Micro/immuno HPR Flashcards
CMV infects 1) first
vascular endothelial cells and leukocytes
HYPOCALCEMIA
DIGEORGE
ATM gene on Chromosome 11 mutation
Ataxia Telangiectasia:
Recipient T-cell with Recipient T-cell receptor DONOR DC with DONOR MHC Both interact with DONOR antigen
Direct allorecognition
Aedes aegypti
Dengue
Diagnosis: impaired integrin activation
LADIII (rare)
donor CD8+ t-cells recognize the MHC I, resulting in the use of granzyme and perforin to cause apoptosis -> result in cell death and recipient tissue cell damage.
GVHD
CMV in Bone marrow transplants
interstitial pneumonia
LOSS of natural killer cells
Ebola
Dengue: monocyte or dendritic cell produce 1) leading to DIC
IL-12, IL-8, and IL-1beta
In CGD, Nitroblue tetrazolium (NBT) test will be 1) indicating that 2)
1) NEGATIVE 2) ROS are not being made by neutrophils
absence or defect in beta 2-integrin (CD18) family
LADI
Endemic in Southern China
Nasopharyngeal Carcinoma
EBV diagnosis:
atypical lymphocytes and heterophile Abs
CGD pts at inc. risk for:
Catalase + organisms (s. aureus, Serratia mercescens) Burkholderia cepcacia Aspergillus fumigatus
enzymes and proteins that are required immediately for viral replication.
Tegument in EBV
absence of CD18 and the associated alpha subunits
LADI
CMV Neonatal infections at or shortly after birth
NO adverse outcomes
used for heterophile Ab negative abs
Serologic test (CMV)
Recipient T-cell with T-cell receptor Recipient DC with Recipient MHC these interact with DONOR antigen
Indirect allorecognition
Autosomal recessive
LAD Ataxia Telangiectasia
periodontitis–> gum infection
LAD1
CVID treatment
IV Immunoglobulin
B-cell infected
EBV
Fetal damage most likely in 1st trimester
CMV
Sinopulmonary infection
DIGEORGE Ataxia Telangiectasia
inhibit anti-viral interferons as well as the increased production of TNFalpha, IL-6 and tissue factor,
Ebola
Occurs >50% of long-term survivors of HLA-identical sibling transplants
Chronic GVHD
defective activation of all beta–integrins; not just the CD18 family
LADIII (rare)
direct vs. indirect allorecognition
Indirect–> Recipient DC and Recipient MHC Direct–> Donor DC and Donor MHC
HYPOgammablobulinemia
CVID
Transmission: Ingestion or inhalation of infected rat urine or feces
Lassa Fever
all viruses that cause hemorrhagic fevers
enveloped; ssRNA
EBV enters B cells by binding to
CR2
eterophile antibody negative mononucelosis syndrome)
CMV
Defective in both cell-mediate and humoral immunity; B-cell and T-cell deficiency
SCID
Infection occurs in a monocyte or dendritic cell.
all Hemorrhagic fevers
human platelet antigen 3
minor histocompatibility antigen; causes GVHD if HLA matches
Adults 30-60 years of age;
CMV
Arenaviridae family
Lassa Fever
latency in CMV where? significance?
in monocytes; means it may be transmitted in transplant
Reduced IgA
Ataxia Telangiectasia:
Autologous best source of HSC
Blood
Occurs >50% of long‐term survivors of HLA‐identical sibling transplants (allogeneic transplantations).
