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Mycoplasmal pneumonia of pigs

Preferred citation: Anipedia, www.anipedia.org: JAW Coetzer and P Oberem (Directors) In: Infectious Diseases of Livestock, JAW Coetzer, GR Thomson,
NJ Maclachlan and M-L Penrith (Editors). P Wallgren, Mycoplasmal pneumonia of pigs, 2019.
Mycoplasmal pneumonia of pigs

Mycoplasmal pneumonia of pigs

Previous authors: P WALLGREN

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

GENERAL INTRODUCTION: MOLLICUTES

Introduction

Mycoplasmal pneumonia of swine (MPS), caused by Mycoplasma hyopneumoniae,39 is an insidious, subacute to chronic pneumonia characterized clinically by a non-productive cough, loss of condition, growth retardation and low mortality. The causative agent was first isolated in 1965 in the USA30 and Europe.18 Mycoplasmal pneumonia of swine occurs worldwide causing great losses to pig producers due to decreased growth of fatteners, either as a result of  the disease itself or in combination with secondary infections.36, 51

Aetiology

Mycoplasma hyopneumoniae is a small, fastidious, slow-growing organism that can only be propagated on special media (see General Introduction: Mollicutes).12, 35 Overgrowth by other faster growing mycoplasmas may jeopardize cultivation. Mycoplasma hyopneumonia should be differentiated from other closely related mycoplasmas (see Diagnosis), such as M. flocculare.14, 39, 40

It may survive in the environment for up to one month under humid conditions.17 but as it is sensitive to heat, sunlight and dehydration it is, in general, rapidly inactivated in the environment.15

Epidemiology

The disease is typically introduced into uninfected herds by subclinically infected pigs which are usually adult breeding animals. Herds  a short distance from an infected herd(s) may become infected by airborne transmission of M. hyopneumoniae, particularly during conditions of cold outdoor temperature and high  humidity.22 Infections with M. hyopneumoniae have not been reported in minimal- disease herds located two miles from the closest infected herd.17

Within herds, M. hyopneumoniae is transmitted either in aerosols45 or by direct contact between pigs, and is often spread from older to younger pigs. Mycoplasma hyopneumoniae infections are most common among fatteners, i.e. those in units housing high numbers of  young pigs.  The disease is exacerbated by poor hygienic conditions, which also pave the way for secondary infections  such as Pasteurella multocida  is frequently isolated from fattening pigs with pneumonia.8, 12, 56

Piglets are susceptible to M. hyopneumoniae infection because of their poor antibody response.54 Nevertheless, piglets of conventional dams (especially older sows16) generally possess some immunity to  M. hyopneumoniae due to protective, colostrum-derived antibodies.23, 54 In contrast, poorly immunized dams or those with no immunity (especially gilts) may  infect their offspring.8

Multiple strains of M. hyopneumoniae are found in  pig populations, but certain strains appear to be responsible for  outbreaks.32 Limited genetic variation was found  among M. hyopneumoniae isolates in a in a herd with commingled pigs from different sources.37 Nevertheless,  infections with multiple strains may occur within herds  associated with increased severity of  pneumonic lesions at slaughter, suggesting that reducing the number of different strains may lead to fewer lung lesions at slaughter and better respiratory health of  pigs.35

Pathogenesis

After inhalation, M. hyopneumoniae colonizes the lungs extracellularly in the vicinity of ciliated epithelial cells and provokes an inflammatory reaction that may develop as early as one week post-infection.23, 27 The extent of the reaction correlates with the severity of infection. Circulating antibodies to M. hyopneumoniae have been demonstrated 14 days post-infection.13, 28, 47 It has been suggested that  cell-mediated immune responses may play a role in the pneumonic process.33, 48 This contention is supported by the fact that an increased ability of mononuclear cells to produce antibodies in vitro after exposure to M. hyopneumoniae has been demonstrated.53 Antibodies provide protection  to animals following challenge, even when pigs are exposed to stressors that affect the general immune response negatively.59

Clinical signs

Mycoplasmal pneumonia of pigs is a chronic, often insidious, disease with high morbidity and low mortality, at least when uncomplicated. The incubation period is one to three weeks43 and the clinical signs comprise a dry, unproductive cough that increases in intensity on physical exertion, unthriftiness and a decrease in appetite. If established early during the fattening period in a group of pigs, MPS will affect a great majority of them before they reach market weight.42, 44, 51, 61 However, the disease may go unnoticed since pigs with active infections decrease their physical activities and show no overt evidence that they are infected. Their inappetence is generally hidden from the farmer since pen mates of the affected pigs will consume the pooled feed ration. As individual pigs in a herd become diseased at different times, this ‘feed stealing’ can, at least to some extent, explain the phenomenon often referred to as ‘compensatory growth’.58

In uncomplicated cases of MPS, the clinical signs gradually decrease and disappear within 30 to 40 days after onset of the disease,43 and the lesions in the lungs heal completely within approximately 10 to 12 weeks.52 However, if the lung lesions are secondarily infected by bacteria, the course of the disease can be considerably prolonged. The most important secondary invader within the respiratory disease complex of pigs appears to be Pasteurella multocida.8, 12, 56

Pathology

In uncomplicated cases of MPS the pneumonic lesions occur predominantly in the ventral aspects of the cranial, accessory and middle lobes but may also be present in the cranio-ventral parts of the caudal lobes. They comprise clearly demarcated areas of consolidation varying in colour from dark reddish-blue to pinkish-grey, and are often associated with some degree of atelectasis. Older lesions are greyer, and often become secondarily invaded by bacteria, the identification of which determines the nature of the subsequent inflammatory reaction which is often purulent or serofibrinous, and may extend to involve the pleura with the development of pleuritis.27, 29, 39  Mycoplasma hyopneumoniae may, however, in itself cause fibrinous to serofibrinous pleuritis. Oedema and lymphoid hyperplasia of the mediastinal lymph nodes may be present.

