Protozoa I - Coccidia Flashcards
Review this image:
Simplified and selective protozoa classification
Describe protozoa in general.
„Proto – zoa“ – first animals,
Single celled Eukaryotes (1-150 μm)
No cell wall, but cell membrane.
Heterotrophs that feed off organic compounds.
Pinocytosis, phagocytosis, mouth (cytostome).
More than 50 000 species
Mostly free-living species
Describe Protozoa motility.
Motility through flagella, cilia, amoebic, alveolata.
Protozoa life form nomenclature.
- zoite
Eg. trophozoite, sporozoite, merozoite, bradyzoite, tachyzoite. - moving, infective, invasive
- feeding, reproducing
“-ont”
- a “bag” of zoites
- meront (=schizont), gamont
- intracellular
Cyst (oocyst)
- resting
- non-motile, stable
Protozoa life cycle type.
Monoxenous (one host cylce) or heteroxenous (two or more hosts in life cycle, this is more common).
In heteroxenous life cycle, arthropod vectors are often second hosts, as well as birds or mammals.
Describe protozoa reproduction.
Asexual reproduction - many possible variations.
Sexual reproduction - gametogony.
Metagenesis when there is both sexual and asexual reproduction. (eg.Eimeria spp.)
Sporogony = sporulation which is a type of asexual reproduction.
define sporozoa
a group of parasitic protozoans that includes *Plasmodium, the malaria parasite.
Most sporozoans do not have cilia or flagella.
define schizogony
asexual reproduction by multiple segmentation characteristic of sporozoans (as the malaria parasite)
define gametogeny
the formation and maturation of gametes
define sporogeny
sporulation
the multiple fission of an encysted zygote or oocyte, resulting in the formation of sporozoites.
Sporozoites are inside a sporocyst
Outside in the environment
flagellated protozoa higher group is officially known as
Excavata
Asexual reproduction – binary fission
Some produce cysts
Flagella and undulating membrane for moving
Kinetoplast (mitochondrial DNA) binding the flagella
Important Orders that belong to Excavata: (3)
- Trypanosomatida
- Diplomonadida
- Trichomonadida
Phylum Apicomplexa are what type of protozoa
sporozoa
Life cycle complex - metagenesis
- asexual and sexual multiplication
- sporogony - produce oocysts
Mostly intracellular parasites
- apical complex helps to get in the cell
3 Important Orders to belong to phylum apicomplexa:
- Cryptosporidia
- Eimeriida
- Piroplasmida
What is TSAR?
Also known as phylum apicomplexa or alveolata.
What phylum and class do Eimeria belong to?
Phylum Apicomplexa
Order Coccidea
define
Eimeriosis;
coccidiosis
Genera Eimeria and Isospora/ Cystoisospora (Synonyms)
eimeriosis -disease caused by Eimeria spp.
coccidiosis -disease caused by Eimeria and Isospora
Eimeriosis is caused by?
Where is it found?
Who does it invade?
Parasite: protozoa,
Apicomplexan Eimeria spp.
Prevalent worldwide.
Many-many hosts! But hosts are eimaria spp. specific.
Also, Very site-specific!
Three important stages in eimeria spp. life cycle:
All 3 of the following repro. strategies are ALWAYS present.
- Asexual schizogony (merogony) - schizont (bag of merozoites).
- Sexual gametogony – gamont (always occurs in the host).
- Sporulation – sporozoites form inside oocysts.
Transmission – fecal-oral (sporulated oocysts).
Eimeria spp. life cycle
Sporulated oocysts causes infection.
Oocysts encyst in SI where sporozoites are released.
When they enter enterocytes, they develop into trophozoites.
Then schizogony/merogony takes place (trophozoites into schizonts).
Merozoites are formed (inside schizonts??). Merozoites spread, and then initiate gametogeny which is the cause of clinical disease.
Unsporulated oocysts are not
infectious
Sporulated oocysts are infectious.
Sporulation takes 2-5 days (with a few exceptions).
Oocyst are very resistant in the environment (up to one year) and very resistant to many disinfectants.
Sporulated Eimeria spp. always have how many sporocysts and each with how many sporozoites?
Sporulated Eimeria spp. has always 4 sporocysts and each with 2 sporozoites.
Eimeriosis pathogenesis is due to
intracellular multiplication, host immune reaction.
Some species highly pathogenic.
