Cases reported "Meningitis, Meningococcal"

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1/58. Meningococcal disease and meningitis: a review of deaths proceeding to coroner directed autopsy in Auckland.

    AIMS: To assist the early diagnosis of meningitis, by finding trends and patient profiles, where delay or other factors may have lead to a fatal outcome. methods: All deaths from meningitis and meningococcal disease, confirmed at autopsy were reviewed. The study involved the Auckland area, in the period January 1988 November 1997. RESULTS: Cases were divided into those caused by N meningitidis and other meningitides. Death due to N meningitidis is often within 12-24 hours of the first symptomatology. Symptoms are often vague and may be indistinguishable from any other infection, often leading to fatal patient or doctor delay. A diagnosis of meningococcal disease cannot be excluded on: no rash (44%), no "meningitis" symptoms as sepsis without meningitis occurs (44%), age (50% were over 15 years old) or the presence of other abnormalities, eg bronchopneumonia or hydrocephalus. Non-N meningitidis menigitis is a disease of the very young or old, its time course is also swift with 30% suffering similar vague symptoms for less than 24 hours before death. CONCLUSIONS: For both categories, treat immediately and treat on suspicion, otherwise conformation of the diagnosis might be postmortem.
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2/58. properdin deficiency in a large Swiss family: identification of a stop codon in the properdin gene, and association of meningococcal disease with lack of the IgG2 allotype marker G2m(n).

    properdin deficiency was demonstrated in three generations of a large Swiss family. The concentration of circulating properdin in affected males was < 0.1 mg/l, indicating properdin deficiency type I. Two of the nine properdin-deficient males in the family had survived meningitis caused by neisseria meningitidis serogroup B without sequel. Two point mutations were identified when the properdin gene in one of the properdin-deficient individuals was investigated by direct solid-phase sequencing of overlapping polymerase chain reaction (PCR) products. The critical mutation was found at base 2061 in exon 4, where the change of cytosine to thymine had generated the stop codon TGA. The other mutation was positioned at base 827 in intron 3. The stop codon in exon 4 was also demonstrated by standard dideoxy sequencing in three additional family members. The question was asked if genetic factors such as partial C4 deficiency and IgG allotypes could have influenced susceptibility to meningococcal disease in the family. No relationship was found between C4 phenotypes and infection. Interestingly, the two properdin-deficient males with meningitis differed from the other properdin-deficient persons in that they lacked the G2m(n) allotype, a marker known to be associated with poor antibody responses to T-independent antigens. This implies that the consequences of properdin deficiency might partly be determined by independent factors influencing the immune response.
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3/58. Unusual cluster of mild invasive serogroup C meningococcal infection in a university college.

    The objective of this study was to describe the epidemiology and public health response to an apparent cluster of neisseria meningitidis serogroup C infection in university students in a residential college. A conventional epidemiological approach was taken, supported by routine and novel diagnostic techniques. Over the two days of 21-22 August 1997, three cases of suspected meningococcal infection were notified from a residential college complex at a university campus in the Sydney metropolitan area. neisseria meningitidis was grown from throat swabs of all three cases, and was isolated from the blood of one case only. All three isolates were typed as C:2a:P1.5,2. Seroconversion was demonstrated by a novel method in the three cases. Rifampicin was given to all identified contacts. Forty-seven days after the index case, a 19 year old female living in the same complex was diagnosed with bacterial meningitis, and identified contacts given rifampicin. When this isolate was found to be group C, it was decided to vaccinate residents of the college complex. Genotyping and serotyping (C:2a:P1.5) later revealed the fourth isolate to be distinct from isolates from Cases 1-3. In conclusion the authors note that australia's increasing capacity to type meningococcal strains is essential to understanding the epidemiology of this disease. Furthermore, typing information is of critical importance when decisions are made regarding mass vaccination. As early antibiotic treatment may inhibit isolation of the organism, development of novel approaches to diagnosis and typing should be supported.
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4/58. Delayed deterioration of hearing following bacterial meningitis.

    Bacterial meningitis is an important cause of acquired sensorineural deafness in childhood. deafness following meningitis may be progressive. Previous reports have shown deterioration in hearing up to 12 years after the illness. We present two cases of sensorineural deafness following meningitis. Severe to profound sensorineural hearing losses were detected immediately after meningitis in these patients. The hearing subsequently deteriorated in both cases. Deterioration in hearing thresholds occurred 17 years after the illness in one case. In the other patient the hearing got progressively worse three years after meningitis. She subsequently required a cochlear implant.
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5/58. Management and prevention of meningococcal disease.

    While many other illnesses affecting children have been contained or even eliminated, meningococcal disease has become a leading infectious cause of death. The major management challenge may be increased intracranial pressure or toxic shock, depending on whether meningitis or septicemia predominates. A new protein-conjugated group C vaccine is expected to reduce deaths by as much as 40%.
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6/58. dexamethasone use in adult meningococcal meningitis.

    The use of dexamethasone in the management of bacterial meningitis in adults remains controversial. This report illustrates the case of a 27-year-old male with severe meningococcal meningitis and meningococcemia who completely recovered after receiving antibiotics and dexamethasone. In adults with suspected bacterial meningitis, especially in high risk cases, the adjunctive use of dexamethasone may be beneficial.
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7/58. disease due to serogroup W135 neisseria meningitidis.

    Five cases of disseminated meningococcal disease due to serogroup W135 Neisseria meningitidis are presented. The cases ranged in age from 16 months to 23 years, and spanned a clinical spectrum from mild meningitis without rash or evidence of meningococcal septicemia to severe meningoencephalitis with fulminant meningococcemia, disseminated intravascular coagulation, and death. These cases demonstrate that serogroup W135 N meningitidis is fully pathogenic for man and capable of producing the full spectrum of disseminated meningococcal disease associated with other serogroups. Since this serogroup has recently emerged as a significant cause of disease in europe, attention should be focused on the correct serogroup designation of strains of N meningitidis isolated from clinical material and reported as "nongroupable" by clinical laboratories, so that additional clinical and epidemiologic information may be obtained.
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8/58. Acute severe spinal cord dysfunction in bacterial meningitis in adults: MRI findings suggest extensive myelitis.

    BACKGROUND: Bacterial meningitis is rarely complicated by acute spinal cord involvement (eg, myelitis, ischemic infarction, spinal abscess, or epidural hemorrhage). In spinal cord dysfunction, magnetic resonance imaging (MRI) is the imaging modality of choice. Still, MRI findings of myelitis due to bacterial meningitis in adults have not been reported. methods: Spinal MRIs were obtained during the acute stage of meningitis and on follow-up in 3 adults with bacterial meningitis that was complicated by paraparesis or tetraparesis and bowel and bladder incontinence. The causative pathogens were streptococcus pneumoniae and neisseria meningitidis; in 1 patient, the pathogen was not identified. RESULTS: In all cases, spinal MRI ruled out a compression of the cord by an extramedullary mass but demonstrated hyperintensities on T2-weighted images that predominantly involved the gray matter and extended from the cervical to the lumbar cord. Leptomeningeal and discrete nodular intramedullary enhancement on T1-weighted images was detected only in 1 patient. Follow-up examinations revealed that hyperintensities resolved completely in 1 patient, while a central cavitation developed in the cervical spinal cord of another, and the MRI findings were progressive during the first 4 weeks in the third patient. In all cases, severe paresis and bowel and bladder incontinence persisted. CONCLUSION: We demonstrate for the first time the MRI findings of adults with acute spinal cord involvement during bacterial meningitis. magnetic resonance imaging showed central intramedullary hyperintensities on T2-weighted images that extended from the cervical to the lumbar cord, indicating myelitis. Clinical follow-up examinations suggest that myelitis during bacterial meningitis has an unfavorable prognosis.
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9/58. Thoracic myelopathy complicating acute meningococcal meningitis: MRI findings.

    spinal cord dysfunction is a rare complication of neisseria meningitidis (meningococcal) meningitis. We report a 17-year-old patient who had a 3-day history of fever, headache and vomiting, agitation, and unresponsiveness. cerebrospinal fluid showed a marked polymorphonuclear pleocytosis. latex particle agglutination was positive for meningococci. The patient was given intravenous antibiotics and intravenous dexamethasone. Over the next 4 days, he developed weakness of the lower extremities, with areflexia and extensor plantar responses. MRI revealed contiguous hyperintensities on T2-weighted images involving the thoracic spinal cord from T4 to T9 and 4 brain abscesses. Five months later, he recovered brain function, but the paraparesis remained. This case illustrates that myelopathy may complicate acute meningococcal meningitis, possibly due to a vasculitis, stroke, autoimmune myelopathy, or direct infection of the spinal cord. patients with myelopathy associated with acute meningitis should receive spinal MRI. In addition, meningitis should be considered in patients presenting with acute myelopathy.
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10/58. Primary (isolated) meningococcal pericarditis.

    A 19-year-old man was admitted with a history and examination findings of probable bacterial pericarditis. blood cultures produced neisseria meningitidis Group C, sensitive to penicillin. The patient was initially treated with intravenous benzylpenicillin. Echocardiogram demonstrated the development of a pericardial effusion which was tapped, and benzylpenicillin was instilled into the pericardial space. Because of failure of clinical resolution, cefotaxime was substituted for benzylpenicillin. Rapid clinical improvement then ensued. Repeat echocardiogram showed evidence of neither reaccumulation nor constrictive pericarditis. Primary (isolated) meningococcal pericarditis is a recognized though rare manifestation of meningococcal disease. It is most common in young adults and is associated with a good prognosis.
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