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Infectious bovine rhinotracheitis: the disease

obovis

Synonym(s): IBR, Bovine herpes virus-type 1


Introduction

  • Cause: Bovine Herpes Virus-type 1 (BHV-1).
  • Signs: acute inflammation of the upper respiratory tract. 
  • Diagnosis: virus or antibody detection.
  • Treatment: supportive therapy.
  • Prognosis: reasonable for the individual animal, losses can be significant at population level.
Print off the farmer factsheet Infectious bovine rhinotracheitis (IBR) to give to your client.

Pathogenesis

Etiology

  • Only a single serotype of BHV-1 is recognized Bovine herpes virus; however, three subtypes of BHV-1 have been described on the basis of endonuclease cleavage patterns of viral DNA:
    • BHV-1.1 (respiratory subtype).
    • BHV-1.2 (genital subtype).
    • BHV-1.3 (encephalitic subtype):
      • BHV-1.3 has been reclassified as a distinct herpesvirus designated BHV-5.

Predisposing factors

General

  •  Times of stress, eg calving.

Pathophysiology

  • BHV-1 enters the animal through the mucous membranes in the respiratory tract or genital tracts.
  • The main mode of disease transmission is direct nose-to-nose contact between an infected and a susceptible animal.
    • This is made possible because of the virus sloughing off into the mucus.
  • Aerosols have to be exhaled, sneezed, or coughed from an infected animal during viral shedding in order for transmission to occur Biosecurity Pathogen transmission: overview.
  • Transmission also originates from contaminated semen; bulls that have been affected genitally may shed the virus in their semen.
  • Once infected it is hard for the animal to get rid of BHV-1 because it has many mechanisms to evade the host’s immune systems involved in both innate and adaptive immunity. Despite a pronounced immune response, the virus is not eliminated from the infected host but establishes life-long latency in the sensory ganglia, from where it may be reactivated at intervals. Therefore, eradication of IBR will always include the destruction of a great number of healthy, seropositive animals, which are considered to represent the virus reservoir because they are persistently infected with BoHV-1.
    • BHV-1 is able to evade adaptive immune cells by inducing apoptosis in CD4+ T cells, which assist in coordinating antigen specifc immune responses. This downregulates the number of immune cells that recognize the virus, allowing the virus to evade detection and elimination.
    • The virus has many other evasion strategies against the host’s immune system contributing to the virus being able to maintain lifelong infection in the animal.
  • After primary infection of BHV-1, the latent infection is quite often found in the trigeminal ganglion of the cow.
    • These latent infections can reactivate, with or without clinical symptoms, under conditions of stress.
  •  Infected animals will shed virus throughout their lifetime when the virus reactivates and are therefore successful in propagating the disease.
  • The virus sheds in such high titers that it will spread rapidly throughout a herd.
  • Even though cattle might not be showing clinical signs, they can still spread the disease.
  • Shedding begins from the nasal mucosa as soon as infection occurs, and the virus has replicated in the upper respiratory tract.
  • During replication in the respiratory tract, epithelial cells will undergo apoptosis.
  • The necrosis of the epithelium leaves the animal susceptible to secondary infections and can make diagnosis of BHV infection difficult in advanced clinical cases.

Timecourse

  • The reported incubation period for the respiratory and genital forms is 2-6 days.

Epidemiology

  • Aside from cattle, studies experimentally infecting animals have shown that goats and buffalo can act as reservoirs for BHV-1, as well as red deer, sheep, swine, and reindeer.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Graham D A (2013) Bovine herpes virus-1 (BoHV-1) in cattle–a review with emphasis on reproductive impacts and the emergence of infection in Ireland and the United Kingdom. Irish Vet J 66 (1) PubMed.
  • De Koeijer A A, Diekmann O & de Jong M C (2008) Calculating the time to extinction of a reactivating virus, in particular bovine herpes virus. Mathematical Biosciences 212 (2), 111-131 PubMed.
  • Ackermann M & Engels M (2006) Pro and contra IBR-eradication. Vet Microbiol 113 (3-4), 293-302 PubMed.
  • Bennett R & Ijpelaar J (2005) Updated estimates of the costs associated with 34 endemic livestock diseases in Great Britain. J Agri Eco 56, 135-144.
  • Schynts F, Meurens F, Detry B, Vanderplasschen A, Thiry E (2003) Rise and survival of bovine herpesvirus 1 recombinants after primary infection and reactivation from latency. J Virol 77, 12535-12542 PubMed.
  • Trapp S, Konig P, Beer M (2003) Conventional and marked BHV-1 vaccines in Germany A brief review. Berl Munch Tierarztli Wschr 116, 208-215 PubMed.
  • Bosch J C, Kaashoek M J, Van Oirschot J T (1997) Inactivated bovine herpesvirus marker vaccines are more efficacious in reducing virus excretion after reactivation than a live marker vaccine. Vaccine 15, 1512-1517 PubMed.

Other sources of information

  • Raaperi K (2012) Epidemiology, impact on herd health and control of bovine herpesvirus 1 in Estonian dairy cattle herds. (Doctoral dissertation).

Organisation(s)

  • School of Veterinary Medicine and Science, University of Nottingham, UK

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