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Micro Flashcards

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USMLE® Step 1 flashcards
1
Q

Classification systems for respiratory infections:

A

Site of infections:

  1. upper respiratory tract (URT)
    - Rhinitis/ rhinosinusitis
    - sinusitis
    - otitis media
    - epiglottis
    - pharyngitis/Tonsilitis
  2. Lower respiratory:
    - Laryngotracheitis
    - Bronchitis
    - Bronchiolitis
    - Pneumonia/ Pneumonitis
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2
Q

Etiology of respiratory tract infections.

A
  1. Strict pathogen :
    exogenous transmission cause primary infection such as virus
  2. Opportunistic pathogen:
    Endogenous microbes cause secondary infection.
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3
Q

High risk gorups increased risk for severity of primary infections?

A
  • Pre existing lung disease like asthma , copd, cystic fibrosis
  • smokers
  • immuno-compromised
    -age (under 5 yrs, over 60)
  • Environmental risk like hospitalization, travel, seasonal
    etc
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4
Q

Individuals with……………………………. are at high risk of primary and seconary infections.

A

pre-existing lung conditions or intubation

  • scar tissue &damaged cilia - binding site for opportunists!!
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5
Q

How’s like innate host response to viral infection?

A

Interferon alpha and beta play a major role initially controlling viral infection,specificially inhibitng translation.

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6
Q

Interferon alpha and beta creates…….

A

non-specific febrile disease like flu-like symptoms are result of type I interferons and t cell proliferation.

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7
Q

How’s like adaptive host response to viral infection?

A 
CD8+ CTL (cytotoxic lymphocytes) detects viral peptides in context of MHC class I and directly kill virus infected cells. 
CTL are able to kill virus infected cells by release of granzymes and perforin with assistance from CD4+T helper cells.
  • CTL destruction of host cells cause collateral damage = symptoms
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8
Q

Common cold virus

A

Rhinovirus,
Coronavirus
Adenovirus

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9
Q

Rhinovirus … what season?

A

summer

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10
Q

Coronavirus…. what season?

A

winter

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11
Q

Adenovirus

A

all season

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12
Q

naked virus — envrionmental surface infection meaning formite mediated transmission and survival in droplet. Which are?

A

Rhinovirus, adenovirus

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13
Q

Rhinovirus is…..

A

Non-enveloped ss+RNA., icosahedral virus
labile at acidic PH meaning degradation in GI tract.
Family: Picornaviridae

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14
Q

Epidemiology of rhinovirus?

A

Transmission is via aerosol, direct contact and indirect contact like nose to hand, hand to hand

  • Most common
  • immunity is transient due to antigenic drift
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15
Q

Pathogenesis of rhinovirus?

A

VAP binds to host receptor ICAM-1 on respiratory epithelium of nares, oropharynx, throat.
- viral replication via ss(+)RNA genome to SS- RNA template via rna dependent rna polymerase. Viral replication triggers interferons, histamine and bradykinin, Replication is preferential to nose at 33 ‘C

  • Contribution of host immune response like interferon alpha natural killer cells and cytotoxic lymphocytes

Infection is transient, self resolving and symptoms are primarily caused by immune response.

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16
Q

Key point of pathogenesis of rhinovirus

A

IFN/ Bradykinin, bradykinin, histamine released leading to swelling, redness.
Interferon cause fever whereas histamine cause allergic symptoms.
- After reaction of immune response, around 3-7 days we have IGA antibody. = resolution of infection

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17
Q

Clinical feature of rhnovirus?

A 
- Onset 12-14 hrs. Resolution 7 days
Watery eyes
- nasal congestion
-runny nose
- sneezing
- scratchy/ sore throat
- dry cough 
- fever
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18
Q

What is coronavirus?

A
  • Family: Coronaviruidae
  • linear, ss +RNA
  • enveloped
  • largest positive strand RNA viruses
  • 2nd most common cause common cold
  • peaks in winter
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19
Q

What is adenovirus?

A
  • Family: adenoviridae
  • linear, ds DNA
  • non-enveloped
  • naked capsid has fiber with penton base (viral attachment protein)
  • Immunity is transient (too many serotypes meaning variation)
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20
Q

Features of adenovirus?

A
  • Endemic throughout the year
  • Affects all age, typically affects children from infancy to school age
  • highly infectious
  • military recruits
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21
Q

Prevention of adenovirus….

LIVE oral vaccine against ……………

A

type 4&7 for military

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22
Q

Epidemiology of adenovirus.

A
  • pharygngo-conjuctival fever
  • mild URTI - 3rd most common
  • Interstitial pneumonia / ARDS
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23
Q

Pathogenesis of Adenovirus?

A
  • fibers protein attaches to CAR(Coxsackie- adenovirus receptor)
  • penton base has cytolytic toxic activity
  • Cell rounding, enlargement, intra-nuclear inclusion.
    Intra-nuclear inclusion is feature of dna virus
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24
Q

Clinical features of adenovirus: of pharyngo- conjunctivitis

A
  • pink eyes
  • onset 3-5 days
  • resolution 10 days
  • low grade fever
  • swollen cervical lymph node
  • sore throat
  • itchy red eyes, often with clear discharge
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25
Q

Outcome and Prevention for viral URTI

A

-No vaccine for rhnovirus, and common coronavirus
- usually mild and self limiting illness
-severe complication not common (less than 10% secondary bacterial)
- Live vaccine for adeno (military)
- hand washing, hand sanitizer
- emphasize other environmental measures to control infection: avoiding finger to eye, finger to nose
mask wearing
social distancing

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26
Q

Epidemiology of sinusitis & otitis media:

A
  • Both are common secondary infection following viral rhinitis
  • Bacteria are common to oropharynx especially children and eldely, transient transmission by respiratory droplet. Think of it as trigger
  • viral rhinitis increases inflammation triggering release of endogenous bacteria
  • Children under 4 years will develop acute otitis media
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27
Q

What are the bacterial agents are common endogenous colonizers of nasal cavity and oropharyns, in persistent biofilm form?

A
  • Streptoccous Pneumoniae
  • Haemophilus influenzae
  • Moraxella catarrhalis
    Chronic: staph aureus
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28
Q

What is streptococcus pneumoniae?

A
  • Gram positive diplococcus
  • Polysaccharide capsule
  • a- hemolytic on blood agar
  • optochin sensitive
  • bile soluble
  • positive quellung reaction : detect capsule
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29
Q

Prevention of S.pneumoniae?

