Microbes, bacteria

8/12/2019 Microbes, bacteria

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Microbes

1. Overview of Bacteriologya. Characteristics of bacteria

i. Single cellii. No nuclear membrane

iii. Single circular DNAiv. No organellesv. 70s ribosomal DNA (different from human)

vi. No membrane sterolsvii. Peptidoglycan cell wall(not present in Euks)

viii. Reproduction by binary fissionix. Susceptible to antibiotics

b. Gram Positive:i. Stain blueii. Have thick outer peptidoglycan cell wall

c. Gram Negativei. Stain pinkii. Have LPS (endotoxin) on outside

iii. Thinner layer of peptidoglycans, sandwiched betweeniv. Porins on outer membrane layer

d. Gram Positive Coccii. Staph

1. Grows in clusters2. Catalase positive3. Facultative Anaerobes4. Coag POSITIVE staph = S.Aureus5. Coag NEGATIVE staph- routinely found on skin. Usually not harmful6. Staph Aureus

a. Skin and soft tissue infections (Abscess)b. Pneumoniac. Bone and joint infectionsd. Bacteremiae. Endocarditisf. Catheter infectionsg. Toxin syndromes

i. TSSTii. Scalded skin

iii. Food poisoning (enterotoxin)h. MRSA

i. Hospital Aquiredii. Community acquired


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1. Increasingly prevalent2. Includes Panton-Valentine Leukocidin

ii. Strep1. Grows in chains2. Catalase Negative3. Facultative Anaerobes4. Ferment carbohydrates producing Lactic Acid5. Types of Strep

a. Group A Strep (Pyogenes)i. Beta Hemolyticii. Bacitracin sensitive

iii. Has a capsuleof hyaluronic acidiv. Usu asx colonization of respiratory tractv. Person-to-person spread

vi. Diseases1. Most are suppurative2. Pharyngitis3. Scarlet Fever4. Skin Infections5. Bacteremia6. TSST7. Rheumatic fever

a. 10 days after GASb. Migratory polyarthritis, carditis, subQ

nodules, erythema marginosum, chorea

(Major Jones Criteria)

8. Glomerulonephritisb. Group B strep (agalactiae)

i. Narrow zone of beta hemolysisii. GI/GU

iii. Babies get it from colonized mothersiv. Now, if positive, put on antibiotics before giving birth

c. Strep Pneumoniaei. Alpha hemolyticii. 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 vaccinevi. Diseases

1. Pneumoniaa. #1 for community acquired pneumonia


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2. Otitis, sinusitis3. Meningitis (ties for #1)4. Bacteremia5. Skin and joint infections

iii. Enterococci1. E. Faecalis, E.Faecium2. Grows in chains/pairs3. Catalse Negative4. Usu non-hemolytic5. Grows in 6.5% NaCl6. Diseases

a. Endocarditisb. UTIc. Nosocomial (Wounds, catheters)

e. Gram Negative Bacillii. MacConkey Agar

1. Grows Gram nega. Lactose fermenters grow PINKb. Non-lactose fermenters grow COLORLESSc. Lactose test helps ID the bacteria

ii. Enterobacteriaciae1. Salmonella, shiglella, e.coli, klebsiella, yersinia, enterobacter2. Often common in the ENVIRONMENT3. Oxidase negative4. Ferment glucose5. Diseases

a. Gastroenteritisb. UTIc. Bloodstream infectiond. pneumoniae. plague

iii. P. aeruginosa1. Obligate aerobe2. Does NOT ferment lactose3. Does NOT ferment glucose4. Oxidase positive5. Sweet odor6. Produces a green color

iv. HACEK group1. H. Influenza

f. Gram Negative Coccii. Neisseria


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1. Grow in pairs2. Prefer high CO23. Oxidase positive4. Species

a. Meningitidesi. Carbohydrate capsule

b. Gonorrheaei. Also encapsulatedii. Uses only GLUCOSE

ii. Moraxella1. Otitis, sinusitis, bronchitis

g. Gram Positive Bacillii. Bacillus

1. Spore forming2. Aerobic3. Catalase POSITIVE4. Persist in soil5. Types

a. B. Anthracisi. Spores- bamboo appearanceii. Non-beta hemolytic

iii. Non-motileiv. Has a capsulev. Pulmonary disease- shows widened mediastinum

ii. Corynebacteria1. Irregular shape (Chinese letter shaped)2. Catalase positive3. Causes Diptheria

iii. Listeria Monocytogenes1. Tumbling motility2. Non-spore forming3. Beta-hemolytic4. Diseases

a. Meningitisb. Endocarditisc. Neonatal infectiond. Infection in pregnant women

2. Antibioticsa. Beta Lactams

i. Inhibit crosslinking of peptide side chains in bacterial cell wallsii. BacterioCIDAL

iii. Safe in pregnancy


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iv. Renally clearedv. Resistance

1. Beta lactamases2. Changes to the binding site (MRSA)

vi. Adverse effects: Rash (anaphylaxis), hematologic toxicityvii. Includes:

1. Penicillinsa. Doesnt go to prostate or intraocular fluid (otherwise good

distribution)

b. Renally cleared (so careful in kidney failure)c. Synergize with aminoglycosidesd. Beta Lactamase inhibitors

i. Clavulanic acid, sulbactam, tazobactamii. Add anaerobiccoverage

2. Cephalosporinsa. Renally excretedb. 1stand 2ndgen do NOT penetrate CSFc. Doesnt cover enterococci, lysteria, MRSAd. Adverse reactions: Rash, fewer platelets, fewer WBCe. First Generation cephalosporins

i. The Surgeons favoriteii. Covers gram positive

iii. Skin, soft tissue infection; surgical prophylaxisiv. Includes:

1. Cefazolin, cephalexinf. Second Generation

i. Sinusitis, Otitisii. Works against Haemophilus

iii. Covers more gram negative, strict anaerobesiv. Includes:

1. Cefoxiting. Third Generation

i. More gram negativeii. Stableto beta lactamases

iii. CeftazidimePseudomonas aeruginosaiv. Ceftriaxonegram POSITIVEs. Meningitis, community

pneumonia

h. Fourth Genreationi. Gram positive and negativeii. Cefepimepseudomonas, gram negative resistant bacteria

i. Fifth generationi. Covers MRSA


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3. Carbapenemsa. Stable to beta lactamasesb. Gram positive and negative

i. Including pseudomonasc. Reserve for serious infectiond. Imipenem; meropenem; ertapenem (doesnt do p.aeruginosa)

4. Monobactamsa. Only gram negative

i. Including pseudomonasb. Can use in penicillin allergic ptsc. Azetreonam- IV

b. Vancomycini. Inhibits elongation step of cell wall synthii. Only gram positive

iii. Not absorbed orally. Used in C. Diff Colitisiv. Renal clearancev. Measure trough levels

vi. Adverse effects: Red Man Syndrome, renal toxicity, hemotologic, ototoxicityvii. Use for:

1. MRSA (hospital acquired)2. Beta lactam allergies3. Second line for staph/strep endocarditis4. 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 SSRIsiv. Adverse effects: headache, nausea, thrombocytopenia, peripheral and optic

neuropathy.

v. Use for:1. MRSA, VRE

vi. Very expensivevii. Reserve

d. Daptomycini. Depolarizes cell wallsii. bacterioCIDAL

iii. gram positive1. MRSA, VRE

3. Antibiotics IIa. Aminoglycosides

i. Enter bacterial cellsii. Bind irreversibly, Inhibit 30s ribosome


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iii. BacterioCIDALiv. Renally exretedv. Resistance due to inactivating enzyles

vi. Narrow therapeutic index1. Monitor peak and trough

vii. Adverse effects: Nephrotoxicity, ototoxicityviii. Use for gram negative bacilli, staph, mycobacteria.

1. Noanaerobesix. Use for synergyx. Includes: Gentamycin (gram pos cocci), streptomycin (TB, plague)

b. Tetracylcinesi. Bind reversibly to 30s, inhibiting protein synthii. bacterioSTATIC

iii. must be transported into celliv. resistance: changes in transportv. does not penetrate CSF

vi. milk, antacids decrease absorptionvii. contraindicated in pregnancy

1. cross placenta, affect fetal bones, teethviii. 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

c. Tigecyclinei. A bigger, better tetracyclineii. Overcomes resistance

iii. Use for resistant gram positive, resistant gram negative , anaerobes, mycobacteria1. Not pseudomonas

iv. Like tetracycline1. Also contraindicated in pregnancy2. Also causes photosensitivity

d. Macrolidesi. Bind reversibly to 50sii. BacterioSTATIC

iii. Metablolized in LIVER1. Cyt P450. Lots of interactions

iv. Doesnt penetrate CSFv. Includes:

1. erythromycin, clarithromycin, azithromicin, dirithromycin.


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vi. Use for: mostly grampositive, some gram neg1. Not pseudomonas2. Erythro- staph, strep, atypical pneumonias3. Community acquired pneumonia

vii. Adverse effects: GI toxicity (frequent), warfarin interaction (bleeding)e. Lincosamides (clindamycin)

i. Covers grampositive, and anaerobes1. no gram neg

ii. metabolized in LIVERiii. does not penetrate CSFiv. use for:

1. community MRSA2. bacterial vaginosis3. staph, strep

f. Quinolonesi. Block DNA synthesis by inhibiting gyrase, topoisomeraseii. Absorbed very well orally

iii. Renally excretediv. Enters the prostate (use ciprofloxacin)v. Contraindicated in pregnancy

1. Can cause tendonitis, tendon rupturevi. Adverse effects

1. CNS, arthropathy, photosensitivityvii. Fluoroquinolones

1. Ciprofloxacin- for gram negatives,a. Only oral option for pseudomonasb. No anaerobesc. Worsk for intracellularpathogensd. Use for:

i. UTIs, Prostatitis, bacterial diarrhea, some STDs, anthrax2. Moxifloxacin and levofloxacin

a. Expand gram positivecoveragei. Use for: Bronchitis, community pneumonia

g. Nitroimidazolesi. Anaerobes, some parasitesii. Is reduced to cyctotoxic intermediates that inhibit DNA synthesis

iii. Includes METRONIDAZOLE1. Good oral absorption2. Enters CSF, BRAIN3. Use for:

a. Anaerobic infection, brain abscess, c.diff colitis, bacterial vaginosis;giardia, trichomonas, amoeba


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4. Adverse effects: nausea, metallic taste, seizures, peripheral neuropathy,antabuse effect

h. Sulfonimidesi. Dont use alone, everythings resistant.

