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70 Cards in this Set
- Front
- Back
General Characteristics of Viruses
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Require LIVING cells for growth and
replication (cell cultures, embryonated eggs, living animals/plants) • Have DNA or RNA…NEVER both! • Multiply by separate synthesis of nucleic acid and protein, combine to form virus particles • Size varies from 10 nm-300 nm |
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Basic Components of Viruses
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Nucleic Acid
-infectious genetic material Protein Coat Surface Antigens -protein or carbohydrate -highly variable |
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Replication
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Adsorption
. Penetration and uncoating Nucleic acid and protein synthesis Assembly Release |
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How do we detect viral infections?
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1. Detect the virus itself!
2. Detect the immune response…antibodies against the virus! |
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Viral Diagnosis- A. Detection in clinical
specimens |
1. Visualisation by
Electron microscopy 2. Cell culture (cytopathic effects, hemagglutination, immunofluorescence) 3. Detection of viral antigens (ELISA) |
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Viral Diagnosis- Detection of patient’s immune responses
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Antibody detection, presence or absence (ELISA)
– IMMUNITY TEST • Rise in antibody titre or high antibody titre – DIAGNOSTIC TEST |
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What types of viruses will we learn about?
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1. Viruses of the breathing
2. Enteric viruses 3. Viruses of diarrhea 4. Viruses of the rashes 1. Viruses of the glands 2. Viruses of the liver 3. Viruses of the brain 4. Viruses of the immune system…aka…HIV |
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Respiratory disease
• Different families |
1. Influenza viruses
2. Parainfluenza viruses 3. Respiratory syncytial viruses 4. Rhinoviruses 5. Adenoviruses 6. Echoviruses, coxsackie viruses, herpes viruses (occasional respiratory tract infection) |
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types of Influenza Viruses
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Influenza virus type A: major epidemics
• Influenza virus type B: milder disease Produce haemagglutinin (diagnostic) • Frequent recombination which means that there are new types which sprea throughout the world causing pandemics of influenza. = High antigenic variability = Pandemics |
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Influenza Viruses clinical, diagnosis, serum, prevention
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Clinical:
– fever, variable respiratory symptoms – Infants and elderly more susceptible • Diagnosis: – Throat washings, naso-pharyngeal aspirate inoculated into cell culture • Serum: – Paired sera (acute and convalescent stage) • Prevention: – Annual vaccination especially for high risk groups |
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The WHO Pandemic response and planning is a
direct reflection of disease SPREAD and not of disease SEVERITY What about disease severity? |
Greater disease burden in <25 yrs than in
>65 yrs – Unusual for seasonal flu • Certain groups have risk of complications – Pregnant women, asthma, diabetes, immune suppression, heart disease, kidney disease – Same as for seasonal flu |
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What does the H1N1 virus look like?
