Veterinary · Clinical · also MSVE VMD-422, Infectious Diseases II
The viral and parasitic diseases of farm and companion animals, national control programmes and the international role of WOAH.
In the exams: ICAR AICE-JRF core group 07 (Medicine); SAVC Paper 4 State veterinary medicine 35; NAVLE veterinary public health 4%; China infectious diseases 30
Preventive veterinary medicine II covers the infectious diseases of animals caused by viruses and by parasites (blood protozoa, trypanosomes and helminths), and the national and international machinery used to control them. For each disease the student learns the same chain: the agent, the hosts, how it spreads and persists, what it looks like in the live and dead animal, which samples to take and which tests confirm it, what else it could be, whether and how to treat, and how it is prevented on a farm and controlled across a country. Viral diseases are rarely treatable, so the weight falls on vaccination, movement control, biosecurity and, for the most serious diseases, stamping out.
The diseases in this subject are the ones that close borders. Foot-and-mouth disease (FMD), peste des petits ruminants (PPR), lumpy skin disease, bluetongue, sheep and goat pox, classical and African swine fever and African horse sickness are all listed by the World Organisation for Animal Health (WOAH), and a single confirmed case can stop a country's exports overnight. Rabies kills tens of thousands of people every year, almost all after dog bites. The blood parasites and helminths rarely make the news but cost livestock owners heavily year after year.
Indian ICAR and state veterinary officer papers ask about agents, vaccine strains and control programmes. NAVLE, BCSE, the RCVS, Australasian and South African licensing exams set clinical vignettes and ask what to sample, what to do next and whom to notify. The Chinese and Korean national examinations weight infectious and parasitic disease heavily.
This manual is written for the practising vet and the state veterinary officer. It gives vaccination schedules in general terms only, because products and national schedules differ, and it gives very few drug doses; where a dose appears it is the standard textbook value and must be checked against the product label and the national formulary.
Foot-and-mouth disease (FMD) is caused by an aphthovirus of the family Picornaviridae, a small non-enveloped RNA virus. There are seven serotypes: O, A, C, Asia 1 and the three South African Territories types SAT 1, SAT 2 and SAT 3. Infection or vaccination with one serotype gives no useful protection against another. Serotype C has not been reported for many years. All cloven-hoofed animals are susceptible: cattle, buffalo, sheep, goats, pigs, deer and camelids to a lesser degree. The three main species play different roles. Cattle are the indicator hosts: they are highly susceptible to inhaled virus and show clear signs. Pigs are amplifiers: an infected pig exhales far more airborne virus than a cow. Sheep and goats are maintenance hosts: signs are often mild and the disease is missed.
The virus spreads by contact, aerosol (far in cool, humid weather), fomites, milk, semen and swill. It survives well in chilled and frozen meat and in lymph nodes and bone marrow, but is inactivated by acid (pH below about 6) and by the fall in pH of muscle after normal slaughter. Many ruminants that recover carry virus in the pharynx for months; African buffalo can carry SAT viruses for years. Pigs do not. The incubation period is usually 2 to 14 days, shorter after heavy exposure.
In cattle the first signs are high fever, dullness and a sharp fall in milk yield, followed within a day or two by vesicles (blisters) on the tongue, dental pad, gums, muzzle, interdigital space, coronary band and teats. Vesicles rupture to leave raw erosions; the animal salivates in ropes, smacks its lips, shakes its feet and is lame. Mortality in adults is low, but young calves, lambs and piglets can die suddenly from myocarditis, which gives the pale-streaked 'tiger heart' at necropsy. Pigs may slough the hoof horn.
The best samples are vesicular epithelium and vesicular fluid. At least 1 g of fresh epithelium from an unruptured or freshly ruptured vesicle is placed in transport medium of equal parts glycerol and phosphate buffer at pH 7.2 to 7.6, kept cool and sent by the approved route to the national or WOAH reference laboratory. Where no epithelium is available, oesophageal-pharyngeal fluid collected with a probang cup, and blood for serology, are used. Laboratory tests include antigen-detection ELISA, real-time RT-PCR and virus isolation for diagnosis and serotyping, and antibody tests: ELISA or virus neutralisation against the structural proteins, which detect both infection and vaccination, and the non-structural protein (NSP, for example 3ABC) ELISA, which detects infection in animals vaccinated with purified vaccine. NSP serology is the basis of surveillance in vaccinated populations.
The main differential diagnoses in ruminants are vesicular stomatitis, bluetongue, bovine viral diarrhoea and mucosal disease, malignant catarrhal fever, infectious bovine rhinotracheitis, bovine papular stomatitis and, historically, rinderpest. In pigs, vesicular stomatitis, swine vesicular disease, vesicular exanthema and Senecavirus A produce identical lesions, so every vesicular disease in pigs must be reported and tested.
Countries free of FMD keep it out by import controls, swill-feeding bans and surveillance, and eliminate an incursion by stamping out: killing infected and in-contact animals with compensation, disposal, cleaning and disinfection, movement standstills and control zones, sometimes with emergency vaccination. In the European Union the minimum zones are a protection zone of 3 km and a surveillance zone of 10 km around an infected premises; other countries set their own distances. Endemic countries rely on mass vaccination with inactivated, adjuvanted vaccines containing the locally circulating serotypes. Immunity is short: a common pattern is a primary dose at about 4 months of age, a booster about a month later and revaccination every 6 months, but schedules are set nationally. Vaccination prevents disease but does not reliably prevent infection or the carrier state.
WOAH grants official status for FMD: country or zone free without vaccination, free with vaccination, and endorsed official control programmes. FAO and WOAH promote the Progressive Control Pathway for FMD (PCP-FMD), in which a country moves stage by stage from understanding where the virus circulates to sustained control and then to an application for official freedom. In an outbreak, field officers age the lesions to estimate when infection entered, trace contacts, and disinfect with acids or alkalis (citric acid, sodium carbonate, sodium hydroxide).
Peste des petits ruminants (PPR), also called goat plague, is caused by small ruminant morbillivirus (peste des petits ruminants virus) of the family Paramyxoviridae, a close relative of rinderpest, measles and canine distemper viruses. There is one serotype and four lineages. Goats are usually more severely affected than sheep; cattle and pigs are infected silently. Spread is by close contact, so outbreaks follow market movements and festivals; the virus is fragile outside the host.