Young animals most susceptible to clinical disease.
Eimeriosis clinical signs
Signs vary from poor weight gain to sudden death.
- diarrhea (watery, mucous, bloody) - mostly in young animals
- dehydration
- loss of weight, anaemia, apathy, possible death
Manifestation of coccidiosis in
● Individual animal versus
● Herd/flock
● Individual animal:
○ asymptomatic/non-clinical disease - but large numbers of oocysts in feces.
or
○ acute, severe, fatal, bloody diarrhea - but no oocysts in feces - prior to patency.
● Herd/flock
○ regularly occurring diarrhea problems with every new cohort of young animals.
Chicken eimeriosis is caused by
Pathogenic spp. are E.brunetti, E.necratrix, E.tenella.
They each affect a diff. portion of the GI tract.
Describe Chicken eimeriosis.
+ e.g. risk factors
Very important infectious disease in chickens due to high economic losses high.
- young birds at greatest risk
Risk factors
- Intensive husbandry
- High stocking density (especially in broiler houses)
- Bad quality litter – too much moisture
- Lighting schedule – intermittent lighting increases risk
- Antinutritional factors
Large intestine eimeriosis in chickens versus small intestine eimeriosis?
Large intestine eimeriosis:
- 2-10 week old chicks
- apathy, gather together, no appetite, thirsty, strong diarrhea (watery, mucous, bloody)
Small intestine eimeriosis:
- in older animals
- milder course, diarrhea, loss of egg production, decreased weight
These Can predispose to secondary diseases such as bacterial infection with Clostridium perfringens which causes necrotic enteritis (NE).
Small ruminant eimeriosis is caused by
Pathogenic species:
E. ovinoidalis and
E. crandallis.
Prepatent period: 1-3 weeks
Describe the age demographic of Small ruminant eimeriosis.
Lambs are primary source of infection and infected.
Shedding of oocysts is highest in lamb weaning period, also symptoms are seen then.
Mostly due to bad hygiene in farm and high stocking density either inside or outside.
Clinical signs of acute vs chronic Small ruminant eimeriosis.
Acute: loss of formed faeces , liquid faeces (yellow to dark), slimy, wool dirty, loss of appetite, weakness, dehydration, weight loss, fever.
Chronic: symptoms of the disease are either absent or mild diarrhea, poor condition, weight loss, may never recover, susceptible to other diseases.
Goats are highly susceptible to Eimeria infection and it should always be suspected in a goat kid with diarrhea for more than two weeks.
Cattle eimeriosis is caused by?
Pathogenic species: E. zuernii and E. bovis
Prepatentperiod: 1-3 weeks
Describe the age demographic of Cattle eimeriosis.
All calves get the infection during the first year of life, often seen in 2-6 months old calves (naive animals).
Not always a connection with diarrhea.
Risk factors for Cattle eimeriosis.
Damp pasture, drinking water from the ground.
Intensive farming
Damp farms, bad water hygiene
Feeding of wet bedding, bedding in feed
Climate system not working in farms
Often a problem with the herd rather than the individual.
Describe Cattle eimeriosis, specifically Large intestine eimeriosis - acute.
Cause by infection with species E. bovis and E.zuernii.
Epithelial loss and mucosal necrosis - ulcerative.
Symptoms: 2-3 week post infection, loss of appetite, but thirsty, dehydration, anaemia, apathy.
Diarrhea: slimy, watery, bloody, acidosis, tenesmus.
Sometimes CNS symptoms, death.
Describe Cattle eimeriosis, specifically Small intestine eimeriosis - subacute.
Caused by species with E. auburnensis and E. ellipsoidalis.
Symptoms: 1-3 weeks post infection, long-term weight loss in calves.
Describe Cattle eimeriosis, specifically mixed infections, subacute.
most common
Species: E. zuernii, E.bovis, E. ellipsoidalis, E.
auburnensis
Symptoms: Mild – catarrhal enteritis, no bleeding.
Describe Rabbit eimeriosis.
Young are more susceptible (5-7 week) - mostly acute disease.
Mostly in group housing – main source of infection drinking and feeding.
Either Liver and biliary tract eimeriosis or Intestinal eimeriosis.
Describe Rabbit eimeriosis: Liver and biliary tract eimeriosis,
Species: E. stiedae in the bile ducts of liver.
Prepatent period 2-3 weeks.
