VIP Test 2

Which viruses are in the family Calciviridae

Vesivirus felis (feline calcivirus) and Varicellocirus felidalpha1 (feline herpesvirus)

What is the aetiology for Upper respiratory tract disease?

Vesivirus felis, Varicellovirus felidalpha1, Bordetella bronchiseptica

Where are Chlamydial infections found in cats?

Conjunctivae and oronasal mucosa

How many serotypes are there for each Calciviradae species?

1 serotype for both Vesivirus felis and Varicellovirus felidalpha with multiple strains of each.

What is the epidemiology of Calciviradae?

Worldwide

What are the hosts of Calciviradae?

Domestic and wild felids, believed to be benign in free-range wild felids, not the case in captive wild felids.

How is Varicellovirus felidalpha1 transmitted?

Intimate contact between shedding and susceptible cats. Normal breathing movements do not create an infective aerosol. Sneezing might spread it over a radius a little more than a meter. In optimal conditions V. felidalpha1 can survive for up to 24 hours outside the host in warm climates.

How is Vesivirus felis transmitted?

Direct close contact, and is shed in large quantities through oculonasal discharge and saliva, as well in smaller amounts in urine and faeces. It can remain active outside the host for 8-10 days.

What is the pathogenesis for Varicellovirus felidalpha1?

Replicates primarily in the superficial epithelium of the conjunctivae and the upper respiratory tract, including turbinate mucosa, soft palate, tonsils and trachea. Causing multifocal necrosis with neutrophilic infiltration and inflammation. Spreads along sensory nerves and reaches neurons, primarily in the trigeminal ganglia, which is the main site of latency. Cats are either latently or actively infected. Latent cats do not shed infectious virus. Under stress conditions (rehousing, cat show, transportation, after corticosteroid administration, etc.), the genome is reactivated and shed intermittently through the oropharynx. These cats are especially hazardous within 3 weeks of the event. Offspring of carrier queens can become subclinically infected and can lead to latent infection or active disease.

What is the pathogenesis of Vesivirus felis?

The oropharynx is the primary site of virus replication and induces necrosis of epithelial cells. Vesicles may develop on the margin of the tongue and rapidly become ulcers. Pneumonia is less commonly found. Carriers shed infectious virus through the oropharynx for weeks, months or years after primary infection. Some carriers might have mild conjunctivitis, gingivitis and periodontal disease. Virus shedding ends abruptly and the recovered cat seems resistant to reinfection. The variable capsid protein is what is believed to help V. felis avoid the immune system.

What are the clinical signs for Calciviradae?

The incubation period for V. felidalpha1 infection is 2 - 6 days and for V. felis, 2 - 10 days.

Clinical signs of many viruses overlap and cannot be distinguished clinically. The hallmark for acute URTI in cats is sneezing. Initially intermittent, the severity and frequency increases in the following 2-5 days. Mild serous nasal and/or ocular discharge may be the first detectable signs after sneezing. In kittens, the discharge becomes mucopurulent within 3-5 days due to bacterial colonisation. In untreated cases, anorexia and dehydration may also be seen. Oral ulceration is accompanied by hypersalivation. Mortalities are common in kittens under 6 months and are usually due to malnutrition, dehydration or secondary bacterial pneumonia. Neonatal ophthalmia, acute conjunctivitis, keratoconjunctivitis sicca and ulcerative keratitis with corneal perforation represent the spectrum of ocular disease attributed to herpesvirus infection

What is the pathology of feline viral rhinotracheitis?

Distribution of gross lesions corresponds to the predilection sites for viral replication, namely the epithelium of nasal passages, pharynx, soft palate, conjunctivae, tonsils, and, to a lesser extent, trachea. The initial serous inflammation becomes mucopurulent or fibrinous within a few days. Lethal cases usually have extensive fibrinous rhinotracheitis. Tonsils are enlarged, and in some, petechiae are observed. The regional lymph nodes are also usually enlarged, reddened, and oedematous. Ulcerations of the tongue are rarely seen, as opposed to calicivirus infection. Some cats develop necrosis and resorption of the turbinates. Ocular involvement is usually limited to purulent conjunctivitis but can progress to ulcerative keratitis.

What is the pathology of feline calicivirus infection?

