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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cryptococcosis, caused by Cryptococcus neoformans, is the most common life-threatening AIDS-related fungal infection. The infection can occur in any organ of the body, although meningitis is its most frequent form. Symptoms of cryptococcal meningitis appear gradually and generally include headache, fever, or malaise. Symptoms may also include memory loss, lethargy, and personality changes. Isolation of the pathogen is done by using microscopy of the cerebrospinal fluid or by testing the serum antigen titer. Appropriate therapy includes amphotericin B or triazole antifungals. Patients with elevated intracranial pressure may be treated by draining cerebrospinal fluid (about 30 ml) daily. Other antifungal agents are being investigated.
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PMID:Cryptococcosis. 1136 41

Bacterial meningitis is one of the major causes of morbidity and mortality in children. A retrospective chart review of all cases of culture-proven bacterial meningitis in children was conducted in a tertiary care facility in the King Fahad National Guard Hospital (KFNGH), Riyadh. Sixty-seven patients with culture-proven meningitis were reviewed. Bacterial meningitis is more common in children under 2 years of age (85%). Haemophilus influenzae type b (Hib) was the most common organism causing meningitis in children (57%). Streptococcus pneumoniae was the second most common organism (31%) followed by group B streptococcus in (7.5%). Fever, lethargy and vomiting were the most common presenting symptoms, occurring in 95%, 72%, and 66% respectively. The calculated incidence of Hib in KFNGH is 40/100,000. This incidence decreased dramatically after the initiation of routine infant vaccination in KFNGH with the conjugate Hib vaccine in April 1998. Outcome of Hib meningitis was good in 85% while outcome of Streptococcus pneumoniae was good in (53%). 43% of S. pneumoniae were resistant to penicillin. There was no cephalosporin-resistant isolate identified during the study period. Mortality due to meningitis was 4 (6%), 3 patients died due to S. pneumoniae and one due to Hib. Since Hib is the most common organism causing meningitis in Saudi Arabian children, mass vaccination of all Saudi children should be mandatory.
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PMID:Bacterial meningitis in Saudi Arabia: the impact of Haemophilus influenzae type b vaccination. 1143 27

The importance of an acute encephalopathy associated with nontyphoidal salmonellosis has recently been recognized, but the disease entity has been poorly established. In this study, we describe two encephalopathic patients associated with nontyphoidal salmonellosis. The patients exhibited a rapid evolution of coma after the onset of lethargy or seizure. Fever and diarrhea due to salmonellosis preceded these events. Secondary factors inducing encephalopathies, such as severe dehydration, sepsis, meningitis, electrolyte or metabolic disturbances, acute renal failure, and multiple organ failure, were excluded in the differential diagnosis at the onset of encephalopathic features. These clinical findings and rapid development of encephalopathic features from localized intestinal infection without any significant abnormalities in a variety of blood tests may suggest a toxic etiology. However, endotoxin was not found in serum from both patients. From these results, we conclude that nontyphoidal salmonellosis can cause a toxic encephalopathy syndrome, like shigellosis or verocytotoxin-producing Escherichia coli infection.
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PMID:Acute encephalopathy associated with nontyphoidal salmonellosis. 1145 56

Treatment of tuberculous meningitis should begin with an anti-tuberculous regimen of at least three drugs: isoniazid, pyrazinamide, and rifampin. Early in the course of therapy, ethambutol or streptomycin may be of some added benefit. If the local incidence of drug resistance to Mycobacterium tuberculosis is greater than 4%, or is unknown, then a fourth drug (ethambutol or streptomycin) should be added. If the patient is from an area with organisms resistant to multiple drugs, or is likely to be infected with a multiply resistant organism for any reason, then the patient should be on enough drugs to insure that at least two active anti-tubercular drugs are included in the therapy. An expert should be consulted Length of therapy is not standardized. For sensitive organisms, a regimen of three drugs daily for 2 months, followed by two-drug therapy (isoniazid and rifampin) has been recommended. The American Thoracic Society (ATS) and the Centers for Disease Control (CDC) have recommended a minimum of 12 months of therapy for tuberculous meningitis. If cultures remain positive for extended periods, or signs or symptoms respond slowly, therapy should be extended to 18 months. Patients with HIV also may need longer courses of therapy. The severity of tuberculous meningitis can be classified based on a system devised by the British Medical Research Council. Stage I patients are fully conscious, rational, and do not have neurologic signs. Stage II patients are confused or have neurologic signs such as cranial nerve palsy or hemiparesis. Stage III patients are comatose or stuporous with more severe neurologic signs. Corticosteroids are recommended if the patient is mentally confused, has neurologic signs, or is comatose (Stages II and III). In patients with moderate disease (Stage II), corticosteroids appear to improve neurologic sequelae and survival. Dexamethasone 6 to 12 mg per day and prednisone 60 to 80 mg per day tapered over 4 to 8 weeks has been used. Symptoms of central nervous system (CNS) inflammation may recur if the corticosteroid taper is implemented too soon or too fast. Steroids and diuretics such as furosemide and acetazolamide are sometimes used to treat hydrocephalus. Ventriculoperitoneal or ventriculoatrial shunting may be required to relieve signs and symptoms of hydrocephalus.
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PMID:Tuberculosis Meningitis. 1148 56

