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330 Cards in this Set

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Bacterial Structures, describe function/composition of:
peptidoglycan--
gram + cell wall--
gram - outer membrane--
plasma membrane--
peptidoglycan--
*Gives rigid support, protects against osmotic pressure.
*Sugar backbone with peptide side chains cross­ linked by transpeptidase.

gram + cell wall--
*Major surface antigen.
*Peptidoglycan for support. Lipoteichoic acid induces TNF and IL-1.

gram - outer membrane--
*Site of endotoxin [LPS]; major surface antigen.
*Lipid A induces TNF and IL-1; O polysaccharide is the antigen.

plasma membrane--
*Site of oxidative and transport enzymes.
*Lipoprotein bilayer.
Bacterial Structures, describe function/composition of:
ribosome--
periplasm--
capsule--
pilus/fimbria--
ribosome--
*Protein synthesis.
*50S and 30S subunits.

periplasm--
*Space between the cytoplasmic membrane and outer membrane in gram-negative bacteria.
*Contains many hydrolytic enzymes, including ß-lactamases.

capsule--
*Protects against phagocytosis.
*Polysaccharide (except Bacillus anthracis, which contains D-glutamate).

pilus/fimbria--
*Mediate adherence of bacteria to cell surface; sex pilus forms attachment between 2 bacteria during conjugation.
*Glycoprotein.
Bacterial Structures, describe function/composition of:
flagellum--
spore--
plasmid--
glycocalyx--
flagellum--
*Motility.
*Protein.

spore--
*Resistant to dehydration, heat, and chemicals.
*Keratin-like coat; dipicolinic acid; peptidoglycan.

plasmid--
*Contains a variety of genes for antibiotic resistance, enzymes, and toxins.
*DNA.

glycocalyx--
*Mediates adherence to surfaces, especially foreign surfaces (e.g., indwelling catheters).
*Polysaccharide.
Bacterial CW diagrams:
List all the cocci:
List all gram + rods:
Clostridium
Corynebacterium
Bacillus
Listeria
Mycobacterium (acid fast) 
Gardnerella (Gram variable)
Clostridium
Corynebacterium
Bacillus
Listeria
Mycobacterium (acid fast)
Gardnerella (Gram variable)
List all the enterics: 13
• E. coli
• Shigella
• Salmonella
• Yersinia
• Klebsiella
• Proteus
• Enterobacter
• Serratia
• Vibrio
• Campylobacter 
• Helicobacter
• Pseudomonas
• Bacteroides
• E. coli
• Shigella
• Salmonella
• Yersinia
• Klebsiella
• Proteus
• Enterobacter
• Serratia
• Vibrio
• Campylobacter
• Helicobacter
• Pseudomonas
• Bacteroides
List the respiratory-acquired bacteria: 3
• Haemophilus (pleomorphic)
• Legionella (silver)
• Bordetella
• Haemophilus (pleomorphic)
• Legionella (silver)
• Bordetella
List the zoonotic bacteria: 4
Zoonotic:
• Francisella 
• Brucella
• Pasteurella 
• Bartonella
Zoonotic:
• Francisella
• Brucella
• Pasteurella
• Bartonella
List the branching filamentous bacteria: 2
Actinomyces
Nocardia (weakly acid fast)
Actinomyces
Nocardia (weakly acid fast)
What are the pleomorphic bacteria?
Rickettsiae (Giemsa)
Chlamydiae (Giemsa)
What are the spiral bacteria?
Spirochetes:
• Leptospira
• Borrelia (Giemsa)
• Treponema
Spirochetes:
• Leptospira
• Borrelia (Giemsa)
• Treponema
Wall-less bacteria?
Mycoplasma (does not Gram stain)
Mycoplasma (does not Gram stain)
Bacteria with unusual cell membranes/walls:
Mycoplasma-- Contain sterols and have no cell wall.

Mycobacteria-- Contain mycolic acid. High lipid content.
Gram stain limitations--These bugs do not Gram stain well: why?

mnemonic?
*These Rascals May Microscopically Lack Color*

Treponema (too thin to be visualized).
Treponemes-- Use dark-field microscopy and fluorescent antibody staining.

Rickettsia (intracellular parasite).

Mycobacteria (high lipid content in cell wall detected by carbolfuchsin in acid-fast stain).

Mycoplasma (no cell wall).

Legionella pneumophila (primarily intracellular).
Legionella-- Use silver stain.

Chlamydia (intracellular parasite; lacks muramic acid in cell wall).
What bugs do you use a Giemsa stain for? mnemonic
*Certain Bugs Really Try my Patience*

Chlamydia, Borrelia, Rickettsiae, Trypanosomes, Plasmodium.
What's a PAS stain and what's it good for?
PAS = periodic acid-Schiff

Stains glycogen, mucopolysaccharides; used to diagnose Whipple's disease (Tropheryma whipplei).

*PASs the sugar.*
What's a Ziehl-Neelsen stain? What's it good for?
ZN = carbol fuchsin

Acid-fast organisms (Nocardia, Mycobacterium).
What's an India ink stain good for seeing?
Cryptococcus neoformans (mucicarmine can also be used to stain thick polysaccharide capsule red).
What's a silver stain good for seeing?
Fungi (e.g., Pneumocystis), Legionella, Helicobacter pylori.
Special culture requirements for:
h. flu--
n. gonorrhoeae, n. meningitidis--
b. pertussis--
c. diphtheriae--
h. flu-- Chocolate agar with factors V (NAD+) and X (hematin)

n. gonorrhoeae, n. meningitidis-- Thayer-Martin (or VPN) media-- Vancomycin (inhibits gram-positive organisms), Polymyxin (inhibits gram-negative organisms except Neisseria), and Nystatin (inhibits fungi); "to connect to Neisseria, please use your VPN client"

b. pertussis-- Bordet-Gengou (potato) agar (Bordet for Bordetella)

c. diphtheriae-- Tellurite plate, Loffler's media
Special culture requirements for:
m. tb--
m. pneumonia--
lactose-fermenting enterics--
legionella--
fungi--
m. tb-- Lowenstein-Jensen agar

m. pneumonia-- Eaton's agar

lactose-fermenting enterics-- Pink colonies on MacConkey's agar (fermentation produces acid, turning colony pink); E. coli is also grown on eosin-methylene blue (EMB) agar as colonies with green metallic sheen.

legionella-- Charcoal yeast extract agar buffered with cysteine and iron

fungi-- Sabouraud's agar. "Sab's a fun guy!"
Discuss obligate aerobes and give examples:
Use an O2-dependent system to generate ATP.

Reactivation of M. tuberculosis (e.g., after immune compromise or TNF-a inhibitor use) has a predilection for the apices of the lung, which have the highest PO2.

P. aeruginosa is an aerobe seen in burn wounds,
complications of diabetes, nosocomial pneumonia, and pneumonias in cystic fibrosis patients.

Examples include Nocardia, Pseudomonas aeruginosa, Mycobacterium tuberculosis, and Bacillus.
*Nagging Pests Must Breathe*
Discuss obligate anaerobes and give examples:

What antibiotic class won't work vs them? Why?
Examples include Clostridium, Bacteroides, and Actinomyces.
*Anaerobes Can't Breathe Air*

They lack catalase and/or superoxide dismutase and are thus susceptible to oxidative damage.

Generally foul smelling (short-chain fatty acids), are difficult to culture, and produce gas in tissue (CO2 and H2).

Anaerobes are normal flora in GI tract, pathogenic elsewhere.

Aminoglycosides are ineffective against anaerobes because these antibiotics require O2 to enter into bacterial cell.
What bugs are intracellular? Why?
Facultative?
OI: Rickettsia, Chlamydia. Can't make own ATP.

FI: Salmonella, Neisseria, Brucella, Mycobacterium,
Listeria, Francisella, Legionella, Yersinia pestis.
*Some Nasty Bugs May Live FacultativeLY*
How do you identify an encapsulated bacterium?

examples of them?

clinical correlation?
Positive quellung reaction-- if encapsulated bug is present, capsule swells when specific anticapsular antisera are added.
*Quellung = capsular "swellung"*

Examples are Streptococcus pneumoniae, Haemophilus influenzae type B, Neisseria meningitidis, Escherichia coli, Salmonella, Klebsiella pneumoniae, and group B Strep.
*SHiNE SKiS*

Their capsules serve as an antiphagocytic virulence factor. Capsule + protein conjugate serve as an antigen in vaccines.

Encapsulated bacteria are opsonized, and then cleared by spleen. Asplenics have decreased opsonizing ability and are at risk for severe infections. Give S. pneumoniae, H. influenzae, N. meningitidis vaccines.
Discuss catalase positive bacteria:

clinical correlation:

examples:
Catalase degrades H2O2 before it can be converted to microbicidal products by the enzyme myeloperoxidase.

People with chronic granulomatous disease (NADPH oxidase deficiency) have recurrent infections with these microbes because they degrade the limited H2O2.

Examples: Pseudomonas, Listeria, Aspergillus, Candida, E. coli, S. aureus, Serratia.

*You need PLACESS for your cats*
Discuss conjugate vaccines. Why do they work?

3 examples?
For vaccines containing polysaccharide capsule antigens, a protein is conjugated to the polysaccharide antigen to promote T-cell activation and subsequent class switching.

A polysaccharide antigen alone cannot be presented to T cells; therefore, only IgM antibodies would be produced.

*Pneumovax (polysaccharide vaccine with no conjugated protein) and Prevnar (conjugated vaccine)

*H. influenzae type B (conjugated vaccine)

*Meningococcal vaccines (conjugated vaccines)
What are the Urease-positive bugs?
mnemonic
Cryptococcus, H. pylori, Proteus, Ureaplasma, Nocardia, Klebsiella, S. epidermidis, S. saprophyticus.

*CHuck Norris hates PUNKSS*
Pigment producing bacteria: 4
Actinomyces israelii-yellow "sulfur" granules, which are composed of filaments of bacteria.
*Israel has yellow sand*

S. aureus-yellow pigment.
*aureus (Latin) = gold*

Pseudomonas aeruginosa-blue-green pigment.
*Aerugula is green*

Serratia marcescens-red pigment.
*Serratia marcescens-think red maraschino cherries*
Main function of bacterial virulence factors?

List 3 and describe how they work. Give an example of what bug they're found in.
*They promote evasion of host immune response.

Protein A: Binds Fc region of Ig. Prevents opsonization and phagocytosis. Expressed by S. aureus.

lgA protease: Enzyme that cleaves IgA. Secreted by S. pneumoniae, H. influenzae type B, and Neisseria (SHiN) in order to colonize respiratory mucosa.

M protein: Helps prevent phagocytosis. Expressed by group A streptococci.
Exotoxins:
source--
secreted?
chemistry--
location of genes--
toxicity--
clinical effects--
mode of action--
antigenicity--
vaccines--
heat stability--
typical diseases-- 3
source-- Certain species of some gram-positive and gram-negative bacteria

secreted? Yes

chemistry-- Polypeptide

location of genes-- Plasmid or bacteriophage

toxicity-- High (fatal dose on the order of 1 µg)

clinical effects-- Various

mode of action-- Various

antigenicity-- Induces high-titer Abs called antitoxins

vaccines-- Toxoids used as vaccines

heat stability-- Destroyed rapidly at 60°C (except staphylococcal enterotoxin)

typical diseases-- Tetanus, botulism, diphtheria
Exotoxins:
source--
secreted?
chemistry--
location of genes--
toxicity--
clinical effects--
mode of action-- 2
antigenicity--
vaccines--
heat stability--
typical diseases-- 2
source-- Outer cell membrane of most gram-negative bacteria

secreted? No

chemistry-- Lipopolysaccharide (structural part of bacteria; released when lysed)

location of genes-- Bacterial chromosome

toxicity-- Low (fatal dose on the order of hundreds of
micrograms)

clinical effects-- Fever, shock

mode of action-- Induces TNF and IL-1

antigenicity-- Poorly antigenic

vaccines-- No toxoids formed and no vaccine available

heat stability-- Stable at l00°C for 1 hour

typical diseases-- Meningococcemia; sepsis by gram-negative rods
Bugs with Exotoxins that Inhibit protein synthesis: 4
name their toxin--
discuss their mechanism--
identify the manifestation of each--
a= Toxin is an ADP ribosylating A-B toxin: B (binding) component binds to host cell surface receptor, enabling endocytosis; A (active) component attaches ADP-ribosyl to disrupt host cell proteins.
Bugs with Exotoxins that increase fluid secretion: 3
name their toxin--
discuss their mechanism--
identify the manifestation of each--
a= Toxin is an ADP ribosylating A-B toxin: B (binding) component binds to host cell surface receptor, enabling endocytosis; A (active) component attaches ADP-ribosyl to disrupt host cell proteins.
Bugs with Exotoxins that inhibit phagocytic ability: 1
name their toxin--
discuss their mechanism--
identify the manifestation of each--

Bugs with Exotoxins that inhibit phagocytic ability: 2
name their toxin--
discuss their mechanism--
identify the manifestation of each--
Bugs with Exotoxins that lyse cell membranes: 2
name their toxin--
discuss their mechanism--
identify the manifestation of each--
Bugs with Exotoxins that are SAgs, causing shock: 2
name their toxin--
discuss their mechanism--
identify the manifestation of each--
What is endotoxin and what does it do?
activates what 3 things and causes what effects?
mnemonic of effects:
*A lipopolysaccharide found in outer membrane
of gram-negative bacteria.

ENDOTOXIN: 
Edema
Nitric oxide 
DIC/Death
Outer membrane 
TNF-a
O-antigen
eXtremely heat stable 
IL-1
Neutrophil chemotaxis
*A lipopolysaccharide found in outer membrane
of gram-negative bacteria.

ENDOTOXIN:
Edema
Nitric oxide
DIC/Death
Outer membrane
TNF-a
O-antigen
eXtremely heat stable
IL-1
Neutrophil chemotaxis
Bacterial growth curve; define these phases:
Lag phase--
Exponential/log phase--
Stationary phase--
Death--
Lag phase-- Metabolic activity without division.

Exponential/log phase-- Rapid cell division. Penicillins and cephalosporins act here as peptidoglycan is being made.

Stationary phase-- Nutrient depletion slows growth. Spore formation in some...
Lag phase-- Metabolic activity without division.

Exponential/log phase-- Rapid cell division. Penicillins and cephalosporins act here as peptidoglycan is being made.

Stationary phase-- Nutrient depletion slows growth. Spore formation in some bacteria.

Death-- Prolonged nutrient depletion and buildup of waste products lead to death.
Bacterial genetics; discuss transformation:

what 4 bacteria are significant for doing this?
Ability to take up naked DNA (i.e., from cell lysis) from environment (also known as "competence").

A feature of many bacteria, especially S. pneumoniae, H. influenzae type B, and Neisseria (SHiN).

Any DNA can be used. Adding deoxyribonuclease to environment will degrade naked DNA in medium --> no transformation seen.
Describe F+ x F- bacterial conjugation:
F+ plasmid contains genes required for sex pilus and conjugation.

Bacteria without this plasmid are termed F-.

Plasmid (dsDNA) is replicated and transferred through pilus from F+ cell.

No transfer of chromosomal genes.
Describe Hfr x F- bacterial conjugation:
F+ plasmid can become incorporated into bacterial chromosomal DNA, termed high-frequency recombination (Hfr) cell.

Replication of incorporated plasmid DNA may include some flanking chromosomal DNA.

Transfer of plasmid AND chromosomal genes.
Describe bacterial transposition:
Segment of DNA that can "jump" (excision and reintegration) from one location to another, can transfer genes from plasmid to chromosome and vice versa.

When excision occurs, may include some flanking chromosomal DNA, which can be incorporated into a plasmid and transferred to another bacterium.
Describe Generalized bacterial transduction:
A "packaging" event. Lytic phage infects bacterium, leading to cleavage of bacterial DNA.

Parts of bacterial chromosomal DNA may become packaged in viral capsid.

Phage infects another bacterium, transferring these genes.
Describe Specialized bacterial transduction:
An "excision" event. Lysogenic phage infects bacterium; viral DNA incorporates into bacterial chromosome.

When phage DNA is excised, flanking bacterial genes may be excised with it.

DNA is packaged into phage viral capsid and can infect another bacterium.
What toxin-encoding genes are encoded in a lysogenic phage? 5

Mnemonic:
• ShigA-like toxin
• Botulinum toxin (certain strains)
• Cholera toxin
• Diphtheria toxin
• Erythrogenic toxin of Streptococcus pyogenes

*ABCDE*
Gram + Lab Algorithm (diagram):
Identification of gram + cocci:
what good is Novobiocin?
NOvobiocin:
Staph Saprophyticus is Resistant
Staph Epidermidis is Sensitive

*On the office's staph retreat, there was NO StRESs*
Identification of gram + cocci:
what good is Optochin?
Optochin:
Strep Viridans is Resistant
Strep Pneumoniae is Sensitive

*OVRPS (overpass)*
Identification of gram + cocci:
what good is Bacitracin?
Bacitracin:
group B strep are Resistant
group A strep are Sensitive

*B-BRAS*
alpha-hemolytic bacteria:
what do they look like on blood agar?
give 2 examples.
Form green ring around colonies on blood agar. Include the following organisms:

• Streptococcus pneumoniae (catalase negative and optochin sensitive)

• Viridans streptococci (catalase negative and optochin resistant)
ß-hemolytic bacteria:
what do they look like on blood agar?
give 4 examples.
Form clear area of hemolysis on blood agar. Include the following organisms:

• Staphylococcus aureus (catalase and coagulase +)

• Streptococcus pyogenes-- group A strep (catalase negative and bacitracin sensitive)

• Streptococcus agalactiae-- group B strep (catalase negative and bacitracin resistant)

• Listeria monocytogenes (tumbling motility, meningitis in newborns, unpasteurized milk)
Staphylococcus aureus
Staphylococcus aureus
Main points about s. aureus:
*Gram-positive cocci in clusters.
*Protein A (virulence factor) binds Fc-lgG, inhibiting complement fixation and phagocytosis.

*TSST is a superantigen that binds to MHC II and T-cell receptor, resulting in polyclonal T-cell activation. Presents as fever, vomiting, rash, desquamation, shock, end-organ failure.

*S. aureus food poisoning is clue to ingestion of preformed toxin.

*Causes acute bacterial endocarditis, osteomyelitis.

*Staph make catalase because they have more "staff." Bad staph (aureus) make coagulase and toxins. Forms fibrin clot around itself; can lead to abscess.
3 bad types of disease that Staph causes:
• Inflammatory disease: skin infections, organ abscesses, pneumonia

• Toxin-mediated disease: toxic shock syndrome (TSST-1), scalded skin syndrome (exfoliative toxin), rapid-onset food poisoning (enterotoxins)

• MRSA (methicillin-resistant S. aureus) infection: important cause of serious nosocomial and community-acquired infections; resistant to ß-lactams because of altered penicillin-binding protein
staph epidermidis. go.
Infects prosthetic devices and intravenous catheters by producing adherent biofilms.

Component of normal skin flora; contaminates blood cultures.
strep. pneumo is the most common cause of what 4 afflictions?
• Meningitis
• Otitis media (in children)
• Pneumonia
• Sinusitis

*S. pneumoniae MOPS are Most OPtochin Sensitive.*
Describe the appearance of s. pneumo:

What is its virulence main factor?
Lancet-shaped, gram-positive diplococci. 

Encapsulated. IgA protease.

Pneumococcus is associated with "rusty" sputum, sepsis in sickle cell anemia and splenectomy.

No virulence without capsule.
Lancet-shaped, gram-positive diplococci.

Encapsulated. IgA protease.

Pneumococcus is associated with "rusty" sputum, sepsis in sickle cell anemia and splenectomy.

No virulence without capsule.
Streptococcus pneumoniae
Streptococcus pneumoniae
Describe the Viridans group strep:
Viridans streptococci are a-hemolytic. They are normal flora of the oropharynx and cause dental caries (Streptococcus mutans) and subacute bacterial endocarditis at damaged valves (S. sanguis).

Resistant to optochin, differentiating them from S. pneumoniae, which is a-hemolytic but is optochin sensitive.

*Sanguis= blood. There is lots of blood in the heart (endocarditis). S. sanguis sticks to damaged valves by making glycocalyx.

*Viridans group strep live in the mouth because they are not afraid of-the-chin (op-to-chin resistant).
Streptococcus pyogenes (group A streptococci):

3 main things it causes:
Causes:
• Pyogenic: pharyngitis, cellulitis, impetigo
• Toxigenic: scarlet fever, toxic shock-like syndrome, necrotizing fasciitis
• Immunologic: rheumatic fever, acute glomerulonephritis

*Pharyngitis can result in rheumatic "phever" and glomerulonephritis.

*Impetigo more commonly precedes glomerulonephritis than pharyngitis.

*Scarlet fever: scarlet rash sparing face, strawberry (scarlet) tongue, scarlet throat

*Bacitracin sensitive. Antibodies to M protein enhance host defenses against S. pyogenes but can give rise to rheumatic fever.

*ASO titer detects recent S. pyogenes infection.
What is the Jones criteria to diagnose rheumatic fever?
Joints-- polyarthritis
O (heart symbol)-- carditis
Nodules (subcutaneous)
Erythema marginatum
Sydenham's chorea
Streptococcus agalactiae (group B streptococci):
discuss:
*Bacitracin resistant, ß-hemolytic, colonizes vagina; causes pneumonia, meningitis, and sepsis, mainly in babies.

*Group B for Babies!*

*Produces CAMP factor, which enlarges the area of hemolysis formed by S. aureus. (Note: CAMP stands for the authors of the test, not cyclic AMP.) Hippurate test positive.

*Screen pregnant women at 35-37 weeks. Patients with positive culture receive intrapartum penicillin prophylaxis.
Enterococci (group D streptococci):
*Enterococci (Enterococcus faecalis and E. faecium) are normal colonic flora that are penicillin G resistant and cause UTI, biliary tract infections, and subacute endocarditis. 

*Lancefield group D includes the enterococci and the nonenterococc...
*Enterococci (Enterococcus faecalis and E. faecium) are normal colonic flora that are penicillin G resistant and cause UTI, biliary tract infections, and subacute endocarditis.

*Lancefield group D includes the enterococci and the nonenterococcal group D streptococci. Lancefield grouping is based on differences in the C carbohydrate on the bacterial cell wall. Variable hemolysis.

*VRE (vancomycin-resistant enterococci) are an important cause of nosocomial infection.

Enterococci, hardier than nonenterococcal group D, can grow in 6.5% NaCl and bile (lab test).

Entero= intestine, faecalis= feces, strepto= twisted (chains), coccus= berry.
Enterococci (group D streptococci)
Enterococci (group D streptococci)
Streptococcus bovis (group D streptococci):
Colonizes the gut. Can cause bacteremia and subacute endocarditis in colon cancer patients.

*Bovis in the blood= cancer in the colon*
Corynebacterium diphtheriae:
it causes what?
sx?
diagnosis?
prevention?
shape?
staining traits on what agar?
mnemonic?
Causes diphtheria via exotoxin encoded by ß-prophage. Potent exotoxin inhibits protein synthesis via ADP-ribosylation of EF-2.

Symptoms include pseudomembranous pharyngitis (grayish-white membrane) with lymphadenopathy, myocarditis, and arrhythmias.

Lab diagnosis based on gram-positive rods with metachromatic (blue and red) granules and Elek's test for toxin.

Toxoid vaccine prevents diphtheria.

Coryne = club shaped.

Black colonies on cystine-tellurite agar.

ABCDEFG:
ADP-ribosylation, Beta-prophage, Corynebacterium, Diphtheria, Elongation Factor 2, Granules
Talk about bacterial spores:

Spore-forming bacteria? 6
Some bacteria can form spores at the end of the stationary phase when nutrients are limited.

Spores are highly resistant to heat and chemicals. Have dipicolinic acid in their core. Have no metabolic activity. Must autoclave to kill spores by steaming at 121°C for 15 minutes.

Spore-forming gram-positive bacteria found in soil: Bacillus anthracis, Clostridium perfringens, C. tetani.
Other spore formers include B. cereus, C. botulinum, Coxiella burnetii.
C. tetani:
Produces tetanospasmin, an exotoxin causing tetanus. Tetanus toxin (and botulinum toxin) are proteases that cleave releasing proteins for neurotransmitters.

TETanus is TETanic paralysis (blocks glycine and GABA release [inhibitory neurotransmitters]) from Renshaw cells in spinal cord. Causes spastic paralysis, trismus (lockjaw), and risus sardonicus.
C. botulinum:
Produces a preformed, heat-labile toxin that inhibits ACh release at the neuromuscular junction, causing botulism.

In adults, disease is caused by ingestion of preformed toxin. In babies, ingestion of spores in honey causes disease (floppy baby syndrome).

BOTulinum is from bad BOTtles of food and honey (causes a flaccid paralysis).
C. perfringens:
Produces a toxin ("lecithinase," a phospholipase) that can cause myonecrosis (gas gangrene) and hemolysis.

PERFringens PERForates a gangrenous leg.
C. difficile:
Produces 2 toxins. Toxin A, enterotoxin, binds to the brush border of the gut. Toxin B, cytotoxin, destroys the cytoskeletal structure of enterocytes, causing pseudomembranous colitis.

Often 2° to antibiotic use, especially clindamycin or ampicillin. Diagnosed by detection of one or both toxins in stool.

DIfficile causes DIarrhea.

Treatment: metronidazole or oral vancomycin.
Talk about anthrax:
Caused by Bacillus anthracis, a gram-positive, spore-forming rod that produces anthrax toxin. The only bacterium with a POLYPEPTIDE capsule (contains D-glutamate).

Causes cutaneous and pulmonary infection.
Cutaneous anthrax:
Contact --> black eschar (painless ulcer); can progress to bacteremia and death.

Black skin lesions-- black eschar (necrosis) surrounded by edematous ring. Caused by lethal factor and edema factor.
Pulmonary anthrax:
Inhalation of spores - flu-like symptoms that rapidly progress to fever, pulmonary hemorrhage, mediastinitis, and shock.

Woolsorters' disease-- inhalation of spores from contaminated wool.
Bacillus cereus:
Causes food poisoning. Spores survive cooking rice. Keeping rice warm results in germination of spores and enterotoxin formation.

Emetic type usually seen with rice and pasta. Nausea and vomiting within 1-5 hours. Caused by CEREULIDE, a preformed toxin.

Diarrheal type causes watery, nonbloody diarrhea and GI pain in 8-18 hours.

Reheated rice syndrome.
Listeria monocytogenes:
describe it--
and what it causes--
and treatment--
Facultative intracellular microbe; acquired by ingestion of unpasteurized milk/cheese and deli meats or by vaginal transmission during birth. Form "actin rockets" by which they move from cell to cell. Characteristic tumbling motility.

Can cause amnionitis, septicemia, and spontaneous abortion in pregnant women; granulomatosis infantiseptica; neonatal meningitis; meningitis in immunocompromised patients; mild gastroenteritis in healthy individuals.

Treatment: gastroenteritis usually self-limited; ampicillin in infants, immunocompromised patients, and the elderly in empirical treatment of meningitis.
Adinomyces vs. Nocardia:
what do they have in common?
what do they argue about?
-O2 requirements
-staining
-natural habitat
-what they cause
-treatment
Diagram describing 1˚ and 2˚ TB:
TB. caseating granuloma. With multinucleated Langhan's
giant cell (arrow).
TB. caseating granuloma. With multinucleated Langhan's
giant cell (arrow).
What does a positive PPD indicate?

What does a negative PPD indicate?
PPD+ if current infection, past exposure, or BCG vaccinated.

PPD- if no infection or anergic (steroids, malnutrition, immunocompromise) and in sarcoidosis.
Mycobacteria:
what do they have in common?
discuss 3 types and junk they cause:
*All mycobacteria are acid-fast organisms.

*Cord factor in virulent strains inhibits macrophage maturation and induces release of TNF-a. Sulfatides (surface glycolipids) inhibit phagolysosomal fusion. 

*Mycobacterium tuberculosis (TB, often ...
*All mycobacteria are acid-fast organisms.

*Cord factor in virulent strains inhibits macrophage maturation and induces release of TNF-a. Sulfatides (surface glycolipids) inhibit phagolysosomal fusion.

*Mycobacterium tuberculosis (TB, often resistant to multiple drugs). TB symptoms include fever, night sweats, weight loss, and hemoptysis.

*M. kansasii (pulmonary TB-like symptoms).

*M. avium-intracellulare (causes disseminated, non-TB disease in AIDS; often resistant to multiple drugs). Prophylactic treatment with azithromycin.
Mycobacteria showing off its acid fast staining trait.
Mycobacteria showing off its acid fast staining trait.
Leprosy (Hansen's disease):
what bug causes it?
talk about the 2 forms:
treatment:
Caused by Mycobacterium leprae, an acid-fast bacillus that likes cool temperatures (infects skin and superficial nerves-"glove and stocking" loss of sensation) and cannot be grown in vitro. Reservoir in United States: armadillos.

Hansen's disease has 2 forms:
• Lepromatous-presents diffusely over skin rn and is communicable; characterized by low cell-mediated immunity with a humoral Th2 response.
• Tuberculoid-limited to a few hypoesthetic, hairless skin plaques; characterized by high cell-mediated immunity with a largely Th1- type immune response.

Multidrug therapy consisting of dapsone and rifampin
for 6 months for tuberculoid form and dapsone, rifampin, and clofazimine for 2-5 years for lepromatous form.
Facial afflictions of leprosy: 4
lesions of a leper
lesions of a leper
Gram negative lab algorithm:
Lactose-fermenting enteric bacteria:
Grow pink colonies on MacConkey's agar.

Examples include:
Citrobacter
Klebsiella
E. coli
Enterobacter
Serratia.

E. coli produces ß-galactosidase, which breaks down lactose into glucose and galactose.

*Lactose is KEE*
*Test with MacConKEE'S agar*

EMB agar-- lactose fermenters grow as purple/black
colonies. E. coli grows purple colonies with a green sheen.
Talk about penicillin's relationship with gram - bugs:
Gram-negative bacilli are resistant to penicillin G but may be susceptible to penicillin derivatives such as ampicillin and amoxicillin.

The gram-negative outer membrane layer inhibits entry of penicillin G and vancomycin.
Talk very generally about Neisseria. We'll get into details later.
Gram-negative diplococci.

Both ferment glucose and produce IgA proteases.

*MeninGococci ferment Maltose and Glucose.
*Gonococci ferment Glucose.
N. gonorrhoeae within polymorphonuclear leukocytes.
N. gonorrhoeae within polymorphonuclear leukocytes.
Compare/contrast Gonococci and Meningococci:
capsule?
maltose fermenter?
is there a vaccine?
how is it transmitted?
what does it cause?
treatment?
Haemophilus influenzae:
it causes?
appearance? transmission?
culture? mnemonic
treatment
vaccine
HaEMOPhilus causes Epiglottitis ("cherry red" in children), Meningitis, Otitis media, and Pneumonia. Does not cause the flu (influenza virus does).

