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;
141 Cards in this Set
- Front
- Back
|
what are the 4 zoonoses?
|
Yersinia: plague
Francisella Pasteurella Brucella |
|
|
what is the cause and course of bubonic plague?
|
Yersinia pestis. enters bloodstream and infects LNs, "buboes" form and then lead to sepsis, HOTN, and cutaneous thrombi ("Black Death")
|
|
|
what are the two diseases caused by Yersinia pestis, how are they causes different?
|
bubonic plague: from flea bites (not person to person)
pneumonic plague: spread person to person |
|
|
what are the animal reservoirs and vectors for Yersinia pestis?
|
reservoirs: urban rats (urban plague), prarie dogs and wild rodents (Sylvatic plague)
vector: fleas |
|
|
how do you diagnose Yersinia pestis infection?
|
IHC
|
|
|
how do you treat Yersinia pestis infeciton?
|
streptomycin and tetracycline
|
|
|
Yersinia pestis replicates...
|
in macrophages
in lymph nodes => buboes |
|
|
Francisella tularensis replicaes...
|
in macrophages
|
|
|
what 5 diseases can francisella tularensis cause?
|
1. Ulceroglandular (skin lesions with lymphadenopathy)
2. Oculoglandular (conjunctival granuloma) 3. Glandular 4. Typhoidal 5. Pneumonic |
|
|
what is the reservoir for Francisella tularensis?
|
wild rodents (esp rabbits)
transmitted by insect bites (ticks) |
|
|
how do you treat/prevent francisella tularensis?
|
streptomycin
live attenuated vaccine given to zookeepers, vets, and people with lots of rabbit exposure |
|
|
how is Pasteurella multocida infection initiated?
|
cat bites or immunocompromised host
|
|
|
how do you treat pasteurella multocida infection?
|
penicillin and ampicillin
|
|
|
what is the key morphologic characteristic of spirochetes?
|
periplasmic flagella (between outer membrane and cell wall)
|
|
|
what is the transmission efficiency of syphilis?
|
60% in MSM contact
low in heterosexual sex |
|
|
syphilis infection increases the rate of transmission of...how??
|
HIV
lesions increase transmission increase in CD4 cells present increases the number of targets |
|
|
what is the progression of Syphilis?
|
primary: lesions and lymphadenopathy at genitals or mouth (depending on initial inoculation site)
secondary: disseminated rash, lymphadenopathy tertiary: GUMMA lesions: cardiovascular and neurologic disease |
|
|
what is secondary syphilis?
|
occurs ~6 weeks later
a CD8 response (CD4 is primary) disseminated maculopapular rash headache, malaise |
|
|
what % of patients with untreated syphilis completely resolve their symptoms?
|
70%
|
|
|
what is the mechanism and result of tertiary syphilis?
|
low infectious load causes hypersensitivity
GUMMA lesions (monocytic infiltrates into many tissues causing rubbery granulomatous lesions |
|
|
what are the characteristic symptoms of congenital syphilis?
|
saddle nose
hutchinson's teeth (double points) saber shins (curved tibia) may cause other very serious defects (abortions, deafness, multiple organ failure) |
|
|
how do you diagnose spirochete infections?
|
Gram stains will not work!
IHC is the best way phase contrast another option |
|
|
what are the two screening tests for syphilis?
|
Rapid Plasmid reagin (RPR)
Venereal disease research laboratory test (VDRL) |
|
|
what are the 2 diagnostic tests for syphilis?
|
Indirect fluorescent antibody
Treponema pallidum particle agglutination test |
|
|
how do you treat syphillis?
|
parenteral syphilis?
|
|
|
how do you diagnose leptospirosis?
|
Microscopic agglutination Test (MAT) with lepto specific pentameric Abs
|
|
|
how are mycoplasma different than other bactertia?
|
they have no cell wall
they have sterols like mamallian membranes they have no paricular morphology the smallest non-viral living organisms |
|
|
what is the most likely causative microbe in summer-time pneumonia?
|
Mycoplasma pneumoniae (it has no seasonality but it is the only one which occurs in summer)
|
|
|
what is the most likely causative microbe in 5-20 year old getting pneumonia?
