Y2B6 Micro

Front 1

what are the 3 basic problems w/ transplantation?

Back 1

1) transplant must be introduced in ways that allow them to function normally
2) health of the recipient and the transplant must be maintained throughout the whole transplantation
3) immune system of the recipient must be prevented from mounting an immune response to ags on grafted tissue.

Front 2

what is the universal rule of transplantation?

Back 2

engrafted tissue will be rejected from the immune system if ANY histocompatibility ags on the graft are absent from recipient.

Front 3

define: alloreaction

Back 3

immune reaction provoked by the alloantigen (which is the ag that differs btwn members of the same species)

Front 4

what is the difference in reaction between a solid organ transplant and a BMT?

Back 4

Solid organ: the recipient's lymphocytes attack the organ donated. SO recipient attacks donor.

BMT: Some of the cells in the donated bone marrow are already mature T lymphocytes and they then attack the recipient's organs (specifically those that are being irritated by the BM prep--> areas of rapid turnover). SO donor attacks recipient

Front 5

mismatch of which MHC is more severe? which one is the most important to match?

Back 5

MHC II mismatch is more rapid and severe Than MHC I.

The major HLA considered for matching: HLA A, B and DR. DR is the most important

Front 6

why does an A blood group form a response against a B blood group?

Back 6

Bc the gut bacteria bear ags that are similar/ identical to blood group ags which stimulate production of ab against the ags.

Front 7

what is the cross match test? Is the serum of the donor important?

Back 7

assessment of reactivity between the recipients serum and the donors blood cells.

serum of donor- no not necessary bc there aren't enough abs present there to cause a hemolytic reaction.

Front 8

how is tissue typing done via serology? DNA? Mixed lymphocyte reaction?

Back 8

serology: microcytotoxicity test (MHC I) or lymphocyte cross match.--> pt's serum is cross-matched w/ potential donor's lymphocytes

DNA: PCR

MLR: for DR (DQ,DP) molecules. In vitro culture contains leukocytes from both donor and recipient

Front 9

In the microcytotoxicity test, how do you deter which one is a better match? how does that occur?

Back 9

Best match is the cell that takes up the dye.

you place the donor cell in a batch with antibodies to HLA-A allele 2. Those HLA ab will bind to the HLA on the surface of the cell and it will cause activation of the complement cascade. That will cause perforin to come in and make holes in the cell making it leaky allowing the dye to be taken up.

Front 10

explain how Mixed lymphocyte reaction/response works.

Back 10

place the lymphocytes of donor and recipients together, but irradiate the donor cells first so they can't replicate. The cells that do replicate must be from the recipient's cells and identifies that this pt has alloreactive T cells which recognize foreign MHC and foreign processed peptide. (1-10% of T cells that leave the thymus are autoreactive). The more the replication the worse the prognosis.

Front 11

Explain hyperacute transplant rejection

Back 11

hyperacute: occurs w/n hrs of transplant. Recipient has preformed abs against donors blood cells or HLA ags--> immediately deposit in endothelial cell. This will lead to compliment activation --> C3a and C5a--> and IL-8 will be released which is chemotactice for neutrophils and lymphocytes---> this leads to a hemorrhagic (purple) engorged and dead graft

pt has preformed abs d/t pregnancy by many daddy's, blood transfusions or previous transplant

Front 12

explain alloreaction

Back 12

alloreaction is the alloag being recognized by recipient's T cells.

directly: ag is presented directly to donor APC

indirectly: donor apc disentigrates and the recipient APC takes it into the cell and it is txed as an expogenous piece of material and processed in phagosome via MHC II.

Front 13

explain acute transplant rejection

Back 13

kidney graft contains dendritic cells, those dendritic cells then travel to the donor's spleen and activates the effector T cells those effector T cells then travel back to the kidney and kill it. (via CTLA ) CAn be CD4 or CD8 depending on which MHC it binds to: CD4-- will kill via activated macrophages exacerbating inflammation, CD8- just attacks

acute takes days to weeks and the MC type of rejection seen.

Front 14

what do you see histologically in acute transplant rejection?

