VIP test 3

What is the scientific name for FMD Virus?

Apthovirus vesiculae in the Family Picornaviridae

How is FMD transmitted?

Predominantly direct contact, affected by:
The quantity, duration and means by which the virus is liberated into the environment. Present in all secretion, even before CS. Highest in saliva. Airborne infection may occur over great distances.
The ability of the virus to survive outside the animal body. It survives, e.g., in aerosols or on fomites such as hay infected with saliva.
The quantities of virus required to initiate infection in the animal body. Very small doses will infect cattle and sheep via the respiratory route. Larger doses are required via the oral route.

Discuss the socio-economic impact of FMD

Low mortality, but high morbidity, antigenetic variation, and high virallity make it hard to control. It may cost the country dearly in loss in exports, costs of disease control, impact of slaughtering infected animals, production losses, etc. Farmers cannot sell infected cows.

What is the pathogenesis of FMD?

The respiratory tract is the usual route of infection in species other than pigs. Initial replication is in the mucosa and lymphoid tissues of the pharynx and soft palate and regional lymph nodes. Viraemia and infection of multiple organs. Characteristic lesions happen when SSE (stratum spinosum) cells become infected and are agitated by friction.

What OIE category is FMD classified under?

Category A

Which animals are primarily affected by FMD?

Ruminants and pigs, less prevalent in Bos indicus cattle. Foot-and-mouth disease in adult sheep and goats is frequently mild or inapparent but can cause high mortality in young animals. In intensively reared pigs, FMD results in severe clinical disease in adult and fattening animals and high mortality in piglets. Recovered ruminants (not pigs) may remain carriers of the virus for varying periods. The African buffalo is the only free-living species known to sustain the virus for indefinite periods, although infections are clinically inapparent. Various other wildlife species are periodically infected through contact with buffaloes.

What are clinical signs of FMD?

Vary with species, breed and strain.
Young my die acutely due to myocarditis (Tiger-heart)

Acute:
First clinical signs include fever, dullness, inappetence and, in lactating cows, a fall in milk production. Followed by signs caused by lesions (lameness and disinclination to stand, and signs of discomfort in the mouth, such as salivation, smacking of the lips and grinding of the teeth). Cattle mouth lesions usually on tip and dorsal surface of tongue, vesicles that pop. Mouth lesions less in other domestic spp. All get foot lesions.

Subacute to chronic:
Healing in mouth is more rapid (duh). Fill with fibrin. Foot lesion may separate the horn from the underlying tissue.

How is FMD diagnosed?

Presumptive diagnosis
This is based on the history, epidemiology, clinical signs and pathology.

Laboratory confirmation
Virus isolation and identification, specimen of choice is the epithelium covering a vesicle.

What are DDs fro FMD?

Vesicular stomatitis, swine vesicular disease and vesicular exanthema, are clinically indistinguishable from FMD. (not in Africa)
Conditions of cattle which produce erosions or ulcerations in the mouth or on the muzzle include bovine viral diarrhoea/mucosal disease, rinderpest, bluetongue (BT), epizootic haemorrhagic disease (EHD), malignant catarrhal fever (MCF), lumpy skin disease, bovine papular stomatitis, infectious bovine rhinotracheitis. In sheep, orf must be considered.
Foot lesions may be caused by bacteria and fungi, e.g., footrot and foot abscess.

How is FMD controlled?

Inactivated vaccines are available

Countries or zones previously free from FMD:
Isolate the outbreak focus, all cloven-hoofed animals in the focus area should be slaughtered in situ and the carcasses disposed of by incineration or burial as quickly as possible. It is impossible to vaccinate against FMD and retain recognition of freedom from the disease, as vaccinated animals may become infected and serve as carriers without clinical signs. Serology cannot distinguish between vaccinated animals and carriers.

Countries or zones in which FMD occurs sporadically:
Establish the type and subtype of the outbreak virus, isolate the outbreak focus, including the quarantine area, after a physical barrier must be placed around the outbreak focus. Once that has been done, cloven-hoofed livestock in the outbreak focus and the surrounding uninfected area should be vaccinated with an appropriate vaccine containing a virus strain closely related to that which caused the outbreak.

