SketchyMicro: Viruses Flashcards
Piconavirus: 3 main features
Piconaviruses:
- positive sense: meaning the RNA is directly translated into proteins
- RNA virus
- naked
3 main subgroups of piconaviruses
Piconaviruses: positive sense RNA viruses w/o capsules (naked)
ABC
- A for Hepatitis A
- B for birds = Enterovirus
- C for common cold = Rhinovirus
Main manifestation of the three classes of piconoviruses
(a) Hep A
(b) Enterovirus
(c) Rhinovirus
(a) Hep A => anicteric acute febrile self limited
(b) Enterovirus = MC cause of aspetic (aka nothing grows on gram stain b/c there’s no bacteria) meningitis
(c) Rhinovirus => common cold
MC cause of aspetic meningitis
Aspetic meningitis = viral meningities, MC cause = enterococcus species = poliovirus, coxsackie A and B, echovirus
Called aseptic b/c the gram stain doesn’t grow anything (b/c it’s viral not bacterial)
Where does the polio virus replicated?
(a) Duration of latency period
Polio virus replicated in Peyers patches of the GI tract
(a) Remains latent for about 2-3 weeks, then infects anterior horn cells of the spinal cord
Differentiate the 2 vaccines for poliomyelitis
- Salk = inactivated, killed vaccine given intramuscularly
- IM so bypass Peyer’s patches => mostly IgG not IgA - Sabin = oral live attenuated vaccine- gives both IgA and IgG but can shed in feces and revert to infectious strain
- rare but this is why we don’t use it in the US (we use Salk)
Where does the poliovirus infect to cause symptoms?
(a) Clinical presentation
(b) Cause of death
Poliovirus infects the anterior horn cells of the spinal cord
(a) Ascending asymmetric paralysis
(b) Paralysis rises to diaphragm => respiratory insufficiency
Compare and contrast coxsackie A and B viruses
Both coxsackie viruses are enteroviruses, which are picornaviruses = positive sense RNA naked viruses
A => hand-foot-mouth disease, red vesicular rash, and aseptic meningitis (like the other enteroviruses)
B => dilated cardiomyopathy and Devil’s grip
Name 3 rashes that involve the hands and feet
- Hand-foot-mouth disease = Cocksackie A
- Syphilis
- Rickettsia Ricketsia
Buzzwords
(a) Devil’s grip
(b) Child immigrant p/w descending rash and lymphadenopathy
(a) Cocksackie B caused syndrome of severe unilateral CP that makes it hard to breathe
(b) Rubella = German measles
Which of the picornaviruses is acid labile?
3 subgroups of picornaviruses = ABC
- A: Hepatitis A
- B: Birds = Enterococcus
- C: Common cold = rhinovirus
Rhinovirus is the only acid labile one of the three => can’t survive gastric acid => not fecal/oral transmitted, instead by fomites and respiratory droplets
While Hep A and enterococcus are acid stable => transmitted fecal/oral
What group of virus causes
(a) Rhinovirus
(b) Cruise ship diarrhea
(c) Dengue fever
Viral group
(a) Rhinovirus = picornavirus- positive sense RNA naked virus
(b) Cruise ship diarrhea = Norwalk virus = Calicivirus = ssRNA naked positive sense
(c) Dengue fever = flavivirus
What group of viruses causes
(a) Yellow fever
(b) Rubella
(c) Hepatitis A
Viral group
(a) Yellow fever = flavivirus
(b) Rubella (German measles) = togavirus
(c) Hepatitis A = picornavirus
What group of viruses causes
(a) West Nile Virus
(b) SARS
Viral group
(a) West nile = Flavivirus
(b) SARS = coronavirus
Explain why rhinovirus infects the location it does
Rhinovirus prefers cooler temps (33 C) as in colder than body temp, so likes the upper respiratory tract where air comes in and is colder
Why don’t we have a vaccine for the
(a) Common cold
(b) Hepatitis C
(a) Ummm b/c there’s literally 113 serotypes of rhinovirus- can’t cover for all of them
(b) Hep C envelop proteins have a ton of antigen variability b/c their virion encoded RNA polymerase lacks 3’ to 5’ exonuclease proofreading activity
MC mode of transmission of Hepatitis A
(a) Underdeveloped countries
(b) US
Hepatitis A
(a) Contaminated water in underdeveloped countries
(b) US- uncooked shellfish
Smoker suddenly develops aversion to smoking
Buzzword for Hepatitis A infection
Describe the clinical presentation of Hepatitis A
(a) Duration
Usually asymptomatic (esp in children), but can be acute febrile illness w/ RUQ pain and jaundice (jaundice esp in adults)
Lasts about 1 mo without a chronic state! No carrier/chronic state
Who gets the Hep A vaccine?
