Veterinary · Para-clinical · also MSVE VMC-311
The bacteria and fungi that cause disease in animals, genus by genus: what they are, where they live, what they cause and how they are identified.
In the exams: ICAR AICE-JRF core group 06; ICAR AIEEA-PG 13 (Microbiology); China preventive paper
Systematic veterinary bacteriology and mycology takes the general principles of microbiology and applies them genus by genus. For each important bacterium and fungus it asks the same questions: which animals does it infect, what disease does it cause in each species, which sample will show it, how a diagnostic laboratory identifies it with stains, culture and a few key tests, how the disease is treated and prevented, and whether it threatens people. This manual is written at the level of a practising veterinarian and a routine diagnostic laboratory. It does not describe research culture methods; where an organism needs a reference laboratory, it says so.
The subject matters because most of the infectious diseases a veterinarian meets daily are bacterial or fungal: mastitis, pneumonia, neonatal diarrhoea, abortion, pyoderma, ringworm and sudden death. It also matters because many of these organisms are zoonoses. Anthrax, brucellosis, bovine tuberculosis, glanders, leptospirosis, listeriosis, salmonellosis, Q fever, chlamydial infection and ringworm all pass from animals to people, and a veterinarian is often the first person to suspect them.
Worldwide the subject is examined in a similar way. In India it is the MSVE course VMC-311 and part of the microbiology group of the ICAR postgraduate (AIEEA-PG, code 13) and doctoral (AICE-JRF/SRF, core group 06) entrance papers and state veterinary officer papers. Licensing examinations in North America, Britain, Australasia, South Africa, China, Korea, Japan, the Philippines and Nepal test it mainly through clinical cases. Drug doses are not given in this manual; where a drug is named, confirm it against the product label and your national formulary, because doses, permitted uses and withdrawal periods vary by country and product.
Two habits run through every chapter. First, the sample decides the diagnosis: take it from the lesion, before treatment, aseptically, keep it cool, put fresh tissue for culture and fixed tissue for histopathology in separate containers, and send a full history. Second, warn the laboratory: Bacillus anthracis, Brucella, Mycobacterium bovis, Burkholderia mallei, Coxiella burnetii and Chlamydia abortus are handled only in containment level 3 laboratories, and many of the diseases here are notifiable to the national veterinary authority and listed by the World Organisation for Animal Health (WOAH). Notifiable lists differ by country.
Staphylococci are Gram-positive cocci arranged in grape-like clusters. They are catalase positive, which separates them from streptococci, and they grow well aerobically on blood agar in 24 hours as round, opaque, white to golden colonies. The coagulase test divides them into coagulase-positive species, which are the main pathogens, and coagulase-negative staphylococci, which are mostly skin commensals but do cause mild mastitis. The important coagulase-positive species are Staphylococcus aureus (all species, especially cattle, small ruminants, poultry and people), Staphylococcus pseudintermedius (dogs and cats) and Staphylococcus hyicus, which is variably coagulase positive and causes exudative epidermitis (greasy pig disease) in piglets. Many S. aureus strains show double-zone haemolysis on sheep or ox blood agar: an inner zone of complete (alpha-toxin) haemolysis and an outer zone of incomplete (beta-toxin) haemolysis. On mannitol salt agar, S. aureus ferments mannitol and turns the medium yellow. Identification to species, particularly separating S. aureus from S. pseudintermedius, is increasingly done by MALDI-TOF or PCR because the two can look alike on simple tests.
S. aureus is a major cause of contagious bovine mastitis. It spreads from cow to cow at milking through hands, cloths and liners, and it forms micro-abscesses in udder tissue, so cure rates during lactation are poor and chronic carriers with intermittently high somatic cell counts are common. Peracute gangrenous mastitis, with a cold, blue quarter, occurs in some cows and in ewes. In poultry S. aureus causes bumblefoot, arthritis and septicaemia; in sheep it causes tick pyaemia in lambs and contributes to mastitis. In dogs S. pseudintermedius is the main cause of pyoderma, otitis externa and wound infection. Methicillin resistance, conferred by the mecA gene, matters greatly: methicillin-resistant S. aureus (MRSA) occurs in horses, pigs (livestock-associated clonal lineages) and people, and methicillin-resistant S. pseudintermedius (MRSP) is a serious problem in dogs because it is often resistant to many drug classes. Treatment of staphylococcal infections should follow culture and susceptibility testing wherever possible. Mastitis control relies on the five-point plan principles: teat disinfection after milking, dry-cow therapy or selective dry-cow therapy, prompt treatment of clinical cases, culling of chronic cases and milking-machine maintenance. Staphylococcal enterotoxins in milk and meat cause food poisoning in people.
Streptococci are Gram-positive cocci in pairs and chains and are catalase negative. Colonies on blood agar are small, translucent and dewdrop-like. Haemolysis is a first sorting tool: beta-haemolysis is complete clearing, alpha-haemolysis is partial greenish clearing, and gamma means none. Lancefield grouping detects a cell-wall carbohydrate antigen by agglutination and assigns groups such as B, C, E and G. The CAMP test identifies Streptococcus agalactiae (group B): a streak of the isolate placed at right angles to a beta-toxin-producing S. aureus streak shows an arrowhead of enhanced haemolysis. Aesculin hydrolysis on Edwards medium helps separate Streptococcus uberis (aesculin positive, dark colonies) from S. agalactiae and Streptococcus dysgalactiae (negative). In cattle, S. agalactiae is an obligate udder pathogen spread at milking; it is very sensitive to penicillin and can be eradicated from a herd by treatment and hygiene. S. dysgalactiae is spread both at milking and from the environment, and S. uberis is an environmental pathogen of bedding and pasture that cannot be eradicated, only managed. In horses, Streptococcus equi subspecies equi causes strangles: fever, nasal discharge and abscessation of the submandibular and retropharyngeal lymph nodes. Complications include guttural pouch empyema with chondroids, bastard strangles (abscesses in other organs) and purpura haemorrhagica, an immune-complex vasculitis. Carriers with guttural pouch infection maintain the disease, so control uses isolation, temperature monitoring of in-contacts, guttural pouch endoscopy and PCR on lavage, and vaccination where available. Streptococcus equi subspecies zooepidemicus is an opportunist in horses (respiratory disease, endometritis) and causes disease in other species. In pigs, Streptococcus suis causes meningitis, arthritis, septicaemia and sudden death in weaners; serotype 2 is the classic type and it is a zoonosis of pig and pork handlers, causing meningitis and deafness. Streptococcus porcinus causes jowl abscesses. Penicillin remains the first choice for most streptococcal infections, subject to the label and national formulary.
Bacillus anthracis is a large Gram-positive rod that forms spores outside the body when exposed to oxygen. In the animal it is capsulated and does not form spores; once released from a carcass that has been opened, it sporulates and the spores can survive in soil for decades. Anthrax districts are therefore linked to soil type, flooding and drought, and outbreaks often follow heavy rain after dry weather or digging that disturbs old burial sites. Virulence depends on two plasmids: one carries the genes for the three toxin components (protective antigen, lethal factor and oedema factor), and the other carries the genes for the poly-D-glutamic acid capsule, which resists phagocytosis. Herbivores, especially cattle, sheep, goats and wild ruminants, are highly susceptible. Pigs, dogs and cats are more resistant and usually develop localised throat and intestinal disease after eating infected meat. Birds are largely resistant. In cattle and sheep the usual form is peracute or acute septicaemia. Animals are often simply found dead, sometimes with dark, unclotted blood from the nostrils, mouth, anus or vulva. Rigor mortis is incomplete and the carcass bloats and decomposes quickly. Live animals in the acute form show high fever, depression, congested mucous membranes, difficulty in breathing, and in cows sudden fall in milk with blood-tinged milk. Horses often show colic and hot, oedematous swellings of the throat, chest and abdomen. Pigs typically develop severe swelling of the throat and difficulty swallowing, with or without intestinal signs. At necropsy, which should not be carried out if anthrax is suspected, the classic findings are a greatly enlarged, soft spleen with dark, tarry blood, widespread haemorrhages and failure of blood to clot. In people, the cutaneous form produces a painless ulcer with a black eschar (malignant pustule), usually in farmers, butchers and wool and hide workers; inhalational (woolsorters' disease) and gastrointestinal forms are less common and more often fatal.
When anthrax is suspected, the carcass is not opened, because doing so lets the bacteria sporulate and contaminate the site. Instead, a drop of blood is taken from a superficial vein (an ear vein or tail vein in cattle) or a swab is taken from a natural orifice, and thin blood smears are made. The M'Fadyean reaction is the classic direct test: a smear fixed and stained with polychrome methylene blue shows large square-ended rods singly or in short chains, surrounded by pink-purple capsular material, against blue bacilli. In pigs and horses with localised lesions, a sample from oedematous tissue or an affected lymph node is used. In the laboratory B. anthracis grows on blood agar as non-haemolytic, grey-white, flat colonies with an irregular, wavy edge often described as a 'medusa head' or 'cut glass' appearance; it is non-motile and sensitive to penicillin and to gamma phage, which help separate it from the haemolytic, motile Bacillus cereus. The Ascoli test is a thermoprecipitation test that detects anthrax antigen in heat-extracted tissue such as hides or putrefied material when organisms can no longer be cultured. PCR is now widely used in reference laboratories. Laboratory work with B. anthracis is restricted to containment level 3.
Early treatment of in-contact or febrile animals with penicillin or oxytetracycline can be effective because the organism is usually sensitive, but treatment is often too late for clinical cases. Anthrax is notifiable in most countries. Control rests on the following steps: notify the authority; do not open or move the carcass; prevent scavengers reaching it; dispose of it by incineration or, where allowed, deep burial with lime according to national rules; disinfect contaminated ground and objects with a sporicidal disinfectant such as formaldehyde or a strong hypochlorite; quarantine the premises; and vaccinate the remaining animals in endemic areas. The standard livestock vaccine is a live spore vaccine of the toxigenic, non-capsulated Sterne strain (34F2), which lacks the capsule plasmid. Because it is a live bacterial vaccine, antimicrobials should not be given around the time of vaccination, as they would kill the vaccine organism; the interval to observe is given on the product label. Annual revaccination is usual in endemic areas. People exposed to infected animals or products should seek medical advice.
Clostridia are large Gram-positive, anaerobic, spore-forming rods that live in soil and in the intestine of healthy animals. Almost all clostridial diseases are caused by toxins, which explains why they are sudden, frequently fatal and best prevented by toxoid vaccines. They fall into three groups: the histotoxic clostridia that invade tissue (blackleg, malignant oedema, black disease, bacillary haemoglobinuria), the enterotoxaemic clostridia that produce toxins in the gut (Clostridium perfringens types), and the neurotoxic clostridia (tetanus and botulism). In the laboratory, samples must be fresh, because clostridia invade tissues rapidly after death and a positive culture from an old carcass means little. Fluorescent antibody staining of smears from affected muscle or liver is a fast and widely used way to identify C. chauvoei, C. septicum, C. novyi and C. sordellii. Culture is on blood agar incubated anaerobically. C. perfringens gives a characteristic double zone of haemolysis and produces a lecithinase reaction on egg-yolk agar (the Nagler reaction, which is inhibited by antitoxin); it is non-motile. C. septicum swarms over the plate. Toxin detection, by ELISA or PCR for toxin genes, is central to diagnosing enterotoxaemia.
Blackleg (blackquarter), caused by Clostridium chauvoei, affects well-grown young cattle, usually between about six months and two years old, and sheep. Spores ingested from soil lie dormant in muscle and are activated by bruising or other injury, producing an acute myositis. Signs are fever, lameness and a hot, then cold, swelling over a heavy muscle mass such as the thigh, shoulder or neck that crackles (crepitates) because of gas; death often occurs within a day or two. Cut muscle is dark red to black, dry and gaseous, with a rancid butter smell. Malignant oedema (gas gangrene) follows contamination of wounds, including castration, shearing and calving injuries, by C. septicum, C. novyi, C. perfringens type A, C. sordellii or C. chauvoei; the swelling is more oedematous and spreads from the wound. Black disease (infectious necrotic hepatitis), caused by C. novyi type B, occurs in sheep and cattle when liver fluke migration damages the liver and lets dormant spores germinate; the skin of the carcass darkens because of venous congestion. Bacillary haemoglobinuria, caused by C. haemolyticum (C. novyi type D), causes intravascular haemolysis and red urine in cattle, again often in fluke areas. Control is by vaccination with multivalent clostridial toxoid/bacterin vaccines and, for black disease, by fluke control.
C. perfringens strains are classified into toxinotypes by the major toxins they produce. The original scheme recognised types A to E using alpha, beta, epsilon and iota toxins, and newer schemes add types F and G based on enterotoxin and NetB toxin. Type B causes lamb dysentery in very young lambs, with haemorrhagic enteritis. Type C causes haemorrhagic, necrotic enteritis in newborn piglets, calves and lambs and struck in adult sheep; beta toxin is destroyed by trypsin, so colostrum, which contains trypsin inhibitors, favours disease in neonates. Type D produces epsilon toxin and causes enterotoxaemia (pulpy kidney disease, overeating disease) in fast-growing lambs on rich diets and in goats; signs include sudden death, convulsions, and in sheep glycosuria, with soft, autolysed kidneys and fluid in the pericardium at necropsy. Goats show a more enteric, diarrhoeic form and respond less completely to vaccination. Type A is associated with necrotic enteritis in poultry (in the newer scheme the NetB-producing strains are type G) and with some enteric conditions in other species. Control is by toxoid vaccination of dams so that colostrum protects the young, vaccination of the young, and gradual changes of diet. Lambs from vaccinated ewes are usually vaccinated twice, a few weeks apart, before maternal protection wanes, according to the product label.
Clostridium tetani produces tetanospasmin, a neurotoxin that travels up nerves to the spinal cord and blocks release of the inhibitory neurotransmitters glycine and GABA. The result is spastic paralysis. Horses are the most susceptible domestic species, followed by sheep and goats; cattle and dogs are more resistant. Signs are stiffness, a sawhorse stance, erect ears, raised tail, prolapse of the third eyelid when the head is raised or tapped, lockjaw and hyperaesthesia. Diagnosis is clinical, often with a wound or recent castration, docking or foaling as a history. Treatment combines wound debridement, penicillin, tetanus antitoxin, sedation and muscle relaxation, a dark quiet stable and nursing; prevention is by tetanus toxoid vaccination, with antitoxin for unvaccinated animals at risk. Clostridium botulinum produces the most potent known toxins, which block acetylcholine release at the neuromuscular junction and cause flaccid paralysis. Cattle develop botulism from carcass-contaminated feed, poultry litter or bone chewing in phosphorus-deficient areas; horses from poorly made haylage or, in foals, from toxicoinfection (shaker foal syndrome); waterfowl from type C toxin in stagnant water ('limberneck'). Signs include progressive weakness, recumbency, reduced tongue and tail tone and difficulty swallowing. Diagnosis rests on history and signs, with toxin detection in feed, serum or gut content; treatment is supportive plus antitoxin early. Vaccination with toxoid is used where the risk is known.
Mycobacteria are slender, non-motile, non-spore-forming rods with a cell wall rich in mycolic acids. This waxy wall makes them acid-fast: once stained with hot carbol fuchsin in the Ziehl-Neelsen method, they resist decolourisation by acid-alcohol and appear red against a blue background. The wall also makes them resistant to many disinfectants and to drying, and it explains their slow growth. The veterinary pathogens are the Mycobacterium tuberculosis complex (including M. bovis, which causes bovine tuberculosis and infects many mammals and people, M. tuberculosis in people and occasionally in animals in close contact, and M. caprae in goats and cattle), the Mycobacterium avium complex (M. avium subsp. avium in birds, and opportunist infections in pigs), and M. avium subsp. paratuberculosis (MAP), the cause of Johne's disease. Culture of these organisms needs special egg-based or other enriched media and takes weeks to months; it is done in reference laboratories under containment level 3 for M. bovis. M. bovis grows better on media containing pyruvate than glycerol, whereas M. tuberculosis is enhanced by glycerol. MAP is dependent on the iron-chelating compound mycobactin for growth in culture, a classic identification feature. Avian tuberculosis (M. avium subsp. avium) affects older backyard poultry and caged birds, producing emaciation and lesions in the liver, spleen and intestine; lungs are usually spared, unlike in mammals. Pigs pick up M. avium complex organisms and develop lesions mainly in the lymph nodes of the head and mesentery, found at slaughter. Dogs and cats can be infected with M. bovis or M. tuberculosis; cats also suffer from M. microti and from non-tuberculous mycobacteria causing skin disease. Because some species react poorly to tuberculin, diagnostic approaches vary by species and country.
M. bovis spreads mainly by aerosol between cattle in close contact, and also by ingestion, including calves drinking infected milk. The typical lesion is the tubercle, a granuloma with a caseous, often calcified, centre surrounded by macrophages, epithelioid cells, Langhans giant cells and a fibrous capsule. Lesions are most common in the lymph nodes of the head and thorax and in the lungs. Clinical signs appear late: progressive weight loss, fluctuating fever, a soft chronic cough, enlarged superficial lymph nodes and, rarely, tuberculous mastitis. Most infected cattle are found by testing, not by clinical signs. The standard live-animal test is the tuberculin skin test, which measures delayed (type IV) hypersensitivity to purified protein derivative (PPD). In the single intradermal test, bovine PPD is injected in the skin of the neck or caudal fold and the increase in skin thickness is read at about 72 hours. The comparative (single intradermal comparative cervical) test injects avian and bovine PPD at two sites and compares the reactions, so that sensitisation to environmental mycobacteria and MAP is not mistaken for M. bovis infection. The interferon-gamma assay is a blood test used alongside skin testing, mainly to increase sensitivity. Cut-off values and interpretation rules are set by each national programme. Control is by test and slaughter, movement controls, meat inspection and abattoir surveillance, and, in some countries, management of wildlife reservoirs such as badgers, brushtail possums, deer or buffalo. Pasteurisation of milk breaks the main route to people. Treatment of infected food animals is not permitted in most countries.
Johne's disease is a chronic granulomatous enteritis of ruminants caused by MAP. Calves are infected mainly in the first months of life by ingesting faeces, colostrum or milk from infected cows, but clinical disease usually appears only at two to five years or older. In cattle the classic sign is chronic, profuse, watery diarrhoea without blood or straining, with progressive weight loss while appetite is maintained, and sometimes submandibular oedema from protein loss. In sheep and goats wasting is the main sign and diarrhoea is less common. At necropsy the terminal ileum, caecum and colon have a thickened mucosa thrown into transverse corrugations, and the mesenteric lymph nodes are enlarged; acid-fast bacteria in clumps are seen in smears of mucosa or node. Laboratory diagnosis uses faecal culture, faecal PCR, serum or milk ELISA and, at necropsy, histology and Ziehl-Neelsen staining. All tests have low sensitivity in young or early infected animals, so they are best used at herd level and repeated. There is no practical cure. Control relies on hygiene at calving, separating calves from adult faeces, feeding colostrum and milk from test-negative cows or pasteurised milk, and testing and culling. Vaccines exist in some countries; they reduce clinical disease and shedding but interfere with tuberculosis skin testing, so their use is regulated. A possible link between MAP and Crohn's disease in people has been proposed but remains unproven.
Brucella organisms are small, Gram-negative coccobacilli that are non-motile, aerobic, and catalase, oxidase and urease positive in most species (B. ovis is an exception for oxidase and urease). They are facultative intracellular parasites of macrophages and of the placenta. With the modified Ziehl-Neelsen stain (using weak acid for decolourisation) they stain red, which is why stained smears of placental cotyledons or fetal stomach content are a classic first test; Chlamydia abortus and Coxiella burnetii also stain red with this method, so the smear is presumptive only. The main species and hosts are Brucella abortus (cattle and buffalo), Brucella melitensis (sheep and goats, and the most pathogenic for people), Brucella suis (pigs, reindeer, hares), Brucella ovis (rams, causing epididymitis, not usually zoonotic), and Brucella canis (dogs). Brucella abortus, melitensis and suis exist as smooth colonies, whereas ovis and canis are naturally rough, which matters for serology because the standard tests detect antibody to smooth lipopolysaccharide. Culture uses selective media and takes several days; all culture work belongs in containment level 3 because laboratory infection is common.
In cattle, B. abortus localises in the pregnant uterus, where erythritol in the placenta favours its growth. The typical sign is abortion in the last third of pregnancy, often only once per cow, followed by retained placenta, metritis and reduced fertility. The placenta shows necrotic cotyledons and a thickened, leathery intercotyledonary area. Bulls may develop orchitis and epididymitis, and hygromas of the knee occur in chronically infected cattle. Infected cows shed enormous numbers of organisms in fetal fluids and the placenta and continue to shed in milk. In sheep and goats B. melitensis causes abortion, stillbirths and weak kids and lambs, and orchitis. In pigs B. suis causes abortion, infertility, orchitis and lameness from spondylitis and arthritis. B. ovis causes epididymitis, usually of the tail of the epididymis, and poor fertility in rams; palpation of the testes is part of ram breeding soundness examination. B. canis causes abortion at about 45 to 55 days of pregnancy, epididymitis, infertility and discospondylitis in dogs. Horses develop fistulous withers or poll evil from B. abortus. In people, brucellosis (undulant or Malta fever) causes recurring fever, sweats, joint pain and fatigue; it is acquired from raw milk and cheese, and by direct contact during assisting births or handling aborted material.
Because culture is slow and hazardous, surveillance relies on serology. The Rose Bengal plate test (RBPT) is a rapid screening agglutination test with buffered antigen at acid pH; it is sensitive and cheap. The milk ring test (MRT) screens bulk tank milk: antibody in the milk binds stained antigen and the complexes rise with the cream to form a coloured ring. Positive screening results are confirmed by the complement fixation test (CFT) or by indirect or competitive ELISA. The serum agglutination test was widely used in the past and is still used in some countries. Vaccination with the smooth strain S19 induces antibody that can confuse these tests, especially when given to adults, which is why calfhood vaccination within a fixed age window is required where S19 is used. B. ovis and B. canis need rough-antigen tests. Cut-off values and confirmatory algorithms vary by national programme and by WOAH guidance.
Treatment of brucellosis in food animals is not recommended or not permitted in most countries because it does not reliably clear infection. Control depends on the disease prevalence and resources: test and slaughter where prevalence is low and compensation is available; vaccination where prevalence is high; and movement control, hygiene at calving, safe disposal of aborted material and pasteurisation of milk in all cases. For cattle the main vaccines are S19, a live attenuated smooth strain given to female calves within the age range set by national rules, and RB51, a live rough strain that does not induce antibody detected by the standard smooth-antigen tests. For small ruminants, Rev. 1 (a live B. melitensis strain) is the standard vaccine. All three live vaccines can infect people and can cause abortion if given to pregnant animals, so they are handled with care. S19 and RB51 are not used in males. B. canis in kennels is managed by testing, removal of positives and neutering, because antibiotic treatment is unreliable and the infection is zoonotic.
Pasteurella multocida and Mannheimia haemolytica are small Gram-negative coccobacilli that often stain more darkly at both ends (bipolar staining) with Giemsa, Leishman or methylene blue. Both live in the upper respiratory tract of healthy animals and become pathogens when stress, viral infection or crowding lowers host defences. P. multocida grows on blood agar as non-haemolytic, greyish colonies with a characteristic 'mousy' smell; it is oxidase positive, indole positive and, importantly, does not grow on MacConkey agar. M. haemolytica produces a narrow zone of beta-haemolysis on blood agar, grows weakly on MacConkey, and is indole negative. Bibersteinia trehalosi (formerly part of Pasteurella haemolytica) causes septicaemia in older lambs. P. multocida is typed by capsule (A, B, D, E, F) and by somatic antigen; serotypes B:2 and E:2 cause haemorrhagic septicaemia, capsule type A causes fowl cholera and pneumonia, and toxigenic type D (and some A) strains cause progressive atrophic rhinitis in pigs.
Haemorrhagic septicaemia (HS) is an acute, highly fatal septicaemia of cattle and especially water buffalo, caused by P. multocida B:2 in Asia and E:2 in Africa. It is a major disease in South and South-East Asia, often in the monsoon or wet season, when animals are crowded, stressed and working. Carrier animals keep it in herds. Signs are sudden high fever, profuse salivation, depression, and a hot, painful oedematous swelling of the throat, brisket and dewlap, with difficult, noisy breathing; death often follows within a day. At necropsy there are petechial haemorrhages on serous membranes and oedema of subcutaneous tissues of the head and neck. Diagnosis is from the clinical picture plus bipolar organisms in a blood smear, culture from heart blood or bone marrow of fresh carcasses, and PCR for HS-specific strains. Very early antimicrobial treatment can save animals, but in practice prevention is by vaccination before the high-risk season, using alum-precipitated or oil-adjuvant killed bacterins; oil-adjuvant vaccines give longer protection. The schedule depends on the national programme and product label.
Bovine respiratory disease (shipping fever) is the commonest reason for treatment and death in feedlot and weaned calves. M. haemolytica serotype A1 is the classic pathogen, aided by viruses such as bovine respiratory syncytial virus, parainfluenza 3 and bovine herpesvirus 1, and by transport, mixing and weather changes. Its leukotoxin kills ruminant leucocytes and causes severe fibrinous pleuropneumonia with marbled lungs. P. multocida type A, Histophilus somni and Mycoplasma bovis also contribute. Samples are nasopharyngeal swabs or bronchoalveolar lavage from untreated early cases, and lung tissue from untreated dead animals. Treatment uses antimicrobials labelled for respiratory disease, ideally guided by herd susceptibility data, with anti-inflammatory drugs; prevention uses vaccination before transport or weaning, management to reduce stress, and good ventilation. Fowl cholera, caused by P. multocida, affects chickens, turkeys and waterfowl; the acute form causes sudden death, cyanosis and diarrhoea, while the chronic form causes swollen wattles and joints. Control combines biosecurity, rodent control and vaccination. Progressive atrophic rhinitis in pigs results from toxigenic P. multocida, often after Bordetella bronchiseptica damage, and produces sneezing, tear staining, twisted snouts and shortened turbinates that are scored at slaughter. Sow vaccination with toxoid-containing vaccines protects piglets through colostrum. P. multocida is also the usual cause of infected cat and dog bite wounds in people.
Salmonella and Escherichia coli belong to the Enterobacterales: Gram-negative, non-spore-forming rods that are oxidase negative, catalase positive, facultatively anaerobic and grow well on MacConkey agar. Lactose fermentation is the first sorting step. E. coli ferments lactose and forms pink colonies on MacConkey; most Salmonella do not and form pale colonies. Salmonella is usually hydrogen sulphide positive, giving black-centred colonies on xylose lysine deoxycholate (XLD) agar and a black butt in triple sugar iron (TSI) agar, whereas E. coli is indole positive and hydrogen sulphide negative. Faeces often contain few salmonellae among many other bacteria, so laboratories use selective enrichment broths before plating; this is part of standard diagnostic culture. Salmonella isolates are confirmed with polyvalent and specific O (somatic) and H (flagellar) antisera and named by serovar under the Kauffmann-White-Le Minor scheme, for example Salmonella enterica serovar Typhimurium. E. coli pathotypes are identified by detecting virulence factors, such as fimbrial adhesins (F4, also called K88, F5 or K99, F18) and toxin genes, usually by PCR.
Most of the more than 2,500 serovars infect many hosts, but some are host-adapted. Host-adapted serovars include Dublin in cattle, Choleraesuis in pigs, Abortusovis in sheep, and Gallinarum and Pullorum in poultry. Host-adapted serovars tend to cause septicaemia, abortion and carrier states; non-host-adapted serovars such as Typhimurium and Enteritidis cause enteritis in many species and are the main food-borne zoonotic serovars. In calves, salmonellosis causes fever, depression and diarrhoea with mucus, fibrin and blood; adults show diarrhoea, fall in milk and abortion, especially with S. Dublin. In pigs, S. Choleraesuis causes septicaemia with cyanosis of the ears and belly, and S. Typhimurium causes enterocolitis and rectal stricture. In horses, stress, surgery and antimicrobial treatment can trigger severe colitis with neutropenia, and equine hospitals use faecal surveillance. In poultry, S. Pullorum causes white diarrhoea and high mortality in chicks under three weeks (pullorum disease), while S. Gallinarum causes fowl typhoid in older birds; both are egg-transmitted and are controlled by testing breeders with whole-blood or serum plate agglutination and removing reactors. S. Enteritidis can colonise the reproductive tract of hens and contaminate eggs without making the hens ill. Samples are faeces (several, because shedding is intermittent), intestinal contents, mesenteric lymph nodes, and fetal stomach contents after abortion. Antimicrobial treatment is reserved for septicaemic animals because it may prolong shedding and select for resistance. Control combines hygiene, rodent control, feed safety, all-in all-out management, vaccination with live or killed vaccines in some species and countries, and national poultry programmes.
E. coli is a normal gut inhabitant, so its isolation means little unless the strain carries virulence factors. Enterotoxigenic E. coli (ETEC) causes watery neonatal diarrhoea in calves, lambs and piglets in the first days of life, and post-weaning diarrhoea in pigs; fimbriae attach the bacteria to the small-intestinal wall and enterotoxins drive secretion of fluid. F5 (K99) strains affect calves and lambs; F4 (K88) and F18 strains affect piglets. Oedema disease of weaned pigs is caused by F18-bearing strains producing Shiga toxin type 2e, which damages blood vessels and causes eyelid and forehead oedema, ataxia and sudden death. Septicaemic E. coli causes colisepticaemia in calves that received too little colostrum. In poultry, avian pathogenic E. coli (APEC) causes colibacillosis: airsacculitis, perihepatitis, pericarditis, yolk sac infection and cellulitis. E. coli is also a major environmental mastitis pathogen in cows, causing acute, sometimes toxic, mastitis around calving, and a common cause of urinary tract infections in dogs and cats and of pyometra in bitches. Prevention of neonatal diarrhoea relies on colostrum, hygiene, and dam vaccination with fimbrial antigens so that colostral antibody blocks attachment. Shiga toxin-producing E. coli (STEC), notably O157:H7, colonises cattle without causing disease but causes haemorrhagic colitis and haemolytic uraemic syndrome in people, so cattle faeces, contaminated beef, raw milk and petting farms are public-health concerns.
Leptospires are thin, tightly coiled, motile spirochaetes with hooked ends. They stain poorly with the Gram stain and are seen live by dark-field microscopy, or in tissue by silver staining or immunohistochemistry. Pathogenic leptospires are grouped into many serovars. Each serovar is maintained by particular maintenance hosts, which carry it in the kidneys and shed it in urine for long periods with few signs, and causes more severe disease in incidental hosts. Examples are serovar Hardjo in cattle, Bratislava and Pomona in pigs, Canicola in dogs, and Icterohaemorrhagiae carried by rats. Infection is through mucous membranes and damaged skin, by contact with urine or urine-contaminated water and soil; warm wet conditions and flooding favour transmission. In cattle, Hardjo causes milk drop syndrome (a sudden fall in yield with a flabby udder and thick milk in all quarters), abortion, stillbirths, weak calves and infertility; incidental serovars such as Pomona cause acute haemolytic disease in calves, with fever, jaundice and red urine. In pigs, leptospirosis causes abortion, stillbirths and weak piglets. In dogs it causes acute kidney injury, liver disease with jaundice, bleeding tendencies and a pulmonary haemorrhage syndrome; vaccinated dogs can still be infected by serovars not in the vaccine. In horses it causes abortion and is associated with recurrent uveitis. In people leptospirosis (Weil's disease in its severe form) ranges from flu-like illness to kidney and liver failure and lung haemorrhage; farmers, abattoir workers, veterinarians, sewer workers and people exposed to flood water are at risk.
The reference serological test is the microscopic agglutination test (MAT): dilutions of serum are mixed with live cultures of a panel of serovars and examined by dark-field microscopy for agglutination; the titre is the highest dilution showing agglutination. A fourfold rise between paired samples taken two to four weeks apart indicates recent infection; a single titre is hard to interpret in vaccinated or endemic populations. ELISA is used for herd screening. PCR on blood in the first week of illness and on urine afterwards detects the organism itself, and fluorescent antibody tests or immunohistochemistry are used on fetal tissues. Culture is slow and is done in specialist laboratories. Treatment uses antimicrobials such as penicillins or doxycycline in dogs and, in cattle, products licensed to clear renal carriage, with supportive care for kidney injury, subject to the label and national formulary. Control combines vaccination with serovar-specific killed vaccines, rodent control, avoiding standing water, and protective clothing and hygiene for people handling urine, placentas and aborted fetuses.
Listeria monocytogenes is a small Gram-positive rod that is catalase positive, shows a narrow zone of beta-haemolysis on blood agar, is CAMP positive with S. aureus, and has a characteristic tumbling motility at room temperature (about 20 to 25 degrees Celsius) but not at 37 degrees. It grows at refrigerator temperature, which is why cold enrichment was historically used and why it is a problem in chilled foods. It lives in soil and in poorly fermented silage, where the pH stays above about 5.5, so ruminant listeriosis is commonly linked to spoiled silage and is seen in winter and spring in housed animals. Three main forms occur in ruminants. Encephalitic listeriosis (circling disease) follows entry through breaks in the oral mucosa and spread up the trigeminal nerve to the brainstem, causing depression, head pressing, circling to one side, and unilateral facial paralysis with a drooping ear, eyelid and lip, and dribbling of feed; histopathology shows microabscesses in the brainstem. Abortion occurs in late pregnancy, and septicaemia occurs in neonates and monogastric animals. Ocular listeriosis (silage eye) causes keratoconjunctivitis and uveitis. Samples are brainstem (medulla and pons) for culture and histology, and fetus and placenta after abortion. High doses of penicillin or oxytetracycline given early can be effective in the encephalitic form, subject to the label and national formulary. Control focuses on making well-fermented silage, discarding mouldy or spoiled silage, and avoiding soil contamination at harvest. In people, Listeria causes abortion, neonatal infection and meningitis in the elderly and immunocompromised; soft cheese, pâté and chilled ready-to-eat foods are the main sources.
Glanders is a contagious, usually fatal disease of horses, mules and donkeys caused by Burkholderia mallei, a small, non-motile, Gram-negative rod. Unlike its relative Burkholderia pseudomallei (the cause of melioidosis), it does not survive long in the environment and is an obligate parasite of equids. Glanders has been eradicated from many countries but persists or has re-emerged in parts of Asia, the Middle East, Africa and South America, including India. Donkeys tend to develop acute disease and die quickly; horses more often develop chronic disease and become carriers. Three forms are recognised and often overlap. The nasal form produces nodules and ulcers on the nasal septum that heal to star-shaped scars, with a sticky nasal discharge and enlarged, hard submandibular lymph nodes. The pulmonary form causes nodules in the lungs, cough and weight loss. The cutaneous form, called farcy, produces nodules along the lymphatic vessels of the limbs and body that ulcerate and discharge a honey-like pus, with corded, thickened lymphatics. Carnivores fed infected meat and people can be infected; human glanders is severe and often fatal without treatment, and the organism is regarded as a potential biological weapon.
Glanders is listed by WOAH and is notifiable. The mallein test is a delayed-hypersensitivity test similar in principle to the tuberculin test: mallein, a protein extract of B. mallei, is injected into the lower eyelid (the intrapalpebral test), and a positive reaction is swelling of the eyelid with a purulent conjunctivitis within about 24 to 48 hours. The complement fixation test is the prescribed serological test for international trade, and ELISA and immunoblot are also used. Culture of nodule pus or nasal discharge gives slow-growing colonies on blood agar and glycerol-containing media, but this work must be done only in containment level 3 laboratories because of the risk to staff. Treatment is not recommended in endemic or free countries because treated animals can remain carriers. Control is by testing, humane destruction of positive animals, disinfection, quarantine and movement controls. Practitioners must not treat suspected cases privately; they must notify the authority.
Mycoplasmas are the smallest free-living bacteria. They have no cell wall, so they do not stain with the Gram stain, are pleomorphic, and are naturally resistant to antimicrobials that act on the cell wall, such as penicillins and cephalosporins. Most need sterols for growth and are cultured on specialised enriched media, where they form tiny 'fried egg' colonies with a dense, embedded centre seen under the low-power microscope. Culture is slow, so PCR and serology are the usual diagnostic tools. Drugs used against them include tetracyclines, macrolides, pleuromutilins and fluoroquinolones, subject to the label, the national formulary and restrictions on critically important antimicrobials. Contagious bovine pleuropneumonia (CBPP), caused by Mycoplasma mycoides subsp. mycoides (small colony type), is a WOAH-listed disease of cattle in parts of Africa. It spreads by close contact and causes fibrinous pleuropneumonia with a marbled lung, distended interlobular septa, and sequestra (encapsulated necrotic lung) in chronic carriers. Control is by movement control, vaccination with live attenuated strains in endemic countries, and test and slaughter in outbreaks in free countries; the CFT and competitive ELISA are used for herds. Contagious caprine pleuropneumonia (CCPP), caused by Mycoplasma capricolum subsp. capripneumoniae, is a highly contagious fatal pleuropneumonia of goats in Africa and Asia. Mycoplasma bovis causes pneumonia, arthritis, otitis media and severe, treatment-resistant mastitis in cattle, often spread by introducing carrier cattle; bulk milk PCR is used for herd screening. Contagious agalactia of sheep and goats, mainly caused by Mycoplasma agalactiae, causes mastitis, arthritis and keratoconjunctivitis. In pigs, Mycoplasma hyopneumoniae causes enzootic pneumonia, a chronic dry cough with cranioventral lung consolidation that reduces growth and is assessed by lung scoring at slaughter; vaccination and all-in all-out management are standard. In poultry, Mycoplasma gallisepticum causes chronic respiratory disease in chickens and infectious sinusitis in turkeys, and Mycoplasma synoviae causes synovitis and airsacculitis; both are transmitted through the egg, so breeder flocks are monitored by the rapid serum plate agglutination test, ELISA and PCR, and kept free by eradication programmes.
Rickettsiae in the broad sense are small, Gram-negative, obligate intracellular bacteria, mostly spread by ticks or other arthropods. They cannot be grown on ordinary bacteriological media, so diagnosis rests on stained blood smears, serology and PCR. Giemsa or other Romanowsky stains show them as small inclusions in particular cells. Anaplasma marginale lives in red blood cells, sitting at the margin of the cell, and causes bovine anaplasmosis: fever, progressive anaemia and jaundice without haemoglobinuria, in adult cattle more severely than calves; it is spread by ticks and mechanically by biting flies and contaminated needles. Anaplasma phagocytophilum infects neutrophils and causes tick-borne fever in sheep and cattle and granulocytic anaplasmosis in horses, dogs and people. Ehrlichia canis infects monocytes, forming clusters called morulae, and causes canine monocytic ehrlichiosis, spread by the brown dog tick; acute fever and lymphadenopathy may progress to a chronic phase with pancytopenia and bleeding. Ehrlichia ruminantium causes heartwater in ruminants in Africa and the Caribbean, spread by Amblyomma ticks, with fever, nervous signs and fluid in the pericardium; it is seen in brain capillary endothelium in crush smears. Rickettsia rickettsii causes Rocky Mountain spotted fever in dogs and people in the Americas. Tetracyclines, especially oxytetracycline in ruminants and doxycycline in dogs, are the drugs of choice, and imidocarb is also used for anaplasmosis in some countries, subject to the label and national formulary. Control relies on tick control, careful use of needles, and in some regions live vaccines for anaplasmosis or heartwater.
Coxiella burnetii, once classed as a rickettsia, is now placed separately. It forms a resistant small-cell variant that survives for long periods in dust and is spread by aerosol, which makes it unusually infectious to people. Sheep, goats and cattle are the main reservoirs; infection is often silent, but in sheep and goats it causes late abortion and stillbirths, with enormous numbers of organisms in placentas and birth fluids. Placental smears stained with modified Ziehl-Neelsen show red coccobacilli, as with Brucella and Chlamydia abortus, so PCR and serology are needed to tell them apart. In people Q fever causes flu-like illness, pneumonia, hepatitis and, rarely, chronic endocarditis; outbreaks have followed abortion storms on goat farms. Control includes vaccination of small ruminants in some countries, safe disposal of birth products, and protection of farm and laboratory workers. Chlamydiae are obligate intracellular bacteria with a two-stage life cycle: an infectious, non-replicating elementary body that enters the cell, and a larger reticulate body that multiplies inside a membrane-bound inclusion. They cannot make enough of their own energy and are grown only in cell culture or eggs in reference laboratories, so diagnosis uses stained smears, antigen tests, PCR and serology. Chlamydia abortus causes enzootic abortion of ewes, a major cause of late-term abortion in sheep and goats in many countries: ewes abort in the last two to three weeks of pregnancy or give birth to weak or dead lambs, and the placenta is thickened with necrotic cotyledons and intercotyledonary areas covered in reddish-brown exudate. Infected ewes usually abort only once and become immune. Diagnosis is by modified Ziehl-Neelsen smears of placenta showing red elementary bodies, PCR, and CFT or ELISA. Live and inactivated vaccines are used before mating, and long-acting oxytetracycline may reduce losses in an outbreak. C. abortus can cause severe illness and abortion in pregnant women, who should avoid lambing ewes. Chlamydia psittaci causes psittacosis (avian chlamydiosis) in parrots, pigeons and ducks, with conjunctivitis, respiratory signs and green diarrhoea; birds may carry it silently. It is a notable zoonosis of bird owners and poultry processors, causing atypical pneumonia. Chlamydia felis causes conjunctivitis in cats.
Dermatophytes are fungi that digest keratin and infect hair, skin and nails or claws. The main veterinary genera are Microsporum and Trichophyton. Microsporum canis is the commonest cause of ringworm in cats and dogs; cats, especially long-haired cats, can carry it with few or no lesions. Trichophyton verrucosum causes ringworm in cattle, typically grey, crusty, circular lesions around the eyes, head and neck of housed calves in winter. Trichophyton mentagrophytes is associated with rodents and affects many species; Microsporum gypseum (now Nannizzia gypsea) lives in soil and infects dogs that dig. Lesions are classically circular areas of hair loss with scale and crust, but presentation varies and itching is variable. Diagnosis starts with Wood's lamp examination: about half of M. canis strains make infected hairs fluoresce apple-green, while Trichophyton species do not, so a negative result does not exclude ringworm. Hairs plucked from the edge of lesions are examined in potassium hydroxide or a clearing agent under the microscope for spores (arthroconidia) around the hair shaft. Culture is on Sabouraud dextrose agar or dermatophyte test medium, which turns red as the colony grows; identification is by colony appearance and microscopic macroconidia (spindle-shaped, thick-walled and rough in M. canis; cigar-shaped and thin-walled in Trichophyton species). In cattle, ringworm is often self-limiting over a few months; topical treatment is used, and vaccination with live attenuated T. verrucosum vaccine is used in some countries. In cats, combined topical treatment (such as lime sulphur or enilconazole rinses where licensed) and systemic treatment (itraconazole or terbinafine) plus thorough environmental cleaning are needed, with treatment continued until repeated cultures are negative, subject to the label and national formulary. Ringworm is a common zoonosis, particularly in children and farm workers.
Aspergillus fumigatus is a saprophytic mould found in soil, hay, straw and litter that causes disease when animals inhale large numbers of spores or when defences are weak. In birds, whose air sacs are poorly cleared of inhaled spores, aspergillosis is important: brooder pneumonia in chicks and poults causes gasping and death, and in older birds, raptors, penguins and parrots it causes chronic air sacculitis with yellow plaques. In dogs, especially long-nosed breeds, sino-nasal aspergillosis causes chronic, often unilateral, nasal discharge, nose bleeds, pain and depigmentation of the nostril; treatment is by debridement and topical antifungal infusion. In horses, guttural pouch mycosis can erode the internal carotid artery and cause fatal nosebleeds. In cattle, Aspergillus causes mycotic abortion, with thickened, leathery placenta and ringworm-like plaques on the fetal skin, and mycotic pneumonia. Diagnosis combines imaging or endoscopy, cytology or histopathology showing septate hyphae with acute-angle (about 45 degrees) dichotomous branching, culture on Sabouraud agar (fast-growing blue-green, velvety colonies with conidial heads), and serology. Because Aspergillus is a common contaminant, a culture result must be matched with lesions. Prevention depends on dry, clean litter and bedding and good ventilation. Azole antifungals are used for treatment in dogs and birds, subject to the label and national formulary.
Candida albicans is a yeast that is a normal inhabitant of mucous membranes and gut and causes disease when the normal flora is disturbed, typically after prolonged antimicrobial treatment, or when immunity is low. In poultry it causes crop mycosis (thrush), with white, raised, 'turkish towel' plaques on the crop mucosa. In pigs and foals it causes oral and oesophageal thrush, and in cattle it is an occasional cause of mastitis after contaminated intramammary infusions. In the laboratory Candida appears as Gram-positive, oval budding yeast cells with pseudohyphae; it grows on Sabouraud agar as creamy white colonies, and C. albicans forms germ tubes when incubated in serum for a few hours. Other important mycoses include Cryptococcus neoformans and C. gattii, capsulated yeasts that cause nasal and nervous disease in cats and are shown in nasal discharge or cerebrospinal fluid by India ink staining or by capsular antigen latex agglutination; Malassezia pachydermatis, a peanut-shaped yeast associated with otitis and dermatitis in dogs; and Histoplasma capsulatum var. farciminosum, the cause of epizootic lymphangitis in equids, which must be distinguished from the farcy form of glanders.
Mycotoxins are toxic metabolites produced by moulds growing in crops in the field or in storage. Disease (mycotoxicosis) is not infectious and does not respond to antimicrobials; it is a feed problem diagnosed by history, clinical signs and lesions, and confirmed by analysing feed. Aflatoxins, produced mainly by Aspergillus flavus and A. parasiticus in groundnut, maize, cottonseed and other feeds stored warm and damp, are hepatotoxic and carcinogenic; aflatoxin B1 is the most potent. Young animals, ducklings, turkeys and pigs are most sensitive; signs include poor growth, jaundice, bleeding and immunosuppression, and aflatoxin M1 appears in the milk of cows fed contaminated feed, which is why milk limits exist. Ochratoxin A, from Aspergillus and Penicillium species, causes kidney damage in pigs and poultry. Fusarium species produce zearalenone, an oestrogenic toxin that causes vulvovaginitis, swollen vulvae and rectal or vaginal prolapse in gilts; trichothecenes such as deoxynivalenol (vomitoxin), which causes feed refusal and vomiting in pigs, and T-2 toxin, which causes oral lesions; and fumonisins, which cause equine leucoencephalomalacia and porcine pulmonary oedema. Claviceps purpurea produces ergot alkaloids in grass and cereal seed heads, causing gangrene of the extremities and hyperthermia; Pithomyces chartarum produces sporidesmin, which damages the liver and causes facial eczema (photosensitisation) in sheep and cattle grazing pastures in some regions. Control depends on proper drying and storage of grain, rejecting mouldy feed, feed testing against national regulatory limits (which vary by country and species), dilution of contaminated feed where regulations allow, and the use of mycotoxin binders, whose effectiveness varies by toxin.
A student uses this subject to link each disease to its organism, host, sample and test, the four facts that are tested again and again. The useful habit is to build, for every genus, a short card: Gram reaction and shape, growth on blood and MacConkey agar, catalase and oxidase, the one classic test (CAMP, coagulase, M'Fadyean, Ziehl-Neelsen, MAT, mallein), the diseases in each species, the vaccine, and whether it is zoonotic. With these cards a student can answer most recall questions and work through clinical vignettes in licensing exams. Students should also learn which organisms must not be cultured outside containment laboratories and which carcasses must not be opened.
A practitioner with five years' experience uses this knowledge every week to choose the right sample and avoid wasted laboratory fees: milk taken aseptically for mastitis culture, paired sera and fetal tissue for abortion, brainstem for suspected listeriosis, an ear-vein blood smear rather than a necropsy for suspected anthrax. They interpret culture and susceptibility reports, recognise a contaminant from a pathogen, and know when an isolate (MRSP, Salmonella Dublin, Streptococcus suis) changes advice to the owner. They also carry the public-health duty: notifying anthrax, brucellosis, tuberculosis and glanders, and warning farm families about ringworm, leptospirosis and Q fever.
A senior clinician or diagnostic laboratory head with 25 years' experience designs herd and regional programmes. They decide whether a brucellosis problem calls for vaccination or test and slaughter, plan haemorrhagic septicaemia and anthrax vaccination ahead of the risk season, set up bulk-milk surveillance for Mycoplasma bovis or Streptococcus agalactiae, and manage feed-testing programmes for aflatoxin. In a laboratory they decide which tests to offer, how to validate them, how to report and how to protect staff working with zoonotic agents. They also train younger vets to see the pattern behind sudden deaths, abortion storms and herd-level wasting.
A researcher with 25 years' experience works where the textbook ends: the epidemiology of carrier states (Pasteurella multocida B:2 in buffalo, Burkholderia mallei in horses, Leptospira serovars in maintenance hosts), the performance of diagnostic tests in different populations, the spread of antimicrobial resistance genes such as mecA between animals and people, and the evaluation of vaccines for Johne's disease, brucellosis and bovine tuberculosis that do not interfere with surveillance tests. They advise national authorities and WOAH reference laboratories and interpret the evidence for contested links, such as Mycobacterium avium subsp. paratuberculosis and Crohn's disease.
This manual covers the sixteen syllabus units and the main mycotoxicoses at a clinical and diagnostic level. It does not give drug doses, withdrawal periods or national vaccination schedules, which vary by country and product. It does not cover several genera that some syllabi include in this course: Actinobacillus, Haemophilus and Histophilus, Corynebacterium and Trueperella, Rhodococcus equi, Erysipelothrix, Dermatophilus, Nocardia and Actinomyces, Fusobacterium and Dichelobacter, Campylobacter, Bordetella, Moraxella, Lawsonia and Brachyspira. Detailed taxonomy, molecular typing schemes and research culture methods are deliberately left out. Diagnostic cut-offs for tuberculin, Brucella and Leptospira tests are set by national programmes and are not given here.
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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