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Infectious Optic Neuropathies
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Imran Rizvi, Ravindra Kumar Garg
Vision loss is a common complication of tuberculosis in South East Asia. Vision loss is seen both in pulmonary as well as in extrapulmonary tuberculosis. Tuberculous meningitis is the most frequent extrapulmonary tuberculosis that leads to vision impairment. Vision impairment occurs in approximately 25% tuberculous meningitis patients.29 In tuberculous meningitis, a variety of causes are responsible for vision loss. Causes include tuberculous optic neuropathy, optico-chiasmatic arachnoiditis, compression by enlarging third ventricle, optic nerve tuberculoma and ethambutol toxicity. Tuberculous optic neuritis can occur as a result of direct Mycobacterium tuberculosis infection, Bacillus Calmette-Guerin vaccination or hypersensitivity reaction.30 Tuberculous optic neuritis often presents with unilateral painless vision loss. Eye examination demonstrates papillitis along with neuroretinitis, optic nerve tubercle and papilledema.31
Tuberculosis in Childhood and Pregnancy
Published in Lloyd N. Friedman, Martin Dedicoat, Peter D. O. Davies, Clinical Tuberculosis, 2020
Lindsay H. Cameron, Jeffrey R. Starke
Confirming a diagnosis of tuberculous meningitis can be extremely difficult. The TST and IGRAs are negative in up to 50% of cases, and 20%–50% of children have a normal chest radiograph.76 The most important laboratory test for the diagnosis of tuberculous meningitis is examination and culture of the lumbar cerebrospinal fluid (CSF). The CSF leukocyte count usually ranges from 10 to 500 cells/μL. Polymorphonuclear leukocytes may be present initially and may portend a poorer prognosis, but a lymphocyte predominance is more typical. The CSF glucose is usually between 20 and 40 mg/dL, whereas the CSF protein level is elevated and may be markedly high (400–5,000 mg/dL). The success of the microscopic examination of stained CSF and mycobacterial cultures correlates with the volume of the CSF sample. When a minimum of 10 mL of lumbar CSF is available, the acid-fast stain of the CSF sediment is positive in up to 30% of cases and the culture is positive in up to 70% of cases. Unfortunately, a volume of 1–2 mL is usually all that can be obtained from a young child. Polymerase chain reaction (PCR) testing of the CSF can improve diagnosis. Cultures of other body fluids can help confirm the diagnosis.
Pulmonary Tuberculosis In Children
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
Miliary disease results when a small caseous focus, often from a lymph node, discharges multiple organisms into the bloodstream. This is the earliest complication of primary tuberculosis, often occurring with the first 3 months. In Lincoln’s series, 90% of children with miliary tuberculosis showed evidence of primary disease. Infants and young children are predominantly affected. The most characteristic symptoms are fever and, later, rapidly progressing weight loss, but there are no respiratory symptoms. The chest physical examination is usually normal, but the spleen is nearly always enlarged. Within 1 to 3 weeks after the onset of fever, multiple small nodules of a uniform size are seen in the chest roentgenogram. The lateral view reveals the tiny lesions in the retrocardiac space as well as the hilar adenopathy of the primary complex. The lesions will increase rapidly in size if diagnosis and treatment are delayed. A positive Mantoux skin test in the presence of this characteristic roentgenogram is diagnostic in the young child. Choroid tubercules on fun-doscopic examination would be further corroboration, but Lincoln found them in only 13% of her cases. Because untreated miliary tuberculosis nearly always progresses to tuberculous meningitis, examination of the cerebrospinal fluid is essential before treatment is started.6
Management of tuberculous meningitis in children
Published in Paediatrics and International Child Health, 2021
H. Simon Schaaf, James A. Seddon
Tuberculous meningitis (TBM) remains the most devastating form of tuberculosis (TB). A systematic review of TBM in children reported an overall mortality risk of almost 20% [1], yet mortality has been found to be <5% in some large paediatric studies [2,3]. In several studies, severe neurological morbidity is reported in more than 50% of survivors, but this depends largely on the stage of TBM at presentation [1,4]. Because many cases go undiagnosed, little is known about the true incidence of TBM in children, and, even if diagnosed, cases may not be reported [5,6]. In Germany, a low TB-burden country, the prevalence of TBM among TB cases from 2002 to 2009 was estimated to be approximately 1% overall, but was 3.9% in children <5 years, 2.2% in children aged 5–9 years and 1.3% in children aged 10–14 years [7]. In a high TB-burden setting in the Western Cape, South Africa, 5.6% of children (<13 years) with bacteriologically confirmed TB diagnosed at hospital level between 2013 and 2017 had TBM [8]. The World Health Organization (WHO) estimated that in 2019 there were 1.19 million new cases of TB in children (0–<15 years); if 2% of these children had TBM, it would account for ~25,000 cases per year globally. This editorial briefly describes the pathogenesis of TBM in children as well as advances in diagnostics, recent developments in antimicrobial therapy and the role of therapeutic drug monitoring.
HIV TB coinfection - perspectives from India
Published in Expert Review of Respiratory Medicine, 2021
Bharat Bhushan Rewari, Amitabh Kumar, Partha Pratim Mandal, Anoop Kumar Puri
Paradoxical TB-IRIS generally develops during the first 4 weeks of starting ART [61]. It usually presents with a worsening of the TB and may manifest as new infiltrate on chest radiograph or worsening of an existing lesion, new onset lymphadenopathy, enlargement of existing lymphadenopathy, serous effusions, soft tissue abscesses [63]. Patients may also have protracted fever, weight loss, and other constitutional symptoms. Neurological manifestations may be tuberculous meningitis, enlarging tuberculomas, brain abscesses and carries a worse prognosis [64]. The most likely pathological mechanism is due to inflammatory response to mycobacterial antigen persisting in the tissues despite TB treatment. Diagnosis is by exclusion of other opportunistic infection, drug resistant TB, poor adherence to TB treatment, malabsorption of drugs, malignancy, etc.
Intensified antibiotic treatment of tuberculosis meningitis
Published in Expert Review of Clinical Pharmacology, 2019
Fiona V. Cresswell, Lindsey Te Brake, Rachel Atherton, Rovina Ruslami, Kelly E. Dooley, Rob Aarnoutse, Reinout Van Crevel
It is widely recognized that TBM is the most severe form of TB – death and severe neurological sequelae are common. Reported outcomes vary drastically by geographical region, prevalence of HIV co-infection, drug resistance patterns, and time period. We reviewed tuberculous meningitis studies published up to 6 June 2018, to examine the risk of death, and neurological sequelae amongst survivors. Full search strategy and search terms are shown in the supplementary material. After manual screening of abstracts, we included 84 studies; 12 included all ages, 35 included adults only, and 37 included children only. We present data from both retrospective and prospective studies which commenced enrolment within the past 30 years (from 1988 onwards) and which enrolled at least 100 participants (n = 28; 4 all ages, 16 adults, 8 children) plus two additional smaller studies which add to limited evidence within a drug-resistant population in Table 1.