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RelA and p50 in airway cells with or without E1A transection,LPS could induce nuclear translocation of NF-B in E1A-transfected cells alone.7 In E1A-transformed airway cells, theNF-B transcription factor is involved in the IL-8 gene andICAM-1 gene expression after LPS stimulation. In addition,Metcalf 8 reported that adenovirus E1A 13S gene product up-regulates TNF- gene. On the other hand, cigarette smokershave increased numbers of neutrophils present in their lowerrespiratory tract. Acute exposure to cigarette smoke induces

infiltration of neutrophils into the airways through NF-

B andIL-8 gene expression.9 Consequently, the latent adenovirusinfection and cigarette smoke synergistically cause chronic airway inflammation through the cytokine genes and adhesion moleculegenes expression, possibly via NF-B activation. Thus, NF-Bactivation may be involved in the pathogenesis of COPD andchronic airway inflammation after chronic cigarette smoke inha-lation and adenovirus infection. These experimental data shouldbe further confirmed in the future by clinical data in humans.

Shinji Teramoto, MD, FCCPHaruki Kume, MD

International University of Health and WelfareSan-no Hospital

Tokyo, Japan

Correspondence to: Shinji Teramoto, MD, FCCP, Department of Internal Medicine, San-no Hospital, 8–10 –16 Akasaka, Mi-

 nato-ku Tokyo 107-0052, Japan; e-mail: [email protected]

References

1 Christman JW, Sadikot RT, Blackwell TS. The role of nuclearfactor-B in pulmonary diseases. Chest 2000; 117:1482–1487

2 Hogg JC. Childhood viral infection and the pathogenesis of asthma and chronic obstructive pulmonary disease. Am JRespir Crit Care Med 1999; 160:S26–S28

3 Matsuse T, Hayashi S, Kuwano K, et al. Latent adenoviralinfection in the pathogenesis of chronic airways obstructions.Am Rev Respir Dis 1992; 146:177–184

4 Elliott WM, Hayashi S, Hogg JC. Immunodetection of ad-enoviral E1A proteins in human lung tissues. Am J RespirCell Mol Biol 1995; 12:642–648

5 Keicho N, Elliott WM, Hogg JC, et al. Adenoviral E1Aupregulates interleukin-8 expression induced by endotoxin inpulmonary epithelial cells. Am J Physiol 1997; 272:L1046–L1052

6 Keicho N, Elliott WM, Hogg JC, et al. Adenoviral E1A genedysregulates ICAM-1 expression in transformed pulmonary epithelial cells. Am J Respir Cell Mol Biol 1997; 16:23–30

7 Keicho N, Higashimoto Y, Bondy GP, et al. Endotoxin-specific NF-B activation in pulmonary epithelial cells har-boring adenovirus E1A. Am J Physiol 1999; 277:L523–L532

8 Metcalf JP. Adenovirus E1A 13S gene product upregulatestumor necrosis factor gene. Am J Physiol 1996; 270:L535–L540

9 Nishikawa M, Kakemizu N, Ito N, et al. Superoxide mediatescigarette smoke-induced infiltration of neutrophils into theairways through nuclear factor-B activation and IL-8 mRNAexpression in guinea pigs in vivo. Am J Respir Cell Mol Biol1999; 21:189–198

Chicken Soup or Jewish Medicine

To the Editor:

The study by Rennard et al (October 2000)1 is the latestattempt at humor on the subject of chicken soup, but it leaves abad taste in one’s mouth with regard to the millennia-olddiscipline of Jewish Medicine. Ancient Jewish literature included

descriptions of folk remedies, even the “Dreckapotheke,” medi-cines that were derived from offensive human and animal partsand excretions (I place the swirling of dead chicken remains in

  vegetable broth in this category). However, in keeping withrespect for educated scientific and medical opinion, Jewish sagesthroughout the ages have warned that one should not rely on thefolk remedies of the Talmud, and some have even stated that it isforbidden to do so.

