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Urease positive bugs
<span style="font-weight:600;">P</span>articular <span style="font-weight:600;">K</span>inds <span style="font-weight:600;">H</span>ave <span style="font-weight:600;">U</span>rease<br /><br /><span style="text-decoration: underline;">P</span>roteus, <span style="text-decoration: underline;">K</span>lebsiella, <span style="text-decoration: underline;">H</span>. pylori, <span style="text-decoration: underline;">U</span>reaplasma
Obligate Intracellular Bugs
Stay Inside when it is <span style="font-weight:600;">R</span>eally <span style="font-weight:600;">C</span>old<br><br>Rickettsia, Chlamydia
Facultative Intracellular
<span style="text-decoration: underline;">S</span>ome <span style="text-decoration: underline;">N</span>asty <span style="text-decoration: underline;">B</span>ugs <span style="text-decoration: underline;">M</span>ay <span style="text-decoration: underline;">L</span>ive <span style="text-decoration: underline;">F</span>acultative<span style="text-decoration: underline;">LY</span><br><br>Salmonella, Neisseria, Brucella, Mycobacterium, Listeria, Francicella, Legionella, Yersinia
Encapsulated Bugs
Some Killers Have Pretty Nice Capsules<br><br>Streptococcus pneumoniae<br>Klebsiella<br>Haemophilus influenzae<br>Pseudomonas aeruginosa<br>Cryptococcus neoformans<br><br>+ others: some E. coli, Streptococcus agalactiae, Yersinia pestis (F1 envelope)
Gram stain limitations
These Rascals May Microscopically Lack Color<br><br><span style="font-weight:600;">T</span>reponema (too thin): dark field microscopy, fluorescent antibody staining<br><span style="font-weight:600;">R</span>ickettsia (intracellular)<br><span style="font-weight:600;">M</span>ycoplasma (no cell wall)<br><span style="font-weight:600;">M</span>ycobacterium (high mycolic acid content): acid fast stain<br><span style="font-weight:600;">L</span>egionella pneumophila (intracellular): silver stain<br><span style="font-weight:600;">C</span>hlamydia (intracellular, lacks muramic acid in cell wall)
Spore forming bacteria
Bacillus anthracis<br>Bacillus cereux<br>C. perfringens<br>C. tetani<br>C. botulinum
Bacteria that require cysteine
Brucella, Francisella, Legionella, Pasteurella
Obligate anaerobes
Anaerobes <span style="font-weight:600;">C</span>an't <span style="font-weight:600;">B</span>reathe <span style="font-weight:600;">A</span>ir.<br><br>Clostridium, Bacteroides, Actinomyces
Microaerophilic
Campylobacter and Helicobacter
Obligate aerobes
Nagging Pests Must Breathe<br><br><span style="font-weight:600;">N</span>ocardia, <span style="font-weight:600;">P</span>seudomonas aeruginosa, <span style="font-weight:600;">M</span>ycobacterium tuberculosis, and <span style="font-weight:600;">B</span>acillus
Which coagulase negative Staphylococcus is Novobiocin <span style="font-weight:600;">resistant</span>? which is <span style="font-weight:600;">sensitive</span>?
On the office's <span style="font-weight:600;">staph </span>retreat, there was <span style="font-weight:600;">NO StRES</span>.<br><br>Novobiocin resistant: S. saprophyticus<br>Novobiocin sensitive: S. epidermidis
Which alpha hemolytic Streptococcus is <br>1. optochin sensitive and bile soluble?<br>2. optochin resistant and not bile soluble?
OVRPS<br><br><span style="font-weight:600;">O</span>ptochin: <span style="font-weight:600;">V</span>iridans is <span style="font-weight:600;">R</span>esistant, <span style="font-weight:600;">P</span>neumoniae is <span style="font-weight:600;">S</span>ensitive
Which beta hemolytic Streptococcus is:<br />1. bacitracin resistant?<br />2. bacitracin sensitive?
<span style="font-weight:600;">B-BRAS</span><br /><br /><span style="font-weight:600;">B</span>acitracin<br /><br />Group <span style="font-weight:600;">B</span> (S. agalactiae) is <span style="font-weight:600;">R</span>esistant<br /><br />Group <span style="font-weight:600;">A</span> (S. pyogenes) is <span style="font-weight:600;">S</span>ensitive
Lactose-fermenting enteric bacteria
<span style="text-decoration: underline;">Test with Mac</span><span style="font-weight:600; text-decoration: underline;">C</span><span style="text-decoration: underline;">on</span><span style="font-weight:600; text-decoration: underline;">KEE</span><span style="text-decoration: underline;">'</span><span style="font-weight:600; text-decoration: underline;">S</span><span style="text-decoration: underline;"> agar</span><br><span style=" text-decoration: underline;"></span><br><span style="font-weight:600;">C</span>itrobacter<br><span style="font-weight:600;">K</span>lebsiella<br><span style="font-weight:600;">E</span>nterobacter<br><span style="font-weight:600;">E</span>. coli<br><span style="font-weight:600;">S</span>erratia<br><br>middle 3 are fast fermenters.
PSEUDOmonas diseases
Wound and burn infections, hot tub folliculitis<br><br><span style="font-weight:600;">P</span>neumonia (especially in CF)<br><span style="font-weight:600;">S</span>epsis (black skin lesions)<br><span style="font-weight:600;">E</span>xternal otitis (swimmer's ear)<br><span style="font-weight:600;">U</span>TI<br><span style="font-weight:600;">D</span>rug use and <span style="font-weight:600;">D</span>iabetic <span style="font-weight:600;">O</span>steomyelitis<br>
Triad of Typhoid fever
Bradycardia, neutropenia, splenomegaly
How to diagnose Typhoid fever during first week and second week?
