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Actinobacillus Peritonitis in a Warmblood Gelding
Vet Clin Equine 22 (2006) e9–16
Actinobacillus Peritonitis in a Warmblood Gelding Tony D. Mogg, BVSc(Hons), PhDa,b,*, Susanne Dykgraaf, BVSc, MVSca,c a
Institute of Veterinary, Animal and Biomedical Sciences, Massey University, Palmerston North, New Zealand b Faculty of Veterinary Science, University Veterinary Centre Camden, University of Sydney, Camden, Australia c Large Animal Clinic, Veterinary Medical Teaching Hospital, University of California, Davis, Davis, CA, USA
Case details History An 8-year-old Warmblood gelding was referred to Massey University Veterinary Teaching Hospital with a history of depression, tachycardia, tachypnea, and acute abdominal pain of approximately 12 hours duration. The gelding had received flunixin meglumine on two occasions and also had been treated with mineral oil and water via nasogastric tube. Abdominocentesis performed by the referring veterinarian on the morning of referral to the hospital yielded yellow, turbid peritoneal fluid suggestive of peritonitis. Physical examination The gelding was in excellent body condition and weighed 570 kg. He was quiet, responsive, and showed no signs of abdominal pain. The heart rate, respiratory rate, and rectal temperature were 44 bpm, 20 bpm, and 38.5 C (101.3 F), respectively. Oral mucous membranes were light pink with a capillary refill time of 1.5 seconds. He had decreased borborygmi and the abdomen appeared splinted. The remainder of the physical examination was unremarkable. * Corresponding author. Faculty of Veterinary Science, University Veterinary Centre Camden, University of Sydney, 410 Werombi Road, Camden, NSW 2570, Australia. E-mail address: [email protected] (T.D. Mogg). 0749-0739/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.cveq.2005.12.031 vetequine.theclinics.com
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Case assessment The following diagnostic procedures were performed on admission to the hospital: Rectal palpationdno significant abnormalities detected. Abdominocentesisdyielded dark yellow, turbid peritoneal fluid, samples of which were submitted for cytology, nucleated cell count, total protein, and aerobic and anaerobic bacterial culture, and sensitivity. Cytologic examination of the fluid revealed a neutrophilia, with intracellular and extracellular bacterial rods. Total protein concentration (6.2 g/dL: normal !2.0 g/dL) and nucleated cell count (434,000/mL: normal !5,000/mL) were elevated. These findings were consistent with a diagnosis of acute septic peritonitis. Routine hematology and serum biochemistrydrevealed no significant abnormalities, other than a mild neutrophilia (Table 1). Fecal egg countdzero. Transabdominal ultrasonographyda small amount of hyperechoic free peritoneal fluid was detected (Fig. 1). There was no evidence of fibrin tags and no other abnormalities were detected. A diagnosis of septic peritonitis was made. Treatment and outcome Initial therapy consisted of procaine penicillin (22,000 IU/kg intramuscularly [IM] every 12 hours), gentamicin sulfate (6.6 mg/kg intravenously [IV] Table 1 Selected hematology and biochemistry results Days of hospitalization Test (reference range)
1
2
4
5
6
7
8
9
PCV (32%–52%) TPP (5.5–8.4 g/dL) White blood cells (6.0–13.0 103/mL) Band neutrophils (0–0.24 103/mL) Neutrophils (2.47–6.96 103/mL) Neutrophil morphology
31 7.6 9.7
36 8.6 ND
35 8.6 6.2
39 8.6 ND
34 8.0 10.4
36 7.4 ND
43 7.4 ND
ND ND ND
0.0
ND
0.0
ND
0.0
ND
ND
ND
7.5
ND
3.0
ND
7.1
ND
ND
ND
Mild toxic changes 400
ND
No toxic changes
ND
No toxic changes
ND
ND
ND
ND
500
ND
500
ND
ND
ND
1.22
1.07
1.75
1.31
1.31
1.06
1.14
0.94
Fibrinogen (200–400 mg/dL) Serum creatinine (1.0–1.7 mg/dL)
Abbreviations: ND, not done; PCV, packed cell volume; TPP, total plasma protein.
ACTINOBACILLUS PERITONITIS IN A WARMBLOOD GELDING
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Fig. 1. Transverse sonogram of ventral abdomen. Small volume of hyperechoic peritoneal fluid (A). Intra-abdominal fat (B). Normal large intestine (C). This sonogram was obtained using a 7-MHz convex linear-array transducer at a displayed depth of 6 cm.
