key: cord-0040492-9dm7z0wv authors: Cohn, Leah A.; Langdon, Paige title: Viral Infections date: 2009-05-15 journal: Handbook of Small Animal Practice DOI: 10.1016/b978-1-4160-3949-5.50116-3 sha: 4d60f8899f3778714bdd6b6299ef2c0e8cf4b4fb doc_id: 40492 cord_uid: 9dm7z0wv nan I. Canine parvovirus II. Parasites, bacterial enteritis III. Canine distemper virus (CDV), canine herpesvirus (CHV) IV. Toxins, foreign bodies, intussusception, or metabolic diseases Treatment I. Supportive care may be instituted, although many dogs require no therapy. II. See Box 112-1 for treatment of GI signs. I. The need for routine CCV vaccination is questionable, although inactivated and modifi ed live virus (MLV) vaccines are available for at-risk populations. II. Avoid exposure of young puppies to potentially contaminated environments. III. CCV is inactivated by various disinfectants (Table 112-1) . IV. Viral shedding may occur for up to 6 months postinfection (Pratelli et al., 2004) . I. CDV is a highly contagious virus with either focal or multisystemic manifestations, and variable morbidity and mortality. II. Respiratory, GI, and neurological tissues are all targets. I. CDV is a SS-RNA virus of the family Paramyxoviridae and is closely related to measles virus of primates and rinderpest in domestic livestock. II. CDV is highly contagious. A. Large viral concentrations occur in respiratory secretions. B. It is commonly spread by aerosolization. I. Canine coronavirus (CCV) causes contagious enteritis of variable severity (rarely fatal) in young dogs. II. The true signifi cance of this pathogen in juvenile diarrhea is not fully known, but it may contribute to the morbidity and mortality of other infectious enteropathies, such as canine parvovirus (CPV) (Pratelli et al., 2004) . I. CCV, a single-stranded (SS) ribonucleic acid (RNA) virus of the family Coronaviridae, is closely related to feline coronavirus and transmissible gastroenteritis virus of pigs. II. CCV is highly contagious via fecal-oral transmission. III. Fecal shedding results in environmental contamination, an important route of exposure. IV. CCV infects any age group, but clinical disease is usually seen only in very young puppies. V. After ingestion, the virus localizes in the villus tips of the small intestines, where it replicates and results in villous atrophy and crypt cell hyperplasia. C. Infective virus is also present in urine and other bodily fl uids. D. Recovered dogs shed the virus for 60 to 90 days postinfection (Greene and Appel, 2006) . III. The virus is viable in cold and freezing environments, but susceptible to heat, drying, and ultraviolet light. IV. Younger animals are most susceptible to infection. V. Susceptibility is enhanced in older dogs not adequately vaccinated and with either concurrent stress or immunosuppressive conditions. VI. During systemic infection, CDV contacts upper respiratory epithelium; replicates within respiratory lymphatics; eventually disseminates to other lymphatic tissues, intestines, and liver; and produces viremia. A. Host immunity may be suppressed by the virus. B. Several outcomes are possible, depending on immunity and antibody (Ab) response. 1. Adequate immunity a. Virus cleared with no illness Box 112-1 Therapy for Gastrointestinal Manifestations of Viral Disease* b. Enrofloxacin 2.5-5.0 mg/kg SC BID for dogs; relatively contraindicated in growing puppies and kittens owing to potential cartilage damage c. Gentamicin 6-6.6 mg/kg IV, IM, or SC SID or amikacin 15-30 mg/kg IV, IM, or SC SID (1) Contraindicated in dehydration, hypotension, or renal failure (2) May cause renal failure, ototoxicity (3) Covers gram-negative bacteria only d. Cefazolin 22 mg/kg IV TID with enrofloxacin or gentocin e. Cefoxitin 22 mg/kg IV TID 6. H 2 -blocker therapy may decrease gastric acidity and its associated complications. a. Famotidine 0.5-1.0 mg/kg IV, SC, or IM SID-BID b. Cimetidine 5-10 mg/kg IV, SC, or IM TID c. Ranitidine 2 mg/kg IV BID 7. Adjunctive therapy includes the following: a. Animals on NPO restrictions for 3 days or longer require parenteral nutrition. b. Whole blood, packed RBCs, or blood substitute are indicated for anemia. c. Routine nursing care is critical to keep IV sites clean and prevent urine or fecal scald. 