1. Use with trimethoprim. Both inhibit steps in folate synthii. Gram positives, some enterobacteraciae

1. Use for: nocardia, toxoplasmosis, pneumocystisiii. Adverse effects: Hypersensitivity (HIV), hemolytic anemia, Jaundice, neutropenia

i. Trimethoprimi. Penetrates prostate

1. Use for prostatitis, certain UTIsj. Trimethoprim Sulfamethoxazole (TMP-SMX)

i. Synergisticii. bacterioCIDAL

iii. used in HIV ptsiv. covers gram positivessome gram neg.v. use for: pneumocystis, toxoplasmosis, nocardia, uncomplicated UTI, prostatitis,

some STDs, MRSA (outpatient. Its oral)

4. Endocarditis, bloodstream infectionsa. Bloodstream infection classification

i. 2 infection: from another infected siteii. 1 infection: from an unknown site

1. Catheter2. Endocarditis

iii. Transientb. Diagnosis of CA- BSI

i. Clinical pictureii. Get blood cultures

iii. No evidence of infection elsewherec. Tx

i. Remove catheters if possibleii. Treat 7-14 days if uncomplicated,

1. 4-6 weeks if complicated (endocarditis, supperative thrombophlebitis,osteomyelitis)

iii. Risk factors1. Imm supp2. Neutropenia3. CHF4. DM5. Being fed through the catheter (TPM)6. Catheter scenario, location, type

iv. Complications


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1. Endocarditis2. Osteomyelitis3. Endopthalmitis4. Septic arthritis5. Septic pulmonary emboli6. Systemic abscesses

d. Endocarditisi. Usually infects valvesii. Pathophysiology

1. Native valves with underlying disease2. damage of valve with fibroblast healing3. transient bacteremia4. colonization of valve5. growth of vegetation

iii. If untreated, fatal. If treated, still probably fataliv. In a native valve, its usually oral strep or staph aureusv. In IVDU, Its usually s.aureus

vi. In prosthetic valve, EARLY, its coag neg staph. LATE its oral strepvii. Culture negative endocarditis

1. HACEK organismsa. Hard to cultureb. Haemofilusc. Actinobacillusd. Cardiobacteriume. Eikenellaf. Kingella

viii. Clinical picture:1. Fever, chills, cardiac murmur, arthralgia/myalgia,2. Vascular signs

a. Osler nodes- tender nodules on fingersi. Indicate chronic endocarditisii. Autoimmune vasculitis

b. Splinter hemorrhages- in the fingernail (usu near base)c. Janeway lesions- look like bruises

i. Palms and solesii. Contain bacteria

d. Roth spots- retinal spotse. Petechiae- hemorrhages on conjunctiva

ix. Diagnosis:1. 2 major criteria: microbiologic (blood culture), evidence of endocardial

involvement


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2. Minor criteria: predisposition, fever, immunologic/vascular phenomenon,microbiologic

3. Trans Esophageal Echois gold standardx. Embolic complications

1. Stroke2. Brain abscess3. Lung abscess4. Spleen problems5. Kidneys

xi. Tx: based on organism1. Empiric Vanc + gentamycin + ceftriaxone2. Use penicillin if sensitive3. Treat for 4-6 weeks4. Surgery if necessary

a. Valve insufficiency causes CHFb. Persistent sepsisc. Valve ring/myocardial abscessd. Others

xii. Prophylaxis for IE1. Dont use for most patients2. Consider if:

a. Prosthetic valveb. Previous IEc. Heart transplant with a valvulopathyd. Unrepaired cyanotic shunte. NOT Mitral valve prolapsed

5. Skin and soft tissue infectionsa. Impetigo

i. Mostly in kidsii. Superficial intraepidermal vesicles

iii. Crusty, weepingiv. Caused by : Group A strep or Staph Aureus

b. Folliculitisi. Inflammation of hair folliclesii. S. aureus is common. Pseudomonas from pools, hot tubs

c. Furunclei. In areas of friction, perspiration. Contain hair folliclesii. A red tender nodule of pus

iii. Risk factors: Obesity, neutropenia, DM, steroidsd. Erysipelas

i. Clearly demarcated, slightly raised area. Peau dorangeii. Older adults, kids


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iii. Lower extremityiv. Caused by: group A strepv. Venous stasis, lymphatic obstruction, DM, alcohol abuse

e. Cellulitisi. More diffuse border, not raisedii. Secondary to trauma, other lesion

iii. Hot, tender, swolleniv. Fever, malaise, chills, leukocytosisv. Caused by: staph aureus or any strep

vi. Drug of choice is vancomycinf. Necrotizing Faschiitis

i. Effects extremities mostlyii. Erythematous, hot, painful, no defined borders (initially)

iii. Fever, leukocytosis positive gram stainiv. Changes quickly: red-purpleblue-graygangrenev. Loses feeling (doesnt hurt anymore)

vi. Fourniers Gangrene1. In males. Involves scrotum, perineum2. Multiple bacteria

vii. Tx: Surgical debridement, antibioticsg. Pyomyositis

i. Infection, abscess of muscleii. Immunocompromised, following blunt trauma

iii. Usu Staph Aureush. Community acquired MRSA

i. Has the P-V Leukocidinii. Usu cutaneous

iii. Use vanc, I guess. Lots of optionsi. Vibrio Vulnificus

i. Liver disease + ingest raw shellfishii. Necrosis in arms, legs. May need amputation

iii. Doxycycline is drug of choicej. Cutaneous Anthrax

i. Direct contactii. Prurituspainless papulevesiclepainless necrotic ulcer with black center

iii. Treat with Ciprofloxacine or Doxyfloxacine for at least 60 daysk. Acute lymphangitis

i. Tracks up lymphaticsii. Seen with Pasteurella (cat bites), Group A strep

l. Mycobacterium Marinumi. Open wounds exposed to freshwater/aquariumsii. Subacute/chronic cellulitis


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iii. Lesions track up lymphaticsm. Toxic Shock mediated disease

i. Fever, nausea/vomiting, diarrhea, confusionii. Staph Aureus (mortality LOW) or Group A strep (mortality HIGH)

iii. Desquamating rashn. Scalded skin syndrome

i. Begins with a known infectionii. Treat with Vanc

6. Bacterial Pneumoniaa. Risk factors

i. Disruption of barriers (anatomical, mechanical)1. Smoking2. CHF3. COPD, Asthma

ii. Increased exposure to pathogens1. Crowding2. Aspiration

iii. Immune Deficiencies1. Infant not breastfeeding2. Very old3. DM4. HIV

iv. Iatrogenic manipulations1. Bronchoscopy2. Sedation3. Immunosuppression

b. Clinical picturei. Fever, productive cough, pleuritic chest painii. Tachypnea, rales, leukocytosis (mostly band)

c. Strep pneumoniaei. most common cause of CAPii. can kill you

iii. most damage is caused by the inflammatory response it createsiv. remember: polysaccharide capsule, diplococcusv. Tx: Ceftriaxone

d. H. Influenzai. Chronic lung diseaseii. Gram neg coccobacillus

iii. Makes a weak beta lactamase.iv. So use 2ndgen cephalosporin

e. Moraxellai. Gram neg diplococcus (just like neisseria)


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ii. Colonizes nasopharynx. When it spreadsdiseasef. Staph Aureus

i. Severe Necrotizing pneumonias in healthy kidsii. Pleural effusions, empyema

iii. CA-MRSA common. Has P-V leukocidiniv. Tx: Vanc

g. Atypicals: Chlamydia, legionella, mycoplasmah. Diagnosis:

i. Blood culture, sputum cultureii. CXR

iii. O2 sati. Tx:

i. Supportive:1. Blood pressure (IV fluids, pressors)2. Ventilatory support (mechanical ventilation, O2

ii. Antibiotics1. First empiric2. Then pathogen-directed

j. Hospital Acquired Pneumoniai. 48-72 hours after admissionii. Usu resistant bacteria (oft gram negative)

1. Enterobacteriaceae, pseudomonas, staph aureusiii. Dx: Sputum gram stain and cultureiv. Tx: empiric, broad spectrum

7. Sepsisa. SIRS:

i. Temperature too low or highii. HR>100

iii. RR> 20/miniv. WBC over 12,000 or under 4000v. Very easy to have this, just by walking up some stairs

b. SIRS + infection = sepsisc. Sepsis + 1 sign of organ failure = severe sepsisd. Sepsis + inability to keep adequate blood pressure despite fluids = septic shocke. Mostly caused by gram positiveorganisms

i. Fungi have been increasingf. Pathogenesis

i. Endotoxin binds to immune cellcell makes inflammatory cytokines (IL-1, IL-6,TNF

1. fever, tachypnea, tachycardia2. capillary leak, neutrophil migration, platelet aggregation3. vasodilation


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ii. inadequate blood pressureiii. Lactic acidosisdeathiv. Hyperreactive immune response to LPS

1. Binds to TLRsa. TLR4 does gram negb. TLR2 does gram pos

i. Gram pos sepsis is usually staph aureus1. Uses peptidoglycan instead of LPS

g. Diagnosisi. At least 2 blood cultures

1. One from each central line, if presentii. Remember, its not always infectious

h. Txi. Early antibiotics, broad spectrumii. Pick based on clinical presentation (transplant? Neutropenic? HIV?)

iii. Drain pus, debride tissue, remove infected materialiv. Activated Protein C

1. Anticoagulant, antiinflammatory2. Expensive, bleeding risk

v. Corticosteroids1. Debated

vi. Maintain normoglycemia in dm pts1. Just keep it reasonable

8. Atypical Pneumoniaa. Typical vs Atypical

Typical Atypical

Onset acute insidious

Sx fever, cough, chest pain Fever, cough, headache

ConstitutionalSx severe moderate

Physicalfindings rales, consolidation minimal rales

Sputum purulent, rust colored scant, clear

Leukocytosis common mild

CXR airspace disease interstitial

Response to penicillin prompt none


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b. Causes:i. Mycoplasma pneumoniae

1. Lacks cell wall2. Contains membrane sterols3. fried egg appearance on microscope4. Long replication time5. School-aged kids, with pneumonia visible on Xray50% chance its mp6. Infects mucus membranes of respiratory tract

a. Not alveolar, Its AIRWAY7. Diagnosis is clinical8. Tx: macrolides (azythromycin)

ii. Chlamydia pneumonia1. Looks similar to m.penumoniae2. May have a long duration.3. Mild sx4. Tx: macrolides (azythromycin)

iii. Chlamydia psittaci1. Chlamydiae are obligate intracellular2. Nuclear inclusions seen3. Psittaci is related to parrots

iv. Legionella pneumophila1. Many strains now2. Fastidious growth requirements3. Found in aquatic environment4. Likes warm5. Lives within amoebas6. Chlorine resistant7. No person to person transmission8. May appear to have multisystem involvement9. Dx test: sputum culture10.Tx: Azythromycin

v. Viral pneumonias1. Esp in kids2. Seasonal

9. Gastroenteritisa. 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. Vomitingtoxin, virus


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ii. Nonbloody diarrheasmall bowel dysfunction (shigella, salmonella)iii. Bloody diarrheabacterial colitis, colon

c. Cholerai. Water-borneii. Toxins:

1. cholera toxina. A subunit: ADP ribosylase

i. Translocates into cell/causes harm to cellb. B subunit: GM1 ganglioside

i. Docking mechanism. Highly immunogenicc. Locks adenylate cyclase in ON position

i. Enhances cAMP levelsii. Enhances Cl secretion

2. pili (attachment)iii. They lose 1-2 LITERS of stool per HOURiv. Tx: Rehydration

1. Water + salt + sugard. E.Coli diarrhea

i. Enterotoxigenic Ecoli- travellers diarrhea1. Secretory diarrhea cholera-lite2. Harms kids more than adults3. antiBio may help, but NOT prophylaxis

ii. Enteropathogenic Ecoli- severe infantile diarrheaiii. Enteroinvasive Ecoli- like shigellaiv. Enteroaggregative Ecoli- chronic diarrheav. Enterohemorrhagic Ecoli (produces shigatoxin)- Ecoli o157:H7

1. Can be lethal2. In foods often (rare burgers)3. Can give hemorrhagic colitis

a. Toxins in bloodstream injure endothelial cellsb. Form clotsc. Frickin everywhere.

