Mononucleosis syndromes Flashcards
immunocompromised pt with CMV: Latently infected 1) contact activated T cells and differentiate into macrophages that produce infectious virus
1) monocytes
microcephaly, chorioretinitis
CMV manifestations in infants:
EBV pathogenesis–>Once B-cells are infected, three things can happen: 1) where the virus replicates in B-cells; ends up in the 2);
1) Lytic infection 2) SALIVA
Seroconversion and presence of IgM
CMV in immunocompetent
Symptomatic illness = hepatosplenomegaly, jaundice, anemia, thrombocytopenia, low birth weight, microcephaly, chorioretinitis
CMV manifestations in infants:
Lymphomas in immunocompromised patients: s/s
Persistent fever, lymphadenopathy, hepatosplenomegaly
infects macrophages
CMV
CMV manifestations in infants: Fetal damage most likely in 1)
1) 1st trimester
Latent CMV in:
Monocytes
Diagnosis of CMV in Immunocompromised
• Viral antigen or DNA in blood • Inclusions or viral antigen in diseased tissue
EBV and Immunity: Capacity to limit proliferation of EBV-infected B cells
Memory T cells
EBV Not good correlation between titer and disease severity
Heterophile antibodies
African Burkitt Lymphoma genetics:
Translocations in B cells = c-myc oncogene and Ig heavy or light loci
protein-filled region; houses Enzymes and proteins required immediately for viral replication
Tegument; refers to EBV
EBV and Immunity: 1)–> Inc. circulating T-cells b/c activated in response to virus-infected B cells
1) Atypical lymphocytosis
Teenagers and young adults
EBV
Cytomegalovirus family and subfamily:
herpesvirus family β-herpesvirus subfamily
Diagnosis of CMV in Congenital infection Culture or 1) positive at birth or within 1-2 weeks
1) viral DNA assay
EBV–> Outside of viral particle covered by 1)
1) lipoprotein envelope
Perinuclear cytoplasmic inclusions
CMV
EBV and Lymphoproliferative Disease: Endemic in southern China
Nasopharyngeal carcinoma
CMV in bone marrow transplants:
interstitial pneumonia leading cause of death
Only used in heterophile antibody negative cases
Serologic tests
Large viral genome = 125-240 kb encoding 75 viral proteins
EBV
Close personal contact Sexual contact Congenital infections Isolated from saliva, cervical secretions, semen, urine, WBCs for months to years after infection
CMV
heterophile antibody–> Sera from 1) agglutinate RBCs from 2)
1) patients 2) sheep and horses
CMV in immunocompetent vs. immunocompromised
Immunocompetent = clinical disease from primary infection, if at all; mostly asymptomatic; Immunocompromised = primary infection and reactivation symptomatic
CMV on histo hallmark
Nuclear inclusions = owl eye cells
Not contained in immunocompromised organ transplant recipients
Memory T cells
Simple slide agglutination tests using animal erythrocytes; Present by end of 1st week of illness o May persist for many months
Heterophile antibodies
Screening for increased IgA to VCA and early EBV Ags used for early diagnostic purposes
African Burkitt Lymphoma
EBV pathogenesis: -Initially infects 1) -Subsequent infection of 2) activation and proliferation -Virus enters B cells by binding 3)
1) epithelial cells 2) B cells and polyclonal B cell 3) CR2
1)detectable in nucleus of infected cells;
1) 18-24h EBNA (Epstein Barr Nuclear antigen)
immunocompromised pt with CMV: Infection of monocytes causes 1)
1) increasing predisposition to fungal and bacterial infections
EBV and Lymphoproliferative Disease: Lymphomas in 1) patients, such as post-renal or lung transplant;
1) immunocompromised
CMV transmission
Close personal contact, sexual contact and congenital infections
EBV Can be used as diagnostic test, but 15% of adults fail to induce detectable levels
Heterophile antibodies
Infects vascular endothelial cells and leukocytes
CMV
Mononucleosis Syndrome clinical feature:
fever and reactive lymphocytes
EBV and Immunity: Heterophile antibodies–> 1) antibodies against antigens on sheep and horse RBCs
1) IgM
CMV has a latent infection; how may this be significant:
it may be transmitted in transfusion and organ transplant
Suggested infectious cofactor, such as malaria that causes immunosuppression and predisposes to EBV-related malignancy such as 1)
African Burkitt Lymphoma
what is CR2;
EBV enters B-cell by binding to CR2
CMV Neonatal infections during or shortly after birth: transmission via 1); not associated with adverse outcome
1) breast milk
10-15% of children infected in 1st 5 years of life
CMV
CMV manifestations: 1)–> 90% normal or asymptomatic but long term 10-20% develop sensory hearing loss, psychomotor mental retardation, or both
1) infants
Febrile prodrome 3-7 days
Mononucleosis Syndrome
Requires multiple contacts between shedding and susceptible persons
EBV
EBV Envelope = 1) protrude like spikes
1) 9 glycoprotein
why do immunocompromised organ transplant recipients have a higher risk of EBV associated malignancies
immunocompromised organ transplant recipients do not have MEMORY T-cells;
In AIDS patients, EBV is associated with:
• Hairy leukoplakia • Interstitial lymphocytic pneumonia • Lymphoma
EBV and Lymphoproliferative Disease: Most common malignancy in young children
African Burkitt Lymphoma
Expression of viral genome associated with immortalization and proliferation Infected B cells produce Ig and express a membrane Ag that is target of host cellular immune reponses
EBV pathogenesis
Two strains circulate widely, both can coinfect a single individual
EBV
Mononuclear leukocytosis–> key feature of Mono syndrome: 1) = greater than 50% of blood cells; At least 10% = 2)
1) Lymphocytes 2) reactive lymphocytes
Clinical manifestations due to vigorous host response to viral infection
Mononucleosis Syndrome
EBV family and subfamily:
Herpesviridae family; γ- herpesvirus subfamily
Diagnosis of CMV in immunocompetent
Seroconversion and presence of IgM
CMV Childhood and adulthood: Usually asymptomatic; may cause 1) In immunocompromised: 2)
1) mono syndrome 2) primary infection and reactivation is severe
Larger than normal with vacuolated cytoplasm, lobulated, and eccentrically placed nucleus
reactive lymphocytes
Environmental carcinogens create precancerous lesions
Nasopharyngeal carcinoma
CMV in AIDS patients:
disseminates to visceral organs causing chorioretinitis, gastroenteritis, and neurologic disorders
EBV: Present at onset of symptoms and disappear with resolution of disease
Atypical lymphocytes
EBV pathogenesis–>Once B-cells are infected, three things can happen: -Priming of the immune response -> production of 1)
1) EBV cytotoxic t-cells or memory t-cells.
Infects B cells
EBV
Adults 30-60 years of age
CMV
Diagnosis of CMV in Perinatal infection: Culture 1) at birth but positive at 2)
1) negative 2) 4 weeks or more after birth
EBV pathogenesis–>Once B-cells are infected, three things can happen: 1) from resting B cell that harbors the virus inside them;
1) Persistent infection
reactive lymphocytes: Larger than normal with vacuolated cytoplasm,1) nucleus
1) lobulated, and eccentrically placed
EBV and Diagnosis: Demonstration of 1) and 2)
1) atypical lymphocytes 2) heterophile antibodies
