AFIP Wednesday Slide Conference - No. 7

14 October 1998
Conference Moderator:
Dr. Catherine Wilhelmsen, Diplomate, ACVP
Geo-Centers, Inc.
U.S. Army Medical Research Institute of Infectious Disease
Department of Aerobiology and Product Evaluation
Ft. Detrick, MD 21702-5011

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Case I - 4312-98 (AFIP 2643733)
Case 7-1. Gross photo. There is diffuse cyanosis of both ears.
Signalment: Ten-day-old, mixed breed, commercial piglets.
History: The piglets were from a first litter sow. Other sows were reported to have had skin lesions that were thought to be erysipelas and were successfully treated with penicillin.

Gross Pathology: The piglets had red-black discoloration of the skin of the ears, hind legs, and feet. The skin sections had dark blood oozing from a layer under the epidermis. The upper hind leg muscle of one piglet had a well-demarcated, 3 to 4 centimeter, dark red, infarcted area immediately under the skin. The spleens of both animals were moderately enlarged. The lungs of one piglet were diffusely, moderately reddened but not consolidated. The other internal organs were grossly normal.

Laboratory Results:
1. Serum was negative for Porcine Reproductive and Respiratory Syndrome virus.
2. Erysipelothrix rhusiopathiae was isolated from: both lungs (1+ and 4+); spleen (4+); infarcted muscle (4+); and foot (2+).

Contributor's Diagnoses and Comments:
1. Moderate necrosuppurative myositis with fibrinoid necrosis and fibrin thrombosis of blood vessels.
2. Multifocal, moderate hemorrhagic dermatitis with fibrin thrombi and intravascular bacteria.
There was also moderate, diffuse subacute interstitial pneumonia consistent with septicemia. Many capillaries contained hyaline thrombi and rare, gram-positive bacilli. Neither microscopic lesions, nor gram-positive bacteria were present within sections of kidney, liver, brain, spleen, and intestine. Gram-positive bacteria and fibrin thrombi are numerous in some sections of the skin. The submitted section of muscle from the leg is not the most severely affected area, but myofiber atrophy, individual necrotic fibers surrounded by neutrophils, and fibrin thrombi in the capillaries are present. The more affected muscle section (not submitted) had more extensive necrosuppurative and hemorrhagic myositis.
All pigs are susceptible to infection with Erysipelas rhusiopathiae, but most cases occur between two months and one year of age. The disease has three forms: acute, subacute, and chronic. Acute infection has septicemia with disseminated intravascular coagulation and hyaline thrombi throughout the body. By four days post infection, the bacteria invade the endothelium, and there is diapedesis of erythrocytes. The purple skin is usually due to congestion, and sometimes thrombosis, of dermal vessels. Fibrinoid necrosis of vessels may be due to a hypersensitivity (Arthus) reaction. Arteriolar fibrinoid necrosis is thought to be the cause of the "diamond skin" lesions and may not be present in our piglets due to the rapid nature of the infection which may not have allowed enough time for full hypersensitivity vasculitis to develop. The discoloration of the skin can be used as a prognosticator. Pigs with pink to red skin lesions usually recover, while those with dark red-purple lesions usually die, as was our experience. In another report of acute erysipelas in piglets, the dermal and hypodermal hemorrhage also occurred mostly on the ears and limbs.

Muscle degeneration is seen with acute erysipelas, but the locally severe pattern of hemorrhagic infarction seen in one of our pigs is unusual. Less specific lesions can be seen in any organ, with leukothrombi or bacterial emboli. The choroid plexus in the brain and the ciliary body of the eye are reportedly the most likely sites to have sequestered bacteria. Synovitis may occur in acute or chronic disease. The subacute form is similar but less severe than the acute disease. Chronic infection is characterized by arthritis or bacterial valvular endocarditis, with the bacteria localized at these sites.
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Case 7-1. Dermis. The 4x view demonstrates a thrombus within a valved vein (left of center). The dermal connective tissue is expanded by hemorrhage beneath the epidermis and around blood vessels. The 40x view shows the thrombus and vessel wall in which there are vague outlines of bacilli.
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Case 7-1. Subcutis, skeletal muscle. Several vessels are occluded by fibrinocellular thrombi and the vessel walls are disrupted by neutrophils and macrophages. Some skeletal muscle fibers have hyaline degeneration and fragmentation.

