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Ivermectin toxicosis in three adult horses. JAVMA, Vol 235, No. 5, September 1,
2009. Clinical Signs- depression, forelimb and hind limb ataxia, drooping of the superior
and inferior lips, and muscle fasciculations. Bilateral mydriasis, decreased pupillary light
reflexes, and absent menace reflexes were evidentOne horse was euthanized, and a high
concentration of ivermectin was detected in its brain tissue at postmortem examination.
Analysis of the ivermectin concentration in the paste product revealed that the
concentration was approximately that indicated on the packaging. Clinical Relevance—
Ivermectin toxicosis is an uncommonly reported condition in equids that should be
considered when acute neurologic impairment develops after ivermectin
administration. Recovery is possible with supportive care and time. Toxic concentrations
of ivermectin have been reported for several animal species, including dogs, cats,
pigs, cattle, horses, chelonians, and frogs. The mechanism of action of ivermectin
involves potentiating the release of the inhibitory neurotransmitter GABA, causing
an influx of chloride ions and hyperpolarization of neuronal membranes. This
sequence of events inhibits neuromuscular transmission and leads to flaccid paralysis of
invertebrates, in which GABA receptors are located in the peripheral nervous system. In
mammals, GABA receptors are located only in the CNS and an intact blood-brain barrier
protects from the neurologic effects of ivermectin. Picrotoxin is recommended as a
reversal agent for ivermectin toxicosis in dogs, and it functions as a GABA-receptor
antagonist by blocking the chloride ion channels. Neuronal excitability caused by
picrotoxin administration may lead to seizures; therefore, the agent has a narrow
margin of safety. For example, Collies have a multidrug-resistance gene (mdr1) that
encodes for P-glycoprotein, which is an integral part of the blood-brain barrier that
functions to keep ivermectin from entering the CNS. Dogs possessing a deletion mutation
of the mdr1 gene are unable to synthesize P-glycoprotein appropriately and have a
high sensitivity to ivermectin.
Severe polymyositis and neuritis in a cat. JAVMA, Vol 235, No. 2, July 15, 2009. In
triceps brachii muscle, areas of mild mononuclear cell infiltration and areas of extensive
myofiber loss, atrophy, and fibrosis were detected within the same sections. Multifocal
areas of cellular infiltration with an endomysial and perimysial distribution as well as
variable fiber atrophy and loss were also present within the other muscle speci mens.
Scattered mononuclear cell infiltrations were evident under the perineurium and within
the endoneurium in the ulnar nerve biopsy specimen (Figure 2). On the basis of these
findings, a diagnosis of inflammatory myopathy (myositis) and neuropathy (neuritis) was
made. Negative for Toxoplasma gondii by serology. .( Vet Pathol 43:257–269 (2006))
The disadvantage of formalin fixation of a highly metabolically active tissue such as
skeletal muscle is that muscle fibers may shrink by as much as 30%, enzyme activity is
reduced or abolished, and storage products such as glycogen and lipids are not
optimally retained. In addition, it is impossible to identify metabolic or contractile
muscle fiber types (Type 1 vs Type 2) in formalin-fixed muscle.
4) Primary Splenic Peripheral Nerve Sheath Tumour in a Dog; splenic mass that
infiltrated the mesentery and composed of spindle-shaped cells arranged in interlacing
bundles, streams, whorls and storiform patterns (Antoni A pattern) and less cellular areas
with more loosely arranged spindle to oval cells (Antoni B pattern). Cells expressed
vimentin, S-100 and GFAP, but did not express desmin, a-smooth muscle actin or factor VIII.
5) Nasal Osteoma in a Dairy Cow: a Combined Clinical, Imaging and
Histopathological Approach to Diagnosis: smooth-surfaced mass within the left nasal
cavity, composed of well-differentiated and interlacing bone trabeculae lined by osteoblasts
and multinucleated osteoclasts.
Expression of Transforming Growth Factor-β1, -β2 and -β3 in Normal and Diseased
Canine Mitral Valves : in chronic valvular disease (endocardiosis) there is activation
and proliferation of valvular stromal cells and transdifferentiation into myofibroblasts
like cells. In mild and strong valvular disease there was increased expression of TGF- β1
and β3 and smooth muscle actin
Systemic Candida albicans Infection in Two Alpacas (Lama pacos) Candida albican is
dimorphic fungus commensal in skin, upper respiratory tract, alimentary tract and genital
tract. Immunosuppresion or disturbance of cutaneous/mucosal barrier for invasion to take
place..Histo: suppurative to necrotizing inflammation in various organs.
Summaries BGC
Visceral and Neural Larva Migrans in Rhesus Macaques. Journal of the American
Association for Laboratory Animal Science Vol 47, No 4 July 2008. Granulomatous
lymphadenitis in the mesenteric and pancreatic lymph node, cerebral granulomas, with
larval nematodes consistent with Baylisascaris procyonis.
3) Malignant catarrhal fever in sika deer (Cervus nippon) in the UK: enlargement
of the super ficial lymph nodes and mesenteric chain. Mineralised caseous
nodules1·5 cm in diameter were present on the right cranial pleura, and segmental
haemorrhagic enteropathy in the small intestine. Histo: multisystemic
granulomatous inflammatory changes associated with lymphocytic vasculitis and
fibrinoid vasculitis, most pronounced in the brain, leptomeninges, lymph nodes,
adrenal glands and liver, consistent with MC
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Epidermolysis Bullosa in Calves in the United Kingdom. J. Comp. Path. 2010, Vol.
142, 336e340. Epidermolysis bullosa (EB) was diagnosed. Lesions included multifocal
erosion and ulceration of the hard and soft palates, tongue, nares and gingiva, with
nychomadesis
(dysungulation). There was alopecia, erosion and crusting of the coronets, pasterns,
fetlocks, carpi, hocks, flanks and axillae. Histopathological findings included segmental
separation of full thickness epidermis from the dermis, with formation of large clefts
containing eosinophilic fluid, extravasated red blood cells and small numbers of
neutrophils. Ultrastructurally, there was evidence of vacuolar change within basal
keratinocytes, corresponding to areas of histological clefting. Preliminary genetic
screening of the candidate keratin genes (bKRT5 and bKRT14) has excluded mutations
of these as the cause of this condition.