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Seroprevalence of Cytomegalovirus in Antenatal Cases with Bad Obstetric History at Warangal, Telangana, India

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Seroprevalence of Cytomegalovirus in Antenatal Cases with Bad Obstetric History at Warangal, Telangana, India Int.J.Curr.Microbiol.App.Sci (2015) 4(11): 422-430 ISSN: 2319-7706 Volume 4 Number 11 (2015) pp. 422-430 http://www.ijcmas.com Original Research Article Seroprevalence of Cytomegalovirus in Antenatal Cases with Bad Obstetric History at Warangal, Telangana, India M. Ram Mohan Rao1* and Syam D Gopal2 Department of Microbiology, SRMC, Akathumuri, Arkala, Kerala, India Department of General Medicine, SRMC, Akathumuri, Varkala, Kerala, India *Corresponding author A B S T R A C T The occurrence of foetal death and malformation is one of the tragedies that confront the physician providing obstetric care, his patient and her family as well. The pregnant woman and her fetus are susceptible to many factors affecting the outcome of pregnancy, notable among which are infections. Some of these infections may be quite serious and live threatening for the mother, where as others may have a profound impact on neonatal outcome by virtue of a high likelihood of fetal infection. Generally speaking, the pregnant woman is immune competent. Considering the possible effects of decreased immune surveillance during K e y w o r d s pregnancy, the rate of susceptibility to infection is high. Among the various infectious agents, viruses are most important followed by bacteria and protozoa. Cytomegalo - Among the viral infections in pregnancy, include Rubella, Cytomegalovirus, Herps virus in simplex, Parvovirus B, Varicella, Hepatitis B and Human Immunodeficiency Virus antenatal (HIV). Cytomegalovirus is reported to occur in high incidence. The causative agent cases, Pregnant Cytomegalovirus is transmitted to body through transplacental, intrapartum and woman through Human Milk. Infection in Pregnancy may cause abortion, still birth and physical defects, growth deficit and physical dysfunction. The Infected infant may be quite normal at birth, but later develop certain sequelae. Considering all the above factors, it is worthwhile to conduct a study to know the seroprevalence of Cytomegalovirus in antenatal women having bad obstetric history with increased incidence of fetal loss either by way of abortions, still births or congenital malformations. The present study is hence attempted to assess the Seroprevalence of Cytomegalovirus in high risk pregnancies in antenatal women attending the Government Maternity Hospital, Hanamkonda with a view to help the Clinician to arrive at a proper diagnosis which will in turn result in a better antenatal care and management. Introduction A number of microbiological agents may The true incidence of infection in pregnant produce pregnancy loss without significant women is not known and the contribution of evidence of maternal disease. infection to abortion, congenital 422 Int.J.Curr.Microbiol.App.Sci (2015) 4(11): 422-430 malformation and fetal disease can only be individuals to a primary CMV infection or guessed. to reactivation of latent inflection, which may lead to fulminant and life-threatening The cytomegaloviruses (CMVS) are a disease that can be difficult to treat despite distinct, widely distributed subgroup of available antiviral drugs. herpes viruses that share common growth characteristics and induce acytopathology Morphology involving characteristic nuclear and cytoplasmic inclusions. Viruses in this group CMV is one of the herpiviruses with a were generally known as salivary gland genome of 240 kb and a virus diameter of viruses until the common name 200nm. It contains double-stranded DNA in cytomegalovirus was proposed by Weller to a 64nm core enclosed by an icosahedral reflect both virus-induced cytopathic effects capsid composed of 162 capsomers. The and the virus role in congenitally acquired core is assembled in the nucleus of the host cytomegalic inclusion disease. cells. The capsid is surrounded by a poorly defined amorphous tegument in which it is Cytomegalo viruses are the principal surrounded by a loosely applied, lipid members of the beta herpes virus subgroup containing envelop. The envelope is and they share several characteristics with acquired during the budding process through other herpes viruses, including virion the nuclear membrane in to a cytoplasmic structure and the ability to establish vacuole which contains the protein persistent and latent infection. The CMV s components of the envelop. Mature viruses exhibit a number of distinguishing biologic exit the cell by reverse pinocytosis. characteristics common to the beta herpes Serologic tests do not define specific viruses, including salivary gland tropism, serotypes. In contrast, restriction strict species specificity, and slow growth in endonuclease analysis of CMV-DNA shows cultured cells, all of which have been that, although all know human strains are reviewed. genetically homologous, none are identical unless they were obtained from In most areas of the world, human CMV epidemiologically related cases. spreads at an early age and infects a large majority of the population. This pattern has It is the most common cause of perinatal been altered by increased hygiene in infection and evidence for foetal infections developed countries, where this virus may is found in from 0.5 to 2% of all neonates. reach only 40% to 60% of the population. In the developed world, a large proportion of The genome, surrounded by a tegment or the adult population remains susceptible to matrix and enveloped in a lipid bilayer primary infection increasing the risk of carrying a large number of virus encoded congenital transmission and subsequent glycoprotein s such a disease. The importance of human CMV as a pathogen has also a reason over the past 3 a. Virion proteins decades with the increase in organ b. Capsid proteins allografting and immunosuppressive post c. Envolop clycoproteins transplant therapies and the increase in d. Tegment proteins acquired immunodeficiency syndrome e. Host proteins (AIDS). Their conditions predispose 423 Int.J.Curr.Microbiol.App.Sci (2015) 4(11): 422-430 Viral DNA are commonly used for propagation and isolation of CMV. The genome of human CMV (235 Kbp) contains internal repeats in a class E genome Pathogenesis, persistence, and latency structure and undergoes inversion of two genome components similar to HSV-1. The Human CMV exhibits a ubiquitous pattern genomes of all other characterized beta of distribution and efficient transmission via herpes viruses, including all the animal direct contact in all areas of the world CMVs, are linear and lack internal repeats. regardless of socio-economic The human CMV genome has two unique conditions. The usually benign primary components, UL and US flanked by inverted infection by this virus is repeats b (TRL/TRL) and C (TRS/TRS). Controlled by a combination of innate and Genome organization adaptive immune control functions, after which latent infectio0n continues for life. The only human CMV strain that has been Primary infection, lifelong latency, and completely sequenced is a laboratory- intermittent shedding resulting from adapted strain, AD 169. reactivation commonly occur without any marked disease consequences. These The AD 169 strain of human CMV chosen characteristics underscore the remarkable for genome sequence analysis is a variant balance this pathogen has developed with its (AD 169 var UK) that was propagated under host. growth conditions to attenuate virulence for its use as a live attenuated vaccine. Its Primary infection typically starts with genome was plasmid cloned following 25 replication in mucosal epithelium as a result yrs. of serial passage in various laboratories. of direct contact with infectious secretions The reported sequence contains errors from an infected individual. A high requiring corrections as well as omissions incidence of infection in the general that complicate its use as a prototype. population and accumulating evidence that hand-washing prevents acquisition of CMV Infectious agent from infants who shed high levels of virus in urine and saliva provide excellent evidence (Propagation and cytopathic effect in cell that this virus reaches a large proportion of culture) the population because it is efficiently transmitted. A systemic phase of infection Although a variety of cell culture systems disseminates virus in the host via a are permissive, human CMV is propagated leukocyte associated viremia that may last best in fibroblasts of human origin. The for several months as assessed using assays growth of human CMV is characterized by a for viral DNA or viral antigen. Cell-free relatively prolonged replication cycle and infectious virus is not found in blood, distinctive focal cytopathic effect (CPE) although viral DNA, somehow protected with cell enlargement and rounding (OWL s from degradation, is detected in plasma from EYE). immune compromised individuals. Peripheral blood (PB) neutrophils, Human foreskin fibroblasts and the human monocytes and endothelial cell have been embryonic fibroblasts, WI-38 and MRC-5 observed to carry infectious virus in 424 Int.J.Curr.Microbiol.App.Sci (2015) 4(11): 422-430 immunocompromised host, but the role of where blood leukocytes are an important particular leukocyte subsets as vehicles for reservoir for transmission. P.B mononuclear dissemination during primary infection in cells in the myeloid lineage support latent the immunocompetent host is still unclear. infection. Latently infected cells most likely The suggestion that neutrophils act as originate from the bone marrow in healthy vehicles to disseminate infectious virus and seropositive individuals and virus has viral products has been supported
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