4. Hemolytic uremic syndromee. Rotavirus

i. Has a capsidii. Nearly everyone gets some rotaviral infections as a kid

iii. The first one is worstiv. It can kill childrenv. Vaccine: they made one, but it had intussiception risknot acceptable in us

1. So other countries (where it couldve saved kids lives) also didnt accept it.f. Giardia

i. Carried in water


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ii. Non-bloody chronic diarrheaiii. Treat with metronidazole

g. Entameba histolyticai. Amebiasisii. Rare in US.

iii. Tx with metronidazoleh. Cryptosporidium parvum

i. Severe chronic non-bloody diarrheaii. Even in immune competent ppl

iii. Treat with nitazoxanidei. C. Diff

i. Healthy ppl often carry itii. Culture is tedious. DONT. just test for toxins

iii. Pseudomembranous colitisiv. Tx: Vancomycin

10.Urinary Tract Infectionsa. Clinical syndromes

i. Bacteuria- bacteria in urine that shouldnt be thereii. Acute cystitis

1. Most common2. Voiding syndrome

a. Burning urinationb. Feeling like you need to go all the timec. Suprapubic tendernessd. Occult URI

iii. Pyelonephritis- upper tract infection1. Flank pain2. Fever, chills3. Nausea, vomiting

iv. Renal abscess1. Abscess around/in kidney2. From untreated pyelo3. Can give fever of unknown origin

v. Uncomplicated UTI- UTI involving normalurinary tract with no functional problemsvi. Complicated UTI- everything else

b. Epidemiology: more in women then meni. Women: starts medium, rises after sexual activityii. Men: starts low (neonate), drops to zero, rises after age 45

c. Caused by:i. Uncomplicated: 80% E.Coli 20% proteus, enterobacteraciaeii. Complicated: 20% e. coli 80% klebsiella, enterobacteraciae, pseudomon

d. Mostly ascending(90%)


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e. Pathogenesisi. Vaginal colonization happens firstii. Entry into urinary tract

iii. Bacterial virulence1. Adherence2. Toxins3. Capular polysaccharides4. Urease production

iv. Host Defense1. Colonization resistance from urogenital flora2. Antimicrobial properties of urine3. Inflammatory response- leads to turnover and sloughing of infected cells4. Micturition, bladder emptying gives mechanical protection5. Specific immune responses6. Barrier method contraception increases risk

v. Risk factors for worse outcome1. Infants, Kids2. Pregnant women3. Compromised adults: DM, imm comp, spinal cord injury

f. Diagnosisi. Internal dysuria, other voiding sx, abrupt onset, no vaginal dischargeii. Urinalysis, microscopy

1. If you dont have pyuria, you dont have cystitisiii. Leukocyte esterase test

1. If negative, they dont have UTI (checks for pyuria)iv. Nitrite test

1. Specific but not sensitiveg. Tx: Bactrim (TMP/SMZ) for 3 days (uncomplicated)

i. 7 days if risk factorsii. 14 days for men

h. Acute uncomplicated pyelonephritis (women)i. Usu ecoliii. Pyuria present

iii. Tx: fluoroquinolonesiv. Culture after therapy is over

i. Recurrent UTIi. Relapse/reinfectionii. Change contraception

iii. Cranberry juice?iv. TMP/SMZ prophylaxis

11.Anaerobic Infectionsa. Gram Negative:


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i. Bacteroides (esp fragilis)1. Give the most greif

b. Gram Positivei. Peptostreptococcusii. Clostridium

iii. Lactobacillusc. Live in mucosal surfaces and GI tract

i. Not in stomachii. Predominate in colon

d. Hallmarksi. Suppurationii. Abscess

iii. Thrombophlebitisiv. Chronicv. Polymicrobial (synergy)

vi. Gas formationvii. Lowered blood supply predisposes

viii. Infection adjacent to mucosal tissueix. Smells like fecesx. Virulence factors: Exotoxins (clostridium), Capsular polysaccharides, beta lactamase

(bacterioides fragilis)

e. Specimens necessaryi. Blood, aspirates, pus, deep tissue. No swabs

f. Tx: ampicillin-sulbactam (include a beta lactamase inhibitor)i. Drain, debride

g. Diseases causedi. Head and neck infection

1. Ludwigs angina (neck spaces)2. Lemierres syndrome (septic thrombophlebitis of jugular vein)3. Gingivitis, dental abscess, to mandible

ii. CNS1. Solitary brain abscessanaerobe2. Spreads from chronic otitis, mastoiditis, sinusitis3. Tx: metronidazole plus ceftriaxone

iii. Pulmonary infection1. Aspiration of oral flora2. Necrotizing pneumonia, abscess, empyema3. Tx clindamycin

iv. Intraabdominal infection1. Perforation

a. You need surgeryb. Treat with combos (polymicrobial)


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v. Pelvic infectionvi. Skin, soft tissue

1. Gas gangrene, nec fasc2. Deep tissue involvement3. Aggressive debridement, antibiotics

h. Clostridium Difficilei. Gram pos, spore forming, anaerobeii. All over hospitals

iii. Causes pseudomembranous colitisiv. Really bloody diarrheav. Toxins A, B- cytoskeleton injurymucosal injuryfluid secretion

vi. Culture not usefulvii. Complications

1. Fulminant colitis, perforation, toxic megacolonviii. Tx: oral vanc

i. Clostridium perfringensi. Gas gangrene, myonecrosis, nec fascii. Enterotoxin (food poisoning)

iii. Aggressive deridementiv. Penicillin + clindamycin

j. Clostridium tetanii. Preventableii. Toxin- tetanosporin. Stops inhibition of motor neurons

k. Clostridium Botulinumi. Foodborneii. Descending paralysis (prevents Ach release)

iii. Makes 7 neurotoxinsl. Actinomycoses

i. Gram positive branching bacillus1. Looks like a fungus but is NOT2. Not acid fast (unlike nocardia)

ii. Sulfur granules in tissuesiii. Extends through tissue planes like malignancyiv. Tx: penicillin

12.Arboviruses, Enterovirusesa. Arthropod-borne virusesb. Potential for explosive epidemicsc. Humans are dead-end hostsd. Usual vectors: mosquitoes, ticks, flease. Dengue fever

i. Most important flavivirusii. Mosquito borne (aedes aegypti)


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iii. Distributed in a belt across the world: tropics, subtropicsiv. Get infected and reinfected. Sequentially worse.v. breakbone fever- fever, rash, HA, severe myalgia, arthralgia

vi. Heals with no sequelae unlessvii. Dengue shock syndrome- 3rdspace fluid into lungs, abdomenhypovolemic

viii. No treatmentix. It takes less than 2 weeks to show up (so if travel was more distant than that, dont

worry)

f. West Nilei. Normally between birds and mosquitoesii. Epidemiology: over 55 higher risk

iii. Fatality is worse for hospitalized ptsiv. Genetic susceptibility: CCR5 mutationv. Pathogenesis

1. Bitten by mosquitotravels to lymph nodeviremiaCNS2. If high enough innoculum, can cross BBB, kill neurons

vi. 5-10 days after mosquito bitevii. Mild: fever, headache, myalgia/arthralgia, anorexia

viii. Sore throatix. Rash (trunk> extremities) (rare in US cases)x. Recovery is usu complete, worse in adults than kidsxi. Tx: no real tx

g. Chikungunya virusi. Mosquito borne (aedes aegypti)ii. Debilitating febrile illness (joint painimpossible to move)

iii. No vaccine/txiv. Possibility of pandemic

h. Enterovirusesi. Many serotypesii. Usu infections are mild: febrile rash, UTI

iii. Very smalliv. Non-envelopedv. Have a protein coat

1. So hard to decontaminate. Alcohol wont help herevi. Mostly in summer and fallvii. Mostly in young kids

viii. Transmission: fecal-oral, respiratory dropletsix. Adults have more severe diseasex. Men2Xxi. Can make vaccines (it worked for polio), but theyre so small, they can be

synthesized.

xii. Diseases caused


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1. Aseptic meningitisa. Coxsackievirus group Bb. Summer and fall meningitis

2. Encephalitisa. Altered mental status, focal neurological signs, seizuresb. Worse prognosis than aseptic meningitisc. Enterovirus 71

3. Cardiac diseasea. Acute myocarditis in young ppl (esp males)

i. Enteroviruses, coxsackieb. Chronic cardiac disease

i. Sporadic dilated cardiomyopathyii. Coxsackie group B

4. Eye infectionsa. Acute hemorrhagic conjunctivitisb. Excessive lacrimation, pain, periorbital swelling, redness, visual

impairment

5. Respiratory syndromesa. Enteroviruses- cause URI

6. Herpanginaa. Febrile illness, acute onset, sore throat

i. Lesions on tonsils, soft palate, uvula, pharynxii. May be part of hand-foot-mouth

7. Hand-Foot and Mouth diseasea. Common in kidsb. Very contagious

xiii. Therapy: supportive care13.DNA Viruses (Herpes)

a. Double-stranded, enveloped DNA virusb. 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 synthesisiv. DNA replication occursv. Late Genes are expressed, genes for structural proteins

c. Latencyi. 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 sxd. Transmission- direct contact w body fluid

i. Does not survive in environmentii. Mucosal surfaces, resp tract, bloodstream are susceptible sites


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e. HSV 1 and 2i. HSV1

1. Orolabial2. Usu get it in childhood3. Up to 90% of adults have it (higher levels in poorer ppl)4. 20-40% recur5. Course:

a. Primary infection- most widespreadi. Fever, malase, myagliasii. Lesions on palate, lips, tongue

b. Latent- noninfectious HSV in the trigeminal ganglionc. Recurrence

i. 20-40% in first yearii. More limited

iii. Triggered by: trauma, light, imm suppression6. Incubation is from 2-14 days7. Many people are asymptomatic carriers

ii. HSV 21. Genital2. Sexually transmitted3. 25% of adults have it4. 60-90% recur5. Painful lesions6. Primary infection can have systemic sx (like HSV1)7. Incubation period of 2-7 days8. Virus can be shed asymptomatically

iii. Diagnosis:1. Viral isolation

iv. In Imm Comp1. Reactivate frequently2. Can involve other systems (gi, etc)3. Is a prominent feature in advanced HIV

v. Tx1. HSV1- analgesics, acyclovir (esp if recurrent)2. HSV2- also acyclovir

vi. Encephalitis1. Most common endemic encephalitis in US2. Usu caused by HSV13. Can happen at any age4. Dx: CSF PCR. MRI if you want5. Tx: high dose acyclovir for 3 wks

f. Varicella Zoster virus


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i. Spread by direct contactii. Primary infection: Chicken pox

1. 5-9 yo2. Respiratory spread3. Fever, URI, malaise; THEN the rash

a. By the time you have the rash, youre not contagious4. Rash: start on face/head, move down

a. Different stages of vesicle will be near each other5. Tx: Antihistamines, acetaminophen, acyclovir (heals faster, fewer lesions)6. Vaccine: Varivax.