A
  1. Pneumococcal polysaccharide vaccine - inactivated vaccine
    - purified capsular antigen of 23 serotypes
    - adults 65 years or order
    - Pneumovax 23
  2. Pneumococcal conjugate vaccine
    - prevnar 13
    - children younger than 2 and adults
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30
Q

Pathogenesis of S>pneumoniae.

A

1 Initial infection: S.pneumoniae colonize epithelium of orpharynx and secrete IgA protease.
- persist asymptomatically in healthy host as biofilm
2. Virulence activation:
primary viral infection triggers inflammation.
- immunological stress disrupts biofilm, inducing release of pneumolysin (cytotoxin)
3. Contribution of host immune response
- resident macrophages recognize GPC with TLR2, releasing TNFa and IL-8. neutrophils are recruited.
- bacteria escape phagocytosis by capsule and can migrate to sinuses, eustachian tubes, inner ear, bronchi, alveolar sac, blood, meninges

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31
Q

Biofilm function

A

Bacteria bind to respiratory epithelium and establish a biofilm on respiratory epithelial cells, contributing to persistent colonization.
- Chronic biofilm is a risk factor for exacerbation in high risk patients esp. COPD.

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32
Q

Function of IgA protease

A

Bacteria secrete an Ig A protease to cleave mucosal IgA, contributing to persistent mucosal colonization.

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33
Q

function of pneumolysin?

A

When induced by immunological stress aka viral infection, bacteria secrete an Pneumolysin (exotoxin) which causes localized host cellular damage.
- cytotoxic for respiratory epithelial and endothelial cells.

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34
Q

S. Pneumoniae pathogenesis: Capsule

A
  • capsule protects bacteria from phagocytes recognition via complement opsonization
  • T independent B1 cells of spleen play important role to generate anti-Capsule IgM to activate complement for bloodstream infection.

SO, Asplenia is a major risk factor for bacteremia, sepsis, and meningitis with encapsulated bacteria.

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35
Q

Clinical features of sinusitis:

A 
VIral UTRI <7 days
Bacterial URTI > 7
- fever
- nasal stuffiness and thick discharge
- bad breadth or loss of smell
-fatigue, headache
- postnasal drip
- sore throat
- viral = thin, clear discharge
where as bacteria has thick, yellow discharge
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36
Q

Clinical features of acute otitis media?

A
  • fever
  • neonates: irritability, feeding difficulties
  • ear pain, and or ear tugging.
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37
Q

Clinical features of chronic otitis media?

A
  • infection persist for more than 3 weeks
  • ear pain
  • hearing loss
  • Air /fluid accumulation
    MRSA is the most common cause
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38
Q

What is Haemophilus influenzae?

A
  • Gram negative coccobacilli/ pleomorphic
  • Non-typeable : non-encapsulated: normal component of Upper RT flora. Associated with sinusitis, otitis media, bronchopneumonia
  • Typeable: capsule
    Haemophilus influenzae type b (Hib)
  • capsule composed of Polyribosyl- ribitol phosphate PRP
    Prevention: Hib- PRP conjugated vaccine
    Associated with epiglottis, sepsis, meningitis
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39
Q

Haemophilus influenzae does not grow?

A

on blood agar whereas it grows on chocolate agar

- requires NAD &Hemin for growth

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40
Q

Pathogenesis of haophilus influenzae:

A
  • Pili
  • non-pilus adhesin
  • biofilm
  • IgA protease
  • LOS: has endotoxic lipid A activity;; endotoxin .. recognized by macrophages and recruits of neutrophils- pus

HiB only, has capsule

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41
Q

Clinical presentation: epiglottis encapsulated Hib ONLY

A
  • neck hyperextended, trunk forward(tripod) , enlarged epiglottis: Thumb sign
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42
Q

What is moraxella catarrhalis?

A
  • gram negative diplococcus
  • oxidase positive,
  • colonize URT, particularly Children
  • associated with sinusitis, otitis media, bronchopneumonia
  • no capsule
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43
Q

Moraxella catarrhalis colony on

A

blood Chocolate agar solid colonies that can be pushed like hockey puck
gamma haemolysis

Haemo : no growth on blood agar
Strep . pneumo: alpha

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44
Q

Pathogenesis of moraxella catarrhalis:

A
  • biofilm

- LOS: induction of inflammation

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45
Q

Bacterial URTI: Outcome and prevention

A
  • Often requires antibiotics fully resolve
  • complication: tympanic perforation, chronic sinusistis, deafness abscess formation, penumonia , exacerbation of COPD.
  • pneumococcal, Hib vaccines esp, infants and high risk
  • antibiotic resistance is becoming more common.
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46
Q

What is Mumps?

A
  • Paramyxoviridae family
  • Enveloped ss_ RNA virion
  • One serotype, endemic
  • Aerosol transmission
  • infection from crowded condition
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47
Q

What are the clinical presentation of mumps parotitis?

A
  • Low grade fever, malaise, myalgia, headache, and anorexia.
  • Parotitis may be unilateral or bilateral
  • swelling of parotid and tenderness
  • difficulty eating, swallowing, talking
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48
Q

What are the complication and prevention for mumps?

A
  • Orchitis- most common complication after parotitis.
    = inflammation of one or both testicles
  • meningoencephalitis = inflammation of the the meninges (covering of the CNS) and inflammation of the brain tissues respectively.
  • Most patients experience complete recovery with no long term effects
  • Prevention : MMR/ MMRV vaccine
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49
Q

What is pharyngitis?

A
  • inflammation of the pharygeal tissues, and tonsils usually associated with pain.
  • ## characterized by triad of - sore throat, fever, pharyngeal inflammation such as edema, ertythema
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50
Q

Difference between viral pharyngitis and bacteria pharyngitis?

A 
* Viral pharyngitis: 
Gradual onset
low grade fever
Less erythema and swelling of the pharynx 
Discrete ulcerative lesion
Tonsils generally not involved
  • Conjunctivitis, coryza, cough may be present.
  • an acute inflammatory contagious disease involving the upper respiratory tract = coryza
  • Bacterial pharyngitis:
    Acute onset
    Sore throat, fever
    nausea, vomiting and headache
    erythematous posterior pharynx and palatine tonsils
    tender cervical lymphadenopathy
    white or yellow exudate in tonsillar crypts
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51
Q

What is S. pyogenes?

