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In this VETgirl blog, we review treatment for canine leptospirosis, including further treatment for canine leptospirosis, along with zoonotic risks and preventive measures (e.g., vaccines, etc.).

Fluid therapy
In the leptospirosis patient, aggressive intravenous (IV) fluid therapy is indicated as many patients are often massively polyuric, dehydrated, and azotemic. In general, a balanced, maintenance, isotonic crystalloid (e.g., LRS, Norm-R) can be used at 2.5-4.5X maintenance, and monitoring of ins and outs may be necessary to guide treatment (based on the severity of polyuria seen in patients with leptospirosis). The patient should be assessed carefully to ensure that volume overload does not occur, particularly in patients with cardiopulmonary disease. Fluid therapy should be continued until azotemia and clinical signs resolve (typically 2-4 days); IV fluids should then be slowly tapered to ensure that polyuria has resolved and the patient can maintain hydration.

Goals of fluid therapy
Serial physical examination is imperative to adequately evaluate a patient’s hydration status—checking for return of skin turgor, appropriate weight gain, and moisture of mucous membranes. However, physical examination findings are subjective, and <5% dehydration is subjective and difficult to assess on physical examination. The concurrent use of evaluation of PCV/TS, blood glucose, blood urea nitrogen (BUN or AZO), weight, urine output (UOP), urine specific gravity (USG), and thirst can be used in conjunction with physical examination findings to better assess hydration status.

Packed Cell Volume/Total Solids, Blood Glucose, and Blood, Urea, Nitrogen (BUN/AZO)
Patients on IV fluids should have daily blood work (including PCV/TS, blood glucose, electrolytes, renal or biochemistry panel) assessed while hospitalized. Because patients often experience hemoconcentration when they are dehydrated (e.g., PCV/TS 55%/7.8 g/dl), the goal of fluid therapy is to ensure that these numbers improve with appropriate therapy (consistent with hemodilution). Ideally, the PCV/TS in a normal, systemically healthy patient on IV fluids at sea level should be 35%/5.0 g/dl. In fact, oxygen delivery is maximal at such a “hemodilute” PCV/TS, as there is less viscosity of red blood cells and “sludginess.” Note that some patients with leptospirosis may have a mild to moderate non-regenerative anemia; the goal should still be to hemodilute the patient, and total protein/solids should be used as a more appropriate guide in this situation. We can still evaluate the PCV/TS in abnormal, metabolically inappropriate patients. Classically, a 10% to 12% dehydrated, cachectic, geriatric cat with chronic renal failure may present to you with a PCV/TS of 28%/11 g/dl. Once that patient is adequately hydrated, the PCV/TS may decrease to 20%/7 g/dl, unmasking the anemia from lack of erythropoietin.

Urine Specific Gravity (USG)
In normal healthy patients, USG can be evaluated in patients on IV fluids to help assess hydration status. Ideally, USG should be measured before fluid administration to allow for evaluation of renal function. Dehydrated patients with concentrated urine demonstrate adequate renal function (cat > 1.040, dog > 1.025) – in other words, the kidneys are working and trying to absorb as much water from the urine as possible. Once started on IV fluids, normal, systemically healthy patients should have isosthenuric urine. Patients on IV fluids for > 6 to 12 hours should have adequate dilution of USG, and the ultimate goal of fluid therapy and adequate hydration should be USG of 1.015 to 1.018 on IV fluids. Patients on IV fluids with USG > 1.020 are still likely dehydrated and should be treated more aggressively with IV fluids if other parameters of dehydration persist (e.g., hemoconcentration). Hydration can be determined by assessing the color, volume, and USG of urine. A patient that is still dehydrated while hospitalized on IV fluids may have decreased UOP and dark-yellow urine (provided, for example, that no pigmentation, myoglobinuria, or bilirubinuria are present). This is a result of antidiuretic hormone release and renin-angiotensin stimulation, resulting in maximum absorption of free water and sodium. Unfortunately, in the leptospirosis patient, PU/PD may occur due to acquired nephrogenic diabetes insipidius, so utilizing USG as a guideline for hydration status will be difficult.

