Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
23 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Herpes simplex 2 --> General Notes
|
Glycoprotein-containing envelope, and therefore susceptible to drying, acid, solvents, and detergents. Space between capsid and envelope contain enzymes and viral proteins that initiate replication and this space is called a tegument. The envelope of Herpes comes from the nucleus of the Golgi membrane. Can be transmitted at time of birth
|
|
|
|
Herpes simplex 2 --> Area of body affected.
|
Type 2 - Usually genital, latent in sacral ganglia. Associated with cervical cancer.
|
|
|
|
Herpes simplex 2 --> Genome and replication
|
Double-stranded DNA envelope virus .LYSOGENIC...1-Latency (asymptomatic) is initiated by transcription by host polymerase in the cytoplasm (not integrated) . Infection initiated in mucous membrane, virus infects cells at site, and virus moves to innervating neurons, traveling to ganglion. Tissue damage is caused by virus infection and host response. Lesions heal with scarring. 2-Lytic cycle is when the genome has completed transcription performed by viral-encoded polymerase. 3-Regulated by viral-encoded and cellular nuclear factors 4-Scavenger enzymes provide DNA substrates to viral polymerase. 5-Recurrence activated by stress, virus travels down nerve and initiates another lesion at the same site. Recurrent infections are generally less severe, more localized, and heal more quickly.
|
|
|
|
Herpes simplex 2 --> epidemiology
|
Infected individuals remain infected (and infectious) for life. HSV is labile (enveloped). Transmitted sexually via vesicle fluid (kissing), saliva. 90% of third-wolrd invididuals have HSV 1 and antibody by age. If transmitted during birth, HSV 2 can cause disseminated and neurologic infection. Both types of herpes simplex cause the lesions in either the oral or genital regions, and can not be differentiated by look.
|
|
|
|
Herpes simplex 2 --> virulence factors
|
Infection initiated in mucous membrane (virus infects cells at site, and vius moves to innervating neurons, traveling to ganglion. Infection returns to the original site and produces vesicles (but may be inapparent). Herpes simplex has clever mechanisms to avoid antibody-mediated inactivation. Glycoprotein C (gC) binds and depletes complement. gE/gl complex binds Fc portion of antibody = camouflage. Infection is controlled by TH1-associated delayed-type hypersensitivity and cytotoxic killer T-cell (culprit = CD8). Humoral immunity (i.e. antibodies) is ineffective. Cell mediated immunity is responsible for many of the symptoms. In immunocompromised pateints HSV can disseminate to vital organs and brain. Tissue damage is caused by virus infection and host reponse and lesions heal without scaring. Encodes a protein which blocks TAP channel, thus can't get viral antigen thru TAP channel in order to be presented on MHC I which prevents recognition by CD8 cells.
|
|
|
|
Herpes simplex 2 --> Signs and symptoms of disease
|
Genital herpes - usually type 2, but can be type 1 (10%). Primary infection is asymptomatic (but maybe accompanied by fever, malaise, myalgia, inguinal adenitis indicating transent viremia); recurrences are painful; patients can usually predict recurrences (burning, itching); patients can be shedding virus even if asymptomatic.
|
|
|
|
Herpes simplex 2 --> Laboratory diagnostic
|
Serology is not useful because it is cell mediated. Tzanck Smear - scrape the base of a lesion, Pap stain shows giant cells and inclusions. Culture - sensitive and rapid (2-3 days), lab will usually tell you if it is type 1 or 2. Biopsy of brain - herpes can be seen by a good pathologist.
|
|
|
|
Herpes simplex 2 --> Treatment
|
The scavenger enzymes are targeted by some antiviral agents because they are different from host cell enzymes. Most drugs are nucleotide analogues and inhibitors of DNA polymerase. Acyclovir is activated by viral thymidine kinase (ON EXAM - acyclovir mechanism of action); incorporated by polymerase into viral DNA instead of tymidine; prevents elongation of DNA molecules; Resistance mechanism = inactivated viral thymidine kinase. Treatment may shorten symptoms but doesn't eliminate latent infection.
|
|
|
|
Varicella zoster --> General Notes
|
Child form: Extremely contageous- kids in daycare. 90+% of adults have serologic evidence of previous infection. The younger the child the milder the disease. Adult form: As older adults 10-20% of us will experience shingles. Adults with shingles may serve as a source of chickenpox in susceptible kids ("zoster form" = varicella).
|
|
|
|
Varicella zoster --> Epidemiology
|
Contract from infected individuals. Enters respiratory tract, then to the skin, and then spreads from skin to sensory neurons/dorsal root ganglia.
