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Herd Health and Management
DIAGNOSIS AND PATHOLOGY OF SOME DISEASES OF RUMINANTS
By Milton McAllister, DVM,
Oct 27, 2002, 11:34pm
DIAGNOSIS AND PATHOLOGY OF SOME DISEASES OF RUMINANTS
August, 2000 Milton McAllister, DVM, PhD, DACVP, Assoc Prof
University of Illinois
There is a great deal of variation of tests used among veterinary diagnostic laboratories. However, many animal diagnostic laboratories in the U.S. do adhere to several common principles: periodic external review and accreditation by the American Association of Veterinary Laboratory Diagnosticians (AAVLD), maintenance of written standard operating procedures, and use of positive and negative control specimens whenever appropriate or practical. The most progressive laboratories also participate in performance examinations by testing materials that are provided by reference laboratories and professional organizations, or are exchanged among colleagues and collaborating diagnostic laboratories.
As a baseline for comparison of diagnostic tests, the closest thing to an international standard is the Manual of Standards for Diagnostic Tests and Vaccines that is published by the Office International des Epizooties. A web form of this manual is also accessible at or more directly at
. Although useful, the OIE manual can be several years behind the latest developments and thus should not be considered to be an ultimate authority. Furthermore, the manual only covers diseases that primarily interfere with international trade. Many common and important diseases, such as pneumonic pasteurellosis (now mannheimiosis), haemonchosis, or hypomagnesemia are not covered.
The focus of this review will be methods of diagnosis and pathology of some of the most common, economically important, or interesting diseases of cattle, sheep, and goats in the U.S. and Canada. Differential diagnoses and several zoonotic diseases will also be discussed.
Bovine viral diarrhea
BVDV is a common and important pathogen of cattle in North America and most of the world. BVDV is a pestivirus of the flaviviridae, related to Border Disease Virus of sheep and Classical Swine Fever Virus (Hog Cholera). The virus is present in most or all body fluids and also easily crosses the placenta. BVDV may cause:
1. subclinical infection
2. fever and inappetance
6. mucosal disease
7. systemic disease with widespread hemorrhage
8. temporary infertility
9. abortion, birth of weak calves, or congenital deformities
10. birth of subclinically, persistently infected calves (PI animals)
Because of variable clinical signs, transient infections, death of virus in autolyzed tissues, complicated epidemiology, and genetic variation, accurate BVDV diagnosis is a challenge. Virus may be detected in blood, serum, milk, or tissues of persistently or acutely infected animals. Standard virus isolation, microplate isolation with ELISA detection, PCR, and immunohistology are all currently used to detect active infections. IFA testing of tissues is also frequently performed, but I personally found this test to be difficult to interpret in a consistent manner. Serology to detect antibody titers is sometimes useful, especially for herd or epidemiological investigations, but is less useful on individual animals and generally costs more than microplate isolation tests. Looking for seronegative cattle in a vaccinated herd, previously used to screen for likely PI animals, is no longer considered to be a reliable method. PCR techniques are being adapted to test bulk tank milk, which appears to be highly useful to screen for PI infections in dairy cows without having to test individuals (unless a positive result is obtained).
Once BVDV is diagnosed in any animal in a breeding herd, then further examination of the herd should be considered in order to detect and remove PI animals. Various schemes may be somewhat complicated because maternal immunity can interfere with diagnostic tests in calves up to six months of age, and because whole-herd tests must ultimately include fetuses. Animals discovered to be infected may be re-tested after 3 weeks to distinguish between acute and persistent infections. An immunohistologic test using a skin biopsy from the pinna is reportedly sensitive and specific for persistent infections using a single test.
In aborted fetuses or weak newborn calves, lesions associated with BVDV infection can be as dramatic as cerebellar hypoplasia and bilateral lenticular opacity, or nonexistent. Many affected fetuses or nonviable calves will have thymic atrophy and mild to minimal infiltrates of lymphocytic-appearing cells in the meninges, epicardium, and hepatic portal triads. The chief differential diagnosis for minor nonsuppurative lesions is neosporosis, but other viral or protozoal agents and possibly Chlamydia can also be incriminated. Care must be taken not to confuse extramedullary hematopoiesis in the liver for leukocytic infiltrates.
Persistent infections are caused by noncytopathic strains of BVDV. Mucosal disease is believed to be the result of superinfection of a PI animal with a second, cytopathic strain (which may have mutated from the original noncytopathic strain). In addition to classical noncytopathic/cytopathic differentiation of viral strains, viral strains have also been divided into two genomic subsets, types I and II. Some highly virulent type II strains are capable of causing ulcerative disease, in non-PI animals, that closely resembles mucosal disease. The chief differential diagnosis of mucosal disease is malignant catarrhal fever. A foreign disease, rinderpest, also is grossly similar. MCF will cause mucosal hemorrhages in the urinary bladder, which grossly distinguishes it from mucosal disease.
Sheep are infected with a pestivirus closely related to BVDV, which results in many of the same conditions. Lambs are often born prematurely or are otherwise unviable. The haircoat may be abnormal and there may be cerebral cavitations. Recovering lambs are persistently infected.
Neosporosis in cattle and goats causes abortion, premature birth, stillbirth, and birth of neurologically impaired neonates. The causative agent, Neospora caninum, is an Apicomplexan protozoan. Dogs are a definitive host and cattle, goats, and several species of deer are known intermediate hosts. There are at least two methods of transmission to cattle: ingestion of oocysts, and transplacentally from congenitally infected dams to their offspring (vertical propagation). Epidemiologic evidence indicates that both methods of transmission are important. Neosporosis abortion is relatively common in both dairy and beef cattle.
The finding of mild to severe mononuclear leukocytic infiltrates in brain, heart, and skeletal muscle warrants a high degree of suspicion of neosporosis. Tissues of aborted fetuses are often highly autolyzed, but this seldom interferes with histological identification of lesions. Classically, cerebral lesions are small necrotic foci surrounded by a rim of mononuclear leukocytes, but in many cases no necrosis is observed and leukocytic infiltrates may be small and sparsely scattered. Meninges are frequently infiltrated multifocally, sometimes diffusely. Ventricular myocardium usually has multifocal, mild to severe infiltration of similar leukocytes, especially in the epicardium or endocardium. Similar leukocytic infiltrates are often found multifocally in skeletal muscle of the tongue, diaphragm, or other sites. Inflammation is sometimes observed in the liver, and infrequently in the interstitium of lung or kidney. Organisms are rarely observed in HE sections, but the presence of oval, thick-walled, 15 to 100 mm tissue cysts in the brain or spinal cord is diagnostic. Immunohistochemistry will often reveal organisms in brain or other tissues. Although very specific, this test is not very sensitive, at least unless you are willing to test numerous sections. The most likely places to find organisms are in inflammatory foci in the brain. These lesions are often most easily observed in the midbrain, but it is not clear if this represents a true predilection site, or if this area of the brain is better preserved in autolyzed fetuses and thus more easily examined.
Isolation of organisms in cell culture, although diagnostic of infection, is usually a difficult and tedious procedure that is too insensitive to use for routine diagnostics. PCR methods to detect parasites in tissues are reasonably sensitive and highly specific tests, although somewhat labor intensive.
Serology of dams at the time of abortion is a useful adjunctive test. Cows aborting from neosporosis should have a high N. caninum titer at the time of abortion. Using IFAT, the titer will be $ 1:800 in the majority of cows aborting from neosporosis, with an increasing degree of suspicion with progressively higher values. Cows with titers of 1:200 or 1:400 are seropositive, but the index of suspicion that the infection is causally related to the abortion should be reduced. An exact cut-off for seronegative animals using the IFAT has not been set, but most seronegative animals will have values below 1:50. At least one ELISA serology kit is commercially available, and several laboratories have developed their own ELISA tests. Most appear to be fairly good. The most significant differences between laboratories involves the cut-off points between seropositive and seronegative animals, which may be somewhat arbitrary. Most are probably set a little high. Although neosporosis is never proven as the cause of abortion based solely upon serology, it can be ruled-out in cows that are seronegative at the time of abortion.
In goats, care must be taken to differentiate neosporosis from toxoplasmosis, which causes nearly identical lesions and has similar appearing organisms. Cross-reaction between N. caninum and T. gondii organisms is possible in immunohistological preparations, depending upon the antibody that is used. PCR and serology can discriminate between the two infections if immunohistologic results are in doubt. Natural cases of neosporosis abortion have not been described in sheep, although they are highly susceptible to toxoplasmosis.
