JPC SYSTEMIC PATHOLOGY
DIGESTIVE SYSTEM
November 2021
D-V11
Signalment (JPC #1210479): An ox
HISTORY: None.
HISTOPATHOLOGIC DESCRIPTION: Superficial oral mucosa: Diffusely, the stratum spinosum is markedly expanded and fragmented by numerous coalescing, variably sized (up to 500um diameter) vesicles and pustules. Vesicles contain homogenous, pale eosinophilic fluid, amorphous eosinophilic cellular debris, basophilic karyorrhectic debris (necrosis), and beaded fibrillar material (fibrin). Pustules additionally contain moderate numbers of viable and degenerate neutrophils, fewer lymphocytes and plasma cells, and eosinophils that infiltrate into the adjacent stratum spinosum. The remaining stratum spinosum epithelium multifocally exhibits intracellular edema (hydropic degeneration) or variable cytoplasmic hypereosinophilia with nuclear pyknosis (necrosis). Multifocally, there are chains of cocci, filamentous bacilli, and plant material adhered to or within the surface epithelium.
MORPHOLOGIC DIAGNOSIS: Oral mucosa: Stomatitis, vesicular and necrotizing, acute, diffuse, severe, breed not specified, bovine.
ETIOLOGIC DIAGNOSIS: Rhabdoviral stomatitis
CAUSE: Vesicular stomatitis virus (rhabdovirus)
CONDITION: Vesicular stomatitis (VS)
GENERAL DISCUSSION:
- Family Rhabdoviridae, genus Vesiculovirus; single-stranded RNA virus
- Two distinct serotypes in the United States:
- VS New Jersey serogroup (VSV-NJ): One subtype; more common and virulent; responsible for most epizootics
- VS Indiana serogroup (VS-IV): Three subtypes
- Two other viruses are known to cause disease:
- VS Alagoas virus (VSV-AV): Formerly Indiana 3
- Cocal virus: Formerly Indiana 2
- Primarily affects horses, cattle, mules, swine and South American camelids;
disease does not occur in sheep and goats
- The only vesicular disease naturally occurring in horses
- Grossly indistinguishable from foot and mouth disease (FMD)
- Enzootic in Central and South America; sporadic in North America
- Seasonal occurrence during warmer weather
- Cattle: Morbidity near 100%; clinical signs in 5-60%; mortality negligible
- Economically important; decreases production in dairy herds
- Young animals rarely show clinical signs
- Self-limiting disease lasting 1-5 weeks
- Secondary infections are common and delay healing; coronary band lesions may
take a long time to heal
PATHOGENESIS:
- Transmission: Abrasions of the skin or mucosa in contact with infected saliva
or vesicular fluid; biting insects feeding on lesions (sand flies and black flies possible reservoirs), non-biting insects and fomites act as mechanical carriers
- Virus probably enters through breaks in the skin or oral mucosa > viral replication in tonsils > viral shedding to oral cavity > epithelial cell destruction and intercellular edema > separation from underlying tissue > local vesiculation and epithelial denudation > spread by local extension to lymph nodes of the head > healing is usually rapid and complete due to neutralizing antibodies and local immunity
- Viremia reported only in swine, laboratory animals, and bats
- Virus cannot penetrate intact skin or mucosa
- The majority of viral replication occurs in the epithelium (stratum spinosum)
- A single surface glycoprotein (G protein) protrudes from the envelope and is the
major antigen enhancing viral infectivity and inducing neutralizing antibody
TYPICAL CLINICAL FINDINGS:
- Incubation period 24-48 hours
- Excessive salivation and vague signs of depression in horses
- Lesions in the mouth lead to salivation, grinding of teeth (bruxism), reluctance
to eat, and weight loss
- Coronary band lesions > lameness (often first sign in swine); rarely sloughing of
claws/hooves
- Teat lesions > sudden drop in milk production; mastitis
TYPICAL GROSS FINDINGS:
- Blanched, flat, raised papules, vesicles, erosions, and ulcers in and around the
mouth, coronary bands, and teats
- Can lead to extensive sloughing of the epithelium
- Oral lesions: Tongue, lips, oral commissures, gingiva, hard palate, and nostrils
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Intercellular edema (spongiosis) of stratum spinosum
- Cells dissociate and become necrotic > forming enlarging coalescing vesicles that
