CANINE FLU VIRUS - H3N8:


In 2004, canine influenza virus subtype H3N8 emerged in greyhounds in the United States. Subsequent
serologic evidence indicated virus circulation in dog breeds other than greyhounds, but the virus had not
been isolated from affected animals. In 2005, we conducted virologic investigation of 7 nongreyhound
dogs that died from respiratory disease in Florida and isolated influenza subtype H3N8 virus. Antigenic
and genetic analysis of A/canine/Jacksonville/2005 (H3N8) and A/canine/Miami/2005 (H3N8) found
similarity to earlier isolates from greyhounds, which indicates that canine influenza viruses are not
restricted to greyhounds. The hemagglutinin contained 5 conserved amino acid differences that distinguish
canine from equine lineages. The antigenic homogeneity of the canine viruses suggests that measurable
antigenic drift has not yet occurred. Continued surveillance and antigenic analyses should monitor possible
emergence of antigenic variants of canine influenza virus.

Influenza A viruses (family Orthomyxoviridae) are known to cause acute respiratory disease in humans,
horses, pigs, and domestic poultry (1,2). Influenza A virus subtype H3N8 has recently emerged as a
respiratory pathogen in dogs, associated with outbreaks of acute respiratory disease in racing greyhounds
(3). The disease is caused by a novel virus closely related to contemporary equine influenza A virus
subtype H3N8. These viruses share >96% nucleotide sequence identity, which suggests direct
transmission of the entire virus from horses to dogs without reassortment with other strains (3).

Canine influenza virus (CIV) was first identified in racing greyhounds in Florida in January 2004 and was
later associated with respiratory disease outbreaks in racing greyhounds in 9 states from 2004 through
2006 (3,4). Most affected greyhounds had clinical signs associated with virus infection of the upper
respiratory tract—cough for 10–30 days, nasal discharge, low-grade fever—followed by recovery.
However, some dogs died peracutely with extensive hemorrhage in the lungs, mediastinum, and pleural
cavity. Histologic examination showed tracheitis, bronchitis, bronchiolitis, and suppurative
bronchopneumonia associated with extensive erosion of epithelial cells and infiltration with neutrophils. The
isolation of 4 closely related influenza A subtype H3N8 viruses from dogs that died in different geographic
locations over a 25-month period, together with substantial serologic evidence of widespread infection
among racing greyhounds in 9 states, suggested sustained CIV circulation in this population by dog-to-dog
transmission (3,4).

The first evidence of CIV infection in dogs other than greyhounds came from serologic testing of dogs with
acute respiratory disease in shelters, boarding kennels, and veterinary clinics in Florida and New York in
2004 and 2005 (3). Since August 2005, a national syndromic serosurvey for canine influenza has been
conducted on >5,000 samples collected from nongreyhound dogs with compatible clinical signs (Cornell
University College of Veterinary Medicine, http://diaglab.vet.cornell.edu/issues/civ-stat.asp). As of April
2008, seropositive dogs have been identified in 25 states and the District of Columbia.

In April and May 2005, an outbreak of respiratory disease occurred in dogs housed in a shelter facility in
northeastern Florida (3). The outbreak involved at least 58 dogs, ranging in age from 3 months to 9 years,
and included purebred dogs as well as mixed breeds; 6 were euthanized. In May 2005, a respiratory
disease outbreak occurred among ≈40 pet dogs at a veterinary clinic in southeastern Florida; 1 died. We
performed molecular analyses on 2 influenza A subtype H3N8 viruses isolated from these 7 nongreyhound
dogs that died and genetically and antigenically compared them with influenza (H3N8) viruses from racing
greyhounds.