A
  • gram positive cocci
  • B hemolytic
    -Lancefield group A
    -PYR positive
    -Bacitratin sensitive
    -
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52
Q

Epidemioloy of S.pyogens?

A

Estimated to cause over 500 million cases of pharyngitis worldwide yearly

  • most common cause of bacterial pharyngitis
  • Humans are the primary reservoir: skin and throat
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53
Q

Clinical presentation of pharyngitis?

A
  • Develops 2-4 days after exposure
  • abrupt onset of fever, sore throat, malaise, headahe, dysphagia
  • erythematous posterior pharynx and palatine tonsils
  • tender cervical lymphadenopathy
  • palatal petechiae
  • tonsils may have white or yellow exudate
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54
Q

What is clinical features of scarlet fever?

A
  • fever, headahce, sore throat, nausea, vomiting, and malaie
  • diffuse, sandpaper- like rash, develops, initially on trunk and groin then spreads to face.
  • accentuation of the rash in flexor creases
  • Initially a thick, white coat and swollen papillae seen on tongue (white strawberry tongue)
  • White coating desquamates leading to red strawberry tongue appearance.
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55
Q

Chronic tonsillitis &peritonsillar abscess

A
  • Complication if initial infection is untreated , potentially due to drug resistance or carrier state
  • Polymicrobial infection : Group A strep
    Staph aureus
    gram negative anaerobic rods
    -
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56
Q

clinical features of peritonsillar abscess?

A
  • Fever, dysphagia,
    Severe throat pain
    hot potato. muffed voice=obstructive voice
    Trismus= restriction of motion of jaw
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57
Q

Pharyngitis leading to

A

acute rheumatic fever.

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58
Q

What are the clinical features of acute rheumatic fever?

A 
Fever, polyarthralgia
caroditis
polyarthralgia=
Erythema marginatum 
susbcutaneous nodu
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59
Q

Diagnosis of acute rheumatic fever:

A
  • evidence of preceding GABHS infection

- clinical criteria like carditis, chorea like irregular movement, erythema marginatum, subcutaneous nodules, arthritis.

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60
Q

Pharyngitis leading to

A 
PSGN..... post strep gramerulnephritis. 
- acute nephritic syndrome
- hematuria
gross hematuria
- edema : protein loss
- hypertension: water retention
type III hypersensitivity.
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61
Q

What is corynebacterium diphtheridae?

A
  • Genus: Corynebacterium
  • Gram positive rods
  • Non- motile, non spore forming
  • aerobic
  • club shaped plemorphic
  • Only strains harboring phage- encoded toxin can cause disease.
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62
Q

Epidemiology of C. Diphtheriade?

A
  • immunization rates are high
  • humans are the primary reservoir
  • trasmitted by droplet spread, direct contact
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63
Q

Pathogenesis of C.diphtheriade?

A
  • organism is non invasive disase is due to local and systemic effects of the toxin
  • Virulence factor= diphtheria toxin
  • genes for toxin acquired via lysogenic conversion -bacteriophage
  • DT is an A-Btoxin that acts in the cytoplasm to inhibit protein synthesis irreversibly
  • causing the necrosis and inflammation, forming an adherent , leathery pseudomembrane.
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64
Q

continued of pathogenesis of C.diphtheriade

A
  • Binding mediated by the B subunit
    -A subunit moves into cytosol and goes to its target,elongatio factor 2
    A subunit inactivates EF-2 by ADP ribosylation - shuts off protein synthesis - cell death.
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65
Q

Clinical presentation of c diphtheriade?

A
  • Usually manifests as pharyngitis or tonsillitis
  • malasise, sore throat and fever
  • extensive lymphadenopathy bull neck
  • Complication: carditis, nerve damage
  • intact pseudomembrane on palate, tonsils or pharynx
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66
Q

complication and prevention for C.diphtheriae

A
  • Complication due to systemic effects of toxin
    myocarditis and nerve damage
  • prevention: Dtap vaccine(Td or tdap)
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67
Q

Tinsdale agar

- Elek test

A

C. Diphtheriade

  • agar contains L-cysteine and sodium thiosulfate that are H2S indicators.
  • Potassium tellurite is selective agent
  • Elek test is functional assay to determine if clinical isolate has phage and is secreting toxin.
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68
Q

What are the examples of Lower respiratory?

A
  • Laryngotracheitis
  • bronchitis
  • bronchiolitis
  • pneumonia/ pneumonitis
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69
Q

What is Bordetella perussis?

A
  • gram negative coccobacillus
  • Regan lowe, Bordet- Genou agar
  • Charcoal blood agar , samples acquired from ciliated nasal epithelium
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70
Q

Epidemiology &prevention for B.pertussis?

A
  • very contagious
  • Neonates &unvaccinated children less than 5 yrs of age
  • asymptomatic carriers
  • acellular pertussis DTAP/Tdap vaccine
  • Recommended for infants
  • tdap booster strongly recommended for pregnant woman to prevent transmission from mom to neonate
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71
Q

Pathogenesis of B. pertussis?

A
  • Filamentous hemagglutinin , pertactin, fimbraiae facilitate right binding to ciliated epithelium of nose, trachea, bronchi.
  • Colonization impairs ciliary function
  • Bacteria secrete Tracheal cytotoxin and pertussis adenylyl cyclase toxin (alters GCPR signaling pathways)
  • Cilia damage contributes to necrosis
  • Leukocytes fail to migrate to infected tissue(leukocytosis)
  • Excessive mucus production contribute to cough severity
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72
Q

Pertussis toxin.

A
  • A-B type exotoxin, inactivates a subunit GCPR via ADP ribosylation
  • inhibits immune signaling and chemotaxiss

Adenylyl Cyclase Toxin: Increases cAMP levels of respiratory epithelium
- contributes to immune cell dysregulation and increased mucus production

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73
Q

Clinical features of B. pertussis: whooping cough aka trachebronchitis.

A
  • stage 1:Catarrhal
    : Common cold/ rhinopharyngitits
    -Stage 2: partoxysmal : Sore throat, intense coughing, epsides followed by a whoop, productive clear sputum , predominant lymphocytosis
    Stage 3: Convalescence: Residual cough.

