Hendra Virus Case Study

Common clinical signs for Hendra virus in horses will include: acute onset illness, increased body temperature, increase heart rate, discomfort/weight shifting between legs, rapid deterioration. Respiratory problems that may occur: pulmonary oedema and congestion, respiratory distress, increased respiratory rate, nasal discharge, weakness, ataxia (the loss of full control of bodily movement), and collapse. Neurological signs include: wobbly gait progressing to ataxia, altered consciousness, and apparent loss of vision in one or both eyes, aimless walking in a dazed state, head tilting, circling, muscle twitching – seen in acutely ill and recovered horses, urinary incontinence, decumbency with inability to rise. Contact with suspected horses should be avoided until a veterinarian has investigated and provided advice on handling affected horses safely. Horses feed and water troughs should not be placed under trees where bats may feed or roost. Hendra is a notifiable emergency animal disease. If you suspect a horse might be infected, you must report it. Even more alarming we now know that infected horses may shed live virus for up to 48 hours before they show any clinical signs of Hendra virus. In addition it appears that the incubation period is increasing – this means that the number of days between when the horse is infected and starts showing signs of disease is increasing. This means that the potential for exposure to Hendra virus exists even in an

One of the main reasons why this topic was selected is that the infections caused by the virus are considerably common with some people having outbreaks several times a year. The risks of infection depend on

Hantavirus was first discovered in 1993 in areas in the southwest United States and found to be transferred by rodent urine, feces, saliva, and by air-born particles containing these items. The latest hantavirus outbreak at Yosemite National Park was because hantavirus’s transfer to humans by mice. Human-to-human exchange of the hantavirus in America has not

Apart from food transmission the virus is most commonly contracted via person-to-person contact. Several other ways of transmission include touching surfaces or objects that are contaminated with the virus and then proceeding to

Flavivirus is a group of single-stranded RNA viruses in Flaviviridae family that are causative agents of public health diseases such as Murray Valley encephalitis and West Nile fever. Since 1917, arboviral encephalitis has some sporadic occurrences in south-eastern Australia due to heavy rainfall following by widespread flooding that caused to enhance the population of water birds and mosquito vectors (Doherty, 1977). MVEV was first found and isolated from the passed away encephalitis patients in 1951 around Murray Valley. It was called ‘Australian encephalitis’ at the time, which covered WNV/KUNV and other flaviviruses infection (Anderson, 1954). However, the investigation later suggested that these viruses are causing different diseases (Doherty

They had came to the conclusion that there is no cure unless these are done following the encounter with the disease, Providing intravenous fluids and balancing electrolytes (body salts), Maintaining oxygen status and blood pressure and Treating other infections if they occur. They also made a list for prevention such as making sure to practice hygiene, self monitoring yourself for 21 days when coming from a country exposed to the virus and avoid areas and contact of treatment areas and people with the virus. In addition they made a list of ways to protect yourself from the disease mainly avoiding bodily

The most widely quoted date for the beginning of recorded history of avian influenza (initially known as fowl plague) was in 1878 when it was differentiated from other diseases that caused high mortality rates in birds. Fowl plague, however, also included Newcastle disease until as recently as the 1950s. Between 1959 and 1995, there were 15 recorded occasions of the emergence of HPAI viruses in poultry, but losses were minimal. Between 1996 and 2008 however, HPAI outbreaks in poultry have occurred at least 11 times and 4 of these outbreaks have involved millions of birds (Alexander and brown, 2009). In the 1990s, the world’s poultry population grew 76% in developing countries and 23% in developed countries, contributing to the increased prevalence

is present for life in the body of the host animal once it is infected. Equids are the only known natural host of the disease and all ages are susceptible. The virus is only infected inside the body of the host but can be present in blood, saliva, milk, feces and serum of diseased horse (North Carolina Department of Agriculture and Consumer Services, n.d.; OIE Terrestrial Manual, 2008; The Center for Food Security and Public Health, 2005).

Bacteria and viruses often mutate, as the H1N1 influenza virus proves, and new pathogens, like the one leading to severe acute respiratory syndrome (SARS), can appear− infecting unprotected populations. By evaluating the viral sources of infection we can begin to better understand these various respiratory afflictions and develop and implement efficacious prevention policies and programs.

For example if we take one cell of our red blood cells and compare the sizes we will find that our red blood cell is 75 times bigger than MERS-CoV. Is very incredible of how a small thing can kill fully-grown adult human being. Viruses are Obligated intracellular parasite, which means they need a host to function. They either contain DNA or RNA. Also have no ribosomes, and No ATP-generating mechanism. The MERS-CoV is covered by a membrane and attached to the membrane are spikes. Spikes are made up from glycoprotein and they are receptors binding. These spiked infect only specific types of cell in host; spike also is a major determinant of pathogenicity of that viral. Also they have Ion channel impeded in the membrane and what that does is it regulates ions in the virus. Inside the membrane is where you find the RNA sequences. The RNA sequences are kept inside Capsomere. But how this small and simple organism

For the Nipah Virus, fruit bats of the Pteropus genus have been identified as the natural reservoir. The virus has been isolated in many bodily locations, such as the brain and spinal fluid, and from environmental prototypes, like bat urine and partially eaten fruit, such as found in cases of Malaysia. Antibodies of the Nipah virus have been found in the sera of fruit bats, which have been collected in India, Indonesia, and many others such as Madagascar and Ghana. The presence of these antibodies indicate that goats, horses, and some cats and dogs have been reported as infected, with a history of exposure to infected pigs in Malaysia. This wide range of locations where NiV has been discovered represents its wide geographic distribution. While

Infected bird populations experience high morbidity and mortality rates. The virus is transmitted among birds by exposure to droppings or close contact with an infected bird (Petsko, 2005). Birds typically present with swollen or bluish wattles, cyanosis, respiratory distress, diarrhea, and pinpoint hemorrhages on the legs. Infected wild birds can spread H5N1 to various locations along their migratory pathway, hence the spread from Asia to Europe (Kilpatrick et al, 2006).

). In the current virus taxonomy NDV, or avian paramyxovirus type 1 (APMV-1), is classified with the other avian paramyxoviruses, in the genus Avulavirus, sub-family Paramyxovirinae, family Paramyxoviridae, order Mononegavirales (Lamb et al., 2005). All APMVs, except avian metapneumovirus, are classified in the genus Avulavirus of the family Paramyxoviridae and are divided into nine serological types (APMV 1-9) (Nayak et al., 2008). In 2007 in survey A.I program the biological, serological, and genomic characterization of a paramyxovirus recently isolated from Rockhopper Penguins (Eudyptes chrysocome) suggested that this virus represented a new APMV group, APMV10. This penguin virus resembled other APMVs by electron microscopy but, its viral HA activity was not inhibited by antisera against any of the nine defined APMV serotypes.

Hantavirus has been identified to cause two distinct illnesses: Hemorrhagic Fever with Renal Syndrome (HFRS) and Human Pulmonary Syndrome (HPS) (Centers for Disease Control and Prevention [CDC], 2013; Willacy & Tidy, 2013). Recent studies have dated Hantavirus to the Middle Ages. However, the first sweeping outbreak of HFRS Hantavirus traces back to the Korean War between 1950 and 1953 where mortality climbed to 12% in soldiers suffering from renal failure. The virus was responsible for the deaths of 3000 United States soldiers. The etiologic agent was not identified until the virus was isolated in 1978 (Jonsson, Figuiredo, & Vapalahti, 2010). The Hantavirus is not new to animal species, but since

The maedi-visna virus (MVV) is a very deadly disease that’s most commonly found in sheep but on rare occasions can also affect goats. MVV is also known as Ovine Progressive Pneumonia in North America but formally it has been called maedi visna because of two traits that an animal may have if it has contracted MVV. Maedi and visna are both Icelandic terms; maedi is to have progressive pneumonia and visna means wasting and withering of the animal. Both scenarios of pneumonia and wasting result in fatality since MVV is currently an incurable disease. Many researchers have looked into vaccinating sheep for MVV but all attempts have failed and actually worsened the condition of the animal in testing. Throughout this report I will be covering what