JPC SYSTEMIC PATHOLOGY

NERVOUS SYSTEM

April 2017

N-V02 (NP)

 

Signalment (JPC# 1446702):  Two near-term ovine fetuses

 

HISTORY:  Both of these animals were from a flock in which adults of both sexes were ill and there had been several deaths.  Abortions had occurred, and many ewes had given birth to small weak lambs.

 

HISTOPATHOLOGIC DESCRIPTION:  Cerebrum:  Diffusely, gyri are markedly thinned, and multifocally the white matter and deep gray matter are lost, often forming areas of cavitation (necrosis).  Within adjacent areas, small caliber blood vessels are closely apposed (stromal collapse) and surrounded by a small amount of vacuolated to amphophilic-fragmented neuropil and high numbers of glial cells, including reactive astrocytes and moderate numbers of microglial cells (gliosis).  Bordering the cavitated areas in the gray matter, are scattered shrunken neurons with hypereosinophilic cytoplasm and loss of nuclei (necrosis).  Multifocally throughout, Virchow-Robin space is mildly expanded by low numbers of lymphocytes and plasma cells (perivascular cuffing).

 

Tongue:  Essentially normal tissue.

 

MORPHOLOGIC DIAGNOSIS:  1. Cerebral cortex, white and deep gray matter: Necrosis and loss, acute, multifocal, marked, with gliosis and perivascular lymphoplasmacytic inflammation, breed unspecified, ovine.

 

2.  Tongue:  No significant lesions.

 

ETIOLOGIC DIAGNOSIS:  Orbiviral encephalopathy

 

CAUSE:  Ovine orbivirus; Bluetongue virus (BTV)

 

CONDITION:  Bluetongue; Soremuzzle

 

GENERAL DISCUSSION:

·       Bluetongue is a non-contagious viral disease of sheep that causes hydranencephaly and porencephaly in lambs and calves

·       Goats and adult cattle are largely asymptomatic

·       Family Reoviridae, genus Orbivirus, nonenveloped, double stranded RNA virus; over 24 serotypes described

 

PATHOGENESIS: 

·       Culicoides sp. (midge, gnat) ingests infected blood meal > virus replicates and infects salivary glands 10-15 days post-ingestion > Culicoides sp. bites sheep > virus replicates in regional lymph nodes and spleen > viremia > virus replicates in endothelial cells throughout body > endothelial cell damage > hemorrhage, edema, thrombosis and infarction

·       Congenital bluetongue occurs in lambs and calves when the dam receives a live, attenuated bluetongue virus vaccine or contracts bluetongue infection during pregnancy

·       Type of congenital CNS anomaly depends on fetal age at time of inoculation or infection

·       Necrosis of the precursor cells in the subventricular zone, which are essential in the formation of the cerebral cortical white matter > cavitation

 

TYPICAL CLINICAL FINDINGS: 

·       Lethargy, circling, head pressing, blindness-loss of normal pupillary light reflexes

·       Hypermetria and spasticity if cerebellum is affected

 

TYPICAL GROSS FINDINGS:

·       Congenital anomalies (lambs) varies with stage of gestation that the dam is infected:

·       < 50 days: Fetal absorption or abortion

·       50 - 55 days: Hydranencephaly and retinodysplasia

·       75 days: Porencephalic cysts (no ocular lesions)

·       > 100 days: Mild focal meningoencephalitis

·       Bluetongue viral infection of fetal calves can cause hydranencephaly

·       Systemic bluetongue: focal hemorrhage of the tunica media at the base of the pulmonary artery, hemorrhage of the ruminal pillars, tongue cyanosis, erosions and ulcers of oral mucosa, laminitis, coronitis, skeletal and cardiac muscle hemorrhage, edema and necrosis

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

·       Lambs infected at 50 - 55 days gestation: Severe necrotizing encephalopathy and retinopathy

·       At 75 days gestation:  Multifocal encephalitis, vacuolation of white matter, formation of a porous cavity lined by astrocytes and hemosiderin-laden macrophages

·       At 100 days gestation:  Focal mild meningoencephalitis

 

ULTRASTRUCTURAL FINDINGS:

·       Virions in the cytosol are icosahedral, nonencapsulated, approximately 75 nms in diameter; inner electron-dense core of 45 nms surrounded by an inner shell

 

ADDITIONAL DIAGNOSTIC TESTS: 

·       ELISA, AGID, complement fixation

 

DIFFERENTIAL DIAGNOSIS: 

Causes of hydrancephaly and porencephaly in sheep:

·       Border disease (Flaviviridae, Pestivirus):  Hypomyelinogenesis, porencephaly, hydranencephaly, cerebellar hypoplasia, microencephaly of lambs and goat kids

·       Cache valley virus (Bunyaviridae, Bunyavirus):  Hydranencephaly, microencephaly, cerebellar hypoplasia, absent ventral horn neurons in spinal cord of lambs in U.S.

