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I created this blog as an instrument of what I have encountered in the world of veterinary medicine as a proud vet student. Comments and suggestions are welcome here at;


Aina Meducci 2012


The following blog posts is not genuinely from my research but through readings and citation from trusted website. I do not own any of the copyright and therefore you may use it at your own risk


Happy reading!
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Why red blood cell has no nucleus?

I came across this terminologies while reading;

" Why red blood cell has no nucleus? "

Here's the answer:

While in the bone marrow, the developing red blood cells are nuclear. They include in order of maturity, the prorubricyte, rubricyte and metarubricyte (being the most matured). Just before being released from the bone marrow, the metarubicyte discard their nuclei.Therefore rbc in most domestic animal (except birds) are anuclear, biconcave, discoid cells.

Hence, with no nucleus, the number oxygen's molecule that can bind to the haemoglobin can be increased up to 4 molecules for each red blood cells.

Erythrocyte maturation diagram

Sources: Veterinary Medical Terminologies 2nd edition, Saunders Elsevier

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Infectious Canine Hepatitis

I remember during my 2nd year where we had virology oral exam with Dr J. So before waiting our names to be called in, we were scampering for notes and memorized the all the virus and the diseases associated with it like nobody business. Until my name was called, I went and sat in front of the examiner. I was doing quite well for the rest of the exam until he came out with the final question;

"Name the virus that causes infectious canine hepatitis?"

Opps...I blown the day :(

At the end of the semester, virology is my favorite subject


Canine infectious hepatitis

Infectious canine hepatitis an acute highly contagious viral disease of dogs which affect the liver and other organs and is characterized by high rise of temperature, diarrhoea, vomiting and convulsion. Dogs of all ages, specially puppies and foxes is affected by this disease. A carrier dog may recover, but continue to spread the virus via its urine for up to six months.Severely affected dogs will have a fever, loss of appetite, depression, diarrhoea, tonsillitis and acute abdominal pain due to an inflamed liver. Death may result within 36 hours. Corneal opacity known as "blue eye" may follow infection.

Abdominal pain in a dog with ICH

Aetilogy and transmission

ICH is caused by a nonenveloped DNA virus, canine adenovirus 1 (CAV-1), which is antigenically related only to CAV-2 (one of the causes of infectious canine tracheobronchitis). CAV-1 is resistant to lipid solvents and survives outside the host for weeks or months, but a 1-3% solution of sodium hypochlorite (household bleach) is an effective disinfectant.

Ingestion of urine, feces, or saliva of infected dogs is the main route of infection. Recovered dogs shed virus in their urine for ≥6 mo. Initial infection occurs in the tonsillar crypts and Peyer’s patches, followed by viremia and infection of endothelial cells in many tissues. Liver, kidneys, spleen, and lungs are the main target organs. Chronic kidney lesions and corneal clouding (“blue eye”) result from immune-complex reactions after recovery from acute or subclinical disease.

Even a dog dish that has been licked clean can carry the virus. The tonsils and lymph nodes are the first body parts effected. The incubation period can last 4-9 days, after which the virus enters the bloodstream.

dog eye diseases photo

Blue eye dog infectious hepatitis


The virus can remain in the kidneys of dogs that have recovered from infection for up to one year, making it all the more difficult to determine what locations might be contaminated. The particles enter the body through the nose or mouth and initially infect the tonsils. Here the virus replicates and proceeds to invade the nearby lymph nodes.This process of replication continues for 4 to 8 days, at which point the virus spreads from the lymphatic system and enters the bloodstream.

Once in the blood, CAV-1 particles infect a varieyt of other target organs – the liver, kidneys, and eyes. The viral particles themselves are cytotoxic which is why they are capable of doing so much damage. The liver is almost always the most severely affected organ, with consequences including disturbance of protein and fat manufacture, problems with bile secretion, and difficulty detoxifying drugs, chemicals, and bacteria from food. ICH is generally not fatal, but when it is, death is usually a result of massive hemorrhage, fluid leakage from a severely damaged liver, and central nervous system trauma which triggers seizure and coma.


Clinical signs

Signs vary from a slight fever to death. The mortality rate is highest in very young dog. The first sign is a fever of >104°F (40°C), which lasts 1-6 days and is usually biphasic (fever associated with 2 different sets of symptoms as it progress) . If the fever is of short duration, leukopenia may be the only other sign, but if it persists for >1 day, acute illness develops. Tachycardia out of proportion to the fever may occur.

On the day after the initial temperature rise, leukopenia develops and persists throughout the febrile period. The degree of leukopenia varies and seems to be correlated with the severity of illness. Signs are anorexia, thirst, conjunctivitis, serous discharge from the eyes and nose, and occasionally abdominal pain and vomiting. Intense hyperemia or petechiae of the oral mucosa, as well as enlarged tonsils, may be seen. There may be subcutaneous edema of the head, neck, and trunk.

Clotting time is directly correlated with the severity of illness. It may be difficult to control hemorrhage, which is manifest by bleeding around deciduous teeth and by spontaneous hematomas, because of underlying disseminated intravascular coagulation. Although CNS involvement is unusual, severely infected dogs may develop convulsions from forebrain damage; brain stem hemorrhages, resulting in paresis, are common.

The fatal form of the disease results in a sudden onset of severe symptoms. Bleeding from the nose and gums, enlarged abdomen due to fluid leaking from the liver, bloody diarrhea and vomit, seizures due to central nervous system association, disorientation, coma, and death may occur. Pets may die suddenly without any obvious illness. Infectious Canine Hepatitis is most severe and the mortality rate is highest in young dogs. Veterinary attention will need to be sought ASAP.


Endothelial damage results in “paint brush” hemorrhages on the gastric serosa, lymph nodes, thymus, pancreas, and subcutaneous tissues. Hepatic cell necrosis produces a variegated color change in the liver, which may be normal in size or swollen. The gallbladder wall may be edematous and thickened; edema of the thymus may be found. Grayish white foci may be seen in the kidney cortex.


Urinalysis and blood tests may be performed in an attempt to detect viral antibodies. Similarly, viral antibodies can be detected using immunofluorescent techniques. In addition, the ELISA test may be used to look for the presence of viral particles in the feces of a sick animal.

Treatment and management

There is no specific treatment for infectious canine hepatitis so treatment is aimed at managing the symptoms until the virus runs its course. Depending on the severity of illness, hospitalization and intravenous fluid therapy may be necessary. Antibiotics don't treat the virus but may be prescribed to ward off secondary bacterial infections. In severe cases, blood transfusions may be necessary

Management for ICH;

(a) Broad spectrum antibiotic -To prevent secondary bacterial infection
(b) Anti emetic - To stop vomiting
(c) Anti diarrhoea- To stop diarrhoea
(d) Anti serum may be tried
(e) Blood transfusion in case of severely infected dog. Dose is 5-8ml/lb of body weight by slow
intra venous infusion
(f) Fluid theraphy - NSS or DNS to restore fluid and electrolyte loss
(g) Anti pyretic – In case of high rise of temperature
(h)Vitamins therapy and protein hydrolysate- To restore vitality
(i) Care nursing of infected dogs


  • Vaccination is the most recommended method of preventing Infectious Canine Hepatitis. While it seems logical to vaccinate using the CAV-1 virus, this can usually cause unwanted side effects such as the bluing of the eye and the shedding of virus. Vaccination with a very closely related virus, CAV-2, is much safer, and will help the dog build immunity against CAV-1. CAV-2 is also thought to play a part in a common condition called kennel cough, so vaccinating with CAV-2 would result in immunity to both conditions.

It is important that all puppies commence a vaccination program from 6-8 weeks of age and that all adult dogs have their boosters.

