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Microbes
Overview of Bacteriology 1.
a. Characteristics of bacteria i. Single cell ii. No nuclear
membrane iii. Single circular DNA iv. No organelles v. 70s
ribosomal DNA (different from human) vi. No membrane sterols vii.
Peptidoglycan cell wall (not present in Euks) viii. Reproduction by
binary fission ix. Susceptible to antibiotics
b. Gram Positive: i. Stain blue ii. Have thick outer
peptidoglycan cell wall
c. Gram Negative i. Stain pink ii. Have LPS (endotoxin) on
outside iii. Thinner layer of peptidoglycans, sandwiched between
iv. Porins on outer membrane layer
d. Gram Positive Cocci i. Staph
1. Grows in clusters 2. Catalase positive 3. Facultative
Anaerobes 4. Coag POSITIVE staph = S.Aureus 5. Coag NEGATIVE staph-
routinely found on skin. Usually not harmful 6. Staph Aureus
a. Skin and soft tissue infections (Abscess) b. Pneumonia c.
Bone and joint infections d. Bacteremia e. Endocarditis f. Catheter
infections g. Toxin syndromes
i. TSST ii. Scalded skin iii. Food poisoning (enterotoxin)
h. MRSA
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i. Hospital Aquired ii. Community acquired
1. Increasingly prevalent 2. Includes Panton-Valentine
Leukocidin
ii. Strep 1. Grows in chains 2. Catalase Negative 3. Facultative
Anaerobes 4. Ferment carbohydrates producing Lactic Acid 5. Types
of Strep
a. Group A Strep (Pyogenes) i. Beta Hemolytic ii. Bacitracin
sensitive iii. Has a capsule of hyaluronic acid iv. Usu asx
colonization of respiratory tract v. Person-to-person spread vi.
Diseases
1. Most are suppurative 2. Pharyngitis 3. Scarlet Fever 4. Skin
Infections 5. Bacteremia 6. TSST 7. Rheumatic fever
a. 10 days after GAS b. Migratory polyarthritis, carditis,
subQ
nodules, erythema marginosum, chorea (Major Jones Criteria)
8. Glomerulonephritis b. Group B strep (agalactiae)
i. Narrow zone of beta hemolysis ii. GI/GU iii. Babies get it
from colonized mothers iv. Now, if positive, put on antibiotics
before giving birth
c. Strep Pneumoniae i. Alpha hemolytic ii. Lancet shaped iii.
Optochin sensitive (viridians is not) iv. Soluble in bile (other
streps are not) v. Have a polysachharide capsule (Candy
coating)
1. Capsule is basis for vaccine vi. Diseases
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1. Pneumonia a. #1 for community acquired pneumonia
2. Otitis, sinusitis 3. Meningitis (ties for #1) 4. Bacteremia
5. Skin and joint infections
iii. Enterococci 1. E. Faecalis, E.Faecium 2. Grows in
chains/pairs 3. Catalse Negative 4. Usu non-hemolytic 5. Grows in
6.5% NaCl 6. Diseases
a. Endocarditis b. UTI c. Nosocomial (Wounds, catheters)
e. Gram Negative Bacilli i. MacConkey Agar
1. Grows Gram neg a. Lactose fermenters grow PINK b. Non-lactose
fermenters grow COLORLESS c. Lactose test helps ID the bacteria
ii. Enterobacteriaciae 1. Salmonella, shiglella, e.coli,
klebsiella, yersinia, enterobacter 2. Often common in the
ENVIRONMENT 3. Oxidase negative 4. Ferment glucose 5. Diseases
a. Gastroenteritis b. UTI c. Bloodstream infection d. pneumonia
e. plague
iii. P. aeruginosa 1. Obligate aerobe 2. Does NOT ferment
lactose 3. Does NOT ferment glucose 4. Oxidase positive 5. Sweet
odor 6. Produces a green color
iv. HACEK group 1. H. Influenza
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f. Gram Negative Cocci i. Neisseria
1. Grow in pairs 2. Prefer high CO2 3. Oxidase positive 4.
Species
a. Meningitides i. Carbohydrate capsule
b. Gonorrheae i. Also encapsulated ii. Uses only GLUCOSE
ii. Moraxella 1. Otitis, sinusitis, bronchitis
g. Gram Positive Bacilli i. Bacillus
1. Spore forming 2. Aerobic 3. Catalase POSITIVE 4. Persist in
soil 5. Types
a. B. Anthracis i. Spores- bamboo appearance ii. Non-beta
hemolytic iii. Non-motile iv. Has a capsule v. Pulmonary disease-
shows widened mediastinum
ii. Corynebacteria 1. Irregular shape (Chinese letter shaped) 2.
Catalase positive 3. Causes Diptheria
iii. Listeria Monocytogenes 1. Tumbling motility 2. Non-spore
forming 3. Beta-hemolytic 4. Diseases
a. Meningitis b. Endocarditis c. Neonatal infection d. Infection
in pregnant women
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Antibiotics 2.
a. Beta Lactams i. Inhibit crosslinking of peptide side chains
in bacterial cell walls ii. BacterioCIDAL iii. Safe in pregnancy
iv. Renally cleared v. Resistance
1. Beta lactamases 2. Changes to the binding site (MRSA)
vi. Adverse effects: Rash (anaphylaxis), hematologic toxicity
vii. Includes:
1. Penicillins a. Doesnt go to prostate or intraocular fluid
(otherwise good
distribution) b. Renally cleared (so careful in kidney failure)
c. Synergize with aminoglycosides d. Beta Lactamase inhibitors
i. Clavulanic acid, sulbactam, tazobactam ii. Add anaerobic
coverage
2. Cephalosporins a. Renally excreted b. 1st and 2nd gen do NOT
penetrate CSF c. Doesnt cover enterococci, lysteria, MRSA d.
Adverse reactions: Rash, fewer platelets, fewer WBC e. First
Generation cephalosporins
i. The Surgeons favorite ii. Covers gram positive iii. Skin,
soft tissue infection; surgical prophylaxis iv. Includes:
1. Cefazolin, cephalexin f. Second Generation
i. Sinusitis, Otitis ii. Works against Haemophilus iii. Covers
more gram negative, strict anaerobes iv. Includes:
1. Cefoxitin g. Third Generation
i. More gram negative ii. Stable to beta lactamases iii.
Ceftazidime Pseudomonas aeruginosa
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iv. Ceftriaxone gram POSITIVEs. Meningitis, community
pneumonia
h. Fourth Genreation i. Gram positive and negative ii. Cefepime
pseudomonas, gram negative resistant bacteria
i. Fifth generation i. Covers MRSA
3. Carbapenems a. Stable to beta lactamases b. Gram positive and
negative
i. Including pseudomonas c. Reserve for serious infection d.
Imipenem; meropenem; ertapenem (doesnt do p.aeruginosa)
4. Monobactams a. Only gram negative
i. Including pseudomonas b. Can use in penicillin allergic pts
c. Azetreonam- IV
b. Vancomycin i. Inhibits elongation step of cell wall synth ii.
Only gram positive iii. Not absorbed orally. Used in C. Diff
Colitis iv. Renal clearance v. Measure trough levels vi. Adverse
effects: Red Man Syndrome, renal toxicity, hemotologic, ototoxicity
vii. Use for:
1. MRSA (hospital acquired) 2. Beta lactam allergies 3. Second
line for staph/strep endocarditis 4. C. Diff Colitis
c. Oxalidinones (Linezolid) i. Inhibits protein synth (binds to
50s subunit) ii. Gram positive iii. Weak MAOinhibitor. So can get
serotonin syndrome with SSRIs iv. Adverse effects: headache,
nausea, thrombocytopenia, peripheral and optic
neuropathy. v. Use for:
1. MRSA, VRE vi. Very expensive vii. Reserve
d. Daptomycin i. Depolarizes cell walls
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ii. bacterioCIDAL iii. gram positive
1. MRSA, VRE e. Aminoglycosides
i. Enter bacterial cells ii. Bind irreversibly, Inhibit 30s
ribosome iii. BacterioCIDAL iv. Renally exreted v. Resistance due
to inactivating enzyles vi. Narrow therapeutic index
1. Monitor peak and trough vii. Adverse effects: Nephrotoxicity,
ototoxicity viii. Use for gram negative bacilli, staph,
mycobacteria.
1. No anaerobes ix. Use for synergy x. Includes: Gentamycin
(gram pos cocci), streptomycin (TB, plague)
f. Tetracylcines i. Bind reversibly to 30s, inhibiting protein
synth ii. bacterioSTATIC iii. must be transported into cell iv.
resistance: changes in transport v. does not penetrate CSF vi.
milk, antacids decrease absorption vii. contraindicated in
pregnancy
1. cross placenta, affect fetal bones, teeth viii. works for
intracellular pathogens
1. Chlamydia, mycoplasma, legionella (causes of atypical
pneumonia) 2. Rickettsia (doxy), lyme disease, STDs
ix. Includes: 1. Tetracycline, Doxycycline, Minocycline
x. Adverse effects: 1. Gastric irritation, nausea, vertigo,
photosensitivity, diarrhea
g. Tigecycline i. A bigger, better tetracycline ii. Overcomes
resistance iii. Use for resistant gram positive, resistant gram
negative , anaerobes, mycobacteria
1. Not pseudomonas iv. Like tetracycline
1. Also contraindicated in pregnancy 2. Also causes
photosensitivity
h. Macrolides i. Bind reversibly to 50s
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ii. BacterioSTATIC iii. Metablolized in LIVER
1. Cyt P450. Lots of interactions iv. Doesnt penetrate CSF v.
Includes:
1. erythromycin, clarithromycin, azithromicin, dirithromycin.
vi. Use for: mostly gram positive, some gram neg
1. Not pseudomonas 2. Erythro- staph, strep, atypical pneumonias
3. Community acquired pneumonia
vii. Adverse effects: GI toxicity (frequent), warfarin
interaction (bleeding) i. Lincosamides (clindamycin)
i. Covers grampositive, and anaerobes 1. no gram neg
ii. metabolized in LIVER iii. does not penetrate CSF iv. use
for:
1. community MRSA 2. bacterial vaginosis 3. staph, strep
j. Quinolones i. Block DNA synthesis by inhibiting gyrase,
topoisomerase ii. Absorbed very well orally iii. Renally excreted
iv. Enters the prostate (use ciprofloxacin) v. Contraindicated in
pregnancy
1. Can cause tendonitis, tendon rupture vi. Adverse effects
1. CNS, arthropathy, photosensitivity vii. Fluoroquinolones
1. Ciprofloxacin- for gram negatives, a. Only oral option for
pseudomonas b. No anaerobes c. Worsk for intracellular pathogens d.
Use for:
i. UTIs, Prostatitis, bacterial diarrhea, some STDs, anthrax 2.
Moxifloxacin and levofloxacin
a. Expand gram positive coverage i. Use for: Bronchitis,
community pneumonia
k. Nitroimidazoles i. Anaerobes, some parasites ii. Is reduced
to cyctotoxic intermediates that inhibit DNA synthesis
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iii. Includes METRONIDAZOLE 1. Good oral absorption 2. Enters
CSF, BRAIN 3. Use for:
a. Anaerobic infection, brain abscess, c.diff colitis, bacterial
vaginosis; giardia, trichomonas, amoeba
4. Adverse effects: nausea, metallic taste, seizures, peripheral
neuropathy, antabuse effect
l. Sulfonimides i. Dont use alone, everythings resistant.
