8
Volume 47. Number I Primed m the 1 IN II liNNIII)\ I^R \ \I ()I I I i'12(PS1 Respiratory System Involvement in Leprosy S. Kaur, S. K. Malik, B. Kumar, M. P. Singh and R. N. Chakravarty All tissues of the body are known to be af- fected by leprosy except lung parenchyma and the central nervous system ("). The in- volvement of the nose with nasal discharge rich in leprosy bacilli was described as early as 1891 by Goldschmidt (17) and later by Koch in 1897 (25), Sticker in 1897 (4(), and Schaffer in 1898 (45). The nasopharynx and larynx are frequently involved in lepromatous patients (I2,2'. '6,41). Various degrees of tracheo-bron- chial involvement have been described (7.1". 37). M. leprae were demonstrated in bronchial washings of two lepromatous patients (3). Nasal involvement akin to that of humans has been described in immunologically com- promised mice experimentally infected with leprosy bacilli. The present study is an attempt to eluci- date the extent of leprous involvement of the respiratory system in patients and its corre- lation with its functional impairment. MATERIALS AND METHODS Twenty-five patients having leprosy were randomly selected from the leprosy clinic of the dermatology department of the Post- Graduate Institute of Medical Education and Research, Chandigarh, India. A detailed his- tory and clinical examination of the patients with particular emphasis on the respiratory system involvement were recorded on a spe- cial chart. Routine investigations of blood, urine, stool and scrum biochemistry, were performed. Smears were made and cultures done thrice for acid-fast bacilli from the spu- tum ()leach patient. Postero-anterior and lat- eral chest X-rays of all patients were taken to exclude pulmonary tuberculosis. Anterior and posterior rhinoscopy and detailed laryn- goscopic examination were carried out to de- tect the presence of nasal obstruction, septal ' Receixed for puhlication 14 June 1978. = S. Kaur,^NI.A.N1.S., Assistant Professor of 1)ermatology, S. K. NIalik, NI.D., F.C.C.P., Assistant Professor of Chest 1)iseases; 13. Kumar, M.D.. Lecturer In DerIllall)10gV: NI. P. Singh. Ex-Resident 1)octor in Internal Nledicine: and K. N. Chakra arty. NIB., B.S., I NI.A.NI.S., F.I.C.A.. D.I.NI.. Associate Professor Ill Experimental Nledicine, Post - (iraduate Institute of NIedical Education ;Ind Research. Chandigarh. India. ulceration and perforation, destruction of the nasal bridge, congestion or pallor, infiltra- tion, nodularity and atrophy of the nasal mu- cosa and turbinates and their sensitivity to painful stimuli. The epiglottis, ary-epiglottic folds, and the false and true vocal cords were examined for thickening and nodulation, con- gestion, pallor and loss of sensation. The oral cavity was examined for involvement of tongue, palate, tonsillar pillars and pharyn- geal wall. Four nasal smears were taken from each nostril (anterior and posterior site on the sep- tum and from in and middle turbi- mites). The smears were stained by the tech- nic of Fite et al (16). The Bacteriologic Index (131) and the Morphologic Index (MI) were calculated according to Ridley's logarithmic scale (42) and by the method of Waters and Rees (55), respectively. Bronchoscopic and laryngoscopic exam- inations were carried out under general an- esthesia, and the presence of infiltration, nodularity, pallor of mucosa or excessive se- cretions in the tracheo-bronchial tree were sought. In the absence of any suspicious area, the mucosa' tissue was biopsied from the right upper and lower bronchi, the free mar- gin of the epiglottis and the false vocal cords. Smears of tracheal and bronchial secretions were studied for the presence of leprosy ba- cilli and Bacterial Indices were claculated as described earlier. Biopsy specimens were stained with hematoxylin-eosin and Ziehl- Neelsen stains. Biopsies were studied for leprous granu- lomas, presence of acid-fast bacilli and non- specific inflammatory reaction. According to the degree of chronic inflammatory response, the histopathologic findings were classified as mild, moderate or severe. RESULTS Twelve patients were classified as lepro- matous (LI), eight were borderline (BT, BB, BE), and five were of the tuberculoid (TT) variety. There were 22 males (88%) and 3 fe- males (12%). The ages ranged from 16 to 70 years. Duration of the symptoms varied from two months to ten years with an average of 18

esiaoy Sysem Ioeme i eosyila.ilsl.br/pdfs/v47n1a04.pdf · S. Kau, S. K. Maik, . Kuma, M. . Sig a . . Cakaay. A issues o e oy ae kow o e a-ece y eosy ece ug aecyma a e cea eous sysem

  • Upload
    others

  • View
    2

  • Download
    0

Embed Size (px)

Citation preview

Page 1: esiaoy Sysem Ioeme i eosyila.ilsl.br/pdfs/v47n1a04.pdf · S. Kau, S. K. Maik, . Kuma, M. . Sig a . . Cakaay. A issues o e oy ae kow o e a-ece y eosy ece ug aecyma a e cea eous sysem

Volume 47. Number IPrimed m the 1

IN II liNNIII)\ I^R \ \I ()I I I i'12(PS1

Respiratory System Involvement in LeprosyS. Kaur, S. K. Malik, B. Kumar, M. P. Singh and R. N. Chakravarty

All tissues of the body are known to be af-fected by leprosy except lung parenchymaand the central nervous system ("). The in-volvement of the nose with nasal dischargerich in leprosy bacilli was described as earlyas 1891 by Goldschmidt (17) and later by Kochin 1897 (25), Sticker in 1897 (4(), and Schafferin 1898 (45). The nasopharynx and larynx arefrequently involved in lepromatous patients(I2,2'. '6,41). Various degrees of tracheo-bron-chial involvement have been described (7.1".

37). M. leprae were demonstrated in bronchialwashings of two lepromatous patients (3).Nasal involvement akin to that of humanshas been described in immunologically com-promised mice experimentally infected withleprosy bacilli.