every 24 hours), metronidazole (20 mg/kg by mouth every 8 hours), flunixin meglumine (0.25 mg/kg IV every 8 hours), and IV fluid therapy (lactated Ringer’s solution supplemented with potassium chloride). Low-dose heparin therapy (40 IU/kg IV every 8 hours) was instituted to help reduce the formation of intraabdominal adhesions. Aspirin (30 mg/kg by mouth every other day) was administered for its antiplatelet activity to reduce thrombus formation associated with the placement of a long-term, indwelling polyurethane jugular catheter. The gelding showed marked clinical improvement with treatment. During the remainder of the hospitalization, he remained bright, alert, and afebrile. Fluid therapy was discontinued after 24 hours when he dislodged the IV catheter. Despite an improved demeanor, he failed to drink enough to maintain optimal hydration. Further fluid therapy was commenced with administration of water via a nasogastric tube and provision ad libitum of a commercial electrolyte solution. The gelding consumed the latter solution readily in quantities sufficient to maintain adequate hydration. Repeat ultrasonographic examination of the abdomen on day 4 again failed to reveal any significant abnormalities. Subjectively less free peritoneal fluid was present, however. Repeat abdominocentesis showed a marked improvement in the nucleated cell count (24,800/mL on day 4 and 3400/mL on day 12) and return of the total protein concentration to within normal range (!2.0 g/dL on days 4 and 12). The peritoneal fluid neutrophilia also improved and bacteria became less evident. Hematology repeated on day 4 revealed a mild increase in plasma fibrinogen concentration (see Table 1). An Actinobacillus organism (species not determined) was grown on enrichment culture from the gelding’s peritoneal fluid. No anaerobes were isolated. The Actinobacillus was susceptible to amoxicillin/clavulanic acid combinations, ceftiofur, enrofloxacin, gentamicin, tetracycline, and
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trimethoprim-sulfonamide (TMS) combinations and moderately susceptible to penicillin and streptomycin. Because of a mild increase in serum creatinine concentration, antimicrobial therapy with penicillin and gentamicin were discontinued and treatment with ceftiofur commenced (3.5 mg/kg IM every 12 hours) on day 7. Oral metronidazole therapy was continued. The gelding was discharged from the hospital on day 9. Body weight at that time was 564 kg. It was recommended that he be treated with metronidazole (30 mg/kg by mouth every 12 hours for 3 days) and ceftiofur (3.5 mg/kg IM every 12 hours for 6 days) and monitored closely. Aspirin, flunixin, and heparin therapies were discontinued immediately before discharge from the hospital. Unfortunately, the owner had difficulties administering the ceftiofur. Thus, on day 10, TMS (30 mg/kg by mouth every 12 hours) was substituted for the ceftiofur. He was treated with oral TMS for a total of 22 days. The owner reported that the gelding remained stable with no depression, signs of colic, reduction in appetite, or fever. Three years after hospitalization, the gelding was reported clinically normal and had no recurrence or complications of the peritonitis. Discussion Actinobacillus spp are normal inhabitants of the equine oral cavity and intestinal tract [1–3]. They are implicated in various disease processes in horses, including neonatal enteritis and septicemia, abortion, abscesses, and respiratory tract disease [1]. A distinct syndrome of acute peritonitis in adult horses associated with Actinobacillus equuli is described in Australia [4–6]; however, Actinobacillus-associated peritonitis seems to be rare in other parts of the world. In several retrospective studies of equine peritonitis from the United States and the United Kingdom, there were no reported cases of infection with Actinobacillus spp [7–9]. An Actinobacillus spp was cultured from a pony that developed diffuse fibrinous peritonitis after abdominal lavage with a povidone-iodine solution [10] at the University of Florida, and a case report from the University of Kentucky describes the gross and microscopic pathology associated with septicemia and peritonitis resulting from A equuli in an adult horse [11]. It is unclear why A equuli–associated peritonitis is most common in Australia. At the time the gelding described in this report was presented to the hospital, Actinobacillus peritonitis had not been reported in New Zealand. The authors were suspicious that the gelding may have Actinobacillus peritonitis (despite the history that the gelding was born in New Zealand and never was transported to Australia), based on the similarities between this case and the syndrome of A equuli–associated peritonitis described in Australia. Other causes of septic peritonitis considered included primary bacterial peritonitis, intraabdominal abscessation, and gastrointestinal tract perforation. Typically, horses with A equuli peritonitis have an acute history of lethargy, depression, inappetance, and mild to moderate colic (including
ACTINOBACILLUS PERITONITIS IN A WARMBLOOD GELDING