Control of FMD in Africa, where it is associated with buffaloes and SAT-type viruses:
Cattle:
Livestock identification and traceability scheme.
Physical separation between livestock and wildlife as far as possible by the use of game fencing,
Immunisation of livestock, especially cattle with the appropriate FMD vaccine and
Regular surveillance for clinical cases of livestock in the threatened area.
Movement control through permits.
Pigs:
Only oil-adjuvant vaccines are effective in pigs.
Excrete up to 3000x as much FMD as a cow, so in high concentration can create virus plumes.
High reproductive rates make achieving acceptable herd immunity levels through vaccination hard.

What diseases do viruses in the Retroviridae family cause and what are their hosts?

Disease	Host animal
Betaretrovirus ovijaa	Sheep (goat)
Deltaretrovirus bovleu	Cattle (sheep)
Lentivirus ovivismae	Sheep (goat)
Lentivirus capartenc	Goat (sheep)
Lentivirus equinfane	Horse, donkey
Gammaretrovirus felleu	Cat
Lentivirus felimdef	Cat (males more, spread through bites)

Dicuss features of Retroviridae.

The possession of a "reverse transcriptase" or RNA-dependent DNA polymerase, thus can make a DNA copy of its RNA genome (provirus). The Provirus Can also act as a natural vector that transmits cellular oncogene from one cell to another, which is one of the mechanisms of oncogenesis. All the diseases associated with this group, including Lentivirus humimdef1/2 (human immunodeficiency virus), have immunopathological changes as the primary lesion.

What is the aetiology of feline aids? What are the characteristics of the genus?

Lentivirus felimdef, lentiviruses have a very long incubation period.

Discuss the pathogenesis of Lentivirus felimdef

Carried to regional lymph nodes, replicate in T lymphocytes, tropism for T4 helpers. Non known if tumour formation is due to immunosuppression or due to direct oncogenicity.

What are clinical signs of FIV?

Generalised lymphadenopathy, fever, and leukopaenia. Following the acute phase, cats will progress to an asymptomatic phase. Chronic phase will result in opportunistic infections that mainly result in disorders of the oral cavity, digestive system, respiratory tract, and skin. Clinical signs in this immunosuppressive phase are lethargy, anorexia, weight loss, pyrexia and lymphadenopathy, gingivitis, periodontitis, stomatitis, diarrhoea, rhinitis, ocular discharge, pustular dermatitis and neoplasia. Neurological signs may include behavioural changes, dementia, facial twitching, peripheral neuropathies, psychomotor abnormalities and seizures.

How is FIV diagnosed?

Cats infected with FIV produce antibodies against viral proteins that can co-exist with the virus, this is insufficient to clear the virus and a persistent infection develops. Detection of antibodies.

How is FIV controlled?

Maintaining the quality of the cat's life is possible if secondary infections are treated, should preferably be kept indoors to reduce the chance of transmission, neuter male cats to reduce urge to fight. A vaccine was authorised, but is not cross-effective with types other than D, and serology cannot distinguish between a vaccinated and infected cat.

What is the Aetiology of Feline leukemia?

Gammaretrovirus felleu (FeLV)

How is FeLV diagnosed?

A group-specific protein, p27, that is produced in excess during viral multiplication. is tested for with ELISA. The envelope contains the major type-specific protein gp70 that allows the subgroups of FeLV to be distinguished and is responsible for the humeral response. The envelope also contains a minor envelope antigen, p15E, that has immunosuppressive properties. It can alter the permeability of lymphocyte membranes, leading to their dysfunction.

How is FeLV transmitted?

Horizontally or vertically, but intimate contact is necessary. Exposure to high concentrations and repeated doses of infectious FeLV at an early age is the most important factor contributing to an exposed cat's risk of becoming persistently viraemic. The virus gains entry, primarily via saliva, through eyes, nose or respiratory tract membranes. It can also be transmitted in milk to kittens, by blood transfusions, and across the placenta to foetuses.

Discuss the pathogenesis of FeLV

Replicates in the regional lymph nodes (head and neck lymph nodes and the tonsils). While FeLV is still confined to these areas, many cats mount an adequate immune response. Cats that do not mount an adequate immune response become persistently infected, and the virus spreads to the bone marrow, where it replicates in nucleated cells. Viraemia ensues. Infects the GIT, salivary glands, pancreas, and respiratory tract.
3 syndromes occur after acute infection:
Uncontrolled proliferation of virus-transformed cells, resulting in lymphosarcoma or leukaemia of lymphoid, myeloid or erythroid cell lines.
Degenerative and necrotic disorders of the myeloid tissues resulting in non-regenerative anaemia, leukopenia, and thrombocytopenia.
Degenerative and necrotic disorders of the lymphopoietic tissues resulting in generalised immunosuppression.

