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Transcript
Nervous System
 The nervous system is composed of
billions of neurons with long,
interconnecting processes that form
complex integrated electrochemical
circuits. It is through these neuronal
circuits that animals experience
sensations and respond appropriately.
Basic Sensory and Motor
Functions:
 The peripheral nervous system (PNS) is
formed by neurons of the cranial and
spinal nerves. The central nervous
system (CNS) is formed by neurons of the
spinal cord, brain stem, cerebellum, and
cerebrum.
 Evidence of disease in other body systems
may be associated with inflammatory,
metabolic, toxic, or metastatic neoplastic
disorders of the nervous system. External
signs of traumatic or toxic exposure may
support these mechanisms of disease.
The neurologic examination consists of
evaluation of the following:
 1) the head.
 2) the gait.
 3) the neck and thoracic limbs.
 4) the trunk, pelvic limbs, anus, and tail.
Initially, an attempt should be made to
relate all deficits to a focal anatomic
lesion.
Mechanisms of Disease:
 Disease processes affecting the nervous
system may be congenital or familial,
infectious or inflammatory, toxic,
metabolic, nutritional, traumatic, vascular,
degenerative, neoplastic, or idiopathic.
 Infections of the nervous system are due
to specific viruses, fungi, protozoa,
bacteria, rickettsia, and algae
Rabies
 Rabies is an acute viral encephalomyelitis that
principally affects carnivores, although it can affect any
mammal including food animals.
 Rabies is most often transmitted by the bite of infected
wild animals including skunks, raccoons and foxes.
 Bats are the important species in which carriers are
known to occur
 Rabies is endemic in Texas.
A raccoon with rabies. Courtesy of Dr.
Thomas Lane
Etiology and Epidemiology:
 Rabies is caused by lyssaviruses in the
Rhabdovirus family. Lyssaviruses are
usually confined to 1 major reservoir
species in a given geographic area,
although spillover to other species is
common.
Transmission and Pathogenesis
 Transmission is almost always by
introduction of virus-laden saliva into the
tissues, usually by the bite of a rabid
animal. Although much less likely, it is
possible for virus from saliva, salivary
glands, or brain to cause infection by
entering the body through other fresh
wounds or through intact mucous
membranes
Clinical signs
 The most reliable signs,
regardless of species, are
acute behavioral changes and
unexplained progressive
paralysis. Behavioral changes
may include sudden anorexia,
signs of apprehension or
nervousness, irritability, and
hyperexcitability (including
priapism). The animal may
seek solitude. Ataxia, altered
phonation, and changes in
temperament are apparent
Clinical signs cont.
 Due to the vagueness of signs and lack
of consideration of rabies as a potential
diagnosis, cattle handlers, veterinarians
and other people in contact are often
exposed to the virus. During the active
course of the disease, the virus is
excreted at high levels in saliva.
 Cattle with furious rabies can be
dangerous, attacking and pursuing
humans and other animals. Lactation
ceases abruptly in dairy cattle. The
usual placid expression is replaced by
one of alertness. The eyes and ears
follow sounds and movement.
Diagnostic
 Rabies testing should be done by a
qualified laboratory, designated by the
local or state health department.
 Fluorescent antibody testing of the brain,
the presence of Neigri bodies on
histopathology.
Control
 Vaccines approved for use in cattle, sheep
and horses are available and should be
seriously considered for high-risk
exposures or high-value animals. Due to
costs of vaccine and relative low incidence
rates, vaccination is not routinely used in
most cattle herds.
Polioencephalomalacia (PEM)
 is an important neurologic disease of
ruminants that is seen worldwide. Cattle,
sheep, goats, deer, and camelids are
affected.
 Historically, PEM has been associated
with altered thiamine status, but more
recently an association with high sulfur
intake has been observed.
Etiology, Pathogenesis, and
Epidemiology
 The disease is seen sporadically or as a herd
outbreak. In general, younger animals are more
frequently affected than adults. Animals on high
concentrate diets are at higher risk, but pastured
animals also develop PEM..
 Thiamine inadequacy can be caused by such
factors as acute dietary deficiency of thiamine or
ingestion of plant thiaminases or thiamine
analogs.
Clinical Findings:
 PEM may be acute or subacute. Animals
with the acute form manifest blindness,
recumbency, tonic-clonic seizures, and
coma. Those with a longer duration of
acute signs have poorer responses to
therapy and higher mortality. Animals with
the subacute form initially separate from
the group, stop eating, and display
twitches of the ears and face.
Lesions
 Acutely affected animals may have brain
swelling with gyral flattening and coning of
the cerebellum due to herniation into the
foramen magnum. Slight yellowish
discoloration of the affected cortical tissue
may be present.
Lesions cont.
 Polioencephalomalacia. Transverse section of the dorsal parietal cortex of a
feedlot steer with PEM viewed under ambient illumination. Affected
segments of the cortical gray matter have a yellowish discoloration and
irregular contours. Courtesy of Daniel H. Gould
Treatment
 The treatment of choice regardless of
cause is thiamine. Therapy must be
started early in the disease course for
benefits to be achieved. If brain lesions
are particularly severe or treatment is
delayed, full clinical recovery may not be
possible. The dosage of thiamine is 10-20,
mg/kg, IM or SC, tid. Initial treatment may
be administered IV.
Listeriosis
 Listeriosis, a disease of the central
nervous system, is caused by
the bacterium Listeria moncytogenes.
 This bacterium can live almost anywhere-in soil, manure piles, and grass.
 Listeriosis is common in cattle, sheep and
goats and can occur in pigs, dogs, and
cats, some wild animals, and humans.
Etiology






Listeria moncytogenes.
Gram-positive
Ovoid to rod-shaped
Facultative anaerobe
Acid but not gas producing from glucose
Can multiply at temperatures between ~0 and 45°C
Reservoirs
L. monocytogenes.
 – decaying vegetation
 – soils
 – animal and human feces
 – sewage
 – silage
 – water
It has been isolated from a wide range of
retail foods.
Pathogenesis:
 Listeria organisms that are ingested or
inhaled tend to cause septicemia,
abortion, and latent infection. Those that
gain entry to tissues have a predilection to
localize in the intestinal wall, medulla
oblongata, and placenta or to cause
encephalitis via minute wounds in bucal
mucosa.
Clinical Findings:

Encephalitis is the
most readily recognized
form of listeriosis in
ruminants. It affects all
ages and both sexes,
sometimes as an
epidemic in feedlot cattle
or sheep. The course in
sheep and goats is rapid,
and death may occur 2448 hr after onset of signs;
however, the recovery
rate can be up to 30%
with prompt, aggressive
therapy
Lesions:

In listeric encephalitis, there are few
gross lesions except for some congestion
of meninges. Microscopic lesions are
confined primarily to the pons, medulla
oblongata, and anterior spinal cord.
Lesions of listerial encephalitis (microabscessation) in the midbrain of a cow. Courtesy of the
Department of Pathobiology, University of Guelph
Diagnostic
 Listeriosis is confirmed only by isolation
and identification of L monocytogenes .
Specimens of choice are brain from
animals with CNS involvement and
aborted placenta and fetus
Treatment and Control:
 L monocytogenes is susceptible to penicillin (the
drug of choice), ceftiofur, erythromycin, and
trimethoprim/sulfonamide. High doses are
required because of the difficulty in achieving
minimum bactericidal concentrations in the brain.
 Penicillin G should be given at 44,000 U/kg body
wt, IM, daily for 1-2 wk; the first injection should
be accompanied by the same dose given IV
Zoonotic Risk
 Whether animals serve as a reservoir of
infection for humans may be questioned,
because Listeria organisms have been isolated
from feces of a significant number of apparently
healthy people as well as other animals.
 L monocytogenes can be isolated from milk of
mastitic, aborting, and apparently healthy cows.
 Listeria also have been isolated from milk of
sheep, goats, and women.