Flashcards in transfusion transmitted diseases Deck (21):
What are the differences between viral and protein infectious agents?
Has filterable infectious agent, presence of nucleic acid, defined morphology, and presence of protein
Only has filterable infectious agent and presence of protein. No defined morphology or nucleic acid
What are the symptoms of classic creutzfeldt-jakob disease (CJD) progression?
-Disease progression: long incubation period (up to 30 years), neurocognitive degeneration, rapid progression to death
-Symptomatology: loss of muscle control, myoclonic jerks/tremors, loss of coordination, rapid dementia, ultimately death
Describe variant CJD.
-age of onset: earlier
-median age of death: 28 yrs
-Psych/sensory symptoms: frequent in early course of illness
-EEG changes: absent
-Duration of illness: 13 months median
-neuropathologic features: florid prion protein plaques, surrounded by spongiform changes
-immunohistochemistry: abnormal prion protein detectable in lymphoid tissues.
Describe classic CJD.
-age of onset: later
-median age of death: 68 yrs
-Psych/sensory symptoms: appear later in course of illness
-EEG changes: diagnostic EEG changes commonly seen
-Duration of illness: 4 months
-neuropathologic features: florid prion protein plaques uncommon
-immunohistochemistry: abnormal prion protein NOT detectable in lymphoid tissues.
What is the difference of lymphoreticular system involvement in CJD vs. vCJD?
Classical CJD: brain and spinal cord
vCJD: brain, eyes, tonsil, spinal cord, thymus, spleen, adrenal gland, lymph nodes, appendix, rectum
Explain the structural and behavioral differences between PrP-C and PrP-Sc
-normal PrP-C is more alpha helix than beta sheet. Cellular proteins found normally on membranes, endogenous form found in many tissues.
-misfolded PrP-Sc is mainly beta sheet. Scrapie prion proteins, infectious isoform of PrP, induces conversion of PrP-C to PrP-Sc
-PrP-C: sensitive to proteoytic degradation, sensitive to chemical and physical inactivation
-PrP-Sc: resistant to most proteolytic degradation, resistant to chemical and physical inactivation, can induce conversion of PrP-C to PrP-Sc
Describe the acute stage of Chagas disease caused by T cruzi.
Chagoma: hardened, red small tumor of the skin at the site of parasite entry
-Romana's Sign: unilateral bipalpebral edema if the port of entry is conjunctiva
Non-specific: Fever, malaise, lymphadenopathy
Describe the intermediate stage of Chagas disease.
-persistently low level of parasite in the blood as well as antibodies
-most persons remain in this phase for life without any progressive change
Describe the chronic stage of Chagas Disease.
-CNS: meningoencephalitis (younger patients), Dementia
-Colon and Esophagus: Megacolon, megaesophagus
What is the pathogenesis of Chagas Disease
Direct damage and inflammation:
-intracellular amastigotes kill host cells
-tissue destruction in neurons, heart, intestines
-damage to cardiac muscle frequently cause of death
-T Cruzi antigens cross react with host antigens causing autoimmune reactions
-cross reactive T cells or B cells become activated and attach host tissue
Describe primary CMV infection.
-Seroconversion: Ab- to Ab+
-productive viral replication and shedding
-CMV may be shed from bodily fluids: blood, breast milk, saliva, semen, tears, urine
Describe latent CMV infection.
-Viruses establishes latency in T cells, macrophages, epithelial cells, etc.
-no viral proliferaiton
-No cell damage caused during latency and thus no clinical illness
-The disease is controlled by surveillance of CD8+ T cells
Describe recurrent CMV disease.
-Control of viral replication is lost due to suppression of immune response: HIV, transplant, immunodeficient patients
-CMV may be shed intermittently from bodily fluids
Why are immunocompromised individuals more prone to CMV recurrences?
-immune surveillance chemically impaired by suppressive therapy
-seropositive patient receive seronegative graft because graft is still naive/not protected
-deficient T cell function, inability to mount response
-loss of CD4 cells leads to functional loss of CD8 cells controlling virus
How does CMV affect immunocompetent individuals?
-acquired after birth
-heterophile negative mononucleosis: prolonged fever, mild hepatitis, sore throat
How does CMV affect fetus/neonates?
-most common cause of congenital abnormalities
-primary infection of mother during pregnancy is dangerous: developmental impairment, congenital defects, death
-Diseases: intrauterine growth restriction, prematurity, microcephaly, jaundice, petechiae, hepatosplenomegaly, pneumonia
What diseases does CMV cause in immunocompromised individuals?
-GI disease: ulcerative lesions, ab pain, hematemesis, diarrhea
-CMV retinitis: blurred vision, eye pain, photophobia, redness, blindness
How does CMV evade host immunity?
1. Decreases viral antigen presentation
-downregulate MHC1 on infected cells and down regulate MHC2 on AP cells
2. Inhibit cell-mediated immunity
-block NK cell activity by inhibiting synthesis of ligand for NK activating receptors
-inhibit TH1 immune response: CMV encodes Il-10 analogue that inhibits Th1 immune responses
Describe the clinical diseases caused by west nile virus.
-majority are asymptomatic (80%)
WEST NILE FEVER
-incubation period 3-15 days
-symptoms severity increases with age
-headache, chills, fever, weakness
-joint pain, drowsiness, nausea, vomiting
-overall very non specific flu like symptoms
-no permanent health effects
WEST NILE ENCEPHALITIS/MENINGITIS
-<1% cases have CNS infections
-severe headache, neck stiffness, disorientation, convulsions
-40% develop neuroinvasive disease after organ transplantation
-neurological impairment may be permanent
List the methods to test for WNV infection.
-WNV IgM antibodies
-WNV IgG neutralizing antibodies
-Nucleic acid amplification technique (NAAT) detects viral RNA
-useful for immunocompromised patients who can't mount antibody immunity