A dog's body is constantly being influenced by the world around it. A canine's behavior and physiology can be greatly influenced by its habitat, enrichments, chemicals, toxins, parasites, bacteria, diet and other important factors. During its life, the physiological systems of the dog endeavor to account for any factors the dog may be exposed to and maintain the animal's body in homeostasis. This site describes the effects of several environmental factors that a dog may encounter. Please be aware that the information in this page intended to be used as advice only; if you have any questions about the content or a medical emergency, please consult your veterinarian immediately.
Use this alphabet bar to quickly browse the listings. Click here for a full list of subjects.
Immediately after ingestion, the poison is rapidly absorbed into the dog’s system and quick begins to affect the brain and spinal fluid. The pet may exhibit drooling, disoriented behavior, uncoordinated movements, depression, lethargy, and coma within 30 minutes to 12 hours after consumption of antifreeze depending on how much was ingested. These signs usually pass after several hours; unfortunately many pet owners assume this means the danger has passed and do not seek further treatment. After the central nervous system symptoms are over, the kidneys are damaged by the antifreeze; in dogs, the kidney problems usually manifest themselves 1 to 3 days after ingestion of antifreeze. As the toxic metabolites of ethylene glycol build up, formation of urine drops off to nothing due to severe renal failure. Also, increased thirst, vomiting, mouth sores, noticeable increase in oral odor, severe depression, and then eventually coma and death may be seen. Some ethylene glycol compounds contain fluorescin, which may give a yellow fluorescence to the urine and vomitus of the dog when viewed with a Wood’s lamp shortly after ingestion.
If an owner suspects their dog has been exposed to antifreeze, it is vital to get the animal to the veterinarian as quickly as possible. Ethylene glycol toxicosis is often fatal if not treated within 4 to 8 hours after ingestion; treatment after 24 hours is often futile. If there is time, it may help to induce vomiting with hydrogen peroxide or syrup of ipecac to expel the toxin from the stomach before it is absorbed. Once at the veterinary clinic, the animal will be evaluated with a complete medical history and physical examination. Also, the veterinarian will conduct several tests including an ethylene glycol blood test, serum biochemistry, urinalysis, blood gas analysis, and an abdominal ultrasound. The ethylene glycol blood test will register high levels of the substance in the blood; however, a negative test result does not mean the dog has not been poisoned, it simply means that the levels present are undetectable by the test. A urinalysis is done to detect characteristic calcium oxalate crystals and other evidence of kidney damage. Examination of urine reveals crystals that are highly indicative of ethylene glycol poisoning; however, the crystals do not show up until about 6 hours after exposure. Waiting for the crystals to show up may put the pet at risk. Looking for crystals is appropriate when the time of exposure is unknown or definitely over 6 hours. Blood gas analysis evaluates blood for the presence of severe acidosis. A serum biochemistry profile will detect electrolyte disturbances in calcium and other ions or abnormal kidney function indicators such as serum nitrogen, creatinin, and phosphorus. Approximately 50% of ethylene glycol toxicosis patients show hypercalcemia, hyperglycemia, hyperurea, and hyperphosphatemia. An abdominal ultrasound is done to examine kidney size and appearance. Deposits of calcium oxalate crystals in the kidney result in very bright appearance (hyperechoic regions) within hours of ingestion. A kidney biopsy may be done to confirm ethylene glycol poisoning.
After testing is complete and the
diagnosis is made, the veterinarian will begin to treat the condition. If the
patient is presented soon enough after consumption, he will use vomiting
induction and gastric lavage to empty the stomach of toxic contents before they
can be broken down into toxic metabolites. Administration of activated charcoal
may be given to bind the ethylene glycol within the digestive tract and prevent
its absorption and metabolism. Intravenous fluids are administered to treat
dehydration. Sodium bicarbonate is necessary with severe acidosis. Specific
drugs such as ethyl alcohol or 4-methylpyrazole (Antizol) inhibit the breakdown
of ethylene glycol. These compounds compete for the liver enzymes that break
down ethylene glycol and slow its metabolism down, keeping the serum levels of
toxin down; this allows them to be excreted safely when applied early enough.
Drugs to treat kidney failure and encourage urine production such as the
diuretic furosemide and the vasodilator dopamine may be given. Unfortunately,
once kidney failure has developed, more than 80% of pets die despite medical
treatment.
It is estimated that 10000 dogs are poisoned each year due to ethylene glycol toxicosis. Studies have shown that most poisonings occur around the pet’s own home because owners have not safely stored or disposed of antifreeze. Prevention is the best treatment. Pet owners should keep containers of antifreeze and other solutions containing ethylene glycol tightly closed and out of the reach of pets. If any is spilled, it should be cleaned up immediately and thoroughly with large amounts of water. Also, pets should never be allowed to roam unsupervised. Further, while more expensive, some products are available that do not contain ethylene glycol but rather consist of the less toxic substance propylene glycol like Prestone LowTox or Sierra.
Dogs are susceptible to aspirin poisoning following the ingestion of aspirin or aspirin- containing
products. Salicylate toxicity may cause gastrointestinal problems, respiratory difficulties, neurological
problems, bleeding disorders, and kidney failure; gastrointestinal problems are most common in dogs.
The most common symptoms of aspirin poisoning are the gastrointestinal effects such as loss of appetite,
abdominal pain, nausea, vomiting, black stools, and
lethargy. Aspirin 
toxicity
can lead to ulceration of
the stomach or intestine and, in extreme cases, stomach or bowel perforation that causes a severe, life
threatening, bacterial infection of the abdomen. Aspirin stimulates the brain’s respiratory center so most
dogs will pant excessively; alternatively, some dogs may experience extreme mental depression with
decreased respiration. Neurological symptoms include restlessness, anxiety, depression, incoordination, and seizures. Acute kidney failure may result with symptoms such as vomiting, diarrhea, loss of appetite, lethargy, extreme thirst, and dilute urine. Finally, aspirin interferes with platelets in the blood, which are vital to the clotting response. This increases the amount of time it takes the blood to clot following an injury. Spontaneous bleeding may occur causing pinpoint bruises to appear on the skin and gums.
If you suspect aspiring poisoning, immediately
take the animal to the veterinarian. He will gather a history of the animal and
perform a physical examination. Your veterinarian will also likely perform a
complete blood count (CBC), a biochemistry profile, a urinalysis, a blood gas
analysis, and an
activated clotting time (ACT) test. The CBC is used to asses
the animal’s white and red cell count; if the dog has intestinal bleeding
secondary to ulceration of the stomach, the red cell count may be decreased. A
biochemistry profile will asses internal organs such as the kidneys. Elevations
in kidney values indicate kidney damage. The urinalysis assesses the kidneys’
ability to produce and concentrate urine; in situations with kidney damage, the
urine becomes more dilute and lighter in color. A blood gas is done to assess
the pH of the blood; acidosis is often seen in patients with aspirin toxicity.
The ACT test measures the dog’s ability to form a clot; salicylate toxicity will
cause an increased clot time. If aspiring poisoning is suspected, the dog will
be hospitalized. Treatment includes induction of vomiting and gastric lavage to
remove undigested pills if therapy is given within four hours after consumption.
Activated charcoal is administered to prevent further absorption of aspirin from
the stomach. Intravenous fluids are given to rehydrate and alleviate kidney
failure. Antacids such as misoprostol (Cytotec), cimetidine (Tagamet),
famotidine (Pepcid AC), or sucralfate (Carafate) are given to treat ulceration
of the stomach. Anti-emetic drugs such as metaclopramide (Reglan),
prochlorperazine (Compazine), or chlorpromazine (Thorazine) are administered to
reduce vomiting.
This condition usually occurs due
to the improperly stored drugs or following the administration of an incorrect
dose of aspirin. Always keep
medicines tightly sealed and out of reach of pets.
If accidental ingestion has occurred, remove any remaining pills from the
environment and take the dog to the veterinarian as soon as possible. It may be
advisable to induce vomiting before leaving your home with hydrogen peroxide or
syrup of ipecac. If you have been administering aspirin under a veterinarian’s
advice and you notice vomiting, black stools, pale gums, or loss of appetite,
immediately stop giving the aspirin and seek veterinary care as soon as
possible.
Canine respiratory bordetellosis (a.k.a.
Kennel Cough) was first recognized in the early 1900s. Bordetella
bronchiseptica is the agent responsible for this disease. Bordetella
bronchiseptica is closely related to B. pertussis, the
etiologic agent of whooping cough in humans; in fact, the two bacteria differ
only in their host specificity. This organism is a gram (–) bacterium well
adapted to colonize a host’s respiratory tract. This organism is considered an
obligate extracellular pathogen because it only colonizes the surface of the
respiratory tract and is unable to survive outside the host. Bordetellosis is
transmitted through the aerolization of the organism in respiratory secretions
and through contaminated fomites. Due to this
mode of distribution, this
disease is common where dogs of different ages and levels of susceptibility
congregate among one air source or in close contact with one another such as
humane societies, boarding and training kennels, veterinary hospitals, research
institutions, and facilities where performance or show dogs are housed. Due to
this association between groups of dogs and the disease, the condition is also
called “kennel cough.” When the dog is exposed to the infected particle, the
bacterium is inhaled; it then attaches to ciliated respiratory epithelium such
as that found on the lining of the dog’s trachea and upper bronchii. The damage
to the epithelium is fairly superficial, but exposes nerve endings that become
irritated simply by the passage of air over the damaged area. These attachments
are made due to the bacterium recognizing specific host cell receptors. Once
colonization has been established, Bordetella bronchiseptica produces
several exotoxins (adenylate cyclase-hemolysin, dermonecrotic toxin, and
tracheal cytotoxin) as well as endotoxins that damage the respiratory tract and
impair the host’s ability to eliminate infection; together these factors
disrupt ciliated cells, disable phagocytic cells, and suppress both humoral and
cell-mediated immune response.
The most characteristic clinical sign associated with Bordetellosis is a dry, hacking, persistent cough that appears three to 7 days after the dog is initially infected. This cough is typically exacerbated by exercise or activity, and can be produce by palpation of the tracheal or laryngeal regions of the throat. The animal’s general state of health and alertness will generally not be affected; they usually will not display a rise in temperature, a reduced appetite, or a decrease in activity. A history of exposure to other dogs in a kennel, veterinary hospital, or other group situation, in addition to this hacking cough, is usually sufficient to make a diagnosis. Nasal discharge may or may not be present. Identification of the etiologic agent(s) is usually not required in most situations, but can be done using endoscopy, bronchoalveolar lavage, transtracheal wash, Schaeler’s enrichment broth, and charcoal blood agar.
Once diagnosis is made, treatment is determined on an individual basis depending on the severity of the infection. Usually, Bordetellosis is self-limiting and does not require extensive treatment. However, in some cases, secondary infections require the use of antibiotics. The tetracyclines, chloramphenicol, erythromycin, clarithromycin, and azithromycin are considered the most effective against Bordetella bronchiseptica. Strict rest, avoidance of excitement, and nominal exercise are indicated to minimize cough—producing situations and avoid perpetuating airway irritation. Antitussives (cough suppressants) and bronchodilators can be used to control coughing.
Despite the availability of several types of vaccines, bordetellosis continues to be a major respiratory tract disease in dogs. As recent as 1999, and on a smaller scale in 2003, major outbreaks of the disease in greyhound racing kennels caused millions of dollars of lost revenue for the industry. Currently, nine types of vaccine are available for the prevention of Bordetellosis. In general, the products are either whole cell bacterin, extracted cellular antigens, or avirulent live cultures. These vaccines may be administered through either injectable or intranasal routes. The necessity, effectiveness, and duration of these vaccines is currently an issue of debate among the veterinary community. While most pet dogs who will not be exposed to high-risk group situations such as boarding or grooming facilities are adequately protected; in this case, the pet dogs may not even need to be vaccinated and are able to rely on natural immunity for protection. However, a more aggressive approach is required for performance animals and dogs that frequent group situations.
Preventative measures should be implemented to reduce a dog’s risk of the disease. Minimizing a dog’s exposure to infectious agents can be achieved through isolating dogs that have recently been exposed to a kennel or group boarding situation. Infected dogs can spread the organisms for days to weeks after they have fully recovered. Also, because Bordetella bronchoseptica may survive severe nutrient deficiency, attention to sanitation and cleanliness by animal caretakers will eliminate the pathogen in the environment. Also, minimizing animal crowding, optimizing hourly air exchange rates and humidity levels, and ensuring proper air flow with respect to population density will help reduce risk of disease.
Calcium is important to the development of strong bones and teeth; excess calcium or calcium deficiencies cause bone abnormalities. Important as calcium is, it usually acts in association with another mineral or vitamin. Too little calcium in association with a vitamin D deficient diet may result in rickets. Rickets is a condition where bones become soft and bend out of shape under a pet’s weight. Calcium is very dependent on phosphorus; an acceptable ration of calcium to phosphorus in a diet is 2:1. An example of calcium/ phosphorus imbalance is found in an all-meat diet. While meat is high in protein, it is deficient in calcium and does not provide the proper calcium/phosphorus ratio. Some lean meats have only one part calcium to 18 parts phosphorus. Supplementing the diets of large breed puppies with excessive amounts of calcium may result in the development of bones that are large but low in density and strength. Females experience increased demands for calcium during pregnancy and lactation. The condition hypocalcemia, also known as milk fever, is characterized by deficiency of calcium during the sudden increased demands of lactation following parturition and results in muscle weakness, trembling and possibly paralysis. The fast and very effective treatment for this condition is intravenous calcium.
the cacao tree. The beans contain the If you suspect chocolate poisoning in your pet, contact your veterinarian
immediately. There is no specific antidote for theobromine toxicity; medical treatment is
supportive and may include IV fluids, emetics, gastric lavage, activated charcoal, anti-seizure medications, and cardiac medications. IV fluids prevent dehydration from vomiting, diarrhea, and/or increased urination and to help flush the theobromine out of the system. Emetics are medications that induce vomiting. Emetics are used within 4 hours of the ingestion of chocolate. Gastric lavage, or pumping the stomach, will remove any further chocolate from the dog’s system. Activated charcoal is used for cases when ingestion was greater than 4 hours prior to treatment; it will prevent further absorption of the toxin. Anti-seizure medications are used in patients having seizures and/or muscle tremors. Cardiac medications will stabilize patients exhibiting irregular heart rhythms.
