CHAPTER 18. Infectious Diseases
Patricia A. Schenck
FELINE LEUKEMIA VIRUS
I. Causes
A. Structure of the virus
1. RNA retrovirus
2. Core contains viral RNA and reverse transcriptase enzyme
3. Core protein p27 is the specific antigen detected by diagnostic tests
4. Envelope glycoprotein (gp70) is important in defining the antigenic subgroup; only subgroup A is infectious
5. Envelope protein p15e mediates feline leukemia virus (FeLV) immunodeficiency
B. Prevalence
1. Young kittens (i.e., younger than 4 months of age) are most susceptible
2. Highest prevalence in free-roaming stray cats
C. Transmission
1. Primarily through saliva. Infected queens shed virus in milk. Exposure is typically by direct contact through grooming, bite wounds, and sharing of food and water bowls
2. Transplacental transmission can occur
3. FeLV survives a maximum of 48 hours in the environment and is readily destroyed by most disinfectants
II. Pathogenesis
A. Sequence of FeLV infection
1. After entry, FeLV replicates in lymphoid tissue throughout the body. Enzyme-linked immunosorbent assay (ELISA) tests may detect antigen in the blood at this stage. If an immune response is effective, the infection may be eliminated
2. FeLV infects bone marrow, causing circulation of infected leukocytes and platelets. These are detectable with immunofluorescent antibody (IFA) testing and indicate that the infection will be persistent
3. FeLV infects glandular cells, and virus is shed in body secretions. At this stage, infected cats are contagious
B. Many cats over 4 months of age resist infection
C. Most exposed cats develop a transient infection that is rejected by an immune response. These cats eliminate virus within 4 to 6 weeks after infection. Vaccinated cats will have a brief transient infection but resist persistent infection
D. Some cats that recover from transient infection become latent carriers of FeLV. The latent stage is usually eliminated with time, but a few remain infected. In latent carriers, there is the rare possibility that FeLV may be reactivated to replicating infection
E. Persistent infection is eventually fatal
III. Clinical signs
A. The immunosuppression effects of FeLV cause many nonspecific clinical signs, including weight loss, fever, dehydration, anemia, diarrhea, stomatitis, lymphadenopathy, and oculonasal discharge
B. FeLV can be a primary cause of lymphoma, including alimentary, mediastinal, multicentric, renal, ocular, neural, and cutaneous lymphoma. Lymphoid leukemia, nonlymphoid leukemia, or myelodysplasia may result from bone marrow infection
C. Nonregenerative anemia is common with FeLV. FeLV-related neutropenia or thrombocytopenia may occur
D. Secondary infections are common and include viral, fungal, protozoal, Mycoplasma, and bacterial causes
E. Peripheral lymph node hyperplasia can be seen, especially in young adult cats. This tends to resolve but may recur or develop into lymphoma at a later date
F. Immune-mediated disorders such as immune-mediated hemolytic anemia, immune-mediated thrombocytopenia, immune-complex glomerulonephritis, polyarthritis, pemphigus, and systemic lupus erythematosus like syndrome may occur
G. Infected queens may have reproductive failure. Infertility, fetal resorption, abortion, stillbirth, fading kitten syndrome, and milk-borne transmission can occur
IV. Diagnosis
A. Test all cats before vaccination and before bringing a new cat into the house or cattery
B. ELISA and immunochromatographic tests
1. Rapid screening tests; detect infection earlier than IFA tests
2. Detect FeLV p27 antigen (a viral core protein); test not affected by vaccination or maternal antibodies
3. Confirm positive results with repeat testing in several weeks
C. The IFA test is preferred for confirmation of FeLV because it is more specific than ELISA testing
1. May be negative in early infections
2. Confirm positive tests with repeat testing in a month
D. Polymerase chain reaction (PCR) testing detects FeLV nucleic acid in blood, bone marrow, or biopsies and may be helpful in detecting latent FeLV infection
E. Virus isolation is the “gold standard” for confirming positive test results with other methods
V. Treatment
