JPC SYSTEMIC PATHOLOGY
Hemolymphatic System
April 2018
H-P05

Signalment (JPC Accession # 1913179):  Bull, age and breed unspecified

HISTORY:  This bull was inoculated with an infectious agent.  On day 8 post-inoculation, there was a slight febrile reaction.  By day 18, the peripheral lymph nodes were enlarged.  The animal became progressively anorectic and emaciated and was euthanized and necropsied on day 25.

HISTOPATHOLOGIC DESCRIPTION:  Slide A:  Lymph node:  Diffusely, the cortical and medullary architecture is expanded and obscured by sheets of large, monomorphic “lymphoblastic cells” that multifocally infiltrate the capsule.  Lymphoblasts have variably distinct cell borders, scant amphophilic cytoplasm, round to oval vesiculate nuclei, and 1-2 prominent nucleoli.  Mitotic figures average 4 per 40X HPF.  Rarely lymphoblasts contain 1-2 um diameter, round, basophilic, intracytoplasmic protozoal schizonts (Koch’s bodies).  There is multifocal lymphocytolysis in both the cortex and paracortical areas.  Cortical germinal centers are often replaced by small foci of fibrin and eosinophilic and karryorhectic debris (necrosis).    Small numbers of tingible body macrophages are randomly scattered within the cortex and medulla.  Multifocally, cortical and medullary sinuses contain mild, draining hemorrhage admixed with low numbers of hemosiderin laden macrophages.  The lymph node capsule is thickened up to 2x normal and expanded by low numbers of lymphocytes, plasma cells, fewer macrophages and hemorrhage.

MORPHOLOGIC DIAGNOSIS:  Lymph node:  Hyperplasia, lymphoblastic, diffuse, severe, with multifocal necrosis and intralymphoblastic protozoal schizonts, breed not specified, bovine.

HISTOPATHOLOGIC DESCRIPTION:  Slide B: Cerebrum: There are multifocal to coalescing areas of necrosis within the cortex and extending into the medulla.  Affected areas are often well demarcated and characterized byloss of grey and white matter and replacement by necrotic debris containing many gitter cells mixed with fewer lymphocytes and plasma cells, and moderate amounts of hemorrhage, fibrin, and proteinaceous fluid (infarct). Adjacent cortical and meningeal vessels are often partially occluded by fibrin thrombi and/or distended by manylymphoblastic cells. Lymphoblasts have distinct cell borders, scant amphophilic cytoplasm, and large, irregularly round, vesiculate nuclei with 1-2 prominent nucleoli. Mitotic figures among lymphoblasts average 1 per 40X HPF; and occasionally, lymphoblasts contain 1-2 um diameter, round, intracytoplasmic protozoal schizonts (Koch’s bodies). Diffusely, blood vessels within the neuropil and meninges are lined by hypertrophied, reactive endothelium; and rarely, vessel walls are disrupted by low numbers of neutrophils, macrophages, fibrin, edema and necrotic debris (vasculitis). Multifocally, Virchow-Robin space and the meninges are expanded up to 3x normal by moderate numbers of lymphocytes, plasma cells, and fewer macrophages and lymphoblasts. Diffusely, there is vacuolation of the gray matter (spongiosis), mild gliosis consisting of low to moderate numbers of astrocytes, fewer gemistocytic astroctytes, and rod-shaped microglia.  Multifocally within the white matter there are dilated myelin sheaths and swollen, eosinophilic axons (spheroids).

MORPHOLOGIC DIAGNOSIS:  Cerebrum:  Encephalomalacia, acute, multifocal to coalescing, marked with multifocal thrombosis (infarct), moderate nonsuppurative meningoencephalitis, many intra and perivascular lymphoblasts, and intralymphoblastic protozoal schizonts, breed not specified, bovine.

ETIOLOGIC DIAGNOSIS:  Lymph nodal and cerebral theileriosis

CAUSETheileria parva parva

SYNONYMS:  East Coast Fever; turning sickness

GENERAL DISCUSSION:

PATHOGENESIS:

TYPICAL CLINICAL FINDINGS:

TYPICAL GROSS FINDINGS:

TYPICAL LIGHT MICROSCOPIC FINDINGS:

ADDITIONAL DIAGNOSTIC TESTS:

DIFFERENTIAL DIAGNOSIS:

COMPARATIVE PATHOLOGY:

References:

  1. Boes KM, Durham AC. Bone marrow, blood cells, and the lymphoid / lymphatic system.  In: Zachary JF, ed. Pathological Basis of Veterinary Disease. 6th ed. Philadelphia, PA: Mosby Elsevier Inc.; 2017:748-749.
  2. Constable PD, Hinchcliff KW, Done SH, Grünberg W. Veterinary Medicine: A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses. 11th ed. London, England, UK: WB Saunders Company LTD; 2017:2144-2145.
  3. Dessauge F, Lizundia R, Baumgartner M, Chaussepied M, Langsley G. Taking the MThyc is bad for Theileria. Trends Parasitol. 2005;21:377-85.
  4. Forsyth LMG, Minns FC, Kirvar E, et al. Tissue Damage in Cattle Infected with Theileria annulata Accompanied by Metastasis of Cytokine-producing, Schizont-infected Mononuclear Phagocytes. J Comp Path. 1999;120:39-57.
  5. Lawrence JA, de Vos AJ, Irvin AD. East Coast Fever; Turning Sickness. In: Coetzer JAW, Thomson GR, Tustin RC, eds. Infectious Diseases of Livestock with special reference to Southern Africa. 2nd ed. Vol 1. Oxford, UK: Oxford University Press; 1994:309-314,331-333.
  6. Mans BJ, Pienaar R, Latif AA. A review of Theileria diagnostics and epidemiology. Int J Parasitol Parasites Wildl. 2015;4(1):104-118.
  7. Miller LM, Gal A. Cardiovascular system and lymphatic vessels.  In: Zachary JF, ed. Pathological Basis of Veterinary Disease. 6th ed. Philadelphia, PA: Mosby Elsevier Inc.; 2017:605.
  8. Stockham SL, Kjemtrup AM, Conrad PA, et al. Theileriosis in a Missouri beef herd caused by Theileria buffeli: Case report, herd investigation, ultrastructure, phylogenetic analysis, and experimental transmission. Vet Pathol. 2000;37:11-21.
  9. Valli VEO, Kiupel M, Bienzle D. Hematopoietic system. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 3. 6th ed. Philadelphia, PA: Elsevier Saunders; 2016:176-178.


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