Parasitology

Question 1

Describe the lifecycle toxoplasma gondi

Answer 1

Intermediate host

• Acute phase - Rapid division & dissemination.Asexual reproduction forming tachyzoites.
• Chronic phase - Host immunity to tachyzoites after 2 weeks, Bradyzoites then form. Walled of in cysts in tissue

Final host (Cats)

• Infected by swallowing sporulated oocyst. (prepatent 3weeks) or eating infected rodents ( prepatent 3-10days).
• Infection is self limiting asitinfects superficial cells of vili.

Facultatively heterxenous - Intermediate host not essential for completion of life cycle

Question 2

Describe pathogenesis of Toxoplasma Gondii and how it diagnosed and prevented

Answer 2

Sheep - If non immune, pregnant ewe infected

• 0-40 days - Foetal death/ absorption
• 40-110 days - Mumified fetus, abortion (focal necrotic placenta)
• 110-145 days - Still born or weak lambs

Humans

• Asymptomatic
• If pregnant, can cause fetal death, hydrocephalus or cerebral necrosis

Cats

• Asymptomatic
• 30-80 % seroprevelance

Diagnosis

Diagnosed via IgG or IgM ELISA

Prevention

• Vaccinate sheep with Toxovac. A live, Avirulent strain. Only forms tachyzoites which immune system responds to and no bradyzoites. Given 6 weeks before tupping. Immunitys wains after 2 years (if thers no re-exposure)
• Avoid raw uncooked meat. Wash hands after handling raw meat.

Question 3

Describe the life cycle, pathogensis, prevention and diagnosis of Neospora caninum

Answer 3

Final host (Dog)

• Dogs pass oocyst, 2 sporocysts with 4 sporozoites. Pre patent of 5days
• Can cause acending paralysis of hindlimb. Also muscle wasting inpups

Intermediate host (Cow)

• Transplacental transmition in all hosts. Can occur in successive progeny. Can give birth to healthy offspring, can give birth to persistently infected offspring (have 2-7x higher chance of abortion) or can cause abortion.

Diagnosis

• PCR
• ELISA

Prevention

• No access to calving cows for dogs
• Cull infected cows/progeny
• Prevent dog defecating in cattle feed areas

Question 4

Describe the problems associated with musca flies and how their controlled

Answer 4

Musca are standard nuiscance flies with labellum. Lays eggs in faeces.

Causes fly worry in live stock => decreased milk yield and weight gain. Also transmits viruses (enterovirus), bacteria (E.coli) & helminths ( poultry tapeworm)

Controlled by good sanitation, collecting dung in heeps and spraying with insecticide

Question 5

Describe problems associated with head flys and how their controlled

Answer 5

H.irritans associated with sheep. eggs layed in decaying vegetation, and larvae emerge over winter and pupate in spring.

Sheep attempt to avoid flys by huddling together and looking towards ground. They bash their heads together in the process causing damage to head, leading to secondary bacterial infection or blowfly strike

Controlled by good sanitation and collecting dung into heeps and spraying with insecticides. Also use a pour on insecticide

Question 6

Describe problems associated with stable flys and how their controlled

Answer 6

Spends alot of time off host. has a forward pointing proboscis. Eggs layed on rotting straw. Life cycle lasts for one month, and adults last a month.

Painful bite => decrease in milk yield. Also transmits bacterial, protozoa (trypanasomes) & helminth disease

Question 7

Describe problems associate with the horn fly and how its controled

Answer 7

Resident biting fly that spends most of its time on the hosts back, feeding on the belly and udders where skin is thinner. Similiar appearance to stable flys (grey stripes) but are smaller. Eggs layed in dung, larvae pupate in dungpat.

Horn flys cluster around head, biting causes wounds which attract blowflys and muscid flies. Also transmits pathogenic bacteria and viruses by mechanical transmission.

Control is easier as fly has more contact time with the host

Question 8

Describe problems associated with the forest fly and how its controlled

Answer 8

Biting fly of cattle and horse. Reddish brown with yellow spots on thorax. deposits larvae in soil and they pupate here. Life cycle takes a year.

Fly bites perineum causing irritation and annoyance. Mechanical vector for trypanasomes.

Controlled by good sanitation and insecticides

Question 9

Describe the sheep ked fly and the problembs associated with it

Answer 9

Sheep ked is a wingless, biting fly associated with sheep and goats. Whole life cycle is on host, single larvae pupate in fleece.

sucks blood and can cause anaemia if present in large numbers, Cause wool damage and intermediate host for trypanasoma melophagium.

Controlled by sheering and dipping sheep

Question 10

Describe problems associated with sandflies and how their controlled

Answer 10

Resemble a miniature mosquito. Eggs laid in cracks in floor, larvae hatch and pupate and flies emerge.

Transmit leishmania.

Controled by spraying (campaigns or household spray)

Question 11

Describe problems associated with tsetse flies and how their controlled

Answer 11

Yellow brown abdomen, with a butchers cleaver wing ventation. Single larvae laid in shrubs and pupates in soil.

Painful irritating bites (both male and female) and transmits trypanosomes responsible for nagana and sleeping sickness

Past methods of control included killing game animals, currently insecticides are sprayed aerialy and baited traps used.

Question 12

What problems are associated with the Simulidae genus of fly and whats their life cycle and how they controlled

Answer 12

Black flies are small black hump backed flys with clear wings.

Life cycle - Eggs laid on plants underwater. emerging larvae attach to submerged rocks and pupate.

Painful bites, Vector for Eastern equine encephalitis and parasitic diseases

Controled by applying insecticides to breeding sites and removing brush that would be resting sites for adults

Question 13

What species of midge is important in veterinary medicine, what are its associatd problems and whats its control measures

Answer 13

CULLICOIDES is a small dark hump backed fly with mottled wings.

Life cycle - Eggs layed on plants near water. Larvae drop into water and pupate.

Most active in the late afternoon/early evening. Causes painful bites, Sweet itch in horses ( a seasonally occuring Allergic dermatitis). Also a vector for Schmallenberg disease and blue tongue.

Controlled by destroying breeding sites, stabling horses in the late afternoon/early evening.

Question 14

Describe problems associated with mosquitos and how their controlled

Answer 14

Eggs layed and larvae and pupal stages can be seen hanging from the surface for oxygen access.

Painful bites, transmit human diseases (malaria (parasitic) and dengue fever (viral)). in animals vector for viral diseases ( rabbit myxmatosis and equine encephalitis) and parastitc diseases ( Dirofiloria immitis [canine heartworm], avian malaria)

Controlled by destroying bredding sites, application of insecticides and education

Question 15

What are tabanidae and what are the problems associated with them

Answer 15

TABANIDAE are horse flies. medium flies with biting mouth parts. Have a Discal cell wing ventation.

Eggs are laid on leaves hanging over water. larvae drop in and return to dry land to pupate. Life cycle take over a year!

Painful irritating bite, mechanical vectors for bacterial diseases (anthrax and pasteurellosis), viral (equine infectious anaemia) and rickettsial. Intermediate hosts for trypanosomes.

Controled by long term insecticide use

Question 16

Whats In flea saliva and what Allergy can it cause and how is it tested for

Answer 16

Saliva contains:

• Histamine like compounds
• Anticoagulants
• Potential allergens

Flea allergic dermatitis - A type I hypersensitivity (IgE) to flea slavia proteins causes IgE to bind to FcER1 on mast cell causing histamine release.

Tests:

1. Serum IgE test for flea antigens. can also test for FCER1 or detect IgE bound to Mast cells in vivo
2. Flea challenge test - Flea allergen, saline (control) & histamine are injected intradermaly, reaction noted after 20 mins. Possible to have delayed hypersensitivity IV , mediated by T-cells, occurs in 24-48 hours

Question 17

What is milary dermatitis

Answer 17

Dermatitis with a millet seed like appearance. Commonly due to Flea allergic dermatitis, atopic dermatitis (heriditary hypersensitivity to common allergens), food allergens & dermatophytosis

Question 18

What is ovine ostertagia and what are its 3 types and epidemiology

Answer 18

O.circumcinta causes a clinical disease in lambs.

1. Type 1 - Main form of PGE. Effects lambs in their first grazing season, causing diarrhoea and weight loss.
2. Type II - Affects lambs >1year old after their first grazing season. Large amounts of Arrested larvae resume development in waves causing intermittent diarrhoea. can cause severe acute disease.
3. Trichostrongylus axei - causes black scour, a dark foul smelling diarrhoea. Affecting lambs <1year. But takes long for L3 to build up as not many offspring produced. affects sheep cattle and pigs.

Epidemiology

• Clean pasture - Ewe releases eggs from april/may onto pasture due to peri-parturient relaxation in immunity. Auto infection of L3.
• Contaminated pasture - Ewes contaminate pasture due to peri-parturient relaxation in immunity, but theres also L3 on pasture that survived from previous year, causing an earlier infection of lambs. Lambs therefore contribute to eggs layed on pasture alot earlier. Small peak of L3 in september due to newly infected lambs releasing eggs.

Question 19

What is Nematodirosis and its epidemiology

Answer 19

N.Battus can cause an acute and fatal disease. Effects lambs 6-10 weeks old. First grazing season (april-june) affected. Sudden onset of profuce diarrhoea. Large brown eggs with parallel sides.

Epidemiology

• Eggs deposited on pasture in spring
• L3 develops inside egg and can survive for 2 years in egg
• Hatches when after a prolonged period of chill is followed by a mean temperature of >10 (spring). Therefore eggs layed in spring can be arrested for a year/2
• Reduced risk of infection if lambs still suckling
• Ewes don’t play a significant role in epidemiology.

Question 20

What is haemonchosis and describe its epidemiology

Answer 20

A sheep nematode with a barber pole appearance due to the red intestines and white uterus intertwined. Has a piercing lancet for blood sucking (causes anaemia)

Epidemiology:

• Tropical climate - Survives dry periods by arresting. development and a subsequent outbreak dependatn on rainful. Several cycles yearly
• Temperate regions (UK) - One cycle annually. Ewe primary source of infection. Few L3 overwintering causes type 2 disease, the larvae ingested in summer arrest and re-emerge in spring)

Question 21

What are the 4 types of Large strongyles

Answer 21

Large strongyles (redworms) affect horses. 3 species belong the the Strongylus species and the other is Triodontophorus. Have large buccal cavitys, a dorsal gutter (secretions) and teeth

• S.Vulgaris - Penetrates intestinal mucosa & migrates to the cranial mesenteric artery. Then migrates to the aorta, causing Verminous endarteritis. This is where the wall of the artery is thickened, Organsied thrombi forms from inflammation which can embolise and cause infarction in SI. Prepatent of 3-4 months.
• S.endentatus - Pops through intestinal mucosa and migrates via the hepatic protal system to the liver. Causes the formation of nodules in liver. Then via falciform ligament migrates to the LI. Prepatent of 11-12 months
• S.equinus - Pops through intestinal wall and swims across peritoneal cavity to liver PPP- 9months
• Triodontophorus - L3 burrows into mucosa to moult to L4. non migratory. PPP - 2-3 months

Large strongyles are plug feeders, penetrate to muscularis layer and blood vessels causing ulceration and anemia if in large numbers. Triodontophorus samage more superficial and feed in herds.

Question 22

What are the most important small strongyles, whats their life cycles, pathogenecity and epidemiology

Answer 22

Cyathostomins are most important.

Life cycle

• Ingest L3 and larvae invade LI mucosa
• Can develop to L4 or arrest at L3
• L4 emerge into gut lumen and mature into adults
• PPP 8-12 weeks

Pathogenecity:

• Initial infection of L3 causes local inflammation
• L4 larvae can been seen as brown flecks in mucosa
• Larval emergence in summer and plug feeding of adults causes wormy horse ( poor coat, anaemia and diarrhoea)
• Emergence of large numbers of arrested larvae in spring can causes severe diarrhoea and weight loss

Epidemiology

• Occurs in young horse (adults if poor hygiene and overcrowding)
• Small amount of overwintered L3 on pasture
• Spring rise in faecal egg output in breeding and non breeding horses

Question 23

What is parascaris equorum, whats its life cycle, pathogenecity and epidemiology

Answer 23

Nematode of horses from the Ascarid family affecting young foals. Distinctive 3 lips of ascarids.

Life cycle

• Infection of ingested embryonated L2 egg (brown thick pitted shell)
• Larvae undergo hepatotracheal migration (liver-heart-lungs-intestine)
• PPP 10-122ks

Pathogenicity

• Larvae cause eosinophilic tracts and haemorrhage in liver and lungs. Causes cough and nasal discharge
• Adults cause weight loss

Epidemiology

• High fecundicy
• Thick pitted shell ensure survival
• Sticky outer shell of egg permits passive spread
• One years foals transmit to the next years.
• Adults are carriers

Question 24

What is strongyloides westeri, its life cycle, pathogenicity and treatment

Answer 24

Is the most commenest in foals <6months. First parasite foals are exposed to. Has a long oesophasgus and only females are parasitic.

Life cycle

• Has non parasitic phases of life cycle
• Infected by ingestion of mares milk or grass or skin penetration

Pathogenicity

• Foals - Severe enteritis and diarrhoea if theres a heavy burden
• Adults are normally immune and act as carriers

Treatment - Regular anthelmintic treatment and good hygiene

Question 25

What is Oxyuris equi, whats its life cycle and pathogenicity

Answer 25

Oxyuris equi is a pin worm effecting the caecum, LI and rectum.

Life cycle

• Adults in lumen of colon
• Female migrates to anus to lay eggs on perianal hair.
• Eggs fall to ground and L3 develops inside egg. Ingested and L3 invades colonic mucosa and L4 emerges. PPP 5months

Pathogenicity

• L4 feed on colon mucosa. nip of epithelium.
• Adults not pathogenic but egg laying is a irritant causing SEAT itch

Question 26

What is hypostongylus Rubidus

Answer 26

Hypostongylus rubidus is the equivalant to porcine ostertagia. similiar life cycle ( L3 ingested , L4 develops in stomach gastric glands) epidemiology and pathogenesis. Seen only in outdoor pigs and fecundicy is low. Was rare in uk but increasing prevelance as free range increases. Cause severe weight loss and death in lactating sows.

Question 27

What is Oesophagostomum and what is thin cow syndrome

Answer 27

Oestophagostomum are typical stongyloid. Found in ther caecum and colon. A periparturient egg rise occurs. Not very pathogenic but large numbers depress milk production and growth rate.

Thin sow syndrome

• Associated with Oestophagostomum
• Quantitiy of feed is inadequate causing sow to eat bedding which cotains larvae
• Aquires large burden
• Intestinal damage and excretes eggs increasing L3 in bedding
• downward spiral causing more intestinal damage and excessive weight loss

Question 28

What is Ascaris suum, whats its life cycle, pathogenesis, 2 mechanisms of infection and problems associated with treatment

Answer 28

Ascaris suum is a typical ascarid. Has a thick brown sticky coating to its egg.

Life cycle - Hepato tracheal migration. Causes Milk spots on liver

Pathogenesis

• Causes lung damage and respiratory distress
• Liver damage by milk spot
• Adults can block intestines or bile ducts if large burden

Mechanisms

1. L4 only killed as they reach intestine. Immunity is developing and milk spots are present on liver. (bacon pigs) takes several months to develop immunity
2. L2 is killed before reaching the liver. Animal already has a solid immunity therefore no milk spot lesions

Control involves decontaminating environment. Eggs however are long lived and can continue to infect pifs after deworming programmes

Question 29

What is trichuris suis, whats its pathonesis and what are the approaches to control

Answer 29

Trichuris suis is a whipworm which prefers warm climates (rare in uk). Can provoke diarrhoea or dysentery, also provides a portal from microbial organisms.

Control approaches

1. Routine dousing - All stock are give medicated feed simultaneously. Initially three monthly intervals, with f.e.c monitored and treatment interval increases as prevelance decreases. Can accelerate anthelmentic resistance in oesophagostomum
2. Strategic dousing - Sows are treated before entering farrowing house. eliminates shedding of ascaris eggs by carrier sows. Eliminates periparutient egg rise. Weaners treated before entry.

Question 30

What is trichostrongylus tenius

Answer 30

a nematode of birds, particularly grouse. Found in the intestine. can arrest over winter. L3 can accumulate in heather tips which are eaten by grouse. lead to cyclical crashes in the population.

Question 31

What is toxocara canis, describe it complicated life cycle and how its controled

Answer 31

Toxocara canis almost all pupies are born with. Small no. of worms is asymptomatic but large burden causes pot belly, diarrhoes, vomiting and weight loss. females can release 250,000 eggs per day

Life cycle:

1. Puppies <2months

• Migrates via hepatotracheal route
• Becomes adult in SI
• PPP of 5 week but can pass eggs at 2-3 weeks of age, can be infected in utero
• After 6 weeks theres spontaneous expulsion of worms

2. > 2 Months

• Larvae migrate from liver-heart-lungs-heart.
• Granulomatous reaction during ‘waiting phase’, this is where Larvae do not develop but are metabolically highly active. Produce large amounts of Es antigen, immune evasion. Lies dormant until pregnancy occurs. If in male dead end host

3. Pregnant bitch

• After 42 day of gestation, proportion of larvae are activated
• Activated larvae either travel to placenta causing prenatal infection or to mammary gland to infect colostrum/milk
• Unactivated larvae activated in subsequent pregnancies

4. Non canids

• Larvae migrate Liver-heart-lungs-heart- somatic tissues (liver/kidney/muscle) causing granulomatous reaction, entering waiting phase
• Wait to be eaten by canid, Paretentic host (maintains natural reservoir)

Can be human infection by swallowing embryonated eggs (L2). Causing unilateral partial impairment of vision.

Control

• Hygiene
• Prevent dogs excreting eggs by dosing pups at 2weeks
• Most anthelminits only active against adults stages, so have to be doesd at 2 week intervals
• Fenbendazole active for both larvae and adult, just two treatment at 3 and 6 weeks.
• Pregnant bitch can be given Fenbendazole everyday from day 40 up until 2d before parturition to stop pups being born with it.

Question 32

What is toxascaris leonina

Answer 32

Similiar to toxocara canis except:

• Infects felines
• No prenatal transmission
• No transmammary transmission
• No hepatotracheal migration

Question 33

What are hook worms, describe their LC and pathogenicity

Answer 33

Bursate nematodes with lare buccal cavity and teeth.

Life cycle

• In uncinaria L3 is ingested & confined to the SI
• In ancylostoma penetrates skin penetration, and migrates to blood and lungs

Pathogenesis

Uncinaria - Common in uk. Relatively non pathogenic. Plug feeders causing protein losing enteropathy. Heavy infestation = intermitten diarrhoea

Ancylostema - Rare in uk, blood sucker causing sever anaemia

Question 34

What is Dipylidium caninum, what is life cycle and recognition

Answer 34

D.canim is very common cestode in cats and dogs. However has little clinical importance causing anal irratation and diarrhoea in heavy burdens. Proglottids are motile. Have two genital pores in the individual segments and have 4 suckers.

Life cycle

• Egg packets are ingested by flea larva. The oncospheres transforms to cysticercoid.
• Flea infestation provokes exaggerated grooming behaviour, then becoming infected with Dipylidium as infected flea ingested

Flea control is vital for preventiona and treatment

Question 35

What us Anoplocephala, How would you recognise it and what is its life cycle

Answer 35

A cestode affecting horses, although it looks like a tapeworm. Found at the ileo-caecal junction and can cause colic in heavy burden. has suckers not hooks. Eggs are rounded triangular shape, with oncospheres contained in pyriform apparatus.

Life cycle - Intermediate host is Pasture mite. Forms a cysticercoid.

Question 36

What is moniezia

Answer 36

Common tapeworm of lambs. can reach up to 2m long. little clinical significance. Spontaneously expelled. Also has rounded triangular eggs. Intermediate host is pasture mite

Question 37

What is Davainea

Answer 37

Tapeworm affecting poultry. Intermediate hosts can be earthworms, beetles or mollusc, therefore seen mostly on free range farms. Causes haemorrhagic enteritis.

Question 38

What is the horse bot fly, its life cycle, Pathogenic significance and control method

Answer 38

Small miasis fly, similiar to drone bees but with one pair of wings

Life cycle

• Females cement eggs onto individual hairs on the horses fore legs and shoulders.
• Eggs hatch spontaneously or stimulated by warmth and moisture from grooming
• Larvae crawl into mouth and penetrate tissues of the tongue or buccal mucosa
• Emerge and swallowed into stomach where they attach to gastric mucosa and refered to as bots
• After 10-12 months, bots detach and passed in faeces.
• Larvae pupate on ground and emerge in one to two months.
• Adults survive a few days/weeks

Pathogenic significance

• Adult flies cause annoyance while egg laying
• Larvae attach to stomach provoking inflammatory reaction
• Large numbers may interfere with the passage of food

Control

• Insecticide treatment over winter, after frost all adult flies should be dead, therefore all larvae killed breaking life cycle
• Sponge horses in summer with warm insecticide containing water to kill eggs

Question 39

What is coccidiosis, what is the most important uk species, What is its life cycle, Pathogenecity

Answer 39

Caused by the protozoa Eimeria. Huge economic importance costing 2bn a year. E.Tenella most relevant in UK, high prevelance and pathogenecity

Life cycle - Direct

• Oocyst not infective until it has undergone sporulation (requires warmth ,moisture & oxygen). They contain 4 sporocyst, each holding 2 sporozoites.
• Oocyst ingested and broken down by grinding of the crop to release sporocysts.
• Sporozoite are released due to intestinal bile & trypsin. Sporozoites invade gut lumen
• Three to four phases of asexual multiplication (shizogony) are followed by gametogeny forming merozoites
• Zygote develops into oocyst which is shed in faeces
• PPP 4-5 days
• Highly host specific and self limiting (cleared of disease unless theres re infection)

Pathogenic significance

• Group 1. - Malabsorption group - Vilous atrophy causes weight decrease and drop in feed conversion
• Group 2 - Highly pathogenic becuase the 2nd gen shizonts form at base of intestinal crypts, destroying them and causing marked haemorrhage. high mortality. E. Tenella in this group

Question 40

Describe how Eimeria is diagnosed, the epidemiology and control methods

Answer 40

Diagnosis

• Oocyst morphology
• Location of infection
• Lesion scoring
• Faecal appearance
• Absence or presence

Epidemiology

• Huge biotic potential, generation time is short and massive infection can build up rapidly
• Immunity develops slowly, so high stocking densitites can cause explosive
• Warmth and moisture essential for sporulation

Control

• Integrated control - Management and hygiene. Litter should be removed between crops and should be dry. lowest stocking density possible and a turnaround time of 10 days between crops
• Ionophores - Causes influx of Na and water. organism depletes energy stores trying to remove Na. Therefore eventually swells. No longer pathogenic but immunity still develops. supress clinical and sub clinical coccidiosis and excert little selection pressure on parasite reducing risk of resistance developing.
• Other chemicals - they either kill the parasite (interfers with immunity build up) or stop asexual reproduction. high selection pressure excerted, increasing chance of resistance.
• Shuttle programe - Different drugs used in sequence to minimise risk of resistance, protect the bird and build immunity
• Vaccine - Has multiple strains in a attenuated live vaccine. Precocious strains feature fewer rounds of asexual replication. Vaccinated once at 1-9 days. oocyst is suscpended in water. can cause sub optimal growth rates so not used for broilers. retains immunogenecity despite reduced pathogenecity.

Question 41

Describe coccidia in bovine, its life cycle, diagnosis and control

Answer 41

Three relevant species in cattle: E.bovis, E.zuernii & E.alabamensis. Usually occuring in young animals (<1year). 2 types of coccidiosis:

1. Stable coccidiosis - Caused by E.bovis & E.zuernii. Mainly occuring in calves in poor, over crowded conditions. Enzootic stability occurs in older animals. More pathogenic coccidiosis, causing dysentery, retarded development and dehydration.
2. Pasture coccidiosis - Caused by E.alabamensis. Causes a mucoid enteritis (malabsorption). Has a lower mortality but a higher morbidity. Enzootic stability also.

Life cycle - Sporulation - Shizogony (only 2 rounds because shizonts are larger) - Gametogony. PPP 17-22 d (longer than E.tenella).

Diagnosis

• History, clinical signs and diarrhoea appearance
• Post mortem of caecum, ileum and colon (inflammation and oocyst)
• Faecal oocyst count (but healthy animals can pass oocysts)

Control

• Improve management and sanitation (increase bedding and ensure faecal contamination of troughs)
• Infeed anticoccidial drugs
• No vaccine because fewer round of shizogony

Question 42

Describe coccidia in sheep, pigs and rabbits

Answer 42

Sheep

2 of importance: E.ovinoidalis & E.crandalis. Frequently seen in lambs <6weeks. Oocysts from ewes (carriers) accumulate in poorly managed litter. Early lambs amplify the parasite population, making later lambs infection larger. Affected lambs may die before oocyst are passed in faeces.

Pigs

Eimeria and Cystoisospora. Sporadic disease in unweaned piglets, causing a profuse diarrhoea and even death.

Rabbits

E.steidae. Infection of the portal blood and then liver causing white nodules. Oocysts passed from bile to faeces. Causes diarrhoea, poluria, ascites and polyuria

Question 43

What is Cryptosporidium, whats its life cycle, pathogenic significance, epidemiology, diagnosis and control

Answer 43

Cryptosporidium is a small protozoan parasite occupying the brush border (C.parvum). Oocyst is very small (4-5um)

Life cycle - Oocyst (sporulated when pasted in faeces) - Shizogony- Gametogony. Produces thick and thin walled oocysts. Thin walled can rupture in vitro, Increasing burden.

Pathogenic significance - Causes outbreaks of diarrhoea in young animals.

Epidemiology - Direct faecal oral transmission and water borne

Diagnosis - Faecal smear with a Ziehl-neelsen stain (oocyst red against blue backround) & immunoassays.

Control:

• Quarantine bought in calves, treat if signs of diarrhoea
• Good hygiene, adequate bedding and disinfection in calf pens
• Treatment - drugs (Halofuginone)

Question 44

What is Giardia, whats its life cycle, pathogenic significance, epidemiology, Diagnosis and control/treatment

Answer 44

Giardia is a flagellate protozoa responsible for chronic diarrhoea. Pear shaped with eight flagella, also has a large adhesive disk used to grasp onto mucosa of SI.

Life cycle

• Trophozoites attach to intestinal vili
• Reproduce by binary fission
• Cysts formed intermittently

Pathogenic significance - Commonest cause of diarrhoea in man. Causes villous atrophy. commonly asymptomatic in most cases in domestic animals

Epidemiology

• Direct oral faecal route or water borne transmission
• Wild animals (beavers) act as resorvoirs

Diagnosis - Faecal examination (cyst excretion intermittent, collect over 3 consecutive days. commercial immunoassays

Control/treatment - Good hygiene. Boil drinking water. Fenbendazole. Vaccine from killed Giardia.

Question 45

What is histomonas, whats its life cycle, pathogenic significance, diagnosis and control

Answer 45

Histomonas is a flagellate protozoan that causes infectious entero-hepatitis (Circular necrotic lesions in liver) in turkeys, and also infect chickens (carriers)

Life cycle

• Carried in larval stage inside the egg of Heterakis (caecum nematode)
• Released from larva when egg hatches in intestine
• Penetrates caecal wall and carried by hepatic portal system to liver
• Intestinal Histomonas infects Heterakis and passes to worm ovary
• Worm passes Histomonas infected eggs
• Eggs swallowed by birds or earthworms (carriers)

Diagnosis - Yellow droppings. Post mortem necrotic mucosa & Circular lesions of liver.

Control - Dont rear turkeys on ground used by chickens (earthworms can be infected)

Question 46

What is Balantidum

Answer 46

A ciliate protozoan found as a commensual of the large intestine of pigs and man. Has kidney shaped macronucleus and a contractile vacuole.

Reproduction by binary fission. Has thick walled cysts. If mucosa is damaged in pigs can cause ulceration of dysentery. In man causes ulceration and dysentry when infected by contaminated food stuffs (hands with pig faeces)

Question 47

What is trichenella spiralis, what is its life cycle and how is it controlled

Answer 47

A non bursate nematode, is a species of trichinellosis. Has zoonotic potential to infect humans causing:

• Myocarditis
• Severe muscle pain
• Facial oedema
• Coma

Main risk to humans is from pigs. Intracellular nematode that gives rise to viviparous offspring. L1 migrates to muscle and moults 4/5 times to adult, causes syncitium formation. In muscle forms nurse cell:

• Accumulation of mitochondria & ER around larva
• Synthesis of collagen capsule
• Secretion of VEGF causing angiogenesis => provides nutrients & metabolites
• Accumulation of granulation tissue & adipocytes

Coiled larvae inside nurse cell are infective and persist for years.

Control - Prevent pig scavenging, cook pork well, meat insepction by microscopy or pepsin digestion

Question 48

What Is taenia multiceps, what is its life cycle and pathogenesis

Answer 48

Is a cestode (tapeworm) affecting the nervous system.

Life cycle:

• Eggs/proglottids shed in environment
• Embryonated eggs ingested by IH (rabbit/possibly human)
• Oncospheres hatch and migrate to the CNS via blood, develop into coenuri (multiple inverted scolex in fluid filled bladder)
• Ingested by dog (FH)

In sheep causes staggers, head turned to one side, ataxia and possibly death

Question 49

What is sarcocystitis, whats its life cycle, pathogensis and how is it diagnosed

Answer 49

Sarcocystitis is a Coccidia. Is obligate heteroxenous (needs to replicate in IH).

Life cycle:

• Gamogony occurs in FH.
• Sporogony (asexual), forming sporocysts containing sporozoites which are infective.
• Sporozoite ingested by IH, formation of tachyzoites in mesenteric lymph and endothelial cells.
• In the muscle, formation of large sarcocysts containing thousands of bradyzoites

Prepatent period of 1-2 weeks in FH. in IH takes 2-3 months for sarcocyst with bradyzoites to form.

Pathogenesis

• No symtoms in FH
• Causes fever, anaemia, CNS disorders and haemorrhage in intermediate hosts.
• Diagnosed by the presence of visible sarcosysts on muscle

Question 50

What is taenia, whats its lifecycle and epidemiology

Answer 50

Taenia is a cestode with a human FH. Teania saginata infects cattle and taenia solium infects pigs.

Life cycle:

• humans shed eggs/proglottids in faeces contaminating environment
• Ingested & oncospheres hatch and penetrate intestinal wall
• Circulate to musculature & develop into cysticerci (one inverted scolex in bladder) in muscle

Cysticercus is supposed to be calcified by normal immune system. most are located on the masseter or tongue

Epedemiology

1. Northern europe - Low human prevelance, low oppertunities for immunity to develop. cattle are susceptible. can cause cysticercosis storm
2. Eastern african - High human preverlance and high transmission to cattle. calves infected at an early age, immunity to reinfection develops. infection persists but small

Question 51

What parasite is responsible for Hydatid cyst, whats its life cycle, epidemiology and principles of control

Answer 51

Echinococcus granulosus is a tapeworm whos definitive host is in the dog. Small adults (0.2-0.7cm).

Life cycle:

• Scolex is buried in a intestinal crypt
• One gravid segment is passed by each tapeworm each week (low biotic potential)
• eggs hatch and oncosperes migrate to form metacestode.
• Intermediate host (sheep, horse & cattle) swallow eggs (40um)
• Metacestode is a Hydatid cyst (fluid filled bladder with 000’s of inverted scolex’s). contains brood capsules with protoscolices

Epidemiology - great evolutionary plasticity. Each strain exists between distinc species.

1. Dog-Sheep - Infective for humans. Dogs become infected when fed offal or by scavenging dead sheep. Flock infected when brought down for lambing
2. Dog-Horse - Diff species, Echinococcus equinus. Hunt dogs fed horse meat.

Principles of control;

• Regular treatment at 6 week intervals of dogs (Praziquantel)
• Regular testing of dogs (Copro-antigen)
• Ensure no access to raw offal

E.multilocularis definitive host is a fox (also effect cat) and a microtine rodents as IH. Metacestode is Alveolar cyst, which bud off as daughter cysts externally

Question 52

What is Fasciola hepatica, what is its life cycle, different clinical diseases, Pathology & epidemiology

Answer 52

Liver fluke. Adults live in the bile ducts causing fibrosis. Affects mainly sheep and younger cattle.

Life cycle:

• Eggs shed in faeces and develop in water
• Miracidium hatch in the presence of light and water
• Miracidium seek out mud snail and penetrates into it. Undergoes Asexual reproduction forming motile sporocysts
• Redia develop inside sporocyst. Inside redia asexual reproduction occurs forming cercaria
• Cercaria emerge from snail and attach to grass forming metacercaria
• Metacercaria ingested and excystation and migration to liver

Pathology: Metacercariae excyst and immature fluke migrates out of SI, across peritoneal cavity and into liver. remain here for 6-7 weeks then move to bile ducts.

1. Acute fasciolosis - Sudden death in september - november. >1000 immature flukes. No eggs produced
2. Sub-acute fasciolosis - Rapid weight loss over 1-2 weeks. Occurs in october-december. Enlarged liver with haemorrhages. >500 flukes. 50:50 immature and adult flukes
3. Chronic fasciolosis - Progressive weight loss of weeks/months. Occurs in jan-march. Hypoalbuminae, anemia. >250 flukes
4. Sub-clinical effects - Fleece weight decrease. Reproductive performance is adversely influenced. liver condemnations cause economic loss at slaughter.

Question 53

Describe the disease manifestation of liver fluke and its epidemiology

Answer 53

• Large numbers of metacercariae = acute disease and low numbers = chronic
• Feed intake decreases with fluke infection
• Species susceptibility - Proportion of flukes that reach bile ducts dependant on fibroblastic potential of liver and effectiveness of protective immune system

Epidemiology

Summer infection of snail

• Eggs passed in spring and hatch in june
• Cercariae develop in snail during summer and are shed late august causing acute disease in sept-nov or chronic from january

Winter infection of snail

• Eggs dropped late summer and infect snail.
• Development halted when temp <10, flukes trapped in hibernating snails
• Development resumes when >10, cercariae shed from july, causing disease in august

Also during a wet summer, theres a larger population of snails = more infected snails = increased risk of disease

Question 54

What is dictyocaulus viviparus, whats its life cycle and epidemiology

Answer 54

Dictyocaulus vivparus is a trichostrongyloidea, bovine lungworm. Found in trachea and larger bronchi.

Life cycle: PPP 3 weeks

• Females in trachea lay embryonated eggs
• Eggs coughed up and swallowed, eggs hatch in abomasum/SI. L1 are passed in faeces
• L2 => L3 develop in dungpat
• Ingestion of infective larvae
• Penetrate wall of intestine and migrate via lymphatics to the lungs

Epidemiology

• Few calves pick up overwintered L3
• These calves then begin to release eggs, then re infected by emerging L3
• translation of L3 by fungus
• Remainder of calves infected, cycles 1-3 times until sufficient L3 on pasture to cause disease
• Many larvae inhibited in lungs of calves over winter, causing contamination the following spring‘carriers’.

Immunity is acquired following heavy exposure to infection withing a few weeks

Question 55

What are the 3 types of ovine lungworm, whats their life cycles and epidemiology

Answer 55

Dictyocaulus filaria is the most pathogenic and the least common. associated with chronic cough. Life cycle is the same as D.viviparus (direct) PPP 5 weeks.

Muellerius and Protostrongylus are common but not pathogenic. Indirect life cycle involving mollusc as intermediate host. L1 passed in faeces and develops in mollusc to L3. Infected mollusc ingested with grass. Travels to lungs via lymphatics. Adults found in alveoli/parenchma (Muellerius) or small bronchioles (Protostongylus). high prevelance due to wide range of intermediate hosts, prolonged survival of larvae in faeces, an long periods of latency

Question 56

What is Dictyocaulus arnfieldi and its epidemiology

Answer 56

Equine lungworm found in the smaller bronchi causing chronic cough.

Main source of infection is donkeys contaminating horse pasture. This is because donkeys release many eggs in faeces and have a patency of 5+ years while being asymptomatic.

Question 57

What is metastongylus spp responsible for & whats its life cycle

Answer 57

Porcine lungworm. found in the bronchioles. Very pathogenic and can cause severe lung damage.

Life cycle

• Intermediate host is earthworm, therefore only affects outdoor pigs
• Larvae migrate via lymphatics to lungs
• Immunity builds up quickly

Only affects free range systems

Question 58

What is angiostongylus vasorum, whats its life cycle and epidemiology

Answer 58

Angiostrongylus vasorum is a canine lungworm of the metastongyloids. lives in pulmonary arteries of right side of heart.

Life cycle

• Eggs released in pulmonary arteries and get trapped in lung capillaries
• Larvae hatch and migrate from alveoli to trachea
• Larvae swallowed and pass in faeces
• Larvae infects slugs which are eaten by dog
• Larvae migrate via mesenteric lymph nodes to blood stream to heart

Epidemiology - Fox acts a an important reservoir

Question 59

What is Filaroides, whats its life cycle and epidemiology

Answer 59

Canine lungworm of the metastonyloid family. Has a direct life cycle and adult worms live in tracheal nodules. Transmission from bitch to pups when grooming.

Question 60

What is Oestrus ovis, whats its life cycle, pathogenic significance and control methods

Answer 60

Nasal bot fly affecting sheep and goats. medium sized grey fly with black spots and clear wings.

Life cycle

• Females squirt a jet of liquid containing larvae into nostrils
• Larvae crawl up nasal passage into frontal sinuses
• Feed on nasal mucosa and mature
• Mature larvae (black bands) Return to nostril and are snezeed out and pupate on the ground

Pathogenic significance - Adults flies are of annoyance. Larvae cause nasal discharge and sneezing. can cause erosion of bones of the sinus and can even enter brain causing neurological signs.

Control - Systemic insecticides in heavy infestation.

Question 61

What is linguatula, whats its life cycle and pathogenic significance

Answer 61

Tongue worm.

• Adults tongue worms are found in nasal passage of dogs.
• Eggs are expelled by coughing and are eaten by herbivores (IH).
• Hatch in intestines and emerging larvae migrate to the mesenteric lymph nodes.
• here they encyst and become infective nymphs.
• Life cycle complete when dog eats uncooked viscera containing infective nymph

Heavy infestations may lead to sneezing and coughing and nasal discharge