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Pre-Midterm Micro > Respiratory > Flashcards

Respiratory Flashcards

1
Q

URT infections

A 
Common cold
SARS
MERS
Pharyngitis
Sinusitis
Otitis media
Epiglottis
Diphtheria
Influenza
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2
Q

LRT Infections

A

Acute Bronchitis
Bronchiolitis
Pneumonia

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3
Q

Cells of URT

A

Ciliated, pseudo stratified columnar epithelial cells.

Mucus secreting cells with secretory IgA

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4
Q

Cells of LRT

A

Nonciliated epithelium with IgG and IgA

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5
Q

Nonspecific defenses of the URT

A

S-IgA
Lactoferrin
Lysozyme (has antimicrobial properties)

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6
Q

Normal flora for the LRT

A 
37C
Streptococcus
Staphylococcus
Haemophilus
Neisseria
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7
Q

Common causes of infectious pharyngitis

A

S. pyogenes

Rhinovirus, adenovirus, coronavirus, EBV

HSV, HPIV, Influenza, Coxsackievirus, C. pneumonias, N. gonorrhea, M. pneumonias, C. albicans

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8
Q

Infections caused by S. pyogenes

A

Infections pharyngitis

Rheumatic fever, post-streptococcal nephritis, carditis

Impetigo, skin and wound infections

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9
Q

Professional and Secondary invaders

A

Professional/Frank pathogens are what cause damage to the epithelial layer and alter it.
May cause:
- epithelial damage
- altered airway fxn
- up-regulation and exposure of receptors
- alter innate immune response.

Then the secondary/opportunistic invaders take advantage of that and enter through the damaged epithelium

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10
Q

Microflora of URT that are likely to cause disease

A 
Corynebacterium
Enterobacteriaceae
Haemophilus
Moraxella
Mycoplasma
Neisseria
Propionibacterium
Staphylococcus
Streptococcus
Treponema
Candida
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11
Q

Examples of enterobacteriaceae

A 
E.coli
Klebsiella
Salmonella
Shigella
Yersinia
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12
Q

Adenovirus persistance on dry inanimate surfaces

A

7d-3m

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13
Q

Rhinovirus persistance on dry inanimate surfaces

A

2h-7d

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14
Q

Coronavirus persistance on dry inanimate surfaces

A

3hrs

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15
Q

RSV persistance on dry inanimate surfaces

A

up to 6 hrs

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16
Q

Factors that predispose to an endogenous infection

A 
Age
Preceding infection
Smoking
Disease: COPD, CF, Asthmaa, CB
Aspiration of URT flora into lungs: aspiration pneumonia
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17
Q

Most common cause of RTIs?

A

Viruses.

Mainly:
Adeno
Rhino
Corona
HPIV
HSV
Influenza
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18
Q

Nucleic acid in Adenovirus

A

linear dsDNA

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19
Q

Nucleic acid in Influenza virus

A

segmented RNA

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20
Q

Common agents and sxs of Rhinitis

A

Rhinovirus
Adenovirus
Coronavirus

Sxs: Rhinorrhea, sneezing, cough, sometimes fever

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21
Q

Common agents and sxs of Pharyngitis

A

Viral:
Rhino, Adeno, Corona
Bacterial:
S. pyogenes, C. diphtheriae, N. gonorrhea

Sxs: cough, sore throat, fever

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22
Q

Common agents and sxs of Sinusitis

A

Bacterial:
S. pneumoniae, H.influ, M.catarrhalis

Sxs: blockage, pressure, HA, nasal discharge, facial pain

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23
Q

Common agents and sxs of Otitis media

A

Bacterial:
S. pneumoniae, H. influ., M. catarrhalis

Sxs: ear ache, hearing loss, sinus blockage, pressure

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24
Q

Infections that may initially manifest as rhinitis

A

Varicella
Rubella
Rubeola

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25
Q

Rhinovirus

A 
Picornaviridae
\+ssRNA, non-enveloped
has IRES element
acid labile
4 viral capsid protein: VP1, VP2, VP3, VP4.

Seasonal: March-October
Risks: smoking, extreme age, infected contact exposure, crowding (day care)

Can cause exacerbation of asthma and COPD.

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26
Q

Rhinovirus pathogenesis

A

HRV binds to ICAM-1 (major) and LDLR (minor) receptors on host cells

Undergoes Antigenic drift– high number of viral serotypes

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27
Q

Adenovirus

A

Adenoviridae
linear, dsDNA, non-enveloped, icosahedral.
Capsid has fiber VAPs
Serotypes based on pentane base and fiber proteins which determine tissue tropism.
Can cause lytic, persistent and latent infections in humans.

Endemic throughout the year.
Most common in children, but affects young adults in close quarters, and those under stress.
Oral vaccine against type 4&7 used in military only.

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28
Q

Assoc. Illnesses of Adenovirus

A

Can cause:

  • ARDS in infants, young ch. and military recruits
  • Pertussis-like syndrome in infants and young children
  • Viral pneumonia in infants, young children, military and IMCP’d.
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29
Q

Adenovirus pathogenesis

A

Fiber protein- attachment to host cell receptor.
CAR (coxsackie adenovirus receptor) is host cell receptor for serotypes 2&5.
Virus undergoes receptor mediated endocytosis.
Penton base has toxic activity:
-inhibits cellular mRNA synth
-cell rounding
-tissue damage

High mortality in IMCP’d

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30
Q

Coronavirus

A

Coronaviridae
linear, +ssRNA, enveloped, helicalnucleocapsid.

Are either a, B, y, or d.
B-coronaviruses include MERS-CoV.
Peak incidence in winter
transmission= airborne

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31
Q

HCoV proteins

A

E2 (peplomer/spike protein)- on the envelope- binds to host cell, facilitates fusion

H1 (hemagglutinin)- on the peplomer

N (nucleoprotein)- found on core- fxns as a ribonucleoprotein

E1 (matrix glycoprotein)- on the envelope- transmembrane protein

L (polymerase)- found on host cell- has polymerase activity

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32
Q

Coronavirus pathogenesis

A

Replication in cytoplasm of ciliated nasal epithelium

Obtains its envelope from the ER, not plasma membrane

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33
Q

SARS

A

SARS-CoV
Epidemic between 2002-2003
Case definition:
-h/o fever AND
- one or more sxs of LRTI (cough, dyspnea, SOB).
AND
- xray evidence of pneumonia/ARDS or autopsy confirmation

Reservoir: bats
Intermediate host: civet cats
Transmission: respiratory droplets

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34
Q

Clinical features of SARS

A

3-7 day prodrome: T>100.5, malaise, HA, myalgia. usually no URT sxs.
Respiratory phase: non-prod cough, dyspnea, res failure. Sometimes: diarrhea, chest pain, pleurisy, sore throat.
Pneumonia by 7-10 days
Lymphopenia in many cases

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35
Q

MERS

A

Outbreaks in Arabian peninsula 2014.
Animal host: Dromedary camel

Probable case:
- febrile acute resp illness w clinical evidence of pulm parenchymal disease.
AND
-direct link with confirmed MERS-CoV case
AND
- testing for MERS-CoV is unavailable or inconclusive.

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36
Q

Clinical features of MERS

A

Fever w/orw/out chills or rigors
Cough, SOB, hemoptysis, sore throat,
GI sxs
Abnormal chest radiograph

Comorbidities:
DM, HTN, Chronic cardiac dx, chronic kidney dx

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37
Q

Enterovirus D68

A 
Recent emergence in 2014.
Non-polio enterovirus. Picornaviridae family.
Non-enveloped, +ssRNA
Tropism for resp. tract
Seasonal: summer and fall
Transmission: resp and GI secretions
Risk: children with asthma
Linked to acute flaccid paralysis
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38
Q

GCStreptococci Pharyngitis

A

Adults and college students

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39
Q

GGStreptococci pharyngitis

A

community outbreaks in older children

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40
Q

Arcanobacterium haemolyticum Pharyngitis

A

Adolescents and young adults
Generalized rash
(scarlatiniform rash)

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41
Q

Clahmydophila pneumoniae Pharyngitis

A

seen in young and healthy

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42
Q

Fusobacterium necrophorum Pharyngitis

A

Seen in young adults

Lemierre syndrome: septic thrombophlebitis of the internal jugular vein

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43
Q

Scleral icterus in pharyngitis

A

Infectious mononucleosis (EBV)

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44
Q

Most common age to see GAS pharyngitis

A

3-14 years

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45
Q

Agar for Bordetella pertusis

A

Bordet-Gengou agar

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46
Q

Agar for C. diphtheriae

A

Tinsdale agar

Tellurite plate: bc diphtheroids contain telluride reductase

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47
Q

Streptococcus characteristics

A

Chains of cocci
G+
Catalase -, non-motile
Facultative anaerobes

Polysaccharide capsule:

  • hyaluronic acid: gives antiphagocytic properties
  • quelling rxn: capsular Ag reacts with Abs and makes the capsule swell.
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48
Q

S. agalactiae

A

Lance field group B
B-hemolytic
Neonatal meningitis, wound infections, UTIs, pneumonia, and sepsis

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49
Q

S. pyogenes

A

Lance field group A
B-hemolytic from Streptolysin S
Bacitracin sensitive
Leukocidin production-induces pus

Pharyngitis, skin and soft tissue infections, sepsis, Rheumatic fever, acute glomerulonephritis.

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50
Q

Identification of Streptococci

A

G+ spheres in chains
Catalase - (aerotolerant anaerobes)
Superoxide dismutase + (aerotolerant)
Growth enhanced by CO2

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51
Q

Virulence factors of S. pyogenes

A 
Avoid phagocytosis by:
- capsule
- C5a peptidase
- M and M-like proteins
- Lipoteichoic acid
- F protein
Adhesion and Invasion:
- M protein
- Lipoteichoic acid
- F protein
Toxins:
- SPE
- Streptolysin S (does B hemolysis)
- Streptolysin O
- Streptokinase
- DNAse
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52
Q

Scarlet fever

A

Complication of GAS pharyngitis.

Diffuse rash beginning on chest–> spreads to extremities.

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53
Q

Rheumatic fever

A

Follows GAS pharyngitis
Type II HS rxn
Non-suppurative inflamm lesion of joints, heart, and subcutaneous tissue and CNS.

Preventable with penicillin prophylaxis

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54
Q

Acute Glomerulonephritis

A

Poststreptococcal glomerulonephritis. Follows GAS pharyngitis or skin infection.
Type III HS rxn
Acute inflamm of renal glomeruli–> edema, HTN, hematuria, and proteinuria.

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55
Q

Corynebacterium characteristics

A

G+ rods
Non-spore forming
Aerobic
Club-shaped, Chinese letter formation
Gray-black colonies of dub-shaped G+ rods in V or L shapes on gram stain.
Granules/Volutin are produced on Loeffler coagulated serum and stain metachromatically.
Toxin-producing strains have B-prophage genes

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56
Q

Respiratory Diphtheria

A

Sudden onset exudative pharyngitis
Sore throat, fever, malaise
Thick pseudomembrane over pharynx– may obstruct resp. tract. Contains large amounts of dead bacteria. May bleed if ruptured

Severely ill: carditis and neuro complications- recurrent laryngeal n. palsy.

57
Q

C. diphtheriae pathogenesis

A

Endemic in tropics/subtropics
NON-invasive
diphtheria exotoxin causes local and systemic sxs: inflammation and formation of pseudomembrane, damage to organs.
Diphtheria exotoxin inactivates EF-2, prevents protein synthesis by the ribosome

58
Q

Identification of C. diphtheriae

A 
G+ rods
Black colonies on tellurite plate
Urease -
Cystinase + 
Elek test: lines of precipitin
59
Q

Causes of sinusitis and AOM

A 
Viral:
- Rhino
- Aden
- Corona
Bacterial:
- S. pneumoniae
- H. influenza
- M. catarrhalis
60
Q

H. influenzae

A

Pleomorphic, G -
Facultative anaerobe
Type B assoc. with invasive disease.
Vaccine against type B only
Most common cause of epiglottis. Shows “thumb sign” on x-ray with thickening of aryepiglottic folds.
Other syndromes: AOM, pneumonia, meningitis

61
Q

Virulence factors of H. influenzae

A

Pili
Non-pilus adhesions:
- P-2: outer membrane prot.– attaches to sialic-acid containing mucin oligosaccharides
-LPS: endotoxin. Impairs ciliary fxn.
- Antiphagocytic capsule composed of Polyribose Ribitol Phosphate (PRP)- what Abs are developed against
- IgA proteases

62
Q

H. influenzae identification

A

G -
Coagulase -
Catalase -
Culture: chocolate agar with X and V growth factors.
- X: acts as hemin
- V: nicotinamide adenine dinucleotide (NAD)

63
Q

Moraxella catarrhalis

A 
G - 
Strictly aerobic, non-motile
Oxidase +
Most have B-lactamases
Common cause of AOM
Acute exacerbation of COPD in elderly.
64
Q

M. catarrhalis pathogenesis

A

AOM:
- colonization of nasopharynx–> migration through eustachian tube to middle ear.
Normally precipitated by viral URI

Exacerbation of COPD:
- altered mucociliary fxn–> colonize/infect airway.
Triggered by acquisition of new strains.

