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Vaccinations: All Veterinary Schools in North America Changing Vaccination Protocols
Recent editions of the Senior Dogs Project's newsletter have reported on the ever-broadening trend of eliminating vaccinations for adult dogs, except for rabies, where required by state law. We have now had a report that all 27 veterinary schools in North America are in the process of changing their protocols for vaccinating dogs and cats. Here, in a nutshell, are the new guidelines under consideration: "Dogs and cats immune systems mature fully at 6 months. If a modified live virus (MLV) vaccine is given after 6 months of age, it produces immunity, which is good for the life of the pet (i.e., canine distemper, parvo, feline distemper). If another MLV vaccine is given a year later, the antibodies from the first vaccine neutralize the antigens of the second vaccine and there is little or no effect. The titer is not 'boosted' nor are more memory cells induced.
"Not only are annual boosters for parvo and distemper unnecessary, they subject the pet to potential risks of allergic reactions and immune-mediated hemolytic anemia. There is no scientific documentation to back up label claims for annual administration of MLV vaccines. Puppies receive antibodies through their mothers milk. This natural protection can last 8-14 weeks. Puppies and kittens should NOT be vaccinated at LESS than 8 weeks. Maternal immunity will neutralize the vaccine and little protection (0-38%) will be produced. Vaccination at 6 weeks will, however, delay the timing of the first highly effective vaccine. Vaccinations given 2 weeks apart suppress rather than stimulate the immune system. A series of vaccinations is given starting at 8 weeks and given 3-4 weeks apart up to 16 weeks of age. Another vaccination given sometime after 6 months of age (usually at 1 year 4 months) will provide lifetime immunity."
Original Doc: vaccinations- latest information.doc
All About Ears, Understanding health and disease of the canine ear
By Sandra A. Priest, D.V.M.
Source: AKC GAZETTE, February 1992. pp 69-73.
The perfect canine ear hears every command right on cue and delivers those commands to the brain for immediate (and obedient) reaction. It never requires grooming, cleaning or medical treatment. In fact, the only attention the perfect ear ever needs is frequent petting. After all, the perfect canine ear is, well, perfect!
But in reality, almost all canine ears fall short of this ideal, and many owners face periodic ear problems in their dogs. These problems can be minimized, however, by regular observation and by seeking prompt medical treatment as soon as problems occur.
Anatomy of the Ear
The canine ear, an organ of hearing and balance, is divided into three portions: external, middle and internal.
The familiar ear flap, or pinna, is part of the external ear, along with the ear canal. Functioning as a sort of cartilaginous funnel, the pinna receives sounds and transmits them to the eardrum (tympanic membrane) via the ear canal. Canine pinnas vary in shape and form depending on the breed, from small and erect to large and pendant.
The ear canal is also made of cartilage, and extends inward in a vertical and horizontal direction until it terminates with the eardrum. Secretory glands are present in the skin which lines the ear canal, except near the eardrum. Some breeds also have hair follicles in this area, and thus have hirsute ears.
The region of the middle ear begins with the eardrum. Behind the eardrum are the auditory ossicles, small bones which transmit sounds from the eardrum to the inner ear. Most of the middle ear is an air-filled cavity lying within an open bony structure called the tympanic bulla. The opening of the Eustachian tube, a short canal which connects the middle ear with the oral cavity, is found within the rounded tympanic bulla.
The deepest part of the canine ear, the internal ear, is responsible for both hearing and equilibrium. Some of the structures in the internal ear convert sounds into nerve impulses, which are then sent to the brain. Other structures transmit impulses which help the brain orient the rest of the body in space.
As the outermost structure of the ear, the pinna is the likeliest candidate for an injury. it's not uncommon to see pinna lacerations, especially in dogs with large or pendulous ear flaps. Most lacerations result from fights, sharp vegetation, and self- trauma.
Because the ear has a rich blood supply, copious bleeding may follow a pinna injury, especially if the dog proceeds to shake its head. Severe head-shaking or scratching may also result in a hematoma, a large, soft, blood-filled swelling that occurs when small vessels rupture within the cartilage of the ear flap. Hematomas can build rather suddenly, and-though not life-threatening in themselves and amenable to surgical repair-can involve virtually the entire ear flap.
Other problems of the pinna include bacterial, fungal and parasitic infections that often occur in conjunction with lesions on other parts of the body. For instance, the ear margins are a preferred site of infection by the Sarcoptes mange mite (though a localized form of Demodex mite may infect the pinna area alone). Hypersensitivity, endocrine and immune-mediated diseases may affect the pinna as well as other body areas. Additional information about these diseases will be discussed later in this article.
Otitis Externa, Media and Interna
Otitis is the medical term used to describe inflammation or infection of ear structures. Otitis may occur in the external, middle and/or internal portions of the ear.
Otitis externa is one of the most common conditions treated by veterinarians. At one time, it was thought to be caused primarily by microorganisms. Recent studies, however, have shown that it almost always occurs secondary to some predisposing factor or other disease state. Common examples of predisposing factors are conformation of the ear canal, frequent wetting of the canal, foreign bodies, parasites and trauma.
Ear type is an important factor in the incidence of otitis externa among breeds. The pendulous ear conformation found in many breeds, particularly spaniels and retrievers, actually restricts air circulation within the ear canal. The canals relatively small diameter and downward sloping direction also allow secretions to accumulate and clog the passageway.
Moisture in the ear canal, which is normally a region of high humidity, softens the epithelial lining of the canal and stimulates increased secretion by local glands. This sets up an environment which favors proliferation of microorganisms that normally reside in the ear. (Low numbers of a variety of organisms live inside the ear canals of most healthy dogs. Staphylococcus intermedius, Mircrococcus species, and occasionally coliforms, are the most common bacteria isolated from normal ears. The yeast Malassezia canis is another common inhabitant of normal canine ears which, given the correct circumstance, can overgrow.) Sources of moisture include environmental humidity, frequent baths, and swimming.
Other potential irritants to the ear are foreign bodies-typical examples are plant awns, foxtails, dirt, matted hair and dried wax- and ear mites. The saliva of these microscopic parasites provokes an intense allergic response in some dogs. Secondary microbial infections are common complications of ear mite infestations. Another parasite, the spinous ear tick of dogs (found in the Southwest) may also cause a severe inflammation. Occasionally, sarcoptic and demodectic mites may infect the ear canal and lead to otitis externa.
Many of these conditions cause a great deal of pain and itching, and dogs will commonly traumatize themselves by pawing and scratching at their head in distress. Medical attention is necessary to ease the dog's discomfort and solve the underlying problem.
A number of different systemic diseases can also ultimately affect the ear canal. Perhaps the most common are allergic diseases such as atopy (inhalant allergic disease), food allergy and flea allergy.
As many as half of all dogs with atopic dermatitis develop chronic otitis externa as part of their disease. This otitis, which may be complicated by secondary bacterial or yeast infection, usually results in severe itching. Many dogs with food allergies develop ceruminous (waxy) otitis externa. In fact, this otitis may be the only observable sign of the patient's initial problem. Some dogs with flea bite hypersensitivity also develop otitis externa, though fleas may be present anywhere on the dog's body.
Endocrine-related otitis is often accompanied by seborrhea in the dog, and the presence of this waxy secretion frequently contributes to otitis. Hypothyroidism is the most common endocrine cause of chronic otitis externa; others include Sertoli cell tumors and ovarian imbalances.
Several immune-mediated diseases are also associated with otitis, which are known to cause lesions on the pinna. Examples of such diseases are systemic and discoid lupus erythematosus, pemphigus foliaceous, and pemphigus erythematosus. These immune-mediated diseases almost always involve lesions on other parts of the body as well.
Lastly, other potential causes of otitis externa include tumors, though this is uncommon, and anal sac disease, fever and the canine distemper virus.
If otitis becomes chronic, the skin lining the ear canal thickens and the outer layer may ulcerate. The diameter of the ear canal may narrow and eventually become obliterated by proliferating bone tissue. Eventually, the eardrum may rupture and permit infection to spread to the middle and inner ears.
Otitis media (infection of the middle ear) most frequently occurs as an extension of otitis externa. In some cases, the infection may ascend to the middle ear through the Eustachian tube or result from blood-borne micro-organisms. An infection of the inner ear, otitis interna, may result from otitis media, systemic infection or meningitis. Other causes include trauma, neoplasia and the administration of antibiotics which are toxic to ear structures.
Most dogs with otitis externa exhibit head shaking and/or pawing and scratching at the ears. The ears themselves may appear red or swollen and have an abnormal odor. A yellow or brown discharge may be obvious on the inner surface of the pinna and within the canal opening.
Dogs with otitis media may have any of the preceding signs plus a head tilt, hearing loss, and/or paralysis of structures of the face (e.g. the lips, eyelids or ears). Some dogs have constricted pupils, drooping eyelids and protruding third eyelids, a collection of signs commonly known as Horners syndrome.
All the signs of otitis media, plus a nystagmus (rapid, abnormal pupillary movements) typically accompany otitis interna, along with incoordination and apparent nausea. Otitis interna can be life-threatening because the infection can spread from the inner ear to the brain.
Because otitis is often due to underlying factors, veterinarians begin searching for clues with a thorough history and a complete physical exam. The history may reveal an environmental cause (frequent bathing or swimming) or indicate the nature of an underlying disorder. A complete physical exam may likewise reveal evidence of systemic disease. If such evidence is found, a blood sample may be drawn for analysis. Other laboratory tests may be performed as indicated by the physical examination findings and results of the blood screen.
The ears should be systematically evaluated, both with and without the use of an otoscope, starting with the pinna and the surrounding region. If only one ear appears suspicious, the normal ear will be examined first. When ears are extremely painful, it may be necessary to sedate or anesthetize the dog before continuing.
Canine ears aren't like human ears in that the canal forms a distinct bend before it reaches the eardrum. For that reason, veterinarians need to gently pull the pinna up to straighten the ear canal while inserting the otoscope. In this way, any secretions, swelling, inflammation or structural abnormalities of the vertical canal become visible as the cone descends toward the horizontal portion of the canal.
If the ears contain excessive debris and secretions, it may be necessary to do some cleaning at this point in order to visualize deeper structures. Before this is accomplished, a small sample may be obtained to examine for ear mites or microorganisms. Sterile samples may also be collected for bacterial or fungal culturing as well as antibiotic sensitivity testing.
Visualization of the ear canal is not complete without an examination of the eardrum. A normal canine eardrum looks like a smooth, translucent, pearly membrane. Cloudiness, opacity, bulging or color changes may indicate an extension of the ear canal disorder to the eardrum or problems in the middle ear. Ruptures should not be apparent.
If otitis media is suspected, radiographs may be taken to look for changes in structures of the external and middle ear. In particular, radiographs of the tympanic bullae are desired to determine whether the middle ear infection has spread to inner ear structures.
Another part of the physical examination of a dog with signs of middle or inner ear disease is a neurological evaluation to detect possible brain involvement.
Types of Therapy
Successful treatment of otitis depends on diagnosis and treatment or correction of the predisposing factors or underlying systemic disorders. This includes the identification of the micro-organisms, parasites or foreign bodies which may be involved, and a thorough cleansing of the ears to remove debris from the pinna and ear canal.
The initial treatment of choice for many ear problems is a medical approach. Surgical treatment is reserved for most hematomas and for medically unresponsive otitis patients as well as those cases where proliferating tissue or tumors obstruct the ear canal. Surgery may also be necessary to drain the tympanic bullae of secretions.
Appropriate medical therapy is consistent with the cause of the ear problem and, if necessary, complements medications used to treat underlying systemic disorders.
Ear mite infections are typically treated with a topical medication containing a parasiticide. Many of these medications also contain an anti-inflammatory agent intended to reduce irritation and pain, as well as an antibiotic, to treat or prevent concurrent bacterial infection. In addition, topical flea powders or sprays should be applied around the ears and neck to kill any mites that have traveled beyond the ear canal. Because ear mites are highly contagious, other animals in the household should be checked for evidence of infestation and treated accordingly. No environmental treatment is necessary.
Ear infestations of Demodex and Sarcoptes mites are treated in conjunction with the rest of the body. Localized pinna lesions due to Demodex mites usually resolve spontaneously.
Bacterial infections are treated with topical antibiotic solutions. A combination product containing an anti-inflammatory agent may be prescribed if irritation and swelling of the ear canal are present. Since many medications used to treat otitis can be damaging to the middle ear, it's important to determine whether the eardrum is intact before selecting an antibiotic.
