Pet Beat BC

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Letter from the Founder

Letter from the Editor's

Rabbit Hemorrhagic Disease

Parvo in BC

Moose Loose in Community

Salmon in BC

This article was written by Dustyn Lindley

Sockeye Salmon

The sockeye salmon (Oncorhynchus nerka), also called red salmon, kokanee salmon, or

blueback salmon, is an anadromous species of salmon found in the Northern Pacific Ocean

and rivers discharging into it. This species is a Pacific salmon that is primarily red in hue

during spawning. They can grow up to 84 cm (2 ft 9 in) in length and weigh 2.3 to 7 kg (5–15

lb). Juveniles remain in freshwater until they are ready to migrate to the ocean, over

distances of up to 1,600 km (1,000 mi). Their diet consists primarily of zooplankton. Sockeye

salmon are semelparous, dying after they spawn. Some populations, referred to as kokanee,

do not migrate to the ocean and live their entire lives in freshwater.

Classification and name origin

The sockeye salmon is the third-most common Pacific salmon species, after pink and chum

salmon. Oncorhynchus comes from the Greek ὄγκος (onkos) meaning "barb", and ῥύγχος

(rhynchos) meaning "snout". Nerka is the Russian name for the anadromous form. The

name "sockeye" is an anglicization of suk-kegh (sθə́qəy̓), its name in Halkomelem, the

language of the indigenous people along the lower reaches of the Fraser River (one of

British Columbia's many native Coast Salish languages). Suk-kegh means "red fish".

Description

The sockeye salmon is sometimes called red or blueback salmon, due to its color. Sockeye

are blue tinged with silver in color while living in the ocean. When they return to spawning

grounds, their bodies become red and their heads turn green. Sockeye can be anywhere

from 60 to 84 cm (2 ft 0 in–2 ft 9 in) in length and weigh from 2.3 to 7 kg (5–15 lb). Two

distinguishing features are their long, serrated gill rakers that range from 30 to 40 in number,

and their lack of a spot on their tail or back.

Range and habitat

Sockeye salmon range as far south as the Columbia River in the eastern Pacific (although

individuals have been spotted as far south as the 10 Mile River on the Mendocino Coast of

California) and in northern Hokkaidō Island in Japan in the western Pacific. They range as

far north as the Bathurst Inlet in the Canadian Arctic in the east and the Anadyr River in

Siberia in the west. The farthest inland sockeye salmon travel is to Redfish Lake, Idaho, over

1,400 km (900 mi) from the ocean and 2,000 m (6,500 ft) in elevation.

Landlocked populations

Some sockeye salmon populations are completely landlocked. Sockeye that live and

reproduce in lakes are commonly called kokanee, which is red-fish name in the Sinixt Interior

Salish language and silver trout in the Okanagan language. They are much smaller than the

anadromous variety and are rarely over 35 cm (14 in) long. In the Okanagan Lake and many

others, there are two kinds of kokanee populations – one spawns in streams and the other

near lake shores. Landlocked populations occur in the Yukon Territory and British Columbia

in Canada, as well as, in Alaska, Washington, Oregon, California, New York, Utah, Idaho,

Montana, Nevada, Colorado, New Mexico, and Wyoming in the United States. Nantahala

Lake is the only place in North Carolina where kokanee salmon are found. The fish, which is

native to western North America, was stocked in Nantahala Lake in the mid-1960s by the NC

Wildlife Resources Commission in an attempt to establish the species as a forage fish for

other predator fishes in the lake. This stock has remained and become a favorite target for

anglers.

In Japan, a landlocked variety termed black kokanee, or "kunimasu" in Japanese, was

deemed to be extinct after 1940, when a hydroelectric project made its native lake in

northern Akita Prefecture more acidic. The species seems to have been saved by

transferring eggs to Saiko Lake, 500 kilometers to the south, however. This fish has been

treated as a subspecies of sockeye Oncorhynchus nerka kawamurae, or even an

independent species Oncorhynchus kawamurae.

Diet

Sockeye salmon use patterns of limnetic feeding behavior, which encompasses vertical

movement, schooling, diel feeding chronology, and zooplankton prey selectivity. They can

change their position in the water column, timing and length of feeding, school formation,

and choice of prey to minimize the likelihood of predation. This also ensures they still get at

least the minimum amount of food necessary to survive. All of these behaviors contribute to

the survivability, and therefore fitness of the salmon. Depending on location and threat of

predation, the levels of aggressive feeding behavior can vary.

Sockeye salmon, unlike other species of Pacific salmon, feed extensively on zooplankton

during both freshwater and saltwater life stages. They also tend to feed on small aquatic

organisms such as shrimp. Insects are part of their diets at the juvenile stage.

Life Cycle

Sockeye salmon exhibit many different life histories with the majority being anadromous

where the juvenile salmon migrate from freshwater lakes and streams to the ocean before

returning as adults to their natal freshwater to spawn. Similar to most Pacific salmon,

sockeye salmon are semelparous, meaning they die after spawning once. Some sockeye,

called kokanee, do not migrate to the ocean and live their entire lives in freshwater lakes.

The majority of sockeye spawn in rivers near lakes and juveniles will spend one to two years

in the lake before migrating to the ocean, although some populations will migrate to saltwater

in their first year. Adult sockeye will spend two to three years in the ocean before returning to

freshwater. Females will spawn in 3–5 redds over a period of several days. The eggs usually

hatch within six to nine weeks and the fry typically rear in lakes before migrating to the

ocean.

Reproduction

Males partake in competitive and sneaking tactics, formation of hierarchies, and

non-hierarchical groupings around females who are ready to mate. Reproductive success

varies more in males than females. The greater variability in male reproduction is associated

with the greater average size and exaggerated shape of males. Reproductive success in

females is determined by the number of eggs she lays, her body size, and the survival of the

eggs, which is due in part to the quality of the nest environment. Male spatial distribution

depends on shifts in reproductive opportunities, physical traits of breeding sites, as well as

the operational sex ratio (OSR) of the environment.

Non-dominant males adopt a subordinate behavior, acting as a satellite to mated pairs.