Small gram-negative (coccobacillary) rod. Aerosol transmission. Most invasive disease caused by capsular
type B.

Nontypeable strains cause mucosal infections (otitis media, conjunctivitis, bronchitis). Produces IgA protease.

Culture on chocolate agar requires factors V (NAD+) and X (hematin) for growth; can also be grown with S. aureus, which provides factor V.
*When a child has "flu," mom goes to five (V) and dime (X) store to buy some chocolate*

Treat meningitis with ceftriaxone. Rifampin prophylaxis in close contacts.

Vaccine contains type B capsular polysaccharide (polyribosylribitol phosphate) conjugated
to diphtheria toxoid or other protein. Given between 2 and 18 months ofage.
Legionella pneumophila:
causes?
appearance of bug?
culture
detection?
transmission? treatment?
Legionnaires' disease = severe pneumonia, fever, GI and CNS symptoms.

Pontiac fever = mild flu-like syndrome.

Gram-negative rod. Gram stains poorly-use silver stain. Grow on charcoal yeast extract culture with iron and cysteine.
*Think of a French legionnaire with his silver helmet, sitting around a campfire (charcoal) with his iron dagger: he is no sissy (cysteine).

Detected clinically by presence of antigen in urine. Labs show hyponatremia.

Aerosol transmission from environmental water source habitat. 

No person-to-person transmission.

Treatment: macrolide or quinolone.
Pseudomonas aeruginosa:
causes what things?
appearance, culture, toxins
treatment
PSEUDOmonas is associated with wound and burn infections, Pneumonia (especially in cystic fibrosis), Sepsis (black lesions on skin), External otitis (swimmer's ear), UTI, Drug use and Diabetic Osteomyelitis, and hot tub folliculitis. Malignant otitis externa in diabetics.

Aerobic gram-negative rod. Non-lactose fermenting, oxidase positive. Produces pyocyanin (blue-green) pigment; has a grape-like odor. Water source. Produces endotoxin (fever, shock) and exotoxin A (inactivates EF-2).

Treatment: aminoglycoside plus extended­ spectrum penicillin (e.g., piperacillin, ticarcillin).

*Aeruginosa-- aerobic. Think water connection and blue-green pigment.
*Think Pseudomonas in burn victims.
*Chronic pneumonia in CF patients is associated with biofilm.
List the e. coli virulence factors: 3
E. coli virulence factors:
fimbriae-- cystitis and pyelonephritis
K capsule-- pneumonia, neonatal meningitis
LPS endotoxin-- septic shock
EIEC:

toxin and mechanism--
presentation--
Microbe invades intestinal mucosa and causes necrosis and inflammation. No toxins produced. Clinical anifestations similar to Shigella.

Invasive; dysentery.
ETEC:

toxin and mechanism--
presentation--
Labile toxin/stable toxin. No inflammation or invasion.

Traveler's diarrhea (watery).
EPEC:

toxin and mechanism--
presentation--
No toxin produced. Adheres to apical surface, flattens villi, prevents absorption.

Diarrhea usually in children (P for Pediatrics).
EHEC:

toxin and mechanism--
presentation--
Ol57:H7 is the most common serotype. Produces Shiga-like toxin and Hemolytic-uremic syndrome (triad of anemia, thrombocytopenia, and acute renal failure).

Endothelium swells and narrows lumen, leading to mechanical hemolysis and reduced renal blood flow; damaged endothelium consumes platelets.

Dysentery (toxin alone causes necrosis and inflammation).

Does not ferment sorbitol (distinguishes it from other E. coli).
Klebsiella:
An intestinal flora that causes lobar pneumonia in alcoholics and diabetics when aspirated.

Very mucoid colonies caused by abundant polysaccharide capsule. Red "currant jelly" sputum.

Also cause of nosocomial UTis.

4 A's:
Aspiration pneumonia
Abscess in lungs and liver
Alcoholics
di-A-betics
Compare/contrast Salmonella and Shigella:
Salmonella typhi:
Caused typhoid fever. Found only in humans.

Characterized by rose spots on the abdomen, fever, headache, and diarrhea. Can remain in gallbladder and cause a carrier state.
Campylobacter jejuni:
Major cause of bloody diarrhea, especially in children. Fecal-oral transmission through foods such as poultry, meat, unpasteurized milk.

Comma or S-shaped, oxidase positive, grows at 42°C ("Campylobacter likes the hot campfire").

Common antecedent to Guillain-Barre syndrome and reactive arthritis.
Vibrio cholerae:
Produces profuse rice-water diarrhea via toxin that permanently activates Gs, increases cAMP. Comma shaped, oxidase positive, grows in alkaline media.

Endemic to developing countries. Prompt oral rehydration is necessary.
Yersinia enterocolitica:
Usually transmitted from pet feces (e.g., puppies), contaminated milk, or pork.

Causes mesenteric adenitis that can mimic Crohn's or appendicitis.
Helicobacter pylori:
Causes gastritis and up to 90% of duodenal ulcers. Risk factor for peptic ulcer, gastric adenocarcinoma, and lymphoma.

Curved gram-negative rod. Urease positive (can use urea breath test for diagnosis). Creates alkaline environment.

Most common initial treatment is triple therapy: proton pump inhibitor; clarithromycin; amoxicillin or metronidazole.
Helicobacter pylori
Helicobacter pylori
Spirochetes:
The spirochetes are spiral-shaped bacteria with axial filaments and include Borrelia (big size), Leptospira, and Treponema.

Only Borrelia can be visualized using aniline dyes (Wright's or Giemsa stain) in light microscopy. Treponema is visualized by dark-field microscopy.
Spirochetes
Spirochetes
Leptospira interrogans:
Found in water contaminated with animal urine, causes leptospirosis: flu-like symptoms, jaundice, photophobia with conjunctivitis.

Prevalent among surfers and in tropics (i.e., Hawaii).

Weil's disease (icterohemorrhagic leptospirosis): severe form with jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, and anemia.
Lyme Disease:
Caused by Borrelia burgdorferi, which is transmitted by the tick Ixodes (also vector for Babesia). Natural reservoir is the mouse. Mice are important to tick life cycle. Common in northeastern United States.

Treatment: doxycycline, ceftriaxone.

3 stages of Lyme disease:
• Stage 1: erythema chronicum migrans (expanding "bull's eye" red rash with central clearing), flu-like symptoms.
• Stage 2: neurologic (facial nerve palsy) and cardiac (AV nodal block) manifestations.
• Stage 3: musculoskeletal (chronic monoarthritis and migratory polyarthritis), neurological (encephalopathy and polyneuropathy), and cutaneous manifestations.
Mnemonic for Lyme Disease symptoms:
FAKE a Key Lyme pie:
Facial nerve palsy (typically bilateral)
Arthritis
Kardiac block
Erythema migrans

or...some people seem to FAKE lyme disease.
Bug that causes syphilis:

treatment:
Caused by spirochete Treponema pallidum.

Treatment: penicillin G.
painless chancre in 1˚ syphilis (treponema pallidum).
painless chancre in 1˚ syphilis (treponema pallidum).
Describe 1˚ syphilis:
Localized disease presenting with painless chancre.

Screen with VDRL and confirm diagnosis with FTA-ABS.
Describe 2˚ syphilis:
Disseminated disease with constitutional symptoms, maculopapular rash (palms and soles), condylomata lata.

Treponemes are present in chancres of 1˚ and condylomata lata of 2˚ syphilis and may be directly visualized through dark-field microscopy.

Screen with VDRL and confirm diagnosis with FTA-ABS.

Secondary syphilis = Systemic.
Treponeme of syphilis visualized through dark-field microscopy.
Treponeme of syphilis visualized through dark-field microscopy.
Describe 3˚ syphilis:
Gummas (chronic granulomas), aortitis (vasa vasorum destruction), neurosyphilis (tabes dorsalis), Argyll Robertson pupil.

Signs: broad-based ataxia, positive Romberg, Charcot joint, stroke without hypertension.

Test spinal fluid with VDRL.
Describe congenital syphilis:
Saber shins, saddle nose, CN VIII deafness, Hutchinson's teeth, mulberry molars.

Early prevention is key, as placental transmission typically occurs after first trimester.
What is an Argyll Robertson pupil?
Argyll Robertson pupil constricts with accommodation but is not reactive to light. Associated with 3° syphilis

*"Prostitute's pupil"-accommodates but does not react*
Discuss the significance of VDRL false positives:
mnemonic--
VDRL detects nonspecific antibody that reacts with beef cardiolipin.

Used for diagnosis of syphilis, but many false positives, including viral infection (mononucleosis, hepatitis), some drugs, rheumatic fever, SLE, and leprosy.

VDRL:
Viruses (mono, hepatitis)
Drugs
Rheumatic fever
Lupus and leprosy
What is the Jarisch-Herxheimer reaction?
Flu-like syndrome immediately after antibiotics are started-- due to killed bacteria releasing pyrogens.
Of the following zoonotic bacteria, identify the disease it causes and the transmission/source:
-bartonella spp.
-borrellia burgdorferi
-Borrelia recurrentis
-Brucella spp.
-Campylobacter
-Chlamydophila psittaci
-Coxiella burnetii
-Ehrlichia chaffeensis
Of the following zoonotic bacteria, identify the disease it causes and the transmission/source:
-Francisella tularensis
-Leptospira spp.
-Mycobacterium leprae
-Pasteurella multocida
-Rickettsia prowazekii
-Rickettsia rickettsii
-Rickettsia typhi
-Yersinia pestis
Gardnerella vaginalis

Clue cells, or vaginal epithelial cells covered with bacteria, are visible under the microscope (arrow).
Gardnerella vaginalis

Clue cells, or vaginal epithelial cells covered with bacteria, are visible under the microscope (arrow).
Discuss Gardnerella vaginalis:
A pleomorphic, gram-variable rod that causes
vaginosis presenting as a gray vaginal discharge with a fishy smell; nonpainful.

Associated with sexual activity, but not an STD. Bacterial vaginosis is characterized by overgrowth of certain bacteria in vagina.

Clue cells, or vaginal epithelial cells covered with bacteria, are visible under the microscope (arrow).

Treatment: metronidazole.

*I don't have a clue why I smell fish in the vagina garden!*
Treatment for all Rickettsial diseases?
doxycycline
Discuss Rickettsial diseases with Rash:
Rocky Mountain spotted fever (tick) -Rickettsia rickettsii. Broadly distributed in US (in spite of name). Rash typically starts at wrists and ankles and then spreads to trunk, palms, and soles. Rickettsiae are obligate intracellular organisms that need CoA and NAD+.

Typhus:
• Endemic (fleas) -R. typhi.
• Epidemic (human body louse) -R. prowazekii. Rash starts centrally and spreads out, sparing palms and soles.

*Classic triad: headache, fever, rash (vasculitis).

*"Rickettsii on the wRists, Typhus on the Trunk."

*Palm and sole rash is seen in Coxsackievirus A infection (hand, foot, and mouth disease), Rocky Mountain spotted fever, and secondary Syphilis (you drive CARS using your palms and soles).
Discuss Rickettsial diseases w/o Rash:
Ehrlichiosis (tick) -Ehrlichia. Monocytes with morula (berry-like inclusions) in cytoplasm.

Anaplasmosis (tick) - Anaplasma. Granulocytes with morula in cytoplasm.

Q fever (tick feces and cattle placenta release spores that are inhaled as aerosols): Coxiella burnetii. No arthropod vector. Presents as pneumoma.

Q fever is ***** because it has no rash or vector and its causative organism can survive outside in its endospore form. Not in the Rickettsia genus, but closely related.
Life cycle of chlamydia (EBs, RBs, all that junk):
Discuss Chlamydiae:
Chlamydiae cannot make their own ATP. They are obligate intracellular organisms that cause mucosal infections.

2 forms:
• Elementary body (small, dense) is "Enfectious" and Enters cell via Endocytosis.
• Reticulate body Replicates in cell by fission; this form seen on tissue culture.

Chlamydia trachomatis causes reactive arthritis, conjunctivitis, nongonococcal urethritis, and PID.

C. pneumoniae and C. psittaci cause atypical pneumonia; transmitted by aerosol.

Chlamys = cloak (intracellular).

Chlamydophila psittaci-notable for an avian reservOir.

The chlamydial cell wall is unusual in that it lacks muramic acid.
How do we diagnose and treat chlamydiae?
Lab diagnosis: cytoplasmic inclusions seen on Giemsa or fluorescent antibody-stained smear.

Treatment: azithromycin (favored because one­ time treatment) or doxycycline.
Discuss the various Chlamydia trachomatis serotypes:
Mycoplasma pneumoniae
Mycoplasma pneumoniae
Discuss Mycoplasma pneumoniae:
Classic cause of atypical "walking" pneumonia (insidious onset, headache, nonproductive cough, diffuse interstitial infiltrate).

X-ray looks worse than patient. High titer of cold agglutinins (IgM), which can agglutinate or lyse RBCs.

Grown on Eaton's agar.

Treatment: macrolide or fluoroquinolone (penicillin ineffective since Mycoplasma have no cell wall).

No cell wall. Not seen on Gram stain.

Bacterial membrane contains sterols for stability.

Mycoplasmal pneumonia is more common in patients <30 years of age.

Frequent outbreaks in military recruits and pnsons.
In general, talk about the Systemic mycoses:
All can cause pneumonia and can disseminate. All are caused by dimorphic fungi: cold (20°C) = mold; heat (37°C) = yeast.

The only exception is coccidioidomycosis, which is a spherule (not yeast) in tissue.

Treatment: fluconazole or itraconazole for local infection; amphotericin B for systemic infection.

Systemic mycoses can mimic TB (granuloma formation), except, unlike TB, have no person-person transmission.
ID and discuss:
ID and discuss:
Mississippi and Ohio River valleys. Causes pneumonia.
Macrophage filled with Histoplasma (smaller than RBC) 

*Histo hides (within macrophages). Bird or bat droppings.
Histoplasmosis-- a systemic mycosis.
Mississippi and Ohio River valleys.

Causes pneumonia.
Macrophage filled with Histoplasma (smaller than RBC)

*Histo hides (within macrophages). Bird or bat droppings.
ID and discuss:
ID and discuss:
Blastomycosis-- a systemic mycosis.
States east of Mississippi River and Central America. 

Causes inflammatory lung disease and can disseminate to skin and bone. Forms granulomatous nodules.
Broad-base budding (same size as RBC)

*Blasto bu...
Blastomycosis-- a systemic mycosis.
States east of Mississippi River and Central America.

Causes inflammatory lung disease and can disseminate to skin and bone. Forms granulomatous nodules.
Broad-base budding (same size as RBC)

*Blasto buds (broadly).
ID and discuss:
ID and discuss:
Coccidioidomycosis-- a systemic mycosis.
Southwestern United States, California. Causes
pneumonia and meningitis; can disseminate to bone and skin. 

Case rate goes up after earthquakes (spores in dust are thrown up in the air and become spher...
Coccidioidomycosis-- a systemic mycosis.
Southwestern United States, California. Causes
pneumonia and meningitis; can disseminate to bone and skin.

Case rate goes up after earthquakes (spores in dust are thrown up in the air and become spherules in lungs).

Spherule filled with endospores (shown; much larger than RBC)

*Coccidio crowds.
*San Joaquin Valley or desert (desert bumps) "valley fever."
ID and discuss:
ID and discuss:
Latin America.
Budding yeast with "captain's wheel" formation (much larger than RBC)

*Paracoccidio parasails with the captain's wheel all the way to Latin America.
Latin America.
Budding yeast with "captain's wheel" formation (much larger than RBC)

*Paracoccidio parasails with the captain's wheel all the way to Latin America.
ID and discuss:
ID and discuss:
Tinea versicolor-- a cutaneous mycosis.

Caused by Malassezia furfur. Degradation of lipids produces acids that damage melanocytes and cause hypopigmented and/or hyperpigmented patches. Occurs in hot, humid weather.

Treatment: topical miconaz...
Tinea versicolor-- a cutaneous mycosis.

Caused by Malassezia furfur. Degradation of lipids produces acids that damage melanocytes and cause hypopigmented and/or hyperpigmented patches. Occurs in hot, humid weather.

Treatment: topical miconazole, selenium sulfide (Selsun). "Spaghetti and meatball" appearance on KOH prep (shown).
Discuss various tineae besides versicolor:
Includes tinea pedis (foot), tinea cruris (groin), tinea corporis (ringworm, on body), tinea capitis (head, scalp), tinea unguium (onychomycosis, on fingernails).

Pruritic lesions with central clearing resembling a ring, caused by dermatophytes (Microsporum, Trichophyton, and Epidermophyton). See mold hyphae in KOH prep, not dimorphic.
Candida albicons. Dimorphic yeast. 

Pseudohyphae and budding yeasts at 20˚C (left).
Germ tubes at 37˚C (right)
Candida albicans. Dimorphic yeast.

Pseudohyphae and budding yeasts at 20˚C (left).
Germ tubes at 37˚C (right)

Opportunistic fungal infection
Candida albicans:
alba= white.

Systemic or superficial fungal infection. Oral and esophageal thrush in immunocompromised (neonates, steroids, diabetes, AIDS), vulvovaginitis (diabetes, use of antibiotics), diaper rash, endocarditis in IV drug users, disseminated candidiasis (to any organ), chronic mucocutaneous candidiasis.

Treatment: topical azole for vaginal; fluconazole or caspofungin for oral/esophageal; fluconazole, amp B, or caspofungin for systemic.
Aspergillus fumigatus. 
Septate hyphae that branch at 45˚ angle (left). Conidiophore with radiating chains of spores (right).
Aspergillus fumigatus.
Septate hyphae that branch at 45˚ angle (left). Conidiophore with radiating chains of spores (right).

Opportunistic fungal infection
Aspergillus fumigatus:
Invasive aspergillosis, especially in immunocompromised and those with chronic granulomatous disease.

Allergic bronchopulmonary aspergillosis (ABPA): with asthma or CF.

Aspergillomas in lung cavities, especially after TB infection.

Some species of Aspergillus produce aflatoxins, which are associated with HCC.

*Think "A" for Acute Angles in Aspergillus. Not dimorphic.

Opportunistic fungal infection
Cryptococcus neoformans. 5-10 µm yeasts with wide capsular halos and unequal budding in lndia ink stain.
Cryptococcus neoformans. 5-10 µm yeasts with wide capsular halos and unequal budding in lndia ink stain.

Opportunistic fungal infection
Cryptococcus neoformans:
Cryptococcal meningitis, cryptococcosis.

Heavily encapsulated yeast. Not dimorphic. Found in soil, pigeon droppings. Acquired through inhalation with hematogenous dissemination to meninges.

Culture on Sabouraud's agar. Stains with India ink. Latex agglutination test detects polysaccharide capsular antigen and is more specific.

"Soap bubble" lesions in brain.

Opportunistic fungal infection
Mucor. Irregular, broad, nonseptate hyphae branching at wide angles (arrows).
Mucor. Irregular, broad, nonseptate hyphae branching at wide angles (arrows).

Opportunistic fungal infection
Mucor and Rhizopus spp.:
Mucormycosis. Disease mostly in ketoacidotic diabetic and leukemic patients.

Fungi proliferate in blood vessel walls when there is excess ketone and glucose, penetrate cribriform plate, and enter brain. Rhinocerebral, frontal lobe abscesses.

Headache, facial pain, black necrotic eschar on face; may have cranial nerve involvement.

Opportunistic fungal infection
Pneumocystis jirovecii
Pneumocystis jirovecii

Disc-shaped yeast forms on methenamine silver stain of lung tissue

Opportunistic fungal infection
Sporothrix schenckii
Sporothrix schenckii

Dimorphic, cigar-shaped budding yeast that lives on vegetation

Opportunistic fungal infection
Pneumocystis jirovecii:
Causes Pneumocystis pneumonia (PCP), a diffuse interstitial pneumonia. Yeast (originally classified as protozoan). Inhaled.

Most infections are asymptomatic. Immunosuppression (e.g., AIDS) predisposes to disease. Diffuse, bilateral CXR appearance. Diagnosed by lung biopsy or lavage. Disc-shaped yeast forms on methenamine silver stain of lung tissue.

Treatment: TMP-SMX, pentamidine, dapsone. Start prophylaxis when CD4 drops < 200 cells/mm3 in HIV patients.

Opportunistic fungal infection
Sporothrix schenckii:
Sporotrichosis. Dimorphic, cigar-shaped budding yeast that lives on vegetation.

When spores are traumatically introduced into the skin, typically by a thorn ("rose gardener's" disease), causes local pustule or ulcer with nodules along draining lymphatics (ascending lymphangitis). Little systemic illness.

