Volume 4 | Issue 1 (January 2002)


Veterinary Neurology and Neurosurgery Journal (VNNJ) Case Study 9

Vet Neurol Neurosurg J. January 2002;4(1):1.
Andrew MacLean Isaacs1, Todd W Axlund2
1 Auburn University Small Animal Clinic; 2 Auburn University Small Animal Clinic

Full Text Article (What's Your Diagnosis?)

December, 2002

Signalment, History, Physical Examination   Neurological Examination   Tests Performed   Case Summary/Final Diagnosis

Signalment, History and Physical Examination

Signalment: 4 year old, castrated male, DSH

History: Two weeks prior to presentation to the referring veterinarian, the cat developed a shifting lameness and anorexia. These signs responded to parenteral corticosteroid treatment. However, three days prior to presentation the lameness returned and progressed to tetraparesis. The referring veterinarian's laboratory investigations yielded no helpful information. A SNAP (in house ELISA) test for FeLV/FIV status yielded negative results. Samples for FCoV and toxoplasmosis titers were submitted and treatment with prednisone and clindamycin was initiated before referral to the Auburn University Small Animal Clinic

At time of presentation to the Auburn University Small Animal Clinic:
Medications: Prednisone: 1 mg/kg PO BID, clindamycin 15 mg/kg PO BID

Physical Examination

 General Condition: Lethargic; obese.

 Rectal temperature: 97.7

 Integument: Within normal limits (WNL)

 Eyes, ears, nose and pharynx (EENT): WNL

 Cardiopulmonary: heart rate = 64/min; respiratory rate=15 per minute with open mouth breathing, normal lung sounds. Capillary refill time = 2s, mucosae pink.

 Abdominal Cavity: Urinary bladder markedly distended, large amount of feces in the colon.

 Musculoskeletal: generally weak, otherwise WNL

 Lymph Nodes: WNL

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Neurological Examination

 Posture: laterally recumbent

 State of Consciousness and apparent mentation: N

 Gait: Can not stand and support weight, tetraparetic

Sensory Systems Examination (note depressed, absent, asymmetric or misdirected responses)

 Somatosensory: N

 Visual: N

 Olfactory: Not examined

 Auditory: N

 Gustatory: Not examined

Placing and Postural Reactions

 Proprioceptive Placing Reactions:

 Thoracic limb: Left: A - Right: A

 Pelvic limb: Left: A - Right: A

 Hopping/Wheelbarrow: A

 Extensor Postural Thrust: A

 Visual & Tactile Placing Reactions: A

Segmental (Spinal) Reflexes: N (Left/Right) (N=Normal, D=Decreased, I=Increased, A=Absent)

 Thoracic Limb

 Tendon Reflexes

 Biceps A/A

 Triceps A/A

Flexor Reflexesand response to deep pain: Decreased withdrawal with good deep pain sensation

 Crossed Extensor Reflex: A/A

 Pelvic Limb

 Tendon Reflexes

 Patellar N/N

 Gastrocnemius N/N

Flexor Reflexes and response to deep pain: Normal with good deep pain sensation

 Crossed-extensor Reflex A/A

 Perineal Reflexes: N

 Cutaneous Trunci Reflex: absent along entire dorsum

Cranial Nerves

 I: Not tested.

 II: Normal visual fields. PLR - Equal pupils with intact direct and consensual responses. Normal menace reflex.

 III, IV, VI: Normal physiological nystagmus present without positional nystagmus or strabismus. Pupils normal and of equal size. Pupillary light reflexes normal bilaterally.

 V: Normal motor and sensory function present on both sides.

 VII: Normal facial symmetry and normal movement of the muscles of facial expression.

 VIII: Normal clinical response to auditory stimuli each ear. No head tilt, positional nystagmus or strabismus noted.

 IX, X, XI: Normal swallowing action was noted with stimulation.

 XII: The tongue musculature was symmetrical and tongue movements were normal.

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Tests Performed

Hematology, Chemistry and Urinalysis

Clinical Chemistry Laboratory Results

Constituent

Patient's Results

Units

Reference Range (Cat)

Alk. Phosphatase

18

U/L

6 - 51

ALT (SGPT)

35

U/L

26 - 52

Bilirubin: total

0.10

mg/dl

0.15 - 0.66

Blood urea nitrogen (BUN)

19.3

mg/dl

5 - 30

Calcium

9.5

mg/dl

9.5 - 11.6

Cholesterol

122

mg/dl

0 - 239

Creatine kinase

393

U/L

100 - 250

Creatinine

0.9

mg/dl

0.0 - 1.5

Glucose

168

mg/dl

58 - 116

Electrolytes:

Anion gap

14.5

mmol/l

6.9 - 22.5

Chloride

109.7

mmol/l

119 - 133

CO2, total

28.9

mmol/l

12 - 30

Potassium

4.05

mmol/l

3.3 - 5.7

Sodium

149.0

mmol/l

150 - 164

Magnesium

2.7

mg/dl

1.46 - 2.20

Phosphorus, inorganic

6.3

mg/dl

4.3 - 5.9

Proteins:

Albumin

3.7

g/dl

2.8 - 3.7

A/G ratio

0.8

 

0.0 - 100.0

Globulin

4.7

g/dl

2.7 - 4.4

Total protein

8.4

g/dl

6.2 - 7.7

Osmolality Calculated

306

MOsm/k

270 - 305

Hemogram Results

Parameter

Patient's results

Reference Values (Cat)

Erythrocytes

8.27

5.0 - 10.0

Hemoglobin (Hb)

12.2

8.0 - 15.0

Hematocrit

37.0

30.0 - 45.0

Mean corpuscular volume

44.7

39.0 - 55.0

Mean corpusc. Hb

14.7

13.0 - 17.0

Mean corpusc. Hb conc.

33.0

30.0 - 36.0

Reticulocytes

0

 

Leucocytes

14.37

5.5 - 19.5

Band

0

 

Neutrophils

13220

2500 - 12500

Lymphocytes

862

1500 - 7000

Monocytes

287

0 - 850

Eosinophils

0

0 - 750

Basophils

0

0 - 100

Platelets

170

300 - 700

PLT EST

Plt. Est. Adequate

 

Cell Morphology

2+ platelet clumps

 

Urinalysis Results

Parameter

Result

Method/Units

Turbidity

Slightly hazy

Visual

Color

Yellow

Visual

Specific gravity

1.035

Refractometer

pH

7.0

Reagent strip

Protein

Negative

Acid PPT

Glucose

Negative

Reagent strip

Ketones

Negative

Reagent strip

Bilirubin

Negative

Reagent strip

Urobilinogen

0.2 EU/dL

 

Bilirubin

Negative

Reagent strip

Occult blood

Negative

Reagent strip

Sediment

   

Leucocytes

Rare

range/high power microscope field

Erythrocytes

None

range/high power microscope field

Epithelial Cells

None

 

transitional

 

range/high power microscope field

squamous

 

range/high power microscope field

renal

 

range/high power microscope field

Casts

None observed

range/low power microscope field

Crystals

 

range: rare/few/moderate/many

Bacteria

Few cocci

range: rare/few/moderate/many

Lipid droplets

 

range: rare/few/moderate/many

Sperm

None

range: none/rare/few/moderate/many

Immunology, Serology and Microbiology

 Acetylcholine Receptor Antibody Titer: 0.03 nmol/L=Negative (Normal = < 0.3 nmol/L)

 Feline Corona Virus Serology: IFA titer: 1:400
Feline Corona Virus Serology Interpretation: 1:400 is a relatively low titer indicating exposure to the feline coronavirus; however the cat's FIP status cannot be determined from this test alone.

 Toxoplasmosis Serology: Latex agglutination: 1:512
Toxoplasmosis Serology Interpretation: 1:512 on latex agglutination test is a relatively high titer and suggests need for re-testing in 1-2 weeks for increased titer.

