The Majestic Tiger

One of the most ferocious and fascinating species of wildlife, the tiger has always conquered people’s imagination. Imagine if future generations did not get a chance to know the royal animal of jungle. It is sad but true that the tiger is facing extinction. Several subspecies, like the Bengal, the Sumatran and the South China tigers, have been designated as endangered species.

The decline of this majestic animal is due to poaching for its fur, deforestation and encroachment into their habitat. Our country has the maximum number of wild tigers in the world. But over population has led to a constant conflict between man and animal. As the numbers dwindled, a conservation effort called Project Tiger was set up in 1973.

Project Tiger has been a successful venture in preserving the existing number of wild tigers. It aims at preventing and fighting poachers, developing tiger reserves and preservation of the jungles ecosystem. Making people aware of the danger to our national animal is the only way by which the tiger can regain its lost glory.

The Tasmanian Taiger

Australia is home to some of the world's most unusual and mysterious wildlife. Our native animals, such as the platypus, the koala and the kangaroo, have been a source of wonder and surprise to people the world over. But perhaps our most mysterious animal is the thylacine, or Tasmanian tiger, which is considered to have become extinct in 1936.

There are many reasons why people are fascinated by this animal. Perhaps it is its name and the romantic notion of Australia having its own 'tiger'. Perhaps it is its sad history since European settlement, or the fact that there are many people who claim they have seen a Tasmanian tiger and believe it may not be extinct after all.

What was a Tasmanian Tiger?

The now-extinct Tasmanian tiger. Image courtesy of Department of Primary Industry, Water and the Environment, Tasmania.

The full scientific name for the Tasmanian Tiger is Thylacinus cynocephalis. Roughly translated, this means pouched dog with a wolf's head.

Modern history records the thylacine as being native to Tasmania. However scientists believe it was once widespread throughout mainland Australia, Tasmania and even Papua New Guinea.

The main evidence for this belief is the presence of thylacine-like animals in Aboriginal rock-paintings from northern Australia, including the Kimberley region of Western Australia, the Upper East Alligator region of Deaf Adder Creek and Cadell River crossing in the Northern Territory.

Numerous thylacine bones have been found in mainland Australia. Some of these bones have been dated at about 2,200 years old. Although we can't be sure what happened to the thylacines of mainland Australia and Papua New Guinea, scientists suspect that competition for food and predators such as the dingo had a lot to do with their disappearance.

By the time Europeans settled in Australia, the thylacine was only found in the coastal and plains regions of Tasmania. Thylacines were quite common and widespread when Tasmania was first settled in 1803, and the Aboriginal people of Tasmania used the thylacine as a food item.

The Lion's Den! - Extreme Animals

Gorilla Population Increases in the Congo

A recent census by the Wildlife Conservation Society indicates there are currently 125,000 western lowland gorillas in the northern part of the Congo. Estimates from the previous two decades placed the entire population of western lowland gorillas found in seven Central African nations at 50,000.

“These figures show that northern Republic of Congo contains the mother lode of gorillas,” said Steven E. Sanderson, president of the Wildlife Conservation Society. “It also shows that conservation in the Republic of Congo is working. This discovery should be a rallying cry for the world that we can protect other vulnerable and endangered species, whether they be gorillas in Africa, tigers in India, or lemurs in Madagascar.”

Paula J. Dobriansky, the under secretary for democracy and global affairs at the U.S. Department of State, agrees: “For the first time in recent memory, we are hearing good news about an endangered species. What that tells us is that conservation strategies are vital, and they are working.” Dobriansky addressed a Wildlife Conservation Society event September 15.

The new results showed more than 125,000 western lowland gorillas living in two adjacent regions covering 47,000 square kilometers (18,000 square miles) in the northern part of the Congo. Population densities ranged as high as eight individuals per square kilometer in one particularly rich forest patch, which ranks as among the highest densities for gorilla populations ever recorded, according to a statement by the Wildlife Conservation Society.

Spring Viremia Carp

Introduction

Spring viremia of carp (SVC) is a viral disease of fish, primarily common carp (Cyprinus carpio). Although the disease and its causative agent, spring viremia of carp virus (SVCV) or Rhabdovirus carpio, was first described in 1971, there is evidence that the disease has been present in Europe for at least 50 years and, potentially, since the Middle Ages. Before the disease was recognized, it was variously called infectious dropsy, infectious ascites, hemorrhagic septicemia, or rubella.

In Europe, the disease has had substantial impact on the production of carp, with estimated losses of 10–15 percent of 1–year–old carp or about 4,000 tons annually. In some cases, mortality rates of young carp can reach 70 percent. This impact of the disease has led to its listing by the Office International des Epizooties (OIE) as notifiable.

Susceptible species and geographical distribution

Although common carp, which includes the variety called koi carp, is the main species of fish affected by SVC, there have been several other species that are susceptible to the disease under non–experimental (natural) conditions. These species include crucian carp (Carassius carassius), grass carp (Ctenopharyngodon idella), silver carp (Hypophthalmichthys molitrix), bighead carp (Aristichthys nobilis), goldfish (Carassius auratus), tench (Tinca tinca), and sheatfish (Silurus glanis).

Under experimental conditions, other species including roach (Rutilus rutilus), pike (Esox lucius), guppy (Lebistes reticulates), pumpkinseed (Lepomis gibbosus), goldfish (Carassius auratus), zebra danios (Brachydanio rerio), and golden shiners (Notemigonus crysoleucas) have been found to be susceptible to the disease.

Many species in the minnow family (Cyprinidae) are indigenous to the United States, including endangered species; the susceptibility of these has not yet been determined either under natural or experimental conditions. A SVC–like virus has been isolated from diseased penaeid shrimp (Penaeus stylirostris and P. vannamei).

Historically, SVC has been reported from many countries in Europe, the Middle East, and Asia, but recently the disease has been reported in South and North America as well.

Clinical signs of SVC

First signs of the disease may be a change in behavioral patterns of the fish. Fish may congregate in slow–flowing water, near pond banks, or lie on the bottom. Over time, the rate of respiration will decrease, as will reaction to stimulation and
swimming speed. As the disease progresses, the fish become sluggish and may swim and lie on their sides.

Externally, the fish can exhibit a number of non–specific physical signs including darkening of the skin, swollen abdomen, exophthalmia (pop–eye), hemorrhages in the skin, gills and anterior eye chamber, anemia and pale gills, and a protruding vent.

Internally, the signs are dominated by building up of fluid (edema) in all organs and in the body cavity, hemorrhages in the swim bladder, and inflammation of the intestines.

Temperature and seasonality

Research has shown that the optimal temperature for development of SVC in experimentally infected carp is between 16 and
17° C. At this temperature, 90 percent of the fish died within 5 to 17 days after being infected. At lower temperatures, 11–15° C, the percent of fish that died was similar but the mortality was delayed (2–3 weeks). Mortality was reduced at temperatures between 17 and 26° C. The optimum temperature for in vitro virus replication is 20–22° C. Other experiments have investigated the influence of increasing and decreasing temperatures on the rate of disease. Research has also demonstrated that a gradual decrease of temperature (11 down to 5° C) caused low mortality, while increasing temperature back to 20° C caused massive mortality as the temperature changed from 7 to 14° C.

These results correspond with the field observations that most SVC outbreaks occur in the spring with warming temperatures.

After water temperatures rise above 15–18° C, the immune system of carp becomes capable of rapid interferon and neutralizing antibody synthesis that suppresses viral replication. Thus, in the countries where SVC has been reported, there are only sporadic reports in June and July. The temperature constraints make tropical and subtropical climates unfavorable for SVC outbreaks. The replication of virus as temperatures rise also has implications for detecting virus in fish populations. All viral isolations for SVC were from samples taken in May when the water temperature was between 10 to 18° C. Virus detection likely would be more difficult during the other seasons of the year.

