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Clinical presentations, laboratory features, and responses to therapy of 102 patients treated at an army medical center for genitourinary tuberculosis between January 1961 and September 1972 are described. During that time, a total of 3109 patients had been treated for tuberculosis of all types. The study group included 72 men aged 18-59 with a mean age of 29, and 31 women aged 17-66, with a mean age of 31. There was often a latent period of 20 years or more between infection with the tubercle bacillus and the expression of genitourinary tuberculosis. The principal means of diagnosis was isolation of Mycobacterium tuberculosis from urine, obtained in 80%, or sputum, obtained in 38%. M. tuberculosis was not cultured in 13 patients. In patients with negative cultures, diagnosis was made by combinations of positive tuberculin skin test, caseating granulomata on biopsy, characteristic changes in the excretory urogram, characteristic bladder lesions on cystoscopy, and the presence of sterile pyuria or microscopic hematuria. A wide variety of signs and symptoms were encountered as was a high frequency of involvement of other organ systems. The most common laboratory abnormalities were pyuria, albuminuria, and hematuria. 75% of patients had an abnormal chest roentgenogram on admission. 88% of patients tested had positive skin tests and 63% tested had abnormal excretory urography. 16% showed renal calcification. Only 1 nephrectomy was done in the latter 5 years of the study, for hypertension. 2 women and 6 men had hypertension, but 1 woman and 2 men had nontuberculous renal disease which could have caused the hypertension. The evidence from the series is that infectivity of genitourinary tuberculosis is low. There was only 1 initial treatment failure, in a 47-year old man with active pulmonary and renal tuberculosis caused by an isoniazid-resistant organism. 2 men, only 1 of whom had had genitourinary disease originally, had recurrences of tuberculous disease after prematurely discontinuing medication.
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PMID:Genitourinary tuberculosis: review of 102 cases. 421 33

Left renal vein hypertension, also called "nutcracker phenomenon" or "nutcracker syndrome," is a rare vascular abnormality responsible for gross hematuria. The phenomenon is attributable to the idiopathic decrease in the angle between the aorta and the superior mesenteric artery with consequent compression of the left renal vein. The entrapment of the left renal vein is not easily detectable by ordinary diagnostic procedures. We report two cases of gross hematuria (persistent in one patient and recurrent in the other) caused by "nutcracker phenomenon." In both cases, no remarkable findings were obtained from medical history, urinary red blood cells morphology, repeated urinalysis, pyelography, cystoscopy, or ureteroscopy. Left renal vein dilation in one case was found with a computed tomography (CT) scan performed on the venous tree of left kidney. The diagnosis of "nutcracker phenomenon" was confirmed by renal venography with measurement of pressure gradient between left renal vein and inferior vena cava in both cases. In one case, the diagnosis was complicated by the presence of Mycobacterium tuberculosis in urine. The "nutcracker phenomenon" is probably more common than thought. Early diagnosis is important to avoid unnecessary diagnostic procedures and complications such as the thrombosis of the left renal vein. Many procedures are available to correct the compression of the left renal vein entrapped between the aorta and the superior mesenteric artery: Gortex graft vein interposition, nephropexy, stenting, and kidney autotransplantation. After surgery, gross hematuria ceases in almost all patients.
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PMID:Gross hematuria of uncommon origin: the nutcracker syndrome. 1007 88

A 79-year old woman, with a history of hypertension, presented with clinical features of congestive heart failure, fever, a purpuric rash, and left lower quadrant abdominal tenderness. Contrast computed tomography scan of the abdomen showed features of acute diverticulitis, and blood culture was subsequently positive for Klebsiella pneumoniae. Histological examination of a biopsy of the rash confirmed a diagnosis of leukocytoclastic vasculitis (LCV). The bacteremia responded to intravenous amoxycillin/clavulanic acid and gentamicin and the rash subsided. This case represents the first case of LCV complicating K. pneumoniae bacteremia in the English literature. The English literature on bacteria-associated LCV is reviewed. Taking aside organisms such as Rickettsia that cause endothelial invasion, the associated bacterial species tends to be subacute or chronic pathogens e.g. Mycoplasma pneumoniae, Mycobacterium tuberculosis, and Yersinia enterocolitica; or the disease process is of a subacute or chronic nature e.g. endocarditis, bronchiectesis, and cystic fibrosis, leading to prolonged exposure to pathogens that apparently cause acute pyogenic infections, such as K. pneumoniae.
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PMID:Leukocytoclastic vasculitis complicating Klebsiella pneumoniae bacteremia. 1097 80

