Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Block 5 - Pulm and Skeletal > Gill Micro > Flashcards

Gill Micro Flashcards

0
Q

What are the basics of herpes viruses?

A

dsDNA, envelope

3 sets of genes - immediate early, early, late

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What viruses are associated with mono?

A 
EBV = HHV5
CMV = HHV4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 subfamilies of herpes viruses?

A

Alpha - latency in neurons, hhv1, 2, and 3 (vzv), type b
Beta - latency in multiple cells usually lymphoid, CMV, HHV 6,7
Gamma - latency in B cells, EBV, HHV8
All establish lifelong latent infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is EBV transmitted?

A

Through saliva
Receptor is CD21 or CR2 - C3d complement receptor on *B cells and mouth epithelial cells
Co receptor is MHC class II on B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the pathogenesis of EBV?

A

Latency - no viral particles, replicates as episome
Polyclonal B cell activation - secrete lots of non EBV related antibodies
B cells incite cytotoxic T cell response and NK response - clear infection and responsible for symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the EBV antigens?

A

Early - polymerase and thymidine kinase, site of antiviral drugs, in lytic inf
Viral capsid - late structural, in lytic inf
Epstein Barr nuclear - maintenance of latent inf, + for life, only after acute phase
Late membrane proteins - LMP1 major oncogene (activate B cells through cd4 receptor), LMP2 (bridge B cell and Ig)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the clinical manifestations of EBV?

A

15-45 day incubation
Sore throat and exudative tonsillitis, fever
Hepatosplenomegaly - watch the spleen!
Shedding of virus can last more than a month - can also be asymptomatic - may not have known sick contact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the demographics and epidemiology of EBV?

A

Most before age 5

Second peak in late teens and early twenties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the relevant labs in EBV that are useful to diagnose it?

A

Heterophile antibodies - igM antibodies that recognize Paul Bunnell antigen on animal RBCs
Mono spot uses equine RBCs - positive by one week and a few months after
Elevated WBC with atypical lymphocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are complications of EBV?

A

Upper airway obstruction from enlarged tonsils
Splenic rupture
CNS involvement
EKG abnormalities and myocarditis
Hemolytic anemia
Granulocytopenia
X linked lymphoproliferative syndrome - defect in SLAM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Of VCA IgM, IgG, anti EA, and anti EBNA which are present before, during the acute phase and during the convalescent phase of EBV?

A

None before
First three acute
Last three convalescent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are other EBV associated illnesses besides mono?

A

Burkitts - endemic in Africa, non endemic less association
Nasopharyngeal carcinoma
Hodgkin’s, non Hodgkin’s in HIV and CNS lymphoma in AIDS
Post transplant lymphoproliferative disorder
oral hairy leukoplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the prevention and treatment of EBV?

A

Mono - antiviral s only work in lytic phase but most cells are latent - ineffective, symptomatic relief
Lymphoproliferative - reduce immune suppression
Leukoplakia - antivirals, treat underlying HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is CMV acquired?

A

Contact with infected body secretions
Across placenta
From a transplant
Most adults in the US are infected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is CMV similar to and different than EBV?

A

Does not immortalized unlike EBV

Does require cell mediated immunity to control infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the clinical manifestations of CMV?

A

Most asymptomatic
Clinically similar to EBV mono but milder
Mono with negative mono spot –> CMV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are complications of CMV?

A

*most common congenital infection - worse if mom gets primary DURING pregnancy
Re activation disease - in immunosuppressed (malignancies, corticosteroids, transplant, HIV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What syndromes are associated with reactivation CMV?

A 
GI - ulcers and esophagitis
Eye - chorioretinitis
Lungs - pneumonitis 
Nervous system
Graft failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is CMV diagnosed?

A

Owls eye inclusions
IgM to CMV positive, IgG only indicates late or past infection
Pp65 can detect virus in blood, PCR is replacing this

19
Q

What is the prevention and therapy for CMV?

A

Ganciclovir - IV, inhibits viral DNA synthesis
Valganciclovir - better bioavailability than ganciclovir
Foscarnet - pyro phosphate analog
Cidofovir - chain terminator

20
Q

What are the basics of paramyxoviruses?

A

Enveloped, negative strand RNA - no latent infection
No genetic reassortment - very little variability
First group - morbillivirus - measles - only hemagglutinin
Second - parainfluenza - mumps and parainfluenza - H and N
Third - pneumovirus - RSV and metapneumovirus - no H or N

21
Q

What is the pathogenesis of mumps?

A

World wide - winter/spring peak
Respiratory transmission in saliva or respiratory droplets
6 days before dev of clinical illness and for several days after dev of parotitis - can transmit when clinically well
Replication in epithelial cells of nasopharynx and regional lymph nodes
Can spread to Stensens duct and parotid
Viremia 12-25 days after exposure

22
Q

What are the clinical features of mumps?

