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Medical Microbiology Enteroviruses Fall, 2009

Medical Microbiology Enteroviruses Fall, 2009. INSTRUCTOR : Dr. J. David Gangemi Chapter 57, Murray, 6 th Edition TEACHING OBJECTIVE : Review of enterovirus biology, pathogenesis, and immune response to infection

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Medical Microbiology Enteroviruses Fall, 2009

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  1. Medical MicrobiologyEnterovirusesFall, 2009 • INSTRUCTOR: Dr. J. David Gangemi • Chapter 57, Murray, 6th Edition • TEACHING OBJECTIVE: Review of enterovirus biology, pathogenesis, and immune response to infection • KEY WORDS: Polioviruses, echoviruses, coxsackie A & B viruses, enteroviruses, aseptic meningitis, paralytic disease, Salk vs Sabin vaccines,herpangina, pleurodynia, myocardiopathy

  2. Outline of Major Teaching Points I. BACKGROUND II. CLASSIFICATION III. BIOLOGICAL PROPERTIES IV. VIRAL PATHOGENESIS V. IMMUNITY VI. DISEASE

  3. Picornaviridae Rhinoviruses Enteroviruses Hepatoviruses 1) Echoviruses 2) Coxsackiviruses 3) Enteroviruses

  4. Enterovirus Prototype: “Poliovirus” Genome ss (+) RNA Capsid VP1 - VP4 (60 Copies each) Size 20-30 nm

  5. Diseases Associated withEnterovirus Infections 1. Non-specific Febrile Illness 2. Perinatal Infection 3. Febrile Disease With Rash 4. Meningitis 5. Myocarditis 6. Hepatitis 7. Pleurodynia 8. Poliomyelitis

  6. I. BACKGROUND The enteroviruses have been among the most intensively studied of all human pathogens. The war on poliomyelitis produced many breakthroughs in the science of virology.

  7. I. BACKGROUND (cont’d) Research on the enteroviruses has led to: • Important discoveries in the replication of RNA viruses • x-ray crystallographic characterization • Fine structure mapping

  8. II. CLASSIFICATION The Enteroviruses: • Are small, nonenveloped, and have a single positive sense RNA strand • Infectious particles are 27- to 30-nm • Capsid made up of 60 copies each of four proteins, VP1-VP4

  9. II. CLASSIFICATION (cont’d) Because the Enteroviruses have no lipids in their capsid: • They are stable against treatment with ether, ethanol, and various detergents • They are heat and acid stable and will stay viable for hours on laboratory surfaces if left moist

  10. General Features Used For Taxonomy Stable in an acid (pH 3-5) environment; replicate in GI tract; isolated from throat or lower intestine, feces. Some cause silent infections or disease and are occasionally isolated from blood or spinal fluid. • 1. Polio (types 1-3) • 2. Coxsackie A: 24 types • 3. Coxsackie B: 6 types • 4. Echoviruses (enteric cytopathic human orphan): 34 types • 5. Enteroviruses (types 68-71) • 6. Hepatitis A virus (Enterovirus 72)

  11. III. Biological Properties 1. Found in feces & spread by fecal- oral route 2. Grow in tissue culture with or without CPE 3. Cause silent infections but also cause a number of important illnesses

  12. III. Biological Properties(cont’d) 4. Several genera of Enteroviruses can cause similar symptoms, e.g. aseptic meningitis or exanthems, but some diseases have a more specific association with a single genus, e.g., pleurodynia and herpangina 5. Isolation of Enteroviruses from the stool provides a basis for suspecting that the virus is responsible for the illness in question.

  13. IV. VIRAL PATHOGENESIS • Virus enters the body through the mucosa of the oropharynx and upper respiratory tract, then begin to multiply in the tissues around the oropharynx. • Because the Enteroviruses are stable in acid they are able to pass through the stomach into the intestines, where they undergo further rounds of replication. • Roughly at the same time as it reaches the intestine, the virus begins to spill into the systemic circulation. This early (primary) viremic phase is usually asymptomatic and involves fairly low titers of virus in the blood.

  14. IV. VIRAL PATHOGENESIS(cont’d) • During the primary viremia, tissues are seeded according to the tropism of the virus • In the case of the polioviruses, the tissues infected include neurons, especially the anterior horn cells of the spinal cord

  15. V. IMMUNITY • Antibodies can be detected in the circulation by the seventh to tenth day after exposure, roughly the same time as the symptomatic disease and secondary viremia occur. • With the exception of the gastrointestinal tract, viral replication in tissues soon slows to a halt. In contrast, gastrointestinal tract viral multiplication and fecal shedding can continue for weeks after the development of high neutralizing antibody titers.

  16. VI. Disease The Enteroviruses: • Cause a variety of clinical syndromes, with a great deal of overlap among the different serotypes • Viral tropism, as determined by the Vp1 capsid protein, ultimately determines tissue involvement and the clinical syndrome which each serotype can cause

  17. Aseptic Meningitis Symptoms- headache, neckache, rigidity of neck and back, malaise Cause- while several viruses can cause aseptic meningitis (enteroviruses, mumps, lymphocytic choriomeningitis, herpes, etc.), there are other causes of nonpurulent meningitis (chlamydia, leptospira). Certain other bacteria and fungi may also cause nonpurulent spinal fluids but with altered chemistry compared to viral meningitis.

  18. Poliomyelitis • Poliovirus was once thought to be the main cause of paralysis before the advent of polio vaccines • Poliovirus did account for a large portion of paralytic cases but many cases were caused by other agents or were due to unknown causes

  19. Poliomyelitis:Disease Characteristics • The vast majority of persons infected with poliovirus have an inapparent or silent infection. • The symptoms, locations, extent and persistence of paralysis depend on the degree of damage to the anterior horn neurons and the number of neurons affected. • If all neurons supplying a given muscle are irreversibly damaged, the result is permanent paralysis; but if the damage to the neurons is incomplete and reversible or if some neurons are spared, the muscle function can be restored or regained.

  20. Poliomyelitis:Disease Characteristics (cont’d) Paralytic disease (spinal form) may begin with excruciating pain or spasms which may precede paralysis of the extremities.

  21. Poliomyelitis:Disease Characteristics (cont’d) • An especially serious form isbulbar polioas it involvescranial nervesandrespiratory and circulatory centers in the medulla. • Post paralytic polio syndrome may occur many years after initial disease and reflects the continued loss of neurons with aging.

  22. Poliomyelitis:Prevention • The Salk polio vaccine is a formalinized whole virus preparation. • The Sabin polio vaccine is a live, attenuated virus. Attenuation means repeated passage of the virulent poliovirus in tissue culture to produce mutants which no longer are neurotrophic. • Immunity from Sabin vaccine seems to be lifelong. Protection with the Salk vaccine requires multiple immunizations and boosters which can cause logistical problems.

  23. Poliomyelitis:Prevention (cont’d) • Questions have been raised about the Sabin vaccine in view of the alleged polio paralysis in a few recipients of the vaccine and their contacts. • Also note susceptibility of populations in which religious beliefs prevent immunization.

  24. Diseases Associated with Coxsackie Viruses 1. Summer Minor Illness - this is an acute febrile illness of short duration and without distinctive features, usually occurring in summer and fall, and may be accompanied by a rubelliform rash on the face, neck and chest. 2. Herpangina - mostly in children; caused by Coxsackie A (types 1-10), B (types 1-5) and some echoviruses; virus is isolated from stool in 86% of cases; epidemic in the summer months; symptoms are mild and patients recover; characterized by abrupt onset of fever, sore throat, anorexia, abdominal pain and tiny, discrete vesicles with red aureola on the anterior pillars of the fauces, the tonsils, pharynx and edges of the soft palate.

  25. Diseases Associated with Coxsackie Viruses (cont’d) 3.Pleurodynia- Coxsackie group B; characterized by acute sudden chest pain, fever, malaise (may present as coronary occlusion); may also be accompanied by abdominal and testicular pain; viremia is followed by seeding of the virus to striated intercostal muscles; recovery is complete but relapses are common.

  26. Diseases Associated with Coxsackie Viruses(cont’d) 4. Aseptic Meningitis - No bacteria cultivated from CNS; caused by Coxsackie A or B; fever, malaise headache, anorexia, abdominal pain and sometimes mild muscle weakness and severe stiff neck. 5. Neonatal Disease – Mostly group B and some group A; ranges from inapparent infection to fatal disease.

  27. Diseases Associated with Coxsackie Viruses(cont’d) 6.Respiratory Infections - Coxsackie A10, A24, B3; common cold-like symptoms. 7. Hand, Foot & Mouth Diseases - Coxsackie A16, A4, A5, A9, A10; vesicular lesions. 8. Myocardiopathy - Involves several Coxsackie B types. 9. Sudden Onset Diabetes - associated with Coxsackie B4 infection.

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