Chlamydia pneumoniae and Acute Chest Syndrome in Patients With Sickle Cell Disease

Dean, Deborah; Neumayr, Lynne; Kelly, D.; Ballas, Samir K.; Kleman, Klara; Robertson, Shanda; Iyer, Rathi V.; Ware, Russell E.; Koshy, Mabel; Rackoff, Wayne; Pegelow, Chuck H.; Waldron, Peter; Benjamin, Lennette J.; Vichinsky, Elliott

doi:10.1097/00043426-200301000-00010

Cited by 54 publications

(30 citation statements)

References 65 publications

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“…Positive controls were: (1) a CHsp60-and lipopolysaccharide-positive sample by IHC, and chlamydial DNAor cDNA-positive sample by kPCR (see below); and (2) Cpn grown in U-937 macrophages and snap-frozen in OCT. Culture for Cpn was performed as described. 13 Negative controls were: (1) a patient carotid plaque sample negative for Cpn by all tests; (2) excess IgG secondary antibody with chromogen DAB reacted against a Cpnpositive sample; and (3) mock-infected U-937 cells. Cpn antigens were similarly counted and normalized to cell number in 20 nonoverlapping fields of the same section as for IL-6.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Chlamydia pneumoniae Burden in Carotid Arteries Is Associated With Upregulation of Plaque Interleukin-6 and Elevated C-Reactive Protein in Serum

Johnston

Zhang

Messina

et al. 2005

ATVB

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Objective-Chlamydia pneumoniae (Cpn) infection of vascular smooth muscle cells increases secretion in vitro. In vivo, IL-6 stimulates liver C-reactive protein (CRP) production. Because serum levels of IL-6 and CRP are independent risk factors for stroke and myocardial infarction (MI), we investigated whether Cpn burden in carotid plaques might provide a link between plaque IL-6 expression and elevated serum levels of IL-6 and CRP. Methods and Results-Consecutive patients undergoing elective carotid endarterectomy were studied. Serum levels of CRP and IL-6 were measured before surgery.

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Section: Immunohistochemistrymentioning

confidence: 99%

Chlamydia pneumoniae Burden in Carotid Arteries Is Associated With Upregulation of Plaque Interleukin-6 and Elevated C-Reactive Protein in Serum

Johnston

Zhang

Messina

et al. 2005

ATVB

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“…Es una bacteria perteneciente al filo Chlamydiae, de la familia Chamydiaceae, relacionado, principalmente, con infecciones del tracto respiratorio superior en el ser humano 11 . Su ciclo de vida es bifásico, ya que una vez que ingresa al huésped en forma de corpúsculo elemental (CE), metabólicamente inactivo, debe desarrollarse a corpúsculo reticular (CR) que es la forma intracelular y metabólicamente activa 6,12,13 .…”

Section: Chlamydophila Pneumoniaeunclassified

Ateroesclerosis asociada a infección por chlamydophila pneumoniae: interacción entre el ser humano y una bacteria

Gudiño-Gomezjurado¹,

Gomezjurado

2015

Duazary

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La ateroesclerosis y sus complicaciones constituyen una de las mayores causas de morbi-mortalidad a nivel mundial. Sin embargo, solo la mitad de los casos se justifica por los factores de riesgo tradicionales. No obstante, desde hace casi cinco décadas se ha intentado encontrar causas no tradicionales asociadas a la enfermedad ateroesclerótica. Varios agentes infecciosos han emergido como posibles candidatos centralizándose la investigación en Chlamydophila pneumoniae por su capacidad de infectar las células endoteliales durante el proceso ateroesclerótico. A lo largo del tiempo, múltiples estudios han tratado de probar la causalidad de C. pneumoniae en el proceso ateroesclerótico y sus complicaciones. A pesar de esto, hasta la fecha las conclusiones son ambiguas y de poca relevancia para la práctica clínica diaria.Palabras clave: Aterosclerosis; Chlamydophila pneumoniae; Enfermedades Cardiovasculares (fuente: DeCS) ABSTRACTAtherosclerosis and its complications are a major cause of morbidity and mortality worldwide. However, only half of the cases are justified by traditional risk factors. Nevertheless for almost five decades ago, has tried to find non-traditional causes associated with atherosclerotic disease. Various infectious agents have emerged as potential candidates being centralized research Chlamydophila pneumoniae by its ability to infect endothelial cells in the atherosclerotic process. Over time many studies have tried to prove the causality of C. pneumoniae in the atherosclerotic process and its complications. Despite this, to date the findings are ambiguous and of little relevance to daily clinical practice.