fill with transudate
- Neutrophil and macrophage infiltration in response to necrosis
- Ruptured vesicles leave erosions
- No inclusion bodies
ULTRASTRUCTURAL FINDINGS:
- Bullet-shaped, 80x20 nm, enveloped virions with an internal helical coil and an
outer membrane with glycoprotein projections
- Virions bud from cytoplasmic membrane into the dilated intercellular spaces
- Submembranous vacuolation; focal separation of the apposed cell surfaces;
lysis of desmosomes occur at sites of virion formation
ADDITIONAL DIAGNOSTIC TESTS:
- Virus isolation from vesicular fluid and associated epithelium
- Serum neutralization, complement fixation, fluorescent antibody tests, IgM-IgG ELISA, PCR
- Titers can persist for years but have a limited protective effect
DIFFERENTIAL DIAGNOSIS:
Vesicular diseases of cattle:
- Foot and mouth disease (Picornaviridae, Aphthovirus): Clinically identical but
affects only cloven-hoofed animals
Vesicular diseases of pigs:
- Vesicular stomatitis
- Foot and mouth disease
- Vesicular exanthema of swine (Caliciviridae, Vesivirus)
- Swine vesicular disease (Picornaviridae, Enterovirus)
- Senecavirus A (Picornaviridae, Senecavirus)
Erosive diseases of cattle:
- Infectious bovine rhinotracheitis (Bovine herpesvirus 1)
- Bovine viral diarrhea (Flaviviridae, Pestivirus)
- Bluetongue (Reoviridae, Orbivirus)
- Rinderpest (Morbillivirus)
- Malignant catarrhal fever (gammaherpesvirus)
- Trauma
- Photosensitization (lightly pigmented skin on the face and muzzle)
COMPARATIVE PATHOLOGY:
- The only vesicular disease naturally occurring in horses
- Sheep and goats often seroconvert; clinical signs are rare
- Deer mouse: Systemic infection in intranasally infected deer mice; disseminated
CNS infection in juveniles infected intradermally; viremia in nestling mice infected by black fly bite; may play a role as a potential reservoir or amplifying host for VSNJV
- Guinea pigs, mice and monkeys can be infected experimentally
- Wildlife: Serologic evidence of viral exposure in numerous species, including
white-tailed deer, elk, raccoons, rodents, and opossums
- Pigs: Senecavirus A (SVA) presents with similar characteristics; mild clinical lesions and signs; cutaneous vesicles that rupture to form ulcers on lips, snout, tongue and feet
- Vesicular stomatitides:
|
Disease |
Cause |
Ruminant |
Swine |
Horse |
|
Foot-and-mouth disease |
Aphthovirus |
+ |
+ |
-- |
|
Swine vesicular disease |
Enterovirus |
-- |
+ |
-- |
|
Vesicular stomatitis |
Rhabdovirus |
+ |
+ |
+ |
|
Vesicular exanthema of swine |
Calicivirus |
-- |
+ |
-- |
|
Seneca virus disease |
Senecavirus |
-- |
+ |
-- |
REFERENCES:
- Berminger ML, O’Hearn E, Lomkin R, Newens K, Havas KA. A post-infection serologic assessment of cattle herd immune status after a vesicular stomatitis outbreak and the agreement of antibody assays. J Vet Diagn Invest. 2018:30(4):510-516.
- Cargnelutti JF, Olinda RG, Maia LA, et al. Outbreaks of vesicular stomatitis Alagoas virus in horses and cattle in northeastern Brazil. J Vet Diagn Invest. 2014;26(6):788-794.
- Gelberg HB. Alimentary system and the peritoneum, omentum, mesentery and peritoneal cavity. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Mosby; 2017:345-347.
- Mesquita LP, Bruhn FRP, Majorka PC, Howerth EW. Expression Kinetics of RANTES and MCP-1 in the Brain of Deer Mice (Peromyscus maniculatus) Infected with Vesicular Stomatitis New Jersey Virus. J Comp Pathol. 2016:155(4):326-338.
- Mesquita LP, Diaz MH, Howerth EW, et al. Pathogenesis of Vesicular Stomatitis New Jersey Virus Infection in Deer Mice (Peromyscus maniculatus) Transmitted by Black Flies (Simulium vittatum). Vet Pathol. 2017:54(1):74-81.
- Segales J, Barcellos D, Alfieri A, Burrough E, Marthaler D. Senecavirus A: An Emerging Pathogen Causing Vesicular Disease and Mortality in Pigs? Vet Pathol. 2017:54(1):11-21.
- Uzal FA, Plattner BL, Hostetter JM. Alimentary system. In: Maxie MG, eds. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 2. 6th ed. St. Louis, MO: Elsevier; 2015:117-158.
- Zachary JF. Mechanisms of microbial infections. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Elsevier; 2017:200, 227.
