Download IHC Detection of Common Viral Infections in Placenta

Winter 2 0 1 4
mikro-graf
Volume
43
01
Issue
O ff ic ial Publ ication of the Mich ig an S o c ie t y of Hi stotech nolo g i sts
IHC Detection
of Common Viral
Infections in Placenta
Amy S. Porter, HT (ASCP) QIHC
Patricia K. Senagore, M.D., Perinatal Pathologist
this issue
President’s Message
2
Editor’s Note
2
Inbox
3
Test Your Knowledge
3
MSH News & Events
9
In the Spotlight
10
Spring Symposium
11
Signals: Dermatopathology
12
Around the Region
14
NSH Update
17
Officers And Chairpersons
19
T
he placenta (plah-senʹtah) is an organ whose presence helps to define
mammals; it develops in the uterus during pregnancy, connects the
uterus to the fetus, and allows nutrient delivery, gas exchange, endocrine hormone production and waste removal to occur during gestation. It is
normally expelled from the uterus following delivery of the infant and is thus
readily available for pathologist examination.
Overview of placental gross examination
The placenta is comprised of three basic components: the disc, the extraplacental membranes that form the birth sac, and the umbilical cord. The
placenta in its entirety may be weighed prior to removal of membrane sac
and cord but by convention, for diagnostic evaluation, the cord and membranes are removed prior to weighing the disc. Measurements will record the
umbilical cord length/diameter, number of cord blood vessels, and distance of
cord insertion to the nearest margin. Also measured is the membrane length
that represents the shortest distance between the membrane rupture site
and the disc margin. Placental disc dimensions to be documented include its
largest diameter, the perpendicular dimension through this diameter at the
cord insertion site, and disc thickness. All examinations should describe and
sample abnormalities of the cord and extra-placental membranes, as well as
non-lesional tissue. The intact maternal (bloody, rough, and dark) and fetal
(smooth and shiny) surfaces of the disc are also inspected for abnormalities
prior to disc dissection.
Cross-sectional samples of the extra-placental membranes are taken from a
“jelly roll” preparation that includes its entire length from site of rupture to disc
margin, and of the umbilical cord taken at its proximal insertion into the disc
and at a distal location.
Gross dissection of the disc involves making slices (“breadloaf”) 1–2cm apart,
parallel to the smaller disc diameter and through its full thickness. Representative tissue sections are taken that include both maternal and fetal surfaces.
Such sections are most often taken to sample lesions but should also include
central disc tissue that is grossly “normal” and without lesions. Research
examinations may require additional sections of the disc from the margin and
through the umbilical cord insertion site.
Whatever examination procedure is followed, it usually represents a routine
protocol, such that information is gathered systematically and without omissions.
[continued on page 4]
Mikro-Graf
President’s Message
Snow, snow and more snow…the flakes keep falling…but Spring is around the
corner and brings with it The MSH Annual Scientific Symposium. On April 11th
and 12th we hope you will join us for education and fun at The Radisson Hotel
of Lansing. This year is sure to be as successful as the last. The committed
technologists involved with the MSH achieved many accolades at last year's
National Society of Histotechnology Symposium Convention in Rhode Island.
After that, our own society hosted a great Fall Seminar spotlighting the newly
renovated histology facility at the Capitol Area Career Center in Lansing, whose
hospitality program prepared our wonderful lunch and break foods.
The newly elected MSH officers will be announced at the Spring Symposium
– keep your eyes open for election materials in this and coming issues of the
Mikro-Graf, on the website, as well as email blasts. Make sure you participate
– the society belongs to its members and your participation is paramount in its
endeavors. Think about becoming involved, if not in an elected office, maybe with
a small responsibility that you could share or be mentored in by an established
board member. It is my sincere hope that will we have a new generation of techs
that become active at the state level who continue to carry the mantle to the
national level.
I have established an email specifically dedicated to all things MSH mihistoprez@
mihisto.org; please consider this an open invitation to communicate with me at
anytime.
Amy Porter, MSH President
Editor’s Note
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MG43.01
Official Publication of the Michigan Society of Histotechnologists
Inbox
Dear Mikro-Graf,
Thought your readers would enjoy hearing about the experiment we
conducted today. We have been having problems with tissues received
from a certain client. Troubleshooting led me to believe that we could have
a fixation problem. But my questions regarding specimen collection were
getting me nowhere! We don't normally see the tissues as the samples come
down in cassettes ready to process. So, I asked for a representative grossed
specimen– a jar filled with the amount of formalin normally used with a piece
of tissue the size they would normally cut. We all gasped when the specimen
was recieved! I couldn't resist sharing the photo (right).
I don't think this follows the rule 20-1 fixative to specimen ratio! Even worse
was the fact that, since it is lung and wants to float, half of the tissue is not
exposed to the formalin. This is the source of our cassetted tissue!
Our experiment consisted of taking multiple samples of lung, roughly the
same size, and put ting them in various amounts of formalin–one of them
being the recommended 20:1. We will gross them after 48 hours of fixation
which is their normal process. I will be making this into a poster for them to
use as a visual aid to reinforce our findings!
Trying all these different things has definitely increased our workload but it's
been a fun learning process! Hopefully it will fix what ails this project and help
others at the same time!
A Loyal Reader,
Dear Reader,
Thank you for an excellent reminder of the importance of PROPER fixation!
We’d love to hear from you!
Submit YOUR technical question for a response from one of our experts!
Comments, suggestions or technical tips are also welcome! Send to:
Mikro-Graf Editor
8476 Pennfield Road
Battle Creek, MI 49017
or email: [email protected]
Test Your Knowledge
Q.
1. Name the tissue.
2. Positive staining showing overamplification of this prognostic marker is required for Herceptin™ therapy.
[answers on page 3]
Winter 2014
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3
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[continued from page 1]
Development of the placental disc
The placental disc tissue is composed of highly vascularized fetal villous tissue that is bathed in maternal blood. A
thin maternal decidua, developed from uterine endometrium, forms the deep surface or “floor” of the disc (decidua
basilis). Fetal membranes, carrying blood vessel branches
of the umbilical cord that give rise to the villous placental
tissue, form the “roof” surface of the disc (chorion fundosum).
Except for the amnion, the tissues of the placenta are
derived from the outer cell layer of the blastocyst, a spherical, hollow, cellular structure that forms several days after
the ovum is fertilized, the result of a series of cell divisions.
The embryo/fetus is derived from the inner cell mass of
the blastocyst. Upon attachment of the blastocyst to the
decidualized endometrium, the trophoblast shell further
differentiates into an inner layer of proliferating cytotrophoblasts that move outward and fuse into a continuous outer
mantle known as the syncytiotrophoblast. Within the syncytiotrophoblast mantle small blood lacunae develop that will
interconnect and form the intervillous space of the maternal
circulation, described below. The syncytiotrophoblast is
involved in the production of many proteins, and exchange
of nutrients and waste between mother and fetus.
The sustained proliferation of cytotrophoblasts into columns, continued formation of its covering mantle of syncytiotrophoblast and eventual ingrowth of mesenchymal
cells that will become villous blood vessels, lead to the
formation of the placenta’s tree-like villous architecture.
Ultimately blood vessels in villi connect to blood vessels
simultaneously forming in the umbilical cord and the fetus,
thus establishing the fetal-placental circulation. The development and growth of the placenta continues throughout
most of pregnancy as the fetus grows in size, guided by
growth factors that allow branching and elongation of the
villous blood vessels.
The maternal blood supply of the placenta is usually completed by the end of the first trimester. Formation of the
maternal- placental circulation is initiated when small uterine
spiral arteries in the decidualized endometrium are invaded
by specialized trophoblasts and then converted into coiled,
large-diameter, and elongated vessels. Maternal arterial
blood begins to flow through the remodeled spiral vessels
into the intervillous space that surrounds the forming villi,
eventually bathing them in the oxygen and nutrient-rich
blood needed for growth of the fetus and its placenta. Delivery of nutrients and removal of waste occurs as substances
move across the vasculo-syncytial membrane of the villi,
a thin tissue barrier that separates the maternal and fetal
circulations. As nutrients are removed and exchanged for
waste, oxygen-poor and nutrient-poor maternal blood is
returned to the uterus through endometrial veins.
amount of maternal blood flowing to the placenta as the
pregnancy advances. Incomplete conversion of these
blood vessels is thought to underlie some abnormal conditions that present later in pregnancy (pre-eclampsia).
Fetal circulation
The three large blood vessels of the umbilical cord seem to
divide into branches within the chorionic connective tissue
membrane that cover the fetal surface of the placental disc
and course deep into the most terminal portions of its villous tissue. Paradoxically, because of their muscular structure, two vessels are actually arteries that carry “venous”
blood from the fetus to the placenta. The third is a vein that
carries “arterial” blood from the placental villi to the fetus. To
explain: capillaries in the most terminal portions of the villi
are the site of nutrient and waste exchange. Villous capillaries that carry oxygen and nutrient-rich blood TO the fetus
(“arterial” blood) gradually join together to form increasingly
larger branches, and finally come together to form one
large thin-walled vein that extends the length of the umbilical cord to the umbilicus. The umbilical vein then delves
deep into the abdomen to deliver its contents into the fetal
liver for processing and eventual delivery TO all body tissues. Fetal capillaries that exist in all tissues and organs
collect blood, from which all nutrients have been removed,
(venous) and gradually join together to become increasingly larger vessels that empty into the fetal heart. Since the
fetus does not “breathe” through its lungs in-utero, venous
heart blood bypasses the lungs and is pumped out of the
heart through muscular arteries, and eventually is carried
through the two umbilical arteries and then the placental
vessel branches to the terminal villi of the placenta for nutrient/waste exchange.
This arterio-capillary-venous system brings the fetal blood
exceptionally close to maternal blood in the intervillous
space that bathes the villi. No true intermingling of fetal and
maternal blood occurs, as the systems are separated by
the vasculaosyncytial membranes of the placental villi.
The early maternal spiral artery conversion process
described above allows for a progressive increase in the
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placental circulation. reproduction from Gray's Anatomy.
MG43.01
Official Publication of the Michigan Society of Histotechnologists
Placental Function
Nutrition, excretion, endocrine, and immune functions are
provided by the placenta during pregnancy. Nutrients are
delivered through active and passive transport to the fetus;
active transport allows vastly different plasma concentrations of a variety of large molecules to be maintained on
both sides of the placental barrier. Excretion carries waste
products from the fetus into the maternal blood via diffusion across the placenta; wastes include urea, uric acid,
and creatinine. Endocrine functions allow for the secretion
of hormones that are necessary to maintain pregnancy,
which can include hCG – (human Chorionic Gonadotrophin,) hPL – (human Placental Lactogen,) estrogen and
progesterone. As part of its immune function, maternal IgG
molecules are allowed to pass across the placenta to the
fetus, usually between week 20 and week 24 of gestation,
providing antibody protection to the fetus while in-utero.
This humoral immunity is identical to that present in the
mother and can remain with the newborn infant for several
months after birth. However, because the much larger IgM
antibodies cannot cross the placenta, some mother-to-child
infections can be transmitted during pregnancy, which may
have detrimental effects on the fetus. Cytomegalovirus and
Parvovirus B19 are two such pathogenic viruses that may
be transmitted vertically from mother-to-child.
Infected infants that are symptomatic at birth (0.1% of all
infants) are more likely to be born to mothers without preexisting immunity (specific antibodies) to CMV. Manifestations include congenital defects, liver and spleen enlargement, jaundice, anemia, low platelets, low birth weight,
microcephaly, and inflammation of the retina and its vascular membrane. Most (90%) infants with in-utero infection
are born without symptoms and are healthy, yet after birth
long term follow-up has shown that 10-20% infants present with conditions that can vary from neurological damage, to learning difficulties (Sherris). Hearing loss due to
sensory nerve damage is the most frequent and long term
outcome. Excretion of CMV in urine and saliva is common
and prolonged, up to 5 years, in children with the congenital
infection and may represent a source of infection for other
children and daycare workers.
