Mononucleosis syndromes Flashcards by Hussain Azizi

immunocompromised pt with CMV: Latently infected 1) contact activated T cells and differentiate into macrophages that produce infectious virus

1) monocytes

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microcephaly, chorioretinitis

CMV manifestations in infants:

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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

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Seroconversion and presence of IgM

CMV in immunocompetent

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Symptomatic illness = hepatosplenomegaly, jaundice, anemia, thrombocytopenia, low birth weight, microcephaly, chorioretinitis

CMV manifestations in infants:

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Lymphomas in immunocompromised patients: s/s

Persistent fever, lymphadenopathy, hepatosplenomegaly

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infects macrophages

CMV

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CMV manifestations in infants: Fetal damage most likely in 1)

1) 1st trimester

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Latent CMV in:

Monocytes

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Diagnosis of CMV in Immunocompromised

• Viral antigen or DNA in blood • Inclusions or viral antigen in diseased tissue

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EBV and Immunity: Capacity to limit proliferation of EBV-infected B cells

Memory T cells

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EBV Not good correlation between titer and disease severity

Heterophile antibodies

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African Burkitt Lymphoma genetics:

Translocations in B cells = c-myc oncogene and Ig heavy or light loci

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protein-filled region; houses Enzymes and proteins required immediately for viral replication

Tegument; refers to EBV

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EBV and Immunity: 1)–> Inc. circulating T-cells b/c activated in response to virus-infected B cells

1) Atypical lymphocytosis

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Teenagers and young adults

EBV

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Cytomegalovirus family and subfamily:

herpesvirus family β-herpesvirus subfamily

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Diagnosis of CMV in Congenital infection Culture or 1) positive at birth or within 1-2 weeks

1) viral DNA assay

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EBV–> Outside of viral particle covered by 1)

1) lipoprotein envelope

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Perinuclear cytoplasmic inclusions

CMV

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EBV and Lymphoproliferative Disease: Endemic in southern China

Nasopharyngeal carcinoma

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CMV in bone marrow transplants:

interstitial pneumonia leading cause of death

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Only used in heterophile antibody negative cases

Serologic tests

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Large viral genome = 125-240 kb encoding 75 viral proteins

EBV

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 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

Mononucleosis syndromes Flashcards

(70 cards)