common viral pathogens Flashcards
What is a major characteristic of the Herpes
following primary infection, the vrius establishes a latent infection in the host and may reactivate at a later time
T or F: Reactivation is not always associated with disease
TRUE
What is the antiviral given for herpes and how does it work?
Acyclovir, inhibitor of viral DNA pol
How many Human herpes viruses (HHV) are there?
8
What are the HHV-1 and HHV-2?
Herpes simplex virus-1 (HSV1) and HSV2
HSV-1 and HSV-2 both cause what?
painful, clear fluid filled vesicles often with a red base on the skin at site of inoculation
What does HSV1 most commonly present as?
orofacial lesions
What does HSV2 most commonly present as?
genital lesions
T or F: HSV1 does not cause genital lesions
FALSE, it causes up to 40% of new genital infections
What is the incubation period of HSV1 and HSV2?
2-12 days (average of 4)
How are HSV1 and HSV2 trasmitted?
close contact with a person shedding virus at a mucosal surface. HSV penetrates susceptible mucosal surfaces or cracks in skin
T or F: primary infection of HSV can be symtomatic or asymptomatic
TRUE
T or F: primary infection of HSV is usually less severe that reactivation
FALSE
T or F: in immune competent hosts, HSV infection remains confined to site of contact, but immunocompromised hosts may spread to new areas
TRUE
When does Prmary HSV-1 infection usually occur?
childhood
Most common symptomatic sign of infection?
Gingivostomatitis (mouth ulcers), commonly associaed with fever and enlarged cervical nodes
What is Herpetic whitlow?
inoculation of HSV from oral secretions to fingers, often transmitted by mother’s kiss to injured finger of child.
What is herpes gladiotorum?
herpes from sports contact
What is genital herpes
sexually-trasmitted, with primary infection making vesicle/ulcers in genital area
How long do genital herpes lesions last?
10-14 days, usulaly very painful
How are genital herpes warts different from syphilis and chancroid?
syphilis are hard and painless ulcers, chancroid are soft painful ulcers associated with swollen inguinal lymph nodes
What is herpes keratitis?
HSV infection/inflammation of the cornea, distictive dendriric pattern, can be primary or reactivation
how does HSV get to cornea during reactivation
opthalmic branch of the trigeminal nerve
What is the most common cause of encephalitis in US?
HSV, and it can be primary or reactivation
Where is encephalitis by HSV usually located and what does it present with?
predilection for temporal lobes, often presents as psychiatric illnes
What is Neonatal HSV?
it is a serious disease transmitted to an infant perinatally, usually from exposure to maternal HSV1 or 2
What 3 different ways can Neonatal HSV present?
1) Skin, eye and mucous membrane disease 2) CNS disease 3) Disseminated
How does neonatal HSV skin, eye and muscous membrane disease present ?
leasons on skin, commonly at sites of trama (scalp, electrode site, wristband site, forceps site), eye lesions can lead to corneal ulcers and blindness
How does CNS neonatal HSV?
severe encephalitis, mortality with treatment about 30%, 75% of survivors with retardation, motor impairment, and/or learning disabilities
How does Disseminated neonatal HSV?
Widespread disease, including pneumonitis, hepatitis, DIC, with or without encephalitis, skin rash, or eye involvement. Most lethal, mortality with treatment 50%
What can you do for pregnant woman with HSV?
give acyclovir or valacyclovir to treat lesions, If leasions at time of delivery, C-section is recommended
T or F: skin vesicle on a neonate less than 1 month of age is a medical emergency
TRUE, assume HSV, treat fast with acyclovir
What does HSV do after primary infection and how does it do it?
establishes latent infection by traveling up sensory nerve ending and axon to sensory ganglia
Where does orofacial latent HSV establish?
trigeminal ganglia
Where does genital latent HSV establish?
sacral ganglia
how long does a latent infection last?
That shit’s for life
how does reactivation of HSV happen?
get stimuli (stress, sunlight, illness, menstration, immunosuppression), goes back down axon, makes lesion (more localized and heal faster)
T or F: reactivated lesions are not infectious
FALSE, people even shed for a period after it heals
T or F: reactivation may produce no lesion
TRUE, virus still sheds and this is how 70% of transmissions occur
how can you confirm HSV lesion?
Tzanck smear, viral culture, direct IFA, PCR
What is HHV-3?
Varicella Zoster Virus (VZV)
Varicella Zoster Virus (VZV) causes what 2 clinical syndromes?
chicken pox (varicella), and Shingles (herpes zoster or zoster)
T or F: varicella is a clinical manifestation of primary infection with VZV
TRUE, common childhood disease
How is VZV transmitted?
primarily respiratory via droplet or aerosolized secretions, or contact with lesions
What is the incubation period of VZV
10-21 days
How does Varicella present?
starts w/ fever, malaise, headache, +/- cough. Then generalized itchy vesicular rash, first on trunk, spread to face and limbs, appear in waves of lesions, illness lasts 7 days.
What are the stages of the classic rash of chicken pox?
appears in crops or waves, first blister or vesicle, then pustule, then scab.
Give a general pathogenesis of Primary VZV infection
entry via respiratory tract, goes to lymphoid system, replicated for 2-4 days, then primary viremia, 4-6day initial inoculation, replicates in liver and spleen and other, secondary viremia spread to skin causing rash
What complications arise with primary VZV?
secondary infections ( group A strep +/- necrotizing fasciitis), pneumonia, encephalitis or encephalomyelitis, hepatits, congenital varicella, adolescents and adults more severe, pregnant woman and immunocompromised patients have higher morbidity and mortality
Varicella treatment
Uncomplicated varicella is self-limited disease, no specific treatment. Acyclovir can resolve chicken pox faster if presents early, immunocompromised always receive treatment
How can prevent we prevent VZV?
Live attenuated varicella vaccine (VAR) given in 2 doses (once at 12-15 months, booster at 4-6 years), but can causes disease in pregnant and immunocompromised. Can be used post-exposure in certain unimmunized kids
Where does VZV remain latent
cranial, dorsal root and/or trigeminal ganglia
T or F: VZV is the ONLY herpesvirus that does NOT have asymptomatic viral shedding
TRUE
T or F: VZV reactivation forms a dermatomal rash
TRUE
T or F: Herpes Zoster or shingle occurs in 90% of people
FALSE, 30%
T or F: shingles is a primary infection of VZV
FALSE, reactivation
symptoms of shingles
radicular pain from site where shingles will erupt in a few days, leasions in a single dermatome that do not cross midline, may itch but are very painful, 2 weeks to heal
What is post-herpetic neuralgia (PHN)?
debilitating neuropathic pain that can last weeks to months after reactivation of VZV
how do you diagnose VZV?
clinically, if unclear do direct IFA, PCR, viral culture
How do we tream shingles?
acyclovir within 48-72 hrs or PPX with recurrent shingles. For PHN give NSAIDs, opiates, and occasionally corticosteroids
T or F: Cell mediated immunity (CMI) to VZV is an important determinant in who is at risk for shingles
TRUE, low CMI =higher risk
HHV-4 is what?
Epstein Barr Vrisu (EBV)
how common is EBV?
95% have it by 40 years of age
T or F: Primary infection with EBV is often symtomatic
FALSE
how is EBV transmitted?
contact with saliva
infectious mononucleosis is caused by what?
EBV
symptoms of Infectious mono
Fever, sore throat, swollen lymph nodes, fatigue
signs of Infectious mononucleosis
Exudative tonsillitis, enlarged cervical nodes (often posterior cervical), splenomegaly and/or mild hepatomegaly
how long til infectious mononucleosis resolves?
4-8 weeks
Where does EBV infect and spread to?
infects nasopharyngeal epithelium, cell lysis causes spread to lymphoid tissue and salivary glads
Where does EBV go dormant/latent?
nasopharyngeal epithelium and B cells
T or F: reactivation is commonly found intermittently in saliva and occurs without symptoms
TRUE
how is diagnosis of infectious mononucleosis done?
typically clinical, but can see atypical lymphocytes in peripheral blood smear, serology tests: IgM to viral capsid antigen (VCA), IgG to VCA is prior infection
monospot/heterophile tests
after acute infection of EBV, 75%-90% of patients develop antibodies that cross-react and agglutinate RBCs. This detects antibodies that bind RBC
What cancers in EBV associated with?
Burkitt’s lynphoma, Hodgkin’s lynphoma, Nasopharyngeal carcinoma, lymphoproliferative disease
How do you treat EBV?
fluids, antipyretics, steroids (lymphode swelling threatens bloodflow. Reduce immunosuppression in the immunocompromised
What is HHV-5?
cytomegalovirus (CMV)
how is CMV spread?
infected body fluids contact (blood, organ, secretions, urine, tears, perinatally, inutero)
what is the prevalence of CMV?
90% in developing countries, 50-80% in developed countries
Where does CMV infect?
spithelial cells of salivary glands or genital tract. Likely viremia shortly after. Intermittent viral shedding also seen
T or F: almost all CMV primary infections come in a mononucleosis-like syndrome
FALSE, this does happen but more often is asymptomatic
T or F: primary infection of CMV in immunocompromised persons is serious and can infect most organs
TRUE, can cause retinitis and colitis
Where is CMV latent?
monocytes and lymphocytes
T or F: Reactivation in persons with normal immune systems is asymptomatic
TRUE, but virus is still being shed in fluids
What is congenital CMV syndrome?
mom gives CMV to baby in utero. Leads to low birthweight, microcephaly, hearing loss, mental impairment, hepatosplenomegaly, skin rash (blueberry muffin spots), jaundice, chorioretinitis. Most often asymptomatic
What affects the severity of CMV disease and where does it hit?
severity parallels the degree of impairment of cell-mediated immunity. Can be general febrile syndrome or organ-specific
Serology with pos IgM and IgG for CMV means what?
recent reactivation
Tissue histology of CMV infection
Infected cells have “owl’s eye” (intranuclear inclusion bodies) and Intracytoplasmic inclusions
Treatment of CMV
In immunocompromised treat with gancyclovir, Ig in pregers, gancyclovir in infants maybe
What is RSV?
Respiratory Syncytial Virus
T or F: RSV is in the paramyxoviridae family
TRUE
What is the structure, genome, and important proteins of RSV?
Enveloped virus with ssRNA genome, 2 important proteins: G-protein for viral attachemtn to host and F-protein allows fusion of infected cells to neighboring cells to form syncytia
What kind of infections does RSV cause?
acute respiratory disease. Bronchiolitis (children <1 yr of age), Viral pneumonia (young children and elderly, Upper respiratory tract infection (children and adults)
T or F: Primary infection is usually symptomatic
TRUE, lasts 7-21 days
How is RSV trasmitted?
contact with droplets on environmental surfaces or objects
T or F: RSV is the most frequent cause of bronchiolitis and viral pneumonia in young children and infants
TRUE
T or F: reinfection with RSV is normally asymptomatic
FALSE, can be but usually looks like a cold
how does RSV Bronchiolitis present?
URI with congestion, sore throat, fever. Cough deepens and becomes more prominent. Lower resp. tract develops with increase RR, retraction, and wheezing. Mucus and inflammation can block airways
T or F: Wheezing in child <2 yrs is most likely bronchiolitis
TRUE
Give pathogenesis of RSV
enters through mucosa of eye and nose, cell-cell transer leading to lower respiratory infection, syncytia, Bronchiolitis
Which infants are at high risk for severe RSV bronchiolitis?
Premature infants (<32 weeks gestation), chronic lung disease, congenital heart disease
how is RSV diagnosed?
usually clinical, rapid test (not very sensitive), Viral culture, Serlogy, Direct fluorescent antibody
What is treatment for RSV?
primarily supportive, Ribavirin is the only antiviral that works (use is controversial
T or F: RSV has no licensed vaccine
TRUE, but there is a monoclonal RSV F-protein antibody
What family is Rotavirus a part of?
Reoviridae
What is the structure, genome, and important proteins of rotavirus?
dsRNA virus with segmented genome (reassortment), several serotypes, 5 strains are responsible for more than 90% of rotavirus disease
What does rotavirus cause?
leading single cause of severe diarrhea and/or gastroenteritis in infants and young children worldwide
Is there a vaccine for Rotavirus?
yup, since 2006. before is was very common
How is Rotavirus transmitted?
Fecal oral is the most common
Why is Rotavirus so infectious?
kids excrete 100 billion rotavirus particles per mL of feces (infectious at just 10-100 particles) it survives on fingers for 60 min
Clinical characteristics of rotavirus
incubation of 2 days, then vomiting, watery diarrhea, freq also fever, addominal pain, lasts 3-8 days
pathogenesis of rotavirus
infects mature absorptive epithelial cells or enterocytes in proximal 2/3 of illem. Cell death. Regen of villi takes 7-10 days
describe immunity in Rotavirus infection
1st infection => severe gastroenteritis. Subsequent infection milder or asymptomatic (incomplere immunity develops after infection, protects against symptoms but not disease.
diagnosis of rotavirus
ELISA on stool sample, or the rest of the typical diagnostics
how is Rotavirus treated?
no antivirals, supportive care given.
how many vaccines are available for rotavirus?
2 oral, live-attenuated.
T or F: Herpetic whitlow is an occupational hazard for doctors, dentist, and nurses
TRUE