a. Live, attenuatedb. Give to kids

iii. Recurrent infection: Zoster (Shingles)1. Follows unilateral dermatomes2. Pain, burningerythema-papulesvesicles3. Mostly in older ppl4. Virus sheds only while theres rash5. If it crosses dermatomes, its disseminated

a. Risk of pulmonary transmission6. Tx: Acyclovir, analgesics7. Vaccine: Zostervax

a. Live, attenuatedb. Give to adults over 60c. More concentrated form of varivax

14.Herpesviruses 2a. CMV

i. Lipid envelope derived from hostii. Largest herpes virus

iii. Infects fibroblasts, endothelial cells, epithelial cells, and macrophagesiv. Can be latentin cells of monocyte/macrophage lineagev. Pathophysiology

1. Primary infection- Usu resp tract. Then it disseminates2. Productive infection- shedding virus from secretions (saliva, urine)3. Adaptive immune respose-controls the virus4. Latency- in hematopoetic cells in bone marrow,5. Reactivation- periodically (from immunosuppression, stress, pregnancy)

vi. Interacts with immune response:1. Inhibits expression of MHC 12. Blocks antigen presentation of MHC 23. Downregulates NK cells4. Inhibits TH1

vii. Epidemiology


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1. Widespread, requires close contact(person to person)a. Saliva, tears, urine, genital secretions, bloodb. Vertical transmission to babies

i. Babies are usu asymptomaticii. more likely to be symptomatic if mom gets CMV during

pregnancy.

viii. Disease:1. In a normal host, asymptomatic, or mono-likeillness

ix. Transplants1. Solid organ: Donor positive, recipient negative is highest risk

a. CMV is common in solid organ transplantsb. Just get systemically sick

2. Stem cells: Donor negative, recipient positive is highest riska. CMV pneumonia is common here

i. Bilateral, diffuse, interstitial3. HIV patients get CMV retinitis

x. Dx1. PCR of blood.2. Amount of virus corresponds to severity of infection

xi. Tx: Gangcylcovirb. Roseola (HHV6)

i. Beta herpes virusii. Infects T lymphocytesiii. Sheds in salivaiv. Everyone gets it within first 3 yrs of lifev. High fever, then as fever breaks, develops rash

1. Some kids dont get the rash2. Can also get febrile seizures

vi. Dx: PCR of bloodvii. Tx: unsure. Gangcyclovir?

c. EBVi. Replicates in B lymphocytes

1. When it infects them, they become immortalii. Exposure to infected saliva

1. pharyngitis2. shedding in saliva3. B cell infection

a. heterophile antibodiesb. T cell activation

i. malaise, spleen enlargement, atypical lymphocytesii. control the B cell population

1. EBV becomes latent


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iii. Transmission: person to person (infected saliva)iv. Diseases

1. Infectious mononucleosisa. Fever, tiredness, lymphadenopathy, sore throatb. 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 Lymphoma3. Oral hairy leukoplakia (HIV)

d. Kaposis Sarcoma (HHV 8)i. Multiple lesionsii. Multiple cell types

iii. Worse risk if imm compiv. Most ppl are asymptomaticv. If youve had it before, then get AIDS, Kaposis is more common

vi. Dx: PCR, histologyvii. Tx: HHV8 is sensitive to foscarnet.

1. Unclear clinical use15.Respiratory viruses

a. Often seasonali. RSV: in the WINTERii. Influenza: in the WINTER

iii. Rhinovirus: in the SPRING and FALLb. Most common respiratory virus is rhinovirusc. Rhinovirus

i. Non-enveloped1. Stable in the environment

ii. Spring and fall peaksiii. Transmitted by particle aerosol, or secretionsiv. Mostly young kidsv. Pathogen of upper respiratory tract

1. Causes common cold2. Can also go down into lower airways and cause asthma exacerbations

vi. Non-cytopathicvii. Dx: clinical

viii. Tx: symptomatic. Antihistamines, NSAIDSd. Influenza

i. Envelopedii. Segmented RNA genome

1. H and N


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2. Can recombine (antigenic shift)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 awfulvii. Cytopathic- damages respiratory epithelium

viii. Dx: Viral cultureix. Tx: Neurominidase inhibitorsx. Vaccine

1. Live attenuated (nasal spray)2. Inactivated (injection3. Grown in eggs4. Reformulated yearly

e. RSVi. Envelopedii. RNA virus

iii. Everyone gets it in first 2 yrs of life1. 1% need hospitalization2. Can get reinfected (immunity is incomplete)

iv. Transmission by large droplets, contaminated secretionsv. Sx: Bronchiolitis, pneumonia

1. Premies- apnea2. Preexisting heart conditions- decompensation

vi. Pathophysiology1. 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/swab1. Antigen test

viii. Tx: mostly symptomatic (o2, hydration, ventilation if needed)1. Ribovirin for imm comp

16.Antiviral agentsa. Herpes drugs

i. Topical:1. trifluorothymidine

a. Drug of choice for hsv keratoconjunctivitis2. Cidofovir

a. Very toxicb. Used for resistant strains of DNA viruses (CMV, HSV, EBV, VSV)

i. For immunocompromised, before it disseminates3. Docosanol


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a. Over the counter.b. Recurrent HSV

ii. Systemic1. Require phosphorylization inside the cell2. Acyclovir

a. Inhibits DNA polymeraseb. Prefers HSV DNAp to host DNApc. 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 acyclovirb. 4X more bioavailable

4. Famicyclovir (prodrug), penicyclovira. Same action as acyclovir.b. Also, hep Bc. Famicyclovir = oral; penicyclovir= topical

5. Gancyclovira. For HSV- same efficacy as acyclovirb. CMV- 10-50X BETTERc. Competitive inhibitor of DNApd. Use for: serious CMV infections, transplant prophylaxise. Renally clearedf. Lots of toxicity

i. Neutropenia, anemiaii. Bone marrow suppression

6. Valcancyclovira. Prodrugb. Oral availability equals IV! (high serum levels)

iii. Foscarnet1. Non-nucleoside inhibitor2. Doesnt require phosphorylation3. Directly inhibits herpes DNAp4. Use for resistant strains esp resistant herpes5. IV only6. Very toxic

a. Nephrotoxic (renally clearedrenal tubular injury)b. Hypo/hyper calcemia, hyperphosphatemiac. Penile ulcers

b. Influenza virusi. Vaccine is most importantii. Prophylaxis if not


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iii. Neurominidase inhibitors1. Zanamivir, Oseltamivir

a. Work for influenza A and Bb. Prevent releaseof virus particles (so new cells arent infected)c. Few side effectsd. Expensivee. Only shortens illness by a few daysf. Theres resistance to oseltamivir

iv. (and amantidines, but resistance is common)v. Ribavirin

1. Only use for Hep Ca. This plus interferon is the treatment

2. Resistance is rare3. Inhibits viral mRNA formation4. Can use the aerosol for RSV pneumonia5. Contraindicated in pregnancy6. Can get concentrated in RBCshemolytic anemia

vi. Interferon-inhibits viral replication1. Adverse effects: fever, chills, acute pneumoniachronic fatigue,

depression, ataxia

17.Acid Fast Organismsa. Lipid rich wall

i. Allows for: resistance to drying, antibiotics, detergentsb. Penetrates macs, lives freely in themc. M. Tuberculosis

i. Rates 2x menii. Crowding, poverty

iii. HIV, Silicosis, IVDU, DM, end stage renal diseaseiv. Person-to-person (small aerosolized droplets)v. Latent TB

1. Positive skin test/assay2. No signs/sx3. Not infectious

vi. TB1. Caseating, granulomatous, usu upper lobes

vii. Pulmonary TB Reactivation1. Cough, hemoptysis, weight loss, night sweats2. Primary: hilar nodules

viii. Extrapulmonary TB1. Pleuritis- hurts to breathe2. Lymphadenitis- more WOMEN. Maybe no systemic sx3. Ostomyelitis- the spine. May have cold abscess of psoas


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ix. Military TB1. Lymphohematogenous spread2. Can happen in infants

x. TB skin test: test sucks1. Measure area of induration2. 5mm:

a. Past TB ptsb. Close contacts of TB ptsc. HIV pts

3. 10 mma. IVdrug useb. Healthcare workersc. Ppl with risk factorsd. Immigrants from endemic countries

4. False negatives- due to anergy5. False positives- BCG vaccine

xi. IFNGamma Release Assays1. Drug of choice for ppl with BCG vaccine2. More specific3. Doesnt require return for reading4. Results in 24 hrs

xii. Anti TB drugs1. Isoconazid

a. Interferes with mycolic cell wall synthb. Hepatotoxicity, renal toxicity

2. Rifampina. Inhibits DNA dependent RNA polymeraseb. Adverse rxns: Hepatitis, hypersensitivity, Drug interactions (cyt

P450)

3. Rifabutina. Similar mech to rifampinb. Fewer drug interactionsc. Better to use in HIV

4. Pyrazinamidea. Adverse effects: nausea, hepatotoxicity, hyperuricemia, arthralgias

5. Ethambutola. Inhibits cell wall synthb. Adverse effects: optic neuritis

xiii. Treat w all four drugs for 2 mo, INH & rifampin after that, total 6 mo1. Directly observed therapy

xiv. Noninfectious: all of:1. 3 separate sputum cultures negative


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2. Responding to therapy3. 2 weeks of therapy

d. Non-tuberculous mycobacteriai. Hansens Disease (m. Leprae)

1. Tuberculoida. Low bacterial burden, low infectivity

2. Lepromatousa. High bacterial burden, high infectivity

3. Anesthetic plaques4. Sensory/motor neuropathy5. Prefers cooler skin6. Does NOT grow in culture

ii. Nocardia1. Found in soil2. opportunist3. Skin, lung, brain4. Tx: TMP-SMX5. Branching, filamentous

iii. Rhodococcus1. Found in soil2. Opportunist3. Exposure to horses4. Grows red on culture5. Causes cavitarypulmonary disease in imm comp6. Tx: Vanc

18.STDs: Genital Ulcer Syndromesa. Syphillis

i. T. pallidumii. Difficult to grow

iii. Humans sole hostiv. Pathogenesis

1. Penetrates skin via microabrasionsa. Replicates w/o inflammationb. Travels to lymph nodesblood streamsystemicc. Causes primary lesion at site of inoculation

i. Painless ulcerii. Indurated

iii. punched outiv. Scant secretion

v. Primary infection: painless ulcer.1. 3 weeks after exposure

vi. Secondary infection: rash on palms, soles. Systemic


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vii. Teritary infection: Neuro, CV (ascending aorta), opthoviii. Congenital: oft causes stillbirth

ix. Tx: Penicillinb. Genital herpes

i. Usu HSV2ii. Initial infection:

1. Systemic: fever, malaise, headache, pharyngitis, myalgias2. 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, serologyvi. Tx: Acyclovir

c. Chancroidi. Haemophilus ducreyiii. Requires break in skin to infect

iii. Pyogenic, painfuliv. box car or school of fish appearance histologicallyv. Disease

