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227 Cards in this Set
- Front
- Back
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What RNA viruses are helical?
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Cornocaviridae (common cold); orthomyoxoviridae (flu); paramyxoviridae (mumps, measles, RSV); Rhabdoviridae (Rabies)
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which RNA viruses are negative
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Orthomyoxoviridae (Flu); Paramyxoviridae (measles, mumps, RSV); Rhabdouridae (rabies)
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All positive RNA viruses are segmented or non-segmented
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non-segmented
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What viruses are segmented?
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BOAR
Bunyaviridae Orthomyxoviridae (flu); Arenaviridae Rhabdoviridae |
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What DNA virus does not replicate in the nucleus
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pox virus
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All negative stranded RNA viruses are
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enveloped
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All positive RNA viruses are segmented or non-segmented
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non-segmented
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What viruses are segmented?
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BOAR
Bunyaviridae Orthomyxoviridae (flu); Arenaviridae Rhabdoviridae |
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What DNA virus does not replicate in the nucleus
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pox virus
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All negative stranded RNA viruses are
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enveloped
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Whipworm
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tricurius
luminal nematode tea tray rectal prolapse eggs in feces mebendazole, albendazole |
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Ascaris clinical presentation
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luminal nematode
malnutrition bowel obstruction Loeffler's syndrome (lungs) |
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hook worm: what phases
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luminal nematode
soil, GI, lung |
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difference between ancylostoma duodenal and necator americanus
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Ancylostoma has 4 sharp teeth
Necator has 2 cutting blades |
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cutaneous larva magna;
treatment |
hookworms from dogs and cats
in cutaneous skin but cannot penetrate Treatment: albendazole (3 days) or ivermectin |
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strongyloides stercolaris: phases
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luminal nematode
soil phase, GI invasion, lung phase and FREE LIVING |
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stongyloides treatment
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ivermectin
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what are the lymphatic filaria?
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Wuchereria bancrofti and Brugia malayi
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How do you test for lymphatic filaria
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during the night. Loa Loa is daytime
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Loa Loa has what vector? when do you test for it?
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deer fly. Daytime. Diurnal periodicity. Pulminary capillaries at night.
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You should not use what drug with loa loa?
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Ivermectin!
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Calabar swellings associated with?
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Loa Loa
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Vector for Onchocerciasis
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black fly near fast moving water
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What is the real problem that happens with onchocerciasis?
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inflammatory response against dead microfilm
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What is contraindicated with onchocerciasis
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DEC
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Dracunculus medinensis = ?
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Guinea worm
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what is the treatment for guinea worm
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put fut in water
wrap worm around stick |
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Trichinosis: clinical and treatment
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asymptomatic, fever, myalgia, myositis, encephalitis
Diagnosis: eosinophilia and serology treatment: albendazole or mebendazole |
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visceral larva migraines causes what three symptoms
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carditis
ocular larva migrans hypereosinophilia |
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prevention of visceral larva migrans
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cover sandbox
deworm pets sanitary disposal of feces |
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What parasite deposites in striated muscle
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trichinosis
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Myiasis is caused by what?
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larvae of fly
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What are the different forms of trypanosomiasis?
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T.b. rhodesiense = E. African
T.b. gambiense = w. and c. african sleeping sickness |
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sleeping sickness: other name and vector
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trypanosomiasis
vector: tsetse fly |
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The tsetse fly injects human with _____ and they get trypanosomiasis
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trypomastigote
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trypanosome resevoir
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cattle, sheep, goats, wild game
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difference between rhodesiense and T. gambiense in trypanosomiasis disease progression
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R: can develop into fulminating infection
G: self-limiting, slowly pogressing |
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Special signs of trypanosomiasis
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1) trypanosomal chancre
2) irregular fever + headache 3) Winterbottom's sign (lymphatics part of disease) |
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What are extreme signs of trypanosmiasis
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parasites can cross blood brain barrier producing motor changes, fatigue, apathy
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What is unique about trypanosmiasis in terms of parasitemia
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it fluctuates. parasites from peaks are antigenic ally different which produce different surface glycoproteins.
