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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Allescheria boydii, a true fungus frequently isolated from soil, is best known as a causative agent of maduromycosis of the foot. In our report we describe two patients under treatment for acute leukemia who died from rapidly progressive A. boydii infections. One patient had signs of central nervous system infection and was found at autopsy to have had a large brain abscess. The second patient had a cavitary necrotizing pneumonia with thoracic inlet obstruction (Pancoast's syndrome) and failed to show improvement despite treatment with amphotericin B. The clinical spectrum of allescheriasis is reviewed with particular emphasis on its role as a pathogen in the compromised host. Since A. boydii may resemble other fungi morphologically in tissue sections and may produce infections clinically similar to other mycoses, culture of the organism is required for definitive diagnosis. Based on recently reported in vitro susceptibility studies, miconazole may have a future role in the therapy of A. boydii infections which are resistant to presently available antifungal agents.
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PMID:Allescheria boydii infections in the immunosuppressed host. 27 Sep 6

The designation of "Infantile Bilateral Striatal Necrosis" (IBSN) was first given by Friede in 1975. However, this unusual condition was first described by Paterson and Carmichael in 1924. The disease is rare with uncertain etiology. The clinical picture includes choreoathetosis, abnormal eye movements, seizures and mental dullness. These circumstances often follow symptoms such as fever, vomiting and impaired consciousness. The final diagnosis is confirmed by pathological examination, which reveals symmetrical degeneration of bilateral basal ganglia. With present technology IBSN can be well demonstrated in the brain Ct scans or MRI scans nowadays. This article reports four cases with clinical manifestations which had appeared before the age of one year. Three cases had prodromal upper respiratory tract infection symptoms with vomiting, while seizure and impaired consciousness ensued. One case had several bouts of pneumonitis followed by seizures, impaired consciousness and abnormal eye movement. Brain sonogram of one of these cases showed hyper-echoic basal ganglia, while CT scans or MRI scans revealed symmetrical hypodensity or signal change over bilateral basal ganglia, respectively. All of these led to a bedridden life. These four cases are reported based on their clinical presentations and brain imaging findings, in spite of the absence of pathological confirmation. Some of the literature are also reviewed. To sum up, IBSN should be kept in mind in the differential diagnosis of symmetrical bilateral basal ganglia lesion after the exclusion of other disorders such as neurometabolic disorders, central nervous system infection, carbon monoxide intoxication, hypoxic-ischemic encephalopathy, tumors and cerebrovascular disorders etc.
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PMID:[Infantile bilateral necrosis of the striatum of corpus: report of four cases]. 151 18

Haemophilus influenzae type b is a human bacterial pathogen that causes approximately 12,000 cases of H influenzae type b meningitis and 7500 cases of other forms of invasive disease annually in the United States. This organism is the leading cause of bacterial meningitis in the United States. The cause of meningitis can be established more accurately than that of other forms of invasive bacterial disease because the isolation of the bacterium from the cerebrospinal fluid or blood and/or the detection of bacterial antigen can correctly attribute the infection to a specific bacterial agent and dictate appropriate antimicrobial therapy. In children, more than 95% of all invasive diseases attributable to Haemophilus species, including septicemia, pneumonia, epiglottis, cellulitis, arthritis, osteomyelitis, and pericarditis, are due to H influenzae type b. It has been estimated that systemic disease caused by H influenzae type b occurs in approximately 1 in 200 children in the United States before the age of five. The case fatality rate for H influenzae type b meningitis is approximately 5%, and substantial morbidity has also been documented to result from central nervous system infection with this agent. Of surviving children reported in a 1969 paper, 40% had significant neurologic sequelae after meningitis. A more recent study demonstrated substantial neurologic improvement during the first few months after hospitalization, but at 1 year of age 8% of the children had neurologic or intellectual sequelae of their meningitis. Milder defects with an array of developmental problems have been reported in as many as one third to one half of all survivors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiology of Haemophilus influenzae type b infections. 217 52