  • Unvaccinated dog should be kept away from public places, dogs outside household, or dirty food bowls that are left outside or belonging to dogs outside household. Keep an eye on the dog during walks to ensure he does not consume urine or feces.
  • Disinfection of contaminated areas with a bleach or iodine solution can kill the virus

Sources: Merks Veterinary Manual, animalhealthcareveterinary.blogspot, ICF; Cornell university college of veterinary medicine, ICF; petsmd.com, Dog eye diseases; dog-health-handbook.com .

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I attended a veterinary seminar last week. Very interesting one. They had a talk on anthrax threat in Malaysia and how the department received the case and processed it. It turned out to be a negative result. I always love microbiology. So this one got my huge attention :)


A zebra with suspected anthracis (note at those bleeding)


Anthrax (also known as Splenic fever, Siberian Ulcer, Charbon, Milzbrand) is a life-threatening infectious disease that normally affects animals, especially ruminants (such as goats, cattle, sheep, and horses). Anthrax can be transmitted to humans by contact with infected animals or their products. In recent years, anthrax has received a great deal of attention as it has become clear that the infection can also be spread by a bioterrorist attack or by biological warfare. Anthrax does not spread from person to person so it is considered to be noncontagious. It is still a large threat, however, because if it isn't recognized and treated quickly enough it can be deadly.

Anthrax is an acute infectious disease that can strike almost all warm-blooded animals, including humans, and affects a variety of tissues including the skin, intestine, kidney, meninges, conjunctiva and lymphatic system.


Bacillus anthracis, the anthrax agent, is a simple rod-shaped bacterium that usually infects domestic animals. Its durable spores lie dormant in soil until consumed by a grazing animal. Once ingested, the bacterium reproduces, often killing the host animal, and then returns to the soil, where it remains dormant again in spore form.

Bacillus anthracis, gram positive slim and long rod-shaped bacteria (spore forming)

Anthrax is found all over the world. It contaminates the ground when an affected animal dies. It spreads when grazing animals pick it up from contaminated dirt or through contaminated food sources such as bone meal that may have been made from contaminated carcasses. There appears to be an increase in the cases of anthrax among grazing animals during droughts, when they tend to graze closer to the ground and consume more dirt with the grass.

Anthrax may also spread when carnivorous animals, such as vultures or even insects, feed on affected herbivores. The bacteria are then transferred to other areas by the host and contaminate the ground when that animal dies. As the animal decays, the bacteria are exposed to oxygen and turn back into the spores that contaminate the soil. The anthrax spores have a very tough outer casing and can remain viable in the ground for decades.

The anthrax cycle

Outbreaks of anthrax tend to occur in association with particular climatic and weather events, such as heavy rainfall, flooding and drought. In anthrax-prone areas, the close grazing of animals on fresh shoots of grass after rainfall often leads to outbreaks of the disease due to the ingestion of organisms picked from contaminated soils.

Incubation of anthrax

The incubation period (the period between contact with anthrax and the start of symptoms) may be relatively short, from one to five days. Like other infectious diseases, the incubation period for anthrax is quite variable and it may be weeks before an infected individual feels sick.

Forms of anthrax (in human and animal)


The cutaneous (skin) form of anthrax starts as a red-brown raised spot that enlarges with considerable redness around it, blistering, and hardening. The center of the spot then shows an ulcer crater with blood-tinged drainage and the formation of a black crust called an eschar. There are swollen glands (lymph nodes) in the area. Symptoms include muscle aches and pain, headache, fever, nausea, and vomiting. The illness usually resolves in about six weeks, but deaths may occur if patients do not receive appropriate antibiotics.

This type of anthrax may also be spread by biting insects that have fed on infected hosts. The head, arms and hands are most often affected.

Skin lesion in human


The pulmonary form of anthrax, due to inhalation of spores, is the most dangerous manifestation of the disease. Pneumonia-like symptoms develop, and the organisms may invade the bloodstream and even the brain. The fatality rate is greater than 90%. Under usual circumstances, pulmonary anthrax is rare, found mainly among people who work with wool or fleeces. Viable, vegetative forms of Bacillus anthracis, although microscopic, are too large to readily enter the alveoli (air sacs) of the human lung. However, the spores are much smaller, and can gain entry to the alveoli, germinate, produce toxic substances, and cause disease.

