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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A mouse hepatitis virus, strain JHM, grown on DBT cell culture was inoculated intranasally into ICR-SLC weanling mice, and histopathological lesions were studied in relation to viral growth. In the spleen virus titer reached a peak of 10(3) PFU/0.2G 48 H after inoculation, and later it decreased gradually. No virus was detected from the liver throughout the experiment, while some early inflammatory reactions appeared in the spleen and liver without any further development. At 48 h postinoculation there existed degeneration and necrosis in the nasal mucosa and submocosa. In the brain and spinal cord active viral growth was seen at 48 h postinfection or later. In the olfactory bulb mitral cells were also affected with accumulation of glial cells and some meningitis. At 72 to 96 h postinoculation, degeneration of neurons and glial cells were remarkable in the tructus olfactorius, cortex of lobus piriformis, septa pellucidum and commissura anterior accompanying meningitis. At 120 h postinfection, pyramidal cells in the hippocumpus were also degenerated and necrotized, and nodular proliferation and collapse of glial cells, small foci of demyelination and perivascular cuffing were seen in the interbrain. At 144 h postinoculation or later, the lesions developed through the whole brain including the pons and medulla oblongata as well as spinal cord. Brain virus titers showed 10(5) PFU/0.2g at 120 h and 10(4) PFU/0.2g at 144 h postinfection. In mice surviving at 168 hr after inoculation severe demyelinating lesions were observed despite of a decreased virus titer. These findings suggest that intranasally inoculated virus might invade the olfactory bulb through the tractus olfactorius and then produce necrotizing lesions, extending later towards the posterior parts of the central nervous system.
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PMID:Nasoencephalopathy of mice infected intrananasally with a mouse hepatitis virus, JHM strain. 19 27

Observations were conducted over 8 children aged 5 months to 3 years and 2 months, in whom the disease developed acutely and was accompanied by collapse. Death occurred within the first 12--36 hours from the onset of the disease. Morphologically, there were revealed haemorrhagic rash, initial phenomena of serous-purulent meningitis, clear-cut disorders of the microcirculation (stasis, thrombosis) in the skin, lungs, myocardium, kidneys. The cause of early death of the children with meningoccaemia turned out to be the Waterhouse-Friderichsen syndrome, the morphological manifestations of the latter being bilateral haemorrhages into the adrenals. In the kidneys capillarothrombosis may develop, which is in accord with the picture of the Sanarelli-Schwartzmann phenomenon, and may lead to the development of acute renal insufficiency with formation of cortical necroses of the kidneys.
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PMID:[Morphological characteristics of meningococcemia in children]. 120 Aug 82

Serum C3 levels were measured in 211 patients with meningococcal disease. Low levels were found in 13 patients with acute meningococcaemia, and complement activation may have contributed to the peripheral circulatory collapse that was responsible for nine deaths. The complement profile of these patients suggested activation of both classical and alternative complement pathways. Patients with meningitis had a higher mean serum C3 level than controls. Serial studies in 13 serum antigen-positive patients with meningitis who subsequently developed arthritis or cutaneous vasculitis showed a transient fall in serum C3 in eight. This fall was probably due to the formation of immune complexes that were responsible for their allergic complications.
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PMID:Complement and meningococcal infection. 126 Mar 36

Clinical studies have demonstrated the prognostic importance of increased intracranial pressure in central nervous system infections. To delineate development of intracranial pressure in meningitis experiments were carried out in rabbits. Meningitis was induced by injecting streptococcus pneumoniae bacteria into the cisterna magna and blood, and intracranial pressures were continuously recorded. In the experimental model, three stages were seen: incubation period (0-8 h)--in which CSF becomes positive for the infecting organism and biochemical changes occur, but there are no hemodynamic or intracranial pressure changes; stage of slowly increasing intracranial pressure - because blood pressure remains normal, cerebral perfusion pressure is maintained adequate for cerebral metabolic need (9-24 h); terminal stage (greater than 25 h)--with hemodynamic collapse, critical reduction of cerebral perfusion pressure, cerebral ischemia, and death of the experimental animals. It is suggested that a similar sequence occurs in human disease. The clinical implication stresses the need for early recognition and treatment of intracranial hypertension as an important adjunct to antibiotic treatment of the infecting organism.
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PMID:Intracranial pressure and cerebral perfusion pressure in experimental streptococcus pneumoniae meningitis. 157 Apr 13

