From: TSS ()
Subject: POSITION STATEMENT MATERNAL TRANSMISSION OF vCJD
Date: May 10, 2005 at 11:54 am PST
MATERNAL TRANSMISSION OF vCJD
1. The Chief Medical Officer for England asked SEAC to consider
current evidence and comment on the potential transmission of
vCJD from mother to child via human breast milk. In utero
transmission was also considered. The committee also
commented on the scientific basis of a risk reduction measure for
possible transmission of vCJD via banked breast milk.
2. No diagnostic test is currently available for the detection of
abnormal PrP in milk. Research is under way to develop tests to
screen for the possible presence of abnormal prion protein (PrP) in
milk samples from cattle experimentally infected with BSE1. These
modified tests may also be applicable to human milk. However, it is
not yet clear when/if a reliable test will be available.
3. A small number of breast milk banks in the UK supply highly
vulnerable premature babies for whom no milk may be available
from the mother. A model developed by the Department of Health
to assess the effect of pooling breast milk from multiple donors on
the possible risks of transmission of vCJD via breast milk banks
4. There is some, albeit limited, published epidemiological and
experimental research on maternal transmission of prion diseases.
There are also unpublished surveillance data of children born to
vCJD cases from the National CJD Surveillance Unit and UK
surveillance of neurological illness in children which might inform on
potential risks of maternal transmission.
1 A joint FSA/SEAC milk working group is monitoring and providing advice
on this research
carried out at the Veterinary Laboratories Agency.
Breast milk banks
5. There is no evidence that vCJD infectivity has ever been
transmitted through breast milk. However, a theoretical risk exists.
Modelling studies clearly show that the practice of pooling breast
milk increases the number of donors to which a recipient is
exposed and thereby increases the potential risk of an infant
receiving milk contaminated with vCJD infectivity. The theoretical
risk of infection can be minimised by not pooling the milk, by the
use of individual hand operated breast milk pumps for single
donors, and by the use of single-use sterilised bottles for collection.
In addition, available evidence suggests that infection/inflammation
of the breast results in increased lymphocytes in milk and therefore
increased risk of infectivity. This risk would be minimised if milk
from donors showing signs of infection is not used.
6. The committee suggested that, if practicable, milk could be stored
for an appropriate period of time to allow the health status of donors
to be monitored, before it is released. However, information was
not available to the committee on whether long-term storage of
human milk is detrimental to its nutritional quality.
7. There is evidence from animal studies for low level maternal
transmission of prions in cattle and sheep. This transmission may
occur in utero, via milk and/or perinatally. However, the possibility
that this putative maternal transmission might have been due to
another mode of transmission, for example through a contaminated
environment or feed, cannot be ruled out.
8. In contrast, in humans there is no evidence for maternal
transmission in cases of familial prion disease, other than the
transfer of a mutant form of the PrP gene, and there is no evidence
of maternal transmission of Kuru. However, compared with other
human prion diseases vCJD may pose a greater risk because of
the greater involvement of the lymphoreticular system in vCJD
pathogenesis. Although, breast tissue (and placenta) from a single
vCJD case tested negative for PrPvCJD, transfer of infectivity to
breast milk may depend on the physiological status of the
mammary gland. Similar tests or infectivity bioassays have not
been conducted on breast tissue from lactating patients with vCJD.
9. A published study suggesting transmission of sCJD in colostrum2
was considered unreliable because tissues not normally associated
with high levels of infectivity (blood and placenta) showed
equivalent infectivity to that of the brain in this study.
10. Analysis of prospective surveillance data of UK children born to
mothers with, or that had subsequently developed clinical vCJD,
provide no evidence for maternal transmission of vCJD. However,
the number of cases is very small and the incubation period of
vCJD, if transmitted from mother to child, is unknown and so the
children may yet be too young to have developed symptoms.
11. The phenotype of BSE infection in humans expressing PrP
genotypes other than M/M at codon 129 is not known. Given
recently published studies in mice expressing the human PrP
gene3, which suggest that the human PrP genotype may affect
disease phenotype, the committee considered it very important that
undiagnosed neurological diseases be carefully monitored. In this
respect, amongst others, it is recommended that the careful
monitoring of neurological illnesses through the PIND surveillance
of children4 continue.
12. In summary, there is currently no epidemiological evidence for
maternal transmission of vCJD, including transmission via breast
milk. However, there is a hypothetical risk. Although available
evidence is limited and mostly indirect rather than direct, this risk, if
any, appears to be low. As a risk cannot be excluded, a watching
brief should be maintained.
2 Tamai Y et al. Demonstration of the transmissible agent in tissue from
a pregnant woman
with CJD. New Eng J Med 1992 327, 649.
3 Wadsworth et al. Human prion protein with valine 129 prevents
expression of variant CJD
phenotype. Science. 2004 306, 1793-1796.
4 Devereux G et al. Variations in neurodegenerative disease across the
UK: findings from the
national study of Progressive Intellectual and Neurological
Deterioration (PIND). Arch Dis
Child. 2004 89, 8-12.
Post a Followup