Brucellosis in Dogs PDF

202 Blackwell’s Five-Minute Veterinary Consult Brucellosis B Physical Examination Findings positive RSAT and negative 2ME, retest in...

202 Blackwell’s Five-Minute Veterinary Consult Brucellosis B Physical Examination Findings positive RSAT and negative 2ME, retest in Peripheral lymphadenopathy. Males— 2–4 weeks. swollen scrotum with scrotal dermatitis, Agar Gel Immunodiffusion (AGID) Test ­ BASICS enlarged firm epididymides, orchitis, Soluble antigen test—recommended; DEFINITION prostatitis. Chronic infection—unilateral or employs antigens highly specific for Contagious disease of dogs caused by bilateral testicular atrophy, spinal pain, antibodies against Brucella spp. (including B. Brucella canis. Rarely caused by B. suis, B. discospondylitis, posterior weakness, ataxia. canis, B. abortus, and B. suis); reactive abortus, or B. mellitensis. Characterized by Chronic recurrent anterior uveitis without antibodies appear 4–12 weeks after infection abortion and infertility in females, epididymitis signs of systemic disease; also iris hyperpig­ and persist; may be positive after other tests and testicular atrophy in males. mentation, vitreal infiltrates, multifocal become equivocal or negative. chorioretinitis. Vaginal discharge—may last ELISA—using purified cytoplasmic PATHOPHYSIOLOGY several weeks after abortion. Fever (rare). B. canis—a small, intracellular Gram-negative antigens; not yet commercially available. bacterium; has propensity for growth in CAUSES PCR—available at some diagnostic lymphatic, placental, and male genital B. canis—Gram-negative coccobacillus; laboratories; high sensitivity and specificity. (epididymis and prostate) tissues. morphologically indistinguishable from other Cell wall antigen test—not recommended; members of genus. highly sensitive but not standardized; frequent SYSTEMS AFFECTED RISK FACTORS false positives. Hemic/lymph/immune—lymph nodes, spleen, bone marrow, mononuclear leukocytes. Breeding kennels, pack hounds. Contact IMAGING Reproductive—target tissues of gonadal with strays in endemic areas. Discospondylitis—radiographic changes slow steroids (gravid uterus, fetus, testes to develop, may not be seen even when spinal epididymides, prostate gland). Other pain is present. tissues—intervertebral discs, anterior uvea, DIAGNOSTIC PROCEDURES meninges (uncommon). ­ DIAGNOSIS Isolation of Organism GENETICS DIFFERENTIAL DIAGNOSIS Blood cultures—when clinical and serologic No known genetic predisposition. Abortions—maternal, fetal, or placental findings suggest diagnosis, can be isolated INCIDENCE/PREVALENCE abnormalities. Systemic infections—canine from blood of infected dogs if they have not Incidence unknown. Seroprevalence—not distemper, canine herpesvirus, B. abortus, received antibiotics; onset of bacteremia 2–4 well defined; false-positive results common hemolytic streptococci, E. coli, leptospirosis, weeks after oral-nasal exposure, persists for 8 with agglutination tests. Prevalence— toxoplasmosis. Inguinal hernia. months to 5.5 years. Culture is preferred 1–18% in United States, Japan; higher in Discospondylitis—fungal infections, method for diagnosis in endemic situations or rural United States; 25–30% in stray dogs in actinomycosis, staphylococcal infections, with known exposure (1–8 weeks ago); must Mexico, Peru. nocardiosis, streptococci, or Corynebacterium specifically request Brucella culture. Culture diphtheroids. or PCR of vaginal fluids or vaginal swab after GEOGRAPHIC DISTRIBUTION abortion. Semen or urine—PCR more United States, Mexico, Japan, South America; CBC/BIOCHEMISTRY/URINALYSIS practical than culture. Tissue samples— Spain, Tunisia, China, Bulgaria; individual Normal in uncomplicated cases. Chronic culture or PCR of prostate, testicle, epididymis, outbreaks in Germany, Czech Republic. infection—hyperglobulinemia and hypo­ lochia, or placenta. Contaminated albuminemia. Cerebrospinal fluid— SIGNALMENT samples—media that contain antibiotics (e.g., neutrophilic pleocytosis, elevated protein Species Thayer–Martin medium) have proven useful. (meningoencephalitis); normal in Dogs discospondylitis. Urinalysis usually Semen Quality Breed Predilections normal. Sperm motility, immature sperm, inflamm­ No evidence of breed susceptibility, atory cells (neutrophils) with epididymitis. OTHER LABORATORY TESTS reportedly high prevalence in beagles. Pure Abnormalities usually evident by 5–8 weeks Serologic testing—most common diagnostic breeds in commercial kennels (“puppy mills”). post infection; conspicuous by 20 weeks. method; subject to error due to false-positive Azoospermia without inflammatory cells Mean Age and Range reactions to several species of bacteria common with bilateral testicular atrophy. Any age. Most common in sexually common with tube agglutination tests; mature dogs. chronically infected dogs may test negative. Lymph Node Biopsy Tissues (lymph node, uterus, testes) should Predominant Sex Rapid 2-Mercaptoethanol Slide be sterilely obtained, cultured on appropriate Most common in females. Agglutination Test (RSAT) media, and submitted for histopathology. Simple, inexpensive, rapid. Detects Lymphoid hyperplasia—large numbers of SIGNS infected dogs 3–4 weeks after infection; plasma cells. Intracellular bacteria—may be General Comments accurate in identifying noninfected dogs. observed in macrophages with special stains Suspect with abortions, reproductive failures, Screening test—sensitive, not specific; high (e.g., Brown–Brenn stain). Histopathologic or genital disease. rate (50%) of false-positive tests. Confirm examination of testes—necrotizing vasculitis, Historical Findings results with other tests. inflammatory cells, granulomatous lesions. Animals may appear healthy or have vague Mercaptoethanol Tube Agglutination PATHOLOGIC FINDINGS signs of illness. Lethargy. Loss of libido. Test (2ME) Gross findings—lymph node enlargement, Swollen lymph nodes. Back or neck pain. Semi-quantitative—similar information to splenomegaly, enlarged and firm epididymides, Abortion—commonly 6–8 weeks after RSAT, but inactivates immunoglobulin (Ig) M. scrotal edema, or atrophy of one or both testes; conception, although pregnancy may Good screening test (lacks specificity). If chronic infection: anterior uveitis and terminate at any stage. discospondylitis. Microscopic changes—  Canine and Feline, Seventh Edition 203 (continued) Brucellosis B diffuse lymphoreticular hyperplasia; chronic chlortetracycline, or minocycline: 25 mg/kg infection: lymph node sinusoids with plasma PO q8h for 4 weeks) or doxycycline (10 mg/ cells and macrophages that contain bacteria, kg PO q12h for 4 weeks) and dihydrostrepto­ diffuse lymphocytic infiltration and granulo­ mycin (10 mg/kg IM q8h during weeks 1 and ­ MISCELLANEOUS matous lesions in all genitourinary organs 4). Enrofloxacin (10–20 mg/kg PO q24h ZOONOTIC POTENTIAL (especially prostate, epididymis, uterus, and for 30 days)—not recommended: variable Human infections possible; usually mild scrotum); inflammatory cell infiltration and results. flu-like symptoms. Severe infections, necrosis of prostate parenchyma, seminiferous