atrophic rhinitis 5

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atrophic rhinitis in livestock


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Atrophic rhinitis is an infectious disease of swine characterised by serous to mucopurulent nasal discharge, shortening or twisting of the snout, atrophy of the turbinate (conchal) bones and reduced productivity. It may occur enzootically or more sporadically, depending on a variety of factors including herd immunity. It is also known as

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Historical information Atrophic rhinitis (AR) was described first in 1830. AR was reported in the US in 1944. It rapidly increased in frequency with expansion and intensification of swine production and stimulated a great amount of research. AR has a complex etiology. It is mainly found in large white yorkshire breeds and cross-breds of this species Large white yorkshire

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The most severe progressive form is caused by infection with toxigenic strains of Pasteurella multocida alone or in combination with Bordetella bronchiseptica. Infections with B. bronchiseptica alone can cause a mild to moderate form with non progressive turbinate bone atrophy. Turbinate atrophy may only be obvious at slaughter or may be detected in the live animal by use of radiography or tomography

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Environmental and management factors also contribute to the severity and incidence of this disease. A large proportion of apparently normal pig herds may be infected with B. bronchiseptica or nontoxigenic P. multocida and show a mild degree or low prevalence of turbinate atrophy.


ETIOLOGY Causal pathogens: Two forms of atrophic rhinitis have been recognised, depending on the causal agent(s) (De Jong, 2006): a) A severe progressive form caused by toxigenic isolates of Pasteurella multocida, most commonly capsular types D or A, alone or in combination with Bordetella bronchiseptica. b) A less severe, nonprogressive form with mild to moderate turbinate atrophy, often without significant snout changes, caused by B. bronchiseptica

Epidemiology :

Epidemiology Numerous factors assure survival of toxigenic  B. bronchiseptica  and  P. multocida  among swine. Atrophic rhinitis results in the establishment of inapparent carriers. Swine introduced into a clean herd from an outside source can be carriers and disseminate the agents that cause AR. Also, carrier sows expose their piglets. When their infected piglets are mingled with others, the agents can be transmitted. Although immune sows provide their piglets with some colostral immunity against the agents that cause AR, waning colostral immunity and weaning soon leave young pigs susceptible to infection. Older sows may provide more colostral immunity (and perhaps less infective dose) than do gilts. Several microbiologic agents, other than  B. bronchiseptica  and  P. multocida  are known to cause or be associated with rhinitis The rhinitis they cause may predispose to colonization by the bacteria that cause AR. Other contributing factors include overstocking, substandard housing or sanitation, continuous use of facilities, and failure to use all in/all out production methods


PATHOGENESIS Initial clinical signs include sneezing, snuffling and eye discharge with resultant dark tear-staining and subsequent nasal discharge, which can vary from serous to mucopurulent; in some cases pigs may show epistaxis. Atrophy of the nasal turbinate and septal deviation may lead to shortening or twisting of the snout and, in severe cases, difficulty in eating

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Increased severity is associated with overstocking and poor management, housing and environmental conditions. Reduced productivity is generally associated with moderate to severe atrophic rhinitis, although the precise relationship between infection with these bacteria and reduced weight gains has not been thoroughly elucidated.

Clinical Findings :

Clinical Findings Acute signs, which usually appear at 3–8 wk of age, include sneezing, coughing, and inflammation of the lacrimal duct. In more severe cases, nasal hemorrhage may occur. The lacrimal ducts may become occluded, and tear stains then appear below the medial canthi of the eyes.

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Some severely affected pigs may develop lateral deviation or shortening of the upper jaw, while others may suffer some degree of turbinate atrophy with no apparent outward distortion. The degree of distortion can be judged from the relationship of the upper and lower incisors if breed variations are considered. In addition to the above clinical signs, outbreaks frequently impair growth rate and feed conversion.

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The severity of atrophic rhinitis in a herd depends largely on the presence of toxigenic strains of  P. multocida , the level of management, and the immune status of the herd. The latter is related to both vaccination status and the parity distribution of the sow herd, because younger sows tend to shed more organisms and produce less lactogenic immunity for their nursing piglets than do older multiparous sows.

Lesions :

Lesions The degree of atrophy and distortion is best assessed by examining a transverse section at the level of the second premolar tooth (the first cheek tooth, up to 7–9 months of age); some recommend additional parallel sections. In the active stages of inflammation, the mucosa has a blanched appearance, and purulent material may be present on the surface

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In later stages, the nasal cavities may be clear, but there may be variable degrees of softening, atrophy, or grooving of the turbinates; deviation of the nasal septum; and asymmetric distortion of the surrounding bone structure.

Biopsy findings:

Biopsy findings Normal mucosa ; Pseudostratified columnar Presence of serous and mucous glands Atrophic rhinitis Squamous metaplasia Atrophy of mucous glands Endarteritis obliterans

Diagnosis :

Diagnosis The signs and lesions are commonly the basis for diagnosis; however, the presence of toxigenic strains of  P multocida  should be confirmed. Routine monitoring is done in some breeding herds by measuring the degree of turbinate atrophy and giving the herd an atrophy score. Atrophic rhinitis must be differentiated from necrotic rhinitis

Control :

Control It is rarely possible to keep herds entirely free from mild outbreaks of sneezing, and a low level of aberrant turbinates and nasal bones at necropsy is common, even in herds that show no clinical signs of rhinitis. When atrophic rhinitis rises to an unacceptable level in a herd, control measures are usually strategic—chemoprophylaxis, vaccination, temporary closure of the herd to introduction of new pigs, and improved management (eg, better ventilation and hygiene, less dusty feed).

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Chemoprophylaxis usually includes administration of antibacterial drugs to all sows, particularly prefarrowing, as well as programs of repeated medications for newborn piglets and sometimes for newly weaned pigs. Medication of weaner and grower rations, and sometimes sow rations, is often helpful. Drugs commonly used are ceftiofur, sulfonamides, tylosin, and tetracyclines.

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Bacterins against toxigenic  P multocida  and  B bronchiseptica  have been developed. Both toxoid vaccines and bacterin-toxoid mixtures are available against  P multocida ; while both give satisfactory results in most herds, infection can be best prevented with bacterin-toxoid mixtures. Typically, sows are vaccinated 4 and 2 wk before farrowing, and the young pigs at 1 and 4 wk of age. However, vaccination schedules recommended by the manufacturer should be followed. A high level of colostral immunity is acquired by piglets nursing vaccinated sows. An intranasal vaccine using modified live strains of  B bronchiseptica  is also available for young pigs.

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