1st week: blood culture<br>2nd week: stool culture
VDRL False positives
VDRL<br /><br />Viruses (mono, hepatitis)<br />Drugs<br />Rheumatic fever<br />Lupus and Leprosy
Features of Lyme Disease
<span style="font-weight:600;">BAKE </span>a Key Lyme pie:<br><br><span style="font-weight:600;">B</span>ell's Palsy<br><span style="font-weight:600;">A</span>rthritis<br><span style="font-weight:600;">K</span>ardiac block<br><span style="font-weight:600;">E</span>rythema migrans
Classic triad of all Rickettsial diseases
headache, fever, and rash (vasculitis)
Palm and Sole Rashes
You drive <span style="font-weight:600;">CARS </span>using your palms and soles<br><span style="font-weight:600;">C</span>oxsackie <span style="font-weight:600;">A </span>virus (hand, foot, and mouth disease)<br><span style="font-weight:600;">R</span>ocky mountain spotted fever<br><span style="font-weight:600;">S</span>yphilis<br>
Thermally dimorphic fungi
<span style="font-weight:600;">B</span>ody <span style="font-weight:600;">H</span>eat <span style="font-weight:600;">C</span>hanges <span style="font-weight:600;">S</span>hape<br><br>Blastomyces<br>Histoplasma<br>Coccidioides<br>Sporothrix
What are pseudohyphae? Which fungus has this morphology?
Pseudohyphae are hyphae with constrictions at each septum. (yeasts that bud but do not separate)<br><br>e.g. Candida albicans
Killed viral vaccines
<span style="font-weight:600;">RIP A</span>lways<br><br><span style="font-weight:600;">R</span>abies<br><span style="font-weight:600;">I</span>nfluenza<br><span style="font-weight:600;">P</span>olio (Salk)<br>H<span style="font-weight:600;">A</span>V
Recombinant viral vaccines
HBV and HPV
Naked viruses
Naked <span style="font-weight:600;">CPR </span>and <span style="font-weight:600;">PAPP </span>smear<br>Calicivirus<br>Picornavirus<br>Reovirus<br>Parvovirus<br>Adenovirus<br>Papilloma<br>Polyoma
DNA enveloped viruses
Herpesviruses (HSV, VZV, CMV, EBV)<br>HBV<br>Smallpox virus
DNA nucleocapsid viruses
Parvovirus<br>Adenovirus<br>Papillomaviruses<br>
RNA enveloped viruses
Influenza, Parainfluenza, RSV<br><br>Measles, Mumps, Rubella<br><br>Rabies, HTLV, HIV<br>
RNA nucleocapsid viruses
Enteroviruses (poliovirus, Coxsackievirus, Echovirus, HAV)<br>Rhinovirus<br>Reovirus
All DNA viruses are double stranded except <span style="font-weight:600; color:#0000ff;">[...]</span>
All DNA viruses are double stranded except <span style="font-weight:600; color:#0000ff;">parvovirus</span>
All DNA viruses have linear DNA except <span style="font-weight:600; color:#0000ff;">[...]</span>
All DNA viruses have linear DNA except <span style="font-weight:600; color:#0000ff;">papilloma and polyoma (circular supercoiled) and hepadna (circular incomplete)</span>
All DNA viruses are icosahedral except <span style="font-weight:600; color:#0000ff;">[...]</span>
All DNA viruses are icosahedral except <span style="font-weight:600; color:#0000ff;">pox virus (complex)</span>
All DNA viruses replicate in the nucleus except <span style="font-weight:600; color:#0000ff;">[...]</span>
All DNA viruses replicate in the nucleus except <span style="font-weight:600; color:#0000ff;">pox virus (carries own DNA-dependent RNA polymerase)</span>
Name the 7 DNA viruses
<span style="font-weight:600;">HHAPPPP</span>y<br><br>Hepadna<br>Herpes<br>Adeno<br>Pox<br>Parvo<br>Papilloma<br>Polyoma
Which Hepatitis virus is associated with PAN and membranous glomerulonephropathy?
HBV
Which hepatitis virus is associated with cryoglobulinemia and MPGN type I
HCV
Most common causes of Neonatal Pneumonia
Group B Streptococci<br>E. coli
Most common causes of Pneumonia in Children (4w to 18 y)
Runts May Cough Sputum<br><br>RSV, Mycoplasma, Chlamydia pneumoniae, Streptococcus pneumoniae
Most common causes of Adult Pneumonia (18-40 y)
M. pneumoniae<br>C. pneumoniae<br>S. pneumoniae
Bloody diarrhea
Campylobacter, Salmonella, Shigella, EHEC, EIEC, Yersinia enterocolitica, C. difficile, Entamoeba histolytica
Watery diarrhea (3 bacteria, 3 viruses, 3 protozoa)
ETEC, Vibrio cholerae, C. perfringens<br><br>Rotavirus, Adenovirus, Norwalk virus<br><br>Giardia, Crytposporidium, Isospora<br><br>
Nosocomial pneumonia
Staph, enteric gram negative rods
Pneumonia in Immunocompromised patients
Staph, enteric gram negative rods, fungi, viruses, PCP
Aspiration Pneumonia
Anaerobes
Pneumonia in Alcoholics and IVDU
S. pneumoniae, Klebsiella, Staph
Pneumonia in Cystic fibrosis
Pseudomonas
Postviral Pneumonia
Staph, H. influenzae
Atypical Pneumonia
Mycoplasma, Legionella, Chlamydia
MCC of neonatal meninigitis
Group B streptococci
MCC of Meningitis in children
S. pneumoniae
MCC of Meningitis in Elderly
S. pneumoniae
MCC of Meningitis in adults (6-60 y)
N. meningitidis
MCC of Osteomyelitis
S. aureus
MCC of Osteomyelitis in sexually active people
N. gonorrhea (rare, septic arthritis is more common)
MCC of Osteomyelitis in Diabetics and IVDU
Pseudomonas
MCC of Osteomyelitis in Sickle Cell anemia
Salmonella
MCC of Osteomyelitis in prosthetic replacement
S. aureus and S. epidermidis
MCC of Vertebral Osteomyelitis
Pott's disease (M. tuberculosis)
MCC of Osteomyelitis following cat and dog bites or scratches
Pasteurella multocida
MCC of ambulatory UTI
E. coli (50-80%) and Klebsiella (10%)<br><br>in sexually active women, 2nd MCC is Staphylococcus saprophyticus (10-30%)
Hospital acquired UTIs
E. coli, Proteus, Klebsiella, Serratia, Pseudomonas
UTI Bugs
SSEEK PP<br><br>Serratia, Staph saprophyticus, E. coli, Enterobacter, Klebsiella, Proteus mirabilis, Pseudomonas
Classic triad of Toxoplasma gondii congenital infection
Chorioretinitis, intracranial calcifications, hydrocephalus
TORCHeS Infections
Toxoplasma gondii<br>Others: Listeria, E. coli, group B streptococci<br>Rubella<br>CMV<br>HSV-2 and HIV<br>Syphilis
Catalase Positive Bugs
If you've got CGD, make <span style="font-weight:600; text-decoration: underline;">SPACE </span>for bugs with catalase!<br><br>Staph<br>Pseudomonas<br>Aspergillus<br>Candida<br>Enterobacteriaceae
1st Signal for Th-cell activation
binding of TCR (Th cell) to MHC II (APC)
2nd Signal of T cell activation
CD4/CD8 bind to MHC II/MHC I <br />Integrin (LFA-1) binds to ICAM-1<br />IgCAMs binds to LFA-3<br />CD28 binds to B7 --&gt; triggers transcription of several cytokine genes<br />
3rd singal for T-cell activation
Cytokines: <br /><br />IL-1<br />IL-2<br />IL-6<br />TNF-alpha
Endotoxin receptor
CD14 located on macrophages
Mechanism of action of Superantigens
nonspecifically bind TCR to MHC II <br>--&gt; activate Th cells <br>--&gt; release of IFN-gamma from Th1 cells<br>--&gt; activate macrophages<br>--&gt; release of IL-1, IL-6, and TNF-alpha from macrophages
Which cytokines are produced by Th1 cells?
<span style="font-weight:600;">IFN-gamma<br />TNF-alpha</span><br />IL-2, IL-3<br />GM-CSF
Which cytokines are produced by Th2 cells?
<span style="font-weight:600;">IL-4, 5, 6, 10</span><br />IL-2, 3<br />GM-CSF<br />
Crossregulation of Th1 and Th2 cells
Th1 --&gt; IFN-gamma --&gt; inhibits Th2<br /><br />Th2 --&gt; IL-4 and IL-10 --&gt; inhibit Th1<br />
What is the first signal for B cell activation?
binding of MHC II-peptide complex (B cell) to TCR (Th cell)
What is the second signal for B cell activation
B7 binds to CD28<br>CD40 binds to CD40L
What is the third signal for B cell activation
IL-2, 4, 5
Activation of B cells includes what 3 processes?<br />
differentiation, memory, and class switching
Deficiency of DAF (GPI)
paroxysmal nocturnal hemoglobinuria
Deficiency of C5-C8 leads to <span style="font-weight:600; color:#0000ff;">[...]</span> bacteremia.
Deficiency of C5-C8 leads to <span style="font-weight:600; color:#0000ff;">Neiserria</span> bacteremia.
Deficiency of C3 leads to
severe, recurrent pyogenic sinus and respiratory tract infections. <br>
Deficiency of C1 esterase inhibitor leads to <span style="font-weight:600; color:#0000ff;">[...]</span>
Deficiency of C1 esterase inhibitor leads to <span style="font-weight:600; color:#0000ff;">hereditary angioedema</span>
Name the 2 primary opsonins
IgG and C3b
Name to complement factors that induce anaphylaxis
C3a and C5a
Which complement factor attracts neutrophils?
C5a
MAC is formed of which complement factors?
C5-C9
Defect in Bruton's agammaglobulinemia
<br><br>XR defect in BTK (a tyrosine kinase gene) --&gt; blocks B-cell differentiation/mutation --&gt; -- production of B-cells
Characteristic lab result in Bruton's agammaglobulinemia
decreased B cells
Defect in Hyper-IgM syndrome
defective CD40L on Th cells --&gt; inability of B cells to class switch
++ IgM and -- IgG, IgA, IgE
Hyper-IgM syndrome <br />(CD40L defect)
most common immune deficiency
IgA deficiency
Anaphylaxis on exposure to blood products with IgA
IgA deficiency
Defect in IgA deficiency
failure in isotype switching to IgA
normal number of B cells, -- plasma cells and immunoglobulins
CVID
Defect in CVID
defect in B-cell maturation (many causes)
B-cell immunodeficiency that presents in the 20s to 30s
CVID
True or false, in CVID there is increased risk of autoimmune diseases.
