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Gross and microscopic lesions of Bolivian hemorrhagic fever (BHF) are described in 10 rhesus monkeys that survived from 30 to 78 days after subcutaneous inoculation with a dose of 10(3) plaque-forming units (PFU) of Machupo virus, a dose which produces a severe and generally fatal disease. Six of the monkeys had been given low doses of homologous immune globulin when initial signs of infection appeared. Monkeys exhibited clinical signs in two phases. The initial signs of acute infection which began to appear about 1 week following inoculation included: diarrhea, depression, anorexia, dehydration, and skin rash. The survivors of this early phase of the illness usually showed improvement before relapsing into the second (or chronic) phase, which was characterized clinically by central nervous system disturbances including incoordination, tremors, convulsions, paresis, and muscle atrophy. Microscopic lesions were similar in both immune globulin-treated and untreated animals. These included widespread lymphoreticular infiltrates in the walls and adventitia of blood vessels of the brain, spinal cord, pancreas, intestine, liver kidney, adrenal, parathyroid, heart, and skeletal muscle. Diffuse lymphocytic infiltrates not confined to the vascular or perivascular tissues were present to a variable degree in many of these and other organs. Several monkeys exhibited lymphocytic inflammation of the choroid, meninges, peripheral nerves, and ganglia.
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PMID:Pathology of chronic Bolivian hemorrhagic fever in the rhesus monkey. 18 94

Estonian shale oil contains about 25--30% phenols, and their action determines the toxicity of shale oils. The clinical symptoms of intoxication are rather similar, regardless of route of administration. Due to neurotropic action, the coordination of movements is impaired, and clonic and tetanic convulsions, paresis and paralysis of extremities, and narcosis are observed. In subacute and chronic toxicity tests, dysfunction of the central nervous system was found. In long-term (4--6 month) experiments, changes in liver and kidney function were found. Shale oil has gonadotropic activity and causes changes in the sexual cycle as well as diminution of the number of primordial folicles in the ovaries or a decrease in the quantity of normal spermatogonia in testicular germinal epithelium. Shale oils produce local irritation of skin and mucous membranes. Shale oil can induce sensitization of the organism after repeated administration. The results of acute intoxication tests have proved that volatile and nonvolatile phenol fractions, isomeric dimethylphenols, and 5-methylresorcinol, must be characterized as moderately toxic substances; the LD50 ranges from 501 to 1500 mg/kg. The clinical symptoms of acute toxication are similar for all studied phenols (restlessness, unsteadiness, clonic tremor, paresis and paralysis of extremities, and death). In spite of the moderate toxicity of phenols in acute experiments, repeated administration of small doses can cause different changes in the nervous system and internal organs of experimental animals. For all the phenols studied, the maximum allowable concentration in water was limited by their effect on the organoleptic properties of water. The nonactive dose for warm-blooded animals is from 100 to 3000 times the threshold limit value of phenols on the basis of their organoleptic properties. The effect of commercial products of oil shale industry is generally determined by the toxicity of the main components: water-soluble oil shale phenols.
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PMID:Toxicological studies of shale oils, some of their components, and commercial products. 57 2

The mercury levels in 69 muscle samples from fish weighing from 0.3 to 200 kg caught in Moreton Bay, Queensland, in the latter half of 1976 ranged from less than 10 to 2,030 ng/g. Mercury levels in blood samples from 53 humans and 100 dogs in Brisbane almost all contained less than 10 ng/ml while the level in 162 cats sampled ranged from less than 10 to 329 ng/ml. Chronic methylmercurialism developed in 2 cats dosed daily with methylmercury, bound to cysteine, at the rate of 0.6 mg/kg body weight for 74 and 77 days respectively. Terminal clinical signs included anorexia, weight loss, knuckling over at the carpus and tarsus, hypermetria initially involving the forelegs and later the hindlegs, sluggish reflexes, paresis involving all limbs, persistent crying, apparent blindness, tonic and clonic convulsions and salivation. Pathological changes were confined to the nervous system and included degeneration of neurones and perivascular cuffing in the cerebrocortical grey matter, focal atrophy of the granular layer, focal spongiosus of the molecular layer and degeneration and loss of Purkinje cells in the cerebellum and demyelination in the fibre tracts of the dorsal funiculus, mainly the fasciculus cuneatus and in the lateral and ventral corticospinal tracts. Terminal blood methylmercury levels were in excess of 18 microgram/ml, while brain methylmercury levels ranged from 21.0 to 28.4 microgram/g. The liver and kidney contained the highest total levels of mercury of 50 to 80 microgram/g, of which 23 to 37% was inorganic.
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PMID:Chronic methylmercurialism in the cat. 68 73

Clinical signs of toxicosis, neurologic lesions, and elevated tissue residues of methylmercury (MM) were produced in 12 pigs by oral administration of 1.29, 0.86, 0.64, and 0.43 mg mercury/kg of body weight daily as methylmercuric hydroxide (MMH). Clinical signs which began on day 17 were ataxia, dysmetria, blindness, convulsions, paresis, and death. Time of onset of signs was inversely related to size of daily dose. Microscopic lesions were found in the cerebrum brain stem, and spinal cord, and correlated well with clinical signs. The cerebrum in which severity of lesions was directly related to length of exposure was the most severely affected region of the central nervous system (CNS). Lesions were neuronal necrosis, neuronophagia, cortical vacuolation, axon swelling, gliosis, leptomeningitis, and vascular fibrinoid necrosis. Neuronal necrosis was most extensive within mid and deep cerebrocortical laminae. Brain residues of MM were directly proportional to the size of daily dose, and statistically significant. Distribution of MM among different tissues was rather uniform with highest concentrations found in liver, followed by kidney, muscle, spleen, and brain.
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PMID:The pathology of subacute methylmerculialism in swine. 125 8

We present a very rare case of 7 year-old-girl who had a pontine glioma with supratentorial meningeal involvement. She complained severe headache with meningeal irritation. She showed fluctuating cranial nerve impairment of the both abducens and glosopharyngeal nerves but no signs of weakness or facial paresis. She also reported two episodes of generalized convulsion with unconsciousness during admission. MRI disclosed a hypointensity intrinsic brainstem mass with an enhancing exophytic component in the prepontine cistern and a sharp contrast uptake is disclosed in the left-meninges of the supratentrial structures. An open biopsy was performed and diagnosed as a high grade astrocytoma.
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PMID:[Brainstem glioma with supratentorial meningeal dissemination--a case report]. 128 96

A study was done of 309 children seen in two ERs with a first seizure and fever to assess whether meningitis could be recognized using readily available clinical information. Among these children, 23 (7%) cases of meningitis were diagnosed. A group of 69 children with seizures and fever but no meningitis served as controls. Signs from ER examinations that discriminated between children with and those without meningitis were: petechiae, nuchal rigidity, coma, persistent drowsiness, ongoing convulsions, and paresis or paralysis; 21 cases were thus identified. Two children with a suspicious history but none of these signs proved to have meningitis. Children whose seizures showed no complex features and whose febrile illness revealed no suspicious features did not have meningitis. Our results indicate that based on available clinical data, meningitis can be ruled out in children presenting with seizures and fever; thus, there is no need for routine investigation of cerebrospinal fluid.
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PMID:Seizures and fever: can we rule out meningitis on clinical grounds alone? 146 67

The clinical profile of 150 hospital based cases (6 months-7 yrs) of measles presenting between May 1986 to May 1987 was analyzed. Nearly a quarter (28%) were less than 1 yr; 60% belonged to 1-3 yrs age group, 8.6% were 3-5 yrs old and 2.6% were in the 5-7 yrs age group. The male:female ratio was 1.2:1. Nearly half (53.3%) were well nourished, 36.6% had Grades I-II PEM and 9.9% had Grades III-IV PEM. About half (47%) showed no complications; 53% had some complications of which 15% had more than one system involvement. Respiratory complications were seen in 50%, nutritional deterioration in 17.3%, gastrointestinal and neurological in 14.6% each and cardiac in 1.3%. The respiratory complications included pneumonia (16%), bronchitis (12.6%), activation of TB (10.66%), otitis (7.3%) and miliary tuberculosis (4%). CNS complications were encephalitis in 8%, meningitis in 3.3%, convulsions -2.6% and limb paresis in 0.6%. Children below 1 yr had a greater incidence of complications and multisystem involvement. Children between 3-5 yrs had respiratory and GI system involvement and children greater than 5 yrs showed respiratory system involvement only. No complications were seen in the well nourished group while early grades of PEM had mild complications. Severe degree of malnutrition had higher incidence and severity of complications. The need for large coverage of measles vaccine in our country especially amongst the malnourished group is obvious.
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PMID:Clinical profile of measles--a prospective study of 150 hospital based children. 160 95

A 48-year-old female suffered from severe headache, vomiting, and disturbance of consciousness. On admission, she was somnolent with mild paresis of the left leg. Precontrast computed tomography (CT) scans showed a high-density area in the left sylvian fissure and the posterior horn of the left lateral ventricle. Angiographically, a right middle cerebral artery aneurysm and a basilar artery aneurysm were recognized. Furthermore, on the venous phase of bilateral carotid angiograms, superior sagittal sinus (SSS) thrombosis was recognized. Subarachnoid hemorrhage (SAH) was probably induced by rupture of a dilated vein associated with SSS thrombosis, because high-density area on CT scan and location of the aneurysms were different. The patient was initially treated conservatively. Two months later, craniotomy was performed which did not disclose any trace of hemorrhage around the aneurysms and aneurysms themselves. Postoperatively, acute brain swelling and generalized convulsion were induced. The patient became ambulatory 5 months after surgery. In SAH cases, the venous phase should be examined at least in one side of the carotid arteries. In such a SAH case induced by venous thrombosis complicated by aneurysms it is very difficult to decide the timing of surgery for aneurysms.
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PMID:[Superior sagittal sinus thrombosis complicated with multiple aneurysms presenting as subarachnoid hemorrhage. Case report]. 172 64

Seventy-six patients with neurologic complications of cat-scratch disease are discussed. Encephalopathy occurred in 61, while 15 had either cranial or peripheral nerve involvement. The average age of the patients with encephalopathy was 10.6 years (range, 1 to 66 years), and almost twice as many males as females were affected in contrast to patients with uncomplicated cat-scratch disease, in which the ratio was almost equal. Fever was not documented in 50% of patients with encephalopathy and only 26% had temperatures higher than 39 degrees C. Convulsions occurred in 46% and combative behavior in 40%. Lethargy with or without coma was accompanied by variable neurologic signs. Results of laboratory studies, including imaging of the central nervous system, were inconsistent and nondiagnostic. Biopsy tissue from 14 patients showed histopathologic findings compatible with cat-scratch disease. The "English-Wear bacillus" was demonstrated by the Warthin-Starry stain in 10 of 14 skin or lymph node specimens. Of the 15 patients without encephalopathy, two children with facial nerve paresis displayed cranial nerve symptoms and/or signs, 10 patients had cat-scratch disease neuroretinitis, and three women had peripheral neuritis. All 76 patients recovered within 12 months; 78% recovered within 1 to 12 weeks. There were no neurologic sequelae. Treatment consisted of control of convulsions and supportive measures. Commonly used antibiotics administered to more than half of the patients were apparently ineffective.
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PMID:Cat-scratch disease. Acute encephalopathy and other neurologic manifestations. 184 21

Each of two horses was dosed by stomach tube with culture material on maize of Fusarium moniliforme MRC 826. One horse developed severe hepatosis and mild oedema of the brain after 6 doses of 2.5 g of culture material/kg body mass/day in 7 days. The second horse, in a similar experiment but at a dosage rate of 1.25 g/kg/day, developed mild hepatosis and moderate oedema of the brain. In both animals the brain oedema was particularly noticeable in the medulla oblongata. The mycotoxin fumonisin B1 was extracted and purified from the culture material of F. moniliforme MRC, 826 which contained approximately 1 g/kg of this compound. A horse was injected intravenously 7 times from Day 0-Day 9 with 0.125 mg of fumonisin B1/kg body mass/day. Clinical signs of neurotoxicosis, which appeared on Day 8, included nervousness followed by apathy, a wide-based stance, trembling, ataxia, reluctance to move, paresis of the lower lip and tongue, and an inability to eat or drink. Euthanasia was performed on the horse on Day 10 while the animal was in a tetanic convulsion. The principal lesions were severe oedema of the brain and early, bilaterally symmetrical, focal necrosis in the medulla oblongata. This report provides experimental evidence that fumonisin B1, produced by F. moniliforme, causes equine leukoencephalomalacia.
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PMID:Leukoencephalomalacia in a horse induced by fumonisin B1 isolated from Fusarium moniliforme. 321 91


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