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189 Cards in this Set
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- Back
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types of infections generally cuased by influenza (orthomyxo) and parainfluenza (paramyxovirus) viruses
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local,
nonsystemic, nonviremic infections |
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mumps (virus type)
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paramyxovirus
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measles (virus type)
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paramyxovirus
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type of infection caused by mumps
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mumps and measles are paramyxoviruses that cause systemic infections with VIREMIA as an ESSENTIAL step in pathogenesis
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type of infection caused by measles
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mumps and measles are paramyxoviruses that cause systemic infections with VIREMIA as an ESSENTIAL step in pathogenesis
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explain the consequences of obligatory viremia on the incubation period and immunity involved in mumps and measles infection
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a) incubation period is longer because cycles of multiplication in several sites in succession are required
b) immunity is generally life-long because the obligatory viremia allows for neutralization by IgG |
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mumps (nucleocapsid)
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typical paramyxovirus
1 molecule (-) ssRNA envelope with virus-specific glycoproteins |
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mumps (but not measles) is antigenically related to what type of virus
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mumps is antigenically related to the paramyxoviruses (and the myomyxoviruses) these viruses agglutinate red cells
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measles (nucleocapsid)
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typical paramyxovirus
1 molecule (-) ssRNA envelope with virus-specific glycoproteins |
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recombination frequency for mumps and measles
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infrequent
viral RNA is in one piece explains absence of antigenic-variation, and long immunity |
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mumps (incubation period)
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3 weeks
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mumps (pathophysiology)
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3 weeks incubation
prodormal period (fever, malaise & anorexia) unilateral or bilateral swelling of the parotid gland virus grows in parotid and is excreted in saliva (before and after swelling begins) pain due to pressure within encapsulated organs (parotid and testis (orchitis)) |
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mumps (transmission)
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salivary droplets infect upper respiratory tract
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mumps (replication)
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primary multiplication in resp. epithelium and local lymph nodes
viremia infects salivary glands and other organs virion produced in salivary glands go down the duct to the mout ahd provide most of the infetious virions spread by coughs and sneezes |
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percentage of mumps cases that are subclinical
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~30%
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mumps (incubation period)
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~18 days (then swelling and fever begin)
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incidence of orchitis in mumps infected males
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~10%
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organs affected in mumps (excluding testis and pancreas)
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meninges (aspetic meningitis), pancreas, ovary (both uncommon)
all have generally benign course |
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immunity after mumps infection
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generally ifelong, even after subclinical infection or infection of only one parotid
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mumps (vaccine)
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live attenuated vaccine (grown in chick embryo culture)
1 subcutaneous dose gives (life?) long protection w/o serious side effects. has reduced incidence in dvpt countries, eradication is a low priority bc morbidity and mortality are low |
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measles is caused by what type of virus?
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paramyxovirus
antigenically UNRELATED to any other paramyxovirus of humans (mumps is related) |
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what is probably the most contagious disease known?
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MEASLES
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incidence of subclinical measles infections
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almost none
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MEASLES
pre-vaccine; when/how often did local epidemics occur? |
every 3 years
in winter each epidemic associated with enough new susceptibles (from new births) to break down herd immunity |
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usual course of measles in the US
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- virus INFECTS via RESPIRATORY TRACT
- MULTIPLIES in epithelium and local lymph nodes (& conjunctiva) - VIREMIA and PRODROMAL symptoms (fever, Koplik spots, conjunctivitis, photophobia) - RASH appears 3 days after viremia, 14 days after infection - Virus EXCRETION from respiratory tract and in tears and urine (a few days before and after rash appears) - Immune reponse eliminates viral excretion and generally confers lifelong immunity |
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PRODROMAL SYMPTOMS
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nonspecific symptoms that appear before definitive symptom
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PRODROMAL SYMPTOMS of MEASLES
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fever, cold-like symptoms, Koplik spots (legions on buccal mucosa), conjuntivitis and photophobia
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definitive symptom of measles
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THE RASH
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Koplik spots
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lesions on buccal mucosa, a prodromal symptom of Measles
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measles (incubation period)
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14 days (rash appears, asymptomatic infections are rare/unknown)
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measles (virus excretion)
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from respiratory tract, tears and urine
for a few days before and after appearance of rash (14 days after infection) |
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measles (immune response)
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eliminates viral excretion
generally confers life-long immunity |
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measles (pathology)
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multi-nucleate giant cells in lymphoid tissue and respiratory mucosa (virus induced cell fusion)
1. infection of four-celled tissue by virion 2. viral Ag in membrane of first infected cell 3. cell fusion spreads the infection to adjacent cells 4. multinucleate giant cell results |
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cell mediated immunity in measles infection
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virus profoundly suppresses cell-mediated immunity (ANERGY)
DTH skin tests become negative for child who was positive before contracting measles |
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ANERGY
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transient loss of cell-mediated immunity
(example: supression of cell mediated immunity by measles infection) |
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cause of secondary infections in some measles infected individuals
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ANERGY (suppression of cell-mediated immunity) by measles infection
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measles; epidemiologic survival depends on:
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measles virus needs a large, concentrated human population to survive (virion is unstable, it must be growing in some individual somewhere at all times.
