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In pigs, as in other animals, the term "lameness" refers to an abnormal gait. The cause of lameness in pigs may be musculoskeletal, neurological, or integumentary in origin, and may be of traumatic, infectious, nutritional, or developmental etiology. Affected pigs may be visibly limping, unable to rise, or simply less inclined to move to feed and water troughs; swollen joints or hoof lesions may also be apparent. Examination for lameness in pigs involves comprehensive evaluation of the facility and herd, as well as the affected individual animals. Diagnostics include necropsy, nutritional analysis, and infectious disease testing. Given the nature of production medicine, treatment for lameness in pigs is most often directed at an appropriate management change to prevent additional cases, rather than treatment of the individual animal.

Lameness is a perennial problem in swine production worldwide. Although lameness can be caused by congenital or developmental abnormalities, most lameness in production animals is due to pain associated with infections, trauma-related injuries, or underlying metabolic diseases. For that reason, lameness has become an area of focus for swine farm audits of animal well-being.

Lameness is also an economic issue, because it is likely to affect the viability, growth, or reproduction of pigs. Lameness in a herd can negatively impact the overall supply of pigs through the production pipeline; eg, if breeding stock is lost because of lameness, farrowing targets may not be met, or if younger pigs are affected by musculoskeletal disease, their growth rates, and therefore time to finishing, may be prolonged.

As with diseases of other body systems, lameness problems in a swine herd require a comprehensive approach if a diagnosis is to be reached so that preventive or curative measures can be instituted. Respectful, objective, and timely communication with stakeholders is an important component of the investigation process.

Signalment of Lameness in Pigs

The types and causes of lameness in pigs can vary widely by the age of the pig and, to a lesser extent, by gender and breed. Traumatic injury can cause lameness in pigs at any age; however, some types of lameness arising from infectious or physiological causes can have a more limited age range or set of circumstances under which lameness develops.

Some infectious agents can affect and cause lameness at multiple ages. Therefore, part of a comprehensive approach to diagnosis is to understand the signalment of not only the group of pigs under evaluation but also other pigs recently in contact or proximity with the affected group.

In addition to the signalment of the affected pigs in a population, the signalment of the entire composite group (ie, demographics) is an important consideration. Examples of group signalment include the proportion of gilts in farrowing groups (because gilts are more likely to pass pathogenic bacteria to their progeny) and the herd immune status with respect to a particular pathogen, based on known endemic presence or vaccination status.

History of Lameness in Pigs

With cases of lameness, the history must be thorough and should include information on the age of onset, presence of clinical signs, and progression of the lameness. Morbidity and mortality associated with any lameness, as well as the number of groups, pens, rooms, or buildings housing affected pigs, are all relevant.

Morbidity information should include treatments and the responses observed. Culling rates can provide information on morbidity; however, recorded reasons for culling sows are notoriously inaccurate.

Condemnations at slaughter can also provide objective data on morbidity. Condemnations for limb abnormalities, joint abscesses, or fractures have a direct bearing on lameness statistics. Condemnations for polyserositis, adhesions, or "downer" pigs have an indirect bearing on lameness statistics.

Mortality data can be evaluated as an absolute rate or, more usefully, as incidence by stage or week of production. For sows, body condition score at the time of death or euthanasia can help reveal underlying lameness conditions because recorded reasons for cause of death are also prone to inaccuracy, and lame sows tend to lose body condition before death or euthanasia.

Investigating a lameness problem on a farm also requires an understanding of how the farm operates. The sources, transport, and placement of the pigs should be explored. The history of replacement breeding stock is relevant, especially if new herds of origin or different genetic lines have been introduced.

Current health programs and practices should be considered. It is important to determine whether vaccination or medication protocols have been changed. It is equally important to determine whether protocols have been followed correctly. Audits of product consumption or antibody testing for vaccine titers, if available, can be used as verification methods.

Reviewing nutrition programs as a possible contributor to lameness problems can be complex. Fundamental questions include which rations were formulated, as well as how and where they were mixed and delivered to the pigs. Problems are relatively rare but possible during each stage of the process:

  • At the formulation stage, lameness problems can result, for example, when book values of phosphorus are different from actual amounts in the product used, or when vitamin D or phytase activities are not at expected concentrations because of storage, processing, or other problems. These discrepancies can ultimately affect calcium and phosphorus ingestion by the animal.

  • At the mixing stage, mills can have time constraints that do not allow adequate mixing of feed batches, so the feed composition can be uneven, or even delivered to the wrong bin.

  • At the point of consumption, feed density differences in sow gestation feed can result in overfeeding or underfeeding when volumetric feeders are not adjusted to keep pace with weight and nutrient density changes in the ration.

Suspected nutritional lameness problems are collectively referred to as metabolic bone disease, which usually involves calcium, phosphorus, and/or vitamin D metabolism. Diagnosis requires testing of feed, feed components, and their availability (see Rickets Rickets Lameness in pigs is of increasing interest in North American swine production. Mycoplasma hyosynoviae in particular has received more attention, in part because of more intensive diagnostic... read more Rickets ).

