Gpvec.unl.edu
TERMINOLOGY
The following is a list of terms dealing with livestock that seem to confuse students that do not have a strong farm background. Please note that some of these definitions will vary depending the facilities and type of management.
Suckler: A pig that is still nursing. Age range depends upon age at weaning in a given management system.
Weaner: A pig that has recently been weaned.
Nursery
pig: A pig that has been weaned but has not reached the grower stage. These pigs may weigh 15 to 70 pounds or so depending on the type of facilities. Pigs in a one stage type of facility will be fed to around 70 pounds. Pigs in a two stage facility will be moved out of the nursery weighing about 40 pounds and placed in a grower unit.
Feeder
pig: A pig that is destined to be fed out and slaughtered. The term usually refers to a young pig that has been weaned but has not entered the finishing stage. Feeder pigs are often thought of as being about 40 pounds or so. This can vary.
Grower: A pig that is in the 40 to 170 pound range or so (see definition of nursery pig).
Finisher: A pig that is in the final stage of feeding prior to marketing.
Fat hog: Also called market hog. One that is ready for slaughter. Most slaughter hogs in this country weigh about 225 to 280 pounds. Individual meat packers have different ideal weights.
Gilt: A female pig. If the gilt is retained in the herd for breeding purposes, she is referred to as a gilt until after she farrows and some refer to her as a gilt until after her first litter is weaned. Then she becomes a sow.
Barrow: A castrated male pig. Essentially all male pigs not used for breeding purposes are castrated.
Carcass basis (grade and yield). Slaughter hogs can be sold on the basis of how good the carcass grades and how much it weighs immediately following slaughter (hot weights). The hogs are killed and eviscerated, the head, feet, tail, hair, etc. removed, and the carcass graded on the basis of the amount of backfat, the size of the loin eye, etc. The farmer is paid a premium for higher quality hogs that yield a higher percentage of quality cuts of meat and less fat. Cattle are often sold on carcass basis also.
Live-weight basis. This is the opposite of the carcass basis. The slaughter hogs are weighed at the point of sale and the farmer is paid a certain amount per pound of live weight.
METHODS FOR ELIMINATION OF INFECTIOUS AGENTS FROM SWINE HERDS
CONVENTIONAL SWINE FACILITIES
These have traditionally been relatively small units on individual farms. The farmer maintains a herd of 50 to several hundred sows and takes care of all their needs himself with the help of hired labor or family members. The adult breeding swine are maintained on the farm, usually in separate facilities from the pigs that are in the nursery or in the grower-finisher facilities. Piglets are weaned at or after 3 weeks of age. Diseases that are present in the sow herd are often transmitted to the piglets as the level of colostral immunity wanes. Also, personnel moving between the units may bring in new diseases. In farrow-to-finish operations, all the functions take place in one building. If infectious agents get into the piglets at or shortly after weaning, serious disease problems can occur because this is often the time of maximum stress and lowest levels of immunity.
CONTINUOUS THRU-PUT
This type of operation may put pigs into barns where the pigs are continually added to existing grower-finisher swine. The slowest growing pigs are often the ones left behind and these are the ones that remain when new pigs are added to the unit. They are also the most likely to have infectious diseases.
ALL-IN-ALL-OUT
Eliminates the exposure of susceptible pigs to potential disease carriers from other age groups.
SPECIFIC PATHOGEN FREE SWINE
Caesarian derived
Maintained separate from all other swine
Used for:
1. Establishment of disease-free breeding stock
2. Preservation of valuable bloodlines that were infected with pathogens that could not be eliminated by other means.
Limitations:
1. Very labor intensive and expensive.
Pigs this young are difficult to rear and there tended to be a high mortality.
2. What happened when SPF pigs were exposed to disease agents?
3. What happened when the SPF pigs were not really SPF (ie. had pathogens that were not detected) and were then introduced into herds?
MEDICATED EARLY WEANING (MEW), MODIFIED MEW and SEGREGATED EARLY WEANING (SEW)
1. Initial programs (1980) used high doses of tiamulin and trimethoprim-sulfa to medicate the sows from the time of their entry into farrowing units until the piglets were weaned. The piglets also received the same antimicrobials for 10 days following birth. The best doing piglets were weaned at 5 days and maintained in isolated units to prevent transmission of diseases from the source herds. This regimen was used to eliminate mycoplasmal pneumonia and Bordetella bronchiseptica. They were also trying to eliminate Serpulina hyodysenteriae but were apparently unsuccessful.
2. Other antimicrobials were later tried in attempts to eliminate other infectious diseases. The main drawbacks of the system were the high mortality in the pigs weaned at 5 days and the labor involved.
3. Vaccination of the sows to maximize their level of immunity to some of the diseases was instituted. This had the effect of increasing the level of immunity in the piglets and allowing the weaning dates to be delayed somewhat. Piglet mortality decreased as the age at weaning was increased. Pigs weaned early have higher levels of maternal antibody remaining. They can be mixed with other pigs while their level of immunity is higher and there should be lower levels of disease if any of the groups of pigs should be harboring an infectious agent.
The breeding, farrowing and maintenance of the sow herd takes place at one site. The piglets are then weaned at 10 to 21 days of age and removed to an isolated farm where they are reared. When the pigs weigh between 45 and 75 lb, they may be moved to another isolated facility for growing and possibly still another unit for finishing. Basically, the pigs are handled much the same as in the medicated early weaning. Specific diseases present in the breeding herd may be targeted for elimination. This allows for specific vaccination schemes and the utilization of specific antimicrobials if necessary. Once the diseases are eliminated from the breeders, the use of the antimicrobials and extensive vaccination programs can be eliminated.
Note on Immunoglobulin levels
Normal adult sow serum immunoglobulin levels are 22 mg/ml (range 18 to 27 or so depending on the study quoted).
Sow immunoglobulin levels at parturition are approximately 14 to 18 mg/ml. Note that the sow is apparently putting her immunoglobulin synthesis efforts into the colostrum.
Pig immunoglobulin levels at 2 days of age: Approximately 16 to 27mg/ml or roughly equal to a normal adult sow. A crude approximation in well-managed pigs that receive higher levels of colostrum puts it at roughly double the level of the sow at parturition.
By 2 weeks of age, the well managed pig will have immunoglobulin levels roughly equal to the sow(s levels at parturition. However, the levels at parturition are only half the normal adult sow immunoglobulin levels. The pig is undoubtably beginning to synthesize its own immunoglobulins at this time in response to exposure to infectious agents.
By 4 weeks of age, the well-managed pig will also have immunoglobulin levels roughly equal to the levels seen in sows at parturition (11 to 13 mg/ml).
Table 1. Diseases that can be theoretically eliminated using a multiple site isolated rearing system.
| | | | | |
|Agent |Breeders and sucklers |Wean Age |Weaners (to 75 lb or so) |Finishers |
| | | | | |
|Pasteurella multocida (toxigenic) |Vaccinate sows |10-15 days |All-in, All-out by site or unit |AIAO by site or unit |
| | | | | |
|Mycoplasma hyopneumoniae |Vaccinate sows |10-19 days |AIAO by site or unit |AIAO by site or unit |
| | | | | |
|Actinobacillus pleuro- pneumoniae |Vaccinate sows |21 d |AIAO by site |AIAO by site |
| | | | | |
|Pseudorabies |Vaccinate sows |21 d |AIAO |AIAO |
| | | | | |
|Transmissible gastro- enteritis |Virus exposure to whole unit |21 d |AIAO by site |AIAO by site |
| | | | | |
|Brachyspira hyodysenteriae |Medicate sows to eradicate or |21 d |Medicate, AIAO, extensive disinfection |Essentially the same as for |
| |depopulate, Sanitation | |and sanitation, Depopulate |weaners. |
If a two or three site system is used there is a continuous supply of pigs coming into the weaner and finisher units. If disease outbreaks occur, one can stop the outbreak by interrupting the flow of susceptible pigs coming into a unit. This would essentially mean a total depopulation. The advantage of a multiple site system over a two or three site system is that at the weaner and finisher stage, all-in-all-out management can be substituted for the depopulation. The flow of pigs from the farrowing unit is not interrupted and a specific weaner or finishing unit can be closed down temporarily for cleanup while piglets go to other units. In both types of units however, the piglets could be sold to allow time for cleanup. The most common type of system in use today is actually a two-site system. The main problem with any high-health status herd is biosecurity. Maintaining biosecurity can be difficult and even those individuals that claim to be very careful, can have breakdowns.
What are some potential sources for breaks in biosecurity?
Potential for elimination of other disease agents using segregated early weaning strategies.
Streptococcus suis. Some studies have found that a relatively high percentage of SEW pigs carry this organism although the incidence of clinical disease may be low. One study used penicillin in an MEW program and had relatively good results. However, S. suis infections remain an important problem in "high health status" herds. The main problem with elimination of this disease is the fact that it is carried in the vagina of some sows and is transmitted to piglets at birth. Generally it is not considered a disease that can be eliminated from high health status herds and is usually considered to be even more troublesome than in (conventional( herds.
Haemophilus parasuis. Also, generally it is not considered a disease that can be eliminated from high health status herds. Weaning by 10 days of age has been successful in a few cases in elimination of this organism in SEW pigs. One study indicated that to "reliably" eliminate this organism, one has to vaccinate the sow and maintain the pigs on one or more antibiotics. Again, however, it has been very difficult if not impossible to eliminate this organism. When disease breaks occur in highly susceptible populations, the economic loss can be high.
Influenza virus. Good success following a vaccination program in the sows. However, this disease remains a problem in many swine units in part because it can apparently get back into such units fairly easily.
PRRS. Current thinking is that PRRS can be eliminated by SEW if the sow herd is not undergoing an active infection in the period between the last trimester and weaning. This is difficult or impossible in large herds. Pigs were weaned at 10, 15, and 20 days in one study and all remained serologically negative. Keeping the herd negative is a problem. More recent work indicates that the virus can be kept out of pigs with strict sanitation measures and a relatively minor barrier between infected and non-infected groups.
PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS (PRRS)
General Description
The disease caused by this virus was first described in the U.S. in 1987. It subsequently spread very rapidly and by the early 1990's had become a major problem in swine. Initial descriptions dealt mainly with the reproductive system problems but currently the disease most often affects the respiratory system of nursery age pigs. In addition, other disease problems are often exacerbated by the presence of this virus.
Etiology
Arterivirus. There are two major variants, the European or Lelystad strains and the American strains. There is a large amount of genetic variation within the two major variants so that there is a lot of antigenic variation and variation in virulence. In addition, this has possibly given rise to differences in published research results.
Epidemiology and Transmission
Virus is carried in the lymphoid tissues and is present in the oropharynx, milk, feces, semen, urine and other tissues. Once excreted, the virus is not particularly resistant and will die out within a day unless present in a moist environment. It has been recovered for up to 11 days in water. It is readily inactivated by disinfectants.
Persistence in the host is a major factor in epidemiology and transmission. The virus has been recovered from sows for 157 days following infection and is present probably equally as long in boars. Virus has been recovered from pigs infected in-utero for up to 210 days following farrowing. However, it is essential to note that the virus may not be shed from these animals in the later stages of recovery. The virus may be shed for several days or weeks during the active infection stage, but it may also be shed only intermittently during this time. The disease may transmit rapidly through a group of pigs or progress slowly. Up to a 37-day lag time has been reported between introduction of the virus and development of clinical disease. Herds may remain infected as long as new susceptible pigs are constantly being introduced to infected animals. It is believed that the virus remains in the herd at least 6 months following cessation of clinical signs. This is probably quite variable and may be dependent on the size of the swine unit in question.
The major mode of transmission is via direct contact from pig to pig. About 60% of outbreaks can be traced to introduction of infected pigs. Fomites account for about 25% of the outbreaks. In-utero transmission accounts for most of the remainder.
Airborne: Conflicting evidence. Orginally thought to transmit long distances, then airborne was not considered to be a likely route. More recent work indicated that airborne transmission can be important in farm to farm transmission. Research at ISU indicated that a one meter air space between groups was a sufficient barrier to prevent transmission if fomite transmission was eliminated. A solid wall works better. Can have positive and negative pens within the same building however, it is best not to rely on this.
Semen from boars with an acute infection contains enough virus to transmit the disease. It has been difficult to transmit the virus by AI but this remains a possibility. Long-term shedding in the semen has not been demonstrated, but also remains a possibility.
Clinical signs
Pigs:
Interstitial pneumonia with a "thumping" type of respiration.
Mouth breathing, nasal discharge, sneezing
Listlessness, lateral recumbency, CNS-signs, paddling
Vomiting
Pre-weaning mortality may be 50% to 60% especially in weakborn pigs that can die of starvation and crushing
Secondary infections are common with Streptococcus suis, respiratory and enteric pathogens.
In chronically infected herds, the clinical disease often occurs 10-14 days following weaning.
Recent studies link PRRSV to mild diarrhea in 1 to 7-day-old pigs but the causal realtionship has not been firmly established.
Sows:
Breeding pigs have a transient fever (104-106(F), anorexia, and listlessness that may last 4-7 days. If this occurs during nursing, agalactia or hypogalactia may occur.
Reproductive failure:
Live-born pigs are often small and weak.
Premature farrowing (5-7days)
Increases in late-term abortions
Stillbirths (50-70%) with fetuses that are often autolysed and edematous and have a tan-brown skin color.
Mummies occasionally seen (these are late term "mummies" and some people do not think they are true mummies.
During recovery there is an poor conception rate (50%) and slow return to heat.
Long term effects: In some herds the litter size remains below pre-infection levels.
Diagnosis: Many different tests are available.
Serotesting: Many tests are available.
IFA was used extensively and is still available in many diagnostic laboratories. Anti-PRRS IgM and IgG titers can be determined in some labs. These can sometimes be used to determine the stage of infection. If these two tests are 1:64 or higher and the serum virus neutralization (SVN) test is negative, it generally means that the animal is undergoing an active infection. If the SVN test is positive, it indicates that the animal is recovering and may not be shedding the virus.
ELISA is usually the standard test performed for detecting the presence of the virus in a herd. It is able to detect antibody against both the American and European strains of the virus and has the advantage of being easily automated and is more standardized. It is not able to differentiate between infection and vaccine titers.
Immunohistochemistry is performed by some labs but was initially said to have a high rate of false negatives. More recent work has indicated that it can be a valuable test for identifying infected animals within a herd.
RT-PCR: Performed on boar semen and feces to detect viral RNA. It has recently been developed for use with tissues and seems to be very sensitive in identifying the virus.
Virus isolation: Pooled serum samples can be tested to lower the cost. Virus can be recovered from live-born and some stillborn pigs but not from (mummies(.
Histopath: Useful but may be complicated by secondary infections in the respiratory form.
Control-Eradication
Depop-repop with PRRSV-negative swine is a possibility. Needs to be done carefully and there is always a chance that the virus can re-enter the herd.
Development/Isolation/Acclimatization: As long as PRRSV is cycling through a breeding swine herd it would be relatively difficult to eliminate the virus from the operation. An essential step therefore is to make sure that none of the breeding swine have (active( infections. All replacement gilts and sows need to be infected with the virus prior to entering the breeding herd and be allowed to recover. If this is done, then SEW is more likely to succeed in elimination of the virus. One possible procedure is to obtain serum from infected animals, have a lab determine the virus titer in the serum and use this serum to infect (IM or orally) naïve replacement gilts.
SEW: May work if there is no active infection cycling through the sow herd and pigs are removed to an all-in all-out facility. Several instances of the virus spontaneously disappearing from a farm have occurred. Elimination of the virus using SEW has been most successful in herds with 300 or fewer sows. Gilts can then be saved and used as replacements. Extensive serologic testing should be done to determine that all swine in a group are negative for PRRSV prior to introduction to the breeding herd.
Seedstock and multipliers: Need to be free of the virus so that it is not transmitted to uninfected herds.
Semen: Transmission has occurred even when the virus could not be detected in the semen. Boar studs should be free of the virus.
McRebel: Management Changes to Reduce Exposure to Bacteria to Eliminate Losses. This is an 11 point program that was originally designed to limit bacterial diseases but which also helps to lessen the impact of PRRS during an acute outbreak. The main points of McRebel are summarized as:
1. Cross-foster piglets only during the first 24 hr. of life and only within the same farrowing unit.
8. Immediately euthanize very sick pigs.
10. Stop all feed-back programs of stillborn or aborted fetuses.**
1. Establish AIAO nursery flow.
** Feedback programs involve the feeding of either feces of clinically affected animals or dead fetuses or little pigs. These are sometimes used to expose gilts and sows to the infectious agents in a herd so as to prevent problems later (for example, stillbirths caused by parvovirus) or boost colostral immunity for preventing disease in offspring.
Prevention
Buy from reputable sources
Good biosecurity is essential
Vaccination. "Modified"live (B.I.-NOBL and Schering-Plough. Vaccination should be limited to infected herds, especially with the modified live. May inhibit eradication by complicating testing. Also may not be completely protective. A killed vaccine is available from Bayer and autogenous vaccines are produced by a subsidiary of Bayer. SAMS (sow abortion mortality syndrome) has been a problem in some vaccinated herds that received the first MLV on the market. This is currently considered to have been a severe form of PRRSV but SAMS has not been a problem recently.
In infected herds, new breeding animals can be exposed to infected animals prior to breeding. Fence to fence contact isn't usually fast enough and you probably need to mix infected, shedding animals with the group. Probably the best procedure is to perform tonsil scrapings of shedding animals and administer this material orally to all animals coming into the breeding herd. Otherwise there are likely to be animals that do not become infected until later and act as a source of the virus for young pigs.
PORCINE CIRCOVIRUS-ASSOCIATED DISEASE [POST-WEANING MULTISYSTEMIC WASTING SYNDROME (PMWS)]
Etiology
PMWS was first described in Canada in 1991. In 1995, a circovirus was isolated and implicated as the cause of the syndrome. This was subsequently named a Type II circovirus (PCV2) to distinguish it from circovirus that had been isolated previously but not associated with disease (PCV1). Typical PMWS has been reproduced with pure circovirus in CDCD pigs at ISU. Another report from Ohio State indicates that minor lesions were produced with pure circovirus infection but full-blown disease occurred when pigs were co-infected with parvovirus. Since circovirus seems to be so widespread in the pig population, it appears that there needs to be some inciting cause to set off relatively widespread viral replication in the pig. Some adjuvants were implicated as inciting causes of PMWS, particularly some of the adjuvants used with Mycoplasma hyopneumoniae vaccines.
It should be emphasized that PCV2 infection doesn(t necessarily cause PMWS. A study of sera from 28 high-health status sow herds indicated that all the herds had antibody to PCV2 but none of these particular herds had PMWS.
Epidemiology
PMWS most often affects pigs between 4 and 16 weeks of age and seems to be more common in pigs around the late nursery to early grower-finisher stage. Large quantities of virus are excreted in the feces, urine, and nasal secretions from pigs in the acute stages of the infection. Infected pigs have high numbers of circovirus in their tissues. Not all of the pigs in a pen will be affected at the same time and in most infected herds there is only a 5-15% morbidity. However, some herds have significantly higher morbidity rates. The disease progresses randomly through a hog facility for a three to five week period before resolving.