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treatment for trypanosomiasis
early late CNS |
early: Suramin, pentamidine
late: eflornithinie, melarsoprol (toxic) |
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what parasite is the leading cause of cardiac disease in s. america
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trypanosoma cruzi = chagas
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key symptoms of chagas
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Romana's sign = swollen eye
Chargoma = ulceration |
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treatment for chagas
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nifurtimox
benznidazole azole antifungal agents |
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in chagas, what replicates via binary vision in the heart
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amastigotes
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Entamoeba histolytica: humans ingest and secrete what?
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cysts
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encystation in E. histolytica happens where? Ameobas feed on what and where?
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small intestine
bacteria in large intestine |
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pathologic signs of amebiasis
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ulcers with raised boarder - flask shaped
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flask shaped ulcers
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ameobiasis
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what do tropozoites ingest?
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RBC
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intestinal perforation is a sign of what
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E. histolytica - invasive
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Amebiasis invades where and presents as what
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1) LIVER: chocolate colored pus
2) Lung - abscess, bacterial infections, 3) Cutaneous - hepatic or intestinal fistula, penile ulcers |
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Chocolate colored pus on liver
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invasive E. histolytica (amebiasis)
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treatment of E. histolytica
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asymptomatic or luminal: iodoquinol or paromomycin
invasive: metronidazole or tinidazole |
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Owl-eyed parasite
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Gardia
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in gardia describe the trophozoite stage vs the cyst stage
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trophozoite: replication stage inhabiting small intestine
cyst: infective stage passed in feces |
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pathogenesis of giardia
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epithelial damage
villus blunting crypt cell hypertrophy cellular infiltration malabsorption lactase deficiency (intolerance) |
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treatment of giardia
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metronidazole
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trichomonas vaginalis
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STD
most women asymptomatic, some with malodorous foamy vaginal discharge |
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treatment for trich
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metrodinazole or tinidazole
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diagnosis of trich
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NAAT
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Brain lysis
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Naegleria fowlerii
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only non icosohedral DNA virus
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poxviridae
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T/F RNA viruses must encode their own polymerases
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T
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Helical viruses:
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coronaviridae (common cold), orthoxyoxoviridae (flu), paramyxoviridae (measles, mumps, RSV), Rhabdoviridae (rabies); Filoviridae, Bunyviridae, Arenaviridae
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what retrovirus is associated with adult T cell leukemia?
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HTLV-I
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Oseltamivir
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Neuroanimase inhibitor, destroys receptors recognized by viral HA, prevents release of virus form infected cells. A and B
High bioavailability |
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Zanamivir
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dry powder
low oral and systemic bioavailability not recommended for people with airway disease no pregnancy |
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what are cytokines?
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low molecular weight peptide or glycoprtoeins of diverse structure and function
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IL-12 acts on?
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NK cells, influences lymphocyte differentiation
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IL-8 acts on
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vascular endothelium; attaction/activation of neutrophils
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IL-1 acts on
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vascular endothelium, increases its permeability, stimulates IL-6 production
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IL-6 acts in
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Liver, produces acute phase proteins
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TNF-alpha
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increases permeability of vascular endothelium
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which complement pathway is antibody dependent
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classical
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chronic granulomatous disease is cause by?
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mutations in phagosomal NADPH oxidase....neutraphils can't kill ingested bacteria
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Chediak-Higashi syndrome results from
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mutation of CHS1 genes that encodes cytoplasmic protein involved in intracellular vacuole and granule fusion. vesicles can't fuse with phagosome and phagocytosis is impaired
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Leukocyte adhesion deficiency lype 1
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B2 integrins impaired. Neutrophils can't leave circulation and extravate into side of infection or injury.
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What complement component is an opsonin
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C3b, binds to CR1
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What diseases provide protection for malaria?
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Sickle-cell anemia, B-thalassemia gene, G-6PD, Duffy blood group antigens
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Oseltamivir
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Neuroanimase inhibitor, destroys receptors recognized by viral HA, prevents release of virus form infected cells. A and B
High bioavailability |
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Zanamivir
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dry powder
low oral and systemic bioavailability not recommended for people with airway disease no pregnancy |
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CD8 binds to what on MHC
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MHC I, alpha 3 subdomain
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what processes pathogens in CD8 T cells?
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Protease cuts it
Tap carries it to ER |
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What part of MHC binds to CD4?
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MHC II, Beta-2 domain
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What is the process of processing antigen in CD4?
