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CANINE INFECTIOUS RESPIRATORY DISEASE (CIRD) Management of Outbreak Situations

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CANINE INFECTIOUS RESPIRATORY DISEASE (CIRD) Management of Outbreak Situations ZOETIS OCTOBER 2017 CANINE INFECTIOUS RESPIRATORY DISEASE (CIRD) Management of outbreak situations Margaret Gober, VMD Manager, Product Support Veterinary Medical Information and Product Support Zoetis, Inc. Robert McCloskey, DVM OVERVIEW his technical bulletin is designed to assist the veterinary practitioner in the management of outbreak situations involving canine infectious respiratory T disease (CIRD). To this end, we have gathered opinions and articles from some of the leaders in the veterinary community. Our goal is to provide clinics with general guidelines regarding the handling, diagnosis, and treatment of their CIRD patients and support in the management of these potentially catastrophic events. We will explore the various pathogens implicated in CIRD, describe some of the currently recommended diagnostic tests, and review potential treatment options. We will discuss some of the current CIRD vaccines in broad terms to increase awareness around use, and lastly, we will outline some of the management factors which need to be undertaken in the face of an outbreak. Since CIRD is a complex syndrome involving a multifactorial etiology, diagnostic testing is always recommended to identify pathogens. Armed with this information, the practitioner may then determine the appropriate steps to help mitigate or reduce the effects associated with an outbreak situation. PATHOGENS Incubation Preclinical Duration of Subclinical Persistent VIRUS Period shedding shedding infection infection1 CRCoV < 1 week Yes 2 weeks Yes No CIV 2-4 days Yes 7-21+ days Yes No CHV < 1 week Yes 2 weeks Yes Yes CPiV < 1 week Yes 1 week Yes No CAV-2 < 1 week Yes 1 week Yes No CDV 1-3 weeks Yes < 1 month Yes No Incubation Preclinical Duration of Subclinical Persistent BACTERIA Period shedding shedding infection infection Mycoplasma 1-4 weeks Yes Several weeks Yes Up to 3 weeks in spp. lung tissue2 Bordetella 3-10 days Yes Several weeks Yes Recovered up to 14 bronchiseptica weeks after clinical signs resolved3 Streptococcus 1-3 weeks Yes 1-2 weeks4 Yes Possible (seen in zooepidemicus other species) Chlamydophila Unknown5 Yes Unknown5 Possible5 Possible (seen in other species) hile these charts highlight many of the environment. None of the canine viruses commonly recognized CIRD establish persistent infection, but several of the Wpathogens, they are by no means bacteria can linger in tissues for weeks to comprehensive. In fact, emerging infectious months. All of the respiratory pathogens are agents such as reovirus and pneumovirus have transmitted by direct contact with respiratory been identified.6 These organisms may act secretions of infected dogs and by contact with alone to cause disease or they may intensify contaminated fomites. Veterinary clinic staff the effects of other known pathogens, resulting members are the most important vector for in more significant CIRD symptoms and fomite spread. In addition, canine viruses are compromising patient outcomes. One effectively distributed over distances >20 feet characteristic that the above etiologic agents in aerosols generated by sneezing and share in common is that they all contribute to coughing, significantly enhancing rapid preclinical shedding during the incubation transmission throughout a kennel.1 Unlike period, meaning infected animals are viruses, Mycoplasma spp. can survive for weeks contagious before they develop clinical signs.1 to months outside the host in the environment; Most of these bacteria and viruses are shed in therefore, the potential for reexposure from an respiratory secretions for 7 to 14 days, untreated environment exists.2 allowing ample opportunity for spread of Environmental factors and host immune disease. A subclinical carrier state may also response play equally important roles in the exist, further compound-ing the problem. development of CIRD. Several pathogens may Dogs with clinical signs shed greater amounts produce mild or subclinical disease in healthy of bacteria and/or virus which significantly animals in the absence of complicating factors increases the infectious dose in the 2 like stress, immunocompromised host, or high Bordetella through direct or indirect contact contact rates. All of the etiologic agents listed with other animals. Contaminated bedding or above can cause a similar clinical presentation water may serve as indirect vehicles of of coughing and/or nasal discharge.7 While transmission. Bordetella is unique in that it can canine parainfluenza virus and Bordetella induce temporary ciliary impairment. This bronchiseptica are classically thought of as allows the bacteria to be a primary, rather than causing only relatively mild disease, more an opportunistic, respiratory pathogen. Most severe illness may occur when secondary, adult dogs develop mild to moderate opportunistic pathogens become involved. tracheobronchitis after exposure, resulting in a Ultimately, in an outbreak situation, the harsh cough. Less frequently, sneezing and/or specific cause of CIRD cannot be definitively oculo-n asal discharge may also be observed. determined based on diagnostics from a single Damage to the respiratory cilia makes dog. Instead, pinpointing the source(s) of conditions ripe for a secondary, opportunistic, illness requires analyzing samples from a larger bacterial or viral infection which can make representative portion of the affected what would usually otherwise be a population of animals. As a result, we self-limiting condition more serious. Presence recommend at least five separate and discrete of contaminated fomites in the environment sample submissions to help determine the is short-lived and is directly related to the pathogenic players. Interpretation of the concentration of infected animals present. diagnostic test results must be made in Bordetella bacteria are readily killed by light of several factors. For instance, many decreased oxidation/reduction potentials, of the CIRD pathogens can be isolated UV irradiation, pH and temperature from clinically normal dogs. Additionally, extremes, and many common chemical if the same pathogen is found in several disinfectants.5 dogs, this raises the index of suspicion that Mycoplasmas a causative relationship exists, but still does Mycoplasmas, the smallest prokaryotic cells not rule out other contributing agents.7 In capable of self-replication, are pleomorphic the face of suspected severe infectious organisms. Since they are seldom identified to respiratory disease resulting in death or a species level during routine testing, they are euthanasia, necropsy should be utilized to often mistakenly thought of as a single entity. investigate the source of illness. If you are However, there are more than 15 different uncertain whether a single death might species of Mycoplasma which have been represent the beginning of an outbreak, isolated from pet animals.2 Most of these are collection of lung specimens and commensal organisms, with only a few serving oropharyngeal swabs for future analysis would as pathogens.2 There is evidence that be recommended. Formalin fixed, frozen, and Mycoplasma cynos can induce upper refrigerated specimens should be obtained for respiratory disease in dogs, and isolation of M. histopathology, viral isolation, and bacterial cynos has been correlated with an increased 7 culture respectively. severity of CIRD.2 One study isolated M. cynos from the air within a kennel, suggesting BACTERIAL PATHOGENS that environmental contamination may be a Bordetella bronchiseptica significant problem with this pathogen. Bordetella bronchiseptica is a Gram Clinical signs may include cough, accumu- negative bacteria that replicates in the lation of mucus and exudate. This pathogen respiratory tract. Dogs encounter does have the potential to develop into pneumonia. Mycoplasma can 3 often evade the immune response, resulting in both tracheal and lung samples in dogs with PATHOGENS a chronic, low grade infection and perhaps CIRD. As is true of many of the other predisposing patients to other, secondary pathogens mentioned above, Chlamydo-p hila bacterial infections.5 may contribute to subclinical infections in some animals, while causing severe signs of Streptococcus equi subspecies CIRD in others.8 At this time, most diagnostic zooepidemicus labs do not have PCR testing available for this Although this organism may occasionally be pathogen. found in the respiratory tract of healthy dogs, in some settings, it can be responsible for a VIRAL PATHOGENS severe, acute to peracute, respiratory infection Canine Adenovirus Type 2 (CAV-2) which may be either primarily airway-related or may cause a fatal hemorrhagic pneumonia. This virus was first identified in 1961 in Co-infection with various respiratory viruses Canada.9 Strain isolation identified the virus as may increase the likelihood of infection or CAV-2, differentiating it from CAV-1, which worsen severity of infection after exposure to S. causes infectious canine hepatitis. Infection zooepidemicus. Several outbreaks in shelter/ occurs via the oronasal route. Respiratory kennel settings have demonstrated that this can signs, which generally result from damage to be a highly contagious, frequently fatal disease. bronchial epithelial cells, include fever, a deep In its peracute form, infected dogs may simply sounding dry cough, watery nasal discharge, be found dead in the morning without having pharyngitis, and tonsillitis.5,9 While widespread acted sick the day prior. Pulmonary vaccination has lessened the prevalence of this hemorrhage, pleural effusion,
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