Treatment: itraconazole or potassium iodide.
*"Plant a rose in the pot."

Opportunistic fungal infection
ID and discuss:
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
Protozoa-GI infections
cyst form of giardia lamblia.
cyst form of giardia lamblia.
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
Protozoa-GI infections
cysts of entamoeba histolytica in stool sample.
cysts of entamoeba histolytica in stool sample.
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
Protozoa-GI infections
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
Protozoa- CNS infections
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
Protozoa- CNS infections
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
Protozoa- CNS infections
Protozoa-Hematologic infections
merozoite forms of plasmodium
Protozoa-Hematologic infections
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
*A protozoa*
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
ID and discuss:
disease--
transmission--
diagnosis--
treatment--
*A protozoa*
Discuss:
disease--
transmission--
diagnosis--
treatment--

of trichomonas vaginalis:
*A protozoa*
Disease= Vaginitis: foul-smelling, greenish discharge; itching and burning; do not confuse with Gardnerella vaginalis, a gram-variable bacterium that causes vaginosis

Tx= Sexual (cannot exist outside human because it cannot form cysts)

Diagnosis= Trophozoites (motile) on wet mount

Treatment= Metronidazole for patient and partner (prophylaxis)
Name 5 prominent Intestinal Nematodes:
Discuss their tx:
and the disease they cause:
and treatment:
Name 5 prominent Tissue Nematodes:
Discuss their tx:
and the disease they cause:
and treatment:
List the nematodes that get ingested:

List the nematodes that infect cutaneously:
Ingested: Enterobius, Ascaris, Trichinella.
*You'll get sick if you EAT these!

Cutaneous: Strongyloides, Ancylostoma, Necator.
*These get into your feet from the SANd.
Name 3 prominent Cestodes (tapeworms):
Discuss their tx:
and the disease they cause:
and treatment:
Name 3 prominent Trematodes (flukes):
Discuss their tx:
and the disease they cause:
and treatment:
Name the associated parasite:

Brain cysts, seizures--
Liver cysts--
Vitamin B12 deficiency--
Biliary tract disease, cholangiocarcinoma--
Hemoptysis--
Portal hypertension--
Hematuria, bladder cancer--
Microcytic anemia--
Perianal pruritus--
Brain cysts, seizures-- Taenia solium (cysticercosis)
Liver cysts-- Echinococcus granulosus
Vitamin B12 deficiency-- Diphyllobothrium latum
Biliary tract disease, cholangiocarcinoma-- Clonorchis sinensis

Hemoptysis-- Paragonimus westermani
Portal hypertension-- Schistosoma mansoni
Hematuria, bladder cancer-- Schistosoma haematobium
Microcytic anemia-- Ancylostoma, Necator
Perianal pruritus-- Enterobius
Viral structure-general features:
Define viral recombination:
Exchange of genes between 2 chromosomes by crossing over within regions of significant base sequence homology.
Define viral Reassortment:
When viruses with segmented genomes (e.g., influenza virus) exchange segments. High-frequency recombination. Cause of worldwide influenza pandemics.
Define viral Complementation:
When 1 of 2 viruses that infect the cell has a mutation that results in a nonfunctional protein. The nonmutated virus "complements" the mutated one by making a functional protein that serves both viruses.
Define viral Phenotypic mixing:
Occurs with simultaneous infection of a cell with 2 viruses. Genome of virus A can be partially or completely coated (forming pseudovirion) with the surface proteins of virus B.

Type B protein coat determines the tropism (infectivity) of the hybrid virus. However, the progeny from this infection have a type A coat that is encoded by its type A genetic material.
What are Live attenuated vaccines?

Give examples.
Induce humoral and cell-mediated immunity but have reverted to virulence on rare occasions.

Live attenuated- smallpox, yellow fever, chickenpox (VZV), Sabin's polio virus, MMR, Influenza (intranasal).

No booster needed for live attenuated vaccines.

Dangerous to give live vaccines to immunocompromised patients or their close contacts.

*"Live! One night only! See small yellow chickens get vaccinated with Sabin's and MMR! It's incredible!"

MMR = measles, mumps, rubella (live attenuated vaccine that can be given to HIV­ positive patients who do not show signs of immunodeficiency).
What are killed vaccines?

Give examples.
Killed/inactivated vaccines induce only humoral immunity but are stable.

Rabies, Influenza (injected), Salk Polio, and HAV vaccines.

*SalK = Killed.
*RIP Always.
What are examples of recombinant vaccines?
HBV (antigen = recombinant HBsAg), HPV (types 6, 11, 16, and 18).
DNA viral genomes:
All DNA viruses except the Parvoviridae are dsDNA.

All are linear except papilloma-, polyoma-, and hepadnaviruses (circular).

*All are dsDNA (like our cells), except "part-of-a­ virus" (parvovirus) is ssDNA.
*Parvus = small.
RNA viral genomes:
All RNA viruses except Reoviridae are ssRNA. Positive-stranded RNA viruses: I went to a retro (retrovirus) toga (togavirus) party, where I drank flavored (flavivirus) Corona (coronavirus) and ate hippy (hepevirus) California (calicivirus) pickles (picornavirus).

All are ssRNA (like our mRNA), except "repeato-virus" (reovirus) is dsRNA.
Naked viral genome infectivity:
Purified nucleic acids of most dsDNA (except pox viruses and HBV) and (+) strand ssRNA (~mRNA) viruses are infectious.

Naked nucleic acids of (-) strand ssRNA and dsRNA viruses are not infectious. They require polymerases contained in the complete virion.
Virus ploidy:
All viruses are haploid (with 1 copy of DNA or RNA) except retroviruses, which have 2 identical ssRNA molecules (~diploid).
Where does viral replication occur for DNA viruses? RNA?
DNA: All replicate in the nucleus (except poxvirus).

RNA: All replicate in the cytoplasm (except influenza virus and retroviruses).
Which viruses are naked?
Papillomavirus, Adenovirus, Picornavirus, Polyomavirus, Calcivirus, Parvovirus, Reovirus, and Hepevirus.

*Give PAPP smears and CPR to a naked Heppy (hippy).

DNA = PAPP; RNA = CPR and hepevirus.
How do enveloped viruses get their envelopes?
Generally, enveloped viruses acquire their envelopes from plasma membrane when they exit from cell. Exceptions include herpesviruses, which acquire envelopes from nuclear membrane.
List some general rules about DNA viruses:
Herpesviruses:
envelope?
DNA structure?
Notes of medical importance:
Hepadnaviruses, Adenoviruses, and Parvoviruses:
envelope?
DNA structure?
Notes of medical importance:
Papillomavirus, Polyomavirus, and Poxvirus:
envelope?
DNA structure?
Notes of medical importance:
Herpes labialis. Grouped and confluent vesicles with an erythematous rim.
Herpes labialis. Grouped and confluent vesicles with an erythematous rim.
Herpes genitalis. Ulcerating vesicles associated with HSV-2 and less frequently HSV-1.
Herpes genitalis. Ulcerating vesicles associated with HSV-2 and less frequently HSV-1.
Zoster. Hemorrhagic vesicles and pustules in dermatomal distribution.
Zoster. Hemorrhagic vesicles and pustules in dermatomal distribution.
CMV. Renal tubular cells in a neonate with congenital CMV infection. Note the "owl's eye" inclusions (arrows).
CMV. Renal tubular cells in a neonate with congenital CMV infection. Note the "owl's eye" inclusions (arrows).
Compare/contrast HSV-1 and HSV-2:
Diseases associated with VZV?

Route of transmission?
Varicella-zoster (chickenpox, shingles), encephalitis, pneumonia. Latent in dorsal root or trigeminal ganglia.

Tx: Respiratory secretions.
Diseases associated with EBV?

Route of transmission?
Infectious mononucleosis, Burkitt's/Hodgkin's lymphoma, nasopharyngeal carcinoma. Latent in B cells.

Tx: Respiratory secretions, saliva.
Diseases associated with CMV?

Route of transmission?
Congenital infection, mononucleosis (negative Monospot), pneumonia, retinitis. Infected cells have characteristic "owl's eye" inclusions. Latent in mononuclear cells.

Tx: Congenital, transfusion, sexual contact, saliva, urine, transplant.
Diseases associated with HHV-6?

Route of transmission?
Roseola: high fevers for several days that can cause seizures, followed by a diffuse macular rash.

Tx not determined.
Diseases associated with HHV-8?

Route of transmission?
Kaposi's sarcoma (HIV patients).

Sexual contact.
Describe identification of HSV:
PCR is test of choice.

Tzanck test: a smear of an opened skin vesicle to detect multinucleated giant cells commonly seen in HSV-1, HSV-2, and VZV.

Infected cells also have intranuclear Cowdry A inclusions.

*Tzanck heavens I do not have herpes.
Discuss EBV--what it causes, age groups affected, detection:
A herpesvirus. Can cause mononucleosis.
Infects B cells. Characterized by fever, hepatosplenomegaly, pharyngitis, and lymphadenopathy (especially posterior cervical nodes).

Peak incidence 15-20 years of age.

Atypical lymphocytes seen on peripheral blood smear are not infected B cells but rather reactive cytotoxic T cells.

Positive Monospot test: heterophile antibodies detected by agglutination of sheep or horse RBCs. Also associated with development of Hodgkin's and endemic Burkitt's lymphomas as well as nasopharyngeal carcinoma.

*Most common during peak kissing years ("kissing disease")
Atypical lymphocytes. Seen with EBV infection. Note "hugging" of RBCs (arrow)
Atypical lymphocytes. Seen with EBV infection. Note "hugging" of RBCs (arrow)
Discuss Reoviruses and Picornaviruses:
envelope?
RNA structure?
capsid shape?
medical importance?
Discuss Hepeviruses, Caliciviruses, Flaviviruses, and Togaviruses:
envelope?
RNA structure?
capsid shape?
medical importance?
Discuss Retroviruses, Coronaviruses, Orthomyxoviruses, and Paramyxoviruses:
envelope?
RNA structure?
capsid shape?
medical importance?
Discuss Rhabdoviruses, Filoviruses, Arenaviruses, Bunyaviruses, and Delta virus:
envelope?
RNA structure?
capsid shape?
medical importance?
What are negative stranded viruses?

Give 6 examples:
Must transcribe negative strand to positive.

Virion brings its own RNA-dependent RNA polymerase.

They include Arenaviruses, Bunyaviruses, Paramyxoviruses, Orthomyxoviruses, Filoviruses, and Rhabdoviruses.

