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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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Toy breed dogs

I am not good in recognizing breeds of dog. I'm not a dog person so only few breeds I can remember. I've tried so hard to remember many breeds of dog and managed to install dogs breed in my tablet and force myself to memorize at least 1 breed per night. Alhamdulillah, making a good progress on it :)


Toy breeds (small breed of dog for petting purposes)


Biewer terrier

Brussels griffon

Cavalier King Charles Spaniel


China crested

English toy spaniel

Havana silk dog


Italian grehound

Japanese Chin


Miniature pinscher




Poodle toy


Shih tzu

Silky terrier

Toy fox terrier

Yorkshire Terrier

Now how you would tell to differentiate them?

Sources: Toy group dog petwave.com

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Foot and Mouth disease (FMD)

I attended a clinical case few days ago. It was supposed to be our avian round but we received an emergency call from a vet whom asked our lecturer to look on the case at the quarantine center Rantau Panjang.

I was thrilled to find out that it was about FMD! So far I have never seen FMD case alive and today was our gold pot.


On the farm..

**Malaysia is one of the FMD countries

Foot-and-mouth disease (FMD) is a severe, highly communicable and economically devastating viral disease of cattle and swine. It also affects sheep, goats, deer, and other clovenhoof ruminants. Many affected animals recover, but the disease leaves them debilitated. FMD causes severe losses in the production of meat and milk. The disease does not effect food safety or humans. Other susceptible species include hedgehogs, nutria, rats, armadillos, elephants, capybaras, and mice. FMD is not recognized as a zoonotic disease.

The disease is characterized by fever and blisterlike lesions followed by erosions on the tongue and lips, in the mouth, on the teats, and between the hooves. Because it spreads widely and rapidly and because it has grave economic as well as clinical consequences, FMD is one of the animal diseases that livestock owner dread most.

Cattle is the most susceptible to FMD


The FMD disease is caused by a virus. The FMD virus (FMDv) is a member of the genus Apthovirus in the family Picornaviridae. The virion is a small (23-nm) single-stranded RNA virus. The virus survives in lymph nodes and bone marrow at neutral pH, but destroyed in muscle when in pH<6.0 i.e. after rigor mortis. The virus can persist in contaminated fodder and the environment for up to one month, depending on the temperature and pH conditions. There are seven serotypes of FMD virus, O, A, C, Asia 1, SAT 1, SAT 2 and SAT 3, distributed throughout the world and many subtypes of the FMD virus. Immunity to one type does not protect an animal against other types.

Serotype O is the most widely distributed, being endemic in many South American, African and Asian countries, affecting all susceptible species. Certain strains of serotype O appear particularly adapted to a particular host species. Within serotype O there are groups of strains (genotypes) that are associated with particular areas of distribution, and species preference.

FMDV can infect most or all members of the order Artiodactyla (cloven-hooved mammals), as well as a few species in other orders. Each species varies in its susceptibility to infection and clinical disease, as well as its ability to transmit the virus to other animals. Livestock susceptible to FMD include cattle, pigs, sheep, goats, water buffalo and reindeer. Lllamas, alpacas and camels can be infected experimentally, but do not appear to be very susceptible. FMDV can also infect at least 70 species of wild animals including African buffalo (Syncerus caffer), bison (Bison spp.), elk, moose, chamois, giraffes, wildebeest, blackbuck, warthogs, kudu, impala, and several species of deer, antelopes and gazelles. Susceptible non clovenhooved species include hedgehogs, armadillos, kangaroos, nutrias, capybaras, guinea pigs, rats and mice. Infections have been reported in African and Asian elephants in zoos; however, African elephants are not considered susceptible to FMD under natural conditions in southern Africa.

On most continents, cattle are usually the most important maintenance hosts for FMDV, but some virus strains are primarily found in pigs, sheep or goats. Cattle and African buffalo are the usual maintenance hosts for FMDV in Africa; African buffalo are currently thought to carry only the SAT serotype. With this exception, wildlife hosts do not seem to be able to maintain FMD viruses, and are usually infected by contact with domesticated livestock. Early reports suggested that transmission also occurred between cattle and European hedgehogs, but there is no evidence that this species has helped to propagate FMDV in the last 40 years.


FMD viruses can be spread by animals, people, or materials that bring the virus into physical contact with susceptible animals. An outbreak can occur when:
  • Animals carrying the virus are introduced into susceptible herds.
  • Contaminated facilities are used to hold susceptible animals.
  • Contaminated vehicles are used to move susceptible animals.
  • Raw or improperly cooked garbage containing infected meat or animal products is fed to susceptible animals.
  • People wearing contaminated clothes or footwear,or using contaminated equipment, pass the virus to susceptible animals.
  • Susceptible animals are exposed to materials such as hay, feedstuffs, hides, or biologics contaminated with the virus.
  • Susceptible animals drink common source contaminated water.
  • A susceptible animal is inseminated by semen from an infected animal

Clinical signs

Vesicles (blisters) followed by erosions in the mouth or on the feet and the resulting excessive salivation or lameness are the best known signs of the disease. Often blisters may not be observed because they easily rupture, leading to erosions. These signs may appear in affected animals during an FMD outbreak:

  • Marked rise in body temperature for 2 to 3 days.
  • Vesicles that rupture and discharge clear or cloudy fluid, leaving raw, eroded areas surrounded by ragged fragments of loose tissue.
  • Production of sticky, foamy, stringy saliva.
  • Reduced consumption of feed due to painful tongue and mouth lesions.
  • Lameness with reluctance to move.
  • Abortions.
  • Low milk production (dairy cows).
  • Myocarditis (inflammation of the muscular walls of the heart) and death, especially in newborn animals. Animals do not normally regain lost weight for many months. Recovered cows seldom produce milk at their former rates, and conception rates may be low.


Blister on the coronary band of the hoof

Blister on the tongue and mouth


The symptoms of FMD vary with the species, but vesicles and erosions in the oral cavity or on the feet, teats or other areas are suggestive. In cattle, suspicion should be raised by simultaneous salivation and lameness, particularly when a vesicular lesion has been seen or is suspected to exist. Profuse salivation is uncommon in pigs or sheep, where lameness is more typical. Suspect or febrile animals should be examined closely for lesions. When sudden death is observed in young cloven-hooved livestock, older animals should also be examined; young animals that die of heart disease may not have vesicular lesions. Tranquilization may be necessary for a thorough examination as vesicles are painful and may be difficult to see. Laboratory confirmation is necessary, as all vesicular diseases have almost identical clinical signs.

FMD cannot be distinguished clinically from other vesicular diseases including vesicular stomatitis, swine vesicular disease and vesicular exanthema. In domesticated animals, the symptoms may also resemble foot rot, traumatic stomatitis, and chemical and thermal burns. In cattle, oral lesions can resemble rinderpest, infectious
bovine rhinotracheitis, bovine viral diarrhea, malignant catarrhal fever and epizootic hemorrhagic disease. In sheep, the lesions can be confused with bluetongue, contagious ecthyma, and lip and leg ulceration.

Samples to collect

In acute disease, the preferred sample for virus detection is epithelium from unruptured or freshly ruptured vesicles, or vesicular fluid. Sedation is generally advisable before these samples are collected. FMDV is extremely sensitive to low pH, and virus isolation is dependent on good buffering; epithelial samples should be shipped in a transport medium, and kept refrigerated or on ice. If vesicles are not available, blood (serum) and esophageal-pharyngeal fluid samples can be collected for virus isolation or RT-PCR. Esophageal–pharyngeal fluids are taken by probang cup from ruminants, or as throat swabs from pigs, and are shipped in transport medium. These samples should be refrigerated or frozen immediately after collection. Vesicles are the preferred sample from animals that died of heart failure, but myocardial tissue or blood can be collected if vesicles are not present. FMDV may also be found in milk, other secretions and excretions, and other organs. Serum should be collected for serology. In animals suspected to be carriers, esophagealpharyngeal fluids should be collected.

Probang cup


FMD has no treatment

Prevention and control

FMD outbreaks are usually controlled by quarantines and movement restrictions, euthanasia of affected and incontact animals, and cleansing and disinfection of affected premises, equipment and vehicles. Effective disinfectants include sodium hydroxide (2%), sodium carbonate (4%), citric acid (0.2%) and Virkon-S®. Iodophores, quaternary ammonium compounds, hypochlorite and phenols are less effective, especially in the presence of organic matter. Infected carcasses must be disposed of safely by incineration, rendering, burial or other techniques. Milk from infected cows can be inactivated by heating to 100°C (212°F) for more than 20 minutes. Slurry can be heated to 67°C (153°F) for three minutes. Rodents and other vectors may be killed to prevent them from mechanically disseminating the virus. Good biosecurity measures should be practiced on
uninfected farms to prevent entry of the virus.

Vaccination may be used to reduce the spread of FMDV or protect specific animals (e.g. those in zoological collections) during some outbreaks. The decision to use vaccination is complex, and varies with the scientific, economic, political and societal factors specific to the outbreak. Vaccines are also used in endemic regions to protect animals from clinical disease. FMDV vaccines must closely match the serotype and strain of the infecting strain. Vaccination with one serotype does not protect the animal against other serotypes, and may not protect the animal completely or at all from other strains of the same serotype. Currently, there is no universal FMD vaccine. Vaccine banks contain a wide variety of strains, particularly those judged to be the greatest threat of introduction, for use in an outbreak.

Humans are thought to carry FMDV mechanically for a short period of time, based on a study that found this
virus in the nasal passages of one of eight people 28 hours after they had been exposed to infected animals and none of the eight people at 48 hours. People who have been exposed to infected animals should avoid susceptible livestock for a designated period, usually a few days to a week. Some recent studies suggest that extended avoidance periods may not be necessary if good biosecurity practices, including effective personal hygiene protocols (showering or washing hands, and changing clothing), are followed. The discrepancy between these studies remains to be resolved, and government authorities should be consulted for the most recent waiting period recommendations.

Sources: 'Van Nostrand’s Scientific Encyclopedia. — 10th ed.- edited by Glenn D.Considine, Published by John Wiley & Sons, Inc., Hoboken, New Jersey, USA, 2008, p. 2057-2059. Adapted and illustrated to be posted by Leopoldo Costa.

FMD: the center for food security and public health, Iowa State of university Fiebre Aftosa

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Calico and tortoiseshell (3 colored cats)

I know, I know, its been a while since my last update. My time schedule doesnt gave me any mercy at all. Till then, I am finally free for a week, and this will be a golden time to brush up my precious masterpiece- vet blog

Ever wonder about the 3 colored cats?

Calico (with white patch)

Tortoiseshell (no white patch)

What is a calico cat? A calico cat is not a breed of cat, it is a color pattern. To be called "calico", three colors must be present: black, white and orange. Variations of these colors include gray, cream and ginger. A "true" calico cat has large blocks of these three colors, a "tortoise shell" or "tortie" cat has a mix of these three colors (blended/swirled together more than distinct blocks of color). Because of the way tortoiseshell is inherited, almost all tortoiseshell and calico cats are female. The very few male tortoiseshell cats are caused by genetic aberration or development abnormalities in the foetus.

How tortoiseshell pattern occur?

The ginger colour of cats (known as "yellow", "orange" or "red" to cat breeders) is caused by the "O" gene. The O gene changes black pigment into a reddish pigment. The O gene is carried on the X chromosome. A normal male cat has XY genetic makeup; he only needs to inherit one O gene for him to be a ginger cat. A normal female is XX genetic makeup. She must inherit two O genes to be a ginger cat. If she inherits only one O gene, she will be tortoiseshell. The O gene is called a sex-linked gene because it is carried on a sex chromosome. Tortoiseshell cats are therefore heterozygous (not true-breeding) for red colour.

The formation of red and black patches in a female with only one O gene is through a process known as X-chromosome inactivation. Some cells randomly activate the O gene while others activate the gene in the equivalent place on the other X chromosome. This only shows up visibly in skin cells as these produce pigment. This occurs early on in the embryo and as skin cells multiply, they form patches. The skin is a mosaic of cells where some have the O gene active (making ginger pigment) and some do not (making black pigment). This can only happen in cats with two X chromosomes. Male cats only inherit one X chromosome so this is active in all skin cells as there is nothing equivalent on the Y chromosome which could "switch off" the O gene.

There are two main theories regarding brindled torties and patched torties. One (the "early/late deactivation theory") suggests that the time at which X chromosome deactivation occurs during foetal growth determines whether the cat has well defined patches or is brindled with intermixed black and orange hairs. Skin cells multiply during growth and spread out across the skin; as the embryo grows the skin cells multiply. If deactivation occurs early on each pigment cell has room to multiply into, a "red" cell will multiply into more red cells while a "black" cell will give rise to patches of black. If it occurs later, the patches are smaller as the cells have less room to multiply into; some "patches" will be no larger than a single hair! All "red" cats are red tabbies - where there are large red patches, the tabby pattern will usually be discernible.

The other theory regarding brindling and patching (the "migration theory") is that brindled torties occur when there are more pigment producing cells produced from the neural crest (which becomes the back and spine area). The cells are assumed to have undergone X chromosome deactivation before migration. The migrating cells carry either O (red) or o (black) and they migrate at the same rate into their final positions. Where there are many pigment producing cells, there is more competition and they become intermingled. Where there are fewer pigment producing cells, each cell has room to grow into patches of colour (imagine plants forming clumps in a flower border).

Tortoiseshell-white (calico pattern)

Calico cats

The white patches in tortie-and-white (tricolour, calico) cats is caused by the piebald spotting gene. This is a semi-dominant gene with very variable expression ranging from nearly all white to nearly all coloured with only a few white hairs. The gene affects the embryo cells which will become pigment-producing skin cells. These cells are initially formed along the "neural crest" - the embryo's backbone area - and migrate to all over the body during formation of the skin. Where these pigment producing cells fail to get in position before the skin is fully formed, there will be areas of skin which lack pigment producing cells i.e. white areas. White areas are usually the areas furthest from the cat's backbone - paws, belly, chest and chin - these areas take longest to reach.

One effect of white spotting in tortoiseshell cats is to change the pattern from brindled to patched. Tortie cats with little or no white tend to have brindled coats. However, the more white there is, the more the black and white will also be separated out into patches instead of being intermingled.

In the developing embryo, the pigment forming cells migrate from the neural crest. If the "migration theory" is right, cells which activate O (red) and those which activate o (black) appear to migrate at the same speed, leading to a brindled pattern. If the embryos also inherit the gene for white spotting, the fur develops as patches of colour. The bigger the white areas, the bigger the and better defined the separate patches of black and red. The presence of the white spotting means fewer pigment producing cells and less competition between them as they migrate into position. One or two cells reach an area and these multiply in situ to form a patch of colour (a clonal patch).

This is basic tri-color variation in cats. To understand more please visit

A dog once said "This person is so kind to me and feed me, he must be a God"
but a cat said "This person is so kind to me and feed me, I must be a God"

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