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Parasitology 3 Flashcards

1
Q

Describe the general cestode life cycle

A
  • Tapeworm egg in proglottid
  • Shed in faeces
  • Ingested by intermediate host
  • Development in intermediate host
  • IH eaten by definitive host or ingested with herbage
  • Larval stage evaginated and attaches in gut
  • Adult worm in GI tract hermaphroditic
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2
Q

What are Peudophyllidea?

A
  • Tape worms of carnivores

- Eggs immature

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3
Q

What are the larval stages of pseudophyllidea?

A
  • Coracidium
  • Procercoid
  • Plerocercoid
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4
Q

What are cyclophyllidea

A
  • Tapeworms of large animals

- Eggs contain embryo

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5
Q

What are the larval stages of cyclophillidea

A
  • Cysticercoid
  • Cysticervus
  • Strobilocercus
  • Coenurus
  • Hydatid cyst
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6
Q

Describe the appearance of cyclophillidae

A
  • Multiple proglottid segments
  • 4 suckers on scoluses
  • Genital openings on one side
  • Compact yolk gland posterior to ovary
  • Multiple segments
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7
Q

Describe the appearance of Pseudophyllidea

A
  • Can identify proglottids as uterine and genital pore on midventral surface
  • Ovary bilobed
  • Flatworm with multipe segments
  • 2 sucking grooves
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8
Q

Explain the role of teh cestode tegument

A
  • No mouth or form of intestine
  • Entire uptake of nutrients through tegument
  • Absorptive surface enlarged by small microvilli or microtriches
  • Microfilaments
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9
Q

Describe the stages of tapeworm development

A
  • Scolex produces new proglottids
  • Immature contain early testes and ovaries
  • Still growing, organs not functional
  • Mature segments have functional reproductive organs
  • Gravid segments detach adn disintegrate to release eggs
  • All segments are eventually just uterus filled with eggs
  • Other organs atrophy
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10
Q

What is the difference between the life cycles of T. saginata and T. solium?

A
  • In T solium humans can act as intermediate hosts

- In T. saginata huamsn act as final host, cattle are intemediate host

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11
Q

How can infection with T. solium or saginata be diagnosed?

A
  • Eggs or proglottids in stool
  • Identify species by proglottid morphology
  • Identify scolex
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12
Q

What is used to treat taeniasis?

A

Praziquantel

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13
Q

List the preventative measures for taeniasis

A
  • Cook meat sufficiently
  • Hygiene and sanitation
  • Strict meat examination
  • Prevent faecal contamination of animal feed
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14
Q

Why is T. soilum dangerous to humans?

A
  • Humans are intermediate host
  • Not natural hosts
  • Migrates through all parts of body and encysts
  • Causes widespread damage
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15
Q

What are the clinical outcomes of taeniasis in humans?

A
  • Vision impairment/blindness
  • Seizures/death
  • Hydrocephalus/coma/death
  • Neurological or other deficits, depending on location of cysts
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16
Q

How is taeniasis in humans diagnosed?

A
  • Differentiate between cysticercosis and other possible lesions
  • Biopsy
  • Palpation
  • Radiology
  • Enzyme linked immunoblot serological test
  • MRI
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17
Q

How is taeniasis in humans treated?

A
  • Surgical removal of cysticercus
  • Steroids
  • Anticonvulsants
  • Antiparasitic antibiotics
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18
Q

How can you differentiate between T. solium and T. saginata

A
  • Scolex

- Number of branches in gravid segment

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19
Q

Describe hydatid cysts

A
  • Lined by multilayered parasite tissue
  • Inner layer is germinal layer
  • Can spawn formation of brood capsules
  • These are also lined by germinal layer
  • Daughter cysts bud into centre of fluid filled cyst
  • May become very large
  • Each smaller body will develop into a worm if eaten by intermediate or final host as needed
  • Hydatid sand may be visible
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20
Q

Describe the general properties of protozoa

A
  • Important consumers of bacteria
  • Parasites and symbiots of multicellular animals
  • Single celled, eukaryotic organisms
  • feed heterotrophically
  • Diverse motility mechanisms
  • Not all pathogenic
  • Divided by form
  • Complex life cycles with different forms
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21
Q

What are the divisons of protozoa?

A
  • Flagellates
  • Ciliates
  • Amoebae
  • Apicomplexa
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22
Q

Describe feeding in protozoa

A
  • Food uptake pby phagocytosis, pinocytosis and simple absorption
  • Mouth openings temporary (amoeba) or permanent (ciliates)
  • Food particles surrounded by membranes forming food vacuole, digestive enzymes secreted into vacuole = phagosome
  • Soluble nutrients absorbed into endoplasm, waste discharge through opening in plasma membrane
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23
Q

Explain the importance of protozoa

A
  • Zoonotic
  • In veterinary medicine
  • Specific and zoonotic
  • Economic importance
  • Many species affected, can have severe consequences
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24
Q

List the important protozoa

A
  • Eimeria
  • Isospora
  • Cryptosporidium
  • Toxoplasma
  • Neospora
  • Balantidium
  • Sprionucleus
  • Giardia
  • Trichomonas
  • Histomonas
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25
Q

What are the causative agents of coccidiosis?

A
  • Eimeria spp.

- Isospora spp.

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26
Q

Describe Eimeria oocysts

A
  • Tetrasprocystic-dizoic
  • 4 sporocysts
  • Each sporocyst has 2 sporozoites
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27
Q

Describe Isospora oocysts

A
  • Disporocystic-tetrazoic
  • 2 sporocysts
  • Each contains 4 sporozoites
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28
Q

Describe coccidiosis in poultry

A
  • oocysts sporulate within 24 hours of excretion, resilient in environment
  • Different clinical signs depending on different species (different gut regions)
  • Diarrhoea
  • Poor growth
  • Death
  • Chicksand young birds
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29
Q

Describe the control of coccidiosis

A
  • Coccidiostats
  • Coccidiocides
  • Vaccines in poultry
  • Biosecurity
  • Disinfection
  • Colostrum
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30
Q

Describe coccidiosis in lambs

A
  • Mainly Eimeria
  • Many species, not all pathogenic
  • Adults asymptomatic sources of infection to young animals
  • Dehydration
  • Diarrhoea
  • Poor growthh
  • Death
  • Relaed to overcrowding and stress
  • Diagnosis by oocyss in faeces and necropsy
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31
Q

Describe the clinical signs of Cryptosporidiosis

A
  • Sticky, fetid diarrhoea

- Dehydration

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32
Q

What is unusual about the life cycle of cryptosporidium?

A

Can carry out self-infection

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33
Q

Describe Cryptosporidiosis

A
  • Caused by Cryptosporidium spp
  • Many hosts
  • Some specific, others wide host range, some zoonotic
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34
Q

What are the important species of Cryptodporidium and their hosts?

A
  • C. parvum - most mammals, zoonotic

- C. hominis - person to person

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35
Q

Describe Cryptosporidiosis in humans

A
  • C. hominis or parvum both infect humans
  • Contaminated water supply (by people or animals), swimming (human contamination of pools)
  • Petting zoos or pets
  • Can be long lasting, mucoid, sticky, fetid diarrhoea
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36
Q

Describe the treatment of cryptosporidiosis

A
  • No vaccine
  • No treatment
  • Usually self limiting
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37
Q

What is the main cause of Neosporosis?

A

Neospora caninum

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38
Q

What is the importance of Neospora caninum in cattle?

A
  • Abortion
  • Epidemic following dog faeces contamination
  • Endemic/sporadic through recrudescence of tissue cysts during pregnancy
  • Vertical transmission maintains infection in herd
  • Offspring permanently infected
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39
Q

Describe neosporosis in dogs

A
  • Only definitive hosts
  • Usually asymptomatic
  • May get muscle/neurological disease associated with tissue cysts
  • Oocysts shed for a few weeks after infection
  • Vertical transmission possible
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40
Q

How is neosporosis diagnosed?

A
  • Abortion mid-late pregnancy
  • Necropsy of foetus and detection by immunohistology/PCR
  • Serology of dam (or foetus) or dog
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41
Q

How can neosporosis be controlled?

A
  • No vaccine
  • No treatment
  • Do not let dog eat placenta or raw beef
  • Do not allow defaecation in fields with cattle
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42
Q

Describe Trichomoniasis

A
  • Trichomonas gallinae and other spp
  • Canker or frounce
  • Common, asymptomatic in wild pigeons
  • Transmitted in crop milk
  • Severe upper GI tract disease
  • Diphtheritic membrane blocks eating, drinking and respiration
  • Death
  • Emerging in garden birds
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43
Q

Describe the diagnosis of trichomoniasis

A
  • Smear and view under LM
  • Distinctive appearance
  • Large “head”, lots of “tails”
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44
Q

Describe histomoniasis

A
  • Mainly caused by Histomonas meleagridis
  • Blackhead in turkeys
  • Amoeboid in tissues, flagellated in gut lumen
  • Unusual life cycle - hyperparasitic
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45
Q

Describe the life cycle of Histomonas meleagridis

A
  • Intemediate stages infect nematodes of birds (e.g. Heterakis gallinarum)
  • Eaten by bird
  • Infect ovaries
  • Oocysts shed in eggs of worms
  • Hyperparasitic
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46
Q

Describe the clinical signs of histomoniasis

A
  • Severe necrosis of caecae and liver
  • Yellow diarrhoea
  • Listless
  • High fatality
  • Diagnosis at necropsy
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47
Q

Describe the control of histomoniasis

A
  • Worming

- Biosecurity

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48
Q

Describe Balantidium spp

A
  • Cilate
  • Forms tough cysts to survive in environment
  • Often found in faeces WITHOUT causing disease
  • Normal part of gut biota of many mammals esp pigs
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49
Q

Disease the clinical signs of Balantidiosis

A
  • Diarrhoea in humans mainly in tropics (also other primates)
  • Diarrhoea in pigs (most likely opportunistic pathogen)
  • Diarrhoea in various reptiles
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50
Q

Describe the treatment and control of balantidiosis

A
  • Metronidazole treatment

- Prevent with better hygiene

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51
Q

What causes Spironucleosis, where is it found and how is it transmitted?

A
  • Sprionucleus spp
  • Live in gut
  • Transmitted via faeces
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52
Q

What are the clinical signs of spironucleosis

A
  • Diarrhoea
  • Depression
  • Weight loss (all 3 in birds and fish)
  • Skin lesions in fish - “hole in the head” disease
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53
Q

Describe the treatment and control of spironucleosis

A
  • Improved hygiene
  • Less crowding
  • Metronidazole
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54
Q

Describe the life cycle of protozoa

A
  • Sporulated oocyst in environment ingested
  • Stomach acid causes oocyst to excyst
  • Sprozoites released, invade host cell, grow, get rounder = schizogony
  • Schizont produced, contains merozoites
  • Schizont ruptures, releases merozoites = merogony
  • merozoites invade more host cells, repeat
  • 2nd gen meronts invade host cells again and either continue cycle or carry out gametogony
  • In gametogoony form macro or microgamonts
  • Micro released, fuse with macro to form zygote (oocyst)
  • Oocyst exits cell, excreted
  • Oocyst sporulated and infective again outside the host
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55
Q

What is a sporozoite?

A

The infectious unit that intiates infection inside the host intestinal cells soon after the ingestion of the oocyst

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56
Q

What is a trophozoite?

A

The intracellular stage of Eimeria sporozoites after they enter the cell and change their morphology. Divides producing merozoites

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57
Q

What is a tachyzoite?

A
  • The free-replicating stage of life cyce in cyst forming coccidian protozoa Toxoplasma, Neospora caninum, Besnoitia
  • Reproduces asexually intracellularly, all pathogenesis
  • Found free in blood/body fluid or in pairs/groups within vacuole in infected cell
  • Rapid replication stage
  • Under stress can form bradyzoite
58
Q

What is a bradyzoite?

A
  • Slow replicating dormant stafe
  • Group of bradyzoites surrounded by thick capsule forming cyst
  • Under stress, reactivate and convert to tachyzoite
59
Q

What is sporulation in protozoa?

A
  • Occurs outside host

- Is process of maturation of undifferentiated oocyst to differentiated (containing sporozoites)

60
Q

Describe enzystation in protozoa

A
  • Occurs inside host (Toxoplasma)
  • Or outside (Entamoeba or Giardia)
  • Process of transformation of free-replicating, vegetative stage to dormant cyst stage
61
Q

Describe the general mechanisms of pathogenesis in protozoa

A
  • Competition with normal commensals
  • Toxin production
  • Hypersensitivity, inflammation
  • Evasion of host immune response via antigenic variation
  • Hide in cells
  • Host mimicry
  • Interfere with cell signalling pathways
  • Cell and tissue damage
  • Bind to host cells
62
Q

Explain the significance of encystment in protozoa

A
  • Hardy, survive in environment
  • Metabolically inactive so drug ineffective
  • Resistant to many disinfectant
  • Infectious
  • May be detected in faeces and used for diagnosis
63
Q

Describe the importance of tachyzoites and bradyzoites in toxoplasmosis

A
  • Tachyzoites infect other cells
  • Bradyzoites replicate slowly or do not replicate at all
  • Tachyzoites able to cross placenta in mice, infected since birth, abortions or malformations
  • In rats, bradyzoites in brain cause rat to lose fear of cat wee - infects cats
64
Q

What are the clinical signs of toxoplasmosis

A
  • Tissue damage
  • Abortion
  • Malformed young
  • Systemic/neurological disease in humans
  • In cats chronic inflammatory lesions e.g. in eyes
65
Q

Describe treatment and control of toxoplasmosis

A
  • Unlikely to treat without clinical signs
  • Pyrimethamin and asuphomide or spiramycin is needed
  • Vaccine available for sheep
  • Acoid cat litter and sheep during pregnancy
  • Cook lamb and porl thoroughly
66
Q

What is the main cause of toxoplasmosis?

A
  • Toxoplasma gondii
  • Cats are the only definitive host - no disease
  • Oocysts shed by younger cat mostly
67
Q

Describe the life cycle of Toxoplasma gondii

A
  • Rodent intermediate hosts
  • Tissue cysts
  • Eaten by cats
  • Shed oocysts
68
Q

What is Johnson Reid lesion scoring and what is it used for?

A
  • Lesion scoring in coccidiosis
  • Based on gross intestinal lesions in infected birds
  • Determine pathogenicity of coccidia
  • Measure effects of anti-coccidials and vaccines
69
Q

List the important species of Oesophagostumum and their host species

A
  • Radiatum (cattle)
  • Columbianum (cattle and sheep)
  • Venulosum (sheep and goats)
  • Dentatum (swine)
  • Quadrispinulatum (swine)
70
Q

Describe the epidemiology of Oesophagostumum spp

A
  • Common in wet temperate climates
  • Hypobiosis/Spring rise occurs to infect young animals
  • Dentatum common in pigs
71
Q

Describe the epidemiology of Oesophagostomum radiatum

A
  • Cattle
  • PPP 35-40 days
  • Typical strongyloid life cycle
  • L1 free living, L3 infectious
  • Large intestine
72
Q

Describe Oesophagostomum radiatum in young animals

A
  • Severe disease in calves
  • Anorexia, anaemia, oedema
  • Very dark diarrhoea due to blood present
  • Weight loss
  • Death
  • Immunity quickly built up
73
Q

Describe Oesophagostomum radiatum in older animals

A
  • Strong protective immunity causes nodule formation
  • Nodules (granuloma) calficy and may cause intestinal itussusceptions
  • May lead to stenosis
  • Usually no problem in older animals
74
Q

Compare Ostertagia and Oesophagostomum in cattle

A
  • Oesophagostomum radiatum has strong protective immunity
  • Ostertagia immunity takes loong time to develop, sterile immunity never reached
  • Different regions of GIT
75
Q

Describe the treatment of Oesophagostomum radiatum

A
  • Common wormers effective
  • Oxfendazole
  • 6 month withdrawal period for meat
  • Cattle dosed prior to turnout or later in season, 1-2 weeks prior to moving to contaminated pasture
76
Q

Describe Oesophagostomum of sheep

A
  • Columbianum and venulosum
  • Large intestine
  • Heavy infections cause severe disease in young lambs
  • PPP 40 days
  • Similar to Chabertia but anterior of adults look different
77
Q

Describe the appearance of adult Oesophagostomum

A
  • Bottle neck appearance
  • Sheath tail long
  • Rounded head
  • 32 gut cells
  • 726-923um
  • Male bursa
78
Q

Describe the clinical signs of Oesophagostomum in young lambs

A
  • Failure to thrive
  • Scouring
  • Weakness
79
Q

Describe the treatment for Oesophagostomum in sheep

A
  • Levamisole/triclabendazole

- 56 day meat withdrawal period

80
Q

Describe Oesophagostomum in pigs

A
  • Dentatum (distal colon), quadrispinulatum (caecum, proximal colon)
  • May coexist in same animal
  • Usually not a clinical problem
81
Q

Describe the clinical signs of Oesophagostomum in pigs

A
  • Weight loss
  • Signs of oedema (pot belly)
  • Intestinal nodules
82
Q

Describe the treatment of Oesophagostomum in pigs

A

Ivermectin

83
Q

Describe diagnosis of Oesophagostomum in ruminants and pigs

A
  • Eggs in faeces

- Nodules on necropsy

84
Q

Describe the appearance of the anterior of Oesophagostomum spp

A

Bottle neck anterior

- Cephalic and cervical vesicle cause this appearance

85
Q

List the important species of Trichuris and their hosts

A
  • Discolor (cattle)
  • Felis (felids)
  • Loporis (rabbits)
  • Muris (rats)
  • Ovis (cattle, sheep)
  • Trichiura (primates)
  • Suis (swine)
  • Vulpis (canids, sometimes humans)
86
Q

Describe the epidemiology Trichuris spp

A
  • Whip-shaped worm
  • Bioperculated eggs, very resistant, viable up to 11 years
  • Burrows into lining of LI
  • Facilitates invasion of pathogenic spirochaetes
  • Affectis young animals especially
  • Light infection in adults
  • Adults usually in caecum
87
Q

Describe the clinical signs of Trichuris infection

A
  • Weight loss
  • Bloody diarrhoea
  • Anaemia
  • Severe infection leads to mucohaemorrhagic colitis and typhilitis
  • Pseudonecrotic membranes and slouhging of colonic mucosa leading to death of young pigs
88
Q

Describe how Trichuris leads to psuedonecrotic membranes in pigs

A
  • Worm under tissue
  • Continual movement searching for food
  • Acts like knife cutting in all directions
89
Q

Describe immunity to Trichuris

A
  • Low dose exposure leads to acquired immunity and high degree of protection
  • Increased blood eosinophils, increased IL-4 in blood and mesenteric lymph nodes
  • Increased crypt length, crypt cell adn goblet cell hyperplasia
  • Localised Type-2 immune response with increased IL-4, IL-5 and IL-13
90
Q

Describe the diagnosis of Trichuris

A
  • Females lay eggs sporadically so McMaster not reliable
  • Eggs in faeces easily recognisable
  • Necropsy shows worm and muco-haemorrhagic colitis
91
Q

Describe the treatment and management of Trichuris

A
  • Benzimidazoles or levamisole
  • Thorough cleaning and disinfection
  • Common anthelmintics e.g. fenbendazole
92
Q

Describe Trichinosis in humans

A
  • Caused by Trichuris trichura
  • Soil transmitted
  • Indisitnguishable from T. suis
  • Both strictly host specific
  • Can be fatal (esp. children)
  • Can be used to treat autoimmune disease (switch from Th1 to Th2 system)
93
Q

Describe Trichuris ovis

A
  • PPP 6-8 weeks
  • Ruminants
  • Failure to thrive, bloody diarrhoea can be fatal)
  • On necropsy thickened intestine (hyperplasia), worms visible, blood mixed with mucus
  • Usually subclinical
94
Q

Describe Trichuris vulpis

A
  • PPP up to 3 months
  • Dogs of any age
  • Adults live 1.5 years
  • High level of egg shedding
  • May need to distinguish from other parasite eggs
95
Q

Describe the eggs of Trichuris

A
  • Bioperculated
  • Resistant
  • Thick shell
  • Tan coloured
  • Lemon shaped
  • Medium size
96
Q

Describe the external features of adult whip worms

A
  • Posterior is wider part
  • Male posterior coiled
  • Male 5cm, female 8cm
  • Terminal portion of female reproductive system may be seen packed with eggs adn muscular ovijector containing 2 eggs awaiting oviposition
97
Q

Explain why dogs in kennels are at risk of reinfection after deworming

A
  • Female produces 2000 eggs per day
  • Hard to kill
  • Can stay in environment for years
98
Q

Describe the epidemiology of Oxyuris equi

A
  • Pinworm
  • Common, relatively benign
  • Parasite of stabled horses (eggs do not survive well outdoors)
  • Very visible on back of horses
99
Q

Describe the appearance of Oxyuris equi eggs

A
  • D shaped (one side flatter than the other)

- Single mucoid plug

100
Q

Describe the life cycle of Oxyuris equi

A
  • Horse ingests infective L3 in egg
  • L3 hatch, moult to L4, L5, adults (male and female)
  • Female crawls to distal end of horse and lays eggs around anus
  • White/yellow and sticky, stick to perianal region
  • Only fall when horse rubs against hard surface
101
Q

Describe the disease caused by Oxyuris equi

A
  • Anal pruritis and skin excoriation and/or myiasis

- Diagnosis using sellotape

102
Q

Describe teh treatment of Oxyuris equi

A
  • All anthelmintics effective

- Topical anti-inflammatories to decrease pruritis

103
Q

Describe the appearance of Strongylus vulgaris

A
  • Large
  • Leaf crown and tooth plates
  • 2cm
104
Q

Describe the epidemiology of Strongylus vulgaris

A
  • Causes verminous arteritis
  • Important cause of surgical colic, frequently fatal
  • Larvae main cause of disease
  • Occasionally migrate aberrantly to brain, kidneys, lungs, liver
  • Can form granulomas
  • May get bleeding on tooth and gums
105
Q

Describe the life cycle of Strongylus vulgaris

A
  • Eggs passed in faeces
  • L1 hatches, L1-L3 free-living
  • L3 migrate up grass, ingested by horse
  • L3 enter SI, cross mucosal wall, moult to L4 in 7 daus
  • L4 migrate to small arterioles of intestine, then colic and caecal arteries, then cranial mesenteric artery
  • L4 larvae cause thrombi, moult to L5 in cranial mesenteric artery
  • Return via blood vessels to LI
  • Form nodules in wall of caecum and colon
  • Adults in 6-8 weeks
  • Eggs shed in faeces
106
Q

Describe the diagnosis of Strongylus equi

A
  • Difficult, is pre-patent disease
  • Disease before eggs shed as larvae are cause
  • May feel thrombi in rectal examination
  • Faecal analysis not always useful
  • History of recurrent colic
107
Q

How is Strongylus vulgaris treated?

A
  • Anthelmintics
  • Benzimidazoles and avermectins kill larvae and adults
  • Pyrantel kills only adults
108
Q

Describe the appearance of Strongylus equinus

A
  • Large strongyle
  • Larger than vulgaris (4-5cm)
  • Leaf crown
  • Tooth plates (one large, 2 smaller)
109
Q

Describe the epidemiology of Strongylus equinus

A
  • PPP 9 months

- Hepatopancreatic strongyle

110
Q

Describe the life cycle of Strongylus equinus

A
  • Eggs in faeces, L1 hatch, L1-L3 free living
  • L3 ingested on herbage
  • L3 penetrate wall of caecum and colon and form nodules
  • Moult to L4 in 2 weeks
  • L4 crosses visceral peritoneum to liver, stays for 4 months
  • Moult to L5, return to LI via pancreas
  • Moult to adults and shed eggs
  • Does not enter blood vessels
111
Q

Describe the disease caused by Strongylus equinus

A
  • Mild colic

- Some pancreatic disease adn primary diabetes mellitus

112
Q

Describe the appearance of Strongylus edentatus

A
  • Larger than vulgaris
  • 4-5cm
  • Leaf crown
  • No teeth plates, just buccal capsule
113
Q

Describe the migration of Strongylus edentatus

A
  • Hepatoperitoneal
  • Through liver via peritoneum
  • PPP 11 months
114
Q

Describe the life cycle of Strongylus edentatus

A
  • Eggs in faeces, L1 hatch, moult L1-L3
  • L3 ingested on contaminated herbage
  • L3 exsheaths in SI, crosses wall of intestine, enters blood stream, travels to liver
  • Moults to L4
  • Migrates to peritoneaum adjacent to liver on right flank
  • Forms oedematous masses where become L5 and then work way back to walls of caecum and colon
  • L5 enter intestinal lumen, develop to adults in 6-8 weeks
115
Q

Describe the clinical signs caused by Strongylus edentatus

A
  • Colic due to liver disease or peritonitis
116
Q

Describe the epidemiology of Cyathostomes

A
  • Overwinter
  • Only susceptible to treatment in adult stages
  • Hypobioses at L3
117
Q

Describe the life cycle of Cyathostomes

A
  • Eggs in faeces, L1 hatch, Free living L1-L3
  • L3 ingested by horse
  • L3 exsheaths in SI, penetrates SI wall
  • Either hypobioses as L3 in Autumn/winter to emerge in Spring
  • Or grows directly and emerges 8-10 weeks later as L5 and then adults in SI lumen
118
Q

Describe the clinical signs of Cyathostomes

A
  • Colic
  • Weight loss
  • Diarrhoea
  • Wasting
  • Death
119
Q

Describe the treatment of Cyathostomes

A
  • Encysted and hypobiotic larvae unaffected by anthelmintic
  • Intensive care for animals with acute disease
  • Steroids, anthelmintics
  • moxidectin, ivermectin, fenbendazole
  • Treat spring to autumn, pick up faeces, separate by age, avoid overgrazing, rotate pastures
120
Q

Describe general equine parasite management

A
  • Harrowing (eggs sensitive to sunlight)
  • Good stable hygiene
  • Avoid overgrazing
  • Rotate filds after treatment to reduce risk of reinfection
  • Pick up faeces regularly
  • Mixed grazing with other species
121
Q

Explain how mixed grazing can be useful in equine parasite management

A
  • Sheep will graze near to faeces (horses won’t)
  • Sheeps eats down grass, exposing eggs to sunlight
  • Egg unable to survive
  • Sheep will also not be affected by ingestion of the eggs so this also removes some of the eggs safely
122
Q

How can an unsporylated oocyst be distinguished from a sporylates one?

A

Sporocyst containing sporozoites will be visible in a sporylated one

123
Q

Describe the appearance of a schizont

A
  • Large structure in epithelial cell
  • Looks a bit like an egg
  • Contains merozoites (circles or banana shapes depening on how they are lying in the schizont
124
Q

What are the important factors in the trnamission of coccidiosis?

A
  • Poor sanitation
  • Poor management
  • Overcrowding
  • Moisture
  • carriers (older animals mixed with younger)
  • Extreme resistance of oocysts in environment
  • Formites
  • Insects/birds
125
Q

Explain the pathogenesis of haemorrhagic coccidian species

A
  • Coccidiosis (Eimeria, Isospora)
  • Direct damage to gut mucosa
  • May also be secondary bacterial infection
126
Q

Explain the pathogenesis of mal-absorptive coccidian species

A
  • Histomonas spp, Balantidium, Spironucleosis
  • Diarrhoea caused by increased intestinal permeabiliy, chloride secretion and decreased absorption due to damage to villi
  • Thought to be caused by host response to pathogen
127
Q

Discuss in general terms the economic importance of coccidiosis to the chicken industry

A
  • Major parasitic disease of poultry
  • Estimated annual cost between £1-2 billion
  • Causes high mortality, morbidity
  • Low growth rate due to malabsorption
  • Temporary reduction of egg production in layers
128
Q

Describe the oocysts of Cryptosporidium

A
  • Very small

- 4 naked sporozoites

129
Q

What are the intermediate stages of Toxoplasma for the FINAL host?

A
  • Bradyzoite cysts
  • Tachyzoites
  • Small oocysts
  • 2 sporocysts each with 4 sporozoites
130
Q

What are the intermediate stages of Toxoplasma for the INTERMEDIATE hosts?

A
  • Bradyzoite cysts
  • Tachyzoites
  • Small oocyst (2 sporocysts, 4 sporozoites in each)
131
Q

Where does the asexual phase of Toxoplasma’s life cycle take place?

A
  • Many different hosts

- (Intermediate hosts)

132
Q

What disease is caused by Sarcocystic neurona

A
  • Protozoan

- Equine protozoal myeloencephalitis

133
Q

What is unusual about the life cycle of Neospora caninum?

A
  • Can undergo vertical transmission if does not cause abortion
  • Calf has persistent infection
  • When that calf goes on to have its own, these will also be persistently infected
134
Q

What are the important features to consider in faecal examination?

A
  • VOlume
  • Colour
  • Composition and consistency
  • Presence of abnormal structure
135
Q

Describe the faecal smear technique, giving pros and cons

A
  • Used for preliminary egg identification
  • Quick, simple
  • Can be used to demonstrate helminth infection
  • Idenify eggs and larvae present
  • Cannot be used to determine level of infection
136
Q

Describe the faecal sedimentation technique

A
  • Qualitative method for detecting trematode eggs in faeces
  • Most trematode eggs to heavy to float
  • Sink to bottom of suspension
  • Can demonstate presence of eggs
137
Q

Describe the simple faecal flotation method

A
  • Qualitative
  • Detection of nematode and cestode eggs
  • Establish which parasite groups are present
  • Eggs separated from faecal materal, concentrated by flotation fluid of appropriate specific gravity
138
Q

Describe the qualitative faecal flotation method

A
  • Quantitative test tube flotation technique
  • Count eggs where concentrations too small for McMaster
  • Eggs separated from faecal material
  • Concentrated by flotation fluid of appropriate specific gravity
  • Takes advantage of low specific gravity of most helminth eggs to separate them from faeces
139
Q

Describe the larval culture method of faecal examination

A
  • Diagnose nematode infection
  • Identify L3 of nematodes in faeces
  • Provide suitable conditions for hatching eggs and larval development to L3
140
Q

Describe how immature worms can be separated from faeces

A
  • Place faeces on screen mesh and examine afer washing solution through mesh
  • Allows observation of immature worms that may be present in faecal samples
141
Q

Describe the Baermann technique to separate larvae from faecal material

A
  • Used to separate larvae from faecal material
  • Based on active migration or movement of larvae
  • Faeces suspended in water while larvae move into water and sink to bottom
  • Can be collected for identification
  • Open clamp and collect sample to view under microscope
  • Stain with iodine to give contrast and immobilise worms

GI (31 decks)

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