Farm staff play a large role in caring for pigs on farms, so they are a key source of information and possible solutions to lameness problems. Personnel working with the pigs may also contribute to lameness problems. Observing the work environment and the interaction between pigs and farm staff can help reveal sources of trauma likely to occur routinely on the farm. The extent of staff training, competence, and compliance is an important component of the case history.

Understanding the farm's hygiene practices is important for identifying risks of injury and disease—eg, from slippery surfaces or from contamination by transport vehicles. If bedding is used, determining its source and management is also important for characterizing disease risks.

Finally, reviewing previous disease history, diagnostic reports, and all test results from the farm is critically important for establishing a starting point for further investigation of lameness problems. If available, the disease histories of neighboring farms can help to elucidate disease risks. At a minimum, a review of all the pertinent diagnostic testing results for the specific herd is required.

Clinical Evaluation of Lameness in Pigs

Diagnosis of lameness can be complex. At least three body systems (musculoskeletal, nervous, and integumentary) may be affected independently or in combination. In addition, there are multiple insult types, risk factors, and specific agents or diseases that can operate sequentially or simultaneously to contribute to lameness expression.

The objective of thorough clinical evaluation in a diagnostic investigation is to characterize the lameness by careful antemortem examination of individuals and groups to formulate accurate case definitions. Strategic necropsy and evaluation of gross lesions also contribute to final case definitions.

Differential diagnosis of lameness is determined by generating a list of suspected primary or contributory insults. Laboratory testing may be necessary to confirm a role for specific agents or disease processes.

The table includes some of the common insult types, disease conditions, and agents that may be considered in lameness investigations.

Table

Examination of a herd with a locomotor problem should include not only the individual affected animals or groups but the environment in general, unaffected groups of animals, and pens adjacent to affected groups. Modification of the “four circle” approach for farm investigations is useful, particularly if the attending veterinarian is not familiar with the farm.

  • Circle 1 is the examination of premises to understand facility design, traffic patterns, external biosecurity, and general impression of management.

  • Circle 2 is the examination of individual barns for environmental features and management practices.

  • Circle 3 is the closer examination of rooms and pens to provide a general sense of the overall health, activity, and behavior of the group.

    Pen-by-pen evaluations provide an opportunity to make counts or estimates of the prevalence and severity of the lameness. Pigs should be made to move around (in pens or into alleyways), to stand, and, if housing allows, to walk while being observed for evidence of lameness.

    The pen ahead and pen behind the last pigs to stand up and first pigs to lie down should be observed. Pigs that take advantage of the diversion caused by the evaluation to access feed or water should be noted. Abnormal gait and posture, body condition (thin pigs are more likely to be lame), and physical evidence of trauma, infection, or malformation (swelling, vesicles, etc) should be watched for in individual pigs.

    This stage of examination should yield a refined case definition with representative lame pigs identified.

  • Circle 4 is in-depth clinical examination of individual pigs that meet the emerging case definitions, with the objective of identifying the specific causes of the lameness (eg, as in the ).

    Physical examination of individual pigs usually requires some restraint. For example, a sorting panel can be used to prevent the pig from moving away. If more restraint is needed, small pigs can be lifted or manually held for examination.

    Larger pigs can be snared or cast using ropes. The advantage of this type of restraint is that it immobilizes the pig. The disadvantages are that the pig is placed in an unnatural posture, excess muscle tone is normally stimulated, and help from additional people is usually required.

    Anesthesia is another possible means of greater restraint. The advantage is that muscles are relaxed, allowing manipulation of skeletal structures such as potential fractures. In addition, muscle mass can be assessed, joint taps or other diagnostic procedures can be performed, and more extensive evaluations, such as radiography or other scanning, are possible, if warranted. The disadvantages are that controlled substances used as anesthetics must be managed, withdrawal times are required, and managing recovery from anesthesia with other pigs present or in facilities that may not be set up for such procedures can be challenging.

    Occasionally, the farm may have lift chutes to immobilize boars, sows, and gilts for foot trimming or other procedures. Lift chutes enable good restraint with full access to the feet and lower limbs.

    A general physical examination of an individual pig for lameness requires a thorough, systematic, and consistent process by individual clinicians. One approach is to proceed from the bottom up and from front to back of the pig. The feet are evaluated first, followed by the limbs and torso, in a front-to-back progression.

The feet can be examined most easily when the pig is lying laterally recumbent or is lifted (manually for small pigs or using a mechanical chute for sows). Standardized guides exist to score foot lesions by type. Prevalence and severity of foot lesions in a sow herd can be estimated by scoring the feet using statistical sampling. A good flashlight is helpful when scoring foot lesions.

Feet may need to be cleaned for pigs housed on nonslatted floors. Exploring lesions by trimming with a hoof knife, clipper, or grinder requires adequate restraint and safety protocols.