Topical antifungal preparations will be prescribed when yeast cells or fungi are suspected of contributing to the otitis. Mixed infections require medications to treat both types of organisms.
When dogs have an uncomplicated case of otitis externa arising from atopy, food allergy or other allergic disorders, topical anti-inflammatory medications without an antibiotic ingredient may be prescribed to help ease the dog's discomfort as management of allergy is explored. This also holds true for other cases of ceruminous otitis. Treatment of foreign body otitis includes removal and treatment with an antibiotic preparation to minimize infection.
When the eardrum has ruptured, systemic antibiotics help prevent the spread of infection to the middle ear. High doses of systemic antibiotics are prescribed to treat middle and inner ear infections. Systemic antibiotics and anti-inflammatory agents may also be used to treat chronic otitis and cases where owners are unable to administer topical medications at home.
Surgical correction is the only way to restore an ear with a hematoma to its former appearance. Left alone, most hematomas will resolve on their own ( the inciting factor, however, should be identified and resolved), but disfigurement, due to contraction of the ear cartilage, will probably occur.
The surgical technique involves making a long incision over the hematoma to remove the blood clot and promote drainage. To prevent refilling of the defect, rows of sutures are placed through the full thickness of the ear. Many practitioners prefer to bandage the repaired ear to facilitate healing.
Three surgical procedures have been described to treat refractory otitis externa. The first and most common is lateral ear canal resection, in which the outside wall of the vertical canal is excised and a permanent opening is created, improving drainage of the horizontal canal and overall canal ventilation. Vertical ear canal ablation, the second option, involves removing the entire vertical ear canal and reclosing the skin, leaving a small drainage hole at the opening of the horizontal ear canal. Finally, total ear canal ablation removes both the horizontal and vertical ear canals, and recloses the skin. These surgical procedures may also be employed for tumor removal. (Radiation therapy may follow surgery, depending on the type of tumor.)
Surgical management of otitis media and interna is directed at removing debris and improving the drainage of the tympanic bullae.
Many canine ear problems are completely preventable, if owners are willing to follow a few simple guidelines.
Perhaps the easiest (and the most valuable) measure is getting to know the normal appearance and odor of the dog's ears. Thereafter, when a change in appearance or odor is noticed, intervention can occur early-before the problem has a chance to grow in scope.
Good grooming is also important. The underside of the pinna and the external opening of the ear canal should be kept free of debris and hair. This is particularly important for pendant ear breeds. If you need to clip this area, first place a small ball of cotton in the opening of the ear canal to prevent clipped hair from falling into the ear and causing an irritation. Hair in the ear canal itself should be plucked out gently.
Dogs that are used for field work or that swim frequently run a higher risk of developing ear disorders due to increased moisture levels in the ear canal. Routine use of otic drying agents or agents which restore normal canal pH after field events or swimming episodes can be beneficial. Such products are available at most veterinary hospitals.
The ear canal is a delicate environment. Shampoo, water, flea sprays, hydrogen peroxide, alcohol and other cleaning agent and many topical ear medications can cause irritation, swelling and pain. Always check with your veterinarian before putting anything in your dog's ears.
Additional Reading: Diseases of the Ear Canal, The Veterinary Clinics of North America. J.R. August (editor). W.B. Saunders Co., 1988.
Dr. Priest, a private practitioner in Tennessee, competes in obedience and tracking with her Welsh Springer spaniel and English Cocker Spaniel.
Beware Pennyroyal Oil Repellents
by Christine Wilford
Source: Journal of the AVMA, Volume 200, Number 6, March 15, 1992
In the never-ending search for the perfect flea product, owners may try almost anything. Advertisements may imply that "natural" products are superior to - and safer than - those that are synthetic or man-made. However, natural products can be toxic, too.
Health food stores, pet shops, feed stores, grocery stores and some veterinary hospitals sell various flea repellents that contain an ingredient called pennyroyal oil, derived from the pennyroyal plant, sqauw mint or mosquito plant ( Mentha pulegium and Hedeoma pulegoides). The toxic ingredient, pulegon, is historically known for repelling fleas. Unfortunately, what appears as a "natural" way to repel fleas (which may be incorrectly interpreted as safer) can cause a dog's death.
Pennyroyal oil is extremely toxic to the liver of many animals, including humans. Symptoms of toxicity result within hours of application, beginning with listlessness, vomiting, diarrhea, and bleeding from the nose, mouth, and intestines. Exposure may possibly culminate with convulsions. Depending upon the amount of exposure, treatment may be futile, and death may ensue within one to two days.
Do not use pennyroyal oil in its pure form. And be cautious with shampoos, powders and any other form of flea product containing pennyroyal oil. Your best bet is to use only approved, reliable flea-products. Ask your veterinarian about new products or those that seem questionable.
Remember . . . natural does not necessarily mean safer or superior. After all, arsenic and cyanide are natural, too!
From the AKC GAZETTE, Veterinary News column, p. 34.
An Ear Full of Auditory Advice
by Dennis W. Thomas, DVM
This article was published in Dog World magazine, November 1996 edition
A wise old doctor once said, "Never put anything in your ear smaller than your elbow." This doctor could have been a veterinarian instructing you about ear care in the dog. Without a doubt, one of the most common problems that crosses the veterinarian's exam table is otitis externa (infection or inflammation of the external ear canal). Surprisingly, most ear infections can be forestalled by proper preventative care by the pet's owner. Often pet owners unknowingly make the problem worse by inappropriately treating the ear with improper medication or by traumatizing the ear during cleaning. The best way of preventing this is to take your dog to your veterinarian once you notice any ear problems and learn proper ear cleaning techniques.
Now HEAR This!
I once had a pet owner complain that she had been treating her dog for what she thought were ear
mites (a parasite found in the ear) for weeks and had not been successful at resolving the problem. Upon examination of her dog's ear canal, I found several pieces of spear grass embedded near the ear drum and gently extracted them. All the ear mite medication in the world would not have re-solved the problem.
To understand the dog's ear problems better, we must initially understand that the dog's ear canal is anatomically different than that of the human ear. Unlike the human ear, the dog's ear has two
compartments. Beginning at the opening of the ear canal, the vertical canal travels downward
towards the dog's jaw. Then it makes a 45 degree turn and travels horizontally towards the ear
drum. This makes visualization and treatment of the entire canal more difficult. Also, as a rule, most breeds have a much longer ear canal than humans. These differences predispose the dog's ear to infection as well as make treatment more difficult.
