Veterinary · Clinical · also MSVE VMD-412, Infectious Diseases I
The bacterial and related infectious diseases of livestock and horses: clinical signs, diagnosis, treatment, prevention and control.
In the exams: ICAR AICE-JRF core group 07 (Medicine); ICAR AIEEA-PG 13; China infectious diseases 30; TNPSC Micro/VPH/Preventive Medicine 30
Preventive veterinary medicine I covers the infectious diseases of animals caused by bacteria and by three groups that are taught alongside them: the mycoplasmas (bacteria without a cell wall), the rickettsia-like Anaplasma, and the dermatophyte fungi that cause ringworm. For each disease the student learns the same sequence: the cause, how it spreads and persists (epidemiology), what it looks like in the live and dead animal, how to confirm it in the laboratory, what else it could be (the differential diagnosis), the principles of treatment, and how it is prevented and controlled on a farm and across a country. Most of the diseases here are old, well described and still common. Their importance lies in production losses (mastitis, Johne's disease), sudden deaths (anthrax, haemorrhagic septicaemia, blackquarter, enterotoxaemia), trade (anything on the list of the World Organisation for Animal Health, WOAH) and human health, because anthrax, brucellosis, bovine tuberculosis, leptospirosis, listeriosis, glanders and ringworm are zoonoses.
The practical skill is recognition and decision. A veterinarian who finds a dead cow bleeding from the nostrils must think of anthrax before opening the carcass. One who sees a buffalo with a hot throat swelling in the monsoon must think of haemorrhagic septicaemia and vaccinate the rest of the herd. One who runs a dairy's mastitis programme must read cell-count data and change milking routines. Treatment matters, but for most diseases in this subject the decisive actions are notification, isolation, vaccination, testing and hygiene. Where a country runs a statutory programme, this manual names the country, because the same disease is handled by test-and-slaughter in one place and by vaccination or by nothing at all in another.
The subject is examined everywhere. In India it is the MSVE course VMD-412, part of the medicine groups of the ICAR postgraduate and PhD entrance papers, and a large share of state veterinary officer papers. Licensing exams from China and Korea to North America, Britain, Australasia and South Africa test it, the latter mainly through clinical vignettes by species. Drug doses in this manual are given only where a value is standard; every dose is followed by a reminder to check the label and national formulary, because doses, permitted uses and withdrawal periods differ by country and product.
Most bacterial diseases of livestock are not new introductions but the expression of an organism the herd already carries or the environment already holds. Three patterns recur. Obligate pathogens that persist in the host, such as Brucella, Mycobacterium bovis, Burkholderia mallei and Mycoplasma mycoides, are maintained by infected animals, often carriers that look healthy. Soil-borne spore formers, such as Bacillus anthracis and the clostridia, persist for years in the ground and cause disease when conditions allow. Opportunists, such as Escherichia coli in mastitis or Pasteurella multocida in stressed buffalo, live on or near the animal and cause disease when defences fall. A carrier is an infected animal that sheds the agent without signs; a reservoir is the population or environment in which the agent is maintained. Control fails when either is ignored.
The tools are few and are combined differently for each disease. Notification tells the veterinary authority that a listed disease is suspected. Movement control and quarantine stop spread between herds. Test-and-slaughter (or test-and-segregate) removes infected animals and is the basis of tuberculosis and brucellosis eradication in countries that can pay compensation. Vaccination raises herd immunity; it works well for clostridial diseases, anthrax and haemorrhagic septicaemia and less well where the agent is intracellular. Hygiene, management and biosecurity break the route of transmission, as in milking routines for contagious mastitis or calf-rearing for Johne's disease. Treatment helps the individual but can create carriers, as in contagious bovine pleuropneumonia, which is why some national rules forbid it. Antimicrobial stewardship means choosing a drug by diagnosis and sensitivity, using it for the labelled species, dose and duration, and observing withdrawal periods for milk and meat.
The World Organisation for Animal Health (WOAH, formerly OIE) keeps a list of diseases that member countries must report. Among the diseases in this subject, anthrax, haemorrhagic septicaemia, brucellosis (Brucella abortus, B. melitensis and B. suis), infection with the Mycobacterium tuberculosis complex, paratuberculosis, glanders, contagious bovine pleuropneumonia, contagious caprine pleuropneumonia, contagious agalactia and bovine anaplasmosis are listed. Mastitis, strangles, caseous lymphadenitis, listeriosis and ringworm are not. Each country has its own law naming notifiable diseases and the powers of officials, for example India's Prevention and Control of Infectious and Contagious Diseases in Animals Act, 2009, the Animal Health Act 1981 in Great Britain, and the Animal Diseases Act 35 of 1984 in South Africa. WOAH also grants official disease-free status for a few diseases, including contagious bovine pleuropneumonia, which matters for export.
Mastitis is inflammation of the mammary gland, almost always caused by bacteria entering through the teat canal. It is the most costly disease of dairy cattle and buffalo worldwide, mainly through subclinical cases that cut yield and raise the somatic cell count (SCC) without visible change in the milk. Clinical mastitis shows abnormal milk (clots, flakes, watery secretion) with or without a hot, swollen quarter; peracute cases add fever, depression and sometimes death. Pathogens are grouped by where they live. Contagious pathogens live in the infected udder and spread at milking through hands, liners and cloths: Staphylococcus aureus, Streptococcus agalactiae, Mycoplasma bovis and, as a minor pathogen, Corynebacterium bovis. Environmental pathogens live in bedding, dung and water and reach the teat between milkings: Escherichia coli, Klebsiella species, Streptococcus uberis and, often classed between the two groups, Streptococcus dysgalactiae. Trueperella pyogenes causes 'summer mastitis' of dry cows and heifers in parts of Europe, spread by flies. The distinction matters because contagious mastitis is controlled at milking and by culling, while environmental mastitis is controlled by housing, bedding and cow cleanliness.
Streptococcus agalactiae is an obligate udder pathogen, highly susceptible to penicillin, and can be eradicated from a herd by blitz treatment and hygiene. Staphylococcus aureus forms deep microabscesses and fibrosis, survives inside cells, and cures poorly during lactation, so chronic cases are culled; some strains cause gangrenous mastitis with a cold, blue-black quarter, seen in cows and especially in ewes and does. Mycoplasma bovis affects several quarters, produces sandy or watery secretion, does not respond to treatment, and is controlled by culture of bulk milk, segregation and culling. Coliform mastitis from E. coli is peracute around calving, when endotoxin causes fever, then subnormal temperature, weakness, diarrhoea and recumbency; the quarter may look only mildly changed. Klebsiella is linked with sawdust bedding. In sows, coliform mastitis is part of the post-partum dysgalactia syndrome; in bitches and queens mastitis is usually staphylococcal or streptococcal and is managed by drainage, hot packing and antimicrobials. Prototheca, an alga, and yeasts can cause mastitis after contaminated intramammary infusion and do not respond to antibacterials.
Clinical mastitis is diagnosed by forestripping and examining the udder. Subclinical mastitis needs a test. The California mastitis test (CMT) adds a detergent that lyses cells; released DNA forms a gel whose thickness is scored. SCC counts cells per millilitre of milk, most of which are neutrophils during infection. An individual cow SCC above about 200,000 cells/mL is widely used as a sign of intramammary infection, though thresholds vary. Bulk-tank SCC is a herd indicator and a legal standard: the European Union limit is 400,000 cells/mL (rolling geometric mean) and the United States Grade A limit is 750,000 cells/mL; other countries set their own. Bacteriological culture of aseptically collected quarter samples identifies the pathogen and its sensitivity and is the basis of a herd plan. Bulk-milk culture and PCR screen for contagious pathogens.
Treat clinical cases by severity. Mild and moderate cases receive an intramammary antimicrobial chosen by likely pathogen, and many herds now culture first and treat only Gram-positive cases, because many Gram-negative mild cases cure spontaneously. Severe coliform cases need supportive care first: intravenous fluids (often hypertonic saline followed by water by mouth), a non-steroidal anti-inflammatory drug, frequent stripping, and a systemic antimicrobial chosen for Gram-negative bacteraemia where permitted. Chronic Staph. aureus and Mycoplasma cases are culled or the quarter dried off. Milk from treated cows is discarded for the labelled withdrawal period, which varies by product and country.
The five-point plan developed in England in the 1960s remains the core of contagious mastitis control: post-milking teat disinfection, antibiotic treatment of all quarters at drying off, prompt treatment of clinical cases, culling of chronically infected cows, and regular milking machine testing and maintenance. Later programmes, such as the ten-point plan of the US National Mastitis Council, add goals, records, biosecurity for bought-in cows, environmental management and review. Modern dairies increasingly use selective dry-cow therapy, treating only infected cows at drying off and giving an internal teat sealant to the rest, to reduce antimicrobial use. Environmental mastitis is controlled by clean, dry bedding, pre-milking teat disinfection, keeping cows standing after milking (feeding fresh feed), and J5-type E. coli core-antigen vaccines, which reduce severity rather than infection. Vaccines against Staph. aureus exist in some countries but give limited protection.
Strangles is an acute, highly contagious infection of the upper respiratory tract and associated lymph nodes of horses, donkeys and mules, caused by Streptococcus equi subsp. equi, a Gram-positive, beta-haemolytic, Lancefield group C coccus in chains. It is not WOAH-listed but is among the most commonly diagnosed infectious diseases of horses worldwide. Young horses and those moving through sales, shows and training yards are most at risk. Spread is by direct contact with nasal discharge or pus and indirectly by shared water troughs, tack, handlers and feed buckets. Around one in ten recovered horses may remain a carrier, usually through infection persisting in the guttural pouch, sometimes as inspissated pus concretions called chondroids. Carriers shed intermittently for months or years and are the usual source of new outbreaks.
After an incubation of a few days to two weeks, horses show fever, depression, loss of appetite and a mucopurulent nasal discharge. The submandibular and retropharyngeal lymph nodes enlarge, become painful and abscess; they burst externally or, for the retropharyngeal nodes, into the guttural pouch. Enlarged nodes can compress the pharynx and larynx, causing difficult swallowing and noisy breathing, which gave the disease its name. Complications include 'bastard strangles', metastatic abscesses in the abdomen, thorax or brain; purpura haemorrhagica, an immune-complex vasculitis with limb oedema and mucosal petechiae, usually two to four weeks after infection or vaccination; myositis; and guttural pouch empyema. Diagnosis is by culture and PCR of nasal swabs, nasopharyngeal washes or pus. Detecting carriers relies on endoscopy of the guttural pouches with lavage for culture and PCR. An ELISA for antibodies to the SeM protein supports diagnosis of recent infection, helps decide whether a horse may develop purpura before vaccination, and screens horses in some biosecurity programmes.
Penicillin is the drug of choice for S. equi, but its use is a judgement. Given very early, before abscesses form, it can stop the disease but may leave the horse without immunity. Once abscesses are forming, antimicrobials can delay maturation; the usual approach is warm packing, lancing mature abscesses, soft feed and nursing, with antimicrobials reserved for severe cases, complications or dyspnoea. Control of an outbreak rests on stopping movement, separating sick, in-contact and clean groups, monitoring temperatures twice daily in in-contacts to detect early cases, disinfecting shared equipment, and clearing carriers by guttural pouch endoscopy and lavage (with treatment of chondroids) before the group is released. Vaccines include a live attenuated intranasal vaccine (licensed in North America), a live deletion-mutant vaccine given in the upper lip submucosa in Europe, and extract vaccines; none gives complete protection, and vaccination of an exposed horse carries some risk of purpura. National and industry codes of practice, such as those used in the United Kingdom, set out outbreak and quarantine rules.
Caseous lymphadenitis (CLA) is a chronic abscessing infection of sheep and goats caused by Corynebacterium pseudotuberculosis biovar ovis, a Gram-positive, pleomorphic facultative intracellular rod. The organism enters through skin wounds, especially at shearing, and through dips and communal handling; pus from ruptured abscesses contaminates the environment and survives for months. It spreads to regional lymph nodes and forms abscesses, the superficial form affecting the parotid, submandibular, prescapular, prefemoral and supramammary nodes, and the visceral form affecting the lungs and mediastinal and other internal nodes. Visceral CLA causes weight loss ('thin ewe syndrome'). In sheep, cut abscesses show concentric laminations like an onion; in goats the pus tends to be pasty. The main virulence factor is phospholipase D, an exotoxin that increases vascular permeability. Losses come from carcass trimming and condemnation, wool and skin damage and wasting. Diagnosis is by culture of pus, and by serology such as the synergistic haemolysis inhibition test and ELISAs for antibody to phospholipase D, used to screen flocks. Treatment of individual animals is unrewarding; abscesses are lanced and flushed only in isolation, because pus is highly infectious. Control uses culling of animals with abscesses, shearing clean flocks first, disinfecting equipment, and vaccination with phospholipase D toxoid, often combined with clostridial toxoids in Australia and elsewhere. Biovar equi causes ulcerative lymphangitis and pectoral abscesses ('pigeon fever') in horses and some disease in cattle. Human lymphadenitis is rare and occupational.
Clostridia are Gram-positive, anaerobic, spore-forming rods found in soil and in the intestine. Their spores survive for years, so disease cannot be removed from a farm by eradication, and control depends on vaccination with toxoids or bacterin-toxoids. They cause three kinds of disease: myonecrosis (blackquarter, malignant oedema), enterotoxaemia (Clostridium perfringens) and neurotoxic disease (tetanus, botulism). Most are rapidly fatal, so treatment is rarely successful and prevention is everything. Multivalent vaccines covering several clostridia are widely used in sheep and cattle; young animals need a primary course of two doses, then boosters, and dams vaccinated before parturition pass immunity through colostrum.
Blackquarter (black leg, BQ) is an acute myonecrosis of cattle caused by Clostridium chauvoei. It typically affects well-grown, well-fed cattle between about six months and two years. Spores are eaten, cross the gut wall and lie dormant in muscle; bruising or other damage creates anaerobic conditions in which they germinate and produce toxins. Cases cluster on particular pastures and seasons; in India outbreaks follow the onset of the monsoon, and state programmes vaccinate before it. Signs are high fever, depression, lameness and a hot, painful swelling of a heavy muscle mass such as the thigh, shoulder or neck that becomes cold, painless and crepitant (gas under the skin). Death follows within about 12 to 48 hours, and many animals are simply found dead. At necropsy the muscle is dark red to black, dry and spongy with gas, and smells of rancid butter. In sheep, blackquarter usually follows wounds at shearing, docking or lambing. Diagnosis uses fluorescent antibody staining of muscle smears, culture and PCR. The main differentials are malignant oedema (Clostridium septicum and others entering through wounds, at any age, with more oedema and less gas), anthrax (do not open a carcass that could be anthrax) and haemorrhagic septicaemia. Penicillin in large doses early, with surgical fenestration of the lesion, occasionally saves a case. Control is by vaccination of all cattle at risk with a formalin-killed, alum-precipitated C. chauvoei bacterin, usually combined with other clostridial antigens; in an outbreak all in-contacts are vaccinated and may be given penicillin, and carcasses are destroyed without opening.
Clostridium perfringens is classified into toxinotypes A to G by the major toxins it produces: type A alpha toxin; B alpha, beta and epsilon; C alpha and beta; D alpha and epsilon; E alpha and iota; F alpha and C. perfringens enterotoxin; G alpha and NetB. Enterotoxaemia caused by type D, called pulpy kidney disease, is the classic form. It strikes the best-grown lambs and kids, often after a sudden change to rich pasture or grain, when starch reaches the small intestine, the organism multiplies and epsilon toxin is absorbed. Epsilon toxin damages vascular endothelium, causing brain oedema, and in subacute cases focal symmetrical encephalomalacia. Many animals are found dead; others show convulsions, opisthotonus and recumbency. Hyperglycaemia and glucosuria are characteristic, and kidneys autolyse rapidly after death. Diagnosis is by detecting epsilon toxin in intestinal contents with ELISA, glucose in urine and histology of the brain. In goats, type D causes enterocolitis with diarrhoea, and vaccinated goats are less well protected than sheep. Type B causes lamb dysentery in young lambs; type C causes haemorrhagic enteritis of piglets and calves and 'struck' in adult sheep; type G, through NetB toxin, causes necrotic enteritis in broiler chickens. Control combines feeding management with vaccination: ewes and does receive a booster toxoid a few weeks before parturition so colostrum protects the young, and lambs and kids begin their own course when maternal antibody falls.
Tetanus is caused by the neurotoxin tetanospasmin of Clostridium tetani, whose spores enter through wounds, the umbilicus, castration and docking sites, or the uterus after dystocia. In the anaerobic wound the toxin is produced, travels by retrograde axonal transport to the spinal cord and brainstem, and blocks release of the inhibitory transmitters glycine and GABA by cleaving synaptobrevin. The result is unopposed muscle contraction. Horses and humans are the most sensitive species, ruminants and pigs are susceptible, dogs and cats are relatively resistant and often show localised tetanus, and birds are highly resistant. Signs are stiffness, a 'sawhorse' stance, raised tail, erect ears, prolapse of the third eyelid when the head is lifted or tapped, trismus (lockjaw), inability to eat and drink, bloat in ruminants, and exaggerated responses to noise and touch; death follows respiratory failure. Diagnosis is clinical. Treatment is to find and debride the wound, give penicillin to kill the organism, give tetanus antitoxin to neutralise unbound toxin, sedate and relax muscles, keep the animal in a quiet, dark place with slings or deep bedding, and support fluids and nutrition, sometimes by stomach tube. Prevention is by tetanus toxoid: a two-dose primary course with boosters. An unvaccinated horse with a wound receives antitoxin for immediate passive protection and a first dose of toxoid at a different site. Tetanus antitoxin of equine origin has been associated with serum hepatitis (Theiler's disease) in horses.
Anthrax is caused by Bacillus anthracis, a large, Gram-positive, aerobic, spore-forming rod. In the host it forms a capsule of poly-D-glutamic acid and produces a tripartite toxin: protective antigen binds cells and carries lethal factor and oedema factor inside. The genes for the toxin lie on plasmid pXO1 and those for the capsule on pXO2; both are needed for full virulence. Vegetative cells in an unopened carcass die within days as it putrefies, but when blood reaches air the organism forms spores, which persist in soil for decades. Outbreaks recur in 'anthrax districts' with alkaline, calcium-rich soils, often after heavy rain follows drought or when animals graze close to the soil. Herbivores are most susceptible: cattle, sheep, goats, buffalo, horses and many wildlife species. Pigs, dogs and cats are relatively resistant, and birds are highly resistant. Anthrax is WOAH-listed and notifiable in most countries.
In ruminants the disease is usually peracute or acute: animals are found dead, or show high fever, trembling and difficult breathing for a few hours before collapse. After death there is dark, tarry, unclotted blood from the nostrils, mouth, anus and vulva, rapid bloating and incomplete rigor mortis. If a carcass is opened, which should not be done, the spleen is greatly enlarged and soft, with haemorrhages throughout. Pigs and carnivores more often have pharyngeal anthrax with swelling of the throat, or intestinal disease. Horses show fever, colic and oedematous swellings. The diagnostic step is a thin blood smear from a peripheral vessel, such as an ear vein, collected without opening the carcass and stained with polychrome methylene blue: B. anthracis appears as square-ended rods in short chains with a pink capsule (the M'Fadyean reaction). Culture, PCR and, for old or processed material such as hides, the Ascoli thermoprecipitation test support the diagnosis. The main differentials of sudden death are blackquarter, haemorrhagic septicaemia, lightning strike, acute poisoning, bloat and enterotoxaemia.
Sick animals may respond to penicillin or oxytetracycline if treated very early, and in-contact animals are often treated or vaccinated. Control rests on the live Sterne spore vaccine (strain 34F2), which makes toxin but no capsule because it lacks pXO2; it is given annually in endemic areas. Antimicrobials kill the vaccine strain, so antimicrobial treatment and vaccination should not overlap; national instructions say how many days to separate them. The carcass is not opened. It is burned where possible, or buried deep in accordance with national rules; the site is fenced and disinfected with a sporicidal disinfectant, and scavengers are kept away. Milk and meat from affected herds are withheld from sale, and movements are restricted until a period set by law has passed since the last case. People in contact are advised to seek medical care.
Human anthrax is mainly occupational: farmers, butchers, veterinarians and workers with hides, wool and bone meal. Cutaneous anthrax, a painless black eschar with oedema (historically 'malignant pustule'), accounts for most cases. Gastrointestinal anthrax follows eating meat from animals that died of the disease, which is why outbreaks in villages often follow sharing of such meat. Inhalational anthrax ('woolsorters' disease') is rare and severe.
Haemorrhagic septicaemia (HS) is an acute, often fatal septicaemia of cattle and water buffalo caused by particular serotypes of Pasteurella multocida, a small Gram-negative coccobacillus that stains bipolar. Serotype B:2 (6:B in the Namioka system) causes the disease in Asia, and serotype E:2 (6:E) in Africa. Buffalo are more susceptible than cattle. HS is endemic in South and South-East Asia, parts of the Middle East and Africa; it causes some of the largest losses of any bacterial disease of large ruminants in these regions and is WOAH-listed. Recovered and vaccinated animals can carry the organism in the tonsils and nasopharynx. Under stress, particularly hot and humid weather, the onset of the monsoon, work, poor nutrition and crowding, carriers shed the organism and susceptible animals become infected through ingestion or inhalation. Outbreaks therefore follow the rains, and mortality in unvaccinated buffalo can be very high once signs appear.
The course is short, from a few hours to a day or two. The animal has a high fever, dullness, profuse salivation, and a hot, painful oedematous swelling in the throat, dewlap and brisket that spreads and becomes cold. Breathing becomes difficult and noisy, the tongue may protrude, and the animal dies. Some are found dead. At necropsy there are widespread petechial haemorrhages on serous surfaces, subcutaneous gelatinous oedema in the throat and brisket, and pulmonary congestion. Diagnosis is by blood smears stained with Leishman or methylene blue showing bipolar organisms, culture of heart blood or bone marrow on blood agar, and PCR assays specific for the HS-associated serotype. The differentials are anthrax (which must be excluded by a smear before opening the carcass), blackquarter, pneumonic pasteurellosis (shipping fever) caused by Mannheimia haemolytica or other P. multocida types, and acute poisoning.
Treatment is effective only in the early febrile stage, before oedema and breathing difficulty develop; sulphonamides, oxytetracycline, penicillin–aminoglycoside combinations and other drugs to which the strain is sensitive are used, with anti-inflammatory support. Control is by vaccination. The traditional vaccines are killed bacterins with alum or aluminium hydroxide adjuvant, which protect for a few months and are given twice a year, and oil-adjuvant bacterins, which protect for longer but cause more injection-site reactions. In India, state animal husbandry departments vaccinate cattle and buffalo before the monsoon, supported under the central scheme of Assistance to States for Control of Animal Diseases. A live intranasal vaccine based on a B:3,4 strain from fallow deer has been used in Myanmar. In an outbreak, the herd is vaccinated, sick animals isolated and treated, movements stopped, and carcasses disposed of properly. Fowl cholera of poultry is a different disease, caused by other P. multocida strains, commonly capsular type A.
Listeriosis is caused by Listeria monocytogenes, a small Gram-positive rod that is facultatively intracellular, grows at refrigeration temperatures and shows tumbling motility at 20 to 25 °C but not at 37 °C. It lives in soil, plant material and the intestine of healthy animals. In ruminants the main source is poorly fermented silage: where the pH stays above about 5.0 to 5.5, often at the surface or in spoiled bales, the organism multiplies. Disease is most common in housed sheep, goats and cattle in winter and spring, and sheep and goats are affected more acutely than cattle. Listeriosis is not WOAH-listed, but it is one of the most serious foodborne zoonoses.
There are five forms. Encephalitis ('circling disease') follows entry through small wounds in the mouth and spread along the trigeminal nerve to the brainstem, producing depression, circling, head deviation, and unilateral facial nerve paralysis with drooping ear, eyelid and lip, and dropped feed ('cudding'). Abortion occurs in late pregnancy, often without other signs. Septicaemia affects neonates and monogastric animals, with focal necrosis in the liver. Keratoconjunctivitis and uveitis ('silage eye') follow direct contact with silage. Mastitis is uncommon but important for milk safety. In the encephalitic form, cerebrospinal fluid shows raised protein and a mononuclear pleocytosis, and histology shows microabscesses and perivascular cuffing in the brainstem, which is diagnostic. Culture from brain tissue may need cold enrichment. The differentials are pregnancy toxaemia, polioencephalomalacia, rabies, coenurosis, middle ear infection and brain abscess. Treatment with high doses of penicillin or oxytetracycline for a prolonged course works in early cases, especially in cattle; sheep and goats often die. Control is good silage making, discarding spoiled silage and feeding from clean faces. The human disease causes abortion, neonatal sepsis and meningitis, particularly in pregnant women, the elderly and immunocompromised people, and is linked to soft cheeses, raw milk and ready-to-eat foods.
Leptospirosis is caused by spirochaetes of the genus Leptospira, of which the pathogenic species include L. interrogans and L. borgpetersenii. They are grouped into more than 250 serovars. Each serovar is adapted to a maintenance host, in which infection is common, mild and chronic, with long-term shedding in urine from the kidney; infection of other, incidental hosts is less common but more severe. Cattle are maintenance hosts for serovar Hardjo, pigs for Pomona and Bratislava, dogs for Canicola, and rats for Icterohaemorrhagiae and Copenhageni. Leptospires survive in warm, wet, neutral or slightly alkaline conditions, so disease is common in the tropics, in wet seasons and after floods. Transmission is by contact of mucous membranes or damaged skin with infected urine or contaminated water, and venereally and transplacentally.
In cattle, Hardjo causes a sudden fall in milk yield with a flabby udder and thick, colostrum-like milk in all four quarters ('milk drop syndrome'), abortion, stillbirth, weak calves and infertility. Incidental infection of calves, for example with Pomona, can cause acute haemolytic disease with fever, haemoglobinuria, jaundice and death. In pigs, infection causes abortion, stillbirths and weak piglets. In dogs, leptospirosis causes acute kidney injury, liver disease with jaundice, bleeding and a severe pulmonary haemorrhage syndrome. In horses it is the most important cause of equine recurrent uveitis and also causes abortion. The microscopic agglutination test (MAT) is the reference serological test; it uses live leptospires of a panel of serovars, and a four-fold or greater rise in titre between paired sera confirms recent infection. PCR on blood (early) or urine (after the first week), fluorescent antibody tests, dark-field microscopy and culture on special media support diagnosis. Treatment uses penicillins or tetracyclines in the acute phase; in dogs a course of doxycycline is used to clear renal carriage. Control in livestock combines serovar-specific killed vaccines, rodent control, fencing off contaminated water, and testing of bought-in stock. In dogs, WSAVA treats leptospira vaccination as non-core but recommended wherever exposure is likely; some national guidelines class it as core. Humans are infected occupationally (dairy farmers, abattoir and sewer workers, rice farmers) and after floods; severe cases (Weil's disease) have jaundice, kidney failure and bleeding.
Brucellosis is caused by small, Gram-negative, facultatively intracellular coccobacilli of the genus Brucella. Each species has a preferred host: B. abortus in cattle and buffalo, B. melitensis in sheep and goats (and camels and cattle where kept together), B. suis in pigs, B. ovis in rams, and B. canis in dogs. B. melitensis is the most important cause of human disease, followed by B. abortus and B. suis; B. ovis is not known to infect people. The organism enters through mucous membranes, spreads to lymph nodes and then localises in the pregnant uterus, udder, testis and joints. The pregnant ruminant placenta contains erythritol, a sugar that B. abortus uses preferentially, which helps explain its concentration in the placenta and fetal fluids. Infection is WOAH-listed (B. abortus, B. melitensis and B. suis as one listed infection; ovine epididymitis due to B. ovis separately).
In cattle the hallmark is abortion in the last third of pregnancy, usually only once; later pregnancies may go to term with a weak calf, and retained placenta, metritis and infertility follow. Bulls develop orchitis and epididymitis. Hygromas of the knee are common in endemic areas of Africa and Asia. Infected cows shed large numbers of organisms in fetal fluids and placenta and continue to shed in milk. In sheep and goats, B. melitensis causes abortion, stillbirth and mastitis. B. ovis causes epididymitis in rams, detected by palpating the tail of the epididymis, and poor fertility. B. suis causes abortion, infertility, orchitis and lameness in pigs. B. canis causes late abortion in bitches, epididymitis and testicular atrophy in dogs, and discospondylitis; it is zoonotic, and breeding kennels are screened.
Direct diagnosis uses smears of cotyledons, fetal stomach contents or vaginal swabs stained with the modified Ziehl-Neelsen (Stamp) method, which shows red coccobacilli in clumps; culture on selective media (such as Farrell's medium) in a biosafety level 3 laboratory; and PCR. Serology is the basis of herd testing. The Rose Bengal plate test is a rapid, sensitive screening test; the complement fixation test and ELISAs (indirect and competitive) are used for confirmation; the fluorescence polarisation assay is another option; the serum agglutination test is older and less specific. The milk ring test and milk ELISA screen herds by bulk milk. Cross-reactions occur with Yersinia enterocolitica O:9, which shares the O-chain antigen of smooth Brucella, and cause false-positive serology in free herds. B. ovis and B. canis are rough species, so tests using smooth antigen miss them and specific tests are needed.
Treatment of livestock is not recommended because cure is unreliable and treated animals remain a risk. Control is by vaccination, test-and-slaughter, or both. Strain 19 (S19) is a live, smooth, attenuated B. abortus vaccine given to female calves; it gives lasting protection, but it can cause abortion in pregnant animals and persistent antibody if given to adults. RB51 is a live, rough, rifampicin-resistant B. abortus mutant that does not induce antibodies to the O-polysaccharide, so it does not interfere with standard serology. Rev.1 is the live B. melitensis vaccine for sheep and goats, preferably given by the conjunctival route to reduce persistent antibody. All three are infectious for people, and RB51 is resistant to rifampicin, one of the drugs used in human brucellosis. India's National Animal Disease Control Programme vaccinates female bovine calves aged four to eight months once in a lifetime with S19. The United States eradicated bovine brucellosis from its domestic herds through a state-federal test, slaughter and vaccination programme; residual infection persists in bison and elk of the Greater Yellowstone Area. Australia declared itself free of bovine brucellosis in 1989. Human brucellosis (undulant or Malta fever) causes recurrent fever, sweats, joint pain and orchitis; it is acquired from raw milk and cheese and through contact with birth products, and it is an occupational disease of veterinarians and farmers. Pasteurisation of milk prevents foodborne infection.
Bovine tuberculosis is caused mainly by Mycobacterium bovis, a member of the Mycobacterium tuberculosis complex, which also includes M. tuberculosis and M. caprae. M. bovis has a wide host range: cattle, buffalo, goats, deer, pigs, cats, many wildlife species and people. Infection spreads mainly by inhalation of aerosols from infected animals in close contact, and by ingestion, including of milk by calves. The lesion is the tubercle, a granuloma with a caseous centre that may calcify, surrounded by epithelioid cells, multinucleate giant cells and lymphocytes. In cattle, lesions are commonest in the lungs and in the lymph nodes of the head and thorax (retropharyngeal, bronchial and mediastinal). The disease is chronic: most infected cattle show no signs, and advanced cases show wasting, cough and enlarged lymph nodes. Infection with the M. tuberculosis complex is WOAH-listed. Wildlife reservoirs complicate control: the badger in Great Britain and Ireland, the brushtail possum in New Zealand, white-tailed deer in Michigan (United States) and wild boar and deer in Spain.
The tuberculin test measures delayed-type hypersensitivity to purified protein derivative (PPD) injected into the skin, with the increase in skin-fold thickness read at 72 hours. The single intradermal test uses bovine PPD, in the caudal fold (as in the United States and New Zealand) or the side of the neck (as in Europe and India); the neck is more sensitive. Under the EU standard interpretation of the single cervical test, an increase above 4 mm, or clinical signs at the site, is positive, 2 to 4 mm is inconclusive, and less than 2 mm is negative. The single intradermal comparative cervical tuberculin test (SICCT) injects avian and bovine PPD at two neck sites to separate M. bovis infection from sensitisation by environmental mycobacteria; it is the standard test in Great Britain and Ireland. Under the standard interpretation, the animal is a reactor if the bovine reaction exceeds the avian by more than 4 mm, inconclusive if by 1 to 4 mm, and negative if the bovine reaction is equal to or less than the avian; some countries use a more severe interpretation in infected herds. The interferon-gamma blood assay is used alongside the skin test to find more infected animals. False negatives occur in advanced cases (anergy), around calving, and when cattle are retested too soon after a previous test (desensitisation).
Treatment of tuberculous cattle is not allowed in countries with programmes. Control is test-and-slaughter with movement restriction of infected herds, meat inspection surveillance at slaughter, trace-back of lesioned animals and, where needed, wildlife control. Australia declared itself free of bovine tuberculosis in 1997 after a national campaign. In England, the government strategy aims for officially TB-free status by 2038, and badger culling and badger vaccination remain contested scientifically and politically. Many low- and middle-income countries, where herd prevalence may be substantial, have no compulsory test-and-slaughter programme because compensation is not affordable. Humans acquire M. bovis mainly from unpasteurised milk, which causes extrapulmonary tuberculosis such as cervical lymphadenitis; pasteurisation and meat inspection are the main safeguards. Dogs can acquire M. tuberculosis from their owners. In poultry, avian tuberculosis caused by M. avium subsp. avium produces tubercles in the liver, spleen and intestine of older birds in backyard flocks, and pigs develop lesions in cervical and mesenteric lymph nodes.
Johne's disease is a chronic granulomatous enteritis of ruminants caused by Mycobacterium avium subsp. paratuberculosis (MAP). MAP is acid-fast, grows very slowly (weeks to months) and needs mycobactin in culture media. It survives for a year or more in soil and water. Calves are infected mainly in the first months of life by swallowing faeces from contaminated teats, bedding and feed, and through colostrum and milk; infection in utero also occurs. Susceptibility falls with age. The organism lives in macrophages of the ileum and associated lymph nodes. After an incubation of usually two to five years or more, a proportion of infected cattle develop disease. Infection is WOAH-listed as paratuberculosis.
In cattle the clinical disease is chronic, intermittent then persistent diarrhoea without fever, with progressive weight loss while appetite remains, and later submandibular oedema ('bottle jaw') from protein loss. Sheep and goats show wasting, and diarrhoea is less common. At necropsy the terminal ileum has a thickened, corrugated mucosa, with enlarged mesenteric lymph nodes and thickened lymphatics. For every clinical case there are several subclinical ones shedding the organism and losing yield. Diagnosis uses faecal culture or PCR, serum or milk ELISA and, in clinical cases, Ziehl-Neelsen stained smears of faeces or rectal scrapings showing clumps of acid-fast organisms; all these tests miss many early infections, so herd testing is repeated. Control focuses on calf rearing: calving in a clean area, removing the calf quickly, feeding colostrum from test-negative cows or pasteurised colostrum, milk replacer, and keeping young stock away from adult faeces; along with this, test-and-cull of shedders and buying from herds of known status. Herd assurance schemes exist in several countries, including Australia, the Netherlands and the United States. Killed oil-adjuvant vaccines reduce clinical disease and shedding, particularly in sheep, but do not prevent infection, cause injection-site lesions and can interfere with tuberculin testing, so their use is regulated. A causal link between MAP and Crohn's disease in people has been proposed and remains unproven.
Glanders is a contagious, usually fatal disease of equids caused by Burkholderia mallei, a Gram-negative, non-motile rod that is an obligate mammalian pathogen and does not persist long in the environment. Donkeys and mules tend to develop acute disease and die quickly, while horses more often develop chronic disease and act as long-term carriers. Carnivores, including cats and captive big cats, can be infected by eating infected meat. Spread is by ingestion of feed and water contaminated by nasal discharge and pus, especially at shared troughs, and by inhalation. Glanders was eradicated from Western Europe and North America in the twentieth century by test-and-slaughter, but it persists or has re-emerged in parts of Asia (including India and Pakistan), the Middle East, Africa and South America. It is WOAH-listed and notifiable, and in India it is a scheduled disease under the Prevention and Control of Infectious and Contagious Diseases in Animals Act, 2009.
Three forms overlap. Nasal glanders gives nodules and ulcers on the nasal septum that heal as star-shaped scars, with unilateral or bilateral mucopurulent discharge and hard, enlarged submandibular lymph nodes. Pulmonary glanders gives nodules in the lungs, cough and debility. Cutaneous glanders ('farcy') gives nodules along thickened lymphatics of the limbs and trunk ('farcy buds' along 'farcy pipes') that ulcerate and discharge a honey-like pus. The mallein test, an intradermo-palpebral injection of mallein into the lower eyelid read for swelling and discharge, is the classical field test. The complement fixation test is prescribed by WOAH for international trade; ELISAs and immunoblot are used for confirmation; and culture and PCR are used on lesion material under biosafety containment. The differentials are strangles, epizootic lymphangitis caused by Histoplasma capsulatum var. farciminosum, ulcerative lymphangitis caused by C. pseudotuberculosis, sporotrichosis and melioidosis caused by Burkholderia pseudomallei. Treatment is not permitted in most countries. Confirmed cases are destroyed, premises are quarantined and disinfected, and equids in contact are tested. Glanders is a severe, sometimes fatal zoonosis, with laboratory workers and animal handlers at risk, and B. mallei is regarded as a potential biological weapon.
Actinomycosis in cattle is caused by Actinomyces bovis, a Gram-positive, branching, filamentous anaerobe that lives in the mouth. It enters through wounds from coarse feed or erupting teeth and causes a chronic, rarefying pyogranulomatous osteomyelitis of the mandible or maxilla. The bone becomes swollen, hard and painless, with a honeycombed internal structure, and discharging sinuses release pus with small yellow 'sulphur granules', which are colonies surrounded by club-shaped deposits. Teeth may loosen, eating becomes difficult and the animal loses condition. Diagnosis is clinical, supported by radiography and by crushed granule smears showing Gram-positive filaments. Treatment is prolonged and often only halts progression: sodium iodide by intravenous injection, often repeated, with or without penicillin or other antimicrobials and surgical debridement. A commonly quoted cattle dose is sodium iodide 70 mg/kg as a 10% solution by slow intravenous injection — confirm against the product label and your national formulary. Iodism, with lacrimation, dandruff-like scurf, coughing and loss of appetite, signals that the limit has been reached. Many advanced cases are culled.
