1. Vesicular Stomatitis

   1. Vesicular stomatitis (“sore nose” or “sore mouth”) is a highly contagious zoonotic infectious disease.
   2. It is caused by a RNA virus in the family Rhabdoviridae and genus Vesiculovirus.
   3. It affects primarily horses, cattle, and swine but other susceptible species include camelids, wildlife, sheep, goats, and humans.
   4. The disease is enzootic in North, Central and South America and parts of Mexico.
   5. It is a reportable disease in the USA.
   6. It is believed to be transmitted by blood-feeding insects and usually occurs during the summer months. It can also be transmitted via direct contact with infected animals with clinical disease.
   7. Morbidity varies from 10 to 95% but mortality is rare.
   8. Clinical signs:
      1. The incubation period can range from 2 to 8 days and ptyalism is often the first clinical sign noticed.
      2. Lesions are characterized by vesicles, erosions and ulcers and may occur in various body regions such as the tongue, oral mucosa, lips, coronary band, teats and prepuce. Some variations in lesion distribution occur among animal species.
      3. Coronitis with erosions in the coronary band can be seen in cattle, horses and pigs leading to the development of lameness.
      4. Secondary bacterial mastitis may develop, which causes losses of meat and milk production leading to significant economic impact.
      5. The disease is generally self-limiting and resolves within 10-14 days.
      6. Some vesicular stomatitis viruses can cause mild influenza-like disease in humans that lasts 3-5 days, although these infections are rare.
   9. Differential diagnoses:
      1. Foot-and-mouth disease of ruminants and pigs, swine vesicular disease, and vesicular exanthema of swine.
   10. Diagnosis:
       1. Confirmation of a suspected clinical diagnosis is commonly done by the following serologic tests: competitive ELISA, virus neutralization, and complement fixation. Competitive ELISA and virus neutralization titers persist for many years after an outbreak. On the other hand, complement fixation titers are relatively short-lived and provide the best serologic evidence of recent infection.
       2. Viral isolation or detection of viral genetic material via PCR tests can also be used.
   11. Treatment:
       1. No specific treatment is available. Symptomatic and supportive care may be warranted.

2. Scrapie

   1. Scrapie is a chronic, progressive and invariably fatal neurodegenerative disorder naturally affecting sheep and goats. In the USA, the disease occurs primarily in sheep with black face such as Suffolk, Hampshire and their crosses.
   2. It belongs to a group of disorders commonly known as prion protein disorders or transmissible spongiform encephalopathies.
   3. The disease has a worldwide distribution but has not been reported in Australia and New Zealand.
   4. Transmissible mink encephalopathy, bovine spongiform encephalopathy, and chronic wasting disease of deer and elk have been linked to scrapie.
   5. The disease is believed to be caused by the intracellular accumulation of an abnormal form of prion protein.
   6. Transmission occurs during lambing via ingestion of infected allantoic fluid or placenta by newborn lambs and flock mates.
   7. Susceptibility of the disease in sheep is genetic related.
   8. Most cases of clinical scrapie occur in sheep 2–4 years old.
   9. The incubation period is probably modulated by the infectious dose, the age at infection, the prion protein (PrP) genotype of the host, and possibly by the infecting strain.
   10. Clinical signs:
       1. The first signs are usually behavioral changes, which are readily evident to shepherds.
       2. These early signs progress to a more definite neurological illness frequently characterized by signs of pruritus and ataxia.
       3. Intense itch is recognized mainly by compulsive rubbing, nibbling at the skin, and scratching with a hind foot.
       4. Pruritus often begins over the tail head and progresses cranially to involve the flanks, thorax, and occasionally the head and ears.
       5. This may result in extensive loss of wool and self-inflicted skin lesions, particularly over the lateral thorax, flanks, and hindquarters.
   11. Diagnosis:
       1. Clinical diagnosis is based on a detailed history and clinical signs.
       2. Immunohistochemistry of brain and lymphoid tissues from infected animals are needed to confirm a presumptive clinical diagnosis
   12. Treatment:
       1. The disease is invariably fatal, thus, no treatment is instituted.

References

Balch SG. Scrapie. Merck Manual 2022; https://www.merckvetmanual.com/nervous-system/scrapie/scrapie.

Doster AR. Skin diseases of swine. J Swine Health Prod 1995; 3: 256-261.

Jeffrey M, González L. Scrapie. In: Diseases of sheep. Blackwell Publishing, Iowa, 2007; 241-250.

Pelzel-McCluskey A. Vesicular stomatitis in large animals. Merck Manual 2024; https://www.merckvetmanual.com/generalized-conditions/vesicular-stomatitis-in-large-animals/vesicular-stomatitis-in-large-animals.

Scott DW.  Large Animal Dermatology.  In: Viral Diseases.  W.B. Saunders, Philadelphia, 1998; 96 – 119.

USDA. Vesicular stomatitis 2016. www.aphis.usda.gov/vs/nahss/equine/vsv/docs/usaha_2006_VSV_presentation.pdf.

Wang J, Zhang T, Lu Y et al. Vesicular stomatitis forecasting based on Google Trends. PloS one. 2018; 13(1): e0192141.