During spawning, a subordinate male will move quickly into the redd and release their

sperm. Nearby dominant males from other redds will also do this. Male social status is

positively correlated to length and dorsal hump size. Larger females tend to spawn in

shallower water, which is preferred over deeper water. There is a dramatic sexual

dimorphism at maturity. Males go through numerous morphological changes at maturation

including, an increase in body depth, hump height, and snout length. Snout size also

increases in females, but hump height and adipose fin length do not increase. This could

mean that longer snout sizes are sexually selected, but hump height and adipose fin length

are not. Females develop large gonads that are about 25% of the body mass.

Females are responsible for parental care. They select, prepare, and defend a nest site until

they die or are displaced. Males do not participate in parental care at all, and they move

between females after egg deposition.

Energy cost

Reproduction is marked by depletion in energy stores. Fat, protein, and somatic energy

stores decrease from the final moments in marine migration through freshwater entry,

spawning, and death. Sockeye salmon do not feed during reproduction. Feeding ends once

they enter into freshwater, which can be several months before spawning. Embryos are

maintained with only endogenous food supplies for about 3–8 months. Reproduction in the

sockeye salmon has to be accomplished with the energy stores brought to the spawning

grounds. How the salmon use their energy during migration and spawning affects how

successful they will be reproductively; energy used for migration cannot also be used for

courtship. If they waste too much energy, they might not be able to spawn. Males must also

make the decision whether to invest energy in fighting for a female or for longevity on the

spawning grounds. Sockeye salmon with longer and more difficult migration routes produce

fewer eggs on the spawning grounds. High water temperatures also increase the energy

expenditure of sockeye salmon as they migrate upriver.

Competition

Aggressive behavior displayed by dominant males is predominantly directed towards

intruding dominant males. Sometimes sockeye salmon males behave aggressively towards

subordinate males. These encounters are short, with the intruding male leaving after one or

two aggressive interactions. Spawning females direct their aggression primarily towards

intruding females or other spawning females that are close by. However, they may also

direct aggression towards intruding or subordinate males. Aggressive interactions between

females only last one or two charges and/or chases. The intruder retreats and the spawning

female settles back in her redd. These acts of aggression are important in terms of

reproductive success, because they determine the quality of the nest site the female obtains

and access to males.

Competition for food or space while the salmon are in their lake residence period can exist.

This happens when there is a more populous class of young sockeye or when there are

multiple classes present. It can also happen when resources are in short supply. Interspecific

competition can also occur and can lead to interactive segregation, which is when species

emphasize their differences in diet and habitat to avoid competition. Interspecific competition

can affect the growth rates of the salmon if their access to resources is limited.

Fisheries and consumption

The total registered fisheries harvest of the sockeye in 2010 was some 170,000 tonnes, of

which 115,000 tonnes were from the United States and the rest was equally divided between

Canada and Russia. This corresponds to some 65 million fish in all, and to some 19% of the

harvest of all Pacific salmon species by weight. Commercial fishermen in Alaska net this

species using seines and gillnets for fresh or frozen fillet sales and canning. The annual

catch can reach 30 million fish in Bristol Bay, Alaska, which is the site of the world's largest

sockeye harvest. Sockeye salmon have long been important in the diet and culture of the

Coast Salish people of British Columbia. The largest spawning grounds in Asia are located

on the Kamchatka Peninsula of the Russian Far East, especially on the Ozernaya River of

the Kurile Lake, which accounts for nearly 90% of all Asian sockeye salmon production, and

is recognized as the largest spawning ground outside of Alaska. Illegal fishing in Kamchatka

is subject to environmental concern. Sockeye is almost never farmed. A facility in Langley,

BC harvested its first salmon in March 2013, and continues to harvest farmed salmon from

its inland facility.

Conservation status

United States

United States sockeye salmon populations are currently listed under the US Endangered

Species Act by the National Marine Fisheries Service as an endangered species in the

Snake River and as a threatened species in Lake Ozette, Washington. The Snake River

sockeye salmon was listed as endangered in November 1991, after the Shoshone-Bannock

Tribe at Fort Hall Indian Reservation petitioned the National Marine Fisheries Service. Other

sockeye populations in the upper Columbia River and in Puget Sound are not listed under

the Act. Sockeye is an exception to 2010's forecast resurgence of Oregonian fish stocks.

Spring Chinook, summer steelhead, and Coho are forecast to increase by up to 100% over

2008 populations. The sockeye population peaked at over 200,000 in 2008 and were

forecast to decline to just over 100,000 in 2010. As an early indication of the unexpectedly

high sockeye run in 2010, on July 2, 2010, the United States Army Corps of Engineers

reported over 300,000 sockeye had passed over Bonneville Dam on the Columbia River.

Lower temperatures in 2008 North Pacific waters brought in fatter plankton, which, along

with greater outflows of Columbia River water, fed the resurgent populations. Proposed

legislative efforts, such as the Northern Rockies Ecosystem Protection Act, are attempting to

protect the headwaters of the sockeye salmon by preventing industrial development in

roadless areas. Record numbers of a once-waning population of sockeye salmon have been

returning to the Northwest's Columbia Basin (as of June 2012), with thousands more

crossing the river's dams in a single day than the total numbers seen in some previous

years.

Canada

The conservation status of sockeye populations in Canada is under review by Fisheries and

Oceans Canada as part of its Wild Salmon Policy strategy to standardize monitoring of wild

salmon status. Salmon runs of particular note are the Skeena and Nass river runs, and the

most famous is the Fraser River sockeye run. The Fraser River salmon run has experienced

declines in productivity since the 1990s, mirroring a similar decline in the 1960s. The return

abundance (population) of Fraser River sockeye in 2009 was estimated at a very low

1,370,000, 13% of the pre-season forecast of 10,488,000. That represented a decline from

the recent (1993) historical cycle peak of 23,631,000 and the return abundance was the

lowest in over 50 years. The reasons for this (former) decline remain speculative. According

to a consortium of scientists assembled to review the problem, the decline highlights the

uncertainty in forecasting salmon returns. After the low returns, the Government of Canada

launched a formal inquiry into the decline, the Commission of Inquiry into the Decline of

Sockeye Salmon in the Fraser River. The Commission has been tasked with investigating all

the factors which may affect Fraser River sockeye salmon throughout their life cycle.

According to the terms of reference, the subjects of investigation are "the impact of

environmental changes along the Fraser River, marine environmental conditions,

aquaculture, predators, diseases, water temperature and other factors that may have

affected the ability of sockeye salmon to reach traditional spawning grounds or reach the

ocean."

