SWINE REPRODUCTION

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PATHOGENESIS, PREVENTION, AND TREATMENT OF LACTATIONAL INSUFFICIENCY IN SOWS Guy-Pierre Martineau, DMV, Bradford B. Smith, DVM, MS, PhD, and Beatrice Doize, DMV, MSc, PhD

Although the periparturient hypogalactia syndrome (PHS) of swine has been recognized for years, effective prophylactic and therapeutic management of the problem has frequently remained an elusive goal for the practitioner. These management difficulties are a reflection of (1) multiple causes producing similar clinical changes, (2) inconsistencies in the identification and classification of herds with lactational insufficiency, and (3) the complex interactions of environmental factors in the development of insufficient milk production at the herd level as well as at the individual level. These difficulties have resulted in many treatment recommendations that have been of questionable efficacy on a long-term basis in commercial pig production facilities. Historically, the approach to the management of PHS has been either antibiotic administration (either to individuals or to the entire herd) for the treatment of a range of ill-defined problems (in sows as well as in piglets) or induction of parturition with F series prostaglandins. Incorporation of bran in the feed is a common feature. Although these treatments sometimes are effective, in a significant percentage of the cases, the treatment is ineffective. Moreover, although the use of antibiotics may be useful in the short-term, it cannot be recommended for long-term usage. There are numerous causes of treatment failure, however, a substantial percentage of the problems can be traced to inaccurate identification of predisposing risk factors. For example, neonatal diarrhea can be diagnosed inaccurately as a cause and not as a consequence of PHS. Therefore, the From the Department of Medicine (GPM), the Groupe de Recherche sur les Maladies Infectieuses du Porc, Department of Pathology and Microbiology (BD), University of Montreal Faculty of Veterinary Medicine, Quebec, Canada; and the Oregon State University College of Veterinary Medicine, Corvallis, Oregon (BBS)

VETERINARY CLINICS OF NORTH AMERICA: FOOD ANIMAL PRACTICE VOLUME 8· NUMBER 3· NOVEMBER 1992

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focus of this article is on the accurate identification and the classification of problems at the herd level and on the role of environmental influences in the development of PHS. Particular emphasis is placed on the identification of specific risk factors predisposing a herd to the development of PHS. DEFINITIONS OF LACTATIONAL INSUFFICIENCY

The multiplicity of etiologies is reflected in the names that have been associated with this disease complex - coliform mastitis, agalactia toxemia, postpartum dysgalactia, puerperal mastitis, dysgalactia, mastitis-metritis-agalactia (MMA), and puerperal toxemia. 6,12,75,86,95,105 Although the term "MMA" has been used extensively, it is a misnomer. Indeed, few sows have a true agalactia, and the role of clinical metritis is of debatable significance. Recent work has suggested that subclinical metritis may, however, be of importance in the development of PHS. The term pariparturient hypogalactia syndrome (PHS) is used in this article. 95 This lack of a precise definition of PHS, at the individual as well as the herd level, has had many consequences. Until now, it has been impossible to provide a single etiologic definition of PHS. The dynamism and multiplicity of the terminology for PHS reflects this situation in the field. As currently seen under field conditions, the syndrome is more frequently associated with less spectacular signs such as poor induction of lactation than previously observed, with consequences of PHS sometimes only having an impact on piglet growth. This gradual change in the clinical presentation of PHS is most likely caused by improved herd health and productivity (Fig. 1). Clinical aspects and severity of PHS may vary from herd to

Incidence of herds with -lactation problems-

1960

1970

1980

1990

c::J Dysgalactia syndrome rllllZll -Classical- MMA syndrome Figure 1. Relative importance of classical mastitis-metritis-agalactia (MMA) syndrome and PHS during the past 30 years. As the total prevalence of lactational insufficiency has increased, the relative contribution of classical MMA syndrome has decreased with a concurrent increase in herds with a relative hypogalactia (PHS).

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herd according to the quantitative and qualitative records available for each herd as well as its health status. Because of the difficulties involved in assessing a single definition of PHS, and to provide a better clinical definition, Miquet et al63 developed an index to rank the severity of PHS in affected sows according to the intensity and duration of the symptoms. This index also provides an approach to classifying the gravity of PHS in a given herd. The parameters used for the construction of this index are listed in Table 1. This index is useful as a guideline for the practitioner. Therefore, it may be possible to follow cohorts of sows from day 0 to day 6 postpartum and develop an index for each sow. Table 2 gives an example of the distribution of the index in a group of 136 sows. In this study, an index greater than 4 was used to identify the presence of PHS, whereas an index greater than 6 identified a severe problem of PHS.

PREVALENCE One of the primary difficulties in assessing the prevalence of PHS is establishing a functional definition of lactational insufficiency. This diversity of classification criteria is reflected in a study by Jorsal,47 who classified animals as having PHS if they had one or more of the following symptoms: agalactia, anorexia, constipation, vaginal discharge, inflammation of mammary gland, or a rectal temperature higher than 39.8°C (l03.6°F). In contrast, Persson 76 classified an animal as having a subclinical case by a normal rectal temperature (less than 39.5 °C [103 ° F]), absence of clinical mastitis, but with a cell count of greater than 10 million/mL in mammary secretions. These examples underline the difficulty in comparing field observations. Microbiologists frequently see PHS as a primary infectious disease, endocrinologists perceive it as an endocrinologic disturbance, and others consider it a nutritional disease, which illustrate the diversity of the definitions, and, therefore, the prevalence. Even to the clinician, there are different levels of definitions according to the quantitative and qualitative nature of the available data, such as total herd productivity, quality of the nursing piglets (growth, homogeneity), health status, and so forth. Therefore, although a definition is difficult to formulate, many criteria may be used to assess the presence of the disease in sows as well as its consequences at the piglet level (at the individual level or at the level of the litter). It is also essential to evaluate the herd's risk for PHS.

Table 1. EXAMPLE OF A PHS INDEX USED TO ASSESS THE SEVERITY OF THE SYNDROME IN A GIVEN HERD* Criteria Rectal temperaturet Anorexia; Mammary gland aspects Vulvar discharge Delayed parturition§

Duration DO DO DO DO DO

to to to to

05 05 05 05

Index

o to 6 o to 6 o to 6 o to 6 o to 2

*An individual index is calculated for each sow during the 5 days after farrowing. A mean for a cohort of sows may then be calculated. For example, a sow with hyperthermia during 3 days, partial anorexia « half meal) during 3 days, 4 days of a vaginal discharge, no' change in the mammary gland aspect, and a normal parturition has an index of 8.5 (3 + 1.5 + 4). t>39.8°C (103.6°F); =1=< half meal = 0.5; > half meal = 1; §5h = 2. From Miquet JM, Madec F, Paboeuf F: Epidemiologie des troubles de la mise bas chez la truie: Premiers resultats d'une etude realisee dans deux elevages. J Rech Porcine en France 22:325, 1990; with permission.

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Table 2. PREVALENCE OF CLINICAL CHANGES IN SOWS WITH PHS (% OF 136 SOWS THAT PRESENTED ONE OR MORE SYMPTOMS AT ANY TIME DURING THE OBSERVATION PERIOD) Symptoms

Percent

Vulvar discharges Hyperthermia· Mammary changes Poor appetite Delayed parturition

47 11 2 45 13

*>39.8°C (103.6°F) From Miquet JM, Madec F, Paboeuf F: Epidemiologie des troubles de la mise bas chez la truie. Premiers resultats d'une etude realisee dans deux elevages. J Rech Porcine en France 22:325 - 332, 1990; with permission.