 Echocardiogram Report: No abnormalities detected.

Imaging

Radiography Report

Examination: routine thorax and routine abdomen:

The cardiac silhouette is enlarged. The right caudal lobar artery is prominent, however tapers normally. There is a mild increase in interstitial opacities in the lung fields. There is a large amount of intra-abdominal fat in this obese patient, giving excellent serosal detail. The liver, stomach, spleen, kidneys, and small bowel are within normal limits. The urinary bladder is greatly distended. The colon is full of fecal material and appears obstipated. The osseous structures are within normal limits.

An incidental finding is the presence of two metallic staples superimposed over the cervical soft tissues.

Impression:

1.  Cardiomegaly. Pericardial fat may be contributing to this appearance in this obese patient. Recommend echocardiography to further define this radiographic abnormality.

2.  Possible enlargement of the right caudal lobar artery.

3.  Obstipated.

4.  Distended urinary bladder.

Magnetic Resonance Imaging

Pre- and post-contrast images of the cervical spine.

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Ultrasound Examination Report

Abdominal ultrasound:

Some loops of small intestine contained a small amount of fluid and motility was slightly decreased. The right adrenal gland was slightly small. The liver was slightly more echogenic than usual (equal to falciform fat). Liver size was normal. The appearance suggested early hepatic lipidosis although there are many other causes of increased hepatic echogenicity including increased levels of glycogen, fibrosis and infiltrative disease.

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Case Summary and Final Diagnosis

Summary: A 5 year old, castrated male, domestic short-hair cat was referred to the Auburn University Small Animal Clinic (AUSAC). It had been presented to the referring veterinarian with the complaint of shifting lameness and anorexia of two weeks duration. The problems had improved after a single corticosteroid injection. Three days prior to presentation to the AUSAC the lameness returned and progressed to tetraparesis. At this point a hemogram and blood chemistry were relatively unremarkable and the feline leukemia virus and feline immunodeficiency virus tests (SNAP: in-house ELISA) were negative.  Specimens for feline corona virus (FCoV) and toxoplasmosis testing were submitted but the results were not yet available when treatment with prednisone (1 mg/kg PO BID) and clindamycin (15 mg/kg PO BID) was initiated.

When the cat was presented to Auburn University Small Animal Clinic physical and neurological examinations were performed and the cat was hospitalized in the intensive care unit (ICU). It remained there overnight and with supportive care improved slightly. However it was still so weak that imaging could be performed with only tape needed for restraint.

Laboratory examinations were not diagnostic. Radiographs of the thorax revealed an 8 cm-diameter soft tissue mass in the caudodorsal aspect of the right cranial lung lobe and an additional 1 cm nodule in the same lobe, with other suspicious soft tissue nodules within the cranial subsegment of the left cranial lung lobe. MRI revealed a contrast enhancing lesion in the cervical spinal cord.

After discussion with the clinicians, the owners elected to have the cat euthanatized and granted permission for necropsy.

Final Diagnosis

Necropsy Findings

Gross Findings: The body is that of a reportedly six-year-old, approximately 4.5 kg, gray, castrated male, Domestic-Shorthair cat in good body condition.

1.  The C5 to T2 spinal cord segment was 1.5 cm in diameter (approximately twice normal diameter) and soft with multiple, irregular, individual to coalescing, tan to gray foci scattered throughout the dorsolateral and ventral funiculi. (See Gross Pathology figure below)

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Gross Pathology, Spinal Cord

Example of soft irregular, individual to coalescing, tan to gray foci found scattered throughout the dorsolateral and ventral funiculi of the cervical spinal cord.

2.  The pulmonary lobes were mottled red-black and rubbery, and the pleural surfaces glistened. Copious amounts of semi-transparent, red-yellow, frothy fluid exuded from the pulmonary parenchyma.
No additional anatomic pathologic alterations were observed.

