PID Flashcards
1
Q
What are Koch’s Postulates?
A
1) The microorganism must be found in abundance in all organisms suffering from the disease, but not healthy organisms
2) The MO must be isolated from a diseased organism and grown in pure culture
3) The cultured MO should cause disease when introduced to a healthy organism
4) The MO must be reisolated from the innoculated, diseased experimental host and identified as being identical to the original causative agent
2
Q
Is an abscess defined as acute or chronic infection?
A
Because of the predominance of neutrophils usually acute - but can be persistent
3
Q
What is the pathogenesis of FMD
A
The causative virus infected epithelial cells and causes lytic infection
4
Q
What pathogens cause atrophic rhinitis
A
Bordatella bronchiseptic (primary) and Pasteurella multocida (secondary - toxigenic type D strain)
5
Q
Describe the pathogenesis of atrophic rhinitis
A
The seondary infection of P.multocida leads to production of heat and trypsin-like labile toxin which reduces osteoblastic activity and increases osteoclastic activity - which causes loss of turbinate structure
6
Q
Give 3 potential agents of kennel cough
A
- B.bronchiseptica
- Canine parainfluenza virus type 2
- CAV2
- Canine respiratory coronavirus
- Canine mycoplasma
7
Q
Describe type 2 meningitis is pigs
A
- Caused by strep suis
- Spreads like a respiratory disease but can enter the CSF via the bloodstream
- Can have a carrier state in the tonsils of immune pigs
- Most common in the post-weaned pig
8
Q
Describe the pathogenesis of Johne’s disease in cattle
A
Caused by a mycobacterium that is quite resistant to host defences so causes a chronic inflammatory response
The organism is ingested by macrophages and causes recruitment and accumulation of them - mainly in the ileum - leads to characteristic thickening - leads to malabsoprtion, diarrhoea and progressive weight loss
9
Q
What type of immunity is stimulated by FIP
A
Type III hypersensitivty - Ab-Ag complexes that cause vasculitis
10
Q
What are the 6 potential mechanisms of parasite harm
A
1) Mechanical (obstruction) - e.g. ascarids
2) Traumatic (e.g ancylostomas - blood sucking hookworm)
3) Inoculation - e.g. tick
4) Malabsorption - e.g. Giardia affecting the epithelium
5) Malnutrition - helminths using host nutrients
6) Pressure and atrophy - eg. cestode larval cysts
11
Q
Define definitive host in terms of protozoa
A
Many protozoa divide asexually - so their vertebrate host is called the definitive host
12
Q
Define definitive and intermediate host (parasites)
A
Definitive host (usually vertebrate) - where the adult or sexual stages of the parasite occur Intermediate - where the intermediate/immature/larval stage occurs (can also see asexual multiplication)
13
Q
Define terminal hosts and give an example
A
An intermediate host that does not allow transmission to the definitive host
E.g. humans and E.granulosus
14
Q
Define paratenic host
A
A host in which the parasite is carried but doesn’t develop - e.g. mouse and toxo
15
Q
GIve examples of parasites which rely on the following as intermediate hosts:
- flies
- ticks
- fleas
A
flies - thelazia spp (eye worm)
ticks - babesia, anaplasma, rickettsia
fleas - dipylidium caninum
16
Q
Describe the life cycle of Dicrocoelium (ruminant - 2 intermediate hosts)
A
Snail is the first intermediate host - it multiplies asexually and kills the snail, which produces a slime ball full of larvae
Ants ingest the slime ball and the larvae move to the CNS and when the temperature rises, the cysts they form expand and cause spastic paralysis -so the ants grip onto blades of grass to be eaten by cattle
17
Q
Name a parasite that has a direct life cycle
A
Ostertagia ostertagi
18
Q
How is Leishmaniosis transmitted
A
Via the sand fly
19
Q
Differentiate:
- Prokaryotes
- Helminths
- Arthropods
A
- Prokaryotes are single eukaryotic cells
- Helminths - include flatworms (trematodes and cestodes) with no body cavity, and nematodes (roundworms) with a body cavity
- Arthropods - insects, ticks and mites
20
Q
Describe the larval moults of nematodes
A
The life cycle has 4 larval moults - the 3rd stage is always the infective stage
21
Q
What is hypobiosis and which parasites can undergo it
A
It is temporary cessation in development, usually in response to adverse environental conditions (remains sexually immature until more favourable conditions arise)
Occurs in nematodes
22
Q
Discuss copulatory bursae and spicules in nematodes
A
Nematodes are sexually dimorphic
Males - can be bursate or non-bursate (which is key for species identification) - the copulatory bursa around the anus is used to hold the female during mating
Males have spicules (2) to guide the sperm during mating
Males - intestines communicate with reproducitive system - not the case in females
23
Q
What is the pre-parturient rise
A
This is where you often see increased numbers of nematode eggs in the faeces of animals around parturition - may link to immune competition
24
Q
Describe the characteristics of trematodes
A
- Hermaphrodites
- Have oral and ventral suckers
- Tegument covered in spines that absorbs most of the nutrients (although they do have a simple oral cavity too)
- Can undergo very fast asexual reproduction (usually kills intermediate host)
25
Describe the characteristics of cestodes
- The have a scolex (head) - with attachment organs (suckers) - some species also have hooks
- Segmental chain (proglottides)
- Form cysts inside the intermediate hosts (when eggs are ingested)
26
Describe the different types of cysts formed by cestodes
- Cysticercus - fluid filled cyst with a single invaginated scolex (e.g. taenia solium)
- Coenurus - similar to cysticercus but with several invaginated scolices
- Strobilocercus - evaginated scolex and there is a chain of asexual proglottids attached to the cyst
- Hydatid - large and fluid filled with a germinal epithelium and invaginated scolices
- Cysticercoid - single evaginated scolex embedded in a small, solid cyst (typically in very small intermediate hosts such as arthropods)
27
What is a gravid proglottid
This links to cestodes (tapeworms) - proglottids are their segments - a gravid one is fully mature and contains eggs that can be shed (reproductive organs have essentially dissolved)
28
What are the characteristics of bovine PGE?
- Diarrhoea and weight loss (with clinical disease)
- Loss of production (with subclinical disease)
- Seasonal appearance of the diseases linked to environmental condition and parasite life cycles
- Hypoalbuminaemia (low protein)
It is a particular problem with grazing and organic herds
Associated with many species of the GI nematodes - but Ostertagia is the main one
29
```
What are the main GI nematodes that affect:
- Abomasum
- SI
- LI
(cattle)
```
Abomasum - Ostertagia, haemonchus and trichostrongylus
SI - Nematodirus (but also cooperia, strongyloids and trichostrongylus)
LI - oesophagostomum
30
Briefly describe the life cycle of a GI nematode
Direct and non-migratory - cattle become infected by ingesting infective L3s from pasture
L3 develop from eggs (shed in faeces) on the pasture
After ingestion -the L3s exsheath in the rumen and then moult further in the abomasal glands to L5 -they then emerge to become sexually mature on the mucosal surface
PPP = 21 days (but can undergo hypobiosis)
31
Where is nematodirus (adult) found in the cow?
In the glandular, fundus part of the abomasum
32
What is the appearance of ostertagia?
Slender, reddish brown worms, around 1m long
Short buccal cavity
Males have brown spicules with 3 hooked processes
Female tail tapers gradually with a rounded tip
33
What factors can extend the PPP in ostertagia?
Overwintering -the L3 sheath protects it from the harsh environmental conditions so they can survive until spring on the pasture
Hypobiosis - arrested development in the host (EL4) when there are harsh environmental conditions
34
What are the main pathogenic effects of ostertagia
- The developing parasites cause a reduction in the functional gastric gland mass
- In particular the parietal cells, which produce HCl, are rapidly replaced by undifferentiated, non-acid secreting cells
- Can lead to a thickened hyperplastic gastric mucosa
- Macroscopically it appears as a raised nodule with a visible central orifice (can coalesce in heavy infections)
35
What is the difference in presentation of type I vs type 2 ostertagia disease
Type 1 - usually seen in calves grazed intensively during their first grazing season -due to larvae ingested 3-4wks previously - usually high morbidity low mortality
Type 2 - occurs in yearlings, usually in late winter or following their first grazing season - due to development of previously hypobiosed larvae - prevalence is generally lower but the cases tend to be more serious
In both cases the main clinical signs of profuse watery diarrhoea and considerable loss of bodyweight (if severe)
36
The basic epidemiology of Ostertagia in cattle is similar to which parasite in sheep?