Back 14

lymphocytes, CD3+ staining T cells (brown), no healthy glomerulus.

comparable to type IV HSN reaction like (CD4- contact dermatitis or CD8- RA/MS)

Front 15

Explain Chronic rejection of transplanted organ

Back 15

Months to years and is likely mediated by indirect pathway of allorecognition. Alloab recruit inflammatory cells in BV walls of transplanted organ and over time those recruit immune effectors that will increasing cause damage. (makes tissues fibrotic--> ischemia and loss of function)

this is correlated w/ anti-HLA abs specific for graft and cells expressing CD40 and CD40L (B and T cell involvement): recipient DC's present MHC II to CD4 which then activates B cells. This interaction results in anti-HLA ab production. --> all downhill

Front 16

what does the outcome of transplantation depend on?

Back 16

matching HLA groups between donor and recipient and successful use of immunosuppressive drugs. (CS, cytotoxic drugs, T cell inactivators)

Front 17

what makes CS different from other biologically active molecules?

Back 17

they diffuse through the plasma membrane and bind to the receptors intracelllarly. (receptor is a/w HSP90)

Front 18

What does Azathioprine affect? WHen do you use it?

Back 18

All cells in active division bone marrow, intestinal epithelium, and hair follicles (inhibits inosinic acid and is a prodrug)

Used in post transplant period

Front 19

SE of cyclophosphamide? What is used as an alternative for? When do you use it?

Back 19

SE: hemorrhagic cystitis

alt: MTX

used: pre and post transplant (cross links DNA molecules and is a prodrug)

Front 20

DOC for inhibiting GVHD

Back 20

MTX

Front 21

how does rapamycin work?

Back 21

Inhibits T cell activation (like cyclosporine or tacrolimus) by preventing signal transduction from IL-2 receptors

Front 22

what are the 4 MC genetic disease in which BMT is a tx?

Back 22

SCID, Fanconi's anemia, Thalassemia Maj, sickle cell anemia

Front 23

what is the main focus of BMT? solid organ transplantation?

Back 23

main focus BMT: Myeloablative thx (ablating the whole immune system)

Solid organ: Ablating T cell response = main focus

Front 24

in order for a successful BMT, what must the donor and recipient have?

Back 24

at least 1 HLA class I and one HLA class II allotype in common

Front 25

what are the characteristics of GVHD? what 3 factors are essential for developing GVHD?

Back 25

rash, diarrhea, pneumonitis, jaundice

acute: post transplant 3 weeks.

3 factors: graft must contain immunocompentent cells, their must be a mismatch in maj or mino histocomp molcules, and recipient must be incapable of rejecting the graft

Front 26

Explain GVHD

Back 26

Allogenic bone marrow transplant contains mature and memory T cells--> T cells circulate to secondary lymphoid tissues and alloreactive cells interact w/ dendritic cells and replicate--> effector CD4 and CD8 T cells enter tissues inflamed by conditioning regimen and cause further tissue damage

Front 27

histology of GVHD

Back 27

lymphocytes exit BVs and attach to basal layer of epidermis--> that layer begins to swell & vacuolate (nuclei condense and cells die)--> advanced GHVD skin is destroyed and epidermis is sloughed out.

Front 28

Explain the order of clinical sxs in GVHD

Back 28

Bright red rash(that usua starts at the face and neck and spreads to involve trunk and limbs Typically accompanied by fever. --> Skin sloughing--> profuse watery diarrhea d/t the destruction of the normal architecture (like in hashimoto's)--> liver is infiltrated--> abnormal liver enzyme level (jaundice)

Front 29

when you do a transplant between twins who happened to be different sexes where do the problems arise?

Back 29

Some peptides are encoded on male specific Y chromosome and if given to sister, her T cells will not be tolerant of it bc her peptides were not made on Y chromosome. --> this is an example of a minor histocompatibility ag (which is d/t bound peptide and not MHC molecules)

Front 30

what are the beneficial effects of alloreaction (GVHD)?

Back 30

subdues residual activity of pt's immune system and helps to eliminate cancer cells that have escaped conditioning regimen.

it takes care of the residual leukemia cells--> therefore GVHD is better that GV tumor or leukemia effecto.

Front 31

what is the problem w/ autologous BMT?

Back 31

freq relapse of cancer compared to allogenic

Front 32

what is the purpose of leukapheresis? what is an additional source of hematopoietic stem cells?

Back 32

Leukapheresis is used to separate the CD3 + CTLA positive stem cells from the G-CSF pumped pts to use as a transplant. other source: umbilical cord cells from placenta after birth.

Front 33

what is the tx for GVHD? where else might you see GVHD besides liver and skin?

Back 33

IV anti-CD3 monoclonal ab and mycophenolate mofetil

GUT!!! D/t large pool of donor lymphocytes

Front 34

WHat is PrPC? What is the healthy protein PrPc a product of? where is it predominantly expressed?

Back 34

PrPC is a glycoproetin anchored to cell membrane. Product of PRNP gene on chr 20 and is predominantly expressed in neuronal cells (Also ganglia, Peripheral nerve cells)

Front 35

How do you convert PrPC to PrPsc? what are the sxs of prions?

Back 35

alpha helical structure change to a predominantly B sheets one

sxs: personality changes, dementia, jerky movements, depression. Later: severe mental impairment, inability to move or speak.

Front 36

MC parasitic infection of CNS? what is the reproductive form What happens to immunocompromised individuals infected w/ toxoplasmosis?

Back 36

Toxoplasmosis gondii; reproductive form: Tachyzoite.

immunocompromised: can lead to necrotizing encephalitis, pneumonitis, hemiparesis, seizures

Front 37

what are the 3 forms of toxo? SXS?

Back 37

Tachyzoites, cysts (in brain), sporulated and unsporulated oocysts

sxs: fever, night sweats, retroperitoneal and mesenteric lymphadenopathy, chorioretinitis

Front 38

Congenital toxo sxs?

Back 38

microcephaly, mental retardation, visual defects, seizures

Front 39

what causes primary amebic meningoencephalitis? What does PAM result from?

Back 39

Naegleria fowleri: thermophilic, free living amoeba (hot springs), which inhabits fresh water ponds, lakes and rivers.

PAM results from: swimming in the summer and the naegleria go up the nose into the olfactory nerve to brain (via cribriform plate)

Front 40

what is the pathophys of Naegleria?

Back 40

It's high phagocytic and ingests RBCs and brain tissue (severe hemorrhagic necrosis of brain)--> produces a "food cup" amebostome which secretes lysosomal hydrolases and phospholipidases into it and produces/ secretes heat stable hemolytic proteins, heat-labile cytolysin, phospholipase A and cysteine protease.

Front 41

how do you differentiate naegleria fowleri meningitis vs bacterial?

Back 41

wet mount positive for motile trophozoites & hemorrhagic CSF

otherwise all the same: High protein, neutrophil predominance.

Front 42

Which trypanosomiasis is the slow progressing one? rapid? what is their mitochondrial DNA called?

Back 42

gambiense (exclusively human)

rapid- rhodesiense (animal reservoir)

mitoDNA: Kinetoplastids

Front 43

what is the disease progression for trypanosomiasis? what type of CNS infection does trypanosomiasis cause?

Back 43

1) 1-2 week incubation
2) acute blood stage (fever HA)
3) invasion of lymphatics
4) relapses (d/t antigenic variation of trypanosomal surface)

causes meningoencephalitis

Front 44

sxs of trypanosomiasis?

Back 44

apathy, confusion, motor changes, changes sleep patterns (BIGGIE)

Front 45

what happens when the larva atatch to the brain in cystercercosis? why does it cause an altered mental status?

Back 45

seizure. --> larval presence allows the brain activity to go uncontrolled.

alt mental status d/t larvae blocking flow of brain fluid

Front 46

who are the definitive hosts for echinococcus granulosus? how about intermediate hosts? How does E. G enter the circulatory sys? what do they develop into?

Back 46

Def: Dogs
interm: Humans

enters circulatory sys by penetrating the gut wall. --< develop into hydatid cysts

Front 47

what is a hydatid cysts made of?

Back 47

protoscolices (each capable of forming a hydatid cysts)

Front 48

What type of cysts does echinococcus multilocularis cause? How does it reproduce?

Back 48

alveolar hydatid cysts

reproduces asexually a via lateral budding. These cysts can spread into surrounding tissue unlike E. granulosus.

Front 49

what do you use to tx Echinococcus hydatidosis and taenia?

Back 49

praziquantel

Front 50

what is the MCC of human eosinophilic meningitis? Where can you find this pathogen?

Back 50

angiostrongylus cantonensis "rat lungworm"

southeast asia and pacific basin, spreading to africa and caribbean

Front 51

What can angiostrongylus invade in a/w the CNS sxs? WHat will you find in CSF that will be diagnostic of angiostrongylus?

Back 51

Ocular (found vitreous humor)

csf: eosinophilia

Front 52

what are the MCC of CNS fungal infections?

Back 52

cryptococcus Neoformans, coccidoides immitus

Front 53

Encapsulated yeast like fungus causing meningoencephalitis dx & name virulence factors

Back 53

Cryptococcus neoformans. (capable of forming mycelia)

VF: polysaccharide capsule, ability to grow at 37 degrees C and production of phenol oxidase enzyme (prevents formation of FRs)

Front 54

where does cryptococcal meningitis usu result from?

Back 54

disseminated fungus from a pulmonary infection

Front 55

who suffers the most serious complications from Cryptococcus? How does Cryptococcys cayse Vision loss and HAs?

Back 55

Suffers: AIDS pts and organ transplant recipients

HA and vision loss: d/t increased ICP d/t C. ag which changes the osmolality affecting flow and adsorption.

Front 56

how does coccidioides disseminate from lungs to CNS? what is the geographical distribution of cocci?

Back 56

hematogenous spread--> resulting in rashes.

geo: san joaquin valley, CA; southwest US, northern mexico

Front 57

What is the most lethal form of coccidioidomycosis? what does it cause?

Back 57

dissemination to CNS --> chronic granulomatous meningitis (basilar meninges), cerebral and cerebellar abscesses, clinical sxs: HA, N/V, alt mental status.

Front 58

WHat does the viral meningoencephalitis panel NOT contain? what must you do instead?

Back 58

enterovirus, EBV, VZV, HHV6, CMV, HSV (basically enteroviruses + herpes viruses)

do PCR

Front 59

Viral or bacterial cause of meningitis

1) WBCs <1000
2) culture positive 65-90%
3) opening pressure >200

Back 59

1) viral
2) bacterial
3) viral

Front 60

Which virus causes acute viral meningitis:
1) Summer-fall: infants
2) Summer fall: swimming pools (1-15yo)
3) summer-fall: Ca, S.Eastern US (1-15 yo)

4) Winter: school exposure (1-15 yo)
5) WInter: college exposure (16-21)
6) Winter: any + mice, rats, hamsters
7) winter: adults

8) Any time: immunocompromised
9) any time: AIDs

Back 60

1) coxsackie B (infected mom)
2) enteroviruses
3) California serogroup virus
4) VZV, measles, mumps (M>F)
5) Measles, mumps, ebv
6) Lymphocytic choriomeningitis virus
7) VZV
8) adenovirus
9) Human immunodeficiency virus

Front 61

MCC of viral meningitis: How is it spread? What other sxs are either preceded or are concurrent?

Back 61

picornaviridae family (enteroviruses-- coxsackievirus, human enterovirus, echovirus)

spread f/o
sxs: GI sxs

Front 62

Which causes of viral meningitis are transmitted via arthropod's?

Back 62

California serogroup virus (bunyaviridae family)

Front 63

which viral cause of meningitis is not recoverable in CSF during acute phase? what is the clinical spectrum of this virus?

Back 63

California serogroup viruses-->

spectrum: nonspecific febrile illness, aseptic meningitis, meningoencephalitis

Front 64

Skin lesions + Meningitis

Back 64

VZV

Front 65

WHat is the MC form of encephalitis a/w measles virus? when does subacute sclerosing panencephalitis occur? sxs?

Back 65

acute encphalitis during convalescent stage of normal course. (paramyxoviridae family)

SSPE: 7 years after infection w/ measles (usu in those infected before 2 yo).

sxs: insidous onset of personality change, myoclonic jerks, poor school performance, loss of coordination, ocular abnormalities

Front 66

parotitis + meningitis/ meningoencphalitis

Back 66

mumps (paramyxoviridae family)

Front 67

meningoencephalitis + focal neuro features

Back 67

EBV

Front 68

Pets/ lab animals + biphasic sxs (meningeal signs -1st phase, HA- 2nd phase)

Back 68

lymphocytic choriomeningitis virus (LCMV)

arenaviridae family

Front 69

MCC of viral encephalitis? sxs? which one is more likely to be sporadic vs recurrent?

Back 69

HSV

sxs: alt consciousness> fever >HA ...... seizures; MRI: temporal lobe findings

HSV-1 : sporadic
HSV-2: MC recurrent benign lymphocytic meningitis

Front 70

Neutrophil predominance (50% of the time) + tremors + parkinsonism + myoclonus + poliomyelitis like paralysis

Back 70

W. nile (flaviviridae family)

Front 71

St. louis virus meningitis/ encephalitis age distribution? what is a distinguishing sx for this virus?

Back 71

<20= 50/50 (meningitis/ encephalitis)

>60= 90% encephalitis

sx: seizures in 47% of pts

(flaviviridae)

Front 72

prodrome (fever, chills, malaise) followed by recovery or encephalitis. dx. what is the mortality associated? via age

Back 72

Eastern/western encephalitis virus

mortality= 33%, >60 yo= 50%

western = MC than eastern

Togaviridae

Front 73

hyperactivity w/ hydrophobia + aerophobia + spasms and hallucinations. High body temp + encephalitis dx and what is the other form of this pathogen

Back 73

Rabies (furious)-80%

dumb rabies-20% paresthesias, weakness, flaccid paralysis

Front 74

Polio subtypes:

1) nonspecific febrile illness for 2-3 days w/o CNS involvement
2) meningeal irritation + signs of #1
3) meningeal irritation + asymmetric flaccid paralysis.

what are the severe cases of #3 sxs.

Back 74

1) abortive poliomyelitis
2) nonparalytic poliomyelitis-- aseptic meningitis
3) paralytic poliomyelitis

severe: paralysis of all 4 limbs & respiratory muscles.

severity of sxs incr w/ age at infection

Front 75

what three causes of viral meningitis/ encephalitis can cause flaccid paralysis?

Back 75

Herpes, West nile and polio

Front 76

pt mutation in a self-protein vs self-peptide

Back 76

Self-protein: allows binding of a new PEPTIDE to MHC molecules

self-peptide: creates a new EPITOPE for recognition by T cells.

Front 77

what are the 6 types of tumor ags?

Back 77

1) mutated genes
2) abnormal expression
3) oncogenic virus genes
4) oncofetal ags
5) alt glycolipid & glucoprotein ags
6) tissue specific differentiation ags

Front 78

how many IDENTICALLY loaded MHC: peptide complexes are req on a target cell to activate a T cell? how many would it take w/o co-receptor CD4 or CD8?

Back 78

10-100

w.o--> 10,000

Front 79

what does overexpression of a normal selfprotein do?

Back 79

overexpression changes density of peptide presentation allowing recognition by T cells.

eg: Tyrosinase, gp100, MART in melanoma

Front 80

what will oncogenic virus infected cells present peptides from? examples of DNA and RNA viruses

Back 80

Viral proteins:

DNA: papilloma, HBV, EBV

RNA: HTLV-1, HIV-1, HHV8

Front 81

what are oncofetal ags?

Back 81

reactivation of germ cell genes in a tumor cell not normally expressed in differentiated cell--> new cells in the immune sys (CEA, AFP)

Front 82

what are the innate immune system responders? WHAT is their MOA and how do they kill?

Back 82

NK cells: MOA: recognition of alt glyoproteins, loss of MHC I, and bound abs. Kill: release cytotoxic granules

macrophages: bound abs, receptor interactions. kill: phagocytosis and NO production

Front 83

which members of the NKG2 family are inhibitory? activating? what about the Ly49 family? These receptors belong in a/w which killer cells?

Back 83

NKG2 inhib: A and B, active: C & D

Ly49: Inhib: A &G, D&H= active

Front 84

what cells are involved as the adaptive immune system responders? MOA, Mech of kill!

Back 84

CD8+: tumor ags present in MHC class I. kill: cytotoxic granules (like NK cells), Fas Recepto Ligand, induction of anti-tumor T cell response.

Treg: MOA: Tumor expressed chemokines (CCR4-9). kill: TGF-b and IL-10 production

B lymph: MOA: Cell surface tumor ag, T helper cell. kill: ADCC (AB dependent cell mediated cytotox), compliment activation

TLRs, T cells and Tumors: TLR-9 = downreg by tumor microenvironment, chronic viral infections; but they can provide add'l co stim to T cells

Front 85

what is the anti-tumor T cell response method of killing done by CD8?

Back 85

tumor cells & ags ingested by APCs--> diff of tumor specific T cells--> anti-tumor response-- death of tumor cell

Front 86

what are the 5 ways in which the tumors evade the immune system?

Back 86

1) Tolerance
2) Tregs
3) loss of class I MHC
4) Loss of tumor ags
5) Local and systemic modulating effects

Front 87

what do most tumor cells lack that aid in tolerance?

Back 87

IL-2 signal which activates CTL--> leading to anergy or death.

Front 88

what CD's are a/w Tregs?

Back 88

CD4/ CD25

Front 89

How does loss of class I MHC protect the tumor cell? how is it non-protective?

Back 89

inhibits CTL killing but also increases NK killing

Front 90

When is a protein no longer necessary for a tumor cell?

Back 90

when it is not essential for growth and is being responded to by the immune system.

Front 91

what are some local immune modulating effects that tumor cells do? how about systemic?

Back 91

local: receptors & secreted factors--> TGFbeta and other immunosuppressive

systemic: exosomes

Front 92

what are the stages involved with systemic exosome formation of tumor cells?

Back 92

exosome--> 1) endocytosed receptor--> 2) early endosome w/ receptor recycling--> 3) multivesicular body --> 4) exosome release + receptor --> 5)late endosome is formed via MVB and autophagosome--> lysosomes.

exosomes block CD14$ monocyte differentiation in myeloid suppressor cells or fasL and TRAIL (elimination of anti-tumor effector T cells)

Front 93

what is the fxn of the multivesicular body joining the plasma membrane? where are they found? what are they released by?

Back 93

releases all the endosomes--> immune cell ag recognition, CA progression

found: serum, breast milk, BALF, urine

released: mast, T,B, dendritic, ntestinal epithelial, tumor & macrophage cells.

Front 94

how does the immune system promote a tumor?

Back 94

Chronic inflammation: macrophage released factors: promote angiogenesis, NDA damage (FR) and Tissue remodeling

Front 95

what are the 5 immune thx techniques?

Back 95

Tumor vaccination
augmentation
blocking inhibitory pathways
nonspecific stimulation
passive immunothx

Front 96

Explain tumor vaccination

Back 96

dendritic cells are removed and loaded w/ tumor ags and then returned. Plasmid will express tumor ag (vaccine) and pt dendritic cells will be transfected w/ same plasmid before return.

Front 97

Explain augmentation of tumor reponses

Back 97

tumor cells removed and forced to express immunomodulating genes and then returned

ie: Il-2, 4 (Renal Ca and melanoma), INF gamma, TNF, GMCSF etc

Front 98

explain blocking inhibitory pathways

Back 98

abs are injected to block CD152/CTLA-4 allowing immune system to respond to tumor.

Front 99

explain nonspecific stimulation

Back 99

non specific stim injected into tumor (cytokines, BCG, anti-CD3)

Il-2: melanoma, renal CA, colon CA
INF-alpha: melanoma
TNF: melanoma, sacroma
Il-12: melanoma

Front 100

explain passive immunothx

Back 100

adoptive cell culture: lymphocytes are removed, activated by tumor ags and expanded and then returned to pt.

Front 101

what 3 pathogens travel via axon cytoplasm causing a NS infection?

Back 101

rabies, HSV, tetanus toxin

Front 102

what pathogens cause chronic meningitis?

Back 102

M tb, fungi and sometimes protozoa

Front 103

epidemic viral encephalitis cause?

Back 103

Arboviruses (all the one's w/ city/ directions in their name)

Front 104

selective destruction of anterior horn cells + perivascular cuffing + asymmetric flaccid paralysis?

Back 104

poliomyelitis

Front 105

what are the 4 pathogens that you can confirm w/ latex agglutination?

Back 105

N. meningitis, S. pneumonia, Hemophilus influenza and cryptococcus.

Front 106

Turbid vs cobweb appearance of CSF

Back 106

turbid= bacterial
cobweb: TB

Front 107

virulence factors of neisseria Meningitidis?

Back 107

IgA protease, Capsule, LPS

Front 108

proinflammatory cytokines? ANTIINFLAMMATOR CYTOKINES?

Back 108

pro: Il-1b, TNF-a

ant: TGF-b and IL-10

Front 109

tx of neisseria? tx close contacts?

Back 109

tx: PCN

close contacts: Rifampin

Front 110

Beta hemolytic pathogens: what are they are how do you tell them apart?

Back 110

GBS, S. pyogenes and S. aureus

Staph vs strept: Catalase
GBS V GAS: Bacitracin, camp test

Front 111

serotypes of GBS most a/w neonatal dz in neonates and adults.

Back 111

1a, 3, and 5- neo

adults: 1a, 5

Front 112

GBS pathogenesis? tx

Back 112

factor h-- accelerates degradation of C3b!

tx: PCN or PCN + gentamycin

Front 113

renal transplants and CA pts. CNS infection

Back 113

listeria

via LLO, internalin

Front 114

Th1 response cytokines, TH2:

Back 114

Th1: IL-2, INF gamma and TNF beta

Th2: IL-4, IL-5, IL-10