The present study is an attempt to eluci-date the extent of leprous involvement of therespiratory system in patients and its corre-lation with its functional impairment.

MATERIALS AND METHODSTwenty-five patients having leprosy were

randomly selected from the leprosy clinic ofthe dermatology department of the Post-Graduate Institute of Medical Education andResearch, Chandigarh, India. A detailed his-tory and clinical examination of the patientswith particular emphasis on the respiratorysystem involvement were recorded on a spe-cial chart. Routine investigations of blood,urine, stool and scrum biochemistry, wereperformed. Smears were made and culturesdone thrice for acid-fast bacilli from the spu-tum ()leach patient. Postero-anterior and lat-eral chest X-rays of all patients were takento exclude pulmonary tuberculosis. Anteriorand posterior rhinoscopy and detailed laryn-goscopic examination were carried out to de-tect the presence of nasal obstruction, septal

' Receixed for puhlication 14 June 1978.= S. Kaur,^NI.A.N1.S., Assistant Professor of

1)ermatology, S. K. NIalik, NI.D., F.C.C.P., AssistantProfessor of Chest 1)iseases; 13. Kumar, M.D.. LecturerIn DerIllall)10gV: NI. P. Singh. Ex-Resident 1)octor inInternal Nledicine: and K. N. Chakra arty. NIB., B.S.,I NI.A.NI.S., F.I.C.A.. D.I.NI.. Associate ProfessorIll Experimental Nledicine, Post -(iraduate Institute of

NIedical Education ;Ind Research. Chandigarh. India.

ulceration and perforation, destruction of thenasal bridge, congestion or pallor, infiltra-tion, nodularity and atrophy of the nasal mu-cosa and turbinates and their sensitivity topainful stimuli. The epiglottis, ary-epiglotticfolds, and the false and true vocal cords wereexamined for thickening and nodulation, con-gestion, pallor and loss of sensation. The oralcavity was examined for involvement oftongue, palate, tonsillar pillars and pharyn-geal wall.

Four nasal smears were taken from eachnostril (anterior and posterior site on the sep-tum and from in and middle turbi-mites). The smears were stained by the tech-nic of Fite et al (16). The Bacteriologic Index(131) and the Morphologic Index (MI) werecalculated according to Ridley's logarithmicscale (42) and by the method of Waters andRees (55), respectively.

Bronchoscopic and laryngoscopic exam-inations were carried out under general an-esthesia, and the presence of infiltration,nodularity, pallor of mucosa or excessive se-cretions in the tracheo-bronchial tree weresought. In the absence of any suspicious area,the mucosa' tissue was biopsied from theright upper and lower bronchi, the free mar-gin of the epiglottis and the false vocal cords.Smears of tracheal and bronchial secretionswere studied for the presence of leprosy ba-cilli and Bacterial Indices were claculated asdescribed earlier. Biopsy specimens werestained with hematoxylin-eosin and Ziehl-Neelsen stains.

Biopsies were studied for leprous granu-lomas, presence of acid-fast bacilli and non-specific inflammatory reaction. According tothe degree of chronic inflammatory response,the histopathologic findings were classifiedas mild, moderate or severe.

RESULTSTwelve patients were classified as lepro-

matous (LI), eight were borderline (BT, BB,BE), and five were of the tuberculoid (TT)variety. There were 22 males (88%) and 3 fe-males (12%). The ages ranged from 16 to 70years. Duration of the symptoms varied fromtwo months to ten years with an average of

18

Page 2: esiaoy Sysem Ioeme i eosyila.ilsl.br/pdfs/v47n1a04.pdf · S. Kau, S. K. Maik, . Kuma, M. . Sig a . . Cakaay. A issues o e oy ae kow o e a-ece y eosy ece ug aecyma a e cea eous sysem

47, 1^ Kaur et al: Respiratory System in Leprosy^ 19

50.84 ± 31.68 months. Eleven patients hadreceived dapsone in the past and one was onantituberculosis treatment as well. Signs andsymptoms pertaining to the respiratory sys-tem are listed in Table I. Fifteen patientshad a dry cough (60%) and II in this groupwere smokers; 12 had a cough with expec-

I \BIT I. Symptoms and signs pertaining tothe respiratory tract in /eprosy patients.

Symptoms and signs^No. of^Percentagepatients^( (:i)

Epistaxis 16 64Cough 15 60Expectoration 12 48Nasal obstruction 12 48Septal perforation & ulceration 8 32Depressed bridge of nose 6 24Anosmia 1 4Pale mucosa of nose 5 20Congested nasal mucosa 5 20Atrophy of turbinates 4 16Pale mucosa of oral cavity 4 16Ilernoptysis 5 20Vocal cord thickening 4 16Nodulation and congestion 4 16Sluggish arytenoid 3 12Pale mucosa of larynx 8Thickening of epiglottis 2 8Diminished sensation of larynx 2 8Pale tracheal mucosa 5 20

toration (48%); 15 had been cigarette smok-ers from 4 to 30 years, the average durationbeing 13.20 ± 6.8 years.

Investigations revealed mild anemia in tenpatients (hemoglobin below 12 gm%) andmoderate in three (hemoglobin below 10gm%). Total serum proteins were low in onepatient ( < 5.5 gm%), serum albumin was low( < 3.2 gm%) in thirteen patients, and hyper-globulinemia ( > 3.5 gm%) was present infive patients.

Nasal smears were positive for acid-fastbacilli in eight patients, seven of these (58.3%)were lepromatous (LL) and one (12.5%) wasborderline (1313). The 131 varied from 1+ to 3+and the MI from 20% to 83%. Sputum smearswere positive for acid-fast bacilli in two pa-tients (Table 2). Cultures did not yield growthon Lowenstein-Jensen medium during sixweeks of observation.

Radiologic examination showed bilateralnodular infiltrations in upper and mid-zonesof the lungs, without cavitation, in one (LL)patient and was interpreted as being tuber-culous in nature. This patient also developederythema norlostan leprosum (ENL) duringthe hospital stay. Sputum and bronchialsmears showed the presence of acid-fast ba-cilli believed to he M. /eprae. Culture onLowenstein-Jensen medium was negative.Evidence of infiltration in the right upperzone was present in another patient, this wasalso considered tuherculous in nature but cor-

TABLE 2. Acid fast bacilli positivity in iltikrent specimens.

Site/ Specimen

Bacillary positive Bacillary negative

Lepromatous n = 12

^

Total^Percentage

^

no.^((ii)

Borderline n= 8

^

Total^Percentage

^

no.^(CO

Tuberculoid n = 5

^

Total^Percentage

^

no.^(%)

Nasal smear 7 58.3 1 12.5 0 0Bronchial

smear3 25 0 0 () 0

Spat= smear 2 16.6 0 0 0 0Laryngeal

biopsy0 0 0 0 0 0

Right upper bronchialbiopsy

I 8.3 0 0 0 0

Right lower bronchialbiopsy

1 8.3 0 0 0 0

Page 3: esiaoy Sysem Ioeme i eosyila.ilsl.br/pdfs/v47n1a04.pdf · S. Kau, S. K. Maik, . Kuma, M. . Sig a . . Cakaay. A issues o e oy ae kow o e a-ece y eosy ece ug aecyma a e cea eous sysem

; • • .• • •

" -2•* ••••••^• •;,!..t•,; ••^•"".•,_ •^.^• •.•^•^-

r.

s cv,

... ;A.^••••.....--...e•m•tio.^,..1 ..,...P

." zo- •^.^-

0 .711rtf:1,j..-•...'••r^

.

- •""-. •^•of- t.

-'^: •.,:„:••••:•,...'4•:,`,:•:ele •

••,4t.r.-Asw„'^• • -^•^-„

‘n ..

,- •• xz.-- •^--'44• •^." • „:.•••1'^,^• ••-•;. -ty•

20^ International Journal of Leivosl•^ 1979

rohorative clinical findings were not present.Bronchial smears yielded acid-fast bacilli

in only three lepromatous patients (Table 2).In the absence of any other evidence of tu-berculosis, these were taken to he leprosy ba-cilli in two patients. The third had nodularinfiltration on radiography hut had no clin-ical evidence of tuberculosis, and culture onLowenstein-Jensen medium was negative.

Laryngoscopic examination showed con-gestion and thickening of the right vocalcord in one patient and the area was hiop-sied. The biopsy specimens from the epiglot-tis as studied for inflammatory reaction wereclassified as mild in six (24%), moderate inten (40%), and severe in three (12%) (Fig. 1);six specimens showed no abnormality (Table3). Two specimens showed foam cell struc-tures without acid-fast bacilli in them. Onebiopsy from a false vocal cord showed a tu-berculoid lesion characterized by collectionsof histocytes, Langhan's giant cells, lymph-ocytes and a few plasma cells, but there wasno caseation (Fig. 2). Mast cells were seen

in two biopsies. Biopsies of false vocal cordsin eleven patients (50%,) showed mild inflam-matory reaction, moderate in three (13.6%),severe in four (18.2%), and another four(18.2%) had normal histology. Tissue wasinadequate for interpretation in three pa-tients.

Bronchial mucosal tissue was not adequatefor study from two upper and five right low-er lobe bronchi. leprous granulomas werenot found in any bronchial biopsy. Four(17.4%) upper lobe bronchial biopsies wereinterpreted as normal, infiltrate was mild infourteen (60.9%), and moderate in five(20.7%) (Table 3). Excess of mucus secretingcells was seen in four specimens, one showedmetaplastic changes, and thickening of thebasement membrane was seen in another.Biopsies from the right lower lobe bronchusshowed normal histology in three (15%),fourteen (70%) revealed mild, two (10%)moderate, and severe inflammatory response(Fig. 3) was seen in only one (5%) (Table 3).Acid-fast bacilli were present in a clump in

AC^••

•••

FIG. I. Section of the epiglottis from LL patientshowing diffuse collection of chronic inflammatorycells in the submucosa. H & E, X 100.

• • . 4' ► • • •

•• ... ^•:•• • o ‘a,/::.,•?: • • •* '‘...' I • 1 i :

,^• I,• ..t ' • • .^,ii ;^'"f 4 '• • b 't^'.';‘• I 4 :4

. •4.^r)^•• • 't • 4 ,1 ,. t .1 ••^4^•

I . . . • •le' . * . I • '-- • - 4 P I^. • 9 ' • •• i'..9' - •^.i f..,

' ♦ 41} . "..■:'!,.'^l'' ' .%•:: . 1 1t1',. 1 II ,Ir'il '•%)„ ..;,....,.,,,^•,,I:^1%•• tAii'14 'i I ,...J•

.,..1. g,-0 # ,•Air:, fr 94% tt'‘‘'‘4 1•

$ C, 1„.. '.et 41

i I IA,

,/, ') ......... Ø.,,:: ,;........ . ...., : ,„,t• • ^I .. i. -

.^,,^,^4 . . . •i . . ;, ,• N., 1s.,,, Jr-^i.. *^: 7^- • ** 't• •''', •^••• •

V I^. I - 0^' .7'4 *** -^•^*-•'-'- -••'.# 4 , ! 4:-‘a .%^..^- ' a: —.* *:"... •• .^`

B' ' ;lc t 1/4 ..t.' --..^1- ---^.*-- :* ..41*-' s .s; ;.••••-•••••.1^.: . •••••••••'' '"‘..a •%•'*‘• "- Z. 1,#.` ..^.-^• I

..;...sid^41,41••••••••444711.;)11%!:":1-44::: qe-::

• 1. ••• ) ....;••T•t;, 111‘4"11% -7.0.— el"'' '4": ': - i :

.. , -....., A .^ ,„..r.:^1„..,^. ...., - - . .!.... .

0.1,,;•'.• .^lit^

4. INaipeseli_evi.**;ga4•L'Ig;;;`,.:::..:

\"'46'liet '0^44 VI 1, *C!. !'‘A• ^ tir ^1 4 .a/0 a* i $‘• .‘" 'i' ir- ;; . li At e: ---4,4 or, Tr; 04,•,e‘f

,

...kJ 1/••;4 •11yir 4^4,...gk .,„444, la.% ^

' it.^ 140. ,••

p ...;,•.• $ fe,717........„ 'IN •-•74,...;1,,rii.. .r,:' st. 't/64SeTh..4',71:4:1:* ..-:.!.#"..

:.-% a''..4:?4)C;.:**.r.8‘ irbi‘.744".4.1: I i'. ,t4,..A.^. 7. I -•... *tr: ...., n..4, ; e ,^_ , . . ,' Re"-^' 'It .4",„,.•.:1 Ns.. • : ....: _^,„ .,, t . s ..^. , ;•1 •• • ,,,....^- , ....? ; . . ... „.^......t. s^,vi.

-^....,. •^••

'^; 7^•^• ...,^..,-_^•^

......, ... . ti.. -^......././' .- ^..IIIII

FIG. 2. Section of false vocal cord from the sameLL patient showing an inflammatory granulomaunder the squamous epithelial layer. H & E,X 100.

Page 4: esiaoy Sysem Ioeme i eosyila.ilsl.br/pdfs/v47n1a04.pdf · S. Kau, S. K. Maik, . Kuma, M. . Sig a . . Cakaay. A issues o e oy ae kow o e a-ece y eosy ece ug aecyma a e cea eous sysem

Site of biopsy"Normal

Epiglottis (25) 6 (24(,i)

False vocal cords (22) 4 (18.2(2)

Right upper bronchus (23) 4 (17.4C)

Right lower bronchus (20) 3 (15)

Degree of inflammation vs. no. of patients

Mild^!Moderate^Severe

6 (24Ci)^

10 (40Ci)^

3 (124i)

11 (5(Ki)^

3 (13.6Ci)^

4 (18.2(A

14 (60.9)^

5 (21.7Ci)^

0 (OCi)

14 (70Ci)^

2 ( IOCi)^

I (5Ci)

47, I^ kaur et al: Respiratory System in Leprosy

the submucosa in one biopsy. l.arge numbersof mucus secreting cells were present in eightbiopsies, metaplastic change in the bronchialepithelium was present in three. Thickeningof the basement membrane and eosinophilswas seen in one specimen.

fr3itt`t"1.scti^-

• .^.0 i;

,Je

•••-r".

*^.111,_1(1'a-NS^100.° •

a 71 legtv:A4140.^ :::;'‘':;:4;4- 4% 4 • :i".4 9;;• 1 ''‘I ,I;: ;:k:::;:: Ci■,7. • .

V • I.; r SO .:■11l..ii: •

. ..., _..14

^

' * ."...... --.. 4.. - ':#/triri,•'4. ;.'t,s,^ %.„7,,.. .-'. k.■i*. A. - .^hi —.^.1 .^. .(., f„.^. , .

*'•

•,.4 4-04,4)/.14.

. .,^- . ... i..f ilf i el.•.^■ ".' .,^• 44, ., ; 4., ... I ..r• .-...... y L.,^• . ". ,,a . • ....;;....

• ',.... 1,0 ‘1^14 if f • • ,. ; • • Ok•%••V sor , ,?; .1,,,, I I / ,1% 7 - r^' N'^'7'. °^,1 '.;,..' ,o, kV '. :„‘III..■•44$ . (...1. ..,- -.• 'e' .. ie - ' ....,14?‘...,re,^•■ • ' ..'• ,^• I Iv; . :tr..

-7., • i r'' . . A 7.^' :: ' • •■^4,4

' : . • . . ea' /of ";414t ". 1 :

.A's ..:.

lo..• '

. ....,,,. '^...7. r^4...! . A t : •

Fin. 3. Section of the right lower bronchusshowing partial desquamation of the columnarepithelium. Subepithelial tissue shows inflamma-tion but no foam cells. II & E, X 100.

DISCUSSIONOne patient with acid-fast bacilli in spu-

tum, bronchial smears and nodular infiltra-tion of lung fields on radiography had noclinical signs of tuberculosis. Ilistopathologydid not show granuloma or acid-fast bacilliin the bronchial mucosa. Another patientwith negative sputum and bronchial smearshad acid-fast bacilli in the bronchial biopsywithout specific granulomas, clinical or ra-diologic signs. It is, therefore, evident thatthere is no correlation between clinical, ra-diologic, sputum and bronchial smear posi-tivity for acid-fast bacilli and histopathologyof bronchitil mucosa in the group of patientsstudied.

Bacilleinia in patients with leprosy hasbeen amply documented (12.14.15,34.4.0.) It is,therefore, quite logical to expect various de-grees of visceral involvement

It was recognized quite early that the nosewas frequently involved in leprosy and thatnasal discharge contained large numbers ofleprosy bacilli (11.17. 25, 4o. 45,.) In the presentstudy the nose was found to be clinically in-volved in 22 patients (88C('). The involvementwas in the form of congestion or pallor, sep-tal perforation, ulceration, atrophy of turbi-nates and depressed nasal bridge. The find-ings are consistent with those of Barton (')who found nasal involvement in 96Ci of pa-tients examined. Positive nasal smears forAFI3 were found in seven (58Ci) 1_1_ patientswhich conforms to the findings of Daveyand Rees (II) whose figure was 53Ci. A pos-itive nasal smear was found in only one pa-tient ( ) having borderline leprosy. How-ever, Pedley (45), Davey and Rees ("), and

1.4 12. 20, 41).

TABLE 3. Incidence of nonspecific inflammatory response in various parts of thetracheo-bronchial tree.

"Figures in parentheses gke total ntanher actually studied.

Page 5: esiaoy Sysem Ioeme i eosyila.ilsl.br/pdfs/v47n1a04.pdf · S. Kau, S. K. Maik, . Kuma, M. . Sig a . . Cakaay. A issues o e oy ae kow o e a-ece y eosy ece ug aecyma a e cea eous sysem

-r)^ International .lourtial of Leprosy^ 1979

McDougall et al (15) did not find AFB in anyborderline leprosy patients.

As early as 1898, Brutzer (7) described acase of nodular leprosy who had stenosis ofthe larynx and on autopsy showed considera-ble thickening of tracheal mucosa with enor-mous masses of leprosy bacilli present whileonly a few bacilli could be detected in thebronchial m LICUS membrane. Involvement ofthe nose, pharynx and larynx has been des-cribed in various studies on 1_1_ patients (4.5, 12, 19, 22„16, 41) In the present study, eight pa-tients (32%) had laryngeal involvement. Bar-ton (2) had the same percentage of his pa-tients similarly involved, the most commonsite of involvement being the epiglottis whilein our study the vocal cords were the mostfrequent site involved. M. leprae and granu-lomas were not found in any of the patients.Powell and Swann (41) found vacuolated his-tiocytes and globi in many of their 50 autopsyspecimens. Desikan and Job (12) found lep-romatous granulomas involving the submu-cosa of the larynx in eight of their nine pa-tients even when none of them showed grossclinical involvement, while Bernard andVazquez (4) found lepromas in only 2 of their60 autopsy specimens.

M. leprae were seen by Bedi et al (3) inbronchial washings in two patients. In ourstudy, only three patients (25%) of the LLtype showed the presence of AFB in bron-chial smears. One patient had coexisting pul-monary tuberculosis but none of his speci-mens grew AFI3 on Lowenstein-Jensenmedium, therefore these were assumed to beleprosy bacilli. Muir (37) stressed the nodularinfiltration of the trachea and bronchi whichcould sometimes rupture to discharge lepro-sy bacilli, leading to a false diagnosis of pul-monary tuberculosis. Lie (27) described tra-cheal and bronchial mucosa] thickening intwo of his three cases, and on microscopyfound leprosy bacilli in the epithelium, con-nective tissue and even in the nerves. Bacilliwere found in the mucosa of medium sizedand finer bronchioles, but less in number thanin the upper portions of the tract. Bernardand Vazquez (4) found M. leprae in alveolarmacrophages in only 1 of 60 autopsies. How-ever, no bacilli were demonstrated in the tra-cheo-bronchial tree by other authors (02. 39'

41 '24') Kirchheimer et al ) in experimentallyproduced leprosy in the armadillo showedthat the lungs had variable histiocytic infil-

tration with many histiocytes containing glo-hi and individual bacilli. In our study nothickening or nodulation of the bronchial mu-cosa was seen, leprosy bacilli were seen intwo bronchial sections only, and there wereno leprous nodules. Culture on Lowenstein-Jensen medium was negative even when onepatient had radiologic evidence of tubercu-losis. Chronic nonspecific infiltrate in thebronchial wall was seen in the majority (88%)of patients. This could be due to smoking(60%) or other poorly recognized causes. Anabundance of mucus secreting cells could alsobe attributed to similar causes. The associa-tion between tobacco smoking and chronicnonspecific lung disease is well recognized.

Negre and Fontan (3") subjected 110 pa-tients to pulmonary radiography and of these3 patients with ENL showed nodular shad-ows which were not subsequently visualizedthe following year. The lesions were consid-ered to be allergic in nature and a manifesta-tion of the general reaction. Two of our pa-tients showed infiltration in the right apicalregion and the upper and mid-zones. Thesewere considered to be tuberculous. In onepatient the lung shadows persisted for sixmonths after the ENL reaction subsided.

Review of the literature reveals a theoryof antagonism between leprosy and tuber-culosis, i.e., tuberculous infection protectsagainst leprous infection. Chaussinand (")was the first to put forward this concept onthe basis of his observation that as tubercu-losis increased in Western countries leprosydecreased. Viel and Dallien (5') also support-ed this concept, observing only a few casesof tuberculoid leprosy in the local populationin the Chuteen mine areas, despite large scalemigration of leprosy patients because of ram-pant tuberculosis in the local population. Therelationship also had further documentation(6,29). A number of reports have been pub-lished from time to time to prove or disprovethe relationship between the two diseases(10. 26 ...33. 43, 49, 50. 52 ) However, some authors(", 31.32) have adopted a guarded attitudeand regard the evidence as inconclusive.

The incidence of tuberculosis in our studywas 80/i; which is consistent with the studiesof other workers (4. 21. 2S, 53. 54) who found theincidence to be 11.7%, 8.5%, 11%, and 13.3%,respectively. However, Mitsuda and Ogawa(3(), Takano (47.4'4), and Desikan and Job (12)

Page 6: esiaoy Sysem Ioeme i eosyila.ilsl.br/pdfs/v47n1a04.pdf · S. Kau, S. K. Maik, . Kuma, M. . Sig a . . Cakaay. A issues o e oy ae kow o e a-ece y eosy ece ug aecyma a e cea eous sysem

47, I^ Kaur et al: Re.spiratory System in Leprosy^ 23

showed involvement with tuberculosis in7()%, 54.7%, and 71%, respectively.

