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Mycoplasma hyopneumoniae: ‘Fix the gilts, fix Mycoplasma’

By James F. Lowe, DVM, MS, Dip ABVP (Food Animal)
Lowe Consulting Ltd, Mahomet, Ill.
Associate Professor and Head, Integrated Food Animal Management Systems
Department of Veterinary Clinical Medicine, College of Veterinary Medicine
University of Illinois at Urbana-Champaign 

 

There’s a lot we think we know about Mycoplasma hyopneumoniae (M. hyo) under field conditions, but there’s a paucity of peer-reviewed literature to support much of the conventional wisdom we swine veterinarians apply to the management of M. hyo as well as its role in porcine respiratory disease complex (PRDC). Our inability to accurately assess infection dynamics limits our ability to design evidence-based M. hyo-management strategies for gilt populations. The result has been many divergent and sometimes conflicting approaches to controlling M. hyo in modern production systems.

In my experience, however, it’s possible to achieve effective M. hyo control, but it depends on five critical, key messages. They focus on the status of gilts at the time of entry to the sow farm because control of M. hyo-associated PRDC late in finishing won’t be achieved until the M. hyo infection status of gilts at the time of entry is adequately managed. That’s why I like to say, “Fix the gilts, fix Mycoplasma.

Key message 1

The number of pigs infected at weaning determines the disease load from M. hyo in growing pigs.

The first step toward understanding the potential impact of an infectious disease in a population is to understand the root mechanisms of the disease source and its transmission. M. hyo is a slow-growing organism with a long incubation prior to the emergence of clinical signs, so infection early in life is an important factor in disease progression. Without sufficient time for the organism to grow in the host before marketing, clinically important disease doesn’t occur. For disease to occur in the population, increased transmission early in the growing period is important.

Key message 2

Shedding sows means infected pigs.

While it’s possible piglets could become infected with M. hyo from horizontal transmission during transport or immediately after weaning, this appears to be unlikely. The dam is the most logical source of infection in pigs at weaning for most diseases, and M. hyo is no exception. It’s logical to assume from available evidence that controlling this transmission link is the key to improving clinical outcomes in late finishing pigs.

Key message 3

Females that are infected in the 200 days prior to farrowing are likely to shed to their piglets.

Even if infection rates in piglets at weaning are low, some sows are shedding M. hyo to their piglets. This raises the question of why some sows are more likely to shed M. hyo than others. There’s clear evidence in the literature that animals that are within 200 days of M. hyo exposure and infection are capable of infecting other pigs.1 In other words, any female infected within the last 200 days is capable and likely to infect her offspring, but those infected more than 200 days previously are not likely to do so. Thus, the ability of a sow to shed M. hyo is strongly dependent on the post-infection interval.

Research has not definitively established M. hyo reinfection and shedding patterns, but it’s speculated that once animals are M. hyo-infected, they are unlikely to be reinfected or to shed the organism again. This assumption suggests that if the herd does not have new exposures to M. hyo for at least 200 days, shedding will stop. In the case of M. hyo-elimination programs, herd closure for extended periods of time has been shown to stop sow-to-piglet transmission.

Key message 4

Gilts are the most likely animals to be infected in the 200 days prior to farrowing.

In typical breeding herds with continuous or intermittent introduction and removals, new animals are the most likely to be infected within 200 days of farrowing. There are two potential ways for this to occur either before or after introduction into the herd. In the first scenario, naive gilts are introduced into an infected herd and become infected during the gestation period. In the second scenario, gilts are recently infected prior to arrival and have not cleared the organism prior to farrowing. Both scenarios have the same clinical outcome, which is transmission to first-parity litters and late-finishing PRDC in susceptible animals.

Key message 5

Vaccination is not effective when used as the sole or primary tool for disease control.

There is clear evidence that conventional, killed M. hyo bacterins do not alter the transmission rates of M. hyo in populations.1,2 An M. hyo bacterin may minimize or prevent clinical signs of M. hyo in pigs,3 but it doesn’t prevent infection or reduce the number of infected pigs in a herd setting. Although M. hyo bacterins remain a valuable tool for mitigating clinical enzootic pneumonia or PRDC, they will not solve the root cause of M. hyo infection or minimize the impact of M. hyo on profitability.

Gilt acclimation scenarios

The objective in commercial swine herds is to have gilts that aren’t shedding M. hyo at the time of farrowing to reduce the rate of M. hyo infection in their offspring. Practically speaking, there are four scenarios for replacement gilt (RG) introduction in commercial swine herds that need to be managed to minimize the impact of M. hyo on the downstream pig flow.

In all four scenarios, it’s critical that acclimation addresses all other microorganisms that can cause production-herd losses. The strategies outlined below are exclusive to M. hyo and need to be incorporated into an individualized, whole-herd, evidence-based acclimation plan that considers other conditions and constraints.

Scenario 1M. hyonaïve RGs, M. hyonaïve breeding herd

This is the simplest scenario to manage. In this case, the acclimation program needs to be preceded by a period of isolation and testing to ensure RGs are M. hyo-free. This can be a challenge because all M. hyo-testing strategies suffer from relatively low sensitivity and specificity.

However, coupling incoming-RG monitoring with a comprehensive source-herd monitoring strategy can produce confidence in the naïve status of RGs. No additional acclimation processes are necessary.

Scenario 2 — M. hyonaïve RGs, M. hyoinfected breeding herd

This scenario is increasingly common due to the steady increase in M. hyo-naïve sources of replacement breeding stock. It’s critical that gilts are exposed to M. hyo no later than 200 days pre-farrowing, which is at least 90 days prior to breeding.

RGs have to be delivered at less than 90 kg (200 lbs) of bodyweight to the acclimation barn so there’s enough time from exposure to farrowing while still maintaining target breeding weights. In addition, because it’s difficult to maintain a consistent M. hyo source for exposure, a continuous-flow acclimation barn is almost always necessary to achieve successful exposure.

Exposure can take from 1 to 30 days after entry, so extended acclimation times produce more consistent exposure patterns than very short acclimation periods. Introduction of RGs no heavier than 25 kg (55 lbs) is necessary to allow for isolation and testing before entry into an acclimation facility.

Scenario 3 — M. hyo-infected RGs, M. hyoinfected breeding herd

You would think this scenario is easy to manage, but it’s actually the most complex. For this model to be successful, RGs need to be exposed using the same time line as for Scenario 2. This is often more difficult than expected because M. hyo-infected herds have variable rates of M. hyo shedding from sow to pig. This means the timing of exposure is not consistent in the RGs coming from that herd.

To ensure M. hyo infection occurs early enough during the development period, RGs have to be delivered to the acclimation barn at less than 90 kg (200 lbs) of bodyweight to ensure there’s enough time between exposure and farrowing while still achieving target breeding weights. In addition, it’s difficult to maintain a consistent M. hyo source for exposure, so for successful exposure, a continuous-flow acclimation barn is almost always necessary.

Again — as in Scenario 2 — exposure can take from 1 to 30 days after entry, so extended acclimation times produce more consistent exposure patterns than very short acclimation periods. The introduction of gilts no heavier than 25 kg (55 lbs) is necessary to allow for isolation and testing before entry into an acclimation facility.

Scenario 4 — M. hyo-infected RG, M. hyo-naïve breeding herd

Avoid this scenario at all cost. The introduction of M. hyo-infected gilts into an M. hyo-naïve population will induce an outbreak of acute M. hyo in the breeding herd and the resulting pig flow because RGs will shed M. hyo to naïve animals after introduction.

If M. hyo-positive gilts are to enter an M. hyo-naïve herd, they need to have enough time to clear the infection. The only way to reliably prove they aren’t still infected is to wait until they no longer have any M. hyo antibodies. Animals that are still M. hyo carriers will always have an antibody titer. (The converse is not true; all antibody-positive animals are not infected because there’s a period between the time that M. hyo clears and antibodies decay to below detectable levels.) Other diagnostic modalities have a high false-negative rate — a low sensitivity — and aren’t useful for determining infection status.

For detailed information on managing M. hyo, see A Contemporary Review of Mycopolasma Hyopneumoniae Control Strategies.

 

 

 

 

1. Pieters M, et al. An experimental model to evaluate Mycoplasma hyopneumoniae transmission from asymptomatic carriers to unvaccinated and vaccinated sentinel pigs. Can J Vet Res 2010;74:157-160.

2. Meyns T, et al. Comparison of transmission of Mycoplasma hyopneumoniae in vaccinated and non-vaccinated populations. Vaccine 2006;24:7081-7086.

3. Okada M, et al. Evaluation of Mycoplasma hyopneumoniae inactivated vaccine in pigs under field conditions. J Vet Med Sci 1999;61:1131-135.

 

 

 


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