Canine distemper

Canine distemper (sometimes termed hardpad disease) is a viral disease that affects a wide variety of animal families, including domestic and wild species of dogs, coyotes, foxes, pandas, wolves, ferrets, skunks, raccoons, and large cats, as well as pinnipeds, some primates, and a variety of other species. Animals in the family Felidae, including many species of large cat as well as domestic cats, were long believed to be resistant to canine distemper, until some researchers reported the prevalence of CDV infection in large felids.[2] Both large Felidae and domestic cats are now known to be capable of infection, usually through close housing with dogs[2][3] or possibly blood transfusion from infected cats,[2] but such infections appear to be self-limiting and largely without symptoms.[3]

In canines, distemper affects several body systems, including the gastrointestinal and respiratory tracts and the spinal cord and brain, with common symptoms that include high fever, eye inflammation and eye/nose discharge, labored breathing and coughing, vomiting and diarrhea, loss of appetite and lethargy, and hardening of nose and footpads. The viral infection can be accompanied by secondary bacterial infections and can present eventual serious neurological symptoms.

Canine distemper is caused by a single-stranded RNA virus of the family Paramyxoviridae (the same family of the viruses that causes measles, mumps, and bronchiolitis in humans). The disease is highly contagious via inhalation.[4] Morbidity and mortality may vary greatly among animal species, with up to 100% mortality in unvaccinated populations of ferrets. In domestic dogs, while the acute generalized form of distemper has a high mortality rate, disease duration and severity depends mainly on the animal's age and immune status and virulence of the infecting strain of the virus.[4][5] Despite extensive vaccination in many regions, it remains a major disease of dogs, and was the leading cause of infectious disease death in dogs, prior to a vaccine becoming available.[6]

The origin of the word "distemper" is from the Middle English distemperen, meaning to upset the balance of the humors, which is from the Old French destemprer, meaning to disturb, which is from the Vulgar Latin distemperare: Latin dis- and Latin temperare, meaning to not mix properly.[7][8]

Canine morbillivirus
Virus classification
(unranked): Virus
Realm: Riboviria
Phylum: Negarnaviricota
Class: Monjiviricetes
Order: Mononegavirales
Family: Paramyxoviridae
Genus: Morbillivirus
Canine morbillivirus

Canine distemper virus

Italian wolf in advanced stage of infection.
Canine distemper
Dog infected with canine distemper: Note the purulent nasal discharge and hyperkeratotic nose.

Clinical signs

In dogs, signs of distemper vary widely from no signs, to mild respiratory signs indistinguishable from kennel cough, to severe pneumonia with vomiting, bloody diarrhea, and death.[9]

Commonly observed signs are a runny nose, vomiting and diarrhea, dehydration, excessive salivation, coughing and/or labored breathing, loss of appetite, and weight loss. If neurological signs develop, incontinence may ensue.[10][11] Central nervous system signs include a localized involuntary twitching of muscles or groups of muscles, seizures with salivation and jaw movements commonly described as "chewing-gum fits", or more appropriately as "distemper myoclonus". As the condition progresses, the seizures worsen and advance to grand mal convulsions followed by death of the animal. The animal may also show signs of sensitivity to light, incoordination, circling, increased sensitivity to sensory stimuli such as pain or touch, and deterioration of motor capabilities. Less commonly, they may lead to blindness and paralysis. The length of the systemic disease may be as short as 10 days, or the start of neurological signs may not occur until several weeks or months later. Those few that survive usually have a small tic or twitch of varying levels of severity. With time, this tic usually diminishes somewhat in its severity.[12][10]

Lasting signs

A dog that survives distemper continues to have both nonlife-threatening and life-threatening signs throughout its lifespan. The most prevalent nonlife-threatening symptom is hard pad disease. This occurs when a dog experiences the thickening of the skin on the pads of its paws, as well as on the end of its nose. Another lasting symptom that is common is enamel hypoplasia. Puppies, especially, have damage to the enamel of teeth that are not completely formed or those that have not yet grown through the gums. This is a result of the virus killing the cells responsible for manufacturing the tooth enamel. These affected teeth tend to erode quickly.[13]

Life-threatening signs usually include those due to the degeneration of the nervous system. Dogs that have been infected with distemper tend to suffer a progressive deterioration of mental abilities and motor skills. With time, the dog can develop more severe seizures, paralysis, reduction in sight, and incoordination. These dogs are usually humanely euthanized because of the immense pain and suffering they face.[13]


Distemper is caused by a single-stranded RNA virus of the family Paramyxoviridae, which is a close relative of the viruses that cause measles in humans and rinderpest in animals.[12][14]

Host range

Distemper, or hardpad disease in canines,[15] affects animals in the families Canidae (dog, fox, wolf, Raccoon dog), Mustelidae (ferret, mink, skunk, wolverine, marten, badger, otter),[12][15] Procyonidae (raccoon, coati), Ailuridae (red panda), Ursidae (bear), Elephantidae (Asian elephant), and some primates (e.g., Japanese monkey),[12] as well as Viverridae (raccoon-like South Asian binturong, palm civet),[12] Hyaenidae (hyena), Pinnipedia (seals, walrus, sea lion, etc.),[16][10] and large Felidae (cats,[12] though not domestic cats.)

