VOL.

No. 3

524,

MYCOPLASMA Downloaded from www.ajronline.org by 187.160.196.170 on 06/21/16 from IP address 187.160.196.170. Copyright ARRS. For personal use only; all rights reserved

CLINICAL

AND

CHARLES

By

JOSEPH

PNEUMONIA*

ROENTGENOGRAPHIC

E. PUTMAN,

M.D.,

NEW

pneumonia

//JYCOPLASMA

ri

I

sent

in

a variety

M.D.,t

F’. SIMEONE,

HAVEN,

may

of ways.

and

is

considered

rare,’9

pre-

ferent clinical and roentgenographic ings. They did not differ significantly age, race or sex (Table i). Forty-eight patients presented symptoms characteristic of an acute

A recent

but

this

monic

years.

The

study

population

has

consisted

process:

non-pleuritic

hemorrhagic.

Two

of

per

2

groups

cent

ber

AND ASPECTS

Presented

‘

24-27,

t

of the

cases

presented at

the

Seventy-fifth

investigated. with Annual

These

distinctly Meeting

Per

OF

Mean

Cent

Age

Group

I

48

(48)

26

Group

II

28

(28)

36

Group

III

24

(24)

28

of

the

American

Roentgen

Ray

Society,

San

Francisco,

1974. Assistant

Professor, Diagnostic Radiology and Internal Resident, Diagnostic Radiology, Yale University Resident, Diagnostic Radiology, Yale University School

II Assistant

Professor,

Diagnostic

Radiology,

Yale

underwent

pul-

CASES

Sex

Race

M2o F28 Mi8

W38

Flo

M3

Bi6 Wi4-

FI3

BI2-

california,

September

BI4 W12

dif-

chief

§

pain,

I

CI.ASSIFICATION

Among ioo patients with Mycoplasma pneumonia we have observed 2 distinct groups of patients who together comprise 76

patients

TABLE

Num-

CLINICAL

with pneu-

monary angiography for diagnosis. Both angiograms were normal. Pulmonary function was evaluated in 14 patients. Hypoxia with PO2 of less than 75 mm. Hg was found in 4 patients. The associated pCO2 was normal. All 14 had normal vital capacity and FEy1 determinations. Patients treated with appropriate antibiotics (erythromycm, tetracycline) responded clinically and roentgenographically, clearing pulmonary

both hospitalized and ambulatory patients. Sera for antimycoplasma antibodies were drawn when Mycoplasma pneumonia was suspected clinically. Titers were measured using the complement fixation technique described by Eng.9 In all cases the dianosis of Mycoplasma pneumonia was made on the basis of clinical and roentgenographic findings as well as a fourfold rise in titer of complement fixing antibody. ROENTGENOGRAPHIC

chest

findas to

cough, myalgias, and fever. Chest roentgenograms showed segmental or lobar consolidation with associated air bronchograms and, occasionally, atelectasis (Fig. i). Unilateral involvement was noted in 31 cases. Pleural effusions, obvious on posteroantenor roentgenograms, were present in 9 cases (Fig. 2). Four ofthese effusions were grossly

recently been reported in 6 of 29 adult cases,’3 and in 6 of6 pediatric cases.’8 Because of these confusing reports and obvious discrepancies, we have recently evaluated retrospectively i 00 consecutive cases ofMycoplasma pneumonia seen at the Yale-New Haven Hospitals over the past 3

ANNE McB. CURTIS, M.D.4 PAMELA JENSEN, M.D.II

CONNECTICUT

paper emphasizes these variations.30 One author has stated that the infiltrate is of a lobar segmental type,’9 while others have found the infiltrates to be mainly reticular or interstitial.1’”’20’27’33 Some authors emphasize bilateral lower lobe involvement,20 while others report unilateral infiltration in 86 to 90 per cent of cases.’4’7 Pleural effusion

PATTERNS

University

Medicine, Yale University School of Medicine. of Medicine. School 417

of Medicine.

School

of Medicine.

Putman,

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418

Curtis,

Simeone

and

Jensen

JULY,

1975

symptoms or the roentgenographic abnormalities over a 2-4 week period. Ten patients continued to have abnormal chest roentgenograms for 3 months following the acute episode of Mycoplasma pneumonia. Within

this

group

of

patients,

8 had

sar-

Hodgkin’s disease. The remaining 24 patients had such variable clinical and roentgenographic findings that specific categorization is not possible. Some presented with classic symptoms of pneumonia, while others presented with less specific complaints. Fifteen of these 24 patients had normal chest roentgenograms; coidosis

and

had

FIG. upper

1.

Chest lobe

roentgenogram segmental

i

had

roentgenograms

demonstrating

local

or diffuse disease or both. Response to antibiotics was variable. In effect, these patients represent an overlap of the popula-

showing

tions

consolidation.

of Group

i

and

Group

II.

DISCUSSION

infiltrates within tients within this lupus

erythematosus,

ease,

and

patients

3

to

group

cell

disease

had

plicated prolonged illnesses. A second group of 28 patients with symptoms oflonger duration: lethargy, and a 1-4 week history ness

of

breath.

In

pa-

systemic

sickle cell disdisease. The

Hodgkin’s

sickle

Four

had

3 had

had

with

days.

14

first

contrast

com-

presented malaise, of shortto

the

first

group, these patients were usually afebrile and free from cough, mvalgia, and chest pain. Chest roentgenograms showed hilateral di ifuse reticulonodular infiltrates extending from the hila to the periphery with occasional Kerley B lines (Fig. 3; and 4).

None

solidation.

showed

lobar

Only

patient

or

segmental had

a pleural

Our other

confirms the findings of many Mycoplasma pneumonia

survey

authors:

may

present

with

either

segmental

con-

solidation or diffuse reticulonodular infiltration.3#{176} Upper lobe involvement occurs frequently enough that this finding by no means excludes Mycoplasma pneumonia from a differential diagnosis.29 Pleural effusion is not an uncommon finding, and is more

commonly

associated

of lobar or segmental tients with accepted tions in our study,

with

the

consolidation.30 autoimmune with systemic

pattern

Paaberralupus

A

conef-

fusion. Pulmonary function was evaluated in 19 patients: hypoxia with PO2 of less than 75 mm. Hg was found in 13 cases. Unlike the hypoxic patients in the first group, these patients also had an associated low pCO2. Sixteen of 19 had a decreased vital capacity with normal FEV1. These abnormalities are consistent with either restrictive or diffusion defects or both together. Appropriate antibiotic therapy did not appear to affect the clinical

I

FIG.

2.

pleural

Chest

roentgenogram

effusion

which

was

showing massive grossly hemorrhagic.

left

VOL.

No.

524,

Mycoplasma

3

erythematosus

on

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Hodgkin’s

disease,

steroids,

and

generally

display

Pneumonia

with

3

lobar

or segmental consolidation. with Hodgkin’s disease had edematous pattern referred et al.2#{176} The 3 patients with

One patient the interstitial to by Jansson sickle cell dis-

ease

courses,

had

been

prolonged

reported

though

difficult

by

response

Shulman

as has

al.28

et

to antibiotics

419

Al-

is difficult

to

evaluate, as the disease may have a short course,22 those patients in Group i treated with erythromycin or tetracycline seemed to have rapid improvement both clinically and roentgenographically, as noted by Kingston et al.23 In some instances, Mycopneumonia

plasma

illness

associated

pulmonary

may

with

be

a

protracted

fuse

Severity

of disease

hila to periphery.

function.2’3#{176}

indolent

lar infiltrates fusing clinical were

considered:

roentgenogram

abnormal

does not correlate with level of antimycoplasma antibody titers.8’3#{176} The existence of 2 distinctive clinical and roentgenographic responses to infection with Mycoplasma pneumoniae remains to be explained. The patients in Group with

Chest

4.

