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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

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1
Q

What viruses are associated with mono?

A 
EBV = HHV5
CMV = HHV4
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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

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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

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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

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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)

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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

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7
Q

What are the demographics and epidemiology of EBV?

A

Most before age 5

Second peak in late teens and early twenties

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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

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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

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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

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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

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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

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13
Q

How is CMV acquired?

A

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

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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

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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

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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)

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17
Q

What syndromes are associated with reactivation CMV?

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

What is the diagnosis of mumps?

A

Clinical diagnosis
Isolation of mumps in culture
PCR detection of virus
Serology - IgM in acute illness, 4 fold rise in IgG

25
Q

What is the treatment and prevention of mumps?

A

No treatment but vaccine of 2 doses

Live virus vaccine - don’t give to immunocompromised

26
Q

What are the basics of the influenza virus?

A

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
Q

What are the basics of type a, b, and c influenza?

A

Type a - animals and humans, annual epidemics and pandemics
Type b - humans only, outbreaks every 2-4 years
Type c - humans only

28
Q

How is influenza transmitted?

A

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
Q

Where does replication of influenza happen?

A

Cytoplasm

30
Q

How is influenza diagnosed?

A 
Epidemiology
Clinical presentation
Viral culture
LCD 
Acute and convalescent serologies
Rapid detection on sputum or nasal cells - fluorescence, ELISA
31
Q

How does genetic variability among influenza strains work?

A

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
Q

What are the M2 inhibitors?

A

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
Q

What are the neuraminidase inhibitors?

A

Oseltamivir (oral) and zanamivir (inhaled)
Effective against types a and b
Prophylaxis and treatment if within 24-48 hrs of symptoms

34
Q

What are complications of influenza virus?

A

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
Q

What are the basics of the flu vaccine?

A 
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
Q

What is the swine flu?

A

Quadruple reassortment virus

2 genes from flu viruses normally in pigs, genes from avian flu and genes from human flu

37
Q

How is RSV spread?

A

Contact - portals of entry are eye, nose, mouth
Secretions and airborne droplets
Hygiene can control a lot of spread - wash hands!
Nosocomial transmission

38
Q

What is the pathology of RSV?

A

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
Q

He is RSV diagnosed?

A

Rapid tests
Culture
Serology
PCR

40
Q

What is the treatment for RSV?

A 
Mainly supportive - oxygens, fluid, suctioning 
Bronchodilators
Ribavirin 
Corticosteroids 
No vaccine
41
Q

What is palivizumab?

A

Antibody used in infants at high risk for RSV

Combo of mouse specific RSV and human non RSV specific

42
Q

What is adenovirus?

A

Double stranded naked DNA virus
Resistant to drying, detergents, GI secretions, chlorine
No treatment or vaccines for civilians

43
Q

How is adenovirus transmitted?

A 
Respiratory
Fecal oral
Fingers
Fomites
Swimming pools
Epidemics in closed environments
44
Q

What kinds of clinical syndromes does adenovirus cause?

A

Pharyngitis
Pharyngoconjunctival fever
Epidemic conjunctivitis
Pneumonia and ARDS, tracheitis, bronchitis
Disease in immunosuppressed
Diarrhea in infants and toddlers (type 40 and 42)

45
Q

How are parainfluenza viruses transmitted?

A

Large respiratory droplets
Only over a couple of feet - require close contact
Viral replication limited to respiratory epithelium - no viremia unless immunocompromised

46
Q

What are the manifestations of parainfluenza?

A 
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)

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