AFIP Diagnoses:
1. Haired skin, dermis and subcutis: Thrombosis, fibrinoid necrosis, and acute vasculitis, multifocal, moderate, with diffuse hemorrhage, mixed breed, porcine.
2. Skeletal muscle: Thrombosis, fibrinoid necrosis, and acute vasculitis, multifocal, moderate, with interstitial edema and myodegeneration.
Conference Note: Erysipelas rhusiopathiae is a small, gram-positive, non-spore forming, unencapsulated, pleomorphic bacillus that is the cause of swine erysipelas. Infection has been reported in several avian and mammalian species, including humans. The organism is a facultative anaerobe that has a worldwide distribution and may be found in alkaline soil, decaying organic matter, and water. The bacterium is resistant to many chemical and food preservative processes, including salting, pickling, and smoking, and may remain viable in the environment for up to several weeks under optimal conditions.
Swine are the most important reservoir hosts, and many pigs carry the organism in the oropharynx; the organism can be cultured from the tonsils of clinically healthy pigs. An infected or subclinically diseased pig is often the source of infection to other herd animals. The bacterium is shed into the environment, and susceptible pigs may acquire the infection by ingestion of contaminated soil or water (most common), percutaneously through skin wounds, or possibly via ticks and flies. Septicemia develops within 24 hours of exposure and produces disseminated intravascular coagulation characteristic of acute disease which may be fatal. Animals surviving the acute phase develop lesions of subacute to chronic infection, including cutaneous necrosis, polyarthritis, and endocarditis. Pregnant sows may abort due to infection, and bacteria have been isolated from aborted and stillborn fetuses.
Infection with E. rhusiopathiae has been reported in a wide variety of domestic and wild birds, cattle, sheep, horses, fish, moose, and dolphins. Erysipelas rhusiopathiae causes polyarthritis in sheep, and is most often seen in lambs in which the organism gains entry through docking or castration wounds. The disease in turkeys is similar to that of swine. In dogs, erysipelosis is caused by E. tonsillarum, a commensal found in the tonsils of pigs. Canine erysipelosis is similar to the disease in pigs, and is clinically characterized by fever, shifting-leg lameness, and cardiac murmur. In humans, E. rhusiopathiae causes a localized skin lesion termed erysipeloid which may progress to septicemia in rare cases. Erysipeloid is characterized by a self-limiting, painful, red swelling of the fingers, with or without lymphadenopathy. Human infections are usually acquired through occupational exposure in meat or chicken slaughterhouses, or fish plants. The term "erysipelas" in human disease is reserved for infections caused by Group A beta-hemolytic streptococci.
Contributor: Arkansas Livestock and Poultry Commission, 1 Natural Resources Drive, Little Rock, AR 72205.

1. Bastianello S, Spencer BT: A report of swine erysipelas in a litter of piglets. J South African Veterinary Assoc 55:195-198, 1984.
2. Palmer, N: Diseases of bones. In: Pathology of Domestic Animals, Jubb, Kennedy, Palmer eds., 4th ed., vol. 1, pp. 164-166, Academic Press, San Diego, 1993.
3. Legendre AM: Streptococcal and other gram-positive bacterial infections. In: Infectious Diseases of the Dog and Cat, 2nd ed., pp. 213-214, WB Saunders Co., 1998.
4. Jones TC, Hunt RD, King NW: Diseases caused by bacteria. In: Veterinary Pathology, 6th ed., pp. 435-438, Williams and Wilkins, 1997.
5. Charlton BR: Erysipelas. In: Whiteman and Bickford's Avian Disease Manual, 4th ed., pp. 101-104, American Association of Avian Pathologists, University of Pennsylvania, PA, 1996.
International Veterinary Pathology Slide Bank:
Laser disc frame #08966; 03453; 21206; 20375; 19720; 20476-77.
Case II - VN 87-98 (AFIP 2642427)
Case 7-2. Gross photo. There is a focal area of pale discoloration affecting 20% of the skeletal muscle (necrosis).
Case 7-2. Gross photo. Within the pericardial sac there is 30-50ml of serosanguinous fluid. The epicadium is pale toward the heart base and contains dull reddish-pink paintbrush like hemorrhages apically. There are scattered bright red 2-3mm petechial hemorrhages within the cranial mediastinal and parietal pleura.
Signalment: Two-year-old, female, quarter horse.
History: On May 13, 1998, three Quarter horses were started on a new batch of commercial ration. This particular batch was from a ration targeted for feeder calves. Affected horses were a six-year-old stallion of 500 kg (horse A), a three-year-old filly of 350 kg (horse B), and a two-year-old filly of 250 kg (horse C). Horses A and B died on May 18, 1998, and horse C died on May 19, 1998. Clinical courses were of 24-48 hours duration and included sudoresis, hindlimb incoordination which progressed to forelimb incoordination, muscle weakness, stumbling and death. The urine of horse A had a dark red discoloration. Horse C was necropsied. The ration manufacturer was contacted by phone and confirmed that monensin was added to this particular ration as a growth promoter for cattle. He stated that the label did not indicate its use in horses and declined to disclose the exact amount of monensin present in the ration, but mentioned that it was the recommended dose for growth promotion in cattle.

