A Little about each of the major infectious diseases in cats
Note; some of the following descriptions of these diseases were copied from professional handouts and contain a lot of medical terms...but they are well written and highly informative. Unfortunately, I don't know who the author(s) are in order to give them credit. But thanks.
Feline Leukemia
Introduction: Despite the widespread use of vaccines, feline leukemia virus (FeLV) remains one of the most important causes of disease and death in cats. It causes a variety of malignancies, but persistent infection can also cause severe immunosuppression and profound anemia. The virus is present worldwide.
The incidence of FeLV infection is directly related to the population density of cats. Infection rates are highest in catteries and multicat households, especially when cats have access to the outdoors. In the USA, 1-2% of seemingly healthy stray cats are persistently viremic.
Persistently infected, seemingly healthy cats are the major reservoir of FeLV. Carriers excrete large quantities of virus in saliva. Lesser amounts of virus are excreted in tears, urine, and feces. Oronasal contact with infectious saliva or urine is the most likely mode of transmission. Nose-to-nose contact, mutual grooming, and shared litter trays and food dishes facilitate transmission. Bite wounds from infected cats are an efficient mode of transmission but occur relatively infrequently in cats kept indoors 100% of the time. Bites may be a more important mode of transmission in indoor-outdoor cats.
Age resistance is significant. Young kittens are much more susceptible than adults. The virus may be transmitted vertically (in utero or by milk) or horizontally (by secretions and excretions). Because FeLV is a fragile, enveloped virus and because of age resistance, horizontal transmission between adults usually requires prolonged, intimate contact. In addition, the dose required for oronasal transmission of the virus is relatively high.
Disorders Caused by FeLV: FeLV-related disorders are numerous and include immunosuppression, neoplasia, anemia, immune-mediated diseases, reproductive problems, and enteritis.
Treatment: Ideally, an FeLV-infected cat would be identified early and treated to eradicate its infection before FeLV-related diseases had time to develop. Unfortunately, eradication of retroviral infections at any stage of disease is extremely difficult. Most infected cats are persistently viremic by the time their infection is diagnosed. Persistent viremia is notoriously difficult to reverse. In addition, FeLV-related disease(s) may already be present at the time of diagnosis, further complicating therapeutic efforts.
Antiviral drugs based on nucleoside analogs have, in general, been of little benefit in the management of FeLV-infected cats. Although AZT at 20 mg/kg, PO, t.i.d., can prevent the development of persistent viremia if given shortly after viral inoculation, it is of little benefit when given to persistently viremic cats. However, in recent studies, the degree of antigenemia was reduced in naturally infected cats treated with AZT at 5 mg/kg, SC, b.i.d., or with PMEA (9-[2-phosphonylmethoxyethyl]adenine) at 2.5 mg/kg, SC, b.i.d. Unfortunately, both AZT and PMEA cause adverse hematologic effects. In another study, PMEA (>6.25 mg/kg/day, SC) enabled cats to resist infection with FeLV.
Interferon, up to 1.6 x 106 u/kg, SC, s.i.d., has been given alone and in combination with AZT (20 mg/kg, PO, t.i.d.) to FeLV-infected cats. In this study, the degree of antigenemia was significantly decreased, beginning 2 wk after treatment with human recombinant interferon alpha-2b, either alone or in combination with AZT administered PO. AZT alone had no effect on the degree of antigenemia. Unfortunately, rapid development of antibodies directed against the interferon molecule limited the efficacy of this treatment to a period of 7 weeks.
In another study, ultralow doses of leukocyte-derived human interferon-ª were given to FeLV-infected cats (0.5 or 5.0 u, PO, s.i.d. for 7 days, every other week for 4 wk). Although the treatment was not effective in preventing persistent viremia, mean survival time was significantly increased in treated cats compared with placebo-treated controls. The lower dose was more efficacious than the higher dose.
Staphylococcal protein A is a bacterial cell wall component that binds the Fc portion of IgG. In one study, extracorporeal immunoadsorption of plasma from FeLV-infected cats was reported. In a few infected cats, viremia was reversed and lymphoma regression was induced. Staphylococcal protein A has also been given (6.6 mg/kg, IV, twice weekly with prednisone) for the treatment of hemolytic anemia associated with FeLV infection.
Other therapeutic options, including acemannan, BCG, diethylcarbamazine, levamisole, mixed bacterial toxins, muramyl peptides, killed parapoxvirus preparations, Propionibacterium acnes, and suramin, have been recommended for consideration in the treatment of FeLV-infected cats. However, relatively little work has been done to establish their efficacy. FeLV-induced lymphoid malignancies can be treated using combinations of antineoplastic drugs; most protocols include prednisone, vincristine, and cyclophosphamide.
Many Leukemia positive cats die from the disease within days to months of making the diagnosis, but many FeLV-positive cats remain completely healthy for years. There is no clear evidence that healthy FeLV-positive cats benefit from any form of therapy during this period. Stress and sources of secondary infection should be avoided. The cat should remain indoors 100% of the time to reduce the risk of exposure to infectious agents and to prevent the infected cat from acting as a source of infection to other cats. Owners should be advised to watch for signs of FeLV-related disease, particularly secondary infections. If an FeLV-related disease develops, it should be diagnosed and aggressively treated.
Prevention and Control: A test and removal program to rid catteries and multicat households of FeLV can be extremely effective if these guidelines are carefully followed: 1) All cats should be tested for FeLV viremia (IFA is best). 2) All viremic cats should be removed. 3) All dishes, litterpans, and bedding should be disinfected. 4) All movement of cats in and out of the cattery should be prevented. 5) All cats should be retested after 12 weeks to detect cats that may have been incubating the virus at the time of the first test. 6) The quarantine can be lifted when all cats have tested negative on two consecutive occasions, 12 weeks apart. 7) All cats should be tested and quarantined before introduction to the cattery. Ideally, two tests 12 wk apart should be done. 8) Breeding should be only to cats known to be FeLV-negative, and cats should be introduced only from FeLV-negative colonies.
FeLV vaccines are intended to protect cats against FeLV infection or, at least, to prevent persistent viremia. Types of vaccines include killed whole virus, subunit, and genetically engineered. Vaccines may vary in protective effect, and manufacturers' claims and independent comparative studies should be carefully noted. The following guidelines for vaccine use have been recommended: 1) Only healthy, afebrile (no fevers) cats should be vaccinated. 2) Cats from a high-risk or unknown background should be tested for FeLV before vaccination. 3) All cats at risk of exposure to FeLV should be vaccinated. 4) Positive and Negative cats should be kept separated, even if the negative cats have been vaccinated.
Feline Panleukopenia (Feline infectious enteritis, Feline distemper)
Introduction: Feline panleukopenia is a highly contagious, often fatal, viral disease of cats; it is most severe in kittens. The disease is seen relatively uncommonly by veterinarians, presumably as a consequence of the widespread use of effective vaccines. However, infection rates remain high in feral, un-vaccinated feline populations.
Etiology, Transmission, and Pathogenesis: The causative parvovirus (feline panleukopenia virus [FPV]) infects and destroys actively dividing cells of all Felids and some members of related families (raccoon, mink, coatimundi, and kinkajou). Rapidly dividing cells in bone marrow, lymphoid tissues, intestinal epithelium, and in very young animals, cerebellum and retina are most affected. In pregnant queens, the virus may spread transplacentally to infect rapidly dividing embryonic or fetal cells, which leads to embryonic death, mummification, abortion, and stillbirth.Alternatively, infection of kittens in the perinatal period may destroy the germinal epithelium of the cerebellum, which leads to cerebellar hypoplasia, incoordination, and tremor. Feline cerebellar ataxia has become a relatively rare diagnosis, because most queens provide protective passive immunity to their kittens during the period of susceptibility.
Virus particles are abundant in all secretions and excretions during the acute phase of illness and may be shed in the feces of survivors for up to 6 wk after recovery. The virus is extremely resistant to inactivation; it may survive > or = 1 yr in a suitable environment and can be transported via fomites (e.g., shoes, clothing, food bowls). However, it can be destroyed by a 6% solution of bleach (aqueous sodium hypochlorite). Cats are infected via the oronasal route by exposure to infected animals or their secretions or to fomites. Most free-roaming cats are exposed to the virus during their first year of life. Those that develop subclinical infection or survive acute illness usually mount a robust, protective immune response.
Clinical Findings: Most infections are subclinical or not obvious. Those cats that do manifest signs of illness are usually <1 yr old. Typically, fever, depression, and anorexia develop after an incubation period of 2-7 days. Vomiting may develop 1-2 days after the onset of fever; it is usually bilious and unrelated to eating.
Diarrhea tends to begin a little later. Extreme dehydration develops rapidly, even in the face of continued drinking. Physical examination reveals severe depression, dehydration, and sometimes abdominal pain. Abdominal palpation may induce vomiting. Thickened, turgid intestinal loops and mesenteric lymphadenopathy may be palpable. In young animals with cerebellar involvement, ataxia and tremors with normal mentation may be seen. Retinal lesions, if present, appear as discrete gray foci. The duration of illness seldom exceeds 5-7 days. Indeed, young kittens with peracute panleukopenia often die within 24 hr of the onset of observed clinical signs. Mortality is high, especially in young kittens; losses of 25-90% are typical.
Differential diagnoses include other causes of profound depression, panleukopenia, and GI signs. Salmonellosis, feline leukemia virus (FeLV), and feline immunodeficiency virus infections should be considered. There is recent evidence to suggest that the panleukopenia-like syndrome previously associated with FeLV infection is in fact caused by concurrent FeLV and FPV infections.
Lesions: There may be few gross lesions in peracute cases, although typically, dehydration and emaciation are marked. The earliest changes are edema and necrosis of the thymus and mesenteric lymph nodes. The bone marrow may appear semifluid and fatty. The bowel walls are usually thickened and turgid; excessive gas may be present in some bowel loops. The serosal surfaces of severely affected bowel loops may be hyperemic, with ecchymotic or petechial hemorrhages. The liver, kidneys, and spleen may appear slightly swollen. Histologically, the intestinal crypts are usually dilated and contain debris consisting of sloughed necrotic epithelial cells. Blunting and fusion of villi may be present. Degeneration of hepatocytes and renal tubular epithelial cells is seen. Eosinophilic intranuclear inclusion bodies may be found in tissues in which viral replication has occurred.
Treatment and Prevention: Successful treatment of acute cases requires careful monitoring, vigorous fluid therapy, and supportive care. Electrolyte disturbances, acidosis, hypoglycemia, hypoproteinemia, anemia, and systemic infections commonly develop in severely ill cats infected with FPV, and appropriate treatment should be administered. In addition to vigorous crystalloid infusion, transfusion of plasma or whole blood from an immune cat will help support plasma oncotic pressure, as well as provide some passive immunity. Parenteral, broad-spectrum antibiotic therapy is appropriate; however, nephrotoxic drugs (eg, gentamicin, amikacin) should be avoided or used with great care in dehydrated cats. Antiemetic therapy (eg, metoclopramide) may provide some relief and allow earlier enteral feeding. Parenteral nutrition may be beneficial in some cases.
Excellent inactivated and modified live vaccines are available for prevention of FPV infection. Live vaccines should not be given to cats that are pregnant, immunosuppressed, or sick, or to kittens <4 wk old. Most vaccine manufacturers recommend that kittens should be vaccinated at 8-10 wk of age and again at 12-14 wk, with annual revaccination thereafter. The last vaccination of the initial series should be given after the kitten is l2 wk old because transferred maternal passive immunity may compromise efficacy if the vaccine is given earlier. Exposure to virus should be avoided until 2 wk after the initial vaccination series has been completed. Vaccination provides solid, long-lasting (perhaps lifelong) immunity.
-Feline Respiratory Disease Complex
Introduction: Feline respiratory disease complex includes those illnesses typified by rhinitis, conjunctivitis, lacrimation, salivation, and oral ulcerations. The principal diseases, feline viral rhinotracheitis (FVR) and feline calicivirus (FCV) infections, affect exotic as well as domestic species. Feline pneumonitis (Chlamydia psittaci) and mycoplasmal infections appear to be of lesser importance. Feline infectious peritonitis and pleuritis typically causes a more generalized condition but may cause signs of mild upper respiratory tract infection. FVR and caliciviruses are host-specific and pose no known human risk. Human conjunctivitis caused by the feline chlamydial agent has been reported.
Etiology: Probably 40-45% of feline upper respiratory infections are caused by FVR virus, which is a herpesvirus; incidence of FCV is similar. Dual infections with these viruses are common. Other organisms such as Chlamydia psittaci, Mycoplasma spp, and reoviruses are believed to account for most of the remaining infections.
Natural transmission of these agents occurs via aerosol droplets and fomites, which can be carried to a susceptible cat by a handler. Convalescent cats may continue to harbor virus for many months. Calicivirus is shed continuously, while infectious FVR virus is released intermittently. Stress may precipitate a secondary course of illness. The incubation period is 2-6 days for FVR and FCV, and 5-10 days for pneumonitis.
Clinical Findings: The onset of FVR is marked by fever, frequent sneezing, conjunctivitis, rhinitis, and often salivation. Excitement or movement may induce sneezing. The fever may reach 105°F (40.5°C) but subsides and tends to fluctuate from normal to 103°F (39°C). Initially, a serous nasal and ocular discharge occurs; it soon becomes mucopurulent and copious, at which time depression and anorexia are evident. Severely debilitated cats may develop ulcerative stomatitis, and ulcerative keratitis occurs in some. Signs may persist for 5-10 days in milder cases and up to 6 wk in severe cases. Generally, the mortality is low and prognosis good except for young kittens and aged cats. The illness often is prolonged, and a marked weight loss may occur. FVR often is complicated by secondary bacterial infections; abortions and generalized infections have been associated with it.
There are many serologically related strains of feline caliciviruses. They appear to have a predilection for the epithelium of the oral cavity and the deep tissues of the lungs. Some caliciviruses are nonpathogenic. Some induce little more than salivation and ulceration of the tongue, hard palate, or nostrils; others produce pulmonary edema and interstitial pneumonia. Two strains may produce a transient "limping syndrome" without signs of oral ulceration or pneumonia. These latter two strains produce a transient fever, alternating leg lameness, and pain on palpation of affected joints. These signs occur most often in 8- to 12-wk-old kittens and usually resolve without treatment. The syndrome may occur in kittens vaccinated against FCV because no vaccine protects against both strains of the caliciviruses that produce the "limping syndrome."
Calicivirus has also been found in cats with lymphocytic-plasmacytic gingivitis and stomatitis. The superficial lesions heal rapidly, and the infected cat regains appetite 2-3 days after onset. The clinical course usually is 7-10 days. An acute febrile response, inappetence, and depression are common signs. Serous rhinitis and conjunctivitis also can occur.
Chlamydia psittaci infections characteristically produce conjunctivitis; infected cats sneeze occasionally. Fever may occur as the disease progresses beyond serous lacrimal discharge to mucopurulent conjunctivitis, lymphoid infiltration, and epithelial hyperplasia. Convalescent cats may undergo relapses.
Mycoplasma may infect the eyes and upper respiratory passages, characteristically producing severe edema of the conjunctiva and a less severe rhinitis.
The occurrence of severe viral upper respiratory disease is rare in adult, properly vaccinated cats. These cats should be tested for concurrent immunodeficiency diseases, including feline leukemia virus and feline immunodeficiency virus.
Lesions: Lesions generally are confined to the respiratory tract, conjunctivae, and oral cavity. In FVR, the conjunctivae and nasal mucous membranes are reddened, swollen, and covered with a serous to purulent exudate. In severe cases, focal necrosis of these membranes may occur. The larynx and trachea may be mildly inflamed. The lungs may be congested, with small areas of consolidation; however, pulmonary changes are rarely remarkable in FVR except possibly in stressed, young kittens. The characteristic histologic lesion of FVR is the acidophilic intranuclear inclusion body. During the early stage of the illness, inclusions may be present in sites of epithelial necrosis on the tongue, nasal membranes, tonsils, epiglottis, trachea, and nictitating membranes. Inclusion bodies are transitory. Inclusions do not occur in calicivirus infections.
The characteristic lesion caused by FCV is ulceration of the oral mucosa. Lesions on the tongue or hard palate initially may appear as vesicles, which subsequently rupture. Ulcerations are occasionally found on the epithelium covering the median nasal septum. The more virulent caliciviruses destroy epithelial cells of the bronchioles and alveoli, which causes acute pulmonary edema that progresses through seropurulent bronchiolar hyperplasia and interstitial pneumonia. Early in the clinical course of feline pneumonitis, the causative organism may be identified in Giemsa-stained conjunctival smears or scrapings. The elementary bodies are intracytoplasmic. Mycoplasmas occur as extracellular coccoid bodies often seen on the surface of conjunctival epithelial cells.
Treatment: Treatment is largely symptomatic and supportive, but broad-spectrum antibiotics are useful against secondary bacterial invaders as well as directly against C psittaci. Tetracyclines are the most effective against C psittaci. Nasal and ocular discharges should be removed frequently for the comfort of the cat. Nebulization or saline nose drops may aid in the removal of tenaceous secretions. Nose drops containing a vasoconstrictor (e.g., two drops of ephedrine sulfate [0.25% solution] in each nostril, b.i.d.) and antibiotics may be helpful in reducing the amount of nasal exudate. Prolonged use of nasal decongestants, however, may result in rebound nasal congestion and worsening of clinical signs. A bland ophthalmic ointment containing antibiotics (tetracyclines in C psittaci infections) is indicated 5-6 times daily to prevent corneal irritation produced by dried exudate. If corneal ulcers occur in FVR infections (herpetic keratitis), ophthalmic preparations containing idoxuridine or acyclovir are indicated in addition to other antibiotic ophthalmic preparations. Lysine (250 mg, PO, b.i.d. to t.i.d.) interferes with herpetic viral replication and may help reduce the severity of FVR infection. If dyspnea is severe, the cat may be placed in an oxygen tent. Fluids may be indicated to correct dehydration, and force-feeding may be necessary. Esophagostomy and gavage may be appropriate for alimentation of severely debilitated cats. Antihistamines (e.g., chlorpheniramine maleate, PO, b.i.d. [8 mg for adults, 4 mg for kittens]) may be beneficial early in the course of the disease.
Prevention: Two types of modified live virus FVR-FCV vaccines are available. The first type is intended for parenteral administration. Cats >9 wk old should be vaccinated twice, with a 3 wk interval. Kittens should be vaccinated at intervals of 3-4 wk until they are > or = 12 wk old. Annual revaccination with a single dose is indicated.
The second type of vaccine is administered to healthy cats by instillation into the conjunctival cur-de-sacs and nasal passages. Owners should be advised that cats inoculated oronasally may sneeze 4-7 days after vaccination. Kittens vaccinated when <12 wk old should be revaccinated on reaching this age. Annual revaccination with a single dose is recommended.
Modified live virus FVR-FCV vaccines intended for parenteral administration are available in combination with either chemically inactivated or modified live virus feline panleukopenia vaccines. A parenterally administered vaccine composed entirely of inactivated viruses also is available.
Vaccines containing either chick-embryo- or cell-line-origin C psittaci are administered parenterally. A single dose is recommended for cats >12 wk old; younger kittens should be revaccinated when they reach 16 wk. All should be revaccinated annually. These vaccines are indicated in catteries or on premises where C psittaci infection has been confirmed. The chlamydial vaccines are available in combination with FVR-FCV and panleukopenia vaccines. Systematic vaccination and control of environmental factors (such as exposure to sick cats, overcrowding, and stress) provide excellent protection against upper respiratory disease.
-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.
FIV Vaccine Released
August 23, 2002
Written by: Erin Harty
For thousands of cats every year, feline immunodeficiency virus is a death sentence.
The American Association of Feline Practitioners estimates that one in 12 cats, usually outdoor cats or those in multiple cat households contracts FIV, which is fatal. But a new medical development may offer hope of bringing the incidence of the disease down.
On Aug. 12, Fort Dodge Animal Health announced the release of the first vaccine effective against FIV. Called Fel-O-Vax FIV, the vaccine will be available at veterinary clinics nationwide.
The road to this point was a long one. The vaccine was more than 10 years in development. Janet Yamamoto, Ph.D., an immunologist and researcher at the University of Florida, developed the patented technology responsible for this medical breakthrough.
Dr. Yamamoto also co-discovered the virus itself, along with Dr. Niels Pedersen, an international authority on retroviruses and immunologic disorders of small animals at the University of California at Davis. The two universities hold joint patents on the vaccine, and Fort Dodge, with approval from the United States Department of Agriculture, utilized the research to develop a commercial vaccine.
"Formal approval of the vaccine is really a tribute to Dr. Yamamoto, who doggedly persisted in pioneering this approach for an FIV vaccine," Dr. Pedersen said in a statement.
Fel-O-Vax FIV has an 84 percent efficacy rate, according to Fort Dodge. Cats require three initial doses of the vaccine, and then an annual booster each year thereafter. The USDA also approved the FIV vaccine for administration to cats 8 weeks of age and older. The vaccine provides protection for a minimum of 12 months.
"It is generally believed that transmission of FIV takes place through bite wounds inflicted during fighting, and no cat-to-human transmission has ever been reported in the literature. We do, however, see the virus spreading rapidly through the cat population with up to 15 percent of at-risk or sick cats already infected with FIV," said Dr. Yamamoto in a statement.
Although FIV is often called "feline AIDS," it is not related to human immunodeficiency virus, or HIV. Researchers do hope, however, that the development of the FIV vaccine will help further the work on a vaccine for HIV.
Now that the FIV vaccine is available, it will be up to pet owners and their veterinarians to decide if they want to use it.
Jeff Werber, DVM, of the Century Veterinary Group in Los Angeles, Calif., is adopting a cautious, wait-and-see approach.
"From the broad picture, you say, 'Oh my God, that's great!' And it very well may be," he said.
But, like most vaccinations, the FIV vaccine is not 100 percent effective. And unlike human vaccines, animal vaccines are not tested on huge groups of subjects, Dr. Werber explained. "In humans, you'd have thousands of test cases. It doesn't have to be nearly that much in a cat."
For now, Dr. Werber said, he is not recommending the FIV vaccine to his entire client base. Most of his feline patients are indoor cats and are at low risk. Even for outdoor or stray cats, he said he would probably not recommend the vaccine as a matter of course. "Would I jump to use it right now? Probably not. I'd be open to using it if there were better numbers," he explained.
He also doesn't routinely use the feline infectious peritonitis or feline leukemia vaccines, for the same reasons, he said.
Veterinarians have to weigh the risk of any particular disease with the risk of vaccination and vaccines are not risk-free. They tax the immune system, Dr. Werber explained.
In recent years, veterinarians and pet owners have become leery about overusing vaccines because of the risk of vaccine-associated sarcomas, a type of cancerous tumor cats develop at injection sites. Many vets now tend to be more conservative with the number of vaccinations they recommend.
Another concern is that if tested, cats vaccinated for FIV will not, at this time, be distinguishable from cats that have actually been exposed to the disease, Dr. Werber said both will have FIV antibodies. "That could cause confusion," he said, in interpreting the test results.
FIV infection (Feline AIDS)
While we, as a profession, were getting a handle on Feline Leukemia, there were some mystery cases...cats that were thought to have leukemia...but the leukemia virus couldn't be isolated. And the disease didn't transmit the same as leukemia. It took 20 years, but in 1986, researchers discovered that a different Retrovirus was responsible for another immune suppressive disease that we mistook for leukemia. This "new" disease was so similar to Human Aids that it quickly became known as Feline Aids. (It wouldn't surprise me if some sharp,research fund raiser didn't purposely tryed to link the two diseases in hopes of getting in on the huge gravy train of Human Aids Research) (Cynicism aside, it may be that the work on feline aids will, in fact, lead to the biggest breakthrough to date on Human Aids: a vaccine)
The facts about Feline Aids are a little sketchy, even now: it's estimated that about 2% of the cat population carry the Aids virus.
Estimates about what types of cats are most likely to have the disease are also sketchy... some publications say mostly young males, some say mostly older males. But any cat can get it, including kittens, but it seems that the number one mode of transmission is through bite wounds. Intact males are at higher risk ONLY because they are more likely to fight and therefore get bitten, but again, any cat can get the disease. And while bite wound transmission is thought to be the primary cause, other means are possible. And the disease can stay dormant in the cat for several years and then start causing trouble. Big Trouble.
The virus itself is easily disinfected and dies within minutes upon exposure to dry surfaces.
FIV is not transmissible to people.
We vets now have a test kit available to test for Feline Aids, and infected cats may become positive one month of exposure and may live for years without signs of illness.
We now have a vaccine for FIV (Feline Aids). It's new and a little expensive (we charge $15, but a series of 3 are recommended the first year.)
Once sick, there is no cure. And the virus can apparently directly cause blood disorders and several types of cancer.
As with leukemia, treatment is mainly supportive and experimental.
Many vets attempt to minimize or slow the disease using the same drugs being used to combat human aids. And again, sometimes there are Veterinary University Experimental Treatment Programs that may accept you cat if it is Feline Aids positive.
I personally have tried immune stimulants to treat feline AIDS. Agents including interferon, staphylococcus Lysate, and Immunoregulin can cause clinical improvement in infected cats. Combination therapy using these drugs with reverse transcriptase
inhibitors can also be of benefit. Your vet may or maynot be comfortable using these unapproved medications.
Feline Infectious Peritonitis (FIP)
coming soon