MSM, travel to endemic area, other chronic liver disease
Viral group
(a) Hepatitis A
(b) Hepatitis C
Viral group
a) Hepatitis A = picornavirus
(b) Hepatitis C = flavivirus (also Dengue, West Nile, Yellow fever
Break bone fever
Break bone fever = Dengue fever, infects bone marrow and can cause thrombocytopenia
Which flavivirus has a vaccine?
Live attenuated vaccine available for yellow fever
-not Dengue or West Nile Virus
Differentiate clinical presentation of Dengue vs. Yellow fever
Dengue fever- break bone fever (infects bone marrow) => thrombocytopenia, hemorrhagic fever, high risk renal failure
Yellow fever- jaundice, back ache, bloody diarrhea
Both by the same species of mosquito
Major complication of West Nile Virus
Meningitis!
Can also cause flaccid paralysis, seizure, coma
More likely to become chronic- hep B or C?
Hep C- like 60-80% become chronic
‘C for chronic’
For Hep B chronicity depends on age of primary infection- 90% chronic in infected as infant, while only 5-10% adult cases become chronic
Hepatitis C
(a) Acute presentation
(b) When does anti-HCV develop
(c) Chronic risk
Hep C = Flavivirus (positive sense, enveloped RNA virus)
(a) Acutely w/ jaundice, can have RUQ pain and elevated LFTs (ALT drops w/in 6 mo), then 60-80% progress to chronic
(b) anti-HCV develops after 2-3 months
(c) Chronic risk = cirrhosis and HCC
Chronic Hep C infection
(a) Histologically
(b) Serum finding
Chronic Hep C (develops in 60-80% of primary infections)
(a) See tons of lymphocytes in the portal tracts
(b) Serologically: Hep C RNA remains positive after 6 months
- also cryoglobulins = IgM that precipitate in cold temps (extremities)
What is cryoglobulinemia?
(a) Differentiate from cold agglutinin
Cryoglobulinemia = blood contains a lot of cryoglobulins = proteins (usually IgM against Fc of IgG) that precipitate at colder temps
(a) While cold agglutinins are precipitates of RBCs (not IgM)
Name 3 classes of disease commonly associated w/ cryoglobulinemia
Cryoglobulinemia = blood contains high concentration of cryoglubulins that precipitate at cold temps, usually IgM
- Multiple myeloma (makes sense b/c it’s a cancer of IgM producing cells)
- Hepatitis C
- AI d/o: RA, SLE
General overview of tx for Hep C
Hep C tx: need to genotype to determine exact regimen, but overall protease inhibitors, previously used ribavarin and interferon alpha
Classic clinical presentation of the most common togavirus
MC togavirus = Rubella = German measles
Classic presentation = immigrant child (aka not vaccinated) w/ descending rash (macpap rash beginning on face) and cervical and postauricular lymphadnopathy
Name the TORCHeS infections
TORCHeS infections = ones that cross the placenta and cause disease in newborn
Toxoplasma gondii Rubella CMV HIV, HSV Syphilis
Also includes Varicella, Parvovirus
Classic triad of congenital rubella
Congenital rubella = congenital blindness (cataracts), sensorineural deafness, patent ductus arteriosis
Also: ID, microcephaly, purpuric blueberry muffin rash
2 contraindications to the MMR vaccine
- Pregnancy
2. HIV w/ CD4 under 200, safe if over 200
Where in the cell do the picornaviruses replicated?
All RNA viruses, esp positive strand that just directly translate into proteins, replicate in the cytoplasm (not the nucleus!)
Classify the HIV virus
(a) Type of genetic material
(b) Diploid
(c) How makes proteins
HIV virus
(a) Technically positive sense RNA virus, but not directly translated into proteins
(b) Diploid b/c two molecules of viral RNA in each virion
(c) positive sense RNA reverse transcriptase into cDNA which is then incorporated into host genomes then made into proteins
Fxn of these 3 key HIV genes
(a) Gag
(b) Env
(c) Pol
HIV genes
(a) Gag codes for p24 protein = capsule for RNA strands
(b) Env codes for glycoproteins 41 (transmembrane protein) and 120 (outer protein)
(c) Pol codes for the reverse transcriptase
Describe the clinical features of the HIV prodrome stage
(a) Latent period?
HIV prodrome: flu or mono-like symptoms w/ cervical lymphadnopathy/fever 2/2 infection of first macrophages then CD4
(a) Latent period of virus replicating in the lymph nodes can last for up to 10 years
HIV increases risk for which malignancy?
HIV increases risk for large diffuse B cell lymphoma (MC type of Non-Hodgkin Lymphoma)
Name the two receptor proteins on CD4 cells used by HIV for access
CD4 cell receptor proteins that HIV binds to for access
Early in disease- CCR5 (hence CCR5 receptor inhibitors used as anti-HIV drug)
Later in disease- CXCR4
Differentiate how to diagnose HIV in adult vs. newborn
In adults: first ELISA to look for HIV Ab, if positive then confirm w/ Western blot
In newborn: will automatically have IgG of mother so ELISA is useless => dx w/ NAT (nucleic acid amplification testing) to look directly for the virus
Which HIV drug is used in pregnant F to prevent vertical transmission?
Zidovudine = NRTI (nucleotide reverse transcriptase inhibitor) aka nucleotide analog
Mechanism of
(a) Maraviroc
(b) Zidovudine
Mechanism
(a) Maraviroc = CCR5 receptor inhibitor
- inhibits the receptor used by HIV to infect CD4 cells
(b) Zidovudine = NRTI = nucleotide reverse transcriptase inhibitor = nucleotide analog
Name some negative sense RNA viruses
Negative sense RNA viruses
- Orthomyxovirus: influenza
- Paramyxovirus: Measles (rubeola), mumps, parainfluenza (croup)
- rhabdovirus: rabies
- filovirus: ebola
- Bunyavirus, arenavirus, reovirus
Name some positive sense RNA viruses
Positive sense RNA viruses
- Picornavirus: hep A, enterococcus, rhinovirus
- Flavivirus: hep C, West Nile, Dengue fever
- Togavirus: Rubella
- HIV/AIDS
Negative sense RNA viruses
(a) How many strands?
(b) Location of replication?
(c) Necessary for replication
Negative sense RNA viruses
(a) All are single stranded except reovirus (ds)
(b) All replicate inside the cytoplasm except orthomyxovirus
(c) Since negative sense they can’t be made directly into proteins => bring their own RNA polymerase
Name the 4 negative sense RNA viruses that form segments
‘BOAR’ mnemonic for segmented viruses- all of which are negative RNA viruses
Bunyavirus: 3 circular segments
Arenavirus: 2 segments
Orthomyxovirus (influenza): 8 segments
Reovirus: 11 segments
Differentiate antigenic drift and antigenic shift
Antigenic drift = point mutation that causes epidemics
ex: seasonal flu
Antigenic shift = gene reassortment (possible in ‘BOAR’ segmented viruses), much more dangerous, causes pandemics
ex: H1N1 swine flu
Mechanism of hemagluttinin
Hemagluttinin is a glycoprotein on viral membranes that bind salic acid reside on host cell membranes in upper respiratory tract and RBC
-called hemagluttinin b/c agglutinates BRC in vitro
So the strain of hemagluttinin determines which cells the virus can infect
-so H1, H2, and H3 are the strains that infect humans
What protein determines which organisms are infected by which influenza strains?
Hemagluttinin protein defines the tropism- hemagluttinin is the viral membrane glycoprotein that binds host membrane
Ex: H1, H2, H3 are the strains that can infect humans
Mechanism of M2 protein
M2 protein of influenza responsible for creating pH needed for viral encoding
Name the three virulence factors of influenza virus
3 virulence factors of influenza A
- Hemagluttinin- allows binding to host cell
- M2 protein- creates pH for viral encoding
- Neuraminidase- release of new virions out of host nucleus
Mechanism of the following against influenza virus
(a) Amantadine
(b) Oseltamivir
(a) Amantadine (but not used b/c of resistance) inhibits M2 protein that codes for the ion channel needed to make the right pH for viral replication
(b) Oseltamivir = inhibits neuraminiase (protein that cleaves sialic acid to release new virions from the nucleus), taken early (w/in 72 hrs) or else not helpful b/c virions already released
3 complications of influenza
(a) Pulm
(b) Aspirin
(c) Neurologic
Complications of influenza
(a) Pneumonia super infection, often staph aureus
(b) Give aspirin to a kid w/ influenza = risk of Reye syndrome = liver failure and encephalitis
(c) Can precipitate Guillain-Barre: ascending paralysis, albuminocytologic dissociation of CSF
4 syndromes caused by paramyxovirus
Paramyxovirus = negative sense ssRNA viruses, enveloped
- Measles (rubella): cough, coryza, conjunctivitis, Koplik spots, fever, rash starting on face
- Mumps- parotitis b/l, possible orchitis and meningitis
- RSV- bronchitis and pneumonia in infants
- Parainfluenza- croup/laryngotracheobronchtiis = seal like cough w/ inspiratory stridor
Prodrome syndrome of Rubeola
Rubeola = Measles = paramyxovirus = -sense ssRNA virus
4 Cs: cough, coryza (runny nose), conjunctivitis, Koplik spots
and fever
2 viral rashes that start on the face then descend
(a) How to differentiate
Both measles (rubeola, paramyxovirus, negative sense RNA) and rubella (German measles, togavirus, positive sense RNA) have rashes that start on face then descend
(A) Rash of measles is confluent (bumps fuse)
What virus causes subacute sclerosing panencephalitis
Subacute sclerosing panencephalitis from chronic measles (rubeola) infection
Meales/rubeola = paramyxovirus: ss, negative sense RNA virus, enveloped, replicates in cytoplasm
Virulence factors present in
(a) Influenza
(b) Measles
(c) Mumps
(d) RSV
(e) Parainfluenza
Virulence factors
(a) Influenza- HA (hemagluttinin), M2 protein, neuraminidase
(b) Measles- HA and fusion protein
(c) Mumps- HA, fusion protein, neuraminidase
(d) RSV- fusion protein only
(e) Parainfluenza- HA, fusion protein, neuraminidase
Antibodies against what molecule protect us from repetitive infection by influenza strains
Anti-HA (hemagluttinin) is what protects from infections of the same strain in the future
CSF findings specific to Guillain-Barre syndrome
GB: albuminocytologic dissociation = high protein w/ low WBC count
Two infectious precipitators of Guillain-Barre
- Campylobacter: s/comma shaped gram negative
2. Influenza (orthomyxovirus)
Describe clinical features of the measles that arise after the prodrome phase
Measles/Rubeola starts w/ conjuncitivits, coryza (runny nose), cough, fever, Koplik spots (blue/gray on buccal mucosa)
Then a few days after Koplik spots appear, get itchy rash starting on face then descends
Virulence factors present in the paramyxoviruses
(a) Measles
(b) Mumps
(c) RSV
(d) Parainfluenza
Virulence factors of the paramyxoviruses
(a) Measles (Rubeola, Koplik spots and rash starting on face): neuraminidase and fusion protein
Vitamin A can help reduce the morbidity/mortality of which viral illness?
VIt A reduces morbidity/mortality of measles (rubeola) = paramyxovirus, negative sense RNA enveloped virus
Function of fusion protein
(a) Present in which viruses?
Fusion protein causes fusion of syncytial cells to form multinucleated giant cells
(a) Fusion protein is produced by Measles, mumps, RSV, and parainfluenza (all 4 paramyxoviruses)
MC cause of bronchitis and pneumonia in infants
(a) Virulence factor
MC cause of bronchitis and pneumona in pts under 6 mo = RSV (respiratory synctial virus)
(a) Virulence factor = only fusion protein
- fusion of syncitial cells to form multinucleated giant cells
Mechanism of infection by RSV
(a) Tx
RSV (respiratory syncytial virus attaches to G protein to infect respiratory epithelial cells => bronchitis and pneumonitis in infants under 6 mo
(a) Tx w/ Ribavarin
MC carrier of rhabdovirus in the US
MC carrier of rhabdovirus (rabies) in the US = bats
-also carried by dogs, rodents etc but we’ve mostly vaccinated those in the US
What does the rhabdovirus bind to?
(a) What determines length of incubation period?
Rhabdovirus (rabies) glycoproteins bind the nicotinic ACh receptors at the post-synaptic motor endplate
(a) Then travel retrograde 1-3mm/day up peripheral nerves to the dorsal root ganglia
- so incubation period duration determined by distance of inoculation to the DRG (how far the virus has to travel), usually weeks to months
Where does the rhabdovirus replicate?