What are clinical signs of Feline leukemia?

The acute phase of the disease is usually subclinical but may rarely be manifested by fever, lymphadenopathy and leukopenia. Clinical signs associated with the chronic phase of the disease are related to the effects on the lymphopoietic tissues, myeloid tissues, kidneys or other organs. Thymic lymphosarcoma will, for example, give rise to coughing, gagging and choking while vomiting may predominate in alimentary forms. Myeloproliferative disease embraces all the non-lymphoid dysplastic and neoplastic conditions arising from the haematopoietic bone marrow stem cell or its progeny. Clinically, it is characterised by anaemia, leukopaenia, thrombocytopenia, and septicaemia. The myelosuppressive diseases most commonly associated with FeLV infection are non-regenerative anaemia and a panleukopaenia-like syndrome. Glomerulonephritic lesions are caused by immune complexes deposited on the glomerular capillary basement membrane (hypersensitivity type III).

What are PM findings in FeLV cases?

Malignant neoplasia is the most serious FeLV-related disease, Lymphoma is the most typical, myeloproliferative disease may give rise to myelogenous leukaemia. Multiple anaplastic fibrosarcoma is caused by feline sarcoma virus (FeSV), which is a recombinant hybrid of a viral oncogene in the host genome and FeLV.

How is FeLV controlled?

Prevent spread: vaccinate, do not introduce infected cats, do not expose susceptible cats to infected cats (at shows etc).

What is the aetiology of bovine leukemia?

Deltaretrovirus bovleu.

Discuss the available FeLV vaccines.

One makes use of an adjuvanted canarypox virus into which was inserted in the FeLV env (envelope) and gag (group antigen) genes along with 1272 base pairs from the pol (polymerase) gene under control of the vaccinia virus H6 promoter. The FeLV recombinant canarypox virus, when absorbed into susceptible cells, expresses the gp70 glycoprotein of FeLV.

Another recombinant vaccine is based on a purified p45 protein that is produced by insertion of the sequence of the gene coding for subgroup A gp 70 synthesis into Escherichia coli.

How is Bovine leukosis transmitted?

Iatrogenic – man is the most important transmitter (bleeding needles, ear tagging instruments, dehorning and castration instruments).

Blood transfusions and blood-based vaccines.

Mechanical spread by insect vectors, e.g., Stomoxys.

Saliva and other excretions (less important).

In utero transmission; in less than 15 % of infected cows (transmission is inconsistent and may vary with successive calves).

Per os infection with colostrum or milk.

Infected animals remain infected for life

Discuss the pathology of Deltaretrovirus bovlue

After infection, there are no signs of viraemia (fever, circulating virus), but the animal develops a strong and persistent humoral response to BLV proteins. The majority of animals remain healthy, with no loss of production.

Persistent lymphocytosis in clinically healthy animals; increased B lymphocytes in circulation.

Lymphomas in a small percentage

Virus enters lymphocytes only and replicates; genome integration and cell transformation.

Both circulating and sessile cells are affected in high concentration; chromosome abnormalities, e.g., polyploidy.

Persistence of the virus is ensured by the transfer of the integrated genome with cell division (there is no free virus in vivo).

Multicentric invasion of a variety of organs and tissues.

Infection might, therefore, produce:

Antibody production (cell antigens)

Antibody production and persistent lymphocytosis

Antibody production, lymphomas and persistent lymphocytosis

What are clinical signs and PM findings of Deltaretrovirus bovlue

Enzootic bovine leukosis

• It is seen in adults

• Proliferation of lymphocytes produces discrete solid tumour masses or a diffuse infiltration of tissues/organs.

• Multicentric invasion

• The first sign is usually enlargement of lymph nodes, followed by loss of weight and decreased milk production. Sometimes exophthalmos, posterior paresis, cardiac failure, anaemia and melaena. Anaemia results from infiltration of haemopoietic organs (particularly bone marrow) and blood loss.

• Clinical signs depend upon the organ involved, tumour growth rate and spread rate.

• Persistent lymphocytosis probably precedes lymphoma cases by several years; persistent lymphocytosis may be a pre-tumour phase.

Sporadic bovine leukosis

• Not associated with bovine leukaemia virus; thought to be non-contagious.

• Of rare occurrence affecting cattle less than 3 years of age.

• Three forms are recognised:

• Calf or juvenile form: < 6 months of age, generalised lymph node involvement and bone marrow infiltration.

• Thymic form: < 2 years of age, thymic enlargement; affects heart.

• Cutaneous or skin form: 1 to 3 years of age, nodular infiltrations of lymphocytes in skin; later spread to lymph nodes.

Sheep:
Tumours arise more commonly after a much shorter incubation period (12 months to 3 years) than in cattle. High antibody titres in sheep but no persistent lymphocytosis.

How is Bovine leukosis diagnosed?

Clinical signs, clinical pathology

Serology: ELISA

How is bovine leukosis controlled?

Control is based on the elimination of carriers or isolation of carriers.

All animals in the herd are regularly tested at intervals of 3 – 6 months; reactors are eliminated

Losses are relatively low; economically, an eradication scheme at this stage is not justified

Natural and experimental infection of sheep, e.g., common grazing/from cattle but not between sheep.

No evidence of infection of man.

What is the aetiology of jaagsiekte?

Betaretrovirus ovijaa

What is the pathology of Jaagsiekte / pulmonary adenomatosis?

The primary lesion is a neoplastic transformation of type II secretory epithelial (pneumocytes) and possibly the non-ciliated terminal bronchiolar epithelial cells. The transformed cells proliferate and form clusters that invade and eventually obliterate the alveolar lumen, leading to death from anoxia. The transformed cells retain their secretory function and produce large amounts of surfactant-containing, clear, viscous fluid, which accumulates in the air passages.

What are clinical signs of jaagsiekte / pulmonary adenomatosis?

Clinical signs are only seen when the lung lesions are advanced. The onset is insidious, and the respiratory rate increases markedly with exercise. Initially, there is no fever. Later, there is a rapid loss of weight. As the infection progresses, affected animals lag behind the flock. Respiratory distress is evident during exercise, and the respiratory movements become jerky and short. Dyspnoea becomes progressive. On auscultation, moist rales are heard. There are spasmodic bouts of coughing. Secretions from the lungs increase, and if the animals are lifted by the hind legs, fluid streams out of the nostrils. This is regarded as a pathognomonic sign for jaagsiekte.

What are PM findings of Jaagsiekte / pulmonary adenomatosis?

Due to secondary bacterial infection, chronic adhesive pleuritis may be seen. The lungs are 3 – 4 times their normal weight. The tumours grow by expansion of a semi-transparent nodule that expands and coalesces with neighbouring nodules until a large part of the lobe is affected.

How is Betaretrovirus ovijaa diagnosed?

Clinical diagnosis is difficult. A copious amount of fluid flowing from the nose when the sheep is lifted by the hind legs is a useful diagnostic sign.

How is jaagsiekte / pulmonary adenomatosis controlled?

The only method of prevention is by maintaining a completely closed flock. No sheep should be introduced into a clean flock.

Quarantine is not practical due to the long incubation period. Once infection is observed in a flock, one can:

• Immediately slaughter all suspected cases. Although this measure will reduce the incidence, it will not necessarily eliminate the disease.

• Maintain a two-flock system. The infected flock is reduced by sale to a butcher. The clean flock is built up. The two flocks must be kept in strict isolation with different drinking troughs, different dosing syringes, etc.

• Use a slaughter-out system. The whole flock is sold to a butcher, and after six weeks in summer or 3 months in winter, a new flock may be introduced. All water and feed troughs must be disinfected, and sheds and kraals used by the previous animals should be avoided for extended periods.

What is the aetiology of ovine progressive pneumonia (Maedi-Visna)?

Lentivirus ovivismae

What is the pathogenesis of Lentivirus ovivismae?

Produce pulmonary (Maedi) and neurological (Visna) disease in sheep. Replicates at the entry site and viraemia ensues. In non-neural tissues, L. ovivismae exclusively infects cells of the monocyte-macrophage lineage, including promonocytes in the bone marrow and macrophages in the lung, spleen, synovium, bone marrow and lymph nodes draining the brain. In the lungs and CNS, tissue is destroyed in areas where inflammatory cells have collected. Eventually, this burden of pathological change becomes apparent as shortness of breath or partial paralysis and weight loss. Viral antigens in cells are not produced in sufficient quantities to detect and destroy the infected cell by immune surveillance mechanisms. Antigenic variation through point mutations in the env gene that encodes the virion envelope glycoprotein adds to the persistence of lentiviruses.

What are clinical signs of Maedi-Visna?

Maedi (chronic interstitial pneumonia) is the more common form of the disease. The onset of clinical signs is insidious, and the disease generally persists for months, resulting in progressive deterioration and eventual death. Early signs consist of a slow progressive loss of condition with dyspnoea. In time, respiration becomes more difficult, accompanied by rhythmic jerks of the head. Sometimes there is a dry cough. No appreciable amount of fluid is found in the respiratory tract, nor is there nasal discharge. In Visna, the onset is likewise insidious. The first signs consist of a slight abnormality when walking, especially the hindquarters, trembling of the lips, unnatural head posture and, in rare cases, blindness. The signs are those of an ascending paralysis, namely abnormal hind limb gait progressing to incoordination and paresis.

What are PM findings in Maedi-Visna?

There is a great increase in the weight of the lungs, lung lesions are diffuse, compact and homogeneous. Irrespective of the site of the inflammatory lesions, there is a consistency in its character and cellular composition. The basic components are lymphoid hyperplasia and an interstitial infiltration of mononuclear cells. Brain lesions include periventricular and subependymal perivascular cuffing of mononuclear cells

How is Maedi-Visna diagnosed?

Diagnosis is confirmed by histological examination. Virus isolation can be attempted. Most infected sheep possess specific humoral antibodies that several different serological tests can detect. After seroconversion, the antibody response usually persists, and antibody-positive sheep are identified as virus carriers.

What is the aetiology of swamp fever (Equine infectious anemia)?

Lentivirus equinfane

What is the pathogenesis of swamp fever?

It is found primarily in macrophages in infected horses, in which it persists for life. The virus may be detected in blood or various other tissues.

It can persist in the presence of high antibody levels.

Recovered animals remain carriers for life, and circulating virus is present in low concentration during the periods between clinical episodes, mainly in the form of immune complexes.

How is swamp fever transmitted?

The most common transmission mode is by infected blood, e.g., contaminated instruments and equipment such as twitches, bridles and gags, but blood-sucking insects are probably the most important transmitters in nature.

What are clinical signs of Swamp fever?

The clinical course of EIA is variable. 
Acute cases develop a high fever for one to three weeks until death occurs in most cases. Severe anaemia, icterus, petechial haemorrhages in the mucosae, and weight loss are commonly seen.

Animals which survive the acute form pass into the subacute form with continuing moderate fever.

Chronic disease with signs varying from failure to thrive to persistent or episodic fever and anaemia, icterus, cachexia, ventral oedema, progressive muscle weakness and incoordination and frequent micturition. Inapparent infection may follow any of the above forms and persist for life or subsequently revert to clinical disease.

What is the Aetiology of rabies?

Family Rhabdoviridae, genus Lyssavirus

What is Rabies virus sensitive to?

Sunlight, UV radiation, heat, detergents, halogens and lipid solvents.

When can rabies be found in the saliva?

Up to 13 days (dogs) or 3 days (cats) before signs, terminates usually 1 to 2 days before death

Discuss the susceptibility of animals to rabies

Foxes, and jackals have been rated as extremely susceptible; skunks, cats, cattle, mongooses and most rodents as highly susceptible and dogs, sheep, goats, horses and primates including humans as moderately susceptible.

How can rabies be transmitted?

Usually saliva with bites. Does not cross unbroken skin. Contact with mucous membranes can cause infection. Raw milk can cause infection. Aerosols have been reported in a cave with over 20mil bats in an endemic rabies zone. Eating infected meat should not cause infection. Organ donation.

Discuss rabies related viruses (rrv)?

Lagos bat virus (bats flying in the day and in houses, caught by dogs and cats), Mokola (Small mammals such as shrews (skeerbekke) or myomorph rodents, not in bats, cats or dogs) virus and Duvenhage virus (bats). Routine diagnostic procedures do not allow rabies and rabies-related viruses to be differentiated with certainty. Not adapted to spread in carnivores but sporadic cases may happen.

Discuss the pathogenesis of rabies.

Following inoculation via a bite wound, virus undergoes a variable period of replication at the site of the bite, before gaining entry into the peripheral nervous system. This occurs though binding to nicotinic acetylcholine receptors at the neuromuscular junction. The most superficial portal for entry of rabies virus into the nervous system is the sensory nerve endings of the epithelial and subepithelial tissues of the skin and mucous membranes. The virus is taken up by parasympathetic oculomotor nerve fibres, and fibres of the ophthalmic branch of the trigeminal nerve; not by the optic nerve. The cornea has only sensory innervation and ocular infection has been recorded after transplantation of infected corneas. Following deep introduction by bite, rabies virus enters the nervous system either through neuromuscular spindles (stretch proprioceptors consisting of modified muscle cells wrapped in unmyelinated nerve endings) or through motor end plates. The virus is capable of entering nerve endings immediately and leaving the site of inoculation rapidly. Once virus has entered nerves, there is passive centripetal transport of subviral genome-containing particles, presumably ribonucleocapsids, by retrograde axoplasmic flow to the central nervous system. Infection can occur via either sensory or motor nerves. Spread of virus in the spinal cord proceeds via axons and dendrites. Infection can reach the brain stem in a matter of days. Occasionally, infection may be limited to the spinal cord. Spread of infection is rapid within the brain. Selective involvement of neurons. From the time that the infection reaches the central nervous system, passive centrifugal spread of virus by anterograde axoplasmal flow proceeds simultaneously with centripetal spread. Centrifugal spread proceeds throughout the body, and virus or antigen has been demonstrated in terminal illness in a range of tissues and organs, including the cornea, nerve fibres surrounding hair follicles, myocardium, lungs, kidneys. Spread to the salivary glands coincides with widespread dissemination of infection in the brain. The response to the administration of inactivated virus or attenuated live virus is three-fold: there is production of interferon and circulating antibody, and induction of cell-mediated immunity. Passively acquired antibody can be protective if adequate amounts are administered prior to infection. Interferon counteracts spread of the virus by conferring resistance to infection on susceptible cells. In natural infection, antibody response only becomes demonstrable after the onset of illness, irrespective of the duration of the incubation period. Early selectivity for the limbic system and relative sparing of the
neocortex result in behavioural changes which promote confrontation between rabid and
susceptible animals. The high mortality serves to ensure that there is minimal accumulation of immune animals in the population, and the occasional occurrence of long incubation periods ensures that the virus survives until susceptible individuals are recruited to the population.

Discuss the pathogenesis of rabies-related viruses (RRV)

The sequence of events observed following peripheral inoculation of Mokola and Lagos bat virus in hamsters is essentially similar to that seen in the pathogenesis of rabies: replication of virus in muscle cells at the site of inoculation, centripetal spread of infection along nerves and dissemination of virus in the central nervous system. However, the rabies-related viruses tend to replicate to a greater extent in non-neural tissues and organs and may produce demonstrable viraemia.

How is rabies diagnosed?

It is more important to be aware that rabies induces abnormal behaviour than to suspect the disease only when animals exhibit the furious behaviour classically associated with it. History (active area, immunisation). If animals are furious and show signs of aggression but is normal on examination, authorised persons may decide to confine the animal, keep it under observation and kill it only if overt signs start. This happens primarily in vaccinated animals and animals where rabies exposure is unlikely. Feral animals, animals showing signs of illness considered to be suggestive of rabies, or animals whose owner and history cannot be traced should be killed for examination. Animals should be killed in such a manner as to avoid damaging the cranium. Brain specimens to be submitted for laboratory examination include 10-20mm3 blocks of cerebrum, cerebellum, hippocampus, medulla, thalamus and brain stem, as well as submaxillary salivary gland, preserved in duplicate in 50 per cent glycerol-saline solution for virological examination and in 10 per cent buffered formalin for histopathological examination. IFAT tests t obe done on brain smears.

How is rabies controlled?

All dogs and cats in South Africa must be vaccinated against rabies by a veterinarian or
authorised person at the age of three months, followed by a second vaccination one to
twelve months later, and thereafter every three years. Dogs and cats younger than three
months may be vaccinated, provided that they are again vaccinated at the age of three
months, followed by normal procedure. It is recommended that fully susceptible domestic pets which are exposed to infection by a proven rabid animal should be destroyed, but dogs which are immunised in conformity with legal requirements may be given a booster and kept under observation. Vaccination of farm herbivores is generally made optional, to be performed at the discretion and expense of the owner when problems with rabies are encountered.

What is the aetiology of Bovine Ephemeral fever?

Ephemerovirus febris of the family Rhabdoviridae

What is Ephemerovirus febris sensitive to?

BEF virus is susceptible to both high and low pH and to environmental temperatures. The virus therefore does not survive long outside its vertebrate or invertebrate host. It is rapidly inactivated by the high concentrations of lactic acid which develop in the muscles of cattle after death. Fomites, body discharges or tissues therefore play no part in the transmission of BEF

Discuss the pathogenesis of BEF

Primarily affects the endothelium of small blood vessels. This leads to effusion of fibrin-rich fluid into joints and tendon sheaths. There is a fall in the total serum calcium, and absorption of calcium from the food which has been ingested ceases (as a result of rumenstasis). High oxalates increase mortality (binds to Ca to create insoluble calcium oxalate crystals). Contained in the leukocyte fraction of the blood during fever and, more particularly, in neutrophils.

The pathogenesis of the pulmonary and subcutaneous emphysema seen in a small proportion of cases is not known but may be due to partial blockage of the air passages with exudate as well as to necrosis of the bronchiolar walls resulting in rupture of bronchioles and alveoli.

What are clinical signs of BEF?

In most cases self-limiting. The onset is always sudden and accompanied by a sharp rise in body temperature. During the first febrile episode, cattle may exhibit nothing more than depression, disinclination to move, and stiffness, but nevertheless maintain their appetite. Many cattle recover completely after this febrile phase. If the disease progresses, animals may become separated, anorexic, and stiff, developing a shifting lameness. The pulse rate accelerates, the respiratory rate increases, and subcutaneous muscles may fasciculate or exhibit tremors. Recumbency is the obvious feature of the next order of severity. The affected animal is at first in sternal recumbency and able to rise in response to a strong stimulus, but is later completely unable to do so. Loss of the swallowing reflex, bloat, ruminal stasis, constipation, and excessive salivation may be evident, and torticollis is seen. An early sign of the disease in lactating cows is an abrupt decline in milk production, and there is a high cell count. Rales can be heard in the lungs in the second febrile stage. Pneumonia may be a secondary complication, and severe pulmonary emphysema has been observed in a small proportion of cases which may eventually result in subcutaneous emphysema. The cause of the temporary infertility and of abnormal spermatozoa in bulls is unknown.

What are PM findings in BEF?

The most conspicuous macroscopic changes are serofibrinous polysynovitis, tendovaginitis, fasciitis, cellulitis and focal necrosis of skeletal muscles. The lesions in both joints and muscles are invariably more severe in the limbs on which the animal was limping. A generalised enlargement of lymph nodes is invariably present.

How is BEF diagnosed?

A reliable presumptive diagnosis of BEF is possible based on the sudden onset of disease in late summer, affecting sizeable numbers of cattle in areas where BEF is known to occur. The most useful direct confirmatory test is a differential leukocyte count which may be performed crudely on a blood smear. If there is no neutrophilia the animal does not have BEF.

What are DDs of BEF?

Aphosphorosis, Crotalaria spp., botulism, black quarter, Diplodia maydis.

Fog fever or acute bovine pulmonary oedema.

How is BEF controlled?

Treatment is based on:

1. Rest, and provision of water and feed.

2. Parenteral rehydration in hot weather.

3. NSAIDS

4. Calcium borogluconate solution (hypocalcaemic)

5. Nothing should be giver per os unless swallowing is seen to be normal

6. Do not stress or work animals.

Vaccinate valuable animals in endemic areas.

What is the aetiology of vesicular stomatitis?

Vesicovirus in the family Rhabdoviridae

How is VS transmitted?

Direct contact does not spread it, except in swine, milking machines, arthropod vectors.

What is the significance of equine infectious metritis?

Important cause of economic losses to Thoroughbred breeding industry

What is the aetiology of EIM? Discuss some characteristics.

Taylorella equigenitalis. Commensal in the genital tract. Fastidious. Gram negative bacterium. Streptomycin resistant

What is the reservoir for EIM?

Persistently infected stallions (indefinitely infected)

How is EIM transmitted?

Venereal transmission to the mare

How do foals get infected?

Persists in the external genital tract of mares for years, so either congenital infection or during birth

What is the pathogenesis of EIM?

Natural breeding or AI can cause infection. Proliferation in uterus, Fallopian tubes and vagina. Endometritis, salpingitis, vaginitis. Failed conception, early embryonic death

What are clinical signs of EIM?