In 2010, there was an outbreak of the H3N8 Canine Flu Virus in Texas.   Sadly it was misdiagnosed by
local Veterinarians as Canine Distemper.  Most of the misdiagnosed dogs either died or were euthanized.  
There is now a vaccine for this virus.
HEALTH
AND
HEALTH CONCERNS
Parvo made its first appearance in the 1970's, Parvo type 2.  In 1980's Parvo type 2a and 2b
emerged.  Recently there has been some discussion concerning a new strain Parvo type 2c.
Scientists in Italy, Vietnam and Spain have reported in scientific literature about the new
strain.  A new strain really means a genetic variant; only  of its 5000 nucleotides needs to be
different than current strains.  CPV-2c diffrees from CPV-2b by only  nucleotide so it is
99.98% identical to CPV-2b according to Dr. Hatler.  This small change allows it to survive
and affect dogs better than the old strain.

Oklahoma State University
has isolated a NEW strain of Canine Parvo Virus, named 2c Parvo from kennels and
reported it at The Western States Veterinary Conference in Las Vegas.  It has not appeared
in US scientific literature at this point.  Until more is known, it is extremely important for you
to be diligent about your Parvo vaccination protocol.  If you have struggled with Parvo in the
past it may be time to switch to another brand of vaccines and review when you are giving
the Parvo vaccine.  If your vaccination protocol is working - don't change.  
Oklahoma Animal Disease
Diagnostic Laboratory

Hot Topics

Canine Parvovirus

  • • Canine parvovirus (CPV) remains the most frequent
infectious disease condition investigated at OADDL
in the canine species (see Animal Health Update Fall
’06).

  • • Of current interest at OADDL is the identification of
numerous 2c and 2b variants in the VP2 region of the
CPV genome. The importance of these genetic differences
in CPV is uncertain with respect to vaccination
and immunity at this time.

  • • The findings may help to explain the endemic occurrence
of CPV in Oklahoma, in the face of vaccination.

  • • Further work on this virus is planned in 2007; and
confirmation of CPV cases using PCR amplification
of viral product in fresh tissue along with histopathology
is recommended in “outbreak” situations.
Naylor MJ, Walia CS, McOrist S, Lehrbach PR, Deane EM, Harrison GA.
School of Science, Food and Horticulture, University of Western Sydney, Penrith South DC,
New South Wales, Australia. m.naylor@garvan.org.au

Canine coronavirus (CCV) UWSMN-1 was originally identified from an outbreak of fatal
gastroenteritis in breeding colonies. In this report, we examined whether UWSMN-1
represents a novel divergent strain or is the result of recombination events between canine
and feline coronavirus strains. Sequencing of various regions of the spike and polymerase
genes confirms that UWSMN-1 is widely divergent from other CCV and feline coronavirus
strains. These data raise the possibility that this strain is the first member of a novel third
subtype of CCV.

PMID: 12202609 [PubMed - indexed for MEDLINE]
COOLIE HEALTH
No dog is without health problems.  Since there is still much discussion, theory, fact, legend
and assumptions about the breeds that were used in the early development of the German
Coolie, it is safe to say they are not without genetic skeletons in their closet.  The breed that
most agree upon, that make up the Coolie, is the "Blue Merle Collie".   Further research
indicates that the breed is a derivative from early herding breeds from the United Kingdom
such as the Scotch Collie (rough collie) though some believe that the German Coolie is a
member of the Border Collie family and known throughout the British Isles as the Blue Merle
Collie and that these dogs can still be found today in Wales, Scotland and England.  

You will read on many sites that the Coolie is the most healthy dog on this planet.  This may
or may not be the complete case.  Depending on whom you obtain your Coolie from, this
dog may have been ancestors, such as the Border Collie, Kelpie, Australian Shepherd, and
one breeder admitted to knowing German Shepherd is in her lines.  Unfortunately, with this,
comes genetic defects that are incorporated into the Coolie breed from other breeds.  There
are many breeders/owners/stockmen who have chosen to ONLY breed Coolie to Coolie;
and those are commended in their efforts to keep the lines pure, for lack of a better word.
Border Collie's are currently being tested for:
  • TNS (Trapped Neutrophil Syndrome)
  • CL (NCL - Neuronal Ceroid Lipofuscinosis)
  • CEA/CH (Collie Eye Anomaly / Choroidal Hypoplasia)

According to the American Border Collie Association (ABCA):
The primary genetic diseases currently thought to be a problem in the breed are as follows:
  • Hip Dysplasia (HD)
  • Collie Eye Anomaly (CEA)
  • Epilepsy

