Characterization and experimental reproduction of peripheral neuropathy in White Leghorn chickens

A clinical neurological syndrome termed peripheral neuropathy (PN) that resembles Marek's disease (MD) occurred at low frequency in a commercial layer strain for several years. Study of chickens from six field cases showed that the PN syndrome could be distinguished pathologically from MD on the basis of several factors, including onset as early as 6 weeks, presence of B-type but not A-type lesions in peripheral nerves, and absence of visceral lymphomas. Serotype 1 MD virus could not be isolated from blood from any chicken or demonstrated in tissues by histochemistry or polymerase chain reaction assays. Moreover, the syndrome was not prevented by MD vaccination, either in the field or in laboratory trials. PN was induced in 3 to 54%of commercial line chickens inoculated at 1 or 6 days of age with whole blood or buffy coat cells from clinically affected donor chickens. Sonicated cells also induced PN, but plasma was ineffective. Chickens did not develop PN if reared in isolators without cellular transfer or when vaccinated solely against MD. However, PN was observed in 9% of 57 B*2/*19 commercial chickens reared in isolators following vaccination against MD, infectious bursal disease, Newcastle disease and infectious bronchitis, suggesting that common vaccines may predispose chickens to PN. The data confirmed a strong influence of the major histocompatibility complex (B-complex) on both naturally occurring and experimentally induced PN with the B*19 haplotype conferring susceptibility compared with other alleles. It is postulated that PN may represent an autoimmune reaction to nerve tissue that may result from response to a combination of common vaccines. These studies confirmed that PN is distinct from MD, provided criteria for its differential diagnosis, identified strategies for its control, and established a model for its experimental induction.     

A disease severity scale for systemic sclerosis: development and testing.

OBJECTIVE: To develop and test a severity scale for individual organ involvements in systemic sclerosis (SSc, scleroderma). METHODS: An international study group completed the following tasks: (1) developed a glossary of terms including all pertinent variables for 9 potentially affected organ systems; (2) collected prospective data to determine the feasibility and practicality of each proposed variable; (3) revised the initial list of variables; (4) determined the association of each variable with mortality (a proxy for morbidity) using 579 patients in an existing comprehensive longitudinal scleroderma databank; (5) developed a severity grading scale for each organ system by discussion and consensus; and (6) externally validated the scale using an independent group of 680 patients from the same databank. RESULTS: Nine organ-specific severity scales were developed from 0 (no documented involvement) to 4 (endstage disease). The data required for scale completion are relatively easy and practical for all physicians to obtain. CONCLUSION: This preliminary severity scale will be useful for assessing disease severity status in individual patients both at one point in time and longitudinally. The severity scale will assist in the design and conduct of clinical trials and the comparison of study populations with one another. The scale will serve as a framework for developing a scleroderma disease activity index.     

Correlation of filiform hair position with sensory afferent morphology and synaptic connections in the second instar cockroach.

An attempt is made to relate the distribution of filiform hairs on the cercus of the second instar cockroach, Periplaneta americana, to the morphology and patterns of synaptic connectivity of their afferents. We studied the most distal 25 of the 39 filiform hairs which are commonly present. Filiform afferent arborizations were stained by cobalt filling from the cell body in the cercus. Three fundamental arbor types were found, two similar to those of the first instar medial (M) and lateral (L) afferents, and a third, novel type. L-type arbors could be divided into four subtypes. The most obvious correlate of arbor type is the circumferential position of the hair on the cercus. The proximodistal position of the sensillum within each cercal segment is also a determinant of its arbor. By comparison of hair positions and afferent morphologies, we were able to ascribe homologies between the second instar hairs and members of adult longitudinal hair columns. The patterns of monosynaptic connections between afferents and giant interneurons (GIs) 1, 2, 3, 5, and 6 were determined by recording synaptic potentials in GIs evoked by direct mechanical displacement of individual filiform hairs. Latency from stimulus onset to the rise phase of the first excitatory postsynaptic potential (EPSP) was used as the criterion of monosynapticity. The EPSP amplitudes of the two original L and M afferents are halved in the second instar, in the absence of a significant decrease in GI input resistance. The other afferents can be divided into two basic classes: those which input to GI5 (M-type), and those which input to GI3 and GI6 (L-type). The former is correlated with a central or medial position, while the latter is associated with a group of afferents situated laterally on the cercus. In segments 3 and 4, input to GIs 1 and 2 also correlates with a medial cercal position, however, in the more proximal segments 5 and 6, afferents at all positions input to these interneurons. The occurrence of afferents of identical morphology and similar connectivity in equivalent positions in different segments suggests that each sensory neuron is determined by its two-dimensional position within a segment. The presence of afferents with the same morphology which display proximodistal differences in synaptic connectivity, and of other afferents which have M-type connectivity despite L-type morphology, means that anatomy is generally a poor predictor of synaptic connectivity.     

Clostridium difficile infection

Summary Considering the current wide use of antimicrobial agents, the general internist is commonly faced with the patient at risk for diarrhea due toC. difficile. The diagnosis should be considered for any patient with diarrhea who has received any type of antibiotic therapy in the preceding 4–6 weeks. Symptoms may range from a minor bout of diarrhea to fulminant and fatal colitis. Diagnosis usually requires demonstration of the toxin in stool; culture of the organism and fiberoptic endoscopy may play an adjunctive role in selected clinical settings. The ultimate goal in the treatment forC. difficile infection is to repopulate the normal colonic flora in the most efficacious manner. Minimally symptomatic patients may respond to discontinuing the offending antimicrobial agent or using nonspecific binding agents. Oral vancomycin continues to be the “gold standard” for specific treatment, while metronidazole therapy is considered the first-line agent for individuals with milder infection. Oral bacitracin shows promise, though large studies are lacking. Patients with multiple relapses ofC. difficile diarrhea can be treated with prolonged courses of vancomycin or a combination of vancomycin and rifampin. Intensive care unit patients who are NPO have few therapeutic options besides intravenous administration of metronidazole and oral administration of vancomycin via clamped nasogastric tube. Preventive efforts are directed at cautious use of antibiotics and the use of vinyl gloves when caring for patients with known infection.     

Effectiveness of ammonia treatment in detoxification of fumonisin-contaminated corn

Corn throughout the world is frequently contaminated by the fungus Fusarium moniliforme, which produces toxic fumonisins. Ammonia has been shown to detoxify effectively aflatoxins in corn and cottonseed. Since corn can be contaminated by both fumonisins and aflatoxins, we investigated the effects of ammoniation of corn either cultured with or naturally contaminated by F. moniliforme. Fumonisin B₁ levels in the culture material and in naturally contaminated corn were reduced by 30 and about 45%, respectively, by the ammonia treatment. Despite the apparent reduction in fumonisin content, the toxicity of the culture material in rats was not altered by ammoniation. Reduced weight gains, elevated serum enzyme levels and histopathological lesions, typical of F. moniliforme toxicity, occurred in rats fed either the ammoniated or non-ammoniated culture material. Atmospheric ammoniation of corn does not appear to be an effective method for the detoxification of F. moniliforme-contaminated corn.