Canine Distemper
(Hardpad disease)
Introduction:
Canine distemper is a highly contagious, systemic, viral disease of dogs seen worldwide. It is characterized by a diphasic fever, leukopenia, GI and respiratory catarrh, and frequently pneumonic and neurologic complications. The disease occurs in Canidae (dogs, foxes, wolves), Mustelidae (eg, ferret, mink, skunk), most Procyonidae (eg, raccoon, coati mundi), and some Viverridae (binturong).
Etiology and Pathogenesis: Canine distemper is caused by a paramyxovirus closely related to the viruses of measles and rinderpest. The enveloped virus is sensitive to lipid solvents and most disinfectants and is relatively unstable outside the host. The main route of infection is via aerosol droplet secretions from infected animals. Some infected dogs may shed virus for several months.
Virus replication initially occurs in the lymphatic tissue of the respiratory tract. A cell- associated viremia results in infection of all lymphatic tissues, which is followed by infection of respiratory, GI, and urogenital epithelium, as well as the CNS. Disease follows virus replication in these tissues. The degree of viremia and extent of spread of virus to various tissues is moderated by the level of specific humoral immunity in the host during the viremic period.
Clinical Findings: A transient fever usually occurs 3-6 days after infection and there may be a leukopenia (especially lymphopenia) at this time, but these signs may go unnoticed. The fever subsides for several days before a second fever occurs, which lasts <1 wk. This may be accompanied by serous nasal discharge, mucopurulent ocular discharge, and anorexia. GI and respiratory signs may follow and are usually complicated by secondary bacterial infections. An acute encephalomyelitis may occur in association with or immediately after the systemic disease, or in the absence of systemic manifestations. Hyperkeratosis of the footpads ("hardpad" disease) and epithelium of the nasal plane may be seen.
Neurologic signs are frequently seen in those dogs with hyperkeratosis. CNS signs include the following: 1) localized involuntary twitching of a muscle or group of muscles (myoclonus, chorea, flexor spasm, hyperkinesia), such as in the leg or facial muscles; 2) paresis or paralysis, often beginning in the hindlimbs evident as ataxia, followed by ascending paresis and paralysis; and 3) convulsions characterized by salivation and chewing movements of the jaw (petit mal, "chewing-gum fits"). The seizures become more frequent and severe, and the dog may then fall on its side and paddle its legs; involuntary urination and defecation (grand mal seizure, epileptiform convulsion) often occur. A dog may exhibit any or all of these neurologic signs in addition to others in the course of the disease. Infection may be mild and inapparent or lead to severe disease manifest by most of the above signs. The course of the systemic disease may be as short as 10 days, but the onset of neurologic signs may be delayed for several weeks or months.
Chronic distemper encephalitis (old dog encephalitis [ODE]), a condition often marked by ataxia, compulsive movements such as head pressing or continual pacing, and incoordinated hypermetria, may occur in adult dogs without a history of signs related to systemic canine distemper. Convulsions and neuromuscular twitching (chorea) do not seem to occur with ODE. Although canine distemper antigen has been detected in the brain of dogs with ODE by fluorescent antibody staining, dogs with ODE are not infectious and replication-competent virus has not been isolated. The disease is caused by an inflammatory reaction associated with persistent canine distemper virus infection in the CNS.
Lesions: Thymic atrophy is a consistent postmortem finding in young puppies. Hyperkeratosis of the nose and foot pads may be present. Depending on the degree of secondary bacterial infection, bronchopneumonia, enteritis, and skin pustules may also be present. Histologically, canine distemper virus produces necrosis of lymphatic tissues, interstitial pneumonia, and cytoplasmic and intranuclear inclusion bodies in respiratory, urinary, and GI epithelium. Lesions found in the brain of dogs with neurologic complications include neuronal degeneration, gliosis, demyelination, perivascular cuffing, nonsuppurative leptomeningitis, and intranuclear inclusion bodies predominantly within glial cells.
