First Report of Brown Root Rot of Alfalfa Caused by Phoma sclerotioides in Colorado and New Mexico.

Brown root rot (BRR), caused by the fungal pathogen Phoma sclerotioides G. Preuss ex Sacc. (synonym Plenodomus meliloti Dearn. & G.B. Sanford), is associated with winterkill, slow emergence from winter dormancy, and yield loss of alfalfa (Medicago sativa L.) (1,2). BRR is a problem in regions with severe winters and is common in Alaska and Alberta, Saskatchewan and Manitoba, Canada. It was first observed in the continental United States in Wyoming during 1996 (2) and has subsequently been found in Idaho, Minnesota, Montana, New Hampshire, New York, Vermont, and Wisconsin. In the intermountain valleys of northern New Mexico and western Colorado, winters can be severe; alfalfa winterkill events occur periodically, but it is unknown if BRR is present. In May 2006, alfalfa plants were collected from production fields in Huerfano, Otero, and Rio Grande counties in Colorado and Rio Arriba and Taos counties in New Mexico and assessed for BRR. Two to three fields were sampled per county and 20 or 40 plants were collected per field. All fields existed for at least two winters. Fields sampled in Rio Grande County exhibited severe winterkill, with most plants completely girdled by crown lesions. Plants from other fields exhibited a range of root and crown rots. Isolation of P. sclerotioides was attempted from all plants with a previously described protocol (4). The pathogen was isolated from crown lesions of one alfalfa plant each from Rio Grande and Taos counties. Both lesions extended into the cortex. On potato dextrose agar and water agar with barley (4), single-conidium cultures of each isolate produced large pycnidia (0.35 to 0.80 mm in diameter) with multiple beaks, white cirri darkening to yellow with age, and unicellular, hyaline, ovoid conidia 5 to 7 µm long by 2 µm wide. Diagnostic PCR of the cultures using P. sclerotioides-specific primers (3) resulted in a single amplicon of expected size (500 bp). The internal transcribed spacer (ITS) 1, 5.8S, and ITS2 of the rDNA were amplified and sequenced using primers ITS1 and ITS4. The ITS sequences (GenBank Accession Nos. EU265669 and EU265670) were >98% identical to P. sclerotioides ATCC isolate 56515 over 503 bp of aligned sequence. Potted 'Vernal' alfalfa was inoculated 4 months after seeding, kept at 4°C for 5.5 weeks, 0 to -2°C for 12 weeks, and 4°C for 3 weeks. Of the 14 plants inoculated with the Colorado isolate, 11 developed cortical lesions and 8 winterkilled. Of the 23 plants inoculated with the New Mexico isolate, 22 developed cortical lesions and 16 winterkilled. Lesions were light to very dark brown, sometimes with a darker border and often containing abundant pycnidia. Winterkill was associated with lesions girdling the crown. P. sclerotioides was isolated from the lesions. To our knowledge, this is the southernmost report of BRR in North America and the first report of BRR in New Mexico and Colorado. The incidence and severity of BRR in the region surveyed appear to be considerably lower than in the more northern regions. References: (1) B. Berkenkamp et al. Can. J. Plant Sci. 71:211, 1991. (2) C. R. Hollingsworth et al. Can. J. Plant Pathol. 25:215, 2003. (3) R. C. Larsen et al. Plant Dis. 86:928, 2002. (4) M. J. Wunsch et al. Plant Dis. 91:1293, 2007.

Treatment of severe complicated Kawasaki disease with oral prednisolone and aspirin.

We report on 7 patients with severe, complicated Kawasaki disease treated with oral prednisolone, after apparently unsuccessful intravenous immunoglobulin treatment. An additional eighth patient was a Jehovah's Witness, who was given steroid and aspirin as first-line treatment. These findings support a beneficial role for steroids in intravenous immunoglobulin-resistant Kawasaki disease.

Urinary supersaturation of calcium oxalate and phosphate in patients with X-linked hypophosphatemic rickets and in healthy schoolchildren.