The range and severity of lesions depend on the virulence and tropism of the particular strain and the mode of infection. Ulceration of the oral epithelium is a common finding. Ulcers are often present on the dorsal surface or lateral margins of the tongue and on the hard palate and external nares. Less consistent findings include serous or mucoid rhinitis and conjunctivitis. Lung lesions are characterised by acute to subacute interstitial pneumonia.

How do we diagnose Calciviradae infection?

Infectious agents can be recovered from cats with upper respiratory disease. Persuing a definitive diagnosis is not needed. In URTI treament knowing the cause rarely assists in treatment, history and physical exam is enough. PCR is the prefered method of detection. Positive PCR may show low level shedding or latency, not confirming the symptoms are from Calciviradae. Using real time PCR can help, as high levels in nasal secretion or tears suggest replication. Viral isolation from nasal or conjunctival swabs also diagnose these viruses. V. felis can be detected with 2 oropharyngeal swabs 5 weeks apart. V. felidalpha can be diagnosed with administration of corticosteroids. Carries can be diagnosed with history. Direct antigen detection can be performed with FA conjugates on cells in smears from the conjunctiva or cornea for herpesvirus and cells from the tonsils, tongue, and transtracheal washes for calicivirus. However, the sensitivity of these tests is lower than for virus isolation in cell cultures. Serology is only of use in non vaccinated cats.

How is Calciviridae controlled?

Broad spectrum antibiotic. Cats with oral ulcers should be fed through a nasogastric tube. Herpetic keratitis can be treated with opthalmic antivirals. Vaccines are considered core vaccines. Vaccinated cats may still get infected and be subjected to milk URTI and can shed virus. Boosters every 12 (inactive) /36 (live) months is recommended. Chlamydia felis and Bordetella bronchiseptica are non core but recommended for patient susceptible to URTI. Other methods include: at least 12 air changes per hour in hospital wards and cateries, new cats and kittens may not enter a household until 3 weeks after vaccination, in boarding facilities cats should be kept in separate cages. Treatment of URTI should be outpatients.

What viruses can be found in the Parvoviridae family?

Protoparvovirus carnivoran1 (canine parvovirus/feline panleukopenia virus), Protoparvivirus ungulate1 (porcine parvovirus)

In which cells do parvovirus mutiply?

Actively replicating cells

In which animals is CPV-2 found?

None, all cases have been replaced by antigenic varients known as CPV-2a, CPV-2b and CPV-2c, but it could only infect Canines

What is the epidemiology of CPV-2?

Worldwide distribution.

What are the hosts for CPV-2?

Cats, minks, artic foxes, dogs, raccoons, etc.

What are the host range variants of Feline panleukopenia virus?

CPV-2 which can infect dogs and FPV which infects cats.

How do most cases of CPV in the wild present?

Mild to subclinical, severe lethal cases are the exception.

Which factors can worsen CPV mortality and morbidity?

Dose of the virus, age of the puppies, stress factors, breed, concurrent infection and internal parasitism.

How is CPV transmitted?

Oronasal route

Explain the pathogenesis of CPV.

Route of entry and initial replication are the cells of the nasal- and oropharynx, including the tonsils and otehr lymphoid tissue. It then spreads haematogenically to other lymphoid tissue, increasing vireamia and causing intestinal epithelial infection. The target cells are teh crypt cells, which have a high mitotic index, even higher in growing puppies, thus CPV would replicate better in pups. Young dogs may also present with myocarditis as the myocardium has a high mitotic index in pups youngert han 8 weeks.

Which breeds suffer more from CPV than others?

Rottweilers and Dobermans

Which concurrent infection can be caused by CPV-2?

Intestical infiltration by gut bacteria causing septicemia.

How do lymph nodes look like with CPV infection?

Lack of T and B lymphocytes as CPV can replicate in these cells.

Up until when can virus be isolated from Faeces?

Up until day 9

What are clinical signs of CPV infection?

Listlessness, anarexia, vomiting and/or diarrhoea. Fever is common. In severe cases weakness and dehydration is also seen. Front feet are soiled with vomitus and saliva, the perenium is soiled with yellow to muco-haemorrhagic faeces. In advanced cases cold extremities and cyanosis.

What ages of dogs get CPV more often, and jow long is the incubation period?

6w-6m, 3 days in test but probably a day or 2 longer in nature.

What PM findings can be seen with CPV?

Dehydration, intestinal lumen is usually empty or contains haemorrhagic fluid. Mild Catarrhal to severe necrotic enteritis could be present. Oemeda and hyperplasia of lymph nodes may be seen. If heart failure caused death, pulmonary oedema, hydrothorax, hydropericard, flabby heart with multifocal pale necrotic areas.

