Int J Gynecol Obstet. 1992, 37: 247-252 International Federation of Gynecology
241 and Obstetrics
Placental malaria and pregnancy S.E. Ibhanesebhor
outcome
and A.A. Okolo
University of Benin Teaching Hospital,
Department
of Child Health, Benin City, Bendel State (Nigeria)
(Received March 7th, 1991) (Revised and accepted July 8th. 1991)
Abstract Malaria parasitemia was assessed in 312 placentae of singleton deliveries in Benin. The prevalence rate was 45.19%. The dominant infecting specie was Plasmodium falciparum. High density parasitemia of placental smear in 44.68% was associated with preterm delivery, low birthweight, intrauterine growth retardation and neonatal mortality. Placental histological diagnosis of malaria in 57.69% was more frequently associated with intrauterine growth retardation. Extraplacentalparasitemia decreased but intraplacental parasitemia increased with gestational age.
Keywords:
Placenta;
Malaria;
Pregnancy
outcome. Introduction
Malaria affects more than 200 million people in the world; and in tropical Africa, the disease is predominantly stable with little or no yearly variation [I]. It continues to be a serious public health problem in tropical countries, accounting for between 5 and 15% of deaths of children in endemic areas [2]. I, 0020-7292/92/$05.00 0 1992 International Federation Printed and Published in Ireland
conditions favorable for the Though transmission of malaria exist throughout the year, the rainy season favors an increase in malaria infection [3,4]. Thus the rates of inoculation by Anopheles gambiae mosquito are 0.03 per person per day for the rainy season and 0.005 per person per day for the dry season [3-61. Higher frequencies of Plasmodium falciparum infections have been highlighted amongst pregnant women in holoendemic malarious areas 161. Because clinical observations indicate that pregnancy exerts a dampening effect on the immunity to malaria, pregnant women suffer from recurrent and severe infections as a result of their increased susceptibility and high density of Plasmodium infection [7,8]. Malaria in pregnancy promotes placental insufficiency, leading to intrauterine growth in addition, it may cause retardation; prematurity, low birthweight and fetal death [7,9]. Various authors highlight the association between the density of placental reduced birthweight parasitization and W,71.
In pregnancy,
maternal
infections
with
Plasmodium falciparum is common and the ex-
amination of a thick smear made from the placental blood at the time of delivery frequently demonstrates parasites and pigments, even when the maternal peripheral blood Article
of Gynecology
and Obstetrics
248
Ibhanesebhor and Okolo
smears are microscopically negative for malaria parasite [3]. The role of the placenta as a barrier in sequestering malaria parasites, thus preventing parasitic invasion of the fetus and newborn is well illustrated by various instances of dense parasitization of this organ, relative to the maternal blood [3,6,7, lo]. Though the placenta acts as a trap for malaria parasites, this organ permits the evolution of parasites within it. The effect of dense [2,8,10] parasitization and inter villous clogging of placenta have been adduced causes of fetal and neonatal mortality and morbidity. The extent of the contribution of placental malaria to these perinatal health problems is largely undetermined in a holoendemic malarious area. Also the relative frequency of parasitization of the placenta and fetus in the various trimesters of gestation has not received attention. This study therefore examines the various issues. Methods Three hundred eighteen consecutive deliveries that occurred from August lst, 1989 to November 30th, 1989 were recruited into the study, following informed consent of the parturients. After each delivery, 0.5 ml of blood was drawn from the placental end of the cord, before separation of the placenta. The blood sample thus obtained was used to prepare a thick and thin blood lilm immediately after it was collected. Each placenta was examined macroscopitally for the presence of gross pathology and it was subsequently weighed with the full length of the cord. Thereafter, 2 cm* of placental tissue was carved from the maternal surface of the placenta. The blood obtained from this site of incision was used for the preparation of a thick and thin blood smear. The placental tissue thus obtained was stored in both 10% formaldehyde in phosphate buffer (pH 7.4) and 10% formaldehyde in saline Int J Gynecol Obstet 37
before fixing [ 111. Each batch of tissue was processed and stained with hematoxylin and eosin within 1 week of fixation, using a standard procedure [12]. Blood films were stained with Giemsa stain and the results read at x 100 oil immersion were graded as follows: (i) low density, when there was one parasite per field, (ii) medium density, when there were 2- 19 parasites per field, (iii) high density, when the parasite load was >20 per lield; as a consequence of this grading, the results were recorded as + , ++ and +++ respectively 1131. Placental histology slides were read at x 40 magnification, with positive slides showing the presence of malaria pigments, histiocytes with ingested malaria pigments in the intervillous spaces or placental parenchyma [ 111. The weight of each neonate and placenta was recorded to the nearest 50 g on a Waymaster Scale, while the crown to heel length was measured to the nearest centimetre on a Holtian measuring table. The head circumference and midarm circumference were measured with a plastic tape to the nearest 0.25 cm [14]. All measurements were carried out within 1 h of delivery. The gestational age was determined by a combination of the maternal dates and gestational age assessment using the methods of Dubowitz [ 161. If there was discrepancy of over 2 weeks between the two methods, the age as determined by the gestational Dubowitz Score was selected [ 161. The intrauterine growth of the newborn was assessed by a comparison of the birthweight for gestational age with the intrauterine growth standards of Battaglia and Bubchenco [ 151. The results were analysed with a computer using the Microstat packages. Significance was at 95% level. Student’s t-test was used for comparison of means and the chi square test for comparison of frequencies, while the 2 score was used for probability testing.
Placental malaria parasitization
Table 1. Frequency
of intervillous
Specific gestational age groups (weeks)
and intraplacental
malaria
Total no. of cases
>28 28-31 32-36 37-41 P42 Total
1 2 27 248 34 312
parasitization Placental
by gestational
histology
lntervillous parasitization
249
age groupings.
criteria Intraplacental parasitization
No.
‘%I
No.
‘%>
I 2 22 138 I7 180
100 100 81.48 55.64 50.00 57.69
0 0 2 58 9 69
0.00 0.00 7.40 23.39 26.47 22.12
The prevalence rate of malaria parasitemia the placenta was 45.19% (141/312). Plasmodium falciparum was identified in 96.45% (1361312) as against Plasmodium malariae in 3.55% (5/312). Though a higher incidence of extraplacental parasitemia persisted through the gestational age groups, the incidence of villous stromal parasitization increased with gestational age (Table 1). The overall incidence of intraplacental parasitization was 38.33%. Table 2 highlights the gestational age trends in rate of cord and placental parasitemia. Significantly there was a positive correlation between intervillous blood parasitemia and intraplacental parasitemia with increasing gestational age r = 0.93; P < 0.025. The results of placental smear parasitemia
Results
of
Three hundred eighteen deliveries occurred during the study period; of these, there were three cases of monozygotic twin deliveries. There were 4 fetal deaths and 308 live births. Eleven neonates died in the early neonatal period, while one neonate died after the first week of life. There were altogether 12 neonatal deaths. Only the 312 singleton deliveries were analysed; 1248 placental histology slides and 624 thick and thin blood films from placental smears were examined. The mean birthweight of the 312 neonates studied was 2.9458 A 0.6286 kg, while the mean birthweight of the preterm neonates was 1.98 kg, term neonates 3.05 kg and postterm neonates 3.19 kg.
Table 2. Gestational Specific gestational age groups (weeks) >28 28-31 32-36 37-41 242 Total
age trends
in rate of cord and placental Total no. of cases
I 2 21 248 34 312
parasitemia. Infected cord blood smear
Infected placental blood smear
No.
‘X,
No.
‘%,
0 0 4 18 4 26
0.00 0.00 14.82 7.26 I I.77 8.33
0 0 13 108 20 141
0.00 0.00 48.15 43.54 58.82 45. I9
Article
250
Ibhanesebhor and Okolo
by gestational age group showed that of 45.19% of the total who were infected, none of the three placentae from those 0.60). Similarly, the mean birthweight of babies with malaria positive placental histology, was significantly lower than that of babies whose placentae were histologically negative (2.83 f 0.64 kg versus 3.1 f 0.57 kg, P < 0.01). When the diagnosis of placental parasitemia was based on the examination of placental blood smear, no difference was observed in the mean birthweight (2.93 f 0.59 kg versus 2.96 f 0.66 kg). There was no significant difference in mean placental weight of the infected and noninfected groups. Table 3 shows the influence of the degree of placental malaria parasitemia on perinatal indices. Significantly, the rates of occurrence of preterm low birthweight, SGA and perinatal were high in high density mortality parasitemia. Discussion This study has highlighted high prevalence rates for both placental smear parasitemia and placental histological parasitization. The observed rate of placental smear parasitemia is higher than has been previously described [7-91. Pre-existing maternal semi-immunity to malaria and the immune effects of pregnancy modulate the function of the placenta as an effective barrier against fetal and neonatal infection, although the effect of sequestration of malaria parasites persists [3,7]. It is therefore possible that lower maternal immune status of the mothers in this study contributed to the high rate of placental infection observed. Although the numbers were too few, it did appear that infection of the early placenta at < 32 weeks gestation was rare; an observation that might find support in the concept of the existence of some maternal factor which suppresses placental infection from the 16th to 32nd weeks of gestation. This factor had been explained on the basis of a surge of immunity
Placental malurio parasilizafion
following the high rate of maternal infection of early pregnancy from 9 weeks to 16 weeks. It is this surge of immunity which protects the early placenta [9]. In effect, it is possible that placental immaturity precluded the development of villous inflammation or destruction. This suggestion is further supported by the observation in this study that the incidence of intravillous parasitemia increased as the gestational age advanced. This phenomenon requires further confirmation in the frame of a carefully designed larger longterm study. Though the infection rate was high in placentae of term neonates, the highest frequency of placental parasitemia was observed in the postterm. This reflects the placental immune status and also agrees with reports from the literature that have shown increased frequency of placental parasitemia with advancing gestational age. The existence of a linear relationship between intervillous blood and intraplacental blood parasitemia as gestational age increased is indicative of an increase in the rate of transplacental transfer of parasites with advancing gestational age; a phenomenon that might have implications for the highest rate of acquisition of fetal and congenital malaria with advancing gestational age. Indeed it would appear that the highest rate of placental infection and transplacental transfer of parasites had been attained at 32-36 weeks. This observation further emphasises the role of maternal and placental immunity status in curtailing placental infection until term gestation is attained. Thereafter placental immune status waned with peak occurrence of parasitemia at postterm gestation. It would be useful to confirm this observation in a future study. Significantly, lighter babies and more SGA babies had positive placental tissue parasitization. This finding might be explained by the fact that repeated infection of the placenta has been associated with intervillous space clogging and consequent decrease m surface area of placenta participating in transfer of nutrients
251
to the fetus [7,1 I]. Contrary to the findings of other workers, placenta weight was not significantly affected by the state of placental infection [3]. It is possible that the degree of parasitization of the placenta in relation to the intensity and duration of infection might have played a role. Infected placentae as identified by histology weighed 19.3 g less than the uninfected; this possibly reflects the effect of chronicity of infection on placental nutrition. High density placental parasitemia was positively associated with higher frequency of preterm deliveries, IUGR, low birthweight babies and perinatal mortality. This phenomenon might be a positive reflection of the effects of the extensive histopathological placental changes that ensued from the degree and density of parasitization [l 11. A higher rate (57.69%) of placental parasitization was obtained when placenta histology was the means of diagnosis for placental infection. This higher rate derived from histological diagnosis possibly highlights the importance of the state of chronicity of placental infection. This agrees with the reports of others who favor placental histology as a means of diagnosis. Because this method of diagnosis in itself has implications for chronicity of infection, it is not surprising that histological diagnosis of malaria infection was made in as much as 71% of the SGA placentae relative to when placental blood smear was the means of diagnosis. Clearly, more SGA placentae were infected. It can be assumed that this association might be a reflection of the effect of fetal malnutrition resulting from a disruption of the fetoplacental relationship. Further questions need to be answered. For example, why is placental infection rare at lower gestational age? What is the maternal immune status of the mothers relative to the placental state? Would infection with species of Plasmodium other than Plasmodium fulciparum be associated with similar morbidity? Further carefully designed studies are required to answer these questions. Article
252
Ibhanesebhor and Okolo
References Bisseru B: Chloroquine resistance in African. Postgrad Doctor Afr 4: 205, 1985. 2 Patwari AK: Childhood malaria - a perspective. Postgrad Doctor Afr I: 333, 1985. 3 Bruce-Chwatt LJ: Malaria in African infants and children in Southern Nigeria. Ann Trop Med Parasitol 46: 173, 1952. 4 Steketee RIW: Recent findings in perinatal malaria. Bull Int Pediatr Assoc 10: 418, 1989. 5 Emujuaiwe SO, Okafor GO, Uche GO, Marshall WC, Njoku-Obi ANU: Some evidence for the occurrence of congenital malaria infection in parts of Nigeria. Nig J Med Sci 2: 81, 1979. 6 Jellife EF: Low birth weight and malaria infection of the placenta. Bull WHO 38: 69, 1968. Lee EV: Parasites and pregnancy. The problem of malaria and toxoplasmosis. Clin Perinatol IS: 351, 1988. Mcgregor IA, Wilson ME, Billewicz WZ: Malaria infections of the placenta in Gambia, West Africa: Its incidence and relationship of still birth, birth weight, and placental weight. Trans R Sot Trop Med Hyg 77: 232, 1983. 9 Brabin BJ: Malaria in pregnancy, its importance and control. Postgrad Doctor Afr II: 57, 1989. 10 Jilly P: Anaemia in parturient women, with special reference to malaria infection of the placenta. Ann Trop Med Parasitol 63: 109, 1969. 1
Ini J Gynecol Obstet 37
11 Galbraith RM, Faulk PW, Galbraith GMP, Holbrook TW: The human materno-foetal relationship in malaria. Identification pigments and parasites in the placenta. Trans R Sot Trop Med Hyg 74: 52, 1980. 12 Baker FJ, Silverton RE, Kilshaw D: Introduction of histology. In: Introduction of Medical Laboratory Technology, vol 6 (eds FJ Baker, RE Silverton, D Kilshaw), p 171. Butterworths, London, 1985. 13 Etienne L: Identification of malaria parasites. In: Manual of Basic Techniques for a Health Laboratory (eds M Cheesbrough, LM Prescott) p 166. WHO, Geneva, 1980. 14 Sasanow SR, Georgieff MK, Pereira CC: Mid-arm and mid-arm/head circumference ratios: standard curves for anthropometric assessment of neonatal nutritional status. J Pediatr 109: 311, 1968. 15 Battaglia FC, Lubchenco LO: A practical classification of newborn infants by weight and gestational age and by neonatal mortality risks. J. Pediatr 71: 159, 1967. 16 Dubowitz LM, Dubowitz V, Goldberg C: Clinical assessment of gestational age in the newborn infant. J Pediatr 77: 1, 1970. Address for reprints: A.A. Okolo University of Benin College of Medical Sciences Department of Child Health PMB 1154, Benin City Bendel State, Nigeria
241 and Obstetrics
Placental malaria and pregnancy S.E. Ibhanesebhor
outcome
and A.A. Okolo
University of Benin Teaching Hospital,
Department
of Child Health, Benin City, Bendel State (Nigeria)
(Received March 7th, 1991) (Revised and accepted July 8th. 1991)
Abstract Malaria parasitemia was assessed in 312 placentae of singleton deliveries in Benin. The prevalence rate was 45.19%. The dominant infecting specie was Plasmodium falciparum. High density parasitemia of placental smear in 44.68% was associated with preterm delivery, low birthweight, intrauterine growth retardation and neonatal mortality. Placental histological diagnosis of malaria in 57.69% was more frequently associated with intrauterine growth retardation. Extraplacentalparasitemia decreased but intraplacental parasitemia increased with gestational age.
Keywords:
Placenta;
Malaria;
Pregnancy
outcome. Introduction
Malaria affects more than 200 million people in the world; and in tropical Africa, the disease is predominantly stable with little or no yearly variation [I]. It continues to be a serious public health problem in tropical countries, accounting for between 5 and 15% of deaths of children in endemic areas [2]. I, 0020-7292/92/$05.00 0 1992 International Federation Printed and Published in Ireland
conditions favorable for the Though transmission of malaria exist throughout the year, the rainy season favors an increase in malaria infection [3,4]. Thus the rates of inoculation by Anopheles gambiae mosquito are 0.03 per person per day for the rainy season and 0.005 per person per day for the dry season [3-61. Higher frequencies of Plasmodium falciparum infections have been highlighted amongst pregnant women in holoendemic malarious areas 161. Because clinical observations indicate that pregnancy exerts a dampening effect on the immunity to malaria, pregnant women suffer from recurrent and severe infections as a result of their increased susceptibility and high density of Plasmodium infection [7,8]. Malaria in pregnancy promotes placental insufficiency, leading to intrauterine growth in addition, it may cause retardation; prematurity, low birthweight and fetal death [7,9]. Various authors highlight the association between the density of placental reduced birthweight parasitization and W,71.
In pregnancy,
maternal
infections
with
Plasmodium falciparum is common and the ex-
amination of a thick smear made from the placental blood at the time of delivery frequently demonstrates parasites and pigments, even when the maternal peripheral blood Article
of Gynecology
and Obstetrics
248
Ibhanesebhor and Okolo
smears are microscopically negative for malaria parasite [3]. The role of the placenta as a barrier in sequestering malaria parasites, thus preventing parasitic invasion of the fetus and newborn is well illustrated by various instances of dense parasitization of this organ, relative to the maternal blood [3,6,7, lo]. Though the placenta acts as a trap for malaria parasites, this organ permits the evolution of parasites within it. The effect of dense [2,8,10] parasitization and inter villous clogging of placenta have been adduced causes of fetal and neonatal mortality and morbidity. The extent of the contribution of placental malaria to these perinatal health problems is largely undetermined in a holoendemic malarious area. Also the relative frequency of parasitization of the placenta and fetus in the various trimesters of gestation has not received attention. This study therefore examines the various issues. Methods Three hundred eighteen consecutive deliveries that occurred from August lst, 1989 to November 30th, 1989 were recruited into the study, following informed consent of the parturients. After each delivery, 0.5 ml of blood was drawn from the placental end of the cord, before separation of the placenta. The blood sample thus obtained was used to prepare a thick and thin blood lilm immediately after it was collected. Each placenta was examined macroscopitally for the presence of gross pathology and it was subsequently weighed with the full length of the cord. Thereafter, 2 cm* of placental tissue was carved from the maternal surface of the placenta. The blood obtained from this site of incision was used for the preparation of a thick and thin blood smear. The placental tissue thus obtained was stored in both 10% formaldehyde in phosphate buffer (pH 7.4) and 10% formaldehyde in saline Int J Gynecol Obstet 37
before fixing [ 111. Each batch of tissue was processed and stained with hematoxylin and eosin within 1 week of fixation, using a standard procedure [12]. Blood films were stained with Giemsa stain and the results read at x 100 oil immersion were graded as follows: (i) low density, when there was one parasite per field, (ii) medium density, when there were 2- 19 parasites per field, (iii) high density, when the parasite load was >20 per lield; as a consequence of this grading, the results were recorded as + , ++ and +++ respectively 1131. Placental histology slides were read at x 40 magnification, with positive slides showing the presence of malaria pigments, histiocytes with ingested malaria pigments in the intervillous spaces or placental parenchyma [ 111. The weight of each neonate and placenta was recorded to the nearest 50 g on a Waymaster Scale, while the crown to heel length was measured to the nearest centimetre on a Holtian measuring table. The head circumference and midarm circumference were measured with a plastic tape to the nearest 0.25 cm [14]. All measurements were carried out within 1 h of delivery. The gestational age was determined by a combination of the maternal dates and gestational age assessment using the methods of Dubowitz [ 161. If there was discrepancy of over 2 weeks between the two methods, the age as determined by the gestational Dubowitz Score was selected [ 161. The intrauterine growth of the newborn was assessed by a comparison of the birthweight for gestational age with the intrauterine growth standards of Battaglia and Bubchenco [ 151. The results were analysed with a computer using the Microstat packages. Significance was at 95% level. Student’s t-test was used for comparison of means and the chi square test for comparison of frequencies, while the 2 score was used for probability testing.
Placental malaria parasitization
Table 1. Frequency
of intervillous
Specific gestational age groups (weeks)
and intraplacental
malaria
Total no. of cases
>28 28-31 32-36 37-41 P42 Total
1 2 27 248 34 312
parasitization Placental
by gestational
histology
lntervillous parasitization
249
age groupings.
criteria Intraplacental parasitization
No.
‘%I
No.
‘%>
I 2 22 138 I7 180
100 100 81.48 55.64 50.00 57.69
0 0 2 58 9 69
0.00 0.00 7.40 23.39 26.47 22.12
The prevalence rate of malaria parasitemia the placenta was 45.19% (141/312). Plasmodium falciparum was identified in 96.45% (1361312) as against Plasmodium malariae in 3.55% (5/312). Though a higher incidence of extraplacental parasitemia persisted through the gestational age groups, the incidence of villous stromal parasitization increased with gestational age (Table 1). The overall incidence of intraplacental parasitization was 38.33%. Table 2 highlights the gestational age trends in rate of cord and placental parasitemia. Significantly there was a positive correlation between intervillous blood parasitemia and intraplacental parasitemia with increasing gestational age r = 0.93; P < 0.025. The results of placental smear parasitemia
Results
of
Three hundred eighteen deliveries occurred during the study period; of these, there were three cases of monozygotic twin deliveries. There were 4 fetal deaths and 308 live births. Eleven neonates died in the early neonatal period, while one neonate died after the first week of life. There were altogether 12 neonatal deaths. Only the 312 singleton deliveries were analysed; 1248 placental histology slides and 624 thick and thin blood films from placental smears were examined. The mean birthweight of the 312 neonates studied was 2.9458 A 0.6286 kg, while the mean birthweight of the preterm neonates was 1.98 kg, term neonates 3.05 kg and postterm neonates 3.19 kg.
Table 2. Gestational Specific gestational age groups (weeks) >28 28-31 32-36 37-41 242 Total
age trends
in rate of cord and placental Total no. of cases
I 2 21 248 34 312
parasitemia. Infected cord blood smear
Infected placental blood smear
No.
‘X,
No.
‘%,
0 0 4 18 4 26
0.00 0.00 14.82 7.26 I I.77 8.33
0 0 13 108 20 141
0.00 0.00 48.15 43.54 58.82 45. I9
Article
250
Ibhanesebhor and Okolo
by gestational age group showed that of 45.19% of the total who were infected, none of the three placentae from those 0.60). Similarly, the mean birthweight of babies with malaria positive placental histology, was significantly lower than that of babies whose placentae were histologically negative (2.83 f 0.64 kg versus 3.1 f 0.57 kg, P < 0.01). When the diagnosis of placental parasitemia was based on the examination of placental blood smear, no difference was observed in the mean birthweight (2.93 f 0.59 kg versus 2.96 f 0.66 kg). There was no significant difference in mean placental weight of the infected and noninfected groups. Table 3 shows the influence of the degree of placental malaria parasitemia on perinatal indices. Significantly, the rates of occurrence of preterm low birthweight, SGA and perinatal were high in high density mortality parasitemia. Discussion This study has highlighted high prevalence rates for both placental smear parasitemia and placental histological parasitization. The observed rate of placental smear parasitemia is higher than has been previously described [7-91. Pre-existing maternal semi-immunity to malaria and the immune effects of pregnancy modulate the function of the placenta as an effective barrier against fetal and neonatal infection, although the effect of sequestration of malaria parasites persists [3,7]. It is therefore possible that lower maternal immune status of the mothers in this study contributed to the high rate of placental infection observed. Although the numbers were too few, it did appear that infection of the early placenta at < 32 weeks gestation was rare; an observation that might find support in the concept of the existence of some maternal factor which suppresses placental infection from the 16th to 32nd weeks of gestation. This factor had been explained on the basis of a surge of immunity
Placental malurio parasilizafion
following the high rate of maternal infection of early pregnancy from 9 weeks to 16 weeks. It is this surge of immunity which protects the early placenta [9]. In effect, it is possible that placental immaturity precluded the development of villous inflammation or destruction. This suggestion is further supported by the observation in this study that the incidence of intravillous parasitemia increased as the gestational age advanced. This phenomenon requires further confirmation in the frame of a carefully designed larger longterm study. Though the infection rate was high in placentae of term neonates, the highest frequency of placental parasitemia was observed in the postterm. This reflects the placental immune status and also agrees with reports from the literature that have shown increased frequency of placental parasitemia with advancing gestational age. The existence of a linear relationship between intervillous blood and intraplacental blood parasitemia as gestational age increased is indicative of an increase in the rate of transplacental transfer of parasites with advancing gestational age; a phenomenon that might have implications for the highest rate of acquisition of fetal and congenital malaria with advancing gestational age. Indeed it would appear that the highest rate of placental infection and transplacental transfer of parasites had been attained at 32-36 weeks. This observation further emphasises the role of maternal and placental immunity status in curtailing placental infection until term gestation is attained. Thereafter placental immune status waned with peak occurrence of parasitemia at postterm gestation. It would be useful to confirm this observation in a future study. Significantly, lighter babies and more SGA babies had positive placental tissue parasitization. This finding might be explained by the fact that repeated infection of the placenta has been associated with intervillous space clogging and consequent decrease m surface area of placenta participating in transfer of nutrients
251
to the fetus [7,1 I]. Contrary to the findings of other workers, placenta weight was not significantly affected by the state of placental infection [3]. It is possible that the degree of parasitization of the placenta in relation to the intensity and duration of infection might have played a role. Infected placentae as identified by histology weighed 19.3 g less than the uninfected; this possibly reflects the effect of chronicity of infection on placental nutrition. High density placental parasitemia was positively associated with higher frequency of preterm deliveries, IUGR, low birthweight babies and perinatal mortality. This phenomenon might be a positive reflection of the effects of the extensive histopathological placental changes that ensued from the degree and density of parasitization [l 11. A higher rate (57.69%) of placental parasitization was obtained when placenta histology was the means of diagnosis for placental infection. This higher rate derived from histological diagnosis possibly highlights the importance of the state of chronicity of placental infection. This agrees with the reports of others who favor placental histology as a means of diagnosis. Because this method of diagnosis in itself has implications for chronicity of infection, it is not surprising that histological diagnosis of malaria infection was made in as much as 71% of the SGA placentae relative to when placental blood smear was the means of diagnosis. Clearly, more SGA placentae were infected. It can be assumed that this association might be a reflection of the effect of fetal malnutrition resulting from a disruption of the fetoplacental relationship. Further questions need to be answered. For example, why is placental infection rare at lower gestational age? What is the maternal immune status of the mothers relative to the placental state? Would infection with species of Plasmodium other than Plasmodium fulciparum be associated with similar morbidity? Further carefully designed studies are required to answer these questions. Article
252
Ibhanesebhor and Okolo
References Bisseru B: Chloroquine resistance in African. Postgrad Doctor Afr 4: 205, 1985. 2 Patwari AK: Childhood malaria - a perspective. Postgrad Doctor Afr I: 333, 1985. 3 Bruce-Chwatt LJ: Malaria in African infants and children in Southern Nigeria. Ann Trop Med Parasitol 46: 173, 1952. 4 Steketee RIW: Recent findings in perinatal malaria. Bull Int Pediatr Assoc 10: 418, 1989. 5 Emujuaiwe SO, Okafor GO, Uche GO, Marshall WC, Njoku-Obi ANU: Some evidence for the occurrence of congenital malaria infection in parts of Nigeria. Nig J Med Sci 2: 81, 1979. 6 Jellife EF: Low birth weight and malaria infection of the placenta. Bull WHO 38: 69, 1968. Lee EV: Parasites and pregnancy. The problem of malaria and toxoplasmosis. Clin Perinatol IS: 351, 1988. Mcgregor IA, Wilson ME, Billewicz WZ: Malaria infections of the placenta in Gambia, West Africa: Its incidence and relationship of still birth, birth weight, and placental weight. Trans R Sot Trop Med Hyg 77: 232, 1983. 9 Brabin BJ: Malaria in pregnancy, its importance and control. Postgrad Doctor Afr II: 57, 1989. 10 Jilly P: Anaemia in parturient women, with special reference to malaria infection of the placenta. Ann Trop Med Parasitol 63: 109, 1969. 1
Ini J Gynecol Obstet 37
11 Galbraith RM, Faulk PW, Galbraith GMP, Holbrook TW: The human materno-foetal relationship in malaria. Identification pigments and parasites in the placenta. Trans R Sot Trop Med Hyg 74: 52, 1980. 12 Baker FJ, Silverton RE, Kilshaw D: Introduction of histology. In: Introduction of Medical Laboratory Technology, vol 6 (eds FJ Baker, RE Silverton, D Kilshaw), p 171. Butterworths, London, 1985. 13 Etienne L: Identification of malaria parasites. In: Manual of Basic Techniques for a Health Laboratory (eds M Cheesbrough, LM Prescott) p 166. WHO, Geneva, 1980. 14 Sasanow SR, Georgieff MK, Pereira CC: Mid-arm and mid-arm/head circumference ratios: standard curves for anthropometric assessment of neonatal nutritional status. J Pediatr 109: 311, 1968. 15 Battaglia FC, Lubchenco LO: A practical classification of newborn infants by weight and gestational age and by neonatal mortality risks. J. Pediatr 71: 159, 1967. 16 Dubowitz LM, Dubowitz V, Goldberg C: Clinical assessment of gestational age in the newborn infant. J Pediatr 77: 1, 1970. Address for reprints: A.A. Okolo University of Benin College of Medical Sciences Department of Child Health PMB 1154, Benin City Bendel State, Nigeria