Transmission

Infected fish can shed virus in feces and possibly in urine and gill mucus. Horizontal transmission likely occurs when virus enters fish through the gills. Research has demonstrated that SVC was easily transmitted horizontally through water from
experimentally infected fish to uninfected fish. Reservoir hosts include sick fish and fish that have survived an outbreak. In addition to carp, other cultured and wild fish may serve as reservoirs for the disease. Vertical transmission may be possible since SVC virus has been found in ovarian fluids, but the lack of outbreaks among fry and fingerlings suggests that it is not an important route of transmission.

Parasites such as the carp louse, Argulus foliaceus, and the leech, Pisciola geometra, have been shown to be passive vectors in the transfer of disease to healthy carp. Mechanical vectors can also be a problem since SVCV can maintain infectivity for a long time in water or mud or after becoming dry.

Diagnosis

In 2000, OIE set the international standards for diagnosing SVC virus. The diagnosis of SVC in clinically infected fish can be accomplished through virus isolation or by using an immunological test such as direct immunofluorescence (IF) test or an enzyme–linked immunosorbant assay (ELISA). A virus neutralization (VN) test is the confirmatory identification test. Immunofluorescence tests and ELISAs should be followed by virus isolation and a VN test.

The OIE has specified criteria for declaring countries, zones, and aquaculture establishments free of SVC. The International Aquatic Animal Health Code and the Diagnostic Manual for Aquatic Animal Diseases have complete details on all of the
requirements so only some general criteria are presented here. The appropriate Web sites for these documents are listed at the end of the document. A country declared free must meet these conditions: 1) no recorded outbreak of SVC for at least 2 years; 2) no detection of virus in any of the susceptible fish species tested during an official surveillance scheme
during the past 2 years; and 3) requirements met for importing live fish from other countries.

For a zone to be declared free of SVC, both aquaculture establishments and wild populations containing susceptible fish species must have been tested in an official surveillance scheme and SVC must not have been detected in the past 2 years.

The zone must also be one or more entire catchment areas or be part of a catchment area where upstream migration of fish from downstream areas cannot occur.

For an aquaculture establishment to be declared free of SVC, it may be part of a free country or zone. An aquaculture establishment in an infected area can still be declared free if it: 1) has been tested under an official health surveillance scheme for at least 2 years without detection of SVCV; 2) is supplied by water from a spring, well, or borehole only and is free from wild fish; and 3) is not connected to a watercourse or there is a natural barrier that prevents the migration upstream of fish from downstream stretches of the waterway.

The OIE Diagnostic Manual for Aquatic Animal Disease has specifications for surveillance programs to achieve and maintain health status. Briefly, fish culture units on aquaculture establishments must be inspected twice annually for 2 years. Each inspection should be conducted in order to detect a 2 percent prevalence with 95 percent confidence level. This
represents collection of approximately 150 appropriate–age fish at times of the year clinical signs are most likely to be observed and isolating pathogens is the easiest. Ovarian fluid samples can be used if available. To maintain free status, twice annual inspections of 30 fish are required. Wild fish populations need to be sampled only once a year for 2 years and 150 fish from different fish crops may be pooled. Maintenance of health status of wild fish can only be attained by annual sampling of 150 fish including as many broodfish as possible.

Prevention

There are several recommendations for preventing the disease from becoming established on commercial farms. Using a source of water that is free from disease such as a spring or a well is necessary, especially in an endemic disease area, to exclude disease. Other on–farm measures include disinfection of eggs by iodophore treatment, regular physical and chemical disinfection of ponds, disinfection of equipment, and proper disposal of dead fish. Also, new fish being brought onto farms should be purchased from an SVC–free source. Movement of ornamental fish to shows and returning to
operations should be undertaken with caution.

Currently, no commercially available vaccine exists for SVC. However, some studies hold promise for the development of a vaccine.

Scrapie

Scrapie is a fatal, degenerative disease affecting the central nervous system of sheep and goats. It is among a number of diseases classified as transmissible spongiform encephalopathies (TSE). Infected flocks that contain a high percentage of susceptible animals can experience significant production losses. Over a period of several years the number of infected animals increases, and the age at onset of clinical signs decreases making these flocks economically unviable. Animals sold from infected flocks spread scrapie to other flocks.

The presence of scrapie in the United States also prevents the export of breeding stock, semen, and embryos to many other countries. TSEs are the subject of increased attention and concern because of the discovery of bovine spongiform encephalopathy in cattle, the link between BSE and variant Creutzfeldt-Jakob disease (vCJD) in people, and feline spongiform encephalopathy (FSE) in cats in Europe.

Pseudorabies

Pseudorabies is a viral disease most prevalent in swine, often causing newborn piglets to die. Older pigs can survive infection, becoming carriers of the pseudorabies virus for life. Other animals infected from swine die from pseudorabies, which is also known as Aujeszky's disease and "mad itch." Infected cattle and sheep can first show signs of pseudorabies by scratching and biting themselves. In dogs and cats, pseudorabies can cause sudden death. The virus does not cause illness in humans.

Equine Piroplasmosis

Introduction

In the fall of 2010, the United States will host the World Equestrian Games (WEG) at the
Kentucky Horse Park in Lexington, Kentucky. Because horses that are positive to equine
piroplasmosis (EP) will be able to participate in all disciplines including endurance, we expect an
increased interest in the disease. We have prepared this document to answer questions about EP
and the measures the United States will take to allow EP-positive horses to participate in the
WEG. If you have additional questions, we have provided references and contact information
for obtaining information below. Finally, we expect to update this document as additional
information becomes available before the WEG.

What is equine piroplasmosis (EP)?

EP is a tick-borne disease caused by two parasites, Babesia caballi and B. equi. Certain ticks are
biological vectors in which the parasite amplifies and then is transmitted to horses under certain
conditions. If horses become affected, fever, anemia, jaundice, hemoglobinuria, central nervous
system disturbances, and sometimes death may result. In the acute phase, some infected horses
are less severely affected and may show little or no symptoms with no decrease in performance.
Those that survive infection in the acute phase may carry the parasites for prolonged periods
during which they are potential sources of infection to other horses via tick-borne transmission or
mechanical transfer by biting ticks, needles, or surgical instruments.

Equine Viral Arteritis

What is EVA?

Equine viral arteritis (EVA) is a contagious disease caused by the equine arteritis virus (EAV). The virus occurs worldwide including mainland Europe.

There is no risk to human health or species other than eqidae.

How does the infection spread?

A. Routes of infection - All horses

Infection spreads through transmission of the virus between horses in 4 main ways:

• venereal infection of mares by stallions during mating
• artificially inseminating mares with semen from infectious stallions
• contact with aborted foetuses and other products of parturition
• direct contact in droplets (eg from coughing and snorting) from the respiratory tract

B. The Shedder Stallion

The stallion is a very important source of the virus. On infection, the virus localises in his accessory sex glands and the virus may be shed in his semen for several weeks afterwards, or for many months or years and possibly for life. After recovery from acute illness, his fertility is not affected and he will show no further clinical signs of infection even though he may still be infectious. Shedder stallions will infect susceptible mares during mating, or after insemination with the stallion's semen, and these mares may, in turn, infect in-contact animals via the respiratory route.

It is important to note that the shedder stallion is always seropositive (ie past or existing infection indicated in a blood test) but that a seropositive stallion is not necessarily a shedder.

Breeders using AI must note that the virus can survive in chilled and frozen semen.

C. Teasers

Teasers are also a potential source of the virus and should be subjected to the same precautions as stallions.

D. Mares

Available evidence indicates that the 'carrier' state does not occur in mares.

What are the clinical signs?