*Always Bring Polymerase Or Fail Replication.
What are segmented viruses?

Give 4 examples:
All are RNA viruses.

They include Bunyaviruses, Orthomyxoviruses (influenza viruses), Arenaviruses, and Reoviruses.

*BOAR
What are picornaviruses?

Give 5 examples:
RNA is translated into 1 large polypeptide that is cleaved by proteases into functional viral proteins.

Can cause aseptic (viral) meningitis (except rhinovirus and HAV). All are enteroviruses (fecal-oral spread) except rhinovirus.

Includes Poliovirus, Echovirus, Rhinovirus, Coxsackievirus, HAV.

*PicoRNAvirus = small RNA virus. PERCH on a "peak" (pico).
What are rhinoviruses?
A picornavirus. Nonenveloped RNA virus.

Cause of common cold; > 100 serologic types.

Acid labile: destroyed by stomach acid; therefore, does not infect the GI tract (unlike the other picornaviruses).

*Rhino has a runny nose.
What is yellow fever virus?

tx:
sx:
A flavivirus (also an arbovirus) transmitted by Aedes mosquitoes.

Virus has a monkey or human reservoir.

Symptoms: high fever, black vomitus, and jaundice.

*Flavi = yellow, jaundice.
What is rotavirus?

tx:
sx:
Rotavirus, the most important global cause of infantile gastroenteritis, is a segmented dsRNA virus (a reovirus). 

Major cause of acute diarrhea in the United States during winter, especially in day-care centers, kindergartens. 

Villous dest...
Rotavirus, the most important global cause of infantile gastroenteritis, is a segmented dsRNA virus (a reovirus).

Major cause of acute diarrhea in the United States during winter, especially in day-care centers, kindergartens.

Villous destruction with atrophy leads to lower absorption of Na+ and loss of K+.

CDC recommends routine vaccination of all infants.
rotavirus
rotavirus
Discuss flu viruses:
Orthomyxoviruses. Enveloped, negative single­ stranded RNA viruses with 8-segment genome. Contain hemagglutinin (promotes viral entry) and neuraminidase (promotes progeny virion release) antigens.

Patients at risk for fatal bacterial superinfection. Rapid genetic changes.

Killed viral vaccine is major mode ofprotection; reformulated vaccine offered each fall.

Vaccine containing live, temperature-sensitive mutant that replicates in the nose but not in the lung is also available. Used in children.
Discuss antigenic shift:
Causes pandemics. Reassortment of viral genome; segments undergo high-frequency recombination, such as when human flu A virus recombines with swine flu A virus.

Sudden shift is more deadly than gradual drift.
Discuss genetic drift:
Causes epidemics. Minor (antigenic drift) changes based on random mutation.
Discuss rubella virus:
A togavirus. Causes rubella, once known as German (3-day) measles.

Fever, postauricular adenopathy, lymphadenopathy, arthralgias, fine truncal rash that starts at head and moves down.

Causes mild disease in children but serious congenital disease (a ToRCHeS infection).
Discuss paramyxoviruses:
Paramyxoviruses cause disease in children. They include those that cause parainfluenza (croup: seal-like barking cough), mumps, and measles as well as RSV, which causes respiratory tract infection (bronchiolitis, pneumonia) in infants.

All contain surface F (fusion) protein, which causes respiratory epithelial cells to fuse and form multinucleated cells.

Palivizumab (monoclonal antibody against F protein) prevents pneumonia caused by RSV infection in premature infants.
Discuss measles virus:
A paramyxovirus that causes measles.

Koplik spots (red spots with blue-white center on buccal mucosa) and descending maculopapular rash are characteristic.

SSPE (subacute sclerosing panencephalitis, occurring years later), encephalitis (1 :2000), and giant cell pneumonia (rarely, in immunosuppressed) are possible sequelae.

Rash presents last and spreads from head to toe. Includes hands and feet (vs. truncal rash in rubella).

Do not confuse with roseola (caused by HHV-6).

3 C's of measles: Cough, Coryza, Conjunctivitis
Discuss mumps virus:
A paramyxovirus.

Symptoms: Parotitis, Orchitis (inflammation of testes), and aseptic Meningitis. [POM]

Can cause sterility (especially after puberty).

*Mumps makes your parotid glands and testes as big as POM-poms.
mumps--swollen neck and parotids
mumps--swollen neck and parotids
rabies virus (rhabdovirus)
rabies virus (rhabdovirus)
negri body--a cytoplasmic inclusion in neurons infected by rabies virus; found in purkinje cells of cerebellum.
negri body--a cytoplasmic inclusion in neurons infected by rabies virus; found in purkinje cells of cerebellum.
Discuss rabies virus:
Bullet-shaped virus. Negri bodies are characteristic cytoplasmic inclusions in neurons infected by rabies virus; commonly found in Purkinje cells of cerebellum.

Rabies has long incubation period (weeks to months) before symptom onset. Postexposure treatment is wound cleansing and vaccination ± rabies immune globulin.

Travels to the CNS by migrating in a retrograde fashion up nerve axons.

Progression of disease: fever, malaise --> agitation, photophobia, hydrophobia --> paralysis, coma --> death.

More commonly from bat, raccoon, and skunk bites than from dog bites in the United States.
Compare/contrast Hepatitis viruses:
-tx
-carriers?
-incubation
-HCC risk?
-Notes
a: HAV and HEV are fecal-oral: The vowels hit your bowels. Naked viruses do not rely on an envelope so they are not destroyed by the gut.

b: In HBV, the virus uses its own DNA-dependent DNA polymerase to make full double-stranded DNA. The host ...
a: HAV and HEV are fecal-oral: The vowels hit your bowels. Naked viruses do not rely on an envelope so they are not destroyed by the gut.

b: In HBV, the virus uses its own DNA-dependent DNA polymerase to make full double-stranded DNA. The host RNA polymerase transcribes mRNA from viral DNA and then makes viral proteins from the mRNAs.
Signs and symptoms of all hepatitis viruses: 4
episodes of fever, jaundice, elevated ALT and AST.
Briefly discuss the 8 serologic markers of hepatitis:
Describe the structure of hepatitis virus:
Discuss the importance of diagnostic tests as a function of time after exposure in hepatitis.

Discuss the levels of serologic markers as a function of time after exposurein hepatitis.
In viral hepatitis, ALT > AST. In alcoholic hepatitis, AST > ALT.

SECES: SE are antigens, CES are antibodies; labeled on figure in order of appearance.
HBV: discuss detection of serologic markers at different points in the disease state--
acute HBV:
chronic HBV:
recovery:
immunized:
Discuss the HIV virus:
Diploid genome (2 molecules of RNA). The 3 structural genes (protein coded for):
• env (gp120 and gp41):
* Formed from cleavage of gp160 to form envelope proteins.
* gp120-attachment to host CD4+ T cell.
* gp41-fusion and entry.
• gag (p24) -- capsid protein.
• pol -- reverse transcriptase, aspartate protease, integrase.

Reverse transcriptase synthesizes dsDNA from RNA; dsDNA integrates into host genome.

Virus binds CCR5 (early) or CXCR4 (late) co-receptor and CD4 on T cells; binds CCR5 and CD4 on macrophages.

Homozygous CCR5 mutation = immunity. Heterozygous CCR5 mutation = slower course.
Structure of HIV particle:
Describe the process of HIV diagnosis:
Presumptive diagnosis made with ELISA (sensitive, high false-positive rate and low threshold, rule out test); positive results are then confirmed with Western blot assay (specific, high false-negative rate and high threshold, rule in test).

HIV PCR/viral load tests determine the amount of viral RNA in the plasma. High viral load associated with poor prognosis. Also use viral load to monitor effect of drug therapy.

AIDS diagnosis 200 CD4+ cells/mm3 or less (normal: 500-1500). HIV positive with AIDS-defining condition (e.g., Pneumocystis pneumonia, or PCP) or CD4/CD8 ratio <1.5.

ELISA/Western blot tests look for antibodies to viral proteins; these tests often are falsely negative in the first 1-2 months of HIV infection and falsely positive initially in babies born to infected mothers (anti-gp120 crosses placenta).
What are the 4 stages of HIV infection?
1. Flu-like (acute)
2. Feeling fine (latent)
3. Falling count
4. Final crisis

During latent phase, virus replicates in lymph nodes.
Time course of HIV infection:
Discuss systemic diseases of HIV + adults:
Discuss dermatologic and GI diseases of HIV + adults:
Discuss neurologic diseases of HIV + adults:
Discuss oncologic diseases of HIV + adults:
Discuss respiratory diseases of HIV + adults:
Discuss Prions:
Prion diseases are caused by the conversion of a normal cellular protein termed prion protein (PrPc) to a ß-pleated form (Prpsc), which is transmissible. Prpsc resists degradation and facilitates the conversion of still more Prpc to PrPsc.

Accumulation of Prpsc results in spongiform encephalopathy and dementia, ataxia, and death.

It can be sporadic (Creutzfeldt-Jakob disease­ rapidly progressive dementia), inherited (Gerstmann-Straussler-Scheinker syndrome), or acquired (kuru).
List dominant normal flora of:
skin--
nose--
oropharynx--
dental plaque--
colon--
vagina--
List 7 bacteria that cause food poisoning. What food are they in?
What bugs can mimic appendicitis?
Yersinia enterocolitica is most common cause of mesenteric adenitis, a disease that mimics appendicitis.

Nontyphoidal Salmonella can also be a cause.

Camplyobacter jejuni may also mimic appendicitis.
Briefly describe 7 bugs that cause bloody diarrhea:
Briefly describe 6 bugs that cause watery diarrhea:
List common causes of pneumonia in different age groups:
neonates-
children-
adults (18-40)-
adults (40-65)-
elderly-
List nosocomial bugs:
Bugs that affect immune compromised:
Bugs assoc with aspiration:
Bugs assoc with alcoholics/IV users:
Bugs assoc with CF:
Bugs associated with postviral infection:
Bugs that are atypical:
Common causes of meningitis by age:
newborn-
children-
6-60yrs-
60+

Discuss treatment:
Viral causes?
HIV associated bugs?
CSF findings in meningitis: bacterial/fungal, TB/viral

opening pressure-
cell type-
pretein-
sugar-
List causes of osteomyelitis associated with specific predisposing circumstances:
Discuss UTIs:

sx:
risk factors:
diagnostic markers:
Cystitis presents with dysuria, frequency, urgency, suprapubic pain, and WBCs (but not WBC casts) in urine. Primarily caused by ascension of microbes from urethra to bladder.

Males:­ infants with congenital defects, vesicoureteral reflux.
Elderly: enlarged prostate.

Ascension to kidney results in pyelonephritis, which presents with fever, chills, flank pain, CVA tenderness, hematuria, and WBC casts.

Ten times more common in women (shorter urethras colonized by fecal flora). Other predisposing factors include obstruction, kidney surgery, catheterization, GU malformation, diabetes, and pregnancy.

Diagnostic markers: positive leukocyte esterase test = bacterial UTI; positive nitrite test = gram­ negative bacterial UTI.
List 7 UTI associated bugs.

list their features

discuss diagnostic markers
What are ToRCHeS infections?
Microbes that may pass from mother to fetus. Transmission is transplacental in most cases, or via delivery (especially HSV-2).

Nonspecific signs common to many ToRCHeS infections include hepatosplenomegaly, jaundice, thrombocytopenia, and growth retardation.

Other important infectious agents include Streptococcus agalactiae (group B strep), E. coli, and Listeria monocytogenes-- all causes of meningitis in neonates. Parvovirus B19 causes hydrops fetalis.
List the bugs in the acronym Torches:

Mode of tx for each:
Maternal manifestations:
Neonatal manifestations:
Congenital syphilis facies. Skin is dry, wrinkled with yellow-brown hue. Note the hemorrhagic rhinitis.
Congenital syphilis facies. Skin is dry, wrinkled with yellow-brown hue. Note the hemorrhagic rhinitis.
Hutchinson's teeth. Note the centrally notched, widely spaced central incisors. A neonatal manifestation of syphilis.
Hutchinson's teeth. Note the centrally notched, widely spaced central incisors. A neonatal manifestation of syphilis.
List 7 causes of red rashes of childhood:
Their associated syndrome/disease:
Clinical presentation:
Erythema infectiosum. Slapped cheek rash of parvovirus B19.
Erythema infectiosum. Slapped cheek rash of parvovirus B19.
Hand-foot-mouth disease. A result of Coxsackievirus type A.
Hand-foot-mouth disease. A result of Coxsackievirus type A.
Clinical features and organism responsible for:
gonorrhea-
1˚ syphilis-
2˚ syphilis-
3˚ syphilis-
Chancroid-
Genital Herpes-
Clinical features and organism responsible for:
Chlamydia-
Lymphogranuloma venereum-
Trichomoniasis-
AIDS-
Condylomata acuminata-
Hepatitis B-
Bacterial vaginosis-
Pelvic Inflammatory Disease:
top bugs-
signs/sx-
risk factors/end results-
Top bugs-Chlamydia trachomatis (subacute, often undiagnosed), Neisseria gonorrhoeae (acute). C. trachomatis-- the most common bacterial STD in the United States.

Cervical motion tenderness (chandelier sign), purulent cervical discharge. PID may include salpingitis, endometritis, hydrosalpinx, and tubo-ovarian abscess.

Can lead to Fitz­-Hugh-Curtis syndrome-- infection of the liver capsule and "violin string" adhesions of parietal peritoneum to liver.

Salpingitis is a risk factor for ectopic pregnancy, infertility, chronic pelvic pain, and adhesions.
Bugs implicated in nosocomial infections:
risk factors for each:
notes:
Bugs affecting unimmunized children:
clinical presentation:
findings/labs:
Bug hints (if all else fails):

characteristic--
organism--
Where do antimicrobials act?
graphic
Mechanism, Clinical use, toxicity, and resistance of penicillin:
What are the penicillinase-resistant penicillins?
Mechanism, Clinical use, toxicity, and resistance of penicillinase-resistant penicillins:
What are the aminopenicillins?
Mechanism, Clinical use, toxicity, and resistance of aminopenicillins:
What are the antipseudomonals?
Mechanism, Clinical use, toxicity, and resistance of antipseudomonals:
What are the ß-Lactamase inhibitors? What are they used for?
*CAST: Clavulanic Acid, Sulbactam, Tazobactam.

Often added to penicillin antibiotics to protect the antibiotic from destruction by ß-lactamase (penicillinase).
Mechanism of Cephalosporins:

what bugs aren't killed by them?
ß-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal.

Organisms typically not covered by cephalosporins are LAME: Listeria, Atypicals (Chlamydia, Mycoplasma), MRSA, and Enterococci. Exception: ceftaroline covers MRSA.
List all cephalosporins by generation:
Clinical use of cepalosporins by generation:
1st generation (cefazolin, cephalexin): gram- positive cocci, Proteus mirabilis, E. coli, Klebsiella pnewnoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections.
*1st generation-PEcK*

2nd generation (cefoxitin, cefaclor, cefuroxime): gram-positive cocci, Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens.
*2nd generation-HEN PEcKS*

3rd generation (ceftriaxone, cefotaxime, ceftazidime): serious gram-negative infections resistant to other ß-lactams.
*Ceftriaxone-meningitis and gonorrhea.*
*Ceftazidime-Pseudomonas.

4th generation (cefepime): increased activity against Pseudomonas and gram-positive organisms.
Describe cephalosporin toxicity:
Hypersensitivity reactions, vitamin K deficiency. Low cross-reactivity with penicillins. They increase the nephrotoxicity of aminoglycosides.
Aztreonam:
mechanism--
clinical use--
toxicity--
lmipenem/cilastatin, meropenem:

mechanism:
Imipenem is a broad-spectrum, ß-lactamase­ resistant carbapenem. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules.

With imipenem, "the kill is lastin' with cilastatin."

Newer carbapenems include ertapenem and doripenem.
lmipenem/cilastatin, meropenem:

clinical use:
Gram-positive cocci, gram-negative rods, and anaerobes. Wide spectrum, but the significant side effects limit use to life-threatening infections, or after other drugs have failed. Meropenem, however, has a reduced risk of seizures and is stable to dehydropeptidase I.
lmipenem/cilastatin, meropenem:

toxicity:
GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.
Vancomycin:
mechanism--
clinical use--
toxicity--
resistance--
What are the protein synthesis inhibitor antibiotics?
where do they act?

graphic
Aminoglycosides:
mechanism--
clinical use--
toxicity--
resistance--
Tetracyclines:
mechanism--
clinical use--
toxicity--
resistance--
Macrolides:
mechanism--
clinical use--
toxicity--
resistance--
Chloramphenicol:
mechanism--
clinical use--
toxicity--
resistance--
Clindamycin:
mechanism--
clinical use--
toxicity--
Sulfonamides:
mechanism--
clinical use--
toxicity--
resistance--
Where do TMP and SMX act?
Trimethoprim:
mechanism--
clinical use--
toxicity--
Fluoroquinolones:
mechanism--
clinical use--
toxicity--
resistance--
Metronidazole:
mechanism--
clinical use--
toxicity--
resistance--
Antimycobaderial drugs:
list prophylaxis against TB, MAI, and leprosy:
list treatment against TB, MAI, and leprosy:
Isoniazid:
mechanism--
clinical use--
toxicity--
Rifampin:
mechanism--
clinical use--
toxicity--
Pyrazinamide:
mechanism--
clinical use--
toxicity--
Ethambutol:
mechanism--
clinical use--
toxicity--
Antimicrobial prophylaxis for:

Meningococcal infection--

Gonorrhea--

Syphilis--

History of recurrent UTIs--

Endocarditis with surgical or dental procedures--

Pregnant woman carrying group B strep--

Prophylaxis of strep pharyngitis in child with
prior rheumatic fever--

Prevention of postsurgical infection due to
S. aureus--

Prevention of gonococcal or chlamydial
conjunctivitis in newborn--
HIV prophylaxis at various CD4 counts:
Preferred treatment for MRSA:

Preferred treatment for Vancomycin-Resistant Enterococci (VRE):
MRSA- vancomycin

VRE- linezolid and streptogramins (quinupristin/dalfopristin)
Sites of action of different antifungal therapies:
Amphotericin B:
mechanism--
clinical use--
toxicity--
Mechanism and clinical use of nystatin:
MECHANISM: Same as amphotericin B. Topical form because too toxic for systemic use.

CLINICAL USE: "Swish and swallow" for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis.
Azoles:
mechanism--
clinical use--
toxicity--
Flucytosine:
mechanism--
clinical use--
toxicity--
Caspofungin, micafungin:
mechanism--
clinical use--
toxicity--
Terbinafine:
mechanism--
clinical use--
toxicity--
Griseofulvin:
mechanism--
clinical use--
toxicity--
List some antiprotozoan therapies:
Pyrimethamine (toxoplasmosis)

suramin and melarsoprol (Trypanosoma brucei)

nifurtimox (T cruzi)

sodium stibogluconate (leishmaniasis).
Chloroquine:
mechanism--
clinical use--
toxicity--
List some antihelminthic therapies:
Mebendazole, pyrantel pamoate, ivermectin, diethylcarbamazine, praziquantel; immobilize helminths.

Use praziquantel against flukes (trematodes) such as Schistosoma.
Antiviral therapies: where do various kinds act?
Zanamivir/Oseltamivir:
mechanism--
clinical use--

Ribavirin:
mechanism--
clinical use--
toxicity--
Acyclovir:
mechanism--
clinical use--
toxicity--
mechanism of resistance--
Gancyclovir:
mechanism--
clinical use--
toxicity--
mechanism of resistance--
Foscarnet:
mechanism--
clinical use--
toxicity--
mechanism of resistance--
Cidofovir:
mechanism--
clinical use--
toxicity--
Describe HAART therapy:
Highly active antiretroviral therapy (HAART): initiated when patients present with AIDS-defining illness, low CD4 cell counts (< 500 cells/mm3), or high viral load.

Regimen consists of 3 drugs to prevent resistance:
[2 nucleoside reverse transcriptase inhibitors (NRTis)] +

[1 non-nucleoside reverse transcriptase inhibitor (NNRTI) OR 1 protease inhibitor OR 1 integrase inhibitor]
List 8 Protease inhibitors used for HIV:
Describe their mechanism:
Describe their toxicity:
List 7 NRTIs used for HIV:
Describe their mechanism:
Describe their toxicity:
List 3 NNRTIs used for HIV:
Describe their mechanism:
Describe their toxicity:
List an important integrase inhibitor used in HIV:
Describe its mechanism:
Describe its toxicity:
Raltegravir inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HTV integrase.

Tox --> Hypercholesterolemia
Interferons:
mechanism--
clinical use--
toxicity--
Antibiotics to avoid in Pregnancy:

List their adverse effect: