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

Nearly one thousand different types of viruses are known to infect humans and it is estimated that they account for approximately 60% of all human infections (Horsfall 1965).

Viruses are spread easily through closed environments such as the home, schools, workplaces, transport systems, etc. Although many of the respiratory and gastrointestinal infections caused by viruses can be asymptomatic or relatively mild and self‐limiting (coughs and colds, etc.), they still represent a significant economic burden. Increasing numbers of people who have reduced immunity to infection, for whom the consequences of infection can be much more serious, are now cared for at home. At risk groups include not only the immunocompromised but also the elderly, neonates, pregnant women, hospital patients discharged into the community, individuals using immunosuppressive drugs and also those using invasive systems (indwelling catheters) or inhalation systems or devices. Otherwise healthy family members with asthma or allergies also have increased susceptibility to infection. In the UK it is estimated that one in six people in the community belong to an ‘at risk’ group (Bloomfield 2001). World Health Organisation estimates suggest that, by 2025, there will be more than 800 million people over 65 years old in the world, two‐thirds of them in developing countries (Anon. 1998).

Viruses are probably the most common cause of infectious disease acquired within indoor environments. Close personal contact within the home and community settings, such as daycare centres and schools, makes them ideal places for the spread of viral infections. Infected individuals can shed up to 1012 virus particles per ml of faeces with the possibility of transfer of the virus by contaminated hands to surfaces in the bathroom or toilet. Viruses that cause tonsillitis, colds, croup, bronchiolitis, influenza, pneumonia and other respiratory tract infections can be spread in aerosolized droplets. Aerosols produced by coughing, sneezing and talking can be inhaled directly by a susceptible host or may settle onto surfaces. Touching hands or fomites, such as eating utensils, towels or doorknobs, inadvertently contaminated with fresh secretions or vomit, etc. from an infected person and then transferring the virus from the hands to the eyes, nose or mouth, are further routes of spread. Infants are especially vulnerable to such infections because they frequently place objects, such as toys, into their mouths. Transfer of viruses to food during handling and preparation via hands and food contact surfaces is an important route of spread of viral gastroenteritis.

Amongst health care professionals there is growing awareness that improved standards of hand, surface and air hygiene in community settings could do much to prevent the spread of viral infections within these environments. The purpose of this paper is to review the evidence base for this assumption. Since viral infections are not easily treated, prevention of infection is still the main route of control. Assessment of the impact of hygiene is made difficult by the general lack of quantitative epidemiological data and, even where evidence for cross‐contamination as a causative factor in an outbreak exists, it is always circumstantial. A further problem in assessing whether contamination found on hands or other surfaces might represent a hazard is that the infectious dose can vary significantly according to the pathogenicity of the organism and the immune status of the host. Thus the case for practising good hygiene in these settings rests largely on evidence showing that cross‐contamination can occur in these environments coupled with laboratory data demonstrating the efficacy of hygiene procedures in minimizing microbiological contamination.

/pdf/spread-and-prevention-of-some-common-viral-infections-in-1nr4q5zs4r.pdf

Spread and prevention of some common viral infections in community facilities and domestic homes

Diarrhea in neonates, followed as a cohort, and their families was studied prospectively. The families were followed for an average of 16.3 months. Stool and serum specimens were obtained at least every three months. Stool specimens were examined for viruses by electron microscopy and cultured for enteropathogens, and serum specimens were tested for antibodies to rotavirus and Norwalk virus. During the study, 237 episodes of gastroenteritis were observed in 104 infants and their 62 siblings. Rotavirus, detected 82 times in 72 children, was by far the most common enteropathogen. It was associated with gastrointestinal symptoms in 72% (with diarrhea in 65%). Rotavirus diarrhea occurred mostly in winter months and was significantly more frequently associated with respiratory symptoms than were diarrheas with other etiologies. Rotavirus infection was uncommon in the first six months of life, but by two years of age, 62% of the infants had had at least one infection. Neither breast feeding nor the presence of antibody to rotavirus in cord blood appeared to be protective.

/pdf/a-prospective-study-of-rotavirus-infection-in-infants-and-1kwdqeh8ss.pdf

A Prospective Study of Rotavirus Infection in Infants and Young Children

Rotaviruses infect mature, differentiated enterocytes of the small intestine and, by an unknown mechanism, escape the gastrointestinal tract and cause viremia. The neonatal rat model of rotavirus infection was used to determine the kinetics of viremia, spread, and pathology of rotavirus in extraintestinal organs. Five-day-old rat pups were inoculated intragastrically with an animal (RRV) or human (HAL1166) rotavirus or phosphate-buffered saline. Blood was collected from a subset of rat pups, and following perfusion to remove residual blood, organs were removed and homogenized to analyze rotavirus-specific antigen by enzyme-linked immunosorbent assay and infectious rotavirus by fluorescent focus assay or fixed in formalin for histology and immunohistochemistry. Viremia was detected following rotavirus infection with RRV and HAL1166. The RRV 50% antigenemia dose was 1.8 x 10(3) PFU, and the 50% diarrhea dose was 7.7 x 10(5) PFU, indicating that infection and viremia occurred in the absence of diarrhea and that detecting rotavirus antigen in the blood was a more sensitive measure of infection than diarrhea. Rotavirus antigens and infectious virus were detected in multiple organs (stomach, intestines, liver, lungs, spleen, kidneys, pancreas, thymus, and bladder). Histopathological changes due to rotavirus infection included acute inflammation of the portal tract and bile duct, microsteatosis, necrosis, and inflammatory cell infiltrates in the parenchymas of the liver and lungs. Colocalization of structural and nonstructural proteins with histopathology in the liver and lungs indicated that the histological changes observed were due to rotavirus infection and replication. Replicating rotavirus was also detected in macrophages in the lungs and blood vessels, indicating a possible mechanism of rotavirus dissemination. Extraintestinal infectious rotavirus, but not diarrhea, was observed in the presence of passively or actively acquired rotavirus-specific antibody. These findings alter the previously accepted concept of rotavirus pathogenesis to include not only gastroenteritis but also viremia, and they indicate that rotavirus could cause a broad array of systemic diseases in a number of different organs.

Rotavirus Viremia and Extraintestinal Viral Infection in the Neonatal Rat Model

A disseminated viral illness was demonstrated by isolating a virus from the CSF, blood or urine in 27% of 73 children who were admitted to hospital after a first febrile convulsion. However, a viral aetiology could be implicated for 86% of the children after combining results of tissue culture, electron microscopy, mouse inoculation, complement fixation tests, and interferon assay. Parallel bacterial cultures showed a possible pathogen in 29% of children, but in only 4% was the pathogen isolated from the CSF, blood, or urine. No correlation was found between the nature of the pathogen (or evidence of its dissemination) and the severity of the convulsion, degree of fever, CSF protein, CSF white cells, or the WBC. The results suggest that a febrile convulsion could be a response to invasion of the blood stream or central nervous system by a micro-organism which is usually a virus. Invasion may be of such brief duration that successful isolation of the virus from the blood, CSF, or urine in not more commonly achieved.

https://adc.bmj.com/content/archdischild/54/11/869.full.pdf

Role of viruses in febrile convulsions.

In a hospital study rotavirus was identified in 51% of 152 children with diarrhoea. These patients showed a clinical pattern that was distinct from patients in whom the diarrhoea was associated with bacteria, other viruses, or no pathogens. A respiratory illness was described in 66% of rotavirus patients and usually preceded the gastrointestinal symptoms. Vomiting lasted between one and 3 days and was curtailed by substituting the normal diet with clear fluids. Watery diarrhoes continued for 4 or 5 days, even when rehydration was by the intravenous rather than the oral route. Prolonged diarrhoea was rare. Most children infected with rotavirus were under 2 years of age, but dehydration was most severe in infants aged between 12 and 18 months. A clinician can thus recognise the rotavirus syndrome and expect spontaneous recovery if adequate rehydration is maintained for a critical few days.

A year's experience oftherotavirus syndrome and its association withrespiratory illness

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A year's experience oftherotavirus syndrome and its association withrespiratory illness