True
Defect in Digeorge syndrome
failure of development of 3rd and 4th pharyngeal pouches (thymus and parathyroid glands)
IL-12 deficiency
decreased Th1 response --&gt; decreased IFN-gamma --&gt; disseminated mycobacterial infections.
Defect in Job's syndrome (Hyper-IgE syndrome)
Th cells fail to produce IFN-gamma --&gt; inability of neutrohils to respond to chemotactic stimuli
Features of Hyper-IgE syndrome
<span style="font-weight:600;">FATED</span><br><br>coarse <span style="font-weight:600;">F</span>acies<br>cold staph <span style="font-weight:600;">A</span>bscesses<br>retained primary <span style="font-weight:600;">T</span>eeth<br>increased Ig<span style="font-weight:600;">E</span><br><span style="font-weight:600;">D</span>ermatologic problems (eczema)
Defect in Chronic mucocutaneous candidiasis
T-cell dysfunction
Defect in SCID
Several types<br><br>IL-2 receptor defect (MC)<br><br>adenosine deaminase deficiency<br><br>failure to synthesize MHC II antigens
Defect in Ataxia-telangiectasia
Defects in DNA repair enzymes
Triad of ataia-telangiectasia
cerebellar defects (ataxia)<br />spider angiomas (telangiectasia)<br />IgA deficiency
Defect in Wiskott-Aldrich syndrome
Progressive deltion of B and T cells. Decreased ability to mount an IgM response.
Triad of Wiskott-Aldrich syndrome
<span style="font-weight:600;">TIE</span><br><br><span style="font-weight:600;">T</span>hrombocytopenic purpura, <span style="font-weight:600;">I</span>nfections, <span style="font-weight:600;">E</span>czema
--IgM and ++ IgE, IgA
Wiskott-Aldrich syndrome
Defect in Leukocyte adhesion deficiency 1
LFA-1 integrin (CD18)
Features of LAD type 1
recurrent bacterial infections<br>absent pus formation<br>delayed separation of umbilicus<br>neutorphilia
Defect in Chediak-Higashi syndrome
AR defect in microtubular function --&gt; decreased fusion of phagocytic vesicles with lysosomes
Partial albinism is seen in which immunodeficiency syndrome?
Chediak-Higashi syndrome
Defect in Chronic granulomatous disease
lack of NADPH oxidase
increased susceptibility to catalase-positive organisms
CGD
test for CGD
negative nitroblue tetrazolium dye reduction test
Explain why in CGD catalase positive organisms cannot be killed.
Catalase positive organisms breakdown any H2O2 they produce by catalase. Therefore, to kill them, a WBC needs myeloperoxidase to produce HOCl. In NADPH deficiency there is no H2O2 production, which is the substrate for myeloperoxidase. <br><br>Catalse negative organisms cannot breakdown the H2O2 they produce. The WBC uses this H2O2 as a substrate for myeloperoxidase to form HOCl which can kill these organisms (bypassing the defective NADPH oxidase).<br><br>
Fever, urticaria, arthrlagia, proteinuria, and lymphadenopathy 5-10 days after antigen exposure
Serum sickness (III)
local edema and necrosis after intradermal injection of antigen
Arthus reaction (III)
Test for each type of hypersensitivity
I: scratch test and RISA<br>II: direct and indirect Coombs<br>III: immunofluorescent staining<br>IV: patch test
4 T's of Type 4 Hypersensitivity
<span style="font-weight:600;">T</span> lymphocytes<br /><span style="font-weight:600;">T</span>ransplant rejections<br /><span style="font-weight:600;">T</span>B skin test<br /><span style="font-weight:600;">T</span>ouching (contact dermatitis)
HLA-A3
Hemochromatosis
HLA-B27
PAIR<br><br>Psoriasis, Ankylosing spondylitis, IBD, Reiter's syndrome
HLA-B8
Grave's disease
HLA-DR2
MS, SLE, Goodpasture syndrome, Hay fever
HLA-DR3
DM type 1
HLA-DR4
Rheumatoid Arthritis, DM type 1
HLA-DR5
Pernicious anemia, Hashimoto's thyroiditis
HLA-DR7
steroid-responsive nephrotic syndrome
After a bone marrow transplant, a patient presents with maculopapular rash, jaundice, hepatosplenomegaly, and diarrhea
GVHD
What is the <span style="text-decoration: underline;">mediator </span>and <span style="text-decoration: underline;">timeframe</span> in Hyperacute rejection
preformed antidonor antibodies<br><br>minutes
What is the <span style="text-decoration: underline;">mediator </span>and <span style="text-decoration: underline;">timeframe</span> in Acute rejection
Tc cells reacting against foreign MHCs of the donor<br /><br />days to weeks
What is the <span style="text-decoration: underline;">mediator </span>and <span style="text-decoration: underline;">timeframe</span> in Chronic rejection
T cell and Ab mediated vascular damage (obliterative vascular fibrosis)<br><br>months to years
Which 2 types of transplant rejection are irreversible? which 1 is reversible?
