Chapter 36 Specific diseases of uncertain etiology
INTRODUCTION 1981
DISEASES CHARACTERIZED BY SYSTEMIC INVOLVEMENT 1981
DISEASES CHARACTERIZED BY ALIMENTARY TRACT INVOLVEMENT 1990
DISEASES CHARACTERIZED BY RESPIRATORY TRACT INVOLVEMENT 1998
DISEASES CHARACTERIZED BY NERVOUS SYSTEM INVOLVEMENT 2006
DISEASES CHARACTERIZED BY INVOLVEMENT OF THE MUSCULOSKELETAL SYSTEM 2023
DISEASES CHARACTERIZED BY INVOLVEMENT OF THE SKIN 2037
It was anticipated that, with time, this chapter would shrink in succeeding editions and, eventually, disappear. As the causes of individual diseases are demonstrated they are removed to other chapters but in the past newly identified diseases have been added at almost the same rate so that the net effect on the chapter has been small. The process could have been hastened by moving diseases when the consensus of opinion, short of proof, was that the cause had been identified. We have thought it preferable to leave those diseases here, together with those in which the combination of causes is complex, such as ‘weaner illthrift’.
Diseases characterized by systemic involvement
A number of different diseases have been associated with this syndrome in both lambs and calves. In many cases an association has been established by a response trial but in others the association has not been established as causal. These include intestinal parasitism, coccidiosis, infection with hemoplasma (eperythrozoonosis), deficiencies of copper, cobalt, selenium, zinc, thiamin, vitamin A, and vitamin D. A combination of these deficiencies has also been suspected.
Etiology Several causes including parasitism, trace element deficiencies, pasture palatability and fungal infestations of pasture.
Epidemiology Loss of weight at weaning and failure to make satisfactory weights subsequently, in spite of the presence of ample feed and when adult sheep are faring well.
Clinical findings Poor body condition and failure to thrive.
Diagnostic confirmation Laboratory testing for specific cause. Correction-response trial.
Palatability of pasture appears a cause of illthrift in some instances, or at least associated with it, and moving the animals to a different pasture will sometimes alleviate the condition. This has been observed with perennial rye-grass (Lolium perenne), setaria grass (Setaria sphacelata), tall fescue (Festuca arundinaceae), and turnips (Brassica repens). Infestation of grass species with endophyte fungi may prove an important cause of illthrift and poor growth rates occur in calves with the ‘summer syndrome’ associated with the endophyte Acremonium coenophialum in tall fescue pastures. Infection of pasture species with toxigenic Fusarium spp. has been associated with ill thrift in lambs in South Africa, New Zealand, and Australia. Pasture and soil fungi have also been suspected of being associated with illthrift in sheep in eastern Canada.
• The problem has seemed to be most severe in the southern hemisphere but this may be because sheep are so prevalent there
• It may also be due partly to the predominance of Merino and Merino-type sheep; the disease is most common in these breeds which have their own particular timorous nature which makes weaning and the need to shift for themselves more traumatic than in most other breeds
• This trait is particularly noticeable if there is overcrowding on pasture
• Lambs that are weaned at light weights are more prone to illthrift following weaning and ideally they should be 45% of mature weight when weaned
• Merino ewes have a low persistency of milk production and consequently management of the flock and the pastures is critical for effective weaning weights
• Other management factors likely to lead to low weaning weights and subsequent unthriftiness are multibirth lambs, small ewes, ewes with little milk, and lambs born late in the season.
Weaner illthrift does occur in breeds other than Merino and is also reported from several countries in the northern hemisphere. Weaner illthrift has been reported on a variety of different pastures and under a variety of different management systems.
In bad years there may be many deaths; in any circumstance there is a gross delay in maturation so that maiden lambing may be delayed to as late as 3 years of age. The economic effects can be disastrous. Illthrift syndromes are also recorded in calves although with less frequency.
As the name indicates the disease in weaned sheep is manifest primarily by poor body condition and failure to thrive. Within an affected group not all lambs are equally affected and there will be a range of conditions. Those lambs in very poor condition are usually anemic, frequently have diarrhea, and there is a sporadic but continuing death loss amongst them. Commonly the sheep have been treated with anthelmintics with no response. There are usually no abnormal findings at postmortem other than those associated with emaciation but villous atrophy is often found on histological examination of the small intestine.
This lack of significant findings is probably the defining factor for placing a problem in this disease category.
When faced with this problem the initial approach should be to examine for the most likely cause which is a deficiency in energy or protein intake.
An examination of the teeth to insure that there is no excessive attrition of the teeth, or even breaking of the incisors if the sheep are being fed roots, is also a logical preliminary step in any investigation of an illthrift problem.
The Parasite Status of the group should be examined by techniques appropriate to their detection as outlined in previous chapters. Clinical or subclinical infestations with nematodes are common occurrences at this time in the sheep’s life, before immunity is properly developed and when pasture contamination can be high.
Infections with coccidia, cryptosporidia, or Mycoplasma (Eperythrozoon) ovis are significant causes of illthrift and should be examined as outlined in previous chapters.
The Trace Element Status of the group should be examined if the cause cannot be found with the above examinations. Many trace element deficiencies are area deficiencies or in an area are strongly associated with certain soil types. If trace element deficiency is a cause it is likely that there will be some prior history of this problem in the area. Diagnosis by response to supplementation is a common approach and the diagnostic aspects of the trace element deficiencies are outlined under their specific headings in this text.
Examination of the above-mentioned possible causes is time-absorbing and costly and, if there is a residuum of unsolved cases, they are likely to remain undiagnosed.
Infectious Agents can produce enteric lesions and illthrift (e.g. coronavirus and yersiniosis) and the malabsorption which results may be manifested by weight loss and by chronic diarrhea. They are differentiated on the initial postmortem examinations.
Etiology Unknown. Behavioral problem of steers in feedlots
Epidemiology Prevalence varies and increases with increasing age and weight at entry.
Clinical findings and lesions Areas of denuded hair, subcutaneous hematomas, other traumatic injuries
The buller steer syndrome is a behavioral problem in cattle confined in feedlots1 of unknown etiology. Within a pen of cattle, one or more cattle persistently ride a particular individual or individuals of the group. The ridden animals are referred to as bullers. There have been several suspect etiogies. Improper placement of hormonal growth implants has been suspected as being associated.
The syndrome occurs only in cattle in feedlots. The prevalence varies, but in one study ranged from 0 to 11% with a mean of 2.7%.1,2 The prevalence increases with increasing weight and age.1,2 The case fatality has been estimated at 1%.3 The incidence of occurrence is higher in the summer and the fall and during the first 30 days of the feeding period.4
Epidemiological studies indicate that bullers occur as a point source epidemic with the cause occurring soon after cattle arrive in the feedlot and mingle into pen groups.1 The peak incidence of bullers occurs much sooner after arrival and declines much quicker in older cattle. Bullers occur significantly sooner after mixing in older cattle than in younger cattle. The pen prevalence also increases as cattle become older on arrival at the feedlot and are more aggressive. As the prevalence of intact bulls increases in pens of cattle, so does the prevalence of bullers, presumably due to more aggressiveness in the bulls.
Postulated causative and risk factors include the incorrect timing and administration of hormonal growth implants, reimplantation and double dosing, estrogenic substances in feeds, pheromones in the urine of certain cattle, improper or late castration of young cattle, daily feedlot management, weather and seasonal factors, disease, group size, and dominance behaviour. However, these factors have not been well substantiated and controlled studies have found little influence of implant type and implant timing on buller incidence.5
The mixing and confinement of unfamiliar cattle into pen groups, with subsequent agonistic interactions as these cattle established a social hierarchy, are considered as important risk factors. Both riding behavior and antagonistic behavior cease once cattle establish a stable social hierarchy. This suggests that riding behavior and subsequent identification of bullers is associated with this dominance behavior. It is possible that when a dominant animal becomes ill in a pen, other more subordinate animals in the pen that were previously subdued in dominance contests may want to fight the sick animal to achieve higher social status
The syndrome has been ranked along with acute undifferentiated bovine respiratory disease and footrot as one of the three most important disease syndromes in beef feedlots in North America. In addition to the economic loss from decreased weight gain, injury, treatment, death, and carcase condemnation, there is economic losses associated with extra handling necessary to accommodate affected cattle, the disruption of uniform marketing of cattle, especially in custom feedlots, and the need for extra pens in which to house the bullers. The importance of the syndrome includes the animal welfare aspects.
Bullers may be at significantly greater risk of illness and mortality (from bacterial pleuropneumonia) than other steers.2 The association between illness, mortality, and bullers among individuals was greatest among the oldest yearling steers.2
Two types of bullers are identified.3
Type 1 or true bullers stand as if they were a heifer in estrus and do not move away or show agonistic behaviour when being mounted by rider cattle. There can be several rider cattle in a pen and type 1 bullers are rapidly damaged.
Type 2 bullers are animals that appear low in social dominance. They use aggression to discourage riders and will lie down to avoid being ridden.
Affected animals show areas of denuded hair and have extensive subcutaneous hemorrhage. The hematomas may become infected and develop to subcutaneous pockets of pus and gas. Other traumatic injuries, such as limb fractures, also occur.
Management of the syndrome has usually involved identification and removal from the pen to prevent injury and even death from riding-related injuries.
The high rate of risk of illness and mortality in bullers relative to other feedlot steers suggests that bullers should always be checked for evidence of illness in addition to their removal from their designated pen to prevent severe riding-related injuries. Treating sick bullers may improve the chance of settling them back into their designated pen by allowing them to resume their original position in the social hierarchy.
Epidemiology Most commonly multiple cases on a farm. Several farms affected in a geographic region in a single season. Problem may not occur for several years and then occur as ‘epidemic’ in a region.
Clinical findings Calves may be born weak and unable to stand. More commonly are born apparently normal and stand but subsequently collapse with hypothermia and die within a few hours of birth.
Lesions Petechial hemorrhages, subcutaneous edema, and hemorrhage commonly in the subcutaneous tissue of the carpal and tarsal joints.
Diagnostic confirmation Specific to cause
A disease of newborn calves called the ‘weak calf syndrome’ was first recognized in Montana in 1964.1 It has been recognized throughout the US and other countries since then, and is considered a major economic loss in beef cattle herds. In the earlier descriptions of the syndrome, calves were affected by 10 days of age, and approximately 20% were affected at birth.2 Morbidity ranged from 6 to 15%. In some herds, sporadic abortions occurred before calving season of the herd began. In some cases, affected calves died within minutes after being born with varying degrees of obstetrical assistance.3
In calves which survived for a few days, clinical findings included lassitude, depression, weakness, variable body temperature, a reddened and crusty muzzle, lameness, and reluctance to stand, enlargement of the carpal and tarsal joint capsules along with periarticular subcutaneous swellings, and a hunched-up back if they stood. Diarrhea occurred in some calves after a few days of illness but was not a major clinical finding. Treatment was ineffective and the case fatality rates ranged from 60 to 80%.
At necropsy, the prominent lesions were hemorrhage and edema of the subcutaneous tissues over the tarsal and carpal joint regions and extending distally. Polysynovitis with hemorrhagic synovial fluid often containing fibrin was also common. Erosive and hemorrhagic lesions of the forestomachs and abomasum also occurred. Several different pathogens were isolated from these calves but no consistent relationship between the pathogens and the lesions was ever determined.1
In retrospect, the case definitions were not well described and it is possible that several different diseases of newborn calves were lumped into the enigma of the weak calf syndrome. As more detailed clinical and laboratory examinations of sick newborn calves have been done over the years, some of the causes of the original syndrome have been identified as certain diseases of newborn calves which are characterized by such non-specific signs as lack of desire to suck, weakness, and failure to respond to therapy.
A wide spectrum of clinical and pathological findings has been associated with the weak calf syndrome. In the most common situation, which is a major diagnostic challenge, calves are born weak and die within 10–20 minutes after birth; sometimes they live for up to a few days. At necropsy there are no obvious or only few lesions to account for the illness. Calves which are weak after birth due to traumatic injuries associated with dystocia or other significant lesions can be accounted for according to the nature and severity of the lesions. Reports from Northern Ireland in recent years indicate that in dairy herds the incidence of the weak calf syndrome has ranged from 10 to 20% of all calves born.4 Field observations in problem herds found that the gestation period is of normal duration but parturition is usually prolonged with the first and second stages of labor lasting 24 hours.5 Affected calves usually are born alive but are unable to sustain breathing following birth. Despite resuscitation efforts, they commonly die within 10 minutes often accompanied by prominent incoordinated movements of the limbs.4 Some calves are stillborn and whether or not this is a variation of the syndrome is uncertain. In a report from the UK, the syndrome occurred in calves born from heifers and was characterized by failure to breathe at birth, or breathing with difficulty, and/or failing to move after birth, and failure to suck.6 The term stillbirth/perinatal weak calf syndrome has been suggested as more appropriate.
A variation of the weak calf syndrome is the dummy calf syndrome reported from the southern US.7 Affected calves appear normal at birth, are generally alert, but lack the instinct or the desire to seek the teat or suck after birth and for up to several hours later. The syndrome may occur in calves of any birth weight. The incidence has been highest in purebred Brahman females but it has also occurred in Aberdeen Angus, Hereford, Chianina, and Brown Swiss breeds of cattle. Field observations indicate that affected calves did not stand for up to 1–2 hours after birth to initiate teat-seeking.7 Dummy calves appear to lack the sensitivity to teat-seek and if they fail to locate a teat by about 4–5 hours after birth they commonly lose the sucking reflex and then require intensive nursing care by bottle feeding to initiate sucking. In calves which fail to suck and ingest colostrum, hypothermia, hypoglycemia, and neonatal infections are common complications. Concurrently, the dam loses interest in the calf and may abandon it. The cause is unknown but is thought to be a behavioral disorder inherent in some breeds; this has not been supported with any scientific evidence.
The etiology of the weak calf syndrome is unclear, but several epidemiological observations have suggested some possible causes.8 These include:
• Underdevelopment because of nutritional inadequacy of the maternal diet during pregnancy
• Maternal dietary deficiencies of selenium and vitamin E
• Traumatic injuries associated with dystocia and excessive force during obstetrical assistance
Fetal infections in the last few days before term can result in stillbirth or weak calves which may die within hours or days after birth. In one series of 293 weak calves in Northern Ireland, leptospiral infection was present in 25% of them.8 Calves in which leptospiral antigen was detected in the placenta were significantly lighter by an average of 6 to 10 kg than calves with no antigen in the placenta.9 Calves infected with Leptospira in the uterus were more likely to be infected by Arcanobacterium pyogenes or Bacillus species, and infection of the placenta is associated with a lower bodyweight. The adrenal gland, lung, and placenta are most useful tissues to examine for leptospiral antigen.9
There is some evidence that an immune inadequacy based on T lymphocyte function may be associated with the weak calf syndrome in Japanese Black calves but the data are not compelling.10
An unidentified type of adenovirus has been associated with the weak calf syndrome on a large dairy farm in Israel.11 At birth the calves were reluctant to suck or drink colostrum and were force fed colostrum with a gastric tube. Affected calves were weak at birth, unable to rise without assistance and when forced to move, walked stiffly, suggestive of polyarthritis. An adenovirus was detected in the feces, synovial fluid, and aqueous humor of affected calves.
Hypothyroidism due to iodine deficiency in the pregnant dam has been considered on the basis of thyroid hyperplasia in some calves.12 Analysis of the laboratory data from 365 calves which died from the stillbirth/perinatal weak calf syndrome in Ireland, found some differences between calves with an abnormal and normal thyroid gland.13 Glands weighing more than 30 g were probably abnormal. Abnormal glands were heavier, consitituted a greater percentage of the calfs bodyweight and had a lower iodine concentration. A higher proportion of calves with an abnormal thyroid gland had uninflated lungs and pneumonia. Abnormal thyroid glands had a lower selenium concentration in the kidneys.
However, the experimental reproduction of iodine deficiency in pregnant heifers by feeding an iodine deficient diet over the last 4 to 5 months of pregnancy resulted in clinicopathological changes and pathological changes in the thyroid glands of both the heifers and their calves, but all calves in the iodine deficient group were born clinically normal.8
A maternal dietary deficiency of selenium in pregnant cattle has also been examined but field trials have failed to show any protective effect from the parenteral administration of pregnant cattle with selenium.4,5 The parenteral administration of both selenium and iodine to pregnant cattle did not have any effect on the incidence of the syndrome between treated and untreated herds where the incidences were 7.9% and 7.4%, respectively.14 A general nutritional inadequacy in the maternal diet can result in underdevelopment of the fetus and the birth of smaller than normal calves but the deficiency usually must be grossly inadequate. Radiographic examination of affected calves found that intrauterine growth retardation is not a common feature in calves dying with the syndrome.15
Intrauterine growth retardation associated with feto-placental dysfunction has been described in Japanese Black beef calves.16 Affected calves were weak when born at term and were underweight compared to normal calves. Anemia due to bone marrow dysfunction was present in affected calves and presumably was associated with intrauterine growth retardation. Dams delivering weak calves had lower serum concentrations of estrone sulfate during late pregnancy than those of normal calves suggesting a feto-placental dysfunction. The dysfunction was influenced by sires and maternal families.
Fetal hypoxemia due to a prolonged parturition or dystocia may be a cause of the weak calf syndrome.17 While asphyxia is not an integral part of normal delivery, it is still an important cause of fetal death during abnormal parturitions. Various predisposing factors can cause prolonged interference with fetal blood or oxygen supply, which results in death during delivery or shortly after.18
In newborn mammals subjected to anoxia, initially there is a period of struggling and rapid gasping during which blood pressure rises and bradycardia becomes profound. A relatively short period of primary apnea follows, after which there is a period of more regular and deeper gasping, which may become more frequent terminally. This is followed by a period of secondary apnea, the heart rate continues to beat at a slowly declining rate, and blood pressure falls slowly. The brain lesions begin in lower brainstem nuclei and, as asphyxia becomes prolonged, progress to involve the cerebellar and thalamic nuclei and the cerebral cortex. Examination of blood gas values on newborn calves has shown that a prolonged parturition or delivery terminated by forced extraction may result in a severe acidosis due to oxygen deprivation. As blood pH drops, first vitality is reduced, subsequently vital organs like the brain are damaged and ultimately the fetus dies.19
The bovine fetus appears relatively susceptible to anoxia which has been studied experimentally by clamping the umbilical cords of fetuses for 4–8 minutes, at 24–48 hours before expected birth, followed by a cesarean section 30–40 minutes later. Calves born following this procedure may die in 10–15 minutes after birth or survive for only up to 2 days. Under these experimental conditions, fetuses can survive anoxia for 4 minutes but most will die following 6 or 8 minutes of anoxia.17 During the clamping of the umbilical cord, there is a decline in the blood pH, PO2 and standard bicarbonate levels and an increase in the PCO2 and lactate levels.17 Hypoxia in neonatal calves can result in high plasma lactate concentrations, which contributes to a progressive primary metabolic acidosis.20
During the clamping there is also increased fetal movement and a release of meconium which stains the calf and the amniotic fluid. Those which survive for a few hours or days are dull, depressed, cannot stand, have poor sucking and swallowing reflexes, and their temperatures are usually subnormal. They respond poorly to supportive therapy.
Some calves whose umbilical cords were clamped for 4 minutes were born weak, and made repeated efforts to raise their heads and move onto their sternum but were unable to maintain an upright position for long. These calves become hypothermic, dull, and their sucking and swallowing reflexes are present but weak. These calves are usually too weak to suck the cow even when assisted, and commonly develop diarrhea and other complications.
Dystocia is a major cause of neonatal mortality in range beef cattle and may be a cause of the weak calf syndrome because of fetal hypoxia or traumatic injuries associated with obstetrical assistance.21,22 In a study of 13 296 calvings over a period of 15 years in two research herds in Montana, calf mortality due to dystocia accounted for the single largest loss category through the first 96 hours postpartum.21 Dystocia accounted for 51% of calf deaths and 53% of dystocia deaths occurred in calves which were born without assistance. Calf deaths from primiparous 2- and 3-year-old dams accounted for 41% of total mortality. Necropsies done on 798 of 893 calves found that 77.7% were anatomically normal and 22.3% abnormal. At necropsy of the calves which died associated with dystocia the findings included a froth-filled trachea, non-functional lungs, bruises, contusions, hemorrhages, bone fractures, and joint dislocations. It was concluded that the provision of adequate obstetrical assistance at the right time could have reduced the mortality associated with dystocia.
Similar reports of weakness following dystocia have been reported; in some cases a collapsed trachea is present.23 In a study of parturient calf mortality in Australia, death rates as high as 44% from heifer groups have been reported.24 The death rate was significantly higher in male calves than female calves. Pathological changes in many of the dystocia-related deaths were minimal but a congested swollen tongue was a definitive lesion.
Traumatic injuries of calves at birth are caused primarily by the mechanical influence of traction during delivery and can result in asphyxia and a high perinatal mortality rate.25 Excessive traction is the most important cause of rib and vertebral fractures in the calf during dystocia. A series of 235 calves which died perinatally were examined by necropsy to determine the possible causes of death related to dystocia. Most of the parturitions were protracted and needed veterinary assistance, and 58% of the calves had pathological evidence of asphyxia. Calves delivered by extraction had pathological evidence of asphyxia more often than those born unassisted or delivered by cesarean section. Intrapulmonary amniotic material may be present in the lungs26 and represent evidence of perinatal respiratory distress.27 The aspiration of small amounts of amniotic fluid with or without meconium is common in calves and is not associated with hypoxemia, respiratory acidosis, or failure of passive transfer.28
Premature expulsion of the placenta has been associated with perinatal calf mortality.29 Field observations indicate that the majority of affected fetuses die from fetal hypoxia during stage two of calving. The most significant risk factor associated with premature expulsion of the placenta was fetal malpresentation and malposture. Prolongation of the second stage of parturition allows for sufficient detachment of the placenta for it to occupy the posterior part of the genital tract. The placenta is frequently expelled together with the calf.30 In one series of cases, there was no significant relationship between the occurrence of premature expulsion of the placenta and parity, calving difficulty, previous calving history, or sex of the calf.29
All calves which die should be examined by necropsy to identify possible causes. It is important to establish if there is one disease complex or several different diseases of newborn calves.
In the weak calf syndrome described in Northern Ireland, at necropsy, many calves had petechial hemorrhages in the thymus gland, on the ventricular epicardium and the parietal pleura and endocardium.8 These lesions were similar to those present in animals which died of acute terminal asphyxiation.18 The gasps made in response to asphyxia in utero result in amniotic fluid being inhaled into the respiratory tract. In one study, 84% of stillborn calves had these lesions of asphyxia. It is well established that asphyxiation during birth is a major factor in intrapartum stillbirth in piglets and contributes to early postnatal mortality.18 Froth may be present in the caudal trachea of some calves which die within 10–20 minutes after birth.
Varying degrees of subcutaneous edema of the head and/or bruising of the rib cage are also common. Fractures of the ribs are common, accompanied by intrathoracic hemorrhage. Vertebral body fractures occur commonly at the thoracolumbar region and may be accompanied by intra-abdominal hemorrhage. The lungs may be inflated normally, partially inflated, or not inflated. Severe bruising and hemorrhage occur around the costochondral junctions, the sternal extremities of the costal cartilages, and over the sternum and shoulder regions. In some cases, the traumatic lesions are severe and may involve primarily the right side of the rib cage.6 Severe subcutaneous hemorrhage and edema may be present over the carpal and fetlock joints due to the pressure applied by the obstetrical chains or ropes.
In the syndrome described in the US, the lesions either appeared at birth or developed in the first few weeks of life.1 At necropsy the prominent lesions are marked edema and hemorrhages of the subcutaneous tissues over the carpal and tarsal joints and extending distally down the limbs. The synovial fluid may be blood-tinged and contain fibrinous deposits. Erosions or ulceration of the gastrointestinal tract, petechial hemorrhage of internal organs, involution of the thymus gland, and hemorrhages in skeletal muscle have also been present.
• Bacteriology – fetal liver, lung, stomach content, adrenal gland; placenta (CULT). Special detection techniques for Leptospira antigens.
• Histology – fixed placenta, lung, spleen, brain, liver, kidney; maternal caruncle (LM, IHC)
Determination of the cause of the weak calf syndrome in a herd is often difficult because the limits of the case definition cannot be determined. Several risk factors may interact to contribute to the disease. The most common definition is a calf that is alive at birth, appears normal otherwise, but either fails to breathe or breathes for less than about 10 minutes and then dies. If they survive for several hours or a few days, affected calves are usually in sternal recumbency, depressed, reluctant to stand unassisted, reluctant to walk, and not interested in sucking. They may not respond favorably to supportive therapy.
When an epidemic of the disease is encountered, an epidemiological investigation of the herd is necessary in an attempt to identify possible risk factors.
The patterns of occurrence should be determined:
• Is the problem more common in calves born to heifers than cows? In some situations, the owner may provide more surveillance for the calving heifers and less for the mature cows with a consequent greater incidence of weak calves born from the cows
• Is there any evidence that parturition is prolonged in the heifers or the cows and what are the possible reasons?
• How long are heifers and cows in the herd allowed to calve unassisted before obstetrical assistance is provided?
• Is it possible that some nutritional, management or environmental factor is interfering with normal parturition?
• Is the condition more common in male or female calves and what are the relative birth weights?
• How soon after birth are the calves affected?
• What is the course of the illness after the first clinical abnormalities are noted?
• What level of calving surveillance and assistance is being provided by the attendants?
• The veterinarian should make every effort to clinically examine a representative number of affected calves.
Calves born weak, unable to stand, lacking the instinct to seek the teat or lacking a suck reflex, need intensive care including force-feeding of colostrum and the provision of warm surroundings to prevent hypothermia and other complications. Affected calves must be assisted to suck the dam normally. Bottle feeding for a few days may be necessary until the calf becomes strong enough to suck the dam on its own.
Control and prevention of the weak calf syndrome is based on empirical observations beginning with insuring adequate nutrition of the dam to avoid any possible nutritional factors affecting neonatal calf vitality. The provision of adequate surveillance at calving time and competent obstetrical assistance when necessary is also crucial to avoid prolonged parturition and fetal hypoxia in calves.
When epidemics of the disease are occurring, the surveillance of calving must be intensified, and it may be necessary to intervene with obstetrical assistance earlier than usual. Determination of the cause may require that the veterinarian attend several calvings, make detailed clinical examinations of the length of parturition and observe the parturition process and the health of the calves at birth.
Meijering A. Dystocia and stillbirth in cattle — A review of causes, relations and implications. Livestock Sci. 1984;11:143-177.
Randall GCB. Perinatal mortality: some problems of adaptation at birth. Adv Vet Sci Comp Med. 1978;22:53-81.
Mee JF. The role of micronutrients in bovine peri parturient problems. Cattle Pract. 2004;12:95-108.
1 Stauber EH. J Am Vet Med Assoc. 1976;168:223.
2 Card CS, et al. Proc 77th Ann Mtg US Anim Hlth Assoc 1974; 67.
3 Ward JK. Proc 6th Ann Mtg Am Assoc Bovine Pract 1973; 97.
4 Logan EF, et al. Vet Rec. 1990;126:163.
5 Rice DA, et al. Vet Rec. 1986;119:571.
6 Simpson VR. Vet Rec. 1990;127:459.
7 Kim Hak-Nam, et al. Agri-Pract. 1988;9:23.
8 McCoy MA, et al. Vet Rec. 1997;141:544.
9 Smyth JA, et al. Vet Rec. 1999;145:539.
10 Ohtsuka H, et al. J Vet Med Sci. 2003;65:793.
11 Brenner J, et al. J Vet Med B. 2005;52:98.
12 Logan EF, et al. Vet Rec. 1991;129:99.
13 Smyth JA, et al. Vet Rec. 1996;139:11.
14 McCoy MA, et al. Vet Rec. 1995;136:124.
15 Smyth JA, Ellis WA. Vet Rec. 1996;139:599.
16 Ogata Y, et al. J Vet Med A. 1999;46:327.
17 Dufty JH, Sloss V. Aust Vet J. 1977;53:262.
18 Randall GCB. Adv Vet Sci Comp Med. 1978;22:53.
19 Meijering A. Livestock Prod Sci. 1984;11:143.
20 Tyler H, Ramsey H. J Dairy Sci. 1991;74:1957.
21 Patterson DJ, et al. Theriogenology. 1987;28:557.
22 Bellows RA, et al. Theriogenology. 1987;28:573.
23 Kasari TR. Agri-Pract. 1989;10:19.
24 Gee CD, et al. Aust Vet J. 1989;66:293.
25 Schuijt GJ. Am Vet Med Assoc. 1990;197:1196.
26 Kelly DF, Rowan TG. Vet Rec. 1993;133:475.
27 Lopez A, Bildfell R. Vet Pathol. 1992;29:104.
28 Lopez A, et al. Am J Vet Res. 1994;55:1303.
Etiology Non-enteropathogenic E. coli endotoxemia predisposed by failure of passive transfer
Epidemiology Higher risk with intensive housing with poor hygiene
Clinical findings Loss of sucking reflex, retention of meconium or feces, excessive mucoid saliva, abomasal distension.
Diagnostic confirmation Nothing pathognomonic.
Treatment Fluids and energy via stomach tube. Antimicrobials.
Control Antimicrobials at birth, pen hygiene, ensure adequate colostral transfer
This disease is believed to be the result of endotoxemia in young lambs. It is postulated that the neutral pH of the abomasum in newborn lambs, coupled with low concentrations of colostral immunoglobulin in the gut, allow rapid multiplication of non-enteropathogenic strains of Escherichia coli in the gut, and to some extent systemically, to result in endotoxemia.1
The syndrome is primarily reported in lambs in Great Britain but has also been reported in New Zealand and in goat kids in Spain and North America.1,2
Lambs 12 to 72 hours of age are affected. The disease is seen under all management systems but is rare in pastured flocks and occurs most commonly in lambs kept in intensive housing where there is poor hygiene of the lambing environment. Lambs from prolific ewes are at risk and the disease is more common in triplets than twins or singles.
Delayed or poor colostral intake is a major risk factor and situations that predispose this may lead to outbreaks. A high prevalence has occurred in ram lambs castrated by the use of an elastic band at a very young age and the resulting pain may have dissuaded them from feeding.
Other risk factors, all of which reduce sucking by the lamb, are inclement weather, mismothering, maternal agalactia, competition between twins or triplets, low vitality, and ewes in poor condition.
An equivalent clinical syndrome is reproducible by administering non-enterotoxic strains of E. coli by mouth to colostrum-deprived lambs, all of whom died within 24 hours.3
Watery mouth disease is a major cause of mortality of housed newborn lambs in Great Britain and is reported to be the cause of approximately 25% of all deaths of lambs in indoor intensive lambing systems.1 Where conditions allow morbidity rates may approach 24% and without early treatment case fatality rates are high.4
Gram-negative bacteria, non-enterotoxigenic and non-enteropathogenic E. coli in the environment, are ingested as a result of a contaminated environment, or from a contaminated fleece, and survive passage through the neutral pH of the abomasums to be absorbed into the systemic circulation by the natural pinocytosis that occurs in the intestinal epithelium of newborn ruminants, to produce an endotoxemia.
Affected lambs are normal at birth but become sick at 24–48 hours and up to 72 hours old. The disease is characterized by dullness, a complete failure to suck, and excessive mucoid saliva around and drooling from the mouth. As the disease progresses there is hypothermia, failure to pass feces, cold extremities, depression to the point of coma, anorexia and, in the late stages, abdominal distension and recumbency, but rarely diarrhea. The alimentary tract is full of fluid and the lamb rattles when it is shaken. Some lambs are hypothermic but the temperature is normal at the onset of the condition and falls to subnormal as the disease progresses. Progress is rapid with death 6–24 hours after the first signs of illness.
Total protein concentrations and base excess values are significantly elevated compared to normal lambs.5 Blood glucose concentrations are normal but may be low in the terminal phase of the disease.
There are no findings specific to the syndrome. The abomasal contents are fluid and mucoid, and contain small milk curds and the intestine is gas filled.
Treatment with intramuscular amoxycillin and clavulanic acid, intravenous flunixin meglumine, and oral rehydration fluid, when administered early in the clinical course, has resulted in a high recovery rate in field cases.5 Dextrose solution should also be given to those lambs that are hypoglycaemic and external warming should be provided. Other recommended treatments include emptying the alimentary tract by purgation or enema.