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Has been termed “swine” flu
• Influenza genome has 8 segments • 2009 H1N1 segments – 3 from classical swine – 2 from asian swine – 2 from avian – 1 from human |
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H1N1 2009 vaccine
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Vaccination is major effort of PHAC to fight
pandemic flu • Canada has a dedicated vaccine manufacturer • Adjuvanted vs. unadjuvanted vaccine – Why adjuvant? • To reduce the amount of vaccine protein per dose – Why new adjuvant? • Existing adjuvants have never worked well for flu shots – Why controversial? • Little data on adjuvant in children, pregnant women • New adjuvant had not been used in other vaccines |
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Parainfluenza viruses
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Infants and young children
• Respiratory infection that could have serious complications • Croup (barking cough, high pitch sound on inhalation) • Bronchiolitis, bronchopneumonia • No vaccine |
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Respiratory syncytial virus
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Major respiratory pathogen for children < 2years
• Pneumonia and bronchiolitis; occasionally fatal • Epidemics • No vaccine • Antiviral: Ribavizine |
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Rhinovirus
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Common colds
• > 100 serotypes; no cross-immunity • Repeated infections |
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Adenovirus
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Pharyngitis and conjunctivitis; pneumonia in
young children • Children most commonly infected • Asymptomatic infection common • Vaccines used in army |
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ENTERIC VIRUSES- general information
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Enterovirus = Enteric virus
• Infect intestinal / lymphoid cells • Poliovirus, coxsackievirus, echovirus • Multiply in GI tract, but RARELY cause gastroenteritis • Infection via respiratory or GI tract • Spread to other target organs in body • 95% inapparent infection, 4-5% minor illness, 1% serious illness |
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Poliovirus
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Humans are the ONLY natural host
• Types 1, 2 and 3 • Causes poliomyelitis – Highly infectious, invades the host nervous system and can cause total paralysis in as little as a few hours |
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Global Polio Eradication Initiative
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– Launched in 1988 by WHO, goal was to eliminate
poliovirus in the same manner as smallpox was eliminated – Since 1988, number of cases has decreased by ~99% (from > 350,000 cases in 1988 to 1997 cases in 2005) – Currently polio is only found in parts of Africa and South Asia (Nigeria, India, Pakistan, Afghanistan) |
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Poliovirus Diagnosis
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Isolation from stool samples (up to 5-6
weeks after infection), CSF and pericardial fluid • Serology: acute and convalescent phases * Carriers with inapparent infection are able to spread the disease to susceptible individuals* |
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Polio Prevention
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VACCINATION
– Salk vaccine (Jonas Salk) • Killed/inactivated vaccine; does not produce local immunity in GI of host (IgA); Virus can still colonize host GI tract and SPREAD to the community!!! • used for immunocompromised – Sabin vaccine (most common; Albert Sabin) • Live attenuated; host will produce IgA and IgG, so is protected against intestinal colonization and virus can NOT replicate and spread • Oral administration |
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Coxsackieviruses
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minor respiratory illness (mainly group B)
aseptic meningitis (both group A and B) herpangina and hand-foot-and-mouth disease (group A) pleuodynia, pericarditis, and myocarditis (group B) |
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Coxsackieviruses
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Groups A and B
• Seasonal variation • Diagnosis by stool sample and paired sera (same as polio) • NO VACCINE |
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Echoviruses
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Several types
• Enteric cytopathogenic human orphan viruses • Minor respiratory illness • Aseptic meningitis • Same diagnosis as coxsackie and polioviruses • NO VACCINE |
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Viruses of Diarrhea
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ROTAVIRUS
– Epidemics in infants (6 months-2yrs); mainly in winter – Replication in small intestine – Acute gastroenteritis vomiting, diarrhea, fever – Highly infectious!!! |
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Rotavirus diagnosis epidemiology and prevention
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Diagnosis
– EM or immunological testing of virus from stool samples (within 3 days) • Epidemiology – Short incubation (2-3days) – Fecal-oral route, aerosols (explosive diarrhea), fomites – Outbreaks in daycare centres, children’s hospitals • Prevention – Rapid diagnosis and isolation of patient – Proper handwashing – No vaccine….. |
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Norovirus diagnosis, epidemiology and prevention
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Outbreaks of gastroenteritis in older children and
adults • Diagnosis: first exclude bacterial cause, then can be differentiated from bacterial gastroenteritis • Epidemiology: VERY CONTAGIOUS; survives well on objects/environment – Fecal-oral route; food-borne outbreaks • Prevention: no vaccine; handwashing and isolation of infected individuals |
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US CDC estimated in 1999 (Mead et
al.) that of all foodborne illness: |
30% is bacterial
3% is parasitic 67% is viral |
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Of viral foodborne outbreaks:
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More than 90% attributed to
Noroviruses |
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Adenoviruses (also a respiratory virus!)