A. Provide good general health care and prevent spread of infection to noninfected cats
B. Zidovudine (AZT) and interferon therapy may have some effectiveness
C. Provide fluid therapy, nutritional support, antibiotics as needed
VI. Prevention and control
A. Vaccination
1. Vaccines are available but are considered “non-core” vaccines
2. Vaccinate cats that go outdoors or negative cats living in a household with infected cats
3. Vaccination is not recommended in adult indoor cats with no exposure to infected cats
4. Local swelling may develop at the site of vaccination and can develop into vaccine-associated sarcomas at a later date
5. Vaccination is not 100% effective
B. Control in multi-cat households and catteries
1. In catteries with FeLV-positive cats, follow a test and removal program to eliminate FeLV from the household
2. In FeLV-negative households or catteries, screen any new cats with ELISA testing, vaccinate (if negative), and isolate for 3 months
FELINE IMMUNODEFICIENCY VIRUS (FIV)
I. Causes
A. Lentivirus subfamily of retrovirus; RNA virus with outer envelope and nuclear capsid. Subtype A is common in the western United States; subtype B is common in the eastern United States
B. Epidemiology
1. Prevalence is higher in free-roaming stray cats
2. Affects all ages but most prevalent in cats 6 years of age or older
3. More prevalent in male cats
4. Wild felids are susceptible to feline immunodeficiency virus (FIV)
C. Transmission
1. Shed in saliva; most infection occurs via a bite wound
2. Can be transmitted via intravenous (IV) transfusion of contaminated blood
D. Pathogenesis
1. Infects T lymphocytes with loss of CD4+ lymphocytes, inversion of the CD4-CD8 ratio with loss of CD8+ cells later
2. Latent period can last for years
3. Progressive loss of T cells results in an immunodeficiency syndrome with recurrent infections
4. Eventually fatal
II. Clinical signs
A. Initial infection occurs within 4 to 6 weeks after exposure; signs are usually mild and include a transient fever, neutropenia, lymphopenia, and lymphadenopathy
B. A latent period follows, usually for several years
C. An immunodeficiency syndrome follows that predisposes the cat to chronic and recurrent infections
1. General signs include weight loss, wasting, recurrent fever, lymphadenopathy, polyclonal hypergammaglobulinemia, recurrent anemia, leucopenia, or thrombocytopenia
2. Chronic infections affect the oral cavity (common), respiratory tract, gastrointestinal (GI) tract, urinary tract, and skin. In the mouth, lesions often begin in the fauces and spread along the maxillary gingivae
3. Common conditions include calicivirus, herpesvirus, poxvirus, papillomavirus, Chlamydophila felis, Mycoplasma haemofelis, Staphylococcus, Pseudomonas, Mycobacterium, Yersinia, Candida, Cryptococcus, Aspergillus, Toxoplasma, Giardia, Cryptosporidium, Demodex, and Notoedres spp.
4. FIV is neurotropic leading to neuronal damage; signs include dementia, behavior abnormalities, circling, gait abnormalities, and abnormal reflexes
5. B-cell lymphoma and myeloproliferative neoplasia occur more frequently in FIV-infected cats
6. Ocular disorders (anterior uveitis, chorioretinitis, glaucoma, retinal hemorrhage, retinal degeneration) and nephropathy may occur in association with FIV
III. Diagnosis
A. Test cats over 6 months of age
B. Assays for antibody
1. The ELISA antibody test is useful for screening. Confirm any positive ELISA results with Western blot
2. IFA test
3. The Western blot test detects antibodies against viral proteins and is the “gold standard” test for confirming FIV
C. Commercial PCR assays are unreliable at this time
IV. Treatment
A. Specific antiviral therapy
1. AZT can be used; however, it is myelosuppressive. Drug-resistant strains may emerge
2. Treatment with feline or human interferon can be attempted but is expensive and may only be effective short-term
B. General supportive therapy includes antibiotics, fluid therapy, and nutritional support. Use metronidazole and clindamycin to treat stomatitis
V. FIV-positive cats can live several years before exhibiting clinical signs
VI. Prevention
A. Prevent exposure to other potentially infected cats
B. Keep infected cats indoors to prevent exposure to noninfected cats
C. A killed vaccine is available that contains subtypes A and D; it is unknown whether there is cross-protection with other subtypes. FIV vaccination is not recommended as a core vaccine
D. Before vaccination, make sure that the cat is FIV antibody negative
FELINE INFECTIOUS PERITONITIS (FIP)
I. Causes
A. Feline coronavirus (FCoV), a single-stranded enveloped RNA virus that infects cells of the respiratory and GI tracts
B. Pathogenesis
1. Feline infectious peritonitis (FIP) occurs when the enterotropic FCoV mutates, which allows FCoV to infect and replicate in macrophages
2. Macrophages carry the mutated virus to peritoneum, pleura, kidney, uvea, and nervous system
3. It is the immune reaction to the virus that causes disease
II. Epidemiology
A. Seroprevalence for FCoV is high, yet few cats develop FIP. Prevalence is highest in catteries and shelters
B. Risk factors
1. Young cats (6 months to 3 years) are at increased risk of FIP
2. Cats in catteries, shelters, or multiple cat households are at higher risk of FIP
3. Anything that causes an increased replication of FCoV in the intestine (stress, concurrent disease, corticosteroids, immuno suppression, surgery) increases the probability of virus mutation
4. Most wild felids (e.g., lions, cougars, cheetahs, jaguars) are susceptible to FCoV and FIP. Cheetahs are particularly susceptible to FIP
5. Genetics may play a role in the susceptibility to FIP
C. Transmission is through oronasal contact with infected feces
1. FCoV can survive for 7 weeks in dried feces; thus contaminated articles (e.g., dishes, shoes, clothing) can serve as fomites. Most disinfectants will destroy FCoV
2. Carriers of FCoV can shed virus in feces for 10 months
3. Cats with FIP shed the nonmutated form of FCoV
III. Clinical signs
A. Incubation period is variable from a few weeks to several years. The onset is usually gradual but may be acute in young kittens
B. Once clinical signs develop, FIP is progressive and fatal usually within 3 to 6 weeks but may result in prolonged illness for 6 months or longer
C. Effusive (wet) form of FIP
1. Inflammatory fluid is predominantly in the abdominal cavity but can also be present in the thoracic cavity
2. Effusion in the peritoneal cavity causes progressive fluid distension, which can be detected by palpation and percussion of a fluid wave. Scrotal swelling may be present in intact males
3. Thoracic effusion causes dyspnea, tachypnea, and exercise intolerance from compression by fluid in the pleural space. Muffled heart sounds are usually noted
4. Thoracic and abdominal effusion can be confirmed by radiography
5. Pericardial effusion also occurs but does not typically cause clinical signs
D. Noneffusive (dry) form of FIP
1. Characterized by pyogranulomatous inflammation and necrotizing vasculitis in multiple organs. The specific organs affected determine which clinical signs are present
2. Organs affected include kidney, liver, spleen, visceral lymph nodes, uvea, retina, brain, lungs, and testicles
3. Meningoencephalitis and myelitis are common. The most common clinical signs are ataxia, tremors, vestibular dysfunction, seizures, paresis, and behavioral changes. Hydrocephalus can occur
IV. Diagnosis of FIP
A. Hematology and serum chemistries
1. Total serum protein and globulins are increased in most cases; albumin is commonly decreased. A decreased serum albumin globulin ratio (A:G < 0.8) strongly suggests FIP
2. Chemistry profiles may reveal a number of abnormalities depending on the organs affected
B. Radiology is useful for confirming the presence of thoracic and abdominal effusions
C. Fluid analysis of effusions
1. If total fluid protein is greater than 3.5 g/dL with more than 50% globulins, FIP is likely
2. FIP fluid usually has a low nucleated cell count
3. Cellular analysis of FIP fluid shows a pyogranulomatous exudate
4. Fluid may be stringy or sticky and may clot when refrigerated
D. Cerebrospinal fluid has a high protein concentration and an elevated nucleated cell count
E. FCoV antibody titers in serum or effusions
1. If the titer is positive but low, FIP is possible (if clinical signs are present)
2. If the titer is positive and high, FIP is probable (if clinical signs are present)
3. If the titer is negative, FIP is unlikely
4. Avoid rapid in-office ELISA tests that do not give titer information
F. The reverse transcriptase-polymerase chain reaction (RT-PCR) test can detect FCoV in blood, effusions, tissues, or feces. This indicates the presence of FCoV but does not distinguish between the mutated (FIP) form and the nonmutated form
H. Immunofluorescence and immunohistochemistry of tissue samples or effusion are definitive for effusive FIP
V. Treatment
A. No treatment has been proven to reduce the risk of FIP development in cats with FCoV
B. Antiviral drugs and immunomodulators have not been successful
C. Interferon therapy may cause remission in some, but is very expensive
D. Supportive care with high-dose corticosteroid with or without cytotoxic alkylating agents (chlorambucil, cyclophosphamide) may cause transient improvement
VI. Prevention
A. A vaccine is available but has not been shown to be effective and is not recommended
B. Control of exposure
1. Use good husbandry practices, reduce stress, avoid overcrowding, clean litter daily, and disinfect feeding and water bowls
2. Do not breed cats that have produced kittens that later developed FIP because of the possibility of genetic susceptibility
3. Wean kittens and remove them from the mother by 5 to 6 weeks of age. Isolate from all other cats until at least 4 months old
4. Any cat that tests positive for FCoV can shed virus in the feces and has the potential for developing FIP
FELINE INFECTIOUS RESPIRATORY DISEASE
I. Causes
A. Viruses: Feline herpesvirus-1 (FHV, feline viral rhinotracheitis, FVR), feline calicivirus (FCV)
B. Bacteria: Chlamydia felis, Bordetella bronchiseptica, Mycoplasma felis
II. Transmission
A. Via aerosol infection, through direct contact or fomites
1. FHV survives about 24 hours outside the host and is susceptible to drying and most disinfectants
2. FCV survives 8 to 10 days outside the host; bleach is the preferred disinfectant
B. Cats that have recovered from FHV and FCV become subclinical carriers, shedding virus for long periods of time
1. FHV persists for life, and carriers shed virus intermittently for approximately 2 weeks
2. FCV is shed for months to years
3. Chlamydophila felis can be shed for up to 18 months
4. Bordetella bronchiseptica can be shed for up to 5 months
III. Clinical signs
A. General signs include sudden onset of naso-ocular discharge, with anorexia, fever, and depression. Signs may be severe in young kittens. Infection with FHV and FCV is typically self-limiting within 10 days
B. FHV attacks conjunctival, nasal, and laryngotracheal epithelium, causing sneezing, lacrimation, naso-ocular discharge, coughing, and excess salivation
1. Secondary bacterial infection can occur
2. Turbinate damage may cause obstruction
3. Ulcerative lesions are not common
4. Abortion may occur in infected pregnant cats. Newborn kittens may have fatal encephalitis or hepatitis. Neonates may develop panophthalmitis, resulting in permanent ocular damage
C. Calicivirus consistently produces oral ulcers
1. Nasal crusting and ulceration may be seen
2. Mild rhinitis and conjunctivitis are commonly seen
3. Other signs associated with FCV include synovitis, fever, joint pain, enteritis, lower urinary tract disease
4. An acute hemorrhagic fever syndrome may occur with high fever, respiratory signs, ulcerative dermatitis, pulmonary edema, abdominal effusion, hepatic necrosis, disseminated intravascular coagulopathy (DIC), vomiting, diarrhea, epistaxis, or jaundice. Mortality is high, and FCV vaccines do not appear to protect against this strain
D. Chlamydia felis causes chronic conjunctivitis. Nasal discharge, sneezing, or pneumonia is uncommon
E. Bordetella bronchiseptica may cause fatal bronchopneumonia but is usually mild. Coughing does not routinely occur as in dogs
F. Complications
1. Cats that have recovered from FHV and FCV are carriers and are infectious for other cats
2. Chronic nasal disease can occur after FHV infection and includes sinusitis, turbinate damage, and obstructed nasal passages
3. Chronic ocular disease can occur after FHV infection and includes keratoconjunctivitis sicca, ulcerative keratitis, tear duct blockage, conjunctivitis, or anterior uveitis
4. Chronic oral disease such as stomatitis and gingivitis may be linked to FCV infection
IV. Diagnosis
A. The general diagnosis of upper respiratory infection is acceptable for the individual cat with mild infection. If infection is severe, or there is an outbreak of disease in a cattery, a confirmatory diagnosis should be attempted
1. Naso-ocular signs and corneal ulceration are more common with FHV
2. Oral ulcers are more common with FCV
3. Persistent conjunctivitis is common with chlamydophilosis
B. Direct immunofluorescence if most useful for FHV. Virus isolation from swabs is best for confirming FCV. PCR is sensitive for FHV determination
D. Intranuclear inclusion bodies (FHV or Chlamydophila) may be seen in conjunctival scrapings or biopsy
E. Evaluate for underlying FIV or FeLV if there are recurring episodes or if signs persist longer than 2 weeks
V. Treatment
A. Treat as an outpatient if possible
B. Treat supportively and provide fluid and nutritional support if needed
C. Ophthalmic therapy
1. Topical antiviral drugs can be used to treat ophthalmic signs of FHV
2. Do not use topical corticosteroids in FHV
3. Use tetracycline ophthalmic ointment for 3 to 4 weeks if Chlamydophila or Mycoplasma spp. are present
D. l-lysine therapy may reduce replication of FHV. Give twice daily with food
E. Broad-spectrum antibiotics (e.g., amoxicillin, doxycycline) can be used to control secondary infections
VI. Prevention
A. Vaccinate for FHV and FCV
B. Intranasal (modified live-virus vaccine [MLV]) vaccines give better protection and avoid adjuvant-related problems (injection site sarcomas). Sneezing and oculonasal discharge are common after intranasal vaccination
C. In shelters, vaccinate and isolate all new cats for 3 weeks. Provide adequate ventilation and disinfection
CANINE INFECTIOUS TRACHEOBRONCHITIS (KENNEL COUGH)
I. Causes
A. Canine parainfluenza virus (CPIV) or Bordetella bronchiseptica primarily. Canine adenovirus (CAV-2), herpesvirus, reovirus, and mycoplasmas may play a role
B. Cats may develop respiratory disease from B. bronchiseptica
C. Highly contagious, transmitted via aerosolized respiratory secretions or fomites
D. More common in dogs confined in facilities with poor ventilation
II. Clinical signs
A. Acute onset of loud, hacking cough. There is usually an increased production of mucus
B. Serous naso-ocular discharge may be present
C. Dogs typically continue to eat, are nonfebrile and active (unless pneumonia is present)
D. The clinical course is about 7 to 14 days
III. Diagnosis is usually based on history and clinical signs
A. Complete blood cell count(CBC) will typically be normal unless pneumonia is present (neutrophilic leukocytosis with left shift)
B. Thoracic radiography may identify the presence of pneumonia
C. Bordetella or Mycoplasma spp. may be found on culture
D. Virus (CPIV, CAV-2) can be isolated from nasopharyngeal or tracheal swabs
IV. Treatment
A. Treat as an outpatient if possible. Treat aggressively if pneumonia is present
B. Most cases are treated with doxycycline, amoxicillin, or azithromycin for possible infection with Bordetella
C. Do not use antitussives if the cough is productive. If the cough is nonproductive (with no fever or pneumonia), use hydrocodone and butorphanol
D. Corticosteroids can be used for a short period (5 days) to control cough, but do not use if there are any signs of pneumonia
E. Bronchodilators (e.g., theophylline, animophylline) may be used
V. Prevention
A. Vaccinate against CAV-2 and CPIV (MLV vaccines). If at high risk, Bordetella vaccination (killed vaccine) may be considered
1. Intranasal vaccines stimulate local immunity, rapid onset of protection, and minimal interference from maternal antibodies
2. Immunity for Bordetella lasts for 6 months or less
B. Isolate affected animals, provide proper ventilation (especially in kennels), use disinfectants
VI. Public health. B. bronchiseptica may infect immunocompromised humans, but risk is minimal
CANINE DISTEMPER
I. Causes and epidemiology
A. Epidemiology
1. RNA Morbillivirus in the Paramyxoviridae family
2. Occurs worldwide, with the highest incidence in dogs 2 to 6 months of age
3. Canidae, Mustelidae (e.g., ferrets, minks), Procyanidae (raccoons), large Felidae (e.g., cheetahs, lions, ocelots), bears, pandas, hyenas are all susceptible to canine distemper (CDV)
B. Transmission
1. Inhalation primarily but virus is shed in all secretions and excretions
2. Virus is shed for up to 1 to 2 weeks after recovery
3. CDV does not survive for more than a few days in the environment and is easily killed by disinfectants
II. Pathogenesis
A. The course of the disease is over a 2-week period
B. After infection of the upper respiratory tract, CDV spreads to lymphoid tissues, including liver, spleen, and GI tract (causing severe immunosuppression). Viremia occurs, and the virus is spread to epithelial tissues and the central nervous system (CNS). The outcome depends on the immune response
1. If the immune response is rapid, there is elimination of CDV with complete recovery (by day 14) and no clinical illness
2. If the immune response is partial, signs are mild and recovery occurs. Neurologic signs may develop from CNS localization
III. Clinical signs are multisystemic
A. Depression, anorexia, fever
B. Rhinitis, nasal discharge, cough, tachypnea (due to pneumonia)
C. Vomiting, diarrhea
D. Keratoconjunctivitis, retinal atrophy, retinal detachment, blindness
E. CNS signs include encephalitis, seizures, ataxia, abnormal reflexes, cranial nerve deficits, eye twitching
F. Enamel hypoplasia of the teeth
G. Hard pad disease: Nasodigital hyperkeratosis of the nose and foodpads
H. Cardiomyopathy
IV. Diagnosis is based on clinical signs in unvaccinated young dogs
A. Lymphopenia is noted early, with neutrophilic leukocytosis occurring later. Intracytoplasmic inclusion bodies may be seen
B. Radiography of the thorax shows diffuse interstitial pneumonitis, and secondary bronchopneumonia may develop
C. Analysis of cerebrospinal fluid may show increased cells (primarily lymphocytes), and antibodies to CDV may be noted
D. Immunoglobulin G (IgG) titer is not beneficial; an IgM titer is suggestive but not diagnostic
E. Viral antigen can be identified in blood cells or epithelial cells
V. Treatment is symptomatic and supportive
A. Broad-spectrum antibiotics
B. Restrict food intake and give antiemetics and antidiarrheals if vomiting or diarrhea is present
C. If seizures occur, give dexamethasone for CNS edema. Consider anticonvulsant therapy
VI. Prognosis
A. High mortality rate in young puppies
B. Neurologic deficits that occur are irreversible
VII. Prevention
A. Passive immunity is derived from colostrums
B. Measles vaccine can give partial protection in young puppies between the ages of 4 and 12 weeks
C. Vaccinate puppies starting at about 6 weeks, and vaccinate every 3 weeks until 12 to 14 weeks of age. Give a booster 1 year later, then every 3 years
D. Postvaccinal encephalitis has rarely occurred within a few weeks of MLV distemper vaccination, mostly in neonatal puppies
INTESTINAL VIRUSES
I. Canine parvovirus (CPV-2)
A. Cause and epidemiology
1. Nonenveloped, single-stranded deoxyribonucleic acid (DNA) virus
2. Probably evolved from feline panleukopenia virus
3. Transmission is fecal-oral
a. Massive amounts of virus are shed in feces, and the virus can survive for 5 to 7 months in the environment. Thus environmental contamination is a major source of infection
b. Signs of infection appear about 4 to 7 days after exposure
c. Clinical disease is most common in puppies between 6 weeks and 6 months of age
d. Rottweilers, Doberman pinschers, pit bull terriers, German shepherd dogs, and Labrador retrievers may be more susceptible to parvoviral infection
B. Parvovirus attacks rapidly dividing cells (GI, hematopoietic, lymphoid tissues). The intestinal mucosal barrier can break down, leading to bacteremia
C. Clinical signs
1. Sudden onset of vomiting and diarrhea, with severe dehydration. Diarrhea can be profuse and foul-smelling and may contain blood
2. DIC may occur
3. Severe cases may result in death, especially in young puppies
D. Diagnosis is usually based on clinical signs. Prior vaccination does not preclude the presence of parvovirus
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