Enteroviruses and Gastroenteritis Viruses
⭐ Definition and members ★★★
A group of viruses that parasitise the enteric tract and cause disease. They are transmitted by the faecal–oral route and occur worldwide.
The Picornaviridae family — six genera
| Genus | Members |
|---|---|
| Enterovirus | Polio, Coxsackie, echovirus — below |
| Rhinovirus | Common cold |
| Hepatovirus | Hepatitis A virus |
| Parechovirus | Echovirus 22, 23 |
| Aphthovirus | Foot-and-mouth disease viruses |
| Cardiovirus | Encephalomyocarditis |
⭐ The enteroviruses and their serotypes
| Virus | Serotypes |
|---|---|
| Poliovirus | 1–3 |
| Coxsackie A | 1–22, 24 |
| Coxsackie B | 1–6 |
| Echovirus — Enteric Cytopathic Human Orphan | 1–9, 11–27, 29–34 |
| Hepatitis A | Enterovirus 72 |
| Other enteroviruses | 68–71 |
- Define enteroviruses. → A group of viruses that parasitise the enteric tract and cause disease, transmitted faecal–orally and occurring worldwide
- Name the six genera of Picornaviridae. → Enterovirus, Rhinovirus, Hepatovirus (HAV), Parechovirus, Aphthovirus (foot-and-mouth), Cardiovirus
- Name the enterovirus members and their serotypes. → Poliovirus 1–3 · Coxsackie A 1–22, 24 · Coxsackie B 1–6 · echovirus 1–9, 11–27, 29–34 · hepatitis A (enterovirus 72) · other enteroviruses 68–71
- What does ECHO stand for? → Enteric Cytopathic Human Orphan
⭐ Common biological properties ★★★
| Property | Detail |
|---|---|
| Size | 24–30 nm |
| Shape | Spherical |
| Structure | NAKED virus; the nucleocapsid is ICOSAHEDRAL |
| Nucleic acid | +ssRNA |
| Replication | Multiply in the CYTOPLASM |
| Resistant to | Ether · ACID (tolerate pH 3–5). Survive for a long period in water and sewage |
| Sensitive to | Drying, heat and UV |
Two rows of that table explain the whole epidemiology of the group, and Unit 18 §3 predicted it.
A virus swallowed on the way to the intestine must survive stomach acid at pH 1–3 and then bile salts and digestive detergents in the duodenum. An enveloped virus — a lipid membrane — is destroyed by both, which is why no enveloped virus spreads faecal–orally.
The enteroviruses are naked, so there is no lipid to dissolve, and their protein capsid tolerates pH 3–5 and ether. They pass the stomach intact and infect the gut.
The same durability keeps them alive for long periods in water and sewage — which is why polio is a disease of poor sanitation, why sewage surveillance detects it, and why the deck's rotavirus prevention advice is handwashing and disinfection of surfaces, toilets and toys rather than anything cleverer.
Contrast: hepatitis A is enterovirus 72, naked and faecal–oral; hepatitis B is enveloped and blood-borne. The structure decides the route.
- Give the common properties of enteroviruses. → 24–30 nm, spherical, NAKED with an icosahedral nucleocapsid, +ssRNA, multiplying in the cytoplasm
- What are they resistant and sensitive to? → Resistant to ether and acid (pH 3–5), surviving long periods in water and sewage; sensitive to drying, heat and UV
- Why does the structure fit the route? → Naked and acid-resistant viruses survive stomach acid and bile, so they can spread faecal–orally
Pathogenesis and clinical findings ★★★
The general sequence is portal of entry → viraemia → target tissue, and different enteroviruses bind to different target cells — Unit 18 §5's tissue tropism.
