Protozoa- Apicomplexa 4: Plasmodium, Babesia, & Sarcocystis Flashcards
(65 cards)
What are the characteristics of the genus Sarcocystis?
Tissue cyst forming, ubiquitous in mammals, birds, and reptiles; free oocyst in feces, sporulate in intestine of definitive host; named for their host (e.g., S. bovicanis, S. ovicanis, S. suihominis).
Describe the pathogenesis of Sarcocystis.
Usually apathogenic; occasionally zoonotic self-limiting diarrhea can be seen; some species have very large, visible cysts.
What are the hosts of S. neurona?
Definitive: opossums; Intermediate: armadillos, skunks, raccoons, and other animals; Aberrent (dead-end): horses.
Describe S. neurona in horses.
Can result in EPM; tropism for development of bradyzoite cysts in neurological tissue; more common than N. hughesi.
What is EPM?
Progressive neurological disease of horses resulting from schizogony of Sarcocystis in neurons.
Where is EPM found?
North, south, and central America.
In what kind of horses is EPM most common?
Arises sporadically mostly in younger horses less than 4 months old.
Describe the neurological signs of EPM in horses.
Varying depending on whether the brain, brainstem, or spinal cord are affected.
What are the initial clinical signs of EPM?
Dysphagia, abnormal upper airway function, unusual or atypical lameness, or even seizures.
What are the clinical signs of EPM seen in severely affected horses?
Difficulty standing, walking, or swallowing; the disease can progress very rapidly.
True or false: Occasionally, the clinical signs of EPM stabilize, only to relapse days or weeks later.
True.
Describe the diagnosis techniques of EPM.
Differential is difficult; rule out other causes; test CSF for antibodies against S. neurona or N. hughesi; definitive diagnosis possible on post-mortem exam.
What is the treatment for EPM?
Ponazuril or similar, sulfonamide/pyrimethamine plus anti-inflammatories.
What are the characteristics of Besnoitia?
Both tissue-cyst forming and vector-borne; low morbidity/mortality in endemic areas; higher numbers of clinical cases in emerging areas: 1% mortality.
What are the clinical signs of severe acute Besnoitia in cattle?
Pyrexia, subcutaneous edema, stiffness of the limbs due to swollen joints; conjunctivitis, nasal discharge, photophobia, inspiratory dyspnoea, reduced milk yield, and orchitis in bulls.
What are the clinical signs of chronic Besnoitia in cattle?
Skin lesions, the presence of macroscopic scleral conjunctival and vestibulo-vulval cysts, and a gradual deterioration in body condition.
What are the methods of diagnosis of Besnoitia in cattle?
Histopathology characteristic cysts in skin biopsies; molecular techniques; ELISA; clinical signs.
What are the characteristics of Besnoitiosis in equids?
Emerging disease in Europe, recognized in USA; clinical signs mostly in donkeys; usually non-fatal.
What are the clinical signs of Besnoitiosis in equids?
Multi-focal white miliary nodular lesions in the skin - over the face and body, within the nares, on the internal and external pinnae, vulva, perineum, and on the legs.
What is the most common and unique feature of Besnoitiosis in equids?
The presence of scleral and conjunctival parasitic cysts - ‘scleral pearls.’
What are the general characteristics of Babesia genus?
Tick vectors are required hosts; mammalian stages found within RBCs; size, appearance, and arrangement particular to different species; clinically important in several veterinary species with high public health relevance.
What are the important Babesia spp in cattle?
B. divergens, B. major, B. bovis, B. bigemina.
What are the important Babesia spp in dogs?
B. canis, B. vogelli, B. gibsoni, B. vulpes (B. microti).
What are the important Babesia spp in humans?
B. microti; others in splenectomized people.