Leptospirosis

Katharine F. Lunn, Raleigh, North Carolina

Leptospirosis is a zoonotic bacterial disease of worldwide importance in human and veterinary medicine. Disease is caused by serovars of the pathogenic species Leptospira interrogans sensu lato. Infection is maintained in nature by mammalian reservoir hosts infected endemically with host-adapted strains. Examples of reservoir hosts include the vole and raccoon (both carrying serovar grippotyphosa), and the rat (serovar icterohaemorrhagiae and serovar bratislava). These hosts serve as a source of infection for incidental hosts, such as humans and dogs, through excretion of organisms in the urine. Survival of leptospires is optimum in warm and wet environments with stagnant or slow-moving water. Transmission to incidental hosts may be direct or indirect, through exposure to contaminated water, soil, food, or bedding.

Case reports and serologic surveys have demonstrated clinical and subclinical leptospirosis in dogs from many locations in North America. Because leptospirosis typically is contracted through indirect contact with the urine of wild animal hosts, it often has been assumed that working dogs, large-breed dogs, or dogs with an outdoor rural lifestyle are more likely to develop the disease. However, many clinicians, including this author, routinely diagnose leptospirosis in small-breed dogs and dogs that rarely leave the house and backyard. In support of this, it recently was shown that dogs in regions of the midwestern United States are at higher risk for leptospirosis if they live in urban areas (Raghavan et al, 2011). Thus any dog should be considered to be at risk, regardless of breed or lifestyle. The manifestations of leptospirosis in dogs range from peracute disease to subclinical infection and include sudden death, renal failure, hepatic failure, vasculitis, and uveitis. Because leptospires have zoonotic potential, veterinarians must maintain a high index of suspicion for this infection, particularly in those cases that do not have typical clinical signs. Feline leptospirosis rarely is recognized as a clinical entity; however, cats can be infected experimentally with the organisms and can seroconvert and shed leptospires in the urine. This chapter focuses on the clinical manifestations, diagnosis, and treatment of leptospirosis in dogs. There have been few new developments in the prevention of canine leptospirosis. Vaccination was discussed in the previous edition of this text (see Chapter 269 in the previous edition of Current Veterinary Therapy), in the 2011 American Animal Hospital Association Vaccine Guidelines (www.aahanet.org), and in the 2010 American College of Veterinary Internal Medicine Small Animal Consensus Statement on Leptospirosis: Diagnosis, Epidemiology, Treatment, and Prevention (Sykes et al, 2011).

Clinical Findings

Common Manifestations

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

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

Polyuria and polydipsia (PU/PD) in the absence of azotemia is a less common manifestation of the renal effects of leptospirosis. PU/PD could result from a decrease in GFR sufficient to cause loss of renal concentrating ability without azotemia. However, this PU/PD also may be 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.

Acute liver disease can accompany acute renal failure in dogs with leptospirosis, or it can occur alone. Affected dogs may be icteric, and serum biochemistry analysis reveals increased bilirubin and alkaline phosphatase (ALP) activity. Alanine aminotransferase (ALT) activity typically is less markedly increased than ALP activity. In humans and dogs, the icterus of acute leptospirosis appears to be associated with minimal histopathologic changes in the liver, suggesting that it is due to “cholestasis of sepsis” rather than hepatocellular damage.

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

Uncommon Manifestations

Petechial hemorrhages, epistaxis, melena, and hematemesis occasionally are seen in dogs with leptospirosis. These findings most likely are due to vasculitis. Affected dogs also may 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.

Pulmonary hemorrhage is one of the most common clinical signs in outbreaks of human leptospirosis. Reticulonodular pulmonary opacities have been described in the thoracic radiographs of dogs with leptospirosis and attributed to pulmonary hemorrhage (Baumann and Fluckiger, 2001). These changes may be diffuse or involve predominantly the caudodorsal lung fields. This was previously believed to be a rare finding in canine leptospirosis; however, clinical or radiographic signs of pulmonary disease have been noted in several dogs with leptospirosis, and recent case series suggest that pulmonary disease may be more common than suspected, at least in Europe (Baumann and Fluckiger, 2001; Klopfleisch et al, 2010; Kohn et al, 2010).

Uveitis is an uncommon manifestation of leptospirosis in dogs, although it may be underrecognized. Although uveitis is associated infrequently with experimental canine leptospirosis and has been reported only rarely in the literature (Townsend, Stiles, and Krohne, 2006), this author has observed it. Uveitis also has been reported in human patients with leptospirosis. In most human cases, uveitis occurs as a late complication after apparent recovery from leptospirosis and is likely immune-mediated. However, leptospirosis also can cause uveitis in the acute phase of the disease, in humans and animals, possibly associated with the vasculitis caused by the organism. In the horse, there is a well-known association between leptospirosis, uveitis, and periodic ophthalmia.

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

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