Dogs with long, pendulous ears, such as Cocker Spaniels, Labrador Retrievers, Basset Hounds and Irish Setters, certainly are more predisposed to ear problems than those breeds with short, erect ears. As the ear folds, it covers the ear canal and prohibits air from entering and drying the canal. The result is a moist, warm ear canal that is a perfect environment for organisms to grow.
Inflammation of the ear canal, or otitis externa, can be caused by a number of factors, such as
parasites, microorganisms, foreign bodies, tumors, and underlying dermatological (skin) disease. Ear mites are parasites that often can cause otitis externa. However, the incidence is much lower than often thought. In my experience, less than 10 percent of all ear problems in dogs that I have treated are the result of ear mites. Ticks and fleas are other examples of parasites commonly found in canine ear canals.
Ear mites can be problematic, however. An elderly gentleman once explained that he thought his dog was "going crazy." He said his old setter would sleep by the fireplace. Suddenly it would jump up yelping and begin to run around the room in circles. After several minutes of hysterical commotion, the dog would lie down again and go back to sleep.
After pondering the situation, I examined the dog's ears and found a heavy infestation of ear mites. It appeared that as the heat from the fire warmed the dog's ear canals, the mites would became agitated and began to move around. As the old setter would run around the room, the ears would cool down and the mites would stop their activity. Then the dog would return to the fireside.
An important point to remember is that ear mites are parasites. Therefore, for your dog to have ear mites, it must have had direct contact with another pet infested with ear mites. So if your veterinarian diagnoses one animal in your house with ear mites, it is best to have all of your animals examined for possible infestations.
Dastardly Yeast Infections
The most common cause of canine ear problems that I see is caused by microorganisms, particularly yeasts. Malassezia pachydermatitis usually is the culprit, and it loves to proliferate in warm, moist environments such as the dog's ear canal.
Owners will notice the dog shaking its head or scratching at its ears. A good sniff near the ears
usually verifies a problem, as most infectious otitis ears are quite pungent. Certain bacteria such as Staphylococci, Streptococci, E coli, and Pseudomonas spp also can cause infections in the dog's ear, and in many cases both bacteria and yeast are present. If the infection persists, the ear canal will become inflamed and often discharge a purulent exudate, a pussy substance.
Your veterinarian usually will take an ear swab and examine it under a microscope to determine the exact cause of the infection. This will enable a specific treatment plan to resolve the problem. Often, treatment will include flushing the ear canal with an antimicrobial solution and drying agent. An anti-inflammatory injection is then administered to reduce swelling and relieve the pain. The appropriate topical medication also will be dispensed for further treatment by the pet owner. Remember, all ear infections are not caused by the same microorganism; therefore, treatment without proper examination is strictly guessing.
As a pet owner, it is important to know that persistent or recurring ear infections in a dog commonly are manifestations of other concurring disease processes. Allergies and hypothyroidism are good examples. Systemic allergies often cause dermatitis and itching in the ear canal, which predispose self-trauma and subsequent ear infection. Hypothyroidism may manifest itself as increased thickness of the skin and continual release of exudate in the ear canal, which favors an environment for otitis externa.
Practicing Proper Ear Care
Proper ear care for the dog can often prevent recurring infection. Dogs with a history of ear disease require routine cleaning of the canals. I recommend plucking all hair that grows in the canal. Hair impedes air flow into the canal that tends to keep the canal dry. Common household tweezers or forceps work well and usually are well tolerated by the dog. Be careful not to grasp the skin of the canal. After hair removal, flush the ear canals with a commercial ear cleaner. These products can be found at most veterinarian clinics or pet shops. After flushing, gently massage the base of the ears to distribute the solution around the normal ear folds.
Most ear cleaners have several functions. They not only clean the ear canal but also have an agent for liquefying exudate, drying the ear canal, and changing the pH (acidity) in the canals. Most microorganisms prefer an environment that is alkaline; therefore, most ear preparations have an acid base. Frequency of treatment will vary among individuals, but once a week during the warm months is a good rule of thumb for those dogs that have had problems with infected ears. Also, any time your dog is bathed or enters the water, an ear cleaning solution should be administered immediately afterward. This preventative is similar to what humans do to ward off "swimmer's ear." Dogs without a history of ear problems may be treated with an ear cleanser after bathing.
It is not wise to use cotton tip applicators in the ear canal. This can be quite painful to the dog. Also, I don't recommend using alcohol in a dog's ear. Alcohol will dry the ear, but if there is inflammation or small scratches in the canal, the alcohol will burn and cause tremendous pain and further inflammation. If you must use a product from the shelf at home, use white vinegar diluted 50:50 with water.
Good preventative ear care can eliminate needless trips to your veterinarian and save a lot of
discomfort for your dog. Watch your dog carefully for scratching at its ears or shaking its head.
Have your groomer check for an ear problem each time you take your dog in, and at home take the time to check your dog's ears for redness, odor or the presence of exudate. If you determine there is a problem with your pet's ears, don't wait. Let your veterinarian do a thorough examination and direct specific treatment before the problem worsens.
Canine Ear Checklist
You may need to take your dog to the vet for a thorough examination if it:
Shakes its head or scratches its ears
Lives with other pets with parasitic infestations
Exudes a pungent odor from its ears
Has long, pendulous ears
Lives in a humid environment
Loves to swim or bathe
Has a history of recurring ear infections
Dr. Thomas has been a practicing veterinarian in Lewisville, Texas, for 15 years. He has
written numerous articles about pet health published in several magazines and newspapers.
This article was published in Dog World magazine, November 1996 edition.
Source: The 36th Annual Gaines Symposium, Gastrointestinal Disorders of Dogs and Cats, Continuing Education Article #4, Vol. 9, No. 12, December 1987.
Sponsored by Quaker, make of
GainesR, Ken-L RationR, and Puss'N BootsR
*Campylobacter jejuni is a common cause of enteritis in humans and is commonly isolated from domestic and pet animals.
*C. jejuni is microaerophilic with special culture and handling requirements; thus "rectal swabs" for routine laboratory cultures are inadequate.
*Differences in strains of both spontaneous and experimental isolates probably account for the inconsistent clinical disease induced by this organism.
*Exposure of both pet and owner to a common source rather than pet- to-owner contamination is a likely scenario if both should develop campylobacter enteritis.
Nonculturable spiral-form gram-negative bacteria were noted in 1886 by Theodor Escherich in stool specimens and intestinal mucus from human neonates with diarrhea and from adult cats. Later, similar organisms that would not grow on solid media were found mainly in the colon or associated with mucus in diarrhea stool specimens were described as "spirilla." These spirilla were reported in cases of "choleralike" and "dysenteric" disease. Growth on solid media was unsuccessful, although bacteria remained viable in liquid culture media for a few days. Based on the morphologic description, the association with enteritis in neonates and infants, the failure to grow on solid media, and the fact that no other bacteria with comparable morphology had been associated with human enteric infections, this initial description of the microorganism probably describes Campylobacter species. "In less than a decade, Campylobacter jejuni has emerged from obscurity as a veterinary pathogen to recognition as a leading cause of enteritis in human beings. When proper culture techniques are used, C. jejuni is isolated in North America and Europe from patients with diarrhea at least as often as Salmonella or Shigella species. Moreover, C. jejuni has been found in virtually every country in which it has been sought.
The genus Campylobacter previously named Vibrio fetus, was recognized in 1909 as a cause of abortion in cattle and sheep. It was not until 1977 that it was generally recognized that Campylobacter was a common cause of acute diarrhea in humans. the genus Campylobacter (campylo meaning curved and bacter meaning rod) was proposed, separating it from Vibrio species initially on the basis of the variation of serologic and biochemical characteristics of the human isolates and ultimately on the DNA composition.
The species that in the past was classified as "related vibrios" and C. fetus subsp. jejuni is now known as Campylobacter jejuni. The other Campylobacter species are listed in Table I according to the host(s) that each infects and their zoonotic potential. Under the present classification, C. fetus subsp. venerealis causes infertility and abortions in cattle; C. fetus subsp. fetus causes abortions in sheep and is a potential human pathogen; C. sputorum subsp. sputorum is a commensal oral microbe in humans; C sputorum subsp. bubulus and C. fecalis are commensals of the bovine reproductive and ovine intestinal tract; and C. sputorum subsp. mucosalis and C. hyointestinalis have been associated with porcine proliferative enteritis. Campylobacter coli, which at one time was believed to be the cause of swine dysentery, and C. jejuni differ only slightly and are often discussed together as potential human pathogens. A recently recognized species, C. laridis, is prevalent in sea gulls and has caused infection in humans; another species, C. pyloridis, is associated with peptic ulcers and chronic gastritis in humans but has unknown potential in animals.
Campylobacter jejuni is a curved, motile, gram-negative rod that requires some oxygen for growth but cannot tolerate normal oxygen concentrations in room air. Special culture techniques are needed, therefore, for its isolation; and that may explain its relatively late discovery. The organism is typical of gram- negative bacteria with its endotoxic properties of the lipopolysaccharide cell wall. Campylobacter has also been implicated as releasing an enterotoxin that is cytotoxic. In veterinary medicine, C. jejuni has generated additional interest because animals might present an important reservoir for the organism.
Campylobacter Enteritis in Humans
Campylobacter jejuni is a major cause of acute diarrhea in children and adults. Recently, C. jejuni has rivaled Salmonella as a cause of enteritis and might actually be present more often than Shigella or Salmonella. The usual incubation period of 24 to 72 hours after ingestion can extend up to 10 days. The disease in humans is usually accompanied by fever and diarrhea (in 90
% of cases), abdominal pain (70%), myalgia, malaise, anorexia, and occasionally vomiting. Feces are loose, usually becoming watery, mucus and blood (in 50% of cases) may be present. The disease usually is self-limiting; recovery is complete in one to two weeks. Deaths have been reported, however, in severe cases of C. jejuni enterocolitis.
The disease can vary and bacteremia, meningitis, and abortions have been reported. In addition to direct tissue invasion of the bowel, the release of endotoxins or enterotoxins has been implicated and may be strain-specific. The pathology is most common in the jejunum and ileum; but the colon, extending to the rectum, may be involved.
After oral ingestion, bacteria that survive the gastric acid barrier reach the bile-rich, microaerobic small intestine, where multiplication enables diarrheic patients to shed 106 to 109 bacteria per gram of stool. The pathology is consistent with a nonspecific colitis with acute inflammation of the lamina propria, degeneration and atrophy in the goblet cells and epithelium, crypt abscesses, and mucosal ulceration. Administration of erythromycin, the drug of choice in C. jejuni infections in humans, results in disappearance of the organism in the stool
Reservoirs for Campylobacter jejuni
Transmission appears to be by a fecal-oral route through contaminated food and water or by direct contact with fecal material from infected animals or humans. In general, person-to-person spread of the organism is believed to be rare. Untreated humans can be carriers for six weeks during convalescence, and shedding can occur for up to one year in some cases.
For the veterinarian, the zoonotic potential of pet-owner contact is important. In domestic animals, the organism is almost ubiquitous. In mammals, C. jejuni has been isolated from healthy cattle, sheep, horse, pigs, goats, dogs, cats, rodents, and monkeys and from diarrheic calves, lambs, dogs, cats, and monkeys. In avian species, C. jejuni has been isolated from 30% to 100% of fecal samples. Once fecal contamination has occurred, viable organisms can be present for up to four weeks. The organism also has been isolated from fresh and salt water and has survived up to five weeks in fresh, untreated water.
Because campylobacter enteritis in humans is clearly a zoonosis with animals as an important reservoir, both dogs and cats are sources of infection. How important they are as sources is still uncertain. Skirrow and Benjamin stated that in Britain no more than 5% of cases of campylobacter enteritis in humans have been associated with dogs and cats, and those zoonoses were associated with newly acquired puppies. Recently, C. jejuni infection in a young woman was associated with infection in an apparently healthy adult cat.
Despite the ubiquitous nature of the organism, the epidemiologic associations of C. jejuni are not well established. Outbreaks with water and milk as the vehicles of transmission have been confirmed. The evidence for ill-cooked chicken as a source is interesting but not conclusive.
Based on matched controlled studies of sporadic human C. jejuni enteritis in Colorado, the odds ratios of increased risk factors were noted for drinking raw water (10.7), drinking raw milk)6.9), eating undercooked chicken(2.8), and living in a household with a cat(3.2).
In a study of human cases of diarrhea in Japan, 188 of 881 cases had C. jejuni isolated from the stool and the rates of positive stool cultures of animals in the area were cattle (12%), chickens (45%), dogs (5%), and cats (10%). The strains found in chickens most closely resembled the human isolates.
Studies on heat-stable antigens using unabsorbed anti-sera of human isolates compared with domestic farm isolates indicated a high similarity index for, in decreasing order, poultry, wild birds, flies, and pigs. The predominant porcine strain was never isolated from humans, and the strains found in flies closely resembled those from animals in the area. Serotyping also showed a close relationship between isolates of human and chicken origin but little relationship between human and pig strains.
Although the sources of human infection are usually poultry, unpasteurized milk, contaminated water, and direct contact with animals with enteritis, food poisoning caused by campylobacter appears to be uncommon, unlike the situation with Salmonella. Campylobacter dies during cooling of pork and beef carcasses because of drying effects of ventilation. Furthermore, the inability of the organism to grow at temperatures below 30oC (86oF) and its microaerophilic nature would make contamination of most foods, except for chicken and vacuum-packed processed meats, uncommon for Campylobacter.
Typing of Campylobacter jejuni
With the increasing interest in the zoonotic potential oC. jejuni, several methods of distinguishing strains have been developed. Criteria for classification of C. jejuni are summarized in the box on this page. Serotyping, biotyping, and phage-typing techniques have helped differentiate pathogenicity of different strains but have not clearly discerned the role fo the small pet animal in the epidemiology. Most of the methods are technically difficult and expensive, and reliance on only one can be confusing.
In a human outbreak of C. jejuni associated with dogs, a litter of 11 puppies was given to local residents of a community. All but 1 of the puppies died with enteritis, and people in most of the household with puppies developed diarrhea. Campylobacter jejuni was diagnosed in nine households involving 16 human cases. Use of 2 serologic methods and 1 biotyping scheme, however, revealed that 3 different strains were involved in the outbreak.
Even with the use of hemagglutination methods of serotyping, a slide agglutination method, and the biotyping scheme of Preston, confusion exists as to the best method for strain classification. Serology involves the separation of strains by the tolerance to heat of the somatic, flagellar, and capsular antigens (O, H, and K). Evaluation of data suggests that heterogenicity within apparently similar strains exists. Strains that are of similar serotypes may be of different biotypes, or strains by the same biotype may be of the same serotype according to one but not another serologic method. Further confusion is inherent in the ability of the strains of Campylobacter to change antigenicity with serial passage in vivo and in vitro. Thus, it has been suggested that a serotyping scheme should always be combined with a biotyping scheme to document an epidemiologic study of an outbreak when human, animal, and environmental isolates are involved.
Plasmids in Campylobacter Isolates
The rate of occurrence of plasmids in Campylobacter isolates in diarrheic humans (9.5%), pigs (83.3%), and poultry 0 % to 100% depending on flock; mean 58%) indicates variability and probably adaptability of the organism.
Animal isolates of Campylobacter species frequently have plasmids of various molecular weights. For plasmids that act as R factors, the high frequency of plasmid DNA may result from the exposure of the organisms to antibiotics present in animal feeds. Under normal conditions, plasmids can be superfluous and tend to be lost; when plasmid function becomes essential for survival, cells containing the appropriate plasmid will be selected. These genetic loci may be transient and unstable and lost or gained based on necessity. In addition to antibiotic resistance, plasmids may encode for phenotypic traits involved in virulence, toxicity, and hydrocarbon catabolism. The pathogenic potential of C. jejuni to invade and produce enterotoxin has been confirmed. The possibility exists, as in Escherichia coli, that there might be a separate plasmid-induced property of either invasiveness or enterotoxigenicity. Several researchers have identified a choleralike enterotoxin produced by strains of C. jejuni.
Screening of C. coli and C. jejuni strains from domestic animals revealed plasmid profiles that varied according to the health status of the animal host. The frequency of plasmids in diarrheic cattle with C. jejuni was higher than in normal cattle. Isolates showing resistance to ampicillin, tetracycline, and gentamicin were more likely to contain plasmids, suggesting a probable plasmid-mediated resistant for tetracycline and perhaps gentamicin. A tetracycline-resistant plasmid has not been associated with enterotoxin or cytotoxic activity.
Plasmid profiles have indicated homology between DNA-encoding tetracycline resistance in Campylobacter species and tetracycline resistance from Streptococcus species indicating a transfer of genetic information between gram-negative and a gram-positive coccus. Tetracycline resistance could not be transferred to E. coli by conjugation or transformation, suggesting that transfer between Campylobacter and unrelated gram-negative organisms is unlikely.
Campylobacter in Dogs and Cats
The interest in C. jejuni in dogs and cats has been directed at documentation of the prevalence of the organism in diarrheic and healthy dogs and cats. Attempts have also been made experimentally to induce infestation or infection.
Although it is clear that C. jejuni can cause enteric disease in humans with relatively few organisms (500 bacteria per os), the pathogenicity is unclear in dogs and cats. Campylobacter species have been isolated from both normal and diarrheic dogs at about the same frequency, suggesting that Campylobacter species are not primary pathogens of dogs. Reported canine isolates indicate that C. jejuni may be a cause of diarrhea in dogs and can be found more frequently in diarrheic dogs.
Conditions associated with increased frequency of isolation of C. jejuni in dogs and cats are summarized in the box below. Differences in the animals' ages, degree of sanitation, and environment of the survey populations might explain the discrepancies in the reported rate of infection. The histories of the dogs surveyed often are not documented. The young puppy in a concentrated population with poor sanitation, such as an ill-kept kennel, has the greatest potential for exposure. Isolation frequency ranges from less than 5% to as high as 90% in puppies.
Conditions Associated with Increased Frequency of Isolation of Campylobacter jejuni in Dogs and Cats
Concentrated housing or poor sanitation
New arrivals in kennel
Other enteric pathogens
Parvovirus, Salmonella, Giardia, parasites
In reported spontaneous Campylobacter-associated diarrhea, dogs developed a mucous, watery, and occasionally bloody stool of 5 to 15 days duration. Anorexia, vomiting, and a febrile response have been noted. In that these are nonspecific signs and the disease reportedly is most common in the young, the differential diagnosis would include all causes of acute enteritis in dogs. The higher incidence of disease in the young, in poor kennel conditions, in stressed adult dogs, and concomitant with other intestinal disease agents would indicate that the organism may be synergistic or opportunistic in the mechanism of disease. The synergistic role of C. jejuni in parvovirus infections has been documented, and there has been speculation on a potential role for other viral agents. Campylobacter jejuni-associated disease in adult dogs can clinically and histopathologically mimic parvovirus infection and should be considered in dogs developing diarrhea after environmental, physiologic, or surgical stress.
In one study, Campylobacter jejuni was isolated from 29% of dogs and 21% of cats with diarrhea as compared with 4% of normal dogs and cats. Campylobacter coli was isolated from dogs (8%) and cats (5%) with diarrhea but rarely from normal dogs (2%) or cats (0%). The rate of occurrence of C. jejuni in positive stools from laboratory beagles was higher in diarrheic (90%) than in normal (63%) dogs. The occurrence in privately owned healthy dogs would generally appear to be low (3.8%) compared with dogs in public kennels (12.8%).
In young (less than six months old) dogs, the influence of stress is supported by finding C. jejuni in 3.1% of healthy dogs, 21.7% of dogs with diarrhea, and 6.7% of dogs without diarrhea but sick from other causes. In a production colony of beagles with a 14.7% infection rate (25% in the young and 3.9% in adults, ) the rate of infection in recently acquired dogs was 32%. Evaluation of age and stress demonstrated that on arrival at the kennels there was no difference in the rate of isolation among dogs less than or over six months of age; however, a significant increase in the rate of isolation by Days 5 to 7 compared with Day 1 was noted, suggesting that while dogs may acquire campylobacter infection in kennels, excretion of the organism may be intermittent and precipitated by stress.
The incidence in cats is less well described than in dogs. Campylobacter jejuni has been isolated from feces of up to 45% of nondiarrheic cats. The infection rate seems to be low, however, in most cat populations in which good hygiene is practiced. No correlation between the environment or age of animal and incidence of infection was noted in a population of cats, 1% of which had campylobacter isolates. Contact of uninfected cats with cats shedding the organism caused a transient diarrhea in the previously healthy cats, and the sporadic pattern of excretion of organisms tends to make diagnosis based on one culture difficult. Clinical signs in another cat with seroconversion abated when treated, and the organism could not be recultured from the stool. In another report, C. jejuni was isolated from 21% of diarrheic cats compared with 4% of normal cats, similar to the rates in dogs (29% of diarrheic dogs versus 4% of normal dogs).
The incidence of positive stool cultures for C. jejuni provides serious confusion and consternation for the veterinarian. Given the fact that the organism can be found in normal, adult dogs but is isolated more frequently in young, diarrheic, stressed dogs, the diagnosis can be elusive as far as a cause and effect relationship.
Variables associated with experimental infection of dogs with C. jejuni include the following:
*Selection of pathogenic strain
*Serial passage of strains versus frozen (-70oC)
*Number of organisms for inoculation
*Route of delivery of infective dose
*Animals host conditioning
Although initially unsuccessful in producing diarrhea in puppies with Campylobacter species of human origin, a mild diarrhea was produced in gnotobiotic beagle puppies using either human or canine isolates of C. jejuni. A moderate, superficial, erosive colitis was noted. Feces from infected puppies became increasingly fluid at the peak of the illness. Other signs were tenesmus, lassitude, and mild anorexia. In contrast with the disease in humans, the clinical disease in dogs appears to be less severe and to require more infective organisms. Reports of induction of enteritis in conventional puppies and fieldwork with natural cases indicate that a 7- to 10-day course of semiformed to watery stools with mucus and occasional blood, tenesmus, and ileus, as in humans, occurs in conventional dogs rather than just a colitis as in the gnotobiotic dogs.
Inconsistencies in the experimental induction of the disease obviously center on the source and method of inoculation of the organism. given the multiple strains and the ability of the organism to change both in vivo and in vitro, laboratory manipulation before inoculation may influence the pathogenicity of the C. jejuni to be tested. The difficulty in inducing the disease in gnotobiotic beagles must also be viewed in reference to the synergistic role of other enteric pathogens. Oral inoculation of up to 8.8 x 109 organisms from diarrheic dogs to puppies did not induce disease, but the organism multiplied in 60% of the cases and was excreted for two to seven weeks.
Organisms that are pathogenic in humans can reproduce, shed and cause seroconversion in dogs. Although this is of public health concern, the role of the bacteria as a primary pathogen is still in doubt. The higher incidence in the young, in animals under stress, and in animals with diarrhea is too compelling to allow veterinarians to ignore the role of C. jejuni as at least a secondary pathogen. Careful challenge with an endotoxin-producing strain with known human pathogenesis would illuminate the role of C. jejuni as a primary pathogen in dogs and cats.
The histologic pattern may depend on the strain of the organism but the ileum, cecum, and colon are primarily involved. Mucosal hyperplasia, blunting of intestinal villi, inflammatory cell infiltrates of the lamina propria, and Peyer's patches have been described in dogs. Campylobacter jejuni can be found, however, in the stools of dogs with diarrhea even when none of the above histologic changes are observed. In one study of 32 strains isolated, 43% were from the rectum, 75% from the colon, and 81% were from the cecum.
In Sweden, thermotolerant, catalase-negative, hippurate- positive Campylobacter species have been isolated from diarrheic humans and dogs that have been considered non-enteropathogenic. Based on DNA studies, this "Swedish catalase-negative or weak strain" closely resembles C. jejuni. Clinical signs ascribed to a similar Campylobacter species in a dog that responded to antibiotics have been described.
Identification of Campylobacter jejuni
Examination of diarrheic feces by dark-field or phase-contrast microscopy can permit a presumptive diagnosis and suggest whether fecal cultures are indicated. The finding by the untrained observer of motile curved rods darting across a microscopic field is nonspecific and not definitive. The use of Gram stain on human stool specimens for early presumptive diagnosis has been reported.
