Respiratory Flashcards
URT infections
Common cold SARS MERS Pharyngitis Sinusitis Otitis media Epiglottis Diphtheria Influenza
LRT Infections
Acute Bronchitis
Bronchiolitis
Pneumonia
Cells of URT
Ciliated, pseudo stratified columnar epithelial cells.
Mucus secreting cells with secretory IgA
Cells of LRT
Nonciliated epithelium with IgG and IgA
Nonspecific defenses of the URT
S-IgA
Lactoferrin
Lysozyme (has antimicrobial properties)
Normal flora for the LRT
37C Streptococcus Staphylococcus Haemophilus Neisseria
Common causes of infectious pharyngitis
S. pyogenes
Rhinovirus, adenovirus, coronavirus, EBV
HSV, HPIV, Influenza, Coxsackievirus, C. pneumonias, N. gonorrhea, M. pneumonias, C. albicans
Infections caused by S. pyogenes
Infections pharyngitis
Rheumatic fever, post-streptococcal nephritis, carditis
Impetigo, skin and wound infections
Professional and Secondary invaders
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
Microflora of URT that are likely to cause disease
Corynebacterium Enterobacteriaceae Haemophilus Moraxella Mycoplasma Neisseria Propionibacterium Staphylococcus Streptococcus Treponema Candida
Examples of enterobacteriaceae
E.coli Klebsiella Salmonella Shigella Yersinia
Adenovirus persistance on dry inanimate surfaces
7d-3m
Rhinovirus persistance on dry inanimate surfaces
2h-7d
Coronavirus persistance on dry inanimate surfaces
3hrs
RSV persistance on dry inanimate surfaces
up to 6 hrs
Factors that predispose to an endogenous infection
Age Preceding infection Smoking Disease: COPD, CF, Asthmaa, CB Aspiration of URT flora into lungs: aspiration pneumonia
Most common cause of RTIs?
Viruses.
Mainly: Adeno Rhino Corona HPIV HSV Influenza
Nucleic acid in Adenovirus
linear dsDNA
Nucleic acid in Influenza virus
segmented RNA
Common agents and sxs of Rhinitis
Rhinovirus
Adenovirus
Coronavirus
Sxs: Rhinorrhea, sneezing, cough, sometimes fever
Common agents and sxs of Pharyngitis
Viral:
Rhino, Adeno, Corona
Bacterial:
S. pyogenes, C. diphtheriae, N. gonorrhea
Sxs: cough, sore throat, fever
Common agents and sxs of Sinusitis
Bacterial:
S. pneumoniae, H.influ, M.catarrhalis
Sxs: blockage, pressure, HA, nasal discharge, facial pain
Common agents and sxs of Otitis media
Bacterial:
S. pneumoniae, H. influ., M. catarrhalis
Sxs: ear ache, hearing loss, sinus blockage, pressure
Infections that may initially manifest as rhinitis
Varicella
Rubella
Rubeola
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.
Rhinovirus pathogenesis
HRV binds to ICAM-1 (major) and LDLR (minor) receptors on host cells
Undergoes Antigenic drift– high number of viral serotypes
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.
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.
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
Coronavirus
Coronaviridae
linear, +ssRNA, enveloped, helicalnucleocapsid.
Are either a, B, y, or d.
B-coronaviruses include MERS-CoV.
Peak incidence in winter
transmission= airborne
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
Coronavirus pathogenesis
Replication in cytoplasm of ciliated nasal epithelium
Obtains its envelope from the ER, not plasma membrane
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
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
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.
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
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
GCStreptococci Pharyngitis
Adults and college students
GGStreptococci pharyngitis
community outbreaks in older children
Arcanobacterium haemolyticum Pharyngitis
Adolescents and young adults
Generalized rash
(scarlatiniform rash)
Clahmydophila pneumoniae Pharyngitis
seen in young and healthy
Fusobacterium necrophorum Pharyngitis
Seen in young adults
Lemierre syndrome: septic thrombophlebitis of the internal jugular vein
Scleral icterus in pharyngitis
Infectious mononucleosis (EBV)
Most common age to see GAS pharyngitis
3-14 years
Agar for Bordetella pertusis
Bordet-Gengou agar
Agar for C. diphtheriae
Tinsdale agar
Tellurite plate: bc diphtheroids contain telluride reductase
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.
S. agalactiae
Lance field group B
B-hemolytic
Neonatal meningitis, wound infections, UTIs, pneumonia, and sepsis
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.
Identification of Streptococci
G+ spheres in chains
Catalase - (aerotolerant anaerobes)
Superoxide dismutase + (aerotolerant)
Growth enhanced by CO2
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
Scarlet fever
Complication of GAS pharyngitis.
Diffuse rash beginning on chest–> spreads to extremities.
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
Acute Glomerulonephritis
Poststreptococcal glomerulonephritis. Follows GAS pharyngitis or skin infection.
Type III HS rxn
Acute inflamm of renal glomeruli–> edema, HTN, hematuria, and proteinuria.
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
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.
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
Identification of C. diphtheriae
G+ rods Black colonies on tellurite plate Urease - Cystinase + Elek test: lines of precipitin
Causes of sinusitis and AOM
Viral: - Rhino - Aden - Corona Bacterial: - S. pneumoniae - H. influenza - M. catarrhalis
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
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
H. influenzae identification
G -
Coagulase -
Catalase -
Culture: chocolate agar with X and V growth factors.
- X: acts as hemin
- V: nicotinamide adenine dinucleotide (NAD)
Moraxella catarrhalis
G - Strictly aerobic, non-motile Oxidase + Most have B-lactamases Common cause of AOM Acute exacerbation of COPD in elderly.
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.
Identification of M. catarrhalis
Hockey puck sign on blood and chocolate agar.
Colonies turn pink after 48hrs.
Differentiate from Neisseria: DNAsa +, Nitrate reduction +
Neurologic syndromes assoc with Influenza virus
GBS
Encephalitis
Reye syndrom in children- made worse by aspirin
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
Lineages of Influenza B
Victoria-like
Yamagata-like
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
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.
Non-specific/Systemic flu sxs
Caused by interferon and cytokine response to virus
Local flu sxs
caused by epithelial damage, including ciliated mucus-secreting cells.
Swine flu
Type A influenzas may jump from domestic fowl to pigs.
Antigenic drift
gradual accumulation of point mutation–> gradual loss of stereospecificity of the Ag-Ab bond.
Happens in Influenza A and B (sometimes C)
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.
Common causes and sxs of bronchitis
Bacterial:
B. pertussis, M. pneumoniae, C. pneumoniae
Viral:
Influenza, Adenovirus, RSV
Sxs: dry cough, fever, myalgia
Common causes and sxs of Bronchiolitis
Bac:
B. pertussis, M. pneumoniae
Viral:
RSV, Rhino, HPIV
Sxs: Dry cough, fever, wheeze
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
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
How to distinguish between acute bronchitis and pneumonia
You can’t.
Systemic sxs suggest pneumonia though
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.
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
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
Most common cause of bronchiolitis
RSV
followed by Rhino
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
P/F protein of HPIV
Inhibits immune response by preventing establishment of cellular antiviral state.
Blocks IFN-a/B production and signaling pathway
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
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.
Risk factors for RSV
<6m Children with: - Underlying lung diseases - Premies - CHD - passive smoking - Down's IMCP'd Asthma
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
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
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
Hospital Acquired pneumonia
Bronchial pneumonia.
Most common agents are viral.
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)
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
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.
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
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
How does K. pneumoniae avoid phagocytosis?
with LPS- impedes complement (C3b) and inhibits opsonization.
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.
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
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.
CARDS toxin
Community acquired respiratory distress syndrome toxin.
Seen in M. pneumoniae
Paralyzes cilia– cough won’t go away.
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.
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.
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
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
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.
Identification of Legionnaire’s disease
Most common lab test: urinary Ag test.
DFAb staining
PCR
Serology- looks for serogroup 1
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.
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.
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.
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.
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.
Primary fungal pathogens
Histoplasma capsulatum
Blastomyces dermatitis
Coccidioides immitis
Paracoccidioides dermatidis
Opportunistic fungal pathogens
Cryptococcus neoformas
Aspegillus spp.
Pneumocystis jiroveci
Normally MONOmorphic
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
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
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
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.
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
Most virulent human mycotic pathogen?
Coccidioides immitis
Opportunistic fungal pathogen assoc. with Chemotherapy
Aspergillus spp.
Pneumocystis
Opportunistic fungal pathogen assoc. with assisted ventilation
Aspergillus spp.
Opportunistic fungal pathogen assoc. with malnutrition
Pneumocystis
C. neoformas
Opportunistic fungal pathogen assoc. with HIV/AIDS
C. neoformans
Pneumocystis
Opportunistic fungal pathogen assoc. with Neutropenia
Aspergillus spp.
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.
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
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.
Ornithosis
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.
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
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.
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.
Pathogenesis of HPS
Increase in capillary permeability results from endothelial damage.
Injury is from host’s immune response.
Melioidosis
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
Clinical features of Meliodosis
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.
Identification of B.pseudomallei
Ashdown’s agar (selective media): cornflower head morphology
Gram stain: G- bacilli, bipolar staining.