While small amounts of milk chocolate do not pose a problem for dogs, it is not a good idea to give a dog chocolate even occasionally or as a treat. Because chocolate is sweet and highly palatable to most dogs, they may develop a taste for it and seek it out in the future which may lead to ingestion of a greater quantity of chocolate if it can get into an improperly stored supply. Also, chocolate is high in calories and sugar and can contribute to obesity and tooth decay.
study,
long-nosed dogs with nasal cancer were 2.5 more likely to live in smoking
households than among non-smokers; short-nosed dogs with lung cancer were 2.4
times more likely to live in smoking households than among non-smokers. Overall,
any dog, regardless of anatomy, is 1.6 times more likely to develop cancer than
a dog that is not exposed to secondhand smoke. Some of the warning signs of lung
cancer in dogs include chronic coughing, weight loss, and abnormal fatigue.
Indicator signs of nasal cancer in dogs include swelling over the nose or sinus
area, frequent sneezing, or bloody nasal discharge. Exposure to second hand
smoke can also cause chronic eye irritation in dogs.
Coccidia are intestinal protozoa that invade and infect the lining of the small intestine. Of the numerous types that can infect dogs, Isospora is the most common. Coccidia spread when an animal eats infected fecal material or an infected host. Most coccidial infections are harmless, cause minimal symptoms, and are eliminated by the body’s normal defense mechanisms. More serious coccidial infections cause severe watery or bloody diarrhea; these problems are common in high density kennel situations or unsanitary conditions. Treatment of the entire population of animals in the environment with sulfa drugs along with a thorough cleaning of the habitat is necessary to eradicate the problem. Animals with compromised immune systems are more likely to contract and experience a severe infection.
Canine coronavirus is the cause of sporadic outbreaks of enteritis in dogs. This virus is a member of the Group I coronaviruses; the viral particles are pleomorphic with a diameter of 60-200nm, spherical in shape and enveloped. The nucleocapsid is filamentous, 9-13nm in diameter, with helical symmetry. Electron micrographs show surface projections spaced widely apart and dispersed evenly over the entire surface; surface glycoproteins are responsible for the attachment of the virus to cells. Like other enveloped virus, canine coronavirus is sensitive to heat, lipid solvents, non-ionic detergents, formaldehyde and oxidizing agents, but acid stable.
Dogs of all ages appear to be susceptible to canine coronavirus; however, young pups are more likely to develop clinical infections. Canine coronavirus is associated with mild to severe gastroenteritis with low mortality rates. The mode of transmission is fecal-oral. Because the virus is acid resistant, it passes unaltered through the stomach and is expelled in the feces. Upon entry of the virus into the cell via endocytosis, coronaviruses replicate entirely in the cytoplasm. Virus replication is relatively slow; maximum virus yield is attained about 24 hours after infection. The surface epithelium of the small intestine is the main target of canine coronavirus, while the colon is resistant to infection. Within 2 days after exposure, the virus can be found in the upper two thirds of the duodenal villi. After the fourth day post infection, there is commonly a patchy distribution of infected villi throughout the small intestine. In exceptional circumstances, canine coronavirus may be present in the brain, pancreas, or the lungs. Commonly, the virus causes a lytic infection resulting in the shortening of the villi. Malabsorption and the deficiency of digestive enzyme follows, resulting in diarrhea which can be seen by 18-72 hours post infection; this condition usually lasts for several days. Feces may be watery, mucoid, hemorrhagic, and extremely malodorous. Vomiting may also be present by one to three days post infection. Infected animals become dehydrated quickly and are often also depressed and anorexic. Normally, no fever is associated with infection. Secondary infections by bacteria, parasites, or other viruses may prolong the illness. Infected dogs shed virus in the feces for 6 to 9 days after clinical signs have ceased. Most dogs recover spontaneously within a week, but the illness may last several weeks. The mortality rate of this virus is low, but may be elevated in cases involving puppies or immunosuppressed individuals.
Animals become immune to reinfection after recovery from canine coronavirus infection. Maternally transferred antibodies in dogs from affected kennels are usually low and only present in puppies for 4 to 5 weeks. For this reason, it is important to vaccinate a young animal before or soon after the maternal antibodies wear off. Currently, inactivated canine coronavirus vaccines are available. Also, prevention is recommended. Avoiding contact with infected dogs and their excretions is the only way to assure avoidance of the disease. Crowding, unsanitary conditions, stress during training or performance and other environmental stressors appear to favor the development of clinical disease. Hygiene in a kennel situation is very important. The virus is inactivated by most germicidal agents effective against enveloped viruses. Disinfection of kennels and equipment with a 3% hypochlorite solution is successful in killing canine coronavirus, but it does not prevent the transmission of the disease. Because the virus is highly contagious, once an infection is established in a kennel, the spread of the disease is very difficult to control.
The ear mite, Otodectes cynotis, is a
common crab-like parasite that lives in the ear canal and on the skin of dogs.
These microscopic insects can occur at any age, but are more common in younger
dogs. Ear mites spend their entire lives on the host. The female lays her
eggs, normally about 5 during her entire adult life, in the ear and on the
surrounding fur. The eggs hatch after a four-day incubation period, and the
larva feed on ear-wax and skin oils for about one week. The larva then molts
into a protonymph, which in turn molts into a deutonymph. Each stage of nymph
feeds for 3 to 5 days and then rests; soon after, it molts to the next stage.
The deutonymph does not develop a gender until it mates with an adult male. If
the result is a female, she will be laden with eggs; the cycle will begin
again. Unlike fleas, they do not pierce the skin or suck blood. With repeated
irritation, the ear canal thickens and debris build up in the ear canal.
Usually, ear mites do not break the ear drum. However, in the presence of
infection and with severe enough infestation of ear mites, the ear drum can be
penetrated. When this occurs, a very severe middle ear disorder can result
where the animal can lose balance, become disoriented, and have severe physical
signs of trouble. In chronic cases of ear mites, there is often secondary
bacterial or yeast infections present that complicate treatment and further
stress the animal.
he most common signs of ear mite infection are scratching at the ear area, irritation, shaking the head, head held at a slight angle, red or inflamed ear, scabs or crust around the ear, and a discharge of brownish black exudate that resembles coffee grounds; due to this exudate, the ears will have an unpleasant odor. Mites can also spread to the skin, and the animals will be seen scratching and itching along their backs and at the base of their tail. To diagnose an ear mite infection, a veterinarian is often able to observe the mites in the ear canal as tiny moving white specks using an otoscope; a sample of ear discharge mixed with mineral oil on a slide can also be examined under a microscope can also be studied to locate ear mite and make a diagnosis. A skin scraping may also be performed if the dog shows general skin lesions. Diagnosis is an important step before treatment because using anti-mite preparations with other ear organisms may aggravate an existing infection. Full treatment of mite infection consists of first cleaning the ear. Cleaning is a mandatory first step in treatment; if the exudates is not removed, it will keep the medication from encountering the mites directly. Moderate to severe infections may require sedation and in-hospital flushing. Next, medication is applied to the infected ears. Topical therapy usually consists of mediations that are placed in the dog’s ears daily or weekly in the form of liquid drops. Tresaderm (thiabendazole) and Acarexx (ivermectin) are two common products used to treat ear mites. Studies have shown Acarexx to be approximately 95% effective in treating adult ear mite infestations after 7 days. Medication may also need to be applied to infected areas of skin. If the mites are causing skin problems, the area is often treated with a flea product topically. Finally, the animal should be taken back to the veterinarian for follow-up examinations. Ear mites are extremely contagious; if one animal in a multiple-pet households is infected, it is highly probable that the rest are as well. In this case, all pets should be taken to the veterinarian for treatment. Dogs with long, floppy ears are more prone to ear mite infections. Air movement is restricted, promoting infection and other bacterial growth. When a dog shakes his head vigorously, blood vessels may rupture and soft swellings form on the ear flap; this conditions is called hematoma, and immediate veterinary treatment is necessary to avoid pain to the animal and possible ear deformity. You can prevent ear mites by drying the dog’s ears after bathing, checking his ears for foreign matter, and promptly visiting the veterinarian at the first sign of anything unusual.
Though once included in a diet as merely filler, or bulk, fiber has proven to have beneficial effects on the gastrointestinal system despite limited digestibility. Fiber is the portion of carbohydrate in a diet that is difficult for the digestive system to break down and use. First of all, fiber can be utilized to help prevent and treat obesity in animals. If included in a weight management food, it helps reduce caloric intake by giving pets a satisfied feeling of fullness so they consume less. Also, fiber can prevent constipation. In the body, fiber absorbs water and gives bulk to the intestinal contents. This stimulates the movement of the gastrointestinal tract and normalizes passage time through the bowels. Fiber also contributes to fecal consistency. Studies also show that a moderate increase in dietary fiber may be helpful in diabetes mellitus management. Certain forms of fiber may slow down the absorption of sugar from the intestine, which aids in blood sugar control. Excessive dietary fiber is associated with adverse effects such as diarrhea and loose stool, flatulence, and increased stool volume or density. Sources of indigestible fiber in pet foods include soybean and peanut hulls, apple, tomato, and citrus pulp, the bran of oats, rice, wheat and cellulose. (Pulp is the sold residue that remains after juices are extracted from fruits or vegetables.)
While the dangers of fireworks to humans are well known, most people forget to consider the safety of their pets when enjoying displays. Fireworks become extremely hot very quickly and a curious pet may be severely burned. They also may try to ingest the firework. Even if unlit, consuming fireworks can be quite dangerous; fireworks contain a variety of toxic agents including potassium nitrate, mercury, antimony, copper, barium, strontium, and phosphorus. In addition, many fireworks contain projectile components that may eject and injure a pet.
Physical examination and a history of recent
exposure to fireworks is usually all that is necessary to diagnose firework
related illness or 
injury. In the case of ingestion, blood tests may be
necessary to determine the effects of the firework’s ingredients on the dog’s
internal organs. Signs of illness or injury include burning of the mouth or
skin, soft tissue injury, vomiting, severe abdominal pain, and respiratory
distress. Treatment of these injuries depends on the kind of damage sustained.
Burns are treated by cleaning the area and administering antibiotics. Ingestion
of fireworks requires intravenous fluids as well as medications such as sucralfate, famotidine, or cimetidine to protect the gastrointestinal tract from
further damage. Emetics are also used to induce vomiting. Depending on the heavy
metal ingested, specific treatment or even an antidote may be available. The
likelihood of survival depends on the extent of injury and the promptness of
medical treatment.
Fleas are small dark brown or black wingless
insects found all over the world. They are bloodsucking parasites which cause
disease through local reactions to bites, generalized reactions to bites due to
hypersensitivity (allergy) to flea saliva, or the transmission of other
infections to the host through the flea. There are over a thousand species of
flea in the world, but only relatively few infest dogs and humans including
Ctenocephalides felis, Ctenocephalides canis, Pulex irritans, Tunga penetrans,
and Echidonophaga gallinacea. Because the insect prefers temperatures of 65
to 80 degrees Fahrenheit and humidity levels of 75-85%, some areas of the
country experience these pests year round while for some they are restricted to
a warm seasonal irritation. The life cycle of a flea is quick and efficient. A
female flea lays hundreds of eggs on or off the host; these eggs then fall off
into the environment (usually where the animal normally sleeps or lays). The
maggot-like larva hatches around ten days after the eggs are laid. The larvae
then move away from the light and downwards in response to gravity; they tend to
radiate to warm and humid environments. The larva feed on organic matter, skin
scales, and even the blood-rich feces of adult fleas. Each larva molts twice to
form a 3rd stage larva which then forms a cocoon and pupates. The
adult flea emerges after a period of 5 to 140 days depending on environmental
conditions; the adult fleas will emerge when they sense a warm, humid habitat as
well as vibrations and exhaled carbon dioxide which indicate a host is near.
Female fleas start l
aying eggs within 5 days of eating her first blood meal and
the cycle begins again. A female typically will remain for several weeks on the
pet. During this time period, she will feed two to three times and lay 20 to 30
eggs each day. The typical life cycle of a flea usually takes 3 to 4 weeks, but
under favorable conditions may be completed in just 14 days. A single female is
able to produce over 20000 adults in 60 days! Adult fleas can survive for 12
months without feeding.
The signs of flea infestation are scratching, hair loss (especially along the top of the back), small crusty areas of skin, erythema, self-trauma scratches to skin, firm nodular swellings in the skin, evidence of flea dirt (brown-black specs on the skin surface that are actually flea feces), and evidence of fleas in the coat. A flea comb is helpful in detecting both flea dirt and the fleas themselves. Flea infestations can cause several major complications. First, the bite can cause itching and irritation for the host. In the case of hypersensitivity, the host develops an allergy to the flea saliva, which causes severe itching, hair loss, inflammation, scabbing, and secondary skin infections. This condition, known as flea allergy dermatitis, is highly uncomfortable for the affected pet. Also, fleas may transmit other disease-causing organisms to the dog such as tapeworm, Dipylidium canium, Dipetalonema reconditum, Francisella tularensis, Haemobartonella felis, and Yersinia pestis. Some of these diseases are zoonotic and can be transferred to humans. Flea bite anemia may occur in severe flea infestations or in small puppies. When a flea bites, it feeds on blood; with many fleas feeding at the same time, significant blood loss can occur. Symptoms of anemia include pale gums, weakness, or lethargy. Blood transfusions, iron supplementation, and hospitalization are occasionally necessary. The most effective way to prevent these conditions is to eliminate the fleas. Modern treatment regimens against fleas are designed to break the life cycle as well as to kill individual fleas.
Flea control can be applied not only to the animal itself, but also the environment. Frequent vacuuming and carpet cleaning may help to remove eggs and larva from the dog’s indoor environment; however, only about 20 percent of the larva may be removed when vacuuming because they wrap themselves around the bottom strands of carpeting. After vacuuming, throw the bag away. Steam cleaning the carpet may kill additional larva. When treating the indoor environment, it is important to wash all bedding in warm soapy water. Professional cleaning or exterminating services may be used in difficult cases. Appropriate yard maintenance can alleviate the problem in backyards. By trimming trees, keeping grass mowed, and raking debris, ideal flea habitats are eliminated. Also, immature stages of the flea lifecycle are sensitive to dryness and heat; they will die in sunny areas. Products containing certain chemicals are used to treat fleas on the host. Benzoyl urea derivatives (lufenuron), carbamates (carbaril, propoxur), fipronil, imadacloprid, organochlorines (fenthion), organophosphates, and pyrethrins are shown to terminate fleas on dogs. It is also a good idea to treat all animals in contact with the animal known to be infected to prevent that other animal harboring the infection. Currently, flea prevention is available in several forms such as oral, topical, or injectable. Also, different varieties offer differing lengths of protection. Program is a monthly oral tablet for dogs; however, this product makes the eggs infertile, but does not harm adults. Due to this fact, it is ideal in situations where infestation is not a problem, but should not be used in dogs with flea allergy dermatitis because the adults will still bite the animal. Advantage, Advantix, Frontline, and Revolution are all topical flea prevention applied to the skin. Each of these products kills the adult fleas and gives month-long protection. Capstar is an oral product intended to kill fleas quickly, but has no residual action. Typically, a longterm product is applied after Capstar. While some online companies advertise these products at cheaper prices, it is not a good idea to obtain these medications in this manner. Click here to read an article describing the problem with this method. Recurrence is likely unless the environmental flea population is eliminated and the dog is effectively protected.
Recent reports of grape and raisin toxicity cases have come to the attention of the ASPCA Animal Poison Control Center. From the data, experts have concluded that grapes and raisins can be toxic to dogs in large quantities So far, about 10 dogs have been officially reported to the ASPCA Animal Poison Control Center. The amount of grapes ingested ranged between 9 ounces and 2 pounds which works out to be between 0.41 and 1.1 oz/kg of body weight. The dogs exhibited signs of gastrointestinal distress including vomiting and diarrhea and then signs of kidney failure about 24 hours after ingestion of grapes or raisins. While a few grapes or raisins in moderation will probably not result in problems, but any dog that ingests a large quantity of grapes or raisins should be treated immediately and aggressively. Treatment includes emetics, activated charcoal, and gastric lavage to try to remove any undigested from the stomach and prevent further absorption of the toxin. Also, blood tests are done to assess renal function. Hospitalization and treatment with intravenous fluids will help alleviate any damage to the kidneys and prevent further injury. Despite testing, the reason for this acute kidney failure and the exact amount required for toxicity is unknown. Further study is necessary.
Heartworm disease is an infection of the parasitic worm called Dirofilaria immitis. These worms are found in all 50 states of the United States as well as all over the world on every continent except Antarctica. Its prevalence has increased due to today’s mobile society – people and their pets are constantly traveling from place to place, and the parasite gets taken along as well. Dogs of any age and breed as well as wolves, coyotes, foxes and cats are susceptible.
Dogs are the definitive host of Dirofilaria
immitis, but two organisms are required to complete the heartworm’s
lifecycle. Mosquitoes of
several species serve as vectors and carry the disease
from infected dogs to healthy ones. When a mosquito bites an infected dog, the
mosquito ingests the heartworm larva, known as microfilaria. Inside the
mosquito, the microfilaria undergo changes that make them infective to a healthy
dog; this process takes two to three weeks; the actual time for this
transformation to occur depends on the temperature and will occur more rapidly
in warmer climates. Development of the microfilaria requires temperatures at or
above 80 degrees Fahrenheit for about two weeks; no larval development will
occur when temperatures are below 57 degrees Fahrenheit. When the mosquito feeds
again on a healthy dog, the infective microfilaria are passed on. The
microfilaria enter the dog’s circulatory system through the mosquito’s bite
wound and migrate throughout the dogs’ body, ending up in the right atrium
approximately four months later. Adult Dirofilaria immitis are long,
thin, white worms that can grow to be about 12 inches long. Once in the dog’s
heart, heartworms can cause significant damage to the dog’s heart and lungs and
may remain there for several years. Also, heartworms may lodge in the veins of
the liver. After adult heartworms mate, a female will produce thousands of live
young in a day. These microfilaria will travel throughout the dog’s bloodstream
and wait, possibly for up to three years, for a mosquito to carry it to another
host dog. The entire lifecycle of the heartworm is approximately six months.
The first signs of heartworm disease may not appear for up to a year after the initial infection. The most common symptom of heartworm disease is a soft cough; unfortunately, many owners make the mistake of disregarding this indication as a minor occurrence and ignore it. Eventually, the cough will worsen and the dog will show a drastic reduction in energy; he will tire easily, be weak and listless, and may actually faint after exertion. Also, the dog will lose weight and condition, show difficulty breathing, and may cough up blood. The degree of infection, the length of time a dog has been infected, and the individual animal’s response to the infection determine the severity of the signs of the disease. If left untreated, congestive heart failure ensues, and the dog may die.
A simple diagnostic blood test can show if a
dog is infected with heartworms; the filtration test detects microfilaria in the
blood while the occult test finds adult worms in the heart. Also, a radiograph
can distinguish the presence of adult heartworms in the heart or lungs.
Once a dog has tested positive, treatment is possible; however, often the success of a given treatment depends on how far the disease has progressed. The first step in treating a dog with heartworms is evaluate the dog and treat any secondary problems such as heart failure or kidney or liver insufficiency so the dog can withstand treatment. Next, the adult worms are killed with a compound containing arsenic. The treatment is administered in two doses each day for two days. It is important to follow the treatment with several weeks of inactivity to allow the dog’s system a chance to recover and to absorb the dead worms. During this time, exertion could cause the dead worms to dislodge from the heart, travel to the lungs, and cause death. Three to four weeks after the adult worms are killed; further treatment is needed to kill the microfilaria. The dog is dosed daily for a week, and then the blood test is repeated to confirm the heartworms are gone. Follow up studies should be done several months later. Surgical removal of adult worms as possible and may be necessary in advanced cases with heavy heart involvement.
Despite relative success with treatment of heartworm infections, a far safer and cheaper approach is prevention. Preventative medicine comes in oral, topical, and injectable doses and is available from any veterinarian. Some products are given daily, but the most popular medicines are given monthly. Some common products are Heartgard, Interceptor, ProHeart, and Revolution. Before starting any prevention plan, you must get the dog tested for heartworms. While the required interval to administer heartworm prevention in this area is considered April through December, it is highly recommended to dose dogs year round due to highly unpredictable winter climate patterns. Also, many preventive products carry a guarantee that if the dog is on year- round prevention, undergoes a blood test annually and still contracts heartworm disease, the company will pay for the treatment. Considering the cost of treatment is 10-20 times the expense of annual medication, this is a wise choice.
Lyme disease has been recognized in Europe for
almost a century, but it was not described in humans in the United States until
1975. The disease also occurs in dogs, horses, cattle, and cats, while many
wildlife mammals and birds serve as reservoirs for the infection. During the
1980’s, the reported disease incidence in both dogs and humans increased
dramatically; lyme borreliosis is now the most common arthropod-borne disease
in the United States.
Lyme disease is caused by a group of Borrelia species. Only one species, B. burgdorferi is known to be present in the United States. B. burgdorferi organisms are corkscrew-shaped, motile, microaerophilic bacteria of the order Spirochaetales. Hard-shelled ticks of the genus Ixodes transmit B.burgdorferi by attaching and feeding on the various mammalian, avian, and reptilian hosts. In the northeastern regions of the United States, the black-legged deer tick is the predominate vector. When the tick attaches and begins to feed on its host, spirochetes are found in the midgut of the tick. Stimulated by the blood meal, they begin to migrate to the tick’s salivary glands. From there, they are introduced into the skin of the host. Studies have shown that it takes the organism at least 24 hours to migrate from the tick hindgut to the host’s skin; therefore, risk of infection increases with the time the tick is allowed to feed on the host. A tick’s lifecyle is complicated and involves three different hosts over four developmental stages. The typical tick life cycle takes approximately two years. The female ticks lays about 2000 eggs in the spring. Usually, only a small portion of the larva that emerge from an infected female carry the B. burgdorferi organism. The larva of Ixodes ticks feed mainly on small mammals such as mice; larva may contract the organism from infected mice. After feeding, they drop off the host and enter a resting state for the winter. The larva molt into nymphs the following spring. During spring and early summer, nymphs feed on new hosts, again usually small mammals but possibly humans or dogs. Again, nymphs may contract B. burgdorferi form an infected host mammal. In the fall, nymphs molt again and enter the adult stage. In some areas of northeastern United States, more than 50% of the adult ticks carry B. burgdorfer; adult ticks are the most important source of infection for dogs. Adult ticks are found on shrubs and other vegetation; from this elevated position, they can detect and attach to large mammals. Adult ticks mate on the host. Females engorge for 5 to 7 days following mating, and then drop off into the leaves where they will hide through the winter. The following spring, the females lay eggs and the cycle continues.
After a blood meal is initiated, spirochetes in the tick hindgut begin to migrate to the salivary glands. During that time, organisms multiply, cross the gut epithelium into the hemolymph, desseminate to the salivary glands, and infect the host through tick saliva. From the site of attachment, the organisms then replicate and migrate through the tissues of the host mammal. Within weeks, they may spread to many tissues where they will commonly invade the closest joints. The interaction of Borrelia organisms and host cells initiates the host’s immune response. Locally produced immune factors accumulate in the joints and may cause arthritis and joint pain. Joints typically contain increased amounts of synovial fluid. This pain typically begins in the joints closest to the site of attachment and spreads throughout the body. This arthritis pain is usually intermittent due to the migration of B. burgdorferi and its interaction with host cells, and the subsequent production of the inflammatory response factors. Not all infected animals develop clinical signs. It is speculated that numbers of organisms in tissue differ from individual to individual and large numbers of spirochetes may be essential to induce a clinically apparent response. The genetic background of the host may also be important. Studies have shown that of dogs kept as pets in endemic areas, approximately 5% of all infected dogs became ill. However, under experimental conditions, up to 75% of infected animals develop clinically apparent Lyme arthritis. In those experiments, dogs developed mono- or oligoarthritis 2 to 5 months after tick exposure in the joints closest to the tick attachment. In dogs and humans, B. burgdorferi establishes persistent infections. Other clinical signs include anorexia and general malaise. In a few cases, heart block, fatal kidney failure, and neurological incidents such as seizures, aggression, and other behavioral changes have been reported.
There are no specific clinical, hematological, or biochemical pathological changes that would confirm the diagnosis of Lyme borreliosis. Therefore, additional tests, such as antibody and organism detection, need to be performed to produce a specific diagnosis. The three criteria important to establishing the diagnosis of Lyme disease in dogs are a history of exposure to ticks in an endemic region, typical clinical signs for Lyme borreliosis, specific antibodies to B. burgdorferi. It is probably that both antibodies and organisms persist in dogs for several years. Several commercial kits are available which allow veterinarians to test for Lyme antibody in dogs without sending samples to diagnostic laboratories, but these tests are moderately unreliable.
Antibiotics are the treatment of choice for Lyme borreliosis. Tetracycline (doxycycline), penicillins (amoxicillin and ceftriaxone, and macrolides (azithromycin) are very effective in improving the clinical status of the patient. Antibiotics should be given for 3 to 4 weeks. The long duration of therapy is necessary because of the very slow multiplication rate of the organisms; it takes 12 hours of more for B. burgdorferi to double in number. Antibiotic therapy reduces the number of organisms in the host. Corticosteroids and other anti-inflammatory drugs are sometime used to treat Lyme disease, but these drugs should be applied cautiously; studies have shown that a persistent subclinical infection may be reactivated to clinical Lyme arthritis by a two-week course of prednisone.
There are currently several approaches to preventing infection in dogs. Tick exposure can be reduced by either modifying the tick habitat—trimming trees, mowing lawns, removing bushes, and reducing deer traffic—or by limiting tick engorgements on pets by using tick repellants such as Frontline or Advantix and by grooming the dog daily. If this is not possible, vaccination against B. burgdorferi may be considered. Vaccines are either based on a single antigen or on a whole-cell bacterin. Both vaccine types noted prevent the transmission of B. burgdorferi to the host. Yearly re-vaccination is required to maintain antibody titers are protective levels.
Mange in the dog is an infestation of the dogs skin by one of two varieties of mite. Mange can be caused by both Sarcoptic mites and Demodex mites. The term mangy describes the ragged and uneven hair coat and damaged skin that results from this disease. Both varieties of mite responsible for mange reside and feed in the hair follicle and oil glands of the skin. This causes intense itching and scratching of the skin which can lead to hair loss, inflammation, self trauma, and dry scabby skin lesions on the body. Because Sarcoptic mites actually burrow into the skin, they tend to cause a more severe mange. Most cases of Demodex are self-limiting and the animal will recover on its own while Sarcoptic mange usually requires veterinary treatment. Once eliminated, most dogs do not acquire another infestation because its natural immune system is prepared to quickly remove any new mites from the animal. However, certain dogs, due to their genetics, are highly susceptible to the disease and may acquire severe, unresponsive episodes of the disease. Many veterinarians believe that all dogs carry mites on the skin, but clinical signs do not appear until hereditary, nutritional, or environmental conditions allow the mites to proliferate and visible skin lesions become apparent; healthy dogs are quite resistant to mites. This condition is most often seen in young dogs or those that are nutritionally deficient or immunosuppressed. It is common for a mother carrying the mite, but not showing clinical signs, to transmit the parasite to her puppies; the pups may or may not develop signs of the disease. Adult-onset Demodex in a dog assumed to be healthy usually indicates an underlying pathological or immune disorder. These cases can be difficult to cure unless the primary condition is treated successfully as well. While caused by a similar organism, diagnosing the two types of mange is very different. Demodex mites are easily seen on a slide prepared from a skin scraping. Because Sarcoptic mites are difficult to diagnose, the condition is commonly mislabeled as allergy dermatitis and the wrong treatment given. Dogs given cortisone therapy may experience a reduction in itching and scratching, but the mites are unharmed and continue to infest the animal. The correct treatment for mange is a topical insecticide such as Mitaban or Revolution. Lime-sulphur dips have been used in the past, but are not used currently in favor of the more effective methods. Recent studies have shown Ivermectin (injected or oral), used currently as a large animal dewormer, to be effective for both Demodex and Sarcoptic mange cases; however, it is important to remember that this medication has not been tested in this application by the manufacturer and is not approved to be used in this manner. Discuss this option with your veterinarian before choosing this treatment. Also, dogs afflicted with mange will benefit from a high-quality, meat-based diet as well as supplements such as fatty acids and vitamins. All dogs in contact with the infected animal should also be treated because they are assumed to be asymptomatic carriers of the mites.
Click here to view pictures of dogs affected with mange.
There are two kinds of fatty acids – nonessential and essential. Nonessential fatty acids can be synthesized within the body of a dog and are therefore not required in its diet. Essential fatty acids cannot be synthesized and must be provided in its food. Dogs require one essential fatty acid – linoleic acid. If provided at proper levels, dogs can synthesize all other necessary fatty acids from linoleic acid. Linoleic acid is classified as an omega-6 fatty acid based on its structure. This fatty acid is found primarily in grain and animal fats. Another important class of fatty acids is the omega-3 fatty acids. While structurally similar to omega-6 fatty acids, omega-3 fatty acids are not considered essential in companion animal nutrition. Because of their similar structures, omega-3 and omega-6 fatty acids compete for the enzymes which convert these fatty acids into their respective metabolites. Interestingly, their specific metabolites differ in intensity as cellular signals; generally the signals derived from omega-6 fatty acids are more powerful than those coming from omega-3 fatty acids. Together, the omega fatty acids work to regulate the blood flow to body tissues, assist an animal’s immune system respond to injury and infection, aid in clotting after injury, boost the inflammation response, aid in normal reproduction, and maintain a normal, attractive hair coat and healthy skin. In addition, dietary fat provides other important functions in a pet’s diet. Besides supplying a concentrated form of energy, it contributes to the palatability and texture of food and carries the fat-soluble vitamins A, D, K, and E.
All forms of onion and garlic are problematic;
this includes raw, dehydrated, cooked, powders, and those in foods. Dogs lack
the enzyme necessary to properly digest onions and garlic; a buildup of the
toxic ingredient in these foods, thiosulphate, can result in anemia, gas,
vomiting, diarrhea, or severe gastrointestinal distress. Treatment would
include fluid therapy, anti-emetics and anti-
diarrhea medications. Also,
stomach lavage may help if performed soon enough after ingestion of the
overdose. If large amounts of onions or garlic are ingested or are a daily part
of the dog’s diet, the red blood cells may become fragile or break apart. Signs
can begin immediately after eating the foods or a few days later. Ingestion of
large quantities of onions or garlic may result in death if left untreated.
PARVOVIRUS (parvoviral enteritis)
Parvovirus, or parvo for short, is a virus causing severe infection in puppies and dogs. It invades and destroys rapidly growing cells in the intestine, bone marrow, and lymphoid tissue resulting in nausea, vomiting, and severe, hemorrhagic diarrhea. The invasion of the bone marrow cells causes a decrease in the white blood cell count leading to increased susceptibility to bacterial infections and sometimes a shock-like condition known as endotoxemia. The disease can vary from mild to fatal if not properly treated. Infection is generally attributed to ingestion of material contaminated with infected dog feces and can occur when a dog smells or licks the ground; direct contact with another dog is not necessary for infection. Parvovirus is shed in the feces of infected dogs for approximately two weeks after initial ingestion and can live in the environment for two years. Dogs of all ages can be infected, but puppies and younger dogs, especially unvaccinated animals, are more susceptible. Unsanitary and/or overcrowded kennel conditions may increase a dog’s chance of infection; concurrent infection with parasites, bacteria, or other viruses may also increase susceptibility to parvo infection. Proper vaccination is the best prevention. Parvovirus is a severe and acute infection; all cases require immediate veterinary attention and hospitalization.
Diagnosis is usually based on clinical signs
such as depression, fever, lethargy, loss of appetite, vomiting, and
foul-smelling, mucuosy diarrhea. Following a complete medical history and
physical exam, the feces of the animal is tested for the presence of the virus
using an ELISA antibody test. Blood tests and X-rays determine the severity of
the infection and exclude other causes of the symptoms such as gastrointestinal
ileus, obstruction of the bowel, foreign body in the gastrointestinal tract, or
intussesception. A CBC will determine the effect of the virus on the bone
marrow; usually a very low white blood cell count is shown. Serum biochemistry
will help the veterinarian determine the animal’s hydration status, blood sugar
level, kidney function, and electrolyte levels. Therapy is dependent upon the
severity of clinical symptoms and is directed at treating the severe
dehydration, controlling vomiting and diarrhea, and preventing secondary
bacterial infection. Therapy may include intravenous fluid therapy and
electrolyte replacement, antibiotics, anti-nausea drugs, anti-emetics, and
possibly transfusion of blood products. Sick puppies should be kept in isolation
because they are highly contagious. All isolation disinfectant procedures should
be followed to prevent cross-contamination of other dogs in the clinic. A bleach
solution has been shown effective at killing the virus on non-porous surfaces;
iodine is also successful at inactivating the virus. The expected prognosis is
that 80-90% of affected dogs will survive and lead normal, healthy lives if the
disease is detected early and the proper treatment given.
After treatment, the dog will need some time to rest and regain his strength. Once vomiting and diarrhea have subsided, encourage water intake and a bland diet. It is important to clean up all stools and disinfect the dog’s area very thoroughly so shed virus is removed and the environment not contaminated. Prevention is possible through a series of vaccinations. Antibodies acquired from the mother can interfere with the development of the puppy’s own immunity to parvovirus; this effect can last up to 16 weeks so it is important that puppies receive the final parvovirus vaccine at 16 weeks of age or older. Immunity is acquired after infection, but it is still necessary to booster the immune system with a vaccination. Also, keep the dog away from fecal waste of other dogs when walking along neighborhood streets or parks.
POISON IVY and POISON OAK
Poison oak and poison ivy belong to a group of plants called toxicodendron; these are also known as the Rhus species. The toxic component in these plants is urushiol; this toxin is an oil resin found in the plant sap. Animals can be affected by the toxin and may also transmit it to a person. Like humans, some animals seem resistant to the toxin while others are highly susceptible.
Dogs typically come into contact with the poison ivy or poison oak plant in wooded areas. They may ingest some of the plant, but are more likely to rub against it while walking. In animals, exposure to urushiol may result in skin irritation or gastrointestinal distress if the plant was eaten. Symptoms include red, inflamed skin, itchiness, raised bumps or swellings on the skin, and anorexia, lethargy, or vomiting and diarrhea if the plant was ingested. Veterinary care is recommended if the animal develops a reaction to the plant. Treatment of urushiol toxicity is based on the severity of the signs. For those animals with skin irritation, prolonged bathing and rinsing is recommended. Hospitalization with intravenous fluids may be necessary for dogs who ingest the plants. Gastric lavage or activated charcoal may be administered to remove any more plant material from the stomach. Preventing a pet’s exposure to the plants is the surest way to avoid urushiol toxicity. Do not allow the dog to freely roam in unfamiliar woods. Frequently check your own property for the presence of these plants.
RAISINS … Please see GRAPES and RAISINS
ROUNDWORM (Ascariasis)
Please click here to view a picture of roundworm.
The roundworm
endoparasites are members of the
ascarid family. Toxocara canis and Toxascaris leonine are the
species known to infect the dog. In Toxocara canis, the adult female
lays large numbers of eggs in the intestine which are then passed in the feces;
females are able to produce more than 200000 eggs in a single day. Adult
roundworms are occasionally seen in feces and vomitus. The eggs are particularly
resistant and can survive in the environment for years. They become infective
in about 4 weeks depending on various environmental factors. After being
ingested by a dog after contact with the infected feces, the eggs hatch in the
small intestine. Larva travel via the blood stream to the liver and the lungs,
and then through the trachea to the intestine where they mature. In pregnant
dogs, the larva are able to infect the fetuses she carries through the
bloodstream; in this way, many puppies are born with roundworm infections.
Also, the mother may shed larva in her milk which is a source of infection to
puppies. In some cases, the larva encyst in the muscle of dogs and remain there
for a period of time. Dogs may also become infected by ingesting small rodents,
mammals, and birds who harbor the parasite. A small number of worms rarely
causes clinical evidence of infection. Heavy infestations can cause intestinal
obstruction. Heavily infected dogs may have digestive disturbances,
intermittent diarrhea, a dull coat, and a pot-belly appearance. Clinical signs
are most common in young dogs (under 3 months of age); infections in adult dogs
are normally asymptomatic. Diagnosis of this parasite is based on seeing adults
in the feces or eggs in fecal smears viewed under the microscope. Adults of
these species may range from 7 to 13 cm in length and are long thin and whitish
in color; the adult worms resemble spaghetti noodles. While helpful, flotation
techniques are not required to visualize eggs on the microscope slide. Two
treatments of an an oral medication such as fenbendazole, febantel, and pyrental
is suggested; these treatments are to be repeated two weeks apart for maximum
efficacy. To reduce a dog’s risk of a roundworm infection, prevent his exposure
to the feces of other dogs or soil that may have been contaminated, and
regularly do a fecal check on the animal.
TAPEWORM (Dipylidium caninum)
Please click here to view a picture of tapeworm and proglottids.
The adult tapeworm lives in the small intestine of the dog. An adult tapeworm is typically about 6 inches in length. It is made up of a head portion called a scolex and many small tail segments. Each tail segment, called a proglottid, is like a separate organism and contains independent digestive and reproductive systems. The tapeworm hooks onto the intestinal wall and absorbs nutrients through its skin as the food eaten and digested by the host moves past. Older segments of the worm are released from the tail and are released in the feces of the dog; these segments contain many eggs. Eventually, the sac breaks and the eggs are released into the environment; the tapeworm eggs themselves are not infections to dogs. Larval fleas are commonly located in the same environment the eggs are found in; flea larva feed on organic debris and consume the tapeworm eggs. As the larval flea develops, the tapeworm also matures. By the time the flea is an adult, the tapeworm is developed enough to infect a dog. A dog acquires a tapeworm infection when it ingests an infected flea. The flea, carrying the adult tapeworm, is carried to the stomach and small intestine of the dog where the cycle begins again. It takes approximately three weeks from the time the flea is swallowed to when tapeworm segments are seen shed in the feces. Tapeworm lifecycle
Mild tapeworm infections do not do major harm to the pet; problems arise when a massive infestation occurs or when the dog is nutritionally deficient. These dogs begin to lose weight and show a decrease in performance and energy. Prevention is the best treatment and involves treating the animal with flea prevention. Also, maintain a high level of nutrition because dogs that are in a generally healthy condition are not threatened by this parasite. Tapeworm infestations are diagnosed by observing adults in the feces of the animal or by detecting the eggs on a slide from a fecal smear. Once diagnosed, tapeworm worm infestations are treated by oral or injectable dewormers; the most common medications used are Drontal and Droncit.
In cases of toad poisoning, the dog has licked or eaten the toad, but the dog doesn’t necessarily have to come into contact with the animal to be exposed. Several cases have been reported where the toad was attracted to the dog’s water dish and merely perched along the rim. Enough toxin can be left behind to make a dog sick.
If you see your pet lick a toad, you should
flush his mouth with water to remove traces of toxin and immediately take him to
the veterinarian to be evaluated. If enough toxin is ingested, the dog may have
an irregular heartbeat and strange behavior; the toxins are hallucinogens. Also,
mouth irritation with foamy salivation, depression, weakness, collapse,
difficulty breathing, seizures, fever, vomiting or diarrhea may be observed. At
the
veterinary clinic, an echocardiogram may be conducted to determine whether
the dog has an abnormal heart rhythm. Currently, there is no test to find the
presence of the toxin and diagnosis is usually based on having seen the pet with
the toad or by finding toad parts in the digestive tract. The veterinarian may
give the dog cardiac drugs such as propranolol to correct abnormal heart
rhythms. Also, intravenous fluids are given. Pets with hyperthermia may benefit
from a cool bath.
Dog toys are intended to enrich the lives of the pet. The best toys will keep life from being boring for the dog, initiate pet-owner play, and entertain the animal when the owner is away. Most animals do not need many toys; it is important to remember that the ideal plaything is largely a matter of personal (canine) preference. However, it is important to select toys for your dog that do not pose a health risk to keep the animal safe. While the vast array of toys at the petstore may seem overwhelming, when choosing a toy, there are many criteria to consider that will allow you to select the correct toy(s) for your animal. First of all, make sure the toy is too large to lodge in the animal’s throat should he try to swallow it. A dog’s primary activities with a toy are carrying it in its mouth, chewing it, tossing it, and catching it, so it is important that it will not become wedged in the animal’s throat. Next, choose a toy made of a tough, durable material so that the dog gets chewing satisfaction without the risk of ingesting bits of plastic. For this reason, Nerf balls and shapes are not a good idea because they are easily shredded; a dog may ingest these pieces and its gastrointestinal system may be irritated or blocked. Also, avoid toys with small parts that may be torn apart and devoured. The key here is supervision; if the dog tears his toy apart, remove the pieces before he can ingest them. On the other hand, you do not want something too hard, or the pet may break his teeth while chewing on the toy. If you intend to play ball outside with the dog, make sure the ball you choose to play with will bounce. If your canine spends a lot of time unattended, look for balls and plastic toys with hard rubbery segments, nubs, depressions, and indentations. These allow the dog to bite onto one end and then flip the toy into the air or across the room; this play action will allow the dog to entertain itself while it’s alone. A knotted rope is good for playing tug and for chewing. Rawhide is generally considered a safe chew toy by veterinarians. As the dog chews, the rawhide softens; in this way the teeth are not damaged and any rawhide swallowed will be digested. While many toys advertise to clean dog’s teeth while they chew, veterinarians agree that the best way to keep teeth clean is to brush them regularly; do not rely on chew toys for dental care.
Yews are evergreen shrubs or small trees with glossy, rigid, dark green, linear leaves 1 ½ to 2 inches long with pointed ends that are closely spaced on the branches. Male and female flowers are produced on separate plants, producing red to yellow fruits containing a single seed. The toxicity of yews to animals and humans has been known for many years. Yews contain a group of 10 or more toxic alkaloids, the most toxic of which are taxine A and B, collectively referred to as taxine. Taxine inhibits normal sodium and calcium exchange across myocardial cells, depressing cardiac depolarization and causing
arrhythmias. Yews also contain nitriles, ephedrine, and irritant oils. All parts of the plant, green or dried, except the fleshy part of the fruit surrounding the seed are toxic. The highest concenterations of alkaloids are found in the leaves during the winter. Animals generally are not attracted to the plant if they are fed a balanced diet. The toxic does is not exactly known, but as little as 200g of dried leaves proved fatal to a 550kg steer. The fatal dose is estimated to be about 0.1 to 0.5 percent of the body weight of the animal.
Clinical signs of yew poisoning include the sudden onset of muscle trembling, incoordination, nervousness, difficulty breathing, slow heart rate, vomiting, diarrhea, convulsions, and unexpected death. Death may occur immediately or several days after the yew was eaten. Diagnosis is based on clinical signs and a history of exposure to the plant. There is no specific treatment or antidote for yew poisoning. If an animal is observed consuming a yew, immediate veterinary attention is indicated. Activated charcoal and magnesium sulfate should be introduced via stomach tube to decontaminate the stomach. Atropine sulfate is reportedly effective in counteracting the slow heartbeat and heart failure, but should be used with caution. When possible, intravenous fluid therapy to support the cardiovascular system should be performed.
References:
Veterinary Technician magazine
