Australia is currently free of many major diseases which cause significant agricultural losses in different parts of the world. Should any of these enter Australia they have the potential to cause significant damage here as well. While entry of exotic disease to Australia could be accidental, there is a distinct possibility in the future that nefarious activity could take place. Australia has in place a broad range of systems to reduce the likelihood of diseased but early recognition of outbreaks will remain of paramount importance. In New South Wales, the role of the District Veterinarian is critical. Not only is it important that we recognise endemic diseases to minimise loss to individual producers but that we have the necessary skills to recognise the unusual and call in the specialists.
Rift Valley fever (RVF), East Coast fever (ECF) and classical swine fever (CSF) are three diseases with differing epidemiology and disease attributes which might be introduced into Australia. This paper aims to provide a summary of these diseases. More complete information can be acquired from AUSVETPLAN and the OIE Terrestrial Animal Health Code.
This peracute or acute disease of domestic ruminants is caused by a Phlebovirus, family Bunyaviridae, and considered one of the most important exotic zoonoses. There is only one serotype but strains of differing virulence exist. Bunyaviruses are enveloped single-stranded RNA viruses, the envelope being a lipid with two glycoproteins - G(N) and G(C). After entry into a cell the virus delivers its genome into host-cell cytoplasm by fusing their envelope with an endosomal membrane.
RVF was first reported in livestock in Kenya 1915 but the virus only identified in 1931. Currently the disease is endemic in tropical regions of eastern and southern Africa but outbreaks have occurred in western Africa and Arabian peninsula.
The disease is spread by contact with the tissue of infected animals as well as mosquitoes. Known vectors are Culex tritaeniorhyncus and Aedes vexans but other species being possibilities – Anopheles, Eretmopodites, Mansonia and others. The virus has been isolated from two bat species which are believed to be reservoir hosts - Peter’s epauletted fruit bat (Micropteropus pusillus) and the aba roundleaf bat (Hipposideros abae). African monkeys and domestic carnivores show a transitory viraemia.
In endemic areas, the disease circulates among ruminants and mosquitoes with inapparent infection. Rain allows explosive hatching of mosquito eggs, many harbouring RVF. Precipitation cycles of 5 – 25 years create both animal and human populations that are immune-naïve with respect to RVF, thus allowing outbreaks involving multiple vector species. To-date no human-human spread has been identified, the majority of human infections result from handling infected animals, especially nasal and vaginal discharges, and meat.
Diagnosis of RVF
The severity of disease varies with species and age. Lambs, kids, puppies and kittens are 'Extremely Susceptible' with mortalities of 70-100%; calves and sheep are 'Highly Susceptible' with mortalities between 20-70%, while cattle and goats are 'Moderately Susceptible'. Mortalities among humans are normally less than 10% while camels, equids, pigs and rabbits are considered resistant.
Young and highly susceptible animals will show a fever (40-41°C) with inappetence, depression and weakness, lachrymation and oro-nasal discharges, bloody or foetid diarrhoea and icterus. Abortion rates may reach 100%, especially in sheep. Lambs usually die within 24-36 hours after showing colic.
People have an influenza-like syndrome – fever (3.8 - 40°C) with headache, muscular pains and photophobia which usually settles after 4-7 days but complications can occur which include meningo-encephalitis, jaundice and death, inter al.
Heparinised or clotted blood (plasma or serum) and tissue samples from liver, spleen, kidney, lymph nodes and brain (both chilled and fomalised) are needed for laboratory diagnosis.
These include, but are not limited to:
Treatment and control
There is no specific treatment but vaccines are available for livestock and people.
East coast fever, an acute disease of cattle, is the single largest cause of mortality and lost production (over 1 million head per annum) in 13 countries of sub-Saharan eastern and central Africa. Caused by Theileria parva - along with Corridor disease and January disease — it is not a zoonosis but is usually characterised by high fever, swelling of the lymph nodes, dyspnoea, and high mortality. Theileria are obligate intracellular protozoan parasites that infect both wild and domestic Bovidae and are spread by ticks. Their complex life-cycle requires both vertebrate and invertebrate hosts.
The T. parva parasite is transmitted by the tick vector, Rhipicephalus appendiculatus, so disease occurrence is limited to its geographic distribution.
Theileria annulata causes tropical theileriosis in large areas of the Mediterranean coast, extending to northern Sudan, southern Europe and across the Middle East to India, China and central Asia. It is transmitted by several species of ticks of the genus Hyalomma.
The endemic regions of T. parva and T. annulata do not overlap because of the separate distribution of their vectors.
The infective sporozoite stage of T. parva is transmitted in the saliva of infected R. appendiculatus, the brown ear tick, as they feed. Sporozoites invade bovine leucocytes (WBCs) and, within a few days, develop to schizonts. T. parva multiplication occurs predominantly within the host WBCs (less pathogenic species like the endemic T. orientalis of Australia) multiply mainly in RBCs. Development of the schizont stage causes the host WBC to divide; at each cell division, the parasite also divides. Thus, the parasitized cell population expands and, through migration, becomes disseminated throughout the lymphoid system. Later in the infection, some of the schizonts undergo merogony, releasing merozoites that infect RBCs, giving rise to piroplasms. Uptake of piroplasm-infected RBCs by vector ticks feeding on infected animals is the prelude to a complex cycle of development, culminating in transmission of infection by ticks feeding in their next instar (trans-stadial transmission).
The African buffalo (Syncerus caffer) is an important asymptomatic wildlife reservoir of T. parva.
After inoculation of T parva sporozoites, an occult phase of 5–10 days follows before infected lymphocytes can be detected in Giemsa-stained smears of cells aspirated from the local draining lymph node. Subsequently, the number of parasitized cells increases rapidly throughout the lymphoid system, and from about day 14 onward, cells undergoing merogony are observed. This is associated with widespread lymphocytolysis, marked lymphoid depletion and leukopenia. Piroplasms in RBCs infected by the resultant merozoites assume various forms, but typically they are small and rod-shaped or oval.
Diagnosis of ECF
Clinical signs vary according to the level of challenge, and range from inapparent, through mild or severe to fatal. The incubation period is generally about 15 days from the time of attachment of the infected tick, but may range from eight to 25 days. Fever continues throughout the course of infection, and may be >106°F (41°C) with increases in pulse and respiration rates. Initially parotid lymph node swelling reflects the sites of inoculation (the ears) and then becomes more pronounced and generalized - the prescapular and precrural nodes become very prominent.
Anorexia and lachrymation commonly occur together with oedema of the eyelids and this may be accompanied by photophobia. The animal is often constipated.
Lymphoblasts in Giemsa-stained smears of needle aspirates from lymph nodes contain multinuclear schizonts. Anorexia develops, and the animal rapidly loses condition; lacrimation and nasal discharge may occur with evidence of pulmonary oedema and hydropericardium. Terminally, dyspnoea is common. Just before death, a sharp decrease in body temperature is usual and pulmonary exudate pours from the nostrils. Death usually occurs 18–24 days after infection. The most striking post mortem lesions are lymph node enlargement and massive pulmonary oedema and hyperaemia. Haemorrhages are common on the serosal and mucosal surfaces of many organs, sometimes together with obvious areas of necrosis in the lymph nodes and thymus. With little division of the parasites in RBCs and no massive destruction, anaemia and icterus are not regular diagnostic signs.
The disease usually progresses over a period of about 15 days, but may terminate after five days or be prolonged to 25 days. Appetite and rumination become increasingly depressed and there is a severe loss of body condition, increasing weakness and ataxia, progressing to recumbency. Constipation is succeeded by diarrhoea and there may be blood and mucus in the faeces. Opacity of the cornea may develop and petechiae may be detected in the mucous membranes, especially beneath the tongue and in the vulva. Pregnant cows may abort.
A small number of animals, usually about five per cent, may recover, but convalescence is prolonged and the animals may remain emaciated and unproductive for months
These include but are not limited to:
Babesiosis, anaplasosis, bovine virus diarrhoea/mucosal disease and bovine malignant catarrhal fever and enzootic bovine leucosis.
Classical swine fever (CSF) is a highly contagious, often fatal, viral disease of pigs clinically characterized by high body temperature, lethargy, yellowish diarrhoea, vomiting and a purple skin discoloration of the ears, lower abdomen and legs.
CSF has the potential to cause devastating epidemics, particularly in countries free of the disease, and so outbreaks are notifiable to the OIE because of their severe economic impact. There have been several historical outbreaks in Australia that have been eradicated with no outbreaks since 1961. Australia is now internationally recognised as free of classical swine fever.
Hog cholera was first described in the early 19th century in the USA after which a condition in Europe termed ‘swine fever’ was recognized to be the same disease. Both names continue to be used, although in most of the world the disease is now called classical swine fever (CSF) to distinguish it from African swine fever which is a clinically indistinguishable disease but caused by an unrelated DNA virus.
CSF is caused by a small, enveloped RNA virus in the genus Pestivirus of the family Flaviviridae, that naturally infects domestic and wild pigs. CSFV is antigenically related to other pestiviruses, especially bovine viral diarrhoea virus (BVDV) and to border disease virus of sheep. These viruses are prevalent in bovine and ovine populations and can infect pigs. Although infections of pigs with ruminant pestiviruses in most cases do not lead to clinical disease and are rapidly cleared, both infections induce an antibody response in swine. Therefore, antibody discrimination tests must be applied to differentiate CSF infections from infections caused by ruminant pestiviruses. Transmission of ruminant pestiviruses to pigs usually requires direct contact with cattle, sheep, or goats.
Significant amounts of CSFV are shed from infected animals into the environment via the oro-nasal route, particularly early during infection. CSFV is moderately fragile and does not persist in the environment or spread long distances by the airborne route. However, it can survive for prolonged periods in a moist, protein-rich environment such as pork tissues or body fluids, particularly if kept cold or frozen. Virus survival times up to several years have been observed in frozen pork meat. CSFV may also survive months in chilled or cured cuts.
CSF is endemic in much of Central and South America, in the Caribbean basin, in eastern Europe and in many pork-producing countries in Asia. Australia, New Zealand, Canada and the USA are free of the disease, as are most countries of western and central Europe (although sporadic outbreaks occur in Europe). The main source of CSFV infection is the pig, either via infected live animals or via uncooked pork products. The disease spreads through endemic areas by movement of infected animals among farms or to slaughter houses which may lead to widespread outbreaks.
In Europe, CSFV is considered endemic in wild boar populations and infected wild boars are a source of outbreaks among domestic pigs. The most probable source of CSFV infection for wild boars is contaminated waste or even ‘spillover’ from infected domestic pigs. Outbreaks in small populations of wild boars living within natural confines, such as valleys, tend to be self-limiting, and the disease fades away over time; in contrast, outbreaks in large areas densely populated with wild boars often become endemic.
The persistence of CSFV within herds for long periods has been observed. Infections of sows during pregnancy with low to moderately virulent strains of CSFV may lead to in utero infections of foetuses. These infections lead to litters born persistently infected with CSFV that are carriers of the virus and source for new infections. Persistently infected carrier pigs usually show no clinical signs but constantly shed CSFV into the environment. Therefore, it is particularly important to consider CSFV infections while investigating herds presenting with unexplained reproductive failures that include clinical manifestations in piglets such as congenital tremor or congenital abnormalities.
Mechanical transmission by vehicles and equipment, as well as by personnel (notably veterinarians) travelling between pig farms, are also significant means of spread of CSF.
A major risk for CSF outbreaks (especially in Australia) is the introduction of CSFV into herds through illegally imported pork meat or pork products that find their way into the porcine food chain. Although, CSFV is readily inactivated by heat (i.e. cooking), swill feeding is banned here. Feral pigs could easily take the place of wild boar in the maintenance of endemic disease.
Awareness and vigilance are essential, so that outbreaks are detected early and control measures instituted rapidly to prevent severe consequences for the swine industry
Diagnosis of CSF
CSF is characterized by fever, haemorrhages, ataxia, and purple discoloration of the skin; however, the clinical presentation varies, depending on host characteristics and the particular virus strain causing the infection. CSF occurs in several forms, including highly lethal, acute, chronic, or subclinical.
Acute forms of CSF, associated with highly virulent CSFV strains, are characterized by an incubation period that is typically 3–7 days, with death occurring within 10 days after infection. Fever >41°C (105.8°F) is usually seen and persists until terminal stages of the disease when body temperature drops and becomes subnormal. Constipation followed by diarrhoea and vomiting is common.
The principal lesion produced by CSFV infection is a generalized vasculitis, clinically manifested as haemorrhages and cyanosis of the skin, notably at the ears, lower abdomen, and extremities. There may also be a generalized skin erythema. Vasculitis in the CNS leads to incoordination or even convulsions. Histologically, non-suppurative encephalitis with a characteristic vascular cuffing is common.
At post mortem, the principal findings are widespread petechial and ecchymotic haemorrhages, especially in lymph nodes (e.g. mandibular and retropharyngeal), tonsils, larynx, kidneys, spleen, urinary bladder, and ileum. Infarction may be seen, particularly in the periphery of the spleen.
Subacute and chronic forms of the disease are also characterized by high fever, staggering gait, cough, diarrhoea, purple discoloration of the skin, and death. In the subacute form, death generally happens within 20–30 days after infection but in the chronic form, death may occur much later. Subacute and chronic forms of the disease are associated with CSFV strains of moderate to low virulence, respectively.
Low virulence strains can be difficult to detect; the only clinical expression may be poor reproductive performance of sows and the birth of piglets with neurologic defects (e.g. congenital tremor). In chronic forms of CSF after an initial acute febrile phase, infected animals may show an apparent recovery but then relapse with anorexia, depression, fever and progressive weight loss. Macroscopically, in addition to the lesions described above, ‘button’ ulcers may develop in the intestine, particularly near the ileo-caecal junction. Histologically, atrophy of the thymus and depletion of lymphoid follicles in lymph nodes are seen.
Laboratory confirmation is always required to confirm field diagnosis of CSF.
This varies according to the course of the disease but includes, though not limited to
Advice on sample submission should be sought from DPI laboratory specialist as part of notification of exotic diseases with suitable tissues being tonsils, lymph nodes (mandibular, retropharyngeal, gastro-hepatic and mesenteric), spleen, kidney, and ileum. Whole blood collected with EDTA as anticoagulant can be used for virus isolation or virus detection, particularly during the viraemic phase of the infection, while clotted blood samples (serum) are taken for serologic tests to detect CSFV antibodies. Nasal swabs and/or tonsil scrapings are commonly collected clinical samples used to detect the virus
CSF is a notifiable disease with so control is highly regulated with strict sanitary measures. No treatment is available – only culling and pre-emptive slaughter of susceptible animals within determined distances from the focus. Restriction of movement within a well-defined radius from the outbreak is applied to contain spread of the infection in the first instance.
The three diseases discussed reflect different aspects of the problems facing District Veterinarians in the field in the first instance and subsequent control should any of the diseases enter Australia.
Any of the three viruses could easily be introduced into susceptible livestock populations. They would probably cause a severe outbreak in the first instance. However, the ability of the virus to remain in circulation would depend on the speed of detection and the population in which each became established.
Rift Valley fever and East Coast fever both require a vector for significant disease survival. The known vectors are not present in Australia but, were a suitable vector to exist here, the wide variety of habitats in the country would potentially allow the disease to become endemic in the way that T. orientalis has become established.
Were classical swine fever to enter a commercial piggery it is highly likely that it would be soon identified and eradicated. However, if its first arrival were into a hobby-farming or life-style herd, then it might remain undetected for considerably longer and this could allow spill-over into feral pigs or even wider dissemination through uncontrolled 'black-market' sales.
The role of frontline field veterinarians to protect Australia, her agriculture and her way of life from the threats of exotic diseases has rarely been greater. As professionals, we need to be prepared for any eventuality and without undue scare-mongering, need to ensure that our producers, ratepayers and other livestock owners are aware of the need for continued vigilance.