Foot lesions have been well defined; however, they do not always correlate with lameness on an individual pig basis, because the pain associated with foot lesions depends on exposure or infection of the sensitive tissues underlying the claw, heel, and sole of the toes.

A consistent approach should be used in palpating and manipulating limbs and joints. As noted in the description of circle 4 above, the amount and type of restraint depend on the size of the pig and other logistical considerations.

Cardinal signs of inflammation—ie, heat, swelling, pain, and redness—should be noted. Strength, range of motion, crepitus, and weight-bearing distribution should be evaluated. Joints embedded in muscle mass (eg, hip, stifle, shoulder) require deep palpation, which may not be possible on large, heavily muscled pigs.

Fracture of the head of the femur, a common cause of downer sows, is difficult to diagnose antemortem because the hip is buried under a large muscle mass. Even infectious arthritis in the stifle, a site commonly affected by Mycoplasma hyosynoviae, can be missed in individual pigs on cursory examination.

The torso can be evaluated and palpated for muscle mass, tone, and symmetry; ribs should be examined for evidence of fractures or knobby thickening (rachitic rosary). The spine can be palpated and examined for kyphosis.

Some of the more common diseases affecting bones, joints, and muscle are described in the tables and .

Table
Table

A neurological examination is indicated in cases when neurological disease is suspected. The examination should be performed in a similar fashion to that for dogs, cows, and horses (see Physical and Neurologic Examinations The Neurologic Examination of Animals The neurologic examination begins the moment the veterinarian first sees the patient. (See a sample neurologic examination form.) If possible, the patient should be observed moving freely in... read more The Neurologic Examination of Animals ).

Necropsy and Sample Collection

Postmortem examination of lame pigs is often required to achieve confidence in the diagnosis of a herd lameness problem. Field necropsies of baby, nursery, and grower pigs are relatively easy. However, for larger finishing pigs, gilts, sows, and boars, the process is laborious because of the size of the animal and the need to examine numerous joints and bones, including the spine.

Examination of greater numbers of pigs improves the odds of accurately characterizing the causes of lameness. Opening the joints even on dead pigs that may not be ideal candidates for diagnostic sampling is good practice; it can help direct diagnostic efforts when more suitable pigs are available.

With a complete history, careful clinical assessments, and detection of gross lesions, one or more case definitions should emerge. Case definitions then drive the formulation and prioritization of differential diagnoses—the agents and risk factors that are possibly causative and suspected as either primary or secondary.

Diagnostic confirmation usually requires some laboratory testing, including agent detection with compatible microscopic lesions.

Ideally, samples for laboratory testing from on-farm necropsies in the field are collected from three acutely affected, nonmedicated, euthanized pigs with characteristic clinical signs that meet the case definitions. Samples should be packaged and identified individually for each pig. Proactive communication with a diagnostic laboratory to determine the appropriate range and types of samples for laboratory testing is prudent.

Another option is to submit freshly euthanized or live, nonmedicated, acutely affected pigs to a full-service diagnostic laboratory. This approach can improve diagnostic accuracy, particularly when multiple agents are involved or differential diagnosis is complex. This approach also increases the odds of successfully isolating offending bacteria, which are needed for antimicrobial susceptibility testing or the production of autogenous vaccines.

Diagnostic laboratories have the facilities and personnel to perform more complete and careful dissections of the joints, spine, and brain of pigs of any age. These submissions should be accompanied by clear communication of an accurate history and a list of differential diagnoses to ensure proper sampling, testing, and interpretation of results.

Steps for field necropsy and sampling of lame pigs include the following:

  • Collect serum and whole blood on ice.

  • Examine joints (eg, carpi, elbows, shoulders, hocks, stifles, coxofemoral, intervertebral):

    • Clean the area or remove skin before attempting synovial fluid collection with syringe and needle. Alternatively, open the joint with clean instruments and collect synovial fluid and/or a swab of any suspicious exudates (see ).

    • Collect synovium and abnormal connective tissue, chilled and in formalin. In smaller pigs, it is often easier to wash or remove skin and submit the intact joint on ice.

  • If brain or spinal cord involvement is suspected, do the following:

    • Collect CSF with syringe and needle, using a dorsal approach from a clean or skinned site. Alternatively, remove the tongue and pharyngeal viscera to expose the atlanto-occipital joint, and collect CSF using a ventral approach.

    • Disarticulate the head; carefully swab meningeswhile the atlanto-occipital joint is being opened.

    • Remove the brain with a saw or hatchet; collect intact cerebrum, cerebellum, and brainstem, half in formalin and half chilled.

    • Alternatively, rapidly chill the head for submission intact.

  • Open thoracic and abdominal cavities to expose the internal organs:

    • Collect fibrin from serosal surfaces with swabs if present.

    • Collect fresh sections of spleen, lymph nodes, heart, kidneys, and/or lungs if gross lesions are apparent or if relevant to testing for agents included in differential diagnosis.

    • Fresh tissues should be ≥ 2- to 3-cm cubes on ice; also collect 1-cm formalin-fixed slices for histological examination.

    • Collect fresh liver, which is useful if analytical chemistry becomes necessary.

  • Examine and collect bones as they become available:

    • Ribs in healthy pigs > 5–6 weeks of age should not bend before breaking with a snap. Collect two or three intact ribs if metabolic bone disease is suspected.

    • Submit fractures and bones with suspected osteomyelitis, deformities, calluses, or swollen growth plates intact and chilled.

    • Examine all opened joints for any abnormal articular surfaces. Submit any affected joints or bones or suspected lesions chilled.

    • Base the selection of bones for density and ash analysis on the recommendation of the testing laboratory.

  • Collect muscle samples if muscular involvement is suspected:

    • Preferred samples are fresh and fixed sections of any gross lesions and/or diaphragm, semimembranosus muscle, longissimus muscle, and heart.

  • Collect spinal cord if there are CNS signs and/or bilateral involvement with paresis or paralysis suspected:

    • Examine muscle and connective tissues for gross lesions as they are being removed from the vertebral column.

    • Remove the spinal cord using a saw, hatchet, or Barnes dehorning device.

    • Collect portions of cord from the cervical, thoracic, and lumbar areas in 5-cm sections in formalin, and chill the remainder.

    • Alternatively, submit the entire vertebral column or portions (two or three vertebrae from each of the cervical, thoracic, and lumbar areas) chilled.

  • Collect and retain additional samples from the farm that may become relevant (eg, feed, water, ration components, vitamin or mineral premix).

Evaluation of lameness problems at slaughter plants is not usually productive, because processing lines run too fast to evaluate all the elements of the musculoskeletal system and not all joints can be thoroughly examined. Condemned carcasses or euthanized “slow or down” pigs can sometimes be made available for examination. Some abattoirs are willing to cooperate on specific projects to retrieve lower limbs for investigative purposes, if asked.

Diagnostic Testing

Samples collected antemortem for laboratory testing can be useful but are limited in scope.

  • Vesicles on coronary bands or the snout should always be pursued using regulatory protocols. Aspirates or swabs of vesicles can be collected concurrently for detection of other viruses.

  • Synovial fluid and needle aspirates from fluctuant masses can be collected for microbial detection and cytology.

  • Serum, whole blood, feed, and water may be useful for clinical pathology, detection of certain agents of relevance, or analytical chemistry.

Molecular diagnostic tests such as PCR are both highly sensitive and highly specific. Therefore, many of the common, potentially pathogenic endemic agents (and some vaccines) are easily detected, yet some variants may be missed.

Distinguishing between the presence of a benign endemic agent and a pathogenic variant of that agent requires the presence of compatible gross and microscopic lesions, along with typical clinical signs. Histological examination also can implicate agents that are not detected in a particular sample or were not sought by testing.

Confirming the presence of and causative role for an agent offers a more precise understanding of exposure and transmission with which to develop more effective control strategies for specific agents.

Bacterial culture is necessary for antimicrobial sensitivity testing and autogenous bacterin production.

Analytical chemistry of bone (eg, density, ash, calcium, phosphorus) is often not diagnostic for cause; however, it can offer support of clinical or pathological observations in cases of suspected metabolic bone disease.

Feed analysis should be interpreted with care because of variations between sources of samples, batches, mixing, and delivery to feeders. The feed currently present may not represent feed from batches over the prior weeks or months. Some feed mills and farms routinely retain feed samples from each batch for this reason.

It is important to collect and retain all relevant samples during the initial herd investigation to ensure that proper samples are available in case additional testing becomes necessary.

The final herd diagnosis is the purview of the attending veterinarian, who has access to and direct knowledge of all available qualitative and quantitative information, including history, clinical signs, gross lesions, case definitions, and laboratory results. An accurate diagnosis and identification of any contributing risk factors drives the success of intervention strategies.

Environment and Management of Lameness in Pigs

The environmental management of pigs is central to potential lameness problems, and includes housing, facility maintenance, cleanliness, and stocking or grouping practices. Flooring type is a major determinant of lameness in pigs, and all types have forms of lameness associated with them:

  • Dirt and pasture lots can range from too dry to too wet, leading to vertical hoof wall cracks or foot infections, or they can serve as a source of bacteria that cause infectious arthritis, such as Erysipelothrix rhusiopathiae in straw bedding.

  • Solid, partially slatted, and fully slatted floors also have relative advantages and disadvantages in terms of associated lameness conditions.

In addition to the type of flooring, its state of repair can have a considerable effect on lameness. Holes, gaps, and sharp edges on concrete floors can traumatize the feet and lower legs. The flooring surface may be not abrasive enough, making floors slippery and leading to injuries, or it may be too abrasive, wearing down the claws and promoting heel overgrowth.

Cleanliness and moisture are additional factors to evaluate. Buildup of feces in bedded areas can lead to foot infections, and excess moisture from misting cooling systems can lead to softening of the claws, hoof wall cracks, and excess wear.

