Yorkshire Terrier Medical Information

What on Earth are Coccidia?

Coccidia are single celled organisms that infect the intestine. They are microscopic parasites detectable on routine fecal test in the same way that worms are but Coccidia are worms and they are not visible to the naked eye. Coccidia infection causes a water diarrhea which is sometimes bloody and can even be a life threatening problem to an especially young or small pet.

Cocysts are passed in stool. In the outside world, cocysts begins to mature or “sporlate”.  After they have adequately matured, they become infective to a host (dog or cat) that accidentally swallows them. They are swallowed when a pet grooms/licks the dirt off itself. In some cases, sporulated occysts are swallowed my mice and the host is infected when it eats the mouse.  Coccidia infection is especially common in young animals hosted in groups (shelters, rescue areas, kennels, etc.) This is a common parasite and is not necessarily a sign of poor husbandry, dirty living conditions, or neglect, especially in kennel; situations.

The sporulated cost breaks open and releases eight sporozoites. These sporozites each finds an intestinal cell and begin to reproduce inside it. Ultimately, the cell is so full of what are called”merozites” that it burst releasing the merozites which seek out their own intestinal cells and the process begins again. It is important to note how thousands of intestinal cells can become infected and destroyed as a result of accidentally swallowing a single occyst. As the intestinal cells are destroyed in larger and larger numbers, intestinal function is disrupted and a bloody, water diarrhea results. The fluid loss can be dangerously dehydrating to a very young or small pet.

A routine fecal test is a good idea for any new puppy or kitten whether there are signs of diarrhea or not as youngsters are commonly parasitized. This sort of test is also a good idea for any patient with diarrhea. Coccidia are microscopic and a fecal test is necessary to rule them out.  It should be noted that small numbers of coccidian can be hard to detect so just because a fecal sample test negative, this does not mean that the pet is not infected. Also, small numbers of coccidian in the stool are not a problem unless there are other symptoms such as diarrhea that are present. Sometimes several fecal tests are performed, especially in a young pet with a refractory diarrhea, and parasites may not be evident until later in the course of the condition.

Stress is a large factor in coccidian. The stress of being moved to a new home, being allowed to play too much and become overtired, a mild cold, or just being held too much can weaken the young, immature immune system and allow the coccidian to begin to multiply in numbers that would be dangerous to a very small pet.

We do not have any medicine that will kill coccidian; only the patient’s immune system can do that.  But we can give medicine called “coccidiostats” which can inhibit the coccidian reproduction.  Once the numbers stop expanding, it is easier for the patient’s immune system to “catch up” and wipe the infection out.  This also means though, that the time it takes to clear the infection depends on how many coccidia organisms there are to start with and how strong the patient’s immune system is.  A typical treatment course last about a week or two, but it is important to realize that the medications should be given until the diarrhea resolves plus an extra couple of days.  Medicine should be given for at least five days total, sometimes courses as long as a month is needed.  Albon (sulfa drug) or Amprollium is the most common coccidiostats used to treat coccidian infections.

The use of sulfa drugs in pregnancy can cause birth defects. The over use of Sulfa Drugs can also lead to false positive test results for urine glucose level.

While there are species of coccidian that can infect people (Toxoplasma and Cryptosporidium for example). The Isospora species of dogs and cats are not infective to people. Other pets may become infected from exposure to infected fecal matter but it is important to note that this is usually an infection of the young (i.e. the immature immune system tends to let the coccidian infection reach large numbers where the mature immune system probably will not). In most cases, the infected new puppy or kitten does not infect the resident adult animal.