Most neonatal disease of lambs is manifest with diarrhea which is not present in watery mouth. The early stages of Colisepticemia and Clostridium perfringens type B or C present with similar clinical signs but are easily differentiated later in the clinical course or at post mortem examination. Hypothermia/starvation/cold stress can present with similar clinical findings but the history and environmental circumstances of occurrence differ.
In outbreaks the administration of antibiotics to all newborn lambs within 15 minutes to 2 hours of birth dramatically reduces the occurrence of further cases.4-6 Fresh or frozen sheep or cow colostrum should be supplemented to lambs at risk. The provision of ewe colostrum at 50 mL/kg body weight within 6 hours of birth prevents the disease.
Lambing areas and associated pens and yards should be kept clean and fresh bedded. Contaminated fleece should be removed from around the udder of the ewe prior to lambing and every effort should be made to insure early and adequate colostral intake by newborn lambs, especially for twins and triplets.
This is a herd disease problem reported from the UK in cows freshly turned out onto lush pasture with a high (27–43%) soluble carbohydrate content.1 There is a high morbidity (up to 80%) and a large number of outbreaks in an area. The syndrome includes hypothermia, dullness, inappetence, agalactia, and profuse diarrhea. Affected cows feel cold to the touch. Some have perineal edema, some collapse. The herd milk yield falls disastrously but there is a quick return to normal if the cows are moved to a different field. The problem may occur on the same pasture each year and recur if the cows are returned to the same pasture. There is no obvious clinicopathological abnormality. It is postulaed that the syndrome might be due to zearalenone or related metabolites produced by field micro fungi in the pasture.2
Etiology The syndrome is the result of inadequate nutrition and unbalanced nutrition in pregnancy and lactation but can also result from parasitic or chronic infectious disease.
Epidemiology Loss of weight to the point of inanition particularly in first and second litter gilts.
Control Recognition of the relation between voluntary feed intake in pregnancy and lactation, feeding based on condition scores.
The ‘thin sow syndrome’ is discussed in this chapter because of its multiple etiology. Regardless of etiology the effects of this syndrome on fertility and overall farm productivity can be formidable. There are a number of causes of wasting and the occurrence of thin sows:
• The major cause of sow abnormality under this heading results from errors in feeding and management, which are likely to be exaggerated and multiplied on farms where intensive management is practiced. The most common errors are incorrect feeding in pregnancy and lactation. These can be exacerbated by cold or drafty housing, fluctuating temperatures, too high a temperature in the farrowing house, low-level feeding to avoid obesity, wet bedding, and lack of drinking water. Early weaning increases the risk for the thin sow syndrome, especially if nutrition is inadequate.
• Parasitic disease, particularly associated with infestation with Oesophagostomum spp. and Hyostrongylus spp. Is a cause of wasting in sows and the occurrence of the thin sow syndrome and is discussed under those headings (Ch. 27)
• Thin sows can be a component of the syndrome of infectious diseases such as cystitis and pyelonephritis.
The syndrome is most common in first and second litter gilts but can affect all parities when nutrition is inadequate. It emerged as a problem in the 1970s as a result of poor understanding of the inter-relation between feed intake in pregnancy and that in lactation, combined with the move to intensive indoor housing of pregnant sows. Penning of sows exacerbated social dominance/submissive relationships. The voluntary intake of food by sows during lactation is inversely related to the intake in pregnancy. Consequently sows that are fed at high levels during pregnancy will gain excessive weight during pregnancy but will voluntarily restrict feed intake during lactation and loose excessive weight during lactation. In contrast sows that are fed what is basically a maintenance ration 2.0–2.5 kg (4.5–5.5 lbs) of a balanced sow ration during pregnancy will gain adequate weight for conceptus and body growth and during lactation will consume adequate feed for lactation requirements and loose minimal weight in this period. Knowledge of sow nutrition has improved such that major problems with this syndrome should not occur but there is still a risk of inadequately feeding sows selected for lean genotype and high litter size and weaning weights. First and second litter gilts may require more feed to provide for body growth.
Within a herd the thin sow syndrome develops over a period of months and often one or two pregnancy cycles, with a gradually declining of body condition of the group until 20% to 30% of sows have a low body condition score. No abnormalities are evident on clinical examination but the sow fails to regain weight after weaning, particularly sows after their first litter. The most critical period for weight loss is the first 2 weeks after weaning. Affected sows have a poor appetite but often show pica and excessive water intake and may be anemic.
Currently the risk for the thin sow syndrome exists where it is assumed that all pregnant sows can be fed a standard amount of ration. Problems are likely to occur when sows are run in groups and fed as a group where timid sows are likely to be bullied out of their required share of food.
The critical issue is to ensure adequate feed and energy intake during lactation. This can be achieved by:
• not feeding to excess during pregnancy
• restricting the feed intake of sows in the first few days after farrowing to encourage better feed intake in later lactation
• ensuring an adequate and constant supply of water
• ad lib feeding during lactation
• a high-energy-density lactation diet
• enclosing the creep with heat for the piglets so that the farrowing house can be kept at a lower temperature 65°F (65°C) for the sow
Condition scoring is a valuable guide to the feeding of individual sows and for a judgement of feeding practices in the herd as a whole. On a score of 1 to 5 it should be very rare to find sows with condition scores of 1 or 5. The optimum is to have sows entering the farrowing house between condition score 3 and 4 and not less than 2.5 at weaning. First and second parity sows in poor condition at weaning are best ‘skipped’ at the first heat and mated on the second heat.
Methods for condition scoring and guidelines can be found at http://www.defra.gov.uk/animalh/welfare/farmed/pigs/pb3480/pigsctoc.htm
An acute hepatopathy of horses often associated with administration of equine biological products such as tetanus antitoxin.
The disease occurs in horses administered equine serum or tissue products. The first reports of the disease were in horses in South Africa administered equine serum as prophylaxis for Africa Horse Sickness. Outbreaks of the disease have occurred in horses in Africa, Europe, and North America administered equine serum as prophylaxis for a variety of diseases including African horse sickness, encephalomyelitis, botulism, Strep. equi infection, tetanus, and influenza and in mares given pregnant mare serum.1 Most sporadic cases of the disease appear to be associated with administration of tetanus antitoxin.
The disease is reported only from adult horses (>1 year of age) and most cases are reported in the summer and autumn.2 There is a suspicion that pregnant mares are at increased risk.
The morbidity rate in outbreaks among horses administered equine serum ranges between 2 and 18%,3 although the rate among horses administered tetanus antitoxin as prophylaxis following injuries is clearly much lower. Acute hepatitis developed in 4 (0.4%) of 1260 horses >1 year of age administered commercial equine plasma at one institution in the United States over a 6-year period.4 The disease can occur after intrauterine infusion of equine serum to mares.
The case fatality rate is between 50 and 90%.
The disease occurs sporadically in horses that have not been administered equine biological products. There are reports of in-contact, non-treated horses developing the disease.
Destruction of hepatocytes results in hepatic dysfunction. Hepatoencephalopathy develops in severely affected horses.
The disease usually occurs after an incubation period of 40–70 days (range 27–165 days). Depression, anorexia, and icterus are evident in mildly affected cases. There may be mild to moderate colic. Body temperature and heart rate are usually normal. Acutely affected, or horses observed infrequently, can die unexpectedly. Signs of hepatoencephalopathy include restlessness, excitement, compulsive walking and head pressing, abnormal head position, seizures, apparent blindness, muscle tremors, and ataxia. Affected horses often injure themselves by walking into fences and troughs.
Leukocytosis with neutrophilia and mild lymphocytopenia is common. The hematocrit and plasma total protein concentrations may be mildly increased. Hyperbilirubinemia and an increase in direct (conjugated) bilirubin concentration are present and serum bile acid concentration is increased, as is serum activity of liver specific enzymes aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), and sorbitol dehydrogenase (SDH). Increases in serum GGT activity is often less than expected for the increases in serum AST, SDH, and bile acid concentrations, likely reflecting the primary insult to hepatocytes.
Hypoglycemia (<2 mmol/L, 40 mg/dL) and hyperammonemia (>150 μmol/L) may be severe. Clotting time, especially the one stage prothrombin time, may be prolonged.
The liver may be enlarged, normal or shrunken and discolored slightly yellow to green. There is severe centrilobular necrosis of hepatocytes with mild infiltration of lymphocytes and plasma cells. Alzheimer type II astrocytes are present in the brains of horses with encephalopathy.
Diagnostic confirmation antemortem is achieved by examination of a liver biopsy, although this should not be performed in animals with coagulation abnormalities.
• Rubratoxicosis (Penicillin rubrum)
• Pyrrolizidine alkaloid intoxication
• Idiopathic hyperammonemia.5
Treatment is essentially supportive and consists of correction of metabolic and acid–base abnormalities, reduction of plasma ammonia concentration, and preventing horses with hepatoencephalopathy from injuring themselves.
Hypoglycemia and dehydration can be corrected by intravenous administration of 5% dextrose and isotonic electrolyte solutions. Metabolic acidosis can be corrected by infusion of sodium bicarbonate. Plasma transfusions may be necessary to correct coagulation abnormalities.
Hyperammonemia can be treated by giving neomycin (20 mg/kg, orally, every 6 hours for 4 doses) or lactulose (0.25 mL/kg, orally every 8 hours) to decrease absorption of ammonia from the gastrointestinal tract.
Sedation with xylazine or similar compounds may be necessary to prevent the animal injuring itself. The affected horse should be housed in an area where it has the least opportunity to injure itself, and may need to be fitted with a padded helmet.
A fairly widespread disease of recent origin, granulocytopenic disease of calves is commonly ascribed to poisoning with furazolidone. Affected calves are those being reared on milk replacer and sometimes, but not always, receiving prophylactic antibiotics.1,2
Affected calves show persistent fever, and increased salivation and nasal discharge, and there are hemorrhages and necrotic lesions in the mouth and lower alimentary tract. The disease is characterized by decreased myelopoiesis in bone marrow, neutropenia, and thrombocytopenia. The course varies from 2 to 5 days, and the mortality rate is high, apparently from bacterial invasion. Pneumonia, peritonitis, and enteritis are common accompaniments. Fusobacterium necrophorum can be isolated from necrotic lesions.1 These clinical, pathological, and hematological findings resemble those of radiation sickness, and poisoning by bracken fern.
The disease has been related to long-term feeding of furazolidone (2 mg/kg BW daily), either in the milk replacer or as specific therapy, and the disease can be reproduced by this means. At higher dose rates (20–30 mg/kg BW) nervous signs, including convulsions, and death follow within a few days; both syndromes may occur at the same time in a group of calves.3
Etiology Unknown, associated with bites of Hyalomma truncatum.
Epidemiology Reported in Africa, India, and Sri Lanka affecting calves 2 to 6 months of age.
Clinical findings Fever, salivation, lacrimation, hyperemia of mucosae, epistaxis, and extensive and severe dermatitis, necrosis of oral epithelium
Lesions Dermatitis and necrotic stomatitis, disseminated intravascular coagulopathy.
The cause has not been identified, but it behaves as though it were an epitheliotropic toxin produced by the salivary glands of certain strains of the tick Hyalomma truncatum. Not all strains of H. truncatum have the ability to produce the disease and antigens unique to sweating sickness-inducing strains are described.1,2
Attempts to transmit the disease between animals by mediate or immediate contact and by injections of tissue or blood are unsuccessful. The disease occurs in Central, East and South Africa, Sri Lanka, and probably southern India. Only calves 2–6 months of age are affected as a rule but rare cases occur in adults. Sheep, pigs, and goats are susceptible, although the disease does not naturally occur in them, and the disease has been produced experimentally in dogs. Sweating sickness occurs at all times of the year but is most prevalent during the wet season when ticks are more plentiful. The morbidity rate varies with the size of the tick population but is usually 10–30%. The case fatality rate is up to 30%.
The clinical signs begin 4–7 days after the ticks attach, probably 3 days in experimental infestations. The effects are dose-specific; if the ticks are removed very early there is no clinical response and the animal remains susceptible; with a longer exposure before the ticks are removed the animal becomes immune but shows no clinical signs. With longer exposure of more than 5 days the subject develops the full-blown clinical disease and may die. If it recovers it has a solid and durable immunity.
There is a sudden onset of fever up to 41°C (106°F), anorexia, hyperemia of the mucosae, and hyperesthesia. The animal is lethargic, depressed, dehydrated, and has a serous then mucopurulent oculonasal discharge, an arched back, and a rough coat. There is an extensive, moist dermatitis commencing in the axilla, groin, perineum, and at the base of the ears which extends to cover the entire body in bad cases. ‘Sweating’ refers to this moist dermatitis. The hair is matted together by exudate and moisture collects in the form of beads on the surface. The eyelids may be stuck together. Subsequently patches of the skin and hair are rubbed off or can be pulled off to leave raw, red areas of subcutaneous tissue exposed. The tips of the ears and tail may slough.
Affected calves seek shade and their skin is very sensitive to touch. Later it becomes dry and hard, and cracks develop. Secondary bacterial infection and infestation with blowflies or screw-worm larvae are common sequelae. The oral mucosa is hyperemic at first and then becomes necrotic with the formation of ulcers and diphtheritic membranes. The calf salivates profusely, cannot eat or drink, and becomes emaciated and rapidly dehydrated. There are similar mucosal lesions in the vagina and nasal cavities, the latter causing dyspnea. The severity of the mucosal lesions appears to vary with different ‘strains’ of the toxin.3 There may be abdominal pain and diarrhea in some calves.
The course may be as short as 2 days but is usually 4 or 5 days. In recovered animals the skin may heal and the hair may regrow, but there may be permanent, patchy alopecia and the calves may remain stunted and unthrifty.
There is a severe neutropenia and eosinopenia and a degenerative left shift. α-globulin and beta-globulin levels are raised. Urinalysis indicates the existence of nephrosis but serum creatinine levels are normal.4 Dermatological examination fails to reveal the presence of any of the usual infectious causes of dermatitis.
The lesions are essentially those seen clinically. There is also evidence of severe toxemia, dehydration, emaciation, and hyperemia of all internal organs and disseminated intravascular coagulation. The necrosis of the oral epithelium extends into the esophagus and may reach the forestomachs.
There is no specific treatment; efforts should be directed at relieving the severity of the dermatitis and mucosal loss. Non-steroidal anti-inflammatory drugs (NSAIDs) and broad-spectrum antibiotic cover is a logical regimen. Hyperimmune serum, produced in sheep and cattle by infesting them with Hyalomma truncatum at 6-week intervals for 2–5 occasions, is an effective treatment in pigs, sheep, and to a less extent calves.2,5
Diseases characterized by alimentary tract involvement
Epidemiology Horses of all breeds and both sexes in the UK, Western Europe, Scandinavia, and southern South America. Greatest incidence in early summer.
Acute grass sickness: Colic, nasogastric reflux, absent gut sounds, depression, dysphagia, and small intestinal distension of <2 days duration at time of death.
Subacute grass sickness: Tachycardia with or without signs of colic, reduced intestinal sounds, impaction of the colon, and clinical course of 2–7 days.
Chronic grass sickness: Insidious onset weight loss, intermittent colic, decreased appetite, rhinitis sicca, patchy sweating, and mild dysphagia.
Clinical pathology None is specific or diagnostic.
Lesions Both forms of the disease have degeneration of neurons of the autonomic nervous system, especially of the myenteric and submucosal plexuses.
Diagnostic confirmation Examination of ileal biopsy.
Acute grass sickness/subacute grass sickness: Supportive. None effective.
The cause is unknown but is suspected to be a neurotoxin, possibly Clostridium botulinum toxin, based on epidemiologic data.1,2 Evidence supporting a role for Cl. botulinum in the etiology of the disease included the isolation of toxin (BoNT/c) producing strains of Cl. botulinum type C from the ileum of 45% of horses with grass sickness and 4% of clinically normal control horses.2 In addition to preventing the release of acetylcholine at cholinergic nerve terminals and thereby causing paralysis, a function that it shares with other botulinum toxins, BoNT/C is neurotoxic. Other studies have demonstrated increased numbers of bacterial organisms, including anaerobes, and number of species of clostridia in feces of horses with grass sickness compared with normal horses.3 Whether these findings represent a causative role of Cl. botulinum in grass sickness, or an effect of the modified gastrointestinal motility and on intestinal flora remains to be determined. Further evidence to support a role for Cl. botulinum in the etiology of grass sickness include the observations that low serum concentrations of antibodies to Cl. botulinum are associated with increased risk of the disease.1,4 However, the hypothesis of a role for toxicoinfectious botulism in grass sickness of horses does not explain the geographic distribution of the disease given that botulism occurs worldwide in horses and grass sickness does not.
