Virology – Microbiology – Flashcards
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| RNA viruses |
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| Poliovirus. Coxsackie virus. Enterovirus. Rhinovirus. Hepatitis A virus. Norovirus. Rubella virus. Eastern equine encephalitis (EEE) Venezuelan equine encephalitis (VEE) Western equine encephalitis (WEE) Flavivirus. Dengue virus. St. Louis encephalitis virus (SLE) West Nile Fever virus. Yellow Fever virus. Hepatitis C virus. Lassa virus. Lymphocytic choriomeningitis (LCM) virus Coronavirus. SARS Coronavirus. Ebola virus. Influenza A. Parainfluenza virus. Mumps. Measles. RSV. Rotavirus. Colorado Tick Fever virus. HTLV 1. HIV. |
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| Symptoms of Poliovirus |
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| Mild disease: Fever, malaise, headache, nausea, vomiting, constipation, sore throat. Aseptic meningitis: Above symptoms, plus stiff neck and back pain. Paralytic polio (Infantile paralysis): Flaccid paralysis. |
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| Pathogenesis of Polio |
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| Orally introduced. Multiplication may initiate in lymphoidal tissue (tonsils, Peyer's patches). Viremia ensues even in presence of circulating Ab. Virus continues to be shed for weeks. Neuronal cells infected via blood stream. Both spinal cord and brain may be affected. Myocarditis may be seen on occasion. |
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| Diagnosis of Polio |
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| Virus isolation in human or monkey cell lines. CPE develops within 3-5 days. Identification through neutralization assays. Serology may be used to show 4-fold rise in Ab to poliovirus. |
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| Specimens used for diagnosis of Polio |
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| Throat swabs and/or fecal specimens. |
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| Treatment for Polio |
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| Supportive |
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| Incubation period for Polio |
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| 1-2 weeks. |
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| Epidemiology of Polio |
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| Vaccines developed in the 1950's (Salk and Sabin) Eliminated from Western Hemisphere in 1994. Currently a target for eradication. Occurs in all age groups. Children affected more seriously. Humans are only known reservoir. Often seen in summer. |
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| Symptoms of Coxsackie virus |
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| Aseptic meningitis (A,B) - Fever, malaise, headache, nausea, paresis. Herpangina (A) - Febrile pharyngitis with vesicular lesions. Hand, foot and mouth disease (A) - Pharyngeal ulcerations coupled with vesicular rash on soles and palms. Pleurodynia (B) - Fever and "stabbing" chest pain. Myocarditis (B) - Acute inflammation of the heart. - Presents in adults and children but more severe in children. Cold-like disease (A, B) - Rhinitis, congestion. |
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| Pathogenesis of Coxsackie virus |
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| Orally introduced. Multiplication initiates in throat and gut. Spread via circulatory system. Virus continues to be shed for weeks. |
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| Diagnosis of Coxsackie virus |
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| Virus isolation in cell culture or newborn mice. CPE develops within 6-12 days (slower than Polio) |
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| Specimens used for diagnosis of Coxsackie virus |
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| Throat swabs. Nasal secretions. Fecal specimens. CSF. (Depends on the disease) |
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| Epidemiology of Coxsackie virus |
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| Worldwide. No vaccines. More common in summer and fall. |
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| Incubation period of Coxsackie virus |
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| 3-9 days. |
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| How many types of Enterovirus are know to cause human disease? |
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| Three. |
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| Symptoms of Enterovirus |
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| Bronchiolitis or pneumonia in children. Acute hemorrhagic conjunctivitis. Aseptic meningitis or encephalitis. |
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| Pathogeneis of Enterovirus |
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| Similar to Coxsackie virus. |
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| Diagnosis of Enterovirus |
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| Virus isolation in cell culture. |
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| Epidemiology of Enterovirus |
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| Worldwide. No vaccines. Humans as reservoir. Waterborne transmission most likely cause. |
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| Incubation period for hemorrhagic conjunctivitis (Enterovirus) |
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| 1 day. |
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| Symptoms of Rhinovirus |
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| Common cold: -Sneezing, lacrimation, pharyngitis, malaise, chills, bronchitis. -Clinically may be indistinguishable from similar conditions caused by coronaviruses, adenoviruses, Coxsackie viruses, parainfluenza, and influenza. |
