Parasitology Flashcards
1
Q
Describe the lifecycle toxoplasma gondi
A
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
2
Q
Describe pathogenesis of Toxoplasma Gondii and how it diagnosed and prevented
A
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.
3
Q
Describe the life cycle, pathogensis, prevention and diagnosis of Neospora caninum
A
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
4
Q
Describe the problems associated with musca flies and how their controlled
A
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
5
Q
Describe problems associated with head flys and how their controlled
A
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
6
Q
Describe problems associated with stable flys and how their controlled
A
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
7
Q
Describe problems associate with the horn fly and how its controled
A
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
8
Q
Describe problems associated with the forest fly and how its controlled
A
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
9
Q
Describe the sheep ked fly and the problembs associated with it
A
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
10
Q
Describe problems associated with sandflies and how their controlled
A
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)
11
Q
Describe problems associated with tsetse flies and how their controlled
A
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.
12
Q
What problems are associated with the Simulidae genus of fly and whats their life cycle and how they controlled
A
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
13
Q
What species of midge is important in veterinary medicine, what are its associatd problems and whats its control measures
A
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.
14
Q
Describe problems associated with mosquitos and how their controlled
A
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
15
Q
What are tabanidae and what are the problems associated with them
A
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
16
Q
Whats In flea saliva and what Allergy can it cause and how is it tested for
A
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:
- Serum IgE test for flea antigens. can also test for FCER1 or detect IgE bound to Mast cells in vivo
- 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
17
Q
What is milary dermatitis
A
Dermatitis with a millet seed like appearance. Commonly due to Flea allergic dermatitis, atopic dermatitis (heriditary hypersensitivity to common allergens), food allergens & dermatophytosis
18
Q
What is ovine ostertagia and what are its 3 types and epidemiology
A
O.circumcinta causes a clinical disease in lambs.
- Type 1 - Main form of PGE. Effects lambs in their first grazing season, causing diarrhoea and weight loss.
- 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.
- 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.
19
Q
What is Nematodirosis and its epidemiology
A
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.
20
Q
What is haemonchosis and describe its epidemiology
A
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)
21
Q
What are the 4 types of Large strongyles
A
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.
22
Q
What are the most important small strongyles, whats their life cycles, pathogenecity and epidemiology
A
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
23
Q
What is parascaris equorum, whats its life cycle, pathogenecity and epidemiology
A
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
24
Q
What is strongyloides westeri, its life cycle, pathogenicity and treatment
A
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
25
What is Oxyuris equi, whats its life cycle and pathogenicity
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**
26
What is hypostongylus Rubidus
**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.**
27
What is Oesophagostomum and what is thin cow syndrome
**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**
28
What is Ascaris suum, whats its life cycle, pathogenesis, 2 mechanisms of infection and problems associated with treatment
**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
29
What is trichuris suis, whats its pathonesis and what are the approaches to control
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.
30
What is trichostrongylus tenius
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.
31
What is toxocara canis, describe it complicated life cycle and how its controled
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.
32
What is toxascaris leonina
Similiar to toxocara canis except:
* Infects felines
* No prenatal transmission
* No transmammary transmission
* No hepatotracheal migration
33
What are hook worms, describe their LC and pathogenicity
**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
34
What is Dipylidium caninum, what is life cycle and recognition
**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
35
What us Anoplocephala, How would you recognise it and what is its life cycle
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.**
36
What is moniezia
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**
37
What is Davainea
**Tapeworm** affecting **poultry**. **Intermediate hosts** can be **earthworms**, beetles or **mollusc**, therefore seen mostly on **free range farms**. Causes **haemorrhagic enteritis.**
38
What is the horse bot fly, its life cycle, Pathogenic significance and control method
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**
39
What is coccidiosis, what is the most important uk species, What is its life cycle, Pathogenecity
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
40
Describe how Eimeria is diagnosed, the epidemiology and control methods
_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.**
41
Describe coccidia in bovine, its life cycle, diagnosis and control
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 lar**ger) - 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
42
Describe coccidia in sheep, pigs and rabbits
_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**
43
What is Cryptosporidium, whats its life cycle, pathogenic significance, epidemiology, diagnosis and control
**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**)
44
What is Giardia, whats its life cycle, pathogenic significance, epidemiology, Diagnosis and control/treatment
**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.
45
What is histomonas, whats its life cycle, pathogenic significance, diagnosis and control
**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)
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What is Balantidum
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)
47
What is trichenella spiralis, what is its life cycle and how is it controlled
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**
48
What Is taenia multiceps, what is its life cycle and pathogenesis
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
49
What is sarcocystitis, whats its life cycle, pathogensis and how is it diagnosed
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 **tachyzoite**s 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 month**s 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
50
What is taenia, whats its lifecycle and epidemiology
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
51
What parasite is responsible for Hydatid cyst, whats its life cycle, epidemiology and principles of control
**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**
52
What is Fasciola hepatica, what is its life cycle, different clinical diseases, Pathology & epidemiology
**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 l**oss 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.
53
Describe the disease manifestation of liver fluke and its epidemiology
* **Large numbers** of **metacercariae** = **acute** disease and **low numbers = chro**nic
* 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**
54
What is dictyocaulus viviparus, whats its life cycle and epidemiology
**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**
55
What are the 3 types of ovine lungworm, whats their life cycles and epidemiology
**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**
56
What is Dictyocaulus arnfieldi and its epidemiology
**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**.
57
What is metastongylus spp responsible for & whats its life cycle
**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
58
What is angiostongylus vasorum, whats its life cycle and epidemiology
**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**
59
What is Filaroides, whats its life cycle and epidemiology
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.
60
What is Oestrus ovis, whats its life cycle, pathogenic significance and control methods
**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.
61
What is linguatula, whats its life cycle and pathogenic significance
**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
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