irreversible: hyperacute and chronic<br>reversible: acute
Anti-basement membrane antibodies
Goodpastur syndrome
Antiacetylcholine receptor antibodies
Myasthenia gravis
Anticentromere antibodies
CREST syndrome
Antiendomysial and antigliadin
Celiac disease
What 3 antibodies may be present in Type 1 DM
anti-insulin<br>anti-islet cell<br>anti-glutamate decarboxylase
Anti-intrinsic factor, anti-parietal cell
pernicious anemia<br>
antimicrosomal antibodies
Hashimoto's thyroiditis
antithyroglobulin antibodies
Hashimoto's thyroiditis
Antimitochondrial antibodies
primary biliary cirrhosis
antimyeloperoxidase antibodies (p-ANCA)
microscopic polyangiitis
Antiproteinase 3 (c-ANCA)
Wegener's granulomatosis
Antiribonucleoprotein (Anti-U1-RNP)
mixed connective tissue disease
anti-TSH receptor
Grave's disease
ANA
SLE
Anti-dsDNA, anti-smith
SLE<br>
antihistone antibodies
Drug induced lupus
Anti-IgG
Rheumatoid factor
Anti-Scl-70
Scleroderma
Anti-desmoglein
Pemphigus vulgaris
Anti-Jo1
Polymyositis, dermatomyositis
Anti-SS-A (anti-Ro), Anti-SS-B (anti-La)
Sjogren's syndrome
Anti-smooth muscle
Autoimmune hepatitis
Agar for Haemophilus influenzae
Chocolate agar with factors V (NAD) and X (hematin)
N. gonorrhoeae agar
Thayer Martin media
B. pertussis agar
Bordet-Gengou (potato) agar
C. diphtheriae culture
Tellurite plate, Loffler's media
M. tuberculosis culture
Lowenstein-Jensen agar
M. pneumoniae culture
Eaton's agar (pyrimidines, purines, cholesterol)
E. coli culture
blue-black colonies with metallic sheen on Eosin-methylene blue (EMB) agar<br>
Legionella culture
Charcoal Yeast Extract agar
Sabourad's agar
Fungi
TCBS agar
V. cholera
Thioglycolate agar
Anaerobes
Enteric pathogens culture
Hektoen enteric agar or xylose-lysine-deoxycholate agar
Bipolar staining
Y. pestis
kidney-shaped diplococci
Neisseria<br>
Lancet-shaped diplococci
S. pneumoniae
Metachromatic staining
Corynebacterium
Gull's wings
Campylobacter
Catalase Positive Organisms
If you've got CGD, make <span style="font-weight:600;">SPACE</span> for organisms with catalase!<br><br>Staph<br>Pseudomonas<br>Aspergillus<br>Candida<br>Enterobacteriaciae
The only Gram positive bacterium that has endotoxin
Listeria
Name the 2 toxins that are Superantigens
Staphylococcus aureus: Toxic Shock Syndrome (TSST-1)<br>Streptococcus pyogenes: Scarlet fever (erythrogenic toxin)
Name the 4 ADP ribosylating (A-B) toxins and their targets
Cholera toxin: Gs (<span style="text-decoration: underline;">activates</span>)<br />ETEC heat labile toxin: Gs (<span style="text-decoration: underline;">activates</span>)<br />Pertussis toxin: Gi (inactivates)<br /><br />Diphtheria: EF-2 (inactivates)<br />Pseudomonas: EF-2 (inactivates)
Name the 4 toxins that increase cAMP
<span style="font-weight:600;">cAMP</span><br><br><span style="font-weight:600;">C</span>=<span style="font-weight:600;"> </span>cholera toxin<br><span style="font-weight:600;">A</span>=<span style="font-weight:600;"> </span>anthrax toxin<br><span style="font-weight:600;">∑</span>= ETEC heat labile toxin<br><span style="font-weight:600;">P= </span>Pertussis toxin
which bacterial toxin is in itself a bacterial adenyl cyclase?
bacillus anthracis toxin
Which 2 toxins cleave host cell rRNA (inactivate 60S ribosome)
Shiga toxin<br>Vero toxin (EHEC)
5 Bacterial toxins encoded in a lysogenic phage
ABCDE<br><br>Shig<span style="font-weight:600;">A</span>-like toxin<br><span style="font-weight:600;">B</span>otulinum toxin<br><span style="font-weight:600;">C</span>holera toxin<br><span style="font-weight:600;">D</span>iphtheria toxin<br><span style="font-weight:600;">E</span>rythrogenic toxin of S. pyogenes
Fungal Pneumonia in Eastern states
Blastomycosis
Fungal Pneumonia in Mississippi and Ohio river valleys
Histoplasmosis
Fungal Pneumonia in Rural Latin America
Paracoccidiomycosis
Fungal Pneumonia in Southwestern states
Coccidiomycosis
45 degree branching septate hyphae
Aspergillus
pseudohyphae + budding yeasts at 20 degrees C
Candida<br>
Pigeon droppings
Cryptococcus
Bat and bird droppings
Histoplasma
irregular nonseptate hyphae branching at obtuse angles
Mucor and Rhizopus<br>
Treatment of toxoplasmosis
sulfadiazine + pyrimethamine
Treatment of most trematodes and cestodes
Praziquantel<br><br>except neurocysticercosis and Echinococcus granulosus: Albendazole
Treatment of Loa loa, Wuchereria bancrofti, and Toxocara canis
Diethylcarbamazine
Treatment of Onchocerca volvulus (rIVER blindness)
IVERmectin
Treatment of Dracunculus medinensis
Niridazole<br>
Treatment of intesitnal nematodes
Mebendazole
rose gardener's disease
sporotrichosis (local pustule or ulcer + ascending lymphangitis)<br><br>cigar shaped budding yeast visible in pus
All DNA viruses are dsDNA except <span style="font-weight:600; color:#0000ff;">[...]</span>
All DNA viruses are dsDNA except <span style="font-weight:600; color:#0000ff;">parvovirus ("part-of-a-virus")</span>
All RNA viruses are ssRNA except <span style="font-weight:600; color:#0000ff;">[...]</span>
All RNA viruses are ssRNA except <span style="font-weight:600; color:#0000ff;">reovirus ("repeato-virus") which is dsRNA</span>
Name the most prominent parvovirus and it's diseases
B19:<br>1. aplastic crisis in sickle cell disease<br>2. fifth disease (erythema infectiosum "slapped cheeks" rash)<br>3. hydrops fetalis
Name the herpes viruses
<span style="font-weight:600;">CHEV</span>rolet<br><br>CMV<br>HSV-1, HSV-2, HHV-6, HHV-8<br>EBV<br>VZV
what is the most prominent Polyomavirus and what diseases does it cause?
