zithromax has been researched along with Meningitis--Bacterial* in 3 studies
3 other study(ies) available for zithromax and Meningitis--Bacterial
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Clinical metagenomic sequencing for rapid diagnosis of neonatal meningitis caused by Ureaplasma parvum: A case report.
It is challenging to obtain favorable results through conventional diagnostic testing for Ureaplasma parvum (UP), a conditional pathogen, because of the atypical clinical phenotype of UP meningitis.. Herein, we report a pediatric case of neonatal meningitis caused by UP in a spontaneously delivered full-term baby. The infant's temperature peak was 38.3°C at the age of 9 days. The patient was diagnosed with neonatal suppurative meningitis.. The pathogen was diagnosed in a timely and accurate manner by metagenome sequencing, and the patient was eventually discharged with azithromycin.. Neonatal Ureaplasma meningitis may be more common than previously suspected. The clinical manifestations were not obvious and were similar to those of neonatal meningitis caused by other bacteria. When conventional treatments and conventional pathogenic tests are negative, mNGS is a better choice for timely and accurate pathogen identification. Topics: Adult; Anti-Bacterial Agents; Azithromycin; Child; High-Throughput Nucleotide Sequencing; Humans; Infant, Newborn; Infant, Newborn, Diseases; Meningitis, Bacterial; Metagenome; Metagenomics; Polymerase Chain Reaction; Ureaplasma | 2022 |
A novel NFKBIA variant substituting serine 36 of IκBα causes immunodeficiency with warts, bronchiectasis and juvenile rheumatoid arthritis in the absence of ectodermal dysplasia.
Genetic studies have led to identification of an increasing number of monogenic primary immunodeficiency disorders. Monoallelic pathogenic gain-of-function (GOF) variants in NFKBIA, the gene encoding IκBα, result in an immunodeficiency disorder, typically accompanied by anhidrotic ectodermal dysplasia (EDA). So far, 14 patients with immunodeficiency due to NFKBIA GOF mutations have been reported. In this study we report three patients from the same family with immunodeficiency, presenting with recurrent respiratory tract infections, bronchiectasis and viral skin conditions due to a novel pathogenic NFKBIA variant (c.106 T > G, p.Ser36Ala), which results in reduced IκBα degradation. Immunological investigations revealed inadequate antibody responses against vaccine antigens, despite hypergammaglobulinemia. Interestingly, none of the studied patients displayed features of EDA. Therefore, missense NFKBIA variants substituting serine 36 of IκBα, differ from the rest of pathogenic GOF NFKBIA variants in that they cause combined immunodeficiency, even in the absence of EDA. Topics: Adult; Arthritis, Juvenile; Azithromycin; Bronchiectasis; Cell Proliferation; Cells, Cultured; Child; Ectodermal Dysplasia; Gain of Function Mutation; Gentamicins; Humans; Immunologic Deficiency Syndromes; Leukocytes, Mononuclear; Male; Meningitis, Bacterial; Neisseria meningitidis; NF-KappaB Inhibitor alpha; Papillomaviridae; Pedigree; Pseudomonas aeruginosa; Pseudomonas Infections; Virus Diseases; Warts; Young Adult | 2020 |
[Meningitis after acute Borrelia burgdorferi infection in HIV infection].
A 39-year-old HIV positive patient developed myalgia, headache and cough 4 weeks after a tick bite. His temperature was 37.4 degrees C and a circular pale erythema was noted over the left lower leg.. C-reactive protein was raised to 120 mg/l, white blood cell count was 5860/microliter, CD4-lymphocyte count 250/microliter. The chest radiogram showed pneumonitic infiltration in the left lower lobe. There were IgM antibodies against Borrelia burgdorferi.. Left lower lobe pneumonia and chronic erythema migrans were diagnosed and he was given oral azithromycin (500 mg on the first day and 250 mg for 4 days). The pneumonia cleared up, but 2 weeks later he developed symptoms of meningitis (496 cells per microliter, 87% lymphocytes, positive Borrelia burgdorferi antibody titer), which quickly and lastingly responded to ceftriaxon (2 g daily by brief infusion for 14 days).. This immune-compromised HIV-infected patient developed disseminated borreliosis with CNS involvement 2 weeks after the occurrence of chronic erythema migrans. The initial treatment of the latter with azithromycin was unable to prevent the meningitis. It is unlikely that there was a causal connection between the borreliosis and the pneumonia. Topics: Adult; Animals; Anti-Bacterial Agents; Antibodies, Bacterial; Azithromycin; Borrelia burgdorferi Group; Ceftriaxone; Cephalosporins; HIV Seropositivity; Humans; Immunocompromised Host; Immunoglobulin M; Insect Bites and Stings; Lyme Disease; Male; Meningitis, Bacterial; Pneumonia; Ticks | 1997 |