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endocytosis.
fragmentation by proteases in endosomal/lysosomal veslles In ER, alpha, beta and invariant chain is produced and sent to golgi. In late endosome, invariant chain broken down into CLIP. HLA-DM exchanges CLIP for antigenic peptide |
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IgA and IgB are accessary proteins on what type of cell that do what?
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On B cells.
They talk to the nucleus |
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Variable region is near what end of the protein
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Amino end
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What talks to the nucleus in terms of T cell receptor
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CD3
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Most versitile immunoglobulin. Acts as a opsonin
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IgG
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What immunoglobulin can cross the placenta
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IgG
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What is the first Ig made by the fetus
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IgM
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What Ig is found in secretions
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IgA
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What Ig has low levels in serum and is produced during parasitic infections
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IgE
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Difference between BCR and TCR
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TCR is attached to the membrane and MHC restricted
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positive vs negative selection
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positive: able to recognize and bind self MHC expressed by cortical thymic cells
negative selection: those that bind with high affinity eliminated |
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self tolerance is the result of
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negative selection
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mhc restriction is the result of
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positive selection
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costimulation
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B7 recognized by CD28
CD40 recognized by CD40 ligand |
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If costimulation is present what receptors are upregulated
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IL-2
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activated TH cells produced what cytokine first?
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IL-2, which allows to to proliferate and differentiate
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CTLs don't produce IL-2 so they rely on?
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cross presentation. need TH help, which is being simulated by APC as well. Produces IL-2
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TH1 cells secrete?
Activated by? |
Interferon gamma, IL-2, TNF
They are activated by: IL-12 from dendritic cell or INF-gamma from NK |
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TH2 cells secrete?
They are activated by? |
IL-4, IL-5, IL-13
Activated by IL-4 |
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TH1 differenciation is produced for what type of infection
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more intracellular: opsinization, phagocytosis
intracellular microbes; inflammatory |
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TH2 differentiation is produced for what type of infection
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more extracellular: humoral response
helminths allergic reactions |
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what does IL-5 do?
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activates eosinophils to kill helminths
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Th2 activates B cells to do what?
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secrete neutralizing IgG antibodies
secret IgE -> mast cell degranulation |
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CTLs kill via
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perforin - hole punching
granzymes - proteases that produce cell death |
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heavy chain rearrangement in B cells occurs when
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Pre-B stage
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light chain rearrangement occurs when
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Immature B
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Mature B cells have what types of receptors at first
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IgM and IgD
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signals for B cell recognition of antigen
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1) multiple epitope repeats -> cross linking
2) CR2 (B cell) binds to C3d on antigen (compliment on virus) |
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B cells are presented with antigen where?
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in lymphoid follicles (in all secondary lymph)
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B cell activation by antigen causes four changes
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1) differentiation into plasma cells -> short lived antibody production
2)increase expression of B-7 (T cell costimulator) 3) increased expression of cytokine receptors 4) increased migration to paracortical areas where TH cells are located |
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long lived plasma cells are produced how?
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with the help of helper T cells in the follicles
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protein antigens can bind to B cells but what else do B cells need to produce a response
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Th cells
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Helper T cell signals
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stimulate heavy chain class switching and affinity maturation
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class switching involves what?
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constant chain rearrangement. does not affect variable region
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somatic hypermutation occurs when
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during rapid proliferation in germinal centers, increased rate of point mutations
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affinity maturation of B cells is what
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increased affinity of antibodies for a protein antigen. B cells that have developed mutations resulting in high affinity receptors will be rescued from apoptosis.
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IIgA is produced in response to what
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mucosal tissues, TGF-B
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IgG is produced in response to what cytokine
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IFN-gamma
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IgE is produced in response to what cytokine
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IL-4
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people with X linked hyper IGm Syndrome suffer from what
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they cannot class switch
intracellular microbe susceptibility bc CD40L is inactivated |
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role of follicular dendritic cells
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display antigen to B cell. B cells are selected for advantageous mutations in T-cell dependent protein reactions
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what type of Ig is more present in first and second responces
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1) IgM> IgG
2) IgG>IgM |
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Negative feedback of B cells
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IgG binds to immune complex. Fc tail recognizes Fc receptor on B cells, inhibiting further antibody product.