Several serovars of Leptospira interrogans may be involved. Leptospirosis is one of the few abortifacient diseases of cattle that often has a gross lesion: icterus. Leptospires are most easily visualized in smears or frozen sections of fetal kidney using a fluorescent antibody test. Care must be taken to observe the characteristic undulating morphology of fluorescing organisms, because cross reactions with non-leptospires are possible. Darkfield examination of body fluids may also reveal leptospires, but this is a less sensitive test that is most likely to succeed in non-autolyzed fetuses soon after abortion, so that organism motility is still present. Serology of the dam at the time of abortion will usually reveal a high titer to one serovar, 1:1,600 or greater. Serology can also be attempted on fetal fluids. A detectable titer is diagnostic, but the lack of a titer is common even in infected fetuses.
Epizootic bovine abortion
This disease primarily occurs in regions of California and Oregon, where it is commonly known as Afoothills abortion.@ The disease is transmitted by the soft shelled tick, Ornithodoros coriaceus. Once thought to be caused by Chlamydia, the latest evidence points to the possible involvement of Borrelia coriaceae. Abortions occur in naive pregnant cattle after they are moved to endemic pastures. If cattle are exposed to endemic regions prior to breeding, they will not abort, and immunity is long-lived.
The diagnosis is based upon geographic location, history, and gross and microscopic lesions. Aborted fetuses are usually late-term, in good condition, and some are born alive. The liver may be enlarged and have a coarsely nodular pattern. Lymph nodes and spleen are markedly enlarged by lymphoid hyperplasia and sinus histiocytosis, with foci of necrosis. The thymus is altered by thymocyte hypoplasia and dense infiltration by macrophages. Granulomatous inflammation is commonly found in lung, meninges, and other organs.
Infectious bovine rhinotracheitis, a bovine herpesvirus, typically causes multifocal necrosis in the liver and adrenal cortex, and often also in the lungs. Intranuclear inclusions are diagnostic, and IFA testing of these organs is quite useful. Virus isolation, although specific, is insensitive compared to IFA. IBR is seen infrequently because commonly used vaccines are effective.
Bacterial causes of abortion will usually cause suppurative placentitis and bronchopneumonia. The best specimens for aerobic culture are abomasal fluid and lung. Special isolation procedures should also be attempted for Campylobacter spp., especially in sheep. Chlamydia is also a cause of infectious abortion in sheep (enzootic abortion of ewes) and goats. Histology, cytology of placental smears, cell culture, IFA, ELISA test kits, and serology are available to detect EAE.
Q fever is a cause of necrotizing placentitis and abortion in ruminants, especially sheep and goats. This is a zoonotic disease which can cause endocarditis or pneumonia in humans. The causative ricketsial agent is Coxiella burnetii. Special attempts to isolate the organism in cell culture are not warranted because of health risks, and because other tests are available, including cytology using a Gimenez stain, IFA, and immunohistology of placenta. The pathologist should become suspicious if placental trophoblasts are distended by a basophilic granular substance, and if there is necrotizing placentitis. This disease is difficult to diagnose without examination of placenta.
Nitrate intoxication can cause abortion, although if there is a herd outbreak, then some of the cows will probably be found ill or dead. Ocular fluid from the fetus is the preferred specimen for nitrate testing.
GASTROINTESTINAL DISEASES OF NEONATES
Abomasal bloat, inflammation, and perforation
Disease of the abomasum of neonatal ruminants is a surprisingly common cause of mortality in some regions, usually before the age of 2 months in cattle or 5 weeks in lambs. I have seen a beef herd with approximately 25% incidence over a several year period, possibly associated with crowding or feeding of silage. A severe epidemic of abomasal bloat was once reported in kids fed milk replacer.