Despite the fact that many worldwide references concerning the prevalence of PHS are available,97 it is important to remember that the prevalence depends on the criteria used to assess the presence and severity of the disease. Moreover, the proportion of sick sows in each herd is another important parameter. Table 2 emphasizes the variability within a single herd in the symptoms of PHS. In this study, only 15 sows had hyperthermia, but more than half of the sows had vulvar discharges and/or poor appetite. The importance of the symptoms vary from herd to herd. Nevertheless, these observations confirm the fact that the unit of investigation is not the individual animal but the herd, as emphasized by Hermansson43 15 years ago. Both the absolute number and relative incidence of subclinical cases of PHS have increased significantly during the past 10 years (Fig. 1). Clinical changes consistently observed in "classic" cases of PHS in the sow included anorexia, constipation, or depression. 12,43,75,82,85 In contrast, recent work27 has demonstrated that the clinical presentation of PHS may be changing significantly; specifically, only the piglets may be affected while the sow is clinically normal. An important ramification of this change is that subtle changes in the piglets have to be more carefully evaluated; specifically, changes in piglet weight and/or litter homogeneity.l08 LACTOGENESIS AND NURSING BEHAVIOR

Understanding the factors influencing lactogenesis and nursing behavior is important in understanding the pathophysiology and diagnosing PHS accurately.97 Although the general periparturient changes in progesterone, estrogens, relaxin, and prolactin have been reviewed elsewhere,97 it is important to note that there is also substantial individual animal variability.2,92 Moreover, the relative hormonal changes are not always synchronous, particularly with relaxin further complicating the issue. 48,99 Timing of the initial increase in the concentration of plasma prolactin coincided with a similar rise in plasma lactose. This observation may be associated with those of Gooneratne et al,39 who reported that lactose concentrations in the colostrum of sows that subsequently became agalactic were higher than in normal sows. These authors suggested that the altered lactose concentrations may be associated with the premature initiation of lactation, an interesting theory that remains to be confirmed even if subsequent work generally has not supported this view. Nevertheless, this premature initiation of lactation may be associated with a

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common clinical observation; that is, "milk let-down" as early as just prior to parturition in sows from herds with a high percentage of PHS (Martineau G-P, personal observation; Dewaele, personal communication). Normal nursing behavior involves a sequence of distinct phases occurring over a 2- to 3-minute interval, with the majority of milk ejection occurring during a 10- to 20-second interval. 34,88 Careful observation is one of the most effective ways to assess the nursing behavior of the sow. Once the sow begins to vocalize, the piglets usually stop jostling for position on the teats and begin to nurse actively. In sows with adequate milk production, the piglets are usually relatively quiet at the end of the milk ejection, with some of the animals falling asleep. Milk around the snout is another indication of adequate milk consumption. Piglets not receiving adequate milk frequently persist in fighting over teat position, do not settle down, and continue attempting to nurse once the sow has ceased vocalizing. These changes, however, are not easy to take into account when visiting a large herd. Although there is substantial individual variability in colostrum volume and immunoglobulin concentration,50,51 most of the colostrum is released in an intermittent manner during the first 4 to 6 hours postpartum.37 In addition to providing a source of immunoglobulins for the neonate, colostrum is also an important source of energy during the periparturient period. Decreased energy availability in PHS sows is an important factor in increasing piglet susceptibility to a range of pathogenic organisms during the periparturient period. 121 These losses are associated with lactational failure as well as with weight loss due to metabolic losses when piglets' attempt to nurse from these sows with PHS. Indeed, metabolic losses are proportional to metabolic body size and are twice as great in moving piglets as in sleeping piglets. Moreover, in the case of unsuccessful sucklings, it has been reported that there was an additional average piglet weight loss of twice that of moving piglets, hence fourfold that of sleeping piglets. 49,71 These losses are attributable to these piglets' higher activity, loss of saliva during stimulation of the mammary gland, and fighting for teats. This is the reason that a high level of teat fidelity is an advantage for piglets, because it reduces teat disputes and the resultant chance of missing a nursing. 28 These results illustrate the need for careful observation of nursing behavior to identifying PHS-affected animals. ll0,120 This is of particular importance during the animal's first week of life. From a clinical examination point of view, these modifications are difficult to quantify and to evaluate on a large scale in a large herd.

CLINICAL PRESENTATION

The primary clinical signs of PHS are associated with the sow's inability to meet the nutritional requirements of her piglets. PHS is observed almost exclusively within the first 3 days postpartum; more than 50% of affected sows show clinical signs of insufficient milk production within the first 24 hours postpartum.43 PHS is rarely observed more than 72 hours postpartum,43,75,82 although the manifestations of early nutritional insufficiency by the piglets more frequently begin 3 days postpartum. The clinical polymorphism of PHS is a prominent feature. With the general increase in herd productivity and health status, "classical" manifestations (often dramatic in clinical terms) are less frequently seen whereas more subtle symptoms are more frequently observed yet are more difficult to analyze. 97 This subclinical PHS can have an important effect on total herd productivity. In a given herd, not all sows have the same symptoms or intensity of clinical manifestations. Furthermore, the number of affected sows may vary. The less perceptible clinical symptoms also have economic repercussions. Table 3

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Table 3. LIST OF SYMPTOMS ACCORDING TO TARGET ANIMALS AND PRODUCTIVITY LEVEL. THE SEVERITY OF THESE SYMPTOMS MAY VARY HERD TO HERD AND ANIMAL TO ANIMAL Symptoms in sows Local symptoms absent "mastitis - agalactia" vaginal discharge General symptoms absent

fever prostration anorexia (total or partial)

Symptoms in piglets 1 Week increased heterogeneity among the litter Low weaning weight

Herd productivity symptoms Decreased PSY Decreased quality of nursing piglets

PSY = piglets/sow/year

summarizes the symptoms that are commonly observed at a herd level. It is uncommon to observe all these symptoms in a given sow and its litter. However, they are present at a herd level. Contrary to general belief, clinical changes in the sow frequently are not obvious. In most herds, fewer than 10% of the PHS animals have a poor appetite and a postpartum fever greater than 39.5°C (103°F). Although fever generally is accepted as an indicator of PHS, the definition of "fever" differs among clinicians and may vary between 39.4°C to 39.8°C (103-104°F). Some authors choose two levels of temperature, 39.8°C (104°F) and 40.5°C (l05°F), to differentiate between mild and severe cases of PHS. Furniss36 measured daily rectal temperatures of normal sows and those that subsequently developed either moderate or severe cases of lactational failure from the day preceding parturition until 2 days following parturition. Rectal temperatures of greater than 39.4 °C (103 OF) on the afternoon of parturition or at approximately 18 hours following parturition were a good predictor of which animals would develop PHS. Furniss36 also reported no difference in the rectal temperatures of normal sows and sows with PHS 1 day prior to parturition, but others4o,41,77 have reported an increase in rectal temperatures of affected sows when examined 1 day prior to parturition. BernerB established a relationship between the fever and the gravity of PHS. Sows classified with mild and moderate disease had rectal temperatures less than 39.8°C (104°F). Despite its limitations, temperature can be used as a monitoring tool in a herd at risk for PHS, where only a few sows exhibit "classical" PHS symptoms such as anorexia and mammary gland symptoms. In litters, PHS increased the risk of pre weaning diarrhea by 90%.47 When present, it may be possible to observe two patterns of diarrhea. One pattern begins prior to 24 hours of age53,58 and is typically self-limiting (Martineau G-P, personal observations), although the other is encountered in piglets at about 2 to 4 days of age. This latter diarrhea is often classified as a primary colibacillosis. Aside from heterogeneity and undersized piglets, there are no other symptoms after 1 week of age in the majority of cases. In litters affected with PHS there is already a perceptible heterogeneity within litters soon after birth, which continues until weaning. 33 In these litters, it is common to observe one or two piglets within each litter that rapidly become emaciated. Restless piglets are another common observation.

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At the productivity level, there sometimes is an increase in the frequency of stillborn or crushed piglets and an increase in total preweaning mortality. Even if clinical symptoms appear minimal, it may be possible to note some "abnormal" daily management rules, such as an increase in the use of drugs in sows (antimicrobial, antipyretic, anti-inflammatory, oxytocin) and in piglets (mainly antimicrobials). Pathophysiology

Although there is still significant debate concerning the origin of systemic change, it appears that interactions between endotoxin produced by gram-negative bacteria and alterations in immune and endocrine function playa central role in the development of PHS (Fig. 2). Furthermore, all these interactions are closely related, and it becomes difficult to study them separately. For example, once absorbed, endotoxins exert profound effects on the immune, cardiovascular, and endocrine systems. Owing to the common metabolic pathways associated with many of these effects, it is impossible to evaluate the relative importance of each change, and in each system, on milk production. Supporting the role of endotoxins in the development of PHS, experimental administration of lipopolysaccharide to periparturient sows has produced clinical and hematologic changes that closely mimic field cases of hypogalactia. 68,69 Only a few experimental studies have been done to establish the exact involvement of this agent in the physiopathologic/biochemical mechanisms involved in maternal hypogalactia or agalactia. 33 Results from a study by De Ruijter et aP9 suggest that the

RISK FACTOR

ENVIRONMENT

EVENTS

ANIMALS

DRINKING

Parturition

Uterus

STRESS and/or INFECTION

Stress

In testin e

Inflammatory mediators

1

Endocrinological dysfunction

PHS

FEEDING

Endotoxem ia

1

PHS·IIII----- Prolactin

Figure 2. A hypothetical approach to the pathophysiology of PHS, taking into account some risk factors, several events that may lead to infection, and stress.