Rennard et al1 mention that chicken soup has been referred to

as Jewish penicillin, and I have no doubt that it is just as effectiveas any antibiotic in the treatment of viral illnesses. But instead of trying to inhibit the function of WBCs to control inflammation,

 which could be harmful, we should be trying to bolster the immunesystem to eradicate the infection and prevent complications.

Aside from his medieval remedies such as chicken soup, whatdid Maimonides feel was the main focus of medicine? The story 2

is told that the Sultan of Egypt asked Maimonides, who was hisphysician, “How do I know you’re such a great physician? Afterall, in all the time you’ve been taking care of me, I’ve never beensick.” Maimonides replied that in the Bible (Exodus 15:26), Godpromised the children of Israel that if they followed all of Hiscommandments, He would protect them from all of the diseasesHe had placed on the Egyptians, concluding, “I am the Lord yourphysician.” Because, in preventing illness, we are emulating God,prevention is the highest form of healing, and preventing illness

is the main role of a physician. Maimonides explained that whena patient follows his physician’s advice on lifestyle (diet andexercise) and the patient does not get sick, that is the greatestproof of a physician’s abilities. And that is what Jewish Medicineis really all about.

 Jay B. Lavine, MDTuscon, AZ

Correspondence to: Jay B. Lavine, MD, PO Box 43126, Tucson, AZ 85733-3126; e-mail: [email protected]

References

1 Rennard BO, Ertl RF, Gossman GL, et al. Chicken soupinhibits neutrophil chemotaxis in vitro. Chest 2000; 118:1150–1157

2 Beifuss YYH, ed. Yalkut lekach tov al parashiyot hashavua (inHebrew). Rechisim, Israel: Tashbar Harav 5748, 1987–88;109

Etiology of Community-AcquiredPneumonia Requiring Hospitalizationin Japan

To the Editor:

Community-acquired pneumonia (CAP) remains a commoncause of morbidity. Because CAP also is a potentially fataldisease, even in previously healthy persons, early appropriateantibiotic treatment is vital. In Japan, pneumonia is the fourthleading cause of death, and from 57 to 70 persons per 100,000population died per year of this disease in the last decade.Because of this high rate of morbidity, guidelines for CAPmanagement have been produced in Japan.1 However, prospec-tive studies on the etiology of CAP among the Japanese popula-tion have been very limited, and only the etiology of CAP hasbeen investigated by Ishida et al (December 1998).2 Therefore,

 we investigated the etiology of CAP requiring hospitalization inJapan based on our findings.

 We undertook a study to determine the etiology of CAP in

CHEST / 119 / 4 / APRIL, 2000 1295

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Japan between April 1998 and September 2000 at three differenthospitals. The microbiological and serologic studies that wereperformed were almost the same as those used in the study by Ishida et al.2 In addition, we also employed other diagnosticmethods for the detection of Chlamydia spp, Coxiella burnetii,and Legionella spp. Chlamydia pneumoniae, Chlamydia psittaci,and Chlamydia trachomatis infections were diagnosed by isola-tion in cell cultures and by serology. Antibodies to Chlamydia spp

  were measured by the microimmunofluorescence test, and cell

cultures were performed in cycloheximide-treated HEp-2 andHeLa 229 cells. Antibodies to C burnetii were measured by theindirect immunofluorescence test. In addition to serology andculturing, the urinary antigen test was used for detection of Legionella spp.

Two hundred patients (128 men and 72 women; age range, 19to 91 years; mean age, 60.9 years) who had had episodes of pneumonia were enrolled in the study. One hundred nine(54.5%) patients had at least one underlying disease. A microbi-ological diagnosis was established in 117 patients with pneumonia(58.5%). The most common pathogens were Streptococcus pneu-

 moniae (41 patients [20.5%]), followed by  Haemophilus influen- zae (22 patients [11.0%]), Mycoplasma pneumoniae (19 patients[9.5%]), C pneumoniae (15 patients [7.5%]), and Staphylococcusaureus (10 patients [5.0%]) (Table 1). Dual pathogens weredetected in 25 patients (12.5%).

Ishida et al2

investigated the etiology of CAP among theJapanese population for the first time, and their findings did notdiffer markedly when compared with those of Western countries.Our results were almost consistent with those of Ishida et al,2

 with the exception of the frequencies of atypical pathogens. The

atypical pathogens, C pneumoniae, Legionella spp, C burnetii,and M pneumoniae, have been recognized as common respiratory pathogens. In several studies,3–6 these organisms have beenfound to account for up to 25% of CAP cases in Westerncountries. In the present study, we were able to detect atypicalpathogens in approximately 20% of CAP cases. The frequencies

 were lower than those in Western countries but were higher thanthose in the study of Ishida et al.2 The difference from the study by Ishida et al may be related to the period in which the survey 

 was conducted or to the traditional diagnostic methods used forthe detection of  C pneumoniae. The difference from findings in Western countries may be due to the low incidence of Legionellaand C burnetii pneumonia in Japan.

In our study, S pneumoniae was the leading cause of CAP, andan emerging or newly recognized pathogen, C pneumoniae, wasalso a significant causative microorganism in Japan. The recog-nition of these results will allow us to treat patients with promptantimicrobial therapy and will promote the formulation of newguidelines for the management of CAP in Japan.

 Naoyuki Miyashita, MD, PhDHiroshi Fukano, MD

Yoshihito Niki, MD, PhD, FCCPToshiharu Matsushima, MD, PhD, FCCP

 Niro Okimoto MD, PhD, FCCP

Kawasaki Medical SchoolKawasaki HospitalOkayama, Japan

Correspondence to: Naoyuki Miyashita, MD, PhD, Departmentof Internal Medicine, Kurashiki Daiichi Hospital, 5–3-10Oimatsu cho, Kurashiki City, Okayama 710-0826, Japan; e-mail:

 [email protected]

References

1 The Japanese Respiratory Society. Basic management of community-acquired pneumonia in adults. In: Matsushima T,Kohno S, Saito A, eds. Guidelines for the management of respiratory tract infection. Tokyo, Japan: The Japanese Re-spiratory Society, 2000; 1–49

2 Ishida T, Hashimoto T, Arita M, et al. Etiology of community-acquired pneumonia in hospitalized patients: a 3-year pro-

spective study in Japan. Chest 1998; 114:1588–15933 Woodhead M. Community-acquired pneumonia guidelines:an international comparison. Chest 1998; 113:S183–S187

4 Ortqvist A, Valtonen M, Cars O, et al. Oral empiric treatmentof community- acquired pneumonia: a multicenter, double-blind, randomized study comparing sparfloxacin with rox-ithromycin. Chest 1996; 110:1499–1506

5 Liberman D, Schlaeffer F, Boldur I, et al. Multiple pathogensin adult patients admitted with community-acquired pneu-monia: a 1-year prospective study of 346 consecutive patients.Thorax 1996; 51:179–184

6 Ruiz-Gonzalez A, Falguera M, Nogues A, et al. Is Strepto-coccus pneumoniae the leading cause of pneumonia of un-known etiology? A microbiologic study of lung aspirates inconsecutive patients with community-acquired pneumonia.Am J Med 1999; 106:385–390

Table 1—  Microbiological Diagnosis of 200 Episodes of CAP*

Pathogen

Cases

No. %

S pneumoniae 41 20.5H influenzae 22 11.0

M pneumoniae 19 9.5C pneumoniae 15 7.5S aureus 10 5.0Anaerobes 8 4.0

  Viruses 6 3.0Moraxella catarrhalis 6 3.0Klebsiella pneumoniae 5 2.5Pseudomonas aeruginosa 4 2.0Streptococcus milleri group 4 2.0

 Legionella pneumophila 2 1.0C psittaci 2 1.0C burnetii 1 0.5Unknown 83 41.5

*Patients with dual infections were included.

1296 Communications to the Editor

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DOI 10.1378/chest.119.4.12952001;119;1295-Chest 

Jay B. LavineChicken Soup or Jewish Medicine

This information is current as of September 7, 2008

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