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why does measles virus disappear from small isolated populations?
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continuous transmission is blocked by immunity or herd immunity
1) life-long measles immunity does not require restimulation by contact with exogenous virus 2) immune individuals do not excrete infectious virus |
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complications of measles in developed countries:
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a. encephalitis
b. pneumonia (sometimes bacterial) and otitis media (generally bacterial) c. Rare GIANT-CELL PNEUMONIA w/o rash when cell-mediated immunity is defective. Thus cell-mediated immunity plays a role in the genesis of the rash |
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GIANT-CELL PNEUMONIA
complication of what virus? how is the disease manifested differently? |
rare complication of measles (without rash, when cell-mediated immunity is defective)
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type of immunity that probably evolved as the primary defense mechanism against viruses
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cell-mediated immunity (at least as important as antibodies in immunity to viral disease)
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describe cell-mediated immune response to viral infection
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-viral proteins synthesized on ribosomes in cytoplasm of infected cells
-occassionally viral proteins degraded and "antigenic fragments" are presented on the cell surface in association with Class I MHC glycoprotein molecules -this triggers an attack by MHC-class-I-restricted cytotoxic T cells that are specific for the viral antigen |
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what happens to patients with congenital agammaglobulinemia when infected with a virus
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generally recover normally from viral infections and have long-term immunity to reinfection (though they are subject to certain recurrent bacterial infections)
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mortality rate of MEASLES in developing countries
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5-25%
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in fatal cases of measles what is seen?
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a severe hemorrhagic rash
death probably results from fatal synergism of measles and malnutrition (treatment with Vit. A can substantially reduce mortality) |
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measles vaccine
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live-attenuated vaccine (part of MMR)
a killed vaccine (no longer used) gave initial immunity, but susceptibility returned and infection resulted in the more severe "atypical measles" |
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status of measles in the US
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has been eradicated, but imported cases are still common
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why is immunization of measles difficult in developing countries?
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many cases occur before 12 months of age, making immunization difficult because of maternal antibody.
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WHO's 2006 goal for measles
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to reduce mortality by 50%, likely to fall short
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SSPE (onset)
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insidious with intellectual deterioration, psychological disturbances with slow decline interrupted by remissions
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SSPE (prognosis)
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generally fatal with paralysis and blindness
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SSPE (population affected)
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rare disease seen in school-age children
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SSPE (appearance of inclusion bodies)
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helical nucleocapsids in the inclusion bodies suggesting viral etiology
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SSPE (what is unusual about patients Ab titers and CNS?)
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very high Ab titers to measles virus
CNS contains measles viral antigen all had measles 4-17 years earlier (many had measles at a very early age (2 years and younger)) |
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measles virus can be isolated from where in SSPE patients
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their brains
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what causes SSPE?
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measles virus apparently, but not well understood.
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compare incidence of SSPE following live measles vaccine and natural measles
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in vaccinated individuals (<1/1 million)
following natural measles (1/100,000) |
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what does the incubation of SSPE suggest about viral illnesses?
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that some human viral diseases can have very long incubation periods.
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slow viruses defined by what 4 characteristics in sheep?
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a. long incubation period (months or usually years)
b. relentless progressive abnormalities c. generally localized to a single organ d. genetic constitution of the host often critical |
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Scrapie
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chronic progressive CNS (especially cerebellum) disorder of adult sheep
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Scrapie (pathology)
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no pathological evidence of an infectious process
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Scrapie (genetics)
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certain inbred lines of sheep are much more susceptible
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Scrapie (infectious agent)
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resistant to UV irradiation, formaldehyde, alkylating agents, etc. No known virus would survive these treatments.
has been transferred to mice with incubation period of less than a year. |
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PRIONS
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infection agents
proteins; highly resistant to proteolytic enzymes |
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heterogenous nature of "slow viruses"
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some are conventional viruses (measles and SSPE) others are caused by PRIONS (scrapie)
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Kuru
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progressive degenerative disorder of the CNS (esp. the cerebellum)
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Kuru (population affected)
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small stone-age tribe in New Guinea
at its peak it caused 1/2 of the total mortality in this tribe |
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Kuru (epidemiology)
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no obvious environmental favors, once considered purely a genetic defect
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Kuru (symptoms and neuropathology)
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SMONGIFORM ENCEPHALOPATHY (reproduced in chips by intracerebral injection of brain material form human cases) Ingestion of infected brains also transmits the disease
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Kuru (infectious agent)
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properties resemble those of scrapie (PRIONS)
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Kuru (incidence)
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low now, because of reduced cannibalism
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Kuru (transmission)
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injestion of infected brains
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CREUTZFELD-JACOB DISEASE
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most common human spongiform encephalopathy (has been transmitted to primates)
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CJD (transmission)
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some cases result of an inherited mutation, but most are SPONTANEOUS with no established cause
some IATROGENIC cases (corneal transplants, contaminated instruments, infected Growth Hormone) |
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Mad Cow Disease
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bovine spongiform encephalopathy
reached epidemic status as a result of use of brains and bone marrow from cows and sheep in bovine feed |
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atypical human Creutzfeld-Jacop disease
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outbreak in England, linked epidemiologically to eating beef from infected cows
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***Prion results from...
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abnormal folding of a protein encoded in the human (or animal) genome
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**Critical hypothesis to explain infectiousness and "multiplication" of prions is that"
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presence of a prion can cause the newly synthesized nroaml protein to fold abnormally to produce a prion
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ARBOVIRUSES
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arthropod-borne viruses (not a formal classification, but an epidemiological subset of viruses)
Examples we will consider: Togaviruses Flaviviruses |
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Shared characteristics of Togaviruses and Flaviviruses
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a. SMALL, ENVELOPED
b. ICOSAHEDRAL nucleocapsid (w/ 1 molecule of + ssRNA) c. most togaviruses and flaviviruses are ARBOVIRUSES (transmitted by blood sucking arthropod vector)(**note, this is NOT true of rubella virus (a togavirus) or HepC (a flavivirus) |
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arbovirus (incubation)
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2 incubation periods, because transmission requires multiplication in the arthropod host
INTRINSIC INCUBATION PERIOD (in humans, ~1 wk) EXTRINSIC INCUBATION PERIOD (in mosquito, ~2 wks of vigorous multiplication (cannot transmit the virus for 14 days post infection, but after that point mosquito is infectuous for life and is not harmed by the virus) |
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INTRINSIC INCUBATION PERIOD
of arboviruses |
in humans, about 1 week
(one of two incubation periods in arboviruses) |
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EXTRINSIC INCUBATION PERIOD
of arboviruses |
in mosquito (or other arthropod)
~14 days (one of two incubation periods in arboviruses) |
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Arbovirus (transmission)
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vertebrate --> arthropod
arthropod--> vertebrate (or sometimes transovarian transmission to arthropod progeny) |
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arbovirus characteristics
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many known arbovriuses
most are tropical antigenic cross-reaction genome sequences and other shared characteristics yield several taxonomic groups (among them togaviruses and flaviviruses) |
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only serious arbovirus disease in the US
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encephalitis, caused by:
Eastern equine encephalitis virus Western equine encephalitis virus St. Louis encephalitis virus West Nile virus the California group of encephalitis viruses |
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arboviral encephalitis (incubation period)
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~ 1 week
instantaneous viremia (from multiplication in vascular endothelium) |
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arboviral encephalitis (multiplication)
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occurs in vascular endothelium
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arboviral encephalitis (disease progression)
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following short (1 wk) incubation period:
brief febrile malaise, followed by encehpalitis with paralysis, coma and death |
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arboviral encephalitis (treatment)
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no specific treatment is available
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Eastern Equine Encephalitis virus
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causes the most deadly arboviral encephalitis
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Eastern Equine Encephalitis (population affected)
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infects mostly children, but also adults living in swampy and wetland areas with high fatality
HORSES die of the same disease |
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DEAD-END HOSTS
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hosts in which viremia does not facilitate further infections (e.g. viremia in humans and horses (infected with E & W equine encephalitis) rarely reaches level required to infect mosquitoes.