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“…Although children may be more likely to have infectious etiologies for their chest syndrome and adults more likely sickle cell-related causes, 4,5 infection and inflammation may well induce sickling, and embolism/infarction may lead to superimposed infection. This is perhaps best illustrated by the fact that 2 common causes of ACS, Chlamydia pneumoniae and Mycoplasma pneumoniae, are associated with a severe clinical course in children with sickle cell disease [6][7][8][9] rather than the "walking pneumonia" that typifies infection in others. It thus makes no sense to try to differentiate between "pneumonia" and ACS.…”

Section: (William Shakespeare)mentioning

confidence: 99%

“…24 That C pneumonia is an obligate intracellular organism and may persist even in patients who mount an antibody response makes a firm establishment of causation difficult. 25 Using PCR on BAL specimens and serology, Dean et al 8 found that C pneumoniae was the most common identifiable infectious agent in the NACSS; it was present in 7.2% of all patients and in 30% of all patients tested at first episode and with a single agent isolated. C pneumoniae infection occurs in young children (Ͻ 5 years of age) 26-28 and can be acquired nosocomially.…”

Section: Nothing Happens Without a Cause (Voltaire)mentioning

confidence: 99%

How I treat acute chest syndrome in children with sickle cell disease

Miller

2011

Blood

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IntroductionAcute chest syndrome is (ACS) the second most common cause of hospitalization and challenges infection 1 as the leading cause of sickle cell-related mortality 2 in children. Still, management is largely determined by the experience of individual practitioners, and there are no conclusive randomized controlled clinical trials to guide therapy. What follows is a review of treatment options and related issues to assist in management; it will likely be especially useful to those who do not regularly encounter children with this potentially life-threatening complication.What is in a name? That which we call a rose by any other name would smell as sweet. (William Shakespeare)ACS is the term used to describe a new pulmonary infiltrate with respiratory findings in a person with sickle cell disease. 3 The etiology of these episodes is often multifactorial and difficult to discern. Although children may be more likely to have infectious etiologies for their chest syndrome and adults more likely sickle cell-related causes, 4,5 infection and inflammation may well induce sickling, and embolism/infarction may lead to superimposed infection. This is perhaps best illustrated by the fact that 2 common causes of ACS, Chlamydia pneumoniae and Mycoplasma pneumoniae, are associated with a severe clinical course in children with sickle cell disease 6-9 rather than the "walking pneumonia" that typifies infection in others. It thus makes no sense to try to differentiate between "pneumonia" and ACS.Chance is a word that does not make sense. Nothing happens without a cause. (Voltaire)The investigators of a multicenter National Acute Chest Syndrome Study (NACSS) 4 published in 2000 made aggressive attempts to identify etiology, including the performance of bronchoalveolar lavage (BAL) on consenting study enrollees; 72% of the 671 enrolled in the study had a lavage or sputum sample available. Despite these efforts, the authors only established potential causation in 38% overall and 70% of those with a complete assessment.The most common identifiable cause of ACS in this study was pulmonary fat embolism (PFE). 4 Originally described in trauma victims, PFE is a frequent complication of bone fracture and may progress to involve the lungs and CNS with multiorgan failure and death. 10,11 The NACSS made the diagnosis by using BAL to identify fat-laden macrophages; less-invasive means of making the diagnosis are not well established, and even the specificity of fat-laden macrophages in BAL specimens has been questioned. 12 Vichinsky et al, 13 in the first systematic, prospective search for PFE in sickle cell disease, found that 44% of patients with moderate-tosevere ACS had PFE as a probable etiology. These patients had longer, more severe hospital courses and a greater decrease in hemoglobin concentration and platelet count than those without fat emboli. Fat from bone marrow, which is typically infarcted during acute pain episodes, 14 embolizes to the lungs and, in its most extreme form, fat embolism syndrome may involve the brain, k...

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Chlamydia pneumoniae and Acute Chest Syndrome in Patients With Sickle Cell Disease

Abstract: C. pneumoniae was the most prevalent pathogen in this study of ACS and was responsible for significant morbidity. Additional research is required to develop effective treatment guidelines for ACS.

Cited by 54 publications

References 65 publications

Chlamydia pneumoniae Burden in Carotid Arteries Is Associated With Upregulation of Plaque Interleukin-6 and Elevated C-Reactive Protein in Serum

Chlamydia pneumoniae Burden in Carotid Arteries Is Associated With Upregulation of Plaque Interleukin-6 and Elevated C-Reactive Protein in Serum

Ateroesclerosis asociada a infección por chlamydophila pneumoniae: interacción entre el ser humano y una bacteria

How I treat acute chest syndrome in children with sickle cell disease

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