Urine Output (UOP)
UOP should be monitored carefully, particularly in azotemic patients with leptospirosis. Fluid therapy should be directed toward achieving a hydrated state and matching ins and outs, based on the patient’s UOP. Note that normal UOP is 1–2 ml/kg/hour, but many of these leptospirosis patients present with severe polyuria. Again, one can assess the hydration status of the patient by evaluating the volume and USG of urine. Excessive urination with dilute, clear urine may indicate copious or excessive IV fluid therapy, whereas hypersenthuria may suggest ongoing dehydration, and aggressive fluid resuscitation may be further warranted. If UOP is decreased (particularly in azotemic patients), fluid therapy and vasopressor support (to increase renal blood flow) should be initiated to prevent anuria (< 0.5 ml/kg/hour) or oliguria (< 1 ml/kg/hour). If UOP is decreasing and renal function is normal (based on creatinine, BUN, and pre–fluid therapy USG), the patient should be reassessed for hydration status, and fluid therapy adjusted as indicated.

• Normal UOP: 1–2 ml/kg/hour
• Oliguria: 0.5–1 ml/kg/hour
• Anuria: < 0.5 ml/kg/hour

Note that underlying diseases such as leptospirosis; postobstructive diuresis (posturethral obstruction); diabetes mellitus (with secondary osmotic diuresis due to glucosuria); diabetes insipidus; hyperthyroidism (increased glomerular filtration rate due to increased metabolic rate); and chronic renal failure (inability to adequately concentrate and absorb water) may result in dramatic water losses through the kidneys, and these patients may need a higher rate of fluids to compensate for ongoing losses. Likewise, these disease processes prevent us from differentiating renal versus prerenal disease on the basis of USG alone, as these patients have isosthenuria due to metabolic disease. Regardless, appropriate fluid therapy and urine monitoring (e.g., “measuring ins and outs”) may be necessary, particularly in azotemic, oliguric renal failure.

Antibiotic therapy
In the patient suspected of having leptospirosis, prompt, appropriate antibiotic therapy should be initiated (ideally after pre-treatment blood work has been submitted). Goals of antibiotic therapy is to eliminate leptospiremia and to eliminate leptospires from the renal tubular cells and renal carrier state). Appropriate antibiotics include penicillins (e.g., including ampicillin, amoxicillin, amoxicillin/clavulanic acid, penicillin, etc.) and doxycycline. In humans, the use of ceftriaxone and cefotaxime are also efficacious. The use of fluoroquinolones is controversial, as efficacy in a hamster model failed to clear leptospires from the kidneys and blood. Based on the ACVIM Consensus Statement, the antibiotic of choice is doxycycline (5 mg/kg PO or IV q. 12 hours for 2 weeks). Leptospires can shed in urine for months if appropriate antibiotic use is not implemented.

Gastrointestinal support
Azotemic patients should be treated with phosphate binders (e.g., aluminum hydroxide) if hyperphosphatemic, along with gastrointestinal protectants (e.g., omeprazole, pantoprazole, famotidine, sucralfate, etc.) for presumptive uremic gastritis. Anti-emetics (e.g., maropitant, ondansetron, dolasetron) should be implemented for patient comfort and to treat nausea.

• Maropitant: 1 mg/kg SQ q. 24 hours
• Ondansetron: 0.1-0.2 mg/kg IV q. 8-12 hours
• Dolasetron: 0.5-1 mg/kg SQ, IV q. 24 hours
• Metoclopramide: 0.1-0.5 mg/kg SC, IV q. 8 hours or 1-2 mg/kg/day as CRI IV

Gastric pH altering medication:
H2 blockers:
• Famotidine: 0.5-1 mg/kg IV, SQ q. 12-24 (least p-450)
• Ranitidine: 0.5-2 mg/kg, IV, PO, SQ q. 8-12 (moderate p-450)
• Cimetidine: 5-10 mg/kg IV, PO, SQ q. 6-8 (most p-450)

Proton-pump inhibitors:
• Omeprazole: 0.5-1 mg/kg PO q. 24 hours
• Pantoprazole: 1 mg/kg IV q. 24 hours

Sucralfate 100-1 g PO q. 8 hours

Zoonotic risks
In animals developing acute leptospirosis, caution must be taken to prevent zoonotic spread. The use of appropriate hygiene (including protective eye ware, gowns, gloves, etc.) should be used when handling the patient and bodily fluids while hospitalized. Pet owners should also be cautioned about the zoonotic risk. A 10% bleach solution, iodine-based disinfectant, accelerated hydrogen peroxide, and quaternary ammonium solutions can all be used against leptospires. Likewise, other pets in the house should be assessed for clinical signs, and if healthy, vaccinated to mount an immune response.