| System | Diseases |
|---|---|
| a · Neurologic infection | Aseptic meningitis · paralysis · encephalitis |
| b · Cardiac and muscular infection | Myocarditis · pericarditis · pleurodynia |
| c · Infection of skin and mucosa | Herpangina · hand-foot-and-mouth disease |
| d · Respiratory infection | Common colds |
| e · Alimentary infection | Diarrhoea in children |
- Give the general pathogenetic sequence. → Portal of entry → viraemia → target tissue, with different enteroviruses binding different target cells
- Name the five clinical categories with examples. → Neurologic (aseptic meningitis, paralysis, encephalitis) · cardiac and muscular (myocarditis, pericarditis, pleurodynia) · skin and mucosa (herpangina, hand-foot-and-mouth) · respiratory (common cold) · alimentary (childhood diarrhoea)
Poliovirus ★★★
| Property | Detail |
|---|---|
| Structure | 30 nm · +ssRNA (INFECTIOUS RNA) enclosed by an icosahedral capsid; the RNA acts as mRNA and is translated to polypeptide |
| Source of infection | Patients or asymptomatic carriers |
| Route | Faecal–oral |
| Causative virus | Type 1 is the commonest and causes most epidemics |
| Incubation | 4 days to 4 weeks, average 10 days |
Poliomyelitis is a highly infectious viral disease of children, with inflammation of the motor neurons of the spinal cord and brainstem, leading to paralysis, muscular atrophy and deformity.
⭐ The pathogenetic pathway — and the numbers
Poliovirus → throat and Peyer's patches of the small intestine → regional lymph nodes → blood. From there: 90% unapparent infection; 1–2% reach the CNS (motor neurons); and 0.1–0.2% develop flaccid paralysis, which may progress to post-poliomyelitis muscle atrophy or, rarely, medullary paralysis → respiratory and heart failure → death.
| Type of illness | Frequency |
|---|---|
| Asymptomatic illness | 90% |
| Abortive poliomyelitis | 5% |
| Non-paralytic poliomyelitis | 1–2% |
| Paralytic polio | 0.1–0.2% |
The paralysed child is the visible tip of a very large iceberg. For every one, roughly 900 people are infected and shedding virus with no symptoms at all — Unit 20 §4's inapparent infection, whose stated significance was exactly this: a source of infection, misdiagnosed or not diagnosed, while conferring immunity.
Three consequences:
• Isolating cases cannot stop transmission, because the cases are a fraction of one per cent of those infected.
• One paralytic case signals a large silent outbreak — which is why a single case is treated as a public health emergency.
• Eradication requires vaccinating everyone, not treating patients — and it requires gut immunity, to stop the shedding, which is precisely the argument of §5.
Note also that the paralysis is flaccid, from destruction of motor neurons — the same clinical picture as botulinum toxin in Unit 11 §4, reached by destroying the neuron rather than silencing it.
- Describe poliovirus. → 30 nm, naked, icosahedral capsid, +ssRNA which is itself infectious and acts as mRNA
- Source, route, type and incubation? → Patients or asymptomatic carriers; faecal–oral; type 1 commonest and causes most epidemics; incubation 4 days to 4 weeks, average 10 days
- Give the pathway. → Throat and Peyer's patches → regional lymph nodes → blood → CNS motor neurons in 1–2%
- Give the four outcomes with frequencies. → Asymptomatic 90% · abortive 5% · non-paralytic 1–2% · paralytic 0.1–0.2%
- What is the pathology of paralytic polio? → Inflammation of the motor neurons of the spinal cord and brainstem, causing flaccid paralysis, muscular atrophy and deformity
⭐ Sabin versus Salk ★★★
Poliovirus vaccines, 1960: the Sabin live attenuated vaccine (OPV), by Albert Sabin, and the Salk killed vaccine (IPV), by Jonas Salk. “What is different when you compare Sabin vaccine with Salk vaccine?” is question 2 on the deck's own focus slide — Section III shape.
| Property | Sabin (OPV, live) | Salk (IPV, killed) |
|---|---|---|
| Safety | Satisfactory | Satisfactory |
| Administration | 3 doses at 6–8 week intervals, given ORALLY | Primary 2–3 doses at 4–6 week intervals, boosters every 3–5 years; by INJECTION |
| Cost | More | Less |
| Nature of immunity | Induces BOTH local and systemic immunity | Systemic antibody only — NO local immunity |
| Duration of immunity | Lifelong | May need periodic booster doses |
| Spread of vaccine | Spreads naturally to unvaccinated individuals by faecal–oral spread | No spread |
| Stability | Less stable; difficult to preserve and transport in tropical areas | Stable; preservation and transport are convenient |
The deck's advantage/disadvantage lists
| Live (OPV) | Inactivated (IPV) | |
|---|---|---|
| Advantages | 1. Effectiveness · 2. Lifelong immunity · 3. Induction of a secretory antibody response similar to natural infection · 4. Ease of administration · 5. No need for repeated boosters | 1. Effectiveness · 2. Good stability during transport and storage · 3. Safe in immunodeficient patients · 4. No risk of vaccine-related disease |
| Disadvantages | 1. Risk of vaccine-associated poliomyelitis in recipients or contacts — the virus reverts to its virulent form; incidence 1 per 4 million doses · 2. Unsafe in immunodeficient patients · 3. Less stable, harder to preserve and transport in tropical areas | 1. Lacks induction of local (gut) immunity · 2. Needs boosters for lifelong immunity · 3. Injection is more painful than oral administration |
Every difference above follows from one fact — OPV replicates in the gut and IPV does not — and two of them decide public policy.
Local (gut) immunity and natural spread. OPV produces secretory IgA in the intestine, so a vaccinated child stops carrying and shedding wild virus. IPV protects the individual from paralysis but leaves the gut susceptible, so the vaccinated child can still be infected and still transmit. And the OPV strain itself spreads faecal–orally to unvaccinated contacts, immunising them for free. For eradicating a faecal–oral virus from a population, OPV is decisively better.
Reversion to virulence, 1 in 4 million doses. The price. Once wild polio is nearly gone, the vaccine causes more paralysis than the disease — at which point the arithmetic reverses and countries switch to IPV.
That is why the world used Sabin to eliminate polio and is using Salk to finish. Not a change of mind — a change of which risk is larger.
Note how exactly this maps onto Unit 21 §5's general live-versus-killed table. Polio is that table's worked example.
- Compare Sabin and Salk. → Oral vs injected · more vs less costly · local AND systemic vs systemic only · lifelong vs boosters needed · spreads to contacts vs no spread · less vs more stable
- Name three advantages of OPV. → Lifelong immunity · secretory antibody like natural infection · ease of administration with no boosters
- Name the key disadvantage of OPV. → Risk of vaccine-associated poliomyelitis by reversion to virulence — 1 per 4 million doses; and it is unsafe in the immunodeficient
- Name the key disadvantage of IPV. → It does not induce local gut immunity, so vaccinated people can still carry and transmit the virus
Coxsackie viruses ★★
Named after the town of Coxsackie, New York. Classification is based on pathogenicity in mice.
| Group | Effect in mice | Human disease |
|---|---|---|
| Group A | Widespread myositis, flaccid paralysis — fatal | Herpangina · hand-foot-and-mouth disease · aseptic meningitis |
| Group B | Generalised — heart, CNS, focal myositis | Myocarditis, hepatitis and encephalitis · pericarditis · pleurodynia |
- How are Coxsackie viruses classified? → By their pathogenicity in mice, into groups A and B
- Group A vs group B in mice? → A: widespread myositis and fatal flaccid paralysis. B: generalised, affecting heart, CNS and focal muscle
- Which human diseases? → A: herpangina, hand-foot-and-mouth disease. B: myocarditis, hepatitis, encephalitis
Rotavirus and the gastroenteritis viruses ★★★
Acute gastroenteritis viruses: rotavirus · Norwalk virus (SRSV — small round structured virus) · “classic” calicivirus · enteric adenovirus · astrovirus. These viruses cause acute gastroenteritis with similar symptoms — diarrhoea and vomiting.