Cough >14 days

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74
Q
  • Paramyxoviridae family biology:
A
  • Enveloped negative ssRNA genome
    -PIV: Parainfluenza virus
  • Respiratory syncytia Virus: RSV
  • Human MEtapnemovirus (HMV)
    , - measels virus
    Mumps virus
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75
Q

Parainfluenza PIV epidemiology:

A
  • 4 serotypes
  • children <5 yrs old
  • predisposing factors: Asthma, vitamin A deficiency, lack of breastfeeding, Environmental smoke or toxin
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76
Q

EPidemiology of parainlfuenza

A

CROUP (Laryngeotracheobronchitits)

77
Q

Pathogenesis of PIV:

A
  • HN on virion acts as VAP; binding to host receptor sialic acid on respiratory epithelial cells
  • Fusion F protein has a hydrophobic fusion pepetide which is exposed after VAP attaches
  • F protein inserts into host membrane, triggering fusion of virion and target cell lipid bilayer membranes.
78
Q

pathogenesis of PIV

A
  • Viral replication leads to surface expression of F protein , leading to fusion to new cells aka : Syncytium formation.
  • Viral replication, syncytia and host response trigger inflammation for lining laryns, trachea, and bronchi
79
Q

Clinical features of PIV:

A 
Croup: Laryngo tracheo bronchitits
- inspiratory stridor : whistle
Subglottic narrowing of the treachea: steeple sign
- Barking cough 
- hoarseness
80
Q

RSV epidemiology:

A
  • leading cause of LRTIs in infants and young children

- infans <6 months or premature birth (<35 weeks)

81
Q

Pathogenesis of RSV:

A

G protein mediate attachment; F protein mediates fusion
- virion directly invade the respiratory epithelium, leading to syncytia formation, which is followed by immnologically- mediated cell injury

  • necrosis of the bronchi and bronchioles leads to the formation of plugs of mucus, fibrin, and necrotic material within smaller airways.
  • infection can progress to alveolar sacs or trigger bacterial secondary super infections
82
Q

RSV ;

A

necrosis, inflammation and syncytial giant cell formation!!

83
Q

Clinical presentation of RSV:

A
  • Bronchiolitis- interstitial pneumonia
  • respiratory distress(RR, retraction and wheezing)
  • atelectasis
  • hypoxia, cyanosis

Chest radiograph : of an infant with a severe case of Respiratory syncytial virus penumonia and bronchiolitis .

84
Q

Human metapneumovirus HMPV and RSV

A

Family: Paramyxoviridae

- confirmatory differential diagnosis requires RT- PCR

85
Q

Bronchitis: outcome and prevention

A
  • 90% bronchitis is viral and does not require antibiotics
  • antibiotics for whooping cough will shorten the course
  • complication include interstital pneumonia (especially infants) exacerbation of asthma and COPD, bronchiectasis, rib frature

Prevention and patient education:
- TDAP/Tdap vaccines, esp for infants and pregnant women

86
Q

Pneumonia classification:

  • typical
  • atypical
A

Typical: gram positive and gram negative bacteria
Atypical: viruses, atypical bacteria, fungi, parasites

Exposure:

  • community acquired pneumonia: no recent hospitalization
  • nosocomial: Hospital acquired pneumonia:>48 hrs post- admission
  • ventilator associated Pneumonia: >48 hrs intubation
  • Pathology:
  • broncho-pneumonia/ lobar: typical pneumonia with focal densities (alveolar sac or multipic alveolar sacs called lobar) CONSOLIDATION
  • Interstital: atypical pneumonia with diffuse, hazy infiltrates (viral , atypical )
  • if infection looks so bad- necrosis
87
Q

Covid 19

A

actute (less than one month)
, community acquired,
interstital (hazy infiltrate)
viral tested by Rt-pcr

88
Q

What is Sars- COv2?

A

Enveloped ss +RNA virus

  • spike protein = vaccine
  • RDRP-antivirals

Diagnosis: Rapid antigen elisa, lateral flow

Rt- PCR,
Serology-

89
Q

Epidemiology and transmission of Covid 19

A
  • aerosol droplet, airborne
  • high risk populations for severe disease
  • unvaccinated 97x risk of death
  • elderly, hypertension, obesity, diabetes
  • prevention: moderna, fpfizer: mrna subunit vaccines encoing spike protein

-

90
Q

Epidemiology : shift versus drift

A
  1. Drift: gradual accumulation of random point mutation

2. Shift: sudden phenotypic change of virus from gene rearrangement with co-infection with 2 strains.

91
Q

pathogenesis of SARS- COV2

A
  1. Spike protein binds to ACE2 host receptor on epithelial cells of URT and LRT and or GI tract
  2. Virus downregulates interferon - alpha
    viral replicates in interstitial tissue, syncytia formation
    virions spread systemically replicating in CD4+ T cells, cardiac, hepatic, renal tissue.
  3. Inflammatory dysregulation and cytokine storm - causing inflammation
    - alterationn of renin- antiotension signaling activates bradykinin.
    Vascular damage accumulates on major organs.

detrimental causing inflammation, if it gets to lung ,oxygen exchange problem.

92
Q

clinical presentation : covid 19

A
  1. Non- specific URTI symptoms. , loss smell(anosmia), loss of taste( ageusia)
  2. Interstitial pneumonia progressing to acute respiratory distress syndrome ARDS is most common cause of mortality.
  3. if it gets into blood, immune- mediated inflammation can cause multi organ tissue damage
93
Q

imaging for covid -19,

A

ground glass opacities are most common.

consolidation can be observed.

94
Q

Complication for covid-19

A
  1. intersittial pneumonia- ARDS- death
  2. Secondary bacterial pneumonia superinfection
  3. long COVID
95
Q

What is influenza?

A
  1. Orthomyxoviridae
    - enveloped segmented ss negative RNA
    - Hamagglutinin glycoprotein (HA)= viral attachment protein
    - Neuraminidase (NA ) surface enzyme- release of new virions by sialic acid cleavage

Three types :A,B , and C
- based on Matrix (M-protein) and nucleoprotein

Rapid antigen test can determine type A/B

96
Q

Biology for inlfuenza:

A
  1. HA- attachment
    Hemagluttanin binds to the sialic acid. (restricted to respiratory tract)- it doesn’t fusion so no syncytia
  2. NA- release neuraminidase cuts sialic acid.
    M2- uncoating
97
Q

Epidemiology &transmission for influenza:

A
  1. Three types:A,B,C
    Type A: Zoonotic:
    More pathogenic than B and C
    Reservoir: humans, birds, swine, horses, seals
    - Antigenic shift : causes pandemic (Swine flue)
    - Antigen drift: cause localized annual epidemic

Type B, and Type C : are human restricted cause milder symptoms and undergo antigenic drift only!!

