Clinical Implications of Viral Infections of the Bowel PDF

Clinical implications of viral infections of the bowel Prof Hilary Humphreys, Emeritus Professor Dept. of Clinical Microbiology, RCSI  RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn SESSION ID: GIHEPMicroL4 Clinical...

Clinical implications of viral infections of the bowel Prof Hilary Humphreys, Emeritus Professor Dept. of Clinical Microbiology, RCSI  RCSI Royal College of Surgeons in Ireland Coláiste Ríoga na Máinleá in Éirinn SESSION ID: GIHEPMicroL4 Clinical implications of viral infections of the bowel Class Year 2 Course Undergraduate Medicine Lecturer Prof Hilary Humphreys Date 10th September 2024 LEARNING OUTCOMES FOR GI VIRUSES & INFECTIONS BY THE END OF THIS LECTURE YOU SHOULD BE ABLE TO…… Discuss the epidemiology of gastrointestinal (GIT) viruses & the infections they cause Describe the pathogenesis of GIT viruses Recognise & describe the clinical features & complications of GIT virus infection Outline the laboratory diagnosis of infections caused by GIT viruses Choose the appropriate measures to treat infections caused by GIT viruses Use the appropriate measures to prevent the acquisition and spread of GIT virus infection  CLINICAL VIGNETTE On a Thursday afternoon, over a period of 3 hours, four hospital patients develop vomiting followed later by diarrhoea One of the patients is on co-amoxiclav for a urinary tract infection Later, a staff nurse goes off sick with similar symptoms Q. What is the likely cause of this? Q. How might it have been acquired? Q. How do you treat the patients & the nurse? Q. What measures should be taken to prevent onward spread?  GASTROINTESTINAL VIRUSES Cause diarrhoeal illness Cause illness elsewhere Rotavirus Hepatitis A (see hepatitis) Hepatitis E (see hepatitis) CMV (see herpes viruses) Caliciviruses Enteroviruses – Noroviruses Cause luminal disease Astroviruses CMV (see herpes viruses) Adenoviruses  ENTEROVIRUSES Family: Picornavirus Genus: Enterovirus 1. Polioviruses – 3 types 2. Coxsackie A viruses – 23 types 3. Coxsackie B viruses – 6 types 4. ECHO viruses – 33 types 5. Other Enteroviruses – at least 5 types VIRUSES TRANSMITTED VIA THE FAECAL-ORAL ROUTE WITHOUT SYMPTOMS OF DIARRHOEA Source Unknown  POLIOVIRUS Enterovirus: – 3 distinct serotypes – Type 1 the most likely to cause paralysis – Paralysis in infected individuals: 1 in 1000 Higher in adults POLIOVIRUS Faecal-oral spread – Virus multiplies in lymphoid tissue of GIT & migrates to the local lymphatic glands – Continues to multiply in the intestine with faecal excretion WHICH ONE OF THE FOLLOWING IS MOST CLOSELY ASSOCIATED WITH A HIGHER PREVALENCE OF POLIO? A. Ethnicity B. Family size C. Seasonal factors D. Socioeconomic factors E. Urban living  POLIOMYELITIS –IRISH DATA (WWW.HPSC.IE) Although rare if non-existent in high-income countries, it could return & it is still a major source of illness & death in income-poor countries or during warfare, e.g. Gaza  EPIDEMIOLOGY Humans the only known reservoir Incubation period: usually 7 days Faecal-oral spread Highly infectious! – Can remain in stool for up to 6 weeks  CLINICAL MANIFESTATIONS 3 manifestations 1. Nil or mild illness (90-95% cases) – Virus is still shed in stool & they are infectious 2. Influenza-like illness (4-8% cases) Fever, lack of energy, pharyngitis Complete recovery usually in 1 week 3. Biphasic illness (1-2%) – with fever & GIT symptoms for 2-3 days, appear to recover then develop fever, severe headache, etc. – Aseptic meningitis [1-5%], usually recover – Paralytic poliomyelitis [1 in 1,000] with acute flaccid paralysis; covered in CNS module  POLIOVIRUS Laboratory diagnosis Early in illness – viral culture (throat + faeces) CSF – PCR Treatment Supportive - pain relief & physical therapy Mechanical ventilation, if respiratory failure Bulbar involvement = monitor blood pressure fluctuations, circulatory collapse – (autonomic dysfunction)  POLIO VACCINE Antibody is the principal protective component of the immune response 1. Live attenuated poliovirus (Sabin) OPV - Administered orally - Induces secretory IgA in addition to other humoral immunity - 3 doses must be given in primary course 2. Inactivated Poliovirus “IPV” (Salk) - Contains 3 polio serotypes - Produces immunity (antibody) to each - produces little secretory IgA - 3 doses must be given in primary course Big global priority by WHO & others  POLIO ERADICATION STRATEGY 2022 - 2026 1. Permanently interrupt all poliovirus transmission in endemic countries – Well functioning vaccination programme – Investment in improving surveillance & detection 2. Stop circulating vaccine-derived poliovirus (cVDPV) transmission & prevent outbreaks in non-endemic countries http://www.who.int/topics/poliomyelitis/en/  NON-POLIO ENTEROVIRUSES Epidemiology Human-only infection Incubation period + clinical presentation variable – Depends on the virus Can be detected for 1-2 weeks in pharyngeal washings – & for several weeks in faeces Transmission Faecal-oral route (enterovirus) – Direct contact – e.g. changing nappies – Indirect contact – e.g. contaminated water Oral-oral route (less common) Peri-natal transmission  PATHOGENESIS Initiate infection by replicating in mucosa of the upper respiratory & GI tracts – Multiply in the intestinal tract; only occasionally cause GI symptoms Virus spreads to lymphoid tissue Viraemia common (hence spread to different target organs) Damage to the target organ – direct cell damage – cell-mediated immunity  CLINICAL PRESENTATION Infections more common in children – 75% in children under 15 years old Most are asymptomatic (90%) Can cause a wide range of symptoms – Mild febrile / flu-like illness – Pharyngitis – Respiratory (D68) – Headache – Conjunctivitis – Rash – Meningitis – Paralysis (D68)  DIAGNOSIS & TREATMENT Diagnosis Treatment Enterovirus PCR Illness usually self- – Stool sample limiting – Clinical specimens Supportive treatment – Rehydration Cell culture, rarely – Analgesia done now – Anti-pyretics Antivirals not Serology indicated – Not available  COXSACKIE VIRUSES Large number of different antigenic types divided into two groups: – Coxsackie A – Coxsackie B Source of infection: – faecal-oral – inhalation – direct contact  CLINICAL MANIFESTATIONS Coxsackie A Coxsackie B Fever Fever Common cold Rash Rash Meningitis Herpangina Epidemic myalgia (vesicular ulcerated (Bornholm’s disease) lesions around soft – severe pleuritic chest palate/uvula) pain Hand, foot & mouth Respiratory disease (vesicles) – bronchitis & pneumonia in children Myocarditis, pericarditis  ENTERIC CYTOPATHOGENIC HUMAN ORPHAN (ECHO) VIRUSES At least 33 antigenic types (1 – 33) Spread: – faecal-oral route – oropharyngeal secretions Clinical Manifestations – Many asymptomatic – Fever – Sore throat with rash – Meningitis – Diarrhoea – Rubella-form rash – Pericarditis, myocarditis  ENTEROVIRUS D68 Non polio enterovirus Clinical manifestations Spread: – Mild upper respiratory – Via tract infection direct inhalation manual transfer of – Severe LRTI infected particles – Acute flaccid paralysis – Cough/Sneeze/Saliva/ Fomites Diagnosis Epidemiology – PCR (Throat/ – Cases peak in Summer Nasopharyngeal swab, and Autumn BAL, CSF) – Children predominantly affected Treatment – Underlying respiratory – Supportive illness (Asthma) – No antivirals VIRAL GASTROENTERITIS OVERVIEW Significant cause of morbidity / mortality worldwide – Overcrowded, poorer socioeconomic regions Faecal-oral spread Occasionally droplet (inhalation from vomit) Food contamination Asymptomatic infection common Gastroenteritis Outbreaks, families, institutions, ships VIRUSES CAUSING GASTROENTERITIS Reoviridae family – RNA viruses – Rotavirus Caliciviridae family – RNA viruses – Norovirus Astroviridae family – RNA viruses – Astrovirus Adenoviridae family – DNA viruses – Adenovirus OUTBREAKS OF ROTAVIRUS ARE MOST COMMON IN WHICH ONE OF THE FOLLOWING SETTINGS? A. Crèches B. Fast food outlets C. Holiday camps D. Large families E. Universities  ROTAVIRUS - EPIDEMIOLOGY 7 serogroups (A-G), Group A most common Most common cause of acute diarrhoeal illness in infants + young children – Main cause of diarrhoea requiring hospitalisation – Outbreaks: crèches, children’s hospitals – Susceptibility greatest between 6 & 24 months – By 3yo most infected & immune Infectious dose very small Incubation period: 2-4 days Tropical regions = year round Temperate climates = peaks during the cooler months  ROTAVIRUS - PATHOGENESIS Multiplies in villi of small intestine – Damaged cells slough into lumen of intestine – Release of large numbers of viruses Shortening & flattening of villi – Decreases the surface area for production of enzymes & absorption Hyperosmotic diarrhoea results from this malabsorptive state  CLINICAL PRESENTATION Diarrhoea for about 5 days – Variable mild diarrhoea & vomiting severe, non-bloody watery diarrhoea with dehydration & electrolyte loss – Dehydration – Circulatory collapse & death occasionally in severe cases In immunocompromised, may cause persistent diarrhoea Rarely, CNS manifestations – Seizure – Encephalopathy ROTAVIRUS IN IRELAND (HPSC) LABORATORY DIAGNOSIS / MANAGEMENT Diagnosis: Stool – Antigen detection – PCR Management: Rehydration May develop post-gastroenteritis lactose intolerance – Persistent diarrhoea exacerbated by milk Prevention: Vaccine now available Oral vaccine (2 & 4 months) Given up to 8 months of age  CALICIVIRUSES Small RNA viruses Calicivirus: cup shaped (‘Calyx’) depression on spherical capsid surface Most well-recognised are the Noroviruses – Very common cause of gastroenteritis worldwide – ‘Winter vomiting’ bug – Norwalk virus, a norovirus, is a major cause of epidemics of diarrhoea in children – Half of non-bacterial acute gastroenteritis in US due to Norwalk  NOROVIRUS: EPIDEMIOLOGY Spread by the faecal-oral route – Contaminated water or food Replication in small intestine Asymptomatic excretion by carriers is not uncommon Short incubation period (12-72hrs) Clinical presentation: – Nausea, abdominal cramps – Malaise, myalgia, headache – Acute vomiting – Diarrhoea may occasionally occur Spontaneous resolution in 24-48h Rehydration important  DIAGNOSIS Clinical presentation – especially in healthcare facilities if staff also have symptoms Faeces: PCR (antigen detection & EM but rarely used now)  PREVENTION & CONTROL Hand hygiene – soap & water Good standards of environmental cleaning & disinfection In hospitals & other healthcare facilities – Surveillance to detect cases & outbreaks – Isolation/cohorting of patients – Closing wards/limiting traffic (visitors, staff) & transfers www.hpsc.ie  ASTROVIRUSES Astrovirus: star-like appearance – Similar symptoms to norovirus – Incubation period slightly longer (3- 4 days) – Illness lasts up to 4 days Numerous outbreaks caused by caliciviruses & astroviruses in bivalve shellfish (oysters, clams, mussels etc.) Acute diarrhoea / vomiting – more prominent in calicivirus infections  ADENOVIRUS Double-stranded DNA virus > 40 serotypes Most adenoviruses multiply in GIT & can be found in faeces – Generally asymptomatic Transmission by: – faecal-oral route – respiratory route – direct inoculation Clinical infection: Infantile diarrhoea – watery diarrhoea and fever lasting up to 2 weeks Respiratory infection (common), meningitis, conjunctivitis  SUMMARY POINTS 1. Polio remains important in low-income countries but can be prevented/eradicated by vaccination 2. Enteroviruses cause a variety of illnesses, including meningitis, especially during childhood, but most are minor & self-limiting 3. Rotavirus is a major cause of diarrhoea amongst infants & for which there is a vaccine 4. Norovirus causes sporadic & epidemic diarrhoea & vomiting in hospitals & the community  CLINICAL VIGNETTE On a Thursday afternoon, over a period of 3 hours, four hospital patients develop vomiting followed later by diarrhoea One of the patients is on co-amoxiclav for a urinary tract infection Later, a staff nurse goes off sick with similar symptoms. WHAT IS THE LIKELY CAUSE OF THIS? HOW MIGHT IT HAVE BEEN ACQUIRED? HOW DO YOU TREAT THE PATIENTS & THE NURSE? WHAT MEASURES SHOULD BE TAKEN TO PREVENT ONWARD SPREAD?