CONTRAINDICATIONS including hepatomegaly, splenomegaly, tubules. Ocular changes—granulomatous Tetracyclines—do not use in immature animals. meningitis, endocarditis reported in iridocyclitis; exudative retinitis; leukocytic immunocompromised children and adults. exudates in anterior chamber. ALTERNATIVE DRUG(S) Gentamicin—6–15 mg/kg IM/SC q12h; PREGNANCY/FERTILITY/BREEDING limited success; insufficient data on efficacy Abortions at 45–60 days of gestation combined with tetracycline. typical. Pups from infected bitches may be infected or normal. ­ TREATMENT SYNONYMS APPROPRIATE HEALTH CARE Contagious canine abortion. Outpatient ­ FOLLOW-UP ABBREVIATIONS ACTIVITY PATIENT MONITORING 2-ME = mercaptoethanol tube agglutination test. Restricted Serologic tests—monthly at least 3 months AGID = agar gel immunodiffusion. CLIENT EDUCATION after completion of treatment; continuous, Ig = immunoglobulin. Goal is eradication of B. canis from animal persistent decline in antibodies to negative RSAT = rapid 2-mercaptoethanol slide (seronegative, no bacteremia for at least 3 status indicates successful treatment. agglutination test. months); sometimes result is persistent low Recrudescent infections (rise in antibody ­Suggested Reading antibody titers with no systemic infection. levels, recurrence of bacteremia after therapy)— Greene CE, Carmichael LE. Canine brucel- Antibiotic treatment is expensive, time retreat, neuter and retreat, or euthanize. losis. In: Greene CE, ed., Infectious Diseases consuming, and controversial (because Blood cultures—negative for at least 3 of the Dog and Cat, 3rd ed. St. Louis, MO: outcomes are uncertain, and organism has months after completion of treatment. Saunders Elsevier, 2012, pp. 398–411. potential to recrudesce). Euthanasia is PREVENTION/AVOIDANCE Johnson CA, Carter TD, Dunn JR, et al. strongly recommended for breeding or Vaccine—none. Testing—all females Investigation and characterization of commercial kennels; treatment is only before estrus if breeding is planned; breeding Brucella canis infections in pet-quality dogs recommended for spayed or castrated dogs if males at frequent intervals. Quarantine and and associated human exposures during a the owner is willing to accept the ongoing test all new dogs twice at monthly intervals 2007–2016 outbreak in Michigan. JAVMA zoonotic risk. Before treatment is attempted before entering breeding kennel; test all 2018, 253:322–336. for an intact household pet or breeding dog, breeding animals yearly. Kauffman LK, Petersen CA. Canine client must clearly agree that animal will be brucellosis old foe and reemerging scourge. neutered and potentially euthanized if POSSIBLE COMPLICATIONS Vet Clin Small Anim 2019, 49:763–779. treatment fails. Zoonotic infection is a Owner reluctance to neuter or euthanize Keid LB, Soares RM, Vasconcellos SA, et al. possibility; discuss proper sanitation and valuable dogs, regardless of treatment failure. Comparison of agar gel immunodiffusion test, prevention of exposure. Remind owners of ethical considerations, rapid slide agglutination test, microbiological obligation not to sell or distribute infected dogs. culture, and PCR for the diagnosis of canine SURGICAL CONSIDERATIONS Neuter/spay plus treatment—when EXPECTED COURSE AND PROGNOSIS brucellosis. Res Vet Sci 2009, 86:22–26. euthanasia is unacceptable to owner. Prognosis guarded. Infected for T) general proprioceptive ataxia; gait shows support a presumptive diagnosis of DM in has been seen only in Bernese mountain dogs. long-strided spastic paraparesis. light of typical clinical signs and normal Lesions may represent a multisystem ◦ Paw replacement deficits. findings on neuroimaging and cerebrospinal central-peripheral axonopathy. ◦ Spinal reflexes usually present or fluid analysis. Predilection for lesion severity in mid- exaggerated (patellar reflex may be thoracic spinal cord may be a result of lower IMAGING reduced). Survey spinal radiography. percentages of radicular artery contributions ◦ Presence of crossed-extensor reflex is and small-diameter vessels when compared to Myelography evaluates for compressive variable. spinal cord disease. other spinal cord regions. ◦ Lack of paraspinal hyperesthesia is key Paucity of vascular supply in thoracic spinal Myelography combined with CT—more clinical feature. sensitive technique to evaluate suspicious cord may predispose it to damage from Later: oxidative and metabolic disturbances. lesions. ◦ Pelvic limb paresis leading to plegia, MRI—preferred technique to evaluate for SYSTEMS AFFECTED eventually progressing to tetraparesis/ extramedullary compressive and intramedul- Central and peripheral nervous systems. plegia. lary lesions. Thoracolumbar spinal cord in early stage. ◦ Mild to moderate loss of muscle mass in pelvic limbs due to neurogenic atrophy. DIAGNOSTIC PROCEDURES Progresses to involve the cervical and ◦ Reduced spinal reflexes in pelvic limbs. CSF analysis evaluates for inflammatory lumbar spinal cord and peripheral nervous ◦ ± Urinary and fecal incontinence. disease. system later in the course of the disease. End stage: Definitive diagnosis is determined by Neurons in the brainstem also may be affected. ◦ Flaccid tetraplegia. post-mortem histopathology of spinal cord. Disease also involves the sensory nerve roots and dorsal root ganglia. ◦ Difficulty with swallowing and tongue PATHOLOGIC FINDINGS movements. Spinal cord axons and myelin affected most GENETICS ◦ Absence of spinal reflexes in all limbs. severely in dorsal and dorsal portion of lateral Most commonly autosomal recessive ◦ Reduced to absent cutaneous trunci funiculi. inheritance. reflex. Vacuolated axon cylinders/myelin sheaths Due to preponderance of purebred dogs ◦ Profound generalized muscle wasting. most extensive in mid-thoracic spinal cord. affected, a familial inheritance is currently ◦ Urinary and fecal incontinence. Astroglial proliferation is prominent in suspected. severely affected areas of lesion distribution. Mutations in SOD1 are causative for DM CAUSES Hereditary disease and genetic predi­- Usually, lesion distribution is described as but are incompletely penetrant. asymmetric and discontinuous; however, Dogs that are homozygous for the mutant sposition. Other hypothesized causes include more recent evidence describes lesion distrib­ allele are at highest risk for developing DM; not ution as symmetric and continuous in dogs all dogs that test homozygous for the mutation immune-mediated, metabolic deficiencies, toxic, and oxidative stress. that survive for long periods with DM. will develop DM, but dogs that test normal Neuronal cell body loss in ventral horn is (clear) are highly unlikely to develop DM; dogs RISK FACTORS evident at terminal or end-stage disease. that test carrier are less likely to develop DM, Dogs homozygous for the mutant allele(s) Nerve specimens show fiber loss resulting but this has been documented in some breeds. are at highest risk. from axonal degeneration and secondary There may be other environmental factors demyelination. INCIDENCE/PREVALENCE Prevalence rate of DM reported for all dogs and modifying genes; studies underway. Muscle specimens show large and small collected from the Veterinary Medical groups of atrophic fibers typical of denervation. Database (1990–1999) was 0.19%.  