Veterinary · Para-clinical · also MSVE VPA-222
Blood and gut protozoa of domestic animals, including trypanosomes, Babesia, Theileria and coccidia, with Anaplasma taught alongside, and their diagnosis and treatment.
In the exams: ICAR AICE-JRF core group 06; ICAR AIEEA-PG 13 (Parasitology)
Veterinary protozoology is the study of the single-celled eukaryotic parasites of animals, together with a few rickettsial blood organisms, chiefly Anaplasma, that are traditionally taught alongside them because they share vectors, signs and diagnostic methods. Protozoa multiply inside their host, so a single infection can become a massive one within days. That is why protozoal disease tends to be acute and explosive.
The subject divides naturally into blood and tissue protozoa that are carried by vectors (trypanosomes, Babesia, Theileria, Leishmania, and Anaplasma alongside them) and gut and genital protozoa that spread through the environment or by contact (Eimeria, Cystoisospora, Toxoplasma, Neospora, Cryptosporidium, Giardia, the trichomonads and Histomonas). For each organism the manual gives host, site, vector or route, life cycle, pathogenesis, signs, diagnosis, treatment by drug class and control; the last two chapters gather the laboratory methods and the drugs.
Protozoology is examined everywhere. Indian postgraduate and research entrance papers (ICAR AIEEA-PG, AICE-JRF/SRF, ASRB) repeatedly ask for vectors, stages, morphology in smears and the drug of choice. Licensing examinations in North America, the UK, Australia, South Africa and Kenya ask clinical questions: a haemolytic cow, an aborting ewe flock, a cat with Tritrichomonas diarrhoea.
Practice differs by country. Which parasites occur depends on the vectors present; which drugs may be used depends on national licensing, and several antiprotozoals (the nitroimidazoles, for example) are banned in food animals in many jurisdictions. Every dose given here must be checked against the product label and national formulary.
Trypanosomes are flagellate protozoa of the order Kinetoplastida. Each cell has one nucleus, a flagellum running along an undulating membrane (sometimes continuing free), and a kinetoplast of mitochondrial DNA near the flagellar base. In the trypomastigote, the blood form, the kinetoplast lies behind the nucleus; the amastigote is a rounded intracellular form with no free flagellum.
The mammalian trypanosomes are divided by where they develop in the vector. In the Stercoraria the infective stage forms in the hindgut of the insect and is passed in its faeces, so infection is by contamination of a wound or mucosa. This group includes T. cruzi (Chagas disease, triatomine bugs) and the large, non-pathogenic T. theileri of cattle. In the Salivaria the infective stage forms in the mouthparts or salivary glands and is inoculated when the vector feeds. This group contains the pathogenic African trypanosomes: T. congolense, T. vivax and T. brucei, which cause nagana and develop cyclically in tsetse flies (Glossina), and two species that have escaped the tsetse: T. evansi and T. equiperdum.
T. evansi is a slender monomorphic trypanosome with a well-developed undulating membrane, a free flagellum and a small subterminal kinetoplast. T. brucei looks the same but is polymorphic, with long slender and short stumpy forms. T. congolense is small, lacks a free flagellum and has a marginal kinetoplast. T. vivax moves very rapidly across a wet film and has a large terminal kinetoplast and a free flagellum.
Surra is the disease caused by Trypanosoma evansi. It is the most widely distributed pathogenic trypanosome, from North Africa and Asia to Latin America. It is transmitted mechanically: biting flies such as Tabanus, Haematopota and Stomoxys carry blood on their mouthparts from one animal to the next when their feeding is interrupted. No development takes place in the fly. In Latin America vampire bats also transmit it, and carnivores can be infected by eating infected meat. Having lost part or all of its kinetoplast DNA, it cannot develop in tsetse.
Camels, horses and dogs usually suffer severe disease. Cattle and buffalo in India and South-East Asia are often infected subclinically, but they carry the parasite and may abort or show disease under stress. The pathogenesis is driven by waves of parasitaemia. Each wave is cleared by antibody against the dominant variant surface glycoprotein, and a new variant then multiplies; this antigenic variation is why the fever is intermittent, why infection becomes chronic and why no vaccine exists. Anaemia, largely from removal of red cells by an expanded mononuclear phagocyte system, is the central lesion.
Clinically there is intermittent fever, progressive anaemia, loss of condition, oedema of the lower limbs, brisket and ventral abdomen, and petechiae on the mucous membranes. Horses may show nervous signs. In camels the disease is chronic and wasting, with abortion. Dogs may develop corneal opacity. Surra is a WOAH-listed disease.
Nagana is the African tsetse-transmitted trypanosomosis of cattle and other livestock, caused mainly by T. congolense and T. vivax, with T. brucei also involved. It is one of the main constraints on cattle keeping in sub-Saharan Africa. West African taurine breeds such as the N'Dama are trypanotolerant. T. vivax is also transmitted mechanically, which is how it spread to South America outside the tsetse belt. T. brucei rhodesiense, which causes human sleeping sickness, has animal reservoirs.
Dourine, caused by T. equiperdum, is the only trypanosomosis transmitted venereally, during coitus. Genital oedema is followed by raised skin plaques and then paralysis. The parasite is rarely found in blood, so diagnosis relies on serology, classically the complement fixation test. It is WOAH-listed, and control is by test-and-slaughter and movement control rather than treatment.
T. cruzi infects dogs in the Americas and causes an acute myocarditis in young dogs and a chronic dilated cardiomyopathy in older ones. Its amastigotes multiply inside heart muscle cells.
Parasitaemia fluctuates, so a single negative film does not rule out infection. In increasing sensitivity, the methods are the wet film, thin and thick Giemsa-stained films, and concentration by microhaematocrit centrifugation or the dark-ground buffy coat method (Chapter 11). Antibody tests (ELISA, card agglutination for T. evansi) show exposure; PCR shows current infection and species.
Trypanocidal drugs are few and old, and resistance to them is widespread. Diminazene aceturate (an aromatic diamidine) is therapeutic; in cattle 3.5 mg/kg by deep intramuscular injection is the standard dose for T. congolense and T. vivax, with higher doses used against resistant strains and T. evansi — confirm against the product label and your national formulary. Camels and horses tolerate diminazene poorly. Isometamidium chloride and homidium are phenanthridinium compounds; isometamidium binds in tissues and gives several months of prophylaxis. Quinapyramine (as the sulphate for treatment and a sulphate-chloride salt for prophylaxis), suramin and the arsenical melarsomine are used against T. evansi in camels and horses. Diminazene and isometamidium have been used as a 'sanative pair': when resistance to one appears, the herd is switched to the other, because cross-resistance between them is usually limited.
Control combines drugs with vector control: insecticide-treated cattle, traps and targets for tsetse, and reduction of fly contact for surra.
Babesia and Theileria are the piroplasms: tick-transmitted protozoa of the phylum Apicomplexa that live in red blood cells, where they appear as pear-shaped (piriform), round or rod-shaped bodies. In Babesia the sporozoites injected by the tick enter red cells directly. There it divides by binary fission into two (sometimes four) merozoites, which infect new red cells. There is no stage in lymphocytes, which separates Babesia from Theileria.
When a tick feeds on an infected animal, some parasites in the ingested blood become gametes (the ray bodies or Strahlenkörper), fuse, and form a motile kinete that invades the tick's tissues, including the ovary. Transmission therefore passes through the egg to the next generation of ticks (transovarial transmission), and the parasite also persists from one tick stage to the next (trans-stadial transmission). Final development (sporogony) happens in the salivary glands when the next stage starts to feed.
The important species are host-specific. Cattle: B. bigemina and B. bovis, carried in the tropics and subtropics by one-host Rhipicephalus (Boophilus) ticks, especially R. microplus and R. annulatus; B. divergens in northern Europe, carried by Ixodes ricinus; and B. major. Horses: B. caballi (and Theileria equi, see next chapter). Dogs: B. canis (Dermacentor reticulatus, Europe), B. vogeli (Rhipicephalus sanguineus, worldwide), B. rossi (Haemaphysalis elliptica, southern Africa, the most virulent) and the small B. gibsoni. Sheep and goats: B. ovis and B. motasi.
The size of the parasite relative to the red cell is the first clue. Large babesias are longer than the radius of the red cell; small ones are shorter. B. bigemina is a large babesia, typically seen as paired pear-shaped bodies joined at their pointed ends at an acute angle, and parasitaemias can be high in peripheral blood. B. bovis is small, with pairs lying at an obtuse angle, and it is usually scanty in jugular blood because infected cells are sequestered in capillaries; a smear from capillary blood of the ear tip or tail tip is more likely to show it. B. divergens is small and often lies near the edge of the red cell. In the dog, B. canis, B. vogeli and B. rossi are large; B. gibsoni is small.
At necropsy, a crush smear of cerebral cortex is the classic way to confirm B. bovis: the brain capillaries are packed with infected red cells, and the grey matter looks cherry-pink.
B. bigemina causes disease mainly by haemolysis. Red cells are destroyed inside blood vessels as parasites leave them, so haemoglobin is released into plasma and passed in urine. The classic signs are high fever, haemoglobinuria ('redwater'), pale then jaundiced membranes and a falling packed cell volume. B. bovis is the more virulent species. Besides haemolysis, it causes hypotension and shock, and infected red cells stick to capillary walls in the brain and other organs. This produces cerebral babesiosis: incoordination, aggression, convulsions and coma.
Age matters. Calves under about six to nine months are relatively resistant, partly through colostral antibody and partly through an innate resistance of young animals. If calves are infected during this window they develop immunity without severe disease. Where ticks are abundant enough for every calf to be infected early, clinical cases are rare: this is endemic stability. Outbreaks occur when the balance breaks: naive adults brought into a tick area, or tick challenge falling (drought, intensive dipping) so calves escape infection and meet it later as adults.
In dogs, B. rossi can cause severe haemolysis with kidney injury and cerebral signs. B. gibsoni is also transmitted by blood contact, including bites during fighting, which is why it is more common in fighting breeds.
Two drugs dominate treatment in cattle. Diminazene aceturate at 3.5 mg/kg by deep intramuscular injection is effective against B. bigemina and B. bovis — confirm against the product label and your national formulary; its use is not permitted in some countries, including the USA and EU member states. Imidocarb dipropionate, a carbanilide, is used at 1.2 mg/kg by subcutaneous injection for treatment in cattle, and at a higher dose (3 mg/kg) it gives several weeks of chemoprophylaxis — confirm against the product label and your national formulary. Imidocarb has anticholinesterase side effects (treated with atropine) and long tissue residues. Trypan blue, an old drug, is active against B. bigemina but not B. bovis. In dogs, imidocarb at 6.6 mg/kg by intramuscular or subcutaneous injection, repeated after two weeks, is a standard regimen for large babesias — confirm against the product label and your national formulary; B. gibsoni responds poorly to it and is usually treated with a combination of a hydroxynaphthoquinone (atovaquone) and a macrolide (azithromycin).
Severe cases also need blood transfusion, fluids and rest. Control relies on tick control, on managing for endemic stability rather than trying to eradicate ticks where that is impossible, and on vaccination. Live attenuated blood-derived vaccines against B. bovis and B. bigemina (often combined with Anaplasma centrale) are used in Australia, southern Africa, Israel and parts of Latin America. They are best given to young calves.
Theileria species are piroplasms transmitted by hard ticks. Their defining feature is a stage in white blood cells. Sporozoites inoculated by the tick enter lymphocytes or macrophages and grow into multinucleate schizonts, the Koch's blue bodies seen in Giemsa-stained smears of lymph node aspirates. The schizont of the pathogenic species transforms its host cell, which begins to divide without control. The parasite divides with it, so each daughter cell carries a schizont: a clonal expansion of infected cells that spread through lymphoid tissue and into organs. Merozoites from schizonts then invade red cells as small piroplasms: rods, commas and rings.
Ticks acquire infection by feeding on an animal with piroplasms. Development proceeds in the tick gut and then the salivary glands, and the parasite is passed only from one tick stage to the next (trans-stadial transmission). It is not passed through the egg, unlike Babesia. A larva or nymph that feeds on an infected animal therefore transmits as the next stage, the nymph or adult. Sporozoites mature only after the tick starts to feed, so transmission takes a few days of attachment.
Theileria parva causes East Coast fever in eastern, central and southern Africa. It is carried by the three-host tick Rhipicephalus appendiculatus. Schizonts are abundant in lymphoid tissue, piroplasms are relatively few, and death is caused mainly by lymphoid destruction and terminal pulmonary oedema; mortality in susceptible cattle is very high. African buffalo carry a form of T. parva that causes Corridor disease when transmitted from buffalo to cattle.
Theileria annulata causes tropical (Mediterranean) theileriosis in North Africa, southern Europe, the Middle East, India and China. Its vectors are Hyalomma ticks, notably H. anatolicum in India. Schizonts develop in macrophages and B lymphocytes, and, in contrast to T. parva, piroplasms are numerous and anaemia is marked. Exotic and crossbred dairy cattle in India are far more susceptible than indigenous zebu cattle.
Theileria orientalis group (including the Ikeda genotype) is carried by Haemaphysalis ticks, especially H. longicornis. It was long considered benign, but the Ikeda genotype causes anaemia and deaths in cattle in Australia, New Zealand, Japan and Korea; the schizont stage is inconspicuous and disease is mainly anaemic. Theileria lestoquardi causes malignant theileriosis of sheep and goats, carried by Hyalomma. Theileria equi (formerly Babesia equi) infects horses; it has a brief lymphocytic stage and forms the Maltese cross in red cells. Together with Babesia caballi it causes equine piroplasmosis, a WOAH-listed disease that restricts the international movement of horses.
Theileriosis begins with enlargement of the lymph node draining the tick bite, usually the parotid or prescapular node, followed by generalised lymphadenopathy, high fever, loss of appetite, drop in milk yield and weakness. In T. annulata infection anaemia and jaundice follow; haemoglobinuria is not typical. Terminal signs include dyspnoea and froth at the nostrils from pulmonary oedema, diarrhoea, corneal opacity and petechiae.
Diagnosis in the field is by a Giemsa-stained smear of a lymph node aspirate, which shows schizonts in lymphoblasts, and a thin blood smear, which shows piroplasms. PCR and serology detect carriers.
Buparvaquone, a hydroxynaphthoquinone, is the drug of choice for clinical theileriosis; 2.5 mg/kg by intramuscular injection in cattle is the standard dose, repeated once after 48–72 hours if needed — confirm against the product label and your national formulary. It works best early. Tetracyclines suppress schizonts if given at infection but do not cure established disease.
Control rests on two things. First, tick control by acaricides, housing and pasture management; for T. annulata, keeping stall-fed dairy cattle free of Hyalomma, which live in cracks in cattle sheds, is effective. Second, vaccination: cell-culture vaccines made from T. annulata schizont-infected cells attenuated by long passage are used in India, the Middle East and North Africa; for T. parva, the infection-and-treatment method inoculates live sporozoites and simultaneously treats with long-acting oxytetracycline, leaving the animal immune but often a carrier.
Anaplasma is not a protozoon. It is an obligate intracellular Gram-negative bacterium of the order Rickettsiales, family Anaplasmataceae, related to Ehrlichia. It is taught with the piroplasms because it shares their vectors, signs and stained blood films.
Anaplasma marginale is the important species in cattle. In a Giemsa-stained film it appears as a dense, dark, round inclusion about 0.3–1.0 micrometres across, usually at the edge of the red cell, with no cytoplasm around it; this is how it was named. A. centrale lies more centrally and causes mild disease; it is used as a live vaccine. A. ovis infects sheep and goats, usually mildly. A. phagocytophilum lives in neutrophils and causes tick-borne fever in sheep and cattle in Europe (carried by Ixodes ricinus) and granulocytic anaplasmosis in horses, dogs and people; A. platys infects platelets of dogs and causes cyclic thrombocytopenia.
A. marginale is transmitted biologically by ticks, including Dermacentor species in North America and Rhipicephalus species in the tropics, and mechanically by biting flies and by people: blood on needles, dehorning equipment, castration and ear-tagging instruments carries it from animal to animal. It can also cross the placenta. Recovered cattle remain carriers for life, which keeps infection in a herd.
Infected red cells are coated with antibody and removed by macrophages in the spleen and liver. The haemolysis is extravascular, so haemoglobin is broken down to bilirubin inside macrophages rather than released into plasma. The result is anaemia and jaundice without haemoglobinuria: this is the clinical point that separates anaplasmosis from babesiosis. Severity rises with age. Calves under about one year usually have mild infections, cattle one to two years old have moderate disease, and cattle over two years may die. Signs are fever, pale then yellow membranes, weakness, weight loss, milk drop, constipation, abortion and, from brain hypoxia, aggression.
Diagnosis in acute cases is by a thin blood film stained with Giemsa or a rapid Romanowsky stain, showing marginal inclusions in a large proportion of red cells, together with a low packed cell volume and a regenerative response. Two artefacts cause errors: stain precipitate, and Howell-Jolly bodies, which are nuclear remnants in red cells and are usually single, smooth and seen in regenerative anaemias. In carriers the organisms are too few to see, so a competitive ELISA based on the major surface protein 5, card agglutination tests or PCR are used for herd testing and export.
Tetracyclines are the drugs of choice. Oxytetracycline at 10 mg/kg once daily for three to five days, by intravenous or intramuscular injection, or a long-acting formulation at 20 mg/kg intramuscularly, are standard regimens in cattle — confirm against the product label and your national formulary. Imidocarb is also active against Anaplasma. Treatment may not clear infection. In-feed chlortetracycline for control is legal only in some countries. Severely anaemic cattle must be moved as little as possible.
Control combines tick and fly control, hygiene of needles and instruments (a fresh needle per animal during herd procedures), testing and segregation or treatment of carriers where the disease is not endemic, and vaccination. Live A. centrale vaccine, often combined with Babesia vaccines, is used in Australia, South Africa, Israel and parts of Latin America.
Coccidia of the family Eimeriidae are intracellular parasites of the intestinal epithelium, with a direct life cycle in one host. The oocyst passed in faeces is unsporulated. It sporulates in the environment given oxygen, moisture and warmth. In Eimeria the sporulated oocyst contains four sporocysts, each with two sporozoites (eight in all). In Cystoisospora (Isospora of mammals) it contains two sporocysts, each with four sporozoites. After ingestion, sporozoites excyst and enter gut cells, where they undergo two or more generations of asexual multiplication (merogony, also called schizogony), each producing many merozoites. Merozoites of the last generation form male and female gametes (gametogony); fertilisation produces the zygote, which becomes a new oocyst. The cycle is self-limiting: each species has a fixed number of merogonic generations, after which infection ends unless the animal ingests more oocysts.
Coccidia are strictly host-specific and each species usually lives in a particular part of the intestine. Damage depends on the dose of oocysts, the species, the depth of the developing stages and immunity; disease follows crowding, wet litter and stress in young animals.
Seven Eimeria species infect the chicken. E. tenella lives in the caeca; its large second-generation meronts develop deep in the mucosa, and when they rupture there is severe haemorrhage, bloody droppings and caeca distended with blood and later with cores of clotted blood and debris. E. necatrix develops its meronts in the middle of the small intestine, causing ballooning, white spots and red petechiae visible through the serosa ('salt and pepper'), and it is the most pathogenic species, affecting older birds; its oocysts are produced in the caeca. E. acervulina causes white, transverse, ladder-like lesions in the duodenum. E. maxima affects the middle small intestine, with thickened wall and orange mucus, and has the largest oocysts. E. brunetti affects the lower small intestine and rectum. Subclinical coccidiosis costs broiler producers more than outbreaks and predisposes to necrotic enteritis.
At necropsy the Johnson and Reid method scores gross lesions from 0 (none) to 4 (most severe) for each intestinal region, and the average score of a sample of birds is used to judge a flock and the efficacy of an anticoccidial programme.
In cattle, E. zuernii and E. bovis are the most pathogenic species. Their later stages develop in the caecum and colon, causing diarrhoea with blood and mucus, tenesmus, and dehydration, mostly in calves from about three weeks to a year old. Some calves with E. zuernii infection develop nervous signs (nervous coccidiosis), especially in winter. In sheep, E. ovinoidalis and E. crandallis cause disease in lambs, typically a few weeks after turnout or in crowded lambing sheds; in goats, E. ninakohlyakimovae and E. arloingi. Many other ovine and caprine species are of low pathogenicity.
Rabbits suffer hepatic coccidiosis from E. stiedae, which develops in the bile duct epithelium and produces white nodules in an enlarged liver, and intestinal coccidiosis from several species. In pigs, Cystoisospora suis causes a pasty to watery diarrhoea in piglets, typically at about one to two weeks of age; because it appears before most oocysts are shed, diagnosis often needs histology of the small intestine. Dogs and cats carry Cystoisospora species that cause diarrhoea in young animals.
Oocysts are found by faecal flotation and counted by the McMaster method as oocysts per gram (OPG). Interpretation needs care: healthy young animals often have high counts, much output may come from non-pathogenic species, and damage can precede shedding, so a low count does not rule out disease. Speciation (after sporulation) and post-mortem lesions and scrapings are often needed.
Anticoccidial drugs are either coccidiostatic (they arrest development) or coccidiocidal (they kill stages). The ionophores (monensin, salinomycin, narasin and maduramicin, which carry monovalent ions, and lasalocid, which carries divalent ions) disrupt ion balance in sporozoites and merozoites. They are toxic to horses, and monensin, narasin and salinomycin must not be given to birds or pigs receiving tiamulin, which interacts dangerously with them. Chemical (synthetic) anticoccidials include amprolium, a thiamine analogue; decoquinate and clopidol, which inhibit mitochondrial respiration; nicarbazin, which can reduce heat tolerance in broilers; robenidine; halofuginone; and the triazines toltrazuril and diclazuril, which act on all intracellular stages. Sulfonamides, alone or potentiated, act on meronts and are used in outbreaks. In piglets, toltrazuril at 20 mg/kg by mouth once at three to five days of age is a standard preventive dose for Cystoisospora suis — confirm against the product label and your national formulary.
Resistance develops readily, so broiler producers use shuttle programmes (different drugs in starter and grower feed) and rotation programmes (changing drugs between flocks). Live vaccines, made from wild-type or attenuated precocious lines of each Eimeria species, are given in the first days of life to breeders and layers, and increasingly to broilers; they are not used with in-feed anticoccidials that would kill the vaccine strains. Dry litter, clean raised feeders and avoiding overcrowding reduce challenge.
Toxoplasma gondii is a coccidian with a two-host (heteroxenous) life cycle. Cats and other felids are the only definitive hosts; almost any warm-blooded animal, including people, can be an intermediate host. In the cat's intestine the parasite goes through merogony and gametogony and produces oocysts. A cat that eats tissue cysts usually sheds unsporulated oocysts for one to two weeks, starting a few days after infection; most cats shed only once, and immune cats rarely shed again. The oocysts sporulate in the environment in one to five days, contain two sporocysts each with four sporozoites, and survive for months.
In intermediate hosts there are two asexual stages. Tachyzoites multiply rapidly in many cell types during acute infection and cause the tissue damage. As immunity develops, the parasite converts to bradyzoites, which multiply slowly within tissue cysts, mainly in the brain and muscles, and persist for the life of the host. There are three routes of infection: eating tissue cysts in meat (carnivorism), ingesting sporulated oocysts in food, water or soil, and transplacental transmission of tachyzoites when a female is infected for the first time during pregnancy.
Toxoplasmosis is a major cause of abortion in sheep and goats worldwide. A ewe infected for the first time in pregnancy passes tachyzoites to the placenta and foetus. Early infection causes foetal death and resorption, which appears as barrenness; mid-gestation infection causes abortion, mummified foetuses, or stillbirths; late infection may produce weak or healthy, infected lambs. The placental cotyledons show characteristic small white foci of necrosis, and the foetal brain shows focal leucomalacia and gliosis. Infected ewes are immune in later pregnancies, so abortions hit young ewes and newly exposed flocks, often via cat faeces in stored feed.
Cats usually show no signs. When disease occurs, it often involves the lungs, liver, eyes (uveitis) and nervous system, especially in kittens and immunosuppressed cats. In people, infection is common and usually mild, but a first infection in pregnancy can cause congenital disease, and immunocompromised patients can develop encephalitis. Undercooked pork and lamb and contaminated food and water are the main sources. Owners are advised to empty litter trays daily, before oocysts sporulate.
In ovine abortion, diagnosis rests on the placenta and foetus: gross cotyledon lesions, histopathology of brain and placenta, immunohistochemistry and PCR, supported by antibody in foetal fluids. Serology of the flock (latex agglutination, ELISA, IFAT, modified agglutination test) shows exposure. The Sabin-Feldman dye test is the historical reference serological test. Toxoplasma oocysts in cat faeces cannot be told apart by light microscopy from those of the non-pathogenic Hammondia hammondi and Besnoitia.
Cats with clinical toxoplasmosis are treated with clindamycin, a lincosamide; about 10–12.5 mg/kg by mouth every 12 hours for about four weeks is widely cited — confirm against the product label and your national formulary. Potentiated sulfonamides are an alternative. In sheep flocks, a live vaccine based on an incomplete strain of tachyzoites that does not form tissue cysts is given before mating (not to pregnant ewes), and gives lasting protection; it is a live organism, so handlers must avoid self-injection. In-feed decoquinate or monensin during pregnancy can reduce losses where permitted. Keeping cats out of feed stores cuts exposure.
Neospora caninum resembles Toxoplasma but its definitive hosts are dogs and some wild canids, and it is one of the most frequently diagnosed causes of bovine abortion worldwide. Cattle are infected horizontally, by eating oocysts shed by dogs, or vertically, by highly efficient transplacental transmission, so a persistently infected heifer can pass infection to calf after calf. Vertical transmission is why infection persists in herds even without dogs. Abortion is most common in mid-gestation, around five to six months. The foetal brain shows non-suppurative encephalitis with focal necrosis, and there may be myocarditis. Diagnosis combines foetal histopathology, immunohistochemistry or PCR, and serology of the dam (a seropositive dam supports but does not prove the cause). There is no licensed effective vaccine or treatment for cattle; control is by keeping dogs away from calving areas, feed and water, disposing of placentas and foetuses, and not keeping replacement heifers from seropositive dams. In puppies, Neospora causes an ascending paralysis with rigid extension of the hind limbs.
Sarcocystis species cycle between carnivore definitive hosts and herbivore intermediate hosts, which carry muscle cysts. Sarcocystis neurona, with the opossum as definitive host in the Americas, causes equine protozoal myeloencephalitis (EPM), a neurological disease of horses with asymmetric ataxia and muscle wasting, treated with triazines (ponazuril, diclazuril) or pyrimethamine with a sulfonamide.
Cryptosporidium is an apicomplexan now placed apart from the true coccidia. It lives on the surface of intestinal epithelial cells, inside a parasitophorous vacuole formed from the host cell membrane: intracellular but extracytoplasmic. Its oocysts are very small, about 4–6 micrometres, and contain four naked sporozoites with no sporocysts. They sporulate inside the host, so oocysts are infective as soon as they are passed. Some oocysts are thin-walled and release sporozoites within the same host, causing autoinfection; the thick-walled oocysts pass out in faeces. The infectious dose is small, and oocysts are resistant to chlorine at concentrations used in drinking water treatment, which is why cryptosporidiosis causes waterborne outbreaks in people.
Several species matter in animals. C. parvum infects the small intestine of young calves, lambs, kids and other mammals, and is the main zoonotic species from livestock. C. andersoni lives in the abomasum of older cattle and reduces milk yield and weight gain. C. bovis and C. ryanae are common in older calves and are of low pathogenicity. C. baileyi infects the respiratory tract and bursa of chickens, and C. meleagridis infects turkeys and people. C. hominis is mainly a human species.
Neonatal calves are affected mostly between about one and three weeks of age. C. parvum destroys and shortens the villi of the lower small intestine, causing malabsorption and a secretory component, with watery yellow diarrhoea, dehydration, depression and loss of appetite. Mortality is usually low unless there are other pathogens (rotavirus, coronavirus, enterotoxigenic E. coli) or poor colostrum intake. Diarrhoea resolves in one to two weeks, but shedding contaminates pens for later calves. In immunocompetent people infection causes self-limiting diarrhoea; it is a recognised occupational risk for farm workers, veterinary students and children on farm visits, and can be severe in immunocompromised people.
Because oocysts are tiny, they are easily missed in routine flotation. A faecal smear stained with a modified Ziehl-Neelsen (acid-fast) method shows them as pink-red round bodies against a blue or green background. Immunofluorescence, antigen ELISA and lateral-flow tests are also used; PCR identifies species and subtype.
No drug eliminates Cryptosporidium. Halofuginone lactate, given by mouth to calves at 0.1 mg/kg (100 micrograms/kg) once daily for seven consecutive days, reduces oocyst shedding and the severity of diarrhoea when started within the first days of life or within 24 hours of the onset of diarrhoea — confirm against the product label and your national formulary. It has a narrow safety margin: toxic effects appear at about twice the recommended dose, and it must not be given to calves that are already dehydrated or weak, or on an empty stomach. Paromomycin, an aminoglycoside, is licensed for calves in some countries. The most important treatment is supportive: oral electrolyte solutions to correct dehydration and acidosis, intravenous fluids for calves that cannot stand or suck, and continuing to feed milk so the calf does not lose weight.
Control is by good colostrum management, hygiene of calving areas and calf pens (removing organic matter and using disinfectants proven against oocysts, which ordinary disinfectants are not), all-in/all-out pens, and individual housing for the first weeks. Staff handling scouring calves should wash their hands.
Giardia duodenalis (also called G. intestinalis or G. lamblia) is a flagellate that lives on the surface of the small intestine. The trophozoite is pear-shaped and bilaterally symmetrical, about 12–15 micrometres long, with two nuclei, four pairs of flagella, a ventral adhesive (sucking) disc by which it attaches to the villi, and median bodies; in a stained film it looks like a face with two eyes. The cyst is oval, about 8–12 micrometres, with a thick wall and four nuclei. Cysts are passed in faeces, are immediately infective, and survive for weeks in cool, moist conditions and in water. Transmission is faecal-oral.
G. duodenalis is divided into genetic assemblages. Assemblages A and B infect people and many animals and are the zoonotic ones. Assemblages C and D are adapted to dogs, E to hoofed livestock, and F to cats. Most dog and cat isolates are host-adapted, so the zoonotic risk from pets is real but modest.
Most infections are subclinical, especially in adult animals. Clinical giardiasis is seen in puppies, kittens, young calves and animals in kennels, shelters and breeding catteries. Trophozoites damage the brush border and shorten the villi, causing malabsorption and maldigestion. Diarrhoea is typically small-intestinal: pale, soft, bulky, malodorous and sometimes fatty (steatorrhoea), with weight loss or poor growth despite a good appetite.
Cysts are shed intermittently, so a single negative sample does not rule out infection; testing three samples over three to five days is recommended. The standard method is centrifugal flotation with zinc sulphate solution (specific gravity about 1.18), which floats the cysts without distorting them as much as saturated sugar or salt solutions do. A direct saline smear of fresh, still-warm faeces may show motile trophozoites moving with a characteristic 'falling leaf' motion; iodine stains cysts and trophozoites. Faecal antigen ELISAs, including rapid in-clinic tests, and direct immunofluorescence are sensitive; PCR identifies assemblages. Tests stay positive for a while after successful treatment, so testing healthy animals after treatment is of limited value.
The two drug classes used in dogs and cats are benzimidazoles and nitroimidazoles. Fenbendazole at 50 mg/kg by mouth once daily for three to five days is a standard regimen in dogs — confirm against the product label and your national formulary. Metronidazole is effective but can cause neurological signs at high doses, and nitroimidazoles are prohibited in food-producing animals in many countries. A combination of febantel, pyrantel and praziquantel is licensed for Giardia in dogs in some countries. Albendazole is effective but is teratogenic and can cause bone marrow suppression, so it is avoided.
Treatment alone often fails because animals re-infect themselves from cysts in the coat and environment. Effective control combines treatment with bathing the animal (particularly the perineum) at the end of treatment to remove cysts, cleaning and drying kennels and runs, removing faeces promptly, and treating in-contact animals that are positive. Guidelines such as those of ESCCAP advise treating animals with clinical signs and a positive test, not routinely treating healthy animals with a positive result.
Trichomonads are flagellates with an undulating membrane and an axostyle, a rigid rod running through the cell. They multiply by binary fission and have no cyst stage, so transmission is direct. Tritrichomonas foetus is pear-shaped, about 10–25 micrometres long, with three anterior flagella and a fourth running back along the undulating membrane and continuing as a free posterior flagellum.
Bovine trichomonosis is a venereal disease transmitted at natural service. In the bull, T. foetus lives on the surface of the penile and preputial mucosa. Bulls show no signs. Older bulls, above about three to four years, have deeper epithelial crypts and tend to remain permanently infected, whereas young bulls may clear infection. In the cow the parasite colonises the vagina, cervix and uterus after mating. It causes early embryonic death with irregular returns to service, low pregnancy rates, a prolonged calving season, occasional abortion in the first half of pregnancy and pyometra. Cows usually clear infection after several months and develop temporary immunity.
Diagnosis is by collecting smegma from the preputial cavity of bulls and examining it directly and after culture in a selective medium, including self-contained pouch culture systems; PCR on the sample increases sensitivity and confirms the species (other, harmless trichomonads can contaminate samples). Because one test misses some infected bulls, a bull is usually declared negative only after several consecutive negative tests, often three at weekly intervals. It is WOAH-listed. There is no approved treatment for cattle: nitroimidazoles are prohibited in food animals in many countries. Control is by artificial insemination, using young virgin bulls, testing and culling infected bulls, and, in some countries, a killed whole-cell vaccine for cows.
A genotype of Tritrichomonas foetus, now sometimes named T. blagburni, causes chronic large-bowel diarrhoea in young cats, especially in breeding catteries and shelters. The faeces are semi-formed with mucus and sometimes fresh blood, the anus may be inflamed, and the cat is otherwise usually well. Diagnosis is by direct smear of fresh faeces, culture and PCR. In a wet smear T. foetus moves in a jerky, forward direction with a visible undulating membrane, unlike the falling-leaf motion of Giardia, with which it is often confused. Ronidazole, a nitroimidazole, is the drug used most often; about 30 mg/kg by mouth once daily for 14 days is the widely cited regimen — confirm against the product label and your national formulary. Ronidazole can cause neurotoxicity and must be handled with care because it is a potential carcinogen.
Trichomonas gallinae has four anterior flagella and infects the upper digestive tract of pigeons, doves, raptors and finches. Adult pigeons are carriers and infect squabs through crop milk; raptors are infected by eating pigeons. Disease, called canker in pigeons and frounce in raptors, presents as yellow caseous (cheesy) masses in the mouth, pharynx and crop, causing difficulty in swallowing and weight loss. A wet smear of the lesion confirms it.
Histomonas meleagridis causes histomonosis (blackhead, infectious enterohepatitis) of turkeys and, less severely, chickens. It is related to the trichomonads. In the caecal lumen it has a single flagellum; in the tissues it is amoeboid, without a flagellum. Its classic route of transmission is inside the eggs of the caecal nematode Heterakis gallinarum: the protozoon enters the worm's ovary and is carried in its eggs, which can survive in soil for years. Earthworms eat the eggs and act as paratenic (transport) hosts, so birds on range pick up infection from soil and earthworms. In turkey flocks, Histomonas also spreads directly from bird to bird through the cloaca ('cloacal drinking'), which explains the rapid spread through a house once disease starts.
The parasite invades the caecal wall, causing thickening and ulceration and the formation of firm yellow cores in the caeca. It then reaches the liver by the portal vein, producing the characteristic lesions: circular, depressed, yellow-green to grey necrotic foci, often with concentric rings like a target. Turkeys show dullness, drooping wings, and sulphur-yellow droppings, and mortality in a flock can approach 100%. Chickens usually have milder disease and act as reservoirs.
Diagnosis is by the gross lesions at necropsy, confirmed by histopathology showing the organisms in tissue, and by PCR. Treatment is the major problem: the nitroimidazoles and nitarsone that once controlled histomonosis have been withdrawn or banned for food-producing birds in the EU and USA, and no effective licensed replacement exists there. Control therefore relies on prevention: separating turkeys from chickens, controlling Heterakis with anthelmintics, avoiding contaminated range, biosecurity, and preventing spread within a house.
Leishmania are kinetoplastid flagellates with two stages. In the vertebrate host they are amastigotes: oval organisms about 2–4 micrometres long, without a free flagellum, living inside macrophages. In a Giemsa-stained smear each shows a nucleus and a small rod-shaped kinetoplast; these are the Leishman-Donovan bodies. In the vector they are elongated, flagellated promastigotes. The vectors are female phlebotomine sand flies: Phlebotomus in the Old World and Lutzomyia in the Americas. The fly ingests infected macrophages while feeding, the parasites develop into infective promastigotes in its gut, and they are inoculated at the next blood meal. Transplacental and transfusion transmission explain cases where there are no sand flies.
Leishmania infantum (known as L. chagasi in the Americas) causes canine leishmaniosis around the Mediterranean, in the Middle East, Central Asia, China and Latin America. The dog is the main reservoir of human visceral leishmaniasis caused by this species, which makes canine leishmaniosis a One Health problem. By contrast, human kala-azar in the Indian subcontinent and East Africa is caused mainly by L. donovani, which is largely anthroponotic (human to human through sand flies), and dogs are not considered its main reservoir.
