Dog Owners and Breeders Symposium

July 27, 2002

University of Florida
College of Veterinary Medicine

Sponsored by

*Cancer Treatment Update

*Endocrine Update
*Neurological Emergencies
*Ten Steps to Breeding Better Dogs
*Ear Disease Update
*Canine Physical Therapy
*Vaccination and the Immune System
*Feeding, Exercise, and Endurance
*Dental Care and Disease
*GDV Update
*Tick-Borne Diseases…An Emerging Threat
*The Importance of Genetics to the Dog Breeder/Enthusiast
*Neurologic Emergencies
*Advanced Reproduction Symposium
 Cancer Treatment Update
Dr. Rowan Milner, BVSc, MedVet
University of Florida
Introduction

Veterinary oncology is undergoing fundamental change. The old paradigm of “if it can’t be
surgically removed then euthanasia is the next step” no longer applies. The reason for this
change is due to the following factors: pet owners are becoming more sophisticated in their
requirements for specialized treatment, improved results due to better treatment protocols and
drugs, a heightened awareness in private practitioner of the early signs of neoplasia leads to
earlier detection of cancer leading to more successful treatment, and an increase in age of the pet
population has lead to a population of pets with a greater risk of developing cancer.

A very important consideration in veterinary oncology is client counseling. Cancer has a very
emotional connotation and requires tact and patience in giving “bad news” to the owner. In the
medical field, physicians are taught to steer the middle course by using language that would
dispel ignorance without dispelling hope. Veterinarians need to communicate clearly the options
available to the owner. A recent report on people’s response to bad news cited most respondents
as retaining only about 15 percent of what was told to them on the first visit. It is therefore
imperative to supply literature and information to owners about their pets’ cancers that can be
read at a leisurely pace. Veterinary oncology has learned a tremendous amount from the human
experience, however there are some major differences. In animals, cure is often not a realistic
goal but rather quality of life, and therefore when chemotherapy is used drug dosages are lower.
As a result, they do not experience the same side effects associated with chemotherapy in man.
However, complications associated with treatment do occur, e.g. drug induced pancreatitis, and
bone marrow suppression.

Cancer is essentially a genetic disease. Two of the most important discoveries have been the
identification of genes called oncogenes (onco meaning cancer) and cancer suppressor genes.
Oncogenes exist in the normal cell but when cancer occurs, depending on the cause, these genes
are modified. These genes are involved in regulating cell activity, e.g. growth and protein
production, and when changed uncontrolled growth occurs. Cancer suppressor genes on the
other hand, act to suppress uncontrolled cell growth. When they are changed cells develop
“immortality.” The normal check and balances that determine if a cell should divide are lost. It
is worth noting that unlike oncogenes, cancer suppressor genes may be found in germ cells,
allowing the defect to be passed from one generation to the next. It has become clear that no
single gene is responsible for the transformation of a cell, but rather two or more oncogenes as
well as cancer suppressor genes are needed.

There are also a number of pathways that may be involved in the generation of a particular
cancer. These are via: heritable carcinogenesis, passive carcinogenesis, chemical carcinogenesis
and physical carcinogens. Cancers are a collection of cells that are always changing. This
phenomenon is termed cancer progression. Cancer progression generally results in disease that
is more aggressive. This may partly explain the poor prognosis of cancers that are detected late.
The major distinguishing feature between benign or malignant cancers is the ability of malignant

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cancers to spread to distant sites.

Clinical Staging

Staging is the process of investigating and documenting the extension of a cancer within the
body. This is achieved by physical examination, X-rays, ultrasound, CT, nuclear medicine MRI
and biopsy.

Treatment of Cancers

Cancers are treated in several ways depending on their position, malignancy and tissue type.
Most solid cancers are treated using surgery followed by chemotherapy and/or radiation.

Chemotherapy

Other than for cancers arising from immune system and bone marrow, chemotherapy is
employed in combination with other treatment options (e.g. radiation and/or surgery).
Chemotherapy’s main function in these cases is to mop up leftover cancer cells or to suppress
distant metastases. Few chemotherapeutic agents are without side effects and in some cases
these toxicities are life threatening. Resistance to treatment, as is seen with antibiotic resistance,
also occurs with chemotherapy and leads to therapy failure.

Radiation Therapy

Radiation therapy involves the treatment of cancers with radiation delivered by way of either
modified X-ray machines (orthovoltage or linear accelerators) or radioactive sources such as
cobalt-60. Radiation therapy works by causing free radicals (reactive molecules), which then
damage the cells’ DNA. Cells then die when they reach the stage of wanting to divide. This
process is dependent on the susceptibility of the tissue and the presence of oxygen. Typically,
tissue such as brain is resistant to the effects of radiation since the cells are not dividing whereas
bone marrow cells are very susceptible due to their rapid division.

Surgery

This is the oldest method and still the most effective of treating cancer in the early stage.
Surgical techniques are advancing all the time, which enable veterinary oncologists to achieve
the ultimate goal of cure. In most cases of malignant cancer, surgery forms part of the therapy
that may include chemotherapy and radiation.

Nutrition

Nutrition is probably the most neglected part of therapy for cancer. Research has shown that
there are substantial changes in the metabolism of fats, carbohydrates and protein that occur in a
patient with cancer. A specific cancer diet has been formulated by Hills known as n/d. This diet
contains high levels of essential fatty acids (FFA) in the form of omega-3 FFA (fish oil is high in
omega-3). Omega-3 has been shown to aid in the reversal of the metabolic changes seen with

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cancer. This diet also has reduced levels of carbohydrate, the reason for this is that cancers
prefer sugars to metabolize and produce less energy from this metabolism. The body has to then
convert the lactic acid from this cancer metabolism back to a usable fuel for cells at a net loss of
energy to the body. Correct nutrition in cancers will starve the cancer of nutrients and thereby
aid in the treatment.

Alternative

Alternative therapy covers all the aspects, from herbal remedies to acupuncture. While these
therapies may be beneficial, the vast majority of them have not been subjected to close scientific
scrutiny. The use of antioxidants are beneficial in preventing cancers, however, they may be
contraindicated during therapy. The reason for this is that most drug and radiation therapy for
cancer work via the production of oxidants (free radicals) and concurrent use of antioxidants may
cause the drugs to work sub optimally.

When we evaluate the effectiveness of therapy, we use the following terminology. The terms
used by definition are:

Complete Response (CR): Disappearance of all cancer in all sites for a defined period of time.
Partial Response (PR): Decrease in size of all cancers by 50 percent or greater as measured by
the sum of the products of two diameters for each cancer. There should be sustained decrease in
cancer size, as defined for CR, and no new cancers should arise.
Stable Disease (SD): Decrease of 50 percent or an increase of 25 percent in the sum of the
products of the diameters as measured for PR.
Progressive Disease (PD): Increase of 25 percent or more in the sum of the products of cancer
diameters or the appearance of a new cancer.

Note: It should be remembered that remission does not necessarily mean cure but rather the
disappearance of clinically detectable disease.

Common Cancer Types

Lymphoma in Dogs:

Dogs with lymphoma (cancer of the lymphoid tissue) typically present with enlarged glands,
either locally or all external glands. Since the body has lymphoid tissue everywhere, it can occur
in any organ. However, the multicentric (all peripheral glands form is the most common). When
veterinarians stage lymphoma in the dog, the most important criteria they look for are: extent of
the disease (does it involve the spleen and/or liver), whether or not the dog has systemic signs
(e.g. weight loss, excess urine production), and type of lymphoid cell involved. These criteria
are used to determine the chances for a meaningful response to treatment. Veterinary
oncologists will treat most lymphomas as the therapy relieves many of the symptoms of the
cancer and response can sometimes be unpredictable.

Treatment can take various forms depending on the site and extent of the lymphoma. However,
chemotherapy remains the mainstay of treatment. Drugs most commonly used are cortisone,

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alkylating agents and anthracycline antibiotics. Most treatments consist of multiple drugs,
although there are single drug treatments. Therapy is divided into an induction period of 4-6
weeks followed by maintenance treatment for 6-24 months. The most effective combination is
known as the Wisconsin-Madison protocol. This protocol gives the best remissions and survival
times. However, since it has multiple drugs it also has a moderate level of toxicity.

The goal of treatment is to achieve a good remission of the cancer. Remission rates vary from
three months to as much as 36 months or longer. Generally, a stage III lymphoma with no
complications can be expected to remain in remission for 6-9 months followed by re-induction of
remission for, on average, another 3-6 months. Cure of canine lymphoma is only rarely
achieved.

Lymphoma in Cats

Lymphoma in the cat is similar to dogs, but with a number of exceptions. When cats are feline
leukemia virus positive, their survival times are reduced. The more common form of lymphoma
in cats occurs in the intestines and chest cavity. Cats generally have longer survival times than
dogs. Therapy is similar albeit at a lower dose.

Perianal Cancers:

These are cancers arising around the anus. They are more common in the male dogs than in
female dogs. The most common cancers are perianal adenoma (80 percent), followed by
adenocarcinoma and anal sac adenocarcinoma (apocrine gland). Perianal adenoma occurs more
commonly in intact males and older large breeds of dog. Testosterone secretion from the adrenal
glands (with or without Cushing’s) may stimulate perianal adenomas. Treatment includes
surgical removal of the mass and castration.

Perianal adenocarcinoma is also seen in male dogs and metastasizes locally to the regional lymph
node. Prognosis is good if the mass is smaller than five centimeters and can be removed
completely with surgery. Castration does not make a difference. Anal sac adenocarcinoma
(apocrine gland) is a highly malignant cancer with an increased occurrence in old female dogs.
The cancer is often associated with increased urine production resulting in increased water
intake. This is due to high calcium levels in the blood. Prognosis is generally poor as the cancer
shows early spread and is often resistant to treatment.

Hemangiosarcoma

Hemangiosarcoma is a highly malignant cancer of the blood vessel wall. It is more common in
the dog and occurs in the spleen, right atrium of the heart and skin. Large breeds of dog appear
to have a greater incidence with German Shepherd Dogs having the highest incidence. Because
this cancer occurs in deep organs, owners are often unaware that their dogs have the tumor until
it suddenly ruptures, which leads to bleeding either in the abdomen or around the heart. These
dogs commonly present in a shocked state with white gums and abnormal rhythm to the heart.
Dogs may even die suddenly for no apparent reason. The best instrument to diagnose the
presence of the cancer is ultrasound. When hemangiosarcoma occurs in the skin it can be due to

5
sun damage or metastasis from a distant site (e.g. spleen). Therapy for this cancer is generally
unrewarding except for the skin (sun-induced) cancer. Average survival following removal of a
spleen is three months.

Mammary Neoplasia

Mammary cancer in dogs is seen most often in older intact females. There is a clear statistical
link between time of spaying a dog in relation to the number of seasons she has had. The earlier
she is spayed the less likely she will develop mammary cancer; so much so that there is even a
difference between first and subsequent seasons. Typical presentation is, as in humans, a lump
that is felt within the mammary gland. Fifty percent of these turn out to be malignant which go
on to spread to the local gland and then to the lungs. Treatment is mainly surgical with radiation
and chemotherapy in some cases. Surgery invariably means radical mastectomy. In benign
tumor lumpectomy can be done.

Breast cancer in the cat is a far more malignant cancer. Seventy-five to ninety-five percent of
mammary cancers in cats turn out to be malignant, with a large number showing spread to the
lungs on presentation to the veterinarian. Treatment in the early stage consists of surgery
followed by chemotherapy.

Osteosarcoma

Osteosarcoma is a cancer of the bone-producing cells of the body. It is a highly malignant

cancer, which results in destruction of the bone and in most cases early spread to the lungs. It is
a particularly painful cancer, as are most bone cancers. The cancer occurs most commonly in
giant breeds of dog, although not exclusively. The most common bones affected are the long
bones of the limbs with the site on the bone being “away from the elbow towards the knee.” The
current gold standard for treatment is surgical amputation followed by chemotherapy using a
drug called carboplatin. The author (University of Florida) is researching alternative therapies in
dogs that cannot undergo amputation. Currently two clinical trials are running.

Mast Cell Cancer (MCT)

Mast cells occur throughout the body and take part in the inflammatory reaction associated with
allergies. They contain histamine and other pro-inflammatory agents. Because of the histamine
contained in MCT, these cancers can cause gastric ulceration and acute allergic reactions. Mast
cell cancer commonly arises on the skin but can occur elsewhere. When veterinarians stage an
MCT, they take into account the following criteria: position on the body, grade of the cancer,
how quickly it grew, and the breed. Criteria that carry a poor prognosis are high grade MCT
located in the inguinal (groin) area that have grown rapidly. Treatment varies depending on the
former criteria but may include at the very least surgery and/or chemotherapy and possible
radiation therapy.

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 Those Interesting Hypercalcemia Syndromes
Michael Schaer, DVM
Hypercalcemia occurs when the serum calcium concentration exceeds 11 mg/dl. In dogs, the
most frequent causes include primary hyperparathyroidism and hypercalcemia of malignancy
(pseudohyperparathyroidism), the latter being the most common. Bony spread of malignant
neoplasms, kidney disease and certain inflammatory diseases can also cause hypercalcemia.
Minor serum calcium elevation can also occur with Addison’s disease, but it is readily rectified
with fluid therapy. Other possible causes include hypervitaminosis D and day-blooming
Jessamine ingestion. The newer cholecalciferol-containing rodenticides pose a particular threat
to the pet animal.

Signs: The patient with hypercalcemia can show anorexia, nausea, vomiting, weakness,
abdominal pain, constipation, increased thirst and urination, dehydration and depression.
Hypercalcemia can adversely affect brain function, nerve conduction to muscles, cardiac
excitation and kidney function.

Diagnosis: The initial medical workup should be extensive and include serum level
determinations of calcium, phosphorus, sodium, potassium, chloride, creatinine or urea nitrogen,
alkaline phosphatase and proteins. A complete urinalysis, CBC, as well as chest and abdominal
radiographs should also be done. Further evaluation might require renal creatinine and
phosphate clearance determinations, radioimmunoassay determination of plasma parathormone
levels and a bone marrow cytology evaluation. Certain cancer syndromes can have increased
plasma levels of parathyroid hormone related protein (PTHrP). The initial objectives are to
stabilize the patient while diagnosing the cause. When all extra-parathyroid causes of
hypercalcemia are eliminated, the primary focus should then concentrate on the parathyroid
glands and their possible removal. It is important to note that the cardinal diagnostic features of
primary hyperparathyroidism are elevated or inappropriately elevated parathyroid hormone
(PTH) levels in the setting of hypercalcemia. Pure PTH levels should be low with the
hypercalcemia of malignancy syndrome.

Treatment: The four management objectives are: 1) correct dehydration, 2) promote calcium
excretion by the kidneys, 3) inhibit accelerated bone resorption, and 4) treat the underlying
disorder. Even when the cause of hypercalcemia turns out to be a surgical disorder, the
following medical guidelines should be done in order to normalize the serum calcium level as
quickly as possible.

A) Saline infusion: Since hypercalcemia is a medical emergency, treatment must not be

delayed while the etiology is being determined. The most important therapeutic measure
is to rehydrate the patient. Since urinary calcium excretion is enhanced by saline infusion
and since 0.9 percent sodium competitively inhibits renal tubular reabsorption of calcium,
sodium chloride solution administered IV is the fluid of choice. The infusion should be
rapid in order to produce an intense diuresis, but care must be taken to avoid plasma
volume overload. Serum electrolytes must be monitored and supplemented (especially
K+) accordingly.

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B) Glucocorticoids are particularly beneficial when treating hypercalcemia associated with
lymphoma or other malignant tumors associated with hypercalcemia. When lymphoma is
suspected it is best to obtain a tissue diagnosis prior to steroid administration. By
counteracting the effect of vitamin D, glucocorticoids are efficacious in treating
hypercalcemia caused by hypervitaminosis D. They might be particularly useful for the
treatment of cholecalciferol rodenticide intoxication and dietary oversupplementation.

C) Other therapeutic measures for hypercalcemia can include the administration of IV and
oral phosphate solutions, Mithramycin (Plicamycin), calcitonin, and bisphosphonates
(etidronate disodium). The use of these agents must be done under close medical
observation.

D) Surgical excision of a parathyroid tumor or hyperplastic parathyroid glands is the

preferred treatment for primary hyperparathyroidism. Since the uninvolved parathyroid
glands will be atrophied due to negative feedback effects from hypercalcemia,
postoperative hypocalcemia should be anticipated as a potential life-threatening
complication. This can occur several hours following the parathyroid tumor removal and
should be counteracted by slowly infusing ten percent calcium gluconate at a dosage of
two ml/kg IV every six hours immediately after surgery. This infusion should be
appropriately titrated during the subsequent postoperative days. Dihydrotachysterol
treatment is commonly needed for several days to weeks postoperatively in order to
maintain normocalcemia. The dosage is titrated to effect pending the results of periodic
serum calcium level determinations.

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 Ten Building Blocks of an Exceptional Breeding Program
I. Deborah A. Lynch
Executive Vice President
AKC Canine Health Foundation

1. Become a Student of Your Chosen Breed

A. Study the breed standard
B. Observe judging at dog shows
C. Practice positive appreciation
D. Interview outstanding breeders
E. Attend your national specialty and regional specialties
F. Remember, for the first five years you are considered a novice

2. Study Canine Genetics and Physiology

A. Attend workshops and seminars
B. Read books about dog breeding and canine genetics
C. Keep informed of new advances and tests currently available
D. Study structure and movement in your breed and all breeds
E. Study dogs and pedigrees in your breed – keep notes

3. Develop a Plan and Target Your Goals

A. Breeding Goals
A. Healthy dogs
B. Advance breed performance and temperament
C. Advance the breed standard
D. Good permanent homes for all dogs produced

B. Performance Goals
A. What are your goals in conformation
B. What are your goals in performance

4. Develop Annual Objectives and Milestones

C. Sample Objectives
A. Finish a champion
B. Put dual titles on your first dog
C. Potential breeders should finish one champion and obtain at least one obedience
title, and if applicable a performance title

a) Sample Milestones
A. First homebred champion
B. First Specialty and Breed Wins
C. Finish with all Specialty Wins

5. Identify a Mentor

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 A. Observe breeders and exhibitors in your selected breed
B. Identify those that are successful and have extensive experience
C. Avoid becoming part of an entourage
D. Seek out breeders who are objective, positive, encouraging and experienced

6. Select Your Foundation Dogs

A. Start with a quality bitch
B. Avoid buying a young puppy
C. Purchase a dog at least six months old with a show record
D. Pay attention to the dam’s record - outstanding producer, natural whelper, good
litter size, excellent health and temperament, predictable pedigree of producing
and performing dogs
E. Pay attention to the sire’s record - quality producer, predictable pedigree of
producing specific qualities, excellent health record
F. Parents clear on appropriate tests

7. Screen All Dogs For Appropriate Health Tests in Your Breed and
Plan With Your Mentor
A. Evaluate your brood bitch
B. Identify strengths and weaknesses in phenotype and genotype
C. Make a list of potential stud dogs, strengths and weaknesses of the dog and its get
D. Learn to analyze a pedigree in your breed
E. Review the pedigree and get with your mentor
F. Make the decision

8. Practice Critical Evaluation and Develop A Network of Friends

A. Continually evaluate your breeding program
B. Practice good sportsmanship
C. Know the strengths of your competition
D. Breed to the competition when it makes sense
E. Develop a group of breeders in your regional area that have similar goals

9. Always Put Your Dogs First

A. Keep your dogs to a reasonable number
B. Know that your home, which is now a show and breeding kennel, is not always
the best home for every dog you produce
C. Make each decision based on what is right for the individual dog
D. Practice good animal husbandry

10. This Is Your Hobby, Enjoy It!

A. There will be ups and down
B. Focus on fun and friendship
C. The happiness of you and your dogs is number one!
D. Always smile when you leave the ring!
E. There may be a Best in Show next litter!
F. THE DOGS WILL LOVE YOU NO MATTER WHAT!

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 II. Ear Care and Disease
III. Rosanna Marsella, DVM

Introduction
Otitis externa is one of the most frequent reasons for owners to seek veterinarians’ help. The
prevalence of otitis externa in dogs has been reported to be between 10-20 percent, although in
more tropical climates it is probably closer to 30-40 percent. Unfortunately, the term otitis does
not refer to a specific disease but to an inflammation of the external ear canal. It is a symptom of
many diseases and not a specific diagnosis. The actual underlying causes of otitis are numerous.
The purpose of this lecture is to review the general principles of ear care and the most important
causes of otitis externa.

Physiology of the Ear Canal

The ear canal in the dog and cat can be divided into a vertical segment (which is continuous with
the pinnae) and a horizontal segment that abuts the tympanic membrane. The canal is almost
entirely surrounded by cartilage that offers stability to the structure. Besides the obvious
auditory function of the external meatus, the canal also offers protection of the tympanic
membrane and the middle ear from direct injury.

Preventative Ear Care and Ear Cleaning

Preventative ear care begins with a complete history and thorough physical examination.
Historical information and physical findings are necessary to identify patients at risk. Specific
information about previous and concurrent medical disorders is essential, because ear disease
may co-exist with other disease or be secondary to systemic diseases.

