612 PUERPERAL AND NEONATAL BACTEREMIA
Puerperal
Bacteremia
and
Neonatal
Sepsis
Due to
Hemophilus
Parain-fluenzae:
Report
of a Case with
Antibody
Titers
Puerperal bacteremia and neonatal sepsis due to the same organism have been reported infrequently.’ Hemophilus parainfluenzae, a
small pleomorphic gram negative bacillus
which differs from H. influenzae by not requir-ing the X (hemin) growth factor, has not been implicated as a pathogen in puerperal or neo-natal sepsis13 (but for one case of meningitis in a newborn1 )
.
We report here a case of ma-ternal bacteremia and neonatal sepsis due to this organism. Because of two ongoing studies, blood was obtained for culture from a mother at delivery and sequential sera from her child were available for antibody studies. The assayof specific 1gM antibody in the infant was
helpful in determining the time of the
infec-tion.
CASE REPORTS
CASE 1
A 27-year-old woman was admitted to the Bos-ton City Hospital in active labor at term. Her two previous full-term pregnancies were complicated
by asymptomatic bacteriuria with E. coil, which also was noted early in this pregnancy and treated with sulfamethoxasole. A subsequent urine culture was negative. After 12 hours of labor, because of transverse occiput arrest and an edematous cervix, mid-forceps rotation and extraction of the fetal head was performed under spinal anesthesia. She was delivered of a 7-pound, 8-ounce male infant 8 hours after spontaneous rupture of th membranes. The mother was asymptomatic and afebrile, but blood was drawn for culture 8 minutes after deliv-ery as part of a prospective study of postpartum fever. The culture subsequently grew a pure cul-hire of H. parainfluenzae. On the evening following
delivery, her temperature rose to 102#{176}F. The lo-chia was described as serosanguinous and foul
TABLE I
IMMUNOOLOBULIN ANTIBODY TITERS
TO H. PARAINFLUENZAE
Serum 1gM IgG
Motheratterm 1:0 1:10-1:0
Cord serum 0 1 : 10-i :0
Infantat7days 1:160 1:160
smelling, and on the second postpartum day, treat-ment with penicillin and streptomycin was initiated for presumed endometritis. A urine culture was
sterile and cultures of the lochia yielded a heavy growth of Mycopiasma hominis, Haemophilus vagi-nalis, and a few colonies of gamma hemolytic
streptococcus and E. coil. The blood was not recul-tured, and no additional cultures were obtained. She became afebrile by the fourth postpartum day
and was discharged on the following day. Patho-logical examination of the placenta revealed acute chorionitis.
CASE 2
A baby boy had no spontaneous respirations at
birth and had a 1 minute Apgar score of 3. He responded to suction, intermittent positive pressure breathing, and oxygen. Physical examination on
admission to the nursery revealed a pale, slightly
cyanotic infant with mild substernal retractions and a respiratory rate of 100/minute. The venous hematocrit was 48I and a chest x-ray demon-strated a left lower lobe infiltrate. At age 60 hours, the baby was noted to be jaundiced, irritable, and febrile to 102#{176}F.The white blood count was 3,960 per cu mm with 47% polymorphonuclear cells, 51%
lmphocvtes, and 2% monocytes. The cerebrospinal
fluid contained 91 red blood cells and 3
lvmpho-cytes per cu mm with a protein of 40 mg/100 ml
and glucose of 40/100 ml. Repeat chest x-ray showed bilateral patchy infiltrates. Blood and cere-brospinal fluid cultures were obtained and the child was treated with ampicillin, 50 mg/kg/day and kanamycin, 15 mg/kg/day. On the next day,
purulent drainage was noted from an area of swell-ing on the scalp in the right parietal area. This drainage and the blood culture grew pure cultures of H. parainfluenzae. The cerebrospinal fluid was sterile. Treatment was continued with ampicillin;
the subsequent course was unremarkable, and the child was discharged well on the 17th day.
ANTIBODY STUDIES
A slide titration modification of the indirect fluorescent antibody (IFA) test was used to
measure specific IgG and 1gM antibodies
directed against the infecting strain of H.
parainfluenzae isolated from these patients. Commercially obtained monospecific fluorescein conjugated goat anti-human 1gM and IgG (Hy-land ) were used. Titers were read in duplicate to the highest dilution which gave clear, bright fluorescence. When incubated with anti-IgM and anti-IgG in the absence of serum, the or-ganisms did not fluoresce.
deliv-EXPERIENCE AND REASON-BRIEFLY RECORDED 613
ery, the cord serum and serum obtained from the infant 7 days after birth (Table I)
.
No 1gMantibody to the infecting organism was present in the cord senim at birth, but the infant
devel-oped a titer of 1gM and IgG of 1 : 160 by 1
week of life. Low, but detectable, titers of
specific 1gM and IgG were present in the
mother at term. The IgG in the cord serum presumably reflected maternal antibody.
DISCUSSION
This report documents maternal and neona-tal bacteremia due to H. parainfluenzae and is unusual not only for the double bacteremia, but also because of the organism isolated. H.
parainftuenzae was first described by Rivers in
192.2” and is distinguished from other
mem-hers of the genus by being nonhemolytic and requiring the V (nicotinamide adenine dinu-cleotide) but not the X (hemin) growth factor, and fermenting maltose, saccharose, and usu-ally dextrin.’6 This organism is a normal
inhab-itant of the upper respiratory tract and in a
recent study’ it was recovered from the phar-ynx of 12% of 490 healthy children and from 13% of a like number of children with upper respiratory tract infections. It has also been iso-lated from the normal vagina,’8 duodenal se-cretions,19 and the blood of patients with endo-carditis.’#{176} Recently, Hable, et al.’ analyzed 16 cases of serious infection due to Haemophilus species occurring over a 16-month period and
H. parainfluenzae was the pathogenic organism
in 10 of these. Two additional cases of menin-gitis due to this organism have been described in a neonate’4 and in a 4.year..old.21
The pathogenesis of the maternal bacter-emia, which was initially asymptomatic, is not
documented and the focus of infection is ob-scure; however, the genital tract or the naso-pharynx are possible sources of the organism.
H. parainfluenzae was not isolated from the
lo-chia possibly because of the overgrowth of the culture by other members of the vaginal micro-flora. The role of bacteremia with this organism
in the development of her postpartum fever is not proven from the available data, and we can only speculate as to the part it played in the
postpartum endometritis.
In all probability, the infant was infected during the difficult labor or delivery. The ab-sence of 1gM antibody against the infecting
or-ganism at birth suggests that there was no
preexisting infection in utero, as 1gM
produc-tion does occur in the fetus in response to ill-tra-uterme infection with a variety of
orga-22 The scalp lesion was a possible portal of entry, but it is equally possible that there was trans-placental hematogenous infection and that the circulating organisms subsequently
be-came trapped in the traumatized area on the
scalp. That the scalp lesion developed after the fever and jaundice favors the latter explana-tion.
This and the other reports cited suggest that
H. parainfluenzae is capable of causing serious
infections, that its pathogenicity should not be
underestimated, and that speciation of the
Haemophilus group is of clinical importance.
SUMMARY
Puerperal bacteremia and neonatal sepsis due to Haemophilus parainfluenzae is described in a mother and her infant. Indirect fluorescent antibody studies for specific 1gM antibody di-rected against the H. parainfluenzae were
per-formed on maternal and infant sera. The rise in infant 1gM antibody titers suggested that the infant acquired the infecting organism during labor or delivery. H. parainfluenzae has not previously been implicated as a pathogen in
either puerperal or neonatal sepsis.
STEPHEN H. ZINNER, M .D.
WILLIAM M. MCCORMACK, M.D.
Yim-HsIuNc LEE, M.D. Channing Laboratory
Thorndike Memorial Laboratory Harvard Medical Unit Boston City Hospital
Departments of Medicine and Pediatrics
Harvard Medical School
MARGUERITE H. ZUCKERSTATTER, M.D.
Department of Pediatrics
Boston University School of Medicine A. KATHLEEN DALY, B.S.
Department of Medical Microbiology
Boston City Hospital
Boston, Massachusetts 02118
W.M.McC. is a recipient of U.S. Public Health Service Post-Doctoral Fellowship 1 F02
AI44394-01.
This work was supported by Research Grant
HD-03693 from the National Institute of Child
Health and Human Development, and Training
Grant TOl AI-00068 from the National Institute of Allergy and Infectious Diseases.
614 SCHONLEIN-HENOCH SYNDROME
Kass, Jerome Klein, and 1)avid Ingall for their
re-view of the manuscript; and to Susan Alpert and Kathleen Browne for technical assistance.
ADDRESS FOR REPRINTS: (S.H.Z.)
Chan-ning Laboratory, Boston City Hospital, 774 Albany Street, Boston, Massachusetts 02118.
REFERENCES
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2. Dunham, E. C. : Septicemia in the newborn.
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3. Ritter, J. A., and Ralph, N. : Streptococcic
sep-ticemia of hematogenous origin in a
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4. Frankenthal, L. E., Jr. : Postnatal infection due to short-chain hemolytic streptococci. Amer.
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Obstet. Cynec., 26:910, 1933.5. Round table discussion on infection in the newborn period. Clifford, S., Chairman. J. Pediat., 30:696, 1947.
6. Calman, R. M., and Gibson,
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: Pvrexia in thepuerperium. Lancet, 2:649, 1953.
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8. Cibberd, C. F. : Puerperal sepsis,
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9. Silverman, W. A., and Homan, W. E. : Sepsis
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10. Smith, R. T., Platou, E. S., and Good, R. A.:
Septicemia of the newborn. PEDIATRICS, 17: 549, 1956.
11. Nvhan, W. L., and Fousek, M. D.:
Septice-mia of the newborn. PEDIATIuC5, 22:268, 1958.
12. Gotoff, S. P., and Behrman, R. E. : Neonatal
septicemia. J. Pediat., 76:142, 1970.
13. Klein, j. 0., and Marc\, S. NI.: Infection in the
newborn. Clin. Obstet. Gvnec., 13:321, 1970.
14. Gullekson, E. II., and Dumoff, M. : Haemophi-his parainflueuzae meningitis in a newborn. J.A.M.A., 198:199, 1966.
15. Rivers, T. M. : Influenza-like bacilli; growth of
influenza-like bacilli on media containing
only an autoclave labile substance as an
ac-cessorv food factor. Bull. Johns Hopkins
11051)., 33:429, 1922.
16. Wilson, C. S., and Miles, A. A.: Topley and
Wilson’s Principles of Bacteriology and
Im-munity, Vol. 1. Baltimore: \Villiams and
Wilkins, Chapter 32, 1964.
17. Hable, K. A., Logan, C. B., and Washington,
J. A., II. : Three Hernophiius species. Amer.
J. Dis. Child., 121:35, 1971.
18. Lapage, S. P. : Hemophilus vaginalis and its role in vaginitis. Acta Path. Microbiol. Scand., 52:34, 1961.
19. Anderson, C. NI., and Langford, R. F. :
Bacte-rial content of small intestine of children in health, in coeliac disease and in fibrocystic
disease of pancreas. Brit. Med.
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1:803, 1958.20. Boughton, C. R. : Subacute bacterial endocar-ditis due to Haeniophilus parainflnenzae.
Med. J. Aust., 1 :804, 1965.
21. Barnshaw, J. A., and Phillips, C. F.:
Haenio-philus parainfluenzae meningitis in a
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22. Sever,
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L. : Immunoglobulin determinations for the detection of perinatal infections. j. Pediat., 75:1111, 1969.Sch#{246}nlein-Henoch Syndrome:
Observations
on Some
Atypical
Clinical
Presentations
Sch#{246}nlein-Henoch purpura is a clinical syn-drome of unknown etiology associated with a widespread acute vasculitis. Involvement of
the skin, kidneys, gastrointestinal tract, and joints is usually observed. A characteristic rash
constitutes the most helpful aid in diagnosis.
The purpose of this report is to review the experience with Sch#{246}nlein-Henoch syndrome seen at our hospital, to detail the frequency
and duration of symptoms prior to the onset of the rash, to describe one child with the clinical features of this syndrome in whom the rash was absent, and finally, to report the frequency of
testicular hemorrhage in a sizable series.
CASE REPORTS
CASE 1
A 23-vear-old Caucasian male presented in the
emergency room with a 5-day history of vomiting,
fever, and abdominal pain, and bloody diarrhea on
the morning of admission. He was taken to the
op-erating room with a diagnosis of intussusception
and was found to have multiple ileal and jejunal intussusceptions which were easily reduced. The bowel was edematous with many focal
hemor-rhages. Post-operatively, the patient became
hyper-tensive with the blood pressure reaching 135/105
mm Hg, and edema, proteinuria, and microscopic