Viral Exanthems (red Rashes) Of Childhood Flashcards
Difference between macules and papules, vesicular, petechiae, purpura
Macules = flat, altered texture with < 5mm
Papules = elevated, solid lesions < 1mm
Petechiae = pinsized purple/red lesions
Purpurae = purple, palpable papules < 2 mm
Vesicular = clear fluid-filled blisters < 5mm
Parvo B19 effects on blood system
As viremia increases, platelets and reticulocytes decrease as well as hemoglobin and hematocrit
- IgG and IgM are produced within 10-14 days at which point the patient is not infectious any more
While viremia is present and infectious
- flu like prodromal
While immune response is active and NOT infectious
- slapped cheek rash in children
- joint pain in adults and children
- lace-like rash on adults and children
What is common with parvovirus in adult women?
Acute arthritis and arthralgia
Transient aplastic crisis
Suspension of erythropoiesis leads to severe anemia and related complications
- really only seen in parvovirus with patients who currently have sickle cell/hereditary spherocytosis or moderate unspecific anemia
Developed severe anemia can rarely be fatal due to CHF, CVAs or acute splenic sequesteration
Is self-limiting (1-2 weeks)
Fetal infection of parvoB19
Exceptionally susceptible and can lead to miscarriage
- caused due to transient pleural/pericardial effusions
- OR hydrops fetalis (accumulation of fluid in the soft tissues and serous cavities)
Highest risk is during 1st half of pregnancy and requires intrauterine blood transfusions
Parvovirus in immunocompromised hosts
Leads to chronic infection with severe chronic anemia. Also pure red cell aplasia will develop.
- NO RASH OR ARTHRALGIA (since they can’t amount an immune response)
Human herpes virus
All are ubiquitous except HHV-8 (kaposi syndrome)
Are large enveloped icosahedral capsids
DsDNA genomes
- replication occurs in the nucleus
- requires viral DNA poly but cellular RNA poly
Viral release = exocytosis and cell lysis
All are latent infections as well and require cell mediated immunity to control
- can replicate in non-growing cells (especially neurons) makes viral scavenging enzymes
Types of proteins transcribed in herpesvirus infections
Immediate early proteins (alpha)
- Latency-associated transcripts (LATs)
- proteins for cell takeover an transcription regulation
Early proteins (beta)
- transcription factors and DNA polymerase
- viral growth
Late protiens (gamma
- structural proteins and glycoprotein
- cell death
What points of a host cell does the herpes virus visit to make new particles?
Nucleus = procapsid
Endoplasmic reticulum = tegument proteins
Golgi membrane = viral envelope
HHV6 details
DsDNA
- herpesviridae family
- had icosahedral capsid and tegument layers
Two sub variants
- HHV-6A = targets CD46 receptor
- HHV-6B = targets CD134 receptor
- both receptors are found on CD4 T cells*
80% of all people are infected with it by 2 yrs old
Transmitted by saliva, respiratory droplets and close contact (horizontal infection)
- when it enters the body it binds to APC cells and causes them to migrate to lymph nodes where the virus then latches onto CD4 T cells where it invades CD4 and replicates
Produces viral proteins and induces the lytic cycle which then infects numerous other immune cells continuously
- can go into latent phase however especially when patients become immunocompromised
incubated period = 1-2 weeks
- casues Roseola infantum/sixth disease (biphasic 3-5 day high fever with maculopapular rash which starts centrally and moves out)
- (this occurs before rash usually) also shows periorbital edema, lymphadenopathy cervical, diarrhea, vomiting
HHV-6 in immunocompromised hosts
Kills hemoglobin and WBCs easier
- can present with febrile neutropenia (<800 neutrophil)/ (<500 lymphocytes)/ (<9.1 hemoglobin)
In transplant patients = reactivates latent HHV6 - unexplained fever, viremia, rash, hepatitis, penumonitis and graft rejection if not caught
Diagnosis of HHV6
Based on clincial presentation usually
Labs confirm
- qPCR and serology (IgG increases in two separate titers)
Treatment: usually benign and just goes away
- IV ganciclovir/Foscarnet if needed (immunocompromised usually)
HHV-7
Attacks CD4-T cells again (lymphotropic)
95% found in most patients once they are 18
Generally asymptomatic unless immunocompromised
Found in saliva and breast milk
Symptoms (if present)
- febrile seizures and nonspecific fever
- URIs
- N/V
- diarrhea
- Roseola infantum
Diagnosis = ELISA and indirect IgM/PCR
Enteroviruses
Icosahedral, naked (+)ssRNA virus
Attaches to cells of the intestinal tract and is cytolytic
Infections more common in children
Commonly asymptomatic and is an immunizing infection (dont get it again once you have had it)
Includes
- polio
- coxsackieviruses A and B
- echoviruses
Coxsackievirus A
Hand/foot/mouth patients
90% primary infections are asymptomatic or is a generalized febrile illness
Mostly causes hand/foot/mouth disease
- fever and oral vesicles
- peripherally distributed small/tender cutaneous lesions on hands/feet/buttocks
- can cause serious complications (encephalitis, pulmonary edema and hemorrhage and HF)
Normal Incubation = 3-5 days - fever <38C - mouth/throat pain - oral enanthem and exanthem vesicular rash that is often on pruritic and non painful and resolves within 3-4 days
coxsackie A6 specific
- more serious and wider distribution
- also runs the risk of palmar and plantar desquamation as well as nail dystrophy