210 Blackwell’s Five-Minute Veterinary Consult Canine Degenerative Myelopathy (continued) Intervertebral Disc Disease, Thoracolumbar. C Lumbosacral Stenosis and Cauda Equina Syndrome. ­ TREATMENT ­ FOLLOW-UP ABBREVIATIONS APPROPRIATE HEALTH CARE PATIENT MONITORING ALS = amyotrophic lateral sclerosis. Supportive care. Repeat neurologic examinations. DM = degenerative myelopathy. Breeds of small size may survive longer with Urine retention. SOD1 = superoxide dismutase 1. DM because the pet owner is able to more Urinalysis and urine culture to monitor for easily give the appropriate care. urinary tract infection. INTERNET RESOURCES www.caninegeneticdiseases.net/dm/ NURSING CARE PREVENTION/AVOIDANCE maindm.htm When dog becomes nonambulatory, keep Decubitus ulceration. www.ofa.org/diseases/dna-tested-diseases/dm on a well-padded surface to prevent decubitus Urine retention. ulceration over bony prominences. Dermatitis from urine scald. ­Suggested Reading Keep hair trimmed, and skin clean and Weight gain. Awano T, Johnson GS, Wade C, et al. dry to prevent urine scald secondary to Genome-wide association analysis reveals a POSSIBLE COMPLICATIONS SOD1 missense mutation canine degenera- incontinence. Urine retention may predispose to urinary Urine should be monitored for odor and tive myelopathy that resembles amyotrophic tract infections. lateral sclerosis. Proc Natl Acad Sci USA color change, which may indicate urinary Local skin infections from decubitus ulceration. tract infection. 2009, 106:2794–2799. Physical therapy using range-of-motion and EXPECTED COURSE Coates JR, March PA, Ogelsbee M, et al. active exercises may help maintain limb AND PROGNOSIS Clinical characterization of a familial mobility and muscle strength. Nonambulatory paraparesis occurs within degenerative myelopathy in Pembroke 9–12 months from time of onset of signs. Welsh Corgi dogs. J Vet Intern Med 2007, ACTIVITY 21:1323–1331. Tetraparesis may be evident within 3 years Exercise is encouraged to slow disuse Coates JR, Wininger FA. Canine degenerative atrophy of pelvic limbs, but fatigue should from time of onset of signs. Long-term prognosis is poor. myelopathy. Vet Clin North Am Small be monitored and exercise intensity Anim Pract 2010, 40:929–950. adjusted. March PA, Coates JR, Abyad R, et al. Hydrotherapy can involve use of an Degenerative myelopathy in 18 Pembroke underwater treadmill setup. Welsh Corgi dogs. Vet Pathol 2009, A wheel cart may assist with patient ­ MISCELLANEOUS 46:241–250. mobility. Ogawa M, Uchida K, Yamato O, et al. ASSOCIATED CONDITIONS DIET Other neurologic diseases associated with Neuronal loss and decreased GLT-1 Maintain balanced diet. old-age onset. expression observed in the spinal cord of Prevent weight gain. Spinal cord neoplasia. Pembroke Welsh Corgi Dogs with canine Intervertebral disc disease. degenerative myelopathy. Vet Pathol 2014, CLIENT EDUCATION Orthopedic disease. 51:591–602. Long-term prognosis is poor. Wininger FA, Zeng R, Johnson GS, et al. Meticulous nursing care is crucial to AGE-RELATED FACTORS Degenerative myelopathy in a Bernese preventing secondary complications in a Older dogs commonly affected. Mountain Dog with a novel SOD1 missense recumbent patient. ZOONOTIC POTENTIAL mutation. J Vet Intern Med 2011, SURGICAL CONSIDERATIONS None 25:1166–1170. None Zeng R, Coates JR, Johnson GC, et al. Breed PREGNANCY/FERTILITY/BREEDING distribution of SOD1 alleles previously N/A associated with canine degenerative myelopa- SYNONYMS thy. J Vet Intern Med 2014, 28:515–521. Canine ALS. Author Joan R. Coates ­ MEDICATIONS DM. DRUG(S) OF CHOICE Degenerative radiculomyelopathy. Clinical trials are underway to determine German Shepherd dog myelopathy.  Client Education Handout effectiveness in slowing or halting disease SEE ALSO available online progression. Intervertebral Disc Disease, Cervical.  Canine and Feline, Seventh Edition 211 Canine Distemper ◦ Gray matter disease—affects cerebral dog are suggestive of infection; may be useful cortex, brainstem, and spinal cord and may for risk assessment of clinically healthy dogs C cause a nonsuppurative meningitis, in shelter environment. ­ BASICS seizures, mentation change, and ataxia; CDV antibody in cerebrospinal fluid DEFINITION dogs may die in 2–3 weeks; some dogs (CSF)—indicative of distemper encephalitis, Acute to subacute, contagious, febrile, often recover (associated with prompt humoral false negatives possible. fatal disease with respiratory, urogenital, and cell-mediated immunity), others IMAGING gastrointestinal, ocular, and CNS manifest- develop white matter disease. Radiographs—evaluate pulmonary disease. ations. ◦ White matter disease—multifocal disease, CT and MRI—may or may not show Caused by canine distemper virus (CDV), a commonly cerebellovestibular signs, paresis, lesions; MRI sensitive for demyelination. Morbillivirus in the Paramyxoviridae family. ataxia, occasionally myoclonus; some dogs Affects many Carnivora species; mortality die 4–5 weeks after initial infection with DIAGNOSTIC PROCEDURES rate varies greatly. noninflammatory, demyelinating disease; some Immunohistochemical detection in haired dogs may recover with minimal CNS injury. skin, nasal mucosa, and footpad epithelium. PATHOPHYSIOLOGY Optic neuritis and retinal lesions may Viral antigen or viral inclusions—in buffy Natural route of infection—airborne and occur; anterior uveitis, keratoconjunctivitis coat cells, urine sediment, conjunctival or droplet exposure; from nasal cavity, pharynx, sicca possible. vaginal imprints, trans-tracheal wash and lungs, virus replication occurs in local Hardening of footpads (hyperkeratosis) and (negative results do not rule out CDV). lymph nodes; within 1 week, viral shedding nose—some virus strains; uncommon. Reverse transcriptase polymerase chain occurs (mainly in respiratory exudates but also Enamel hypoplasia of teeth after neonatal reaction (RT-PCR)—on buffy coat, urine urine) and virtually all lymphatic tissues infection. sediment cells, respiratory secretions, become infected; spreads via viremia to surface epithelium of respiratory, gastrointestinal, and CAUSES conjunctival swabs, CSF; false negatives urogenital tracts and to CNS. CDV exposure. possible, false positives with recent Disease progression depends on virus strain Incompletely attenuated vaccines (rare). vaccination (uncommon). CSF—moderate mononuclear pleocytosis, and host immune response: RISK FACTORS ◦ Strong cellular and humoral immune elevated concentrations of CDV-specific Contact of nonimmunized animals with antibody, interferon, and viral antigen early in response—subclinical infection. CDV-infected animals (dogs, wild carnivores). ◦ Weak immune response—subacute disease course. infection; longer survival. PATHOLOGIC FINDINGS ◦ Failed immune response—death within 2–4 weeks after infection; frequently due to Gross CNS manifestations. ­ DIAGNOSIS Thymus—greatly reduced in size (young Viral excretion can occur for up to 2–3 months. animals); sometimes gelatinous. DIFFERENTIAL DIAGNOSIS Lungs—patchy consolidation. SYSTEMS AFFECTED Diagnosis based on clinical suspicion; Footpads, nose—hyperkeratosis. Multisystemic—all lymphatic tissues, combination of respiratory and gastrointestinal, Mucopurulent discharges—from eyes and surface epithelium in respiratory, alimentary, ± CNS disease, in unvaccinated dog. nose, bronchopneumonia, catarrhal enteritis, and urogenital tracts, skin, endocrine and Respiratory signs—can mimic kennel cough. skin pustules (secondary bacterial infection). exocrine glands. Enteric signs—differentiate from canine CNS—brain and/or spinal cord. parvovirus, coronavirus, parasitism (giardiasis), Histologic bacterial infections, gastroenteritis from toxin Intracytoplasmic eosinophilic inclusion INCIDENCE/PREVALENCE ingestion, inflammatory bowel disease. bodies—in epithelium of bronchi, stomach, Dogs—sporadic outbreaks. CNS form—differentiate from auto­ urinary bladder; also in reticulum cells and Wildlife (raccoons, skunks, fox, tigers)— immune meningoencephalitis (granulomatous leukocytes in lymphatic tissues. fairly common. meningoencephalomyelitis, necrotizing Inclusion bodies in glial cells and neurons— GEOGRAPHIC DISTRIBUTION encephalitis, meningoencephalitis of frequently intranuclear; also in cytoplasm. Worldwide unknown etiology), protozoal (e.g., Immunofluorescence and/or immunocyto­ toxoplasmosis, neosporosis), fungal (e.g., chemistry, virus isolation, and/or RT-PCR SIGNALMENT cryptococcosis), and rickettsial (e.g., performed on tissues from lungs, stomach, Species ehrlichiosis, Rocky Mountain spotted fever) urinary bladder, lymph nodes, brain. Most species of the order Carnivora; has been meningoencephalitis, rabies. reported in large exotic cats. CBC/BIOCHEMISTRY/URINALYSIS Mean Age and Range Lymphopenia in early infection; rare Young, especially unvaccinated animals are thrombocytopenia; intracytoplasmic ­ TREATMENT most susceptible. inclusions in white and red blood cells. APPROPRIATE HEALTH CARE SIGNS OTHER LABORATORY TESTS Inpatient medical management to intensive Fever—intermittent peaks starting 3–6 days Serology—positive antibody tests do not care as indicated; isolate patient to prevent after infection. differentiate between vaccination and spread to other dogs. Gastrointestinal and/or respiratory signs— exposure to virulent virus; patient may die nasal and ocular discharge, depression, NURSING CARE from acute disease before neutralizing Symptomatic. anorexia, vomiting, diarrhea; often exacer­ antibody is produced. Immunoglobulin (Ig) IV fluids—for hypovolemia, support. bated by secondary bacterial infection. M responses may occur up to 3 months after Oxygen therapy, nebulization, and CNS—common; generally after systemic exposure to virulent virus, up to 3 weeks after disease (depends on virus strain). coupage—for pneumonia. vaccination; rising IgG titers in unvaccinated Clean ocular, nasal discharges.  212 Blackwell’s Five-Minute Veterinary Consult Canine Distemper  (continued) ACTIVITY Modified live vaccine for CDV (MLV-CD)— AGE-RELATED FACTORS C Limited, to reduce spread. prevents infection and disease; two types Young puppies—more susceptible; DIET available: mortality rate is higher. ◦ Canine tissue culture-adapted vaccines Nonimmunized old dogs—highly Depends on extent of gastrointestinal involvement. (e.g., Rockborn strain)—induce complete susceptible to infection and disease. immunity in virtually 100% of susceptible ZOONOTIC POTENTIAL CLIENT EDUCATION dogs; rarely, a postvaccinal fatal encephalitis Inform client that mortality rate is about 50%. Possible that humans may become subclini- develops 7–14 days after vaccination, cally infected with CDV; immunization Inform client that dogs appearing to recover especially in immunosuppressed animals. from early catarrhal signs may develop fatal against measles virus also protects against ◦ Chick embryo-adapted vaccines (e.g., CNS disease. CDV infection. Lederle strain)—safer; postvaccinal Presenting neurologic abnormalities usually encephalitis does not occur; only about PREGNANCY/FERTILITY/BREEDING not reversible. 80% of susceptible dogs seroconvert. In utero infection—occurs in antibody-nega- ◦ Other species—chick embryo can safely tive bitches; rare; may lead to abortion or to be used in variety of wildlife species (e.g., persistent infection; infected neonates may gray fox); Rockborn type fatal in these develop fatal disease by 4–6 weeks of age. ­ MEDICATIONS animals. SYNONYMS Killed vaccines—useful for species in which Canine distemper. DRUG(S) OF CHOICE either type of MLV-CD is fatal (e.g., red Hard pad disease. Antiviral drugs—none known to be effective. panda, blackfooted ferret). Broad-spectrum antibiotics—for secondary Canarypox recombinant CDV vaccine. SEE ALSO bacterial infection (CDV is immuno­ Myoclonus suppressive), beta-lactams or cephalosporins Maternal Antibody Important. ABBREVIATIONS are good initial choices. CDV = canine distemper virus. Anticonvulsant therapy—phenobarbital, Most puppies lose protection from maternal antibody at 6–12 weeks of age; 2–3 CSF = cerebrospinal fluid. potassium bromide, levetiracetam. Ig = immunoglobulin. Myoclonus—no proven treatment; single vaccinations should be given during this period. MLV-CD = modified live virus of canine case report describes use of botulinum toxin distemper. type A. Heterotypic (measles virus) vaccination— recommended for puppies that have maternal RT-PCR = reverse transcriptase polymerase CONTRAINDICATIONS antibody; induces protection from disease but chain reaction. Corticosteroids—use anti-inflammatory not from infection. INTERNET RESOURCES dosages with caution; may provide short-term https://www.uwsheltermedicine.com/library/ control. Immunosuppressive dosages may POSSIBLE COMPLICATIONS Possibility of CNS signs developing for 2–3 resources/canine-distemper-cdv enhance viral dissemination. months after catarrhal signs have subsided. ­Suggested Reading PRECAUTIONS Greene CE, Vendevelde M. Canine distem- Tetracycline, fluoroquinolones—avoid in EXPECTED COURSE per. In: Greene CE, ed., Infectious Diseases growing animals. AND PROGNOSIS of the Dog and Cat, 4th ed. St. Louis, MO: Depends on strain and individual host Saunders Elsevier, 2012, pp. 25–42. response—subclinical, acute, subacute, fatal, Lempp C, Spitzbarth I, Puff C, et al. New or nonfatal infection. aspects of pathogenesis of canine distemper Mild CNS signs—patient may recover; ­ FOLLOW-UP myoclonus may continue for several months leukoencephalitis. Viruses 2014, 6:2571–2601. PATIENT MONITORING or indefinitely. Loots AK, Mitchell E, Dalton DL, et al. Monitor for CNS abnormalities, partic­ Death—2 weeks to 3 months after Advances in canine distemper virus ularly seizures. infection; mortality rate ~50%. pathogenesis research: a wildlife perspective. Monitor for respiratory distress or Euthanasia—owner may elect if or when J Gen Virol 2017, 98:311–321. dehydration in acute phase. neurologic signs develop; indicated if Pesavento PA, Murphy BG. Common and PREVENTION/AVOIDANCE uncontrollable seizures occur. emerging infectious disease in the animal Vaccination. shelter. Vet Pathol 2014, 51:478–491. Isolate puppies to prevent infection from Author Michelle C. Tensley wildlife (e.g., raccoons, foxes, skunks), Consulting Editor Amie Koenig CDV-infected dogs, ferrets. ­ MISCELLANEOUS Acknowledgment The author and book Recovered dogs may shed virus for up to 4 editors acknowledge the prior contribution of ASSOCIATED CONDITIONS months; isolate for this time period or until Stephen C. Barr. Persistent or latent Toxoplasma gondii multiple negative RT-PCR tests. infections—may be reactivated due to Vaccines immunosuppressive state.  