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systemic signs in mastitic sows are predominantly the results of the formation of inflammatory endogenous mediators in the mammary gland and their subsequent release into the circulation subsequent to the absorption of endotoxin. Prolactin (PRL), an anterior pituitary hormone, is involved in the initiation and maintenance of lactation in numerous species. 15 Under normal conditions, it primarily is under inhibitory control by dopamine released from the medial basal hypothalamus. Threlfall et aP03 reported that PRL concentrations were suppressed in hypogalactic sows. The interaction between LPS and PRL concentrations was further clarified in another study93 that demonstrated a concurrent decline in PRL concentrations and milk production following LPS administration. Indeed, tolerance to endotoxin can be induced rapidly. Sows that became tolerant to endotoxin are still quite susceptible to the pyrogenic action of endogenous mediators such as interleukine. Stress seems important in the pathophysiology of the syndrome. 109 Stress may also exert a significant effect in the stimulation of the beta-2 receptors, resulting in uterine inertia and a delay in parturition. Stress has other direct effects on lactation as it induces the release of epinephrine, which has been shown to block oxytocin-induced milk ejection. 20 The role of LPS in the pathogenesis has been examined by Truszczynski et aP07 and Morkoc et a164 using the limulus amebocyte lysate test (LAL test). Although fewer than 40% of the clinically affected PHS sows had detectable LPS concentrations, this may be the result of the relative insensitivity of the LAL assay and the rapid absorption of LPS from the circulation, probably by macrophages. Indeed, LPS has a half-life of less than 10 minutes in the pig. 122 The origin of the endotoxemia may differ from herd to herd and theoretically can originate from the mammary gland, uterus, urinary tract, or gastrointestinal tract. The target organ (mammary glands, uterus, gut, or bladder) that may lead to a resorption of endotoxin has to be identified at the herd level. This is not always easy, because only some sows exhibit enough symptoms to give clinical information, and more than one target organ may be involved. Mammary Glands and Mastitis

Numerous experiments have established the role of gram-negative mammary infections in the development of PHS.13,82,85,86 To better characterize this group of animals, Bertschinger et aP2 introduced the term coliform mastitis (CM) to describe gram-negative coliform mammary infections in the periparturient sow caused by bacteria of the genus Escherichia, Klebsiella, Enterobacter, or Citrobacter. Studies involving the experimental infusion of a field isolate of E. coli into the lactiferous sinus of sows has been shown to produce an acute mastitis and a concurrent increase in serum LPS concentrations. 96 The clinical changes closely mimic field cases of acute onset of PHS. Experimental intramammary inoculations with field strains of E. COli 87 and K. pneumoniae52 have produced similar results of PHS that closely mimic naturally occurring cases of hypogalactia. Therefore, sytemic changes observed in CM may be the result of endotoxin production within the mammary glands or inflammatory endogenous mediators,29 perhaps interleukine1 (IL-1). There is also an association between the isolation of E. coli from the mammary glands and the presence of fever. The presence or absence of hyperthermia is not, however, a pathognomonic sign of PHS. For example, in one study/3 no bacterial isolates were found in 15% of the hyperthermic animals, whereas significant coliform isolates were collected from mammary glands in an additional 26% of the herd that did not have an elevated rectal temperature. The number of affected mammary glands also may vary significantly, both

669 from sow to sow and from herd to herd, In the study by Wegmann et al 116 involving 59 sows from 15 herds, 83% of the sows were affected with mastitis in at least one mammary gland, with an average of three affected glands. In this study, it is also interesting to note that fewer than 40% sows had a fever (>39.5°C, 103°F). The predisposing factors leading to bacterial colonization of the mammary gland are not fully understood. Natural predisposition may occur: the milk composition appeared to influence the growth characteristics of E. coli in one study.114 Several coliform strains grew significantly better in whey samples collected on the day of farrowing than in whey samples collected later during lactation. These results suggest that, 1 week after parturition, E. coli is difficult to isolate from mammary glands with a history of previous E. coli infection. 1l4 This may be explained on the basis of the impaired growth conditions for E. coli in secretions from mastitic glands. 114,117 Likewise, bacterial growth was greater in whey samples collected from sows with elevated temperatures, with or without signs of PHS.81 Similar observations have been reported in the cow when comparing bacterial growth in normal and mastitic milk. 62 Coliform mastitis also is influenced by the degree of fecal contamination of teat ends and the surroundings. 116 Therefore, it seems logical that dirty floors are an important factor. 114,115 Wegmann et aP16 postulated that the incidence of PHS is due, to a significant extent, to the system of stalling. It must be emphasized, however, that PHS is also very common in high health status herds. One of the reasons for the correlation between flooring and the incidence of PHS may be that the comparison was performed between sows individually housed in conventional farrowing crates bedded with straw and wood shavings and those given access to outdoor runs for defecation and urination. The behavior of the sow, however, is significantly different in the two types of housing. As a result, high floor and teat-end bacterial counts may reflect the behavioral changes, which may explain why the prevalence of PHS is lower in sows farrowing outside, as reported by Backstrom et al. 5 LACTATIONAL INSUFFICIENCY IN SOWS

Uterus - Metritis

The role of uterine infection in the development of PHS is controversial. Both direct and indirect arguments, however, are in favor of the involvement of the uterus in the pathophysiology of PHS, such as arguments associated with the positive results obtained by the use of prostaglandins and/or ft-blocking agents. 10 Not all cases of puerperal fever appear to be due to mastitis. 79 Although metritis was originally considered to be a significant component of the disease complex,4,64,66,75,105 examinations of the reproductive tracts of normal and affected animals generally have not supported this conc1usion. 46,67,82,84,100 These conflicting results may reflect a uterine reaction, which differs from those of the mammary gland. Indeed, in contrast to mastitis, which almost always causes a severe general disorder, endometritis is more frequently subclinical. Bemer1 detected symptoms of mastitis 6 to 24 hours later than those of endometritis, and the highest concentration of bacteria in the uterus was found following delayed parturition. This is perhaps one of the reasons for the discrepancy about the role of uterus in PHS. The origin of the uterine tract infection (UTI) is controversial. Some epidemiologic observations seem to emphasize primary urinary tract infection and the subsequent development of PHS when infection of the uterus occurs during the postpartum period. Indeed, a positive correlation was established between bacterium and albuminuria prepartum and the subsequent development of a lactational insufficiency.72 It is also common to observe UTI in high health status herds in

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which PHS is an important problem. If both gram-negative bacteria and protein were detected in urine samples prepartum, there was a 97% probability of the sow developing PHS postpartum. Likewise, if both prepartum tests were negative, there was a 74% probability of the sow not developing lactational problems. Based on other field investigations, Berner and Jochle lo stated that UTI always preceded urinary tract infection. For these authors, the majority of the sows suffering from puerperal endometritis showed no bacteriuria or cystitis prepartum. For this latter group, puerperal endometritis appears to provide the nidus for infection of the urinary bladder, and thus the cause of puerperal cystitiS. I8 They conclude that quantitatively defined bacteriuria has no clinical value. Nonsignificant bacteriuria «105 bacteria/mL) is mainly produced by extracystic bacterial additions. 19 One other indirect proof of uterine involvement concerns the results from Peter et al,78 who suggest that inhibition of uterine secretion of PGF 2a after delivery may remove an important stimulus to prolactin secretion in the immediate postpartum period. An altered uterine PGF2a secretion influencing prolactin secretion may play an important role in the onset of some cases of PHS in sows.