Gross Pathology: The main necropsy findings were confined to the skeletal muscles. Large, patchy areas of white-yellow discoloration (color transparency A) were present in the heavy muscle groups (quadriceps femoris, adductor, semitendinosus, semimembranosus, longissimus dorsi, subscapularis, pectineus, and gastrocnemius). Abundant yellowish gelatinous edema was present in the intermuscular fasciae. There was an accentuation of the hepatic lobular pattern and marked hydropericardium. The myocardium was diffusely pale (color transparency B).
Laboratory Results: Analysis of two samples of the ration performed at an independent laboratory revealed 174 ppm and 180 ppm of monensin.
Contributor's Diagnoses and Comments:
1. Skeletal muscle, degenerative myopathy, subacute, moderate to severe, Quarter Horse, equine. Etiology: Ionophore antibiotic (monensin) toxicosis.
2. Skeletal muscle, Sarcocystis sp., Quarter Horse, equine (incidental finding).
3. Liver, centrilobular fatty degeneration, moderate, diffuse, Quarter Horse, equine (slides not included).
4. Cardiomyopathy, degenerative, toxic, minimal to mild, acute, Quarter Horse, equine (slides not included).

Ionophore antibiotics are compounds that form lipid-soluble, dipolar reversible complexes with cations (Ca++, K+, Mg++), enhancing ionic transport through biological membranes with resultant disturbances in intracellular ionic homeostasis. The main therapeutic uses of ionophores include coccidiostasis for several animal species, growth promotion, and anti-bloat therapy for cattle. A large spectrum of other therapeutic uses has been described.
The best known ionophores in veterinary practice are monensin, lasalocid, salinomycin, and narasin. Although these drugs are reportedly safe when used in target species within the recommended dosage range, many cases of accidental or intentional poisoning by ionophores have been reported in horses, cattle, sheep, dogs, pigs, rabbits, poultry, and ostriches. In general, the hallmark of toxicosis is degenerative/necrotic myopathy and/or cardiomyopathy.
Factors determining the occurrence of ionophore toxicosis include overdosage and misuse (e.g., inadequate mixture of the premix, administration to non-target animal species). The latter is no doubt the cause of the poisoning of the horses in this report. Susceptibility to ionophores varies among species: LD50 (mg/kg or ppm) of monensin is 50-80 for cattle and only 2-3 for horses. The amount of monensin found in the ration in this case is too high even for cattle (maximum recommended amount as growth promoter in the ration for cattle is usually 33 ppm).
Clinical signs described for horses vary according to the location of lesions (skeletal muscle versus myocardium). Usually, there is profuse sweating, reluctance to move, repeated rising up and lying down, restlessness, and muscular weakness. Horses with cardiomyopathy may exhibit ill-thrift, intolerance to exercise, and sudden death. The dark discoloration of the urine found in one horse (not necropsied) of this report was most likely due to myoglobinuria, frequently present in cases of myodegeneration and also reported in association with ionophore toxicosis.
The gross and histologic lesions found in this case, although not pathognomonic for the condition, are the ones typically described. The lesions seen in the skeletal muscles of this case are degeneration and necrosis. Affected myofiber segments are markedly swollen, lack normal striation, and are transformed into coagulated proteinaceous tubes (hyaline necrosis). Frequently, fragmented necrotic segments of myofibers are seen as irregularly-shaped clumps of eosinophilic material (floccular necrosis) with invasion of fibers by neutrophils and macrophages. Edema between fibers is marked. A regenerative component is also observed characterized by proliferation of the satellite cells.
Ionophore antibiotic poisoning in horses induces myopathy and, commonly, cardiomyopathy. Myocardial lesions of the necropsied horse of this report were only mild. This might be related to the amount of the toxicant present in the ration. Differential diagnosis for ionophore antibiotic toxicity should include exertional rhabdomyolysis (azoturia), coffee senna poisoning, and colic.
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Case 7-2. Skeletal muscle. Muscle fibers are hyalinized, fragmented, and have a loss of cross striations, and are infiltrated and separated by neutrophils, macrophages, serocellular debris.
AFIP Diagnoses:
1. Skeletal muscle: Degeneration and necrosis, diffuse, with multifocal histiocytic and neutrophilic inflammation, quarter horse, equine.
2. Skeletal muscle: Sarcocysts, few.
Conference Note: Cases of ionophore antibiotic toxicity have been reported in numerous species, but monogastric animals, in particular the horse, are more sensitive than ruminants or domestic poultry. Monensin alters the membrane transport system for sodium and potassium, leading to disruption of the electrolyte modulated calcium gating mechanism. Mitochondrial failure and energy depletion ensue, with subsequent failure of calcium ion sequestration from the cytosol. Constantly elevated levels of cytosolic calcium lead to myofiber hypercontraction and degeneration. Marked mitochondrial swelling and disintegration are the earliest ultrastructural changes of monensin toxicity. The heart is particularly susceptible to disruption of cellular physiology due to its high energy requirements.
Clinical signs and lesions in the horse are due to cardiac, skeletal muscle, renal, and hepatic disturbances. Gross and microscopic lesions are varied depending upon dose and duration of exposure. In peracute cases, death may occur before gross and histologic changes become evident, particularly if there is extensive involvement of the cardiac mitochondria. Complicating the cardiac mitochondrial disturbance are the derangements in serum electrolyte levels that can occur due to extensive skeletal muscle necrosis. Skeletal muscle composes up to 55% of the total body mass of a horse and is a major reservoir for potassium and phosphorous, while containing very little sodium, chloride, and calcium. Necrosis of muscle causes disruption of the boundary between the intracellular fluid (ICF) and extracellular fluid (ECF), resulting in an efflux of potassium into the ECF and an influx of water, sodium, chloride, and calcium. Hyperkalemia, hyponatremia, and hypocalcemia may follow, causing myocardial conduction disturbances that exacerbate the disturbance of mitochondria. Influx of significant quantities of water into necrotic muscle from the ECF may cause hypovolemia, potentiating the toxic effects of myoglobin on the kidney.
The severity and distribution of lesions also varies among species. Myocardial lesions reportedly predominate over skeletal muscle lesions in cattle, the reverse is true in swine, and there is equivalent severity of lesions in both types of muscle in chickens and sheep. The long term prognosis for horses surviving the initial toxic insult probably depends upon the extent of myocardial lesions. Some horses may suffer from delayed monensin toxicity. Myocardial fibrosis leads to conduction disturbances and cardiac arrhythmias, pleural effusion, poor performance, unthriftiness, muscular weakness, and subcutaneous edema. Signs may not become evident until the animal is returned to work. Cardiac abnormalities have been seen in horses three to six months after toxic exposure.
Differential diagnosis considered by conference attendees for the skeletal muscle lesions in this horse included ionophore antibiotic toxicity (monensin), vitamin E/selenium deficiency, exertional rhabdomyolysis, and ingestion of Cassia sp. plants. Because the histological lesions in monensin toxicity differ very little from nutritional or exertional myopathy, clinical history and feed analysis are critical in the diagnosis. Simultaneous onset of pronounced clinical signs in multiple, especially adult, animals suggests exposure to a toxic agent. Owner reports of recent purchase of a new or "bitter smelling" feed is an additional helpful historical finding. Vitamin E/selenium deficiency most often occurs in young foals, commonly involves the masticatory muscles and tongue, and concurrent steatitis is often present.
Nutritional myopathy occurs sporadically in older horses, and steatitis is usually absent. Myocardial lesions may be present in both foals and adult horses with nutritional myopathy. The myocardium is infrequently involved in exertional rhabdomyolysis, and there is usually significant damage to the renal proximal convoluted tubules secondary to myoglobinuric nephrosis and ischemia. In addition to the muscle lesions induced by ingestion of Cassia sp., hepatic lesions are also found, characterized by extensive hepatocellular degeneration and necrosis.

Contributor: Universidade Federal de Santa Maria, Departamento de Patologia, 97105-900, Santa Maria RS, Brazil.
1. Amend JF, et al.: Equine monensin toxicosis: Some experimental clinicopathological observations. Comp Cont Ed Pract Vet 11:S173-S182, 1980.
2. Boemo CM, et al.: Monensin toxicity in horses. An outbreak resulting in the deaths of ten horses. Aust Eq Vet 9:103-106, 1991.
3. Doonan GR, Brown CM, Mullaney TP, Brooks DB, Ulmanis EG, Slanker MR: Monensin poisoning in horses - an international incident. Can Vet J 30:165-169, 1989.
4. Hanson LJ, Eisenbeis AB, Givens SV: Toxic effects of lasalocid in horses. Am J Vet Res 42:456-461, 1981.
5. Irigoyen LF, Graça DL, Barros CSL: Intoxicação experimental por Cassia occidentalis (Leg. Caes.) em eqüinos [Experimental poisoning by Cassia occidentalis (Leg. Caes.) in horses]. Pesq Vet Bras 11:35-44, 1991.
6. Ordidge RM, Schubert FK, Stoker JW: Death of horses after accidental feeding of monensin. Vet Rec 104:375, 1979.
7. Rollinson J, Taylor FGR, Chesney J: Salinomycin poisoning in horses. Vet Rec 121:126-128, 1987.
8. Salles MS, Barros CSL, Barros SS: Ionophore antibiotic (narasin) poisoning in rabbits. Vet Human Toxicol 36:437-444, 1944.
9. Hulland TJ: Muscle and tendon. In: Pathology of Domestic Animals, Jubb KVF, Kennedy PC, Palmer N, eds., 4th ed., vol. 1, pp. 217-244. Academic Press, San Diego, CA, 1993.
10. Perkins G, et al.: Electrolyte disturbances in foals with severe rhabdomyolysis. J Vet Intern Med 12:173-177, 1998.
International Veterinary Pathology Slide Bank:
Laser disc frame #05232 through 05235; 04273.
Case III - 98-746-11 (AFIP 2640640)
Signalment: A third trimester abortus and placenta from a 5-year-old Swiss Braunvieh cow.
History: Two years ago, several abortions occurred in the herd of origin. At that time the submitting practitioner suspected an infection with the bovine virus diarrhea virus (BVDV).

Gross Pathology: Necropsy findings were nonspecific, and consisted of generalized edema in the subcutaneous tissue and moderate autolytic changes of fetal organs. Intercotyledonary areas of submitted placental portions were edematous and thickened.
Laboratory Results: Arcanobacterium pyogenes was isolated from lung, liver, kidney and placenta. Routinely applied immunohistochemistry for BVD virus infection was negative. A mixed infection with Chlamydia sp. was excluded by immunohistochemistry of placental tissue sections.

Contributor's Diagnoses and Comments:
1. Placenta: Placentitis, necrotizing, subacute, multifocal to diffuse, moderate, with numerous intra- and extracytoplasmic bacteria.
2. Placenta: Vasculitis, subacute, focal, mild and calcification of villous mesenchyme, focal to diffuse, mild.
3. Lung: Alveolitis and bronchiolitis, necrotizing, multifocal, moderate, with numerous intra- and extracytoplasmic bacteria.
4. Lung: Intrauterine asphyxia with aspiration of chorionepithelium and meconium (bovine abortion due to fetal infection with Arcanobacterium pyogenes).
5. Intrahepatic cholestasis and extramedullary hematopoiesis in liver and spleen were additional microscopic findings.
Arcanobacterium (A.) pyogenes (formerly Actinomyces pyogenes and Corynebacterium pyogenes respectively) is widespread throughout the world as a common cause of pyogenic infection in a variety of domestic animals. In cattle, it is one of the most common causes of sporadic bacterial abortion. Abortions can occur at any stage of gestation, but are most often observed during the last trimester and usually occur as a single event in the herd.
A. pyogenes is a small, pleomorphic, gram-positive bacterium and is a common inhabitant of the nasal, conjunctival, vaginal, and preputial mucous membranes of clinically healthy cattle. A. pyogenes is believed to reach the pregnant uterus by a hematogenous route and produces suppurative endometrial lesions; the fetus may become septicemic by transplacental transmission. Fetal death may be caused by hypoxia following placental destruction.
A yellow to brown exudate covering swollen, edematous cotyledons and marked autolysis are the main gross lesions. The lungs of infected fetuses less than five months of gestation are dark red and swollen, and yellow foci are visible on the pleural surface.
Microscopic examination of the placenta reveals a necrotizing, suppurative placentitis, which is a consistent, but not pathognomonic lesion. In some cases, large numbers of bacteria can be found in sections of placenta with minimal changes. Not as consistently as placental lesions, an acute, fibrinous fetal bronchopneumonia occurs, and bacterial colonies within these lesions are probably due to aspiration of contaminated amniotic fluid. Inconsistently, a fibrinous pericarditis, pleuritis, or peritonitis may be present; bacteria may colonize in vessels and the surface of the skin and conjunctiva, with destruction of the epithelium. A. pyogenes is not often present as a contaminant or commensal in tissues of aborted fetuses or their placentas, and thus, its presence is usually of significance. Diagnosis of abortion induced by A. pyogenes is based on typical lesions and the isolation of the organism, preferably from the placenta, lung, and abomasal contents. In the absence of lesions, A. pyogenes induced abortion can only be suspected.
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Case 7-3. Placenta. Trophoblastic cells are detached from the surface of the fetal placenta and placenal villi. The intervillus space contains abundant necrotic cellular debris, scattered yellow-orange pigment (meconium), and occassional macrophages and neutrophils. Villous connective tissue is thickened and hyalinized.
40x obj H&E
Case 7-3. Lung. There are abundant coccobacilli and fewer neutrophils filling scattered bronchioles. Occassional plump macrophages contain bacteria which compress the nucleus against one pole of the cell. The interstitium is expanded by macrophages, fewer lymphocytes and fibroblasts admixed with finely granular proteinaceous debris.
40x obj B&H stain
Case 7-3. Lung. Brown and Hopps staining demonstrate aggregates of Gram positive bacilli within many of the bronchioles. Periarteriolar connective tissue is expanded by clear space (edema).

AFIP Diagnoses:
1. Chorioallantois: Placentitis, acute to subacute, diffuse, mild to moderate, with multifocal necrosis, vasculitis, and numerous intracellular and extracellular bacilli, Swiss Braunvieh, bovine.
2. Lung (fetus): Intrabronchiolar and intra-alveolar bacteria, histiocytes, amorphous debris, yellow pigment, and epithelial cells, multifocal, consistent with aspiration of contaminated amniotic fluid and meconium.
Conference Note: This case was studied in consultation with the Department of Neonatal and Pediatric Pathology. Conference participants agreed with the description of the histologic lesions in the placenta; however, several did not recognize conclusive evidence of an inflammatory response or pneumonia within the examined sections of fetal lung. Clumped within alveoli and bronchioles are abundant intracellular and extracellular bacteria, mononuclear cells (histiocytes), amorphous debris, small amounts of yellow pigment (meconium), and a few desquamated epithelial cells. The clumping of this material, along with the lack of interstitial inflammatory infiltrates and vascular changes, is consistent with aspiration of contaminated amnionic fluid and meconium. In human fetal pathology, the differentiation between aspiration of infected amniotic fluid and fetal pneumonia is, likewise, often problematic.
Several conference participants identified prominent, wide interlobular septa in the fetal lung and speculated whether this was the result of edema. In humans, the fetal lung has very wide interstitial septa during the 1st and 2nd trimesters. These septa remain wider than those of adults throughout the 3rd trimester and the first months of postpartum life. The expanded pulmonary interstitium of this bovine fetus likely represents normal development.
Recently, phylogenetic analysis of 13 bacterial species within the genus Actinomyces was performed; the 16S ribosomal RNA gene sequences were determined in this study. Based on the results, the study proposed that Actinomyces pyogenes be assigned to the genus Arcanobacterium as Arcanobacterium pyogenes comb. nov. While the results of this genetic analysis are certainly enlightening, we will refer to the organism throughout the remainder of this text by its more commonly known name, Actinomyces pyogenes, to avoid confusion.
Reports of natural infection and experimental evidence suggest that A. pyogenes may be a cause of sporadic abortion in cattle and sheep. In most cases, the organism is presumed to reach the placenta hematogenously. Infected animals may or may not have signs of systemic illness. Placentitis develops and leads to placentomal dysfunction, fetal hypoxia, fetal death, and abortion. An ascending route of placental infection is possible, but is less likely as this would require disruption of the cervical plug.
The fetus may become infected during the progression of placental lesions, but this is not a consistent feature. In aborted bovine fetuses in which A. pyogenes has been isolated, colonies of gram-positive bacteria are often present in the lungs. The bacteria are frequently confined to the bronchioles and are generally unaccompanied by inflammation. The gross and microscopic changes in experimentally infected ovine fetuses are primarily autolytic in nature. Widespread autolysis is noted grossly in the viscera and musculature, while microscopic findings include congestion, the presence of bacteria, and varying degrees of autolysis.
Contributor: Institute of Veterinary Pathology, University of Zurich, Winterthurerstrasse 286, CH-8057 Zurich, Switzerland.
1. Addo PB, Dennis SM: Experimental production of Corynebacterium pyogenes abortion in sheep. Cornell Vet 69:20-32, 1979.
2. Hinton M: Bovine abortion associated with Corynebacterium pyogenes. Vet Bull 42:753-756, 1972.
3. Sorensen GH: Studies on the occurrence of Peptococcus indolicus and Corynebacterium pyogenes in apparently healthy cattle. Acta Vet Scand 17:15-24, 1976.
4. Ramos CP, Foster G, Collins MD: Phylogenetic analysis of the genus Actinomyces based on 16S rRNA gene sequences: Description of Arcanobacterium phocae sp. nov., Arcanobacterium bernardiae comb. nov., and Arcanobacterium pyogenes comb. nov. Int J Syst Bacteriol 47:46-53, 1997.
Case IV - X-1555 (AFIP 2642319)
Signalment: 13-year-old, Tennessee walking horse, male (intact), equine.
History: The stallion had cutaneous lesions of three months duration on the caudal surfaces of the pasterns of both rear legs and one front leg. Otherwise, the horse was in good condition. This stallion was housed individually in a stall and was infrequently taken out as needed to service mares.
Gross Pathology: The lesions consisted of raised, coalescing, nodular and papillomatous masses, with multifocal areas of erosion, crusts, and hemorrhage that covered most of the distal caudal aspect of the affected pasterns.

Laboratory Results: None.
Contributor's Diagnoses and Comments:
1. Chronic, moderate to severe, exudative, papillomatous dermatitis with intraepidermal bacterial rods and spirochetes, haired skin, pastern.
2. Mild verminous folliculitis due to Pelodera strongyloides, haired skin, pastern.
Differential diagnosis for the gross lesions in this case included: Staphylococcal folliculitis/furunculosis, dermatophilosis, dermatophytosis, deep dermal mycosis, pythiosis, habronemiasis, acariasis, sarcoid, papilloma, exuberant granulation tissue, squamous cell carcinoma, allergic contact dermatitis, contact irritant dermatitis, and autoimmune disease. In addition to the epidermal hyperplasia and inflammatory changes visible in H&E stained sections, there are small to moderate numbers of nematode larvae in crevices of the hyperplastic epidermis and in hair follicles (nematodes are not present in all microslides; see enclosed 2x2 color transparency). Fresh tissue from the lesions was digested and yielded 3rd stage larvae of Pelodera strongyloides.
Due to similarity grossly and histologically between the lesions in this horse and papillomatous digital dermatitis (PDD) of cattle, a modified Steiner stain was applied to histologic sections of the pastern lesions and revealed numerous spirochetes within the superficial epidermis (see enclosed 2x2 color transparency). Numerous gram-negative rods that often form linear associations are also present; the rods are often visible in the H&E sections. Transmission electron microscopy of the affected tissue confirmed the location of both the rods and the spirochetes within epidermal cells. No viral particles were seen in the electron micrographs.
PDD is a contagious, painful, wart-like digital dermatitis of unknown etiology in dairy cattle. One of the defining characteristics of PDD histologically is the presence of an eroded acanthotic epidermis attended by parakeratotic papillomatous proliferation colonized by spirochete-dominant bacterial flora. Using molecular techniques, researchers have recently determined that the spirochetes associated with PDD are closely related to Treponema denticola, an oral treponeme of humans that is commonly associated with human periodontal disease. PDD has been associated with housing of cattle in persistently wet, unsanitary conditions.
Pelodera dermatitis in the horse has previously been reported, and it presents as a dry, exfoliative dermatitis with pustules on the underline and forelegs. Pelodera strongyloides is a free-living nematode found in decaying organic matter or moist soil. The nematodes may invade skin and cause dermatitis in animals maintained on dirty, persistently moist bedding such as soiled straw. The lesions on the pasterns of the stallion in the present case appeared more compatible with PDD, and the Pelodera folliculitis was interpreted to be a concurrent, but slightly less significant, factor in the pastern dermatitis.
Additional history revealed that this stallion's stall was rarely cleaned and was very dirty and moist with urine and feces. The stallion was treated with IV tetracycline, and an unspecified ointment was applied topically to the debrided pastern lesions. The horse's stall was cleaned, and the lesions did not recur.
2x obj40x obj
Case 7-4. The 2x view demonstrates papillomatous to polypoid character of the epidermis in affected areas. The 40x view has cross-sections of 3 nematodes within a hair follicle. An unusual feature of Pelodera (Rhabditis) strongyloides is the minute double lateral alae extending from each side of the larva. The musculature is platymyarian, and the gut has a simple low epithelium (lumen not visible here).
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Case 7-4. There are multiple rabditiform larva surrounded by keratin scale.
Steiner Stain 100x obj
Case 7-4. There are abundant argyrophilic (silver positive) spirochetes within and between multiple squamous epithelial cells.

AFIP Diagnoses:
1. Haired skin: Dermatitis, proliferative and verrucous, chronic-active, diffuse, moderate, with multifocal epidermal hydropic degeneration, and moderate numbers of intraepidermal filamentous bacilli and argyrophilic spirochetes, Tennessee walking horse, equine.
2. Haired skin: Intrafollicular and superficial rhabditid nematodes, few.
Conference Note: The clinical and pathological syndrome of PDD in dairy cows is incompletely understood, and intense study is in progress to characterize the disease, its pathogenesis, and the relationship of the intraepithelial spirochetes to the cutaneous proliferative lesions. The lesions are often grossly and histologically indistinguishable from squamous papillomas, hence the name. Interdigital dermatitis (IDD) is histologically similar to PDD, but lesions are found in the interdigital space. Lesions of both PDD and IDD occur on the digits below the level of the dewclaws, and the hindlimbs are most frequently affected.
While Treponema-like organisms have been isolated from PDD lesions, their pathological significance is unknown. In a study of affected California dairy cows4, a few animals had either deep ulcers or cutaneous lesions consistent with PDD in the flexural skin folds of the pastern. The lesions differed histologically from PDD, but the predilection for the same anatomical site under similar environmental conditions suggests a common pathogenesis. Deep ulcers or fissures also occur on the lower limbs of cattle housed in wet, unsanitary conditions. Studies in southern California dairies strongly linked muddiness of corrals to a high prevalence of PDD. Poor foot hygiene and prolonged contact of the lower limbs with manure has been associated with digital dermatitis in Europe and England. These findings suggest that PDD is multifactorial, and further study is needed to define the mechanisms and etiologies of the disease.
The significance of intraepidermal spirochetes in this horse is uncertain. The unsanitary conditions in which the horse was housed, coupled with the potential of a multifactorial etiology, make the pathogenesis of this lesion difficult to determine. However, the response to treatment, husbandry conditions, anatomical location, and histological features of the cutaneous pastern lesion in the horse seem to parallel the syndrome described in dairy cattle. Continuing research is needed to identify similar equine cutaneous lesions and to determine whether an entity comparable to PDD exists in horses.
Contributor: Diagnostic Laboratory Services, College of Veterinary Medicine, Box 9825, Mississippi State University, Mississippi State, MS 39762.
1. Armed Forces Institute of Pathology Wednesday Slide Conference 1996-1997 (AFIP 2550164). Papillomatous digital dermatitis in a Holstein cow.
2. Choi B-K, et al.: Spirochetes from digital dermatitis lesions in cattle are closely related to treponemes associated with human periodontitis. International Journal of Systemic Bacteriology 47:175-181, 1997.
3. Farrington DL, Lundvall RL, Greve JH: Pelodera strongyloides dermatitis in a horse in Iowa. Veterinary Medicine/Small Animal Clinician 71:1199-1201, 1976.
4. Read DH, Walker RL: Papillomatous digital dermatitis (footwarts) in California dairy cattle: Clinical and gross pathologic findings. J Vet Diag Invest 10:67-76, 1998.
5. Rijpkema SG, David GP, Hughes SL, Woodward MJ: Partial identification of spirochetes from two dairy cows with digital dermatitis by polymerase chain reaction analysis of the 16S ribosomal RNA gene. Vet Rec 140:257-259,1997.
Ed Stevens, DVM
Captain, United States Army
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
* The American Veterinary Medical Association and the American College of Veterinary Pathologists are co-sponsors of the Registry of Veterinary Pathology. The C.L. Davis Foundation also provides substantial support for the Registry.
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