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Fatal potomac horse fever (Ehrlichial colitis) in a foal: A case report from Connecticut
Refereed
FATAL POTOMAC HORSE FEVER (EHRLICHIAL COLITIS) IN A FOAL: A CASE REPORT FROM CONNECTICUT
G. A. John, DVM1; H. J. Van Kruiningen, DVM, PhD, MD2; D. Reim, DVM2; A. W. Wachtel, PhD~
SUMMARY A 4-month-old Quarter Horse Idly died after only 3 hours of illness. An autopsy revealed transmural congestion and hyperemia of cecum and colon consistent with acute colitis. Histologic and electron microscopic studies demonstrated lesions of Potomac horse fever and an abundance of Ehrlichia organisms within diseased tissue.
with Ehrlichia sennetsu antigen?Later that year, an Ehrlichia was cultured from experimentally infected horses. 6,7 This organism was shown to reproduce the disease in susceptible ponies. 2 Originally reported in Maryland, the disease has also been documented in Virginia, West Virginia, Kentucky, Pennsylvania, New Jersey, New York, Connecticut, Ohio, Illinois, Wisconsin, Minnesota, Florida, Idaho and California? ~'s There is a seasonal incidence of Potomac horse fever; most cases occur from June to September.9The disease is more frequent in older horses, and is seldom seen in foals and weanlings?
INTRODUCTION Potomac horse fever is a recently recognized (1979) infectious disease of horses characterized by fever, anorexia, depression, leukopenia, diarrhea and 30% mortality. Whitlock et al.11 transmitted the disease by the inoculation of whole blood from affected horses. The etiologic agent, an Ehrlichia, was initially suspected in 1984 when infected horses were found to produce antibodies which reacted Authors' address: 'Dr. John's present address: 45 Card Road, Freeville, NY 13068.2Department of Pathoblology,The University of Connecticut, Storrs, CT 06269-3089. Address reprint requests to Dr. H. J. Van Kruinlngan. Scientific Contribution No 1206, Storm Agricultural Experiment Station, The University of Connecticut, Storrs, CT 06269-3010. Acknowledgements: The authors acknowledge and thank Lamia HadcladKhairallah, PhD, for technical assistance with ultrastructural studies. Date of acceptance:June 1989
250
CASE REPORT On July 25, 1986, a 4-month-old Quarter Horse filly (180 kg) from Andover, CT was presented for autopsy. History indicated that the animal had been weaned 3 weeks earlier and was in good health until 3 hours prior to death. The clinical signs were partial anorexia and a watery diarrhea. A temperature had not been recorded, and there was not time to have the animal examined by a veterinarian. Twelve other horses, all greater than 1-year-of-age, were kept in relatively close contact with this animal, but none showed evidence of disease. Poslmortem examination conducted 3 hours after death indicated a well-fleshed animal. Lesions were limited to EQUINEVETERINARYSCIENCE
Figure 1. Reddened mucosal surface of the ventral colon. Cecal mucosa had a similar appearance.
Figure2. Cecal mucosa. Note the loss of surface epithelium, reduced mucosal thickness, decrease in the number of intestinal crypts, and collapse of connective tissue stroma. Surface pseudomembrane co~ists of necrotic cells, fibrin and bacteria. H&E; X63. the cecum, ventral colon and small intestine. The tip of the cecum, ventral colon and entire small intestine had pronounced hyperemia. Contents of all portions of the large intestine were normal. The mucosal surface of the cecum and ventral colon was dark red (Fig 1). Several areas of the cecal mucosa were covered by a thin, gray pseudomembrahe. Contents of the small bowel were rich with mucus. Throughout the small intestine there were many 4 to 8 cm areas of reddened mucosa. Based on the lesions and peracute course of the disease, salmonellosis, colitis X and Potomac horse fever were considered. Contents of the ventral colon were cultured for Salmonella and none were found. Tissue samples from affected areas were appropriately labelled, fixed in 10% buffered formalin and later processed, embedded in paraffin, sectioned at 6 micrometers, and stained with hematoxylin and eosin. Histologically, sections of the cecum and ventral colon had reduced mucosal thickness, loss of surface epithelium, a marked deVolume 9, Number 5, 1989
Figure 3. Lymphocytic depletion and karyorrhexis in a lymphoid follicle of the ventral colon. H&E; X160. crease in the number ofintestinalcrypts,and collapse of the remaining connective tissue stroma (Fig 2). Capillaries and veins in these areas were engorged with blood. Intestinal crypts that were present had intact epithelium and rarely contained necrotic debris. Cecal mucosa had apseudomembrane consisting of fibrin, necrotic cells and bacteria (Fig 2). The lamina propria of the mucosa had a mild hypercellularity which was most notable at the base of the intestinal crypts. Macrophages were prominent among the increased cells and they were also found in the edematous submucosa. Submucosal lymphoid follicles of the colon had depletion of lymphocytesin germinal centers and associated karyorrhexis (Fig 3). The small intestine was free of such lesions, but did contain a mycobacterial granuloma in 1 segment, which was undoubtedly unrelated. A modified Steiner's silver stain was applied to selected sections of cecum and ventral colon?° In both, the lamina propria around the bases of intestinal crypts contained numerous macrophages, 7 to 14 microns in diameter, which were filled with ring-likeorganisms (Fig4). Electron microscopy was performed on samples of cecum and ventral colon which had been fixed in 10% neutral buffered formalin. Ehrlichia, approximately 0.4 to 0.9 microns in diameter, were found in macrophages of the laminapropria at the base of the mucosa (Fig 5).