Interactions among the pigs are also important factors to evaluate. The sourcing and mixing of discrete pig populations can influence whether infectious diseases are maintained as endemic within the population or become epidemic outbreaks; pigs may become susceptible over time as maternal immunity wanes and they are exposed by commingling with externally sourced pigs.

Stocking density and space for animals to exhibit social behaviors can influence the amount of aggressive social behavior within groups of pigs. The distance that pigs have to walk to access feed and water, as well as the conditions of that space, can affect wear on the feet and trauma to joints.

Group size and stability also have an impact on the development of lameness:

  • Sows housed in individual stalls are restricted in terms of movement; however, they tend to develop fewer lameness problems than do confined group-housed sows.

  • Pigs kept in very large groups have fewer aggressive interactions than do pigs housed in small groups.

  • Sorting growing pigs to allow for more variation in size within pens can decrease the time required for social structures to become established at weaning or regrouping times.

Nutrition of Lameness in Pigs

Skeletal development in pigs may be affected by relatively short-term nutritional deficiencies, especially considering expectations for rapid growth and muscle development in modern hybrid pigs. Problems early in the production cycle may be reflected as abnormal bone growth in nursery or growing pigs. Recurrent deficiencies or those that occur later in the finishing phase may result in weak bones in slaughter pigs or replacement breeding stock.

During the growing phase of pigs, the goal of the nutritional program should be to ensure the development of a strong skeleton so that the incidence of spontaneous bone fractures in the finishing barn or during the slaughter process is low, thus preventing large numbers of culls or condemnations of carcasses.

Fractures of the femur, humerus, ribs, or vertebrae of pigs may be induced by strong muscle contractions during the slaughter process, and may occasionally occur as postmortem artifacts. However, the detection of multiple or frequent fractures in a herd should raise suspicions of metabolic bone disease. Clinical signs of hypocalcemia can develop before pigs are slaughtered and can include lameness, spiral fracture of the femur, leg weakness and posterior paresis, recumbency and paddling, and even sudden death.

In breeding pigs especially, foot lesions can cause lameness. Excessive water hardness or high concentrations of iron or heavy metals in water can antagonize trace mineral absorption, leading to foot lesion development. Diets should be carefully balanced for macronutrients and trace minerals, as well as for key vitamins, such as vitamin D and biotin.

Common Bacterial Causes of Lameness in Pigs

A variety of bacteria can cause or contribute to lameness in pigs of all ages (see the table ). Several of the more common agents associated with lameness outbreaks are discussed below.

There is considerable variation between and within the genera and species of bacteria that colonize pigs, the virulence of pathogens that infect pigs, the expression of protective epitopes important for immunity, and the efficacy of maternal immunity or active immunity from either colonization or vaccination. This nuanced complexity is magnified when multiple risk factors and coinfections are present, as is common in population medicine.

Table

Streptococcus suis

Streptococcal infections are a major concern to the pig industry in the US, particularly disease caused by Streptococcus suis, which is also zoonotic. S suis is resident in the nasopharynx, is an opportunist in pneumonia, and is a frequent cause of sepsis. With sepsis, S suis causes not only arthritis but also severe outbreaks of suppurative meningitis Meningitis, Encephalitis, and Encephalomyelitis in Animals Meningitis, encephalitis, and encephalomyelitis are terms used to describe inflammatory conditions of the meninges, brain, or brain and spinal cord, respectively. These inflammatory processes... read more Meningitis, Encephalitis, and Encephalomyelitis in Animals and polyserositis. The predominant lesion in joints is fibrinopurulent synovitis (see ). Outbreaks can occur in suckling piglets or finishing pigs; however, they are much more common and severe in the postweaning and nursery phases.

Diagnosis of streptococcal infection is based on bacterial isolation and, importantly, histological evaluation of the affected tissues (eg, synovium, brain, spinal cord, serosal surfaces) because S suis is quite diverse in virulence and is a common contaminant.

Treatment of streptococcal infection relies on early, aggressive administration of antimicrobials based on antimicrobial sensitivity data.

The approach to preventing and controlling streptococcal infection is comprehensive. It includes but is not limited to controlling primary viral infections, paying attention to commingling of sources, ensuring proper nutrition, and establishing herd immunity in sow herds through proper acclimation of gilts.

In some pigs, marginal or deficient amounts of micronutrients (eg, vitamins A, D, and E, as well as some trace minerals) may be risk factors for increased susceptibility to streptococcal disease expression.

S suis shows considerable intraspecies antigen and virulence diversity. For this reason, strategic vaccination with autogenous products is often attempted, with the goal of providing more targeted, specific immunity; however, the efficacy varies considerably. Other streptococci (eg, S porcinus, S dysgalactiae equisimilis, S equi zooepidemicus, and others) are often opportunists in joint infections and can induce pyogenic lesions throughout the body as well. S equi zooepidemicus can cause severe outbreaks of sepsis, with high mortality.

Glaesserella parasuis

Glaesserella parasuis causes clinical signs and lesions very similar to those resulting from infection by S suis. These signs can be quite severe in naive populations. Disease expression is a threat throughout the postweaning and growing-finishing stages, occasionally occurring in young adults or commingled breeding stock.

There is considerable antigenic diversity within and between G parasuis serotypes. Therefore, this agent causes particularly severe disease when populations from different sources are commingled or with new introductions of breeding stock. Outbreaks are exacerbated by environmental stresses and viral coinfections.

Like S suis, G parasuis is an endemic agent in most swine herds, and the same general comments about diagnosis, treatment, and control noted above for S suis apply to G parasuis as well.

G parasuis is fastidious and sometimes difficult to isolate from field samples; therefore, PCR assay is frequently relied on for detection and is coupled with histological examination of typical lesions to confirm a causative role.

Vaccines are commercially available; however, the diversity of G parasuis strains often requires the use of autogenous products for improved efficacy.

Mycoplasma hyorhinis

Mycoplasma hyorhinis is a very common endemic agent of infection in swine and may be clinically silent within herds. Disease is most often expressed during the periweaning phase and nursery period.

The predominant clinical sign of infection by M hyorhinis is lameness or ill thrift, with gross lesions of polyserositis and fibrinous arthritis prominent; meningitis is uncommon with this agent.

Some pigs are colonized by M hyorhinis from their dams in the suckling phase, and lateral transmission can also occur as maternal immunity wanes.

Disruption of herd immunity with modern production practices, including elimination strategies for Mycoplasma hyopneumoniae, may contribute to increases in disease expression. In addition, risk factors are likely similar to those noted above for S suis and G parasuis.

M hyorhinis can be detected from lesions by PCR assay or culture, with diagnosis confirmed by compatible histological findings.

Because Mycoplasma spp lack a cell wall, treatment requires antimicrobials that are appropriate for mycoplasmas (eg, tylosin, lincomycin, tetracyclines) and is based on current or historical antimicrobial sensitivity data.

Commercial and autogenous vaccines against M hyorhinis are available and of benefit in some cases. As with infections by other endemic bacteria discussed in this section, the control of viral coinfections and attention to details of nutrition, environment, and management are important in the prevention of clinical disease.

Actinobacillus suis

Actinobacillus suis is the fourth relatively common bacterium that can cause polyserositis, sepsis, and joint infections, as well as pneumonia. Disease tends to be less common and more acute, and it often occurs as a sporadic individual pig disease or in small outbreaks associated with other stresses or viral coinfections (again, similar to those mentioned for other agents of polyserositis).

Early recognition and aggressive antimicrobial treatment can be effective against A suis. Seeking and controlling risk factors is the first priority for control and prevention of infection. When cases are ongoing, autogenous vaccines may have value.

Pasteurella multocida is infrequently reported to cause signs and lesions similar to those caused by A suis. Actinobacillus pleuropneumonia causes sudden deaths, pneumonia, and fibrinous pleuritis; however, it is not commonly associated with arthritis or joint lameness.

Mycoplasma hyosynoviae

Mycoplasma hyosynoviae is a common and usually endemic commensal in most swine herds.

Infected dams can occasionally infect offspring, which then serve as a source for lateral transmission to cohorts in growing and finishing stages. Maternal immunity probably keeps transmission low until weaning, with gradual transmission among cohorts and disease expression most commonly occurring in pigs 12–26 weeks old.

M hyosynoviae commonly colonizes the nasopharynx, and stress or waning immunity allows transient bacteremia and sometimes localization of the organism in the synovium.

Generally, morbidity associated with M hyosynoviae infection is low to moderate; however, morbidity can exceed 50% when naive groups of pigs are exposed. The mortality rate due to infection is very low; however, lame pigs fall behind and/or develop secondary infections, leading to market losses or culling.

Clinically, acute lameness due to M hyosynoviae infection lasts about 10 days in susceptible pigs or breeding stock. Clinical expression of arthritis is exacerbated by trauma, transport, or other common stresses and risk factors. Affected pigs are afebrile, with pain in major joints (eg, elbows, stifles, hocks) and soft, fluctuant swelling of joints.

On necropsy, M hyosynoviae lesions are restricted to the joints, especially the stifles, and include an excess of clear, yellow synovial fluid that may contain fibrin flakes. Polyserositis and pneumonia are not features of this disease. The synovium may be thickened by obvious villous hypertrophy. Articular surfaces and periarticular tissues usually are unaffected.

As an endemic opportunist, M hyosynoviae may be detected concurrently with other joint insults, including trauma or osteochondrosis, in a seemingly additive effect.

Definitive diagnosis is based on the PCR detection of M hyosynoviae on the synovium and/or in synovial fluid collected from acutely affected pigs, accompanied by histological examination of the synovium to confirm compatible lesions.

Vaccines against M hyosynoviae are not generally available.

Erysipelothrix rhusiopathiae

Erysipelothrix rhusiopathiae infection, or erysipelas, can occur in pigs at all ages. However, outbreaks are most common in growing-finishing pigs. Clinical signs and disease severity are directly related to the amount of passive or active immunity present in individual pigs.

