MOBILE VIEW  | 

FOODBORNE ILLNESS-NOROVIRUS

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Noroviruses are nonenveloped, single-stranded RNA viruses in the genus Norovirus and the family Caliciviridae. They are the most common cause of epidemic gastroenteritis, and are believed to be responsible for at least half of all gastroenteritis worldwide, in addition to being a major source of foodborne illness and a significant cause of traveler's diarrhea.

Specific Substances

    1) Norovirus (synonym)
    2) Norwalk-like virus (synonym)
    3) NLV (synonym)
    4) Small round-structured viruses (synonym)
    5) SRSVs (synonym)
    6) Food poisoning norovirus (synonym)
    7) Norovirus food poisoning (synonym)

Available Forms Sources

    A) FORMS
    1) Noroviruses are divided into at least 5 genogroups, designated GI through GV, based on the amino acids in their major structural protein. The strains GI, GII, and GIV infect humans. The GIII strain infects cows and GV infects mice. There have been GII and GIV strains responsible for diarrhea in dogs, and there are GII strains that infect pigs, but interspecies transmission has not been documented to date. Noroviruses can be further subclassified into genotypes. The GII.4 viruses have been responsible for the most viral gastroenteritis outbreaks worldwide (Hall et al, 2011).
    2) Pandemics caused by new genotypes of norovirus, particularly the GII.4 genotype, have been reported about every 2 years since 2002. This is believed to be related to the ability of norovirus to mutate; the mutation rate is said to be higher than that of influenza viruses (Apelt et al, 2010).
    B) SOURCES
    1) Humans are the only known reservoir for norovirus. Transmission can occur from person-to-person, foodborne or waterborne spread. Spread from person-to-person may be through the fecal-oral route, ingestion of aerosolized vomitus, or indirectly via fomites or contaminated surfaces. Foodborne spread is most commonly from infected food handlers during food preparation or service. It may also occur from agricultural contamination with human waste or during food processing. Well water can become contaminated from leaking of septic tanks or sewage systems. Recreational water can become contaminated from inadequate chlorination (Hall et al, 2011; Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    2) SPORADIC DISEASE
    a) Norovirus is the leading cause of sporadic gastroenteritis in people of all ages. It is estimated that noroviruses account for 10% to 15% of severe gastroenteritis cases in children younger than 5 years, and for 9% to 15% of cases of mild to moderate diarrhea in people of all ages (Hall et al, 2011).
    3) OUTBREAKS
    a) In the United States, an estimated 5.5 million norovirus infections (estimated range, 3.2 million to 8.3 million cases of foodborne illness) occur annually, accounting for 58% of all foodborne illnesses. This results in approximately 0.03% of patients (range, 8097 to 23,323; mean, 14,663) requiring hospitalization and less than 0.1% of these illnesses resulting in death (range, 84 to 237 deaths; mean, 149) (Center for Food Safety and Applied Nutrition (CFSAN), 2012).
    b) Noroviruses are the most common cause of gastroenteritis outbreaks worldwide. Outbreaks often occur in the following settings: long-term care facilities, other healthcare facilities, restaurants, catered events, schools and other institutions, and cruise ships (Hall et al, 2011).
    c) About 30% to 50% of norovirus outbreaks occur in closed facilities (eg, hospitals, retirement centers, nursing homes). During 2000-2001 the CDC estimates that 28% of norovirus outbreaks occurred in restaurants or catered events, 16% on cruise ships, and 8% in daycare centers (Said et al, 2008). One outbreak was reported at a catered conference in a hospital setting (Vinnard et al, 2012).
    d) Duration of outbreaks is generally longer in healthcare facilities than in other settings. In a meta-analysis of outbreaks in closed settings published through June 2008, outbreaks in hospitals lasted a mean of 19 days (range: 6 to 92 days), in nursing homes the mean duration of an outbreak was 16 days (range: 3 to 44 days) and in non-healthcare settings the mean duration of outbreaks was 7 days (range: 1 to 26 days) (Harris et al, 2008).
    4) SOURCES OF CONTAMINATION
    a) Most foodborne infections develop from fecal-oral transmission in one of two ways. Primary contamination develops when food is contaminated prior to harvest, for example shellfish grown in sewage contaminated waters or vegetables or soft fruits sprayed or irrigated with contaminated water. Secondary contamination occurs at harvest, or during food processing or serving, and results from use of contaminated water, contaminated preparations surfaces, or transmission of infection from a food handler (Tuan Zainazor et al, 2010).
    b) Food handlers have been implicated as the most common source of contamination leading to outbreaks, in those cases where the source of the outbreak could be identified (Dreyfuss, 2009).
    c) Commonly implicated foods include prepared foods such as salads, sandwiches and baked goods, and raw or poorly cooked meat or seafood. Fruits and vegetables that are usually consumed without heating are also common sources (Tuan Zainazor et al, 2010). Sandwiches, potato chips, and ice were implicated in one outbreak (Vinnard et al, 2012).
    d) Fruits and vegetables may be contaminated prior to harvest from use of irrigation water contaminated with feces, or organic fertilizers. Bivalve shellfish can become contaminated from fecally contaminated seawater. Other seafood is generally secondarily contaminated during processing or serving (Tuan Zainazor et al, 2010).
    5) SEASONAL VARIATION
    a) Studies show that there is an increase in norovirus outbreaks by up to 25% in the colder months of the year and a decrease in the warmer months (Dreyfuss, 2009).
    6) COINFECTION
    a) Coinfection with norovirus and bacteria causing gastroenteritis has been reported, particularly in cases of traveler's diarrhea (Ajami et al, 2010). Coinfection with other gastroenteritis causing viruses has also been reported in both outbreaks and sporadic cases (Liu et al, 2010).
    7) FATALITIES
    a) Fatalities are rare and occur almost exclusively in the elderly. A study in England and Wales suggested that norovirus infection might be associated with about 80 deaths a year in patients over the age of 65 (Harris et al, 2008).

