congenital kala-azar

[ANDRADE at NPD.UFPE.BR]

Does anyone know other references than the ones listed below on transplacentary
kala-azar? I would be grateful. Please direct your information back to leish-L.
Thanks in advance.  Paulo Andrade    RECIFE, Department of Genetics, Universi-
dade Federal de Pernambuco, BRAZIL    ANDRADE at NPD.UFPE.BR

Transplacentary and congenital kala-azar

TI: Visceral leishmaniasis in a 6-week-old infant: possible congenital transmission.
AU: Elamin-A; Omer-MI
SO: Trop-Doct. 1992 Jul; 22(3): 133-5

TI: Congenital kala-azar and leishmaniasis in the placenta.
AU: Eltoum-IA; Zijlstra-EE; Ali-MS; Ghalib-HW; Satti-MM; Eltoum-B; el-Hassan-AM
SO: Am-J-Trop-Med-Hyg. 1992 Jan; 46(1): 57-62
AB: During an epidemic of visceral leishmaniasis in the Sudan, two cases of congenital kala-azar were seen. The 
first child, whose mother had contracted kala-azar in southern Sudan, was born in Khartoum, where no 
transmission of leishmaniasis is currently occurring. At seven months, the child had fever, lymphadenopathy, and 
hepatosplenomegaly; leishmania parasites were detected in the bone marrow. The child died and an autopsy 
showed leishmania parasites in all tissues including the lungs, kidneys, and thymus. In the second case, parasites 
were found in the placenta of a five-month-old fetus. These two cases demonstrate the importance of follow-up of 
infants born to mothers with leishmaniasis.

TI: Visceral leishmaniasis in a six month old child: is congenital transmission of disease possible?
AU: Rab-MA; Mahmood-MT; Bux-D; Hassan-M; Hassan-K
SO: JPMA-J-Pak-Med-Assoc. 1991 Aug; 41(8): 191-3


AU: Mittal-V; Sehgal-S; Yadav-TP; Singh-VK
TI: Congenital transmission of kala-azar.
SO: J Commun Dis [IBN] 1987 Jun; 19(2): P 184-5
MJ: Leishmaniasis Visceral:CN. Pregnancy Complications Infectious:PS
MN: Adult:. Animal:. Bone Marrow:PS. Case Report:. Female:. Human:. Infant:.
Leishmania donovani:. Male:. Pregnancy:


And not directly a report on congen. transm.

TI: Sensitization of offspring of Leishmania donovani-infected hamsters to immunization and of offspring of 
immunized hamsters to challenge.
AU: Herman-R; Nolan-TJ; Fahey-JR
SO: Am-J-Trop-Med-Hyg. 1982 Jul; 31(4): 730-9
PY: 1982
AB: Female hamsters, infected intracardially (i.c.) with 1.0--2.0 x 10(5) amastigotes of Leishmania donovani 
produced offspring, following mating, which, when immunized subcutaneously with 1.0 x 10(7) amastigotes at 8 
weeks of age, were more resistant to i.c. challenge 6 weeks later than were hamsters born to non-infected mothers. 
Offspring of mothers infected with as many as 6.0 x 10(6) amastigotes demonstrated no greater capacity for 
immunization than did those of mothers infected with 1.0 x 10(5) amastigotes. Sensitization of offspring of 
infected mothers apparently is transplacental since the effect could only be seen in offspring of infected mothers 
and not in those of normal mothers weaned by infected dams. Offspring of female hamsters immunized by footpad 
inoculation of 1.0 x 10(7) amastigotes exhibited reduced spleen parasite burdens when challenged at 8.5 weeks of 
age and reduced spleen and liver parasite burdens when challenged at 16 weeks of age, compared to offspring of 
nonimmunized hamsters; this effect was not noted following challenge of offspring of the two groups within 1 day 
of weaning. The passage of parasites from mother to young during gestation and/or nursing apparently does not 
occur since, at 125 days of age, no parasites were observed in spleen or liver impression smears of offspring of 
hamsters infected i.c. with 6.0 x 10(6) amastigotes while parasites were seen in such smears of hamsters infected, 
120 days previously, with 10 amastigotes i.c. Thus, sensitization to immunization in offspring of infected 
hamsters and to challenge of offspring of immunized hamsters is apparently transplacental, effected either by 
soluble leishmanial antigen, soluble lymphocyte (or transfer) factor, or by cells.

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