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Block 5 - Pulm and Skeletal > Gill Micro > Flashcards

Flashcards in Gill Micro Deck (47)
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What viruses are associated with mono?



What are the basics of herpes viruses?

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


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


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


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


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)


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


What are the demographics and epidemiology of EBV?

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


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


What are complications of EBV?

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


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


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


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


How is CMV acquired?

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


How is CMV similar to and different than EBV?

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


What are the clinical manifestations of CMV?

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


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)


What syndromes are associated with reactivation CMV?

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


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


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


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


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


What are the clinical features of mumps?

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


What are the complications of mumps?

Orchitis - infertility
Oophoritis - but no infertility


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


What is the treatment and prevention of mumps?

No treatment but vaccine of 2 doses
Live virus vaccine - don't give to immunocompromised


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


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


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)


Where does replication of influenza happen?