PATHOGENIC VIRUSES
Cytomegalovirus or CMV is from the viral family Herpesviridae or herpesviruses; with the name from the Greek
being cyto–, “cell” and –megalo, “large”. The viral species
that infects humans is commonly known as human CMV
(HCMV) or human herpesvirus-5 (HHV-5). This species
is the most commonly studied of all cytomegaloviruses
and is the most common congenitally-acquired infection in
infants. About 1% of pregnant women become infected with
CMV and of these; about 40% transmit the infection to the
fetus. Placental infection most often occurs during primary
infection of the mother within the period of viremia, when
the virus can pass from the maternal to fetal circulation
across a destroyed trophoblast layer. The resulting placental inflammatory response is a lympho-plasmacytic chronic
villitis. CMV viral cytopathic effect (CPE) can be histologically identified with Hematoxylin and Eosin staining, represented by the classic morphology of large “owls–eye”
nuclear inclusions plus cytoplasmic inclusions that add to
the enlarged size of infected cells. However, inclusions are
often so widely scattered that careful inspection of many
sections is required for diagnosis.
Most likely to be infected and show inclusions are villous
capillary endothelial cells, and stromal cells. Immunohistochemistry will confirm the infection in most instances.
Because capillaries are destroyed by the virus, the finding
of hemosiderin pigment plus plasma cells in villi is strongly
suggestive of CMV infection and should prompt a search
for the inclusions. The CMV virus can also be detected in
maternal cervical secretions and breast milk.
Cytomegalovirus (CMV) infection. the dramatically enlarged nuclei are
characteristic of CMV.
Parvovirus B19 (from Latin word ”parvus” for small) is
sometimes known as erythrovirus B19 (it replicates in
the nucleus of erythroid cell precursors), erythema infectiousum, or “Fifth Disease” (it is the fifth disease known to
commonly cause a viral skin rash in childhood). This was
the first and only virus in the family of parvoviruses known
to infect humans until 2005. The B19 virus most frequently
affects children, however infection can also be contracted
by adults; about 20% of infected individuals are asymptomatic (CDC). This virus is the cause of the classic rash
in children known as “slapped cheek syndrome” accompanied by runny nose, fever, headache, and sometimes painful swollen joints. It was discovered by chance in 1975 in
Australia by virologist Yvonne Cossart, who named it for the
infected sample’s position in “well B19” of a large number
of micro-titer plates. Parvovirus is transmitted primarily by
respiratory droplets from an infected individual.
[continued on page 6]
Winter 2014
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Mikro-Graf
[continued from page 5]
The virus preferentially targets and infects the nuclei of
erythroid (red blood cell) precursors, which leads to the
destruction of these cells and severe anemia. By adulthood, approximately 50% of the population is thought to
be B19 immune due to a previous infection; re-infection is
possible in a minority of cases.
Maternal parvovirus B19 infection that occurs prior to the
20th week of pregnancy may result in pregnancy loss in
about 5% of cases; but losses become minimal in the
second half of pregnancy (CDC). Prenatal antibody testing enables a pregnant mother to determine her immune
status and risk of infection. In infected fetuses, intrauterine
transfusion therapy to treat anemia has been successful,
and cases have been reported in which recovery occurred
without treatment.
Congenital Parvovirus B19 infection acquired by the fetus
during pregnancy may lead to hydrops fetalis, a lifethreatening form of body-wide tissue edema resulting from
severe fetal anemia, which sometimes leads to miscarriage
or stillbirth. The placenta also appears hydropic; it is large,
heavy, pale, and edematous. Because the chronic hemolysis of infected erythroid precursors results in a compensatory increase in erythrocyte production (erythroblastosis),
large numbers of nucleated red blood cell precursors are
evident in fetal blood vessels of the placenta, especially
villous capillaries
The hallmark histologic finding in cases of hydrops fetalis
caused by Parvovirus B19 infection is viral inclusion bodies
within erythroid precursor nuclei (“lantern cells”) that can
be identified with routine Hematoxylin and Eosin staining
and later confirmed by immunohistochemistry. The classic
morphology is of a nucleus with a dark, thin, peripheral
rim of chromatin surrounding a central, glassy (“groundglass”), amphophilic cleared area, filled with viral particles.
The cells are resistant to autolysis and may be detected in
cases of stillbirth in which tissues are macerated; immunohistochemistry can highlight infected cells even in autolysed
tissue. There is no accompanying inflammatory response to
parvovirus infection. Placenta. H&E. 60x
6
placenta parvovirus infection, specifically no chronic villitis.
Immunohistochemistry can be routinely performed to detect
these two common viral inclusions utilizing the following
protocols; please keep in mind that every laboratory is different and all immunohistochemical protocols should be
developed and validated at the laboratory performing the
assay. Polymerase chain reaction (PCR) is a more sensitive detection method that can be performed on paraffin
embedded tissue in cases of CMV and parvovirus infection
(nested PCR).
Routinely fixed, processed and embedded samples are
sectioned at 4 to 5 microns; placed onto adhesive or
charged slides; once sectioned slides are dried in a slide
drying oven with the temperature not to exceed 60°C to
preserve antigenicity. Slides are handled in the following
manner:
1. Deparaffinize slides in 2 changes of Xylene – 10 minutes each
2. Absolute Ethanol – 2 changes of 2 minutes each
3. 95% Ethanol – 2 changes of 2 minutes each
4. Distilled water – several changes
5. Tris Buffered Saline without surfactant – 5 minutes at
room temperature to adjust the pH for epitope retrieval
with heat or enzymes if needed for immunohistochemical staining.
Staining protocols are performed on an Autostainer. See
Table 1 Staining Protocols, next page.
6. Slides are counterstained with Gill 2 Hematoxylin for
1½ minutes, differentiated in 1% Glacial Acetic Water,
then blued followed by dehydration through 95% ethanol, absolute ethanol and cleared through xylene.
7. When using Fast Red Phosphatase chromogen, these
reactions must be coverslipped with Fisher Scientific™
Permount™ Mounting Medium–other mounting medias
will remove the reaction and cause staining to breakdown. This recommendation has been given by more
than one vendor of chromagens in relation to the Fast
Red compounds.
This protocol is reflective of what we perform in our laboratory. The development of polymer technology has allowed
many changes to occur with reduced incubation times and
reagents. Working with archival samples and specimens
that have been fixed in aldehyde fixatives for an extreme
period of time sometimes requires staining with increased
incubations. With this protocol, our laboratory has been
able to detect Parvovirus B19 in archived wet tissue fixed
for up to one year without the need for retrieval. Please
refer any questions related to vendor information to me
directly if you wish to have more information as we do not
wish to promote any specific vendor in this article at [email protected].
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MG43.01
Official Publication of the Michigan Society of Histotechnologists
TABLE 1. Staining protocols
Cytomegalovirus
Parvovirus B19
0.04% Pepsin in 0.2N HCl – 20 minutes at 37°C
No retrieval required
Rinse in running tap water – 5 minutes
Rinse in several changes of distilled water
Place in Tris Buffered Saline + Tween 20 – 5 minutes
Place in Tris Buffered Saline + Tween 20 – 5 minutes
Normal Horse Serum – 30 minutes
Normal Horse Serum – 30 minutes
Tris Buffered Saline + Tween 20
Tris Buffered Saline + Tween 20
Avidin D – 15 minutes
Avidin D – 15 minutes
Tris Buffered Saline + Tween 20
Tris Buffered Saline + Tween 20
d-Biotin – 15 minutes
d-Biotin – 15 minute
Tris Buffered Saline + Tween 20
Tris Buffered Saline + Tween 20
Monoclonal Mouse anti – Cytomegalovirus diluted 1:40 – Monoclonal Mouse anti – Parvovirus B19 diluted 1:40 – 60
60 minute – Room temperature
minute – Room temperature
Tris Buffered Saline + Tween 20
Tris Buffered Saline + Tween 20
Biotinylated Horse anti-Mouse IgG H+L diluted
to 11µg/ml – 40 minute – Room temperature
Biotinylated Horse anti-Mouse IgG H+L diluted
to 11µg/ml – 40 minute – Room temperature
Tris Buffered Saline + Tween 20
Tris Buffered Saline + Tween 20
Alkaline Phosphatase Enzyme Reagent –
60 minutes – Room temperature
Alkaline Phosphatase Enzyme Reagent –
60 minutes – Room Temperature
Tris Buffered Saline + Tween 20
Tris Buffered Saline + Tween 20
Fast Red Phosphatase Chromogen – 8 to 15 minutes
Fast Red Phosphatase Chromogen – 8 to 15 minutes
Tris Buffered Saline + Tween 20
Tris Buffered Saline + Tween 20
Distilled Water – Rinse
Distilled Water - Rinse
References
•
Early Development of the Placenta. Pathology of the Human Placenta
6th Ed, Benirschke K, Ed Burton G,J and Ed Baergen RN. Heidelburg: Springer (2012) pages 41–45.
•
Parvovirus Anemia and Other Causes of Myocarditis. Pathology of
the Human Placenta 6th Ed, Benirschke K, Ed Burton G,J and Ed
Baergen RN. Heidelburg: Springer (2012) pages 447–450.
•
Virus Infections and Villitides. Pathology of the Human Placenta 6th
Ed, Benirschke K, Ed Burton G,J and Ed Baergen RN. Heidelburg:
Springer (2012) pages 599—603, 608–609.
•
Kindelberger DW, Sirois KF, and Boyd TK . Evaluation of the Placenta. Diagnostic Gynecologic and Obstetric Pathology 2nd Ed.
Christopher P. Crum, Marisa R Nucci, Kenneth R. Lee. Philadelphia:
Saunders Elsevier (2011) p. 1046, 1069, 1072-1074, 1076.
Winter 2014
•
Boyd TK, Parast MM, Tantbirojin P, and Saleemuddin A. Placental
Correlates of Unanticipated Fetal Death. Diagnostic Gynecologic
and Obstetric Pathology 2nd Ed. Christopher P. Crum, Ed Marisa R
Nucci, ED Kenneth R. Lee. Philadelphia: Saunders Elsevier (2011)
pages 1097, 1099–1101, 1106–1107.
•
Parast MM and Boyd TK. Complications of Previable Pregnancy.
Diagnostic Gynecologic and Obstetric Pathology 2nd Edition Ed.
Christopher P. Crum, Ed Marisa R Nucci, Ed Kenneth R. Lee. Philadelphia: Saunders Elsevier (2011) pages 1011–1012.
•
Mumps Virus, Measles, Rubella, and Other Childhood Exanthems.
Sherris Medical Microbiology 5th Edition. Ed Ryan KJ and Ed. Ray
CG, New York : McGraw Hill Medical, (2011) pages 189-190, 201-203
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DATE OF ARTICLE:
Winter 2014
TITLE:
IHC Detection of Common Viral Infections in Placenta
Amy Porter, HT (ASCP) QIHC; Patricia K. Senagore, M.D., Perinatal Pathologist
AUTHOR: DIRECTIONS:
1. Answer the following questions by circling the one (1) BEST answer for each question.
2. Complete the information required at the bottom of the page.
3. Submit questions & check made out to “MSH”(in US funds) to: Sarah Bajer 35669 Impala Dr, Sterling Heights, MI
48312
To earn Continuing Education credit from MSH, completed form must be submitted within
Three (3) years of original date of the article.
1.
In which of the following organs does the placenta develop during pregnancy?
A. Cervix
B. Fallopian Tube
C. Ovary
D. Uterus
2.
TRUE or FALSE (circle one): The vein located in the umbilical cord carries venous blood from the placental villi to the
fetus.
3.
TRUE or FALSE (circle one): No true comingling of fetal and maternal blood occurs in the placenta.
4.
All of the following are provided to the fetus by the placenta, EXCEPT:
A. Genes
B. Endocrine functions
C. Excretion functions
D. Nutrients
5.
CMV viral cytopathic effect can be identified on a routine H&E as:
A. Large clusters of infected cells
B. Lantern Cells
C. Owl Eye Inclusions
D. Small Cells
6.
Which of the following testing methods is most sensitive for detecting CMV and Parvovirus B19?
A. Enzyme Histochemistry
B. IHC
C. PCR
D. Routine H&E staining
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