Clinical Manifestations of Leptospirosis in Dogs
ACVIM 2008
Katharine F. Lunn, BVMS, MS, PhD, MRCVS, DACVIM
Fort Collins, CO, USA

Introduction

Leptospirosis is a zoonotic bacterial disease of worldwide importance in both human and veterinary medicine.1 Disease is caused by serovars of the pathogenic species Leptospira interrogans sensu latu.2 Infection is maintained in nature by mammalian reservoir hosts that are endemically infected with host-adapted strains.3 Reservoir hosts do not typically develop clinical disease, but serve as a source of infection for incidental hosts, such as humans, through excretion of organisms in the urine. Survival of organisms is optimum in warm and wet environments with stagnant or slow-moving water, and transmission to incidental hosts may be direct or indirect, through exposure to contaminated water, soil, food or bedding.

Leptospiral organisms enter the host through intact mucosal surfaces or damaged skin. During the first week of infection, organisms multiply and spread throughout the vascular space, leading to vascular damage and invasion of many organs and tissues. During this initial leptospiremic phase organisms can be isolated initially from the blood, and later from cerebrospinal fluid. The immune phase of infection begins in the second week, with the appearance of serum antibodies. This leads to clearing of leptospires from the blood and many organs; however organisms may be protected from the systemic antibody response in sites such as the renal tubules and the eye. Leptospiruria develops in the second week after infection and can persist for days to months, depending on the species of the mammalian host and the infecting serovar.1-5

Pathological changes in leptospirosis include vasculitis and endothelial cell damage. Inflammatory infiltrates in tissues and organs may include neutrophils, monocytic cells, plasma cells and histiocytes.4 The precise mechanisms by which leptospires cause tissue damage and disease are not well understood.4 Several toxins and enzymes produced by the organisms likely contribute to disease pathogenesis. These may include lipopolysaccharide, hemolysins, and cytotoxins.4 The pathogenicity of leptospires may also be related to their motility and their ability to adhere to, and penetrate, cells.

Case reports and serological surveys have demonstrated both symptomatic and asymptomatic leptospirosis in dogs from many locations in the US and Canada.6-15 The manifestations of leptospirosis in dogs range from peracute disease to asymptomatic infection, and include sudden death, renal failure, hepatic failure, vasculitis, and uveitis.2 This discussion will review the common and uncommon clinical features of canine leptospirosis. Because this is a zoonotic disease, it is essential that veterinarians maintain a high index of suspicion for this infection, particularly in those cases that do not have typical clinical signs.

Common Clinical Manifestations of Canine Leptospirosis

Renal Disease

Acute renal failure has been the most common presentation for canine leptospirosis in recent years. Affected animals may present with lethargy, anorexia, vomiting, abdominal pain, and history of polyuria, oliguria, or anuria. Dogs that survive acute renal failure may return to normal, or progress to chronic renal failure. Leptospirosis should also be considered in any dog with previously diagnosed chronic renal disease that develops "acute-on-chronic" renal failure.

Acute renal failure may result from interstitial nephritis, renal swelling, and vasculitis, leading to decreased renal perfusion and decreased glomerular filtration rate (GFR). The leptospiral organisms also penetrate and colonize renal tubular cells. Renal tubular damage in leptospirosis may manifest as cylindruria, proteinuria or glycosuria.1

In humans, the acute renal failure of leptospirosis is often non-oliguric,16,17 and can be associated with hyponatremia and hypokalemia. These electrolyte changes have also been noted in canine leptospirosis, along with the expected changes of azotemia, hyperphosphatemia and acidosis of renal failure.15 The hypokalemia of acute renal failure in leptospirosis may be the result of decreased proximal tubular reabsorption of sodium leading to increased distal tubular sodium delivery with associated increased distal potassium secretion.17,18 These abnormalities may be caused by a Na+/K+ ATPase inhibitor associated with leptospiral endotoxin.19

Polyuria and polydipsia (PUPD) in the absence of azotemia is a less common manifestation of the renal effects of leptospirosis.8 PUPD may be due to a decrease in GFR that is sufficient to cause loss of renal concentrating ability without azotemia. However it is also possible that this PUPD is a form of nephrogenic diabetes insipidus. In guinea pigs experimentally infected with leptospirosis, the inner medullary collecting ducts of the renal tubules appear to be resistant to the effects of vasopressin.18

Hepatic Disease

Acute liver disease may accompany acute renal failure in dogs with leptospirosis, or it may occur alone. Affected dogs may be icteric, and serum biochemistry analysis reveals elevated bilirubin and ALP. ALT is typically less markedly elevated than ALP.8 In humans and dogs, the jaundice of acute leptospirosis appears to be associated with minimal histopathological changes in the liver, suggesting that it is due to the "cholestasis of sepsis" rather than hepatocellular damage.4,9,13,16 Chronic hepatitis has also been associated with leptospirosis in at least two groups of dogs.20,21 These patients may present with signs of liver failure.

Musculoskeletal Disease

Muscle pain, stiffness, weakness, trembling or reluctance to move can be seen in dogs with leptospirosis. These may be the result of vasculitis, myositis or nephritis. Myalgia is commonly reported in human leptospirosis, and is associated with the septicemic phase of the disease.4,5,16

Uncommon Clinical Manifestations of Canine Leptospirosis

Bleeding Disorders

Petechial haemorrhages, epistaxis, melena and hematemesis are occasionally seen in dogs with leptospirosis. These findings are most likely due to vasculitis. Affected dogs may also be thrombocytopenic, however platelet counts are rarely low enough to be responsible for spontaneous bleeding. The causes and mechanisms of bleeding disorders in leptospirosis are poorly understood, but they have been suggested to be associated with endothelial cell damage.22 Disseminated intravascular coagulation does not appear to be responsible for the thrombocytopenia seen in leptospirosis in humans.4

Respiratory Disease

Pulmonary haemorrhage is now one of the most common clinical signs in outbreaks of human leptospirosis.22 This is a rare finding in canine leptospirosis, however, along with other authors, we have noted cough or dyspnea, or radiographic abnormalities in some affected dogs.7,8,23

Uveitis

Uveitis is an uncommon manifestation of leptospirosis in dogs. It appears to be infrequently associated with experimental canine leptospirosis, but rare case reports exist in the literature,24,25 and it has been observed by this author. Uveitis has also been reported in human patients with leptospirosis.4,16,24 In most human cases, uveitis occurs as a late complication after apparent recovery from leptospirosis, and it is believed to be an immune-mediated disease. However, leptospirosis can also cause uveitis in the acute phase of the disease, both in humans and animals, and this may be associated with the vasculitis caused by the organism. In the horse, there is a well-known association between leptospirosis, uveitis, and periodic ophthalmia.24

Other Signs of Canine Leptospirosis

Additional clinical signs that have been reported in dogs with leptospirosis include vomiting, diarrhea, weight loss, fever, hypothermia, oculonasal discharge, lymphadenopathy, effusions, and edema.

Clinical Laboratory Findings in Canine Leptospirosis

CBC changes may include neutrophilia, lymphopenia, monocytosis, anemia (due to blood loss) and thrombocytopenia. Serum chemistry may reveal increases in blood urea nitrogen, creatinine, phosphorus, ALP, ALT, AST, CK, bilirubin, lipase and amylase.7,13 Electrolyte changes can include hyponatremia, hypochloremia and hypokalemia, or hyperkalemia. Metabolic acidosis may be present. Coagulation abnormalities may include increased fibrin degradation products and prolonged PT or APTT. Urinalysis may reveal hyposthenuria, isosthenuria or hypersthenuria, depending on the degree of renal involvement. Other changes may include proteinuria, glucosuria, cylindruria, hematuria, and pyuria. Leptospirosis could also potentially be associated with renal tubular acidosis.

Radiographic and Ultrasonographic Findings in Canine Leptospirosis

Reticulonodular pulmonary opacities have been described in the thoracic radiographs of dogs with leptospirosis, and attributed to pulmonary hemorrhage.23 These changes may be diffuse, or predominantly involve the caudodorsal lung fields. Abdominal radiographs may be unremarkable, or may show renomegaly or hepatomegaly.7,8

Changes noted on ultrasonography include renomegaly, pyelectasia, increased cortical echogenicity, perinephric effusion, and a hyperechoic medullary band.10 These changes are however not specific for leptospirosis, and absence of these findings does not rule out the diagnosis.

References

1.  Langston CE, et al. Vet Clin North Am Small Anim Pract 2003;33(4):791.

2.  Greene CE, et al. In: Infectious Diseases of the Dog and Cat, Greene (Ed), 3rd Ed, W. B. Saunders, Philadelphia, 2006; 402.

3.  Heath SE, and Johnson R. JAVMA 1994;205(11):1518.

4.  Levett, PN. Clin Microb Rev 2001;14(2):296.

5.  Farr, RW. Clinical Infectious Diseases 1995;21:1-8.

6.  Nielsen JN, et al. JAVMA 1991;199(3):351.

7.  Rentko VT et al. J Vet Intern Med 1992;6(4):235-244.

8.  Harkin KR, and Gartrell CL. J Am Anim Hosp Assoc 1996;32(6):495.

9.  Brown CA, et al. JAVMA 1996;209(7):1265.

10. Forrest LJ, et al. Vet Radiol Ultrasound 1998;39(4):337.

11. Adin CA, and Cowgill LD. JAVMA 2000;216(3):371.

12. Lunn KF, and Sawchuk SA. Proceedings of the 82nd Annual CRWAD Meeting, 2001.

13. Prescott JF, et al. Can Vet J 2002;43:955.

14. Stokes JE, et al. JAVMA 2007;230(11):1657.

15. Goldstein RE, et al. J Vet Intern Med 2006;20:489.

16. Bharti AR, et al. Lancet Infect Dis 2003;3:757.

17. Seguro AC, et al. Nephron 1990;55:146.

18. Magaldi AJ, et al. Nephron 1992;62:332.

19. Burth P, et al. Infect Immun 1997;65(4):1557.

20. Bishop L, et al. AJVR 1979;40(6):839.

21. Adamus C, et al. J Comp Pathol 1997;117(4):311.

22. Wagenaar JFP, et al. Trop Med Int Health 2007;12(1):111.

23. Baumann D, Flückiger M. Vet Radiol Ultr 2001;42(4):305.

24. Dziezyc J. Vet Clin N Am: Small An Prac 2000;30(5):1103.

25. Townsend WM, et al. Vet Ophthalm 2006;9(3):169.

Speaker Information
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Katharine Lunn, BVMS, MS, PhD, MRCVS, DACVIM
Laporte, CO


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