(a) Clinical features
Rhabdovirus (rabies) replicates in the motor neurons
(a) Foaming of mouth, fever, rabies encephalitis
Tx of rhabdovirus
Tx of rabies- can’t do much once you have the symptoms, so need to quickly tx w/ passive immunity for post exposure prophylaxis
Passive immunity is giving preformed antibodies, then also give killed vaccine for active immunity
Give passive immunity to ppl even after simple exposure to bats, even w/o obvious bit (b/c so dangerous and can’t just treat later)
What kind of virus is ebola?
(a) Shape
(b) Another of this class
Ebova and (b) Marburg are Filoviruses
(a) Negative sense single stranded helical RNA virus, enveloped
Clinical features of filovirus
(a) Cause of death
Filovirus = Ebola and Marburg
Hemorrhagic fever: fever and petechial rash, w/ end-organ failure
(a) Death usually from hypovolemic shock from all the blood loss
- super infectious thru all body secretions, so gotta be really careful w/ the dead body or it’ll just spread everywhere (ugh ew)
Bunyavirus
(a) Unique about its envelope
(b) Feature in common w/ influenza
(c) Mechanism of pulm and renal involvement
Bunyavirus: negative sense ss RNA virus w/ envelope
(a) Gets its envelope from the golgi apparatus of host cell
(b) Like influenza (orthomyxovirus), BUnyavirus is segmented (‘BOAR’)
(c) Causes pulmonary capillary leak => pulmonary edema and pre-renal azotemia 2/2 loss of fluid to third space
Name the single ambisense RNA virus
Arenavirus (‘BOAR’ of segmented viruses)
Ambisense meaning it’s technically negative sense but can also translate gene from a positive strand
3 virus species that have helical-shaped capsid
- Arenavirus
- Rhabdovirus- causes rabies
- Filovirus- Ebola
RNA double stranded virus
(a) Location of replication
Only reovirus is double stranded
(a) Still replicates in the cytoplasm: only RNA virus that doesn’t replicate in the cytoplasm is orthomyxoviruses (influenza)
MC cause of severe diarrhea in children
Reovirus = Rotavirus = #1 cause of severe diarrhea in children
-typically in winter months, highest risk in children
How to clinically distinguish Rocky Mtn spotted fever and Colorado Tick virus
Both have myalgias, fever, vomiting, but Colorado tick virus doesn’t cause rash
While Rocky mtn spotted fever classically causes rash starting on hands/feet that then spreads to trunk
Reovirus
(a) Clinical syndrome
(b) Toxin mechanism
(c) Transmission
Reovirus = Rotavirus
(a) Clinically: secretory diarrhea
(b) NS-P4 toxin increases Cl- permeability of enterocytes => secretory, explosive diarrhea
(c) Oral fecal transmission
Rotavirus vaccine
(a) Type
(b) When to give first dose
(c) Risk
Rotavirus vaccine
(a) Live attenuated virus vaccine given orally
(b) Give first dose before 3 months of age
(c) Slight risk of intussusception due to Peyer’s patch hypertrophy acting as a lead point
Characteristics of the herpes virus family
Herpes virus family = double stranded DNA virus- all remain latent and are enveloped
DNA virus => replicates in the nucleus
Herpes family: HSV, CMV, VZV, HHV6 and HHV8
Differentiate histologic findings of poxvirus vs. herpes virus family
Poxvirus has eosinophilic inclusions but they’re in the cytoplasm
While Herpes virus family (HSV, CMV, VZV) has Cowdry bodies = intranuclear eosinophilic inclusion bodies
Presentation of HSV-1
(a) in children
(b) in the eye
HSV-1 => oral herpes (herpes labialis)
(a) In children initially presents as gingivostomatitis = inflamed lips and gums
(b) Keratoconjunctivitis- serpiginous ulcers on the cornea under slit lamp
MC cause of sporadic encephalitis in the US
Herpes (HSV)
Where do the following lay dormant
(a) HSV-1
(b) HSV-2
(c) EBV
(d) CMV
(e) VZV
(a) Trigeminal ganglia
(b) Sacral ganglia
(c) EBV dormant in B cells
(d) CMV in mononuclear cells = white cells w/ one nucleus = lyphocytes (T and B) and macrophages
(e) VZV in dorsal root ganglion
Dew drops on a rose petal rash
Dew drops on a rose petal = clear vesicles on a red erythematous base describes the rash on HSV and VZV
-both herpes and varicella
Erythema ___ rash seen 2/2 HSV infection
Erythema multiforme = hypersensitivity target lesions 1-2 weeks after infection w/ primary HSV
Clinical presentation of HSV-2
(a) Serious complication
HSV-2 => genital herpes
-painful genital vesicular lesions w/ painful inguinal lymphoadenopathy
(a) Aseptic meningitis in adolescents and adults
Smear for visualization of HSV
(a) What other virus?
Tzank smear of HSV scrapings show multinucleated giant cells
(a) Also diagnostic for VZV
Tx of HSV-1/2 infection
Oral (HSV-1) and genital (HSV-2) herpes can’t be cured, but can prevent outbreaks w/ acyclovir or valcyclovir
EBV
(a) Type of virus
(b) Peripheral smear findings
EBV
(a) Herpes virus family: dsDNA (replicated in nucleus), enveloped, remains latent
(b) Peripheral smear: irregular/atypical lymphocytes = reactive cytotoxic CD8 T cells
Mechanism by which EBV infect B cells
EBV has envelope glycoprotein that binds to CD21 receptor on B cells
Clinical hallmarks of EBV infection
EBV infection (infectious mono MC cause): fever, lymphadenopathy (usually cervical but can also be generalized), pharyngitis and tonsillar exudates
Why do you not want to confuse pharyngitis from EBV w/ strep pharyngitis?
B/c giving Ampicillin or amox to pt w/ EBV can cause macpap rash
So yes both present w/ pharyngitis
but also more lymphadenitis in EBV, longer duration and fatigue, dif exudate?
EBV increases risk of which cancers?
EBV increases risk of 3 cancers
- Hodgkin Lymphoma (Reed Sternberg cells)
- Burkitt non-Hodkins Lymphoma
- Nasopharyngeal carcinoma (in Asian pts)
Oral lesion associated w/ EBV infection
Hairy oral leukoplakia- non-precancerous lesion
-lateral tongue white plaque that can’t be scraped off usually seen in HIV pts
Explain the monospot test
EBV virus activates B cells to secrete heterophile anti-sheep RBC antibodies
So monospot test looks for these antibodies: add to sheeps blood to see if the blood clots (aka if the sheep anti-RBC abs are present)
CMV
(a) Type of virus
(b) Where latent
CMV
(a) Herpes virus family => ds DNA (replicated in nucleus), enveloped, latent phase
(b) Latent in mononuclear cells = macrophages and T/B lymphocytes
Congenital CMV
(a) Appearance
(b) Neuro
(c) Sensory loss
(d) MC outcome
Congenital CMV
(a) Blueberry muffin: thrombocytopenia, jaundice, and HSM
(b) Neuro: periventricular calcifications and ventriculomegaly => seizures and MR
(c) Sensorineural deafness
(d) 80-90% clear infection w/o symptoms, the other 10-20% develop above
MC congenital viral infection
CMV = MC congenital viral infection
MC of the TORCHeS infection
MC cause of sensorineural hearing loss in children
MC cause of sensorineural hearing loss in children = congenital CMV
Increased risk of what infection due to CMV in post-transplant pts?
CMV pneumonia in post-transplant pts
Name the 3 infectious caused by CMV in HIV pts
CMV infection in HIV pts
- CMV esophagitis- see single deep ulceration
- CMV colitis- ulcerated colonic wall
- CMV retinitis (MC***): full thickness retinal necrosis w/ ‘pizza pie’ retinopathy
Tx for CMV infection
CMV tx: Gancyclvori and Foscarnet
Use Foscarnet for viruses w/ UL97 gene causing resistance to gancyclovir
MC CMV infection in non-immunocompromised pt
CMV mononucleosis- same clinical presentation as EBV mono but persistently negative monospot test
Endoscopy findings of CMV vs. HSV esophagitis
CMV esophagitis- single deep linear ulceration
HSV esophagitis- multiple shallow lesions
How to differentiate varicella from small pox rash
Both varicella and small pox have vesicular rash “dew drop on a rose petal”, but small pox are all in the same stage
While varicella rash has vesicles in all dif phases: some just forming, some crusted etc
Varicella vs. Human Zoster
(a) Vaccine
(b) Tx
Varicella (chicken pox) primary infection, then when reactivated called Herpes Zoster (Shingles)
Chicken pox
(a) Live attenuated vaccine
(b) Tx: acyclovir for children over 12, adults, and immunocompromised
Shingles
(a) Live attenuated vaccine for adults over 60
(b) Acyclovir, famciclovir, or valcyclovir
Where does VZV remain latent?
(a) Describe rash
VZV remains latent in dorsal root ganglia
(a) Then travels thru sensory nerves to cause painful vesicular rash in dermatomal distribution
Complication of Varicella Zoster in V1 distribution
VZV in V1 = Zoster opthalmicus
which can cause blindness (unilateral)
So pt w/ vesicular rash in V1 distribution and unilateral blindness = Zoster opthalmicus
Describe the clinical features of congenital varicella syndrome
Congenital varicella: limb hypoplasia, cutaneous dermatomal scarring, blindness
Differentiate clinical presentation or Roseola and measles
Roseola (HHV-6, Sixth disease, ds DNA virus) starts w/ 4 days of high fever (like 104F, so high that associated w/ febrile seizures), then as child defervesces they get diffuse lacy rash that spares the face
While measles (paramyxovirus, negative sense RNA virus) rash starts on face and fever and rash occur simultaneously
Virus that causes Roseola
(a) Type of virus
(b) Infects what cells?
Roseola ‘ros-six-ola’ from HHV-6 (human herpes virus 6)
(a) Herpes family virus, ds DNA virus (replicates in the nucleus), encapsulated
(b) Roseola infects CD4 helper T cells
MC location of lesions 2/2 HHV-8
(a) Pathogenesis of lesions
MC location of Kaposi’s sarcoma = hard palate
Other common places: nose, extremities, mucous membranes (including GI tract)
(a) HHV-8 virus causes aberrant angiogenesis 2/2 dysregulation of VEGF => high vascularity gives the purple color to these lesions
HHV-8 infection increases risk of what malignancy?
HHV-8 virus (cause of Kaposi’s sarcoma) increases risk Primary Effusion Lymphoma = B-cell lymphoma (non-Hodgkins)
How to differentiate HHV-8 from bartonella henselae lesion?
Kaposi’s sarcoma viral => lymphocytic infiltrate on biopsy
Bartonella henselae => neutrophilic infiltrate since bacterial
BK vs. JC virus
Both polyomaviruses naked circular ds DNA
JC: progressive multifocal leukoencephalopathy- non-enhancing lesions in white matter of HIV pts
BK: nephropathy and hemorrhagic cystitis in post-transplant pts
MRI findings of PML vs. toxo
Two intracranial opportunistic infections
PML 2/2 JC virus- non-enhancing multifocal lesions in the white (leuko) matter
vs. ring-enhancing lesions seen in toxo
Are most DNA viruses ds or ss?
Almost all DNA viruses are ds, exception is parvovirus B19 which is ss
-and hepB which is partially ds
Clinical syndrome caused by
(a) HPV strains 1-4
(b) HPV 6 and 11
(c) HPV 16, 18
Clinically
(a) HPV 1-4 cause verruca vulgaris = cutaneous common wart usually on hands and feet
(b) HPV 6 and 11 => Laryngeal papillomatosis- benign papilloma tumors in the airway acquired at birth
(c) HPV 16, 18, 31, 33 increase risk of anogenital squamous cell carcinomas: cervical, penile, anal
Which strains of HPV are covered by Gardasil
(a) Type of vaccine
Gardasil covers 6, 11, 16, and 18
indicated for M and F 9-26
(a) Inactivated subunit vaccine
Mechanism by which HPV increases risk of cancer
HPV creates E6 and E7
E6 causes proteolysis of p53 (cell cycle checkpoint at G1S) and E7 causes proteolysis of Rb (retinoblastoma tsg) => uninhibited cell growth
Exact place where pap smear takes cells from
Pap smear samples cells from transformation zone of squamous cells of exocervix to columnar epithelium of endocervix
DNA virus
(a) Smallest
(b) Largest
DNA virus
(a) Smallest = parvovirus B19
(b) Poxvirus = largest
5th disease- what virus?
(a) Clinical feature
5th disease “5 finger slap” = Slapped cheek fever = Parvovirus B19
(a) Rash that starts on cheeks and moves downwards
Differentiate rash caused by parvovirus B19 and Roseola
Parvovirus B19 (naked ss DNA virus) = Erythema Infectiosum- rash starts on face (‘slapped cheek’) and is simultaneous w/ fever
Roseola (HHV-6 ds DNA enveloped) = Exanthum Subitum- starts w/ super high fever associated w/ febrile seizure, then as child deferveses rash starts- lacy reticular rash that SPARES the face
In addition to slapped cheek fever in children, parvovirus B19 clinical features
(a) Adults
(b) SCD
(c) Neonates
Parvovirus B19- ss DNA naked virus
(a) Joint pain, arthritis, and edema in adults
(b) Transient aplastic anemia in SCD
(c) Neonates- hydrops fetalis
MC cause of tonsilitis
(a) Type of virus
(b) Transmission
Tonsilitis MC 2/2 adenovirus
(a) Naked DNA virus
(b) Transmission of adenovirus via respiratory droplets and fecal-oral
Adenovirus- 3 clinical features
Adenovirus
- # 1 cause of infection in adenoids and tonsils (tonsillitis)
- Hemorrhagic cystitis
- Viral conjunctivitis (pink eye)
Unique features of Poxvirus
(a) Envelope
(b) Location of replication
Poxvirus = largest DNA virus
-pox virus brings everything they need with it!!!
(a) Makes its own envelope (doesn’t take it from membrane or golgi of host)
(b) Replicates fully in the cytoplasm
-only DNA virus that replicates fully in the cytoplasm
=> brings its own DNA-dependent RNA polymerase (allows it to fully replicate outside the nucleus)
Diagnostic histologic feature of smallpox
Smallpox/cow pox = poxvirus- Guarnieri bodies = intracytoplasmic inclusions that are sites of viral replication in the cytoplasm
Take skin biopsy of small pox skin lesions (now eradicated in US) and see intracytoplasmic inclusions
-reminder that they replicate fully in the cytoplasm
Molluscum contangiosum
(a) Type of virus
(b) Appearance
Molluscum contagiosum
(a) Poxvirus, enveloped DNA virus
(b) Appearance- flesh colored, dome-shaped umbilicated skin lesion MC on trunk/axilla
Type of viruses
(a) Hep A
(b) Hep B
(c) Hep C
(d) Hep D
(a) Hep A- Picornavirus- positive sense naked RNA virus
(b) Hep B- enveloped DNA virus, circular and partially ds DNA, replicates both in and out of the nucleus
(c) Hep C- Flavivirus positive sense enveloped RNA virus
(d) Hep D is an enveloped negative sense RNA virus w/ circular genome
Hepatitis B
(a) Type of virus
(b) Location of replication
Hep B
(a) DNA virus w/ circular partially ds DNA
(b) Replicates both in and out of the nucleus
Difference btwn Hep B and retroviruses
Hep B is a circular partially ds DNA that replicates in and out of the nucleus- does make intermediate ssRNA w/ reverse transcriptase
-so carries reverse transcriptase but doesn’t integrate into host genome
HIV- carries reverse transcriptase to make cDNA to integrate into host genome
Hep B
(a) First antigen on the scene
(b) Antigen that indicates infectivity
(c) First antibody on the scene
(d) Indicative of recovery
Hep B
(a) HBsAg = surface antigen
(b) HBeAg indicates infectivity
(c) anti-HBc Ab = Hep B core antibody is first on the scene
(d) anti-HBs Ab = Hep B surface antibody that indicates recovery (no longer has acute or chronic infection)
Explain the window period seen in Hep B
(a) Serum marker
Hepatitis B- starts w/ HBsAg then anti-HBs Ab develops, but short bit of time where Ab production is revving up and binding antigen to which neither are detectable in blood
(a) In this window period the anti-HBc Ab (Hep B core antibody) is present
Hep B- serum titers to differentiate vaccinated vs. infected and recovered
Vaccinated: anti-HBs w/o anti-HBc or anti-HBe (so recovered w/o ever being infected)
Recovered = anti-HBs w/ either positive anti-HBc or positive anti-HBe
Why does Hep D required Hep B infection?
(a) Better prognosis- coinfection or superinfection?
B/c Hep D requires HBsAg (Hep B surface antigen) to infect host cells
(a) Coinfection (get both Hep B and D at the same time) is less dangerous, worse prognosis when get Hep D infxn on top of pre-existing Hep B
Tx for neonates w/ vertical transmission of HepB
Neonates w/ Hep B vertical transmission: give HBig (Hep B Ig passive immunity) and vaccination
So give both active and passive immunity