8. Recovery and realimentation are important. a. Small amounts of water are offered 12-24 hours after cessation of vomiting. b. If no vomiting occurs within 12-24 hours of water administration, small amounts of a bland diet are offered every 2-3 hours. c. Animals are gradually weaned onto maintenance requirements of a bland diet over 2-4 days. d. Bland diet is maintained for 1-3 weeks, followed by gradual reintroduction of a diet appropriate for age. I. Isolate sick dogs. II. Maternal Ab is usually gone by 12 weeks of age, but may interfere with initial vaccination (Greene and Appel, 2006) . III. MLV vaccines are administered 3 to 4 weeks apart, with at least one vaccine given after maternal Ab has waned. A. Annual to triennial vaccines are currently recommended to booster protection (Table 112 -2). B. Measles vaccine provides cross-protection against CDV and may be given as an initial puppy vaccination at 6 to 12 weeks, when maternal Ab interferes with CDV vaccine response. C. Inactivated (i.e., killed virus) vaccine is used in pregnant or immunosuppressed animals, but it confers a lower degree and duration of immunity than MLV vaccines. D. MLV vaccines are contraindicated in pregnant or immunosuppressed animals. IV. Vaccination complications can occur. A. Encephalitis may develop in severely immuno suppressed puppies or in puppies whose dam received MLV vaccination while pregnant. B. CDV vaccine is inactivated by hyperthermia, and an attenuated response may occur with concurrent parvovirus infection or chemotherapy (Greene and Appel, 2006) . V. Recovery from natural infection provides prolonged immunity. VI. CDV is inactivated by various disinfectants (see Table 112 -1). I. CHV is a relatively common infection, but an uncommon cause of disease. II. When disease occurs, it causes abortions in pregnant bitches or a fatal hemorrhagic disease in puppies <3 weeks of age. III. CHV, a double-stranded DNA virus of the family Herpesviridae, infects only Canidae. I. CHV requires close contact for transmission. II. It spreads transplacentally at birth or through direct dog-to-dog contact (e.g., during breeding). III. It is unstable in the environment, so it is rarely transmitted through fomites. I. Consequences of rare, transplacental infection include abortions, stillbirths, weak puppies, and puppies that succumb to neonatal infection. II. Neonatal infection occurs via exposure to the dam's vaginal secretions at birth or to infected littermates, and is most common during the fi rst 3 weeks of life (Anvik, 1991) . III. Signs in puppies 3 to 5 weeks old may be less severe and include neurological signs, such as trigeminal neuropathy, ataxia, and blindness. IV. Adults are usually asymptomatic. A. Females that appear healthy may experience infertility, abortion, or stillbirths. B. Genital lesions include papulovesicular lesions that regress and reappear in both males and females. C. CHV may play a minor role in canine respiratory infections. D. Latent infections recrudesce in some immunosuppressed dogs (Okuda et al., 1993) . A. Limited usefulness in neonates because of sampling diffi culty and lack of specifi city B. Puppies: thrombocytopenia, evidence of disseminated intravascular coagulopathy and increased liver enzyme activity (particularly alanine aminotransferase) II. CHV-specifi c testing A. Virus isolation from tissues of affected puppies is diagnostic. B. Serological testing indicates exposure, but does not diagnose active infection in adults. C. Multifocal hemorrhages and necrosis with inclusion bodies in epithelial tissues, or CHV identifi ed in tissue via FA, EM, or polymerase chain reaction (PCR) assays are also conclusive. I. Neonatal death A. Bacterial septicemia with Salmonella spp., Streptococcus spp. B. Other viral infections: CPV-1, CPV-2, CDV C. Protozoal diseases II. Abortion and stillbirths: brucellosis, leptospirosis, bacterial metritis, CDV, protozoal diseases, endocrinopathies Treatment I. Supportive therapy is typically unsuccessful. II. Provide parenteral fl uids with oral or IV dextrose, nutritional support, nursing care, animal warming, and broadspectrum antibiotics. III. Hyperimmune serum from recovered dogs may protect other puppies (<5 weeks of age) in an affected litter; administer 1 to 2 mL intraperitoneally (Anvik, 1991; Greene and Carmichael, 2006) . IV. Rapid progression of neonatal disease makes the role of antiviral therapy questionable. V. Infected adult dogs remain latently infected because there is no way to clear all virus from the body. I. Puppies that are kept warm (37° to 38° C [99° to 100° F]) have lower morbidity and mortality. II. Although bitches that have recovered from infection usually raise subsequent litters without problems, it is recommended they not be bred again. III. Isolate young puppies from dogs that might shed viral particles. IV. A preventative vaccine is available only in Europe. V. CHV is easily inactivated by most disinfectants (see Table 112 -1). I. CPV causes acute contagious enteritis with a high morbidity and mortality in immunologically naive dogs. II. Rarely, myocardial disease results from perinatal infection. I. Canine parvovirus-2 II. SS-DNA virus of the family Parvoviridae III. CPV-2b: most common disease-causing strain in the United States IV. CPV-2: distinct from CPV-1 (including disease manifestations) A. This highly contagious virus is shed primarily in the feces of infected and recovering animals. B. Fomites are a more common source of exposure than direct contact with feces, and CPV-2 persists in the environment. C. Incidence is higher in summer and late fall (Houston et al., 1996) . D. Immunologically naive animals (young puppies) are the most susceptible to CPV-2 infection; however, older, immunocompromised animals are also at risk. E. Reported breed predispositions include the rottweiler, American pit bull terrier, Doberman pinscher, and German shepherd dog (Houston et al., 1996) . A. After oronasal exposure (primary route) initial replication occurs in local lymphoid tissues, with subsequent viremia in 2 to 5 days. B. Rapidly dividing tissues (e.g., intestinal crypt cells, bone marrow leukocyte precursors) are preferentially infected; dissemination to the lungs, kidneys, and myocardium is possible. A. Adjunctive therapy involves hyperimmune plasma transfusions (1.1 to 2.2 mL/kg IV) from recovered dogs (Cohn LA, unpublished data, 2006) . B. Empirical deworming is used to eliminate concurrent intestinal parasites. C. Treatment with recombinant human granulocyte colony-stimulating factor (G-CSF) is not benefi cial (Rewerts et al., 1998) . D. CPV-2 infection may be fatal, but many animals fully recover. III. Myocardial disease is extremely diffi cult to treat. A. Because the disease is rapidly progressive and fatal, therapeutic intervention is rarely attempted. B. Treat congestive heart failure in survivors. I. Quarantine unvaccinated animals. II. Passive immunity is important in neonates. A. Maternal Ab titers >1:80 (hemagglutination-inhibition) are protective (McCaw et al., 1997) . B. Maternal Ab typically protects for 6 to 12 weeks and may interfere with vaccination responses up to 18 weeks of age (Coyne, 2000) . III. Good acquired immunity is achieved through vaccination. A. High-titer potentiated MLV CPV-2 vaccines are preferred. 1. They induce protective immunity in puppies when maternal Ab is present (Larson and Schultz, 1997 ). 2. Annual (McCaw et al., 1997) to triennial booster vaccines (see Table 112 -2) are recommended. B. Low-titer, MLV CPV-2 vaccines do not always protect puppies with high maternal Ab levels, even at 20 weeks of age, but the vaccines do provide adequate protection for older puppies and adults (Hoskins, 1998) . IV. Following natural infection, recovered animals have longlasting immunity. V. The virus is resistant to most disinfectants (see Table 112 -1). I. The onset of CNS signs is usually with in 2 to 24 weeks, but depends on the viral load inoculated, the degree of innervation at the site, the proximity of the site to the CNS, and the strain of RV. II. Classic clinical presentation is either "furious" or "paralytic," but not all cases fi t these categories, and a combination of signs is possible. III. With the furious form of rabies, the disease course lasts only days. A. Behavioral changes, hyperexcitability, hyperesthesia, and aggression occur. B. Ataxia and seizures develop and are followed by death. IV. With the paralytic form, the disease course typically lasts about 1 week. A. Progressive ascending lower motor neuron paralysis begins at the inoculation site and leads to dysphagia, masticatory muscle paralysis, and laryngeal and pharyngeal dysfunction, with classic signs of salivation. B. Death is caused by respiratory paralysis. I. History of a recent bite wound and classic clinical presentation may be helpful. II. Clinical pathologic fi ndings are nonspecifi c. III. Antemortem testing may confi rm RV infection, but cannot adequately rule it out. IV. Owing to the serious public health implications, euthanasia of animals suspected of RV infection is urgently recommended and often required by law. V. Postmortem testing confi rms or denies the diagnosis. A. Submit the brain-chilled but not frozen-as soon as possible to a state diagnostic laboratory. B. Direct FA testing of the brain is the diagnostic method of choice. C. Additional tests on brain specimens include PCR for viral particles, histopathologic evaluation (intracellular inclusions or Negri bodies), and mouse inoculation (Kasempimolporn et al., 2000) . D. RV strains may be identifi ed to help determine the source of exposure. I. Vaccination provides excellent protection against the disease. A. Vaccination in most states is initiated by a killed vaccine at 12 to 16 weeks of age, with a booster vaccination at 1 year of age followed by triennial boosters. B. Some states require yearly vaccination; some vaccines are approved for yearly use only (e.g., canary poxvectored vaccines). C. The use of rabies vaccine has been associated with injection-site sarcomas in cats. II. In most municipalities, rabies vaccination for dogs and cats is required by law. III. Recommendations for preexposure vaccination and management and postexposure management are available yearly from the American Veterinary Medical Association (AVMA; www.avma.org/issues/policy/rabies_control.asp) and from the Centers for Disease Control and Prevention (CDC; www.cdc.gov/ncidod/dvrd/rabies; see Table 112 -2). IV. Use extreme care when handling an animal or its bodily fl uids if RV infection is suspected. V. RV is susceptible to most disinfectants and does not survive well in the environment (see Table 112 -1). I. Feline coronavirus (FCoV) causes either subclinical infection or mild, transient diarrhea in exposed cats. II. Spontaneous mutation of enteric FCoV may lead to clinical FIP, which is associated with very high morbidity and mortality. III. FCoV is an SS-RNA virus of the family Coronaviridae. I. FCoV is highly contagious via fecal-oral transmission, but salivary, urinary, and transplacental sources of exposure are uncommon. II. Most infected cats shed the virus intermittently and then stop shedding, although some shed persistently. III. FCoV that has mutated to an FIP-causing form is seldom shed in feces, so epizootics are rare. IV. Although inactivated by most disinfectants, FCoV may persist in the environment (see Table 112 -1). V. Enteric infection results in villous atrophy and mild, selflimiting diarrhea. VI. With FIP, a history of recent stress or illness may precede the disease. A. Mutated FCoV invades intestinal epithelium and enters macrophages, resulting in disseminated spread of mutated viral particles. B. Immunological response is ineffective and pathologic changes occur. C. Two forms of FIP are recognized. 1. Effusive (wet) form a. Immune complexes circulate and are deposited in endothelia. b. A vasculitis ensues with exudation of proteinrich fl uid into body cavities. c. The wet form is usually more rapidly progressive than the dry form. a. An ineffective cell-mediated immune response is mounted against the virus. b. Pyogranulomatous infl ammation in a variety of tissues results in disease. c. The dry form may become effusive in its terminal stages. I. Enteric FCoV: often subclinical or mild diarrhea II. FIP A. Young (<2 years) and elderly cats more commonly affected B. Sexually intact and purebred cats more commonly affected C. Effusive FIP 1. 4. Remove kittens from seropositive queens at 5 to 6 weeks of age. A. The available intranasal vaccine appears safe when used as directed. 1. Temperature-sensitive vaccine virus replicates only in respiratory epithelium, inducing mucosal immunity. 2. Vaccine effi cacy is 50% to 75% for previously unexposed cats (Pederson, 1995) . 3. It is not indicated in low-risk cats, such as adults or cats in single-cat households. 4. At-risk kittens possibly benefi t from vaccination, with two doses given 3 to 4 weeks apart and followed by yearly booster vaccinations. 5. Currently, the vaccine is not recommended for routine use (Table 112 -3). B. Vaccination does not prevent mutation of FCoV in an infected cat. I. FIV causes chronic infections with a long subclinical period, and eventual development of acquired immunodefi ciency with associated clinical syndromes. II. FIV, a lentivirus, is a SS-RNA virus of the family Retroviridae that only infects Felidae and is closely related to human immunodefi ciency virus. I. Epidemiological fi ndings A. Horizontal and vertical transmission occur, but vertical spread is not epidemiologically important. B. Close contact is required for transmission, and fomites are involved only minimally. C. Horizontal transmission occurs primarily via bite wounds, and also occurs via blood transfusions, contaminated needles and instruments, or other contact with bodily fl uids. D. Males, particularly intact, outdoor cats that fi ght, are more commonly infected than females. E. Adults (middle aged and older) are infected more often than kittens. F. A higher seroprevalence of FIV occurs in areas with large outdoor cat populations. A. FIV initially replicates in lymphoid (including thymic) and salivary tissue, with subsequent dissemination to many tissues. B. As the cat mounts a partially effective immune response, the number of circulating viral particles lessens and the cat appears healthy. C. During the subclinical period (possibly many years), gradual deterioration in immune function occurs (not a true latency). D. Secondary infections and associated illness eventually occur, resulting in the terminal phase of disease. I. Acute infection may be inapparent, but can cause selflimiting fever, neutropenia, and lymphadenopathy. II. Lymphadenopathy is variably present during the subclinical period (months to years). III. Clinical illness has a variety of manifestations. A. Recurrent fevers, anorexia, malaise, gingivitis, stomatitis (common) B. Secondary infections of the GI, respiratory, and urinary tracts C. Infl ammatory diseases of the eye (Hartmann, 1998) D. A variety of malignancies (Hutson et al., 1991) E. Rare peripheral or central neurological dysfunction (Podell et al., 1993) F. Severe weight loss and cytopenia (terminally) A. Lymphopenia and neutropenia acutely, and during later stages of disease B. Anemia and thrombocytopenia II. Serum biochemistry profi le: hyperglobulinemia or fi ndings related to secondary diseases III. Cytological evaluation of fi ne-needle aspirates of enlarged lymph nodes: hyperplasia or mimic lymphoma IV. FIV-specifi c diagnostic testing A. In-hospital ELISA tests identify Abs. 1. FIV is not always detected during acute infection or during terminal stages. 2. False positives can occur from maternal Ab, so retest positive kittens after 6 months of age (Sellon, 2006) . 3. False positives can occur in vaccinated cats. B. Although Western blot is used as a confi rmatory test for a positive ELISA result, it cannot distinguish Ab formed in response to infection from maternal Ab or Ab formed in response to vaccination (Levy et al., 2004) . C. PCR assays are available but vary greatly in reliability (Crawford et al., 2005) . A. Provide supportive care and prompt therapy for secondary infections. B. Human recombinant G-CSF may be helpful for severe neutropenia (see Treatment under Feline Leukemia Virus). C. The use of recombinant human granulocyte-macrophage colony stimulating factor may lead to increased FIV load (Arai et al., 2000) . D. Other immune modulators and antiviral therapy may be tried (see Treatment under Feline Leukemia Virus). I. A vaccine is available but does not confer perfect protection (Huang et al., 2004 Table 112 -3). II. Discourage fi ghting, and do not breed infected cats. III. Ideally, separate FIV-positive cats from FIV-negative housemates; however, unless they fi ght, the risk of transmission with normal contact (e.g., sharing litter boxes, food bowls) is low. (Arai et al., 2000) . 3. Address other causes of anemia, such as hemotrophic Mycoplasma spp. infection and IMHA. B. Neutropenia 1. The use of human recombinant G-CSF (5 mg/kg/day SC for ≤2 weeks) in severe neutropenia is controversial (Obradovich et al., 1993; Hartmann, 2006; Arai et al., 2000) , because at higher doses or for longer periods it may cause production of antibodies to feline colony stimulating factors. 2. Consider prophylactic antibiotics. IV. Secondary bacterial infections require prompt therapy with appropriate antibiotics. V. Immune modulator and antiviral therapy may be tried, but evidence of effi cacy is slim (McCaw et al., 2001) . A. Staphylococcus aureus protein A 10 mg/kg IP twice weekly B. Human recombinant interferon-a 30 U PO SID on alternating weeks C. Feline recombinant interferon omega 1 μ 10 6 U/kg/day SC for 5 consecutive days in 3 series, beginning on days 0, 14, and 60 (de Mari et al., 2004) . I. Isolate cats with FeLV from noninfected cats; keep infected cats indoors, vaccinate them for other infectious diseases, and do not breed them. II. Vaccination involves the following (see Table 112 -3). A. Test before FeLV vaccination, because vaccination of positive cats provides no benefi ts. B. Vaccination is not indicated for low-risk cats (e.g., indoor cats, single-cat households, or households in which all cats test negative). C. Killed and subunit vaccines are equally effi cacious. D. Vaccine effi cacy is <100%, and estimates of true efficacy vary (Legendre et al., 1991; Jarret and Ganiere, 1996) . E. Initially give two vaccines 3 to 4 weeks apart, with annual booster vaccinations. F. Use of FeLV vaccine has been associated with injectionsite sarcomas in cats. I. Feline panleukopenia is a highly contagious, acute enteric disease of young cats, typically accompanied by severe leukopenia and high morbidity and mortality. II. In utero or early neonatal infection may cause cerebellar disease. III. Feline parvovirus (FPV), an SS-DNA virus of the family Parvoviridae, is related to CPV-2, which is rarely isolated from cats with panleukopenia. A. FPV is highly contagious to all domestic and wild members of the family Felidae. B. Virus is shed in all body secretions, with fecal shedding being the primary source of infection. C. Transmission is from contact with infected animals, contaminated environment, or fomites. D. FPV is seldom encountered in vaccinated domestic cats, but is problematic in feral, shelter, and stray cats. E. Disease is most common in 3-to 5-month-old kittens, because most cats >1 year old are immune from subclinical infection and younger kittens are protected by maternal Abs. II. Pathogenesis A. After oronasal exposure, the virus replicates in regional lymph nodes and causes viremia. B. FPV preferentially infects rapidly dividing cells (e.g., intestinal epithelial cells, lymph tissue, hematopoietic cells of bone marrow). C. Secondary GI bacterial infection, translocation of gut bacteria, and increased susceptibility to bacterial infection and sepsis all contribute to the clinical signs produced. Immunologic abnormalities in pathogen-free cats experimentally infected with feline immunodefi ciency virus Clinical considerations of canine herpesvirus infection The use of human hematopoietic growth factors (rhGM-CSF and rhEPO) as a supportive therapy for FIV-infected cats Plasma granulocyte colonystimulating factor concentrations in neutropenic, parvoviral enteritisinfected puppies Seroconversion of puppies to canine parvovirus and canine distemper virus: a comparison of two combination vaccines Accuracy of polymerase chain reaction assays for diagnosis of feline immunodefi ciency virus infection in cats Treatment of canine parvoviral enteritis with interferon-omega in a placebo-controlled fi eld trial Therapeutic effects of recombinant feline interferon-omega on feline leukemia virus (FeLV)-infected and FeLV/feline immunodefi ciency virus (FIV)-coinfected symptomatic cats Development of clinical disease in cats experimentally infected with feline immunodefi ciency virus Canine coronavirus-associated puppy mortality without evidence of concurrent canine parvorirus infection Environmental factors in infectious disease Infectious canine hepatitis and canine acidophil cell hepatitis Infectious Diseases of the Dog and Cat Infectious Diseases of the Dog and Cat Feline immunodefi ciency virus infection: an overview Infectious Diseases of the Dog and Cat Use of propofol to manage seizure activity after surgical treatment of portosystemic shunts Focal mesangialsclerosing glomeruloneprhitis and acute-spontaneous infectious canine hepatitis: structural, immunohistochemical and subcellular studies Feline leukaemia provirus load during the course of experimental infection and in naturally infected cats Infectious Diseases of the Dog and Cat Risk factors associated with parvoviral enteritis in dogs: 283 cases (1982-1991) Effi cacy and safety of a feline immunodefi ciency virus vaccine Neoplasia associated with feline immunodefi ciency virus infection in cats of Southern California Comparative studies of the effi cacy of a recombinant feline leukaemia virus vaccine Detection of rabies virus antigen in dog saliva using a latex agglutination test Infectious canine hepatitis: detection of canine adenovirus type 1 by polymerase chain reaction Comparison of selected canine vaccines for their ability to induce protective immunity against canine parvovirus infection Comparison of the effi cacy of three commercial feline leukemia virus vaccines in a natural challenge exposure Effect of vaccination against feline immunodefi ciency virus on results of serologic testing in cats Kirk's Current Veterinary Therapy XIII: Small Animal Practice Immunomodulation therapy for feline leukemia virus infection Infectious Diseases of the Dog and Cat Early protection of puppies against canine parvovirus: a comparison of two vaccines Effect of recombinant canine granulocyte colony-stimulating factor on peripheral blood neutrophil counts in normal cats Virus reactivation in bitches with a medical history of herpesvirus infection AAHA canine vaccine guidelines An overview of feline enteric coronavirus and infectious peritonitis virus infections Clinical overview of feline immunodefi ciency virus AIDS-associated encephalopathy with experimental feline immunodefi ciency virus infection Two related strains of feline infectious peritonitis virus isolated from immunocompromised cats infected with a feline enteric coronavirus Two genotypes of canine coronavirus simultaneously detected in the fecal samples of dogs with diarrhea Recombinant human granulocyte colony-stimulating factor for treatment of puppies with neutropenia secondary to canine parvovirus infection Feline immunodefi ciency virus infection Studies on the epizootiology of canine coronavirus Enzyme-linked immunosorbent assay for the detection of canine coronavirus and its Ab in dogs I. Passive immunity A. Colostral Ab prevents infection and interferes with vaccination up to 12 weeks of age. B. Plasma provides passive immunity (up to 4 weeks) if the kitten is colostrum-deprived. II. Active immunity A. Inactive (killed virus) vaccine 1. Requires at least two administrations to be effective 2. Safe in pregnant queens or young kittens (<4 weeks of age) B. MLV vaccines 1. They provide long-lasting immunity, although yearly booster vaccinations are still recommended by manufacturers. 2. They are not safe in pregnant queens and potentially cause neurological dysfunction in kittens. 3. Give kittens at least two vaccines, with at least 1 dose occurring after 12 weeks of age. 4. For current recommendations, see Table 112 -3. III. Natural infection produces lifelong immunity. IV. FPV is resistant to environmental degradation and to many disinfectants (see Table 112 -1). See Table 112 -4.