Clinical signs
Initially, many pigs develop a high fever are listless and seek a cool area of the pen. Pigs may be dyspneic, have a light cough, and there may be diarrhea in some cases. Often the lymph nodes are sufficiently enlarged to be palpapated on physical exam. A small percentage of animals look pale or yellow due to jaundice (bilirubin levels are quite high in these pigs). Pigs develop a rough hair coat and become emaciated. Many of the affected pigs die but it may take several weeks for them to do so. Pigs that recover are often 50 to 100 pounds lighter than the non-affected pigs in the same group.
Postmortem findings
Gross lesions: Enlarged inguinal, mesenteric, bronchial, and mediastinal lymph nodes are generally observed. These have a white, homogeneous appearance on cut surface. Lungs are often firm, noncollapsed, rubbery and mottled with gray nodules. The lungs may have a patchy interstitial pneumonia that is more characteristic of PRRSV infection. The liver may be diffusely atrophied and mottled with yellow-orange areas. Kidneys may have no lesions or may be grossly enlarged, waxy and contain diffuse white foci.
Histopathology: Lymph nodes may have a loss of B-cell follicles, infiltration of T-cell areas by histiocytic cells, and vasculitis. Suggestive lesions also occur in the liver and kidneys.
Culture: Culture often reveals secondary bacterial infections with Pasteurella multocida, Actinobacillus pleuropneumoniae or Haemophilus parasuis in animals that die.
Diagnosis
Immunohistochemistry is the standard test used in the ISU Diagnostic Lab. It has the advantage of allowing one to visualize virus antigen in characteristic lesions.
In-situ hybridization is used as a back-up for the IHC when results are equivocal.
Virus isolation is relatively slow and not as sensitive
Lesions: Helpful but similar lesions can be produced by PRRSV, salmonellosis and others.
Treatment
Good supportive care. Otherwise none.
Prevention
Vaccination: Early indications are that the available vaccines are highly efficacious but as of 2007, they are still in short supply.
Good management practices such as all-in/all-out pig flow and provision of good sanitation, air quality, and nutrition are helpful.
Isolate PMWS-suspect pigs from the rest of the group.
Minimize cross-fostering of piglets (McRebel?). This would decrease the chances of transmission if the disease needs to be transmitted early in life.
Allow replacement gilts time to generate immunity to the diseases in a given herd.
SWINE RESPIRATORY DISEASES
As with most of the respiratory disease associated with domestic livestock, the etiology of swine respiratory diseases is often multifactorial. Good management practices, adequate ventilation and good building design, prevention of crowding and stress, and prevention of the introduction of new pathogens are extremely important in controlling respiratory disease. Where disease does occur, more than one pathogen may be involved.
Mycoplasmal Pneumonia
(Enzootic Pneumonia)
General description
Mycoplasma hyopneumoniae causes a chronic pneumonia characterized by a persistent, nonproductive cough, loss of condition and growth retardation. It is thought to be a major factor in the development of respiratory disease in swine and its control is key to overall respiratory disease control.
Etiology
M. hyopneumoniae is the etiologic agent but many bacterial and viral agents usually contribute to the production of disease and vice-versa. If these secondary (or primary) invaders are controlled, clinical disease can be markedly decreased. A poor environment with excessive pit gases and heavy microbial air loads also contribute to disease.
Epidemiology and transmission
The organism is found worldwide in almost all swine herds and 30 to 80% of market-weight pigs have pneumonic lesions consistent with infection. It is estimated that 10-20% of sows are chronic carriers. Transmission is assumed to be primarily by droplet and contact although movement into clean units by airborne infection from other units is suspected. Most young pigs probably do not become infected prior to 5 to 6 weeks of age and may not show clinical disease until much later. Spread of disease through a unit is generally slow. The incubation period is 10 days to 3 weeks although it can be much longer in some cases. With boostering of colostral immunity (sow vaccination) clinical disease may be delayed.
Clinical Signs
Clinical disease is seen mainly after 5-7 weeks of age and persists 6 weeks or longer. There may be bouts of recrudescence in pigs up to market weight. Pigs have a dry, nonproductive cough, unthrifty appearance, fever (if secondary invaders are involved), and normal appetites. There is generally a high morbidity. Mortality depends upon complicating factors but is usually low to moderate. In well-managed herds the disease may be clinically silent.
Infected pigs may have up to a 30% decrease in rate of gain and a 20% decrease in feed conversion.
Lesions
Purple to tan or gray areas of consolidation primarily in the cranioventral portions of the lungs. These portions of the lungs are atelectatic and appear smaller in size than surrounding lung. The bronchi and bronchioles often have some catarrhal exudate and bronchial lymph nodes may be swollen and edematous. Microscopically there are collections of lymphocytes around the airways and blood vessels and extensive destruction of tracheal cilia. Uncomplicated lesions may resolve within 6 weeks, but may be present 3 months after onset.
Secondary invaders are common and many lesions reflect this mixed infection.
Diagnosis
Clinical signs: Chronic coughing with loss of condition.
Lesions: Gross and histologic
FA test: Demonstrate the M. hyopneumoniae lining the airways.
Culture: Not routine since isolation of M. hyopneumoniae is tedious and not generally available.
Prevention
Management
All in-All out reduces the severity and seems to be the most important factor in recent studies. Improvement of air quality and decreased crowding are key control measures. Vaccination of sows or gilts in combination with AIAO seemed to give the best results. Gilts generally have higher antibody titers in their colostrum than sows (possibly due to more recent exposure) and vaccination for gilts may not be needed. When combined with SEW or MEW and maintenance of good air quality, mycoplasmal pneumonia often becomes economically non-significant. SEW, MEW and AIAO have been combined to (eradicate( the disease from some farms. Control measures can also markedly reduce it's impact by limiting secondary invaders.
Vaccination
Sixty to 80% control in some controlled studies. Mixed reviews from practitioners but the vaccines are generally considered to be effective. Some regard vaccination against this organism as a cornerstone of their respiratory disease control program and don(t believe they can do without it. It is currently the most commonly administered vaccine in pigs.
Antibiotics
Tetracyclines suppress development of disease if started at time of exposure. Other antibiotics can be beneficial if
Treatment
Quinolones are effective but not approved for use in the U.S. Several others are used such as Lincomycin, Tylocin and Tiamulin but have not been proven to have any effect on the M. hyopneumoniae itself. These may be more effective against some of the secondary invaders and therefore be of value in treating the clinical disease.
SWINE INFLUENZA
Etiology
Type A influenza virus is similar to influenza A virus of humans. About 25% of midwestern US swine have antibodies to the classical strain (H1N1). Some studies indicate up to an 80% incidence of serologically positive swine. Recombination of virus strains in mixed infections is thought to play a role in the generation of new virus types but this has not occurred in swine to the extent as that of human influenza virus. The H3N2 virus had been a problem in Europe and Asia but until 1998 there were no outbreaks associated with this serotype in the U.S. Since the fall of 1998, a number of outbreaks have occurred in the U.S. and it recent figures indicate that it is the strain involved in a marked resurgence in clinical swine influenza. Older surveys indicated that thirty-five percent of U.S. swine have antibody to this virus, but it had not been seen as a clinical problem here. Apparently, there are other genetic differences that contribute to virulence. In addition, the H1N1 and H3N2 viruses have undergone recombination and we now have H1N2 strains showing up. Some H1N7 virus has also been detected. There has been considerable antigenic drift in the swine influenza viruses.
Epidemiology
The first outbreaks reported in the US coincided with the human pandemic of 1918. Since then influenza viruses have been suspected to move between avian species (turkeys harbor a similar virus), pigs, humans, and others. The major source of the virus for pigs is other pigs. Large numbers of viral particles are shed in the nasal mucus of acutely infected pigs. It rapidly moves through a group and will spread progressively through a large facility. Apparently, some pigs in a group may shed the virus for longer periods of time and may be responsible for transmission to new facilities when these pigs are sold. There is also some evidence that the virus can be wind-blown and move to other sites.
Disease
Classically occurs in autumn or winter and is often associated with inclement weather. Interestingly there is another peak (much lower in severity) around May. It can infect swine of all ages. There is a sudden onset of anorexia, depression, muscular pain, fever, dyspnea with "thumpy or jerky" respiration, cough, conjunctival discharge. Pigs may be very reluctant to move and frequently will not eat. Morbidity is usually high but mortality is usually low in uncomplicated disease. Other pathogens such as PRRSV, Erysipelothrix, etc., that may be endemic in the herd may become clinically apparent. Uncomplicated recovery is very rapid and occurs at about 6 days.
May see disease in several farms in a given area at the same time. Carrier pigs are the most likely source for some of these outbreaks but can(t explain the majority.
"Chronic" disease is less common. Infection of pregnant sows results in higher neonatal mortality, smaller litters with slower growth rates. Recent anecdotal information that the virus is a cause of abortion may not be true in the sense that the organism has not been found in the fetus except for one case on record. Sows that have a high fever and other problems associated with influenza infection may abort, but it is not thought to be due to the effects of the virus on the fetus. However, the virus may not survive long enough in the fetus to be recovered. With the recent H3N2 outbreak, 2-4% abortions and sow deaths of 1-4% per week per group have been reported.
There has been an overall increase in the incidence and importance of swine influenza in the past several years possibly due to the effects of the PRRS virus and Mycoplasma hyopneumoniae and definitely related to the new H3N2 strain.
Diagnosis
Clinical: Unique disease when a full blown outbreak occurs
FA test: Rapid and reliable.
Immunohistochemistry is available in VDL
Virus isolation: Inoculation of material from nasal swabs or acutely affected lung tissue into embryonated eggs.
Hemagglutination inhibition (HI) test: Test for antibodies in paired sera. Acute stage vs 3-4 weeks later.
Lesions: Very helpful. Necrotizing bronchiolitis and bronchitis.
Treatment
Supportive, antibiotics for complicated disease, expectorants, etc.
Control and prevention
Vaccine is available commercially for both H1N1 and H3N2 virus. They reduce clinical severity but are not completely protective. A suggested vaccination program could include the following:
Vaccinate all sows and boars in the herd in the summer (priming dose).
Re-vaccinate all sows 3 weeks pre-farrowing to booster immunity. Boars should be booster vaccinated at this time as well
Replacement gilts and boars should receive two vaccinations 3 weeks apart during the isolation/acclimatization period and then be boostered as above.
If necessary to break the disease cycle, depopulate the nursery after the sow herd has been stabilized by vaccination or infection.
Vaccinate finishing pigs during late fall in high risk situations but this is frequently not warranted on farms with relatively low risk.
Good sanitation, prevent mixing of livestock. All-in all-out by site is necessary to break the cycle of infection. AIAO by room or building is not sufficient.
The possibility of the introduction of type A virus from humans, turkeys, etc., should be considered but these appear to be minor sources at the present time.
PASTEURELLOSIS
Etiology
Pasteurella multocida is considered to be a common and important secondary invader in pneumonias in swine. Initial damage to the pulmonary defenses is caused by Mycoplasma sp., other bacterial agents and viruses.
Type A serotype 3 (A3) P. multocida is the most common serotype reported from pneumonic lesions, however, other serotypes are reported.
Epidemiology
P. multocida is frequently found in the upper respiratory tract of normal swine. It is transmitted shortly after birth to young pigs. Type A3 organisms can be isolated from other species of animals and these animals may serve as a source of infection for swine.
Disease
Lesions are typically those of a purulent bronchopneumonia and are often superimposed on the lesions of the primary disease agent such as a mycoplasma. In field cases, lung abscesses due to Arcanobacterium pyogenes, Streptococcus, spp. or Haemophilus spp. are not uncommon.
Diagnosis
Bacteriologic culture
Prevention
Control other diseases: In addition to mycoplasmal diseases, atrophic rhinitis, influenza, inclusion body rhinitis, ascarid larvae migration, and lungworms may serve to help initiate disease.
Management
Treatment
Early treatment with antibiotics may be beneficial. The organism is usually quite susceptible to antibiotics in vitro but an antimicrobial susceptibility test is recommended because resistant isolates are common.
Naxcel 2-3 mg/kg
Tiamulin
Tetracycline 200-400 g/ton
Tilmicosin in feed (Do not give Tilmicosin parenterally to swine - very low margin of safety - kills pigs).
Actinobacillus pleuropneumoniae
A. pleuropneumoniae causes acute pleuropneumonia in pigs characterized by fever, respiratory distress and a high rate of mortality in some outbreaks.
Etiology
A. pleuropneumoniae has 12 different capsular serotypes. Serotypes 1, 3, 4, 5, 7, 9 and 10 are present in the U.S. Serotypes 1, 5 and 7 are the most commonly seen. There is some serological crossreactivity between serotypes 3, 6 and 8; 4 and 7; 1 and 9. The crossreactivity is between the LPS antigens. A. pleuropneumoniae can be typed based on capsule, LPS and ApX toxins.
biotype 1: requires NAD (V Factor).
biotype 2: Same as biotype 1 but does not require NAD.
The organism is capable of producing severe disease without the interaction of other agents. However, P. multocida, M. hyopneumoniae and other respiratory disease agents may influence the severity of disease.
Epidemiology and Transmission
A. pleuropneumoniae resides in the tonsils of chronic carrier pigs and is probably spread by droplet and contact. The organism does not survive long outside of the host. Sows may transmit the organism to their piglets but colostral immunity usually protects against clinical disease in suckling pigs. In a susceptible herd, the organism may spread subclinically until stress factors occur which cause expression of overt disease. Overt disease usually occurs in feeder pigs and growing and finishing pigs.
Clinical signs
The disease seen in herds where the organism has been present for some time is usually less severe than when a completely naive herd becomes infected. Morbidity can vary from 8 to 40% with mortality up to 25%.
In peracute disease, pigs develop a 104 to 106(F temperature, suddenly become apathetic, anorexic, may vomit, develop severe dyspnea with a blood-stained frothy discharge from the nose and mouth, have a moist suppressed cough, cyanosis of the skin and mucous membranes, and die acutely.
An acute form is also seen where pigs may die or develop chronic disease.
In chronic disease, pigs may have a chronic cough, reduced appetite and a retarded growth rate. Milder cases may be hard to recognize.
Arthritis, abortion and septicemia with CNS signs may occasionally be observed.
Pathogenesis
The organism initially proliferates in the upper respiratory tract but quickly spreads widely in the lung to produce a diffuse fibrinous pleuropneumonia. There is edema, hemorrhage, and a neutrophilic exudate with foci of coagulative necrosis. The lesions are raised with an irregular surface and are dark red, firm and swollen. In the chronic stages, pulmonary abscesses and adhesions develop. Pleuritis is very common and pericarditis, although rare, is sometimes seen. There are three RTX class toxins produced by this organism that are apparently major factors in the production of disease. The leukotoxin (ApX1) causes the neutrophils to lyse and release their lysosomal enzymes onto the pulmonary tissues helping to give rise to the acute nature of the disease. The ApX toxins are also directly toxic to pulmonary tissue.
Diagnosis
Differentials are Streptococcus suis, Pasteurella multocida, and Salmonella choleraesuis.
Clinical. Sudden deaths of fattening pigs with pneumonia.
Lesions of patchy areas of consolidated lung - raised, distributed randomly over lung.
Bacterial culture from lesions. Use media containing NAD or staphylococcus "nurse" culture. The organisms die quickly in tissues and in transport. If P. multocida is present in tissues one may need to dilute the inoculum to isolate A. pleuropneumoniae.
Determine serotype in order to enhance chances for successful vaccination.
Serologic tests. High percentage of pigs acquire antibody via colostrum which persists 5-12 weeks, depending on sensitivity of assay.
CF antibodies detectable 10 days after infection, persist several months.
ELISA's based on LPS or capsule are used as a good screening test then followed with the CF test.
Treatment
Base treatment on antimicrobial susceptibility testing when possible and treat all the pigs in a pen when extensive losses are occurring. Commonly used antimicrobials are:
Penicillin at high dosage rates, sulfonamides, 400-500g/ton tetracycline in feed, LA 200, Tiamulin in water and Naxel.
Control
All-in all-out production, SEW or MEW, minimize stress, improve ventilation.
CF or ELISA to detect adult carriers. Cull seropositive adults.
Vaccination: Autogenous and commercial vaccines are used with mixed reports on efficacy. The presence of ApX toxin(or toxoid)is needed for good protection but unfortunately, none of the currrent vaccines has enough ApX to induce a titer. The organism produces very little toxin under conditions used in vaccine production. Need to include the common serotypes occurring in an area. To be most effective, the vaccines need to be in an oil-based adjuvant that may cause a high incidence of abscesses.
A modified live vaccine has been marketed since about 1998. The parent organism was a serotype 5 that lost the ability to produce a capsule but which retained production of ApX1 and ApX2 toxins. Current information from the manufacturer (B.I. Vetmedica) indicates good efficacy especially against serotype 5 but other serotypes as well, however some breaks in protection against serotype 1 strains. A major problem apparently exists with adverse reactions. In some groups of pigs, there is an immediate adverse reaction, 10 to 30% of pigs may vomit, shudder/shake, 100% may be lethargic. The reaction disappears within a couple of hours. This seems to be peculiar to some groups of pigs while others may have no problems. The reaction is apparently due to endotoxin in the vaccine strain and not due to strain virulence or the presence of the RTX toxins. The reactions are seen with the first dose only and are found in both infected and non-infected herds. The vaccine is not commonly used currently.
Haemophilus parasuis
Haemophilus parasuis causes septicemia and acute polyserositis, arthritis and meningitis in young swine (Glasser's disease). Infection of the nasal and tracheobronchial mucosa is common in young pigs. Infections in high health status swine units are difficult to control and can cause significant economic losses.
Epidemiology
Haemophilus parasuis is found worldwide in swine populations. It is carried in the upper respiratory tracts of sows although the percentage is not known. It is readily transmitted by contact and droplet to young pigs by 2 to 5 weeks of age and spreads laterally through a group of pigs. Over 70% of pigs in conventional and continuous thru-put operations are infected. In SEW operations it is thought that many pigs do not become infected until after being mixed with carrier pigs the same age. SPF swine are also highly susceptible.
Stresses associated with transport, mixing, fighting, weaning and diet changes are important factors in the onset of disease.
Viral infections such as swine influenza markedly increase the severity of clinical disease.
Clinical disease
Glasser's disease is a polyserositis and septicemia. The clinical appearance of the disease depends on the tissues affected. There is usually an incubation period of 12 to 72 hours followed by a sudden onset of fever (106 to 107(F). There may be abdominal distention or tenderness, labored breathing, coughing, lameness, orchitis, and CNS signs.
Lesions are found on any serosal surface and include peritonitis, pleuritis, pericarditis, meningitis, arthritis, orchitis. Hemorrhages may be found in the liver, spleen and kidneys due to the septicemia.
The organism is extremely common in pneumonias of baby pigs and somewhat less frequent in pneumonias of older pigs.
Diagnosis
Clinical signs. A history of acute onset following some type of stress and the typical signs of polyserositis.
Culture. H. parasuis is readily recovered from fresh tissues using blood agar with a staphylococcal nurse colony or media containing NAD.
Postmortem lesions
Rule-outs
Streptococcal infection
Erysipelas
Mycoplasma hyorhinis polyserositis and arthritis
Prevention
Minimize stress: Optimize environment and management.
Commercial bacterins are available and autogenous bacterins may be used. Some evidence that protection is mainly type specific but there is a lack of research information on this organism.
Expose new swine by fence contact 2-3 weeks prior to commingling with conventional stock.
Experimental: Infecting all pigs at 5 days of age with the strains present in the herd has been done experimentally and has resulted in a marked decrease in incidence of disease.
Treatment
Penicillin, ampicillin, tetracyclines, sulfathiazole or potentiated sulfonamides, where approved.
STREPTOCOCCAL DISEASES
S. equisimilis, Lancefield's group L streptococci and occasionally other streptococci can be responsible for septicemia, arthritis, endocarditis, and other sporadic conditions in swine.
Epidemiology
S. equisimilis, and the other organisms involved are common in the URT, oral cavity, vaginal secretions and milk of normal swine. They are spread to young piglets from the sow via wounds, the umbilicus, and tonsils. Contamination of instruments for clipping needle teeth and tail docking can result in large numbers of pigs being infected.
Disease
Most common in piglets 1 to 3 weeks of age. One sees joint swelling and lameness most commonly. Elevated temperatures and unthriftiness may be observed.
Endocarditis may occur in older pigs. The pigs are usually more severely ill, depressed, show pain on handling, and redness and cyanosis of extremities.
Diagnosis
Bacteriologic culture: Joints may have low numbers of organisms in advanced disease. Organisms grow readily from the vegetative lesions in the heart.
Control
Since the organism is widespread, good management is essential.
Disinfect equipment used for clipping needle teeth and tail docking
Adequate colostrum
Reduced abrasiveness of flooring
Navel dipping
Vaccination of sows may be beneficial in problem herds. Autogenous and commercial bacterins have been used and have resulted in a reduction of infections.
Treatment
Penicillin has worked well in the past, but resistance has been reported. Tetracyclines.
Streptococcus suis
Common cause of septicemia, meningitis, arthritis and bronchopneumonia in pigs.
Potential human pathogen.
Etiology
About 35 serotypes of S. suis have been recognized. The organisms are all in Lancefield's group D. Type 1 is endemic in most herds but only sporadically affects pigs. The majority of disease is caused by type 2. The common serotypes are 2, 3, 4, and 7.
Disease: Three clinical forms in young pigs. The first two are often combined, but all three can be seen together.
Neonatal septicemia: Seen in young pigs in the absence of colostral immunity. Pigs die in 24 h.
Suppurative meningitis: Pigs 10 days to 4 months of age. One theory on the appearance of meningitis is that there has to be some other agent such as Bordetella bronchiseptica present to cause irritation of the nasal mucosa before the organism can cause meningitis.
Bronchopneumonia: In all ages but much more common in pigs 6 to 12 weeks of age; more severe in young pigs. There is currently some controversy over whether this agent is the cause of bronchopneumonia. It has been reported that pure infections with this agent in pigs do not cause a bronchopneumonia, however, the bronchopneumonia is frequently present and probably requires some type of inducing agent such as swine influenza virus.
S. suis can also cause endocarditis, arthritis, vaginitis, and abortions in sows but the incidence is low.
Transmission
Large, intensive swine rearing operations are more commonly affected by type 2 S. suis. Recent work indicates that the organism can be transmitted from the sow to her piglets as they pass through the birth canal. The organism is transmitted between herds by carrier pigs and possibly by flies and fomites. The organism survives long periods in feces, dust, and dead carcasses.
Diagnosis
Bacterial culture. Lancefield typing.
Differential Diagnosis
Pseudorabies, Haemophilus parasuis, and Streptococcus equisimilis.
Prevention and control
Good management to minimize stress from overcrowding, poor ventilation and mixing and moving of pigs. Temperature stress has been identified as a major factor by some. The suggestion is that a goal of 2 degrees fluctuation in temperature be established. Mixing of pigs with greater than 2 weeks age difference in the nursery is discouraged. Use all in/all out methods with good disinfection between groups.
Treat clinically affected pigs: Penicillin or ampicillin (about 5% are resistant to penicillin).
Depopulation/repopulation with SPF or medicated early weaning pigs has been tried but all have ultimately failed. Essentially all herds have Streptococcus suis.
Vaccination
Commercial bacterins are available for types 1, 1.5, and 2. Killed bacterins and autogenous bacterins for sows to boost colostral immunity have relatively low efficacy. They have reduced the mortality in the piglets in some cases from about 6% to around 2% but are generally not considered to be of significant value. Vaccination of the piglets at weaning and 2 weeks later has given highly variable results. Vaccination seems to be even less efficacious in PRRSV-infected herds. Recent studies indicate that experimental modified live vaccines have not been successful either.
Atrophic Rhinitis
Progressive Atrophic Rhinitis is a chronic disease of swine characterized by rhinitis, atrophy of the nasal turbinates, deviation of the nasal septum, malformation of facial bones and growth retardation. Type D organisms have been eliminated from many high health status swine herds but are still a problem in some continuous thru-put facilities. Prior to the use of SEW, etc., most surveys revealed at least 50-% of slaughter pigs had lesions.
Etiology
The main etiologic agents are Pasteurella multocida (toxigenic capsular type D or A) and/or Bordetella bronchiseptica. Poor air quality and noxious gases, certain other bacterial agents such as Haemophilus parasuis, Pseudomonas aeruginosa and Fusobacterium necrophorum, and probably some viral agents play major contributing roles in the development of disease. Infection with Bordetella bronchiseptica alone may cause a non-progressive type of disease that is considered to be much less severe.
Epidemiology
Toxigenic Pasteurella multocida and Bordetella bronchiseptica are found worldwide in swine. Both are carried in the upper respiratory tract. The numbers of organisms are usually much higher in acutely affected pigs than in carrier swine. Transmission from infected sows to piglets occurs very early in life. Pigs that are not infected shortly after birth are readily infected by lateral transmission. Transmission is by contact and airborne droplets. Air in infected farrowing units may contain several hundred toxigenic P. multocida per cubic meter.
B. bronchiseptica can be carried by other animals including rats, rabbits, cats and dogs but these normally are not the source of the organism for pigs.
Clinical Signs
In early or mild disease there will be sneezing and snuffling during quiet periods that may be exacerbated when pigs are stirred up. There is a serous nasal discharge, excessive lacrimation and a roughened hair coat. The pigs may cough if the trachea and bronchi are colonized (often with secondary invaders and pneumonia may develop. As the disease becomes chronic in the progressive form, there is a shortening and deviation of the snout, folding/wrinkling of skin over snout, malapposition of teeth, epistaxis, sneezing, pneumonia, and decreased growth rate. The degree of these changes depends on the severity of the disease. As far as the effect on growth rate, some investigators found no reduction, others found 2 to 12% reductions in daily gain. When combined with other diseases, the impact of atrophic rhinitis could be even more significant.
Pathogenesis
Initial infection with B. bronchiseptica causes an acute inflammation of the nasal mucosa. H. parasuis, ammonia or other pit gases may play a role in the initial damage. The B. bronchiseptica causes squamous metaplasia of the epithelium, loss of cilia and inflammation of epithelium and submucosa resulting in impairment of mucociliary clearance.
Infection with toxigenic P. multocida causes the majority of the chronic alterations. The toxin is thought to activate mature bone cells to release cytokines such as IL-6 that enhance bone resorption while impairing new bone formation. The P. multocida toxin has systemic effects among which are hepatotoxicity. Experimentally, the toxin reduced weight gain in pigs and may be largely responsible for the decreased growth rate that occurs. The P. multocida toxin may also predispose to other disease, such as sublethal pseudorabies virus infection. Depending upon the agents involved in the disease, there may be severe alteration in structure of turbinate, premaxillary, frontal, etc. bones. The most severe atrophy may be seen in pigs slaughtered during the summer months
Diagnosis
Clinical signs are characteristic.
Culture: Following the acute phase, toxigenic P. multocida may not be detectable by culture from nasal tissues, however, it may be present in the tonsils. Just finding P. multocida is not generally sufficient for diagnosis since non-toxigenic strains are often present. Toxigenic strains can be identified using a Western immunoblot and this is the procedure that is employed at NVSL and on a research basis at ISU. An ELISA kit for detection of toxigenic strains has been used in Europe but is not licensed for use in the U.S. According to the ISU Diagnostic Laboratory, there are very few requests for testing.
Slaughter checks:
If a slaughter plant will cooperate you might be able to use slaughter checks to evaluate the status of atrophic rhinitis in a herd. Use a bandsaw to cross section the snout just anterior to second upper premolar teeth or at first premolar teeth. Changes to look for: The inferior scroll of ventral turbinate is most often and most severely affected. The ethmoid and dorsal turbinates may also be involved. There may be a catarrhal exudate on the nasal mucosa and the mucosa itself is often pale. There is hypoplasia of the turbinates to a variable extent, deviation of the median septum and malformation of the of the maxillary, premaxillary and frontal bone. More frequently, the importance of atrophic rhinitis is evaluated clinically and on post-mortem.
Control
It is essential that control programs include monitoring atrophic rhinitis in the herd. Disease can vary with the season and with groups of pigs, etc.
Improve management and environment. Use all-in all-out production and proper ventilation.
Segregated or medicated early weaning programs can be used to help eliminate toxigenic P. multocida from the breeding herd.
Vaccination - many products contain B. bronchiseptica and toxigenic P. multocida. Immunization with P. multocida toxoid appears to be the most effective. Generally, it is recommended that sows receive 2 doses prior to farrowing and the pigs one dose at 7 days and one at 14 -28 days of age. Vaccines usually yield the best results when the disease is more severe and may not be indicated if the economic loss from the disease is less than the cost of vaccination.
Biosecurity for negative herds includes prevention of exposure to infected swine, cats, dogs, rodents, vehicles and personnel from infected units, and complete confinement.
Treatment
It is extremely important to improve the environment, management and nutrition.
Tetracycline antibiotics may be useful, especially if given early or if there is pneumonia present. The recommended dose is 20mg/kg long acting oxytetracycline at day 1, day 7, day 14 and at weaning. Tetracyclines are more effective when used in combination with a vaccination program.
Naxel is effective against P. multocida and is commonly used.
Inclusion Body Rhinitis
An acute systemic viral disease of swine causing lesions throughout the body but especially in the nasal submucosa. Infection with this virus was previously thought to be largely inapparent or subclinical. Recently, however, the infection seems to be causing disease especially in "high health status herds". The virus is not known to cause turbinate atrophy.
Etiology: Cytomegalovirus (Herpesvirus)
Epidemiology
The virus is found worldwide and virtually all swine in conventional herds are infected based on serological evidence. SPF herds and segregated early weaning herds may not be infected. Transmission is assumed to be by contact or aerosol from nasal secretions of carriers, which probably include sows. Infections may be more common in PRRS infected herds and the cytomegalovirus itself is immunosuppressive.
Clinical Signs
Usually seen in 1 to 4 week-old pigs. There may be a moderate fever, anorexia, weakness, plugging of the nasal passages with mouth breathing. There may be coughing and piling.
Lesions
Highly inflamed and hemorrhagic nasal mucosa is almost pathognomonic. There may be excessive mucus present. The tubuloalveolar gland cells in the nasal submucosa are greatly enlarged and contain large intranuclear inclusions. Inclusion bodies are seen in various other locations such as the lungs and kidneys.
Diagnosis
Gross lesions are almost pathognomonic.
Histopathologic exam of the turbinates (use the ventral turbinate).
Control
One of the theories on why we may be seeing more disease is that infection may be occurring in susceptible pigs after colostral immunity is lost. More attention to this disease in high health status herds may be necessary. Control measures used for other respiratory agents should work against this virus.
Treatment
None currently available.
Sanitation to minimize secondary disease
SWINE ENTERIC DISEASES
Diarrhea and enteric diseases are probably the most important causes of economic loss to the swine industry. The approach the differential diagnosis of swine enteric diseases is best done by age at which the pigs are affected. Some of the enteric diseases have very specific age ranges of pigs that they affect while others are quite broad. The following is a listing of some of the main causes of enteric disease broken down by age of pig and the most prominent clinical presentations:
1-6 Days of Age
C. perfringens 1-4 days; Claret red-colored diarrhea, acute deaths,
Type C high mortality, may have subacute and chronic forms.
Type A increasingly recognized as a cause of watery diarrhea in this age group (out to a week or ten days) The diarrhea is generally mild but can be a cause of economic loss.
C. difficile 1-7 days; Mesocolonic edema, mild diarrhea, feces with a (creamy( consistency.
E. coli 1-3 days; Profuse watery diarrhea and dehydration; gastric distention, watery contents in small intestine.
TGE Profuse watery greenish-gray diarrhea without blood, vomiting is prominent, high mortality, older pigs may be affected but not as severely.
Rotavirus Severity depends upon antibody levels in the sow's milk, presence of secondary invaders, and the level of exposure. Subclinical to severe watery diarrhea.
S. choleraesuis Rare
7-21 Days of Age
Coccidiosis 7 to 15 days of age. Yellowish to grayish diarrhea that may progress to watery diarrhea; no blood in feces; No response to antibiotics.
E. coli Usually less severe than neonatal disease. May respond well to antibiotics.
TGE Pigs at the upper age range may survive. Others die.
Rotavirus Most severe in 7 to 41-day-old pigs. Can see severe disease, especially in early weaned pigs that get a high infectious dose and when E. coli is also present.
Salmonella
choleraesuis Not as common as in post-weaning pigs. See more problems as pigs near weaning. May see sporadic acute deaths.
Strongyloides Diarrhea followed by progressive dehydration, death usually occurs before 10 -14 days in heavy infestations. Stunting and unthriftiness are more common.
Weaners-Nursery Pigs
Rotavirus Combined with E. coli, it is said to be the most common cause of postweaning diarrhea.
E. coli Hemolytic strains, usually mild to moderate diarrhea when uncomplicated.
TGE Diarrhea without high mortality, depending on the age.
Salmonella
choleraesuis Usually see occasional septicemic deaths and little to moderate diarrhea. May have some blood in the feces.
Trichuris suis Mucohemorrhagic diarrhea, large intestine only. Diagnose by finding the parasites.
Brachyspira
hyodysenteriae Bloody dysentery. May appear to have one to three cycles of disease at about 3 week intervals.
Proliferative
enteropathy Problems usually begin about 7 weeks of age or so. Subclinical to pigs with anorexia, dullness, severe diarrhea and death.
Grower-Finisher
Brachyspira
hyodysenteriae Bloody dysentery
Trichuris suis Mucohemorrhagic diarrhea.
Proliferative
enteropathy Subclinical to severe diarrhea. May have moderate mortality with the more severe forms. Replacement gilts often have severe problems with the PHE form of the disease.
COLIBACILLOSIS
Etiology
Escherichia coli associated with the production of diarrheal diseases in pigs are characterized by the production of a number of important virulence attributes. Listed below are those that seem to be of some importance:
Fimbriae are essential for the attachment of E. coli in the small intestine. E. coli that are normally found only in the distal 2/3 of the intestinal tract are not associated with diarrheal disease. Certain fimbrial types are associated with the attachment in the small intestine and therefore are essential for the production of disease in neonatal pigs.
F4 (K-88) strains adhere throughout the intestinal tract.
F5 (K-99), F6 (987P), and F41 strains adhere in greater numbers in the distal half of the small intestine.
Enterotoxins are essential in the production of diarrheal disease. STa is produced by all strains of E. coli that produce diarrhea in neonatal pigs. STb is associated with strains that produce postweaning diarrhea. Some strains produce the LT toxin.
Epidemiology
Problems with E. coli enteritis in neonatal pigs increased dramatically with the advent of swine confinement buildings. Pathogenic strains of E. coli are maintained in the intestinal tract of swine and to a lesser extent the environment. Baby pigs come in contact with the organisms from the sow's feces. The cleanliness, dryness, and design of farrowing units has been demonstrated to have an effect on the incidence of neonatal diarrhea in pigs. E. coli do not survive as long in dry environments. Poorly designed farrowing crates where piglets come in contact with feces from the sow have been shown to result in a higher incidence of diarrhea. Drafts that result in chilling of the baby pigs are an extremely important predisposing cause of colibacillosis in baby pigs.
Clinical signs
E. coli usually kills pigs because of the extensive fluid loss from the intestines and the resulting severe dehydration. Whole litters or individual pigs may be affected within a few hours of birth and up to 2 to 3 weeks later. The initial signs can vary from acute death without signs of diarrhea to a mild diarrhea with no evidence of dehydration. Up to 40% of body weight may be lost. The feces may vary from an almost clear fluid to white or brown depending on the diet. The immune status of the sow, the age of the pig and, to some extent, the infectious dose of the organism are important factors in determining the severity of the clinical disease.
In post-weaning E. coli diarrhea, the clinical signs are the same as in the pre-weaning diarrhea, but are milder and the mortality is normally not high. Recently, cases of E. coli diarrhea have been occurring in pigs 3 to 4 weeks following weaning.
Lesions
Distention of the small intestine and loss of tone of the intestinal wall. On histopath, the villi are normal and there is heavy bacterial adherence to the intestinal epithelium.
Diagnosis
It is important to recognize that more than one agent may be contributing to a diarrhea.
Clinical signs
Bacteriologic culture of an acutely ill, untreated animal. Strains from post-weaning diarrheas are almost always hemolytic K88 strains.
Rule out other causes (histopath, FA)
Rule-outs
In neonatal diarrhea
Clostridium perfringens types A and C
Rotavirus
TGE
Coccidiosis
In post-weaning diarrhea
Salmonellosis
Bloody dysentery
Rotavirus
TGE
Treatment
Temperature: Has a big effect on normal intestinal motility in piglets; should be 32( to 34(C for unweaned pigs.
Antibiotics: E. coli develops resistance readily. Base on antimicrobial susceptibility test if possible. Probably best to treat the whole litter.
Fluids: Electrolytes with glucose and vitamin C are recommended.
Prevention
Sanitation and a dry warm environment.
Design of the farrowing crate: raised crates with perforated floors that allow the fecal material to drop through have a lower incidence.
Immunity is primarily via the blockage of adherence by anti-fimbrial antibodies in the sow's milk. A continuous supply of IgA is required to protect the pigs. Just getting colostrum isn't enough. Hypogalactia and nutritional imbalances (low vitamin E levels) can have a dramatic effect on the incidence of diarrhea.
Vaccination of the sows has been very beneficial in helping boost protective antibody levels in milk. Bacterins have replaced most of the live oral vaccines at the present time. However, it should be noted that vaccination against one fimbrial type often leads to an increased incidence of disease caused by other fimbrial types. Piglets start to produce their own antibodies at about 10 days of age and will develop active immunity to the various types of E. coli as the levels of protective antibodies in the milk decline.
CLOSTRIDIUM PERFRINGENS TYPE C ENTERITIS
A severe, usually hemorrhagic enteritis that usually affects pigs within the first week of life (usually the first 3 days). Infections may be observed in pigs 2 to 4 weeks of age but these are not hemorrhagic.