1. Use with trimethoprim. Both inhibit steps in folate synth ii.
Gram positives, some enterobacteraciae
1. Use for: nocardia, toxoplasmosis, pneumocystis iii. Adverse
effects: Hypersensitivity (HIV), hemolytic anemia, Jaundice,
neutropenia
m. Trimethoprim i. Penetrates prostate
1. Use for prostatitis, certain UTIs n. Trimethoprim
Sulfamethoxazole (TMP-SMX)
i. Synergistic ii. bacterioCIDAL iii. used in HIV pts iv. covers
gram positives some gram neg. v. use for: pneumocystis,
toxoplasmosis, nocardia, uncomplicated UTI, prostatitis,
some STDs, MRSA (outpatient. Its oral)
Blood stream Infections o. Bloodstream infection
classification
i. 2 infection: from another infected site ii. 1 infection: from
an unknown site
1. Catheter 2. Endocarditis
iii. Transient p. Diagnosis of CA- BSI
i. Clinical picture ii. Get blood cultures iii. No evidence of
infection elsewhere
q. Tx i. Remove catheters if possible ii. Treat 7-14 days if
uncomplicated,
1. 4-6 weeks if complicated (endocarditis, supperative
thrombophlebitis, osteomyelitis)
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iii. Risk factors 1. Imm supp 2. Neutropenia 3. CHF 4. DM 5.
Being fed through the catheter (TPM) 6. Catheter scenario,
location, type
iv. Complications 1. Endocarditis 2. Osteomyelitis 3.
Endopthalmitis 4. Septic arthritis 5. Septic pulmonary emboli 6.
Systemic abscesses
Endocarditis r.
i. Usually infects valves ii. Pathophysiology
1. Native valves with underlying disease 2. damage of valve with
fibroblast healing 3. transient bacteremia 4. colonization of valve
5. growth of vegetation
iii. If untreated, fatal. If treated, still probably fatal iv.
In a native valve, its usually oral strep or staph aureus v. In
IVDU, Its usually s.aureus vi. In prosthetic valve, EARLY, its coag
neg staph. LATE its oral strep vii. Culture negative
endocarditis
1. HACEK organisms a. Hard to culture b. Haemofilus c.
Actinobacillus d. Cardiobacterium e. Eikenella f. Kingella
viii. Clinical picture: 1. Fever, chills, cardiac murmur,
arthralgia/myalgia, 2. Vascular signs
a. Osler nodes- tender nodules on fingers i. Indicate chronic
endocarditis
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ii. Autoimmune vasculitis b. Splinter hemorrhages- in the
fingernail (usu near base) c. Janeway lesions- look like
bruises
i. Palms and soles ii. Contain bacteria
d. Roth spots- retinal spots e. Petechiae- hemorrhages on
conjunctiva
ix. Diagnosis: 1. 2 major criteria: microbiologic (blood
culture), evidence of endocardial
involvement 2. Minor criteria: predisposition, fever,
immunologic/vascular phenomenon,
microbiologic 3. Trans Esophageal Echo is gold standard
x. Embolic complications 1. Stroke 2. Brain abscess 3. Lung
abscess 4. Spleen problems 5. Kidneys
xi. Tx: based on organism 1. Empiric Vanc + gentamycin +
ceftriaxone 2. Use penicillin if sensitive 3. Treat for 4-6 weeks
4. Surgery if necessary
a. Valve insufficiency causes CHF b. Persistent sepsis c. Valve
ring/myocardial abscess d. Others
xii. Prophylaxis for IE 1. Dont use for most patients 2.
Consider if:
a. Prosthetic valve b. Previous IE c. Heart transplant with a
valvulopathy d. Unrepaired cyanotic shunt e. NOT Mitral valve
prolapsed
Skin and soft tissue infections 3.
a. Impetigo i. Mostly in kids
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ii. Superficial intraepidermal vesicles iii. Crusty, weeping iv.
Caused by : Group A strep or Staph Aureus
b. Folliculitis i. Inflammation of hair follicles ii. S. aureus
is common. Pseudomonas from pools, hot tubs
c. Furuncle i. In areas of friction, perspiration. Contain hair
follicles ii. A red tender nodule of pus iii. Risk factors:
Obesity, neutropenia, DM, steroids
d. Erysipelas i. Clearly demarcated, slightly raised area. Peau
dorange ii. Older adults, kids iii. Lower extremity iv. Caused by:
group A strep v. Venous stasis, lymphatic obstruction, DM, alcohol
abuse
e. Cellulitis i. More diffuse border, not raised ii. Secondary
to trauma, other lesion iii. Hot, tender, swollen iv. Fever,
malaise, chills, leukocytosis v. Caused by: staph aureus or any
strep vi. Drug of choice is vancomycin
f. Necrotizing Faschiitis i. Effects extremities mostly ii.
Erythematous, hot, painful, no defined borders (initially) iii.
Fever, leukocytosis positive gram stain iv. Changes quickly:
red-purpleblue-graygangrene v. Loses feeling (doesnt hurt anymore)
vi. Fourniers Gangrene
1. In males. Involves scrotum, perineum 2. Multiple bacteria
vii. Tx: Surgical debridement, antibiotics g. Pyomyositis
i. Infection, abscess of muscle ii. Immunocompromised, following
blunt trauma iii. Usu Staph Aureus
h. Community acquired MRSA i. Has the P-V Leukocidin ii. Usu
cutaneous iii. Use vanc, I guess. Lots of options
i. Vibrio Vulnificus
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i. Liver disease + ingest raw shellfish ii. Necrosis in arms,
legs. May need amputation iii. Doxycycline is drug of choice
j. Cutaneous Anthrax i. Direct contact ii. Prurituspainless
papule vesicle painless necrotic ulcer with black center iii. Treat
with Ciprofloxacine or Doxyfloxacine for at least 60 days
k. Acute lymphangitis i. Tracks up lymphatics ii. Seen with
Pasteurella (cat bites), Group A strep
l. Mycobacterium Marinum i. Open wounds exposed to
freshwater/aquariums ii. Subacute/chronic cellulitis iii. Lesions
track up lymphatics
m. Toxic Shock mediated disease i. Fever, nausea/vomiting,
diarrhea, confusion ii. Staph Aureus (mortality LOW) or Group A
strep (mortality HIGH) iii. Desquamating rash
n. Scalded skin syndrome i. Begins with a known infection ii.
Treat with Vanc
Bacterial Pneumonia 4.
a. Risk factors i. Disruption of barriers (anatomical,
mechanical)
1. Smoking 2. CHF 3. COPD, Asthma
ii. Increased exposure to pathogens 1. Crowding 2.
Aspiration
iii. Immune Deficiencies 1. Infant not breastfeeding 2. Very old
3. DM 4. HIV
iv. Iatrogenic manipulations 1. Bronchoscopy 2. Sedation 3.
Immunosuppression
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b. Clinical picture i. Fever, productive cough, pleuritic chest
pain ii. Tachypnea, rales, leukocytosis (mostly band)
c. Strep pneumoniae i. most common cause of CAP ii. can kill you
iii. most damage is caused by the inflammatory response it creates
iv. remember: polysaccharide capsule, diplococcus v. Tx:
Ceftriaxone
d. H. Influenza i. Chronic lung disease ii. Gram neg
coccobacillus iii. Makes a weak beta lactamase. iv. So use 2nd gen
cephalosporin
e. Moraxella i. Gram neg diplococcus (just like neisseria) ii.
Colonizes nasopharynx. When it spreadsdisease
f. Staph Aureus i. Severe Necrotizing pneumonias in healthy kids
ii. Pleural effusions, empyema iii. CA-MRSA common. Has P-V
leukocidin iv. Tx: Vanc
g. Atypicals: Chlamydia, legionella, mycoplasma h.
Diagnosis:
i. Blood culture, sputum culture ii. CXR iii. O2 sat
i. Tx: i. Supportive:
1. Blood pressure (IV fluids, pressors) 2. Ventilatory support
(mechanical ventilation, O2
ii. Antibiotics 1. First empiric 2. Then pathogen-directed
j. Hospital Acquired Pneumonia i. 48-72 hours after admission
ii. Usu resistant bacteria (oft gram negative)
1. Enterobacteriaceae, pseudomonas, staph aureus iii. Dx: Sputum
gram stain and culture iv. Tx: empiric, broad spectrum
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Sepsis 5.
a. SIRS: i. Temperature too low or high ii. HR>100 iii.
RR> 20/min iv. WBC over 12,000 or under 4000 v. Very easy to
have this, just by walking up some stairs
b. SIRS + infection = sepsis c. Sepsis + 1 sign of organ failure
= severe sepsis d. Sepsis + inability to keep adequate blood
pressure despite fluids = septic shock e. Mostly caused by gram
positive organisms
i. Fungi have been increasing f. Pathogenesis
i. Endotoxin binds to immune cell cell makes inflammatory
cytokines (IL-1, IL-6, TNF
1. fever, tachypnea, tachycardia 2. capillary leak, neutrophil
migration, platelet aggregation 3. vasodilation
ii. inadequate blood pressure iii. Lactic acidosis death iv.
Hyperreactive immune response to LPS
1. Binds to TLRs a. TLR4 does gram neg b. TLR2 does gram pos
i. Gram pos sepsis is usually staph aureus 1. Uses peptidoglycan
instead of LPS
g. Diagnosis i. At least 2 blood cultures
1. One from each central line, if present ii. Remember, its not
always infectious
h. Tx i. Early antibiotics, broad spectrum ii. Pick based on
clinical presentation (transplant? Neutropenic? HIV?) iii. Drain
pus, debride tissue, remove infected material iv. Activated Protein
C
1. Anticoagulant, antiinflammatory 2. Expensive, bleeding
risk
v. Corticosteroids 1. Debated
vi. Maintain normoglycemia in dm pts
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1. Just keep it reasonable
Atypical Pneumonia 6.
a. Typical vs Atypical Typical Atypical
Onset acute insidious
Sx fever, cough, chest pain Fever, cough, headache
Constitutional Sx severe moderate
Physical findings rales, consolidation minimal rales
Sputum purulent, rust colored scant, clear
Leukocytosis common mild
CXR airspace disease interstitial
Response to penicillin prompt none
b. Causes: i. Mycoplasma pneumoniae
1. Lacks cell wall 2. Contains membrane sterols 3. fried egg
appearance on microscope 4. Long replication time 5. School-aged
kids, with pneumonia visible on Xray 50% chance its mp 6. Infects
mucus membranes of respiratory tract
a. Not alveolar, Its AIRWAY 7. Diagnosis is clinical 8. Tx:
macrolides (azythromycin)
ii. Chlamydia pneumonia 1. Looks similar to m.penumoniae 2. May
have a long duration. 3. Mild sx 4. Tx: macrolides
(azythromycin)
iii. Chlamydia psittaci 1. Chlamydiae are obligate intracellular
2. Nuclear inclusions seen
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3. Psittaci is related to parrots iv. Legionella pneumophila
1. Many strains now 2. Fastidious growth requirements 3. Found
in aquatic environment 4. Likes warm 5. Lives within amoebas 6.
Chlorine resistant 7. No person to person transmission 8. May
appear to have multisystem involvement 9. Dx test: sputum culture
10. Tx: Azythromycin
v. Viral pneumonias 1. Esp in kids 2. Seasonal
Gastroenteritis 7.
a. Mechanisms of pathogens i. Secretory toxin: inhibit
absorption, enhance secretion (cholera) ii. Cytotoxins: destroy
absorptive cells, giving diarrhea (shiga toxins, c.diff) iii.
Invasion: Burrow into mucosa, inhibit structural resorbing ability
(campylobacter) iv. Neurotoxins: vomiting predominates. Bug may be
dead already (staph enterotoxin)
b. Sx: i. Vomiting toxin, virus ii. Nonbloody diarrhea small
bowel dysfunction (shigella, salmonella) iii. Bloody
diarrheabacterial colitis, colon
c. Cholera i. Water-borne ii. Toxins:
1. cholera toxin a. A subunit: ADP ribosylase
i. Translocates into cell/causes harm to cell b. B subunit: GM1
ganglioside
i. Docking mechanism. Highly immunogenic c. Locks adenylate
cyclase in ON position
i. Enhances cAMP levels ii. Enhances Cl secretion
2. pili (attachment) iii. They lose 1-2 LITERS of stool per HOUR
iv. Tx: Rehydration
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1. Water + salt + sugar d. E.Coli diarrhea
i. Enterotoxigenic Ecoli- travellers diarrhea 1. Secretory
diarrhea cholera-lite 2. Harms kids more than adults 3. antiBio may
help, but NOT prophylaxis
ii. Enteropathogenic Ecoli- severe infantile diarrhea iii.