The variety and severity of clinical signs of EVA vary widely. Infection may be obvious or there may be no signs at all. Even when there are no signs, infection can still be transmitted and stallions might still become shedders.

EVA can cause abortions. Other signs include fever, depression, lethargy, stiff movement, runny nose, conjunctivitis, (‘pink eye’), swelling of the lower parts of the legs, around the eye and of the reproductive organs.

How is the Disease diagnosed?

Because of the variability or the possible absence of symptoms, clinical diagnosis is not always possible.
Laboratory diagnosis is therefore essential. This requires appropriate samples, which are nasopharyngeal swabs, heparinised or EDTA blood, semen, serum and possibly urine, to be taken by a veterinary surgeon and sent to a specialist laboratory. In blood samples, laboratories look for antibodies to the virus (serological test); in blood and other samples, they look for the virus itself (virus detection tests).

Where abortion may be EVA-related, detailed clinical information must be sent to the laboratory with the foetus and its membranes.

How is EVA treated?

A. There is no treatment available for EVA itself, although there may be treatments to alleviate some of its symptoms.

Is EVA is a notifiable disease?

In Great Britain, EVA is a notifiable disease under the Equine Viral Arteritis Order 1995.
It is a legal requirement to notify a Divisional Veterinary Manager (DVM) of the Department for Environment, Food and Rural Affairs (Defra) when:

• it is known or suspected that a stallion has the disease or is a carrier of the virus
• it is known or suspected that a mare which has been mated or subjected to Artificial Insemination in the last 14 days has become infected with the virus.

Full details of the exact notification requirements are in the EVA Order 1995.

EVA Vaccine

A vaccine (Artervac, Fort Dodge) is available on an Animal Test Certificate (or similar licence) in the UK, Ireland, France and Germany, but with different national restrictions on use. Consult your veterinary surgeon on uses allowed in your country. In the UK, the vaccine can be used for all horses.

There are data to show that Artervac is safe. There is also experimental efficacy data to show that it can protect horses 3 weeks after the second dose of vaccine is given. However, it is not yet clear how the vaccine will perform in the field. If it performs well, it will be an effective way of protecting stallions. Veterinary advice should be sought on vaccination timings and administration.

Vaccinated horses will become seropositive. Horses should therefore be blood tested immediately before vaccination to show that they were previously seronegative.

Details about the prior blood test and the vaccination, both primary and booster, should be recorded in the horse's passport.

Pre-Vaccination Blood Test

If the passport includes a section titled Laboratory Health Test, details about the test should be recorded in that section by a veterinary surgeon.

If the passport does not include a section titled Laboratory Health Test, or the horse does not have a passport, the following records, certified by a veterinary surgeon, should be kept:

1. Date when the pre-vaccination blood sample was taken.
2. Type of test.
3. Certificate from the laboratory showing the blood test result, and the identity of the laboratory that carried out the test.

Vaccination

Details should be recorded by a veterinary surgeon in the section of the passport titled Vaccinations Other Than For Equine Influenza. The details are the date and place when the vaccination was given, and the name and batch number of the vaccine.

If these details cannot be entered in a passport, a record of the same details, certified by a veterinary surgeon, should be kept.

A post-vaccination blood sample may be taken to confirm seroconversion as a result of either primary or booster vaccination. The same records as set out above for pre-vaccination tests should be kept.

The above records are important as evidence of previous seronegativity for breeding and export purposes. Some importing countries require this information for vaccinated horses, either in passports or official export certificates.

For official export certification purposes, samples for EVA blood testing must be sent to a Government laboratory, i.e. the Veterinary Laboratories Agency, Addlestone.

As the vaccine's efficacy is not yet fully known, owners should monitor the horse's antibody response after vaccination, in consultation with the veterinary surgeon.

Vaccination is not an alternative to good management.

The code of practice remains essential to prevent EVA.

Equine Piroplasmosis

Equine Piroplasmosis is present in South and Center America, the Caribbean (including Puerto Rico), Africa, the Middle East, and Eastern and Southern Europe. Only the United States, Canada, Australia, Japan, England and Ireland are not considered to be endemic areas.

This disease is a disease of Equidae (horses, donkeys, mules, and zebras), and is caused by two parasitic organisms, Babesia equi and Babesia caballi. Although, Equine Piroplasmosis is primarily transmitted to horses by ticks, this bloodborne disease has been spread mechanically from animal to animal by contaminated needles.

Once infected, an equine can take 7 to 22 days to show signs of illness. Cases of Equine Piroplasmosis can be mild or acute, depending on the virulence of the parasite. Acutely affected equine can have fever, anemia, jaundiced mucous membranes, swollen abdomens, and labored breathing. Equine Piroplasmosis can also cause equine to have roughened hair coats, constipation, and colic. In its milder form, Equine Piroplasmosis causes equine to appear weak and show lack of appetite.

The greatest risk for introduction of this disease is through trading of animals or international equestrian sports, where infected and non-infected animals are in contact. Many disease free countries have the climate suitable for a foreign tick vector, or have ticks which could act as vectors.

Equine Infectious Anemia

Introduction

Equine infectious anemia (EIA), also known as Swamp Fever, is a virus disease known to occur in all members of equidae, including horses, mules and donkeys. This virus has the unique capability of infecting the horse for life, producing intermittent attacks of illness (during which the horse may die) followed by periods during which the horse may appear normal.

Occurrence

The disease has been diagnosed in many areas of the world and the infection may exist worldwide.

Transmission of the EIA Virus

The EIA virus is spread mechanically. That is, blood, containing the virus has to be transmitted from an infected horse to a susceptible horse by a vector, such as an insect, infected syringes, needles or surgical equipment. The virus can cross the placental barrier and cause fetal infection and a symptomatic stallion can infect healthy mares during breeding.

(a) Insect Vectors

The EIA virus is mechanically transmitted from one horse to another by the bloodsucking horse flies, deer flies (Tabanids), stable flies (Stomoxys spp.), mosquitoes and possibly midges. For transmission of the EIA virus to occur, the horse fly (vector) must first find and begin feeding on an infected horse, be interrupted in its feeding, and then transfer the virus during a subsequent feeding on a susceptible horse. Feeding must occur within a short period of time. Tabanids’ large size and noisy flight attract attention and their cutting/slashing rnouthparts inflict considerable pain, therefore, their feeding is frequently interrupted. Research has indicated that the EIA virus can be transmitted up to 30 minutes after the first feeding, however, transmission after 4 hours was unsuccessful.

Horse flies may have a home range or flight distance of up to 4 miles and therefore, in Canada, permanent quarantine requires complete isolation in a fly proof building.

(b) Placental Barrier

The virus apparently can cross the placental barrier and cause fetal infection. Mares with signs of acute EIA during pregnancy run the greatest risk of carrying infected fetuses. Infected fetuses can be aborted or be born alive "virus positive" and possibly be a seropositive virus carrier. The fetal response may be related to the age of the fetus at the time of the virus infection.

(c) Other Vectors and Factors Affecting Virus Transmission

The trading of horses and the indiscriminate use of non-disposable hypodermic needles, teeth floats, gags, nose twitches and stomach tubes all contribute to the spread of the EIA virus. During the fall when horses are changing hands, the spread of the disease is more prevalent.

EIA Virus Characteristics

The EIA virus is a slow acting virus of the lenti-retrovirus group. Retroviruses cause leukemia in cats, mice and cattle, arthritis, pneumonia and neurologic diseases in small ruminants and acquired immune deficiency syndrome (AIDS) in humans. These viruses localize and multiply in macrophages of many organs, especially in the spleen, liver, kidney, and lymph nodes, where they take over the cell and sit and wait to become activated. Upon activation, the cell reproduces more virus, which bursts free from the cell to infect other cells. This causes recurring cycles, in which the horse seems normal and then ill.

