Behçet's syndrome associated with pregnancy.

A case of Behçet's syndrome diagnosed during pregnancy is reported. It is believed that this condition is more common in the United States than previously thought. It should be considered in the differential diagnosis of genital ulceration.

Persistence of cellulitis-associated Escherichia coli DNA fingerprints in successive broiler chicken flocks.

Avian cellulitis in broiler chickens is primarily caused by Escherichia coli. Previous research found that the E. coli isolates of cellulitis origin were unique to each ranch, suggesting that these E. coli were endemic within the ranch environment. To test the hypothesis that the E. coli associated with cellulitis are endemic in the litter of the broiler house, we designed a study to determine whether E. coli DNA fingerprints associated with cellulitis persist over successive flocks that are grown in the same house. In addition, we assessed the impact of different cleaning and disinfection strategies on this persistence. Two broiler houses were followed on each of five farms over 3-4 flocks. A total of 353 E. coli isolates from cellulitis lesions were analyzed in this study, and 314 of these isolates (89%) were DNA fingerprinted by PFGE. In each ranch, there were several DNA fingerprint patterns that were present over successive flocks, regardless of the cleaning and disinfection strategy utilized. Isolates persisted as long as 191 days, implying that these E. coli are capable of persisting in the broiler house environment for long periods of time. In addition, these E. coli isolates were associated with cellulitis lesions in successive flocks. Thus, the isolates of E. coli that are associated with cellulitis in broiler chickens appear to be endemic in the litter environment of the broiler house.

Multiplex polymerase chain reaction for distinguishing Taylorella equigenitalis from Taylorella equigenitalis-like organisms.

It is difficult to distinguish isolates of Taylorella equigenitalis, the cause of contagious equine metritis, from a T. equigenitalis-like organism isolated from asymptomatic donkeys and horses. Although T. equigenitalis is responsible for a severe, contagious disease of the reproductive tract of equids, the T. equigenitalis-like organism, although contagious, does not appear to produce disease. Because of the economic consequences of correctly distinguishing isolates of these 2 microorganisms, a polymerase chain reaction (PCR)-based assay was developed that will distinguish isolates of T. equigenitalis from the T. equigenitalis-like microorganism. The primers used in the PCR assay were designed to amplify unique regions of the gene encoding the 16S ribosomal RNA.

Spatial heterogeneity of Escherichia coli DNA fingerprints isolated from cellulitis lesions in chickens.

Avian cellulitis in broiler chickens is characterized by subcutaneous lesions that result in economic losses because of the partial or complete condemnation of the carcasses at processing. Escherichia coli is the primary causative agent of this condition. Previous research with a biotyping system found that the E. coli of cellulitis origin were unique to each ranch, suggesting that these E. coli were endemic within the ranch environment. The objective of our study was to analyze the genetic variability of E. coli isolates associated with cellulitis. We analyzed the genetic relatedness of the isolates in relation to the houses, ranches, and complexes in which the broilers were grown. This analysis enabled us to assess the spatial heterogeneity, or genetic diversity on a spatial scale, of the isolates. Forty-nine broilers with cellulitis lesions were necropsied. These broilers came from six houses on four ranches on three complexes that had been placed with chicks from the same hatchery within a 2-wk period. Isolates of E. coli from the lesions were DNA fingerprinted by pulsed-field gel electrophoresis. Relatedness among isolates was determined with the Dice coefficient and an unweighted pair group method with average linkages cluster analysis. The complexes possessed isolates with a variety of DNA fingerprints, yet each complex appeared to have isolates with a unique set of DNA fingerprints. Isolates from the same complex tended to form clusters with similarity coefficients greater than 90%. Isolates from different complexes were genetically distinct. This heterogeneity at the level of the complex suggests that isolates were not disseminated from a source common to the complexes. The spatial heterogeneity of the E. coli isolates in this study implies an endemic population of cellulitis-associated E. coli exists in the broiler house environment.

Sex-specific effects of low protein diet on in utero programming of renal G-protein coupled receptors.

Intrauterine growth restriction (IUGR) is an important risk factor for development of hypertension, diabetes and the metabolic syndrome. Maternal low protein (LP) intake during rat pregnancy leads to IUGR in male and female offspring, although females may be resistant to the development of effect. Current evidence suggests that changes in the renin-angiotensin system (RAS) in utero contribute to this programmed hypertension, via sex-specific mechanisms. The previously orphaned G-protein coupled receptor (GPR91) was identified as a central player in the development of hypertension in adult mice, through a RAS-dependent pathway. However, whether the GPR91 pathway contributes to fetal programming is unknown. Furthermore, the nature of involvement of downstream modulators of the RAS including Gqα/11α and GαS has not been investigated in IUGR-LP rats. Therefore, we postulated that renal GPR91, in conjunction with RAS, is differentially impacted in a sex-specific manner from LP-induced IUGR rats. Pregnant Wistar rats were fed control (C, 20% protein) or LP (8% protein) diet until embryonic day 19 (E19) or postnatal d21. At E19, GPR91 protein and mRNA were increased in both male and female LP kidneys (P<0.05), whereas renin and angiotensin converting enzyme (ACE) were only increased in males (P=0.06 and P<0.05, respectively). On d21, AT1R and Gqα/11α were increased in LP males, while in LP females, AT2R protein was elevated and renin expression was decreased (P<0.05). This study demonstrates that in IUGR-LP rats, up regulation of GPR91 in fetal kidney is mirrored by increased ACE and renin in males. These in utero alterations, when combined with postnatal increases in AT1R-Gqα/11α specifically in male offspring, may predispose to the development of hypertension.

Case report: fatal gastrointestinal hemorrhage in mixed connective tissue disease.

We have presented the case of a young woman with MCTD who died of gastrointestinal bleeding due to fibrinoid necrosis of blood vessels of the small and large intestine. This appears to be the first recorded occurrence of such findings in MCTD.

Rapidly progressive glomerulonephritis in Behçet's syndrome.

Rapidly progressive glomerulonephritis developed in a patient with Behçet's syndrome while he was being treated with transfer factor. The therapy did not prevent development of this disease and thus cannot be recommended in patients who have Behçet's syndrome with renal involvement.

Spastic long-lasting reflexes in the awake rat after sacral spinal cord injury.

Following chronic sacral spinal cord transection in rats the affected tail muscles exhibit marked spasticity, with characteristic long-lasting tail spasms evoked by mild stimulation. The purpose of the present paper was to characterize the long-lasting reflex seen in tail muscles in response to electrical stimulation of the tail nerves in the awake spastic rat, including its development with time and relation to spasticity. Before and after sacral spinal transection, surface electrodes were placed on the tail for electrical stimulation of the caudal nerve trunk (mixed nerve) and for recording EMG from segmental tail muscles. In normal and acute spinal rats caudal nerve trunk stimulation evoked little or no EMG reflex. By 2 wk after injury, the same stimulation evoked long-lasting reflexes that were 1) very low threshold, 2) evoked from rest without prior EMG activity, 3) of polysynaptic latency with >6 ms central delay, 4) about 2 s long, and 5) enhanced by repeated stimulation (windup). These reflexes produced powerful whole tail contractions (spasms) and developed gradually over the weeks after the injury (< or =52 wk tested), in close parallel to the development of spasticity. Pure low-threshold cutaneous stimulation, from electrical stimulation of the tip of the tail, also evoked long-lasting spastic reflexes, not seen in acute spinal or normal rats. In acute spinal rats a strong C-fiber stimulation of the tip of the tail (20 x T) could evoke a weak EMG response lasting about 1 s. Interestingly, when this C-fiber stimulation was used as a conditioning stimulation to depolarize the motoneuron pool in acute spinal rats, a subsequent low-threshold stimulation of the caudal nerve trunk evoked a 300-500 ms long reflex, similar to the onset of the long-lasting reflex in chronic spinal rats. A similar conditioned reflex was not seen in normal rats. Thus there is an unusually long low-threshold polysynaptic input to the motoneurons (pEPSP) that is normally inhibited by descending control. This pEPSP is released from inhibition immediately after injury but does not produce a long-lasting reflex because of a lack of motoneuron excitability. With chronic injury the motoneuron excitability is increased markedly, and the pEPSP then triggers sustained motoneuron discharges associated with long-lasting reflexes and muscle spasms.

Complexation of iron cation by sodium urate crystals and gouty inflammation.

Gouty inflammation can be suppressed by an iron chelator. We therefore hypothesized that arthritis associated with sodium urate crystal deposition could follow the incomplete complexation of iron cation with subsequent oxidant generation as the metal cycles through reduced and oxidized states. Urate crystals adsorbed Fe3+ in vitro and crystals collected from a human tophus had significant concentrations of ionizable iron. Urate crystals oxidized deoxyribose to a thiobarbituric acid (TBA)-reactive product, augmented luminol chemiluminescence by neutrophils, released leukotriene B4 from neutrophils, activated complement, and promoted neutrophil chemotaxis. All of these events increased with the concentration of complexed iron and were suppressed by the iron chelator deferoxamine or the .OH scavenger dimethylthiourea. These results suggest that some portion of gouty inflammation after urate crystal deposition could result from the incomplete complexation of iron with subsequent catalytic generation of reactive oxygen species.