Cases reported "Bacterial Infections"

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1/14. Superficial temporal artery dilatation in a patient with infectious temporal headache clinically mimicking temporal arteritis.

    A 57-year-old woman noticed a pulsatile shooting headache in her right temporal region 3 days after extraction of a tooth from the right mandible. The following day, a localized headache over the right superficial temporal artery (STA), low grade fever, and jaw claudication appeared and progressed subacutely. Seven days after the onset, magnetic resonance imaging and angiography (MRI/MRA) disclosed inflammatory swelling of the right temporal muscle and dilatation of the right STA. All the symptoms disappeared following antibiotic treatment, and neuroimaging findings were improved. In conclusion, MRA is thought to be useful to non-invasively identify reversible inflammatory dilatation of extracranial vessels.
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2/14. Awake craniotomy for microsurgical obliteration of mycotic aneurysms: technical report of three cases.

    OBJECTIVE AND IMPORTANCE: Infectious (mycotic) aneurysms that do not resolve with medical treatment require surgical obliteration, usually requiring sacrifice of the parent artery. In addition, patients with mycotic aneurysms frequently need subsequent cardiac valve repair, which often necessitates anticoagulation. Three cases of awake craniotomy for microsurgical clipping of mycotic aneurysms are presented. Awake minimally invasive craniotomy using frameless stereotactic guidance on the basis of computed tomographic angiography enables temporary occlusion of the parent artery with neurological assessment before obliteration of the aneurysm. CLINICAL PRESENTATION: A 56-year-old woman presented with progressively worsening mitral valve disease and a history of subacute bacterial endocarditis and subarachnoid hemorrhage 30 years previously. A cerebral angiogram revealed a 4-mm left middle cerebral artery (MCA) angular branch aneurysm, which required obliteration before mitral valve replacement. The second patient, a 64-year-old woman with a history of rheumatic fever, had an 8-mm right distal MCA aneurysm diagnosed in the setting of pulmonary abscess and worsening cardiac function as a result of mitral valve disease. The third patient, a 57-year-old man with a history of fevers, night sweats, and progressive mitral valve disease, had an enlarging left MCA angular branch aneurysm despite the administration of antibiotics. Because of their location on distal MCA branches, none of the aneurysms were amenable to preoperative test balloon occlusion. INTERVENTION: After undergoing stereotactic computed tomographic angiography with fiducial markers, the patients underwent a minimally invasive awake craniotomy with frameless stereotactic navigation. In all cases, the results of the neurological examination were unchanged during temporary parent artery occlusion and the aneurysms were successfully obliterated. CONCLUSION: Awake minimally invasive craniotomy for an infectious aneurysm located in eloquent brain enables awake testing before permanent clipping or vessel sacrifice. Combining frameless stereotactic navigation with computed tomographic angiography allowed us to perform the operation quickly through a small craniotomy with minimal exploration.
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3/14. debridement of periumbilical necrotizing fasciitis: importance of excision of the umbilical vessels and urachal remnant.

    The operation of a neonate with periumbilical necrotizing fasciitis consisted of (1) excision of infected skin, fat, and fascia (including the umbilicus); (2) a limited laparotomy, with ligation and excision of the umbilical vessels and urachal remnant; and (3) placement of a temporary silastic patch over the central abdominal defect. Pathological sections confirmed the spread of infection along the vessels and urachal remnant. Excision of the vessels and urachal remnant may be crucial to survival from periumbilical necrotizing fasciitis.
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4/14. Histopathology of bacillary angiomatosis of lymph node.

    Bacillary angiomatosis, a recently characterized pseudoneoplastic vascular proliferation caused by a bacterium identical or related to the cat-scratch disease bacillus, usually presents as cutaneous lesions. We report the histologic findings of this disease involving the lymph nodes of two immunocompromised patients. The lymph nodes showed patchy involvement by coalescent nodules of proliferated blood vessels lined by plump endothelial cells with pale cytoplasm. There were foci exhibiting mild to moderate nuclear atypia. Although neutrophil infiltration was prominent in one case, it was minimal in the other. The interstitium was formed by pink-staining material in hematoxylin-eosin-stained sections, and this proved to be aggregated bacilli on Warthin-Starry stain. Recognition of this potentially fatal disease is important because it is curable with antibiotics.
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5/14. The agent of bacillary angiomatosis. An approach to the identification of uncultured pathogens.

    BACKGROUND. Bacillary angiomatosis is an infectious disease causing proliferation of small blood vessels in the skin and visceral organs of patients with human immunodeficiency virus infection and other immunocompromised hosts. The agent is often visualized in tissue sections of lesions with Warthin-Starry staining, but the bacillus has not been successfully cultured or identified. This bacillus may also cause cat scratch disease. methods. In attempting to identify this organism, we used the polymerase chain reaction. We used oligonucleotide primers complementary to the 16S ribosomal rna genes of eubacteria to amplify 16S ribosomal gene fragments directly from tissue samples of bacillary angiomatosis. The dna sequence of these fragments was determined and analyzed for phylogenetic relatedness to other known organisms. Normal tissues were studied in parallel. RESULTS. Tissue from three unrelated patients with bacillary angiomatosis yielded a unique 16S gene sequence. A sequence obtained from a fourth patient with bacillary angiomatosis differed from the sequence found in the other three patients at only 4 of 241 base positions. No related 16S gene fragment was detected in the normal tissues. These 16S sequences associated with bacillary angiomatosis belong to a previously uncharacterized microorganism, most closely related to Rochalimaea quintana. CONCLUSIONS. The cause of bacillary angiomatosis is a previously uncharacterized rickettsia-like organism, closely related to R. quintana. This method for the identification of an uncultured pathogen may be applicable to other infectious diseases of unknown cause.
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6/14. Post-cannulation radial artery aneurysm--a rare complication.

    The following case report describes an expanding aneurysmal dilatation of the radial artery which developed 17 days following cannulation. Possible causes of this complication are: abnormal state of the vessel wall, multiple attempts at cannulation, and haematoma or infection at cannulation site. Other major and minor sequelae following arterial cannulation are reviewed.
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7/14. Microvascular injury and repair in acute human bacterial pyelonephritis.

    Acute inflammatory cell-capillary endothelial cell interactions, related to injury and repair, were investigated light and electron microscopically in acute human bacterial pyelonephritis. In inflammatory infiltrate-adjacent microvessels, the small capillaries were completely occluded by leukocyte plugs and the large capillaries were densely filled with acute inflammatory cells adhering to the endothelium. Severe damage to small and large capillaries was observed around endothelium adherent, degranulated neutrophil granulocytes containing phagocytosed bacteria. There were spaces in the endothelium, degradation of the vascular basement membrane, of the perivascular interstitial matrix and of collagen fibrils, with fibrin deposition and vessel wall fragmentation. In the small capillaries relatively distant from the interstitial infiltrates, emigration of leukocytes was frequently seen. Around the escaping cells the endothelial lining displayed occasional discontinuities, allowing leakage of vascular fluid into the interstitial space. Some small capillaries not related to the infiltrate were occluded by fibrin thrombi with apparent damage to the endothelial cells and disruption of the capillary wall. Various reparative changes were noticed in association with this change including capillary neovascularization. The findings confirm the existence of polymorphonuclear leukocyte-mediated injury of capillaries during the development of inflammatory responses in acute pyelonephritis.
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8/14. survival following rupture of a pancreatic abscess in a heart transplant recipient.

    A 43-year-old man underwent orthotopic heart transplantation for end-stage ischemic cardiomyopathy. Immunosuppressive therapy consisted of cyclosporine and corticosteroids. The diagnosis of acute pancreatitis was made on the ninth postoperative day and was based on clinical symptoms and an upper gastrointestinal barium study. Both serum and urine amylase values were normal. Abdominal ultrasound examination was nondiagnostic. Two weeks postoperatively, the patient's clinical condition deteriorated sharply. Chest and abdominal roentgenograms revealed free intraperitoneal air, as well as air in the lesser sac. diagnosis of a ruptured pancreatic abscess was made, and he underwent immediate exploratory laparotomy. Four liters of purulent fluid were present in the peritoneal cavity. A ruptured pancreatic abscess was found, and it had dissected above the superior mesenteric vessels and down the right gutter over the inferior vena cava. After extensive retroperitoneal debridement and copious irrigation, multiple surgical drains were placed. The patient is now well and is performing normal daily activities 16 months after the transplantation procedure. The incidence and proposed causes of pancreatitis occurring after heart transplant are reviewed, and we discuss our management of this complication.
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9/14. Cutaneous and soft-tissue manifestations of sepsis due to gram-negative enteric bacilli.

    Four patterns of tissue involvement can be distinguished in sepsis due to gram-negative enteric bacilli. When intense local inflammation predominates, cellulitis or thrombophlebitis results, often with venous or arterial obstruction. bacteria are present in the affected tissues, but not in sufficient numbers to be seen microscopically. When bacterial proliferation is unchecked by an appropriate leukocyte response, ecthyma gangrenosum, erythema multiforme, or diffuse bullous lesions may occur with minimal clinical or histologic signs of inflammation. In symmetric peripheral gangrene associated with disseminated intravascular coagulation, bland fibrinous deposits are seen in small vessels but neither inflammatory cells nor bacteria are present. The fourth kind of lesion is that seen in bacterial endocarditis. In all four patterns a vascular component is prominent clinically and histologically. The pathogenesis of these lesions is multifactorial; in each individual case the interaction between bacterial and host factors probably determines which clinical picture will result. The appearance of symmetric soft tissue lesions of the extremities in the absence of predisposing local conditions suggests the possibility of sepsis due to gram-negative bacilli, especially if other clinical features indicate that sepsis might be present.
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10/14. Acute acalculous cholecystitis. An increasing entity.

    Acute acalculous cholecystitis was observed to increase in frequency between 1950 and 1979, an increase that was statistically significant. The greatest part of this increase occurred between 1965 and 1979. Acute acalculous cholecystitis was also found to be associated with a higher mortality rate, more than twice that of acute calculous cholecystitis. Acute acalculous cholecystitis occurred in a variety of clinical settings including bacterial sepsis, severe trauma including surgical trauma and burns, multiple transfusions, and severe debilitation. The lesion in the gallbladder consists of intense injury of blood vessels in the muscularis and serosa similar to those induced experimentally by in vivo activation of factor xii dependent pathways. Possibly because of the intensity of vascular injury, acute acalculous cholecystitis with minimal clinical manifestations may rapidly progress to gangrene with perforation. Undelayed surgical treatment, which has become more widely accepted over the past 50 years, is essential. It may have also contributed to the increased recognition of this clinical entity.
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