Cattle - Haemolymphatic Dz

Question 1

In what breeds is Factor XI deficiency reported? What is the mode of inheritance and genetic defect which causes the condition?

Answer 1

• Holstein, Holstein-Friesian and Japanese Black cattle.
• Autosomal recessive inheritance.
• Mutation of F11 gene.

Question 2

What are the clinical manifestations reported in cattle with Factor XI deficiency?

Answer 2

• Asymptomatic.
• Prolonged bleeding.
• Decreased resistance to infection.
• Increased prevalence of repeat breeding.
• Prolonged APTT, normal PT (intrinsic pathway only).

Question 3

In what breeds is Factor VIII deficiency (Haemophilia A) reported? What is the mode of inheritance of this condition?

Answer 3

• Japanese Brown and Hereford cattle; QHs.

- X-linked recessive; clinical disease usually occurs in males but is possible in females.

Question 4

What are the clinical manifestations reported in cattle with Factor VIII deficiency (Haemophilia A)?

Answer 4

• Factor VIII conc 5% normal: may see excessive haemorrhage post-trauma.
• Prolonged APTT, normal PT (intrinsic pathway only).

Question 5

Does vasculitis occur commonly in cattle? What agents has it been associated with?

Answer 5

• Vasculitis occurs rarely in cattle.

- Has been reported secondary to septicaemic diseases incl MCF and Bluetongue.

Question 6

List the aetiologic agent of Bovine Anaplasmosis.

Answer 6

• Anaplasma marginale.
• Obligate intraerythrocytic, gram-negative bacteria of the order Rickettsiales, family Anaplasmataceae, genus Anaplasma.

Question 7

Describe the epidemiology of Bovine Anaplasmosis.

Answer 7

• Transmitted by tickes of the ixodid spp, mainly Dermancentor in US and Rhipicephalus in tropical/subtropical climates.
• Maintained by asymptomatic carrier state in cattle and possibly in wild ruminants.
• Disease occurs in Summer and Spring.
• Severity of CSx related to strain virulence, breed resistance, age-related susceptibility (younger).
• Incubation period 15-30d.

Question 8

List clinical signs of Anaplasmosis in cattle.

Answer 8

• Fever, lethargy, anorexia.
• Dec milk production.
• Dec rumination.
• Dry muzzle.
• MM pallid or icteric if survive first 2-3d.
• +/- neuro signs.
• +/- constipation w dark brown, mucus-covered faeces.
• +/- pollakiuria w dark yellow urine.
• +/- abortion if infected during late gestation.
• If survive: 3-4wk convalescence; infected for life (–> asymptomatic carrier).

Question 9

Describe diagnostic test findings in cattle with Anaplasmosis.

Answer 9

• Acute: rapid drop in PCV; 5-70% RBCs contain A. marginale morula on Wrights or Giesma stain.
• Chronic: regen anaemia: anisocytosis, basophilic stippling, poikilocytosis, polychromatophilia, reticulocytosis.
• Serology: cELISA highest sens/spec (OIE/USDA test for carriers) > complement fixation.
• PCR on whole blood during acute infection.

Question 10

Describe the pathophysiology of Bovine Anaplasmosis.

Answer 10

• Most commonly ticks transfer to cattle; may be trans by biting flies, dehorning/castration etc equi, blood trans.
• Bacteria rapidly replicates in vesicles in RBCs –> 10-90% infected.
• Anaemia occurs secondary to splenic and hepatic macrophage phagocytosis of infected and non-infected RBCs.
• Immune-reaction: auto-ABs against erythrocyte surface antigens and activation of macrophaghes to enhanve phagocytosis –> remove many but not all bacteria from blood (antigenic variants) –> recurring waves of bacteraemia and immune reactions.

Question 11

Describe findings on necropsy of cattle that have died from Anaplasmosis. What finding differentiates this disease from Bovine Babesiosis, Leptospirosis, Copper toxicity and Clostridial infection?

Answer 11

• No pathognomic findings.
• Blood is thin, icterus, splenomegaly, hepatomegaly.
• Lack of haemoglobinuria and haemoglobinaemia differentiates from other listed diseases as haemolysis is intravascular in Anaplasmosis.

Question 12

Outline treatment and prevention methods for Bovine Anaplasmosis.

Answer 12

• Tetracyclines NB do not prevent persistent infection.
• +/- blood transfusion.
• Endemic area: expose cattle when young –> asymptomatic carriers.
• Non-endemic areas: live vacc of young cattle (only licensed in California in USA).
• Tick spray, fly ear tags.

Question 13

What other names is Babesiosis known by in cattle?

Answer 13

• Piroplasmosis.
• Tick fever.
• Texas fever.
• Redwater.
• Tristeza.

Question 14

List the aetiologic agents of Babeiosis in cattle.

Answer 14

• > 6 species of Babesia can cause dz in cattle.
• Intra-erthyrocytic protozoa.
• USA:
  i) B. bigemina: big, pale, pear-shaped, acute angle paired inclusions.
  ii) B. bovis (more virulent): small, pleomorphic, round or pear-shaped, obtuse-angle paired inclusions.

Question 15

Outline the epidemiology of Babesiosis in cattle.

Answer 15

• Tick-bourne dz.
• Transmitted by Boophilus spp in USA.
• Trans by adults, nymphs, larvae of ticks or mechanical vectors e.g. biting flies, contained dehorning etc equip.
• Incubation period: 5d->3wk.
• Bos indicus and

Question 16

List the clinical signs of Babesiosis in cattle.

Answer 16

• Fever, depression, anorexia.
• Icterus.
• Tachypnoea.
• Tachycardia.
• Haemoglobinaemia and haemoglobinuria.
• Abortion.
• Death.
• +/- central babesiosis (secondary to anoxia): hyperexciteability, opisthotonus, coma, death.
• Outcome: death, asymptomatic carrier or persistent infection w recrudescence of infection and death.

Question 17

Describe the pathophysiology of Babesiosis in cattle.

Answer 17

• Babesia enters bloodstream, infects RBCs.
• Intravascular haemolysis due to emergency of merozoites from infected RBCs and osmotic fragility of whole (incl uninfected) RBC population.
• +/- autoimmune removal of infected RBCs by spleen.
• Results in rapid anaemia despite low parasitaemia.

Question 18

How is Babesiosis diagnosed in cattle?

Answer 18

• Blood smear: organisms identified in RBCs following Giesma stain.
• IFA or complement fixation.

Question 19

List necropsy findings in cattle with Babesiosis.

Answer 19

• Pallor, icterus.
• Enlarged liver.
• Distended gall bladder.
• Dark red urine (acute).
• +/- hydropericardium.
• +/- subepi, subendo, GI petechiae.

Question 20

Outline treatment of Babesiosis in cattle.

Answer 20

• Supportive care: blood transfusion, IVFT, prophylactic ABs, minimal handling.
• Anti-protozoals: imidocarb (tx and prev), diminazene diacturate, phenamidine diisethionate, amicarbalide diisethionate.

Question 21

Outline prevention of Babesiosis in cattle.

Answer 21

• Young animals: live vaccine.
• Older animals: live vaccine + imidocarb.
• Sub-unit vaccines may modify severity of dz.
• Tick control: acaricide, controlled range burning, cultivation, pasture rest.

Question 22

List causes of Heinz body haemolytic anaemia in cattle which are unique to those reported in horses.

Answer 22

• Grazing selenium deficient pastures.

- Grazing rye grass (Secale cereale) pastures.

Question 23

Describe water intoxication as a cause of haemolytic anaemia in cattle.

Answer 23

• Reported in milk-reared calves when first allowed water –> excess water consumption; 4-5mo at highest risk.
• Prod marked hypotonicity of body fluids –> intravascular haemolysis due to osmotic lysis of RBCs.
• CSx: neuro deficits, resp distress, haemoglobinuria and death in some cases.
• Clin path: haemolytic anaemia, hypoproteinaemia, hypochloraemia, hyponatraemia, hyposmolality, haemoglobinuria, hyposthenuria.
• Tx: restrict access to water; if profound hyponatraemia may need hypertonic saline, mannitol, corticosteroids.

Question 24

What is the aetiology of postparturient haemoglobinuria?

What is the signalment of cows most commonly affected?

Answer 24

• Phosphorus deficiency –> low intracellular phosphate conc interferes w energy metab –> affects cell viability and ability of RBCs to cope w potential haemolysins.
• High-producing multiparous cows that dev CSx within one month of calving.

Question 25

Describe the clinical presentation of postparturient haemoglobinuria in cattle.

Answer 25

• Depression, dec feed consumption, dec milk prod.
• Haemoglobinuria and icterus.
• Marked anaemia w marked regen response after 4-5d.

Question 26

Describe treatment of postparturient haemoglobinuria in cattle.

Answer 26

• Blood transfusion.
• IVFT.
• IV sodium acid phosphate followed by oral phosphorus supplementation.
• Correct herd dietary imbalances.

Question 27

Describe the effect of bracken fern ingestion of the bone marrow of cattle and the subsequent clinical condition seen after 2-8wks on an affected pasture.

Answer 27

• Bone marrow suppression –> pancytopaenia.
• CSx: fever, melena, epistaxis, haematuria, mucosal petechiation, hyphema, bleeding from the eyes and vulva.
• CBC: platelet count

Question 28

Describe the bacteria responsible for causing Anthrax.

Answer 28

• Bacillus anthracis.
• Vegetative form: large, rectangular-shaped, gram positive rod.
• Vegetative form predominately found in infected animal tissues but can exist in enviro.
• Forms spores under nutritionally limited conditions (aerobic process) –> stable in enviro for decades.

Question 29

Describe the epidemiology of Anthrax in livestock.

Answer 29

• Found worldwide.
• Soils with elevated pH, Mn++, Ca++ and rich in organic material favour spore survival.
• Drought followed by heavy rain or earth-disturbing activities often –> outbreak.
• Outbreaks usually during warmer part of year.
• Bloodsucking insects transfer B. anthracis b/w animals.
• Scavengers disseminated bacteria and carcasses of infected animals contaminate the enviro.
• Susceptibility: ruminants > horses > pigs.

Question 30

Describe the pathophysiology of Anthrax in livestock.

Answer 30

• Exposure: grazing contaminated pastures (spores), forage grown on contam pastures, animal by-products, insects.
• Ingested anthrax spores gross mucosal barriers, phagocytosed by macro, travel to LNs –> convert to vegetative stage and kill host cell –> enter extracellular enviro.
• Virulence factors:
  i) Poly-D-glutamic acid capsule: evade phagocytosis.
  ii) Three-component toxin: protective antigen - attaches to cell and on of other 2 factors, enters cell by endocytosis and forms pore to let other 2 factors in; lethal factor and oedema factor - interrupt cells immune functions, phagocytic capacity, cAMP prod –> oedema, cell death, expression of pro-inflamm cytokines.
• B. anthracis proliferates rapidly in the host –> overwhelming septicaemia –> death due to hypotensive shock and multi-organ failure.

Question 31

List clinical signs of Anthrax in sheep, goats and cattle.

Answer 31

• Typically peracute form –> sudden death.
• May see fever, depression, resp distress, MM congestion, convulsions, bloody dxa, haematuria, localised tissue swelling.

Question 32

List clinical signs of anthrax in pigs.

Answer 32

• Most common form: oropharyngeal form w swelling of head, neck, cervical LNs; may obstruct breathing and swallowing.
• GI form present as dysentary.
• Pregnant sows may abort.

Question 33

Describe findings on necropsy of animals that have died from Anthrax.

Answer 33

• Carcass decomposes rapidly.
• May see bloody exudates from body cavities and blood may not clot.
• Spleen enlarged with ‘blackberry jam’ consistency.
• LNs and internal organs may be oedematous and haemorrhagic.
• Localised exposure may result in enteritis, regional LN involvement, peripheral tissue oedema.
• Histo: large numbers of bacilli in affected tissues.

Question 34

Outline diagnostic test findings in Anthrax cases.

Answer 34

• DO NOT OPEN CARCASS!!! –> sporulation of vegetative cells and contam of enviro; use PPE!!!
• Dx based on microscopic exam of blood or tissue smears, bacterial culture; NB warn lab personnel (zoonotic risk).
• Samples: blood, AQ, whole eye; LN if localised dz.
• B. anthracis cells are destroyed during decomp, so take samples early.
• Large, gram pos, square-ended rods found singly or in chains of 2-4; polychrome methylene blue (M’Faydean stain) identifies capsule surrounding the organism.

Question 35

Describe measures for treatment and control of Anthrax in large animals.

Answer 35

• Report suspected case to local/state vet ASAP.
• Tx often unrewarding/not possible due to peracute nature of dz; can try penicillin or oxytet for at least 5 days.
• Carcasses should not be opened or moved; burn carcass and contam bedding/soil > deep burial.
• Premise quarantined; clinically normal animals vaccinated w live acapsular vacc, vaccinate neighbouring herds, control insects and scavengers to limit spread.
• Endemic areas: vacc 4 weeks prior to turning out on pasture where previous outbreak has occurred; rpt in 2-3 weeks if heavily contam area; goats and llamas may have severe adverse reactions to vaccine!
• Ideally do not graze contam areas.

Question 36

Describe C. pseudotuberculosis infection in cattle.

Answer 36

• Sporadic herd problem, doesn’t affect production.
• Most common form is cutaneous excoriated granulomas’ mastitis, visceral and mixed infections also reported.
• Granulomas: ulcerative, exuding, granulomatous lesions up to 20cm diam that can be excised to leave underlying granulation tissue bed; lesions usually on face, neck, thorax, flanks; spontaneous heal in 2-4wks.