Shih Tzu dogs

 

Shih Tzu dog information

The name Shih Tzu is pronounced shee-tzoo and means Lion Dog in Chinese. The name is believed to originate from the dog's vague resemblance to the Asian Snowlion, and this breed is also known as Chrysanthemum Dog since its face looks somewhat like the flower. The Shih Tzu was developed in Tibet and is one of the oldest and smallest of the Tibetan holy dogs. It is actually one of the oldest breeds of dog in the entire world. The Shih Tzu was bred as a pet dog, not a working dog, and it is believed to hail, at least in part, from the Tibetan Lhasa Apso and Chinese Pekingnese, but no one knows for sure. Over the centuries, a tradition developed where the Dalai Lama of Tibet would send dogs to the Emperor of China and receive dogs or other gifts in return. This is probably how the Lhasa Apso came to breed with the Pekingese.
In ancient China, the Shih Tzu could be found next to the Emperor where it would keep him company and bark if people or animals approached.
The Shih Tzu was a much guarded national treasure in China and exporting Shih Tzu dogs was prohibited until China became a republic in 1912. The first official record of a Shih Tzu being imported to the United Kingdom dates back to 1931, and the breed was recognized by The Kennel Club in 1934.

Shih Tzu dog care

Since the Shih Tzu originates from the Imperial Palace of China, it comes as no surprise that this breed requires more care than any ordinary peasant would have time to lavish on it. If you are looking for a low maintenance dog, the Shih Tzu is not a good choice.  
One essential part of Shih Tzu dog care is naturally to brush its long coat on a daily basis to avoid tangles. Some owners cut the coat short to save some time, but if you live in a cold climate you should ideally allow your Shih Tzu to keep its long coat at least during the winter. In addition to this, the Shih Tzu is adapted to cool Chinese and Tibetan conditions and is very sensitive to high temperatures. Being a snub-nosed dog (brachycephalic), it can suffer from breathing problems and heat stroke if exposed to high temperatures. Many airlines refuse to ship Shih Tzu dogs if they suspect that the temperature will exceed 75 degrees F (24 degrees C) at any point during the journey.
Another important part of good Shih Tzu dog care is to clean the area around the eyes each day. You can use cotton and some warm water, no soap is necessary. Some owners claim that giving their dogs chlorine-free water to drink reduces the amount of eye mucus, but this has not been scientifically proven.
Just like most other dog breeds, the Shih Tzu dog needs to have its claws cared for on a regular basis.
Unless the weather is too warm, the Shih Tzu is an energetic dog that will enjoy regular walks to burn off energy and explore the neighbourhood.

Shih Tzu dog puppy

All puppies are adorable, but do not settle for the first breed you happen to come across. A lot of animals end up in shelters every year simply because their owners did not choose a suitable breed. A Shih Tzu dog puppy is a great choice if you want to dog that stays comparatively small and does not need excessive amounts of exercise. (This doesn’t mean that you can put it in a dog crate and never exercise it at all, it simply means that it needs less exercise than huge working dogs.) Like any other small breed, the Shih Tzu does not require large amounts of food and you will be able to easily fit it into a carrying crate when you travel. A Shih Tzu dog puppy is however only a good choice if you are willing to spend time on coat maintenance throughout its entire life.

Shih Tzu dog training

As mentioned above, the Shih Tzu was bred to be a house pet and a close companion, and this becomes very clear when you start training it. It loves human company and will often love training sessions since it means it gets to spend time with its owner. Never yell at your Shih Tzu during training, since this will only serve to frighten it. Despite being a little stubborn at times, this breed responds extremely well to praise and if you spend enough time with your dog it will become very devoted to you. Use praise, affection and perhaps some treats during Shih Tzu dog training and you will notice much faster improvements than were you to yell and scare the dog.
Shih Tzu housetraining can start early, but keep in mind that the puppy can not be expected to control its bladder for an extended period until 12 weeks of age. Even at this age, it is still a very young baby and accidents will happen. This does not indicate that your dog is stupid or disobedient; it is simply a matter of physical bladder control. If you catch your dog in the act of urinating or defecating in an improper place, simply say NO in a firm voice and bring the dog outside where you want it to go. By saying NO in a firm voice you can startle your dog into stop what it’s doing. Remember, there is no need to yell or become upset. One firm NO is enough. Give your Shih Tzu puppy a lot of praise when it finishes its business outdoors.

Shih Tzu dog breeding

According to the American Kennel Club (AKC) American Shih Tzu Club (ASTC), Shih Tzu dog breeding should strive to develop specimens weighing from 9 to 16 pounds as adults. According to this Shih Tzu dog breeding standard, the dog should have a short snout, big eyes and a palm-like tail that waves above its torso. All coat colours are allowed, the important thing is a long and flowing double coat. In addition to this, the Shih Tzu should be sturdy built.

Since the original purpose of the Shih Tzu was to serve as a companion for the Emperor, it was bred to be an intelligent, friendly and lively pet dog that loved to spend time with both its owner and other people. Today, all reputable Shih Tzu breeding programs strive to keep these temperamental characteristics and create dogs that are happy, friendly, affectionate, trusting and well socialized.

Shih Tzu dog breeders

Several health problems are known to plague Shih Tzu dogs and it is therefore important to purchase only from Shih Tzu dog breeders that strive to breed out genetic problems. Reputable Shih Tzu breeders will also make sure that your dog undergoes a comprehensive veterinary exam prior to purchase. Common health issues in the Shih Tzu dog breed is portosystemic liver shunt, hip dysplasia, renal dysplasia and various eye problems. They can also be allergic to red dye #40, which is present in many types of commercial dog foods. The most common sign of red dye allergy is excessive scratching.

Shih Tzu dog price

The Shih Tzu dog price varies a lot from breeder to breeder. When you compare the Shih Tzu dog price always check what you actually get for your money. Has the dog been vet checked, vaccinated and de-wormed? Are the puppies well socialised? Is this a reputable breeder that strives to breed out genetic disease and temperamental problems? The life span of a well cared for Shih Tzu dog is 9-15 years and spending some extra money on getting a healthy, well socialized specimen is definitely

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Dogs Walking in Circles

Normal dogs don't typically walk in circles, except when they are either preparing to urinate or defecate, or their attention is drawn by a smell or another animal to the extent that they are forced to do so to avoid losing the scent or direct contact. If you discover your dog walking in circles without any such reason for it, be immediately suspicious and try to figure out what the cause is.

What to Look For

Dogs with neurological reasons for circling typically find it difficult to turn in the direction opposite the one they are circling in. Start your investigation by attempting to get your dog to turn away from the direction in which she is circling. Next, conduct a neurological exam. This should include an evaluation of her eyes, ears, spine, and limbs.
What to Do

Now ask yourself these few questions:

•  Did your exam reveal evidence of an ear infection? If so, the circling might be due, in part, to the imbalance that sometimes results from an acute middle ear infection. See your vet for the appropriate course of action and that should help resolve the circling behavior.

• Did your exam uncover any eye asymmetry? Different pupil sizes often indicate neurological problems that are best handled by a veterinary neurologist. The sooner your dog sees one the better.

•  Was every aspect of your physical exam completely normal? If it was, there is a strong possibility that the circling behavior is just that; a behavioral issue only. If it persists for more than a few days, it might be worthwhile to consult an animal behaviorist.

When to Get the Vet

A recent head trauma can easily be the cause of a dog's circling behavior. Because these effects may be the beginning of something significantly worse, it is always wise to seek the immediate attention of a veterinary neurologist any time your dog exhibits even the slightest behavioral abnormality following head trauma.

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Why Your Pets Are Suffering Common Deficiencies?

