Veterinary Clinical Pathology ISSN 0275-6382

What is your diagnosis? Blood smear from a cat

Mary Leissinger1, Stuart Walton2, Jon Fletcher2, Stephen Gaunt1
Departments of 1Pathobiological Sciences and 2Veterinary Clinical Sciences, Louisiana State University School of Veterinary Medicine, Baton Rouge, LA,
USA

Correspondence
M. Leissinger, Department of Pathobiological Sciences, Louisiana State
University School of Veterinary Medicine, Skip Bertman Drive, Baton
Rouge, LA 70803, USA
E-mail: Mleiss1@lsu.edu

DOI:10.1111/vcp.12160

Case Presentation
A 2-year-old male neutered Domestic Shorthair cat was
presented to the emergency medicine service of the Louisi-
ana State University veterinary teaching hospital for acute
onset of cluster seizures. The cat presented in lateral recum-
bency with prolonged capillary refill time (> 2 seconds)
and hypothermia (96.7 F/35.9°C). Neurologic examination
revealed obtunded mentation, anisocoria, opisthotonus,
and lack of menace and palpebral reflexes bilaterally. Rele-
vant abnormalities on a CBC included the presence of an
inflammatory leukogram with a left shift (segmented neu-
trophils 7.2 9 103/lL, reference interval [RI] 2.5–
12.5 9 103/lL; band neutrophils 2.2 9 103/lL, RI 0–
0.3 9 103/lL; lymphocytes 0.2 9103/lL, RI 1.5–7 9 103/
lL) (Figure 1). Blood glucose was 68 mg/dL (RI 80–
115 mg/dL). The cat was placed in lateral recumbency with
head elevation. It also received supplemental oxygen (oxy-
gen cage 39%) and was warmed using a warm water bath
(37°C). Symptomatic treatment included a crystalloid bolus
of 0.9% sodium chloride (50 mL/kg IV), followed by 0.9%
sodium chloride (21 mLs/h), valium (2.5 mg IV), dextrose
50% (3 mLs IV), mannitol (0.5 g/kg IV), and thiamine
(250 mg SQ). Despite aggressive medical intervention, the
cat suffered cardiac arrest. Although cardiopulmonary
resuscitation was successful, the cat was unable to maintain
a normal body temperature or ventilate unassisted, and the
owner elected for humane euthanasia without necropsy.
Upon extubation, the endotracheal tube contained a green
frothy liquid. Figure 1. Blood smear from a cat. Wright–Giemsa, 9 100 objective.

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Blood smear from a cat
Figure 2. Blood smear from a cat. Neutrophils within the body of the smear contain low-to-moderate numbers of bacterial cocci (left, middle) and
demonstrate cytoplasmic vacuolation and basophilia. At the feathered edge, bacteria are present extracellularly among ruptured cells (right).
Wright–Giemsa, 9 100 objective.
Interpretation: left shift with bacteremia
The blood smear contained many toxic segmented and band
neutrophils with basophilic foamy cytoplasm and moderate
numbers of D€ohle bodies. Some neutrophils contained vari-
able numbers of basophilic cytoplasmic inclusions, which
ranged from coccoid to coccobacillary (< 1 lm in diameter)
(Figures 1 and 2), considered consistent with bacteria given
morphology and staining characteristics.
Additional tests
Aerobic culture on blood samples from 2 peripheral veins and
on fluid from the endotracheal tube yielded Streptococcus canis
susceptible to a broad range of antibiotic classes. PCR and
sequencing for bacterial 16s rRNA performed on colonies
confirmed 100% sequence homology with S canis strains
1–82 MP, 8–87 MP, and ATCC 43496.
Discussion
Streptococcus canis is a Lancefield group G b-hemolytic Strepto-
coccus considered normal flora of the canine and feline uri-
nary, reproductive, and gastrointestinal tract.1 In cats, S canis
causes a wide spectrum of disease including necrotizing fasci-
itis, arthritis, sinusitis, meningitis, sepsis, and Streptococcal
toxic shock-like syndrome (STSS).1,2 STSS, as originally
defined in people, includes a positive culture of Streptococcus
spp. from a sterile site, hypotension, and 2 or more indicators
of systemic organ dysfunction.3 The term has been applied to
cases of S canis in acutely ill dogs and cats presenting in
shock-like states progressing to death rapidly.1,2,4 To date,
conserved S canis genotypic determinants, which correlate
with disease manifestation or severity, have not been identi-
fied.1 As in other S canis infections in animals, the inciting
factor for disease in this case is unknown.1,2,4 Unfortunately,
the neurologic and respiratory signs consistent with sinusitis
and associated meningitis (as previously reported) could not
be confirmed by necropsy. Mild hypoglycemia was con-
sidered another sequela of sepsis, and less likely a cause for
466 Vet Clin Pathol 43/3 (2014) 465–466 ©2014 American Society for Veterinary Clinical Pathology and European Society for Veterinary Clinical Pathology
Leissinger et al
seizures. S canis cultured from the endotracheal tube may
reflect direct extension from the upper respiratory tract or a
septic embolic pneumonia as previously reported in S canis
infected cats.4 Positive blood culture and acute onset of
clinical signs with rapidly deteriorating condition are sup-
portive of STSS. Bacteremia on peripheral blood smears
reflects disease severity.5 In models of pneumococcal septi-
cemia, mortality, lack of antibiotic responsiveness, and
identification of bacteria on peripheral blood smear were
positively correlated with a blood concentration of 106
pneumoccoci/ml.5 Bacteremia should be interpreted with
caution in samples collected without use of aseptic tech-
nique, or if extended storage time elapses after sample col-
lection until smear preparation, allowing bacterial
proliferation. A Gram stain could provide additional rapid
information prior to culture results; however, culture is
necessary for definitive diagnosis.
Key Words: Bacteremia, left shift, Streptococcal toxic shock-like
syndrome, Streptococcus canis, toxic changes
References
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