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J Med Microbiol 55 (2006), 1601-1603; DOI: 10.1099/jmm.0.46614-0
© 2006 Society for General Microbiology
ISSN 1473-5644

Case Report

Molecular evidence for vertical transmission of listeriosis, Taiwan

Yu-Tsung Huang1, Shee-Uan Chen2, Mu-Zon Wu2, Chien-Yir Chen2, Wuu-Shiun Hsieh2, Buor-Niarn Tsao2, Chieh Jou Horng2 and Po-Ren Hsueh2,3

1 Department of Internal Medicine, Far Eastern Memorial Hospital, Taiwan

2 ,3 Department of Internal Medicine2 and Department of Laboratory Medicine3 , National Taiwan University Hospital, National Taiwan University College of Medicine, Taiwan

Correspondence
Po-Ren Hsueh
hsporen{at}ha.mc.ntu.edu.tw

Received 8 March 2006
Accepted 1 August 2006

The case is presented of a pregnant woman at the 31st week of gestation with Listeria monocytogenes bacteraemia and microabscess formation in the endometrium, who delivered an infant with disseminated infection (meningitis and bacteraemia). The two patients were successfully treated with intravenous ampicillin and gentamicin. Molecular typing using random amplified polymorphic DNA (RAPD) analysis disclosed that three isolates from the mother (blood) and infant (blood and cerebrospinal fluid) had identical RAPD profiles.

Abbreviations: CSF, cerebrospinal fluid; ICU, intensive care unit; RAPD, random amplified polymorphic DNA; WBC, white blood cell.


   Introduction
TOP
 Introduction
Case report
 REFERENCES
 
Infections (sepsis or meningitis) due to Listeria monocytogenes mainly occur at the extremes of life, and in pregnant women and patients with various underlying medical conditions (AIDS, diabetes mellitus, malignancy, and hepatic and renal failure) (Gellin & Broome, 1989; Southwick & Purich, 1996). In Taiwan, three patients with perinatal listeriosis have been reported, but to the best of our knowledge, feto-maternal infection has not been described (Chen et al., 1998, 2003; Cheng et al., 1990).


   Case report
TOP
 Introduction
 Case report
REFERENCES
 
A 38-year-old woman (gravida 1, para 0) was at her 31st week of gestation. She had previously been well, except that she was a hepatitis B virus carrier and was regularly monitored at our clinic. She was admitted to the hospital because of fever (38.2 °C) and chills for 3 days. Her pregnancy course was uneventful until 1 week prior to admission, when she suffered from one episode of chills at home. There was no fever or any symptoms and signs of respiratory, urinary or gastrointestinal tract infection at that time. Chills recurred again accompanied by general malaise 3 days prior to this admission. Decreased fetal movement and fetal tachycardia were also noted.

On admission, leukocytosis [white blood cell (WBC) count 20 220 cells µl–1) and hyponatraemia (129 mmol l–1) were found. Levels of serum creatine and aminotransferase were normal. Ritodrine (67 µg min–1) was given for tocolysis and betamethasone (12 mg per day) was given for fetal pulmonary maturation after admission. Intravenous cefazolin (1 g every 8 h) and gentamicin (80 mg every 12 h) were administered empirically for possible amnionitis. Rupture of membrane with meconium stain was noted 12 h after admission. Fourteen hours after admission, the fetal heart rate suddenly decelerated from ~150 to 90 beats min–1, and this episode lasted for 2 min. Decreased fetal movement was also noted. A male infant was delivered by emergent caesarean section 15 h after admission, giving the impression of fetal distress. The endometrium was noted to be thickened during the Caesarean section, and a sample of endometrium from the uterine portion was sent for histopathological examination. The latter revealed acute chorioamnionitis with microabscess formation without visible micro-organisms (Fig. 1Go). Intravenous clindamycin (600 mg every 8 h) was added to the patient's treatment on the basis of the diagnosis of acute chorioamnionitis.


Figure 1
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  		Fig. 1. Pathological examination (haematoxylin and eosin stain) of the endometrium revealing microabscess formation and accumulation of pus cells with fibrinoid necrotic substances (x200). Bar, 100 µm.

 
The infant was 1558 g in weight and had a head circumference of 29 cm. The Apgar scores were 4 at 1 min and 7 at 5 min after delivery. Generalized bleachable papules and pustules were found over the trunk and extremities. He was transferred to the neonatal intensive care unit (ICU) for possible neonatal sepsis. Seizure developed after admission to the neonatal ICU. Laboratory tests revealed a WBC count of 7990 cells µl–1 (84 % normoblast), haemoglobin 13.9 g dl–1 and hematocrit 43.1 %. The C-reactive protein level was 12.84 mg dl–1. Cerebrospinal fluid (CSF) was yellow and turbid. The total CSF WBC count was 87 cells µl–1 with neutrophil predominance (mononuclear cells, 20 cells µl–1 and polymorphonuclear cells, 67 cells µl–1). The CSF protein level was 693 mg dl–1 and the glucose level was 3 mg dl–1. Ampicillin (100 mg kg–1 per day) and cefotaxime (200 mg kg–1 per day) were used initially for treatment of neonatal meningitis. A brain echo of the infant on the second ICU hospitalization day revealed grade II bilateral intra-ventricular haemorrhage, which could have been due to the prematurity of the infant, and suspected ventriculitis and cerebritis.

The blood cultures of the mother (isolate A) and her infant (isolate B) both yielded L. monocytogenes. The CSF culture of the infant also yielded the same organism (isolate C). Culture of the amniotic fluid was negative. The mother's fever subsided after delivery. The skin rash of the infant disappeared 2 days after the start of antimicrobial treatment. After the notification of positive cultures for L. monocytogenes, antibiotic regimens including ampicillin and gentamicin were administered to the infant (for 21 days) as well as his mother (for 14 days). The progress of the infant remained uneventful and he started on oral feeding on the eighth day of his ICU stay.

The three isolates of L. monocytogenes were haemolytic on sheep blood agar plates and exhibited a positive Christie–Atkins–Munch-Petersen (CAMP) reaction with Staphylococcus aureus (Bille et al., 2003). These organisms were further identified to species level using standard biochemical methods as well as the API Coryne system (bioMérieux). Molecular typing of the three isolates and six other isolates (control strains) was performed by random amplified polymorphic DNA (RAPD), using a method described elsewhere (Boerlin et al., 1995). Three primers, M13, OPA-2 and ERIC2, were used. The three isolates from the infant and his mother had identical RAPD profiles, which were different from those of the six control strains.

The mother reported here had L. monocytogenes bacteraemia and had evidence of endometrial infection, and delivered an infant with disseminated infection (meningitis and bacteraemia) caused by the same species of bacterium with a RAPD profile identical to that of his mother. The incidence of listeriosis among pregnant women is 17-fold higher than that among the general population (Mylonakis et al., 2002). The common presentations of maternal listeriosis are usually non-specific and benign, with fever and flu-like symptoms (Benshushan et al., 2002; Evans et al., 1985; McLauchin, 1990; Silver, 1998; Sirry et al., 1994). Involvement of the central nervous system in pregnant women is rare (Sirry et al., 1994). The micro-organism has been reported to be present in blood (43 %), cervical or vaginal swabs (34 %), placenta (12 %), amniotic fluid (8 %), lochia (8 %) and urine (2 %) (McLauchin, 1990). Maternal listeriosis may result in stillbirth or spontaneous abortion (20 %), and the rate of vertical transmission with subsequent fetal infection is high (68–77 %) (McLauchin, 1990; Sirry et al. 1994). Examination of the placenta usually reveals chorioamnionitis and microabscess formation (Benshushan et al., 2002; Evans et al., 1985; McLauchin, 1990; Silver, 1998; Sirry et al., 1994).

Clinical presentations of infants with listeriosis include respiratory distress, meconium staining at birth, fever, lethargy, jaundice and skin rashes (McLauchin, 1990). The skin rashes are usually distributed on the trunk and extremities, and are maculopapular or papulovesicular lesions. The overall case fatality rate is high (24.5 to ~46.5 %). Disseminated neonatal infection (granulomatosis infantisepticum) due to L. monocytogenes presents with widespread abscess formation, involving the liver, placenta and skin, and involvement of the brain, spleen, kidney, lungs, adrenal glands and gastrointestinal tract can result in a high mortality (McLauchin, 1990).

Antepartum treatment of listeriosis has been found to have a better outcome for neonates, and ineffective initial treatment might result in a poor outcome in pregnant women (Gellin & Broome, 1989; McLauchin, 1990; Posfay-Barbe & Wald, 2004). High-dose ampicillin and gentamicin remain the drugs of choice for listeriosis. Trimethoprim-sulfamethoxazole is used for those with penicillin allergy, but is not suitable for pregnant women. Cephalosporins and clindamycin, which are usually recommended for treating chorioamnionitis and septic abortion, are ineffective against L. monocytogenes. Our patients responded well to the conventional therapy with ampicillin and gentamicin.

RAPD analysis has been extensively evaluated by Boerlin et al. (1995) for typing L. monocytogenes isolates alongside other typing methods. They conclude that RAPD analysis is a highly discriminating, timesaving and relatively simple technique for the epidemiological typing of L. monocytogenes. Using three primers in this study, the three isolates recovered from our patients were successfully demonstrated to belong to the same strain.

Our observations demonstrated that maternal and perinatal listeriosis responded well to conventional antimicrobial therapy, and provided molecular evidence of vertical transmission of listeriosis.


   REFERENCES
TOP
 Introduction
 Case report
 REFERENCES
 
Benshushan, A., Tsafrir, A., Arbel, R., Rahav, G., Ariel, I. & Rojansky, N. (2002). Listeria infection during pregnancy: a 10 year experience. Isr Med Assoc J 4, 776–780.[Medline]

Bille, J., Rocourt, J. & Swaminathan, B. (2003). Listeria and Erysipelothrix. In Manual of Clinical Microbiology, 8th edn, pp. 461–471. Edited by P. R. Murray, E. J. Baron, J. H. Jorgensen, M. A. Pfaller & R. H. Yolken. Washington, DC: American Society for Microbiology.

Boerlin, P., Bannerman, E., Ischer, F., Rocourt, J. & Bille, J. (1995). Typing of Listeria monocytogenes: a comparison of random amplification of polymorphic DNA with 5 other methods. Res Microbiol 146, 35–49.[Medline]

Cheng, B. R., Kuo, D. M. & Hsieh, T. T. (1990). Perinatal listeriosis – a case report. Changgeng Yi Xue Za Zhi 13, 152–156 (in Chinese).[Medline]

Chen, Y. Y., Hsieh, K. S., Lin, S. M. & Huang, Y. F. (1998). Early-onset listeriosis in prematurity: a case report. Clin Neonatol 5, 32–34.

Chen, J. M., Chen, M. H. & Yang, W. (2003). Early-onset listeriosis in prematurity. Acta Paediatr Taiwan 44, 106–108.[Medline]

Evans, J. R., Allen, A. C., Stinson, D. A., Bortolussi, R. & Peddle, L. J. (1985). Perinatal listeriosis: report of an outbreak. Pediatr Infect Dis 4, 237–241.[Medline]

Gellin, B. G. & Broome, C. V. (1989). Listeriosis. JAMA (J Am Med Assoc) 261, 1313–1320.[Abstract/Free Full Text]

McLauchin, J. (1990). Human listeriosis in Britain, 1967–85, a summary of 722 cases. 1. Listeriosis during pregnancy and in the newborn. Epidemiol Infect 104, 181–189.[Medline]

Mylonakis, E., Paliou, M., Hohmann, E. L., Calderwood, S. B. & Wing, E. J. (2002). Listeriosis during pregnancy: a case series and review of 222 cases. Medicine 2002 81, 260–269.[CrossRef][Medline]

Posfay-Barbe, K. M. & Wald, E. R. (2004). Listeriosis. Pediatr Rev 25, 151–159.[Free Full Text]

Silver, H. M. (1998). Listeriosis during pregnancy. Obstet Gynecol Surv 53, 737–740.[CrossRef][Medline]

Sirry, H. W., George, R. H. & Whittle, M. J. (1994). Meningo-encephalitis due to Listeria monocytogenes in pregnancy. Br J Obstet Gynaecol 101, 1083–1084.[Medline]

Southwick, F. & Purich, D. (1996). Intracellular pathogenesis of listeriosis. N Engl J Med 334, 770–776.[Free Full Text]




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