Enteroinvasive Ecoli- like shigella iv. Enteroaggregative Ecoli-
chronic diarrhea v. Enterohemorrhagic Ecoli (produces shigatoxin)-
Ecoli o157:H7
1. Can be lethal 2. In foods often (rare burgers) 3. Can give
hemorrhagic colitis
a. Toxins in bloodstream injure endothelial cells b. Form clots
c. Frickin everywhere.
4. Hemolytic uremic syndrome e. Rotavirus
i. Has a capsid ii. Nearly everyone gets some rotaviral
infections as a kid iii. The first one is worst iv. It can kill
children v. Vaccine: they made one, but it had intussiception risk
not acceptable in us
1. So other countries (where it couldve saved kids lives) also
didnt accept it. f. Giardia
i. Carried in water ii. Non-bloody chronic diarrhea iii. Treat
with metronidazole
g. Entameba histolytica i. Amebiasis ii. Rare in US. iii. Tx
with metronidazole
h. Cryptosporidium parvum i. Severe chronic non-bloody diarrhea
ii. Even in immune competent ppl iii. Treat with nitazoxanide
i. C. Diff i. Healthy ppl often carry it ii. Culture is tedious.
DONT. just test for toxins iii. Pseudomembranous colitis iv. Tx:
Vancomycin
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Urinary Tract Infections 8.
a. Clinical syndromes i. Bacteuria- bacteria in urine that
shouldnt be there ii. Acute cystitis
1. Most common 2. Voiding syndrome
a. Burning urination b. Feeling like you need to go all the time
c. Suprapubic tenderness d. Occult URI
iii. Pyelonephritis- upper tract infection 1. Flank pain 2.
Fever, chills 3. Nausea, vomiting
iv. Renal abscess 1. Abscess around/in kidney 2. From untreated
pyelo 3. Can give fever of unknown origin
v. Uncomplicated UTI- UTI involving normal urinary tract with no
functional problems vi. Complicated UTI- everything else
b. Epidemiology: more in women then men i. Women: starts medium,
rises after sexual activity ii. Men: starts low (neonate), drops to
zero, rises after age 45
c. Caused by: i. Uncomplicated: 80% E.Coli 20% proteus,
enterobacteraciae ii. Complicated: 20% e. coli 80% klebsiella,
enterobacteraciae, pseudomon
d. Mostly ascending (90%) e. Pathogenesis
i. Vaginal colonization happens first ii. Entry into urinary
tract iii. Bacterial virulence
1. Adherence 2. Toxins 3. Capular polysaccharides 4. Urease
production
iv. Host Defense 1. Colonization resistance from urogenital
flora 2. Antimicrobial properties of urine 3. Inflammatory
response- leads to turnover and sloughing of infected cells 4.
Micturition, bladder emptying gives mechanical protection
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5. Specific immune responses 6. Barrier method contraception
increases risk
v. Risk factors for worse outcome 1. Infants, Kids 2. Pregnant
women 3. Compromised adults: DM, imm comp, spinal cord injury
f. Diagnosis i. Internal dysuria, other voiding sx, abrupt
onset, no vaginal discharge ii. Urinalysis, microscopy
1. If you dont have pyuria, you dont have cystitis iii.
Leukocyte esterase test
1. If negative, they dont have UTI (checks for pyuria) iv.
Nitrite test
1. Specific but not sensitive g. Tx: Bactrim (TMP/SMZ) for 3
days (uncomplicated)
i. 7 days if risk factors ii. 14 days for men
h. Acute uncomplicated pyelonephritis (women) i. Usu ecoli ii.
Pyuria present iii. Tx: fluoroquinolones iv. Culture after therapy
is over
i. Recurrent UTI i. Relapse/reinfection ii. Change contraception
iii. Cranberry juice? iv. TMP/SMZ prophylaxis
Anaerobic Infections 9.
a. Gram Negative: i. Bacteroides (esp fragilis)
1. Give the most greif b. Gram Positive
i. Peptostreptococcus ii. Clostridium iii. Lactobacillus
c. Live in mucosal surfaces and GI tract i. Not in stomach ii.
Predominate in colon
d. Hallmarks
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i. Suppuration ii. Abscess iii. Thrombophlebitis iv. Chronic v.
Polymicrobial (synergy) vi. Gas formation vii. Lowered blood supply
predisposes viii. Infection adjacent to mucosal tissue ix. Smells
like feces x. Virulence factors: Exotoxins (clostridium), Capsular
polysaccharides, beta lactamase
(bacterioides fragilis) e. Specimens necessary
i. Blood, aspirates, pus, deep tissue. No swabs f. Tx:
ampicillin-sulbactam (include a beta lactamase inhibitor)
i. Drain, debride g. Diseases caused
i. Head and neck infection 1. Ludwigs angina (neck spaces) 2.
Lemierres syndrome (septic thrombophlebitis of jugular vein) 3.
Gingivitis, dental abscess, to mandible
ii. CNS 1. Solitary brain abscessanaerobe 2. Spreads from
chronic otitis, mastoiditis, sinusitis 3. Tx: metronidazole plus
ceftriaxone
iii. Pulmonary infection 1. Aspiration of oral flora 2.
Necrotizing pneumonia, abscess, empyema 3. Tx clindamycin
iv. Intraabdominal infection 1. Perforation
a. You need surgery b. Treat with combos (polymicrobial)
v. Pelvic infection vi. Skin, soft tissue
1. Gas gangrene, nec fasc 2. Deep tissue involvement 3.
Aggressive debridement, antibiotics
h. Clostridium Difficile i. Gram pos, spore forming, anaerobe
ii. All over hospitals iii. Causes pseudomembranous colitis iv.
Really bloody diarrhea
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v. Toxins A, B- cytoskeleton injurymucosal injuryfluid secretion
vi. Culture not useful vii. Complications
1. Fulminant colitis, perforation, toxic megacolon viii. Tx:
oral vanc
i. Clostridium perfringens i. Gas gangrene, myonecrosis, nec
fasc ii. Enterotoxin (food poisoning) iii. Aggressive deridement
iv. Penicillin + clindamycin
j. Clostridium tetani i. Preventable ii. Toxin- tetanosporin.
Stops inhibition of motor neurons
k. Clostridium Botulinum i. Foodborne ii. Descending paralysis
(prevents Ach release) iii. Makes 7 neurotoxins
l. Actinomycoses i. Gram positive branching bacillus
1. Looks like a fungus but is NOT 2. Not acid fast (unlike
nocardia)
ii. Sulfur granules in tissues iii. Extends through tissue
planes like malignancy iv. Tx: penicillin
Arboviruses, Enteroviruses 10.
a. Arthropod-borne viruses b. Potential for explosive epidemics
c. Humans are dead-end hosts d. Usual vectors: mosquitoes, ticks,
fleas e. Dengue fever
i. Most important flavivirus ii. Mosquito borne (aedes aegypti)
iii. Distributed in a belt across the world: tropics, subtropics
iv. Get infected and reinfected. Sequentially worse. v. breakbone
fever- fever, rash, HA, severe myalgia, arthralgia vi. Heals with
no sequelae unless vii. Dengue shock syndrome- 3rd space fluid into
lungs, abdomenhypovolemic viii. No treatment
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23
ix. It takes less than 2 weeks to show up (so if travel was more
distant than that, dont worry)
f. West Nile i. Normally between birds and mosquitoes ii.
Epidemiology: over 55 higher risk iii. Fatality is worse for
hospitalized pts iv. Genetic susceptibility: CCR5 mutation v.
Pathogenesis
1. Bitten by mosquitotravels to lymph nodeviremiaCNS 2. If high
enough innoculum, can cross BBB, kill neurons
vi. 5-10 days after mosquito bite vii. Mild: fever, headache,
myalgia/arthralgia, anorexia viii. Sore throat ix. Rash (trunk>
extremities) (rare in US cases) x. Recovery is usu complete, worse
in adults than kids xi. Tx: no real tx
g. Chikungunya virus i. Mosquito borne (aedes aegypti) ii.
Debilitating febrile illness (joint pain impossible to move) iii.
No vaccine/tx iv. Possibility of pandemic
h. Enteroviruses i. Many serotypes ii. Usu infections are mild:
febrile rash, UTI iii. Very small iv. Non-enveloped v. Have a
protein coat
1. So hard to decontaminate. Alcohol wont help here vi. Mostly
in summer and fall vii. Mostly in young kids viii. Transmission:
fecal-oral, respiratory droplets ix. Adults have more severe
disease x. Men 2X xi. Can make vaccines (it worked for polio), but
theyre so small, they can be
synthesized. xii. Diseases caused
1. Aseptic meningitis a. Coxsackievirus group B b. Summer and
fall meningitis
2. Encephalitis a. Altered mental status, focal neurological
signs, seizures b. Worse prognosis than aseptic meningitis
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24
c. Enterovirus 71 3. Cardiac disease
a. Acute myocarditis in young ppl (esp males) i. Enteroviruses,
coxsackie
b. Chronic cardiac disease i. Sporadic dilated cardiomyopathy
ii. Coxsackie group B
4. Eye infections a. Acute hemorrhagic conjunctivitis b.
Excessive lacrimation, pain, periorbital swelling, redness,
visual
impairment 5. Respiratory syndromes
a. Enteroviruses- cause URI 6. Herpangina
a. Febrile illness, acute onset, sore throat i. Lesions on
tonsils, soft palate, uvula, pharynx ii. May be part of
hand-foot-mouth
7. Hand-Foot and Mouth disease a. Common in kids b. Very
contagious
xiii. Therapy: supportive care
DNA Viruses (Herpes) 11.
a. Double-stranded, enveloped DNA virus b. Gene expression
i. VP16 stimulates transcription of IE genes (doesnt require
protein synth) ii. IE genes code for proteins that stimulate Early
Gene expression iii. Early Genes encode nonstructural proteins that
help DNA synthesis iv. DNA replication occurs v. Late Genes are
expressed, genes for structural proteins
c. Latency i. Virus persists for life as an episome (limited
viral gene expression, noninfectious) ii. Latency is failure to
stimulate IE gene expression iii. Reactivation may or may not have
signs and sx
d. Transmission- direct contact w body fluid i. Does not survive
in environment ii. Mucosal surfaces, resp tract, bloodstream are
susceptible sites
e. HSV 1 and 2 i. HSV1
1. Orolabial
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25
2. Usu get it in childhood 3. Up to 90% of adults have it
(higher levels in poorer ppl) 4. 20-40% recur 5. Course:
a. Primary infection- most widespread i. Fever, malase, myaglias
ii. Lesions on palate, lips, tongue
b. Latent- noninfectious HSV in the trigeminal ganglion c.
Recurrence
i. 20-40% in first year ii. More limited iii. Triggered by:
trauma, light, imm suppression
6. Incubation is from 2-14 days 7. Many people are asymptomatic
carriers
ii. HSV 2 1. Genital 2. Sexually transmitted 3. 25% of adults
have it 4. 60-90% recur 5. Painful lesions 6. Primary infection can
have systemic sx (like HSV1) 7. Incubation period of 2-7 days 8.
Virus can be shed asymptomatically
iii. Diagnosis: 1. Viral isolation
iv. In Imm Comp 1. Reactivate frequently 2. Can involve other
systems (gi, etc) 3. Is a prominent feature in advanced HIV
v. Tx 1. HSV1- analgesics, acyclovir (esp if recurrent) 2. HSV2-
also acyclovir
vi. Encephalitis 1. Most common endemic encephalitis in US 2.
Usu caused by HSV1 3. Can happen at any age 4. Dx: CSF PCR. MRI if
you want 5. Tx: high dose acyclovir for 3 wks
f. Varicella Zoster virus i. Spread by direct contact ii.
Primary infection: Chicken pox
1. 5-9 yo
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2. Respiratory spread 3. Fever, URI, malaise; THEN the rash
a. By the time you have the rash, youre not contagious 4. Rash:
start on face/head, move down
a. Different stages of vesicle will be near each other 5. Tx:
Antihistamines, acetaminophen, acyclovir (heals faster, fewer
lesions) 6. Vaccine: Varivax.
a. Live, attenuated b. Give to kids
iii. Recurrent infection: Zoster (Shingles) 1. Follows
unilateral dermatomes 2. Pain, burningerythema-papulesvesicles 3.
