Coccidosis Flashcards
1
Q
Coccidia
A
- Coccidiosis: name of the disease produced
- All need to have at leasr one lifecycle
- Protosomes: single celled organisms
- Toxoplasma spp. (cyst)
- Eimeria spp. (Non-Cyst)
2
Q
Eimeria spp.
A
Eimeria Species
- Broad range but are completely species specific (only affects cattle, birds, sheep or reptiles etc)
- Can affect almost all livestock but are HOST SPECIFIC!
One kind can only infect sheep
One kind can only infect chicken
So on…..
- Not zoonotic, not transferrable between species & none affect humans
- ↑ prevalence in chickens due to ↑ stocking densities large economic impact (>£2billion/year)
- 62 billion born a year–> CAN INFECT VAST NUMBER OF POULTRY
3
Q
Chickens and Eimeria spp.
A
Problem:
- The settings that chicken are in are cramped and in close quarters
- One host will host the replication ofthe parasite and then the poultry surrounding will get sick from infection
- Backyard system would probably get an infection, but you wouldn’t see disease
- Vaccines can include all 7 but there is a cost issue, with broilers you would want to include the 3-5 species of coccidia that you would see
- A third of antimicrobials sold for use in UK agriculture arecoccidiostats!! –> becoming a big issue
- ranked in top 20 veterinary disease/pathogens globally based upon impact on the poor –> If you cant afford to have cattle/pigs and only can get chickens, large impact
4
Q
Life Cycles of Coccidia
A
- Direct: goes from host to host of same host type e.g. Eimeria
- Indirect: has a definitive/ intermediate host, e.g. Sarcocystis
- Facultative: can do either, e.g. Toxoplasma
5
Q
Eimeria Life Cycle
A
- Sporulation occurs outside the host (requires several days and oxyfgen
- Must go through sporulation process to be infectious! It is a metabolic process
- In one egg (oocyst) you are looking at 8 parasites (sporozoites)- 2 sporozoites per sporocyst
- After sporocysts have been released from the oocyst in the gut through excytation, sporocysts will pass into intestines and the sporozoites will emerge
6
Q
Excystation
A
- Sporocyst excysting from oocyst, sporozoite emerging from sporocyst
7
Q
Sporozoite
(Eimeria)
A
- 1st motile stage of parasites life cycle will move around until it finds a cell to invade to initiate infection (in the intestine)
- Apical Complex: Shared by other parasites of the phylum
- Series of organelles that secrete proteins that allow that parasite to attach and invade
- when the sporozoite comes out of the sporocyst it will glide along the intestine until it finds a cell to invade
- at that point stands on its head and drives itself into the cell
- depending on parasite actinomyosin is a pretty quick process (about 10-15 seconds)
- parasite basically holds on a pulls itself into the cell
- once it is in the cell it become a Trophozoite and undergoes a round of asexual replication to form a Schizont
- within the schizont it produces merozoites and those are the second motile stage of the parasites life cycle
8
Q
Schizogany
A
- asexual reproduction by multiple fission, found in some protozoa, especially parasitic sporozoans
- The parasite undergoes asexual replication in the schizont
- the schizont will end up being packed with merozoites, those will invade neighboring cells and continue the infection process
- They have several rounds of this asexual replication, the amount of rounds depends on the species! (either 3 or 4 rounds)
- After 3 or 4 rounds they differentiate into gametes (the sexual stage of replication) -male gamete packed with sperm and female macrogametes that are like ova
- male gametes will emerge and fertilize the female macrogamete
- from the zygote, secretes an oocyst wall and it is released into the environment through faeces!!
9
Q
Eimeria
Sporulation
A
- Non-infectious egg (oocyst) is excreted environment
- Oocyst sporulates (20-30um) outside of host & becomes infectious
- Conditions: temps >2 degrees, humidity and oxygen, takes several days (>2)
- –>a round of meiosis then mitosis –> 4 sporocysts (each containing 2 sporozoites)- so one oocyte contains 8 parasites & can survive environment for long periods of time (6 months- >1 year)
10
Q
Eimeria Spp.
(Key Facts)
A
- Many Species (hundreds of thousands)
- Direct Life Cycle (no intermediate hosts or vectors)
- Faecal- oral transmission
- Sporulated oocyst 20-30 um (very small, stongyle is 80um) has 4 sporocysts each containing 2 sporozoites
- Host specific
- Self- Limiting:
3 or 4 rounds of replication
- then sexual replication before leaving the host
- not driven by the host immune response , parasite life cycle terminates!
- “hit and run” parasites, get in and replicate quickly
11
Q
Pathogenecity
A
- Some are more pathogenic than others
- But some effect is dose dependent (amt of parasite)
- 2 groups:
- Malabsorptive Group (Biggest issue in U.S. -E. maxima) - E. acervulina and E. maxima (low pathogenicity: E. mitis & E. praecox) - malabsorptive because later stages of the lifecycle (gametes, zygotes, oocysts) will actually cause problems in the gut). Form a physcial barrier that disrupts gut function and absorption of nutrients.
- also stimulate the production of mucus
- result in villous atrophy and mucoid enteritis–> decreased weight gain & increased feed conversion ratio
- these are located more at the top of the cells they invade (above nuclei)
- Haemorrhagic group E. tenella, E. necatrix & E. brunetti
- these cause much more damage in the gut
- will see haemorrhage, not just damage
- earlier stages of the lifecycle cause problems here (asexual)
- cells rupture to release merozoites causing deep erosions and haemorrhage –> bloody faeces, high morbidity, high mortality
- these go much deeper, even below the nuclei –> when they rupture tehy cause much more damage!!
12
Q
Invasion
A
Invasion
- Once in the gut, the Eimeria drive their way into the epithelial cells- fairly quick process (10-15secs)
- Dependent on parasite actionmyosin
13
Q
Schizogony (asexual reproduction)
A
Schizogony (asexual reproduction)
- Sporozoites–> trophozoites and undergo schizogony
- Schizonts produce large numbers of merozoites- which are released & invade other parts of the gut
- Number of times this cycle occurs is hardwired- different species have different numbers of rounds of
- asexual replication, its normally 3/4, after that they differentiate into male/ female gametes
14
Q
Gametology
A
Gametology
- ♂ gametes have 2 flagella
- fuse with ♀ –> zygote
- –> oocyst which is shed–> environment
15
Q
Summary of Eimeria Life Cycle
A
Summary
Eimeria replicate in intestine, are excreted into environment (oocyst) undergo rounds of sporulation and are the ingested and start life cycle again
- Direct life cycle
- Self-limiting- leave host once gamete
stage is reached so no residual infection
- Faecal-oral transmission
- PPP= 138hours (E. tenella)
16
Q
Seven Species of Eimeria Infect Chickens
A
- E. nefatrix= most pathogenic but fecundity & prevalence is low, therefore
- E. tenella is the most clinically relevant type as its highly pathogenic & common
(Fecundity= number of oocysts produced from number ingested)
17
Q
Pathogenecity
A
- Malabsorptive species- doesn’t cause much harm directly but large volume of parasites in gut villous atrophy and mucoid enteritis –> ↓ nutrient uptake–> ↓ weight gain & ↑feed conversion ratio
- Replicate in the superficial parts of the enterocytes (above the nucleus)
- E. maxima, E. acervulina, E. praecox, E. mitis
Haemorrhagic species- more serious- Cells rupture to release merozoites causing deep erosions & haemorrhage –>bloody faeces, high morbidity, mortality
- Replicate deeper within the enterocytes (under the nucleus) –> much deeper erosions
- E. tenella, E. brunetti, E. necatrix
Fecundity: if you are very pathogenic, you cant be too fecundic or else you will kill your host
3 worst species: Et-Ema-Ea . (due to balance of pathogenecity, fecundity, and prevalence)
**Wherever you find chickens you will find eimeria
18
Q
Diagnosis
A
- Usually see mixed infections! -It’s a fecal oral life cycle so you may see biological properties
- Can tell its eimeria but not the species
- Oocyst Morphology, Mucosal Scrapings- E.maxima oocysts=large, E.mitis= small, the rest are relatively indistinguishable from one another. Very specific parasites!! Still overlap though so not definitive
- Infection Location- each species also only infects one specific area of the gut i.e. E. acervulina only affects the duodenal loop, E. tenella is found in ceca, E. maxima in midgut etc. Can get some overlap
- Lesion Scoring- preferred method (cost-effective)- rate lesions in each section (of intestine and ceca) on a 0 to 4 scale, post mortem. White ladder lesions indicate E. acervulina . (in upper intestine)
- E. maxima- still malabosorptive, but is larger than other so can still cause damage (see replication near jejunum or ileum, orange mucus, some blood clotting)
- E. necatrix: Hemorrhagic species!! (distended intestine, blood, brown mucus, thickened wall in jejunum-ileum)
- Faeces Examination- blood & mucus present indicates haemorrhagic types & orange mucus is indicative of malabsorptive types
- PCR assays & Histopathology:
PCR assays are available, but they are not routinely used
- -nature of oocyst is very tough and it can be hard to get out DNA
19
Q
Control
A
Immunity - Eimeria= highly immunogenic–> very strong host IR- exposure to a few oocytes is enough to develop immunity but this is species specific, strain specific (Infection of E. maxima will only cause immunity to that ONE species!-can have strains of species as well. They are highly mutagenic)
-no cross protection & no passive immunity to chicks, any age suceptible (Really about the first time they are exposed. Pretty much every broiler chicken will be exposed at some time)
- Will stimulate a sterile immune response (innate). This is why they are a hit and run parasite. Once this immune response is created, any post infection of eimeria will be eliminated by the immune system
- species specific (E. maxima >>>> E. tenella)
Influencing Factors of coccidosis
- oocysts= ubiquitous & robust (resistant to bleach etc), Really large numbers excreted per gram/liter, They are REALLY tough. They can last through bleach and most chemicals, besides ammonia! Be careful with what you use
- large susceptible host population, Large population of naïve hosts
warmth and moisture is needed for sporulation (can dry out bedding to try and prevent)
- good ventilation, reasonable stocking density & good quality litter will ↓ risk. can dampen sporulation process but not stop the sporulation completely
- Immunity can develop slowly per ‘flock’: Flock wise it takes a while to develop.
- Chemoprophylaxis: ionophores, oher chemicals
20
Q
Chemoprophylaxis
A
- Ionophores= dominant (most important)- dose related response: suppress infection but don’t completely stop it so inclusion rate is important, ‘leaky’ so allows chickens to develop immunity
- Forms molecular pore on parasite–> Na+ enters–> parasite must pump the Na+ out, but it requires energy, once they have run out they try & balance out the concentration by absorbing water instead –> swollen parasite- much harder to invade cells/ replicate. the parasite life cycle can’t really continue, but the host can still build up an immune response by recogntion of the parasite
- How we include in diets is important as they are toxic
- Highly toxic particularly to species such as horses (very susceptible!)- safety precautions regarding litter
- Classed as antibiotics (ZFAs-zootechnical feed additives/MFS- medicated feed supplements)- so there’s a big drive to ↓ their use
- Withdrawal period: 3-5 days
- “leaky” –> ISSUE
- Other chemicals = (anticoccidials) all or nothing (kill parasite or don’t) so can select for resistance
- chemical drugs are a kill or no kill method
-Most commonly give a mix of an ionophore and a chemical (Maxiban)
Not really any new coccidial drugs, problem as we see new forms of parasite
Resistance develops very fast
21
Q
Vaccines
A
- Broilers- vaccines not commonly used- not fast/ cheap enough & can ↓ growth so use drugs (ionophores) instead throughout lifecycle.
- Can use shuffle programs instead: aim to ↓ resistance by switching between different drugs
- Can vaccinate as part of a rotation- popular in US, not used in uk
- Layers & Breeders- vaccines are used as growth rate is less important than immunity
-In UK- attenuated parasites- paracox, livacox and hipracox- select precocious lines which have a shorter
PPP & produce less oocytes (have fewer rounds of schizogony)
-In US- live oocysts used (coccivac) or immunocox which is given in gel/ water- can overdose themselves
**Resistance develops very fast
- old Gel using WT vaccines (purified oocysts) can make the chickens very sick
- there is a Vaccine that purifies the gametocytes: don’t see immunity pass from hens to chicks, doesn’t seem to work too well
22
Q
Eimeria tenella
A
- MOST IMPORTANT SPECIES OF EIMERIA TO REMEMBER
- Oocysts: ~22x19um
- PPP: 138hours (Time from infection and when it excretes oocysts)
- Sporulation takes at least 2 days:
Occurs in env’t to be from non-infectious to infectious
- Massive biotic potential
- Self-limiting life cycle
- Very Important:
- The worst pathology occurs before oocysts are produced
- Can check birds before they die, but it is hard
- Usually the post mortem of one will give you a sign
- tends to be on a FLOCK basis, if one bird is infected the rest easily will be
23
Q
Major Feature of Precocious Lines
A
less production, but the same protection
- If you take these and infect the animal again and again, get a lower PPP (blue line). You can select for a subpopulation of parasites for less productive (attenuated) parasites with a shorter PPP period- also much lower levels of replication
Enter sexual stage much earlier than normal!!
Less asexual replication- less numbers
- Shorter prepatent time
- Attenuated
- Produce fewer progeny
- Immunogenic
24
Q
GIT of a chicken
A