In a captive population of giant pandas in China (Shanxi Rare Wild Animal Rescue and Research Center), six of 22 captive pandas were infected by CDV. All but one infected panda died; the survivor had previously been vaccinated.[17]


Canine distemper virus affects nearly all body systems.[18] Puppies from 3-6 months old are particularly susceptible.[19] CDV spreads through aerosol droplets and through contact with infected bodily fluids, including nasal and ocular secretions, feces, and urine, 6 to 22 days after exposure. It can also be spread by food and water contaminated with these fluids.[20][21] The time between infection and disease is 14 to 18 days, although a fever can appear from 3 to 6 days after infection.[22]

Canine distemper virus tends to orient its infection towards the lymphoid, epithelial, and nervous tissues. The virus initially replicates in the lymphatic tissue of the respiratory tract. The virus then enters the blood stream and infects the respiratory, gastrointestinal, urogenital, epithelial, and central nervous systems, and optic nerves.[12] Therefore, the typical pathologic features of canine distemper include lymphoid depletion (causing immunosuppression and leading to secondary infections), interstitial pneumonia, encephalitis with demyelination, and hyperkeratosis of the nose and foot pads.

The virus first appears in bronchial lymph nodes and tonsils 2 days after exposure. The virus then enters the bloodstream on the second or third day.[21] A first round of acute fever tends to begin around 3-8 days after infection, which is often accompanied by a low white blood cell count, especially of lymphocytes, as well as low platelet count. These signs may or may not be accompanied by anorexia, a runny nose, and discharge from the eye. This first round of fever typically recedes rapidly within 96 hours, and then a second round of fever begins around the 11th or 12th day and lasts at least a week. Gastrointestinal and respiratory problems tend to follow, which may become complicated with secondary bacterial infections. Inflammation of the brain and spinal cord, otherwise known as encephalomyelitis, either is associated with this, subsequently follows, or comes completely independent of these problems. A thickening of the footpads sometimes develops, and vesicular pustular lesions on the abdomen usually develop. Neurological signs typically are found in the animals with thickened footpads from the virus.[12][10] About half of sufferers experience meningoencephalitis.[10] Less than 50% of the adult dogs that contract the disease die from it. Among puppies, the death rate often reaches 80%.[23]


Canine Distemper Virus Cytoplasmic Inclusion Body (Blood smear, Wright's stain)
Canine distemper virus cytoplasmic inclusion body (blood smear, Wright's stain)

The above signs, especially fever, respiratory signs, neurological signs, and thickened footpads, occurring in unvaccinated dogs strongly indicate canine distemper. However, several febrile diseases match many of the signs of the disease and only recently has distinguishing between canine hepatitis, herpes virus, parainfluenza, and leptospirosis been possible.[10] Thus, finding the virus by various methods in the dog's conjunctival cells or foot pads gives a definitive diagnosis. In older dogs that develop distemper encephalomyelitis, diagnosis may be more difficult, since many of these dogs have an adequate vaccination history.[24]

An additional test to confirm distemper is a brush border slide of the bladder transitional epithelium of the inside lining from the bladder, stained with Diff-Quik. These infected cells have inclusions which stain a carmine red color, found in the paranuclear cytoplasm readability. About 90% of the bladder cells will be positive for inclusions in the early stages of distemper.[25]


A number of vaccines against canine distemper exist for dogs (ATCvet code: QI07AD05 (WHO) and combinations) and domestic ferrets (QI20DD01 (WHO)), which in many jurisdictions are mandatory for pets. Infected animals should be quarantined from other dogs for several months owing to the length of time the animal may shed the virus.[12] The virus is destroyed in the environment by routine cleaning with disinfectants, detergents, or drying. It does not survive in the environment for more than a few hours at room temperature (20–25°C), but can survive for a few weeks in shady environments at temperatures slightly above freezing.[26] It, along with other labile viruses, can also persist longer in serum and tissue debris.[21]

Despite extensive vaccination in many regions, it remains a major disease of dogs.[27]

