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15 Cards in this Set
- Front
- Back
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anaplasmosis
a. etiology b. transmission c. pathophysiology |
a. Anaplasma marginale, A. caudatum (rickettsial)
b. ticks**, biting flies, blood contaminated fomites c. infects mature RBCs parasitized RBCs removed by reticuloendothelial system (extravascular hemolysis) --> release of acute phase proteins --> fever |
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anaplasmosis
a. stages of infection b. signs |
a. incubation stage: time from infection until 1% of RBCs parasitized (3-8 wks)
developmental stage: development of anemia; goes until reticulocytes appear in blood (4-9 d.) convalescent stage: goes until all blood values return to normal (variable: weeks to months) carrier stage: begins w/ disappearance of Anaplasma bodies to end of animal’s life b. mortality & severity increase w/age: high mortality in cattle > 3 yo signs not seen until > 15% of RBCs parasitized fever (up to 106º F), anorexia, depression, pale mucus membranes, watery blood, icterus (late stages) -death or abortion occurs around time of peak parasitemia (~90% RBCs infected) |
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anaplasmosis
a. dx b. tx c. immunity & resistance d. possible control program |
a. cytologic examination of blood smears: basophilic punctate bodies on margins of RBCs
clinical signs serology: herd level b. oxytetracycline: single injection is very effective IF < 15% of RBC’s parasitized c. long lasting cell-mediated immunity d. injection of oxytetracycline every 30 d. during vector season continuous feeding of chlortetracycline during vector season vaccination: 2 doses that end at least 2 wks before vector season begins: ↓ severity only |
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babesiosis
a. etiology b. transmission c. pathophysiology d. signs e. dx |
a. Babesia bovis, B. bigemina (rickettsia): eradicated from US
b. ticks c. initially multiples in blood vessels & destroys RBCs (intravascular hemolysis) d. fever, anemia, icterus, hemoglobinuria** more severe in older animals e. cytology |
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leptospirosis
a. etiology b. transmission c. dz in maintenance vs. incidental hosts |
a. Lepto hardjo, L. pomona
b. direct contact w/ infected urine or fluids or by venereal/transplacental route c. maintenance host: efficient transmission, chronic dz of low virulence incidental host: low susceptibility but high pathogenicity |
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leptospirosis
a. pathophysiology b. signs: acute c. signs: chronic |
a. organisms invade thru mucus mems & skin lesions --> circulate in blood & replicate in kidney, liver & lungs
hemolysins produced --> intravascular hemolysis b. most common: transient fever, ↓ milk production for 2-10 d. other possible signs: fever, hemolytic anemia, hemoglobinuria, icterus, occ. meningitis c. most common dz syndrome in ruminants renal dz, abortions, infertility, stillbirths |
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leptospirosis
a. dx b. tx c. prevention |
a. serology: most common method used (1 high titer = acute, limited use w/ chronics)
detection of organism in tissues &/or body fluids: dark field, PCR, etc. b. acute: tetracycline for 3-5 d. (or ceftiofur) chronic: single injection of tetracycline c. routine vaccination recommended in endemic areas can also vaccinate during outbreaks to limit mortality |
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copper toxicosis
a. epidemiology b. etiology c. signs: acute (rare) |
a. sheep
b. exposure to excess copper or low dietary levels of molybdenum &/or sulfur c. severe gastroenteritis, abdominal pain, severe diarrhea (green to blue), icterus if animal survives > 24 hrs. |
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copper toxicosis
a. pathophysiology b. signs c. dx |
a. sheep fed excess Cu store it in liver: can occur for weeks to months w/o clinical dz
stress --> sudden release of Cu from liver --> acute hemolytic crisis (intravascular hemolysis) --> hemoglobinuria, methemoglobinuria --> renal tubular nephrosis & severe renal failure b. hemoglobinuria, anorexia, icterus, depression, death w/in 24-48 hrs of onset of signs c. gold standard: liver bx w/ Cu analysis necropsy: gunmetal blue kidneys inc. serum Cu |
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copper toxicosis
a. tx b. prevention c. px |
a. Cu chelators: ammonium tetrathiomolybdate (IV or SQ) OR ammonium molybdate (PO) OR sodium sulfate (PO)
b. maintain proper copper:molybdenum ratio in diet, don't graze sheep on pastures fertilized w/ swine manure, don't feed sheep horse or pig feed c. 70-80% die |
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What are some causes of secondary copper toxicosis?
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phytogenous Cu toxicosis: subterranean clover ingestion
hepatogenous Cu toxicosis: Heliotrope ingestion --> excess Cu retention |
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water intoxication
a. epidemiology b. pathogenesis c. signs d. necropsy findings e. tx |
a. young calves (2-4 mo.) that have had limited access to water & are suddenly given unlimited access to water
b. hypotonicity --> RBC lysis (intravascular hemolysis) c. seen w/in 3-10 hrs hemoglobinuria, +/- salivation, +/- CNS signs d. cerebral edema, red urine in bladder, renal cortical necrosis e. most recover spontaneously temporarily restrict access to water & restore sodium concentration w/ hypertonic saline |
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postparturient hemoglobinuria
a. epidemiology b. etiology c. pathogenesis |
not common
a. mature dairy cows that have been housed for long periods or in animals on poor quality hay b. dietary phosphorous deficiency c. P deficiency --> ATP deficiency --> ↑ RBC fragility as cells pass thru capillary beds --> IV hemolysis |
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postparturient hemoglobinuria
a. signs b. dx c. tx |
a. hemoglobinuria, anorexia, weakness, followed by dehydration, tachycardia, dyspnea, +/- icterus
mortality rates can approach 50% b. signs + confirmation of P deficiency c. parenteral phosphorous |
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anthrax
a. etiology b. epidemiology c. transmission d. signs e. dx |
a. Bacillus anthracis
b. large outbreaks in permanently infected areas c. ingestion of contaminated feed d. animals usually found dead w/ tarry blood coming from body orifices e. don't open carcass if you suspect anthrax!! reportable dz |