The aetiology of Takayasu's arteritis is unknown, but an association with tuberculosis has been reported. We report the case of a 12-year-old-boy with Takayasu's arteritis: his blood pressure was 150/90 mmHg and fundoscopic examination showed grade I hypertensive changes. A tuberculin test was positive and acid-fast bacteria were seen in the urine. Angiography revealed involvement of the descending aorta, thoracic aorta and upper abdominal aorta, with fusiform enlargement and no filling of the left renal artery. He was started on prednisolone therapy, with cyclophosphamide being added subsequently. Despite vigorous treatment, including three courses of nitroprusside infusion, the severe hypertension persisted and his blood pressure became regulated only after left nephrectomy. Acid-fast bacteria were seen in the nephrectomy material. The exact role of Mycobacterium tuberculosis in the pathogenesis of Takayasu's arteritis is still unknown. In this patient the tuberculin test was positive and acid-fast bacteria were seen in both the urine and nephrectomy material. This finding is suggestive of the association between tuberculosis and the disease process.
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PMID:Takayasu's arteritis and tuberculosis: a case report. 1114 63

A 73-year-old African American female presented to our clinic with painful lower extremity lesions of 2 weeks duration. She was in her usual state of health until 3 months prior to presentation when she reported symptoms of fatigue and weakness. She also noticed an enlarging mass on the left side of her neck. She denied fevers, chills, night sweats or cough. Her symptoms were unresponsive to a course of oral dicloxacillin. The neck mass enlarged over 8 weeks and she was referred to our institution for evaluation. CT scan of the neck showed an enlarged lymph node. Ten days prior to her presentation in dermatology, a fine needle aspirate of the enlarging lymph node revealed necrotizing granulomas. Tissue was sent for routine mycobacterial and fungal cultures. Routine blood work, chest radiograph, and a tuberculin skin test were also performed. At the time of her dermatology visit she described the development of multiple new painful, non-pruritic lesions, bilaterally on the lower extremities. She also reported a red crusted area that appeared at the site of her tuberculin test that was placed subsequent to the development of her lower extremity lesions. Her past medical history was significant for Parkinson's disease, hypothyroidism and hypertension. Her current medications included l-thyroxine, estrogen and diltiazem. Her travel history was only remarkable for a trip to Jamaica the previous spring. She was born and raised in Haiti. She reported a history of a positive tuberculin skin test 20 years ago, but received no therapy. Physical examination revealed a 2 x 3 centimeter firm, nontender left lateral neck mass (Fig. 1). Her right forearm revealed an erythematous, ulcerated, indurated plaque 1.5 cm in diameter (Fig. 2.). Her lower extremities revealed tender 0.5 to 1 cm erythematous nodules below the knees bilaterally (Fig. 3). A punch biopsy of a lower extremity nodule revealed a mild pervisacular dermal infiltrate. Within the subcutaneous tissue there was septal widening. There was also a lymphohistiocytic infiltrate with a slight admixture of neutrophils within the septa of the fat lobules. There was no evidence of necrotizing vasculitis or collagen necrosis. An acid-fast stain was not performed. The histologic findings were consistent with a diagnosis of erythema nodosum. Her laboratory evaluation including CBC, electrolytes, thyroid studies, angiotensin converting enzyme level and chest radiograph were normal. Approximately 1 week after her dermatological evaluation, the fine-needle aspirate culture grew Mycobacterium tuberculosis. A diagnosis of tuberculous lymphadenitis associated with erythema nodosum was confirmed. The patient was started on quadruple therapy of isoniazid, rifampin, ethambutol and pyrazinamide. Her lower limb skins lesions rapidly resolved over the subsequent month and her neck mass also diminished in size. She completed 6 months of antituberculous therapy with complete resolution of her lymphadenopathy.
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PMID:Erythema nodosum associated with reactivation tuberculous lymphadenitis (scrofula). 1201 Mar 45