DISCUSSION Potomac horse fever has been described as an acute diarrheal syndrome with a course of several days to weeks and a 30% mortality late.4 The case presented here was outstandingfor its peracute or clinically unapparent course. Our pathologic findings concur with those ofCordes et al.i The damaged mucosa is tattered from necrosis of crypt and surface epithelial cells, the mucosa is engorged with blood, mucosal thickness is reduced, and the slroma is collapsed. The lamina propria contains many leukocytes, some of which are macrophages filledwith the causativeorganisms. 2Sl
Fig ure 4. Cecal mucosa. Macrophages filled with organisms were located around the bases of intestinal crypts. Steiner's silver stain; X1000.
Potomac horse fever has been recognized in Connecticut since 1983 ?The case reported here representes the first example of this disease autopsied at the Department of Pathobiology, University of Connecticut. The incidence of this entity in New England has not been defined, and current vaccination of some horses promises to influence the epidemiology.
REFERENCES 1. Cordes DO, Perry BD, Rikihisa Y, Chickerin9 WR: Enterocolitis caused by Ehrlichia sp. in ~e horse (Potomac horse fever). Vet Patho123:471-477,1986. 2. Holland CC, Ristic M, Cole AI, Johnson P, Baker G, Goetz T: Isolation, experimental transmission and characterization of the causative agent of Potomac Horse Fever. Science227:522524,1985. 3. Jenny AL: Report on Potomac horse fever (AEDS) Seminar. Am Assoc EquinePract Newsletter2:64-65,July 1984.
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Figure 5. Electron microg raph of a single Ehrlichiaorganism demonstrated in the ventral colonic mucosa. X74,000. 4. Knowles RC, Anderson CW, Shipley WD, Whitlock RH, Perry BD, Davidson J P:Acute equine diarrhea syndrome (AEDS): A preliminary report. Proc 29th An MeetAm Assoc Equine Pract. pp. 353-357,1983. 5. Palmer J E, Whitiock RH, Benson CE: Equine ehrlichia/ colitis (Potomac horse fever): Recognition of the disease in Pennsylvania, New Jersey, New York, Ohio, Idaho and Connecticut. J Am Vet MedAssoc 189:197-199,1986. 6. RikJhisey, Perry B, Cordes D: Rickettsial link with acute equine diarrhea. VetRec 115:390,1984. 7. Rikihisa Y, Perry BD: Causative agent of Potomac horse fever. Vet Rec 115:554,1984. 8. Ristic M, Holland CJ, Dawson JE, Sessions J, Palmer J: Diagnosis of equine monocytic ehrlichiosis (Potomac horse fever) by indirect immunofluorescanca. J Am Vet IViedAssoc 189:3946,1986. 9. Robl MG: Potomac horse fever: Closing in on an unknown killer. VetMed80:49-58,0ct.1985. 10. Steele KE, Rikihisa Y, Walton AM: Ehrlichia of Potomac horse fever identified with a silver stain. VetPa~o123:531-533,1986. 11. Whitiock RH, Palmer JE, Benson CE, Ackland HM, JennyA, Ristic M: Potomac horse fever: Clinical characteristicsand diagnostic features. Proc 27th An Meet, Am Asso Vet Lab Diag, pp.103-124,1984.
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.Reports complete In2daye .Free self.addressed sample bags
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3559 U.S. 62-Star Route, Millersburg, Ohio 44654 (216) 893-2933
EQUINE VETERINARY SCIENCE
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FATAL POTOMAC HORSE FEVER (EHRLICHIAL COLITIS) IN A FOAL: A CASE REPORT FROM CONNECTICUT
G. A. John, DVM1; H. J. Van Kruiningen, DVM, PhD, MD2; D. Reim, DVM2; A. W. Wachtel, PhD~
SUMMARY A 4-month-old Quarter Horse Idly died after only 3 hours of illness. An autopsy revealed transmural congestion and hyperemia of cecum and colon consistent with acute colitis. Histologic and electron microscopic studies demonstrated lesions of Potomac horse fever and an abundance of Ehrlichia organisms within diseased tissue.
with Ehrlichia sennetsu antigen?Later that year, an Ehrlichia was cultured from experimentally infected horses. 6,7 This organism was shown to reproduce the disease in susceptible ponies. 2 Originally reported in Maryland, the disease has also been documented in Virginia, West Virginia, Kentucky, Pennsylvania, New Jersey, New York, Connecticut, Ohio, Illinois, Wisconsin, Minnesota, Florida, Idaho and California? ~'s There is a seasonal incidence of Potomac horse fever; most cases occur from June to September.9The disease is more frequent in older horses, and is seldom seen in foals and weanlings?
INTRODUCTION Potomac horse fever is a recently recognized (1979) infectious disease of horses characterized by fever, anorexia, depression, leukopenia, diarrhea and 30% mortality. Whitlock et al.11 transmitted the disease by the inoculation of whole blood from affected horses. The etiologic agent, an Ehrlichia, was initially suspected in 1984 when infected horses were found to produce antibodies which reacted Authors' address: 'Dr. John's present address: 45 Card Road, Freeville, NY 13068.2Department of Pathoblology,The University of Connecticut, Storrs, CT 06269-3089. Address reprint requests to Dr. H. J. Van Kruinlngan. Scientific Contribution No 1206, Storm Agricultural Experiment Station, The University of Connecticut, Storrs, CT 06269-3010. Acknowledgements: The authors acknowledge and thank Lamia HadcladKhairallah, PhD, for technical assistance with ultrastructural studies. Date of acceptance:June 1989
250
CASE REPORT On July 25, 1986, a 4-month-old Quarter Horse filly (180 kg) from Andover, CT was presented for autopsy. History indicated that the animal had been weaned 3 weeks earlier and was in good health until 3 hours prior to death. The clinical signs were partial anorexia and a watery diarrhea. A temperature had not been recorded, and there was not time to have the animal examined by a veterinarian. Twelve other horses, all greater than 1-year-of-age, were kept in relatively close contact with this animal, but none showed evidence of disease. Poslmortem examination conducted 3 hours after death indicated a well-fleshed animal. Lesions were limited to EQUINEVETERINARYSCIENCE
Figure 1. Reddened mucosal surface of the ventral colon. Cecal mucosa had a similar appearance.
Figure2. Cecal mucosa. Note the loss of surface epithelium, reduced mucosal thickness, decrease in the number of intestinal crypts, and collapse of connective tissue stroma. Surface pseudomembrane co~ists of necrotic cells, fibrin and bacteria. H&E; X63. the cecum, ventral colon and small intestine. The tip of the cecum, ventral colon and entire small intestine had pronounced hyperemia. Contents of all portions of the large intestine were normal. The mucosal surface of the cecum and ventral colon was dark red (Fig 1). Several areas of the cecal mucosa were covered by a thin, gray pseudomembrahe. Contents of the small bowel were rich with mucus. Throughout the small intestine there were many 4 to 8 cm areas of reddened mucosa. Based on the lesions and peracute course of the disease, salmonellosis, colitis X and Potomac horse fever were considered. Contents of the ventral colon were cultured for Salmonella and none were found. Tissue samples from affected areas were appropriately labelled, fixed in 10% buffered formalin and later processed, embedded in paraffin, sectioned at 6 micrometers, and stained with hematoxylin and eosin. Histologically, sections of the cecum and ventral colon had reduced mucosal thickness, loss of surface epithelium, a marked deVolume 9, Number 5, 1989
Figure 3. Lymphocytic depletion and karyorrhexis in a lymphoid follicle of the ventral colon. H&E; X160. crease in the number ofintestinalcrypts,and collapse of the remaining connective tissue stroma (Fig 2). Capillaries and veins in these areas were engorged with blood. Intestinal crypts that were present had intact epithelium and rarely contained necrotic debris. Cecal mucosa had apseudomembrane consisting of fibrin, necrotic cells and bacteria (Fig 2). The lamina propria of the mucosa had a mild hypercellularity which was most notable at the base of the intestinal crypts. Macrophages were prominent among the increased cells and they were also found in the edematous submucosa. Submucosal lymphoid follicles of the colon had depletion of lymphocytesin germinal centers and associated karyorrhexis (Fig 3). The small intestine was free of such lesions, but did contain a mycobacterial granuloma in 1 segment, which was undoubtedly unrelated. A modified Steiner's silver stain was applied to selected sections of cecum and ventral colon?° In both, the lamina propria around the bases of intestinal crypts contained numerous macrophages, 7 to 14 microns in diameter, which were filled with ring-likeorganisms (Fig4). Electron microscopy was performed on samples of cecum and ventral colon which had been fixed in 10% neutral buffered formalin. Ehrlichia, approximately 0.4 to 0.9 microns in diameter, were found in macrophages of the laminapropria at the base of the mucosa (Fig 5).