Teladorsagia
37
Describe the development of immunity against ostertagia in cattle
Acquired immunity is slow to develop - calves often don't have a significant level until the end of their first grazing season
Housing over winter may also allow the immunity to wane by the following spring
But usually during this second spring immunity is rapidly re-established, and usually by second and third year of grazing, adult stock in endemic areas are highly immune to reinfection (but remember they can still shed -- although generally lower numbers than calves)
38
Describe how the epidemiology of ostertagia differs in beef cows (compared to dairy)
In beef herds calves usually graze with their mothers, and often the spring mortality of L3s has occured before the calves ingest a significant amount of grass
Mothers eat most of the grass and are immune - with sloer production of eggs - so spring disease (type 1) is unlikely
Autumn calvers turned out in spring with the mothers - risk is slightly higher but mothers will still eat most of the grass
39
How would you diagnose Ostertagia infection in cattle?
- Clinical signs (inappetence, weight loss and diarrhoea)
- The season (type 1 vs type 2)
- Grazing history - in type I disease, the calves have been usually set-stocked in one area for several months; in contrast, Type II disease often has a history of calves being grazed on a field from spring to mid-summer, then moved and brought back to the original field in the autumn
- FEC (type 1 >1000epg, type 3 is more variable)
- Plasma pepsinogen levels (>3 - normal is 1)
- PM exam of abomasum
40
What is the main treatment for ostertagia?
Type 1 - responds well to a standard dose of any BZ, levamisole or avermectins/milbemycins - these are all effective against developing larvae and adult stages
Type 2 disease - requires drugs that are effective against arrested larvae as well as developing larvae and adult stages
Modern BZs and ML will work
The offending pasture can be grazed by sheep or rested until the following june to rid it of any L3s
41
What are the pros and cons of the 'dose and move' strategy for ostertagia treatment
Calves are dosed and then moved in early summer (becasue in early summer they have been infected but won’t have disease yet because the L3 levels won’t be high enough) - however, this will not control for type 2 disease, and increases the risk of anthelmintic resistance
42
What strategies can be used to allow young cattle to develop immunity to ostertagia but not get clinically ill?
- Use anthelmintics to limit pasture contamination during optimal larval growth periods (spring and summer)
-Rest pastures of graze with sheep until most of the existing L3s have diet off
(or a combo)
43
How might prophylactic anthelmintic treatment be used to combat Ostertagia
Giving anthelmintics on 2 or 3 occasions between April and July to minimise the number of eggs deposited on the pasture
(at 3 week intervals - the number depends on how early they are turned out -may be longer interval if longer acting anthelmintics are used)
Could also use rumen boluses
44
What is the relationship of lice with the host?
They reside on the host for almost their entire lifespan, only leaving it to infect another host of the same species
45
What are the 3 main lice species that affect dogs
- Heterodoxus spiniger (C)
- Linognathus setosus (S)
- Trichodects canis (C)
46
What are the main differences between chewing and sucking lice
Sucking lice (anoplura) - only infect mammals
- Tend to be larger
- Head smaller than thorax
- Legs with robust claws
- Mouth shaped to pierce and suck
- Move slowly
Chewing lice
- Mainly infect birds
- Flat body, head larger than thorax
- Mouth shaped to chew
- Legs with robust claws
47
What is the main louse to affect cats and what are its characteristics
Felicola subrostratus
Has a point triangular head, localises on face, ears and neck
Life cycle 30-40days
48
What are the 3 main lice affecting small ruminants and how might you differentiate them?
- Bovicola ovis - localises on shoulders - red/brown in colour (3mm long) - head as wide as it is long and ventral mouth
- Bovicola caprae - similar to above - localises to shoulders and back and causes intense irritation
- Linognathus pedalis - blackish, 2.5mm long, 2nd and 3rd pair of legs larger than the first - localised on legs and abdomen
49
What disease can be transmitted by the cattle louse linognathus vituli (S)
Anaplasmosis, theileriosis and dermatomycosis
50
What are the 5 major lice affecting cattle and how might you differentiate them?