Microscopically the nature of the lung reaction varies because the lesions in most field cases are secondarily invaded by bacteria, and the inflammatory reaction will reflect that provoked by both the secondary and primary pathogens. Two to three weeks after infection in uncomplicated experimentally induced disease, the lesions comprise alveolar interstitial thickening due mainly to lymphocyte and neutrophil infiltrations and to proliferation of cells in the septa, giant cell formation and perivascular lymphoid hyperplasia.27, 29, 39  In older cases, six to eight weeks after infection, the predominant lesion is pronounced peribronchial and peribronchiolar lymphoid hyperplasia.

Diagnosis

A presumptive diagnosis can be made on the basis of the clinical signs and macro-and microscopic pathology, but as other pathogens can elicit similar signs and lesions, it is necessary to confirm the diagnosis.29

Mycoplasma hyopneumoniae grows slowly in cultures and is easily overgrown by other mycoplasmal species, therefore bacteriological culture of diseased lung tissue is not a reliable method for diagnosing MPS. Other more efficient methods for detecting the organism in lung tissue include immunofluorescence,19 DNA probes,1, 46 oligonucleotide probes complementary to ribosomal RNA,15, 21 and the use of the polymerase chain reaction (PCR).31, 43, 45 Also, gene sequencing can be used to type M. hyopneumoniae directly from clinical material without prior isolation and culture.11, 32, 35

Mycoplasma hyopneumonia may, however, be absent from the lungs of immune pigs, which remain seropositive for a long period. Therefore, the detection of circulating antibodies has been found to be superior to the diagnostic methods described above when performing epidemiological studies in pig herds. Circulating antibodies to M. hyopneumoniae can be detected using several methods, but the indirect or blocking enzyme-linked immunosorbent assay (ELISA)  is preferred. Cross-reactions with other Mycoplasma spp. are minimized either by treating the antigen with Tween6 or by performing blocking ELISAs based on monoclonal antibodies to the microbe.13

Differential diagnosis

The differential diagnosis should include pneumonia caused by Bordetella bronchiseptica and Mycoplasma hyorhinis, and swine influenza virus.

Control

Because MPS is a chronic, insidious disease, chemotherapy has generally not been successful in controlling it. Nevertheless, M. hyopneumoniae is sensitive to lincomycin, quinolones, tetracyclines and tiamulin.2, 62 These drugs can be used for individual treatment during outbreaks of MPS in naive herds or strategically in control programmes. The long-term use of antibiotics aimed is not recommended due to increasing minimal inhibitory concentration (MIC) values toward the antimicrobials, which has been demonstrated for drugs such as tetracyclines.62

As M. hyopneumoniae is generally transmitted in aerosols within herds, appropriate management practices should be employed to prevent its spread, including an appropriate  stocking density and  acceptable air quality, ventilation, and temperature. Since the disease is often spread from older to younger pigs, the introduction of age segregated rearing systems is  important.9, 20 Despite the presence of M. hyopneumoniae within the breeding stock, some farrow-to-finish herds have   been reared to market size without any pigs developing either macroscopic pneumonic lesions or becoming seropositive to M. hyopneumoniae by housing only one age category of growers per unit.25, 56

Inactivated vaccines9, 22, 32  may be used to control the disease but do not totally prevent the development of lung lesions following experimental challenge with M. hyopneumoniae.10, 11, 24, 38, 60 Similar results, together with increased daily weight gains, have been reported in vaccination trials in conventional pig herds.23, 27 The vaccines have been shown to stimulate the cellular immune response.5, 7  The vaccination of piglets during the first week of life has been recommended by some researchers, but others  obtained better results  when older piglets were vaccinated,49 possibly due to an increased age-related ability to mount an immune response towards M. hyopneumoniae.54 Under field conditions a higher level of protection was obtained when piglets nine weeks of age were vaccinated compared to littermates vaccinated for the first time at three weeks of age.59 If piglets are vaccinated once at the age of nine to ten weeks but before they have been exposed to M. hyopneumoniae, subsequent natural infection may act as a form of a ‘booster vaccination’, after which they will possess a high level of protection against MPS. However, if vaccinated twice, i.e. at nine to ten weeks and again at 13 weeks of age, they will be even better protected.55

The protective role of colostrum from older sows has been investigated.16 By transferring older sows to new facilities prior to farrowing and not restocking the previously used buildings for a year, it was  possible to eradicate MPS.50 The administration of antibiotics has considerably increased the efficiency of such programmes, and successful eradication attempts have been carried out in a number of countries.4, 26, 34, 41, 57, 64 Generally, such programmes include the isolation of pigs older than 10 months and the strategic treatment of sows before farrowing and their transfer to cleaned and disinfected units.

Another method of protecting the piglets from infection by M. hyopneumoniae (and certain other infections) in infected herds is the introduction of  medicated early weaning (MEW).3 Medicated piglets are weaned from their medicated dams at the age of 14 days, and the piglets are transferred to new facilities that have been disinfected. If the sows are also transferred to disinfected facilities, this method may be used to establish disease-free herds.

The ultimate way to eradicate M. hyopneumoniae is to establish specific pathogen-free (SPF) or ‘minimal disease’ herds.63 The first generation of pigs within these systems is obtained by caesarean section of the dams. The subsequent generations of pigs may be mated by artificial insemination, which also ensures the maintenance of genetic improvement of the breeding stock. However, careful consideration  should be given to the introduction of new pure-bred stock. Specific pathogen-free herds should be monitored continuously with respect to freedom from infection.

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