Disorders of the Hematopoietic System Food Animal 2024 PDF
Document Details
2024
Dr. Emily John
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Summary
This presentation discusses disorders of the hematopoietic system in food animals, including topics like regenerative anemia, hemorrhage, oxidative hemolysis, and copper toxicity. The information is relevant to veterinary medicine professionals.
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Disorders of the Hematopoietic System VHM 322 Dr. Emily John Outline Red blood cells Coagulation disorders White blood cells Anthrax Caseous lymphadenitis Camelids Regenerative Anemia Ruminants do display regenerative response in...
Disorders of the Hematopoietic System VHM 322 Dr. Emily John Outline Red blood cells Coagulation disorders White blood cells Anthrax Caseous lymphadenitis Camelids Regenerative Anemia Ruminants do display regenerative response in peripheral blood Increased MCV, decreased MCHC Marked anisocytosis Polychromasia Basophilic stippling Howell-Jolly bodies, nucleated RBCs Case Study 3 week Holstein heifer 5 day history diarrhea, sometimes hemorrhagic; 8% dehydrated Referred in for plasma transfusion rDVM bloodwork, day 1 AM: PCV 24% Total protein 50 g/L Case Study - Bloodwork Day 1 PM Day 2 AM Day 2 PM Day 3 AM PCV 19 % 18% 16% 10% TP 42 g/L 39 g/L 47 g/L 47 g/L Dehydration 7% 5% 6% 8% Hemorrhage Internal External Clotting abnormalities Abdominal Endoparasitism Hereditary deficiencies - Neoplasia - Haemonchus - Platelet function - Splenic rupture Ectoparasitism - Clotting factor Thoracic Abomasal ulcer deficiencies - Pulmonary trauma - Diet Chronic bracken fern - neoplasia - Neoplasia toxicity Severe coccidiosis Caudal vena cava syndrome Hemorrhage Hemorrhage Hypoxic dementia Keep in mind for patients with hemorrhage as well as blood donors Fecal occult blood testing Blood transfusion Impractical to find “universal” donor Disease-free donor Herd/flock-mate Oxidative Hemolysis Plant or chemical toxicities Allium spp. Brassicas Selenium deficiency Copper toxicity Copper Toxicity Sheep most sensitive Calves; adult cattle, goats Molybdenum and sulfur protective Inhibit copper absorption Copper Toxicity Sources: Feeds formulated for other species Pastures treated with chicken/swine manure Orchard crops – copper-containing fungicides Copper fencing, piping Copper Toxicity - Pathogenesis Hepatic accumulation Massive liver necrosis See increased hepatocellular leakage enzymes Copper in bloodstream causes oxidative hemolysis Intravascular hemolysis Pigment nephropathy, Hb-uria Death due to anemic crisis, organ failure Copper Toxicity – Clinical Signs Copper Toxicity – Diagnosis Post-mortem findings History of exposure Blood/tissue copper levels Copper Toxicity – Treatment and Prevention Supportive care Medications to encourage copper excretion Blood transfusion Guarded prognosis Prevention: Appropriate feed Molybdenum supplementation Bovine Anaplasmosis A. marginale Tickborne disease (Dermacentor) Present in USA; immediately notifiable in Canada Anaplasmosis – Clinical Signs Infected as calf: Mild malaise 1-2 d then lifelong inapparent infection Infected as adult: High fever with anorexia, lethargy, depression Marked anemia (extravascular hemolysis) with icterus – no Hb-uria! High mortality rate; prolonged convalescence Anaplasmosis – Diagnosis History, geographic location, clinical signs Anemia with intra-RBC morulae cELISA (OIE-approved test) Anaplasmosis – Treatment and Control Supportive care and tetracyclines Will not 100% clear infection Control strategies: Tick control Endemic areas, high transmission – expose cattle when calves Endemic areas, low transmission – blood-based vaccine Non-endemic areas – screening and quarantine of imports Babesiosis Reportable disease in Canada Intravascular hemolysis = will have hemoglobinuria (unlike Anaplasma) Other causes of Hemolytic Anemia Infectious: Hemobartonellosis, Eperythrozoonosis Leptospirosis Bacillary hemoglobinuria Miscellaneous: Water intoxication Postparturient Congenital erythropoietic porphyria Depression Anemia Information in notes Also for polycythemia Platelet Disorders Hereditary Chediak-Higashi syndrome Thrombocytopenia Bone marrow insult Decreased survival DIC Immune-mediated Thrombocytosis Common with systemic inflammation Dicoumarol Toxicity Conversion of coumarin in forage to dicoumarol via mold growth Clinical signs consistent with impaired coagulation Vitamin K1 for treatment Remove feed; “cycle” with other feed if impossible Caudal Vena Cava Syndrome CVC thrombosis secondary to hepatic abscess (secondary to rumenitis) Sudden death or respiratory signs (acute or chronic) Diagnosis via necropsy Ultrasonographic changes Caudal Vena Cava Syndrome Bluetongue Orbivirus of sheep Cattle are amplifier hosts; rare clinical disease Clinical signs due to systemic vasculitis Considered ovine equivalent of human viral hemorrhagic fevers (Ebola, Marburg) Bluetongue – Clinical Signs Bluetongue – Prevention Bovine Leukocyte Adhesion Deficiency (BLAD) First report: 1983 Almost absent from Holstein breed now 2018: BLAD confirmed in Lineback cattle in US Bovine Lymphoma Two main forms Sporadic Generally young animals B or T cell involvement Enzootic Usually older animals B cell involvement Sporadic Bovine Lymphoma Juvenile 3-6 months old Acute onset, rapid progression Anemia, lymphocytosis Sporadic Bovine Lymphoma Thymic 6 months – 2 years Signs due to space-occupying mass Bloodwork unremarkable Sporadic Bovine Lymphoma Cutaneous Wider age range Painful nodules +/- ulceration Anemia, atypical lymphocytes Enzootic Bovine Leukosis Adult form of bovine lymphoma Bovine leukemia virus: deltaretrovirus Persistent infection Dairy > beef EBL – Clinical Signs Infection ≠ clinical disease 30% of infected cattle develop persistent lymphocytosis Up to 5% develop lymphoid tumors Nonspecific clinical signs: Anorexia Lethargy Decreased milk production Enlarged superficial LNs EBL – Clinical Signs EBL – Epidemiology Retrovirus spread by blood contamination Shared needles/syringes Rectal sleeves? Live bull breeding Biting flies? Virus (and antibodies) in colostrum In utero infection EBL – Epidemiology Immune system genotype influences Susceptibility to infection Tendency to develop clinical disease Development of high proviral load Prevalence high in North America EBL – Economics BLV-positive cows: Earlier culling Increased susceptibility to disease Decreased response to vaccination Other costs: Reduced milk production (herd level) Carcass condemnation Export restrictions EBL – Diagnosis Physical examination of clinically affected cows Histopathology on LNs Serology ELISA for anti-BLV antibodies PCR for viral antigens Serology for individual and herd status EBL – Control and Prevention Minimize blood transfer between animals Colostrum management Fly control Segregate BLV-positive and negative cows Test bulls used for live breeding Closed herd/buy only BLV-negative animals Targeted culling of high-PVL animals Anthrax Bacillus anthracis Regional disease based on soil characteristics “Anthrax corridor” of North America Important differential for sudden death in ruminants and horses 3-part toxin involved in pathogenesis Anthrax – Clinical Signs Ingested or inhaled forms Found dead Fever, depression, respiratory distress Cutaneous Dark-coloured external lesions Anthrax – Diagnosis Lack of rigor mortis Unclotted blood at orifices Characteristic bacterial appearance on smear Anthrax – Treatment and Prevention Systemic antimicrobials for affected animals Live spore vaccine for at-risk populations Move animals to different pasture Prevent soil contamination Proper carcass disposal Discourage scavenging Caseous Lymphadenitis C. pseudotuberculosis Major cause of abscesses in small ruminants Widespread prevalence CL – Clinical Signs External abscesses Enlarged superficial LNs May spontaneously rupture; white/green pus Internal abscesses Chronic weight loss most common sign Respiratory compromise, colic CL – Clinical Signs CL – Epidemiology Infection via bacteria/pus entering skin abrasion/wound Fly bites Fighting Shearing/vaccination/castration Exposure very common “Tip of the iceberg” disease CL – Diagnosis Assume any external abscess in a small ruminant is CL until proven otherwise! Culture of abscess fluid Diagnostic imaging to identify internal abscesses Valuable breeding stock/pets Characteristic abscess appearance SHI serology – US laboratories CL – Treatment Drain abscesses, flush with iodine Properly dispose of any contaminated materials Surgical LN removal Antimicrobial therapy CL – Prevention and Control Isolate or cull affected animals Vaccination with regular examination of flock/herd and culling animals with external abscesses Shearing/vaccination Young animals first, affected animals last Single-use needles Camelid Hematology Camelids – Anemia Red maple toxicity Mycoplasma haemolamae Endoparasitism C3 ulceration Juvenile Llama Immunodeficiency Syndrome Suspected hereditary immunodeficiency Young llamas (+/- alpacas) Stunted growth Chronic or recurrent infections Low circulating B-cell levels