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Some types cause gastroenteritis in children
– Can NOT cultivate diarrhea type in cell culture – Diagnosis by EM |
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Calici- and Astro- viruses
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Sporadic gastroenteritis in children
– EM diagnosis – Fecal-oral route of transmission |
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Viruses Causing Rashes
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Common epidemiological features of
viruses causing rashes: – Humans are the only reservoir – Highly contagious! |
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5 virus names causing rashes
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Measles
• Rubella (German measles) • Varicella (chickenpox) • Herpes simplex (HSV) • Papilloma virus |
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Measles
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One of the highest infectivity rates
• Clinical: rash first appears behind ears, forehead and nostrils then spreads to whole body; BLOTCHY appearance • Lifelong immunity after natural infection • Complications: secondary bacterial infections ie bronchopneumonia – Encephalitis (rare) – Exacerbation of TB and leukemia |
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Measles diagnosis and prevention
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• Diagnosis:
– Serological – Confirmation of Suspected Case: • IgM Ab in single blood specimen against measles OR a rising IgG Ab titer against measles in paired blood – Immune status • Circulating measles specific Ab IgG • Prevention – Immunoglobulin: can suppress disease if given within 5 days of contact with virus – Live attenuated vaccine: very effective, widely used. Administer after 12 months of age • MMR |
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Rubella (German Measles)
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VERY dangerous for non-immune pregnant
women birth defects • Largest danger is in first trimester – 50% chance of damage to the fetus if non-immune mother is infected between 0-4 weeks • Birth defects: – General: abortion, death of newborn – Localized: cataracts (infection during 6 th week) deafness (infection during 9 th week) heart defects (infection during 5 th -10 th week) Other: low birth weight, cleft palate, mental deficiency |
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Rubella epidemiology
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Clinical: similar to measles but milder; lifelong immunity
• Epidemiology and Immunity: pre-vaccine era, seen in school children during winter in spring, outbreaks every 7-10 years, lead to life-long immunity – Now most cases (60%) are seen in those 15 years and olderRub |
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Rubella diagnosis
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Lab Diagnosis:
– Suspected cases: detection of rubella specific IgM or rising Ab titer in paired sera – Immunity status: detection of circulating Rubella Ab (IgG) |
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Rubella prevention
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Prevention of congenital rubella:
– Check immune status of women of childbearing age – Diagnosis in hospitals – Rubella serology screening of men and women starting work in hospitals – Vaccination of non-immune – Isolation of rubella cases in hospitals • Vaccination-live attenuated vaccine – Do NOT give vaccine to women who are already pregnant! |
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Varicella
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Chickenpox: Varicella
Zoster Virus (VZV) • Clinical: childhood febrile illness with characteristic rash – Successive crops of fresh vesicles appear within 3- 4 days of onset – In non-immune adults, occasional pneumonia, may be fatal |
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Varicella (shingles portion)
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Herpes Zoster (Shingles)
– LIMITED rash, along trajectory of ONE nerve – Late recurrence of latent VZV (chicken pox) infection • Diagnosis: ID of virus particles in pustules by EM or immuno methods, followed by cell culture • Prevention: no vaccine; detection of susceptible persons by serological methods |
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Herpes Simplex Virus (HSV)
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Widespread
• Become LATENT after initial infection; lesions reappear periodically • High percentage of inapparent infections • Epidemiology: – HSV1: “cold sores” oral and ocular lesions; transmitted via oral and respiratory secretions – HSV2: “herpes genitalis” associated with genital tract; infected females can transmit to the newborn • Diagnosis: ID of virus particles by EM or immuno methods; cell cultures; Serology NOT usefu |
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Herpes clinical forms and prevention
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Clinical forms (other than cold sores):