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| Pathogenesis of Rhinovirus |
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| Enters via respiratory tract. Replicates in cells of nasal mucosa. Symptoms are related to host response. |
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| Diagnosis of Rhinovirus |
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| Based on clinical symptoms. |
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| Treatment of Rhinovirus |
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| Symptomatic. |
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| Epidemiology of Rhinovirus |
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| Worldwide. Adults average 1-2 colds per year. Over 100 serotypes. Transmission is likely to be via contact as through respiratory droplets. Being "chilled" is not a predisposing factor. |
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| Incubation period of Rhinovirus |
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| 2-4 days. |
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| Viruses considered Picornaviridae |
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| Enteroviruses: - Poliovirus - Coxsackie virus - Enterovirus - Rhinovirus - Hepatovirus (Hepatitis A Virus) |
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| Virus considered Calciviridae |
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| Norovirus |
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| Symptoms of Hepatitis A virus |
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| (Infectious Hepatitis) Rapid onset; jaundice occurs in prodromal stage - jaundice not always present. Fever, malaise, anorexia, nausea, abdominal discomfort. Hepatitis may be caused by: Hep. A, B, C; EBV; Yellow Fever; CMV; HSV; Rubella; some enteroviruses. |
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| Pathogenesis of Hep. A |
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| Orally introduced. Multiplication in cells lining alimentary tract. Transcytosis brings virus to blood stream. Spreads to hepatocytes. Symptoms related to cell mediated immune response. Virus passed in bile and feces. |
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| Diagnosis of Hep. A |
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| Serology: -Detection of anti HAV IgM. -Not recommended to screen asymptomatic cases (False positives) -Anti HAV IgG useful only as pre vaccine screen. |
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| Treatment of Hep. A |
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| Supportive. |
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| Incubation period of Hep. A |
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| About 1 month. |
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| Epidemiology of Hep. A |
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| Widespread. Outbreaks associated with families, institutions, camps, daycares and military settings. Fecal-oral spread (Food workers pose threat) Raw oysters or clams are a potential source Anicteric cases more common in children About 1/3 of US adults have HAV Ab. |
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| Prevention of Hep. A |
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| Human immunoglobulin. Vaccination. |
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| Symptoms of Norovirus |
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| Gastroenteritis: - Rapid onset; diarrhea, nausea, vomiting, fever, abdominal cramps, headache, malaise. |
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| Properties of Norovirus |
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| Icosahedral. RNA, single stranded. Non-enveloped. Replicates in cytoplasm. |
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| Pathogenesis of Norovirus |
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| Orally introduced. Low ID (~10 viral particles). Multiplication in cells of small intestine. Little else understood about pathogenesis of Norovirus infections. |
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| Diagnosis of Norovirus |
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| Electron microscopy: - Used in stool specimens. - Requires relatively high numbers of virus. Direct detection: - EIA for Norovirus Ag - PCR |
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| Incubation period for Norovirus |
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| 24-48 hours. |
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| Epidemiology of Norovirus |
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| Widespread. Most common cause of adult viral gastroenteritis. More associated with outbreaks than sporadic cases. Estimated 23 million cases per year in US. Outbreaks associated with restraunts, long term care facilities, schools, cruises. |
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| Arenaviridae viruses |
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| Lassa virus. Lymphocytic choriomeningitis (LCM) virus. |
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| Coronaviridae viruses |
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| Coronavirus. SARS Coronavirus. |
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| Filoviridae virus |
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| Ebola virus. |
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| Symptoms of Lassa virus |