| Rotavirus (HRV) | Detail |
|---|---|
| Discovery and name | Described in 1959 by Albert Sabin; belongs to the Reoviridae — respiratory enteric orphan virus; from the Latin rota, a WHEEL |
| Structure | 60–80 nm · NAKED · TWO concentric icosahedral capsid shells · a DOUBLE-STRANDED SEGMENTED RNA genome of 11 discrete segments |
| Classification | 7 groups, A–G. A–C: human and animal diarrhoea — A: infantile acute gastroenteritis · B: outbreaks in adults · C: only sporadic diarrhoea. D–G: animal diarrhoea |
| Epidemiology | One of the most common causes of infantile diarrhoea worldwide. High-risk group: children 6 months to 2 years. Faecal–oral; contagious from before the onset of diarrhoea to a few days after it ends; many cases and outbreaks are NOSOCOMIAL |
| Pathogenesis | Infects cells in the VILLI of the small intestine, multiplies in the cytoplasm of enterocytes, and damages their transport mechanisms so as to interrupt SODIUM AND WATER ABSORPTION |
| Clinical | Incubation 1–4 days; abrupt onset with diarrhoea, fever, abdominal pain, vomiting and dehydration. The diarrhoea is WATERY, with no blood or leukocytes, lasting 3–9 days. In children and infants severe loss of electrolytes and fluid may be fatal until treated |
| Immunity | Rotaviruses are ubiquitous — by age 6, 60–90% are seropositive |
| Diagnosis | Rapid — antigen detection in stool by ELISA; also electron microscopy |
| Prevention and treatment | Handwashing with good technique; disinfection of surfaces, toilets and toys. Vaccine — Rotashield, first licensed for infants in 1998. Supportive: oral or intravenous rehydration. Antiviral agents are not known to be effective |
The acute gastroenteritis viruses compared
| Virus | Shape and size | Nucleic acid | Transmission | Season | Clinical |
|---|---|---|---|---|---|
| Rotavirus | Spherical, 60–80 nm | dsRNA | Faecal–oral | Late autumn, winter | Infants <2 y, watery diarrhoea |
| Enteric adenovirus | Spherical, 70–90 nm | dsDNA | Faecal–oral | Whole year, summer | Infantile diarrhoea |
| SRSV (Norwalk) | Spherical, 27 nm | +ssRNA | Faecal–oral AND respiratory tract | Winter | Any age |
| Classic calicivirus | Spherical, 31–38 nm | +ssRNA | Faecal–oral | Whole year | Infantile watery diarrhoea |
| Astrovirus — a “5 or 6 pointed star” | Spherical, 28–30 nm | +ssRNA | Faecal–oral | Winter | Infants <5 y |
That phrase is a diagnostic instruction, not a description.
Rotavirus does not invade. It infects the enterocytes on the villi and damages their transport mechanisms so sodium and water are not absorbed. Nothing is ulcerated, so there is nothing to bleed and no neutrophils are recruited.
Contrast Unit 10's Shigella and EIEC, which invade and destroy the colonic epithelium: blood, mucus and faecal leukocytes.
So the stool answers the question. Watery, no blood, no leukocytes → a non-invasive, secretory or malabsorptive process — rotavirus, ETEC, cholera. Blood and leukocytes → an invasive process — Shigella, EIEC, Salmonella.
And the treatment follows from the mechanism, which is why the deck says antiviral agents are not effective but rehydration is: the problem is lost water and electrolytes, so replacing them is the treatment. Oral rehydration works because the glucose-coupled sodium transporter survives even when the damaged villus cannot absorb sodium alone.