Epidemiology
Clostridium perfringens type C is maintained in the intestinal tract of carrier sows and transmitted to piglets through the feces. Transmission probably occurs within a few hours of birth. The intestinal tract of the young pig has not established it's normal flora at this time and C. perfringens is able to multiply to high numbers.
Clinical signs
May have peracute, acute, subacute and chronic manifestations of the infection.
Peracute disease is characterized by a hemorrhagic diarrhea and pigs may die within a few hours of onset. Occasionally, pigs may die without showing diarrhea.
Acute cases commonly survive about 2 days and characteristically have reddish-brown liquid feces that contain shreds of necrotic debris.
Subacute cases survive 5 to 7 days and do not have a hemorrhagic diarrhea. Their feces may be yellow but then change to a clear fluid. The pigs become progressively emaciated and dehydrated even though their appetites are relatively normal.
Chronic cases may be difficult to characterize. The pigs may have an intermittent diarrhea and merely be stunted or die after several weeks.
Necrosis of the intestinal mucosa usually does not occur in either the subacute and chronic forms of the disease.
Pathogenesis
Clostridium perfringens colonizes the small intestine and but does not invade the intestinal mucosa.
The organism produces a potent ß-toxin and antibody against this toxin is highly protective. The toxin is susceptible to proteolytic cleavage and is protected by the trypsin inhibitors in the sow's milk.
The jejunum is the most consistently affected and the lesions are generally confined to the small intestine and mesenteric lymph nodes. They may vary in location; however, and lesions have been observed in the colon.
Diagnosis
Gross lesions are highly suggestive. In the acute hemorrhagic form the lesions are almost pathognomonic.
Bacterial culture-easy in the acute cases, all but impossible to obtain a diagnosis using this in the chronic cases.
Mucosal scrapings--> Gram stain, should see large Gram-positive rods, often in large numbers.
Diagnosis of subacute and chronic forms of the disease usually requires histopathologic examination to demonstrate colonized villi.
Mixed infections: Once secondary bacteria invade the necrotic villi, it becomes impossible to differentially diagnose the disease from severe coccidiosis. Therefore histopath is needed on necrotic and non-necrotic areas of the intestine.
Treatment
Can treat with penicillin and antiserum orally and this may be of some benefit if the infection is detected very early. Once clinical signs become evident in the acute disease, it is difficult to treat.
Prevention
Antitoxin. In an outbreak one can give Type C antitoxin parenterally. This needs to be done soon after birth.
Vaccination of sows with toxoid: One dose at breeding or mid-gestation and a second dose 2-3 weeks before farrowing. Booster 3 weeks before each farrowing. Provides good protection for most farms. On some farms clostridial enteritis is a difficult disease to control, even with a good vaccination program.
CLOSTRIDIUM PERFRINGENS Type A
Produces disease in both neonatal and post-weaning swine. The type of disease depends upon the age of the pigs and whether the infecting strain produces an enterotoxin. The beta-2 toxin seems to be the most important in production of disease. In neonatal pigs, disease usually begins within 48 hr. of birth and may last up to 5 days. The feces are usually pasty, soft and mucoid. Infections with C. perfringens type A cause only a transient watery diarrhea. Pigs 5 to 7 weeks of age may develop diarrhea or soft feces. The diarrhea does not result in death but may suppress the rate of gain.
Diagnosis is based on culturing C. perfringens type A from the affected areas of the intestine and subsequent laboratory demonstration of the beta-2 toxin.
Vaccination. A toxoid for C. perfringens Type A is currently being marketed with a conditional license (as of 2006).
Clostridium difficile
C. difficile is being recovered from neonatal pigs (1-7 days of age) and is apparently a common cause of mesocolonic edema. Affected pigs develop a relatively mild diarrhea with dehydration and unthrifiness. Recent figures from the ISU VDL indicate that it is currently one of the most common organisms associated with diarrhea in neonatal pigs.
Epidemiology: Fecal oral transmission is assumed. There is some indication that antimicrobial therapy may play a role in development of disease similar to the situation seen in humans with pseudomembraneous colitis. However, the gut of the neonatal pig probably has not established its normal competitive microflora and this may provide adequate opportunity for the organism to multiply.
Toxins: The organism produces two toxins, A and B that are associated with disease production. Toxin A is an enterotoxin and B is a cytotoxin.
Clinical signs: Usually a mild diarrhea that may have a (creamy( consistency.
Lesions: The most consistent finding is mesocolic edema although this is generally considered to be a non-specific finding. This is currently the most common cause of colitis in neonatal piglets.
Diagnosis: The toxins are apparently labile and submission of live pigs or colonic contents that have been immediately frozen is essential. A commercially available ELISA (TechLab Tox A/B) is used. Culturing the organism is difficult. If colitis is seen on histopath in this age group of pigs, the probability is about 84% that it is associated with C. difficile.
Prevention and Treatment?
TRANSMISSIBLE GASTROENTERITIS
A highly contagious enteric disease of swine characterized by vomiting, severe diarrhea and a high mortality in piglets under 2 weeks of age. All ages of pigs are susceptible to infection but the mortality rate drops dramatically with increasing age. The disease is most costly when outbreaks occur during farrowing time and the majority of clinical disease is observed in the winter months.
Etiology
TGE virus is a coronavirus that is antigenically related to canine coronavirus (CCV) and FIP virus of cats. It is apparently not antigenically related to hemagglutinating encephalomyelitis virus (HEV) or porcine epidemic diarrhea virus (PEDV) which are also coronaviruses infecting swine. Recently, a porcine respiratory coronavirus (PRCV) has been described which is antigenically related to TGEV. Initial data indicate that PRC is not associated with the production of enteric disease. However, antibody against this virus is cross-reactive with TGEV and can lead to false positive serologic test results.
Epidemiology
The virus is transmitted readily by aerosol and also shed in the feces. Infection occurs when the virus is swallowed. The incubation period is 18 hours to 3 days and the virus spreads rapidly through a group of swine.
Surveys have indicated from 19 to 54% of swine in the US and Europe have been infected based on serologic evidence. The virus is quite labile when exposed to sunlight, drying, heat, and disinfectants. However, it survives for long periods of time in frozen tissues. This has been used as an explanation for the appearance of the disease primarily during the winter months. In addition, reduced or fluctuating ambient temperatures predispose pigs to infection with the virus and the resulting diarrheic state leads to increased shedding. The virus may also be shed in milk and possibly via a respiratory route.
The virus may also spread subclinically through a group of susceptible swine (especially older pigs) and be maintained in a herd. Continuous or frequent farrowing operations will maintain the virus in this manner. Carriers have been demonstrated but the role of the long-term carrier has not been determined. Pigs have been shown to harbor the virus for up to 104 days but not transmit it to sentinel pigs. TGE may also be transmitted by other hosts. Starlings have been shown to shed the virus for up to 32 h following experimental exposure. Cats, dogs, and foxes may shed the virus for long periods in their feces. The virus from the dog was found to be infectious for pigs.
Clinical signs
In young piglets one sees transient vomiting, watery and usually profuse yellowish diarrhea, rapid dehydration and weight loss. Growing and finishing pigs and sows have anorexia and diarrhea for a short period (1 to a few days) and an occasional animal may vomit.
Epizootic TGE occurs where most of the swine in a herd are susceptible. It spreads rapidly to all ages of pigs, especially during the winter.
Suckling pigs become very sick, dehydrated, and die rapidly with mortality rates of almost 100%. Pigs 2-3 weeks of age have a high mortality rate but this drops dramatically by 5 weeks of age.
Some lactating sows become very sick, have an elevated temperature, vomiting, diarrhea and agalactia which leads to increased baby pig mortality.
Enzootic TGE results when susceptible swine are frequently or continually introduced into a herd (such as in continuous farrowing operations or where feeder pigs are purchased). Even in operations that do not use a continuous farrowing system, the infection can become enzootic. As colostral immunity wanes, pigs become infected and show mild but typical signs of TGE. Mortality may be as high as 10 to 20% depending upon the age when infected. Most pigs with clinical disease are going to be between 6 days and 2 weeks of age. A factor complicating diagnosis is that most pigs normally scour a little when weaned.
Intermittent Enzootic TGE is caused by the re-entry of the virus into a herd which contains immune sows. This is seen in areas of concentrated swine production. Each winter the herd becomes re-infected and disease is seen primarily in growing and finishing swine. If the disease is transmitted into the farrowing house, young pigs will develop disease typical of the enzootic form.
Lesions
Dehydration and distention of the small intestine with yellow and frequently foamy fluid with flecks of curdled milk.
Marked shortening or atrophy of the villi in the jejunum and, to a lesser extent, the ileum. This is usually much more extensive and severe than that seen in rotavirus diarrhea.
Diagnosis
Detection of viral antigen in frozen sections with immunofluorescence or immunoperoxidase tests. This is best done on pigs in the early state of diarrhea because the epithelium is lost as the disease progresses and the peak amount of virus is present at this time.
Serologic diagnosis can be useful if paired serum samples are used.
Differential Diagnosis
Rotavirus
E. coli
Coccidiosis
Treatment
In very young pigs, the mortality rate is going to be almost 100 percent no matter what the treatment regimen.
Increase the ambient temperature (above 32(C) and provide dry, draft free environment.
Symptomatic: Water, milk replacer, and electrolyte solutions freely available to infected pigs to alleviate dehydration, acidosis, and starvation.
Cross-suckling pigs onto immune sows was found to be helpful.
Prevention and Control
Vaccination
Oral administration of virulent autogenous virus (feedback) to sows at least 3 weeks before farrowing. Stimulates high IgA levels and is relatively successful.
When confronted with an outbreak of TGE in a large farrowing operation, it has been proposed that all sows more than 2 to 3 weeks from farrowing be exposed to the virulent virus at the same time. The strategy is to have the whole population of breeding swine develop immunity simultaneously and prevent the development of enzootic TGE. This seems to work as long as each sow or gilt is individually dosed with the live virus so that infection can be ensured. Putting the virus in the feed may not be sufficient.
Oral or intranasal attenuated vaccines have not been as successful: May not survive the stomach and may not replicate sufficiently in the gut.
Parenteral vaccination of sows with commercial vaccines resulted in a decreased (but still high) mortality in piglets. IM vaccines result in high IgG titers but little or no IgA which is important for intestinal immunity. The same was true of intramammary vaccination. However, vaccination of infected sows resulted in an increase in IgA and IgG in the milk.
Management
Prevent introduction into a herd. Isolate swine coming into a clean herd. Swine recovering from an outbreak of disease can be introduced 4 weeks after the last clinical signs disappear. Control starlings and other birds, cats, dogs, etc. The virus can be transmitted on boots, feed trucks, etc. and this may constitute the major means of spread. Control access and supply clean footwear.
After an outbreak, vaccinate all sows that have more than 2 to 2 1/2 weeks before farrowing. Vaccination closer to farrowing may be beneficial but there may be a high percentage of sows that do not pass sufficient immunity to their pigs. One can try to control the exposure of these sows to the virus.
With enzootic TGE, vaccination with an attenuated virus may help, but changes in management practices to eliminate the continual influx of susceptible swine are probably warranted. One may wish to alter the farrowing schedule, temporarily utilize other facilities, or have smaller farrowing units to facilitate an all-in all-out system.
COCCIDIOSIS
General description
Coccidiosis was not generally recognized as a disease problem in swine until the middle 1970's. It generally produces a yellowish to grayish diarrhea in 7 to 14-day-old piglets but may affect pigs on concrete as young as 5 days of age in the summer months. The parasite is considered to be worldwide in distribution.
Etiology
Isospora suis is by far the major cause of porcine coccidiosis. Sows that are raised in dirt lots also carry Eimeria spp. but these are rarely involved.
Epidemiology and Transmission
It appears that little pigs become infected from residual organisms that build up in farrowing crates from previous litters of pigs. The sow apparently does not play a major role in the transmission of the parasites. Most clinical studies have been able to demonstrate the organism in only 1% to 3% of sows. The sporulated oocysts are very resistant to disinfectants and survive in high numbers in the farrowing crates. When neonatal pigs ingest the organism in high numbers, clinical disease is produced. Diarrheic pigs amplify the dose of organisms for other pigs.
Clinical signs
Yellowish to grayish diarrhea in usually in 7-14-day-old piglets.
Loose, pasty feces that become more fluid as the disease progresses. Piglets may become covered with the feces and remain wet and have a rancid odor. They continue to nurse but become dehydrated, develop a roughened haircoat and do not gain weight well. The severity of the disease varies among the pigs in a given litter.
The severity of disease is due primarily to the infectious dose of the parasite. Experimental inoculation of 200,000 oocysts of Isospora suis results in a relatively severe clinical disease and moderate to high mortality. A lesser inoculum may result in only diarrhea or the absence of clinical disease.
Lesions
Gross: Fibrinonecrotic membrane in the jejunum and ileum in severely affected pigs. The necrotic membrane is not seen in pigs that are not severely affected.
****Lack of hemorrhage- even in severe disease.****
Microscopic: Villous atrophy, villous fusion, crypt hyperplasia, necrotic enteritis and loss of enterocytes at the tips of the villi.
Diagnosis
Main differential diagnosis is chronic clostridial enteritis.
Histopath: Most accurate method. Demonstrate the paired Type 1 merozoites. If the intestine is necrotic, one must examine both necrotic and non-necrotic areas.
Mucosal scrapings: Better than fecal samples. Demonstrate the paired Type 1 merozoites.
Fecal samples: Demonstrate the oocysts on direct exam or flotation. Hard to do unless on removes the lipid from the sample with solvents. Sample several litters that have had diarrhea for 2 to 3 days. This is the peak period of oocyst production. Oocysts usually do not appear in the feces until a day or so after onset of clinical signs.
Treatment
Supportive. Coccidiostats have not produced good results.
Prevention
Sanitation is the key. Farrowing crates need to be steam cleaned and thoroughly disinfected between litters. Strong bleach (50% solution) or ammonia compounds are active against Isospora suis but the steam cleaning seems to be the most important part.
Concrete and wood floors harbor large numbers of the organisms and can be very difficult to deal with. One can seal surfaces with waterseal or paint to break the cycle. Coccidiosis is the main reason that raised, wire bottom farrowing crates were developed. We now use coated metal for farrowing crates that is easier to clean.
PORCINE ROTAVIRUS
Most rotavirus infections of young pigs are either subclinical or mild and piglets recover without treatment. However, rotaviruses have been associated with outbreaks of severe clinical disease in the absence of other demonstrable agents, especially in newly weaned pigs. In addition, disease can be seen in new gilts or in very young pigs when a new virus strain enters the herd. Other agents such as E. coli and TGEV and adverse environmental conditions seem to enhance the severity of the disease.
Etiology
Rotaviruses are widespread in many animal populations and the rotaviruses of several other animals are capable of infecting gnotobiotic piglets and causing seroconversion. The virus is quite resistant to many normal disinfectants, heat, and adverse environmental conditions. Rotaviruses in pigs are divided into Groups A, B, and C and there have been at least 4 serogroups identified within Group A alone. Groups B and C probably have serogroups as well. Thus rotaviruses are actually a whole series of viruses that are not cross-protective. About 75% to 80% of pre-weaning rotavirus infections are Group A. About half of postweaning infections are caused by Groups B and C. Pigs may undergo multiple rotavirus infections.
Epidemiology
Porcine rotavirus is widespread in swine; most animals become infected early in life from viruses that are circulating through the population. Almost all pigs will shed rotavirus within 5 days after weaning. Spread of the virus is through ingestion of fecal-contaminated material.
Clinical signs
The severity of the disease is quite variable. Concurrent infection with rotavirus and hemolytic (usually K88) E. coli is the most common cause of postweaning diarrhea. The incubation period is 12 to 24 h. Depression, anorexia, and reluctance to move are observed. Vomiting may occur immediately after feeding. A profuse diarrhea develops and pigs become severely dehydrated and have up to a 30% weight loss. Mortality depends upon the age of the pigs at weaning and the amount of specific antibody in the sow's milk. Pigs weaned at a few days of age may have a very high mortality rate. Generally clinical signs in suckled piglets 10 to 21 days and older are mild. If infection occurs after weaning, the disease can be quite severe in pigs up to 3 to 8 weeks of age (mortality from 3 to 10% and occasionally up to 50%). Most adult sows have antibody to rotavirus but adult gilts occasionally may not.
Pathogenesis
Lesions are similar to those of TGEV but not as severe. Desquamation of villous epithelial cells results in loss of intestinal enzymes and interference with digestion and malabsorption.
Diagnosis
FAT on sections from the intestine of pigs in the earliest stages of the disease.
EM can be used
ELISA is used at ISU. It only detects Group A rotaviruses.
Treatment
Electrolyte-glucose or sucrose solutions have been demonstrated to be of benefit. A high quality diet following infection may lessen the impact of the disease in the recovery phase.
Prevention and Control
Thorough disinfection and a high level of cleanliness help to keep exposure to the virus low. It is a very difficult virus to eliminate and it is virtually impossible to eliminate from a whole farm.
Vaccination has been tried but the presence of multiple serotypes and the fact that colostral immunity is not especially protective make the vaccines questionable. Vaccination of piglets is complicated by the presence of colostral immunity. Commercial vaccines are available but they are usually considered to be of little value.
Feedback of farrowing barn manure to sows can be used to booster the level of colostral immunity.
SWINE DYSENTERY
General description
A muco-hemorrhagic enteritis that usually affects 30 to 150 lb pigs but has been observed occasionally in all ages of pigs. It is very rare in nursing pigs. The disease was at one time relatively widespread in the swine population (a 1982 study revealed that it was present in 40% of herds in Iowa, Illinois and Missouri). It is now seen infrequently because of the severe economic impact forced producers to either eliminate the disease or quit raising swine. It can be a cause of serious economic loss from mortality, poor growth performance, poor feed conversion, and the cost of treatment and control.
Etiology
Brachyspira hyodysenteriae (Formerly Serpulina hyodysenteriae) is the causative agent of swine dysentery. Other spirochaetal agents are commonly present in the intestinal tract of pigs and some of these have been associated with a relatively mild disease. Recent attempts to classify many of the intestinal Brachyspira of swine have led to the recognition of a large number of proposed species, almost all of which have not been incriminated in disease. The presence of these organisms as normal flora makes diagnosis more difficult. One of the main weakly-beta-hemolytic sprirochetes (WBHS) is Brachyspira pilosicoli and it has been associated with relatively mild disease in swine.
Epidemiology
Disease seems to occur most commonly in late summer or fall and is often associated with stress. The incubation period is variable but is usually in the range of 10 to 14 days in naturally exposed pigs.
The organism is shed from the intestinal tract of swine for long periods of time following infection. Introduction of the organism into a herd is often through a carrier pig. Pigs were found to be shedding the organism in the feces 70 days following recovery from clinical disease. The organism can be transmitted to suckling pigs from the sow.
B. hyodysenteriae has been shown to survive for long periods of time in lagoon water, soil, feces, and in the intestinal tracts of mice and dogs.