Client Education Handout Duration of immunity from most vaccines Respiratory infections with Bordetella available online is >3 years. bronchiseptica (kennel cough).  Canine and Feline, Seventh Edition 213 Canine Infectious Diarrhea loss, hyporexia; no history of dietary indiscretion. Hypoglycemia—parvoviral enteritis and Physical examination findings—depends on systemic salmonellosis. C etiology and severity; may include dehydration, Panhypoproteinemia and hypocholesterol­ ­ BASICS poor body condition, borborygmus, flatulence, emia if secondary protein-losing enteropathy DEFINITION hematochezia, melena, visualization of worms or GI blood loss. Viral, enteropathogenic bacterial, protozoal, on rectal exam or peri-anal, signs of sepsis or IMAGING or parasitic etiologies; small, large, or mixed- systemic inflammatory response syndrome Abdominal radiographs if no response to bowel diarrhea. (SIRS). symptomatic care to rule out other causes of Secondary systemic signs with canine CAUSES diarrhea. parvovirus (CPV)-2 and salmonellosis. Viral—coronavirus, CPV-2, circovirus. Abdominal ultrasound recommended in Presence of organisms on diagnostic Bacterial—Campylobacter spp., Clostridium nonpediatric patients with diarrhea that is screening does not indicate causation; perfringens enterotoxin, Clostridium difficile nonresponsive to symptomatic care. patient factors (clinical signs, age, toxins, Salmonella spp. environmental exposure) should be DIAGNOSTIC PROCEDURES Parasitic—Toxocara spp., Ancylostoma considered before treatment. Fecal flotation—for intestinal parasitism; spp.,Toxascaris leonine, Dipyldium caninum, false negatives possible (ova are intermittently Some dogs will have self-resolution; Trichuris vulpis. diagnostic testing appropriate for more shed); dogs suspected to have intestinal Protozoal—Giardia spp. parasitism should have multiple fecal flotations severely affected animals or if clinical signs are Coccidial—Cryptosporidium spp., persistent having ruled out other causes of performed or be treated with anthelmintics. Cystoisospora spp. Fecal cytology—bacterial morphology acute or chronic diarrhea. Puppies with acute diarrhea should be RISK FACTORS (frequent spirochetes, spores) or presence of screened for CPV-2. Pediatric and young adult dogs more fungal or protozoal organisms. commonly affected, particularly for viral Giardia ELISA. PATHOPHYSIOLOGY enteritis, Cryptosporidium spp., roundworm Infectious diarrhea PCR panels detect a Typically, fecal–oral route of infection. (Toxocara and Toxascaris), Cystoisospora spp., range of possible causes of diarrhea; however, Diarrhea from enterotoxins, osmotic and Campylobacter spp. caution should be used in interpretation of diarrhea, or invasion of epithelium resulting Administration of antimicrobials and these assays, as a positive result does not in inflammation. immunosuppressive drugs increase risk for necessarily indicate causation and false- Up to 50% of dogs may have coinfections. hospital-associated colonization of C. difficile. negative results are possible. Crowding and poor sanitation. PATHOLOGIC FINDINGS SYSTEMS AFFECTED Lack of regular parasiticide administration. Gastrointestinal (GI)—vomiting, diarrhea. Gross examination of intestinal mucosa Dogs with environmental exposure to may demonstrate parasites attached to Cardiovascular—fluid balance. livestock or wildlife for Cryptosporidium spp., intestinal mucosa with multifocal hemor- INCIDENCE/PREVALENCE Campylobacter spp., Giardia spp. rhagic ulcerations, submucosal congestion or Prevalence of most pathogens similar in hemorrhage, intestinal wall thickening. dogs with or without diarrhea. Histopathology of intestine may show ◦ Coronavirus more common in dogs with eosinophilic, neutrophilic, or lymphoplasmacytic diarrhea. ◦ Dogs with diarrhea more likely to have ­ DIAGNOSIS enteritis with varying degrees of hemorrhage and necrosis, depending on etiology. >1 enteropathogen. DIFFERENTIAL DIAGNOSIS Specific prevalence in dogs in United States: Acute diarrhea—dietary indiscretion, foreign ◦ 0–6%—CPV-2, Salmonella spp., body, pancreatitis, GI neoplasia; non-GI Cystoisospora spp., Dipylidum caninum, diseases: hepatotoxicity, renal disease, other Campylobacter spp., C. difficile toxin A systemic diseases (commonly other clinical ­ TREATMENT and B, ascarids. signs such as hyporexia, vomiting, icterus). APPROPRIATE HEALTH CARE ◦ 7–20%—whipworms, Giardia spp., Chronic diarrhea—chronic enteropathy Mildly affected dogs—outpatient basis. Cryptosporidium, circovirus. (dietary responsive, antibiotic responsive, or Moderate to severely affected dogs may ◦ 35–60%—C. perfringens enterotoxin A inflammatory bowel disease), chronic require IV administration of isotonic or alpha toxin gene, hookworm. pancreatitis, primary GI neoplasia, and balanced electrolyte solution for dehydration. GEOGRAPHIC DISTRIBUTION non-GI diseases of other organs. Electrolyte and acid-base imbalances should Widespread. CBC/BIOCHEMISTRY/URINALYSIS be corrected with fluid therapy and moni- Prevalence of etiologies varies by location. Eosinophilia—possible with intestinal tored closely. SIGNALMENT parasitism. Dextrose should be supplemented Anemia and/or microcytosis—GI hemor- parenterally in dogs with hypoglycemia. Species—dog. Breed predilections—none. rhage or iron deficiency, particularly with Packed red blood cell or plasma transfusions Mean age and range—largely pediatric and high worm burden (e.g., T. vulpis) or GI should be given as needed for severe anemia or young adult dogs; older animals if in high-risk mucosal shedding (e.g., CPV). coagulopathies from sepsis (rare). Leukopenia—parvoviral enteritis (bacterial environments. DIET translocation or bone marrow suppression) or Easily digestible diets until clinical signs SIGNS systemic salmonellosis. General comments—range from mild to have resolved, followed by slow transition Hyponatremia and hyperkalemia with large (3–4 days) to maintenance diet. severely affected. bowel diarrhea—T. vulpis. In anorexic pediatric patients, nasogastric Historical findings—acute or chronic, small or Azotemia and electrolyte derangements large bowel diarrhea; possibly vomiting, weight tube feeding of liquid diet recommended if with dehydration. anorexia persists ≥48 hours.  214 Blackwell’s Five-Minute Veterinary Consult Canine Infectious Diarrhea  (continued) CLIENT EDUCATION POSSIBLE INTERACTIONS ZOONOTIC POTENTIAL C For most infectious organisms, environ- Metronidazole given at higher doses for Giardiasis—low risk of transmission. mental decontamination prevents transmis- giardiasis or long-term use can lead to Cryptosporidiosis. sion to other pets/people and reinfection; vestibular signs. Salmonellosis. isolation during hospitalization may be Some dogs may be sensitive to sulfa- Campylobacter jejuni. warranted depending on underlying cause. containing medications used for treatment of Toxocara spp. (ascarids)—visceral larval Appropriate vaccination and deworming coccidiosis. migrans in humans, most common in schedules should be followed. children. Dogs with identified infectious causes of Ancylostoma (hookworms)—cutaneous diarrhea should be isolated from other dogs if larval migrans in humans, most common in possible until clinical signs resolve. children. ­ FOLLOW-UP SURGICAL CONSIDERATIONS PREGNANCY/FERTILITY/BREEDING PATIENT MONITORING Viral and parasitic enterocolitis can result in If heavy endoparasite load, fenbendazole can Case-based, may include reassessment of intussusceptions, especially in puppies. be administered to pregnant bitches from anemia, leukopenia, or electrolyte derange- 14th day of gestation through to 14th day of ments as appropriate. lactation. If risk of infection is high, all Persistent clinical signs after appropriate puppies (and mothers) should be treated with treatment is suggestive for alternative cause of appropriate anthelmintics at 2, 4, 6, and 8 ­ MEDICATIONS diarrhea. weeks of age. Patients with recurrent clinical signs should DRUG(S) OF CHOICE be retested, particularly if environmental SEE ALSO Many cases will self-resolve with supportive reinfection is possible (e.g., giardiasis, Acute Diarrhea. care and time. campylobacteriosis). Campylobacteriosis. Empiric therapy pending diagnostics, if Canine Coronavirus Infections. clinical signs persist—probiotics, or metroni- PREVENTION/AVOIDANCE Canine Parvovirus. dazole (10 mg/kg PO q12h) and fenbenda- Routine vaccination. Clostridial Enterotoxicosis. zole (50 mg/kg PO q24h for 5 days). Monthly flea/tick or heartworm preventa- Coccidiosis. Anthelmintics—fenbendazole (50 mg/kg tive with combination anthelmintic therapy. Diarrhea, Chronic—Dogs. PO q24h for 5 days), pyrantel pamoate Avoid subjecting poorly vaccinated or Giardiasis. (5–10 mg/kg PO for 3 days). immunocompromised animals to high-traffic Hookworms (Ancylostomiasis). Coccidiostatic—sulfadimethoxine areas, including but not limited to pet supply Roundworms (Ascariasis). (50–60 mg/kg PO q24h for 5–10 days), stores, dog parks, or newly introduced poorly Salmonellosis. ponazuril (50 mg/kg PO once). vaccinated pets. Whipworms (Trichuriasis). Antiprotozoal drugs—fenbendazole POSSIBLE COMPLICATIONS (50 mg/kg PO q24h for 5 days). ABBREVIATIONS Sepsis. Campylobacteriosis with persistent clinical CPV-2 = canine parvovirus. Anemia. signs—erythromycin (10–15 mg/kg PO q8h) GI = gastrointestinal. Electrolyte disturbances. or azithromycin (5–10 mg/kg PO q24h). SIRS = systemic inflammatory response Aspiration pneumonia if concurrent Probiotics may be of benefit for dogs with syndrome. vomiting (uncommon). bacterial enteritis with acute or chronic signs; ­Suggested Reading probiotics should be selected with evidence of EXPECTED COURSE AND PROGNOSIS Gookin JL. Infection, large intestine. In: efficacy (e.g., Visbiome®). Usually good to excellent; underlying Washabau RJ, Day MJ, eds., Canine & Patients with systemic illness, leukope- immunosuppressive conditions may increase Feline Gastroenterology. St. Louis, MO: nia, or suspected GI mucosal barrier susceptibility to infection and worsen prognosis. Saunders Elsevier, 2013, pp. 745–757. breakdown (evidenced by blood in the Parvoviral enteritis carries guarded to poor Lappin MR. Infection, small intestine. In: feces) should be treated with broad-spec- prognosis without treatment; appropriate Washabau RJ, Day MJ, eds., Canine & trum antimicrobial agents and as indicated supportive care provides full recovery rates of Feline Gastroenterology. St. Louis, MO: by specific etiology. 90% or more. Saunders Elsevier, 2013, pp. 683–695. Dogs with confirmed salmonella should Authors Kasey E. Mabry and Tracy Hill not be treated with antibiotics unless Consulting Editor Amie Koenig systemically ill. PRECAUTIONS ­ MISCELLANEOUS Metronidazole dose should be reduced in AGE-RELATED FACTORS animals with hepatic insufficiency. Puppies and young dogs affected.  Canine and Feline, Seventh Edition 215 Canine Infectious Respiratory Disease Physical Examination Findings OTHER LABORATORY TESTS Uncomplicated—cough readily induced with Pulse oximetry and arterial blood gas analysis— C minimal tracheal pressure; lung sounds often can reveal hypoxemia in pneumonia. ­ BASICS normal; systemically healthy. Complicated— IMAGING DEFINITION low-grade or intermittent fever (39.4–40.0 °C; Uncomplicated disease—radiographs: A multifaceted disease whereby infectious disease 103–104 °F); increased intensity of normal unremarkable; most useful for ruling out and environment contribute to the genesis of lung sounds, crackles or wheezes possible. other differential diagnoses. Complicated cough and other respiratory signs in dogs. CAUSES disease—radiographs: interstitial and PATHOPHYSIOLOGY Viral—canine distemper virus (CDV); canine alveolar lung pattern with a cranioventral Initiated by injury to the respiratory adenovirus (CAV-2); canine parainfluenza distribution typical of bacterial pneumonia; epithelium by viral infection followed by (CPIV); canine respiratory coronavirus can see diffuse interstitial lung pattern invasion of damaged tissue by bacterial, (CRCoV), canine reovirus; canine herpesvirus-1 typical of viral pneumonia; mixed lung mycoplasmal, or other virulent organisms, (CHV-1); canine influenza virus (CIV; H3N8 pattern can be present. resulting in further damage and clinical signs. or H3N2); canine bocavirus, canine hepacivirus; DIAGNOSTIC PROCEDURES canine pneumovirus (CnPnV). Most viral In cases with severe disease—ideally SYSTEMS AFFECTED pathogens (except CHV and CDV) primarily Respiratory—upper and lower airways can be perform bronchoalveolar lavage via infect epithelial and lymphoid tissue of the bronchoscopy for cytology and microbial involved. Multisystemic—cases that develop upper and lower respiratory tract; in severe sepsis. culture; tracheal wash sample acceptable, but cases, causing desquamation of the epithelium increased likelihood for upper airway GENETICS and aggregation of inflammatory cells in the contamination. Antimicrobial sensitivity None lungs, leading to secondary bacterial coloni­ pattern of cultured bacteria—identification INCIDENCE/PREVALENCE zation and infection; CRCoV infection leads to aids markedly in providing an effective Most common in areas of high density with loss of cilia associated with the respiratory treatment plan. PCR from bronchoalveolar immunologically naïve or immunosuppressed epithelium, increasing the severity and duration lavage, nasal, ocular, or pharyngeal secretions patients (i.e., training kennels, shelters, of secondary infections. Bacterial—Bordetella can be used to detect virus, though there is veterinary hospitals). bronchiseptica, with no other respiratory difficulty in interpreting results as many pathogens, produces clinical signs healthy animals shed virus in the absence of GEOGRAPHIC DISTRIBUTION indistinguishable from those of other bacterial Worldwide clinical signs. causes; Streptococcus equi subsp. zooepidemicus is SIGNALMENT associated with a particularly virulent course PATHOLOGIC FINDINGS that can progress to death; Pseudomonas, CPIV—causes few to no clinical signs; Species Escherichia coli, Klebsiella, Pasteurella, lungs of infected dogs 6–10 days after Dog Streptococcus, Mycoplasma, and other species exposure may contain petechial hemorrhages Breed Predilections equally likely. that are evenly distributed over the surfaces; None detected by immunofluorescence in RISK FACTORS columnar epithelial cells of the bronchi and Mean Age and Range Substandard hygienic conditions and bronchioles 6–10 days after aerosol Most severe in puppies 6 weeks–6 months overcrowding—encountered in some pet exposure. CAV-2—lesions confined to the old. Can develop in dogs of all ages, partic­- shops, shelters, research facilities, and respiratory system; large intranuclear ularly with preexisting airway disease. boarding and training kennels. Coexisting inclusion bodies found in bronchial Predominant Sex subclinical airway disease—congenital epithelial cells and alveolar septal cells; None anomalies; chronic bronchitis; bronchiectasis. clinical signs tend to be mild and short- SIGNS lasting; lesions persist for at least a month after infection. CIV (H3N8, H3N2)— General Comments fulminant disease characterized by secondary Related to the degree of respiratory tract ­ DIAGNOSIS Mycoplasma or bacterial infection and damage and age of the affected dog and virulence pulmonary hemorrhage. CRCoV— of infectious organism. Can be subclinical, DIFFERENTIAL DIAGNOSIS characterized by marked inflammation of mild, or severe with pneumonia. Most viral, In systemically well dogs—parasitic the trachea and nares with cilia loss in the bacterial, and mycoplasmal agents spread rapidly bronchitis, irritant tracheobronchitis, airway former; detected by immunohistochemistry from seemingly healthy dogs to others in the foreign body, airway collapse. In a dog with of the trachea or bronchioles. Streptococcus same environment; signs usually begin about 3–7 systemic signs—fungal or bacterial (aspiration) equi subsp. zooepidemicus infection—acute, days after exposure to the infecting agent(s). pneumonia, primary or metastatic neoplasia, fibrinosuppurative pneumonia with large congestive heart failure, migrating foreign Historical Findings numbers of cocci found within the pulmonary body. Provisional diagnosis of infectious Uncomplicated—acute-onset cough in an parenchyma and, often, septic thomboemboli. tracheobronchitis is made in a dog with otherwise healthy animal; dry and hacking, Bordetellosis and severe bacterial compelling clinical signs and a history of soft and dry, moist and hacking, or paroxysmal, infection—evidence of purulent bronchitis, exposure to the implicated organisms. See followed by gagging, retching, and expecto­ tracheitis, and rhinitis with hyperemia and Cough. ration of mucus; excitement, exercise, and enlargement of the bronchial, mediastinal, pressure on the trachea induce coughing spells. CBC/BIOCHEMISTRY/URINALYSIS and retropharyngeal lymph nodes; may see Complicated (severe)—inappetence to Early, mild leukopenia (5,000–6,000 cells/ large numbers of Gram-positive or Gram- anorexia; cough is moist and productive; dL)—can be detected; suggests viral cause. negative organisms in the mucus of the lethargy, difficulty breathing, hemoptysis, and Neutrophilic leukocytosis with a toxic left tracheal and bronchial epithelium. exercise intolerance can occur. shift—frequently found with severe pneumonia.  216 Blackwell’s Five-Minute Veterinary Consult Canine Infectious Respiratory Disease (continued) CONTRAINDICATIONS shortens the course. Typical course of severe C Do not use cough suppressants in patients disease—2–6 weeks; patients that die often with pneumonia. Employ glucocorticoids only develop severe pneumonia that affects ­ TREATMENT in cases with significant inflammatory disease multiple lung lobes and multiple organ APPROPRIATE HEALTH CARE refractory to conventional supportive care. dysfunction due to sepsis. Outpatient—strongly recommended for PRECAUTIONS uncomplicated disease. Inpatient—strongly None recommended for complicated disease and/or pneumonia. POSSIBLE INTERACTIONS Fluoroquinolones and theophylline deriva- ­ MISCELLANEOUS NURSING CARE tives—concurrent use causes high and ASSOCIATED CONDITIONS Fluid administration—indicated for possibly toxic plasma theophylline concentra- May accompany other respiratory tract complicated disease and/or pneumonia. tion. Dose reduce theophylline while anomalies. ACTIVITY concurrently administering fluoroquinolones. AGE-RELATED FACTORS Enforced rest—14–21 days with uncompli- ALTERNATIVE DRUG(S) Most severe in puppies 6 weeks–6 months old cated disease; for at least the duration of None and in puppies from commercial pet shops radiographic evidence of pneumonia in and humane society shelters. severely affected dogs. ZOONOTIC POTENTIAL DIET Potential zoonotic risk of Streptococcus equi Good-quality commercial food. ­ FOLLOW-UP subsp. zooepidemicus and B. bronchispetica CLIENT EDUCATION PATIENT MONITORING reported in single case reports. Isolate patient from other animals; infected Uncomplicated disease—should resolve PREGNANCY/FERTILITY/BREEDING dogs can transmit the agent(s) before onset of spontaneously or respond to treatment in 10–14 High risk in dogs on extensive medical clinical signs and afterward until immunity days; if patient continues to cough 14 days or treatment; especially risky for dogs in develops. Dogs with uncomplicated disease more after establishment of an adequate treat­- overcrowded breeding facilities. should respond to treatment in 10–14 days. ment plan, question the diagnosis of uncompli- Once infection spreads in a kennel, it can be SYNONYMS cated disease. Complicated disease— Kennel cough. Infectious controlled by evacuation for 1–2 weeks and repeat thoracic radiography until at least 7 days disinfection with commonly used chemicals, tracheobronchitis—uncomplicated disease. beyond resolution of all clinical signs. such as sodium hypochlorite (1 : 30 dilution), ABBREVIATIONS chlorhexidine, and benzalkonium. PREVENTION/AVOIDANCE CAV-2 = canine adenovírus. CDV = Shedding of the causative agent(s) of infectious canine distemper vírus. CHV-1 = canine respiratory disease in airway secretions of dogs herpesvirus-1. CIV = canine influenza undoubtedly accounts for the persistence of virus. CnPnV = canine pneumovirus. this problem in kennels, animal shelters, CPIV = canine parainfluenza. CRCoV = ­ MEDICATIONS boarding facilities, and veterinary hospitals. canine respiratory coronavirus. DRUG(S) OF CHOICE Viral and Bacterial Vaccines Amoxicillin/clavulanic acid (12.5–25 mg/kg INTERNET RESOURCES Modified live CDV and CAV-2 vaccines https://www.cdc.gov/flu/other/canine-flu PO q12h) or doxycycline (5 mg/kg PO q12h or provide reliable protection and are considered 10 mg/kg PO q24h)—initial treatment of core vaccines for all puppies; can be admin­ ­Suggested Reading uncomplicated disease. Penicillin (ampicillin istered at 6 weeks of age, every 2–4 weeks. B. Bemis DA. Bordetella and Mycoplasma 10–20 mg/kg IV q6–8h or ticarcillin 40–50 mg/ bronchiseptica and CPIV vaccine—can vaccinate respiratory infection in dogs. Vet Clin kg IV q6–8h) with aminoglycoside (gentamicin puppies mucosally or intranasally as early as 2–4 North Am Small Anim Pract 1992, 2–4 mg/kg IV/IM/SC q6–8h or amikacin weeks of age without interference from maternal 22:1173–1186. 6.5 mg/kg IV/IM/SC q8h) or fluoroquinolone antibody and follow with annual revaccination; Buonavoglia C, Martella V. Canine respira- (enrofloxacin 5–10 mg/kg PO/IM/IV q24h)— can vaccinate mature dogs with a one-dose tory viruses. Vet Res 2007, 38(2):355–373. usually effective for severe disease. intranasal vaccination (at the same time as their Chalker VJ, Owen WM, Paterson C, et al. Antimicrobial therapy—continue for at least puppies or when they receive their annual Mycoplasmas associated with canine 10 days beyond radiographic resolution. B. vaccinations). Inactivated B. bronchiseptica infectious respiratory disease. Microbiology bronchiseptica and other resistant species—some parenteral vaccine—administered as two doses, 2004, 150(Pt 10):3491–3497. antimicrobials may not reach adequate 2–4 weeks apart; initial vaccination of puppies is Erles K, Dubovi E, Brooks HW, Brownlie J. therapeutic concentrations in the lumen of the recommended at or about 6–8 weeks of age; Longitudinal study of viruses associated lower respiratory tract, so oral or parenteral revaccinate at 4 months of age. Inactivated with canine infectious respiratory disease. J administration may have limited effectiveness; CIV vaccines (H3N2 and H3N8) available to Clin Micro 2004, 42:4524–4529. nebulization with gentamicin (3–5 mg/kg) can reduce severity and duration of clinical signs but Priestnall SL, Mitchell JA, Walker CA, et al. decrease bacterial numbers when administered considered noncore; can be administered New and emerging pathogens in canine daily for 3–5 days; use in conjunction with starting at 6 weeks as two doses, 2–4 weeks infectious respiratory disease. Vet Path systemic antibiotics in dogs with parenchymal apart; results in seroconversion. 2014, 51(2):492–504. disease. Butorphanol (0.55 mg/kg PO Author Jonathan D. Dear q8–12h) or hydrocodone bitartrate (0.22 mg/kg POSSIBLE COMPLICATIONS Consulting Editor Elizabeth Rozanski PO q6–8h)—effective suppression of dry, N/A nonproductive cough not associated with EXPECTED COURSE AND PROGNOSIS bacterial infection. Bronchodilators (e.g., Natural course of uncomplicated disease, if  Client Education Handout terbutaline 0.625–5 mg/dog q8–12h)—may be untreated—10–14 days; simple restriction of available online used to control bronchospasm and wheeze. exercise and prevention of excitement  Canine and Feline, Seventh Edition 217 Canine Parvovirus Higher fatality rates are seen in hounds, Severely affected dogs exhibit severe gundogs, and nonsporting pedigree groups. neutropenia with onset of intestinal damage. C Leukocytosis during recovery. ­ BASICS Mean Age and Range Serum chemistry profiles help assess Illness occurs at any age. DEFINITION Most severe in dogs 6–24 weeks of age. electrolyte disturbances (especially An acute systemic illness characterized by hypokalemia), presence of azotemia, vomiting, hemorrhagic enteritis, and Predominant Sex panhypoproteinemia, hypoglycemia. leukopenia. None OTHER LABORATORY TESTS Myocardial form was observed in puppies SIGNS Virus antigen detection in stool at onset of in late 1970s, now rare. disease and for 2–4 days afterward; many General Comments Most puppies protected against neonatal commercial point-of-care ELISA assays Suspect CPV-2 infection whenever puppies infection by maternal antibodies. available, also PCR and quantitative PCR have an enteric illness. Monoclonal antibodies have revealed methodologies. antigenic changes in canine parvovirus Historical Findings Serologic tests are not diagnostic because (CPV)-2; CPV2a, b, and c strains have been Sudden onset of bloody diarrhea, anorexia, dogs often have high titers from vaccination identified. and vomiting. and/or maternal antibodies. Original virus now virtually extinct in Some dogs may collapse in a shock-like domestic dogs. state and die without enteric signs. IMAGING CPV2c viruses are more virulent, and In breeding kennels, several littermates may Abdominal radiographs—generalized small mortality rates higher. become ill simultaneously or within a short intestinal ileus; exercise caution to prevent CPV-2 is closely related to feline panleuko­ period. misdiagnosis of intestinal obstruction, but penia virus (FPV). Occasionally, one or two puppies in a litter have intussusception may cause obstructive pattern. minimal signs, followed by death of littermates, Abdominal ultrasound—fluid-filled, atonic PATHOPHYSIOLOGY small and large intestines, duodenal and which may reflect degree of virus exposure. Parvoviruses require actively dividing cells jejunal mucosal layer thinning with or for growth. Physical Examination Findings without indistinct wall layers and irregular After ingestion of virus there is a 2–4-day Hypovolemic shock—weak pulse, tachy­- luminal-mucosal surfaces, extensive duodenal period of viremia. cardia, dull mentation. and/or jejunal hyperechoic mucosal speckling, Early lymphatic infection is accompanied Severe hemorrhagic diarrhea. and duodenal and/or jejunal corrugations; by lymphopenia and precedes intestinal Fluid-filled intestinal loops may be palpated. intussusceptions can be identified. infection and clinical signs. Dehydration, weight loss, abdominal By postinfection (PI) day 3, rapidly dividing discomfort. DIAGNOSTIC PROCEDURES crypt cells of small intestine are infected. May have fever or hypothermia. Electron microscopy detects fecal virus Viral shedding in feces starts ∼3–4 days PI, during early stages of infection. CAUSES Samples for virus detection should be peaks with clinical signs. CPV-2. submitted during acute phase of infection; Virus ceases to be shed in detectable amounts by PI days 8–12. RISK FACTORS ship specimens refrigerated, not frozen. Absorption of bacterial endotoxins from Unvaccinated dogs. PATHOLOGIC FINDINGS damaged intestinal mucosa plays a role in Dogs 0.2 μg/dL at 24 hours after admission is endotoxemia. gentamicin) and antiemetics (e.g., ondanse- associated with 100% survival. An HDL- Fecal microbiota transplant may speed tron, maropitant). cholesterol concentration >50.2 mg/dL at resolution of diarrhea. PRECAUTIONS admission is associated with 100% survival. Prompt, intensive inpatient care leads to Gentamicin may cause renal toxicity in treatment success. dehydrated puppies. Proper, strict isolation procedures are essential. Exercise care to prevent spread of CPV-2, a ­ MISCELLANEOUS very stable virus. ASSOCIATED CONDITIONS Antiviral drugs have not yet been shown to ­ FOLLOW-UP