Case 9

Presentation:
A 6 month old intact male mix breed canine was presented to AcaseAweek Clinic as an emergency after being hit by car (HBC) the previous night. On physical exam the dog was bright, alert and responsive (BAR), has abrasions distal to the hock and on the metatarsal region of both hind limbs. Mild weight bearing lameness on the right hind limb was observed. Radiographs of the abdomen and pelvic region were normal. The abrasions were cleaned and dog was discharged on Rimadyl 25 mg BID for 5 days. Three weeks later the dog was brought to the clinic again with chief complaint of dyspnea and exercise intolerance.


Physical examination:

  • Temp: 101.5
  • HR/PR: 96
  • Respiration: Laboured breathing
  • Auscultation of thorax revealed muffled heart sounds and harsh lung sounds.
CBC, chemistry and electrolytes were all within normal range.

Thoracic radiographs were taken (lateral and VD view) and are shown below:


Give interpretation of the radiographs.
What is your diagnosis?
How will you treat and manage this case?

Solution for case 8


Tentative diagnosis: Hepatitis. An increase in AP, ALT and total bilirubin is indicative of liver problems. The mild elevation in total bilirubin explains the slightly yellow mucus membranes. The generalized lymphadenopathy and increased globulins could be indicative of a systemic infection that in this case is affecting primarily the liver, causing hepatitis.

Further diagnostic tests:
  • Paired serum samples
  • Serology
  • Immunofluorescence
  • Ultrasound
  • Liver biopsy
Differentials:
  • Infectious hepatitis: bacterial, fungal or other
  • Leptospirosis
  • Granulomatous hepatitis
  • Toxic hepatopathy
  • Fulminant infectious disease: parvovirus, canine distemper
  • Portosystemic shunting
Hepatitis can have many different causes. The main disease suspected to be causing the hepatitis is leptospirosis. Leptospira interrogans serovar Bratislava is very prevalent in the area and is not covered by the leptospirosis vaccine. The vaccine only includes serovars Canicola, Icterohemorrhagiae, Grippotyphosa, and Pomona. No cross protection exists between serovars. The typical clinical signs of leptospirosis are fever, depression, lethargy, anorexia, myalgia, vomiting, lumbar pain from renomegaly and nephritis, icterus, bilirubinuria, cholestasis and/or hepatic necrosis, renal failure. It has been reported that many young dogs suffer more from liver problems and not the kidney when infected with leptospirosis.
Extrahepatic bacterial or fungal infections could also cause hepatitis, but this case was not showing clinical signs of having an infection in other body systems that could have traveled to the liver. However, since the owner was not with the dog during the entire summer the patient could have developed a primary infection, that later traveled to the liver, but at the present time is not evident.

Many hepatotoxins such as high amounts of acetaminophen, aflatoxins, blue-green algae, heavy metals; certain herbicides, fungicides, insecticides and rodenticides could cause liver problems. No ingestion or access to any of these was reported by the owner.

Other causes of hepatitis are Canine Adenovirus-1, but this patient vaccinated. Toxoplasmosis is a rare disease because the body is usually able to eliminate the infection. However some young dogs are not able to control the infection and Toxoplasma tachyzoites invade tissues throughout the body and replicate intracellularly until cells burst, causing necrosis. If the Toxoplasma tachyzoites invade the liver clinical signs associated with hepatitis could be seen.

Canine cholangiohepatitis is rare and associated with ascending biliary tract infections (Salmonella sp., Campylobacter jejuni), choleliths, coccidiosis, and surgery of the biliary tract. Clinical signs include anorexia, vomiting, diarrhea, lethargy, PU/PD, fever, abdominal pain, hyperbilirubinemia and elevated AP and GGT. To make a definitive diagnosis samples should be submitted for aerobic and anaerobic cultures and sensitivity.

Idiopathic hepatic fibrosis is a rare disease in young dogs, usually less than 2 years of age, is not associated with any underlying inflammatory conditions. Clinical signs include ascites, hepatic encephalopathy, weight loss, vomiting, diarrhea, portal hypertension, portosystemic shunt, microcytic anemia, elevated AP and ALT and hypoalbuminemia. Microhepatica can be noted on radiographs.

Hepatic amyloidosis is a rare familial disease. Clinical signs include anorexia, PU/PD, vomiting, icterus and hepatomegaly. Diagnosis is made by identifying amyloid deposits in a liver biopsy. Glycogen storage disease is caused by a rare deficiency in glucose-6-phosphatase or in amylo-1,6-glucosidase, this results in a failure of glycogen to be released from the cell. Therefore, glycogen accumulates within the liver and other organs. Enzyme analysis of fresh frozen samples of liver, muscle or skin is needed for diagnosis. Prognosis is poor and most dogs succumb to these diseases at a young age.

Treatment of possible leptospirosis: Administration of 0.9% NaCl fluids IV to prevent dehydration was started along with antibiotic treatment with Ampicillin 500mg orally TID (three times a day). The patient is to be fed three times a day l/d diet in order to prevent any further liver damage and to try to increase body weight. A CBC test is to be repeated in three days to determine if the treatment plan is being effective and assess the health status of the patient.

Need to assess the health and degree of clinical signs in patient's kins. There may be need to look into familial disease.

Case 8

Presentation: 
A six month old, intact, male, mix breed dog (pothound) was presented to AcaseAweek Clinic with a history of anorexia, weight loss and lethargy. The dog has an indoor/outdoor lifestyle, is fed puppy Science Diet, is up to date on its vaccinations and is treated for ectoparasites with Adam’s spray. The owner was away during the summer and upon return found ticks on the dog. There are four other dogs in the household, one of them is showing similar clinical signs and happens to be this patient’s brother. 


Physical examination revealed that the patient was mildly depressed, alert and responsive, had a temperature of 100.4ºF, heart rate was 100bpm, respiratory rate was 12bpm and weighted 18.2 kg.

Ears, eyes, nose, throat: mild black, thick, tarry exudate on both ears. No ocular or nasal discharge observed.
Mucus membranes: grey, pale and slightly yellow (icterus). CRT<2>
Lymph nodes: generalized lymphadenopathy.

Laboratory tests:
Snap test: Ehrlichia, Heartworm, Anaplasma and Lyme disease negative.
CBC: unremarkable, except for mild eosinophilia.

Chemistry profile:
  • AP 1259 U/L (46-337)
  • ALT 673 U/L (8-75)
  • Glob: 4.1 g/dL (2.3-3.8)
  • TBIL: 1.3 g/dL (0.0-0.8)
Urinalysis- unremarkable.

What is your tentative diagnosis? Give list of differentials.
What diagnostic test(s) will you perform to confirm your diagnosis?
How will you treat and manage this case?


Solution for case 7



Radiographs showed that stomach has ingesta in it with some radiopaque materials. Large amount of gas was found in small intestine. Colon was full of fecal material with some radiopaque material.



Tentative diagnosis: Ehrlichea (because of thrombocytopenia) and foreign body in stomach



Further diagnostic tests:


4Dx SNAP test: Heart Worm - negative, Ehrlichea canis + Positive, Anaplasma – negative, Lyme – negative


Coagulation panel: to rule out the rodenticide poisoning.



Ehrlichea: Active infection confirmed by SNAP test, fever and thrombocytopenia are likely responsible for the epistaxis. Epistaxis is the most frequent hemorrhage due to ehrlichea. Increased BUN suggests the possibility of a GI bleed. The Ehrlichea also accounts for the fever and lymphodonopathy. Trauma and rodenticide poisoning are differentials.


Abdominal pain: With a Hx of being fed chicken bones and the multiple opacities in the lower GIT a foreign body (FB) is suggested. The radiographs showed a substantial amount of feces in the large colon with a large amount of gas in the small intestine which may suggest ileus/obstruction from a FB or constipation.

Treatment:

Doxycyline 10mg/kg (88mg) IV SID to treat Ehrlichea.

20cc warm soapy water enema and repeated later in the day to empty the bowel and see if that helps to evacuate the feces from the bowel and resolve the gas and abdominal discomfort. No fluid treatment was done due to the severe anemia.

Day 2:

The patient is QAR and still seems painful in the abdomen. The epistaxis has stopped.

Good appetite with no vomiting.

40cc warm soapy water enema was given but no defecation.

DAY 3:

QAR. Painful around the abdomen, reluctant to move. Pain seems to have become generalized. No further epistaxis.

Good Appetite without vomiting

Urinated on her own but still without defecation. 60cc warm soapy water enema was given, which in 15-20 minutes produced a moderate amount of liquid/soft feces.

PCV = 8%

TP = 6 g/dL

The patient was radiographed again and showed multiple FB in the stomach and increased gas in the small and large intestine as shown in the figure below:


Evening of Day 3


Temperature decreased sharply to 97.9.


Blood transfusion was given very slowly at a rate of 4mL/hr (0.5mL/kg/hr) for 30 minutes while checking TPR, MM, CRT every 5min as to ensure the patient was not having a transfusion reaction of increased respiratory effort, injected MM, or tachycardia. The only change was the temperature increased by 1 degree from 97.9 to 98.9.


After the initial 30minute transfusion trial the rate was increased to 6mL/kg/hr at 50mL/hr.


Two hours later the patient developed profuse diarrhea and respiratory distress.


The blood transfusion was stopped immediately.


Dexamethasone and Diphenhydramine were given IV in case of a delayed transfusion reaction. However, at night the patient died.

Case 7

Presentation:
A 7 month old, intact female mixed breed canine was presented to AcaseAweek Clinic as an emergency with epistaxis of one night duration and abdominal pain of about 5 days duration.
The owner has recently placed rat bait (Klerat = Bradisacoum) under the house. The owner does not believe the patient ingested any but is not certain.
The dog is fed people food and chicken bones.
The owner does not and is unable to monitor urination and defecation as the dog lives outside.
The owner does not believe there was any trauma to the patient.

Physical Exam:
  • Weight = 8.8kg
  • T = 104
  • mm = pale
  • P = 210
  • R = 40
  • EENT: Pale conjunctiva, epistaxis x1 day
  • C/V: Tachycardia, no other abnormalities heard
  • U/G: Brown/mucoid vaginal d/c.
  • GI: Very painful on abdominal palpation, mostly caudal abdomen.
  • LNN: Mildly enlarged pre-scapular and popliteal LN’s
  • The patient had a “hunched” appearance. The dog was shivering and had bloody nasal discharge (epistaxis). The epistaxis was more pronounced from the Right nare. The dog was also groaning.
CBC:
  • PCV = 9.0%
  • TP 6.0
  • WBC = 3.1
  • Plt = 41
  • CBC revealed a severe hemorrhagic regenerative anemia with severe thrombocytopenia, leucopenia and granulocytopenia. MCHC was borderline normal/elevated.
Blood Chemistry revealed hypoalbuminemia along with borderline normal/high BUN and borderline normal/low Creatinine and ALT. All other values were within normal limits.
Radiographs of abdomen were taken as shown in following pictures:Give interpretations of the radiographs.
What is your tentative diagnosis? Give your differentials.
What further tests you will do to confirm your diagnosis?
How will you treat and manage this case?

Solution to this case

Solution for case 6

Tentative diagnosis: Leptospirosis; Clinical signs with history of exposure to contaminated urine suggest leptospirosis.
Differential diagnosis:
  • Immune-mediated hemolytic anemia
  • Infectious canine hepatitis virus
  • Canine herpesvirus
  • Hepatic neoplasia
  • Trauma/bacteremia
  • Rocky Mountain spotted fever
  • Ehrlichiosis
  • Toxoplasmosis
  • Renal neoplasia/renal calculi
Leptospirosis is an infectious disease that can cause renal azotemia as the bacteria cause damage to the renal tubules decreasing the capacity of the kidneys to excrete urea. Also Creatinine levels could be high if the glomerular filtration rate of the kidney decreases in a renal failure. Usually dogs with subacute Leptospirosis will present azotemia, high liver enzymes (AP more high than ALT), icterus, dehydrated, mild anemic (Leptospirosis damaging RBC walls and endothelium) and 20% of dog with thrombocytopenia do to vasculitis. High liver enzymes are also observed in dogs with leptospirosis. All these signs make this patient a suspect of subacute leptospirosis. Also clinical signs and history of “rats around the environment” increase the suspicion of leptospirosis.
Urinary tract obstruction, a post renal condition (frequently in male dogs) can also increase BUN/Creatinine levels but usually clinical signs as hematuria and urinary incontinence will be seen in the dog. This was not in this case, as he was urinating with no signs of hematuria and no urinary incontinence.
Further diagnostic tests:
  • Leptospira isolated from blood and urine after 7-10 days of infection 
  • 2 weeks after infection use liquid culture to growth
  • Dark field microscopic, FA, Silver impregnation technique for tissue (Kidney, liver, lung) with the organism
  • Serology
  • Microscopic agglutination test
  • Not good if the dog was previously vaccinated, or infected or had passive immunity
  • ELISA (anti-lepto-antibodies), DNA probes, PCR
Treatment:
  • Supportive therapy (IV fluids) and antibiotics
  • Ampicillin: Leptospiremia
  • Dosage 5-10 mg/Kg IV, IM, SQ BID
  • Ampicillin 300 mg à 0.3 ml SQ BID
  • Doxycycline: eliminate renal carrier state
  • Dosage 5-10 mg/kg PO, SID
  • Doxycycline (100mg)tablets BID
  • Should be given for 1 month
Prevention:
  • Vaccination at yearly intervals and more often in enzootic areas
  • Be aware of new vaccines for Leptospirosis that induce immunity for new serovars
Be concern that it is a Zoonotic disease!!
  • Owner of the pet should be oriented about how to manage the dog and give the complete dose of antibiotics to eliminate the carrier stage
  • Clean the cage with bleach or diluted iodine
If the dog does not recover after the treatment further diagnostic test should be performed as kidney and/or liver biopsy, ultrasound, and x-rays.

Case 6

Presentation:
A 9 months old neuter male pothound dog that was brought to AcaseAweek Clinic for being lethargic, anorexic (not eating since 2 days), and vomiting. On the next day of hospitalization, the patient continued to be lethargic, anorexic, vomiting and became icteric. On detailed history the owner reported presence of rats around the patient’s environment.

Physical examination:
On the day of presentation:
  • T: 102.1
  • HR: 104
  • RR: 40
  • Tacky mucous membrane
  • Fleas
  • Vomiting
Next day:
  • T: 101.0
  • HR: 96
  • RR: 30
  • CRT: <2sec
  • Icteric
  • Lethargic
  • Not eating
CBC:
  • HCT: 32% (37.0-55.0)
  • HGB: 11.5 g/dl (12-18)
  • MCHC: 35.9 g/dl (30-36.9)
  • WBC: 10.8 x109/L (6.0-16.9)
  • Granulocytes: 9.3 x109/L (3.3-12.0)
  • PLT: 37 x109/L (175-500)
Biochemistry:
  • ALB: 2.6 g/dl (2.3-4.0)
  • ALKP: 879 U/L (23-212)
  • ALT: 184 U/L (10-100)
  • AMYL: 1260U/L (500-1500)
  • CREA: 7.9 mg/dL (0.5-1.8)
  • BUN: 130 mg/dL (7-27)
  • GlOB: 5.6 g/dL (2.5-4.5)
  • TP: 8.2 g/dL (5.2-8.2)
  • TBIL: 9.5 mg/dL (0.0-0.9)



What is your tentative diagnosis?
What are your differentials?
What further tests you will do to confirm your diagnosis?
How will you treat and manage this case?

Solution for case 5

Tentative diagnosis: Transmissible Venereal Tumor (TVT).
Differentials: Canine Herpesvirus, Lymphoma, or preputial blockage.
Further diagnostic tests: Fine needle aspirate to look at the cells of the lesion. 
After the aspirate was stained with Wright’s stain, large round cells with central nucleoli were seen. TVT is related to other round cell tumors such as a lymphoma or a mast cell tumor.  The round cell tumors appear microscopically as single cells, usually described as “discrete” because they are separate from each other.
Other diagnostic tests: Impression smear or biopsy of the lesion for histopathology
Transmissible Venereal Tumor is contracted through physical contact between animals.  They are found mostly on genitals, but also reported on nose, mouth, and anus.  The tumor presents as a cauliflower-like, pedunculated mass that is nodular in appearance, can often be ulcerated, inflamed and bleed easily.  Sometimes misdiagnosed as hematuria due to bloody discharge, which is why it is important to look closely at genitals and take appropriate samples.  TVT can initially grow quickly, but metastasis is uncommon (5%).    A complication of this tumor is urinary retention.  The urethra can be blocked and cause urine to retained in the body, which could lead to an acidosis.
On the top of our differential diagnosis list is Transmissible Venereal Tumor, but after that it was possible for this lesion to be Canine Herpesvirus, Lymphoma, or preputial blockage. 
Canine Herpesvirus could be ruled out because this is typically a disease of puppies less than 2-3 weeks old.  This virus is released in penile or vaginal secretions and could present as a raised sore on the penis, but this is very rare.  If it were, the most important thing to do immediately is to keep the pup warm as a low body temperature allows the virus to spread throughout the body. 
Lymphoma can be seen in extragenital lesions, but it could be ruled out after doing a fine needle aspirate of the lesion and due to the clinical signs.  A lymphoma or lymphosarcoma would show with enlarged lymph nodes and if a CBC would show a leukocytosis, along with the necrosis of the tumor inducing a neutrophilia.  Clinical signs would have been much more severe, affecting the spleen, liver or CNS.
Preputial blockage is a problem with intact males.  This is an accumulation of urine, secretions and debris in the prepuce which leads to infection and necrosis.  This could be ruled out because the lesion was on the penis and even if this infections spread to the penis, then necrosis would look black instead of fleshy and cauliflower-like. 
Treatment:
Vincristine sulfate was given weekly, while alternating the left and right cephalic veins.  After about 6 injections the lesions have been greatly reduced and once the tumor was resolved, one more injection was given. 
Vincristine is a mitotic inhibitor originally derived from the Vinca rosea plant.  It has an antineoplastic effect by disrupting and disassembling the microtubules in the cells.  It was given intravenously with a catheter in the left cephalic vein.  It was important that Vincristine is not administered perivascularly because it causes tissue sloughing.  It would cause such severe vesication and ulceration it could be so deep that tendons and bone would be exposed.  The other side effects of Vincristine are neurological. 
Doxorubicin is another chemotherapy drug used in the treatment of TVT.  This is an antineoplastic antibiotic, which destroys DNA.  Along with the similar side effect of myelosuppression, this drug can also cause perivascular sloughing as well as phlebitis and urticaria around injection site.   But the vesication caused by vincristine will eventually heal with proper bandaging while the damage done with Doxorubicin is beyond repair. Doxorubicin is cardio-toxic too.  
Surgery is not recommended for transmissible venereal tumors mostly due to the anatomic locations of the tumors.  It would be difficult to excise the lesions and ensure that the entire mass was removed.  Likelihood of recurrence is also more after surgery.

Case 5

Presentation:
One year old male intact Beagle/Pothound Mix was presented at AcaseAweek clinic for dripping of blood in urine. Eating and drinking of the patient was reported normal.


Physical Exam:

  • Weight: 14.1 kg
  • Temperature: 101.1°F
  • Heart rate: 108 bpm
  • Respiratory rate: 60 rpm
  • Mucous membranes were pink and moist and CRT was less than 2 seconds.
  • Popliteal lymph nodes were enlarged.  
  • A growth on the penis was observed as shown in the following picture:




What is your tentative diagnosis? Give differentials for your diagnosis.
What further tests you will perform to confirm your diagnosis?
How will you treat and manage this case?



Solution for case 4


Tentative diagnosis: Azotemia due to chronic renal failure (CRF).


Further diagnostic tests:
* Abdominal radiography/ultrasound to demonstrate decreased size of kidneys.


* Urine creatinine:protein ratio.


* Renal biopsy (not commonly performed).


* Blood pressure to demonstrate hypertension.


Isosthenuria is a common finding in chronic renal failure when two thirds of the functioning nephrons are lost.


Azotemia is seen when at least three fourths of the functioning nephrons are lost. Azotemia presents with increased BUN, creatinine, GI, and neurological clinical signs. This patient’s presentation would suggest that she has lost at least three fourths of her functioning nephrons.


Predisposing factors for CRF are age, chronic obstruction, infection, heart failure, and tubular disease. A urine sample taken from this patient, via a cystocentesis, ruled out bacterial infection. Patient’s heart sounded normal on auscultation. The renal failure was attributed to her age.


Management of chronic renal failure is a multifactor process. Most importantly hydration and electrolytes must be maintained with in normal limits. An appropriate renal diet will be low in protein, phosphorous, and sodium. Some other factors which must be addressed in the management of chronic renal failure include anemia, proteinuria, and gastrointestinal processes.


Anemia is due to decreased production of erythropoietin by renal peritubular cells. The anemia could also be from blood loss via GI ulcers, or iatrogenic from blood draws. The anemia is non-regenerative normochromic normocytic.


Treatment of anemia with erythropoietin (EPO) is indicated when the PCV falls below 18% and the patient is showing clinical signs of anemia/hypoxia. Caution must be used with EPO since it is of human origin. Dogs can produce antibodies against it. In severe anemia requiring immediate relief of clinical signs a blood transfusion can be done.


Proteinurea is seen because glomeruli have been damaged enough to allow loss of protein and anti-thrombin III. This decreases oncotic pressure, leading to edema. The loss of anti-thrombin III causes coagulation issues. Many of these patients have pulmonary thromboembolism as a complication.


These patients can be treated with angiotensin converting enzyme inhibitors which decreases the pressure in the glomeruli by dilating the efferent renal artery. This decrease in pressure helps prevent loss of proteins into the urine. Canine patients with CRF and proteinuria tend to have a decreased survival.


GI ulcers and nausea and vomiting are the common clinical signs seen. Uremic toxins activate the chemoreceptor trigger zone which leads to the nausea and vomiting. These uremic toxins also increase gastrin production which increases hydrochloric acid production in the stomach, leading to GI ulcers.


These complications are treated by decreasing the uremic toxins via hydration; protecting the stomach by decreasing acid production, and controlling the nausea and vomiting by blocking the chemoreceptor trigger zone. Acid production can be decreased using histamine blockers or proton pump inhibitors. Sucralfate can be used to protect/coat ulcers. The nausea can be controlled with medication targeted at dopamine antagonism, serotonin, or neurokinin.


Treatment:
Hospitalize patient
– NPO
– Fluid diuresis to decrease azotemia
* * Maintenance: 60ml/kg/24 hours = 2100ml
* * Deficit (5%) = 1715ml
* * Total fluid/day = 3850ml (160ml/hr)
– Decrease gastric acid and control N/V
* * Famotidine 20mg Q12 hours
* * Anti-emetic - Cerenia (maropitant citrate)
– Re-evaluate
* * BUN, Creatinine, Phosphorus every 48 hours
* * PCV and TP daily

The patient remained azotemic.
– After 3 days, fluids increased to 250ml/hr during the day and 160ml/hr during the evening.
– NPO
– Continue H2 blocker and Cerenia
– Continue to monitor BUN, SCr, TP, PCV, Phosphorus
The patient did not improve and was euthanized on consultation with owner.


See following Links for more info on CRF:


http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/130603.htm


http://courses.vetmed.wsu.edu/vm552/urogenital/crf.htm


http://www.marvistavet.com/html/body_chronic_renal_failure.html


http://www.felinecrf.com/what0.htm

Case 4

Presentation:
A 12 year old spayed female Labrador was presented to AcaseAweek Clinic with one week history of vomiting, decreased appetite and lethargy. Bad breath of the pet was also a complaint. The patient was brought to clinic 4 month back for ehrlichia and mild azotemia. She is currently on Hill’s k/d diet.
Physical exam:
  • Weight: 34.8 kg
  • Temperature: 100.7
  • Pulse: 136
  • Respiration rate: 28
  • Mucus membranes: pale
  • Capillary refill time: > 2 seconds.
  • Dehydration: ~5%
  • Abdomen was tender upon palpation.
Lab tests: (Reference Values)
  • BUN: 112 mg/dl
  • Creatinine: >13.6 mg/dl
  • Phosphorous: 16.1
  • PCV: 25%
  • USG: 1.011
  • TP: 6.4 mg/dl
  • Albumin: 2.7 mg/dl
  • Non-regenerative anemia was also noted.



What is your tentative diagnosis?
Give differentials for your diagnosis.
What further diagnostic test(s) will be performed to confirm the tentative diagnosis?
How will you treat and manage this case?

Solution for case 3


Diagnosis:
A 4Dx snap test was performed and was positive for Anaplasma. Normal clinical signs seen with Anaplasma are fever, lymphadenopathy, splenomegaly, weight loss with a history of tick infestation. Lab finding are normally thrombocytopenia, non-regenerative anemia and decrease in white blood cells, hyperproteinemia, hyperglobulinemia, hypoalbuminemia, and increase ALT. Lymphadenopathy and polyarthritis is sometimes seen and petechial hemorrhages or epistaxis due to the thrombocytopenia.

The snap 4DX test identifies both IgM (acute exposure) and IgG (chronic exposure) antibody responses to Anaplasma platys (previously known as Ehrlichia platys) and it infects the platelets leading to thrombocytopenia.

Dogs become infected with Anaplasma spp. when a feeding tick inoculates the organisms. The rickettsia enters the granulocytes, platelets, or macrophages, where it survives and multiplies, and spreads throughout the body. Anaplasma is maintained in a tick vector/vertebrate reservoir host system. 

Other diagnostic tests:
Urinanalysis, bone marrow or lymph node biopsy, abdominal radiographs. We can also go for blood smear stained with Giemsa stain. PCR has also been developed for this condition. 

Differentials:
Rocky mountain spotted fever, multiple myeloma, chronic lymphocytic leukemia, lymphoma, ehrlichia and immune mediated thrombocytopenia. But, since this patient was positive for Anaplasma on the 4Dx snap test, the differentials can be ruled out.

Treatment:
Anaplasma species infections in dogs usually respond to treatment with doxycycline, a treatment regimen of 10mg/kg for 28 days is currently recommended. This patient was admitted to the clinic and IV LRS fluids were given at 180 ml/hr. He was also given doxycycline at 200 mg PO BID for 28 days. This will help clear the infection, but some side effects you must watch out for are nausea, diarrhea, vomiting, upset stomach, loss of appetite, dysphagia, and a possible hypersensitivity to the drug.

Protective immunity does not develop and re-infection may occur following treatment, which would require additional courses of therapy. Vaccines are not available to prevent infections. Therefore, control and prevention of ticks is the key.  Brown dog ticks transmit this infection.

Click here to see image of Anaplasma morula in a Neutrophil and diagnostics.

Click here for a case report of Anaplasma in young dog. 

Click here for more description about Anaplasma.

Case 3

Presentation:
A 5 year old castrated male Rottweiler Labrador mix canine was presented at AcaseAweek Clinic for lethargy and inappetence for the past 4 days. He was still drinking water, and urinating normally. The diet consists of adult dry food, Alpo, of which he is eating less of. He has also lost a lot of weight recently.  Vaccinations were giving 12 days ago, and the dog is currently on ivermectin.
Physical Exam:
The patient weighed 20 kg (44 lbs) on physical exam, he was lethargic. His temperature was 103.2, pulse rate was 100 and respiration rate was 40. Mucus membranes were pink, and CRT was less than 2 seconds.  On physical exam there were enlarged pre-scapular and popliteal lymph nodes.  All other systems were within normal limits.
CBC and Blood Chemistry:
On general blood chemistry, all the values fell within normal limits except for ALT which was slightly increased, 166 (10-100).         The complete blood count revealed a hematocrit of 28.1 (37.0 – 55.0), hemoglobin of 10.2 (12.0 – 18.0), granulocytes of 3.1 (3.3 – 12.0), neutrophils of 1 (2.8 – 10.5), eosinophils of 2.1 (0.5 - 1.5) and platelets of 36 (175 – 500).

What is your tentative diagnosis?
Give differentials for your diagnosis.
What further diagnostic test(s) will be performed to confirm the tentative diagnosis?
How will you treat and manage this case?

Solution for case 2


Problem List:Hemoperitoneum
Cardiac arrhythmia and murmur
Poor peripheral perfusion
Mild anemia with marked regeneration
Moderate leukocytosis due to moderate neutrophilia
Mild lymphopenia
Mild thrombocytopenia
Mild↑ALKP, ALT
Mild↑amylase
Mild↑total bilirubin
Marked↑BUN and creatinine
Marked↑phosphate
Isosthenuria (single reading)
Moderate hematuria and bilirubinuria
Mild proteinuria
Anorexia, depression, lethargy
Vomiting
Marked weight loss and muscle atrophy


Primary problems on this patient are hemoperitoneum and acute renal failure.


Differentials for hemoperitoneumHemangiosarcoma (spleen/liver)
Coagulopathy (rodenticide)
Abdominal trauma


Differentials for acute renal failure
Ischemia due to hypovolemia, hypotension, shock or DIC
Nephrotoxicity (exogenous or endogenous toxins)
Immune mediated glomerulonephritis
Infectious (e.g. Leptospirosis, pyelonephritis)


Regarding the differentials for hemoperitoneum, hemangiosarcoma is the most likely. Hemangiosarcoma is most common in middle-aged to older dogs. Marked weight loss and muscle atrophy noted on physical exam may be suggestive of neoplasia.

The patient’s history and clinical signs are consistent with sudden rupture of splenic hemangiosarcoma causing hemorrhagic effusion into the abdominal cavity. Dogs with ruptured splenic hemangiosarcoma will commonly have abdominal enlargement due to hemoabdomen, pallor and hypotension. Poor peripheral perfusion and hypovolemia are evidenced by increased CRT and pulse deficit on physical exam. CBC with ruptured splenic hemangiosarcoma typically shows evidence of a recent bleed (marked regeneration with a mild decrease in PCV). Leukocytosis due to mature neutrophilia and thrombocytopenia are common CBC abnormalities noted in dogs with hemangiosarcoma of the spleen or liver. Mild lymphopenia may be a ‘stress’ response. High liver enzyme activity may be seen with hemangiosarcoma involving the liver. Mildly elevated liver enzymes are more likely pre-hepatic in origin; secondary to hypovolemia, hypotension and poor perfusion of hepatocytes. The icterus is most likely hepatic in origin, due to impaired uptake and conjugation by the underperfused liver. Mild pancreatic amylase increase is likely also secondary to decreased perfusion.

Regarding other differentials for hemoperitoneium, coagulopathy associated with rodenticide toxicity is less likely than hemangiosarcoma since there was not evidence of intrathoracic bleeding. With hemothorax, clinical signs of coughing, thoracic pain and/or dyspnea would be expected. There was also no history of possible ingestion. Abdominal trauma was ruled out on lack of history or any other evidence of a traumatic event.

