246
AUST.AND N.Z. JOURNALOF OBSTETRICS AND GYNAECOLOGY
8. Seyberth HW, Rascher W, Hackenthal R, Wille L. Effect of prolonged indomethacin therapy o n renal function and selected vasoactive hormones in very low birth weight infants with symptomatic ductus arteriosus. J Pediatr 1983; 103: 979-984. 9. Mari G, Moise KJ, Deter RL, Kirshon B, Carpenter RJ. Doppler assessment of the renal blood flow velocity waveform during indomethacin therapy for preterm labor and polyhydramnios. Obstet Gynecol 1990; 75: 199-201. 10. Wlodek ME, Harding R, Hooper SB, Thorburn GD. How does indomethacin cause oligohydramnios? Proceedings of 9th Annual Congress of the Australian Perinatal Society, Melbourne 1991; A33. 11. Kitterman JA, Liggins GC. Fetal breathing movements and inhibitors of prostaglandin synthesis. Semin Perinatol 1980; 4 97-100.
12. ltskovitz J, Abramovici H, Brandis JM. Oligohydramnios, meconium, and perinatal death concurrent with indomethacin treatment in human pregnancy. J Reprod Med 1980; 24: 137-140. 13. Heymann MA, Rudolph AM. Effects of acetylsalicylic acid on the ductus arteriosus and circulation in fetal lambs in utero. Circ Res 1976; 38: 418-422. 14. Harlass FE, Duff P, Brady K, Read J. Hydrops fetalis and premature closure of the ductus arteriosus: A review. Obstet Gynecol Surv 1989; 44: 541-543. 15. Turner GR, Levin DL. Prostaglandin synthesis inhibition in persistent pulmonary hypertension of the newborn. Clinic Perinatol 1984; 11: 581-589. 16. Kirshon B, Mari 0, Moise KJ, Wasserstrum N. Effect of indomethacin on the fetal ductus arteriosus during treatment of symptomatic polyhydramnios. J Reprod Med 1990; 35: 529-532.
Aust NZ J Obstet Gynaecol 1992; 32: 3: 246
Campylobacter Jejuni in Pregnancy J. Goh', MBBS and M. Flynn', MBBS Department of Obstetrics and Gynaecology, Mater Misericordiae Hospital, South Brisbane, Queensland EDITORIAL COMMENT: We accepted this paper for publication since it reinforces the message carried by the paper by D. 1 Farrell and M. 7: Harris (Aust NZ J Obstet Gynaecol 1992; 32: 172-174) that Campylobacter species can cause perinatal infection and deaths. Irma Kruszelnicki, the senior microbiologist at the Mercy Hospital for Women, provided the information that at this hospital faecal samples from patients presenting with clinical symptoms of diarrhoea are routinely screened for Campylobacter species using selective media. Specimens which are mucoid, bloody or purulent are examined by direct preparation microscopy since this often gives an indication of the presence of Campylobacter namely seeing numerous leucocytes and characteristically vibrantly-motilecurved organisms. Since 1982 there have been 8 cases of Campylobacter species isolated, 7from faeces (all Campylobacterjejuni) in patients (4 adults, 3 neonates) with clinical symptoms or signs of enteritisand one positive blood culture (Campylobacter fetussubspeciesfetus) from an infant who had clinicalfeatures of septicaemia andsurvived after treatment with gentamicin.
Summary: Case notes of pregnancies with proven Campylobacter jejuni infections were collected from 2 Queensland teaching hospitaIs and reviewed. Of these cases, 2 pregnancies (3 fetuses) resulted in stillbirths, 2 neonates required treatment with antibiotic therapy within 2 days of birth, while the remaining 2 pregnancies were treated at the time of the infection and were not associated with adverse outcome. Maternal Campylobacter infection should be actively sought for in the patient with suspected infectious diarrhoea.
1. Registrar.
Address for correspondence: Dr. J. Goh, Department of Obstetrics and Gynaecology, Mater Misericordiae Hospital, South Brisbane, Queensland.
J. GOHAND M. FLYNN
247
Table 1. Clinical Details of 6 Cases of Compylobacter Infection
Presenting symptoms
Culture Slides
Gestation
Maternal
Fetal/ neonatal
Placental
Fetal/ neonatal
Maternal
Placental oathologv
26 weeks
Diarrhoea for 1 week
Stillbirth
N/A
23 weeks twin
Abdominal pain. Bloody diarrhoea. Fevers.
Stillbirth twins 331g and 3358
No pathogens No pathogens grown
Faeces Jejuni Faeces jejuni
41 weeks
Asymptomatic
N/A
Faeces jejuni
36 weeks
Diarrhoea at 27 weeks. Nausea/abdominal pain. Febrile. Not treated.
Not done
Not done
40 weeks
Diarrhoea at 33 weeks' gestation, treated with erythromycin. Diarrhoea at 29 weeks. I.U.G.R. Treated with erythromycin. Threatened premature labour.
Bloody stools on day 2, 3,5408 Respiratory distress day 1. Treated IV amoxil/gentamicin Apgar score 8 ' , 9' Healthy 3,310g female Live 2,8808
Infarction, haematoma Acute suppurative villitis. Placental necrosis. N/A
No pathogens N/A
N/A
38 weeks
No pathogens
N/A
-
Faecal culture negative Faeces jejuni
Faeces jejuni Faeces jejuni
N/A
-
Normal
-
Normal
N/A=not available; IUGR = intrauterine growth retardation
In veterinary medicine, Campylobacter has long been known to be a cause of abortion (1,2). The first human case of Campylobacter bacteraemia was reported in 1947 in a woman in the second trimester of pregnancy who subsequently aborted. Worldwide, Campylobacter jejuni is the commonest cause of human infectious diarrhoea (2-4). Although reports are infrequent in the literature, Campylobacter infections acquired during pregnancy have been associated with spontaneous abortion, stillbirth, prematurity and neonatal sepsis (3). Research using a sheep model suggests that the organism localizes and grows preferentially in placental tissue and specific placental changes have been described (1). The aim of this study was to review the management and outcome of cases and highlight the importance of Campylobacter infection as a cause of fetal mortality and morbidity and to stress the importance of early diagnosis and treatment.
METHODS The case notes of women whose pregnancies were known to be complicated by Campylobacter infection during 1990-1991 were retrospectively reviewed from the Gold Coast Hospital and Mater Misericordiae Hospital, Brisbane. Information was collected on gestational age, presenting maternal signs and symptoms, fetalheonatal complications and outcomes along with microbiological cultures and placental histology. RESULTS Six pregnancies with proven maternal and/or neonatal Campylobacter infection were identified. A summary of these cases is shown in table 1.
In cases 1 and 2 Campylobacter jejuni was grown from maternal faeces after admission for investigation of diarrhoea and pyrexia. These progressed to premature labour and delivery of 3 mid-trimester stillborn fetuses (Case 2 was a twin pregnancy) with common placental pathology of infarction, necrosis and inflammation. In these cases the mothers were untreated prior to fetal death. In Case 3, an asymptomatic mother delivered spontaneously and on day-2 postdelivery, the baby developed bloody stools which were positive for Campylobacter j ej uni. In Case 4 the mother was admitted with diarrhoea, abdominal pains and a raised temperature at 27 weeks' gestation and although faecal culture showed Campylobacter jejuni, she was not treated and subsequently delivered prematurely at 36 weeks. This neonate developed a febrile illness and respiratory distress within 1 day of delivery and was treated with intravenous antibiotics. Microbiological cultures specifically for Campylobacter were not performed on the neonate. In Cases 5 and 6 the mothers were diagnosed and treated antenatally with erythromycin and subsequently had uncomplicated pregnancies; in these 2 cases placental histology was normal.
DISCUSSION The Campylobacter (meaning curved rod) genus is a spiral motile gram-negative bacillus with the species Jejuni separated from other species because it grows at 42 "C and is resistant to cephalothin and is inhibited by nalidixic acid (4). Failure to isolate Campylobacter may occur as these organisms require prolonged incubation
248
AUST.A N D N.Z. JOURNAL OF OBSTETRICS AND
under microaerophilic environment for optimal growth (2). Transmission in humans has been reported via the faecal/oral route, through ingestion of contaminated food or water or milk or by direct contact with faeces of infected humans or animals. Clinical manifestations range from asymptomatic to dysentery and septicaemia after an incubation period of 2-11 days. Bacteraemic patients often present with abdominal pain, fever, nausea, weight loss and dehydration. Faecal excretion in the convalescent phase lasts 2-3 weeks. The asymptomatic carrier rate is less than 1% (4-6). In the study by Young and Roberts (9,Campylobacter jejuni was grown from 28 of the 12,521 (0.2%) . rectal swabs obtained from women in labour; 24 of the 28 mothers were asymptomatic. Where possible, faecal samples from babies with culture-positive mothers were investigated. Of these, 13% were positive for Campylobacter jejuni. Campylobacter infection associated with mid-trimester abortion has been prospectively studied in sheep by Hedstrom et a1 (l), where abortion occurred at a predictable time postinoculation of the organism. Bacteraemic symptoms and histological examination of the placenta from these sheep revealed macroscopic infarction, perivillous fibrin deposition and marked polymorph infiltration. This closely replicates other literature reports (7). Fetal death in the sheep was attributed to Campylobacter placentitis with inflammatory damage in villous tissue (7,s). Campylobacter has also been implicated in human miscarriages and stillbirths (2,9,10). The placentas were infarcted, and necrotic with acute inflammation (2,lO). Campylobacter has been isolated from the placenta (2,lO) and fetus (2,9,10). Gribble et a1 (2) reviewed 7 cases of maternal Campylobacter infection. Three of the 7 pregnancies resulted in premature labour and stilbirths, 3 premature deliveries (1 neonatal death, 1 neonatal sepsis but recovered, 1 healthy premature baby) and 1 healthy term delivery. Intrapartum infection of the neonate typically produces symptoms on day-2 postdelivery and if jejuni species is involved, it is usually a self-limiting diarrhoea with bloody stools. Oral-faecal contamination occurs during the birth process (5,9). Other possible neonatal complications secondary to Campylobacter infection include pyrexia, respiratory distress, and convulsions (11). There seem to be 2 modes of transmission to the fetus: (1) Maternal septicaemia with transplacental spread of organisms to the fetus.
GYNAECOLOGY
(2) Contamination during delivery with subsequent neonatal infection. We have found no reports in the literature of the effectiveness of treatment nor the outcome or placental pathology after treatment of Campylobacter bacteraemia. The aim of antenatal diagnosis and treatment is to prevent or eradicate fetoplacental infection (9). Our recommended management modified from Grandien et a1 (11) is as followi: 1. Patients with diarrhoea should be investigated with specific Campylobacter cultures. 2. Women with positive cultures should be treated with erythromycin 50 mg/kg/day in 4 divided doses for 4 weeks. Gentamicin may be used. 3. Asymptomatic carriers should be treated in the 3rd trimester to prevent intrapartum transmission. 4. Preventive measures include attention to strict enteric and excretion precautions in hospitalized patients. 5. Screen a pregnant mother if there is a family history of infectious diarrhoea. The cases presented illustrate some of the complications of Campylobacter infection in pregnancy and suggest that early diagnosis and treatment may help prevent neonatal sequelae.
References 1. Hedstrom OR, Sonn RJ, Lassen E D et al. Pathology of
2. 3.
4. 5.
6. 7. 8. 9. 10.
11.
Campylobacter jejuni Abortion in sheep. Vet Pathol 1987; 24: 419-426. Gribble MJ, Salit IE, Isaac-Renton J, Chow AW. Campylobacter infections in pregnancy. Am J Obstet Gynecol 1981; 140: 423-426. Simor AE, Ferro S. Campylobacter jejuni infection occurring during pregnancy. Eur J Clin Microbiol Infect Dis 1990; 9: 142-144. Amin NM. Campylobacter caused diarrhoea. Postgraduate Medicine 1984; 7: 89-97. Youngs ER, Roberts C. Campylobacter carriage and pregnancy. Br J Obst Gynaecol 1985; 92: 541-542. Chowdhury M. Campylobacter Jejuni Enteritis; A review. Tropical and Geographical Medicine 1984; 36: 215-222. Gilbert GL, Davoren RA, Cole ME, Radford NJ. Midtrimester abortion associated with septicaemia caused by Campylobacter Jejuni. Medical Journal of Australia 1981; 1: 585-586. Coid CR, Fox H. Short Review: Campylobacters as Placental Pathogens. Placenta 1983; 4: 295-305. Simor AE, Karmali MA, Jadavji T, Roscoe M. Abortion and perinatal sepsis associated with campylobacter infection. Rev Infect Dis 1986; 8: 397-402. Kist M, Keller KM, Niebling W, Kilching W. Campylobacter coli septicaemia associated with septic abortion. Infection 1984; 12: 88-90. Grandien M, Sterner G, Kalin M, Engardt L. Management of pregnant women with diarrhoea at term and of healthy carriers of infectious agents in stools at delivery. Scand J Infect Dis Suppl 1990; 71: 9-18.
AUST.AND N.Z. JOURNALOF OBSTETRICS AND GYNAECOLOGY
8. Seyberth HW, Rascher W, Hackenthal R, Wille L. Effect of prolonged indomethacin therapy o n renal function and selected vasoactive hormones in very low birth weight infants with symptomatic ductus arteriosus. J Pediatr 1983; 103: 979-984. 9. Mari G, Moise KJ, Deter RL, Kirshon B, Carpenter RJ. Doppler assessment of the renal blood flow velocity waveform during indomethacin therapy for preterm labor and polyhydramnios. Obstet Gynecol 1990; 75: 199-201. 10. Wlodek ME, Harding R, Hooper SB, Thorburn GD. How does indomethacin cause oligohydramnios? Proceedings of 9th Annual Congress of the Australian Perinatal Society, Melbourne 1991; A33. 11. Kitterman JA, Liggins GC. Fetal breathing movements and inhibitors of prostaglandin synthesis. Semin Perinatol 1980; 4 97-100.
12. ltskovitz J, Abramovici H, Brandis JM. Oligohydramnios, meconium, and perinatal death concurrent with indomethacin treatment in human pregnancy. J Reprod Med 1980; 24: 137-140. 13. Heymann MA, Rudolph AM. Effects of acetylsalicylic acid on the ductus arteriosus and circulation in fetal lambs in utero. Circ Res 1976; 38: 418-422. 14. Harlass FE, Duff P, Brady K, Read J. Hydrops fetalis and premature closure of the ductus arteriosus: A review. Obstet Gynecol Surv 1989; 44: 541-543. 15. Turner GR, Levin DL. Prostaglandin synthesis inhibition in persistent pulmonary hypertension of the newborn. Clinic Perinatol 1984; 11: 581-589. 16. Kirshon B, Mari 0, Moise KJ, Wasserstrum N. Effect of indomethacin on the fetal ductus arteriosus during treatment of symptomatic polyhydramnios. J Reprod Med 1990; 35: 529-532.
Aust NZ J Obstet Gynaecol 1992; 32: 3: 246
Campylobacter Jejuni in Pregnancy J. Goh', MBBS and M. Flynn', MBBS Department of Obstetrics and Gynaecology, Mater Misericordiae Hospital, South Brisbane, Queensland EDITORIAL COMMENT: We accepted this paper for publication since it reinforces the message carried by the paper by D. 1 Farrell and M. 7: Harris (Aust NZ J Obstet Gynaecol 1992; 32: 172-174) that Campylobacter species can cause perinatal infection and deaths. Irma Kruszelnicki, the senior microbiologist at the Mercy Hospital for Women, provided the information that at this hospital faecal samples from patients presenting with clinical symptoms of diarrhoea are routinely screened for Campylobacter species using selective media. Specimens which are mucoid, bloody or purulent are examined by direct preparation microscopy since this often gives an indication of the presence of Campylobacter namely seeing numerous leucocytes and characteristically vibrantly-motilecurved organisms. Since 1982 there have been 8 cases of Campylobacter species isolated, 7from faeces (all Campylobacterjejuni) in patients (4 adults, 3 neonates) with clinical symptoms or signs of enteritisand one positive blood culture (Campylobacter fetussubspeciesfetus) from an infant who had clinicalfeatures of septicaemia andsurvived after treatment with gentamicin.
Summary: Case notes of pregnancies with proven Campylobacter jejuni infections were collected from 2 Queensland teaching hospitaIs and reviewed. Of these cases, 2 pregnancies (3 fetuses) resulted in stillbirths, 2 neonates required treatment with antibiotic therapy within 2 days of birth, while the remaining 2 pregnancies were treated at the time of the infection and were not associated with adverse outcome. Maternal Campylobacter infection should be actively sought for in the patient with suspected infectious diarrhoea.
1. Registrar.
Address for correspondence: Dr. J. Goh, Department of Obstetrics and Gynaecology, Mater Misericordiae Hospital, South Brisbane, Queensland.
J. GOHAND M. FLYNN
247
Table 1. Clinical Details of 6 Cases of Compylobacter Infection
Presenting symptoms
Culture Slides
Gestation
Maternal
Fetal/ neonatal
Placental
Fetal/ neonatal
Maternal
Placental oathologv
26 weeks
Diarrhoea for 1 week
Stillbirth
N/A
23 weeks twin
Abdominal pain. Bloody diarrhoea. Fevers.
