blood to the CDC in Atlanta, USA, which confirmed Nipah virus infection in one of them. Bangladesh does not have adequate research facilities for diagnosing the virus or working on ways of controlling it. One constraint is that there are no laboratories in which the virus can be studied safely, without a risk of it escaping and infecting more people. The IEDCR, however, is trying to find out how the outbreak began. Although the researchers suspect fruit bats are the main carriers of Nipah virus, they are also collecting samples of blood, tissue and droppings from other species including cats, dogs, poultry, cattle and rodents to see whether the virus has other hosts. By sampling fruit trees, they hope to determine whether the virus can be transmitted through contact with fruit touched by the bats^ref

Proteomics :

• attachment (G) glycoprotein
• fusion (F) glycoprotein
• V and W proteins, which are encoded by the P gene via RNA editing, have a common N-terminal domain but unique C-terminal domains. They localize to the cytoplasm and nucleus, respectively, and have both been shown to function as inhibitors of JAK/STAT signaling. Nuclear localization of the W protein allows for inhibition of both virus- and TLR3-triggered STP^ref.
• receptor : Ephrin-B2, located on brain cells and cells lining the blood vessels, is critical to nervous system development and the growth of blood vessels in human and animal embryos. Ephrin-B2 is found in humans, horses, pigs and bats, which may explain why the infection can jump so easily from one species to another^ref

Transmission : a zooanthroponosis from Sus scrofa (healthy resérvoir : Pteropus spp.). Antibodies to Nipah viruses were identified in other animals (Canis familiaris, Felis catus, Equus caballus and Capra hircus), but transmission from these animals to humans was not documented. Human-to-human transmission has not been reported, although respiratory secretions contain the virus. Not particularly resistant to heat or chemicals.

outbreaks of encephalitis, both caused by Nipah/Hendra-like viruses, occurred in separate areas in western Bangladesh since 2001 and 2003. All outbreaks occurred over brief periods and had high CFRs.

