Wednesday, 27 November 2013

Lower respiratory tract infection (Respiratory Disease) – Bronchitis – The Causes

Lower respiratory tract infection
The lower respiratory tract infection are the infection consisting of the trachea (wind pipe), bronchial tubes, the bronchioles, and the lungs, including the bronchitis and pneumonia. According to  The World Health Report 2004 – Changing History(1), in 2002 lower respiratory track infection were still the leading cause of deaths among all infectious diseases, and accounted for 3.9 million deaths worldwide and 6.9% of all deaths that year.
Bronchitis is defined as a condition of an inflammation of the mucous membranes of the bronchi, the larger and medium-sized airways that carry airflow from the trachea into the lung parenchyma(7). Most cases of Bronchitis are as a result of recurrent injure to the airways caused by inhaled irritants and cigarette smoking(6). There are 2 types of bronchitis
A.1. Causes
A.1.1. Acute bronchitis
The most common causes of acute brochitis are as result of the infection due to the invasion of Virus, (influenza and cold). Prolonged activity of the presence of the virus can have many deteriorative effects.Young adults with underlying medical conditions who are infected with the H1N1 virus are at risk of quickly progressing from mild upper airways infection to severe ARDS within 4 to 5 days after the onset of the illness. According to the study by Dr. Homsi S and the research team, there is a report of a case  a 46-year-old morbidly obese and diabetic woman infected with the H1N1 virus who developed acute bronchitis that lasted for 4 weeks and then progressed to ARDS. The month-long persistence of the H1N1 viral bronchitis and its late progression to ARDS which may reflect prolonged viral activity. Such a prolonged, rather than quick, course of deterioration can cause clinicians to misdiagnose the etiology of the ARDS and may cause the patient to receive a prolonged treatment with steroids to treat bronchitis symptoms(8).
Other in the reviewed study of reported eight cases of influenza A (H1N1) 2009 admitted to themedical intensive care with severe respiratory failure between November and December 2009 and in January 2011. All patients were older than 30 but younger than 50 years, had clinical and radiological evidence of an Acute Respiratory Distress Syndrome (ARDS) and needed invasive ventilatory support. The clinical course of severe cases of influenza A (H1N1) 2009-infection is markedly different from the disease pattern seen during epidemics of seasonal influenza. Most of the patients admitted to our intensive care unit due to influenza A (H1N1) 2009 associated ARDS were previously healthy young people, according to the University Hospital of Muenster(9).
A.1.2. Chronic bronchitis
Most common causes of chronic bronchitis are as result of chronically smoking cigarettes, air pollution, dust. toxic gases, etc.
1. Smoking
In the case-control study in Beirut in 2009/2010 to evaluate the relationship: 274 cases of chronic bronchitis and 559 controls without the condition aged > or = 40 years, conducted by Lebanese University Beirut, found that current waterpipe dependence was significantly associated with chronic bronchitis (OR = 3.74, P < 0.001). After adjustment for covariates/confounders, ever waterpipe smoking > 20 WP-years (P < 0.001) was significantly associated with chronic bronchitis(10).
Other study indicated that in a retrospective clinical and morphological study on a group of 17 smoker patients with symptoms of chronic bronchitis, eight non-smokers diagnosed with chronic bronchitis and five non-smokers and asymptomatic subjects. CB developed especially in men of 65-year-old or older, especially in smokers with a median FEV1% at around 71. Histopathologically, patients with symptoms of CB, regardless of smoking status, presented on bronchial biopsies with focal squamous metaplastic change, goblet cell hyperplasia and enlargement of the bronchial gland mass because of the inflammatory process, consisting predominantly of mononuclear cells in the bronchial wall. The statistical testing proved a significant correlation between the densities of different inflammatory cell classes (with the exception of mast cells in the bronchial epithelium) and FEV1% values on epithelium and submucosa regions in all investigated groups(11).
2. Air pollution, dust. toxic gases and other occupational chemical exposures
In the study to ascertain chronic obstructive pulmonary disease (COPD) prevalence among industrial workers in the Russian Federation and determine relative contribution of smoking and occupational factors to COPD of 1,375 workers aged 30 or over, found that those with airfl ow limitation of FEV1/FVC<0.70 were considered having COPD and those with presence of cough and sputum production for at least three months in each of two consecutive years were considered having chronic bronchitis (CB), with no overlapping between these 2 groups. Data on occupational history and VGDF levels in the working area were collected from all participants. In total, 105 cases of COPD and 170 cases of CB were diagnosed in the cohort of examined workers. Occupational exposure to VGDF was twice as often present among COPD patients than among both patients with CB and the control group of healthy workers (p<0.05). More than 40 % of COPD patients were occupationally exposed to VGDF above the value of 3.0 of the occupational exposure limit (OEL) and more than 20 % to 6.0 OEL and higher. Overall odds ratio for COPD development due to occupational VGDF exposure was 5.9 (95 % CI=3.6 to 9.8, p=0.0001). Both smoking and VGDF seem to be important for the development of COPD. Analysis of the combined effect of tobacco smoking and occupational noxious particles and gases on COPD development has shown the following order of risk factors based on the strength of their influence: VGDF levels, smoking index, age, and heating microclimate(12).

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