|
Mycoplasma pneumoniae
|
|
|
why does Primary Atypical Pneumonia have unremarkable symptoms and auscultory signs?
|
it is an interstitial disease so it doesn't cause rales, crackles etc.
|
|
|
how do you diagnose Mycoplasma pneumoniae infection?
|
"cold agglutination" test. For some patients, RBCs agglutinate
|
|
|
all rickettsial disease is spread by ____ except
|
arthropod (i.e. flea) vectors
except! Q fever: spread by milk or aerosoled afterbirth |
|
|
what type of lung disease does rickettsia cause?
|
pneumonitis (lung infection with NO pus)
it is an intracellular infection which doesn't make pus because PMNs make pus when they ingest extracellular pathogens |
|
|
what is unique about the life cycle of Chlamydacea?
|
they are obligate intracellular pathogens (can't make ATP) that form Elementary Bodies (EBs, non-replicative) that are like canons going to the next cell
|
|
|
what are the names for the two life stages of chlamydia/
|
reticulate body (intracellular replicating)
elemental body (extracellular 'canon" which is non-replicative) |
|
|
epidemiology of Chlamydophila pneumoniae:
|
40% of the world is seropositive
uncommon in young children becomes more common in late childhood and adulthood |
|
|
atherosclerotic plaques may be associated with what infectious organism?
|
Chlamydophila pneumoniae
|
|
|
what infectious agent do birds (i.e. pet parrots) often transmit to humans?
|
Chlamydia psittaci
Psittacosis pneumonia is an atypical pneumonia (no pus) because it is an obligate intracellular pathogen |
|
|
what is the causative microbe of nongonococcal urethritis?
|
Chlamydia trachomatis
|
|
|
what two microbes commonly coinfect the urethra?
|
N. gonorrhea and Chlamydia trachomatis (so if you test positive for one you should also get tested/treated for the other
|
|
|
yeasts reproduce by ______ and molds reproduce by _____
|
yeasts: budding
moulds: forming aerial hyphae and conidia |
|
|
mycelium:
|
a mass of hyphae
|
|
|
propagule:
|
a unit of fungi that can give rise to another organism
|
|
|
conidia:
|
a propagule formed asexually
|
|
|
athroconidia:
|
a conidia (asexual propagule) formed by fragmentation of a hyphae
|
|
|
how are spores different from conidia?
|
spores are formed in a group in sporangium, can be sexual or asexual
conidia: asexual propagule |
|
|
dematiaceous:
|
a fungus with black or brown pigments in the wall
|
|
|
what is the only fungus with an antiphagocytic polysaccharide capsule?
|
Cryptococcus neoformans
|
|
|
what is the unique sterol in fungal membranes?
|
ergosterol
|
|
|
what are the two methods of visualing fungi in tissue? how do they work?
|
Calcofluor white: binds chitin in cell wall
Gomori methenamine silver (GMS): |
|
|
what are the important notes for culture and ID of Malassezia furfur?
|
requires lipid source to grow (olive oil)
bats and balls (both yeast and hyphae) causes tinea versicolor |
|
|
how do you treat both black and white piedra?
|
shaving
|
|
|
onchomycosis (also called tinea unguium)
|
tinea of the nails
|
|
|
what are the 3 genera of dermatophytes and how do they get their energy?
|
Microsporum, epidermophyton, tricophyton
they hydrolyze keratin as an energy source |
|
|
how can you diagnose dermatophytosis?
|
clinical appearance
UV lamp (tinea will lumenesce) |
|
|
topical antifungals will not work for which types of dermatophytoses?
|
tinea capitis, tinea barbae, tinea unguium (onchomycosis), or any extensive cutaneous involvement
|
|
|
how do you treat sporotrichosis?
|
if local: itraconizole + heat
if systemic: Amphotericin B +/- Itraconizole |
|
|
candida is normal flora of...
|
human GI
|
|
|
which fungi often causes bloodstream infections as a result of CVCs?
|
Candida
grows well on plastic and forms biofilms |
|
|
what are the risk factors for Candidiasis?
|
1. antibiotic use: competes off bacteria
2. catheterization: CVC, dialysis 3. nosocomial 4. abdominal surg |
|
|
what is the microscopic appearance of candida?