To prevent canine distemper, puppies should begin vaccination at 6-8 weeks of age and then continue getting the “booster shot” every 2-4 weeks until they are 16 weeks of age. Without the full series of shots, the vaccination does not provide protection against the virus. Since puppies are typically sold at the age of 8-10 weeks, they typically receive the first shot while still with their breeder, but the new owner often does not finish the series. These dogs are not protected against the virus, so are susceptible to canine distemper infection, continuing the downward spiral that leads to outbreaks throughout the world.[28]


No specific treatment for the canine distemper is known. As with measles, the treatment is symptomatic and supportive.[12] Care is geared towards treating fluid/electrolyte imbalances, neurological symptoms, and preventing any secondary bacterial infections. Examples include administering fluids, electrolyte solutions, analgesics, anticonvulsants, broad-spectrum antibiotics, antipyretics, parenteral nutrition, and nursing care.[29]


The mortality rate of the virus largely depends on the immune status of the infected dogs. Puppies experience the highest mortality rate, where complications such as pneumonia and encephalitis are more common.[21] In older dogs that develop distemper, encephalomyelitis and vestibular disease may be present.[24] Around 15% of canine inflammatory central nervous system diseases are a result of CDV.[27]


The prevalence of canine distemper in the community has decreased dramatically due to the availability of vaccinations. However, the disease continues to spread among unvaccinated populations, such as those in animal shelters and pet stores. This provides a great threat to both the rural and urban communities throughout the United States, affecting both shelter and domestic canines. Despite the effectiveness of the vaccination, outbreaks of this disease continue to occur nationally. In April 2011, the Arizona Humane Society released a valley-wide pet health alert throughout Phoenix, Arizona.[30]

Outbreaks of canine distemper continue to occur throughout the United States and elsewhere, and are caused by many factors, including proximity to wild animals and lack of vaccinated animals. This problem is even greater within areas such as Arizona, owing to the vast amount of rural land. An unaccountable number of strays that lack vaccinations reside in these areas, so are more susceptible to diseases such as canine distemper. These strays act as a reservoir for the virus, spreading it throughout the surrounding area, including urban areas. Puppies and dogs that have not received their shots can then be infected in a place where many dogs interact, such as a dog park.


In Europe, the first report of canine distemper occurred in Spain in 1761.[31] Edward Jenner described the disease in 1809,[31] but French veterinarian Henri Carré determined that the disease was caused by a virus in 1905.[31] Carré's findings were disputed by researchers in England until 1926, when Patrick Laidlaw and G.W. Dunkin confirmed that the disease was, in fact, caused by a virus.[31]

The first vaccine against canine distemper was developed by an Italian named Puntoni.[32] In 1923 and 1924, Puntoni published two articles in which he added formalin to brain tissue from infected dogs to create a vaccine which successfully prevented the disease in healthy dogs.[32] A commercial vaccine was developed in 1950, yet owing to limited use, the virus remains prevalent in many populations.[33]

The domestic dog has largely been responsible for introducing canine distemper to previously unexposed wildlife, and now causes a serious conservation threat to many species of carnivores and some species of marsupials. The virus contributed to the near-extinction of the black-footed ferret. It also may have played a considerable role in the extinction of the thylacine (Tasmanian tiger) and recurrently causes mortality among African wild dogs.[14] In 1991, the lion population in Serengeti, Tanzania, experienced a 20% decline as a result of the disease.[34] The disease has also mutated to form phocid distemper virus, which affects seals.[10]