Although Streptococcus salivarius is one of the normal flora in the oral cavity and gastrointestinal tract, the agent may cause bacteremia, meningitis, endocarditis and sinusitis under certain circumstances. We report a 3-year-old female with meningitis after oral trauma by a skewer due to penicillin resistant S. salivarius. The girl injured her throat accidentally with a skewer. Four hours later, she became febrile and came to our emergency room. Plain CT scan was normal, and cefalexin was prescribed. The next day, she had fever, lethargy, meningeal signs, and her cerebrospinal fluid (CSF) showed neutrophilic pleocytosis. The blood culture was negative, but the CSF culture was positive for S. salivarius. The minimal inhibitory concentrations (MIC) for panipenem, penicillin G, ampicillin, cefotaxime, ceftriaxone, vancomycin were 0.125 microgram/ml, 2 micrograms/ml, 2 micrograms/ml, 0.5 microgram/ml, 0.5 microgram/ml, 0.5 microgram/ml, respectively. Intravenous administration of panipenem betamiprom (PAPM/BP) 2 g/day for 7 days and 8 courses of dexamethasone 0.15 mg/kg/dose were effective, and she has had no apparent sequelae except for a slight abnormality in her electroencephalogram. Traumatic meningitis is often caused by S. pneumoniae, but may be also caused by the normal flora pathogens including S. salivarius. In addition, our case suggests that not only S. pneumoniae but also S. salivarius can be penicillin resistant. Taking the drug resistance into consideration, we have to be careful in choosing antibiotics for treating such patients.
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PMID:[Streptococcus salivarius meningitis after oral trauma by a skewer: a case report]. 1185 78

Group B beta-hemolytic streptococci and Escherichia coli strains account for approximately two thirds of all cases of neonatal meningitis, while bacteria that typically account for meningitis in older age groups (Haemophilus influenzae type B, Neisseria meningitidis, and Streptococcus pneumoniae) are infrequent causes of meningitis in the neonatal population. As with other medical problems in neonates, signs and symptoms of bacterial infection of the central nervous system are generally few in number and nonspecific in nature. Manifestations that can suggest meningitis, as well as other serious illnesses, include temperature instability, lethargy, respiratory distress, poor feeding, vomiting, and diarrhea. Signs suggestive of meningeal irritation, including stiff neck, bulging fontanelle, convulsions, and opisthotonus, occur only in a minority of neonates with bacterial meningitis and cannot be relied on solely to identify such patients. Ampicillin and either gentamicin or cefotaxime are recommended for initial empiric therapy of neonatal meningitis. When the results of the cerebrospinal fluid (CSF) culture and susceptibilities are known, therapy can be narrowed to cover the specific pathogen identified. In general, penicillin G or ampicillin is preferred for group B streptococcal meningitis, ampicillin for Listeria monocytogenes meningitis, and ampicillin plus either an aminoglycoside or cefotaxime for gram-negative meningitis. For the very low birth weight neonate who has been in the nursery for a prolonged period of time, organisms such as enterococci and gentamicin-resistant gram-negative enteric bacilli must also be considered. In patients with long-term vascular catheters, Staphylococcus aureus or coagulase-negative staphylococci must also be considered. Empiric combinations of antibiotics for such patients would include ampicillin or vancomycin, plus amikacin or cefotaxime. All neonates should undergo repeat CSF examination and culture at 48 to 72 hours after initiation of therapy. If organisms are observed on gram stain, modification of the therapeutic regimen should be considered, and neuroimaging should be performed. In general, therapy should be continued for 14 to 21 days for neonatal meningitis caused by group B streptococci or L. monocytogenes, and for at least 21 days for disease caused by gram-negative enteric bacilli. All patients with neonatal meningitis should have hearing and development monitored serially. The first audiologic evaluation should occur 4 to 6 weeks after resolution of the meningitis.
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PMID:Meningitis in the Neonate. 1193 31