Some Common Vitamin Deficiencies in Pets
Here are some common deficiencies can lead to serious issues on your pet. These are as follows.
Iodine deficiency:
Most important chemicals required for the existence of living things is Iodine. It stimulates the thyroid which will lead to numerous critical issues. In most of the dogs hypothyroidism has been recognized due to the deficiency of iodine. This deficiency can cause due to lack of Iodine in food. Thyroxin is the best supplement to prevent your dog from Iodine deficiency.
Zinc deficiency:
In your pets; Zinc deficiencies can cause due to inflammation; also called bowel sickness. Zinc does not get properly absorbed in the body of your pets which can cause Zinc deficiencies. This may happen due to some genetic problem. Consumption of excessive amount of calcium can lead to zinc deficiencies. Meat and bone have a greater percentage of zinc so by giving it to your pets zinc deficiencies may reduce.
Thiamine Deficiency:
It is easy to treat thiamine deficiency as there are different kinds of cheap pet meds available in the market. Consumption of excessive amount of over processed food can lead to thiamine deficiencies. Raw fish eaters are prone to this deficiency. It is frequently found in cats.
Taurine:
Taurine or amino acid deficiency is caused due to eating over processed vegetarian diet. This deficiency may affect the eyes and heart in your pets. You can overcome with this deficiency by consulting veterinarian for appropriate Pet Meds.
Pet Vaccinations for pet meds
Pet Vaccinations are really very important for your pets to stay away from various diseases or deficiencies and health related issues as they can badly affect people who are enclosed by them. Consult your veterinary to get more information on suitable vaccination available for your pets’ health. The government has pushed a compulsory law for vaccination in countries where rabies occurs naturally.
A few vaccinations for pets are as follows…
Rabies vaccination: It is an essential vaccination for a dog as per the law.
Vaccination like Canine distemper and canine hepatitis virus are important.
Tips to improve immune system of your pet
You can improve the immune system of your pet by giving them proper food. Some tips are as follows.
Protein and wheat in the diet will definitely improve your pet’s health. Provide steamed or boiled wheat to your pet. Beef is also a good source to get protein. For dogs 50% wheat and 20% protein are important.
Oatmeal, millet also as brown rice can be the best source of energy for pets.
To improve energy level brown rice and Oatmeal is essential.
Eggs can be added occasionally to the diet.
60% of protein and 20% wheat are necessary to keep cats healthy.
Vegetarian diet is recommended for cats for healthy routine.
Avoid the deficiency symptoms of your pet by providing a good diet to them.
Cheap Pet Meds
Medication is important for pets to stay away from deficiencies. The best quality product gives fast effect to improve your pet’s health and also keeps them happy and stronger. Now a days online marketing provides different and better quality medication for fleas and ticks control and vitamin deficiency.

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Controlling an Aggressive Dog

Even the calmest of dogs has the propensity of being really aggressive and unruly if it (or its nose) is rubbed the wrong way. Owners and handlers should ensure these steps are taken to develop emotionally stable dog behavior.
Prevention is always better than cure, and an obvious step to take in handling an aggressive dog is to watch for signs of hostility. If your dog is emitting low growls, tensing up or not wagging its tail, it is sending up a red flag and its behavior needs dealing with. In addition, its ears may flatten and its hairs may stand. Further, it may tilt its head in the direction of the source of the aggression. Recognizing the warning signs it displays is a first step in controlling canine aggression.
Safety always comes first when controlling an aggressive canine. If you own a dog with a propensity for aggression, make sure that it is taken out only when it has a muzzle on. If you wish to give your dog a little freedom from the muzzle, ensure that it is not reacting aggressively to its surroundings. When it shows that it can react properly to stimuli, the muzzle can be removed accordingly.
Let your dog interact as much as it can with other dogs, especially when it is a puppy. Familiarity, in the case of dogs, does not breed contempt. With other dogs which are exhibiting calm behavior, an aggressive dog will be more likely to tone down. Keep your dog on a short leash; this allows you to pull back when it lunges at another dog. Say “no” firmly and calmly when aggressive behavior is observed.
Train your dog to be in the “sit” or “stay” position when seeing another person approaching. Reinforcing the “stay” command with your dog helps it remember that it must behave in a pleasant way to people whenever they approach. Use praise liberally when your dog shows that it knows how to sit or stay. This provides positive association towards both the command and people the dog may come in contact with.
Always watch your own reaction when a dog is hostile. If you show that you are in a frenzy when your dog is aggressive, it picks up vibes from you and will tend to be even more excited than it already is. Maintaining calm assertiveness is the key in combating dog aggression.
Get a gentle but firm lead for your dog. The dog will not have any negative association with it and love its walks. If it likes the leash, it heightens the enjoyment of going out for walks. A happy dog is a calm dog.
Dog aggression may be a problem, but it certainly can be controlled. With the right steps in place, you and your canine can have longer, more pleasant walks

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5 Ways to Rid Your Pet of Fleas or Ticks

As a pet owner you are aware of how detrimental it can be for your pet to have fleas or ticks on their body or within your home. With the implementation of the following tips you will undoubtedly be provided with the opportunity to understand how to get rid of fleas or ticks both naturally and with the use of a variety of different chemical-based treatments.
Tip #1: Flea/Tick Shampoo
The most popular form of getting rid of ticks and fleas is to purchase the appropriate flea and/or tick shampoo from your local pet supply store. There are an ample amount of different brands that can be utilized to your advantage which can be quite beneficial. Whether you are looking for a formula specified for your pet or if you are looking to gather a formula that you can use for your furniture as well, the options are relatively endless.
Tip #2: Dish Soap and Hot Water
For a more cost effective solution, many different pet owners utilize dish soap and hot water to rid their pets of fleas and ticks. Rather than having to venture to the store to purchase a new formula, bathing your pet in an abundance of dish soap will help to kill all of the fleas that are on their bodies. It is also preferred that you comb through your pets hair after treatment to ensure that all of the bugs have been killed.
Tip #3: Consistent Bathing
As more of a flea preventative and a tick preventative, ensuring that your pet is cleaned on a daily basis can be quite advantageous. Whether you are interested in purchasing specialized shampoos or if you prefer to use generic soap brands, the option is up to your personal preferences. With a weekly bath your pet will have clean and luxurious hair that will be less likely to become a home for ticks and fleas.
Tip #4: Treat your Surrounding Area
Although becoming aware of the ways that you can rid your pet of fleas and ticks can be beneficial, treating the environment can also prove to be a great flea preventative and tick preventative. You will be provided with the opportunity to purchase specific chemical-based or organic grass sprays and tree sprays that will deter all different types of ticks and fleas from your property. This will help to ensure that your pet does not contract these bugs while it is playing outside.
Tip #5: Oral Medicine
As a more drastic measure, treating your pet with oral medicine can be an advantageous way to prevent ticks and fleas from affecting your home. Essentially you will provide your pet with an oral dose of medication that will enter their blood stream to help deter ticks and fleas from attaching onto their bodies.

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Grieving for Pets

The loss of a pet is an often underestimated source of trauma and sadness. People are often stunned to find out how empty their house can feel after the passing of a pet. Pet’s play a unique role in our lives. Pet’s can be companions and friends. They cheer us up when we are down and they make us feel like the most important person in the world the second we walk through the door. Petting pets has shown to reduce stress in humans. Studies by the University of Hawaii’s animal science department showed grief over the loss of a pet lasting over six months for 30-percent of test subjects.
History is filled with humans mourning the passing of their animal companions. The ancient Egyptians mummified their cats to acknowledge their importance. Contemporary methods of pet memorialization include small grave-stones, and porcelain memorial plaques.
Everyone grieves for pets in their own way. Some cope by expressing themselves through poetry, music, or writing letters to their deceased pets. Talk to family and friends about what the pet meant to you and how they dealt with the loss of a pet. Grieving for a pet is a process. During this process you may experience guilt, denial, anger, and depression. These are perfectly normal emotions to got through. Blaming yourself is not the answer. Coming to terms with your feelings is the only way to deal with the loss of a pet and move on.
How one experiences grief is unique. Scientific time-tables for grief do not necessarily dictate how long one’s personal journey through grief will last. Ignoring pain will only make it worse in the long run. Reaching out to others and keeping a normal routine can help in dealing with grief. Remember that there are no right or wrong feelings. One should reflect on his/her feelings to really understand what is bothering him/her.
Animals are very sensitive to any change in the household. One may notice a change in behavior among pets in the household. This is because animals grieve as well.
There are those who feel guilty for wanting to get a new pet. A new pet is not a replacement for an old pet. One way to look at getting a new pet is as a tribute. You loved your first pet so much, that you though a new pet could be a comfort as well.

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Coccidiosis, Upper Intestinal, E acervulina

Introduction

This is probably the commonest cause of coccidiosis in chickens and occurs worldwide. It is seen in layers and in broilers, both alone and in association with other species of coccidia and is caused by Eimeria acervulina, which is moderately pathogenic. Morbidity is variable and mortality low or absent. Eimeria mivati is currently considered not to be a valid species distinct from E. acervulina.

Signs

• Depression.
• Ruffled feathers.
• Closed eyes.
• Inappetance.
• Poor production.
• Diarrhoea.
• Depigmentation.