  1. ^ "ICTV Taxonomy history: Canine morbillivirus". International Committee on Taxonomy of Viruses (ICTV). Retrieved 15 January 2019.
  2. ^ a b c Ikeda, Yasuhiro; Nakamura, Kazuya; Miyazawa, Takayuki; Chen, Ming-Chu; Kuo, Tzong-Fu; Lin, James A; Mikami, Takeshi; Kai, Chieko; Takahashi, Eiji (May 2001). "Seroprevalence of Canine Distemper Virus in Cats". Clin Vaccine Immunol. 8 (3): 641–644. doi:10.1128/CDLI.8.3.641-644.2001. PMC 96116. PMID 11329473. Archived from the original on 18 January 2018. Retrieved 30 September 2015.
  3. ^ a b Greene, Craig E; Appel, Max J (2006). "3. Canine distemper". In Greene, Craig E (ed.). Infectious Diseases of the Dog and Cat (3rd ed.). St Louis, MO: Elsevier. ISBN 978-1-4160-3600-5.
  4. ^ a b Deem, Sharon L.; Spelman, Lucy H.; Yates, Rebecca A.; Montali, Richard J. (December 2000). "Canine Distemper in Terrestrial Carnivores: A Review" (PDF). Journal of Zoo and Wildlife Medicine. 31 (4): 441–451. doi:10.1638/1042-7260(2000)031[0441:CDITCA]2.0.CO;2. Archived (PDF) from the original on 2017-05-17. Retrieved 2017-12-05.
  5. ^ Andreas, Beineke; Baumgärtner, Wolfgang; Wohlsein, Peter (13 September 2015). "Cross-species transmission of canine distemper virus—an update". One Health. 1: 49–59. doi:10.1016/j.onehlt.2015.09.002. PMC 5462633. PMID 28616465.
  6. ^ "Animal Health" (PDF). Archived (PDF) from the original on 2017-11-07. Retrieved 2017-10-30.
  7. ^ "distemper (definition)". Oxford Living Dictionaries - English. Oxford University Press. Archived from the original on 2017-12-06. Retrieved 2017-12-06.
  8. ^ "distemper (definition)". American Heritage Dictionary. Houghton Mifflin Harcourt. Archived from the original on 2018-05-09. Retrieved 2017-12-06.
  9. ^ Greene, CE; Vandevelde, M (2012). "Chapter 3: Canine distemper". In Greene, Craig E. (ed.). Infectious diseases of the dog and cat (4th ed.). St. Louis, Mo.: Elsevier/Saunders. pp. 25–42. ISBN 978-1-4160-6130-4.
  10. ^ a b c d e f g Jones, T.C.; Hunt, R.D.; King, N.W. (1997). Veterinary Pathology. Blackwell Publishing.
  11. ^ Hirsh DC, Zee YC (1999). Veterinary Microbiology. Blackwell Publishing. ISBN 978-0-86542-543-9.
  12. ^ a b c d e f g h i j Kate E. Creevy, 2013, Overview of Canine Distemper, in The Merck Veterinary Manual (online): Veterinary Professionals: Generalized Conditions: Canine Distemper, see "Canine Distemper Overview - Generalized Conditions". Archived from the original on 2014-12-23. Retrieved 2014-12-15., accessed 15 December 2014.
  13. ^ a b "Canine Distemper: What You Need To Know". Veterinary Insider. 2010-12-06. Archived from the original on 2012-05-02. Retrieved 2012-04-09.
  14. ^ a b McCarthy AJ, Shaw MA, Goodman SJ (December 2007). "Pathogen evolution and disease emergence in carnivores". Proc. Biol. Sci. 274 (1629): 3165–74. doi:10.1098/rspb.2007.0884. PMC 2293938. PMID 17956850.
  15. ^ a b Otto M. Radostits, David A. Ashford, Craig E. Greene, Ian Tizard, et al., 2011, Canine Distemper (Hardpad Disease), in The Merck Manual for Pet Health (online): Pet Owners: Dog Disorders and Diseases: Disorders Affecting Multiple Body Systems of Dogs, see "Canine Distemper (Hardpad Disease) - Dog Owners". Archived from the original on 2014-12-16. Retrieved 2014-12-15., accessed 15 December 2014.
  16. ^ Kennedy, Seamus, et al. "Mass die-off of Caspian seals caused by canine distemper virus." Emerging infectious diseases 6.6 (2000): 637.
  17. ^ Feng, Na; Yu, Yicong; Wang, Tiecheng; Wilker, Peter; Wang, Jianzhong; Li, Yuanguo; Sun, Zhe; Gao, Yuwei; Xia, Xianzhu (16 June 2016). "Fatal canine distemper virus infection of giant pandas in China". Scientific Reports. 6 (1): 27518. Bibcode:2016NatSR...627518F. doi:10.1038/srep27518. PMC 4910525. PMID 27310722. Archived from the original on 12 March 2017. Retrieved 9 May 2018.
  18. ^ Beineke, A; Baumgärtner, W; Wohlsein, P (December 2015). "Cross-species transmission of canine distemper virus-an update". One Health. 1: 49–59. doi:10.1016/j.onehlt.2015.09.002. PMC 5462633. PMID 28616465.
  19. ^ Editorial Staff at remedy's, 2001-2014, "Health Topics: Pet Health: Canine Distemper: Canine Distemper Overview, Canine Distemper Signs & Symptoms, Canine Distemper Transmission," see "Archived copy". Archived from the original on 2014-12-20. Retrieved 2014-12-15.CS1 maint: Archived copy as title (link), accessed 15 December 2014.
  20. ^ Carter, G.R.; Flores, E.F.; Wise, D.J. (2006). "Paramyxoviridae". A Concise Review of Veterinary Virology. Retrieved 2006-06-24.
  21. ^ a b c d Hirsch, D.C.; Zee, C.; et al. (1999). Veterinary Microbiology. Blackwell Publishing.
  22. ^ Appel, M.J.G.; Summers, B.A. (1999). "Canine Distemper: Current Status". Recent Advances in Canine Infectious Diseases. Archived from the original on 2005-09-01. Retrieved 2006-06-24.
  23. ^ "Archived copy". Archived from the original on 2015-02-02. Retrieved 2015-04-13.CS1 maint: Archived copy as title (link)
  24. ^ a b Dewey, C.W. (2003). A Practical Guide to Canine and Feline Neurology. Iowa State Pr.
  25. ^ "NDV-Induced Serum". Kind Hearts in Action. November 5, 2009. Archived from the original on June 25, 2012. Retrieved October 31, 2012.
  26. ^ "Canine Distemper (CDV)". UC Davis Koret Shelter Medicine Program. 2004. Archived from the original on 2015-10-10. Retrieved 2013-08-17.
  27. ^ a b Elia G, Belloli C, Cirone F, et al. (February 2008). "In vitro efficacy of ribavirin against canine distemper virus". Antiviral Res. 77 (2): 108–13. doi:10.1016/j.antiviral.2007.09.004. PMID 17949825.
  28. ^ "Canine Distemper: Prevention of Infections". MarvistaVet. Archived from the original on 2012-04-21. Retrieved 2012-04-09.
  29. ^ "Overview of Canine Distemper: Canine Distemper: Merck Veterinary Manual". Kenilworth, N.J., U.S.: Merck Sharp & Dohme Corp. 2009. Archived from the original on 2016-10-05. Retrieved 2016-02-13.
  30. ^ "AHS ISSUES VALLEYWIDE PET HEALTH ALERT". Arizona Humane Society. Archived from the original on 2012-04-15. Retrieved 2012-04-09.
  31. ^ a b c d Appel, MJG; Gillespie, JH (1972). "Canine Distemper Virus". Volume 11 of the series Virology Monographs / Die Virusforschung in Einzeldarstellungen. Vienna: Springer Vienna. pp. 1–96. ISBN 978-3-7091-8302-1.
  32. ^ a b Tizard, I (1999). "Grease, anthraxgate, and kennel cough: a revisionist history of early veterinary vaccines". Advances in Veterinary Medicine. 41: 7–24. PMID 9890006.
  33. ^ Pomeroy, Laura W.; Bjørnstad, Ottar N; Holmes, Edward C. (2008). "The Evolutionary and Epidemiological Dynamics of the Paramyxoviridae". Journal of Molecular Evolution. 66 (2): 98–106. Bibcode:2008JMolE..66...98P. doi:10.1007/s00239-007-9040-x. PMC 3334863. PMID 18217182.
  34. ^ Assessment, M.E. (2005). Ecosystems and human well-being. World Resources Institute.

Further reading

ATCvet code QI07

ATCvet code QI07 Immunologicals for Canidae is a therapeutic subgroup of the Anatomical Therapeutic Chemical Classification System for veterinary medicinal products, a system of alphanumeric codes developed by the WHO for the classification of drugs and other medical products for veterinary use. Subgroup QI07 is part of the anatomical group QI Immunologicals.National issues of the ATC classification may include additional codes not present in this list, which follows the WHO version.

Animal virus

Animal viruses are viruses that infect animals. Viruses infect all cellular life and although viruses infect every animal, plant and protist species, each has its own specific range of viruses that often infect only that species.

Black-footed ferret

The black-footed ferret (Mustela nigripes), also known as the American polecat or prairie dog hunter, is a species of mustelid native to central North America. It is listed as endangered by the IUCN, because of its very small and restricted populations. First discovered by Audubon and Bachman in 1851, the species declined throughout the 20th century, primarily as a result of decreases in prairie dog populations and sylvatic plague. It was declared extinct in 1979 until Lucille Hogg's dog brought a dead black-footed ferret to her door in Meeteetse, Wyoming in 1981. That remnant population of a few dozen ferrets lasted there until the animals were considered extinct in the wild in 1987. However, a captive breeding program launched by the United States Fish and Wildlife Service resulted in its reintroduction into eight western states, Canada and Mexico from 1991 to 2009. There are now over 1,000 mature, wild-born individuals in the wild across 18 populations, with five self-sustaining populations in South Dakota (two), Arizona, Wyoming and Saskatchewan. It was first listed as "Endangered" in 1982, then listed as "Extinct in the Wild" in 1996 before being downgraded back to "Endangered" in 2008.The black-footed ferret is roughly the size of a mink, and differs from the European polecat by the greater contrast between its dark limbs and pale body and the shorter length of its black tail-tip. In contrast, differences between the black-footed ferret and the steppe polecat of Asia are slight, to the point where the two species were once thought to be conspecific. The only noticeable differences between the black-footed ferret and the steppe polecat are the former's much shorter and coarser fur, larger ears, and longer postmolar extension of the palate.It is largely nocturnal and solitary, except when breeding or raising litters. Up to 91% of its diet is composed of prairie dogs.The black‐footed ferret Mustela nigripes experienced a recent population bottleneck in the wild followed by a more than 30 year recovery through ex situ breeding and then reintroduction into its native range. As such, this sole, endemic, North American ferret allows examining the impact of a severe genetic restriction on subsequent biological form and function, especially on reproductive traits and success. The black‐footed ferret was listed as endangered by the United States Fish & Wildlife Service (USFWS) in 1967. Declared extinct in 1979, a residual wild population was discovered in Meeteetse, WY in 1981. This cohort eventually grew to 130 individuals and was then nearly extirpated by sylvatic plague Yersinia pestis and canine distemper virus Canine morbillivirus (Carr, 1986), with eventually 18 animals remaining (Carr, 1986; Miller, Reading & Forrest, 1996). These survivors were captured from 1985 to 1987 to serve as the foundation for the black‐footed ferret ex situbreeding program. Seven of those 18 animals produced offspring that survived and reproduced and, with currently living descendants, are the ancestors of all black‐footed ferrets now in the ex situ (n = ~320) and in situ (n = ~300) populations.


CDV may refer to:

cdv Software Entertainment, a German video game publisher

Canine distemper virus, a viral disease affecting several families of animals

Carte de visite, a nineteenth-century photograph format

CD Video, a short-lived video format

Comcast Digital Voice, a telephone service

CDV Records, the record label created by Australian Idol competitor Cosima De Vito

Merle K. (Mudhole) Smith Airport in Cordova, Alaska (IATA Code: CDV)

Check Digit Verification - A form of redundancy check used for error detection.

Clutch delay valve, an automotive device

Committee draft for vote, a stage in the standardization process, used by International Electrotechnical Commission

Criminal Domestic Violence, a criminal charge

Childhood Domestic Violence Association, a nonprofit organization dedicated to help children of domestic violence

405 in Roman numerals

Caspian seal

The Caspian seal (Pusa caspica) is one of the smallest members of the earless seal family and unique in that it is found exclusively in the brackish Caspian Sea. They are found not only along the shorelines, but also on the many rocky islands and floating blocks of ice that dot the Caspian Sea. In winter, and cooler parts of the spring and autumn season, these marine mammals populate the Northern Caspian. As the ice melts in the warmer season, they can be found on the mouths of the Volga and Ural Rivers, as well as the southern latitudes of the Caspian where cooler waters can be found due to greater depth.

Evidence suggests the seals are descended from Arctic ringed seals that reached the area from the north during an earlier part of the Quaternary period and became isolated in the landlocked Caspian Sea when continental ice sheets melted.

Craniomandibular osteopathy

Craniomandibular osteopathy, also known as lion's jaw, is a developmental disease in dogs causing extensive bony changes in the mandible and skull. In this disease, a cyclical resorption of normal bone and replacement by immature bone occurs along the inner and outer surfaces of the affected bones. It usually occurs between the ages of 3 and 8 months. Breeds most commonly affected include the West Highland White Terrier, Scottish Terrier, Cairn Terrier, and Boston Terrier. It is rare in large-breed dogs, but it has been reported. Symptoms include firm swelling of the jaw, drooling, pain, and difficulty eating.

It is an inherited disease, especially in Westies, in which it has been recognized as an autosomal recessive trait. Canine distemper has also been indicated as a possible cause, as has E. coli infection, which could be why it is seen occasionally in large-breed dogs. Growth of lesions will usually stop around the age of one year, and possibly regress. This timing coincides with the normal completion of endochondral bone growth and ossification. If the disease is extensive, especially around the tympanic bulla (middle ear), then the prognosis is guarded.

A similar disease seen in young Bullmastiffs is known as calvarial hyperostotic syndrome. It is also similar to human infantile cortical hyperostosis. It is characterized by irregular, progressive bony proliferation and thickening of the cortical bone of the calvaria, which is part of the skull. Asymmetry of the lesions may occur, which makes it different from craniomandibular osteopathy. Symptoms include painful swelling of the skull, fever, and lymph node swelling. In most cases it is self-limiting.

DA2PPC vaccine

DA2PP is a multivalent vaccine for dogs that protects against the viruses indicated by the alphanumeric characters forming the acronym: D for canine distemper, A2 for canine adenovirus type 2, which offers cross-protection to canine adenovirus type 1 (the more pathogenic of the two strains) (see Canine adenovirus), the first P for canine parvovirus, and the second P for parainfluenza. Because infectious canine hepatitis is another name for canine adenovirus type 1, an H is sometimes used instead of A. In DA2PPC, the C indicates canine coronavirus.

This vaccine is usually given to puppies at 8 weeks of age, followed by 12 weeks of age, and then 16 weeks of age. This vaccine is given again at 1 year of age and then annually, or every 3 years. Some veterinarians' recommended vaccine schedules may differ from this.

DA2PPC does not include Bordetella. But the combination of Bordetella with DA2PPC prevents kennel cough, by preventing adenovirus, distemper, parainfluenza, and Bordetella.

Feline morbillivirus

Feline morbillivirus comes from the family Morbillivirus, specifically influencing wild and domestic cats. The first report of a Feline morbillivirus outbreak occurred in Hong Kong in 2012. Approximately 10% of stray cats in Hong Kong and mainland China were reported to possess the virus at the time with additional infections found in Japan as well. 40% of cats tested in Japan were Fmo-PV positive and exhibited early symptoms of renal failure. While the first cases of Feline morbillivirus were found in China, Hong Kong and Japan, the virus can also be found in Italy, Germany, and the United States. Feline morbillivirus exhibits a substantial amount of genetic diversity, yet cases in Japan and Hong Kong proved to have identical nucleotide sequences. It is also hypothesized that the morbillivirus has high adaptability due to its presence in multiple species. It is often found in dogs, cats, cattle, whales, dolphins, porpoises, and even humans. It likely originated from an ancestral version and underwent viral evolution to adapt to transmission in different species. Other common morbilliviruses include: measles, rinderpest virus, canine distemper virus and peste des petits ruminants virus.

Ferret health

The domestic ferret is known to be affected by several distinct ferret health problems. Among the most common are cancers affecting the adrenal glands, pancreas, and lymphatic system. Viral diseases include canine distemper and influenza. Certain health problems have also been linked to ferrets being neutered before sexual maturity was reached. Certain colors of ferret may also carry a genetic defect known as Waardenburg syndrome. Similar to domestic cats, ferrets may also be affected by hairballs, or dental problems.

Granulomatous meningoencephalitis

Granulomatous meningoencephalitis (GME) is an inflammatory disease of the central nervous system (CNS) of dogs and, rarely, cats. It is a form of meningoencephalitis. GME is likely second only to encephalitis caused by canine distemper virus as the most common cause of inflammatory disease of the canine CNS. The disease is more common in female toy dogs of young and middle age. It has a rapid onset. The lesions of GME exist mainly in the white matter of the cerebrum, brainstem, cerebellum, and spinal cord. The cause is only known to be noninfectious and is considered at this time to be idiopathic. Because lesions resemble those seen in allergic meningoencephalitis, GME is thought to have an immune-mediated cause, but it is also thought that the disease may be based on an abnormal response to an infectious agent. One study searched for viral DNA from canine herpesvirus, canine adenovirus, and canine parvovirus in brain tissue from dogs with GME, necrotizing meningoencephalitis, and necrotizing leukoencephalitis (see below for the latter two conditions), but failed to find any.


Hyperesthesia is a condition that involves an abnormal increase in sensitivity to stimuli of the sense. "When a non-noxious stimulus causes the sensation of pain the area will be termed hyperaesthetic". Stimuli of the senses can include sound that one hears, foods that one tastes, textures that one feels, and so forth. Increased touch sensitivity is referred to as "tactile hyperesthesia", and increased sound sensitivity is called "auditory hyperesthesia". Tactile hyperesthesia may be a common symptom of many neurologic disorders such as herpes zoster, peripheral neuropathy and radiculopathies. In 1979, and then in 1994, Merskey, Bogduk, Noordenbos, Devor and others (a subcommittee of International Association for the Study of Pain) proposed, instead of hyperaesthesia, the concept of allodynia, meaning "other pain", defined as a pain resulting from a stimulus that does not normally provoke pain.In psychology, Jeanne Siaud-Facchin uses the term by defining it as an "exacerbation des sens" that characterizes gifted children (and adults): for them, the sensory information reaches the brain much faster than the average, and the information is processed in a significantly shorter time.

Hypertrophic osteodystrophy

Hypertrophic Osteodystrophy (HOD) is a bone disease that occurs in fast-growing large and giant breed dogs. The disorder is sometimes referred to as metaphyseal osteopathy, and typically first presents between the ages of 2 and 7 months. HOD is characterized by decreased blood flow to the metaphysis (the part of the bone adjacent to the joint) leading to a failure of ossification (bone formation) and necrosis and inflammation of cancellous bone. The disease is usually bilateral in the limb bones, especially the distal radius, ulna, and tibia.The Weimaraner, Irish Setter, Boxer, German Shepherd, and Great Dane breeds are heavily represented in case reports of HOD in the veterinary literature, but the severity of symptoms and possible etiology may be different across the breeds. For example, familial clustering of the disease has been documented in the Weimaraner, but not in other breeds. The disease in the Weimaraner and Irish Setter can be particularly severe, with significant mortality observed in untreated dogs. The classical age of onset is typically 8 to 16 weeks of age, with males and females equally affected.

Juliette de Baïracli Levy

Juliette de Baïracli Levy (11 November 1912 – 28 May 2009) was an English herbalist and author noted for her pioneering work in holistic veterinary medicine. After studying veterinary medicine at the Universities of Manchester and Liverpool for two years, Bairacli Levy left England to study herbal medicine in Europe, Turkey, North Africa, Israel and Greece, living with Romani people, farmers and livestock breeders, acquiring a fund of herbal lore from them in the process, most notably from the Romani people. She has written several well-known books on herbalism and nomadic living in harmony with nature, in addition to fiction and poetry illustrated by Olga Lehmann. After living for some time on the Greek island Kythira, de Bairacli Levy resided in an old age home in Burgdorf, Switzerland.

Ovine rinderpest

Ovine rinderpest, also commonly known as peste des petits ruminants (PPR), is a contagious disease primarily affecting goats and sheep; however, camels and wild small ruminants can also be affected. PPR is currently present in North, Central, West and East Africa, the Middle East, and South Asia. It is caused by small ruminants morbillivirus in the genus Morbillivirus, and is closely related to, among others, rinderpest morbillivirus, measles morbillivirus, and canine morbillivirus (previously known as canine distemper virus). The disease is highly contagious, and can have an 80–100% mortality rate in acute cases in an epidemic setting. This virus does not infect humans.

This disease was first described in 1942 in Côte d'Ivoire. Now, PPR has spread to more than 70 countries in the world.In 2017, the disease was reported to be affecting saiga in Mongolia, causing near-catastrophic herd depletion for the endangered species.In 2018, the disease was reported to be in Bulgaria close to the border with Turkey.


Paramyxoviridae is a family of viruses in the order Mononegavirales. Vertebrates serve as natural hosts; no known plants serve as vectors. Currently, 49 species are placed in this family, divided among seven genera. Diseases associated with this negative-sense, single-stranded RNA virus family include measles, mumps, and respiratory tract infections.


Rinderpest (also cattle plague or steppe murrain) was an infectious viral disease of cattle, domestic buffalo, and many other species of even-toed ungulates, including buffaloes, large antelope and deer, giraffes, wildebeests, and warthogs. The disease was characterized by fever, oral erosions, diarrhea, lymphoid necrosis, and high mortality. Death rates during outbreaks were usually extremely high, approaching 100% in immunologically naïve populations. Rinderpest was mainly transmitted by direct contact and by drinking contaminated water, although it could also be transmitted by air. After a global eradication campaign since the mid-1900s, the last confirmed case of rinderpest was diagnosed in 2001.On 14 October 2010, the United Nations Food and Agriculture Organization (FAO) announced that field activities in the decades-long, worldwide campaign to eradicate the disease were ending, paving the way for a formal declaration in June 2011 of the global eradication of rinderpest. On 25 May 2011, the World Organisation for Animal Health announced the free status of the last eight countries not yet recognized (a total of 198 countries were now free of the disease), officially declaring the eradication of the disease. In June 2011, the United Nations FAO confirmed the disease was eradicated, making rinderpest only the second disease in history to be fully wiped out (outside laboratory stocks), following smallpox.Rinderpest is believed to have originated in Asia, later spreading through the transport of cattle. The term Rinderpest is a German word meaning "cattle-plague". The rinderpest virus (RPV) was closely related to the measles and canine distemper viruses. The measles virus emerged from rinderpest as a zoonotic disease between 1000 and 1100 AD, a period that may have been preceded by limited outbreaks involving a virus not yet fully acclimated to humans.

Sarah Cleaveland

Sarah Cleaveland is a veterinary surgeon and Professor of Comparative Epidemiology at the University of Glasgow.

Toxocara cati

Toxocara cati, also known as the feline roundworm, is parasite of cats and other felids. It is one of the most common nematodes of cats, infecting both wild and domestic felids worldwide. Adult worms are localised in the gut of the host. In adult cats, the infection – which is called toxocariasis – is usually asymptomatic. However, massive infection in juvenile cats can be fatal.

Feline roundworms are brownish-yellow to cream colored to pink and may be up to 10 cm in length. Adults have short, wide cervical alae giving their anterior ends the distinct appearance of an arrow (hence their name, toxo, meaning arrow, and cara meaning head). Eggs are pitted ovals with a width of 65 μm and a length of about 75 μm making them invisible to the human eye. The larvae are so small that they are easily transmitted from an adult female to her nursing kittens through her milk.

This page is based on a Wikipedia article written by authors (here).
Text is available under the CC BY-SA 3.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.