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Block 5 - Pulm and Skeletal > Gill Micro > Flashcards

Flashcards in Gill Micro Deck (47):
0

What viruses are associated with mono?

EBV = HHV5
CMV = HHV4

1

What are the basics of herpes viruses?

dsDNA, envelope
3 sets of genes - immediate early, early, late

2

What are the 3 subfamilies of herpes viruses?

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

3

How is EBV transmitted?

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

4

What is the pathogenesis of EBV?

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

5

What are the EBV antigens?

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)

6

What are the clinical manifestations of EBV?

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

7

What are the demographics and epidemiology of EBV?

Most before age 5
Second peak in late teens and early twenties

8

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

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

9

What are complications of EBV?

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

10

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

None before
First three acute
Last three convalescent

11

What are other EBV associated illnesses besides mono?

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

12

What is the prevention and treatment of EBV?

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

13

How is CMV acquired?

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

14

How is CMV similar to and different than EBV?

Does not immortalized unlike EBV
Does require cell mediated immunity to control infection

15

What are the clinical manifestations of CMV?

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

16

What are complications of CMV?

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

17

What syndromes are associated with reactivation CMV?

GI - ulcers and esophagitis
Eye - chorioretinitis
Lungs - pneumonitis
Nervous system
Graft failure

18

How is CMV diagnosed?

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

What is the prevention and therapy for CMV?

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

20

What are the basics of paramyxoviruses?

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

What is the pathogenesis of mumps?

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

What are the clinical features of mumps?

Incubation 14-18 days
Sudden fever, parotid gland swelling with pain

23

What are the complications of mumps?

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