Post-mortem lesions

• Thickening, and other lesions, restricted to upper third of small intestine - the duodenum and part of the ileum.
• Petechiae.
• White spots or bands in the mucosa. In severe infections they become confluent and cause sloughing of the mucosa.
• Poor absorption of nutrients/pigments.
• A system of assessing the severity of coccidial challenge by attributing a 'score' is often used. A detailed description is beyond the scope of this book. In general terms a score of 0 indicates no lesions and a score of 4 indicates maximal severity of lesion or death. Various publications provide a photographic key to severity of lesion.

Diagnosis

Signs, lesions, microscopic exam of scrapings. Differentiate from necrotic and non-specific enteritis.

Treatment

Toltrazuril, Sulphonamides, Amprolium, in feed or water.

Prevention

Coccidiostats in feed, vaccination by controlled exposure, hygiene. Immunity is quite short lived (about 30 days) in the absence of continued challenge.

Figure 12. Moderate Eimeria acervulina infection (score 2) in chicken duodenum. In milder infections there may be scattered white spots, in severe the entire surface is pale or denuded of epithelium.

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Coccidiosis, Mid-intestinal, E necatrix

Introduction

A highly pathogenic form of coccidiosis, caused by Eimeria necatrix, in which the parasite is present in the small intestine and in the caecum. It occurs in chickens worldwide and has variable morbidity but mortality is high in severely affected birds.

Signs

• Reduced feed consumption.
• Depression.
• Ruffled feathers.
• Closed eyes.
• Inappetance.
• Poor production.
• Diarrhoea, blood in faeces.

Post-mortem lesions

• Petechiae and thickening, of middle to posterior third or more of small intestine.
• 'Sausage-like' intestine.
• Severe necrotising enteritis.
• Schizonts seen as white spots through the serosa interspersed with petechiae. Deep scrapings necessary to show large schizonts. Oocyts in caecal scrapings.

Diagnosis

Signs, lesions, microscopic examination of scrapings Differentiate from necrotic enteritis, other types of coccidiosis.

Treatment

Toltrazuril, Sulphonamides, Amprolium, Vitamins A and K in feed or water.

Prevention

Coccidiostats in feed, vaccination, hygiene. This is one of the less immunogenic species, commercial vaccines commonly contain more than one strain of E. maxima.

Figure 14. Moderate Eimeria necatrix infection in the jejunum of a chicken (Score 3). In this case the intestine is thickened and can become ballooned and sausage-like. Haemorrhages and white spots are visible from the outside of the intestine.

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Coccidiosis, Mid-intestinal, E maxima

Introduction

One of the more common forms of coccidiosis in commercial broilers. Because of the area of intestine affected it tends to have a significant effect on productivity and susceptibility to necrotic enteritis. Caused by Eimeria maxima, of moderate to high pathogenicity it is seen worldwide. Morbidity and mortality are variable.

Signs

• Depression.
• Ruffled feathers.
• Closed eyes.
• Inappetance.
• Poor production.
• Blood or pigment in the faeces.
• Depigmentation of skin and plasma is especially evident in this form of cocccidiosis and this is commercially important in some markets.

Post-mortem lesions

• Petechiae and thickening of middle third of intestine.
• Poor absorption of nutrients/pigments.
• Mild to severe enteritis, contents often orange in colour, mucosa tends to be pinker than normal.
• This infection is often associated with E. acervulina coccidiosis and there may be large numbers of characteristic oocysts in smears.

Diagnosis

Signs, lesions, microscopic examination of scrapings. Differentiate from necrotic enteritis, non-specific enteritis.

Treatment

Sulphonamides, Amprolium, Vitamins A and K in feed or water.

Prevention

Coccidiostats in feed, vaccination, hygiene. This is one of the less immunogenic species, commercial vaccines commonly contain more than one strain of E. maxima.

Figure 13. Moderate Eimeria maxima infection in the jejunum of a chicken (Score 2). The lesions are subtle compared to other forms of coccidiosis. The intestine is slightly thickened and there are scattered haemorrhages in the mucosa when seen from the inside.

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Coccidiosis, Kidney

Introduction

A disease of geese caused by Eimeria truncata that can cause high mortality in geese of 3-12 weeks of age, it can also infect Barbary ducks and swans.

Signs

• Depression.
• Weakness.
• Diarrhoea - faeces tend to be whitish.
• Reduced feed intake.

Post-mortem lesions

• Enlarged kidneys.
• Kidneys light grey to greyish pink.
• Tiny white foci and petechiae in the kidneys.

Diagnosis

Lesions, presence of coccidial stages in fresh scrapings of kidney lesions.

Treatment

Controlled trials of treatments have not been published.

Prevention

Good Hygiene.

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Coccidiosis, Intestinal, of Ducks and Geese

Introduction

Young ducks and geese may suffer from Eimeria spp infection. In the goose E. anseris is the most important, while in ducks Tyzzeria perniciosa is most pathogenic. Tyzerria has eight sporocysts in each oocyst, compared to four per oocyst for Eimeria. Coccidiosis occurs only very rarely in commercially reared ducks in the UK.

Signs

• Sudden death.
• Depression.
• Blood-stained vent.
• Tucked appearance.

Post-mortem lesions

• Massive haemorrhage in upper small intestine.

Diagnosis

Signs, lesions, microscopic examination of scrapings (usually few or no oocysts, large number of merozoites). Differentiate from Duck viral hepatitis, Duck viral enteritis, anatipestifer.

Treatment

Sulphonamides (e.g. Sulphadimidine 30-600gm/100 birds/day, 3 days on, 2 days off, 3 days on), Amprolium, Vitamins A and K in feed or water.

Prevention

If required coccidiostats could be used in feed, however this is not routinely practised. Hygiene.

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Coccidiosis, Ileorectal, E brunetti

Introduction

A relatively rare form of coccidiosis affecting chickens worldwide caused by Eimeria brunetti. Of moderate to high pathogenicity, it is found in the terminal ileum, caecum and rectum. Morbidity and mortality are variable.

Signs

• Depression.
• Ruffled feathers.
• Closed eyes.
• Inappetance.
• Poor production.
• Diarrhoea, blood in faeces.

Post-mortem lesions

• Petechiae and thickening of the distal third or more of intestine, extending into caecal tonsils.
• Severe necrotising enteritis.
• Oocysts in caecum and rectum.

Diagnosis

Signs, lesions, microscopic examination of scrapings. Differentiate from ulcerative enteritis, caecal coccidiosis.

Treatment

Toltrazuril, Sulphonamides, Amprolium, Vitamins A and K in feed or water.

Prevention

Coccidiostats in feed, vaccination by controlled exposure, hygiene. This species is not usually included in vaccines for broilers. There is good immunity to the same parasite in recovered birds.

Figure 16. Moderate Eimeria brunetti infection in the terminal ileum and rectum of a chicken. There is thickening of the intestinal mucosa and there are lines of haemorrhagic spots in the mucosa.

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Coccidiosis, E praecox

Introduction

Infection of chickens with the protozoan parasite Eimeria praecox is spread in exactly the same as that with E. mitis but is practically non-pathogenic.

Signs

• Normally asymptomatic but may cause reduced feed efficiency and reduced weight gain, and predispose to other intestinal conditions.

Post-mortem lesions

• Minimal, but usually excess liquid and mucus in the duodenal loop.
• Severe infection can cause dehydration through excessive fluid loss.
• The cells of the sides of the villi (not tips) are usually parasitised.

Diagnosis

Identification of characteristic slightly ovoid oocysts in the duodenum in the absence of E. acervulina lesions. It has a very short pre-patent period (c. 80 hours).

Treatment

Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis.

Prevention

Normally controlled by anticoccidials in feed. Not usually included in vaccines.

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Coccidiosis, E mitis

Introduction

This condition of chickens, seen worldwide, is caused by the protozoan parasite Eimeria mitis, which colonises the small intestine.

The infective agent is found in litter, faeces and on fomites and birds are infected by the oral route with an incubation period of 2-5 days. The disease occurring is proportional to the amount of infective agent ingested.

The parasite is moderately resistant in the environment and highly resistant to conventional disinfectants.

Predisposing factors include exposure to faeces and litter conditions that favour development of the parasite (temperature, humidity).

Signs

• Reduced feed conversion efficiency and weight gain. May predispose to wet litter, secondary bacterial enteritis.

Post-mortem lesions

• The lesions are minimal and located in the lower small intestine (ileum) which tends to be pale and flaccid with scattered petechiae.

Diagnosis

Mild lesions, identification of typical small round oocysts and other stages in fresh scrapings from the small intestine.

Treatment

Not usually treated but susceptible to the products used for other forms of intestinal coccidiosis.

Prevention

Normally controlled by anticoccidials in feed. May be included in vaccines.

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Coccidiosis, Caecal, E tenella

Introduction

This was at one time the commonest type of coccidiosis and is certainly the most easily diagnosed. It is caused by Eimeria tenella and results in lesions in the caecum of chickens worldwide. Morbidity is 10-40% and mortality up to 50%. Transmission as for E. mitis (see above).

Signs

• Depression.
• Ruffled feathers.
• Closed eyes.
• Inappetance.
• Diarrhoea, blood in faeces.
• Production less affected than in some of the other forms of coccidiosis.

Post-mortem lesions

• Petechiae.
• Thickening, ecchymoses, of caecal mucosa.
• Accumulation of varying quantities of blood and caseous necrotic material in the caecum.

Diagnosis

Signs, lesions, microscopic examination of scrapings. Differentiate from ulcerative enteritis, histomonosis.

Treatment

Toltrazuril, Sulphonamides, Amprolium, Vitamins A and K in feed or water.

Prevention

Coccidiostats in feed, vaccination by controlled exposure, hygiene. E. tenella is more common when 'straight' ionophore programmes are used. Shuttle programmes with chemicals in the starter diet usually improve control. In some markets the organic arsenical compound 3-Nitro is used as an aid in the control of caecal coccidiosis. Vaccines are used mainly in breeders but increasingly in broilers. Recovered birds have good immunity to the same parasite.

Figure 15. Moderate Eimeria tenella infection in the caecae of a chicken (Score 3). The caecal walls are thickened and haemorrhagic and there is a mass of blood in the caecal lumen.

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Coccidia of Turkeys

Introduction

Infection of turkeys with Eimeria spp. This disease is not very common in commercially reared turkeys though most turkey growers receive preventative medication for at least part of their lives. Five species of Eimeria have been identified that cause lesions in turkeys, of which two are associated with significant disease effects. E. meleagrimitis affects the upper small intestine, while E. adenoides affects the caecae and rectum. E. gallopavonis and E. meleagridis affect the lower small intestine rectum and caecae, while E. dispersa is found in the small intestine.

Signs

• Huddling.
• Weight loss.
• Depression.
• Watery diarrhoea that may occasionally be blood stained or contain clumps of mucus or shed mucosa.
• Tucked appearance, ruffled feathers.

Post-mortem lesions

• The affected area of intestine shows thickening of the wall and dilation. The contents may be haemorrhagic or be watery with white material shed from the mucosa.

Diagnosis

Signs, lesions, microscopic exam of scrapings (oocysts, gamonts). Differentiate from necrotic enteritis.

Treatment

Toltrazuril, Sulphonamides (e.g. Sulphaquinoxaline), Amprolium.

Prevention

The ionophore coccidiostats lasalocid and monensin are routinely used in turkey growers, typically to 12 weeks of age. Diclazuril is also used for this purpose. Dosage levels of ionophores may be critical to efficacy and safety. Exposure of previously unmedicated birds to these compounds can cause toxicity. Salinomycin is toxic for turkeys even at very low doses. Avoid use of tiamulin in ionophore treated birds.

Figure 37. Turkey coccidiosis of the upper small intestine caused by E. meleagrimitis. The intestines are dilated, show some spotty congestion and have abnormal contents due to the sloughed epithelium.

Figure 38. Turkey caecal coccidiosis caused by E. adenoides. The exudate can range from semi-liquid to solid white cores.

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11:40 AM

اقرأ المزيد

Slipped Tendon or Perosis

Introduction

Caused by deficiency of manganese, choline, zinc, either singly or in combination (although deficiencies of pyridoxine, biotin, folic acid, niacin may also be involved).

This condition is seen in chickens, ducks and turkeys. In turkeys it may be an inherited deficiency of galactosamine.

Signs

• Short legs.
• Lameness.
• Distortion of hock.
• Slipping of Achilles tendon (or perosis).
• Malposition of leg distal to hock.
• In embryos parrot beak, shortened bones.

Post-mortem lesions

• Shortening and thickening of long bones.
• Tibia and metatarsus bowed.
• Shallow trochlea.
• Lateral slipping of tendon.

Diagnosis

Lesions, analysis of feed.

Differentiate from twisted leg, infectious synovitis, rickets, infectious arthritis, ruptured ligaments.

Treatment

For flock proceed as for prevention, no value to affected bird.

Prevention

Addition of manganese, choline, vitamins, correct mineral balance.

Unknown

11:39 AM

اقرأ المزيد

Chlamydiosis, Psittacosisof poultry

Introduction

An infection of turkeys, ducks, psittacines, pigeons, man, rarely chickens, caused by Chlamydia psittaci, a bacterium of highly variable pathogenicity. It is a 'Scheduled Disease' rarely diagnosed in UK, but occurring probably worldwide. Morbidity is 50-80%, mortality 5-40%.

It is transmitted by contact, faecal dust and wild bird carriers, especially pigeons and robins. Egg transmission does not occur.

Elementary bodies are highly resistant and can survive in dried faeces for many months.

Iodophores and formaldehyde are effective disinfecting agents, phenolics are less so. Intercurrent salmonellosis and, perhaps, other infections may be predisposing factors.

Signs

• Respiratory signs.
• Greenish-yellow diarrhoea.
• Depression.
• Weakness.
• Inappetance.
• Weight loss.
• Nasal discharge.
• Conjunctivitis.
• Occasional transient ataxia in pigeons.
• Production drops in naive laying flocks

Post-mortem lesions

• Vascular congestion.
• Wasting.
• Fibrinous pericarditis.
• Airsacculitis.
• Perihepatitis.
• Spleen enlarged and congested, may rupture in pigeons.
• Necrotic foci in liver.
• Fibrinous pneumonia.
• Congested lungs and air sacs in the turkey.

Diagnosis

History, signs, lesions. Intracytoplasmic inclusions are helpful but confirmation requires demonstration of causal organisms (Giemsa stain, IFA).

Serology: complement fixation, Elisa and gel diffusion.

Differentiate from Duck viral hepatitis, Duck septicaemia.

Treatment

Tetracycline (200-800 ppm in feed for 3-4 weeks) and/or quinolone medication and supervised slaughter.

Prevention

Biosecurity, exclusion of wild birds.

Live and inactivated vaccines are protective although the former result in carriers and the latter require several applications.

Unknown

9:18 AM

اقرأ المزيد

Chicken Anaemia

Introduction

A viral disease of chickens caused by Chicken Anaemia Virus or CAV. Prior to confirmation that it is in fact a virus it was known as Chicken Anaemia Agent or CAA.

Mortality is typically 5-10% but may be up to 60% if there are predisposing factors present such as intercurrent disease (Aspergillosis, Gumboro, Inclusion body heptatitis etc.) or poor management (e.g. poor litter quality).

Transmission is usually vertical during sero-conversion of a flock in lay, lateral transmission may result in poor productivity in broilers.

The virus is resistant to pH 2, ether, chloroform, heat (70°C for 1 hour, 80°C for 5 minutes) and many disinfectants even for 2 hours at 37°C. Hypochlorite appears most effective in vitro.

Signs

• Poor growth.
• Pale birds.
• Sudden rise in mortality (usually at 13-16 days of age).
• No clinical signs or effect on egg production or fertility in parent flock during sero-conversion.

Post-mortem lesions

• Pale bone marrow.
• PCV of 5-15% (normal 27-36%).
• Atrophy of thymus and bursa.
• Discoloured liver and kidney.
• Gangrenous dermatitis on feet, legs wings or neck.
• Acute mycotic pneumonia.

Diagnosis

Gross lesions, demonstration of ongoing sero-conversion in parent flock, virus may be isolated in lymphoblastoid cell line (MDCC-MSB1).

Treatment

Good hygiene and management, and control of other diseases as appropriate, may be beneficial. If gangrenous dermatitis is a problem then periodic medication may be required.

Prevention

Live vaccines are available for parents, their degree of attenuation is variable. They should be used at least 6 weeks prior to collecting eggs for incubation. Their use may be restricted to those flocks that have not sero-converted by, say, 15 weeks.

Immunity: there is a good response to field challenge (in birds over 4 weeks of age) and to attenuated live vaccines.

Serology: antibodies develop 3-6 weeks after infection, and may be detected by SN, Elisa, or IFA.

Unknown

9:17 AM

اقرأ المزيد

Cellulitis

Introduction

Cellulitis is literally an inflammation of connective tissues. It typically occurs between skin and muscles and between muscles and may be an incidental finding in a range of conditions. However its main importance is as a cause of condemnation in meat poultry, particularly broiler chickens.

In the USA it is called 'Inflammatory Process'. The condition is caused by infection of, often minor, skin wounds by particular strains of E. coli, which can replicate in the tissues.

Signs

• Affected flocks tend to have poorer than average productivity and uniformity, but the affected birds are not readily detectable prior to slaughter.

Post-mortem lesions

• Typically it presents as exudate ranging from liquid and pale cream pus to yellowish solid plaques of caseous material under the skin of the abdomen and/or in the leg. Many affected birds have no other lesions and are reasonably well grown. Many meat inspectors become skilled at detecting subtle differences in skin colour in the affected birds.

Diagnosis

Typical lesions.

Treatment

Treatment would not be possible if the problem is identified at a final depletion. If identified at a thinning there may be time for antibacterial treatment to have some benefit for those birds in the early stages of the problem.

Prevention

Toe scrapes at 15-25 days of age when feather cover is poor are the most likely predisposing factors. Careful flock management with a view to reducing toe wounds has the greatest impact in controlling cellulitis. Routine monitoring of skin damage at about 25 days of age may be helpful in fostering good practices, though most of the birds showing toe scrapes will not go on to develop cellulitis.

Unknown

9:16 AM

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Hairworm Infection

Introduction

Nematode parasitic worms of poultry, game birds and pigeons of Capillaria species. C. obsignata in the small intestine, C. contorta in the crop and oesophagus.

The worms are 7-18 mm long, about 0.05 mm wide and hair-like in appearance. Morbidity and mortality are usually low. Infection is by the oral route. Worm eggs take about 20 days to embryonate with an L1 larvae, prepatent period about 21-25 days according to species.

Some species have earthworms as intermediate hosts; some are transmitted direct from bird to bird. Worm eggs in the environment are resistant.

Signs

• Diarrhoea.
• Wasting
• Poor growth.
• Dejection.

Post-mortem lesions

• Enteritis.
• Hairworms in mucosa of crop, small intestine or caecum.

Diagnosis

This may be by a combination of macroscopic examination, seiving intestinal contents, or characteristic worm eggs in faeces in patent infections. Differentiate from other causes of enteritis.

Treatment

Coumphos has been licensed in some markets. Fenbendazole has been shown to have high efficacy - other approved benzimidazoles can be expected also to have activity. Levamisole.

Prevention

Separation of birds from possible transport and intermediate hosts, effective cleaning of houses.

Unknown

9:14 AM

اقرأ المزيد

Cannibalism

Introduction

A complex multifactorial behavioural problem of poultry and game birds seen worldwide. Morbidity is usually low but mortality is high among affected birds. Predisposing factors include overcrowding, excessive light intensity or variation (e.g. through shafts of light in the house), high temperatures, nutritional deficiencies, feed form (mash takes longer to consume than pellets), tenosynovitis and other diseases affecting mobility, boredom, and strain of bird.

Signs

• Pecking at feet (especially young chicks) and vents (adult layers and turkey poults 8-12 days old), head, face, wings.
• Feather-pulling.

Post-mortem lesions

• Skin wounding related to particular signs exhibited.
• Generalised anaemia.

Diagnosis

Age, distribution of lesions, anaemia. Differentiate from bacterial dermatitis, post-mortem cannibalism.

Treatment

Correct any husbandry problems. Soluble multivitamins and/ or methionine may be of some benefit in some circumstances. Beak trimming may be necessary. If so it should be carried out carefully by trained operators, complying with local regulations and any relevant codes of practice.

Prevention

Proper density and temperature, low light level, control ectoparasites. Provision of a diet that closely matches the nutritional requirements of the stock concerned.

Unknown

9:13 AM

اقرأ المزيد

Candidiasis,Thrush of poultry

Introduction

A disease of the alimentary tract of chickens, turkeys, and sometimes other birds and mammals, characterised by thickening and white plaques on the mucosa, especially in the crop but sometimes in the proventriculus, intestine and cloaca, and associated with gizzard erosion.

The cause is a fungal yeast, Candida albicans and the condition is seen worldwide. Morbidity and mortality are usually low.

The route of infection is normally oral and the organism is often present in healthy animals with disease occurring secondary to stress and poor hygiene. The fungus is resistant to many disinfectants.

Signs

• Dejection.
• Poor appetite.
• Slow growth.
• Diarrhoea, possibly confused or masked by signs of the primary disease.

Post-mortem lesions

• White plaques in mouth, oesophagus, crop, occasionally proventriculus and intestine.
• Raised focal lesions may slough into lumen as caseous material.

Diagnosis

Lesions, histopathology, microscopic examination of a digested smear (heat in 10% potassium hydroxide) to demonstrate the hyphal forms of the yeast in the tissues. Colonies of this fungus appear as white to ivory colour, smooth and with a yeasty smell.

Treatment

Nystatin (100 ppm in feed) for 7-10 days, copper sulphate (1 kg/tonne feed) for 5 days, or copper sulphate 1gm/2 litre water for 3 days if approved locally.

Prevention

Avoid excessive use of antibiotics and other stressors. Ensure good hygiene, proprionic acid, sodium or calcium proprionate at 1 kg per tonne continually. A finely divided powder of copper sulphate (where approved) at 200gm/tonne continually or to 14-16 weeks in replacement pullets.

Control of Candida through drinking water is sometimes practised with chlorination (e.g. Chlorox, sodium hypochlorite) at 5 ppm. This is economical and effective. It should be repeated periodically. Take care to provide fresh clean feed and water, uncontaminated by fungi.

Unknown

9:12 AM

اقرأ المزيد

Campylobacter Infection

Introduction

Campylobacter spp. are bacteria that commonly infect a broad range of livestock species, pets and wild animals. In poultry they tend to multiply in large numbers in the hindgut, principally in the caecae. Campylobacters are a significant cause of enteritis in man. Infected poultry are a potential reservoir of this zoonosis.

Campylobacter jejuni is the commonest species found in poultry. All campylobacters are delicate organisms that survive for relatively short periods outside the host unless protected by organic material, biofilm or engulfed by protozoa.

Campylobacter jejuni infection is not currently considered to be pathogenic in poultry though a Campylobacter-like organism is considered to be the cause of 'Vibrionic Hepatitis'.

There are indications that plantar pododermatitis, carcase quality and litter quality are better on farms which tend to have Campylobacter-negative stock. The reason for this is unclear. It may be that management that favours dry litter reduces the risk of infection and/or transmission within the flock.

There is an annual cycle with increased risk of infection in the summer months in some countries.

Signs

• None.

Post-mortem lesions

• None.

Diagnosis

Isolation of the organism from caecal contents, cloacal swabs or composite faeces. The organism is sensitive to air so swabs should be collected into transport medium and other samples placed in airtight containers with minimal airspace. Samples should be tested as quickly as possible after collection.

Treatment

Not required on clinical grounds.

Prevention

In principle, housed poultry can be maintained free of Campylobacter infection by consistent application of excellent biosecurity. Key aspects of this include effective sanitation of drinking water, sourcing of water from high quality supplies, avoidance of contact with pets and other farmed species, good hand hygiene by stockmen, and changing of overalls and boots on entering bird areas.

In practice the success of this will also depend upon the degree of environmental contamination by the organism. For this reason it may be difficult to stop the spread of infection between houses once it becomes established in one house.

Many infections are introduced during thinning or other forms of partial depopulation. Insects and rodents may act as a means of transfer of the infection from the general environment into the poultry buildings.

Research is ongoing on the development of vaccines, phage treatments and competitive exclusion approaches, as well as processing plant technologies to reduce carcase contamination.

Unknown

9:30 AM

اقرأ المزيد

Calcium Tetany

Introduction

A metabolic disease of chickens, especially broiler parents. Predisposing factors include heat stress with reduced feed intake and panting.

Signs

• Paralysis.
• Death from respiratory and cardiac failure.

Post-mortem lesions

• Cyanosis.
• Congested lungs.
• Active ovary with egg in oviduct.

Diagnosis

This is made on signs, lesions, lack of other significant lesions, and response to treatment. Differentiate from IB 793b, other acute infections and other causes of sudden death.

Treatment

Provide 5 gm of oyster shell per hen on 3 successive days along with vitamin D in drinking water.

Prevention

Keep pullet flocks on low calcium diet until 5% production hen/day, managing birds for maximum uniformity.

Unknown

9:29 AM

اقرأ المزيد

Caecal Worm

Introduction

Heterakis gallinae, nematode parasites of poultry and game birds, are small whitish worms with a pointed tail, up to 1.5 cm in length that occur in the caecum. They are found worldwide. Morbidity is high but it is not associated with mortality. Infection is by the oral route. Earthworms may be transport hosts for eggs, or paratenic hosts with partially developed (L2) larvae. There is an incubation period of 2 weeks for eggs to embryonate, and a four-week prepatent period. The meaning of the technical terms relating to parasite life cycle are defined in the glossary. Heterakis gallinae eggs and larvae are a transport hosts for Histomonas, the cause of Blackhead.

Signs

• None.

Post-mortem lesions

• Inflammation of caecum, possibly with nodule formation.

Diagnosis

Adults can be seen in caecal contents at post-mortem examination.

Treatment

Flubendazole, Levamisole, are effective.

Prevention

Avoiding access to earth and earthworms. Routine anthelmintic treatment.

Figure 11. The life cycle of Heterakis showing the location of adults, an undeveloped egg as found in fresh faeces, and the embryonated egg. The egg may be ingested directly by a chicken, or by an earthworm which is in turn ingested by a chicken.

Unknown

9:28 AM

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Breast Blister

Introduction

A complex condition of chickens and turkeys occurring worldwide associated with trauma, leg weakness, and infection with Staphylococcus spp. bacteria. Morbidity may reach more than 50% but the condition is not fatal. Poor feather cover and caked or wet litter are predisposing factors.

Signs

• Swelling over the keel bone with bruising and discolouration.

Post-mortem lesions

• Inflammation of sternal bursa along the keel bone which may, in chronic cases, give way to scar tissue.

Diagnosis

Based on lesions.

Treatment

Not usually appropriate.

Prevention

Good litter management and handling, control of leg problems.

Unknown

9:26 AM

اقرأ المزيد

Botulism

Introduction

A condition of chickens, turkeys, ducks and other waterfowl occurring worldwide and caused by a bacterial toxin produced by Clostridium botulinum mainly types A / C. The toxin is produced in decaying animal (usually carcases) and plant waste, and toxin-containing material (pond-mud, carcases, maggots) is consumed by the birds. Toxin may also be produced by the bacteria in the caecum. Morbidity is usually low but mortality is high. The toxin and bacterial spores are relatively stable and may survive for some time in the environment. It has also been suggested that poultry carcases lost in litter can be a cause of botulism in cattle grazing land or consuming silage where poultry litter has been spread.

Signs

• Nervous signs, weakness, progressive flaccid paralysis of legs, wings then neck, then sudden death.
• Affected broilers tend to settle with eyes closed when not disturbed.
• A soiled beak, because it rests on the litter, is also quite typical.

Post-mortem lesions

• Possibly no significant lesions.
• Mild enteritis if has been affected for some time.
• Feathers may be easily pulled (chicken only).
• Maggots or putrid ingesta may be found in the crop.

Diagnosis

History, signs, mouse toxicology on serum or extract of intestinal contents. Differentiate from acute Marek's disease ('Floppy Broiler Syndrome') by histology of the brain.

Treatment

Remove source of toxin, supportive treatment if justifiable, antibiotics, selenium.

Prevention

Preventing access to toxin, suspect food and stagnant ponds, especially in hot weather. The single most important measure is careful pick-up and removal of all dead birds on a daily basis. This will reduce the risk of botulism both in the poultry and in any grazing animals on land where poultry litter is spread.

Unknown

9:20 AM

اقرأ المزيد

Blackfly Infestation

Introduction

Grey-black hump-backed flies, 5 mm long and found in North and South America that are external parasites of birds and mammals. The flies transmit leucocytozoonosis and also a filarial parasite in ducks. The condition tends to occur near to rapidly flowing streams, although these insects can travel up to 15 miles. Eggs and larvae survive through the winter to cause new infestations in the following year.

Signs

• Anaemia in young birds.
• Swarms of flies.

Post-mortem lesions

• Anaemia.

Diagnosis

Anaemia, season, local history.

Treatment

Treatment is difficult.

Prevention

Similar measures as for mosquito control. Biological control using a strain of Bacillus thuringensis has had some success and is preferable to insecticides. Weekly treatments are required.

Unknown

9:19 AM

اقرأ المزيد

Biting Lice

Introduction

Various species of lice are common external parasites of poultry worldwide. They are spread by direct contact between birds and by litter etc. Away from birds adults survive about 4-5 days. The parasites are 1-6 mm in size and their life cycle takes about 3 weeks. Menocanthus stramineus is the most pathogenic and is said to be capable of causing anaemia in heavy infestations. Check flocks regulary for rapidly moving insects at the base of the feathers on the abdomen or around the vent. Crusty clumps of eggs ('nits') may be visible at the base of feathers.

Signs

• Lack of thrift in young birds.
• Lice eggs stuck to feathers.
• Parasites on birds, especially around vent.
• Irritation.
• Loss of vent feathers.
• Scabs around vent.
• Loss of condition.
• Drop in egg production.

Post-mortem lesions

• Usually none, may be some feather damage and crustiness of skin.

Diagnosis

Identification of the parasites. Differentiate from mites, bedbugs.

Treatment

Malathion powders and pyrethroid sprays where approved for bird application.

Prevention

Avoid direct contact with wild and backyard poultry. Examine for lice regularly, especially in autumn and winter and treat if required. It is usually necessary to treat twice at a 7-10 day interval to fully control the condition, as the larvae within eggs are not killed by most products. Effective removal of all organic material at flock depletion should be practised in all-in/all-out production systems.

Unknown

9:18 AM

اقرأ المزيد

Biotin Deficiency, Fatty Liver and Kidney Syndrome

Introduction

Biotin deficiency has occured in turkeys and chickens in many countries but is now rare in birds consuming properly formulated feeds. Reduced feed intake and blood sugar can precipitate fatty liver and kidney syndrome.

Signs

• Poor growth.
• Leg weakness.
• Scabs around eyes and beak.
• Thickened skin under foot pad, in embryos, webbing between toes.
• Chondrodystrophy.
• Sudden deaths in fatty liver and kidney syndrome.

Post-mortem lesions

• See signs.
• Pale livers and kidneys in fatty liver and kidney syndrome.

Diagnosis

Signs, lesions, response to treatment/prevention. Differentiate from pantothenic acid deficiency (skin lesions).

Treatment

Addition of biotin in feed or water.

Prevention

Supplementation of diets with biotin - naturally present in many raw materials, has very low bioavailability.

Unknown

9:15 AM

اقرأ المزيد

Big Liver and Spleen Disease

Introduction

This condition was first seen in Australia in 1980. It is now known to be caused by an Avian Hepevirus. Related viruses have been reported to cause a hepatitis/splenomegaly syndrome in the USA, sub-clinical infection in pigs and Type E Hepatitis in man. The pig origin virus can cause disease in man, but avian hepeviruses are believed not to be zoonotic. The lesions are associated with deposition of antigen/antibody complexes in tissues. Only chickens are known to be naturally affected, most commonly broiler parents in lay. Natural infections have only been demonstrated in chickens over 24 weeks of age though it is possible that vertical transmission and/or infection in rear occurs with a subsequent period of latency. Transmission is usually by the faecal/oral route. Faecal contamination of drinking water is likely to be an efficient means of spread of this infection. Embryos inoculated intravenously become persistently antigen positive.

Signs

• Chronic under production or egg drops of up to 20%.
• Mortality of up to 1% per week for 3-4 weeks.
• Anaemia.
• Premature moulting.

Post-mortem lesions

• Enlarged spleen (over 1gm/kg bodyweight, often with pale foci).
• Liver usually enlarged, sometimes with subcapsular haemorrhage.
  
  Affected birds may also have:
  
• Lung congestion
• Ovarian regression
• Yolk peritonitis
• Pale foci and haemorrhages in pancreas.

Diagnosis

Typical signs and lesions. Must be confirmed by laboratory tests. Serological tests (agar gel immunodiffusion) may be used to detect either the specific antigen (which is likely to be positive first) or the antibody response to it. Elisa tests have been developed experimentally. A RT-PCR test may be used to detect viral RNA in tissues. Viral particles may be demonstrated in bile. Histopathology may also be used but the findings are not specific to this condition.

Treatment

No specific treatment known. It may be helpful to control other conditions which may be occurring at the same time. Drinking water which is well chlorinated should be helpful in reducing challenge by this route.

Prevention

Thorough cleaning and disinfection after depletion of an affected flock. Good biosecurity. All-in/all-out production.

Unknown

9:13 AM

اقرأ المزيد

external parasite Infestation

Introduction

A condition of poultry, pigeons (and mammals) caused by infestation with the external parasite Cimex lectularius. The parasites are up to 5 mm long and feed at night. It occurs mainly in subtropical and some temperate areas. Adult parasites can survive for 1?12 months in the environment without feeding. Eggs laid by the adult parasites hatch in 4?20 days, there are five nymphal stages each of which feed on birds. Growth to adult parasite takes 1?3 months, depending on temperature.

Signs

• Lack of thrift.
• Anaemia.
• Reduced production when infestation is serious.

Post-mortem lesions

• Anaemia.

Diagnosis

Identification of the parasite. Differentiate from other blood?sucking parasites.

Treatment

Appropriate insecticide treatment of the environment, in particular the cracks and crevices where the parasites hide during the daytime.

Prevention

Thorough treatment of the empty building at turn-around with an appropriate insecticide. Fumigation is also helpful.

Unknown

9:11 AM

اقرأ المزيد

Beak Necrosis

 

Introduction

A condition seen in chickens and turkeys caused by excessively fine mashed feeds.

Signs

• Feed accumulates along edges of lower beak leading to distortion and necrosis of horny tissue.
• Has been associated with curled tongue in turkeys in the past.
• This may also be associated with ulcers in the roof of the mouth (palate) which can be confused with some forms of mycotoxicosis.

Post-mortem lesions

• See signs.

Diagnosis

Clinical signs, exclusion of other causes of similar signs.

Treatment

Not usually sufficiently severe to justify medication. Mild water sanitation may help control secondary infections in the affected tissues.

Prevention

Check feed particle size by granulometry, grind less finely.

Unknown

11:53 AM

اقرأ المزيد

Flea And Tick Prevention

A person can examine their pet at home to determine if there is a need for flea and tick prevention. However, it is important to follow application directions of a product closely to avoid accidental poisoning of the pet. It may also be necessary to treat the yard and home if the pets stay outdoors most of the time. Here are some guidelines to help any pet owner with this common issue.
Use bath time to find ticks. The water on their coat makes it tough for the ticks to hide. Another way to find the pest is to examine their entire body with your hands. This can be done while petting them. However, be certain to examine the entire body and include their ears. You may have to also separate their fur in order to find any ticks that have burrowed more deeply.
Fleas are just as easy to find. Simply use a flea comb on their coat and examine closely. Even if you do not find any fleas but think there may be a problem, you can still treat them for it. However, it they continue to scratch, have hair loss, or scabs on their skin, have your veterinarian test them for mites or bacterial diseases.
Most prevention options will need to be repeated for continued control. Topical treatments are most often applied to the back of the neck to prevent dogs or cats from licking it off. Shampoos are best to use when a young animal has a severe infestation. There are also oral products that work well.
It is vital to use caution when ever using one of the flea and tick prevention products. Pets can sometimes have a reaction to the toxins used or they are sometimes accidentally poisoned. If they develop ear twitching, mild depression, diarrhea, vomiting or excessive salivation, contact your veterinarian immediately.
To prevent accidental poisoning, it is vital to follow the products directions closely. If using a spray, first apply to a grooming brush then evenly brush through the animal's coat. Use caution to not accidentally spray any product into the animal's mouth. If the product is in liquid form, do not submerge the animal into the liquid. Instead, pour it over their body and use a sponge to cover all areas.
You will probably have to also treat your entire yard if your pet stays outdoors most of the time. It is important to use a product regularly for flea and tick prevention. It will kill the larvae and eggs of the pest and hinder their return.

Unknown

1:01 PM

اقرأ المزيد

Skin Cancer In Dogs

Skin cancer in dogs is very common and is found in different forms. It is not always possible to see any changes to the cancer cell, unlike in humans where we can see changes in color etc. Therefore a biopsy is the only guaranteed way to confirm if they are benign or malignant. A biopsy is simply the removal of a small sample of the tumor which is sent off for pathology testing. If the tumor is small your vet may remove all of it to be used for the biopsy.
If the growth is larger, over an inch in diameter, then your vet will take a cell sample by aspiration. This is a simple procedure where they insert a fine needle into the tumor and withdraw a small amount of the cell for further testing.
Skin Papillomas
Skin papillomas on dogs are growths similar to warts which are usually benign and occur on the torso, on the foot pads, and underneath the nails. Canine oral papilloma virus is the usual cause of these lumps, and they tend to be found in older dogs, especially all breeds of Poodle and similar breeds of dogs.
No treatment is usually necessary other than keeping a watchful eye on them. Removal is not required unless they are causing a problem because of their location on the body. Rarely, will they become infected or bleed, but if they did removal would be recommended.
Hematomas
A hematoma is a blood clot beneath the skin, caused by a blow or contusion. These are not a skin cancer in dogs. You may need to have large ones drained. Hematomas on the ears requires special attention, please consult with your vet for advice as each case will be different.
If you find a hard mass that looks like bone then it is likely to be calcifying hematoma. They are often found near an old fracture site, and may occur as a lump on the head especially tall dogs who strike their head on the dining room table or other household furniture.
Because they have the potential turn into a canine bone cancer, calcifying hematomas should to be biopsied and possibly removed. They vary from other types of dog cancer as they are often difficult to treat and may reoccur.
Epidermal Inclusion Cysts (Sebaceous Cysts)
Another type of skin cancer in dogs is an epidermal inclusion cyst, also known as sebaceous cysts, these are common skin tumors found all over the body. Spaniels, Poodles, Schnauzers & Terriers are breeds of dogs more likely to be affected. Canine epidermal inclusion cysts form when dry secretions block hair follicles, this causes a build-up of hair and sebum (an oily/greasy matter), which leads to the formation of a cyst.
They are a dome like growth that can vary in size, anything up to an inch and a half but usually smaller. If they become infected drainage is recommended which occasionally leads to a cure. One option is to have it removed but this is rare.
Treatment and Prevention Of Skin Cancer In Dogs
Now that you are aware of the different types of dog skin cancer what should you do next?
1. Check your canine's body regularly, looking for any signs of tumors or lumps. I usually do it when I bath or groom my dog
2. Ensure your loyal companion has a check up with a veterinarian at least once a year
3. Be mindful of their diet. A good balanced diet will help prevent many ailments and help build up natural immunities to many skin problems and canine cancers.
4. Do research on common illnesses and cancers that occur in your breed of dog
5. Lots of TLC, walks and bonding. Not a cure or prevention but it will make you both feel good;

It is not possible to cover all there is to know about skin cancer in dogs in such a short article, but you can learn more by going to http://cancertreatmentfordogs.com this covers all forms of skin cancer in dogs, their treatment, prevention and onward care. Well worth investigating

Unknown

12:54 PM

اقرأ المزيد

Swollen Head Syndrome

Introduction

A viral disease of chickens, turkeys (see separate summary), guinea fowl and possibly pheasants seen in Europe, Africa, South America and North America. It is caused by a pneumovirus of the Paramyxoviridae family, first isolated from poults in South Africa in 1978. Two subgroups have been identified on the basis of the G-protein sequence: A (original UK isolates) and B (original southern Europe isolates). There is rapid lateral transmission with infection by aerosol through the respiratory route; vertical transmission is uncertain. As for many infections, fomites can be important in moving infection between farms. The incubation period is 5-7 days, morbidity is 10-100% and mortality can be 1-10%.

Signs

• Decreased appetite, weight gain and feed efficiency.
• Facial and head swelling (though this can occur in other conditions).
• Loss of voice.
• Ocular and nasal discharge.
• Conjunctivitis.
• Snick.
• Dyspnoea.
• Sinusitis.

Post-mortem lesions

• Serous rhinitis and tracheitis, sometimes pus in bronchi. If secondary invasion by E. coli then pneumonia, airsacculitis and perihepatitis.
• Congestion, oedema and pus in the air space of the skull occurs in a proportion of affected birds due to secondary bacterial infections.

Diagnosis

Clinical signs, serology, isolation of ciliostatic agent. Differentiate from Infectious Bronchitis, Lentogenic Newcastle disease, low virulence avian influenza, Ornithobacterium rhinotracheale. Serology - Elisa normally used, not all commercial kits are equally sensitive to response to both A and B challenge viruses.

Treatment

Antibiotic not very effective. Control respiratory stressors, chlorination of drinking water, multivitamins.

Prevention

All-in/all-out production, vaccination (degree of cross protection between A and B types remains to be established). Live vaccines can reduce clinical signs and adverse effects, inactivated vaccines may be used in breeders prior to lay.

Figure 10. Pus in skull bones. This is a common sequel to avian pneumovirus infection in both chickens and turkeys.

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3:44 PM

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Avian Leukosis, Lymphoid Leukosis

Avian Leukosis, Lymphoid Leukosis, Leukosis/Sarkoma Group

 

Introduction

A complex of viral diseases with various manifestations such as lymphoid leukosis, myeloblastosis (see Sero-type J), erythroblastosis, osteopetrosis, myxosarcomas, fibrosarcomas, other tumours. It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock - egg layers are generally more susceptible to lymphoid leukosis.

Morbidity is low but mortality high. Mortality tends to be chronically higher than normal for a prolonged period. Egg production is somewhat reduced. There may be increased susceptibility to other infectious diseases due to damage to the immune system. Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers), lateral transmission is poor but infection may occur by the faecal-oral route, especially in young birds. In lymphoid leukosis the incubation period is about 4-6 months; it may be as short as 6 weeks for some of the other manifestations. The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants.

Signs

• Depression.
• Emaciation.
• Loss of weight.
• Persistent low mortality.
• Enlargement of abdomen, liver or bursa.
• Many are asymptomatic.

Post-mortem lesions

• Focal grey to white tumours, initially in the bursa, then liver, spleen, kidney etc. Liver may be very large.
• Microscopic - cells lymphoplastic

Diagnosis

History, age, lesions, cytology. Differentiate from Marek's disease, coligranuloma.

Treatment

None.

Prevention

Good hygiene, all-in/all-out production, control arthropods, eradication - checking of antigen in the albumen is a basis for eradication (see Sero-type J for details).

Figure 9. Diffuse lymphoid tumours in an enlarged liver from a mature broiler parent hen. This was a case of Myelocytoma Avian Leukosis (Sero-type J)

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10:33 AM

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Avian Leukosis

 

Avian Leukosis (Serotype J), Myelocytomatosis

Introduction

Caused by an avian retrovirus. This condition has until now been seen only in meat-type chickens, with considerable strain-to-strain variation. It has occured in Europe, North and South America. Morbidity is low, though there is high mortality of affected birds.

Transmission is by congenital infection from antibody-negative females, bleeding and vaccination needles; lateral transmission by faecal-oral route (this declines as the bird ages). The incubation period is 10-20 weeks. Congenitally infected birds tend to remain antibody negative, shed virus and develop tumours. Virus survival is poor but sufficient to allow cross contamination in hatcheries and on farm in rear.

Signs

• Depression.
• Emaciation.
• Loss of weight.
• Persistent low mortality.
• Enlargement of abdomen, liver.
• Many are asymptomatic.

Post-mortem lesions

• Liver enlargement, often with tumour foci.
• Splenomegaly and enlarged kidneys also occur.
• Most characteristically are chalky white tumours in the bone marrow, particularly of the sternum, ribs, sacral joint.
• Microscopic - tumours usually contain well-differentiated myelocytes. Two cell types may be found in the same tumour.

Diagnosis

History, age, lesions, histology, ultimately identification of virus by isolation and/or PCR. Differentiate from Marek's disease, Lymphoid Leukosis.

Treatment

None.

Prevention

Checking of antigen in the albumen is a basis for eradication - most but not all, birds with egg antigen will be antibody negative. 'Shedders' - 80% produce infected chicks, 'non-shedders' - only 3% produced infected chicks. PCR testing of embryonally infected chicks using DNA testing is uniformly positive for blood and faecal samples. There is also evidence that it is slightly more sensitive than conventional testing. Serology - an Elisa test is aviailable to identify antibody positive birds. Prevent/ reduce cross-infection in hatchery and on farm.

Critical hatchery practices:

• Separate infected and uninfected lines.
• Handle clean lines before infected lines, preferably on separate hatch days and in separate machines.
• Separation in vaccination.
• Minimise stress.

Farm practices:

• Brood and rear lines separately and maintain separate for as long as possible.
• Minimise group sizes.
• Delay live vaccine challenges.
• Avoid migration errors (birds unintentionally moving between pens).

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10:27 AM

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Avian Influenza-Highly Pathogenic

 

Avian Influenza-Highly Pathogenic (HPAI), Fowl Plague

Introduction

One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE, the equivalent of the World Health Organisation for animal diseases. This viral disease can cause exceptionally high mortality, especially in turkeys. In addition official control measures disrupt trade in poultry products from affected areas. The cause is a virus, Orthomyxovirus type A, its pathogenicity is variable, and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). Highly pathogenic forms are usually of the H groups 5 and 7 and may now be identified (if H5 or H7) by the presence of a sequence at the haemagglutinin cleavage site that codes for multiple basic amino acids.

The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1.2 . This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. The higher the proportion of the chickens dying or showing signs the higher the IVPI. The virus infects chickens, turkeys, ducks, partridges, pheasants, quail, pigeons, and ostriches. Effectively all birds are considered to be at risk of infection. Apathogenic and mildly pathogenic influenza A viruses occur worldwide.

Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. Outbreaks due to HPAI were recorded in the Pennsylvania area, USA, in the years 1983-84. More recently outbreaks have occurred in Australia, Pakistan, Mexico and, from December 1999, in northern Italy. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania, Italy). Because of this, and the high mortality that 'low-path' AI can cause in turkeys, OIE and other bodies are currently examining ways to improve control of LPAI. See current OIE records for up to date information on distribution of HPAI. Morbidity is high but mortality usually relatively low, 5-50%.

The route of infection is probably oral initially, but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. Transmission is by direct contact with secretions from infected birds, especially faeces, waterfowl, equipment, clothing, drinking water. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. Avirulent in one species may be virulent in others. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. The virus is moderately resistant, can survive 4 days in water at 22°C, over 30 days at 0°C. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min, by acid pH, by oxidising agent and by formalin and iodine compounds. It can remain viable for long periods in tissues. Infections with other pathogens (e.g. Pasteurella) may increase mortality, even with 'low pathogenicity' strains.

Avian Influenza is a potential zoonosis. It can result in inapparent infection, conjunctivitis or severe pneumonia. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets.

Signs

• Sudden death.
• Marked loss of appetite, reduced feed consumption.
• Cessation of normal flock vocalisation.
• Drops in egg production.
• Depression.
• Coughing.
• Nasal and ocular discharge.
• Swollen face.
• Cyanosis of comb/wattles.
• Diarrhoea (often green).
• Nervous signs such as paralysis.

Post-mortem lesions

• Inflammation of sinuses, trachea, air sacs and conjunctiva.
• Ovarian regression or haemorrhage.
• Necrosis of skin of comb and wattles.
• Subcutaneous oedema of head and neck.
• Dehydration.
• Muscles congested.
• Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract.
• Turkey lesions tend to be less marked than those of chickens, while ducks may be symptomless, lesionless carriers of highly pathogenic virus.

Diagnosis

A presumptive diagnosis may be made on history and post­mortem lesions. Confirmation is by viral isolation in chick embryo, HA+, NDV-, DID+. Commercial Elisa test kits are now available. However, as with many such tests occasional false positive reactions can occur. The agar gel precipitation test is non-group-specific and is used to confirm any positives. Differentiate from Newcastle disease, fowl cholera, infectious laryngotracheitis, other respiratory infections, bacterial sinusitis in ducks.

Treatment

None, but good husbandry, nutrition and antibiotics may reduce losses. Eradication by slaughter is usual in chickens and turkeys.

Prevention

Hygiene, quarantine, all-in/all-out production, etc. Minimise contact with wild birds, controlled marketing of recovered birds. Vaccination is not normally recommended because, although it may reduce losses initially, vaccinated birds may remain carriers if exposed to the infection. Vaccines have been used in recent outbreaks in Mexico and Pakistan. To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). In outbreaks a regime of slaughter, correct disposal of carcases, cleaning, disinfection, isolation, 21-day interval to re-stocking should be followed. Survivors can be expected to have a high degree of immunity but may harbour virulent virus.

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10:24 AM

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