Treatment: Treatments are directed at limiting secondary bacterial invasion, supporting the fluid balance and overall well-being of the dog, and controlling nervous manifestations. Antibiotics, electrolyte solutions, protein hydrolysates, dietary supplements, antipyretics, nasal preparations, analgesics, and anticonvulsants are used. No one treatment is specific or uniformly successful. Dogs may recover completely from systemic manifestations, but good nursing care is essential. Despite intensive care, some dogs do not make a satisfactory recovery. Unfortunately, treatment for neurologic manifestations of distemper are unsuccessful. If the neurologic signs are progressive or severe, the owner should be appropriately advised.
Prevention: Successful immunization of pups with canine distemper modified live virus (MLV) vaccines depends on the lack of interference by maternal antibody. To overcome this barrier, pups are vaccinated with MLV vaccine when 6 wk old and at 2-to 4-wk intervals until 16 wk old. Measles virus induces immunity to canine distemper virus in the presence of relatively greater levels of maternal distemper antibody. An MLV measles vaccine and a combination of MLV measles and MLV canine distemper vaccine are available. These vaccines must be administered IM. Pups 6-7 wk old should receive the measles or combination vaccine and at least two more doses of MLV distemper vaccine when 12-16 wk old. Many varieties of attenuated distemper vaccine are available and should be used according to manufacturers' directions. Annual revaccination is suggested because of the breaks in neurologic distemper that can occur in stressed, diseased, or immunosuppressed dogs.
Canine Parvovirus
Find additional information on how I treat Parvo cases at our clinic on our Intestinal Page
Introduction, Etiology and Pathophysiology: The origin of the canine panvovirus has not been established. The virus is very stable in the environment, able to withstand wide pH ranges and high temperatures. It is resistant to a number of common disinfectants and may survive for several months in contaminated areas. Rottweilers, American Pit Bull Terriers, Doberman Pinschers, and German Shepherd Dogs are at increased risk of disease. Toy Poodles and Cocker Spaniels appear at decreased risk for developing the enteric disease. Mortality associated with canine parvovirus infection is reported to be 16-35%.
The virus is transmitted by direct contact with infected dogs. Indirect transmission, eg, by fecal-contaminated fomites, is also an important source of infection. The virus is shed in the feces of infected dogs for up to 3 wk after infection. Recovered dogs may serve as carriers and shed the virus periodically.
After ingestion, the virus replicates in lymphoid tissue of the oropharynx; from there, it spreads to the bloodstream. It attacks rapidly dividing cells throughout the body, especially those in the bone marrow, lymphopoietic tissue, and the crypt epithelium of the jejunum and ileum. Replication in the bone marrow and lymphopoietic tissue causes neutropenia and lymphopenia, respectively. Replication of the virus in the crypt epithelium of the gut causes collapse of intestinal villi, epithelial necrosis, and hemorrhagic diarrhea. Normal enteric bacteria, eg, Clostridium perfringens and Escherichia coli enter the denuded mucosa and gain entry to the bloodstream, resulting in bacteremia.
Clinical Findings: Infected dogs are often asymptomatic. Clinical disease may be triggered by stress (eg, boarding), and clinical signs may be exacerbated by concurrent infection with opportunistic enteric pathogens (eg, Salmonella, Clostridium perfringens, E coli, Campylobacter, coronavirus, and various parasites). The dose of virus required to cause clinical disease may also be a factor. Prolonged contact with a dog shedding high levels of virus increases the likelihood of disease. The incubation period is 3-8 days. Viral shedding may begin on day 3, before the onset of clinical signs.
Initially, two common clinical forms of the disease were recognized - myocarditis and gastroenteritis. Myocarditis was seen in young pups, especially in the early neonatal period. Infection lead to myocardial necrosis with either acute cardiopulmonary failure (causing pulmonary edema, cyanosis, and collapse) or scarring of the myocardium and progressive cardiac insufficiency. However, Myocarditis is no longer seen because effective immunization of bitches protects pups during this early period of life.
Gastroenteritis is most common in pups 6-20 wk old, ie, the period when maternal antibody protection falls and vaccination has not yet adequately protected the pup against infection. Most affected dogs (~85%) are <1 yr old. In dogs >6 mo old, intact males are more likely to develop enteritis than intact females, reflecting the tendency of male dogs to roam. Dogs with the enteric form suffer from an acute onset of lethargy, anorexia, fever, vomiting, and diarrhea. The feces are loose and may contain mucus or blood. The severity of clinical signs varies. Most dogs recover within a few days with appropriate supportive care; others can die within hours of the onset of clinical signs. A common complication is pulmonary edema or alveolitis.
Other clinical problems that have been associated with canine parvovirus include birth defects and infertility. However, supportive evidence is lacking.
Treatment: There is no specific therapy to eliminate the virus. Most dogs recover with appropriate supportive care directed to restoration of fluid balance. Oral electrolyte solutions may be used in mildly dehydrated dogs without a history of vomiting. More severely affected dogs should receive IV fluid therapy (lactated Ringer's and 5% dextrose with additional potassium chloride [10-20 mEq/L]) to counter dehydration and maintain fluid balance. Monitoring of electrolyte changes is advisable. Most dogs that survive the first 2-3 days of disease recover. Persistent vomiting can be controlled with metoclopramide, 0.2-0.5 mg/kg, q.i.d., PO or SC, or 1-2 mg/kg/day, slow IV).
Routine use of antibiotics is discouraged. In more severe cases (eg, those with severe blood loss, fever, or loss of intestinal integrity), intestinal integrity is compromised, and these dogs are predisposed to bacteremia and septicemia. In these cases, trimethoprim-sulfa (15 mg/kg, b.i.d., SC or PO) for 5-10 days is advisable; in more severe cases, ampicillin (20 mg/kg, t.i.d., IV) and gentamicin (2.2 mg/kg, t.i.d., SC) for a maximum of 5 days is advisable.
Food and water should be withheld until vomiting has subsided. After this, small amounts of a bland diet (eg, cottage cheese and rice or a commercially available prescription diet such as Canine i/d-® [Hill's]) should be offered frequently. A small volume of warm, salted meat broth should be given concurrently. If GI signs recur after feeding, the dog should be fasted for an additional 12-24 hr before feeding again. If food can be tolerated, the bland diet is continued for 7-14 days, after which the dog's regular diet can be gradually reintroduced.
Prevention and Control: Contaminated areas should be thoroughly cleaned. Household bleach (1:30 dilution) or commercial products labeled for use against parvovirus are potent inactivators of the virus. The same solutions may be used as foot baths to disinfect boots. Disinfection of hands, clothing, and food and water bowls is recommended. Pups should be kept isolated from adult dogs returning from shows or field trials.
Vaccination is critical in the control of the disease. Variants of the virus have appeared since the disease was first recognized, but current vaccines protect dogs against all strains of the virus. Vaccines containing live attenuated canine parvovirus generally induce more effective immunity than inactivated virus vaccines. The high-titer canine parvovirus vaccines now available effectively protect puppies against viral challenge, even during the period when maternal antibody titers remain high enough to interfere with active immunization but have declined enough to predispose pups to infection. Three doses of vaccine are recommended at 6, 9, and 12 wk of age.
Infectious Canine Hepatitis
Introduction: Infectious canine hepatitis (ICH) is a worldwide, contagious disease of dogs with signs that vary from a slight fever and congestion of the mucous membranes to severe depression, marked leukopenia, and prolonged bleeding time. It also occurs in foxes, wolves, coyotes, and bears; other carnivores may become infected without developing clinical illness.
Etiology and Pathogenesis: ICH is caused by a nonenveloped DNA virus, canine adenovirus 1 (CAV-1), which is antigenically related only to CAV-2 (one of the causes of infectious canine tracheobronchitis). CAV-1 is resistant to lipid solvents and survives outside the host for weeks or months, but a 1-3% solution of sodium hypochlorite (household bleach) is an effective disinfectant.
Ingestion of urine, feces, or saliva of infected dogs is the main route of infection. Recovered dogs shed virus in their urine for > or = 6 mo. Initial infection occurs in the tonsillar crypts and Peyer's patches, followed by viremia and infection of endothelial cells in many tissues. Liver, kidneys, spleen, and lungs are the main target organs. Chronic kidney lesions and corneal clouding ("blue eye") result from immune-complex reactions after recovery from acute or subclinical disease.
Clinical Findings: Signs vary from a slight fever to death. The mortality rate is highest in very young dogs. The incubation period is 4-9 days. The first sign is a fever of >104° F (40° C), which lasts 1-6 days and is usually biphasic. If the fever is of short duration, leukopenia may be the only other sign, but if it persists for >1 day, acute illness develops. Tachycardia out of proportion to the fever may occur. On the day after the initial temperature rise, leukopenia develops and persists throughout the febrile period. The degree of leukopenia varies and seems to be correlated with the severity of illness.
Signs are apathy, anorexia, thirst, conjunctivitis, serous discharge from the eyes and nose, and occasionally abdominal pain and vomiting. Intense hyperemia or petechiae of the oral mucosa, as well as enlarged tonsils, may be seen. There may be subcutaneous edema of the head, neck, and trunk.
Clotting time is directly correlated with the severity of illness. It may be difficult to control hemorrhage, which is manifest by bleeding around deciduous teeth and by spontaneous hematomas, because of underlying disseminated intravascular coagulation. Respiratory signs usually are not seen in dogs with ICH; however, CAV-1 has been recovered from dogs with signs of infectious tracheobronchitis and from dogs with respiratory signs induced by exposure to the nebulated isolate. Although CNS involvement is unusual, the severely infected dog may have a terminal convulsion, and brain-stem hemorrhages are common. Foxes more consistently have CNS signs and intermittent convulsions during the course of illness, and terminal paralysis may involve one or more limbs or the entire body.
On recovery, dogs eat well but regain weight slowly. Seven to 10 days after the acute signs disappear, ~25% of recovered dogs develop bilateral corneal opacity, which usually disappears spontaneously. In mild cases of ICH, transient corneal opacity may be the only sign of disease.
Chronic hepatitis may develop in dogs having low levels of passive antibody when exposed. Simultaneous infection with CAV-1 and distemper virus is sometimes seen.
Lesions: Endothelial damage results in "paint brush" hemorrhages on the gastric serosa, lymph nodes, thymus, pancreas, and subcutaneous tissues. Hepatic cell necrosis produces a variegated color change in the liver, which may be normal in size or swollen. The gallbladder wall may be edematous and thickened; edema of the thymus may be found. Grayish white foci may be seen in the kidney cortex.
Treatment: Blood transfusions may be necessary in severely ill dogs. In addition, 5% dextrose in isotonic saline should be given, preferably IV. In dogs with prolonged clotting time, SC administration of fluids may be dangerous. A broad-spectrum antibiotic should be given. Because tetracyclines may cause discoloration of the teeth during tooth development, they should not be used in puppies before their permanent teeth erupt. Although the transient corneal opacity (which may occur during the course of ICH or be associated with vaccination with attenuated CAV-1 vaccines) usually requires no treatment, atropine ophthalmic ointment may alleviate the painful ciliary spasm that is sometimes associated with it. The dog should be protected against bright light if corneal clouding occurs. Systemic corticosteroids are generally contraindicated for treatment of corneal opacity associated with ICH.
Prevention: Modified live virus vaccines are available and are often combined with other vaccines. Vaccination against ICH is recommended at the time of canine distemper vaccinations. Attenuated CAV-1 vaccines have produced transient unilateral or bilateral opacities of the cornea, and the virus may be shed in urine. CAV-2 attenuated live virus strains, which provide cross protection against CAV-1, are preferentially used because they have very little tendency to produce corneal opacities or uveitis, and the virus is not shed in urine. Annual revaccination against ICH is often practiced. Maternal antibody from immune bitches interferes with active immunization in puppies until they are 9-12 wk old.
Infectious Tracheobronchitis of Dogs (Kennel cough)
Introduction: Infectious tracheobronchitis results from inflammation of the upper airways. Generally, it is a mild, self-limiting disease but may progress to fatal bronchopneumonia in puppies or to chronic bronchitis in debilitated adult or aged dogs. The illness spreads rapidly among susceptible dogs housed in close confinement, eg, veterinary hospitals or kennels.
Etiology: Canine parainfluenza virus, canine adenovirus 2 (CAV-2), or canine distemper virus can be the primary or sole pathogen involved. Canine reoviruses (types 1, 2, and 3), canine herpesvirus, and canine adenovirus 1 (CAV-1) are of questionable significance in this syndrome. Bordetella bronchiseptica may act as a primary pathogen, especially in dogs <6 mo old; however, it and other bacteria (usually gram-negative organisms such as Pseudomonas sp, Escherichia coli, and Klebsiella pneumoniae) may cause secondary infections after viral injury to the respiratory tract. Concurrent infections with several of these agents are common. The role of Mycoplasma sp has not been clearly established. Stress and extremes of ventilation, temperature, and humidity apparently increase susceptibility to, and severity of, the disease.
Clinical Findings and Diagnosis: The prominent clinical sign is paroxysms of a harsh, dry cough, which may be followed by retching and gagging. The cough is easily induced by gentle palpation of the larynx or trachea. Affected dogs demonstrate few if any additional clinical signs except for partial anorexia. Body temperature and WBC counts usually remain normal. Development of more severe signs, including fever, purulent nasal discharge, depression, anorexia, and a productive cough, especially in puppies, indicates a complicating systemic infection such as distemper or bronchopneumonia. Stress, particularly due to adverse environmental conditions and improper nutrition, may contribute to a relapse during convalescence.
Tracheobronchitis should be suspected whenever the characteristic cough suddenly develops 5-10 days after exposure to other susceptible or affected dogs. Usually severity diminishes during the first 5 days, but the disease persists for 10-20 days. Tracheal trauma secondary to intubation may produce a similar but generally less severe syndrome.
Treatment: Preferably, affected dogs should not be hospitalized because the disease is usually highly contagious (and also self-limiting). Appropriate management practices, including good nutrition, hygiene, and nursing care, as well as correction of predisposing environmental factors, hasten recovery. Cough suppressants containing codeine derivatives, such as hydrocodone (0.25 mg/kg body wt, every 6-12 hr, PO) or butorphanol (0.05-0.1 mg/kg, every 6-12 hr, PO or SC), should be used only as needed to control persistent nonproductive coughing. Antibiotics are usually not needed except in severe chronic cases; cephalosporins, chloramphenicol, and tetracycline are preferable because they reach effective concentrations in the tracheobronchial mucosa. When needed, the antibiotic should be selected by culture and sensitivity tests of specimens collected by transtracheal aspiration or bronchoscopy. Antibiotics given PO or IM may not significantly reduce the numbers of B bronchiseptica in the distal trachea or major bronchi. Thus, in severely affected dogs that are not responsive to parenteral antibiotics, kanamycin sulfate (250 mg) or gentamicin sulfate (50 mg) diluted in 3 mL of saline may be administered by aerosolization b.i.d. for 3 days. Aerosolization treatment should be preceded by administration of bronchodilators. Endotracheal injection of antibiotics (eg, gentamicin) is a possible alternative to aerosolization. Corticosteroids may help alleviate clinical signs but should be used concurrently with an antibacterial agent; they are contraindicated in severely ill, coughing dogs.
Prevention: Dogs should be immunized with modified live virus vaccines against distemper, parainfluenza, and CAV-2, which also provides protection against CAV-1. Commercial products frequently combine these agents and often include modified live parvovirus and leptospiral antigen vaccines. An initial vaccination should be given at 6- 8 wk and repeated twice at 3- to 4-wk intervals until the dog is 14-16 wk old. Revaccination should be performed annually. When the risk of B bronchiseptica infection is considered to be significant, use of a live, avirulent, intranasal vaccine is preferable to parenteral products containing inactivated bacteria or bacterial extracts. A combination of an avirulent B bronchiseptica and a modified live parainfluenza vaccine is available for intranasal use. One inoculation is administered (intranasally) to puppies >3 wk old.
Leptospirosis in Dogs
(Canine typhus, Stuttgart disease, Infectious jaundice)
Introduction: The most common Leptospira serovars infecting dogs were reported to be canicola and icterohaemorrhagia in older studies, but pomona and grippotyphosa have been the most common isolated in recent studies. This shift may represent exposure of pet dogs to infected wildlife such as raccoons and opossums, which inhabit suburban and urban areas.
Clinical Findings: Dog of all ages may be affected, and there is no sex predilection. The incubation period is 4-12 days. Nonspecific signs such as fever, depression, anorexia, and generalized pain may be seen during this time. Vasculitis, thrombocytopenia, and coagulopathy may develop. Within a few days, additional signs of uremia such as dehydration, vomiting, and oral ulceration, are seen. The liver is variably affected, and the degree of icterus often reflects the severity of the disease. Meningitis, uveitis, and abortion have been rarely reported.
Hematologic abnormalities include leukocytosis, lymphopenia, monocytosis, and thrombocytopenia. Serum chemistry may reveal azotemia and electrolyte disturbances secondary to the renal failure, including hyponatremia, hypochloremia, and hyperphosphatemia. Serum levels of hepatic enzymes (AST, ALT, alkaline phosphatase) and serum bilirubin increases if the liver is affected. Urine sediment usually contains RBC, WBC, and granular casts. Isosthenuria, proteinuria, and glucosuria reflect tubular damage.
Lesions: In acute disease, the kidneys or liver, or both are swollen. Hemorrhages may be present in any organ. Other lesions may include any of those seen with acute uremia. In chronic cases, white or gray foci or streaks may be seen in the kidney and liver. Histologically, lesions in acute disease are those of acute uremia, including acute interstitial nephritis and possible hepatitis. In chronic disease, the only lesions may be chronic interstitial nephritis or chronic active hepatitis, or both.
Treatment: Renal failure and liver disease are treated with fluid therapy and other supportive measures to maintain normal fluid, electrolyte, and acid-base balance. Antibiotic therapy consists of penicillin, tetracycline, or doxycycline to eliminate leptospiremia, followed by tetracycline or doxycycline to eliminate the renal carrier phase. Tetracycline should be used with caution in azotemic animals. The fluoroquinolone antibiotics such as enrofloxacin also appear to be leptospirocidal.
Prevention/Prophylaxis: To reduce the chances of exposure, owners are advised to engage in rodent control and keep their dogs leashed. During epidemics, confinement to the owner's premises should be recommended. Bivalent bacterins are available and should be administered q6-8mo to maintain a protective titer for dogs at high risk, e.g., show, stud, or hunting dogs. If leptospirosis is diagnosed in a kennel, treatment and vaccination of all dogs in the kennel should be considered. Dogs in contact with wildlife should receive bacterins containing grippotyphosa and pomona antigens.
-Rabies
Introduction: Rabies is an acute viral encephalomyelitis that principally affects carnivores and insectivorous bats, although it can affect any mammal. It is almost invariably fatal once clinical signs appear. Although rabies occurs throughout the world, a few countries are free of the disease due to successful eradication programs or to their island status and enforcement of rigorous quarantine regulations.
Etiology and Epidemiology: Rabies is a rhabdovirus that characteristically is confined to one species in a given geographic area, although extension to other species is common. Identification of different variants, or ecotypes, by laboratory procedures such as monoclonal antibody analysis and polymerase chain reaction (PCR) has greatly enhanced understanding of rabies epidemiology. Generally, each ecotype is responsible for rabies transmitted between members of the same species in a given geographic area. From an epidemiologic perspective, it is preferable to use the name of the species acting as the reservoir as an adjective: rabies maintained by dog-to-dog transmission is canine rabies, whereas rabies in a dog as a result of extension from a different reservoir, eg, skunk (or fox), should be referred to as skunk (or fox, etc) rabies in a dog.
No cat-to-cat transmission of rabies has been recorded, and no feline ecotype is known. However, cats are very susceptible to all ecotypes, and extension is common. Virus is present in the saliva of rabid cats, and there have been reports of people developing rabies after being bitten by a rabid cat. Reported cases in domestic cats have outnumbered those in dogs in the USA every year since 1987.
Transmission and Pathogenesis: Transmission is almost always by introduction of virus-laden saliva into the tissues, usually by the bite of a rabid animal. However, virus from saliva or tissue fluids may be introduced into fresh wounds or through intact mucous membrane (eg, ingestion). Virus may be present in the saliva and transmitted by an infected animal several days before onset of clinical signs (usually 3-5 days in domestic dogs and cats and up to 8 days in striped skunks). Rabies virus has not been isolated from skunk musk (spray).
The incubation period is both prolonged and variable; typically, the virus remains at the inoculation site for a considerable time. The unusual length of the incubation period is why postexposure treatment, including in man the practice of locally infiltrating hyperimmune serum, is possible. Most cases in dogs occur within 21-80 days after exposure, but the incubation period may be shorter or considerably longer.
After replication within muscle cells near the site of inoculation, the virus travels via the peripheral nerves to the spinal cord and ascends to the brain. After reaching the brain, the virus usually travels efferently via peripheral nerves to the salivary glands. Therefore, it is assumed that if an animal was capable of transmitting rabies via its saliva, virus will be detectable in the brain.
Clinical Findings: Clinical signs of rabies are rarely definitive. Rabid animals of all species exhibit typical signs of CNS disturbance, with minor variations among species. The most reliable signs, regardless of species, are behavioral changes and unexplained paralysis. Behavioral changes may include anorexia, signs of apprehension or nervousness, irritability, and hyper excitability (including priapism). The animal may seek solitude. Ataxia, altered phonation, and changes in temperament are apparent. Uncharacteristic aggressiveness may develop-a normally docile animal may suddenly become vicious. Commonly, rabid wild animals lose their fear of man, and species that are normally nocturnal may be seen wandering about during the daytime.
The clinical course is divided into three phases-prodromal, excitative, and paralytic. However, this division is of limited practical value because of the variability of signs and the irregular lengths of the phases. During the prodromal period, which lasts 1-3 days, animals show only vague CNS signs, which intensify rapidly. The disease progresses rapidly after the onset of paralysis, and death is virtually certain within 10 days after the initial onset of signs. Some animals die rapidly without marked clinical signs.
The term "furious rabies" refers to animals in which aggression (the excitative phase) is pronounced. "Dumb or paralytic rabies" refers to animals in which the behavioral changes are minimal or absent, and the disease is manifest principally by paralysis.
Furious Form: This is the classical "mad-dog syndrome," although it occurs in all species. There is rarely any evidence of paralysis during this stage. The animal becomes irrational and, with the slightest provocation, may viciously and aggressively use its teeth, claws, horns, or hooves. The posture and expression is one of alertness and anxiety, with pupils dilated. Noise invites attack. Such animals lose all caution and fear of natural enemies. Carnivores with this form of rabies frequently roam extensively, attacking other animals, including people, and any moving object. They commonly swallow foreign objects, e.g., feces, straw, sticks, and stones. Rabid dogs chew the wire and frame of their cages, breaking their teeth, and will follow a hand moved in front of the cage, attempting to bite. Young pups apparently seek human companionship and are overly playful, but bite even when petted, usually becoming vicious in a few hours. Rabid skunks appear to seek out and attack litters of puppies or kittens. Rabid domestic cats and bobcats attack suddenly, biting and scratching viciously. As the disease progresses, muscular incoordination and seizures are common. Death is the result of progressive paralysis.
Paralytic Form: This is first manifest by paralysis of the throat and masseter muscles, often with profuse salivation and inability to swallow. Dropping of the lower jaw is common in dogs. Owners frequently examine the mouth of dogs and livestock searching for a foreign body or administer medication with their bare hands, thereby exposing themselves to rabies. These animals are not vicious and rarely attempt to bite. The paralysis progresses rapidly to all parts of the body, and coma and death follow in a few hours.
Control: Comprehensive guidelines for control in dogs have been prepared by the World Health Organization and include the following: 1) notification of suspected cases, and destruction of dogs with clinical signs and dogs bitten by a suspected rabid animal; 2) reduction of contact rates between susceptible dogs by leash laws, dog movement control, and quarantine; 3) mass immunization of dogs by campaigns and by continuing vaccination of young dogs; 4) stray dog control and destruction of unvaccinated dogs with low levels of dependency on, or restriction by, man; and 5) dog registration.
The Compendium of Animal Rabies Control, compiled and updated annually by the National Association of State Public Health Veterinarians (NASPHV), summarizes the most current recommendations for the USA and lists all USDA-licensed rabies vaccines. Many effective vaccines, both modified live virus and inactivated types, are available for use in dogs throughout the world; in the USA, all currently marketed vaccines (for any species) are inactivated. Recommended vaccination frequency is 1 or 3 yr. Several vaccines are also available for use in cats, and a few for use in ferrets, horses, cattle, and sheep. Because of the increasing importance of rabies in cats, vaccination of cats is extremely important. No vaccine is approved for use in wildlife kept as pets, and protective immunity from the commercially available vaccines has not been demonstrated in these species.
Management of Suspected Rabies Cases-Exposure of Pets: Where terrestrial wildlife or bat rabies is known to occur, any animal bitten or scratched by a wild, carnivorous mammal (or a bat) not available for testing should be regarded as having been exposed to rabies. The NASPHV recommends that any unvaccinated dog or cat exposed to rabies be destroyed immediately. If the owner is unwilling to do this, the animal should be placed in strict isolation for 6 mo and vaccinated against rabies 1 mo before release. Some rabies authorities recommend vaccination at the beginning of the isolation period. If an exposed animal is currently vaccinated, it should be revaccinated immediately and closely observed for 45 days.
Canine Herpesviral Infection
Introduction: Canine herpesvirus is a fatal, viral infection of puppies worldwide. It also may be associated with upper respiratory infection or a vesicular vaginitis or posthitis in adult dogs. Only canids (dogs, wolves, coyotes) are known to be susceptible.
Etiology: The disease is caused by an enveloped DNA canine herpesvirus (CHV), which is sensitive to lipid solvents and most disinfectants. CHV is relatively unstable outside the host. Transmission usually occurs by contact between susceptible puppies and the infected oral, nasal, or vaginal secretions of their dam or oral or nasal secretions of dogs allowed to commingle with puppies during the first 3 wk of life. In utero transmission may occur. Infection of newborn susceptible puppies results in replication of CHV in the surface cells of the nasal mucosa, pharynx, and tonsils. If the pups become hypothermic, viremia and invasion of visceral organs occur.
Clinical Findings: Deaths due to CHV infection usually occur in puppies 1-3 wk old, occasionally in puppies up to 1 mo old, and rarely in pups as old as 6 mo Typically, onset is sudden, and death occurs after an illness of <24 hr. Older dogs exposed to or experimentally inoculated with CHV may develop a mild rhinitis or a vesicular vaginitis or posthitis. In utero infections may be associated with abortions, stillbirths, and infertility.
Diagnosis: CHV infection may be confused with infectious canine hepatitis, but it is not accompanied by the thickened, edematous gallbladder often associated with the latter. The focal areas of necrosis and hemorrhage, especially those that occur in the kidneys, distinguish it from hepatitis and neosporosis. CHV causes serious disease only in very young puppies. The rapid death and characteristic lesions distinguish it from canine distemper. The virus can be isolated from fresh lung, liver, kidney, and spleen by cell culture techniques. The tissues should be submitted to the laboratory refrigerated but not frozen.
Control: No vaccine is available. Infected bitches develop antibodies, and litters subsequent to the first infected litter receive maternal antibodies in the colostrum. Puppies that receive maternal antibodies may be infected with the virus, but disease does not result. Removal of puppies from affected bitches by cesarean section and rearing them in isolation has prevented deaths under experimental conditions. However, infections have been noted even in puppies delivered by cesarean section. Deaths may be reduced when infected puppies are reared in incubators at increased temperatures (95°F [35°C], 50% relative humidity) and given adequate fluids and supportive therapy. The prognosis of puppies that survive neonatal infections of CHV is guarded because damage to lymphoid organs, brain, kidneys, and liver may be irreparable.