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| Malaise, fever, headache, sore throat, nausea, vomiting, diarrhea, myaglia. 80% of cases are asymptomatic. Disease is more severe during pregnancy. Fetal loss is 80%. In severe cases: Shock, pleural effusion, hemorrhage, seizures. Deafness is a complication. |
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| How is Lassa virus acquired? |
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| Via aerosol of rodent excreta. Transmissible human to human. |
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| Treatment of Lassa virus |
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| Ribavirin. |
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| Incubation period of Lassa virus |
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| About 1-3 weeks. |
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| Symptoms of Lymphocytic choriomeningitis (LCM) virus |
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| Many subclinical cases. Acute disease manifested as meningitis. May appear as mild "flu-like" illness with fever, chills, malaise, weakness, headache, sore throat. Rarely will develop into encephalitis. |
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| Pathogenesis of Lymphocytic choriomeningitis (LCM) virus |
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| Transmitted via urine, saliva or excreta of infected mice. Spread throughout body similar to adenoviruses. Often will spread to meninges. Cell mediated response of host may actually exacerbate disease. |
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| Diagnosis of Lymphocytic choriomeningitis (LCM) virus |
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| Serology. Virus isolation or detection. |
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| Incubation period of Lymphocytic choriomeningitis (LCM) virus |
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| 1-2 weeks. |
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| Epidemiology of Lymphocytic choriomeningitis (LCM) virus |
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| Widely seen in Europe and the Americas. Reservoir is house mice. No evidence of human to human spread. |
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| General characteristics of Lymphocytic choriomeningitis (LCM) virus |
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| Pleomorphic (spherical) viral particles. RNA genome. Enveloped. Replication occurs in cytoplasm. |
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| Symptoms of Coronavirus |
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| Afebrile "common colds"; considered relatively harmless viruses for humans. Unique strain causes Severe Acute Respiratory Syndrome (SARS-CoV) -Fever, malaise, chills, headache, dizziness, cough, followed by shortness of breath. -May require ventilation. Fatality rate is ~10%. |
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| Pathogenesis of Coronavirus |
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| Highly species specific. Tropism for epithelial cells of respiratory tract. SARS agent may represent jumping the "species barrier". |
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| Diagnosis of Coronavirus |
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| Serology - Ab or Ag detection with EIA or HI Isolation - Challenging, rarely used. |
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| Incubation period for Coronavirus |
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| About 5 days. |
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| Epidemiology of Coronavirus |
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| Worldwide. Cause of perhaps 20% of all colds. Ab found in >90% of adults. Concept of "Super spreaders". |
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| General characteristics of Coronavirus |
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| Pleomorphic (long filamentous) viral particles. RNA genome. Enveloped. Replication occurs in cytoplasm. |
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| Symptoms of Ebola |
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| Severe, acute illness with fever, malaise, myalgia, headache, followed by vomiting, diarrhea, rash. In most serious form, progresses to hemorrhagic disease with hepatic and renal involvement leading to organ failure and death. |
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| Pathogenesis of Ebola |
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| Highly virulent. Propism for endothelial cells, macrophages and hepatocytes. High virus titers in all major organs. Mortality rate up to 90%. |
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| Diagnosis of Ebola |
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| Serology. Isolation: BSL-4 required. |
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| Epidemiology of Ebola |
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| Central and West Africa. First recognized in 1976 (Hot Zone - Preston) Reservoir likely non-human primates, possibly bats. |
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| Incubation period of Ebola |
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| 1-2 weeks. |
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| Orthomyxoviridae virus |
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| Influenza A |
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| Paramyxovirdae viruses |
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| Parainfluenza virus. Mumps. Measles. RSV. |
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| Symptoms of Influenza A (also B and C) |
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| Chills, headache, cough, fever, myalgia, malaise, anorexia. Complications of influenza are associated with age, debilitating disease, pregnancy. Secondary pneumonia may develop: Frequently related to bacterial disease. |