SUMMARYRespiratory system involvement was stud-

ied in 25 leprosy patients, irrespective of age,sex, duration of disease and treatment. Nasalbleeding, cough, expectoration and nasal ob-struction were present in 64%, 60%, 48%, and48% of patients respectively. Sixty percentof the patients were cigarette smokers. Twoviews of chest skiagrams were taken whichshowed nodular shadows in upper and mid-zones in two LI. patients. Nasal involvementwas present in 88%, chiefly LL and BL pa-tients. Nasal smears taken from four siteswere positive for leprosy bacilli in 70.5% ofthe patients, again LL and I3L variety. Ante-rior and posterior rhino- and laryngoscopicexaminations were carried out under generalanesthesia and biopsies were taken from theepiglottis, false vocal cords, and the right up-per and lower bronchi. Laryngeal involve-ment was seen in 33(;i) of the patients, chief-ly of the LL and BL type. The vocal cordswere the most common lesion site. Bronchialsmears were positive for leprosy bacilli inthree Ll_ (25%) patients. Two epiglottic andone vocal cord biopsy showed foam cell andtuberculoid granuloma. Leprous granulomawas not seen in any bronchial biopsy. Acid-fast bacilli were present in one right upperand lower bronchial biopsy but were absentin laryngeal biopsies. Coexistent pulmonarytuberculosis was present in two LL (8%) pa-tients. No correlation was found betweenclinical, radiologic, sputum and bronchialsmear positivity for acid-fast bacilli and his-topathology of bronchial mucosa.

R ESU MENSc estudid la afeccidn del sistema respiratorio

en 25 pacientes con lepra, independientemente desu edad, sex°, duracidn de la enfermedad y trata-miento. Sangrado nasal, tos, expectoracidn y ob-struccidn nasal, afecta roil al 64(;,i, 60Ci , 48% yde los pacientes, respectivamente. El 60%; de lospacientes eran furnadores. El ex:tmen radioldgicodel tOrax indicd, en dos pacientes LL, la presenciade sombras nodulares en las zonas superior y me-dia. La itleccidn nasal se encontrd en el 88%de loscasos, principalmente en los pacientes LL y I31..Los raspados nasales tornados de 4 sitios, mo-straron bacilos de la lepra en el 70.5% de los pa-cientes, otra VC/ de las variedades LL y Bl.. Bajoanestesia general, se hicieron exAmenes rino-

laringoscdpicos anteriores y posteriores y setomaron biopsias de la epiglotis, de las cuerdasVOCalCS falsas y de los bronquios derechos supe-rior c inferior. En el 33(,' de los pacientes, princi-palmente de los tipos LL y BL, se encontraronafecciones laringetts. Las cuerclits vocales fueronel sitio mils comdn de lesidn. Las muestras bum-quiales de 3 pacientes LL (25%) tuvieron bacilosde la lepra. Dos biopsias epigldticas y una decuerdits vocales most raron cdlulas espumosas ygranulomas tuberculoides. En ninguna biopsiabronquial se encontraron granulomas tubercu-loides. Se encontraron bacilos dcido-resistentesen unit biopsia bronquial derecha superior e in-ferior pero no se encontritron en las biopsias larfn-geas. Dos pacientes con LL (8Cii) tuvieron adernifstuberculosis pulmonar. No se encontrd correla-cidn alguna entre la demostracidn clinica, radio-Idgica o tintorial en los exudados bronquiales oen el esputo, de bacilos tfcido resistentes y la his-topatologla de la mucosa bronquial.

1217:SUM17:

Chez 25 malades atteints de lepre, l'atteinte dusysteme respiratoire a dtd dtudide, sans qu'ilsoit tenu compte dc rage, du sexe, de la durde dela maladie ou du traitement. On a constatd unsaignement nasal chez 64% des malades, de latoux chez 60%, des expectorations chez 48%, etune obstruction nasale chez 48% dgalement. Laproportion de fumeurs de cigarettes chez les ma-lades atteignait 60%. Deux clichds de skiagrammedu thorax furent pris. us montraient des ombresnodulaires dans les zones supdrieure et mddianechez 2 malades atteints de lepre LL. Une atteintenasale dtait prdsente chez 88%, principalementchez des sujets atteints de lepre LL et BL. Des frot-tis nasaux prdlevds i partir de quatre sites dtaientpositifs pour le bacille de la lepre chez 70,5% desmalades, de noveau appartenant aux types LL etBE,. Des examens rhinoscopiques et laryngosco-piques antdrieurs et postdrieurs ont dtd pratiquessous anesthdsie gdndrale, et des biopsies ont dtdprdlevdes au niveau de I'dpiglotte, des faussescordes vocales, et des bronches droites supdri-eure et infdrieure. Une atteinte laryngde a dtdconstatde chez 33% des malades, principalementdes types LL et BL. La lesion la plus communese situait dans les cordes vocales. Des frottis bron-chiques sont rdvdlds positifs pour be bacillede la lepre chez 3 malades LL (25%). Des cellulesspumeuses et des granulomes tuberculdfdes ontdtd notds au niveau de 2 biopsies de I'dpiglotteet (rune biopsie de la corde vocale. Aucun granu-lome ldpreux n'a dtd observe dans les biopsiesbronchiques. Des bacilles acido-rdsistantesdtaient prdsents dans une biopsie de la bronchedroite superieure et dans une biopsie de labronche drone infdrieure, mais us dtaient parcontre absents dans les biopsies larynOes. Une

Page 7: esiaoy Sysem Ioeme i eosyila.ilsl.br/pdfs/v47n1a04.pdf · S. Kau, S. K. Maik, . Kuma, M. . Sig a . . Cakaay. A issues o e oy ae kow o e a-ece y eosy ece ug aecyma a e cea eous sysem

24^ International Journal of Leprosy^ 1979

tuberculose pulmönaire coexistait chez 2 maladesLL (8%). Aucune correlation n'a ete observeentre les manifestations cliniques, les images radi-ologiques, les expectorations, Ia positivite desfrottis bronchiques pour des bacilles acido-rdsis-tants, et I'aspect histo-pathologique de la mu-queuse bronchique.

