Up until now 25 named mycoplasma species have been isolated from the various poultry species. Mycoplasma gallisepticum (MG) and Mycoplasma synoviae (MS) both occur in chickens, turkeys and other avian species and cause severe economic losses.
Although Mycoplasma gallisepticum has been largely freed from poultry breeding stocks and is well controlled in broiler breeders, broilers and layer breeders, it still continues to persist in many multi-age commercial layer operations globally, resulting in losses in egg production, poorer feed conversion rates and mortality. With the sustained focus on Mycoplasma gallisepticum, much less attention has been given to Mycoplasma synoviae, until more and more global markets experienced economic losses from Mycoplasma synoviae positive flocks. This and other factors are the reasons why recently there has been an increased interest in understanding the consequences of Mycoplasma synoviae infections in commercial layers.
Mycoplasma synoviae (MS) is an important pathogen of domestic poultry, causing economic losses to the poultry industry and is considered the second most important avian Mycoplasma species for chickens and turkeys. Both M. gallisepticum and M. synoviae are egg-transmitted pathogens and/or spread horizontally via the respiratory pathways, usually affecting 100% of the birds. Following infection, the birds become persistently infected with M. gallisepticum and M. synoviae and remain carriers for life. Infection most frequently occurs as a subclinical upper respiratory infection, which can progress to respiratory lesions, and aggravated by other respiratory pathogens (e.g. Newcastle Diseases Virus, Infectious Bronchitis Virus, Ornithobacterium rhinotracheale and E.coli infections). In a Mycoplasma synoviae positive flock, it can be very difficult to achieve ideal pullet weight profiles in the rearing phase (Figure 1) with consequent later deleterious effects on egg production and egg size when weights are hampered by infection.
The disease has also been associated with respiratory disease and subsequent egg peritonitis and mortality in egg producing commercial layer hens. The major cause of layer mortality globally is secondary E.coli peritonitis, and is characterised by acute mortality. Peritonitis with yolk material deposited in the body cavity and polyserositis are the two main necropsy findings associated with this disease. The occurrence of E. coli peritonitis in layer flocks often creates two mortality peaks along the laying cycle. The first increase in mortality occurs around the pecking period in egg production and is suspected to be of respiratory origin. The second increase in mortality is observed during the later laying period at an age of 50 week and onwards, and is suspected to be of vent origin attributable to vent trauma. The hypothesis is that the injured trachea would allow the avian E.coli a greater level of colonisation and systemic penetration that would result in higher levels of peritonitis. Furthermore, Mycoplasma synoviae can also cause infectious synovitis in chickens and turkeys. Obviously, such affected birds have difficulties in getting sufficient feed intake and egg production is of course affected.
Since the year 2000, a novel syndrome, called ‘Eggshell Apex Abnormality’ (EAA), has been more and more observed in broiler breeders and in table egg laying chickens globally and is again caused by Mycoplasma synoviae strains. The upper portion of the eggshell is translucent, thinner and more fragile to break. In addition, affected flocks show an increase of speckling and discolouration of eggs. Other causes, such as IBV, contribute more strongly to a higher number of much more abnormal eggs (up to 25%). From Table 1, it’s clear that the economic losses for layer producers can be substantial with increased number of smaller and second quality eggs, to be sold at much lower value and re-directed as liquid eggs. Eggs with cracks, breaking easily, contaminate the egg collection system with a substantial increase of labour cost for cleaning.
As the role of Mycoplasma synoviae infection in the layer chicken industry is still a bit controversial, usually it seems to produce somewhat less severe damaging effects than a Mycoplasma gallisepticum infection. However, progressively declining egg production numbers can be observed as demonstrated in Figure 2, and a significant decline in performance can be seen as demonstrated in Table 2, when comparing Mycoplasma synoviae positive layer flocks with negative flocks.
As a result of the expansion of poultry production and the concentration of large, multi-age production complexes within a restricted geographic area, it is becoming more and more difficult to maintain flocks free from Mycoplasma synoviae. Mycoplasma synoviae control should primarily be based on the eradication of the organism, using negative replacement stock and disciplined biosecurity measures to maintain a Mycoplasma synoviae-free status in commercial layer breeders and their progeny.
Live vaccines that are currently used to control Mycoplasma MG and MS (F-strain, 6/85 strain, Ts-11, MS-H) and inactivated vaccines (bacterins), have not been able to completely prevent the occurrence of Mycoplasma in commercial layers.
A Mycoplasma gallisepticum outbreak has been reported in Jordan from July 2004 to January 2005. 70% of broiler flocks suffered from respiratory disease and were found positive for MG by enzyme-linked immunosorbent assay (ELISA). All the isolates from this time period were indistinguishable from the F-strain vaccine. Theses isolates were all from non-vaccinated flocks. The hypothesis here is that the F-strain vaccine is transmissible to unvaccinated flocks and persist for long periods in these flocks, becoming the predominant genotype in the field during the above period.
The first field case of apparent increased virulence and vertical transmission of the ts-11 vaccine strain, a live MG vaccine, in flocks in North Eastern Georgia has been reported. Live vaccines should not cause disease in vaccinated animals and certainly not cause disease in neighbouring flocks. Attenuated strains should not revert to a virulent form. Another inconvenience of vaccination is that the serological response to vaccination may make it very difficult to differentiate with a field mycoplasma infection in vaccinated flocks using serological tests as diagnostics.
While there is a lack of association between levels of antibody and protection against Mycoplasma spp., serology is still used to determine whether a vaccine has elicited an immune response or not. More importantly, serology is also used to determine if a flock has or has not been infected prior to vaccination. Detection of antigen by PCR in oropharyngeal-choanal swabs will however give a more accurate indication of the flock’s infection status and is recommended.
It would be up to the individual layer companies to make their own decisions if they are to vaccinate or not for one or the two main Mycoplasma species. Those which operate in multi-age commercial layer flocks need to be particularly mindful of vaccinated flocks becoming a source of infection for non-vaccinated flocks at the same production site or geographical area. Moreover, birds that are already infected cannot be vaccinated effectively anymore and who wants to vaccinate laying hens in production, seeing the side effects on production?
The companies should perhaps focus more on monitoring the infection status for MS and MG of their flocks via serology (ELISA) and PCR at regular times to identify when and how heavy the flocks are, or become, infected in the rearing phase or early or later in lay with consequent substantial economic losses. Failure to implement disease monitoring greatly increases the risks. Given all of the challenges of dealing with Mycoplasma infections in commercial layers, it is very reasonable and economical to consider responsible therapeutic treatment with effective anti-microbials having a zero-egg withdrawal time, for Mycoplasma spp., when infections have been clearly identified.
References available upon request.