Concerns of the Maltese and Maltese Puppy
1) Maltese and Internal Parasites:
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
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
Giardiasis - an organism which infects
the digestive system of dogs. It can be transmitted to people,
too. Water supplies can harbor it.
2) Maltese and External
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.
3) Maltese and Luxating
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
To get a good idea of patellar luxation, I am adding information
gathered from the OFA (Orthopedic Foundation for Animals).
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
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.
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
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
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.
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.
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.
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.
4) Maltese and Eyelids:
Entropion and Extropion, Trichiasis and Distichiasis
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
5) Maltese and Cleft
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.
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.
6) Maltese and Cryptochidism
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.
7) Maltese and Liver
from the University of Tennessee College of Veterinary
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
For more information, see http://www.vet.utk.edu/clinical/sacs/shunt/faq.shtml.
8) Maltese and Maltese
puppies and Hernias, umbilical:
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.