Liver and abdomen enlargement – jaundice, stomach hard when palpated, back slimming, apathy, thirsty
High mortality – very pathogenic.
Describe Rabbit eimeriosis: Intestinal eimeriosis (large and small intestine).
E. intestinalis and E. flavescens very pathogenic.
Diarrhea and losing weight, stomach soft and large when palpated.
Pig coccidiosis is caused by
Caused by Several Eimeria species
Cystoisospora suis mostly but occasionally by other Eimeria spp.
Describe Pig coccidiosis.
Main cause of diarrhea in suckling piglets.
Prepatent period 1 week
Risk factrs:
Intensive pig-farming
newborn piglets (susceptibility decreases quickly)
Bad feed ratio
Symptoms:
Decreased weight gain
Small intestine diarrhea - pasty to watery, yellow to gray, usually not bloody.
Dehydration
Other intestinal pathogens affect morbidity and mortality.
Diagnosis of eimeriosis.
Anamnesis and clinical signs.
Fecal flotation method in which there must be many oocysts to be diagnostic (species differentiation also possible with PCR.
Diagnostic finding of OPG can begin from
5000 OPG to 100 000 OPG. (oocysts per gram of feces)
+ Histopathology
+ Post mortem analysis
Mixed infections with trichostrongyloid nematodes are common.
Histopathology in eimeriosis diagnostics.
- rectal mucosal smear
- Post mortem intestine mucosal smear
Eimeria different stages:
- schizont (merozoites inside)
- macrogametocytes
- immature oocysts
Hemorrhages
Finding Eimeria spp. oocysts from faeces is not sufficient for
diagnosis
- healthy animal can shed large numbers of oocysts (Eimeria spp. are ubiquitous but don’t need to progress to eimeriosis)
- clinical and severe coccidiosis can occur during the prepatent period
- clinical disease may last longer than oocyst shedding
- many reasons for diarrhea - always the cause is not Eimeria spp. even though you find oocysts from faeces .
Low number of oocysts build up an immunity, but high number of oocysts causes morbidity!
control and prevention of eimeriosis
Drugs administered prophylactically cause resistance problems.
Improve hygiene and husbandry.
Reduce stress.
Do not mix different animal species and different ages in one pen.
“all in - all out”
When first symptoms occur: sick animals should be separated and start treatment to the whole herd.
Protozoal vaccinations!
Genus Cystisospora belongs to what family?
Family Sarcocystidae
Order Eimeriida
Class Coccidea
Phylum Apicomplexa
Cystoisospora spp. cause what disease in dogs and cats?
cystoisosporosis
cystisospora and isospora are essentially synonyms so don’t let this mix you up
technically belong to diff families, however, share so many similarities, in practice they are interchangeable.
Describe what Cystoisospora spp. resembles.
Cystoisospora spp. resembles Sarcocystis spp. and Toxoplasma gondii species
Has 2 sporocysts, each with 4 sporozoites, inside an oocyst.
Describe Cystoisospora spp. in general.
Worldwide prevalence
Localizes in small and large intestine.
Problem in kennels and animal shelters.
Species and hosts:
Dogs:
C. canis , C. ohioensis, C. burrowsi, C. neorivolta
Cats:
C. felis , C. rivolta
Paratenic hosts: rodents, birds, and other animals.
NOT zoonotic
Cystoisospora spp. life cycle
Monoxenous or facultatively heteroxenous.
Sporulated oocyst or dormozoite from prey infects the final host.
Sporozoites then invade epithelial cells.
Reproduction then occurs via multiple methods.
repeated merogony (asexual division)
gametogony (sexual replication)
shedding non-sporulated oocysts
sporulation outside (1+ days)
Paratenic host is infected with extraintestinal dormozoites (sporozoites) in liver, spleen, lymph nodes.
Cystoisospora spp. of Dogs:
C. canis , C. ohioensis, C. burrowsi, C. neorivolta
Cystoisospora spp. of Cats:
C. felis , C. rivolta
Pathogenesis of cystoisosporosis
Destruction of enterocytes, mucosal lesions in the intestines, haemorrhagic ulcers.
Atrophy of the villi, permeability increases.
Hypersecretion due to immune response.
Catarrhal to fibrinous-necrotizing enteritis.
Canine and feline cystoisosporosis clinical signs.
Canine (puppy diarrhea): diarrhea, anorexia, vomiting, apathy, fever, growth disorders.