During the commission, hundreds of thousands of documents and scientific research papers

were reviewed. Twelve technical reports were published using that information, looking at

the possible impacts of diseases and parasites, hatchery diseases, contaminants, marine

ecology, salmon farms, fisheries, predators, climate change and government management

on the productivity of Fraser River sockeye runs.

The commission submitted its final report on October 29, 2012.

While the commission was holding public hearings, in the late summer of 2010, the largest

run of sockeye since 1913 returned to the Fraser River system. Final counts show that

approximately 30 million salmon returned to the Fraser River and its tributaries in 2010. In

total, approximately 11,591,000 Fraser sockeye were caught by Canadian fishers and

1,974,000 Fraser sockeye were caught by American fishers. The final projected escapement

(fish which were not caught) was 15,852,990 fish.

Rent unpredictable fluctuations in runs are speculated to be due to changing water

temperatures. There is high variation in thermal tolerance among the different sockeye

salmon populations that migrate up the Fraser River. The Chilko River sockeye salmon

population is able to maintain cardiorespiratory function at higher temperatures, which may

make them more resilient to the effects of rising river temperatures. In one study examining

possible physiological mechanisms underlying these population differences in thermal

tolerance, juvenile sockeye salmon from the Chilko River and Weaver Creek did not show

any differences in force-frequency response of the heart or cardiac pumping capacity when

reared in common garden temperatures at 5 °C and 14 °C. Therefore, the physiology

underlying these differences in thermal tolerance has yet to be determined.

This article was written by Makala Jackson Johnson

Young moose wanders through neighbourhood in Canoe

Photographer Kristall Burgess and her spouse Rob were enjoying an early morning coffee in their Canoe home earlier this week when an unexpected visitor passed by.

It was about 5:15 a.m. on Monday, June 3. Rob, a hunter, recognized the pitter patter of large feet outside and suggested she grab her camera.

The passerby, a cow moose, was strolling around in the vicinity of 50th and 70th Streets NE so Kristall followed her, giving the animal lots of space as she knows they can be dangerous.

“I was probably 100 feet away, being really respectful,” she says.

Kristall followed it down an alley and then it ducked into a lot. She assumed it was going to keep going through.

However, the moose, out of view, had stopped, so they found themselves closer than either had expected.

“It just stood there and looked at me – I took a couple of steps backward, it took a couple of steps backward.”

And then off it went.

She says it was shedding some hair but looked good and healthy.

A couple of people saw a young moose running around the Canoe area last year, so they think it might be the same one.

This article was written by Kami Martz McDonnel

Canine parvovirus

Canine parvovirus (also referred to as CPV, CPV2, or parvo) is a contagious virus mainly affecting dogs. CPV is highly contagious and is spread from dog to dog by direct or indirect contact with their feces. Vaccines can prevent this infection, but mortality can reach 91% in untreated cases. Treatment often involves veterinary hospitalization. Canine parvovirus often infects other mammals including foxes, wolves, cats, and skunks. Felines are also susceptible to panleukopenia, a different strain of parvovirus.

Signs

Dogs that develop the disease show signs of the illness within three to ten days. The signs may include lethargy, vomiting, fever, and diarrhea (usually bloody). Generally, the first sign of CPV is lethargy. Secondary signs are loss of weight and appetite or diarrhea followed by vomiting. Diarrhea and vomiting result in dehydration that upsets the electrolyte balance and this may affect the dog critically. Secondary infections occur as a result of the weakened immune system. Because the normal intestinal lining is also compromised, blood and protein leak into the intestines, leading to anemia and loss of protein, and endotoxins escape into the bloodstream, causing endotoxemia. Dogs have a distinctive odor in the later stages of the infection. The white blood cell level falls, further weakening the dog. Any or all of these factors can lead to shock and death. Younger animals have worse survival rates.

Diagnosis

Diagnosis is made through detection of CPV2 in the feces by either an ELISA or a hemagglutination test, or by electron microscopy. PCR has become available to diagnose CPV2, and can be used later in the disease when potentially less virus is being shed in the feces that may not be detectable by ELISA. Clinically, the intestinal form of the infection can sometimes be confused with coronavirus or other forms of enteritis. Parvovirus, however, is more serious and the presence of bloody diarrhea, a low white blood cell count, and necrosis of the intestinal lining also point more towards parvovirus, especially in an unvaccinated dog. The cardiac form is typically easier to diagnose because the symptoms are distinct.

Treatment

Survival rate depends on how quickly CPV is diagnosed, the age of the dog, and how aggressive the treatment is. There is no approved treatment, and the current standard of care is supportive care, involving extensive hospitalization, due to severe dehydration and potential damage to the intestines and bone marrow. A CPV test should be given as early as possible if CPV is suspected in order to begin early treatment and increase survival rate if the disease is found.

Supportive care ideally also consists of crystalloid IV fluids and/or colloids (e.g., Hetastarch), antinausea injections (antiemetics) such as maropitant, metoclopramide, dolasetron, ondansetron and prochlorperazine, and broad-spectrum antibiotic injections such as cefazolin/enrofloxacin, ampicillin/enrofloxacin, metronidazole, timentin, or enrofloxacin. IV fluids are administered and antinausea and antibiotic injections are given subcutaneously, intramuscularly, or intravenously. The fluids are typically a mix of a sterile, balanced electrolyte solution, with an appropriate amount of B-complex vitamins, dextrose, and potassium chloride. Analgesic medications can be used to counteract the intestinal discomfort caused by frequent bouts of diarrhea; however, the use of opioid analgesics can result in secondary ileus and decreased motility.

In addition to fluids given to achieve adequate rehydration, each time the puppy vomits or has diarrhea in a significant quantity, an equal amount of fluid is administered intravenously. The fluid requirements of a patient are determined by the animal's body weight, weight changes over time, degree of dehydration at presentation, and surface area.

A blood plasma transfusion from a donor dog that has already survived CPV is sometimes used to provide passive immunity to the sick dog. Some veterinarians keep these dogs on site, or have frozen serum available. There have been no controlled studies regarding this treatment. Additionally, fresh frozen plasma and human albumin transfusions can help replace the extreme protein losses seen in severe cases and help assure adequate tissue healing. However, this is controversial with the availability of safer colloids such as Hetastarch, as it will also increase the colloid osmotic pressure without the ill effect of predisposing that canine patient to future transfusion reaction.

Once the dog can keep fluids down, the IV fluids are gradually discontinued, and very bland food slowly introduced. Oral antibiotics are administered for a number of days depending on the white blood cell count and the patient's ability to fight off secondary infection. A puppy with minimal symptoms can recover in two or three days if the IV fluids are begun as soon as symptoms are noticed and the CPV test confirms the diagnosis. If more severe, depending on treatment, puppies can remain ill from five days up to two weeks. However, even with hospitalization, there is no guarantee that the dog will be cured and survive.

Treatments in development

Kindred Biosciences, a biopharmaceutical company, is developing a monoclonal antibody as a prophylactic therapy to prevent clinical signs of parvovirus infection and also as treatment of established parvovirus infection. Completion of an upcoming pivotal efficacy study for the therapeutic indication is expected in the first quarter of 2021.

Unconventional treatments

There have been anecdotal reports of oseltamivir (Tamiflu) reducing disease severity and hospitalization time in canine parvovirus infection. The drug may limit the ability of the virus to invade the crypt cells of the small intestine and decrease gastrointestinal bacteria colonization and toxin production. However, due to the viral DNA replication pattern of parvovirus and the mechanism of action of oseltamivir, this medication has not shown to improve survival rates or shorten hospitalization stay. Recombinant feline interferon omega (rFeIFN-ω), produced in silkworm larvae using a baculovirus vector, has been demonstrated by multiple studies to be an effective treatment. However, this therapy is not currently approved in the United States.

An unpublished 2012 study from Colorado State University showed good results with an intensive at-home treatment using maropitant (Cerenia) and Convenia (a long acting antibiotic injection), two drugs released by Zoetis (formerly Pfizer). This treatment was based on outpatient care, and would cost $200 to $300, a fraction of the $1,500 to $3,000 that inpatient care cost. However, the more-effective care is intravenous (IV) fluid therapy. In the CSU study, survival rate for the new treatment group was 85%, compared to the 90% survival for the conventional inpatient treatment. The outpatient dogs received initial intravenous fluid resuscitation, and had aggressive subcutaneous fluid therapy and daily monitoring by a veterinarian. The dogs required being taken to the vet every 12 hours for successful treatment and recovery.

History

Parvovirus CPV2 is a relatively new disease that appeared in the late 1970s. It was first recognized in 1978 and spread worldwide in one to two years. The virus is very similar to feline panleukopenia (also a parvovirus); they are 98% identical, differing only in two amino acids in the viral capsid protein VP2. It is also highly similar to mink enteritis virus (MEV), and the parvoviruses of raccoons and foxes. It is possible that CPV2 is a mutant of an unidentified parvovirus (similar to feline parvovirus (FPV)) of some wild carnivore. CPV2 was thought to only cause diseases in canines, but newer evidence suggest pathogenicity in cats too.

Variants

There are two types of canine parvovirus called canine minute virus (CPV1) and CPV2. CPV2 causes the most serious disease and affects domesticated dogs and wild canids. There are variants of CPV2 called CPV-2a and CPV-2b, identified in 1979 and 1984 respectively. Most of canine parvovirus infection are believed to be caused by these two strains, which have replaced the original strain, and the present day virus is different from the one originally discovered, although they are indistinguishable by most routine tests. An additional variant is CPV-2c, a Glu-426 mutant, and was discovered in Italy, Vietnam, and Spain. The antigenic patterns of 2a and 2b are quite similar to the original CPV2. Variant 2c however has a unique pattern of antigenicity. This has led to claims of ineffective vaccination of dogs, but studies have shown that the existing CPV vaccines based on CPV-2b provide adequate levels of protection against CPV-2c. A strain of CPV-2b (strain FP84) has been shown to cause disease in a small percentage of domestic cats, although vaccination for FPV seems to be protective. With severe disease, dogs can die within 48 to 72 hours without treatment by fluids. In the more common, less severe form, mortality is about 10 percent. Certain breeds, such as Rottweilers, Doberman Pinschers, and Pit bull terriers as well as other black and tan colored dogs may be more susceptible to CPV2. Along with age and breed, factors such as a stressful environment, concurrent infections with bacteria, parasites, and canine coronavirus increase a dog's risk of severe infection. Dogs infected with parvovirus usually die from the dehydration it causes or secondary infection rather than the virus itself.

The variants of CPV-2 are defined by surface protein (VP capsid) features. This classification does not correlate well with phylogenies built from other parts of the viral genome, such as the NS1 protein.

Intestinal form

Dogs become infected through oral contact with CPV2 in feces, infected soil, or fomites that carry the virus. Following ingestion, the virus replicates in the lymphoid tissue in the throat, and then spreads to the bloodstream. From there, the virus attacks rapidly dividing cells, notably those in the lymph nodes, intestinal crypts, and the bone marrow. There is depletion of lymphocytes in lymph nodes and necrosis and destruction of the intestinal crypts. Anaerobic bacteria that normally reside in the intestines can then cross into the bloodstream, a process known as translocation, with bacteremia leading to sepsis. The most common bacteria involved in severe cases are Clostridium, Campylobacter and Salmonella species. This can lead to a syndrome known as systemic inflammatory response syndrome (SIRS). SIRS leads to a range of complications such as hypercoagulability of the blood, endotoxaemia and acute respiratory distress syndrome (ARDS). Bacterial myocarditis has also been reported secondarily to sepsis. Dogs with CPV are at risk of intussusception, a condition where part of the intestine prolapses into another part. Three to four days following infection, the virus is shed in the feces for up to three weeks, and the dog may remain an asymptomatic carrier and shed the virus periodically. The virus is usually more deadly if the host is concurrently infested with worms or other intestinal parasites.

Cardiac form

This form is less common and affects puppies infected in the uterus or shortly after birth until about 8 weeks of age. The virus attacks the heart muscle and the puppy often dies suddenly or after a brief period of breathing difficulty due to pulmonary edema. On the microscopic level, there are many points of necrosis of the heart muscle that are associated with mononuclear cellular infiltration. The formation of excess fibrous tissue (fibrosis) is often evident in surviving dogs. Myofibers are the site of viral replication within cells. The disease may or may not be accompanied with the signs and symptoms of the intestinal form. However, this form is now rarely seen due to widespread vaccination of breeding dogs.

Even less frequently, the disease may also lead to a generalized infection in neonates and cause lesions and viral replication and attack in other tissues other than the gastrointestinal tissues and heart, but also brain, liver, lungs, kidneys, and adrenal cortex. The lining of the blood vessels are also severely affected, which lead the lesions in this region to hemorrhage.

Infection of the fetus

This type of infection can occur when a pregnant female dog is infected with CPV2. The adult may develop immunity with little or no clinical signs of disease. The virus may have already crossed the placenta to infect the fetus. This can lead to several abnormalities. In mild to moderate cases the pups can be born with neurological abnormalities such as cerebellar hypoplasia.

Virology

CPV2 is a non-enveloped single-stranded DNA virus in the Parvoviridae family. The name comes from the Latin parvus, meaning small, as the virus is only 20 to 26 nm in diameter. It has an icosahedral symmetry. The genome is about 5000 nucleotides long. CPV2 continues to evolve, and the success of new strains seems to depend on extending the range of hosts affected and improved binding to its receptor, the canine transferrin receptor. CPV2 has a high rate of evolution, possibly due to a rate of nucleotide substitution that is more like RNA viruses such as Influenzavirus A. In contrast, FPV seems to evolve only through random genetic drift.

CPV2 affects dogs, wolves, foxes, and other canids. CPV2a and CPV2b have been isolated from a small percentage of symptomatic cats and is more common than feline panleukopenia in big cats.

Previously it has been thought that the virus does not undergo cross species infection. However studies in Vietnam have shown that CPV2 can undergo minor antigenic shift and natural mutation to infect felids. Analyses of feline parvovirus (FPV) isolates in Vietnam and Taiwan revealed that more than 80% of the isolates were of the canine parvovirus type, rather than feline panleukopenia virus (FPLV). CPV2 may spread to cats easier than dogs and undergo faster rates of mutation within that species.

Prevention and decontamination

Prevention is the only way to ensure that a puppy or dog remains healthy because the disease is extremely virulent and contagious. Appropriate vaccination should be performed starting at 7–8 weeks of age, with a booster given every 3–4 weeks until at least 16 weeks of age. Pregnant mothers should not be vaccinated as it will abort the puppies and could make the mother extremely sick. The virus is extremely hardy and has been found to survive in feces and other organic material such as soil for up to 1 year. It survives in extremely low and high temperatures. The only household disinfectant that kills the virus is bleach. The dilute bleach solution needs to be in a 1:10 ratio to disinfect and kill parvovirus.

Puppies are generally vaccinated in a series of doses, extending from the earliest time that the immunity derived from the mother wears off until after that passive immunity is definitely gone. Older puppies (16 weeks or older) are given 3 vaccinations 3 to 4 weeks apart. The duration of immunity of vaccines for CPV2 has been tested for all major vaccine manufacturers in the United States and has been found to be at least three years after the initial puppy series and a booster 1 year later.

A dog that successfully recovers from CPV2 generally remains contagious for up to three weeks, but it is possible they may remain contagious for up to six. Ongoing infection risk is primarily from fecal contamination of the environment due to the virus's ability to survive many months in the environment. Neighbours and family members with dogs should be notified of infected animals so that they can ensure that their dogs are vaccinated or tested for immunity. A modified live vaccine may confer protection in 3 to 5 days; the contagious individual should remain in quarantine until other animals are protected.

This article was written by Abby Martz McDonnel

Facts About FIV

What is FIV (Feline Immunodeficiency Virus)?

FIV is a lentivirus, a slow-progressing virus that can compromise a cat’s immune system, reducing its ability to fight off illnesses. The virus has a long latent period then progresses so slowly that it may never affect a cat. That’s why long-term studies show what guardians and rescuers have known for decades—that FIV cats can live just as long and as healthy, and ultimately die of the same causes as Non-FIV cats. And, FIV cats can live with Non-FIV cats without spreading the virus.

FIV is a rare virus affecting an estimated 2-3% of cats in the U.S. and 3-4% worldwide. For healthy, domesticated, indoor cats, the percentage is even lower.

How is FIV transmitted?

FIV is difficult to spread. The virus is fragile and does not survive long in the environment. It is killed by air, light, heat and regular household disinfectants.

FIV is primarily transmitted through a deep, penetrating bite (FIV cat to Non-FIV cat) where the virus (in the saliva) is injected directly into the bloodstream of the Non-FIV cat. Bites of this kind are extremely rare, except in free-roaming, un-neutered tomcats.

It can also be spread through blood transfusions (very rare since a Veterinarian would not use an FIV cat to give blood to a Non-FIV cat).

Kittens rarely get it from their mothers. Some inherit their Mom’s antibodies (the good guys that fight the virus) so kittens testing positive should be retested between 6 and 8 months of age, at which time most will test negative. Which means they never had the virus, just the antibodies from Mom.

FIV is not passed through open wounds. And, FIV is not passed casually such as the sharing of food or water dishes or toys, mutual grooming, snuggling, mock fighting, shared litter boxes, scratches, not even sneezes. You can cuddle FIV and Non-FIV cats at the same time and not spread the virus.

Can FIV cats live with other cats?

Yes, FIV cats can live with both FIV and Non-FIV cats without spreading the virus as long as all are non-aggressive. This is usually a matter of introducing cats SLOWLY. Any time a new cat is added to a household, there should be a slow introductory period whether cats are FIV or Non-FIV.

FIV cats can live just as long and as healthy as Non-FIV cats.

FIV cats can live with Non-FIV cats without spreading the virus.

Can my kids or other animals catch FIV?

NO. FIV is a feline disease. There is no evidence FIV can be transmitted to humans or other mammals.

How is a cat tested for FIV?

A simple blood test called ELISA looks for antibodies to FIV. However, due to many false results, if a cat tests positive, it should be retested using an IDEXX PCR test. (The PCR looks for the actual virus itself.)

Is there a cure or treatment for FIV?

No. There are actually no cures for any of the thousands of viruses in cats or humans, and no specific treatments for FIV except good care. (see below: Do FIV cats need special Care?)

Is there a vaccine?

A vaccine was created. However, it is no longer available in the US because it did not work for all strains of the virus. Also, the screening tests cannot tell the difference between a vaccinated cat and one that has the virus. So if a vaccinated cat was lost and ended up at a shelter, the cat could lose its life because some shelters routinely “euthanize” FIV cats as unadoptable. (Thankfully, more people running shelters now know that FIV cats are just cats and they are finding homes for them.)

Cats who have been vaccinated AGAINST FIV

will test positive FOR FIV antibodies.

This leads to false readings all of their lives.

Is FIV the same as Feline AIDS?

Some people, including veterinarians, still use the misleading terminology that FIV=Feline AIDS. The facts are that FIV is NOT “Feline AIDS.” (Just as we have learned that HIV is NOT “AIDS” in people.) FIV is a slow-progressing virus that could (though rarely does) allow a disease to progress unchecked.

FIV is NOT “Feline AIDS.”

Just as HIV is NOT “AIDS” in people.

How long can an FIV cat live?

Several long-term studies show what guardians and rescuers have known for decades, that cats can live as long, and as healthy as non-FIV cats and ultimately die of the same causes.

Do FIV cats need special care?

FIV cats have the same needs as Non-FIV cats. ALL cats should be neutered, live only with other non-aggressive cats, kept as healthy as possible, live in a safe environment (either indoor and/or outdoor cat- proofed area), stress levels kept down (all cats are hypersensitive), a quality diet (the best you can afford), regular vet exams, treat any health problems when they arise. And LOVE.

This article was written by Sarah Crossley Johnson

CANINE PARVOVIRUS IN BRITISH COLUMBIA

Canine parvovirus is a disease of canids, or dog-like animals such as dogs, coyotes and wolves. It only infects these

species so is not a danger to humans or other species. All ages of dogs may be affected, but puppies and older dogs

appear to be most susceptible.

The virus is related to feline panleukopenia, which is also known as feline distemper, and raccoon parvovirus. It is

transmitted between animals by oral contact with fecal material from infected animals. Infected dogs shed the virus

in their feces for approximately 2 weeks and the virus can survive in the environment for a very long time.

Canine parvovirus causes an intestinal infection resulting in severe diarrhea and often vomiting. The diarrhea

typically contains blood and has a very characteristic odor. Affected animals will not eat, are extremely weak and

usually have vomiting and bloody diarrhea. Death often follows as a result of dehydration, shock and secondary

infections.

Treatment includes intensive support with intravenous fluids, good nursing care and antibiotics in domestic dogs.

Animals have been reported to survive without treatment but this is not common. Affected dogs should be isolated

to prevent infection of other dogs.

Prevention of the disease by vaccination of dogs as puppies has reduced the occurrence of canine parvovirus in the

dog population, however outbreaks are reported in areas of British Columbia where vaccination is not commonplace

or groups of susceptible dogs exist. Outbreaks or suspected outbreaks have been reported in wild coyotes and

wolves as well. It is believed that these outbreaks may be associated with outbreaks in domestic dogs. Reports in

wild canids usually involve a number of dead animals found in an area, with or without sick animals reported. In

many cases confirmation of the disease is not possible because appropriate samples are not available. Wolves or

coyotes found in poor dehydrated condition with fecal material on their hindquarters may have been affected by canine parvovirus. Carcasses should be isolated from other canids and incinerated or buried deeply.

This article was written by Stephanie Crossley Johnson

Rabbit Hemorrhagic Disease Information Sheet - for Pet Rabbit Guardians

What is Rabbit Hemorrhagic Disease?

Rabbit Hemorrhagic Disease (RHD) is caused by a virus in the calicivirus family. RHD was first reported in B.C. in February 2018 in

the Nanaimo area of Vancouver Island. Follow-up laboratory work identified an RHD virus. Since then, the disease was confirmed

in BC in 2018 and 2019 (limited to the Island and Lower Mainland) in feral European or domestic rabbits. In 2020, a different strain

of RHD began spreading rapidly across the United States and Mexico. In addition to domestic rabbits, this strain can also infect wild

rabbits, such as cottontails. RHD has not yet been reported in BC in 2021, but was recently reported in AB. Pet rabbits are at risk. RHD

is a serious and extremely contagious disease with high mortality rates. Most infected rabbits will die. The disease does not affect

humans or other species including dogs and cats. The virus can persist in the environment for several weeks and may survive both

heat and freezing.

How does RHD virus spread?

RHD virus spreads easily between rabbits through direct contact with bedding,

feed and water as well as feces and body fluids. It can also spread between areas

through contaminated materials (food, bedding, water, surfaces, human clothing/

hands, vehicles), dead rabbits, insects and wildlife (flies, birds, mammals) that have

contacted or fed on infected rabbits.

What are the symptoms of RHD?

The virus causes hemorrhages by affecting the blood vessels and attacks the liver and

other organs. Most affected rabbits die suddenly, but can show signs of listlessness,

lack of co-ordination, behavioural changes, or trouble breathing before death. There

is often bleeding from the nose at the time of death. Once infected, signs of illness

usually occur within 1-9 days.

How can I protect my pet rabbit?

• Minimize exposure to the virus

o Limit human visitors who have been in areas where the disease was reported and avoid your travel to these areas.

o Avoid taking your rabbit to shows/fairs or introducing any new rabbits into your home.

o Ask visitors to remove footwear before entering your home and wash their hands before handling your rabbit.

o Use designated clean clothing (washed and dried in a dryer) that has not been outside when caring for your rabbit.

o Clean and disinfect any rabbit supplies entering your home (see below).

o Use only high-quality commercial feed from manufacturers with good quality control.

o Don’t use wild plants or vegetables or grass grown in areas accessed by feral rabbits or other wildlife, as food.

o Remove or tightly secure anything outside (feed, garbage) that could attract feral rabbits, wildlife, or flies.

o Exercise rabbits outdoors only in secured areas with no possibility of contamination.

o Do not allow cats or dogs who go outside to potentially contaminated areas to access your rabbit’s housing area.

• Monitoring and prevention

o Vaccinate your rabbit. Ask your vet about vaccines available to BC veterinarians on a special government permit.

o Monitor your rabbit daily for signs of illness and contact your veterinarian immediately with any concerns.

How do I clean and disinfect rabbit supplies?

Feeding and housing supplies should be cleaned with soap and water, and then disinfected

with a disinfectant that is effective against caliciviruses following manufacturer instructions.

Most household cleaners are not effective against this type of virus. Disinfectants considered

effective include: bleach (1:10 dilution), potassium peroxymonosulfate (Virkon), accelerated

hydrogen peroxide (Prevail, Accel, and Peroxigard). The latter disinfectants are more userfriendly than bleach and may be obtained from your veterinarian.

Who do I contact with questions?

Contact your local veterinarian with questions about

your rabbit. If you find a dead rabbit or rabbits outside,

do not handle the rabbit(s), and contact your local

animal control. Veterinarians and shelters have access

to additional professional resources and support.

For more information, visit www.spca.bc.ca/rhd.

This article was written by Ivy Martz McDonnel

* Now just to let everyone know that this article is done on a Dog Breed from BC that has gone extinct and for some reason I thought that it would be cool to see if I could find more info on this dog but there is not alot out there but I was able to find enough for the article.*

Salish Wool Dog

The Salish Wool Dog or Comox dog is an extinct breed of white, long-haired, Spitz-type dog that was developed and bred by the Coast Salish peoples of what is now Washington state and British Columbia. The small, long-haired wool dog and the coyote-like village dogs were deliberately maintained as separate populations. The dogs were kept in packs of about 12 to 20 animals, and fed primarily raw and cooked salmon. To keep the breed true to type and the preferred white color, Salish Wool Dogs were confined on islands and in gated caves.

The fur of the Salish Wool Dog was prized for making the famous and rare "Salish" blankets, as the Salish peoples did not have sheep and wild mountain goat wool was difficult to gather. The dogs were sheared like sheep in May or June. The sheared fur was so thick that Captain George Vancouver could pick up a corner and the whole fleece would hold together. Ceremonial blankets were prized items in the precontact potlatch distribution economic system, almost as valuable as slaves. The dog hair was frequently mixed with mountain goat wool, feathers, and plant fibers to change the yarn quality and to extend the supply of fiber.

The National Museum of Natural History received a specimen of the Salish Wool Dog in 1859, which remains in their collection after being rediscovered in 2003.

Osteometry

Skull total length: 162.0 mm (6.38 in)

Condylobasal skull length: 154.6 mm (6.09 in)

Femur GL: 154.3 mm (6.07 in)

Tibia GL: 150.0 mm (5.91 in)

Humerus GL: 143.5 mm (5.65 in)

Radius GL: 136.0 mm (5.35 in)

Ulna GL: 157.5 mm (6.20 in)

Shoulder height of standing dog: 44 cm (17 in)

The Salish Woolly dog was an important part of Coast Salish life throughout southern Vancouver Island, the Strait of Georgia, and Washington State, as the dogs’ hair was used to weave clothing and blankets. Due to the increased presence of European settlers and their machine-spun sheep wool, the Salish Woolly dog population declined in the 1800s until its extinction around 1900.

Description

The Salish Woolly dog was a small, usually white, long-haired dog with prick ears, curled tail, fox-like face, and a thick coat.

When Captain George Vancouver observed the Salish Woolly dog around the Puget Sound in 1792, he thought that it looked like a larger version of a Pomeranian. According to Spanish naval officers Cayetano Valdés y Flores and Dionisio Alacalá Galiano on their visit to the Pacific Northwest in 1792, the dogs did not bark, but instead “simply [had] a miserable howl.”

Today, many scholars have compared the Salish Woolly dog to the contemporary dog breeds of the Japanese Spitz and the American Eskimo.

Evolution

Just over 14,000 years ago, domestic dogs evolved from two separate wolf populations: one in Asia and the other in Europe. Between 14,000 and 6,400 years ago, humans started to bring Asian domestic dogs westward, breeding them with the European domestic dogs.

Salish Woolly dogs are more closely related to early Asian breeds of domestic dogs than European ones. Nineteenth-century naturalist John Keast Lord believed that the dogs originated from a Japanese shipwreck on the Pacific Coast, but had no evidence for this claim. Scholars do know that the Salish Woolly dog was a breed developed before European contact; the oldest remains of the dog were found in Puget Sound and the Strait of Georgia, and date from 4,000 years ago.

Distribution and Habitat

The Salish Woolly dogs lived throughout the Coast Salish territories, including on the southern end of Vancouver Island, the Strait of Juan de Fuca, Puget Sound, the Olympic Peninsula, the Strait of Georgia, and the Lower Fraser River. Often the dogs would live in packs of about 20 to 30. The dogs were fed a diet of fish and elk tallow (rendered fat) to keep their coats strong so their hair could be used for wool. In order to maintain the breed, Coast Salish peoples kept Salish Woolly dogs from other domestic dogs. This meant that the Salish Woolly dogs were often confined to small islands around Vancouver Island and the San Juan Islands. When the dogs lived on isolated islands, they were often left alone during the spring and summer, with their owners returning in the autumn to shear them. For the Twana-speaking peoples of Puget Sound, the Salish Woolly dogs would share plank houses with their owners while the hunting dogs would live outside. Like other domestic dogs, the Salish Woolly dog would most likely have bred about every six months.

Coast Salish Clothing and Blankets

It is believed that the dogs were raised for their hair, which Coast Salish peoples mixed with mountain goat hair to produce clothing and blankets. When the dogs’ coats were long enough, female weavers washed the animals’ hair with a white clay to remove dirt. The weavers then used a sharp stone or knives made of mussel shells to shear the dogs like sheep, cutting the hair close to the skin. The cut hair was then stored with dried clay to extract oil and kill any parasites. The dogs may have produced up to three coats a year.

Although there is both Indigenous oral history and settler written history of dog hair being used for blankets, very few examples of dog hair blankets have been found. Some believe that because dog hair was so common it was likely used for less important blankets. As such, these blankets may have been used more often and therefore deteriorated faster. It is also believed that dog hair was mainly used in textiles woven before 1862, when sheep wool became common in the Coast Salish territories. While some examples of blankets of dog hair mixed with other fibres (e.g. mountain goat) exist, researchers are only aware of one surviving blanket of primarily dog hair. This blanket is housed at the Burke Museum of Natural History and Culture in Seattle, Washington.

Relationship with Humans

Salish Woolly dogs were most likely owned by high-ranking families within Coast Salish communities. Among the Olympic Peninsula Indigenous nations, the dogs were owned by women and inherited through the female line.

The dogs were highly valued in Coast Salish societies since blankets made of their fur were considered a basic source of wealth during potlatches. Salish Woolly dogs were often buried wrapped in a blanket to honour them.

Extinction

The Salish Woolly dog’s population declined throughout the 1800s. The increased presence of Europeans meant the settlers’ dogs bred with the Salish Woolly dogs, decimating the latter’s population. In addition, Indigenous populations also declined due to land displacement and disease caused by settler colonization. Finally, by the 1820s, fur-trading posts had introduced inexpensive, machine-made blankets from England. These European blankets meant there was no need to keep the dogs for their hair, especially since feeding a herd of dogs required salmon that could otherwise be used to feed people. By 1900, the long, woolly fur characteristics of the Salish Woolly dog had disappeared, though there were a number of rare sightings of woolly dogs on reservations up to 1940.

There is currently not much physical evidence left of the Salish Woolly dog. Artist Paul Kane painted “A Woman Weaving a Blanket” between 1849 to 1856, which depicts either a Songhees or Saanich weaver and a prominent woolly white dog. The painting and other sketches of the dog by Kane can be found at the Royal Ontario Museum. In 1859, naturalist C.B.R. Kennerly collected the pelt of the American ethnologist George Gibbs’ “famous Indian dog, Mutton” for the Smithsonian Institution’s National Museum of Natural History. This pelt is thought to be the only remaining Salish Woolly dog specimen.

This article was written by Kami Martz McDonnel

* Now like the article that Ivy did this puppy is now extinct. I was able to find some good info in it so I am gonna let you all read that now. *

Tahltan Bear Dog

The Tahltan (pronounced tall-tan) bear dog was a domesticated dog indigenous to North America. Now extinct, it was one of five uniquely Canadian dog breeds. Although the name of the breed suggests it was only kept by the Tahltan Nation of Northwestern British Columbia, the dog was common among other First Nations in the region, too. These included the Tlingit, Tagish, Kaska and Sekani. The Tahltan people referred to it as “our dog,” which gave the breed its name. Indigenous peoples used the Tahltan bear dog in sustenance hunting— primarily for bear— an activity in which it excelled.

Appearance

The Tahltan bear dog was small, measuring 30 to 40.5 cm and weighing 4.5 to 8 kg — about the size of a fox terrier. The breed was typically black and white, with pricked-up ears, a sharp nose and a short, upright tail resembling a shaving brush. Its mid-length coat was dense, with a longer ruff around the neck.

Origins and Breeding History

According to Tahltan oral history, the bear dog was present among the Tahltan people since time immemorial. Legends describe how it was created by magic to protect Indigenous peoples living in what now is Northwestern British Columbia.

Explorer Samuel Black documented the Tahltan bear dog in 1824 — the first written records of the breed. In the early 1900s, ethnographer James Teit also documented the dog, during his studies of Tahltan culture.

The Canadian Kennel Club (CKC) recognized the Tahltan bear dog as a distinct breed in 1941. The efforts made by BC police officer J.B. Grey, posted to Telegraph Creek in the late 1930s, greatly contributed to this recognition.

The Tahltan bear dog was widely traded, resulting in a number of crossbred dogs. In addition, white people arriving on Tahltan territory introduced a variety of dogs to the area, and the breed became increasingly mixed. In 1969, the Tahltan bear dog was still present in slim numbers in Telegraph Creek, Iskut and Atlin in BC, and in Carcross, Whitehorse and Keno in Yukon.

Various factors led to the demise of the dog, including modern firearms, illnesses and people neglecting to breed it. The last registration of a Tahltan bear dog with the CKC was in 1953. While no official date exists, the breed went extinct sometime in the 1970s or 80s.

Temperament and Traits

Tahltan bear dog owners valued the breed’s bravery, agility, intelligence and tenacity. The dogs were often bred for specific abilities, including hunting certain prey.

Although fearless, the Tahltan dog didn’t do well when removed from its northern habitat. According to testimonies from members of the Tahltan Nation, the dogs died or became ill once away from their native land. The reasons for this remain unclear, but may have included the change in diet and climate, and exposure to new diseases.

Hunting

The Indigenous peoples of Northwestern British Columbia used the Tahltan bear dog for sustenance hunting. Although small, they were feisty and excelled in hunting big game. As their name suggests, they were primarily known for hunting bears. However, they also hunted other animals, including moose, rabbit, porcupine, lynx, grouse and ptarmigan. The Tahltan dog barked relentlessly during hunting to signal where the prey was located. Its bark had different pitches for different kinds of animals.

Hunters often carried the dogs on their backs in a sack before releasing them, to preserve their energy. Two or three dogs were used in bear hunting, which took place in winter or spring. At this time of year, because of their small size, Tahltan dogs could run on top of the hard snow while the bears sunk and struggled. One dog ran ahead of the bear while the other harassed it from behind, trapping the bear until the hunter arrived.

Role in Local Indigenous Economy

Tahltan bear dogs were highly valued by Indigenous peoples of Northwestern British Columbia and Southern Yukon. Ethnographer James Teit states that they were “as indispensable to the Tahltan as snowshoes.” When interviewed by researcher Leslie Kopas, Tahltan elder John Carlick put it this way: “If you had a bear dog you could find game. If you didn’t have a bear dog, you starved.” Unlike other working dogs, owners revered the Tahltan dogs, making shelters for them and even welcoming them into their tents.

The Tahltan dog’s bravery is celebrated in the region’s mythology. Local stories tell of the dog’s role in sustenance hunting, and portray the close-knit relationships between humans and dogs.

Factors Leading to Extinction

When traders introduced firearms to Northwestern British Columbia, the role of the Tahltan bear dog in the livelihood of the region’s Indigenous peoples greatly diminished. Hunters were able to shoot big game without the assistance of dogs. Sled dogs became more important than bear dogs in hunting activities. Sled dogs also killed bear dogs when they caught them.

In addition to firearms, other factors contributed to the eventual extinction of the Tahltan bear dog. A number of them died in the late 1940s during a distemper outbreak. In 1942, an epidemic of flu and measles in Telegraph Creek killed many elders who owned bear dogs. Following the epidemic, many Tahltan dogs were shot because they were running loose. The arrival of the snowmobile also contributed to the demise of the bear dog. Last but not least, the small number of Tahltan bear dogs still present in the late 1960s stopped being bred.