State veterinary Medicine Flashcards
List the notifiable diseases in GB?
Anthrax, aujeszkys disease, avian influenza, BSE, blutongue, brucellosis, brucellosis melitensis, chronic wasting disease, classical swine fever, contagious bovine pleuopneumonia,, contagious equien metritis, enzootic bovine leuoksis, epizootic lymphangitis, equine infecitous anaemia, equine viral arteritis, european bat lyssavirus, foot and mouth didsease, glanders, Newcastle disease paramyxovirus of pigeons, rabies, rinderpest, scrapie, sheep poox, sheep scab, swine vesicular disease, TB, warble fly, West Nile virus.
What are OIE former list A diseases?
Office international des epizooties - communicable diseases which have the potential for very serious and rapid spread irrespective of the national borders, which are of serious socio-economic or public health consequence and which are of major importance in international trade; - foot and mouth disease, vesicular stomatitis, rinderpest, Rift Valley fever, lumpy skin disease, contagious bovine pleuropneumonia, blue tongue, peste petitis ruminants, sheep & goat pox, Newcastle disease, fowl plague, swine vesicular disease, classical swine fever, african swine fever, teschen disease, african horse sickness.
What is foot and mouth disease?
A highly contagious viral disease characterised by vesicles in the mouth and on the feet affecting all domestic and wild ruminants and swine. Foot and mouth disease is caused by an aphtovirus of the family picornaviridae. the virus is table under a range of conditions surviving well in a cool moist environment of medium pH.
What are the clinical signs of foot and mouth disease?
Initially pyrexia, anorexia, salivation, severe lameness, reduced milk yield, erous occulo nassal discharge which then becomes mucopurulent. Early lesions in the mouth are seen on the tongue and dental pad appearing as blanched, circular areas which swell with fluid and become vesicles. those on the dorsum of the tongue often coalesce until the whole surface of the tongue appears corrugated. Vesicles usually rupture within one or two days of their formation leaving shallow deep red sharp edged ulcers. handling of the tongue causes the animal much pain and results in large pieces of epithelium becoming detached. Vesicles also develop on the hard palate, lips, muzzle, snout and teats. Vesicles develop on the coronary band and interdigital cleft which rupture leaving shallow ulcers. The lesions may extend to the bulbs of the heel resulting in under running and loosening of the hooves, sloughing of the horns and hooves in piglets. within 3-4 days the base of the ulcers become covered with a sero fibrinous exudate and regeneration of the epithelium is complete within about 10 days. Cattle move their tongue and jaw producing a characterising champing which churns saliva into a froth which hangs in string from the mouth. Affected animals paddle from one foot to the other and lie down frequently. pigs are very lame. sheep may show little more than a day or twos lameness. pregnant animals may abort.
How is diagnosis of FMD made?
Usually based on clinical signs with a history of contact with imported animals, infected animals or reports of diseae in the area. Laboratory confirmation using ELISa and PCR and virus isolation readily available. Vesicular epithelium is a particularly good source of virus, virus can also be recovered from many excretions and secretions and whole blood. antibody is produced about 4 days after clinical signs appear and can be detected in serum samples. Portable pen side test kits are being developed for on farm diagnosis. At least 2sq cm of vesicular epithelium should be collected, kept away from disinfectants and transported in chilled glycerol phosphate buffer. suspect material is tested against all 7 serotypes of FMD using ELISA or PCR. At the same time samples are cultured on bovine thyroid and pig kidney cells serving to amplify virus.
What are the possible DDx for cattle, pigs and sheep?
Mouth lesions - malignant catarrhal fever, Ibr, mucosal disease, vesicular stomatitis, rinderpest, bovine papular stomatitis, necrotic stomatitis, trauma, irritant agents such as caustic treated fodder, bluetongue.
in pigs - swine vesicular disease, vesicular stomatitis, enterotoxaemia in piglets, encephalomyocarditis virus.
Sheep - foot rot, bluetongue, orf, enterotoxaemia in lamb.
Describe the pathogenesis of Foot and mouth disease?
Virus usually enters the body through the mucosae and lymphoid tissues of the pharyngeal and tonsillar regions where a primary replication phase lasting 2-3 days takes place. Virus then enters the bloodstream where it circulates for 3-5 days seeding its predilection sites and initiating a secondary replication phase. These sites include the lymph nods, adrenal glands, kidneys, mammary gland, thyroid gland, heart, lungs and skin. Virus is present in large quantities in these tissues and some bodily secretions. milk and semen are known to contain virus for up to 4 days before clinical signs appear. the amount of virus excreted increases dramatically during the early vesicular stage of the disease when all body secretions and excretions contain huge amounts of virus resulting in heavy widespread contamination of the environment.
How is foot and mouth disease transmitted?
Natural infection is most frequently by inhalation of droplets containing virus or by ingestion of virus contaminated material. infection of cattle and sheep by the respiratory route requires as little as 10 infectious units of virus, pigs require about 15 i.u. Once one or more animals in a herd has been infected the quantity of virus in the environment will be greatly amplified then transmission by several different routes will be possible. the remaining animals in a herd will therefore be exposed to ever increasing amounts of virus resulting in shorter incubation periods as the infection gains momentum. the drop in pH pm due to lactic acid and pyruvic acid formation inactivates the virus in skeletal muscles however virus will persist in offal or bone marrow where no such pH changes occur.
Does vaccination for foot and mouth disease work?
Yes -but only effective against the homologous or closely related strains. vaccine virus is grown in cell cultures, chemically inactivated and mixed with an adjuvant. immunity develops within 14 days of primary vaccination and lasts for 4-6 months when revaccination can extend immunity up to one year. Pigs are more difficult to immunise requiring higher concentrations of virus and different adjuvants such as double oil emulsions..
How is foot and mouth disease controlled and eradicated?
Isolate countries such as UK have relied on stamping out policy which requires a well developed state veterinary service, swift slaughter and disposal and efficient cleansing and disinfection of premises and effective movement controls supported by the police, import controls on animals and their products, by the regulation or prohibition of feeding waste food to susceptible livestock and by continuous surveillance.
Describe Bluetongue infection
Caused by an orbivirus. Vector is culicoides species. (midge) . midge activity governed by factors such as high temperature, humidity and rainfall, soil type, so tends to be seaonal. Midge infected when feeding on a viraemic animal, virus passes from midge gut to salivary gland where viral replication occurs. infection is life long. mammalian hosts - sheep, cattle goats and other ruminants. Cattle natural reservoir, latent and inapparent infections. sheep - inapparent infections in indigenous naimals. severest clinical disease seen in introduced animals or old infirm or immunocompromised animals. Transient viraemia, virus spreads to other lymphatic organs, secondary replication occurs in endothelial cells, generalised Viraemia follows, virus closely associated with erythrocytes, protected from immune response. Virus replication in endothelial cells causes cell lysis allowing serum and lymphatic fluid to leak out producing oedema and haemorrhages. Cliniical signs - fever, anorexia, respiratory distess, oedema, swollen head and lower legs, encrusted or bleeding lips, swelling and cyanosis of tongue, ulcers in mouth, conjuctivitis, coronitis, serous oculonasal discharge. Diagnosis by blood spleen lymph glands for virus growth and isolation and detection of viral RNA (PCR ) & antibody (ELISA). Control: attenuated vaccines very effective.
Describe african horse sickness
It is an orbivirus, there are nine distinct serotypes, family reoviridae. vector is culicoides imicola. Zebras are natural reservoir of infection, inapparent infection. Domestic equines and camels are suspected. Infection maintained by longeivity of culicoides and prolongeed viraemias in infected mammals. Inapparent infections in indigenous animals. Serious disease with high mortality in exotics. Epidemics occur when vector extends its normal range. Incubation 2-21 days. High fever, severe respiratory distress, subcutaneous oedema of head especially supra orbital fossa, also neck, abdomen. Annual vaccination for exotic horses in endemic areas.
