ORNITHOSIS
IN
INFANCY
By Shimon Berman, M.D.,* Emil Freundlich, M.D., Kurt Glaser, M.D., Abraham
Abrahamov, M.D., Erela Ephrati-Elizur, Ph.D., and Hans Bernkopf, M.D.
752
P
RIMARY atypical pneumonia may be caused by a variety of agents, amongthem rickettsias and viruses. Of the known
viruses there are members belonging to the
psittacosis-lymphogranuloma group. They
were first isolated from parrots, but then were found distributed throughout the ani-mal kingdom in a variety of wild and do-inesticated birds, and in some mammals
(
cats, mice and cattle).These viruses are endemic in many
spe-cies of birds. Man contracts the disease
usu-ally by intimate contact with birds, or
through inhalation of dust containing virus
particles from their excreta.1’ The infected
bird may not show signs of disease but still be a healthy carrier. Human-to-human transmission is also known to exist, and
“humanized” strains of these viruses were
reported during some epidemics.4’
The name psittacosis is usually reserved for the disease transmitted by parrots or
parakeets. Ornithosis is the term proposed
by Meyer” 2 for virus strains infecting other
species of birds. These strains are generally thought to he less virulent to man.46
Children are believed to be much less
susceptible to ornithosis than adults.1, ‘S
Reports on ornithosis in children are very scarce, and no case report in a child
younger than 13 years has been found in
the literature. From 1 1 1 cases of ornithosis,
(liagnosed at the Hooper Foundation of the
University of California, not a single case
was discovered under the age of 10 years.3
A l)rother and sister aged 5 and 8 years
with interstitial pneumonia and a
3-year-From tile I)epartment of Pediatrics, Hadassah
Ilebrew University Ilospital, and the Virus Labora.
tory, hebrew University Hadassab Medical School, Jerusalem, Israel.
(Submitted for publication I)ecemher 7, 1954;
revision accepted February 1, 1955.)
0 ADDRESS: P.O.B. 499, Jerusal(.ul1, Israel.
old child with pleuropneumonia were
re-ported from Germany and Holland
respec-tively.8’ The youngest patient found with
ornithosis was an 18-month-old infant from Italy.1#{176} Recently 37 cases were reported
from a rural area in Illinois; only 2 of them
were children, aged 7 and 9 years.’1 The
diagnosis of omithosis in all these cases
was based on serological evidence only. Ornithosis viruses were suggested as a possible etiological agent of interstitial pneumonias in Israel when Komarow and Goldsmit isolated an ornithosis virus from
sick pigeons.” A human case of ornithosis in Israel was reported by Valero in an aduht.’ The diagnosis was established by a positive complement-fixation test and
con-tact with infected pigeons was
demon-strated in this case. Five cases of fatal inter-stitial giant cell pneumonia were previously
reported in infants in Israel by Wolman and others.14 The disease was suggested to be of a virus origin but serological and cultural studies for the identification of the virus were not performed.
This article deals with ornithosis in in-fants hospitalized in the Children
Depart-ment of the Hadassah Hebrew University
Hospital, Jerusalem, Israel.
In late winter of 1953 an infant died in our department of a severe pulmonary
in-fection that did not respond to antibiotic
treatment (Case 1 of our series). At about the same time a 1-month-old infant died suddenly at home without signs of previous illness (this infant was not hospitalized and
is not included in our series). A virus
be-longing to the psittacosis-lymphogranuloma
group was isolated from the lung tissue in
both cases.’5 These cases directed our at-tention to the possibility of more frequent occurrence of ornithosis in infants.
There-fore, we started to examine sera of infants and children in our department with
METHODS
ISOLATION OF THE AGENT. Whole blood or serum, taken at the beginning of the illness and/or lung and spleen suspensions from fatal cases were inoculated amniotically into 12 to
13-day-old developing chick embryos. Penicillin
and streptomycin were added to the inocuhum.
The eggs were incubated for 4 additional days and tile virus was then passed to eggs, by the
amniotic and yolk sac routes and to mice by the
intracerebral and intranasal routes.
COMPLEMENT-FIXATION TEST. The antigen for complement-fixation test was prepared from
ahlantoic fluid with the virus isolated from Case
1. At the beginning of this study all sera were
tested in the dilution of 1 :8 or more. Later,
lower dilutions, 1:2 and 1:4, were also tested.
Normal allantoic fluid served as control antigen.
PROPERTIES OF ISOLATED AGENTS. Virus was
isolated from 5 cases by inoculating serum,
l)lOod or organ suspensions from fatal cases into fertilized eggs. Chick embryos died 4 to 5 days
following yolk sac inoculation. Mice inoculated
intracerebrally died within 3 to 6 days. Pigeons died within 7 to 10 days following intracerebral
inoculation. Organs of infected mice and egg material were found to be sterile by ordinary bacteriological methods.
Identification of the isolated agents as
orni-thosis virus was based on the following criteria: 1. Macchiaveiho stained smears from ma-terial of infected eggs and mice showed
dc-mentary and inclusion bodies typical of the
psittacosis-lymphogranuloma group.
2. Fatal infection was produced in mice by the intracerebral route only, in contradistinc-tion to psittacosis virus which produces fatal
infection in mice by both intraperitoneal and
intracerel)ral routes.
3. Fatal infection was produced in pigeons
following intracerebral inoculation, a property attributed to ornithosis virus mainly.
4. A cross immunization test carried out
with the isolated virus and a strain of
orni-thosis virus isolated from sick pigeons in
Israel, did not reveal any immunological
dif-ferences.
A detailed description of the biological and serological properties of the isolated viruses
will be published.’6
CASE REPORTS AND RESULTS
The cases which are reported will be
di-vided in 2 groups according to the
corn-pheteness of the laboratory data. The first
group (Cases 1 to 6, Table I) includes cases in which the diagnosis of ornithosis is con-sidered certain, based on the isolation of a
virus of the psittacosis-lymphogranuhoma
group, or on an increasing antibody titer
in the serum during the illness. The second group (Cases 7 to 9, Table II) includes pa-tients in whom a diagnosis of ornithosis
could not be made with certainty because of incomplete data. In no case was isolation
of the virus attempted. In these cases, the early ones in this series, the only blood
sample examined gave a positive comple-ment-fixation test. A second sample either
was not obtained, or did not reach the
laboratory in good condition.
First Group (Cases 1 -6, Table I)
CASE 1. B. M. A 2-year-old girl was ad-mitted February 9, 1953, because of a corneal
ulcer. The infant was malnourished but no
other abnormal findings were revealed on physical examination. The corneal ulcer
im-proved after 2 weeks of local treatment, but
at this time a severe cough with fever
ap-peared. Coarse rales could be heard over both lungs. Her condition deteriorated; she became
dyspneic and cyanotic, and developed severe
diarrhea with signs of dehydration. Parenteral fluid therapy, oxygen, penicillin, Aureomycinit,
and streptomvcin did not improve her
condi-tion and the infant died 5 days after the
ap-pearance of the first signs of respiratory
dis-ease.
On post-mortem examination interstitial pneumonia with areas of atelectasis was found.
A virus belonging to the psittacosis-lympho-granuloma group was isolated from the lung
tissue.
CASE 2. A.J. A 19-month-old boy was
ad-mitted on April 21, 1954. He suffered from
coughing for 1 month before admission. A few days before he entered the hospital his
condition deteriorated and on admission he
was severely cyanotic and dyspneic. Coarse
rales were heard over both lungs. The liver was enlarged, palpable 3 cm. below the costal
margin, and the spleen was just palpable. A
roentgenogram revealed accentuation of the lower branches of the bronchi and increased hilar markings on both sides, especially the
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lung field, possibly atelectasis of the right
lower lobe. The heart was slightly enlarged in
all directions.
The infant received antibiotics and oxygen
but his condition got worse. Diarrhea occurred on the 9th day and signs of paralytic ileus ap-peared 3 days later. In spite of treatment with parenteral fluids, blood transfusion, panto-theme acid, penicillin, Aureomycin#{174}, and streptomycin the infant died on the 14th day of hospitalization.
A virus belonging to the psittacosis-hympho-granuloma group was isolated from the blood
on the 14th day of hospitalization. The corn-plement-fixation test was negative in a 1:8 titer from the same blood specimen. On post-mortem examination foci of
bronchopneu-monia and interstitial myocarditis were found.
Comment on Cases 1 and 2. These 2
cases were the only deaths in our series.
In both cases virus isolation was successful.
The clinical picture was that of a severe
pulmonary infection which did not respond
to antibiotic therapy. Both infants were malnourished and developed a severe
gastroenteritis with dehydration in the hos-pital and in Case 2, paralytic ileus.
CASE 3. L. R. This male infant was 1 month old on admission April 1, 1954. His mother
re-. ported that she had had a persistent cough
during the last month of pregnancy, without
c fever. His older brother had a mild upper respiratory infection 1 week after the patient’s
. birth. The patient was breast fed
supple-- mented with half skimmed milk and gained
t satisfactorily. At the age of 2 weeks he started
:
to cough and 1 week later developed fever butnevertheless continued to gain weight.
He was cyanotic on admission but in good
. general condition. There was dullness on
per-cussion over the left lung base. The spleen was palpable 1 cm. below the costal margin. A roentgenogram showed decidely increased
]m hilar markings on both sides, especially on the
‘! left, and pleural effusion along the left chest
. border.
. The infant received penicillin, streptomycin
and chhoramphenicol. His condition improved
slowly; the temperature became normal after
. 1 1 days but the left hilar shadow was still markedly increased in the roentgenogram after
con-dition when he heft the hospital 25 days after
admission.
A virus of the psittacosis-hymphogranuloma
group was isolated from the infant’s blood on
the 4th hospital day, 2 weeks after the
begin-ning of the disease. The complement-fixation
test was twice negative in the 1 : 8 dilution.
CASE 4. A.
J.
A 1-year-old boy was admittedOH November 20, 1953, 2 days after his illness
began with cough, high fever and dyspnea.
The infant’s mother had had a cough without
fever 2 weeks before. On admission he was
dyspneic and cyanotic; there was dullness over
the right lung on percussion. A roentgenogram on admission revealed a dense shadow in the
middle lobe (atelectasis?) and a slight pleural
effusion on the right. There were no
patho-logical findings in the left chest.
The infant received penicillin, streptomycin,
Aureomycin#{174}, Terramvcin#{174}, and oxygen. Ten
ml. of clear, bacteria-free fluid were extracted
from the right pleural space. On the 7th day of hospitalization, a roentgenogram showed
marked effusion in the left pleural space and
a round shadow in the right middle hung field. The hilar shadows were markedly increased
on both sides.
There was no improvement during the first 10 days of hospitalization. Afterwards the
temperature became normal and the cyanosis
disappeared ; however, the roentgenological
findings still persisted. The infant was seen
in the outpatient clinic after being discharged
an(l was in excellent condition.
The complement-fixation test on the 6th day of the disease was positive in the 1:8 dilution;
On the 27th (lay the titer rose to 1 :64.
Isola-tion of the virus was not attempted.
Comment on Cases S and 4. These 2
cases represent a moderate to severe
pul-monary infection. The diagnosis was proved
in Case 3 by the isolation of a virus, in
Case 4 by an eight-fold rise of the titer in
the complement-fixation test. Both infants were cyanotic, had fever for nearly 2 weeks
and did not respond to antibiotics. Both had increased hilar markings, a pleural effusion
and persistent roentgenological signs after clinical improvement. The white blood cell count was high in both infants (Table I). The young age of Case 3 is noteworthy.
In both cases the mother had had a
respira-tory infection before the infants’ illness.
CASE 5. 5. C. This infant was admitted on
February 20, 1954, at the age of 40 days. The pregnancy and the birth were normal. He was breast fed and gained satisfactorily. His dis-ease began 3 days before admission with fever, cough, vomiting and diarrhea. On ad-mission, he was in very good condition,
with-out fever. There were no other pathological findings, aside from ronchi and moist rales throughout both lungs. The roentgenogram of
the chest was negative. The infant received penicillin and was discharged after 6 days. A virus belonging to the
psittacosis-lympho-granuloma group was isolated from patient’s
blood on the 5th day of the disease. The com-phement-fixation test was twice negative but was tested in the dilution of 1 : 8 only.
CASE 6. K. E. A 2-year-old boy was admitted on February 20, 1954, with the history of fever for 1 day, cough and respiratory stridor.
The pharynx was mildly inflamed and moist
rales were heard throughout both lungs. A roentgenogram of the chest was negative. The infant received penicillin, streptomycin and Terramycin#{174}, and steam. The temperature became normal the day after admission. He
was discharged after 5 days at his parents’ request though at this time there still were signs and symptoms of a mild upper
respira-tory infection.
A virus was isolated from his blood on the 4th day of the disease. The complement-fixa-tion test was negative in the 1 :8 dilution on
the 4th and 22nd days of the disease; 3 months later it was positive in the 1 :4 dilution.
Comment on Cases 5 and 6. These 2
cases had only a mild upper respiratory
infection with a negative roentgenogram
of the chest. They had mild fever for the first few days of the disease. The infants
were in very good general condition during the illness. The spleen and liver were not enlarged and the white blood cell count was normal. In both cases a virus belonging to
the psittacosis-lymphogranuloma group was isolated from the blood, the
complement-fixation test was negative in the 1 :8
dilu-tion in both cases at first and positive in a
dilution of 1:4 in Case 6 three months after the disease. The young age of Case 5 is
‘l’ABLE HI
COMPLEMENT-FIXING ANTIBODY TITE1IS IN FAMILY MEMBERS
4 1:16 I.5 months
5.5 uimontlus
ORIGINAL ARTICLES
Second Group (Cases 7-9, Table II)
These are the cases with a single positive
complement-fixation test. The interpretation
of the serologic tests requires some cati-tion because non-specific serological
reac-tions are known to appear in cases with
atypical pneumonia. However, the serum
reactions with normal control antigen were
always negative in our cases. Moreover
taking into consideration the young age
of our patients, it seemed unlikely that the
positive serologic tests could be connected
with a former infection. It was assumed, therefore, that the presence of antibodies
was caused by the present disease.
Comment on Cases 7-9. These cases
rep-resent a mild to moderate pulmonary in-fection. They had a history of cough and
fever for a few days before entering the hospital. On admission they had high fever and were dyspneic but improved clinically
after 1 to 3 days. The physical findings in
the lungs were dullness over part of the
lung or a few rales. The roentgenograms revealed density of part of the lung, pleural
effusion or increased hilar markings. The
white blood cell count was normal or slightly elevated. Additional findings were
diarrhea and malnutrition in Case 7, anemia
and purulent conjunctivitis in Case 8, and
congenital heart disease in Case 9.
Serological Findings in Family Members
Family members of some of our patients
were examined for the presence of
comple-ment-fixing antibodies against ornithosis
viruses. As reported earlier, the history of a
recent respiratory infection was elicited in
Sonic family members.
The results are presented in Table III. It is seen that in 2 cases sera of the
par-ents and, in 1 case the mother’s serum
con-tamed specific complement fixing
anti-bodies. In Case 3 the mother reported
hay-ing had a cough during the last month of
pregnancy and the infant’s older brother
had had an upper respiratory infection 1
week before the patient’s illness began. The
patient was 1 month old at the beginning
(‘ase A1otiiei Father
Time of Ixam. after Patient’s
Disease
1 1:16 1:8 ‘3 months
3 1:10 1:10 1nmonth
*
* Could not he examined because of
anticonlple-unentary reaction.
of the disease. In Case 4 the mother’s serum
showed a titer of 1 : 16 which dropped to 1:2 4 months later, a finding which may be explained on the assumption that the titer observed in the first sample was due to a recent infection. In this case, the mother
had a severe cough some 10 days before the infant’s illness.
The presence of complement-fixing anti-bodies in other members of the family may
be due to an infection from a common source, but the possibility of a human-to-human transmission of the disease should also be considered.
DISCUSSION
The experience with ornithosis which has been described definitely demonstrates that clinical ornithosis occurs in infants and that this disease, far from being rare in this age period, may have a predilection for early childhood. The number of cases reported here probably constitutes the minimum
rather than the true number coming in our department, as no doubt other cases were overlooked, especially in the beginning of
this study.
A number of problems have arisen from
our experience with omithosis:
The clinical course was so varied that one
can easily assume infections occur without
chil-(Iren in our series may be dtie either to the
mildness of the infection in this age group
or to an immunity, not necessarily of
demonstrable type, resulting from an
un-recognized infection in the past.
The severity and prolonged duration of
SOI1T1 of the cases cannot be ascribed to a
supenmposed bacterial infection; the
in-effectiveness of the antibiotics is against
such an argument.
Three of our cases had a pleural effusion
(3, 4, and 9), bilateral in one (Case 4),
while all pulmonary findings (clinical and
roentgenologicah) were on the right side only. These findings may indicate that in
the course of a viremia the infection lo-cahized directly in the pleura. No attempt
was made to isolate the agent from the
pleural effusion.
In a disease with such varied clinical
courses, it is difficult to evaluate the effec-tiveness of antibiotic therapy. There is no
basis in any of the cases for ascribing the
termination of the illness to the therapy. Some cases (2, 3, and 4), remained febrile
for 10 or more days and 2 (lied (Cases 1, 2) in spite of antibiotic treatment. This is
contrary to reports in the hiterature’7’#{176}
which claim the broad spectrum antibiotics
have a favorable influence on ornithosis.
On the other hand Aureornycin#{174} in a dose of
1 mg. per egg inhibited completely the mul-tiphication of the strain of ornithosis virus isolated from Case 1.
More should be learned about the evalua-tion of the serological test. The absence of
a rise in the titer of the complement-fixing
antibodies in some of our cases in which
a virus was isolated is not clearly
under-stood; the time of persistence of a positive
complement-fixation test after the disease
has run its course seems to differ from case to case. Two of our youngest patients
(
Cases 3 and 5) showed a very poor serologi-cal response. More study will be necessary before we can attribute this to pooranti-body production in young infants. The low
titer in the complement-fixation test in those
cases can probably not be explained by
treatment, because in most of these cases
there was no clinical response to antibiotics.
In considering the possibility of
human-to-human infection, pathways of the
excre-tion of the virus should be known. If such infection had taken place in our series, from
the mother to infant, droplet transmission seems probable. Two of the fatal cases had
diarrhea which may have been one of the casual infections so common in malnour-ished children. However, the fecal excre-tion of the viruses would have to be
con-sidered, even without diarrhea, especially in infants in whom virus coughed up was
probably swallowed.
In our small series the cases were
dis-tributed between the months October and April. In none of our patients could
in-timate contact with birds be demonstrated. The children could have easily come in
con-tact with infected pigeons’ droppings as pigeons are found all over Jerusalem and
other places in Israel. Over 25 per cent of more than 100 pigeons examined had a positive complement-fixation test for orni-thosis virus.’6 Here too we do not know how long the complement-fixation test
re-mains positive after the infection, nor do we
know how long an apparently healthy bird
may excrete virus. Virus isolation from
birds’ droppings was not attempted. We can
say that pigeons represent a reservoir of
ornithosis infection in our area although
the importance of this reservoir could not be estimated. Sparrows, starlings, chickens, etc. were not examined.
SUMMARY
This report deals with 6 certain and 3 possible cases of ornithosis in infants. All
cases were under 2% years of age; 2 of them
were 1 month old.
In 5 cases a virus belonging to the
psit-tacosis-lymphogranuloma group was iso-lated and the sixth case showed an eightfold rise of the antibody titer in the complement-fixation test during his illness. In other cases the diagnosis was suggested by a single
All these infants had manifestations of
respiratory tract infection. There was a
great \rariatjon in the clinical picture; 2
cases were fatal and 2 others suffered
moderate to severe respiratory disease
while the others had only a mild respiratory
infection. In severe cases the broad
spec-trum antibiotics had no obvious effect upon
the course of the disease.
Infected birds may have been the source
of the disease but in some cases
human-to-llunlan transmission appeared possible.
ACKNOWLEDGM ENTS
\Ve wish to express our thanks to Dr.
S. Schorr, X-ray Department of the
Hadas-saIl Hebrew University Hospital, Jerusalem,
for his helpful a(lyice in the evaluation of
the roentgenologic findings.
Our thanks are due to Drs. M. Wolman
and \I. G. Goldberg, Department of
Pathology, Hebrew University Medical
School, who performed the autopsies on
CaSeS 1 and 2.
REFERENCES
1. Meyer, K. F. : The ecology of psittacoSis
.311(1 Ornitllosis. Iedicine, 2 1:175, 1942.
2.
Meyer, K. F., Eddie, B. , and Yanamura,H. Y.: Ornithosis (Psittacosis) in pigeons
dIl(l its relation to human pneumonitis.
Proc. Soc. Exper. Biol. & Med., 49:609,
1942.
:3. Meyer, K. F., and Eddie, B. : The knowl-edge of human virus infection of animal
Origin. J.A.M.A., 133 : 822, 1947.
4. Bedson, S. P. : Recent work On the viruses
of the psittacosis-lvmphogranuloma
group and its importance with special
reference to primary atypical
pneu-inonia. Irish
J.
M. Sc., 322:385, 1952.5. Bedson, S. P. : The psittacosis-lympho-granuloma group of viruses. Brit. M. Bull., 9:226, 1953.
6. L#{233}pine, P. R.: L’ornithose (#{233}tiologie,
svmptomatologie et diagnostic). Semaine
hop. Paris, 26:3376, 1950.
7. \Volins, W. : Ornithosis (Psittacosis).
Re-,iew, with report of 8 cases resulting from contact with domestic pekin duck. Am.
J.M.
Sc., 216:551, 1948.8. Strobel, W. : Beitrag zum Krankheitsbild (her Ornithose im Kindesalter. Deutsche med. Wchnschr., 79: 176, 1954.
9. Prakken, H. H. : Ecu Ceval van Psittacosis
(
Ornithosis). Maandschr. kindergeneesk.,18:341, 1950.
10. Toscano, F., Angela, C. C., and Di Nola, F. : Pneumopatie da ornitosi nell’infan-zia. Minerva pediat., 5:930, 1953. 1 1. Ward, C. C., Hildinger, A. L., Morrissey,
R. A., and Birge,
J.
P. : Psittacosis-lymphogranuloma venereum virus anti-bodies in man. J.A.M.A., 155:1146, 1954.12. Komarov, A., and Goldsmit, L. : The isola-tion of the causative agent of ornithosis (psittacosis) in Israel. Harefuah, 43:85,
1952.
13. Valero, A. : Human Ornithosis in Israel. Harefuah, 45:102, 1953.
14. Wolman, M., Izak, G., Freund, E., an(I Shamir, Z. : Studies on interstitial giant cell pneumonia. Am.
J.
Dis. Child., 83:573, 1952.
15. Ephrati-Elizur, E., Bernkopf, H. and Wol-man, M. : Isolation of virus belonging to the psittacosis-lymphogranuloma group
from two fatal cases of interstitial pneu-monia in children. Harefuah, 45:199, 1953.
16. Ephrati-Elizur, E., and Bernkopf, H. : To be published.
17. Sigel, M. M., Cole, L. S., and Hunter, 0.: Mounting incidence of psittacosis. Am.
J.
Pub. Health, 43:1418, 1953.18. Wirth,
J.
: L’ornithose. Helvet. med. acta,19:314, 1952.
19. MacLachlan, W. \V. C., Crum, C. E.,
Kleinschmidt, R. F., and Wehrle, P. F.: Psittacosis. Am.
J.
M. Sc., 226:157, 1953.20. Horsfall, F. L. : Chemotherapy of respira-tory viral diseases. PEDIATRICS, I 3:593,
1954.
SPANISH ABSTRACT
Ornitosis
en la Infancia
Los virus determinantes de cua(lrOs respi-ratorios son end#{233}micos en muchas especies (IC
ayes; el hombre los adquiere par contacto Intimo con tales ayes o bien por Ia inhalaci#{243}n de polvo contaminado por eh virus de los
cx-creta de las ayes infectadas. Estas adem#{225}s pueden ser simplemente portadores asinto-m#{225}ticos. Se supone que el virus se transmite
tambi#{233}n de hombre a hombre; los 1111105 son
menos susceptibles que los adultos.
mes de edad, con el objeto de se#{241}alarel hecho de que Ia ornitosis puede ser m#{225}sfrecuente en lactantes y niflos de Jo que comunmente se
supone. A fines de 1953 observaron un nino
it1e muri#{243} con infecci#{243}n pulmonar severa,
resistente a los antibi#{243}ticos; aproximadamente
en Ia misma fecha un lactante de mes de edad falleci#{243} bruscamente en su domicilio sin
mani-festaci#{243}n de enfermedad; en ambos casos se
aisl#{243}del tejido pulmonar un virus del grupo
psitacosis-hinfogranuloma. Desde entonces los autores iniciaron tin estudio del suero de los niflos hospitahizados por infecciones
respira-tori iS.
En cinco de los casos aqul presentados se aisl#{243}el virus; en el sexto los tItulos de aglutinaci#{243}n se encontraron muy elevados y en otros tres ci diagn#{243}stico fue sugerido por una sola prueba de fijaci#{243}n del complemento. Todos presentaron sIntomas y signos de
mIce-ci#{243}nrespiratoria, benigna y higera en algunos y muy grave en otros; 2 fallecieron. En los casos severos no se observ#{243}beneficio sobre el curso de la enfermedad con ci empleo de antibi-#{243}ticosde espectro amphio.