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The Puking Puppy


A 12-week-old, partially vaccinated, 1.1kg poodle mix presented to me with vomiting, diarrhea, inappetence and lethargy. My pattern-recognition loving mind jumped to two primary differentials, parvovirus and dietary indiscretion (and all the complications that brings in a 1.1kg puppy). However, after reviewing the record, I determined that the patient had multiple normal blood glucoses and a negative parvo test over the prior 72 hours.

This patient had two distemper/parvovirus vaccines, two routine dewormings, and had not received any heartworm, flea, or tick medications. Blood work at the primary veterinarian was performed on the first day of the puppy’s illness (3 days prior to presentation). A complete blood count (CBC) and serum biochemistry chemistry profile showed the following abnormalities: an elevated leukocytosis (total WBC 18.9 X 103 ) characterized by a mature neutrophilia (12.9 X 103 cells/µL) and monocytosis (1.5 X 103 cells/µL); normocytic, normochromic anemia (hematocrit 33%); an elevated serum alkaline phosphatase (ALKP) (456 U/L), gamma glutamyl transaminase (GGT) (17 IU/L), total bilirubin (TBILI) (1.3mg/dL), urea nitrogen (BUN) (35 mg/dL) and BUN/creatinine ratio (88). A low creatinine of 0.3mg/dL was noted. Additionally, a fasting bile acid was performed (49.7umol/L). While these results were pending, the patient was started on amoxicillin and lactulose. No improvement was noted with this treatment. When she failed to improve, the patient was referred for further assessment.

On presentation to me, the puppy was depressed, dehydrated (7-8%), tachycardic (188bpm), and in emaciated body condition with melena present on rectal exam. A parvovirus SNAP test, CBC, and chemistry were repeated. The SNAP test was negative. The CBC showed similar changes to the leukogram as previously noted, but also showed progression to a severe microcytic, hypochromic, non-regenerative anemia (HCT 14%). The chemistry showed elevated (ALKP) (166 IU/L), (TBILI) (0.5mg/dL), (BUN) (40mg/dL), BUN/creatinine ratio (200) and panhypoproteinemia- (ALB) (2.5mg/dL) and (GLOB) (1.5mg/dL).

An abdominal ultrasound showed no evidence of an extrahepatic shunt. A fecal float and leptospirosis PCR and titers were submitted.  Fluid resuscitation, antibiotics, and a packed red blood cell transfusion were performed. After twenty-four hours of care the puppy was significantly brighter, began to eat, had no vomiting, and improved stool consistency. Blood work showed improvements in all values. The fecal float was negative for observed parasites. Treatment was continued for an additional twenty-four hours. The next morning the leptospirosis PCR and titers were available for review. The PCR was positive and the titer panel showed a 1:200 value for L. grippotyphosa and L. icterohaemorrhagiae. All other serovars were less than 1:100. At that time further discussion with the owner indicated that the patient was allowed to play in a flooded drainage ditch near the home. We recommended changing antibiotics to doxycycline (5mg/kg PO Q12).

One week later the patient returned for a repeat exam and PCR. At home the patient was doing very well with no vomiting or diarrhea. The owner reported a ravenous appetite and on exam we noted that her weight had increased by nearly 0.5kg. The leptospirosis PCR was negative at that time.


Patients with leptospirosis most frequently develop renal or hepatic failure.

Patients with renal failure can have clinical signs of dehydration, vomiting, diarrhea, polyuria, polydipsia, and lethargy. Oliguira or anuria may also occur if renal failure progresses. The puppy discussed in this report had signs of dehydration, vomiting, diarrhea, and lethargy. While these signs can be associated with renal failure they are non-specific and can be associated with many other disease processes- including gastroenteritis. This puppy never developed a creatinine outside of the reference range but did experience a 4-fold increase in creatinine value. This degree of increase is consistent with an acute kidney injury. 

Dogs with leptospirosis that develop liver involvement may show vomiting, diarrhea, lethargy, hypoglycemia, clotting abnormalities, and icterus. As previously mentioned, vomiting, diarrhea, and lethargy were present in this puppy. Liver pseudofunction markers (albumin, cholesterol, BUN, tbili, glucose) had variable changes in this patient. Albumin was initially normal on blood work performed by the primary care veterinarian, but when the patient developed gastrointestinal bleeding both the albumin and globulin became decreased. The BUN was persistently elevated, but given the presence of gastrointestinal bleeding it is difficult to say if the liver’s production of BUN was adequate or if the level was falsely elevated. Cholesterol remained within the reference range. We noted a persistent elevation in bilirubin levels and an elevated fasted bile acids value. While the signalment and the elevated bile acids may raise suspicion for a portosystemic shunt, the elevated bilirubin and normal abdominal imaging make this unlikely. There was no evidence of a pre-hepatic or post-hepatic source for the elevated bilirubin making primary hepatic disease the likely cause of the patient’s elevation in bilirubin.

This case is an unusual presentation of leptospirosis. The patient was a young, incompletely vaccinated puppy with clinical signs most consistent with viral gastroenteritis. Initially, we presumed that the first Parvoviral SNAP test was a false negative and this spurred our decision to repeat the test. After the second negative result we pursued further investigation of her mildly elevated liver values. Given her age, an infectious disease process was suspected. We also noted that, while normal, the patient’s creatinine increased from 0.2mg/dL to 1.1mg/dL. At the time, the Veterinary Health Center at Kansas State University had seen a rise in the number of leptospirosis cases. The recent increase in leptospirosis cases combined with the patient’s elevated liver values and increasing creatinine level prompted submission of the leptospirosis titers and PCR.

So what is the moral of the story? Puking puppies are probably parvo or dietary indiscretion. But, if these differentials are excluded, consider other infectious disease testing based on outbreaks in your local area and clinical signs.

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