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Patho > Fungal and sepsis > Flashcards

Fungal and sepsis Flashcards

1
Q

Mycoses

A

Structure: Eukaryotes
Metabolism: aerobes
Environ: slightly acidic environment- soil, geographically endemic in areas
Reproduction: fungi of medical interest= asexually by forming conidia

Types of infections fungi:
Yeasts- single cells and asexual budding
Molds- hyphae and a mat (mycelium)

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2
Q

Epidemiology

A

many infxn goes undiagnosed
No public health surveillance for:
common fungal - ringworm or vaginal candidiasis
serious fungal- aspergillosis and cryptococcosis

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3
Q

Fungal morphology

A
  1. Blastoconidia and pseudohyphae- candida
  2. chlamydospores- candida
  3. arthrospores- coccidioides
  4. sporangia and sporangiospores- mucor
  5. microconidia- aspergillus
  6. microconidia and macroconidia- microsporum

familiar dont mem

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4
Q

fungi vs bacteria

A

fungi:
Eukaryotic
cellwall= chitin and Beta glucan- caspofungin target
sterols in cell membrane- amphotericin B and azole target
sexual and asexual spores
Organic carbon for metabolism

Bacteria:
Prokaryotic
cellwall= peptidoglycan
sterols absent
endospores for survival not repro
many dont require organic carbon

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5
Q

Pathogenesis

A
  1. low virulence- opportunists in immunocomprom
  2. Adherence- adhere and colonization and virulence
  3. Invasion- mechanical breaks in skin with enzymes, small size allows for penetration of airways, live and multiply w/in macrophages
  4. Dimorphism-change shape to more invasive form
  5. tissue injury/destruction- from inflammatory response of host
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6
Q

dimorphism in yeast

A

yeast<->pseudohyphae<-> hyphae

budding vs hyyphae

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7
Q

Immunity

A

1st line defense: skin, fatty acids in skin, hormonal environment
Innate immunity: Neutrophils, macrophages, PRRs/PAMPs, some live in macrophages until activated by cytokines from Th1 cells
Adaptive: T cell mediated is most important, deficiencies lead to systemic progressive dx in immunocomprom

summary:
intact barrier defenses stop
neut and macro do a good job killing
fungi escape by growing in macro
th1 cellular imm activat macrophages via cytokines to clear infxn
need Cell mediated response

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8
Q

Manifestations of fungal disease

A

3 kinds:
1. mycotic infxn- opportunistic
2. mycotoxicosis- ingested toxins
* Ergotism- grain contam by mold= Nvd seizures
* Alflatoxin- aspergillus contam grain and peanuts
3. Allergy- asthmatic rxn

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9
Q

classifying Mycotic infxn: consider the source

A

Acquisition:
Exogenous- airborne, cutaneous-> acquired from environ, inhaled conidia, injxn past skin
Endogenous- colonization or reactivation from latent-> normal flora- trauma, invasion of mucosa, imbalance of flora

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10
Q

classifying: Where is it

A
  • superficial: infxn limited to stratum corneum-> Black piedra, white piedra, pityriasis versicolor, tinea nigra
  • Cutaneous: corneum or deeper, integument, appendages, hair nail-> Dermatophytoses, Dermatomycoses
  • Subcutaneous: subcutaneous tissues-> Chromoblastomycosis, Mycetoma, Sporotrichosis
  • Deep: lungs, abdominal viscera, bones, CNS-> primary systemic or opportunistic systemic
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11
Q

classifying: how aggressive is it?

A

Type of virulence:
Primary: infection in immunologically normal host- higher virulence, access via respiratory tract, asym or mild
Opportunistic: requires some compromise of host defense- take advantage, invade via resp, gi tract, intravascular devices

SYSTEMIC MYCOSES: affect whole body, immunosuppression is common-> “overwhelming inoculum”

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12
Q

Systemic Mycoses due to Primary pathogens

A
  • inhalation of virulent spores
  • Geo regions significant
  • immunocomp increases risk for widespread infxn

EX:
1. Blastomycosis
2. Coccidioidomycosis
3. Cryptococcosis- opportunistic
4. Histoplasmosis- OHIO River Valley

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13
Q

Systemic mycoses Opportunistic pathogens

A
  1. Candida albicans- cadidiasis
  2. Aspergillus fumigatus- site of indwelling catheter

Others:
Pneumocystis jirovecii- pneumocystosis= lung colonizer, HIV CD4<200, SPORADIC DX IN IMMUNODEF NEONATES
Zygomycetes- transplant pts

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14
Q

Testing

A
  1. Direct examination- 10% KOH, H&E stains, Silver stains
  2. Culture- selective media to grow
  3. NAAT- dna probes
  4. Serology-> Direct ag detection= immunoassays or Antibody detection= serum abs
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15
Q

Dermatophytes: keratin eaters

ring worm

A
  1. Epidermophyton
  2. Trichophyton
  3. Microsporum

Transmission: Human contact
Sxs:
skin= erythema, induration, itching, sclaing
hair= itchy scalp and hair loss
nails= thickened and dislodged from nailbed

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16
Q

Tinea (Pityriasis) Versicolor

Malassezia furfur

A

component of skin microbiome
Affects: teens, ya, males over females
sxs: patches of hypo or hyperpigmentation on torso and upper arms
Wood’s lamp= yellow/orange fluorescence

not a dermatophyte

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17
Q

Wood’s lamp exam

A

Non specific
Most Trichophyton species= DONT FLUORO
Directions: skin should be clear w/out makeup, cream, deodorant, and not recently washed
Warm up lamp
darken surroundings
place 10-30 cm away from skin
painless and safe

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18
Q

Fluorescence pattern

Wood’s lamp

A

Tinea versicolor: yellowish or orange glow
Malassezia folliculitis: hair follicles bluish white
Tinea capitis: microsporum= blue green, trichophyton=dull blue to absent
Erythrasma: Corynebacteria- rash in skin folds = coral pink
Pseudomonas: hot tub folliculitis and wound infection= green
Acne: propionibacteria= orange red
Porphyria cutanea tarda= red-pink

know these

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19
Q

Sporotrichosis

Sporothrix schenckii

A

mold form lives on plants, yeast for is on human tissue
Subcutaneous mycosis
Rose gardener’s disease- pricked by thorn deposits fungi
DX: fungal cultures
SXS: skin lesion begins as painless papule wks to months after inoculation-> papule slowly enlarges and ulcerates-> firm nodules develop along lymphatic drainage

add picture

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20
Q

Candida

c. albicans MC

A

Opportunistic infxn
C. auris emerging multidrug resistant candida:
serious threat, severe infxns, spread in healthy facilities

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21
Q

Candidiasis

common in babies

A

Thrush and Friends
immunosuppression in adults and mc babies
white caseous chees like plaque, loosely adherent to mucosal surface

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22
Q

Candidiasis in areas the sun dont shine

A
  1. Vulvaginal candidiasis-> think curd lik discharge around period time
  2. intertrigo- skin folds/wet, erythema and tenderness w/ satellite lesions= diaper rash “beefy red” inflammation w/ satellite lesions
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23
Q

Erythrasma

looks like candida intertrigo

A

Not fungus= Corynebacteria
often sign of type 2 diabetes

add pictures

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24
Q

Aspergillus

A

4 presentations:
1. Aspergillus pneumonia- rapid progression, fever, cough, hemoptysis, resp failure
2. Disseminated aspergillosis- primary infxn immunocomp that dissem to any organ and cns
3. Allergic respiratory disease- spores potent allergens-> progressive inflammation
4. Aspergilloma- fungus balls form in lungs-> pulmonary scarring adn cavities from prior healed infxns

other manifest: range from dissem to direct invasion from site
cutaneous aspergillosis- skin
Aspergillus endophthalmitis- eye

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25
Q

Pneumocystis jirovecii pneumonia

A

“yeast like”- inhalation colonizer of human airway
low virulence-> can cause lethal pneumonia immunocompro
* seen in HIV and sporadic sick infants
* SXS gradual:
* fever, nonproductive cough, SOB esp DOE
* bilateral rales on exam
* cxr shows symmetric “ground glass” pattern from hila outward
* Hypoxia in 3-4 wks and death
* DX: cysts in BAL washings

26
Q

Cryptococcus neoformans

cryptococcosis

A

MC Life threatening invasive fungal disease
inhalation of pigeon bird droppings
C. neoformans-> in hiv pts
C. gattii-> less dx
Pulmonary infection:
* asymp
* pneumonia
* fever, cough, SOB, headache, night sweats

Extrapulmonary infxn: CNS-> meningitis or skin-> subcutaneous nodules
DX: serum cryptococcal ag

27
Q

Coccidioidomycosis

coccidioides immitis

A

Southwest US- inhale spores
immunocomp-> mild flu like, no need to tx
immunocompromised-> more severe pneumonia and disseminated dx
DX: skin test for CMI response
SYNDROME OF SEVERE PNEUMONIA + ERYTHEMA NODOSUM + ARTHRALGIAS= “VALLEY FEVER”

28
Q

Histoplasmosis

H. capsulatum

A

Endemic= OHIO/MISSISSIPPI RIVER VALEYS
Acute sympt= flu like sxs
Progressive pulmonary dx= resembles TB- SPUTUM, WT LOSS, NIGHT SWEATS, LUNG CAVITIES
Disseminated dx- immunocomp- painless ulcers on mucous membranes- involve CNS

29
Q

Blastomycosis

B. dermatitidis

A

east central and Great lakes region
landscapers and farmers high risk-> bc spores from moist soil
immunocomp->w/ collagen vascular dx high risk
sequelae
1. Asymp/mild sxs-> self limiting w/ mild fever and cough
2. Acute or chronic pneumonia
3. Exrapulmonary/dissem dx-> any organ->skin lesions mc

30
Q

Interface dermatitis (ID) reactions

A

pruritic, eczematous dermatitis- btwn epidermis and dermis away from actual starting place
MC causes: Dermatophyte (tinea) infxns of feet or stasis dermatitis
Not specific to fungi

31
Q

Sepsis and SIRS

A

1 cause of death from infxn

Focus on:
1. early recognition
2. timely assessment and follow up
3. prompt action and tx

Organ failure is the primary cause of mortality

32
Q

US sepsis figures

A

incidence increasing due to:
* increased awareness and tracking
* aging population
* immunosuppression
* antibiotic resistant infxn

33
Q

Mortality figures

sepsis

A

systemic inflammatory response syndrome (SIRS): up to 7% of mortality figures
lowest risk-> UTI source
HIghest risk-> GI, Lung, or unknown

34
Q

General themes and definition

sepsis

A

sepsis-> dysregulated host immune response to infection -> exists on a continuum
organ dysfunction- SOFA score-increased 2 or more points related to organ failure
Sepsis= dynamic state-> frequent reassessment for changes

35
Q

Continuum of sepsis

A
  1. Early sepsis-> infxn or bacteremia-> SOFA and NEWS
  2. Sepsis-> Life threatening organ dysfunction caused by dysreg host
  3. Septic shock- circulatory, cellular, and metabolic abnormalities
  4. MODS (multifunction organ dysfunction syndrome)- progressive organ dysfunction without homeostasis and intervention
36
Q

Pathophys of sepsis

A
  1. Binding of TLRs on surface of immune cells-> cascade signals
  2. increased transcription of inflamm mediators
  3. Proinflamm cyto incide direct cytopathic injury-> tissue injury
  4. Nitric oxide released-> vasodilation-> ischemia and shock
36
Q

Pathophys of sepsis

A
  1. Binding of TLRs on surface of immune cells-> cascade signals
  2. increased transcription of inflamm mediators
  3. Proinflamm cyto incide direct cytopathic injury-> tissue injury
  4. Nitric oxide released-> vasodilation-> ischemia and shock
37
Q

Clinical sigs of sepsis

A

Alterations in vitals:
* arterial hypotension-> systol 90, MAP <70, Temp >38.3 or <36, tachycardia >90 bpm or tachypnea>20 bpm
* Sigs of end organ perfusion
* Decreased cap refil/cyanosis/mottling, atlered mental status, obtundation, Ileus

38
Q

Lab values that point to sepsis

A
  • hyperglycemia- glucose>140
  • arterial hypoxemia
  • acute oliguria- urine output<0.5 ml/kg/hour
  • creatinine over .05
  • thrombocytopenia
  • hyperbilirubinema>4
  • hyperlactatemia-> sign of acidosis-> sign of organ hypperfusion
  • Procalcitonin high
39
Q

Procalcitonin (ProCT)

A

Calcitonin-from thyroid-> decreases Calcium by inhib clasts
Procalcitonin- not detectable in healthy individuals
Elevated plasma procalc-> occurs when tissue control of calcitonin breaks down and ProCT secreted
* bacterial sepsis triggers
* severe localized bacterial infxn
* major burns, severe trauma, acute multiorgan failure, major abdominal or cardiothoracic surgery
* medullary thyroid carcinoma

Viral: block TNFalpha blocking the release of procalc

40
Q

SOFA score

A

1.PaO2/FiO2 ratio- comparison btwn O2 level in blood and conc breathing
2.platelet count
3.bilirubin
4.hypotension
5.glasgow coma score
6.creatinine

41
Q

qSOFA

quick assessment to get a rough idea of prognosis

A
  1. tachypnia- greater than 22 RR
  2. Altered mental status- GCS 15 or less
  3. Hypotension- sbp less than 100

one point each:
0-1= not high risk
2-3= high risk

42
Q

Risk factors of sepsis

A

1= Pneumonia cause of sepsis

icu admission
recent hospitalization- pt tx with antibiotic
bacteremia
extremes of age
immunosuppression- diabetes, HIV
Malignancy
CAP
inappropriate antibiotic use especially broad spectrum
genetic factors/innate immuno factors
Covid 19
maternal/perinatal period
trauma/burns

43
Q

Nosocomial infection

A

RF: debillitated condition of pts, colonization of environ
inpatient sepsis-> from skin contaminants with UTIS, CENTRAL LINES, MECHANICAL VENTILATION/PNEUMONIA
G+ organisms increasing

follow protocols for indwelling devices:
1. CLABSI- central lines replaced no more fre than every 4 days but no longer than 7
2. CAUTI-urinary catheter should be 3-8 days

cauti- catheter assoc uti
Clabsi- central line assoc bloodstream infxn

44
Q

Sources of infection

sepsis

A

Cardiovascular- Endocarditis, myocarditis, injxn drug use
HEENT- sore throat/pharyngitis
LUNGS- CF
SKIN- hospitalized pts

45
Q

Common bacteria imp in sepsis

A

-
1. E. coli- uti and prostatitis
2. Klebsiella pneumoniae- uti pneumonia
3. enterobacter species- uti
4. pseudomonas aeruginosa- infected burns/pneumonia in CF/ ALL pts/diabetes- highest mortality rate
5. Proteus mirabilis- utis
6. bacteroides fragilis- peritoneal infxn
+
1.streptococcus pneumoniae- pneumonia and meningitis-> MC cause of pneumonia and meningitis in adults
2.streptococcus pyogenes- skin and soft tissue infection-> super antigen
3.staphylococcus aureus- skin and soft tissue infection-> superantigen
4.enterococcus species- utis

46
Q

Systemic inflammatory response syndrome

SIRS

A

INFXN - common cause
RF:
* extensive trauma, hemorrhage, burns
* thromboembolism (PE)
* anaphylaxis
* MI/CABG/surgery
* autoimmune
* addison’s disease

all trigger dysregulated inflamm response

DOES NOT MEAN THERE IS AN INFECTION

47
Q

Clinical signs of SIRS

A

need 2 or more:
1. temp >38 or <36
2. heart rate >90 bpm
3. respiratory rate >20 bbp
4. WBC >12K

48
Q

Problems with SIRS criteria

A

emphasis on inflamm ocmponents without considering dysregulation-> many sxs are adaptive (fever, tach, wbcs)

sepsis definition: life threatening organ dysfunction caused by dysregulated response to infection (maladaptive)

TOO LOOSE

49
Q

Sepsis- maladaption

A

Sepsis is a coagulation trigger-> release pro inflamm cytokines
increases PA-1: plasminogen activator

49
Q

Sepsis- maladaption

A

Sepsis is a coagulation trigger-> release pro inflamm cytokines
increases PA-1: plasminogen activator

50
Q

Disseminated intravascular coagulation (DIC)

ALL PURPLE

A
  1. release of tissue factor is critical-> bleeding more likely in acute DIC, thrombosis in CHRONIC
  2. Clotting factors rapidly consumed

2ndary to:
* infection
* extensive trauma
* malignancies
* OB complications

difficult to recognize until late stages

consumptive of clotting factors lead to excessive bleeding-> shock, hypotension, increased vascular permeability
excessive clotting- ischemia, impaired organ perfusion, end organ damage

51
Q

Signs and symptoms of DIC

A
  1. Clotting:PE, DVT, MI, renal failure, ischemic stroke
  2. Bleeding: petechiae, blood oozing, accumulation of blood in serous vacities, hematuria, hemorrhagic stroke
52
Q

Septic shock

A
  • Circulatory, cellular, and metabolic abnormalities assoc w/ greater risk of mortality than with sepsis alone

Clinically:
* vasopressor requirement to maintain MAP greater than 65
* lactate level higher than 2 in abscence of hypovolemia

Hospital mortality rates over 40%
sock and hypoxemia may result in transient tranaminitis

53
Q

Surviving sepsis

A

1 hour bundle:
1. measure lactate
2. obtain blood culture b4 ab
3. administer broad spec ab
4. rapid administration of cystalloid for hypotension
5. apply vasopressors if hypotensive

54
Q

Pediatric causes and tx

sepsis

A

Neonatal up to 3 months:
Group B strep
E. coli

55
Q

further workup and tx

A
  • fluids- crystalloids- maintain BP
  • pressors- norepinephrine to maintain BP
  • steroids-when fluids and pressors are insuff exept in peds
  • albumin- controversial
56
Q

effects of Norepinephrine

A

BO= COxPR
vasoconstriction
increased renin
increased chronotropic and ionotropic effects

57
Q

Blood related products and glucose

PR

A

PRBC for HB<7
Platelets <10,000
Enoxaparin if dvt considered

glucose:
insulin for BG>180
monitor frequently to ensure stability

58
Q

Prevention of sepsis

A
  • remove foreign bodies, drain abscesses, remove infected tissues
  • use ab prophylactic in pts with liquid tumors
  • topical agents prophylactic in burn pt
  • indwelling catheters should be properly cared for and frequently examined for the possibility of infection

Patho (4 decks)

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