Genetic diseases not considered to be a significant problem in the breed at this time:
  • Progressive Retinal Atrophy (PRA)
  • Elbow dysplasia

Common diseases with questionable heritable cause:
  • Osteochondritis Dissecans (OCD)

Common diseases with no known heritable contribution:
  • Focal/Multifocal Acquired Retinopathy (FMAR):

Color Related Defects:
  • Deafness


Australian Working Kelpie:


Australian Cattle Dog:
  • Polioencephalomyelopathy (Abstract)
  • Hip dysplasia
  • Progressive Retinal Atrophy (PRA)
  • Deafness
  • Luxating Patella



Currently, no markers have been located specifically for the Coolie.  With the possibility of
infusions of the above mentioned dog breeds - DNA tests that are specifically for these
breeds, could (might) work for the Coolie.  

Some Coolie owners/breeders are under the impression that there is a DNA test that can
clear the Coolie for every single genetic disease and hip dysplasia (is an actual claim on a
website) that the canine can carry -- this is very misleading and is not true.  Hip dysplasia is
not a DNA test (yet).  It is a simple x-ray that is taken by a licensed Veterinarian and then
sent to the OFA for reading by three board-certified veterinary radiologists.  Again, no
markers have been located specifically for the Coolie.  
With the infusion of the Kelpie into some lines of the Coolie breed, the Coolie is not immune
to this genetic defect.

Cerebellar Abiotrophy is strongly suspected to be an autosomal recessive mode of inheritance and
affects the cerebellum part of the brain. The cerebellum is the part of the brain that regulates the control
and coordination of movement. In this condition, cells in the cerebellum mature normally before birth,
but then deteriorate prematurely causing clinical signs associated with poor coordination and lack of
balance. The Purkinje cells in the cerebellum are primarily involved; cells in other areas of the brain
may also be affected.

Symptoms of cerebellar abiotrophy (CA) include ataxia or lack of balance, an awkward wide-legged
stance, a head tremor (intention tremor) (in dogs, body tremors also occur), hyperreactivity, lack of
menace reflex, stiff or high-stepping gait, apparent lack of awareness of where the feet are (sometimes
standing or walking with a foot knuckled over), poor depth perception, and a general inability to
determine space and distance. The symptoms are, taken as a group, fairly unique and not easily
mimicked by other illnesses, though certain types of injury and infection do need to be ruled out.
However, verifying the diagnosis in terms of laboratory evidence is only possible by examining the
brain post-mortem to determine if there has been a loss of Purkinje cells.

Most affected animals have normal intelligence and mildly affected animals can, in theory, live out a
normal lifespan. However, affected animals are prone to falling and other accidents, and for this reason
many affected animals, are euthanized for humane reasons. Dogs may need lifetime assistance with
tasks such as climbing stairs, stepping up and over objects, and may fall easily.

CA cannot be prevented, other than by selective breeding to avoid the gene, and it cannot be cured. In
some dog breeds, symptoms appear to progressively worsen, but research is not consistent on this
point. There also is some evidence that affected animals learn over time to partially compensate for the
condition and appear to improve because they are less accident-prone.

Routine diagnostic tests are normal with this condition and a definitive diagnosis can only be made by
brain biopsy or on post-mortem. MRI may be helpful in dogs in which there is gross cerebellar
malformation; however generally with this condition, the cerebellum appears grossly normal.
Histopathologic abnormalities are often minimal and do not seem to correlate with the severity of
cerebellar signs.There is no treatment for this condition. Dogs do not recover from this disorder and
usually at some point (depending on the rate of the progressive deterioration that occurs), euthanasia
becomes the best option.

Dr. Alan Wilton has begun to look for a mutation in the Kelpie genome that is causing this disease.
Eventually, it is hoped that a sample of blood can be used to discern the affected, carrier and clear-of-
gene status in every dog sampled. The Working Kelpie Council (Australia) is the registry for Working
Kelpies. At the WKC October Board meeting it was agreed, in principal, that the WKC would help fund
a project to develop a "DNA Test" for Cerebellar Abiotrophy (sometimes called Ataxia) in Working
Kelpies under the stewardship of Dr Allan Wilton working at the University of NSW.

Any Kelpie owner wishing to submit samples or make a donation to keep the research going should
contact Dr. Wilton.

UPDATE: From the WKC “News Bulletin”

November 2007, No 513ATAXIA (CA) PROGRESS REPORT.

Dr Alan Wilton advises:
The cerebellar abiotrophy research is on track. Half of the 15 ataxic dogs and 15 controls have been
typed successfully for the 50,000 DNA markers and the remainder will be done before the Melbourne
Cup.

Recent publications in the journal Nature Genetics show that this technique works well for as few as 10
affected and 10 controls so we are expecting to have a location for the gene in a few weeks time. Then
we need to search the disease gene region for the DNA defect that causes CA. This requires looking
for one difference in millions of bits of DNA. Since we do not know what we are looking for, it is not
always a simple task, but with luck and persistence we will be able to develop a test by early in 2008.
We greatly appreciate the support of the WKC and donations from breeders that allow us to continue
this work, especially the funding from Terry Snow that has allowed us to take the fast track and develop
a test over months instead of years.

WKC Editorial note: This progress report is very encouraging and we look forward to having the
answer in the not too distant future and to being able to guide breeders with a program to gradually
eliminate the disease from the working Kelpie breed. We take this opportunity to thank all members
who have supported with the supply of samples from affected and/or suspected affected and donations
to help cover the on going costs of the research.

As members are aware the WKC entered into a three year funding agreement with Dr Alan Wilton and
the NSW University. Under the terms of the agreement the WKC was committed to 3 annual amounts
comprising cash and in kind contributions. With Terry Snow extremely generous donation that enabled
the use of the very latest technology equipment research has been sped up and the WKC has been
brought forward and is handing over its 2008 funding commitment in advance.

Whilst we are not actually handling the receipt of donations we have nevertheless received and have
handed over $1000.00 from Swedish Working Kelpie fans, $60 from one of our American members
and a $19.00 donation from a local member. Dr Alan Wilton advised that he had received a generous
donation of over $1000.00 from a WKC breeder/member in Queensland and a number of other
amounts.

Research of this nature is a very expensive process and members generally are encouraged to assist
by sending in donations, no matter how small - an investment which will be in the best interests of all
who rely on sheepdogs in the everyday management of stock.

Donations are still needed to continue this very valuable research. Any Kelpie owner wishing to submit
samples or make a donation to keep the research going should contact Dr. Wilton.
Alan Wilton
School of Biotechnology and Biomolecular Sciences
University of New south Wales
NSW 2052
Phone +61 2 9385 2019
Fax + 61 2 9385 1483
Mobile 0422 736 425



UPDATE ON CEREBELLAR ABIOTROPHY IN KELPIES:

Pups affected by Cerebellar Abiotrophy (CA) have abnormal development of parts of the brain in
purkinje cells and molecular cells, which leads to motor difficulties manifesting as ataxia. Symptoms
range from severe, where the animal cannot walk, to mild where the pup will have an odd stance or
gait. A donation from Terry Snow has allowed use of high-throughput genetic typing to identify a small
region of 5 million bases with 40 genes, any of which could be the cause of CA (PhD student Jeremy
Shearman and Honours student Paulina Kowalczyk).

Ataxia in kelpies is caused by Cerebellar Abiotrophy (CA), which is a loss of Purkinje brain cells. A
small number of litters are born each year with this condition, but they are not restricted to one line of
closely related animals. This suggests that the defect is recessive and widespread in the breed, with
perhaps as high as a few per cent of dogs as carriers (have one good copy of the gene and one
defective and are perfectly healthy but can pass on the defective gene to offspring). It is only when two
carriers mate that a proportion of the offspring (one quarter on average) will inherit two defective
copies of the gene, one from each parent, and manifest symptoms of the disease.