Mostly in older ppl 4. Virus sheds only while theres rash 5. If it
crosses dermatomes, its disseminated
a. Risk of pulmonary transmission 6. Tx: Acyclovir, analgesics
7. Vaccine: Zostervax
a. Live, attenuated b. Give to adults over 60 c. More
concentrated form of varivax
g. CMV i. Lipid envelope derived from host ii. Largest herpes
virus iii. Infects fibroblasts, endothelial cells, epithelial
cells, and macrophages iv. Can be latent in cells of
monocyte/macrophage lineage v. Pathophysiology
1. Primary infection- Usu resp tract. Then it disseminates 2.
Productive infection- shedding virus from secretions (saliva,
urine) 3. Adaptive immune respose-controls the virus 4. Latency- in
hematopoetic cells in bone marrow, 5. Reactivation- periodically
(from immunosuppression, stress, pregnancy)
vi. Interacts with immune response: 1. Inhibits expression of
MHC 1 2. Blocks antigen presentation of MHC 2 3. Downregulates NK
cells 4. Inhibits TH1
vii. Epidemiology 1. Widespread, requires close contact (person
to person)
a. Saliva, tears, urine, genital secretions, blood b. Vertical
transmission to babies
i. Babies are usu asymptomatic
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ii. more likely to be symptomatic if mom gets CMV during
pregnancy.
viii. Disease: 1. In a normal host, asymptomatic, or mono-like
illness
ix. Transplants 1. Solid organ: Donor positive, recipient
negative is highest risk
a. CMV is common in solid organ transplants b. Just get
systemically sick
2. Stem cells: Donor negative, recipient positive is highest
risk a. CMV pneumonia is common here
i. Bilateral, diffuse, interstitial 3. HIV patients get CMV
retinitis
x. Dx 1. PCR of blood. 2. Amount of virus corresponds to
severity of infection
xi. Tx: Gangcylcovir h. Roseola (HHV6)
i. Beta herpes virus ii. Infects T lymphocytes iii. Sheds in
saliva iv. Everyone gets it within first 3 yrs of life v. High
fever, then as fever breaks, develops rash
1. Some kids dont get the rash 2. Can also get febrile
seizures
vi. Dx: PCR of blood vii. Tx: unsure. Gangcyclovir?
i. EBV i. Replicates in B lymphocytes
1. When it infects them, they become immortal ii. Exposure to
infected saliva
1. pharyngitis 2. shedding in saliva 3. B cell infection
a. heterophile antibodies b. T cell activation
i. malaise, spleen enlargement, atypical lymphocytes ii. control
the B cell population
1. EBV becomes latent iii. Transmission: person to person
(infected saliva) iv. Diseases
1. Infectious mononucleosis a. Fever, tiredness,
lymphadenopathy, sore throat
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b. Rare complications: autoimmune hemolytic anemia,
thrombocytopenia, splenic rupture, encephalitis, meningitis,
guillan barre
c. Tx: supportive care. Acyclovir has no clinical help. i.
Corticosteroids for SEVERE complications
2. Burketts Lymphoma 3. Oral hairy leukoplakia (HIV)
j. Kaposis Sarcoma (HHV 8) i. Multiple lesions ii. Multiple cell
types iii. Worse risk if imm comp iv. Most ppl are asymptomatic v.
If youve had it before, then get AIDS, Kaposis is more common vi.
Dx: PCR, histology vii. Tx: HHV8 is sensitive to foscarnet.
1. Unclear clinical use
Respiratory viruses 12.
a. Often seasonal i. RSV: in the WINTER ii. Influenza: in the
WINTER iii. Rhinovirus: in the SPRING and FALL
b. Most common respiratory virus is rhinovirus c. Rhinovirus
i. Non-enveloped 1. Stable in the environment
ii. Spring and fall peaks iii. Transmitted by particle aerosol,
or secretions iv. Mostly young kids v. Pathogen of upper
respiratory tract
1. Causes common cold 2. Can also go down into lower airways and
cause asthma exacerbations
vi. Non-cytopathic vii. Dx: clinical viii. Tx: symptomatic.
Antihistamines, NSAIDS
d. Influenza i. Enveloped ii. Segmented RNA genome
1. H and N 2. Can recombine (antigenic shift)
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iii. Main reservoir is birds (its a zoonosis) iv. Seasonal
(winter) v. Airborne transmission (doesnt require close contact)
vi. Sx: Fever, malaise, cough, sore throat, feel awful vii.
Cytopathic- damages respiratory epithelium viii. Dx: Viral culture
ix. Tx: Neurominidase inhibitors x. Vaccine
1. Live attenuated (nasal spray) 2. Inactivated (injection 3.
Grown in eggs 4. Reformulated yearly
e. RSV i. Enveloped ii. RNA virus iii. Everyone gets it in first
2 yrs of life
1. 1% need hospitalization 2. Can get reinfected (immunity is
incomplete)
iv. Transmission by large droplets, contaminated secretions v.
Sx: Bronchiolitis, pneumonia
1. Premies- apnea 2. Preexisting heart conditions-
decompensation
vi. Pathophysiology 1. Infection of respiratory epithelial
cells
a. blockage of airways (edema, cellular debris) b. asthma-type
sx (air in, but cant escapehyperexpansion) c. Cell mediated
immunity clears it
vii. Dx: nasopharyngeal aspirate/swab 1. Antigen test
viii. Tx: mostly symptomatic (o2, hydration, ventilation if
needed) 1. Ribovirin for imm comp
Antiviral agents 13.
a. Herpes drugs i. Topical:
1. trifluorothymidine a. Drug of choice for hsv
keratoconjunctivitis
2. Cidofovir a. Very toxic b. Used for resistant strains of DNA
viruses (CMV, HSV, EBV, VSV)
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30
i. For immunocompromised, before it disseminates 3.
Docosanol
a. Over the counter. b. Recurrent HSV
ii. Systemic 1. Require phosphorylization inside the cell 2.
Acyclovir
a. Inhibits DNA polymerase b. Prefers HSV DNAp to host DNAp c.
Use for HSV, VZV (VZV requires higher doses) d. Adverse effects:
rare, reversible
i. Watch out for CNS (confusion, seizures. More in elderly) 3.
Valacylcovir
a. Prodrug of acyclovir b. 4X more bioavailable
4. Famicyclovir (prodrug), penicyclovir a. Same action as
acyclovir. b. Also, hep B c. Famicyclovir = oral; penicyclovir=
topical
5. Gancyclovir a. For HSV- same efficacy as acyclovir b. CMV-
10-50X BETTER c. Competitive inhibitor of DNAp d. Use for: serious
CMV infections, transplant prophylaxis e. Renally cleared f. Lots
of toxicity
i. Neutropenia, anemia ii. Bone marrow suppression
6. Valcancyclovir a. Prodrug b. Oral availability equals IV!
(high serum levels)
iii. Foscarnet 1. Non-nucleoside inhibitor 2. Doesnt require
phosphorylation 3. Directly inhibits herpes DNAp 4. Use for
resistant strains esp resistant herpes 5. IV only 6. Very toxic
a. Nephrotoxic (renally clearedrenal tubular injury) b.
Hypo/hyper calcemia, hyperphosphatemia c. Penile ulcers
b. Influenza virus
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31
i. Vaccine is most important ii. Prophylaxis if not iii.
Neurominidase inhibitors
1. Zanamivir, Oseltamivir a. Work for influenza A and B b.
Prevent release of virus particles (so new cells arent infected) c.
Few side effects d. Expensive e. Only shortens illness by a few
days f. Theres resistance to oseltamivir
iv. (and amantidines, but resistance is common) v. Ribavirin
1. Only use for Hep C a. This plus interferon is the
treatment
2. Resistance is rare 3. Inhibits viral mRNA formation 4. Can
use the aerosol for RSV pneumonia 5. Contraindicated in pregnancy
6. Can get concentrated in RBCshemolytic anemia
vi. Interferon-inhibits viral replication 1. Adverse effects:
fever, chills, acute pneumonia chronic fatigue,
depression, ataxia
Acid Fast Organisms 14.
a. Lipid rich wall i. Allows for: resistance to drying,
antibiotics, detergents
b. Penetrates macs, lives freely in them c. M. Tuberculosis
i. Rates 2x men ii. Crowding, poverty iii. HIV, Silicosis, IVDU,
DM, end stage renal disease iv. Person-to-person (small aerosolized
droplets) v. Latent TB
1. Positive skin test/assay 2. No signs/sx 3. Not infectious
vi. TB 1. Caseating, granulomatous, usu upper lobes
vii. Pulmonary TB Reactivation 1. Cough, hemoptysis, weight
loss, night sweats
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32
2. Primary: hilar nodules viii. Extrapulmonary TB
1. Pleuritis- hurts to breathe 2. Lymphadenitis- more WOMEN.
Maybe no systemic sx 3. Ostomyelitis- the spine. May have cold
abscess of psoas
ix. Military TB 1. Lymphohematogenous spread 2. Can happen in
infants
x. TB skin test: test sucks 1. Measure area of induration 2.
5mm:
a. Past TB pts b. Close contacts of TB pts c. HIV pts
3. 10 mm a. IVdrug use b. Healthcare workers c. Ppl with risk
factors d. Immigrants from endemic countries
4. False negatives- due to anergy 5. False positives- BCG
vaccine
xi. IFNGamma Release Assays 1. Drug of choice for ppl with BCG
vaccine 2. More specific 3. Doesnt require return for reading 4.
Results in 24 hrs
xii. Anti TB drugs 1. Isoconazid
a. Interferes with mycolic cell wall synth b. Hepatotoxicity,
renal toxicity
2. Rifampin a. Inhibits DNA dependent RNA polymerase b. Adverse
rxns: Hepatitis, hypersensitivity, Drug interactions (cyt
P450) 3. Rifabutin
a. Similar mech to rifampin b. Fewer drug interactions c. Better
to use in HIV
4. Pyrazinamide a. Adverse effects: nausea, hepatotoxicity,
hyperuricemia, arthralgias
5. Ethambutol a. Inhibits cell wall synth
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33
b. Adverse effects: optic neuritis xiii. Treat w all four drugs
for 2 mo, INH & rifampin after that, total 6 mo
1. Directly observed therapy xiv. Noninfectious: all of:
1. 3 separate sputum cultures negative 2. Responding to therapy
3. 2 weeks of therapy
d. Non-tuberculous mycobacteria i. Hansens Disease (m.
Leprae)
1. Tuberculoid a. Low bacterial burden, low infectivity
2. Lepromatous a. High bacterial burden, high infectivity
3. Anesthetic plaques 4. Sensory/motor neuropathy 5. Prefers
cooler skin 6. Does NOT grow in culture
ii. Nocardia 1. Found in soil 2. opportunist 3. Skin, lung,
brain 4. Tx: TMP-SMX 5. Branching, filamentous
iii. Rhodococcus 1. Found in soil 2. Opportunist 3. Exposure to
horses 4. Grows red on culture 5. Causes cavitary pulmonary disease
in imm comp 6. Tx: Vanc
STDs: Genital Ulcer Syndromes 15.
a. Syphillis i. T. pallidum ii. Difficult to grow iii. Humans
sole host iv. Pathogenesis
1. Penetrates skin via microabrasions a. Replicates w/o
inflammation b. Travels to lymph nodesblood streamsystemic
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c. Causes primary lesion at site of inoculation i. Painless
ulcer ii. Indurated iii. punched out iv. Scant secretion
v. Primary infection: painless ulcer. 1. 3 weeks after
exposure
vi. Secondary infection: rash on palms, soles. Systemic vii.
Teritary infection: Neuro, CV (ascending aorta), optho viii.
Congenital: oft causes stillbirth ix. Tx: Penicillin
b. Genital herpes i. Usu HSV2 ii. Initial infection:
1. Systemic: fever, malaise, headache, pharyngitis, myalgias 2.
Local: pain, itching, discharge, pyuria, lymphadenopathy
iii. Recurs in 80% 1. Has a prodrome (itching, burning)
iv. Lesions: 1. Papulevesiclecrustinghealing with no scar
v. Dx: viral culture, serology vi. Tx: Acyclovir
c. Chancroid i. Haemophilus ducreyi ii. Requires break in skin
to infect iii. Pyogenic, painful iv. box car or school of fish
appearance histologically v. Disease
1. Genital ulcer 4-7 days post exposure a. Soft, ragged border
b. Tender c. Usu multiple d. Painful regional lymphadenopathy
vi. Tx: cephtriaxone
Candida and antifungals 16.
a. Most common is albicans b. Only present where animal
contamination is possible c. Present in hospitals d. Grows white on
agar
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e. Human oropharynx, GI tract f. Diseases
i. Candidemia 1. Candida isolated from one or more blood
cultures 2. Can be a sign of acute disseminated candidiasis
ii. Disseminated candidiasis 1. Histologic evidence of tissue
invasion AND 2. Culture positive at 2 different normally sterile
sites 3. New fever, or septic in a seriously ill person 4.
Candiduria (wo catheter) 5. Rash: nonspecific, popular. Can biopsy
them and find candida 6. Retinal lesions 7. Lesions in liver 8. Tx:
Echinocandin
a. Fluconazole for Albicans i. DONT USE if unstable or c.
glabrata
iii. Vulvuvaginal candidiasis 1. Vaginal discharge
a. May just have pruritis, no discharge iv. Thrush, Diaper
rash
g. Antifungals i. Polyenes
1. Nystatin a. Topical, b/c too toxic to give otherwise
2. Amphotericin B a. Binds to ergosterol in cell membrane b.
Increases permeabiliby c. gold standard d. Nephrotoxic e. Lipid
preparations
i. Less toxic ii. Bigger therapeutic window
ii. Azoles 1. Inhibit ergosterol synthesis cells leak 2.
Oral
a. Fluconazole b. Itraconazole c. Voriconazole d.
Posaconazole
3. Topical a. Ketoconazole b. Clotrimazole
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36
c. miconazole iii. echinocandins
1. Inhibit cell wall crosslinking (glucans) 2. Used for Candida
3. Well tolerated 4. Expensive 5. IV 6. Includes:
a. Caspofungin b. Micafungin c. Anidulofungin
iv. Other 1. Allylamines
a. Topical b. Inhibit sterol synth
2. Flycytosine a. Inhibits DNA synthesis b. Treats cryptococcal
meningitis c. Bone marrow toxicity
Opportunistic Mycoses 17.
a. Cryptococcus Neoformans i. India ink stain shows a capsule
ii. Encapsulated yeast iii. Narrow-based budding iv. Transmission
via inhalation v. Risk factors: SEVERE HIV. CD4 < 50. Less so,
other immunosuppression vi. Clinical presentation
1. Meningitis (esp HIV) a. Subacute b. Elevated opening pressure
c. High white cells d. Tx: Amphotericin B and Flucytosine, then
fluconazole
2. Pulmonary disease: nodules, cavitary lesions, miliary, others
3. Disseminated 4. Skin 5. GI
vii. Everyone w/crypto gets an LP 1. Rule out meningitis
viii. Tx: AIDS pts: lifelong suppression w fluconazole
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b. Pneumocystis Jiroveci i. Whispy interstitial infiltrates ii.
Cant grow in vitro iii. Transmission via inhalation iv. Seen in:
HIV patients (CD4 < 200); corticosteroid pts v. Tx: TMP/SMX, add
predisone for serious cases
c. Aspergillus i. Septated acute angle hyphae ii. Ubiquitous
iii. Fumigatus is most common iv. Can be caused by problems in
ventilation. Demolition v. Seen in: Neutropenic pts. Rarely in HIV.
vi. Pulmonary:
1. Low grade fever 2. Hemoptysis (sometimes severe) 3. Chest
pain 4. Cough 5. Pulmonary infiltrates 6. CXR, CT shows halo
sign
vii. Non-pulmonary: 1. Sinusitis (w nosebleeds) 2. CNS disease
(focal neural signs) 3. Skin
viii. Tx: reduce immunosuppression 1. Voriconazole
d. Zygomycosis (mucormycosis) i. Grows in the environment (on
strawberries
1. Rhinocerebral 2. Pulmonary 3. Cutaneous
ii. Risk factors 1. Diabetic ketoacidosis 2. Neutropenia 3.
Hematological malignancies 4. Iron chelating therapy
iii. Pathogenesis 1. Inhaled (or cutaneous inoculation)direct
invasion (nonhemotogenous) 2. Can cross tissue planes 3. Likes
vascular invasion
iv. Clinical 1. Facial pain, headache, fever 2. Orbital
cellulitis, necrosis of the palate, black nasal discharge,
proptosis
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38
3. Can also be: Pulmonary, cutaneous, GI v. Dx: Broad,
non-septate, right angle branching
1. Culture may be negative vi. Tx: correct risk factors
(DKA)
1. debridement. e. Sporotrichosis
i. Rose gardens ii. Dimorphic fungi (mold cold, yeast hot) iii.
Clinical
1. Lesion at site of inoculation a. Sub Q nodules w/ulceration,
may get more in lymphatic distribution
iv. Tx: Itraconazole
Endemic mycoses 18.
a. Histoplasmosis i. Dimorphic fungus: outside mold, in the body
yeast ii. Mississippi and Ohio river valleys iii. Bat guano, bird
roosts iv. Transmission: like TB. Easy to cough out, hangs in
air
1. Inhaled v. Pathophysiology
1. Alveolar macrophages engulf it 2. They divide and disseminate
in macs
vi. Clinical 1. Acute Histoplasmosis
a. May be asymptomatic b. Maybe flu-like c. Calcified granulomas
indicate past infection
2. Progressive Disseminated Histoplasmosis a. Acute- HIV, imm
supp b. Subacute- immunocompetent ppl
i. Fever, weight loss, malaise ii. Oral ulcers iii.
Hepatosplenomegaly iv. Can look like miliary TB
c. Dx: Serology d. Tx: Amphotericin B for severe
i. Itraconazole for less severe(drug of choice) 3. Other
disease:
a. Isolated pulmonary disease
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39
i. Cavitary or nodule ii. Can look like TB iii. Check for
serology and culture iv. Often in smokers v. Treat with
itraconazole
b. Aseptic meningitis i. Chronic ii. Serology on CSF iii. Treat
with Amphotericin B, then fluconazole
c. Mediastinal Fibrosis i. An overaggressive immune response to
histo ii. Little treatment
d. Erythema Nodosum i. Assosciated with histo
b. Blastomycosis i. Broad-based budding ii. Dimorphic fungus
iii. Eastern and central US
1. Waterways iv. Transmission: enters via lungs v.
Pathophysiology
1. Incubation- 30-45 days asymptomatic vi. Disease: lung, bone,
skin
1. Pulmonary a. Focal lesions
2. Cutaneous a. Get a rash b. Non-healing lesions that
ulcerate
3. bone and joint a. Invasive, destructive focal lesions
4. CNS a. Aseptic meningitis
vii. Dx: biopsy and culture 1. Serology and urine antigen test
arent reliable
viii. Tx: itraconazole. Amphotericin B for severe c.
Coccidiomycosis
i. Dimorphic fungus ii. Spherules full of endospores iii.
Southwestern US iv. Risk: Filipino ppl> African American >
white v. Transmission: inhaled vi. Disease
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40
1. Most are asymptomatic 2. Nonspecific respiratory illness 3.
Infiltrates, hilar adenopathy on CXR 4. Dx: Serology: look for a
change from neg to pos
vii. Tx: Controversial. Maybe or maybe not treat everyone 1.
Definitely treat:
a. HIV pts b. Organ transplant pts c. Pregnancy d. Filipino,
African ppl
2. Itraconazole viii. Chronic coccidio
1. Chronic fibrotic pneumonia 2. Extrapulmonary
a. Cutaneous b. Bone/joint c. Meningitis d. (sounds like
blasto)
3. Dx: Biopsy, culture, serology (titer indicates severity) 4.
Tx: we cant cure this like we can blasto and histo
a. Chronic suppression b. Amphotericin B initially c.
Itraconazole
d. Penicilliosis i. Thailand, Vietnam, southern China ii.
Dimorphic fungus iii. Opportunistic iv. Clinical:
1. Fever, malaise, weight loss > 4 weeks 2. At least one
cutaneous lesion 3. Maybe lymphadenopathy, hepatosplenomegaly,
cough
v. Dx: Pathology, culture vi. Tx: Amphotericin B, then
itraconazole
e. Paracoccidiomycosis i. South American Blasto ii. Looks just
like blasto, but with more cutaneous lesions, esp face
Helminths 19.
a. Host specific b. Dont multiply in humans
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41
c. Many infections are asymptomatic d. Pathogenesis
i. Tissue invasion ii. Compete with hosts for nutrients iii.
Create obstructions iv. Incite harmful immune response
e. Ascaris Lumbricoides i. Pathophys:
1. Ingest eggs a. Stable in environment b. Fecal-oral
2. Larvae penetrate bloodstream a. Can cause eosinophilic
pneumonia
3. Go to lungpenetrate capillariescrawl up airspace 4. Are
swallowedlive in intestine 5. Produce thousands of eggs
ii. Tx: Mebendazole 1. Binds to tubulin, intefrees with motility
2. Poorly absorbed: so it can hit intestinal worms
iii. Southwestern US, Developing countries f. Pinworms
(enterobius vermicularis)
i. Eat eggs ii. Hatch in intestine iii. Live in cecum iv. Adults
come out of anus at night to lay eggs v. Dx: scotch tape test- see
eggs vi. Many ppl are asymptomatic
1. Treat the whole family g. Whipworm
i. Soil transmitted ii. Eat the eggs
1. Barrel shaped, mucus plug at both ends iii. Hatch, live in
intestine
1. Produce more eggs into stool iv. More common in:
1. Kids, developing world v. Can cause: anemia, mental
retardation, growth delay vi. Blanket tx of all kids with
albendazole in developing world
h. Hookworm (ancyclostoma duodenale) i. Pathophys
1. Larvae penetrate skin (of foot) (this itches_ a. Travel in
bloodstream to lung
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42
b. Penetrate capillariescoughed upswallowed c. Reach intestine,
penetrate
i. Bloody diarrhea, abdominal pain on initial penetration d.
Eggs released into stool, hatch in stool e. Larvae can survive in
environment for several weeks
ii. Disease: Anemia (worse with heavier infection) iii. Tx:
Albendazole, mebendazole, and Fe (to help the anemia)
i. Cutaneous Larva Migrans i. Because of host specificity of a
dog/cat hookworm ii. Serpiginous border of rash.
j. Strongyloides stercoralis i. Similar cycle to hookworm,
except can cause autoinfection (hyperinfection)
1. Can be very dangerous in immunosuppressed ii. Walking
barefoot where there are feces iii. Clinical manifestations
1. Oft asymptomatic 2. Lower abdominal rash (where parasites
have entered) 3. Eosinophilia (maybe 4. Abdominal bloating, weight
loss 5. Immunosuppressed (esp steroids) are at risk of
hyperinfection
iv. Dx: larvae (not eggs) in stool v. Tx: Ivermectin
k. Trichinosis i. Eat muscle with larvae in them
1. Oft uncooked pork ii. Hatch in intestinepenetrate
intestinemusclecysts iii. Clincial: fever, severe muscle aches,
periorbital edema, heliotrope rash
1. If severe, myocarditis iv. Tx: Unnecessary. Albendazole can
kill worms, but theyll die on their own anyway
l. Filariasis i. Pathophys
1. Infected mosquito bites 2. Travels to lymph nodes
a. Grow long- block lymph nodes 3. On ultrasound, can be seen
flailing around 4. Can live in blood
a. Only come out at night ii. Disease: edema, Hydrocele,
elephantiasis iii. Dx: look in blood at night OR antigen test iv.
Tx: Albendazole + Ivermectin
m. River-Blindness Onchocerciasis i. South Africa, Yemen
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43
ii. Transmission: Black fly (breeds in rapid streams) iii. Live
in subQ nodules (oft on the head) iv. Inflammitory response causes
blindness v. Can also cause skin changes/inflammation in skin
1. leopard skin vi. Dx: microfilariae in blood vessels vii. Tx:
Ivermectin
1. Blocks neurotransmission in worms 2. Clears it from skin and
eyes, safely 3. But only temporarily. Spares adult worms. 4. So
kill the blackflies 5. Other:
a. There is a bacterium IN the worm: Wolbachia i. Kill thatkills
O. Volvulus ii. Doxy
n. Schistosomiasis i. A fluke (trematode) ii. Liver disease due
to inflammatory response to eggs iii. Pathophysiology
1. Intermediate host: snail 2. Forms circariae (w fork-like
tails)
a. Can penetrate human skin 3. Entersdifferentiates into
adultmigrates to specific tissue
a. If it enters the wrong host, it dies i. Swimmers itch is from
Avian Schistosomiasis
iv. S. Mansoni 1. Eggs have a lateral spine 2. Goes to myenteric
plexus, Portal circulation
a. Causes portal hypertension i. pipe stem fibrosis ii. Caput
medusa, esophageal varices, etc
b. Granulomas surrounding eggs c. In intestine, each egg causes
a polyp
i. Can bleed 3. Can lead to malnutritionpoor development, low IQ
4. Can help with allergies. 5. Tx: not much. Kill the snails
a. Drugs help expose more s. mansoni antigens to the immune
system b. Praziquantel
v. S. Hematobium 1. Eggs have a terminal spine 2. Only in Africa
(esp sub-Saharan)
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44
3. This one goes to the BLADDER PLEXUS a. Can cause fibrotic,
dilated ureters, fibrotic bladderrenal
failuredeath b. Can also get them on the cervixprone to
bleeding
i. More susceptible to other infections like HIV o. Paragonimus
infection
i. Pathophys 1. Ingest raw crayfish 2. Hatch in intestinemigrate
to lungscoughswalloweggs in feces
p. Tapeworms i. Have scolexes, proglottids ii. Cysticercosis
1. Clinical: a. Headache, focal deficits, new onset seizures
2. Pathophys a. Ingest cystercerci in tissues of undercooked
meat
i. Usu pork b. Larva attaches to intestineadultreleases eggs
i. This is asymptomatic c. Ingest eggs
i. Larvae can travel to 1. Brain: Cerebral cysticercosis 2.
Muscle/soft tissue: calcify, seen on Xray
3. Dx: CT/MRI, CSF serology 4. Tx: not always necessary.
a. Albendazole w/ dexamethacin b. Surgery
iii. Diphyllobothrium Latum (Fish tapeworm) 1. Eating
undercooked freshwater fish 2. Can be 10 meters long 3.
Clinical
a. Anemia, B12 deficiency 4. Tx: Niclosamide
STDs II (cervicitis, urethritis, vaginitis, etc) 20.
a. Urethritis/cervicitis i. Urethritis: Discharge, disuria,
PMNs
1. If gram negative Diplococci seengonorrhea 2. If notNGU
ii. Cervicitis: Cervical mucopurulent discharge, cervical
friability
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45
1. Gram stain isnt as specific iii. Gonorrhea
1. Caused by Neisseria Gonorrhoeae a. Gram negative nonmotile
Diplococcus b. INSIDE the PMN c. Oxidase positive d. Likes CO2
environment
2. Has pili with antigenic variation 3. Outer membrane proteins
help it invade cells 4. Pathogenesis
a. Mucosal contact necessary b. Incubation 7 days (closer to
3-4) c. Pili attachendocytosisinflammatory responsepus (yellow-
green) d. Naturally clear it in 1-2 mo
i. But can get scarring, infertility from it 5. Clinical
a. Urethritis- can lead to epididimitis b. Cervicitis- can lead
to PID, perihepatitis (w normal LFTs) c. Disseminated- can be
serious. Dermatitis (nodules) d. Conjunctivitis e. Pharyngitis
6. Tx: cephtriaxone a. Can co-treat for Chlamydia
(azythromycin)
iv. Chlamydia 1. Obligate intracellular 2. Infectious particle
is the elementary body
a. Invades cell, prevents fusion with lysosome 3. Clinical
a. NGU i. Discharge is white or clear, more mucoid ii. Can
progress to epididimitis
b. Mucopurulent Cervicitis- can become salphingitis i. Discharge
is less purulent
c. Lymphadenitis venerum i. Matted inguinal lymph nodes ii.
Groove sign
4. Tx: single dose azythromycin b. Vaginitis, vaginosis
syndromes
i. Copious vaginal discharge ii. Normal vaginal flora:
lactobacillus
1. Keeps pH low
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46
2. Protects against pathogens, keeps other normal flora in check
3. Loss of lactobacillusincreased infection, other bacterial
overgrowth
iii. Vaginitis: 1. Inflammatory response (irritated vagina) 2.
WBCs present
iv. Vaginosis: 1. Decreased lactobacillus, increased anaerobes
2. WBCs absent 3. Non-inflammatory
v. Include 1. Bacterial vaginosis
a. Thin discharge i. Adherent, greyish
b. Elevated pH c. Fish-like odor with KOH d. clue cells
i. Epithelial cells with ragged borders e. Tx: metronidazole
(flagil)
2. Trichomaniasis a. Trichomaniasis Vaginalis
i. Motile, seen on wet mount b. Frothy vaginal discharge
(profuse) c. Itching d. Elevated pH e. Cervical petechiae f. Men
have no sx
i. Treat the partner g. Tx: metronidazole (flagyl)
3. Vulvovaginal candidiasis a. yeast infection from candida b.
Pseudohyphae/budding yeast on wet mount c. Thick white cottage
cheese discharge d. Itching e. Low pH f. Tx: OTC stuff
c. Exophytic syndromes i. HPV
1. 6 and 11 cause warts a. Rough, cauliflower appearance
2. 16 and 18 cause cervical dysplasia 3. Vaccine 4. Tx: ablate
the warts
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47
a. This doesnt cure the virus ii. Molluscum contagiosum
1. Common pox virus in kids (not necessarily sexual) 2. Smooth
domed lesions 3. Dx: visual 4. Tx: ablate the warts
d. Ectoparasitic infections i. Pubic lice
1. Can see lice, eggs on hairs with naked eye 2. Tx: anti-lice
shampoos
a. Treat spouse, house too ii. Scabies
1. See the burrows 2. Can look like eczema
e. Systemic STDs i. Pelvic Inflammatory Disease
1. See disease outside genital tract 2. Manifestations of
a. Chlamydia, gonorrhea, anaerobes ii. Hep B
1. Vaccine-preventible 2. Blood-borne
iii. HIV
HIV pathogenesis 21.
a. Doublestranded RNA virus b. 2 kinds of tropism
i. Human coreceptors necessary to gain entry into cell ii.
CCR5
1. Early infection 2. Most of whats transmitted
iii. CCXR4 1. Late infection
c. Transmission i. Directly into bloodstream
1. Needles 2. Blood transfusion
ii. Mucus membranes 1. Sex
iii. Vertical transmission
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48
1. In utero (uncommon); during delivery (MOST); breastfeeding d.
Natural history
i. First infected 1. Flu-like symptoms
a. Ppl may think they have mono 2. Viral load very high
a. Your body doesnt know how to fight it 3. Very infectious 4.
MANY CD4 cells destroyed
ii. Immune response (quiescent phase) 1. Steady state
equilibrium, immune system fights back 2. HIV antibody level stable
3. Steadily losing CD4 cells 4. High level of inflammation 5. Few
symptoms
e. Dx: ELISA or rapid HIV test (fingerstick)positive, then
western blot to confirm i. To diagnose acute HIV
1. HIV RNA test in plasma f. Always test HIV resistance
i. Dynamic genome g. Tx: Anti-Retroviral Therapy
i. When they have: 1. An AIDS defining illness (regardless of
CD4) 2. CD4 LESS than 500 or 350 3. Nephropathy 4. Pregnancy
ii. 3 drugs of 2 classes (at least) h. Drugs:
i. Reverse transcriptase inhibitors 1. Nucleoside
a. Compete with natural nucleosides for inclusion into DNA 2.
Non-nucleoside
a. Bind to reverse transcriptasechange binding site ii. Protease
inhibitors
1. Causes protease to lock, preventing cleavage iii. Fusion
inhibitor iv. CCR5 receptor blocker v. Blocking integration
i. Pregnancy: all should be on HAART. AZT j. Chronic effects of
HIV
i. Metabolic complications 1. Lipodystrophy
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49
a. Loss of fat in limbs, face b. Central obesity. Buffalo
hump
ii. Ostopenia iii. Increased CV risk iv. Increased malignancies
v. Coinfection with hepatitis
k. Prognosis is improving
HIV epidemiology, clinical manifestations 22.
a. Subsaharan Africa b. Lots of new infections in youth c. Those
unaware of infection are most likely to spread d. Presentations
i. Wasting syndrome 1. Uncommon now 2. Depletion of both fat and
lean tissues
ii. Oral Candidiasis 1. Very common 2. NOT an AIDS defining
illness
a. Esophageal candidiasis is i. Cobblestone-looking lesions
3. Pseudomembranous 4. Treat actutely, do not prophylax
iii. Oral Hairy Leukoplakia 1. Non-movable white plaques on
margins of tongue 2. EBV related 3. Oft shows up in non-symptomatic
HIV 4. Doesnt require treatment
iv. Cutaneous manifestations 1. Syphilitic chancre
a. Higher syphilis rates b. More lesions c. More 2ndary, 3iary
syphilis d. Tx: aggressively. e. Do an LP if severe or neuro
manifestations
2. Bartonella henselae a. Looks like kaposis sarcoma b. Fever,
night sweats, anemia c. Liver, spleen d. Treat with Doxy
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3. Varicella Zoster a. Comes out as imm system wanes b. Tx
acyclovir to avoid post-herpetic neuraligia
4. HPV a. Warts (disfiguring), cancer (increased dysplasia
rates) are both
concerns 5. Molluscum contagiosum
a. Smooth, umbilicated lesions b. Sign of advanced disease c.
Groin, face
6. Seborrheic dermatitis a. Nasolabial folds, eyebrows, back,
chest, scalp b. Responsive to antifungals
7. Psoriasis a. Not more likely to get it, but if they have it,
its SEVERE
8. Kaposis Sarcoma a. Heaped up vascular lesions
i. Arms, gingival, anywhere b. HHV8
i. Reactivates causing malignancies in mucosal surfaces ii.
Rarely becomes pulmonaryvery bad iii. Treat localized lesions
1. Cryotherapy etc 2. Systemic HCG- trial. Pregnancy helps.
Weird
v. Pulmonary syndromes 1. Community acquired pneumonia
a. Much higher risk i. Young person w 2 CAPHIV test
2. Pneumococcal pneumonia a. Most common cause of pneumonia in
HIV b. Focal usually, diffuse if advanced c. HIV+ ppl get a
vaccine
3. Pneumococcus Jiroveci (PCP) a. Most common AIDS defining
opportunistic infction b. First: hilar infiltrates
i. Hydrate 1. Then diffuse interstitial infiltrates
c. Progressive exertional dyspnea d. Subacute e. Hypoxic f. Dx:
induced sputum demonstrating organism g. Tx: high dose bactrim
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i. Side effects are bad. Dont give this unless its proven h.
Prophylax with low dose bactrim
4. TB a. Oft atypical presentation b. Put them on isolation til
youve ruled it out
vi. Disseminated infections 1. Tuberculosis 2.
Histoplasmosis
a. Diffuse pulmonary infiltrates b. Non-necrotizing granulomas
c. Bone marrow infiltration d. Dx: urine antigen test
3. Mycobacterium Avium Complex a. Advanced immunosuppression b.
Inhale itdissemination c. Fever, night sweats, fatigue, weight
loss, anorexia d. Granulomatous infiltration of liver, bone
marrow
4. Lymphoma vii. Ocular
1. CMV Retinitis a. ketchup on eggs lesions
i. White plaques on retina, hemorrhages on top b. May or may not
have visual complaints
viii. CNS manifestations 1. Guillan Barre
a. Happens early 2. Chronic meningitis
a. Somewhat later 3. Late disease:
a. HIV Dementia b. HIV neuropathy
i. Similar to DM c. Toxo d. Cryptococcus
i. Meningitis 1. Sometimes just cryptococcemia
ii. CSF: High opening pressure, High protein, low glucose iii.
Dx: antigen test
e. CNS Lymphoma i. Ring enhancing lesions ii. Neuro findings,
seizures
f. Toxoplasma Gondi Encephalitis
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i. Protozoan reactivation 1. Reactivation of latent cysts
ii. MULTIPLE Ring enhancing lesions iii. Dx: CSF PCR iv. Also
causes ocular manifestations v. Tx: Pyrimethamine, sulfadiazine vi.
Prophylaxis: TMP-SMZ
g. Progressive Multifocal Leukoencephalopathy i. JC virus ii.
Deep white matter lesions iii. No mass effect iv. No Tx. HAART
helps (immune reconstitution)
Protozoans 23.
a. Can multiply in humans b. Not assosciated with eosinophilia
c. Malaria
i. Fever, Malaise, headache, anemia ii. Normal WBC, decreased
platelets iii. Splenomegaly iv. Plasmodium Falciparum
1. Most severe infections a. Can infect RBCs of all ages
i. Higher parasitic load b. Can lead to sequestration
i. Ischemic events ii. Microvascular damage
2. Extracellular banana-shaped gametocytes 3. Ring forms 4.
Maternal immunity protects infants 5. Young children are most
severe 6. Quotidian fever 7. Malarial CNS infections- VERY
SEVERE
a. Dystonus v. Plasmodium Vivax
1. Less severe disease a. Infects YOUNG RBCs
2. Requires duffy antigen 3. Hypnozoites in liver
a. Allow for relapse months/years later
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4. Tertan fever vi. Plasmodium Ovale
1. Less severe disease a. Attacks IMMATURE RBCs
2. Mostly in Africa 3. Doesnt require Duffy
vii. Dx: Thick and Thin smear viii. Tx: Uncomplicated
1. Oral combination therapy a. Quinine/doxy b. Mefloquin c.
Malarone d. If Vivax or Ovale,
i. Primaquine-eradicate hepatic hypnozoites ii. Check for G6PD
first
ix. Prophylaxis 1. Chloroquine- doesnt work against Falciparum
(resistance) 2. Doxy- daily. Photosensitivity 3. Mefloquin- weekly.
Psychosis 4. Malarone- weekly. Expensive.
x. Pregnant 1. Dont go 2. Dont take Doxy. Take mefloquine,
maybe
d. Tripanomiasis (Chagas disease) i. Life cycle:
1. Transmitted by kissing bug. Bites you at nightdefecates on
skinunconscious scratchinginoculation
2. Trypamastigotes travel to cardiac myocytesamastigotes a. Can
go back into bloodtrypamastigotesget sucked out of blood
by kissing bug again ii. Mostly south America iii. Acute
Chagas:
1. Painless swelling of inoculation site. Romanas sign. Fever,
malaise 2. Self-limited
iv. Chronic 1. Continued infestation in cardiac myocites 2.
Dilated cardiomypopathy, conduction blocks 3. Mega-esophagus,
megacolon (rarer)
v. Dx: 2 out of 3 independent serological tests vi. Tx: actually
does help
1. Benznidazole 2. Nefurtomox
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54
vii. HIV- can get it really bad. Can be Fatal. e.
Leishmaniasis
i. In the us, Military personnel from Iraq etc ii. Life
cycle
1. Sandfly bites a. Promastigotes enter b. Enter cells c. Become
amastigotes d. Replicates in cells
iii. Cutaneous 1. Most common form 2. Lesion happens weeks after
infection
a. Starts out looking like a pimple b. Ulcerates w raised
border
3. Heals in months, leaving a scar iv. Mucocutaneous
1. Braziliensis 2. Occur years after initial cutaneous infection
3. Occur on any mucosal surface (usu nose, mouth, pharynx) 4. Very
disfiguring 5. Difficult to treat 6. Can be fatal
v. Visceral (Kala Azar) 1. India, Africa, brazil 2. L. Dovani,
L. infantum 3. Subacute: fever, weightloss
a. Hepatomegaly, splenomegaly b. Can infect bone. c. (Liver,
spleen, bone)
4. Hyperpigmentation (black fever) 5. Die from secondary
infection 6. Dx: splenic needle aspirate
vi. Tx: Pentavalent antomonials 1. Amphotericin B
f. Toxoplama Gondii i. Intracellular parasite ii. Cat is
definitive host
1. Cat feces (can be on unwashed vegitables) 2. Can infect fetus
3. Can infect other animals
iii. Acute: usu asx 1. Mono-like
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2. Generalized lymphadenopathy iv. Congenital
1. Worse in later trimesters 2. Hydrocephalus 3. Retinal
choroiditisblindness
v. Transplants (donor positive, recipient negative) vi. HIV:
Severe disease
1. Necrotizing brain lesions 2. Represent reactivation 3.
Pyramethamine, sulfadiazine
g. E. Histolytica i. Bloody diarrhea ii. Oft travelers to
endemic areas (like Mexico) iii. Ingest cysts
1. become trophozoites in intestine a. become more cysts, exit,
OR b. invasion: liver, heart lungs
iv. Diagnosis by serology (looking at cysts in stool doesnt
help) v. Flask shaped ulcer in mucosa vi. Clinical:
1. Amoebic Dysentery a. Bloody, small volume stools b. Tx:
metronidazole (to kill trophozooites) AND
i. tromomidacin (to eradicate cysts) 2. Amoebic Liver
Abscess
a. anchovy paste as you drain it b. May be fatal c. Biopsy to
prove its not neoplasm
h. Giardia i. Children in daycare, Campers, hikers ii. Feces,
water contaminated with feces iii. Secretory diarrhea, flatulence
iv. 60% asymptomatic v. 30% self-limited diarrhea vi. 10% chronic
diarrhea vii. Dx: stool microscopy viii. Tx: metronidazole
i. Cryptosporidiosis i. Community swimming pools ii. Animal
reservoirs transmit disease iii. Intracellular iv. Intestinal
parasite
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1. Forms cysts 2. Resist chlorination
v. Immunocompetent- self-limited watery diarrhea vi.
Immunocompromised- severe, cholera-like diarrhea
j. Trichomoniasis i. Yellow vaginal discharge, itching. Can be
bubbly ii. Strawberry cervix iii. Wet mount-motile pear shaped
cells iv. Men are asxtreat them to prevent reinfection v. Tx:
metronidazole
Bioterrorism 24.
a. Features of a bioweapon i. High morbidity/mortality ii.
Available iii. Dispersible
b. Anthrax i. the perfect weapon ii. Gram positive bacillus
1. bamboo appearance iii. Aerobic, encapsulated. iv. Forms
spores
1. Very hardy 2. Can survive in nature for decades 3. Become
active when in the respiratory tract 4. Shit.
v. Produces toxins (doesnt invade tissue) 1. Edematoxins- causes
influx of fluids 2. Lethal toxin- creates massive cytokine
response
vi. Disease forms: 1. Cutaneous:
a. Spore lands on damaged skin b. Most common, low fatality c.
Painless papuleedema (from edematoxin) black ulcervery
black escharheals without scar 2. Gastrointestinal
a. Ate an infected animal b. Aerosolized form got into
nasopharynxswallowed c. Mortality 50%
3. Inhalational
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57
a. Mortality up to 95% b. Incubation is usu around 7 days (can
be up to 6 weeks) c. Prodromal phase: Influenza w/nausea and
vomiting d. Flu improves, quickly becomes fulminant
i. sepsis ii. Respiratory failure, shock iii. Death
e. Dx: Blood culture. It grows quickly. f. Widened mediastinum
on clear lungs
i. Bacteria get into lungs ii. Macs engulf them iii. Go to
mediastinal lymph nodes iv. Get hemorrhagic necrosis
g. Tx: ciprofloxacin or doxycycline i. wont respond to CAP
drugs
4. no person-to-person transmission c. Smallpox
i. Incubation: 7-14 days ii. Person to person transmission iii.
Rash marks infectiveness iv. Prodrome:
1. Sudden, severe, flu-like sx 2. 3-5 days long
v. Rash: 1. Face, hands, feet worst (even palms and soles) 2.
Stages: maculopapulardeeperpustulesdryscabscar 3. All the same
age
vi. Tx: none vii. Vaccine, prophylaxis work
d. Plague (yersinia pestis) i. Zoonosis with flea vector ii.
Only pneumonic form is person-to-person iii. Incubation 2-8 days
iv. Lesion at site of inoculation v. Bubonic:
1. After bite, get enlarged painful lymph nodes a. May suppurate
b. You may be very sick c. You may be septic d. You may die e. It
may spread to the lungspneumonic plague
vi. Pneumonic
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58
1. Rapid onset pneumonia 2. Hemoptysis 3. Sputum culture shows
gram negative rods
a. Look like red safety pins 4. Tx: streptomycin, gentamycin
vii. Septic- you get gangrene at the ends of your digits e.
Tularemia
i. Very very small gram negative bacillus ii. Intracellular iii.
Mostly in MO, KS iv. rabbit fever v. Vector is fleas vi. Incubation
3-5 days vii. Fever w/o tachycardia viii. Ulcer at inoculation ix.
Regional lymphadenopathy x. Pneumonic disease
1. Non-productive cough 2. Pleuritic chest pain
xi. Dx: serology takes weeks, cultures are poorly sensitive. 1.
Lab hazard. Warn them.
xii. Tx: Streptomycin, Gentimycin
Zoonoses f.
i. Rabies 1. Bats, dogs 2. Pathogenesis
a. Bite. Replication at site of inoculation i. Retrograde axonal
spread ii. 10 cm/day iii. Goes to the brainstem/thalamus iv. Negri
bodies
3. Prodrome: influenza-like a. Percussion myoedema,
parasthesias
4. Non-mammals are no risk ii. Bartonellosis (cat scratch)
1. Gram negative intracellular bacillus 2. Febrile lymphadenitis
3. Mostly kids 4. Rarely severe
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5. Dx: clinical, tissue PCR 6. Tx: Azythromycin
iii. Q fever 1. Coxiella burnetii 2. Cows, goats, sheep
a. Direct contact b. Inhalational
3. Very contagious 4. Acute:
a. Flulike sx b. Atypical pneumonia c. Tx: doxycycline
5. Chronic a. Endocarditis, osteomyelitis b. Tx: doxycycline and
rifampin
iv. Brucellosis 1. Intracellular gram neg coccobacillus 2. Cows,
goats, sheep 3. Direct contact, aerosol (placenta), unpasteurized
cheese 4. Dx: serology 5. Fever, malaise, malodorous sweat,
Sacroiliac joint involvement 6. Tx: doxycycline and
aminoglycoside
v. Leptospirosis 1. Gram negative helical bacteria 2.
Triathalons 3. Dog, rodent urine 4. Self-limited 90%
a. High fever, headache, conjunctival suffusion 5. Severe,
biphasic 10%
a. Weils disease b. Icterus, renal failure, hepatic failure
6. Dx: Serology 7. Tx: oral doxycycline
a. Jarisch-Herxheimer reponse- you killed LOTS of cells at
oncecytokine response
vi. Psittacosis 1. Chlamydia psitacci 2. From birds
a. Parrots spit on you! Erm 3. Aerosolized 4. Very infectious 5.
Mono-like illness, fever, fatigue
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a. Consolidation in lower lobe 6. Dx: serology 7. Tx:
doxycyline
Immune deficient 25.
a. Infections caused by loss: i. Physical/mechanical barriers:
staph, strep, pseudomonas, aspergillus, candida ii. Neutrophils:
Extracellular bacteria (staph, strep, enterobacteraciae,
pseudomonas),
a. Candida, aspergillus iii. Complement: encapsulated
extracellular bacteria
1. N. meningitides, s.pneumo iv. T cells: intracellular
bacteria, viruses, broader spectrum of fungi
1. Nocardia, legionella, mycobacteria v. B cells: enteroviruses,
giardia, s.pneumo, h.flu, n.meningitidis, s.aureus
b. Immunosuppression i. Congenital ii. Acquired
1. Cancer chemotherapy- neutropenia, mucositis 2. Solid organ
transplant- Cell mediated immunity 3. Bone Marrow Transplant all
lost
c. Cancer chemotherapy i. Neutropenia
1. Greatest risk of infection 2. Sudden dropworse 3. Longer
durationworse 4. Empiric treatment is very important
a. Pseudomonas, s.aureus b. Anaerobes (if a likely area)
d. Solid Organ Transplant i. Specific organ transplanted
matters
1. Greatest risk: lung, heart-lung transplants ii. Long or
demanding surgeries more risk iii. Rejection of transplant more
immunosuppressionmore risk iv. 1st month post transplant
1. Increased risk of NOSOCOMIAL infections a. Long hospital stay
b. Immunosuppressed
i. Candida, c. diff, catheter assosciated infections, etc 2.
Organ specific infections
a. Ex: Kidney transplantUTI
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v. 1-6 Mo 1. T cell defects
a. Viruses: CMV, herpesvirus b. Bacteria: TB c. Fungi: endemic
mycoses, aspergillus d. Protozoans: toxoplasmosis
vi. CMV 1. Most common in transplants 2. Highest risk with Donor
Positive, Recipient Negative 3. Early onset (3-6 mo post
transplant)- pneumonitis 4. Late onset (after that)- enteritis
e. Bone marrow/stem cell transplant i. Autologous: minimal
immune suppression ii. Allogeneic:
1. VERY immune suppressed 2. Long term 3. Stages
a. Pre-engraftment i. Risks:
1. Neutropenia 2. Mucositis 3. Central venous catheter
ii. Possible infections 1. Staph, strep, ecoli, klebsiella,
pseudomonas 2. Aspergillus, candida 3. Give cefapime. Or Vanc (if
MRSA)
b. Early post-engraftment i. B and T cell defects ii. Risks
1. Lymphopenia 2. Hypogammaglobulinemia 3. Central venous
catheter
iii. Infections 1. Viruses (CMV, HSV, EBV, etc) 2. Bacteria
(intracellular) 3. Fungi (many, including aspergillus)
c. Late post engraftment i. Risks
1. Minimal GVHD 2. Chronic GVHD (organ failure, etc)
ii. Infections 1. VZV
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2. Encapsulated community pathogens a. Strep pneumo
4. CMV: risk if donor negative, recipient positive a. Nave
immune system going into a CMV + body
5. Aspergillus: Biphasic a. First because of neutropenia b.
Second because of B and T cell dysfunction
i. Donor matching helps
Neonatal infections 26.
a. In utero infections i. TORCHES
1. Toxoplasmosis 2. Other (west nile virus, lymphangitic
choriomenintitis, malaria) 3. Rubella 4. Cytomegalovirus-most
common. Can lead to deafness 5. HIV, Hepatitis, HSV (but usually
intrapartem) 6. Enteroviruses 7. Syphilis
ii. Oh. And also, Chicken Pox, Lyme disease and Parvovirus b.
Fever in a neonate:
i. Bacterial 1. Order of frequency
a. Group B Strep b. E. coli (tied) c. Other gram negs d. Strep
Pneumo e. N. Meningitis
2. 67% are UTI 3. 2% are meningitis (dont miss this! LP all
babies!)
a. There are no signs of this 4. Most were gram negative 5. Most
were ampicillin resistant
a. Tx with ceftaxipime (3rd gen cephalosporin, gets into CSF) i.
Plus ampicillin to cover Listeria
ii. Viral (MOST LIKELY) 1. Varies with seasons
iii. Group B Strep 1. Ascending infection. 2. Screen moms from
35-37 weeks
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3. Low weight, premature, africanworse 4. Early onset (w/in 7
days of birth)
a. FAST onset. 6 hours of birth, theyre grunting and retracting
b. Respiratory failure
5. Late onset (after 7 days) a. More insidious b. Bone, joint
infections, bacteremia c. 50% will have meningitis
iv. HSV 1. Baby presented as floppy, with hepatitis 2. Mom
primary infection during pregnancy, lesions during deliveryworse 3.
Most are HSV2 4. Skin, eye, mucus membrane disease 5. If treated
with acyclovir good prognosis, no longterm sequelae 6. If
untreatedbecomes disseminated. Often fatal. 7. CNS: Encelphalitis,
fever, lethargy, seizures
a. Most dont have rash 8. Disseminated: Liver, lung, brain,
skin, adrenals
a. Looks like bacterial sepsis b. Mortality 50-80%
9. Happens within first couple weeks of life v. Enterovirus
1. Coxsackievirus A, B, enterovirus 2. Peak in Summer, fall 3.
Virus from moms blood crosses placenta, disseminates in baby 4.
Hyper/hypothermia, poor feeding, irritability, flat, red rash 5.
Dx: stool culture 6. Tx: ? 7. Prevention: handwashing
vi. Hepatitis B virus 1. Neonates who get it at birth become
chronic carriers
a. Have a higher mortality 2. We vaccinate now
Osteomyelitis 27.
a. Difficult for antibiotics to get to the site b. Acute osteo:
prior to formation of sequestrum (dead bone) c. Chronic osteo:
after formation of sequestrum. Not duration dependent.
i. Body puts out new bone (involucrum) d. Mechanism
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i. Bacteria causes inflammation 1. Inflammation squeezes
vascular
channelsischemianecrosissequestrum 2. inflammation strips the
subperiosteum from boneperiosteal
elevationstimulates new bone formation ii. Sequestrum can extend
out through skin and drain
e. Adhesion plays crucial role i. S.aureus is most common bug
ii. Anything that can make biofilms (coag neg staph)
1. Antibiotics cant penetrate them 2. Take out prosthesis.
f. Classification i. Hematogenous
1. Kids a. Symptoms
i. Pain on passive mvmt ii. Inability to move limb iii. May be
warm iv. fever
b. Staph aureus i. Brodies abscess
1. Drain it c. Long bones
i. Capillary loop- stasis d. Neonates: can involve joint b/c of
incompletely closed epiphysis
2. Vertebral in adults a. Sx: back pain, maybe neuro signs (BAD)
b. Discitis and two adjacent vertebrae c. Usu in lumbar area, but
can be anywhere d. Gram pos: from skin, soft tissue e. Gram neg:
from urinary tract f. Can compress spinal chord
i. So check for neurological signs. ii. This is a surgical
emergency.
3. Development of sequestrum is slow. a. Acute osteo
ii. Contiguous 1. Sx:
a. May have a draining sinus b. Persistent pain c. Oft no
fever
2. Trauma, surgery
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a. Usu staph aureus 3. Infected prosthesis, hardware
a. Esp coag negative staph b. Sx: loosened implant
4. Biofilms 5. Rapid sequestral formation
a. Chronic osteo iii. Vascular insufficiency
1. DM, neuropathy a. Oft start as foot ulcers b. Osteo will HURT
though (finally) c. Avoid ill-fitting shoes
2. Usually chronic 3. Osteo if:
a. Persistent ulcer or b. Bone is exposed/can be probed
4. Polymicrobial a. Staph aureus, gram negatives, anaerobes.
iv. Other osteo 1. Sickle cell: salmonella
a. Encapsulated bacteria (strep pneumo) i. b/c they have no
spleen
2. Sneaker: pseudomonas 3. Endemic mycoses: Histo,
blasto,coccidio, TB
v. Dx 1. Xray (but takes 2 weeks to show signs on an Xray) 2.
Bone scan (shows up faster, but shows any inflammation) 3. MRI-
good but expensive 4. Bone Biopsy- gold standard
a. Aerobic and anaerobic cultures b. dont bother culturing the
sinus tract
vi. Tx: 1. Acute:
a. IV antibiotics for 4-6 weeks b. Switch over to oral faster in
kids c. Surgery rarely necessary
2. Chronic a. Much more difficult b. Culture wont help. Need a
bone biopsy to find organism c. Surgery to remove dead tissue d. IV
antibiotics for at LEAST 6 weeks
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Tic-borne Diseases 28.
a. Lyme Disease i. Borrelia burgdorferi
1. Spirochete 2. Multiple plasmids
a. Some are linear (weird) 3. Natural reservoir: white-footed
mouse
ii. Vector: Ixodes scapularis 1. Mostly the nymph stage 2. Must
be attached 24 hours to transmit
a. B.burgdorferi multiplies in tick midgut b. Travels to saliva
during the blood meal
iii. Transvarial transmission: no iv. Geography: MN, WI,
northern CA
1. Not around here. v. Early manifestations
1. Erythema migrans a. 6 cm in diameter, at the site of bite b.
A week after the bite
2. Carditis, aseptic meningitis, bells palsy vi. Late
manifestations
1. Arthritis- usu single knee a. Months after the bite
2. CNS- encephalitis a. Will have a positive blood test
vii. Dx: Serology may not be helpful (not enough bug to make
test positive) a. ELISA, Western Blot
2. Culture skin lesions, joint involved viii. Tx:
Doxycycline
b. Southern Tick Assosciated Rash Illness (STARI) i. Rash looks
like Erythema Migrans ii. But its the lone star tick
c. Rocky Mountain Spotted Fever i. Caused by Rickettsia
1. Small gram negative bacilli 2. Obligate intracellular 3.
Replicate freely in cytoplasm
ii. Assosciated with arthropods iii. Happens mostly in summer,
mostly in kids iv. Geography: a belt across the central US
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v. Sx: 1. Incubation 2-14 days 2. Early: fever, headache,
myalgia, abdominal pain 3. Rash: peripheral petechiae
(nonblanching)
a. Can be on palms and soles b. Petechiae are areas of intense
vasculitis
i. Can eventually cause shock vi. Tx: IMMEDIATE. Dont wait for
tests.
1. Tick exposure + rash = treat, and get labs 2. Doxycycline,
chloramphenicol
d. Ehrlichiosis i. Human Monocytic Ehrlichiosis- involves the
monocyte line
1. Caused by Ehrlichia chafeensis ii. Human Granulocytic
Ehrlichiosis- involves neutrophils
1. Caused by Ehrlichia ewingii iii. Ehrlichia
1. Intracellular- lives in phagosomes a. Replicates (forms a
morula)
iv. Vectors: Lone star tick and I.scapularis (same as lyme
disease) v. Common in
1. May, June 2. Middle aged, elderly
vi. Sx: Fever, headache, myalgia 1. Rash in about 1/3 of pts 2.
Low WBC, low platelets 3. Cytoplasmic inclusions in neutrophils 4.
Severe: Meningitis, pneumonitis, hepatitis, disseminated
intravascular
coagulation vii. Dx: PCR viii. Tx: doxycycline
Healthcare Risks 29.
a. N. Meningitidis i. The only form of meningitis that shows
person-to-person transmission ii. Droplet transmission iii. Risk is
small, but higher than in the general population iv. Risk:
unprotected exposure to respiratory secretions
1. Cough, intubation, CPR v. Anyone with evidence of bacterial
meningitisdroplet precautions vi. Post exposure prophylaxis
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1. HCW with a high risk exposure before pt was on antibiotics 2.
Household members 3. Roommates 4. Anyone who shared eating utensils
5. Day care classmates 6. Ciprofloxacin
b. Tuberculosis i. Pt goes on airborne isolation ii. HCW post
exposure assessment
1. TB skin test now, 2. TB skin test in 8-10 weeks
iii. No minimum infection time. Entering the room= exposure iv.
High risk: pt is coughing, youre intubating, bronchoscopy, induced
sputum
c. Body Substance Exposures i. Happens mostly in residents in
and house staff ii. Happens mostly in OR iii. Standard
Precautions
1. Gowns, gloves, masks, eyewear 2. Wash hands after removing
gloves 3. Do not put hand in front of contaminated