FIG.

markedly

symptoms

presented picture.

and

heart

The

association

of

antibodies

and

been

ii

failure,

sarcoidosis, collagen vascular disease, hvpersensi ti vity pneumoni tis, and even lymphangi tic spread of tumor. This apparently modified response to Mycoplasma pneumoniae may be the result of underlying lung disease, previous exposure to Mycoplasma pneumoniae, or differing immune responses.

anti

in patients

of

those

either

no

case is

with

had

lung

8

lung

diffusion

tional

beyond

genogram

study FIG.

3. Chest

peripheral

roentgenogram

reticulonodular

showing

infiltrate.

bilateral

of

of restrictive

defects,

to

in some

return

of the limits.

similar

functional

period.

chvmal disease, may modify the

far That

a comand

dur-

These

normal

cases

or

illness

persisted,

the

demonstrated

ties

In

abnormalities

convalescence.

abnormalities

cases,

of sarcoidosis.

acute

prolonged

pa-

28

pattern,

indicative

bination,bothduring

ing

segmental our

parenchymal

had

function

disease,

or Of

form

others

pulmonary

pneu-

parenchymal

lobar

underh’ing

in the

titers

demonstrated

reticulonodular

obvious

addition,

in

Mycoplasma

described.

the

disease

rise

bed, of

obnorof

roentgenograms

or increased

No

titers

and with incidence

with chest

with

consolidation 8

compared the

descri

change,

markings. tients

an ti body

The

patients

au-

significantly

bronchitis

associated

when

monia,

disease

several

fou nd

chronic

low.

very

antimvco-

by

disease However,

illness

acute

diffrom

lung

mvcoplasma

with

structive lung mal controls. was

elevated chronic

Lambert24

elevated

bilateral extending

investigated

thors.3’24’34

reticulonodu-

showing

infiltration

plasma

has

a particularly conMultiple diagnoses

congestive

reticulonodular

beyond

funcin some chest roent-

Berven2

has

abnormali-

the

3

month

underlying

paren-

in this case roentgenographic

sarcoidosis, appear-

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420

Putman,

Curtis,

ance is hardly surprising. Long term followup of patients in Group II not having sarcoidosis is needed to evaluate the possibility of early underlying parenchymal disease. A second explanation for differing roentgenographic and clinical response to Mycoplasma pneumoniae may be related to a history of previous exposure to the organism. Chanock3’4 and Rifkind et al.26 have demonstrated that the presence of antimycoplasma antibody in titers of greater than I to 10 confers protection from illness but not infection, as shown by fourfold increase in antibody titer following challenge, positive culture of throat specimens, and the absence of associated illness. There is one report of naturally acquired reinfection with Mycoplasma pneumoniae,15 but unfortunately, no roentgenogram is described. To date, there is no good method of serologic detection of prior infection with Mycoplasma pneumoniae. Complement fixing antibody tends to disappear with time,24 and thus the historical significance of a negative antimycoplasma antibody titer is not known. Other assays for Mycoplasma infection such as tetrazolium reduction inhibition to measure growth inhibiting antibody,2’ or hemagglutination inhibition’0’31 may be of help in this regard. The latter may be positive for 10 years.3’ Pre-infection antimycoplasma antibody titers are not, of course, available for either groups of our patients. In a susceptible population, with a high incidence of Mycoplasma infection, serologic evidence Should be sought to evaluate the possibility that a modified clinical and roentgenographic response to Mycoplasma pneumoniae may be the result of an anamnestic reaction. A third possibility relates to the “role” of humoral and cellular immunity. Clyde and Bienenstock,6 working with Syrian hamsters, have shown that initial infection with Mycoplasma pneumoniae introduced intranasally produces a peribronchial infiltrate with numerous immunoglobulin staining cells. Rechallenge produces an infiltrate of similar distribution, but with immunoglobu-

Simeone

and

Jensen

lin negative cent of a

JULY,

small delayed

lymphocytes hypersensitivity

sponse.”6 In another logic response was

organisms challenge

paper,” induced

“reminisre-

a similar with

given intraperitoneally, with intranasal innoculation

duced

clinical

have

reported

fense

mechanisms

pneumonia.

that

Other

serokilled

yet

repro-

authors

antimycoplasma include

5975

de-

“lymphokine”

mediated macrophage 611 a characteristic of delayed hypersensitivity. Eight of the patients in Group II had sarcoidosis and were shown to be anergic. Unfortunately, none of the other patients in Group II was evaluated in this regard. The manifestations of Mycoplasma pneumonia in immunodeficiency states have been previously reported.’6 The relationship of anergy to the clinical and roentgenographic expressions of Mycoplasma pneumonia warrants a further investigation. Mycoplasma pneumonia provides a unique example of an infectious disease in which autoantibody directed against lung tissue appears early in convalescence. Likewise, false positive serological tests for syphilis, cold hemagglutinins, and agglutinins for a serologically distinct streptococcus have been demonstrated in some phase of active

infection.32

It

is

quite

conceivable

that Mycoplasma pneumoniae possesses special immunological problems for certain hosts. The variability of the pulmonary infiltrates may be the result of antigenantibody reaction in areas of the lung adjacent to the bronchial tree, whereas the organisms themselves have been located primarily in the bronchial epithelium.7 It is conceivable that a few infected individuals may develop a hypersensitivity reaction to a modified tissue product, possibly of pulmonary origin. The roentgenographic response of patients in Group ii to Mycoplasma pneumoniae may not be a manifestation of infection with the organism, but rather an altered host response to some form of antigenic stimulus. SUMMARY

Our

study

of

ioo

patients

with

Myco-

VOL.

124,

Mycoplasma

3

No.

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plasma pneumonia has confirmed ings ofmany other authors. Mycoplasma pneumonia may upper

as

well

as

lateral pleural

or bilateral, effusions,

lower

lobes,

the

be

may be associated and may appear

genographically

as segmental

infiltrates. noted

distinct

2

syndromes:

E. Putman,

Department

of Radiology Avenue

New

Connecticut

Haven,

F. W.

Mycoplasma

tracheal

organ

I I .

J. Studies

12.

2.

H. Studies

BERVEN,

tion

in

ical”

on

pneumonia.

acute

Icta

med.

IS.

5962,

i6.

for

plasma

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CHANOCK, GUTEKUNST, TERFIT,

R. M., FOX, H. H., JAMES, W. D., R. R., WHITE, R. J., and SENL. B. Epidemiology of Mycoplasma

pneumoniae 4.

infection

meeting N.

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17.

H. M.,

R., Mycoplasma

after

yrs.

J. T.,

GRAYSTON,

D.,

H., and

GRIX,

D., WILLERS, A. C. Search for Myco-

19.

HEBERT,

TAYLOR-ROBINSON,

STENHOUSE,

plasma infections bronchitis. Thorax, CLYDE,

i8.

Nat. ilcad.

47, 887-890.

Sc., 1961, CHERRY,

W. A.,

JR.,

in 5975,

and

patients

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chronic

26, 62-67. BIENENSTOCK,

CLARKE,

pneumoniae 1971,

G. E.,

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216,

671-672.

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S., and CIAMMONA, S. Pneumonitis with pleural effusion in children due to Mycoplasma pneumoniae. Am. Rev. Resp. Dis., 5974, 109, 665-671. agent

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283, 790-793.

MACCOLL,

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infected annual na-

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H. M., KENNY, MANSY, A. M., and

FOY,

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Soc., Dec. Va. To be published. L. R., and SHEEDY, P. F.

FOY,

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of

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1nn.

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CLYDE,

immune

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g.

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