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Equine encephalitis (virus maintained by what species?)
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birds and mosquitos (both largely unaffected by the infection, although some birds do die)
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hints of an impending epidemic of Eastern Equine Encephalitis
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excessive rainfall and abnormally high mosquito populations
best warning from finding a high prevalence of antiviroal Ab in wild birds |
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Eastern Equine Encephalitis (control measures)
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a) reduction of mosquito population
b) avoidance of mosquitoes during epidemic |
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St. Louis Encephalitis (virus type)
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flavivirus
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West Nile Virus (type)
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flavivirus
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2 related flaviviruses, antigenically related to one another
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st. louis encephalitis and west nile virus
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St. Louis encephalitis and West Nile virus both cause what?
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encephalitis
fatal cases are mostly in the elderly |
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how are St. Louis encephalitis and West Nile virus maintained?
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by bird --> mosquito --> bird cycles
humans are dead-end hosts, rarely have viremia high enough to infect mosquitos |
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St. Louis encephalitis (found where?)
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indigenous to N. America
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W. Nile virus (where did it come from)
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native to N. Africa and the Middle East, recently imported to the NE US and rapidly spread across the US, likely to be permanatly established in US
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arbovirus, found in rural US
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Western equine encephalitis
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abrovirus, found in rural forests in the US
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LaCrosse encephalitis
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the names of arboviruses indicate what?
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where the virus was first recognized, NOTHING about where it is now found
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St. Louis Encephalitis (virus type)
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flavivirus
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St. Louis Encephalitis (habitat of major mosquito vector)
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urban/rural
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St. Louis Encephalitis (major vertebrate host)
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wild and domestic birds
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St. Louis Encephalitis (age incidence)
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adults over 50
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St. Louis Encephalitis (fatality of clinical cases)
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~10% (many subclinical infections)
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West Nile Virus (virus group)
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flavivirus
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West Nile Virus (hapitat of major mosquito vector)
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urban/rural
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West Nile Virus (age incidence)
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adults over 50
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West Nile Virus (major vertebrate host)
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wild and domestric birds
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West Nile Virus (fatality of clinical cases)
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~10% (many subclinical infections)
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Western equine encephalitis virus (group)
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togavirus
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Western equine encephalitis virus (habitat of major mosquito vector)
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rural
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Western equine encephalitis virus (major vertebrate host)
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wild birds
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Western equine encephalitis virus (age incidence)
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infants and adults over 50
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Western equine encephalitis virus (fatality of clinical cases)
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~10% (many subclinical infections)
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Eastern equine encephalitis virus (group)
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togavirus
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Eastern equine encephalitis virus (habitat of major mosquito vector)
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rural swamp and wetland
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Eastern equine encephalitis virus (major vertebrate host)
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wild birds
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Eastern equine encephalitis virus (age incidence)
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mostly children under 10
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Eastern equine encephalitis virus (fatality of clinical cases)
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75% (some subclinical cases)
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LaCrosse Virus (habitat of major mosquito vector)
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rural forest
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LaCrosse Virus (maj. vertebrate host)
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hares and rodents
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LaCrosse Virus (age incidence)
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children
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fatality of clinical cases
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ab 10% (many subclinical infections)
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characteristics of arbovirus epidemics in temperate zones
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focal epidemics of short duration (conditions have to be just right to allow transmission)
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disease patterns associated with arboviruses outside the US (in addn to encephalitis):
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a. severe systemic disease with degeneration of liver, etc.. (yellow fever)
b. non-fatal systtemic disease with muscle pain and rash (classical form of dengue fever) |
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Dengue Fever (virus group)
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flavivirus
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"bone-break fever"
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classical dengue fever
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Dengue Fever (geographic distribution)
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severe, but not usually life threatening disease of the tropics and subtropics (esp. SE Asia and the Caribbean islands)
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Dengue Fever (incubation period)
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one week
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Dengue Fever (symptoms)
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fever, muscle and joint pains, and a rash appear after 1 week incubation period
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Dengue Fever (antigenic types)
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FOUR CROSS-REACTING ANTIGENIC TYPES:
Types 1, 2, 3, 4 |
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Dengue Fever (transmission)
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pattern is exactly like that of yellow fever (humans are NOT dead end hosts)
Aedes aegypti (mostquito) --> humans --> Aedes aegypti (mostquito) --> humans |
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hemorrhagic Dengue fever
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massive Macrophage infection, results in overproduction of lymphokines and cytokines resulting in increased vascular permeability and hemorrage
seen in S.E. Asia (since ~1950) and in the Carribean (more recently) characterized by hemmorhage, vomiting blood and shock seen primarily in the native population most visitors get the classical mild disease |
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Yellow Fever (virus group)
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a flavivirus
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Yellow Fever (incubation period)
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~7 days
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Yellow Fever (viral multiplication)
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multiplies first in vascular endothelial cells, resultant VIREMIA serves to infect the liver and other organs
multiplication is extensive in LIVER, spleen and kidney |
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Yellow Fever (characteristic symptoms)
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fever, nausea, jaundice (from viral damage to liver cells)
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Yellow Fever (mortality rate)
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high, but there are some subclinical infections
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Yellow Fever (geographic distribution)
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now found ony in rural tropical Africa and S. America where it is endemic
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Yellow Fever (transmission)
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humans are NOT dead end hosts (for yellow or dengue fever)
Aedes aegypti (mostquito) --> humans --> Aedes aegypti (mostquito) --> humans |
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Jungle Yellow Fever
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yellow fever is perpetuated in tropical forests by another cycle:
monkey --> tree mosquito --> monkey --> tree mosquitos (MULTIPLE) ---> Humans ---> Aedes aegypti ---> humans |
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Yellow Fever (vaccine)
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live attenuated vaccine 17-D vaccine, gives long-term protection
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17-D vaccine
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live attenuated vaccine that gives long-term protection
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Yellow Fever (susceptible regions)
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danger of epidemics wherever Aedes aegypti is present
if an infected unvaccinated person enters the US during the incubation period, the yellow fever virus may spread to the mosquitoes and then to the susceptible population (e.g. the siutation in the SE USA today) |
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VERTICAL INFECTIONS
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neonatal infections aquired from the mother
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HORIZONTAL INFECTIONS
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all infections (not including those acquired from the mother)
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2 Pathways that lead to VERTICAL INFECTIONS
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a) PERINATAL PATHWAY- neonate infected during birth, similar to horizontal pediatric infections (HBV, HIV, HERPES simplex type 2
b) TRANSPLACENTAL PATHWAY- virus crosses the placenta (different from horizontal peds infections) (e.g. parvovirus B-19, rubella virus, cytomegalovirus, and lymphocytic choriomeningitis virus) |
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PERINATAL PATHWAY
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one of two pathways that lead to vertical infection (neonatal infections acquired from mother)
neonate infected during birth by contact with maternal blood or other fluids infections resemble horizontal pediatric infections with the same virus examples: HBV, HIV and HERPES SIMPLEX type 2 |
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TRANSPLACENTAL PATHWAY
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one of two pathways that lead to vertical infection (neonatal infections acquired from mother)
virus crosses the placenta to invade the developing fetus fetal infection can distort normal development and result in congenital anomalies. Ex: parvovirus B-19, rubella virus, cytomegalovirus, and lymphocytic choriomeningitis virus |
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why is fetal viral infection uncommon?
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placenta is a barrier to most viruses
embryonic cells and embyros are excellent hosts for growth of all types of virus |
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how does a virus infect a fetus?
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placental barrier is impermeable to particles the size of the smallest viruses, but some virsues can penetrate this barrier by replicating in placental tissue
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what happens if a virus gets through the placenta?
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infection is not inevitable:
fetus has defense mechanisms: a. maternal IgG b. fetal Ab after 4th month (mostly IgM) c. interferon (probably adequate after 4th month) d. cell-mediated immunity? |
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parvovirus (nucleocapsid)
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small
NAKED ICOSAHEDRAL virions linear ssDNA |
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parvovirus (nucleic acid)
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ssDNA (linear)
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parvovirus B-19 (transmission)
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inhalation of respiratory aerosol from infected person
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parvovirus B-19 (replication)
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primary growth (S phase cells of respiratory epithelium)
Bone Marrow (PREFFERED site of replication) |
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parvovirus B-19 (symptoms of infection in normal individuals)
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in normal individuals: asymptomatic, fever, malaise, and a rash ERYTHEMA INFECTIOSUM (prob. from immune complexes: virions + Ab deposited in capillaries)
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ERYTHEMA INFECTIOSUM
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rash associated with parvovirus B-19
"slapped cheek rash" probably caused by immune complexes: virions + Ab deposited in capillaries |
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Parvovirus B-19 (tropism)
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for erythroid precursors (RBC precursors), thus infection inhibits RBC production for about a week, by viral growth in these precursors (tolerated in normals, causes transient aplastic crisis in those already compromised RBC production or high rate of RBC destruction)
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TRANSIENT APLASTIC CRISIS
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associated with infection with B-19 virus
in individuals with compromised RBC production or high rate of RBC destruction (Sickle-Cell Anemia) |
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B-19 in those with immunological defects
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can cause prolonged anemia that they cannot erradicate
can be treated with pooled IgG |
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B-19 Virus during preganancy
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can lead to fetal death (no matter at what time in gestation inection takes place)
1st/2nd trimester (sometimes hydrops fetalis) 3rd trimester (still fatalities, but no hydrops) |
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HYDROPS FETALIS
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severe edema, sometimes associated with fetal deaths from B-19 infection in 1st or 2nd trimester
(uncommon event and B-19 is an uncommon cause) |
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B-19 infection 3rd trimester
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can result in death, but hydrops fetalis is not seen
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Rubella (aka...)
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German Measles, THE CHILDHOOD RASH
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Rubella (virus group)
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togavirus
same structure and pattern, but NO ARTHOPOD TRANSMISSION |
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Rubella (transmission)
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respiratory aerosols from an infected person
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Rubella (replication)
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local multiplication in the respiratory epithelium
followed by viremia **Rubella is less contagious than measles allowing for the persistence in seronegative adults |
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Rubella (susceptible populations)
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any age, seronegative adults susceptible (more of them than measles- because less contagious)
sometimes more severe in adults with transient arthritis |
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Rubella (incubation period)
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18 days
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Rubella (symptoms)
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rash (lasts ~3 days)
fever lymphadenopathy sometimes subclinical and even with the rash the clinical diagnosis can be difficult |
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Rubella (infectiousness)
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excreted from respiratory tract one week before and after the rash
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Rubella (immunity)
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even subclinical infections produce lifelong immunity
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Rubella (incidence currently)
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rare, bc of widespread use of live vaccine
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Congenital Rubella
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virus from the viremia of primary infection during pregnancy crosses the placenta
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anomalies associated with congenital rubella
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a. cataracts
b. heart defects (esp. PDA) c. deafness (progresses in early life) d. retardation **also spontaneous abortion |
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Fetal Rubella Infection % malformation...
First month gestation: Second month gestation: Third month gestation: Fourth month gestation: |
First month gestation: 50%
Second month gestation: 25% Third month gestation: 9% Fourth month gestation: 4% |
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Response of fetus to Rubella infection
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a. virus production throughout gestation and gradually decreasing through first two years of life (mostly in urine)
b. |
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major purpose of the live vaccine for RUBELLA
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to prevent congenital rubella
in the US, the tactical plan is to interrupt the natural pattern of rubella epidemics by immunizing school children to provide herd immunity for non-immune pregnant women |
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requirements for USA plan to interrupt natural pattern of rubella epidemics
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a. nearly all children must be immunized
b. invidiual immunity must be maintained through the child-bearing years to reduce the number of susceptible women |
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risk of rubella vaccine to pregnant women
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though none has been seen so far, risk exists for transplacental infection or congenital anomalies from teh vaccination of pregnant women
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major concerns about potential failures in herd immunity
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a) kids whose parents do not allow immunization
b) rubella cases in immigrant children c) sero-negative immigrant women of child-bearing age |