Giardia and Zoonotic Disease

The incidence of Infection in Humans and Cats and Dogs: 

• Giardia duodenalis (also G. lamblia) is recognized as the most common human intestinal parasite.  Annually, in the U.S., it is estimated that 2.5 million cases of giardiasis occur in humans.
• As many as 25% of cats and dogs are infected with Giardia duodenalis.
• Since 1979, the World Health Organization has recommended that giardiasis be recognized as a zoonotic disease

Transmission of Giardia between Animals and Humans Occure Easily:

• Fecal-oral transmission of Giardia is common in both animals and humans.
• Processed drinking water, raw municipal water and back-country streams and lakes all may contain infective Giardia cysts due to contamination of water sources with human effluent and/or infected animal feces.
• Ingestion of as few as 10 cysts can lead to infection – the number of cysts in raw and processed drinking water samples can exceed 1000 cysts/liter.
• The risk of Giardia infection is enhanced with high population density, poor hygiene and certain feeding behaviors.
• The prevalence of giardiasis is higher in children, as they are immunological naïve and more prone to ingestion of fecal matter.  Immunocompromised adults are also at high risk for infection.

Clinical Symptoms and Diagnosis of Giardiasis:

• Infection with Giardia can be asymptomatic (no symptoms) or can cause severe clinical symptoms of diarrhea, abdominal pain and bloating in both humans and animals.
• Giardiasis is often difficult to diagnose due to inappropriate methodology and intermitten fecal shedding of Giardia cysts (50-70% of cases).
• To diagnose using fecal floatation, 2 grams of feces should be mixed with concentrated Zinc sulfate or sucrose solution and centrifuged to concentrate Giardia cysts.
• There also are humans ELISA test kits available that can detect Giardia antigens from trophozoites in feces.
• Microscopic examination of fresh feces mixed with a drop of normal saline may reveal the motile trophozoites.

Treatment and Control of Giardia:

• All animals with giardiasis should be treated, whether or not they show clinical symptoms.
• Infected animals are a source if infection for other animals and humans with whom they come into contact.
• The feces of infected animals may also contaminate the environment, leading to infection of water sources.
• Reinfection in animals usually occurs, unless infective cysts are removed from the environment.
• Bathing of infected animals and thorough cleaning and disinfecting of the animals environment should be done.
• Quaternary ammonium compounds, high concentrations of chlorine, and other phenolic compounds will inactivate Giardia cysts in the environment.
• Traditional treatment using metronidazole can have undesirable side effects, and development of resistance to metronidazole has been documented.
• Use of albendazole to treat Giardiasis has been associated with severe bone marrow suppression and birth defects in pregnant dogs.

This is a central nervous system disorder caused by low blood sugar levels.  It occurs mainly in toy breeds between 6 and 16 weeks of age.  Stress is the leading cause.

The first signs of listlessness and depression.  They are followed by muscular weakness, vomiting and/or diarrhea, tremors (especially in the facial muscles), and later convulsions, coma, and probably death.  The entire sequence of symptoms is not always seen.  The dog may simply appear to be depressed or he may be weak, wobbly and jerky, or he may be found stiff, unable to coordinate or in a coma.

Hypoglycemia can occur without warning when is placed in a new home or while being shipped.  It might appear after a puppy misses a meal, chills, becomes exhausted from too much playing, or has a digestive problem.  These problems cause an added strain on the energy reserves of the liver and bring on the symptoms.

TREATMENT; Begin at once! 
Treatment is directed at restoring blood levels of glucose.  Give the puppy a mouthful of Nutri-Stat.  If he cannot swallow it all at once, it will begin to absorb under the tongue to begin bringing him back to conscious state so that he will be able to swallow the rest.  When he can swallow, give him water (about 1 cc at a time so he doesn’t choke).  Continue to give him Nuti-Stat and water about every 10 minutes.  Until he is conscious and moving about.
CALL US IMMEDIATELY!  If we cannot be reached, call your Vet immediately.  If the puppy does not respond, call your emergency Animal Vet Clinic. The puppy will need sub-q injections of lactated ringer’s solution every 4 hours for about 2 days to restore it to a normal state.  He may also need some antibiotics to combat secondary infections that can arise from the lowered immune system that results from the hypoglycemia.

If you do not have Nuti-Stat, honey or syrup can be used until you get some Nuti-Stat.  The dose is 1 cc every 10 minutes till recovered.  You will also need to begin some pepto bismol to help keep him from getting bad diarrhea.  The large dose of Nuti-Stat or syrup will probably cause some diarrhea to occur, but it is usually self limiting.

Prevent recurrent attacks by making sure the puppy eats at regular intervals.  He should have dry food available at all times and should be fed canned food at least 2 times a day.  A daily vitamin should be given, (Nuti-Stat 1 cc 2 or 3 times a day) also cottage cheese or yogurt can be added to the diet.

Owners of toy puppies should not allow them to become overtired or chilled.  Play time should be limited and controlled to prevent undue stress and tiring.  Hypoglycemia must be offset by frequent feedings.  A puppy, who does not eat frequently, for whatever reason, is heading for trouble.

WE DO NOT GUARANTEE AGAINST THIS CONDITION!

Patella Luxation is common in Yorkies. It is therefore advisable that breeders have their dogs and puppies tested by a vet.

What is it?
Luxating means out of place, or dislocated. The patella is the equivalent to the human kneecap and part of the stifle structure, and therefore a luxating patella is a kneecap that moves out of its normal location. The patella normally moves up and down in a groove in the lower femur bone called the trochlear groove. In patella luxation the groove is often shallow and this shallow groove prevents the patella from sitting deeply, predisposing it to dislocation. A patella that is not stable but does not slip out of joint is said to be subluxating, while one that comes out of joint on its own is said to luxate.

There are two types of luxation, medial and lateral. Medial luxation is the most common and is where the patella dislocates to the inside of the knee. One knee can be more severely affected than the other. This type of luxation is mainly congenital (present at birth) and trauma is not usually associated with it.

With lateral luxation the patella dislocates to the outside of the knee. Lateral patellar luxation can be congenital or the result of trauma to the knee. In some cases the patella can luxate both medially and laterally. Again, this disorder can affect one or both knees and to varying degrees.

What are the Symptoms?
Signs of luxation may appear as early as weaning or may go undetected until later in life. Signs include intermittent rear leg lameness, often shifting from one leg to the other, and an inability to fully extend the stifle. The dog may frequently stop to stretch his rear leg behind him to allow the patella to pop back into its normal groove. Mildly affected animals can have a hopping or skipping action. This is due to the patella luxating while the dog is moving and by giving an extra hop or skip the dog extends its stifle and is often able to replace the patella until the next luxation, when the cycle repeats.

Diagnosis:
A veterinarian can usually confirm diagnosis by manipulating the stifle joint and pushing the patella in and out of position. Thiscan be done as early as 8 weeks of age to ensure that congenital patella luxation is not present before the puppy leaves for his new home. This type of examination is best left to the veterinarian, as an overzealous examination can stretch the ligaments.

The degree of patella luxation is graded from 1 to 4 depending on the relative ease with which the patella luxates. Grade 1 is the mildest and grade 4 the most severe. With grades 1 and 2 patella luxation the dog may not show any symptoms and can be incidental findings in mature dogs who have never been lame. Grade 3 and 4 dogs are usually lame. Severe cases may develop abnormal growth of the long bones of the leg or a non-functional knee.

Grade 1:
Occasional carrying of the leg is seen, often described as skipping or hopping, which may be transient, often returning to normal by itself. Your veterinarian may easily luxate the patella manually and return it to its normal position. Pain may be evident only when the knee cap is luxated.

Grade 2:
The frequency of luxation increases, becoming more or less permanent. The dog will usually carry its leg, but will occasionally bear weight on it. When palpated by the veterinarian, a dry, crackling sensation (crepitation) may occur in the joint. A grade 2 luxation can increase in severity, and if not surgically treated, can develop into degenerative joint changes.

Grade 3:
Permanent dislocation that occurs though weight bearing may still be possible, however the stance will appear somewhat crouching or bowlegged. Surgical intervention should not be delayed, especially if this is found in a young, growing dog. Rapid growth of abnormalities results in progressive deformities.

Grade 4:
Permanent luxation, with the affected limb always being carried, creates a bowlegged / crouching stance. Early surgery is strongly recommended at this stage for bone deformities of the femur and tibia may occur.

What Causes It?
Patella luxation is strongly suspected of being inherited, but it can also be caused by trauma.