Animals that die with acute severe gaseous distension of the abomasum often have no evidence of abomasitis. In these cases, large numbers of very large, basophilic, coccoid bacteria that grow in clusters are usually observed on the lumenal surface. These have been isolated from calves and lambs and identified as Sarcina ventriculi, a bacterium that is peculiarly able to grow in an acid medium. These bacteria are seldom observed in specimens from animals dying of unrelated conditions. Calves and lambs without severe bloat may die with severe abomasitis, which can vary from emphysematous, to ulcerative, to hemorrhagic. Histologically, ulcers and emphysematous regions are typically infiltrated by large rod-shaped bacteria characteristic of Clostridium spp., and have numerous neutrophils and often granulation tissue associated with ulcerations. Sarcina may also be observed in many of these calves, although in fewer numbers and a lesser percentage. Perforated ulcers generally are surrounded by granulation tissue in the tunica mucosa and submucosa, and there is abundant fibrinous abdominal fluid with admixed ingesta. Histologically, Sarcina is frequently entrapped within fibrin along serosal surfaces, even though it may not be observed within the abomasal lumen.
A causative role for Sarcina ventriculi has not been established. Other factors that have been inconsistently implicated in various studies include copper deficiency, BVDV infection, Clostridium perfringens type A, Clostridium fallax and Clostridium sordellii.
Enterotoxigenic Escherichia coli
The great majority of these cases in calves are caused by strains with K99 pilus antigen, and diarrhea occurs in calves # 5 days old. Grossly, the small intestine is distended with fluid. Histologically, villous enterocytes in the jejunum and ileum will be multifocally coated with small adherent coccobacilli, giving a thin shag carpet appearance. Gram's stains can help to highlight the bacteria, which are Gram negative. Small numbers of neutrophils may be scattered within the lamina propria of villi. Villous atrophy is questionable. Except in freshly killed animals, enteric histopathology routinely requires examination of sloughed enterocytes in the lumen, caused by autolysis. Experienced pathologists learn to carefully examine this sloughed epithelium for the presence of adherent E. coli or Cryptosporidium. Similarly, leukocytic infiltrates and dilated crypts (not associated with enterotoxic E. coli) are changes that can often be observed in autolyzed intestines.
A severe diarrhea that usually affects calves less than 3 weeks of age. In contrast to coronavirus of pigs (TGE), the worst lesions of bovine coronavirus are found in crypts in the colon, rather than villi of the small intestine. Many crypts are dilated, eroded or lined by flattened or necrotic epithelium, often with regenerative hyperplasia, and crypt lumens contain necrotic cellular debris. There may be a variable leukocytic infiltrate in the lamina propria, and intestinal lymphoid tissue is usually atrophied or hypoplastic. The histological lesions are nearly pathognomonic. Coronavirus particles can be observed in feces or colonic scrapings using negative stain preparations observed with a transmission electron microscope, and fluorescent antibody tests are available for fresh samples of colon and small intestine. Mixed enteric infections are common, so care should be taken not to overlook other possible pathogens. Bovine coronavirus is also sometimes implicated as a cause of diarrhea in adult cattle, the so-called winter dysentery. It is not clear if these are similar viral strains.
As a pathologist, I believe that the diagnosis of clostridial enteritis requires appropriate gross lesions and/or microscopic lesions. It affects all species of domestic ruminants. The offending agent is Clostridium perfringens, usually type C. Mortality is very high even in treated animals. Affected animals often die without diarrhea, but may exhibit hemorrhagic diarrhea or melena. Grossly, a variably sized segment of small intestine will usually be dark red-purple (i.e. Apurple gut@), with or without transmural or serosal emphysema and fibrinous serositis. The mucosal surface will vary from a fibrinonecrotic exudate to severe hemorrhage. Histologically, there is segmentally diffuse mucosal erosion or ulceration, and large numbers of large bacterial rods, which are Gram-positive, will be entrapped within the fibrinonecrotic exudate, invaded into the lamina propria and submucosa, or coating denuded remnants of intestinal villi like an overgrown lawn. Numerous neutrophils will be in the underlying tissue and inflammation may extend into all tunics.
Anaerobic culture will yield C. perfringens, but similar culture of intestines from calves with other causes of diarrhea will frequently yield C. perfringens, so isolation is not sufficient for diagnosis. Microbiology reports will often state if the clostridial growth is heavy, but I do not give this any weight. In a preliminary study of calves with histological evidence of clostridial enteritis and unrelated conditions, genotyping of C. perfringens isolates using PCR revealed type C in most cases with clostridial lesions, while type A was isolated in many other intestines.
