Chest ACCP Education Calendar
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ashkin, D.
Right arrow Articles by Narita, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ashkin, D.
Right arrow Articles by Narita, M.
(Chest. 1999;116:856-857.)
© 1999 American College of Chest Physicians

"Won't Get Fooled Again" (by Tuberculosis)

David Ashkin, MD; Elena S. Hollender, MD and Masahiro Narita, MD

Drs. Ashkin, Hollender and Narita are from A. G. Holley State Tuberculosis Hospital, the Florida Department of Health. In addition, Drs. Ashkin and Narita are Clinical Assistant Professors, Division of Pulmonary and Critical Care Medicine, University of Miami School of Medicine.

Correspondence to: David Ashkin, MD, A. G. Holley State Hospital, 1199 W. Lantana Rd, Lantana, FL 33462; e-mail: Daskin@aol.com

We must be honest. When we first read the article by Pérez-Guzmán et al in this issue of CHEST (see page 961), we all had the same impression: there was nothing "new" in this article. There was nothing fancy or "high tech" that immediately caught our attention. But then we all remembered a recent case of a 75-year-old man from a nursing home who presented with cachexia. Only after an exhaustive medical workup was pulmonary tuberculosis (TB) diagnosed. The patient was presumed to have cancer, and no other differential diagnoses were entertained. Chest roentenograms and CT scan were read as neoplasm, and abdominal CTs were read as metastatic disease.

Once again, clinicians were fooled by TB. It changed its "face" (typical presentation), which delayed the diagnosis for months. This critical delay allowed the organism to potentially spread to dozens of new, vulnerable individuals who were exposed while he was in the nursing home and the hospitals. By the lack of early recognition, we once again missed an opportunity to stop the spread of this disease. It is the continued "missed opportunities" that have made TB one of the most successful microbiological pathogens in the world today. In order to reduce these missed opportunities and, thereby, the continued spread of this disease, it is imperative that clinicians always be on the alert for TB in all of its different guises.

That is why we believe this article to be important. Pérez-Guzmán et al present a meta-analytic review of the effects of aging on the clinical presentation of TB. In their analysis, elderly patients had a lower prevalence of fever, sweating, hemoptysis, cavitary disease, and purified protein derivative (PPD) positivity, as well as lower levels of albumin and blood leukocytes. We note that there was a potential bias in the selection of the patients because a significant number of them were inpatients, and thus the criteria for admission may have been different for younger vs elderly patients. Nevertheless, these findings serve as a warning to clinicians who usually rely on a standard clinical picture to point them to the diagnosis of TB. In addition, the older population had a greater prevalence of dyspnea and concomitant medical conditions, such as cardiovascular disease, COPD, diabetes, history of gastrectomy, and malignancies. While similar findings have been published before in separate reports, the compilation of these studies utilizing a meta-analysis study design should serve to reaffirm and solidify the nuances of the presentation of this disease in the elderly for the practicing clinician.

This study also reminds us that the clinical presentation of TB is intimately dependent on the status of the host's immune system. In the past, clinicians could expect that 95% of all patients with TB disease would present with upper lobe infiltrates and/or cavities on chest radiography. HIV, with its significant effect on the host immune system, has unfortunately taught us much about how the "classic" TB presentation can change. Up to 35% of HIV patients with TB disease have clear lung fields on chest radiograph.1 In fact, 5% of HIV-infected TB patients were smear positive despite "normal" chest radiographs.2 Up to 72% of patients with CD4 counts < 200 cells/µL are anergic and have no reaction to PPD.3 Before the widespread recognition of this modified clinical presentation, many clinicians did not diagnose TB in a timely manner, causing a delay in the isolation and treatment of these patients. This, in turn, led to subsequent nosocomial spread in congregate settings, at times with multidrug resistant strains.4

Over the past few years, much has been learned concerning the factors responsible for the differing clinical presentations, namely the immunologic response of the host. Through the elaboration of cytokines (such as tumor necrosis factor-{alpha}, interleukin-2, and interferon-{gamma}), macrophages, fibroblasts, and other cells form granulomata at the site of infection in an attempt to contain Mycobacterium tuberculosis. These cytokines also contribute to the induction of fever, sweating, cachexia, reduced albumin, delayed-type hypersensitivity with subsequent cavity formation, and PPD reactivity.5 Recent research has pointed to the importance of T-helper lymphocytes, specifically TH1 lymphocytes, in the containment of TB.6 When there is a defect in host cellular immunity, as occurs with the loss of T-helper lymphocytes in HIV disease, the TB progresses from infection to disease. Without proper function of TH1 lymphocytes, the clinical presentation of the disease may be altered, manifesting a decrease or absence of fever, and/or an attenuation of delayed-type hypersensitivity that may result in reduced cavity formation and lack of PPD response.

It may therefore be deduced that a corresponding underlying mechanism is responsible for the similar clinical presentation in elderly patients. It has been shown that the elderly are more likely to have detectable defects in cellular immunity.7 As was also shown in this study, elderly individuals are more likely to have concomitant illnesses that cause varying degrees of cellular immunodeficiency. It has long been known that patients with diseases such as diabetes, malignancies, and renal disease, or who were receiving medications that suppress their cellular immunity, were more likely to progress from TB infection to disease.8 Interestingly, while these concomitant illnesses only produce a "minor" cellular deficiency, it is enough to make patients more susceptible to TB disease. Furthermore, one could postulate that this altered immune function might predispose the elderly to potential reinfection with TB, which would then present clinically as primary TB disease instead of reactivation.9 10

Thus, it is essential to consider the diagnosis of TB in any person with a possible deficit in cellular immunity, including the elderly, who presents with a chronic wasting or respiratory illness. It is important to recognize that in these individuals the disease may not present in the "classic" form. Clinicians must therefore consider the diagnosis and take appropriate infection control measures until the disease has either been excluded or confirmed. It is also important to screen, provide, and ensure completion of preventative therapy to vulnerable populations in order to preclude subsequent active disease. This needs to be continuously reemphasized to all physicians, particularly those who treat patients in congregate settings such as hospitals, nursing homes, and correctional facilities, so as not to allow a further spread of the disease. This is especially true now that people are living longer with illnesses that cause or, through their treatment, induce deficiencies of the host's cellular immunity. We just can't afford to be fooled again.

References

  1. Pitchenik, AE, Rubinson, HA (1985) The radiographic appearance of tuberculosis in patients with the acquired immune deficiency syndrome (AIDS) and Pre-AIDS. Am Rev Respir Dis 131,393-396[ISI][Medline]
  2. Perlman, DC, el-Sadr, WM, Nelson, ET, et al (1997) Variation of chest radiographic patterns in pulmonary tuberculosis by degree of human immunodeficiency virus-related immunosuppression: the Terry Beirn Community Programs for Clinical Research on AIDS (CPRCA) Clin Infect Dis 25,242-246[ISI][Medline]
  3. Markowitz, N, Hansen, NI, Wikosky, TC, et al (1993) Tuberculin and anergy testing in HIV-seropositive and HIV-seronegative persons. Ann Intern Med 119,185-193[Abstract/Free Full Text]
  4. Beck-Sagué, C, Dooley, SW, Hutton, MD, et al (1992) Hospital outbreak of multidrug-resistant Mycobacterium tuberculosis infections: factors in transmission to staff and HIV-infected patients. JAMA 268,1280-1286[Abstract]
  5. Schluger, NW, Rom, WN (1998) The host immune response to tuberculosis. Am J Respir Crit Care Med 157,679-691[Free Full Text]
  6. Molloy A, Kaplan G. Cell-mediated immune response. In: Rom WN, Garay S, eds. Tuberculosis. Boston, MA: Little, Brown and Co., 1996; 305
  7. Ben-Yehuda, A, Weksler, ME (1994) Host resistance and the immune system. Clin Geriatric Med 8,701-711
  8. . American Thoracic Society/Centers For Disease Control (1990) Diagnostic standards and classification of tuberculosis. Am Rev Respir Dis 142,725-735[ISI][Medline]
  9. Stead, WW, To, T, Harrison, RW, et al (1987) Benefit-risk considerations in preventive treatment for tuberculosis in elderly patients. Ann Intern Med 107,843-845
  10. Stead, WW, Kerby, GR, Schlueter, DP, et al (1968) The clinical spectrum of primary tuberculosis in adults: confusion with reinfection in the pathogenesis of chronic tuberculosis. Ann Intern Med 68,731-744




This Article
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ashkin, D.
Right arrow Articles by Narita, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ashkin, D.
Right arrow Articles by Narita, M.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS