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99 Cards in this Set
- Front
- Back
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What are the clinical manifestions of prion diseases?
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Prion diseases are different from slow viral diseases in that there are no foreign antigens.
-they produce no immune response -no inflammation -no INF or cytokine production -Amyloid plaque is associated with prion disease |
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Kuru disease manifestations
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-Kuru means shivering
- tremors, ataxia, postural instability - Long incubation period (2-20yrs) -Fatal over 2mo – 2yrs |
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Creutzfeld Jacob Diseases disease manifestations
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Progressive neurodegenerative disease with dementia and early motor signs
Death in 4-5 months |
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Creutzfeld Jacob Diseases
Subtypes |
Sporadic (sCJD) – 85-95%
Familial (fCJD) – 5-15% Iatrogenic (iCJD) - < 1% New variant (nvCJD, BSE) – rare |
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Describe Pox Virus (virus itself)
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- i.e - variola virus
- infect invertebrate and invertebrates - Large brick shaped virus - Large complex ds DNA genome - Replicated in the cytoplasm of host cells |
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Small pox clinical manifestations
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i. Incubations = 7-17 days
ii. Patient presents with prodromal syndrome of malaise, fever, vomiting and headache (delirium in 15% of prodromal phase iii. 2-3 days later a vesicular rash involving face, hands and forearms 1. mucous membrane lesions noted 2. rash spreads to trunk and lower extremities (centripetal) iv. lesions: 1. progress from vesicle to pustules 2. found in mucous membranes (as is varicella) 3. All in the same stage of development (unlike varicella) 4. Have umbilication, dimpling 5. more commonly involve extremities rather than trunk 6. lesion may scab and till contain infectious virus a. in contrast to varicella where scabs = no longer infected 7. Mortality is often greater than 70% |
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What is polyclonal gammopathy?
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Nonspecific antibody response to multiple antigens.
HIV1 Humoral Immune Defect |
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When CD4 drops below 100, these are more frequent:
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cryptococcal meningitis
CMV infection of major organs M. avium cerebral toxoplasmosis |
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HIV Pharmacogenetic considerations include:
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P450 isoforms
CYP2B6 polymorphism HLA B*5701 (increased drug hypersens) |
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AIDS immune reconstitution syndrome is the worsening of what, after the initiation of antiretroviral therapy?
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mycobacterial infections
CMV retinitis PCP **treat with steriods! |
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gag
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group specific antigen:
p24 capsid |
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pol gene
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HIV:
protease polymerase integrase |
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Gp41
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HIV transmembrane (env gene)
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p24
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HIV:
gag gene structural forms the shell of capsid **antibodies are formed during acute response. |
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nef
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HIV regulatory protein
down regulates CD4 and MHC-I expression. Helps viral release from cells. |
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rev
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HIV regulatory protein
promotes nuclear export of incompletely spliced/unspliced viral RNA |
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CXCR4
CCR5 |
HIV
chemokine co-receptors required for entry into cell CXCR4 is syncytium inducing and thus a bad prognostic sign. It is on lymphocytes. CCR5 is not syncytium inducing. It is on macrophages, microglia and lymphocytes. |
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gp120
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HIV
ligand for CD4 |
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HTLV1
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Deltaretrovirus
oncoretrovirus Tcell lymphoma prolonged asymptomatic period cellular transformation Causes 2 syndromes: T-cell lymphoma Tropical spastic paralysis (myelopathy) Infects Tcells, endothelial cells, fibroblasts (Japan, Caribbean) |
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HTLV1 clinical illness
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human T cell lymphoma
(bone involvement, hypercalcemia) HTLV-1 associated myelopathy (tropical spastic paraparesis) |
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Relationship of:
HIV1, HIV2 HTLV1, HTLV2 SIV PTLV |
HIV1, HIV2, SIV are related
HTLVs and PTLV are related |
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what neurologic manifestations occur in HIV versus HTLV-1?
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HIV:
central nervous, encephalopathy, dementia peripheral neuropathy, pain, numb spinal cord disease HTLV-1: Human T-cell Lymphoma virus myelopathy (tropical spastic paralysis) |
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Picornavirus (describe)
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small (pico)
+ RNA naked icosohedral includes enterovirus, poliovirus, coxsackievirus, ECHO, hepA, rhinovirus |
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life cycle of + RNA virus
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+ --> +- --> +
**brief period as double stranded |
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Pathogenesis of non-polio enterovirus
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*shed in feces
*replicate in UResp or ileum *transient viremia *meningitis, myocarditis, exanthem *neutralizing antibodies are good! |
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Highest rates of non-polio enteroviruses occur when?
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summer and early fall
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These symptoms make you think:
fever, sores in the mouth, and a rash with blisters herpangina encephalitis acute hemorrhagic conjunctivitis |
Hand, foot, and mouth disease
Cox A herpangina is vesicular eruption on palatte tonsils |
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Which of the non-polio enteroviruses tend to cause these cardiac and skeletal muscle problems:
pleuordynia myositis myopericarditis |
Cox B
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Parvovirus B19 causes what disease in:
Children |
Erythema infectiosum
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Parvovirus B19 causes what disease in:
Adults |
Arthralgia/arthritis
1-3 weeks symmetrical involving small joints |
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Parvovirus B19 causes what disease in:
Patients with decreased RBC |
Acute RBC aplasia (transient aplastic crisis)
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Parvovirus B19 causes what disease in:
Immunocompromised patients |
Chronic infection with anemia
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Parvovirus B19 causes what disease in:
In utero |
Asymptomatic or arthralgia in mom
Child in utero: Low RBC results in hydrops (anasarca) anemia. Also myocarditis. DX: PCR or DNA hybridisation of amniotic fluid or tissues and persisting IgG antibody TX: transfusion and digoxin |
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Eating beef tartare, may give you:
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Toxoplasmosis
Pregnant women may give babies chorioretinitis, seizures, hydrocephalus, HSM, lymphadenopath, jaundice fever |
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Viral Core Proteins are:
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NONSTRUCTURAL! Early Genes!!
They are expressed before replication. function in assembly and replication. |
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The only dsRNA virus is:
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Reovirus
(Rotavirus) gastroenteritis |
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What is a "defective virus interaction"?
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HDV requires HBV
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What is a "non-defective virus interaction"?
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HIV + HepC get liver disease quickly!
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How are Picornaviruses transmitted?
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Fecal-oral (polio)
Aerosol (rhinovirus) |
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Example of Picornaviruses that cause aseptic meningitis?
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Non-polio Enterioviruses
LYMPHOCYTES! |
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CNS infections of Non-Polio Enteroviruses include:
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Aseptic Meningitis (B, Echo)
Encephalitis (A, B, Echo, Entero) |
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Which gives herd immunity:
Sabin or Salk? |
OPV in stool is SABIN
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Complication of Influenza
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Primary and Secondary Pneumonia
1- hemorrhagic 2- biphasic illness with pneumococcus, H. flu, staph 2 = more common |
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Only vaccine that should be given to pregnant:
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Influenza
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Steeple sign:
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Croup
(may be Paramyxo) |
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What does COOL AIR help?
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Croup!
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What kind of vaccine is Mumps?
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Live Attenuated
(like: polio, measles, mumps, rubella, yellow fever, varicella, influenza, rotavirus) |
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CNS manifestions of MUMPS
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Aseptic meningitis (10%)
Encephalitis (rare!) Facial nerve palsy Transverse myelitis Guillane-Barre syndrome Poliomyelitis-like syndrome Aqueductal stenosis and hydrocephalus |
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RSV pathogenesis:
spread LRTI |
Onoculate nose or eye
Lymphocytic peribronchile infiltration (endothelial cell sloughing) Pneumonia characterized by mononuclear cell infiltration |
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RSV manifestions in:
Children Adults Immuncompromised |
Children: tracheobronchitis, bronchiolitis, pneumonia
Adults: URI, irritates asthma, bronchitis (bad cold) Immuncompromised: diffuse pneumonia |
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Koplik's spots
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Measles!
enanthum |
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Complication of Herpes Zoster
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Dissemination may occur
Post Herpatic neuralgia - greater than a month - more likely with advancing age - possible prevention through antiviral therapy |
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Prevention of Herpes Zoster
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Vaccinate if 60+
(live vaccine can't be given to immunocompromised hosts) use VZIG in immunocompromised! |
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This virus disseminates through lymphoreticular system, gives sore throat, fever, big tonsils with exudate, palatal petechiae, big LN's.
(all lymphatic tissue is engorged) |
EBV!
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CMV in immunocompromised host manifests as:
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Retinitis
Pneumonitis GI: colitis, esophagitis CNS: encephalitis, myelitis |
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What is roseola infantum?
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caused by Human Herpes Virus 6
Exanthem subitum (viral maculopapular rash) |
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What are predominant causes of viral infantile disrrhea?
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Rotavirus
Adenovirus |
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Adenovirus can involve 3 types of interactions with cells:
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Lytic infection
Latent infection (lymphoid, tonsils) Oncogenic infection (integrated into DNA) |
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Pharyngoconjuntival Fever that occurs in small outbreaks of kids at summer camp:
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Adenovirus
(contaminated swimming pool) |
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Epidemic Keratoconjunctivitis (frequently bilateral), is caused by:
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Adenovirus
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Bloody UTI's
Hemorrhagic Cystitis that is more common in boys than girls |
Adenovirus
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Spectrum of Adenovirus disease:
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Respiratory Infection
Pharyngoconjuntival Fever Epidemic Keratoconjunctivitis Hemorrhagic Cystitis **involves transplant organs! **may disseminate |
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This virus has narrow target range and only affects:
erythroid progenitor cells |
Parvovirus B19
can cause aplastic crisis in those with high RBC turn-over. |
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Erythema Infectiosum is also called, what?
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Fifth Disease
Parvo B19 |
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Genetic material for Rotavirus is, what?
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DS RNA
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NSP4 causes what?
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Intusseption in Rotavirus infection
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Epidemiology of Rotavirus:
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Most common cause of severe diarrhea in young children!
Childcare outbreaks Peaks during winter Nosocomial in kids hospital! |
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Dermal erythropoiesis is:
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"blueberry muffin" spots of erthrocyte precursors, found on children born with Rubella/German Measles/Rubivirus
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What is the Rubella vaccine consist of?
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Live attenuated in diploid fibroblasts.
Part of MMR Neutralizing antibodies |
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Which virus is bullet-shaped?
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Rabies (Rhabdovirus)
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Clinical manifestion of Rabies:
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Asymp (10-90 days)
Nonspecific (resp or GI) Brain infection Paralytic Coma Death from resp arrest or heart |
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Rabies vaccine and postexposure treatment:
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Vaccine requires booster (to G-protein)
Postexposure gets RIG at bite site and also vaccine |
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Rabies and viremia... what happens?
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No viremia!
Crawls up nerve! |
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Chlamydia causes what type of arthritis?
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Reactive arthritis: immune mediated (not septic, like G)
aseptic (as part of Reiter's syndrome) |
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What is lymphgranuloma venereum?
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Caused by chlamydia
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What causes Chancroid?
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Haemophilus decreyi (GNR)
Tender papule |
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Syphilis Primary:
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painless chancre that goes away
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Syphilis Secondary:
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disseminated disease, causing maculopapular rash that can coalesce to form plaques called Condylomata Lata, that go away!
Epitrochlear nodes CNS in 40% of cases: mening or CNs glomerulonephritis, hepatitis, uveitis, proctitis, synovitis |
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What stage of Syphilis:
Highly infectious patches and large epitrochlear nodes (elbow) CNS in 40%: meningitis |
Secondary Syphilis
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Clinical Manifestions of latent Syphilis:
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None
Positive Serology! |
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Teriary Syphilus is:
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A progressive inflammatory diesease that can affect any organ:
parenchymatous degeneration neuro cardiac (PARESIS) gummas in any organ tabes dorsalis Charcot joints (deformed feet from misuse) Otitis CN palsy in 7, 8 Can be asymptomatic neuro or sympto neuro with meningitis. Do lumbar puncture for VDRL (non-specific). Confirm with FTA-abs (positive for life) |
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Diagonosis of Syphilus:
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Serological tests: will give false positives because they're non-specific.
VDRL in CSF RPR in serum RPR is a titer that takes a long time to fall. Specific test: FTA-abs & MHA-TP are the confirmatory tests. FTA will permanently be positive. More specific test! Less false positives. |
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Diagnosis of neurosyphilus:
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Often made in suspected individual with +RPR and/or FTA and CSF abnormalities.
+VDRL is proof of CNS involvement -VDRL won't R/O |
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Which Hepatitis is RNA vs DNA?
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B is DNA
all others are RNA |
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Who gets Hep A?
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poor hygiene
crowding travelers oral-anal contact |
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Hep A is easy to diagnose! How?
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ALT>AST
IgM first IgG confers immunity (never get again) |
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Which Hepatitis may present with rash and arthritis?
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Hep B *unique!
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Extrahepatic manifestations of Hep B may include:
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HBsAg : HBsAb complexes
Polyarteritis nodosa Glomerulonephritis |
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What percentages of persistent Hep B infections are CHP or CAH?
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70% CPH (more benign, no progression)
30% CAH (marked symptoms, cancer possible!) Chronic Persistent Hep Chronic Active Hep |
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HBeAg marks what?
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HBeAg marks:
Active viral replication It means you're contageous! |
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Which Hep B antibody protects against re-infection?
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HBsAb appears several months after the antigen disappears and protects against re-infection.
Surface antibody confers immunity! |
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What are the steps of Hep B antigen, antibody formation?
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1- surface antigen detected
2- HBe antigen means person is contagious 3- Ab forms for core antigen 4- window period of a few weeks 5- Ab forms for surface antigen and confers immunity * if 6mo pass and HBsAg is still high, person has chronic form. |
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How is Hep D diagnosed?
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HBsAg and HDV-Ab
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Extrahepatic manifestations of Hep C include:
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Cryoglobinemia with vasculitis and glomerulonephritis
Porphyria cutanea tarda (presence of thyroid antibodies) |
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How is severity of Hep C disease determined?
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Histologically
Liver function: serum albumin and prothrombin time (ALT levels may be normal) anti-HCV Ab does not distinguish between acute and chronic infection. PCR detection of viral RNA |
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What are the steps of Hep B antigen, antibody formation?
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1- surface antigen detected
2- HBe antigen means person is contagious 3- Ab forms for core antigen 4- window period of a few weeks 5- Ab forms for surface antigen and confers immunity * if 6mo pass and HBsAg is still high, person has chronic form. |
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How is Hep D diagnosed?
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HBsAg and HDV-Ab
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Extrahepatic manifestations of Hep C include:
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Cryoglobinemia with vasculitis and glomerulonephritis
Porphyria cutanea tarda (presence of thyroid antibodies) |
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How is severity of Hep C disease determined?
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Histologically
Liver function: serum albumin and prothrombin time (ALT levels may be normal) anti-HCV Ab does not distinguish between acute and chronic infection. PCR detection of viral RNA |