This characteristic of Bacillus anthracis spores, plus the high resistance to environmental stress, makes these bacteria ideal agents for biological warfare. Large-scale production and dispersal of Bacillus anthracis spores has the potential for causing high mortality in a target population. On the positive side, however, is the fact that dispersal of spores can be difficult, and it takes about 10,000 spores to initiate an infection. This latter fact may contribute to the fact that anthrax is not considered to be communicable.

Inhalation form


Ingestion of Bacillus anthracis, or its spores, can result in intestinal anthrax; the form most commonly seen in animals. The clinical signs are pain, vomiting, and bloody diarrhea. This form of the disease has a 25% to 50% fatality rate. Eating undercooked meat that is infected with the anthrax bacteria, or drinking unchlorinated water that harbors the spores, can introduce the bacteria into the gastrointestinal tract. Infection can occur in either the upper or lower GI tract. This form of anthrax is rare.

GI form

How anthrax attacks?

How Anthrax Attacks: As anthrax bacteria burst out of a macrophage, released PA first attaches to the infected cell’s surface, forming a channel through which EF and LF enter the cell. Once inside, the low pH of a lysosome frees the LF, allowing it to spread its toxic effects throughout the cell’s interior.

Taken from Yale University

The virulence of B. anthracis lies not in the bacterium itself but rather in the toxins it produces. The three major toxins released by B. anthracis are proteins known as Protective Antigen (PA), Edema Factor (EF), and Lethal Factor (LF), which work together to kill blood cells. As part of a normal immune response, a macrophage first engulfs a spore, which quickly germinates. As active bacteria burst out of the macrophage, they release PA. PA attaches to the surface of a T-cell, interacting with the cell membrane to form vesicles that can transport EF and LF into the cytoplasm. Once inside, the cyclase EF overwhelms the cell by producing massive amounts of signaling protein cAMP. The protease LF, on the other hand, destroys the MAP kinases’ signaling proteins, thereby disrupting cell cycle regulation and killing the cell. Without T-cells, the body cannot effectively combat the intruders and falls severely ill.

Clinical findings in animals

Typically, the incubation period is 3-7 days (range 1-14 days). The clinical course ranges from peracute to chronic. The peracute form (common in cattle and sheep) is characterized by sudden onset and a rapidly fatal course. Staggering, dyspnea, trembling, collapse, a few convulsive movements, and death may occur in cattle, sheep, or goats with only a brief evidence of illness.

In acute anthrax of cattle and sheep there is an abrupt fever and a period of excitement followed by depression, stupor, respiratory or cardiac distress, staggering, convulsions, and death. Often, the course of disease is so rapid that illness is not observed and animals are found dead. The body temperature may reach 107F (41.5C), rumination ceases, milk production is materially reduced, and pregnant animals may abort. There may be bloody discharges from the natural body openings. Some (chronic?) infections are characterized by localized, subcutaneous, edematous swelling that can be quite extensive. Areas most frequently involved are the ventral neck, thorax, and shoulders.

The disease in horses may be acute. Signs may include fever, chills, severe colic, anorexia, depression, weakness, bloody diarrhea, and swellings of the neck, sternum, lower abdomen, and external genitalia. Death usually occurs within 2-3 days of onset.

Although relatively resistant, pigs may develop an acute septicemia following ingestion of B anthracis , characterized by sudden death, oropharyngitis, or more usually a mild chronic form. Oropharyngeal anthrax is characterized by rapidly progressive swelling of the throat, which may cause death by suffocation. In the chronic form, pigs show systemic signs of illness and gradually recover with treatment. Some later show evidence of anthrax infection in the cervical lymph nodes and tonsils when slaughtered (as apparently healthy animals). Intestinal involvement is seldom recognized and has nonspecific clinical characteristics of anorexia, vomiting, diarrhea (sometimes bloody), or constipation.