|
budding yeast with pseudohyphae
|
|
|
what is the mainstay of candidiasis treatment?
|
fluconazole
|
|
|
Aspergilli are normal flora of...
|
the environment...NOT normal human flora
|
|
|
what is Allergic BronchoPulmonary Aspergillosis (ABPA)
|
IgE formed against the ubiquitous aspergilli so you get an asthma like delayed hypersensitivity rxn
|
|
|
how can you diagnose invasive aspergillosis
|
serial monitoring of serum for galactomannan
blood cultures ineffective, only transient episodes of fungemia |
|
|
what is the first line treatment for invasive aspergillosis
|
voriconazole
|
|
|
the goal of prophylactic voriconzale is to prevent ____
it can cause _____ |
prevents invasive asperillosis in patients post HSCT
can cause zygomycoses (YIKES!) |
|
|
how do you diagnose pneumocystis jiroveci infection?
|
bronchoalveolar lavage
good sens and spec |
|
|
how do you treat pneumocystic jiroveci infection?
|
trimethoprim-sulfamethoxazole (an antibacterial!)
|
|
|
the viral genome lacks...
|
encoding the machinery for protein synthesis (ribosomes etc)
|
|
|
virion:
|
non-replicating extracellular viral particle
|
|
|
enveloped viruses have...
|
a lipid bilayer with many glycoproteins (with receptor-interaction fx)
|
|
|
which is more sensitive to dessication/heat/acid, enveloped or naked viruses?
|
enveloped
|
|
|
capsomere:
|
one of the protein faces of a viral icosahedron
|
|
|
all human pathogen helical viruses are (enveloped/naked)?
|
enveloped
|
|
|
what type of virus is neither icosahedral or helical?
|
poxviruses (enveloped and huge)
|
|
|
what is the reference size for a medium and small virus?
|
medium ~100nm
small: <30nm |
|
|
what is the difference between + sense RNA viruses and -sense RNA viruses?
|
+sense: the viral genome RNA is the same polarity as the mRNA (it can act as mRNA)
-sense: the viral genome is the opposite polarity to the mRNA (complement strand is the mRNA) |
|
|
what are the proteins responsible for viral tropism?
|
Viral Attachment Protein (VAP)
interact with host receptors...determine which types of cell the virus can infect |
|
|
how are VAPs different in enveloped vs. naked viruses?
|
enveloped: membrane glycoproteins
naked: capsomere proteins |
|
|
why are antibodies ineffective against some naked viruses?
|
the Ab binding site cannot enter the capsid clefts for binding specificity
|
|
|
how does HIV gain entry into host CD4 cells?
|
gp120 binds CD4
changes conformaiton of gp41 (which attaches cell to gp120) then recruits CCR5 gp41 then inserts into host membrane allowing for MEMBRANE FUSION |
|
|
how does influenza virus gain entry into host cells?
|
influenza VAP: hemagluttinin
host receptor: sialic acid gets taken up into endosome (no membrane fusion) acidification of endosome releases viral genome |
|
|
what is the central dogma of retroviruses and how is it different than -strand RNA viruses?
|
retrovirus: +senseRNA -> DNAincorporated into host DNA-> mRNA -> protein
-strand virus: RNA -> -mRNA -> protein |
|
|
which DNA virus does NOT replicate in the nucleus?
|
poxvirus
encodes its own DDDP and DDRP |
|
|
how is the RDRP different for -sense vs. +sense RNA viruses?
|
RDRP must be packaged wtih -sense RNA virsues
RDRP must only be encoded by +sense RNA viruses |
|
|
provirus:
|
viral DNA sequence incorporated into the host genome
|
|
|
which RNA virus does not replicate in the cytoplasm?
|
orthomyxovirus
|
|
|
how do enveloped viruses get assembled?
|
their glycoproteins get targeted to cell membranes, then the capsid buds out through that part of the membrane
|
|
|
influenza only occurs during the _______ and coxsackie virus only occurs during the ____
|
influenza: winter
coxsacke: summer |
|
|
what is an inclusion body and what types of viruses cause it?