Fifty-six neonates with enterococcal septicemia in a single hospital from 1977 through 1986 were studied. The incidence was low and constant until 1983, when an increase, attributable to infections in infants older than 7 days of age (late-onset), was noted. These infants were more premature (mean gestational age 29.5 vs 36.9 weeks) and had lower birth weights (mean 1250 vs 2700 g) than those with early-onset enterococcal sepsis, and in most the infections were characterized by a nosocomial origin. Infants with early-onset infection had a mild illness with respiratory distress typical of other etiologic agents or diarrhea without focal infection. By contrast, late-onset enterococcal sepsis was heralded by severe apnea, bradycardia, circulatory collapse, and increased ventilatory requirements. Focal infections, including scalp abscess or catheter-related infection (23% each), meningitis or pneumonia (15% each), were common. Rapid clinical improvement and clearance of bacteremia resulted from therapy with an aminoglycoside and either ampicillin or vancomycin, but only if abscesses were drained and intravascular catheters were removed. Mortality rates for early-onset, late-onset, and necrotizing enterocolitis-associated infection were 6, 8, and 17%, respectively. Enterococcus is a frequent cause of late-onset septicemia in premature neonates, and empiric therapy should include appropriate antimicrobial agents.
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PMID:Enterococcal sepsis in neonates: features by age at onset and occurrence of focal infection. 210 74

Vasoactive intestinal polypeptide (VIP) and endotoxin (lipopolysaccharides, LPS) were measured in plasma samples from 11 patients with bacteriologically verified meningococcal disease. Five patients suffered fulminant septicaemia, developed severe septic shock, and 2 died due to circulatory collapse. Initially, all 5 had levels of VIP above 4 pM and plasma endotoxin above 200 ng/liter. Five patients were diagnosed as meningitis and 1 as having meningococcaemia, all with a normal circulatory state. None of these 6 patients had initially levels of VIP above 2.5 pM or endotoxin levels above 25 ng/liter (P less than 0.001). A correlation existed between plasma endotoxin and VIP levels (r = 0.735, P = 0.01). Sequentially collected samples from 3 patients showed rapidly declining VIP levels after initiation of antibiotic and fluid treatment. These results are in agreement with previous animal experiments, suggesting that endotoxin directly or indirectly stimulates the VIP-ergic nervous system in the initial phase of gram-negative septic shock in man.
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PMID:Elevated VIP and endotoxin plasma levels in human gram-negative septic shock. 250 Jun 80

In late 1984, 10 children in a small, rural town in Brazil had high fever associated with vomiting and abdominal pain. Within 12-48 h of the onset of fever, purpura developed associated with vascular collapse and peripheral necrosis. All 10 children died. Cerebrospinal fluid examinations did not suggest meningitis and, when done, tests were negative for Neisseria meningitidis. Other culture, serological, and necropsy examinations did not reveal a cause. Case-finding uncovered another cluster of similar illness in children in a second town and sporadic cases in five other cities. Two case-control studies demonstrated that children who became ill were significantly more likely than control children to have had conjunctivitis during the month before illness. This conjunctivitis was purulent, preceded the onset of more severe disease by 3-15 days, and had resolved before fever began. Although no conjunctival cultures were obtained from case-children, Haemophilus aegyptius was the most common pathogen isolated from other conjunctival cultures during the epidemic. This organism was also isolated from a non-aseptic skin scraping from 1 case child. A 25-megadalton plasmid distinguished the H aegyptius isolates epidemiologically associated with illness from other Brazilian conjunctival isolates. Brazilian purpuric fever is a newly recognized syndrome of epidemic purpura fulminans associated with antecedent purulent conjunctivitis, possibly caused by H aegyptius.
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PMID:Brazilian purpuric fever: epidemic purpura fulminans associated with antecedent purulent conjunctivitis. Brazilian Purpuric Fever Study Group. 288 85

This article has overviewed complications of rhinoplasty. Generally, these complications fall into two categories: aesthetic (that is, cosmetic sequelae that may require a revision rhinoplasty) and nonaesthetic. Of the nonaesthetic complications, infection has the widest span of severity. A localized Staphylococcus aureus abscess or Pseudomonas infection of the nose may occur postoperatively. Owing to the proximity of the nose to the cranium, a cavernous sinus thrombosis or basilar meningitis may result. Postoperative toxic-shock syndrome is a rare occurrence that surgeons should be aware of; most cases have occurred with the presence of nasal packing, but a case using only plastic nasal splints has been reported also. Bacteremia seems to be uncommon during rhinoplasty. Infection after rhinoplasty is generally much less frequent than one would expect from an operation in an unsterile field. Antibiotics are frequently utilized electively. Postoperative nasal-periorbital edema and ecchymosis are regarded as unavoidable but may be lessened significantly by postoperative head elevation and cold packs. The possibility of postoperative bleeding must be evaluated by the surgeon preoperatively. This sequela usually occurs either within 72 hours postoperatively or at around 10 days postoperatively. Many different causes exist for chronic postoperative nasal obstruction, from poorly supported nasal valves closing upon inspiration to an enhanced allergic rhinitis leading to chronic nasal mucosal edema. The latter may be treated by injection of steroid into the turbinates. Among aesthetic complications, supratip prominence, saddle deformity, and persistent hump are among the more commonly reported. Supratip prominence--"polly-beak"--can be caused by inadequate reduction of tip cartilaginous or soft-tissue elements, especially in relation to the reduction of the dorsum. An over-reduced dorsum will leave an otherwise normal nasal tip with a relative prominence. An accumulation of blood or a mucous cyst occurring under the skin of the tip will produce a prominence. Poor tip projection, tip ptosis, and alar collapse are the result of overreduction of tip elements. A dislocated alar cartilage can appear as an asymmetric nasal bossa. Saddle-nose deformity occurs after overaggressive bony and/or cartilaginous hump removal. Infractured nasal bones that subsequently drop into the piriform aperture can create a bony saddle. Persistent hump is due to inadequate reduction of a bony or cartilaginous hump. If the septal cartilage reduction is disproportionate to the bony septum reduction, the appearance of either a hump or a saddle is possible.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Postoperative sequelae and complications of rhinoplasty. 332 Aug 72

Traditionally, frontal mucoceles were treated with open obliterative procedures such as collapse of the forehead soft tissues into the sinus or the more cosmetically appealing osteoplastic flap technique. When a frontal mucocele expands intracranially, these surgical procedures become difficult and with higher risk of cerebrospinal fluid leak and/or meningitis. In cases of a mucocele that extends both intracranially and anteriorly into the soft tissues, osteoplastic flap procedure may not be possible. We present our experience with telescopic intranasal surgery for the treatment of frontal mucocele with intracranial extension. The technique, which is based on intranasal marsupialization and stenting, was used in four patients with large mucoceles eroding into the cranium and the anterior soft tissues. The results were excellent and the patients are free of disease 1 to 4 1/2 years after surgery.
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PMID:Telescopic extracranial approach to frontal mucoceles with intracranial extension. 760 79

In a series of 12 patients with syringomyelia associated with Chiari's malformation, the authors quantitatively analyzed cerebrospinal fluid (CSF) dynamics in the subarachnoid space of the craniospinal junction, using cine MRI combined with pre-saturation method. In most of subjects, cine MRI revealed (1) decreased or increased maximum velocity of CSF in the caudal direction and (2) disturbed CSF motion in the caudal direction (delayed % cardiac cycle) in the craniospinal junction, strongly suggesting disturbed CSF dynamics in the craniospinal junction because of the tonsilar herniation. Of 12 subjects, 8 patients underwent foramen magnum decompression and 4 underwent syringo-subarachnoid shunt (SS shunt). In the patients who showed marked collapse of syrinx after foramen magnum decompression, follow-up cine MRI revealed the normalization of % cardiac cycle, representing postoperative improvement of CSF dynamics in the craniospinal junction. On the other hand, % cardiac cycle did not improve significantly in the patients who did not show marked collapse of the syrinx or suffered from meningitis after surgery. Significant changes were not observed in the patients who underwent SS shunt. In summary, these results suggested that cine MRI combined with pre-saturation method could detect the pathophysiological changes and evaluate the efficacy of the surgery, especially foramen magnum decompression, in the patients with syringomyelia associated with Chiari's malformation.
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PMID:[CSF dynamics in the patients with syringomyelia associated with Chiari's malformation--quantitative analysis on cine MRI]. 813 2


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