The acute disease begins with high fever, depression and serous then mucopurulent discharge from the eyes and nose, which mats the eyelids and blocks the nostrils. Erosions and necrosis appear on the gums, dental pad, tongue and palate, with foul breath, then profuse watery diarrhoea and bronchopneumonia (often complicated by Mannheimia or Pasteurella). This combination is called the stomatitis-pneumoenteritis syndrome. At necropsy there are erosions along the digestive tract, congestion along the folds of the colon and rectum ('zebra stripes'), and consolidation of the anteroventral lungs. Differentials include contagious caprine pleuropneumonia, pasteurellosis, bluetongue, orf, FMD, sheep and goat pox and helminthosis.
Samples are ocular, nasal and mouth swabs and EDTA blood from febrile animals, and lymph node, lung and spleen from fresh carcasses. Tests include RT-PCR, antigen-capture (immunocapture) ELISA, rapid pen-side antigen tests and, for antibody, competitive ELISA and virus neutralisation. There is no specific treatment; supportive care and antibiotics against secondary pneumonia reduce deaths. Live attenuated vaccines grown in cell culture (the Nigeria 75/1 strain, and Indian strains such as Sungri 96) give strong immunity for at least three years after one dose. PPR is WOAH-listed with official status recognition. FAO and WOAH launched the PPR Global Control and Eradication Strategy in 2015 with the goal of global eradication by 2030, built on the lessons of rinderpest.
Rinderpest (cattle plague) was a morbillivirus disease of cattle, buffalo, yak and many wild artiodactyls, with fever, erosive stomatitis, profuse diarrhoea, dehydration and mortality that could approach total loss in naive herds. An incursion into Belgium in 1920 led to the founding of the Office International des Epizooties, now WOAH, in 1924.
Eradication rested on several pillars. The first was a safe, cheap vaccine: Plowright's tissue culture rinderpest vaccine gave lifelong immunity after one dose, and a thermostable freeze-dried version allowed vaccination in hot areas without a cold chain. The second was coordinated regional campaigns, such as the Pan-African Rinderpest Campaign and national programmes in South Asia, brought together from 1994 under the FAO-led Global Rinderpest Eradication Programme (GREP). The third was a shift from blanket vaccination to targeted surveillance: participatory disease searching, community animal health workers in pastoral areas, wildlife sampling, and serosurveillance after vaccination stopped, so that antibody meant infection. The fourth was a formal pathway in which each country proved freedom to WOAH. India was recognised free of rinderpest infection in 2006. The last confirmed case was in Kenya in 2001, and WOAH (May 2011) and FAO (June 2011) declared the world free, the second disease after smallpox and the first animal disease ever eradicated. The lessons for PPR are that eradication needs no long-term carrier, a durable vaccine, a diagnostic test, political commitment over decades and surveillance that finds the last foci. Remaining virus stocks are held in a few approved facilities, and any suspicion must still be reported.
Lumpy skin disease (LSD) of cattle and water buffalo is caused by a capripoxvirus closely related to sheep pox and goat pox viruses. Long confined to Africa, it reached south-eastern Europe in 2015-16 and South and East Asia from 2019, with very large epidemics in India in 2022. It is transmitted mainly mechanically by blood-feeding arthropods: stable flies (Stomoxys), mosquitoes and probably ticks, so outbreaks peak in the warm wet season and spread along cattle movement routes. Direct contact is a minor route; infected bulls can shed virus in semen.
After an incubation of about one to four weeks there is fever, enlarged superficial lymph nodes, lacrimation and nasal discharge, a sharp drop in milk, and then firm, round skin nodules usually 1 to 5 cm across over the head, neck, udder, perineum and limbs. Nodules involve the full skin thickness and may become necrotic 'sitfasts'. Limb and brisket oedema is common. Mortality is usually low but production losses are large. Differentials are pseudo-lumpy skin disease (bovine herpesvirus 2), dermatophilosis, insect bites and urticaria, ringworm, demodicosis, besnoitiosis, photosensitisation and bovine papular stomatitis.
Samples for PCR are skin biopsies or scab material from nodules and EDTA blood in the febrile stage; serology is less useful because antibody can be low. Treatment is supportive. Control is by vaccination, movement control and vector control. Homologous live attenuated vaccines based on the Neethling strain protect well. Heterologous sheep pox or goat pox vaccines have been used in some countries, including goat pox vaccine in India, and national authorities decide which is permitted. LSD is WOAH-listed and notifiable.
Sheep pox and goat pox are capripoxvirus diseases endemic across North and Central Africa, the Middle East and Asia, including India. They are the most serious pox diseases of livestock: fever, papules that develop into nodules over the woolless skin, eyelids, muzzle and udder, lesions in the lungs and digestive tract, and mortality that can be high in young or naive animals. Live attenuated vaccines are used in endemic areas. Both are WOAH-listed.
Several other pox and pox-like infections are seen in practice. Contagious ecthyma (orf) is a parapoxvirus infection of sheep and goats causing proliferative scabs on the lips, muzzle, teats and coronets; it is zoonotic, causing a painful nodule on the hand of shepherds and vets, and is controlled with a live scab vaccine applied by scarification, which should only be used on farms where the disease already exists. Pseudocowpox, also a parapoxvirus, causes ring-shaped scabs on cows' teats and 'milker's nodules' in people. True cowpox is an orthopoxvirus of wild rodents, now seen in Europe mainly in cats. Buffalopox, a vaccinia-like orthopoxvirus, causes teat and udder lesions in buffalo and cows in South Asia and lesions on the hands of milkers. Fowlpox, an avipoxvirus spread by mosquitoes and contact, appears in a cutaneous (dry) form with scabs on the comb and wattles and a diphtheritic (wet) form with yellow plaques in the mouth, pharynx and trachea that can suffocate the bird; it is controlled by vaccination by wing-web stab.
Bluetongue is a non-contagious disease of ruminants caused by bluetongue virus, an orbivirus of the family Sedoreoviridae (formerly placed in Reoviridae), transmitted by biting midges of the genus Culicoides. More than 24 serotypes are recognised, and protection is serotype-specific. Sheep suffer the most severe disease; cattle and goats are usually infected silently, although serotypes 8 (northern Europe, 2006) and 3 (from 2023) caused disease in cattle. Cattle are important reservoirs because viraemia can last several weeks; WOAH uses an infective period of 60 days for trade purposes. Bluetongue is seasonal: it follows the vector, and a 'seasonally vector-free period' in cold winters is used to permit movement.
