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Thrombosis is a rare situation in pediatric practice. That makes it impossible to have homogenous series and therefore treatment regimens are difficult to be well defined. In this article the authors present: - neonatal thrombosis (arterial and venous), thrombosis in infants and older children; - treatment regimens (indications regarding the etiology) in neonates, infants, children; - thrombolitic treatment (dosage, duration of treatment, precautions and biologic follow-up); - conclusions. [ABSTRACT FROM AUTHOR]

Beside several malformations, especially cerebral (neurulation disorders, agenesia of the corpus callosum, neuronal migration disorders, etc.), the main neonatal causes of neurological sequelar handicaps are: hipoxya, intracerebral hemorrhage, nuclear icterus, hypoglycemia, CNS infections, and iatrogenic pathology. [ABSTRACT FROM AUTHOR]

Group B Streptococcus (Streptococcus agalactiae). Infections colonizes the maternal urethra, vaginal tract and rectum; it is sexually transmitted but colonization is usually asymptomatic. In the mother, group B Streptococcus can cause puerperal sepsis, endometritis and preterm delivery. The biggest risk, however, is to the newborn. The risk of infection appears enhanced in twins. The most devastating form of infection is early-onset bacteremia with shock, pneumonia and, occasionally, meningitis. All three serotypes (I, II, III) can cause early-onset infection although type III is most common in infections that are seen after the first week of age. All three serotypes (I, II, III) can cause early-onset infection although type III is most common in infections that are seen after the first week of age (see table 1). The author presents: morphopathology (pneumonia, especially in early onset group B Streptococcus infections; meningitis, meningoencephalitis in late onset group B Streptococcus infections); clinical manifestations; diagnosis (positive, differential); evolution and treatment; prevention and prognosis. [ABSTRACT FROM AUTHOR]

Pathogenetic mechanisms in neonatal infections The author reviewed the pathogenetic mecanisms of ante- intra and postnatal infections of the newborn. They also discussed the results of the antenatal infections on embrion and foetus, and the clinical variants of intra- and postnatal infections. The attention is focussed on the relationship between pathogenetic mechanisms and the relevant clinical and paraclinical alteration for the diagnosis of the most frequent encountered infections of the newborn. [ABSTRACT FROM AUTHOR]

Infections are a frecvent and important cause of morbidity and mortality in the newborn period. Infections in the newborn infant may be required in utero (congenital), at the terme/or birth (perinatal), or after birth and during the neonatal period (postnatal). The transplacental route is the most common means by which microorganisms reaches the fetus in utero. Some viruses: Toxoplasma gondii, Treponema pallidum, and occasionally other bacteria are transmitted by this route. Infection acquired in utero may result in resorption of the embryo, absorbtion, stillbirth, congenital malformations, intrauterine growth retardation, premature birth, acute diseases in the immediate neonatal, prenatal, or on asymptomatic, but persistent infection that cause neurologic sequelae later in life. Further on the author presents: Viral infections: rubella virus, cytomegalovirus, - herpes virus hominis, hepatitis B, Coksackie, HIV, measles virus, mumps virus, Varicella-zoster virus; - bacterial infections; - rickettiene infections; - infections with mycoplasme and chlamydia; - mycotic infections; - protozoar infections (toxoplasma, malaria, leishmaniasis - Kala - Azar, trypanosomiasis); - parasitic infections (echinococosis, schistosomiasis, ankilostomiasis). [ABSTRACT FROM AUTHOR]

Although the term ‟congenital„ is inaccurate it is so widely accepted that it is used interchangeably with ‟prenatal„ as signyfing syphilis acquired in utero or at birth. Prenatal (congenital) syphilis, reported among infants under a year of age, is estimates with a incidence in growing during the past decade, result from environmental factors of climate and culture and, possibly also, genetic differences in parasit or host, or both (Finberg L. 2000). The author presents: etiology; transmission of prenatal syphilis; pathogenesis and clinical manifestation in early congenital (prenatal) syphilis; in late congenital syphilis; diagnosis; treatment and prophylaxy. [ABSTRACT FROM AUTHOR]

A generic group of parasitic (toxoplasmosis), viral pathogens [rubella, cytomegalovirus (CMV) and herpes simplex] and ‟other„ agents responsible for fetal infections, such as varicella zoster, parvovirus, human immunodeficiency virus (HIV), hepatitis B virus and Borrelia burgdorferi that produce congenital or perinatally acquired infections represents the acronym ‟TORCH„. Many of the clinical manifestations of TORCH infections are similar and include intrauterine growth retardation, nonimmune hydrops, anemia, thrombocytopenia, jaundice, hepatosplenomegaly, chorioretinitis and congenital malformations. In this article the author presents toxoplasmosis, rubella, cytomegalovirus infection and herpes simplex infection. [ABSTRACT FROM AUTHOR]