A major difficulty in developing a vaccine for EIA, is the capacity of the virus to vary antigenically, meaning, the virus changes its protein make-up, making successful antibody development difficult. Therefore, an effective vaccine must protect the horse against all of the variants to which it will be exposed. Research is underway to develop a vaccine for EIA. In light of the concerns over AIDS and an interest in using the EIA virus as a model, there could be significant advances in the development of a vaccine.

Clinical Disease

Following the first exposure to the virus, acute cases experience fever and hemorrhaging 7-30 days post infection. Very few horses with this initial fever are detected by owners. The more classical case of EIA is that of a chronically infected horse. These animals experience episodes of fever, weight loss, depression, progressive weakness, anemia and edema. These signs occur every two weeks in recurring cycles.

Other symptoms which may occur during the course of the disease include: loss of appetite. frequent urination, diarrhea, weakness, paralysis of the hindquarters, paleness of the mucous membranes, yellowish discoloration of the conjunctiva, small pinpoint hemorrhages beneath the tongue, rapid breathing and accelerated pulse. Pregnant mares may abort.

The onset of these signs is often associated with stresses such as hard work, hot weather, racing, pregnancy or use of steroid drugs. The most difficult animals to identify are the inapparent carriers. These horses show no clinical signs associated with the infection and go undetected unless subjected to the Coggins’ blood test.

On occasion, an apparently healthy horse may harbor the virus, but never exhibit any symptoms of the disease. This is referred to as a carrier animal and is a constant source of infection.

Treatment and Prevention

There is no known treatment that can eliminate the virus from the body. To date there are no satisfactory vaccines for EIA.

The key to prevention is the identification and control of infected horses. An eradication program would be only possible, if all members of the equine population were tested, and infected horses euthanized, or placed under complete permanent quarantine in a fly proof building.

Regulations

EIA is a reportable disease and subject to control under the Animal Disease and Protection Act and Regulations administered by the Health of Animals Division of Agriculture Canada. The voluntary control program was initiated in 1972. Private veterinarians accredited by Agriculture Canada, collect blood samples and submit them to accredited laboratories. All results are reported to Agriculture Canada. Positive or atypical reactions to the Coggins’ test will be investigated by Agriculture Canada.

Once a suspect horse has been identified, an Agriculture Canada veterinarian will assume full control of the case. The owner will be advised that a free retest can be run at his or her request. Upon identification of a positive retest, the premise where the reactor is housed is quarantined. The reactor horse is identified by applying a cold "R" brand on a clipped area of the right shoulder. The owner has the option to have the horse:

(a) euthanized on the premises with compensation

(b) euthanized at a registered establishment with compensation

(c) placed into permanent quarantine with no compensation

Equine Herpesvirus

Introduction

Abortion associated with equine herpesvirus type 1 (EHV1) has occurred sporadically in horses in Australia since 1977. Prior to then only the respiratory form of the disease has been recognised in this country. Abortions due to EHV1 are common in England and the USA and the virus is found worldwide. Cases of EHV abortion have been confirmed in Queensland in mares allegedly coming from southern states where other cases of abortion due to EHV1 have been diagnosed.

While there are many causes for abortion in mares, EHV1 is a serious contagious disease and one that horse breeders should be aware of. Basic information on the disease is provided below to assist breeders to institute sensible precautions to prevent the introduction of the disease and to recognise and manage the disease should it occur on their farm.

In Queensland, EHV abortion is a notifiable disease and must be reported to the Department of Primary Industries and Fisheries.

The cause

There are five herpes viruses that cause disease in horses and donkeys in Australia. Of the equine herpesviruses types 1 to 5, only EHV1 causes outbreaks of abortion. EHV1 is also a common cause of respiratory disease in young horses and has occasionally caused neurological disease with incoordination, paralysis and subsequent death. EHV3 causes equine coital exanthema which is a mild vaginal infection spread venereally. EHV4 is a major cause of respiratory infection (usually called rhinopneumonitis) and EHV2 and EHV5 have been associated with mild respiratory disease. There is no evidence that any of these equine viruses will affect humans.

The signs

Abortion in horses due to EHV1 usually occurs between 7 and 11 months of gestation, and occasionally, as early as 4 months in gestation. The incubation period is highly variable with abortions occurring from 10 days to 12 weeks after virus infection. The mare seldom shows signs of respiratory infection or other illness.

Abortion occurs suddenly with no warning signs and the foetus is expelled sometimes still covered with the placenta.

Mares infected late in pregnancy may have a live foal that may be weak, jaundiced and have difficulty breathing, seldom surviving more than a few days.

Sources of infection

EHV1 virus is endemic in Australia. It is one of the common causes of 'colds' in young horses and most have antibodies to it by the time they are 2-3 years old. Older horses seldom show clinical signs of infection. Once infected, horses carry the virus for life and when they are stressed, the virus is reactivated and excreted.

It is unclear whether there is a separate strain of EHV1 virus that causes abortion or whether there is only one strain which, for some unknown reason, moves beyond the respiratory system.

Infection leading to both respiratory disease and abortion occurs mainly by inhalation but also by ingestion. The aborted foetus, foetal membranes and fluids and uterine discharges from the mare contain large amounts of infective virus. Nasal and eye discharges and aerosols from the respiratory tract of a mare that has aborted, clinically affected young horses and carrier horses are also sources of virus infection. Virus contamination of pasture, feed, feed bins, halters, rugs, bedding, transport vehicles and staff clothing can lead to infection. Weak EHV1 infected foals can be a source of infection to other foals that were born healthy.

After aborting, the virus in the mare's genital tract disappears in a few days, but she may shed virus through the respiratory route for up to 2 weeks. Virus may remain infective in the environment and on horse hair for up to 2 weeks in cool moist conditions if cleaning and disinfection are not adequate.

Actions if an aborted foal is found

Until the cause of the abortion is known, it is prudent to take action to reduce the potential risk of spread of EHV1 infection to mares in close contact with the aborted mare. Initial measures are:

* Isolate the aborted mare from contact with all other horses
* Leave her halter and lead rope with her in quarantine
* Call your veterinary surgeon
* Wear gloves to pick up the foetus and placenta and put it in a strong plastic bag
* Keep the foetus and placenta cool (not frozen) for the veterinarian to examine and to preserve it until it, or samples from it, can be sent to the laboratory
* If pasture has been contaminated with foetal fluids, the area should be treated with lime and fenced off

Anyone who has had contact with the aborted mare or the foetus or placenta should

* Disinfect hands and boots with a good surface disinfectant e.g. iodophors (Iovone Scrub), hexachlorophenes (Hibitane, or other chlorhexidine disinfectant) or phenols (Polyphen Polyphenolic Microbiocide)
* Shower and change clothes. Washing and sun drying clothes will effectively kill the virus
* Disinfect the vehicle used to transport the aborted mare to quarantine (inside and wheels) and anything that has come in contact with the foetus or foetal fluids or discharge from the mare
* Keep the mare completely isolated until a diagnosis has been made. If possible avoid entering the quarantine yard at all or use a 5% formalin footbath outside the yard to disinfect footwear
* Provide the quarantined mare with her own feed bin and other equipment and do not use them for any other horse
* The quarantined mare should be cared for by someone who does not work with other horses or who disinfects, showers and changes before they do

Treatment if EHV1 is confirmed

There is no specific treatment for EHV1 infection in mares. Most foals infected with EHV1 before birth succumb within a few days despite nursing and antibiotic administration.

Management if EHV1 is confirmed

* The aborted mare must be isolated for at least 30 days. After that (provided there are no further abortions) she can be treated as a dry mare and bred.
* In contact pregnant mares should be isolated until they foal and for 30 days after foaling or if another mare aborts, 30 days after the last abortion
* In contact mares include those in the same paddock as the aborted foetus and those in direct contact with the mares in the same paddock e.g. sharing a water trough or in direct contact over a single fence line
* Consult your veterinarian about a vaccination program. A combined EHV1/EHV4 vaccine (Duvaxyn EHV 1,4) is available. While this does not induce total immunity to these viruses, it may prevent some abortions and it will reduce the risk of spread of infection.
* Communication with other stud farms is essential. Simple precautions will reduce the risk of disease spread to other farms and minimise disruption to horse movements usual during the stud season.

Where there is only one case of abortion and the mare has been rigorously isolated and thorough disinfection has occurred, there is minimal risk of spread of infection and the management of the unexposed mares can continue as normal.

The long term prospects for the mare that aborted are good. Her conception rate is not adversely affected and it is rare her to abort again due to EHV1.

Preventative management

Disease introduction can be prevented and disease spread restricted by good management practices such as the following:

* Keep weanlings and yearlings and non-breeding stock in a separate part of the farm with their own facilities and staff
* Separate pregnant mares from non-pregnant mares and from mares with foals
* Keep resident mares separated from mares visiting only for the stud season
* Isolate visiting mares on arrival at stud for 3-4 weeks. Keep them in small groups of 2 or 3 which can be combined if they remain disease free
* Minimise stress factors for pregnant mares such as overcrowding and transport in the last 2 months of gestation and provide access to good quality feed and ensure adequate parasite control
* Establish isolation and quarantine facilities and equip it with gloves, plastic bags, disinfectant etc.
* Clean and disinfect horse floats after each journey
* Train staff so they understand about quarantine and the principles of preventing disease spread
* Keep accurate records of mares (e.g. date of arrival, where from, previous stud details) and of movements of horses on the farm. These are essential for identifying the source of infection
* Vaccination of pregnant mares in the 5th, 7th and 9th months of pregnancy will help reduce the risk of abortion

Contagious Equine Metritis

Introduction

CEM is a venereally transmitted bacterial disease of horses. CEM was first reported in the UK in 1977. CEM still occurs in a number of other EU countries, including the Scandinavia countries, as well as in Morocco and Japan.

The following Code of Practice is reproduced by permission of the Horserace Betting Levy Board.

What are the causative agents of CEM?

Three species of bacteria are recognised as liable to cause outbreaks of infectious reproductive disease in the horse:

• Taylorella equigenitalis (the CEM Organism, or the CEMO)
• Klebsiella pneumoniae
• Pseudomonas aeruginosa

Infection with these bacteria can be highly contagious.

How does infection spread?

Infection spreads through direct transmission of bacteria from mare to stallion or teaser or from stallion or teaser to mare at the time of mating or teasing. It is also transmitted to mares if semen used in artifical insemination (AI) comes from infected stallions.

Indirect infection also occurs, for example:

• through contaminated water, utensils and instruments
• on the hands of staff and veterinary surgeons who handle the tail and genital area of the mare, or the penis of the stallion or teaser
• genital to genital or nose to genital contact between stallions/teasers and mares

Indirect infection is a significant risk for the transmission of the CEMO, and of Klebsiella pneumoniae and Pseudomonas aeruginosa between horses.

What are the clinical signs?

In the mare, the severity of disease caused by the CEMO varies. The main outward clinical sign is a discharge from the vulva, resulting from inflammation of the uterus, usually 1 to 6 days after infection at mating. There are 3 states of infection:

In the acute state, there is active inflammation and obvious discharge, seen 1-6 days after infection at mating.

In the chronic state, the signs may be less obvious but the infection is often deep seated and may be difficult to clear. Discharge may not be seen for up to 80 days after infection.

There is also the carrier state. The bacteria have become established as part of the bacterial flora in the genital areas and there are no signs of infection. However, the mare is still infectious.

Infected stallions and teasers are usually passive carriers, meaning that they do not show clinical signs of infection but have the bacteria colonised as part of the flora on their external genital organs. Stallions pass the bacteria on to mares during mating. Bacteria may also pass to mares, directly or indirectly, from infected teasers.

Although internal spread in the male is rare, the bacteria may occasionally invade the urethra and sex glands, causing pus and bacteria to contaminate the semen.

How is infection prevented and controlled?

You are advised to consult the Industry Common Code of Practice for the Prevention and Control of CEM.

The main ways of preventing infection are:

• check stallions, teasers and mares for infection before they are mated: this is done through swabbing
• if a horse proves to be infected, do not use it for mating until the infection has been successfully treated
• always exercise strict hygiene measures when handling mares, stallions and teasers
  
  The main ways of stopping the spread of infection if it does occur are to:
• stop mating by the infected horse(s)
• treat the infection and re-swab to check that the infection has cleared up before resuming mating
• exercise strict hygiene measures when handling the horses involved

NB: For non-Thoroughbreds, Artificial Insemination (AI) is a useful disease control measure. However, mare owners should only use semen collected from stallions proven free of infection at the time of semen collection.

CEM is a notifiable disease

In the UK, isolation of the CEM organism is notifiable by law, meaning that a suspicion or isolation of the organism must be reported to a Divisional Veterinary Manager (DVM) of the Department for Environment, Food and Rural Affairs (Defra).

This is a statutory requirement under the Infectious Diseases of Horses Order 1987. Copies of the Order (reference: 1987 No. 790) are obtainable from HMSO.

Hygiene

Owing to the risk of indirect infection, stud staff should be made aware that CEM, and disease caused by Klebsiella pneumoniae and Pseudomonas aeruginosa can be highly contagious. Staff should wear disposable gloves at all times when handling the genitalia of mares and stallions/teasers, and should change gloves between each horse.

Separate utensils should be used for each stallion/teaser.

If mares are infected when pregnant or foaling, hygiene is very important to prevent the transmission of infection through contaminated utensils or discharges from the mare.

Further information is available in Equine Veterinary Education 1996 Volume 8 (3) 166-170.

Controlling infection-recommendations

When infection is suspected or confirmed, mating, teasing, collection and insemination of semen must cease until treatment has taken place under veterinary direction and subsequent swabbing has proved that the infection has cleared up. The first swabs should be taken 7 or more days after the treatment has ended. Repeat clitoral and penile swabs should subsequently be taken at intervals of 7 or more days. Repeat endometrial swabs should ideally be collected during the next 3 oestrous periods.

In countries where CEM is notifiable, the government must be informed (for the UK, see Section 5 above). You should also inform your breeders' association.

If the CEM organism is suspected or confirmed in mares, stallions or teasers before mating, teasing or AI:
a. Seek veterinary advice and notify the Divisional Veterinary Manager (DVM) of Defra immediately.
b. Isolate the mares, stallions or teasers and treat as advised by the veterinary surgeon.

If the CEM organism is suspected or confirmed in mares, stallions or teasers after mating, teasing or AI:

• Seek veterinary advice and notify the DVM of Defra immediately.
• Stop mating/teasing and collecting and inseminating semen from the stallion/teaser.
• Isolate and treat the stallion/teaser under veterinary direction.
• Isolate and treat the infected mares as advised by the veterinary surgeon.
• Check and deal with any other mares implicated in the outbreak as advised by the veterinary surgeon; this may include blood tests.
• Notify all owners of mares booked to the stallion, including any which have already left the stud.
• Notify people to whom semen from the stallion has been sent.
• Notify the breeders' association.
• Do not resume mating, teasing or collecting and inseminating semen from the stallion/teaser until negative results from 3 full post-treatment sets of swabs have been obtained.
• Thereafter, the first 3 mares mated to him should be swabbed 3 times at intervals of at least 7 days.

Classical Swine Fever

Definition

Classical swine fever (CSF) is a highly contagious viral disease of pigs. In its acute form the disease generally results in high morbidity and mortality.