An organism, identified as Mycobacterium phlei GTIS10, was isolated based on its ability to use dibenzothiophene (DBT) as a sole source of sulfur for growth at 30-52 degrees C. Similar to other biodesulfurization-competent organisms, M. phlei GTIS10 converts DBT to 2-hydroxybiphenyl (2-HBP), as detected by HPLC. The specific desulfurization activity of the 50 degrees C M. phlei GTIS10 culture was determined to be 1.1+/-0.07 micromol 2-HBP min(-1) (g dry cell)(-1). M. phlei GTIS10 can also utilize benzothiophene and thiophene as sulfur sources for growth. The dszABC operon of M. phlei GTIS10 was cloned and sequenced and was found to be identical to that of Rhodococcus erythropolis IGTS8. The presence of the R. erythropolis IGTS8 120-kb plasmid pSOX, which encodes the dszABC operon, has been demonstrated in M. phlei GTIS10. Even though identical dsz genes are contained in both cultures, the temperature at which resting cells of R. erythropolisIGTS8 reach the highest rate of DBT metabolism is near 30 degrees C whereas the temperature that shows the highest activity in resting cell cultures of M. phlei GTIS10 is near 50 degrees C, and activity is detectable at temperatures as high as 57 degrees C. In M. phlei GTIS10, the rate-limiting step in vivo appears to be the conversion of DBT to dibenzothiophene sulfone catalyzed by the product of the dszC gene, DBT monooxygenase. The thermostability of individual desulfurization enzymes was determined and 2-hydroxybiphenyl-2-sulfinate sulfinolyase, encoded by dszB, was found to be the most thermolabile. These results demonstrate that the thermostability of individual enzymes determined in vitro is not necessarily a good predictor of the functional temperature range of enzymes in vivo.
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PMID:Isolation and characterization of a moderate thermophile, Mycobacterium phlei GTIS10, capable of dibenzothiophene desulfurization. 1222 34

One third of cases of cerebral ischemia have no clear etiology. A humoral response to the atherosclerotic plaques components beta2-glycoprotein l (beta2-gpl) and heat-shock proteins (Hsp) might be involved in the pathogenesis of stroke. This case-control study includes a complete profile of anti-beta2-gpl antibodies and testing of IgG antibodies to the 60/65 kilodaltons (kDa) Hsp in stroke patients. Ninety-three patients with acute ischemic stroke and 93 controls were evaluated for age, sex, race, hypertension, smoking, previous cardiopathy, diabetes mellitus, hypercholesterolemia and previous history of cerebral ischemia. lgG/lgM/lgA anticardiolipin (aCL) and anti-beta2-gpl antibodies, as well as lgG antibodies to human 60 kDa Hsp and to Mycobacterium bovis 65 kDa Hsp, were detected by immunoassay. Adjusted odds ratios (OR) were calculated by logistic regression. The adjusted OR for IgA anti-beta2-gpl antibodies was 4.6 (90%Cl 1.5 to 14.3; p = 0.025). The non-adjusted OR for IgG antibodies to Hsp 60 was 26.1. The adjusted OR for IgG antibodies to Hsp 65 was 3.2 (90%Cl 1.2 to 8.3; p = 0.044). The adjusted OR for lgG to any Hsp (60 or 65) was 4.8 (90%Cl 1.9 to 12.1; p = 0.006). This study demonstrates that elevated IgA anti-beta2-gpl and lgG anti-Hsp 60/65 antibodies are associated with increased risk of ischemic stroke. The association occurred independently of other risk factors. This humoral response might link autoimmunity, thrombophilia and atherosclerosis in stroke patients.
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PMID:Antibodies to the atherosclerotic plaque components beta2-glycoprotein I and heat-shock proteins as risk factors for acute cerebral ischemia. 1459 78