UNLABELLED: Nephrocalcinosis (NC) is a complication of the treatment of X-linked hypophosphatemic rickets (XLHR). Some studies have found that treated patients have enteric hyperoxaluria caused by phosphate therapy and have implicated calcium oxalate, whereas others have found only calcium phosphate in renal biopsy tissue. AIM AND METHODS: We aimed to study the urinary supersaturation of calcium oxalate and calcium phosphate and to determine whether these measures are risk factors for NC. We collected 24-hour urine samples from 20 patients (12 girls) with XLHR, mean +/- SD age 8.2 +/- 4.7 years, and from 79 age-matched members of a healthy control group prospectively. RESULTS: The median 24-hour urine excretions of oxalate, phosphate, and citrate (mmol/1.73 m(2) per day) were significantly increased in patients compared with the control group (oxalate 0.38 vs 0.28, P =. 0012; phosphate 63.1 vs 25.8, P <.0001; citrate 4.18 vs 2.7, P =. 0002). However, no significant differences were seen in the calcium oxalate or calcium phosphate between patients and the control group. No significant differences were seen in 24-hour urine calcium or magnesium excretion between patients and the control group; however, 8 patients had hypercalciuria. A significant higher urine volume in patients compared with the normal group (826 mL/m(2) 24-hour vs 597 mL/m(2) 24-hour; P <.005) was found. Twelve patients had NC at the time of investigation, and although the oxalate excretion was significantly higher in these patients, no significant difference was seen in the relative supersaturation of calcium oxalate monohydrate (CaC(2)O(4).H(2)O) compared with the 8 without NC. CONCLUSIONS: Although 24-hour urine oxalate and phosphate excretion are increased in treated patients with XLHR, there is no increase in the supersaturation of either calcium oxalate or phosphate. Determination of the supersaturation of calcium oxalate or calcium phosphate does not predict the development of NC in XLHR.

Atypical (non-diarrhea-associated) hemolytic-uremic syndrome in childhood.

We describe the clinical and laboratory features of 20 children who were seen during the past 20 years with idiopathic nondiarrhea-associated hemolytic-uremic syndrome. There was no seasonal variation in time of onset; a genetic pre-disposition seemed likely in two of the cases. The prodromal illness was nonspecific and by definition did not include diarrhea. Hypertension was a major problem in the majority of the patients. Five died, three during the initial illness; four are in end-stage renal failure, and all but two of the survivors have residual nephropathy. Eleven patients had a "relapsing" course; up to eight additional documented episodes of hemolytic-uremic syndrome occurred in individual patients. Of the nine children treated before 1980, three died shortly after onset, two never recovered function after the initial illness, one had a relapsing course and died later, and one had residual nephropathy. Plasma exchange was introduced for the management of non-diarrhea-associated hemolytic-uremic syndrome in 1980; since then, all of the 11 patients have recovered function after the initial episode, but 10 of them had relapses. It appears that with the introduction of plasma exchange there has been an improved outcome in the initial phase, but the survivors tend to have relapses. Atypical (non-diarrhea-associated) hemolytic-uremic syndrome is a heterogeneous yet distinct subgroup of hemolytic-uremic syndrome that differs from diarrhea-associated hemolytic-uremic syndrome on epidemiologic, clinical, laboratory, histologic, and prognostic grounds.

Renovascular disease in childhood.

Fifty-four children referred for investigation of hypertension had renovascular disease. In eight patients it was associated with neurofibromatosis, in three with idiopathic hypercalcemia of infancy, and in five cases it followed an arteritic illness. Fibromuscular dysplasia was the underlying abnormality in the majority of cases (46%). Twenty-six patients (48%) were first seen with accelerated hypertension; 38 children (70%) had bilateral renal arterial disease, and in 41 (76%), disease of the small intrarenal vessels was found. Renal vein renin ratios indicated unilateral disease in 31 cases; the results correlated with arteriography findings in 32 (62%) of 51 patients. Eleven children also had the middle aortic syndrome, and 9 of 16 patients, investigated by cerebral arteriography because of cranial bruits or focal neurologic signs, had cerebral vascular abnormalities. Twenty patients were treated surgically--10 by reconstructive procedures, 11 by nephrectomy or heminephrectomy, and 6 by transluminal angioplasty. Of these, 9 (45%) are normotensive with no treatment, 10 have a decreased requirement for antihypertensive drugs, and 1 had no improvement. Thirty-four patients were treated medically because of the extent of their disease; two patients have died of hypertensive complications. We conclude that renal vascular disease in children is often widespread, may be associated with intracerebral vascular disease, frequently affects both kidneys, including both intrarenal and extrarenal vessels, and is therefore not always amenable to surgical intervention and cure.

Clinicopathologic review of twelve children with nephropathy, Wilms tumor, and genital abnormalities (Drash syndrome).

The clinicopathologic and radiologic features of 12 children with complete and incomplete forms of Drash syndrome are reported. Their common denominator was a nephropathy. Four had the full triad, consisting of nephropathy, Wilms tumor, and genital abnormalities; five had nephropathy and genital abnormalities, and three had nephropathy and Wilms tumor. Of the 11 children who had proteinuria, eight had the nephrotic syndrome. Of the 10 whose condition progressed to end-stage renal failure, seven were less than 3 years of age. The histologic features of Wilms tumor were favorable in all seven children, and the tumor was bilateral in three. Of the nine patients who had genital abnormalities, eight had 46,XY karyotype and either ambiguous genitalia (six patients) or normal female phenotype (two). One other patient had a normal 46,XX female karyotype and phenotype but had both müllerian and wolffian structures and a streak ovary. Nine patients had a distinct pelvicaliceal abnormality not previously reported as a feature of this syndrome. Other congenital abnormalities were aniridia, mental retardation, deafness, nystagmus, and cleft palate. This syndrome must be considered in any infant with unexplained nephropathy, particularly in young phenotypic female infants and in those children with ambiguous genitalia or Wilms tumor with an early presentation.

Condroma simulando asma bronquial. / Chondroma simulating bronchial asthma

Se presenta un caso de obstruccion traqueal severa por un condroma originado en el bronquio del lobulo superior izquierdo con extension luminal. La paciente comenzo 5 anos antes, con episodios ocasionales de disnea y sibilancias. Se catalogo el cuadro como asma bronquial a pesar de la respuesta erratica a la administracion de broncodilatadores y corticoides. Se interno en el Centro Respiratorio por una crisis intensa de disnea encontrandose escasas sibilancias y un ruido inspiratorio y respiratorio en cara anterior del torax. El examen funcional (Tabla 1) demostro una severa obstruccion de la via aerea de tipo variable intratoracica sin respuesta a los broncodilatadores. Este dato asociado a los hallazgos semiologicos y la mala respuesta a la terapeutica broncodilatadora decidieron la realizacion de una broncoscopia que demostro la existencia del tumor. Luego de una reseccion endoscopica parcial la enferma mejoro notablemente (Tabla 1). El examen histologico mostro un estroma mixoide con placas de cartilago maduro y tejido adiposo rodeado de epitelio respiratorio, efectuandose el diagnostico de condroma (Fig. 2). Se discuten las causas de error diagnostico y algunas peculiaridades de estos raros tumores, en particular su relacion nosologica con los hamartomas haciendose hincapie en la necesidad de un enfoque diagnostico completo y minucioso en todo caso de obstruccion bronquial intratoracica para la deteccion precoz de los mismos

Condroma simulando asma bronquial. / Chondroma simulating bronchial asthma

Se presenta un caso de obstruccion traqueal severa por un condroma originado en el bronquio del lobulo superior izquierdo con extension luminal. La paciente comenzo 5 anos antes, con episodios ocasionales de disnea y sibilancias. Se catalogo el cuadro como asma bronquial a pesar de la respuesta erratica a la administracion de broncodilatadores y corticoides. Se interno en el Centro Respiratorio por una crisis intensa de disnea encontrandose escasas sibilancias y un ruido inspiratorio y respiratorio en cara anterior del torax. El examen funcional (Tabla 1) demostro una severa obstruccion de la via aerea de tipo variable intratoracica sin respuesta a los broncodilatadores. Este dato asociado a los hallazgos semiologicos y la mala respuesta a la terapeutica broncodilatadora decidieron la realizacion de una broncoscopia que demostro la existencia del tumor. Luego de una reseccion endoscopica parcial la enferma mejoro notablemente (Tabla 1). El examen histologico mostro un estroma mixoide con placas de cartilago maduro y tejido adiposo rodeado de epitelio respiratorio, efectuandose el diagnostico de condroma (Fig. 2). Se discuten las causas de error diagnostico y algunas peculiaridades de estos raros tumores, en particular su relacion nosologica con los hamartomas haciendose hincapie en la necesidad de un enfoque diagnostico completo y minucioso en todo caso de obstruccion bronquial intratoracica para la deteccion precoz de los mismos

Renal vein renin measurements in normotensive children.

Renal venous PRA was measured in 49 normotensive children without renal disease undergoing routine cardiac catheterization. PRA levels did not differ significantly between both renal veins and were significantly higher in the renal veins than in the IVC. There was a constant mean ratio of 1.21 between the renal veins and the IVC at low, intermediate, and high absolute PRA levels. Three patients had a renal venous PRA ratio greater than 1.4 and the highest ratio observed was 1.55. This fidning supports 1.5 as an acceptable upper limit of normality for the interpretation of renal vein PRA ratios in the investigation of patients with suspected renal hypertension. In four patients, PRA in the renal veins was significantly lower than in the IVC. The possibility of renin removal by these kidneys is discussed.