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abdominal splinting). Most affected horses are tachycardic, tachypneic, febrile, and have decreased borborygmi [4–6]. The history and physical examination findings in the gelding described in this case report were consistent with these symptoms, although he had not had a significant fever. The gross and microscopic findings of the gelding’s peritoneal fluid also were consistent with those reported previously in horses with A equuli peritonitis. Typically, these horses have turbid, grossly discolored (creamy yellow to orange) [5] peritoneal fluid, which has a high total protein concentration and nucleated cell count. Cytologically, the fluid is characterized by a neutrophilia, and intracellular or extracellular pleomorphic Gram-negative rods may be detected [4–6]. Horses with A equuli peritonitis have inconsistent hematologic changes, with most having normal leukocyte and neutrophil counts [4–6]. Approximately 50% of those tested had hyperfibrinogenemia [5,6]. The mild hematologic abnormalities detected in this gelding were not inconsistent with these findings. Rectal examination in most cases of A equuli peritonitis is unremarkable [4–6], as was the case in this gelding. Firm, dry feces may be palpated in the large intestine or rectum in some cases [5,6]. Ultrasonographic examination of the gelding’s abdomen documented that the peritonitis was not effusive or fibrinous. Also, no underlying primary pathology (eg, intraabdominal abscess) was detected. Abdominal ultrasonography is invaluable in cases of peritonitis to assess the volume and nature of the peritoneal fluid, and to detect any underlying disease [12]. Ultrasonographic examination of horses with A equuli peritonitis is not reported in the literature, so it is unclear whether or not the low volume of free peritoneal fluid and lack of fibrin detected in this gelding were typical of that syndrome. Similarly, there are no reports of the investigation of sequential peritoneal fluid samples in horses with A equuli peritonitis. Thus, it is unclear whether or not the rapid improvement in peritoneal fluid total protein concentration and nucleated cell count observed in this case were consistent with that syndrome. The rapid response to medical therapy described in horses with A equuli peritonitis [4–6] makes it likely that such changes in peritoneal fluid may occur. The authors recommended that the gelding be treated conservatively while awaiting the peritoneal fluid culture results. The factors that contributed to the decision not to recommend exploratory surgery or peritoneal lavage included the gelding’s stable clinical condition, the noneffusive and nonfibrinous nature of the peritoneal fluid, and the failure to identify any underlying pathology. Bacterial isolates from cases of acute septic peritonitis in adult horses described in the literature include streptococci, enterobacteriaceae, corynebacteria, staphylococci, and obligate anaerobes (eg, Bacteroides spp) [7–9,13,14]. The combination of penicillin, gentamicin, and metronidazole, initially chosen in this case provided broad-spectrum antimicrobial coverage while awaiting peritoneal fluid culture and sensitivity results. Isolates of A equuli from horses with peritonitis in Australia commonly are susceptible
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to a range of antimicrobial agents. Most (90%) were susceptible to penicillin [5,6]. In this case, the Actinobacillus was susceptible to all of the antimicrobial agents tested (albeit only moderately susceptible to penicillin and streptomycin). After availability of the culture and sensitivity results, it was decided not to alter the original antimicrobial regimen. Justifications for continuing penicillin therapy were the possibility that the in vitro susceptibility result may not have been representative of the organism’s in vivo susceptibility and that the potential synergistic effects of concurrent penicillin and gentamicin therapy [15] may have been clinically advantageous. Metronidazole therapy was continued because of the possibility that obligate anaerobes may have been present but not cultured. There was a mild increase in plasma creatinine concentration detected on day 4 and the gelding was having difficulties voluntarily maintaining hydration. These factors resulted in the decision to discontinue penicillin/gentamicin therapy, so as to limit potential aminoglycoside nephrotoxicity, and begin treatment with ceftiofur. Ceftiofur was chosen on the basis of the culture and sensitivity results and its bactericidal activity and ease of administration (at least in the hospital environment). Compliance issues after discharge from the hospital necessitated a further change in antimicrobial therapy to oral TMS. The latter was chosen on the basis of its ability to be administered orally and its low cost, after consideration of the culture and sensitivity results and the stable clinical status of the patient. It was decided to treat the gelding with TMS for a longer period than was recommended for ceftiofur because of the concerns that the in vivo efficacy of TMS may be diminished by the presence of any residual exudates within the abdomen [16]. Supportive therapies in this case included IV and enteral fluid therapy, flunixin meglumine, aspirin, and heparin. Fluid therapy was deemed necessary to correct the initial dehydration and then provide for maintenance fluid requirements, because of the subsequent poor voluntary water intake. Flunixin was administered primarily for its antiendotoxic properties [17]. Aspirin and heparin were administered for their antithrombotic effects, as attempted prophylaxis for the development of thrombophlebitis associated with an indwelling IV catheter [18–20]. Heparin also is advocated to help prevent intra-abdominal adhesions [20,21]. The rapid clinical response to conservative medical therapy and lack of complications observed in this case are typical of horses described previously with A equuli peritonitis. In this syndrome, most horses respond favorably within 48 hours, and the long-term prognosis is excellent [4–6]. Neither surgical exploration nor peritoneal lavage was performed in any of the reported cases of A equuli peritonitis in Australia [4–6]. Unlike many other causes of septic peritonitis, which have a guarded to poor prognosis, cases associated with A equuli usually do not progress to develop endotoxic shock, die, or require euthanasia [4–6]. In this respect, the two cases of Actinobacillus peritonitis reported in the United States [10,11] may not be typical of the previously described A equuli peritonitis syndrome, as both of the horses died.
ACTINOBACILLUS PERITONITIS IN A WARMBLOOD GELDING
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Several retrospective studies of horses with non-Actinobacillus peritonitis have reported high mortality rates [7–9]. The highest mortality rate was in horses with gastrointestinal rupture (100%) and in those that developed peritonitis after abdominal surgery (56%) [8]. The mortality rate was lower (30% to 42.9%) for peritonitis not associated with gastrointestinal rupture or abdominal surgery [7–9]. In comparison, none of the 69 horses in Australia with acute A equuli–associated peritonitis died or required euthanasia [4–6]. One of two horses in Australia with chronic A equuli peritonitis was euthanized at the owner’s request [4]. The pathogenesis of A equuli peritonitis is unclear. Most reports suggest that parasitic larval migration from the intestinal tract may play a role [1,4–6], as Actinobacillus spp are part of the normal equine intestinal flora [1,3]. The gelding had a zero fecal egg count and a good deworming history, although this does not rule out parasitism conclusively as a factor in this case. To this end it was recommended that he be treated with a larvicidal dose of an appropriate anthelmintic after discharge from the hospital. In summary, this case was typical in many respects of the syndrome of acute A equuli–associated peritonitis described in Australia. Because of the rapid response to conservative medical therapy and excellent longterm prognosis, it is important for all equine clinicians to be aware of this syndrome, even though peritonitis resulting from Actinobacillus spp remains uncommon outside of Australia. References [1] Kowalski JJ. Bacterial and mycotic infections. In: Reed SM, Bayly WM, editors. Equine internal medicine. Philadelphia: WB Saunders; 1998. p. 61–2. [2] Sternberg S. Studies on equine Actinobacillus spp. Doctoral thesis. Uppsala (Sweden): Swedish University of Agricultural Sciences; 1999. [3] Al-Mashat RR, Taylor DJ. Bacteria in enteric lesions of horses. Vet Rec 1986;118:453–8. [4] Gay CC, Lording PM. Peritonitis in horses associated with Actinobacillus equuli. Aust Vet J 1980;56:296–300. [5] Golland LC, Hodgson DR, Hodgson JL, et al. Peritonitis associated with Actinobacillus equuli in horses: 15 cases (1982–1992). J Am Vet Med Assoc 1994;205:340–3. [6] Matthews S, Dart AJ, Dowling BA, et al. Peritonitis associated with Actinobacillus equuli in horses: 51 cases. Aust Vet J 2001;79:536–9. [7] Dyson S. Review of 30 cases of peritonitis in the horse. Equine Vet J 1983;15:25–30. [8] Hawkins JF, Bowman KF, Roberts MC, et al. Peritonitis in horses: 67 cases (1985–1990). J Am Vet Med Assoc 1993;203:284–8. [9] Mair TS, Hillyer MH, Taylor FGR. Peritonitis in adult horses: a review of 21 cases. Vet Rec 1990;126:567–70. [10] Schneider RK, Meyer DJ, Embertson RM, et al. Response of pony peritoneum to four peritoneal lavage solutions. Am J Vet Res 1988;49:889–94. [11] Patterson-Kane JC, Donahue JM, Harrison LR. Septicemia and peritonitis due to Actinobacillus equuli infection in an adult horse. Vet Pathol 2001;38:230–2. [12] Reef VB. Adult abdominal ultrasonography. Diseases of the peritoneal cavity. In: Ree VB, editor. Equine diagnostic ultrasonography. Philadelphia: WB Saunders; 1998. p. 339–46. [13] Sweeney RW, Sweeney CR, Weiher J. Clinical use of metronidazole in horses: 200 cases (1984–1989). J Am Vet Med Assoc 1991;198:1045–8.
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[14] Moore RM. Pathogenesis of obligate anaerobic bacterial infections in horses. Compend Contin Educ Pract Vet 1993;15:278–87. [15] Prescott JF. Beta-lactam antibiotics. Penam penicillins. In: Prescott JF, Baggot JD, Walker RD, editors. Antimicrobial therapy in veterinary medicine. 3rd edition. Ames (IA): Iowa State University Press; 2000. p. 105–33. [16] Prescott JF. Sulfonamides, diaminopyridines, and their combinations. In: Prescott JF, Baggot JD, et al, editors. Antimicrobial therapy in veterinary medicine. 3rd edition. Ames (IA): Iowa State University Press; 2000. p. 290–314. [17] Semrad SD, Hardee GE, Hardee MM, et al. Low dose flunixin meglumine: effects on eicosanoid production and clinical signs induced by experimental endotoxaemia in horses. Equine Vet J 1987;19:201–6. [18] Cambridge H, Lees P, Hooke RE, et al. Antithrombotic actions of aspirin in the horse. Equine Vet J 1991;23:123–7. [19] Heath MF, Evans RJ, Poole AW, et al. The effects of aspirin and paracetamol on the aggregation of equine blood platelets. J Vet Pharmacol Ther 1994;17:374–8. [20] Moore BR, Hinchcliff KW. Heparin: a review of its pharmacology and therapeutic use in horses. J Vet Intern Med 1994;8:26–35. [21] Parker JE, Fubini SL, Car BD, et al. Prevention of intraabdominal adhesions in ponies by low-dose heparin therapy. Vet Surg 1987;16:459–62.
Actinobacillus Peritonitis in a Warmblood Gelding Tony D. Mogg, BVSc(Hons), PhDa,b,*, Susanne Dykgraaf, BVSc, MVSca,c a
Institute of Veterinary, Animal and Biomedical Sciences, Massey University, Palmerston North, New Zealand b Faculty of Veterinary Science, University Veterinary Centre Camden, University of Sydney, Camden, Australia c Large Animal Clinic, Veterinary Medical Teaching Hospital, University of California, Davis, Davis, CA, USA
Case details History An 8-year-old Warmblood gelding was referred to Massey University Veterinary Teaching Hospital with a history of depression, tachycardia, tachypnea, and acute abdominal pain of approximately 12 hours duration. The gelding had received flunixin meglumine on two occasions and also had been treated with mineral oil and water via nasogastric tube. Abdominocentesis performed by the referring veterinarian on the morning of referral to the hospital yielded yellow, turbid peritoneal fluid suggestive of peritonitis. Physical examination The gelding was in excellent body condition and weighed 570 kg. He was quiet, responsive, and showed no signs of abdominal pain. The heart rate, respiratory rate, and rectal temperature were 44 bpm, 20 bpm, and 38.5 C (101.3 F), respectively. Oral mucous membranes were light pink with a capillary refill time of 1.5 seconds. He had decreased borborygmi and the abdomen appeared splinted. The remainder of the physical examination was unremarkable. * Corresponding author. Faculty of Veterinary Science, University Veterinary Centre Camden, University of Sydney, 410 Werombi Road, Camden, NSW 2570, Australia. E-mail address: [email protected] (T.D. Mogg). 0749-0739/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.cveq.2005.12.031 vetequine.theclinics.com
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Case assessment The following diagnostic procedures were performed on admission to the hospital: Rectal palpationdno significant abnormalities detected. Abdominocentesisdyielded dark yellow, turbid peritoneal fluid, samples of which were submitted for cytology, nucleated cell count, total protein, and aerobic and anaerobic bacterial culture, and sensitivity. Cytologic examination of the fluid revealed a neutrophilia, with intracellular and extracellular bacterial rods. Total protein concentration (6.2 g/dL: normal !2.0 g/dL) and nucleated cell count (434,000/mL: normal !5,000/mL) were elevated. These findings were consistent with a diagnosis of acute septic peritonitis. Routine hematology and serum biochemistrydrevealed no significant abnormalities, other than a mild neutrophilia (Table 1). Fecal egg countdzero. Transabdominal ultrasonographyda small amount of hyperechoic free peritoneal fluid was detected (Fig. 1). There was no evidence of fibrin tags and no other abnormalities were detected. A diagnosis of septic peritonitis was made. Treatment and outcome Initial therapy consisted of procaine penicillin (22,000 IU/kg intramuscularly [IM] every 12 hours), gentamicin sulfate (6.6 mg/kg intravenously [IV] Table 1 Selected hematology and biochemistry results Days of hospitalization Test (reference range)
1
2
4
5
6
7
8
9
PCV (32%–52%) TPP (5.5–8.4 g/dL) White blood cells (6.0–13.0 103/mL) Band neutrophils (0–0.24 103/mL) Neutrophils (2.47–6.96 103/mL) Neutrophil morphology
31 7.6 9.7
36 8.6 ND
35 8.6 6.2
39 8.6 ND
34 8.0 10.4
36 7.4 ND
43 7.4 ND
ND ND ND
0.0
ND
0.0
ND
0.0
ND
ND
ND
7.5
ND
3.0
ND
7.1
ND
ND
ND
Mild toxic changes 400
ND
No toxic changes
ND
No toxic changes
ND
ND
ND
ND
500
ND
500
ND
ND
ND
1.22
1.07
1.75
1.31
1.31
1.06
1.14
0.94
Fibrinogen (200–400 mg/dL) Serum creatinine (1.0–1.7 mg/dL)
Abbreviations: ND, not done; PCV, packed cell volume; TPP, total plasma protein.
ACTINOBACILLUS PERITONITIS IN A WARMBLOOD GELDING
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Fig. 1. Transverse sonogram of ventral abdomen. Small volume of hyperechoic peritoneal fluid (A). Intra-abdominal fat (B). Normal large intestine (C). This sonogram was obtained using a 7-MHz convex linear-array transducer at a displayed depth of 6 cm.
every 24 hours), metronidazole (20 mg/kg by mouth every 8 hours), flunixin meglumine (0.25 mg/kg IV every 8 hours), and IV fluid therapy (lactated Ringer’s solution supplemented with potassium chloride). Low-dose heparin therapy (40 IU/kg IV every 8 hours) was instituted to help reduce the formation of intraabdominal adhesions. Aspirin (30 mg/kg by mouth every other day) was administered for its antiplatelet activity to reduce thrombus formation associated with the placement of a long-term, indwelling polyurethane jugular catheter. The gelding showed marked clinical improvement with treatment. During the remainder of the hospitalization, he remained bright, alert, and afebrile. Fluid therapy was discontinued after 24 hours when he dislodged the IV catheter. Despite an improved demeanor, he failed to drink enough to maintain optimal hydration. Further fluid therapy was commenced with administration of water via a nasogastric tube and provision ad libitum of a commercial electrolyte solution. The gelding consumed the latter solution readily in quantities sufficient to maintain adequate hydration. Repeat ultrasonographic examination of the abdomen on day 4 again failed to reveal any significant abnormalities. Subjectively less free peritoneal fluid was present, however. Repeat abdominocentesis showed a marked improvement in the nucleated cell count (24,800/mL on day 4 and 3400/mL on day 12) and return of the total protein concentration to within normal range (!2.0 g/dL on days 4 and 12). The peritoneal fluid neutrophilia also improved and bacteria became less evident. Hematology repeated on day 4 revealed a mild increase in plasma fibrinogen concentration (see Table 1). An Actinobacillus organism (species not determined) was grown on enrichment culture from the gelding’s peritoneal fluid. No anaerobes were isolated. The Actinobacillus was susceptible to amoxicillin/clavulanic acid combinations, ceftiofur, enrofloxacin, gentamicin, tetracycline, and
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trimethoprim-sulfonamide (TMS) combinations and moderately susceptible to penicillin and streptomycin. Because of a mild increase in serum creatinine concentration, antimicrobial therapy with penicillin and gentamicin were discontinued and treatment with ceftiofur commenced (3.5 mg/kg IM every 12 hours) on day 7. Oral metronidazole therapy was continued. The gelding was discharged from the hospital on day 9. Body weight at that time was 564 kg. It was recommended that he be treated with metronidazole (30 mg/kg by mouth every 12 hours for 3 days) and ceftiofur (3.5 mg/kg IM every 12 hours for 6 days) and monitored closely. Aspirin, flunixin, and heparin therapies were discontinued immediately before discharge from the hospital. Unfortunately, the owner had difficulties administering the ceftiofur. Thus, on day 10, TMS (30 mg/kg by mouth every 12 hours) was substituted for the ceftiofur. He was treated with oral TMS for a total of 22 days. The owner reported that the gelding remained stable with no depression, signs of colic, reduction in appetite, or fever. Three years after hospitalization, the gelding was reported clinically normal and had no recurrence or complications of the peritonitis. Discussion Actinobacillus spp are normal inhabitants of the equine oral cavity and intestinal tract [1–3]. They are implicated in various disease processes in horses, including neonatal enteritis and septicemia, abortion, abscesses, and respiratory tract disease [1]. A distinct syndrome of acute peritonitis in adult horses associated with Actinobacillus equuli is described in Australia [4–6]; however, Actinobacillus-associated peritonitis seems to be rare in other parts of the world. In several retrospective studies of equine peritonitis from the United States and the United Kingdom, there were no reported cases of infection with Actinobacillus spp [7–9]. An Actinobacillus spp was cultured from a pony that developed diffuse fibrinous peritonitis after abdominal lavage with a povidone-iodine solution [10] at the University of Florida, and a case report from the University of Kentucky describes the gross and microscopic pathology associated with septicemia and peritonitis resulting from A equuli in an adult horse [11]. It is unclear why A equuli–associated peritonitis is most common in Australia. At the time the gelding described in this report was presented to the hospital, Actinobacillus peritonitis had not been reported in New Zealand. The authors were suspicious that the gelding may have Actinobacillus peritonitis (despite the history that the gelding was born in New Zealand and never was transported to Australia), based on the similarities between this case and the syndrome of A equuli–associated peritonitis described in Australia. Other causes of septic peritonitis considered included primary bacterial peritonitis, intraabdominal abscessation, and gastrointestinal tract perforation. Typically, horses with A equuli peritonitis have an acute history of lethargy, depression, inappetance, and mild to moderate colic (including
ACTINOBACILLUS PERITONITIS IN A WARMBLOOD GELDING