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) CAUSATIVE ORGANISM
    1) Noroviruses are nonenveloped, single-stranded RNA viruses in the genus Norovirus and the family Caliciviridae.
    B) EPIDEMIOLOGY
    1) In the United States, an estimated 5.5 million norovirus infections (estimated range, 3.2 million to 8.3 million cases of foodborne illness) occur annually, accounting for 58% of all foodborne illnesses. This results in approximately 0.03% of patients (range, 8097 to 23,323; mean, 14,663) requiring hospitalization and less than 0.1% of these illnesses resulting in death (range, 84 to 237 deaths; mean, 149). Noroviruses are the leading cause of sporadic gastroenteritis, and the leading cause of gastroenteritis outbreaks worldwide. It is extremely contagious. Infections are common, but fatalities are very rare and generally only occur in patients with severe underlying health problems. Approximately, 10% of patients are ill enough to seek medical attention. Common settings for outbreaks include long-term care facilities, other healthcare facilities, restaurants, catered events, schools and other institutions, and cruise ships. Outbreaks generally peak in cold weather.
    C) TARGET POPULATION
    1) Norovirus affects people of all ages. Outbreaks involve people in settings that encourage person-to-person spread (ie, semiclosed environments, military, schools, recreational activities). Children under age 5 and adults over age 65, as well as patients with significant underlying medical problems, are at higher risk for complications such as dehydration requiring hospitalization.
    D) MECHANISM
    1) The exact pathogenic pathway of infection is unknown. Noroviruses cause the inflammation of the stomach and the small and large intestines.
    E) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) Illness is typically self-limiting. Severe nausea and vomiting are usually the first sign of illness. Other symptoms include nonbloody watery diarrhea and abdominal cramps. Low-grade fever, headache and myalgias may also develop. Dehydration, hyponatremia, hypokalemia, acute renal insufficiency and mild elevations in aminotransferases may develop in patients with severe gastroenteritis. Up to 30% of patients with norovirus infection are asymptomatic.
    2) CHRONIC SYMPTOMS
    a) Norovirus may exacerbate inflammatory bowel disease, but evidence is inconclusive.
    3) ROUTE OF EXPOSURE
    a) Transmission can occur from person-to-person, or by foodborne or waterborne spread. Spread from person-to-person may be through the fecal-oral route, ingestion of aerosolized vomitus, or indirectly via fomites or contaminated surfaces. Foodborne spread is most commonly from infected food handlers during food preparation or service. It may also occur from agricultural contamination with human waste or during food processing. Well water can become contaminated from leaking of septic tanks or sewage systems. Recreational water can become contaminated from inadequate chlorination. Commonly implicated foods include: prepared foods such as salads, sandwiches and baked goods, and raw or poorly cooked meat or seafood, and fruits and vegetables that are usually consumed without heating.
    4) TIME TO ONSET
    a) Generally 24 to 48 hours (median: 33 to 36 hours) after exposure; onset times within 12 hours have been reported.
    5) DURATION
    a) Symptoms last 12 to 60 hours (mean, 24 to 48 hours) in healthy adults and older children, may resolve within 72 to 96 hours in the elderly, very young children, or hospitalized patients; non-specific symptoms (eg, headache, thirst, vertigo) may last up to 19 days.

