Role of Chlamydia pneumoniae in acute chest syndrome of sickle cell disease

Miller, Scott T.; Hammerschlag, Margaret R.; Chirgwin, Keith; Rao, Sumathi; Roblin, Patricia M.; Gelling, Maureen; Stilerman, Tziporah; Schachter, Julius; Cassell, Gail H.

doi:10.1016/s0022-3476(05)81839-6

Cited by 76 publications

(24 citation statements)

References 13 publications

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“…First described over 30 years ago (Charache et al 1979), ACS has a complex pathophysiology that remains poorly defined. Numerous etiologies have been proposed including typical and atypical bacterial pathogens (Miller et al 1991;Vichinsky et al 2000;Neumayr et al 2003), viral infection (Lowenthal et al 1996), fat embolism (Vichinsky et al 1994), intrapulmonary sequestration of erythrocytes (Vichinsky et al 1994), and nitric oxide -hemoglobin interactions (Gladwin et al 1999).…”

Section: Acute Chest Syndromementioning

confidence: 99%

Current Management of Sickle Cell Anemia

McGann

Nero

Ware

2013

Cold Spring Harbor Perspectives in Medicine

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Proper management of sickle cell anemia (SCA) begins with establishing the correct diagnosis early in life, ideally during the newborn period. The identification of affected infants by neonatal screening programs allows early initiation of prophylactic penicillin and pneumococcal immunizations, which help prevent overwhelming sepsis. Ongoing education of families promotes the early recognition of disease-released complications, which allows prompt and appropriate medical evaluation and therapeutic intervention. Periodic evaluation by trained specialists helps provide comprehensive care, including transcranial Doppler examinations to identify children at risk for primary stroke, plus assessments for other parenchymal organ damage as patients become teens and adults. Treatment approaches that previously highlighted acute vaso-occlusive events are now evolving to the concept of preventive therapy. Liberalized use of blood transfusions and early consideration of hydroxyurea treatment represent a new treatment paradigm for SCA management.

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Section: Acute Chest Syndromementioning

confidence: 99%

Current Management of Sickle Cell Anemia

McGann

Nero

Ware

2013

Cold Spring Harbor Perspectives in Medicine

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“…However exceptions can occur. Acute chest syndrome due to C. pneumoniae in children with sickle disease is frequently severe with significant hypoxia [24]. The chest radiograph may show interstitial or lobar infiltrates.…”

Section: Clinical Presentationmentioning

confidence: 99%

Chlamydia pneumoniae and the lung

Mr¹

2000

European Respiratory Journal

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Chlamydia pneumoniae and the lung. M.R. Hammerschlag. #ERS Journals Ltd 2000. ABSTRACT: Chlamydia pneumoniae is a frequently occurring respiratory pathogen affecting all age groups. It may cause 5±20% of community-acquired pneumonias in adults and children. The organism has also been implicated as an infectious trigger for asthma. Furthermore, new studies suggest that it may play a role in the pathogenesis of several chronic diseases including atherosclerosis.However, despite the growing significance of C. pneumoniae as a pathogen, progress is hampered by the lack of standardized diagnostic methods including serology and polymerase chain reaction. This makes it practically impossible for the practitioner to make a specific microbiological diagnosis. The lack of standardized methods has also had an adverse effect on treatment trials. The dependence on serology for diagnosis in treatment studies has generated some questionable results.Unless cultures are performed, microbiological efficacy cannot be assessed and it may never be possible to survey for or document the emergence of resistance.

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“…In a series of studies, 10% of cases of pneumonia and approximately 5% of cases of bronchitis, sinusitis and, in Finland, pharyngitis have been attributed to the organism (30). In addition, C. pneumoniae has been proposed to be a risk factor for immune-reactive disorders such as adult-onset asthma, reactive arthritis, and acute chest syndrome of sickle cell anemia (21,40). Patients with human immunodeficiency virus infection or other immunosuppressive diseases have increased incidences of seropositivity and isolation of bacteria from the lungs, although the role of C. pneumoniae as an opportunistic pathogen in immunocompromised persons is not well defined (1,14).…”

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confidence: 99%

Roles of Interleukin-12 and Gamma Interferon in MurineChlamydia pneumoniaeInfection

et al. 2000

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BALB/c and strain 129 mice infected intranasally with Chlamydia pneumoniae displayed a moderate-to-severe inflammation in the lungs and produced interleukin-12 (IL-12), gamma interferon (IFN-␥), tumor necrosis factor alpha (TNF-␣), and IL-10, with peak levels on days 1 to 3 postinfection (p.i.), returning to basal levels by day 16 p.i. Anti-IL-12 treatment resulted in less-severe pathological changes but higher bacterial titers on days 3 and 7 p.i. By day 16 p.i., the inflammatory responses of control antibody-treated mice subsided. The bacterial titers of both anti-IL-12-and control antibody-treated mice decreased within 3 weeks to marginally detectable levels. Anti-IL-12 treatment significantly reduced lung IFN-␥ production and in vitro spleen cell IFN-␥ production in response to either C. pneumoniae or concanavalin A. In ␥-irradiated infected mice, cytokine production was delayed, and this delay correlated with high bacterial titers in the lungs. Following C. pneumoniae infection, 129 mice lacking the IFN-␥ receptor ␣ chain gene (G129 mice) produced similar IL-12 levels and exhibited similarly severe pathological changes but had higher bacterial titers than 129 mice. However, by day 45 p.i., bacterial titers became undetectable in both wild-type 129 and G129 mice. Thus, during C. pneumoniae lung infection, IL-12, more than IFN-␥, plays a role in pulmonary-cell infiltration. IFN-␥ and IL-12, acting mostly through its induction of IFN-␥ and Th1 responses, play an important role in controlling acute C. pneumoniae infection in the lungs, but eventually all mice control the infection to undetectable levels by IL-12-and IFN-␥-independent mechanisms.

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Role of Chlamydia pneumoniae in acute chest syndrome of sickle cell disease

Cited by 76 publications

References 13 publications

Current Management of Sickle Cell Anemia

Current Management of Sickle Cell Anemia

Chlamydia pneumoniae and the lung

Roles of Interleukin-12 and Gamma Interferon in MurineChlamydia pneumoniaeInfection

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