Bladder and Urinary Tract Infection

Although UTI should be considered as a predisposing risk factor,54,55 its role in the pathophysiology of PHS is less well-established. Based on clinical observations, it appears that there also may be a correlation between low water consumption, the fat sow syndrome, and the development of UTI or postpartum uterine infection in the sow. The low water consumption may be due to an inadequate water supply, lameness, excessive weight, or any other factor limiting normal water consumption. 56 With decreased water consumption and subsequent decreased urination, it has been hypothesized that ascending infections can develop much more readily in contaminated environments. Adding indirect support to the role of UTI in the development of PHS, Pejsak et aF4 tested a human polyvalent vaccine on sows in herds with high incidence of UTI. This vaccine was found to be effective in one reported study9 in reducing the number of pathogens found in urine samples collected from sows at parturition but another study found it less effective. In contrast, although the vaccine did not eliminate UTI in the chronic nonpregnant animals, it did eliminate bacterial contamination in the genital tract in 5 of 12 pregnant animals. Although the sample size in both studies was not sufficient to evaluate the efficacy of UTI vaccinations adequately, the work does support the concept of UTI playing a significant role in the development of PHS. One other indirect support for the role of UTI in the development of PHS concerns the low frequency of PHS in prostaglandin-treated sows, which may be the result of frequent urination and defecation after giving birth. 21 Those observations also illustrate the importance of checking water availability in pregnant SOWS. 57

Gut, Nutrition, and Absorption of Endotoxin

Some results have suggested that endotoxin may be produced in the intestinal tract and can lead to PHS,23 which perhaps explains why constipation and low intestinal transit may be risk factors for the development of PHS. Although nutritional disorders are clearly a significant factor in the development of PHS,

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prior to 1980 there was relatively little research that examined the correlation between nutrition and PHS. A major exception was the work of Ringarp,82 who demonstrated that it was possible to produce "agalactia toxemia" by making drastic dietary changes during the last week of gestation. Ringarp82 also reported a high incidence of constipation in agalactic sows and indicated that wheat bran in the diet reduced the incidence of PHS by functioning as a laxative, an approach extensively used by many producers. Following this approach, Wallace et al ll1 reported a decline in the incidence of PHS with the inclusion of alfalfa meal in the diet. However, the positive effect seems dependent on the gravity of the syndrome. 112 The results from the literature are conflicting, but not all parameters were reported and hence were insufficient to assess for or against the validity of this approach. 1,68 One of the major difficulties in interpreting the conflicting results of various dietary studies is the different chemical definitions of llfiber" and the fact that inclusion of a high-fiber feedstuff results in changes in the relative amounts of other components. 40 ,41,45,90,91 Sandstedt and Sj ogren90 reported that a very low feed allowance in combination with free access to straw during the last 3 weeks prior to parturition significantly reduced the incidence of PHS, a conclusion supported by Jensen45 in a similar experiment. With increased dietary fiber content, there is also a concurrent decrease in the incidence of constipation, a problem reported in approximately 25% of the sows classified as having PHS.43 Other researchers have suggested that the dietary protein concentration and type of protein, rather than the fiber content, are critical factors in the development of PHS. Sandstedt89 concluded that a high dietary protein content was the most common cause of PHS, a conclusion that differs from Thurman,104 who suggested that as long as the dietary protein content was between 10 and 18%, it did not affect the development of PHS. Although the interaction of dietary protein concentration and the development of PHS is unresolved, increasing dietary fiber content usually results in a lower protein concentration, an approach widely used under field conditions to reduce the incidence of PHS. The type of protein also may influence the incidence of PHS, and use of a therapeutical vegetal diet is well-recognized. 41 Results from Goransson40 suggest that total dietary energy is probably a more important factor than the protein concentration in the development of PHS. In practice, decreasing food consumption during late gestation appears to be most effective in herds with a high incidence of PHS (>30-35 % ). In herds with a relatively low incidence of lactational insufficiency «10-15%), this approach is less likely to be effective. A growing body of research has suggested a relationship between selenium and vitamin E deficiencies and lactational insufficiency in the SOW. 106,119 In several studies, sows on a selenium- and/or vitamin E-deficient diet had a significantly higher incidence of PHS than control animals. The mechanism of vitamin Eand/or selenium-induced lactational deficiency has not been established, although it has been shown that both playa role in normal leukocyte function 31 and in the protection of the cell membrane, which may be affected by endotoxins. With the general use of vitamin E and selenium supplementation, the primary deficiency is uncommon, although subdeficiency carence may occur. It is unclear, however, whether increasing either vitamin E or selenium concentrations above generally accepted dietary concentrations will reduce, let alone prevent, the incidence of PHS. Beside endotoxin-prolactin interaction, stress-prolactin interaction is probably another group of causative factors. The importance of this interaction is not as well-characterized as it is for the endotoxin-prolactin interaction. Recent work suggests that stress can be an important factor. For example, the change of housing system is unavoidable, but some studies emphasize this factor as a risk factor. For

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example, multiparous sows kept in gestation crates 60 cm in width have a PHS scoring index higher than those kept in crates with a width of 67 cm. 22 Furthermore, the complete opposite applies to primiparous sows. There are many other sources of stress. Although it has not been documented in swine operations, stray voltage may be a source of stress. The following are reported in individual cases of PHS: teat malformation, hypoplastic mammary glands of unknown etiology, psychogenic agalactia, failure of milk ejection, and mammary gland edema. 97 The reasons are unknown or, at best, only vaguely recognized. Overheating of the mammary glands can occasionally cause a decrease in milk production. One study65 reported that placement of heat lamps too close to the glands resulted in localized burning of the latter. Ketosis and hypocalcemia occasionally have been reported as causes of lactational insufficiency.75,82 Treatment for both conditions is similar to that used in other species. At the herd level, two conditions lead to acute agalactia syndrome. Although infrequently observed, ergot toxicity can produce PHS. Grain contamination with ergot derivatives produced by Claviceps purpurea has been reported to cause lactation failure in the SOW. 3,75 These cases usually were acute, and affected sows had typically flaccid mammary glands, normal rectal temperatures, increased excitability, and carpal erosions. 3,75 Ergot derivatives are known to suppress prolactin release. 15,94,118 A general systemic disease with a high fever pattern also may lead to agalactia. We have observed this frequently with the swine reproductive and respiratory syndrome. 16,17,59,60,80,102 RISK FACTORS

The key element in reducing the incidence of PHS in a herd is identification of specific risk factors. Unfortunately, because the underlying cause of PHS in many herds is still uncertain, establishing a hierarchy of risk factors is difficult. Risk factors are related to certain characteristics, which have been identified as being different in healthy and sick ecosystems (a herd with PHS is considered as a sick ecosystem). These risk factors are not necessarily of an etiologic nature. In fact, taken individually, they are rarely the origin of the problem. The interplay between some of these risk factors, however, can lead to PHS. Many factors associated with the pathophysiology of PHS also may be considered in the group of risk factors even though their direct implication is more obvious. Animals

The relationship between parity and the incidence of PHS is unclear. For example, in an epidemiologic survey, Jorsal47 concluded that the incidence of PHS declined with increasing parity. In the same study, a case of PHS increased the sow's risk of developing PHS at the following parity, irrespective of the age of the SOW.47,123 These observations are supported by Bertschinger and Buhlmann,l1 who concluded that infection of a mammary gland does not protect this gland against proliferation of the same organisms in a subsequent lactation. In contrast, other studies97 have shown that the occurrence of PHS does not appear to predispose the sow to lactational problems during subsequent lactations. Nevertheless, the consequences of these factors are important because they affect the culling decision for a PHS-affected sow. Other individual factors such as litter size,47,63 obesity, the fat sow syndrome (FSS),61,63 or locomotor disturbances55,63 may have to be considered. Another risk factor is associated with the duration of parturition.

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Prolonged farrowing is a common but multifactorial problem. Jorsal47 reported that obstetric aid by either herd managers or veterinarians resulted in a fourfold increase in the sow's risk of acquiring PHS. Many factors may lead to a prolonged farrowing period at the herd level. They must be considered when investigating PHS at the herd level. One of the more common observations of a prolonged parturition occurs with high temperature in the farrowing unit, FSS, and stress. The low locomotor activity is another individual factor that is difficult to analyze. Many of these factors are confounding variables and therefore must be confirmed.

Housing

Housing during gestation and lactation are important factors in the development of PHS.6,23,63 Stray voltage is another stress factor often present in swine operations. However, despite the fact that many allegations from producers and others38,39 support its role in farrowing problems, scientific backing has yet to be confirmed. 83 Many of these factors are not easy to change or should not be modified. They must, however, be taken into account in order to understand herd susceptibility to PHS.