1. Genital ulcer 4-7 days post exposurea. Soft, ragged borderb. Tenderc. Usu multipled. Painful regional lymphadenopathy

vi. Tx: cephtriaxone19.Candida and antifungals

a. Most common is albicansb. Only present where animal contamination is possiblec. Present in hospitalsd. Grows white on agare. Human oropharynx, GI tractf. Diseases

i. Candidemia1. Candida isolated from one or more blood cultures2. Can be a sign of acute disseminated candidiasis

ii. Disseminated candidiasis1. Histologic evidence of tissue invasion AND2. Culture positive at 2 different normally sterile sites3. New fever, or septic in a seriously ill person4. Candiduria (wo catheter)5. Rash: nonspecific, popular. Can biopsy them and find candida


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6. Retinal lesions7. Lesions in liver8. Tx: Echinocandin

a. Fluconazole for Albicansi. DONT USE if unstable or c. glabrata

iii. Vulvuvaginal candidiasis1. Vaginal discharge

a. May just have pruritis, no dischargeiv. Thrush, Diaper rash

g. Antifungalsi. Polyenes

1. Nystatina. Topical, b/c too toxic to give otherwise

2. Amphotericin Ba. Binds to ergosterol in cell membraneb. Increases permeabilibyc. gold standardd. Nephrotoxice. Lipid preparations

i. Less toxicii. Bigger therapeutic window

ii. Azoles1. Inhibit ergosterol synthesiscells leak2. Oral

a. Fluconazoleb. Itraconazolec. Voriconazoled. Posaconazole

3. Topicala. Ketoconazoleb. Clotrimazolec. miconazole

iii. echinocandins1. Inhibit cell wall crosslinking (glucans)2. Used for Candida3. Well tolerated4. Expensive5. IV6. Includes:

a. Caspofunginb. Micafunginc. Anidulofungin


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iv. Other1. Allylamines

a. Topicalb. Inhibit sterol synth

2. Flycytosinea. Inhibits DNA synthesisb. Treats cryptococcal meningitisc. Bone marrow toxicity

20.Opportunistic Mycosesa. Cryptococcus Neoformans

i. India ink stain shows a capsuleii. Encapsulated yeast

iii. Narrow-based buddingiv. Transmission via inhalationv. Risk factors: SEVERE HIV. CD4 < 50. Less so, other immunosuppression

vi. Clinical presentation1. Meningitis (esp HIV)

a. Subacuteb. Elevated opening pressurec. High white cellsd. Tx: Amphotericin B and Flucytosine, then fluconazole

2. Pulmonary disease: nodules, cavitary lesions, miliary, others3. Disseminated4. Skin5. GI

vii. Everyone w/crypto gets an LP1. Rule out meningitis

viii. Tx: AIDS pts: lifelong suppression w fluconazoleb. Pneumocystis Jiroveci

i. Whispy interstitial infiltratesii. Cant grow in vitro

iii. Transmission via inhalationiv. Seen in: HIV patients (CD4 < 200); corticosteroid ptsv. Tx: TMP/SMX, add predisone for serious cases

c. Aspergillusi. Septated acute angle hyphaeii. Ubiquitous

iii. Fumigatus is most commoniv. Can be caused by problems in ventilation. Demolitionv. Seen in: Neutropenic pts. Rarely in HIV.

vi. Pulmonary:1. Low grade fever


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2. Hemoptysis (sometimes severe)3. Chest pain4. Cough5. Pulmonary infiltrates6. CXR, CT shows halo sign

vii. Non-pulmonary:1. Sinusitis (w nosebleeds)2. CNS disease (focal neural signs)3. Skin

viii. Tx: reduce immunosuppression1. Voriconazole

d. Zygomycosis (mucormycosis)i. Grows in the environment (on strawberries

1. Rhinocerebral2. Pulmonary3. Cutaneous

ii. Risk factors1. Diabetic ketoacidosis2. Neutropenia3. Hematological malignancies4. Iron chelating therapy

iii. Pathogenesis1. Inhaled (or cutaneous inoculation)direct invasion (nonhemotogenous)2. Can cross tissue planes3. Likes vascularinvasion

iv. Clinical1. Facial pain, headache, fever2. Orbital cellulitis, necrosis of the palate, black nasal discharge, proptosis3. Can also be: Pulmonary, cutaneous, GI

v. Dx: Broad, non-septate, right angle branching1. Culture may be negative

vi. Tx: correct risk factors (DKA)1. debridement.

e. Sporotrichosisi. Rose gardensii. Dimorphic fungi (mold cold, yeast hot)

iii. Clinical1. Lesion at site of inoculation

a. Sub Q nodules w/ulceration, may get more in lymphatic distributioniv. Tx: Itraconazole

21.Endemic mycosesa. Histoplasmosis


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i. Dimorphic fungus: outside mold, in the body yeastii. Mississippi and Ohio river valleys

iii. Bat guano, bird roostsiv. Transmission: like TB. Easy to cough out, hangs in air

1. Inhaledv. Pathophysiology

1. Alveolar macrophages engulf it2. They divide and disseminate in macs

vi. Clinical1. Acute Histoplasmosis

a. May be asymptomaticb. Maybe flu-likec. Calcified granulomas indicate past infection

2. Progressive Disseminated Histoplasmosisa. Acute- HIV, imm suppb. Subacute- immunocompetent ppl

i. Fever, weight loss, malaiseii. Oral ulcers

iii. Hepatosplenomegalyiv. Can look like miliary TB

c. Dx: Serologyd. Tx: Amphotericin B for severe

i. Itraconazolefor less severe(drug of choice)3. Other disease:

a. Isolated pulmonary diseasei. Cavitary or noduleii. Can look like TB

iii. Check for serology and cultureiv. Often in smokersv. Treat with itraconazole

b. Aseptic meningitisi. Chronicii. Serology on CSF

iii. Treat with Amphotericin B, then fluconazolec. Mediastinal Fibrosis

i. An overaggressive immune response to histoii. Little treatment

d. Erythema Nodosumi. Assosciated with histo

b. Blastomycosisi. Broad-based buddingii. Dimorphic fungus


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iii. Eastern and central US1. Waterways

iv. Transmission: enters via lungsv. Pathophysiology

1. Incubation- 30-45 days asymptomaticvi. Disease: lung, bone, skin

1. Pulmonarya. Focal lesions

2. Cutaneousa. Get a rashb. Non-healing lesions that ulcerate

3. bone and jointa. Invasive, destructive focal lesions

4. CNSa. Aseptic meningitis

vii. Dx: biopsy and culture1. Serology and urine antigen test arent reliable

viii. Tx: itraconazole. Amphotericin B for severec. Coccidiomycosis

i. Dimorphic fungusii. Spherules full of endospores

iii. Southwestern USiv. Risk: Filipino ppl> African American > whitev. Transmission: inhaled

vi. Disease1. Most are asymptomatic2. Nonspecific respiratory illness3. Infiltrates, hilar adenopathy on CXR4. Dx: Serology: look for a change from neg to pos

vii. Tx: Controversial. Maybe or maybe not treat everyone1. Definitely treat:

a. HIV ptsb. Organ transplant ptsc. Pregnancyd. Filipino, African ppl

2. Itraconazoleviii. Chronic coccidio

1. Chronic fibrotic pneumonia2. Extrapulmonary

a. Cutaneousb. Bone/jointc. Meningitis


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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 suppressionb. Amphotericin B initiallyc. Itraconazole

d. Penicilliosisi. Thailand, Vietnam, southern Chinaii. Dimorphic fungus

iii. Opportunisticiv. Clinical:

1. Fever, malaise, weight loss > 4 weeks2. At least one cutaneous lesion3. Maybe lymphadenopathy, hepatosplenomegaly, cough

v. Dx: Pathology, culturevi. Tx: Amphotericin B, then itraconazole

e. Paracoccidiomycosisi. South American Blastoii. Looks just like blasto, but with more cutaneous lesions, esp face

22.Helminthsa. Host specificb. Dont multiply in humansc. Many infections are asymptomaticd. Pathogenesis

i. Tissue invasionii. Compete with hosts for nutrients

iii. Create obstructionsiv. Incite harmful immune response

e. Ascaris Lumbricoidesi. Pathophys:

1. Ingest eggsa. Stable in environmentb. Fecal-oral

2. Larvae penetrate bloodstreama. Can cause eosinophilic pneumonia

3. Go to lungpenetrate capillariescrawl up airspace4. Are swallowedlive in intestine5. Produce thousands of eggs

ii. Tx: Mebendazole1. Binds to tubulin, intefrees with motility2. Poorly absorbed: so it can hit intestinal worms

iii. Southwestern US, Developing countries


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f. Pinworms (enterobius vermicularis)i. Eat eggsii. Hatch in intestine

iii. Live in cecumiv. Adults come out of anus at night to lay eggsv. Dx: scotch tape test- see eggs

vi. Many ppl are asymptomatic1. Treat the whole family

g. Whipwormi. Soil transmittedii. Eat the eggs

1. Barrel shaped, mucus plug at both endsiii. Hatch, live in intestine

1. Produce more eggs into stooliv. More common in:

1. Kids, developing worldv. Can cause: anemia, mental retardation, growth delay

vi. Blanket tx of all kids with albendazole in developing worldh. Hookworm (ancyclostoma duodenale)

i. Pathophys1. Larvae penetrate skin (of foot) (this itches_

a. Travel in bloodstream to lungb. Penetrate capillariescoughed upswallowedc. Reach intestine, penetrate

i. Bloody diarrhea, abdominal pain on initial penetrationd. Eggs released into stool, hatch in stoole. 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 Migransi. Because of host specificity of a dog/cat hookwormii. Serpiginous borderof rash.

j. Strongyloides stercoralisi. Similar cycle to hookworm, except can cause autoinfection (hyperinfection)

1. Can be very dangerous in immunosuppressedii. Walking barefoot where there are feces

iii. Clinical manifestations1. Oft asymptomatic2. Lower abdominal rash (where parasites have entered)3. Eosinophilia (maybe4. Abdominal bloating, weight loss5. Immunosuppressed (esp steroids) are at risk of hyperinfection


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iv. Dx: larvae (not eggs) in stoolv. Tx: Ivermectin

k. Trichinosisi. Eat muscle with larvae in them

1. Oft uncooked porkii. Hatch in intestinepenetrate intestinemusclecysts

iii. Clincial: fever, severe muscle aches, periorbital edema, heliotrope rash1. If severe, myocarditis

iv. Tx: Unnecessary. Albendazole can kill worms, but theyll die on their own anywayl. Filariasis

i. Pathophys1. Infected mosquito bites2. Travels to lymph nodes

a. Grow long- block lymph nodes3. On ultrasound, can be seen flailing around4. Can live in blood

a. Only come out at nightii. Disease: edema, Hydrocele, elephantiasis

iii. Dx: look in blood at night OR antigen testiv. Tx: Albendazole + Ivermectin

m. River-Blindness Onchocerciasisi. South Africa, Yemenii. Transmission: Black fly (breeds in rapid streams)

iii. Live in subQ nodules(oft on the head)iv. Inflammitory response causes blindnessv. Can also cause skin changes/inflammation in skin

1. leopard skinvi. Dx: microfilariae in blood vesselsvii. Tx: Ivermectin

1. Blocks neurotransmission in worms2. Clears it from skin and eyes, safely3. But only temporarily. Spares adult worms.4. So kill the blackflies5. Other:

a. There is a bacterium IN the worm: Wolbachiai. Kill thatkills O. Volvulusii. Doxy

n. Schistosomiasisi. A fluke (trematode)ii. Liver disease due to inflammatory response to eggs

iii. Pathophysiology1. Intermediate host: snail


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2. Forms circariae (w fork-like tails)a. Can penetrate human skin

3. Entersdifferentiates into adultmigrates to specific tissuea. If it enters the wrong host, it dies

i. Swimmers itch is from Avian Schistosomiasisiv. S. Mansoni

1. Eggs have a lateral spine2. Goes to myenteric plexus, Portal circulation

a. Causes portal hypertensioni. pipe stem fibrosisii. Caput medusa, esophageal varices, etc

b. Granulomas surrounding eggsc. In intestine, each egg causes a polyp

i. Can bleed3. Can lead to malnutritionpoor development, low IQ4. Can help with allergies.5. Tx: not much. Kill the snails

a. Drugs help expose more s. mansoni antigens to the immune systemb. Praziquantel

v. S. Hematobium1. Eggs have a terminal spine2. Only in Africa (esp sub-Saharan)3. This one goes to the BLADDER PLEXUS

a. Can cause fibrotic, dilated ureters, fibrotic bladderrenalfailuredeath

b. Can also get them on the cervixprone to bleedingi. More susceptible to other infections like HIV

o. Paragonimus infectioni. Pathophys

1. Ingest raw crayfish2. Hatch in intestinemigrate to lungscoughswalloweggs in feces

p. Tapewormsi. Have scolexes, proglottidsii. Cysticercosis

1. Clinical:a. Headache, focal deficits, new onset seizures

2. Pathophysa. Ingest cystercerci in tissues of undercooked meat

i. Usu porkb. Larva attaches to intestineadultreleases eggs

i. This is asymptomaticc. Ingest eggs


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i. Larvae can travel to1. Brain: Cerebral cysticercosis2. Muscle/soft tissue: calcify, seen on Xray

3. Dx: CT/MRI, CSF serology4. Tx: not always necessary.

a. Albendazole w/ dexamethacinb. Surgery

iii. Diphyllobothrium Latum (Fish tapeworm)1. Eating undercooked freshwater fish2. Can be 10 meters long3. Clinical

a. Anemia, B12 deficiency4. Tx: Niclosamide

23.STDs II (cervicitis, urethritis, vaginitis, etc)a. Urethritis/cervicitis

i. Urethritis: Discharge, disuria, PMNs1. If gram negative Diplococciseengonorrhea2. If notNGU

ii. Cervicitis: Cervical mucopurulent discharge, cervical friability1. Gram stain isnt as specific

iii. Gonorrhea1. Caused by Neisseria Gonorrhoeae

a. Gram negative nonmotile Diplococcusb. INSIDE the PMNc. Oxidase positived. Likes CO2 environment

2. Has pili with antigenic variation3. Outer membrane proteins help it invade cells4. Pathogenesis

a. Mucosal contact necessaryb. Incubation 7 days (closer to 3-4)c. Pili attachendocytosisinflammatory responsepus (yellow-

green)

d. Naturally clear it in 1-2 moi. But can get scarring, infertility from it

5. Clinicala. Urethritis- can lead to epididimitisb. Cervicitis- can lead to PID, perihepatitis (w normal LFTs)c. Disseminated- can be serious. Dermatitis (nodules)d. Conjunctivitise. Pharyngitis

6. Tx: cephtriaxone


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a. Can co-treat for Chlamydia (azythromycin)iv. Chlamydia

1. Obligate intracellular2. Infectious particle is the elementary body

a. Invades cell, prevents fusion with lysosome3. Clinical

a. NGUi. Discharge is white or clear, more mucoidii. Can progress to epididimitis

b. Mucopurulent Cervicitis- can become salphingitisi. Discharge is less purulent

c. Lymphadenitis venerumi. Matted inguinal lymph nodesii. Groove sign

4. Tx: single dose azythromycinb. Vaginitis, vaginosis syndromes

i. Copious vaginal dischargeii. Normal vaginal flora: lactobacillus

1. Keeps pH low2. Protects against pathogens, keeps other normal flora in check3. Loss of lactobacillusincreased infection, other bacterial overgrowth

iii. Vaginitis:1. Inflammatory response (irritated vagina)2. WBCs present

iv. Vaginosis:1. Decreased lactobacillus, increased anaerobes2. WBCs absent3. Non-inflammatory

v. Include1. Bacterial vaginosis

a. Thin dischargei. Adherent, greyish

b. Elevated pHc. Fish-like odor with KOHd. clue cells

i. Epithelial cells with ragged borderse. Tx: metronidazole (flagil)

2. Trichomaniasisa. Trichomaniasis Vaginalis

i. Motile, seen on wet mountb. Frothyvaginal discharge (profuse)c. Itching


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d. Elevated pHe. Cervical petechiaef. Men have no sx

i. Treat the partnerg. Tx: metronidazole (flagyl)

3. Vulvovaginal candidiasisa. yeast infection from candidab. Pseudohyphae/budding yeast on wet mountc. Thick white cottage cheese discharged. Itchinge. Low pHf. Tx: OTC stuff

c. Exophytic syndromesi. HPV

1. 6 and 11 cause wartsa. Rough, cauliflower appearance

2. 16 and 18 cause cervical dysplasia3. Vaccine4. Tx: ablate the warts

a. This doesnt cure the virusii. Molluscum contagiosum

1. Common pox virus in kids (not necessarily sexual)2. Smooth domed lesions3. Dx: visual4. Tx: ablate the warts

d. Ectoparasitic infectionsi. Pubic lice

1. Can see lice, eggs on hairs with naked eye2. Tx: anti-lice shampoos

a. Treat spouse, house tooii. Scabies

1. See the burrows2. Can look like eczema

e. Systemic STDsi. Pelvic Inflammatory Disease

1. See disease outside genital tract2. Manifestations of

a. Chlamydia, gonorrhea, anaerobesii. Hep B

1. Vaccine-preventible2. Blood-borne

iii. HIV


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24.HIV pathogeneissa. Doublestranded RNA virusb. 2 kinds of tropism

i. Human coreceptors necessary to gain entry into cellii. CCR5

1. Early infection2. Most of whats transmitted

iii. CCXR41. Late infection

c. Transmissioni. Directly into bloodstream

1. Needles2. Blood transfusion

ii. Mucus membranes1. Sex

iii. Vertical transmission1. In utero (uncommon); during delivery (MOST); breastfeeding

d. Natural historyi. First infected

1. Flu-like symptomsa. Ppl may think they have mono

2. Viral load very higha. Your body doesnt know how to fight it

3. Very infectious4. MANY CD4 cells destroyed

ii. Immune response (quiescent phase)1. Steady state equilibrium, immune system fights back2. HIV antibody level stable3. Steadily losing CD4 cells4. High level of inflammation5. Few symptoms

e. Dx: ELISA or rapid HIV test (fingerstick)positive, then western blot to confirmi. To diagnose acute HIV

1. HIV RNA test in plasmaf. Always test HIV resistance

i. Dynamic genomeg. Tx: Anti-Retroviral Therapy

i. When they have:1. An AIDS defining illness (regardless of CD4)2. CD4 LESS than 500 or 3503. Nephropathy4. Pregnancy


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ii. 3 drugs of 2 classes (at least)h. Drugs:

i. Reverse transcriptase inhibitors1. Nucleoside

a. Compete with natural nucleosides for inclusion into DNA2. Non-nucleoside

a. Bind to reverse transcriptasechange binding siteii. Protease inhibitors

1. Causes protease to lock, preventing cleavageiii. Fusion inhibitoriv. CCR5 receptor blockerv. Blocking integration

i. Pregnancy: all should be on HAART. AZTj. Chronic effects of HIV

i. Metabolic complications1. Lipodystrophy

a. Loss of fat in limbs, faceb. Central obesity. Buffalo hump

ii. Ostopeniaiii. Increased CV riskiv. Increased malignanciesv. Coinfection with hepatitis

k. Prognosis is improving25.HIV epidemiology, clinical manifestations

a. Subsaharan Africab. Lots of new infections in youthc. Those unaware of infection are most likely to spreadd. Presentations

i. Wasting syndrome1. Uncommon now2. Depletion of both fat and lean tissues

ii. Oral Candidiasis1. Very common2. NOT an AIDS defining illness

a. Esophageal candidiasis isi. Cobblestone-looking lesions

3. Pseudomembranous4. Treat actutely, do not prophylax

iii. Oral Hairy Leukoplakia1. Non-movable white plaques on margins of tongue2. EBV related3. Oft shows up in non-symptomatic HIV


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4. Doesnt require treatmentiv. Cutaneous manifestations

1. Syphilitic chancrea. Higher syphilis ratesb. More lesionsc. More 2ndary, 3iary syphilisd. Tx: aggressively.e. Do an LP if severe or neuro manifestations

2. Bartonella henselaea. Looks like kaposis sarcomab. Fever, night sweats, anemiac. Liver, spleend. Treat with Doxy

3. Varicella Zostera. Comes out as imm system wanesb. Tx acyclovir to avoid post-herpetic neuraligia

4. HPVa. Warts (disfiguring), cancer (increased dysplasia rates) are both

concerns

5. Molluscum contagiosuma. Smooth, umbilicated lesionsb. Sign of advanced diseasec. Groin, face

6. Seborrheic dermatitisa. Nasolabial folds, eyebrows, back, chest, scalpb. Responsive to antifungals

7. Psoriasisa. Not more likely to get it, but if they have it, its SEVERE

8. Kaposis Sarcomaa. Heaped up vascular lesions

i. Arms, gingival, anywhereb. HHV8

i. Reactivates causing malignancies in mucosal surfacesii. Rarely becomes pulmonaryvery bad

iii. Treat localized lesions1. Cryotherapy etc2. Systemic HCG- trial. Pregnancy helps. Weird

v. Pulmonary syndromes1. Community acquired pneumonia

a. Much higher riski. Young person w 2 CAPHIV test

2. Pneumococcal pneumonia


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a. Most common cause of pneumonia in HIVb. Focal usually, diffuse if advancedc. HIV+ ppl get a vaccine

3. Pneumococcus Jiroveci (PCP)a. Most common AIDS defining opportunistic infctionb. First: hilar infiltrates

i. Hydrate1. Then diffuse interstitial infiltrates

c. Progressive exertional dyspnead. Subacutee. Hypoxicf. Dx: induced sputum demonstrating organismg. Tx: high dose bactrim

i. Side effects are bad. Dont give this unless its provenh. Prophylax with low dose bactrim

4. TBa. Oft atypical presentationb. Put them on isolation til youve ruled it out

vi. Disseminated infections1. Tuberculosis2. Histoplasmosis

a. Diffuse pulmonary infiltratesb. Non-necrotizing granulomasc. Bone marrow infiltrationd. Dx: urine antigen test

3. Mycobacterium Avium Complexa. Advanced immunosuppressionb. Inhale itdisseminationc. Fever, night sweats, fatigue, weight loss, anorexiad. Granulomatous infiltration of liver, bone marrow

