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Herpes viruses cause epidemic as well as latent or persistent diseases in almost all animal species. The name is derived from the Greek word “herpein” (to creep). Common to all herpesviruses is lifelong latency in the host organism.
The so-called “puppy death” in dogs is caused by canine herpesvirus 1 (CHV-1). Puppies under 3 weeks of age die of a general haemorrhagic disease. Massive lytic viral replication occurs with subnormal body temperature of 36 – 37° C and death within 48 hours. The morbidity rate is 100%, the mortality rate is almost 95%!
Older puppies usually show mild respiratory symptoms, therefore CHV is attributed an aetiological involvement in the kennel cough complex.
Adult animals usually undergo clinically inapparent infections. CHV-1 results in latent infection; the viruses retract into the trigeminal and lumbosacral ganglion cells after primary cell lytic infection. In stressful situations (such as parturition or the onset of lactation), reactivation may occur, followed by shedding of virus in saliva and nasal and ocular secretions. Bitches can transmit the virus intrauterinally to the foetuses, rarely resulting in abortions and stillbirths. In adult, immunosuppressed animals, peracute courses with fatal consequences may occur. Diagnosis in breeding animals is recommended.
Infection with suid herpesvirus 1 leads to Aujeszky’s disease (pseudorabies). For further information see herpesviruses swine.
The main signs of feline herpesvirus 1 (FHV-1) are respiratory symptoms such as rhinitis and sinusitis with ocular and nasal discharge. Conjunctivitis, corneal ulcers, dyspnoea and anorexia may occur. Co-infections, for example with feline caliciviruses and bacteria, are possible. After the primary infection, a lifelong latent infection develops which may be reactivated under stress at any time and thus lead to recurrent symptoms. In kittens, apart from very high fever and general weakness, there may also be deaths (fading kitten syndrome).
There are very many different herpes viruses that occur in birds, including commercial poultry, ornamental birds, wild birds and zoo birds. New viruses are also regularly found in these animal groups. Several herpesviruses have also been described in parrots. The best known and perhaps most clinically relevant is psittacid herpesvirus 1 (PsHV-1).
PsHV-1 is responsible for Pacheco’s disease in parrots and is therefore also called Pacheco virus. The clinical course depends on the genotype or serotype and the psittacid species affected. Mild to subclinical courses with virus excretion are described in waved and cockatiels. In large parrots such as macaws, amazons, cockatoos or grey parrots, infection often ends in death. If symptoms occur, they are usually non-specific and consist of anorexia, apathy and poorly developed plumage. Altered faeces and increased uric acid excretion may also occur. Occasionally, CNS symptoms are also observed. The disease breaks out particularly in stressful situations, e.g. capture and quarantine of imported birds, change of ownership, hospitalisation, start of breeding or onset of sexual maturity. Therefore, appropriate pre-screening of birds to be introduced into the flock is recommended to avoid endangering the other birds.
Other birds with systemic diseases, diseases of the respiratory system, liver or with skin or mucosal lesions on the cloaca or around the beak may also need to be tested for herpesviruses.
Psittacine herpesviruses may also be detected in papillomas in the throat and cloaca of Amazons and Cockatoos.
Herpesvirus infections are most common in a wide range of turtle species including land, water and sea turtles. In veterinary practice, the herpesviruses of tortoises of the genus Testudo play a role in veterinary practice. As it is a highly contagious virosis, animals should be routinely examined for infection before being introduced into a population.
Clinical signs include nasal and ocular discharge, regurgitation, anorexia and lethargy. Necrotic coatings in the mouth cavity and on the tongue are also typical.
So far, 4 different types of herpes virus, testudinid herpesvirus (TeHV) 1 – 4, are known in tortoises. In Europe, mainly TeHV-1 and TeHV-3 occur. TeHV-3 has a broad host range among tortoises and infections are usually associated with very high morbidity and mortality rates. TeHV-1 can be detected mainly in four-toed tortoises. Often these are single-animal diseases, as TeHV-1 has a much lower tendency to spread in the population than TeHV-3. TeHV-2 (mainly in desert tortoises) and TeHV-4 (in African tortoises) have been detected in individual cases in Europe in recent years.
In aquatic turtles, herpesvirus infections are mainly associated with liver inflammation. In live animlas, dry pharyngeal and cloacal swabs, and in dead animals, liver samples can be examined by PCR.
In sea turtles, herpesviruses cause fibropapillomatosis and other diseases. Virus detection by PCR is possible from altered tissue.
In lizards, herpesviruses are mainly seen in connection with oral lesions.
EHV-1 and EHV-4
In horses, donkeys, mules and zebras, infections with EHV-1 as well as with EHV-4 are caused by droplet infection or direct contact. The severity of the clinical symptoms depends on the age and immune status of the infected animal. Particularly infections with EHV-1 are able to spread beyond the respiratory mucosa and cause severe manifestations of the disease: abortions, perinatal foal death, neurological diseases.
In case of foals infected with EHV-4, morbidity rates of up to 100% are possible, especially during the weaning period. More than 80% of the isolates come from animals with rhinopneumonitis.
Once horses are infected with herpesviruses, they remain carriers of the virus throughout their lives, and the virus can be reactivated endogenously under unfavourable conditions (stress, etc.). Lymph organs, the leukocyte fraction and trigeminal ganglion cells are the main latency organs. If the vaccinated horses are also taken into account, seroprevalence in the horse population is high.
In recent years, EHV-1-associated neurological diseases, for which a “neurotropic” strain of EHV-1 is held responsible, have been reported with increasing frequency and severity of the clinical disease. This much-feared clinical picture is referred to as EHM (equine herpesvirus myeloencephalopathy).
Two different variants of EHV-1 have been described in horses (DNApol D752 vs. DNApol N752) Each is associated with a different level of neuropathogenicity. The D752 variant is associated with most outbreaks of neurological disease and is considered neuropathogenic. However, only a fraction of the horses infected with this virus will develop neurological signs.
The N752 variant is most commonly isolated in conjunction with abortions, but also in a smaller number of neurological diseases. The differentiation is particularly interesting from an epidemiological point of view.
EHV-2 and EHV-5
The involvement of EHV-2 and/or EHV-5 in keratoconjunctivitis has long been suspected and these viruses are indeed regularly detected in conjunctival swabs. In recent years, it has increasingly been shown that EHV-2 and 5 are precursors of other viral and bacterial infections of the respiratory tract. Especially in young animals, EHV-2 and/or EHV-5 were detected in treatment-resistant, partly catarrhal-purulent, partly necrotising or abscessing bronchopneumonia. EHV-5 was recently presented as aetiological agent of “equine multinodular pulmonary fibrosis” (EMPF).
Coital exanthema caused by equine herpesvirus type 3 (EHV-3), which only sporadically occurs in Germany, is a mildly progressing breeding infection in horses. Clinically, blisters, pustules and erosions appear on the mucous membrane of the vestibulum, penis or prepuce as well as on adjacent skin areas. Healing takes place spontaneously after approximately 2 – 3 weeks, but can be complicated by secondary infections. Transmission mainly occurs through mating, but is also possible through close contact as well as rectal and vaginal examinations. Infected animals remain carriers of the virus for life.
Bovine herpesvirus 1 (BHV-1) is the causative agent of infectious bovine rhinotracheitis (IBR), (IBR), which – depending on where the disease occurs in the individual organ systems – is also known as infectious pustular vulvovaginitis (IPV) and infectious balanoposthitis (IBP).
In Germany, it is an epizootic disease that is notifiable upon suspicion!
Suid herpesvirus 1 causes Aujeszky’s disease (pseudorabies) and is also called Aujeszky’s disease virus (ADV) or pseudorabies virus (PrV). Pigs are the natural host; they develop different clinical signs depending on age and can survive the infection, while the infection is fatal in other animals. In domestic pigs, Germany has been free of Aujeszky‘s disease since 2003, but the virus occurs in the wild boar population and can mainly infect hunting dogs – also via meat waste of healthy, but latently infected wild boars. In dogs, an infection causes central nervous disorders, mostly itching and death after 1 – 3 days.
Aujeszky’s disease is notifiable in Germany in domestic cattle and domestic pigs.
Koi herpesvirus (KHV) is a highly infectious virus that has caused epidemic disease in carps (koi and common carps) in recent years, depending on the water temperature. Morbidity and mortality rates can be as high as 100% within 1 – 2 weeks after the pathogen has been introduced. The incubation period ranges from a few weeks to several months. It depends on various external and internal factors such as stress and condition of the fish. Fish of all age groups are affected at water temperatures between 18 – 29 °C. Clinically, the main signs are gill necrosis, increased mucus production, haemorrhages of the skin, liver, spleen and kidneys. Surviving fish probably remain latent carriers of the virus for years and represent a potential hazard in the trade with live fish in pond management and hobby animal keeping. Immunisation by means of live attenuated vaccine is currently rejected from a scientific point of view.
In Germany, it is an epizootic disease that is notifiable upon suspicion!