Mechanisms:
- adheres to resp. epithelium, intracellular invasion, complement resistance, biofilm formation, induces inflamm.

65
Q

Identification of M. catarrhalis

A

Hockey puck sign on blood and chocolate agar.
Colonies turn pink after 48hrs.

Differentiate from Neisseria: DNAsa +, Nitrate reduction +

66
Q

Neurologic syndromes assoc with Influenza virus

A

GBS
Encephalitis
Reye syndrom in children- made worse by aspirin

67
Q

Influenza virus

A 
Orthomyxoviridae
Spherical, enveloped 
Eight segments of -ssRN
(type C only has 7)
Type A: subtypes based on H and N proteins.
All have M1 matrix protein
Type A only has Ion channel M2 protein.
Segmented genome gives diversity and allows mutations and reassortment
Replicates in nucleus
Buds from plasma membrane
68
Q

Lineages of Influenza B

A

Victoria-like

Yamagata-like

69
Q

Influenza A

A

Disease of birds, but can infect mammals.
Wild ducks/sea birds are reservoir.
Passed to chickens where it causes sweeping epidemics.
Once transmitted to man, can be passed person-person
Subtyped based on H and N present.
H- adheres to epithelium
N-penetrates

70
Q

Influenza A hemagglutinins

A

Major Ag which host Abs are directed
Responsible for evolution of new strains
Requires protease cleavage to be active– proteases define tropism.
HA (as well as NA) can undergo major reassortment/shift as well as minor mutation/drift

drift happens in Type B as well.

71
Q

Non-specific/Systemic flu sxs

A

Caused by interferon and cytokine response to virus

72
Q

Local flu sxs

A

caused by epithelial damage, including ciliated mucus-secreting cells.

73
Q

Swine flu

A

Type A influenzas may jump from domestic fowl to pigs.

74
Q

Antigenic drift

A

gradual accumulation of point mutation–> gradual loss of stereospecificity of the Ag-Ab bond.
Happens in Influenza A and B (sometimes C)

75
Q

Antigenic shift

A

sudden rearrangement/reassortment of the eight genetic subunits of the Influenza A virus.
Normally result of co-infection of 2 different A strains in a single intermediate host.

Only occurs in Influenza A.

76
Q

Common causes and sxs of bronchitis

A

Bacterial:
B. pertussis, M. pneumoniae, C. pneumoniae
Viral:
Influenza, Adenovirus, RSV

Sxs: dry cough, fever, myalgia

77
Q

Common causes and sxs of Bronchiolitis

A

Bac:
B. pertussis, M. pneumoniae
Viral:
RSV, Rhino, HPIV

Sxs: Dry cough, fever, wheeze

78
Q

Common causes and sxs of Pneumonia

A 
Bacterial:
S. pneumoniae, H. influx., M. catarrhalis
Viral:
RSV, Influenza, Aden
Fungal:
Histoplasma, blastomyces

Sxs: productive cough, fever, pleuritic chest pain, resp. insufficiency

79
Q

Acute Bronchitis

A

Inflammation of bronchi due to URI.
Cough lasting >5days
Most common cause: viral- Influenza A and B, Parainfluenza, Corona, Rhink, RSV
Can’t distinguish between acute bronchitis and pneumonia, but systemic sxs suggest pneumonia

80
Q

How to distinguish between acute bronchitis and pneumonia

A

You can’t.

Systemic sxs suggest pneumonia though

81
Q

Croup

A

aka laryngotracheitis: Inflammation in larynx and sub-glottic area.
Most common cause: HPIV-1 (then RSV and adeno)
6m-3y most common
Characterized by:
- Inspiratory stridor
- Barking cough
- Hoarseness
Shows “steeple sign” on X-ray of the subglottic narrowing of the trachea.

May cause secondary bacterial infection.

82
Q

Paramyxoviridae

A 
-ssRNA enveloped, helical nucleocapsid.
VAPs on envelope:
- Fusion protein
- HN (PIV, and mumps)
Just H for measles
- Glycoprotein G for RSV
Replicates in cytoplasm and buds from plasma membrane
Transmitted in resp droplets
2 families:
Paramyxovirinae:
- Respovirus: HPIV-1 and -3
- Rubulavirus: HPIV-2, and -4
Pneumovirinae:
- Pneumovirus: RSV
83
Q

HPIV

A 
Enveloped
have HN activity
F protein for viral entry
- Abs against F protein= neutralizing
-Syncytia formation

Risks:

  • Vitamin A deficiency
  • lack of breastfeeding
  • malnutrition
  • overcrowding
  • environmental smoke

Transmission: resp. droplets, person-person

84
Q

Most common cause of bronchiolitis

A

RSV

followed by Rhino

85
Q

HPIV pathogenesis

A 
Linear -ssRNA
P/F proteins- immune evasion
F protein: syncytium formation
HN: structural and penetration
L protein: multifxnl polymerase
M protein: matrix structural protein
86
Q

P/F protein of HPIV

A

Inhibits immune response by preventing establishment of cellular antiviral state.
Blocks IFN-a/B production and signaling pathway

87
Q

Bronchiolitis

A

Inflamm of bronchioles and small bronchi.
<2yr in fall and winter
URI sxs followed by LRI with inflammation–> wheezing and/or crackles/rales.
Virus infects terminal bronchiolar epithelial cells–> damage and inflammation–> edema and xs mucus–> sloughed cells –> obstruction of small airways and atelectasis.

Common cause: RSV
Risks: premie, low birth wt., CHD, Ch. pulm disease, passive smoking, overcrowding, daycare

88
Q

RSV

A

Enveloped, helical nucleocapsid -ssRNA. Replicates in cytoplasm of nasopharyngeal epithelium.
Has direct CPE–> loss of fxn.

leading cause of LRIs in children.
RSV LRIs in infancy is linked with subsequent reactive airway disease.
Infection limited to RT.
Seasonal: fall/winter. Except FL: July-Feb.

89
Q

Risk factors for RSV

A 
<6m
Children with:
- Underlying lung diseases
- Premies
- CHD
- passive smoking
- Down's
IMCP'd
Asthma
90
Q

Bordetella pertussis

A

G - coccobacillus
Adults are reservoir
children <10 most affected
Whooping cough

Pathogenesis:

  • Adhesion: FHA, PT, fimbriae
  • Growth/toxin release: PT, ACT, TCT
  • Local/Systemic pathology: TCT, PT, DNT, LOS
91
Q

Identification of B. pertussis

A

Nasopharyngeal swab or secretions (must come from ciliated epithelium)
Organism is v susceptible to drying
Culture on Bordet-gengou agar (charcoal blood agar + cephalosporin)
PCR

92
Q

Community acquired pneumonia aka “typical”

A

Lobar pneumonia. Normally bacterial
S. pneumoniae most common cause.
Others: M. pneumoniae, H.influ., C. pneumoniae, viruses.

Clinical features:
- one lobe involvement
- acute onset, high fever, pleuritic chest pain, productive cough
- signs of consolidation.
Dx: CXR
93
Q

Hospital Acquired pneumonia

A

Bronchial pneumonia.

Most common agents are viral.

94
Q

Streptococcus pneumoniae

A

G +
a-hemolytic on blood agar
Optochin sensitive, Bacitracin resistant.
Most common cause of CAP
Part of nasopharyngeal flora
Exog or Endog transmission
Winter and early spring incidence (only for exogenous transmission)

95
Q

Pathogenesis of S. penumoniae

A

Capsule: gives anti-phagocytic properties

IgA protease: breaks down secretory IgA- helps sustain the infection

Pneumolysin: exotoxin- inhibits epithelial activity, is cytotoxic for alveolar and endothelial cells, causes inflammation and decreases PMN effectiveness.

Autolysin: endotoxin- supplements axn of pneumolysin

Transformation

96
Q

Pneumovax

A 
polyvalent vaccine for pneumococcal pneumonia
For protection of high risk individuals:
- >65yr
- Chronic disease
- HIV
- Alcoholism
- Asplenic patients

Have 7-valent vaccine dependent on T-cell response for children.

