Signs Of Paralysis Research Articles

The effect of feeding immature Karoo paralysis ticksIxodes rubicundus (Acari: Ixodidae) on the metabolic rate of the rock elephant shrew

The effect of feeding immature Karoo paralysis ticks (Ixodes rubicundus) on the resting metabolic rate (RMR) of their principal natural host, the rock elephant shrew (Elephantulus myurus), was investigated under laboratory conditions. The elephant shrews were artificially infested with numbers of ticks simulating natural burdens. The RMR of the elephant shrews was quantified by measuring the oxygen consumption in an open through-flow system. The RMR of hosts infested only with larvae did not differ from that of the control group. Those infested with nymphs, or nymphs and larvae, had significantly lower RMR's compared to the control animals. There were no signs of paralysis in any of the infested hosts.

Herpes simplex virus infection and damage in the central nervous system: Immune response to myelin basic protein

Two models of herpes simplex virus (HSV) infection in the mouse (inoculation of the ear pinna or intravenous inoculation) were used to assess immune responses to the virus and myelin basic protein (MBP). In both models demyelination in the central nervous system (CNS) can be assessed by clinical signs; ear paralysis (ear inoculation) and hind limb paralysis (intravenous inoculation). In the ear model, low levels of antibody to MBP were detected at 7 and 14 days after inoculation. The incidence of such antibody was low and bore no correlation with signs of paralysis. Cells from draining lymph nodes of mice inoculated in the pinna showed a proliferative response to HSV and MBP in vitro. In both models, delayed-type hypersensitivity reactions were demonstrated against HSV and MBP but such reactions were most significant after i.v. inoculation. This may reflect the greater CNS damage associated with hind limb paralysis.

Correlation between presence of lactate dehydrogenase-elevating virus RNA and antigens in motor neurons and paralysis in infected C58 mice

Lactate dehydrogenase-elevating virus (LDV) induces poliomyelitis in immunosuppressed C58 mice resulting in fatal paralysis. We have synthesized and cloned cDNA complementary to the LDV genome, and used the cDNA clones as in situ hybridization probes for the detection of LDV RNA in tissue sections. Direct fluorescent antibody staining using IgG from chronically infected mice was used for the detection of LDV antigens. Using these methods, we have detected LDV RNA and antigens in anterior horn neurons of paralyzed mice. The appearance of LDV RNA and antigen positive motor neurons and their location in the spinal cord correlated with the development of paralytic symptoms. No positive neurons were detected in LDV-infected, susceptible mice without signs of paralysis, but some glial cells of the white and gray matter in the spinal cords of these mice were found to contain LDV RNA. These analyses broaden the host cell range of LDV to include neuronal and other cells in the CNS and support the hypothesis of LDV replication in neurons as the cause of poliomyelitis and paralysis.

Aspects moleculaires et cellulaires de la pathogenie dans la rage

The true causes of the beginning of the symptoms and the eventual mortality of rabies are not very well known. Immunopathological factors certainly intervene, but they only complete a process of neuronal alteration. Contrary to other viruses which lyse the infected cells, the rabies virus does not necessarily destroy the neurones which are the preferential target cells. On the contrary. RNA synthesis is stimulated during CNS infection by the rabies virus. Synthesis is not stimulated by the multiplication of the rabies virus in the cell lines of fibroblastic or neuronal origin, which suggests the existence of regulations on neuronal level functions in the CNS. Nevertheless, the protein virus synthesis seemed equally submitted to specific neuron regulations or neuronal populations. The traces of a neuronal dysfunction during infection by the rabies virus have been investigated, using as a probe, variations of muscarinic acetyl choline receptors in the CNS. The presence of these receptors is revealed by the use of an antagonistic ligand of acetyl choline, quinuclidinyl benzylate. We were able to show that as regards the rat, the appearance of the first signs of paralysis is correlated with the diminution of the receptor binding. Thus, it seems that the presence of the virus in the CNS provokes neuronal alteration which can in itself condition the viral multiplication and eventually modulate the viral pathogenesis expression.

The mast cells of the mammalian central nervous system

The central nervous system (CNS) of two mammalian species was studied autoradiographically using tritium-labeled thymidine; the rat, whose brain contains few localized mast cells (MCs) but many ubiquitous neurolipomastocytoid cells (NLMs), and the guinea pig, whose brain contains only ubiquitous NLMs. A few guinea pigs were also injected with an MC discharger compound 48/80 and the response of the NLMs, which are thought to be allied to MCs, as well as of neuroglial and vascular endothelial cells, was noted. The rats were 3 days to 6 weeks old whereas all the guinea pigs were young adults. Both MCs and NLMs took up the label, and much more so in the babies, paralleling similar uptakes in only very small immature MCs outside the CNS. Neuroglial elements, especially subependymal and oligodendroglial, as well as endothelial, perivascular, leptomeningeal and ependymal cells demonstrated some uptake. This was considerably increased upon receipt of compound 48/80, especially in the case of the subependymal glia, the NLMs and the endothelial cells; capillary neoformations were seen in the spinal cords of guinea pigs that had shown signs of paralysis. The cause of this increase is discussed in terms of mild stress induced by that compound. The subependymal response is also discussed with reference to periventricular plaques seen in multiple sclerosis and lymphoreticular and glial tumors seen in that region. It is concluded that both MCs and NLMs are capable of DNA replication and mitosis in immature animals. The NLMs can also divide upon stimulation in adult CNS.

Antibodies to acetylcholine receptors in rabbits: immunochemical and electrophysiological studies.

Acetylcholine receptors (AChR), purified from electric eel and Torpedo by affinity chromatography using a synthetic quaternary ammonium ligand, bound 10 nmole alpha-bungarotoxin (alpha-BuTx) per mg of protein and demonstrated a common subunit. Rabbits, immunized with either eel or Torpedo/AChR, developed flaccid paralysis barely altered by anticholinesterases and died 48 hours after the first sign of paralysis. In paralyzed animals, repetitive stimulation at low rates induced a 50% to 90% decrement of evoked potentials, temporarily reversed by edrophonium. Extracellular and introcellular MEPP amplitudes were 40% to 50% of controls. Serum and isolated IgG formed single immunoprecipitin lines against the antigens. AChR-antibody complexes did not bind alpha-BuTx, whereas alpha-BuTx-AChR complexes bound antibody if the antibody was specific for that AChR. Torpedo and eel AChR showed partial idenity with both antisera. Rat diaphragms and eel electroplax incubated with antisera to Torpedo and eel AChR showed a 50%-60% reduction in carbamylcholine depolarization. These studies demonstrate differences between eel and Torpedo AChR induce a block in neuromuscular transmission in rabbits with features of myasthenia gravis.

PASSIVE NEUTRALIZING ANTIBODIES IN EXPERIMENTAL COXSACKIE B-1 VIRUS INFECTION.

Passive neutralizing antibodies specific to Coxsackie B-1 virus are transmitted from immune mice to the litters both before and after birth.Before birth the antibodies are transmitted via the mother"s blood; their presence could not be detected by the age of 17 days. After birth, the antibodies apparently are transmitted by milk. The ND50of these antibodies is maintained if the litter is suckled by an immune mother.Although the immune 4-day-old litters survive after intracerebral inoculation and there are no signs of paralysis or other severe damage to the CNS, the brain lesions on microscopical examination appear to be as extensive as in the non-immune controls. The brain tissues of the immune mice are spared if the virus is introduced by the subcutaneous route.The damage observed in the interscapular brown fat in either the immune 4- or the 17-day-old mice, irrespective of the route of virus inoculation, is considerably reduced or minimal, if the presence of the passive antibody can be demonstrated in the blood.When the offspring are born of and suckled by an immune mother, the multiplication of the Coxsackie B-1 virus in the brown fat appears to be completely blocked, and there is no evidence of an immediate antigenic stimulus by the challenge virus.

Further observations on the pathogenesis of rabies in guinea-pigs after experimental infection with the Flury strain.

Following inoculation of guinea-pigs with the Flury strain of rabies virus in the muscles of the foreleg, the virus could be recovered from the cervico-thoracic cord on the 4th day. From the 6th day on the virus spread in both directions, to the brain and to the lumbosacral cord. There was a close parallelism between the virus distribution and the clinical symptoms: the first signs of paralysis were observed in the inoculated leg.

Inhibition of rat cholinesterase by tritolyl phosphates.

Summary1) In contrast to previous reports, TOTP was found to be an active inhibitor of true cholinesterase in erythrocytes and brain of rats. Cholinergic signs were noted when activity in either tissue fell to less than 20% of normal. Maximum inhibition occurred 24 hours after single injection and exceeded inhibition of the plasma enzyme. Repeated sublethal doses also produced greater inhibition of true than of pseudocholinesterase. 2) On the other hand, the plasma enzyme was inhibited 24 hours after a single dose of TMTP while the cholinesterase of erythrocytes and brain was not significantly affected. TPTP failed to inhibit the enzyme of any of the 3 tissues. 3) No signs of paralysis were elicited, and no histologic lesions were discovered in the peripheral or central nervous system.

Nutrition of the cat. II. Protein requirements for growth of weanling kittens and young cats maintained on a mixed diet.

From time to time during the past century reference has been made to the effects of meat diets on various animal species. The earliest papers refer to lions maintained on carcass meat in the collection of the Zoological Society of London. Crisp (1864) observed enlarged thyroids in lion cubs born at the zoo, and Bland Sutton (1888) described skeletal changes referred to as ‘rickets’ in cubs and young lions. Of an %weekold cub Bland Sutton wrote: ‘instead of playing with its companions it preferred to remain quiet. . . ; when attempting to walk it advanced a few paces, then staggered. . . the hindquarters rolled over. . .convulsions sometimes occurred’. This cub died at 12 weeks: its skull was found to be softened and much thickened. Bland Sutton noticed that cubs of 6 months or more suffered a less severe form of the disease, often surviving a year or two, the only constant sign being a slow progressive paraplegia. Some cubs, to which he gave supplements of bone dust and cod-liver oil, made a good recovery, and were alive and active without any signs of paralysis 2 years later. In spite of this observation, some 25 years later Marine (1914) wrote: ‘In zoological gardens where carnivores are held and bred in captivity and the diet is for the most part beef, goitre, rickets and osteomalacic states are quite common.’ Baumann (1896) observed that dogs fed on flesh diets frequently had enlarged thyroids of low iodine content. Watson (1904) found that fowls fed on raw lean meat and water died, in 3-16 months, with terminal paralytic signs; their thyroids were ten times the normal weight, though histologically normal apart from occasional hyperaemia. The parathyroids were also enlarged, but of normal structure. Watson (1906) reported marked thyroid hyperplasia in suckling rats whose mothers had been fed on meat, compared with the normal thyroids of those whose mothers received a mixed diet. Heitzmann (1873) noticed that rickets developed in cats fed on milk, boiled meat, white bread, boiled potatoes and fat. He was interested in lactic acid as a factor in the aetiology of rickets, but the diet he used was certainly deficient in calcium and probably also in vitamin D. The cats showed swelling and distortion of the long-bone epiphyses after 4-5 weeks on the diet; rickets was confirmed microscopically. After 4-5 months the long bones were soft ‘ . . .elastic, like a fish’, and at post-mortem the * Paper No. 3 : Brit. y. Nutr. (1960), 14, 361.

Influence of hyper and hypothyroidism on susceptibility of mice to infection with Lansing poliomyelitis virus.

SummaryThe influence of hyper- and hypothyroidism upon susceptibility of mice to infection with Lansing poliomyelitis virus has been studied. In one series hypothyroidism seemed to favor a higher incidence of paralysis, but this was not substantiated in two other series. The only consistent deviation from the normal course of infection was an increased incidence of deaths without previous signs of paralysis in hyperthyroid mice.

THE TRUMBLE OPERATION FOR FUSION OF THE HIP

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Observations on Fowl Paralysis (Neurolymphomatosis)

There are many reports on transmission experiments with fowl paralysis. Some workers have found a greater incidence of paralysis in chickens inoculated with tissues from paralyzed chickens than in uninoculated controls; e. g., Pappenheimer, Dunn and Seidlin found paralysis in 25% of the inoculated chickens and 7% of the uninoculated controls. Similar but somewhat more successful were the transmission experiments of Dalling and Warrack. Biely, Palmer and Asmundson found that the incidence of paralysis depends on inherited susceptibility, and is not conspicuously influenced by inoculation with tissues from paralyzed chickens. There is no report of a readily transmissible strain of fowl paralysis and the relation of fowl paralysis to leukosis is not clearly defined in the literature. Two transmissible strains of fowl paralysis have been isolated. Of one strain (Strain 5) 15 successful passages were made, of the other (Strain 6) 10 passages were made. Chart 1 shows only the results of inoculations of the first 5 passages of Strain 5. The inoculations were made in most instances by intravenous injections of blood from paralyzed chickens, into healthy young chickens. The transmitting agent circulates in the blood of paralyzed chickens throughout the course of illness as shown by the following experiment: No. 3946 was inoculated and showed beginning paralysis of legs and wings 42 days later. At this time three chickens were injected with 0.5 to 5 cc. of its blood. Two of these chickens developed paralysis and the third remained healthy. Eighteen days later the signs of paralysis were more conspicuous and another two chickens were injected with 0.5 to 5 cc. of blood of chicken No. 3946. Both of these chickens developed paralysis. Thirteen days later both extremities and one wing of No. 3946 were completely paralyzed, and the chicken was killed in extremis; two more chickens were injected with 0.5 cc. of its blood and both died with neurolymphomatosis.