Nutrition and Feeding

Extremely dry feces prior to farrowing have previously been shown to be related to the syndrome as well as to nutritional changes (fiber, energy, protein) prior to farrowing such as changes in fiber content and/or fiber quality, protein and/ or energy content, protein quality, vitamins, and oligo-elements. These have been discussed elsewhere, and more complete references are available. 97

Management

Changes in certain management operations within the gestation section, as well as within the farrowing section, are important factors that must be considered. Management is probably the most difficult factor to evaluate, because there is often a great discrepancy between what the producer does and how he or she perceives what has been done.

Microorganisms

The main objective when evaluating this risk factor is to evaluate the importance of endotoxemia in PHS at the herd level and to identify its origin(s): urinary tract, and/or mammary gland, and/or uterus, and/or gut.

Drinking

Low water intake and changes in drinking troughs between gestation and farrowing sections are commonly encountered in the field. Despite its difficulty to assess, low water intake could be evaluated. 56

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ASSOCIATIONS BETWEEN RISK FACTORS

Taken separately, many risk factors are not sufficient to lead to PHS. However, from field observations, the associations between risk factors are probably not additive but synergistic.

Association between primiparous sows, locomotor disturbances, obesity, and changes in housing and floor-type (Fig. 3). It is common to see" obese" primiparous sows. The severity of "leg weakness" (osteochondrosis) is greater in heavy and young animals and is aggravated when sows are kept on a slippery floor or a floor very different from those found in the gestation bam. These features (primiparous, obesity, leg weakness, stress) lead to relative inactivity and a modification in nursing behavior. This inactivity may increase constipation and low water intake. In addition, obesity is a predisposing factor to a prolonged parturition. Associations of some of these risk factors may lead to PHS.

Association between multiparous sows, urinary tract infection, and locomotor disturbances (Fig. 4). UTI is more common as parity increases. 26 There is a relationship between UTI with locomotor disturbances or uterine infection postpartum. 57 Associations of some of these risk factors may lead to PHS. Association between drastic changes in housing, floor, or temperature (Fig. 5). These changes are obviously a source of stress and may easily cause prolonged farrowing and modified nursing behavior, and ultimately may lead to PHS. Association between the FSS, leg weakness, and slow farrowing (Fig. 6). FSS alone generally is insufficient to lead to PHS. It is, however, common to diagnose PHS in a herd in which this syndrome is present. 61 FSS has many consequences in gestation (vaginitis, locomotor problems) and during farrowing (delayed parturition). Association between low water intake and PHS. Low water intake while the sow is occupying the farrowing crate 1 week before parturition is a common observa-

Primiparous sows

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Figure 3. Association of some risk factors such as primiparous sows, locomotor disturbances, obesity, and change of floor type. It is a common observation to see obese primiparous sows. These animals often have locomotor disturbances, especially if the floor type of the farrowing crate is very different from the gestation section. These three characteristics lead to relative inactivity and a modification in nursing behavior. This inactivity may increase constipation or lower water intake. Association of some of these recognized risk factors may lead to PHS.

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Multiparous

Sf \

I

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Urinary

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Figure 4. Association of various risk factors leading to PHS.

tion. Although water quality is often emphasized, the quantitative aspect is far more important. The consequences are obvious: constipation, low activity, urinary tract infection, and so forth. DIAGNOSIS Clinical Diagnosis

The objectives of the diagnosis are an accurate identification of the affected animals, the identification of herds affected by PHS (herds at risk), the determination of the severity, and the prediction of the evolution of a PHS problem. Determination of all the risk factors often is not easy. Care should be taken to avoid simplifying by associating it with a single risk factor. The use of a few therapeutic approaches may lead to a partial cure and a decrease in the severity of the condition in many cases, however. It should be emphasized that careful observation of nursing behavior is one of the best methods used to identify PHS animals.

Changes in flooring systems or slipery floors

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Figure 5. Relationship of some risk factors of PHS associated with housing.

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Figure 6. AssOCiation of some risk factors of PHS with the fat sow syndrome.

Laboratory Findings Bacteriology

Microbiologic examination of the mammary glands, uterus, and bladder can be performed. There does not appear to be a dominant serotype(s) of E. coli collected from field cases of PHS. There does, however, appear to be significant differences in strain pathogenicity.87 Bacteriuria is a questionable finding, and only a concentration exceeding a certain threshold may be significant. Clinical Pathology

Differences in total cell count and content, taken together with the change in polymorphonuclear (PMN) cell content from unaffected mammary glands of healthy sows, must be considered. When both cell count and pH were evaluated, healthy and PHS sows could be differentiated clearly.72 Elevated somatic cell counts, however, can be misleading in the diagnosis of PHS.ll The somatic cell counts per gland are affected by the time period between farrowing and sample collection. 72,113 Despite their limitations, Persson 76 used cell counts in mammary secretions to differentiate subclinical from normal cases. Many hematologic changes have been observed consistently in hypogalactic SOWS. 96,97 Their use as a diagnostic tool is still limited. PROPHYLAXIS AND TREATMENT

When PHS occurs in a sow, the main objectives are to avoid piglet dehydration, provide an alternate source of energy, and stimulate milk production. For instance, recent observations suggest that piglets will drink appreciable amounts of tap water on the first day following birth, particularly if milk intake is limited. 35 These authors speculate that, under these conditions, water intake may help prevent dehydration and promote the survival of piglets with low early milk intake. In sporadic cases of PHS in which the cause is uncertain, the most likely cause of PHS is eM. Antibiotic administration following an initial oxytocin injection is probably the most effective treatment. Selection of an antibiotic should be based

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on its spectrum of activity against gram-negative organisms and previous experience and exposure on the farm. If mammary edema is a problem, a low dose of a diuretic (e.g., furosemide), or glucocorticoid may be effective. Treatment with flunixin meglumine often is beneficial. Dosages of 5 to 10 USP units of oxytocin are sufficient to initiate milk ejection and result in circulating oxytocin concentrations greater than those normally produced by suckling. If necessary, repeated dosages can be given safely at hourly intervals for at least 6 hours. Prostaglandins

PGF 2a is a natural luteolytic agent in sows, causing a prepartum decline in progesterone and the release of relaxin from the corpea lutea,70 which results in an immediate and sharp increase in prolactin concentrations that last about 6 hours. 101 In many herds in which a significant percentage of the gilts and sows have PHS, induction of labor with the F series of prostaglandins (PGF) has proved effective in reducing the incidence of PHS.24,44 Induced parturition probably reduces ascendant infections of the puerperal uterus with E. coli. This reduced bacterial count may result from more frequent and complete micturitions and hence a consequently lower bacterial count in urine and the mucous membranes of the urogenital sinus. 10 The mechanism by which PGF induced parturition reduces PHS is unknown, although it has been speculated that premature mammary engorgement is prevented. With less engorgement, the incidence of mastitis caused by contamination of the dilated teats and the subsequent development of PHS is reduced. Some authors,3o,42 however, reported that PGF administration had no effect on the incidence of PHS. It may be possible that this failure could be due to other PHS pathways. Prostaglandin Synthetase Inhibitors

The prostaglandin synthetase inhibitors are effective in the treatment of endotoxemia in a wide range of species and probably function in a similar manner in the sow affected with PHS. Administration of flunixin meglumine, a prostaglandin synthetase inhibitor, resulted in a decrease in mammary edema and anorexia and an improvement in piglet weight at 7 days following treatment. 25 P-Blocking Agents

One of the more interesting developments in the past few years has been the use of P-blocking agents to accelerate the onset of parturition. Administration of the P-2 blocking agent carazolol has a positive effect on PHS.20,21 In one study,21 Busse noted that the frequency of urination and defecation increased following drug administration and speculated that this might account for the decline in PHS. Another explanation is that by accelerating the onset and duration of parturition, the potential for fecal contamination of the engorged mammary gland is thereby decreased. Antibiotics

There are many references on the beneficial aspects of antibiotics administration. Because most of the bacterial isolates from both the mammary glands and the

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urinary system of PHS animals are coliforms, a wide selection of antibiotics may be used.

Glucocorticoids

The efficiency of glucocorticoid usage for the management of PHS has not been clearly demonstrated,l1O although early work by Ringarp82 reported a moderate improvement (7.6%) in piglet survival following treatment of the sow with prednisolone. In comparison to the nonpregnant and nonlactating sow, glucocorticoid concentrations normally are elevated in the periparturient sow and further increased in PHS animals. Glucocorticoid administration may be effective in the treatment of mammary gland edema but should be used with caution in the treatment of the sow with CM. Prolactin Stimulators

Because purified porcine PRL is available only in minute quantities, most research has focused on stimulating PRL release. Although administration of various phenothiazine and butyrophenone tranquilizers (e.g., chlorpromazine, acetylpromazine, haloperidol, and azaperone) significantly increases PRL concentrations in various species, they generally have not been effective in stimulating PRL release in the pig94 for reasons that have not been elucidated. Thyrotropinstimulating hormone (TRH) has been shown to be effective in increasing PRL concentrations but was of such short duration «45 minutes) that it is unlikely to be clinically useful. 94

Vaccinations

The use of autogenous or mixed bacterins in PHS has produced conflicting results. 87 Based on a recent study by Bertschinger and Buhlmann,l1 it does not appear that the mammary glands develop resistance to subsequent infections. These results suggest that the eventual development of a vaccine for the prevention of CM is unlikely. Work by Pejsak et al,74 however, suggests that the development of vaccines against specific UTIs may provide an effective management tool for reducing the incidence of PHS. Management

Control of infection pressure is an important factor. However, it generally is not sufficient in severe PHS, especially when a high health status herd is affected. Management of feeding and housing also are very important. In fact, correction of the risk factors are essential for a long-term cure of PHS. All of the risk factors must be evaluated and the physiopathologic pathways that lead to PHS must be identified.

References 1. Aherne FX: Dietary laxatives for sows during gestation and lactation. In 62nd Annual Feeders Day Report, Department of Animal Sciences, University of Alberta, Canada, 1983

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2. Mele S, Bryant-Greenwood GD, Charnley WA, et al: Plasma relaxin immunoactivity in the pig at parturition and during nuzzling and suckling. J Reprod Fertil 56:451, 1979 3. Anderson JF, Werdin RE: Ergotism manifested as agalactia and gangrene in sows. JAm Vet Med Assoc 170:1089, 1977 4. Armstrong GH, Hooper BE, Martin CE: Microflora associated with agalactia syndrome of sows. Am J Vet Res 29:1401, 1968 5. Backstrom L, Connors J, Price W, et al: Mastitis-metritis-agalactia (MMA) in the sow: A field survey of MMA and other farrowing disorders under different gestation and farrowing housing conditions. In Proceedings of the Seventh International Pig Veterinary Society Meeting, Mexico City, Mexico, 1982, p 175 6. Backstrom L, Morkoc AC, Connor J, et al: Clinical study of mastitis-metritis-agalactia in sows in Illinois. J Am Vet Med Assoc 185:70, 1984 7. Berner H: Importance of urinary tract infections in development of puerperal endometritis in the sow. Theraztliche Umschau 39:450, 1984 8. Berner H: Bacteriological and clinical investigations in pathogenesis endometritis in the sow. In Proceedings of the Eighth International Pig Veterinary Society, Ghent, Belgium, 1984, p 284 9. Berner H, Bossart W, Jochle W: Immunotherapy in infertile sows with urogenital infections and effects on MMA. In Proceedings of the 11th International Pig Veterinary Society Congress, Lausanne, Switzerland, 1990, p 308 10. Berner H, Jochle W: Influence of induction of parturition in the sow with a PGF analog (Alfaprostol) on bacterial ascendence into and colonization of the puerperal uterus. In Proceedings of the Ninth International Pig Veterinary Society, Barcelona, Spain, 1986, P 103 11. Bertschinger HU, Buhlmann A: Absence of protective immunity in mammary glands after experimentally induced coliform mastitis. In Proceedings, of the 11th International Pig Veterinary Society Congress, Lausanne, Switzerland, 1990, p 175 12. Bertschinger HU, Pohlenz J: Coliform mastitis. In Leman AD, Straw B, Glock RD, et al (eds): Diseases of Swine, ed 5. Ames, lA, Iowa State University Press, 1980, p 491 13. Bertschinger HU, Polhenz J, Ross RF: Coliform mastitis. In Leman AD, Straw B, Glock RD, et al (eds): Diseases of Swine, ed 6. Ames, lA, Iowa State University Press, 1986, p 541 14. Bertschinger HU, Eng V, Wegmann P: Relationship between coliform contamination of floor and teats and the incidence of puerperal mastitis in two types of farrowing accommodations. In Proceedings of the Sixth International Congress Animal Hygiene, 1988, p 86 15. Bevers MM, Willemse AH, Kruip TAM: The effect of bromocryptine on luteinizing hormones levels in the lactating sow; Evidence for a suppressive action by prolactin and the suckling stimulus. Acta Endocrinoll04:261, 1983 16. Bilodeau R, Dea S, Sauvageau R, et al: A severe reproductive outbreak with neonatal losses in a Quebec SPF swine herd. In Proceedings of the Am Assoc Swine Pract, St Paul, MN, 1990, P 307 17. Bilodeau R, Dea S, Martineau G-P, et al: The situation of the "porcine reproductive and respiratory syndrome" in Quebec. Vet Rec 126:54, 1991 18. Bollwahn W, Vopelius-Feldt AV, Arnhofer G.: The clinical value of bacteriuria in sows. In Proceedings of the Eighth International Pig Veterinary Society, Ghent, Belgium, 1984, p 149 19. Bollwahn W, Arnhofer G, Wendt W: The influence of feeding, housing and treatment on the contents of porcine urine. In Proceedings of the 10th International Pig Veterinary Society, Rio de Janeiro, Brazil, 1988, p 305 20. Bostedt H, Rudloff PR: Prophylactic administration of the beta-blocker carazolol to influence the duration of parturition in sows. Theriogenology 20:191, 1983 21. Busse FWI: A study about I.M. injection of IlireneR and SuacronR to induce farrowing and to influence the MMA syndrome. In Proceedings of the 11th International Pig Veterinary Society Congress, Lausanne, Switzerland, 1990, p 176 22. Cariolet R: Etude des postures en phase de repos chez des truies bloquees en gestation: Relation entre la largeur de la stalle et la pathologie de la mise bas. J Rech Porcine en France 23:189, 1991 23. Cereza J, Rosell V, Nievas M, et al: MMA syndrome in sows. Hormonal levels and antibiotic therapy. In Proceedings International Pig Veterinary Society, Barcelona, Spain, 1986, p 94

