Infectious Diseases in Cats PDF

Infectious Diseases 18 CHA P TE R Patricia A. Schenck...

Infectious Diseases 18 CHA P TE R Patricia A. Schenck D. Some cats that recover from transient infection FELINE LEUKEMIA VIRUS become latent carriers of FeLV. The latent stage is I. Causes usually eliminated with time, but a few remain in- A. Structure of the virus fected. In latent carriers, there is the rare possi- 1. RNA retrovirus bility that FeLV may be reactivated to replicating 2. Core contains viral RNA and reverse transcrip- infection tase enzyme E. Persistent infection is eventually fatal 3. Core protein p27 is the specific antigen de- III. Clinical signs tected by diagnostic tests A. The immunosuppression effects of FeLV cause 4. Envelope glycoprotein (gp70) is important in many nonspecific clinical signs, including weight defining the antigenic subgroup; only subgroup loss, fever, dehydration, anemia, diarrhea, stoma- A is infectious titis, lymphadenopathy, and oculonasal discharge 5. Envelope protein p15e mediates feline leuke- B. FeLV can be a primary cause of lymphoma, in- mia virus (FeLV) immunodeficiency cluding alimentary, mediastinal, multicentric, re- B. Prevalence nal, ocular, neural, and cutaneous lymphoma. 1. Young kittens (i.e., younger than 4 months of Lymphoid leukemia, nonlymphoid leukemia, or age) are most susceptible myelodysplasia may result from bone marrow 2. Highest prevalence in free-roaming stray cats infection C. Transmission C. Nonregenerative anemia is common with FeLV. 1. Primarily through saliva. Infected queens shed FeLV-related neutropenia or thrombocytopenia virus in milk. Exposure is typically by direct may occur contact through grooming, bite wounds, and D. Secondary infections are common and include vi- sharing of food and water bowls ral, fungal, protozoal, Mycoplasma, and bacterial 2. Transplacental transmission can occur causes 3. FeLV survives a maximum of 48 hours in the E. Peripheral lymph node hyperplasia can be seen, environment and is readily destroyed by most especially in young adult cats. This tends to re- disinfectants solve but may recur or develop into lymphoma at II. Pathogenesis a later date A. Sequence of FeLV infection F. Immune-mediated disorders such as immune- 1. After entry, FeLV replicates in lymphoid tissue mediated hemolytic anemia, immune-mediated throughout the body. Enzyme-linked immuno- thrombocytopenia, immune-complex glomerulo- sorbent assay (ELISA) tests may detect antigen nephritis, polyarthritis, pemphigus, and systemic in the blood at this stage. If an immune lupus erythematosus like syndrome may response is effective, the infection may be occur eliminated G. Infected queens may have reproductive failure. In- 2. FeLV infects bone marrow, causing circulation fertility, fetal resorption, abortion, stillbirth, fad- of infected leukocytes and platelets. These are ing kitten syndrome, and milk-borne transmission detectable with immunofluorescent antibody can occur (IFA) testing and indicate that the infection will IV. Diagnosis be persistent A. Test all cats before vaccination and before bring- 3. FeLV infects glandular cells, and virus is shed ing a new cat into the house or cattery in body secretions. At this stage, infected cats B. ELISA and immunochromatographic tests are contagious 1. Rapid screening tests; detect infection earlier B. Many cats over 4 months of age resist infection than IFA tests C. Most exposed cats develop a transient infection 2. Detect FeLV p27 antigen (a viral core protein); that is rejected by an immune response. These test not affected by vaccination or maternal cats eliminate virus within 4 to 6 weeks after in- antibodies fection. Vaccinated cats will have a brief transient 3. Confirm positive results with repeat testing in infection but resist persistent infection several weeks 260  CHAPTER 18 Infectious Diseases 261 C. The IFA test is preferred for confirmation of FeLV 3. Progressive loss of T cells results in an immuno- because it is more specific than ELISA testing deficiency syndrome with recurrent infections 1. May be negative in early infections 4. Eventually fatal 2. Confirm positive tests with repeat testing in a II. Clinical signs month A. Initial infection occurs within 4 to 6 weeks after D. Polymerase chain reaction (PCR) testing detects exposure; signs are usually mild and include a FeLV nucleic acid in blood, bone marrow, or biop- transient fever, neutropenia, lymphopenia, and sies and may be helpful in detecting latent FeLV lymphadenopathy infection B. A latent period follows, usually for several years E. Virus isolation is the “gold standard” for confirm- C. An immunodeficiency syndrome follows that ing positive test results with other methods predisposes the cat to chronic and recurrent V. Treatment infections A. Provide good general health care and prevent 1. General signs include weight loss, wasting, re- spread of infection to noninfected cats current fever, lymphadenopathy, polyclonal hy- B. Zidovudine (AZT) and interferon therapy may pergammaglobulinemia, recurrent anemia, leu- have some effectiveness copenia, or thrombocytopenia C. Provide fluid therapy, nutritional support, antibi- 2. Chronic infections affect the oral cavity (com- otics as needed mon), respiratory tract, gastrointestinal (GI) VI. Prevention and control tract, urinary tract, and skin. In the mouth, le- A. Vaccination sions often begin in the fauces and spread 1. Vaccines are available but are considered along the maxillary gingivae “non-core” vaccines 3. Common conditions include calicivirus, herpes- 2. Vaccinate cats that go outdoors or negative virus, poxvirus, papillomavirus, Chlamydophila cats living in a household with infected cats felis, Mycoplasma haemofelis, Staphylococcus, 3. Vaccination is not recommended in adult in- Pseudomonas, Mycobacterium, Yersinia, Candida, door cats with no exposure to infected cats Cryptococcus, Aspergillus, Toxoplasma, 4. Local swelling may develop at the site of vacci- Giardia, Cryptosporidium, Demodex, and nation and can develop into vaccine-associated Notoedres spp. sarcomas at a later date 4. FIV is neurotropic leading to neuronal damage; 5. Vaccination is not 100% effective signs include dementia, behavior abnormali- B. Control in multi-cat households and catteries ties, circling, gait abnormalities, and abnormal 1. In catteries with FeLV-positive cats, follow a reflexes test and removal program to eliminate FeLV 5. B-cell lymphoma and myeloproliferative neopla- from the household sia occur more frequently in FIV-infected cats 2. In FeLV-negative households or catteries, 6. Ocular disorders (anterior uveitis, chorioretini- screen any new cats with ELISA testing, vacci- tis, glaucoma, retinal hemorrhage, retinal de- nate (if negative), and isolate for 3 months generation) and nephropathy may occur in association with FIV III. Diagnosis FELINE IMMUNODEFICIENCY VIRUS (FIV) A. Test cats over 6 months of age I. Causes B. Assays for antibody A. Lentivirus subfamily of retrovirus; RNA virus with 1. The ELISA antibody test is useful for screening. outer envelope and nuclear capsid. Subtype A is Confirm any positive ELISA results with common in the western United States; subtype B Western blot is common in the eastern United States 2. IFA test B. Epidemiology 3. The Western blot test detects antibodies 1. Prevalence is higher in free-roaming against viral proteins and is the “gold stan- stray cats dard” test for confirming FIV 2. Affects all ages but most prevalent in C. Commercial PCR assays are unreliable at this time cats 6 years of age or older IV. Treatment 3. More prevalent in male cats A. Specific antiviral therapy 4. Wild felids are susceptible to feline immunode- 1. AZT can be used; however, it is myelosuppres- ficiency virus (FIV) sive. Drug-resistant strains may emerge C. Transmission 2. Treatment with feline or human interferon can 1. Shed in saliva; most infection occurs via a bite be attempted but is expensive and may only be wound effective short-term 2. Can be transmitted via intravenous (IV) trans- B. General supportive therapy includes antibiotics, fusion of contaminated blood fluid therapy, and nutritional support. Use metro- D. Pathogenesis nidazole and clindamycin to treat stomatitis 1. Infects T lymphocytes with loss of CD4 lym- V. FIV-positive cats can live several years before exhib- phocytes, inversion of the CD4-CD8 ratio with iting clinical signs loss of CD8 cells later VI. Prevention 2. Latent period can last for years A. Prevent exposure to other potentially infected cats 262 SECTION II