Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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Chapter | 26 Cerebrospinal Fluid
orange-red color to body fluids. Rifampin is 90% bound to
protein; hypoproteinemia may result in rifampin staining of
CSF in patients receiving this drug ( Fishman, 1992 ).
3 . Viscosity
Increased viscosity is usually due to a very high CSF protein
content, particularly fibrinogen. If pleocytosis is present,
a surface pellicle or a clot may form. In this situation, collection
of the CSF in a heparinized or EDTA tube may be
necessary to obtain an accurate cell count. Cryptococcosis
may increase CSF viscosity because of the polysaccharide
capsule of the yeast. Epidural fat or nucleus pulposus in the
CSF may also increase viscosity or result in globules within
the fluid ( Fishman, 1992 ; Kjeldsberg and Knight, 1993 ).
B . Cytology
An increase in the cellularity of CSF is termed pleocytosis. In
general terms, the degree of pleocytosis depends on several
factors, including the nature of the inciting cause and the severity
and location of the lesion with respect to the subarachnoid
space or ventricular system ( Cook and DeNicola, 1988 ). A
normal CSF analysis does not exclude the presence of disease
( Fishman, 1992 ; Kjeldsberg and Knight, 1993 ). This is especially
true with deep parenchymal lesions that do not communicate
with the leptomeninges, and hence the subarachnoid space,
or the ependymal surfaces. In these cases, despite the presence
of neurological disease that is often severe, the lesion may not
affect the CSF cellularity ( Cook and DeNicola, 1988 ). Abnormal
CSF findings always indicate the presence of pathology.
1 . Neutrophilia
A marked pleocytosis with neutrophil predominance suggests
either bacterial meningitis ( Kjeldsberg and Knight, 1993 ;
Kornegay et al. , 1978 ) or suppurative, nonseptic (corticosteroid
responsive) meningitis ( Meric, 1988, 1992a ; Tipold and
Jaggy, 1994 ). Total leukocyte counts in excess of 2000 cells
per microliter are frequently encountered in these diseases
and may even exceed 10,000 cells per microliter ( Meric,
1992a ). Observation of bacteria or a positive culture confirms
septic meningitis. In our experience, bacteria are more commonly
observed in the CSF of large animals afflicted with
septic meningitis than in dogs or cats with septic meningitis.
Neutrophil nuclear morphology is often used as criteria for
determining the likelihood of sepsis with nuclear degenerative
changes or karyolysis interpreted as evidence of bacterial
disease. However, the neutrophils in confirmed cases of septic
meningitis in dogs and cats are frequently well preserved,
especially if there has been prior therapy. Therefore, absence
of bacteria or degenerative nuclear changes in neutrophils
cannot be used to unequivocally exclude a diagnosis of septic
meningitis, although it does make it less likely. In people,
acute viral meningoencephalitis initially causes a neutrophilic
pleocytosis ( Converse et al. , 1973 ; Fishman, 1992 ; Kjeldsberg
and Knight, 1993 ) that may persist from a few hours to several
days before the development of the more typical mononuclear
reaction. A similar phenomenon is documented in
animals (Green et al. , 1993). Occasionally, distemper virus
infection causes massive encephalomalacia ( Vandevelde and
Spano, 1977 ) resulting in a neutrophilic pleocytosis, in contrast
to the more typical moderate mononuclear pleocytosis.
Central nervous system neoplasia may result in a neutrophil
predominance in the CSF, especially if there is significant
necrosis and inflammation associated with the tumor.
Moderate to marked pleocytosis with neutrophil predominance
may be noted in dogs with meningioma ( Bailey and
Higgins, 1986b ). However, in another study of dogs with
meningioma, about 30% of dogs had a normal CSF analysis
( Dickinson et al. , 2006 ). In this study, a significant association
between meningiomas in the caudal portion of the
cranial fossa and an elevated CSF nucleated cell count was
found; but only 19% of the dogs had an elevated total nucleated
white cell count with a predominance of neutrophils
(Dickinson et al. , 2006 ).
Canine intervertebral disk disease is associated with variable
alterations in CSF that depend on factors such as disease
severity and chronicity ( Thomson et al. , 1989 ). Acute severe
disease may result in counts greater than 50 cells per microliter
with more than 50% neutrophils ( Thomson et al. , 1989 ).
This finding may be a reflection of acute inflammation secondary
to trauma that may be exacerbated by myelomalacia
in some instances. The authors have seen a similar phenomenon
associated with fibrocartilaginous embolic myelopathy
in dogs. A neutrophilic pleocytosis of varying severity often
occurs following myelography with iodinated contrast agents
(Carakostas et al. , 1983 ; Johnson et al. , 1985 ; Widmer et al. ,
1992 ). These changes usually peak at 24 h postmyelogram (see
Section VII for further details). Similarly, a neutrophilic pleocytosis
has been observed postictally in people. We have occasionally
observed similar findings in dogs (see Section VII).
2 . Lymphocytosis
Alterations in both numbers and morphology of lymphocytes
(see Section III.B) in the CSF occur in a variety of diseases.
Central nervous system viral infections often result in a predominantly
lymphocytic pleocytosis, documented in dogs
( Vandevelde and Spano, 1977 ), cats ( Dow et al. , 1990 ; Rand
et al. , 1994b ), horses (Green et al. , 1992 ; Hamir et al. , 1992 ;
Wamsley et al. , 2002 ), sheep, goats (Brewer, 1983 ), and
numerous other species. In people, CSF lymphocytosis has
been observed in bacterial meningitis following antibiotic
therapy ( Cargill, 1975 ; Converse et al. , 1973 ; Fishman, 1992 ;
Kjeldsberg and Knight, 1993 ), indicating that therapy and
chronicity can alter the CSF findings. A similar finding has
been reported in dogs ( Sarfaty et al. , 1986 ; Tipold and Jaggy,
1994 ) and calves ( Green and Smith, 1992 ). We have noted
that dogs with chronic or acute on chronic type I intervertebral
disk disease have a pleocytosis that is more commonly lymphocytic
than neutrophilic ( Windsor et al. , 2007 ). The CSF