How do we diagnose CPV?

History usually reveals acute onset before reaching 6 months of age. Transmission electron microscope of faeces can be used to diagnose CPV. Viral antigen can be found in faecal smears using direct fluorescence antibody test, ELISA and haemagglutination-haemagglutination inhibition tests. Serum antibody test can be done but has little use in such an acute disease.

How is CPV treated?

Fluid and electrolyte replenishment, antibiotics to prevent secondary infection.

How is CPV controlled?

Vaccines have great effect, inactivated, attenuated and heterotypic vaccinesaare available. Hypochloride-based disinfectants are used.

What are the hosts of Feline panluekopenia virus?

Cats, raccoons, minks, artic foxes, honey badger, wildcat, captive cheetah cubs, but not dogs.

What is the distribution of FPV?

Worldwide

How is FPV transmitted?

Between direct contact of infected and susceptible cats. High viral loads are found in acutely infected cat's vomitus, saliva, urine and faeces. The virus us very persistant in the environment.

Explain the pathogenesis of FPV.

After oral or nasal exposure replication in the lympoid tissue of the oropharynx. Systemic infection follows and infect lymph nodes, stem cells and crypts of Lieberkuhn. Lymphoid tissue is highly mitotically active in all ages of cats, thus the spleen, thymus, peyer's patches and lymph nodes become damaged. Mitotically active precursors to leukocytes get destroyed.

Why do gnotobiotic cats have milder infections of FPV?

The bacteria in normal guts cause “physiological inflammation" as they accelerate the loss of absorptive cells. The crypts respond to this loss by increasing in size, increasing the amount of crypt cell mitosis and decreases the generation time of crypt cells. Endotoxaemia may also occur.

How does FPV affect cats in utero or early in life?

Infections in late gestation or in the first 3 weeks of life can destroy the external germinal layer, purkinje cells, and can cause dysplasia of the granule cell layer, causing cerebellar hypoplasia. Hydranenchephaly may also develop.

What are clinical signs of FPV?

Fever, depression, vomiting, diarrhoea and dehydration. Ataxia and tremors are seen in kitten infected in utero or in the first 3 weeks.

What PM changes can be found in FPV?

Intestinal loops are firm and hyperaemic with petechia and ecchymosis on the serosa. Thymic and Cerebellar hypoplasia, hydrocephaly and hydrancephaly found in congenitally and neonatally infected kittens. Older susceptable cats may have catarrhal to necrotic ileitis, oedema of lymph nodes and bone marrow atrophy is also found.

How do we diagnose FPV?

History and clinical signs may be non-specific, viral antigens can be found in faeces through latex agglutination and immunochromatographic tests. PCR-tests on whole blood and faeces.

How is FPV controlled?

Vaccination from 12w. New kittens should not be introduced to a household where FPV has been reported before being vaccinated. 0.5% Formaldehyde or 1:32 hypochlorite solution destroys FPV.

How does Porcine parvovirus effect each gender of pig?

Sows are immune and gilts get infected before they conceive, so develop an active immunity.

What are the routes of transmission for PPV?

Oronasal and transplacental.

What is the major reservoir for PPV?

Contaminated spaces. Persistent carries may also arise if gilts are infected before day 55 of gestation.

What is the pathogenesis of PPV?

The initial replication site is in the upper respiratory tract (oropharynx), from which the virus can be disseminated into intestinal lymphoid tissues, crypt cells, or other sites via the bloodstream, free or in leucocytes. The virus can cross the placental barrier in pregnant sows and infect embryos and foetuses. Apothogenic in adult pigs, may cause stillbirths and mummification of fetuses.

What are the clinical signs of PPV?

Infertility, returning to oestrus, and give birth to not many piglets or a large litter of mummified piglets.

How do we diagnose PPV?

The laboratory diagnosis of PPV in pigs is mainly performed using serology because virus isolation is difficult. The test used most commonly is the haemagglutination-inhibition test. Aborted, stillborn or mummified foetuses can also be tested.

How do we control PPV?

Parvoviruses are extremely stable and infective, and parvovirus-free farms remain uninfected only when high standards of hygiene are practised, and the entry of new stock is restricted. Susceptible gilts should be naturally infected or vaccinated before they are bred by mixing gilts and "Back-feeding" of placentas.

What viruses can be found in the family Coronaviridae?