SMALL ANIMAL 1. Spay and neuter cats that go outdoors to mini- C. Effusive (wet) form of FIP mize fighting 1. Inflammatory fluid is predominantly in the ab- 2. Minimize exposure to stray cats dominal cavity but can also be present in the B. Keep infected cats indoors to prevent exposure to thoracic cavity noninfected cats 2. Effusion in the peritoneal cavity causes pro- C. A killed vaccine is available that contains sub- gressive fluid distension, which can be de- types A and D; it is unknown whether there is tected by palpation and percussion of a fluid cross-protection with other subtypes. FIV vacci- wave. Scrotal swelling may be present in intact nation is not recommended as a core vaccine males D. Before vaccination, make sure that the cat is FIV 3. Thoracic effusion causes dyspnea, tachypnea, antibody negative and exercise intolerance from compression by fluid in the pleural space. Muffled heart sounds are usually noted FELINE INFECTIOUS PERITONITIS (FIP) 4. Thoracic and abdominal effusion can be con- I. Causes firmed by radiography A. Feline coronavirus (FCoV), a single-stranded en- 5. Pericardial effusion also occurs but does not veloped RNA virus that infects cells of the respi- typically cause clinical signs ratory and GI tracts D. Noneffusive (dry) form of FIP B. Pathogenesis 1. Characterized by pyogranulomatous inflamma- 1. Feline infectious peritonitis (FIP) occurs when tion and necrotizing vasculitis in multiple or- the enterotropic FCoV mutates, which allows gans. The specific organs affected determine FCoV to infect and replicate in macrophages which clinical signs are present 2. Macrophages carry the mutated virus to 2. Organs affected include kidney, liver, spleen, peritoneum, pleura, kidney, uvea, and nervous visceral lymph nodes, uvea, retina, brain, system lungs, and testicles 3. It is the immune reaction to the virus that 3. Meningoencephalitis and myelitis are common. causes disease The most common clinical signs are ataxia, II. Epidemiology tremors, vestibular dysfunction, seizures, pare- A. Seroprevalence for FCoV is high, yet few cats de- sis, and behavioral changes. Hydrocephalus velop FIP. Prevalence is highest in catteries and can occur shelters IV. Diagnosis of FIP B. Risk factors A. Hematology and serum chemistries 1. Young cats (6 months to 3 years) are at in- 1. Total serum protein and globulins are increased creased risk of FIP in most cases; albumin is commonly decreased. 2. Cats in catteries, shelters, or multiple cat A decreased serum albumin globulin ratio (A:G households are at higher risk of FIP 0.8) strongly suggests FIP 3. Anything that causes an increased replication 2. Chemistry profiles may reveal a number of ab- of FCoV in the intestine (stress, concurrent dis- normalities depending on the organs affected ease, corticosteroids, immuno suppression, B. Radiology is useful for confirming the presence of surgery) increases the probability of virus thoracic and abdominal effusions mutation C. Fluid analysis of effusions 4. Most wild felids (e.g., lions, cougars, cheetahs, 1. If total fluid protein is greater than 3.5 g/dL jaguars) are susceptible to FCoV and FIP. Chee- with more than 50% globulins, FIP is likely tahs are particularly susceptible to FIP 2. FIP fluid usually has a low nucleated cell count 5. Genetics may play a role in the susceptibility 3. Cellular analysis of FIP fluid shows a pyogranu- to FIP lomatous exudate C. Transmission is through oronasal contact with in- 4. Fluid may be stringy or sticky and may clot fected feces when refrigerated 1. FCoV can survive for 7 weeks in dried feces; D. Cerebrospinal fluid has a high protein concentra- thus contaminated articles (e.g., dishes, shoes, tion and an elevated nucleated cell count clothing) can serve as fomites. Most disinfec- E. FCoV antibody titers in serum or effusions tants will destroy FCoV 1. If the titer is positive but low, FIP is possible (if 2. Carriers of FCoV can shed virus in feces for clinical signs are present) 10 months 2. If the titer is positive and high, FIP is probable 3. Cats with FIP shed the nonmutated form of (if clinical signs are present) FCoV 3. If the titer is negative, FIP is unlikely III. Clinical signs 4. Avoid rapid in-office ELISA tests that do not A. Incubation period is variable from a few weeks to give titer information several years. The onset is usually gradual but F. The reverse transcriptase-polymerase chain reac- may be acute in young kittens tion (RT-PCR) test can detect FCoV in blood, effu- B. Once clinical signs develop, FIP is progressive sions, tissues, or feces. This indicates the pres- and fatal usually within 3 to 6 weeks but may re- ence of FCoV but does not distinguish between sult in prolonged illness for 6 months or longer the mutated (FIP) form and the nonmutated form  CHAPTER 18 Infectious Diseases 263 G. Histopathology is definitive for confirmation of A. General signs include sudden onset of naso- FIP. Lesions of vasculitis and pyogranulomatous ocular discharge, with anorexia, fever, and inflammation are characteristic. FCoV can be depression. Signs may be severe in young kittens. identified in tissue specimens by PCR and IFA Infection with FHV and FCV is typically self- H. Immunofluorescence and immunohistochemistry limiting within 10 days of tissue samples or effusion are definitive for ef- B. FHV attacks conjunctival, nasal, and laryngotra- fusive FIP cheal epithelium, causing sneezing, lacrimation, V. Treatment naso-ocular discharge, coughing, and excess sali- A. No treatment has been proven to reduce the risk vation of FIP development in cats with FCoV 1. Secondary bacterial infection can occur B. Antiviral drugs and immunomodulators have not 2. Turbinate damage may cause obstruction been successful 3. Ulcerative lesions are not common C. Interferon therapy may cause remission in some, 4. Abortion may occur in infected pregnant cats. but is very expensive Newborn kittens may have fatal encephalitis or D. Supportive care with high-dose corticosteroid hepatitis. Neonates may develop panophthal- with or without cytotoxic alkylating agents (chlo- mitis, resulting in permanent ocular damage rambucil, cyclophosphamide) may cause tran- C. Calicivirus consistently produces oral ulcers sient improvement 1. Nasal crusting and ulceration may be seen VI. Prevention 2. Mild rhinitis and conjunctivitis are commonly A. A vaccine is available but has not been shown to seen be effective and is not recommended 3. Other signs associated with FCV include syno- B. Control of exposure vitis, fever, joint pain, enteritis, lower urinary 1. Use good husbandry practices, reduce stress, tract disease avoid overcrowding, clean litter daily, and dis- 4. An acute hemorrhagic fever syndrome may oc- infect feeding and water bowls cur with high fever, respiratory signs, ulcer- 2. Do not breed cats that have produced kittens ative dermatitis, pulmonary edema, abdominal that later developed FIP because of the possi- effusion, hepatic necrosis, disseminated intra- bility of genetic susceptibility vascular coagulopathy (DIC), vomiting, diar- 3. Wean kittens and remove them from the rhea, epistaxis, or jaundice. Mortality is high, mother by 5 to 6 weeks of age. Isolate from all and FCV vaccines do not appear to protect other cats until at least 4 months old against this strain 4. Any cat that tests positive for FCoV can shed D. Chlamydia felis causes chronic conjunctivitis. virus in the feces and has the potential for de- Nasal discharge, sneezing, or pneumonia is veloping FIP uncommon E. Bordetella bronchiseptica may cause fatal bron- chopneumonia but is usually mild. Coughing does FELINE INFECTIOUS RESPIRATORY not routinely occur as in dogs DISEASE F. Complications I. Causes 1. Cats that have recovered from FHV and FCV A. Viruses: Feline herpesvirus-1 (FHV, feline are carriers and are infectious for other cats viral rhinotracheitis, FVR), feline calicivirus 2. Chronic nasal disease can occur after FHV in- (FCV) fection and includes sinusitis, turbinate dam- B. Bacteria: Chlamydia felis, Bordetella bronchisep- age, and obstructed nasal passages tica, Mycoplasma felis 3. Chronic ocular disease can occur after FHV in- II. Transmission fection and includes keratoconjunctivitis sicca, A. Via aerosol infection, through direct contact or ulcerative keratitis, tear duct blockage, con- fomites junctivitis, or anterior uveitis 1. FHV survives about 24 hours outside the host 4. Chronic oral disease such as stomatitis and and is susceptible to drying and most disin- gingivitis may be linked to FCV infection fectants