When the luxation is from trauma, something has occurred that has caused the knee to be forced out of normal alignment. Usually the traumatic injury occurs when the dog's leg gets caught somehow and he struggles to pull free. Or during an overly enthusiastic playtime when the playmate grabs the foot and holds tight while the excited puppy tries to get away. Any other similar accident can permanently injure this small joint.

If the luxation is believed to be of a genetic nature, it is due to an abnormal development of the leg. The possible mode of inheritance is at present undetermined, but it is believed that it may be polygenic. This means that any number of genes may be involved, and that dogs are not "carriers" as such but it is merely an unfortunate specific combination of certain genes from the parents that produce patella luxation.

As with all polygenic traits, affected dogs should not be bred from as the risk of producing puppies with patella luxation would then be increased.

How is it treated?
Treatment is based on the severity of signs as well as the dog's age and weight, and ranges from rest (decreasing your pet's activity for 1-2 weeks) to surgical reconstruction of the knee joint.

Grade 1 luxations may respond well to anti-inflammatory therapy and restricted exercise. These may or may not progress to worsening grades.

Grades 2 through 4 luxations tend to require surgical corrections. The worse the luxations the more reconstructive surgery required to provide a functional joint.

“Trachea” is the scientific name for “windpipe,” the tube that connects the nose, mouth, and throat to the lungs. The trachea is meant to be a fairly rigid tube. It consists of muscle connecting a group of cartilage rings. The rings are actually not complete circles; they form a “C” with the open end of the “C” facing towards the animal’s back. This muscle covering the open end of the “C” is called the “tracheal membrane.”

When the diaphragm (the flat muscle separating the abdomen from the chest cavity) flattens and the intercostal muscles (the muscles between the ribs) move, air is sucked into the lung. The muscles move the opposite direction and air is pushed out of the lung. The trachea serves as a pipeline bringing air into the chest. Part of the trachea is in the throat but it extends into the chest as well so that we can look at the trachea as having an “intrathoracic” portion and an “extrathoracic” portion.

WHY WOULD A TRACHEA COLLAPSE?

Tracheas collapse due to a flattening of the “C” cartilage due to weak cartilage. When the “C” loses its curvature, the tracheal across the gets loose and floppy. Instead of being a tight muscle covering, the membrane moves as air passes through the trachea. When air rushes into the chest, the membrane of the intrathoracic trachea balloons outward and when air rushes out, the membrane of the intrathoracic trachea droops down into the “C” cartilage causing an occlusion. The tickling sensation of the membrane touching the tracheal lining generates coughing and if the obstruction interrupts breathing, the patient may become distressed. If the collapse is in the extrathoracic (also called the “cervical”) trachea, the opposite occurs; the collapse occurs during inhalation and the ballooning during exhalation.

Panting or rapid breathing for any reason makes the collapse and anxiety worse which unfortunately tends to generate more rapid breathing and a vicious cycle of distress.

Making things worse still, is the inflammation generated in the trachea. The collapse creates increased secretion and inflammation thus promoting yet more coughing which creates yet more inflammation Ultimately the tissue of the trachea changes and loses its normal characteristics and the condition gets
worse and worse.

The trachea may be collapsed along its entire length, only in the intrathoracic section, or only in the extrathoracic section. Most commonly the collapse is at its worse right where the trachea enters the chest.

WHAT ANIMALS ARE AFFECTED?

The victim is almost always a toy breed dog, especially poodles, Yorkshire terriers, and Pomeranians. The disease usually becomes problematic in middle age but can occur at any age. The cartilage defect that leads to the flattened “C” rings seems to be hereditary. Many dogs with collapsed tracheas do not ever show symptoms, however, until a second problem complicates things. Factors that bring out symptoms might include:

• Obesity

• Anesthesia involving the placement of an endotracheal tube

• Development of kennel cough or other respiratory infection

• Increased respiratory irritants in the air (cigarette smoke, dust, etc.)

• Heart enlargement (the heart can get so big that it presses on the trachea)
  

If a secondary factor such as one of those listed above should occur and make a previously incidental collapsed trachea a problem, often removal of the secondary factor (weight loss program, getting an air filter, etc.) may clear up the symptoms of the collapsed trachea.

TREATMENT:
The following steps are often helpful in long term management of the tracheal collapse patient:

• If any of the above listed secondary problems are of concern, they must be addressed. This may mean that the owner gives up cigarettes or that the dog goes on a formal weight loss program or other treatment to resolve the exacerbating problem.

• Dogs with collapsed tracheas become unable to efficiently clear infectious organisms from their lower respiratory tracts. Antibiotics may be needed to clear up infection.

• Cough suppressants such as Hydrocodone or Torbutrol may be handy.

• Corticosteroids such as prednisone and related hormones cut secretion of mucus effectively but are best used on a short term basis only due to side-effects potential. Long term use may promote infection and weaken cartilage further.

• Airway Dilators such as theophylline or terbutaline are controversial as they may dilate lower airways but not the actual trachea. By dilating lower airways, however, the pressure in the chest during inhalation is not as great and the trachea may not collapse as greatly.

EMERGENCY:
The patient’s distress can reach a level so severe that the normally pink mucous membranes become bluish and collapse can result. When this occurs, tranquilization is helpful to relieve the anxiety that perpetuates the heavy breathing and coughing. Oxygen therapy and cough suppressants also help. If the patient reaches the point where distress seems extreme or if collapse results, treat this a emergency and rush the pet to emergency veterinary care.

SURGERY?
If medical management does not produce satisfactory results, it is possible that surgery may be of benefit. Basically, a rigid prosthesis is placed and bonded around the trachea effectively creating a non-collapsible tube. This is largely effective as long as the portion of trachea which is collapsed is external to the chest. Should the intrathoracic trachea be involved, the surgery becomes far less successful, more expensive, and the prosthesis must be ordered according to the specific patient’s measurements.

In all surgery cases, the younger the patient, the more successful the surgery is likely to be with success dropping off in patients over age 6 years. Severity of the collapse prior to surgery is not a tremendous factor in obtaining a successful outcome.

This type of surgery requires a surgery specialist. If one is not on staff or cannot be scheduled, referral can be arranged.

There are several types of mites that can invade the ear canals of dogs, puppies, cats, and kittens. The same mite can affect both dogs and cats. In the puppy and kitten, the most common ear mite is Otodectes cynotis. It is not important in the diagnosis and treatment of ear mites to identify the exact scientific type of mite. Regardless of the exact mite species involved, we usually refer to mites of the ear canal simply as ear mites. Contrary to popular belief, however, is the fact that ear mites can live anywhere on the animal's body.

How are the mites transmitted?
Ear mites are extremely contagious. They can be passed from the mother animal to her offspring. Additionally, the mites are easily spread to other pets within the household including cats, dogs, rabbits, hamsters, gerbils, mice, ferrets, etc. Humans are not affected.

What are the symptoms?
Puppies and kittens with ear mites will scratch around their ears and/or shake their heads. The amount of scratching and shaking depends on the severity of the mite infestation. With more advanced infestation, the ear canals will bleed and either fresh or dried blood will appear inside the canal. Dried blood resembles coffee grounds. If you peer into your pet's ears and notice a build-up of a material that looks like 'coffee grounds,' then your pet probably has ear mites, although a bacterial and/or yeast infection is also a possibility.

Ear mites are very common, but still serious. Left untreated, they severely damage the ear canals and eardrum and can cause permanent hearing loss.

If mites spread out of the ears to other areas of the body, the animal may or may not scratch the area.

What is the management?
Various commercial ear preparations are available to kill the mites. These products contain an insecticide, usually pyrethrin. Ear products without an insecticide will not kill the mites. Ivermectin, fipronil (Frontline), and selamectin (Revolution) have also been used by some veterinarians. (Milbemycin (Interceptor) and Acarexx, a form of ivermectin have recently been approved for the treatment of ear mites in cats.) Depending upon the medication used, the ears may need to be treated two to four weeks until all mites are killed. As previously mentioned, many ear mites live all over the body, including the feet and tail. These areas should also be treated. Most products designed for fleas and ticks such as sprays, dips, and shampoos, which contain one of the above ingredients will be effective. Be sure to use products approved for use on dogs, and to treat the tail. This is because while sleeping, the tail is curled around the puppy's body where it lies in close contact with the ear. Because mites are very easily transferred between pets, it is best if all pets in the household receive simultaneous treatment. Most types of mites do not survive long off the pets, so the treatment of the house and yard is usually not necessary.

Can I get ear mites from my pet?
Ear mites are not considered to be a zoonotic disease (disease which can be transmitted from animals to humans).

A portosystemic shunt (PSS), also known as a liver shunt, is a bypass of the liver by the body's circulatory system. It can be either a congenital (present at birth) or acquired condition.

Congenital PSS is a hereditary condition in dogs and cats, its frequency varying depending on the breed. The shunts found mainly in small dog breeds such as Miniature Schnauzers and Yorkshire Terriers, and in cats such as Persians, Himalayans, and mix breeds are usually extrahepatic (outside the liver), while the shunts found in large dog breeds such as Irish Wolfhounds and Labrador Retrievers tend to be intrahepatic (inside the liver).

Acquired PSS is uncommon and is found in dogs and cats with liver disease such as cirrhosis causing portal hypertension, which is high blood pressure in the portal vein.

Pathology:
Congenital PSS is caused by the failure of the fetal circulatory system of the liver to change. Normally, the blood from the placenta bypasses the liver and goes into circulation via the ductus venosus, a blood vessel found in the fetus. A failure of the ductus venosus to close causes an intrahepatic shunt, while extrahepatic shunts are usually a developmental abnormality of the vitelline veins, which connect the portal vein to the caudal vena cava. Thus in the juvenile and adult animal with PSS, blood from the intestines only partly goes through the liver, and the rest mixes into general circulation. Toxins such as ammonia are not cleared by the liver. Most commonly, extrahepatic shunts are found connecting the portal vein or left gastric vein to the caudal vena cava.

Congenital shunts are usually solitary. Acquired shunts are usually multiple, and are caused by portal hypertension in dogs with liver disease. This is most commonly seen in older dogs with cirrhosis, but may also be seen in younger dogs with liver fibrosis caused by lobular dissecting hepatitis.

Symptoms and diagnosis:
Symptoms of congenital PSS usually appear by six months of age and include failure to gain weight, vomiting, and signs of hepatic encephalopathy (a condition where toxins normally removed by the liver accumulate in the blood and impair the function of brain cells) such as seizures, depression, tremors, drooling, and head pressing. Urate bladder stones may form because of increased amounts of uric acid in circulation and excreted by the kidneys. Initial diagnosis of PSS is through laboratory bloodwork showing either elevated serum bile acids after eating or elevation of fasting blood ammonia levels, which has been shown to have a higher sensitivity and specificity than the bile acids test. Rectal portal scintigraphy using 99mtechnetium pertechnetate, a technique of imaging involving detection of gamma rays emitted by radionuclides absorbed through the rectum and into the bloodstream, demonstrates the blood vessel bypassing the liver. Surgery definitively shows the shunt if it is extrahepatic.

Treatment:
Surgical treatment is best, when it can be performed. Pressure within the portal vein is measured as the shunt is closed, and it must be kept below 20 cm H2O or else portal hypertension will ensue. Complete closure of extrahepatic shunts results in a very low recurrence rate, while incomplete closure results in a recurrence rate of about 50 percent. However, not all dogs with extrahepatic shunts tolerate complete closure (16 to 68 percent). Intrahepatic shunts are much more difficult to surgically correct than extrahepatic shunts due to their hidden nature, large vessel size, and greater tendency toward portal hypertension when completely closed. When surgery is not an option, PSS is treated as are other forms of liver failure. Dietary protein restriction is helpful to lessen signs of hepatic encephalopathy, and antibiotics such as neomycin or metronidazole and other medicines such as lactulose can reduce ammonia production and absorption in the intestines. The prognosis is guarded for any form of PSS.

Heredity:
The intrahepatic shunts found in large dog breeds are passed on in a simple autosomal recessive way, while the extrahepatic shunts of the small breeds are inherited on a polygenic basis.