Diseases Test 1 Flashcards
Parvovirus B19
“Fifths Disease”
Genomic organization: ssDNA (-), small non-enveloped, icosahedral
Tropism: Erythroid progenitor cells. Blood group P antigen (some people are group P antigen deficient and therefore innately immune)
Transmitted via respiratory system and replicates in eyrthroid progenitors. Viral protein NS1 induces erythroid apoptosis
Clinical presentation: Macular rash and arthralgia “slapped cheek”
Rx: Supportive care (IVIG for immunocompromised)
Transient aplastic crisis can occur in pts w/: hemolytic disorders.
Can also cause: chronic anemia/ pure red cell aplasia, hydrops fetalis (fetal loss)
X linked lymphoproliferative disease
Recessive disorder of young boys develop a fatal lymphoproliferative disorders after EBV. Present with severe sx of mono.
Most die.
Colorado Tick Fever Virus
Genomic organization: linear DS RNA virus. (uses negative strand for transcription and as a template for replication of positive strand) No envelope. Icosahedral capsid.
Tropism: Erythroid progenitor cells.
Animal vectors: Rocky Mt Wood Tick (small mammal resevoir)
Found in Rockies and West Coast from May to September (peak in june)
Clinical presentation: Fever, chills, body aches, malaise.
Dx by history, viral RNA (RT-PCR), and IGM
Rx: Supportive care
Complicating onset of meningitis and encephalitis (rare)
Epstein Barr Virus
Genomic organization: dsDNA (Gamma-1 Herpes virus) Evoloped virus w/ icosahedral head.
Tropism: lytic cycle in epithelial tissue. Latent infx in B-cells.
Associated malignancies: Burkitt’s lymphoma, Anaplastic nasopharyngeal carcinoma, Hodgkin’s disease, lymphomatoid granulomatosis.
EBV oncogene LMP1 is a homolog of CD40 and LMP2 is a homolog for BCL2.
LMP1 activates epidermal growth factor receptor transcription factors.
LMP2 activates B-cell proliferation/anti-apoptotic.
EBV gains entry to B cells by contact w/ CD21 on the surface of B-cells. Directly on tonsillar regions. Indirectly through contact with epithelial.
EBV oncogene EBNA3C down-regulates p53 transcriptional activity resulting in increased B cell transformation.
Clinical presentation: Classic triad = mild fever (10-14 days) , severe sore throat (3-5 days), and swollen glands (esp. posterior cervical lymph nodes).
VCA-IgM antibody is diagnostic (Viral Capsid Antigen)
Atypical lymphocytes with deformed nuclei and dark rimmed cytoplasm is also diagnostic. (Downey cells)
Severe if X linked lymphoproliferative disease.
Cytomegalovirus
Genomic organization: dsDNA. Enveloped w/ Icosahedral capsid.
Tropism:
Systemic infx: epithelial cells, endothelial cells, smooth muscle cells, macrophages, and neurons.
Latent infx: lifelong latency in pCD34 myeloid progenitor cells.
Tranmitted congenitally and by tranfusion, sexual contact, saliva, urine, or transplant.
Effective at evading host immune response via preventing antigens from being presented on MHC-1
Clincal presentation:
Congenital sx: microcephaly, seizures, deafness, jaundice, and purpura (blueberry muffin) due to thrombocytopenia. Hepatosplenomegaly and mental retardation.
Heterophil-negative mononucleosis: fever, lethargy, abnormal lymphocytes.
Can cause pneumonitis, esophagitis, hepatitis in immunocompromised
Dx w/ ELISA and presence of OWL’s EYEs cells in blood smears.
Rx: supportive care, or ganciclovir (severe/congenital)
HHV 6 and HHV 7
Exanthem subitum, Roseola, or sixth disease.
Genomic organization: dsDNA (beta herpes virus), enveloped w/ icosahedral capsid
Tropism: hematopoetic stem cell, leukocytes, epithelial cells.
Clincal course: Infancy and childhood. Faint pink, nonpruritic morbilliform rash on trunk which develops after a high fever (72hrs.).
Rx: ganciclovir and foscarnet
Can also cause: Adult- mononucleosis, pityriasis rosea.
immunocompromised - encephalitis, pneumonitis, sycytial giant-cell hepatitis, and disseminated disease
Kaposi Sarcoma Virus
HHV - 8
Genomic organization: dsDNA, enveloped w/ icosahedral, capsid.
Malignacies: Kaposi Sarcoma (vFLIP, vBCL-2, and vCyclin are homologs of normal protein that regulates apoptosis. VGPCR is homolog for protein that regulates cell fate.)
People affected immunocompromised.
Tropism: B cells
Rx: Ganciclovir, Cidofovir, and foscarnet. Goal is to attack lytic phase preventing reinfection only.