CA occurs in a large number of dog breeds. The symptoms of CA in kelpies are quite variable, from
animals that cannot stand to those where the condition goes almost unnoticed except for an unusual
gait or instability in some circumstances. A characteristic sign is constant head bobbing while at rest.  
This variation in presentation has made the disease hard to track and recognise as a genetic problem
because symptoms similar to CA can also result from viral infections in young pups. It is only when the
cases are brought into the open and discussed that comparisons can be made and an idea of the
extent of the problem can be obtained.

Kelpie breeders are fortunate in that the symptoms do not progressively worsen with time as they do in
some other breeds. The symptoms in kelpies remains stable until illness or age reduces the animal's
strength and further weakens the animals coordination. Don Robertson in Western Australia has
produced a video showing the presentation of the diseases in kelpies, copies are available on DVD
from the Working Kelpie Council.

CA in kelpies occurs in both working kelpies and bench kelpies. This further demonstrates how widely
spread the condition is. It is a particular problem in working dogs where even mild cases can affect
performance. It is distressing for any breeder to have severely affected pups that need to be destroyed.

The success of the Wilton lab in developing tests for two different fatal diseases in Border collies and
their application to rid the breed of these inherited defects has encouraged other breeders to look at
the problem in their own breed.  At the request of members, the Working Kelpie Council approached
our lab to help them develop a DNA test for CA in kelpies so that they can detect the carriers and avoid
matings that would produce animals with ataxia, and eventually allow them to eliminate the problem
from the breed altogether.

Developing DNA tests requires application of molecular biology techniques very similar to forensics
and is quite expensive to perform, but recent developments in the field have made the process much
simpler than it once was. We now have the DNA sequence of all of the genes in the dog. The question
is, however, which of the 20,000+ genes is causing the problem. New technology is available to short-
cut the disease gene discovery process, but it is costly to implement. This type of research requires
several thousand dollars of funding each year for a number of years.

Microarray technology allows us to look at 50,000 places spread around the dog DNA at the same
time. Each place is a Single Nucleotide Polymorphism (SNP, pronounced snip) where there are two
possible choices for the DNA bases at that spot, for example, A or G. (The four possible bases are A,
C, G and T.)  Use of this technology was made possible by a donation from Terry Snow. In addition, the
Working Kelpie Council and Swedish Kelpie Club continue to support the research with donations.

We tested 13 affected dogs and18 unaffected controls with SNP microarrays, and identified the
regions where the affected genes are all similar but different to the controls. This should be where  the
CA disease gene is located. There are 40 genes in the region of interest that could be the CA gene;
testing of these genes is ongoing.

A video has been made by Terry Snow about the disease and the research in order to educate
breeders so that they can be prepared when the test becomes available. (A DVD copy is available
through the Working Kelpie Council).  

Shearman, JR, Lau VM, Wilton AN. Elimination of SETX, SYNE1 and ATCAY as the cause of
cerebellar abiotrophy in Australian Kelpies.  Animal Genetics 39: 573, 2008 IF 2.53 doi:10.1111/j.
1365-2052.2008.01753.x
 Aujeszky's Disease
(Pseudo-rabies)
Click here to read the article

It is strongly suggested that you never feed your dog meat from feral (wild) pigs.  
If you use your dogs to hunt feral hogs, you may be interested in this article.


Two short paragraphs from the article above:  
"Aujeszky’s disease (pseudorabies) is a highly contagious, economically significant
disease of pigs. This viral infection causes central nervous system (CNS) signs
and high mortality rates in young animals, and respiratory illness in older pigs. Other
species may be infected when they come in contact with pigs, resulting in a universally
fatal CNS disease. Aujeszky’s disease can result in trade restrictions where it is
endemic. Eradication programs are underway or have been successful in many countries.
In the United States, all states are now considered to be free of the virus in domesticated
swine, and a surveillance program is ongoing.
The presence of the virus in feral pigs remains a concern.

Pigs are the natural host for Aujeszky’s disease virus and the only animals to become
latent carriers. However, the virus can infect nearly all domesticated and wild
mammals including cattle, sheep, goats, cats and dogs. It does not infect humans or
the tailless apes, and infections in horses are rare".