97
Q

Klebsiella pneumoniae

A 
G - bacillus with large polysaccharide capsule- gives mucoid appearance.
Non-motile
Facultative anaerobe/Microaerophilic
Catalase +
Ferments lactose
LPS causes narcotization of lung tissue
At risk: for CAP- Alcoholics, DM, COPD. For nosocomial- ventilators, IV catheters
Have "red currant jelly" sputum
98
Q

K. pneumoniae pathogenesis

A

Causes CAP typical- necrotizing pneumonia (lung abscesses/aspiration pneumonia)
>1 area of lung parenchyma replaced by debris-filled cavities.
Putrid odor to breath and sputum
NOT spread through air. Exposure to bacteria required

Has high affinity Fe uptake systems: aerobactin and enterochelin– helps with growth.
Thick capsule
LPS (O Ag)- prevents phagocytosis and detection by host Abs. Impedes complement (C3B) and inhibits opsonization
Carbapenemase production
Pili- attachment and biofilm formation

99
Q

How does K. pneumoniae avoid phagocytosis?

A

with LPS- impedes complement (C3b) and inhibits opsonization.

100
Q

CAP “atypical” pneumonia

A

Most common from:
Mycoplasma spp.
C. pneumoniae
L. pneumophila

features: gradual/insidious onset with milder sxs than typical
Fever w chills
SOB
Dry (sometimes productive) cough
Scratchy sore throat
Confusion
GI sxs
Loss of appetite, Low E, fatigue.
101
Q

Mycoplasma pneumoniae

A

“Walking Pneumonia”
most common cause of atypical CAP
<40yrs
Outbreaks in crowded institutions

G - rods, lack cell wall so unreactive to gram stain, and are v susceptible to desiccation, but resistant to B-lactams
Gliding motility

102
Q

M. pneumoniae virulence factors

A

P1 adhesin- for attachment
H2O2 production- mediates tissue destruction
CARDS toxin- cytotoxic effect on resp. epithelium during acute infection. Paralyzes cilia.

103
Q

CARDS toxin

A

Community acquired respiratory distress syndrome toxin.
Seen in M. pneumoniae
Paralyzes cilia– cough won’t go away.

104
Q

M. pneumoniae pathogenesis

A

Transmission: airborne, person-person
Incubation: 1-4 wks.
Prolonged paroxysmal cough due to inhibition of ciliary movement (CARDS toxin)
Damages resp epithelial cells at base of cilia– activates innate immunity– produces local cytotoxic effect.
Activates cytokines
Has selective affinity for resp epithelium
ProducesH2O2– initial disruption and RBC membrane damage.

105
Q

M. pneumoniae dx

A

Culture: not common. Slow growth on special media

Serology:
- Serum cold agglutination
May produce cross-ran w adenovirus, EBV or Measles
- >4fold increase or decrease in titters supports diagnosis.

106
Q

Chlamoydophila pneumoniae

A 
aka TWAR
atypical CAP
Middle-age children
No risk groups
Re-infection is common

Has biphasic life cycle:
Elementary bodies- extracellular, infective, but metabolically inactive
Reticulate bodies- intracellular, non-infective, but metabolically active.
Both are released from the cell via reverse endocytosis

107
Q

Legionella pneumophila

A

causes Legionaire’s disease (atypical CAP)

G - motile (polar flagella) rod. 
Non-spore forming
Facultatively intracellular in alveolar macrophages
Infections due to serogroup 1
Cultured on BCYE agar

May also cause pontiac fever

108
Q

L. pneumophila pathogenesis

A

Inhalation of contaminated aerosols– exposure to contaminated water source is KEY!
Person-person transmission is rare.

Uptake via phagocytosis- prevents fusion of phagolysosome.
Most damage is from host response.
Virulence factor: intracellular growth.

109
Q

Identification of Legionnaire’s disease

A

Most common lab test: urinary Ag test.
DFAb staining
PCR
Serology- looks for serogroup 1

110
Q

Pseudomonas spp.

A 
G - rods
Strictly aerobic
Highly motile (many flagella)
Non-hemolytic
Mucoid colonies on conventional agar
- some produce pigments: pyocyanin and fluorescein- turn colorless media green.

Environmental opportunist
Found in still fresh water sources
Most common infection: Otitis externa.

Risks: pts w structural defects in body defenses

  • burn victims
  • CF
  • Ventilator pts.– causes ventilator assoc. pneumonias.
111
Q

Pseudomonas in CF patients

A

P. aeuruginosa and Burkholderia cepacia both cause Necrotizing bronchial pneumonia in CF patients.

Abnormal mucus of CF pts acts as biofilm for the organisms.
These are highly drug-resistant.
Often fatal infections.

112
Q

Mycobacterium tuberculosis

A 
Grows in cords
Aerobic, non-spore forming
Resists drying, sensitive to heat
causes TB
worldwide. affects all age groups
Cell wall:
Lipoarabinomannan
Mycolic acid- gives AF properties
Arabinogalactan
PDG
Cytoplasmic membrane

HIV pts susceptible bc they have less CD4+ T cells, so less IFN-a, so less macrophage activity which is responsible to phagocytizing M. tuberculosis.

113
Q

Pathogenesis of M. tuberculosis

A

Transmitted by droplet nuclei and dust.

Intracellular survival in alveolar macrophages.

  • Sulfolipids prevent oxidative burst & inhibit phagolysosome fusion.
  • resists lysosomal enzymes and ROS through cell wall lipids, LAM, and superoxide dismutase

LAM and mycolic acids

Secrete siderophores: exochelins for Fe acquisition

After initial exposure, the bac is contained in a granuloma and can stay there for life.

114
Q

Identification of M. tuberculosis

A

Lowenstein-Jensen agar
Oleic acid- albumin broth

Ziehl-Neelsen stain
Rhokdamine-Auramine fluorescent stain

PPD test: Type IV HS rxn. Gives info about prior exposure.

115
Q

Primary fungal pathogens

A

Histoplasma capsulatum
Blastomyces dermatitis
Coccidioides immitis
Paracoccidioides dermatidis

116
Q

Opportunistic fungal pathogens

A

Cryptococcus neoformas
Aspegillus spp.
Pneumocystis jiroveci

Normally MONOmorphic

117
Q

Features of fungal RTIs

A 
Acquired via inhalation- no person-person
Assoc w systemic mycoses
Endemic to specific areas
ALL are dimorphic
These may mimic TB
118
Q

Pathogenesis of fungal RTIs

A

Reach alveoli
Convert from mycelial–> yeast form (capable of replication)
Colonize respiratory mucosa.
Some can live inside macrophages:
- H. capsulatum- increases phagolysosomal pH, interferes w Ag processing.

Yeast are less susceptible to phagocytosis

119
Q

Histoplasma capsulatum

A

Causes histoplasmosis

H. capsulatum var capsulatum:
- pulm and disseminated infections
- E USA and latin america
H. capsulatum var duboisii
- skin and bone lesions
- tropical Africa

Found in soil- enriched w bird or bat droppings (old buildings etc)
Microconidia and hyphae are aerosolized and inhaled into alveolar macrophages.

High intensity exposure: fever, cough, chest pain –> dissemination

120
Q

Blastomyces dermatitidis

A

Causes blastomycosis
Assoc. with large skin lesions

Found in decaying organic matter. Assoc. with soil contact.
Most infections in Mid. and E. N.America.
- SE and S-central states bordering MS and OH river basins
Presents as pulmonary, and extra pulmonary (skin lesions), disseminated.

121
Q

Coccidioides immitis

A

Coccidioidomycosis
Exposure through inhalation of arthroconidia from soil
Exposure highest in late summer/early fall– dry conditions

Endemic to desert US states, N. Mexico, and certain central and S america
In tissue it is SPHERULES (seen w calcofluor stain) and not true yeast. This protects the spores from phagocytosis

Presents as self-limited flu-like illness

122
Q

Most virulent human mycotic pathogen?

A

Coccidioides immitis

123
Q

Opportunistic fungal pathogen assoc. with Chemotherapy

A

Aspergillus spp.

Pneumocystis

124
Q

Opportunistic fungal pathogen assoc. with assisted ventilation

A

Aspergillus spp.

125
Q

Opportunistic fungal pathogen assoc. with malnutrition

A

Pneumocystis

C. neoformas

126
Q

Opportunistic fungal pathogen assoc. with HIV/AIDS

A

C. neoformans

Pneumocystis

127
Q

Opportunistic fungal pathogen assoc. with Neutropenia

A

Aspergillus spp.

128
Q

Cryptococcus neoformas

A

Cryptococcosis
Encapsulated yeast (only one)
Worldwide
Grows in soil enriched w pigeon droppings
Transmission: inhalation
Common in: AIDS, sarcoidosis, liver disease

Visualized with India Ink

Pathogenesis:
Inhalation–> capsule production (composed of GXM)
Neurotropic.
Down regulates immune system
Oxidizes exogenous CAs–> melanin, and prevents phagocytic oxidative damage.

129
Q

Pneumocystis jirovecii

A

Pneumocystosis- pneumonia
Lacks ergosterol in walls– has cholesterol instead
Worldwide.
Causes interstitial mononuclear infiltrates
HIV patients w CD4+ <200

Doesn’t respond to anti-fungals, but instead to anti-protozoals

130
Q

Aspergillus spp.

A

Worldwide
In decaying matter, air and soil.

Allergic aspergillosis: asthma and CF pts.
Invasive aspergillosis: hyphae invade tissue- seen in pre-existing lung diseases w cavities. Fungi invade the cavity, erode BV walls. Causes aspergilloma formation.
Causes acute pneumonia in severely IMCPd

Sxs: deadly, invasive pneumonia, hemoptysis, high mortality.

131
Q

Ornithosis

A 
Cause: C. psittaci
Obligate intracellular.
Reservoir= birds
Have EBs and RBs
No PDG in cell wall- has LPS instead. MOMP- major cell wall component, as well as OMP.

The EBs penetrate the cells and inhibit phagolysosome fusion. Then RBs rupture host cell.

Transmission: inhalation of excreta from birds
Spreads to RES of liver and kidneys–> necrosis
Seeding to lung–> edema, thickening of alveolar wall–> macrophage infiltration, necrosis and hemorrhages.
Mucus plugs bronchioles–> cyanosis and anoxia (atelectasis?)

Worldwide
Risk: vets, zookeepers, etc.

132
Q

Clinical features of Ornithosis

A

Incubation: 5-14 days
HA, high fever, chills, myalgia
Non-prod cough, consolidation
CNS involvement: encephalitis, convulsions, coma, death
GI: N/V/D
Others: hepatomegaly, splenomegaly, follicular keratoconjunctivitis.

Diagnosed by serology.
Treat both pt and birds w antibiotics

133
Q

Hantavirus Pulmonary Syndrome

A

Four corners disease
Febrile prodrome-> acute resp failure, and death from circulatory collapse.
Rodents are vector

Hantavirus= bunyaviridae, circular, segmented genome. -ssRNA. Enveloped
Sin Nombre virus most common cause of HPS.
- deer mouse is vector of sin hombre
NO person-person transmission
Airborne transmission is most common.
Primarily in the fall.

134
Q

Clinical features of HPS

A

Incubation: 1-8wks.

1- Prodromal phase (3-5d): fever, HA, myalgia, V/D. Some confusion w/ viral gastroenteritis.
2- Cardiopulmonary (24-48hr): dyspnea, dry cough, pulm edema, circulatory collapse.
- rare: ATN–> renal failure
3- Convalescent: significant diurese w improvement of sxs

50% fatality.

135
Q

Pathogenesis of HPS

A

Increase in capillary permeability results from endothelial damage.

Injury is from host’s immune response.

136
Q

Melioidosis

A 
Aka Whittemore's disease
Cause: Burkholderia pseudomallei
- G - 
- Rod, motile, aerobic
- facultative intracellular
- non-spore forming
Endemic: SEA, N. Australia
Found in soil and fresh water.
Main transmission: percutaneous inoculation during exposure to wet soils or contaminated water.
- also could be: inhalation, aspiration

Risk factors: CF, DM, alcoholics, ch. renal disease, ch. lung disease, thalassemia

137
Q

Clinical features of Meliodosis

A 
Incubation: 1-21 days
Can be:
- asymptomatic
- acute and chronic infection
- latent w reactivation
Most common manifestation:
- pneumonia (adults)
- skin infection (children)

Can present as:
pneumonia, skin ulcer/abscess, GU, septic arthritis, osteoarthritis, encephalomyelitis, organ abscess, parotitis, sepsis.

138
Q

Identification of B.pseudomallei

A

Ashdown’s agar (selective media): cornflower head morphology
Gram stain: G- bacilli, bipolar staining.

Pre-Midterm Micro (8 decks)

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