4. Lymphomavii. Ocular

1. CMV Retinitisa. ketchup on eggs lesions

i. White plaques on retina, hemorrhages on topb. May or may not have visual complaints

viii. CNS manifestations1. Guillan Barre

a. Happens early2. Chronic meningitis

a. Somewhat later3. Late disease:


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a. HIV Dementiab. HIV neuropathy

i. Similar to DMc. Toxod. Cryptococcus

i. Meningitis1. Sometimes just cryptococcemia

ii. CSF: High opening pressure, High protein, low glucoseiii. Dx: antigen test

e. CNS Lymphomai. Ring enhancing lesionsii. Neuro findings, seizures

f. Toxoplasma Gondi Encephalitisi. Protozoan reactivation

1. Reactivation of latent cystsii. MULTIPLE Ring enhancing lesions

iii. Dx: CSF PCRiv. Also causes ocular manifestationsv. Tx: Pyrimethamine, sulfadiazine

vi. Prophylaxis: TMP-SMZg. Progressive Multifocal Leukoencephalopathy

i. JC virusii. Deep white matter lesions

iii. No mass effectiv. No Tx. HAART helps (immune reconstitution)

26.Protozoansa. Can multiply in humansb. Not assosciated with eosinophiliac. Malaria

i. Fever, Malaise, headache, anemiaii. Normal WBC, decreased platelets

iii. Splenomegalyiv. Plasmodium Falciparum

1. Most severe infectionsa. Can infect RBCs of all ages

i. Higher parasitic loadb. Can lead to sequestration

i. Ischemic eventsii. Microvascular damage

2. Extracellular banana-shaped gametocytes3. Ring forms4. Maternal immunity protects infants


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5. Young children are most severe6. Quotidian fever7. Malarial CNS infections- VERY SEVERE

a. Dystonusv. Plasmodium Vivax

1. Less severe diseasea. Infects YOUNG RBCs

2. Requires duffy antigen3. Hypnozoites in liver

a. Allow for relapse months/years later4. Tertan fever

vi. Plasmodium Ovale1. Less severe disease

a. Attacks IMMATURE RBCs2. Mostly in Africa3. Doesnt require Duffy

vii. Dx: Thick and Thin smearviii. Tx: Uncomplicated

1. Oral combination therapya. Quinine/doxyb. Mefloquinc. Malaroned. If Vivax or Ovale,

i. Primaquine-eradicate hepatic hypnozoitesii. Check for G6PD first

ix. Prophylaxis1. Chloroquine- doesnt work against Falciparum (resistance)2. Doxy- daily. Photosensitivity3. Mefloquin- weekly. Psychosis4. Malarone- weekly. Expensive.

x. Pregnant1. Dont go2. Dont take Doxy. Take mefloquine, maybe

d. Tripanomiasis (Chagas disease)i. Life cycle:

1. Transmitted by kissing bug. Bites you at nightdefecates onskinunconscious scratchinginoculation

2. Trypamastigotes travel to cardiac myocytesamastigotesa. Can go back into bloodtrypamastigotesget sucked out of blood

by kissing bug again

ii. Mostly south Americaiii. Acute Chagas:


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1. Painless swelling of inoculation site. Romanas sign. Fever, malaise2. Self-limited

iv. Chronic1. Continued infestation in cardiac myocites2. Dilated cardiomypopathy, conduction blocks3. Mega-esophagus, megacolon (rarer)

v. Dx: 2 out of 3 independent serological testsvi. Tx: actually does help

1. Benznidazole2. Nefurtomox

vii. HIV- can get it really bad. Can be Fatal.e. Leishmaniasis

i. In the us, Military personnel from Iraq etcii. Life cycle

1. Sandfly bitesa. Promastigotes enterb. Enter cellsc. Become amastigotesd. Replicates in cells

iii. Cutaneous1. Most common form2. Lesion happens weeks after infection

a. Starts out looking like a pimpleb. Ulcerates w raised border

3. Heals in months, leaving a scariv. Mucocutaneous

1. Braziliensis2. Occur years after initial cutaneous infection3. Occur on any mucosal surface (usu nose, mouth, pharynx)4. Very disfiguring5. Difficult to treat6. Can be fatal

v. Visceral (Kala Azar)1. India, Africa, brazil2. L. Dovani, L. infantum3. Subacute: fever, weightloss

a. Hepatomegaly, splenomegalyb. Can infect bone.c. (Liver, spleen, bone)

4. Hyperpigmentation (black fever)5. Die from secondary infection6. Dx: splenic needle aspirate


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vi. Tx: Pentavalent antomonials1. Amphotericin B

f. Toxoplama Gondiii. Intracellular parasiteii. Cat is definitive host

1. Cat feces (can be on unwashed vegitables)2. Can infect fetus3. Can infect other animals

iii. Acute: usu asx1. Mono-like2. Generalized lymphadenopathy

iv. Congenital1. Worse in later trimesters2. Hydrocephalus3. Retinal choroiditisblindness

v. Transplants (donor positive, recipient negative)vi. HIV: Severe disease

1. Necrotizing brain lesions2. Represent reactivation3. Pyramethamine, sulfadiazine

g. E. Histolyticai. Bloody diarrheaii. Oft travelers to endemic areas (like Mexico)

iii. Ingest cysts1. become trophozoites in intestine

a. become more cysts, exit, ORb. 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 stoolsb. Tx: metronidazole (to kill trophozooites) AND

i. tromomidacin (to eradicate cysts)2. Amoebic Liver Abscess

a. anchovy paste as you drain itb. May be fatalc. Biopsy to prove its not neoplasm

h. Giardiai. Children in daycare, Campers, hikersii. Feces, water contaminated with feces

iii. Secretory diarrhea, flatulence


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iv. 60% asymptomaticv. 30% self-limited diarrhea

vi. 10% chronic diarrheavii. Dx: stool microscopy

viii. Tx: metronidazolei. Cryptosporidiosis

i. Community swimming poolsii. Animal reservoirs transmit disease

iii. Intracellulariv. Intestinal parasite

1. Forms cysts2. Resist chlorination

v. Immunocompetent- self-limited watery diarrheavi. Immunocompromised- severe, cholera-like diarrhea

j. Trichomoniasisi. Yellow vaginal discharge, itching. Can be bubblyii. Strawberry cervix

iii. Wet mount-motile pear shaped cellsiv. Men are asxtreat them to prevent reinfectionv. Tx: metronidazole

27.Bioterrorism and Zoonosisa. Features of a bioweapon

i. High morbidity/mortalityii. Available

iii. Dispersibleb. Anthrax

i. the perfect weaponii. Gram positive bacillus

1. bamboo appearanceiii. Aerobic, encapsulated.iv. Forms spores

1. Very hardy2. Can survive in nature for decades3. Become active when in the respiratory tract4. Shit.

v. Produces toxins (doesnt invade tissue)1. Edematoxins- causes influx of fluids2. Lethal toxin- creates massive cytokine response

vi. Disease forms:1. Cutaneous:

a. Spore lands on damaged skinb. Most common, low fatality


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c. Painless papuleedema (from edematoxin)black ulcerveryblack escharheals without scar

2. Gastrointestinala. Ate an infected animalb. Aerosolized form got into nasopharynxswallowedc. Mortality 50%

3. Inhalationala. Mortality up to 95%b. Incubation is usu around 7 days (can be up to 6 weeks)c. Prodromal phase: Influenza w/nausea and vomitingd. Flu improves, quickly becomes fulminant

i. sepsisii. Respiratory failure, shock

iii. Deathe. Dx: Blood culture. It grows quickly.f. Widened mediastinumon clear lungs

i. Bacteria get into lungsii. Macs engulf them

iii. Go to mediastinal lymph nodesiv. Get hemorrhagic necrosis

g. Tx: ciprofloxacin or doxycyclinei. wont respond to CAP drugs

4. no person-to-person transmissionc. Smallpox

i. Incubation: 7-14 daysii. Person to person transmission

iii. Rash marks infectivenessiv. Prodrome:

1. Sudden, severe, flu-like sx2. 3-5 days long

v. Rash:1. Face, hands, feet worst (even palms and soles)2. Stages: maculopapulardeeperpustulesdryscabscar3. All the same age

vi. Tx: nonevii. Vaccine, prophylaxis work

d. Plague (yersinia pestis)i. Zoonosis with flea vectorii. Only pneumonic form is person-to-person

iii. Incubation 2-8 daysiv. Lesion at site of inoculationv. Bubonic:


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1. After bite, get enlarged painful lymph nodesa. May suppurateb. You may be very sickc. You may be septicd. You may diee. It may spread to the lungspneumonic plague

vi. Pneumonic1. Rapid onset pneumonia2. Hemoptysis3. Sputum culture shows gram negative rods

a. Look like red safety pins4. Tx: streptomycin, gentamycin

vii. Septic- you get gangrene at the ends of your digitse. Tularemia

i. Very very small gram negative bacillusii. Intracellular

iii. Mostly in MO, KSiv. rabbit feverv. Vector is fleas

vi. Incubation 3-5 daysvii. Fever w/o tachycardia

viii. Ulcer at inoculationix. Regional lymphadenopathyx. Pneumonic disease

1. Non-productive cough2. Pleuritic chest pain

xi. Dx: serology takes weeks, cultures are poorly sensitive.1. Lab hazard. Warn them.

xii. Tx: Streptomycin, Gentimycinf. Zoonoses

i. Rabies1. Bats, dogs2. Pathogenesis

a. Bite. Replication at site of inoculationi. Retrograde axonal spreadii. 10 cm/day

iii. Goes to the brainstem/thalamusiv. Negri bodies

3. Prodrome: influenza-likea. Percussion myoedema, parasthesias

4. Non-mammals are no riskii. Bartonellosis (cat scratch)


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1. Gram negative intracellular bacillus2. Febrile lymphadenitis3. Mostly kids4. Rarely severe5. Dx: clinical, tissue PCR6. Tx: Azythromycin

iii. Q fever1. Coxiella burnetii2. Cows, goats, sheep

a. Direct contactb. Inhalational

3. Very contagious4. Acute:

a. Flulike sxb. Atypical pneumoniac. Tx: doxycycline

5. Chronica. Endocarditis, osteomyelitisb. Tx: doxycycline and rifampin

iv. Brucellosis1. Intracellular gram neg coccobacillus2. Cows, goats, sheep3. Direct contact, aerosol (placenta), unpasteurized cheese4. Dx: serology5. Fever, malaise, malodorous sweat, Sacroiliac joint involvement6. Tx: doxycycline and aminoglycoside

v. Leptospirosis1. Gram negative helical bacteria2. Triathalons3. Dog, rodent urine4. Self-limited 90%

a. High fever, headache, conjunctival suffusion5. Severe, biphasic 10%

a. Weils diseaseb. Icterus, renal failure, hepatic failure

6. Dx: Serology7. Tx: oral doxycycline

a. Jarisch-Herxheimer reponse- you killed LOTS of cells atoncecytokine response

vi. Psittacosis1. Chlamydia psitacci2. From birds


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a. Parrots spit on you! Erm3. Aerosolized4. Very infectious5. Mono-like illness, fever, fatigue

a. Consolidation in lower lobe6. Dx: serology7. Tx: doxycyline

28.HIV Negative Opportunistic Infectionsa. Infections caused by loss:

i. Physical/mechanical barriers: staph, strep, pseudomonas, aspergillus, candidaii. Neutrophils: Extracellular bacteria (staph, strep, enterobacteraciae, pseudomonas),

a. Candida, aspergillusiii. Complement: encapsulated extracellular bacteria

1. N. meningitides, s.pneumoiv. T cells: intracellular bacteria, viruses, broader spectrum of fungi

1. Nocardia, legionella, mycobacteriav. B cells: enteroviruses, giardia, s.pneumo, h.flu, n.meningitidis, s.aureus

b. Immunosuppressioni. Congenitalii. Acquired

1. Cancer chemotherapy- neutropenia, mucositis2. Solid organ transplant- Cell mediated immunity3. Bone Marrow Transplantall lost

c. Cancer chemotherapyi. Neutropenia

1. Greatest risk of infection2. Sudden dropworse3. Longer durationworse4. Empiric treatment is very important

a. Pseudomonas, s.aureusb. Anaerobes (if a likely area)

d. Solid Organ Transplanti. Specific organ transplanted matters

1. Greatest risk: lung, heart-lung transplantsii. Long or demanding surgeriesmore risk

iii. Rejection of transplantmore immunosuppressionmore riskiv. 1stmonth post transplant

1. Increased risk of NOSOCOMIAL infectionsa. Long hospital stayb. Immunosuppressed

i. Candida, c. diff, catheter assosciated infections, etc2. Organ specific infections


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a. Ex: Kidney transplantUTIv. 1-6 Mo

1. T cell defectsa. Viruses: CMV, herpesvirusb. Bacteria: TBc. Fungi: endemic mycoses, aspergillusd. Protozoans: toxoplasmosis

vi. CMV1. Most common in transplants2. Highest risk with Donor Positive, Recipient Negative3. Early onset (3-6 mo post transplant)- pneumonitis4. Late onset (after that)- enteritis

e. Bone marrow/stem cell transplanti. Autologous: minimal immune suppressionii. Allogeneic:

1. VERY immune suppressed2. Long term3. Stages

a. Pre-engraftmenti. Risks:

1. Neutropenia2. Mucositis3. Central venous catheter

ii. Possible infections1. Staph, strep, ecoli, klebsiella, pseudomonas2. Aspergillus, candida3. Give cefapime. Or Vanc (if MRSA)

b. Early post-engraftmenti. B and T cell defectsii. Risks

1. Lymphopenia2. Hypogammaglobulinemia3. Central venous catheter

iii. Infections1. Viruses (CMV, HSV, EBV, etc)2. Bacteria (intracellular)3. Fungi (many, including aspergillus)

c. Late post engraftmenti. Risks

1. Minimal GVHD2. Chronic GVHD (organ failure, etc)

ii. Infections


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1. VZV2. Encapsulated community pathogens

a. Strep pneumo4. CMV: risk if donor negative, recipient positive

a. Nave immune system going into a CMV + body5. Aspergillus: Biphasic

a. First because of neutropeniab. Second because of B and T cell dysfunction

i. Donor matching helps29.Neonatal infections

a. In utero infectionsi. TORCHES

1. Toxoplasmosis2. Other (west nile virus, lymphangitic choriomenintitis, malaria)3. Rubella4. Cytomegalovirus-most common. Can lead to deafness5. HIV, Hepatitis, HSV (but usually intrapartem)6. Enteroviruses7. Syphilis

ii. Oh. And also, Chicken Pox, Lyme disease and Parvovirusb. Fever in a neonate:

i. Bacterial1. Order of frequency

a. Group B Strepb. E. coli (tied)c. Other gram negsd. Strep Pneumoe. N. Meningitis

2. 67% are UTI3. 2% are meningitis (dont miss this! LP all babies!)

a. There are no signsof this4. Most were gram negative5. Most were ampicillin resistant

a. Tx with ceftaxipime(3rdgen cephalosporin, gets into CSF)i. Plus ampicillinto cover Listeria

ii. Viral (MOST LIKELY)1. Varies with seasons

iii. Group B Strep1. Ascending infection.2. Screen moms from 35-37 weeks3. Low weight, premature, africanworse4. Early onset (w/in 7 days of birth)


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a. FAST onset. 6 hours of birth, theyre grunting and retractingb. Respiratory failure

5. Late onset (after 7 days)a. More insidiousb. Bone, joint infections, bacteremiac. 50% will have meningitis

iv. HSV1. Baby presented as floppy, with hepatitis2. Mom primary infection during pregnancy, lesions during deliveryworse3. Most are HSV24. Skin, eye, mucus membrane disease5. If treated with acyclovirgood prognosis, no longterm sequelae6. If untreatedbecomes disseminated. Often fatal.7. CNS: Encelphalitis, fever, lethargy, seizures

a. Most dont have rash8. Disseminated: Liver, lung, brain, skin, adrenals

a. Looks like bacterial sepsisb. Mortality 50-80%

9. Happens within first couple weeks of lifev. Enterovirus

1. Coxsackievirus A, B, enterovirus2. Peak in Summer, fall3. Virus from moms blood crosses placenta, disseminates in baby4. Hyper/hypothermia, poor feeding, irritability, flat, red rash5. Dx: stool culture6. Tx: ?7. Prevention: handwashing

vi. Hepatitis B virus1. Neonates who get it at birth become chronic carriers

a. Have a higher mortality2. We vaccinate now

30.Osteomyelitisa. Difficult for antibiotics to get to the siteb. 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

i. Bacteria causes inflammation1. Inflammation squeezes vascular

channelsischemianecrosissequestrum

2. inflammation strips the subperiosteum from boneperiostealelevationstimulates new bone formation


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ii. Sequestrum can extend out through skin and draine. Adhesion plays crucial role

i. S.aureus is most common bugii. Anything that can make biofilms(coag neg staph)

1. Antibiotics cant penetrate them2. Take out prosthesis.

f. Classificationi. Hematogenous

1. Kidsa. Symptoms

i. Pain on passive mvmtii. Inability to move limb

iii. May be warmiv. fever

b. Staph aureusi. Brodies abscess

1. Drain itc. Long bones

i. Capillary loop- stasisd. Neonates: can involve joint b/c of incompletely closed epiphysis

2. Vertebral in adultsa. Sx: back pain, maybe neuro signs (BAD)b. Discitis and two adjacent vertebraec. Usu in lumbar area, but can be anywhered. Gram pos: from skin, soft tissuee. Gram neg: from urinary tractf. 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. Contiguous1. Sx:

a. May have a draining sinusb. Persistent painc. Oft no fever

2. Trauma, surgerya. Usu staph aureus

3. Infected prosthesis, hardwarea. Esp coag negative staphb. Sx: loosened implant

4. Biofilms


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5. Rapidsequestral formationa. Chronic osteo

iii. Vascular insufficiency1. DM, neuropathy

a. Oft start as foot ulcersb. Osteo will HURT though (finally)c. Avoid ill-fitting shoes

2. Usually chronic3. Osteo if:

a. Persistent ulcer orb. Bone is exposed/can be probed

4. Polymicrobiala. Staph aureus, gram negatives, anaerobes.

iv. Other osteo1. Sickle cell: salmonella

a. Encapsulated bacteria (strep pneumo)i. b/c they have no spleen

2. Sneaker: pseudomonas3. Endemic mycoses: Histo, blasto,coccidio, TB

v. Dx1. 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 expensive4. Bone Biopsy- gold standard

a. Aerobic and anaerobic culturesb. dont bother culturing the sinus tract

vi. Tx:1. Acute:

a. IV antibiotics for 4-6 weeksb. Switch over to oral faster in kidsc. Surgery rarely necessary

2. Chronica. Much more difficultb. Culture wont help. Need a bone biopsy to find organismc. Surgeryto remove dead tissued. IV antibiotics for at LEAST 6 weeks

31.Tic-borne Diseasesa. Lyme Disease

i. Borrelia burgdorferi1. Spirochete2. Multiple plasmids

a. Some are linear (weird)


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3. Natural reservoir: white-footed mouseii. Vector: Ixodes scapularis

1. Mostly the nymph stage2. Must be attached 24 hours to transmit

a. B.burgdorferi multiplies in tick midgutb. Travels to saliva during the blood meal

iii. Transvarial transmission: noiv. Geography: MN, WI, northern CA

1. Not around here.v. Early manifestations

1. Erythema migransa. 6 cm in diameter, at the site of biteb. A week after the bite

2. Carditis, aseptic meningitis, bells palsyvi. Late manifestations

1. Arthritis- usu single kneea. Months after the bite

2. CNS- encephalitisa. 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 involvedviii. Tx: Doxycycline

b. Southern Tick Assosciated Rash Illness (STARI)i. Rash looks like Erythema Migransii. But its the lone star tick

c. Rocky Mountain Spotted Feveri. Caused by Rickettsia

1. Small gram negative bacilli2. Obligate intracellular3. Replicate freely in cytoplasm

ii. Assosciated with arthropodsiii. Happens mostly in summer, mostly in kidsiv. Geography: a belt across the central USv. Sx:

1. Incubation 2-14 days2. Early: fever, headache, myalgia, abdominal pain3. Rash: peripheral petechiae (nonblanching)

a. Can be on palms and solesb. Petechiae are areas of intense vasculitis

i. Can eventually cause shockvi. Tx: IMMEDIATE. Dont wait for tests.


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1. Tick exposure + rash = treat, and get labs2. Doxycycline, chloramphenicol

d. Ehrlichiosisi. Human Monocytic Ehrlichiosis- involves the monocyte line

1. Caused by Ehrlichia chafeensisii. Human Granulocytic Ehrlichiosis- involves neutrophils

1. Caused by Ehrlichia ewingiiiii. Ehrlichia

1. Intracellular- lives in phagosomesa. Replicates (forms a morula)

iv. Vectors: Lone star tick and I.scapularis (same as lyme disease)v. Common in

1. May, June2. Middle aged, elderly

vi. Sx: Fever, headache, myalgia1. Rash in about 1/3 of pts2. Low WBC, low platelets3. Cytoplasmic inclusions in neutrophils4. Severe: Meningitis, pneumonitis, hepatitis, disseminated intravascular

coagulation

vii. Dx: PCRviii. Tx: doxycycline

32.Risks to healthcareworkersa. N. Meningitidis

i. The only form of meningitis that shows person-to-person transmissionii. Droplet transmission

iii. Risk is small, but higher than in the general populationiv. Risk: unprotected exposure to respiratory secretions

1. Cough, intubation, CPRv. Anyone with evidence of bacterial meningitisdroplet precautions

vi. Post exposure prophylaxis1. HCW with a high risk exposure before pt was on antibiotics2. Household members3. Roommates4. Anyone who shared eating utensils5. Day care classmates6. Ciprofloxacin

b. Tuberculosisi. Pt goes on airborne isolationii. HCW post exposure assessment

1. TB skin test now,2. TB skin test in 8-10 weeks


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iii. No minimum infection time. Entering the room= exposureiv. High risk: pt is coughing, youre intubating, bronchoscopy, induced sputum

c. Body Substance Exposuresi. Happens mostly in residents in and house staffii. Happens mostly in OR

iii. Standard Precautions1. Gowns, gloves, masks, eyewear2. Wash hands after removing gloves3.

Microbes, bacteria

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