• between 26 Apr and 26 May 2001, 28 cases including 9 deaths occurred among people with febrile illnesses and neurologic symptoms in Chandpur village, Sadarthana, Meherpur district, 17 km from the border with India; 7 deaths occurred among people within the same family who lived within the same home or whose homes were adjacent to each other. The mean age was 40 years (range 32-60 years); 6 were males. During the same time interval, 18 other residents of the village were reported to have a similar illness and survived. An investigation led by the Director General of Health Services (DGHS) in May 2001 was followed by a 2nd investigation from 26 May to 1 Jun 2001 by a team that included staff from DGHS, the WHO, and ICDDR,B. Results of antibody testing by ELISA done at the CDC in the USA suggested that at least 2 people in the Chandpur outbreak were infected with Nipah/Hendra-like viruses
• between 11 and 28 Jan 2003, another outbreak of severe illness including features of encephalitis was reported affecting at least 17 residents (range 4 to 42 years) of Chalksita and Biljoania villages (located 45 km northeast of Rajshahi) in Naogaon district; 8 people died. In February 2003, an investigative team from ICDDR,B and CDC-Atlanta visited Chandpur to learn more about the scope and risk factors for the 1st outbreak. Upon concluding studies in Chandpur, the team visited Naogaon District with the objective of defining the etiology and scope of the 2nd outbreak. The team collected specimens of blood from 119 residents of Chandpur and 89 residents of Chalksita and Biljoania villages who reportedly had been ill and recovered and those who were contacts (family members, close acquaintances, and neighbours of cases) of residents who had died, during either of the outbreaks. Sera were not available from any of the patients who died during the outbreaks. 4 people from Chandpur had evidence of antibodies (by ELISA) to Nipah antigen; all 4 had been ill during the outbreak period and were relatives of patients who died. Similarly, in Chalksita and Biljoania, 4 residents were found to have antibodies reactive with Nipah virus antigen; all 4 had been ill and had contact with patients who died. No health care workers were identified with illness during the outbreak periods. A case of Nipah/Hendra-like virus infection was defined as a resident of one of the villages where the outbreaks occurred who died during the outbreak periods or who had measurable antibodies to Nipah virus antigen. A total of 13 cases (including 9 deaths) were identified from the 1st outbreak  and 12 cases (including 8 deaths) were identified from the 2nd outbreak. Fever, headache, and altered consciousness were the most common symptoms. Cases in the Naogaon outbreak were more likely than non-cases to have had contact with a herd of pigs that had passed through the villages. In the Meherpur outbreak, cases were more likely than non-cases to report contact with a cow during the 2 weeks before illness. Close contact with ill people in the Meherpur outbreak, including contact with patient secretions, was reported much more commonly in cases than in non-cases. Sera were collected from a variety of animals with the goal of identifying the source of the virus for these outbreaks. Antibodies reactive with Nipah virus antigens were found in 2 of 44 Pteropus giganteus bats tested, while none were found in the remaining animals tested, including 2 other species of bats, pigs, rodents, shrews, pigeons, and dogs in areas near case-households. Findings of this report suggest that Nipah/Hendra-like viruses were the etiological agents of both outbreaks. Because diagnoses were dependent on serologic tests in both outbreaks, the precise etiological agent is not known and may be due to a pathogen that cross-reacts with Nipah virus antigens in antibody assays.
• from 4 Jan to 26 Feb 2004 : on 17 Jan 2004, a 9-year-old child from Kazipara village was brought to the emergency room of Goalanda health complex in Rajbari district, Bangladesh. The patient had a 3-day history of fever and worsening neurological signs. He died within 15 minutes of admission. Between 17 and 21 Jan 2004, 6 additional children (aged between 2 and 15 years) and a 28-year-old woman (mother of the youngest child) also died with the same symptoms. All patients came from the neighboring Kazipara and Juran Molla Para villages and lived in 2 groups of houses located within 1 km of each other. On 4 Feb 2004, SPB-CDC detected IgM antibodies against Nipah virus in the serum of 5 patients. The laboratory investigations included ELISA tests for IgG and IgM antibodies, RT-PCR to detect the viral genome, and viral isolation. CDC was able to culture the virus from 2 of the patients. Viral RNA was amplified to show that a Nipah virus -- with about a 95% homology with that isolated during the Malaysian outbreak in 1999 -- was the cause of the outbreak. As at 23 Feb 2004, 23 Nipah cases -- including 11 laboratory-confirmed cases -- had been identified in 6 districts (Faridpur, Golpagonj, Manikgonj / Manikganj (7 cases, 4 deaths : 50 km to the south west of Rajbari, and at a distance from Meherpur, the site of the 1first recorded outbreak of Nipah-like virus infection in Bangladesh in 2001), Joypurat, Naogaon, Rajbari (35 cases, 10 deaths; in the southwest of Dhaka Division, bordering with both Kulna and Barisal Divisions)). It can be inferred, therefore, that this Nipah-like paramyxovirus is prevalent throughout central Bangladesh. 17 of the 23 cases died (CFR = 74%). In all the affected districts, cases were clustered geographically and in time. The 1st identified case developed the 1st symptoms of the disease on 11 Jan 2004. Most of the detected cases occurred between 12 and 25 Jan 2004 (for 20 out of 23 cases) suggesting a common source of contamination. The main focus, with 12 Nipah cases, was identified in Goalanda, Rajbari district, where an in-depth investigation was undertaken. Of the 12 cases, 9 were male (75%) and aged under 19 years. Previous reports suggested that children were most affected, which suggests that this may be a unique virus, distinct from either Hendra virus or Nipah virus. The investigation failed to establish any link between these cases and sick pigs -- or other types of sick mammals -- as was observed during the Malaysian Nipah outbreak. Conversely, it was noted in Goalanda that young boys collected and ate fruits in the trees before dawn. This observation gave rise to the hypothesis that contamination could have occurred while eating the same fruits that fruit bats (Pteropodidae) fed on during the night. Among 11 patients with laboratory-confirmed Nipah virus infection, the most commonly reported signs and symptoms included fever (11/11), headache (4/11), vomiting (5/11), dizziness (5/11), altered consciousness or total or partial loss of consciousness (11/11), coma (9/11), focal neurological signs (3/11), disorientation/hallucination (4/11), seizure (8/11), respiratory distress (6/11) and cough/cold (3/11). Preliminary results confirm that several Pteropus flying foxes have evidence of Nipah virus infection.Given the results of the epidemiological investigation, it was proposed that several health education messages be prepared to improve hygiene while eating fruits (washing, peeling, cooking fruits before eating them, and hand-washing at home) in order to break the primary infection and transmission of the disease
• from 13 Mar to 14 Apr 2004 : 30 Nipah cases, including 18 deaths (CFR = 60%) in Faridpur district. The Centers for Disease Control and Prevention (CDC) confirmed Nipah virus infection in 16 of the cases. All cases lived in Guha Laksmipur village or were in contact with a spiritual leader living in this village who was himself a case. Direct contact with ill patients is suspected to have played a role in the transmission of the disease and the spread of this outbreak. Symptoms were respiratory problems, high fever, unconsciousness, headache and vomiting

Natural Nipah viral antibody has been found in healthy fruit bats. Virus has been isolated from the urine of fruit bats. Normally, flying foxes live deep in the jungle, feeding off succulent fruit like jambu air [also known as Jambu mawar, water apple, or rose apple, a small red succulent fruit with pink or white flesh] and mango. Local hunters shoot and eat them. In Cambodia, they are prized as aphrodisiacs, and the bats are used as good luck talismans in Filipino wedding ceremonies. So, how did the pig acquire the virus? Researchers have tried to link the emergence of Nipah virus to El Nino. During 1997-1998, El Nino brought drought and dry weather to the Indonesian peninsula, which led to massive forest fires and the haze that shrouded the region for months. Consequently, haze blocked sunlight, reducing the ability of trees to flower and bear fruit. This forced fruit bats to travel great distances in search of sustenance. They settled in places outside their usual habitat such as the fringes of forests, close to pig farms. They may have passed the virus on to pigs via their urine, as well as their saliva in the half-eaten fruit that fell to the ground and was then eaten by the voracious pigs. The presence of Nipah virus antibodies indicate that bats were infected with the virus, as were pigs, cats, and dogs. In contrast, pigs farming is uncommon in the outbreak areas in Bangladesh. That implies that other intermediary sources other than pigs were the source of infection. In the recent Bangladesh outbreak, fruit bats are also the suspected reservoir for Nipah virus. A significant number of victims in Bangladesh were under age 19. It has been hypothesized that young boys may have collected and eaten fruits harvested from trees [in the early morning] and could have contracted infection by eating the same fruits that fruit bats fed on during the night. in addition many of the cases in Bangladesh have occurred within households -- with victims having had no direct contact with animals or bats. This implicates that human-to-human transmission might be possible, which is a matter of great concern, but transmission of infection within households may be indicative of a common source of infection, which could be fruit or bat urine-contaminated material rather than a single infected human family member. Because of the clustering of cases among family members and neighbours, the secondary peaks of cases following a period of no illnesses, and an epidemiologic suggestion of increased risk for illness among people who had exposure to secretions of other sick patients, person-to-person transmission cannot be ruled out. However, absence of illness among health care workers creates some uncertainty about this possibility. Increased risk of illness following exposure to pigs in one outbreak and a sick cow in the other raise the potential of animal-to-human transmission, but this possibility cannot be validated with the limited data available. Systematic surveillance for encephalitis is not routinely done in Bangladesh. It is possible that other outbreaks and sporadic cases of Nipah/Hendra-like virus encephalitis have occurred or will occur. More information will be needed to define the magnitude of the problem and to identify strategies to prevent illness and deaths^ref.