RISK FACTORS FOR EARLY RELAPSE OF TUBERCULOSIS

In a study involving 12,183 patients who had completed treatment for tuberculosis, researchers found that a thrice-weekly drug regimen was associated with disease relapse. The study, conducted by Kwok Chiu Chang, MB, BS, MSc, of Yaumatei Chest Clinic in Hong Kong, and colleagues, was aimed at evaluating treatment-related risk factors of relapse of tuberculosis. Results were published in the November 15 American Journal of Respiratory and Critical Care Medicine.

A total of 113 patients relapsed within 30 months after ending therapy, with an overall relapse rate of 0.9%. These patients were then matched with 226 control subjects. Univariate conditional logistic regression analysis revealed that “thrice-weekly treatment increased the risk of relapse in comparison with daily treatment.” The researchers noted, however, that a thrice-weekly drug regimen could be a cost-effective treatment when no cavitation is found on initial chest x-ray. Among patients receiving thrice-weekly treatment, the 30-month relapse rate for those with no cavitation shown on initial x-ray was 1.1%, compared with 7.8% for those with cavitation present on initial chest x-ray. Comparatively, the relapse rate for those with cavitation present on initial x-ray and who were receiving daily treatment was 3.3%.

Researchers said the superior efficacy of daily treatment compared with thrice-weekly treatment is not surprising for two reasons: “First, most of the risk factors of relapse are ultimately related to the bacterial load of lesions. Second, Mycobacterium tuberculosis replicates approximately once daily when it is actively dividing. Faster sterilization is expected when actively dividing bacteria are killed daily.”

The researchers also pointed out that prolonging both intensive phase and overall treatment by 50% or more protected against relapse; however, prolonging either the intensive phase or overall treatment alone did not seem to protect against relapse.

Other risk factors for relapse of tuberculosis that were identified in the study included “history of opiate use, coexisting extrapulmonary tuberculosis, higher radiographic extent and cavitation on initial chest radiograph, body weight below 50 kg … and persistence of positive culture after two to three months of treatment.”

Chang KC, Leung CC, Yew WW, et al. A nest case-control study on treatment-related risk factors for early relapse of tuberculosis. Am J Respir Crit Care Med. 2004;170:1124-1130.

FAMILIAL RISK OF DEVELOPING LUNG CARCINOMA

Researchers have found that genetic factors contribute to the development of lung carcinoma, according to a report in the December 22/29 JAMA. Steinn Jonsson, MD, and colleagues found an increased risk for lung carcinoma among first-, second-, and third- degree relatives of patients with lung carcinoma, with a stronger effect for relatives of patients with early-onset disease.

The researchers estimated risk ratios of lung carcinoma for relatives of patients with the disease by linking records of 2,756 patients with lung carcinoma within the Icelandic population with a genealogical database of all Icelanders and their ancestors.

Results showed that parents, siblings, and children had risk ratios of 2.69, 2.02, and 1.96, respectively; uncles/aunts and nephews/ nieces had risk ratios of 1.34 and 1.28, respectively; and cousins had a risk ratio of 1.14. Parents, siblings, and children of patients with early-onset disease had risk ratios of 3.48, 3.30, and 2.84, respectively.

After assessing the risk ratios for smoking in a cohort of 10,541 people who had smoked for more than 10 years, the researchers rejected the hypothesis that this increased risk of developing lung carcinoma is solely due to the effects of smoking for all relatives, except cousins and spouses.

The researchers concluded that “these results underscore the importance of genetic predisposition in the development of lung carcinoma.... However, tobacco smoke plays a dominant role in the pathogenesis of the disease, even among those individuals who are genetically predisposed to lung carcinoma.”

Jonsson S, Thorsteinsdottir U, Gudbjartsson DF, et al. Familial risk of lung carcinoma in the Icelandic population. JAMA. 2004;292:2977-2983.

DENTAL PLAQUES ASSOCIATED WITH RESPIRATORY PATHOGEN COLONIZATION IN THE ELDERLY

Dental plaques may be a reservoir for respiratory pathogens responsible for hospital-acquired pneumonia in elderly patients, according to a study in the November Chest. The study is the first “to confirm the association between the colonization of dental plaques and lower respiratory infection in institutionalized patients using molecular genotyping.”

Ali A. El-Solh, MD, MPH, FCCP, and colleagues from the University at Buffalo in New York, examined the dental status of 49 critically ill residents of long-term care facilities who required mechanical ventilation and found a high prevalence of colonization of dental plaques with aerobic respiratory pathogens. They then performed protected bronchoalveolar lavage (PBAL) on 14 patients who subsequently developed hospital-acquired pneumonia. Pulsed-field gel electrophoresis was used to genetically compare respiratory pathogens recovered from PBAL fluid to those isolated from dental plaques.

The researchers were able to identify 33 respiratory pathogens from the dental plaques—11 from patients with clinical evidence of hospital-acquired pneumonia and 22 from patients without hospital-acquired pneumonia. “Staphylococcus aureus (45%) accounted for the majority of the isolates, followed by enteric Gram-negative bacilli (42%) and Pseudomonas aeruginosa (13%),” noted the researchers.

Pulsed-field gel electrophoresis revealed that nine respiratory pathogens recovered from PBAL fluid genetically matched those isolated from corresponding dental plaques in eight patients. “These included Staphylococcus aureus, Escherichia coli, Enterobacter cloacae, and Pseudomonas aeruginosa,” said the researchers.

Dr. El-Solh and colleagues pointed out that “future studies are needed to delineate whether daily oral hygiene in hospitalized elderly would reduce the risk of nosocomial pneumonia in this frail population.”

In an accompanying editorial, Gene R. Pesola, MD, MPH, said, “El-Solh et al have added another piece to the pathophysiologic puzzle of how pneumonia develops by demonstrating that ventilator-associated pneumonia can originate from organisms in dental plaque, something that has not been demonstrated before.”

Dr. Pesola also posed several important questions: Will improved daily oral hygiene result in a reduced risk of pneumonia? Does poor dental hygiene harbor respiratory pathogens that colonize the respiratory tract, or does colonization of the respiratory tract result in the transfer of bacteria to dental plaques, or both? And are elderly patients without teeth less likely to develop pneumonia?

He emphasized that understanding the pathophysiology of pneumonia and developing methods for the prevention of the condition will ultimately help to reduce costs and improve health outcomes.

El-Solh AA, Pietrantoni C, Bhat A, et al. Colonization of dental plaques: a reservoir of respiratory pathogens for hospital-acquired pneumonia in institutionalized elders. Chest. 2004;126:1575-1582.
Pesola GR. Ventilator-associated pneumonia in institutionalized elders: are teeth a reservoir for respiratory pathogens? Chest. 2004;126:1401-1403.

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