The prognosis for leptospirosis is fair to good, provided aggressive treatment can be initiated. The survival is reported to be approximately 80% in dogs, both with dogs treated conservatively (e.g., IV fluids) and those treated more aggressively with hemodialysis. In those dogs developing pulmonary complications, the prognosis is poorer, with reported mortality rates (from Europe) of 36-42%.1 Pet owners should be cautioned about the risks for chronic renal insufficiency as a secondary consequence of chronic renal inflammation.

As shedding of organisms can persist (e.g., leptospuria) for weeks to months, prevention is imperative. Despite the good prognosis for leptospirosis, aggressive preventative care is warranted in dogs. This will help minimize zoonotic risk to pet owners and veterinary professionals; help minimize the chronic carrier state in dogs (which can result in further spread); prevent costly hospitalization; and minimize the risk of chronic injury (chronic renal failure). A leptospirosis prevention package should be initiated with the following:

• Environmental changes: This should be initiated to include rodent control; appropriate fencing; and landscaping changes to remove stagnant/standing water.
• Annual vaccination: The decision to vaccinate should be based on an endemic area, exposure of the dog, and risk factors (e.g., access to streams/stagnant water or urbanized wildlife). Ideally, vaccination with a 4-way leptospirosis strain should be utilized. Vaccination is important to help prevent/aid in the prevention of shedding to reduce infection of other animals and possible human exposure.

Copyright, VETgirl, 2014.

1. Skyes JE, Hartmann K, Lunn KF, et al. 2010 ACVIM Small Animal Consensus Statement on Leptospirosis: Diagnosis, Epidemiology, Treatment, and Prevention. J Vet Intern Med 2011;25:1-13.
2. Winzelberg SE. Leptospirosis treatment and prevention with data on an ongoing leptospirosis prevalence study at the Animal Medical Center in New York City. Atlantic Coast Veterinary Conference Proceedings, 2013.
3. Goldstein RE, Lin RC, Langston CE. Influence of infecting Serogroup on clinical features of leptospirosis in dogs. J Vet Intern Med 2006;20:489-494.
4. Ward MP, Glickman LT, Guptill LF. Prevalence of and risk factors for leptospirosis among dogs in the United States and Canada: 677 cases (1970-1998). J Am Vet Med Assoc 2002;220-53:58.
5. Ward MP, Guptill LF, Prahl A, et al. Serovar-specific prevalence and risk factors for leptospirosis among dogs: 90 cases (1997-2002). J Am Vet Med Assoc 2004;224(12):1958-1963.
6. Ward MW, Guptill LF, Wu CC. Evaluation of environmental risk factors for leptospirosis in dogs: 36 cases (1997-2002). J Am Vet Med Assoc 2004;225(1):72-77.
7. Lee HS, Guptill LF, Johnson AJ, et al. Signalment changes in canine leptospirosis between 1970 and 2009. J Vet Intern Med 2014;28(2):294-299.
8. Stokes JE, Kaneene KB, Schall WD, et al. Prevalence of serum antibodies against six Leptospira serovars in healthy dogs. J Am Vet Med Assoc 2007;230(11):1657-1664.
9. Gautam R, Guptill LF, Wu CC, et al. Spatial and temporal-spatial clustering of overall and serovar-specific Leptospira microscopic agglutination test (MAT) seropositivity among dogs in the United States from 2000 through 2007. Prev Vet Med 2010;96:122-131.
10. Arbour J, Blais MC, Carioto L, et al. Clinical leptospirosis in three cats (2001-2009). J Am Anim Hosp Assoc 2012;48(4):256-60.
11. Zaitsev SV, Chernukha IuG, Evdokimova OA, et al. Survival rate of Leptospira pomona in the soil at a natural leptospirosis focus. Zh Mikrobiol Epidemiol Immunobiol 1989;2:64-68.
12. Barr SC, McDonough PL, Scipioni-Ball RL, et al. Serologic responses of dogs given a commercial vaccine against Leptospira interrogans serovar Pomona and Leptospira kirschneri serovar Grippotyphosa. Am J Vet Res 2005;66:1780-1784.
13. Truccolo J, Charavay F, Merien F, et al. Quantitative PCR assay to evaluate ampicillin, ofloxacin, and doxycycline for treatment of experimental leptospirosis. Antimicrob Agents Chemother 2002;46:848-853.

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