Infections of the central nervous system in patients at risk are relatively uncommon when compared with pneumonia, bacteremia, and soft tissue infection. However, they carry serious morbidity and are frequently fatal. Each of the diverse conditions that can place a patient at risk for central nervous system infection is associated with a fairly predictable spectrum of etiologic organisms. Various forms of trauma (including blunt and penetrating injuries and neurosurgery, especially when a cerebrospinal fluid shunt is implanted) predispose to infection with common pathogenic bacteria. Defects of cellular immunity including congenital immune deficiencies, immunosuppressive drug therapy, leukemia, lymphoma, and the acquired immune deficiency syndrome are more likely to give rise to infection with a distinctive spectrum of opportunistic viruses, fungi, and protozoa. Other underlying conditions include sinus, ear, and mastoid infections, congenital heart disease, intrathoracic suppuration, endocarditis, and bacteremia, hypogammaglobulinemia, and complement deficiencies. Some preventive measures including vaccines, antibiotics, and surgical procedures are available. However, for many of these central nervous system infections, preventive measures are lacking or less effective than those for infections in other organs. In the future, opportunistic central nervous system infections will increase in frequency as the number of patients at risk continues to grow.
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PMID:Prevention of central nervous system infections in patients at risk. 637 75

CRP level was determined in the cerebrospinal fluid in 40 cases of bacterial meningitis. Similar determination in serum was done in 32 of these patients. Aetiological verification was possible in 90% of cases. Meningitis caused by Str. pneumonia and Neisseria meningitides prevailed (52.5% and 27.5% respectively). The control group comprised 20 subjects. For CRP demonstration immunochemical and turbidimetric methods were used. CRP in CSF was raised in 62.5% of the study cases while in the serum it was raised in all of them. CRP detection in serum in acute phase of central nervous system infection is diagnostically important since CRP increase suggests a purulent process.
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PMID:[C-reactive protein (CRP) and its significance in purulent meningitis]. 858 95

A retrospective review of cases seen in the Diarrhea Treatment and Training Unit (DTU) of Bangalore (India) Medical College's Vani Vilas Children's Hospital during 1992-1994 confirmed the efficacy of the standard case management approach. This strategy entails oral rehydration therapy (ORT), continued feeding, and selective use of intravenous fluids and antibiotics. Of the 7966 children (4374 males and 3592 females) reporting to the DTU during the 2-year study period, only 2412 (30.5%) had received oral rehydration solution (ORS) or home-available fluids before admission. Acute watery diarrhea was present in 7316 cases (91.84%). Death occurred in 59 acute watery diarrhea cases, 6 dysentery cases, and 7 persistent diarrhea cases. The average time for cases managed in the ORT area was 2 hours and 45 minutes, while the hospital stay for admitted cases averaged 3 days. In 6957 cases (87.33%), ORS was sufficient treatment. Of the 1009 children (12.67%) who required intravenous fluids, 254 had dehydration attributable to conditions such as persistent vomiting and inability to drink due to oral thrush. Only the 512 children (6.2%) with cholera and dysentery received antibiotics. Of the 72 children who died (case fatality rate, 0.9%), 43 had associated severe malnutrition with pneumonia and anemia, 14 had a central nervous system infection, and 13 had septicemia; in only 2 cases could death be directly ascribed to diarrheal disease. One of these cases was due to shigella encephalopathy and the other to severe dehydration with acidosis. The average cost of treatment per patient was Rs 2.91 when only ORS was used compared with Rs 24.28 when intravenous rehydration was required. The finding that less than one-third of children had received ORS before admission suggests a need for the establishment of more DTUs in large hospitals that can train community-based health personnel in diarrhea case management.
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PMID:Management of diarrhea in a DTU. 905 85

To determined the safety and efficacy of prophylactic antibiotics in head-injured patients requiring intracranial pressure monitors, the files of 30 consecutive patients with isolated, severe head injuries admitted over a 1-year period were reviewed. Patients .15 years with severe closed-head injury who did not have severe concomitant, extracranial injury (Abbreviated Injury Score, 3) and survived .48 hours following hospital admission were included. Fourteen patients underwent intracranial pressure monitor placement and received prophylactic antibiotics for the duration of monitoring and the remaining 16 patients were neither monitored nor given prophylactic antibiotics. Length of hospital stay, length of intensive care stay, overall and septic complication rate, and death rate were compared for the two treatment groups. The groups were similar with regard to patient characteristics, associated injuries, and injury severity. Patients who received prophylactic antibiotics demonstrated statistically higher septic morbidity rates (78.6% versus 31.3%) and statistically higher pneumonia rates (57.1% versus 18.8%) compared with patients who did not. No patient developed central nervous system infection related to the monitor itself. These results indicate that the administration of prophylactic antibiotics to head-injured patients for the duration of intracranial pressure monitoring is unnecessary and potentially detrimental. Antibiotics, if given at all, should be limited to the period immediately surrounding intracranial pressure monitor placement.
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PMID:Antibiotic prophylaxis for intracranial pressure monitors. 968 77

Sixty nosocomial infections caused by Pseudomonas aeruginosa and Acinetobacter baumannii resistant to aminoglycosides, cephalosporins, quinolones, penicillins, monobactams, and imipenem were treated with colistin (one patient had two infections that are included as two different cases). The infections were pneumonia (33% of patients), urinary tract infection (20%), primary bloodstream infection (15%), central nervous system infection (8%), peritonitis (7%), catheter-related infection (7%), and otitis media (2%). A good outcome occurred for 35 patients (58%), and three patients died within the first 48 hours of treatment. The poorest results were observed in cases of pneumonia: only five (25%) of 20 had a good outcome. A good outcome occurred for four of five patients with central nervous system infections, although no intrathecal treatment was given. The main adverse effect of treatment was renal failure; 27% of patients with initially normal renal function had renal failure, and renal function worsened in 58% of patients with abnormal baseline creatinine levels. Colistin may be a good therapeutic option for the treatment of severe infections caused by multidrug-resistant P. aeruginosa and A. baumannii.
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PMID:Intravenous colistin as therapy for nosocomial infections caused by multidrug-resistant Pseudomonas aeruginosa and Acinetobacter baumannii. 1222 36

Capsulate bacteria cause the majority of community-acquired pneumonia presenting to hospital world-wide, at all ages. They are united by the virulence factor of their differing capsular polysaccharides, enabling them to evade phagocytosis. All cause invasive disease beyond the respiratory tract, including septicaemia and central nervous system infection. Recent advances in vaccine development have made the capsular polysaccharide an achievable target for vaccine strategies across all ages, with impacts already seen upon Streptococcus pneumoniae and Haemophilus influenzae type b pneumonia in countries able to afford these new vaccines.
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PMID:Capsulate bacteria and the lung. 1199 99

Melioidosis is an emerging infection in Brazil and neighbouring South American countries. The wide range of clinical presentations include severe community-acquired pneumonia, septicaemia, central nervous system infection and less severe soft tissue infection. Diagnosis depends heavily on the clinical microbiology laboratory for culture. Burkholderia pseudomallei, the bacterial cause of melioidosis, is easily cultured from blood, sputum and other clinical samples. However, B. pseudomallei can be difficult to identify reliably, and can be confused with closely related bacteria, some of which may be dismissed as insignificant culture contaminants. Serological tests can help to support a diagnosis of melioidosis, but by themselves do not provide a definitive diagnosis. The use of a laboratory discovery pathway can help reduce the risk of missing atypical B. pseudomallei isolates. Recommended antibiotic treatment for severe infection is either intravenous Ceftazidime or Meropenem for several weeks, followed by up to 20 weeks oral treatment with a combination of trimethoprim-sulphamethoxazole and doxycycline. Consistent use of diagnostic microbiology to confirm the diagnosis, and rigorous treatment of severe infection with the correct antibiotics in two stages; acute and eradication, will contribute to a reduction in mortality from melioidosis.
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PMID:Clinical guideline for diagnosis and management of melioidosis. 1654 71


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