Respiratory Flashcards
(138 cards)
1
Q
URT infections
A
Common cold SARS MERS Pharyngitis Sinusitis Otitis media Epiglottis Diphtheria Influenza
2
Q
LRT Infections
A
Acute Bronchitis
Bronchiolitis
Pneumonia
3
Q
Cells of URT
A
Ciliated, pseudo stratified columnar epithelial cells.
Mucus secreting cells with secretory IgA
4
Q
Cells of LRT
A
Nonciliated epithelium with IgG and IgA
5
Q
Nonspecific defenses of the URT
A
S-IgA
Lactoferrin
Lysozyme (has antimicrobial properties)
6
Q
Normal flora for the LRT
A
37C Streptococcus Staphylococcus Haemophilus Neisseria
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
8
Q
Infections caused by S. pyogenes
A
Infections pharyngitis
Rheumatic fever, post-streptococcal nephritis, carditis
Impetigo, skin and wound infections
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
10
Q
Microflora of URT that are likely to cause disease
A
Corynebacterium Enterobacteriaceae Haemophilus Moraxella Mycoplasma Neisseria Propionibacterium Staphylococcus Streptococcus Treponema Candida
11
Q
Examples of enterobacteriaceae
A
E.coli Klebsiella Salmonella Shigella Yersinia
12
Q
Adenovirus persistance on dry inanimate surfaces
A
7d-3m
13
Q
Rhinovirus persistance on dry inanimate surfaces
A
2h-7d
14
Q
Coronavirus persistance on dry inanimate surfaces
A
3hrs
15
Q
RSV persistance on dry inanimate surfaces
A
up to 6 hrs
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
17
Q
Most common cause of RTIs?
A
Viruses.
Mainly: Adeno Rhino Corona HPIV HSV Influenza
18
Q
Nucleic acid in Adenovirus
A
linear dsDNA
19
Q
Nucleic acid in Influenza virus
A
segmented RNA
20
Q
Common agents and sxs of Rhinitis
A
Rhinovirus
Adenovirus
Coronavirus
Sxs: Rhinorrhea, sneezing, cough, sometimes fever
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
22
Q
Common agents and sxs of Sinusitis
A
Bacterial:
S. pneumoniae, H.influ, M.catarrhalis
Sxs: blockage, pressure, HA, nasal discharge, facial pain
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
24
Q
Infections that may initially manifest as rhinitis
A
Varicella
Rubella
Rubeola
25
Rhinovirus
```
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.
26
Rhinovirus pathogenesis
HRV binds to ICAM-1 (major) and LDLR (minor) receptors on host cells
Undergoes Antigenic drift-- high number of viral serotypes
27
Adenovirus
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.
28
Assoc. Illnesses of Adenovirus
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.
29
Adenovirus pathogenesis
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
30
Coronavirus
Coronaviridae
linear, +ssRNA, enveloped, helicalnucleocapsid.
Are either a, B, y, or d.
B-coronaviruses include MERS-CoV.
Peak incidence in winter
transmission= airborne
31
HCoV proteins
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
32
Coronavirus pathogenesis
Replication in cytoplasm of ciliated nasal epithelium
| Obtains its envelope from the ER, not plasma membrane
33
SARS
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
34
Clinical features of SARS
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
35
MERS
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.
36
Clinical features of MERS
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
37
Enterovirus D68
```
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
```
38
GCStreptococci Pharyngitis
Adults and college students
39
GGStreptococci pharyngitis
community outbreaks in older children
40
Arcanobacterium haemolyticum Pharyngitis
Adolescents and young adults
Generalized rash
(scarlatiniform rash)
41
Clahmydophila pneumoniae Pharyngitis
seen in young and healthy
42
Fusobacterium necrophorum Pharyngitis
Seen in young adults
| Lemierre syndrome: septic thrombophlebitis of the internal jugular vein
43
Scleral icterus in pharyngitis
Infectious mononucleosis (EBV)
44
Most common age to see GAS pharyngitis
3-14 years
45
Agar for Bordetella pertusis
Bordet-Gengou agar
46
Agar for C. diphtheriae
Tinsdale agar
| Tellurite plate: bc diphtheroids contain telluride reductase
47
Streptococcus characteristics
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.
