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Puerperal Bacteremia and Neonatal Sepsis Due to Hemophilus Parainfluenzae: Report of a Case with Antibody Titers

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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 assay

of 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.

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deliv-EXPERIENCE AND REASON-BRIEFLY RECORDED 613

ery, the cord serum and serum obtained from the infant 7 days after birth (Table I)

.

No 1gM

antibody 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.

(3)

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

1. Laffont, L., M#{233}l#{233},B. : Passage do

staphylo-CO(jUC P voir placentaire au cours d’une

staphvlococi#{233}mie mortelle avec m#{233}ningite. Bull. Soc. Obstet. Gvnec. Paris, 24:566,

1926.

2. Dunham, E. C. : Septicemia in the newborn.

Amer. J. Dis. Child., 45:229, 1933.

3. Ritter, J. A., and Ralph, N. : Streptococcic

sep-ticemia of hematogenous origin in a

new-born infant. J.A.M.A., 101:771, 1933.

4. Frankenthal, L. E., Jr. : Postnatal infection due to short-chain hemolytic streptococci. Amer.

J.

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,

J.

: Pvrexia in the

puerperium. Lancet, 2:649, 1953.

7. Goplerud, C. P., and White, C. A. : Postpartum

infection, a comparative study for the period 1926 through 1961. Obstet. Cvnec., 25:227, 1965.

8. Cibberd, C. F. : Puerperal sepsis,

1930-1965. J. Obstet. Cvnec. Brit. Comm., 73:1.

1966.

9. Silverman, W. A., and Homan, W. E. : Sepsis

of Ol)sCure origin in the newborn.

PEDIAT-RICS, 3:157, 1949.

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.

J.,

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

4-year-old boy. PEDIATRICS, 45:856, 1970.

22. Sever,

J.

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

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1972;49;612

Pediatrics

and A. Kathleen Daly

Stephen H. Zinner, William M. McCormack, Yhu-Hsiung Lee, Marguerite H. Zuckerstatter

of a Case with Antibody Titers

Report

Hemophilus Parainfluenzae:

Puerperal Bacteremia and Neonatal Sepsis Due to

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1972;49;612

Pediatrics

and A. Kathleen Daly

Stephen H. Zinner, William M. McCormack, Yhu-Hsiung Lee, Marguerite H. Zuckerstatter

of a Case with Antibody Titers

Report

Hemophilus Parainfluenzae:

Puerperal Bacteremia and Neonatal Sepsis Due to

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The online version of this article, along with updated information and services, is located on

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