Clinical signs
Diarrhea with variable severity is the most consistent sign. The disease progresses gradually through a group of swine. The initial diarrhea is characterized by a large amount of mucus often containing flecks of blood. As the disease progresses, watery stools containing blood, mucus, and shreds of fibrinous exudate are seen. Abdominal pain evidenced by an arched back may occur. Prolonged diarrhea results in dehydration and eventual emaciation.
The disease may give the appearance of being cyclic in a group of swine. Clinical signs will disappear and then reappear at 3-4 week intervals. This is especially true if the pigs are stressed at these times (respiratory disease, etc.).
In peracute disease, animals may be found dead without previous clinical signs but this is relatively rare. Also rare, disease in suckling pigs may be characterized by a catarrhal colitis without hemorrhage.
Pathogenesis
The causative organisms do not invade beyond the lamina propria. Lesions are confined to the large intestine. The roles of endotoxin and the hemolysin in the pathogenesis of the lesions have not been thoroughly defined. No enterotoxins have been described. Fluid losses appear to be the result of a failure of the colonic mucosa to reabsorb endogenous secretions because of a failure to actively transport sodium and chlorine from the lumen to the blood.
Diagnosis
Clinical signs
Direct exams of colonic mucosal scrapings: Crystal violet stain. Other spirochaetes can be quite numerous so one must be cautious not to over-interpret direct smears.
Bacteriologic culture: Best to rely on this. The numbers of organisms present may be low in chronically diseased or treated pigs.
Differential diagnosis
Salmonellosis: Usually see lesions and bacteria in sites in addition to the large intestine.
Intestinal adenomatosis: Lesions in the small intestine and colon. Thickening of the gut wall.
Trichuriasis: Heavy infestations can look very similar to swine dysentery. Should be able to find Trichuris suis in the large intestine (may hide in mucus and necrotic debris). May have mixed infections with B. hyodysenteriae.
Prevention
Herds infected with Brachyspira hyodysenteriae should be quarantined and no animals allowed to move from them unless to slaughter. Given the current market situations, it is economically not viable to have a swine unit where B. hyodesenteriae is a problem. If a herd is identified as having B. hyodysenteriae, isolation of the herd and rigid sanitation are essential because of the ease of transmission of the organism on boots, equipment, etc.
Quarantine of new stock.
Depopulate in warm dry weather and repopulate with SPF swine. Thorough disinfection is a must and it may be impossible to rid some facilities of the organism. The organisms can live in small cracks in concrete, in lagoons and in the intestinal tracts of other animals.
Medicate the sows with Denagard (tiamulin), increase sanitation, and early weaning may be successful in some herds but the organisms are not completely killed by this method.
Prophylactic medication is usually too costly.
Treatment
A number of drugs were commonly used therapeutically. These included Bacitracin, Carbadox, Mecadox, Gentamicin, Lincomycin, Tiamulin, Tylosin, Virginiamycin and others. Resistance has been reported with some of these.
Medication in acutely affected swine must be given in the drinking water (the pigs aren't eating) or parenterally. Parenteral injections in a large group of swine are time consuming an may not be practical.
Brachyspira pilosicoli
General. Causes porcine intestinal spirochetosis, PIS and human intestinal spirochetosis, HIS and is possibly involved in intestinal infections in other animals.
Distribution. Worldwide in swine, humans and can be demonstrated in other animals. It is one of the organism referred to as a weakly beta-hemolytic intestinal spirochete. Most of these organisms were formerly referred to as Brachyspira innocens, a non-pathogenic spirochete, but most of these isolates were actually B. pilosicoli.
Disease.
Swine. Characteristically, it attaches in large numbers to the colonic epithelium by one end of the bacterial cell. Produces a diarrheal disease most commonly seen in the immediate postweaning period in pigs but can occur anywhere from 4 to 20 weeks of age. The major clinical signs include weight loss, poor growth rate, and diarrhea with occasional flecks of blood. Generally thought to produce a milder disease than B. hyodystenteriae.
Humans. Human intestinal spirochetosis is also characterized by the end-on attachment of large numbers of the organism. The disease is most commonly seen in people in lesser developed countries and AIDS patients, May be associated with a variety of intestinal disorders, but most commonly with rectal bleeding and chronic diarrhea. There is still some doubt in the literature as to whether this is the same organism as seen in PIS although it has been demonstrated experimentally that organisms isolated from humans can cause disease in pigs.
Others. May be associated with intestinal damage in other species of animals especially dogs. Experimentally at least, the organism can cross species barriers and produce disease in other animals.
Other intestinal spirochetes
Brachyspira innocens. Most of the isolations of this organism were actually B. pilosicoli. The organism was thought to not be significant in intestinal disease.
Many other intestinal spirochetes exist but have not currently been associated with disease production.
SALMONELLOSIS
Etiology
The clinical disease seen in salmonellosis of swine is greatly dependent upon the particular serotype of Salmonella involved. The great majority of the clinically significant infections (>90%) are caused by S. choleraesuis var. Kunzendorf. Infections with this organism are most often characterized by a septicemia with accompanying respiratory and systemic signs. The presence of enteric disease is quite variable. S. typhimurium is much more likely to produce enteric disease and is much less frequently isolated as a cause of acute clinical illness. S. typhisuis is relatively rare and is not usually involved in enteric disease. Other serotypes are occasionally involved. Since the two serotypes produce somewhat different diseases they will be presented separately.
Salmonella choleraesuis
Epidemiology
Infected, shedding pigs are the most important source of S. choleraesuis.
Length of carrier period
Numbers of organisms shed in feces
Role of stress and transport in shedding
Crowding
Intestinal hypermotility
Disease
Most common in weaned pigs less than 4 months old but will occasionally occur in market age and older swine. Infections in suckling pigs are considered to be very rare but, recently, infections have been recognized in very young pigs. In these pigs, there is often a marked petechiation of the intestinal serosa.
Septicemia (endotoxemia, DIC)
Sudden death in one or more animals
High fever: 105( to 108(F
Mortality usually less than 5 to 10% of a group. In farrow-to-finish operations the mortality is commonly about 2-3% but where feeder pigs are purchased and there is more stress, mortality can be high. Dr. Kunesh has seen 100% mortality in highly stressed pigs under poor housing conditions.
Enterocolitis: Diarrhea is sporadic and more frequent in nursery age pigs.
Pneumonia: Frequent complaint
Meningoencephalitis
Gross lesions
Cyanosis of ears, feet, tail and ventral abdominal skin. Splenomegaly, hepatomegally, swollen lymph nodes (especially mesenteric). Lesions are often present in the intestinal tract in animals that have survived for a few days following the onset of severe disease.
Diagnosis
Culture: Mesenteric lymph nodes, lungs, liver, spleen, ileocecal junction.
Fecal cultures
Histopath
Treatment
Acute septicemic disease: Separate the affected animals. Probably some benefit to antibiotic therapy. It may buy some time. Anti-inflammatories may be indicated.
Studies have shown little effect of antimicrobial therapy on shedding.
Prevention
Management
Sanitation
Crowding
Vaccination: Modified live vaccine is thought to be efficacious. There are live oral and parenteral (IM) vaccines on the market. The S. choleraesuis vaccines appear to have had a fairly major impact on the decreasing prevalence of clinical disease.
Antibiotics? These can be useful but are probably not the answer in the longer term.
Salmonella typhimurium
Epidemiology
Thought to be more widespread in the general swine population than is S. choleraesuis but it is isolated from clinically diseased pigs much less frequently. Maintained in the intestinal tract and associated lymphoid tissues for long periods of time. It is a common cause of salmonellosis in many other species of animals, thus it can be transmitted to swine rather easily. It can also be transmitted through the feed. Most recovered pigs remain as carriers and intermittent shedders for several months.
Disease
Enterocolitis: Watery, yellow diarrhea, initially without blood or mucus. May last 3-7 days and recur 2 or 3 times. Blood may appear in the feces but not in profuse amounts as is seen in swine dysentery.
Septicemia: Some outbreaks of disease may mimic infections with S. choleraesuis.
Some pigs may remain unthrifty and develop rectal strictures. Rectal strictures are thought to be secondary to rectal prolapse. Some work indicates that severe enteric disease may precede the development of the strictures.
Lesions
Diffuse ulceration and less commonly button ulcers in the small intestine and colon.
Mesenteric lymphadenitis
Rectal strictures?
Salmonella typhisuis
Causes a relatively specific chronic disease syndrome with necrotic colitis, caseous lymphadenitis, and bronchopneumonia. The organism is not often isolated (grows more slowly than other Salmonella). Intestinal lesions may have healed leaving only the lymphoid and pulmonary lesions.
Salmonella dublin and S. enteritidis
Both of these have been described as causes of meningitis in suckling pigs.
PORCINE PROLIFERATIVE ENTEROPATHIES
General Description
Group of conditions that differ markedly in gross appearance but which all involve a thickening of the mucous membrane of the small and sometimes the large intestine. They are characterized by proliferation and immaturity of the intestinal epithelium.
Etiology
Lawsonia intracellularis. Australian workers have also described a different organism, Campylobacter hyoilei as a causative agent but little work has been done on this organism since its initial description in 1995. L. intracellularis is found intracellularly in the apical cytoplasm of affected epithelial cells. L. intracellularis apparently does not cause disease in germ-free pigs and there is apparently some type of (permissive( role for normal gut flora.
Epidemiology and Transmission
The condition affects swine worldwide and the organism is most likely transmitted through the feces. Recent serologic studies in the U.S. using NAHMS (National Health Monitoring Service) have indicated a very high percentage of swine herds have the organism present (98%) with about 20 to 30% of the swine in an infected herd having the organism. This does not necessarily mean that they are showing clinical disease. There is evidence that other species of animals may be affected by an identical or similar organism but the role of these animals in transmission of the organism is probably minimal.
Transmission is by the fecal-oral route. PCR has detected infection in piglets as young as 7 days of age, indicating that vertical transmission from the sow occurs rapidly. Also, attempts to use MEW to prevent the transmission of the agent to a group of pigs have failed, leading one to believe that it is transmitted from the sow to the pigs at an early age. Once in a group of pigs lateral transmission is the most important route. Infected pigs excrete the organism for at least 10 weeks post infection. If sows are acting as the original source of the organism, they must remain infected for much longer periods and perhaps for life.
Colostral antibody is at least partially protective. In infected herds, most natural infections (as measured by seroconversion or clinical disease) occur after 8 weeks of age suggesting that maternal immunity may be protective for this length of time. In infected herds, slow, progressive seroconversion occurs during the grow-finish stage with clinical disease rates being highly variable.
One of the major problems with this organism seems to be with outbreaks of the disease in replacement gilts during the acclimation/early breeding/gestation periods.
The organism may survive 1 to 2 weeks in the environment under cool conditions. Survival under moist, warm conditions is apparently quite good. Approximately 75% of cases of PPE occur between May and September. The organism is susceptible to quaternary ammonium and iodine-based disinfectants when not protected by fecal material.
Clinical Signs and Lesions
PIA: Porcine intestinal adenomatosis. Uncomplicated proliferation upon which NE, RI and PHE conditions may be superimposed. Occurs most commonly in the 6 to 20 week age range but some feel it occurs most commonly in the grow-finish stage. In many cases the clinical signs may be very slight and the swine not considered to have a problem. Most often there is a variable percentage of a given age group affected. In other cases the disease may result in a marked dullness, apathy and anorexia. There may be little or no diarrhea. Recovery from uncomplicated PIA occurs in 4 to 6 weeks and the pigs regain their appetite and rate of growth.
Lesions: Most commonly in the terminal 50 cm of the small intestine and upper 1/3 of the colon. The wall is visibly thickened, some serosal and mesenteric edema is common, deep folds in the mucosa of the large intestine.
RI: Regional ileitis. Occurs most commonly in the 6 to 20 week age range with pigs about 12 weeks of age most commonly affected. More severe clinically than PIA; severe loss of condition and persistent diarrhea. Smoothly contracted, almost rigid lower small intestine: "hose-pipe gut", usually with prominent granulation tissue and a striking hypertrophy of the outer muscle coats.
NE: Necrotic enteritis. Occurs most commonly in younger pigs (early nursery age) but has been reported in the 6 to 20 week age range. More severe clinically than PIA; severe loss of condition and persistent diarrhea. Coagulative necrosis with inflammatory exudate that appears as yellow-gray cheesy masses that tightly adhere to the intestinal wall. In chronic cases, granulation tissue may become prominent. Many pigs never fully recover.
PHE: Proliferative hemorrhagic enteropathy. The diarrhea is described as having the appearance of (A-1 Sauce(. Occurs most commonly in young adults. The disease is particularly troublesome in replacement gilts and sows. These animals can develop a severe hemorrhagic enteritis and die acutely in some cases. Lesions in the large intestine are rare. The lumen of the ileum may contain a well-formed blood clot and the colon may contain black, tarry feces. Bleeding points, ulcers and erosions are not evident and the mucosa may show little damage except for the adenomatous changes and congestion. Histologically there is extensive degeneration of the epithelium, accumulation of cellular debris in the crypts and the formation of goblet cells in the deep crypts.
Diagnosis
Clinical signs are suggestive but are not well correlated with severity of lesions except in the PHE form of the disease.
Gross lesions are highly suggestive but there can be a normal thickening of the ileum adjacent to Peyer's patches subsequent to chronic inflammation due to other causes.
Immunohistochemistry on formalin-fixed tissues has been adopted by the ISU VDL. The sensitivity of this method is said to be far better than the old silver staining technique. Many labs do IHC on fecal samples. Antimicrobial treatment apparently does not diminish one(s ability of diagnosing the infection, especially with IHC.
PCR is performed on fecal samples by some labs but the feces need to be from clinically affected animals to be reliable.
Silver stains, FA, ELISA and others if available. Mucosal smears: Ziehl-Neelsen
Treatment
Several antibiotics have been demonstrated to be effective in treatment. Tylan, Tiamulin and chlortetracycline,lincomycin and Carbadox are used for treatment. Tylan and lincomycin are currently the only drugs approved for use against Lawsonia intracellularis in the U.S.
Prevention
Increased attention to sanitation and biosecurity plus AIAO strategies with thorough cleaning and disinfecting between groups are a good idea, but are not especially valuable with PPE. This is one disease that remains a problem even in high health status herds.
Vaccination. Apparently the vaccines can lessen the disease by decreasing the magnitude of colonization. Not all pigs receiving the vaccine seroconvert. Also, the vaccine organism cannot be differentiated from field stains and is shed from the vaccinated animals. Animals must not be receiving antibiotics at the time of vaccination.
Tetracyclines seem to be effective but there is some evidence for the development of resistance. However, the information may be compounded by poor diagnosis. Generally, intracellular organisms related to Lawsonia have few transferable plasmids and do not readily develop antimicrobial resistance.
NE may respond to Tylocin/sulfonamide combinations.
Continuous medication to slaughter with some antimicrobials has been tried but the value of this is difficult to evaluate. The method is costly and may not be wise in light of prudent antimicrobial use. When the medication is discontinued prior to slaughter, a large population of susceptible pigs may result.
Pulse (intermittent) medication is beneficial. The intermittent medication allows the pigs to develop an infection and respond immunologically.
NOTE:
A condition known as hemorrhagic bowel syndrome occurs in 120+ lb pigs. The pigs die quite suddenly and the intestinal tracts cotain blood. The cause or causes of this syndrome are not definitively known. Some feel that the bloody contents of the bowel is the result of volvulus or some other intestinal accident. Sometimes there is a history of the animals not having access to feed for a time and then overeating when they get a new batch of feed. Anecdotal evidence indicates that antibiotics may help (BMD-bacitracin, or tylan) and these are often tried. Hemolytic E. coli or other bacteria could possibly play a role. The disease tends to be sporadic and there is usually a low mortality rate.
EDEMA DISEASE
A complex disease characterized by the production of a vasoactive toxin and resultant CNS signs and edema at various body locations. The toxin is a variant of the Shiga-like toxin II or verotoxin and is also referred to as "edema disease principle".
Etiology
Edema disease-producing Escherichia coli usually have the following serotypes: O138:K81, O139:K82, and O141:K85. These three have been found to produce the vasotoxin. Other serotypes have been implicated. Fimbrial types F18ab and F18ac are commonly seen in E. coli from edema disease. Edema disease is apparently (enjoying( a resurgence in the swine population. Strains bearing the F18 fimbriae have recently been detected that carry genes for both vasotoxin and enterotoxin. Some of these can produce a combined disease.
Clinical signs
Sudden death of one or more pigs usually 1 to 2 weeks after weaning; Often the best-doing pigs in the group.
Incoordination, staggering gait, knuckling of the forelimbs, ataxia, paralysis, tremors, and paddling.
Edema: May be difficult to demonstrate or absent. Palpebral edema may be seen prior to the onset of CNS signs.
Diagnosis
Clinical signs: CNS
Edema, when present. Rarely seen in the stomach or colon any more.
Large numbers of hemolytic E. coli in the small intestine and colon. These can be serotyped if necessary.
Treatment
Restrict feed consumption and increase the fiber content of the diet. Increasing the fiber content may result in a pH change in the intestine as well as a decreased protein content and the normal flora may be altered as a result (theory).
Antimicrobials may be useful especially in the susceptibility pattern of the E. coli is known.
Prevention
Genetics: We now have the ability to genotype breeding swine and eliminate those animals that possess the receptor for F18 fimbria and are most likely to give birth to susceptible offspring. If a producer is having serious problems with edema disease CHANGE BOARS.
Good creep feeding program
Restricted feeding at weaning or feeding of higher fiber diets.
Vaccination with F18ab-bearing strains of E. coli has had reasonable success but F18ac strains are increasingly causing problems and the current vaccines do not include this fimbrial type.
HEMAGGLUTINATING ENCEPHALOMYELITIS VIRUS
Two forms of the disease: Acute encephalomyelitis and a chronic vomiting and wasting disease (VWD). Caused by a single serotype of a coronavirus. The disease appears in different forms probably because of differences in susceptibility of pigs and strain differences in the virus.
Epizootiology
Pigs are the only known host. The virus is apparently very widespread in the pig population with survey results varying from 0 to 98%. In one US study, the incidence of antibodies in sows at slaughter was 98%. Disease is relatively uncommon, however. Neonatal pigs are usually protected by colostral antibody and they subsequently develop an age-related resistance to potential clinical effects of the virus.
Clinical signs
Confined almost entirely to pigs less than 3 weeks of age. Sneezing and coughing may be noticed initially. The acute encephalomyelitic form has been described only in the US and Canada. In the VMD form, pigs may suckle for a short time, stop, and then vomit milk. The pigs may look listless, have an arched back, and huddle. Rectal temperature may be slightly elevated at first but quickly returns to normal. Abdominal distention may be noted in some pigs. Clinical signs may vary in severity from the acute form to VWD. Mortality approaches 100% within a litter and survivors remain stunted.
Pathogenesis
The virus initially replicates in the epithelial cells of the respiratory and small intestine, spreads via the peripheral nerves to the CNS. The vomiting is due to a disturbance in stomach emptying.
Diagnosis
Virus isolation is the best (has to be within 2 days of developing disease).