Grass sickness is not common and appears to be restricted in its distribution to all parts of Great Britain (including possibly Ireland), Sweden, and the northern and western coasts of Europe. A clinically and histologically indistinguishable disease, mal seco occurs in the Patagonia region of Argentine, southern Chile, and in the Falkland (Malvinas) Islands.5,6
Horses, ponies, donkeys, zebra, Prrzewalski’s horses, rabbits, and hares are the predominant species affected.7 The morbidity and mortality rates are not reported, but the incidence on farms with a history of the disease ranges between 0.4 and 16% per year8 or 2.1 grass sickness cases per 100 horses per year.9
The case fatality rate for acute grass sickness is 100%, while that for the chronic form of the disease in horses treated at a referral hospital is 60–70%.10,11 Horses that survive the chronic form of the disease are often destroyed because of weakness and emaciation, although make complete recoveries.12 However, given the difficulty in establishing an antemortem diagnosis, it is unclear whether horses that fully recovered actually had chronic grass sickness.
The risk of disease is greatest in 4–5 year old horses (adjusted odds ratio of 1.9 compared with 0–3 year olds) and then declines such that the risk of disease is lowest in horses >12 years old (odds ratio 0.02 compared to that of 0–3 year olds).1 Cases in horses 10 months to 20 years of age have been encountered. Foals born of affected mares are clinically normal.13 There is no apparent breed predilection.8
Horses at pasture are at increased risk (hence the colloquial name of the disease), although the disease does occur rarely in stabled horses. A recent (<14 day) change of pasture carries an increased risk (odds ratio 24) of development of the disease.14 Horses that have been on the farm for less than 2 months are at increased risk of developing the disease.8 Horses on farms with previous cases of the disease are at increased risk (odds ratio 2.2–45) of the disease,14,15 although horses that have been in contact with animals with the disease are at reduced risk (odds ratio 0.1) of developing the disease.14
There is a marked seasonal distribution of cases, with the peak incidence occurring in early summer in the British Isles.8,9,16 Outbreaks of the disease are associated with the occurrence of cooler and drier weather than normal during the 2 weeks preceding the outbreak,9,17 although this is not consistently reported.15
As mentioned, farms with a history of horses with the disease are at increased risk of having further cases. For premises with previous cases of grass sickness there is an increased risk of the disease developing as the number of horses on the farm increases, with the presence of young horses, on stud farms and livery/riding schools, on farms having sandy or loamy soil, and those rearing of domestic birds and using mechanical fecal removal.9 The risk of recurrence of disease on a farm decreased with presence of chalk soil, cograzing ruminants, grass cutting of pastures, and manual removal of feces.9 There is no association between the disease and the type of pasture, nor with provision of supplementary feeds.8 Feeding hay or haylage is associated with a decreased risk of the disease.1 Any disturbance of the soil, such as by ploughing, increases the risk of disease.
The clinical signs are attributable to widespread damage to the autonomic nervous system, resulting in sympathetic and parasympathetic dysautonomia that is most clinically evident in the gastrointestinal tract. Coincident with damage to the autonomic nervous system are increases in plasma concentrations of dihydroxyphenylalanine, epinephrine, norepinephrine, and dopamine,18 possibly because of increased secretion of these compounds from affected sympathetic ganglia and neurons.19 Lesions in the cranial nerves and brain stem are probably responsible for dysphagia and drooling evident in most cases. Rhinitis is associated with diminished nonadrenergic, noncholinergic (NANC) innervation, greatest in neurons positive for substance P or calcitonin gene-related peptide, of the nasal mucosa in subacute and chronic cases.20
Electrocardiographic examination of affected horses reveals evidence of loss of parasympathetic innervation of the heart, which is consistent with lesions in the terminal cardiac ganglia.21 Splanchnic lesions are most severe in the myenteric and submucosal plexuses of the ileum, with less severe changes in the large colon and celiaco-mesenteric ganglion.22 There is also a reduction in interstitial cells of Cajal (cells involved in pacemaker activity and autonomic transmission within the gut).23 These neuronal changes are associated with a marked impairment of cholinergic activity in ileal tissue of affected horses.24 Because of the altered autonomic activity, peristalsis decreases (in chronic cases) or ceases (in acute cases) with subsequent accumulation of ingesta in the small intestine, stomach, and large colon. Death is due to emaciation in chronic cases or rupture of the stomach or intestine in acute cases.
The clinical signs of grass sickness are varied, and accurate diagnosis on clinical signs alone is very difficult. The incubation period of the disease is approximately 10–14 days17. Acute, subacute, and chronic forms of the disease are recognized,25 although some authorities use a designation of acute and chronic.26 In all cases, there is some dysphagia, resulting in drooling of saliva and trickling of ingesta from the nose. Dried food is impacted between the cheeks and the teeth and the animal plays at drinking. These signs are attributable to lesions in the cranial nerves. Most animals are depressed.
Acute cases the onset is sudden and the course of the disease is 1–4 days. Abdominal pain may be severe but also may be absent even in the presence of severe tachycardia. There is tachycardia (80–90/min may be >100), decreased to absent gut sounds, lack of defecation, and abdominal distension. On rectal examination, there are hard, dry pellets of feces, the large colon contains firm ingesta which has a corrugated feel that is quite distinct to the smooth surface of a primary colonic impaction. The small intestine is distended with fluid and readily palpable in the caudal abdomen. Nasogastric intubation yields a large (20 L) quantity of fluid. Urination is frequent and may be accompanied by tenesmus. Affected horses may wander about in a restless manner and a fine muscle tremor occurs constantly, especially in the upper forelimb. Periodic attacks of patchy sweating occur commonly. There is noticeable salivation. Esophageal endoscopy reveals linear ulcerations resulting from reflux esophagitis.
Subacute cases have signs of mild colic, or may not have any signs of colic, in the presence of tachycardia, depression, reduced gastrointestinal sounds, and impaction of the large colon with characteristic corrugated appearance.25 The clinical course is 2 to 7 days and death is inevitable. Esophageal endoscopy reveals the presence of linear erosions in many affected horses.
Chronic cases the course is usually >7 days and is characterized by weight loss, patchy sweating, and intermittent colic. Horses stand with all four feet close together under them (‘elephant on a tub stance’) and have a tucked up abdoment. Dysphagia is evident and the gut is empty except for the colon and rectum which contain dry, hard feces. In the late stages the patient snores, the penis droops, and attempts are made to eat abnormal materials. Most cases of the chronic form have rhinitis, characterized by crusting of mucopurulent material on the turbinates and this is considered, in the presence of appropriate history and other clinical signs, almost pathognomonic for grass sickness.
Application of phenylephrine (0.5 mL of a 0.5% solution) into one eye causes a dorsal deviation of the eyelashes of the upper eyelid in horses with grass sickness, but not in normal horses.27
There is a radiological discernible defect in esophageal motility in horses with grass sickness.28
Serum biochemical profiles and hematological examinations do not demonstrate pathognomonic changes.29 Signs of dehydration, electrolyte imbalances, hyperbilirubinemia, and elevations of serum activity of liver derived enzymes are all secondary to the disease.30 Urine from horses with grass sickness has higher specific gravity, protein and creatinine concentrations, and lower pH than that from unaffected horses,31 consistent with dehydration and electrolyte imbalances that occur with the disease. Peritoneal fluid is often abnormal, having an increased protein concentration and leukocyte count but, because of the considerable overlap with values in horses with lesions of the gastrointestinal tract requiring surgery, is of limited diagnostic value.32
Antemortem diagnostic confirmation can only be achieved by examination of biopsy specimens of the ileum,33 although biopsy of nasal mucosa has been suggested as an alternative.18 Examination of rectal biopsy is specific, but not sensitive, for the disease.
In cases of short duration, the stomach and small intestines are distended with an excess of fluid and gas, and the colon is often impacted with corrugated ingesta coated with black material. In chronic cases, the alimentary tract is empty.
Histologically there is extensive degeneration of neurons of the autonomic nervous system without evidence of inflammation.33 These neurons include those of the ganglia (cranial cervical, stellate, coeliaco-mesenteric, etc.) and those of the myenteric and submucosal plexi of the intestines. Degenerative neuronal changes may also be observed in the central nervous system, including the oculomotor, facial, lateral vestibular, hypoglossal and vagal nuclei, the ventral horns of spinal cord and the dorsal root ganglia. This neuropathy is difficult to confirm unless fresh, well-fixed samples are submitted for histological examination. Immunohistochemical staining for synaptophysin aids in the differentiation between autolytic tissue and tissue from horses with grass sickness.34
Samples for light microscopic examination: formalin-fixed sympathetic ganglia, brain stem, spinal cord with dorsal root ganglia, gastric fundus, duodenum, jejunum, distal ileum, ventral colon, and dorsal colon.
Acute cases respond transiently to gastric decompression and intravenous fluid administration, but death is inevitable. Selected chronic cases may benefit from careful nursing care and the administration of the promotility, indirect acting cholinergic agent, cisapride (0.5–0.8 mg/kg orally every 8 hours for 7 days).35 Administration of brotizolam (a putative appetite stimulant), acetylcysteine (antioxidant and neuroprotectant), and aloe vera gel (antioxidant, anti-inflammatory and laxative) was without beneficial effect in 29 cases.36
Successful measures have not been satisfactorily established and no definitive recommendation can be made. However, consideration should be given to the factors identified as increasing the risk of disease, such as pasturing, movement to new properties and especially those on which previous cases of this disease have occurred, and the disturbance of soil. Feeding of hay and haylage is associated with a reduced risk of developing the disease. Although administration of ivermection is associated with an increased risk of the disease, appropriate parasite control should not be ignored in horses in areas in which grass sickness is endemic.
1 McCarthy HE, et al. Equine Vet J. 2004;36:123.
2 Hunter LC, et al. Equine Vet J. 1999;31:492.
3 Garrett LA, et al. Vet Microbiol. 2002;87:81.
4 Hunter LC, Poxton IR. Equine Vet J. 2001;33:547.
5 Uzal FA, Robles CA. Vet Res Communn. 1993;17:449.
6 Araya O, et al. Vet Rec. 2002;150:695.
7 Hahn CN, et al. Vet Rec. 2005;156:778.
8 Doxey DL, et al. Equine Vet J. 1991;23:365.
9 Newton JR, et al. Equine Vet J. 2004;36:105.
10 Milne EM, et al. Br Vet J. 1996;152:537.
11 Milne EM, et al. Vet Rec. 1994;143:438.
12 Doxey DL, et al. Vet Rec. 1999;144:386.
13 Whitwell KE. Br Vet J. 1992;148:81.
14 Wood JLN, et al. Vet J. 1998;156:7.
15 McCarthy HE, et al. Equine Vet J. 2004;36:130.
16 French NP, et al. Epidemiol Infect. 2005;133:343.
17 Doxey D, et al. Equine Vet J. 1991;23:370.
18 McGorum BC, et al. Equine Vet J. 2003;35:121.
19 John HA, et al. Vet Rec. 2001;148:180.
20 Prince D, et al. Equine Vet J. 2003;35:60.
21 Perkins JD, et al. Vet Rec. 2000;146:246.
22 Scholes SFE, et al. Vet Rec. 1993;132:647.
23 Hudson N, et al. Auton Neurosci. 2001;92:37.
24 Murray A, et al. Vet Res Commun. 1994;18:199.
25 Hudson NPH, Pirie RS. Equine Vet Educ. 2005;17:19.
26 Proudman CJ. Equine Vet Educ. 2005;17:25.
27 Hahn CN, Mayhew IG. Vet Rec. 2000;147:603-606.
28 Greet TRC, Whitwell KE. Equine Vet J. 1986;18:294.
29 Doxey DL, et al. Res Vet Sci. 1992;53:106.
30 Marrs J, et al. J Vet Med. 2001;48:243. Vet Rec 2001;151:381.
31 Fintl C, et al. Vet Rec. 2002;151:721.
32 Milne EM, et al. Vet Rec. 1990;127:162.
33 Hahn CN, et al. Acta Neuropathol. 2001;102:153.
34 Hilbe M, et al. J Comp Pathol. 2005;132:223.
A syndrome of combinations of weight loss, ill thrift, diarrhea, intestinal malabsorption, and hypoproteinemia attributable to chronic inflammatory disease of the small and/or large intestine of horses is well described. The syndrome has been subdivided into granulomatous enteritis, eosinophilic enteritis, lymphocytic-plasmacytic enterocolitis, basophilic enterocolitis, and multisystemic eosinophilic epitheliotropic disease.1 Other causes of chronic inflammatory bowel disease in horses include alimentary lymphosarcoma, tuberculosis, pithyosis, and histoplasmosis.2
The etiology of granulomatous enteritis is unknown. Infection with Mycobacterium spp. is suggested as a cause but demonstration of acid fast bacteria in tissue sections or by culture of gut or mesenteric lymph nodes of affected horses is rare and inconsistent. The disease occurs with greatest incidence in Standardbred horses between 1 and 6 years of age, although it does affect other breeds of horses. The disease is usually sporadic, although it has been recorded in siblings raised on the same farm.1 Estimates of incidence are not available. The disease has an almost 100% case fatality rate.
Accumulation of lymphocytes and multinucleated giant cells in the lamina propria is associated with villous blunting in the small intestine. There is malabsorption of carbohydrates and fats and excessive loss of protein in feces2 with subsequent hypoalbuminemia, edema, and weight loss. Weight loss and anorexia are the most common presenting signs. Fever is uncommon. Approximately one-third of horses have diarrhea or a history of abdominal pain. Affected horses may have a diffuse, scaling alopecia and excoriations especially of the coronary band. Rectal examination may reveal enlarged, soft mesenteric lymph nodes. Exploratory laparotomy in horses with signs of colic attributable to inflammatory bowel disease often reveals constricting circumferential bands in the large or small intestine.3
Hematological and serum biochemical examination reveals:
• A mild, macrocytic anemia (hemoglobin <100 g/L, hematocrit <30%) with a normal leukogram
• Hypoalbuminemia is a consistent finding (<25 g/L, <2.5 g/dL) while the globulin concentration may be normal, low or, more commonly, high (>50 g/L, >5.0 g/dL)
• Plasma fibrinogen concentration is usually increased (>4 g/L, 400 mg/dL)
• There are no characteristic changes on serum biochemical analysis
Absorption tests using (D(+)-xylose, glucose, or starch) may indicate diminished absorption of carbohydrate by the small intestine. The D(+)-xylose absorption test is performed by administering D(+)-xylose at a dose of 0.5 or 1 g/kg as a 10% solution by nasogastric intubation after an overnight fast. The concentration of D(+)-xylose in blood samples collected at 0, 1, 2, 3, 4, and 5 hours after dosing is determined. An abnormal test is one in which there is not an obvious peak in the D(+)-xylose curve and in which the peak concentration is lower than expected for a normal horse on a similar diet. Administration of a 10% glucose solution orally at a dose of 1 g/kg body weight results in an increase in plasma glucose concentration of >85% the baseline values in horses with normal small intestine. An increase of <15% over baseline is found in horses with small intestinal disease that impairs glucose absorption. Intermediate values are found in both normal and diseased horses.4
Diagnostic confirmation is achieved by histological examination of biopsy of rectum or small intestine. Rectal biopsy has a low sensitivity (less than 50%) but high specificity for diagnosis of granulomatous enteritis.5 Biopsy of small intestine and mesenteric lymph nodes has a much higher sensitivity than rectal biopsy and is the recommended test.
Necropsy examination reveals that the intestinal wall is thickened uniformly especially in the jejunum and ileum. Mesenteric lymph nodes may be enlarged. There is villous atrophy with a diffuse and patchy granulomatous infiltration of the lamina propria of the small intestine. Crypt abscesses are common. Granulomas are also present in the liver, spleen, kidney, and bone marrow of many cases. The predominant cell types are macrophages and epitheliod cells with occasional giant cells. The disease may be difficult to distinguish from alimentary lymphosarcoma.
The differential diagnosis includes:
• Gastric squamous cell carcinoma
• Small intestinal adenomatous polyposis.6
Attempts at treatment with a variety of anti-inflammatory and antimicrobial drugs, including prednisone and sulfasalazine, have been almost university unsuccessful.7 Resolution of the disease occurred for up to 7 months while a horse was treated with a decreasing dose of dexamethasone, beginning at 40 mg (0.1 mg/kg) intramuscularly every 4 days for 4 weeks, and then slowly decreasing.7 Surgical resection of defined, solitary lesions is reported but this is an unusual manifestation of the disease.
1 Sweeney RW, et al. J Am Vet Med Assoc. 1986;188:1192.
2 Lindberg R, et al. Zbl Vet Med A. 1985;32:526.
3 Scott EA, et al. J Am Vet Med Assoc. 1999;214:1527.
4 Mair TS, et al. Equine Vet J. 1991;23:344.
5 Lindberg R, et al. Equine Vet J. 1996;28:275.
This is an uncommon disease of horses, in contrast to dogs, affecting horses of any age and without discernible breed or sex predilection.1,2 The etiology is unknown. Presenting signs include weight loss, diarrhea, and lethary. Clinicopathologic abnormalities include hypoproteinemia and hypoalbuminemia in approximately one-half and three-quarters of cases, respectively.2 Results of an oral glucose tolerance test are abnormal in approximately 75% of cases. Histologic examination of a rectal mucosal biopsy reveals abnormal tissue suggestive of the disease in about one-half of cases. The diagnosis is confirmed by biopsy of ileum or necropsy examination. Differential diagnoses are similar to those for granulomatous enteritis. There is marked infiltration of the lamina propria with lymphocytes and plasma cells. Effective treatment has not been described. Control measures are not available.
Eosinophilic enterocolitis occurs either as part of the multisystemic, eosinophilic, epitheliotropic disease complex or as a lone entity. Multisystemic, eosinophilic, epitheliotropic disease is characterized by eosinophilic infiltrates in the gastrointestinal tract and other organs, while horses with eosinophilic enterocolitis have no evidence of extraintestinal disease.
Multisystemic, eosinophilic, epitheliotropic disease occurs in adult horses of any age and without apparent breed or sex predilection. The etiology is unknown, but some cases are associated with lymphosarcoma, suggesting that the disease in these horses is due to clonal expansion of a T-lymphocyte population that secretes interleukin-5.1 The disease is idiopathic in most horses. Clinical signs include weight loss in all cases and diarrhea or dermatitis in approximately two-thirds of cases.2 The dermatitis occurs mainly on the face, limbs, and ventral abdomen and is exudative with alopecia, hyperkeratosis, and lichenification.3 Lesions of the coronary band and mouth are common. Urticaria occurs in some horses. Most affected horses have low serum protein and albumin concentrations. Hypereosinophilia is not a consistent feature of the disease and blood leukocyte concentrations are usually within the reference range. There are often elevations in serum activity of gammaglutamyl transpeptidase (GGT) and alkaline phosphatase, consistent with lesions in the biliary tree. This can be useful in differentiating horses with this disease from horses with granulomatous enteritis.2 Histologic examination of tissues reveals eosinophilic infiltration of skin, liver, and gastrointestinal tract. Rectal biopsy can reveal the presence of eosinophilic granulomas, but these must be differentiated from the more common eosinophilic infiltrate secondary to parasitism. Treatment is usually ineffective and the prognosis for recovery is very poor. Affected horses should be administered an anthelmintic in case the disease is due to nematodiasis. Administration of corticosteroids (dexamethasone, prednisolone) is the usual treatment but is only transiently effective in most cases. Hydroxyurea, which is used to treat a similar syndrome in people, was only transiently effective in one horse.4 There are no recognized control measures.
Idiopathic eosinophilic enteritis is a sporadic disease of horses of any age. Affected horses rarely have weight loss or diarrhea.2 The common form of the disease is one in which the infiltration is segmental and associated with acute colic due to obstruction of the small intestine or large colon by mural lesions.5,6 The D(+)-xylose absorption curve is usually normal in affected horses.7 Histologically, the disease is characterized by the presence of eosinophilic infiltrates in a chronic inflammatory reaction affecting the small or large intestines. The infiltrates are restricted to the intestinal tract. The cause has not been identified but the lesion suggests a continuing hypersensitivity reaction to an ingested allergen. Antemortem diagnostic confirmation is achieved by rectal or small intestinal biopsy. Successful treatment is usually surgical. Control measures are not reported.
During the outbreak of foot-and-mouth disease (FMD) in the UK in 2001, field investigations reported the appearance of oral lesions, initially in sheep and then in cattle which complicated the diagnostic process.1,2 While the lesions appeared to have a common, though obscure, etiology, prior to that they had not been identified as a differential diagnosis for FMD. The lesions were usually singular, located predominantly (but not exclusively) in the gingival mucosa ventral to the incisors, often in the midline; circular to nearly circular in shape and usually ranging in diameter from 4 to 10 m; never vesicular but always erosive with a raised edge, giving the ulcer a crater-like appearance; and were more prevalent in adult sheep than in lambs.2
Experienced sheep veterinarians in the UK have reported ulceration of the gums of sheep as a regular occurrence in late winter and spring.1 It has been suggested that grazing sparse rough or short pasture, the provision of feed or salt blocks, and the use of feeding troughs with sharp edges, could be predisposing causes.
An abattoir survey of sheep in New Zealand examined the lesions of the anterior lips and gums of the animals after slaughter.3
Lesions of the midline of the lips and gums of traumatic or irritant etiology were common, and the prevalence was higher in adult sheep than in lambs. The lesions probably arose from the fright/flight response behaviour of sheep, resulting in the mouth impacting against wire fences or yard railings while being handled. A smaller percentage of lesions may have been due to abrasive or irritant feed or soil. The presence of plant material and bacteria in lesions delayed healing and contributed to the formation of ulcers.
Naturally occurring ulcers of the stomach in swine occur in the pars esophagea (non-glandular part) of the stomach. They are single or multiple bleeding ulcers often associated with hyperkeratosis. Experimental lesions in the stomach are usually produced in the glandular part of the stomach as a model for the condition in humans. The condition was first reported in Illinois in 1897.
Etiology Fine particle and pelleted feed. Certain bacterial species may contribute.
Epidemiology Highly variable incidence but has increased with greater intensification of swine industry, emphasis on improving digestibility and feed efficiency and use of fine particle and pelleted feed. Growing and finishing pigs, adult sows, and boars.
Signs Sudden death from peracute gastric hemorrhage. Subacute form causes anemia, pallor, unthriftiness, black tarry feces.
Clinical pathology Hemorrhagic anemia.
Lesions Hyperkeratosis, erosions, ulcers of pars esophagea, gastric hemorrhage, anemia.
Diagnostic confirmation Lesions at necropsy.
Control Use of diets prepared through hammer mill screen of at least 6 mm. Incorporate S-methylmethionine-sulphonium chloride in diet.
The etiology is multifactorial. Finely ground and pelleted feed are important causes. Helicobacter heilmannii1 and Gastrospillium suis,2 have been found in gastric ulcers, but not ulcers of the pars esophagea of pigs and are unlikely to be the primary cause of the lesion.3 Certain environmental stressors may also be contributing factors.
The disease is most common in pigs of 45–90 kg BW4 but the disease may also occur in pigs after weaning and in adult sows and boars. All breeds are susceptible. Prevalence in groups of pigs may vary anywhere in the world from 5 to 90%. In some countries the rate is 1% and in others 87%.5
Most gastric ulcers of pigs are localized in the pars esophagea and are referred to as esophagogastric ulceration. Examination of the stomachs of pigs at abattoirs in various countries has revealed a high proportion of pigs with varying degrees of hyperkeratosis, erosions, and ulcers of the pars esophagea. Extensive erosions of the pars esophagea may be present in up to 63% of sows and 36% of finishing pigs.6
The incidence is variable between countries which may reflect differences in feeding or husbandry methods. In the Netherlands 11% of the pigs may be affected.7 The incidence of ulceration may be increasing in pigs in the UK compared to earlier studies.8 An abattoir survey of the stomachs of pigs in the UK found ulceration of the pars esophagea in 23% with a range from 4 to 57%.8 The ulcers were mild in 9.5% and severe in 13.4%.
The disease has assumed increased economic importance with increased intensification of the swine industry.9 The feed manufacturing industry is faced with the dilemma of finely ground pelleted feed providing high digestibility and feed efficiency in growing and finishing pigs but with a high incidence of lesions of the pars esophagea which may affect performance. Pelleting swine feed is also advantageous because it flows more easily and effectively in automated distribution systems in swine farms compared to finely ground meal which may bridge and clog in distribution systems, decrease dustiness and segregation of ingredients and increase bulk density. Meal is less damaging than pellets.
The incidence of clinical disease is low but the case fatality rate is high when severe hemorrhage occurs. The effects of the lesions on performance may vary considerably. In one study, pigs with extensive lesions gained 50–75 g/day less than pigs with no lesions10 while in another the presence of ulcers as determined at the abattoir did not influence growth rate.8 The disease has increased in significance with the occurrence of PMWS and PDNS associated with porcine circovirus 2. There is also an increased occurrence where there is a problem with porcine respiratory disease complex (PRDC) particularly during summer months.
Anything that causes an empty stomach which potentially increases the acidity in the pars esophagea region of the stomach is a risk factor.7 Back in the 1960s all that was needed to produce an esophageal ulcer in a pig was to keep the pig restricted in a feeding or farrowing crate and deprive it of water for 24 hours and it would have an ulcer. This would therefore include intermittent feeding and watering, respiratory disease and hot weather.
The disease occurs primarily in penned pigs receiving a grain diet and growing rapidly. It has also occurred in pigs fed large quantities of cheese whey or skimmed milk. Too much copper and not enough zinc may also be a factor. The incidence is highest in pigs receiving diets containing a higher proportion of corn (maize) than other grains. The incidence is even greater if the corn is finely ground or is gelatinized or expanded. Ulceration in some pigs may be associated with Ascaris suis infection, but in other studies there is no significant association between the parasite and ulcers.
This is the most important risk factor.11 One of the explanations of this may be the rapid emptying of the stomach when fine particles are used.12 There is normally a gradation of ascending pH from the cardia to the oesophagus but with rapid emptying there is the possibility of the low pH reaching the esophageal region.11,12
Feeding a diet based on finely ground barley to pigs beginning at 10–11 weeks results in lesions as early as 1 month later, and the incidence and severity of lesions increased progressively over the next 2 months. Diets high in wheat or corn starch may be worse than diets based on barley. The incidence and severity of hyperkeratosis may be greater in some breeds compared to others, but the effects of previous diets and environmental factors may have influenced the results.
The particle size and the physical form of the feed are important risk factors. Finely ground diets and pelleting have detrimental effects on the gastric mucosa of finishing pigs.13 A pelleted diet uses grain that is finely ground before it is compressed into a pellet but on reaching the stomach it reverts to the fine particles. A diet finely ground through a 3 mm screen in a hammer mill and then pelleted will be associated with a 75% incidence of pigs with hyperkeratosis of the pars esophagea and 11% of the pigs may have severe erosions and ulceration of the pars esophagea.10 The incidence of lesions decreases when the diet is ground through a 6 mm screen.14 Finely ground barley or wheat is associated with a marked increase in gastric abnormalities compared to the use of coarsely ground grains. The size of particles in feed is significant whatever feed is used, even straw; coarsely ground barley straw at 5–10% of the ration gives almost complete protection. In growing pigs, dietary fiber rich in structural polysaccharides has been shown to be important in preventing the development of parakeratotic lesions in the pars esophagea.15 But an increase in the crude fiber content of a diet which is finely ground does not affect the occurrence of severe erosions and/or ulcers of the pars esophagea.
Grinding barley through a 1.56 mm screen results in finely ground feed, which is associated with an increased incidence and severity of gastric ulcers in pigs. Grinding through a 4.68 mm screen approximates the screen size used most frequently for grinding barley for pigs in practice and is associated with a low incidence of ulcers.15
Reducing particle size and pelleting improves growth performance of finishing pigs.16 For every 100 microns of decrease in size of the particle size there is an approximately 1.3% increase in gain efficiency but each time the level of ulcers increases.17 The processes have additive effects on digestibilities of dry matter, nitrogen, and energy, with maximum nutrient digestibility in pelleted diets with corn milled to a particle diameter size of 400 μm. Reducing the particle size to below 400 μm causes practical problems with milling and an increased incidence of gastric lesions and it is suggested that a particle size of 600 μm, or slightly less, is optimal for corn in either meal or pelleted diets for finishing pigs.
Using endoscopic examination of the stomachs of pigs fed a fine particle diet (geometric mean size of 578 μm) it was found that as ulcer severity increases, the growth performance of individually fed pigs decreases. Feeding a coarse particle diet (geometric mean size of 937 μm) for 3 weeks resulted in a decrease in the severity of the ulcers.18
High levels of unsaturated dietary fat are not helpful especially if they are accompanied by low levels of vitamin E. Similarly pigs fed waste food had more severe gastric lesions.19
It has been suggested that confinement, crowding, transportation, changes in environment, and exposure to other pigs, were important in the etiopathogenesis of gastric ulcers of pigs. All of these stresses and many others including anxiety, fear, pain, fatigue, fasting, etc., will be associated with an increase of ulcers. There is an even greater occurrence in summer when water demands are higher. Males are always more affected in prevalence and severity but that may be that they are more easily stressed. One of the most important factors is time in the lairage. Pre-mortem handling is extremely important.20 Pigs kept overnight in the lairage have more ulcers than pigs killed on the day of arrival.21 Similarly there is no difference in the prevalence of lesions in small and medium farms but there is a considerable increase in the prevalence in these two groups compared to the larger producer.22 Larger herds always show more of the problem23 and it is probably a reflection of the different diets that they use (based on wheat and pelleted). The larger farms also have more infection pressure, more selection pressure, and more feed-related factors.
Pigs that receive porcine somatotrophin may have an increased level of ulcers possibly due to the elevated circulating gastrin.24
There are a variety of foreign bodies reported from the pigs’ stomach including stones, which outside sows chew all the time, and also sand. The majority of stones is probably passed in the feces, but may accumulate in and stretch the stomach. The stomach capacity is normally about 3–6 L. This may lead to reduced appetite and gastritis but is not believed to be a contributor to esophageal ulceration. Similarly, hairballs are a common finding, reaching 10–15 cm in size in the stomach. The occurrence of rubbish indicates pica or a depraved appetite which is often an indicator of inadequate feeding. One of the other substances found in outdoor pigs stomachs is the flakes of bitumen that remain from clay pigeon shooting, which are toxic.
Increased frequencies of any of four combinations of behavioral indicators of stress, recorded 4 weeks after weaning, were weakly associated with increased risk of acute fundic ulcers in slaughter pigs from a conventional farrow-to-finish herd.25
The spiral-shaped Gastrospirillium suis has been found in 84% of the stomach of pigs with frank gastric ulcers of the pars esophagea. The organisms were mainly in the mucus layer and in gastric foveolas of the antral and oxyntic mucosa and only occasionally in the cardiac-pars esophagea region.2 The presence of the organism has been associated with lesions of the pyloric mucosa in pigs.26
There is no known cause and effect relationship but the gastric environment associated with gastric ulcer may favor colonization of the organism. The oral inoculation of Gastrillium-like bacteria into laboratory animals is capable of inducing gastric ulceration.27 Helicobacter heilmannii type 128 has been found more frequently in the stomachs of pigs with ulcers (100%) and in those with pre-ulcer lesions (90%) than in stomachs with macroscopically normal pars esophagea (35%).1 It has been suggested that Helicobacter heilmannii may play a role in the pathogenesis of gastric ulcers in swine by causing increased acid secretion. H. pylori can colonise the pig stomach. Experimental reproduction of Helicobacter suis infection has recently been described.29 The pigs had no ulcers and infection was only accompanied by a mild superficial gastritis.
In pigs, nearly all naturally occurring gastroduodenual ulcers are localized in the pars esophagea of the stomach. Excessive gastric acid production, depletion of the gastric buffering system resulting in prolonged activation of pepsinogens, and changes in mucus composition are suggested as important factors related to gastric ulceration in swine. The physical texture of the feed can influence pepsin and acid secretion, and the fluidity of the stomach contents induced by ulcerogenic diets may alter the normal pH gradient within the stomach. This allows greater pepsin and acid contact to the esophagogastric area.
The concentrations of short chain fatty acids are high in the proximal gastric contents of pigs and associated with intakes high in readily fermentable carbohydrates, like ground corn. These products of bacterial metabolism, principally acetate and lactate, reach high concentrations within 4 hours after feeding because of high pH in the proximal gastric contents which may allow some types of bacteria to proliferate. These weak acids are lipid soluble in their undissociated form and could penetrate and acidify underlying tissue more readily than free hydrogen ions. In this way, rapid production of short chain fatty acids, followed by their absorption and tissue acidification, may be similar to ruminal acidosis and rumenitis in ruminants following the ingestion of large quantities of readily fermentable carbohydrates.30
The rumen epithelium, also a stratified squamous mucosa, is easily injured by short chain fatty acids at pH ≤ 5.0. The breaking of the barrier by short chain fatty acids could result in underlying inflammation and widespread tissue destruction. Experimentally, exposing undissociated short chain fatty acids to swine gastric mucosa results in rapid penetration of the outer barrier and acidification of the underlying viable tissue.30 This results in cell swelling and vesicle formation, followed by sloughing of the outer barrier, erosion into deeper zones, and finally, ulceration.30
Weak organic acids, at pH ≤ 2.5 induce a greater degree of functional and histological injury in 3 stomach zones (squamous, cardiac, and oxyntic) than does hydrochloric acid. The predilection for the squamous mucosa in naturally occurring ulcers may be attributed to the lack of defense or repair mechanisms that are present in the cardiac and oxyntic mucosa, which are capable of HCO3- and mucus secretion, which may raise the pH adjacent to these epithelial layers.30 Thus the increased digestibility associated with decreased particle size of the diet may promote rapid fermentation following eating resulting in the production of increased concentrations of short chain fatty acids. Any increase in fluid content will also contribute to the changes in pH gradient that exist in the stomach. Excessive gastrin is then stimulated and more acid secretion follows.
Normally, the pars esophagea is white, smooth, and glistening and may be bile stained. The first stage in ulceration is hyperkeratosis. This is followed by erosions, ulcerations, and hemorrhage. The erosions may heal, resulting in a fibrous contraction. Chronic ulceration may occur with the development of several ulcers in combination with fibrous tissue involving all of the squamous mucosa. Advanced hyperkeratosis may cause partial stenosis of the terminal esophagus.
The erosion of a blood vessel within the ulcer will result in acute to subacute gastric hemorrhage. These cases are usually sporadic, causing deaths of individuals within a group, with cases occurring over a period of several weeks. Clinical signs are often not observed, affected pigs being found dead from acute hemorrhage into the stomach.
The regurgitation of bile into the stomach and the intensity of bile staining of esophagogastric tissue have been linked to the pathogenesis of esophagogastric ulcers in pigs. Almost all stomachs of pigs contain bile and bile staining of the pars esophagea; there is no evidence for the hypothesis that the regurgitation of bile into the stomach is associated with esophagogastric lesions in finishing pigs.31 There is no evidence of an association between gastritis and ulcer.32
Most cases are sub-clinical but sows will die from blood loss. Pigs frequently die from ulcers during concurrent disease such as respiratory disease33 and in this case anorexia may disturb the gastric contents and allow material of high acidity to reach the cardia. Similarly where there is a reduced consumption of water the integrity of the mucus may be broken by the dessication that results on mucosal surfaces.
Gastric ulceration is most common in pigs over 6 weeks of age and occurs in adult sows and boars; the clinical findings are dependent on the severity of the ulcers. The effects of ulceration on production may be highly variable. Most pigs with esophagogastric ulcers are clinically normal, and growth rate and feed intake appear unaffected. Some observations suggest that there is no effect of ulceration on growth rate, while others indicate that the presence of esophagogastric ulcers results in a marked decrease in growth rate and an increase in the length of time required for the pig to reach market weight. Some affected pigs also eat slowly and regurgitate frequently. Endoscopic monitoring of the stomachs of pigs fed ulcerogenic diets found that as the severity of the ulcer increased growth performance was decreased.18 The greatest economic losses were associated with sudden deaths due to hemorrhage and marked decreases in performance associated with fine particle size.
The erosion of a blood vessel within the ulcer will result in acute to subacute gastric hemorrhage. These cases are usually sporadic, causing deaths of individuals within a group, with cases occurring over a period of several weeks. Clinical signs are often not observed, affected pigs being found dead from acute hemorrhage into the stomach. When pigs are found dead from peracute hemorrhage, inspection of the in-contact pigs may reveal other animals with pallor and black tarry feces which represent those with subacute hemorrhage.
Cases with subacute gastric hemorrhage may survive for a few days and there is evidence of marked pallor, weakness, anorexia, and black pasty feces changing to mucus-covered pellets in small amounts. The weakness may be sufficient to cause recumbency. Vomiting frothy bile-stained fluid and grinding of the teeth may occur. Abdominal pain may be elicited by deep palpation over the xiphisternum and there may be a reluctance to walk along with a rigid back indicative of pain.6 Animals that survive are often unthrifty, usually due to anemia from chronic blood loss with a few cases affected by chronic peritonitis. When the disease is occurring careful observation may detect early cases. Suggestive signs are a darkening of the feces and the development of pallor.
Laboratory testing is not indicated. Animals with gastric ulceration generally have lower hematocrit values, haemoglobin concentrations, and erythrocyte counts than normal. The black tarry feces can be examined for the presence of blood.
Ascarids have been found in the stomach but these are not a factor in the field.34
At necropsy, the ulcers are confined to the esophageal region of the stomach. Affected stomachs consistently have more fluid contents than unaffected ones. If severe blood loss from the ulcer has been the cause of death then the carcass is pale and fresh blood is usually present in the stomach (there may be large blood clots) and intestines. The colonic contents may also appear melenic. Early lesions in clinically unaffected animals include hyperkeratinization of the mucosa (usually pale raised areas without bile staining initially) which progresses to epithelial erosion without actual ulceration. Ulcers usually initially occur along the junction of the pars esophagea with the glandular stomach but may enlarge to efface the entire squamous portion of the stomach. These more diffuse ulcers are easily missed on cursory examination due to their uniform appearance. Chronic gastric ulcers develop thickened, raised edges due to ongoing fibrosis, occasionally resulting in a gastroesophageal stricture. The histological appearance varies with the stage of lesion development but in fatalities there is typically complete loss of the epithelial layer, with exudation of neutrophils from a bed of mature granulation tissue. Recent studies have demonstrated Helicobacter-like bacteria in porcine stomachs but further research is required to determine if this infection plays a significant role in ulcer formation. Small clusters of H. hellmanii have been seen in the gastric crypts,35 but are not associated with histological changes.36 A recent survey suggested no correlation between infection in the cardiac mucosa and the severity of the lesions shown by the esophagogastric region.37 The macroscopic findings are usually sufficient for the confirmation of a diagnosis of esophagogastric ulceration. The initial lesion of hyperkeratosis leads to parakeratosis with fissures and the lamina propria is then exposed. The epithelium sloughs off and then ulcers of the epithelium develop with haemorrhage from the vessels.
Severity and extent of esophagogastric lesions can be graded according to the following scheme6:
1: small degree of hyperkeratosis (< 50% of total surface)
2: distinct hyperkeratosis (= 50% of the total surface)
3: hyperkeratosis and less than 5 erosions smaller than 2.5 cm in size
4: hyperkeratosis and more than 5 erosions or erosions larger than 2.5 cm in size
5: hyperkeratosis and more than 10 erosions or erosions larger than 5 cm in size, and/or an ulcer (with or without bleeding) or stenosis of the esophagus towards the stomach.
No difference in lesion score was found between Duroc, Landrace, and Iberian pigs.38
The occurrence of sudden death with a carcass that shows extreme pallor and a marble-white skin suggests the possibility of peracute hemorrhage from an esophagogastric ulcer. The disease must be differentiated at necropsy from proliferative hemorrhagic enteropathy, swine dysentery, and salmonellosis. Black tarry feces in growing and finishing pigs are characteristically due to subacute hemorrhage associated with esophagogastric ulceration.
It is possible to detect stomachs with Helicobacters by covering the stomach with urea gel containing an indicator sensitive to pH change. If there are large numbers of urease-positive bacteria then the pH changes.39
Severe infestation with whipworms is a differential. The clinical diagnosis can be confirmed by endoscopy40 which requires an empty stomach (may cause ulceration in itself) and anesthesia.
Vitamin K and hematinics have been tried with little success. Bovine serum concentrate given as a 1% solution is supposed to have reduced the extent and severity of signs associated with ulcers in growing pigs but in general medication does not help.41 If a diagnosis is made euthanasia is advised.
Control of esophagogastric lesions of growing and finishing pigs is dependent on using diets with a particle size and physical form which will provide the most economical performance in terms of digestibility and feed efficiency and minimize the incidence of lesions.
The most desirable particle size or physical form of diet, meal, or pelleted form, has not been determined. The use of a diet ground through a 6 mm screen instead of 3 mm screen is recommended. However, screen size is not the only factor affecting particle size. Other factors include the condition of the screen and hammer, the type and variety of grain and its moisture content, the speed of the mill, the pelleting process and the flow rate in the distribution of the feed to the pigs. A particle size of 600 μm, or slightly less is suggested as optimal for corn in either meal or pelleted diets for finishing pigs.16
The incorporation of S-methyl-methionine-sulphonium chloride (MMSC), a nutritional component of many vegetables such as cabbage and carrots, has anti-gastric ulcer properties. Its addition to the diet, ground through a 3 mm screen, and fed to grower pigs from 45 to 107 kg liveweight, at 400 ppm decreased the incidence of severe erosions or ulcers by about 50%.14 The addition of lucerne meal to increase the crude fiber content of one of the experimental diets did not have an effect on the incidence or severity of the lesions.
The diet should contain adequate amounts of vitamin E and selenium. Where applicable a reduction of the amount of corn in the ration and the feeding of meal rather than pellets may also be of value. The reduction of environmental and managemental stressors with attention to stocking rates may be of value.
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Friendship RM, Melnichouk SI, Smart NL. Helicobacter infections; What should a swine practitioner know? Swine Health and Production. 1999;7:167-172.
Friendship RM. Gastric ulceration in swine. Swine Health and Production. 2004;12:34-35.
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25 Dybkjer L, et al. Prev Vet Med. 1994;19:101.
26 Mendes EN, et al. J Med Microbiol. 1991;35:345.
27 Eaton KA, et al. Vet Pathol. 1995;32:489.
28 Melnichouk SI, et al. Swine Hlth Prod. 1999;7:201.
29 Hellemans A, et al. Proc 17th Int Pig Vet Soc 2002; 192.
30 Argenzio RA, et al. Am J Vet Res. 1996;57:564.
31 Elbers ARW, et al. Vet Quart. 1995;17:106.
32 da Silva JCP, et al. Rev Bras Cien Vet. 2001;8:403.
33 Dionisopoulos L, et al. Can J Anim Sci. 2001;81:779.
34 Hani H, Indermuhle NA. Vet Pathol. 1979;16:617.
35 De Groote D, et al. Proc 15th Int Pig Vet Soc Cong Birmingham 1998; 84.
36 Szeredi L, et al. Proc 18th Int Pig Vet Soc Cong Hamburg 2004; 609.
37 Choi Y, et al. Proc Allen J Leman Conf Univ Minn 2001;28:1.
38 Ramis G, et al. Proc 17th Int Pig Vet Soc Cong 2002; 282.
39 Melnichouk SI, et al. Swine Hlth Prod. 1999;9:201.
This syndrome of unknown etiology is manifest with wasting, ill thrift and mortality, or culling for poor production, and is reported in England and Canada.1,2 It affects both housed and pastured sheep predominantly in their first year of life, but cases up to 3 years of age have been seen. Affected sheep are dull and anorectic with pale mucous membranes and have fecal staining of the perineum. The rumen fill is reduced and the feces are soft and malodorous. Blood examination shows hypoalbunimemia, an elevated blood urea nitrogen, and leukocytosis with neutrophilia. On post mortem there is lymphocytic enteritis with gross thickening of segments or the entire or distal part of the small intestine. There is no evidence for Johne’s disease or parasitic gastroenteritis and the syndrome has similarities to the proliferative enteropathies of swine and horses.
Diseases characterized by respiratory tract involvement
Interstitial pneumonia of cattle has been known for many years under many different terms including: atypical interstitial pneumonia, acute pulmonary emphysema and edema, bovine pulmonary emphysema, ‘panters’, ‘lungers’, bovine asthma, pneumoconiosis, and ‘fog fever’.
Diffuse or patchy damage to alveolar septa is the essential feature of interstitial pneumonia which may be acute or chronic and can be caused by many forms of pulmonary injury. There is an obvious lack of lesions of the small airways which differentiates interstitial pneumonia from bronchopneumonia. Traditionally it was thought that interstitial pneumonias were characterized by chronic inflammation in which there is a predominantly proliferative response involving the alveolar walls and supporting stroma. However, acute diffuse damage of the alveolar walls accompanied by an early intra-alveolar exudative phase, which can be followed by proliferation of type 2 alveolar epithelial cells and fibroblasts, is now commonly recognized.
The recognition that interstitial pneumonia can have an acute exudative phase was the reason for the designation of acute interstitial pneumonia in cattle as ‘atypical’ interstitial pneumonia. The use of the word ‘atypical’ may create some confusion in the interpretation and diagnosis of lesions and in the conveying of information. It may be more appropriate to use the term interstitial pneumonia and specify where possible, clinically, epidemiologically, and pathologically the various forms of interstitial pulmonary disease in cattle.
The diseases in which interstitial pneumonia is the essential lesion are listed in Table 36.1. Pulmonary congestion and edema, alveolar exudation, hyaline membrane formation, interstitial emphysema, and alveolar epithelial cell hyperplasia and fibrosis of the supporting stroma without lesions of the smaller airways are the characteristic lesions, with their presence and extent varying according to the stage of the disease process.
Table 36.1 Diseases of the lungs of cattle in which the essential lesion is interstitial pneumonia
The term atypical interstitial pneumonia as originally proposed is still useful in describing some of the diseases clinically and sets them apart from the common acute infectious diseases, especially the viral diseases of the respiratory tract of cattle. Clinically, they are atypical with regard to most clinical signs, especially when compared to the bacterial pneumonias:
• Some are acute, like fog fever, while others are chronic as in ‘bovine farmer’s lung’
• There is usually acute or chronic respiratory distress and a relative absence of toxemia
• Most are progressive and non-responsive to treatment
• Pathology consists of varying degrees of pulmonary emphysema, edema, hyaline membrane formation, and alveolar epithelial cell and interstitial tissue hyperplasia.
While there are obvious clinical, and particularly epidemiological, differences between the various diseases, there are fewer differences between the pathological findings which tend to merge from one to another.
Etiology d, l-tryptophan in forage. Inhalation of certain gases. Hypersensitivity to molds. Mycotoxicosis and plant poisonings. Viral and bacterial infections.
Epidemiology Primarily in adult cattle moved from dry to lush pasture. Outbreaks of acute pulmonary emphysema and edema occur primarily in adult cattle moved from dry to lush pasture in autumn in North America. In UK and Europe other interstitial pneumonias due to hypersensitivity to molds occur.
Signs Outbreaks of acute respiratory distress in pasture form of disease; severe dyspnea, mouth breathing, expiratory grunt, subcutaneous emphysema, and rapid death. Subacute form less severe and may survive but develop cor pulmonale later. Individual cases of interstitial pneumonia in UK and Europe are subacute and chronic.
Clinical pathology None clinically applicable.
Lesions Enlarged firm lungs which do not collapse, diffuse congestion and edema, interstitial and bullous emphysema, cranioventral consolidation, hyaline membrane formation, alveolar epithelial hyperplasia, fibrosis.
Diagnostic confirmation Lesions at necropsy.
• Organophosphatic insecticide poisoning
• Other interstitial pneumonias
• Bovine farmer’s lung or extrinsic allergic alveolitis
• Verminous pneumonia caused by aberrant migration of Ascaris suis larvae
Control Grazing management. Use of antimicrobials to control conversion of tryptophan to 3-methylindole. Adequate housing and ventilation to control hypersensitivity pneumonias.