Campylobacter jejuni are gram-negative, slender, curved (vibrio), S-shaped, or "sea gull-shaped" bacteria with tapered ends. They are 0.2 to 0.4 um in width and vary from 1.5 to 3.5 um in length, depending on the shape of the particular bacterium. The organism is microaerophilic with an optimal growth temperature from 37o to 42oC (98.6o to 107.6oF). Campylobacter jejuni will not grow at 25oC (77oF) nor does it tolerate atmospheric concentrations of oxygen, thus it is very important that fecal specimens or swabs be processed soon after collection. The specimens should be kept chilled (4oC [39.2oF]); if the sample is a swab it should be placed in an anaerobic transport medium.
Isolation of C. jejuni from stool specimens can be difficult and requires from two to five days. Special requirements include selective techniques to reduce the growth of competing organisms and microaerophilic (not anaerobic) incubation conditions (5% oxygen, 10% carbon dioxide, and 85% nitrogen). The use of selective campylobacter-specific medium (commonly known as "Campy-BAP") gives better recovery of the isolation and identification of campylobacters have been published.
Antibody titer techniques being developed will augment the current knowledge and provide a clearer prospective of the clinical importance of campylobacters in dogs and cats. The isolation of Campylobacter jejuni does not confirm the organism as the causative agent in dogs and cats with diarrhea. Specific serum antibodies in humans can be detected after C. jejuni infections using tube agglutination, bactericidal assays, and indirect immunofluorescence.
Antibiotic therapy for C. jejuni enteritis in dogs or cats has not been experimentally evaluated. Therapy of spontaneous cases has resulted in elimination of the organism in the stools. In that the disease is usually self-limiting and rarely disseminated, therapy may not affect the clinical course of the disease but might decrease the duration of bacterial shedding.
Based on a series of experiments of antibiotic sensitivity patterns of C. jejuni, high concentrations of ampicillin, penicillin, tetracycline, and metronidazole were required to inhibit growth. Because Campylobacter is believed to produce B-lactamase, most strains are relatively resistant to ampicillin and other related antibiotics. More isolates containing plasmids were resistant to tetracycline, gentamicin, and ampicillin than were isolates not carrying plasmids. This tendency has been shown especially for tetracycline and gentamicin. In general, most isolates were susceptible to gentamicin, kanamycin, neomycin, erythromycin, and sulfonamide. Erythromycin is the drug of choice for therapy in humans, although resistant strains have been noted in human and animal isolates. In a retrospective trial in children with campylobacter enteritis, erythromycin did not alter the course of the disease but did decrease the duration of bacterial shedding. The use of erythromycin in dogs with campylobacter enteritis did not change the clinical signs when compared with fluid therapy alone. Furazolidone was affective at low minimum inhibiting concentrations (MIC), and resistance to the antibiotic apparently is rare. Chloramphenicol and doxycycline were effective, but canine isolates resistant to both antibiotics have been reported. The use of chloramphenicol for one week in a dog with campylobacter enteritis (the organism was catalase-negative and sodium hippurate-negative but was not C. jejuni) did result in abatement of clinical signs and in the elimination of the organism from the stool. Resistance to sulfamethoxazole and trimethoprim was high (60.2%) in isolates of C. jejuni and C. coli.
With the increased incidence of transmission of antibiotic- resistant Salmonella to humans and the apparent increase in plasmid- mediated resistance in other enteric bacteria in response to the widespread use of antibiotics, the zoonotic potential of campylobacters in obvious. It would appear, however, that transmission of plasmid-mediated resistance among strains of E. coli and C. jejuni does not occur. Comparison of the antibiotic sensitivity of C. jejuni/C. coli strains isolated from dogs and cats with acute enteritis from 1981 to 1986 with the exception of chloramphenicol, which did show, however, an increase in isolates that were only moderately sensitive. Increases in percentages of antibiotic-resistant isolates from 1981 to 1986 included 56.4% to 85.7% for benzylpenicillin, 17.9% to 41.3% for ampicillin, 0% to 9.5% for tetracycline, 0% to 8% for erythromycin, 10.3% to 65.1% for streptomycin, 2.6% to 4.8% for gentamicin, 0% to 4.8% for kanamycin, 0% to 9.5% for neomycin, and 7.7% to 14.3% for polymyxin B. All of these antibiotics had been used in the area of Germany in the years examined and the increases in resistance may reflect the bacterial response to the antibiotic pressure.
From the data, erythromycin or chloramphenicol would appear to be the therapeutic drug of choice; however, C. jejuni susceptibility can be variable. In vitro antibiotic testing should be performed before therapy is instituted. The isolation of the causative organism and determination of antibiotic sensitivity are of increased importance because of the zoonotic potential of C. jejuni.
The Role of the Small Animal Practitioner
A C. jejuni infection in dogs or cats cannot be clinically distinguished at this time. Furthermore, isolation of the organism from healthy or diseased dogs or cats is not sufficient to warrant a diagnosis of enteritis. With the increased awareness of the organism, however, pets should be considered a potential reservoir for human infection and child-puppy contact may be questioned in the future. Although less than 5% of human C. jejuni enteritis cases are reportedly acquired from dogs, the history of development of diarrhea in the owner(s) after a previous bout of diarrhea in a puppy is suggestive. This implication would be strengthened if the pet were newly acquired or had been recently stressed or if poor sanitation were suspected.
Small numbers (500) of C. jejuni potentially can cause infection in humans; therefore, the possibility of acquiring an infection from contact with feces from an infected or carrier pet animal is real. This hazard would appear to be more likely than with Salmonella species in which large numbers (105 to 107) usually are required for human infection. The zoonotic potential of campylobacter enteritis is compared with that of Salmonella enteritis in Table II. The large reservoir and multiple modes and vehicles of transmission would dictate that clients developing C. jejuni enteritis should examine water, meats, and foodstuffs, and milk for contamination before the pet dog or cat is incriminated as the source. If both pet and owner are affected, the most likely scenario would be the exposure of both pet and owner to a common source.
For both pet and owners and veterinarians, the basics of good hygiene and the necessity for hand-washing after contact with diarrheic animals or feces are reinforced by this disease. For the practitioner, the isolation of hospitalized puppies with enteric disease and the careful handling of their feces is recommended for the benefit of both the animal handlers and other hospitalized pets. When it is determined that a diarrheic pet is shedding C. jejuni, antibiotic sensitivity testing and the initiation of erythromycin therapy are indicated. Good client education and professional awareness should avoid potential problems until more answers are available.