- Describe rotavirus. → 60–80 nm, naked, two concentric icosahedral capsids, dsRNA in 11 segments; named from Latin rota, a wheel
- Which groups affect humans? → A–C; group A causes infantile acute gastroenteritis, B outbreaks in adults, C sporadic diarrhoea
- Who is at risk, and how does it spread? → Children 6 months to 2 years; faecal–oral, contagious from before onset to a few days after, often nosocomial
- Give the pathogenesis. → Infects villous cells of the small intestine, multiplies in enterocyte cytoplasm, damages transport so sodium and water are not absorbed
- Describe the illness. → Incubation 1–4 days, abrupt diarrhoea, fever, abdominal pain, vomiting, dehydration; watery stool with no blood or leukocytes for 3–9 days
- How is it diagnosed and treated? → Stool antigen ELISA or electron microscopy; oral or IV rehydration — antivirals are ineffective
- Name the five gastroenteritis viruses. → Rotavirus, Norwalk/SRSV, classic calicivirus, enteric adenovirus, astrovirus
Revision
THE TYPES (with serotype numbers, which are worth marks): poliovirus 1–3 · Coxsackie A 1–22 and 24 · Coxsackie B 1–6 · echovirus 1–9, 11–27, 29–34 · hepatitis A virus (enterovirus 72) · other enteroviruses 68–71. They belong to the family Picornaviridae.
THE CHARACTERISTICS: 24–30 nm, spherical, NAKED, with an icosahedral nucleocapsid · +ssRNA · multiply in the cytoplasm · resistant to ether and to acid (pH 3–5), surviving long periods in water and sewage · sensitive to drying, heat and UV · transmitted by the faecal–oral route and occurring worldwide.
Close with the diseases, since the deck pairs them: neurologic (aseptic meningitis, paralysis, encephalitis) · cardiac and muscular (myocarditis, pericarditis, pleurodynia) · skin and mucosa (herpangina, hand-foot-and-mouth) · respiratory (common cold) · alimentary (childhood diarrhoea).
The one sentence that shows understanding: because they are naked and acid-resistant they survive the stomach, which is why the route is faecal–oral.
The whole unit on one screen
| Question | Answer |
|---|---|
| Enterovirus properties? | 24–30 nm, naked, icosahedral, +ssRNA, cytoplasmic, acid- and ether-resistant |
| Members? | Polio 1–3 · Coxsackie A 1–22,24 · Coxsackie B 1–6 · echovirus · HAV = enterovirus 72 · 68–71 |
| Polio outcomes? | 90% asymptomatic · 5% abortive · 1–2% non-paralytic · 0.1–0.2% paralytic |
| Polio pathway? | Throat and Peyer's patches → lymph nodes → blood → motor neurons |
| ⭐ Sabin? | Live, oral, local + systemic immunity, lifelong, spreads to contacts, can revert (1 in 4 million) |
| ⭐ Salk? | Killed, injected, systemic only, boosters needed, stable, safe in immunodeficiency |
| Coxsackie A / B? | Herpangina, hand-foot-and-mouth / myocarditis, hepatitis, encephalitis |
| Rotavirus? | dsRNA in 11 segments, two capsid shells, wheel-shaped; villous enterocytes; watery diarrhoea, no blood or leukocytes |
| Rotavirus age? | 6 months – 2 years; late autumn and winter |
| Rotavirus treatment? | Rehydration — antivirals ineffective |
- Answer the 2020 question. → Types: polio 1–3, Coxsackie A and B, echovirus, HAV (enterovirus 72), enteroviruses 68–71. Characteristics: 24–30 nm, spherical, naked, icosahedral, +ssRNA, cytoplasmic replication, acid- and ether-resistant, sensitive to drying, heat and UV, faecal–oral spread
- Compare Sabin and Salk. → Live oral vs killed injected; local and systemic vs systemic only; lifelong vs boosters; spreads to contacts vs not; unstable vs stable; reversion risk vs none
- Give the polio outcome percentages. → 90% asymptomatic, 5% abortive, 1–2% non-paralytic, 0.1–0.2% paralytic
- Describe rotavirus pathogenesis and its clinical signature. → Damages transport in villous enterocytes so sodium and water are not absorbed → watery diarrhoea with no blood or leukocytes
- Which viruses cause human gastroenteritis? → Rotavirus, Norwalk/SRSV, classic calicivirus, enteric adenovirus, astrovirus