Clinical manifestations and diagnosis of rotavirus infection

Author:: Miguel G O'Ryan, MD
Section Editor:: Morven S Edwards, MD
Deputy Editor:: Diane Blake, MD

Literature review current through: Jan 2024.

This topic last updated: Nov 03, 2023.

INTRODUCTION — Before national vaccination programs, rotaviruses were among the first viral agents identified as important causes of viral gastroenteritis, particularly in children between the ages of six months and two years.

The pathogenesis, epidemiology, clinical manifestations, and diagnosis of rotavirus gastroenteritis will be reviewed here. The prevention of rotavirus infection is discussed separately. (See "Rotavirus vaccines for infants".)

The management of rotavirus infection is as described for other types of viral gastroenteritis and is discussed separately. (See "Acute viral gastroenteritis in children in resource-abundant countries: Management and prevention", section on 'Management' and "Acute viral gastroenteritis in adults", section on 'Treatment'.)

PATHOGENESIS AND HISTOPATHOLOGY

●Pathogenesis – At least three factors are thought to play a role in the pathogenesis of rotavirus-induced diarrhea [1]:

•Necrosis of the gut epithelium leading to villous atrophy and loss of microvilli, mononuclear cell infiltration, endoplasmic reticulum and mitochondrial engorgement in enterocytes, and loss of intestinal brush border enzymes (eg, maltase, sucrase, lactase)

In the setting of acute infection, necrosis of the gut epithelium results in malabsorption of electrolytes, fluids, and nutrients (eg, D-xylose, lactose) [2-4]. Osmotic diarrhea likely occurs as a result of villous epithelial cell destruction with resulting brush border enzyme deficiency and complex sugar malabsorption [5,6]. The success of oral rehydration under these circumstances may reflect the patchy nature of mucosal involvement [4].

•The direct effect of the rotavirus enterotoxin NSP4 and other viral proteins

NSP4 has direct toxic effects on the gastrointestinal mucosa [7], and the antibody to this protein may be associated with protection from rotavirus-induced diarrhea [8]. However, sequence variation in the gene for NSP4 does not always correlate with differences in virulence among strains or with the clinical severity of infection [9-11]. In addition to acting as an enterotoxin, NSP4 protein regulates calcium homeostasis and virus replication.

Other proteins relevant to viral pathogenesis are the capping enzyme (which affects levels of viral ribonucleic acid [RNA] replication), the outer capsid proteins (which are required to initiate infection), and NSP1 protein, which functions as an interferon antagonist [12].

•Activation of the enteric nervous system

Rotavirus may activate the enteric nervous system, resulting in net intestinal fluid and electrolyte secretion [13]. The effectiveness of the drug racecadotril (an inhibitor of enteric enkephalinase) in treatment of rotavirus diarrhea supports the hypothesis that the enteric nervous system plays a role in rotavirus diarrhea [14]. Serotonin liberation due to rotavirus stimulation of enterochromaffin cells may play a role in the intense vomiting characteristically associated with this infection [15].

●Histopathology – Descriptions of the histopathology of rotavirus-induced gastroenteritis have been obtained from peroral small intestinal biopsies performed 24 to 129 hours after the onset of illness [16]. On small intestinal biopsy performed one to five days after onset of illness, the jejunal and duodenal mucosa have patchy irregularities consisting of villous shortening and blunting, as well as infiltration of the lamina propria with mononuclear cells. Electron microscopy demonstrates numerous rotavirus particles in the epithelial cells. Biopsies obtained four to eight weeks after onset of illness demonstrate normal histology [17]. Rotaviral antigen can be demonstrated by immunofluorescence in the cytoplasm of terminal villous epithelial cells in the duodenum and jejunal mucosa [18].

EPIDEMIOLOGY

●Burden of disease – Rotavirus has historically been the most common worldwide cause of severe gastroenteritis in children <5 years of age [19-23]; however, in countries that successfully immunize a large fraction of infants against rotavirus, rotavirus gastroenteritis has decreased substantially [24,25]. (See "Rotavirus vaccines for infants", section on 'Efficacy/effectiveness'.)

The incidence of acute rotavirus infection declined during the coronavirus disease 2019 (COVID-19) pandemic, likely associated with the widespread seclusion of infants and children at home [26,27].

Most older children and adults have serum antibodies to rotavirus, indicative of past infection or immunization [28]. Repeat infection among older children and adults is usually asymptomatic or mild to moderate in severity but can be severe in a subfraction [29-32].

●Risk factors – Young children are at increased risk of rotavirus infection. Severe rotavirus gastroenteritis usually occurs in immunologically naïve, unimmunized children between six months and two years of age [33,34].

All persons, including health care providers, caring for infected patients are at risk for infection (which is generally mild to moderate). Nosocomial infection occurs commonly in the absence of precautions [29]. Others at risk for rotavirus infection include immunocompromised patients and residents of long-term care facilities, in whom disease may be more severe.

Rotavirus binds to histo-blood group antigens (HBGA) on the mucosal surface through specific virus P protein-HBGA interactions. The population prevalence of HBGA type may influence the type of circulating rotavirus. For example, the higher prevalence of P4 and P8 infections in Europe, North and Central America, and Asia is associated with more common secretory-positive individuals [35], while P6 infections, which tend to be more common in Africa, may be, in part, due to the higher prevalence of Lewis-negative phenotype in this population [36].

●Transmission – Rotavirus transmission occurs via the fecal-oral route, with an exposure time of <20 minutes and incubation period of less than 48 hours [29]. A small inoculum is needed for transmission. No more than 100 colony-forming units per gram are necessary for contagion, whereas the stool of the ill person may contain 10⁶ to 10⁹ times that infectious burden.

Viral shedding in stool lasts approximately 10 days; one study noted shedding for at least 21 days among one-third of immunocompetent children [37].

Rotavirus gastroenteritis can be associated with disease in household contacts. In a multicenter surveillance study, 16 percent of household contacts of 829 children with rotavirus-positive acute gastroenteritis reported acute gastroenteritis; contacts younger than five years of age were at particular risk [38]. Acute gastroenteritis illness was more common among household contacts of children with rotavirus-positive gastroenteritis than children with rotavirus-negative gastroenteritis (35 versus 20 percent).

●Seasonality – In tropical regions, infection occurs year-round. In temperate climates, rotavirus infection peaks during the cooler months (for example, during December to April in the United States) [39]. In the United States and Europe, rotavirus infections spread across the country in a wave from west to east each year; the reason for this is not fully understood [39]. Whether such waves of infection still occur in regions with mass immunization is unknown.

CLINICAL MANIFESTATIONS — Rotavirus infection occurs most frequently among children but also occurs in adults. Immunocompromised hosts are more likely to develop a severe and protracted infection.

Children — Typical symptoms and signs among children with rotavirus infection include: vomiting; watery, nonbloody diarrhea; and fever [40-44]. In severe cases, dehydration, seizures, and death can occur [34,45-47].

The frequency of signs and symptoms reported in various series of infants hospitalized with acute gastroenteritis are summarized in the table (table 1). The average duration of symptoms observed in one study of hospitalized children was eight days [42]. However, mild disease can last for just a few days and, conversely, protracted illness can occur.

Respiratory signs and symptoms may be observed in 30 to 50 percent of children with rotavirus infection, although whether these symptoms are caused by rotavirus is unclear and, if present, may reflect underlying acidosis [48]. Simultaneous infection with both respiratory and gastrointestinal viruses can also occur [49].

Neurologic complications occur in 2 to 3 percent of children with rotavirus gastroenteritis. Seizures are the most common manifestation; less commonly, rotavirus can cause an acute encephalopathy or frank encephalitis [50]. One hospital-based survey in Japan noted approximately 41 cases of rotavirus-associated encephalitis/encephalopathy per year [51].

Adults — Rotavirus infection in adults is typically mild and generally occurs among household members of affected children [48,52-54]. Rotavirus has been implicated as a cause of travelers' diarrhea [55-57] and in outbreaks of gastroenteritis in colleges [58] and nursing homes [59].

The clinical manifestations in adults are similar to those in children but are usually less severe [48,60]. Severe diarrhea with hypovolemia among adults has been described [30].

Patients with immunosuppression — Immunocompromised children (eg, those with T cell immunodeficiency, severe combined immunodeficiency, or cancer; recipients of hematopoietic cell or solid organ transplants) are more likely to have severe disease (high fever, acidosis, dehydration) and/or persistent disease with more prolonged excretion of virus than immune-competent children [61-68].

Rotavirus is not a common cause of severe or persistent diarrhea in patients with human immunodeficiency virus (HIV) infection [69,70].

Laboratory findings — Laboratory findings are usually normal. Laboratory studies may be useful for circumstances in which there is suspicion for metabolic acidosis, electrolyte depletion, and severe and/or prolonged lactose intolerance. Dehydration with elevated blood urea nitrogen and metabolic acidosis are common findings [71,72]. Hypocalcemia has also been observed [73].

Peripheral blood leukocyte counts are usually normal in uncomplicated cases, which may help differentiate rotavirus infection from certain bacterial causes of gastroenteritis, in which neutrophilia with immature forms may be observed. Mild elevations in the serum aspartase aminotransferase have been observed during acute illness without other evidence of hepatic injury; these elevations may reflect damage to intestinal epithelial cells [74].

Minimal to moderate numbers of fecal leukocytes are seen in approximately one-third of samples [44,60,75]. A high number of fecal leucocytes may suggest infection or coinfection with an invasive pathogen such as Salmonella, Campylobacter, or Shigella [76].

Associated manifestations with uncertain causality — Rotavirus gastroenteritis has been observed in association with other clinical syndromes; it is uncertain whether rotavirus is an etiologic cause of these manifestations.

●Necrotizing enterocolitis – Although necrotizing enterocolitis (NEC) has been associated with nosocomial rotavirus infection in neonates [77], causality has not been established. (See "Neonatal necrotizing enterocolitis: Pathology and pathogenesis".)

Cytokines may play a role in the pathogenesis of concomitant NEC and rotavirus infection; one study noted that patients with NEC and rotavirus infection had increased interleukin (IL)-8 and tumor necrosis factor and decreased IL-6 relative to patients with NEC in the absence of rotavirus infection [78]. The severity of NEC was not associated with the presence of rotavirus.

●Intussusception – The relationship between rotavirus infection and intussusception is uncertain [79]. Gastrointestinal obstruction due to small bowel intussusception has been described in association with rotavirus gastroenteritis; the mechanism has been attributed to development of localized edema of the small bowel in the setting of viral infection [80,81]. However, subsequent studies have not established a definitive relationship between the two conditions [82,83]. In an Australian case-control study, human adenovirus C, enterovirus B, and rotavirus were associated with intussusception (42, 15, and 10 percent of cases, respectively), although there was no differentiation between wild-type and vaccine-derived rotavirus [84].

Issues related to rotavirus vaccine and intussusception are discussed separately. (See "Rotavirus vaccines for infants", section on 'Intussusception'.)

●Biliary atresia – The relationship between rotavirus infection and biliary atresia is uncertain [85]. Biliary atresia has been described in association with rotavirus infection, and rotavirus antigen has been detected in biliary tissue in some patients [86]. However, other studies have not established a definitive relationship between the two conditions [87]. In one study, there was no difference in serum antibodies levels against rotavirus A and C in cholestatic neonates with or without biliary atresia [88].

●Central nervous system involvement – Rotavirus gastroenteritis may be associated with central nervous system complications, including seizures and encephalopathy [47,51,89-93]. Rotavirus has been detected via polymerase chain reaction (PCR) in cerebrospinal fluid (CSF) in some cases [94,95]. However, it is uncertain whether such detection reflects viral replication in the central nervous system, contamination at the time of lumbar puncture, or carriage of viral RNA in CSF lymphocytes [96]. In one case series including 18 neonates admitted with seizures or apnea and white matter injury, stool was positive for rotavirus PCR in 94 percent of cases; no patients had CSF or serum positive for rotavirus [97]. Rotavirus vaccination has been associated with decreased risk of seizures. (See "Rotavirus vaccines for infants", section on 'Other potential benefits'.)

Protracted gastrointestinal symptoms – Most individuals recover from rotavirus gastroenteritis completely. In some cases, persistent symptoms such as protracted diarrhea or gastroparesis have been observed [98-100]. In addition, carbohydrate or lactase intolerance may persist after resolution of diarrhea [101].

●Diabetes mellitus – It is unknown whether rotavirus induces diabetes mellitus in humans. Rotavirus infection has been associated with an increase in islet autoantibodies in children at risk for diabetes [102], and in a mouse model, rotavirus infection activated islet autoreactive T cells [103]. In addition, universal infant immunization against rotavirus has been associated, albeit not uniformly, with decreased incidence of type 1 diabetes mellitus. (See "Rotavirus vaccines for infants", section on 'Other potential benefits'.)

DIAGNOSIS — A definitive diagnosis of rotavirus is not usually necessary. Situations where it is clinically important to make the diagnosis are discussed separately (See "Acute viral gastroenteritis in children in resource-abundant countries: Clinical features and diagnosis", section on 'Etiologic diagnosis'.)

It is not possible to diagnose rotavirus infection by clinical presentation. Diagnostic methods include detection of intact virus through virus culture; detection of rotavirus proteins through enzyme-linked immunosorbent assays (ELISA), immunochromatography (ICT), or latex agglutination; and detection of rotavirus RNA through real-time polymerase chain reaction (RT-PCR).

For clinical purposes, the most commonly used are ELISA and ICT. Both have high sensitivity and specificity, and ICT provides a rapid result (within minutes) and does not require any equipment [104,105]. PCR-based multipathogen detection systems that include rotavirus are in common use but require somewhat more sophisticated equipment and expertise [106-108].

If latex agglutination is used, a negative result should be interpreted with caution because it is less sensitive than other tests. Stool culture is available in some research and reference laboratories, but it is no longer used for clinical diagnosis of rotavirus diseases.

The decision about which diagnostic test to use is generally made based on which test is available to the clinician.

●ELISA – Rotavirus can be detected by ELISA one to two days prior to onset of clinical illness. The sensitivity is 94 percent during days 1 to 4 of illness and decreases to 76 percent during days 4 to 8 of illness [40,109]. In some cases, virus can be detected ≥2 weeks following resolution of illness [40,110], and severe episodes of diarrhea may be associated with viral shedding for 25 to 30 days [37].

●ICT – ICT has high sensitivity and specificity, provides a rapid result (within 15 minutes) at the point of care, and does not require any equipment.

●PCR – Viral shedding is detectable via PCR for a longer period than via ELISA or ICT; however, the clinical significance of this is unclear [107,111]. Asymptomatic excretion of rotavirus in stool is relatively common and most probably plays a role in transmission [112-114].

Of note, all three of these tests may also detect vaccine virus in recently vaccinated infants.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of rotavirus infection includes bacterial and noninfectious causes of diarrhea. A high number of fecal leucocytes may suggest an invasive pathogen such as Salmonella, Campylobacter, or Shigella.

The differential diagnosis and clinical approach to acute diarrhea in children and adults are discussed separately:

●Children – (See "Diagnostic approach to diarrhea in children in resource-abundant settings" and "Approach to the child with acute diarrhea in resource-limited settings".)

●Adults – (See "Approach to the adult with acute diarrhea in resource-abundant settings" and "Approach to the adult with acute diarrhea in resource-limited settings".)

TREATMENT — The clinical management of rotavirus infection is as described for other types of viral gastroenteritis; these are discussed separately. (See "Acute viral gastroenteritis in adults", section on 'Treatment' and "Acute viral gastroenteritis in children in resource-abundant countries: Management and prevention".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute diarrhea in children".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient education" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Viral gastroenteritis in adults (The Basics)" and "Patient education: Rotavirus infection (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Pathogenesis – Acute rotavirus infection is associated with cellular necrosis leading to decreased levels of intestinal brush border enzymes such as maltase, sucrase, and lactase, leading to malabsorption of D-xylose and lactose in the setting of acute infection. Osmotic diarrhea likely occurs as a result of villous epithelial cell destruction with resulting brush border enzyme deficiency and complex sugar malabsorption. (See 'Pathogenesis and histopathology' above.)

●Epidemiology – Rotavirus is the most important viral cause of gastroenteritis among children worldwide in countries that have not adopted universal use of rotavirus vaccines. (See 'Epidemiology' above.)

●Clinical manifestations

•Typical signs and symptoms among children with rotavirus infection include vomiting, nonbloody diarrhea, and fever. In severe cases, dehydration, seizures, and death can occur. (See 'Children' above.)

•Rotavirus infection among adults is typically mild and generally occurs among household members of affected children. Rotavirus has been implicated as a cause of travelers' diarrhea and in outbreaks of gastroenteritis in colleges and nursing homes. (See 'Adults' above.)

•Prolonged rotavirus gastroenteritis and/or shedding has been reported in children with immunodeficiency; however, rotavirus does not appear to be a common cause of diarrhea in HIV-infected individuals. (See 'Patients with immunosuppression' above.)

•Common laboratory findings include elevated blood urea nitrogen and hypochloremic metabolic acidoses. Peripheral blood leukocyte counts are usually normal, which may help to differentiate rotavirus infection from some forms of bacterial gastroenteritis. (See 'Laboratory findings' above.)

•Rotavirus gastroenteritis has been observed in association with other clinical syndromes, including necrotizing enterocolitis, intussusception, biliary atresia, and central nervous system involvement. It is uncertain whether rotavirus is an etiologic cause of these manifestations. (See 'Associated manifestations with uncertain causality' above.)

●Diagnosis – A definitive diagnosis of rotavirus gastroenteritis is not usually necessary. For patients who require definitive diagnosis, it requires detection of rotavirus antigen or genetic material in the stool. (See 'Diagnosis' above.)

The choice of diagnostic test is generally based on availability. Options include:

•Enzyme-linked immunosorbent assays (ELISA), which requires laboratory processing.

•Immunochromatography (ICT), which provides a rapid result at the point of care.

•Polymerase chain reaction (PCR)-based multidetection systems, which require more sophisticated equipment and expertise.

In recently vaccinated infants, a positive result in any of these tests may be due to the vaccine and not an active infection. (See 'Diagnosis' above.)

●Differential diagnosis – The differential diagnosis of rotavirus infection includes bacterial and noninfectious causes of diarrhea. (See 'Differential diagnosis' above.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges John Treanor, MD, and David O Matson, MD, PhD, who contributed to earlier versions of this topic.

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Topic 2681 Version 33.0

خرید پکیج

Clinical manifestations and diagnosis of rotavirus infection

References