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Infectious Disease Test 3

Terms in this set (388)

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). 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 Aeradicate@ the disease from some farms. Control measures can also markedly reduce its impact by limiting secondary invaders.


Vaccination

Timing of vaccination, especially in PRRS cases, is critical in maximizing the protective immune response. 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.

Growing pigs are usually vaccinated at weaning and 3 weeks later.
Replacement gilts are routinely immunized.

Antibiotics

Tetracyclines suppress development of disease if started at time of exposure. Other antibiotics can be beneficial if given early.

Treatment


Quinolones (Baytril) and tulathromycin (Draxxin) are effective against mycoplasmal pneumonia. 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.
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 much in swine to the extent as that of human influenza virus. However, in March 2009 an H1N1 human influenza virus dubbed swine flu that had genetic elements of swine and avian flu strains was detected in Mexico and caused international alarm. In Mexico, the mortality rate was high and most deaths were in people 25 to 45 years of age (hallmark of pandemic flu). This strain had elements of 4 different viruses: Human influenza virus, North American swine influenza, North American avian influenza and swine influenza typically found in Asia and Europe. Interestingly, from December 2005 to February 2009, there were 12 diagnosed human infections with the classical strain of swine influenza virus in the U.S.

H3N2 viruses are common in humans as well as swine. The H3N2 swine 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 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.
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.
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.
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. On the other hand, in antibiotic-free herds, clinical signs can be seen in piglets as early as 3 - 5 weeks of age. In infected herds, slow an 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
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.

Immunization. Good results have been reported with the live oral product. Immunization at mid-nursery stage and for replacement gilts is used on some farms. Immunization can lessen the disease by decreasing the magnitude of colonization. Not all immunized pigs 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 least a few days before and after 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.

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 has been 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 contain blood. The bloody contents of the bowel does not clot. The cause or causes of this syndrome are not definitively known. Some feel that the blood in 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.
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.

Grow-finishers: Predominantly respiratory signs in this group and in breeder swine with only sporadic CNS signs. Pigs have temperatures of 41 to 42C 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.
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. Vaccination is not practiced in Iowa and some states have actually banned it. In countries where pseudorabies is present, vaccines can be helpful in preventing widespread infection. 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 that 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 had eradicated pseudorabies from Iowa, however, it was probably still present at least for a short period of time. The official declaration of free status was in 2004 for Iowa and the entire U.S.

Gene deletion vaccines: Any vaccine used in the State of Iowa had to have a gI deletion. The only way an animal could have antibody against the gI glycoprotein was to have been infected with the field virus.

Modified-live pseudorabies vaccines had to be used with caution. Although they were avirulent for swine, some of them were capable of producing disease in other animals. Syringes and needles used for vaccination led to fatal infections in other animals.
Leptospiral infections in swine used to be relatively common but clinical disease was not recognized frequently because most of the infections were subclinical or inapparent. Modern swine facilities, the use of routine immunization and antibiotics tend to limit the impact and many swine herds remain free of infection. 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.

Contaminated, untreated surface water used as a water source for swine has been responsible for some outbreaks.
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.
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.
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.
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.
Coliform mastitis

There is usually a high fever (105-107F) 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.