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| Pathogenesis of Influenza A |
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| Spread through airborne droplets. Tropism for resp. epithelial cells. Virus spreads to adjacent cells. Cell death and desquamation ensue. Edema and monomuclear infiltration leads to many of influenza's symptoms. Systemic effects related to cytokine action. |
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| Diagnosis of Influenza A |
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| Virus isolation or detection. - Embryonated eggs, cell culture. - Requires hemadsorption or hemagglutination to detect. FA techniques may be used with shell vial culture. Direct detection lacks sensitivity and specificity. Serology: HI, EIA, Neutralization assays. |
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| Treatment for Influenza A |
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| Amantadine Prevention - Vaccines. |
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| Incubation period of Influenza A |
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| 2-5 days. |
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| Epidemiology of Influenza A |
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| Annual outbreaks with predictable pattern. Up to 5 million cases annually with ~500,000 deaths. Antigenic drift and shift. Species variation, genetic recombination. Pandemic risk. |
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| Paramyxo vs. Orthomyxo: Which is larger? |
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| Paramyxo. |
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| Replication in the nucleus? (Orthomyxo or Paramyxo) Other is in the cytoplasm. |
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| Orthomyxo. |
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| Symptoms of Parainfluenza |
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| Varies by age and type. Infants and children: Croup like illness, bronchitis, bronchiolitis, pneumonia. Fever, rhinitis, pharyngitis, otitis media. Adults: Laryngitis, rhinitis. |
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| Incubation period of Parainfluenza |
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| About one week. |
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| Epidemiology of Parainfluenza |
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| Widespread, common cause of serious respiratory illness in infants and children (2nd to RSV), frequently spread on close settings (daycare, etc.) |
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| Symptoms of Mumps |
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| Infants and children: Acute, febrile disease with enlargement of salivary glands (parotitis) Adults: Fever, malaise, anorexia. Complications - Meningitis, orchitis. |
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| Pathogenesis of Mumps |
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| Spread via resp. route. Localized in nasal passages and upper resp. tract. Viremia followed by involvement of parotid glands. Virus shed in saliva. Virus may spread to certain visceral organs, particularly kidneys. |
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| Diagnosis of Mumps |
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| Virus isolation: -Cell culture with FA detection. -CPE shows syncytia. -Detection using Hemadsorption inhibition. Serology: -HI or EIA |
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| Incubation period of Mumps |
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| About 2 weeks. |
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| Epidemiology of Mumps |
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| Worldwide. Mortality rate is low (~3/10,000 - Often related with mumps encephalitis). Live, attenuated vaccine available. |
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| Symptoms of Measles |
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| Acute, highly communicable disease with fever, conjunctivitis, coryza, cough, Koplik spots, rash. Rash begins on face. More severe in infants and adults than children. Infectious during prodromal phase. |
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| Pathogenesis of Measles |
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| Spread via resp. route. Localized in upper resp. tract. Spreads to regional lymph nodes. Viremic spread through RES cells. Virus secreted in tears, nasal secretions, urine, blood. Encephalitis is a potenial complication. Sub-acute sclerosing panencephalitis is a fatal sequela seen rarely. |
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| Diagnosis of Measles |
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| Often made clincally. -Antigen detection. -Virus isolation. -Serology. |
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| Incubation period of Measles |
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| About ten days. |
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| Epidemiology of Measles |
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| Worldwide. Very low infectious dose. Mortality rate may be up to 5%. Measles deaths are still a major issue in developing countries. Live, attenuated vaccine available. |
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| Symptoms of Respiratory Syncytial Virus (RSV) |
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| Primarily affects children. Ranges from subclinical to cold to pneumonia. Otitis media is common complication. Hospitalization of infant may be required (2:100) Death of admitted infants occurs 1:100 |
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| Pathogenesis of RSV |
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| Spread via resp. route. Localized in nasopharynx. Spreads to lower resp. tract. Viremia is rare. Risk to infants is related to small air passages. |
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| Diagnosis of RSV |
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| Antigen detection. Virus isolation. Serology. |
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| Incubation period of RSV |
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| About 3-5 days. |
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| Epidemiology of RSV |
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| Worldwide. No vaccine. Reinfection may occur, but with less serious symptoms. |
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| Reoviridae viruses |
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| Rotavirus. Colorado Tick Fever virus. |
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| Retroviridae viruses |
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| HTLV 1 HIV |
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| Symptoms of Rotavirus |
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| Diarrhea, fever, abdominal pain, vomiting, dehydration. Loss of electrolytes can be fatal in infants and young children. Symptoms in adults are mild or not evident. |
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| Pathogenesis of Rotavirus |
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| Virus attaches to cells in villi of small intestine. Multiply in these cells and disrupt transport mechanisms. Sodium and glucose absorption are disrupted. Infected cells and viruses are sloughed off in the intestine and shed in stool. Shedding may occur for up to two weeks. |
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| Diagnosis of Rotavirus |
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| Virus isolation: Cell culture not used. Virus detection: EM, EIA, LA. Serology: Uncommon. |
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| Treatment of Rotavirus |
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| Supportive. Restore electrolytes. |
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| Incubation period of Rotavirus |
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| 1-3 days. |
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| Epidemiology of Rotavirus |
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| Worldwide. Single most important cause of gastroenteritis in children worldwide. Fecal-oral spread. Reservoir likely humans. ~5 billion cases per year; ~5 million deaths per year. Outbreaks more common in winter. |
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| Symptoms of Colorado Tick Fever |
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| Fever, myalgia, headache, nausea, vomiting. Fever is normally dyphasic. |
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| Pathogenesis of Colorado Tick Fever |
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| Spread via Tick bite. Viremia occurs. Blood cells are infected. Disease in self limited. |
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| Incubation period of Colorado Tick Fever |
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| 3-4 days. |
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| Human T-lymphotropic virus (HTLV) |
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| Cause of Adult T-cell Leukemia. Most commonly seen in Japan. Likely acquired via breast milk. Latency up to 50 years. |
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| Symptoms of Human Immunodeficiency Virus (HIV) |
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| Fatigue, rash, headache, nausea, night sweats (may occur 3-6 weeks after infection) Immunosuppression: Opportunistic infections - PCP, Candidiasis, Kaposi's sarcoma. |
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| Pathogenesis of HIV |
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| Very slow progressing. Blood borne acquisition. Viremia with seeding of lymphoid organs. T helper lymphocytes (CD4) are the target cell. Ultimately, CD4 count drops. Viral load increases. Individuals succumb to opportunistic infections and other effects of immunosuppression. |
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| Diagnosis of HIV |
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| Serology: -Antibody detection: Screening test (EIA) followed by confirmatory test (WB) -Western Blot. -Problem with "window" -Testing used is influenced by prevalence of disease. -PCR now being used more routinely. Cell counts: -CD4 counts. -<200 cells per microliter (AIDS) Viral load: Used to monitor treatment and disease progression. |
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| Treatment of HIV |
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| Antiretroviral drugs. -Nucleoside analog reverse transcriptase inhibitor (NRTI) -Non-nucleoside reverse transcriptase inhibitor (NNRTI) -Protease inhibitor (PI) -Fusion inhibitor -Chemokine co-receptor antagonists -Nucleoside inhibitors Highly active antiretroviral therapy (HAART) Suppress viral replication. Does not cure HIV infection/AIDS |
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| Incubation period of HIV |
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| About 2-3 months to display antibody. 1-15 years to progress to HIV stage 3. |
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| Epidemiology of HIV |
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| Worldwide; disproportionate distrobution. Recognized in 1981; Virus isolation in 1983; Test release in 1985. Routes of transmission vary by population. |