Transmission : aerosol droplet - human to human, animal to human.

98
Q

Influenza type A H1N1 is

A

has tropism for humans, pigs, horses, and ducks.

99
Q

Influenza shift epidemiology:

A
  • Flu pandemic are result of cross species shift events.

- The global swine flu pandemic in 2009 resulted from genetic reassortment.

100
Q

prevention for influenza virus

A
  1. prevention annual drift necessitates yearly booster
    - Live, attenuated nasal spray: Induces strong IgA response. Recommended for > 2yrs , <50 yrs
  • Killed, inactivated shot : induces IgG response
  • recommended for health are worker, Age extreems, immunocompromised.
101
Q

Pathogenesis of influenza virus

A
  • Influenza HA targets sialic acid on mucus secreting, ciliated cells and replicates in respiratory tract
  • Infection in lower respiratory tract leads to cytokine storm and desquamatin of bronchial epithelium cells
  • virus infection facilitates primary viral pneumonia and onset of secondary bacterial infection
102
Q

Clinical features: the flu

A

Preceded by or with a cold

  • dry sputum cough
  • dyspnea
  • high fever
  • intense muscle pain
103
Q

Complication of influenza:

A

” Secondary bacterial superinfections including sinusitis, otitis media(children), typial bacterial pneunmenia(elderly) - most common

104
Q

Complication of COvid-19 and flu

A

Covid -19: ARDS, sepsis, multi-organ damage
Flu: post- flu bacterial pneumonia, ARDS
Approximately 1/3 COVID-19 patients experience symptoms for months

  • Annual influenza vaccines(attenuated spray, killed shot)
  • SARS- COV2 subunit vaccines
105
Q

What are the typical pneumonia: risk factors ?

A

underlying lung disease or compromised muco-ciliary function - risk of bronchopneumonia especially smokers, COPD/CF, alcoholics, ventilation.

  • preceding viral infection (trigger)- risk of secondary superinfection.
  • Suppressed immune system - risk of bacteremia and meningitis with encapsulated bacteria esp. asplenia
  • Risk of sepsis with S.pneumoniae is 500x higher in children with sickle cell compared to healthy children.
106
Q

Typical pneumonia: gram positive and gram negative

A
  • Streptococcus pneumoniae is most common for community- acquired
  • Drug resistant gram-negative baclli are common for hospital acquired.
107
Q

Bacteria pneumonia distinguished into

A
  1. Bacterial typical pneumonia

2. Bacteria atypical pneumonia

108
Q

What are the bacteria are in bacteria typical pneumonia?

A
  1. community acquired: Strep pneumoniae - gram positive diplococci, alpha, quelling, optochin positive
    - Haemophilus influenzae (gram negative coccibacillli)
    - Moraxella catarrhalis- gram negative cocci, oxidase
    - Klebsiella pneumoniae- gram negative bacillus
  2. Hospital acquired- staph aureus MRSA - gram positive cocci , catalase +, beta
    - Klebsiella pneumoniae- gram negative bacillus, lactose fermenter
    - Pseudomonas aeruginosa- gram negative bacillus, lactose non-fermenter
109
Q

What is Klebsiella pneumoniae?

A
  • Family: Enterobacteriaeceae
    gram negative bacillus, prominent capsule
  • lactose fermenter (macconkey agar- big capsule)
    In the sputum sample: gram negative with capsule
  • capsule bacteria can lead to sepsis
110
Q

What is epidemiology of Klebsiella?

A
  • Part of microbial flora (intestine)
  • asymptomatic carriage if bacteria remains in colon
    Community acquired , aspiration - chronic alcohol abuse
  • hospital acquired, ventilator associated- intubated COVID patients
111
Q

Pathogenesis of klebsiella?

A
  1. LPS(Endotoxic effect of LipidA)
    - Triggers robust inflammatory response via TLR 4 signaling (IL-8, TNFalpha leads to neutrophil recruitment)
  2. Capsular polysaccharide- K antigen
    - Anti-phagocytic, immune evasion contributes to progression from pneumonia to sepsis
  3. MDR (multiple drug resistant) plasmid- highly mobile passed by horizontal gene transfer
    - extended spectrum- beta lactamase ESBL - Klebsiella
    - Carbapenemase CR- Klebsiella or CR0 enterobacteriaceae
112
Q

Klebsiella pathogenesis: Aspiration pneumoniae(subset of typical pneumonia with high mortality) ?

A
  • microbes originate from GI tract, and aspirated in patient with loss of gag reflex ex vomiting CAP or intubation HAP.
  • > 1 area of lung parenchyma replaced by cavities filled with debris.
  • putrid odor to breath and sputum
  • Large % of cases are polymicrobial and can progress o lung abscess formation.
  • facultatitve anaerboes eat all the oxygen and allowing growth of anaerobes(gram negative anaerobic Roods with GNAR, ex0 bacteroides)
113
Q

clinical presentation for typical pneumonia/ lobar bbronchopneumonia?

A
  • productive cough, sputum is thick, viscous due to high neutrophil influx.
  • dyspnea
  • hemoptysis!! - S. Pneumoniae- rust colored sputum
  • Klebsiella- current jelly sputum
  • high fever
  • signs of sepsis: tachycardia, hypotension, edema

Rapid onset of hours to days

114
Q

typical bacterial pneumonia:

A

inflammation progresses esp. virulent, drug resistant bacteria (getting worsen X ray)

  • Strep pneumoniae, MRSA
  • Klebsiella pneumoniae, psedomonas aeruginosa.
  • Bronchopneumonia- lobar consolidation- necrotizing abscess
115
Q

Acute exacerbated chronic bronchitis AECB epidemiology &etiology

A

Subset of typical bbacterial pneumonia in patient with pre-existing cough

  • Patients with COPD and cystic fibrosis are very high risk categories for bacterial LRTI
  • bacterial agents are chronic endogenous biofilm colonizer of oropharynx and bronchi, exacerbation of symptoms are often triggered by viral infection.
  • Patients should get routine pneumococcal vaccination!!
116
Q

Streptococcus pneumoniae, NTHi, and Moraxella are “normal” benign colonizers in the nasopharynx, especially in the pediatric population. In a healthy host, these bacteria will remain senescent in biofilm form indefinitely. They will not have the inherent ability to gain access to the lungs as our muco-ciliary escalator and mucus will prevent any attachment or colonization below the trachea in a healthy person.

A

Pseudomonas is not considered a highly representative species for our respiratory mucosal tissue and it is strictly dependent on opportunities in a person with depressed defenses, ESPECIALLY persons with Cystic Fibrosis. The excessive mucus production in a relatively “sterile” environment of the bronchi is beneficial to Pseudomonas colonization; whereas, the normal flora in the URT will always out complete Pseudomonas.
Of note, Pseudomonas can cause soft tissue disease in healthy host such as hot tub folliculitis or swimmers ear aka otitis externa, but it will almost always be in context of exposure to water.

117
Q

Pseudomonas Biology

A
  • Gram negative rods
  • Lactose Non-fermenter, oxidase
  • produces mucoid green colonies (pyocyanin) on conventional agar
  • lung infections produce fruity smelling, yello green sputum
118
Q

Epidemiology of pseudomonas

A
  • Opportunistic pathogen, dependent on altered host immune status
  • pseudomonas is leading cause of mortality in CF patients
  • At risk: COPD and CF
  • ventilator associated VAP superinfection in COVID-19 patients
  • Complication: Untreated or drug resistant VAP or AECB can progress to necrotizing bronchial pneumonia, sepsis and meningitis.
119
Q

clinical presentation : acute exacerbated chronic bronchitis AECB aka complicated Bronchopneumonia

A
  1. Sudden onset of worsening of symptoms
  2. Dyspnea
  3. High fever
  4. Productive sputum with abundant neutrophils

Sputum cultures are often poly microbial
- Biofilm with pnenumococcus, pseumonas, NTI, Moraxella

120
Q

Atypical pneumonia:

A

Agents are not visualized by gram stain or cultured on blood agar
Mycoplasma pneumoniae

121
Q

What is mycoplasma pneumoniae?

A
  • pleomorphic, lacking cell wall
  • due to lack of cell wall: resistant to Betalactam antibiotics.
  • does not gram stain, requires NAAT
    Cold- agglutinin test is screening tool
  • fastidious, requires special media with sterols.
122
Q

Epidemiology of mycoplasma

A

1st MCC atypical bacterial CAP community acquired penumonia
65 , asthma is high risk
Outbreak lasting months occur in crowded institutional settings. Slow presentation!!

123
Q

Pathogenesis of mycoplasma?

A
  • P1 adhesin= attachment organeele
  • attaches to and damages the respiratory epithelial cells at the base of the cilia,
  • produce hydrogen perioxide and cytotoxin for localized inflammation.
  • molecular mimicry induces production of cross reactive antibodies (cold agglutinin reaction), associated with extrapulmonary complication.
124
Q

Clinical presentation: atypical pneumonia aka WALking pneumonia

A
  • gradual and insidious onset of several days to weeks.
  • dry persistent cough
  • pleuritic chest pain
    -shortness of breath
  • fever, usually low
  • headache, myalgias, arthralgias
    ;mild form of pneumonia
125
Q

What is bacillus anthracis

A
  • gram positive rod
  • inhalation of spores Wool sorter’s disease
  • pulmonary anthrax
    Widened mediastinum
126
Q

Outcome and prevention for bacteria pneumonia!

A

Prognosis: typical : usually serious and may require hospitalization
atypical: can sponetaneously resolve
Complication ARE common: ARDS, pulmonary edema, abscess, sepsis
Multiple antibiotic resistant

Prevention: vaccines are available for S. pneumoniae
chronic colonization is common in COPD.

127
Q

What is mycobacterium tuberculosis?

A
  • Acid fast bacilli
  • strict aerobe
    -catalse and SOD positive
    Thick lipid rich cell wall
  • mycolic acid and cord factor
128
Q

M. tuberculosis epidemiology and prevention?

A
  • Endemic region esp SE Asia m Sub saharan afrian
  • children more likely to present Primary active
  • immunocompromised at high risk of reactivated.
    Prevention: BCG vaccine
129
Q

M.tuberculosis epidemiology: HIV

A
  • MTB- HIV co infection has very poor prognosis if person has subsequently developed AIDS immunosuppression
  • MCC of mortality in persons living with HIV.
    50-70% AIDs patient develop extrapulmonary TB infection
  • disseminated infection can occur in any tissue
130
Q

Pathogenesis of primary:

A
  • bacteria gain access to the alveolar sacs and bind C3b on cell wall, enhancing opsonization,.
  • REsident alveolar macrophage engulf MTB.
  • MTB modifiy phagosomal compartment to replicate intracellar.
  • Prevent oxidative burst & inhibit phagosome- lysosome fusion (cord factor/ mycolic acid)
  • Macrophages secrete IL-12 &TNF-alpha triggering local inflammation.
  • TH1 cells, secrete robust amounts of IFN-y
  • Activated macrophages, Th1 ,PMNs(neutrophils), surround infected macrophages.
  • Healthy individuals form microscopic granuloma - latent
    But patients with low CD4+ fail to control infection, forming larger granuloma(Ghon focus).
  • cytokines and PMNs contribute to DTH (delayed hypersensitivity) tissue damage.
131
Q

M. Tuberculosis pathogenesis of re-activated:

A
  • Live bacteria remain dormant in granuloma
  • Reduction of CD4+ T cells destabilizes encased granuloca
  • MTB begins replicating
  • Bacteria preferentially migrate to lung apex(high oxygen)
  • macrophage attempt to form granuloma , fail without Th1 - IFN-y
  • Extensive host mediate tissue damage result in cavitation and extensive necrosis
  • damage to vascular barrier can result in dissemination of MTB
  • ## Infection overwhelms host
132
Q

Clinical presentation: active pulmonary tuberculosis:

A
  • dyspnea, productive cough, sputum can be scant, clear or bloody,
  • primary- mid lung, reactivated- apex, miliary- dispersed
  • anorexia and weight loss
  • slow onset weeks to months
  • symptoms correspond to affected organ
  • cancer like wasting
133
Q

diagnosis of M. Tuberculosis:

A

microscopy of sputum (bronchoalveolar lavage ) or tissue biopsy:
Ziehl-Neelsen stain
Rhodamine0auramine fluorescent stain higher sensitivity
`

134
Q

Cuture for M.tuberculosis diagnosis:

A
  • Lowenstein Jensen medium

- Antimicrobial susceptibility testing= increasing importnat

135
Q

TB skin test

A

Tuberculin Mantous PPD test: prior exposure to MT will result in delated type 4 hypersenssitivity DTH reaction

  • doesn’t differentiate active/latent TB or previous vaccination
136
Q

Quantiferon &ELispt: m

A

more senstivie in vitro immunoassays to detect MTB - specific memory CD4+ T cells.

137
Q

Difference between TB and Nocardia asteroides?

A

TB : Acid fast bacilli

Acid fast filamentous : nocardia.

138
Q

Fungal infection especial fungal RTI

A
  1. Primary pathogens: histoplasma capsulatum
    - blastomyces dermatidis
    - coccidioides immitis
139
Q

General features of primary fungal mycoses:

A
  • high percentage are asymptomatic

- if symptomatic, community- acquired pneumonia

140
Q

Pathogenesis of systemic fungal mycoses:

A
  1. Initial infection: exposure via inhalation, fungal attachement, dimorphic conversion and or extension of hyphae
  2. Virulence factor:
    Incomplete killing of inhaled conidia- germination
    - tissue invasion
    - enter bloodstream and disseminate
  3. damage results from : inflammatory response, direct damage to tissues, fungal enzymes
141
Q

Lab dianosis of fungal mycoses:

A
  • ## sputum, bronchoalvolar lavage, transtracheal aspirate, lung biopsy.
142
Q

clinical features of histoplasmosis:

A
  • Acute syndrome: pneumonia, disseminated disease (immunocompromised inidividuals)
  • diverse range of presentation: asymptomatic
143
Q

Histoplasma capsulatum:

A

H.capsulatum var capsulatum - pulmonary &disseminated infections, eastern US &Latin america
0 thinner cell walls

H.capsulatum var duboisii- skin and bone lesison, tropical afria, thick walled

144
Q

BIology of histoplasmosis:

A
  • In the environment, Histoplasma capsulatum exists as a mold with aerial hyphae. The hyphae produce macroconidia and microconidia and spores that are aersolized and dispersed.
    3. The warmer temperature inside the host signals a transformation to a oval, budding yeast. 4. The yeast are phagocytized by immune cells and transported to regional lymph nodes. 5. From there they traveled in the blood to other parts of the body.
145
Q

Epidemiology of Histoplasmosis:

A

Most common endemic fungal infection in humans

  • Fungus naturally found in acidic soil with high nitrogen content- enriched with bird or bat droppings.
  • Outbreak therefore associated with - areas where birds/bast roost, caves old buildings.

Pathogenesis: microconidia and hyphae are aeroslized and inhaled.
- phagocytized by alveolar macrophages.

146
Q

Histological finding for Histoplasma capsulatum:

A

non-encapsulated, thick walled and narrow base budding yeast in alveolar macrophages. (facultatively intracellular)

147
Q

Clinical features of blastomycosis:

A
  • Acute: illness resembles bacterial pneumonia, with mucopurluent or purulent sputum

Chronic: resembles TB(low fever, cough , fatigue, chest pain, night sweats)

  • Cutaneous lesion are the most common extrapulmonary form : verrucous or ulcerated in appearance.
148
Q

Biology of blstomycosis:

A
  • in the environment, Blastomyces exists as mold with septae aerial hyphae,. The hyphae produce spores. These spores are either inhaled or inoculated into the skin. The warmer temperature inside the host signals a transformation into a broad based budding yeast. The yeast may continue to colonize the lungs or disseminate in the bloodstream to other parts of the body, such as skin, bones and joints, organs and other CNS>
149
Q

Epidemiology of blastomyces dermatitids:

A
  • soil, decaying organic material : not usually associated with exposure to bird or bat droppings.
  • outbreak associated with contact with disturbed soil
150
Q

Histopathological findings for balstomyces dermatitidis:

A

broad base budding yeast

151
Q

clinical presentation: coccidioidomycosis(valley fever)

A
  • Primary ccoccidioidal pneumonia:
    1. resembles a community acquired pneumonia- cough chest pain, fever
    2. Genralized systemic symptoms: fever drenching night sweats, weight loss,
152
Q

Pathogenesis of coccidioidomycosis:

A

In the environment, coccidioidomycosis exist as a mold with septae hyphae. The hyphae fragment into arthroconidia which measure only 2-4cm in diameter and easily aerosolized when disturbed. 3. Arthroconidia are inhaled by susceptible host. 4 and settle into the lungs. The new environment signals a morphologic change, and the arthroconidia becomes spherules. Spherules divide internally until they are filled with endospores When a pherule ruptures the endospores are released and disseminate within surrounding tissue. Endospores are ten able to develop into new spherules and repeat the cycle.

153
Q

Coccidioides : valley fever

Epidemiology:

A 
dry season (following rainy season)
Pathogenesis: inhalation of arthroconidia
after inhalation, enlarge into barrel shaped spherules.
154
Q

Clinical presentation: paracoccidioidomycosis:

A
  1. chronic form : reactivation of primary infection
    more common form.
    Paracoccidioides brasiliensis
155
Q

Opportunistic fungal pathogens: -

A
  1. cryptococcus neoformans
  2. Pneumocystis jirovecii
  3. Aspergillus spp.
156
Q

Who do these opportunistic fungal infection occur in?

  1. crytoccocus neoformans
  2. penumocystis jirovecii
  3. Aspergilus spp.
A

Immunocompromised individuals including
- malignancies, bone marrow transplantation, solid organ transplantation on immunosuppressive treatment, prolonged corticosteroid therapy.

157
Q

Clinical presentation: cryptoccocus:

A
  • India ink prep: polysaccharide capsule is clear halo around yeast cells.
158
Q

cryptococcus neoformans: encapsulated yeast

A

Epidemiology: grows well in decaying wood, soil especially soil enriched by bird dropping.
- common fungal infection inAIDS patients with CD4+tcell count less than 100

159
Q

Pathogenesis of cryptococcus neoformans:

A
  • inhalation trigger production of capsule

- strong affinity for CNS - neurotropic

160
Q

Pneumocystis jirovecii

A
  • has cholesterol in place of erogsterol in cell wall.

- common fungal infection in AIDS

161
Q

Aspergillus sp:

A
  • septae hyphae, acute- angle branching
  • Afumigatus
    decaying organic matter, air and soil
    pathogenesis: inhaled conidia are phagocytosed.
162
Q

What is atypical clinical features?

A
  • gradual and insidious onset
  • milder symptoms compared to typical pneumonia:
    fever with chills, shortness of breath, dry to mildly productive cough , headache, myalsgias, arthralgias, loss of appetitie, low energy, and fatigue
  • mild pharygeal injection, skin rash (mycoplasm)
163
Q

Community Acquired Pneumonia (atypical)

A

: Mycoplasma pneumoniae

  • chlamydia pneumoniae
  • legionella pneunophila
164
Q

What is Legionella pneumophila:

A
  • clinical syndrome:
  • legionnarire disease
  • pontia feer
  • gram negative rod, motile, non spore forming
  • cultured buffered charcoal yeast extract agar.

Look for GI/ CNS involvement along with respiratory disease plus water

165
Q

Pathogenesis of Legionella pneumophila:

A
  • exposure= inhalation of contaminated aerosols
  • facultatively intracellular (alveolar macrophages)
  • prevent fusion of phagosomelysosome
  • virulence factors: intracellular growth
166
Q

factors increase the risk of infection (legionella pneumophila)

A
  • Decreased local or systemic cellular immunity
  • activates that increase the chances of exposure to an infectious of contaminated water.
  • Environmental and bacterial factors
167
Q

Diagnosis and laboratory testing for legionaries disease?

A
  • GI and CNS symptoms
  • hematuria
  • hyponatremia
  • elevated hepatic transminases. \
  • most commonly used laboratory test for dianosis is the urinary antigen test.
  • Methlyamine silver staining for lung tissue.n
168
Q

What is chlamydia pneumoniae:

A
  • outer cell wall resembles G negative , weakly endotoxic LPS , lacks peptidoglycan
    Major outer membrane protein
  • common to all chlymydia and unique to each species
169
Q

Life cycle of chlamydia:

A
  • Elementary body attaches to surface of cell,
    endocytosis of EB occurs
    , EBis in endosome which does not fuse with lysosome. -EB reorganizes into reticulate body in endosome
  • RB replicates by binary fission.
    -RBs are reorganized to EBs
  • Inclusion granule has both RBs and EBS
  • C. pneumoniae and C trachomatis: reverse endocytosis.
  • C. psittaci: lysis of cells.
170
Q

Replication for chlamydia:

A
  • Intact EB outer membrane inhibits fusion to the lysosomes thus no killling of Chlamydia.
171
Q

Chlamydia pneumoniae:

A
  • school aged children, obligate intracellular, gram negative, diagnosis: PCR, culture, no special risk groups.
172
Q

What is ornithosis: chlamydia psittaci:

A
  • obligate intracellular bacteria

- birds are the natural reservoir

173
Q

Ornithosis: chlamydia psittaci pathogenesis:

A
  • ## transmitted to humans through inhalation of excreta urine or respiratory droplets of birds
174
Q

High risk groups of clamydia psittaci:

A
  • veterinarians, zookeepers, pet shop owners, employers of poultry processing plants.
175
Q

Clinical features of chlamydia psittaci:

A
  • headache, high fever, chills. myalgia
  • nonproductive cough and consolidation
  • CNS involvement
    GI symptoms

Diagnosis by serology.
- antibiotics

176
Q

What is hantavirus pulmonary syndrome:

A
  • cluster of deaths in the southwest US

- four corners disease

177
Q

Biology and epidemiology of hantavirus:

A
  • RNA virus, spherical , lipid envelope with 2 major glycoproteins.
  • Sin nombre virus- commonest cause of HPS>
  • 96% reported cases of hantavirus pulmonary syndrome in states west of Mississippi river
178
Q

Hanta virus pulmonary syndrome:

A

rodents carry hantavirus primarily rats mouse.

  • rodents infestation is priamry risk for virus exposure
  • Cases of HPS occur sporadically, usually in rural areas.
  • Peridomestic settings, barns, outbuildings, and sheds are potential sites.
179
Q

Disease transmission for HPS:

A

Rodents shed the virus in their urine, droppings, and saliva

  • virus is mainly transmitted to humans when they breathe in air contaminated with the virus- airborne transmission
  • HPS occurs in the fall
180
Q

Pathogenesis of HPS:

A
  • generalized increase in capillary permeability that results from endothelial damage
181
Q

Clinical features of HPS:

A
  • divided into 3 clinical phases
    : 1. prodromal - resembles viral illness
    2. Cardiopulmonary: dyspnea, dry cough
182
Q

What is melioidosis, AKA whitemore’s disease?

- infection caused by burholderia pseudomallei

A

Endemic regions are South Asia, SE asia including China, northern austrailia.

  • gram negative bacterium, rod shaped, found in soil and fresh water.
  • transmission: percutaneous inoculation, inhalation, aspiration
  • common in rainy season
  • Risk factors: cystic fibrosis
183
Q

Clinical features of melioidosis:

A
  • Infection can be acute and chronic infection
  • latent infection with reactivation like tuberculosis
  • most common clinical manifestation: localized skin infection
184
Q

Lab diagnosis of melioidosis:

A
  • Sputum culture

: cornflower head morphology

185
Q

Lab diagnosis of melioidosis:

A
  • cultue is the mainstay of diagnosis
  • Ashdown’s agar (selective media)
  • Gram negative bacilli, bipolar staining.
186
Q

Prevention of melioidosis:

A
  • Avoid direct contact with soil and standing water if risk factors present and in endemic region
187
Q

Q fever: Coxiella burnetii

A

Zoonosis
Coxiella burnetii
- Obligate intracellular organisms
- Cattle, sheep, goats are improtant reservoirs

188
Q

3 main clinical presentation of Q fever

A
  • self limiting flu like illness
  • pneumonia
  • hepatitis
189
Q

Chronic Q fever:

A

sometimes present years after primary infection, culture negative endocarditis
- risk groups: pre existing heart defects
- pregnancy, immunocompromised
Diagnosis is seriological, phase I and II.

usmle (7 decks)

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