New World Discovery: Virus Kills Horses and Threatens Human Life

Imagine yourself as an owner of several horses. As a proud owner, you tend to their needs by feeding them, brushing them, and bathing them. As an owner, you realize you also have to deal with the horses' urination and feces. All of a sudden your horses die and you have no clue why. You kept their pens clean, and you kept them clean. Hygienically, you had no problems with maintaining the horses. You had healthy horses. What, you wonder, would suddenly make your precious horses die? A virus. Similar to your pretend horse situation, Australia had an outbreak of a virus called "Hendra Virus." Never before did Australia know of the virus until racehorses and people started dying in 1994. The Hendra virus has significance because of its history, transmission, composition, symptoms, research, and treatment.

Hendra virus first came to attention in 1994, in a suburb called "Hendra" in Brisbane, Australia, when fifteen racehorses and three humans became infected with the virus and died. Because Hendra can infect horses and people, the virus is considered zoonotic, meaning Hendra can infect more than just people. Hendra virus (HeV), formerly called equine Morbillivirus (examples of Morbillivirus include measles and canine distemper), is a newly recognized member of the Paramyxovirus family. Paramyxo comes from the Greek "para" and "myxa," which combined mean "by the side of mucus." The disease is considered serious because Hendra can cause brain and lung disease, similar to measles. The virus replicates inside of a person's brain and lungs causing circulatory problems and necrosis - localized death to cells due to disease. Although highly virulent, the virus is not highly contagious. The Hendra virus outbreak had minimal affects on the Queensland, Australia racehorse industry due to fast recognition of the newfound virus. Had diagnosis taken longer, restrictions on transporting racehorses from region to region could have occurred, resulting in nearly catastrophic financial impacts for the racehorse industry in Australia. The appearance of the virus may have also resulted in the cancellation of the Melbourne Spring Carnival and the Melbourne Cup in 1994. Afterthe initial discovery of the disease, several reports followed. Since 1994, reports followed in 1995 and 1999 reporting more deaths because of Hendra. Scientists, in 1999, discovered a Hendra like virus in Malaysia (called Nipah), and analysis of the virus showed Nipah and Hendra as not the same, but Nipah is also a Paramyxovirus. Approximately 100 people died and a large number of pigs became infected with Nipah and later slaughtered. Had the Hendra virus spread around the world by 1999? No, the Hendra virus outbreak is confined to Australia, and no recent reports indicate the spreading of the virus since 1999 when someone found a horse dead in Cairns, Australia. The horse died after only 24 hours of showing symptoms of having Hendra.

The exact transmission of the Hendra virus is unknown, however, reported cases show individuals have acquired the infection via close contact with body fluids of infected horses. Also, one can potentially get the virus from blood and body fluids of infected fruit bats. The suspected reservoir, a place where a virus multiplies and grows, is fruit bats, also called "flying foxes." The Hendra Virus poses little harm to bats. Once transmitted to other animals, including horses and people, an infection can cause death. The virus' virulence is attributed to hosts, including humans, not producing antibodies to fight the virus, which means the virus can cause severe affects including death of its host, usually within a few days. Studies about Australian fruit bats revealed bats having antibodies to the Hendra virus, which means the fruit bats have previous exposure to the newfound disease, and also explains why they do not die from infection. Animals infected with the virus can excrete the virus in their urine, and horses have picked up the virus in such a manner. Horses can also pick up the virus from eating contaminated foods. Individuals at greatest risk to getting Hendra include fruit bat handlers, farmers, who come in contact with bats and other animals, and racehorse handlers. The "average" person does not need to fear infection of Hendra. Fortunately, the outbreak in Australia never spread or became a tremendous issue and is currently under control, with the most recent infection reported in 1999.

Understanding the composition of the Hendra virus can help in understanding its significance. The virus is enveloped and between the size of 38 nanometers and 600 nanometers covered with approximately 18 nanometers of surface projections. Double-fringed surface projections give the virus a distinct appearance. As noted earlier, the virus is included in the paramyxovirus family. The paramyxovirus family consists of a large group of enveloped, negative-stranded RNA viruses. Because Hendra is a paraymxovirus, the virions, virus particles, have both haemagglutinin and neuraminidase activities and encode a c protein. Haemagglutinin and Neuraminidase, as two types of receptors, stick out of the virus, giving the cell the ability to adhere to host cells.