IV. Diagnosis 2. FCV survives 8 to 10 days outside the host; A. The general diagnosis of upper respiratory infec- bleach is the preferred disinfectant tion is acceptable for the individual cat with mild B. Cats that have recovered from FHV and FCV be- infection. If infection is severe, or there is an out- come subclinical carriers, shedding virus for long break of disease in a cattery, a confirmatory diag- periods of time nosis should be attempted 1. FHV persists for life, and carriers shed virus in- 1. Naso-ocular signs and corneal ulceration are termittently for approximately 2 weeks more common with FHV 2. FCV is shed for months to years 2. Oral ulcers are more common with FCV 3. Chlamydophila felis can be shed for up to 3. Persistent conjunctivitis is common with chla- 18 months mydophilosis 4. Bordetella bronchiseptica can be shed for up to B. Direct immunofluorescence if most useful for FHV. 5 months Virus isolation from swabs is best for confirming III. Clinical signs FCV. PCR is sensitive for FHV determination 264 SECTION II SMALL ANIMAL C. Bordetella, Chlamydia, and Mycoplasma spp. can D. Virus (CPIV, CAV-2) can be isolated from nasopha- be identified by culture ryngeal or tracheal swabs D. Intranuclear inclusion bodies (FHV or Chlamydophila) IV. Treatment may be seen in conjunctival scrapings or biopsy A. Treat as an outpatient if possible. Treat aggres- E. Evaluate for underlying FIV or FeLV if there are sively if pneumonia is present recurring episodes or if signs persist longer than B. Most cases are treated with doxycycline, amoxi- 2 weeks cillin, or azithromycin for possible infection with V. Treatment Bordetella A. Treat as an outpatient if possible C. Do not use antitussives if the cough is productive. B. Treat supportively and provide fluid and nutri- If the cough is nonproductive (with no fever or tional support if needed pneumonia), use hydrocodone and butorphanol C. Ophthalmic therapy D. Corticosteroids can be used for a short period 1. Topical antiviral drugs can be used to treat (5 days) to control cough, but do not use if there ophthalmic signs of FHV are any signs of pneumonia 2. Do not use topical corticosteroids in FHV E. Bronchodilators (e.g., theophylline, animophyl- 3. Use tetracycline ophthalmic ointment for 3 to line) may be used 4 weeks if Chlamydophila or Mycoplasma spp. V. Prevention are present A. Vaccinate against CAV-2 and CPIV (MLV vaccines). D. L-lysine therapy may reduce replication of FHV. If at high risk, Bordetella vaccination (killed vac- Give twice daily with food cine) may be considered E. Broad-spectrum antibiotics (e.g., amoxicillin, 1. Intranasal vaccines stimulate local immunity, doxycycline) can be used to control secondary rapid onset of protection, and minimal interfer- infections ence from maternal antibodies VI. Prevention 2. Immunity for Bordetella lasts for 6 months A. Vaccinate for FHV and FCV or less B. Intranasal (modified live-virus vaccine [MLV]) B. Isolate affected animals, provide proper ventila- vaccines give better protection and avoid tion (especially in kennels), use disinfectants adjuvant-related problems (injection site VI. Public health. B. bronchiseptica may infect immuno- sarcomas). Sneezing and oculonasal discharge compromised humans, but risk is minimal are common after intranasal vaccination C. In shelters, vaccinate and isolate all new cats CANINE DISTEMPER for 3 weeks. Provide adequate ventilation and disinfection I. Causes and epidemiology A. Epidemiology 1. RNA Morbillivirus in the Paramyxoviridae family CANINE INFECTIOUS TRACHEOBRONCHITIS 2. Occurs worldwide, with the highest incidence (KENNEL COUGH) in dogs 2 to 6 months of age I. Causes 3. Canidae, Mustelidae (e.g., ferrets, minks), Procy- A. Canine parainfluenza virus (CPIV) or Bordetella anidae (raccoons), large Felidae (e.g., cheetahs, bronchiseptica primarily. Canine adenovirus lions, ocelots), bears, pandas, hyenas are all (CAV-2), herpesvirus, reovirus, and mycoplasmas susceptible to canine distemper (CDV) may play a role B. Transmission B. Cats may develop respiratory disease from B. 1. Inhalation primarily but virus is shed in all bronchiseptica secretions and excretions C. Highly contagious, transmitted via aerosolized re- 2. Virus is shed for up to 1 to 2 weeks after spiratory secretions or fomites recovery D. More common in dogs confined in facilities with 3. CDV does not survive for more than a few days poor ventilation in the environment and is easily killed by disin- II. Clinical signs fectants A. Acute onset of loud, hacking cough. There is usu- II. Pathogenesis ally an increased production of mucus A. The course of the disease is over a 2-week period B. Serous naso-ocular discharge may be present B. After infection of the upper respiratory tract, CDV C. Dogs typically continue to eat, are nonfebrile and spreads to lymphoid tissues, including liver, spleen, active (unless pneumonia is present) and GI tract (causing severe immunosuppression). D. The clinical course is about 7 to 14 days Viremia occurs, and the virus is spread to epithelial III. Diagnosis is usually based on history and clinical signs tissues and the central nervous system (CNS). The A. Complete blood cell count(CBC) will typically be outcome depends on the immune response normal unless pneumonia is present (neutrophilic 1. If the immune response is rapid, there is leukocytosis with left shift) elimination of CDV with complete recovery B. Thoracic radiography may identify the presence (by day 14) and no clinical illness of pneumonia 2. If the immune response is partial, signs are C. Bordetella or Mycoplasma spp. may be found on mild and recovery occurs. Neurologic signs culture may develop from CNS localization  CHAPTER 18 Infectious Diseases 265 3. If the immune response is poor, there is wide- in the environment. Thus environmental spread dissemination of the virus, with clinical contamination is a major source of infection signs and a high mortality rate b. Signs of infection appear about 4 to 7 days III. Clinical signs are multisystemic after exposure A. Depression, anorexia, fever c. Clinical disease is most common in puppies B. Rhinitis, nasal discharge, cough, tachypnea (due between 6 weeks and 6 months of age to pneumonia) d. Rottweilers, Doberman pinschers, pit C. Vomiting, diarrhea bull terriers, German shepherd dogs, and D. Keratoconjunctivitis, retinal atrophy, retinal de- Labrador retrievers may be more suscepti- tachment, blindness ble to parvoviral infection E. CNS signs include encephalitis, seizures, ataxia, B. Parvovirus attacks rapidly dividing cells (GI, hema- abnormal reflexes, cranial nerve deficits, eye topoietic, lymphoid tissues). The intestinal muco- twitching sal barrier can break down, leading to bacteremia F. Enamel hypoplasia of the teeth C. Clinical signs G. Hard pad disease: Nasodigital hyperkeratosis of 1. Sudden onset of vomiting and diarrhea, with the nose and foodpads severe dehydration. Diarrhea can be profuse H. Cardiomyopathy and foul-smelling and may contain blood IV. Diagnosis is based on clinical signs in unvaccinated 2. DIC may occur young dogs 3. Severe cases may result in death, especially in A. Lymphopenia is noted early, with neutrophilic young puppies leukocytosis occurring later. Intracytoplasmic in- D. Diagnosis is usually based on clinical signs. Prior clusion bodies may be seen vaccination does not preclude the presence of B. Radiography of the thorax shows diffuse intersti- parvovirus tial pneumonitis, and secondary bronchopneumo- 1. CBC: About 50% of dogs with parvovirus have nia may develop severe leukopenia (lymphopenia, granulocyto- C. Analysis of cerebrospinal fluid may show in- penia). The PCV can be decreased because of creased cells (primarily lymphocytes), and anti- intestinal blood loss or may be elevated from bodies to CDV may be noted dehydration D. Immunoglobulin G (IgG) titer is not beneficial; an 2. Serum chemistries typically show electrolyte IgM titer is suggestive but not diagnostic abnormalities and evidence of dehydration E. Viral antigen can be identified in blood cells or 3. Radiography shows gas and fluid distention of epithelial cells the GI tract V. Treatment is symptomatic and supportive 4. Indirect fluorescent antibody test detects IgM A. Broad-spectrum antibiotics antibodies giving evidence of recent infection B. Restrict food intake and give antiemetics and an- 5. Demonstration of excretion of virus or viral an- tidiarrheals if vomiting or diarrhea is present tigen in the feces provides definitive diagnosis C. If seizures occur, give dexamethasone