By the turn of the last century, flying in the face of over a hundred years of research and clinical observation to the contrary, medicine abandoned the link between infection and atherogenesis; not because it was ever proven wrong, but because it did not fit in with the trends of a medical establishment convinced that chronic disease such as heart disease must be multifactorial, degenerative and non-infectious. Yet it was the very inability of 'established' risk factors such as hypercholesterolemia, hypertension and smoking to completely explain the incidence and trends in cardiovascular disease that resulted in historically repeated calls to search out an infectious cause, a search that began more than a century ago. Today, half of US heart attack victims have acceptable cholesterol levels and 25% or more have none of the "risk factors" associated with heart disease, including smoking, high blood pressure or obesity, most of which are not inconsistent with being caused by infection. Even the case of the traditionalist's latest 2003 JAMA assault to 'debunk' what they call the "50% risk factor myth" falls woefully short under scrutiny. In one group 30% died of heart disease with a cholesterol of at least 240 mg/dl, a condition which also existed in 21% who did not die during the same period. And the overlap was obvious throughout the so-called risk categories. Under such scrutiny, lead author Greenland conceded that if obesity, inactivity and elevated cholesteriol in the elderly are included, just about everyone has a risk factor and he likened the dilemma of people who do or do not wind up with heart disease akin to the susceptibility of people who are exposed to tuberculosis but do not get the disease. In Infections and Atherosclerosis: New Clues from an old Hypothesis? Nieto stressed the need to extend the possible role of infectious agents beyond the three infections which have in recent years been the focus of research: Cytomegalovirus (CMV) Chlamydia pneumoniae and Helicobactor pylori. Mycobacterial disease shares interesting connections to heart disease. Not only is tuberculosis the only microorganism to depend on cholesterol for its pathogenesis but CDC maps for cardiovascular disease bear a striking similarity to those of State and regional TB case rates. Ellis, Hektoen, Osler, McCallum, Swartz, Livingston and Alexander-Jackson all saw clinical and laboratory evidence of a causative relationship between the mycobacteria and heart disease. And Xu showed that proteins of mycobacterial origin actually led to experimental atherosclerosis in laboratory animals Furthermore present day markers suggested as indicators for heart disease susceptibility such as C-Reactive Protein (CRP), interleukin-6 and homocysteine are all similarly elevated in tuberculosis. It therefore behooves us to explore the link between heart disease and typical and atypical tuberculosis.
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PMID:Heart disease: the greatest 'risk' factor of them all. 1508 5

Thermophilic bacteria Bacillus subtilis WU-S2B and Mycobacterium phlei WU-F1 desulfurize dibenzothiophene (DBT) and alkylated DBTs through specific cleavage of the carbon-sulfur bonds over a temperature range up to 52 degrees C. In order to identify and functionally analyze the DBT-desulfurization genes, the gene cluster containing bdsA, bdsB, and bdsC was cloned from B. subtilis WU-S2B. The nucleotide and amino acid sequences of bdsABC show homologies to those of the other known DBT-desulfurization genes and enzymes; e.g. a nucleotide sequence homology of 61.0% to dszABC of the mesophilic bacterium Rhodococcus sp. IGTS8 and 57.8% to tdsABC of the thermophilic bacterium Paenibacillus sp. A11-2. Deletion and subcloning analysis of bdsABC revealed that the gene products of bdsC, bdsA and bdsB oxidized DBT to DBT sulfone (DBTO(2)), converted DBTO(2) to 2'-hydroxybiphenyl-2-sulfinate (HBPSi), and desulfurized HBPSi to 2-hydroxybiphenyl (2-HBP), respectively. Resting cells of a recombinant Escherichia coli JM109 harboring bdsABC converted DBT to 2-HBP over a temperature range of 30-52 degrees C, indicating that the gene products of bdsABC were functional in the recombinant. The activities of DBT degradation at 50 degrees C and DBT desulfurization (2-HBP production) at 40 degrees C in resting cells of the recombinant were approximately five times and twice, respectively, as high as those in B. subtilis WU-S2B. The recombinant E. coli cells also degraded alkylated DBTs, such as 2,8-dimethylDBT and 4,6-dimethylDBT. The nucleotide sequences of B. subtilis WU-S2B bdsABC and the corresponding genes from M. phlei WU-F1 were found to be completely identical to each other although the strains are genetically different.
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PMID:Identification and functional analysis of the genes encoding dibenzothiophene-desulfurizing enzymes from thermophilic bacteria. 1522 Dec 22

Sarcoidosis is a systemic disease with multiorgan involvement. In children, renal impairment of sarcoidosis usually is caused by either hypercalcemia leading to nephrocalcinosis or interstitial nephritis with or without granulomata. We report the case of a 13-year-old boy presenting with severe arterial hypertension and acute renal failure caused by an isolated sarcoid granulomatous interstitial nephritis (GIN). Other known causes of GIN, eg, drug intake or fungal or mycobacterial infection, were excluded, and there was no evidence of extrarenal sarcoid involvement. Renal function improved initially with prednisone treatment. Blood pressure was controlled using ramipril, nifedipine, furosemide, dihydralazine, and metoprolol. Later, the patient showed signs of severe steroid toxicity and progressive renal failure. Monthly treatment with infliximab, a tumor necrosis factor-alpha antibody, was started, resulting in steady improvement in renal function and resolution of renal granulomata. In addition, antihypertensive medication could be reduced, and low-dose prednisone therapy was maintained. To our knowledge, this is the first report of successful treatment with infliximab of a patient with sarcoid GIN.
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PMID:Isolated sarcoid granulomatous interstitial nephritis responding to infliximab therapy. 1568 21


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