48
S. agalactiae
Lance field group B
B-hemolytic
Neonatal meningitis, wound infections, UTIs, pneumonia, and sepsis
49
S. pyogenes
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.
50
Identification of Streptococci
G+ spheres in chains
Catalase - (aerotolerant anaerobes)
Superoxide dismutase + (aerotolerant)
Growth enhanced by CO2
51
Virulence factors of S. pyogenes
```
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
```
52
Scarlet fever
Complication of GAS pharyngitis.
| Diffuse rash beginning on chest--> spreads to extremities.
53
Rheumatic fever
Follows GAS pharyngitis
Type II HS rxn
Non-suppurative inflamm lesion of joints, heart, and subcutaneous tissue and CNS.
Preventable with penicillin prophylaxis
54
Acute Glomerulonephritis
Poststreptococcal glomerulonephritis. Follows GAS pharyngitis or skin infection.
Type III HS rxn
Acute inflamm of renal glomeruli--> edema, HTN, hematuria, and proteinuria.
55
Corynebacterium characteristics
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
56
Respiratory Diphtheria
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
C. diphtheriae pathogenesis
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
Identification of C. diphtheriae
```
G+ rods
Black colonies on tellurite plate
Urease -
Cystinase +
Elek test: lines of precipitin
```
59
Causes of sinusitis and AOM
```
Viral:
- Rhino
- Aden
- Corona
Bacterial:
- S. pneumoniae
- H. influenza
- M. catarrhalis
```
60
H. influenzae
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
Virulence factors of H. influenzae
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
H. influenzae identification
G -
Coagulase -
Catalase -
Culture: chocolate agar with X and V growth factors.
- X: acts as hemin
- V: nicotinamide adenine dinucleotide (NAD)
63
Moraxella catarrhalis
```
G -
Strictly aerobic, non-motile
Oxidase +
Most have B-lactamases
Common cause of AOM
Acute exacerbation of COPD in elderly.
```
64
M. catarrhalis pathogenesis
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
Identification of M. catarrhalis
Hockey puck sign on blood and chocolate agar.
Colonies turn pink after 48hrs.
Differentiate from Neisseria: DNAsa +, Nitrate reduction +
66
Neurologic syndromes assoc with Influenza virus
GBS
Encephalitis
Reye syndrom in children- made worse by aspirin
67
Influenza virus
```
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
Lineages of Influenza B
Victoria-like
| Yamagata-like
69
Influenza 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
Influenza A hemagglutinins
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
Non-specific/Systemic flu sxs
Caused by interferon and cytokine response to virus
72
Local flu sxs
caused by epithelial damage, including ciliated mucus-secreting cells.
73
Swine flu
Type A influenzas may jump from domestic fowl to pigs.
74
Antigenic drift
gradual accumulation of point mutation--> gradual loss of stereospecificity of the Ag-Ab bond.
Happens in Influenza A and B (sometimes C)
75
Antigenic shift
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
Common causes and sxs of bronchitis
Bacterial:
B. pertussis, M. pneumoniae, C. pneumoniae
Viral:
Influenza, Adenovirus, RSV
Sxs: dry cough, fever, myalgia
77
Common causes and sxs of Bronchiolitis
Bac:
B. pertussis, M. pneumoniae
Viral:
RSV, Rhino, HPIV
Sxs: Dry cough, fever, wheeze
78
Common causes and sxs of Pneumonia
```
Bacterial:
S. pneumoniae, H. influx., M. catarrhalis
Viral:
RSV, Influenza, Aden
Fungal:
Histoplasma, blastomyces
```
Sxs: productive cough, fever, pleuritic chest pain, resp. insufficiency
79
Acute Bronchitis
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
How to distinguish between acute bronchitis and pneumonia
You can't.
| Systemic sxs suggest pneumonia though
81
Croup
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
Paramyxoviridae
```
-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
HPIV
```
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
Most common cause of bronchiolitis
RSV
| followed by Rhino
85
HPIV pathogenesis
```
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
P/F protein of HPIV
Inhibits immune response by preventing establishment of cellular antiviral state.