History and spread of the disease in Great Britain

CSF was first confirmed in this country in 1864 and was initially allowed to spread unchecked until 1878, when legislation for its control was introduced. The disease persisted for many years until it was finally eradicated from Great Britain in 1966 (see below for details of outbreaks). Since then there have been sporadic outbreaks in 1971 and 1986.

A more serious outbreak in East Anglia in 2000 affected 16 farms. A total of 74,793 pigs including those on contact farms were slaughtered to eradicate the disease. The cause of this most recent outbreak was not finally established but was most likely the result of pigs eating a contaminated imported pork product.

Clinical signs

The symptoms of CSF and African swine fever (ASF) are almost identical and either may occur in chronic or acute form. Laboratory diagnosis is necessary to distinguish CSF from ASF. The incubation period for CSF is variable but is usually between five and ten days. In the acute form pigs develop a high temperature (40.5 degrees C or 105 degrees F), then become dull and go off their food. Other symptoms seen can vary but will include some or all of the following:

• Constipation followed by diarrhoea
• Gummed-up eyes
• Coughing
• Blotchy discolouration of the skin
• Abortion, still births and weak litters
• Weakness of hindquarters.
• Nervous signs including convulsions and tremors in new born piglets.

Differential diagnosis

• African swine fever
• Infection with bovine viral diarrhoea virus
• Salmonellosis
• Erysipelas
• Acute pasteurellosis
• Other viral encephalomyelitis
• Streptococcosis
• Leptospirosis
• Coumarin poisoning
• Porcine Dermatitis and Neopathy Syndrome (PDNS)

How is this disease spread?

The main source of CSF appears to be from pigs eating infected pork or pork products. In this form the CSF virus can remain active for many months.

The movement of infected pigs is a common method of spreading CSF. Apparently healthy pigs may be incubating disease and recovered pigs can excrete the virus for long periods of time.

The virus can exist outside the pig for a long time, so the movement of contaminated vehicles, clothing, footwear and equipment can also spread disease.

Vaccination

Vaccination would not normally be considered as a control measure in the current CSF control strategy. CSF vaccination is restricted by legislation which states that no person shall administer a CSF vaccine to any pig unless authorised to do so by the Secretary of State.

It is possible that vaccination might be used in areas of very high pig density to prevent the occurrence of unrecognised infection in such areas during a prolonged epidemic.

There are currently no operational arrangements in place to mount a widescale CSF emergency vaccination programme in the event of an outbreak in Great Britain.

Brucellosis

What is brucellosis?

Brucellosis is an infectious disease caused by the bacteria of the genus Brucella. These bacteria are primarily passed among animals, and they cause disease in many different vertebrates. Various Brucella species affect sheep, goats, cattle, deer, elk, pigs, dogs, and several other animals. Humans become infected by coming in contact with animals or animal products that are contaminated with these bacteria. In humans brucellosis can cause a range of symptoms that are similar to the flu and may include fever, sweats, headaches, back pains, and physical weakness. Severe infections of the central nervous systems or lining of the heart may occur. Brucellosis can also cause long-lasting or chronic symptoms that include recurrent fevers, joint pain, and fatigue.

How common is brucellosis?

Brucellosis is not very common in the United States, where100 to 200 cases occur each year. But brucellosis can be very common in countries where animal disease control programs have not reduced the amount of disease among animals.

Where is brucellosis usually found?

Although brucellosis can be found worldwide, it is more common in countries that do not have good standardized and effective public health and domestic animal health programs. Areas currently listed as high risk are the Mediterranean Basin (Portugal, Spain, Southern France, Italy, Greece, Turkey, North Africa), South and Central America, Eastern Europe, Asia, Africa, the Caribbean, and the Middle East. Unpasteurized cheeses, sometimes called "village cheeses," from these areas may represent a particular risk for tourists.

How is brucellosis transmitted to humans, and who is likely to become infected?

Humans are generally infected in one of three ways: eating or drinking something that is contaminated with Brucella, breathing in the organism (inhalation), or having the bacteria enter the body through skin wounds. The most common way to be infected is by eating or drinking contaminated milk products. When sheep, goats, cows, or camels are infected, their milk is contaminated with the bacteria. If the milk is not pasteurized, these bacteria can be transmitted to persons who drink the milk or eat cheeses made it. Inhalation of Brucella organisms is not a common route of infection, but it can be a significant hazard for people in certain occupations, such as those working in laboratories where the organism is cultured. Inhalation is often responsible for a significant percentage of cases in abattoir employees. Contamination of skin wounds may be a problem for persons working in slaughterhouses or meat packing plants or for veterinarians. Hunters may be infected through skin wounds or by accidentally ingesting the bacteria after cleaning deer, elk, moose, or wild pigs that they have killed.

Can brucellosis be spread from person to person?

Direct person-to-person spread of brucellosis is extremely rare. Mothers who are breast-feeding may transmit the infection to their infants. Sexual transmission has also been reported. For both sexual and breast-feeding transmission, if the infant or person at risk is treated for brucellosis, their risk of becoming infected will probably be eliminated within 3 days. Although uncommon, transmission may also occur via contaminated tissue transplantation.

Is there a way to prevent infection?

Yes. Do not consume unpasteurized milk, cheese, or ice cream while traveling. If you are not sure that the dairy product is pasteurized, don't eat it. Hunters and animal herdsman should use rubber gloves when handling viscera of animals. There is no vaccine available for humans.

My dog has been diagnosed with brucellosis. Is that a risk for me?

B. canis is the species of Brucella species that can infect dogs. This species has occasionally been transmitted to humans, but the vast majority of dog infections do not result in human illness. Although veterinarians exposed to blood of infected animals are at risk, pet owners are not considered to be at risk for infection. This is partly because it is unlikely that they will come in contact with blood, semen, or placenta of the dog. The bacteria may be cleared from the animal within a few days of treatment; however re-infection is common and some animal body fluids may be infectious for weeks. Immunocompromised persons (cancer patients, HIV-infected individuals, or transplantation patients) should not handle dogs known to be infected with B. canis.

How is brucellosis diagnosed?

Brucellosis is diagnosed in a laboratory by finding Brucella organisms in samples of blood or bone marrow. Also, blood tests can be done to detect antibodies against the bacteria. If this method is used, two blood samples should be collected 2 weeks apart.

Is there a treatment for brucellosis?

Yes, but treatment can be difficult. Doctors can prescribe effective antibiotics. Usually, doxycycline and rifampin are used in combination for 6 weeks to prevent reoccuring infection. Depending on the timing of treatment and severity of illness, recovery may take a few weeks to several months. Mortality is low (<2%),>

Bovine Spongiform Encephalopathy

Bovine Spongiform Encephalopathy (BSE) is one variety of a group of diseases known as "Transmissible Spongiform Encephalopathies" (TSEs). TSEs cause microscopic holes in the brain, giving it a sponge-like appearance under a microscope. TSEs are always fatal and affect both humans and animals.

BSE is the type of TSE that occurs in cattle. Scientists believe cattle are infected when they eat feed that contains remnants of infected animals. FDA has feed rules to prevent the spread of BSE.

The most common human TSE is Creutzfeldt-Jakob disease (CJD). Scientists believe a new variant form of CJD is caused by consuming the brain and spinal cord of animals infected with BSE.

Chronic Wasting Disease

Chronic Wasting Disease (CWD) is a transmissible spongiform encephalopathy (TSE) affecting elk and deer (cervids) as well as moose, in North America.