The aim of this study was to present neurological complications of influenza infections. Infections caused by influenza viruses can be very serious and may lead even to death resulted from the post-infectious complications. The most often occurring complications are pneumonia, bronchitis, bronchiolitis, myocarditis and otitis media. The other group is neurological post-influenza complications, including dementia, epileptic disorders, cerebrovascular disease, febrile convulsions, toxic encephalopathy, encephalitis, meningitis, subarachnoid hemorrhages, lethargic encephalitis, psychosis or increase in the number of cases of Parkinson's disease. The first way of prevention of influenza is vaccination that results in healthy, social and economic benefits.
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PMID:[Neurological complication of influenza infections]. 1219 26

Tuberculous meningitis (TBM) presents clinically as either acute meningitis syndrome characterized by coma, raised intracranial pressures, seizures, and focal neurological deficits, or as a slowly progressive dementing illness. When the infection presents as the former, characteristic signs and symptoms are headache, malaise meningismus, papilloedema, vomiting, confusion, seizures, and cranial nerve deficits. Patients admitted with lethargy or stupor may enter coma in a matter of days, and fever may or may not be present. However, TBM more commonly presents as a slowly progressive dementing illness, with memory deficits and personality changes typical of frontal lobe-like disease. TBM is described with regard to its history, clinical presentations, complications, diagnosis, C.S.F. abnormalities, treatment, prognostic factors, and indications of steroids. Combination drug therapy involving isoniazid, rifampin, pyrazinamide, and pyridoxine is the recommended treatment strategy for adults. The patient's level of consciousness at the start of therapy is the most important prognostic factor reported in TBM cases, with the greater the change in mental status, the worse the outcome. The mortality rate of patients who are comatose before the initiation of therapy is 50-70%.
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PMID:Tuberculous meningitis. 1229 51

From 1996 to 2001, nineteen episodes of bacteremia due to group B Streptococci (GBS) were diagnosed in Siriraj Hospital, Mahidol University. The incidence of early onset group B streptococcal disease (EOD) was 0.27 cases/1,000 live births in 1996, and decreased to 0.10 cases/1,000 live births in 2001. The incidence of the late onset disease (LOD) was 0.05 cases/1,000 in 1996, and there has been none since 1998. All of the infants were inborn. Low birth weight was found in 53 per cent of the infants. Fifty-eight per cent of infants were male. Forty-seven per cent of the infants were born prematurely. None of the mothers had antenatal GBS screening. Only one mother received one dose of intrapartum antibiotic prophylaxis. No risk factor could be identified in 72 per cent of the mothers. EOD accounted for 79 per cent of all infants with GBS infections, with a mortality rate of 40 per cent. All of them died within the first 72 hours of life. Most EOD infants developed disease manifestations within 12 hours of life. Most common clinical manifestations were respiratory distress (74%), temperature instability (68%), cyanosis (63%), hypotension (42%) and lethargy (42%). Only one infant with EOD had meningitis. There were two infants in the LOD group; one of whom had cellulitis, and the other had meningitis. Neutropenia was noted in 42 per cent of all infants. Radiographic studies suggested a diffuse reticulogranular pattern or ground glass appearance in 38 per cent. The chest X-ray was interpreted as normal in 25 per cent of the infants. In conclusion, the incidence of GBS infection in newborn infants in Thailand is still very low but with a very high mortality. Prematurity accounts for almost half of the cases. Even though antepartum screening with intrapartum antibiotic chemoprophylaxis has been recommended in developed counties, its benefit and cost needs to be further investigated in Thailand.
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PMID:Neonatal group B streptococcal infection: incidence and clinical manifestation in Siriraj Hospital. 1240 23

Coccidioidal meningitis is lethal in humans. A reproducible murine model was established by lumbar intrathecal injection of Coccidioides immitis arthroconidia. Cerebrospinal fluid (CSF) samples were obtained by cisternal puncture. Lethal infection developed in all mice given 10-60 colony-forming units (cfu). Lethargy, ataxia, or paralysis preceded death. Temporal studies after challenge with 27 cfu revealed positive brain (4/5 mice) and spinal cord (2/5 mice) cultures on day 3; CSF samples contained 688 leukocytes/mm(3) and 33 cfu/mL. The results of histopathologic analysis were unremarkable. By day 8, all mice were culture positive (5.0 log(10) cfu in brain tissue and 4.1 log(10) cfu in spinal cord tissue); CSF samples contained 4833 leukocytes/mm(3) and 3425 cfu/mL. Histopathologic examinations showed acute meningitis of the brain and spinal cord, some parenchymal invasion and abscesses, and meningeal arteritis. Groups of mice given ketoconazole had prolonged survival and suppressed lung disease; histopathologic examination demonstrated granulomatous meningitis, possibly a more chronic form. With the development of these models, studies of pathogenesis, host response, and therapy are possible.
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PMID:A murine model of coccidioidal meningitis. 1255 29


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