Rigor mortis is frequently absent or incomplete. Dark blood may ooze from the mouth, nostrils, and anus with marked bloating and rapid body decomposition. If the carcass is inadvertently opened, septicemic lesions are seen. The blood is dark and thickened and fails to clot readily. Hemorrhages of various sizes are common on the serosal surfaces of the abdomen and thorax as well as on the epicardium and endocardium. Edematous, red-tinged effusions commonly are present under the serosa of various organs, between skeletal muscle groups, and in the subcutis.

Hemorrhages frequently occur along the GI tract mucosa, and ulcers, particularly over Peyers patches, may be present. An enlarged, dark red or black, soft, semifluid spleen is common. The liver, kidneys, and lymph nodes usually are congested and enlarged. Meningitis may be found if the skull is opened.

In pigs with chronic anthrax, the lesions usually are restricted to the tonsils, cervical lymph nodes, and surrounding tissues. The lymphatic tissues of the area are enlarged and are a mottled salmon to brick-red color on cut surface. Diphtheritic membranes or ulcers may be present over the surface of the tonsils. The area around involved lymphatic tissues generally is gelatinous and edematous. A chronic intestinal form involving the mesenteric lymph nodes is also recognized.


Specific diagnostic tests include bacterial culture, PCR tests, and fluorescent antibody stains to demonstrate the agent in blood films or tissues. Western blot and ELISA tests for antibody detection are available in some reference laboratories. Lacking other tests, fixed blood smears stained with Loefflers or MacFadean stains can be used and the capsule visualized; however, it can result in some 20% false positives.

Differential diagnosis

Peracute blackquarter (clostridium chauvoi) and septicaemic form of other diseases. In splenic enlargement as seen in babesiosis, anaplasmosis and leucosis, spleen consistency is firm. In anthrax, the spleen is soft and upon incision the pulp exudes like thick blackish-red blood.

Treatment in animal

Early treatment and vigorous implementation of a preventive program are essential to reducing losses among livestock. Livestock at risk should be immediately treated with a long-acting antibiotic to stop all potential incubating infections. Domestic livestock respond well to penicillin if treated in the early stages of the disease. Oxytetracycline given daily in divided doses also is effective. Other antibacterials, including amoxicillin, chloramphenicol, ciprofloxacin, doxycycline, erythromycin, gentamicin, streptomycin, and sulfonamides also can be used, but their effectiveness in comparison with penicillin and the tetracyclines has not been evaluated under field conditions.

Control in animal

Anthrax is controlled through vaccination programs, rapid detection and reporting, quarantine, treatment of asymptomatic animals (postexposure prophylaxis), and burning or burial of suspect and confirmed cases. In livestock, anthrax can be controlled largely by annual vaccination of all grazing animals in the endemic area and by implementation of control measures during epizootics. The nonencapsulated Sterne-strain vaccine is used almost universally for livestock immunization. Vaccination should be done 2-4 wk before the season when outbreaks may be expected. Because this is a live vaccine, antibiotics should not be administered within 1 wk of vaccination. Before vaccination of dairy cattle during an outbreak, all of the procedures required by local laws should be reviewed and followed.

In addition to therapy and immunization, specific control procedures are necessary to contain the disease and prevent its spread. These include the following:

1) notification of the appropriate regulatory officials
2) rigid enforcement of quarantine (after vaccination, 2 wk before movement off the farm, 6 wk if going to slaughter)
3) prompt disposal of dead animals, manure, bedding, or other contaminated material by cremation (preferable) or deep burial
4) isolation of sick animals and removal of well animals from the contaminated areas
5) cleaning and disinfection of stables, pens, milking barns, and equipment used on livestock
6) use of insect repellents
7) control of scavengers that feed on animals dead from the disease; and
8) observation of general sanitary procedures by people who handle diseased animals, both for their own safety and to prevent spread of the disease.

Contaminated soils are very difficult to completely decontaminate, but formaldehyde will be successful if the level is not excessive. The process generally requires removal of soil.

Sources: How Anthrax works; Lee Ann Obringer, Hijacking nature's agents; Andrew Chang Yale Scientific, Anthrax; VETNEXT, Anthrax in human; www.medicine.net.com. Anthrax in animals; ww.foa.org

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Von Willebrand's disease (vWD) bleeding disorder

I found this in someone external hard disk haha


A bleeding dog (unknown source)

What is Von Willebrands's disease (vWD)?

Von Willebrand's is an inherited bleeding disorder. In fact, it is the most common inherited bleeding disorder among dogs. The formation of a blood clot is a very complex and involved mechanism. A clot is formed by a cascade of reactions happening in a certain order. For a clot to form, all the factors involved in the cascade must be present and in working order. In Von Willebrand's the factor known as von Willebrand's Factor (vWF) either is not present or is defective. The condition is similar to hemophilia in humans.

What is von Willebrand's factor?

Von Willebrand's factor is a protein complex produced both by platelets (the blood cells involved in clotting) and by the cells lining blood vessels. It is made up of several smaller proteins bound together and von Willebrand's disease results when there is a defect in any one of these proteins. When a blood vessel tears and bleeding occurs, platelets are called to the area to clump upon each other, thus plugging up the hole and staunching the bleeding. While the platelets are in place, a cascade of blood clotting factors activates ultimately leading to production of fibrin, the material scars are made of, to more permanently seal the vessel. Von Willebrand's factor acts as glue holding the platelets together and holds them onto the surface of the torn blood vessel. Von Willebrand's factor also serves to stabilize clotting factor VIII, one of the proteins involved in forming the fibrin clot.When there is something wrong with one's von Willebrand's factor, platelets to do not stick together properly and inappropriate prolonged wound bleeding occurs.

Arrow shows platelets

Why it is called Willebrand's?

Von Willebrand's was discovered in humans and called a "disease" in the 1920s by a Finnish doctor coincidentally named, von Willebrand. Von Willebrand's seldom happens in cats but it is very common in various breeds of dogs.

Causes of Von Willebrand's Disease

Von Willebrand's disease is inherited. This means that it is passed down from parents to offspring.

Breed of dogs predispose to vWD

Certain breeds have a higher incidence of vWD than others. German Shepherds, Doberman Pinschers, Shetland Sheepdogs, Chesapeake Bay Retrievers, German Shorthaired Pointers, Golden Retrievers, Standard Poodles, and Scottish Terriers all have a higher than normal incidence, showing that it can be inherited. In all, some sixty different purebred breeds have been commonly linked to von Willebrand's with the Doberman Pinscher having the highest incidence.

Doberman Pinscher

Types of vWD

There are three types of von Willebrand's disease.


In Type I, all the proteins making up von Willebrand's factor are present but only in very small amounts. This is the type common in the Doberman Pinscher, the Shetland Sheepdog, the German Shepherd Dog, and the Standard Poodle.

It is thought to be an autosomal trait with incomplete dominance. This means offspring may inherit the disorder if either parent carries the gene, but not all offspring will be affected to the same extent. Dogs with type I disease have reduced but measurable levels of Von Willebrand factor (1 to 60 per cent). Animals that inherit the gene for type I vWD from both parents (homozygotes) die before birth or shortly thereafter.

**Although Dobermans are the most commonly affected by von Willebrand's Disease, they usually have the milder forms (type 1)

Shetland sheepdog


In Type II, the larger proteins making up von Willebrand's factor are completely absent, leaving only the smaller proteins to do the job. This creates more severe bleeding episodes and represents the type of von Willebrand's disease usually seen in German Short-Haired and Wire-Haired Pointers.

Type II vWD is very rare. It is an autosomal recessive trait.

Wire-haired pointers

German Short-haired


In Type III, there is simply no von Willebrand's factor at all. This is the most severe form and is usually seen in Scottish Terriers, Chesapeake Bay Retrievers, and Shetland Sheepdogs. Von Willebrand's disease is not limited to the breeds listed here; forms of von Willebrand's disease have been found in over 50 breeds and in cats and humans as well.

Chesapeake Bay Retrievers

Scottish Terrier

Type III vWD is relatively rare. This form is autosomal recessive. Animals are only affected if they inherit the abnormal gene from both parents, who are clinically unaffected carriers. Affected dogs have zero levels of vWF, while carrier parents have 15 to 60 per cent of normal levels.

Clinical signs

In dogs, the most common clinical signs are spontaneous bleeding from the gums or nose, blood in the urine or gastrointestinal tract, or excessive bleeding at the time of surgery. Clinical signs also include epistaxis (nose bleed), prolonged estrus or postpartum bleeding, hematuria, melena, excessive bleeding after toe-nail cutting and sometimes hemorrhaging into body cavities and organs.

As with most diseases symptoms can range from mild, with bleeding times only being extended slightly, to severe, where bleeding cannot be stopped.

Epistaxis (nose bleed) in a dog


To diagnose von Willebrand's Disease a veterinarian will often conduct a CBC (complete blood count), urinalysis, blood clotting time or a "buccal mucosal" screening time. The buccal mucosal bleeding time uses a test strip that is tied around the maxilla (upper jaw) that then causes engorgement in the folded-back area. Normal blood clotting time is somewhere between 1.5 to 2.6 minutes.

Blood clotting time procedure:

The dog is positioned in sternal or lateral recumbency. The upper lip is everted and secured using a strip of gauze wrapped snugly around the muzzle. The template device (Surgicutt)is placed on the buccal mucosa and triggered as the timer or stopwatch is started. Simplate incisions are made parallel and Surgicutt incision is made perpendicular to the lip margin.

Blood flow from the incision(s) is blotted using filter paper held directly below, but not touching the wounds. The time from triggering the device until blood no longer appears on the paper is recorded as the bleeding time. The muzzle gauze is removed and pressure applied to the wounds until active bleeding ceases. If needed, topical tissue adhesive (cyanoacrylate) can be applied to prevent rebleeding.

Normal Range: Two to four minutes.

Interpretation: Lip bleeding time is expected to be prolonged in patients with severe acquired or inherited platelet dysfunction or severe von Willebrand disease. There is a variable response in dogs with DIC or mild forms of vWD. Dogs with even severe coagulation factor deficiencies usually have normal lip bleeding time.

"Mucosal bleeding time is the best screening test for a potential defect in platelet function, and is prolonged in dogs with a deficiency in vWF. However the test is non-specific for vWD because it is also prolonged in dogs with thrombocytopenia or functional platelet defects. (Bleeding times are normal in animals with warfarin toxicity, hemophilia A or B, or a deficiency of Factor VII.)"


There is no cure for Von Willebrand's disease. If a dog is found to have this condition owners should take special precaution to make sure the dog does not injure themselves.

Avoid drugs that are known to inhibit platelet functions. Aspirin is a prime example of one of these drugs. Others include antihistamines, sulfa- or penicillin based antibiotics, Ibuprofen, the tranquilizer phenothiazine, heparin and theophylline.

Veterinarians have found that thyroid supplementation can lower the tendency in some dogs to bleed while raising the level of vWF concentration.There is also a drug called desmopressin acetate DDAVP that can also increase the vWF protein concentration although the response to the drug is variable. It has been shown to raise the concentration in dogs that do not have von Willebrand's disease. The use in these dogs may not be apparent until it is realized it takes a dog to donate blood for a transfusion to another dog.

In case of an emergency or severe trauma, this donated blood is often the only thing that can save the dog's life.

For owners of breeds that are more prone to having von Willebrand's disease, there is a specialized test that can determine the exact amount of the von Willebrand protein that is present in the blood. If the test comes back positive for the disease, it won't necessary help the dog on a daily basis but will come in handy to know if the dog ever requires emergency treatment or undergoes any type of surgery.

Sources: Animal health diagnosis center; Cornell University College of Vet Medicine, vWD Canine Health Foundation, Canine vWD www.essortment.com, Canine vWD www.therealjackrussell.com, vWD, Wendy C. Brooks, DVM, dipAPVB, vWD www.upei.ca

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