A fetus with a parvovirus B19 infection and congenital anomalies

Tiessen, R. G.; Elsacker‐Niele, A. M. W. Van; Vermeij-Keers, Chr.; Oepkes, Dick; Roosmalen, Jos van; Gorsira, M. C. B.

doi:10.1002/pd.1970140305

Cited by 57 publications

(30 citation statements)

References 8 publications

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“…Two possible initiators are exogenous factors or genetically encoded morphological errors. Exogeneous causes of facial anomalies include (1) factors causing environmental stress early in embryological development, such as hyperthermia and hypoxia 9 , nutritional deficiencies and hormonal imbalances 16 , (2) viral and toxoplasma infections 5,13 and (3) toxins, drugs and chemicals 15 . In the present case, the role of infectious agents, parasites and drugs could not be obtained because there were no records and history of husbandry of the dam and sire.…”

Section: Discussionmentioning

confidence: 99%

Partial facial duplication (diprosopus) in a goat kid : clinical communication

Mukaratirwa

Sayi²

2006

J. S. Afr. Vet. Assoc.

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The anatomical and clinical features of a live-born diprosopic goat kid are described. The kid had two faces with two eyes each, two complete oral cavities and nostrils and two ears. Caudal to the neck, the kid grossly appeared normal. Both mouths of the kid showed synchronous suckling motions. Elevated respiratory and heart rates were recorded and the temperature was subnormal. Radiological examination showed a single trunk and vertebral column, normal limbs, two sets of jaws, three orbits, and contrast radiography revealed a single patent oesophagus. There was maxillary and mandibular duplication resulting in two faces. There was a cleft palate. The oropharyngeal regions of each face merged to form a single laryngopharynx and oesophagus. There was a single brain with hypoplasia of the cerebellum. The left and right cerebral hemispheres were fused rostrally, and there was duplication of the optic chiasma and the pituitary gland. The olfactory tract was absent and the superficial origins of most of the cranial nerves were not discernible.

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Section: Discussionmentioning

confidence: 99%

Partial facial duplication (diprosopus) in a goat kid : clinical communication

Mukaratirwa

Sayi²

2006

J. S. Afr. Vet. Assoc.

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“…It has since been found that fetal B19 infection may also cause fetal or congenital anemia, abortion, or stillbirth or result in an asymptomatic self-limiting episode. A few case reports have speculated on B19 causing congenital malformations (158,335; Weiland et al, Letter, Lancet i:682-683, 1987), though systematic studies have failed to substantiate this hypothesis (47,117,261).…”

Section: B19 Infection In Pregnancy (I) Hydrops Fetalismentioning

confidence: 99%

Human Parvovirus B19

2002

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Parvovirus B19 (B19) was discovered in 1974 and is the only member of the family Parvoviridae known to be pathogenic in humans. Despite the inability to propagate the virus in cell cultures, much has been learned about the pathophysiology of this virus, including the identification of the cellular receptor (P antigen), and the control of the virus by the immune system. B19 is widespread, and manifestations of infection vary with the immunologic and hematologic status of the host. In healthy immunocompetent individuals B19 is the cause of erythema infectiosum and, particularly in adults, acute symmetric polyarthropathy. Due to the tropism of B19 to erythroid progenitor cells, infection in individuals with an underlying hemolytic disorder causes transient aplastic crisis. In the immunocompromised host persistent B19 infection is manifested as pure red cell aplasia and chronic anemia. Likewise, the immature immune response of the fetus may render it susceptible to infection, leading to fetal death in utero, hydrops fetalis, or development of congenital anemia. B19 has also been suggested as the causative agent in a variety of clinical syndromes, but given the common nature, causality is often difficult to infer. Diagnosis is primarily based on detection of specific antibodies by enzyme-linked immunosorbent assay or detection of viral DNA by dot blot hybridization or PCR. Treatment of persistent infection with immunoglobulin reduces the viral load and results in a marked resolution of anemia. Vaccine phase I trials show promising results

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“…Hepatic disease has also been related to intrauterine infection by parvovirus [10,11]. Furthermore, a fetus with a bilateral cleft lip, alveolus as well as palate, micrognathia and webbed joints after proven fetal B19 infection was reported [12].…”

Section: Discussionmentioning

confidence: 99%

Fetal Parvovirus B19 Infection and Meconium Peritonitis

et al. 1998

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A 33-year-old primigravida at 26 weeks gestation presented with fetal hydrops and fetal anemia following prior parvovirus B19 infection. The fetus required two intrauterine transfusions of packed red cells. At 35 weeks gestation, a cesarean section was performed for obstetric reasons. As a consequence of a prenatal bowel perforation, the neonate developed meconium peritonitis, for which she needed laparotomy. This case demonstrates that there may be an association between intrauterine parvovirus infection and meconium peritonitis, the latter possibly caused by vascular injury in fetal life.

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A fetus with a parvovirus B19 infection and congenital anomalies

Cited by 57 publications

References 8 publications

Partial facial duplication (diprosopus) in a goat kid : clinical communication

Partial facial duplication (diprosopus) in a goat kid : clinical communication

Human Parvovirus B19

Fetal Parvovirus B19 Infection and Meconium Peritonitis

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