Many dogs in endemic areas are infected but remain healthy for long periods; whether a dog becomes ill depends on its immune response. A strong cellular (Th1) response controls infection; a predominantly humoral response with high antibody levels is associated with disease. Skin lesions are the most common: non-itchy exfoliative dermatitis with silvery scales, alopecia around the eyes ('spectacles'), ulcers on the ear tips and pressure points, and overgrown, brittle claws (onychogryphosis). Systemic signs include weight loss, generalised lymph node enlargement, splenomegaly, pale mucous membranes, epistaxis, lameness from polyarthritis, and eye lesions such as uveitis and keratoconjunctivitis. Immune-complex glomerulonephritis leading to proteinuria and chronic kidney disease is the main cause of death. Laboratory findings typically include a non-regenerative anaemia, hyperglobulinaemia with hypoalbuminaemia, and proteinuria.
Diagnosis combines clinical and laboratory findings with confirmation of infection. Cytology of lymph node, bone marrow or skin aspirates may show amastigotes in macrophages. Quantitative serology (IFAT, ELISA) is central: a high antibody titre in a dog with compatible signs confirms the diagnosis, whereas a low titre needs further testing. PCR on bone marrow, lymph node or skin is sensitive and confirms infection, but a positive PCR in a healthy dog does not mean disease. LeishVet clinical stages (I–IV), based on signs, serology and kidney function, guide treatment and prognosis.
Treatment improves signs and prolongs life but rarely eliminates the parasite; relapse is common, and treated dogs may still infect sand flies. The standard first-line protocols combine a leishmanicidal drug for about four weeks with allopurinol for many months. Meglumine antimoniate, a pentavalent antimonial, at 100 mg/kg by subcutaneous injection once daily for about four weeks, or miltefosine, an alkylphosphocholine, at 2 mg/kg by mouth once daily for 28 days, are the standard leishmanicidal regimens; allopurinol, a purine analogue that is leishmaniostatic, is given at 10 mg/kg by mouth twice daily for at least six to twelve months — confirm against the product label and your national formulary. Antimonials can be nephrotoxic, and allopurinol can cause xanthine uroliths. Availability and legality of these drugs for dogs differ widely between countries.
Prevention focuses on the sand fly. Collars or spot-on products containing synthetic pyrethroids (deltamethrin, permethrin) repel sand flies and reduce bites; permethrin is highly toxic to cats. Keeping dogs indoors from dusk to dawn during the sand fly season, fine-mesh netting, and vaccination (vaccines are licensed in some European countries) add protection. Blood donors should be screened.
A good thin blood film is the most useful single test for blood protozoa. A small drop of blood is spread with a second slide held at about 30–45 degrees into a film that thins to a feathered edge. It is air-dried quickly, fixed in methanol and stained, usually with Giemsa (commonly diluted to about 10% in buffered water at pH 7.2 for 20–30 minutes) or a rapid Romanowsky stain. Parasites are sought under oil immersion in the monolayer near the feathered edge. A thick film, a larger drop spread over a small area, is not fixed with methanol before staining, so the red cells lyse and parasites are concentrated; it is more sensitive for detecting organisms but worse for identifying them.
Where to take the sample matters. Blood from the ear tip or tail tip capillaries is preferred for B. bovis, because infected cells are sequestered in capillaries. Samples should be taken before treatment, since babesicides and tetracyclines rapidly clear organisms from the blood. Lymph node aspirates are smeared and stained for Theileria schizonts and for Leishmania amastigotes; bone marrow and spleen aspirates for Leishmania.
Reading a film asks: is there a parasite, where is it (red cell, white cell, plasma), and what does it look like (size, shape, pairing, position, kinetoplast)? Artefacts include stain precipitate, platelets over red cells and Howell-Jolly bodies.
The degree of parasitaemia is expressed as the percentage of red cells infected: count infected cells among a known total (for example 500 or 1,000 cells) across several fields, then divide and multiply by 100.
For trypanosomes, the microhaematocrit centrifugation technique (Woo's method) spins blood in a capillary tube; motile trypanosomes are seen at the junction of the buffy coat and plasma. Breaking the tube and expressing the buffy coat onto a slide for dark-ground or phase-contrast microscopy (Murray's method) improves sensitivity and species identification.
For intestinal protozoa, faecal flotation separates cysts and oocysts from debris using a solution denser than they are. Saturated salt (specific gravity about 1.20) and sugar solutions (Sheather's, about 1.27) float coccidial oocysts; zinc sulphate at about 1.18 is preferred for Giardia cysts. The McMaster technique counts oocysts per gram of faeces. A known weight of faeces is mixed with a known volume of flotation fluid, a counting chamber of known volume is filled, and the count is multiplied by a factor. For example, if 2 g of faeces are made up to 30 ml in total and both grids of the chamber (0.15 ml each, 0.30 ml together) are counted, the counted volume contains 0.02 g of faeces, so each oocyst represents 50 oocysts per gram. The factor changes with the recipe, so it must be worked out, not memorised. Fresh direct saline smears show motile trophozoites (Giardia, trichomonads). Acid-fast staining by modified Ziehl-Neelsen is used for Cryptosporidium. Sporulation of oocysts in 2.5% potassium dichromate allows species identification by morphology.
Antibody tests detect exposure and are used for herd surveys, carrier detection and certification: indirect fluorescent antibody tests (IFAT) for Babesia, Theileria, Toxoplasma, Neospora and Leishmania; ELISAs, including competitive ELISA for Anaplasma marginale and equine piroplasmosis; card and latex agglutination tests (for example for T. evansi and Toxoplasma); and the complement fixation test (dourine, and historically equine piroplasmosis). A positive antibody result in an endemic area often reflects past or carrier infection rather than the cause of current illness, and young animals may carry maternal antibody. Paired samples showing a rising titre, or high titres with compatible signs, are more informative.
PCR and related molecular methods detect parasite DNA, identify species and genotypes (for example Cryptosporidium species, Giardia assemblages, Theileria orientalis Ikeda), and find carriers with parasitaemias too low to see. PCR is highly sensitive, but a positive result shows infection, not necessarily disease. Histopathology and immunohistochemistry confirm protozoal abortion and tissue lesions. Animal inoculation (mouse or rat subinoculation for T. evansi) and culture (T. foetus, Leishmania) are still used in reference laboratories.
Antiprotozoal drugs differ from antibacterials in one important respect: many target stages inside host cells, so the drug must reach the parasite inside a red cell, lymphocyte, macrophage or gut cell without harming the host. Most are narrow in spectrum. Some drugs cure; others only suppress, leaving a carrier state that may be useful (premunition, the protection from a low-grade persisting infection) or harmful (a reservoir for others). In food animals, residues, withdrawal periods and bans, which differ between countries, matter as much as efficacy. Resistance, a problem for trypanocides and anticoccidials, is slowed by dosing by weight, rotating classes and non-drug control.
For blood protozoa and Anaplasma, the main classes are these. Aromatic diamidines: diminazene aceturate (trypanosomes, Babesia) and imidocarb dipropionate (a carbanilide with a similar diamidine structure; Babesia, Anaplasma, Theileria equi). They interfere with parasite DNA. Diminazene is poorly tolerated by camels, horses and dogs at higher doses, and in dogs can cause neurological signs. Imidocarb has anticholinesterase side effects and long residues. Phenanthridinium compounds: isometamidium and homidium, trypanocides with a prophylactic effect from tissue depots. Quinapyramine and suramin: for T. evansi in camels and horses. Arsenicals: melarsomine for T. evansi in camels. Hydroxynaphthoquinones: parvaquone and buparvaquone for Theileria, and atovaquone (with azithromycin) for B. gibsoni; they block the mitochondrial electron transport chain (cytochrome b). Tetracyclines: oxytetracycline for Anaplasma (and tetracyclines in the Theileria parva infection-and-treatment method).
Anticoccidials fall into ionophores and synthetic (chemical) compounds. Ionophores (monensin, salinomycin, narasin, maduramicin, lasalocid, semduramicin) form lipid-soluble complexes with cations and disrupt the parasite's ion balance; they are toxic to horses and interact with tiamulin. Triazines (toltrazuril, diclazuril; ponazuril, the sulfone metabolite of toltrazuril, for EPM in horses) act on all intracellular stages. Amprolium competitively antagonises thiamine uptake; very high or prolonged doses can contribute to thiamine deficiency (polioencephalomalacia) in ruminants. Quinolone anticoccidials (decoquinate) and pyridinols (clopidol) inhibit mitochondrial respiration of sporozoites and are coccidiostatic. Sulfonamides and their potentiated combinations (with trimethoprim or pyrimethamine) block folate synthesis and act on developing meronts; they are used for outbreaks and for Toxoplasma.
Nitroimidazoles (metronidazole, ronidazole, dimetridazole) are activated in anaerobic organisms to toxic radicals that damage DNA; they are effective against Giardia, trichomonads and Histomonas but are banned in food-producing animals in the EU, USA and many other countries because of concerns about carcinogenicity. Benzimidazoles (fenbendazole, albendazole) bind parasite tubulin and are used for Giardia. Halofuginone lactate and paromomycin are used for cryptosporidiosis in calves. Lincosamides (clindamycin) and potentiated sulfonamides are used for toxoplasmosis in cats and dogs. For Leishmania: pentavalent antimonials (meglumine antimoniate), miltefosine, and allopurinol.
Before using any of these, check legality for the species, the withdrawal period and known toxicities (ionophores in horses, halofuginone overdose, ronidazole neurotoxicity, permethrin in cats).
Learn each organism as a card: host, site, vector or route, the stage seen in diagnosis, the key sign, the confirmatory test and the drug class. Practise making and reading Giemsa-stained thin films until you can tell B. bigemina from B. bovis, Anaplasma from a Howell-Jolly body, and a trypanosome's species from its kinetoplast and flagellum. Do McMaster calculations from the recipe rather than memorising a factor. Draw the Babesia and Theileria cycles side by side and mark where they differ (lymphocyte stage, transovarial versus trans-stadial). Link Eimeria species to their gut site and lesion. Know which drugs are banned in food animals, because examiners test it.
In field practice the microscope is your fastest tool: an ear-tip smear and a lymph node aspirate, stained in the clinic, separate babesiosis, theileriosis, anaplasmosis and surra in a febrile, anaemic cow the same day, and the treatment differs for each. Weigh or tape the animal, calculate the dose, and check withdrawal periods before treating dairy cows. In small animal practice, test diarrhoeic puppies and kittens for Giardia and Tritrichomonas, treat and clean the environment together, and give zoonotic advice on Toxoplasma to pregnant owners. Investigate abortion storms properly: submit placenta and foetus, not just serum.
Senior clinicians and advisers design herd and flock programmes: vaccination windows for Babesia and Theileria, maintaining endemic stability instead of chasing tick eradication, anticoccidial shuttle and rotation programmes with lesion-score monitoring, colostrum and hygiene protocols against cryptosporidiosis, bull testing and AI schemes for trichomonosis, and cat and dog control on sheep and dairy farms. They audit drug use, track treatment failures that suggest resistance, handle notifiable and WOAH-listed diseases (surra, dourine, trichomonosis, equine piroplasmosis) with the authorities, and advise on the movement of animals between endemic and free regions.
Research at this level addresses the unsolved problems: vaccines against Theileria, Babesia, Eimeria, Cryptosporidium and Neospora that are safe, cold-chain-friendly and do not create carriers; replacement drugs for histomonosis and trypanosomosis; the molecular basis of drug resistance and field tests for it; host genetics of trypanotolerance and theileriosis resistance in indigenous cattle; parasite genotyping for epidemiology and zoonotic risk (Cryptosporidium subtypes, Giardia assemblages, T. orientalis Ikeda); and modelling how climate change and tick spread will alter endemic stability.
This manual stays at clinical and diagnostic level. It does not cover the protozoa of fish, bees and laboratory animals; Besnoitia, Hepatozoon, Cytauxzoon, Balantidium, Entamoeba, amoebae, Plasmodium of birds (avian malaria), Leucocytozoon and Haemoproteus are omitted or mentioned only in passing, as are Ehrlichia and other rickettsiae apart from Anaplasma. Prepatent periods of individual Eimeria species, oocyst dimensions for species keys, detailed molecular biology (VSG switching, Theileria host-cell transformation pathways) and vaccine strain details are left out because they vary between sources or go beyond the syllabus. Doses are given only where a standard textbook figure is well established; quinapyramine, suramin, melarsomine, isometamidium, amprolium and in-feed anticoccidial inclusion rates are described by class only, because rates vary by product and country. Withdrawal periods and licensing status are not given because they differ by jurisdiction. No images of smears, oocysts or lesions are included yet.
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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