Laboratory Monitoring

    A) Monitor serum electrolytes and urine output in patients with severe vomiting and diarrhea.
    B) Reverse transcriptions-polymerase chain reaction assays are sensitive for noroviruses. These assays are sometimes used to identify outbreaks, but not used to guide clinical management of individual patients.
    C) Enzyme immunoassays have been developed, but are generally of low sensitivity and are not widely used.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) SUPPORTIVE CARE
    1) Care is symptomatic and supportive. Administer antiemetics, and intravenous or oral fluids to prevent dehydration.
    B) STANDARD PRECAUTIONS
    1) Always use standard precautions with all patients. Meticulous hand hygiene is imperative for patients, visitors and staff to control transmission. Wash hands well with soap and water for one minute, rinse for 20 seconds and dry with a disposable paper towel. Hands should be washed after eating or drinking, using the bathroom, or contact with patients. An alcohol-based hand sanitizer may not be effective against noroviruses. Use gloves, gown, mask and/or face shield when caring for ill patients depending on the anticipated exposure.
    C) CONTACT PRECAUTIONS
    1) Acutely ill patients should be isolated as much as possible during the acute stage of illness and for 24 to 72 hours after recovery, during the peak period of viral shedding. Do not share equipment between patients. Use gown, gloves and mask or face shield for all interactions that may involve contact with a patient or contaminated areas of the patient's environment. Isolate ill patients to single rooms, or if that is not possible cohort ill patients together. Do not allow visits by sick individuals. Provide different toilet facilities for ill and non-ill patients. Remove supplies from a room before an infected patient is admitted.
    D) ENVIRONMENTAL DISINFECTION
    1) Clean spill with detergent to remove particulate material and then with a hospital approved disinfectant. Chemical disinfectants (ie, at least a 1:50 sodium hypochlorite:water solution) should be used on potentially contaminated environmental surfaces, particularly in bathrooms or on high-touch surfaces like doorknobs, light switches, tables, counter tops, keyboards, and hand rails, every shift. Clean bathrooms every shift. Clean common areas, and staff rooms, including refrigerators. Clean rooms every 24 hours and at patient discharge. Clean floors with approved disinfectant, change cleaning solution and mop head every 3 rooms. Clean rooms that have housed patients with vomiting and/or diarrhea last, change the mop head and solution after cleaning a room that housed an infected patient. Remove and replace curtains, if soiled or contaminated.
    E) PATIENT DISPOSITION
    1) HOME CRITERIA: The vast majority of patients with self-limited vomiting and diarrhea who can tolerate oral fluids can be managed at home.
    2) OBSERVATION CRITERIA: Patients with persistent vomiting, severe diarrhea and those who can not tolerate oral fluids should be referred to a healthcare facility for treatment with antiemetics and intravenous hydration.
    3) ADMISSION CRITERIA: Patients with severe dehydration, electrolyte abnormalities, and those with vomiting that persists despite therapy, may require hospital admission. Infants, the elderly, and patients with significant underlying health problems are more likely to require admission.
    4) CONSULT CRITERIA: Consult an infections disease specialist and the local health department in the event of a significant outbreak, to help identify the source of exposure and reduce further transmission.

Range Of Toxicity

    A) INFECTIVE DOSE: The estimated infectious dose is as low as 1 to 10 viral particles; as high as 1 x 10(12) million viral particles/g feces are excreted by both symptomatic and asymptomatic people. FATALITIES: Fatalities are rare and occur almost exclusively in the elderly.

Summary Of Exposure

    A) CAUSATIVE ORGANISM
    1) Noroviruses are nonenveloped, single-stranded RNA viruses in the genus Norovirus and the family Caliciviridae.
    B) EPIDEMIOLOGY
    1) In the United States, an estimated 5.5 million norovirus infections (estimated range, 3.2 million to 8.3 million cases of foodborne illness) occur annually, accounting for 58% of all foodborne illnesses. This results in approximately 0.03% of patients (range, 8097 to 23,323; mean, 14,663) requiring hospitalization and less than 0.1% of these illnesses resulting in death (range, 84 to 237 deaths; mean, 149). Noroviruses are the leading cause of sporadic gastroenteritis, and the leading cause of gastroenteritis outbreaks worldwide. It is extremely contagious. Infections are common, but fatalities are very rare and generally only occur in patients with severe underlying health problems. Approximately, 10% of patients are ill enough to seek medical attention. Common settings for outbreaks include long-term care facilities, other healthcare facilities, restaurants, catered events, schools and other institutions, and cruise ships. Outbreaks generally peak in cold weather.
    C) TARGET POPULATION
    1) Norovirus affects people of all ages. Outbreaks involve people in settings that encourage person-to-person spread (ie, semiclosed environments, military, schools, recreational activities). Children under age 5 and adults over age 65, as well as patients with significant underlying medical problems, are at higher risk for complications such as dehydration requiring hospitalization.
    D) MECHANISM
    1) The exact pathogenic pathway of infection is unknown. Noroviruses cause the inflammation of the stomach and the small and large intestines.
    E) WITH POISONING/EXPOSURE
    1) ACUTE SYMPTOMS
    a) Illness is typically self-limiting. Severe nausea and vomiting are usually the first sign of illness. Other symptoms include nonbloody watery diarrhea and abdominal cramps. Low-grade fever, headache and myalgias may also develop. Dehydration, hyponatremia, hypokalemia, acute renal insufficiency and mild elevations in aminotransferases may develop in patients with severe gastroenteritis. Up to 30% of patients with norovirus infection are asymptomatic.
    2) CHRONIC SYMPTOMS
    a) Norovirus may exacerbate inflammatory bowel disease, but evidence is inconclusive.
    3) ROUTE OF EXPOSURE
    a) Transmission can occur from person-to-person, or by foodborne or waterborne spread. Spread from person-to-person may be through the fecal-oral route, ingestion of aerosolized vomitus, or indirectly via fomites or contaminated surfaces. Foodborne spread is most commonly from infected food handlers during food preparation or service. It may also occur from agricultural contamination with human waste or during food processing. Well water can become contaminated from leaking of septic tanks or sewage systems. Recreational water can become contaminated from inadequate chlorination. Commonly implicated foods include: prepared foods such as salads, sandwiches and baked goods, and raw or poorly cooked meat or seafood, and fruits and vegetables that are usually consumed without heating.
    4) TIME TO ONSET
    a) Generally 24 to 48 hours (median: 33 to 36 hours) after exposure; onset times within 12 hours have been reported.
    5) DURATION
    a) Symptoms last 12 to 60 hours (mean, 24 to 48 hours) in healthy adults and older children, may resolve within 72 to 96 hours in the elderly, very young children, or hospitalized patients; non-specific symptoms (eg, headache, thirst, vertigo) may last up to 19 days.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) Low grade fever develops in some patients (Hall et al, 2011).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) Hypotension might develop in patients with severe volume loss from vomiting and diarrhea, but is not common.
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) Tachycardia might develop in patients with severe volume loss from vomiting and diarrhea, but is not common.