This degenerative neurological illness has affected both farmed and wild cervids in the US, thus impacting the hunting and wildlife industries as well as domestic and international markets for farmed cervids and cervid products. APHIS' response to this disease includes support of surveillance in both farmed and wild populations and assistance to State agencies for quarantine of affected animals and premises, humane euthanasia, and testing affected and exposed animals. In addition APHIS provides indemnity to animal owners for the value of positive and exposed animals euthanized in disease control efforts. A Herd Certification Program (HCP) is being developed by APHIS in coordination with states, the farmed cervid industry, and the US Animal Health Association (USAHA) to support this effort. APHIS also has assisted, and continues to assist, States with CWD surveillance and management in wild cervid populations. Finally, APHIS is working with the US Department of Interior, Tribes, and States to implement an interagency, national plan to help manage CWD in captive and wild cervids. For more detailed information on CWD and APHIS response, read the fact sheets listed above. See also the VS approach to free-ranging wildlife.

CWD Diagnostics

The "gold standard" diagnostic test for CWD is the Immunohistochemistry (IHC) test performed on the obex tissue of the brain (right) or specific lymphoid tissues.

IHC testing is a method utilizing antibody based staining which is evaluated using light microscopy. This test is both sensitive and specific. In addition, the microscopic methods used to detect positive staining also allow confimation that the correct tissue and location within the tissue are present to detect the earliest accumulations of the prion agent. Other diagnostic tests utilizing enzyme-linked immunosorbent assay (ELISA) and other technologies that allow more rapid testing of larger numbers of samples have been, and continue to be, developed. Several test kits using ELISA and other technologies have recently been licensed by USDA's Center for Veterinary Biologics for CWD diagnosis in wild elk and deer. CWD testing can only be performed by approved laboratories that are part of the USDA Contract Laboratory system. A tonsillar biopsy (live-animal) test has been developed by researchers in Colorado and appears promising for certain CWD disease control or management situations. This technique utilizes the current IHC testing technologies described above.

Click here to view a map (pdf 48kb) showing the locations of the 26 USDA Contract laboratories for CWD, or view the National Veterinary Services Laboratories listing of laboratories and contact points.

Interagency National Plan

The Management Plan for Assisting States, Federal Agencies, and Tribes in Managing Chronic Wasting Disease (CWD) in Wild and Captive Cervids was developed by a task force including USDA, the US Department of Interior, Tribal, and State representatives at the request of Congress. This plan establishes a coordinated approach to performing research and management actions and for sharing information across geographic boundaries and agency jurisdictions. It includes information on communications, scientific and technical information dissemination, diagnostics, disease management, research, and surveillance. To read the Management

Bluetongue Disease Information

Disease and Cause

Bluetongue is an insect-borne, viral disease primarily of sheep, occasionally goats and deer and, very rarely, cattle. The disease is non-contagious and is only transmitted by insect vectors. The disease is caused by a virus belonging to the family Reoviridae.

Species Affected

Primarily a disease of sheep but other species such as goats, cattle, buffaloes, camels, antelopes and deer can be infected. Humans are not infected.

Distribution

The virus is present in most countries of Africa, the Middle East, India, China, the United States, and Mexico. Bluetongue virus infection, without associated clinical disease, is present in Southeast Asia, Papua New Guinea, northern South America and northern Australia.

Key Signs

The disease is characterized by fever, widespread haemorrhages of the oral and nasal tissue, excessive salivation, and nasal discharge. In acute cases the lips and tongue become swollen and this swelling may extend below the lower jaw. Lameness, due to swelling of the cuticle above the hoofs and emaciation, due to reduced feed consumption because of painful inflamed mouths, may also be symptoms of this disease. The blue tongue that gives the disease its name occurs only in a small number of cases. Convalescence of surviving sheep is slow. The high fever in sheep results in wool breaks, which adds to production losses.

Spread

The virus cannot be transmitted between susceptible animals without the presence of insect carriers. The incidence and geographical distribution of bluetongue depends on seasonal conditions, the presence of insect vectors, and the availability of the susceptible species of animals. The insect carriers, biting midges, prefer warm, moist conditions and are in their greatest numbers and most active after it rains.

Persistence of the Virus

Bluetongue virus does not survive outside the insect vectors or susceptible hosts. Animal carcases and products such as meat and wool are not a method of spread. Survival of the virus within a location is dependent on whether the vector can over winter in that area.

Control Strategy

1. using a combination of quarantine and movement controls to prevent spread
2. treatments and husbandry procedures to control vectors, reduce transmission and protect susceptible animals
3. tracing and surveillance to determine the extent of virus and vector distribution
4. zoning to define infected and disease-free areas

Avian Influenza

Worldwide, there are many strains of avian influenza (AI) virus that can cause varying amounts of clinical illness in poultry. AI viruses can infect chickens, turkeys, pheasants, quail, ducks, geese and guinea fowl, as well as a wide variety of other birds. Migratory waterfowl have proved to be a natural reservoir for the less infectious strains of the disease known as low-pathogenicity avian influenza.

AI viruses can be classified into low-pathogenicity (LPAI) and high-pathogenicity (HPAI) based on the severity of the illness they cause. HPAI is an extremely infectious and fatal form of the disease that, once established, can spread rapidly from flock to flock. However, some LPAI virus strains are capable of mutating under field conditions into HPAI viruses.

The U.S. Department of Agriculture’s (USDA) Animal and Plant Health Inspection Service (APHIS) works to keep HPAI from becoming established in the U.S. poultry population.

Pet Vaccination

What vaccinations are necessary to keep my pets healthy?

Pets need the following vaccinations to keep them healthy:

Dogs: 6 in 1 vaccination (DHLPP: Distemper, Hepatitis, Leptospirosis, Parainfluenza and Parvovirus) and Bordetella every 12 months. Rabies vaccination every 3 years.

Puppies: 6 in 1 vaccination (DHLPP: Distemper, Hepatitis, Leptospirosis, Parainfluenza and Parvovirus) and Bordetella at eight weeks of age and then once every three to four weeks until the puppy reaches 4 months of age. Then once each year. Rabies vaccination is given at 4 months of age, then again within 12 months, then every 3 years.

Cats: FVRCP (Feline Viral Rhinotracheitis, Calicivirus, Panleukopenia) and Chlamydia every 12 months. Rabies every 1-3 years depending on vaccination.

Kitten: FVRCP (Feline Viral Rhinotracheitis, Calicivirus, Panleukopenia) and Chlamydia at eight weeks of age, then once every 3 to 4 weeks until the kitten reaches 4 months of age. Then once each year. Rabies is due at 4 months, then again within 12 months, then every 1-3 years depending on vaccination.

Seals and sea-lions

Seals, sea-lions and walruses belong to the order Pinnipedia. There are 33 species of pinnipeds, divided into three families. The family Otariidae contains 14 species, including the fur seals and sea-lions. Otariid species are typically more upright when on land, and can move with reasonable agility. The family Phocidae is made up of the 'true seals' and contains 18 species. Unable to 'walk' on land like the otariids, they move in a lunging caterpillar-like motion. The third family, Odobenidae, contains only the walrus.

Seals in Australian Waters

The Australian sea-lion, New Zealand fur seal and Australian fur-seal breed on the coast of the Australian mainland (including Tasmania) and its nearshore islands. The remaining species breed on Antarctic pack-ice or Sub-Antarctic Australian territories, and occasionally haul out on Tasmanian mainland beaches or reefs.
Important Habitat

Important habitat for seals within the Australian jurisdiction comprises:

* breeding colonies of the terrestrial breeding species, Australian sea-lion, New Zealand fur-seal and Australian fur-seal, on the Australian coast;
* breeding colonies of the terrestrially breeding species, Antarctic fur-seal, Sub-Antarctic fur-seal and southern elephant seal, on Sub-Antarctic islands;
* waters adjacent to breeding colonies on the Australian coast and waters adjacent to Sub-Antarctic islands; and
* favoured feeding places of seals.

Diet and breeding

Diet differs between species but usually includes squid and fish and, for Antarctic species, krill. Some seals, like the leopard seal, are known to eat seabirds such as penguins, and even other seals. Seals usually breed on land or on ice, with peak mating and pupping taking place in the summer months for most species. Seal pups become independent from their mothers at ages varying in Australian seals from 10 weeks to about a year and a half in Australian sea-lions.
Threatening Processes

Seals were hunted in Australia in the last century for their meat, oil and fur. By 1820, seal populations had been reduced to remnants. Some breeding colonies, such as the Australian sea-lion colony in Bass Strait, were completely destroyed. Today, all seals are protected in Australia and populations are generally recovering from this over-harvesting.

However, seals may be affected by several human activities including:

* conflict with commercial fishing
* entanglement in fishing gear and other debris
* reduction in food supply
* human disturbance, including tourism, aircraft and vessels
* oil spills and chemical contaminants
* diseases

Seismic survey activity and climate change may potentially impact seals, although little is known about the effects of these at this time.
Legislative Protection

Australia's main piece of conservation legislation is the Environment Protection and Biodiversity Conservation Act 1999 (Australian Government) (the EPBC Act), which came into force on 16 July 2000.

Seals located in all Australian Commonwealth waters are protected under the EPBC Act, and seals located south of 60°S are protected under the Antarctic Treaty (Environment Protection) Act 1980 and associated conventions including the Seals Convention. In addition, seals in Commonwealth marine protected areas that surround the world heritage listed sub Antarctic islands of Macquarie Island, and Heard and Macdonald Islands are also protected under the EPBC Act. Read more information about seal protection under the Antarctic Treaty .

Under the EPBC Act all marine mammals occurring within Australian waters are listed 'Marine' (section 248). It is an offence to kill, injure, take, trade, keep, or move any member of a listed marine species on Australian Government land or in Commonwealth waters without a permit. Where these animals occur in State/Territory waters or on State/Territory land, relevant State /Territory legislation applies.

Three species of seal are listed under the EPBC Act as 'Vulnerable' — the Subantarctic Fur-seal (Arctocephalus tropicalis), the Southern Elephant Seal (Mirounga leonina) and the Australian Sea-lion (Neophoca cinerea) (section 178). In accordance with the EPBC Act, a recovery plan for the Sub-antarctic fur seal and southern elephant seal was made by the Australian Government in 2004. Read the Sub-antarctic fur seal and southern elephant seal recovery plan and a supporting background document.

In addition to the levels of protection afforded to listed 'Marine' and 'Threatened' species, the EPBC Act also requires that any action that has, will have or is likely to have a significant impact on listed species in the threatened or migratory categories must be referred to the Department of the Environment, Water, Heritage and the Arts for assessment — this applies in States and Territories as well as Commonwealth land and waters. Any action that may have a significant impact on a Commonwealth marine area should also be referred for assessment under the EPBC Act. Criteria for considering whether an action impacts on the environment in a Commonwealth marine area includes whether populations of marine species will be substantially adversely affected.

Where to see Seals

There are many places along the coastline of southern Australia where seals can be seen in the wild. Visitors must take a great deal of care not to disturb seals or place themselves in any danger — seals can bite! Some of the best places where organised viewing of seals takes place include Seal Bay on Kangaroo Island, Montague Island on the New South Wales South Coast, Seal Rocks in Victoria, various places in Tasmania and on accessible islands around Perth and Albany in Western Australia.

Water Dragons

Water Dragons in Australia can be up to 1 metre, with long powerful legs and claws. Their tail forms 2/3 of their length and is almost all muscle. It is laterally compressed to help act like an oar when swimming. The Water Dragon has a nuchal crest – a central row of enlarged spikey spines at the back of the head. These spikes continue down the spine, decreasing in size to the base of the tail. At the tail the spines divide into two rows.

The Water Dragon’s upper body is a grey-green with cream and black transverse bands on the body and tail. Underneath the body is creamy brown-grey. They have loose folds of skin under the jaw, giving them an almost Bearded Dragon appearance.

Subspecies differences: The Eastern Water Dragon (Physignathus lesueurii lesueurii) has a dark stripe from ear to eye, that the Gippsland Water Dragon (Physignathus lesueurii howittii) lacks. The Eastern Water Dragon male has a red flush on its chest and darker bands. The Gippsland Water Dragon male has an olive-grey chest, and is distinguished with a colourful throat that is blotched or striped with various colours; orange, blue and yellow.

Sexual and age differences: Juvenile Water Dragons are light brown in colour, with head and feet disproportionately large compared with the adults. The female Water Dragons lack the bright colourations on the chest and throat, and have narrower, more delicate heads. The male Water Dragon’s head is much larger and angular.

photo: Water Dragon
In the Botanic Gardens we have Gippsland Water Dragons, lacking the dark stripe from ear to eye. This is a male.

photo: Swimming Water DragonSwimming: Water Dragons as their name suggests are semi-aquatic lizards. They spend a lot of time perching in trees along creeks and rivers. At any sign of danger they will dive into the water and either remain underwater or swim away. Water Dragons have been known to remain underwater for up to 90 minutes. Water Dragons when underwater slow their heart rate and conduct some gas exchange across their skin, both O2 and CO2.

Running: Water Dragons at slow speeds run on all four legs, but to increase their running speed they can run on their back legs only (bipedally). Their long powerful back legs and sharp claws help in their abilities to climb trees and dig holes for hibernation and nesting.

Eating: Water Dragons are omnivorous (eat both plant and animal matter). They generally feed on insects, frogs, yabbies, other aquatic organisms, fruits, berries and flowers. They can eat under water. There has been recorded incidents of cannibalism occurring to young hatchlings

Mountain Lion

Mountain lions are quiet, solitary and elusive, and typically avoid people.

Mountain lion attacks on humans are extremely rare. However, conflicts are increasing as California’s human population expands into mountain lion habitat.

* Do not hike, bike, or jog alone.
* Avoid hiking or jogging when mountain lions are most active—dawn, dusk, and at night.
* Keep a close watch on small children.
* Do not approach a mountain lion.
* If you encounter a mountain lion, do not run; instead, face the animal, make noise and try to look bigger by waving your arms; throw rocks or other objects. Pick up small children.
* If attacked, fight back.
*

Scrapie Disease

Goats with scrapie sometime present with a hunched back and raised tail giving the appearance of back pain.

Scrapie is a fatal, degenerative disease affecting the central nervous system of sheep and goats. It is among a number of diseases classified as transmissible spongiform encephalopathies (TSE). Infected flocks that contain a high percentage of susceptible animals can experience significant production losses. Over a period of several years the number of infected animals increases, and the age at onset of clinical signs decreases making these flocks economically unviable. Animals sold from infected flocks spread scrapie to other flocks.

The presence of scrapie in the United States also prevents the export of breeding stock, semen, and embryos to many other countries. TSEs are the subject of increased attention and concern because of the discovery of bovine spongiform encephalopathy (BSE) in cattle, the link between BSE and variant Creutzfeldt-Jakob disease (vCJD) in people, and feline spongiform encephalopathy (FSE) in cats in Europe. See Factsheet for more detail.

Animal Diseases

Each of the links below shows relevant animal health information for that disease, including disease information related to conditions that APHIS is working to manage:

Avian influenza
Bluetongue
Bovine spongiform encephalopathy
Brucellosis
Chronic wasting disease
Classical swine fever
Contagious equine metritis
Equine herpesvirus
Equine infectious anemia
Equine piroplasmosis
Equine viral arteritis
Piroplasmosis
Pseudorabies
Scrapie
Spring viremia carp
Tuberculosis
Venezuelan equine encephalomyelitis
Vesicular stomatitis
West Nile virus

Refer: http://www.aphis.usda.gov/animal_health/animal_diseases/