Actinobacillosis is caused by Actinobacillus lignieresii, a Gram-negative rod that is also a commensal of the mouth. Unlike Actinomyces, it infects soft tissue: in cattle, classically, the tongue, which becomes hard, swollen and protruding ('wooden tongue'), with drooling and difficulty prehending feed; also lymph nodes of the head and neck, and, in sheep, the lips, face and nose. Pus contains small granules that are Gram-negative. Soft-tissue lesions respond much better than bone lesions: sodium iodide intravenously, sometimes with oral potassium iodide, and antimicrobials chosen by sensitivity usually produce rapid improvement. Other actinobacilli cause different diseases: A. pleuropneumoniae causes porcine pleuropneumonia, and A. equuli causes septicaemia in neonatal foals ('sleepy foal disease').
Mycoplasmas are the smallest free-living bacteria. They have no cell wall, so beta-lactam antibiotics have no effect on them, and they are pleomorphic and need rich media containing serum; many produce 'fried egg' colonies. They cause chronic respiratory, joint, udder and genital disease across species. Beyond the two diseases in this chapter, contagious agalactia of sheep and goats (mainly M. agalactiae) is WOAH-listed, M. bovis causes pneumonia, arthritis and mastitis in cattle, M. hyopneumoniae causes enzootic pneumonia of pigs, and in poultry M. gallisepticum (chronic respiratory disease of chickens and infectious sinusitis of turkeys) and M. synoviae are WOAH-listed as avian mycoplasmosis and controlled by breeder-flock testing and eradication.
Contagious bovine pleuropneumonia (CBPP) is caused by Mycoplasma mycoides subsp. mycoides (formerly the small-colony type) and affects cattle and water buffalo. It spreads by aerosol through close contact, so outbreaks follow cattle movement, trekking and common watering and night enclosures. It is endemic in much of sub-Saharan Africa. It was eradicated from the United States in 1892 and from Australia in 1973; Europe had outbreaks until the late 1990s; and India is recognised by WOAH as free. Acute cases show fever, cough, laboured breathing, extension of the neck and reluctance to move; many cases are chronic, with loss of condition. Calves may have arthritis. The characteristic lesion is fibrinous pleuropneumonia, usually of one lung, with widened, oedematous interlobular septa separating lobules in different stages of consolidation, a 'marbled' appearance, together with pleural fluid and fibrin. Recovered animals may carry sequestra, encapsulated pieces of necrotic lung that hold live organisms and can reactivate. Diagnosis combines necropsy findings with culture and PCR, and serology (the complement fixation test and competitive ELISA), which is interpreted at herd level. Antimicrobial treatment is discouraged or forbidden in many countries because it may produce carriers and mask disease. Control is by movement control, slaughter of affected and in-contact herds in free countries, and vaccination in endemic countries with live attenuated strains T1/44 or T1sr, given by injection at the tip of the tail so that the severe local reaction (Willems reaction) does not spread to vital tissues. CBPP is WOAH-listed, and WOAH grants official free status.
Contagious caprine pleuropneumonia (CCPP) is caused by Mycoplasma capricolum subsp. capripneumoniae, historically called the F38 biotype. It is a disease of goats; sheep are not usually clinically affected, and some wild ruminants are susceptible. It occurs in Africa, the Middle East and parts of Asia. It spreads by aerosol and causes very high morbidity and mortality in naive herds: fever, cough, laboured breathing, frothy nasal discharge and death. The lesion is fibrinous pleuropneumonia, often of one lung, with straw-coloured pleural fluid; unlike CBPP, the interlobular septa are not greatly thickened, and the disease is confined to the thorax. Culture is difficult, so PCR is the preferred confirmation; latex agglutination and competitive ELISA are used for serology. Unlike CBPP, early treatment with tetracyclines or macrolides such as tylosin is effective and is used. Inactivated, saponin-adjuvant vaccines are used in endemic areas, together with movement control. CCPP is WOAH-listed. M. mycoides subsp. capri causes similar disease in goats and is separated by laboratory tests.
Bovine anaplasmosis is caused by Anaplasma marginale, an obligate intracellular bacterium of the order Rickettsiales that infects red blood cells. It appears in stained smears as small dense inclusions at the margin of red cells. A. centrale sits nearer the centre of the cell and is much less pathogenic; A. ovis affects sheep and goats. Ticks transmit A. marginale biologically: in tropical regions mainly Rhipicephalus (Boophilus) species, and elsewhere Dermacentor species. It is also transmitted mechanically by biting flies such as tabanids and stable flies, and iatrogenically by needles, dehorning, castration and ear-tagging equipment shared between animals. It occurs across the tropics and subtropics and in parts of temperate countries. Bovine anaplasmosis is WOAH-listed.
Calves under about a year are infected with little disease and become immune carriers; cattle over two years develop severe and often fatal disease. This inverse age resistance means that in endemic areas, where calves are infected young, clinical disease is uncommon ('endemic stability'), while outbreaks occur when adult cattle without immunity enter an infected area or when the tick or fly population changes. Infected red cells are removed by macrophages in the spleen and liver, so anaemia is extravascular, and there is no haemoglobinuria. This is the main clinical difference from babesiosis, in which intravascular haemolysis produces red urine. Signs are fever, severe anaemia with pale then yellow mucous membranes, weakness, rapid breathing and heart rate, weight loss, drop in milk, abortion and sometimes aggression or excitement caused by cerebral hypoxia. Stress and handling can precipitate death. Survivors remain carriers for life.
In acute cases, Giemsa- or rapid Romanowsky-stained blood smears show the marginal bodies, and packed cell volume is low. Carriers, whose parasitaemia is very low, are detected by serology (competitive ELISA against the MSP5 protein, the card agglutination and complement fixation tests) or PCR. The differentials are babesiosis, theileriosis, trypanosomosis, leptospirosis in calves and bacillary haemoglobinuria. Treatment uses tetracyclines, with oxytetracycline the standard choice, and imidocarb, which is also active against Babesia; clearance of the carrier state requires a longer course and is not always achieved. Very anaemic animals may need blood transfusion, and must be handled calmly. Control combines tick and fly control, hygiene of needles and instruments, and, in some countries, vaccination. Live A. centrale blood vaccines have been used in Australia, South Africa, Israel and parts of South America; they carry the risk of transmitting other blood-borne agents and of reactions in adult cattle. Related agents include Anaplasma phagocytophilum, which infects granulocytes and causes tick-borne fever in sheep and cattle and granulocytic anaplasmosis in horses, dogs and people, and A. platys, which infects platelets of dogs.
Ringworm, or dermatophytosis, is a superficial fungal infection of keratinised tissue (hair, skin and claws) caused by dermatophytes. They are grouped by where they live: zoophilic species adapted to animals, geophilic species in soil, and anthropophilic species in people. In cattle the main cause is Trichophyton verrucosum; in horses, T. equinum and Microsporum equinum; in dogs and cats, Microsporum canis, which is the most important zoonotic species, with T. mentagrophytes (from rodents) and Nannizzia gypsea (formerly Microsporum gypseum, from soil) also involved; and in poultry, Microsporum gallinae, which causes favus of the comb and wattles. Infective arthrospores survive in the environment, on bedding, fences, grooming kit and in houses for many months, which explains persistent problems. Ringworm is not WOAH-listed but is a common zoonosis: farm workers catch T. verrucosum from calves, and children and owners catch M. canis from kittens and cats.
In cattle, ringworm is most common in housed calves in winter. Lesions are round, grey-white, thick crusts ('ashy' plaques), commonly around the eyes, on the head and neck and on the trunk; itching is usually mild. Cattle generally recover in a few months as immunity develops, often at turnout. In horses, lesions appear where tack and grooming equipment contact the skin. In cats the classic lesion is patchy, scaly hair loss on the face, ears and forelimbs, but cats, especially longhaired ones, can carry M. canis without signs. Diagnosis combines several tests. A Wood's lamp (ultraviolet light at about 365 nm) shows apple-green fluorescence of hairs infected with M. canis (older texts say about half of strains; recent studies find most infected cats fluoresce when examined carefully); T. verrucosum and most other species do not fluoresce, so a negative result does not rule out ringworm. Direct microscopy of plucked hairs cleared in potassium hydroxide or mineral oil shows arthroconidia around the hair shaft. Culture on dermatophyte test medium changes the colour of the medium to red, but some contaminant fungi do the same, so colonies must be identified microscopically. PCR is quick but can detect spores on a carrier or from the environment. The Mackenzie toothbrush technique (brushing the entire coat and culturing the brush) screens cats without lesions and confirms cure.
In cattle and horses, the disease is often self-limiting, and treatment aims to shorten it and limit spread: topical enilconazole or other azole washes where registered, and removing crusts. In dogs and cats, current guidelines combine systemic treatment (itraconazole or terbinafine) with topical therapy (lime sulphur dips or miconazole-chlorhexidine shampoo) and environmental cleaning, until repeated cultures are negative. Griseofulvin, an older systemic drug, is teratogenic and must not be given to pregnant animals, and it is not permitted for food-producing animals in many countries. Environmental decontamination means removing hair and debris by vacuuming, washing with detergent, then applying a disinfectant proven against spores, such as diluted sodium hypochlorite or enilconazole, repeated. Live attenuated T. verrucosum vaccines are used for cattle in Europe; Norway and Sweden have used systematic vaccination programmes to reduce cattle ringworm to low levels. Handlers should wear gloves, and people with suspicious lesions should see a doctor.
Learn each disease on the same frame: agent, host, spread, signs, lesions, test, differentials, treatment, control, zoonotic and WOAH status. Most exam questions test a single link in that chain, such as which vaccine strain is rough, which test detects antigen in hides, or which serovar is maintained by cattle. Make a one-page table for sudden death in ruminants (anthrax, HS, BQ, enterotoxaemia, lightning, poisoning) and for abortion (brucellosis, leptospirosis, listeriosis), because these comparisons are asked everywhere. Practise interpreting a SICCT result, a bulk-tank SCC and a paired MAT titre with numbers.
In practice the decisions are: is this notifiable, and whom do I call; is it safe to open this carcass; which samples, in what container, to which laboratory; treat, cull or vaccinate? A five-year practitioner should run a herd mastitis investigation from SCC records and culture, advise a vaccination calendar for HS, BQ and clostridial disease before the risk season, manage a strangles outbreak on a yard with isolation zones and guttural pouch screening, and protect staff from zoonoses (gloves for abortions, no raw milk, anthrax caution). Know your national rules on withdrawal periods and on which drugs may be used in food animals.
Senior veterinarians design and defend programmes. That means choosing between test-and-slaughter and vaccination given the budget for compensation, setting targets for brucellosis vaccination coverage of female calves, deciding when a district has become endemically stable for anaplasmosis and should not be disrupted, and managing wildlife reservoirs of tuberculosis with stakeholders. They audit mastitis programmes in large dairies for antimicrobial use, respond to anthrax in a village with the public health service, and handle trade certification that depends on WOAH-listed disease status.
Research questions are about better tools and evidence. Examples include DIVA vaccines and tests for tuberculosis and brucellosis, the true efficacy of HS and CBPP vaccines under field conditions, the role of MAP in human disease, the genomics of S. aureus and S. equi transmission, selective dry-cow therapy and antimicrobial resistance, models of anthrax spore persistence in soils, and cost-benefit analysis of eradication versus control. A senior researcher also judges the quality of the evidence behind current policy, such as badger culling, and advises WOAH, FAO and national authorities.
This manual covers the sixteen curriculum units and names related diseases only in passing. It does not give full accounts of other bacterial diseases often taught nearby: salmonellosis, colibacillosis, pneumonic pasteurellosis (bovine respiratory disease), botulism, bacillary haemoglobinuria, foot rot, dermatophilosis, Q fever, heartwater, ehrlichiosis, swine erysipelas, fowl cholera, infectious coryza and other poultry bacterial diseases, canine and feline bacterial infections apart from leptospirosis, brucellosis and ringworm, and systemic mycoses. It deliberately gives very few drug doses, because doses and permitted uses vary by country and product; treatment is described by drug class. National vaccination schedules for HS and BQ vary by state and country and are described in outline only. Whether leptospirosis is on the current WOAH list is not stated because the writer could not confirm it. Country programme dates and status should be checked against the current national source.
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.
These notes are free to read here, with no account.
What the Laisha app adds:
Free for ten days, then a subscription. We would rather write that here than have you find it later.