Tapeworms - most often tape worms are contracted by a dog that eats an infected flea. So, while treating the tape worm problem, the flea problem must also be treated. Tape worms are not often seen on fecal exam, but if your dog or puppy has them,you will notice the segments, which look like grains of rice flattened out, aroundthe anus.

Roundworms - probably the most common worm that affects dogs. Most puppies have them in their intestines, and so breeders treat the puppies as soon as safe to do so. Roundworms are contracted by eating infected soil and feces. Causes diarrhea, vomiting and digestive upset. They can also harm the liver and lungs.

Hookworms - these worms hook onto the intestine of the dog and suck the blood, hence the name. They can be contracted by eating contaminated soil or feces. They can migrate to the lungs and the dog will contract bronchitis or pneumonia. They are more common in young puppies than in adult dogs.

Whipworms - they have a three-month life cycle. Dogs infected with them may have bloody diarrhea with mucus. The colon makes mucus to lubricate the stools, but whipworms irritate the lining of the colon, making it discharge the mucus. It is difficult to get rid of a whipworm infestation in a lawn.

Heartworms - they have a five-year life cycle. Dogs get them from the bite of an infected mosquito. They lodge in the heart and grow. It is imperative to use preventative measures to insure a dog against this dreaded infestation. Treatment, if caught early, is pretty straight-forward, but if caught after symptoms occur (coughing, exhaustion, weight loss), treatment is expensive and difficult.

Coccidiosis - another organism that inhabits the intestinal tract of dogs and puppies. It is not always seen on fecal examination. Bloody diarrhea is seen with the infestation. Recurrence is common unless surrounding areas are disinfected. The effects are most often seen in puppies, although adult dogs can harbor the organism and symptoms are not always apparent unless the dog is under stress.

Giardiasis - an organism which infects the digestive system of dogs. It can be transmitted to people, too. Water supplies can harbor it.

Fleas - well, pretty much everyone knows what a flea is. So lets talk about fighting them. A flea on your pet can mean that there are eggs on your pet and in your home. Likely they are in the bedding of the dog. Cleaning the pet's bedding on a regular basis and treating with a long-lasting larvicide is recommended. Treat the outdoors, too. Your veterinarian can recommend products that contain insect growth regulators.

Ticks - ticks can cause disease, and anemia. There are many ways to remove a tick. One easy way is to grasp the entire visible part of it with tweezers and pull it straight out.

Sarcoptic Mange - the mites are contagious to humans but do not live long on humans. It is highly contagious to other dogs. Intense itching results, along with hair loss, red bumps and crusty skin.

Demodetic Mange - passed from the mother to her puppies. It affects the puppies/dogs up to one year old. Yellow scales, looking like dandruff, are seen.

Mites - also see are "ear mites." You will see the black droppings of the mites in the ear canal. These are contagious. There is a bad smell. It can cause tear staining, too. See your veterinarian for the treatment of these mites.

Lice - I've never heard of a dog with lice but they can certainly get them. If your child picked them up at school, then check your Maltese for them, too. They suck the blood. You will need to treat the dog for lice just like in humans.

Patella problems are very common in small breeds of dogs. Maltese are no exception. The problem can arise from something inherited and present at birth, or it can be the result of injury. Keeping your Maltese in good weight, and keeping him/her from jumping from extremely high areas, is a good idea.

To get a good idea of patellar luxation, I am adding information gathered from the OFA (Orthopedic Foundation for Animals). www.ofa.org/patluxgeninfo.html

What is patellar luxation?
The patella/kneecap, is part of the stifle joint (knee). In patellar luxation, the kneecap luxates, or pops out of place, either in a medial or lateral position.

Bilateral involvement is most common, but unilateral is not uncommon. Animals can be affected by the time they are 8 weeks of age. The most notable finding is a knock-knee stance. The patella is usually reducible, and laxity of the medical collateral ligament may be evident. The medial retinacular tissues of the stifle are often thickened, and the foot can be seen to twist as weight is placed on the limb.

Although the luxation may not be present at birth, the anatomical deformities that cause these luxations are present at that time and are responsible for subsequent recurrent patellar luxation. Patellar luxation should be considered an inherited disease.

Clinical Signs:
Three classes of patients are identifiable:
1. Neonates and older puppies often show clinical signs of abnormal hind-leg carriage and function from the time they start walking; these present grades 3 and 4 generally.

2. Young to mature animals with grade 2 to 3 luxations usually have exhibited abnormal or intermittently abnormal gaits all their lives but are presented when the problem symptomatically worsens.

3. Older animals with grade 1 and 2 luxations may exhibit sudden signs of lameness because of further breakdown of soft tissues as a result of minor trauma or because of worsening of degenerative joint disease pain.

Signs vary dramatically with the degree of luxation. In grades 1 and 2, lameness is evident only when the patella is in the luxated position. The leg is carried with the stifle joint flexed but may not be touched to the ground every third or forth step at fast gaits. Grade 3 and 4 animals exhibit a crouching, bowlegged stance withthe feet turned inward and with most of the weight transferred to the front legs.

Permanent luxation renders the quadriceps ineffective in extending the stifle. Extension of the stifle will allow reduction of the luxation in grades 1 and 2. Pain is present in some cases, especially when chondromalacia of the patella and femoral condyle is present. Most animals, however, seem to show little irritation palpation.

Grades of Patellar Luxation:
The Patellar Luxation Database is for dogs 12 months and over. Examinations performed on dogs less than 12 months will be treated as Consultations and no OFA breed numbers will be assigned.

A method of classifying the degree of luxation and bony deformity is useful for diagnosis, and can be applied to either medical or lateral luxations by reversing the medial-lateral directional references. The position of the patella can easily be palpated starting at the tibial tubercle and working proximal along the patellar ligament to the patella.

Grade 1
Manually the patella easily luxates at full extension of the stifle joint, but returns to the trochlea when released. No crepitation is apparent. The medial, or very occasionally, lateral deviation of the tibial crest (with lateral luxation of the patella) is only minimal, and there is very slight rotation of the tibia. Flexion and extension of the stifle is in a straight line with no abduction of the hock.

Grade 2
There is frequent patellar luxation, which, in some cases, becomes more or less permanent. The limb is sometimes carried, although weight bearing routinely occurs with the stifle remaining slightly flexed. Especially under anesthesia it is often possible to reduce the luxation by manually turning the tibia laterally, but the patella reluxates with ease when manual tension of the joint is released. As much as 30 degrees of medial tibial torsion and a slight medial deviation of the tibial crest may exist. When the patella is resting medially the hock is slightly abducted. If the condition is bilateral, more weight is thrown onto the forelimbs.

Many dogs with this grade live with the condition reasonably well for many years, but the constant luxation of the patella over the medial trochlear ridge of the trochlea causes erosion of the articulating surface of the patella and also the proximal area of the medial lip. This results in crepitation becoming apparent when the patella is luxated manually.

Grade 3
The patella is permanently luxated with torsion of the tibia and deviation of the tibial crest of between 30 degrees and 50 degrees from the cranial/caudal plane. Although the luxation is not intermittent, many animals use the limb with the stifle held in a semi flexed position. The trochlea is very shallow or even flattened.

Grade 4
The tibia is medically twisted and the tibial crest may show further deviation medially with the result that it lies 50 degrees to 90 degrees from the cranial/caudal plane.The patella is permanently luxated. The patella lies just above the medial condyle and a space can be palpated between the patellar ligament and the distal end of the femur. The trochlea is absent or even convex. The limb is carried, or the animal moves in a crouched position, with the limb flexed.

Taken from Genetics - An Introduction for Dog Breeders by Jackie Isabell

Entropion is an inward rotation of the eyelid that is characterized by watery eyes, blinking, conjunctivitis, sensitivity to sunlight, pain, and inflammation. Ectropion is the drooping or sagging of the lower eyelid (sometimes called the haw) that is characterized by excessive drying of the cornea with overflow of tears. Chronic conjunctivitis aggravates the problems, and surgical correction is necessary if the symptoms are severe and persistent.

Trichiasis is the term for normal eyelashes that curve inward, irritating the cornea and causing chronic eye inflammation. It is considered a probable genetic disorder because of the high incidence in some breeds, though the mode of inheritance is not reported in the literature. However, trichiasis can also be acquired through chronic irritation.

Distichiasis - is the term for extra eyelashes that emerge from the meibomian glands along the margin of the eyelid - from one to ten hairs may emerge from a single gland. The number of affected glands varies, ranging from a few extra eyelashes to what appears to be a complete second row. most of the lashes lack pigmentation, which makes detection difficult.

Taken from Genetics - An Introduction for Dog Breeders by Jackie Isabell

A cleft palate is the failure of the bony plates forming the roof of the mouth to close normally during embryonic development, usually leaving a fissure between the palate and the nasal passages. It is often accompanied by a cleft lip (harelip). Cleft palates have long been considered a genetic disorder because they occur more frequently in families, but the incidence ratios do not conform to any hereditary mode. The genetic relationship was further confused by cases of Siamese twins in which only one twin had the abnormality. Human genetic studies clarified the difficulty of identifying the hereditary basis, and it turned out that cleft palates can be caused by autosomal genes, sex-linked genes, and chromosomal aberrations. Of the 153 different human syndromes associated with cleft palates and lips, 79 are caused by single-gene inheritance; the 79 syndromes account for only 5 percent of the total cases. Many environmental agents are linked with the defect, including vitamin A deficiency, vitamin A overdose, riboflavin and folic acid deficiency, aspirin, hypothermia, oxygen insufficiency, and cortisone. Occasional cleft palates occur in most breeds. Affected puppies can be identified shortly after birth because they cannot nurse properly; the fissure prevents effective suction on the nipple, and frothy bubbles appear at the nostrils. Studies of cleft palates in dogs variously conclude that it is an autosomal recessive or a dominant trait. Overall, the incidence is so low that breeders should not be unduly concerned when one crops up, as most are probably accidents of embryonic development or exposure to teratogenic agents. Nevertheless, if cleft palates occur with any frequency or regularity, a genetic cause must be considered.

From Successful Dog Breeding 2nd Edition; The Complete Handbook of Canine Midwifery by Chris Walkowicz and Bonnie Wilcox, D.V.M.

Cleft Palate/Harelip

A harelip is very obvious; the upper lip is split, sometimes through the nose. A cleft palate forms a crack in the roof of the mouth. Check the puppy by looking into the mouth with a penlight and feeling the roof. Some clefts are far back in the throat. Neither defect is unusual, and they often appear together. Nursing is hampered by either condition; bubbles of milk appear from the nose. Death results from starvation or pneumonia when milk is inhaled into the lungs. Mild cases can be saved by tube-feeding. Surgical corrections can be performed but are not practical in most cases.

Cryptochidism is the failure of one or both testicles to descend. It is considered "he most common disorder of sexual development. The testes normal descend into the scrotum at about ten days, although they are hard to feel or see at that age. A puppy with undescended testicles can make an excellent pet, if neutered. Chances of testicular cancer greatly increase if such a puppy is not neutered, and neutering is more invasive than the typical neuter.

What is Liver Shunt?
A liver shunt is a blood vessel that carries blood around the liver instead of through it. In some In some animals a liver shunt is a birth defect. In others, multiple small shunts form because of severe disease.

Why do congenital shunts develop?
All mammalian fetuses have a large shunt ("ductus venosus") that carries blood quickly through the fetal liver to the heart. Since the mother's liver does the work of filtering out toxins, storing sugar, and producing protein for her unborn babies, liver function is not needed in the fetus. This ductus venosus is supposed to close down shortly before or after birth as the baby's liver begins to work. In some individuals the shunt doesn't close down; it is then called a "Patent Ductus Venosus", or an intrahepatic shunt. In other animals, a blood vessel outside of the liver develops abnormally and remains open after the ductus venosus closes. This is called a congenital extrahepatic shunt.

Why do animals with shunts have problems?
In the normal animal, food and other ingested materials are broken down or digested in the intestines and absorbed into the portal blood stream, where they are carried to the liver. The liver stores some of the food for energy, processes some of it into safe chemicals, and uses some of it to make proteins and other substances. Because the blood bypasses the liver in dogs with shunts, toxins may build up in the bloodstream or kidneys. Additionally, the animal lacks the necessary materials to give it a ready source of energy and to help it grow.

What are the clinical signs of liver shunt?
Clinical signs are often seen at a young age and include small stature, poor muscle development, behavioral abnormalities (circling, disorientation, unresponsiveness, staring into space, head pressing), seizures, and quiet demeanor. Other less common signs include drinking or urinating too much, apparent blindness, diarrhea, and vomiting. In some animals the signs are associated with eating protein. Other animals are diagnosed when they take a long time recovering from anesthetics (i.e. barbiturates) or sedatives (i.e. acepromazine). Some animals show no signs until they are older, when they develop bladder and kidney infections and stones.

What breeds are commonly affected with shunts?
Small breed dogs tend to have shunts that form outside of the liver ("extrahepatic"). In the United States, Yorkshire terriers have almost a 36 times greater risk of developing shunts than all other breeds combined. Extrahepatic shunts can be seen in any small breed but are also reported commonly in schnauzers, Maltese, dachshunds, Jack Russell terriers, Shih Tzu, Lhasa apso, Cairn terriers, and poodles. Large breed dogs tend to retain the fetal liver shunt (patent ductus venosus), or "intrahepatic" shunts. In the Netherlands, about 2% of Irish Wolfhounds are born with intrahepatic shunts. Intrahepatic shunts can be seen in any large breed dog and have been reported in some small breed dogs (especially poodles); in the United States, we see them most often in Labrador retrievers. Australian shepherds, Australian cattle dogs, Samoyeds, and Old English sheepdogs are also commonly reported.

Are shunts hereditary?
A disease is likely to be hereditary if it occurs more commonly in one breed than others; if it occurs in a family of dogs; or if it or a closely related disease is proven hereditary in other breeds or species. Liver shunts are considered hereditary in Irish wolfhounds, Cocker spaniels, Maltese, and Yorkshire terriers, and are probably hereditary in several other breeds. The affected dog should be castrated or spayed and, because the mode of inheritance is not known, it is best to avoid breeding the parents.

How is shunt diagnosed?
On blood work, dogs with congenital liver shunts usually have low blood urea nitrogen (BUN) and albumin concentrations. They may be slightly anemic or have red blood cells that are smaller than normal ("microcytosis"). They also may have increases in liver enzymes ("AST", "ALT"). Their urine may be dilute or infected and contain small spiky crystals ("ammonium biurate"). None of these laboratory changes are specific for a liver shunt; however, when veterinarians see these abnormalities, they will usually measure bile acid or ammonia concentrations to evaluate liver function. A liver shunt cannot be definitively diagnosed by blood work; shunting can only be found with advanced techniques such as scintigraphy, ultrasound, portography, Cat scan ("CT"), MRI, or exploratory surgery.

What are bile acids?
Bile acids are produced in the liver and stored in the gallbladder between meals. They are released into the intestines to help break down and absorb fats, and are reabsorbed and stored again until they are needed. Dogs with liver shunts have increased blood bile acid concentrations because the liver does not get a chance to remove and store these chemicals after they are reabsorbed.

Do all dogs with shunt have high bile acids?
Dogs with shunts will almost always have high bile acids 2 hours after eating, and usually at least 95% of dogs will have high bile acids after a 12 hour fast. Samples are taken at both time periods ("fasting" or "preprandial", and "fed" or "postprandial") for several reasons. Some dogs normally release bile acids in the middle of the night and therefore naturally have a higher than normal fasting sample. Other dogs may have fat in their blood ("lipemia") after eating, which can interfere with the test. If only one blood sample can be obtained, it is best to take it 2 hours after eating.

Do all dogs with high bile acids have shunts?
Bile acids can be increased with any liver disease. Bile acids can also be mildly increased in normal dogs, particularly in some breeds (such as Maltese) where chemicals in their blood interfere with the test. Most dogs with liver shunts have fed bile acids over 100 (normal <15-20). If the bile acids are only mildly increased or the animal seems normal, many veterinarians will simply rerun the test in 3-4 weeks.

For more information, see http://www.vet.utk.edu/clinical/sacs/shunt/faq.shtml.

There are two kinds of umbilical hernias. They appear like "outie" belly buttons. The first kind is "reducible" meaning that you can push it in with your finger and flatten the belly button, and "non-reducible," meaning that the "outie" is hard and cannot be compressed manually. A reducible umbilical hernia is caused by incomplete closure of the muscle wall. The insides of the puppy (usually a small portion of fat) actually bubble out through the open muscle wall. This is serious and needs to be repaired surgically. The non-reducible kind, where you cannot compress it manually and it is hard, is merely a portion of fat that has formed over where the umbilical cord used to be, and is nothing to worry about.

This is a hot topic among Maltese owners, and always will be. I can tell you that Maltese puppies tend to stain when they are cutting teeth, and again when they are cutting their adult teeth. Maltese dogs and puppies can stain due to allergies, inhalant or otherwise. They can stain because they have ear infections. They can stain because they have gum or teeth issues not related to teething. They can stain, also, because of blocked tear ducts. Blocked tear ducts seem to be pretty common in Maltese. There are surgical solutions to this problem, but they may or may not be effective, and if they are, the effects may not last. Blocked tear ducts seem to be related to eye structure. Tear stains are actually caused by a red yeast. What happens is the eye tears, because of irritation or for whatever reason, and the muzzle hair gets wet with tears. Well this is an ideal environment in which to grow this yeast, which happens to be red. There are many products out there that say they get rid of tear stain. I have found that most of them are not worth the money. The BEST advice I can give is be vigilant. Keep the muzzle clean and dry. Keep hair out of the eyes, either by clipping the hair around the eyes, or by keeping the hair pulled back away from the face. Keep the muzzle dry. Kleenex soaks up excess moisture quite well. If you notice a smell to the muzzle, then the yeast is effecting the skin. Get an antifungal from your veterinarian. But hopefully you won't let it get to this point. Boric Acid powder, if you can get it to stick to the muzzle hair (facial furnishings) is quite good. But, I would make very sure none gets in the eyes. Witch hazel is also good for getting out any crusty "eye boogers." And it is a natural anti-fungal. I do not recommend using antibiotics for any length of time. I do not recommend bleaching, unless you are about ready to put the dog in the ring. Bleaching will dry the hair incredibly, and if you have not gotten rid of the tear staining BEFORE you bleach, then since you have just made the hair more porous and dry, the yeast will come back with a vengeance. The best advice I can give is to be vigilant in your care of your Maltese dog or puppy. Keep it clean. Keep it dry.