The terminology of enteric clostridial diseases is somewhat confusing and not used in a consistent manner. I prefer to call ulcerative or hemorrhagic enteritis associated with Clostridium, Aclostridial enteritis.@ Others refer to this as Aenterotoxemia.@ I prefer to reserve Aenterotoxemia@ for clostridial overgrowth that is not associated with severe enteric lesions, but is associated with hyperglycemia and death, with or without lesions of focal symmetrical encephalomalacia. This form of clostridial disease has classically been associated with Clostridium perfringens type D, which elaborates exotoxins, including e toxin, that are absorbed systemically. This disease is most common in fattening lambs, but also occurs in adult sheep, calves, and goats. It is often called Apulpy kidney disease@ due to the frequent autolysis and softening of these organs. However, well-conditioned sheep with wool and perirenal fat will frequently have soft, autolytic kidneys, even if dying from disparate causes. Hyperglycemia can be diagnosed post-mortem by testing the excessive pericardial fluid, often with fibrin clots, that is usually present in cases of enterotoxemia. Another moniker for this condition is Aovereating disease,@ because it is usually seen in fat animals on high grain diets. It is my impression that pulpy kidney disease tends to be used as a catch-all diagnosis in inadequately worked-up cases of unexpected death in feeder lambs that have autolyzed carcasses. Bacterial isolation and PCR genotyping for type D can be a useful exercise in these cases.
Can be a secondary or primary cause of diarrhea. Cryptosporidia are often found in conjunction with the nearly ubiquitous rotavirus. Diagnosis is by microscopic analysis of fecal smears, flotations, or ileal scrapings using either acid-fast or FA stains, and by histology. The organisms are thought to interfere with absorption, as there is little associated inflammation. This is a common zoonosis.
Ubiquitous pathogens of cattle and sheep (species-specific strains) are not usually fatal in uncomplicated infections. It is easily diagnosed using negative stain transmission electron microscopy of feces or using a commercially available latex agglutination test or a commercial immunoassay. Villous blunting is a difficult lesion to observe in clinical specimens, barring meticulous examination of freshly killed animals with acute infections (i.e. rarely).
Infection with Salmonella spp., especially Salmonella typhimurium (precise nomenclature of salmonellae is controversial), should be included in the differential diagnosis of diarrhea in just about any species or age. In calves, the disease is usually seen in animals older than 1 week and is associated with fibrinosuppurative or ulcerative enterocolitis, sometimes with melena. Mesenteric lymph nodes will be enlarged due to reactive hyperplasia and excessive neutrophils and histiocytes. There may be fibrinous cholecystitis, and histologic evidence of multifocal hepatic necrosis and histiocytic or granulomatous inflammation (paratyphoid nodules). There may also be systemic lesions (e.g. interstitial pneumonia). Enteric salmonellosis can be a problem in feedlot sheep and must be differentiated from coccidiosis, which is more common. Diagnosis is primarily by bacterial culture for Salmonella. Of course, beware of its zoonotic threat.
METABOLIC DISEASES ASSOCIATED WITH RUMINAL METABOLISM
PEM affects all species of ruminants. It occurs in both isolated cases and herd outbreaks of variable morbidity and mortality. Some feedlots have a seasonal increase in the summer. Clinical signs include visual impairment or blindness, head pressing, anorexia, aimless wandering, coma, seizures, and death. Gross lesions are restricted to gray matter, primarily within the cerebral cortex. In acute cases, there may or may not be cerebral edema. When edema is present, cerebral gyri will be swollen, flattened, and soft, and if edema is severe, the cerebellum will be pushed into the foramen magnum and deformed (coning defect). The surface of the cerebral cortex may have multifocal pale yellow-tan discoloration, or this change may only be visible on cut section within the ribbon of gray matter. Examination under long UV light will usually reveal bright creamy-white, autofluorescent strips that are restricted to the gray matter, although in severe cases focal lesions may also be found in the thalamus and midbrain. Histologically, acute lesions consist of bands of necrotic neurons that have slightly shrunken, eosinophilic perikaryonic soma and pyknotic nuclei, usually with perineuronal vacuolation. Intervening neuropil is often condensed initially, but may be vacuolated, and underlying white matter may be edematous. Close inspection of blood vessels may reveal either mild hypertrophy or pyknosis of endothelial cells, and rarely fibrinous thrombi within capillaries. As lesions progress in time, affected neuropil begins to fragment and is infiltrated by foamy Gitter cells. Malacia is characterized by the nearly complete fragmentation or loss of neuropil, with large numbers of Gitter cells and remnant blood vessels. Eventually, a glial scar may form, but such brains are seldom examined as the animal has survived.
The most common predisposing factor observed in North America is excessive dietary sulfur. This can be in the feed, e.g. when ammonium sulfate is added to the diet as a urinary acidifier or when diets are high in molasses, or the source of excessive sulfur may be in groundwater, which is a common problem in the Great Plains and Rocky Mountains. Excessive sulfate salts in drinking water is a likely explanation of the summer increase in the incidence of PEM, because animals drink more water in hot weather. Although there are no absolute cut-off points between safe and unsafe levels of dietary sulfur, it appears that animals consuming diets above 0.40% sulfur (expressed on a dry matter basis, even if the source is the water) are predisposed to development of PEM.
The pathogenesis involves ruminal metabolism of sulfur to hydrogen sulfide (H2S). The sulfide anion is a metabolic poison with a mechanism of action similar to cyanide (inhibition of cytochrome oxidase in the electron transport chain). Animals that develop PEM experience abnormally high peak concentrations of H2S in ruminal fluid and in the ruminal gas cap. Measurement of H2S levels in the ruminal gas cap has been described as a simple method of examining a herd for this risk factor. Experimental administration of sulfide into the rumen of sheep caused rapid onset of clinical signs of PEM and classical gross lesions within 20 hours. Thiamine metabolism does not appear to be involved in this form of the disease.
Lead poisoning can also cause blindness, seizures, and lesions that closely resemble PEM. Interestingly, symptoms of lead poisoning respond clinically to administration of thiamine. Altered thiamine metabolism, with thiamine destruction in the rumen, was previously the dominant hypothesis of PEM pathogenesis. It is possible that there are several initiating causes of PEM that end in a final common pathway. PEM in pre-ruminant calves is infrequent, and is possibly a result of hypoglycemia or lead poisoning.
Acute interstitial pneumonia (acute pulmonary emphysema and edema, atypical interstitial pneumonia, fog fever)
This disease of cattle is classically associated with a sudden change of diet to lush grass pasture (foggage), which is high in protein containing the amino acid, L-tryptophan. Microbial metabolism of L-tryptophan in the rumen produces indoleacetic acid, which is further metabolized to 3-methylindole. 3-methylindole is absorbed into the bloodstream and is further metabolized by mixed function oxidase enzymes in the lung. This toxicant damages pulmonary endothelium and causes diffuse edema and fibrinous effusion that forms alveolar casts. Emphysema may result from the mechanical effects of labored breathing. Subacute lesions may progress to type II pneumocyte hyperplasia, with cuboidal epithelium lining alveolar spaces. Other toxicants, besides L-tryptophan, include 4-ipomeanole in moldy sweet potatos, and Perilla ketone in purple mint. The differential diagnosis for diffuse interstitial edema includes bovine respiratory syncitial virus, and for widespread emphysema includes a severe infestation of bovine lungworms (Dictyocaulus viviparus).
This condition is a recurrent problem in some feedlots, and the incidence has been suggested to be increased in association with feeding of melengestrol acetate to heifers (to suppress the estrus cycle). Although lush pasture is not involved, evidence nevertheless indicates excessive localization of 3-methylindole in the lungs.
OTHER DISEASES OF PARTICULAR INTEREST
This transmissible spongiform encephalopathy (TSE) occurs in sheep and goats. Although there is no evidence of transmission to humans, it is still not possible to conclude that there is no risk. Scrapie was originally incriminated as the source of the disastrous bovine spongiform encephalopathy epidemic in the United Kingdom, but this was speculative and subsequent biotyping in mice indicates that BSE and known scrapie strains are distinct. Because of the mounting evidence that BSE agent has been transmitted to humans as a fatal new variant Creutzfeldt-Jakob disease, the public wants to know more about other TSE's such as scrapie, and the USDA has stepped-up its eradication efforts.
TSE's are currently believed to be caused by prions, which are a normal cellular protein, PrP, with an abnormal conformation that is self-perpetuating. The presence of abnormally folded PrP (designated PrPsc) will cause newly synthesized PrP to also fold abnormally, forming digestion-resistant b-pleated sheets. The agent is present in fetal fluids and placenta and will contaminate an area during lambing. Lambs may be infected by ingestion of the agent, and may develop clinical disease after 2 to 4 years. Genotype is important, as animals with certain PrP alleles (in U.S. Suffolk sheep, QQ at codon 171), or are more susceptible to the development of scrapie. A blood test is available to determine the PrP genotype of individuals, for the purpose of selection for scrapie resistance.
Pre-clinical diagnosis is difficult, but no longer impossible. PrPsc can be detected immunohistochemically in tonsil biopsies about 1 year prior to the onset of clinical signs in sheep that are incubating the scrapie agent. Also, a recently developed capillary electrophoresis assay for detecting PrPsc in blood is showing promise, but it isn't yet clear if it can detect infection prior to the onset of clinical signs.
Clinical signs are slowly progressive and result in death within 2 to 5 months. Animals may show progressive weight loss, hind limb weakness, often subtle behavioral changes such as nervousness, fine tremors of the head, frequent pruritus, loss of wool in large patches, and characteristic lip movements when the tailhead is scratched. There are no specific gross lesions although the brain may be slightly atrophied. Diagnostic lesions are microscopic and consist of large clear cytoplasmic vacuoles within neurons, especially in the thalamus, midbrain, and medulla oblongata. Lesions are bilaterally symmetrical and may be associated with a diffuse astrogliosis. There may be a reduction in the number of neurons. The distribution of lesions has predilection for certain nuclei. The finding of rare vacuolated neurons in sheep, without other features, is not diagnostic of scrapie. Scrapie can be confirmed by an immunohistochemical test for the PrPsc protein that resists digestion with proteinase K (normal PrP will be destroyed and will therefore not stain).
It is preferable to have histology personnel use disposable knives when trimming tissues that may have the scrapie agent. The agent resists many chemical and physical disinfectants, but is destroyed by strong sodium hypochlorite or hot sodium hydroxide. Treatment of formalin-fixed tissues with concentrated formic acid can reduce the level of infectivity. Sheep and goat carcasses in diagnostic laboratories should be incinerated or perhaps digested in sodium hydroxide, but cannot be rendered for animal consumption.
Scrapie has it's highest incidence in Suffolk sheep. The USDA has a semi-voluntary eradication program, although restricted sale and movement is enforced in flocks known to have infected animals within the last 5 years, even if they do not wish to be involved in the program. Ultimately it is in the interests of the sheep industry, public health, and international trade to eradicate scrapie, but there are serious impediments such as universal owner compliance and pre-clinical detection of infected animals. Scrapie is a reportable disease.
Abomasal emptying defect of Suffolk sheep
This may be a minor disease, but I think it is under-diagnosed because affected sheep are often destroyed. It often occurs sporadically but can occur in herd outbreaks. Affected animals are between 1 and 8 years of age, and with a few exceptions they are Suffolks. Most cases are fatal but some recoveries have been recorded. Affected animals have a decreased appetite and may regurgitate ingesta into small piles. The animal loses weight while at the same time the lower right abdomen may noticeably swell. Analysis of ruminal fluid may reveal an elevated chloride concentration. The abomasum becomes steadily distended and compacted with thick doughy ingesta containing long stem forage, resembling ingesta in the rumen. The abomasum may become larger than the rumen and extend from the liver to the pelvis, with a wall that is stretched thin. The omaso-abomasal orifice is greatly dilated, big enough to fit a fist through.
Histologically, there are no consistent lesions in the wall of the abomasum, other than being stretched thin. One or two case reports associated this condition with scrapie, although the great majority of reported cases have not had scrapie and the occurrence of outbreaks in a wide age range is not epidemiologically consistent with scrapie. Inheritance has been suggested, but again the occurrence of outbreaks and lineage analysis has not supported this, other than the general observation that Suffolks are at risk compared to other breeds. In preliminary exams, I have found central chromatolysis and reduction of neurons in the celiaco-mesenteric ganglion, which is an autonomic ganglion that innervates the abomasum. In this way, the disease may resemble grass sickness of horses in the UK.
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