TRANSPLACENTAL (HEMATOLOGIC) INFECTIONS
Most parasitic (e.g., toxoplasma, malaria) and viral infections and a few bacterial infections (i.e., Listeria, Treponema) gain access to the fetal bloodstream transplacentally via the
chorionic villi. This hematogenous transmission may occur at any time during gestation or occasionally, as may be the case with hepatitis B and HIV, at the time of delivery via maternalto-
fetal transfusion. The clinical manifestations of these infections are highly variable, depending largely on the gestational timing and microorganism involved.
Some infections, such as those with parvovirus B19 (which causes fifth disease in the mother), may induce spontaneous abortion, stillbirth, hydrops fetalis, and congenital anemia.
While the virus can bind to different cell types, replication occurs only in erythroid cells, and diagnostic viral cytopathic effect can be recognized in late erythroid progenitor cells of
infected infants ( Fig. 10-9 ).
The TORCH group of infections (see above) are grouped together because they may evoke similar clinical and pathologic manifestations, including fever, encephalitis, chorioretinitis,
hepatosplenomegaly, pneumonitis, myocarditis, hemolytic anemia, and vesicular or hemorrhagic skin lesions. Such infections occurring early in gestation may also cause chronic sequelae
in the child, including growth and mental retardation, cataracts, congenital cardiac anomalies, and bone defects.
ONSET OF SEPSIS
Perinatal infections can also be grouped clinically by whether they tend to result in early-onset (within the first 7 days of life) versus late-onset sepsis (from 7 days to 3 months). Most cases
of early-onset sepsis are acquired at or shortly before birth and tend to result in clinical signs and symptoms of pneumonia, sepsis, and occasionally meningitis within 4 or 5 days of life.
Group B streptococcus is the most common
Figure 10-9Bone marrow from an infant infected with parvovirus B19. The arrows point to two erythroid precursors with large homogeneous intranuclear inclusions and a surrounding
peripheral rim of residual chromatin.
Figure 10-10Schematic outline of the pathophysiology of the respiratory distress syndrome (see text).
Figure 10-11Hyaline membrane disease. There is alternating atelectasis and dilation of the alveoli. Note the eosinophilic thick hyaline membranes lining the dilated alveoli.
Figure 10-12Necrotizing enterocolitis. A, Postmortem examination in a severe case of NEC shows the entire small bowel is markedly distended with a perilously thin wall (usually this
implies impending perforation). B, The congested portion of the ileum corresponds to areas of hemorrhagic infarction and transmural necrosis microscopically. Submucosal gas bubbles
(pneumatosis intestinalis) can be seen in several areas (arrows).
Figure 10-13Hydrops fetalis. There is generalized accumulation of fluid in the fetus. In B, fluid accumulation is particularly prominent in the soft tissues of the neck, and this condition
has been termed cystic hygroma. Cystic hygromas are characteristically seen, but not limited to, constitutional chromosomal anomalies such as 45,X0 karyotypes. (Courtesy of Dr. Beverly
Rogers, Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX.)
TABLE 10-5-- Selected Causes of Hydrops Fetalis (in decreasing order of frequency)
Trisomy 21, trisomy 18
Cystic adenomatoid malformation
Immune hydrops (Rh and ABO)
Date: 2016-04-22; view: 443