Routine cleaning of the ear canal is not necessary and may be contraindicated in the healthy dog
and cat. Most dogs do not require cleaning of the ears. Mild to moderate amount of wax is
normal. Cerumen has antibacterial properties that help to reduce the over population of bacteria
and yeast. Cleaning, when necessary, should be complete and non-irritating. A mixture of
vinegar/water (1/10) is a good degreasing solution to remove wax and dry the excessive moisture
in the ear canal. The liquid should be gently applied in the canal, the ear massaged to allow
breakage of the cerumen and cotton balls used to remove the cerumen and wipe out the excess of
liquid. Extreme care should be used when mechanically cleaning the ears. The use of cotton
applicators should be avoided or limited as they may cause rupture of the tympanic membrane.
Also powders should not be applied in the canal as they build up predisposing to the
development of secondary infections.

Accumulations of cellular debris and exudates indicate the presence of ear disease. Swabs of this
material should be collected and the canal should be cleaned. The color, texture and odor of the
exudates from a diseased ear can provide clues regarding the underlying primary cause of the
otitis and the perpetuating factors that may be involved. Dark brown or black, granular, dry (like
coffee grounds) exudates characterizes infestations due to ear mites. A moist brown discharge
tends to be associated with bacteria (cocci) and yeast infections. Purulent creamy to yellow
exudates are most often seen with bacteria such as Pseudomonas. Waxy, greasy, yellow to tan
debris is typical of a ceruminous otitis.

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Thorough cleaning of the ear canals is vitally important for successful management of otitis for
several reasons. Examination of the external ear canal and the tympanum cannot be complete
until the canal is cleaned. Wax, oil and cellular debris may be irritating, prevent medication
from contacting the canal epithelium, and produce a favorable environment for microorganisms
to proliferate and inactivate certain antibiotics. Several products are available on the market and
they should be used as directed by a veterinarian as some of them may interfere with the efficacy
of the topical medications. Also some of them may be irritating if not completely removed thus
appropriate flushing by a veterinarian might be required. These products are usually classified as
either ceruminolytic or drying agents.

1. Ceruminolytic agents (e.g. Cerumene) emulsify the waxes and lipids to

help flush them more readily from the ear canal. They contain surfactants
and detergents (e.g. diotyl sodium sulfosuccinate or DSS, squalene,
carbamide). In general such products should be applied 5-15 minutes
prior to cleaning. General massage improves their effect. Most of these
products are contraindicated with ruptured tympanum. However,
frequently the condition of the tympanum cannot be determined until after
the canal has been cleaned. In those cases the probability of ototoxicity
may be decreased by flushing with water after the application of such
agents. In a recent study several cerumuminolytic agents were applied in
the middle ear and squalene was the only one that did not cause any
damage.1 However, it should be realized that there is no completely safe
solution for cleaning the middle ear. Even water can cause ototoxicity.
Some disinfectant cleansers, such as chlorhexidine, are contraindicated
with ruptured tympanums.
2. Drying agents (e.g. Epi-Otic) are applied after the ear has been cleaned
and is relatively dry. Most contain alcohol and one or more of the
following: boric acid, benzoic acid and acetic acid. Some products are a
combination and they tend to have less drying agents and mildly
ceruminolytic than the standard desiccants (e.g. Epiotic, Oticlens).

When flushing an ear with a ruptured tympanum the use of saline of 1:1 or 1:3 dilutions of five
percent acetic acid (white vinegar) are recommended. The fluid is discarded with every flush
and suck cycle and the canal is filled again with clean saline. This is repeated multiple times
using a fair amount of saline. The best results for deep ear cleaning or flushing are obtained with
the patient under general anesthesia.

Cleaning cannot be done on very swollen, stenotic, ulcerated or painful ears. Such cases need to
be treated symptomatically initially and cleaned at a later date when the inflammation has been
reduced and the canals have opened.

Causes of Otitis Externa

1
Mansfield PD, et al. The effects of four commercial ceruminolytic agents on the middle ear. JAAHA 97; 33: 479-
86.

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Otitis may have numerous causes and a common classification is to break them down into
predisposing, primary and perpetuating.1 Predisposing factors are those that place a patient at
risk but by themselves are not able to cause otitis externa. Primary causes are usually the actual
inciting agent that directly causes otitis externa. Perpetuating factors are those that prevent the
resolution of otitis externa once the problem has been established.

Predisposition Factors and Risk Assessment

The most successful management requires that these factors are recognized and, whenever
possible, controlled. Early detection may prevent unnecessary pain/hearing loss and reduce the
prevalence of chronic and refractory disorders.

1. Breed Predisposition and Anatomic Conformation

Otitis occurs more frequently in breeds of dogs that have pendulous ears (e.g. Cocker Spaniel)
and those with hair growth in the ear canal. Originally this difference was thought to be
secondary to variations in the temperature and/or humidity of the ear’s microenvironment in
dogs with different ear types, however no difference in temperature was found between ear
types. It is becoming more and more evident that variations in the anatomy and the number of
glands may predispose certain breeds to otitis externa. Dogs with longhair coats and pendulous
ears should have the hair clipped frequently around the auricular orifice and the concave surface
of the pinnae. Hair in the ear canal should be removed with a forceps and twisting (rather than
plucking, which is more painful) the hairs out by twirling the forceps to improve ventilation in
the canal. Great care should be used when removing these hairs as excessive trauma to the area
may predispose to an infection. Stenosis of the ear canal (e.g. Shar-Pei) is another variation in
the anatomy that can predispose dogs to otitis externa. In Shar-Peis the stenotic canal and the
conformation of the pinna that is tightly folded over the external orifice increases the risk of
otitis externa. Stenosis of the canal can also be acquired (e.g. abscess, neoplasm).

2. Climatic variations

In a recent study monthly variation in ambient temperature, rainfall, and relative humidity
correlate positively with increases in the number of first-time otitis externa cases seen.

3. Life Style

Dogs used for activities that involve exposure to field are at increased risk of ear disease.
Foreign bodies, especially plant material, often become trapped in the canal. These animals
should be examined frequently.

4. Maceration of the Ear Canal

Any increase in the moisture of the ear canal can lead to maceration. Moisture in the canal,
whether introduced by swimming, bathing, or inappropriate treatment may cause otitis externa of

1
Griffin CE, Kwochka KW, MacDonald JM. Current Veterinary Dermatology: the art and science of therapy.
Mosby Year Book, St. Louis, 1993.

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inflammation of the external part of the ear canal. A combination of water retention, epidermal
maceration, increased ceruminous gland activity and secondary infections may be responsible for
disease. Dogs that swim may benefit from prophylactic treatment with a drying agent (e.g. acetic
acid).

5. Excessive Ear Cleaning

Mechanical trauma of the ear canal through vigorous hair plucking and the use of cotton swabs
or other objects to remove wax, as well as the use of irritant topical solutions and excessive
cleaning that alters the normal micro-flora, are all factors that predispose to the development of
infections.

Primary Causes of Otitis Externa

When discussing the primary causes of otitis externa, it is important to remember that the
epithelium of the external ear canal is simply an extension of the rest of the skin. Most causes of
otitis externa are associated with generalized dermatologic conditions. A complete dermatologic
history and work up may therefore be necessary in the diagnosis of many primary otitis externa
cases. The most common causes seen in dermatology are atopy (inhalant allergies), food allergy,
diseases of keratinization (e.g. primary seborrhea of Cocker Spaniels), and ear mites. It is
critical to long-term management of otitis externa that a primary cause can be found.

1. Parasites

The ear mite (e.g. Otodectes) is the most common mite, being responsible for up to 50 percent of
the cases of otitis externa in cats; in dogs the incidence is controversial but most authors agree
that it is responsible for 5-10 percent of cases. They are most commonly found in the external
ear canal, but can survive for some time on the surface of the skin, typically of the head and
neck. In the ear the mites are protected by desiccation by a typical dark brown crust. In
recurrent cases, it is possible that other in contact animals can act as asymptomatic carriers.
Other mites that can be responsible for otitis include Sarcoptes (mite that causes scabies),
Demodex (mite that causes the so-called red mange), Eutrombicula (chiggers) and Otobius (the
spinous ear tick of dogs).

2. Micro-organisms

Dermatophytes (which cause “ringworm”) are a relatively common cause of disease of the pinna
and in rare occasions may cause otitis externa. Bacteria are most commonly perpetuating
factors.

3. Allergies

Allergies are the most common underlying cause for otitis externa in dogs. They include
inhalant allergy (also called atopy), food allergy and contact allergy.

14
Inhalant allergy is extremely common in dogs and cats and is the most common underlying cause
for recurrent otitis externa in dogs. At least 50 percent of atopic dogs have bilateral otitis
externa. In up to five percent of cases, otitis may be the only complaint. Atopic dogs tend to
have itchy feet (e.g. they lick and chew their feet), itchy face (e.g. they rub their face against the
carpet or pieces of furniture) and itchy ears. They are predisposed to secondary skin and ear
infections that tend to recur after treatment unless the underlying allergy is well controlled. A
familial history is present in most cases and strong breed predilection has been reported (e.g.
Dalmatians, Terriers, Golden Retrievers). Clinical signs are initially seasonal. Progressive
worsening with time is also typical. Diagnosis is based on history, clinical signs, exclusion of
other diseases and intradermal skin test.

Food allergy is not as common as the inhalant allergy, but over 20 percent of these cases start
with just otitis externa, and ear disease is present in 80 percent of the cases. Food allergy should
be considered as a top differential for otitis externa in any young dog (less than one year of age).
Food allergy is diagnosed by appropriate food trial (a novel source of protein is selected based on
the individual history and used for a minimum of two months).

Contact allergy can result from medications used to treat otitis externa. Whenever a case of otitis
externa fails to improve with therapy or worsens after therapy, a contact dermatitis should be
suspected.

4. Foreign bodies

Plant material (fox tails), dirt, sand, impacted wax, loose hair and dried medications are
frequently responsible for otitis externa. In most cases this is a unilateral otitis.

5. Diseases of keratinization (e.g. primary seborrhea of Cocker Spaniels)

Excessive and abnormal composition of cerumen in these cases is responsible for the
development of otitis externa and secondary infections of skin and ears. It is usually seen in
young animals.

6. Endocrine disorders

Hypothyroidism (decreased production of thyroid hormone) and Cushing’s disease (disease

associated with excessive production of steroid hormones) are the most common endocrine
diseases that can cause otitis externa. If a middle-aged dog keeps relapsing with otitis externa
and is not itchy, then endocrine diseases should be considered as possible underlying causes.

7. Autoimmune disorders

Pemphigus (disease in which the organism produces antibodies against component of its own
skin) affects the pinna and may extend to the ear canal causing otitis. Lupus (other autoimmune
disease in which the organism produces antibodies against various components of the body) can
also cause ear disease.

15
Perpetuating Factors

They include anything that prevents the resolution of an already present otitis externa.
Perpetuating factors are a major reason for poor response to therapy regardless of the
predisposing factors and the primary cause. In early cases treating the primary cause might be
sufficient to resolve the otitis, while in more chronic cases perpetuating factors have to be
addressed to resolve the case.

1. Bacteria

In most normal ear canals a variety of bacteria can be cultured. Once predisposing and primary
factors cause alterations in the ear canal environment, these bacteria may proliferate and
perpetuate an inflammatory reaction. In most cases of chronic otitis externa bacteria such as
Staphylococcus and Pseudomonas are present. Aggressive treatment is warranted as resistance
to antibiotic may easily occur, especially in cases when Pseudomonas is cultured. Although
bacteria are not a primary cause of otitis, once the infection is established, they can cause
significant inflammation and damage. These dogs often present with purulent discharge in the
ears. Pain on palpation of the ears is quite common and a strong odor is usually present.
Diagnosis is based on cytology and culture. Initial topical therapy for a case of otitis externa is
based on the results obtained from the cytology of the exudates, while in chronic cases is best
based on results of culture and sensitivity.

Pseudomonas-related infections are extremely frustrating and difficult to treat. Most effective
treatments include topical Polimixin B and systemic enrofloxacin or ciprofloxacin. Doses that
are used are higher than the ones suggested on the label as resistance occurs rapidly. A
commonly used dose for these drugs is eleven mg/kg twice daily. Dogs with OM frequently
require two months of systemic antibiotic. As Polimixin B is rapidly inactivated by the exudates,
aggressive cleaning is an essential part of therapy. Other topical treatments used for
Pseudomonas include acetic acid (vinegar/water 1:1) and silver sulfadiazine (one gram of silver
sulfadiazine is mixed with 100 ml of sterile water and 0.5 ml of the mixture is applied twice
daily). Also pre-soaking the ear with edetate trisodium (tris-EDTA) 15 minutes prior to
application of the antibiotic increases the efficacy. Finally, topical enrofloxcin (Baytril otic) can
be used in Pseudomonas infections.

In cases where Staphylococcus is the cause of otitis, other antibiotics are usually used including
cephalexin (22 mg/kg twice daily) and trimethoprim-sulfa (25 mg/mk twice daily).

2. Yeast

Malassezia is the most common perpetuating yeast that contributes to otitis externa. It is a
budding organism with the shape of a peanut and is part of the normal flora (both skin and ears)
of dogs and cats. It is a common complication with allergic otitis (80 percent of cases) and may
result as a super-infection following antibiotic therapy. Grossly the discharge is thick, dark, and
sweet smelling. Diagnosis is usually based on the physical findings and microscopic
examination of the exudates (cytology). Topical therapy is usually sufficient and miconazole
and clortrimazole (e.g. Conofite, Lotrimin) are the most commonly used ingredients. In rare

16
cases of otitis media due to Malassezia, systemic treatment is necessary and ketoconazole
(Nizoral tablets) is used at five mg/kg twice daily for three to four weeks. Side effects include
anorexia, vomiting and diarrhea.

3. Progressive pathological changes

Chronic inflammation stimulates the proliferation of the skin lining the ear canal. As a
consequence, thickening of the canal occurs leading to stenosis of the canal. More importantly
the skin is thrown into numerous folds, which inhibits effective cleaning and the application of
medications. These folds act as a site for the perpetuation and protection of secondary
microorganisms (e.g. bacteria). Laser surgery has been used successfully to correct excessive
stenosis and thickening of the canal.

4. Otitis media

Otitis media (inflammation of the middle ear) results from chronic inflammation of the external
part of the ear canal, rupture of the tympanic membrane, and establishment of infection in the
middle part of the ear. Exudate in the tympanic cavity is difficult to treat with topical therapy
and often remains as a source for infection. Otitis media is usually bacterial in origin. Clinical
signs suggestive of otitis externa include head shyness and pain on palpation of the ears. Some
cases of otitis media might present with head tilt, circling and dry eyes, but the vast majority
does not have neurological abnormalities. As the tympanic membrane quickly grows back after
rupture, otitis media may also be present even if an intact membrane is seen on otoscopic
examination. Radiography cannot be used to completely rule out the presence of otitis media
since 25 percent of confirmed cases had no radiographic evidence of the disease. In a study otitis
media was present in 80 percent of cases of chronic, relapsing otitis externa therefore it must be
considered as a possible cause of any refractory or relapsing otitis externa. Treatment of otitis
media is based on bacterial culture/sensitivity results. Most cases require long-term antibiotic
therapy (minimum of two months) and aggressive topical therapy.

Conclusions

Otitis externa is a very common clinical presentation in small animals.

A good history is very important in every case of otitis externa to identify predisposing and
primary factors.

Aggressive treatment is needed in most cases of relapsing otitis externa as an infection of the
middle ear might be present.

17
 Canine Physical Therapy
Jason Wheeler, DVM
IV. University of Florida

Physical therapy or rehabilitation is a relatively new field in veterinary medicine. In human

patients, physical therapy is a common and well-accepted form of treatment for conditions such
as postoperative rehabilitation, osteoarthritis, and neuromuscular disorders. Until recently, there
has been limited study of physical therapy in animals. Knowledge of physical therapy modalities
in human patients has enabled veterinarians to adopt some of the techniques and procedures to
small animals.

Rehabilitation of patients with acute and chronic musculoskeletal injuries involves the
application of controlled challenges to tissues to improve strength, condition and function. The
tissues most affected by injury are cartilage, muscle, ligaments, tendons and bone. Ultimately
the goal of physical rehabilitation is to facilitate and maximize recovery and functional mobility
following a neuromuscular insult. This can be accomplished in a variety of ways: 1) reduce pain
and accelerate healing of injured and inflamed tissues; 2) maintain and restore normal range of
motion in affected joints; 3) prevent fibrosis or soft tissue contractures in injured, weak and
paralyzed limbs; 4) prevent disuse atrophy during the healing phase of neurologic or
musculoskeletal insult; 5 gain strength and improve function in weak or paralyzed muscles; 6)
provide a positive psychological effect maximizing both patient and owner well-being; and 7)
provide the owner with individualized home care programs to maximize the animal’s functional
mobility and prevent injury to the owner and possibly further injury to the animal.

In order to detect functional limitations and primary impairments, an initial patient assessment is
crucial prior to administering physical therapy. A thorough evaluation is required to document
current baseline status as well as to document the efficacy of therapeutic interventions and
protocols. Assessment tools may include a goniometer to measure range of motion, a
girhtometer to measure limb girth and effusion measurements, and a method of measuring
weight bearing status (force plate) and observational gait analysis. Factors affecting the type of
physical therapy include the age and physical condition of the patient, the nature of the surgical
condition, concurrent injuries, owner compliance, and the expertise of the person performing the
physical therapy. Whenever possible, preemptive analgesia should be instituted to allow
physical therapy to be performed to a patient that is as comfortable and pain free as possible.

Massage

Massage is the manipulation of superficial and deep soft tissues. Different types of massage
include gentle gliding over the skin without moving the underlying tissues to vigorous cross fiber
friction over muscles or ligaments to break up adhesions. Strokes may be linear, circular, or
applying direct compression, while directing strokes toward the heart to help promote venous
return. The beneficial effects of massage include relaxation of soft tissues, decreased muscle
spasm and trigger points, increase muscle flexibility, improved venous and lymphatic flow with
reduction of edema, and increased local blood flow. Massage is helpful in increasing blood flow
to muscles to help “warm up” an area prior to activity as well as decrease stiffness after activity.

18
Passive Range of Motion

Passive range of motion is an important post-injury modality to reduce tissue adhesions, promote
normal joint dynamics, enhance venous and lymphatic drainage, and prevent muscle and joint
capsular contractures. This type of therapy should ideally begin the day of surgery and continue
for two to three weeks. However, in the acute injury phase, full pain free use of joints may be
limited. It is very important to reestablish full range of motion (ROM) as soon as possible.
Permanent loss of motion can occur in as little as two weeks following some surgical procedures,
which ultimately limits an animal’s functional ability in the future.

Proper technique is very important when performing ROM. Over-aggressive ROM exercises
will result in pain, reflex inhibition, delayed use of the limb and increased joint fibrosis. The
goal is to stretch and realign soft tissues, not to tear tissues. Begin by flexing the joint until the
first signs of discomfort, and hold for ten seconds while continuing to stretch. Repeat this
exercise with extension of the joint. Repeat for ten to 30 repetitions of flexion and extension,
three to six times daily. These exercises should be performed on all joints in the affected limb.
ROM therapy is especially important for any joint surgery and in young dogs.

Cryotherapy

Cryotherapy (ice packing) is important following acute injuries or in the immediate postoperative
period. Cryotherapy decreases blood flow, and reduces pain, swelling, inflammation,
hemorrhage, and metabolic activity. Cryotherapy is most effective if applied for the first 72 to
96 hours, for 15 to 20 minutes, every four to six hours following injury or surgery. It is also
beneficial for up to two weeks following physical therapy sessions. Although cryotherapy is
beneficial for acute injuries, it is also sometimes helpful for chronic conditions because it
reduces pain and edema, and it may reduce collagen destruction, and synovial or joint
inflammation.

Cryotherapy can be performed with commercially available ice packs or by filling a sealable
waterproof bag with crushed ice and wrapping it in a towel.

Heat

After 72 to 96 hours, heat application may be beneficial, especially prior to initiating therapy
sessions. Heat increases blood flow, tissue extensibility of joint capsules, tendons, and scar
tissue, and promotes general relaxation. Superficial heating agents generally heat the skin and
subcutaneous tissues to a depth of one to two centimeters. This can be done with commercially
available hot packs or warm moistened towels. Circulating warm water blankets may be used for
large areas. Electric heating pads should not be used. Be careful applying heat to areas with
reduced sensation or in animals that cannot move away from a painful stimulus. Heat is
generally contraindicated if swelling or edema is present; cold therapy is typically used in these
instances.

19
Therapeutic Ultrasound

When deeper tissue heating than can be accomplished with warm packs is warranted, therapeutic
ultrasound is indicated. Ultrasound penetrates tissues up to five centimeters and heats tissues to
40-45ºC. Ultrasound offers all the beneficial effects of traditional heat therapy to deeper tissues
as well as many non-thermal effects. These include increased cell diffusion and membrane
permeability, increased calcium ion transport, facilitation of the inflammatory process, and
increased production of fibroblasts, glucosaminoglycans and hydroxyproline. Therapeutic
ultrasound typically uses a 1 or 3.3 MHz transducer. 3.3 MHz transducers are effective for
heating superficial tissues and 1 MHz transducers penetrate deeper tissues. Variation in pulsed
or continuous ultrasound can also vary the therapeutic outcome. Pulsed ultrasound produces
primarily non-thermal effects, as the average energy is much lower. In continuous mode, the
thermal effects are much greater.

Rehabilitative Exercises

As edema and inflammation begin to subside, the animal is more tolerant of manipulation to the
surgical site. The pain begins to resolve, and additional activities may be added to the
rehabilitation protocol. These activities include exercises, such as standing (neurologic patients
or patients with pelvic trauma), walking with sling assistance, walks at slow speeds to encourage
weight bearing, walking up or down inclines, climbing stairs, treadmill, wheel barrowing
(encourage use of forelimbs), and dancing (encourage hind limb use). Therapeutic exercises are
limited only by one’s imagination. These exercises help to facilitate the speed of recovery,
maintain pain-free range of motion and quality of movement, enhance performance and
endurance, increase muscle mass and strength, improve daily function and prevent further injury.

Aquatic Therapy

Following removal of any sutures and complete sealing of the incision, aquatic therapy can be
added. For small dogs a bath tub may be sufficient. If a whirlpool is available, it may also be
used for medium to large breeds. Alternatively a swimming pool, lake or pond (with clean water
and no alligators) may be used to allow animals to swim. Some dogs do not tolerate swimming
and there is some risk to the handler and to the animal by damaging tissues if the animal thrashes
around too much. Animals undergoing aquatic therapy should also be assisted into and out of
the water and should not be allowed to freely run and jump into the water. However, swimming
is an excellent means of improving muscle strength and joint mobility in a non-weight-bearing
environment. Underwater treadmills have recently been developed for dogs which allows active
use of muscles, appropriate gait patterning with limited weight-bearing, and enhanced
cardiovascular fitness, while taking advantage of the buoyant effects of aquatic therapy to reduce
weight-bearing stress on bones and joints. It should be noted that many patients are not well
conditioned and they may only be able to tolerate two to five minutes of swimming when starting
an aquatic program.

20
Summary

Optimal protocols for physical therapy and postoperative rehabilitation in animals are unknown.
This is an exciting new area of patient management and has the potential to improve outcomes,
increase patient quality of life, and enhance owner satisfaction and enjoyment of their
companions.

21
 The Current Status of Canine Vaccinations:
Are We Vaccinating Dogs with Too Many Vaccines Too Often?
Cynda Crawford, DVM, PhD
University of Florida

Introduction

Since the 1950’s, veterinary medicine has done an excellent job in educating pet owners on the
importance of vaccination. There is no debate over the health benefits that millions of dogs have
derived from vaccination against distemper, parvovirus, infectious hepatitis, and rabies. The
decrease in number of human, canine, and farm animal cases of rabies in recent years, despite an
increasing incidence in wildlife, is largely attributable to vaccination of dogs.1 Vaccination not
only protects the individual dog, but also decreases disease prevalence and transmission in the
canine population as a whole, even if some of the dogs are not vaccinated. For example, rabies
is not effectively transmitted if more than 70 percent of the canine population is vaccinated.1
Outbreaks of disease occur when the proportion of immune individuals decreases below a
threshold, either because of decreasing immunity in vaccinated dogs or decreased number of
dogs vaccinated. Thus, the population’s immunity to an infectious agent needs to be maintained
by vigilant vaccination of individuals at risk for exposure and transmission of disease.

More than 20 years ago, the American Veterinary Medical Association (AVMA) recommended
annual revaccination of all dogs, a practice still common today. This recommendation was based
on the assumption that immunity would dwindle in some dogs, so that frequent revaccination of
all dogs was required to insure immunity in the population. Recommendation for annual
revaccination of all dogs with multivalent or “combo” vaccines assumes that every dog is at
significant risk for exposure to every infectious agent in the vaccine, and that each agent in the
vaccine will stimulate the same degree of immunity that lasts the same amount of time.1 Today,
we know that these assumptions are neither rational nor scientifically justified, but are
convenient for the veterinarian and pet owner alike.

Vaccination should not be a regimented, one-fits-all procedure.1 The objective of vaccination is

simply to give the right vaccine at the right time to the right individual to protect that individual
from an infectious disease. To accomplish this objective, each dog should be evaluated with
regard to age, lifestyle, disease prevalence in the community, potential for exposure to infected
dogs and environments, and the severity of clinical disease, if any, after infection.2 The benefit
of vaccination is questionable if the potential for exposure is limited by lifestyle, the prevalence
of disease in the community is low, and the clinical disease is either unapparent or mild.
Vaccination is a medical procedure, and as such, requires individual assessment of each patient.

Fortunately, the most common effect of vaccination is stimulation of a protective immune

response. Despite the intended benefits, vaccination does carry with it attendant risks. Now, a
growing awareness of vaccine-related health problems is motivating veterinarians and pet
owners alike to question the benefit of annual revaccination or “boosters” for adult dogs. The
concern, controversy, and confusion centers around the question “Are we vaccinating dogs with
too many vaccines too often?” 2

22
Vaccine Types

There are three types of vaccines: killed vaccines, modified live vaccines, and recombinant
vaccines.1,3 Vaccines that contain killed viruses or bacteria also contain an adjuvant, usually
aluminum hydroxide, to nonspecifically boost the immune response to the vaccine. The
advantages of killed vaccines include lack of replication in the host, no chance of reversion of
the infectious agent to virulence, and safer for use in dogs that are immunosuppressed or in
breeding bitches housed in contact with neonates. The disadvantages include a higher incidence
of adverse reactions to the killed organisms suspended in adjuvant, formation of lower amounts
of antibody that do not remain at protective levels for very long, and requirement for frequent
vaccinations to boost the immunity to protective levels. In addition, killed vaccines must be
administered by intramuscular or subcutaneous injection. Examples of killed vaccines
commonly used in dogs include those for coronavirus, leptospirosis, kennel cough, Lyme
disease, giardia, and rabies.

Modified live vaccines (MLV) contain live viruses or bacteria whose virulence has been
modified to allow replication in the host without causing disease. These vaccines simulate
natural immune responses in that they stimulate rapid humoral and cell-mediated immunity that
is sustained at high levels for long periods of time. Some of these vaccines can be given at the
site where the pathogen normally invades the body, such as the nostrils, thus inducing a localized
immune response that acts quickly to prevent invasion. Examples of commonly used modified
live vaccines in dogs include those for distemper, parvovirus, canine infectious hepatitis,
parainfluenza, and kennel cough. Both killed and modified live vaccines can be monovalent or
multivalent. Monovalent vaccines contain only one infectious agent, whereas multivalent
vaccines contain two or more.

Recombinant vaccines are genetically engineered vaccines created by inserting selected genes
from an infectious agent into a nonpathogenic carrier agent that serves as a production factory.
The proteins made from the selected genes are those that are critical in stimulating protective
immunity to the infectious agent, and thus focus the immune response. The proteins can be
harvested after production by the carrier agent and used as a purified protein vaccine, with or
without adjuvant. An example of this type of recombinant vaccine is the new one for Lyme
disease. Alternatively, a nonpathogenic virus into which the selected genes of the pathogen have
been inserted can serve as the actual vaccine. Replication of the nonpathogenic carrier virus in
the dog produces the pathogen proteins that induce a protective immune response. An example
of this is the new recombinant vaccine for canine distemper.

Duration of Vaccine-Induced Immunity

Vaccine manufacturers in the United States are required by the USDA to conduct efficacy and
safety studies for their vaccines prior to licensure.1 The efficacy studies are challenge studies,
the “gold standard” for demonstrating protective immunity provided by a vaccine. In challenge
studies, non-vaccinated and vaccinated dogs are exposed to the virulent organism at various
times after vaccination to determine the extent and duration of protection against disease. The
manufacturer is not required to establish the full duration of immunity for the vaccine, but only
to provide documentation of what they claim on the label, hence the recommendation for annual

23
revaccination.1 However, minimum duration of immunity challenge studies are required for all
rabies vaccines, and for all new vaccines using antigens that were not in use prior to 1995.1
Vaccines produced by different companies may induce different durations of immunity against
the same diseases. Trials to determine the duration of immunity beyond that of one year that
would meet USDA guidelines can be cost-prohibitive. However, recent challenge studies
performed by independent research groups have demonstrated that the minimum duration of
immunity induced by modified live virus vaccines for distemper, parvo, canine infectious
hepatitis, and parainfluenza is actually five to seven years, not one year!1 Furthermore, annual
revaccination in these challenge studies did not provide any additional benefit in terms of the
strength of the humoral immune response elicited, improved resistance to disease, or extension
of the duration of immunity.

Thus, based on duration of immunity, annual revaccination of adult dogs is probably not
necessary for protection against distemper, parvovirus, canine infectious hepatitis, and
parainfluenza.1, 2

Who Should be Vaccinated with What and When?

Puppies less than six months old are more susceptible to the common infectious diseases than
adults, and therefore are the primary target population for vaccination.1 In the US, the incidence
of clinical disease from distemper, infections hepatitis, and parvovirus in dogs older than one
year of age is virtually zero.1

In 2001, the American Veterinary Medical Association Council on Biologic and Therapeutic
Agents (COBTA) presented guidelines for vaccination of dogs.2 The guidelines emphasized that
there are inadequate data at this time to support a single best vaccination protocol, so
veterinarians should perform a risk to benefit analysis for the use of each vaccine in each patient.
The guidelines divide currently available vaccines into “core” and “non-core.” Core vaccines are
selected based on the prevalence of the infectious agent in the environment, the severity of the
clinical disease that results from infection, the ease with which the infectious agent is transmitted
between animals, and the zoonotic potential. Core vaccines include canine distemper,
parvovirus, infectious hepatitis virus, and rabies. Non-core vaccines are those that are useful in
situations where the risk of exposure is high and disease can be debilitating. These include
vaccines for leptospirosis, parainfluenza, coronavirus, kennel cough, Lyme disease and giardia.

High levels of maternal antibodies acquired from ingestion of colostrums protect puppies from
disease for the first six to eight weeks of life. After six to eight weeks of age, a window of
susceptibility to infection is created because maternal antibodies are high enough to interfere
with the vaccine-induced response, but not high enough to protect the pup from infection and
disease.1 This maternal antibody blockade is the most common cause of vaccine failure in
puppies. Therefore, immunizations are repeated at timed intervals during the first four to six
months of the puppy’s life to insure development of a protective immune response. The
pediatric series include the core vaccines for distemper, parvovirus, and infectious canine
hepatitis starting with an initial immunization at six to eight weeks of age, followed by boosters
every three to four weeks until 16 weeks old. Certain breeds have a higher frequency of
individuals that do not develop vaccine-induced antibody titers during the routine pediatric

24
series. These breeds include the Rottweiler, Doberman Pinscher, Labrador Retriever, Alaskan
sled dog, Pomeranian, and American Staffordshire Terrier.4 For puppies of these breeds,
boosters are recommended every three to four weeks until 24 weeks of age.

The most popular core vaccines are modified live vaccines that contain a combination of
distemper virus, canine adenovirus type 2 for protection against infectious hepatitis,
parvovirus and parainfluenza virus (DHPP or DA2PP). Contrary to popular belief, combining
these viruses into multivalent vaccines does not alter the immune response to each – no scientific
study has shown that one virus suppresses the immune response to the other viruses given at the
same time, so it is not necessary to alternate vaccination with each separately.1 Several
potentiated monovalent vaccines are available for parvovirus. Potentiated vaccines contain very
high titers of parvovirus, and are most effective in overcoming the maternal antibody blockage in
young puppies. The original parvovirus, CPV2, has been replaced over the years by two
antigenic variants or biotypes called CPV2a and CPV2b. The CPV2b biotype is more prevalent
in the US, while the CPV2a is more prevalent in Europe. Most licensed parvovirus vaccines still
contain the original CPV2 virus, but the induced immunity is cross protective against both
biotypes.1, 5 A recently marketed recombinant vaccine for distemper (Recombitek CDV, Merial)
uses the canarypox virus as a vector for a distemper virus gene that codes for a protein associated
with protective immune responses.3 The vaccine is effective but the minimum duration of
immunity beyond one year has not been established.

The last core vaccine administered during the pediatric series is rabies. The rabies vaccine is the
only one that is legally required due to the health threat to humans. Most states require an initial
vaccination at 12-16 weeks of age, followed by a booster one year later. State laws vary on
revaccination intervals for adult dogs, with intervals ranging from one to three years. Rabies
vaccines contain large amounts of killed virus suspended in adjuvant, and have a minimum
duration of immunity of one year or three years.

Based on the long duration of immunity for the core vaccines against distemper, canine
infectious hepatitis, and parvovirus, Dr. R.D. Schultz at the University of Wisconsin proposed
that a more ideal vaccination program would be one in which dogs were revaccinated one year
after completion of the pediatric series, then at three-year intervals thereafter.1 However,
revision of current protocols for these vaccines should not be done without accurate
epidemiological data about the prevalence of each disease in the community, and a careful risk
assessment for each dog.

Non-Core Vaccines

Non-core vaccines are recommended only for dogs in situations where the risk of exposure is
high and the disease can be debilitating.2 These include vaccines for coronavirus, leptospirosis,
parainfluenza, kennel cough, Lyme disease, and giardia. Most non-core vaccines require annual
revaccination due to their short duration of immunity. In addition, most of these vaccines
contain killed organisms suspended in adjuvant, which increases the risk for vaccine-associated
reactions.

25
Canine coronavirus can cause clinical disease in pups less than six weeks old, but most are
protected by maternal antibodies.1 The clinical disease is very mild compared to parvo, and
unlike parvo, is confined to the intestinal tract without any systemic involvement. Concurrent
infection with coronavirus can contribute to the severity of clinical disease in puppies infected
with parvovirus, but vaccination of puppies against parvovirus will prevent disease from both.1
Therefore, it is difficult to rationalize the use of a coronavirus vaccine, but more doses of
multivalent vaccines containing killed coronavirus are sold than those without, indicating that
most pups and adult dogs are routinely vaccinated anyway. The vaccine, which contains killed
virus in adjuvant, may be most useful for brood bitches in kennels where diarrhea is a problem in
young pups prior to weaning. Vaccines containing killed coronavirus combined with killed
leptospirosis bacteria targeted for use in puppies should not be used due to increased frequency
of hypersensitivity reactions.1

Canine leptospirosis is a bacterial infection that causes kidney and liver failure in dogs of all
ages. The bacterial species, Leptospira, has several different variants, called serovars, which are
antigenically distinct from each other, thus antibodies to one will not protect against infection
with other serovars. Vaccines for leptospirosis contain killed bacteria from the L. canicola and
L. icterohemorrhagie serovars. The killed bacteria are usually incorporated into multivalent
vaccines containing modified live distemper virus, parvovirus, adenovirus, and parainfluenza
virus (DHLPP, DA2LPP). The killed bacteria suspended in adjuvant are responsible for many
hypersensitivity reactions, particularly in Dachshunds and other small breeds, and only induce a
short-lived immunity of six to eight months.1 However, widespread use of multivalent vaccines
containing L. canicola and L. icterohemorrhagie for many years has been credited with the
reduced prevalence of these two serovars in the canine population. New serovars, such as L.
Pomona and L. grippotyphosa have now emerged as the predominant cause of canine
leptospirosis, and the old vaccines do not induce protective immunity to these bacteria.1
Recently, Fort Dodge has developed a new killed vaccine that contains L. Pomona and L.
grippotyphosa for use in dogs at risk for exposure, but the duration of immunity is still less than
12months.1

Kennel cough, or infectious tracheobronchitis, is an upper respiratory tract disease caused by

Bordetella bronchiseptica bacteria alone, or in concert with a variety of viruses such as
parainfluenza, distemper, canine adenovirus type 2, and herpesvirus. The intranasal vaccine
contains live avirulent B. bronchiseptica combined with modified live parainfluenza virus. This
vaccine rapidly stimulates mucosal and cell-mediated immunity in the upper respiratory tract
where the pathogens enter the body, so that vaccination three to five days prior to anticipated
exposure provides protection. The intranasal vaccine can also be given to pups after three weeks
of age, and is not subject to the maternal antibody blockade. However, replication of the
attenuated bacteria and virus in the upper respiratory tract can cause mild clinical signs that
resolve in a few days. The parenteral vaccines given by injection contain killed B.
bronchiseptica, and thus require boosters two to four weeks apart to generate protective levels of
immunity. These killed vaccines induce systemic immune responses that contribute to protection
of the respiratory tract without inducing a mild clinical disease like the modified live vaccine, but
do cause more vaccine-associated hypersensitivity reactions. Parenteral vaccines are safe to use
in breeding bitches, but are subject to maternal antibody blockade when given to puppies. The
duration of immunity for both the intranasal and parenteral vaccines is probably less than 12

26
months.1 It is generally thought that stimulation of local immunity in the respiratory tract with
an intranasal vaccine is superior to use of parenteral vaccines. Others have proposed that
protocols incorporating both types of vaccines are superior to either vaccine alone. A recent
study6 found that administration of both the intranasal and parenteral vaccine once each in
sequence afforded better protection and less severe clinical signs from B. bronchiseptica
challenge than either vaccine alone.

Lyme disease is caused by Borrelia burgdorferi bacteria transmitted by tick bites. The vast
majority (99 percent) of cases are in the northeastern, middle Atlantic and upper Midwestern
states. Vaccination is recommended for dogs in these endemic areas, but not for dogs in areas of
low prevalence, such as the southeast.1 The Lyme vaccine contains killed bacteria suspended in
adjuvant, and has produced postvaccinal lameness in dogs. In addition, the vaccine contains
limited strains of the bacteria and may not induce cross protective immunity to other strains that
cause disease. A new recombinant vaccine licensed for use in dogs contains purified bacterial
out surface protein A (OspA) instead of whole bacteria, does not have an adjuvant, and challenge
studies have shown a minimum duration of immunity of one year.3

Giardia is a protozoan that infects the gastrointestinal tract of birds and mammals worldwide,
and causes explosive diarrhea, gas, and pruritic skin lesions in dogs. The infection responds to
medical therapy, but reinfection rates are high because the infectious cysts shed in fecal material
persist on the dog and in the environment. There is a new killed vaccine (GiardiaVax, Fort
Dodge) licensed for use in dogs and pups older than six weeks that contains inactivated giardia
trophozoites. Challenge studies have shown that the vaccine stimulated a strong antibody
response within three weeks, and vaccinated dogs were less severely affected clinically and shed
cysts for a shorter time compared to non-vaccinated dogs1. The decreased shedding of cysts was
maintained for up to one year. In a clinical trial supported by the manufacture7, six pet dogs with
chronic giardia infections for months to years received two doses of the vaccine given three
weeks apart, which eliminated clinical signs and shedding of cysts with two to eight weeks.
However, in a recent independent study8 in which digs infected with giardia were treated
medically with or without the vaccine, medical treatment alone was effective without the
vaccine, as long as the dogs were bathed and put in a different environment. The vaccine did not
prevent recurrence of infection in dogs that were not bathed and moved to a different
environment.

Assessment of Immune Status by Antibody Titers

One method to assess the adequacy of humoral immunity induced by vaccination is measurement
of antibody titers to the infectious agent vaccinated against. The vaccine-induce antibody titer is
compared to a standard titer associated with prevention of infection. Antibody titers are
increasingly recommended as an objective method for determining the need for revaccination.
However, antibody titers do not necessarily correspond to protection against disease.1, 2 A high
antibody titer does not guarantee immune protection, and a low or negative antibody titer does
not mean loss of immunity and susceptibility to infection. Certain breeds have higher numbers
of individuals that do not develop antibody titers after vaccinations. These breeds include the
Rottweiler, Doberman Pinscher, Labrador Retriever, Alaskan sled dog, Pomeranian, and
American Staffordshire Terrier.4 Yet, dogs in these breeds with no or low antibody titers remain

27
healthy, presumably because of vaccine stimulation of other important immune system
compartments such as cell-mediated immunity, mucosal immunity, and immune memory cells,
all of which cannot be accurately or practically measured at this time. Unfortunately, there are
no standardized tests for measuring antibody titers with reliable interpretations, so that
submission of a serum sample to three different labs most likely would yield three different
results with three different interpretations.2

In a recent study4, serum antibody titers to distemper and parvovirus were measured in 1,441
dogs of various ages and breeds located across the US and Canada. In this population, more than
95 percent had adequate titers to distemper and parvo. For the 468 dogs with known vaccination
histories, the interval of time after the last vaccination was one to two years for the majority (60
percent), two to seven years for 30 percent, and less than one year for ten percent. Based on
these results, the authors concluded that annual revaccination of adult dogs may not be
necessary, and that an acceptable alternative approach is antibody titer screening to determine the
need for vaccination on an individual basis. An alternate vaccination protocol has also been
proposed for puppies from families with known genetic predisposition to adverse vaccine
reactions or immune-mediated diseases.9 This protocol suggests using only monovalent vaccines
for distemper and parvovirus with alternating administration every three to four weeks until the
puppy has received a total of three doses of each vaccine. The vaccines are boosted at one year
of age, again using monovalent vaccines given at least two weeks apart, followed by
measurement of antibody titers to determine future need for revaccination.

Adverse Vaccine Reactions

Just as no vaccine is 100 percent effective in preventing disease, no vaccine is 100 percent free
from causing an adverse reaction. An adverse event is defined as any undesirable consequence,
including illness or a reaction, after the use of a vaccine, whether or not a cause-and-effect
relationship can be established.2 The most commonly recognized adverse reactions are the
nonspecific reactions of immune system stimulation, including fever, anorexia, and stiffness for
24-36 hours after vaccination.10 Another common systemic reaction, most frequently reported
with killed vaccines, is immediate hypersensitivity of anaphylaxis, indicated by urticaria (hives)
and pruritis of the face and ears followed by vomiting and/or diarrhea in some dogs.10 These
signs can occur immediately after vaccination or several hours later. Local reactions to vaccines
with adjuvants include swelling, pain, lumps, and hair loss at the vaccine site. Other reactions
include abortions and birth defects due to vaccination of pregnant dogs, and illness in neonates
exposed to dogs recently vaccinated with modified live vaccines that are shedding the vaccine
viruses into the environment.

For most currently available vaccines, the benefits derived far outweigh the risks for an adverse
event when vaccination is performed in accordance with published standards.10 With the
technology available today, there is no way to accurately predict what vaccine will pose a threat
to which dog and when.

Manufacturers of human vaccines are required to list on the vaccine label the type and frequency
of adverse events that occurred during safety trials.10 There are approximately 12,000 reports of
adverse events annually for human vaccines, all of which must be forwarded to the FDA, the

28
federal agency that regulates drugs and vaccines for humans.10 In contrast, animal vaccine
manufacturers are neither required to list possible adverse reactions on vaccine labels, nor keep
records of adverse events reported directly to them, nor forward reports to the USDA, the federal
agency that regulates drugs and vaccines for animals.10 There are approximately 10,000 reports
of adverse events associated with animal vaccines annually in the US, but the vast majority of
these are communicated directly to the manufacturers.10 However, veterinarians and pet owners
can report concerns directly to the USDA or to the Veterinary Practitioners Reporting Program,
which is a volunteer watchdog organization that forwards reports of adverse reactions to the
USDA, vaccine manufacturer, and the AVMA in an effort to protect animal health.

One of the best-developed surveillance schemes in the world for monitoring adverse reactions to
veterinary vaccines is in the United Kingdom. In contrast to the US, vaccine manufacturers in
the UK are legally required to record reports of adverse reactions and submit the reports to a
regulatory agency.11 The Veterinary Products Committee, an independent group that gives
advice on the safety, quality, and efficacy of veterinary vaccines to the regulatory agency,
recently published a report on vaccine-associated adverse events in the UK.11 The overall annual
incidence of adverse events in dogs from 1995 – 1999 was less than 0.1 percent per 10,000 doses
of vaccines sold, which is similar to that reported in Australia. Toy breeds and puppies less than
six months old had the highest incidence of the five-year reporting period. Anaphylaxix
reactions were the most common type reported. The group concluded that there are insufficient
scientific data to warrant changing revaccination intervals from that already approved by the
regulatory agencies, and that the very low incidence of adverse reactions sdtronly supports
continued vaccination. However, the group strongly emphasized that dogs should be
individually assessed with regard to the need for each vaccine as well as the frequency of
administration.

Immune-Mediated Diseases and Vaccinosis

There is increasing evidence suggesting that vaccination, particularly “overvaccination,” is

associated with development of immune-mediated disorders and chronic diseases, or
“vaccinosis,” in individuals that are genetically predisposed. Certain breeds appear more
genetically predisposed to developing adverse reactions and immune-mediated diseases
following vaccination, including the Old English Sheepdog, Akita, American Cocker Spaniel,
Standard Poodle, Scottish Terrier, Shetland Sheepdog, Shih Tzu, Vizsla, Weimaraner, Irish
Setter, Doberman Pinscher and Dachshund.9 There are two published studies12, 13 that linked
vaccination and development of immune-mediated hemolytic anemia. More recent reports9, 14
have suggested vaccine-induced development of Hypertrophic Osteodystrophy in Weimaraner
puppies that were genetically predisposed to the disease. Other reports linking vaccination to
development of joint diseases, neurological diseases, and thyroid disease are largely anecdotal,
and await rigorous scientific validation. To date, there are no controlled scientific studies that
prove a cause and effect relationship between vaccination and development of immune-mediated
diseases or chronic diseases.10, 11

Due to concern about vaccination overload of the immune system with development of
autoimmune diseases and “vaccinosis,” there has been a proliferation of anti-vaccination
websites offering alternatives to conventional vaccinations. One of the alternatives is “nosodes”

29
which are products prepared from infected tissues or discharges given orally.2 General
recommendations for use of nosodes include administration orally for three days the first week,
then once weekly for three weeks, then once monthly for six months, then every six months
thereafter. The dose is three drops for small dogs and six drops for large dogs. The nosode does
not cause disease because of “homeopathic dilution,” where the product is diluted enough that
the amount of infectious material remaining is too little to cause disease. There has been only
one controlled study on the efficacy of nosodes for protection against disease. This study2
examined a nosode for parvovirus and found that 100 percent of the non-vaccinated as well as
vaccinated puppies became infected when challenged with the virus.

Conclusion

Are we vaccinating dogs with too many vaccines too often? Probably. No doubt, there will
be changes in the who, what, when and how for canine vaccinations. In general, canine vaccines
are effective and safe, with benefits that far outweigh the risks. However, more rigorous
controlled studies are needed on vaccine efficacy, duration of immunity, and safety to point out a
scientifically sound direction for change. Change is hard, and human nature resists change
unless there is compelling evidence to do so. It is important to remember that the overall goal
of vaccination is protection of the population as a whole, which can be achieved by
vaccinating more dogs, but vaccinating each dog less. To date, the best protocol for
vaccination is individual assessment of every dog with regard to age, health status, risk of
exposure to the infectious agent, prevalence of the infectious agent in the community, and
severity of illness caused by the infectious agent.

Selected References

1. Greene CE, Schultz RD, Ford RB. Canine Vaccination. In: North American Veterinary
Clinics 2001. Ford RB, ed. 31(3): 473-492.
2. Ford RB. Vaccines and vaccination: The strategic issues. In: North American Veterinary
Clinics 2001. Ford RB, ed. 31(3): 439-453.
3. Van Kampen KR. Recombinant vaccine technology in veterinary medicine. In: North
American Veterinary Clinics 2001. Ford RB, ed. 31(3): 535-538.
4. Twark L, Dodds WJ. Clinical use of serum parvovirus and distemper virus antibody titers for
determining revaccination strategies in healthy dogs. JAVMA 2000; 217: 1021-1024.
5. Pratelli A, Cavalli A, Martella V, et al. Canine parvovirus (CPV): comparison of
neutralizing antibody responses in pups after inoculation with CPV2 or CPV2b modified live
virus vaccine. Clin and Diag Lab Immunol 2001; 8:612-615.
6. Ellis JA, Haines DM, West KH, et al. Effect of vaccination on experimental infection with
Bordetella bronchiseptica in dogs. JAVMA 2001; 218:367-375.
7. Olson ME, Hannigan CJ, Gaviller PF, et al. The use of a Giardia vaccine as an
immunotherapeutic agent in dogs. Can Vet J 2001; 42:865-868.
8. Payne P, Ridley RK, Dryden MW, et al. Efficacy of a combination febantel-praziquantel-
pyrantel product, with or without vaccination with a commercial Giardia vaccine, for
treatment of dogs with naturally occurring giardiasis. JAVMA 2002; 220:330-333.
9. Dodds WJ. Vaccination protocols for dogs predisposed to vaccine reactions. J Am Anim
Hosp Assoc 2001; 37:211-214.

30
10. Meyer EK. Vaccine-associated adverse events. In: North American Veterinary Clinics 2001.
Ford RB, ed. 31(3):493-514.
11. Gaskell RM, Gettinby G, Graham SJ, et al. Veterinary Products Committee working group
report on feline and canine vaccination. Vet Rec 2002; 150:126-134.
12. David D, Giger U. Vaccine-associated immune-mediated hemolytic anemia in the dog. JVIM
1996; 10:290-295.
13. Hogenesch H, Azcona-Olivera J, Scott-Moncrieff C, et al. Vaccine-induced autoimmunity in
the dog. Adv Vet Med 1999; 41:733-747.
14. Harrus S, Wainer T, Aizenberg I, et al. Development of Hypertrophic Osteodystrophy and
antibody response in a litter of vaccinated Weimaraner puppies. J Small Animal Practice
2002; 43:27-31.

31
 Nutrition for Working Dogs
V. Richard Hill, MA, VetMB, PhD, DACVIM, MRCVS

What factors are important?

1. Type of Exercise: Endurance vs. sprinting; most working dogs are endurance athletes.
2. Training: Slow increases in exercise and slow adjustment to new nutritional needs are best.
Being a “weekend warrior” and suddenly increasing exercise and diet can result in injuries
and digestive upset.

What is unique about the exercising dog?

Fat Metabolism:
1. Dogs do not get heart attacks and do not need to worry about increased fat.
2. Dogs burn fat twice as fast as people do.
3. All dogs’ muscle fibers burn fat whereas some muscle fibers in horses and people do not
4. Stamina improves when dogs are fed a high fat diet (50% energy). This is the
opposite of people who need increased carbohydrate for stamina.

Effect of diet on stamina in Beagles on a treadmill (Downey et al. 1989)

Dietary Protein Dietary Fat Time (min) to Distance
(%energy) (%energy) exhaustion (miles)
20% 30% 100 15
20-40% 50-70% 140 20

5. Dogs sprint faster when fed increased fat.

6. Dogs “tie up” less when fed high fat diets.

How much protein?

7. Dogs require at least 30% energy as protein for endurance exercise to prevent anemia.
8. Dogs do not require more than 24% energy as protein for sprint exercise.

Types of Pet foods

9. Dry foods are formed by an extruder and are mostly low fat (~ 25% energy as fat)
because the extruder requires a low fat mixture. These are fine for dogs that are couch
potatoes but do not contain enough fat for working dogs undertaking endurance exercise.
More expensive dry diets have fat sprayed on after extrusion and tend to contain more fat
(40% energy as fat). They are packaged in special greaseproof bags and are greasy to the
touch. These should provide the staple diet for a working dog. It is enough on its own if
the dog is not working. It is not necessary to feed diets designed for large breed dogs.
10. Canned foods contain 75% moisture and are more expensive but usually contain more
fat and protein. The analysis on the bag cannot be compared with that on a dry food
because the amount of water is greater in canned food. For a rough comparison, multiply
the analysis on the canned food by four to compare with that of a dry diet. Working dogs
which are normally fed dry food should be supplemented with canned food when they are
working. Foods designed for growing dogs mostly contain increased protein and fat.
11. Soft-moist and soft-dry (e.g. Kibbles and Bits): These are intermediate but mostly low
fat and are not suitable for working dogs.

32
Note that high fat is here defined as greater than 40% energy which is equivalent on the
label to greater than 5% fat for a canned diet, greater than 13% in a semi-moist diet and
greater than 18% fat in a dry diet. High protein is defined as greater than 30% energy,
which is equivalent on the label to greater than 9% in a high fat canned diet or greater
than 33% in a high fat dry diet.

Differences between pet foods

Differences between pet foods are often small. Foods with different names do not necessarily
differ in composition. Some terms such as “premium” and “super-premium” have no definition
and do not guarantee better performance. The major differences are:
12. Dry vs. canned: Canned usually contain more fat and protein than dry diets.
13. Generic vs. proprietary: Generic diets are usually made with poorer quality ingredients
and are not necessarily tested on animals. Proprietary (popular & premium) brands made
by national manufacturers are made with better ingredients and are usually tested on
animals. “Generic” diets are inexpensive private label of a local or regional
manufacturer. Pet food is well regulated but there is no policing of label claims within
the state of Florida. It is therefore better to use a food that is sold nationally.
14. Life stage and therapeutic diets: These sometimes have different compositions and
should be used only with a veterinary recommendation.

Supplements and treats

15. Unbalance balanced diets. Do not feed supplements. Treats should comprise less than
10% of the diet
a. Too much meat can result in thin bones and fractures.
b. Too much liver can cause stiff neck and joints.
c. Too much calcium can cause joint problems.
16. Some treats and supplements may be beneficial:
a. Chews: may be beneficial for dental hygiene.
b. Antioxidants may be beneficial especially in dogs that are not properly trained or
are eating a lot of extra fat but very high doses are not recommended. Some
manufacturers are including increased antioxidants in their dog foods. If feeding
a diet without increased antioxidants, 10 IU/kg vitamin E (as alpha-tocopheryl
acetate) may be given daily or 50 IU/kg every week by mouth. Vitamin C may
also be beneficial. It is probably best to give vitamin C immediately before
exercise as it does not last long in the blood and 100 mg may be sufficient for the
average medium to large sized dog. It should be noted, however, that high doses
of antioxidants may have detrimental effects. Very high daily doses of vitamin E
(1000 IU) and C (1 gram) are not recommended because our laboratory team
found that these high doses appeared to slow racing greyhounds weighing 25-30
kg. Additional vitamin C in particular may not be beneficial and could exacerbate
injury.
c. Glucosamine or green lipped mussel powder may help dogs with arthritis but
should only be used in consultation with your veterinarian.
d. Fish oil may reduce inflammation of the feet in dogs working in snow. Some
diets already contain fish oil and should not be supplemented.

33
Human food
17. Not complete and balanced so must have supplements such as vitamins and minerals
added of more than 10% of the diet. This is not recommended unless diet has been
formulated to be balanced by a professional with nutritional experience.
18. Uncooked meat represents a likely source of infection especially in young, pregnant, or
infirm animals, or stressed animals such as working dogs.
19. Bones, especially spiky bones such as the vertebrae found in chicken necks, can get
lodged in the esophagus. Too many bones can also cause constipation.

Neutraceuticals and Herbs

Quality, consistence, absorption, potency and efficacy are uncertain. Toxicity and therapeutic
index have not been established. Some may prove beneficial in the future but are not currently
recommended.

How much to feed?

Adjust food intake to maintain optimum body weight and condition. Do not feed too much. The
slim-line model is best. Ribs should be felt but not seen. There should be a waist visible from
the side and from above. The recommendation on the back of the packet can provide a guide but
there is much individual variation. There is some evidence that lean dogs perform better than
heavier ones. Lean dogs also live longer and have fewer joint problems.

Weigh your dog every two weeks and keep a record. Always use the same scale and do it before
a meal but after urinating and defecating at the same time each day and not after exercise.
Sudden changes in body weight are an indication of dehydration. Slow changes will give some
indication of whether you are feeding too little or too much. Also keep a record of body
condition score. Take a photo for comparison so you can see how things change over time.
Your dog should have a body condition score of five on the nine point Purina scale.

A working dog, such as a Collie, working sheep needs almost twice as much food as a couch
potato pet dog. A racing sled dog has the most extreme work out and may need twice as much
again. When starting training, add ½ 16 oz. can for each 8 oz. cup of dry food normally fed.
Over three days, reduce dry by half and double canned food. Then increase canned food as
necessary to maintain weight, body condition and stamina.

When and how often to feed?

Do not feed directly before or during exercise. Do not exercise within 8-12 hours of a large meal
or 4-6 hours of a moderate sized mea. Racing sled dogs have long bouts of exercise and short
rests. The custom in these dogs is to race for 4-6 hours then take a rest for 2-4 hours during
which a high fat and protein snack is fed. Dogs then race for an additional 4-6 hours before
eating a full meal.

Water
Dehydration must be avoided. Offer water continuously during exercise. Pet dogs on average
need 50 mL/kg per day (2-5 pints per day for a 45-100 lb working dog). Working dogs may
need four or five times that amount (1-3 gallons/day). Adding three level tablespoons of table

34
sugar to a liter of water may help water absorption and will increase the recuperation of dogs at
rest stops.

Salt and other electrolytes

There should be enough salt in the food if a balanced diet is being fed. Salt may improve water
absorption in dehydrated animals. A recipe for oral electrolyte replacement solutions is provided
below which can be used if a dog becomes dehydrated but a recent study showed no benefit of
such a solution over plain water in working dogs. Giving sodium bicarbonate (a “shake”) before
exercise also has been shown not to be beneficial in dogs.

Oral rehydration recipe (level spoonfuls)

To one liter of drinking water add:
1. 3 Tablespoons of table sugar or 1 ½ tablespoons of glucose
2. ½ teaspoon of table salt
3. ¼ teaspoon of salt substitute
4. ½ teaspoon of baking soda
Use immediately.

Gastric Dilatation-Volvulus: “Bloat”

20. Predisposing factors suggested by epidemiology (Glickman et al):

a. Large size
b. Large depth to width ration for body conformation
c. Male gender
d. Being underweight
e. Eating only one meal per day
f. A faster rate of eating
g. Fearful or nervous temperament
h. An event perceived
21. Reduced risk:
a. Table scraps or canned food included with a dry dog food
b. Happy and easy-going character
22. Recommendation:
a. Feed twice daily
b. Add some canned food to dry diet
c. Avoid stress associated with eating
d. Do not allow to be underweight

Recommendation:
23. Feed a national brand pet food that says on the label that it has been tested using AAFCO
approved feeding and is complete and balanced.
24. Feed a high fat dry food for maintenance. Add a canned food during periods of work.
25. Feed enough to keep dog lean.
26. Do not feed supplements such as meat, bones, calcium or vitamins.

35
27. Give 50 IU/kg vitamin E once a week by mouth. You may also give 100 mg vitamin C
one hour before exercise and repeat every 6-8 hours during exercise but this may not be
beneficial and could exacerbate injury.
28. Keep treats to a minimum (greater than 10% of the diet). Most of the diet should be pet
food.
29. Give a dental chew once daily.
30. Make sure access to water at least every half hour during exercise.
31. Feed after exercise not before or during exercise.
32. Rest dogs after 4-6 hours work. If the dog is expected to work again within a few hours
then give sugar water and a high protein, high fat snack.

36
 Overview of Canine Dental Health and Disease
Susan E. Anderson, DVM, DABVP
(1) University of Florida

Why is veterinary dentistry important?

• Every pet has a mouth
• 85 percent of pets over two years have some evidence of periodontal disease
• Dental health contributes to overall health
• Goal should be prevention rather than treatment

Dental Disciplines
• Pedodontics: puppy dentition
• Orthodontics: guidance and correction of malocclusion
• Periodontics: treatment of supporting tissues of teeth
• Endodontics: treatment of disease affecting tooth pulp
• Exodontics: extraction of teeth
• Oral surgery: surgery of the oral cavity
• Restorative Dentistry: restoration of form and function
• Prosthodontics: construction of appliances to replace missing teeth and/or adjacent
structures

Anatomy

Head
• Mesocephalic: German Shepherd Dog, Labrador
• Brachycephalic: Boxer, Bulldog
• Dolichocephalic: Collie, Greyhound

Dentition
• Incisors: nibbling, grooming
• Canines: holding, tearing; largest and strongest teeth
• Premolars: cutting, holding, shearing
• Molars: grinding

Tooth Structure
• Teeth designed to be self-cleaning
• Natural diets of fiber, sinews, tendons
• Conical in shape
• Few contact points to trap debris
• Alkaline pH of saliva deters bacteria

Periodontium
• Supporting structures of the teeth
• Gingiva, periodontal ligament, alveolar bone

37
Tooth Anatomy
• Crown
• Root
• Enamel: covers the crown, hardest substance in body
• Dentin: bulk of the tooth structure
• Pulp: blood and nerve supply
• Gingival sulcus: space between gingival and tooth, 1-3 mm
• Cementum: covers root

Dental Formula

Deciduous

3 1 3
2{l3C1P3}

Permanent

3 1 4 2
2{l3C1P4M3}

Eruption Times

Deciduous teeth
• Incisors: 3-4 weeks
• Canines: 3 weeks
• Premolars: 4-12 weeks

Permanent teeth
• Incisors: 3-5 months
• Canines: 4-6 months
• Premolars: 4-6 months
• Molars: 5-7 months

Normal Occlusion
• Upper incisors in front of lower incisors (scissors bite)
• Lower canine fits evenly between upper canine and 3rd incisor
• Premolars fit in a “pinking shear” fashion, interdigitate
• Upper 4th premolar fits outside (lateral) to lower 1st molar

38
Malocclusion
Class 0 occlusion: normal or normal for breed
Class 1 occlusion: jaw relationship normal but one or more teeth out of position
• Base narrow canines
• Anterior crossbite
• Lance canine (spear, tusk)
• Posterior crossbite
Class 2 occlusion: mandible short in relation to maxilla – brachygnathic
• Overbite
• Unilateral wry (1/2 maxilla short)
Class 3 occlusion: maxilla short in relation to mandible – prognathic
• Underbite
• Unilateral wry (1/2 mandible short)

Pedodontics
Missing teeth
• Never developed, never erupted, trauma
• Radiograph (x-ray)
Retained deciduous teeth
• No 2 teeth of the same type should occupy the same space!
• Causes malocclusion, crowding
• Increased incidence of periodontal disease and tooth loss
• Extraction as soon as possible
• Caution not to disturb developing permanent tooth
Interceptive orthodontics
• Early extraction of deciduous teeth to prevent “interlock”
• Removes interference to allow for maximal jaw growth
• Will not cure a pre-existing genetic problem
• DO NOT trim or cut deciduous teeth – pain, infection, potential damage to permanent
tooth
Fractured deciduous teeth
• Frequent: running into objects, catching hard toys, overzealous play or tug-o-war
• Requires extraction
• If untreated: pain, infection, damage to permanent tooth especially enamel
Supernumerary teeth
• Extra teeth
• Usually incisors or premolars but can be canines
• Can cause crowding; if so, extract
Cranial mandibular osteopathy
• Inherited condition, most common in West Highland White Terriers
• Non-neoplastic (not cancerous) bone formation of the temporomandibular joint and occ
spreads to mandible
• Pain, fever, reluctance to eat, difficulty opening jaw
• Treat symptoms of pain, lessens with age

39
Periodontal Disease
• Inflammation of the structures supporting the teeth
• Normal gingival: smooth, coral pink, well attached, sulcus 1-3 mm
• Plaque: accumulation of bacteria, glycoproteins, polysaccharides that adhere to tooth
• Tartar (calculus): plaque mineralizes within 48 hours, forms more readily in alkaline
saliva

Predisposing Factors for Periodontal Disease

• Overcrowded, rotated teeth
• Retained deciduous teeth
• Soft, sticky diet with no brushing
• Slab fracture of tooth exposing rough surface for plaque accumulation
• Malocclusions
• Trauma
• Chemical irritants
• Systemic disease (uremia, diabetes)
• Open mouth breathing (dries saliva)

Clinical Signs of Periodontal Disease

• Halitosis
• Inflamed gums and/or bleeding
• Asymmetrical facial swelling
• Mobile teeth
• Gingival recession
• Nasal discharge
• Exposed roots
• Gingival pockets (> 3mm)
• Vertical and horizontal bone loss

Smaller Breeds More Predisposed to Periodontal Disease

• Closer teeth decreases tooth’s self-cleaning ability
• Smaller the dog the thinner the supporting bone
• Bacterial and inflammatory by-products can damage thin bone quickly
• Bone thinnest at incisors, frequent location of disease loss
• Smaller dogs live longer
• Open mouth breathing more frequent

Stages of Periodontal Disease

Stage 1: Gingivitis
• Only reversible state
• Gingival becomes swollen, rolled and red

Stage 2: Early periodontitis

• Increased gingival pocket depth

40
 • Up to 25 percent attachment loss
• Bacteria begins to change from aerobic to anaerobic
• Teeth stable
Stage 3: Moderate periodontitis
• Deeper pockets
• More cirulent anaerobic bacteria colonizes
• Up to 50 percent attachment loss (bone and gingival)
• Slight mobility of teeth
Stage 4: Severe periodontitis
• More than 50 percent attachment loss
• Increased severity of infection
• Salvageability of teeth is questionable
• Tooth mobility can be great

Treatment of Periodontal Disease

• Thorough prophylaxis – complete oral exam, supra gingival scaling, root
planning/subgingival curettage, polish, flush, repeat exam
• Radiographs
• Root planing – closed (<5 mm) vs. open (>5 mm)
• Extractions, periodontal surgery, endodontics (root canal)
• COMMITMENT to home care
• Reassess in 1-3 months

Indications for Antibiotic Use

• Oral ulceration
• Severe periodontitis
• Evidence of systemic disease (renal, cardiac, diabetes, Cushing’s)
• Additional surgery being performed
• Bone implants (hip replacement)
• Pulp capping

Antibiotics
• Ampicillin
• Amoxicillin
• Amoxicillin-clavulanate (clavamox)
• Clindamycin (antirobe)
• Metronidazole (Flagyl)
• Doxycycline

Other Dental Abnormalities

Caries (cavities)
• Bacterial degradation of enamel, not common in dogs
• Maxillary 1st molar most common

41
Abrasions (external source)
• Excessive grooming
• Toys especially tennis balls
• Rocks, fences, cages
Attrition (wear from other teeth)
• Malocclusion especially level bite
• Increased risk of fracture if mid tooth (canine)
Enamel hypoplasia (reduced formation of enamel, enamel dysplasia)
• Hereditary
• Systemic infection causing high fever during tooth formation
• Viral infection during tooth formation (distemper)
• Enamel organ damaged during early extraction of deciduous tooth
• Other trauma during formation
Discolored teeth
• Pink – purple – tan
• Pulpal hemorrhage and/or tooth death usually due to trauma
Inapparent oral nasal fistula
• Pocket that communicates with nasal cavity
• Lingual side of upper canine
• Rest of tooth may have little disease present
• More common in small dogs
Foreign bodies
• Wedged between upper 4th premolars
• Sticks, bones

Home Care
Brushing
• Gradual training with reward/positive reinforcement
• Ideal is daily
• Cleaning under edge of gums most important (gingival sulcus)
• Nothing truly replaces the mechanical disturbance of plaque
• Finger brush, gauze over finger (doesn’t clean sulcus well)
• Pet designed brush or small, soft child’s brush
• DO NOT use hand scalers or curettes regardless of training
o Trauma to gingival
o Excessive wear to enamel (not that thick)
o Without polishing, roughened surface of the enamel allows plaque to return
that much faster

Toothpastes
• Many choices
• Avoid human toothpaste
o Too much fluoride – dogs don’t spit
o Foaming agents can cause vomiting

42
Rinses
• Chlorhexiding gluconate 0.12 percent oral rinse
o CHX, Nolvadent, Hexarinse
o Inhibits plaque formation
o Bacteriostatic and bactericidal
• Zinc gluconate/Vitamin C
o Maxiguard
o Promotes healing of ulcerated oral tissues
Chew Toys
• Monitor to avoid swallowing, fractured teeth, choking
• Kong toys – dental
• Nylabone products
• Rawhides, some have tartar control coating (CET)
Diets and Treats
• T/D (Hill’s Pet Nutrition) fibers designed to squeegee teeth
• Tartar Check (Heinz) coated with hexametaphosphate
• Dentabone (Waltham)
• Dental Chew (Waltham)

43
 What’s New With GDV?
Christopher A. Adin, DVM, DACVS
University of Florida
Background:

Gastric distention and volvulus (GDV) is an acute, life-threatening disease that primarily affects
large and giant breed dogs. In dogs with GDV, the stomach rapidly fills with gas and fluid.
Rotation of the stomach on its axis (volvulus) prevents emptying of the stomach contents and
occludes the blood supply. Clinical signs in affected dogs include sudden swelling of the
abdomen, non-productive retching and lethargy. Severe distention of the stomach can decrease
the amount of blood returning to the heart, compromise breathing, and cause death of the
stomach wall.

Diagnosis and Treatment:

Due to advancements in the medical and surgical treatment of dogs with GDV, mortality rates
have decreased from 42 percent in the 1980s1 to 18 percent in recent years.2 Early diagnosis by a
veterinarian followed by rapid intravenous fluid treatment and decompression of the stomach has
become the standard of care. Dogs that are recovering from GDV require critical care and 24
hour monitoring due to the risks of irregular heart rhythms, bleeding tendencies and sepsis
(infection).

Recurrence:

The rate of GDV recurrence approaches 70 percent if the stomach is not surgically fixed to the
body wall (gastropexy) after the first incident. Fortunately, surgical gastropexy prevents
recurrence in 90-100 percent of dogs. As a result, it is recommended that surgical gastropexy be
performed after treatment for shock in dogs with GDV. At the time of surgery, the veterinarian
is able to evaluate the viability of the stomach wall and other organs which may need to be
removed or repaired, depending upon the degree of damage that has occurred.

New developments… The newest trend that I can foresee in veterinary medicine is a shift in
focus from the treatment of GDV that has already occurred to the prevention of GDV in high
risk breeds.

1
Muir W. Gastric dilatation and volvulus, with an emphasis on cardiac arrhythmias. J Am Vet Med Assoc
1982;180:739-742.
2
Brourman JD, Schertel ER, Allen DA, et al. Factors associated with preoperative mortality in dogs with surgically
managed gastric dilatation-volvulus: 137 cases (1988-1993). J Am Vet Med Assoc 1996;208:1855-1858.

44
Risk factors and epidemiology

Recent studies by Dr. Larry Glickman at Purdue University1 have identified a number of risk
factors for GDV which include: increasing age, having a first degree relative with GDV, faster
speed of eating, raised food bowl, and specific breed-related risks (e.g. Great Dane). Overall, a
pure-bred large or giant breed dog had a lifetime risk of 24 percent and 21.6 percent of
developing GDV, with a 30 percent chance of death from this incident. For Great Danes, this
lifetime risk increased to 42.4 percent.

Prophylactic gastropexy

Based on the aforementioned statistics, many surgeons (myself included) feel that prophylactic
gastropexy is indicated for high-risk large and giant breed dogs. Prophylactic gastropexy is an
elective procedure involving surgical attachment of the stomach to the abdominal wall in an
attempt to prevent the occurrence of GDV. The procedure is typically recommended at the time
of elective ovariohysterectomy or castration in pet dogs. Though elective gastropexy may be
performed at any time in breeding animals, it would be most reasonable to perform the procedure
early in life, as the incidence of GDV increases with age.

Prophylactic gastropexy may be performed through a standard midline abdominal incision or by

laparoscopic techniques.2 Laparoscopy involves the use of a tiny camera and light source so that
the surgeon may operate through small incisions, avoiding some of the pain and prolonged
recoveries that can be associated with more invasive surgical procedures. Elective ovariectomy
may be combined with the laparoscopic procedure in non-breeding animals. Depending upon the
technique employed, the complications associated with prophylactic gastropexy are minimal and
are infrequent. When the risks of the occurrence of GDV and the associated cost and mortality
rate of this condition are considered, prophylactic gastropexy would appear to be an excellent
option for dog owners with large or giant breed dogs.

1
Glickman LT, Glickman NW, Perez CM, et al. Analysis of risk factors for gastric dilatation and dilatation-volvulus
in dogs. J Am Vet Med Assoc 1994;204:1465-1471.
Glickman LT, Glickman NW, Schellenberg DB, et al. Non-dietary risk factors for gastric dilatation-volvulus in
large and giant breed dogs. J Am Vet Med Assoc 2000;217:1492-1499.
Glickman LT, Glickman NW, Schellenberg DB, et al. Incidence of and breed-related risk factors for gastric
dilatation-volvulus in dogs. J Am Vet Med Assoc 2000;216:40-45.
2
Hardie RJ, Flanders JA, Schmidt P, et al. Biomechanical and histological evaluation of a laparoscopic stapled
gastropexy technique in dogs. Vet Surg 1996;25:127-132.

45
 Tick-Borne Diseases: An Emerging Threat
Dr. Brian J. Luria
University of Florida
Introduction

Our awareness in human and veterinary medicine that certain insects and arthropods transmit
disease has been established for many years. In recent years, our knowledge has increased
dramatically, mostly due to advancements in our ability to diagnose these diseases.

For a variety of reasons, ticks are appearing in greater numbers than ever. Ticks are a very
important cause of debilitating and deadly diseases and conditions in both humans and domestic
animals. Almost equal to the disease transmitting potential of ticks, is the fear and concern that
arise among many owners and veterinary staff members when a tick is found on a dog or cat.

This discussion will focus on education regarding the diseases that ticks can transmit, how to
diagnose and treat them, and how to prevent your dogs from acquiring ticks and the diseases they
transmit.

Brief Review of Ticks

Ticks are blood feeding external parasites of mammals, birds, and reptiles throughout the world.
Ticks are second only to mosquitoes as vectors of pathogens. A vector is simply an organism
that transmits a pathogen. For this discussion, we will focus on four tick species, based on the
diseases that they transmit.

1. The Black-legged or Deer Tick (Ixodes scapularisI)

This tick is concentrated in both the North and Southeastern United States as well as in areas
surrounding the Great Lakes. It is the tick that transmits Borrelia burgdorferi, the causative
agent of Lyme disease as well as the agents of Babesiosis.

2. The Brown Dog Tick(Rhipicephalus sanguineus)

This tick has a widespread distribution. It is the tick that transmits Ehrlichia canis, one of
the causative agents of Ehrlichiosis as well as Babesia canis and Babesia gibsonii.

3. The American Dog Tick (Dermacentor variabilis)

This tick is widespread throughout the US as well as parts of Canada and Mexico. It is the
most important vector of Rickettsia rickettsii, the causative agent for Rocky Mountain
spotted fever in the eastern US.

4. Rocky Mountain Wood Tick (Dermacentor andersoni)

This tick is found mostly in the Northwestern parts of the United States. It is an additional
vector for Rocky Mountain spotted fever.

46
Basic Tick Lifecycle

Depending on the tick and environmental conditions, the lifecycle of a tick can range from a few
months to two years. Each developmental stage of a tick’s life requires a blood meal in order to
reach the next stage. Some species can survive for years without feeding.

Egg Stage
Female ticks lay eggs in secluded areas where vegetation is dense and several inches high. Adult
females of some tick species lay about 100 eggs at a time; others lay 3,000 to 6,000 eggs per
batch. Regardless of species, tick eggs hatch in about two weeks.

Larval Stage
After hatching, the larvae move into grass or shrubs in search of their first blood meal. If you or
your pet passes by, they attach themselves and crawl upward in pursuit of an area of the skin that
they can feed from. Then they drop off the host, back into the environment.

Nymphal Stage
After finding their first blood meal, the larvae molt into their nymph stage and begin searching
for another host. Nymphs are the size of a freckle and often go undetected, increasing the chance
for disease transmission.

Adult Stage
Once the nymph has had its blood meal, it matures into adulthood. Adult female ticks feed on a
host for eight to twelve days. In some cases, they will increase to 100 times their original weight
while feeding. While still on the host, the female will mate, fall off and lay her eggs in a
secluded place – beginning the lifecycle again.

Review of Common Diseases

I. Lyme Disease (Lyme Borreliosis)

A. Introduction
Lyme disease was named in 1977 when arthritis was observed in a cluster of children in
and around Old Lyme, CT. The first case of canine Lyme disease was reported in 1984.
Lyme disease is caused by the bacterium, Borrelia burgdorferi. These spiral shaped
bacteria are transmitted to humans and animals by the bite of infected deer ticks in the
genus Ixodes (Deer ticks). Ticks, small rodents, and other non-human vertebrate animals
all serve as natural reservoirs for B. burgdorferi. This means that the Lyme disease
bacteria can live and grow within these hosts without causing them to die.
B. Transmission
1. Black-legged ticks, also known as Dear ticks (Ixodes scapularis) are
responsible for transmitting Lyme disease bacteria to humans and animals in the
northeastern and north-central United States. On the Pacific Coast, the bacteria
are transmitted by the western black-legged tick (Ixodes pacificus). Ixodes ticks
are much smaller than common dog ticks. In their larval and nymphal stages,
they are no bigger than a pinhead. Ticks feed by inserting their mouths into the

47
 skin of a host and slowly taking in blood. Ixodes ticks are most likely to transmit
infection via saliva after feeding for two or more days. This amount of time is
needed for the Borrelia organism to travel from the tick’s midgut to the salivary
glands where it is transmitted.
2. In the spring, about 35 percent of ticks are thought to be harboring Borrelia,
whereas up to 50 percent of adult ticks may be infected with the Borrelia
organism in the fall.
C. Signs of Disease
1. Within days of the initial tick bite, animals will show flu-like symptoms
(fever, malaise) and possibly enlarged lymph nodes (in humans, a “bull’s-eye”
lesion can be seen on the skin at this stage). Up to two to three months later, signs
of an acute inflammatory process is seen (joints, heart, brain, eyes can all be
affected). Over years of being affected, chronic arthritic changes can be seen.
2. About 75 percent of dogs will get acute arthritis which usually lasts two to
four days and will often resolve on its own. However, dogs can have recurrent
bouts of arthritis. After about 100 days post tick exposure, signs of acute arthritis
resolve, even though animals are still infected.
D. Diagnosis
1. History, along with clinical signs, positive serology (see below), and prompt
response to antibiotic therapy are usually the criteria for the diagnosis of Lyme
disease in dogs. If animals are having acute arthritic signs, a sample of joint fluid
can be taken for analysis. Affected animals often have high numbers of
neutrophils (a white blood cell often present when fighting bacteria) in their joint
fluid.
2. Serologic testing is the most common modality used for diagnosis. Serum is
the liquid part of the blood that is left when the blood cells are removed. It is
comprised of water (naturally) as well as a very high content of various proteins.
These include albumin – a protein that aids in the proper retention of water in the
bloodstream and globulins – which are antibodies. Serological tests refer to a
laboratory test done on blood serum to measure antibodies to infections.
a. The most common screening serologic test for Lyme disease, as well as many
other infectious diseases, is called an enzyme-linked immunosorbent assay (or
ELISA) which quantifies the presence of specific antibody produced by the
immune system against specific organisms, such as Borrelia.
**A positive serology detecting antibodies directed against Borrelia
burgdorferiI is merely an indication of exposure to the organism or to a
vaccine which contains antigen (single subunit vaccine) or multiple antigens
(bacterin) to the spiorchete. An antigen is a substance capable of stimulating
an immune response. A positive serology by itself does not constitute a
diagnosis of Lyme disease. Antibodies persist in infected animals and do not
decrease after antibiotic therapy.
b. The ELISA test cannot distinguish between antibodies produced against
exposure to a natural infection and those produced against the vaccine for
Lyme disease. In order to separate these two, another serologic test called
Western blot testing is traditionally done to confirm natural exposure.

48
 c. Recently, a test has been developed that detects the presence of antibody
directed against a very specific surface antigen of Borrelia burgdorferi that is
produced only in response to active infection. This antigen is called the C6
antigen. The only commercially available test for this is made by IDEXX
Laboratories, Inc., and is called the SNAP3Dx™. It is a combination test that
also tests for Dirofilaria immitis antigen (Heartworm) and Ehrlichia canis
antibody (see below). This test should help veterinarians determine if a dog
has anti-Borrelia burgdorferi antibody induced by infection, rather than by
vaccination.
E. Treatment
1. It is important to remember that prevention measures can be effective in
reducing exposure to infected ticks, and most patients can be successfully treated
with antibiotic therapy when diagnosed in the early stages of Lyme disease.
2. Antibiotics are the treatment of choice for Lyme disease in dogs, as in
humans. Tetracyclines such as Doxycycline or lactam antiobiotics such as
Amoxicillin have been found to be very effective. Animals should be treated for
at least four weeks.
3. Dogs usually respond with clinical recovery within 24 – 48 hours; however
the organism can persist, hence the duration of antibiotic therapy. Evidence to
date indicates that in spite of adequate antibiotic therapy, infected individuals may
be infected for life.
4. Anti-inflammatory medications, such as carprofen or etodolac can be used to
alleviate arthritic pain in the short term. Corticosteroids, such as prednisone,
should be avoided because of their ability to suppress the immune system.
F. Prevention, Tick Control and Public Health Concerns
1. Vaccinating dogs for Lyme disease is still a controversial issue in veterinary
medicine and arguments for and against have been postulated over time. There
are strong arguments in favor of vaccinating dogs in endemic areas against Lyme
disease.
2. There are currently 2 different types of Lyme vaccines for dogs:
a. Whole-cell bacterin vaccine (LymeVax®, Fort Dodge; Galaxy Lyme®,
Schering-Plough Animal Health), which consists of a complete killed B.
Burgdorferi. This vaccine has been available for several years, however,
with recent advancements in vaccine technology, it is the less preferable
vaccine if one is to vaccinate their dogs.
b. Recombinant vaccine (rLyme®, Merial), which consists of only parts of
B. burgdorferi that are thought to provide protection from infection and/or
disease in dogs. This vaccine consists of outer surface protein A (OspA)
of B. burgdorferi. The mode of protection appears to involve killing the
bacteria in the tick, prior to its transmission into the host animal.
c. So, what dogs should be vaccinated? It is clear, based on the mode of
action of these vaccines, particularly the recombinant vaccine, that
vaccinating already infected or exposed dogs will not cure them and may
not prevent them from being infected. Naïve, or unexposed, dogs in
endemic areas appear to be the best candidates for vaccines.

49
 d. A fatal kidney infection by B. burgdorferi has been reported in some dogs
in endemic areas where antibiotic treatment had little effect. There has
been no convincing evidence that vaccines could be related to this disease,
however, the possibility of a connection does exist.
3. Tick control is discussed in detail at the end of these notes.
4. Dogs do not appear to be reservoirs for human infection.
II. Ehrlichiosis
A. Introduction
Canine ehrlichiosis is an infectious rickettsial disease of dogs caused by a variety
of different ehrlichial species, the most notable one being Ehrlichia canis.
Rickettsia are rod-shaped, coccoid, or diplococcus-shaped, often pleomorphic
bacteria that cause various diseases. E. canis was first recognized in Algeria in
1935 and first reported in the United States in 1963. The disease gained
prominence due to devastating losses of military working dogs stationed in
Vietnam. Ehrlichiosis is an illness characterized by a reduction in cellular blood
elements.
B. Transmission
1. Ehrlichia canis is transmitted by the vector tick Rhipicephalus sanguineus, or
brown dog tick. This tick is also responsible for spreading Babesiosis (see
below). This tick prefers to feed on dogs over humans.
2. Canine infection occurs when salivary secretions from the tick contaminate
the attachment site during ingestion of a blood meal.
C. Signs of Disease
1. There are three phases of disease seen with Ehrlichiosis: acute, subclinical and
chronic:
a. Acute: After an incubation period of 8 – 20 days, the infected dog enters
into the acute phase, which lasts about two to four weeks. During this
time, the organism multiplies within circulating white blood cells and is
transported to all areas of the body. Fever, depression, malaise, anorexia
and weight loss, discharge from the eyes and nose, enlarged lymph nodes
and occasionally swelling of the legs can all be seen during this time.
Platelets, a cell line responsible in part for blood clotting, often are
decreased during this phase of disease by a variety of mechanisms.
b. Subclinical: Occurs six to nine weeks post-infection and is characterized
by persistence of low platelet count, variably low white and red blood cell
counts in the absence of obvious illness. Dogs with an adequate immune
system may eliminate the infection during this phase.
c. Chronic: Dogs unable to effectively rid the organism become chronically
infected. Elevated globulin levels in the blood are often seen. In this
stage of disease, many dogs develop bone marrow suppression (the bone
marrow is where the majority of our cells are made). Clinical signs in this
stage are variable. Some dogs show no signs of illness, while others can
show a variety of clinical signs, including many bleeding abnormalities,
particularly from the nose.

50
 2. Laboratory abnormalities that can be seen include deficiencies in all cell lines,
red, white and platelet. Occasionally a dramatic increase in the lymphocyte white
blood cell line is seen.
3. Bone marrow examination usually reveals low cell numbers with varying
degrees of suppression of all cell lines. However, elevation in the number of
plasma cells, another white blood cell, is a frequently reported finding.
4. Serum proteins are often abnormal. Elevated globulins are commonly seen.
Sometimes this is seen as elevation of all of the globulins equally, or just one of
them. If only one globulin is elevated, described as a monoclonal gammopathy,
this can easily be confused with a type of cancer called Multiple Myeloma. Often
plasma albumin is low.
D. Diagnosis
1. Morulae (intracellular inclusions composed of clusters of organisms) are
observed rarely and almost exclusively during the acute stage of infection.
However, if these are observed, they are definitively diagnostic.
2. Serologic testing is again the most common means of diagnosing Ehrlichiosis.
The indirect fluorescent antibody (IFA) technique is currently recommended. The
only drawback is that there is often cross-reactivity amongst different species of
Ehrlichia.
3. Polymerase chain reaction (PCR) can be used to confirm diagnosis, as this is a
molecular test that tests for the presence of DNA of the ehrlichial organism.
4. As discussed in the Lyme disease discussion, IDEXX Laboratories has
marketed an in-house ELISA antibody test for E. canis that is calibrated at
approximately 1:100. Again, it needs to be said that a positive test should be
interpreted in combination with history, clinical signs, or laboratory abnormalities
since a positive test does not necessarily mean that the dog has active disease.
E. Treatment
1. Tetracyclines or Doxycycline, administered for at least three weeks is the
treatment of choice for Ehrlichiosis. Dramatic clinical improvement generally
occurs within 24-48 hours after initiation of appropriate antibiotics.
2. If an animal is in the chronic phase of the disease and has bone marrow
changes, it can take up to 120 days for the bone marrow to regenerate following
treatment.
F. Public Health Concerns
There is no evidence that direct transmission of ehrlichial species from dogs to
humans occurs.
III. Rocky Mountain Spotted Fever
A. Introduction
1. Rocky Mountain spotted fever (RMSF) is an infectious rickettsial disease of
dogs, which is characterized by sever vascular damage. Canine susceptibility to
Rickettsia rickettsii was demonstrated in 1933. Recent reports emphasize that,
contrary to previous literature, untreated naturally-occurring RMSF can result in
death. Clinical reports suggest that RMSF is a much more common cause of
disease in dogs than was previously recognized.
2. Despite its name and original description as a disease of humans in the
western United States, the majority of human cases of RMSF occur in the

51
 southeastern US. Human cases of RMSF have been reported from nearly every
state in the US, western Canada, Mexico, and South America. Distribution of the
disease is related to the distribution of the vector ticks Dermacentor variabilis, the
American dog tick found in the eastern US, and Dermacentor andersoni, the
wood tick, which is the principal vector in the western US. Canine RMSF has
been recognized in most southeastern states, New York, Massachusetts, and Ohio.
3. Rocky Mountain spotted fever is caused by Rickettsia rickettsii, a very small
bacterium that must live inside the cells of its hosts. They are difficult to see in
tissues by using routing histologic stains and generally require the use of special
staining methods. Rocky Mountain spotted fever was first recognized in 1896 in
the Snake River Valley of Idaho and was originally called “black measles”
because of the characteristic rash. It was a dreaded and frequently fatal disease
that affected hundreds of people in this area.
B. Transmission
R. rickettsii is a small intracellular parasite in the family Rickettsiaceae. The
organism is a member of the spotted fever group rickettsiae, which includes both
pathogenic and nonpathogenic rickettsiae. Dogs and rodents comprise the
mammalian reservoir for R. rickettsii. Following tick bite, infection may occur in
humans, dogs and cats. Within the general tick population, few ticks contain
infective R. rickettsii. However, there are geographic centers that contain large
numbers of infective ticks. Attachment of a tick to a host for five to 20 hours is
required before infection can take place.
C. Signs of Disease
1. R. rickettsii is transmitted to the dog by a tick bite. The rickettsiae enter the
circulatory system and replicate. Rickettsiae cause direct damage to cells lining
the vascular system, resulting in vascular inflammation and death of the cells,
swelling of the skin, hemorrhage, which if severe can cause low blood pressure,
shock and death. Central nervous system swelling may contribute to the
development of neurologic signs, rapid clinical deterioration, and death. Fluid
accumulation in the lungs may occur, and may be detected with an X-ray.
Clinical signs include rapid breathing, difficult breathing or coughing in some
dogs. In severe cases, acute kidney failure may occur. Due to increased vascular
permeability, fluid therapy should be used with caution, when treating dogs with
Rocky Mountain spotted fever.
2. Some dogs develop mild illness following experimental and naturally
occurring infection with R. rickettsii. In addition to the infective dose or strain
variation in rickettsiae, breed predisposition may play a role in determining the
severity of illness. For example, some have observed severe disease in Siberian
Huskies, whereas Deerhounds sustain high antibody titers without prior evidence
of associated illness.
3. Clinical signs in canine infection are identical to human cases of RMSF.
Unlike Ehrlichiosis in which chronic infection can persist, the total duration of
illness following R. rickettsii infection is generally short (two weeks or less). For
this reason, canine RMSF is a disease that presents in the spring and summer
(April to September). Fever, loss of appetite, depression, vomiting, diarrhea, and
neurologic abnormalities are typically associated with the clinical presentation of

52
 the animal. Redness and discharge from the eyes, nasal discharge and coughing
are frequent findings. In some dogs, weight loss is very severe, considering the
short duration of illness. Joint pain and/or muscle pain may represent the only or
most prominent clinical finding.
4. Bloody nasal discharge, blood in stools, blood in the urine and areas of
bruising occur in some dogs, but may not develop unless diagnosis and treatment
are delayed for five or more days after the onset of clinical signs. Bleeding into
the eye is a consistent finding, even early in the course of the disease. Scrotal
swelling, hemorrhage, and testicular pain are frequently observed in mail dogs.
This finding correlates with the disease in man and experimental infections in
rodents.
5. Neurologic signs including pain, loss of balance, tilting of the head, stupor,
seizures, and coma may occur in dogs with RMSF. Similar to Ehrlichiosis, this
presentation can mimic canine distemper in the young dog.
D. Diagnosis
1. The marked variation in clinical presentation allows RMSF to mimic
numerous other infectious and noninfectious diseases. Seasonal occurrence,
history of tick infestation, fever, or the previously described clinical findings
would suggest the possibility of RMSF.
2. Decreased platelets, generally mild in degree, are the most consistent finding
in blood counts. Biochemical abnormalities reflect the effects of generalized
vascular damage and vary with the severity and duration of infection. Low
protein levels, elevated kidney function tests, and increased liver enzymes (serum
alkaline phosphatase, alanine animotransferase) may occur in dogs with RMSF.
In general biochemical abnormalities are mild. If joint swelling is present,
inflammatory cells may be present.
3. Confirmation of a diagnosis requires either direct immunofluorescent testing
for R. rickettsii antigen in tissue biopsies, or serologic testing utilizing an indirect
fluorescent antibody test. Evaluation of acute and convalescent sera with greater
than or equal to a fourfold increase in antibody titers confirms a diagnosis of
RMSF. Timing of sample collection for acute and convalescent sera will greatly
influence the serologic results. Cross reaction with other spotted fever group
rickettsiae and persistent tick exposure to R. rickettsii complicates the
interpretation of serologic results from clinical patients with suspected RMSF.
Direct immunofluorescent testing of tissue biopsies provides the opportunity for
rapid diagnosis of RMSF. R. rickettsii are generally more readily demonstrated in
human patients in areas of hemorrhage prior to initiation of treatment. This also
appears applicable to canine patients, although organisms may be more readily
identifiable in clinically unaffected skin from dogs. If acute phase sera are
obtained several days after the onset of clinical signs, antibody titer to R. rickettsii
antigens will be high.
E. Treatment
Tetracycline or doxycycline is the treatment of choice. However,
chloramphenicol and enrofloxacin are equally effective. A rapid clinical response
occurs in dogs without neurologic signs following the initiation of treatment. If
fever persists, another diagnosis should be considered likely. Delay in diagnosis

53
 and initiation of tetracycline of the use of antibiotics lacking efficacy for treating
rickettsial diseases may result in a fatal outcome. Due to sever vascular damage,
fluid therapy should be utilizes with caution.
IV. Babesiosis
A. Introduction
1. Babesiosis is a tick-borne hemoprotozoan (blood) disease. The organism is
called Babesia, the disease is called Babesiosis. There are two primary infecting
species: Babesia canis and Babesia gibsonii. Babesia species can cause an acute
hemolytic anemia in dogs. This is a low red blood cell count caused by the
destruction of the red blood cells within the animal’s body. Babesia has
worldwide distribution. In a high percentage of dogs with acute or potentially
chronic babesiosis, it will contribute to an immune-mediated hemolytic anemia,
where the red blood cells are destroyed by the animal’s own immune system.
Babesiosis is a cyclical disease, similar to malaria. Dogs that recover from the
initial infection show variable and unpredictable patent periods alternating with
dormant periods.
2. Historically, Babesia gibsonii was considered endemic in Asia, Africa and the
Middle East, but was not recognized in the United States until 1979.
Subsequently, B. gibsonii infection was recognized in dogs from California and
most recently in Pit Bull Terriers in the southeastern US. In most instances, the
presenting problem was immune-mediated hemolytic anemia. To date, a
competent tick vector for the organism has not been identified in the US;
therefore, establishment of the organism within the tick population may not be
possible. As the efficacy of currently available drugs for treatment of B. gibsonii
is limited, veterinarians should report any suspected cases to the State
Veterinarian. Should B. gibsonii become established within a tick population in
the US, the consequences could be serious.
B. Transmission
Babesiosis is thought to be transmitted by the vector tick Thipicephalus
sanguineus, or brown dog tick, the same tick that transmits Ehrlichia canis. This
has not been definitively demonstrated.
C. Signs of Disease
Acute phase is of short duration, and is where the dog is initially infected with the
disease. If the dog does not die outright from the infection, then it moves on to
the next phase. Subclinical phase can last months or years. It is characterized by
a fine equilibrium between the parasite and the immune system of the host. This
equilibrium can be disturbed by a number of things: environmental stress,
additional diseases/infections (especially Ehrlichiosis), immunodeficiency, spleen
removal, surgery, stress, hard work, immunosuppressive treatment, or use of
corticosteroids. The dog may exhibit few clinical symptoms during this phase,
beyond intermittent fever and loss of appetite. If the equilibrium is disturbed, the
parasite will begin to slowly grow in number and the dog will move into the next
phase. In the chronic phase, if the dog’s system remains unable to clear the
parasite, it enters this final phase. The most obvious initial signs to an owner are
a cycle of: lethargy, loss of interest in food, and a gradual loss of body condition
especially evident around the eyes and along the spine. Other symptoms are:

54
 upper respiratory problems (coughing or labored breathing), vomiting,
constipation, diarrhea, ulcerative stomatitis (sores in the mouth), edema
(swelling), abdominal swelling (ascites), bleeding under the skin or a rash
(purpura), low white blood cell count, clotting problems, joint swelling, back
pain, seizures, weakness, increased liver enzyme, low platelet count, hyper
reflective eyes, enlarged lymph nodes, enlarged spleen, septic shock, depression.
D. Diagnosis
1. A combination of a regenerative anemia, elevated bilirubin, low platelet
count, elevated kidney values, elevated globulins and urinary “casts” are all
common with Babesiosis.
2. Indirect fluorescent antibody tests are available and will demonstrate antibody
titers against the organism.
3. Definitive diagnosis is based on organism demonstration in red blood cells.
E. Treatment
1. Until recently, there has not been an approved anti-babesia drug available in
the United States for treatment of canine babesiosis. Imidocarb diproprionate
(Imizol®, Schering-Plough Animal Health) is currently available for the treatment
of babesiosis in dogs. In acute babesiosis, the therapeutic response is rapid, with
increasing production of new red blood cell values documented within 12 to 24
hours. In Africa and other regions of the world, imidocarb diproprionate is
considered efficacious for treatment of E. canis, as well as B. canis infections.
Some reports of success using metronidazole or clindamycin have been reported.
2. Although multiple therapies are being studied, there is no definitive treatment
established for B. gibsonii infections in dogs.

Preventive Care
V. Tick Control
A. Advancements in the products available to control fleas and ticks have revolutionized
their prevention in veterinary medicine. In the past, we were recommending multiple
products, from whole house flea bombs to topical powders, all containing chemicals less
than ideal regarding exposure to our pets and to their owners. Now, more safe and
effective products have been developed for use in dogs and cats.
B. Topical “spot-on” products
1. Frontline and Frontline Plus
A topical product which kills both fleas and ticks. The active
ingredient is Fipronil. It is marketed to prevent fleas for up to three
months, and prevent ticks for up to one month. Although not
established, the label claims that ticks will die prior to beginning a
blood meal. Frontline PLUS contains an insect growth regulator as
well, which prevents eggs laid by fleas from developing into adults.
2. KillTix® (Bayer)
a. Label claims a single application will repel and kill ticks for up to
four weeks. Apply KillTix® montly when ticks are a threat in
your area. In more acute infestations, repeat applications can be
made, but not more than every three weeks.
b. Can ONLY be used in dogs.

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 C. Tick Collars
Preventic® Collar
Active ingredient is amitraz. Label claims that it kills ticks for up to three
months. Studies have shown similar efficacy between fipronil and
amitraz.
D. Revolution® is not effective at preventing ticks.
E. Vaccination
Other than the Lyme disease vaccine discussed above, no other vaccines are available to
prevent infection.

How do I remove ticks from my dog?

If possible, use blunt forceps or tweezers. Place tips around the tick where it is attached to the
skin. Remove tick with a steady pull away from the skin. DO NOT JERK OR TWIST THE
TICK. Take care not to crush or puncture the body of the tick or to get any fluids form the tick
on you. After removing the tick, cleanse the area with mild soap and water and wash your hands
with soap and water. Remedies such as matches, petroleum jelly or nail polish do not cause ticks
to detach.

Other Resources

1. American College of Veterinary Preventive Medicine (ACVPM) www.acvpm.org

2. Centers for Disease Control and Prevention (CDC) www.cdc.gov

56
 Basic Genetics for the Dog Breeder
Anne P. Lannon, DVM

Basic Principles of Genetics

One of the basic principles of genetics involves the difference between phenotype (i.e., a dog’s
physical makeup/appearance) and genotype (a dog’s genetic makeup, which is passed on to the
offspring). Dog breeders try to assess the genotype of a dog based on its phenotype. As we all
know, the top winners are not always the best producers for just this reason. It is important to
examine not only the dog you are interested in using but also its littermates, parents, and
offspring, if possible. Try to determine what traits the dog possesses and how strong (prepotent)
is the potential for transmission of these traits to its offspring.

Disorders that puppies are born with are referred to as congenital disorders. Remember that a
genetic disorder is one that is determined by genes, whereas a congenital disorder is merely one
that is present at birth and may or may not have a genetic basis. Some genetic disorders manifest
themselves prior to birth and thus are both genetic and congenital. One example is renal
dysplasia, a disease in which the kidneys do not fully develop. Other genetic disorders, such as
primary lens luxation, as seen in some of the terrier breeds, may not be expressed until later in
life. An example of a disorder that would be congenital but not genetic would be herpes virus, or
puppies born with defects such as missing limbs because their dam received corticosteroids
during pregnancy.

Fundamentally, genetic diseases are due to abnormalities in deoxyribonucleic acid (DNA),

which is the material of which genes are made. Genes occur in pairs – one allele or member of
the pair is inherited from the mother and one from the father. Abnormalities in genes, called
mutations, can involve one or both members of a pair. A dog with different alleles in regard to a
given characteristic (e.g., one mutant allele and one normal allele) is called a heterozygote. A
dog with two identical alleles, whether mutant or normal, is called a homozygote.

Each genetic disease is inherited in a particular way. With a recessive pattern of inheritance,
both alleles of the pair must be abnormal to produce the disease. Affected animals have
inherited one mutant allele from each parent, both of which appear clinically (phenotypically)
normal. Mendel taught us that when two of these “carriers” of the gene are bred, a certain
percentage (25 percent) of their offspring will show the trait.

One example of a recessively inherited disease is cystinuria in the Newfoundland. Cystinuria

results from a kidney disorder that allows cystine crystals, or “stones,” to form in the urine. The
stones can potentially block the urinary tract, especially in males due to their anatomy.

Another example of a recessively inherited disease is phosphofructokinase (PFK) deficiency in

English Springer Spaniels. This disorder is caused by an enzyme deficiency that causes affected
dogs to have diseased red blood cells and muscle cells. The hallmark of the disease is
pigmenturia (dark urine), which commonly develops after strenuous exercise. Jaundice or
anemia can also occur during these episodes. Fortunately, these episodes are rarely fatal, but
care must be taken to avoid any stressful situations that could precipitate a crisis.

57
A second mode of inheritance is the dominant pattern, in which only one member of the gene
pair needs to be mutant to produce the disease. In classic dominant inheritance, every affected
dog in a pedigree has an affected parent, which also has an affected parent, and so on.

One example of a dominantly inherited disease is dermatomyositis, a disease of the skin and
muscle seen in Collies and Shetland Sheepdogs. The syndrome is characterized by skin lesions
such as vesicles (blisters), redness, ulcers, crusts, scales, and hair loss. These lesions are most
commonly seen on the face, ears, and the bony areas of the feet and legs, as well as the tips of
the tail. In very mild cases where there is no muscle involvement, the skin lesions may
spontaneously resolve, or may even be missed by the owner, but if these dogs are bred they can
produce the disease.

Another, less common mode of inheritance is X-linked, which refers to genes located on the X
chromosome. In X-linked recessive diseases, the affected animals are usually male. They
receive the mutant gene from their mothers, which are heterozygous carriers that do not have the
disease. Two examples of X-linked diseases are Hemophilia A (seen in some lines of German
Shepherd Dogs) and X-linked severe combined immunodeficiency (SCID), which has been seen
in the Basset Hound and the Cardigan Welsh Corgi.

Sex limited inheritance is a mode of inheritance in which an autosomally transmitted trait (one
not transmitted on the sex chromosomes) is expressed in only one sex. One example is
persistent mullerian duct syndrome in the Miniature Schnauzer.

Finally, we see diseases that are inherited in a complex pattern not fitting any single gene mode.
These defects result from the cumulative action of a number of different genes (polygenic) rather
than from abnormalities in a single pair. Cleft palate, bite problems, and hip dysplasia are
examples of defects inherited in this manner.

Avoiding Genetic Diseases

First, it is vitally important that you know what genetic diseases are a problem in your particular
breed. Breed clubs are doing an excellent job of keeping abreast of health concerns in their
respective breeds. Also, the American Kennel Club has created the Canine Health Foundation,
which devotes significant resources to canine health research in the areas of genetics and breed-
related health problems.

If you breed a litter and suspect a problem with one or more puppies, have your veterinarian
examine the litter carefully. If he or she is unsure of what the problem is or whether it is a
genetic problem, have your veterinarian refer you to someone who can help. There are
universities in all areas of the country now that are working on genetic diseases in dogs.

Screening for Disorders

Your breeding stock should be screened for those genetic diseases for which tests exist. Hip and
elbow dysplasias, eye disorders such as progressive retinal atrophy (PRA), heart defects, and

58
bleeding disorders are examples of genetic diseases for which routine screens are conducted in
breeds shown to have these problems. Keep in mind that the age at which these defects can be
detected varies by breed.

Screening for recessive genes is much more difficult. Several diseases (and I’m happy to say
more all the time) have been identified at the biochemical or molecular level, and a laboratory
test utilizing a few drops of blood or a few cells can be used to identify animals affected by
and/or carrying the gene for these diseases.

We need to make a distinction between a direct DNA test and a linkage based DNA test. With a
direct DNA test, the disease gene itself has been clearly identified and it is the presence or
absence of that gene that is used to identify affected, carrier, and/or clear dogs. Linkage based
tests measure the presence of microsatellites (large chunks of DNA consisting of repetitive
sequences that stand out from the rest and serve as markers) that may be located close to the
gene for a genetic disorder on a chromosome rather than identifying the gene itself.

One example of a direct DNA test available to detect a genetic disease is the test for PFK
deficiency. This test was developed at the University of Pennsylvania by Drs. Urs Giger and
Bruce Smith. The test is based on the fact that diseased (affected) dogs have two mutant PFK
gene copies, carriers have one normal and one mutant PFK gene copy but are clinically normal,
and normal dogs have 2 PFK genes with the correct code. The test requires only a few drops of
blood from which the DNA is extracted and tested by the use of a polymerase chain reaction
(PCR), a modern laboratory technique that results in bands showing up in the area of either the
mutant allele, the normal allele, or in the case of carriers, both.

For recessive diseases (or traits) for which there is no laboratory test for carriers, test breeding
remains the only way to identify carriers. Test breeding consists of breeding a dog that is
suspected to be a carrier either to a dog that has the disease or to a proven carrier. If even one
puppy is affected, then the dog in question is a confirmed carrier. However, if no puppies are
affected, you still cannot be absolutely certain of the test dog’s status – in any one litter the
actual ratio of affected to normal animals may be very different from what was expected. The
more normal puppies born, the greater the likelihood that the dog is normal and not a carrier.

There are several problems with test mating, including the fact that many genetic disorders are
not recognized until the offspring are several years of age. Another problem is that test breeding
may produce affected and/or carrier pups. Finally, in most breeding programs it is unrealistic to
think that only noncarrier, normal animals can be used for breeding. In some breeds, this is
virtually impossible. A more realistic approach would be to identify carriers so that if they are
vitally important to a breeding program they can be bred only to noncarriers; the breeding
program can then be continued using the normal noncarrier offspring from these crosses.

Pedigree Evaluation

Careful evaluation of pedigrees should also be done prior to breeding. There are three basic
types of breeding programs one can undertake based on pedigrees:

59
The first type of breeding program is inbreeding. The general definition of inbreeding is the
mating of two individuals that are related to each other through one or more common ancestors.
The closer the relationship, the greater the degree of inbreeding.

The second type, linebreeding, is actually just a form of inbreeding that usually involves the
breeding of a sire with more distantly related relatives than its daughters, sisters, or dam.

Finally, outcrossing is a third type of program that involves breeding two dogs with no common
ancestors. This may be almost impossible in breeds with a limited foundation but can be used in
breeds where foundation stock came from various sources. Although there is less chance of
recessive genes being expressed, there also tends to be less uniformity in the litter. This could,
however, be a way to introduce desirable traits that your stock is lacking.

Conclusion

Many people feel that genetic diseases are on the rise. Certainly more genetic diseases are
recognized today because there are more sophisticated methods of diagnosis available. The
development and institution of diagnostic tests, therapies, and preventive strategies for acquired
diseases (such as infection, nutritional imbalances, and toxicities) have greatly reduced
morbidity and mortality in puppies, hence the inherited diseases have become relatively more
apparent.

The availability of genetic testing and counseling for breeders is also on the rise. Such services
are expected to increase nationwide over the coming years as veterinarians, researchers,
breeders, and breed organizations focus increasingly on the problems (and solutions!) to genetic
defects in dogs.

I strongly feel that by working together to solve these problems we will continue to enjoy and
extol the virtues of purebred dogs for many generations to come!

Recommended Readings

1. Ackerman L: The Genetic Connection: A Guide to Health Problems in Purebred Dogs.

Lakewood, CO, AAHA Press, 1999.
2. Bell, Jerold: Choosing Wisely, American Kennel Club Gazette, vol. 117, no 8. New York,
American Kennel Club, 2000.
3. Lynch, D: Mapping the Future of Canine Health. , American Kennel Club Gazette, vol.
117, no 8. New York, American Kennel Club, 2000.
4. Mostoskey UV, Padgett GA, Stinson AW, et al: Canine Molecular Genetic Diseases.
Compendium on Continuing Education for the Practicing Veterinarian, vol. 22, no 5.
Trenton, NJ, Veterinary Learning Systems, 2000.
5. Paddock A: Joining Hands for Breed Health. , American Kennel Club Gazette, vol. 117,
no 8. New York, American Kennel Club, 2000.
6. Willis, MB: The Road Ahead. , American Kennel Club Gazette, vol. 117, no 8. New
York, American Kennel Club, 2000.

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Websites of Interest

AKC Canine Health Foundation: www.akcchf.org

Canine Genome Project: www.fhcrc.org/science/dog_genome/dog.html

Cornell Genetics Course: www.ansci.cornell.edu/cat/cg01/dogcourses.html

Optigen, Inc.: www.optigen.com

VetGen, LLC: www.vetgen.com

61
 Neurologic Emergencies
R.M. Clemmons, DVM, PhD
University of Florida
The development of neurologic disease in dogs and cats can be stressful to the owner, since the
clinical signs may be acute and severe. Some conditions do represent clear emergencies
whereby immediate intervention can not only be life saving, but also can reduce the suffering of
the pet and reduce the recovery time if treated decisively and swiftly. On the other hand, a
number of neurologic problems look serious, but are not truly emergencies. Understanding
when a neurologic problem is a true emergency as compared to when it is only something that
should be tended to as soon as possible can be important. This distinction prevents delaying
treatment, while not unduly costing the owner in needless emergency fees and procedures. Here
are a few examples of true neurologic emergencies and some conditions that are not. Overall,
seizures, coma, paralysis, vestibular disease and nervous system trauma are examples of
conditions that may be true emergencies regardless of cause along with the important aspects of
treatments.

Seizures

A reproducible change in behavior can be called a seizure. Most commonly, seizures are
associated with an increase in voluntary motor activity, an alteration in consciousness, and an
increase in involuntary motor behavior. Severe seizures result in what most people recognize as
“grand mal” seizures when the animal is on its side and shows alternating extension and flexion
of the limbs. A single, simple seizure that lasts less than two minutes is probably not of
immediate concern. Contact with your veterinary team in a timely manner is indicated and
discussion about what should be done for diagnosis and treatment. On the other hand, more than
three seizures in an hour or a single seizure that lasts more than five minutes probably constitutes
a true neurologic emergency. This may be called status epilepticus, a special case where
seizures occur one after another without abatement. If these seizures are not stopped, the
resultant hypoxia may result in irreparable brain damage. The goal, then, is to stop the seizures.
This requires injectable medications, including diazepam, pentobarbital and Phenobarbital.
Although pentobarbital is not an anticonvulsant, it can sedate the patient long enough for
phenobarbital to work. Give diazepam (to effect) at 0.5-1.5 mg/kg IV. If the seizures continue,
repeat and give both pentobarbital and phenobarbital at 2 mg/kg IV. Remember to check the
glucose level and give if low and consider calcium glucconate if the seizures don’t seem to be
controlled. Once the seizures are under control, the patient should be examined to determine the
cause of the seizures and anticonvulsant therapy with phenobarbital and/or KBr continued while
achieving the diagnosis. Since there may have been hypoxia from the seizures, use of
antioxidant steroids (Solu Medral or Solu Delta Cortef) may be given at 15-30 mg/kg and
repeated every five to eight hours as needed for 24-48 hours. In most referral centers, status
epilepticus is now treated with Constant Rate Infusions (CRI) of diazepam at 0.25-0.5
mg/kg/hour. Once the seizures are controlled, the rate is reduced and oral medication with
maintenance anticonvulsants is begun. Caution with CRI of diazepam is that it should be given
separately from fluid infusion and by a central intravenous line that reduces the risk of peripheral
vasculitis from the diazepam. After the emergency is controlled, then diagnostic tests can be
performed to find the underlying disease process that led to the seizures.

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Flow Chart for Treatment of Status Epilepticus:

• Give IV diazepam 0.25-0.5 mg/kg

• If continues:
o Give IV pentobarbital 2 mg/kg and IV phenobarbital 2 mg/kg
o OR Start CRI IV diazepam .025 - .05 mg/kg/hour
• Start maintenance anticonvulsants

Coma

Acute loss of consciousness (coma) or onset of stupor (almost complete unconsciousness but
arousable with vigorous stimuli) is usually an emergency. Initial evaluation should take care of
the “ABC’s” of emergency medicine: make sure there is an Airway, support Breathing and assist
Cardiac function as needed. Once this has been evaluated, consideration should be give to the
location and cause of the problem. Cerebral diseases usually have normal to small pupils,
Cheynes-Stokes respiration (crescendo-decrescendo breathing pattern) and a slow heart rate.
Mid-brain diseases have fixed pupils that are midrange or dilated, hyperventilation and rapid
heart rate. Caudal brain stem lesions have myotic pupils and irregular respiration and heart rate.
The common causes include head trauma, intoxication (organophosphate, ethylene glycol, etc.),
hypoglycemia, hepatic encephalopathy, meningoencephalitis, hydrocephalus, neoplasia and
cerebrovascular disease. So, treatment may depend upon finding the causative factor and
developing an appropriate treatment plan. Initially, provide support with oxygen therapy if
blood gasses indicate problem or to potentially reduce cerebral edema. Give methylprednisolone
(Solu Medral ) 30 mg/kg. If meningitis is suspected, consider support with IV sulfadimethozine
at 15 mg/kg every twelve hours and cefazolin at 22 mg/kg every eight hours. If cerebral edema
is suspected give IV mannitol at 0.25 – 2 gm/kg over 10 – 15 minutes followed in 15 minutes by
furosemide at 0.5 – 1 mg/kg. This can be repeated every four hours, if needed. Once the patient
is stable, referral to a center where CT scan or MRI, CSF analysis and 24-hour tertiary care can
be provided.

Paralysis

Acute loss of function of two or four legs resulting in paralysis is a common emergency
situation. The “dynamic factor” (how quickly the spinal cord is damaged and with what force
creates the damage) dictates the severity of clinical signs. The amount of traumatic force
imparted by a small amount of material traveling rapidly is greater than a larger amount going
slowly. In the worst case, this means that time for intervention is also quite short. In most cases
of paralysis, definitive treatment must be started before 24 hours in order to achieve the greatest
success. In some cases, this time is shorter and treatment may need to be started within four
hours of the initial injury. Unfortunately, delaying treatment to see the outcome may preclude
success. We treat severe paralysis as a medical and surgical emergency. In patients with
complete motor and sensory paralysis, the patient should be treated for acute spinal injury and be
immediately referred to a center that can diagnose and definitively treat the problem. In patients

63
who are paralyzed but retain deep pain, then it is possible to treat them for acute spinal injury
and observe them for signs of improvement. If they are worse or no better within 24 hours, they
then constitute an emergency referral. On the other hand, it is best to treat these patients as true
emergencies at the outset. In patients with mild paresis or mere back pain, they can be worked-
up for the rule/out and referred if they do not make improvements in five to seven days. These
later patients may benefit from surgical intervention, but may not represent immediate
emergencies, as do patients with paralysis. In general, paralysis of a single limb is not an
emergency if the patient is stable, but may need methodic work-up during the first few days to
weeks.

Initial medical management of acute paralysis consists of giving 30 mg/kg of

methylprednisolone (Solu Medral or Solu Delta Cortef) IV, initially; followed by 15 mg/kg
every eight hours for the first 24 – 48 hours. Also during this time, referral can be arranged and
initial diagnostics performed. The patient is stabilized and referred to a facility capable of
emergency surgery. There is probably no rational reason to give these patients dexamethasone
since the antioxidant action of the short-acting methylprednisolone is superior in the eventual
outcome, a fact established over the last decade. There is also not place for the use of NSAID
(non-steroidal anti-inflammatory drugs) medication in acute spinal injury. With rapid surgical
intervention, patients who are paralyzed with deep pain have a 90 percent chance of significant
recovery if treated in the first 24 hours. In dogs with no deep pain, the chances for recovery are
less and probably around 75 percent in the first 24 hours. In the next 48 hours, these dogs have a
50 percent chance of recovery; while, after 72 hours, their chances fall to around 25 percent
(which is essentially the same as without surgery).

Vestibular Disease

All cranial nerves have the potential to develop specific syndromes that are clinically classified
as idiopathic disorders. This is probably due to the fact that each cranial nerve represents a
unique developmental anatomy from their respective brachial arches. This also gives them a
unique antigenic signal allowing very specific immune attack upon them. Idiopathic vestibular
disease represents one of these cranial nerve syndromes.

Clinically, idiopathic vestibular disease presents as an acute onset of vestibular signs with severe
imbalance, due to its sudden onset and the severe nystagmus, which is associated with the onset
of the disorder. Since the eyes are unable to fix on the horizon and the vestibular mechanism is
defective, there is severe vertigo. This often results in the rolling described by the owners. This
can be mistaken for a seizure, which it is not. During the early phases of idiopathic vestibular
disease, the patient often experiences nausea to the point of frequent vomiting and inappetence.
The head tilt will be toward the side of dysfunction and the nystagmus will be horizontal or
rotatory with the fast-phase away from the head tilt. If supported, there are no other neurologic
deficits and proprioception is normal.

The diagnosis of idiopathic vestibular disease is tentatively made by the presence of acute
clinical signs in the absence of other physical findings. The minimum database includes
physical examination, otoscopic examination and neurologic examination. The lack of findings
(other than the peripheral vestibular signs) supports the diagnosis. The signs of idiopathic

64
vestibular disease are regressive, meaning that they disappear without treatment over time. As
such, the fact that the disease is self-limiting is how the final diagnosis is achieved. The
nystagmus will usually improve or disappear all together within three to five days of the onset.
The patient will, then, improve in their imbalance and be more able to function normally. This
improvement will continue until minimal deficits will remain. It is possible that there will be a
residual head tilt. If the head tilt persists beyond six months following the onset of signs, it is
likely to be permanent.

There is no treatment that will hasten the recovery from idiopathic vestibular disease.
Corticosteroids probably do not offer an effective treatment. On the other hand, since idiopathic
vestibular disease may represent an immune disease, anti-oxidant steroids (such as Solu Medral)
may decrease severe symptoms. During the early phases, anti-vertigo drugs might make the
patient more comfortable. Generally, I use dephenhydramine at 2 – 4 mg/kg every eight hours as
needed. Diphenhydramine is a centrally active anticholinergic, antihistamine that helps reduce
vertigo and nausea. Assuming that the regressive course becomes evident, then I monitor the
patient periodically for the signs of continued improvement.

Anecdotal evidence suggests that idiopathic vestibular disease may represent toxicity to eating
certain strains of lizards. Owners often notice the cat with a lizard in its mouth just prior to the
onset of clinical signs. However, experimental feeding of the suggested lizard species to cats
does not lead to the disease. It is still possible that laboratory conditions do not mimic field
conditions. On the other hand, idiopathic vestibular disease occurs in many animals and in
animal species where exposure to lizards plays no role in the condition. It is most likely that
idiopathic vestibular disease is an immune-related condition affecting the unique antigens
presented by the vestibular nerve. It can recur and is often more severe on recurrence.

So, while acute idiopathic vestibular disease is a common problem and frightens the owners, it
represents (generally) a good disease that will go away on its own. On the other hand, since the
signs are so severe, it usually is “treated” as an emergency if only to make the owner feel better.
If the vertigo can be reduced, the patients are more comfortable. That is the actual goal of initial
assessment. If the signs do not regress, then more aggressive diagnostics can be done.

Trauma

Central nervous system trauma is a common cause of neurologic emergency and may lead to
stupor or coma or paralysis as discussed above. Fractures should be stabilized. Pain should be
controlled. Shock and fluid disturbances should be prevented and normal tissue perfusion should
be maintained. IV methylprednisolone (Solu Medral) should be given at 30 mg/kg to protect the
nervous system and to prevent further neurologic damage. In cranial injuries, IV mannitol (0.25
– 2 gm/kg) followed by furosemide (0.5 – 1 mg/kg) should be given. With cranial trauma,
sedative drugs should be avoided so that levels of consciousness can be monitored. Once the
patient is stable, referral for appropriate diagnostics and surgical corrections should be done.
Remember that trauma often affects other systems as well as the nervous system. On the other
hand, waiting for those systems to heal before treating the neural injuries will probably decrease
the chances for neural repair. The neural injuries may take precedence, treating the other injuries
at the same time.

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 Advanced Reproduction Symposium
Ann Lannon, DVM

Artificial Insemination from the “Male Perspective”

Some of the advantages of artificial insemination include the ability to breed to stud dogs no
matter where they are located. Obviously we are referring to fresh cooled or “chilled” semen or
frozen semen. Certainly, if the dog is local, a natural or fresh semen breeding is easily achieved.
Also many popular stud dogs are not always readily available due to being on show/trial circuits,
or if he is a heavily used stud dog the choice of frozen semen may be the only option. A huge
advantage of using chilled or frozen semen is elimination of the need to transport the bitch,
especially distances that would involve air travel. It is becoming increasingly difficult to find
inexpensive ways to ship these days, and the stress (to owner and bitch!) is decreased.

Other indications for doing an artificial breeding would include a temperament problem such as
a very sensitive, shy young stud and/or a non-receptive bitch. Structural problems in some
breeds may preclude a natural breeding. For example, some standards call for very straight
stifles which may make mounting difficult, or some of the giant breeds are so heavy that it is
difficult for the bitch to support the male. Also, a structural problem due to trauma may make it
necessary to do an artificial breeding.

I think a big indication for A.I. for many breeders is fear of infection, and I think it is very
important to stress that neither the sheath/penis of the male or the vagina of the female are
sterile. If you are getting back totally negative cultures, something is wrong with the culture!
The normal flora of the vagina contains a huge cross section of normal bacteria, including the
dreaded mycoplasma. Also in true cases of a severe sheath infection or vaginal infection,
breeding should probably be delayed anyway until the infection is treated.

Finally, an artificial insemination is relatively quick (other than surgical insemination of frozen
semen) – we’ve all experienced those hour-long ties and you wonder of your back and legs will
give out as you assist!

There are also disadvantages to artificial insemination. First of all, your insemination timing
becomes critical with chilled or frozen semen breeding. If you have the dog and bitch available
and are doing either natural breedings or fresh semen A.I., you can pretty much cover the cycle
starting with either the first day of an estrus vaginal cytology slide or when the bitch accepts the
male. With chilled or frozen semen, it is critical to time ovulation, utilizing more extensive
testing. In these cases, costs can really go up. Costs include semen collection and preparation,
semen shipment, and for the bitch, veterinary exams, vaginal cytology/vaginoscopy, and serum
progesterone and/or LH testing to determine optimum breeding time.

In addition, in some cases, depending on the skill of those involved, you may see decreased
conception rates and litter sizes with artificial insemination.

My feeling is that if you have the dog and bitch available and there are no problems precluding a
natural breeding, then that is the way to go. At Guide Dogs for the Blind I managed a breeding

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colony of Labradors, Golden Retrievers and German Shepherds. We averaged ten litters a
month to meet the needs of the training program for our blind clientele. We had 150 bitches and
50 stud dogs who lived in family homes in the community and went everywhere with their
families. They would come in for breeding as needed, and we did almost exclusively natural
breedings. We had a conception rate of 97 percent and an average litter size of nine! Certainly
there are times when artificial breeding is needed and it’s great that our technology has improved
so much in these areas, but let’s not forget about natural breeding.

The use of fresh cooled or chilled semen has some additional AKC regulations involved, so let’s
touch on those. First of all, the semen must be collected and extended by a licensed veterinarian.
In addition, the insemination of the bitch must be performed by a licensed veterinarian in order
for the resulting litter to be registerable. The certification form for a chilled semen breeding
contains certifications from the owner, co-owner, or lessee of the dam on the date of mating,
owner or co-owner of the sire on the date of mating, the veterinarian collecting and extending the
semen, and the veterinarian inseminating the bitch. Nothing like a little paperwork!

We discussed the collection of fresh semen in the article concerning the breeding soundness
exam. Obviously, it is vitally important that a complete semen evaluation be completed after
collection of semen that is going to be used for a chilled breeding. Assessment of motility,
concentration, volume, and morphology should be completed and it is important that the semen
be normal in all respects to optimize results.

The collected semen (collected in the same manner as for a fresh semen breeding or semen
evaluation) is evaluated and then immediately mixed with an extender. The extender prolongs
the life span of the sperm and is either skim milk based or egg yolk based. Commercial
extenders are available from companies such as Synbiotics but recent studies have shown that
milk based equine extenders are also suitable (and much cheaper!). The dilution of semen to
extender is normal 1:1 to 1:3, depending on the amount of the semen. Remember that we want
to utilize only the first and second fractions of the ejaculate for a volume of 2-3 cc’s max. If
more than that is collected the ejaculate should be centrifuged and then extended.

Packaging can utilize commercial canine or equine systems but any container that will maintain
a temperature of four degrees (refrigerator temperature) will suffice. Examples are thermos
bottles of Styrofoam boxes containing cold packs. Obviously the semen must be shipped to
arrive to the bitch at the proper time for inseminations (ideally two days after ovulation or four
days after the LH peak). Semen is generally viable for up to 48 hours (24-48 hours) once
packaged for shipment; therefore overnight shipping is used most commonly. Some things to
keep in mind regarding shipping: check whether the company will deliver and/or pick up on
Saturdays. If the company won’t pick up on Saturday then you won’t be able to do a Sunday or
Monday insemination. Airline “counter to counter” service may need to be utilized if weekend
service is necessary. An official AKC litter registration application form should be included
with the shipment with the appropriate information filled out and the signature of the
veterinarian who collected and extended the semen. It is also a good idea to have the results
from the initial semen analysis included.

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On the bitch’s end, the veterinarian should always check the motility of the semen after it has
been warmed and prior to insemination. If there has been a problem during shipment and the
sperm are all dead, the stud owner will need to be contacted as soon as possible!

As far as timing the inseminations it is recommended that there be two inseminations either three
and five days or four and six days after the LH peak (which is most commonly estimated
utilizing progesterone kits). If only one insemination is possible it is recommended that it be
four days after the estimated LH peak.

The chilled semen should be warmed for a minute or so in a warm water bath, after which the
semen is deposited vaginally at the cervix. Sterile insemination pipettes are attached to plastic
syringes for insemination. The pipette is inserted at the top of the vulva, first vertically and then
horizontally to follow the normal anatomy of the bitch to the level of the cervix. Following
insemination some people recommend “feathering” or tickling the dorsal part of the vagina with
the inseminator’s finger and elevation of the bitch’s hindquarters to maximize the insemination.
Keep in mind that research has shown that elevation for more than one minute was no more
useful that five, ten or fifteen minutes, so keep it short!

Communication between all involved parties is the most important aspect of utilizing fresh
chilled semen successfully!

Conception rates with chilled semen A.I. depend on appropriate timing, appropriate handling of
semen during collection, extension, and shipment, and correct semen placement. Conception
rates are estimated at 59 – 80 percent depending on these factors.

Frozen semen breedings present their own set of challenges, and truly timing is everything!
Timing is even more critical when you are dealing with frozen semen due to the short life span
of semen post-thaw. If the bitch is to be inseminated surgically and hence only one insemination
will be possible, we recommend that the inseminations be done three to four days post ovulation
or five to six days after the LH peak. It is recommended that both LH and progesterone testing
be done to insure insemination at the proper time. With trans-cervical insemination two
inseminations can be done, on days three and five or four and six post LH peak.

The freezing process begins with collection of the sperm-rich fraction and extension but the
process is much more involved than with chilled semen. Basically, the process involves
centrifugation in order to decrease the number of straws needed, and then the semen is extended
for the first time at a 1:1 ratio and refrigerated for one hour. Then a second extender is added
over a 30-minute period. Finally, the straws are filled, sealed, and refrigerated for about two
hours before being placed on a freezing rack suspended above liquid nitrogen for six minutes
before finally being placed directly into the liquid nitrogen for storage. Quite a process! Semen
that has been frozen in liquid nitrogen is good indefinitely. It is always a good idea to thaw a
straw after freezing to ascertain how well this particular dog’s semen freezes.

Usually frozen semen is shipped in a vapor shipper, also know as a dewar. The shipper does not
contain any free liquid nitrogen but the vapor is enough to keep the straws at the appropriate
temperature during shipping.

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Prior to use, the straws are thawed in a 37 degree centigrade water bath for 60 seconds. It is
important that the veterinarian evaluate post-thaw motility before insemination. Thawed sperm
have a maximum life span of 12 – 24 hours after insemination into the bitch.

There are two methods of insemination of frozen semen. The first is surgical, and a laparotomy
incision is made while the bitch is under general anesthesia, the same as if she were going to be
spayed. The semen is drawn into a syringe through an insemination rod and a 22-gauge needle is
utilized to inject the semen directly into the uterine body or horns.

The disadvantages of this approach would be the risks of general anesthesia and the stress to the
bitch; however, there are many who have great success with this approach.

The other method is trans-cervical insemination, where semen is deposited into the uterus in an
awake and standing bitch utilizing one of two catheterization methods. The Norwegian method
utilizes a long steel catheter with an outer protective nylon sheath. The inseminator palpates the
cervix and the tip of the catheter is inserted vaginally and then through the cervix into the uterus.
This method has not been utilized much in this country as the cervix is very difficult to palpate
abdominally and hence there is a steep learning curve – perhaps those Norwegians have
especially sensitive fingers!

In this country, the New Zealand method first introduced by Dr. Marion Wilson is gaining
growing favor and is the method I was taught while I was at Guide Dogs for the Blind. This
method utilizes a vaginal fiber optic endoscope (actually a cystoscope commonly used to
examine the bladder) to visualize the cervix and then a plastic urinary catheter is inserted via the
endoscope and the semen is deposited through the catheter by attaching the syringe with the
thawed semen to the end of the catheter.

Conception rates vary considerably for frozen semen due to the many variables, and have been
estimated to be anywhere for 11 – 80 percent.

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 The Canine Male Breeding Soundness Exam
Anne P. Lannon, DVM
There are many reasons why a dog may be presented to a veterinarian for a breeding soundness
exam. This may be a young, unproven dog that the owner wants to be assured is fertile prior to
introducing him at stud. Perhaps it is an older proven dog that has recently had a few “misses.”
Alternatively, this could just be a serial examination of a popular stud dog. It is a great idea for
these popular males to have an exam every six months or so and then the owner can present the
results as proof of his fertility.

It is important to consider the age and breed of the dog presented for several reasons. First, a
very young dog with fertility issues brings congenital defects into the picture. On the other hand,
an older dog may have other health issues to deal with. Plus it is important to realize that the
AKC requires that a semen evaluation and breeding soundness exam be performed by a
veterinarian for dogs under seven months or older than twelve years of age who have sired a
litter. In addition, breed related health or genetic issues may play a part in a fertility problem,
and certainly different breeds mature at different rates.

A complete breeding history is very important. If the dog is proven, we want to be sure to check
on the bitches they have been bred to and ascertain their reproductive history before
incriminating the male. Who did the breedings, how were the breedings performed, and how
often were they bred? How often has the dog in question been used and what was the
environment? Medical history and any medications being used must be known, as well as the
status of the last brucellosis test and when it was done. Genetic history may also be important –
any history of infertility in the family?

A complete physical examination is indicated for all dogs, starting with body condition and body
weight. Eyes, ears, nose and throat, heart and lungs, abdomen, musculoskeletal, coat, and skin
are all examined for signs of abnormalities. Special attention is paid to skin conditions that may
indicate an underlying endocrine disease that may have an effect on the reproductive system.

Special attention is, of course, paid to the reproductive tract. First the prepuce is examined for
tumors, abrasions, or abnormal discharge. The normal prepuce contains a small amount of
yellow-green discharge but it should not be profuse (which would indicate a condition known as
balanoposthitis) or bloody. The penis should be easy to extrude from the prepuce. Pain or
failure of the prepuce to be moved may signal an anatomic abnormality such as persistent
frenulum or preputial stenosis. The non-erect penis should be light pink and examined for
abnormalities such as tumors or signs of trauma. The scrotum should be examined for
thickening, lesions, tumors, or dermatitis (skin disease). Scrotal dermatitis can be very painful
and can cause the dog to severely self-traumatize the area by licking and chewing. This is often
caused by harsh cleaning substances used on runs. The testicles are palpated carefully for size,
which should correlate to the size of the dog, symmetry (they should be symmetrical),
consistency (firm but not hard), and pain. Soft, small testicles may signal testicular atrophy,
whereas enlarged, painful testicles may indicate orchitis, or an inflammation or infection of the
testicles. The epididymes are palpated as the testicles are palpated and any swelling or
asymmetry is noted. Last, but certainly not least, the prostate should be palpated digitally via the

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rectum to determine size, consistency and evidence of pain. Prostatitis is a common problem
and can be due to many causes.

The semen collection is sometimes done prior to the examination of the reproductive tract,
especially with a sensitive dog. It is recommended that there be five to ten days of sexual rest
prior to collection. If the dog has never been used or it has been a long interval since the dog has
been bred or collected we will usually recommend collection of a second ejaculate because you
may see an increase in detached heads and distal droplets (both are secondary defects of sperm)
due to prolonged storage in the epididymis.

Collection equipment consists of a latex or plastic cone (artificial vagina), plastic collection tube,
and a small amount of water soluble, sterile lubricating jelly. Obviously many of us have had
successful collections with much simpler equipment, i.e., manual stimulation and a Dixie cup!

We want the dog to be as relaxed as possible, and footing should be secure. In a veterinary
clinic it is optimal to cover the linoleum flooring with rubber nonskid mats. A bitch in estrus is
essential to get an optimum, complete ejaculation. If an estrus bitch is not available you can
utilize the vaginal secretions of an estrus bitch that have been collected onto gauze pads and
frozen. When needed, these pads can then be thawed and given to the stud dog to smell or
spread on the vulva of an anestrus teaser bitch.

Manual stimulation is utilized first to create an erection and then, once strong thrusting has
begun, the prepuce is slipped behind the bulbus glandis and pressure is applied behind the bulbus
to simulate the “tie.”

When the dog ejaculates, there are three fractions to the ejaculate. The first fraction is the clear
pre-sperm fluid. The second fraction, the sperm rich fluid, is easily identified because of its
milky appearance. These first two fractions are usually produced during rapid thrusting by the
male and are usually collected together. Normally the first two fractions will result in 1 – 3 ml
of fluid. The third fraction mainly consists of prostatic secretions and is usually collected
separately for analysis of prostate abnormalities. The semen should be evaluated immediately
after collection.

The semen evaluation consists of evaluating color and volume, motility, concentration and
morphology of the semen/sperm cells. Color and volume can be easily assessed immediately.
The color of the semen should be milky white. A yellow or reddish color suggests
contamination with urine or blood. The volume is easily estimated if a graduated cylinder was
used for collection. If you have over 3 ml of volume you have included prostatic fluid in the
collection.

Motility (sperm movement) is estimated immediately because sperm slow down as they get cool.
A drop of semen is placed on a clean glass slide and examined under the microscope. The
percentage of sperm swimming rapidly forward is then estimated. Samples containing greater
than 70 – 80 percent of progressively motile sperm are considered to be normal.

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The total sperm count is determined by multiplying the volume by the sperm concentration.
Sperm concentration is determined by utilizing a counting chamber called a hemocytometer.
First the cells are diluted, and then they are placed in the hemocytometer and counted
microscopically. Normal dogs should have greater than 200 million sperm per ejaculate.

Morphology, or the structure of the sperm, is evaluated by preparing smears of the semen and
then staining them with special stains. One hundred sperm are observed both for primary
abnormalities, which are more serious (examples are proximal droplets, double heads, or double
tails) or secondary abnormalities such as bent tails, distal droplets, or separated heads or tails. It
is generally felt that 80 percent of sperm in an ejaculate should be morphologically normal.

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 Infertility in the Stud Dog
Anne P. Lannon, DVM

It is important to realize that ejaculates can vary tremendously on a daily basis depending upon
use of the dog. Therefore, several collections should be taken on separate days before a semen
abnormality is diagnosed. Frequent ejaculation may decrease sperm counts, which is why it is
recommended that the dog be rested for at least 48 hours prior to semen evaluation. Also, a dog
that is inexperienced or frightened during the collection procedure may give an incomplete
ejaculate, and collection on a different day under different conditions may yield a better result.

Once a representative sample is obtained, the first piece of information to be derived is whether
sperm are present or absent in the ejaculate, what are their numbers, and are they normal in
appearance.

Aspermia is a complete lack of sperm in the semen sample because the dog failed to ejaculate.
Aspermia can have several causes. First of all, an inexperienced dog may fail to ejaculate due to
nervousness, or a very young dog of a late maturing breed may not have reach sexual maturity
and so physically is incapable of ejaculation. Pain, a second cause of aspermia, may be caused
by an infected prostate, joint pain due to arthritis, or an injury. Psychological factors may
include a very subordinate or passive male, or a more experienced dog that has a strong
preference for certain surroundings. There are some drugs such as amitriptyline, which are
sometimes used for behavioral disorders, and naproxin, which is used as a non-steroidal anti-
inflammatory medication, which have been reported to cause ejaculatory dysfunction. Finally,
retrograde ejaculation is an example of a neurologic dysfunction that causes the dog to ejaculate
backwards into the bladder instead of through the reproductive tract. This is caused by blockage
of nervous system receptors in the bladder neck, and is easily diagnosed by obtaining a urine
sample by systocentesis immediately after semen collection.

In contrast to aspermia, azoospermia involves normal ejaculation of seminal fluid, but the fluid
does not contain sperm cells. Azoospermia must be differentiated from an incomplete
ejaculation where the dog only ejaculates the pre-sperm fraction of semen. This can happen with
a young, inexperience, or very nervous dog. We can differentiate the two by measuring a
substance called alkaline phosphatase in the collected fluid. Alkaline phosphatase is found in
very high levels in epididymal fluid, therefore if the alk phos level is very high, then the fluid
collected is from the epididymis and the dog did have a complete ejaculation.

Causes of azoospermia can be divided into pre-testicular, testicular, and post-testicular causes.
Pre-testicular causes of azoospermia would be non-reproductive tract diseases or physical
problems that affect sperm production. Examples would be endocrine diseases such as
Cushing’s Disease, pituitary problems, or hypothyroidism. Inguinal or scrotal hernias are
physical abnormalities that can affect sperm production. Finally, a high fever can definitely kill
sperm and shut down sperm production (as can high external temperatures for that matter).

Disorders involving the testicle are common causes of azoospermia and hence infertility. These
disorders include intersex states, such as female pseudohermaphrodites that have male external

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genitalia and female gonads. These problems are uncommon and are usually caused by
administration of androgens (testosterone producing substances) to the dam. There is also a
phenomenon of XX sex reversal which is inherited as a recessive trait in the American Cocker
Spaniel, Kerry Blue Terrier, German Shorthaired Pointer, and a few other breeds. These dogs
have male external genitalia and testicular and/or ovarian gonadal tissue but have two X
chromosomes.

Traumatic testicular injury can certainly cause azoospermia, as can a disease called autoimmune
orchitis, where the dog is producing antibodies against his own testicular tissue and sperm cells.

Testicular hypoplasia and degeneration refers to testicles that become shrunken due to any
disease process or disorder. Sperm production decreases and finally fails as cells die and
degenerate.

Finally, testicular cancer or neoplasia may also be a cause of azoospermia by direct destruction
of testicular tissue by causing inflammation and elevation of testicular temperature, or by
producing hormones that have a negative influence on sperm production.

Post-testicular causes of azoospermia in the dog are those causing outflow obstruction of sperm
from the reproductive tract and include epididymal segmental aplasia, which just means that
there is a portion of the epididymis that was either never formed during development or is no
longer present due to trauma. A spermatocele can also cause obstruction and is an area of
swelling in the epididymis due to a blockage that will not allow the semen to continue through
the tract. This results in a sperm granuloma, which presents as a firm, non-painful swelling in
the epididymis. Testicular size is normal with these problems, and they may be unilateral or
bilateral, but if they affect only one side the dog may still be fertile.

A more common presentation than azoospermia is oligospermia, which means that there are
sperm cells in the ejaculate but they are reduced in number from what would be considered
normal. Any of the causes of azoospermia that we have previously discussed may cause a
decrease in sperm numbers as opposed to a total absence of sperm, especially if the problem is
diagnosed in its earlier stages.

A decrease in sperm numbers is a common sign of inflammation and/or infection in the

reproductive tract such as prostatitis due to benign prostatic hypertrophy, prostate
infection/abscess, or even prostatic cancer. Infection or inflammation in the testicles is referred
to as orchitis and may be caused by bacterial infections and, in the epididymis, by brucellosis.
Autoimmune orchitis is also a common problem, and we previously talked about high
temperatures, or hyperthermia, causing decreased sperm numbers.

Asthenospermia refers to reduced motility in the ejaculate. This is most commonly due to
collection and handling procedures such as too much water soluble lubricant, exposure to latex,
or allowing the semen to become too cool. However, reduced motility can also be caused by
testicular tumors or infections in the reproductive tract. In very rare cases it may be caused by
immotile cilia syndrome, which is a congenital abnormality causing absent or irregular,
asynchronous motility of all ciliated cells in the body. Heritability of this syndrome is unknown

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but breeds in which affected littermates have been reported include the Bichon Frise, Springer
Spaniel and Old English Sheepdog.

A few other, less common, abnormalities include teratospermia, which is when we see increased
morphological or structural problems with the sperm cells themselves. These may be secondary
abnormalities that may still allow normal fertility but usually indicate a problem in storage or
transport, or primary abnormalities which are more serious and usually indicate a problem with
sperm production. Hematospermia, or blood in the semen, may be seen with benign prostatic
hypertrophy, penile lacerations, or infection/inflammation of the testes or epididymis. Finally,
pyospermia, or pus in the semen, may be seen with prostatic, epididymal, or testicular infections,
or may also be contamination from a sheath infection.

So now we have discussed all of the different abnormalities that may be noted when evaluating
semen, and we may or may not have a good idea of what may be causing the problem. We may
need to do some diagnostics so that we can figure out what the problem is. We should start out
testing with a few basics, the first being brucellosis testing if it has not been performed recently.
Secondly, we need to rule out any underlying systemic problems by doing a CBC (complete
blood count) and chem. screen. The CBC may give us a clue to infection of inflammation if the
white blood cell count is high, or it may clue us in to anemia if the red blood cell count is low, or
even parasites if there is a high count of cells called eosinophils. We should also include a
heartworm screen if this has not been performed recently. The chem. screen tells us about
kidney function, liver function, blood sugar level, and other internal systems. Thyroid testing is
a must if there is a history of skin disease, unexplained weight gain, and/or lethargy.
Hypothyroidism does not just cause reproductive problems and is very unusual in young dogs.
Finally, it is important not just to do a T4 level, as this is the total amount and may not indicate
the amount of thyroid hormone available for your dog to use. Free T4 is a better measure of that
and is included in most thyroid panels.

The sex hormones FSH, LH and testosterone are all necessary for normal sperm production, so it
stands to reason that these would be great things to measure to ascertain the reproductive health
of our dogs. Unfortunately, it isn’t easy!

Observation of normal libido (sex drive) gives a rough estimation of normal testosterone levels.
If libido is low you can measure testosterone levels but you must realize that testosterone is
released in a pulsatile manner, therefore a single random sample is not diagnostic. You would
have to do three blood samples at 30-minute intervals, and it is still rarely of diagnostic value in
evaluating sperm production as levels remain in the normal range in dogs with a wide variation
in the health of the tubules in the testicles that produce testosterone.

Canine specific assays of LH and FSH are not readily available commercially and hence are
rarely of help in ascertaining a problem.

Ultrasound is an excellent tool to use to diagnose prostate or testicular problems. Neoplasia

(cancer), cysts, and abscesses can all be diagnosed via ultrasound, and an ultrasound-guided
biopsy can be done. The epididymes can also be ultrasounded to check for the presence of a
spermatocele or sperm granuloma.

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Cytology of both the sperm-rich and prostatic fractions of the semen can be evaluated by just
putting a drop on a slide, and then preparing a thin film using another slide, allowing it to dry,
staining it, and looking under the microscope. A prostatic wash is another way to collect
prostatic fluid if a dog is in too much pain to collect a semen sample. A urinary catheter is
advanced to the level of the prostate and is flushed with sterile saline and the fluid aspirated with
a syringe for analysis. If bacteria or other abnormal cells are seen a sample should be submitted
to the laboratory for culture and sensitivity. I recommend culturing for aerobic bacteria,
anaerobic bacteria, and mycoplasma.

We may also want to check the alkaline phosphatase level of the semen sample. This is the test
we mentioned earlier that can be used to differentiate azoospermia, or no sperm in the ejaculate,
from an incomplete ejaculation, from an incomplete ejaculation. We simply submit a semen
sample to the lab to ascertain the level of this enzyme, which is found in very high levels in the
epididymis. It can also be sued to differentiate an obstructive problem causing azoospermia
from a degenerative process.

A urinalysis should be performed to ascertain kidney function and evaluate for a possible urinary
tract infection. The sample should be obtained via a cystocentesis (needle introduced into the
bladder) to avoid contamination from elsewhere in the tract. The urine is evaluated for the
presence of WBCs, RBCs, bacteria, crystals, sugar, and to see if the dog is concentrating his
urine normally. If there are WBCs and bacteria present in the sample this is indicative of
infection and a culture and sensitivity should be done. Finally, as we discussed, a urinalysis can
be very helpful in diagnosing the problem of retrograde ejaculation. The urine should be
collected by cystocentesis immediately after semen collection to look for the presence of large
numbers of spermatozoa.

Let’s say your testing has all come up non-diagnostic to this point. You may then consider doing
an epididymal and/or testicular biopsy and submit it for histopathology to see if you can get a
diagnosis. However, these are invasive procedures and may themselves result in damage and
failure of spermatogenesis. These procedures are usually used in the case where the owner
wants an answer but realizes we are at the end of the line anyway as far as future fertility goes.

I just want to mention one other test that is available through several universities. The karyotype
test is generally used in the case of a young dog when a congenital abnormality is suspect (like
the XX sex reversal). Certainly if the animal has abnormal or ambiguous genitalia this test
should be run. Either a blood sample or a skin biopsy can be submitted and the test involves a
process that allows the individual chromosomes to be evaluated for abnormalities. Normal
males have a karyotype of 78 XY and normal females are 78 XX.

So what treatments are available in cases of canine male infertility? To be honest, the prognosis
is poor for many types of azoospermia. For example, a congenital problem in a young dog with
no evidence of ever having produced spermatozoa is unlikely to respond to therapy. On the
other hand, a problem such as hypothyroidism or other systemic illnesses can certainly be
treated. Bacterial prostatitis, epididymitis, and orchitis can be treated with long term (often 6-8
weeks) antibiotic treatment, and toxins or drugs causing problems can be removed. Treatment

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for obstruction would be surgical but this has rarely been done in dogs. Retrograde ejaculation
was mentioned earlier and this condition is sometimes reversible with administration of
pseudoephedrine or phenylpropanolamine at appropriate levels.

This is one instance where time can be the most appropriate therapy because spermatogenesis
(sperm formation) and maturation take approximately 75 days in the canine, and it may take
several cycles before sufficient numbers of functional sperm appear in the ejaculate. Therefore,
several months of sexual rest may be necessary to treat some disorders. Semen evaluations can
be done every six weeks or so to ascertain progress.

Oligospermia has a better prognosis than azoospermia and generally reflects infection/
inflammation of the reproductive tract causing decreased numbers of sperm in the ejaculate.
Infection again can be treated with antibiotics, and prognosis depends on the chronicity of the
condition, i.e., how much inflammation, fibrosis, and degenerative changes have already
occurred.

Breeding management can be done with oligospermic dogs since they are not necessarily
infertile. Breeding should be by natural mating if possible and progesterone testing of the bitch
should be done to maximize each breeding by being as close to the time of fertilization as
possible. Intrauterine insemination may be beneficial for these breedings, and the dog should be
collected every two to four days to maximize fertility.

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