Norovirus, reactive arthritis and should a child with diarrhea be vaccinated?


Below is a wonderful, detailed, thorough excerpt from the Centers of Disease Control about the Norovirus. When infected, the symptoms include diarrhea, vomiting and cramping.  In some individuals, perhaps with a genetic predisposition, a reactive arthritis appears following a norovirus attack. As a result of the infection by the norovirus the body’s immune system continues to attack “self” cells believing they are enemy “norovirus” cells. Read the detailed original description of the Norovirus here. Cruise ships, nursing homes, college dorms are places were a norovirus infection spreads quickly where people live in enclosed conditions.

A cruise ship with a reported norovirus infection during a year when there were several diarrhea epidemics on cruise ships. Photo inlay of Norovirus. Photo ABC news

My question was that should a child with diarrhea or gastroenteritis be allowed to be vaccinated say perhaps with MMR vaccine or should this child wait until the child is fully recovered? How long should this gap be? The MMR vaccine contains components of three viruses to prevent three diseases. The vaccine aims to train the child’s immune system to recognize the foreign material and train in advance to prepare against an infection. Is the child with gasteroenteritis or diarrhea compromised in any way prior to being vaccinated? I could not find any scientific study published to answer this question. Is there any study on how many children had an infection upto one month prior to any immunization? How did they fare after that?

The second question which follows is which is more dangerous – losing a child to measles given a 1 in 1000 chance or having a child live a dependent life forever with Autism Spectrum Disorder with a 1 in 100 chance? I wonder which is more of a public burden. Should it be safer to ask a family with a norovirus infection to give a far lengthier gap prior to vaccinating a child? Except for an Italian court ruling a connection between a child with autism and a MMR vaccine (following a gastroenteritis infection), all official scientific studies have ruled out a connection between the MMR vaccine and autism. Yet, most parents continue to insist that their child was a normal baby who was able to communicate prior to the MMR vaccine. Could the norovirus provide one more clue to this puzzle?

Quote:

Biology and Epidemiology

The Virus

Noroviruses are a group of nonenveloped, single-stranded RNA viruses classified into the genus Norovirus (previously referred to as Norwalk-like viruses [NLVs] or small round-structured viruses [SRSVs]) of the family Caliciviridae. Other genera within the Caliciviridae family include Sapovirus (previously referred to as Sapporo-like viruses [SLVs]), which also cause acute gastroenteritis (AGE) in persons, as well as Lagovirus, Vesivirus, and Nebovirus, which are not pathogenic for humans (11). Noroviruses can be divided into at least five genogroups, designated GI–GV, based on amino acid identity in the major structural protein (VP1) (12). The strains that infect humans (referred to collectively as “human noroviruses”) are found in GI, GII, and GIV, whereas the strains infecting cows and mice are found in GIII and GV, respectively (Figure 1). Although interspecies transmission of noroviruses has not been documented, strains that infect pigs are found in GII (13), and a GIV norovirus was discovered recently as a cause of diarrhea in dogs (14), suggesting the potential for zoonotic transmission. On the basis of >85% sequence similarity in the complete VP1 genome, noroviruses can be classified further into genotypes, with at least eight genotypes belonging to GI and 21 genotypes belonging to GII (12,13; CDC, unpublished data, 2011). Since 2001, GII.4 viruses have been associated with the majority of viral gastroenteritis outbreaks worldwide (15). Recent studies have demonstrated that these viruses evolve over time through serial changes in the VP1 sequence, which allow evasion of immunity in the human population (15,16).

Clinical Features

Noroviruses cause acute gastroenteritis in persons of all ages. The illness typically begins after an incubation period of 12–48 hours and is characterized by acute onset, nonbloody diarrhea, vomiting, nausea, and abdominal cramps. Some persons might experience only vomiting or diarrhea. Low-grade fever and body aches also might be associated with infection, and thus the term “stomach flu” often is used to describe the illness, although there is no biologic association with influenza. Although symptoms might be severe, they typically resolve without treatment after 1–3 days in otherwise healthy persons. However, more prolonged courses of illness lasting 4–6 days can occur, particularly among young children, elderly persons, and hospitalized patients (17,18). Approximately 10% of persons with norovirus gastroenteritis seek medical attention, which might include hospitalization and treatment for dehydration with oral or intravenous fluid therapy (7,19,20). Norovirus-associated deaths have been reported among elderly persons and in the context of outbreaks in long-term–care facilities (21,22). Necrotizing enterocolitis in neonates, chronic diarrhea in immunosuppressed patients, and postinfectious irritable bowel syndrome also have been reported in association with norovirus infection (23–25); however, more data from analytic studies are needed to confirm a causal link with these conditions.

Norovirus is shed primarily in the stool but also can be found in the vomitus of infected persons, although it is unclear if detection of virus alone indicates a risk for transmission. The virus can be detected in stool for an average of 4 weeks following infection, although peak viral shedding occurs 2–5 days after infection, with a viral load of approximately 100 billion viral copies per gram of feces (26). However, given the lack of a cell culture system or small animal model for human norovirus, whether these viruses represent infectious virus is unknown, and therefore the time after illness at which an infected person is no longer contagious also is unknown. Furthermore, up to 30% of norovirus infections are asymptomatic, and asymptomatic persons can shed virus, albeit at lower titers than symptomatic persons (26–28). The role of asymptomatic infection in transmission and outbreaks of norovirus remains unclear.

Immunity

Protective immunity to norovirus is complex and incompletely understood. In human challenge studies, infected volunteers were susceptible to reinfection with the same strain as well as to infection with heterologous strains (29–32). In addition, those with preexisting antibodies were not protected from infection unless repeated exposure to the same strain occurred within a short period. Two of these studies demonstrated that homologous antibody protection might last anywhere from 8 weeks to 6 months (30,31). However, the infectious dose of virus given to volunteers in these challenge studies was several-fold greater than the dose of virus capable of causing human illness, and thus immunity to a lower natural challenge dose might be greater and more cross-protective.

Because preexisting antibodies among challenged volunteers did not necessarily convey immunity, and some persons seemed to remain uninfected despite significant exposure, both innate host factors and acquired immunity have been hypothesized to contribute to the susceptibility to infection (31). Histo-blood group antigens (HBGAs), including H type, ABO blood group, and Lewis antigens have been proposed as candidate receptors for norovirus. Expression of HBGAs is associated with strain-specific susceptibility to norovirus infection (17,33–38). Resistance to norovirus infections has been associated with mutations in the 1,2-fucosyltransferase (FUT2) gene leading to a lack of expression of HBGAs on the surface of intestinal cells (33–35,39). Thus, persons who have the normal FUT2 gene and who express these antigens are termed “secretors” whereas mutations in the FUT2 gene leading to the absence of HBGA expression result in “nonsecretor” persons who are less susceptible to infection. However, secretor status does not completely explain the differences seen among infected and uninfected persons for all strains of norovirus. Thus, additional mechanisms of immunity are likely involved, and this remains an ongoing field of research. In addition, evidence suggests that new GII.4 variants evolve to escape the build-up of acquired immunity and innate resistance in the human population (16,40).

Transmission

Norovirus is extremely contagious, with an estimated infectious dose as low as 18 viral particles (41), suggesting that approximately 5 billion infectious doses might be contained in each gram of feces during peak shedding. Humans are the only known reservoir for human norovirus infections, and transmission occurs by three general routes: person-to-person, foodborne, and waterborne. Person-to-person transmission might occur directly through the fecal-oral route, by ingestion of aerosolized vomitus, or by indirect exposure via fomites or contaminated environmental surfaces. Foodborne transmission typically occurs by contamination from infected food handlers during preparation and service but might also occur further upstream in the food distribution system through contamination with human waste, which has been demonstrated most notably by outbreaks involving raspberries and oysters as vehicles (42–46). A recent outbreak involving consumption of delicatessen meat also demonstrated the potential for norovirus contamination during processing (47). Finally, recreational and drinking water can serve as vehicles of norovirus transmission and result in large community outbreaks (48,49). These outbreaks often involve well water that becomes contaminated from septic tank leakage or sewage (50) or from breakdowns in chlorination of municipal systems (51).

Sporadic Disease

As diagnostic methods have improved and become more widely available, the role of noroviruses as the leading cause of sporadic gastroenteritis in all age groups has become clear. Approximately 21 million illnesses caused by norovirus are estimated to occur each year in the United States, approximately one quarter of which can be attributed to foodborne transmission (52). A recent systematic review of 31 community, outpatient, and hospital-based studies in both developed and developing countries estimated that noroviruses accounted for 10%–15% of severe gastroenteritis cases in children aged <5 years and for 9%–15% of mild and moderate diarrhea cases among persons of all ages (53). Although laboratory-based data on endemic norovirus disease in the United States are sparse, recent studies suggest that norovirus is the leading cause of acute gastroenteritis in the community and among persons seeking care in outpatient clinics or emergency departments across all age groups (54,55; CDC, unpublished data, 2011).

Serosurveys have demonstrated that norovirus infections are prevalent throughout the world, with initial exposure typically occurring early in life (5). In population-based studies from Australia, England, Hong Kong, and the Netherlands, norovirus infection has accounted for 9%–24% of gastroenteritis cases (19,20,56–58). In these studies, infection was more frequent in certain age groups (e.g., children aged <5 years and adults aged >65 years). In studies that have used sensitive molecular assays, a relatively high prevalence of norovirus-positive samples in asymptomatic persons has been detected, ranging from 5% in the Netherlands to 16% in England (20,56). This background rate of asymptomatic infection, coupled with innate resistance attributable to secretor status and acquired immunity, helps explain why attack rates rarely exceed 50% in outbreaks.

Outbreaks

Noroviruses are the predominant cause of gastroenteritis outbreaks worldwide. Data from the United States and European countries have demonstrated that norovirus is responsible for approximately 50% of all reported gastroenteritis outbreaks (range: 36%–59%) (5). Outbreaks occur throughout the year although there is a seasonal pattern of increased activity during the winter months. In addition, periodic increases in norovirus outbreaks tend to occur in association with the emergence of new GII.4 strains that evade population immunity (Table) (40,59). These emergent GII.4 strains rapidly replace existing strains predominating in circulation and can sometimes cause seasons with unusually high norovirus activity, as in 2002–2003 and 2006–2007. Because the virus can be transmitted by food, water, and contaminated environmental surfaces as well as directly from person to person, and because there is no long lasting immunity to norovirus, outbreaks can occur in a variety of institutional settings (e.g., nursing homes, hospitals, and schools) and affect people of all ages. Whereas prior national estimates of outbreak attribution by mode of transmission were likely biased toward foodborne disease (60,61), more recent data from individual states indicate that the majority of norovirus outbreaks primarily involve person-to-person transmission (62,63). Multiple routes of transmission can occur within an outbreak; for example, point-source outbreaks from a food exposure often result in secondary person-to-person spread within an institution or community. Of the 660 norovirus outbreaks laboratory confirmed by CDC during 1994–2006 that indicated the setting, 234 (35.4%) were from long-term–care facilities (e.g., nursing homes); 205 (31.1%) were from restaurants, parties, and events; 135 (20.5%) were from vacation settings (including cruise ships); and 86 (13.0%) were from schools and communities (59). Although GII.4 variants predominate overall, the role of GI and other GII genotypes appears to be greater in settings that involve foodborne or waterborne transmission (Figure 2).

Long-Term Care and Other Health-Care Facilities

Health-care facilities including nursing homes and hospitals are the most commonly reported settings of norovirus outbreaks in the United States and other industrialized countries (59,60,63–65). Virus can be introduced from the community into health-care facilities by staff, visitors, and patients who might either be incubating or infected with norovirus upon admission or by contaminated food products. Outbreaks in these settings can be prolonged, sometimes lasting months (66). Illness can be more severe in hospitalized patients than for otherwise healthy persons (18), and associated deaths have been reported (21,22). Strict control measures (including isolation or cohorting of symptomatic patients, exclusion of affected staff, and restricting new admissions into affected units) are disruptive and costly but might be required to curtail outbreaks (9,67,68).

Restaurants and Catered Events

Norovirus is now recognized as the leading cause of foodborne disease outbreaks in the United States. Norovirus accounted for 822 (35%) of the 2,367 foodborne disease outbreaks reported to CDC during 2006–2007 (Figure 3) and half of the 1,641 foodborne disease outbreaks with a confirmed or suspected etiology (69,70). Food can become contaminated with norovirus at any point during production, processing, distribution, and preparation. Thus, a variety of products have been implicated in outbreak investigations; foods eaten raw (e.g., leafy vegetables, fruits, and shellfish) are identified most commonly (69,70). Handling of ready-to-eat foods by infected food employees is commonly identified as a contributing factor in outbreaks of foodborne norovirus associated with food-service establishments (71,72). Norovirus outbreaks also have resulted from fecal contamination of certain food products at the source. For example, oysters harvested from fecally contaminated growing waters and raspberries irrigated with sewage-contaminated water have been implicated in outbreaks (44,73). Because gross sewage contamination will contain a collection of viruses circulating in the community, multiple norovirus genotypes often are detected in such outbreaks. Contamination with norovirus also can occur during processing, as demonstrated by a recent outbreak involving delicatessen meat (47). Only a small dose of virus is needed to cause infection, and thus infected food handlers can contaminate large quantities of product. For example, approximately 500 cases of gastroenteritis were reported during a 2006 outbreak caused by a foodhandler who vomited at work (74). Drinking water or ice also might become contaminated with norovirus and result in outbreaks in food-service settings. Secondary person-to-person transmission is common following point-source food or water exposures.

Schools and Other Institutional Settings

Norovirus outbreaks occur in a range of other institutional settings including schools, child care centers, colleges, prisons, and military encampments. Outbreaks of gastroenteritis in child care centers also are caused by other pathogens, including rotavirus, sapovirus, and astrovirus, as a result of a lack of immunity to these viruses in young populations (75). Outbreaks have been reported recently from multiple universities in different states and have led to campus closures (76). An intervention study in elementary schools demonstrated that improved hand hygiene and surface disinfection can lead to lower rates of absenteeism caused by nonspecific gastroenteritis and reduced surface contamination with norovirus (77). Norovirus was also the most common cause of gastroenteritis in U.S. marines during Operation Iraqi Freedom (78) and a common cause of outbreaks among deployed British troops (79).

Cruise Ships and Other Transportation Settings

Passengers and crew aboard cruise ships are affected frequently by norovirus outbreaks (80). Virus generally is introduced on board by passengers or crew infected before embarkation but might also result from food items contaminated before loading or persistently contaminated environmental surfaces from previous cruises. Virus also might be acquired when ships dock in countries where sanitation might be inadequate, either through contaminated food or water or passengers becoming infected while docked. Repeated outbreaks can occur in subsequent sailings as a result of environmental persistence or infected crew, particularly if control measures have not been implemented consistently and thoroughly. Genotyping of outbreak strains from repeated outbreaks has demonstrated that this can occur through the introduction of new virus or recrudescence of virus from one sailing to the next (81,82). CDC’s Vessel Sanitation Program assists the cruise ship industry in preventing and controling the introduction and transmission of gastrointestinal illness by inspecting cruise ships, monitoring gastrointestinal illnesses, and responding to outbreaks (http://www.cdc.gov/nceh/vsp). Outbreaks also have been reported in association with bus tours and air travel, in which environmental contamination and proximity to ill passengers facilitated norovirus transmission (83,84).

Unquote
Read the entire original article here by Centers of Disease Control of the United States.

Related Articles

Autism walks in 2012
Norovirus infection among children with acute gastroenteritis in Recife, Brazil: disease severity is comparable to rotavirus gastroenteritis by scientists in the journal Archives of Virology, 2008
147 frozen brains thawed and lost to research; one third of those were from autism patients.

Advertisements

Leave a comment

Filed under Research, Science

Comments and Any Questions

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s