DISCUSSION Potomac horse fever has been described as an acute diarrheal syndrome with a course of several days to weeks and a 30% mortality late.4 The case presented here was outstandingfor its peracute or clinically unapparent course. Our pathologic findings concur with those ofCordes et al.i The damaged mucosa is tattered from necrosis of crypt and surface epithelial cells, the mucosa is engorged with blood, mucosal thickness is reduced, and the slroma is collapsed. The lamina propria contains many leukocytes, some of which are macrophages filledwith the causativeorganisms. 2Sl
Fig ure 4. Cecal mucosa. Macrophages filled with organisms were located around the bases of intestinal crypts. Steiner's silver stain; X1000.
Potomac horse fever has been recognized in Connecticut since 1983 ?The case reported here representes the first example of this disease autopsied at the Department of Pathobiology, University of Connecticut. The incidence of this entity in New England has not been defined, and current vaccination of some horses promises to influence the epidemiology.
REFERENCES 1. Cordes DO, Perry BD, Rikihisa Y, Chickerin9 WR: Enterocolitis caused by Ehrlichia sp. in ~e horse (Potomac horse fever). Vet Patho123:471-477,1986. 2. Holland CC, Ristic M, Cole AI, Johnson P, Baker G, Goetz T: Isolation, experimental transmission and characterization of the causative agent of Potomac Horse Fever. Science227:522524,1985. 3. Jenny AL: Report on Potomac horse fever (AEDS) Seminar. Am Assoc EquinePract Newsletter2:64-65,July 1984.
~
-Hn~
.
FORAGE"
.
.
.
.
FEEDSTUFF " WATER"
.
.
SOIL"
AM LY I "
"
"
Figure 5. Electron microg raph of a single Ehrlichiaorganism demonstrated in the ventral colonic mucosa. X74,000. 4. Knowles RC, Anderson CW, Shipley WD, Whitlock RH, Perry BD, Davidson J P:Acute equine diarrhea syndrome (AEDS): A preliminary report. Proc 29th An MeetAm Assoc Equine Pract. pp. 353-357,1983. 5. Palmer J E, Whitiock RH, Benson CE: Equine ehrlichia/ colitis (Potomac horse fever): Recognition of the disease in Pennsylvania, New Jersey, New York, Ohio, Idaho and Connecticut. J Am Vet MedAssoc 189:197-199,1986. 6. RikJhisey, Perry B, Cordes D: Rickettsial link with acute equine diarrhea. VetRec 115:390,1984. 7. Rikihisa Y, Perry BD: Causative agent of Potomac horse fever. Vet Rec 115:554,1984. 8. Ristic M, Holland CJ, Dawson JE, Sessions J, Palmer J: Diagnosis of equine monocytic ehrlichiosis (Potomac horse fever) by indirect immunofluorescanca. J Am Vet IViedAssoc 189:3946,1986. 9. Robl MG: Potomac horse fever: Closing in on an unknown killer. VetMed80:49-58,0ct.1985. 10. Steele KE, Rikihisa Y, Walton AM: Ehrlichia of Potomac horse fever identified with a silver stain. VetPa~o123:531-533,1986. 11. Whitiock RH, Palmer JE, Benson CE, Ackland HM, JennyA, Ristic M: Potomac horse fever: Clinical characteristicsand diagnostic features. Proc 27th An Meet, Am Asso Vet Lab Diag, pp.103-124,1984.
.
7F
MANURE
Holmes ~_~
252
Labora.,,.y.
/
I
"
An important tool ,. monltonng relationships between trace and major minerals .I.~,,'lrtn'
~
lnrMl'
.Reports complete In2daye .Free self.addressed sample bags
~l
I ! RUeho','. 1;Uo . .,ab,. I
t ~"
J "
c a , orwr/te for free information brochure: Inr,, ,, , ~ .
3559 U.S. 62-Star Route, Millersburg, Ohio 44654 (216) 893-2933
EQUINE VETERINARY SCIENCE
~j~
M