Stillbirth twins 331g and 3358
No pathogens No pathogens grown
Faeces Jejuni Faeces jejuni
41 weeks
Asymptomatic
N/A
Faeces jejuni
36 weeks
Diarrhoea at 27 weeks. Nausea/abdominal pain. Febrile. Not treated.
Not done
Not done
40 weeks
Diarrhoea at 33 weeks' gestation, treated with erythromycin. Diarrhoea at 29 weeks. I.U.G.R. Treated with erythromycin. Threatened premature labour.
Bloody stools on day 2, 3,5408 Respiratory distress day 1. Treated IV amoxil/gentamicin Apgar score 8 ' , 9' Healthy 3,310g female Live 2,8808
Infarction, haematoma Acute suppurative villitis. Placental necrosis. N/A
No pathogens N/A
N/A
38 weeks
No pathogens
N/A
-
Faecal culture negative Faeces jejuni
Faeces jejuni Faeces jejuni
N/A
-
Normal
-
Normal
N/A=not available; IUGR = intrauterine growth retardation
In veterinary medicine, Campylobacter has long been known to be a cause of abortion (1,2). The first human case of Campylobacter bacteraemia was reported in 1947 in a woman in the second trimester of pregnancy who subsequently aborted. Worldwide, Campylobacter jejuni is the commonest cause of human infectious diarrhoea (2-4). Although reports are infrequent in the literature, Campylobacter infections acquired during pregnancy have been associated with spontaneous abortion, stillbirth, prematurity and neonatal sepsis (3). Research using a sheep model suggests that the organism localizes and grows preferentially in placental tissue and specific placental changes have been described (1). The aim of this study was to review the management and outcome of cases and highlight the importance of Campylobacter infection as a cause of fetal mortality and morbidity and to stress the importance of early diagnosis and treatment.
METHODS The case notes of women whose pregnancies were known to be complicated by Campylobacter infection during 1990-1991 were retrospectively reviewed from the Gold Coast Hospital and Mater Misericordiae Hospital, Brisbane. Information was collected on gestational age, presenting maternal signs and symptoms, fetalheonatal complications and outcomes along with microbiological cultures and placental histology. RESULTS Six pregnancies with proven maternal and/or neonatal Campylobacter infection were identified. A summary of these cases is shown in table 1.
In cases 1 and 2 Campylobacter jejuni was grown from maternal faeces after admission for investigation of diarrhoea and pyrexia. These progressed to premature labour and delivery of 3 mid-trimester stillborn fetuses (Case 2 was a twin pregnancy) with common placental pathology of infarction, necrosis and inflammation. In these cases the mothers were untreated prior to fetal death. In Case 3, an asymptomatic mother delivered spontaneously and on day-2 postdelivery, the baby developed bloody stools which were positive for Campylobacter j ej uni. In Case 4 the mother was admitted with diarrhoea, abdominal pains and a raised temperature at 27 weeks' gestation and although faecal culture showed Campylobacter jejuni, she was not treated and subsequently delivered prematurely at 36 weeks. This neonate developed a febrile illness and respiratory distress within 1 day of delivery and was treated with intravenous antibiotics. Microbiological cultures specifically for Campylobacter were not performed on the neonate. In Cases 5 and 6 the mothers were diagnosed and treated antenatally with erythromycin and subsequently had uncomplicated pregnancies; in these 2 cases placental histology was normal.
DISCUSSION The Campylobacter (meaning curved rod) genus is a spiral motile gram-negative bacillus with the species Jejuni separated from other species because it grows at 42 "C and is resistant to cephalothin and is inhibited by nalidixic acid (4). Failure to isolate Campylobacter may occur as these organisms require prolonged incubation
248
AUST.A N D N.Z. JOURNAL OF OBSTETRICS AND
under microaerophilic environment for optimal growth (2). Transmission in humans has been reported via the faecal/oral route, through ingestion of contaminated food or water or milk or by direct contact with faeces of infected humans or animals. Clinical manifestations range from asymptomatic to dysentery and septicaemia after an incubation period of 2-11 days. Bacteraemic patients often present with abdominal pain, fever, nausea, weight loss and dehydration. Faecal excretion in the convalescent phase lasts 2-3 weeks. The asymptomatic carrier rate is less than 1% (4-6). In the study by Young and Roberts (9,Campylobacter jejuni was grown from 28 of the 12,521 (0.2%) . rectal swabs obtained from women in labour; 24 of the 28 mothers were asymptomatic. Where possible, faecal samples from babies with culture-positive mothers were investigated. Of these, 13% were positive for Campylobacter jejuni. Campylobacter infection associated with mid-trimester abortion has been prospectively studied in sheep by Hedstrom et a1 (l), where abortion occurred at a predictable time postinoculation of the organism. Bacteraemic symptoms and histological examination of the placenta from these sheep revealed macroscopic infarction, perivillous fibrin deposition and marked polymorph infiltration. This closely replicates other literature reports (7). Fetal death in the sheep was attributed to Campylobacter placentitis with inflammatory damage in villous tissue (7,s). Campylobacter has also been implicated in human miscarriages and stillbirths (2,9,10). The placentas were infarcted, and necrotic with acute inflammation (2,lO). Campylobacter has been isolated from the placenta (2,lO) and fetus (2,9,10). Gribble et a1 (2) reviewed 7 cases of maternal Campylobacter infection. Three of the 7 pregnancies resulted in premature labour and stilbirths, 3 premature deliveries (1 neonatal death, 1 neonatal sepsis but recovered, 1 healthy premature baby) and 1 healthy term delivery. Intrapartum infection of the neonate typically produces symptoms on day-2 postdelivery and if jejuni species is involved, it is usually a self-limiting diarrhoea with bloody stools. Oral-faecal contamination occurs during the birth process (5,9). Other possible neonatal complications secondary to Campylobacter infection include pyrexia, respiratory distress, and convulsions (11). There seem to be 2 modes of transmission to the fetus: (1) Maternal septicaemia with transplacental spread of organisms to the fetus.
GYNAECOLOGY
(2) Contamination during delivery with subsequent neonatal infection. We have found no reports in the literature of the effectiveness of treatment nor the outcome or placental pathology after treatment of Campylobacter bacteraemia. The aim of antenatal diagnosis and treatment is to prevent or eradicate fetoplacental infection (9). Our recommended management modified from Grandien et a1 (11) is as followi: 1. Patients with diarrhoea should be investigated with specific Campylobacter cultures. 2. Women with positive cultures should be treated with erythromycin 50 mg/kg/day in 4 divided doses for 4 weeks. Gentamicin may be used. 3. Asymptomatic carriers should be treated in the 3rd trimester to prevent intrapartum transmission. 4. Preventive measures include attention to strict enteric and excretion precautions in hospitalized patients. 5. Screen a pregnant mother if there is a family history of infectious diarrhoea. The cases presented illustrate some of the complications of Campylobacter infection in pregnancy and suggest that early diagnosis and treatment may help prevent neonatal sequelae.
References 1. Hedstrom OR, Sonn RJ, Lassen E D et al. Pathology of
2. 3.
4. 5.
6. 7. 8. 9. 10.
11.
Campylobacter jejuni Abortion in sheep. Vet Pathol 1987; 24: 419-426. Gribble MJ, Salit IE, Isaac-Renton J, Chow AW. Campylobacter infections in pregnancy. Am J Obstet Gynecol 1981; 140: 423-426. Simor AE, Ferro S. Campylobacter jejuni infection occurring during pregnancy. Eur J Clin Microbiol Infect Dis 1990; 9: 142-144. Amin NM. Campylobacter caused diarrhoea. Postgraduate Medicine 1984; 7: 89-97. Youngs ER, Roberts C. Campylobacter carriage and pregnancy. Br J Obst Gynaecol 1985; 92: 541-542. Chowdhury M. Campylobacter Jejuni Enteritis; A review. Tropical and Geographical Medicine 1984; 36: 215-222. Gilbert GL, Davoren RA, Cole ME, Radford NJ. Midtrimester abortion associated with septicaemia caused by Campylobacter Jejuni. Medical Journal of Australia 1981; 1: 585-586. Coid CR, Fox H. Short Review: Campylobacters as Placental Pathogens. Placenta 1983; 4: 295-305. Simor AE, Karmali MA, Jadavji T, Roscoe M. Abortion and perinatal sepsis associated with campylobacter infection. Rev Infect Dis 1986; 8: 397-402. Kist M, Keller KM, Niebling W, Kilching W. Campylobacter coli septicaemia associated with septic abortion. Infection 1984; 12: 88-90. Grandien M, Sterner G, Kalin M, Engardt L. Management of pregnant women with diarrhoea at term and of healthy carriers of infectious agents in stools at delivery. Scand J Infect Dis Suppl 1990; 71: 9-18.
