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Major Infectious Diseases of Dogs and Cats (Listed Alphabetically) - Part 1 (A through D)
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Read
- Introduction
- General Recommendations
- Locating a Disease
- Major Infectious Diseases: A to D
- Major Infectious Diseases: E to L
- Major Infectious Diseases: M to Z
- Internal Parasitic Diseases
- External Parasitic Diseases
- Diseases Caused by Protozoa in Dogs and Cats
Infectious Diseases - Part 1
This is Part 1 of the alphabetically listed descriptive summaries of major infectious diseases of dogs and cats. Individual diseases can be accessed by browsing Sections I, II and III of this chapter or by the links to individual diseases at the top of each section. Parasitic disease are covered in separate chapters on Internal Parasites and External Parasites. See Chapter 1 for notes on abbreviations, use of subheadings and disclaimer. See Chapter 4 for drug dosages.
Part 1 - Diseases Entities - A through D
- Actinomycosis
- Adiaspiromycosis
- Anaerobic Infections
- Anthrax
- Aspergillosis
- Bite Wound Infections (Human)
- Blastomycosis
- Botulism
- Campylobacteriosis
- Candidiasis
- Canine Abscess and Cellulitis
- Canine Adenovirus 2 Infection
- Canine Brucellosis
- Canine Calicivirus Infection
- Canine Coronavirus Infection
- Canine Cyclic Thrombocytopenia
- Canine Distemper
- Canine Ehrlichiosis
- Canine Granulocytic Ehrlichiosis
- Canine Hemobartonellosis
- Canine Hemorrhagic Gastroenteritis
- Canine Herpesvirus Infection
- Canine Influenza
- Canine Leptospirosis
- Canine Papillomatosis
- Canine Parainfluenza Virus
- Canine Parvovirus Infection
- Canine Parvovirus Type 1 Infection
- Canine Respiratory Disease: General
- Canine Rotavirus Infection
- Cat-scratch Disease
- Canine Streptococcal Toxic Shock Syndrome
- Chromoblastomycosis
- Coccidioidomycosis
- Cryptococcosis
- Dermatophilosis
- Dermatophytosis
Actinomycosis
Actinomycosis of dogs and cats is a chronic, sporadic, bacterial disease manifested most frequently in two principal forms: a localized granulomatous abscess(es) involving the skin and subcutis; and a pyogranulomatous thorax, with suppurative lesions involving the lungs, pericardium and pleura and occasionally the peritoneal cavity.
Etiology
The gram-positive rod Actinomyces viscosus and/or A. hordeovulneris (very rarely by A. bovis) and occasionally unnamed Actinomyces. These actinomycetes occur as commensals in the oral cavity of dogs and cats.
Distribution
Occurrence is probably worldwide. A moderately common infection; seen most often in hunting dogs.
Mode of Infection/Transmission
Infection is by inhalation and via wounds, often from bites and occasionally due to gunshot or grass awns.
Clinical Features
The disease is chronic but rarely disseminated; the course is variable.
In the thoracic form: abnormal lung and pleural sounds, low-grade fever, dullness, dyspnea, anorexia, vomiting, abdominal swelling and tenderness, ascites and weight loss. In the skin form there are pyogranulomatous abscesses and nodules in various locations.
Diagnosis
- The disease resembles nocardiosis clinically which is also seen in the two forms mentioned above. Other diseases to be considered are blastomycosis, cryptococcosis, other fungous infections, abscesses due to other causes and various pulmonary and pleural infections.
- Abscesses and cellulitis initiated by bites and caused by a wide variety of microorganisms, including anaerobes, are frequent in dogs and even more common in cats.
- Because the treatment of actinomycosis and nocardiosis is different, it is advisable to seek a diagnosis, preferably, by the isolation and identification of the causative organism.
- Fresh material from the localized form (skin, subcutis); the granulomatous abscess may have to be opened surgically.
- A tracheal wash and/or fluid obtained by thoracocentesis should be submitted in the thoracic form.
- Demonstration of the organism in gram-stained smears of material from lesions. Actinomyces viscosus, A. hordeovulneris and Nocardia asteroides resemble one another morphologically; however, the latter organism can be distinguished from the other two in that it is partially acid-fast. A highly presumptive diagnosis of these diseases can be made on the basis of the Gram and acid-fast staining of smears from typical lesions.
- Isolation and identification of A. viscosus or A. hordeovulneris from characteristic lesions are definitive.
Treatment
- Surgical debridement and drainage including placement of a chest tube for pyothorax.
- Prolonged treatment with penicillin G, amoxicillin, tetracyclines, or chloramphenicol is usually effective; however, because there may be a difference between the antimicrobial susceptibility of A. viscosus and A. hordeovulneris, all significant isolates should be subjected to drug susceptibility tests.
- Penicillin is not effective in the treatment of nocardiosis.
Control
Vaccines are not employed.
Public Health Significance
Dog bites have resulted in infrequent A. viscosus human infections; however, its zoonotic potential is not considered significant.
Adiaspiromycosis (Haplomycosis)
This disease is caused by the soil-borne fungi Chrysosporium parvum and C. crescens. The conidia are inhaled resulting in a respiratory infection that has been reported in many species of rodents and other wild animals. There are reports of several canine cases.
The conidia do not replicate in the lungs but develop into spherules without endospores. Lesions result from the granulomatous inflammation.
Diagnosis is based on demonstration of conidia and spherules in tissue sections and isolation and identification of the fungi. The fungi are dimorphic with a yeast-like phase growing at 37°C and a mycelial phase at 25°C on appropriate media.
Thus far the disease is rare and information on treatment is not available. Amphotericin B or one of the imidazoles would most likely be effective.
Anaerobic Infections
(Related Topics are Canine Abscess and Cellulitis and Feline Abscess and Cellulitis).
Many infections involving anaerobic bacteria are polymicrobial as is noted below. Almost all of the anaerobes involved in infections of dogs and cats are part of the normal mucosal flora. Infections result from traumatic injury, bites and other penetrating wounds. Suppurative conditions frequently yield anaerobes. Cellulitis and abscessation which are frequent and osteomyelitis, may be caused by anaerobes and/or facultative anaerobes.
Etiology
The anaerobic bacteria most commonly involved are the gram-negative species of Bacteroides, most common and Fusobacterium. The anaerobic streptococcus, Peptostreptococcus, is occasionally involved. The large gram-positive rod Clostridium perfringens, type A is sometimes implicated. Among the facultative anaerobes frequently involved in these often mixed infections are E. coli, Pasteurella, Staphylococcus, Streptococcus and Klebsiella.
Clinical Signs
These vary greatly depending on the type and extent of the infection. Cellulitis, edema; crepitation when Clostridia are involved; abscessation, discharging sinus tracts; exudates and pus may have a foul odor. Fever, toxemia, anorexia, depression and lymphadenopathy may be evident. Dyspnea or tachypnea is characteristic of pyothorax, attributed at least in part to anaerobic bacteria. Pyothorax is seen most frequently in cats.
Diagnosis
- A clinical diagnosis based on clinical signs should be confirmed by laboratory means as there are a number of causes of abscesses in dogs and cats other than anaerobes.
Laboratory Procedures: - Submission of specimens for the isolation of anaerobes is discussed in Chapter 1. Every effort must be made to prevent clinical material from contacting oxygen. Special transport systems for suspected anaerobes are available commercially.
- In pyothorax aspirates are taken for culture from both sides of the chest.
- The Gram stain of exudates may be helpful in selecting the primary antibiotic.
- Clinical material should be cultured for anaerobes and facultative anaerobes (those that grow in the presence or absence of oxygen) and antimicrobial susceptibility tests conducted on isolates.
Treatment
- Abscesses should be drained when practicable. Debridement of necrotizing lesions may be indicated.
- Treatment should, when possible, be based on the results of antimicrobial susceptibility tests on both anaerobes and facultative anaerobes. The treatment of pyothorax may involve installation of a thoracostomy tube or repeated thorocentesis for drainage.
- The most effective antimicrobial drugs for anaerobic infections are as follows:
- Amoxicillin combined with clavulanic acid is recommended for empiric treatment. Duration of antimicrobial treatment will depend upon the nature and extent of the infection.
- Amoxicillin with metronidazole for at least one month is used to treat pyothorax in cats.
- Clindamycin is effective against most Bacteroides isolates.
- Penicillin G is effective against many anaerobes with the exception of Bacteroides.
- Chloramphenicol and metronidazole are effective against Bacteroides.
- Cefoxitin is effective against many anaerobes. - Prolonged treatment may be necessary.
Anthrax
Anthrax is most often an acute, toxemic disease of warm-blooded animals and humans, caused by Bacillus anthracis and characterized by septicemia, sudden death, exudation of tarry blood from body orifices and absence of rigor mortis. It is a rare disease of the dog and cat.
Etiology and Source
Bacillus anthracis, a large gram-positive, sporeforming bacillus. Virulence of strains depends on possession of a capsule and the capacity to produce toxin. Spores can survive for years in the soil; flooding may disseminate them. Contaminated oil-cake, tankage, bone meal and leather goods are other possible sources of spores.
Distribution
Worldwide, in endemic regions where the spores are present.
Susceptibility
The disease is rare in dogs and cats; ruminants and horses manifest the acute disease.
Mode of Infection/Transmission
Most often by ingestion; rarely by inhalation; fomites. Mechanical transmission by biting flies.
Incubation Period and Course
The incubation period is 2 - 3 days and the course 1 - 4 days. Death may ensue as early as 48 hours.
Clinical Features
Animals may be found dead. High temperature, depression, dyspnea, edema of the neck, ventral chest and abdomen. Blood is frequently discharged from body openings.
Diagnosis
- Anthrax is rare in dogs and cats.
- Among the diseases and conditions that should be considered are acute infectious, febrile diseases such as salmonellosis, canine parvovirus infection, leptospirosis, distemper, feline panleukopenia, acute poisonings, and causes of sudden death such as lightning and heatstroke.
- To prevent sporulation, the carcass should not be opened.
- Two swabs and two smears of peripheral blood from a convenient vein.
- With experience, a diagnosis of anthrax can be made on the basis of finding typical large, capsulated rods in smears stained by Giemsa, Wright's, or Loeffler's methylene blue. However, it is advisable when possible to isolate and identify B. anthracis.
- It should be remembered that clostridia (large gram-positive rods) invade carcasses shortly after death and can be confused with B. anthracis.
Treatment
- If anthrax is suspected the animal should be isolated and great care taken to avoid contact with potentially infectious clinical materials. Those at risk should wear masks, gloves and appropriate clothing.
- Treatment of sick animals with penicillin G, tetracyclines, erythromycin or chloramphenicol. Only those animals treated in the early stage of infection survive.
- Tetracyclines for in contact animals.
Control
- Vaccination is not practiced in dogs and cats.
- Anthrax is a reportable disease in many countries requiring notification of regulatory officials who apply strict regulatory measures.
Public Health Significance
Humans are highly susceptible to anthrax. Clinical materials containing B. anthracis are highly infectious.
Aspergillosis
Aspergillosis is a noncontagious disease of a number of animal species caused by fungi of the genus Aspergillus (usually A. fumigatus). Other potentially pathogenic species are A. flavus, A. nidulans, A. deflectus, A. niger and A. terreus. These fungi occur widely in nature and the usual mode of infection is by inhalation with the production of granulomatous lesions and nodules in the respiratory tract from which there may be dissemination to other tissues and organs.
Infections may also, but less frequently, begin in the alimentary tract. Disseminated aspergillosis originating from pulmonary or intestinal aspergillosis is a rare disease of dogs and cats. It is more common in immunosuppressed animals and in those under prolonged antibiotic treatment. Disseminated aspergillosis is probably most often diagnosed following necropsy. If diagnosed antemortem it is treated long term with itraconazole or amphotericin B.
Nasal or paranasal aspergillosis is seen most commonly in the dog (see Nasal Aspergillosis).
Diagnosis
This is discussed under Nasal Aspergillosis. In general diagnosis is usually based on the isolation and identification of the Aspergillus species from appropriate clinical specimens and the demonstration of typical septate hyphae in biopsies or tissue sections. Because this fungus is very widespread in nature, mere isolation may not indicate significance.
Bite Wound Infections (in Humans)
Although these are not infections of dogs or cats they are zoonotic infections originating from these species and thus are of interest to practicing veterinarians. They are bite wounds resulting from dogs and cats biting humans. Scratch wounds occur less frequently. The bacteria involved are of veterinary interest because they are part of the normal flora of dogs and cats. The most common bacterium involved in these infections is the gram-negative, small rod, Pasteurella multocida, which can frequently be recovered from the mouths of normal dogs and cats.
Other Pasteurella spp. that are involved in bite wounds are:
P. dagmatis: Occurs in the canine and feline oral cavity
P. canis: Occurs in the canine oral cavity
The gram-negative bacteria listed below, which are part of the normal flora of dogs and/or cats, are occasionally involved in bite wounds:
Bartonella henselae: The cause of cat-scratch disease which is discussed separately.
Bergeyella zoohelicum (was Weeksella zoohelcum): Occurs as part of the normal flora of the mouth and paws of dogs and cats. It is involved in scratch infections as well as bite infections.
Bisgaard's Taxon 16: This unnamed Pasteurella-like bacterium is occasionally recovered from dog bite wounds.
Eikenella corrodens: Part of the normal flora of the canine and human mouth.
Neisseria weaveri (Was CDC Group M5): Part of the oral flora of dogs.GROUP EF4a (was Ef4), EF4b (was EF4): These organisms are commensals in the mouth and nasopharynx of dogs and cats.
Capnocytophaga: Species of this genus are slender, pleomorphic, gram-negative rods that are found as commensals in the mouth and nasopharynx of dogs and cats.
Two species are recognized:
Capnocytophaga canimorsus (formerly designated DF-2): Produces infections following dog bites. Serious and even fatal infections may develop in variously compromised human patients.
C. cynodegmi: Less virulent than the aformentioned species; the cause of dog-bite infections and keratitis resulting from cat scratches.
Bite Wounds (Cats)
see Feline Abscess and Cellulitis.
Blastomycosis (North American Blastomycosis)
Blastomycosis is usually a severe disease, principally of the dog and human (rarely the cat and other animals), caused by the fungus Blastomyces dermatitidis and characterized by an infection that usually begins with the formation of granulomatous nodules in the lungs.
The infection may be confined to the lungs and regional lymph nodes or metastasize to produce the disseminated disease with involvement of the skin, bone and other tissues and organs.
Although there are usually numerous nodules in the lungs, in some instances metastases may come from very limited pulmonary involvement. Occasionally the infection is confined to lesions involving the skin and subcutis. Such infections may persist for months.
Etiology/Source
Blastomyces dermatitidis is a soil-borne, dimorphic fungus. The mycelial phase occurs in nature and the yeast form in vivo.
Distribution/Occurrence
It is probably worldwide in distribution, although the number of cases reported outside of North America is relatively small. The endemic area in the United States includes the middle western, southeastern and Appalachian states. Although single cases are most frequent, multiple cases have been reported in hunting dogs.
Susceptibility
The disease occurs most frequently in dogs; it is rare in cats. Humans are susceptible.
Mode of Infection/Transmission
Inhalation of spores. Infrequently via skin wounds leading to cutaneous lesions. Most often cutaneous lesions are derived from pulmonary infection.
Incubation Period/Course
The incubation period is variable and may be as long as several months. The course likewise is variable.
Clinical Features
These depend on the stage of the disease. Fever, coughing, dyspnea, anorexia, nasal discharge and progressive loss of condition may be present. Subcutaneous purulent, ulcerative granulomas may also be seen. As the disease spreads, signs reflecting involvement of various organs are observed. Ocular involvement with anterior uveitis and subretinal effusion may be seen. Without treatment the disseminated disease is invariably fatal. Radiographs disclose swollen bronchial lymph nodes and nodular pulmonary lesions.
Diagnosis
- Cryptococcosis, nocardiosis, canine actinomycosis, coccidioidomycosis, histoplasmosis, tuberculosis, chronic granulomatous infections of the skin due to other agents and pneumonia due to other agents should be considered.
- Chest radiographs may suggest blastomycosis.
- Material is taken by transtracheal aspiration, transthoracic biopsy and from granulomatous nodules or abscesses involving the skin. An ocular tap can be used if the eye is thought to be involved. Examination of materials in wet mounts for the characteristic thick-walled, single-budding yeasts. Gram-stained smears are examined and culture at room and incubator temperature (37°C) on appropriate media.
- The finding of the typical organisms in sections of biopsies or affected lung is highly diagnostic and is the usual means of diagnosis.
- Serum. Paired samples preferable.
- Paired samples are preferable. The agar gel immunodiffusion test for antibody indicates a current or recent infection with a reliability of about 90%.
- Definitive diagnosis depends on the isolation and identification of B. dermatitidis; however, because it is very time-consuming it is not always carried out.
Treatment
- Itraconazole is the drug of choice; ketoconazole is an alternative. Prolonged treatment, 2 - 3 months, is essential. The recurrence rate may be as high as 20%.
- A combination of amphotericin B with ketoconazole or itraconazole is used for dogs with severe infections.
- In cases confined to the skin and subcutaneous tissue, lesions are removed surgically.
Control
There are no practicable preventive measures.
Public Health Significance
Blastomycosis is not considered contagious, but one should avoid contact with infectious material. There are rare reports of humans acquiring the disease while performing necropsies.
Botulism
Botulism is a noncontagious, intoxicative disease of animals caused by the neurotoxins of Clostridium botulinum and characterized by progressive motor paralysis due to the effect of the neurotoxin blocking the release of acetylcholine at motor end-plates.
Etiology/Source
Clostridium botulinum is a large, gram-positive, sporeforming, anaerobic rod. The highly resistant spores occur widely in nature. The neurotoxins are produced in decomposing food, dead animals (carrion) and plant materials (rarely in the alimentary tract and wounds). Types A, B, C, D, E, F and G of C. botulinum have been identified on the basis of antigenic differences in neurotoxins. Types C and D toxins have been identified in canine botulism. The toxins are inactivated by heating at 100°C for 20 minutes; spores are killed by heating at 121°C for 15 minutes.
Distribution
Botulism occurs worldwide where ever spores occur. The case fatality rate may reach 100%.
Suscepibility
Dogs and cats are relatively resistant to botulism. Cases are seen in dogs occasionally but rarely in cats.
Mode of Infection and Transmission
Ingestion of food containing the toxin. Botulism is not contagious. Dogs and other carnivores usually develop the disease after consuming carrion or spoiled meat.
Incubation Period/Course
The incubation period is variable depending upon the amount of toxin consumed. Signs usually appear 3 - 7 days after ingestion. Peracute cases may die without showing clinical signs. Ordinarily death ensues within 1 - 5 days of the appearance of signs.
Pathogenesis
Clostridium botulinum multiplies in the anaerobic milieu provided by spoiled or decaying organic material, including necrotic tissue. Botulism resulting from toxin produced in tissues is called toxicoinfectious botulism. Examples are wound and infant botulism (gastrointestinal); these forms of the disease do not appear to have been reported in dogs or cats. The toxin prevents presynaptic release of acetylcholine at the neuromuscular junction.
Clinical Signs
These depend on severity. Among the signs are: progressive, ascending motor paralysis, weakness. difficulty in chewing and swallowing, impaired vision and finally death due to cardiac or respiratory failure.
Diagnosis
- Rabies, pseudorabies, coonhound paralysis, tick paralysis and other diseases affecting the nervous system should be considered.
- Botulism has been called a catch-all clinical diagnosis; a definitive diagnosis is rather involved.
- Specimens:
Food including carrion suspected of harboring botulinus toxin (handle with care).
Serum; at least 5 ml, preferably more.
Tied-off stomach and a portion of small intestine if gastrointestinal botulism (rare) is suspected. Liver or a large portion thereof.
Canine feces. - The specimens, except serum, are processed in order to obtain toxin. The filtrate obtained or serum is used in animal tests to demonstrate toxicity.
- Suspected food is sometimes fed to laboratory animals or animals of the same species as those that are affected.
- If botulinum toxin is demonstrated in the serum, liver extract, or food by animal inoculation, a strongly presumptive diagnosis of botulism can be made.
- A definitive diagnosis depends on the identification of the type of C. botulinum involved by toxin neutralization tests in mice.
- Recovery of C. botulinum alone from food is not sufficient for a diagnosis, for the organism is ubiquitous in its occurrence. An animal may die of botulism and not have a demonstrable level of toxin in its serum.
Treatment
Botulinum antitoxin of the appropriate type, or a polyvalent product, has been used in treatment with variable success; however, once signs have developed and toxin is fixed to receptors, the efficacy of antitoxins is questionable.
Control
- Avoid feeding spoiled feed; prevent exposure to decomposing animal and plant materials.
- Dogs and cats are not vaccinated.
Public Health Significance
Great care should be exercised in handling materials suspected of containing botulinus toxin.
Campylobacteriosis
Campylobacteriosis is a contagious disease of dogs and cats caused by Campylobacter jejuni and characterized by enteritis and a diarrhea of variable duration and severity.
Etiology
The cause is Campylobacter jejuni, a small, fragile, gram-negative rod. A considerable percentage of dogs carry and shed C. jejuni (up to 10% or more) but most of them do not develop enteritis and diarrhea. A considerable number of cats are also carriers of C. jejuni.
Distribution
Distribution of C. jejuni is probably worldwide in dogs, cats and other animals.
Susceptibility
Dogs less than six months of age are more severely affected. Kittens are sometimes susceptible. There is some question as to whether or not this organism causes enteritis and diarrhea in normal cats other than kittens. Debilitated cats and those with parasitic or microbial infections are thought to be susceptible. Immunosuppression may also have a predisposing role.
C. coli and C. upsaliensis can also be occasionally recovered from the feces of cats. Their disease significance is not clear.
Clinical Features
The diarrhea in dogs may last 1 - 2 weeks or become chronic. Among the signs are: low fever, anorexia, vomiting and regurgitation, weight loss, poor condition and diarrhea. The organism has been reported to cause abortion in bitches.
Diagnosis
- Among the diseases and agents that should be considered are salmonellosis, canine parvovirus infection, pancreatitis, intestinal parasites and poisons.
- Direct microscopic examination of fresh feces may reveal characteristic curved organisms with darting motility. In gram-stained fecal smears Campylobacter appear as gull-wing shaped gram-negative rods. The aforementioned procedures are used for a quick presumptive diagnosis.
- For culture rectal/fecal swabs in transport media (Cary and Blair medium preferred); or feces in sealed containers. Specimens should be refrigerated and delivered to the laboratory so they can be cultured within 48 hours of collection. Failing this, feces should be frozen on dry ice.
- Special media, incubated in a microaerophilic atmosphere, must be used to isolate this fragile and fastidious organism. Without special selective media the organism is rapidly overgrown by other enteric bacteria.
- Antimicrobial susceptibility tests should be performed.
- Isolation of the organism in itself does not necessarily mean the dog has campylobacteriosis. Such an isolation should be considered along with the clinical picture, the results of other diagnostic tests and the results of antimicrobial therapy.
Treatment
It would seem that most cases of canine campylobacteriosis recover without treatment, although the course is probably shortened by the administration of erythromycin, chloramphenicol, tetracyclines, or other drugs shown to be effective in susceptibility tests.
Control
There are reports that shedding of the organisms can be reduced and possibly eliminated by erythromycin administration. Several negative cultures are required before the dog is no longer considered a carrier.
Public Health Significance
Campylobacter jejuni is an important cause of gastroenteritis in infants, children and adults. Potential sources of this organism for humans include carrier poultry and a number of animals, in addition to dogs and cats. Owners of dogs with diarrhea should be advised to exercise appropriate hygienic measures to prevent possible exposure to C. jejuni.
Candidiasis (Candidosis, Moniliasis, Thrush)
Candidiasis is an infrequent disease of dogs and cats, usually caused by the yeast-like fungus Candida albicans and characterized most frequently by infection of the skin and mucous membrane of the alimentary tract (occasionally the genital tract).
Etiology
The disease is caused by the yeast-like fungus Candida albicans, a commensal in the alimentary tract.
Distribution
Worldwide in occurrence.
Susceptibility
Young and debilitated animals are most often affected. Prolonged antibiotic treatment and immunodeficiency may predispose animals to candidiasis, particularly the systemic form.
Clinical Features
Candidiasis is most frequently an infection of the skin and mucous membrane of the alimentary tract and occasionally of the genital tract. The infrequent disseminated form may involve the lungs, heart, kidneys, placenta and other tissues. The oral form of the disease with ulcerative pseudomembranous inflammation of the mouth, extending sometimes to the esophagus and stomach is seen infrequently in dogs and cats.
Diagnosis
- Candidiasis has to be distinguished from a number of other diseases affecting mainly the mucous membranes of the alimentary and genital tracts. White to gray, discrete patches of pseudomembranous inflammation on the skin and mucosa are characteristic.
- Collect material by deeply scraping the surface of affected tissue below the pseudomembrane or other extraneous material. Smears and wet mounts are examined for the characteristic yeast-like cells and pseudohyphae. If present a highly presumptive diagnosis can be made. Definitive diagnosis requires the isolation and identification of C. albicans.
- Systemic infections are usually only diagnosed after necropsy by cultural and histopathologic examination of tissues.
- Immunodiffusion, latex agglutination and counterimmunoelectrophoresis are used to aid in the diagnosis of human infections.
Treatment
- Nystatin may be administered topically or orally.
- Clotrimazole and natamycin are used topically to treat chronic candidiasis.
- Ketoconazole or itraconazole for four weeks, are effective for systemic infections.
Control
Because of the ubiquity of the organism no control measures are applicable.
Canine Abscess and Cellulitis
This infectious process occurs much less frequently in dogs than in cats. As in cats initiation is by bites or other injuries including gunshot wounds in hunting dogs. Many of the same infectious agents are involved.
Diagnosis and Treatment
Diagnosis and treatment are essentially the same as for Feline Abscess and Cellulitis.
Canine Adenovirus 2 Infection
This virus is associated with respiratory disease (see Infectious Canine Tracheobronchitis).
Canine Brucellosis
Canine brucellosis is a contagious disease of dogs caused, almost always, by Brucella canis and characterized by a bacteremia leading frequently to abortion and other sequellae.
Etiology
Canine brucellosis is caused by the gram-negative, intracellular bacterium, Brucella canis. Brucellosis in dogs due to B. abortus, B. suisand B. melitensis acquired from livestock is rare.
Distribution
Canine brucellosis is widely distributed in North and South America and Europe; it has not been reported from Australia.
Susceptibility and Incidence
Dogs of all ages and both sexes are equally susceptible. The incidence of the disease is not high except in some kennels and colonies.
Mode of Infection and Transmission
Ingestion, direct (organisms shed from the male and female genital tracts) and via fomites; venereally and congenitally. The disease spreads rapidly in kennels.
Clinical Features
Brucellosis is characterized in the bitch by metritis, abortion, prolonged bacteremia and vaginal discharge and in the male by infection of the testicles and accessory sex glands, leading occasionally to irreversible sterility. Sequellae include bone and joint infections, particularly the intervertebral discs. Abortion during the last trimester of pregnancy is the cardinal sign followed by mucopurulent vaginal discharge. In kennels there are usually multiple abortions and bitches abort in subsequent pregnancies. Stillbirths and failure to conceive also suggest canine brucellosis. Epididymitis, orchitis and prostatitis are frequent. Discospondylitis, meningitis, splenomegaly, anterior uveitis and osteomyelitis occur infrequently.
Diagnosis
- Infectious abortion due to other agents is infrequent.
- Females: Blood (heparinized), fetus (lung and liver preferred), placenta, vaginal swabs, urine
- Male: Blood (heparinized), semen, testes, epidydymis, prostatic fluid, urine.
- Isolation and identification of B. canis: Positive cultures, and most conveniently blood cultures, are the most reliable evidence of B. canis infection. Dogs may be bacteremic for long periods.
The following serological procedures are employed but they are not as reliable as culture: - Rapid Slide Agglutination Test (RSAT) - The original form of this office screening test used stained B. ovis as antigen. Serum was treated with 2-mercaptoethanol. This test was reliable when negative, but about 40% of positive samples were false.
- M-RSAT - An improved test uses a B. canis strain(mucoid negative) and has greater specificity.
Dogs positive to the screening test should be retested with the improved AGID test or ELISA.
Positive reactions to the latter tests are particularly significant when there are clinical signs of the disease. - Agar Gel Immunodiffusion Test (AGID) - This test using cell wall antigens is subject to false positives. When highly specific protein antigens are used the procedure has been found to be sensitive and accurate in detecting infection. Antibodies appear 4 - 12 weeks post infection and persist for some months.
- Tube Agglutination Test (TAT) - This procedure is widely used but is also prone to false positives.
- ELISA - This procedure using "specific antigens" has been reliable and may be adapted to commercial kits.
- Indirect Fluorescent Antibody Test - This procedure has also been found to have a high rate of false-positive reactions.
Treatment
Treatment is not usually attempted; however, it may be employed to save valuable bloodlines. The regimen of combined tetracycline and streptomycin or tetracycline and gentamycin for four weeks has been effective, particularly if begun early. Doxycycline alone or the combination of minocycline and gentamycin can be effective; however, antimicrobial treatment is not always successful.
Control
Elimination of animals presumed to be infected based on serologic testing. An animal is presumed to be negative after two negative tests one month apart. Negative blood cultures are confirmatory.
Public Health Significance
Humans are susceptible to B. canis so great care should be taken to avoid contact with infectious materials.
Canine Calicivirus Infection
There have been a small number of caliciviruses isolated from cases of glossitis and enteritis in dogs. Their significance in these diseases is not yet clear. Some isolates appear to be closely related to feline caliciviruses whereas others are distinctly different and more closely related (genetically) to San Miquel sea lion virus.
Laboratory diagnosis involves isolation and identification of the canine calicivirus from feces and oral lesions.
Canine Coronavirus Infection
Canine coronavirus infection is a relatively mild enteric disease of mainly young dogs although all ages may be infected.
Etiology
The causal agent is an RNA virus referred to as canine coronavirus (CCV) which is relatively labile and can surive outside the animal for 1 - 2 days. This coronavirus is carried by many dogs. Disease is thought to occur in young dogs in the absence of sufficient protection acquired from the bitch. This virus resembles closely feline coronavirus.
Distribution
Probably worldwide. It appears to be more common in kennels and colonies.
Mode of Infection
Virus is shed in the feces and the mode of infection is by ingestion.
Clinical Signs
Clinical signs are anorexia, depression and loose stools. Occasionally, there is sudden onset with vomiting and diarrhea. Mucus is usually present in the foul-smelling feces.
Diagnosis
- Enteric infections such as coccidiosis, cryptosporidiosis, salmonellosis, campylobacteriosis, hookworm infection, acute pancreatitis and renal or hepatic failure should be considered. Canine parvovirus infection is more severe than CCV infection.
- Fresh feces and/or fresh and fixed portions of small intestine. The virus is difficult to isolate. A diagnosis is most readily made by the demonstration of coronavirus in fecal lysates with the electron microscope.
- Direct fluorescent antibody staining is used to identify coronavirus in frozen sections of small intestine and in feces.
- Finding the characteristic histopathologic changes (particularly villus atrophy) in the small intestine is supportive.
Treatment
Supportive. Fluid therapy.
Control
- An inactivated virus vaccine is available.
- The virus retains its infectivity for at least 1 - 2 days under cool conditions.
Canine Cyclic Thrombocytopenia
(see Infectious Cyclic Thrombocytopenia).
Canine Distemper
Canine distemper is a highly contagious viral disease, usually of young dogs, characterized by profound involvement of the respiratory, alimentary and nervous systems.
Etiology
The cause is a Morbilivirus (Paramyxoviridae) which is relatively labile and unstable apart from the host.
Distribution
This disease occurs worldwide and is endemic in urban areas.
Susceptibility
Dogs, wolves, coyotes, racoons, ferrets. mink, weasels, skunks, dingos and some other wild and exotic animals.
Mode of Infection/Transmission
The mode of infection is inhalation and transmission is by direct contact and fomites. Large numbers of virus particles are shed in secretions and excretions during the active stage of the disease. Because of maternal antibody, many infections are subclinical.
Clinical Features
The incubation period is 3 - 7 days but may be as long as four weeks. Signs include: a diphasic fever, leukopenia, acute coryza, later bronchitis, catarrhal pneumonia and gastroenteritis. Recovery from the acute phase may be followed by neurologic signs including rhythmic jerking of a muscle or muscles (myoclonus). Nasal and digital hyperkeratosis (hard pad disease) usually occur when CNS signs are present. Dogs with neurological signs rarely recover. A condition referred to as "old dog encephalitis" (ODE) is sometimes seen,even years after recovery from distemper. Occasionally there is no history of previous clinical distemper. Live virus has not been recovered from ODE. The clinical signs can include ataxia, incoordinated movements and compulsive head pressing and pacing. Recovered puppies may display multifocal enamel hypoplasia or agenesis.
Diagnosis
- Infectious canine hepatitis, leptospirosis, lead poisoning and granulomatous meningoencephalomyelitis are among the diseases that should be considered. A number of viral, bacterial and parasitic infections may flare up during the course of distemper, complicating the clinical diagnosis.
- The disease is usually diagnosed clinically or after necropsy examinations.
- Live animals: Conjunctival, tracheal, vaginal scrapings and buffy coat are taken early in the course of the disease for fluorescent antibody (FA) examination.
Inclusion bodies can sometimes be demonstrated in scrapings with appropriate stains. The later the course, the more difficult it is to demonstrate virus by the FA procedure because of antibody production.
Necropsy: Fixed and fresh portions of intestine, pancreas, stomach, bladder, brain and lung.
Histopathologic examination of tissues for the characteristic cytoplasmic inclusion bodies in the bladder, lung, stomach and pancreas. In the neurologic form the microscopic lesions located in the white matter near the ventricular and meningeal surface are diagnostic. They involve demyelination with inclusions in glial cells and neurons.
- The FA test on frozen sections of tissues taken at necropsy is very reliable.
- Paired sera or plasma. An ELISA is performed in some diagnostic laboratories. An indirect fluorescence assay test kit is available to detect antibodies in serum or plasma. Rising IgG titers in the ELISA are significant, but single titers are not reliable. Antibodies in cerebrospinal fluid are diagnostic of distemper. Some laboratories perform a serum-neutralization test.
- The virus is not readily cultivated in cell cultures or embryonated eggs. Ferrets are very susceptible and are occasionally used for virus isolation.
Treatment
Supportive. Antimicrobial drugs for secondary bacteria.
Control
- Vaccination of in contact dogs.
- Isolation of infected dogs. Thorough cleaning and disinfection of premises, cages and utensils.
- Vaccination is effective after loss of maternal immunity, which is usually by 12 weeks of age.
- Modified live vaccines are administered between 6 - 12 weeks of age at intervals of 2 - 3 weeks. These multiple doses are needed because maternal antibodies reduce the efficacy of vaccination.
- Modified live vaccines should not be administered to pregnant bitches.
- It is recommended that dogs older than three months with unknown immune status be vaccinated twice with an interval of 2 - 4 weeks.
- Traditionally it was recommended that all confined dogs receive an annual booster. This need is being reassessed and a longer interval between vaccinations may be indicated.
- Rarely, a viral encephalitis is seen 1 - 2 weeks after vaccination with attenuated live virus vaccine.
Canine Ehrlichiosis (Canine Monocytic Ehrlichiosis, Tropical Canine Pancytopenia)
Canine ehrlichiosis is an acute to chronic rickettsial disease characterized by infection of monocytes and lymphocytes, resulting in various clinical signs including recurrent fever.
Etiology
The cause is a rickettsia (bacterium), Ehrlichia canis. Ehrlichiosis may be complicated by concurrent infection with babesia and haemobartonella.
Distribution
Worldwide. Occurs in many regions of the US.
Susceptibility
Puppies and German Shepherds appear to be particularly susceptible.
Mode of Infection/Transmission
The brown dog tick Rhipicephalus sanguineus is the vector and reservoir. Ticks may harbor the organism for as long as five months.
Clinical Features
These may include recurrent fever, epistaxis, mucopurulent nasal discharge, vomiting, subcutaneous hemorrhages and edema, depression, emaciation, anemia, splenomegaly, polyarthritis, generalized lymphadenopathy, meningoencephalitis, convulsions, paralysis and weight loss.
Diagnosis
- Babesiosis and other infectious diseases produce some clinical signs similar to those of ehrlichiosis. Rocky Mountain spotted fever, a relatively uncommon disease of dogs, is clinically similar to ehrlichiosis and also immune-mediated thrombocytopenia. A clinical diagnosis should be confirmed by laboratory means.
- Unclotted blood for buffy coat and regular smears. In necropsied dogs, smears should be made from the lungs and other organs. Smears stained by Giemsa and fluorescent antibody procedures.
The characteristic morulae of E. canis in monocytes and lymphocytes are frequently not present in Giemsa-stained smears. The optimum time for their demonstration is about 13 days postinfection.
- Thrombocytopenia, hyperglobulinemia, non-regenerative anemia and neutropenia are supportive of a diagnosis.
- A PCR procedure and in situ DNA hybridization have been used in the identification of E. canis in tissues.
- Serum is tested for antibody by an indirect fluorescence assay. A titer of 1:10 or greater with the indirect fluorescent assay test is considered positive. The test may be negative early in the disease.
Treatment
- Doxycycline, tetracycline and oxytetracycline are effective if the disease is diagnosed early; treatment should be given for at least two weeks. Additional treatment may be necessary, particularly in the chronic disease.
- Without antibiotic therapy, dogs may remain carriers for many months.
Control
- Isolation, treatment, or elimination of seropositive animals.
- Spraying and dipping to eradicate ticks.
- Avoid tick infested areas.
- Remove ticks using gloves.
Public Health Significance
A considerable number of human infections have been reported. Infection is not thought to be acquired directly from dogs. Ticks are the probable vector.
Canine Granulocytic Ehrlichiosis
This is a milder and much less common ehrlichiosis than canine monocytic ehrlichiosis. It is caused by the rickettsia Ehrlichia ewingii and characterized clinically by anorexia, muscle stiffness, polyarthritis, lameness, neck pain and weight loss. Anemia and thrombocytopenia may be present.
Diagnosis is based on finding the characteristic morulae in neutrophils and eosinophils and serologic differentiation from E. canis using the indirect fluorescence assay.
Treatment is the same as for canine monocytic ehrlichiosis.
Canine Hemobartonellosis
Dogs can be infected with Haemobartonella canis but clinical disease is rare.
Canine Hemorrhagic Gastroenteritis
This infrequent, sporadic, noncontagious disease is characterized by rapid onset and course with a severe bloody diarrhea. Toy, miniature breeds and young dogs are particularly susceptible.
The etiology is not known. The presence of Clostridium perfringens in large numbers in the feces has suggested a clostridial enterotoxemia. Bacterial endotoxemia has also been suggested. Toxigenic strains of E. coli have not been implicated. The increase in bowel permeability in the absence of inflammation and necrosis have suggested a type I hypersensitivity reaction (immediate hypersensitivity and anaphylaxis). Possible contributing factors are stresses and changes in diet.
The cardinal clinical sign is the copious bloody diarrhea of rapid onset. There are usually vomiting, anorexia, profound depression with a normal or subnormal temperature.
Diagnosis
- Other causes of bloody diarrhea should be considered including parvovirus, coronavirus, Salmonella, Campylobacter and Leptospira. Bloody diarrhea may also be seen with giardiasis, coccidiosis, hookworm and whipworm infestations, pancreatitis and hypervolemic shock.
- The clinical signs, particularly the sudden onset and copious bloody diarrhea are especially significant.
- Radiographs show gas and fluid in the small and large intestines.
- Hemoconcentration with a PCV usually greater than 60% is characteristic. The biochemical profile is usually normal.
- Appropriate diagnostic tests may be indicated to rule out other diseases.
Treatment
- Most dogs respond to fluid replacement therapy and ampicillin.
- Glucocorticosteroids may be administered for hypovolemic shock.
- With excessive blood loss a transfusion may be indicated.
- With appropriate treatment the mortality rate is about 10%. The disease recurs in about 10% of patients.
Canine Herpesvirus Infection
Canine herpesvirus infection is a contagious, often fatal disease of puppies (three weeks of age or less).
Etiology
Canine herpesvirus 1 (Herpesviridae). The virus is carried by many adult dogs; puppies are usually protected by maternal antibody.
Distribution
Occurrence is probably worldwide.
Mode of Infection/Transmission
Infection of puppies is considered to take place transplacentally or by contact during or shortly after parturition.
Clinical Features
The disease in susceptible puppies is characterized by a viremia with disseminated necrosis and hemorrhages involving the kidney, liver, lungs and other organs. Among the clinical signs are a soft, yellowish green stool, anorexia, labored breathing, abdominal pain and finally death or recovery.
The disease in previously unexposed adults is characterized by mild rhinitis and conjunctivitis. In females the virus may cause vesicular vaginitis, abortion and infertility. Male dogs may have vesicular lesions on the penis and prepuce.
Diagnosis
- Canine herpesvirus infection should be suspected if young puppies (three weeks of age or less) have an acute, frequently fatal, febrile disease that does not respond to antibiotics.
- Distemper, canine hepatitis, toxoplasmosis and canine parvovirus-1 should be considered.
- Portions of lung and kidney, fixed and fresh, are submitted for virus isolation, fluorescent antibody staining of tissues and histopathologic examination. The latter involves finding of the characteristic inclusion bodies in the lung, liver and kidney.
Treatment
- No specific treatment.
- Supportive measures are not thought to alter the course of the acute disease.
Control
- No practicable measures are available for prevention.
- Vaccination is not practiced.
Canine Influenza
Canine influenza or dog flu is of recent occurrence (2004) and is an acute, highly contagious respiratory infection of relatively short duration and low mortality caused by an influenza A virus thought to be of equine origin.
Etiology
Influenza A virus, closely related to subtype H3N8 and presumed to have been acquired from a horse(s). Subtype H3N8 virus is a frequent cause of equine influenza.
Distribution/Occurrence
Dog flu first occurred in greyhounds in Florida, USA in January 2004. Of the dogs affected by the outbreak about 30% died. The disease was first seen in race tracks but has since spread to veterinary clinics, boarding facilities and animal shelters. Infections have also been confirmed in New York and a number of other states.
Susceptibility
Susceptibility is broad in unexposed dogs. Older dogs and puppies may be more severely affected.
Mode of Infection/Transmission
Infection is via the respiratory tract and spread is mainly by infectious aerosols resulting from coughing but also indirectly by fomites.
Incubation Period/Course
The incubation period is 2 - 5 days and the course in uncomplicated cases is 1 - 3 weeks.
Clinical Features
It appears that the disease is less severe than earlier thought and about 80% of those infected come down with a mild disease. Among the clinical signs are fever, coughing, dyspnea, anorexia, depression and mucoid to purulent nasal discharge. The severe, infrequent form is characterized by pneumonia with secondary bacterial infection. The fatality rate has ranged from 5 - 8% in the early outbreaks among greyhounds but somewhat less in later outbreaks in other breeds.
Diagnosis
Dog flu can only be distinguished from other respiratory infections, such as kennel cough which it resembles clinically, by laboratory means.
- Specimens: Nasopharyngeal swabs as soon as possible. Paired sera with a three-week interval.
- The virus can be readily isolated in chicken embryos and identified by hemagglutination-inhibition (HI).
- An HI procedure can be used to detect antibody in paired sera.
- There are several rapid commercial tests for influenza A virus used for diagnosis of human influenza which may have application for the canine disease.
Treatment
- The antiviral drug oseltamvir (Tamiflu) has been used in the treatment of human influenza. To be effective it must be administered within 48 hours of evidence of infection. There is as yet no information on its efficacy in dog flu.
- Antibiotics are indicated for secondary bacterial infections.
Control
- A vaccine is not yet available.
Public Health Significance
Transmission of dog flu to humans has not been reported.
Canine Leptospirosis
Canine leptospirosis is a contagious disease of varying severity, from latent to acute, caused by spirochetes of the species Leptospira interrogans.
Etiology
Leptospira interrogans, serovar canicola (L. canicola) and less frequently serovar icterohaemorrhagiae (L. icterohaemorrhagiae). In recent years there have been increasing infections with L. pomona, L. bratislava and L. grippotyphosa possibly due to protection afforded by vaccination with principal servars. Outbreaks of the hemorrhagic type of leptospirosis are considered to be due to L. canicola, while the disease in which icterus more often occurs is thought to be caused by L. icterohaemorrhagiae.
Distribution
The disease is worldwide in distribution and common in occurrence.
Source and Mode of Infection
The reservoir for L. canicola is mainly carrier dogs and for L. icterohaemorrhagiae, rats and mice. The organism may be shed in the urine for months from dogs and other animals with asymptomatic kidney infections. Infection occurs by direct or indirect contact via the skin, conjunctiva, or oral mucous membrane.
Pathogenesis
In the acute disease, a bacteremia follows introduction of the leptospira with later localization in various tissues and organs, including the liver, spleen, kidney and lymph nodes.
Clinical Features
Among the clinical signs are anorexia, vomiting and fever; followed by depression, reluctance to move, labored breathing, sometimes icterus, hemorrhages and necrotic patches involving the oral mucosa, muscular tremors, bloody feces and vomitus resulting from a severe gastroenteritis. Frequent urination results from acute nephritis. Renal failure is common and often is the most serious manifestation of infection. Uremia may also develop. The mortality rate is approximately 10%.
Diagnosis
- Canine hepatitis, distemper, ehrlichiosis, babesiosis and sporadic febrile diseases caused by various bacteria and viruses, should be considered.
- Dark-field examination of urine to which formalin has been added at the rate of 0.75 ml of 10% formalin to 10 ml of urine.
- Serologic tests, preferably the microscopic agglutination, on paired sera. A fourfold increase in titer is usually significant. Leptospira antigens are available commercially for this procedure.
- Culture of fresh urine and heparinized blood. Not all diagnostic laboratories are prepared to do this.
- Histopathologic examination of sections of liver and kidney for leptospiras (silver impregnation staining). Microscopic tissue changes alone are not usually characteristic.
- Fluorescent antibody staining of tissues, particularly the kidney and urine.
Treatment
- Penicillin G in particular, ampicillin, streptomycin, chloramphenicol and erythromycin given early and continued for two weeks.
- Streptomycin (unless renal failure is present) in large doses for two weeks along with vaccination is used to eliminate latent kidney infections and urine shedding.
- General supportive treatment.
Control
- Exposure can be reduced by leashing and restricting access to other dogs.
- Bacterins prepared from L. canicola and L. icterohaemorrhagiae are of value, although the duration of immunity is less than one year and there is no cross protection for other serovars.
Vaccines containing the serovars L. pomona and L. grippotyphosa are also available for dogs.
Public Health Significance
The leptospira of dogs can cause serious infections in humans.
Canine Papillomatosis (Canine Warts)
Canine papillomatosis, or warts, is a contagious viral disease of dogs. Cats are not susceptible to the wart virus.
Etiology
It is caused by a host-specific papillomavirus and is characterized by the formation of benign tumors involving the skin and oral mucous membrane.
The virus is resistant and remains viable for long periods of time in contaminated kennels and environs. Warts and affected tissue are highly infectious.
Distribution
Canine papillomatosis is a common disease of worldwide distribution.
Clinical Features
Transmission is by direct and indirect contact. Canine warts are usually found on the mucous membrane of the lips, mouth, tongue and pharynx of young dogs. These warts usually disappear spontaneously in several months. The infection begins as small papules. These enlarge to form small, cauliflower-like warts which may appear on the lips, tongue, gums. buccal mucosa and occasionally the conjunctivae. Skin warts, which may be caused by another papillomavirus, are mostly seen in older dogs. They do not regress spontaneously. Dogs more than two years of age are usually immune to oral papillomatosis. Warts may interfere with chewing and swallowing.
Diagnosis
- A laboratory diagnosis is not ordinarily carried out, as the lesions (warts) are clinically characteristic.
- Histopathologic examination of tissue biopsies is confirmatory.
- The causal agent has not been grown in cell cultures.
Treatment
- Surgical excision.
- The value of commercial and autogenous wart vaccines is questionable. Warts frequently disappear spontaneously within a few weeks.
Control
Vaccination for prevention is not practiced.
Canine Parainfluenza 2
This virus (Paramyxoviridae) which frequently infects the respiratory tract of dogs is associated with infectious canine tracheobronchitis. In the absence of secondary invaders infections are mild (see Infectious Canine Tracheobronchitis).
Canine Parvovirus Infection (Canine Parvovirus Enteritis)
Canine parvovirus infection is a contagious disease of dogs, characterized by vomiting, diarrhea (usually hemorrhagic), fever, weakness, dehydration and marked leukopenia.
Etiology
The cause is canine parvovirus 2 (Parvoviridae), a DNA virus which is closely related to the parvovirus causing feline panleukopenia.
Distribution
Canine parvovirus would appear to be worldwide in distribution.
Susceptibility
The disease is seen in household dogs and may involve whole litters and kennels. Young (2 - 16 weeks) and aged dogs are most susceptible. Doberman Pinschers and Rottweilers are thought to be more susceptible. Myocarditis may occur in susceptible puppies up to eight weeks of age.
Mode of Infection
The virus is shed in the feces and the mode of infection is by ingestion.
Diagnosis
- Among other causes of infectious diarrhea in dogs are canine coronavirus, hookworm infection, Salmonella spp. and Campylobacter jejuni.
- Feces and portions of fresh intestine and heart. Virus identification is accomplished by electron microscopic (EM) examination of feces or fluorescent antibody staining of frozen sections of intestine or heart. The characteristic morphology of the parvovirus allows it to be readily recognized by EM examination.
- Viral hemagglutination (HA): Canine parvovirus agglutinates certain species of red blood cells. An HA titer of 1:64 (dilution of feces) provides presumptive evidence of infection. The higher the titer the more virus present.
- ELISA is also used to detect parvovirus in feces and commercial kits for this purpose are available, e.g., Cite test. False negative results are common with both the HA test and ELISA in the later stages of the illness; developing antibodies interfere with the tests.
- The CPV antigen-capture CITE (Iddex Corp.) assay referred to above is considered sensitive and reliable.
- Unclotted blood samples. A leukopenia is suggestive.
- Formalin-fixed portions of intestine and heart. Crypt epithelial necrosis with collapse of mucosal architecture and villus loss is diagnostic. Intranuclear inclusion bodies are infrequent to rare in the gut, but can be numerous in the myocardium of very young puppies that die suddenly from the myocardial form of the disease.
- Because the virus presents some difficulty in cultivation, virus isolation and identification are not generally carried out.
Treatment
Intensive care, fluid therapy and antimicrobial drugs for secondary bacteria, e.g., amoxicillin or penicillin G.
Control
- Isolation of infected animals.
- Killed virus vaccines and modified live virus vaccines are used. Maternal antibody can interfere with vaccination.
- The virus can persist for long periods on the premises.
- Formalin, gluteraldehyde and chlorine based disinfectants are effective against the two canine parvoviruses.
Canine Parvovirus 1 Infection (Minute Virus of Canines Infection)
Canine parvovirus 1 (CPV-1), which differs antigenically from canine parvovirus 2, is the cause of as yet infrequent enteric and respiratory infections in young puppies. The virus has been isolated from the feces of normal dogs and that it is widespread in dogs in the United States is clear from antibody surveys. Limited studies suggest that the virus is also prevalent in Europe and Japan. The virus appears to be quite variable in its pathogenicity and the extent of significant infections in dogs is not yet known.
Although mild diarrhea has been observed in dogs other than puppies the most significant infections have been in puppies up to about one month of age. A number of puppies in a litter may be infected and the outcome may be fatal. The signs include dullness, anorexia, diarrhea, vomiting and dyspnea. Enteritis, myocarditis and pneumonitis may be present. Unless a particular cell line (Walter Reed canine cell line) is employed for isolation or special immunological reagents employed, laboratory diagnosis will probably be unsuccessful.
Canine Respiratory Disease: General
Most of the bacteria and viruses listed below may be involved in infections of the upper and/or the lower respiratory tract.
The following are the principal etiological categories of canine respiratory disease:
- The following viruses have been implicated in canine respiratory infections: canine adenovirus 2, canine herpesvirus, canine reovirus and canine parainfluenza virus.
- Bordetella bronchiseptica is a primary agent in infectious canine tracheobronchitis (discussed separately) or the kennel cough syndrome. It is also a secondary invader in canine distemper and some other viral respiratory infections.
- The following bacteria appear to be mainly secondary invaders in canine respiratory infections: Pasteurella multocida, P. pneumotropica, E. coli, Pseudomonas aeruginosa, Klebsiella spp., streptococci, staphylococci and mycoplasmas.
- Respiratory infection may be an important feature of the following diseases: actinomycosis, aspergillosis, blastomycosis, coccidioidomycosis, cryptococcosis, distemper, histoplasmosis and nocardiosis.
Diagnosis
This usually involves the isolation and identification of the causative agent from material taken by transtracheal or transthoracic aspiration, nasal and throat swabs.
Note
See the specific diseases and causal agents mentioned above for further details on laboratory diagnosis.
Canine Rotavirus Infection
This double-stranded RNA virus (Reoviridae) occurs widely in the intestine of dogs but infections are generally subclinical. Enteritis with diarrhea has been reported in puppies. Rotavirus can be detected in feces with electron microscopy.
Canine Streptococcal Toxic Shock Syndrome
This is an infrequent disease which has been recognized in the last two decades. It results from a severe, invasive streptococcal infection and resembles streptococcal toxic shock syndrome in humans.
Etiology
It is mainly due to the toxins of Streptococcus canis (Group G). The disease is considered to be initiated by minor trauma followed by local cellulitis and then progressing to shock and necrotizing fasciculitis.
Distribution
Although reported from North America the disease is potentially widespread given the ubiquity of S. canis.
Susceptibility
Outbreaks have occurred in racing greyhounds, in other breeds and in captive coyotes. It has not been shown to be associated with kennels, shows or performance events. Given the fact that many dogs carry S. canis infections may be endogenous.
Clinical Features
Apparently healthy dogs can become seriously ill within a few hours and the course may be as short as seven hours. Among the signs are: vomiting, lateral recumbency, too weak to move or moving rigidly, mild convulsions, intense pain and rapid uncontrolled muscle fasciculation. Particularly characteristic is a high temperature, > 105°F. As the disease progresses there is non-productive coughing, which may later include blood due to spontaneous hemorrhaging, epistaxis and bloody diarrhea. If not treated aggressively at this stage death may ensue.
Diagnosis
This is based; on clinical signs including particularly, the short course, rapid onset, intense pain, hypotension and high fever. Isolation of S. canis from tissue is confirmatory.
Treatment
- Early treatment with injectable antibiotics, penicillin G or clindamycin.
- Supportive and shock therapy.
- Surgical debridement of necrosis resulting from the necrotizing fasciculitis.
Cat-scratch Disease (Cat-scratch Fever, Benign Lymphoreticulosis) of Humans
Cat-scratch disease (CSD) is not an animal disease, but is of interest because the cat is the source of this common zoonosis. The disease, which is not contagious, is most often acquired from cats less than one year old, due to a lick, a scratch, or a bite. Some infections have been initiated via the conjunctiva. In 10% of cases there is no evidence of contact with a cat. There is some evidence that fleas can transmit the infection. It is thought that claws acquire the organism from saliva during grooming.
Etiology
Multiple cases have been reported in families and attributed to the same cat. Children are more frequently affected than adults. It is estimated that about 40% of cats are carriers.
The principal cause is an obligate intracellular bacterium (rickettsia), Bartonella henselae, which is thought to be a frequent commensal in the mouth of cats. The latter show no evidence of infection. The incubation period may range from 3 - 90 days and the course usually ranges from 2 - 4 months. The principal sign is regional lymphadenopathy, usually accompanied by a low-grade fever and mild, systemic symptoms. The lymph nodes involved depend upon the location of the bite or scratch. It has been found recently that some cases of CSD are caused by B. clarridgeiae.
Clinical features
The disease causes serious illness including bacillary angiomatosis and peliosis hepatitis in immunocompromised patients; however, in normal individuals it is usually self-limiting and complications are rare. Disseminated infections are seen in some AIDS patients.
Diagnosis
- This is carried out in medical diagnostic laboratories.
- Characteristic organisms are seen in sections of biopsies stained with the Warthin-Starry silver procedure.
- Indirect fluorescence assay and enzyme immunoassay procedures are employed to detect antibody.
- The organism can be cultured from pus taken from lymph nodes after prolonged incubation on rabbit blood agar in 5% CO2 at 36°.
- A PCR procedure has been used to amplify the DNA of the causal agent in tissue samples.
Treatment
- Most cases of uncomplicated CSD recover without treatment.
- Inflamed, fluctuant abscesses may be aspirated or excised for the relief of symptoms.
- Tetracycline, erythromycin, rifampin and ciprofloxacin have been effective in disseminated forms of the human infection.
Control
Disposal of the suspected cat is not ordinarily indicated. However, removal of cats from the household may be recommended for at-risk, immunosuppressed individuals. A vaccine is now available to prevent CSD in humans.
Chromoblastomycosis (Chromohyphomycosis, Phaeohyphomycosis)
Chromoblastomycosis is an infrequent cutaneous and subcutaneous fungal infection of dogs, cats, horses and humans. To avoid confusion the closely related diseases chromohyphomycosis and phaeohyphomycosis are included here under chromoblastomycosis. They have similar lesions but are caused by different saprophytic fungi.
Etiology
This disease is caused by a number of saprophytic, dematiaceous (dark pigmentation) fungi. Among those involved are a number of species of the genera Cladosporium, Phialophora and Fonsecaea including Cladosporium carrionii, Phialophora verrucosa, Fonsecaea pedrosoi and F. campacta. Species of other genera may also be involved.
Pathogenesis
The fungi, some of which are listed above, enter via a wound or at the site of trauma and produce a granulomatous mass at or near the site of entry. It may spread peripherally and, on occasion, to the lymphatics and other tissues and organs. The disease is chronic and if not treated it may persist and progress.
Diagnosis
- Chromoblastomycosis should be suspected when chronic granulomatous lesions resulting from wounds and trauma are seen involving the skin, lymphatics and regional lymph nodes.
- Blastomycosis, nocardiosis, canine actinomycosis and eumycotic mycetoma (also caused by dematiaceous fungi) are among the diseases that should be considered.
- Material from granulomatous and/or ulcerous lesions. Biopsies or portions of lesions, fixed.
- The characteristic brown-pigmented, or hyaline branching, hyphal elements can be seen in wet mounts of material from granulomatous and/or ulcerous lesions.
- The same fungal structures are seen in stained sections of lesions. Finding the characteristic fungal elements in tissue sections is supportive.
- Definitive diagnosis is based upon the cultivation, isolation and identification of the fungus, which may take as long as six weeks to grow.
Treatment
- Surgical excision when the disease is confined to the skin and subcutaneous tissues.
- Amphotericin B, locally and systemically.
- Flucytosine, ketoconazole and itraconazole have been effective; the latter is preferred for cats.
- Cure may require treatment for weeks to months.
Coccidioidomycosis (Coccidioidal Granuloma)
Coccidioidomycosis is a noncontagious disease of domestic animals, humans and various wild animals, caused by the soil- or dust-borne dimorphic fungus, Coccidioides immitis.
Distribution
The disease occurs in the arid, acid-soil regions of the United States (mainly Arizona and California) and in some regions of South America.
Susceptibility
Dogs are affected most significantly; cats rarely develop the clinical disease.
Mode of Infection
Inhalation of spores.
Pathogenesis
It occurs in a benign, subclinical form with the formation of tuberculosis-like granulomas in the lung which infrequently progresses to the disseminated form with granulomas developing in various tissues and organs. The latter form is seen not infrequently in dogs.
Clinical Signs
These depend upon the stage of the disease. Signs of the disseminated disease may include: fever, chronic cough, lameness, anorexia, enlarged joints, draining skin lesions, ocular inflammation and diarrhea.
Diagnosis
- Blastomycosis, histoplasmosis, nocardiosis (dog), canine actinomycosis, pneumonic infections caused by other agents and metastatic neoplasia should be considered.
- Most diagnoses of coccidioidomycosis, with the possible exception of cases in the dog, are made by microscopic examination of material from lesions or histopathologic examination after necropsy. Pulmonary nodules can be seen in radiographs.
- Exudate and biopsies taken from nodules and lesions involving the liver, spleen and lymph nodes in the disseminated disease.
- Transthoracic aspirates if pulmonary disease is suspected.
- From necropsy: Fresh and fixed portions of tissues and organs with granulomatous lesions
Employing the above materials, demonstration of the yeast-like forms in wet mounts and smears using fluorescent antibody and other stains. Culture, isolation identification and histopathologic examination.
- Paired sera, or sequentially drawn sera are preferred. Complement Fixation (CF) test; the titer usually rises as the disease progresses. The Agar Gel Immunodiffusion (AGID) test and the ELISA are useful.
- It should be kept in mind that many animals in areas where the fungus occurs in nature will have antibodies to this fungus. If the CF and AGID tests are positive, it indicates a recent or active infection.
Treatment
- Ketoconazole is currently the drug of choice. Prolonged treatment (8 - 12 months) is required for disseminated infections. Other imidazoles may be equally effective. There is evidence that itraconazole is better tolerated by cats than ketoconazole.
- Amphotericin B is reserved for patients that do not respond to or cannot tolerate imidazoles. Amphotericin B can also be used along with ketoconazole.
Public Health Significance
Although human infections are not ordinarily traced to animals, it is advisable to prevent human exposure to infected animals. Arthrospores that are particularly infectious could possibly develop on dressings.
Cryptococcosis
Cryptococcosis is a subacute to chronic, frequently fatal, fungal disease of dogs, cats, horses, cattle, sheep, goats and other animals.
Etiology
The cause is C. neoformans a soil-borne, yeast-like fungus. It multiplies to large numbers in the feces of pigeons and other birds where it can remain viable for months; however, it is not found in the intestinal tract of live birds.
Distribution
Worldwide.
Susceptibility
Cryptococcosis is seen more frequently in cats than in dogs.
Mode of Infection
Inhalation of spores.
Pathogenesis
The disease is manifested most commonly as nasal and frontal sinus infections, particularly in cats, that often extends to the meninges, brain and lungs. The characteristic tumor-like granulomatous lesions may also involve the skin and subcutis. In the disseminated disease, lesions develop in various tissues and organs including the central nervous system and in the absence of treatment terminates fatally.
Clinical Signs
These will depend on the stage of the disease. They include: sneezing, cough, nasal and ocular discharge and with CNS involvement, ataxia, circling, blindness and locomotor dysfunction.
Diagnosis
- Paranasal cryptococcosis must be distinguished from other respiratory diseases. The subcutaneous and nasal forms must be distinguished from a number of diseases such as blastomycosis, nasal aspergillosis (dogs), nocardiosis and canine actinomycosis that may produce discharging, granulomatous lesions and from bacterial/viral rhinitis and nasal tumors in cats.
- Head and thoracic radiographs provide evidence of possible cryptococcal infection.
- The paranasal and subcutaneous forms of the disease can be diagnosed on the basis of clinical signs and the demonstration of yeast-like cells (different from those of blastomycosis and coccidioidomycosis) in wet mounts and gram- or Geimsa- stained smears of material taken from lesions.
- Material is collected aseptically from the nasal passages in the paranasal form and from the granulomatous lesions in the subcutaneous form.
- It may be advisable in certain cases to take biopsies. If there is evidence of involvement of the brain and meninges, cerebrospinal fluid (CSF) should be collected.
- Necropsy: Portions of affected tissues, fresh and fixed, are submitted.
- All materials collected, including CSF, are examined by stains and wet mounts, then cultured for C. neoformans.
- Fixed tissues are examined for the typical lesions containing the yeast-like organisms.
- Although C. neoformans is not the only capsulated cryptococcus, the association of a thickly capsulated yeast-like organism with the morphology of cryptococci from an animal with typical clinical signs or lesions is considered sufficient for a firm diagnosis.
- Sensitive serologic tests, e.g., the tube agglutination and latex agglutination tests, are available for the detection of C. neoformansantibody and antigen, respectively. An indirect fluorescence assay for antibody has also been used although a negative test does not exclude cryptococcosis.
Treatment
- Amphotericin B and flucytosine are used, alone or in combination; the latter in life-threatening cases. Resistance may develop to either drug.
- Fluconazole, itraconazole and ketoconazole are the preferred drugs; the latter appears to be less well tolerated by cats.
- Treatment should be continued for several months after the absence of clinical signs. A fall in the titer of the latex agglutination test indicates a favorable response to treatment.
- Supportive therapy and assisted feeding may be indicated in some patients.
Control
Cases should be isolated.
Public Health Significance
Because humans contract this disease, human exposure to infected animals should be avoided. However, human cases ordinarily are not thought to be acquired from infected animals.
Dermatophilosis (Streptothricosis)
This contagious bacterial disease of domestic and other animals is characterized by dermatitis of the superficial layers of the skin. It is rare in dogs and cats.
Distribution
Worldwide; more prevalent in tropical and subtropical countries.
Etiology
The cause is the gram-positive actinomycete, Dermatophilus congolensis. Its natural habitat is not known; it is thought to be soil. The zoospores of D. congolensis can survive in scabs for as long as three years.
Mode of Infection/Transmission
Direct and indirect contact; fomites. Moist and wet conditions contribute to its spread. Biting arthropods and trauma, e.g., puncture wounds, may initiate infections.
Clinical Signs
Crusts and scabs are characteristic of dermatophilosis. Initial lesions may be circumscribed but later they may coalesce resulting in extensive encrustation. Additional signs may be alopecia, matted and dirty hair, cracked skin, skin pustules and ulcers. Granulomatous lesions involving the subcutis and submucosa are seen in cats.
Diagnosis
- Although the encrustations and scabs allow for a presumptive clinical diagnosis in horses and farm animals, because of the rarity of the disease in dogs and cats laboratory confirmation is recommended.
- Scabs, crusts and plucked hair are collected. Skin biopsies may be taken after removal of scabs but are not usually necessary.
- A definitive diagnosis can usually be made by demonstrating D. congolensis in gram- or Giemsa-stained smears in the aforementioned clinical materials.
- Culture, isolation and identification of D. congolensis. Although culture is not usually difficult, it is not required for diagnosis. There is a good correlation between the results of smear examination and culture.
- The characteristic morphologic elements can be seen in Gram-stained sections of skin biopsies.
Treatment
- Cases should be isolated. Acute cases are often of short duration and clear up without treatment.
- Short term treatment with penicillin, tetracyclines or amoxicillin is usually effective.
- Washing and using disinfectant solutions may reduce spread, although topical treatment is not effective. Mild cases may respond to good, regular grooming.
Control
Isolation of infected animals.
Public Health Significance
The disease has been acquired infrequently from infected animals. Pustules develop on the hands and forearms.
Dermatophytosis (Ringworm)
Dermatophytosis is a contagious disease caused by fungi of the genera Microsporum and Trichophyton which infect the keratin-containing tissues (skin, nails and hair) of domestic animals, humans and other animals.
Etiology
The principal dermatophytic fungi affecting dogs and cats are as follows.
Microsporum canis (Hosts: dog and cat)
M. gypseum (Source: soil. Host: dog)
Trichophyton mentagrophytes (Source: rodents. Host: dog)
Microsporum canis causes more than 95% of ringworm in the cat and about 70% in dogs.
Other species of dermatophytes rarely cause ringworm in dogs and cats.
Distribution
Worldwide. Microsporum gypseum occurs naturally in soil.
Mode of Infection
Direct and indirect contact. Infected animals and fomites are the usual source of the dermatophytes. Inapparent infections are common in kittens.
Pathogenesis
The infections are superficial, starting in the stratum corneum and invading hair follicles and hair, with the production of hyphae and spores within (endothrix) and/or on (ectothrix) hairs. The lesions spread out from a central locus resulting in circular and patchy lesions. Some heavily infected cats may develop cutaneous nodules called pseudomycetomas that ulcerate.
Clinical Signs and Diagnosis
The circular or roughly circular lesions of ringworm are variable in size and develop from raised plaques on the skin. The hair becomes thin, broken and finally there is bareness that may become scaly and scabby. Most lesions occur on the head and neck. Bald patches and hair loss are characteristic of feline ringworm. Lesions of M. gypseum in the dog are mainly on the muzzle. Some heavily infected cats may develop cutaneous nodules called pseudomycetomas which may ulcerate.
Eczema, dermatitis, pyoderma, dermatophilosis and mange are among the diseases which should be considered in diagnosis.
- If feasible, examine lesions with a Wood's lamp (ultraviolet light source); M. canis fluoresces (greenish color). Negative fluorescence does not exclude ringworm.
- Plucked hair (especially those that fluoresce) and skin scrapings from the edge of lesions. These are sent to the laboratory in a paper envelope (to prevent moisture and the growth of saprophytic fungi).
- Some veterinarians inoculate one of the several commercial media (Dermatophyte Test Media, Fungassay, etc...) that are available for the selective growth of dermatophytes. If the results are equivocal, the media may be submitted to a diagnostic laboratory for interpretation.
- The specimen is first examined microscopically in wet mounts for the presence of spores and other fungal elements. Appropriate media are inoculated. Isolation and identification may take several weeks.
Treatment
- Isolation of infected animals if feasible. It is often a self-limiting disease.
- Treatment may vary somewhat between dogs and cats but the following general approaches are recommended.
Local: clipping and shampoo with mild soap to remove crusts, exudate, etc. Whole-body baths with ketoconazole, enilconazole, miconazole, or lime-sulphur solutions.
Systemic: particularly for severe and chronic cases: griseofulvin - not for pregnant cats or cats with FIV - . Ketoconazole and itraconazoleare also effective; ketoconazole is not recommended for pregnant animals. The treatment period for griseofulvin and the imidazoles is 3 - 6 weeks.
Control
- Infected animals should be separated from those showing no signs of infection although the latter may have inapparent infections. In contact dogs and cats can be treated with griseofulvin for two weeks.
- As dermatophyes can survive for long periods, cages and premises must be scrupulously cleaned and disinfected to prevent reinfection. Disinfectants must be fungicidal; bleach diluted 1:10 is effective.
- A fungal cell wall vaccine is available; it is used for prevention and as an adjuvant to treatment particularly in cats.
Public Health Significance
Humans are frequently infected with ringworm fungi of animal origin. Contact with infected animals, their hair clippings, bedding, cages and other potential fomites, should be avoided.
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Affiliation of the authors at the time of publication
Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, Virginia, USA.
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