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abdominal splinting). Most affected horses are tachycardic, tachypneic, febrile, and have decreased borborygmi [4–6]. The history and physical examination findings in the gelding described in this case report were consistent with these symptoms, although he had not had a significant fever. The gross and microscopic findings of the gelding’s peritoneal fluid also were consistent with those reported previously in horses with A equuli peritonitis. Typically, these horses have turbid, grossly discolored (creamy yellow to orange) [5] peritoneal fluid, which has a high total protein concentration and nucleated cell count. Cytologically, the fluid is characterized by a neutrophilia, and intracellular or extracellular pleomorphic Gram-negative rods may be detected [4–6]. Horses with A equuli peritonitis have inconsistent hematologic changes, with most having normal leukocyte and neutrophil counts [4–6]. Approximately 50% of those tested had hyperfibrinogenemia [5,6]. The mild hematologic abnormalities detected in this gelding were not inconsistent with these findings. Rectal examination in most cases of A equuli peritonitis is unremarkable [4–6], as was the case in this gelding. Firm, dry feces may be palpated in the large intestine or rectum in some cases [5,6]. Ultrasonographic examination of the gelding’s abdomen documented that the peritonitis was not effusive or fibrinous. Also, no underlying primary pathology (eg, intraabdominal abscess) was detected. Abdominal ultrasonography is invaluable in cases of peritonitis to assess the volume and nature of the peritoneal fluid, and to detect any underlying disease [12]. Ultrasonographic examination of horses with A equuli peritonitis is not reported in the literature, so it is unclear whether or not the low volume of free peritoneal fluid and lack of fibrin detected in this gelding were typical of that syndrome. Similarly, there are no reports of the investigation of sequential peritoneal fluid samples in horses with A equuli peritonitis. Thus, it is unclear whether or not the rapid improvement in peritoneal fluid total protein concentration and nucleated cell count observed in this case were consistent with that syndrome. The rapid response to medical therapy described in horses with A equuli peritonitis [4–6] makes it likely that such changes in peritoneal fluid may occur. The authors recommended that the gelding be treated conservatively while awaiting the peritoneal fluid culture results. The factors that contributed to the decision not to recommend exploratory surgery or peritoneal lavage included the gelding’s stable clinical condition, the noneffusive and nonfibrinous nature of the peritoneal fluid, and the failure to identify any underlying pathology. Bacterial isolates from cases of acute septic peritonitis in adult horses described in the literature include streptococci, enterobacteriaceae, corynebacteria, staphylococci, and obligate anaerobes (eg, Bacteroides spp) [7–9,13,14]. The combination of penicillin, gentamicin, and metronidazole, initially chosen in this case provided broad-spectrum antimicrobial coverage while awaiting peritoneal fluid culture and sensitivity results. Isolates of A equuli from horses with peritonitis in Australia commonly are susceptible
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to a range of antimicrobial agents. Most (90%) were susceptible to penicillin [5,6]. In this case, the Actinobacillus was susceptible to all of the antimicrobial agents tested (albeit only moderately susceptible to penicillin and streptomycin). After availability of the culture and sensitivity results, it was decided not to alter the original antimicrobial regimen. Justifications for continuing penicillin therapy were the possibility that the in vitro susceptibility result may not have been representative of the organism’s in vivo susceptibility and that the potential synergistic effects of concurrent penicillin and gentamicin therapy [15] may have been clinically advantageous. Metronidazole therapy was continued because of the possibility that obligate anaerobes may have been present but not cultured. There was a mild increase in plasma creatinine concentration detected on day 4 and the gelding was having difficulties voluntarily maintaining hydration. These factors resulted in the decision to discontinue penicillin/gentamicin therapy, so as to limit potential aminoglycoside nephrotoxicity, and begin treatment with ceftiofur. Ceftiofur was chosen on the basis of the culture and sensitivity results and its bactericidal activity and ease of administration (at least in the hospital environment). Compliance issues after discharge from the hospital necessitated a further change in antimicrobial therapy to oral TMS. The latter was chosen on the basis of its ability to be administered orally and its low cost, after consideration of the culture and sensitivity results and the stable clinical status of the patient. It was decided to treat the gelding with TMS for a longer period than was recommended for ceftiofur because of the concerns that the in vivo efficacy of TMS may be diminished by the presence of any residual exudates within the abdomen [16]. Supportive therapies in this case included IV and enteral fluid therapy, flunixin meglumine, aspirin, and heparin. Fluid therapy was deemed necessary to correct the initial dehydration and then provide for maintenance fluid requirements, because of the subsequent poor voluntary water intake. Flunixin was administered primarily for its antiendotoxic properties [17]. Aspirin and heparin were administered for their antithrombotic effects, as attempted prophylaxis for the development of thrombophlebitis associated with an indwelling IV catheter [18–20]. Heparin also is advocated to help prevent intra-abdominal adhesions [20,21]. The rapid clinical response to conservative medical therapy and lack of complications observed in this case are typical of horses described previously with A equuli peritonitis. In this syndrome, most horses respond favorably within 48 hours, and the long-term prognosis is excellent [4–6]. Neither surgical exploration nor peritoneal lavage was performed in any of the reported cases of A equuli peritonitis in Australia [4–6]. Unlike many other causes of septic peritonitis, which have a guarded to poor prognosis, cases associated with A equuli usually do not progress to develop endotoxic shock, die, or require euthanasia [4–6]. In this respect, the two cases of Actinobacillus peritonitis reported in the United States [10,11] may not be typical of the previously described A equuli peritonitis syndrome, as both of the horses died.
ACTINOBACILLUS PERITONITIS IN A WARMBLOOD GELDING
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Several retrospective studies of horses with non-Actinobacillus peritonitis have reported high mortality rates [7–9]. The highest mortality rate was in horses with gastrointestinal rupture (100%) and in those that developed peritonitis after abdominal surgery (56%) [8]. The mortality rate was lower (30% to 42.9%) for peritonitis not associated with gastrointestinal rupture or abdominal surgery [7–9]. In comparison, none of the 69 horses in Australia with acute A equuli–associated peritonitis died or required euthanasia [4–6]. One of two horses in Australia with chronic A equuli peritonitis was euthanized at the owner’s request [4]. The pathogenesis of A equuli peritonitis is unclear. Most reports suggest that parasitic larval migration from the intestinal tract may play a role [1,4–6], as Actinobacillus spp are part of the normal equine intestinal flora [1,3]. The gelding had a zero fecal egg count and a good deworming history, although this does not rule out parasitism conclusively as a factor in this case. To this end it was recommended that he be treated with a larvicidal dose of an appropriate anthelmintic after discharge from the hospital. In summary, this case was typical in many respects of the syndrome of acute A equuli–associated peritonitis described in Australia. Because of the rapid response to conservative medical therapy and excellent longterm prognosis, it is important for all equine clinicians to be aware of this syndrome, even though peritonitis resulting from Actinobacillus spp remains uncommon outside of Australia. References [1] Kowalski JJ. Bacterial and mycotic infections. In: Reed SM, Bayly WM, editors. Equine internal medicine. Philadelphia: WB Saunders; 1998. p. 61–2. [2] Sternberg S. Studies on equine Actinobacillus spp. Doctoral thesis. Uppsala (Sweden): Swedish University of Agricultural Sciences; 1999. [3] Al-Mashat RR, Taylor DJ. Bacteria in enteric lesions of horses. Vet Rec 1986;118:453–8. [4] Gay CC, Lording PM. Peritonitis in horses associated with Actinobacillus equuli. Aust Vet J 1980;56:296–300. [5] Golland LC, Hodgson DR, Hodgson JL, et al. Peritonitis associated with Actinobacillus equuli in horses: 15 cases (1982–1992). J Am Vet Med Assoc 1994;205:340–3. [6] Matthews S, Dart AJ, Dowling BA, et al. Peritonitis associated with Actinobacillus equuli in horses: 51 cases. Aust Vet J 2001;79:536–9. [7] Dyson S. Review of 30 cases of peritonitis in the horse. Equine Vet J 1983;15:25–30. [8] Hawkins JF, Bowman KF, Roberts MC, et al. Peritonitis in horses: 67 cases (1985–1990). J Am Vet Med Assoc 1993;203:284–8. [9] Mair TS, Hillyer MH, Taylor FGR. Peritonitis in adult horses: a review of 21 cases. Vet Rec 1990;126:567–70. [10] Schneider RK, Meyer DJ, Embertson RM, et al. Response of pony peritoneum to four peritoneal lavage solutions. Am J Vet Res 1988;49:889–94. [11] Patterson-Kane JC, Donahue JM, Harrison LR. Septicemia and peritonitis due to Actinobacillus equuli infection in an adult horse. Vet Pathol 2001;38:230–2. [12] Reef VB. Adult abdominal ultrasonography. Diseases of the peritoneal cavity. In: Ree VB, editor. Equine diagnostic ultrasonography. Philadelphia: WB Saunders; 1998. p. 339–46. [13] Sweeney RW, Sweeney CR, Weiher J. Clinical use of metronidazole in horses: 200 cases (1984–1989). J Am Vet Med Assoc 1991;198:1045–8.
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[14] Moore RM. Pathogenesis of obligate anaerobic bacterial infections in horses. Compend Contin Educ Pract Vet 1993;15:278–87. [15] Prescott JF. Beta-lactam antibiotics. Penam penicillins. In: Prescott JF, Baggot JD, Walker RD, editors. Antimicrobial therapy in veterinary medicine. 3rd edition. Ames (IA): Iowa State University Press; 2000. p. 105–33. [16] Prescott JF. Sulfonamides, diaminopyridines, and their combinations. In: Prescott JF, Baggot JD, et al, editors. Antimicrobial therapy in veterinary medicine. 3rd edition. Ames (IA): Iowa State University Press; 2000. p. 290–314. [17] Semrad SD, Hardee GE, Hardee MM, et al. Low dose flunixin meglumine: effects on eicosanoid production and clinical signs induced by experimental endotoxaemia in horses. Equine Vet J 1987;19:201–6. [18] Cambridge H, Lees P, Hooke RE, et al. Antithrombotic actions of aspirin in the horse. Equine Vet J 1991;23:123–7. [19] Heath MF, Evans RJ, Poole AW, et al. The effects of aspirin and paracetamol on the aggregation of equine blood platelets. J Vet Pharmacol Ther 1994;17:374–8. [20] Moore BR, Hinchcliff KW. Heparin: a review of its pharmacology and therapeutic use in horses. J Vet Intern Med 1994;8:26–35. [21] Parker JE, Fubini SL, Car BD, et al. Prevention of intraabdominal adhesions in ponies by low-dose heparin therapy. Vet Surg 1987;16:459–62.