This patient’s remaining problems are consistent with acute renal failure (ARF). The patient demonstrated a marked azotemia and hyperphosphatemia due to build up of nonprotein nitrogenous waste products and phosphate which are normally removed by the kidneys. Hypovolemia indicates that there is at least a partial pre-renal component to the azotemia. However if her azotemia was strictly pre-renal with tubular function intact, urine should be concentrated (SG >1.030) in the face of reduced renal perfusion. Patient’s urine SG of 1.013 is in the isosthenuric range, implying that kidneys are unable to adequately concentrate urine despite azotemia. Unlike pre-renal azotemia, renal azotemia is usually irreversible and is caused by extensive morphological or functional glomerular lesions with a loss of more than 75% of functional nephrons. On urinalysis, proteinuria and hematuria are supportive of glomerular damage.

Clinical signs of ARF are mostly caused by severe uremia and include lethargy, vomiting, anorexia and dehydration. The rapid build up of uremic toxins often causes the animal to become profoundly systemically unwell. Severe metabolic derangements are common, particularly hyperkalemia and metabolic acidosis. Electrolytes were not run on this patient, however hyperkalemia likely contributed to the arrhythmia noted on physical exam and being non-tachycardic despite being hypovolemic/hypotensive. Diagnosis of ARF relies on evidence of a sudden elevation in urea and creatinine, but definitive diagnosis would require renal biopsy or post mortem.

The cause of ARF is debatable. The most likely scenario is that this patient had a splenic hemangiosarcoma which ruptured 2-3 days before she was presented. Subsequent uncorrected hypovolemia and hypotension caused secondary insult to abdominal organs and renal failure due to prolonged ischemia. Multiple factors may have contributed to acute renal failure, and it is possible that patient had some degree of renal insufficiency prior to the ischemic insult which merely pushed her over the edge.


Emergency treatment:
IV catheter (20 G) – L cephalic vein
LRS @ 40 mL/hour (maintenance)
Urinary catheter – closed system


Owner did not want any other diagnostic tests performed and requested euthanasia and necropsy.


Further diagnostics (if patient was not euthanized):
Coagulation panel (OSPT to rule out rodenticide toxicity)
Abdominal ultrasound (hemangiosarcoma search)
Cardiac ultrasound (splenic HSA – often concurrent R atrium involvement)
Electrolyte panel (potassium level) → correct imbalances
Repeat urinalysis (confirm isosthenuria, monitor ARF)


Treatment of hemagiosarcoma is supportive and anti-neoplastic drugs. However, prognosis is Grave.


Necropsy findings:
About 500 ml of fluid was reported in abdominal cavity. Ruptured splenic mass of about 12 cm in size was also found and submitted for histopathology. Histopathology confirmed hemangiosarcoma.
Follow these two links for more information about the hemangiosarcomas:



Case 2

A 13 year old, female spayed, mixed breed dog was presented to AcaseAweek Clinic with history of collapse, depression, lethargy and vomiting 3 times the night before presentation. The patient had been anorexic for the past 2 days and appeared healthy previously. The patient lives mostly inside and her owner reported no possibility of accidental ingestion of foreign body or chemicals. Her vaccination status is current and she is on heartworm preventative. She was treated for Ehrlichiosis with doxycycline two months back.

Physical Exam:
Remarkable weight loss and muscle atrophy.
T: 98
P: 88
R: 44
MM: pale pink
CRT> 2 sec

Cardiovascular: murmur, cardiac arrhythmia, pulse deficit.
Respiratory: lungs sound clear
Abdomen: distended, positive succession, moderately painful

CBC/Cytology:
PCV: 23% [37-55]
WBC: 28.9 x103/μL [6-16.9]
Mature Neutrophils: 26.3 x103/μL [3.3-12]
Band Neutrophils: 0.6 x103/μL
Lymphocytes: 0.3 x103/μL
NRBC: 0.9 x103/μL
Smear: Platelets: 1-4/hpf
RBC morph: marked polychromasia, moderate anisocytosis

Biochemistry:
ALKP: 267 U/L [23-212]
ALT: 164 U/L [10-100]
AMYL: 2490 U/L [500-1500]
BUN: 130 mg/dL [7-27]
CREA: 6.1 mg/dL [0.5-1.8]
PHOS: >16.1 mg/dL [2.5-6.8]
TBIL: 1.4 mg/dL [0-0.9]

Urinalysis:
Bilirubin: ++
SG: 1.013
Blood: +++
pH: 5.0
Protein: +

Abdominocentesis:10 mL fluid was withdrawn.
Abdominal Fluid Analysis/Cytology:
Color: red
Turbidity: 3+
Protein: 7.2 g/dL
PCV: 23%
Smear: many RBCs, neutrophils and macrophages, moderate lymphocytes, almost no platelets seen, few reactive mesothelial cells.
What will be your tentative and differential diagnosis?
What further diagnostic test(s) you will perform to confirm your diagnosis?
What will be your treatment plan(s)?



Solution to this case