for CNS of parvovirus. Rapid in-office tests are com- edema. Consider anticonvulsant therapy mercially available VI. Prognosis 6. At necropsy, characteristic intestinal lesions of A. High mortality rate in young puppies intestinal crypt cell necrosis are observed B. Neurologic deficits that occur are irreversible E. Treatment VII. Prevention 1. IV fluid therapy is the most important aspect A. Passive immunity is derived from colostrums of treatment B. Measles vaccine can give partial protection in a. Use a balanced crystalloid young puppies between the ages of 4 and 12 weeks (e.g., Normosol-R, lactated Ringer’s) C. Vaccinate puppies starting at about 6 weeks, and b. Add potassium to avoid hypokalemia; moni- vaccinate every 3 weeks until 12 to 14 weeks of tor serum potassium daily age. Give a booster 1 year later, then every 3 years c. Possibly add magnesium because in severe D. Postvaccinal encephalitis has rarely occurred cases magnesium is often deficient within a few weeks of MLV distemper vaccination, d. Add dextrose to control hypoglycemia; mostly in neonatal puppies monitor serum glucose concentrations e. Use hetastarch if balanced crystalloid solu- tions are not maintaining stability INTESTINAL VIRUSES 2. Broad-spectrum antibiotics (parenterally) help I. Canine parvovirus (CPV-2) to control bacterial complications. Use cefazo- A. Cause and epidemiology lin or ampicillin alone for mild cases or in com- 1. Nonenveloped, single-stranded deoxyribonucleic bination with aminoglycosides or fluoroquino- acid (DNA) virus lones in severe cases. Beware of nephrotoxicity 2. Probably evolved from feline panleukopenia with aminoglycoside use virus 3. Diet 3. Transmission is fecal-oral a. Give nothing orally for the first 12 to a. Massive amounts of virus are shed in feces, 24 hours. Partial parenteral nutrition may and the virus can survive for 5 to 7 months be needed if vomiting is prolonged 266 SECTION II SMALL ANIMAL b. When starting to refeed, give small feedings B. Clinical signs of a bland, highly digestible diet (commer- 1. Acute enteritis is seen in young puppies. This cial GI diet). Transition gradually back to is usually self-limiting normal feedings 2. Infection is subclinical in adult dogs 4. For vomiting, treat with metoclopramide. Gas- C. Diagnosis: Can be detected in feces by EM, PCR, tric acid secretion can be controlled with ranit- or virus isolation idine or famotidine D. Treat with supportive therapy a. Chlorpromazine can be used if metoclo- E. There is no vaccine. Ensure that neonates receive pramide is unsuccessful but only after dehy- colostrums dration has been corrected IV. Feline panleukopenia virus (FPV) b. Do not use anticholinergics A. Causes 5. Antidiarrheals are not usually needed as long 1. Infects all felines and also raccoons, ferrets, as fluid therapy is intensive; loperamide can be and minks used if necessary 2. Shed in body secretions for 6 weeks 6. Blood transfusion can be considered if there is 3. Resistant to inactivation but is inactivated with anemia, and plasma infusion may be used in dilute sodium hypochlorite. FPV can survive in cases of concurrent DIC the environment for over a year 7. Treat for septic shock if necessary 4. Affects rapidly dividing cells, especially intestinal F. Prognosis and complications crypt epithelium, lymphoid tissue, hemopoietic 1. If survive the first few days, most recover tissue, and nervous system in the developing 2. Mortality is highest in young puppies fetus 3. Complications include bacterial infections, B. Clinical signs other viral infections, liver disease, DIC, CNS 1. Young kittens usually show a high fever, vomit- signs ing, diarrhea, dehydration, and anorexia G. Prevention 2. In susceptible adult cats, infection is usually 1. Minimize exposure subclinical a. Keep an infected dog isolated for at least a 3. Infection can occur in utero near the end of week after recovery gestation or within the first few weeks of life. b. Keep young puppies isolated from other Infection at this time usually results in cere- dogs and potentially infected areas until bellar hypoplasia with ataxia and intention completely vaccinated tremors 2. Vaccination C. Diagnosis is based on clinical signs in an unvacci- a. Maternal antibodies interfere with protec- nated kitten tion by vaccination; thus there is a 2- to 1. Leukopenia can be profound and lasts 2 to 4-week period during which puppies may 4 days. If leukopenia lasts more than 5 days or be susceptible to infection but refractory nonregenerative anemia is also present, con- to vaccination sider FeLV infection b. Vaccinate puppies with MLV CPV-2 vaccines 2. Definitive diagnosis requires fecal PCR or virus every 3 to 4 weeks until about 14 weeks of isolation age. Booster 1 year later, then every 3 years D. Treat supportively (intensive fluid therapy, antibi- thereafter otics, antiemetics, dietary restriction) c. Used killed vaccine to vaccinate pregnant E. Prognosis is poor if hypothermia, shock, jaundice, dogs or for puppies less than 5 weeks of age or DIC develops II. Canine coronavirus F. Prevention A. Causes 1. Vaccination is highly effective 1. Transmission is fecal-oral 2. Use killed vaccine in kittens less than 4 weeks 2. Coronavirus is shed in feces for months after old or in pregnant cats infection 3. With MLV vaccine, vaccinate kittens twice, 3 B. Clinical signs: Acute mild diarrhea is most com- weeks apart. Give a booster 1 year later, then mon, and there may be mild anorexia, depression, revaccinate every 3 years or vomiting V. Feline coronavirus C. Diagnosis is based on clinical signs. Coronavirus A. Inapparent infection is very prevalent and may can be detected in feces using electron micros- cause mild enteritis copy (EM), virus isolation, or PCR B. In kittens 1 to 3 months of age, there is an acute D. Treat with supportive therapy. Antibiotics are not mild enteritis with diarrhea. Signs are typically usually necessary. Diarrhea may persist for 3 to self-limiting after 2 to 4 days 4 weeks C. Serology can measure a coronaviral titer but E. Prevention: Vaccines are available, but their effi- cannot distinguish between active or previous cacy and duration of immunity are questionable infection III. Canine rotavirus D. Treatment is supportive and often not A. Causes necessary 1. Transmission is fecal-oral E. An intranasal vaccine is available but is not 2. Highly infectious and persists in the environment effective  CHAPTER 18 Infectious Diseases 267 VI. Feline rotavirus B. Postexposure management (animal bitten by A. Has been isolated from normal cats and from cats known rabid animal) with diarrhea. Subclinical infection is frequent 1. Report human and animal exposure to public B. Clinical signs include a mild diarrhea in neonates health authorities for a few days 2. If the exposed animal has been previously C. Diagnosis: Detected in feces by EM, PCR, or ELISA vaccinated, revaccinate immediately and have D. Treat with supportive measures (fluid therapy, the owner observe for 45 days for any illness diet restriction) suggestive of rabies VII. Feline astrovirus 3. If the exposed animal is unvaccinated, eutha- A. Transmission: Fecal-oral route nasia is recommended so that tissues may be B. Clinical signs include a mild diarrhea for 4 to examined. If euthanasia is not allowed, isola- 14 days tion is required for 6 months. If signs sugges- C. Diagnosis: Detected in feces by EM or PCR tive of rabies occur, euthanasia and testing are D. Treat with supportive measures (fluids, diet re- required striction) VII. Prevention in humans is critical as clinical cases are fatal A. Preexposure prevention for humans at high risk in- RABIES clude immunization with human diploid cell vaccine I. Rabies is caused by a rhabdovirus that attacks the B. Animal bites to humans nervous system and is shed in saliva. Reservoir ani- 1. If a healthy dog or cat bites a human (if there is mals are skunks, raccoons, bats, foxes, and coyotes. possibility of that animal having contact with a Some can shed rabies for a long time with no evi- rabid animal), the animal is confined, isolated, dence of clinical signs. Rabies is inactivated by most and observed by the owner for 10 days. Any disinfectants signs of illness must be reported II. Pathogenesis. Rabies enters through a bite wound 2. If a wild animal or dog or cat with unknown usually and travels along peripheral nerves to the vaccination status bites a human, euthanasia CNS. Signs usually occur within 2 to 8 weeks. Virus is with examination of tissues is recommended shed in the saliva for about 10 days before clinical 3. Human wounds should be cleansed vigorously; signs appear, and shedding continues until death. ethanol or benzalkonium chloride are good dis- Once clinical signs start, death occurs within 3 to infectants 10 days a. Nonimmunized humans are given five doses III. Clinical signs of vaccine, and rabies immunoglobulin A. The first phase is prodromal and lasts for a b. Immunized humans are given two doses of few days. There may be subtle signs of erratic vaccine behavior B. The furious phase lasts 2 to 4 days, and signs of PSEUDORABIES erratic behavior (such as aggression, irritability, pica, roaming) are evident. There may be ataxia, I. Causes seizures, and paralysis A. Herpesvirus that infects pigs (Aujeszky disease) C. The paralytic phase lasts 2 to 4 days, and there is B. Results from ingestion of contaminated raw pork ascending paralysis of the limbs and laryngeal II. Clinical signs and pharyngeal paralysis. This phase is followed A. Fatal within 3 to 5 days after exposure by death B. Signs are similar to rabies or other encephalitis. D. Atypical rabies has occurred in dogs, cats, bats, Signs include intense pruritus (especially of the and skunks in which they develop subclinical or head and neck), depression, inactivity, anxiety, chronic infections restlessness, fever, diarrhea, vomiting, hypersali- IV. Diagnosis is accomplished postmortem. Chill the vation, ataxia, seizures. Death within 48 hours of animal’s head, but do not freeze onset of clinical signs A. Direct fluorescent antibody test is the test of III. Diagnosis choice. Brain or salivary glands can be tested A. Serologic tests used in pigs are not useful in dogs B. Negri bodies (intracytoplasmic neuronal inclu- and cats sions) can be seen in most rabid dogs (but not B. Diagnosis is made postmortem, based on testing cats) of unfixed brain tissue for virus V. Treatment is not recommended, as rabies is fatal and IV. Treatment. There is no known effective treatment poses a public health hazard. Any suspected case V. Prevention should be quarantined or euthanized A. Prevent direct contact with pigs VI. Prevention in dogs and cats B. Never feed raw pork A. Vaccination is protective. Only inactivated and re- combinant vaccines are available in the United MISCELLANEOUS VIRAL DISEASES States. Do not use rabies titers in animals, as they may not correlate with protection. Do not vacci- I. Infectious canine hepatitis (ICH) nate wild animals or hybrids against rabies, as A. Caused by canine adenovirus type 1 (CAV-1). ICH there are no vaccines licensed for these animals is rare because of vaccination. Foxes, coyotes, 268 SECTION II SMALL ANIMAL wolves, and bears are susceptible to ICH. Infec- B. Oral papillomatosis is most common, with multi- tion is via oronasal exposure. CAV-1 is very resis- ple nodules on the lips, oral mucosa, tongue, pal- tant to disinfection ate. These increase in size and number for about B. Clinical signs: There is usually a week-long course 4 to 6 weeks, then regress. Ocular or cutaneous with fever, vomiting, diarrhea, abdominal pain, papillomatosis are uncommon pharyngitis, lymphadenopathy, pneumonitis, and C. History and physical examination are diagnostic. hemorrhage. CNS signs may occur. Ocular disease PCR can confirm papillomavirus such as corneal edema or anterior uveitis may be D. Treatment is not necessary for the oral form. Oc- present. Persistent chronic hepatitis may develop ular nodules and some oral nodules should be re- C. Diagnosis is based on clinical signs in unvacci- moved. If nodules do not regress, vincristine can nated dogs. ICH can be confirmed by serology, be used weekly virus isolation, or histopathology (intranuclear V. Feline poxvirus viral inclusions) A. Caused by cowpox virus (orthopoxvirus); has D. Treatment is supportive been seen only in Europe and Asia in cats. Infec- E. CAV-2 vaccination is very effective for prevention. tion is from exposure to rodents CAV-1 vaccines are not recommended as they can B. After the primary lesion (usually a bite wound), cause an anterior uveitis, mild nephritis, and viremia occurs, with mild systemic signs. Pox le- urine shedding of virus sions develop that are small (1 mm) and numer- II. Canine acidophil cell hepatitis ous (10 or more) and are covered with scabs A. Etiology. Transmissible; distinct from CAV-1 and C. Diagnosis is based on history and clinical signs and CAV-2 can be confirmed with fluorescent antibody staining B. Clinical signs include acute hepatitis, chronic D. There is no specific treatment as skin lesions usu- hepatitis, cirrhosis, and hepatocellular carcinoma. ally regress. Cowpox virus is potentially transmis- Signs reflect liver involvement sible to humans C. Diagnosis VI. Other viruses 1. Tests reflect liver disease, with alanine amino- A. West Nile virus is a flavivirus in bird populations. transferase and alanine phosphatase elevations It is transmitted by mosquitoes to birds, humans, most consistent horses, dogs, and cats. Meningoencephalitis oc- 2. Diagnosis depends on liver biopsy curs in birds, humans, and horses, but most dogs D. Treatment and prevention: Provide supportive and cats have few clinical signs treatment for liver failure B. Bornavirus can cause fatal neurologic disease in III. Canine herpesvirus (CHV) dogs and cats, mostly in Europe and Japan. Hu- A. Once infected, dogs remain carriers for life. CHV man infection can occur, and transmission is pre- is readily inactivated in the environment. Trans- sumed to be through a vector mission occurs in utero, during birth (contact C. Other vector-borne viruses that can infect dogs with vaginal secretions), or by oronasal contact and cats include equine togaviruses (equine en- with secretions from an infected mother cephalitis), flaviviruses, bunyaviruses (Rift Valley B. Clinical signs fever), and orbiviruses (African horse sickness) 1. Fetal infection results in fetal resorption, late- D. Avian influenza H5N1 can cause fatal pneumonia gestation abortion, or stillbirth in cats 2. Neonatal systemic infection occurs from birth E. Hantavirus is endemic in rodents and has been to about 3 weeks of age and leads to virus dis- found in cats in North America, Europe, and Asia. tribution to all tissues. Necrosis and hemor- In cats the infection is subclinical, but in humans rhage of many organs occur. Clinical signs in- Hantavirus is life-threatening, causing hemor- clude refusal to nurse, continuous crying, low rhagic fever, renal or pulmonary syndromes body temperature, petechial hemorrhages, G. Feline foamy virus (spumavirus) was formerly with death within 24 to 72 hours called feline syncytium-forming virus. Infection is 3. Adults and older puppies are resistant to infec- very common but does not cause clinical signs tions because of their higher body tempera- H. Feline spongiform encephalopathy has been ob- tures. Infection usually causes mild signs in the served in cats in the United Kingdom and is con- respiratory and genital tracts sidered to be caused by the same prion that C. Diagnosis in newborn puppies is via clinical signs. causes bovine spongiform encephalopathy (mad Virus can be isolated from the oropharynx or gen- cow disease). Cats are infected via ingestion of ital lesions in adults infected meat. Cats develop neurologic signs after D. Treatment is not effective. Puppies that do re- a long incubation period, and there is a slow cover have neurologic dysfunction progression to death. There is no treatment E. Isolate infected bitches and litters, disinfect the premises, and maintain warm ambient tempera- RICKETTSIOSIS, EHRLICHIOSIS, tures for newborn puppies ANAPLASMOSIS, NEORICKETTSIOSIS IV. Canine viral papillomatosis A. Caused by canine papillomavirus and occurs I. Rocky Mountain spotted fever (Rickettsia rickettsiae) most commonly in young dogs. Transmission is A. Caused by R. rickettsiae and in the United States by direct contact, and incubation is 1 to 2 months is most prevalent in the Southeast, Midwest, and  CHAPTER 18 Infectious Diseases 269 Great Plains regions. It is transmitted by the German shepherd dogs and Doberman pinschers. American dog tick (Dermacentor variabilis) and Nonregenerative anemia, thrombocytopenia, leu- the wood tick (Dermacentor andersoni). Rodents kopenia, lymphocytosis, or plasmacytosis may be are the reservoir. Most infections occur in April present. Some cases show a polyclonal gammopa- through October (tick season) thy, or protein-losing nephropathy. Many signs B. Once bitten by a tick, the organism invades vas- may resemble multiple myeloma cular endothelial cells, causing necrotizing vascu- F. Diagnosis litis, edema, and damage of multiple organs. The 1. Serology using IFA is reliable; however, titers incubation period is a few days to a few weeks, may not be detected until 2 to 4 weeks after and clinical illness lasts 1 to 2 weeks with a high infection. An antibody titer persists for about mortality rate 9 to 12 months and does not protect against C. Clinical signs are usually acute and may include reinfection. Serology using the ELISA test kit general signs of fever, anorexia, lethargy, joint only detects infection by E. canis. pain, ocular signs, neurologic signs, vasculitis, pe- 2. PCR testing can identify the Ehrlichia species techial to ecchymotic hemorrhages, pneumonitis, present and myocarditis 3. Intracellular Ehrlichia can be identified in D. Thrombocytopenia is common, as is leukocytosis blood leukocytes, and morulae can be seen in with a left shift, anemia, and toxic granulation of bone marrow cells or aspirates of lymph neutrophils nodes. E. canis and E. chaffeensis are found E. Diagnosis can be confirmed by serum antibody ti- in monocytes, and E. ewingii is found in ters and PCR. The IFA test is diagnostic if there is neutrophils a single high titer, or a four-fold increase in paired G. Doxycycline is the treatment of choice. Clinical serum samples. There can be crossreactivity with signs should improve within 48 hours, and plate- other Rickettsia spp. lets should start to increase within 2 to 7 days. G. Doxycycline is the drug of choice for treatment. The prognosis is good unless there is severe hy- The prognosis is good if treatment is initiated poplasia of the bone marrow early in the course of the disease H. Ehrlichiosis is prevented by minimizing exposure H. Minimize exposure to ticks. Rocky Mountain to ticks. Ticks can transmit Ehrlichia occasionally spotted fever is an important tickborne disease in to humans humans, but dogs are a minimal zoonotic risk III. Anaplasmosis II. Canine ehrlichiosis A. Caused by Anaplasma phagocytophilum that is A. Caused by a variety of species of Ehrlichia, transmitted by Ixodes ticks. The mouse is a reser- including E. canis, E. ewingii, and E. chaffeensis. voir. Most cases occur in the Northeast, upper Ehrlichia is a gram-negative cocci that infects Midwest, and Pacific Coast of California. Ticks leukocytes can infect humans, dogs, cats, horses, small rumi- B. E. canis is transmitted via the brown dog tick nants, and other wildlife (Rhipicephalus sanguineous) most frequently in B. Clinical signs are usually seen in acutely infected the Southeast. E. ewingii is transmitted by the animals. Signs are nonspecific and include fever, lone-star tick (Amblyomma americanum) and pos- lethargy, arthralgia, and polyarthritis. Morulae sibly other ticks most frequently in the Southern may be observed in neutrophils and are identical and Central United States. E. chaffeensis occurs in in appearance to E. ewingii the South and is transmitted by the lone-star tick C. Serum antibody titer or PCR can identify C. E. canis and E. chaffeensis infect monocytes and A. phagocytophilum phagocytes in lymph nodes, spleen, liver, and D. Doxycycline is the treatment of choice bone marrow. E. ewingii infects granulocytes. E. Anaplasmosis is prevented by minimizing tick E. canis typically causes a long subclinical phase exposure that can last for years before developing clinical IV. Canine cyclic thrombocytopenia signs of chronic infection A. Caused by Anaplasma platys, which replicates in D. Acute signs of infection occur a few weeks after a platelets. It is thought to be spread via ticks and tick bite, and signs last 2 to 4 weeks. Clinical is most common in the Southeast and Gulf Coast signs of acute infection include fever, anorexia, states lethargy, oculonasal discharge, lymphadenopathy, B. Few clinical signs are observed. Moderate to splenomegaly, hepatomegaly, and thrombocytope- severe thrombocytopenia develops in 14-day nia. Neurologic signs are infrequent. E. ewingii intervals commonly causes polyarthritis. Antibody titers C. Diagnosis is by serology or PCR. A. platys morulae may be negative during the acute phase are sometimes seen as inclusions within platelets E. After the acute phase, a long subclinical phase D. Doxycycline is the treatment of choice follows and can last from months to years. A vari- E. Minimize exposure to prevent ety of vague clinical signs occur in the chronic V. Neorickettsiosis (Potomac horse fever) phase, including weight loss, fever, spontaneous A. Caused by Neorickettsia risticii and can infect bleeding, anemia, lymphadenopathy, splenomeg- dogs and cats aly, hepatomegaly, uveitis, polyarthritis, and limb B. The vector is a fluke that uses snails as an inter- edema. Clinical signs may be more severe in mediate host. Infection is from ingestion of the 270 SECTION II SMALL ANIMAL trematode stage in water or ingestion of infected C. Most cases occur in the Northeast states and also snails in Wisconsin and Minnesota, where as many as C. Clinical signs include lethargy, vomiting, petechial 80% of ticks may carry Borrelia hemorrhages and bleeding, polyarthritis, edema, D. Clinical signs of disease are present in only 5% of and posterior paralysis. Anemia, thrombocytope- infected dogs; subclinical infection is common nia, and coagulopathy may be present II. Clinical signs develop 2 to 5 months after exposure D. Diagnosis is by demonstration of a positive anti- A. Polyarthropathy causing shifting-leg lameness is body titer against N. risticii the most common sign E. Doxycycline is the recommended treatment 1. Swelling and joint pain may be observed F. Minimize exposure to standing water and snails 2. Chronic arthritis may develop to prevent transmission 3. Synovial fluid examination shows suppurative VI. Salmon poisoning disease inflammation A. Caused by Neorickettsia helminthoeca and found B. Protein-losing glomerulopathy and renal failure only in dogs in the Pacific Northwest. Cats are not have been associated with borreliosis, especially susceptible in Labrador retrievers and golden retrievers B. The vector is a fluke (Nanophyetus salmincola) in- C. Borreliosis is not well documented in cats, but fected with N. helminthoeca. Dogs are infected by many cats are seropositive for Borrelia ingesting raw salmon (or other fish) containing III. Diagnosis the infected fluke. An intermediate host snail that A. Serologic tests for Borrelia antibodies only lives in the Pacific Northwest is required for 1. ELISA and IFA antibody titers the life cycle a. These tests do not differentiate between C. After ingestion, the flukes mature within the dog’s natural infection and vaccination titer intestine and infect the intestinal epithelium and b. A titer increases within 4 to 6 weeks after mononuclear cells. They then disseminate to exposure lymph nodes, spleen, liver, CNS, and lungs. This c. Positive titers can persist for years. IgG and incubation period is from 5 to 21 days IgM titers are not useful D. Clinical signs include high fever, anorexia, hemor- d. A negative titer rules out borreliosis, as rhagic diarrhea, vomiting, weight loss, and lymph- false-negative titers are rare adenopathy. The acute onset can resemble canine 2. C6 Antibody test is highly specific for B. burg- parvovirus infection dorferi E. Fluke ova are usually seen on direct fecal smears. a. This test uses a C6 antigen that can detect Lymph node aspirates often show reactive lym- C6 antibodies against an outer surface pro- phocytes with intracytoplasmic rickettsial bodies tein of Borrelia spp. in macrophages b. This test distinguishes between natural in- F. Doxycycline and tetracycline are the antibiotics fection and vaccination, as only naturally in- of choice. Praziquantel eliminates flukes fected dogs have C6 antibodies. This test G. Do not allow dogs to eat raw fish also does not crossreact with antibodies VII. Feline Ehrlichia-like diseases against other spirochetes (Leptospira) A. Cats can be infected with E. canis, N. risticii, and c. Early infections can be detected with the C6 A. phagocytophilum. Tick vectors are likely for antibody test, before the development of Ehrlichia and Anaplasma clinical signs B. Clinical signs include fever, lethargy, anorexia, 3. Western blot assay gives similar information as GI signs, weight loss, polyarthritis. There may be the C6 antibody test but is more cumbersome a nonregenerative anemia, thrombocytopenia, or and expensive pancytopenia B. PCR and culture can be used to identify organisms. C. Diagnosis has been confirmed by direct visualiza- It is best to use a skin biopsy from around the tick tion of organisms in blood, serology, and PCR bite site. Borrelia can be difficult to culture D. Doxycycline, tetracycline, or imidocarb have been IV. Treatment used for treatment A. Doxycycline orally is the treatment of choice for E. Minimize tick exposure to prevent dogs exhibiting clinical signs of borreliosis. The response is usually rapid. Use nonsteroidal antiinflammatory drugs to treat joint pain BORRELIOSIS (LYME DISEASE) B. Dogs that are seropositive but asymptomatic do I. Causes not require treatment but should be monitored A. Borreliosis is caused by the spirochete Borrelia for lameness burgdorferi and is transmitted primarily by the V. Prevention deer tick (Ixodes spp.). Ticks must attach to skin A. Vaccinate dogs at high risk (hunting dogs, out- for at least 48 hours to transmit Borrelia. Once in door dogs) in tick-infested areas the skin, Borrelia spreads through connective B. Avoid tick bites with topical fipronil, permethrin, tissue or amitraz B. Deer are not usually infected. Mice and other ro- VI. Public health dents are the reservoir hosts. Migratory birds A. Most cases occur in the Northeast states and in may carry deer ticks long distances Wisconsin and Minnesota  CHAPTER 18 Infectious Diseases 271 B. Reduce tick exposure to prevent human F. Humans are infected primarily through contami- infection nated water. Rodent control is important in pre- vention of leptospirosis. Urine should be avoided from infected dogs. Use an iodophor as a disinfec- SYSTEMIC BACTERIAL INFECTIOUS tant to clean urine DISEASE II. Brucellosis I. Leptospirosis A. Caused by Brucella canis, which is a gram- A. Leptospira are spirochetes that colonize in the negative coccobacillus proximal renal tubules. In the United States, lepto- B. Transmission is via semen, vaginal discharge, spirosis is usually caused by serovars L. ictero- urine, or aborted fetal tissue haemorrhagiae, L. canicola, L. pomona, L. bratislava, C. Brucella organisms can live for long periods L. grippotyphosa, and L. autumnalis within mononuclear phagocytes. Bacteremia usu- 1. Wild animals such as rodents, raccoons, ally occurs about 1 to 4 weeks after infection and skunks, and squirrels are sources of infection can last more than 5 years 2. Infection is via skin penetration with environ- D. Most dogs have no clinical signs, but there may mental organisms, especially in contaminated be lymphadenopathy, splenomegaly, and repro- water. Infection can also come from contami- ductive failure. Males typically have testicular at- nated food, bedding, or soil rophy, epididymitis, and sterility. Infected females 3. The prevalence of leptospirosis is increasing fail to conceive, or they abort dead fetuses late in and is most common in periurban areas; how- gestation ever, all dogs are at risk. Late summer and E. Diagnosis early fall or after wet periods are the most 1. A rapid slide agglutination test (RSAT) is used common times of infection for screening, but false-positives are common. 4. Bacteremia occurs about 4 to 12 days after in- Any animal that shows a positive reaction on fection, and the most common organ targets the RSAT should be confirmed by a more spe- are the kidney and liver cific test. False-negatives are rare B. Clinical signs are acute in nature and mostly due 2. Agar gel immunodiffusion (AGID) is the best to acute renal failure or acute hepatic failure in test for confirmation of a positive RSAT result conjunction with DIC 3. The tube agglutination test can be used to C. Diagnosis confirm a positive RSAT result; however, false- 1. Azotemia and increased serum concentrations of positive results do occur liver enzymes are common. Thrombocytopenia 4. A positive blood culture is the most definitive can be severe proof of brucellosis 2. On ultrasound, kidneys show increased F. Treatment is difficult because Brucella is refractory echogenicity in 75% of cases and may have to antibiotics as a result of being intracellular. Re- demarcation of the corticomedullary border lapses occur, so several courses of antibiotics may (medullary rim sign) be needed. Minocycline and dihydrostreptomycin 3. Serology are used in combination. Ovariohysterectomy or a. Microscopic agglutination titer can indicate castration is recommended current or past infection, or leptospiral G. All breeding animals should be screened for bru- vaccination. A high single titer (i.e., 1:800) cellosis before each breeding for females and at or a four-fold increase in paired serum sam- least twice yearly in stud dogs. Brucellosis- ples suggests current infection. Different positive dogs should be removed from a serovars can be tested breeding program b. Combined immunoglobulin titers can distin- H. Canine brucellosis has a low public health risk, guish natural infection from prior infection but human infection from infected dogs has been or vaccination but cannot distinguish be- documented tween serovars III. Bartonellosis 4. Leptospira organisms can be identified by dark- A. Feline bartonellosis (cat scratch disease) field microscopy of fresh urine. Culture is diffi- 1. Cause cult and is rarely used for diagnosis a. Cats are the main reservoir for Bartonella D. Treatment can be effective in 75% to 90% of cases, henselae but may also be a reservoir for although chronic renal failure is a common out- B. clarridgeiae, B. koehlerae, and B. bovis come. In the initial phase, supportive care is given b. Transmission is through fleas but can occur for acute renal failure, and penicillin or amoxicillin through blood transfusions. Prevalence is is used. After the amoxicillin therapy, doxycycline high in flea-infested areas. Cats younger is used to eliminate the renal carrier state than 1 year are most commonly infected E. Vaccines can reduce the incidence of leptospirosis. 2. Clinical signs are rare in cats, and most with A multivalent vaccine containing the serovars bacteremia are clinically healthy. Occasionally L. pomona, L. grippotyphosa, L. canicola, and fever, lymphadenopathy, uveitis, gingivitis, L. icterohaemorrhagiae give the broadest protec- endocarditis occur tion. Anaphylactic reactions can occur, especially 3. Diagnostic testing should be performed only in in small breeds and puppies under 9 weeks of age those exhibiting clinical signs 272 SECTION II SMALL ANIMAL 4. Serology indicates exposure. Blood culture or B. Clinical signs are related to the site of the granu- PCR can prove active infection lomatous inflammation and are usually chronic. 5. Antibiotics such as macrolides (azithromycin) Pulmonary infection is common in dogs with or fluoroquinolones (enrofloxacin) are indi- M. tuberculosis. Cats more commonly have cated only if clinical signs are present M. bovis, and the GI tract is affected. M. avium 6. Flea control is the best method of prevention can cause disseminated mycobacteriosis 7. In humans, bartonellosis is characterized by a C. Diagnosis is based on finding club-shaped acid- small granuloma at the site of a cat scratch after fast bacteria in lesions. Culturing Mycobacteria 7 to 12 days. A few weeks later there is regional may take 6 weeks lymphadenopathy, which usually resolves within D. Infections with M. avium are treated with a combi- 2 to 3 months. Signs can be more severe in im- nation of rifampin, enrofloxacin, and azithromy- munocompromised people. Immunocompro- cin. Euthanasia is recommended in those with mised owners should avoid cats younger than systemic disease or infected with M. tuberculosis 1 year and avoid being scratched; pets need to or M. bovis as a result of zoonotic potential be kept free of fleas V. Tularemia B. Canine bartonellosis A. Caused by Francisella tularensis, a gram-negative 1. Causes coccobacillus. In the United States, most cases a. Infection is most often due to Bartonella occur in Arkansas, Missouri, Oklahoma, and henselae or B. vinsonii (ssp. berkhoffii). B. South Dakota. Transmission can be via a number vinsonii (berkhoffii) is more commonly asso- of routes, including tick and deerfly bites, bites ciated with clinical signs from infected animals, inhalation, or ingestion. b. B. vinsonii (berkhoffii) is transmitted by Ticks, rodents, and rabbits are the primary reser- ticks (usually Rhipicephalus sanguineous), voir, but cats, dogs, livestock, and humans are and coyotes are a major reservoir in also susceptible California. B. vinsonii (berkhoffii) has B. Clinical signs are more common in cats and in- been found worldwide clude anorexia, depression, fever, oral ulcers, c. B. henselae and other Bartonella species are pneumonia, and hepatic necrosis transmitted by fleas. There is a high sero- C. Diagnosis is by serologic testing. Bone marrow, prevalence in the southeastern United States, lymph nodes, or blood can also be cultured where there are many fleas D. Affected animals can transmit infection to people. 2. Clinical signs include a transient fever with a Gentamicin, enrofloxacin, or doxycycline is used persistent bacteremia and immunosuppres- VI. Feline plague sion. A number of conditions are showing asso- A. Caused by Yersinia pestis, a gram-negative cocco- ciation with bartonellosis, especially aortic bacillus. The primary reservoirs are rodents, and valve endocarditis, unexplained granulomatous fleas transmit the disease to pets and humans. In disease, unexplained epistaxis, or immune- the United States, it is most common in the west- mediated disease ern states. Cats are more commonly affected than 3. About half the dogs with clinical bartonellosis are dogs have thrombocytopenia, and about one third B. Clinical signs rapidly progress, with an incubation have eosinophilia. ANA tests can be positive period of 1 to 4 days with bartonellosis 1. Bubonic plague is most common in cats, most 4. Diagnosis is based on serum antibody titers or often affecting submandibular lymph nodes on PCR. Culture of blood is rarely successful 2. Pneumonic plague causes pneumonia and 5. Severe disease is treated with aminoglycosides abscessation in the lung. Animals with pneu- and a penicillin derivative. Chronic disease is monic plague are a serious public health risk treated with azithromycin or a combination of 3. In septicemic plague there is widespread fluoroquinone and amoxicillin dissemination to organs 6. Reduce the exposure to ticks to prevent C. Diagnosis is based on finding gram-negative coc- bartenellosis cobacilli in lymph node exudates. Serology, anti- 7. Do not use dogs with Bartonella as blood donors gen detection, or culture can be used to confirm IV. Mycobacteriosis D. Affected animals can transmit infection to people. A. Causes Parenteral gentamicin is the drug of choice. 1. Mycobacteria are acid-fast, gram-positive bac- Doxycycline can also be used teria that cause persistent infection that leads to granulomatous inflammation SYSTEMIC MYCOSES 2. M. tuberculosis is transmitted from humans to pets via inhalation; pulmonary infection is common I. Histoplasmosis 3. Infection with M. bovis is from unpasteurized A. Causes milk or raw meat. More common in cats; the in- 1. Caused by Histoplasma capsulatum, which is testinal tract is usually involved found in the soil 4. M. avium infection is from contaminated soil or 2. In the United States, it is most prevalent in water. Basset hounds and Siamese cats are the Mississippi, Ohio, and Missouri River genetically predisposed regions  CHAPTER 18 Infectious Diseases 273 3. Route of infection is by inhalation of spores; in- 5. Cytology is the best method for diagnosis. Or- testinal infection from ingestion can also occur ganisms are usually within the cytoplasm of B. Pathogenesis macrophages and appear as round to oval 1. Incubation period of 12 to 16 days structures, 2 to 4 m in diameter, surrounded 2. Invades the lungs and then spreads to the by a clear halo mononuclear phagocyte system (i.e., spleen, 6. Histopathology usually shows granulomatous liver) inflammation, but organisms can be difficult 3. More prevalent in young animals (i.e., younger to find than 4 years) 7. Culture: Grows on Sabouraud’s dextrose agar 4. More common in sporting and hound breeds at room temperature in 7 to 10 days C. Clinical signs E. Treatment 1. Subclinical infection of the respiratory tract is 1. Itraconazole is the treatment of choice. Treat the most common outcome. May see multiple, for a minimum of 4 to 6 months calcified interstitial foci in the lungs 2. Itraconazole plus amphotericin B is used when 2. Acute pulmonary infection severe infection is present. The combined ther- a. Causes severe pneumonia, and death may apy is followed by use of itraconazole alone for occur at least 2 to 4 months b. Radiographically, diffuse or nodular intersti- 3. Fluconazole is used for ocular and neurologic tial pulmonary infiltrates are observed infections 3. Chronic pulmonary infection 4. Ketoconazole is not as effective as itraconazole a. Causes chronic pneumonia and is more but is less expensive common than an acute pulmonary infection II. Blastomycosis b. Clinical signs include chronic cough, exer- A. Cause cise intolerance, mild dyspnea 1. Cause is Blastomyces dermatitidis in the soil c. Enlargement of the tracheobronchial lymph 2. Distribution is in the Great Lakes regions of nodes and nodular interstitial infiltrates are the United States, especially around the seen on radiographs Mississippi and St. Lawrence Rivers. The 4. Intestinal infection organisms live in sandy, acidic soil near a. Occurs more commonly in dogs water b. Can affect small or large intestine, with 3. Infection is via inhalation of spores. Focal skin granulomatous thickening of the bowel wall infection can also occur by direct contact c. Signs include diarrhea, progressive weight 4. Dogs are very susceptible to blastomycosis. loss, anorexia, lethargy, fever, anemia, vom- Young large-breed, sporting, and hound breeds iting, and abdominal effusion are most commonly affected because of in- 5. Disseminated infection creased exposure opportunities. Blastomycosis a. Clinical signs include anorexia, depression, is rare in cats fever, weight loss, and signs dependent on B. Clinical signs the organs involved 1. Pulmonary infection is present in 85% of cases b. Organs involved can include bone marrow, and can include pyogranulomatous pneumo- lymph nodes, liver, spleen, peritoneum, nia, alveolar consolidation, solitary lung eyes, CNS, skin, bone, or oral cavity masses, and pleural effusion D. Diagnosis 2. Disseminated infection is common to lymph 1. Hematology nodes, skin, eyes, and bone. Infection can also a. Normocytic, normochromic nonregenera- occur in the CNS, male genitalia, oral or nasal tive anemia is common cavities, and abdomen b. Subclinical thrombocytopenia is common C. Diagnosis c. May see neutrophilic leukocytosis or neu- 1. Hematology and serum chemistries tropenia. Pancytopenia is occasionally seen a. Neutrophilic leukocytosis, monocytosis, in cats lymphopenia, and mild regenerative anemia 2. Serum chemistry evaluation may reveal hyper- are most common calcemia, hypoalbuminemia, or elevated liver b. Hypercalcemia is noted in some cases enzymes if there is hepatic involvement c. Mild hypoalbuminemia may be noted 3. Imaging 2. Imaging: Radiographs of the lungs show diffuse a. Radiographs show tracheobronchial lymph- interstitial infiltrate or nodular patterns in adenopathy, diffuse or nodular interstitial most cases pulmonary infiltrates, or calcified pulmo- 3. Serology: The AGID test is the most reliable nary interstitial nodules (if inactive) 4. Cytology is the most useful tool for diagnosis b. Depending on organs involved, there may a. Thick-walled extracellular yeast bodies be splenomegaly, hepatomegaly, abdominal (5 to 20 m) with broad-based budding effusion, bone lesions, or thickening of the are observed intestinal wall b. Organisms can also be identified in biopsy 4. Serology is unreliable, and it is better to con- specimens firm infection by identifying the organism 5. Culture: Growth occurs after 1 to 4 weeks 274 SECTION II SMALL ANIMAL D. Treatment IV. Cryptococcosis 1. Itraconazole is the treatment of choice. Treat A. Causes for at least 2 to 3 months 1. Cryptococcus neoformans 2. Itraconazole plus amphotericin B is used in 2. High concentrations can be found where severe infections pigeons roost 3. Amphotericin B alone can be used, but has a 3. Route of infection is by inhalation high risk of nephrotoxicity B. Clinical signs 4. Fluconazole is less effective than itraconazole 1. Nasal infection but is used for infections of the eyes, CNS, or a. Chronic upper respiratory signs are common prostate with cryptococcosis, including sneezing, snif- 5. Ketoconazole is less effective but is less fling, or mucopurulent nasal discharge expensive b. Obstructing masses may occur in the nostrils 6. Treatment is successful in about 75% of cases. 2. Disseminated infection Blindness can result from ocular infection, and a. Organs involved may include skin, CNS, relapses can occur in about 20% of recovered eyes, lungs, peripheral lymph nodes, bone cases marrow, kidneys, liver, spleen, heart, and III. Coccidioidomycosis (Valley fever) s