Serologic: Antibody is widespread in normal pigs. Rise in titer is difficult to demonstrate (pigs die).
Differential diagnosis
Pseudorabies
Teschen/Talfan
Streptococcal infections
All of these are usually more severe than HEV and often affect older pigs. Pseudorabies produces respiratory signs in older pigs and abortions in sows.
Prevention
Maintain the infection in the subclinical form so that sows pass protective antibody to the piglets.
ERYSIPELAS
An acute to chronic disease of swine characterized in its various forms by septicemia, arthritic and/or skin lesions.
Etiology: Erysipelothrix rhusiopathiae
Epidemiology
Distributed worldwide and of economic significance in the swine and turkey industries in the US. It is estimated that 30 to 50% of swine carry the organism. Pigs carry the organisms in their tonsils and shed it in their feces. Acutely affected swine shed the organism in most body fluids.
The organism can survive up to 35 days in the soil and feces in a hog lot. The organism is very widespread in a number of animal species but the disease that we see in swine is quite serotype specific (predominantly serotypes 1 and 2).
Incidence is highest in swine 3 months to 3 years of age. (Passive immunity in the young and subclinical infections as immunity wanes?)
Infection probably occurs most commonly from ingestion and introduction through wounds.
Acute disease
Characterized by septicemia, high fever, stiffness and reluctance to move (arthritis), depression, splenomegaly, petechial hemorrhages, and sudden death. Sows may abort. Diamond skin disease is considered to be a milder form of the acute disease.
Chronic disease
Characterized by arthritis that can progress to ankylosis. Valvular endocarditis can lead to cardiac insufficiency and sudden death under stress.
Disease in both forms may be due to the production of neuraminidase which cleaves neuraminic acid (sialic acid) found on host cell surfaces.
Diagnosis
Clinical exam
Bacteriologic culture: The organism is readily cultured in the acute disease from many organs. The organism can be recovered from arthritic joints for up to 3 to 6 months following initial infection.
Response to penicillin
Differential diagnosis
Acute ASF and HCV
Salmonellosis
Actinobacillus
Swine pox: Generally a mild disease seen occasionally in the US.
Prevention
Management, housing, etc, are very important. Concrete floors are better than dirt floors.
Eliminate chronically infected animals
Vaccination
Attenuated live vaccines: Strains with low virulence for swine. Antibody and antibiotics interfere with the vaccination.
Killed bacterins: Formalinized whole cultures of selected strains of serotype 2 are used. These contain an important soluble immunizing glycolipoprotein that is released into the medium. Lysate bacterins have been widely used. Protective in 2 to 3 weeks.
Efficacy: Adequate long-term protection is not provided by any of the current products. Immunity wanes in 3 to 6 months. None of the products protect against the arthritic form of the disease, although by reducing the incidence of the acute disease, the chronic form is reduced. Vaccine failures may be partially due to serotype differences.
Mycoplasma hyorhinis polyserositis and arthritis
General
Acute, subacute and chronic polyserositis and arthritis occurring in swine from 3 to 10 weeks of age. Characterized by serofibrinous inflammation of the serous membranes and joints. Occurs occasionally in highly susceptible (SPF) young adult swine.
Etiology and transmission
Mycoplasma hyorhinis. Adult swine are carriers but the percentage in an infected herd is probably fairly low. The organism spreads rapidly within a litter and many pigs have a nasal and tracheobronchial infection without clinical signs of pneumonia. If seen, clinical disease occurs at 3-10 weeks of age and occasionally in young adult swine. It is a frequent secondary invader in M. hyopneumoniae pneumonia as well as other types of respiratory and enteric disease.
Clinical signs
There is a progressive onset of disease with labored breathing, abdominal tenderness, decreased feed intake, lameness, temperature of 104 to 107(F and sternal recumbency. Some pigs recover rapidly while others have clinical signs of disease for several weeks. There is generally a low to moderate mortality. Poor sanitation, movement into a new herd, and other environmental and management factors predispose to clinical disease.
Gross lesions
There is a serofibrinous inflammation of membranes lining the pericardial, pleural and peritoneal cavities. Synovial membranes are swollen, edematous and hyperemic. Affected joints contain a serofibrinous to serosanguineous fluid. In chronic disease, adhesions develop in on the serosal surfaces. A chronic arthritis with villous hypertrophy and articular damage may be seen.
Diagnosis
Gross lesions. Very suggestive but there are other causes
Bacteriologic culture of the joint fluid or exudate from serosal surfaces. The organism may persist for several months in the lesions.
Prevention
Minimize stress and control other respiratory diseases.
There is no vaccine available.
Treatment
Not very beneficial on an individual animal basis. Treatment of the whole herd or affected group with tylosin, lincocin, or tiamulin may be of some aid.
Mycoplasma hyosynoviae ARTHRITIS
M. hyosynoviae is the cause of acute, subacute and occasionally chronic, non-suppurative arthritis occurring in swine from 80 lb. to market weight. The condition occasionally affects young adult swine.
Transmission
M. hyosynoviae is carried in the pharyngeal secretions and tonsils of many adult swine. It is intermittently shed in nasal secretions and usually transmitted to a few piglets in a litter prior to weaning. The organism spreads laterally through the group. Management and environmental factors that cause stress predispose to disease.
Clinical signs
Many infected pigs show no disease. In those that show signs, there is a sudden onset of lameness in one or more limbs that may shift from one limb to another. There is usually little evidence of joint swelling. The acute stage of the disease lasts 3 to 10 days and some pigs may develop chronic lameness. There is no mortality but morbidity can range from 5 to 50% in a group. Heavily muscled pigs with poor leg conformation and angularity are predisposed to joint damage and osteochondrosis and are more commonly affected.
Lesions
Affected joints have increased synovial fluid that is serofibrinous to serosanguineous in nature. The synovial membranes are edematous, hyperemic and have a yellowish coloration. As the disease becomes chronic, there may be damage to the articular surfaces but this is most likely due to osteochondrosis.
Diagnosis
Clinical signs are suggestive but not sufficient for etiologic diagnosis.
Culture. Preferably submit 2 untreated pigs with typical acute disease to a diagnostic laboratory. Samples can also be collected from live animals or at slaughter. Synovial fluid should be aseptically removed, frozen and submitted to a diagnostic laboratory. The organism disappears from the joints rapidly.
Prevention
Purchase breeding stock with no history of arthritis or leg conformation problems.
Prevent stress when the pigs are most susceptible to disease (12 to 24 weeks of age).
Treatment
Separate affected animals.
Antibiotics: Tylosin, Lincocin, or Tiamulin
SWINE REPRODUCTIVE DISEASES
OVERVIEW
There are many documented causes of reproductive failure in swine. It is wise to keep in mind that illness of any type including septicemia and toxemia can be a cause of decreased reproductive performance. The following is a list of possible causes:
Brucellosis
Has not been reported from Iowa since 1972 and we are a "Validated brucellosis-free area". Regulations regarding testing of swine have recently been relaxed. One may see abortions in all stages of gestation, arthritis, and orchitis.
Leptospirosis
Abortions in the third trimester, stillbirths, weak piglets. When infection enters a "clean" farm one sees acute forms of the disease. L. pomona has traditionally been the most common cause.
Pseudorabies
Abortions in any stage of pregnancy, stillbirths, young pigs with CNS signs, respiratory signs in others.
Influenza
Explosive febrile outbreaks affecting almost all pigs in a group. Abortion and infertility have been described but may not have been due to the direct effects of the virus.
Parvovirus
Fetal death and mummification depending upon the stage of gestation (must be prior to 70 days or the fetus will develop an immune response and survive).
SMEDI
Stillbirth, Mummification, Embryonic Death and Infertility: Caused by a group of enteroviruses. Disease was supposedly similar to parvovirus-caused disease. This term has fallen out of favor with almost everyone and is no longer used.
EMC
Encephalomyocarditis virus causes acute abortions and sudden deaths with myocarditis.
Eperythrozoonosis
Somewhat controversial as a cause of abortion. Acute abortions at term or chronic infertility (both are infrequent).
Campylobacter
Fifty percent of Danish abortions are isolation positive. The strains are different from swine intestinal campylobacters.
HEV
Hemagglutinating encephalomyelitis virus (Coronavirus). A prevalent virus but disease is seldom reported. Infrequent cause of term abortions and stillbirths.
Blue eye
A paramyxovirus reported in Mexico in 1986. Stillbirths, mummification, infertility. The main clinical presentations are CNS signs in pigs under 30 d of age and corneal opacities in older pigs.
Chlamydia
Abortions in any species of animal.
PRRS
Abortions, stillbirths, weakborns and occasional mummies. Respiratory disease in nursing pigs.
Mycotoxins - Vomitoxin
Streptococcal
Beta-hemolytic streptococci are often isolated from the vagina of both normal and infected sows and from aborted fetuses. Streptococcal metritis is linked to abortions and piglets that have a high incidence of streptococcal joint ill and navel ill. Some herds can have up to a 70% mortality in baby pigs. Antibiotics in the feed are useful in prevention. Vaccination has not been very successful in controlling the disease.
PSEUDORABIES
General
With the advent of more intensive swine-rearing operations and continuous thru-put, this disease became a serious problem in the U.S. Prior to the 1960's this was a relatively sporadic disease. We were making good progress in Iowa until 1999 when we had a rather massive outbreak that continued into 2001. Very aggressive eradication measures have drastically decreased the incidence of disease in Iowa. The state was declared free of pseudorabies in 2004. The disease is basically one of reproductive failure in breeding swine, CNS disease in suckling pigs or respiratory disease in older swine. Once the virus has established itself in a herd, infection may be asymptomatic or produce only respiratory disease in finishing age swine.
Etiology
An alpha Herpesvirus. There is essentially only one serotype of the virus but there are a number of minor differences between isolates that can be demonstrated with monoclonal antibodies or analysis of DNA.
The roles of a number of different viral proteins have been described.
gII, gIII, and gp50 glycoproteins seem to be the most important for induction of immunity.
The genes for gI, gIII, gX, and TK (thymidine kinase) can be deleted and the virus remains viable although reduced in virulence. Deletion of one or more of these proteins has been utilized in generation of vaccines.
Transmission and Epidemiology
Herpesvirus: Latency: Stress
The primary means of transmission into a herd is through introduction of actively shedding or latently infected pigs (95% of cases).
Does not survive well on fomites under dry, warm conditions but will survive up to a month under cold, moist conditions.
Dogs, cats, rodents, and raccoons are all dead-end hosts and can play a role in transmission.
Recent evidence from our most recent outbreak indicates that the virus can become airborne and travel at least mile or so. The (epidemic( of pseudorabies that occurred in 2000 in Iowa occurred in the areas where swine were intensively reared. Unusually moist, warm weather in the late fall and winter months apparently allowed the virus to remain viable an be transmitted on the prevailing winds.
Once in a herd, the virus spreads by direct contact, inhalation, ingestion, breeding, and transplacentally.
The virus may be spontaneously eliminated from a herd under some types of management systems (may take 2 years or so), but will continue to thrive under continuous thru-put systems with a constant supply of susceptible animals.
Clinical signs
Age of the host is very important but signs also vary with the particular strain of virus and the infectious dose.
Also depends greatly on prior exposure of the herd.
Neonatal pigs: High fever, CNS signs (trembling, incoordination, dog-sitting due to posterior paralysis, head tilt, ataxia, paddling, etc.) and sometimes vomiting and diarrhea.
When dams have varying immune status, some litters will be affected and others will be normal. Individual litters may have both normal and unaffected pigs.
Mortality is usually 100% in affected pigs.
Once the infection has gone through a herd and the sows are routinely exposed, infection of the neonates and weaners does not usually occur.
Weaners (3-9 weeks of age): CNS involvement in the younger pigs in this age group but it becomes progressively less severe as the age at infection increases. May have up to 50% mortality in 3-week-old pigs. Respiratory signs in older pigs become more prominent. Often, the disease is characterized by marked depression and sneezing. Nasal discharge and coughing are often observed. Secondary bacterial infections are common and make the clinical picture more complicated. Some pigs may show relatively little long-term effect. Severely affected pigs will often be stunted and take significantly longer to grow to market weight.
Grower-finishers: Predominantly respiratory signs in this group and in breeder swine with only sporadic CNS signs. Pigs have temperatures of 41 to 42(C and the respiratory signs run from mild to severe. The pigs may take a week or two longer to reach market weight and secondary infections can lead to more severe problems.
Sows: The rate of reproductive failure is about 20% in newly infected herds. Infection in the first trimester may result in abortion and a return to estrus. Infection in the second or third trimester results in abortion or stillborn or weakborn pigs (the latter only if infection occurs close to the farrowing date). Weakborn pigs that are infected before birth usually die. Note that there are usually no mummies, the virus is more likely to cause abortion although it is described as a cause of mummies in the literature.
Other species affected
Cattle have an intense pruritus and die. They do not shed the virus so usually the only method for them to contract the infection is through swine. Infections tend to be sporadic unless swine and cattle are housed together or in close approximation.
Sheep can transmit the virus to other sheep.
Dogs often self-mutilate.
Diagnosis:
Clinical signs and herd history: CNS + Respiratory + Reproductive
FA test: Rapid and reliable. Tonsil is the tissue of choice. Best in neonatal pigs.
Virus isolation: More sensitive than FA in older swine. Brain, spleen, lung, nasal swabs: Refrigerate samples or freeze on dry ice. Identify the virus in cultures with an FA test.
Serodiagnosis: ELISA has been the standard. Companion diagnostic. Latex agglutination test seems to be a little more sensitive and detect infection earlier.
Lesions: Often minimal or not present. May see serous to fibrinonecrotic rhinitis and tracheitis, necrotic tonsillitis, swollen and hemorrhagic lymph nodes of the oral cavity and upper respiratory tract. Lower respiratory tract lesions may range from scattered "blotchy" hemorrhages to areas of necrosis.
Keratoconjunctivitis
Focal necrosis of the liver and spleen
Histopathology: Should submit tissues in formalin. Send them along with tissues for virus isolation.
Treatment: Supportive.
Prevention
Vaccination: The use of vaccines had been controversial in the face of the eradication program that was underway until the (blowup(in late 1999-2000. The vaccines are capable of markedly reducing the clinical signs and resultant losses from pseudorabies. They do not prevent infection. However, by reducing clinical signs and shedding they are able to reduce transmission off site. When producers stopped vaccinating, we were left with a large population of highly susceptible swine. As of Jan. 2001, there were 116 infected and quarantined herds in the northern 66 counties of Iowa. That was down from a high of over 800. Vaccination in this area was required 4 times a year in the sow herd and once or twice in finishing swine depending on the infection status of the herd. Periodic testing of swine has been mandatory in the 66 northern counties. In the year 2000, the ISU VDL ran over one million serum samples for pseudorabies. By early 2002, some officials were claiming that we have eradicated pseudorabies from Iowa, however, it was probably still present at least for a short period of time.
Gene deletion vaccines: Any vaccine used in the State of Iowa must have a gI deletion. The only way an animal can have antibody against the gI glycoprotein is to have been infected with the field virus.
Modified-live pseudorabies vaccines must be used with caution. Although they are avirulent for swine, some of them are capable of producing disease in other animals. Syringes and needles used for vaccination should not be used for injection of other animals.
PORCINE PARVOVIRUS
General description
Reproductive problems are the only clinical manifestations of parvovirus infection in swine. The virus crosses the placenta and infects the fetus at all stages of gestation.
Etiology
All porcine parvovirus isolates are antigenically very similar or identical. They are also antigenically similar to parvoviruses from other species of animals but can be differentiated using very specific serologic tests.
Epidemiology and Transmission
The virus is very stable in the environment and is difficult if not impossible to eliminate from a swine facility. It is highly resistant to most disinfectants and heat. The virus multiplies in the intestine and is found in high titers in recently infected animals. There is also considerable evidence that immunotolerant carriers result from in-utero infection. Boars pass the virus in their semen and it has been shown that they can infect gilts at breeding. Essentially all swine herds are infected with this agent and sows pass high titers of antibody through their colostrum to their piglets. Antibody against this virus is very long-lived (at least 3-6 months) and in some cases it prevents replacement gilts from becoming naturally infected until after they are bred and conceive. If infection occurs following conception and before development of immunocompetence in the fetus, reproductive failure results.
Clinical signs
Infection with the virus usually produces no clinical signs other than reproductive failure even though the virus multiplies to high titers in rapidly dividing cell types especially the lymphoid tissues. It does not affect the intestinal crypt cells like the parvoviruses of other animal species.
Maternal reproductive failure is highly dependent upon the stage of gestation at which infection occurs. Dams may return to estrus, fail to farrow despite being in anestrus, farrow only a few pigs per litter, or farrow a large proportion of mummified fetuses (see below). One may see a decrease in the abdominal girth as the fetuses die and the associated fluids are absorbed. Infertility, abortion, stillbirth, and neonatal death have occasionally been associated with parvovirus infection. When mummified fetuses are present, gestation length and farrowing interval may be increased.
If dams are infected prior to 70 days gestation, the fetuses are susceptible to the virus and will die and be resorbed or will mummify. After 70 days the fetus will develop a protective immune response to the virus. Often, only a portion of the litter will be infected transplacentally.
The stage of gestation at which infection occurs determines the type of clinical picture seen:
Days of gestation
Skeletal Fetus starts to be
mineralization Immunocompetent
0 30-35 65-70 114
a,b,c d, e f
a=repeat breeders
b=pseudopregnancies
c=small litters
d=mummies
e=increased stillborn
f=normal litters
Diagnosis
Clinical signs: Reproductive problems in gilts but not sows is highly suggestive. A relative lack of maternal illness, abortions, and fetal anomalies is not seen with most other causes.
FA test: Submit several mummified fetuses (or fetal lungs) less than 70 days of gestational age. Antibody develops in later term fetuses that interferes with virus isolation and antigen detection.
Virus isolation: Not as reliable. The virus is widespread in swine populations and can easily contaminate cultures. Also takes longer.
Serology: Used when fetuses are not available. Need paired or sequential sera. Most animals have antibody. If gilts lack antibody, a diagnosis of parvovirus is ruled out. Can test for antibody in fetuses.
Prevention
Natural infection prior to breeding: Gilts can be exposed to seropositive sows or placed in pens that have been recently occupied by seropositive animals. Infection spreads rapidly in a susceptible population.
Vaccination: Only killed products are available and are reported to be effective; however, the vaccines apparently do not work especially well in the face of residual maternal immunity.
PORCINE ENTEROVIRUS
Enteroviruses are ubiquitous in the swine population and usually infection is not associated with clinical signs. However, a variety of clinical conditions including polioencephalomyelitis, female reproductive disorders and possibly enteritis and pneumonia have been described. The role of the virus in the latter two is not thought to be of great importance. Enteroviruses are commonly found in piglets with or without diarrhea or pneumonia.
Polioencephalomyelitis
Teschen disease occurs sporadically in Europe and to a lesser extent in Africa. This is the most severe disease and is produced by a relatively virulent virus. The disease is characterized by CNS signs and a high mortality.
Talfan disease is caused by a related but much less virulent virus. This virus is essentially found worldwide. Clinical disease takes the form of a benign enzootic paresis and rarely progresses to paralysis.