Alphacoronavirus suis (feline coronavirus, canine coronavirus, transmissible gastroenteritis virus, porcine respiratory coronavirus), A. porci (porcine epidemic diarrhoea virus), Betacoronavirus gravednis (bovine coronavirus and porcine haemagglutinating encephalomyelitis virus)

What disease does Feline Coronavirus and other Alphacoronavirus suis strains cause?

Feline infectious peritonitis (FCoV) transmissible gastroenteritis, porcine respiratory infections of swine, and canine coronavirus infections

Where are FIP-causing strains and Feline enteric coronaviruses found?

FIP-causing strains target macrophages wile FECV are found in villous epithelial cells

How are FIP causing strains transmitted?

Faecal-to-oral passage between the carrier and susceptible cats. Shedding cats have high viral load in the faeces, when it dries and it disturbed, a cloud of particles is released.

What are the differences between FCoV I and II

Type I	Type II
Is purely a feline-type coronavirus	Arose by recombination of canine coronavirus and type I FECV
Most prevalent in the field	Represents less than 10% of field isolates
Probably cell-associated and therefore more difficult to grow in cell cultures	Grows more easily in cell cultures
Can represent both enteric biotypes and virulent mutants	Can represent both enteric biotypes and virulent mutants

What are the hosts of FIPV?

Domestic cats and wild felids, such as the lion, leopard, cheetah, cougar, jaguar, bobcat, lynx, caracal, sand cat, and Pallas cat.

What factors influence if a cat gets FIP?

Endogenous exposure to a mutant FECV, i.e., FCoV, and

Failure of the immune system to contain the mutant virus.

In what classes can cats shedding FCoV be placed in?

• Transient shedders that shed for a few months. The majority of cats fall in this class.

• Intermittent shedders that shed on and off for an indefinite period.

• Carrier cats that shed continuously without becoming sick.

• Resistant cats that will not become infected even if they come into contact with shedding cats.

What is the distribution of FCoV?

Worldwide

What is the pothogenesis of FCoV

The development of an immunological response that is non-protective to the patient is necessary to produce typical pathological changes. When cats are infected with a virulent feline coronavirus, they will invariably develop FIP. The course of the disease depends on the virus strain. Only high virulence strains cause disease before protective immunity levels are induced. Opsonisation enhances its uptake into the cells in which it replicates. A strong humoral immunity and no cellular response is detrimental, as it results in a complement-mediated necrotising vasculitis and perivasculitis after the deposition of immune complexes in blood vessel walls. A stronger cellular response causes a less severe, non-effusive (dry), pyogranulomatous form of FIP.

What are the clinical signs of FCoV?

2 Forms are noted, effusive and non-effusive.

The effusive form is characterised by ascites, icterus, vomiting, diarrhoea, thickened intestines and a palpable omentum. Pericardial involvement leads to muffled heart sounds due to pericardial effusion. Periorchitis manifests as a bilateral scrotal enlargement and pleural involvement, accompanied by dyspnoea, coughing, pleural effusion, and myocarditis. Chronic fluctuating fever and progressive loss of weight, activity and appetite.

In the non-effusive or dry form, signs are vague and consist of chronic weight loss, anorexia and fluctuating fever. Signs in the non-effusive form result from the development of focal pyogranulomas in various organs. Central nervous system involvement is characterised by posterior incoordination, paresis, lumbosacral hyperaesthesia, personality changes, convulsions, and radial, facial, or trigeminal nerve paralysis. Renal involvement may manifest as enlarged kidneys with palpable irregular surfaces

How do we diagnose FCoV?

In the living cat:

Clinical signs supported by laboratory tests. Organ biopsy remains the sole definitive test for FIP, which involves exploratory laparotomy. Full blood counts in cats with FIP may reveal normocytic, normochromic anaemia, thrombocytopaenia, lymphopenia and neutrophilia. Total plasma proteins usually exceed 80 g/l due to polyclonal globulopathy. Pyogranuloma formation in the kidneys and liver can lead to increased BUN and creatinine, hyperbilirubinaemia and elevated hepatic enzymes. Microscopy of stained smears of peritoneal or pleural fluid sediments reveals a mixture of intact neutrophils, macrophages, plasma cells, lymphocytes and a few erythrocytes, with a foamy layer macroscopically and is glucose positive. Indirect fluorescent antibody test is a sensitive and recognised serological technique for detecting coronavirus antibodies, however, it cannot distinguish between infection with non-mutated and mutated (FIP-causing) feline coronaviruses. The IFA test can confirm dry FIP in cats with neurological signs.

What are PM findings of FCoV?

Microscopically, diffuse peritoneal/pleural/pericardial surface-oriented pyogranulomatous lesions are typical of wet FIP. Larger, more focal, surface-oriented granulomatous lesions, are typical of dry FIP.

How is FCoV controlled?

Catteries:

Cease breeding for 6 - 12 months, and no young kittens will be present on the premises. Identify carriers after 2-3 months, by testing serum antibody status to FECV at three-month intervals for a year. Avoid overcrowding, more than 5-6 breeding cats in one house is too many. Isolate seronegative gravid queens.

Shelters:

Target younger cats. Use separate litter boxes for each group and daily litter removal. Treatment includes supportive care (intermittent peritoneal or pleural drainage) and immunosuppressive therapy.

What is the status of the future of FCoV and FECV vaccines?

No promising prospects in the near future, based on the poor immunity that develops to both these viruses in cats following natural exposure.

What are the clinical signs of Transmissible gastroenteritis?

The clinical signs of TGE in fully susceptible pigs differ from those observed in endemically infected herds. In the epidemic situation, TGE is a rapidly spreading disease that is characterised by the sudden onset of acute diarrhoea in pigs of all ages, with neonatal animals being most severely affected.

How is Porcine Respiratory coronavirus spread?

Through respiratory aerosols containing the virus, which may be wind-borne between farms situated several kilometres apart. SA is free of infection.

What ist he pathogenesis of Porcine respiratory coronavirus?

Replication occurs mainly in alveolar epithelial cells but also in epithelial cells of nasal, tracheal, bronchial and bronchiolar pathways.

Porcine respiratory coronavirus replicates to a limited degree in enterocytes located on the villi or in the crypts of the small intestine in one-week-old piglets.

What are clinical signs of Porcine respiratory coronavirus?

Most cases are subclinical

What are clinical signs of Alphacoronavirus porci infection (Porcine epidemic diarrhea)?

Where it is endemic pigs develop watery diarrhoea within two to three weeks of weaning. Although diarrhoea does not always lead to mortality, it may retard the growth of affected animals. In naïve pig populations, the clinical signs may lead to severe diarrhoea and high mortality rates.

What are the clinical signs of Betacoronavirus gravednis infection in pigs (Porcine haemagglutinating encephalomyelitis)?

Two clinical syndromes are caused by infection with the HE virus: acute encephalomyelitis and vomiting and wasting disease.

Vomiting and wasting disease: The piglets continue to suckle but soon withdraw from the sow and vomit. Initially, there are no other clinical signs except for some depression and constipation. As the disease progresses, vomiting occurs after each intake of milk and results in dehydration, loss of condition and, often, death. Piglets that survive several days or weeks of persistent vomition become emaciated and have markedly distended abdomens.

Encephalomyelitis: Only occurs in piglets over three days old. Initially, there may be vomition, but that is soon followed by motor disorders such as muscle tremors and hyperesthesia. As the disease progresses, signs include walking backwards, sitting dog-like, and paddling movements of the legs. Piglets may develop opisthotonus and become blind. Finally, the animals become paralysed, and they are often dyspnoeic. Mortality is 100% if infected within a few days of birth.

How do we control Porcine haemagglutinating encephalomyelitis?

Gilts should ideally be exposed to the virus before the first farrowing. Their offspring will then be protected by antibodies acquired in the colostrum.

What viruses can be found in the Sedoreoviridae family?

Orbivirus alphaequi (African horse sickness), Orbivirus betaequi (Equin encephalosis virus), Orbivirus caerulinguae (bluetongue virus)

What transmits the genus Orbivirus?

Culicoides midges, specifically Culicoides imicola and C. bolitinos

When does AHS appear?

Seasonal, starts in Dec/Jan, peaks in Mar/Apr, following the first frost the illness dissappears until summer. May be present throughout the year in frost free areas.

What are the 4 forms of AHS?

Peracute, “pulmonary” or “dunkop” form, i.e., cases in which subcutaneous swelling of the head is absent. Most common in fully susceptible horses and dogs.

The acute or “mixed” form

The subacute, oedematous, “cardiac” or “dikkop” form

The horse sickness fever form. Occurs in horses immune to one or more serotypes of O. alphaequi, which become infected with a heterologous serotype against which there is some cross-protection.