Chronic GVHD
Previous splenectomy inc. risk of
Chronic GVHD
Bombay blood group
LADII (rare)
T-cell deficient
DiGeorge Syndrome
tropic for B-cells and epithelial cells
EBV
Latent infection –>transfusion and organ donation transmission
CMV
EBV lytic infection
(virus is shed to infect other B-cells;
CMV in immunocompetent
asymptomatic
degranulation of neutrophils, that leads to inflammation
Ebola
Chronic Granulomatous Disease (CGD) diagnosis:
Dihydrorhodamine 123 (DHR) test Nitroblue tetrazolium (NBT) test
fever (greater than 38.6°C), severe headache; unexplained hemorrhage
Ebola
deafness
Lassa Fever
nfection of adrenal cortical cells results in hypotension and metabolic disorders
Marburg
Delayed separation of umbilical cord; leads to bleeding
LAD III
hepatosplenomegaly, jaundice, anemia, thrombocytopenia, low birth weight, microcephaly, chorioretinitis.
CMV in infants
Impaired phagocytic killing mechanisms of neutrophils and macrophages
Chronic Granulomatous Disease (CGD)
CD34+Thy-1+
HSC) specific markers
severely mentally retarded; short in stature and some facial anomalies
LAD2
EBV persistent infection due to:
resting B-cells that harbor the virus
Treatment: fucose supplementation
LADII (rare)
African Burkitt Lymphoma: Screening for increased1) and early EBV Ags
1) IgA to VCA
treatment using IgG from serum of previously recovered
Ebola
lichen planus or scleroderma, dry oral mucosa with ulcerations
Chronic GVHD s/s
bleeding gums, nose and eyes
Dengue
tropics and subtropics
Dengue
x-linked inheritance
CGD Wiskott-Aldrich
high IgA and IgE low to normal IgG and IgM
Wiskott-Aldrich
β-herpesvirus subfamily
CMV
CMV diagnosis in immunoCOMPETENT: immunocompromised?
Immunocompetent: Seroconversion and IgM presence; Immunocompromised: Viral antigen/DNA in blood; inclusions or viral Ag in diseased tissue
no pus formation –>impaired wound healing.
LAD1
MHC I vs MHC II
MHC on all nucleated cells MCH II on immune cells
VERY LOW IgG; low IgA
CVID
affects the sticking process of neutrophils 1) affects the rolling process (selectins) 2) affects the activation process 3)
1) LAD1 2) LAD2 3) LAD3
Wiskott-Aldrich Syndrome pneumonic: WATER
water: Wiskott Aldrich Thrombocytopenic purpura Eczema; Recurrent infection
BATS
Ebola
CMV: Viral antigen/DNA in blood; inclusions or viral Ag in diseased tissue
this is CMV in immunoCOMPROMISED
Lack of a NADPH oxidase
(CGD
polyclonal B cell activation and proliferation.
EBV:
Low CD3+ T cells
DiGeorge Syndrome
IL-2 receptor abnormality; gamma receptor implicated
SCID
22q11.2
DiGeorge Syndrome diagnosis:
monocytes producing IL-12, IL1-beta and IL8 thus DIC
Dengue
Adenosine deaminase deficiency
SCID
Less intensive RECIPIENT chemotherapy before transplantation of allogeneic stem cells
Non-myeloablative HSC transplant
class I myosin family member
minor histocompatibility antigens; recipient and donor are matched for MHC antigens, these can cause GVHD
Nairovirus
Crimean-Congo
G-CSF, GM-CSF, IL-3, thrombopoietin and CXCR4 antagonist (AMD3100)
Blood: Source for Autologous transplants; HSC is mobilized
Reservoir = African fruit bat, Rousettus aegyptiacus
Marburg
Diagnosis: bleeding complications from birth
LADIII (rare)
Pneumocystis jiroveci
causes acute interstitial pneumonitis; seen in SCID pts
In GVHD, principal antigenic targets of graft T cells are 1) if they differ • If graft is matched at MHC, 2) underlie GVHD
1) host MHC molecules 2) minor histocompatibility antigens
Affects teenagers and young adults
EBV
petechiae on the palate
Crimean-Congo
absence of fucosylated carbohydrate ligands for selectins
LADII (rare)
Mobilized 1) are superior for autologous transplants
1) PBPCs (peripheral blood progenitor cells)
Hyalomma tick reservoir and vector.
Crimean-Congo
(+) sense, ssRNA
Flaviridae family causing Denge
virus infecting monocytes, macrophages, neutrophils and natural killer cells.
Ebola
capacity to limit proliferation of EBV-infected B-cells; immunoCOMPROMISED pts dont have it
Memory T-Cells
CMV in immunocompromised
primary infection and reactivation symptomatic
lack of viral response bc no antivirals
Ebola and Marburg
Filoviridae family
Ebola and Marburg
human platelet antigen 3
minor histocompatibility antigens; recipient and donor are matched for MHC antigens, these can cause GVHD
Clinical Features of Mono. syndromes:
Fever and reactive lymphocytes
Cerebellar Ataxia
Ataxia Telangiectasia:
higher risk of relapse for leukemias and lymphomas
Identical Twin:
allogeneic best soruce of HSC
Best Source: Bone marrow
SMALL THYMUS
DIGEORGE
GVHD pathogenesis: Stress causes 1) to mature; Recipient mature DC present antigen to 2) 2) becomes T helper cell which activates 3) Result–> Recipient tissue damage aka GVHD
1) RECIPIENT DC 2) DONOR CD4+; 3) DONOR CD8+ T-cells;
(-)sense ssRNA genome.
all but Dengue
Heterophile antibodies –>1) against antigens on sheep and horse RBCs
1) IgM antibodies
what is one clinical use of allorecognition?
Graft-Versus-Tumor Effect–> the cells that may not have been killed off w/ chemotherapy and radiation are killed off by graft cells
CMV seropositivity inc. risk of:
Chronic GVHD
fever progresses to severe bruising, severe nosebleeds, and uncontrolled bleeding at INJECTION SITES
Crimean-Congo
polymorphism of PECAM
minor histocompatibility antigens; recipient and donor are matched for MHC antigens, these can cause GVHD
Vector = Mastomys natalensis rat
Lassa Fever
Progresses to jaundice, severe weight loss, delirium
Marburg
West Africa including Sierra Leone, Liberia, Guinea and Nigeria
Lassa Fever
blood of infected animal (bats) or bushmeat.
Ebola
CMV in AIDS patients EBV?
CMV–>chorioretinitis, gastroenteritis, and neurologic disorders EBV–>Hairy leukoplakia; Interstitial lymphocytic pneumonia;Lymphoma
infects macrophages
CMV (monocytes cause the latency seen in CMV)
activation of natural killer cells which produce IFN-gamma
Dengue
Nuclear inclusions (owl eye
CMV
facial swelling,
Lassa Fever
Tonsils: reddening, swelling and white patches
Mononucleosis Syndrome
Aedes albopictus mosquitoes.
Dengue
perinuclear cytoplasmic inclusions
CMV
Mono: etiologic agent
Epstein-Barr virus
Maculopapular rash on the trunk
Marburg
Low immunoglobulin due to impaired B-cell differentiation;
Common Variable Immunodeficiency Disorder (CVID)
Graft-Versus-Tumor Effect pathogenesis: 2) interacts with a dendritic cells and releases 1) –> leads to apoptosis of the tumor cell.
2) T-cell 1) granzyme and perforin (CD8+)
EBV: Initially infects 1) then 2);
1) epithelial cells 2) B cells
EBV: Tegument (protein-filled region) surrounds the 1)
1) nucleocapsid
virus infects dendritic cells, macrophages, hepatocytes and adrenal cortical cells
Marburg
most important in initiation of GVHD
HLA-A, B, and DR; these have to be a match
member of Bunyaviridae family
Crimean-Congo
Acute GVHD vs. chronic time period
acute–>First 100 days post-transplant chronic–>After 100 days post-transplant
red eyes, flushed face, and red throat.
Crimean-Congo
autoimmune disorders and lymphoma
CVID
Plasmodium:
Reproduce 1) in RBCs of vertebrate host;
Reproduce 2) in gut of mosquito
1) Asexually
2) sexually
Malaria transmitted by:
Anopheles mosquitoes
Brownish-black pigment = hemozoin
helps ID RBCs in malaria;
Morphology of infected RBC:
fimbriated
P. ovale
P. malariae
Trophozoites seen as: 1)
Mereozoites seen as: 2)
1) band forms
2) rosettes around central pigment
Rings = very small and may contain 2 chromatin dots
P. falciparum
Gametocytes = large, banana-shaped;
Parasites lying along margin of cell
P. falciparum
Trophozoites = band forms
P. malariae
P. vivax and P. ovale invades what subpopulation of RBCs?
immature cells/reticulocytes
P. malariae invades what subpopulation of RBCs?
senescent cells
Schuffner’s dots/granulocytes in RBCs
P. vivax
P. ovale
Trophozoites are band forms;
merozoites are rosettes
P. malariae
irregular in shape and is fimbriated
P. ovale
How does malaria induce damage?
Changes the RBC membrane;
P. falciparum binds to what type of antigen?
glycoprotein A; found on all RBCs, which is why P. falciparum does not discriminate subpopulation of RBCs
Malaria Affected by RBC abnormalities
Hemoglobin S associated with sickle cell;
Thalassemias;
Glucose-6-phosphate dehydrogenase deficiencies
how does P. falciparum cause microinfarcts?
produces a high molecular weight adhesive protein that binds receptors on endothelium leading to obstruction and microinfarcts
Pathogenesis of Fever in malaria;
macrophages release:
IL-1 and/or TNF-α
Fever early in malaria vs later
early–> irregular fever;
Later–> fever at 48 hr intervals
Cytokines in malaria:
High concentrations of TNF-α precipitate 1) by increasing sequesteration of parasitized RBCs in the 2)
1) cerebral malaria
2) cerebral vascular endothelium
Initial immune response to malaria:
premunition–>Initial immune response limits parasite multiplication, but does not eliminate infection
malarial paroxysm;
Cold stage for 20-60 minutes;
Hot stage for 3-8 hours due to vasodilation;
Wet stage = decrease in fever and profuse sweating
Life-cycle stages and the immune response:
Sporozoite stage
antibodies
Life-cycle stages and the immune response:
Liver stage
Cytotoxic T-cells and inflammatory cytokines (TNF, INF-alpha, and IL-1)
Life-cycle stages and the immune response
Asexual erythrocyte stage
antiboides
ROS
TNF alpha
Splanchnic capillaries involved –>vomiting, abdominal pain, diarrhea w/ or w/o bloody stools.
complication of malaria
detects protein excreted by P. falciparum
ParaSight F
Distinguishes between P. falciparum and P. vivax
OptiMAL Card antigen detection tests
detects parasite lactate dehydrogenase
OptiMAL Card antigen detection tests
Babesia microti Transmission
bite of Ixodes tick
which pts do Babesia affect more severely
asplenic patients
Babesia microti Often co-infection with 1)
1) Borrelia burgdorferi
Diagnosis of Babesia:
Maltese cross formation – tetrad of protozoa
Intraerythrocytic ring-shaped parasites on Giemsa-stained blood smears
Giemsa-stained blood smears of Babesia appearance
ID types of hookworms that cause anemia
Necator americanus
Ancylostoma duodenale
Epigastric pain and abnormal peristalsis;
Pruritus at site of skin penetration
Manifestations of hookworm:
Leishmania donovani
i. Parasitology
Obligate intracellular, flagellated parasite
Leishmania donovani Transmitted:
by phlebotomine sandflies
Transmitted by Lutzomyia verrucarum (phlebotomine sandfly)
Bartonella bacilliformi
Leishmania donovani
Red, hemangioma-like, cutaneous vascular lesions
Verruga peruana (chronic phase of infection) by Bartonella bacilliformis: