Many of the common illnesses we think of as `human’ diseases actually began in other species, and only later migrated to humans. The age of emerging infectious diseases in humans really began in earnest about 10,000 years ago when man began to domesticate – and live in close proximity to – other animals.
- The scourge of Tuberculosis, which now infects 1/3rd of humanity, probably jumped to humans when man began to coral and raise its traditional hosts; goats and cattle.
- Measles appears to have evolved from canine distemper and/or the Rinderpest virus of cattle.
- Influenza, as most of you know, is native to aquatic birds – but jumped species thousands of years ago and many strains have adapted to humans, pigs, and other species.
The list of zoonotic diseases (those shared between humans and animals) is long and continually expanding, and includes: SARS, Babesiosis, Borrelia (Lyme), Nipah, Hendra, Malaria, Hantavirus, Ebola, Bartonella, Leptospirosis, Q-Fever, bird flu and many, many others.
Yet despite these disease overlaps, viruses generally adapt to a fairly narrow range of species.
Horse viruses generally attack equines, and not say, cats and dogs. Cat viruses tend to attack felines, and not birds. Bird viruses usually only infect avian species.
The species that a virus will infect is known as its host range. And while usually limited, it isn't always the case.
Rabies is a good example of a virus that can infect an extraordinarily wide range of species.
We know that every once in awhile, viruses will suddenly jump to a new species. A couple of recent examples include:
The H5N1 bird flu virus, which has been unusually promiscuous: showing up in cats (including tigers), dogs, martens, civets, and of course humans. Researchers have successfully infected cattle with the H5N1 virus, along with ferrets and mice for testing.
H3N8 Canine influenza, which only showed up in dogs in 2004, had been known to infect horses for the past 40 years.
All of which serves as prelude to a report that appears in the latest edition of the Journal of General Virology, that finds a recently emerged canine H3N2 influenza virus common in Korea has now adapted to infect domestic cats.
D.S. Song, D.J. An, H.J. Moon, M.J. Yeom, H.Y. Jung, W.S. Jung, S.J. Park, H.K. Kim, S.Y. Han, J.S. Oh, B.K. Park, J.K. Kim, H. Poo, R.G. Webster, K. Jung and B.K. Kang
In the last 4 years, incidences of endemic or epidemic respiratory diseases associated with canine influenza H3N2 virus in Asian dogs have been reported in countries such as South Korea and China. Canine species were considered to be the new natural hosts for this virus.
However, at the beginning of 2010, influenza-like respiratory signs, such as dyspnea, were also observed among cats as well as in dogs in an animal shelter located at Seoul, South Korea. The affected cats showed 100% morbidity and 40% mortality.
We were able to isolate a virus from the lung specimen of a dead cat that had suffered from the respiratory disease, in embryonated chicken eggs. The 8 viral genes isolated were almost identical to those of the canine influenza H3N2 virus suggesting interspecies transmission of canine influenza H3N2 virus to the cat.
Moreover, 3 domestic cats infected with intranasal canine/Korea/GCVP01/07 (H3N2) all showed elevated rectal temperatures, nasal virus shedding, and severe pulmonary lesions, such as suppurative bronchopneumonia.
Our study for the first time shows that cats are susceptible to canine influenza H3N2 infection, suggesting that cats may play an intermediate host role in transmitting the H3N2 virus among feline and canine species, which could lead to the endemic establishment of the virus in companion animals.
Such a scenario raises a public health concern, as the possibility of the emergence of new recombinant feline or canine influenza viruses in companion animals with the potential to act as zoonotic infection cannot be excluded.
The canine H3N2 virus only just appeared in Korea in 2007, and unlike the canine H3N8 virus seen in the United States, appears to have jumped directly from an avian source.
Daesub Song, Bokyu Kang, Chulseung Lee, Kwonil Jung, Gunwoo Ha, Dongseok Kang, Seongjun Park, Bongkyun Park, and Jinsik Oh
In South Korea, where avian influenza virus subtypes H3N2, H5N1, H6N1, and H9N2 circulate or have been detected, 3 genetically similar canine influenza virus (H3N2) strains of avian origin (A/canine/Korea/01/2007, A/canine/Korea/02/2007, and A/canine/Korea/03/2007) were isolated from dogs exhibiting severe respiratory disease.
To determine whether the novel canine influenza virus of avian origin was transmitted among dogs, we experimentally infected beagles with this influenza virus (H3N2) isolate. The beagles shed virus through nasal excretion, seroconverted, and became ill with severe necrotizing tracheobronchitis and bronchioalveolitis with accompanying clinical signs (e.g., high fever).
Consistent with histologic observation of lung lesions, large amounts of avian influenza virus binding receptor (SAα 2,3-gal) were identified in canine tracheal, bronchial, and bronchiolar epithelial cells, which suggests potential for direct transmission of avian influenza virus (H3N2) from poultry to dogs.
Our data provide evidence that dogs may play a role in interspecies transmission and spread of influenza virus.
The good news is that so far, these new canine viruses haven’t shown the ability to infect humans.
But as the author’s of the EID study above point out:
Transmission of avian influenza A virus to a new mammalian species is of great concern, because it potentially allows the virus to adapt to a new mammalian host, cross new species barriers, and acquire pandemic potential.
Companion animals, such as dogs and cats, are of particular concern because of how closely humans interact with them.
While pigs might be biologically better suited as a `mixing vessel’ for influenza (see The (Swine) Influenza Reassortment Puzzle), there are far more opportunities for transmission between humans and their pets.
In terms of their potential to spread rapidly among humans, and cause significant morbidity and mortality, few viruses can compete with influenza. As we saw in 2009, a new influenza virus can jump species and spread around the globe in a matter of months.
A recurring theme in this blog is that nature’s bio lab is open 24/7, and that it is constantly trying out new genetic combinations looking for an evolutionary advantage.
And for a virus, jumping to a new, immunologically naive species is like hitting the jackpot; a fresh supply of hosts and an opportunity to adapt further.
Which is why we watch these species jumps with more than a passing interest.