What are the only 2 species that can be fataly infected by Orbivirus alphaequi?

Dogs and Equids

What is the distribution of AHS?

Endemic to Sub-Saharan Africa, with some reports in Northern Africa, The Middle east and the Iberian Peninsula

How do we prevent and control AHS?

Annual vaccination of horses is a practical means of control, however it cannot be relied upon fully to protect horses against infection or disease. Immunisation with a live polyvalent attenuated vaccine before the peak AHS season should be done. Infection can be prevented by stabling them some hours before sunset and letting them out a few hours after sunrise, as Culicoides spp. are nocturnal and are not inclined to enter buildings. Applying insect repellents and using insecticides on animals' coats will also discourage Culicoides from feeding on them. Horses should not be excessively exerted for about three weeks after the first course of immunisation. To ensure the broadest protection, annual polyvalent vaccines should be given. Animals should be vaccinated every six months in their first and second years of life.

How do otehr equids respond to AHS?

Horses are usually fataly infected (70%-90%), mules are more resistant (50%-70%), Donkeys and Zebras are very resistant.

What is the reservoir for AHS?

Transovarial transmission has not been shown to be true, Zebras and donkeys are the reservoir.

Where does O. alphaequi replicate?

Regional lymph nodes.

What is the pathogenesis of AHS?

Primary viraemia, infects target organs (lungs and lymphoid tissue).

What are PM findings with AHS?

Effusions into body cavities and oedematous changes of various tissues (particularly of the lungs), as well as serosal and visceral haemorrhages. Severe oedema of the lungs and hydrothorax. Several litres of pale yellow fluid that may coagulate on air exposure are found in the thoracic cavity. The mediastinum, and often the loose connective tissue around major blood vessels in the thorax, oesophagus, trachea and thymus, may also be oedematous.
Dikkop: yellowish gelatinous oedema of the head and neck's subcutaneous and intermuscular connective tissues. In severe cases, this extends to the back, shoulders and chest. The oedema is particularly severe around the ligamentum nuchae. Pale greyish blanched areas of varying size may rarely be noticed in the myocardium. Severe hydropericardium is almost invariably present. The liver is engorged, and its lobulation is distinct, but lungs and thoracic cavity is only mildly oedematous.

How do we Diagnose AHS?

The epidemiology, clinical signs and gross lesions of AHS are often sufficiently specific to allow a provisional diagnosis of the disease to be made. Virus isolation from blood or from specimens of the lungs, spleen and lymph nodes. Virus isolation may be achieved by using a variety of cell cultures, by intracerebral inoculation of suckling mice or by intravenous inoculation of embryonated hens' eggs. Isolates are identified by group-specific tests such as complement fixation (CF), agar gel immunodiffusion (AGID), direct and indirect immunofluorescence (IFA) or enzyme-linked immunosorbent assay (ELISA). Serotyping is performed using virus neutralisation (VN) tests employing type-specific antisera. Several conventional reverse transcription polymerase chain reaction (RT-PCR) assays and real-time reverse transcription PCR assays have been developed for the detection of O. alphaequi and to differentiate between the serotypes.

What are the clincal signs for all 4 types of AHS?

Pulmonary (Dunkop): severe dyspnoea, paroxysms of coughing, and sometimes, discharge of large quantities of frothy, serofibrinous fluid from the nostrils. In most cases, the dsicharge appears after death. The appetite remains good despite the high fever and respiratory distress. The animal may take a mouthful of hay without chewing it. The onset of dyspnoea is sudden, and death often follows.

Cardiac (Dikkop): subcutaneous oedema of the head and neck, particularly the supraorbital fossae. The oedema usually appears late in the course of the disease, but if it appears early, the condition is more serious, more acute and has a higher mortality rate. There may be oedema of the eyelids, lips, cheeks, tongue, intermandibular space, and sometimes also the neck, chest and shoulders, but usually not the lower parts of the legs. Animals may lie down repeatedly or are restless when standing and frequently paw the ground due to colic. Unfavourable prognostic signs are petechiae in the mucosa of the conjunctivae and mouth on the ventral aspect of the tongue. This form is less severe than the Pulmonary form.

Mixed: is rarely diagnosed clinically; one of the other preceding forms predominates

Horse sickness fever: very mild disease and is frequently not diagnosed clinically. The most characteristic finding is a rise of the rectal temperature.

What are DD for AHS?

It is not possible to differentiate the AHS fever form of the disease from the early febrile stages of other forms of AHS or the early febrile stages of many other equine infectious diseases. May be confused with equine encephalosis, however, the mortality rate of AHS is much higher than that of equine encephalosis. Virus isolation and identification or serological tests on paired serum samples are essential to confirm either diagnosis. Disseminated small haemorrhages and the oedema may be very similar to those found in cases of purpura haemorrhagica and equine viral arteritis, however In horses affected by these conditions, subcutaneous oedema often occurs ventral to the elbow and stifle joints. Early stages of piroplasmosis, when Babesia/Theileria parasites may be difficult to demonstrate in blood smears, are occasionally confused with AHS. AHS may also be complicated by piroplasmosis, and in such cases, ventral oedema may be severe.

How do we treat AHS?

Supportive treatment. As piroplasmosis may be a complication of AHS, blood smears and the rectal temperature should be taken regularly.

What is the impact of AHS?

Before automobiles horses played a vital role in transportation, was essential in military operations and was used for draught power in agriculture and mining. Modern horses include performance horses or animals used for other forms of recreation. Up to the late 1950's up to 350’000 horses were exported out of SA for the war efforts. AHS imposed a 4 decade ban on exporting horses out of SA. Currently about R250m is made in annual revenue from horse exports, so far there hsa been 5 outbreaks, stopping exports.

What is the distribution of Equine encephalosis?

Endemic to SA and Botswana, may spread further.

Which horses are more susceptible to Equine encephalosis virus?

Weanlings and horses older than 7

What are clinical signs of Oribivirus betaequi infection?

90% of animals show no or very mild symptoms. Most affected horses show either a slightly elevated rectal temperature, may be accompanied by varying degrees of listlessness and inappetence. Congestion and mild icterus may be found. Less common manifestations: degrees of swelling of the eyelids and of the supraorbital fossae and entire face; central nervous system involvement such as mild to severe ataxia, reluctance to walk and stiffness, a wild expression in the eyes, changes in temperament, respiratory distress sometimes accompanied by a frothy, clear or slightly blood-tinged, discharge from the nose and petechiae in the conjunctivae.

How do we daignose Equine encephalosis?

clinical signs are usually non-specific. Isolation from blood collection, tissue from fatal cases or aborted fetuses. Orbivirus betaequi can be isolated by inoculating cell cultures or intracerebral inoculating day-old mice.

What is the impact of Orbivirus caerulinguae?

Deaths (up to 30 % mortality), lowered production (lowered weight gain, poor milk production, shedding of fleece), temporary infertility in rams (natural disease or vaccination), and cost to control disease (vaccination, treatment). Losses are also caused by embargoes on the movement of animals and semen and by serological testing necessary in the international livestock trade.

What is the distribution of Bluetongue?

Africa, Europe, USA, most Central and South America states in the Near, Middle and Far East, Japan, and northern regions of Australia (worldwide)

What are the hosts of Bluetongue?

sheep, cattle, goats, deer, bighorn sheep, most species of African antelope and various other artiodactyls. Goats, cattle, and wild antelope are more resistant to BT than sheep, and they are usually subclinical infections. Indigenous sheep breeds (Dorper, Karakul, Persians, etc.) are more resistant than European breeds (Merinos, etc.).

Which animals are invloved in the BT cycle?

Historically, Culicoides midges (biological vectors) and species of African antelope were in the primary cycle. With agricultural development in large parts of Africa, the role of wild animals has been taken over mainly by cattle. Virus overwinters in subclinical cattle

Sheep involved in a secondary cycle. The infection progresses in the cattle‑midge cycle (cattle are amplifier hosts). Once a certain level of infection is attained, it spills over to sheep (late summer, autumn), with simultaneous outbreaks in sheep in various regions of the country.

What is the pathogenesi of BT?

Infection ‑ of regional lymph nodes (replication in lymphocytes) and other lymph nodes of lymphocytes. The virus also affects lymphoreticular tissues and endothelial cells, causing vasculitis and thrombosis.

BT virus is mostly cell-associated (erythrocytes and leukocytes), with a small amount free in plasma.

Panleukopenia.

Lesions in stratified squamous epithelium (lips, mouth, tongue, skin, rumen) – haemorrhages, oedema, erosions, ulcers.

Transplacental infection by the modified virus (vaccine strain) may give rise to teratology of the foetus.