- Bovicola bovis (C) - red and brown with dark stripes on abdomen - head as wide as it is round - localises on head and dorsum - causes intense irritation
- Haematopinus eurysternus - yellow-brown with dark stripes on the abdomen 3-5mm long - small and pointy head - mainly on head, horn base and tail
- Haematopinus quadripertusus - dark with obvious sternal plaques - legs of equal length and robust hooks
- Linognathus vituli - yellow brown louse (2.5mm), short 1st pair of legs
- Solenopotes capillatus - very small, brown, short first pair of legs
51
Describe the most common louse of pigs
Haematopinus suis
Large (5-6mm), brown/grey with dark patches on the side of the abdomen, long and pointy head
Vector of rinderpest, smallpox and eperythrozoon suis
Localises to skin folds of neck, cheeks, sides and legs
Short life cycle (5-20d)
52
What is the main louse found in horses
Haematopinus asini
Yellow-brown, long and slender head, 3mm long
Localises on head, legs and chest
53
What are the characteristics of sheep PGE?
Diarrhoea and weight loss with clinical disease
Or decreases productivity with subclinical disease
Seasonal appearance
Hypoalbuminaemia
54
What are the 3 most important GI parasites in sheep?
| and where are they found in the GI tract
Teladorsagia circumcincta (abomasum), haemonchus contortus (ab.) and Naematodirus battus (SI)
55
What is characteristic about naematodirus battus (in terms of appearance)
Has a cephalic inflation (bubble) found only in this genus
56
Describe the general life cycle of sheep GI parasites
- Direct and non-migratory
- Sheep ingests infective L3s from pasture
- The larvae moult (after ex-sheathing) in the GI tract mucosa and emerge to the surface as L5s
- Females lay eggs that are excreted in the faeces and develop to L3s on the pastrure (dependent on humidity and temperature)
Also has links to hypobiosis and the pre-parturient rise
57
Why is the pre-parturient rise important in sheep
Because the eggs they shed become the main source of infection for lambs as the peak continues through lactation
If severe it can also cause a reduced lactation
58
What is the appearance of Teladorsagia circumcincta
Adults are slender, reddish brown worms around 1cm long
Males have a well developed bursa and long thin spicules
split into two branches at the end
59
Describe the generally epidemiology of Teladorsagia in sheep
Similar to Ostertagia in cattle - but the PPR is key for contaminating pasture and causing disease in lambs
Hypobiosed and overwintered L3s may play some role in early lamb infection - but likely only if the lambs are >4-8wks old in May-June
60
Describe the difference in epidemiology of Teladorsagia in a clean pasture vs a dirty one
Clean pasture - no overwintered larvae so the only source of infection is the resumed development of hypobiotic larvae that lead to PRR in faecal egg counts
Tend to get type 1 disease peak (not autoinfection) in lambs from July
Contaminated pasture - also have the overwintered L3s - may have an earlier infection peak or two peaks of infection
Type II disease is not common in sheep
61
What is the pathogenesis for Teladorsagia in sheep
- A reduction in the acidity of the abomasum (as a direct consequences of the reduction in numbers of acid and pepsin secreting cells due to damage by parasites)
- pH therefore rises - which inhibits pepsinogen to pepsin activation
- Lose the bacteriostatic effect and increase permeability of gut wall
- See pepsinogen in the circulation and loss of plasma proteins to the gut
62
How would you diagnose Teladorsagia in sheep?
- Clinical signs - inappetance, weight loss and diarrhoea
- The season
- Grazing season
- Faecal egg counts
- Plasma pepsinogen levels
- PM of abomasum
63
Describe the appearance of the sheep parasite haemonchus contortus
Adult worms can reach 2-3cm in length
In fresh specimens, the white ovaries of the females winding spirally around the blood filled intestines produce a 'barbers pole' appearance
The male has asymmetric lobes and barbed spicules
64
Describe the epidemiology of haemonchus contortus
It is usually suited to warmer climates than the UK - so generally has a single annual cycle - also linked to humidity and rainfall
Infective L3s that develop from eggs deposited by ewes in spring tend to become arrested and do not complete development until the following spring
65
Describe the process of self cure for Teladorsagia in sheep
This is where a large number of adult worms are expelled at the same time - via IgE mediated hypersensitivity
It follows infection by a large number of L3s (often a period of intense rain)
66
Describe the pathogenesis of haemonchus contortus
Causes acute haemorrhagic anaemia due to the blood sucking habits of the worms
This can be chronic and consistent, or in some cases hyperacute and cause death within a week
67
What are the clinical signs of haemonchus contortus infection
Anaemia (pale mm and sclera), loss of condition, lethargy and degrees of oedema (bottle jaw)
If chronic may see weight los, weakness and lethargy
68
How do you diagnose haemonchus contortus
- History and clinical signs
- FEC
- Necropsy
69
Describe the appearance of naematodirus battus
Slender adults, up to 2cm in length
Have a small but distinct cephalic vesicle
Spicules of the male are fused and much longer than the bursa
Eggs are much larger than those of strongyles
70
Describe the lifecycle of nematodirus battus
Direct lifecycle
Pre-parasitic phase is unusual - development of L3s takes place within the egg shell
Hatching eggs requires a long period of chill followed by a mean day/night temp of >10
So most eggs from a season will remain on pasture unhatched until the next year
Ingested L3s penetrate the mucosa of the SI and moult - inhabit the lumen as L5s
PP - 14-16d
Very large recognisable eggs
71
What is so key about the epidemiology of naematodirus battus
The free-living stages, especially the eggs containing L3s, can survive on pasture for up to 2 years
And the critical hatching requirements mean that there is often a simultaneous appearance of large numbers of larvae - usually in May-June
Considered a lamb to lamb disease - ewes don't really play any role
May see a second peak in later summer/early autumn if the weather conditions are right - if not the larvae will over winter
72
What are the clinical signs of naematodirus battus infection
- Yellow-green diarrhoea (can start during the PPP)
- As dehydration proceeds, the affected animals become thirsty
- Black colour of intestines on PM
- Reduced growth and lethargy
All linked to disruptuon of the mucosa and damage to villu and inflammation caused by the larvae moulting
73
How do you diagnose naematodirus battus
FEC aren't that ueful because clinical signs appear during the PPP
Best to use grazing history, clinical signs and PM if possible
Can assess faeces for characteristic eggs, or do a larval culture
74
What are the 6 major ways to reduce AR in sheep GI parasites
- Test for it - FERT, inhibition assays
- Use effective quarantine procedures for new sheep
- Use anthelmintics sparingly to reduce further selection pressures
- Dose correctly - for weight and check that the equipment works properly
- Avoid broad spectrum anthelmintics if you can
- Keep worms in refugia to dilute resistant populations
75
What are the 3 main ways of testing for AR in sheep parasites?
- FEC reduction test on samples taken before and 7-14days after treatment
- Egg hatch assay with BZs as they should kill eggs
- Larval inhibition assay
76
What are the 3 major classes of anthelmintic used to treat sheep parasites
- Group 1 - benzimidazoles
- Group 2 - Imidothiazoles/tetrahydropyrimidines
(levamisole, pyrantel, morantel)
- Group 3 - Macrocyclic lactones/milbemycins (avermectins)
77
What anthelmintics are effective/not effective against Teladorsagia
- There is resistance developing in all classes
| - Can use monepantel (but resistance is already developing) - but should do an AR test first (try and use others first)
78
What anthelmintics are effective/not effective against Naematodirus battus
```
Group 1 (BZs) - variable - tends to be better against immature stages
Group 2 - (IM) - highly efficacious against larvae and adults
Group 3 - Avermectins have variable efficacy
```
79
What are the two main anthelmintics used to treat haemonchus contortus
Closantel and Nitroxynil
80
What are the general prophylactic treatments given to sheep for PGE
- Ewes dosed at 4th month of pregnancy
- Can dose them at lambing and then again 4-5wks later but can contribute to AR - better to leave a proportion in refugia
- Lambs should be treated at weaning and moved to clean grazing
- If not possible - then give prophylactic treatment monthly into autumn