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24. Cerne F, Jochle W: Clinical evaluations of a new prostaglandin analog on pigs: 1. Control of parturition and of the MMA-syndrome. Theriogenology 16:459, 1981 25. Cerne F, Jerkovic I, Debeljak C: Influence of FinadyneR on some clinical signs of MMA. In Proceedings of the Eighth International Pig Veterinary Society, Ghent, Belgium, 1984, p 290 26. Chagnon M, D' Allaire 5, Drolet R: A prospective study of sow mortality in breeding herds. Can J Vet Res 55:180, 1990 27. de Pasille A-MB, Rushen J: Using early suckling behavior and weight gain to identify piglets at risk. Can J Anim Sci 69:535, 1989 28. de Pasille A-MB, Rushen J, Hartsock TG: Ontogeny of teat fidelity in pigs and its relation to competition at suckling. Can J Anim Sci 68:325, 1988 29. de Ruijter K, Verheijden JHM, Pipers A, et al: The role of endotoxin in the pathogenesis of coliform mastitis in sows. Vet Q 10:186, 1988 30. Ehnvall R, Einarsson 5, Larson K: Prostaglandin-induced parturition in swine. A field study on its accuracy after treatment with different amounts of PGF2. Nord Vet Med 29:376, 1977 31. Elmore RG, Martin CE: Mammary glands. In Leman AD, Straw B, Glock RD, et al: Diseases of swine, ed 6. Ames, lA, Iowa State University Press, 1986, p 32. Farmer C, Martineau G-P: Les cages de mise bas en production porcine: Entre Ie my the et la science. Med Vet du Quebec 21:173, 1991 33. Fergusson FG, Confer F, Pinto A, et al: Long-term endotoxin exposure in the sow and neonatal piglet-a model for MMA. In Proceedings of the Eighth International Pig Veterinary Society, Ghent, Belgium, 1984, p 289 34. Fraser D: A review of the behavioral mechanism of milk ejection of the domestic pig. Appl Anim Behav Sci 6:247, 1980 35. Fraser D, Phillips PA, Thompson BK, et al: Use of water by piglets in the first days after birth. Can J Anim Sci 68:603, 1988 36. Furniss SJ: Measurement of rectal temperature to predict "Mastitis, metritis and agalacatia" (MMA) in sows after farrowing. Prev Vet Med 5:133, 1987 37. Gadd J: Filling voids on feeding. Pig Farming April 15, 1991 38. Gillespie TG: Stray electrical voltage. In Proceedings of the Swine Herd Health Programming Conference, St Paul, MN, 1984, P 260 39. Gooneratne AD, Hartmann PE, Nottage HM: The initiation of lactation in sows and the mastitis-metritis-agalactia syndrome. Anim Reprod Sci 5:135, 1982 40. Goransson L: The effect of dietary crude fibre content on the frequency of postpartum agalactia in the sow. J Am Vet Med Assoc 36:474, 1989 41. Goransson L: The effect of feed allowance in late pregnancy on the occurrence of agalactia post-partum in the sow. J Am Vet Med Assoc 36:505, 1989 42. Hansen LH: Reproductive efficiency and incidence of MMA after controlled farrowing using a prostaglandin analogue, cloprostenol. Nord Vet Med 31:122, 1979 43. Hermansson I, Einarsson 5, Larson K, et al: On the agalactia post partum in the sow: A clinical study. Nord Vet Med 30:465, 1978 44. Holtz W, Hartmann JF, Welp C: Induction of parturition in swine with prostaglandin analogs and oxytocin. Theriogenology 19:583, 1983 45. Jensen HM: Forebyggelse af farefeber (MMA) komplekset vet reduktion af fodret til den draektige sode sidste 3 uger for faring. Dansk Vet Tidskr 64:659, 1981 46. Jones JET: Bacterial mastitis and endometritis in sows. In Proceedings of the Fourth International Pig Veterinary Society Congress, Ames, lA, 1976, P E6 47. Jorsal SE: Epidemiology of the MMA-Syndrome. A field survey in Danish sow herds. In Proceedings of the Ninth International Pig Veterinary Society, Barcelona, Spain, 1986, P 93 48. King GJ, Wathes DC: Relaxin, progesterone and estrogen profiles in sow plasma during natural and induced parturitions. Anim Reprod Sci 20:213, 1989 49. Klaver J, van Kempen GJM, deLange PGB, et al: Milk composition and daily yield of different milk components as affected by sow condition and lactation/feeding regimen. J Anim Sci 52:1091, 1981 50. Klobasa F, Butler JE: Absolute and relative concentrations of immunoglobulins G, M, 51. Klobasa F, Habe F: The duration of intestinal uptake of colostral immunoglobulins in newborn piglets. In Proceedings of the 11th International Pig Veterinary Society, Lausanne, Switzerland, 1990, p 287

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52. Lake SG, Jones JET: Post-parturient disease in sows associated with Klebsiella infection. Vet Res 87:484, 1970 53. Un PS, Huang S, Fang WS: Effect of Uncomycine and sulfametahzine in combination in sow rations on the reproductive performance of sows and the growth of baby pigs. In Proceedings of the Ninth International Pig Veterinary Society, Barcelona, Spain, 1986, pp 5, 419 54. Madec F: Abreuvement des truies en elevage confine intensif: Observations epidemiologiques. Le Point Vet 611, 1987 55. Madec F: Quelques observations epidemiologiques a propos des metrites chez la truie en elevage intensif. Rec Med Vet 163, 1987 56. Madec F: Comparaison de differentes methodes d'estimation des quantites d'eau bues par les truies gestantes a partir de l'examen de leurs urines. Bull Lab Vet 15/16:1, 1984 57. Madec F, David F: Les troubles urinaires des troupeaux de truies: Diagnostic, incidence et circonstances d'apparition. J Rech Porcine en France 14:413, 1982 58. Maffeo G, Redaelli G, Ballabio R, et al: Evaluation of milk production and MMA complex in sows treated with PGF-2a analogues on day 111 of pregnancy. In Proceedings International Pig Veterinary Society, Ghent, Belgium, 1984, p 288 59. Martineau G-P, Bilodeau R, Sauvageau R, et al: Syndrome "Hyperthermie-AnorexieAvortement de la Truie" et de Pneumonie interstitielle virale au Quebec". J Rech Porcine en France, 1991, p 179 60. Martineau G-P, Bilodeau R, Sauvageau R, et al: Le syndrome reproducteur et respiratoire porcin (SRRP) au Quebec: Donnees cliniques, pathologiques et virologiques. J Rech Porcine en France, 1992, in press 61. Martineau G-P: Body building syndrome in sows. In Proceedings Am Assoc Swine Pract, Denver, CO, 1990, P 345 62. Mattila T, Syviijiirvi J, Sandholm M: Bacterial growth in whey from mastitic and nonmastitic quarters. Am J Vet Res 45:2504, 1984 63. Miquet JM, Madec F, Paboeuf F: Epidemiologie des troubles de la mise bas chez la truie: Premiers resultats d'une etude realisee dans deux elevages. J Rech Porcine en France 22:325, 1990 64. Morkoc A, Backstrom L, Lund L, et al: Bacterial endotoxin in blood of dysgalactic sow in relation to microbial status of uterus, milk and intestine. J Am Vet Med Assoc 183:786, 1983 65. Muirhead M: Mastitis: How to deal with a problem 1. Recognition and definition. International Pigletter 1:1, 1981 66. Nachreiner RF, Ginther OJ: Current studies on the Mastitis-Metritis-Agalactia Complex of swine in Wisconsin. J Am Vet Med Assoc 155:1860, 1969 67. Nachreiner RF, Ginther OJ: Gestational and periparturient periods of sows: effects of altered environment, withholding of bran feeding and induced mastitis on serum chemical, hematologic and clinical variables. Am J Vet Res 33:2221, 1972 68. Nachreiner RF, Ginther OJ: Induction of agalactia by administration of endotoxin (Escherichia coli) in swine. Am J Vet Res 35:619, 1974 69. Nachreiner RF, Garcia MC, Ginther OJ: Clinical hematologic and blood chemical changes in swine given endotoxin (Escherichia coli) during the immediate postpartum period. Am J Vet Res 33:2489, 1972 70. Nara BS, First NL: Effect of indomethacin and prostaglandin F2a on parturition in swine. J Anim Sci 52:1360, 1981 71. Noblet J, Etienne M: Effect of energy level in lactating sows on yield and composition of milk and nutrient balance of piglets. J Anim Sci 63:1888, 1986 72. Pedersen A, Persson A: Udder status during the post-partum period in sows. In proceedings of the Fifth International Conference on Production Disease in Farm Animals, Uppsala, Sweden, 1983, p 217 73. Pedersen A, Krovacek K, Ekwall H: Virulence factors in strains of Escherichia coli isolated from mastitic milk from agalatic sows. In Proceedings of the Eighth International Pig Veterinary Society, Ghent, Belgium, 1984, p 286 74. Pejsak A, Tarasuik K, Jochle W: Immunoprophylaxis against MMA and/or CM in sows with a vaccine against urinary tract infections (Urovac R). In Proceedings, of the 11 th International Pig Veterinary Society Congress, Lausanne, Switzerland, 1990, p 307 75. Penny RHC: The agalactia complex in the sow: A review. Aust Vet J 46:153, 1970 76. Persson A: Udder status during the lactation period in healthy sows and in sows