Blocks IFN-a/B production and signaling pathway
87
Bronchiolitis
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
RSV
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
Risk factors for RSV
```
<6m
Children with:
- Underlying lung diseases
- Premies
- CHD
- passive smoking
- Down's
IMCP'd
Asthma
```
90
Bordetella pertussis
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
Identification of B. pertussis
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
Community acquired pneumonia aka "typical"
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
Hospital Acquired pneumonia
Bronchial pneumonia.
| Most common agents are viral.
94
Streptococcus pneumoniae
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
Pathogenesis of S. penumoniae
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
Pneumovax
```
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
Klebsiella pneumoniae
```
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
K. pneumoniae pathogenesis
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
How does K. pneumoniae avoid phagocytosis?
with LPS- impedes complement (C3b) and inhibits opsonization.
100
CAP "atypical" pneumonia
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
Mycoplasma pneumoniae
"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
M. pneumoniae virulence factors
P1 adhesin- for attachment
H2O2 production- mediates tissue destruction
CARDS toxin- cytotoxic effect on resp. epithelium during acute infection. Paralyzes cilia.
103
CARDS toxin
Community acquired respiratory distress syndrome toxin.
Seen in M. pneumoniae
Paralyzes cilia-- cough won't go away.
104
M. pneumoniae pathogenesis
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
M. pneumoniae dx
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
Chlamoydophila pneumoniae
```
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
Legionella pneumophila
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
L. pneumophila pathogenesis
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
Identification of Legionnaire's disease
Most common lab test: urinary Ag test.
DFAb staining
PCR
Serology- looks for serogroup 1
110
Pseudomonas spp.
```
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
Pseudomonas in CF patients
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
Mycobacterium tuberculosis
```
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
Pathogenesis of M. tuberculosis
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
Identification of M. tuberculosis
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
Primary fungal pathogens
Histoplasma capsulatum
Blastomyces dermatitis
Coccidioides immitis
Paracoccidioides dermatidis
116
Opportunistic fungal pathogens
Cryptococcus neoformas
Aspegillus spp.
Pneumocystis jiroveci
Normally MONOmorphic
117
Features of fungal RTIs
```
Acquired via inhalation- no person-person
Assoc w systemic mycoses
Endemic to specific areas
ALL are dimorphic
These may mimic TB
```
118
Pathogenesis of fungal RTIs
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
Histoplasma capsulatum
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
Blastomyces dermatitidis
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
Coccidioides immitis
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
Most virulent human mycotic pathogen?
Coccidioides immitis
123
Opportunistic fungal pathogen assoc. with Chemotherapy
Aspergillus spp.
| Pneumocystis
124
Opportunistic fungal pathogen assoc. with assisted ventilation
Aspergillus spp.
125
Opportunistic fungal pathogen assoc. with malnutrition
Pneumocystis
| C. neoformas
126
Opportunistic fungal pathogen assoc. with HIV/AIDS
C. neoformans
| Pneumocystis
127
Opportunistic fungal pathogen assoc. with Neutropenia
Aspergillus spp.
128
Cryptococcus neoformas
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.
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Pneumocystis jirovecii
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
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Aspergillus spp.
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.
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Ornithosis
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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.
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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.
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Clinical features of Ornithosis
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
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Hantavirus Pulmonary Syndrome
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.
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Clinical features of HPS
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.
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Pathogenesis of HPS
Increase in capillary permeability results from endothelial damage.
Injury is from host's immune response.
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Melioidosis
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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
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Risk factors: CF, DM, alcoholics, ch. renal disease, ch. lung disease, thalassemia
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Clinical features of Meliodosis
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Incubation: 1-21 days
Can be:
- asymptomatic
- acute and chronic infection
- latent w reactivation
Most common manifestation:
- pneumonia (adults)
- skin infection (children)
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Can present as:
pneumonia, skin ulcer/abscess, GU, septic arthritis, osteoarthritis, encephalomyelitis, organ abscess, parotitis, sepsis.
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Identification of B.pseudomallei
Ashdown's agar (selective media): cornflower head morphology
Gram stain: G- bacilli, bipolar staining.
