JPC SYSTEMIC PATHOLOGY
Signalment (JPC #1848505): 14-day-old Duroc pig
HISTORY: Suckling pigs and sows were sick. Only the suckling pigs died following a disease characterized by anorexia, depression, diarrhea or constipation, and staggering gait.
- Adrenal gland: Multifocally affecting 10% of the cortex, medulla and the corticomedullary junction are individual to coalescing areas of lytic necrosis, up to 0.5 by 0.3 mm, characterized by loss of normal architecture with replacement by eosinophilic cellular and karyorrhectic debris. Primarily on the periphery of the necrotic foci, there are multifocal cortical cells that contain an eosinophilic, 2-6 um, round to oval, intranuclear viral inclusion body that often marginates the chromatin. There is scattered single cell necrosis characterized by cells that are shrunken, hypereosinophilic, with pyknotic nuclei. There are few viable and degenerate neutrophils scattered within the cortex, minimal multifocal hemorrhage, and rare mitotic figures within the zona glomerulosa.
- Eye (not present on all slides): There are focally extensive areas of predominantly neutrophilic inflammation admixed with necrotic debris and variably sized aggregates of basophilic, mixed bacteria that replace the corneal epithelium (ulceration) and the corneal stroma (keratitis). Corneal stromal fibers are disorganized and often separated by increased clear space (edema), reactive fibroblasts, low numbers of lymphocytes, macrophages and small caliber blood vessels (vascularization). Diffusely, the bulbar conjunctiva is similarly affected. Multifocally, there are colonies of 1 um diameter cocci along the conjunctival surface.
- Adrenal gland, cortex: Adrenalitis, necrotizing, acute, multifocal, moderate, with intranuclear eosinophilic viral inclusion bodies, Duroc, porcine.
- Eye, cornea and bulbar conjunctiva: Keratoconjunctivitis, necrosuppurative, acute, diffuse, with edema and vascularization.
ETIOLOGIC DIAGNOSIS: Alphaherpesviral adrenal necrosis
CAUSE: Suid herpesvirus 1 (SuHV-1)
CONDITION / SYNONYMS: Pseudorabies;Aujeszky’s Disease; Mad Itch; infectious bulbar paralysis; porcine herpesvirus infection
- This is primarily a disease of swine that can spread both vertically and horizontally, causing abortions and respiratory disease in older pigs and CNS signs in neonatal pigs
- It lacks host specificity and can infect a wide range of secondary hosts and is lethal due to nonsuppurative meningoencephalomyelitis; secondary hosts include horses, cattle, sheep, dog, cat, rabbit (lab animal spp), many feral species – people are refractory
- Causes an intense pruritus in secondary hosts – mad itch - especially in cattle
- Endemic in swine (domestic and feral) worldwide
- Epitheliotropic and neurotropic
- Latent infections in trigeminal ganglion, olfactory bulb and tonsil
- Transmission: Direct contact (contaminated saliva and nasal secretions), fomites or aerosol, inhalation or ingestion, abraded skin; regardless of route, virus found in nasal secretions; non-porcine/secondary carnivore hosts are infected thru ingestion of infected pig meat and ruminants via direct contact, aerosol or contaminated feed
- Inhalation: Primary viral replication in upper respiratory epithelium (pharynx, nasal cavity, tonsil)
- Invades sensory nerve endings > transported in axoplasm to the olfactory bulb and up the trigeminal, glossopharyngeal, facial, and vagus nerves to cerebral interpretive centers; it causes a ganglioneuritis at many sites
- The virus may also spread to the spinal cord and then to peripheral nerves, and may circulate in blood
- Can also infect tonsils and lungs > viral dissemination either in free form or via infected leukocytes > visceral infection > nervous system invasion via autonomic nerves
- Inoculation: Local reaction > centripetal spread along nerve to spinal cord > outward spread along peripheral nerves and concurrent spread up spinal cord to the brain
- Ingestion: (usually of infected pig meat) Transport across epithelium via M cells to mononuclear cells of Peyer's patches; also localizes in myenteric plexus > Nervous system along autonomic nerves
TYPICAL CLINICAL FINDINGS:
- Neonatal and weaned piglets (<9 weeks old)
- Very young piglets – rapid prostration and death with no premonitory signs
- Older piglets – incoordination, paralysis, tremors, convulsions and respiratory signs; may recover in 5-10 days
- “Dog sitting” posture due to respiratory distress
- Mortality may reach 100% in neonatal piglets infected in the first two weeks of life, decreasing to 50% in the 3rd and 4th weeks
- Grower-finisher and adult pigs: fever, rhinitis, coughing and anorexia
- Sows: fetal resorption (<30 days gestation), mummification, stillbirth or abortion
- Intense cutaneous pruritus in other animals (i.e. “mad itch” at point of inoculation), which eventually results in death
TYPICAL GROSS FINDINGS:
- May be minimal or absent with no specific gross lesions
- Necrotizing rhinitis, tonsillitis, esophagitis, and tracheitis
- Tiny foci of hemorrhagic necrosis in the liver, spleen, lungs, intestines, placenta and adrenal glands in suckling pigs
- Necrotizing endometritis, placentitis, oophoritis
- May see keratoconjunctivitis
- Site of cutaneous infection in cases of pseudorabies (non-specific gross lesions): Epithelial necrosis, ballooning degeneration, serofibrinous inflammation with rare viral intranuclear viral inclusions
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Reflect the epitheliotropic and neurotropic nature of the virus
- CNS lesions (brain lesions more common in ruminants and carnivores)
- Non-suppurative inflammatory lesions in the brain
- Acidophilic intranuclear inclusions in neurons and astroglia
- Solid and amphophilic in swine
- Granular, small and multiple in nuclei of other species
- Marked perivascular cuffing with nonsuppurative meningoencephalitis, ganglioneuritis (in paravertebral ganglia)
- Necrosis of neurons with neuronophagia and gliosis
- Piglets develop panencephalitis, most severe in brainstem, cerebral cortex and spinal ganglia; in other species lesions dependent on route of exposure
- Epithelial lesions (more common in young and aborted piglets)
- Tiny areas of coagulative or lytic necrosis of liver, tonsils, lung, spleen, placenta and adrenals with INIB’s; hemorrhage is variable
- Adrenal glands: INIB’s, necrosis and hemorrhage of the cortex and medulla with lymphohistiocytic infiltrate in later stages
- Lung: mild edema with diffuse cellular infiltrate to necrohemorrhagic pneumonia
- Lymphoid necrosis
- Stillborn/aborted fetuses: no encephalitis; foci of necrosis in liver with bronchiolar necrosis and interstitial pneumonia
- Approximately 180nm diameter virions with a nucleocapsid core surrounded by three concentric shells: inner, middle and outer capsids; nonenveloped virions in the nucleus that acquire an envelope during passage through the nuclear membrane
ADDITIONAL DIAGNOSTIC TESTS:
- Enzyme immunoassay, fluorescent antibody, virus isolation
DIFFERENTIAL DIAGNOSIS: (Adrenal cortical necrosis)
- High concentration of local anti-inflammatory steroids in cortex > suppression of local cell-mediated immunity > preferential growth of fungi, bacteria and protozoa > necrosis and inflammation
- Protozoa (Toxoplasma gondii, Neospora caninum, Sarcocystis spp.): focal necrosis with minimal inflammation
- Bacterial septicemia: often gram negative organisms; focal necrosis and suppuration
- Mycobacteria: cattle and humans
- Systemic fungal organisms (Histoplasma capsulatum, Coccidiodes immitis, Cryptococcus neoformans): dogs and cats in endemic areas; cortical granulomas with cortical hypertrophy
- Rickettsia rickettsii (Rocky Mountain Spotted Fever): dogs and people
- Uniformly fatal in secondary hosts
- Transmission typically via ingestion
- Typically causes intense pruritus in secondary hosts - mad itch
- Nonsuppurative meningoencephalomyelitis: cattle, sheep, dogs, cats, rabbits (most susceptible lab animal), guinea pigs, raccoons, rats, mice, opossum, skunk
- Fatal degenerative angiopathy in mink (viremia and endotheliotropism)
- Rare reports in horses and goats
- Not reported in humans
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