There are several different possible causes.
This is an acute atypical interstitial pneumonia also known as acute respiratory distress syndrome of cattle. The cause in adult cattle which have been moved from a dry to a lush pasture in the autumn season is related to the ingestion of a toxic level of d,l-tryptophan in the forage.1 The experimental oral administration of toxic amounts of d,l-tryptophan to cattle causes clinical and pathological findings similar, if not identical, to those of the naturally occurring disease. d,l-tryptophan is converted in the rumen to 3-methylindole which, when given orally or intravenously, also produces the characteristic lesions in cattle and goats. The 3-methylindole exerts a direct effect upon cells and cell embranes of bronchioles and alveolar walls, perhaps as a result of strong lipophilic properties.
Specific forages have not been implicated, but affected cattle have often been consuming alfalfa, kale, rape, turnip tops, rapidly growing pasture grass, and several other feeds. However, pasture levels of tryptophan are not necessarily higher in those associated with the disease compared to normal pastures. In some naturally occurring cases of fog fever in beef cows changed from a dry summer range to a lush green pasture, there is a marked increase in the ruminal levels of 3-methylindole while in other cases the levels are not abnormal. Failure to detect abnormally high levels in the rumen and plasma of naturally occurring cases may be related to the rapid metabolism and elimination of 3-methylindole.
The levels of tryptophan in lush pasture are sufficient to yield toxic doses of 3-methylindole. A 450 kg cow eating grass at an equivalent DM intake of 3.5% of BW/day with a tryptophan concentration of 0.3% of DM would ingest 0.11 g tryptophan/kg BW/day. The total amount ingested over a 3-day period would approximate the single oral dose of 0.35 g/kg BW needed to reproduce the disease experimentally.
This is a chronic interstitial pneumonia of cattle which occurs sporadically and is suspected of being caused by repeated subclinical incidents of ABPEE or from recovered cases of the disease. Experimentally, repeated oral doses of 3-methylindole can result in diffuse pulmonary fibrosis and alveolitis in cattle.
For many years it was thought that massive infestation of the lungs by large numbers of lungworm larvae in a lungworm-sensitized animal could cause an allergic reaction resulting in the development of acute bovine pulmonary emphysema. The possibility of such hypersensitivity as being associated cannot be totally ignored but at the present time there is no evidence to support such a theory. Such hypersensitivity may occur when the level of larval infestation of pasture is extremely high but it is not involved in the great majority of cases. In most cases of naturally occurring fog fever there is no laboratory evidence of lungworms in the lungs or feces of affected and in-contact animals. Reinfection of cattle with lungworm will occur 2–3 weeks following introduction to an infected pasture and cause acute respiratory distress which is indistinguishable clinically from fog fever. The migration of abnormal parasites, particularly Ascaris suum, has been observed to cause an acute interstitial pneumonia in cattle which were allowed access to areas previously occupied by swine.1
The experimental inhalation of nitrogen dioxide gas is capable of causing acute interstitial pneumonia in cattle1 and severe alveolar edema and emphysema in pigs but it seems unlikely that animals of either species would be exposed naturally to a significant concentration of the gas for a sufficiently long period to produce such lesions.
Pigs which survived experimental exposure to silo gas did not have the lesions seen in silo-fillers’ disease in man, and experimental exposure of cattle to nitrogen dioxide gas produces lesions which do not occur in naturally occurring fog fever. Acute pulmonary emphysema and deaths have occurred in cattle exposed to zinc oxide fumes produced by the welding of galvanized metal in an enclosed barn housing cattle.
The ingestion or inhalation of molds may be a cause of the disease in cattle.1 The disease has been associated with hypersensitivity to moldy hay based on the presence of serum precipitins of the thermophilic antigens of Thermopolyspora polyspora, Micropolyspora faeni, and Thermoactinomyces vulgaris in cattle affected with extrinsic allergic alveolitis or bovine farmer’s lung.
In Switzerland, a high incidence of serum precipitins against Micropolyspora faeni (60%) and moldy hay antigen (80%) was demonstrated in exposed but apparently healthy cattle from an area where ‘allergic pneumonia’ is common. The precipitins decreased during the pasture season and increased during winter housing.
Outbreaks of acute respiratory disease in adult cattle due to acute allergic pneumonitis can occur 15 hours after the introduction of severely moldy hay. Serological investigation and provocative challenge may reveal a hypersensitivity pneumonitis due to allergens of Micropolyspora faeni. A hypersensitivity pneumonitis has been produced experimentally in calves by exposure to aerosols of Micropolyspora faeni with or without prior sensitization by subcutaneous injection of the antigen.
In some Canadian cattle barns the disease occurred in cattle located near the hay chute from which hay and bedding are thrown down from the hay storage above the floor where the animals are kept. It has been suggested that the degree of exposure to dusty hay was greater in these cattle but that has not been substantiated. Similarly, it has been proposed that feeding finely ground feed may be associated with interstitial pneumonia in feedlot cattle but there is little evidence to support the observation.
The high incidence of ABPEE in the autumn when many legumes and other pasture plants are flowering, and the common occurrence at this time of allergic rhinitis in cattle, suggest that the inhalation of pollen may cause an allergic response of the alveolar epithelium. However, many outbreaks of the disease have occurred in cattle solely on grass pasture with no flowers; intradermal tests of sensitivity to many pasture plants and to the ruminal contents of affected animals have been negative, and blood histamine levels are within the normal range.
In North America, the ingestion of sweet potatoes infested with the mold Fusarium solani has been incriminated as a cause of acute interstitial pneumonia in cattle. Growth of the mold on the potatoes produces the toxins ipomeamarone and ipomeamaronol, and a lung edema factor. The latter is a collective term for a group of substances capable of causing death associated with severe edema and a proliferative alveolitis of the lungs of laboratory animals. It produces a respiratory syndrome which is clinically and pathologically indistinguishable from ABPEE.
The fungus Fusarium semitectum growing on moldy garden beans, Phaseolus vulgaris, which were discarded on pasture, was associated with acute pulmonary emphysema in cattle that consumed the beans and their vines. The fungus produces a pulmonary toxin. The pulmonary toxin, 4-ipomeanol (ipomeanol), accumulates in mold-damaged sweet potatoes and induces pulmonary edema, bronchiolar necrosis and interstitial pneumonia in many mammalian species. Outbreaks have occurred in lactating cows following ingestion of sweet potatoes damaged by Myzus tersicae.2 Other Fursarium spp. have been found in peanut-vine hay, which has been associated with acute respiratory distress and atypical interstitial pneumonia in adult beef cattle.3 The population mortality rate due to respiratory disease was about 12% and the case fatality rate 77%. Clinical signs occurred within a few days to 2 months after the animals were fed the peanut-vine hay.
A weed, Perilla frutescens, is considered to be a cause of the disease in cattle in the US and wherever the plant is found. High morbidity and high case fatality rates are characteristic, and the plant contains a perilla ketone which can be used to produce the disease experimentally.
Turf-quality perennial ryegrass straw (Lolium perenne) infected with the endophyte (Acremonium lolii) which yields toxic substances, including lolitrem-B has been associated with atypical pneumonia in weaned beef calves.4 However, feeding the suspect hay resulted in typical ryegrass staggers but not atypical interstitial pneumonia.
There is no evidence that any of the common bacterial pathogens of cattle such as Mannheimia haemolytica, Pasteurella multocida, Histophilus (Haemophilus) somni, or Mycoplasma spp. are primaily associated with acute interstitial pneumonia. In a series of feedlot cattle with clinical findings consistent with acute interstitial pneumonia, the pathogens were present in the lung tissues of some animals at necropsy but their presence was not considered as a primary cause of the pneumonia but rather secondary to the initial injury of the lung which was undetermined.5
Certain viral infections of the lung may result in interstitial pneumonia. In the interstitial pneumonias caused by the bovine respiratory syncytial virus (BRSV) there is a bronchiolitis and alveolitis and these should be termed bronchiointerstitial pneumonias. The BRSV is an important cause of outbreaks of acute interstitial pneumonia in beef calves 2–4 weeks after weaning. Pathologic evaluation of the lung tissues of feedlot cattle which had acute interstitial pneumonia found that BRSV was not a causative agent.6 In a series of cases of interstitial pneumonia in feedlot cattle in Saskatchewan the presence of the BRSV antigen was demonstrated in only 7% of cases and there was more severe bronchiolar epithelial necrosis than in the other cases which were negative for the virus.7
Acute pulmonary emphysema and edema (ABPEE) or fog fever occurs almost exclusively in adult cows and bulls, usually 4–10 days after they are moved abruptly from a dry or overgrazed summer pasture to a lush autumn pasture. The new pasture may or may not have been grazed during that summer and the species of grass or plants does not seem to make a difference, but usually there is some lush regrowth of grass, legume or other palatable plants. Merely changing pasture fields in the autumn has precipitated the disease. In the mountainous areas of North America the disease occurs commonly in cattle brought down from high altitude grasslands to the cultivated and perhaps irrigated lush pastures.
ABPEE usually occurs in outbreaks, the morbidity ranging from 10% in some herds up to 50% and higher in others, with a case fatality ranging from 25 to 50%. It is not unusual to observe a mild form of the disease in about one-third of the adults at risk but only 10% of those at risk may be severely affected. Often, a number of cows are found dead without premonitory signs; many others are severely ill and die within 24 hours and the owner believes that the entire herd will die because of the sudden onset and the large number of animals which are affected at once. Calves and young growing cattle up to 1 year of age grazing the same pasture are usually unaffected.
A retrospective analysis and random sample survey of cattle ranches in northern California found that the type of forage management has a significant effect on the occurrence of the disease. The greatest occurrence of the disease was in herds where the cattle were moved from summer ranges to second-growth hay fields or to irrigated pastures, or from one irrigated field to another. The adult morbidity rate was 2.6% and the case fatality rate about 55%. The disease did not occur on ranches with limited or no movement of cattle from summer ranges to lush autumn pastures.
Placing cattle on rape or kale forage fields or in fields where turnips have been pulled and the cattle allowed access to the tops may have the same effect. The disease has also occurred commonly in western Canada when cattle have been placed in a stubble field following harvesting of any of the cereal crops. Veterinarians have noted that the timespan over which the disease occurs during the autumn months is only 2–4 weeks and that, following the first frost in the fall, the incidence of the disease declines rapidly. The disease has also occurred in the same herd on the same pasture in successive years.
ABPEE in adult cattle in autumn has been recorded in Canada and the US, Great Britain, Holland, and New Zealand. The disease is rare in Australia. The chronic form of the disease in housed cattle appears to be the predominant form of the disease in Switzerland, but the acute form in cattle which have been changed from a dry to lush pasture is now reported. The disease has been recognized in France for many years as aftermath disease or aftermath emphysema, especially in the Normandy region. Some reports have suggested a breed incidence, Herefords being more commonly affected than the Jersey, Holstein, Shorthorn, and Angus breeds, but there are few exact epidemiological data to support the observation. One report suggested that the chronic type in housed cattle was more common in the Channel Island breeds.
Acute interstitial pneumonia in feedlot cattle.
Interstitial pneumonia is recognized as important cause of economic loss in feedlot cattle in western Canada and the United States.8 The disease occurs sporadically and the incidence is about 3.1% of all cattle placed in feedlots.9 Cases occur most commonly during the summer and fall months and new cases occur in an even distribution across all stages of the finishing period. In southern Alberta, the disease is most common during hot, dry, dusty, spring and summer days, and typically affects animals expected to be ready for slaughter within 15 to 45 days. Some feedlot operators have observed that the disease is more common in cattle exposed to excessive dust from bedding.
In southern Alberta feedlots the disease occurred late in the finishing period, when animals had been on feed an average of 114 days and weighed 475 kg.10 All confirmed cases were in heifers and plasma concentrations of 3-methylindole metabolites (adducts) were higher in heifers with interstitial pneumonia than in controls. Most of the heifers were receiving melengestrol (MGA) to suppress estrus. The BRSV antigen was not found in lung tissue of confirmed cases. The odds of an animal with acute interstitial pneumonia being a heifer were 3.1 times greater than the odds that an animal with the disease was a steer.9 In some large feedlots the estimated relative risk was 4.9.
The role of 3-methylindole (3MI) has been examined as a possible cause of interstitial pneumonia in feedlot cattle.10 Anaerobic ruminal fermentation of large amounts of tryptophan leads to a surge in 3-methylindole concentrations, which is readily absorbed across the ruminal and intestinal wall and disseminated throught the body. Bioactivation of 3MI by Clara cells leads to profound cellular injury in Clara and type-1 alveolar epithelial cells and, ultimately, acute interstitial pneumonia. It is postulated that the compound responsible for causing the injury is the electrophilic metabolite of 3MI, 3-methylenedolenine (3MEIN) which forms stable adducts with cellular macromolecules. (Adducts are compounds formed by an addition reaction.)
Concentrations of 3-methyleneindolenine (3MEIN) in lung tissue and blood were higher in feedlot cattle that had died of acute interstitial pneumonia than in healthy feedlot cattle.9 However, lung tissue concentrations of 3MEIN were similar in samples from cattle with interstitial pneumonia and bronchopneumonia.9 Time-dependent patterns and magnitudes of plasma concentrations of 3MI and blood concentrations of 3MEIN-adduct in feedlot cattle during the first 8 weeks after arrival have been followed.11 Mean concentration of 3MEIN-adduct increased to a maximum value on day 33 and then decreased to a minimum on day 54. Plasma 3MI concentrations initially decreased and remained low until after day 54. Neither 3MEIN-adduct concentrations nor plasma 3MI concentrations were associated with deleterious effects on weight gains. A single dose of acetylsalicylic acid (aspirin) to feedlot cattle on arrival did not affect serum or rumen concentrations of 3MI.12 The combination of aspirin and vitamin E fed daily to feedlot cattle did not decrease the risk of developing respiratory tract disease.13
Acute interstitial pneumonia has been recorded in sheep and there was extensive alveolar epithelialization. In Norway, an acute respiratory distress syndrome has occurred in lambs moved from mountain pastures onto lush aftermath pasture. The lesions were those of acute interstitial pneumonia and alveolar epithelial hypersensitivity to molds in the grass is being explored. The experimental oral administration of 3-methylindole to lambs will result in acute dyspnea and lesions similar to those which occur in cattle and adult sheep following dosing with 3-methylindole. However, the lesions in experimental lambs are different from those which occur in lambs affected with the naturally occurring disease.
The other types of interstitial pneumonia occur sporadically and may affect only a single animal or several over a period of time. There is not necessarily a seasonal incidence except in areas where cattle are housed and fed dusty and moldy hay during the winter months. The disease has occurred in feedlot cattle in open feedlots and in young cattle fed on fattening rations indoors.6 Acute interstitial pneumonia occurs in weaned beef calves about 4 weeks after weaning. The interstitial pneumonia which may be the result of anaphylaxis also occurs sporadically and therefore not in outbreaks.
Because of the number and variety of circumstances in which acute or chronic interstitial pneumonia occurs, it is difficult to suggest a basic underlying cause, or to explain the mechanisms for the development of the lesions and the variations which occur from one circumstance to another. The reaction which occurs is a non-specific but fundamental reaction of the pulmonary parenchyma to a wide variety of insults which may be ingested, inhaled or produced endogenously. The reaction to sublethal injury is a combination of congestion, edema, an outpouring of protein-rich fluid into the alveolus, hyaline membrane formation, alveolar and interstitial emphysema which is secondary, and proliferation of alveolar septal cells and fibrosis of the interstitial spaces. Unlike the bacterial pneumonias, the emphasis is on edema and proliferation rather than on necrosis. Because mild cases of ABPEE may recover completely, it is suggested that the lesion can be reversible.
There has been considerable effort to experimentally induce ABPEE similar to the naturally occurring disease, by the oral administration of d,l-tryptophan or one of its metabolites, 3-methylindole, to cattle, sheep, and goats. The l-isomer of tryptophan is metabolized by ruminal microorganisms to indolacetic acid which is then converted to 3-methylindole. The conversion of l-tryptophan to 3-methylindole is maximal at a ruminal pH near neutrality. When cattle are moved from a relatively dry pasture to a lush green pasture, there is an increase in ruminal ammonia, a decrease in ruminal pH, and a decrease in ruminal buffering capacity. The 3-methylindole is absorbed from the rumen and metabolized by a mixed-function oxidase system to an active intermediate which has pneumotoxic properties.
Pulmonary edema is the first morphological change occurring in ruminants given 3-methylindole, and the severity and extent of the lesion is probably the single most important factor which determines the severity of the clinical response and the likelihood of survival. The edema is preceded by degeneration, necrosis, and exfoliation of type I alveolar septal cells. During the acute phase, there is flooding of the alveoli with serofibrinous exudate, congestion, and edema of alveolar walls, and hyaline membrane formation. Varying degrees of severity of interstitial emphysema also occur. The interstitial emphysema may spread within the lymphatics to the mediastinum and into the subcutaneous tissues over the withers, over the entire dorsum of the back and, occasionally, over the entire body including the legs. If the acute phase is severe enough there is marked respiratory distress and rapid death from hypoxemia.
In the experimental disease, the typical clinical signs of respiratory disease appear within 24–36 hours after the oral administration of l-tryptophan to adult cattle and within 4 days 50% of the dosed cows will die. The predominant pulmonary lesions include edema, interstitial emphysema, hyaline membranes, and hyperplasia of alveolar lining cells. The l-tryptophan is converted to indolacetic acid, which is decarboxylated to 3-methylindole, which is absorbed and metabolized by a mixed function oxidase system in the lung to produce pneumotoxicity.
The lesions have also been produced in cattle, sheep, and goats following oral or IV administration of 3-methylindole. Calves may be more resistant to experimental toxicity with 3-methylindole than adults, which supports the observation that the naturally occurring disease is uncommon in calves grazing the same pasture in which adults are affected. Young calves, 30–45 days of age, are susceptible to pulmonary injury induced by 3-methylindole characterized by pulmonary edema and damage to type-1 alveolar epithelial cells and non-ciliated bronchiolar epithelial cells. The 3-methylindole injury does not make the bovine lung more susceptible to the bovine respiratory syncytial virus as is the case for the parainfluenza-3 virus.
If the animal survives the acute phase, proliferation of alveolar type II cells marks the beginning of the shift from the exudative to the proliferative stages of pneumonia. There is alveolar epithelialization and interstitial fibrosis, the latter being progressive and irreversible. The central features of chronic interstitial pneumonia are intra-alveolar accumulation of mononuclear cells, proliferation and persistence of alveolar type 2 cells, and interstitial thickening by accumulation of lymphoid cells and fibrous tissue. Diffuse fibrosing alveolitis is a form of chronic interstitial pneumonia of uncertain etiology, but possibly the chronic form of ABPEE. Repeated oral administration of 3-methylindole in cattle provides a good experimental model for diffuse pulmonary fibrosis.
The effects of 3-methylindole on pulmonary function and gas exchange have been examined in cattle, goats, and horses. In cattle there is impairment of sympathetic pulmonary vasconstriction, and changes in intra-acinar pulmonary arteries which may be related to a sudden elevation in arterial and venous pressures in the pulmonary system. There are large increases in respiratory rate, minute viscous work, PCO2 and large decreases in tidal volume dynamic lung compliance, and PO2. All of these are compatible with the severe pulmonary edema and alveolar injury.
In goats there is a pronounced decrease in lung compliance, a moderate increase in airway resistance, a concomitant hypoxemia, a progressive decrease in tidal volume and alveolar ventilation and an increase in the dead-space-to-tidal volume ratio. These changes are characteristic of a restrictive type of respiratory tract disease in goats in which pulmonary edema and the pulmonary function changes are similar to those of adult respiratory distress syndrome in man.
This disease, also known as ‘fog fever’, is usually obvious, because of its characteristic clinical presentation. The onset is sudden. Within 4–10 days after adult cattle have been moved onto a new pasture, they may be found dead without any premonitory signs. Many cattle exhibit labored breathing, often with an expiratory grunt, open-mouthed breathing, frothing at the mouth, and anxiety. Severely affected cattle do not graze, stand apart from the herd, and are reluctant to walk. If forced to walk they may fall and die within a few minutes. Often, removal of the affected herd from the pasture will result in an increased number of deaths. Moderately affected cattle continue to graze but their respirations are increased above normal. Coughing is infrequent regardless of the severity. The temperature is normal to slightly elevated (38.5–39.5°C, 102–103°F) but may be up to 41–42°C (106–108°F) during very warm weather. There is a similar variation in the heart rate (80–120/min) and those with a rate of more than 120/min are usually in the terminal stages of the disease. Bloat and ruminal atony are common in severe cases. Subcutaneous emphysema is common over the withers and may extend to the axillae and ventral aspects of the thorax. The nostrils are flared and the nasal discharge is normal. Diarrhea may occur but is mild and transient.
Loud, clear breath sounds audible over the ventral aspects of the lung, indicating consolidation without bronchial involvement, are the characteristic findings on auscultation in the early stages of the acute disease. The intensity of the breath sounds may be less than normal over the dorsal parts of the lung if involvement is severe, but in animals which survive for several days the loud crackles characteristic of interstitial emphysema are of diagnostic significance. Most severely affected cases will die within 2 days of onset but less severe cases will live for several days and then die from diffuse pulmonary involvement. Those which survive longer than 1 week will often have chronic emphysema and remain unthrifty. Of those moderately affected cattle which recover in a few days, some will develop congestive heart failure a few months later, due to chronic interstitial pneumonia (cor pulmonale). Calves running with their adult dams will usually not be affected.
These diseases usually occur sporadically, but several animals may be affected over a period of time. There may or may not be a history of a change of feed or the feeding of moldy or dusty feed. In many cases, a few days elapse after the appearance of signs before the owner is aware of the affected animals. The animal may have been treated with an antimicrobial for a bacterial pneumonia with little or no response. Dyspnea, increased respiratory effort sometimes with a grunt, deep coughing, a fall in milk production, an absence of toxemia, a variable temperature (38.5–40°C, 102–104°F) and a variable appetite are all common. On auscultation there are loud breath sounds over the ventral aspects of the lungs and crackles over both dorsal and ventral aspects. The presence of moist crackles suggests secondary bacterial bronchopneumonia. Subcutaneous emphysema is uncommon in these and most will become progressively worse.
Yearling cattle with acute interstitial pneumonia which may be viral in origin may become much worse and die in a few days in spite of therapy. Mature cattle affected with bovine farmers’ lung will survive in an unthrifty state with the chronic disease for several weeks and even months.
The major clinical features of all these other interstitial pneumonias are obvious respiratory disease, lack of toxemia, poor response to treatment, progressive worsening, and abnormal lung sounds distributed over the entire lung fields.
There are no abnormalities of the hemogram or serum biochemistry which have any diagnostic significance. Examination of feces and forage for lungworm larvae will aid in differentiation from verminous pneumonia if past the prepatent period. The observed high levels of ‘farmer’s lung hay’ antibodies in serum are not of much value diagnostically because of the similar levels found in many clinically normal cows; many cases of classic fog fever have negative serum precipitin levels.
In ABPEE, the lungs are enlarged and firm and do not collapse on cutting. In the early stages of acute cases they contain much fluid which is more viscid than usual edema fluid. The pleura is pale and opaque and appears to be thickened. In peracute cases, the entire lungs are homogeneously affected in this way. Such cases usually have edema of the larynx.
In the more common acute case, the lung has a marbled appearance. Adjacent lobes may be affected with any one of four abnormalities. Areas of normal, pink lung are restricted to the dorsal part of the caudal lobes. There are areas of pale tissue indicative of alveolar emphysema, areas of a dark pink color affected by early alveolar exudation, yellow areas in which the alveoli are filled with coagulated protein-rich fluid, and dark red areas where epithelialization has occurred. The latter two lesions are firm on palpation and resemble thymus or pancreas. They are more common in the ventral parts of the cranial lobes.
In chronic cases, as a sequel to the acute form described above, the obvious differences in the age of the lesions suggest that the disease progresses in steps by the periodic involvement of fresh areas of tissue. In all cases there is usually a frothy exudate, sometimes containing flecks of pus, in the bronchi and trachea, and the mucosa of these passages is markedly hyperemic.
Histologically, the characteristic findings are an absence of inflammation, except in the case of secondary bacterial invasion, and the presence of an eosinophilic, protein-rich fluid which coagulates in the alveoli, or may subsequently be compressed into a hyaline membrane. This is more apparent in acute cases and, if animals live for a few days, there is evidence of epithelialization of the alveolar walls. In longstanding cases, there is extensive epithelialization and fibrosis.
The pathology of bovine farmer’s lung and diffuse fibrosing alveolitis has been described and consists of variations of the lesions of chronic interstitial pneumonia.
Bacteriological examination of the lungs is often negative, although in long-standing cases in which secondary bacterial pneumonia has developed Pasteurella multocida, Mann. haemolytica, Streptococcus spp., and Arcanobacterium pyogenes may be found. A careful search should be made for nematode larvae.
The treatment of fog fever in cattle is empirical and symptomatic. The lesion is irreversible in severe cases and treatment is unlikely to be effective. When outbreaks of the disease occur on pasture the first reaction is to remove the entire herd from the pasture to avoid the development of new cases. However, almost all new cases will usually occur by the 4th day after the onset of the outbreak and removal from the pasture usually will not prevent new cases. Conversely, leaving the herd on pasture usually will not result in additional cases. Severely affected cattle should be removed from the pasture with extreme care, very slowly and only if necessary, and moved to shelter from the sun. Immediate slaughter for salvage may be indicated in severe cases. Mild or moderately affected cases will commonly recover spontaneously without any treatment if left alone and not stressed, a fact that has not been given due consideration when claims are made for the use of certain drugs.
Acute bovine pulmonary emphysema and edema is usually obvious when presented with an outbreak of acute respiratory disease in adult cattle which have recently been moved onto a new pasture. The onset is sudden, many cattle are found dead and many are dyspneic. ABPEE must be differentiated from:
Pneumonic pasteurellosis is characterized by fever, toxemia, mucopurulent nasal discharge and less dyspnea; young cattle are more commonly affected and there is a beneficial response to therapy within 24 hours.
Organophosphatic insecticide poisoning may resemble the pasture form of pulmonary emphysema because of the dyspnea but additionally there is pupillary constriction, mucoid diarrhea, muscular tremor and stiffness of the limbs, and no abnormal lung sounds.
Nitrate poisoning may occur in cows moved into a new pasture with high levels of nitrate. Many cows are affected quickly, they are weak, stagger, gasp, fall down, and die rapidly. The chocolate brown coloration of the mucous membranes, the lack of abnormal lung sounds, and the response to treatment are more common in nitrate poisoning.
All of the other types of acute interstitial pneumonia in cattle not associated with a change of pasture in the autumn are difficult to diagnose clinically and pathologically, especially when they occur in a single animal. Their epidemiological characteristics summarized on p. 513 will often offer some clues.
The chronic and subacute types of interstitial pneumonia are difficult to differentiate from each other and from other pneumonias of cattle.
Bovine farmer’s lung or extrinsic allergic alveolitis occurs in housed cattle exposed to dusty or moldy feeds for a prolonged period and is characterized by a history of chronic coughing, weight loss, poor milk production, occasionally green-colored nasal discharge, and dry crackles over most aspects of the lungs. Not infrequently, acute cases occur and die within a week after the onset of signs.
Lungworm pneumonia occurs in young cattle on pasture in the autumn months and causes subacute or acute disease which may resemble bovine farmer’s lung clinically but not epidemiologically. Necropsy is necessary for the diagnosis.
Verminous pneumonia caused by aberrant migration of Ascaris suis larvae may be indistinguishable from acute interstitial pneumonia, but a history of previous occupation of the area by pigs may provide the clue to the diagnosis which can only be confirmed on histological examination of tissues. It is impossible to differentiate clinically between verminous pneumonia and some of the acute interstitial pneumonias seen in yearling cattle except by identification of the larvae in the feces or tissues of affected animals.
Feedlot interstitial pneumonia occurring in recently weaned beef calves or feedlot cattle is characterized by the sudden onset of acute respiratory distress, absence of toxemia, lack of abnormal nasal discharge, and a poor response to treatment with antibiotics. It is difficult to differentiate clinically from acute viral interstitial pneumonia or pneumonic pasteurellosis. However, in acute interstitial pneumonia there is marked dyspnea and the abnormal lung sounds are usually distributed over the entire lung fields.
Several different drugs have been advocated and used routinely for the treatment of ABPEE in cattle. However, none has been properly evaluated and definitive recommendations cannot be made.
Treatment of the chronic interstitial pneumonias is unsatisfactory because the lesion is progressive and irreversible.
There are no known reliable methods for the prevention of ABPEE in pastured cattle but there are some strategies which merit consideration.
If lush autumn pasture contains toxic levels of the substance that causes the acute disease it would seem rational to control the introduction of cattle to the new pasture. This can be done by controlling the total grazing time during the first 10 days: allow the cattle to graze for 2 hours on the first day, increasing by increments of 1 hour per day, and leave them on full time at the end of 10–12 days. Such a management procedure is laborious, requires supplementation with other feeds and daily removal of cattle from the pasture, and may not be practical depending on the size and terrain of the pasture and the holding yards which are available.
Controlling the conversion of d,l-tryptophan in forage to 3-methylindole is a plausible control strategy. Experimental tryptophan-induced ABPEE can be prevented by the simultaneous oral administration of chlortetracycline or polyether antibiotics such as monensin. The daily oral administration of 2.5 g/head of chlortetracycline beginning 1 day before and for 4 days following administration of a toxin of l-tryptophan will prevent clinical signs.14
The daily oral administration of monensin at the rate of 200 mg/head/day beginning 1 day before and for 7 days after an abrupt change from a poor quality hay diet to a lush pasture reduced the formation of 3-methylindole during the 7 days of treatment, but the effect of the drug was dimished on day 10, 3 days after its withdrawal. Because the effects of monensin on ruminal 3-methylindole are diminished within 48 hours after withdrawal of the drug, effective prevention of acute pulmonary edema and emphysema may require continuous administration of monensin for the critical period of approximately 10 days after the mature animals are exposed to the lush pasture. The daily feeding of monensin in either an energy or protein supplement will effectively reduce ruminal 3-methylindole formation in pasture-fed cattle.
Successful prevention of the disease requires monensin supplementation with organized grazing management to reduce the intake of lush pasture by hungry cows. This may be accomplished in several ways: feed dry, mature hay ad libitum to adult cattle just before and during the transition period of a pasture change, then continue to feed hay for at least 4 days into this grazing period; cut all lush forage and allow to wilt before allowing adult cattle access to the pasture. Alternatively, over a 7-day period, gradually increase the amount of time cattle spend grazing lush pasture. If possible, this may be accomplished by rotating cattle back and forth, either between the summer and fall pastures, or between the fall pasture and a drylot where ample supply of dry, mature hay is available. Any combination of these management practices while providing monensin at 200 mg/head per day in an energy or protein supplement may reduce 3-methylindole production to a greater extent than just providing monensin or implementing grazing management techniques.6
To maximize the effectiveness of monensin in reducing 3-methylindole formation, dry hay plus wilted forage should be fed to pastured cattle for at least 4 days after they are allowed access to lush pasture. Lasalocid at a dose of 200 mg per head once daily in ground grain for 12 days reduced the conversion of tryptophan to 3-methylindole and prevented pulmonary edema.15
The daily administration of inhibitors during the critical period immediately before and after the cattle are turned onto the lush pasture may be a practical problem.
The control of non-pasture cases of interstitial pneumonia depends on the suspected cause and removal of it from the environment of the animals. Every attempt must be made to control the concentration of dust and moldy foods to which cattle are exposed. Feed supplies must be harvested, handled, and stored with attention to minimizing dust and molds. In the preparation of mixed ground feed for cattle, the fineness of grind must be controlled to avoid dusty feed particles which may be inhaled. Because of the creation of dust, the grinding and mixing of dry feeds like hay, straw, and grains should not be done in the same enclosed area in which cattle are housed. If dusty feeds must be used they should be wetted to assist in dust control.
Lungworm control is essential in endemic areas where the disease occurs. This may necessitate careful monitoring and regular treatment to reduce the level of infestation on pasture.
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11 Loneragan GH, et al. Am J Vet Res. 2002;63:591.
12 Bingham HR, et al. Am J Vet Res. 2000;61:1209.
13 Loneragan GH, et al. Am J Vet Res. 2002;63:1641.