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures have been reported in young children with norovirus infection (Medici et al, 2010; Tsuge et al, 2010; Glass et al, 2009).
    b) INCIDENCE: In a study of 173 children between the ages of 1 month and 6 years with confirmed norovirus gastroenteritis, 15 patients (8.67%) had afebrile seizures (Chan et al, 2011). In another study of 64 children aged 3 months to 18 years with confirmed norovirus gastroenteritis, 19 (30%) had seizures (Chen et al, 2009). Some of these patients had fevers and/or hyponatremia that may have contributed to the seizures.
    B) DISORDER OF BRAIN
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A previously healthy 15-month-old girl presented with a 2 day history of vomiting and mild dehydration. Blood work was normal, she was treated and sent home. She returned the following day with recurrent seizures. She was febrile (39.8 C), tachycardic (223 beats/min), with a respiratory rate of 62 and a blood pressure of 81/46 mmHg. She was unresponsive to pain and her pupils were sluggish. Laboratory evaluation showed a glucose of 29 mg/dL, lactate 17.4 International Units/L, leukocytosis, normal serum electrolytes and moderately elevated liver enzymes. Tests for influenza and rotavirus were negative, but norovirus immunochromatography was positive. Bacterial cultures (blood, stool and CSF) were negative. The child was treated with intravenous dextrose and hypoglycemia did not recur. MRI showed high intensity areas in the right occipital cortex, and subcortical white matter of the frontal, temporal and parietal lobes. EEG showed generalized slowing. Norovirus genome was detected in plasma and stool by reverse transcription polymerase chain reaction, but not in the CSF. Herpes virus and enterovirus evaluations were negative. Cytokine concentrations in CSF were markedly elevated on the third day of illness. She developed severe brain atrophy that was confirmed on MRI by day 101, and had severe developmental delay and seizures on follow-up at age 2. The authors felt that this represented norovirus encephalopathy. It is not clear how much of the observed sequelae were secondary to hypoglycemia (Obinata et al, 2010).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTROENTERITIS
    1) WITH POISONING/EXPOSURE
    a) Illness is typically self-limiting. Severe nausea and vomiting are usually the first sign of illness. Other symptoms include nonbloody watery diarrhea and abdominal cramps (Center for Food Safety and Applied Nutrition (CFSAN), 2012; Hall et al, 2011). Some patients may only have diarrhea or vomiting (Hall et al, 2011). Vomiting is more common in children, and diarrhea is more common in adults (Glass et al, 2009). Flatulence and fecal urgency are also reported (Ajami et al, 2010).
    B) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Mild elevations in liver enzymes and bilirubin have been reported early in the course of infection (Pazdiora et al, 2009; Yu et al, 2007).
    b) In a series of 4 children with norovirus-induced gastroenteritis, 3 developed symptoms severe enough to require hospitalization. Patients initially had mild elevations in AST and ALT, and clinically improved. Evaluation 8 to 13 days after the onset of illness (at which point the patients were asymptomatic) revealed more significant elevations of AST (119 to 749 units/L) and ALT (172 to 707 units/L), that gradually resolved over the next 2 weeks. All children had norovirus on reverse transcriptase polymerase chain reaction testing (performed after gastroenteritis had resolved) and no other pathogens isolated. It is unclear from these reports if the norovirus was responsible for the observed lab abnormalities (Tsuge et al, 2010).
    C) INFLAMMATORY BOWEL DISEASE
    1) WITH POISONING/EXPOSURE
    a) Case reports have suggested that norovirus infection may exacerbate inflammatory bowel disease in children, but causality is not clear (Glass et al, 2009). Chronic diarrhea has also been reported as a sequelae of infection (Said et al, 2008).
    D) IRRITABLE BOWEL SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Several studies suggest that norovirus infection is associated with the later development of irritable bowel syndrome (Cremon et al, 2010)
    E) NECROTIZING ENTEROCOLITIS IN FETUS OR NEWBORN
    1) WITH POISONING/EXPOSURE
    a) Case reports have suggested an association between norovirus infection and necrotizing enterocolitis in infants, but causality is not clear (Glass et al, 2009).
    b) A retrospective case-control study of infants in a neonatal intensive care unit (NICU) with and without necrotizing enterocolitis (NEC) was performed to evaluate the etiology of an outbreak of NEC involving 8 infants with 2 deaths. Norovirus-like particles were identified in the 6 stool samples available from the NEC cases, and norovirus was confirmed by reverse transcriptase polymerase chain reaction in 4 of these samples. Evaluation of stool samples for bacteria, parasites, Clostridium difficile toxin, viral cultures and rotavirus antigen enzyme immunoassays were negative. NEC cases were younger, had lower APGAR scores at birth, and longer courses of antibiotics than did controls. Three NICU personnel had more contact with cases than with controls, and one of these workers had gastroenteritis symptoms at the time of the outbreak (Turcios-Ruiz et al, 2008).
    c) Another case control study evaluated an outbreak of necrotizing enterocolitis (NEC) in a NICU involving 15 infants over 6 months. Stool samples were available from 10 NEC patients and compared with 45 controls. Four out of 10 NEC patients (40%) had norovirus detected in stool by reverse transcription polymerase chain reaction, compared with 4 out of 45 (9%) of control subjects (Stuart et al, 2010).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache may accompany the gastrointestinal symptoms (Apelt et al, 2010).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) MUSCLE PAIN
    1) WITH POISONING/EXPOSURE
    a) Body aches develop in some patients, often along with low grade fever (Hall et al, 2011).

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor serum electrolytes and urine output in patients with severe vomiting and diarrhea.
    B) Reverse transcriptions-polymerase chain reaction assays are sensitive for noroviruses. These assays are sometimes used to identify outbreaks, but not used to guide clinical management of individual patients.
    C) Enzyme immunoassays have been developed, but are generally of low sensitivity and are not widely used.
    4.1.2) SERUM/BLOOD
    A) Monitor serum electrolytes and urine output in patients with severe vomiting and diarrhea.
    B) Four criteria may be used to diagnose norovirus-associated illness without having a diagnostic test: (1) in an outbreak, more than 50% of affect persons are vomiting; (2) a mean or a median incubation period of 1 to 2 days; (3) a mean or a median duration illness of 12 to 60 hours; (4) lack of identification of a bacterial pathogen in stool culture (Center for Food Safety and Applied Nutrition (CFSAN), 2012).

Methods

    A) Reverse transcription-polymerase chain reaction (RT-PCR) assays are sensitive for noroviruses. These assays are sometimes used to identify outbreaks, but not used to guide clinical management of individual patients (Hall et al, 2011). One study found a difference in viral load (detected by RT-PCR) between symptomatic and asymptomatic norovirus infection (Phillips et al, 2009). This suggests that norovirus may not always be the cause of illness when it is detected by RT-PCR. Determining viral load and establishing a cut-off may help distinguish disease caused by norovirus from incidental carrier states, but this is not currently done in clinical practice.
    B) Enzyme immunoassays have been developed, but are generally of low sensitivity and are not widely used (Kirby et al, 2010) .
    C) Noroviruses cannot be grown in cell culture, and there is no animal model of the disease. While noroviruses have been detected in food, water and environmental specimens via reverse transcription polymerase chain reaction assays, validated methods are available only for water (CDC) and seafood (FDA Gulf Coast Seafood Laboratory) (Hall et al, 2011). These methods are only used for epidemiologic investigation, not clinical management.
    D) Analytical tests on serum, stool, and vomitus can be performed to confirm the clinical diagnosis of norovirus infection. In addition, blood serum samples can be measured by enzyme immunoassay (ie, ELISA or EIA) to diagnose norovirus infection. This analysis can identify an increase in virus-specific serum antibody titers (usually a 4-fold increase of IgA, IgG, and IgM) against the presumed viral antigen in acute or convalescent sera; however, multiple sera samples are needed from patients. This method has been marketed and used to detect norovirus in fecal material with only a 55% level of accuracy, when compared with a RT-PCR method (Center for Food Safety and Applied Nutrition (CFSAN), 2012).

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with severe dehydration, electrolyte abnormalities, and those with vomiting that persists despite therapy, may require hospital admission. Infants, the elderly, and patients with significant underlying health problems are more likely to require admission.
    6.3.1.2) HOME CRITERIA/ORAL
    A) The vast majority of patients with self-limited vomiting and diarrhea who can tolerate oral fluids can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult an infections disease specialist and the local health department in the event of a significant outbreak, to help identify the source of exposure and reduce further transmission.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with persistent vomiting, severe diarrhea and those who can not tolerate oral fluids should be referred to a healthcare facility for treatment with antiemetics and intravenous hydration.

Monitoring

    A) Monitor serum electrolytes and urine output in patients with severe vomiting and diarrhea.
    B) Reverse transcriptions-polymerase chain reaction assays are sensitive for noroviruses. These assays are sometimes used to identify outbreaks, but not used to guide clinical management of individual patients.
    C) Enzyme immunoassays have been developed, but are generally of low sensitivity and are not widely used.

Oral Exposure

    6.5.3) TREATMENT
    A) SUPPORT
    1) Care is symptomatic and supportive. Administer antiemetics, and intravenous or oral fluids to prevent dehydration.
    B) INFECTION CONTROL PROCEDURE
    1) Unfortunately, no single infection control method has been shown to shorten the duration of outbreaks, and outbreaks in healthcare facilities tend to last the longest (Harris et al, 2010). The following infection control measures are generally recommended.
    C) STANDARD PRECAUTIONS
    1) Always use standard precautions with all patients. Meticulous hand hygiene is imperative for patients, visitors and staff to control transmission. Wash hands well with soap and water for one minute, rinse for 20 seconds and dry with a disposable paper towel (Said et al, 2008). Hands should be washed after eating or drinking, using the bathroom, or contact with patients. An alcohol-based hand sanitizer may not be effective against noroviruses (Liu et al, 2010). Use gloves, gown, mask and/or face shield when caring for ill patients depending on the anticipated exposure.
    D) CONTACT PRECAUTIONS
    1) Acutely ill patients should be isolated as much as possible during the acute stage of illness and for 24 to 72 hours after recovery, during the peak period of viral shedding. Do not share equipment between patients. Use gown, gloves and mask or face shield for all interactions that may involve contact with patient or contaminated areas of the patient's environment. Isolate ill patients to single rooms, or if that is not possible cohort ill patients together. Do not allow visits by sick individuals. Provide different toilet facilities for ill and non-ill patients (Heijne et al, 2009). Remove supplies from a room before an infected patient is admitted (Said et al, 2008).
    2) INFECTED HEALTHCARE WORKERS: In one outbreak that occurred among hospital personnel attending a conference, infected employees were instructed to stay home until 72 hours after symptoms resolved, and the environment was decontaminated rapidly. This resulted in successful prevention of secondary outbreaks or infections (Vinnard et al, 2012).
    E) DISINFECTION
    1) Clean spill with detergent to remove particulate material and then with a hospital approved disinfectant. Chemical disinfectants (ie, at least a 1:50 sodium hypochlorite:water solution) should be used on potentially contaminated environmental surfaces, particularly in bathrooms or on high-touch surfaces like doorknobs, light switches, tables, counter tops, keyboards, and hand rails, every shift. Clean bathrooms every shift. Clean common areas, and staff rooms, including refrigerators. Clean rooms every 24 hours and at patient discharge. Clean floors with approved disinfectant, change cleaning solution and mop head every 3 rooms. Clean rooms that have housed patients with vomiting and/or diarrhea last, change the mop head and solution after cleaning a room that housed an infected patient. Remove and replace curtains if soiled or contaminated (Said et al, 2008).

Summary

    A) INFECTIVE DOSE: The estimated infectious dose is as low as 1 to 10 viral particles; as high as 1 x 10(12) million viral particles/g feces are excreted by both symptomatic and asymptomatic people. FATALITIES: Fatalities are rare and occur almost exclusively in the elderly.

Minimum Lethal Exposure

    A) FATALITIES: Fatalities are rare and occur almost exclusively in the elderly. A study in England and Wales suggested that norovirus infection might be associated with about 80 deaths a year in patients over the age of 65 (Harris et al, 2008). In the United States, an estimated 5.5 million norovirus infections (estimated range, 3.2 million to 8.3 million cases of foodborne illness) occur annually, accounting for 58% of all foodborne illnesses. This results in approximately 0.03% of patients (range, 8097 to 23,323; mean, 14,663) requiring hospitalization and less than 0.1% of these illnesses resulting in death (range, 84 to 237 deaths; mean, 149) (Center for Food Safety and Applied Nutrition (CFSAN), 2012).

Maximum Tolerated Exposure

    A) INFECTIVE DOSE: The estimated infectious dose is as low as 1 to 10 viral particles; as high as 1 x 10(12) million viral particles/g feces are excreted by both symptomatic and asymptomatic people (Center for Food Safety and Applied Nutrition (CFSAN), 2012). During peak viral shedding, a gram of feces may contain 5 billion infectious doses (Hall et al, 2011).

Toxicologic Mechanism

    A) The exact pathogenic pathway of infection is unknown. Noroviruses cause the inflammation of the stomach and the small and large intestines (Center for Food Safety and Applied Nutrition (CFSAN), 2012).

General Bibliography

    1) Ajami N, Koo H, Darkoh C, et al: Characterization of norovirus-associated traveler's diarrhea. Clin Infect Dis 2010; 51(2):123-130.
    2) Apelt N, Hartberger C, Campe H, et al: The Prevalence of Norovirus in returning international travelers with diarrhea. BMC Infect Dis 2010; 10:131-.
    3) Center for Food Safety and Applied Nutrition (CFSAN): Noroviruses. In: Bad Bug Book Foodborne Pathogenic Microorganisms and Natural Toxins Handbook Second Edition. U.S. Food and Drug Administration (FDA). College Park, MD. 2012. Available from URL: http://www.fda.gov/downloads/Food/FoodSafety/FoodborneIllness/FoodborneIllnessFoodbornePathogensNaturalToxins/BadBugBook/UCM297627.pdf. As accessed 2013-03-06.
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