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239 Cards in this Set

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can be a primary or secondary manisfestation of several infections (Yellow fever, EBV, HSV, CMV, Lassa Fever) and/or noninfectious conditions (alcoholic cirrhosis)
viral hepatitis
inflammation of the liver
viral hepatitis
RQ: detectable signs of viral hepatitis
RQ: elevated liver enzyme levels, jaundice (icterus), malaise, fever
primary viral hepatitis agents
Hepatitis A-G
Hepatitis A Virus (HAV)
aka ...
taxonomic group?
enterovirus 72 of the picornaviradae
Hepatitis B Virus (HBV)
TQ: *RNA or DNA?*
which taxonomic group?
TQ: *DNA* virus of the Hepadnaviradae
Hepatitis C Virus (HCV)
taxonomic group?
nee NonAnonB (NANB) an enteriovirus
TQ: Hepatitis D Virus (HDV)
taxonomic group?
TQ: *aka Delta agent*
defective RNA virus
currently only member of Deltaviridae
Hepatitis E Virus (HEV)
taxonomic group?
provisionally in caliciviridae
TQ: Hepatitis F (HFV)
variant of what virus?
TQ: variant of HBV
TQ: Hepatitis G Virus (HGV)
homologous to ...
TQ: 25% homologous to HCV genome but doesn't cause symptoms
how many serotypes?
enveloped or not?
thermotolerant or not
single serotype,
unenveloped- since's there's no envelope it's thermotolerant and cold tolerant
acid stable
TQ: how is HAV spread?
TQ: it's in stool 2-3 weeks before and 1 week after jaundice
*fecal-oral* or contaminated food (*shellfish*) or *water*, oro-anal sex
why is parenteral transmission of HAV rare?
parenteral "around the gut"
rare b/c of short viremic phase
where does HAV grow then spread and multiply
assumed to grow in intestinal epithelium then spread to liver and multiply in parenchymal cells
which antibody responds first to HAV?
TQ: is there life-long immunity to HAV?
TQ: IgM - largest, most efficient. then switches to IgG -giving *life long immunity*
is HAV a zoonoses
no, shellfish are intermediate hosts, use chimps as experiemental hosts
does severity of HAV increase or decrease with age?
increases: 75% of adult cases have jaundice
childhood infection tend to be anicteric (milder)- less jaundics cases
is mortality of HAV high or low
low. 90% of pts recover fully w/in 3 months
5% have recurrence of milder dx, then recover
TQ: do people chronically carry HAV
TQ: no, *no chronic carrier state* known. endemicity requires sporadic subclinical infection
responsible for 25% of clinically apparent hepatitis worldwide
highest incidence of HAV found in which populations
Amer. Indians, Alaskan natives, institutionalized children and in daycare
in undeveloped countries when do people have anti HAV antibodies?
how by are seropositive by 50 yrs in developed countries?
undevl. most have antibody by 10 yrs
devel. 50% seropostive by 50 yrs old
what's given in the passive immunization of HAV? is it long term or temporary
Immune Serum Globulin, it's expensive and temporary but you won't become ill and doesn't interfere with natural immunization
who's given the HAV vaccine?
is it active or inactive?
inactivated formalin, universally recommended b/c it's less expensive.
Before it was given at 2 yrs, recommended for those at risk and living in states with high annual incidence (CA)
TQ: *HBV is also known as or causes what?*
how is it spread?
TQ: *serum hepatitis*
spread from sexual contact (50%) or from blood transfusion
is HBV a zoonoses?
no but it can infect chimps and gibbons - can't be cultured b/c cells don't retain wild type markers used for viral attachment
RQ: Dane particle is associated with what virus?
how many layers does it have
two layers
what is strange about the DNA of HBV?
one of the strands is incomplete so that 15-50% is single stranded
has 4 genes
DNA polymerase with reverse transcriptase activity
what antigens are associated with HBV?
HBsAg = surface antigen (AKA Australia antigen)
HBcAG, HBeAg = core antigens
chronic carriers of HBV have a large excess of what antigen? - it's a source of HBV vaccine antigen
HBsAg, a positive or prolonged presence indicative of carrier status and a way to diagnose
how do you tell when a person + for HBV has a low risk of transmission?
when does it "arise"
when anti-HBeAb is found in high amounts, "arises" during incubation
HBcAg and HBeAg are dimers
how long is the incubation of HBV?
long: 6 weeks to 6 months (average is 10 weeks)
what's going on in the proliferative phase of HBV?
viral DNA in hepatocyte - actis as an episomal template (part of the chromosome) for complete virions but replication is inefficient, makes more empty capsids than comple virions
what happens in hepatocytes infected by HBV that are not destroyed by the host's immune system?
viral DNA may be integrated with host DNA, stops viral replication and liver damage
still have risk of hepatocellular carcinoma (Primary Liver Cancer)
which phase of HBV includes jaundice?
icteric (preicteric, icteric, convalescent)
symptoms of preicteric (prodromal) HBV
malaise, lethargy, anorexia, nausea, vomiting, abdominal and upper right quandrant pain
what might you find in an HBV patient in the icteric phase?
bilirubinemia and bilirubinuria (dark urine) followed by jaundice
HAV and HBV are dramatically differnt in that the convalescent stage may be protracted with malaise lasting for weeks, months, or in older folks-a year
HBV - malaise lasting for weeks, months or longer
the severity of HBV is affected by 3 things:
1. portal of entry-needle most serious
2. infective dose (0.0001mL sufficient for disease)
3. intensity of host's CMI response (massive response produces more severe disease but assoc w/ lower carrier rate)
what are the 6 outcomes of HBV
1. transient subclinical infection
2. acute hepatitis
3. fulminant hepatitis
4. healthy carrier
5. persistent infection
6. chronic active hepatitis
which HBV 'outcome' is fatal
fulminant hepatitis
are transient subclinical HBV infected people healthy carriers or non-infective
they are not healthy carriers and are non-infective
what antigen is found in HBV healthy carriers?
how often are they fully resolved?
50% are resolved, others remain as asymptomatic carriers for life
do most persistant HBV infections resolve?
what can they develop into?
extrahepatic disease (polyarteritis nodosum, glomerulonephritis)
Chronic active hepatitis (10-30%)
TQ: chronic active hepatitis from HBV can progress into..
TQ: *cirrhosis* or *primary hepatocellular carcinoma (PHC)*
TQ: when are most HBV infections acquired
TQ: early in life: *perinatally* (not transplacentally)
{HBV- B for Birth}
TQ: how is HBV virus shed from healthy carriers
TQ: semen, saliva, tears, breast milk (*not stool*)
TQ: are many of those infected with HBV at birth become chronic carriers
TQ: 95% - develop either chronic active hepatits, cirrhosis, or PHC
what reduced the infection of HBV
RIA blood screening
TQ: how is HBV 'historically transmitted'?
TQ: tatooing, piercing, venereally, *IV drug use*, *blood transfusions*
TQ: how is HBV prevented?
TQ: *Recombivax*~recombinant subtype vaccine - given to baby, can be given 12 hours after birth
~HBIG (hep B immunoglobulin) - given to mom or others that may have been exposed
is HCV RNA or DNA, ss or ds?
enveloped or not
what was HCV's former name
NonA NonB
TQ: which Hepatitis strain is most known for *post-transfusion hepatits (PTH) and IV drug use*
TQ: Hepatitis C
TQ: most frequent reason for liver transplant
TQ: HCV (leading cause of liver disease in the Western world) {lame mneumonic: C as in Cut you open for a new liver, tell me you won't remember that!}
TQ: what's a characteristic feature of HCV?
TQ: *episodic elevation of liver enzymes/they're sometimes normal
TQ: is jaundice with HCV more or less severe than HBV?
TQ: less severe jaundice but more frequently leads to chronic active hepatitis--> *cirrhosis in 5-10 years*
~*HCV is also most frequent reason for liver transplant in the US*
TQ: what is done for the prevention or to cure HCV?
TQ: no cure or prevention b/c the *virus is unstable* --many variants
TQ: *high titers of what do not protect against subsequent infection or recurrent illness from endogenous strain?
TQ: anti-HCV IgG
TQ: HDV aka...
TQ: Delta agent
the capsid of HDV has which antigen
TQ: HDV is entirely dependent on what for its survival
TQ: *HBV for reverse transcriptase
TQ: when a person has a superinfection with HDV, what other disease is often included?
TQ: HDV can only be transmitted from *host to host* that's what Johnny said was a test question
TQ: what could be the outcomes of HDV/HBV superinfection
TQ: *self-limiting*, *high rate of chronic active hepatitis*, or severe hepatitis (high mortality)
TQ: where is HDV commonly found?
TQ: *{think D for desert} *africa, middle east, southern italy (also russia, romainia, parts of S. america)
where is HBV commonly found?
TQ: is HDV found there also
China and South east Asia
TQ: No, ironically HDV is not common there
who has HDV in the US?
IV drug users (in NE) and hemophiliacs (from blood transfusions)
is HEV DNA or RNA?
enveloped or not
TQ: member of what taxonomic group?
ss RNA
TQ: *Caliciviridae* {remember CALI: cal-E}
TQ: how is HEV spread?
TQ: who is most commonly affected?
TQ: ~*fecal-oral, like *HAV {mneumonic:E, E, E for feeeecal. HAV: A: anus (assoc w/ fecal matter), TV channel A&E}
TQ: ~ *young adults most commonly affected*
TQ: what are some similiarities and a difference b/t HEV and HAV?
similarities: fecal-oral, acute and often severe dx *w/out chronic sequelae*), uncommon in children

TQ: differences: *HEV high mortality rate among pregnant women*, *HEV uncommon in elderly*
{don't worry.. about HEV.. if you're elderly. but oh no.. if you're prego} you're all going to ace this test with my rhyming skillz
why are STDs now called STIs?
can any come from animals/zoonoses?
~b/c many are acute or asymptomatic
all are infectious
~no zoonoses
Herpes Simplex Virus-I (HSV-I)
4 conditions:
herpes labialis
encephalitis and meningits
2 conditions:
genital herpes
herpes neonatorum
do any STIs evoke permanent portective immunity?
Herpes Virus:
enveloped or not?
TQ: is Herpes Virus prevalent?
does Herpes Virus persist in the host indefinitely?
TQ: ~yes, very prevalent -almost everybody has become infected *familial transmission* but majority not symptomatic
~yes, you have the host indefinitely but it's typically latent.
*recurrent symptoms associated with immunosuppressive therapy*
where does the HSV multiply?
slowly in the nucleus of the host cell so it doesn't kill it
buds from nuclear membrane
TQ: how can you tell the area where HSV is replicating?
TQ: *a histopathological lesion* - intranuclear inclusions idential (*Cowdry type A*) [i don't know what that means]
what virus is most responsive to chemotherapy?
herpes viruses- only for symptomatic relief
TQ: how do primary infections of HSV present?
what are recurrences called?
TQ: ~*often inapparent*- you can have it awhile before having symptoms
~*it's considered reactivation, not reinfection* (b/c you have it for life)
what is the portal of entry for HSV?
TQ: *where are virions shed from?
~skin and mucus membranes-direct contact
TQ: ~virions shed in *saliva*
TQ: what the most common disease manisfestation caused by HSV-1?
when is it acquired?
TQ: ~*herpes labialis - 70% of pop seropositive by 45 y/o
~acquired early in life
TQ: what manisfestation of HSV-1 is moslty seen in young children?
what are the symptoms?
TQ: how does it present in young adults?
TQ: ~children: fever, drooling, sore mouth (b/c of *pharyngeal erythema* and edema), mouth and gums covered with vesicles that rupture (*resemble chicken pox*)
TQ: ~young adults: *pharyngitis* or tonsillitis (also occurs with genital herpes with orogenital contact)
TQ: what are complications AIDS patients might have if also infected with HSV-1?
TQ: *esophagitis*-acute onset, painful, difficult swallowing, substernal pain
can get secondary candidiasis
TQ: where is HSV-1 retained for life?
how does it reappear?
TQ: in sensory nerve root ganglia of the *trigeminal nerve* - stressors may reactivate disease --> cluster of vesicles around the mucocutaneious junction of the lips
TQ: what manisfestation of HSV-1 can cause blindness?
how might you get it?
TQ: keratoconjunctivitis- from autoinoculation (from yourself)
dendritic ulcer of cornea and conjunctiva -->scarring -->blindness (*most common cause of corneal damage and blindness in the industrialized world*)
what is the rare but fatal manisfestation of HSV-1?
encephalitis and meningitis - currently the major cause of fatal sporadic encephalitis in US, survivors suffer permanent neurological damage
TQ: what are some local symptoms of HSV-2?
TQ: what are some systemic symptoms?
TQ: ~local: painful vesiculopustular lesions -burst and form *genital ulcers*; in females-discharge, itching, *inguinal lymphadenopathy*
TQ: ~systemic: fever, malaise, myalgias, *photophobia*, small amt may develop menigitis
TQ: *where is HSV-2 retained in your body?
*are recurrences more common with HSV-1 or 2
TQ: *lumbar and sacral sensory ganglia* {remember Dr. Dain's drawing of roman numeral two, II -->between the legs}
~*more common recurrences with HSV-2 but episodes are shorter and milder* *self-limiting*
primary infection may be subclinical but severe disease often occurs, esp in females
does HSV-2 cause cervical carcinoma?
no, but there is a high association. may be a cofactor for development of cancers but is not likely to be a sole cause of it
TQ: is herpes neonatorum passed transplacentally?
TQ: no, herpes 2 *doesn't cross the placenta*
*greatest risk is when there's a primary maternal infection during labor*
TQ: what is the most common infection worldwide?
~what number Herpes virus is it? HHV_
TQ: Epstein-Barr Virus (aka Human Herpes Virus 4: *HHV4)* 90-95% of adults are seropositive

[chicken pox is HHV3]
TQ: ~*what do half of those infected with Epstein-Barr virus develop?
~*heterophile + or -?
TQ: ~*infectious mononucleosis* (*aka glandular fever*)
~*heterophile + {mneumonic: going to the bar is a positive experience: Barr, hetero +}
how is Epstein-Barr virus spread?
is it contagious with "household contacts"?
~oral contact, virus is in saliva and B cells (not in feces, urine or genital secretions)
~not very contagious with household contacts- the secret to its success is that only some people have symptoms and they shed the virus months after recovery
most common manifestation of Epstein-Barr virus infection?
infectious mononucleosis (gladular fever)-initial development in lymphoid tissue of oropharynx (esp tonsils) hard to distinguish from other infections
what is the target cell for Epstein-Barr virus resulting in infectious mononucleosis?
B lymphocyte - the envelope glycoprotein attaches to CD 21 receptor on the B cell (polyclonal activation)
causes them to proliferate and make plasma cells and antibodies but not neccessarily the right ones- takes lots of energy (why pt is tired)
TQ: symptoms of infectious mononucleosis (EPV)
willl they have life long immunity to recurrence?
TQ: -fever (104F or 40 C)
-convalescence, depression, don't want to overexert self
-sore throat
-enlarged lymph glands
-*hepatosplenomegaly* (elevated enzyme levels (AST, ALT) *mimics viral hepatitis*
~most have life long immunity to recurrence
what is seen in immunosuppressed (impaired Tc cell activity) in someone with Epstein-Barr Virus?
progressive lymphoproliferative disease
who develops progressive lymphoproliferative disease from Epstein-Barr virus?
-kids with primary immunodeficiency (SCID-severe combined immunodeficiency)
-transplant pts on cyclosporin A (drug that suppresses T cells)
-AIDS pts
TQ: *E. Africa'*s most common childhood cancers -affects node in jaw
TQ: *Burkitt's lymphoma* -associated with *Epstein-Barr virus*
the kids are immunosuppressed b/c of malaria
two cancers associated with Epstein-Barr virus
~Burkitt's lymphoma-E. Africa, affecting nodes in jaw
~Nasopharyngeal Carcinoma (NPC)-most common cancer in certain parts of China, SE Asia, Africa and eskimos
aka Human Herpes Virus 5 (HHV5)
is it better to 'get this' as a child
~cytomegalovirus- about 40% in US are seropositive, up to 100% in undeveloped countries
~usually subclinical if acquired during early childhood
what does cytomegalic inclusion disease (CID) resemble? {Boss will try to confuse you with SCIDS: associated with Epstein-Barr Virus/progressive lymphoproliferative dx}
TQ: symtoms of CID?
~resembles *erythroblastosis foetalis*:Rh incompatible dx b/t mom and baby, but CID can't be "cured" with transfusions. *infant can shed virus for years
TQ:~*hepatosplenomegaly*, CNS abnormalities (hearing, IQ), *jaundice*, thromobcytopenia, petechiae, pneumonities (but only 10-20% infect manifest with some signs of disease)
TQ: what the major viral cause of congenital abnormalities?
TQ: cytomegalovirus : causing cytomegalic inclusion disease (CID), infant can shed virus for years
how can cytomegalovirus be spread?
during delivery or from breast milk
mostly asymptomatic, possibly b/c infant acquired mom's antibodies
TQ: how are EBV mononucleosis and CMV mononucleosis different?
TQ: EBV : *pharyngitis and lymphadenopathy. CMV-neither of those
CMV- *heterophile - (heterophile antibody is absent) {lame mneumonic CMV sounds like DMV, which is well known as being a negative experience DMV-->CMV heterophile -}
EBV heterophile +{a Bar is a + positive experience}
how is cytomegalovirus shed?
is it spread for life?
~in saliva: urine, semen, cervical secretions, breast milk, transplanted organs
~shed intermittently for life
TQ: how does risk of infecting unborn baby with cytomegalovirus increase?
TQ: if mom has CMV before preganancy-baby has little chance of getting it
-big risk if mom gets mono whle pregnant, but most asymptomatic b/c *mom passes on antibodies*
TQ: how can CMV be passed on?
TQ: *intrauterine* (transplacentally?), *perinatal* (during delivery, breast feeding), oral contact with fomites (esp in day cares), venereal, blood transfusion
{CMV- M- Mom's uterus & V- vagina}
most frequent cause of transfusion-acquired mononucleosis
CMV cytomegalovirus
is Human Papillomavirus (HPV)
enveloped or not?
which taxonomic group?
dsDNA, nonenveloped, Papovaviridae

certain types infect certain types of tissues-(papillomas or warts: common, flat, plantar anogenital and laryngeal papillomatosis)
TQ: second leading cause of cancer related death in women (after lung cancer)
TQ: *Human Papillomavirus -->cervical cancer*
implicated in development of squamous cell dysplasias and carcinomas of the genital tract
TQ: how does cancer develop from HPV?
TQ: ~infection of basal cells in strat. squamous epithelium - causes proliferation
~*Koilocytosis -a cytopathic effect: enlarged vacuolated cytoplasm with shrunken nuclei*
TQ: *condyloma acuminatum aka...
how does it grow?
how does it metastasize?
~* aka anogenital warts* from HPV {the only semi helpful way to remember it is to think of condyleeza rice, it's more helpful if you don't like the Bush administration} {keep this straight from condylomata lata- which if from syphilis}
~exophytic growth (grows outward) but also grows into myometrium
~can metastisize through lymph
TQ: which types of HPV are most common?
~*which accounts for most of the cancer cases?*
TQ: HPV 16 and 18
*HPV 16 accounts for half of cancer cases*
TQ: typical form of anogenital warts:
*atypical form:
~typical: soft, raised, fleshy, lesions (HPV 6, 10, 11, 40-45)
~atypical:flat (*HPV 16*, 18, 31) TQ: *associated with increased risk of cervical, penile and anal carcinoma*
~treatment:caustics, cauterization or surgical excision
TQ: most prevalent STI in the US
TQ: HPV- but it's not tracked by the CDC
TQ: prevention of HPV
TQ: *vaccine against HPV 16*, inoculation of virus like particles, done prior to puberty
leading cause of death in Africa and 4th leading cause of death worldwide
is HIV
enveloped or not?
taxonomic group?
+ or - sense
~2 copies of ssRNA
~group D Lenitvirus- related to a group of nontransforming cytopathic retroviruses {vs transforming retroviruses that are cancer causing}
~ +sense
TQ: how is HIV transmitted?
TQ: ~venereally
~IV drug use
~*blood transfusions* *Like HBV but HIV requires greater exposure b/c free infectioius virus is present in small quantities*
~*in utero* (transplacental?) and *perinatal* (*some in breast milk*)
TQ: highest risk group for HIV in US and worldwide...
*fastest growing risk group...*
TQ: ~in US: homosexual/bisexual males with multiple partners
~worldwide:70-75% of infections acquired heterosexually
*fastest growing risk group is female sex parteners of male IV drug users*
this transmission account for almost all childhood cases
in utero and perinatal
-all infants of HIV+ moms have antibodies at birth but only 25-40% are infected with the virus
TQ: can HIV be passed on by casual contact, air-borne transmission and arthropod vectors (ie mosquitos)
TQ: no ( HBV is also not tranmissable this way)
what's the 'secret to HIVs success'?
is the incubation time variable?
~antigenic diversity
~very variable 2-15 years (avg 5-8 years)
depends on how well you can regenerate T Helper cells
TQ: what is the target cell for HIV?
what happens?
TQ: ~targets cells with *CD4 receptors* (*T4 or helper lymphocytes*, certain *macrophages*, *monocytes* and *Langerhans cells*)
~viral envelope glycoprotein120-CD4 contact results in conformational change of glycoprotein so it can attach to CCR coreceptor which allows viral entry
how does HIV enter cell? (short answer)
via receptor-mediated endocytosis or fusion - often involving syncytia or giant cell formation
TQ: HIV replication kills what directly and indirectly?
TQ: *T4 cells - indirectly via apoptosis
*doesn't kill macorphages and monocytes* but infects them early on-they're used as *vehicles for transport of HIV to lymph nodes and CNS*, they are resistant to cytolytic infection (esp isolated in CNS from immune effector cells)
why is there a higher incidence of Pneumocystis pneumonia in AIDS than in other immunosuppressed conditions?
poor antigen presentation and defective chemotaxis in infected aleolar macrophage
the secretion of what in AIDS patients explains chronic fevers?
enhanced secretion of Interleukin-1, an endogenous pyrogen
Tumor Necrosis Factor Alpha-could explain the 'wasting' slimness see in Africa
TQ: where is the primary resevoir of infectious HIV?
TQ: *in the lymph nodes* - where it's predominately found in the middle (chronic or latent phase) and they're mostly asymptomatic
why is there such a considerable genomic diversity seen with HIV
b/c of hypervariable regions of envelope glycoprotein- gradually changes HIV from M tropic to more T tropic agent
TQ: in what stages is HIV most contagious?
~*in the chronic or latent phase, where does viral replication take place?*
~in the early (acute) and final (crisis) stages. has highest viremia (detectable virus in the blood)
~*replication of virus is predominately in the lymphoid tissue*
when is a person said to have AIDS
when CD4+ counts are below 200
what is Kaposi's sarcoma associated with?
what is it?
~HIV - a rare skin cancer, might be cause by a separate infectious agent (HHV8 or Kaposi sarcoma HV)
~proliferation of endothelial cells lining lymph channels
what is B cell lymphoma (non-Hodgkins) accociated with?
~HIV- thought to be a comlication of Epstein-Barr infection
TQ (matching):what is a common cause of death in early cases of HIV? (in about 60% of the cases)
TQ: *Pneumocystis jiroveci (nee carinii) pneumonia (PCP)*
TQ(matching): name of the systemic infection involving several organ systems in people with HIV?
TQ: *toxoplasmosis*- causes encephalitis, responsible for half of mass lesions found in CNS
TQ (matching):*most common fungal agent infecting AIDS patients
~(matching) *what causes chronic diarrhea in AIDS pts <1month
TQ: *C. albicans or Candidiasis*
candidiasis- esophageal, tracheal or pulmonary
TQ: can HSV-2 cause aseptic meningitis?
TQ: yes, it's usually mild and self-limiting
TQ: can HSV-2 cause aseptic meningitis?
TQ: yes, it's usually mild and self-limiting
TQ: what drugs can be used for Herpes viruses?
TQ: chemotherapy drugs *Acyclovir* or Zovirax-for symptomatic relief only
TQ: what is used to transcribe vRNA (of HIV) to cDNA?
TQ: *enzymes: *reverse transcriptase
then the DNA is incorporated into the host's genome
TQ: heterophile + and - both lead to what infectious disease?
TQ: infectious mononucleosis
TQ: ~*interstitial cell pneumonia* and *chorioretinitis* is associated with what virus
~chorioretinitis is it also known as?
TQ: ~assoc with CMV mononucleosis
~AKA *pizza pie retinitis*
~the person may also have hepatitis, arthritis and carditis
TQ: if a mother was infected with HSV-2 prior to her pregnancy, will the baby become infected?
TQ: the greatest risk of infection at birth (intrapartum) is associated with active primary maternal infection {tricky Boss question, no clear answer, I think the baby won't be infected b/c at birth the mom would not still be in the active primary state}
TQ: where is HEV commonly found?
TQ: blood borne in *Asia, India, sub-Saharan Africa and Mexico*
TQ: 80% of liver cancer among Asian Americans is due to...
TQ (matching): what three bacteria(?) are associated with AIDS and skin lesions?
TQ: *Cryptococcosis, Histoplasmosis or Coccidioiodomycosis* - extrapulmonary and/or disseminated with skin lesions
TQ (matching): in patients with AIDS, what age do you see disseminated *CMV*?
TQ: >1 month old, commonly affects eyes (25% have chorioretinitis-pizza pie retinitis, 10% have GI lesions)
TQ (matching):in patients with AIDS, what other virus might they have if they have persistent mucocutaneious ulcers or pulmonary infections?
TQ: in patients >1month old with *HSV* and AIDS
TQ (matching): leading cause of death worldwide among HIV + people
disseminated *mycobacteriosis*, cause by typical TB or atypical species (eg. MAI complex)
TQ: many AIDS pts have neurological symptoms caused by what?
TQ: ~*AIDS encephalopathy or dementia complex*
~gliosis of cerebral cortex, necrosis or gray and white matter, demyelination of white matter
~may involve inflammation b/c of infected monocytes and macrophages
what's the treatment for people with HIV/AIDS?
what are the side effects
~chemotherapy, a "cocktail" of AZT, ddi and protease inhibitors
reduces viral activity enough to be undetectable, increases T cell count
~neg. effects: diabetes, heart disease, vascular necrosis-->hip replacement
do we have drugs to cure viral diseases?
NO, we only have vaccines to prevent infection. drugs don't cure you once you have the virus
signs of hepatitis (A-G)
malaise, jaundice, fever, increased liver enzymes
compare the Australia antigen and the Dane antigen
Australia: on the surface of the virus
Dane: the complete virus, consists of 2 concentric layers
which virus has oncogenic potential and is associated with cervical cancer?
HSV-2, but doesn't neccessarily cause cervical cancer
True or False: Epstein-Barr virus is largely asymptomatic in childhood.
what virus is associated with inguinal lymphodenopathy?
what virus is assoc w/ cervical lymphodenopathy?
HSV-2 - inguinal
EBV - cervical
True or False: Epstein-Barr virus targets Tcells.
False: targets B cells
what are the target sites of infective mononucleosis?
B lymphocytes
cytomegalovirus is shed for life in...
breast milk, saliva, urine, semen
most prevalent STI in the US
HPV - Human Papilloma Virus
what harbors HIV?
lymphocytes (monocytes) and macrophages
which virus is associated with herpes labialis
TQ: which virus is assoc. with pharyngeal erythema and edema
TQ:which virus is assoc with photophobia?
TQ: which virus is assoc with Burkitt's lymphoma?
which viruses are dsDNA?
All herpes viruses: HSV-1 and 2, EBV, CMV, Varicella Zoster
which virus is assoc with nasopharyngeal carcinoma
which herpes virus is spread sexually?
HSV-2. the rest can be spread by kissing/saliva or mucus membranes
which virus reporduces in the host cell nucleus?
which virus is assoc with gingivomastitis?
which virus is assoc with interstitial cell pneumonia?
which virus is assoc with keratoconjunctivitis?
which virus is assoc. with hepatosplenomegaly and jaundice?
95% of adults are seropositive for what virus?
which virus is associated with herpes neonatorum?
most common manisfestation of tertiary syphillis
aortic aneurysm
associated with condylomata lata
syphilis (don't get confused with the condy--anogenital warts)
TQ: world's leading cause of treatable blindness:
TQ: *chlamydia-a chronic suppurative follicular keratoconjunctivitis*, lesions heal with scarring
{HSV-1 most common cause of corneal damage and blindness in industrialized world}
causes genital elephantiasis, rectal strictures, acute epididymus, PID
chlamydia- i didn't couldn't find acute epididymus but an old final review had this question twice
-gonorrhea also causes PID
True or False: infective mononucleosis can be caused by the same virus as Burkitt's carcinoma
true: EBV
True or False: with infective mononucleosis the circulating cell that's infected is the T lymphocyte.
False: B lymphocyte
True or False: the microscopic changes in the liver in infective mononucleosis resemble viral hepatitis
True or False when regarding infective mononucleosis: exposure during childhood often results in asymptomatic infection
True or False: the microscopic changes in the lymph nodes in a pt with infective mononucleosis resemble Hodgekin's Disease
primary resevoir of this virus is in lymph nodes
~may also be found in monocytes and macrophages
what is the hypothesis of why some people are not infected by HIV
they lack CCR5 receptor
or if they are heterozygous- slows the onset of AIDS
causative agents of Pelvic Inflammatory disease (PID)
Neisseria gonorheoeae
Chlamydia trachomatis
TQ: bacterial STI that's 'famous for having a short incubation time'
~*can it be spread by fomites?*
TQ: gonorrhea: 2-7 days
*can be spread by fomites but it's rare*
TQ: True or False: gonorrhea is* tissue type specific*
True: hangs around mucosal surfaces lined by*transitional* or *columnar epithelium* (urethra, cervix, anal canal, throat, conjunctiva ) doesn't go into gonads
what does this pertain to "attachment to microvilli by pili and multiplication evokes a chronic purulent inflammatory response"
gonorrhea- neutrophils predominate
diagnosis: finding lots of phagocytosed diplococci in gram-stained smears of the exudate
TQ: there's no protective immunity induced by gonorrhea and healing of gonorrhea involves scar, what's the importance?
TQ: repeated infection may lead to extensive scarring/fibrosis
*ORCHITIS* (shouldn't it be no orchitis b/c it doesn't involve the testis)
can scar tissue from gonorrhea impair fertility?
yes; but it's functional sterility, doesn't involve testis
what does salpingitis mean?
what's causes it?
what organs are not involved in women?
~inflammed fallopian tubes- can progress and burst
~caused by gonorrhea
~doesn't involve uterus or ovaries
TQ: ectopic pregnancy, bacteremia, endocarditis, arthritis, infertility and sterility can all be cause by...
TQ: gonorrhea-->*PID pelvic inflammatory disease* *by Neisseria gonorrhea* and *Chlamydia trachomatis*
how do you diagnose gonorrhea?
men: smear
women (or if rectal or pharyngial infection): do a culture or lacroscopy
TQ: what does chemoprophylactic eyedrops in newborns prevent?
TQ: *conjunctival infection* *opthalmia neonatorum*- gonorrhea infection
TQ: second most commonly reported STD
TQ: *gonorrhea* (behind chlamydia)...herpes would be first but that's not reportable
factors contributing to spread of gonorrhea:
-human resevoirs can be asymptomatic
-penicillin resistant strains (absolute refractoriness PPNG strains (Penicillinase Producing N. gonorrhea)
-birth control pills-create salutary environment, b/c of horomone shift?
how is trachoma transmitted?
direct contact, fomites, and filth flies (mechanical vectors)
TQ: most frequent form of chlamydial infection in US, *may be most common bacterial STI in the world*
TQ: chlamydial urethritis or cervicitis
-also causes 50% of *non-gonococcal urethritis (NGU)*
-*chlamydia may be most common STI in world*
compare the incubation time and duration of symptoms of gonorrhea and chlamydia
chlamydia: incubation time is longer, symptoms more prolonged (and hidden)
which STI is Teiter's syndrome the most severe complication in men
chlamydia: genital infection, polyarthritis, conjunctivitis
TQ: how can one acquire inclusion conjunctivitis?
TQ: newborns from *mom with chlamydial cervicitis*. baby can also get neonatal pneumonia {inClusion ConjunCtivitis: Chlamydia Cervicitis}
adults: contaminations with genital secretions or unchlorinated pools
TQ: what is primarily found in tropics:
*begins as genital ulcer*, granulomatous and suppurative (pus) -->inflammation of inguinal lymph nodes-->*bubos* that drain.
*genital elephantiasis*
but most resolve w/out treatment
TQ: *lymphogranuloma venereum* : from chlamydia trachomatis
TQ:~what STI is an intracellular parasite of columnar epithelial cells
~*does it resolve on it's own?*
TQ: ~chlamydia
~*yes, self-limiting*
TQ: which morphological form of chlamydia is the* infectious form*?
which is the *dividing form*?
TQ: infectious: elementary body
dividing: reticulate body
why is chlamydia rigid?
what does this mean it's resistant to?
rigidity maintained by disulfide bonds so it's resistant to penicillin
TQ: why is syphilis known as *'the great imposter'*
*what's the causative agent?*
it's often misdiagnosed as something else, b/c it occurs in so many areas- in blood vessels
*causative agent: treponema pallidum*
how is syphilis transmitted?
most often by sexual intercourse, rarely transplacentally
it's never casually transmitted
TQ: primarily an infectious of blood vessel walls
TQ: syphilis: *inflammation of blood vessel endothelium, blocks lumen causing obliterative endarteritis which underlies all damage seen*
repair involves scarring and *fibrosis*
TQ: chancres (primary lesion)
*when does it appear*
*how does it heal?*
only 30% of males and 50% of females have them, otherwise they'll move onto secondary phase
*appears b/t 10-90 days (avg 3 weeks)
*heals spontaneously, self-limiting*
TQ: -*condylomata lata*-around moist areas
-macular skin rashes commonly involving palms and soles
-oral lesions that appear as white patches
TQ: syphilis- *most infectious when chancres and condylomata latas are present* (*secondary phase*)

oral lesions look like candida
in latent phase of syphilis, what might cause a chronic slowly developing damage
an endotoxin and DH (i don't know what that is)
TQ: *aortic aneurysm* and mesaortitis are associated with what stage of what STI
TQ: *tertiary stage of syphilis
mesaortitis is the dialation of the media of the vessel -->weakening
TQ: *neurosyphilis may present as...

affects which part of CNS
chronic meningitis, tabes dorsalis or general paralysis
~affects posterior roots and columns of spinal cord, atrophy of brain
TQ: *gumma is associated with what STI?
what does it resemble?
TQ: ~*syphilitic gumma*- lesions of liver, bones, testis or skin with rubbery necrotic center
~resembles granulomas of TB
can syphilis be transmitted transplacentally?
yes- during second trimester
characteristic triad of congenital syphilis
1. interstitial keratits and choroiditis (saddle nose)
2. Hutchinson teeth (barrel incisors)
3. 8th cranial nerve deafness
spirochete who's growth can be slowed by PPNG (penicillin producing N. gonorrhea).
associated with cocaine trafficking
this STI is dropping to new lows in most places, except San Fran. LA and Seattle
can non-syphlitic treponematoses be transmitted transplacentally?
TQ: *Yawa (frambesia): agent
~*what resembles Yaws and what does it look like?
TQ: ~t. (pallidium) pertenue: Non-syphlitic treponematoses: *strawberry lesion* (initial lesion called *mother yaw* (framboise)*
~bejel (endemic syphilis) -*primary and secondary lesions in oral cavity*
TQ: causative agent of *chancroid* (soft chancre)
what does it look like?
*where is it found in the world?*
TQ: *haemophilus ducreyi* a bacteria
-red lesion, becomes pustular, ulcerates and has soft ragged edges,
*found in tropics and subtropics*
treatment for chancroid
antibiotics-clears all bacteria and lesions heal in 1-2 weeks
TQ: STI that is a *protozoan, has *flagellates*
TQ: *trichomoniasis : trichomonas vaginalis **it's eukaryotic**
irritates but doesn't penetrate mucosal surfaces
TQ: *strawberry mucosa*
*seen in what stage only?*
TQ: *trichomoniasis: small blisters on surfaces of urogenital tracts
*seen only in the trophozoites stage*
TQ: heavy, greenish, thick, foul-smelling, foamy dishcarge in females
*typically asymptomatic in males*
*males are vectors* in this situation
{men are tricky: trich-omoniasis}
what predisposes one to a symptomatic infection of trichomoniasis?
loss of normal vaginal acidity (an increase of pH)
TQ: *often coexists with gonorrhea
TQ: *trichomoniasis
Are these Gram + or -
staph aureus
gram +
Are these gram + or -
E. coli
gram -
TQ: incubation time for HCV
TQ: 2-26 weeks (avg 6-12 weeks)
TQ: most common enterics in US
TQ: rotavirus, Norwalk virus and *E. coli*