In sheep the signs are fever, hyperaemia and oedema of the lips, muzzle, face and ears, excess salivation and nasal discharge, ulceration of the mouth, and in some cases a swollen, cyanotic tongue, which gives the name but is not the commonest sign. Coronitis causes lameness; muscle damage causes stiffness and torticollis; wool breaks later. At necropsy haemorrhage at the base of the pulmonary artery is characteristic. Infection of the pregnant ewe or cow with some strains causes abortion and congenital brain defects such as hydranencephaly. Differentials are FMD, PPR, orf, sheep pox, photosensitisation, epizootic haemorrhagic disease (a related orbivirus in cattle and deer) and foot rot.
Samples are whole blood in EDTA for RT-PCR, which detects viral RNA for a long time, and serum for the competitive ELISA (group-specific) and virus neutralisation (serotype-specific). Treatment is nursing: shade, soft feed, water and anti-inflammatory drugs. Control relies on vaccination with vaccines matched to the circulating serotypes (inactivated vaccines in most of Europe; live attenuated vaccines in South Africa and elsewhere, which can cause viraemia and fetal damage and must not be used in pregnant ewes), movement restrictions and housing at dusk and dawn when midges are active. Bluetongue is WOAH-listed.
Bovine viral diarrhoea virus (BVDV) is a pestivirus of the family Flaviviridae, with species BVDV-1, BVDV-2 and the HoBi-like pestiviruses, and two biotypes defined in cell culture: non-cytopathic, which causes most field infection, and cytopathic. When a susceptible cow is infected with non-cytopathic virus roughly between the second and fourth months of gestation, before the fetal immune system can recognise the virus, the calf is born immunotolerant and sheds huge amounts of virus all its life. PI animals are the main source of herd infection. Infection at other stages causes embryonic death, abortion, congenital defects such as cerebellar hypoplasia, or a normal calf with antibody.
Acute infection in non-pregnant cattle is often subclinical but suppresses immunity and predisposes to respiratory and enteric disease; some BVDV-2 strains cause severe acute disease with thrombocytopenia and haemorrhage. Mucosal disease occurs when a PI animal, usually aged 6 to 24 months, is superinfected with a cytopathic virus antigenically similar to its own; it is invariably fatal, with fever, profuse diarrhoea, and erosions throughout the mouth, oesophagus and intestine, especially over Peyer's patches.
Diagnosis in a herd uses bulk milk antibody or antigen testing, serology of a few young unvaccinated stock to detect recent circulation, and antigen-capture ELISA or PCR on ear-notch tissue or blood to find PI animals. A single positive result does not prove persistent infection: a transiently infected animal also tests positive, so a positive animal is retested after at least three weeks, and a PI animal stays positive. In calves under about a month old, colostral antibody can mask antigen in blood, so ear-notch tests or PCR are preferred. Control rests on removing PI animals, preventing new ones by biosecurity (testing purchased cattle and the calves of purchased pregnant cows, the 'Trojan cow') and vaccination of breeding females before service with vaccines that protect the fetus. Programmes in Scandinavia, Switzerland and Ireland have greatly reduced BVD by ear-notch testing every newborn calf and removing PIs. BVD is WOAH-listed.
Rabies is an acute, almost always fatal encephalomyelitis caused by rabies virus, a lyssavirus of the family Rhabdoviridae, with a characteristic bullet shape. All mammals are susceptible. In most of Asia and Africa the domestic dog is the reservoir and the source of about 99% of human cases; elsewhere wildlife reservoirs dominate (foxes, raccoons, skunks, jackals, mongooses) and in the Americas bats, including vampire bats that transmit rabies to cattle. Transmission is almost always by a bite introducing saliva. The virus travels along peripheral nerves to the central nervous system and then outward to the salivary glands, so saliva becomes infective shortly before signs appear. The incubation period is very variable, usually weeks to a few months, and depends on the dose and site of the bite.
After a short prodromal phase of behavioural change comes either a furious form (restlessness, aggression, biting at objects, roaming, a change of voice, pica) or a paralytic, 'dumb' form (dropped jaw, drooling, inability to swallow, ascending paralysis). Most animals show elements of both and die within about 7 to 10 days of the first signs. Cattle bellow, strain, salivate and are easily mistaken for choke, a classic way people are exposed. Differentials include distemper, choke, lead poisoning, listeriosis, polioencephalomalacia and Aujeszky's disease.
Rabies cannot be confirmed reliably in the live animal. The animal is humanely killed or allowed to die under observation, and brain tissue (brainstem, cerebellum and hippocampus; the brainstem can be sampled through the foramen magnum without opening the skull) is sent chilled, or in glycerol-saline where cooling is not possible, to an approved laboratory. The direct fluorescent antibody test on brain smears is the WOAH and WHO reference test; RT-PCR and direct rapid immunohistochemistry are also used. Negri bodies on histology or Seller's stain are specific but miss many cases and are no longer relied on. The sampler should be vaccinated and wear protective equipment.
When a dog or cat that appears healthy bites a person, the standard practice in many countries is to confine and observe it for 10 days: if it is still healthy, it was not shedding virus at the time of the bite. Any animal that develops signs is euthanased and tested. Human post-exposure care is a medical decision, not the vet's, but the vet must make sure the wound is washed at once with soap and plenty of water for about 15 minutes and that the person is referred for vaccination and, for severe exposures, rabies immunoglobulin. Vets, laboratory staff and animal handlers should receive pre-exposure vaccination.
Prevention in animals is by vaccination with inactivated vaccines: dogs and cats are commonly given a first dose at about 12 weeks of age, a booster within a year, and then revaccination at the interval on the product licence and national law, often one or three years. Elimination of dog-mediated rabies depends on mass dog vaccination reaching at least about 70% of the dog population each year, plus dog population management, bite surveillance and public education. The global strategy 'Zero by 30', backed by WHO, WOAH, FAO and the Global Alliance for Rabies Control, aims to end human deaths from dog-mediated rabies by 2030. International pet travel to rabies-free countries usually needs a microchip, vaccination and, for many destinations, a rabies neutralising antibody titre of at least 0.5 IU/ml in a fluorescent antibody virus neutralisation test, followed by a waiting period. Rabies is WOAH-listed and notifiable in most countries.
Classical swine fever (CSF, hog cholera) is caused by a pestivirus of the family Flaviviridae, related to BVDV. African swine fever (ASF) is caused by a large, complex DNA virus, the only member of the family Asfarviridae, and the only known DNA arbovirus, being transmitted by soft ticks of the genus Ornithodoros as well as by contact. Both affect only pigs, domestic and wild, and cannot be told apart reliably on clinical or post-mortem signs, so every suspicion must be reported and tested.
Acute CSF causes high fever, huddling, conjunctivitis, constipation followed by diarrhoea, a staggering gait and convulsions, and purple discoloration of the ears, snout, limbs and belly. Lesions include petechial haemorrhages in the kidneys ('turkey-egg kidney'), the bladder and the larynx, haemorrhagic lymph nodes, infarcts at the margin of the spleen, and in subacute cases 'button ulcers' in the caecum and colon. Low-virulence strains in sows cause abortion, mummies, congenital tremor and persistently infected piglets.
ASF in its acute form causes high fever, loss of appetite, reddening and cyanosis of the skin, vomiting, bloody diarrhoea and death within about a week in most of the herd. The classic lesions are a greatly enlarged, dark, friable spleen, lymph nodes that look like blood clots, especially the gastrohepatic and renal nodes, petechiae on the kidneys and oedema of the gall bladder wall and lungs. Subacute and chronic forms occur with less virulent strains. ASF spread from Africa to Georgia in 2007 and from there through eastern and central Europe, to China in 2018 and across much of Asia, including north-eastern India from 2020. It spreads through pigs, wild boar, pork products (where it survives for months), swill, vehicles and ticks. Differentials include PRRS, porcine dermatitis and nephropathy syndrome, erysipelas, salmonellosis and Aujeszky's disease.
Samples are whole blood in EDTA from febrile pigs and serum from pigs that have been ill for longer, and spleen, tonsil, lymph nodes and kidney from dead pigs. Real-time PCR is the main test for both; antigen ELISA, virus isolation and antibody ELISA support it. In acute ASF pigs die before antibody appears.
Control is mainly by biosecurity and stamping out. Farms should fence out wild boar, control entry of people and vehicles, never feed catering waste and buy pigs only from known sources. In an outbreak, all pigs on the infected premises are humanely killed and disposed of, the premises cleaned and disinfected, contacts traced, and control zones with movement bans set up; in wild boar areas carcass search and removal and fencing are added. National plans set the zone sizes, often an infected zone around the outbreak and a wider surveillance zone. For CSF, live attenuated vaccines such as the lapinised C-strain are safe and effective and are used in endemic countries, including India; marker (DIVA) vaccines exist; free countries generally ban vaccination and rely on stamping out. For ASF there is no internationally approved, widely used vaccine, although live attenuated candidates have been licensed in one country and their safety is still debated. Both diseases are WOAH-listed, and CSF is one of the diseases for which WOAH grants official freedom status.
Canine distemper virus (CDV) is a morbillivirus that infects dogs, ferrets, foxes, raccoons, mink and large cats. It spreads by aerosol and contact with discharges and is fragile in the environment. Disease is commonest in unvaccinated puppies aged 3 to 6 months. Signs begin with fever and serous then mucopurulent oculonasal discharge, cough and pneumonia, followed by vomiting and diarrhoea. Nervous signs may follow weeks later, or appear without earlier disease: myoclonus (rhythmic twitching of muscle groups, which is very suggestive), seizures ('chewing-gum fits'), ataxia and paralysis. Hyperkeratosis of the footpads and nose ('hard pad') and enamel hypoplasia of the permanent teeth in survivors are characteristic. Diagnosis is by RT-PCR on conjunctival swabs, blood, urine or cerebrospinal fluid; inclusion bodies in blood cells or conjunctival cells are seen in some cases. Recent live vaccination can give a positive PCR. Treatment is supportive and the prognosis for nervous disease is poor.
Infectious canine hepatitis is caused by canine adenovirus type 1 (CAdV-1), which is very resistant in the environment and shed in urine for months. Acute disease causes fever, abdominal pain, vomiting, bleeding tendencies and sudden death in puppies, with gall bladder wall oedema and intranuclear inclusions in hepatocytes. During recovery some dogs develop an immune-complex anterior uveitis with corneal oedema, the 'blue eye'. Vaccines use canine adenovirus type 2 (CAdV-2), which protects against both CAdV-1 and the CAdV-2 component of infectious respiratory disease, without the blue-eye reactions seen with old CAdV-1 vaccines.
Canine parvovirus type 2 (CPV-2, with variants 2a, 2b and 2c) arose in the late 1970s from a feline panleukopenia-like virus. It is a small non-enveloped DNA virus that survives for months or years in the environment and is shed in enormous amounts in faeces. It replicates in rapidly dividing cells: the intestinal crypt epithelium, bone marrow and lymphoid tissue. The typical case is an unvaccinated puppy aged 6 weeks to 6 months with depression, anorexia, vomiting, then foul-smelling, often haemorrhagic diarrhoea, dehydration and leucopenia (marked neutropenia), with risk of septicaemia and intussusception. Diagnosis is by faecal antigen ELISA in practice (which may be negative early in disease and can be weakly positive shortly after vaccination with live vaccine), confirmed by PCR where needed, with a complete blood count. Treatment is supportive: intravenous fluids, antiemetics, early enteral nutrition and parenteral antibiotics for neutropenic dogs. The kennel must be isolated and cleaned with a disinfectant active against non-enveloped viruses, such as diluted sodium hypochlorite after removing organic matter, or an accelerated hydrogen peroxide or potassium peroxymonosulfate product.
Feline panleukopenia virus (FPV) is the cat parvovirus and causes the same pattern: fever, vomiting, diarrhoea, severe leucopenia and high mortality in kittens. Infection in late pregnancy or the first weeks of life damages the developing cerebellum, giving kittens with cerebellar hypoplasia, which show intention tremor and wide-based ataxia once they begin to walk; retinal lesions may also occur. CPV-2 variants can also infect cats.
Vaccination guidance from the World Small Animal Veterinary Association (WSAVA) lists core vaccines for all dogs as CDV, CAdV and CPV-2, and for all cats as FPV, feline herpesvirus-1 and feline calicivirus, with rabies core wherever it is endemic or required by law. Puppies and kittens start at about 6 to 8 weeks of age and are revaccinated every 2 to 4 weeks until 16 weeks of age or older, because maternal antibody blocks vaccination for a variable time; a further dose follows at 26 weeks or at one year, and after that modified live core vaccines need to be given no more often than every three years.
Equine influenza is caused by influenza A virus subtype H3N8. It is highly contagious and causes sudden fever, a harsh dry cough and nasal discharge, with outbreaks at shows, sales and racing yards. Secondary bacterial pneumonia is the main complication. Diagnosis is by nasopharyngeal swab RT-PCR early in fever, or paired serology. Many racing and competition authorities require vaccination. Equine influenza is WOAH-listed.
Equine herpesvirus 1 (EHV-1) and EHV-4 are alphaherpesviruses that establish lifelong latent infection. EHV-1 causes respiratory disease, late-term abortion (often in several mares, as 'abortion storms'), weak neonatal foals, and equine herpesvirus myeloencephalopathy: a vasculitis of the spinal cord giving ataxia, hindlimb weakness, bladder paralysis and urine dribbling, and recumbency. Diagnosis is by PCR on nasal swabs and buffy coat, and on aborted fetal tissues, which show intranuclear inclusions. Outbreaks are controlled by isolation, twice-daily temperatures of in-contacts and movement restriction. Vaccines reduce respiratory disease and abortion but do not reliably prevent the neurological form.
Equine viral arteritis (an arterivirus) spreads by aerosol and venereally. It causes fever, oedema of the limbs, scrotum and ventral body, conjunctivitis and abortion. Many infected stallions become long-term carriers that shed virus in semen. Stallions are tested by serology and, if positive, by virus isolation from semen or test mating. It is WOAH-listed.
Equine infectious anaemia (EIA) is caused by a lentivirus of the family Retroviridae. It is transmitted mechanically in blood by large biting flies, especially horse flies (Tabanus) and deer flies, and by reused needles, instruments and blood products. Some horses develop recurrent fever, anaemia, oedema and weight loss ('swamp fever'); most become inapparent carriers for life. There is no treatment and no vaccine in most countries. Diagnosis is by the agar gel immunodiffusion (Coggins) test or ELISA, with positives confirmed by immunodiffusion or immunoblot. Positive horses are usually destroyed or kept permanently isolated at a distance from other horses, depending on national law. EIA is WOAH-listed and testing is required for movement and trade in many countries.
African horse sickness (AHS) is caused by an orbivirus with nine serotypes, transmitted by Culicoides midges. It is endemic in sub-Saharan Africa and has caused epidemics beyond it, including in Spain, Portugal and Thailand. Horses suffer the most severe disease; mules are less affected and donkeys and zebras rarely show signs, zebras acting as a reservoir. There are four forms: the pulmonary form ('dunkop') with severe dyspnoea, frothy nasal discharge and death within days; the cardiac form ('dikkop') with swelling of the supraorbital fossae, eyelids and head; a mixed form; and a mild horse sickness fever. AHS is WOAH-listed with official status recognition, and live attenuated polyvalent vaccines are used in endemic areas.
The arboviral encephalitides are mosquito-borne. West Nile virus, a flavivirus maintained in birds, causes ataxia, weakness, muscle fasciculation and behavioural change in horses, which are dead-end hosts. Eastern and Western equine encephalitis (alphaviruses) are also maintained in birds, and horses and people are dead-end hosts; Eastern equine encephalitis has very high mortality. In Venezuelan equine encephalitis, horses amplify epidemic strains. Inactivated vaccines exist for several of these. Differentials include rabies, EHV-1 myeloencephalopathy and equine protozoal myeloencephalitis.
Babesia species are tick-borne protozoa that multiply inside red blood cells. In cattle the main species are Babesia bigemina and Babesia bovis, transmitted by one-host ticks of the Rhipicephalus (formerly Boophilus) microplus group, and Babesia divergens in Europe, transmitted by Ixodes ricinus. Babesia passes through the tick's eggs (transovarial transmission). Calves are relatively resistant for their first months of life, partly because of colostral antibody and partly because of an innate age resistance; if they are infected while young they become immune with little disease, a situation called endemic stability. Outbreaks occur when susceptible adult cattle are brought into a tick area or when intense tick control left young stock unexposed.
Signs are high fever, anaemia, jaundice, haemoglobinuria ('redwater', port-wine urine), rapid heart and breathing rates and a fall in milk; B. bovis also causes cerebral babesiosis, with incoordination, convulsions and coma, as infected red cells stick in brain capillaries. Diagnosis is by thin and thick blood smears stained with Giemsa. B. bigemina is large, often in pairs at an acute angle; B. bovis is small, often paired at an obtuse angle, scarce in jugular blood and best found in capillary blood from the ear or tail tip or, after death, in a smear of cerebral cortex. PCR and serology are used for carriers and surveys. Differentials of haemoglobinuria include leptospirosis, bacillary and postparturient haemoglobinuria and copper poisoning; anaplasmosis causes anaemia and jaundice without haemoglobinuria.
Treatment: diminazene aceturate (commonly 3.5 mg/kg by deep intramuscular injection — confirm against the product label and your national formulary) or imidocarb dipropionate (commonly 1.2 mg/kg subcutaneously for treatment — confirm against the product label and your national formulary). Imidocarb persists in tissues and also protects for some weeks, so withdrawal periods for meat and milk are long and some countries do not permit it in food animals. Severely anaemic animals may need blood transfusion. Prevention uses tick control (balanced against endemic stability), live attenuated blood-derived vaccines in some countries such as Australia, South Africa and parts of South America, and chemoprophylaxis when moving susceptible stock. In dogs, B. canis, B. vogeli, B. rossi and the small B. gibsoni cause similar disease. In horses, Theileria equi and Babesia caballi cause equine piroplasmosis, which is WOAH-listed and tested before export.
Theileria species multiply first as schizonts in lymphocytes, transforming them, and then invade red cells as piroplasms. Tropical theileriosis, caused by Theileria annulata and transmitted by Hyalomma ticks, occurs from North Africa and southern Europe across the Middle East to India and China; exotic and crossbred cattle are far more susceptible than local breeds. East Coast fever, caused by Theileria parva and transmitted by Rhipicephalus appendiculatus, is a major killer of cattle in eastern, central and southern Africa; when it comes from African buffalo it is called Corridor disease. Theileria orientalis (including the Ikeda type), transmitted by Haemaphysalis ticks, causes anaemia and abortion in cattle in Australia, New Zealand and East Asia.
The typical case of tropical theileriosis or East Coast fever shows high fever, marked enlargement of the superficial lymph nodes (especially the prescapular and prefemoral), lacrimation, nasal discharge, petechiae on mucous membranes, laboured breathing from pulmonary oedema, and later anaemia and jaundice in T. annulata. Death is common in susceptible cattle. Diagnosis is by Giemsa-stained smears of lymph node aspirate, which show schizonts (Koch's blue bodies) in lymphocytes, and blood smears showing small comma, rod, ring and 'signet ring' piroplasms in red cells, supported by PCR and serology.
Treatment with buparvaquone (commonly 2.5 mg/kg by intramuscular injection, sometimes repeated after 48 to 72 hours — confirm against the product label and your national formulary) is effective if given early; parvaquone and halofuginone have also been used; tetracyclines have limited value except when given very early. Control combines tick control, keeping cattle away from tick habitat, and vaccination: live attenuated schizont cell-culture vaccines against T. annulata are used in India, the Middle East and North Africa, and the 'infection and treatment method' against T. parva, in which cattle are infected with live sporozoites and simultaneously treated with long-acting oxytetracycline, is used in eastern Africa. Theileriosis (T. annulata, T. parva and T. orientalis) is WOAH-listed.
Trypanosomes are flagellate protozoa that live in the blood and tissue fluids. African animal trypanosomosis (nagana) is caused mainly by Trypanosoma congolense, T. vivax and T. brucei brucei, transmitted cyclically by tsetse flies (Glossina) across a belt of sub-Saharan Africa. T. vivax has also spread to South America, where it is transmitted mechanically by biting flies. Surra, caused by T. evansi, is transmitted mechanically by tabanids and Stomoxys; it affects camels, horses, buffalo, cattle and dogs from North Africa to Asia and South America, and is the most important trypanosomosis in India. Dourine, caused by T. equiperdum, is a venereal disease of horses and donkeys with genital oedema, characteristic 'plaques' on the skin and progressive paralysis.
Disease brings intermittent fever as waves of parasites appear in the blood, anaemia (the central sign), wasting, oedema, infertility, abortion and death. Surra is often acute in horses and dogs and chronic in camels. Some West African breeds, notably N'Dama cattle and West African dwarf goats, are trypanotolerant: they control parasitaemia and anaemia and remain productive in tsetse areas.
Because parasitaemia fluctuates, a negative blood test does not rule out infection. Methods are wet blood films, Giemsa-stained smears, and the far more sensitive concentration methods: the microhaematocrit (Woo) centrifugation technique, which looks at the buffy coat zone in the capillary tube, and the dark-ground buffy coat (Murray) method. Inoculation of mice or rats can detect low parasitaemia of T. evansi and T. brucei. Antibody tests (ELISA, card agglutination test for T. evansi) show exposure, and PCR is used for species and for low parasitaemia.
The main trypanocides are diminazene aceturate (curative), isometamidium chloride (curative and prophylactic, protecting for some months), homidium salts, quinapyramine (curative and prophylactic, used especially against T. evansi in camels and horses), suramin (horses and camels) and melarsomine (T. evansi in camels). Doses differ by trypanosome species, host and product, and several of these drugs are toxic at slightly higher doses or in particular species (for example, diminazene in camels, horses and dogs), so follow the product label and national formulary. Drug resistance is widespread in Africa. The 'sanative pair' approach uses two drugs that do not share resistance, such as diminazene and isometamidium, switching to the other when resistance to one is suspected.
Control of tsetse-borne disease combines chemotherapy and chemoprophylaxis with vector control: insecticide-treated cattle (pour-on or spray on the legs and belly, where tsetse feed), insecticide-impregnated traps and targets, aerial or ground spraying, and the sterile insect technique, which eliminated Glossina austeni from Unguja Island, Zanzibar, in the late 1990s. For surra, control relies on treatment, fly control and screening of animals moved into free areas. Surra, dourine and tsetse-transmitted animal trypanosomosis are WOAH-listed.
Parasitic gastroenteritis of sheep, goats and cattle is caused by a community of trichostrongyle nematodes. Haemonchus contortus, the barber's pole worm of the abomasum, sucks blood; heavy infection causes anaemia, submandibular oedema ('bottle jaw'), weakness and sudden death, often without diarrhoea. It thrives in warm, wet climates and has a very high egg output. Teladorsagia (Ostertagia) and Trichostrongylus cause diarrhoea, weight loss and hypoproteinaemia. In cattle in temperate climates, Ostertagia ostertagi causes type I disease in calves in their first grazing summer, and type II disease in late winter or spring when larvae that had stopped developing in the abomasal wall (hypobiosis) emerge together; the abomasum looks like 'Morocco leather'. The lungworm Dictyocaulus viviparus causes husk in cattle, and a live vaccine of irradiated larvae exists.
Diagnosis uses faecal egg counts by the McMaster method, where each egg counted represents a fixed number of eggs per gram (commonly 50, depending on the dilution and slide), larval culture to identify genera, packed cell volume, and the FAMACHA system for Haemonchus in small ruminants: the colour of the lower eyelid conjunctiva is scored from 1 (red, healthy) to 5 (white, severely anaemic), and only animals scoring 4 or 5, and sometimes 3, are drenched. Plasma pepsinogen is raised in ostertagiosis.
Anthelmintic resistance is now common worldwide, especially in Haemonchus of sheep and goats. Broad-spectrum classes include benzimidazoles, levamisole, macrocyclic lactones and monepantel; closantel is narrow-spectrum against Haemonchus and fluke. Sustainable control relies on refugia: leaving a proportion of the worm population unexposed to drug, by not treating every animal (targeted selective treatment) and not moving treated animals straight onto clean pasture. Other measures are dosing to the heaviest animal's weight, quarantine drenching of purchased stock, and grazing management. Resistance is measured by the faecal egg count reduction test, comparing counts before and after treatment; under the long-used guideline of the World Association for the Advancement of Veterinary Parasitology, resistance was suspected when the reduction was below 95% and the lower 95% confidence limit below 90%, and the method was revised in 2023.
Fasciolosis is caused by the liver flukes Fasciola hepatica, in temperate regions and highlands, with the mud snail Galba (Lymnaea) truncatula as intermediate host, and Fasciola gigantica, in the tropics, with Radix (Lymnaea) species. Cattle, buffalo, sheep and goats ingest metacercariae on wet pasture and forage. Acute fasciolosis in sheep, caused by large numbers of immature flukes migrating through the liver, causes sudden death with a swollen, haemorrhagic liver, and can trigger black disease (Clostridium novyi type B). Chronic fasciolosis causes anaemia, bottle jaw, weight loss and lower production; in cattle the bile ducts thicken and calcify ('pipe-stem liver'). Diagnosis is by faecal sedimentation for eggs, coproantigen ELISA, serology and abattoir findings. Triclabendazole is the drug that kills early immature as well as adult flukes; others (closantel, nitroxynil, oxyclozanide, albendazole) act on older stages. Resistance to triclabendazole is reported. Control combines strategic dosing timed to the snail season and fencing off wet areas.
Amphistomes (rumen flukes, such as Paramphistomum and Cotylophoron) are common in the tropics; the adults in the rumen do little harm, but large numbers of immatures in the duodenum cause acute enteritis with foul diarrhoea and death in young stock, diagnosed by finding immature flukes in the faeces or at necropsy. Oxyclozanide is effective against them.
Cystic echinococcosis (hydatid disease) is caused by Echinococcus granulosus: dogs carry the adult tapeworm and pass eggs, and sheep, cattle, buffalo, camels, pigs and people develop hydatid cysts in the liver and lungs. Control relies on regular treatment of dogs with praziquantel, stopping dogs being fed raw offal, safe disposal of condemned organs, and meat inspection. Toxocara canis passes to puppies across the placenta and in milk, so puppies are dewormed from about two weeks of age to guideline schedules; its eggs cause larva migrans in children. Dirofilaria immitis, the canine heartworm, is transmitted by mosquitoes; adults in the pulmonary arteries cause pulmonary hypertension, right heart failure and caval syndrome. Dogs are screened with an antigen test (which detects adult female worms) plus a microfilaria test and protected with monthly or long-acting macrocyclic lactone preventives; adulticide treatment follows the current American Heartworm Society or equivalent protocol under a vet's direction.
A national disease control programme turns knowledge of a disease into sustained action across a country. Its building blocks are: a legal basis (in India, the Prevention and Control of Infectious and Contagious Diseases in Animals Act, 2009, and state rules; elsewhere an animal health act and its regulations), a list of notifiable diseases and a duty on owners and vets to report them, surveillance (passive reporting, active surveys, abattoir and laboratory data, and participatory surveillance with livestock keepers), a laboratory network linked to national and WOAH reference laboratories, animal identification and movement records, vaccination where appropriate, rules for outbreak response, and compensation so that owners report rather than hide or sell sick animals.
A programme can choose vaccination, test-and-remove, stamping out, movement control, vector control or a combination, and the choice depends on the disease's biology, the existence of a DIVA test or marker vaccine, the budget for compensation, the cultural acceptability of killing animals, and whether trade freedom is the goal. WOAH recognises zoning and compartmentalisation, so part of a country can be free while disease remains elsewhere.
When a notifiable disease is suspected, the field officer's duties follow a set pattern: isolate the premises and stop movement of animals, products, people and vehicles; examine all animals and record signs and lesion ages; take and send the correct samples to the designated laboratory by secure, cooled transport with a full history; report to the higher authority; trace contacts forward and back; and, once confirmed, carry out the measures in the national contingency plan: culling or ring vaccination, disposal, cleaning and disinfection, infected and surveillance zones, and lifting restrictions only after the required surveillance.
India's National Animal Disease Control Programme (NADCP), launched in 2019 with full central funding, targets FMD and brucellosis. For FMD it aims to vaccinate all cattle and buffalo, and also sheep, goats and pigs, every six months, with ear-tag identification and registration of each vaccinated animal in a national database, and serological monitoring of vaccine response and of NSP antibodies; the stated aim is control by 2025 and eradication by 2030, starting with FMD-free zones. For brucellosis it vaccinates female bovine calves aged 4 to 8 months once in their lifetime with Brucella abortus strain 19 vaccine. Other vaccinations are supported under Assistance to States for Control of Animal Diseases. Many high-income countries eradicated bovine brucellosis by test-and-slaughter with compensation, which requires slaughter to be acceptable and affordable. Brucellosis vaccines are strain 19 and RB51 for cattle (RB51 is rough, so it does not interfere with standard serological tests) and Rev.1 for sheep and goats, and all are infectious to people and must be handled with care.
For rabies, India's National Action Plan for Dog Mediated Rabies Elimination by 2030 combines mass dog vaccination, dog population management under animal birth control rules, access to human post-exposure prophylaxis and joint surveillance between health and veterinary services.
Haemorrhagic septicaemia (HS), caused by Pasteurella multocida serotypes B:2 in Asia and E:2 in Africa, and black quarter (BQ), caused by Clostridium chauvoei, are seasonal killers of cattle and buffalo in the monsoon and are controlled mainly by annual or six-monthly vaccination before the monsoon. HS vaccines are bacterins: alum-precipitated vaccines give shorter immunity than oil-adjuvant vaccines, which give longer protection but cause more injection-site swelling. BQ vaccine is a formalin-killed whole-culture vaccine with alum, given to young stock typically between about 6 months and 2 to 3 years of age, the age most at risk. Combined HS and BQ vaccines are used in some states. An outbreak in vaccinated stock is investigated for cold-chain failure, missed animals or a vaccine mismatch.
The World Organisation for Animal Health (WOAH) is the intergovernmental body responsible for improving animal health worldwide. It was founded in 1924 as the Office International des Epizooties (OIE), with its headquarters in Paris, and adopted the acronym WOAH in 2022. It has more than 180 Members. Each Member is represented by a Delegate, usually the Chief Veterinary Officer; the World Assembly of Delegates adopts standards each year. Reference laboratories and collaborating centres provide expertise.
WOAH's mandate covers transparency about the world disease situation, collection and distribution of veterinary scientific information, international solidarity in disease control, safe international trade in animals and animal products, strengthening national Veterinary Services, food safety at the animal production stage and animal welfare. Its standards are set out in the Terrestrial Animal Health Code and the Aquatic Animal Health Code, which cover trade measures, surveillance, zoning, veterinary certification and welfare, and in the Manual of Diagnostic Tests and Vaccines for Terrestrial Animals and the Aquatic Manual, which describe approved tests and vaccine standards. Under the World Trade Organization's Agreement on the Application of Sanitary and Phytosanitary Measures (the SPS Agreement), WOAH is the recognised reference for animal health and zoonoses: a country that bases its import rules on WOAH standards is presumed to comply, and stricter measures must be justified by science-based risk assessment. WOAH works with FAO, WHO and UNEP on One Health and with FAO on global strategies for FMD, PPR and rabies.
Members must report animal diseases through the World Animal Health Information System (WAHIS). An immediate notification, within 24 hours of confirmation, is required for a listed disease's first occurrence in a country or zone, its reoccurrence after the country or zone was declared free, the first occurrence of a new strain, a sudden and unexpected change in its distribution, incidence or severity, and for an emerging disease with significant morbidity or mortality or zoonotic potential. Follow-up reports continue until the event is resolved. Six-monthly reports give the presence or absence of each listed disease, and annual reports describe Veterinary Services. WOAH-listed diseases include many in this manual: FMD, PPR, rinderpest, lumpy skin disease, sheep and goat pox, bluetongue, rabies, bovine viral diarrhoea, classical and African swine fever, African horse sickness, equine infectious anaemia, equine influenza, equine viral arteritis, bovine babesiosis, theileriosis, equine piroplasmosis, surra, dourine, tsetse-transmitted trypanosomosis and echinococcosis.
For a small group of diseases WOAH officially recognises the status of countries or zones after reviewing a dossier: FMD, PPR, classical swine fever, African horse sickness, contagious bovine pleuropneumonia and the bovine spongiform encephalopathy risk status. It also endorses national official control programmes for FMD, PPR, contagious bovine pleuropneumonia and dog-mediated rabies, which signals to trading partners that a credible plan is in place. Status lost after an outbreak is regained after the Code's waiting periods and surveillance.
The Performance of Veterinary Services (PVS) Pathway helps countries evaluate their Veterinary Services against WOAH standards through external evaluation, costed gap analysis and follow-up support. WOAH also maintains vaccine banks, for example for FMD, PPR and rabies. The reporting chain to WAHIS starts with the field vet who suspects the disease.
Learn each disease on one frame: agent and family, hosts, spread or vector, signs, lesions, samples and tests, differentials, treatment, vaccine, control programme and WOAH status. Exams test single links in that chain, such as which species amplifies FMD, which tick carries Theileria annulata, or which canine vaccine component prevents blue eye. Build comparison tables for vesicular diseases, for the swine fevers, for haemoglobinuria in cattle, and for canine and feline core vaccines. Practise the numbers: McMaster egg counts, faecal egg count reduction, vaccination coverage and drug volumes, because these appear as short calculations and are easy marks if you have done them by hand.
In practice the first decision is whether a case could be notifiable, because that changes everything you do next: a lame, salivating cow, a dying pig herd or a horse with sudden respiratory distress means stop, isolate, report and sample before anything else. A five-year practitioner should run a puppy and kitten vaccination clinic to current guidance, manage a parvovirus case and the kennel clean-up, recognise rabies risk and handle a bite incident correctly, diagnose babesiosis and theileriosis from smears and treat early, use FAMACHA and egg counts to drench selectively, and plan pre-monsoon HS, BQ and FMD vaccination with a working cold chain.
Senior state and district officers run campaigns and outbreaks. They plan FMD and brucellosis vaccination rounds, ear-tagging and data entry so that coverage is real rather than reported, set up serological monitoring, and decide when a zone is ready for a freedom claim. In an LSD, PPR or ASF outbreak they set infected and surveillance zones, organise culling or ring vaccination, compensation, disposal and movement control, and brief politicians and the press. They also argue for budgets: compensation that is fast enough to keep reporting honest, laboratory capacity, and staff for rabies elimination and dog population management. They write the reports that feed WAHIS.
A researcher with long field experience works where evidence is thin: the role of carriers in FMD persistence, PPR transmission in mixed flocks and wildlife, the vectors of LSD, BVD and ASF virus survival in feed and pork, drug resistance in trypanosomes and helminths and how fast refugia-based programmes slow it, and the economics of vaccination versus stamping out. They design surveillance that can prove freedom with known confidence, evaluate DIVA vaccines and tests in the field, model the effect of vaccination coverage and animal movement on spread, and advise WOAH, FAO and national governments on standards and on eradication strategies for PPR and dog-mediated rabies.
This manual covers the seventeen curriculum units and names related diseases only in passing. It does not give full accounts of avian viral diseases (avian influenza, Newcastle disease, infectious bursal disease, Marek's disease), aquatic animal diseases, Aujeszky's disease, PRRS and porcine circovirus disease, IBR, malignant catarrhal fever, bovine leukosis, feline retroviruses and feline infectious peritonitis, canine infectious respiratory disease beyond the adenovirus, coccidiosis and other protozoa apart from Babesia, Theileria and Trypanosoma, or ectoparasites; several of these sit in other subjects of this track. Drug doses are given only for diminazene aceturate, imidocarb dipropionate and buparvaquone, and doses for trypanocides are deliberately omitted because they differ by trypanosome species, host and product and several drugs are toxic in particular species. Vaccination schedules are given in general terms; national schedules and product licences differ. Country programme dates, targets and WOAH status lists change and should be checked against the current national and WOAH sources. The writer did not state the exact number of WOAH Members or listed diseases because these change.
Original practice questions written to the syllabus and pattern of the exams named in each question's examTags. They are not past papers and do not reproduce any board's questions.
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