Gastrointestinal Protozoa

What stage of protozoa is the dispersal & infective stage?

cyst stage - shed in feces

what is the lifecycle of giarida?

• cysts shed in feces, immediately infective for other hosts → cyst ingested from contaminated water, food, environment → trophozoites attach to intestinal villi → reproduce by binary fission → form cysts

disease of giardia

• lighter infections → inappetance

• likely occurs in young animals infected for the first time

  • young dogs & cats are main hosts that are likely to be clinically affected & put out large numbers of cysts

• diarrhea ± foul smelling flatulence → main clinical sign

• slow growth rates in young lambs but not detected on FEC (undiagnosed)

zoonotic potential for giardia

• most common cause of protozoal diarrhea in humans

• ingestion of cysts

• strain types & host specificity unclear

• preventative → practice good hygiene around infected pets (especially children)

how to diagnose giardia

• finding of large numbers of cysts in fecal floats prepared with 33% Zinc Sulphate solution → improved results with centrifuging

• PCR

• antigen tests

what causes infectious enterohepatitis in young turkeys?

histomonas melagridis

aka blackhead → cyanosis of wattles in very sick birds, clinical signs is uncommon

lifecycle of histomonas melagridis

trophosoites are present in intestinal ceca → ingestion of heterakis transport host, ingestion of second transport host (earthworm that ate heterakis), or direct bird to bird transmission by ‘cloacal drinking’

pathogenesis of histomonas melagridis

multiplying trophozoites may penetrate into mucosal tissue → inflammatory reaction → ceca fills with necrotic yellow material & feces changes from dark to yellow color → organisms may travel to liver → formation of ‘bullseye’ abscesses → necrotic liver disease → likely results in mortalities

diagnosis of histomonas meleagridis

• PM material (gross lesions of liver)

• PCR of fecal samples, gut contents, tissues

trichomonads in birds (pathology, transmission)

• parasites of upper alimentary tract (oropharynx, crop)

• ulcerative, necrotic lesions develop on the mucosal surface → infection may spread to surrounding bones, causing lytic lesions

• infections often transmitted from parents to young birds via regurgitated food

tritrichomonas foetus in cats

• causes chronic large bowel diarrhea in cats

• older cats may be healthy carriers, helping maintain infection in colonies

diagnosis of tritrichomonas foetus

• trophozoites may be observed in fresh fecal smears → numbers are usually low, unreliable means of diagnosis

• PCR

what are apicomplexa?

• coccidians, piroplasms, malarial organisms

• produce spores

• found in epithelium of intestines, blood cells, tissues

• move via undulations & gliding

• banana, comma, or boomerang shape

how do apicomplexa reporduce?

• cells divide in stages

  • oocyst → cyst stage

  • sporogony → sporulation outside host

  • schizogony → asexual reproduction in host

  • gametogony → sexual reproduction in host

what is the main genera of coccidia of veterinary importance?

• Eimeria (ruminants, birds, horses)

• Cystoisospora (dogs, cats, pigs)

lifecycle of coccidia

• infective stages (fully developed sporulated oocysts) are ingested → each oocyst liberates 8 individual zoiets in the gut → zoiets immediately penetrate host cells (epithelial cells in anterior parts of the gut) & reproduce by asexual repoduction → next generation of zoiets exit the original cell & re-enter flow of digesta → next phase of asexual reproduction tends to occur downstream of the first

• after 2 cycles of asexual reproduction, male & female gamets produce → forms oocyst → oocyst shed in feces → oocysts develop (sporulate) to become infective outside of host → needs warm environment, can persist in environment for a long time

how is coccidia different than other protozoa?

once coccidia form oocysts, they must leave the host → further build up of numbers require reinfection

what is the difference in lifecycles between Eimeria and Cystoisospora?

eimeria → direct lifecycles

cystoisospora → potential for indirect transmission involving intermediate hosts

• mouse ingests oocysts from dog or cat → oocyst can encyst in tissues of mouse & remain dormant until eaten by the correct definitive host

what has a big impact on the pathogenicity of coccidiosis?

• site of replication!

  • superficial epithelial cells → limited damage

  • actively dividing enterocytes → loss of these cells is consequential

  • deeper in the tissues → large structures busrting into the lumen breaches epithelial integrity

what phases of the life cycle of coccidosis are the most pathogenic & why

later stages are most pathogenic → later stages are more numerous & destroy more host cells & occur in the large intestine

large intestine heals slowly due to low mitotic rate

what direct & indirect damage occurs in coccidiosis?

direct damage → direct destruction of host cells & tissues

indirect damage → cell-mediated immunity leads to destruction of infected cells

clinical signs of coccidiosis

• damage to the gut → diarrhea

  • large intestine predominately affected → small volumes of feces, increased frequency, straining

  • presence of mucus & reasonably fresh blood in diarrhea (especially in calves)

• pyrexic

• anorexic

• dehydration

• depression

important factors in epidemiology of coccidiosis

• oocysts are very resistant: once contaminated, environments remain for long periods

• adult animals can be constant shedders of oocysts even if clinically unaffected

• high biotic potential & rapid generation times inside the host mean animals can reinfect themselves before sufficient immunity has built up

• rapid sporulation of oocysts in environment, especially in warm, wet conditions favors rapid reinfection

• can be a problem in housed animals → deep litter systems

  • significant problem with young chicks put into sheds with high oocyst contamination

diagnosis of coccidiosis

• standard fecal egg counting method

• fecal float with saturated NaCl

• PM diagnosis

  • examination of intestinal mucosa

  • tissue can be scraped to liberate organism/oocysts in abundance

what will be the end point of the coccidia-like development of Toxoplasma gondii & Neospora caninum in dogs & cats?

oocyst output

• usually only young dogs & cats infected for the first time shed oocysts

what type of lifecycle do T. gondii & N. caninum favor?

indirect life cycle

oocysts shed by dogs & cats are not meant to infect other dogs & cats

pathogenesis of T.gondii & N. caninum in intermediate hosts

• organisms often replicate initially in the cells of the gut rapidly → develops tachyzoites → organism can stay in this place & infect more cells until immune system is activated

• immune system activated → organism switches to forming tissue cysts of slowly dividng bradyzoietes → immune system can eliminate tachyzoiete infected cells, but not bradyzoiete tissue cysts

• tachyzoiete development can be very destructive phase, especially in animals that do not have an effective immune system → more likely to lead to clinical issues

diagnosis of T. gondii & N. caninum

uncommon finding in canine & feline fecal samples

presence can be confirmed by antibody tests or PCR on tissues → tissue scrapes

What are the two species of cryptosporidium & how are they transmitted to humans?

C. parvum → exposure to young calves on farm

C. hominis → passed from human to human

both species can be transmitted by direct contact or by contaminated water or food

what is the pathogenesis of crypto?

• targets epithelial cells with a microvillar brush border → organisims penetrate inside of a single microvillus → oocyst leave the cells already fully developed & infective → autoinfection can occur as some oocysts are thein-walled & can rapidly break open before exiting host, other oocysts are shed into the environment

• immunity develops rapidly, most infections are self-limiting, autoinfective cycle can continue in immunosuppressed individuals

epidemiology of crypto

• infections can build dramatically & rapidly in animals, & the infective dose required to produce disease is very low

• rapid fecal-oral trannsmission

• oocysts can survive many water purification processes & may not be removed by filtration

• rapid development in most cases of protective immunity limits disease to first infections in very young animals

diagnosis of crypto

• acid-fast staining fecal smears

• PCR

what are the differences between a protozal cyst, an oocyst & an oocyte?

• protozoal cyst → hardy dispersal stage of protozoa, or accumulations of the organisms hiding in tissues

• oocyst → egg-like dispersal stage of apicomplexans (coccidia), result of sexual repoduction in these organisms

• oocyte → female gamete in an ovary

what clinical sign of coccidiosis would not be expected to be seen in calves with heavy nematode burdens?

fresh blood in feces