6.5 Protists 2 Flashcards
what is the smallest parasite commonly diagnosed? Is it a zoonotic threat?
Cryptosporidium; yes
when we think of Cryptosporidium what age group are we commonly thinking about
young and immunosuppressed; typically neonatal cattle
why is hygeine not an effective control measure against Cryptosporidium
the oocysts come into the environment sporulated; thin walled-cysts created in the host give rise to autoinfection
what is unique about the LOCATION of Cryptosporidium replication
epicellular (wraps the cell around it like a blanket, so cozy)
what is Cryptosporidium life cycle and what are the modifications
typical Apicomplexan (coccidian) life cycle - sporogony, merogony, gametogony
differences:
- sporogony occurs inside the host before the sporulated oocyst is shed into the environment, making it immediately infectious
- both thin walled and thick walled oocysts are formed; thin-walled will initiate the cycle within the host again (autoinfectious)
what are the clinical signs of Cryptosporidium
- SI villous atrophy
- enteritis
- malabsorptive diarrhea (non-bloody, watery)
- dehydration (biggest threat to neonates)
how long does the diarrhea induced by Cryptosporidium last
1-3 weeks in healthy animals, longer if immunocompromised
what is the appearance of Cryptosporidium oocysts in feces that helps us diagnose
refractile and small
how can we diagnose Cryptosporidium
- fecal float
- acid-fast staining of feces
- IFA of fecal smears
- puddle technique
- fecal antigen tests available
how do we treat Cryptosporidium
- no effective drugs (in contrast to Eimeria and Cystoisospora)
- fluid replacement
what are some characteristics of heteroxenous coccidia
- infects animals in a predator-prey relationship
- extra-intestinal in the intermediate host (prey) and intestinal in the definitive host (predator)
- dogs and cats are usually the definitive hosts, therefore have the intestinal phase
T/F the heteroxeous coccidia are also the tissue coccidia and the monoxenous coccidida are also the intestinal coccidia
T, with one exception…
Intestinal coccidia/monoxenous coccidia: Eimeria, (Cystoisospora), Cryptosporidium
Tissue coccidia/heteroxenous coccidia: Neospora, Sarcocystis, Toxoplasma, (Cystoisospora)
Cystoisospora has the paratenic host route whereby ingestion of sporulated oocysts causes an extra-intestinal cyst production that gets ingested by the definitive host…
Describe the intermediate and definitive hosts of the following heteroxenous coccidia:
- Sarcocystis
- Toxoplasma
- Neospora
Sarcocystis: One intermediate host, one definitive host
Toxoplasma: Many intermediate hosts, cats are definitive hosts
Neospora: Many intermediate hosts, definitive hosts unknown
How is the apicomplexan life cycle broken down into the intermediate hosts, definitive hosts, and environment for heteroxenous coccidia (ex. Sarcocystis, Toxoplasma, Neospora)
Merogony occurs in extra-intestinal tissue in the intermediate host, gametogony and sporogony occur in the intestinal tissue of the definitive host, and the environment will contain the sporocysts
What are the definitive and intermediate hosts (specific) of SARCOCYSTIS
Intermediate hosts are herbivorous or omnivorous tetrapods
Definitive hosts are predatory reptiles, mammals and birds of prey
Where does Sarcocystic form sarcocysts in the intermediate hosts (the herbivorous and omnivorous tetrapods)
in the endothelium and muscles
Sarcocystis is usually non-pathogenic in what host and pathogenic in what host
non-pathogenic in the definitive host; pathogenic in the intermediate host (makes predation easier and assists with transmission of the pathogen)
Describe the life cycle of Sarcocystis
Intermediate host ingests sporulated oocysts or sporocysts from the environment -> 2 cycles of merogony occur in the vascular endothelium -> merozoites enter muscle or nerve cells and form a cyst containing bradyzoites -> intermediate host eaten by definitive host -> bradyzoites penetrate the intestinal epithelium and undergo gametogony -> zygote/oocyst formation -> sporulation occurs within the host
Why might you see sporulated oocysts or sporocysts within the feces of a definitive host infected with Sarcocystis
The sporulated oocysts often break in the host, releasing the sporocysts
What stage of Sarcocystis life cycle causes disease
the vascular phase (merogony - replication in the endothelium) in the intermediate host
how is Sarcocystis commonly diagnosed in the definitive host and in the intermediate host
in the definitive host by finding oocysts or sporocysts in a fecal floatation
in the intermediate host infrequently diagnosed unless EQUINE PROTOZOAL ENCEPHALITIS
What causes equine protozoal encephalitis? Describe why the disease has the clinical signs of ataxia, muscle atrophy
Caused by accidental ingestion of sarcocystis sporocysts by horses; the 2 cycles of merogony occur in the vascular endothelium but eventually escape to the muscles and brain; the key factor is NO sarcocyst formation so tachyzoites undergo extended replication in the brain in spinal cord causing tissue damage and the clinical signs
how do you treat equine protozoal encephalitis
pyrimethamine/sulfas - long term therapy
how is Toxoplasma different from Sarcocystis
- range of intermediate hosts (vs Sarcocystis which only intermediate hosts are omnivorous/herbivorous tetrapods or horses accidentally)
- Toxoplasma can move asexually between intermediate hosts
what is the only definitive host of Toxoplasma
felids
Where are the extra-intestinal phases of Toxoplasma in kittens
lungs (primarily), also liver, muscle, heart, pancreas
what are the clinical signs of Toxoplasma in cats
pneumonia, depression, anorexia
rapid death in severe cases
what are signs of Toxoplasma in humans
lymphadenopathy, encephalitis, myocarditis, pneumonia
fatal in immunocompromised
what is the most serious form of toxoplasmosis
congenital - abortion and neonatal death
what are the lesions of congenital toxoplasma
inflammation and necrosis of fetal cotyledons; lesions in the liver and brain of the liver; abortion and neonatal death
how is toxoplasma usually diagnosed and how do we interpret active/recent infection vs past infection
Serology
Active/Recent: elevated IgM in the absence of IgG
Past: low IgM and high IgG (IgGONE)
T/F Congenital toxoplasmosis is treatable
F
What is the definitive host of Neospora caninum
Dogs
Neospora caninum is ______tropic
neurotropic
Neospora caninum is most important in dogs for causing ______________ and cattle for causing ______________
ascending paralysis; abortions
what is the main difference between toxoplasma and neospora in terms of infection potential
neospora can cause congenital infection in an animal that was already exposed once, whereas toxoplasma will only cause congenital infection in an animal that was exposed for the first time during pregnancy
how do we diagnose neospora caninum
- clinical signs (ascending rigid paralysis in puppies)
- organisms in CSF or brain of puppies
- parasite-specific ELISA in cattle
how do we treat neospora caninum
- drugs undergoing testing but currently no treatment for calves
how do we prevent neospora caninum
block transmission: prevent exposure to dogs, cull endogenously infected cows,