Diagnosis of polioencephalomyelitis is usually based on isolation of the virus or demonstration of viral antigen in pigs showing early nervous signs.
Prevention against Teschen disease can be provided by vaccination, but less-virulent forms of enteroviral infection are not vaccinated against.
SMEDI
This is a term that was coined to describe a group of enteroviruses implicated in stillbirth, mummification, embryonic death, and infertility. These viruses have been shown to produce the clinical signs experimentally. The exact importance of them is unknown but they are thought to not be nearly as important as porcine parvovirus. The ISU Diagnostic Lab doesn't look for them routinely. Older literature discusses these as being very important but much of what was ascribed to SMEDI was probably parvovirus and other problems.
Diagnosis is based upon finding viral antigen in the fetus.
Prevention of infection in gilts or sows is usually accomplished by making sure gilts are naturally exposed prior to breeding. Gilts should be exposed to the feces of recently weaned piglets and there should be sufficient virus to infect. There are several serogroups involved and this has hampered vaccine development.
LEPTOSPIROSIS
Etiology
Leptospira interrogans serovar pomona is the major cause of leptospirosis in swine throughout the world. Other serotypes, such as canicola, icterohemorrhagiae, grippotyphosa, and sejroe infect swine. Only pomona and sejroe produce clinical disease. Some work indicates that L. bratislava is involved in disease in swine but this has not been well demonstrated.
Epidemiology
Leptospiral infections in swine are relatively common but clinical disease is not recognized as frequently because most of the infections are subclinical or inapparent. The epidemiology varies somewhat with the serovar.
A large number of species of wild and domestic animals have been shown to be capable of carrying L. pomona and spreading it to swine. Wildlife is the major source of infection for autumnalis and grippotyphosa. Serovar icterohemorrhagiae has the rat as its primary host.
Transmission occurs through breaks in the skin, direct penetration of mucous membranes, or through conjunctiva. A relatively low infectious dose is required. The organism disseminates and grows in many tissues but has a definite predilection for the kidney. Antibody can be detected in the blood in 5 to 10 days and the organisms disappear from the bloodstream at that time. The organisms survive in the proximal convoluted tubule and are shed in the urine of infected animals for long periods of time following the initial septicemic phase. Leptospires are able to survive in the undiluted urine of swine for several hours if the urine is neutral or slightly alkaline. If the urine is diluted by water or falls in poorly drained soil, the organisms remain viable for long periods of time.
Transmission from infected boars into a sow herd has occurred. However, transmission may not have occurred through breeding. Transmission from cattle to swine and vice versa has been demonstrated.
Oral exposure from the feed is a concern and may be a method of introduction of the infection into a confined herd.
Clinical signs
Most of the sows that become infected do not show marked clinical signs. Most often, the effects are not observed. The disease spreads gradually through the herd and only a few animals will be in the acute phase at any given time.
Infection with leptospira during the last half of gestation may lead to abortions, stillbirths, and neonatal deaths. Pigs may be born prematurely and survive for a short period of time. The organisms readily pass through the placenta to the fetal fluids and some or all of the fetuses may be infected. Abortions and stillbirths usually occur one to four weeks following infection of the sow and thus most sows have antibody titers by the time of abortion.
Diagnosis
Diagnosis can present a problem because of the relatively mild clinical disease that occurs and the low numbers of organisms that persist following generation of specific antibody.
Culture: Definitive but difficult. Can be found in freshly aborted fetuses but the organisms die quickly.
Serology: Microscopic agglutination test (MAT) is the standard test for detecting antibody. Interpretation of the test is dependent upon knowledge of the vaccination history and herd health. Some animals develop only low, short-lived titers. It is best to use the test on a herd basis, rather than on individual animals.
Infected swine usually develop titers of 1:100 or greater.
Vaccinated swine may develop titers but only a few may develop titers of 1:100 or greater.
RFLP patterns (Restriction Fragment Length Polymorphism)
Prevention and Control
Maintain animals in a clean environment without standing water.
Segregate known infected animals from others: Difficult because of the lack of clinical signs. Test any animals coming into the breeding herd. This may not be very useful if done on an individual basis. It is better to buy stock from herds free of the organism.
Vaccination is probably the best. Commercial bacterins containing the most common serovars are readily available and are often included in vaccination programs for breeding swine. Gilts should be given 2 doses prior to breeding. Protection may last for only 6 months and it is best to repeat the vaccination at this interval.
Other animals and humans may be infected. As with many other diseases, it is best to keep other animals out.
Treatment
Tetracyclines
BRUCELLOSIS
Swine brucellosis was once thought to be widespread in the U.S. especially in areas of concentrated swine production. This was based almost entirely upon serological testing of swine herds and to some extent on clinical signs. In reality, the plate agglutination test has a high rate of false positives and the true incidence may not have been anywhere near the incidence reported in the literature. In addition, the plate test used for diagnosis does not differentiate between Brucella suis and Brucella abortus and the majority of the cases of swine brucellosis may have been due to B. abortus. The state-federal cooperative program to eliminate B. abortus and Brucella suis has resulted in a dramatic decrease in the numbers of infected herds in the U.S. Swine brucellosis is esentially confined to the states that have feral swine. Iowa has been free of brucellosis for 30 years. However, a negative serologic test is still required for interstate shipment.
Etiology
Brucella suis biovars 1 and 3 account for the disease seen in the U.S. Biovar 2 occurs in Europe. Biovar 4 is widespread in reindeer and caribou but is apparently not pathogenic for swine.
Epidemiology
Swine are the most common hosts for B. suis biotypes 1 and 3 and essentially all infections are a result of swine to swine transmission. Feral swine are able to maintain the infection and can serve as a source of the organism for other animals. Transmission of the organism in swine is almost entirely by a venereal route, although it can readily be transmitted by ingestion. The organism does not survive long in the environment and is readily killed by sunlight and many commonly used disinfectants. They will survive in the frozen state in organic material for up to 2 years, however. Infected sows that abort have shed the organism in the vaginal discharge for years but usually the shedding only lasts 30 days or so. The organism tends to be more persistent in boars and most of these never completely clear the organism.
Clinical signs
The clinical signs can vary greatly. The majority of herds may have no clinical signs at all that are readily recognized. Abortion may occur at any time in gestation with the highest rate occurring when the sow or gilt is infected at breeding. Many of the early abortions can easily be missed unless one looks at the breeding records and finds a high percentage of sows returning to estrus at 30 to 45 days. Boars may have orchitis but usually the secondary sex organs are affected. Infertility can result. Suckling and weaning pigs may develop spondylitis and become paralyzed or lame. This can occasionally occur in older swine.
Diagnosis
Culture: Said to be the most accurate. Routine lymph node culture is as good as serologic testing and can serve very well as a routine epidemiologic tool.
Serology: Used most frequently. Must be used on a herd basis. Studies have shown up to 18% of normal swine may be serologically positive at a low dilution (1:25). Some infected swine may be incapable of ever forming detectable antibody against the organism and thus test falsely negative. In addition, titers may be slow to develop.
Prevention and Control
The organism has essentially been eliminated from most of the intensive swine rearing areas of the U.S. The most successful method of eliminating the disease is to depopulate known infected herds, clean up the facilities, and then repopulate with non-infected swine. The disease does not recur when these procedures are followed rigorously. If there are only a few seropositive animals in a herd, these could be removed and then the herd retested in case these were false positives.
The cooperative state-federal-industry program utilizes routine monitoring of sows and boars that go to slaughter. Details of the program can be found in the Uniform Methods and Rules for Brucellosis Eradication and from the State Veterinarian(s office.
TUBERCULOSIS
Etiology
Tuberculosis in swine can be caused by any of the three main species of mycobacteria, M. avium, M. tuberculosis and M. bovis. The vast majority of the infections are caused by M. avium serovars 1, 2, 4, and 8 in the U.S. However, many other serotypes have been isolated from tuberculous lesions in swine.
Epidemiology
The majority of infections in the past in the U.S. have been associated with contact with infected poultry. Because of changes in management and the decreased cross-species contact there has been a decrease in the incidence of swine tuberculosis. Also, current practices for raising poultry results in a rather short lifespan even for laying hens and the organisms do not have as great a chance to build up in the environment. Wild birds have also been documented as sources of the organism for swine. Once in the environment, the organisms can persist for long periods of time (up to 4 years in one study). Infection is almost always by ingestion. When M. tuberculosis is found, one needs to consider humans as the most likely source. M. bovis can be transmitted by a number of animals but the marked decrease in incidence of bovine tuberculosis in this country has limited the number of swine infected with this organism.
Lesions and Incidence
There is no routine tuberculin skin testing performed in swine similar to the program in cattle. Swine can be skin tested on the ear or vulva. Some infected swine will be non-reactive and the test should be repeated especially when testing a herd with known infected animals. Infection is detected at the time of slaughter with routine meat inspection. The lymph nodes of swine are carefully examined for the presence of gross lesions of tuberculosis. Tuberculous lymph nodes are almost always cervical or mesenteric nodes. The lesions are usually caseous and yellowish white and vary from a few millimeters in size to involvement of the whole node. Lesions caused by M. tuberculosis and M. bovis are more likely to be calcified and more encapsulated. The encapsulation makes it easier to separate the lesion from the surrounding tissue.M. bovis tends to cause a much more disseminated infection than the other two organisms. In some studies, a relatively high percentage of the tuberculous lymph nodes were actually infected with Rhodococcus equi rather than Mycobacterium sp.
There are basically four categories or dispositions that swine fall into:
Swine with no lesions
Swine with lesions attributable to tuberculosis: These are passed for consumption if the lesions are not disseminated.
Swine passed for cooking, PFC: These have disseminated lesions but the carcass is not emaciated.
Swine with disseminated lesions with an emaciated carcass: Condemned
Figures on incidence vary a little. The most recent numbers available indicate about 3 to 4 animals per 100,000 slaughtered are condemned, about 12 to 18 per 100,000 are PFC, and about 0.6% of all swine slaughtered in the U.S. have lesions attributable to tuberculosis. These figures represent only gross, meat inspector interpretation of lesions and probably include swine infected with other organisms that may cause similar lesions. These figures are the result of a steady and somewhat dramatic decrease in the incidence of disease from the 1970's to the 1990's.
Swine that are condemned represent an obvious loss, but the PFC category represents a major decrease in carcass value. The carcass is only worth about 1/3 of its normal value.
Diagnosis
Gross lesions are suggestive.
Histopathologic exam plus staining for acid fast bacteria
Bacteriologic culture
Tuberculin skin test
Prevention and control
Elimination of contact between swine and poultry and wild birds.
Thorough disinfection of premises that have had swine with tuberculosis. Elimination of dirt floors is beneficial since the organism is better able to survive in the soil.
Thorough cooking of garbage or meat byproducts that go into swine feed.
CYSTITIS: Actinobaculum suis
Etiology
Actinobaculum suis (Eubacterium suis, Corynebacterium suis and Actinomyces suis have all been used as names) has been recognized as a cause of pyelonephritis/cystitis in sows for over 30 years. Work in Europe has indicated that it is a major cause of death loss in sows, especially in certain types of housing. Infections are increasingly being recognized in this country. The organism is an obligate anaerobe and is relatively difficult to culture.
Epidemiology
The organism is apparently widespread in the swine population and some consider it to be a normal component of the porcine microflora. The disease is more common in sows housed in gestation stalls, due to the greater likelihood for spread from one sow to the next and a reduction in activity, water intake and urination. The organism is carried in the prepuce of the boar.
Clinical signs
The organism produces urease which splits urea into ammonia which, in turn, damages the bladder mucosa. A wide range of clinical signs may be observed. They range from sudden death to acute or chronic renal failure.
In acute disease the sow may have hematuria and pyuria, be reluctant to get up and appear lame in the rear. The mortality is high unless treated aggressively. If the animal survives the acute disease, it may show vaginal discharge, be a repeat breeder and be culled because of poor reproductive performance.
Lesions
These consist of a thickened bladder wall with a hemorrhagic epithelium. The bladder may contain purulent exudate and deposits of sand-like material that are usually composed of struvite.
Diagnosis
Bacterial culture: Field isolation works best. Do not expose to oxygen. Cut a small slit in the bladder wall and collect the sample on a special anaerobic swab.
Treatment
Ampicillin works the best.
In chronic infections, response to therapy is disappointing.
Prevention and control
Management: Maximize water consumption, increase salt in the ration, frequent watering and twice a day feeding to get sows on their feet, general cleanliness and good ventilation.
Cull affected animals or isolate them from the other swine in the unit.
EPERYTHROZOONOSIS
Historically it has been considered a cause of acute icterus and anemia in young pigs under stress. More recently it has been observed in a wide age range from piglets to pregnant sows.
Etiology
Mycoplasma haemosuis (formerly Eperythrozoon suis). The anemia produced is very similar to that observed with bovine anaplasmosis and feline Mycoplasma haemofelis infection.
Epidemiology
M. haemosuis is a pathogen only of pigs. Experiments proving arthropod transmission in swine have not been reported although disease occurs mostly in summer. Transmission through needles and equipment is likely. In-utero and oral transmission have been demonstrated. The overall incidence is less than 8% seropositive by the indirect hemagglutination test (IHA).
Clinical signs
Pigs under 5 days of age are most likely to show clinical signs of anemia and icterus. Most pigs recover within a week but, in some, anemia may persist after weaning especially if there are concurrent bacterial or parasitic infections. General unthriftiness may occur and complicate enteric or respiratory infections.
Feeder pigs are rarely observed with clinical disease although reports used to be more common. Probably due to the use of medicated feed.
Sows (usually those under stress immediately prepartum) may be acutely affected and may have a high fever and anorexia for 1-3 days. Chronically infected sows show anemia, icterus and unthriftiness. A portion of the herd may become debilitated and some may die of secondary infections. Sows with either acute or chronic disease show decreased conception rates.
Diagnosis
Blood smears: Used in acute cases where the organism can be demonstrated in the blood. Organisms are easier to demonstrate in young pigs. Diff-Quick or other stains can be used.
IHA: Indirect hemagglutination is used for diagnosis of subclinical infections.
Treatment
Arsenicals and tetracyclines show beneficial effects.
Iron dextran in anemic piglets
Control other diseases
Prevention
Vaccines are not available
EXOTIC VIRAL DISEASES OF SWINE
Hog cholera and African swine fever are the two major exotic viral diseases pose a threat to the swine industry of the US. Both of these are characterized by:
High fever High mortality
Lymphoid involvement Skin erythemas to effusions
HOG CHOLERA
Classical swine fever or European swine fever
Pestivirus (enveloped) that is closely related antigenically to BVD virus of cattle. The virus is not particularly resistant but will survive for relatively long periods in some substrates.
Acute and chronic strains of the virus exist: Seems to be related to virulence with acute forms being more virulent. The chronic forms are inhibiting eradication efforts because they do not cause severe terminal illness in a short period of time. During the US eradication program, 55% of isolates were of low virulence during the period 1965 to 1975.
Eradication efforts
The disease was costing $50 million/year when US eradication efforts began in 1962. The last case was reported in 1976. The cost of eradication was about $140 million (vs. $1.1 billion to live with the disease for the same period).
Epidemiology
Worldwide distribution but has been eliminated from the US, Canada and several European countries. There was a significant outbreak of disease in the United Kingdom in 2000 followed by FMD in 2001. Both diseases have apparently been present in China and Southeast Asia. HCV is present in Romania and Serbia.
Hosts: Domestic swine, wild boar
Transmission: Direct contact via the oro-nasal route. Primary site of invasion is the tonsillar crypt with viremia and spread to the lymphoid tissues.
Garbage feeding
The virus can remain viable in pork and pork products and be introduced into HCV-free countries by this route.
Mechanical vectors: Personnel, equipment, pets, birds, and arthropods.
Wild pigs. This has been the problem in Serbia where wild pigs coming over the border from Romania have brought the disease into the country.
If exposed in-utero to a HCV of low virulence, some piglets may remain healthy for many months and shed virus continuously. They may also have a "late onset" disease.
Clinical signs
Incubation period 2-4 days
High fever
Excitable at first followed by apathy and anorexia
Marked ocular discharge: Severe conjunctivitis
Hind leg incoordination, huddling, diarrhea, dyspnea, recumbency with paddling.
Morbidity and mortality 100% with survival only 10 to 20 days PI. In subacute HC, pigs show less severe signs of disease and succumb within 30 days. In chronic disease, pigs may survive 100 days or more.
Congenital tremors in piglets with cerebellar hypoplasia due to infection with strains of low virulence.
Pathogenesis
Endothelial damage including CNS cuffing
Disseminated petechiae and ecchymoses especially in the skin, larynx, bladder, brain, and kidney (turkey-egg kidney). Multifocal infarcts of the margin of the spleen are characteristic but inconstant.
Button ulcers (because of infarcts) of the colon
Lymphopenia
Diagnosis: Relatively easy in the acute form.
Reportable disease
FA on tissues (tonsil is the first tissue to become positive). This is the standard test in many countries. Pigs can be infected with BVDV and the FA test will not distinguish these.
SN test: Best in the chronic forms because antibody titers may be low or absent in the acute and late onset disease. Can distinguish BVDV infections.
VI
Differential diagnosis:
African swine fever: Rarely see button ulcers and spleen infarcts. Edema of the lungs and gall bladder wall and excessive pericardial, pleural, and peritoneal fluids not seen with HCV.
Salmonellosis
Erysipelas
AFRICAN SWINE FEVER (ASF)
An acute to chronic disease of swine and wild boars with a high morbidity and mortality. Caused by an Iridovirus, an enveloped DNA virus. In Africa wart hogs and possibly giant forest hogs and bush pigs serve as reservoirs of the virus but do not show clinical signs even when inoculated with the most virulent strains ASFV. These animals may be persistently viremic.
The disease was initially confined to Africa, but spread to Portugal in 1957, Spain in 1960, Cuba in 1971, and Brazil, Dominican Republic and Haiti in 1978. Periodic outbreaks have occurred in France, Italy, Holland and Belgium but the disease was eradicated from these countries. A 1999 outbreak in Portugal was apparently the last time the disease occurred in Europe as of 2006.
Epidemiology
The virus survives for prolonged periods under most environmental conditions especially when protected in meat or blood. South American outbreaks were most likely the result of feeding improperly processed garbage containing pork scraps (The first outbreaks were in pigs fed garbage from international airlines). Survives 5-6 months in processed hams.
Does not survive well on premises after depopulation (3 days to 3 months)
All secretions and excretions from acutely infected domestic pigs are infectious.
Transmission
May occur via ticks or hematophagous insects. This was important in the outbreaks in Spain and Portugal. Transmission commonly occurs by introduction of infected swine or indirectly through contaminated personnel and equipment.
Clinical signs
Incubation period of 1-4 d
Fever: 105 - 108oF
Hyperemia of the skin
Abortions
Mortality 100% with virulent forms, but mortality drops rapidly as the virus circulates in swine herds. The outbreaks in Spain, France, Brazil, and the Caribbean had mortality rates of 10% with primarily chronic respiratory forms and persistent viremia. Surviving pigs with the chronic form are poor doers.