·       Copper deficiency (Swayback, enzootic ataxia):  Can cause porencephaly in lambs

·       Akabane disease (Bunyaviridae, Bunyavirus):  Porencephaly, hydranencephaly, ventral horn neuronal degeneration in spinal cord of ruminants; Japan, Australia and Israel

·       Rift valley fever (Bunyaviridae, Phlebovirus):  Hydranencephaly of lambs in Africa

·       Wesselsbron disease (Flaviviridae, Flavivirus):  Hydranencephaly of lambs in Africa

·       Schmallenberg virus (Orthobunyavirus):  Hydranencephaly, porencephaly, hydrocephalus, cerebellar hypoplasia and micromyelia in calves, goat kids and lambs

·       Deer, antelope, elk:  Epizootic hemorrhagic disease (Reoviridae, Orbivirus): Causes lesions similar to bluetongue, but often does not result in coronitis

 

COMPARATIVE PATHOLOGY: 

·       Numerous domestic livestock (Cattle, goats  wildlife species are serologically positive for Bluetongue virus yet are usually subclinical or minimal clinical signs

 

References: 

1.      Allen AJ, et al. Bluetongue disease and seroprevalence in South American camelids from the northwestern region of the United States. J Vet Diagn Invest. 2015;27(2):226-230.

2.      Balaro MF, et al. Outbreak of bluetongue virus serotype 4 in dairy sheep in Rio de Janeiro, Brazil. J Vet Diagn Invest. 2014;26(4):567-570.

3.      Cantile C, et al.  Nervous system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 2. 6th ed. Philadelphia, PA: Elsevier Saunders; 2016: 138-139.

4.      Cheville NF, et al. Cytopathology of Viral Diseases. In: Cheville NF, ed. Ultrastructural Pathology: The Comparative Cellular Basis of Disease. 2nd ed. Ames, IA: Wiley-Blackwell; 2009:377.

5.      Dubovi EJ, et al. Isolation of bluetongue virus from canine abortions. J Vet Diagn Invest. 2013; 25(4):490-492.          

6.      Gaudreault NN, et al. Whole genome sequencing and phylogenetic analysis of bluetongue virus serotype 2 strains isolated in the Americas including a novel strain from the western United States. J Vet Diagn Invest. 2014; 26(4):553-557.

7.      Gu X, et al. Longitudinal study of the detection of bluetongue virus in bull semen and comparison of real-time polymerase chain reaction assays. J Vet Diagn Invest. 2014; 26(1):18-26.

8.      Herder V, et al. Salient Lesions in Domestic Ruminants Infected With the Emerging So-called Schmallenberg Virus in Germany. Vet Pathol. 2012; 49(4):588-591.

9.      Laguardia-Nascimento M, et al. Detection of multiple viral infections in cattle and buffalo with suspected vesicular disease in Brazil. J Vet Diagn Invest. 2016; 28(4):377-381.

10.   Maclachan NJ, et al. The pathology and pathogenesis of bluetongue. J Comp Pathol. 2009; 141(1):1-16.

11.   Masters NJ, et al. Tragulidae, moschidae, and cervidae. In: Miller RE, et al, eds. Fowler’s Zoo and Wild Animal Medicine. Vol 8. St. Louis, MO: Elsevier Saunders; 2015: 617-620.

12.   Schroeder ME, et al. Development and performance evaluation of a streamlined method for nucleic acid purification, denaturation, and multiplex detection of Bluetongue virus and Epizootic hemorrhagic disease virus. J Vet Diagn Invest. 2013; 25(6):709-719.

13.   Vandevelde M, et al. Veterinary Neuropathology. Ames, IA: Wiley-Blackwell; 2012: 97, 98.

14.   Zachary JF.  Mechanisms of microbial infections.  In: Zachary JF, eds.  Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Mosby Elsevier; 2017:214.

 


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