Blood and lung equine worms

Question 1

Dictyocaulus arnfeldi

Answer 1

Lungworm, mostly in donkeys.eggs hatch immediately after defecation. L3 on grass is infective, travels to lungs via lymphatics and blood stream, do not reach maturity in horses, only donkeys but is not pathogenic in them!

Question 2

Clinical signs and treatment of lungworms

Answer 2

Inflammation block smallest bronchi and cause death. worms migrate to larger areas after death. chronic cough, nasal discharge, increased respiratory rate. Look for larvae in feces (like D. vivparus but larger and have pointed tail). usually no eggs in feces. do tracheal wash and endoscopy. Donkeys develop immunity and macrolide can eliminate them. Use macrocyclic lactone in horse.

Question 3

Babesia caballi

Answer 3

Reportable foreign animal disease, larger, occur as piriform pairs, single spherical trophozoite in RBC 3-4 microns, ticks are DH and transovarian/transstadial transmission occurs, sporozoites in tick saliva go to horse and invade RBC to produce merozoites that destroy them. Tick ingests merozoites while feeding. Dermacentor nitens and albipictus. pathological changes due by intravascular hemolysis and thrombocytopenia. mild to severe, death, no clinical signs.

Question 4

Theileria equi

Answer 4

Reportable foreign animal disease, seen as four in a maltese cross formation, ticks are DH and transovarian/transstadial transmission occurs. Multiplies in lymphocytes and then in RBC, merozoites destroy RBC and tick ingests these while feeding. Amblyomma cajennense, Rhipicephalus microplus and Dermacentor variabilis. pathological changes due by intravascular hemolysis and thrombocytopenia. more pathogenic, incubation period of a week, fever, animal carrier, death 1-2 days after clinical signs

Question 5

Equine piroplasmosis

Answer 5

no tick vector recognized, from blood transfusions,all animals that survive can transmit organism,

Question 6

Clinical signs and treatment for piroplasmosis

Answer 6

Signs from acute infection: from intravascular hemolysis and thrombocytopenia (fever, lethargy, petechiations, edema). REPORTABLE. blood must be sent to Iowa. Conduct several tests to ensure transmission. Horses are quarantined and either enrolled in treatment, quarantined for life, euthanized. Clearance from treatment needs negative PCR and have naive splenectomized horse test negative when given blood transfusion. Give imidocarb diproprionate.

Question 7

Sarcocystis neurona

Answer 7

Causes Equine Protozoal myeloencephalitis. Toxoplasma like. sarcocysts in muscle of IH. tachyzoites in horse CNS. Opossum is DH. Gametogony in SI of opossum, sporocysts released from intestinal epithelial cells, sporocysts in feces infective stage. IH eats sporocysts and sporozoites invade vascular endothelial cells, undergo schizogony, release tachyzoites, form bradyzoites in muscle cells. Horses become IH when ingest sporocysts in feed/water. Neural cells invaded and destroyed as parasite multiplies. Horses cannot transmit disease

Question 8

Clinical signs and treatment for S. neurona

Answer 8

Brain and spinal cord have areas of necrosis, hemorrhage, and inflammation. damage to neurons, edema. mononuclear cell cuffing. begins insidiously and signs of spinal cord involvement more noticed than brain involvement. Progressive ataxia, rapid muscle atrophy, asymmetric gait abnormalities, dysphagia. use marquis paste (ponazuril). Secure feed. Risk factors are stress, previous health problems. Rule out rabies, west nile, other neuro diseases.

Question 9

Diagnosis of S. neurona

Answer 9

Definitive hard because of high seroprevalence (like N. caninum), confirm neurological signs, rule out other diseases, confirm intrathecal antibody production against protozoan. Serologic tests for S. neurona or S. neurona merozoite surface antigens.