Feline (kitten diarrhea): watery diarrhea, lasting for many weeks, seldom bloody.
Note: Infection in cats with Cystoisospora spp. induces reexcretion of
Toxoplasma gondii oocysts!
cystoisosporosis:
prepatent period?
oocyst shedding lasts for how long?
- prepatent period is 5 days
- oocyst shedding lasts 1-3 weeks
Control of cystoisosporosis
Disinfection of kennels and boxes!
- hot water over 70 degrees
Rodent control
No feeding or raw meat and internal organs of the paratenic hosts.
Limit hunting
Lower stress
Diagnosis of cystoisosporosis.
Detecting oocysts in fecal flotation (requires multiple sampling days due to sporadic shedding).
Oocysts resemble other species in this family (Sarcocystidae):
- Toxoplasma gondii, Neospora caninum, Hammondia hammondi, Besnoitia besnoiti
Thus, for species identification PCR is needed.
Post mortem: histological findings from intestinal mucosa.
Image left: unsporulated oocysts, right: sporulated oocyst.
Family Sarcocystidae consist of?
cyst-forming parasites
Cystoisospora, Sarcocystis, Toxoplasma, Neospora, Hammondia, Besnoitia
They cause sarcocystiosis.
Characterize Sarcocystis spp. life cycle.
Heteroxenous life cycle
Carnivores as definitive host.
Herbivores as intermediate host in which formation of cysts.
Size of the cysts vary from microscopic to macroscopic.
Describe Sarcocystis spp. & sarcocystiosis in general.
Very prevalent worldwide.
Excreted sporocysts are instantly infectious and survive for months to years.
Fecal stage sporocysts can survive sewage treatment without damage.
No cross-immunity between species.
ZOONOTIC Humans can be final host and accidental intermediate host!
Describe Sarcocystis spp. life cycle
Letters correspond to image.
A: Intermediate host ingests oocysts/sporocysts. Sporozoites released.
B: Sporozoites invade small endothelial cells in arterioles - asexual division. Many generations. After, merozoites released.
C: In striated muscles, heart muscles; merozoites turn into bradyzoites inside sarcocysts.
C1: Final host ingests tissues with sarcocysts.
D: Bradyzoites are released in small intestine.
E: Bradyzoites infect epithelial cells - sexual
replication - formation of oocysts.
G: Oocysts/ sporocysts shed in feces.
Shedding occurs for several months.
Duration: prepatent period is 8–33 days in dogs and 10–14 days in cat
Pathogenesis of sarcocystosis
II generation schizogony in capillary endothelial cells causes pathology:
- Endothelial cell destruction
- Inflammatory cells surrounding the cysts
- Hemorrhages in various organs and lymphadenopathy
Clinical signs of sarcocystosis
In intermediate hosts - systemic disease (endothelial and muscle phase).
1 month after infection: anorexia, fever, anemia, hepatitis, loss of weight, hair loss, ataxia, stiffness, CNS symptoms, abortions, death in young animals, submandibular oedema in ruminants, decreased milk yield, changes in blood count.
Final hosts get intestinal sarcocystosis:
Mostly apathogenic infection
Mild diarrhea
Diagnosis of sarcocystiosis in herbivores.
During routine meat inspection in slaughterhouses you may find large cysts (whitish streaks running muscle fibre direction).
Clinical symptoms when infection is acute.
Histology/biopsy from kidneys and heart muscle - meronts may be found in capillaries.
Serological testing: presence of antibodies might not show an active infection.
Blood samples: lymphocytosis, anemia, low albumin, lactate dehydrogenase, AST increased, bilirubin increased.
Diagnosis of sarcocystiosis in carnivores.
Fecal flotation to farm cats and dogs for finding the sporocysts.
Oocysts: 14x19μm and sporozoites 9x15μm
Treatment of sarcocystosis
no specific antiparasitic drug is indicated for final and intermediate hosts.
Some options that might work:
for final hosts: toltrazuril, albendazole, sulfonamides and corticosteroids
for Intermediate hosts: Amprolium can be used for prophylactic treatment.
prevention of sarcocystosis
Animals for human consumption, should not be exposed to contaminated water and feed.
- No raw meat to final hosts: dogs, cats and humans!
In intermediate hosts:
- Limit access of dogs and cats to animal feed and drinking water.