|
|
|
|
Varicella zoster --> Virulence Factors
|
Becomes latent in the dorsal root or cranial nerve ganglia. Controlled by CMI, and produces blisters. Spread by respiratory route
|
|
|
|
Varicella zoster --> Signs and symptoms of disease
|
Childhood primary varicell - incubation of 2 weeks. Initial site is the mucosa of the respiratory tract. Spread via circulatory system to cells of RES. Secondary viremia on day 10-13. Infects skin - itchy maculopapular/vesicular rash in successive crops with fever lasting 3-5 days. (more severe on trunk than on extremities, all stages observable at once, unlike smallpox, occur in mouth, vagina, and conjunctivae), vesicle becomes pustular and crust over, becomes latent in dorsal root or cranial nerve ganglia. Adult primary varicella - usually more severe than childhood disease. 20-30% get interstitial pneumonia, possibly fatal. Due to increased inflammatory response in adult. Reye's syndrome (encephlopathy and liver damage) due to increased inflammatory response in adult. Shingles (herpes zoster) - reactivation of infection. Rash follows a single dermatome. Very painful, 30% will have postherpetic neuralgia lasting years! Disseminated disease in immunocompromised hosts - potentially fatal
|
|
|
|
Varicella zoster --> Laboratory Diagnosis
|
You will not usually need to the lab to help make this diagnosis. Cytology of lesion base. Direct antigen test (FAMA = fluorescent antibody to membrane antigen), not widely available. Culture - just like herpes simplex and too expensive. PCR - expensive, but available. Serology - test for immunity (i.e. Serology = good).
|
|
|
|
Varicella zoster --> treatment
|
Treat with acyclovir, but it is less effective for VZV. Disease can be prevented with varicella-zoster immune globin (VZIG) - if child has been inoculated with it, then give immune globin against it to prevent outbreak. Vaccinate Chickenpox in kids doesn't need treatment unless immunocompromised
|
None
|
|
|
Varicella zoster --> Genome and Replication
|
Double-stranded DNA envelope virus. Incubation of 2 weeks. Initial site is the mucosa of the respiratory tract. Spread via circulatory system to cells of RES. Secondary viremia on day 10-13. Infects skin - itchy maculopapular/vesicular rash in successive crops with fever lasting 3-5 days. (more severe on trunk than on extremities, all stages observable at once, unlike smallpox, occur in mouth, vagina, and conjunctivae), vesicle becomes pustular and crust over, becomes latent in dorsal root or cranial nerve ganglia.
|
|
|
|
Parvovirus-->General Notes
|
Smallest ssDNA virus. Just one human pathogen - B19 attacks RBCs. Some Parvoviruses called Dependoviruses can only infect humans if they co-infect with an adenovirus, needed for replicative machinery. TRANSPLACENTAL
|
|
|
|
Parvovirus -->Area of Body Affected
|
RBC's
|
|
|
|
Parvovirus--> Genome and replication
|
Single-stranded DNA non-eveloped virus. Replicates in erythroid-progenitor cells, receptor is blood-group P anitgens
|
|
|
|
Parvovirus--> Epidemiology
|
Most common in young kids, 50% have antibody by age 15. Spread by droplet nuclei, later winter, spring.
|
|
|
|
Parvovirus--> Virulence Factors
|
Haemotopoeisis stops in four days, decline in hemoglobin. In adults, B19 causes acute, symmetric polyarthritis, often without rash (mediated by immune complexes). Severe effects in fetus, because RBC turnover is high and cell-mediated immunity is low.
|
|
|
|
Parvovirus--> Signs and Symptoms
|
Fifth Disease ON EXAM = Erythema infectiosum: aplastic crisis in patients with chronic hemolytic anemia, and acute polyarthritis in adults. "SLAPPED CHEEK SYNDROME" ON EXAM - distinctive rash that develops and spreads to arms and legs (subsides in 1-2 weeks). Fetus may develop myocarditis, severe anemia, secondary cardiac failure If fetus survives, no long-term sequelae ON EXAM. Some have fever, sore throat, malaise. Transient aplastic crisis in patients with chronic hemolytic anemia (sickle cell); dypsnia, lassitude, confusion
|
|
|
|
Parvovirus--> Laboratory diagnostics
|
Serology for Parviovirus B19 IgG and IgM; PCR for parvovirus DNA
|
|
|
|
Parvovirus-->Treatment
|
No Treatment
|
|