– Genital infections: recurrent in both sexes – Herpetic encephalitis: RARE (see CNS viruses) – Neonatal Herpes: acquired during birth from asymptomatic mother; difficult to prevent; can result in death or severe sequelae (see CNS viruses) – Herpetic Whitlow: affects fingers, occupational hazard of health care workers; nosocomial infections in neonates – Corneal and Conjuntival Infection: can cause ulceration of cornea and blindness • Treatment and Prevention: antivirals; C-section for symptomatic mothers; NO VACCINE |
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Papilloma Viruses
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Cause different types of warts
– Common warts on hands and feet – Genital warts: sexual transmission, asymptomatic carriers – Some types associated with cancer: cervix, vulva, penis • Diagnosis: immuno techniques and DNA hybridization techniques; no cell cultures available • Prevention: Vaccine now available (Gardasil) |
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Viruses Causing Glandular Enlargement
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MUMPS
– Childhood disease; bilateral inflammation of parotid glands; many inapparent infections – Complications: meningitis, orchitis (can lead to sterility), ovaritis – Epidemiology: spread by salivary and respiratory secretions; incubation 18-21 days – Prevention: MMR vaccine (live, attenuated) |
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facts about MMR
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As of January 2008, 777 confirmed cases…
Mostly 23 and 24 year old people (university students) Many potentially exposed while celebrating St. Patrick's Day packed bars can you tell someone to “self-isolate” when they had no symptoms? Is this an exercise in futility? In old days, many only had 1 MMR shot (nowadays you get 2) Handling of vaccine by physicians |
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Infectious Mononucleosis (Epstein-Barr Virus)
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Belongs to Herpes virus family
• Mild disease; children and young adults; can be prolonged and debilitating • Transmission by saliva (kissing disease) • Symptoms: lymphadenopathy, fever, sore throat, atypical lymphocytes, enlargement of liver and spleen • Latent virus – Chronic disease (rare) or asymptomatic shedding (common) for lifetime of host • Diagnosis: blood picture ( in atypical lymphocytes) Monospot Test (detects RBC agglutination) Presence of EBV antigens • NO VACCINE |
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Cytomegalovirus (CMV)
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Herpes family, infection usually asymptomatic
and latent BUT dangerous for – Pregnant women: neonatal infection with jaundice, enlarged liver and spleen, mental retardation and motor disorders – Transplant patients: disseminated infection can cause transplant rejection – AIDS and other immunocompromised patients: frequent infection, GI tract ulceration and retinitis |
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CMV diagnosis
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Diagnosis:
– Isolation of virus from urine, blood, organ biopsies (slow process, but accurate) – CMV antigen detection, DNA hybridization and PCR in leucocytes much faster – Serology screening for donors and recipients before transplant • Treatment: antivirals • Prevention (immunocompromised): – Match CMV immune status between donor and recipient in transplants – Preventative administration of antivirals – Universal precautions to prevent transmission – NO VACCINE |
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Hepatitis Viruses
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Hepatitis = Inflammation of the liver
– Malaise, fatigue, nausea, loss of appetite and jaundice • Hep A, B most common and well characterized – Hep C, E, G less common • *Other viruses and bacteria can cause hepatitis as a complication of infection* • Diagnosis: serological |
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Hepatitis A
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Mainly children and young
adults • Sporadic cases and small epidemics • Epidemiology: – Transmission by fecal-oral route – Incubation 15-50 days – Stools infectious 2-3 weeks before onset – Mild or inapparent infection in children – No chronic hepatitis – Life-long immunity |
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Hepatitis A diagnosis
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Diagnosis:
– Suspected clinical cases: detection of IgM – Immunity: detection of IgG (before travel) • Prevention: – Vaccine for high risk populations – Commercial γ-globulin for prevention after exposure |
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Hepatitis B
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Sporadic cases; all ages
• Epidemiology: – Contaminated blood/blood products; saliva, urine, semen – Avg. incubation 90 days – Infective serum 30-60 days before onset of symptoms – Carriers • Clinical – More severe than HepA – Chronic hepatitis and chronic carrier-state |
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Hepatitis B Diagnosis
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• Diagnosis:
– Blood test for HepB surface antigen (HBsAg) – Antibodies are produced several months after onset of symptoms • Used as markers of infection and immunity |
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Hepatitis B Prevention
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Prevention
– Universal precautions for blood and body fluids – Proper handling of needles – Screening – Vaccination – HepB immunglobulins after exposure – HepB carriers |
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Hepatitis C
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Epidemiology:
– Blood and sexual transmission – Initially mild disease but can cause chronic hepatitis • Diagnosis: – Serological • Prevention: – Same as HepB – NO VACCINE – Treat with recombinant interferon and ribavirin |
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Hepatitis Delta Agent
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• Epidemiology:
– Blood and sexual transmission – “Viroid”-relies on HepB presence for replication in cells – Increases severity of HepB infection • Diagnosis: – Serological • Prevention: – Vaccination against HepB |
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Hepatitis E
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Transmission via fecal-oral route
• Incubation 15-50 days • Symptoms similar to HepA BUT 20% mortality in pregnant women • Endemic in India, Pakistan, Nepal, Burma, North Africa and Mexico |
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Hepatitis G
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Epidemiology:
– Blood and sexual transmission – Incubation 14-180 days – Initially mild and no jaundice, can cause chronic hepatitis • Diagnosis: – Detection of viral DNA by PCR or other molecular methods • Prevention: – NO VACCINE |
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Yellow Fever Virus
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Haemorrhagic fever with hepatitis
• Endemic in Africa, South America and Caribbean • Mortality rates as high as 50% • Transmitted by mosquito • Travellers to endemic countries receive live attenuated vaccine |
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Viruses affecting the CNS
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Clinical Manifestations
– Aseptic meningitis – Encephalitis – Meningo-encephalitis – Poliomyelitis – Slow progressive, persistant infections |
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CNS Viruses general diagnosis
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*Always first exclude possibility of
bacterial or fungal infection* – Lumbar puncture X4 – Other specimens • Blood, urine, aspirates, • throat swabs • stools, sera |
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CNS Viruses with a Human
Resevoir |
Usually an extension of a primary infection in
another part of the body – Mumps-aseptic meningitis in children – Enteroviruses-aseptic meningitis in infants and children – HSV1-RARE cause of herpetic encephalitis in young adults – HSV 1 or 2-RARE cause of meningo-encephalitis in neonate or young adult – Vaccination for mumps, measles and polio (entero) |
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CNS Viruses with an Animal
Reservoir |
RARE: Humans are accidental or dead-end
hosts – Arbovirus: • over 200 different types • Tropical rainforest areas • Encephalitis • Eg. West Nile – Rabies virus • Fatal, acute encephalitis • Infects mammals, transmitted via saliva • Long incubation (30-60 days) • Combined active and passive immunization • Prevention by vaccination of wildlife and pets |
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HIV and AIDS
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Severe immunosuppressive condition;
often fatal; predisposition to opportunistic infections and cancers • HIV causes depletion in helper T-cells making the host very susceptible to other infections • Frequent antigenic changes |
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HIV inactivation, pathogenesis
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Inactivation
– Virus often protected by living inside cells, protect it from disinfecting action • Transmission – Sexual, blood/blood products, congenital, organ transplants, sperm donation – Lengthy asymptomatic period increases spread of disease • Pathogenesis – Virus is cytocidal to helper T4 cells – AIDS develops from decreasing immune status |
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HIV clinical diagnosis
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• Clinical
– Incubation 6 months-several yrs – AIDS-related Complex disease, progress to AIDS – Terminal stage patients develop dementias, other neurological problems, many opportunistic infections • Lab Diagnosis – Serology based; seropositivity can take months to occur – Isolation of virus from blood, plasma, semen, cervical, vaginal secretions |
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HIV prevention
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Prevention
– Universal precautions for healthcare personnel – Screen blood, organ and semen donors – Heat inactivation of plasma for haemophilia patients – Sexual education – Education of drug users – Testing pregnant women at risk – NO VACCINE yet, but is a key focus of current research |
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HIV treatment
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Treatment
– MANY forms of treatment – Most effective is cocktail of treatments • HAART – Protease inhibitor (stops viral maturation) – Reverse transcriptase (stops viral replication) – Bad side-effects – Expensive – Treatment and Prevention in developing countries very difficult |