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T regulatory cells do what?
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express high levels of CD25
Some express TGFB and IL-10 Contact-dependent inhibition of T cell response |
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Peripheral T cell tolerance
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1) Anergy via costimulation deficiency or CTLA-4:B7 interaction
2) Death via Fas-Fas L mediated reaction or activation w/out co-stimualtion leading to expression of proapoptotic proteins |
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B-Cell central tolerance
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Negative selection
Receptor editing |
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Peripheral B cell tolerance
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Anergy or death by neglect
B cells are exiled from follicles |
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Genes involved in autoimmunity
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HLA/MHC mostly
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Environmental factors in autoimmunity
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a) induction of costimulation on APC by Microbes
b) mimicry via microbial antigens cross reacting with self. processes initiated by microbes can become directed at self cells or tissues |
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myathenia gravis
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autoantibodies to AcH receptors
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Hashimotos
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autoantibodies for thyroid protein
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Tumor recognition occurs how?
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T cell activation requires TCR recognition of tumor Ag on MHC
No costimulation so need cross-priming (presentation of presented on MHC 1 by CD4 cells or APCs) |
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how do tumors evade detection?
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divide rapidly
anti-tumor response is weak develop strategies such as - stop expressing antigen recognized by CTLs - no longer express MHC 1 - express immunosupressive cytokines (TGF-B, IL-10) and inhibit CTLA-4 |
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Role of NK cells in tumor
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mediate cytotoxicity on cells with low or no MHC
No prior activation needed |
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Role of macrophage in tumor
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immune surveillence for solid tumors
can engulf tumor cells, become activated, recruit others |
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Immunotherapy options
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1) give patient anti-tumor effectors such was antibodies and anti-tumor effector cells
2) boost or create patients own immunity to tumors via vaccination/immunization or stimulation of own anti-tumor responses |
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Direct alloregulation
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Donor dendritic cells present alloantigen to T cells
Reaction: CTL toxicity is intact , causing graft damage. Acute damage |
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what are passenger leukocytes
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dendritic cells/other APCs expressing high levels of MHC II from the graft to enter a nearby lymph node an stimulate recipient/host T cell activation
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Indirect allorecognition
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Host T cells recognize alloantigen presented by host dendritic cells;
Response: CD4+ mediated rejection involving hypersensitivity reaction bc CTL cannot directly kill. |
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Acute rejection of transplant
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anitbody mediated
thrombus formation Must test for antibodies |
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sub-acute rejection
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T-ecll mediated with some antibody involvement
Direct damage, plus cytokine damage of vascular |
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Chronic rejection (months to years)
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chronic delayed hypersensitivity reaction
Tcell/macrophage mediated growth and proliferation of fibroblasts, vascular smooth muscle cells |
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Tests for transplants
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Microcytotoxicity test
Mixed lymphocyte reaction (reaction = possible rejection) |
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graft vs host is what kind of hypersensitivity reaction
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type 4
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what is graft vs host
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when allogenic T cells are transferred with bone marrow, they react to host tissues
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croup is characterized by what?
what type of virus |
Parainfluenza
barking cough, difficulty breathing, stridor |
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Epliglottitis vs croup
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epiglottitis = bacterial, muffled voice
croup = viral, below viral cord |
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therapy for croup
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supportive care, oral corticosteroids, inhaled epinephrin
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infection of oropharynx vs nasopharynx
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ORO: EBV, adenovirus, HSV, enterovirus
NASO: Rhinovirus, cornavirus, |
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nasopharynx infections are: viral or bacterial
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mostly viral
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common cold pathogenesis: attachment via
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ICAM-1
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what is the malaria vector
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anopehline mosquito, female
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malaria cycle
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sporozoite -> hepatocytes -> asexual reporduction -> merzoites -> RBC infection -> rupture.
Every once in a while a merozoite will differentiate into a gametocyte and be ingested by another mosquito |
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malaria incubation
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7-30 days
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what malaria strands can remain dormant in liver
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P.Vivax and P. ovale
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why can P. faciparum kill
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red cells have knob like projections, parasite protein sticks to blood vessel walls
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bed nets have the most efficacy in the
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first year of life
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How is malaria past in placenta
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CSA protein on syncytiotropoblas
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malaria spenomegaly cause by
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P. Vivax
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chloroquine resistance, treat with
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quinine plus doxycycline
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leishmania: intra or extra cellular
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intracellular protezoa
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leishmania: vector
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sand flea
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what type of leishmania should be considered in every chronic fever patient
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visceral leishmania: fever, weight loss, enlarged spleen, anemia, lymphadenopathy, thrombocytepenia
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rodents are reservoirs for what type of leishmania
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L. tropica and L. chagais
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treatment: leishmania
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Miltefosine
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how does the humeral immune response work?
|
1. neutralization of microbes and microbial toxins (binding, transmission)
2. Opsonization and phagocytosis; tags microbes or Ag-Ab complex binds to Fc receptors and microbe is ingested 3. antibody mediated cellular toxicity (NK and eosinophils) 4. activation of compliment via classical pathway |
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antibody depended cellular toxicity is what
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NK cells and leukocytes bind to antibody coated cells and destroy them
Eosinophils and Ig kill helminths |
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mucosal immunity mediated by
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IgA
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neonatal immunity
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passive immunity: maternal antibodies cross palcenta to fetus and across gut epithelium during lactation. IgG
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conjugated vaccines are what?
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antigens coupled to proteins so that Th cells are activated and high affinity antibodies are made (example Hib vaccine)
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Type 1 hypersensitivity
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Ag binds to IgE on mast cells and basophils. Cross linking of IgE receptors results in release of chemical mediators
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Il-4 and IL-13 do what?
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turn on IgE production
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Il-3, Il-5 and Gm-CSF do what
|
promote eosinophil survival
|
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What interaction between B and T cell stimulates B cells to proliferate and differentiate?
|
CD40 and CD40L (on T cell)
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Cause of edema, vasodilation, bronco constriction, nausea, etc in Type I hypersensitivity
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1) Histamine (incr. vascular permaeability, vasodilation, bronoconstriction, mucus secretion)
2) Proteases and acid hydroxylases: kinins (vasodilation, s. musc. contraction); cleave complement; degrade blood vessel basement membrane 3) Chemotactic factors: attracts neutrophils and eosinophils 4) TNF: upregulates adhesion molecules 5) Leukotriene C3 and D4 - Increase vascular permeability, bronchial smooth muscle contraciton 6) Leukotriene B4: chemotactic 7) Prostaglandin D2: Intense bronchospasm, mucus secretion 8) PAF -> everythign |
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When do pre-formed granule contents kick in type 1 hypersensitivity
|
1-5 minutes
histamine, proteases, chemotactic factors, TNF |
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When do lipid mediators kick in type 1 hypersensitivity
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5-30 minutes via activation of arachadonic acid pathway
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when do cytokines kick in in type 1 hypersensitivity
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hours
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TNF does what
|
upregulates adhesion molecules
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What is the most powerful bronchospasm agent
|
leukotriene C4 and D4
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what happens during the late phase of type 1 hypersensitivity reactions?
|
allergic rhinitis, bronchial asthma with the infiltration into the tissues of eosinophils, neutophils, basophils, monocytes
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Eosinophils are recruited and produced via what cytokines
|
TH2 -> Il-3, IL-5, GMCSF
Mast cells-> Il-3, Il-5 TNF-> epithelium to produce Eotaxin |
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what type of cells plays the most important role in late phase reactions?
|
eosinophils: secrete highly toxic granules like a) Major Basic Protein (triggers histamine release but is also toxic to cells)
b) enzymes like peroxidase and collagenase c) cytokines that attract more eosinophils and lipid mediators like Leukotrienes C4,D4,E4 and PAF |
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What type of hypersensitivity reaction: food allergy
|
Type 1
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What type of hypersensitivity reaction: allergic asthma
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Type 1
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Chronic changes in asthma
|
BM thickening with collagen deposition in submucosa
Goblet cell hyperplasia cellular infiltrates in bronchial wall edema increase number of has cells |
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treatments for asthma
|
bronchodilator = epinephrin
mast cell stabilizer = crumbly block inflammation = corticosteroids Leukotriene inhibitor = montelukast |
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what are atrophic individuals?
|
they are prone to produce IgE antibodies. usually a triad of asthma, allergic rhinitis and atopic dermatitis
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what is desensitization therapy:
|
subcutaneous shots of antigen 1-2x weekly for several months
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what is the mechanism of Xolair
|
monoclonal antibody that binds to IgE before it can sit on mast cell
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Type II hypersensitivity reactions
|
IgM or IgG binding to fixed tissue surface antigens
4 mechanisms: A) opsonization and phagocytosis B) complement mediated inflammation C) Antibody mediated cellular dysfunction |
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What type of hypersensitivity reaction: major transfusion reaction
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Type II
Direct lysis via complement activation and MAC |
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What type of hypersensitivity reaction: Rh disease of the newborn
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Type II: cell becomes susceptible to phagocytosis by fixation of antibody or C3b fragment to cell surface
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What type of hypersensitivity reaction: autoimmune hemolytic anemia
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Type II
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What type of hypersensitivity reaction: drug induced reaction
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Type II
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What type of hypersensitivity reaction: Good pastures syndrome or anti-glomerulare BM nephritis
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Type II - complement mediated inflammation with Ab depositing onto extracellular tissue
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What type of hypersensitivity reaction: myasthenia gravis
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Type II: inhibition of receptor via Ab blocking
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What type of hypersensitivity reaction: Graves Disease
|
autoantibody to TSH receptors, mimic TSH and get hyperthyroidism
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Type III hypersensitivity reactions
|
circulatory soluble Ag-Ab complexes that deposit in vessel walls and activate complement
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What type of hypersensitivity reaction: serum sickness
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Type III
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What is immune complex disease?
|
ag-ab complexes increase phagocytosis and clearance by macrophages in liver and spleen. Some complexes bind to Fc or 3b receptors and you get vasodilation, deposition of complexes in the vessel walls and WBC recruitment and inflammation 10 days later.
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Ab-Ag complexes do what in type III hypersensitivity reactions
|
Fc receptor engagement
complement activation platlet aggregation haggerman factor |
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if you see vasculitis with edema and fibrin deposition
|
Type III hypersensitivity (vessels become necrotic)
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What type of hypersensitivity reaction: systemic lupus
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Type III
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Lupus: what is it
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mostly women,
autoantibodies to nuclear antigenbs antibodies bind to double stranded DNA and anti-smith |
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what type of immune complexes are removed by the liver quickly?
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large complexes
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What type of hypersensitivity reaction: post infectious glomerulonephritis
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from strep, rheumatic heart disease, and polyarthritis nodosa
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What type of hypersensitivity reaction: arthur reaction
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type III: reaction to tetanus booster
edema with severe hemorrhage, possible ulceration |
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Type IV hypersensitivity reactions
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cell mediated immunity with sensitized T lymphocytes. damage to the host is done inadvertently when fighting off intracellular pathogens
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What type of hypersensitivity reaction: Tb test
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Type IV: accumulation of CD4 cells around small veins = perivascular cuffing
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perivascualr cuffing is a sign of which hypersensitivity reaction
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Type IV
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What does a positive Th2 test mean?
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individual has mounted an antigen specific Th1 response
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What type of hypersensitivity reaction: contact dermatitis like poison ivy
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type IV
Th1 cells cause damage to keratinocytes causing cell separation |
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what is a haptan
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something that is only capable of becoming a full antigen when it reacts with proteins in the skin
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What type of hypersensitivity reaction: viral hepatitis
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type IV: HBV does not injure the host. liver injury is from immune response to viral Ags on infected hepatocytes
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What type of hypersensitivity reaction: transplant rejection
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Type IV: CTLs directed against cells surface HLA
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What happens to the following with age:
IL-2 IL-6 TNF-alpha CRP |
IL-2: decrease
IL-6: increase but decrease peak TNF-alpha: decrease but longer duration CRP: increase |
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What happens to B cell mediated immunity with age
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B cell number stays the same, circulating Igs are the same but Paraprotanemia is seen with more monoclonal Igs
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Does immune surveillance change with age?
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no
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how does immune response to vaccines change with age?
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vaccination decrease with age
pacs activate less efficeinty and macs activate less efficiently and NK, Macrophage, and NO producing pathways are not down regulated as effectively |
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after a vaccine your risk of heart attack
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decreases
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after respiratory tract infection,
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you have an increased risk of clotting
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