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388 Cards in this Set
- Front
- Back
Paroxysmal cough is characteristic of which microbe?
|
Bordetella
|
|
Paroxysmal cough for _ days (CDC) and _ days (WHO) are used for making the dx of pertussis
|
14 and 21
|
|
small, nonmotile, aerobic gram negative rod, nutritionally fastidious
|
Bordetella pertussis
|
|
Who or what is an important reservoir for Bordetella pertussis?
|
Adults and Adolescents
|
|
Transmission of Bordetella is by?
|
respiratory route
|
|
How does pertussis toxin(s) act?
|
1.)Irreversibly inactivates Gi-protein via ADP ribosylation, resulting in prolonged stimulation of adenyl cyclase and a rise in cAMP which increases protein kinase activity.
2) tracheal cytotoxin kills ciliated cells 3)hemolysin kills mucosal epithelial cells |
|
Pertussis causes what type of exudate?
|
mucopurulosanguineous (yellow-greenish, pussy, with RBCs)
|
|
Pertussis vaccine:
|
is in combination with diptheria and tatanus toxoids (DTap) and shoul dbe given to all ages 6 weeks to 6 years.
|
|
Are blood cultures positive or negative in acute exacerbation of chronic bronchitis?
|
negative usually
|
|
Haemophilus influenzae clinical features:
|
otitis media, sinusitis, epiglottitis (eliminated since vaccine), meningitis, bacteremia (endotoxic shock), pneumonia, cellulitis
*normally occurs in children <2 years who are not vaccinated |
|
Haemophilus is characterized by:
|
gram negative coccobacillary rods
|
|
species of Hi vary by requirements for X and V which are?
|
heme and NAD respectively
|
|
Species designated para-
|
require factor V
|
|
H. influenzae specifically requires:
|
both X and V
|
|
2 different groups of H. influenzae determined by the presence or absence of
|
polysaccharide capsule
|
|
group 1 subtype Hi
|
capsulated, 6 subtypes (a-f)
|
|
group 2 subtype Hi
|
unencapsulated, called NTHi (nontypable Hi.)
|
|
previously was major invasive pathogen of H. influenzae
|
Hib
|
|
NTHi are nontypable because:
|
they cannot be serotyped with antisera to the capsule
|
|
Are Haemophilus part of the normal flora?
|
yes, in the upper respiratory tract
|
|
group 2 causes disease in _ while group 1 causes disease in _
|
adults and children
|
|
transmission of Hi
|
respiratory droplets from a carrier
|
|
Who is at greatest risk of AECB?
|
ppl with COPD and heavy smokers
|
|
What 3 bacterial species are found in pts with COPD
|
S. pneumoniae, H. influenzae (NTHi) and Moraxella catarrhalis
|
|
IgA protease is associated with what bacteria?
|
NTHi
|
|
Tx of Hib or NTHi:
|
macrolides (clarithromycin and azithromycin) and cephalosporins. If due to Hib- parenteral admin of 3-generation cephalosporin (cefotaxime and ceftriaxone)
|
|
Is there a vacine for NTHi?
|
No
|
|
K. pneumoniae is seen in?
|
Alcoholics
|
|
What is a likely pathogen for postinfluenza?
|
S. aureus
|
|
gram positive, lancet shaped diplococci
|
S. pneumoniae (aka pneumococcal pneumonia)
|
|
catalase negative and Optochin sensitive
|
S. pneumonia alpha-hemolytic colonies
|
|
Does S. pneumoniae have a capsule?
|
Yes
|
|
S. pneumonia is transmitted via
|
respiratory
|
|
mulitfactorial pathogenesis:
|
1) upper airway colonization
2) aspiration 3) failure of normal host defenses 4) bacterial proliferation 5) inflammatory response |
|
What does bacterial generated IgA protease do?
|
degrades IgA antibody produced by the host and favors mucosal adherence and colonization
|
|
What do pneumococcal adhesins bind to?
|
GlcNac B1,3-Gal disaccharide groups on epithelial cell glycoproteins and platelet activating factor receptors on epithelial cells
|
|
Important for opsonization and phagocytosis of bacteria
|
IgG and C3 (complement)
|
|
pneumolysin
|
is released during bacterial lysis; forms pores and is cytotoxic to every cell in the lung.
|
|
1st stage of lobar pneumonia:
|
Congestion: serous exudation, vascular engorgement, bacterial proliferation
|
|
2nd stage of lobar pneumonia
|
Red Hepatization: reflects liver-like appearance of the lung, PMNs, vascular congestion, extravasation of RBCs causes reddish color
|
|
3rd stage of pneumonia
|
Grey Hepatization: accumulation of fibrin, WBCs and RBCs, inflammatory exudates
|
|
4th stage of pneumonia
|
Resolution: resorption of exudate
|
|
Tx for S. pneumoniae
|
penicillin! if resistant: 3rd generation cephalosporin (ceftriaxone or cefotaxime) plus a macrolide or floroquinolone (levoflaxacin). If highly resistant - vancomycin.
|
|
empyema
|
bacteria spreading to pleural space, resulting in an abscess which is detected by the presence of pleural effusion on CXR
|
|
cavity lesions imply:
|
polymicrobial abscess or TB
|
|
bacteria of cause in the homeless population
|
K. pneumoniae
|
|
what should rule out TB?
|
homelessness
|
|
k. pneumoniae properties
|
short, plump gram negative, urease-positive, lactose-fermenting (anaerobic), nonmotile, No H antigens but has a polysaccharide capsule ("K" antigen; there are 77 "K" antigens) which is antiphagocytic, LPS with lipid A portion being endotoxic and "O" antigen (10 "O's")
|
|
lives in water, soil, and occasionally food.. sometimes found in intestinal flora of humans
|
K. pneumoniae
|
|
who is at risk of getting K. pneumoniae?
|
alcoholics, people with increased risk of seizures, and those who are hospitalized (since it is a nosocomial pathogen)
|
|
adhesive properties are found on what in K. pneumoniae
|
fimbriae (nonflagellar, filamentous projections)
|
|
How does the capsular polysaccharide of Kp inhibit the activation of complement?
|
It causes antigenic mimicry by selective deposition of C3b onto LPS, which results in inhibition of the formation of the membrane attack complex (C5B-C9)
|
|
What usually follow Kp infection?
|
bronchopneumonia
|
|
How is Kp becoming more resistant to antibiotics?
|
acquisition of transferable plasmids possessing the genes for B-lactamases
|
|
Are vaccines available for Kp?
|
No
|
|
Bacteremia, hypotension due to LPS (endotoxin-mediated sepsis), DIC, UTIs, hospital-acquired wound infections and intra-abdominal infections are clinical features of?
|
Klebsiella pneumoniae
|
|
a CXR of what is consistent with atypical pneumonia?
|
patchy infiltrates
|
|
Which bacteria have no pulmonary clinical findings?
|
Mycoplasma
|
|
Causes GI symptoms and headache?
|
Legionella
|
|
What bacteria has a hx of exposure to birds, domestic animals or environment?
|
Coxiella, Legionella, and C. psittaci
|
|
known as "walking pneumonia"
|
Mycoplasma pnuemonia
|
|
isolation of Mycoplasma can take up to:
|
6 weeks
|
|
smallest, free-living, self-replicating organism?
|
mycoplasma
|
|
has no cell wall (and therefore does not gram stain)
|
mycoplasma
|
|
4 most important characteristics of atypical pneumonia?
|
nonproductive cough, variable CXR (patchy infiltrates), no bacteria on smear, no response to B-lactam antibiotics
|
|
Are gram stains and cultures useful for dx of Mycoplasma or any other atypical pathogen?
|
No
|
|
Is Mp seasonal?
|
No, can get it throughout the year
|
|
How do you transmit Mp?
|
person-to-person; respiratory
|
|
General risk age group for Mp?
|
5-20 years (school age to young adults)
|
|
Especially common in crowded military and institutional settings
|
Mp
|
|
Bacterial adherence leads to inhibition of ciliary movement (ciliostasis)- and prolonged cough
|
Mycoplasma
|
|
what is responsible for hemolytic anemia with mycoplasma?
|
production of H2O2 which destroys erythrocytes (its cytotoxic)
|
|
Mycoplasma stimulates what host immune responses?
|
T and B lymphocytes, inducing the formation of IgM antibodies
|
|
Drug of choice for mycoplasma?
|
erythromycin or doxycycline
|
|
Is there a vaccine for mycoplasma?
|
No
|
|
In untx pts with Mp, what are some clinical findings?
|
tracheobronchitis, pericardtis, myocarditis, and Steven-Johnson syndrome (young males develop rash involving the mucus membranes)
|
|
motile, flagellated, gram negative but stain faintly, aerobic, pleomorphic rods
|
Legionellae
|
|
definitive method for dx of Legionellae
|
culture of BAL (bronchoalveolar lavage) with special medium
|
|
Are Legionellae nutritionally fastidious
|
Yes, grows slowly in 3-7 days on buffered charcoal yeast extract
|
|
How many legionellae species?
|
20 - based on fermentative rxns
|
|
Most pathogenic Legionellae to humans?
|
L. pneumophila, followed by L. micdadei
|
|
Which serotype of L. pneumophila has been most common in causes legionellosis?
|
LPS serogroup 1
|
|
Legionelliosis occurs most often during what season?
|
summer
|
|
Where does the organism that causes Legionellosis survive?
|
tap water and cooling towers in association with slimy growth of ameba and other protozoans.
|
|
3 primary sources of infection for legionellosis
|
1. environment (showers, humidifiers, whirlpools)
2. aerosolizing equipment (nebulizers) 3. aspiration (from contaminated water) |
|
Legionellosis is transmitted person-to person... true or false
|
false
|
|
Risk factors for Legionellosis
|
COPD, age, smoker, alcoholic, immunosuppressed, taking corticosteroids, malignancy
|
|
strictly intracellular - by binding to C3 and favoring opsonization
|
legionella
|
|
Are legionella flagellated?
|
Yes
|
|
What gene allows legionella to survive in the phagosome?
|
dot - delayed organelle trafficking, which prevents phagosome-lysosome fusion
|
|
Primary host defense against legionella
|
Cell-mediated immunity - activation of macrophages which produce cytokines
|
|
What is responsible for lung tissue damage from legionella?
|
cytokines and other reactive mediators of PMN's and T-cells -
|
|
What would you see on CXR with legionella?
|
patchy,diffuse infiltrates
|
|
What meds do you tx legionella with? What med is NOT effective?
|
a macrolide, quinolone, or doxycycline. B-lactams are not effective bc they cannot penetrate host cells
|
|
Legionnaire's Disease
|
the more severe form of legionellosis, presents with severe fibrinopurulet pneumonia with alveolitis and bronchiolitis
|
|
Pontiac Fever
|
acute onset, flu-like, non-pneumonic illness occuring after infection with L. pnrumophila, BUT NO SIGN OF PULMONARY INFILTRATES ON CXR
|
|
ss-RNA genome with 8-segmented pieces that code for 10 proteins
|
Influenza
|
|
Is RNA positive or negative in Influenza?
|
Negative
|
|
helical or icosahedral capsid?
|
helical
|
|
enveloped or nonenveloped?
|
enveloped with hemagglutin (attachment protein) and neuraminidase (severs virus as it buds from host)
|
|
Current Human types of A type influenza?
|
H1N1 and H3N2
|
|
Occurs due to a genetic reassortment that results in a complete change in configuration of an epitope
|
antigenic shift
|
|
occurs when a point mutation results in a change in the configuration of a specific epitope
|
antigenic drift
|
|
leads to generation of new strains
|
antigenic shift
|
|
causes epidemic disease
|
A and B
|
|
causes sporadic disease
|
C
|
|
How does influenza spread?
|
Person-to-person via coughing and sneezing
|
|
incubation period of influenza?
|
28-72 hours, avg is 48
|
|
Active immunization of influenza produces which host immune response?
|
humoral
|
|
How many H spikes of influenza bind to sialic acid receptors in the host?
|
500
|
|
What degrades mucus?
|
neuraminidase
|
|
What initiates infection?
|
fusion of the viral envelope to the cell's plasma membrane
|
|
Is viremia common with influenza?
|
No
|
|
Where does influenza replicate?
|
in mucus secreting ciliated cells
|
|
What causes the symptoms of influenza?
|
Cytokines
|
|
Tx of influenza
|
rimantidine or amantadine (if given within 48 hours) and given for 3-5 days
|
|
Influenza predisposes the host to
|
secondary bacterial infection
|
|
neuraminidase inhibiting drugs (zanamivir or oseltamivir) are useful for which Type of influenza?
|
B
|
|
Reye syndrome is a rare, often fata childhood hepatoencephalopathy associated with analgesic use and is associated with
|
influenza B
|
|
Common in children less than 6 months old during certain times of the year
|
RSV
|
|
enveloped or nonenveloped RSV?
|
enveloped
|
|
negative or positive sense RNA?
|
negative ss-RNA (nonsegmented)
|
|
helical or ocosahedral capsid?
|
helical
|
|
Does RSV have hemeagluttin protein?
|
No
|
|
Why is RSV named so?
|
bc its replication in vitro leads to fusion of neighboring cells and a characteristic alarge mutlinucleated syncytium
|
|
How many antigenic types of RSV?
|
2: A and B
|
|
Is RSV stable in the environment?
|
No and is easily killed with soap and water
|
|
What months of the year is RSV most likely to occur?
|
November through April w/ peak activity in January/February
|
|
most frequently affected age group?
|
2-6 months
|
|
Transmission?
|
through infectious material contact of eyes, nose or mouth
|
|
This disease may involve an immunopathogenic mechanism with IgE and histamine
|
RSV
|
|
Integral to immune response in RSV
|
F (fusion) protein and G (decond glycoprotein)
|
|
bronchiolitis
|
inflammation of the terminale bronchioles, necrosis, and sloughing of the epithelial lining of the bronchioles. commonly seen in RSV
|
|
Tx of RSV
|
only symptoms with acetaminophen
|
|
Is vaccine available for RSV?
|
on experimental basis
|
|
Required for prevention of RSV
|
Contact isolation and hand washing
|
|
Any pt with exposure hx (emigration from an endemic country) with apical infiltrates and who does not respond to antibacterial agents should have studies done to rule out
|
TB
|
|
Fever, cough, night sweats and blood in sputum should suggest
|
TB
|
|
Pulmonary infiltrates are commonly found in the __lobes of TB
|
upper
|
|
Aspiration pneumonia is usually seen in pts with
|
poor dentition and altered mental status, i.e. dementia or alcholism
|
|
PPD skin test results show with in
|
48 hours
|
|
Positive TB test shows
|
thickening of skin and redness at the injection site
|
|
Mycobacterium is what kind of bacteria? (Gram +/_/acid-fast)
|
acid fast
|
|
the cell wall of mycobacteria contain
|
mycolic acid
|
|
Mycobacteria grows on
|
Lowenstein-Jensen agar
|
|
What is the characteristic pattern of virulent mycobacteria growth?
|
in parallel and serpentine patterns due to presence of cord factor
|
|
What is cord factor
|
a virulence factor; 6,6' trehalose-dimycolate
|
|
surface macromolecules of TB
|
PPD (purified protein derivative); a glycolipid - is antigenic!!!
|
|
What contribute to enhanced virulence?
|
LAM (lipoarabinomannan)
|
|
Mycobacteria are resistant to dehydration, but not heat....True or False?
|
True
|
|
Transmission of TB
|
Respiratory
|
|
Mycobacteria are: facultative anaerobes, obligate anaerobes, or obligate aerobes?
|
obligate aerobes!
|
|
LAM is recognized by
|
macrophage mannose receptor
|
|
What triggers phagocytosis in Mycobacteria?
|
they express cell-wall C3 convertase activity, forming C3b on its surface which is recognized by the macrophage complement receptor CR4
|
|
How does Mycobacteria evade phagocytotic killing?
|
Inhibits fusion of the phagosome and lysosome.- mediates by a tryptophan-aspartate coat protein
|
|
Hallmark of TB
|
granulomas
|
|
what stimulates formation of granulomas?
|
Cord factor - causes irreversible structural and functional damage to mitochondria
|
|
What releases IFNy and what does it do?
|
CD4+ T cells release it, IFNy stimulates macrophage activation
|
|
What are granulomas?
|
collections of macrophages that have taken on properties of epithelial cells (and are called epithelioid cells)
|
|
What coalesces with in the granuloma to cause a multinucleated giant cell?
|
epitheloioid cells
|
|
A fully developed granuloma encapsulated with fibrin; consists of a central area of large multinucleated giant cells containing tubercle bacilli, a midzone of epithelial cells, and a peripheral zone of fibroblasts, lymphocytes, and monocytes.
|
a tubercle
|
|
Ghon focus or perihilar lymph node involvement reflects
|
primary infection
|
|
cytokines for controlling TB
|
IFNy, IL-12 and TNF
|
|
key molecule needed to kill TB
|
nitric oxide (released by macrophages)
|
|
>5 mm skin rxn from PPD proves positive
|
FALSE, only in HIV or immunocompromised pts. >15mm is key
|
|
Majority of TB infections are latent or lytic?
|
latent
|
|
When do granulomas become caseous?
|
during reactivation of infection
|
|
Causes TB in cows and humans (rarely)
|
M. bovis
|
|
causes pulmonary TB-like disease
|
M. kansasii
|
|
found in water
|
M. marinum
|
|
causes cervical lymphadenitis in children
|
M. scrofulaceum
|
|
found in hot water tanks
|
M. xenopi
|
|
Causes cervical lymphdenitis in children, DIC in AIDS pts, and pulomary disease in elderly
|
MAC (mycobacterium avium-intracellulare)
|
|
causes skin ulcers
|
M. ulcerans
|
|
rapid growers
|
M. fortuitum- chelonae
|
|
uncultivable mycobacteria, armadillos are reservoirs in Lo and Tx, causes tuberculoid and lepromateous leprosy
|
Leprosy (M. leprae)
|
|
Tx of TB
|
4 drug regiment: isonaizid, rifampin, pyrazinamind, and ethambutol
|
|
Multidrug resistant TB is resistant to
|
INH and RIF (required 5 drugs instead)
|
|
Who is at greatest risk of hepatic toxicity and in response to what drug?
|
>50 years, INH (isonaizid)
|
|
Characteristic of miliary TB
|
PPD +; CXR has appearance of millet seeds scattered in all lung fields
|
|
Pott Disease
|
untx infection disseminates to vertebral bodies, causing osteomyelitis.
|
|
Cultures for TB show up in
|
3 weeks
|
|
Vaccine for TB? in US?
|
Yes, BCG but not readily available in US
|
|
leukopenia and thrombocytopenia characteristic of
|
fungi
|
|
halo sign on CT characteristic of
|
Aspergillus fumigtus
|
|
cytology staining for fungal elements
|
KOH/calcofluor, Giemsa, and silver stain
|
|
Nocardia should always be considered in what pts?
|
immunocompromised
|
|
Most common mold that causes human infection
|
Aspergillus species
|
|
Characteristics of Aspergillus
|
thin hyphae that branch a V-shape (45 degree) angle
|
|
Aspergillus dimorphic?
|
Nope
|
|
Most common Aspergillus species
|
A. fumigatus
|
|
Aspergillus epidemiology
|
found in nature and associated with decaying vegetation
|
|
major mode of transmission
|
inhalation of spores (conidia)- NOT TRANSMITTED FROM PERSON TO PERSON
|
|
What drugs increase susceptibility to this fungus?
|
cytotoic drugs that cause neutropenia (radiation, chemotherapy)
|
|
involved in phagocytosis of Af
|
neutrophils and macrophages
|
|
Af also is characterized by this symptom found in TB
|
granulomas
|
|
Cause of hemoptysis in Af
|
fungal hydrolases (serine protease of phospholipase) and toxic molecules (hemolysin) cause endothelial damage
|
|
Tx of Af
|
Amphotericin B - but if invasive pulmonary aspergillosus=voriconazole
|
|
Second line agent for invasive pulmonary Af
|
caspofungin
|
|
Vaccine for Aspergillus?
|
Nope
|
|
Recovery from Af requires
|
TX OF NEUTROPENIA- by reducing levels of cytotoxic chemotherapy and admin of GCSF (to improve neutrophil counts)
|
|
enlarged hilar and mediastinal nodes with hilar infiltrates suggests
|
fungal infection
|
|
associated with pigeon droppings
|
Histoplasmosis
|
|
Histoplasma capsulatum properties
|
dimorphic fungus, grows as a mold in the environment but converts to yeast in the human
|
|
Where is H. capsulatum found in the environment?
|
Soil; around ohio regions
|
|
Giemsa or Wright stains are taken from what tissues?
|
bone marrow, sputum, blood or lung biopsy
|
|
Growth of mold take up to
|
4 weeks
|
|
thick walled, finger-like projections that grow from the fungus
|
macroconidia (aerial mycelial growth)
|
|
Mold produces what 2 glycoproteins?
|
H and M
|
|
Where is Hc endemic?
|
in Central Eastern US, around Ohio and Mississippi river valleys.
|
|
Hc grows in...
|
soil contaminated with bat or bird droppings
|
|
Is Hc transmitted via respiratory?
|
It is NOT person-to-person, BUT conidia can become airborne and infection results form inhalation from the source
|
|
When do microconidia transform to budding yeast?
|
When they reach the alvelo and bind to CD2/CD18 family of integrins and are engulfed by both macrophages and neutrophils
|
|
What is the most critical determinant of establishing infection in Hc?
|
transformation of mold-->yeast
|
|
The yeasts grow intracellulary within the macrophages
|
True story
|
|
What finding occurs with Hc that also occurs with TB?
|
granuloma formation which produces fibrinous calcified granulomas with areas of caseous necrosis in the lungs
|
|
Ctyokine response to Hc produce what symtoms?
|
fatigue and weight loss
|
|
How does Hc travel to distant sites such as reticuloendothelial system (liver, spleen, and bone marrow)?
|
by lymph via lymph nodes
|
|
Tx of Hc?
|
most are self-limited and resolve on own. Oral itraconazole in immunocompromised pts
|
|
In pts with unresolving infecting due to lung disease, their disease may resemble...
|
TB
|
|
For severe disseminated Histoplasmosis, tx with
|
amphotericin B IV
|
|
Vaccine for Hc?
|
No
|
|
How do you reduce risk?
|
Use protective gear
|
|
Verrucous lesion that is tender and erythematous is characteristic of:
|
Blastomyces dermatitidis
|
|
What would you see on CXR with Blastomyces dermatitidis?
|
multiple nodular lesions, some which cavitate in the upper lobe
|
|
Endemic mycoses (3)
|
histoplasmosis, blastomycosis, and coccidioidomycosis
|
|
All endemic mycoses may cause a pulmonary infection that is indistinguishable from... based on clinical presentation
|
TB
|
|
Upper-lobe disease is characteristic of
|
TB
|
|
What should you consider if culture for a fungus is negative?
|
Sarcoidosis or malignancy
|
|
What temperature must the yeast grow at on culture? hence, why they can only grow in humans...
|
37 degrees Celsius
|
|
B. dermatitidis is what kind of fungus?
|
dimorphic
|
|
Bd on culture is characteristic of:
|
white fluffy mold that grows slowly at room temp (25C) on Sabouraud agar
|
|
How many microcinidium are formed on culture?
|
a single terminal microconidium which is round or oval
|
|
If grown on blood agar at 37C, the fungus grows as
|
brown, wrinkled colonies
|
|
On biopsy with Bd
|
large yeast forms with borad-bases budding
|
|
Bd is endemic where?
|
southeastern US (east of mississippi)
|
|
Bd is also known as
|
North American Blastomycosis
|
|
South American blastomycosis is caused by which agent?
|
Paracoccidioides braziliensis
|
|
What kind of environment is Bd found?
|
Wooded areas along waterways of decaying vegetation in warm, moist soil
|
|
Infection of Bd results from
|
inhalation of microconidia
|
|
Shift from infection mold form to pathogenic yeast form occurs at what temp?
|
37C
|
|
Incubation time for Bd
|
4-6 weeks
|
|
Tissue response to Bd
|
suppurative and granulomatous inflammation in lung parenchyma
|
|
Spread to other organs by Bd occurs
|
lymphohematogenously
|
|
Skin involvement shows:
|
pseudoepitheliomatous hyperplasia with focal micro-abscesses in papillary dermis. has pustular features
|
|
Tx bd with
|
Itraconazole for 6 months!! (Amphotericin B in really ill pts)
|
|
Is Bd transmissible from person to person?
|
Nope, and no vaccine either
|
|
Erythema nodosum lesions are characteristic of
|
Coccidioides immitis (coccidioidomycosis)
|
|
CXR of Ci is characteristic of
|
infiltrates in both lung fields with large cavities in upper lobes
|
|
C. immitis is a
|
dimorphic fungus that grows in soil as a mold with branching septate hyphae
|
|
When the soil is disturbed with Ci fungus, what forms?
|
arthroconidia (fragmented hyphae) that become airborne
|
|
when arthroconidia reach alveoli they transform to
|
thick-walled, nonbudding spherules (pathogenic form) which form septa and produce many uninucleate endospores
|
|
Culture os Ci requires how long for incubation?
|
very long, which is why it is usually not done when suspected bc it can be a danger to the lab... otherwise, looks like a fluffy white mold
|
|
Test of choice if coccidioidomycosis is suspected?
|
serology
|
|
Ci is endemic:
|
In southerwestern us, CALIFORNIA "valley fever" and western half of texas; maybe Mexico
|
|
Reservoir for Ci
|
soil in and around rodent burrows
|
|
infection from Ci results from
|
inhalation of athroconidia
|
|
Where does the athroconidia settle in the lungs?
|
terminole bronchiole b/c of its small size
|
|
Recovery from Ci involves:
|
Cell-mediated immunity
|
|
Ci has a characteristic simular to TB which is:
|
chronic granulomatous inflammation - caseation without calcification
|
|
What is really cool about Ci?
|
you have lifelong immunity after infection
|
|
Tx of Ci
|
fluconazole or itraconazole for 3-6 months (again, ampotericin B is really sick)
|
|
Who is at higher risk of dissemination to the skin?
|
anyone that is immunocompromised: pregnany women, HIV pts, caner pts, those receiving corticosteroids or undergoing organ transplants
|
|
Sites of disemination:
|
skin, meninges, bones, joints
|
|
Which med is preferred for tx of fungus b/c it can enter CSF for meningitis?
|
fluconazole- must tx is for life to prevent reactivation!
|
|
CXR of Nocardia asteroides (nocariosis) shows
|
extensive nodular infiltrates in R. middle and upper lobes and cavitary disease
|
|
Chronic symptoms are associated with
|
fungus and nocardia
|
|
mycoplasma does or does not show up as a unilateral disease on CXR
|
Does NOT!! usually B/L
|
|
What is gram + and partially acid-fast positive?
|
Nocardia
|
|
Characteristics of Nocardia
|
filamentous (beaded) bacteria, aerobic
|
|
Most medically important Nocardia
|
N. asteroides and N. brasiliensis
|
|
Culture of nocardia takes:
|
up to 4 weeks (grow slowly!)
|
|
Mode of acquisition?
|
inhalation of contaminated dust from soil environment
|
|
Who is especially at high risk for disease by Nocardia?
|
immunocompromised pts taking cytotoxic or immunosuppresive drugs as well as HIV pts
|
|
Nocardiosis occurs as a skin lesion in tropical countries called
|
Madura foot
|
|
Nocardia on gram stain looks similar to
|
fungi: have long branching filaments that resemble hyphae
|
|
Are nocardia intracellular bacteria?
|
Yes- facultative intracellular, they remain inside inactivated macrophages by preventing phagosome-lysosome fusion
|
|
Major mechanism of host resistance to Nocardia
|
activated macrophages and T-lymphcytes
|
|
what contributes to symptoms of pulmonary illness by Nocardia?
|
cytokines!!!!
|
|
Lung pathology in unconrolled infection includes
|
inflammatory endobronchial masses or diffuse pneumonitis and abscess
|
|
Is CNS involement rare with Nocardia?
|
No, it is common and takes the form of one or more abscesses
|
|
Symptoms of CNS involvement?
|
headache, lethargy, confusion, seizures, and sudden onset neurologic deficit
|
|
Tx of nocardia
|
improve pt's immune status and 6-12 months of sulfonadmides (first-line of defense)
|
|
Which Sulfonamides are preferred with nocardia?
|
Trimethoprim or sulfamethoxazole
|
|
Any vaccine for nocardia?
|
Nope
|
|
Productive cough with foul-smelling sputum is a sign of
|
Actinomyces israelii (thoracic actinomycosis)
|
|
drainage of Actinomycosis in the chest wall contains what color granules? This is practically dx of this bacteria!!!
|
Yellow
|
|
CXR of Actinomycosis
|
lung infiltrates in upper lobes
|
|
Examine what in dx for Actinocyces
|
sulfur granules in pus from sinus tract
|
|
foul-smelling sputum should reveal diff dx of
|
anaerobic bacteria/abscess
|
|
What is usually seen in immunocompromised pts?
|
Nocardia
|
|
Gram + filamentous bacteria (that may resemble fungi); anaerobic
|
Actinomyces
|
|
Are actinomyces acid fast?
|
NO
|
|
Are they spore forming?
|
NO
|
|
In tissues, actinomyces forms
|
sulfur granules
|
|
How long does it take to grow actinomyces on culture?
|
Up to 4 weeks b/c they are slow-growing
|
|
Periodontal disease is common with Ai
|
True
|
|
what type of colonies from sulfur granules from a draining sinus infection are formed with Ai...this is diagnostic!!!
|
"Molar tooth"
|
|
Where is Ai found
|
oral cavity (saliva, dental suraces, and tonsillar crypts) and GI tract as normal flora
|
|
Transmission is
|
Endogenous
|
|
Who is as risk of getting cervicofacial abscesses?
|
ppl with poor oral hygiene
|
|
Who is at risk of getting pelvic/abdominal actinomycosis?
|
Women with IUDs
|
|
How do you get Ai
|
aspiration of oropharyngeal species
|
|
The Ai is unable to cause disease on their own.. what do they require?
|
synergistic presence of other commensals - fusobacterium, prevotella, prophyromanas, capnocytophaga, and actinobacillus
|
|
So Actinomycosis is therefore a polymicrobic infection?
|
True
|
|
A chronic suppurative abscess spreads mainly by direct extension to their tissue planes involving the chest wall - drains sulfur granules
|
True
|
|
Tx of Ai
|
prolonged high dose iv therapy with penicillin followed by amoxicillin for 6-12 months; surgical if severe
|
|
How can you prevent Ai?
|
good oral hygiene for lung infection
|
|
patchy B/L infiltrates with rales and wheezing, immunocompromised by CF (or any other chronic illness) is most likely caused by which microbes?
|
A. fumingatus, atypical mycobacteria, H. influena, S. aureus, B. cepacia, P. aeruginosa
|
|
gram negative rod
|
Psudomonas aeruginosa
|
|
What other species are in the family Psudomonadaceae?
|
Burkholderia, stenotrophomonas, and aeruginosa
|
|
P. aeruginosa characteristics
|
motile with one flagella, strictly aerobic, nonfermentative, oxidase positive, nonspore forming
|
|
P. aeruginosa makes a water-soluble pigment called what?
|
pyocyanin ("blue pus")
|
|
Has a characteristic fruit odor
|
P. aeruginosa
|
|
What kind of capsule does Pa have?
|
alginate capsule
|
|
Are psudomonads nutritionally fastidious?
|
nope, they are flexible int heir nutrient requirements
|
|
Where can Pa be found in the environment?
|
common inhabitants of the soil and water (tap water and ice)
|
|
nosocomial or community acquired Pa?
|
nosocomial
|
|
What bacteria is found in disinfectants, soap, aqueous solns, ointments, eye drops, dialysis fluids, or any equipment that requires a wet body temperature environment
|
Pa
|
|
Transmission of Pa
|
by ingestion of or of contact with contaminated water or ice; aerosolization of contaminated liquids; penetration by contaminated objects and ingstion of Pseudomonas-laden foods
|
|
What is an example of a Pseudomonas-laden food?
|
tomatoes
|
|
Receptor on tracheal epithelial cells for psudomonas pili is...
|
sialic acid
|
|
What also serves as a surface-bound adhesin for glycolipids on respiratory epithelial cells?
|
exoenzyme S
|
|
When does Pa undergoes a phenotypic shift?
|
When they move down to the bronchi and become MUCOID (due to the alginate capsule)
|
|
Why is Pa mucoid?
|
b/c of the alginate capsule
|
|
What composes the alginate capsule?
|
mannuronic and glucuronic acid
|
|
Name 2 host factors what favor the colonization of Pa
|
1. impaired ability of bronchial epithelial cells to clear Pa
2. increased mucin production by bronchial epithelial cells; stimulated by Pa LPS |
|
What is host defense is stimulated by the Pa LPS?
|
a chronic neutrophilic inflammatory response which interferes with pulmonary function
|
|
In CF pts infected with Pa, what is the major cause of morbidity?
|
the neutrophilic inflammatory response that interferes with pulmonary function
|
|
Is bacteremia common with infection by Pa?
|
NO; very rare b/c of a high level of antibodies to antigens by Pa
|
|
3 secreted products of Pa that cause lung damage
|
elastase, phospholipase and exotoxin a
|
|
What does exotoxin A do?
|
ADP-ribosylates EF2 - results in inhibition of protein synthesis and ultimately cell death
|
|
What does elastase do?
|
hydrolyzes elastin and collagen
|
|
What does phospholipase do?
|
hydrolyze phospholipids of eukaryotic cell membranes
|
|
How do you tx Pa?
|
extended-spectrum penacilli (piperacillin), cephalosporin (ceftazidime), or carbapenem (imipenem) AND a antipseudomonal aminoglycoside (tobramycin)
|
|
True or false: Pa is typically resistant to many commonly used antibiotics
|
TRUE
|
|
In Pa infection in an abnormal host (immunocompromised), what is seen that is typically RARE in a normal host and is associated with an indwelling catheter?
|
UTI's - associated with a Foley catheter
|
|
Which microbe would be responsible in an immunocompromised individual in the ICU on respirator-therapy equipment?
|
Pseudomonas aerginosa (pneumonia)
|
|
Is there a vaccine for Pa?
|
No
|
|
Unilateral erythematous palpebral conjunctiva, watery eye and purulent exudate is characteristic of what infection?
|
S. aureus (secondary bacterial pneumonia and concurrent acute conjunctivitis)
|
|
most likely to cause infiltrates in the posterior lower lobe segment?
|
S. aureus
|
|
What can cause lung collapse due to mucus plugging and acute pulmonary edema
|
S. aureus
|
|
S. aureus characteristics:
|
Gram positive cocci that occur individually, in pairs, or in grape-like clusters; nonmotile; nonspore forming; catalase positive
|
|
Are Sa resistant to high temperatures?
|
Yes
|
|
Are Sa resistant to high [salt]'s
|
Yes
|
|
Are Sa resistant to drying?
|
Yes
|
|
Describe the colonies of Sa
|
large, smooth, translucent, and pigmented (cream orange to yellow)
|
|
3 clinically important species of Staphlococcus?
|
1. Sa 2. S. epidermdis (coagulase negative) and 3. S. saprophyticus (coagulase negative and novobiocin resistant)
|
|
What is coagulase activity?
|
The ability to clot plasma
|
|
What is the most important criteria in identifying S. aureus
|
coagulase activity
|
|
What is extracellular coagulase
|
reacts with prothrombin to form thrombin, which then turns fibrinogen to fibrin
|
|
Who or what is the reservoir for Sa?
|
Human nasal carriers; as well as on the surface of the skin
|
|
Transmission of Sa?
|
endogenously or exogenously; aspiration (usually common after viral infection) or hematogenous mode (in pts with illicit IV drug use)
|
|
How does influenza allow for secondary bacteria infection?
|
It destroys the mucocilliary ladder, thereby destroying the ciliary defense, which normally keeps bacteria out of the lower respiratory tract
|
|
How does S. aureus adhere to host cells?
|
via teichoic acid
|
|
Wat is the hallmark of S aureus infection?!?!?!?!
|
ABSCESS, which consists of a fibrin wall surrounded by inflamed tissues enclosing a central core of pus containing the organisms
|
|
How do you tx Sa?
|
high IV dose of antistaphlococcal penicillin (nafcillin) for a minimun of 2 weeks. Vancomycin is used in highly resistant strains
|
|
Extremely low BP, low pO2, and low platelet count is associated with which infection?
|
Sin Nombre virus (hantavirus pulmonary syndrome [HPS])
|
|
Hantaviruses belong to which family of viruses?
|
bunyavirus family
|
|
bunyacirus, phlebovirus, nairovirus, tospovirus are ____ borne?
|
athropod borne
|
|
hantavirus is the exception of athropod borne infection; instead it is
|
rodent borne
|
|
Characteristics of hantavirus
|
enveloped, spherical, triple-segmented & circular (-)ss-RNA
|
|
how many circular, helically symmetrical nucleocapsids does hantavirus have?
|
3
|
|
HFRS stands for
|
hemorrhagic fever with renal syndrome - precedes pulmonary edema and DIC
|
|
Lab detection of HPS consists of 3 measures: what are they?
|
1. detection of hantavirus-specific IgM (even in prodrome)
2. rising-titers of hantavirus-specific IgG 3. detection of hantavirus-specific ribonucleic acid by PCR |
|
pan-american zoonosis
|
HPS
|
|
Transmission of HPS is by:
|
rodent droppings or urine that is disturbed and inhaled
|
|
Is HPS associated with person=to-person transmission?
|
nope, at least not in america
|
|
Who is at risk for HPS?
|
adult men and individuals bearing B-locus allele (B*35)
|
|
Can HPS be used in bioterrorism?
|
Could possibly
|
|
Incubation period after exposure to infective rodent droppings:
|
1-5 weeks
|
|
What are the cellular receptors for pathogenic hantavirus?
|
b3 integrins
|
|
What cytokines are involved in hantavirus?
|
TNF and IL-2
|
|
HPS clinically resembles what?
|
ARDS
|
|
The key hallmark of early hantavirus infection?
|
thrombocytopenia
|
|
Tx of hantavirus:
|
aggressive ventilator management and use of systemic vasopressors
|
|
Any vaccines for hantavirus?
|
Nope
|
|
Characteristics of SARS-associated coronavirus
|
large, enveloped, (+)ss-RNA, with club-shaped peplomers providing a crown-like appearance, nonsegmented
|
|
Longest of any RNA virus:
|
SARS-CoV
|
|
3 groups of coronavirus have been known to cause upper respiratory and enteric disease:
|
Groups 1 and 2 are mammalian viruses and group 3 includes only avian viruses
|
|
SARS-CoV belongs to which group or coronaviruses?
|
group 4
|
|
Mode of transmission of SARS?
|
large-droplet aerosolization; contact (direct AND fomite); and fecal-oral route
|
|
Incubation period for SARS
|
2-10 days
|
|
What is seen in the lungs of people infected with SARS?
|
pathological cytoarchitectural changes: diffuse alveolar damage (DAD) with mulinucleated giant cells with no conspicuous viral inclusions; desquamation of pneumocytes. With progression, there is increased fibrosis and squamous metaplasia.
|
|
How do you tx SARS?
|
supportive care
|
|
Are steroids helpful in SARS?
|
Nope
|
|
Mortality rate of SARS?
|
10.5%
|
|
What is of upmost importance in a potential SARS outbreak?
|
Infection control measures! airborne precautions, hand washing, contact precautions (glove and gowns) and environmental cleaning
|