REFERENCESI. Amu& P., BAJAJ-MAL1K, G. and Gum, M.

Lepromatous leprosy-a case report of an au-topsy study. Lepr. India 47 (1975) 121-125.

2. BARTON, R. P. E. A clinical study of the nosein lepromatous leprosy. Lepr. Rev. 45 (1974)135-144.

3. BLOC, B. M. S., NARAVANAN, P. S., MANJA,

S. K., KiRcnimmER, W. F. and BALASUBRA-

MANYAM, M. M. hi/rat' in the cells of bron-chial washings. Lepr. India 45 (1973) 228-234.

4. BERNARD, J. C. and VAZQUEZ, C. A. J. Vis-ceral lesions in lepromatous leprosy. Studyof sixty necropsies. Int. J. Lepr. 41 (1973)94-101.

5. BLACK, S. H. The pathology of leprosy. In:Tuberculosis and Leprosy, the MycobacterialDiseases. Symposium Series, The AmericanAssociation for the Advancement of Science.Lancaster, Pa.: The Science Printing Press,1938, vol. I, pp 97-105.

6. BRowN, . A. and STONE, M. M. A trial of BCGvaccination in the prophylaxis of leprosy.Lepr. Rev. 34 (1963) 118-122.

7. Brutzer (1898) quoted by Lie, H. P. Trachei-tis and bronchitis leprosa. Int. J. Lepr. 4(1936)281-288.

8. CHAUSSINAND, R. A propos de la thdorie del'antagonisme entre tuberculose et Ipre. [Onthe theory of the antagonism between tuber-culosis and leprosy.] Sem. Hop. Paris 37(1961)2304-2307. Abstract in Int. J. Lepr. 31 (1963)127.

9. CHAUSSINAND, R. Tuberculose et 14re, mala-dies antagoniques. Eviction de lit 1(s.pre par Iatuberculose. Int. J. Lepr. 16 (1948) 431-438.

10. CONALL, .1., GONZALES, C. L. and RAssi, E.Estudios sobre lepra en el grupo etnico ale-man de Ia Colonia Tovar, Venezuela. I. Pre-Valencia de la enfermedad. Int. J. Lepr. 20(1952) 185-193.

I I. DAvEy, T. F. and Regis, R. J. W. The nasaldischarge in leprosy. Presented at 10th Int.Leprosy Congress, Bergen, Norway. Abstractin Int. J. Lepr. 41 (1973) 512.

P. DLsIRAN, K. V. and Jolt, C. K. A review ofpost-mortem findings in 37 cases of leprosy.Int. J. Lepr. 36 (1968) 32-44.

13. DEsiRAN, K. V. and Jon, C. K. Visceral le-sions caused by .11. leprae-a histopathologi-cal study. Indian. J. Pathol. Bacteriol. 13( 1970) 100-108.

14. DR uTz, D. J. , CHEN, T. S. N. and WEN-

HSIANG, Lu. The continuous bacteraemia oflepromatous leprosy. N. Engl. J. Med. 287(1972) 159-164.

15. DRu -tz, D. J. and 'ANN, L. Further studies ofleprosy bacteraemia. Clin. Res. 19 (1971) 457.

16. FITE, G. L., CANUIRE, P..). and TURNER, NI. II.Procedure for demonstrating lepra bacilli inparaffin sections. Arch. Pathol. 43(1947) 624-625.

17. GOLDSCIIMIDT, J. Der nasale ursprung derlepra. In: Die Lepra auf Madeira, Leipzig:F. C. W. Fogel, 1891.

18. GuiN -ro, R. S., Douu., J. A. and MARALAY,

E. P. Tuberculization and reactivity to lepro-min, association between lepromin and tuber-culin reactions in schoolchildren in Cordovaand Opon, Cehu, Philippines. Int. J. Lepr. 23(1955) 32-47.

19. HANSEN, G. and Loon- , C. Die lepra corn kli-nischen and Pathologisch anatomischen.s. tandpunke-te, T. G. Cassell, ed.,: Fischer &Co., 1894, p 45. Translated by N. Walker,Leprosy in its Clinical and Pathological As-pects, Bristol: John Wright & Co., 1895.

20. JUNNARKAR, R. V. Late lesions in leprosy.Lepr. India 29 (1957) 148-154.

JtrriKov, B. R. Experience in treatment of lep-rosy patients with accompanying pulmonarytuberculosis. Nauch. Sap. Inst. (such. Lepr.(Artrakhan) 5/10 (1968) 252-253.

22. KEAN, B. II. and CHILDREss, M. E. A summa-ry of 103 autopsies on leprosy patients on theIsthmus of Panama. Int..). Lepr. 10 (1942) 51-59.

23. Kii.ANol.RAR, V. R. Pathology of leprosy. In:Leprosy in Theory and Practice, 2nd edit.,R. 0. Cochrane and T. F. Davey, eds., Bristol:John Wright & Sons, Ltd., 1964, p 134.

24. KIRCIDIEINIER, W. F., STORRS, E. E. and BIN-FORD, C. H. Attempts to establish the armadil-lo (Dasypus noveincinctus Linn.) as a modelfor the study of leprosy. II. Histopathologicand bacteriologic post-mortem findings in lep-romatoid leprosy in the armadillo. I nt. J. Lepr.40 (1972) 229-242.

25. Kocn, R. Die lepra erkran. Kungen in kreisememel. Klin. Jahrbuch. 6 (1897).

26. LEwis, N. 0., JR., Era, 0. L. and BoGLN, E.Comparison of reactions to human and aviantuberculins in leprosy patients. Int. J. Lepr.29 (1961) 355-358.

27. LIE, H. P. Tracheitis and bronchitis leprosa.Int. J. Lepr. 4 (1936) 281-288.

28. 1.1mA, S. DE 0. and MAGARAO, M. F. Treat-ment° da tuberculose pulmonarem doente deHansen. Rev. Bras. Tuberc. 21(1953) 397-408.

29. LONG, E. R. Leprosy, some analogies and con-trasts with tuberculosis. Arch. Environ.Health 14 (1967) 242-243.

Page 8: esiaoy Sysem Ioeme i eosyila.ilsl.br/pdfs/v47n1a04.pdf · S. Kau, S. K. Maik, . Kuma, M. . Sig a . . Cakaay. A issues o e oy ae kow o e a-ece y eosy ece ug aecyma a e cea eous sysem

30. 1.0wL^. Rat leprosy. A critical review of the 44.literature. Int. J. 1.epr. 5 (1937) 311-328, 463-481.

3. LowE, .1. and DivEv, T. F. Tuberculin and lep-romin reactions in Nigeria. An analysis of the 45.data of Lowe and McNulty. Int. .1. Lepr. 24(1956) 419-423.LowE, .1. and MACFADZEAN, .1. A. Tubercu- 46.losis and leprosy. Further immunological stud-ies. I.epr. Rev. 27 (1956) 140-147.

33. LowE, J. and McNuurv, F. Tuberculosis and 47.leprosy: immunological studies in healthy per-sons. Br. Med..1. 2(1953) 579-584. Also Lepr.Rev. 24 (1963) 61-70.^ 48.

34. MANTA, S. K., REDI, B. NI. S., KASTURI, G.,KIRCHHEINIER, W. F. and BA I. ASUBR A NI AN-

YANI, M. DeIllOnStratIOn of .1/. /eprac and itsviability in the peripheral blood of leprosy pa-tients. Lepr. Rev. 43 (1972) 181-187.^49.

35. Mc )(^A. C., REFS, R. J. W., WEDDELL,

pathology of lepromatous leprosy in the nose..1. Pathol. 115 (1975) 215-226.

36. Mit SVILs, K. and 06 AwA, NI. A. A study of150 autopsies of cases of leprosy. Int. J. Lepr.5 (1937) 53-60.

37. NIt•IR, E. leprosy of the lungs. Lepr. India 5(1933) 72.

38. NIrik, E. Relationship of leprosy to tubercu-losis. Lepr. Rev. 28 (1957) 11-19.

39. NEGRE, A. and Fox IAN, R. Images radiolo-gigues de 14re pulmonaire. Int. J. Lepr. 24(1956) 167-170.

40. PEDLEA-„1. C. The nasal mucus in leprosy.I.epr. Rev. 44 (1973) 33-35.

41. PowEI.1., C. and Sw ANN, L. Pathologicalchanges observed in 50 consecutive necrop-sies. Am..1. Pathol. 31 (1955) 1131-1147.

42. RIDLEY, D. S. Bacterial Indices. In: Leprosyin Theory and Practice, 2nd edit., R. G. Coch-rane and T. F. Davey, eds., Bristol: JohnWright & Sons, Ltd., 1964, pp 620-622.

43. RIAGER, A. W. F. Lepra en Tuberkulose.[Lep-rosy and Tuberculosis.] Doctorate Thesis, U ni- 55.versity of Amsterdam. Zaandijk: Uitgeverijder Firma .1. Ileijnis Tst., 1956, 217 pp. Ab-stract in Int..1. I.epr. 25 (1957) 78-79.

50.

51.

52.

53.

54.

47, 1^ kaur ci al: Respiratory .Sistein in Leprosy^ 1 5

SAXENA, 11.. AJWANI, K. D., PRADHAN, S.,

CHANDRA, 3. and KVNI.AR, A. A preliminarystudy on bacteraemia in leprosy. Lepr. India47 (1975) 79-84.SCHAFFER. Uber de Verbeitrung der Lepra-bacillen von den oberen luftwegen aus. Arch.Dermatol. Syphilol. 44 (1898) 159.SinCKER, G. M HtheitlIngerl uher lePla nacherfahrungen in Indien und Aegypten. Nlunch.Med. W'ochenschr. 44 (1897) 1063.TAK AM), K. Anatomo-pathological study oncompletion of tuberculosis seen in human lep-rosy. Report I. Lepro 28 (1959) 233-241.TAKAND, K. Anatomo-pathological study oncompletion of tuberculosis seen in human lep-rosy. Report II. Lepro 28 (1959) 242-257. Ab-stracts for Report 1 and Report II in Int. J.Lepr. 28 (1960) 337.TANY0R, C. E. Contributions from animal ex-periments to the understanding of sensitivityto ,t/. leprae. Int. J. Lepr. 31 (1963) 53-67.TRAPPNIAN, R. A study of the lepromin andtuberculin reactions. The correlation betweentwo reactions and the influence of BCG vac-cination on non-reactors in healthy leprosycontact children in Djakarta. Int. J. Lepr. 26(1958) 102-1 ID.

B. and DAELIEN, II. Relaciones entre lep-ra y tuberculosis. [The relationship betweenleprosy and tuberculosis.] Acta Med. Costar-ricense 1 (1958) 167-176. Abstract in Int. J.Lem. 28 (1960) 483.WADE, II. W. Reactions to tuberculins in lep-rosy. A review. Int..1. Lcpr. 18(1950)373-388.WATANABL, Y. Clinical studies on the pulmo-nary tuberculosis complicated with leprosy.Report I. Lepro 28 (1959) 258-267. Abstractin I nt..1. Lepr. 28 (1960) 337.WAIANABL, Y. Clinical studies on the pul-monary tuberculosis complicated with lepro-sy. Report 2. The results of mass examinationon tuberculosis from 1948-1959. Lepro 29(1960) 200-208. Abstract in Int. J. I.epr. 29(1961) 537.WATERs, M. F. R. and REEs, R. J. W. Changesin the morphology of Mycobacterium lepraein patients under treatment. Int. J. Lepr. 30(1962) 266-277.