Acute erysipelas in suckling piglets and young nursery pigs usually occurs when sows lack immunity or when passive transfer of immunity fails—ie, when herd immunization practices are deficient.

Erysipelas usually manifests as acute sepsis, with fever, cyanosis of extremities, and rapid progression to death. Necropsy may reveal splenomegaly or focal hemorrhages in kidneys or lymph nodes, but little else of diagnostic importance. Bacterial isolation or PCR assay of the spleen, synovium, or other tissue confirms diagnosis.

In the nursery phase, acute erysipelas has a presentation similar to that in suckling piglets, with sepsis, fever, cyanosis, the aforementioned acute gross lesions, and often excess synovial fluid. Diamond skin lesions and arthritis are less common at this age than in older animals. Infections can be subclinical but later manifest as valvular endocarditis or chronic proliferative arthritis.

Most clinical outbreaks of erysipelas occur in the growing-finishing period, and these outbreaks are most likely to show the typical clinical signs of acute disease. Clinical signs include sudden death, fever, lethargy, recumbency, vocalization, and pain when prodded to move, as well as, usually, swelling of joints, which contain abundant, less viscous synovial fluid.

Subacute erysipelas infections (2–3 days) may develop rhomboid (diamond-shaped) skin lesions (urticaria); affected skin may later slough in severe cases. If there is no intervention, chronically affected pigs can develop swollen, firm stifles or hocks as a result of proliferative arthritis with villous hypertrophy and fibrosis of the synovia, accompanied by a painful gait. Less frequently, valvular endocarditis or diskospondylitis can occur; the latter is important in boars and sows and can interfere with breeding.

Erysipelas in late finishing and sow herds can, but often does not, demonstrate typical acute clinical signs. Acute infections may be subclinical and thus go unnoticed until characteristic rhomboid skin lesions are observed, either by caretakers or by slaughter inspectors. Although pigs appear otherwise healthy, the typical skin lesions result in carcass condemnations.

Confirmation of E rhusiopathiae infection is challenging in many subacute to chronic cases; however, nearly all cases will be confirmed as erysipelas if vigorously pursued. Rarely, rhomboid urticarial lesions have been reported infrequently with infections by other bacteria, such as A suis.

Isolation of the causative organism is important for a definitive diagnosis of erysipelas, and it is most successful when samples are collected during the acute phase of disease. Untreated pigs are necropsied, and joint fluid, synovium, and spleen are cultured. PCR testing of subacute or chronic lesions can sometimes be used to confirm the presence of the bacteria in chronic cases.

E rhusiopathiae and other Erysipelothrix spp can reside subclinically in tonsils. Therefore, detection of the organism by PCR assay of samples from mucosal surfaces, tonsils, or the environment does not confirm disease.

Timely treatment of acute cases of erysipelas with penicillin, with or without erysipelas antisera, can be remarkably effective; rapid response to injection is a diagnostic aid. Concurrent administration of killed vaccine is also warranted in outbreaks. Other antimicrobials are also useful; treatment selection should be based on isolation antimicrobial susceptibility testing.

Proper vaccination with either modified live or killed organisms effectively controls erysipelas in most pig herds. Outbreaks are often related to noncompliance or inadequate vaccination protocols rather than to changes in virulence of the causative organism or in the nature of the disease. Therefore, any investigation of the problem should begin with a detailed history to ensure that sows are regularly vaccinated.

Sow vaccination often is not sufficient to prevent disease in growing-finishing pigs in endemic herds or herds known to be at risk. Therefore, vaccination during the nursery-grower phase is often warranted.

Viral Agents Affecting Locomotion in Pigs

Many viral agents either directly or indirectly contribute to lameness outbreaks in pigs of all ages. In particular, vesicular viral diseases can cause lameness in breeding and growing swine. Foot-and-mouth disease Foot-and-Mouth Disease in Animals Foot-and-mouth disease is one of the world's most economically important viral diseases of livestock. The virus infects cattle, pigs, and sheep and many cloven-hoofed wildlife species. The infection... read more Foot-and-Mouth Disease in Animals , Seneca Valley virus disease Seneca Valley Virus Disease in Pigs Seneca Valley virus disease is a viral vesicular disease of pigs caused by a picornavirus related to the viruses that cause foot-and-mouth disease and swine vesicular disease. Clinically affected... read more , swine vesicular disease Swine Vesicular Disease Swine vesicular disease is a viral vesicular disease of pigs caused by an enterovirus closely related to human coxsackie virus B5. It is generally a mild disease that was endemic in Italy until... read more , vesicular stomatitis Vesicular Stomatitis in Large Animals Vesicular stomatitis is a viral disease of primarily horses and cattle, transmitted mainly by biting flies and midges. The disease results in characteristic vesicular lesions that can occur... read more Vesicular Stomatitis in Large Animals , and vesicular exanthema Vesicular Exanthema of Swine Vesicular exanthema of swine (VES) is an acute, highly infectious disease characterized by fever and formation of vesicles on the snout, oral mucosa, soles of the feet, coronary bands, and between... read more all fit this clinical picture. The concern over foot-and-mouth disease means that any episode of vesicular disease in pigs warrants a complete diagnostic investigation involving regulatory personnel.

The prevalence and severity of clinical signs vary among the viruses that affect pig locomotion.

Table

Several different types of viruses, historically referred to as enteroviruses, can directly affect ambulation in pigs by infecting the spinal cord or brainstem, particularly in naive herds. Depending on the location of the lesions, clinical signs range from bilateral hind limb or forelimb weakness to posterior paresis, paralysis, or ataxia. Most affected pigs are afebrile and remain centrally aware. Several of these enteroviruses are now categorized in the genera Sapelovirus or Teschovirus.

Diagnosis requires submission of spinal cord and brainstem for histological examination and virus detection.

Licensed vaccines against viral agents that cause lameness in pigs are not available; efficacy data for autogenous products are lacking. Usually, clinical signs associated with these viruses diminish with the onset of herd immunity. As with other endemic agents, proper gilt acclimation and avoidance of commingling are often recommended.

Therapeutic Considerations in Lameness in Pigs

Production practices and conditions for growing pigs are constantly changing. In some areas, pig farming is becoming more intensive; in other areas, more extensive. These changes can alter the epidemiology of diseases, posing both a challenge and an opportunity to intervene more effectively to decrease lameness through biosecurity practices, as well as improved management, environment, and nutrition.

The regulatory landscape for the use of products to treat or prevent lameness in pigs is a major consideration. This is true not only for federal regulations regarding the use of antimicrobials and analgesics, but also for various restrictions in place from commercial marketing programs or contracts. Thus, the type, dose, form, and use of any product should be carefully considered in light of pertinent regulations for the jurisdictions in which the pigs are being raised and marketed. The use of any drugs in pigs must adhere to withdrawal times recommended by the manufacturer or required by regulation.

Pigs with acute infectious bacterial disease typically require timely, aggressive parenteral therapy with an effective antimicrobial. The initial treatment selection is usually based on a tentative diagnosis and the clinician’s experience, until necropsy results, diagnostic testing results, and antimicrobial sensitivity profiles become available.

Antimicrobials should be injected in the neck behind the ear in all age categories, with the caveat that injections too close to cervical vertebrae, particularly in young pigs, can cause spinal cord damage. Medication administered in water or feed may be appropriate for prevention, ongoing control, or treatment in early stages of a disease outbreak.

Beyond targeted antimicrobial treatment or immunization, supportive treatment has a role in the management of lameness in pigs. Examples include moving lame pigs out of a competitive pen to a recovery pen, or providing analgesia. Injectable anti-inflammatory agents to relieve pain in pigs with lameness can be useful and beneficial.

  • Flunixin meglumine is available for use in pigs as supportive care for fever in outbreaks of swine respiratory disease; anti-inflammatory and analgesic qualities of the drug can help relieve pain in a swollen joint or bruised muscle (extra-label).

  • Dexamethasone has benefit for some conditions in which infectious agents do not play a role.

  • Isoflupredone acetate is approved for musculoskeletal pain that causes lameness in pigs.

  • Meloxicam has proved useful to alleviate painful, noninfectious lameness in pigs where approved.

  • Acetylsalicylic acid and sodium salicylate may be a useful adjunct therapy as a water treatment.

Vaccination is a useful intervention for a few of the common infectious agents contributing to lameness in pigs; however, the availability and efficacy of licensed products vary considerably.

Licensed vaccines are generally unavailable for many of the bacterial agents associated with lameness in pigs. Therefore, autogenous vaccines or bacterins are frequently prepared in attempts to stimulate some amount of immunity.

Autogenous vaccines are prepared from farm-specific isolates acquired from clinically affected pigs with typical lameness lesions. The perceived benefit is that farm-specific isolates better represent variation in “strains” (eg, biotypes, genotypes, serotypes, or antigenic configurations) for the particular infectious agent involved, and thus they are better able to augment specific immune responses. Such products are generally regarded as safe; however, efficacy data are not a requirement for manufacture.

The manufacture of autogenous products is allowed for only a limited period with each isolate; therefore, regular monitoring for causative organisms and variants is important for both vaccine renewal and possible changes in antimicrobial sensitivities.

S suis, A suis, G parasuis, and M hyorhinis are examples of organisms against which autogenous products may be useful. Newer antigen selection and delivery technologies have enabled the expansion of autogenous products to include other bacteria, as well as some viruses.

Key Points

  • Lameness in pigs can result from a variety of infectious, nutritional, or environmental causes.

  • A comprehensive analysis of the history, implementation of nutritional and vaccination strategies, examination of affected and unaffected animals, and diagnostic sampling are all required components of lameness evaluation in pigs.

  • Differentiating which pathogens are causing lameness can be challenging because many organisms may also be endemic in swine production.

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