CNS Infections: Polio and Coxsackie PDF
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University of the West Indies
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This presentation provides information on CNS infections, focusing on poliovirus and Coxsackie viruses. It covers various aspects, including etiology, clinical manifestations, diagnostic approaches, and treatment strategies.
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CNS Infections : Poliovirus and Coxsackie Objectives Be able to list the common causes of bacterial vs viral meningitis Basic knowledge on viral structure and clinical effect Discuss transmission and effects and patient population of polio and Coxsackie viruses Basic knowledge on the vaccines availa...
CNS Infections : Poliovirus and Coxsackie Objectives Be able to list the common causes of bacterial vs viral meningitis Basic knowledge on viral structure and clinical effect Discuss transmission and effects and patient population of polio and Coxsackie viruses Basic knowledge on the vaccines available Acute meningitis Syndrome characterized by: Meningeal symptoms – headache, neck stiffness, vomiting, photophobia Cerebral dysfunction – confusion, coma CSF – WBC, proteins, glucose abnormalities Aseptic Meningitis First described in 1925- acute community-acquired meningitis with negative CSF gram stain and culture. Most common causes: Enterovirus, Arbovirus, HSV2 Clinical Features of Aseptic Meningitis A few days history of fever Headache Neck stiffness Unlike bacterial meningitis-no altered mental status Onset less acute Lethargy, but cerebral function is normal Causes of Meningitis Adapted from Oxford handbook of Infectious Diseases and Microbiology, 2nd edition, 2017 Causes of Bacterial Meningitis Adapted from Oxford handbook of Infectious Diseases and Microbiology, 2nd edition, 2017 Bacterial Meningitis Clinically – fever, headache, meningism (neck stiffness, photophobia, Kernig and Budzinski sign) +/- Cranial nerve palsies, rash, hemiparesis Rare – papilloedema Rhinorhoea/otorrhoea Neonates – nonspecific symptoms Elderly – insidiously Investigation CSF sample Elevated opening pressure >18mmHg Elevated WBC (neutrophil predominant) Elevated protein Low glucose Gram stain (positive in 60-90%) Culture (positive in 70-85%) PCR (positive in 90%) Treatment Adapted from Oxford handbook of Infectious Diseases and Microbiology, 2nd edition, 2017 Viral Meningitis Picornaviridae leading cause – echovirus, Coxsackie virus, enterovirus 70, 71, Arboviruses - St. Louis encephalitis, California, Eastern equine, Western equine, Venezuelan equine, Colorado tick fever Mumps Herpes viruses HIV Other-Rabies,inflenza,arboviruses,parechoviruses,lymphocytic choriomeningitis virus Viral Meningitis Symptoms depend on causative agent Enterovirus – respiratory tract symptoms Usually occurring in community outbreaks Mumps – parotitis HSV – urinary retention, dysaesthesia, paraesthesiae, neuralgia, motor weakness Diagnosis and Elevated WBC – lymphocytosis Protein - normal or mildly elevated Glucose – normal or mildly reduced Viral culture – enteroviruses Serology Molecular methods (PCR) Treatment Poliovirus Group C human enterovirus and member of Picornaviridae family. Naked virus Faeco-oral RNA virus Icosahedral Poliovirus Three serotypes – infection by one confers protective immunity ONLY to that type Paralytic disease mainly type 1 Transmission – mainly faeco-oral Pharyngeal in epidemics Targets anterior horn cells Poliovirus Initially sporadic, later developed into epidemics Children 5-9 most commonly 1/3rd in >15yrs Rates fell dramatically after vaccine Global Polio Eradication Initiative Number of countries in which polio transmission has never been interrupted Afghanistan and Pakistan Nigeria, Ethiopia, Iraq, Somalia, South Sudan Pathogenesis Enters through the GI tract, replicating in the gut and adjacent lymphoid tissue Reaches susceptible reticulo-endothelial tissuevia the bloodstream. Asymptomatic cases stop at this point with type-specific antibodies formed. Otherwise, replication and viraemia occur causing a “minor illness” CNS becomes infected by retrograde axonal transport from muscle to nerve to cord. Neurons throughout the grey matter, especially anterior horn of the spinal cord Motor nuclei of the medulla and pons. Distribution of lesions is similar in all cases—it is their severity that determines clinical disease. Poliovirus Clinical Features Incubation: 9–12 days from acquisition to prodrome “Minor illness” 2–3 days of fever, headache, sore throat, anorexia, vomiting, abdominalpain, 11–17 days until the onset of paralysis “Major illness”. Manifestations: inapparent—95% of cases are asymptomatic; abortive—4–8% of infections experience just the prodrome; non-paralytic polio—severe, abortive, with signs of viral meningitis; spinal paralytic polio—frank paralysis occurs in 0.1% of infections. Polio-Risk Factors Risk factors for paralysis : Prepubertal male, pregnancy, B-cell deficiency (increases the risk of oral polio vaccine (OPV)- associated disease), strenuous exercise within first 3 days of major illness, IM injections (paralysis localizes to the limb injected or injured within 2–4 weeksbefore infection), the tonsillectomized (eight times the risk of those with tonsils). Polio-Complications Complications: Respiratory compromise (diaphragmatic and intercostal muscle paralysis, upper airway obstruction, respiratory centre impairment), myocarditis, GI hemorrhage, ileus, complications of paralysis. Differential - other enteroviruses, West Nile, Guillain– Barré, herpes zoster, rabies, botulism, diphtheria, cord lesions, neuropathies, myopathies. Diagnosis CSF - viral identification by PCR or culture (less sensitive) is gold standard. Throat—the virus may be detected in the first week of illness. Faeces—may be detected for several weeks. In areas of low incidence, it is important to identify the viral strain (wild-type or vaccine-related), as the presence of vaccine-virus is not uncommon in the healthy and does not conclusively prove the aetiology. Serology—paired sera; cannot distinguish wild-type from vaccine. Treatment No specific antiviral therapy. Management is supportive. Bed rest is essential in the acute phase to reduce the extension of paralysis. Avoid IM injections. Ventilatory assistance is required once vital capacity falls to 5 Most cases are asymptomatic Some cases result in herpangina – with involvement of tonsils, palate Rash appears several days after high temperature and painful sore throat Itchy, painful, especially on the hands/fingers and bottom of feet. Acute haemorrhagic conjunctivitis (A24 specifically) Aseptic meningitis (both Coxsackie A and B viruses). Coxsackievirus A7 infrequently causes polio-like permanent paralysis. Coxsackie B Viral prodrome – fever, headache, sore throat, extreme fatigue Worst case scenario – myocarditis, pericarditis, permanent cardiac damage, sudden death Aseptic meningitis Incubation 2-6 days Can last 2 days to 6 months if severe Bornholm Disease AKA Epidemic pleurodynia Diaphragmatic pleurisy Epidemic myalgia “Devils Grip” Coxsackie B Supportive treatment May use anti-inflammatories to prevent/reduce carditis No vaccine available Handwashing! Handwashing! Handwashing! VIRUS IS HIGHLY CONTAGIOUS Bathe after swimming pool ?Diabetes Mellitus type 1 Summary Adapted from Medical Microbiology by Murray et al Summary Summary Adapted from Medical Microbiology by Murray et al Questions?