|
a darkened spot in the nucleus
cytomegalovirus rabies virus |
|
|
why do some viruses cause cancer?
|
if they promote progress through the cell cycle they can keep mitotic machinery around
in short lived cells, if they prolong life they can life longer themselves |
|
|
which herpes viruses can cause cancer?
|
Epstein-Barr: burkitt's lymphoma
Kaposi Sarcoma Herpesvirus |
|
|
which hepatitis viruses can cause cancer?
|
hepatitis B virus (a DNA virus)
hepatitis C virus (a RNA virus) |
|
|
what is the main host defense of all cells against viruses?
|
type 1 interferons
all cells can make IFN-beta all cells can react to both IFN-beta and IFN-alpha |
|
|
what are the effects of Type 1 interferons on host cells?
|
induces an antiviral expression profile
induces expression of MHC I stops translation |
|
|
what is the role of type 2 interferons in virus defense?
|
Type 2 interferons induce cytotoxic T cells against intracellular pathogens
|
|
|
Th1 cells produce cytokines favoring...
Th2 cells produce cytokines favoring... |
Th1: cytotoxic T cell response
Th2: B cell Ab response |
|
|
how do some viruses prevent killing of host cell by CD8 T cells?
|
they can downregulate expression of MHC I
|
|
|
almost all RNA viruses employ what immunosuppressive defense mechanism?
|
they produce type 1 IFN blockers
|
|
|
how does human cytomegalovirus prevent its host cell from being killed?
|
it expresses a MHC-1 like molecule that does NOT bind CD8 cells (no killing) but does bind NK cells (prevents NK killing)
|
|
|
why is rhinovirus restricted to the upper respiratory tract?
|
even though all cells can get infected by rhinovirus, it replicates best at cooler temperatures and is sensitive to low pH of GI tract
|
|
|
how does poliovirus cause disease?
|
fecal-oral spread
GI infection viremia travels up motor neurons to produce flaccid paralysis |
|
|
what are the 2 polio vaccines and which is given today?
|
Attenuated (Sabin)
Inactivated (Salk): the only one given today |
|
|
how do you diagnose acute Hepatitis A?
|
anti-HepA-IgM
IgG not helpful...continues to rise slowly after infection |
|
|
why is the 2nd infection with Dengue Fever more dangerous?
|
primary infection: intense muscle pain, low mortality
secondary infection: Abs to IMMATURE particles of 1st strain FACILITATE entry of 2nd strain, which WILL kill you |
|
|
which Flavivirus has a vaccine?
|
yellow fever
|
|
|
how do you treat hepatitis C, is this effective in the U.S.?
|
IFN-alpha and ribavirin
not effective against the serotypes in the U.S., types 1 and 2 |
|
|
how are togaviruses different than flaviviruses?
|
togavirusese are bigger and have subgenomic RNA which encodes structural proteins (processed RNA, only transcribe part of the RNA genome...all of Flavivirus genome is transcribed)
|
|
|
what is the VAP for influenza and what does it bind?
|
HA: hemagluttinin
inactive adn must be activated by serine proteases in the lung binds Sialic acid |
|
|
what determines type (A, B) of influenza virus?
|
the type of M1, M2, or NP protein in the envelope
|
|
|
what is the purpose of influenza M2 protein?
|
it pumps protons into the endosome to allow for low pH dependent uncoating of viral genome
|
|
|
what is the only group of RNA viruses that MUST go to the nucleus for replication?
|
orthomyxoviruses: they steal the 5' methyl-guanine cap of host mRNAs
|
|
|
what is the purpose of influenza neuraminidase (NA)?
|
it removes sialic acid from infected host cell, allows the eggressed virion to get AWAY without HA binding
|
|
|
how does antigenic shift of influenza happen?
|
only happens to influenza A
coinfection and picking up of a completely new surface protein (HA, NA, M) because of segmented genome |
|
|
Amantidine and Ramantidine: mechanism and use
|
M2 channel blockers
prevent low pH dependent uncoating of influenza genome only work for influenza A |
|
|
Zanamivir, Relensa, and oseltamivir: mechanism and use
|
inhibit Neuraminidase (NA) so you can't get release of eggressed influenza virus
|
|
|
what is the key histologic characteristic of rhabies infected nerves?
|
negri bodies: inclusion in nerves
|
|
|
what does HIV require in order to enter a cell?
|
host cell must have CD4 and either CCR5 or CXCR4
both are bound by gp120 |
|
|
what is the process of retroviral RNA getting into the genome?
|
RT synthesizes -DNA from +RNA
degrades viral -RNA as it goes error prone forms complementary +DNA adds Long Terminal Repeats (LTRs) at the ends LTRs (with Integrase) allow for insertion of sequence into genome |
|
|
what are the major gene products of the HIV genome?
|
RT and Integrase
gp41 gp120 gag (spliced to) gp24 makes the capsid |
|
|
how does tropism of HIV commonly change through infection
|
CCR5 tropic (macrophage, monocytes, and memory CD4 T cells) is more effective at transmission
evolve to CXCR4 (CD4 effector T cells) which is more deadly |
|
|
what two factors can increase the progression in an HIV infected person?
|
evolving to a CXCR4 tropic strain
formation of syncytiae which rupture |
|
|
what allele is protective against HIV infection?
|
a mutation in the CCR5 receptor
homozygotes don't get infected hets have slower progression |
|
|
when does HIV become AIDS?
|
when either
1. your CD4 T cell count falls below 200/u 2. you get a pathognmonic opportunistic infection 3. unusual malignancy (i.e. kaposi sarcoma) 4. HIV encephalopathy and neuropathy |
|
|
what is the name of the therapy regimen for HIV/AIDS?
|
HAART (highly active anti retroviral therapy)
at least 3 therapies, good at reducing viral load protease inhibitors most important |
|
|
why is development of an HIV vaccine so difficult?
|
Abs formed against HIV (usually against gp24, the capsid) are useless, need to active the cytotoxic T cell arm
|
|
|
what are the key features of the herpesvirus lytic lifecycle?
|
genome is linear and circularizes in host
3 phases of gene expression: 1. proteins to initiate transcription 2. genome replication proteins 3. production of viral particles |
|
|
what is unique about herpesvirus Dna synthesis?
|
herpesvirus provide their own thymidine kinase to make dNMP
a target of antiviral therapy |
|
|
what is the only herpesvirus with a vaccine?
|
VZV varicella zoster virus
recommended for people over 60 to prevent shingles |
|
|
what is the classic finding on peripheral blood smear of a person with mononucleosis?
|
atypical lymphocytosis
large lymphocytes with large nuclei and abnormal shapes |
|
|
how are poxviruses unique?
|
they are huge
they are the only DNA viruses which replicate in the cytoplasm (they carry their own DDDP and DDRP) |
|
|
what is the classic histological sign of adenoviral cellular infection?
|
intranuclear inclusions
|
|
|
what is the progression of HPV infection in cervical mucosa?
|
must get to basal layer to replicate
then moves back up through the layers to shed onces it gets to the surface layers (clear, granular, horny) |
|
|
what is the classic histologic appearance of HPV infected cells?
|
koliocytosis: large fluid filled cells with distorted nuclei
|
|
|
what are the high risk HPV strains and why?
|
16, 18, 31
have high E6 (p53 blocking) and high E7 (Rb blocking) activities |
|
|
the gardasil vaccine is composed of...
|
empty capsids of the high risk HPV strains
|
|
|
B-19 virus infection is especially dangerous for...
|
people with an existing thalassemia
the B-19 virus targets erythroid progenitor cells |
|
|
what determines whether a person will get an acute or chronic Hep B infection?
|
infants don't have a good T cell response, they don't develop anti-HBsAg antibodies and the infection persists
usually older people do have those and clear the infection, but the acute T cell response is HEPATOTOXIC |
|
|
B-19 virus infection is especially dangerous for...
|
people with an existing thalassemia
the B-19 virus targets erythroid progenitor cells |
|
|
what determines whether a person will get an acute or chronic Hep B infection?
|
infants don't have a good T cell response, they don't develop anti-HBsAg antibodies and the infection persists
usually older people do have those and clear the infection, but the acute T cell response is HEPATOTOXIC |