A

Incubation 14-18 days

Sudden fever, parotid gland swelling with pain

23
Q

What are the complications of mumps?

A 
Meningitis
Encephalitis
Orchitis - infertility
Oophoritis - but no infertility
Pancreatitis
24
What is the diagnosis of mumps?
Clinical diagnosis Isolation of mumps in culture PCR detection of virus Serology - IgM in acute illness, 4 fold rise in IgG
25
What is the treatment and prevention of mumps?
No treatment but vaccine of 2 doses | Live virus vaccine - don't give to immunocompromised
26
What are the basics of the influenza virus?
Enveloped, negative RNA Segmented - can reassort N allows maturing virus to bud, H acts as attachment, M helps remove envelope for replication Types a, b and c - only a and b cause disease
27
What are the basics of type a, b, and c influenza?
Type a - animals and humans, annual epidemics and pandemics Type b - humans only, outbreaks every 2-4 years Type c - humans only
28
How is influenza transmitted?
Aerosols - distances of meters, short incubation 1-4 days Infectious from 1 day before to 7 days after symptoms appear Multiple in URT and and bud from apical side of epithelial cells - desquamation of epithelial cells can lead to superinfection Spread to LRT to cause pneumonia T cell response correlates to onset of symptoms, antibodies near end of resolution (protect against re infection rather than resolve)
29
Where does replication of influenza happen?
Cytoplasm
30
How is influenza diagnosed?
``` Epidemiology Clinical presentation Viral culture LCD Acute and convalescent serologies Rapid detection on sputum or nasal cells - fluorescence, ELISA ```
31
How does genetic variability among influenza strains work?
Antigenic drift - small ongoing point mutations and lack of proofreading by viral RNA polymerase, year to year new strains Antigenic shift - effect of reassortment, novel strains of type a can cause pandemics
32
What are the M2 inhibitors?
Amantidine and rimantadine Inhibits acidification and prevents dissociation of genome from matrix, no uncoating Only act on type a in vivo - work for prophylaxis and treatment Must be taken during incubation or first 48 hrs for treatment Rimantadine has less CNS side effects
33
What are the neuraminidase inhibitors?
Oseltamivir (oral) and zanamivir (inhaled) Effective against types a and b Prophylaxis and treatment if within 24-48 hrs of symptoms
34
What are complications of influenza virus?
Bacterial pneumonia superinfection - s. pneumonia, s aureus, h flu Can exacerbate underlying lung disease Reye's syndrome - acute encephalopathy and fatty infiltration of liver - after kids take lots of aspirin
35
What are the basics of the flu vaccine?
``` Killed vaccine (IM) - children over 6 mos, healthcare workers, pregnant, people with lung or heart conditions Live virus (nasal) - between 2-49, healthy and nonpregnant, no contact with immunocompromised, cold adapted ```
36
What is the swine flu?
Quadruple reassortment virus | 2 genes from flu viruses normally in pigs, genes from avian flu and genes from human flu
37
How is RSV spread?
Contact - portals of entry are eye, nose, mouth Secretions and airborne droplets Hygiene can control a lot of spread - wash hands! Nosocomial transmission
38
What is the pathology of RSV?
Fusion protein allows for syncytia formation and formation of giant cells Most children recover in 8-15 days but reinfection common - severe lower respiratory tract disease may occur in certain individuals
39
He is RSV diagnosed?
Rapid tests Culture Serology PCR
40
What is the treatment for RSV?
``` Mainly supportive - oxygens, fluid, suctioning Bronchodilators Ribavirin Corticosteroids No vaccine ```
41
What is palivizumab?
Antibody used in infants at high risk for RSV | Combo of mouse specific RSV and human non RSV specific
42
What is adenovirus?
Double stranded naked DNA virus Resistant to drying, detergents, GI secretions, chlorine No treatment or vaccines for civilians
43
How is adenovirus transmitted?
``` Respiratory Fecal oral Fingers Fomites Swimming pools Epidemics in closed environments ```
44
What kinds of clinical syndromes does adenovirus cause?
Pharyngitis Pharyngoconjunctival fever Epidemic conjunctivitis Pneumonia and ARDS, tracheitis, bronchitis Disease in immunosuppressed Diarrhea in infants and toddlers (type 40 and 42)
45
How are parainfluenza viruses transmitted?
Large respiratory droplets Only over a couple of feet - require close contact Viral replication limited to respiratory epithelium - no viremia unless immunocompromised
46
What are the manifestations of parainfluenza?
``` Autumn peak Similar to influenza, not as sick Common in infants - croup Incubation 2-6 days, resolves in 2-3 No vaccine or treatment - transient IgA but reinfection common ```

Block 5 - Pulm and Skeletal (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions