Parasitology 3 Flashcards
(141 cards)
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
2
Q
What are Peudophyllidea?
A
- Tape worms of carnivores
- Eggs immature
3
Q
What are the larval stages of pseudophyllidea?
A
- Coracidium
- Procercoid
- Plerocercoid
4
Q
What are cyclophyllidea
A
- Tapeworms of large animals
- Eggs contain embryo
5
Q
What are the larval stages of cyclophillidea
A
- Cysticercoid
- Cysticervus
- Strobilocercus
- Coenurus
- Hydatid cyst
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
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
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
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
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
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
12
Q
What is used to treat taeniasis?
A
Praziquantel
13
Q
List the preventative measures for taeniasis
A
- Cook meat sufficiently
- Hygiene and sanitation
- Strict meat examination
- Prevent faecal contamination of animal feed
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
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
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
17
Q
How is taeniasis in humans treated?
A
- Surgical removal of cysticercus
- Steroids
- Anticonvulsants
- Antiparasitic antibiotics
18
Q
How can you differentiate between T. solium and T. saginata
A
- Scolex
- Number of branches in gravid segment
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
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
21
Q
What are the divisons of protozoa?
A
- Flagellates
- Ciliates
- Amoebae
- Apicomplexa
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
23
Q
Explain the importance of protozoa
A
- Zoonotic
- In veterinary medicine
- Specific and zoonotic
- Economic importance
- Many species affected, can have severe consequences
24
Q
List the important protozoa
A
- Eimeria
- Isospora
- Cryptosporidium
- Toxoplasma
- Neospora
- Balantidium
- Sprionucleus
- Giardia
- Trichomonas
- Histomonas
25
What are the causative agents of coccidiosis?
- Eimeria spp.
| - Isospora spp.
26
Describe Eimeria oocysts
- Tetrasprocystic-dizoic
- 4 sporocysts
- Each sporocyst has 2 sporozoites
27
Describe Isospora oocysts
- Disporocystic-tetrazoic
- 2 sporocysts
- Each contains 4 sporozoites
28
Describe coccidiosis in poultry
- 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
29
Describe the control of coccidiosis
- Coccidiostats
- Coccidiocides
- Vaccines in poultry
- Biosecurity
- Disinfection
- Colostrum
30
Describe coccidiosis in lambs
- 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
31
Describe the clinical signs of Cryptosporidiosis
- Sticky, fetid diarrhoea
| - Dehydration
32
What is unusual about the life cycle of cryptosporidium?
Can carry out self-infection
33
Describe Cryptosporidiosis
- Caused by Cryptosporidium spp
- Many hosts
- Some specific, others wide host range, some zoonotic
34
What are the important species of Cryptodporidium and their hosts?
- C. parvum - most mammals, zoonotic
| - C. hominis - person to person
35
Describe Cryptosporidiosis in humans
- 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
36
Describe the treatment of cryptosporidiosis
- No vaccine
- No treatment
- Usually self limiting
37
What is the main cause of Neosporosis?
Neospora caninum
38
What is the importance of Neospora caninum in cattle?
- Abortion
- Epidemic following dog faeces contamination
- Endemic/sporadic through recrudescence of tissue cysts during pregnancy
- Vertical transmission maintains infection in herd
- Offspring permanently infected
39
Describe neosporosis in dogs
- 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
40
How is neosporosis diagnosed?
- Abortion mid-late pregnancy
- Necropsy of foetus and detection by immunohistology/PCR
- Serology of dam (or foetus) or dog
41
How can neosporosis be controlled?
- No vaccine
- No treatment
- Do not let dog eat placenta or raw beef
- Do not allow defaecation in fields with cattle
42
Describe Trichomoniasis
- 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
43
Describe the diagnosis of trichomoniasis
- Smear and view under LM
- Distinctive appearance
- Large "head", lots of "tails"
44
Describe histomoniasis
- Mainly caused by Histomonas meleagridis
- Blackhead in turkeys
- Amoeboid in tissues, flagellated in gut lumen
- Unusual life cycle - hyperparasitic
45
Describe the life cycle of Histomonas meleagridis
- Intemediate stages infect nematodes of birds (e.g. Heterakis gallinarum)
- Eaten by bird
- Infect ovaries
- Oocysts shed in eggs of worms
- Hyperparasitic
46
Describe the clinical signs of histomoniasis
- Severe necrosis of caecae and liver
- Yellow diarrhoea
- Listless
- High fatality
- Diagnosis at necropsy
47
Describe the control of histomoniasis
- Worming
| - Biosecurity
48
Describe Balantidium spp
- 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
49
Disease the clinical signs of Balantidiosis
- Diarrhoea in humans mainly in tropics (also other primates)
- Diarrhoea in pigs (most likely opportunistic pathogen)
- Diarrhoea in various reptiles
50
Describe the treatment and control of balantidiosis
- Metronidazole treatment
| - Prevent with better hygiene
51
What causes Spironucleosis, where is it found and how is it transmitted?
- Sprionucleus spp
- Live in gut
- Transmitted via faeces
52
What are the clinical signs of spironucleosis
- Diarrhoea
- Depression
- Weight loss (all 3 in birds and fish)
- Skin lesions in fish - "hole in the head" disease
53
Describe the treatment and control of spironucleosis
- Improved hygiene
- Less crowding
- Metronidazole
54
Describe the life cycle of protozoa
- 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
55
What is a sporozoite?
The infectious unit that intiates infection inside the host intestinal cells soon after the ingestion of the oocyst
56
What is a trophozoite?
The intracellular stage of Eimeria sporozoites after they enter the cell and change their morphology. Divides producing merozoites
57
What is a tachyzoite?
- 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
What is a bradyzoite?
- Slow replicating dormant stafe
- Group of bradyzoites surrounded by thick capsule forming cyst
- Under stress, reactivate and convert to tachyzoite
59
What is sporulation in protozoa?
- Occurs outside host
| - Is process of maturation of undifferentiated oocyst to differentiated (containing sporozoites)
60
Describe enzystation in protozoa
- Occurs inside host (Toxoplasma)
- Or outside (Entamoeba or Giardia)
- Process of transformation of free-replicating, vegetative stage to dormant cyst stage
61
Describe the general mechanisms of pathogenesis in protozoa
- 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
Explain the significance of encystment in protozoa
- Hardy, survive in environment
- Metabolically inactive so drug ineffective
- Resistant to many disinfectant
- Infectious
- May be detected in faeces and used for diagnosis
63
Describe the importance of tachyzoites and bradyzoites in toxoplasmosis
- 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
What are the clinical signs of toxoplasmosis
- Tissue damage
- Abortion
- Malformed young
- Systemic/neurological disease in humans
- In cats chronic inflammatory lesions e.g. in eyes
65
Describe treatment and control of toxoplasmosis
- 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
What is the main cause of toxoplasmosis?
- Toxoplasma gondii
- Cats are the only definitive host - no disease
- Oocysts shed by younger cat mostly
67
Describe the life cycle of Toxoplasma gondii
- Rodent intermediate hosts
- Tissue cysts
- Eaten by cats
- Shed oocysts
68
What is Johnson Reid lesion scoring and what is it used for?
- Lesion scoring in coccidiosis
- Based on gross intestinal lesions in infected birds
- Determine pathogenicity of coccidia
- Measure effects of anti-coccidials and vaccines
69
List the important species of Oesophagostumum and their host species
- Radiatum (cattle)
- Columbianum (cattle and sheep)
- Venulosum (sheep and goats)
- Dentatum (swine)
- Quadrispinulatum (swine)
70
Describe the epidemiology of Oesophagostumum spp
- Common in wet temperate climates
- Hypobiosis/Spring rise occurs to infect young animals
- Dentatum common in pigs
71
Describe the epidemiology of Oesophagostomum radiatum
- Cattle
- PPP 35-40 days
- Typical strongyloid life cycle
- L1 free living, L3 infectious
- Large intestine
72
Describe Oesophagostomum radiatum in young animals
- Severe disease in calves
- Anorexia, anaemia, oedema
- Very dark diarrhoea due to blood present
- Weight loss
- Death
- Immunity quickly built up
73
Describe Oesophagostomum radiatum in older animals
- 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
Compare Ostertagia and Oesophagostomum in cattle
- Oesophagostomum radiatum has strong protective immunity
- Ostertagia immunity takes loong time to develop, sterile immunity never reached
- Different regions of GIT
75
Describe the treatment of Oesophagostomum radiatum
- 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
Describe Oesophagostomum of sheep
- 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
Describe the appearance of adult Oesophagostomum
- Bottle neck appearance
- Sheath tail long
- Rounded head
- 32 gut cells
- 726-923um
- Male bursa
78
Describe the clinical signs of Oesophagostomum in young lambs
- Failure to thrive
- Scouring
- Weakness
79
Describe the treatment for Oesophagostomum in sheep
- Levamisole/triclabendazole
| - 56 day meat withdrawal period
80
Describe Oesophagostomum in pigs
- Dentatum (distal colon), quadrispinulatum (caecum, proximal colon)
- May coexist in same animal
- Usually not a clinical problem
81
Describe the clinical signs of Oesophagostomum in pigs
- Weight loss
- Signs of oedema (pot belly)
- Intestinal nodules
82
Describe the treatment of Oesophagostomum in pigs
Ivermectin
83
Describe diagnosis of Oesophagostomum in ruminants and pigs
- Eggs in faeces
| - Nodules on necropsy
84
Describe the appearance of the anterior of Oesophagostomum spp
Bottle neck anterior
| - Cephalic and cervical vesicle cause this appearance
85
List the important species of Trichuris and their hosts
- Discolor (cattle)
- Felis (felids)
- Loporis (rabbits)
- Muris (rats)
- Ovis (cattle, sheep)
- Trichiura (primates)
- Suis (swine)
- Vulpis (canids, sometimes humans)
86
Describe the epidemiology Trichuris spp
- 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
Describe the clinical signs of Trichuris infection
- 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
Describe how Trichuris leads to psuedonecrotic membranes in pigs
- Worm under tissue
- Continual movement searching for food
- Acts like knife cutting in all directions
89
Describe immunity to Trichuris
- 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
Describe the diagnosis of Trichuris
- Females lay eggs sporadically so McMaster not reliable
- Eggs in faeces easily recognisable
- Necropsy shows worm and muco-haemorrhagic colitis
91
Describe the treatment and management of Trichuris
- Benzimidazoles or levamisole
- Thorough cleaning and disinfection
- Common anthelmintics e.g. fenbendazole
92
Describe Trichinosis in humans
- 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
Describe Trichuris ovis
- 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
Describe Trichuris vulpis
- 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
Describe the eggs of Trichuris
- Bioperculated
- Resistant
- Thick shell
- Tan coloured
- Lemon shaped
- Medium size
96
Describe the external features of adult whip worms
- 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
Explain why dogs in kennels are at risk of reinfection after deworming
- Female produces 2000 eggs per day
- Hard to kill
- Can stay in environment for years
98
Describe the epidemiology of Oxyuris equi
- Pinworm
- Common, relatively benign
- Parasite of stabled horses (eggs do not survive well outdoors)
- Very visible on back of horses
99
Describe the appearance of Oxyuris equi eggs
- D shaped (one side flatter than the other)
| - Single mucoid plug
100
Describe the life cycle of Oxyuris equi
- 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
Describe the disease caused by Oxyuris equi
- Anal pruritis and skin excoriation and/or myiasis
| - Diagnosis using sellotape
102
Describe teh treatment of Oxyuris equi
- All anthelmintics effective
| - Topical anti-inflammatories to decrease pruritis
103
Describe the appearance of Strongylus vulgaris
- Large
- Leaf crown and tooth plates
- 2cm
104
Describe the epidemiology of Strongylus vulgaris
- 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
Describe the life cycle of Strongylus vulgaris
- 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
Describe the diagnosis of Strongylus equi
- 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
How is Strongylus vulgaris treated?
- Anthelmintics
- Benzimidazoles and avermectins kill larvae and adults
- Pyrantel kills only adults
108
Describe the appearance of Strongylus equinus
- Large strongyle
- Larger than vulgaris (4-5cm)
- Leaf crown
- Tooth plates (one large, 2 smaller)
109
Describe the epidemiology of Strongylus equinus
- PPP 9 months
| - Hepatopancreatic strongyle
110
Describe the life cycle of Strongylus equinus
- 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
Describe the disease caused by Strongylus equinus
- Mild colic
| - Some pancreatic disease adn primary diabetes mellitus
112
Describe the appearance of Strongylus edentatus
- Larger than vulgaris
- 4-5cm
- Leaf crown
- No teeth plates, just buccal capsule
113
Describe the migration of Strongylus edentatus
- Hepatoperitoneal
- Through liver via peritoneum
- PPP 11 months
114
Describe the life cycle of Strongylus edentatus
- 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
Describe the clinical signs caused by Strongylus edentatus
- Colic due to liver disease or peritonitis
116
Describe the epidemiology of Cyathostomes
- Overwinter
- Only susceptible to treatment in adult stages
- Hypobioses at L3
117
Describe the life cycle of Cyathostomes
- 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
Describe the clinical signs of Cyathostomes
- Colic
- Weight loss
- Diarrhoea
- Wasting
- Death
119
Describe the treatment of Cyathostomes
- 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
Describe general equine parasite management
- 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
Explain how mixed grazing can be useful in equine parasite management
- 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
How can an unsporylated oocyst be distinguished from a sporylates one?
Sporocyst containing sporozoites will be visible in a sporylated one
123
Describe the appearance of a schizont
- 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
What are the important factors in the trnamission of coccidiosis?
- Poor sanitation
- Poor management
- Overcrowding
- Moisture
- carriers (older animals mixed with younger)
- Extreme resistance of oocysts in environment
- Formites
- Insects/birds
125
Explain the pathogenesis of haemorrhagic coccidian species
- Coccidiosis (Eimeria, Isospora)
- Direct damage to gut mucosa
- May also be secondary bacterial infection
126
Explain the pathogenesis of mal-absorptive coccidian species
- 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
Discuss in general terms the economic importance of coccidiosis to the chicken industry
- 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
Describe the oocysts of Cryptosporidium
- Very small
| - 4 naked sporozoites
129
What are the intermediate stages of Toxoplasma for the FINAL host?
- Bradyzoite cysts
- Tachyzoites
- Small oocysts
- 2 sporocysts each with 4 sporozoites
130
What are the intermediate stages of Toxoplasma for the INTERMEDIATE hosts?
- Bradyzoite cysts
- Tachyzoites
- Small oocyst (2 sporocysts, 4 sporozoites in each)
131
Where does the asexual phase of Toxoplasma's life cycle take place?
- Many different hosts
| - (Intermediate hosts)
132
What disease is caused by Sarcocystic neurona
- Protozoan
| - Equine protozoal myeloencephalitis
133
What is unusual about the life cycle of Neospora caninum?
- 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
What are the important features to consider in faecal examination?
- VOlume
- Colour
- Composition and consistency
- Presence of abnormal structure
135
Describe the faecal smear technique, giving pros and cons
- 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
Describe the faecal sedimentation technique
- 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
Describe the simple faecal flotation method
- 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
Describe the qualitative faecal flotation method
- 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
Describe the larval culture method of faecal examination
- Diagnose nematode infection
- Identify L3 of nematodes in faeces
- Provide suitable conditions for hatching eggs and larval development to L3
140
Describe how immature worms can be separated from faeces
- 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
Describe the Baermann technique to separate larvae from faecal material
- 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
