Mycoplasmal polyserositis and arthritis of pigs

Previous authors: P WALLGREN

Current authors:
P WALLGREN - Professor, State Veterinarian, Dipl ECPHM, Department of Animal Health and Antimicrobial Strategies, National Veterinary Institute, Uppsala, 75195, Sweden

GENERAL INTRODUCTION: MOLLICUTES

Introduction

Mycoplasma hyorhinis was the first mycoplasma to be isolated from pigs.²⁵ It occurs worldwide and is mainly associated with development of polyserositis and arthritis in pigs less than three months of age.^{17, 23} However, the agent is also able to induce pneumonia in gnotobiotic pigs,^{8, 10} and dual infections with porcine reproductive and respiratory syndrome virus (PRRSV) and M. hyorhinis can cause severe outbreaks of pneumonia.¹²

Aetiology

For information on the characteristics of the mollicutes the General Introduction: Mollicutes should be consulted.

Mycoplasma hyorhinis is readily isolated from specimens collected from diseased pigs in fluid media containing sterols, and forms typical mycoplasmal colonies on solid media that measure 0,5 to 1mm in diameter after one to five days.²² It requires sterols and ferments glucose but does not utilize arginine or hydrolyse urea.²²

Epidemiology

Mycoplasma hyorhinis is commonly found in the upper respiratory tract of fattening pigs,⁹ but does not appear to have  significant pathogenic effects in them¹⁶ unless they are also infected with other pathogens such as Pasteurella multocida,⁶ porcine reproductive and respiratory syndrome virus (PRRSV),¹⁵ influenza virus or Haemophilus parasuis.²⁷ Mycoplasma hyorhinis is a frequent inhabitant of the upper respiratory tract of apparently healthy sows:²⁴ older pigs serve as a reservoir for the organism. The shedding of M. hyorhinis by carriers may be enhanced by stress  such as overcrowding.

Piglets younger than three to four weeks of age rarely develop the disease.²³ This age- related reduced susceptibilityis probably as a result of maternally- derived immunity  as antibodies to M. hyorhinis have been proved to protect from the development of the disease.¹⁰

As the disease is seldom seen among animals older than 10 to 12 weeks, it appears that  piglets probably  mount a protective acquired immunity to M. hyorhinis by that age. A partial, but not total, resistance may develop with ageing since lesions in M. hyorhinis infected and colostrum- deprived piglets were less severe in pigs aged 13-16 weeks  than in piglets aged 10 weeks, which in turn were less severely affected than piglets 7 weeks old.¹⁸

Pathogenesis

Mycoplasma hyorhinis may be an inhabitant of the upper respiratory tract of apparently healthy pigs. It appears that stress induced by adverse environmental factors or other diseases may trigger septicaemia in pigs that are carriers of M. hyorhinis.²³ Thus, when causing disease in piglets, M. hyorhinis primarily colonizes the upper and lower respiratory tract and may then disseminate to other parts of the body.¹⁰ Lesions  are seen in the lungs, serosal surfaces and joints of affected piglets.

Clinical signs and pathology

Diseased piglets 3 to 12 weeks old initially manifest inappetance and a moderate fever, signs which are easily overlooked. Subsequently, an obvious discomfort is noticed which is characterized by a roughened hair coat, abdominal pain caused by serositis and/or stiffness as a result of arthritis. Long-term signs comprise lameness and swollen joints. The number of affected joints may vary from one to several:²¹ the tarsal, stifle, carpal and shoulder joints in particular being affected.²⁶ If more than one joint is affected the pigs may shift their weight between different legs due to the pain.²¹ Sudden deaths during the acute course of the disease may occur, but the mortality rate is generally low. Chronic signs comprise lameness and swollen joints  that may persist for up to six months, resulting in suffering and poor performance of the affected animals:²³ consequently, the overall mortality due to M. hyorhinis infections may become substantial due to the culling of diseased pigs for humane reasons.

Mycoplasma hyorhinis has been isolated from the lungs of piglets one month of age with  pneumonia,⁸ and has, under experimental conditions, induced pneumonic lesions involving the apices of the cranial and middle lung lobes of gnotobiotic piglets,^{8, 10, 18} as well as pleuritis, serositis and pericarditis.¹⁰ Following experimental infections, clinical signs included dyspnoea, anorexia and drowsiness  in some animals, while in others no apparent clinical signs of respiratory disease were evident.^{12, 15} The clinical signs associated with Mycoplasma hyorhinis infections are exacerbated by mixed infections Severe dyspnoea with abdominal breathing has been reported in piglets aged one to two months suffering from a dual infection with M. hyorhinis and PRRSV.¹² Varying pathogenicity between different strains of M. hyorhinis has been suggested,^{5, 13} as  indicated by the different clinical signs seen among experimentally infected gnotobiotic pigs.^{8, 10, 15} Mycoplasma hyopneumoniae should probably not   be considered as the sole  aetiologic agent of porcine catarrhal pneumonia as M. hyorhinis is commonly isolated also from pneumonic lesions of M. hyopneumoniae infections.^{1, 2, 20} Consequently, it has been suggested that M. hyorhinis  contributes to the porcine respiratory disease complex and  aggravates the pneumonia caused by porcine reproductive and respiratory syndrome virus (PRRSV) and other agents.^{15, 18} Nevertheless, M. hyorhinis is commonly isolated from lungs of fattening pigs with pneumonic lesions.^{1, 2, 20}

The lesions seen in the acute stage of the disease caused by M. hyorhinis infections are those of a serofibrinous (occasionally purulent) polyserositis, i.e. lesions in the pleura, peritoneum, pericardium and joints. In affected joints the acute lesions consist of swelling due to increased amounts of synovial fluid, together with hyperaemia, oedema and occasional fibrin deposits.^{10, 21} Histopathological lesions include hyperaemia, enlargement of synovial epithelial cells, and infiltration of plasma cells, macrophages and lymphocytes.²¹ In chronic cases persisting for five to six months, thickening of the joint capsule and articular lesions consisting of erosions of the cartilage and pannus formation are common.^{17, 23}

Lung lesions in gnotobiotic pigs comprise catarrhal bronchopneumonia that affects the apices especially of the cranial lung lobes.⁸ Histopathologically affected areas include infiltration of macrophages and neutrophils into the bronchial lumens and alveoli. In dual infections with PRRSV macroscopical lesions may involve the entire lung resulting is consolidation with moderate interlobular oedema.¹² A severe proliferative and interstitial pneumonia with a marked infiltration of mononuclear cells develops. If complicated, a suppurative bronchopneumonia with thickened alveolar septa and infiltration of neutrophils and macrophages into alveoli may be seen.¹²

Diagnosis

Typical clinical signs (see Clinical signs)in pigs aged 3 to 12 weeks and gross lesions of serofibrinous to fibrinopurulent polyserositis may indicate infections caused by M. hyorhinis. The  diagnosis can be confirmed by isolating M. hyorhinis from the exudate collected from joints or body cavities. The presence of complement fixing antibodies to M. hyorhinis in the serum of pigs in the affected herd may assist in confirming the diagnosis,⁷ as well as antibodies detected by ELISAs.³ However, it must be borne in mind that M. hyorhinis is a ubiquitous organism in pigs and the finding of such antibodies only provides supportive evidence.⁷ For this reason, also PCR results that detect presence of M. hyorhinis^{4, 7, 11} must be interpreted with care.

Differential diagnosis

Diseases in young pigs that cause similar lesions such as Mycoplasma hyosynoviae, Haemophilus parasuis, Streptococcus equisimilis, Streptococcus suis, Trueperella pyogenes infections and Staphylococcus spp. infections should be considered in the differential diagnoses.

Control

Mycoplasma hyorhinis is sensitive to several antibiotics, including lincomycin, quinolones, tetracyclines, tiamulin and tylosin.²⁴ However, none of these drugs has been successfully used to control the disease. Indeed, initiating  treatment when pigs show signs of serositis and arthritis is generally not satisfactory.

Since only a minority will develop disease most of the pigs infected with M. hyorhinis will develop disease, efforts to control infections with M. hyorhinis should focus on managemental pratices. Avoidance of overcrowding and adverse climate factors  and age-segregated rearing systems will considerably decrease the load of the pathogen by preventing the spread of infection from older pigs to younger growing animals. Such efforts may in future be complimented by vaccination since recent reports  described protection of pigs to M. hyorhinis by immunization.^{3, 14, 19}

References

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