Acute T-cell lymphoma (ATL)
2-4% or patients infected w/ HTLV develop this malignancy.
Sx: Malaise, Night sweats, Fever, Cachexia, Adenopathy
Human T-cell Lymphotrophic Virus (HTLV-1 and HTLV-2)
Genomic organization: + ssRNA w/ reverse transcriptase. Enveloped w/ icosahedral capsid.
Tropism: T-cells.
HTLV-1 - causes T-cell leukemia, and HTLV-1 associated myelopathy/tropical spastic paraparesis.
HTLV-2 - non pathogenic
HTLV-2 - more common in Carribean, Eastern S. America, Western Africa, and Southern Japan.
HTLV binds host gp46 and fuses w/ host cell membrane –> integrates into DNA –> TAX-induced (affects CREB, CREM, NFKB, and NSF) viral gene transcription and REX induced tranlation or viral mRNA
Malignancies: Acute T-cell lymphoma (ATL) occurs in 2-4% or HTLV-1 Associated Myelopathy/Tropical Spastic Parapesis
HTLV-1 Associated Myelopathy (HAM) or Tropical Spastic Parapesis (TSP)
Pathology: infected T cells lead to astrocytosis and inflammation of gray and white matter of spinal cord resulting in progressive demyelination.
Sx: Gait disturbance, Stiffness/ weakness in legs, back aches, weak bladder, constipation
HIV
Genomic organiztion: Group VI + ssRNA w/ RT. Lentivirus subgroup. Enveloped w/ Icosahedral capsid.
Tropism: CD4+ T cell primarily. Also Macrophages, and dendritic cells. CD4, CCR5, or CXCR4.
HIV-2 has a lower transmissibility and less potential to progress to AIDS (confined to W. Africa).
Cell counts: CD4+ 500-1500 cells/ cubic mm (normal) Below 500 (immunocompromised) Below 200 AIDS
Rx: Zidovudine, efavirenz, raltegrovir, ritonavir, maroviroc
Dx w/ rapid ELISA test. Confirmed w/ Western Blot. Monitor patient’s status w/ CD4 tests and RT PCR viral load tests. `
Ebola
Genomic organization: - RNA virus. Enveloped with helical capsid.
Tropism: monocytes, macrophages, and dendritic cells
Clinical signs: fever (always and before infectious stage), myalgia, and malaise. Initial period followed by flu-like symptoms and sometimes rash, melena, hematemesis, shock, and encephalopathy.
Cause of death is sever organ dysfunction, encephalitis, anuria, seizures, and ultimately death.
Rx: Supportive care especiall replacement of fluid and lytes. Oxygen and vasopressors to maintain adequate bodily bodily function.
Iron-Deficiency Anemia
Things you must know:
- Most important cause: GI bleeding
- Microcytic, hypochromic anemia
- Increased anisoctyosis and poikilocytosis
- Abnormal iron studies
Causes: GI bleed, menses, hemorrhage, pregnancy, poor diet, poor absorption (celiac’s), pregnancy, gastric bypass, crohn’s, H. pylori, PNH
Clinical symptoms: pale, Koilonychia (spoon nails), smooth tongue, pica, reduced work productivity, Angular cheilitis, dsyphagia secondary to esophogeal webs.
Morphology: hypochromic, microcytic anemia, anisocytosis, poikilocytosis, decreased reticulocytes, increased platelets.
Labs: decreased serum iron, increased iron-binding capacity, and decreased ferritin (run first –> if positive = iron deficiency), decreased transferrin saturation, decreased hemoglobin
Bone marrow aspirate w/ prussian blue stain is gold standad.
Rx: Find out why patient is iron-deficient. Then give oral iron.
Megaloblastic Anemia
Retarded DNA synthesis w/ unimpaired RNA synthesis resultin in BIG cells w/ immature nucleus and mature cytoplasm.
Secondary to: B12 deficiency (dietary, lack of intrinsic factor, tapeworm), Folate deficiency (diet, alcoholism)
Morphology: oval macrocytes, hypersegmented neutrophils*
Symptoms: atrophic glossitis
Hemolytic anemia
Both chronic and acute; inherited and acquired.
Signs: Increased RBC destruction (Increased unconjugated/indirect bilirubin (jaundice), Increased LDH, Decreased haptoglobin (binds free hemoglobin in blood, hemoglobinemia/uria.) Increased RBC production (Reticulocytosis, and nucleated red cells in blood)
Labs: Direct Antiglobulin Test, DAT (do this right away. Positive = immune process.)
Morphology: Normochromic, normocytic, spherocytes, other poikilocytes.
Treatment: Acute: treat shock, transfusions w/ caution. Splenectomy may help.