JC virus: PML (in HIV)
PML
progressive multifocal leukoencephalopathy (caused by the JC virus)
Segmented viruses
BOAR (all are RNA viruses)<br><br>Bunyaviruses, Orthomyxoviruses, Arenaviruses, Reoviruses
Name the 2 Reoviruses and their diseases
Reovirus: Colorado tick fever<br>Rotavirus: MCC of fatal diarrhea in children
Picornaviruses
<span style="font-weight:600;">PERCH </span>on a "peak"<br><br>Poliovirus<br>Ecohvirus (meningitis)<br>Rhinovirus<br>Coxsackievirus (meningitis, herpangina, hand foot &amp; mouth disease, myocarditis)<br>HAV
Caliciviruses
Norwalk virus: gastroenteritis
Flaviviruses
HCV<br>Yellow Fever<br>Dengue<br>St. Louis encephalitis<br>West Nile virus
Togaviruses
Early Romans Wore Togas<br><br>EEE (Eastern equine encephalitis)<br>Rubella<br>WEE (Western equine encephalitis)
Retroviruses
have reverse transcriptase<br><br>HIV<br>HTLV
Coronavirus
common cold and SARS
Paramyxoviruses
<span style="font-weight:600;">P</span>a<span style="font-weight:600; text-decoration: underline;">R</span>a<span style="font-weight:600;">M</span>yxoviruses<br><br><span style="font-weight:600;">P</span>arainfluenza: croup<br><span style="font-weight:600;">R</span>SV: bronchiolitis in rabies <span style="color:#ff208c;">(Rx is ribavirin)</span><br><span style="font-weight:600; color:#000000;">R</span><span style="color:#000000;">ubeola: Measles</span><br><span style="font-weight:600; color:#000000;">M</span><span style="color:#000000;">umps</span>
Filoviruses
Ebola/Marburg hemorrhagic rever
Arenaviruses
LCMV (lymphocytic chroiomeningitis virus)<br>Lassa fever encephalitis
Bunyaviruses
Bunyaviruses viciously destroy <span style="font-weight:600;">CH</span>u<span style="font-weight:600;">RCH</span>e<span style="font-weight:600;">S</span><br><br><span style="font-weight:600;">C</span>alifornia encephalitis<br /><span style="font-weight:600;">H</span>antavirus<br><span style="font-weight:600;">R</span>ift valley fever virus<br /><span style="font-weight:600;">C</span>rimean-<span style="font-weight:600;">C</span>ongo <span style="font-weight:600;">h</span>emorrhagic fever<br /><span style="font-weight:600;">S</span>andfly fever virus
Deltavirus
HDV
HIV-associated infections when CD4 count is &lt;400
Superficial infections: oral thrush, tinea pedis, hairy leukoplakia<br>Reactivation of: TB, VZV<br>Other bacterial infections (H. influenzae, S. pneumoniae, Salmonella)
HIV-associated infections when CD4 count is &lt;200
Cysts: Pneumo<span style="font-weight:600;">cyst</span>is pneumonia, Crytposporidium and Isospora (acid fast <span style="font-weight:600;">cysts</span>)<br>Reactivation of HSV<br>disseminated coccidiodomycosis<br>
HIV-associated infections when CD4 count is &lt;100
Candidal esophagitis, toxoplasmosis, histoplasmosis
HIV-associated infections when CD4 count is &lt;50
CMV Retinitis and esophagititis<br>disseminated MAI<br>Cryptococcal meningoencephalitis
Identify 1, 2, and 3<br><img src="ccff52a1f20f6cf06a716f77639c51ed.jpg" />
1: gp120<br>2: gp41<br>3: lipid membrane
Identify 4 and 5<br><img src="ccff52a1f20f6cf06a716f77639c51ed.jpg" />
4: p17 matrix protein<br>5: p24 capsid
Identify 6 and 7<br><img src="ccff52a1f20f6cf06a716f77639c51ed.jpg" />
6: RNA<br>7: reverse transcriptase
Structure of the Spleen
White Pulp:<br>1. PALS: T cells<br>2. Follicles: B cells<br><br>Red pulp: <br>1. Splenic cords: reticular cells, B and T cells, macrophages, blood cells (RBCs, platelets, granulocytes) [basically everything]<br>2. Sinusoids: Macrophages
LNs that drain stomach
celiac
LNs that drain duodenum, jejunum
superior mesenteric
LNs that drain sigmoid colon
colic --&gt; inferior mesenteric
LNs that drain upper limb and breast
axillary
LNs that drain rectum (lower part) and anal canal (above pectinate line)
internal iliac
LNs that drain anal canal below pectinate line
superficial inguinal
LNs that drain scrotum and thigh
superficial inguinal
LNs that drain Testes
para-aortic
LNs that drain lateral side of dorsum of foot
popliteal
Function of Th1 cells
Make IL-2, IFN-gamma<br>Activate macrophages and Tc cells<br><br><br>Inhibited by IL-10
Functions of Th2 cells
Make IL-4, IL-5, IL-10<br />Help B cells make antibody<br /><br /><br />Inhibited by IFN-gamma
Activity of Natural Killer cells is enhanced by:
IL-12, IFN-alpha, IFN-beta
Main function of Interleukins 1, 2, 3, 4, and 5
<span style="font-weight:600;">Hot T</span>-<span style="font-weight:600;">Bone</span> st<span style="font-weight:600;">EA</span>k<br /><br />IL-1: fever (Hot)<br />IL-2: growth of <span style="font-weight:600;">T</span> cells (Th and Tc)<br />IL-3: growth and differentiation of <span style="font-weight:600;">bone </span>marrow stem cells<br />IL-4: Ig<span style="font-weight:600;">E</span> production (class switching)<br />IL-5: Ig<span style="font-weight:600;">A</span> production (class switching) + activates eosinophils
IL-6
production of acute phase reactants and immunoglobulins
IL-8
Chemotactic factor for neutrophils
IL-10
inhibits Th1 cells
IL-12
activates NK cells and Th1 cells
IFN-gamma
stimulates macrophages
TNF
mediates septic shock<br>- leukocyte recruitment<br>- vascular leak
CD4, TCR, CD3, CD28, CD40L
Th cell
CD8, TCR, CD3
Tc cell
IgM, B7, CD19, CD20, CD21, CD40, MHC II
B cell
MHC II, B7, CD40, CD14, Fc receptor, C3b receptor
Macrophages
receptors for MHC I, CD16, CD56
NK cell
MHC I
all nucleated cells + platelets
MHC II
APCs (B cells, macrophages, dendritic cells)
Cefepime
4th generation cephalosporin
Ceftriaxone
3rd generation cephalosporin
Cefoperazone
3rd generation cephalosporin
Cefoxitin
2nd generation cephalosporin
Cefaclor
2nd generation cephalosporin
Cefotaxime
3rd generation cephalosporin
Cefuroxime
2nd generation cephalosporin
Cefotetan
2nd generation cephalosporin<br>
Cephalexin
1st generation cephalosporin
Cefazolin
1st generation cephalosporin
Ceftazidime
3rd generation cephalosporin
Spectrum of 1st generation cephalosporins
PECK<br><br>Proteus<br>E. coli<br>Cocci (gram positive)<br>Klebsiella
Spectrum of 2nd generation cephalosporin
HEN PECKS<br><br>Haemophilus influenzae<br>Enterobacter<br>Neisseria<br><br>Proteus<br>E. coli<br>Cocci (gram positive)<br>Klebsiella<br>Serratia
Use of 3rd generation cephalosporin
serious gram negative infections resistant to other beta lactams<br><br>e.g. meningitis (ceftriaxone)
Cephalosporins used to treat Pseudomonas
Taz, Fep, Fop<br><br>Ceftazidine<br><br>Cefepime<br><br>Cefoperazone
Lipid-soluble cephalosporins (eliminated in bile)
Ceftriaxone<br>Cefoperazone<br>Cefomandole
Lipid-soluble penicillins
Nafcillin and Oxacillin (excreted in bile)<br><br>Amoxicillin (enterohepatic cycling but excreted by kidneys)
Magic bullet for Gram negative <span style="font-weight:600;">Aerobes</span>? e.g. Klebsiella, Pseudomonas, Serratia
Aztreonam<br><br>(no activity against gram positives or anaerobes)
Imipinem is always adiminstered with <span style="font-weight:600; color:#0000ff;">[...]</span>
Imipinem is always adiminstered with <span style="font-weight:600; color:#0000ff;">cilastatin</span>
Cilastatin
inhibitor of renal dihydropeptidase I (which inactivates impinem in renal tubles)
Spectrum of Imipenem and meropenem
Widest spectrum of any antibiotic: Gram positive cocci, gram negative rods, anaerobes (drug of choice for Enterobacter)<br><br>But <span style="font-weight:600; text-decoration: underline;">NOT</span>: MRSA, atypical bacteria, some Pseudomonas
Side effects of Imipenem
GI stress<br>Skin rash<br>Seizures (less with meropenem)
Spectrum of Linezolid
Gram positives (including anaerobes) e.g. VRSA, VRE, drug-resistant pneumococci<br><br>but NOT Gram negatives
Side effects of Linezolid
bone marrow suppression (platelets)<br>
Streptogramins (Quinupristin, Dalfopristin)
VRSA, VRE, drug-restistant pneumococci<br><br>MOA similar to TTC
VRE (faecalis and faecium)
Streptogramins treat only E. faecium<br>Lenezolid treats both.
Aminoglycosides
"Mean" <span style="font-weight:600;">GNATS </span>canNOT kill anaerobes<br><br>Gentamycin<br>Neomycin<br>Amikacin<br>Tobramycin<br>Streptomycin<br><br>
Bugs resistant to Aminoglycosides
Amin<span style="font-weight:600;">O2</span>glycosides<br><br>Require O2 for uptake, therefore ineffective against anaerobes
Streptomycin
Aminoglycoside used to treat<br><br><span style="font-weight:600;">TB</span><br><span style="font-weight:600;">T</span>ularemia<br><span style="font-weight:600;">B</span>ubonic plague
Side effects of Vancomycin
Nephrotoxic<br>Ototoxic<br>Thrombophlebitis<br>Red man syndrome (diffuse flushing): can be prevented by pretreatment with antihistamines and slow infusion rate.
Side effects of Aminoglycosides
Nephrotoxic<br>Ototoxic<br>Teratogenic<br>Neuromuscular blokade (decreases acetylcholine release) --&gt; increases effects of skeletal muscle relaxants
Uses of Tetracyclines
A<span style="font-weight:600;">T</span>ypicals (chlamydia, ureaplasma, mycoplasma)<br><span style="font-weight:600;">T</span>ick-borne diseases (Rickettsia, Tularemia, Borrelia)<br>Acne<br>Vibrio<br><br>Doxyclicline: Prostatitis<br>Demeclocycline: SIADH<br>Minocycline: meningococcal carriers (or Rifampin)
Macrolides
Erythromycin, Azithromycin, Clarithromycin<br><br>Gram-positive cocci<br>Mycoplasma<br>*Legionella*<br>Chlamydia<br>Neisseria<br><br>URIs, Pneumonias, STDs
Treatment of Osteomyelitis (bone penetrating drugs)
Gram positive: Vancomycin<br>Gram negative: Quinolones
Lipid soluble Tetracycline
doxycycline
Lipid soluble Macrolide
Azithromycin
Antibiotics that potentiate neuromuscular blockers
Aminoglycosides<br>Clindamycin
Use of Clindamycin
<span style="font-weight:600;">Anaerobic infections above the diaphragm</span><br><br>Bacteroides fragilis<br>Clostridium perfringens
MCC of clostridium difficile pseudomembranous colitis?
Clindamycin
MOA of sulfonamides
inhibit dihydropteroate synthetase
Use of of SMX-TMP
Nocardia<br />UTIs<br />PCP<br /><br />Gram positives<br />Gram negatives (shigella, salmonella)
Sulfasalazine
Sulfonamide<br><br>prodrug of salicylate used in <span style="font-weight:600;">ulcerative colitis </span>and <span style="font-weight:600;">rheumatoid arthritis</span>
Mechanism of Drug resistance to Aminoglycosides
conjugation: acetylation, adenylation, or phosphorylation
Mechanism of Drug resistance to Penicillins/Cephalosporins
1. Penicillinase<br>2. PBP changes (MRSA)<br>3. porins (gram negatives)
Mechanism of Drug resistance to Vancomycin
D-ala-D-ala to D-ala-D-lactate
Mechanism of Drug resistance to Chloramphenicol
acetylation
Mechanism of Drug resistance to TTC
pumped out of bacteria
Mechanism of Drug resistance to Sulfonamides
1. altered enzyme (dihydropteroate synthetase)<br>2. -- uptake<br>3. ++ PABA synthesis
Mechanism of Drug resistance to Quinolones
1. altered enzyme (gyrase)<br>2. -- uptake
Antibiotic used to treat hypercortisolism
Ketoconazole
Side effects of Protease Inhibitors
GI upset<br>Hyperglycemia<br>Lipodystrophy<br>Thrombocytopenia<br>P450 inhibitors
Which HIV drugs causes pancreatitis
Ritonavir<br>Didanosine<br>Zalcitabine
Which HIV drug causes kidney stones
Indinavir
ZDV
Zidovudine
ddI
Didanosine
ddC
Zalcitabine
d4T
stavudine
3TC
lamivudine
Which HIV drugs causes peripheral neuropathy and pancreatitis
Didanosine<br>Zalcitabine
ANtibiotics to Avoid in pregnancy
SAFE Moms Take Really Good Care<br><br>Sulfonamides: kernicterus<br>Aminoglycosides: ototoxicity<br>Fluoroquinolones: cartilage damage<br>Erythromycin estolate: acute cholestatic hepatitis in mom<br><br>Metronidazole: mutagenesis<br>Tetracyclines: discolored teeth, inhibit growth<br>Ribavirin: teratogenic<br>Griseofulvin: teratogenic<br>Chloramphenicol: "gray baby"
Cerebellar defects (ataxia)<br>Spider angiomas (telangiectasia)<br>IgA deficiency
ataxia-telangiectasia (defect in DNA repair enzymes)
MOA of cyclosporine
forms complex with cyclophilins --&gt; inhibit calcineurin --&gt; block T-cell activation and differentiation
MOA of Muromonab
Binds to CD3 --&gt; inhibits T-cell activation (2nd signal)
MOA of Azathioprine
antimetabolite (precursor of 6-MP)
Immunosuppressant that is nephrotoxic
Cyclosporine
Immunosuppressant that is nephrotoxic, neurotoxic, causes hypertension, hyperglycemia, and pleural effusion
Tacrolimus
Immunosuppressant that causes bone marrow suppression
Azathioprine
Immunosuppressant that causes cytokine release syndrome
Muromonab
Immunosupressant that leads to hyperlipidemia, thrombocytopenia, leukopenia
Sirolimus
MOA of Tacrolimus
forms complex with FK-binding proteins --&gt; inhibit calcineurin --&gt; -- IL-2 --&gt; -- T-cell activation and differentiation
MOA of Daclizumab
Mab against IL-2 receptor