Miscarriage and pre-eclampsia are the most common disorders of human pregnancy. Both are placental-related and exceptional in other mammalian species. Ultrasound imaging has enabled events during early pregnancy to be visualized in vivo for the first time. As a result, a new understanding of the early materno-fetal relationship has emerged and, with it, new insight into the pathogenesis of these disorders. Unifying the two is the concept of placental oxidative stress, with associated necrosis and apoptosis of the trophoblastic epithelium of the placental villous tree. In normal pregnancies, the earliest stages of development take place in a low oxygen (O2) environment. This physiological hypoxia of the early gestational sac protects the developing fetus against the deleterious and teratogenic effects of O2 free radicals (OFRs). In miscarriage, development of the placento-decidual interface is severely impaired leading to early and widespread onset of maternal blood flow and major oxidative degeneration. This mechanism is common to all miscarriages, with the time at which it occurs in the first trimester depending on the aetiology. In contrast, in pre-eclampsia the trophoblastic invasion is sufficient to allow early pregnancy phases of placentation but too shallow for complete transformation of the arterial utero-placental circulation, predisposing to a repetitive ischaemia-reperfusion (I/R) phenomenon. We suggest that pre-eclampsia is a three-stage disorder with the primary pathology being an excessive or atypical maternal immune response. This would impair the placentation process leading to chronic oxidative stress in the placenta and finally to diffuse maternal endothelial cell dysfunction.

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Placental-related diseases of pregnancy: involvement of oxidative stress and implications in human evolution

Animal models of human placentation - : A review

Preeclampsia is a pregnancy-specific disorder characterized by hypertension and excess protein excretion in the urine. It is an important cause of maternal and fetal morbidity and mortality worldwide. The disease is almost exclusive to humans and delivery of the pregnancy continues to be the only effective treatment. The disorder is probably multifactorial, although most cases of preeclampsia are characterized by abnormal maternal uterine vascular remodeling by fetally derived placental trophoblast cells. Numerous in vitro and animal models have been used to study aspects of preeclampsia, the most common being models of placental oxygen dysregulation, abnormal trophoblast invasion, inappropriate maternal vascular damage and anomalous maternal-fetal immune interactions. Investigations into the pathophysiology and treatment of preeclampsia continue to move the field forward, albeit at a frustratingly slow pace. There remains a pressing need for novel approaches, new disease models and innovative investigators to effectively tackle this complex and devastating disorder.

Preeclampsia: multiple approaches for a multifactorial disease.

Respiratory syncytial virus.

In developing countries rotavirus infections account for nearly 6% of all diarrheal episodes and for 20% of diarrhea-associated deaths of young children. Even in industrialized countries rotavirus diarrhea in the young is among the leading causes of hospitalization. In temperate regions institutional outbreaks of the disease occur mainly in cold dry weather, whereas in tropical settings the seasonality is less well defined. Waterborne outbreaks of rotavirus gastroenteritis have been recorded; air, hands, fomities, and food may also act as vehicles for this infection. Rotaviruses can survive for weeks in potable and recreational waters and for at least 4 hours on human hands. In air and on nonporous inanimate surfaces, the survival of rotaviruses is favored by a relative humidity of less than or equal to 50% and viral infectivity can be retained for several days. Rotaviruses are relatively resistant to commonly used hard-surface disinfectants and hygienic hand-wash agents.

Survival and Vehicular Spread of Human Rotaviruses: Possible Relation to Seasonality of Outbreaks

Diarrhea developed in five newborn rhesus monkeys(Macaca mulatta) inoculated orally on the first day of life with the human reovirus-like agent of infantile gastroenteritis. Incubation period ranged from 2–5 days; virus particles were detected in stools in association with illness, and virus shedding lasted between 1 and 3 days. Virus derived from monkeys that developed illness following inoculation was infectious for other monkeys but did not induce diarrhea which could be associated temporally with virus shedding. Viral antigens were also detected in tissues of the grossly abnormal small intestine of an acutely-ill monkey. Serum antibody responses were demonstrated in two of the ill animals by complement-fixation and/or immunofluorescence.

Induction of diarrhea in colostrum-deprived newborn rhesus monkeys with the human reovirus-like agent of infantile gastroenteritis

A disease characterized by edema, proteinuria, hypoproteinemia and hypertension was seen in late gestation in patas monkeys. The initial sign was edema of the perineum, ankles and lower trunk. The onset was abrupt, occurring 7 days or less prepartum. The affected animals were not depressed, and convulsions were not seen. In 6 of the 98 pregnancies during a 1-year period, symptoms of the disease were present. The highest incidence was manifested by primiparous animals with 3 of 36 pregnancies affected. Two of 38 second pregnancies and 1 of 24 third pregnancies were also affected. Five of the animals recovered spontaneously and were normal 14 days postpartum. Edema persisted for 30 days in one female. This animal continued to be hypertensive and had persistent mild proteinuria and hypoproteinemia. She was killed approximately 1 year postpartum due to severe renal disease. The spontaneous disease seen in patas monkeys resembled toxemia of pregnancy in humans more closely than the experimentally induced disease in other animals.

Spontaneous preeclamptic toxemia of pregnancy in the patas monkey (Erythrocebus patas).

Respiratory syncytial virus antibodies in nonhuman primates and domestic animals.

Data from 338 blood samples of 31 patas monkeys is presented to show the normal hematolgoic development from birth to one year of age, and is compared to 120 samples from normal adults. Marked changes in hematocrit, hemoglobin, red cell numbers, and leukocyte distribution which occurred during the first month were followed by a slow progression to adult values. Body weight data is also presented which shows a linear growth rate during the first year of life.

Growth and hematologic development of the patas monkey (Erythrocebus patas) to one year of age.

Cryptococcosis was diagnosed in an adult male patas monkey (Erythrocebus patas) 9 months after importation. The disease was characterized by an open lesion on the buttock and epileptiform seizures. Diagnosis was confirmed through immunologic identification of the organism in serum and cerebrospinal fluid and by mycologic procedures performed on the cultured organism. The monkey was killed and cryptococcal organisms were found in the lung, brain, subcutaneous lesions, thyroid, pancreas, adrenals, and spinal cord. Retrospective analysis of stored serum indicated that the monkey was infected at the time of importation.

Disseminated cryptococcosis in a patas monkey (Erythrocebus patas).

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