Pathogenesis
Enters via mouth or URT-->tonsils and spreads quickly to the mandibular lymph nodes and throughout the body via blood and lymph. When injected (tick bites) the virus spreads rapidly to the RES and lymphocytes.
Lesions
In acute ASF due to highly virulent virus, the lesions are usually marked; whereas in subclinical, mild, or chronic disease, the lesions may be minimal or absent.
Severely hemorrhagic and edematous lymph nodes (look like hematomas, often with little discernable lymphoid tissue.
Splenomegaly
Petechial hemorrhages throughout the body. Lungs, kidneys and lymph nodes are often examined for characteristic lesions. Kidneys may be very hemorrhagic.
Immune response
Antibody forms readily but is not protective. No vaccine currently exists.
Diagnosis
Hemadsorption (HAd) test is the standard test but some strains of virus, especially low virulence strains, may not adsorb RBCs or will do so only after several passages in the laboratory.
Direct FA test: Useful but may not be positive in clinically mild disease.
Pig inoculation with suspected tissues is one of the most sensitive and reliable tests.
Once the disease has been diagnosed in an area, observation of the clinical disease and gross lesions is reliable.
Control
Slaughter all infected and exposed swine. Cuban outbreak resulted in slaughtering 400,000 pigs. Dominican Republic and Haiti: All domestic and most of the feral swine were eliminated.
Restrict swine and pork movement
Thorough cooking of garbage before feeding it to swine.
VESICULAR DISEASES
Foot and Mouth Disease
General
A vesicular disease affecting cloven-hoofed animals including wild and domestic ruminants and swine. It has the broadest host range of the vesicular diseases affecting domestic animals and is the most easily transmitted. In addition to cloven-hoofed animals, elephants, hedgehogs, and even humans have been infected with the virus. Horses are totally resistant to infection. FMD outbreaks have occurred in the U.S. on at least nine separate occasions and have been stamped out aggressively using total slaughter of all affected and contact animals. There have been no outbreaks in the U.S. since 1929. The disease is said to be one of the most economically important worldwide when one includes the adverse effects on trade.
Etiology
Foot and Mouth Disease virus, an Aphthovirus (picornavirus). There is a great deal of genetic rearrangement of the various strains of FMDV resulting in multiple antigenic variants. Some strains develop genetic variants and a rate of 10-4 . The classic European types (A, O, and C) are the most widespread and are the types found in South America. South African types (SAT1, 2, and 3) are found in Africa and the Asia 1 type is found in Asia.
Epidemiology and Transmission
Most of the virus particles are found in the epithelial lesions of affected animals and the majority of transmission is thought to be through infected saliva. During the early febrile period however, all tissues, excretions and secretions contain the virus including semen. The virus does not survive long in muscle tissue because of the acidic environment but will survive in bone marrow and in organ meats. Several outbreaks have been traced to the importation of fresh meat or to meat scraps in uncooked garbage. The U.S. currently has an embargo on any fresh meat, hides or offal originating from countries infected with FMD.
Following an outbreak and total depopulation of all the animals on a farm, the virus disappears fairly rapidly except from protected dark, moist areas. In countries endemic for FMD, the virus can apparently persist in recovered animals but is not readily transmitted by natural means. However, several outbreaks have been observed in isolated areas and the chronic carrier state has been implicated as a source of the virus. Cattle and sheep have been found to harbor the virus for 1 to 5 months and, in one study in cattle, up to 15 months. Vaccinated cattle can be subclinically infected with virulent virus and carry the virus for long periods. Calves from cows immunized with modified live virus have been shown to carry the virus up to a year of age. It is theorized that the various chronic carrier states may be important in the development of variants of the virus. No good data exists for the role of birds in transmission but they may act strictly as mechanical vectors. Virus in milk has been associated with transmission through trucks picking up milk at various farms. Humans can inhale the virus and carry it in their throats and nasal passages for up to 28 hours. Humans can also become infected with the FMD virus and develop vesicular lesions although this seems to be relatively uncommon. Because of this, it is wise to wear protective, boots, gloves and clothing when handling infected animals. The clothing must be thoroughly disinfected following use.
Clinical disease and lesions
The sudden onset of lameness in a group of animals and the finding of vesicular lesions is characteristic and warrants immediate notification of the State Veterinarian. In cattle, the disease is characterized by depression, elevated temperature, and the appearance of vesicles containing a clear fluid on the epithelium of the mouth, tongue, muzzle, interdigital space, tops of the claws, teats and sometimes the surface of the udder. Other mucous membranes may develop vesicles as well. The vesicles contain large numbers of virus particles and those in the mouth are especially prone to rupture within a few hours after formation. Following rupture, large whitish flaps of epithelium may be found partially covering the affected areas. In many animals, a large part of the epithelium of the tongue may be lost. The virus is rapidly transmitted to other animals in the herd. The incubation period ranges from less than 48 hr to no more than 4 days.
About 24-48 hours after the formation of vesicles, the virus enters the blood and multiplies in various organs. The heart muscle of calves is particularly affected by some strains of the virus and high mortality can result from myocardial necrosis (yellowish streaks are found in the heart muscle).
Affected cattle become lame and champ their jaws and drool because of the mouth lesions. Most lose condition rapidly. Secondary bacterial infection especially in the foot area complicates the recovery. The claws may be totally undermined and eventually sloughed. Mastitis in lactating dairy cattle can be a major cause of economic loss. Mortality in due to the virus infection is generally low (1 to 3%) but has been as high as 50% in some outbreaks.
Disease in swine is generally similar to that in cattle. Pigs develop lameness initially as the most conspicuous sign. Large vesicles may appear on the snout and other epithelial surfaces. Sheep and goats also show lameness most commonly but usually are not as severely affected as cattle.
Diagnosis
Clinical signs
Serologic tests- preferred due to rapid turnaround time. Recently recognized that other viruses serologically cross-react with FMD and some normal cattle have antibody.
Animal inoculation
Animal FMD VS VE
Horse (intradermal-intralingual) - + -*
Cow (intradermal-intralingual) + + -
Cow (intramuscular) + - -
Guinea pig (intradermal-footpad) + + -
*Small local lesions produced without generalized disease.
Swine are not used in the above scheme because they are susceptible to all the viruses.
Control and prevention
During an outbreak, aggressive quarantine measures need to be instituted immediately for several miles around affected farms. This means that sufficient personnel to enforce the quarantine need to be immediately mobilized. No livestock should be allowed to move within the quarantine area and of course none should be allowed to leave. Dogs, cats, and other pets should be confined. Humans are also confined and allowed to move from one place to another only with special permission and only after thorough disinfection. All affected animals and all animals that have had contact with them are slaughtered and buried on the farm with quick-lime.
The U.S., Canada, Japan, Australia, New Zealand, Great Britain and Ireland have consistently dealt with FMD using aggressive total depopulation of affected and contact animals. As a result, the disease has never gained a firm foothold in these areas. In the U.S., a policy of gradual restocking of a farm beginning 30 days following total disinfection has been used. A few animals are re-introduced to the premises and inspected every other day for the first 10 days then twice a week for the next 20 days. Additional animals may be added to the herd at that time but it is kept under close surveillance and quarantine for 90 days following the initial disinfection. Because of the potential impact of FMD on the U.S. animal industry, the U.S. currently stockpiles sufficient vaccine for use in slowing an epidemic should one occur.
Ships and planes originating in countries where FMD is found are not allowed to offload garbage in the U.S. Only canned or cured meat is allowed to be imported from FMD countries.
In areas where FMD is enzootic, vaccination has been the method of choice for controlling outbreaks. The traditional inactivated vaccines, are generally produced in cell cultures (in monolayers or in suspension), inactivated with first-order kinetic inactivants, and formulated with an adjuvant. These vaccines have been successful when applied systematically and a rigorous quality control (i.e. efficacy or potency tests) were carried out . While most of the control and eradication of FMD from Western Europe was based on the use conventionally adjuvanted vaccines in cattle ( aluminum hydroxide), significant progress has been made in South-America through the utilization of double oil emulsion adjuvant FMD vaccines for cattle. The oil adjuvant concept for FMD vaccines has also been used with success in pigs in other parts of the world. Argentina successfully eradicated FMD by 1994 using a trivalent vaccine (O, A and C) in a single oil adjuvant. Infected herds were slaughtered and surrounding herds were vaccinated.
Historically, problems with vaccination have arisen. The immunity generated by many of the vaccines is relatively short lived and it is thought that having animals partially immune to certain virus types has provided the necessary pressure on the virus to allow antigenic variants to arise.
Vesicular Exanthema of Swine
General
Causes vesicular lesions in swine that are grossly indistinguishable from those of foot and mouth disease. The disease was first described in California in 1932 and was thought to be FMD until two years later when it was determined to be a separate virus. The virus does not spread as rapidly as FMD and the only domestic animals routinely infected are swine which is very different from FMD. The virus was confined to the state of California for 20 years without the institution of any control measures. In 1952, the virus suddenly spread eastward and within a few months, outbreaks had been reported in 42 states. An eradication program was instituted and the virus was (eradicated( from the U.S. in 1959.
Etiology
Calicivirus.
Epidemiology and transmission
A very similar virus was isolated in 1972 from sea lions on San Miguel Island off the coast of California. This virus produced lesions in swine identical to those of VES and VESV produced lesions in the sea lions identical to those of San Miguel Sea Lion virus (SMSV). SMSV was isolated on several occasions from opaleye fish and it has been postulated that the original outbreaks arose from feeding raw garbage containing scraps from infected fish. The disease was then transmitted to swine through garbage feeding. Once established in the swine population, the disease was spread by two routes: through the garbage and by introduction of infected swine into a clean herd. Almost all the outbreaks occurred in swine fed raw garbage. The virus apparently does not last long in the environment since swine placed in pens where actively infected pigs had recently been housed, did not develop infection. The infection also spreads relatively slowly through a group of swine and fully susceptible swine may not develop disease in a given group. Lesions may take three or more weeks to completely heal,
Unlike FMD, other domestic animals are not routinely infected. Horses and dogs have been infected with some of the four serotypes by intralingual injection, but this is not easily done. Guinea pigs are not affected by the virus.
Clincal disease and lesions
About 12 hours before the appearance of vesicles, swine will have a fever and will be off feed. Vesicles of varying size appear on the lips, tongue, snout, footpads and the skin between the claws, coronary band, dew claws, and teats of nursing sows. The vesicles rupture easily, leaving a raw surface often with flaps of whitish skin attached. The animals can become quite lame and will refuse to rise when prodded and may walk knuckled over on their fetlocks or knees. The lameness can persist for several weeks although the mouth lesions heal rather quickly. Swine experience a rapid and extensive weight loss.
Mortality is low in adult swine. Nursing pigs may have a high mortality rate due to the development of lesions in the oral and nasal cavities that may cause suffocation or from starvation because of agalactia in the sows.
Control and Prevention
Because of the similarity of the infection to FMD, depopulation is required. Feeding of raw garbage is prohibited. The reservoir still exists in the sea lion and fish populations.
Swine Vesicular Disease
General
Disease was first described on two farms in Italy in 1966. The disease was rapidly disseminated to many countries in Europe, Japan and Taiwan. The disease produces lesions that are clinically indistinguishable from other vesicular diseases of swine. The disease has not been reported in the U.S.
Etiology
An enterovirus that is closely related to the Coxsackie B5 virus that affects humans.
Epidemiology and transmission
Less is known about this virus that the other vesicular diseases. In the outbreak in Italy, about 25 % of swine in contact with the infected group developed lesions. No new cases were seen after about 3 weeks. In Japan, the virus was isolated from the feces of healthy pigs. Apparently, subclinical infections occur and carrier pigs may be an important part of the transmission.
Disease and Lesions
Indistinguishable from other vesicular diseases. Morbidity in natural outbreaks has been reported at 25 to 65%. A mild non-suppurative meningoencephalitis throughout the CNS was observed in both natural and experimental disease.
Control and prevention
Cooking all garbage or no garbage feeding
Strict quarantine and slaughter of all affected and exposed swine
Vesicular Stomatitis
General
Cause of fever and vesicular and ulcerative lesions primarily in horses, cattle and swine. Lesions in cattle and swine cannot be readily distinguished from those of FMD.
Etiology
Vesicular stomatitis virus, a Rhabdovirus. There are two main serotypes of virus (New Jersey and Indiana). The Indiana serotype seems to be more diverse and is divided into three subtypes but even the New Jersey serotype possesses a lot of genetic variation. The New Jersey serotype is thought to be the most virulent.
Epizootiology and transmission
Not as clear-cut as the other vesicular diseases. Disease occurs only in the Western Hemisphere and is more prevalent in tropical and subtropical areas. In some cases there appears to be an arthropod reservoir and/or vector involved because of the occurrence of the disease in late summer. Epidemics have occurred in winter months as well however. A wide variety of animals can be infected with the virus, but all of those studied did not develop sufficient viremia to account for infection of arthropod vectors. In other outbreaks, it seems that the virus has somehow (seeded down( pastures and multiple cases occur at separate sites within a given area. In some cases, the virus seems to move down river valleys. It seems to be more common in areas that are shaded and moist. Direct transmission between animals is apparently not important, because animals on neighboring farms often are unaffected. Disease tends to recur from year to year on certain farms and pastures.
Disease and lesions
In horses and cattle, oral lesions are more common than lesions on the feet. The lesions may appear as blanched areas with little or no vesiculation. Even when vesicles are present on the oral mucosa, they rupture rapidly and leave raw denuded ulcers. Drooling, teeth grinding, lip smacking and rubbing affected areas are most commonly observed. Lactating cattle experience a sudden drop in milk production and develop lesions on the teats that can be quite extensive and severe.
Lameness characterized by hyperemia and ulceration of the coronary band are most common in horses and swine.
The disease course is usually only 3-4 days and most animals recover without complications. Lesions usually heal with 2-3 weeks. Persistent lameness can occur due to damage to the coronary band.
Humans are susceptible and can develop a fever and vesicles. Most of the human cases have involved those working with the virus in the laboratory or with vaccine production where large numbers of virus particles are present. Otherwise, most of the human infections are subclinical. In certain areas where the incidence in animals is high, 50% of the human population may have antibody titers.
Diagnosis
Notification of state or federal authorities is essential as with all vesicular diseases
Demonstration of viral antigen in tissues
Paired serum samples for antibody titers.
Virus isolation and identification
Control and prevention
Complicated by lack of understanding of the epidemiology and transmission.
Quarantine of affected premises until all clinical signs disappear.
Once diagnosed, extensive control measures are not as warranted as with other vesicular diseases.
Vaccination can assist in control and are primarily used to protect dairy cattle. Vaccines were used in the 1982-83 outbreak in the U.S.
Agalactia Syndrome of Sows (MMA)
This problem was initially termed "mastitis, metritis, agalactia (MMA) syndrome. It had historically been a major factor in piglet mortality but is not as common as it was 15 or 20 years ago. The syndrome is an acute problem, occurring 12 to 72 hours after parturition and characterized by agalactia or hypogalactia.
Etiology
Physiologic factors. Hormone imbalances have been blamed for many cases but the exact nature of the imbalances have not been clarified.
Coliform mastitis may be involved in some of the cases. E. coli, Klebsiella pneumoniae or Enterobacter spp. are the most common.
Vitamin E - Selenium deficiency has a role in resistance to infectious mastitis. Adequate supplementation has been shown to have a beneficial effect.
Toxemia associated with retained pigs is an occasional cause.
Mycotoxins have been implicated but many believe mycotoxins to be unlikely causes. Both ergot and zearalenone have been studied and experimentally cause agalactia.
Hypocalcemia and ketosis are involved only rarely.
Clinical signs
Coliform mastitis
There is usually a high fever (105-107(F) in the early acute stages that may decline rapidly in severe disease. The sows may be depressed and lethargic. The mammary glands are swollen, hyperemic and have a pitting type edema. Milk flow is markedly reduced, and may be coming only from unaffected portions of the gland. The affected glands usually involute rapidly. Total milk flow from the sow will be adversely affected. If the sow recovers, milk flow will return to relatively normal levels except in the affected glands.
Inappetence may be a contributing factor. Many sows don't eat during the first 12-24 hours after farrowing. Sows affected with coliform mastitis or other diseases such as TGE may not eat for several days.
Constipation often occurs in coliform mastitis but has also been implicated as a primary cause of agalactia in it's own right.
Metritis.
Usually not associated with the syndrome. There may be excess vaginal discharge (lochia) but this varies a lot between normal sows. If the discharge is purulent or bloody, there is probably an infection.
Agalactia. Detection requires knowledge of normal nursing behavior and careful observation of the clinical condition of the piglets. Diarrheal diseases in the piglets and other conditions can mimic starvation.
The behavior of the piglets is important to note. Nursing can take place during farrowing because milk is continually available. Normally, during the first 12-24 hours after birth the piglets sleep and nurse at irregular intervals. After this, nursing occurs every 40 to 60 minutes. It is important to note that not all normal nursings result in milk letdown. Sows with agalactia may not allow nursing this frequently, have fewer successful nursings and may produce little milk. Glands with mastitis may produce no milk.
There are five phases in normal piglet nursing.
1. Jostling for position on the udder.
2. Nosing the udder with vigorous up and down movements of the head.
3. The quiet phase during which piglets suck on the teats with slow mouth movements (about 1 per second).
4. Suckling with rapid mouth movements (about 3 per second). Milk can be expressed only during this short time.
5. A brief return to sucking with slow mouth movements and nosing the udder.
When pigs are squealing a lot, are continuously trying to nurse and drink water from the sows' watering cup, they are probably not getting enough milk. The pigs progressively lose weight and eventually become lethargic, pile up in a warm area, become emaciated, and die. Death generally occurs between 2 and 5 days of age due to hypoglycemia, diarrhea and being overlain by the sow. The severity of the agalactia or hypogalactia determines the clinical progession of starvation. Necropsy of the piglets reveals dehydration, emaciation, empty stomachs and serous atrophy of body fat.
The course of the disease in a sow varies with the cause of the agalactia or hypogalactia, it's severity, continued nursing attempts by the piglets so that the sow will resume lactation, and medication given to the sow.
Diagnosis - Coliform mastitis
Clincal signs of agalactia based on close observation of sow and piglet behavior during nursing attempts.
Bacteriologic culture is possible but somewhat difficult. Because the mammary gland is segmented, milk collected from a single gland may not contain any secretion from the infected portion of that gland. One must collect milk from several glands during the period of milk letdown.
Rule out other causes such as TGE, erysipelas, pseudorabies.
Prevention
It is essential to maintain good sanitation in the farrowing unit to minimize contamination of the teats. Avoid damage to the teats from fighting and other problems. Select sows with low incidence of lactational problems.
Autogenous bacterins are generally of questionable value. No data available on core-mutant vaccines.
Vitamin E, Selenium supplementation may be useful. Vitamin E at 50 IU/kg selenium at 0.1 ppm.
Treatment
Oxytocin 20-30 units several times a day to maintain milk flow. Gently!
Antimicrobials may be of some use, especially aminoglycosides.
Banamine at 1 mg/lb - 2 doses.
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