Microscopic Findings: Heart, lung, liver, spleen, kidney, adrenal gland, gastrointestinal tract, spinal cord, brain were examined. (see Histopathology, Spinal Cord below)

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Histopathology, Spinal Cord

The normal gray matter architecture is obscured by a diffuse inflammatory infiltrate consisting of numerous small to medium lymphocytes, oligodendrogliocytes, gitter cells, degenerated neutrophils and prominent type II astrocytes. The intervening neuropil is composed of proteinaceous cellular debris and irregular vacuolar spaces (malacia). The malacic foci are outlined by an intense accumulation of degenerated neutrophils. Numerous tachyzoites and microgamonts are scattered throughout the necrotic foci and the remaining neuropil and perivascular parenchyma. The majority of neurons are not identifiable; however an occasional faint outline of an angulated neuron is present. The inflammatory infiltrate extends into the adjacent white matter and several surrounding myelin sheathes are irregularly dilated and many lack axons or contain ellipsoids. Virchow-Robins' spaces surround the majority of arterioles, venules and capillaries and are expanded by a mononuclear inflammatory infiltrate, lymphocytes and an occasional plasma cell. Many of the affected vessels are lined by prominent endothelium and a rare zoite is present in the endothelium. This mononuclear inflammatory infiltrate extends through the ventral median fissure, communicating with the meninges, and several lymphocytic nodules are scattered throughout the leptomeninges. Immunohistochemical staining for Toxoplasma gondii was strongly positive.

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Lung: The alveoli are filled with pale eosinophilic, proteinaceous material and contain an occasional pulmonary alveolar macrophage. The intervening capillaries are moderately ectatic and filled with erythrocytes.

No other histopathologic abnormalities are observed.

Final Diagnoses:

1.  Spinal cord, C5-T2 segment: Nonsuppurative, necrotizing myelitis with intralesional protozoan parasites consistent with Toxoplasma gondii and secondary lymphocytic perivasculitis/leptomeningitis, diffuse, subacute to chronic, severe.

2.  Lung; congestion and edema, diffuse, subacute, moderate.

Discussion

The obligate intracellular parasite, Toxoplasma gondii (T gondii) infects many species. Felidae, including the domestic cat, are the definitive hosts. Species other than Felidae are intermediate hosts and are infected either directly (ingestion of sporulated oocysts from cat feces) or indirectly (ingestion of tissue cysts or transplacental infection).1

The life cycle of T gondii consists of three stages: oocyst, tachyzoite, and bradyzoite. Oocysts are shed in cat feces in the unsporulated form. Then, over 24 hours, the oocyst sporulates, producing two sporocysts, each with four sporozoites. The sporulated oocyst is the infective stage of the organism in the environment and can remain viable in the environment for several years. After the oocyst is ingested, the sporozoites are released and divide asexually to form tachyzoites that are able to penetrate the intestinal boundary and invade other organs. The tachyzoites divide intracellularly until the host cell either ruptures, releasing more tachyzoites, or forms a cyst, containing many tachyzoites. After encysting, the tachyzoites transform into bradyzoites and grow slowly. The cyst, containing bradyzoites, can either remain dormant, be ingested, or rupture. If the cyst is ingested the bradyzoites will be released and transform into tachyzoites in the new host. Within the original host, rupture of the cyst can lead to transformation from bradyzoites to tachyzoites and subsequent reactivation of infection.

Felidae have two stages of infection, enteroepithelial and extraintestinal. The enteroepithelial stage is unique to Felidae and terminates in the production of oocysts that are excreted in the feces. In this stage T gondii infects only the enterocytes in the small intestine and undergoes both sexual and asexual replication. The extraintestinal stage is similar to that found in intermediate hosts after ingestion of sporulated oocysts and has the potential to cause clinical disease in cats just as in other species.

Clinical disease in cats infected extraintestinally with T gondii occurs in the organ system(s) where the tachyzoites have infiltrated and are replicating. In 100 cats with clinical toxoplasmosis, the most frequent signs were dyspnea, polypnea, and signs of abdominal discomfort.2 Ocular lesions (uveitis and retinochoroiditis) are also seen commonly.2 In one paper, interstitial pneumonia was the most common lesion noted, 97.7 %, (84 of 86), while only 7 of 100 cats had clinically detectable neurological involvement.3 Notably, the brains of 53 (96.4%) of 55 cats with clinical toxoplasmosis had microscopic lesions at necropsy, most of which were not detectable grossly.3 Disseminated, starburst-shaped, glial-histiocytic granulomas were the most common lesion noted, with mononuclear perivascular cuffing noted less frequently.3

Neurological lesions can occur in some cases without lesions in other organ systems. A 10 year old, castrated male, domestic short-haired cat with signs of transverse myelopathy in the T3 to L3 region was found to have a 4mm, brown discolored lesion located ventrally at T10. Microscopically, T gondii tachyzoites and tissue cysts were found and confirmed with special stains. Importantly, no organisms were noted in sections of lung, brain, lumbar and cervical spinal cord, lymph nodes, stomach, intestines, urinary bladder, spleen, and heart. This cat was FIV positive using an ELISA for FIV antibodies.4 FIV infection has been shown to markedly enhance susceptibility to a primary T gondii infection, presumably due to the effect of FIV on lymphocyte function.5

A presumptive diagnosis of toxoplasmosis can be made on the basis of clinical signs, serologic evidence of a recent infection, and response to therapy.2 Thoracic radiographs may demonstrate signs of alveolar and interstitial pneumonia. Titers generally do not develop until two weeks after infection and can stay high for many years. Therefore, an increase in titer over a 2-3 week period must be demonstrated to indicate active infection reliably. Measurement of T gondii antibodies in the CSF may be helpful when used with other diagnostic tests; however, it must be noted that IgG specific for T gondii has been found in the CSF of clinically normal cats.6 Finally, the organisms can sometimes be seen on CSF cytology.

Clindamycin or sulfonamides plus either pyrimethamine or trimethoprim have been shown to be effective in the treatment of T gondii infections in cats. The course of treatment needed is usually around four weeks.1

Toxoplasmosis in cats is usually a subclinical disease. However, cats can develop extraintestinal infection with T gondii and with such infections neurological signs sometimes occur. Toxoplasmosis needs to be considered when a cat has signs consistent with encephalitis or myelopathy. Diagnosis, however, can be difficult due to the lack of diagnostic tests that are reliable and can be reported to the clinician quickly. Response to therapy may be useful diagnostically in suspected toxoplasmosis cases.

References

1.  Lindsay DS, Dubey JP: Toxoplasmosis and neosporosis. Infectious Diseases of the Dog and Cat, 2nd ed. Edited by Craig E. Greene. Philadelphia, W.B. Saunders Company, pp 493-509, 1998.

2.  Lindsay DS, Blagburn BL, Dubey JP: Feline toxoplasmosis and the importance of the Toxoplasma gondii oocyst. Compendium 19:448-461, 1997

3.  Dubey JP, Carpenter JL: Histologically confirmed clinical toxoplasmosis in cats: 100 cases (1952-1990). JAVMA 203:1556-1566, 1993.

4.  Heidel JR, Dubey JP, Blythe LL, et al: Myelitis in a cat infected with Toxoplasma gondii and feline immunodeficiency virus. JAVMA 196:316-318, 1990.

5.  Davidson MG, Rottman JB, English RV, et al: Feline immunodeficiency virus predisposes cats to acute generalized toxoplasmosis. Am J Path 143:1486-1497, 1993

6.  Munana KR, Lappin MR, Powell CC, et al: Sequential measurement of Toxoplasma gondii specific antibodies in the cerebrospinal fluid of cats with experimentally induced toxoplasmosis. Prog Vet Neurol 6:27-31, 1995.

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