A symptom for Hendra is different for each animal, although they do share some similarities. Symptoms include fever, drowsiness, and coma in people. Advanced stages of the disease include respiratory disease (lesions in the lungs caused by the virus attacking blood vessels), "oedema (fluid in the lungs)," changing blood pressure and body temperature. Lesions in the lungs can lead to an individual developing pneumonia. Hendra can also lead to encephalitis, inflammation of the brain caused by a viral infection. Horses have various symptoms including breathing difficulties, fever and foaming blood at the nostrils.

Through researching the Hendra virus, over a period of about four years, Australian researches further developed knowledge of the virus, but much research is still needed to further development in technologies, treatments, and general knowledge of the newfound virus. Initially, Hendra became identified through viral comparisons - looking at similar viruses for similarities through gene sequencing. In 1995, researchers injected horses with infected tissue of the Hendra virus to test the disease for transmissibility, and shortly after, the horses with the diseased tissue became ill, showing definite signs of Hendra. The incubation period for the virus is approximately 16 days. Also, in 1995, a test of approximately 2,000 horses in Queensland, Australia revealed the disease did not spread naturally among other horses, which means the risk of spreading is unlikely. Only through injecting animals with infected tissue, did those animals become ill from Hendra. Researchers could not show spreading of the virus in clinical trials of horse-to-horse, bat-to-person, and bat-to-horse. However, research has proven horses can pick up the virus from eating contaminated food. Tests have shown animals including horses, guinea pigs, and cats have urinated with the Hendra virus present in their urine. Thus, some researches have an inclined notion to believe in transmissibility through urine, which they have yet to prove. Lastly, a rather interesting and most important find revealed fruit bats infected with the virus display no symptoms of disease. In response to the finding, researchers extensively and vigorously attempted to develop antibodies for humans to fight off Hendra, but have yet to succeed.

Although not currently a great threat and not much of a threat in general, researchers created various guidelines to follow for treatment and prevention. If one's horses become infected with the virus, researchers suggest the killing of the infected animals to prevent the spreading of the disease, as no cure is known. Ribavirin, an antiviral drug, can reduce both the duration of fever and the severity of disease in people. No cure or vaccine exists against the Hendra virus. Avoiding contact with known infected animals and people may reduce one's risk to infection of Hendra. Various hygiene practices including hand washing can help prevent infection and spreading of the disease, as the virus is susceptible to varying detergents. Tending to flesh wounds can also help prevent one from getting Hendra. An open wound is certainly an easy entrance for any virus.

From 1994, to present day, the Hendra virus is virtually unknown to the world. Only a few cases ever emerged from Australia and at one time did people believe the virus began to spread globally. Although the virus did not kill millions upon millions of people, the virus somehow existed in fruit bats for a long time, eventually emerging to Australian researchers' eyes. Hendra virus is certainly new, never seen before anywhere in the world. Just as quickly did the virus appear as the virus disappeared. The virus showed up in 1994, with the last reported case in 1999; making an appearance for roughly 5 years, and in essence vanished.

Sources:

Australian Veterinary Association. Information on Zoonotic Bat Viruses for Veterinary Practitioners. September 1999. Department of Agriculture. Viewed October 27, 2002.

Murray, Keith. A Novel Morbillivirus Pneumonia of Horses and its Transmission to Humans. March 1995. CSIRO Australian Animal Health Laboratory. Viewed November 2, 2002.

National Center for Infectious Diseases. CDC. October 26, 2002. Viewed October 27, 2002.

Queensland Health and the Department of Primary Industries. Animal and Plant Health. Viewed October 27,
2002.

Selvey, L. A. Infection of Humans and Horses by a Newly Described Morbillivirus. Medical Journal of Australia 162. 1995. 642-645.

Sompayrac, Lauren. How Pathogenic Viruses Work. Jones & Bartlett. September 2002. 95-115.

Strauss, James H. and Strauss, Ellen G. Viruses and Human Disease 1st edition. Academic Press. December 2001. 285-300.

Thibodeau, Gary A and Patton, Kevin T. Structure and Function of the Body. 10th edition. Mosby-Year Book, Inc., 1997. 263-268.

Young, Peter. Isolation of Hendra Virus from Pteropid bats: a Natural Reservoir of Hendra Virus. Journal of General Virology. April 2000.