682

MARTINEAU et al

affected with agalactia post partum. In Proceedings of the Eighth International Pig Veterinary Society, Ghent, Belgium, 1984, p 285 77. Persson A, Pedersen E, Gorensen L, et al: A long term study on the health status and performance of sows on different feed allowances during late pregnancy. 1. Clinical observations with special reference to agalactia post partum. Acta Vet Scan 30:9, 1989 78. Peter AT, Huethe P, Doble E, et al: Prostaglandin F2a and prolactin in experimental hypogalactia in sows. Res Vet Sci 39:222, 1985 79. Plonait H, Wilms-Schulze K, Schoning G: Prophylaxis of the MMA-syndrome by antibacterial medication and restricted feeding. In Proceedings International Pig Veterinary Society, Barcelona, Spain, 1986, p 1:108 80. Pol JMA, van Dijk JE, Wensvoort G, et al: Pathological, ultrastructural, and immunohistochemical changes caused by Lelystad virus in experimentally induced infections of mystery swine disease (synonym: porcine epidemic abortion and respiratory syndrome [PEARS]). Vet Q 13:137, 1991 81. Raekallio M: N-acetyl-B-D-glucosaminidase (NaGase) in porcine milk. Acta Vet Scand 28:173, 1987 82. Ringarp N: Clinical and experimental investigation into a postparturient syndrome with agalactia in sows. Acta Agric Scand Suppl 7, 1960 83. Robert S, Matte H, Bertin-Mahieux J, et al: Effects of continuous stray voltage on health, growth and welfare of fattening pigs. Can J Vet Res 55:371, 1991 84. Ross RF, Christian LL, Spear ML: Role of certain bacteria in mastitis-metritis-agalactia sows. J Am Vet Med Assoc 155:1844, 1969 85. Ross RF, Zimmermann BJ, Wagner WC, et al: A field study of coliform mastitis in sows. J Am Vet Med Assoc 167:231, 1976 86. Ross RF, Orning AP, Woods RD, et al: Bacteriologic study of sow agalactia. Am J Vet Res 42:949, 1981 87. Ross RF, Harmon RL, Zimmerman BJ, et al: Susceptibility of sows to experimentally induced Escherichia coli mastitis. Am J Vet Res 44:949, 1983 88. Rushen F, Fraser D: Nutritive and nonnutritive sucking and tahe temporal organization of the suckling behavior of domestic piglets. Develop Psychobiol 22:789, 1989 89. Sandstedt H: Agalakti hos sugga. Medlemsbl Sveriges Vet Forb 5:103, 1983 90. Sandstedt H, Sjogren U: Forebuggande atgarder vid hog frekvens av MMAI I suggbesattningar. Sv Vet Tidn 34:487, 1982 91. Sandstedt H, Sjogren U, Swahn 0: Foreguggande atgarder mot MMA (agalakti) hos sugga. Sv Vet Tidn 31:193, 1979 92. Sherwood OD, Nara BS, Welk FA, et al: Relaxin levels in the maternal plasma of pigs before, during and after parturition and before, during and after suckling. BioI Reprod 25:65, 1981 93. Smith BB, Wagner WC: Suppression of prolactin in pigs by Escherichia coli endotoxin. Science 224:605, 1984 94. Smith BB, Wagner WC: Effect of dopamine agonists or antagonists, TRH, stress and piglet removal on plasma concentrations of prolactin in lactating sows. Theriogenology 3:282, 1985 95. Smith BB, Wagner WC: Effect of Escherichia coli endotoxin and TRH on prolactin in lactating sows. Am J Vet Res 46:175, 1985 96. Smith BB, Lassen ED, Mulrooney D: Hematologic changes associated with E. coli endotoxin induced lactation failure in the periparturient sow. In Proceedings of the 11 th International Congress Reproduction Artificial Insemination, Dublin, Ireland, 1988, p 525 97. Smith BB, Martineau G-P, Bisaillon A: Mammary gland and lactation failure. In Leman AD, Straw B, D'Allaire S (eds): Diseases of Swine, ed 7. Ames, lA, Iowa State University Press, 1992, p 40 98. Stetson LE, Beccard AD, DeShazer JA: Stray voltage in a swine farrOwing unit. A case study (Abstract 3502). In Proceedings of the Am Soc Agric Eng. Winter Meeting. 1979 99. Stone BA, Petrucco OM, Seamark RF, et al: Concentration of steroid hormones, and of relaxin, in utero-ovarian venous plasma of periparturient sows. Anim Reprod Sci 15:227, 1987 100. Swarbrick 0: The porcine agalactia syndrome: Clinical and histological observations. Vet Res 3:241, 1968

LACTATIONAL INSUFFICIENCY IN SOWS

683

101. Taverne M, Willemse AH, Dieleman SJ, et al: Plasma prolactin, progesterone and oestradiol-17B concentrations around parturition in the pig. Anim Reprod Sci 1:257, 1978/1979 102. Terpstra C, Wensvoort G, Pol JMA: Experimental reproduction of porcine epidemic abortion and respiratory syndrome (mystery swine disease) by infection with Lelystad virus: Koch's postulates fulfilled. Vet Q 13:131, 1991 103. Threlfall WR, Dale H, Martin CE: Serum and adenohypophyseal concentrations of prolactin in sows affected with agalactia. Am J Vet Res 35:313, 1974 104. Thurman JC: The metritis-agalactia-mastitis syndrome of sows (PhD thesis). 1967 105. Thurman JC, Simon J: A field study of 12 sows affected with the MMA syndrome. Vet Med Small Anim Clin 65:263, 1970 106. Trapp AL, Keahy KK, Whitenack DC, et al: Vitamin E-selenium deficiency in swine: Differential diagnosis and nature of field problems. J Am Vet Med Assoc 157:289, 1970 107. Truszczynski M, Pejsak 2, Tarasiuk K: Role of endotoxin, measured with the LAL test, in coliform mastitis of sows. In Proceedings of the 10th International Pig Veterinary Society Rio de Janeiro, Brazil, 1988, p 302 108. Van der Lende T, de Jager D: Death risk and preweaning growth rate of piglets in relation to the within-litter weight distribution at birth. livestock Prod Sci 28:73, 1991 109. Verhulst A, Ottowicz G: Le stress et la pathologie des troubles post-partum chez la truie. Ann Med Vet 118:307, 1974 110. Wagner WC: Mastitis-metritis-agalactia. Vet Clin North Am Large Anim Pract 4:333, 1982 111. Wallace HD, Thieu D, Combs GE: Alfalfa meal as a special bulky ingredient in the sow diet at farrowing and during lactation. Research Report, Department of Animal Science, Gainesville, FL, 1974 112. Wallace HD, Thieu D, Combs GE: Wheat bran as a sow ration ingredient during the farrowing and lactation period. Research Report, Department of Animal Science, University of Florida, Gainesville, FL, 1974 113. Weber, JA, Ferguson FG: Analysis of the cellular components of swine colostrum and milk. In Proceedings of the Seventh International Pig Veterinary Society Congress, Mexico City, Mexico, 1982, p 169 114. Wegmann P, Bertschinger HU: Sequential cytological and bacteriological examination of the secretions from sucked and unsucked mammary glands with and without mastitis. In Proceedings of the Eighth International Pig Veterinary Society, Ghent, Belgium, 1984, p 287 115. Wegmann P, Bertschinger HU, Eng V: Relationship between contamination of the teat ends with coliform bacteria and incidence of coliform mastitis. In Proceedings of the 11th International Pig Veterinary Society Congress, Lausanne, Switzerland, 1990, p 302 116. Wegmann P, Bertschinger HU, Eng V: Relationship between contamination of the teat end with coliform bacteria and incidence of coliform mastitis (MMA). In Proceedings of the 10th International Pig Veterinary Society, Rio de Janeiro, Brazil, 1988, p VII: 302 117. Wegmann P, Bertschinger HU, Jecklin H: A field study on the prevalence of coliform mastitis (MMA) in Switzerland and antimicrobial susceptibility of the coliform bacteria isolated from the milk. In Proceedings of the Ninth International Pig Veterinary Society Barcelona, Spain, 1986, p 1:96 118. Whitacre MD, Threlfall WR: Effects of ergocryptine on plasma prolactin. Luteinizing hormone and progesterone in the periparturient sow. Am J Vet Res 42:1538, 1981 119. Whitehair CK, Miller ER: Nutritional deficiencies. In Diseases of Swine, ed 6. Ames, lA, Iowa State University Press, 1986, p 746 120. Whittemore CT, Fraser D: The nursing and suckling behavior of pigs. II. Vocalization of the sow in relation to suckling behavior and milk ejection. Br Vet J 130:346, 1974 121. Wilson MR: Dealing with enteric diseases in pigs. In Proceedings Guelph Pork Symposium, Waterloo, Ontario, 1991, p 1 122. Youngberg JA, Smith BB, Reed PJ: Clearance characteristics of Escherichia coli lipopolysaccharide in the pig. In Proceedings of the Conf Res Workers Anim Dis, 1988, P 79

684

MARTINEAU et al

123. Zyczko K, Kureman B, Gierej W: Secretion disorders of mammary glands in sows. Zootechnica 29:45, 1986

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