Norwalk virus and srsv symptoms

However, foodhandlers might contaminate food items during preparation. The risk for contamination through foodhandlers is increased when the food item is consumed without further cooking e. Passengers and crew members on cruise ships and naval vessels are frequently affected by outbreaks of NLV gastroenteritis 35,92, These ships dock in countries where levels of sanitation might be inadequate, thus increasing the risk for contamination of water and food taken aboard or for having a passenger board with an active infection.

After a passenger or crew member brings the virus on board, the close living quarters on ships amplify opportunities for person-to-person transmission. Furthermore, the arrival of new and susceptible passengers every 1 or 2 weeks on affected cruise ships provides an opportunity for sustained transmission during successive cruises.

NLV outbreaks extending beyond 12 successive cruises have been reported Consequently, efforts to prevent both the initial contamination of the implicated vehicle and subsequent person-to-person NLV transmission will prevent the occurrence and spread of NLV gastroenteritis outbreaks. Theoretically, any food item can potentially be infected with NLVs through fecal contamination.

However, certain foods are implicated more often than others in outbreaks of NLV gastroenteritis. Shellfish e. In addition, cooking e. Until reliable indicators for routine monitoring of viral contamination of harvest waters and shellfish are available, measures to prevent the contamination of harvest waters with human waste e. Food contamination by infectious foodhandlers is another frequent cause of NLV gastroenteritis outbreaks. Because of the low infectious dose of NLVs and the high concentration of virus in stool, even a limited contamination can result in substantial outbreaks.

Ready-to-eat foods that require handling but no subsequent cooking e. Previously, the exclusion of ill foodhandlers for hours after resolution of illness was recommended to prevent outbreaks caused by foodhandlers Data from recent human volunteer and epidemiologic studies demonstrate that viral antigen can be shed for a longer duration after recovery from illness and in the absence of clinical disease.

Although data are limited regarding whether this detectable viral antigen represents infectious virus, foodhandlers should be required to maintain strict personal hygiene at all times. Although waterborne outbreaks are far less common than foodborne outbreaks, NLV gastroenteritis outbreaks have been associated with sources of contaminated water, including municipal water, well water, stream water, commercial ice, lake water, and swimming pool water.

Because current analytic methods do not permit direct monitoring of NLVs in water, indicator organisms e. However, because the size, physiology, and susceptibility to physical treatment and disinfection of bacterial indicators differ from those of NLVs, inherent limitations of this approach exist.

Until reliable methods for assessing the occurrence and susceptibility to treatment of NLVs are available, prevention methods should focus on reducing human waste contamination of water supplies. If drinking or recreational water is suspected as being an outbreak source, high-level chlorination i. Person-to-person spread of NLVs occurs by direct fecal-oral and airborne transmission.

Such transmission plays a role in propagating NLV disease outbreaks, notably in institutional settings e. Although interruption of person-to-person transmission can be difficult, certain measures might help.

Frequent handwashing with soap and water is an effective means of prevention. Because spattering or aerosols of infectious material might be involved in disease transmission, wearing masks should be considered for persons who clean areas substantially contaminated by feces or vomitus e. Soiled linens and clothes should be handled as little as possible and with minimum agitation.

They should be laundered with detergent at the maximum available cycle length and then machine dried. Because environmental surfaces have been implicated in the transmission of enteric viruses, surfaces that have been soiled should be cleaned with an appropriate germicidal product e.

In situations in which the epidemic is extended by periodic renewal of the susceptible population e. The following sections provide a summary of the commonly available diagnostic methods, which are extensively reviewed elsewhere Under the electron microscope, NLVs can be identified by their characteristic morphology.

In one type of IEM, convalescent-phase serum from patients is coated on the examination grid of the microscope before stool specimens are applied. The antibody on the grid traps homologous virus, thereby increasing diagnostic yield.

However, IEM has certain disadvantages, the greatest of which is that success is highly dependant on the skill and expertise of the microscopist. Furthermore, the virus might be totally masked if a large excess of antibody is present, resulting in a false-negative test. The expression in baculoviruses of the capsid proteins of NLVs that self-assemble into stable virus-like particles has allowed the detection of these viruses by ELISAs. To develop assays to detect virus in fecal specimens, the expressed capsid antigens have been used to generate hyperimmune antibodies in laboratory animals.

To date, these assays have been type-specific, but broadly reactive tests are under development. The baculovirus-expressed viral antigen can be directly used for detection of antibodies to NLVs in patient's sera by enzyme immunoassay. Because certain adults have preexisting immunoglobulin G IgG antibodies to NLVs, a single serum specimen is insufficient to indicate recent infection.

In outbreak settings, if at least half of affected persons seroconvert to a specific NLV, that viral strain can be designated as etiologic. Titers can begin to rise by the fifth day after onset of symptoms, peak at approximately the third week, and begin to fall by the sixth week. Hence, for IgG assays, the acute-phase serum should be drawn within the first 5 days and the convalescent-phase serum during the third to sixth weeks. In certain cases where diagnosis is critical e.

In addition to potential difficulties in obtaining an adequate number of serum specimens during outbreaks, serologic assays are currently limited by the fact that the available array of expressed NLV antigens is insufficient to detect all antigenic types of NLVs.

High sensitivity of these assays i. Efforts are ongoing to develop universal or degenerate primers that would detect the majority of NLV strains that cause gastroenteritis outbreaks. Application of new molecular diagnostics has expanded the scope of outbreak investigations, as demonstrated in recent outbreaks Table 2 , because outbreak source vehicles e. However, these methods are not sufficiently developed to be routinely applied. Through nucleotide sequencing, establishing an irrefutable genetic link between outbreaks that occur through a single contaminated vehicle that is distributed in multiple geographic locations is possible.

Specimen collection for viral testing should begin on day 1 of the epidemiologic investigation. Any delays to await testing results for bacterial or parasitic agents could preclude establishing a viral diagnosis. Ideally, specimens should be obtained during the acute phase of illness i.

With the development of sensitive molecular assays, the ability to detect viruses in specimens collected later in the illness has been improved. In specific cases, specimens might be collected later during the illness i. If specimens are collected late in the illness, the utility of viral diagnosis and interpretation of the results should be discussed with laboratory personnel before tests are conducted.

Number and Quantity. Bulk samples i. Serial specimens from persons with acute, frequent, high-volume diarrhea are useful as reference material for the development of assays.

The smaller the specimen and the more formed the stool, the lower the diagnostic yield. Rectal swabs are of limited or no value because they contain insufficient quantity of nucleic acid for amplification. Storage and Transport. Because freezing can destroy the characteristic viral morphology that permits a diagnosis by EM, specimens should be kept refrigerated at 4 C. At this temperature, specimens can be stored without compromising diagnostic yield for weeks, during which time testing for other pathogens can be completed.

If the specimens have to be transported to a laboratory for testing, they should be bagged and sealed and kept on ice or frozen refrigerant packs in an insulated, waterproof container. If facilities for testing specimens within weeks are not available, specimens can be frozen for antigen or PCR testing. Vomiting is the predominant symptom among children, and specimens of vomitus can be collected to supplement the diagnostic yield from stool specimens during an investigation.

Recommendations for collection, storage, and shipment of vomitus specimens are the same as those for stool specimens. Acute-phase specimens should be obtained during the first 5 days of symptoms, and the convalescent-phase specimen should be collected from the third to sixth week after resolution of symptoms. Ideally, 10 pairs of specimens from ill persons i. Adults should provide ml of blood, and children should provide ml.

Specimens should be collected in tubes containing no anticoagulant, and the sera should be spun off and frozen. If a centrifuge is not available, a clot should be allowed to form, and the serum should be decanted and frozen.

If this step cannot be accomplished, the whole blood should be refrigerated but not frozen. NLVs cannot be detected routinely in water, food, or environmental specimens. Nevertheless, during recent outbreaks , NLVs have been detected successfully in vehicles epidemiologically implicated as the source of infection. If a food or water item is strongly suspected as the source of an outbreak, then a sample should be obtained as early as possible and stored at 4 C.

If the epidemiologic investigation confirms the link, a laboratory with the capacity to test these specimens should be contacted for further testing.

If drinking water is suspected, special filtration 45 of large volumes i. If, after consultation, viral diagnostic services would be useful, specimens may be shipped to CDC's Viral Gastroenteritis Section with the following provisions: A unique identifier for each patient preferably not the patient's name should be included on each specimen. Stool specimens should be shipped as soon as they can be batched. Individual containers should be verified as being leak proof and then enclosed in a plastic bag.

The entire collection should be bagged in plastic and placed in a padded, insulated box with refrigerant packs. Frozen acute- and convalescent-phase serum samples should be batched and sent in a single shipment.

Waterproof, padded, insulated boxes should be used, with dry ice added to maintain freezing. Whole-blood samples should not be frozen, and refrigerant packs should be used instead of dry ice. Final notification should be made by telephone to immediately before shipping. All suspected foodborne outbreaks of viral gastroenteritis for which specimens are sent to CDC for laboratory testing should be reported to CDC on a standard form.

Visualization by immune electron microscopy of a nm particle associated with acute infectious nonbacterial gastroenteritis. J Virol ; Virus particles in epithelial cells of duodenal mucosa from children with acute non-bacterial gastroenteritis. Lancet ; Appleton H, Higgins PG. Viruses and gastroenteritis in infants [Letter]. Viruses in infantile gastroenteritis [Letter]. Stool viruses in babies in Glasgow. Hospital admissions with diarrhoea. J Hyg ; Solid-phase microtiter radioimmunoassay for detection of the Norwalk strain of acute nonbacterial, epidemic gastroenteritis virus and its antibodies.

J Med Virol ; There appeared to be no secondary cases among household contacts to suggest person to person spread. Two controls at one of the above functions ate oysters but did not develop any symptoms.

All other controls did not consume oysters. No other food item or beverage listed on function or restaurant menus were significantly associated with illness.

The number of oysters consumed by individuals was not consistently reported to enable the calculation of a dose-response effect. Figure 1. Number of cases of gastroenteritis following oyster consumption, by date of onset.

Seven faecal samples, including two collected during the acute phase of illness, were submitted for laboratory analysis.

All were negative for ova, cysts and parasites, and for bacterial pathogens including Salmonella spp. Faecal specimens examined by electron microscopy and immune electron microscopy failed to detect any virus particles. None of the above bacterial pathogens were detected in any of the raw oyster specimens.

However, faecal coliform counts were elevated in some oyster samples Australian Food Standards Code recommends a maximum E. A composite oyster sample was positive for adenovirus by PCR. Norwalk virus was not detected in this oyster sample. Environmental investigations indicated that the oysters associated with this food-poisoning outbreak were harvested from a common source, the Terranora Broadwater area at Tweed Heads.

Water quality testing of numerous sampling sites near oyster harvest areas during a two week period showed faecal coliform counts varying between 4 per ml and per ml National Health and Medical Research Council, United States Food and Drug Authority and New South Wales Environmental Protection Agency guidelines recommend maximum faecal coliform levels of 14 per ml. These included leaking sewerage pipes, a leaking sub-marine sewerage pipe, septic tanks in the residential development on one side of the Broadwater, and stormwater drain discharges.

Any contamination would be exacerbated by the poor tidal exchange in the Broadwater area. The timing of tidal discharge outgoing tide by the sewage treatment plants was in accordance with regulations. Two out of five oyster purification plants on the Tweed River were currently in use and found to have unsatisfactory purification and sterilisation techniques, although the limitations of these in removing viruses is widely acknowledged.

The findings from this investigation clearly implicated oysters as the likely vehicle of transmission for this outbreak. Although the wide confidence interval around the odds ratio indicates a small study sample, it is unlikely that any other food or beverage item would be causally associated with this illness given the strength of the association with oysters. Similarly, the poor questionnaire response rate of the controls and the different approaches to data collection by each public health unit may have introduced biases into the study.

However, it is unlikely that these would change the findings of this investigation. The number of cases related to this outbreak was probably considerably greater than the 97 cases identified, either because patients experienced only mild symptoms, or health authorities were not informed.

However, the management of media releases assisted in the identification of unknown cases. The bimodal epidemic curve reflects two separate large functions held on consecutive weekends. Of the 94 persons known to eat oysters, all but two developed gastroenteritis. In contrast, only one out of 30 persons who were known not to consume oysters developed the illness. It is possible that the two subjects who did not become ill ate uncontaminated oysters, or both may have had asymptomatic infection.

The aetiological agent responsible for gastroenteritis appears to be Norwalk virus. This is a small round structured RNA virus SRSV which has previously been implicated as the aetiological agent in a number of acute non-bacterial gastroenteritis outbreaks. Oysters have also been shown to transmit bacterial and other viral pathogens including Shigella spp.

The incubation period and clinical symptoms of cases were consistent with a Norwalk-like infection, according to 'Kaplan's criteria'. These criteria have been shown to have a relatively high specificity and sensitivity for a Norwalk-like infection during outbreaks of gastroenteritis. Although the gastroenteritis is usually self-limiting and not life-threatening, the likelihood of more severe disease may be increased for immunocompromised persons and the elderly. Norwalk virus was not detected in seven faecal specimens tested by electron microscopy.

However, the sensitivity of electron microscopy is limited if faecal specimens for viral examination are not collected within 48 hours of onset of illness.

The recent development of RT-PCR as a diagnostic tool has improved detection rates, and the sensitivity of this test enables faecal specimens to be submitted up to seven days after the onset of illness. The application of Kaplan's criteria as a screening tool would be helpful in determining whether faecal specimens should be sent for molecular diagnostic testing during outbreaks, particularly if there is a delay in the collection time of specimens rendering them unsuitable for electron microscopy.

Serological testing was not requested for any of the cases involved in this outbreak. Enzyme immunoassay EIA and radioimmunoassay RIA techniques have been used for the detection of Norwalk virus during foodborne outbreaks. This would complement faecal diagnostic testing, and also address the difficulty in detecting Norwalk virus in stools, and the poor compliance with submitting stool specimens during gastroenteritis outbreaks. The elevated faecal coliform counts in some of the oyster samples, and the identification of adenovirus in a composite oyster sample, indicate probable sewage contamination.

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