Chapter 4: pulmonary infections Flashcards
what are the factors that predispose the host to develop pneumonia
viral infections damage the cilia and predispose to secondary bacterial infection
smoking damages the ciliary function
alcohol and other drugs depress coughing and epiglottal function
elderly patients have reduced humoral and cell mediated immunity, and may have impaired swallowing
because of stroke
immunosuppressed patient
patients with chronic disease
cold weather dries the mucous membranes and increases person to persons spread of infection
what are the symptoms, signs and diagnostic tests that help differentiate viral from bacterial pneumonia
predominance of mononuclearis in sputum cultures is suggestive of mycoplasma
chlamydophila
or virus
predominance of PMNs is suggestive of bacterial infection
how useful is sputum gram stain, what are the parameters that are used to assess the adequacy of a sputum sample
adequacy of the sample is assessed by the number of epithelia cells present, more than 10 means extensive contamination with mouth flora
more than 25 PMNs or bronchial epithelial cells per low power field indicated adequate sample
how should the clinician interpret the sputum culture, and should sputum cultures be obtained in the absence of sputum gram stain
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how often should chest x-ray be repeated and how long do the radiologic changes associated with acute pneumonia persist
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which antibiotic regimens are recommended for elmiric therapy of community acquired pneumonia and why
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what is nonproductive cough or a cough productive of scanty sputum suggestive of?
atypical pneumonia
what is a rusty-colored sputum suggestive off?
S. pneumoniae
what’s the pathogenesis of pneumonia, which organisms cause permanent damage and which don’t
pathogens are aspirated or inhaled as small aerosolized droplets
bacterial invasion of the alveoli induces 1) edema fluid that spreads to other alveoli though the pores of Kohn, 2) infiltration by polymorphonuclear leukocytes and red bloods cells, followed by macrophages
infection spreads centrifugally(red hepatization: newer regions in the periphery; grey hepatization: older central regions)
strep pneumonia does NOT cause tissue destruction
staphylococcus aureus(usually happens in ventilator associated pneumonia), Causes permanent damage
what is hemoptysis suggestive of
tuberculosis, lung abscess and lung carcinoma
what are the things to check for during history taking in pneumonia
- cough: frequency, production of sputum.. color and thicccccness of sputum
- chest pain: pain on deep inspiration, usually sharp, suggest pleural involvement. seen in strep pneumoniae, staph aureus, strep pyogenes. anaerobs like coxsackievirus and chovirus
- shortness of breath: worrisome symptom; may be the result of pleuritic chest pain rather than poor gas exchange.
- epidemiology: travel history, animal exposure, exposure to people with respiratory illnesses, occupational and sexual history
whats pleuritic chest pain classically associated with
S. pneumoniae. stabbing sharp pain
associated with friction rub and dull breath sounds during auscultation
since pulmonary parenchyma has no pain sensing nerves, its always associated with pleural inflammation.
diaphragmatic inflammation mimics cholecystitis or appendicitis
bad prognostic signs on physical examination
respiratory rate >30/min, blood pressure <90mmhg, temperature <35and>40 and depressed mental status
what are the patterns of pneumonia
typical patterns:
lobar pattern: streptococcus pneumoniae. Haemophilus influenzae and legionella
bronchopneumonia pattern: staphylococcus aureus, G- organisms, mycoplasma, chlamydophila and viral
interstitial pattern: influenza, cytomeglovirus, pneumocysitis, miliary tuberculosis
lung abscess: anaerobes, S.aureus
nodular lesion: fungal
P.s. radiographic patterns may be atypical in the immunosuppressed and AIDS patients
what are the patterns of pneumonia
typical patterns:
lobar pattern: streptococcus pneumoniae. Haemophilus influenzae and legionella
bronchopneumonia pattern: staphylococcus aureus, G- organisms, mycoplasma, chlamydophila and viral
interstitial pattern: influenza, cytomeglovirus, pneumocysitis, miliary tuberculosis
lung abscess: anaerobes, S.aureus
nodular lesion: fungal
P.s. radiographic patterns may be atypical in the immunosuppressed and AIDS patients
blood tests in pneumonia, whats associated with a bad prognosis
blood tests are used for people >50 years of age to assess the severity
a peripheral white blood cell count below 6000/mm3 in S. pneumoniae is a bad prognostic finding
anemia (hematocrit <30%), BUN above 30 mg/dl serum sodium below 130 mEq/L and glucose above 250mg/dl is associated with worse prognosis
arterial blood O2 below 60mmHg and pH below 7.35 worsen prognosis
two blood samples should be drawn before antibiotics are stated
what does the predominance of PMNs suggestive of
bacterial infection
what does the predominance of mononuclear cells suggestive of
mycoplasma
chlamydophila
or virus
treatment of pneumonia, what you shouldn’t do
treatment must start within 4 hours of diagnosis, delays increases mortality
use CRB classification
empiric therapy is different for disease and patient characteristic
1) outpatient with no comorbidity and no previous antibiotics use macrolides (azithromycin or clarithromycin)
2) hospitalized patient: use a third gen cephalosporin (ceftriaxone, ceftaxime)
3) aspiration outpatient: penicillin or clindamycin
4) aspiration inpatient: third gen cephalosporin or respiraor fluroquinolone plus metronidazole
you should NOT use x-ray to monitor improvement, it takes weeks
blood tests in pneumonia, what’s associated with a bad prognosis
blood tests are used for people >50 years of age to assess the severity
a peripheral white blood cell count below 6000/mm3 in S. pneumoniae is a bad prognostic finding
anemia (hematocrit <30%), BUN above 30 mg/dl serum sodium below 130 mEq/L and glucose above 250mg/dl is associated with worse prognosis
arterial blood O2 below 60mmHg and pH below 7.35 worsen prognosis
two blood samples should be drawn before antibiotics are stated
what increases mortality rate in patients with pneumonia
age >65 liver disease neoplastic disease CHF renal disease cerebrovascular accident
pathogenesis of S. pneumoniae. (Virulent factors)
thickcapsule prevents phagocytosis, thiccccest capsule is type 3
immunoglobulins are important opsonin that help phagocytose it
strep pneumoniae does not produce protease and seldom destroys lung parenchyma
it does not corss anatomic barriers such as lung fissures
disease manifestation are caused primarily by the hosts inflammatory response to the organism
pathogenesis of S. pneumoniae
thickcapsule prevents phagocytosis, thiccccest capsule is type 3
immunoglobulins are important opsonin that help phagocytose it
strep pneumoniae does not produce protease and seldom destroys lung parenchyma
it does not corss anatomic barriers such as lung fissures
disease manifestation are caused primarily by the hosts inflammatory response to the organism
what increases mortality rate in patients with pneumonia
age >65 infants liver disease neoplastic disease CHF renal disease cerebrovascular accident
who is specially at risk of S. pneumoniae
patients with opsonins deficiency:
complement deficiency
HIV
hypogammaglobinemia
who is specially at risk of S. pneumoniae
patients with opsonins deficiency: complement deficiency HIV hypogammaglobinemia asplenic/ patients with slpeen dysfunction
patients with cirrhosis alcoholism nephrotic syndrome CHF COPD
what are the clinical manifestation of S. pneumoniae
3 classic features:
abrupt onset and rigor(abrupt feeling of coldness and raise in temp)
rusty colored sputum
pleuritic chest pain
how do you diagnose S. pneumoniae
sputum culture with more than 10 lancet shaped G+ diplococci
blood culture should always be performed
urine pneumococcal antigen test
CXR shows lobar pattern with a little pleural effusion
treatment of S. pneumoniae
for penicillin sensitive strains use ampicillin and ampicillin
cephalosporins and high dose parenteral penicillin for intermediately sensitive strains
for highly sensitive strains use respiratory fluoroquinolone [gentiflloxacin, moxifloxacin] (except in those with meningitis, for that use vancomycin)
vaccinate those older than 65
Haemophilus influenzae pneumonia treatment
G- pleomorphic(it occurs in more than one distinct form) cobacilii
treat with parenteral ceftriaxone or cefotaxime in hospitalized patients.
in outpatient: multiple oral amoxicillin-clavulanate/macrolides/fluoroquinolones are useful
treatment of Staphylococcus aureus pneumonia
G+ arobic rare, follows influenza or AIDS patient Destructive bronchopneumonia complicated by lung abscesses pneumothora empyema
legionella pneumonia, characteristics and clinical presentation
G-, found in soil (but dont form spores)
elderly, smokers and immunocompromised are at increased risk
clinical presentation
minimal presentation
confusion and headache
GI symptoms and hyponatremia
treatment and diagnosis of legionella pneumonia
diagnosis
culture on buffered charcoal yeast extract agar
direct fluoresscent antibody stain (low sensetivity)
polymerase chain reaction
urinaryantigen to serotype I which is sensetive and specific
treatment of choice with azithromycin and fluroquinolone
atypical pneumonia: causes, treatment and diagnosis
physical findings nonproductive cough
CXR findings are worse than physical
causes are:
mycoplasma
chlamydophila
respiratory viruses:influenza, adenovirus, RSV
treatment with macrolide or tetracycline
if influenza is diagnosed, treat with amantadine within 48h of illness
atypical pneumonia: causes, treatment and diagnosis
physical findings nonproductive cough
CXR findings are worse than physical
causes are:
mycoplasma
chlamydophila
respiratory viruses:influenza, adenovirus, RSV
treatment with macrolide or tetracycline
if influenza is diagnosed, treat with amantadine within 48h of illness
syndromes associated with aspiration and treament
chemical burn pneumonitis: aspiration of acidic contents, acid damage causes pulmonary capillaries to leak fluid and release cytokines and permit infiltration by PMNs, eventually cause ARDS
Bronchial obstruction resulting from aspiration of food particles
Pneumonia resulting from a mixture of anaerobic and aerobic mouth flora, especially in patients with gingivitis which have higher bacteria colony counts
treatment: penicillin for community acquired infection
third generation cephalosporin for hospital acquired infection
bronchoscopy for obstructing foreign bodies
actinomycosis
G+, slow growing modified acid fast negative, microaerophillic or anaerobic
infection associated with poor oral hygene
slowly progressive infection, breaks though fascial planes, causes pleural effusions and fistula tracks, forms sulfure granules
alert clinical microbiology to hold anaerobic cultures
treatment must be prolonged high dose IV penicillin for 2-6 weeks followed by 6-12mont of oral penicillin
nosocomial pneumonia risk factors and causative agents
endotracheal intubation age >70 depressed mental status underlying disease or malnutrition metabolic acidosis
causes are G- bacilli and S. aureus
how to differentiate colonization from infection in nosocomial pneumonia
worsening fever and leukocytosis with left shift
sputum gram stain with increased PMNs predominance of one organism
decreasing PaO2, indicative of pulmonary shunting(perfusion is fine but ventilation is fucked)
expanding infiltrate on chest radiographs
treat with broad spectrum antibiotics after blood samples are obtained
empyema definition, when do you suspect it, organisms associated and treatment and diagnosis
purulent pleuritis.
suspect if fever persists after pneumonia treatment
common organisms, s pneumoniae, s. aureus, s. pyogenes and mouth anaerobes
diagnose with chest radiograph in decubitus (lying on the side) then thoracentesis
when pH is <7.2, glucose <40mg/dl, lactate dehydrogenase exceeds 1000IU/L, empyema is strongly suggested
early diagnosis and drainage prevent lung and pleural compromise
mortality is high in young patient and elderly ones
how is tuberculosis contracted and how can the disease be prevented
humans are the onl reservoir of this disease. spread by person to person aerosolized droplets laryngeal tuberculosis is highly infectious those people are at high risk: immigrants alcoholic urban poor single men intravenous drug abusers migrant farm workers prison inmates HIV elderly
what is primary tuberculosis
first eposure to inhaled infectious particles
flu like illness
spread is controlled over 4-8 weeks with cell mediated immunity
Ghon foci are calcified lung lesions at the site of primary infection
bacteremia develops and seeds the kidneys, epiphyses of long bones and vertebral bodies (areas with high oxygen content)
what is reactivation tuberculosis
occurs in 10% of patients
most common in men 30-50
apical infection is most common (high O2)
symptoms progress slowly over months, worsening cough, sputum production, low grade fever, night sweats, fatigue and weight loss
hemoptysis or pleuritic pain indicates severe disease
CXR shows apical cavities without fluids
cavitary disease is highly infectious, isolate all patients. in HIV infection, chest doesn’t show cavities. all patients with AIDS are considered to have tuberculosis until proven otherwise
what are the characteristics pathogenesis of tuberculosis
not gram stainable because of the lipid mycolic acid. acid fast bacteria because it takes red dye fuchsin
lipid wall lets the M. tuberculosis survive disinfectant and macrophages thus they are trasported wtihin the macrophages to lymph nodes where a cell mediated immune response is generated
caseating granulomas forms as a consequence of cell mediated immunity and the accumulation of lipid rich bacteria
increase in IL1 causes fever and weight loss
what are the typical symptoms and findings in miliary tuberculosis
develops in very young, very old HIV patients
associated with alcoholism, malignancy, connective tissue disease, renal failure, and pregnancy
in children it presents with high fever, night sweats and weight loss, hepatosplenomegaly, and lymphadenopathy
adults show moderate to low grade fever, night sweats, malaise, anorexia, weakness, and weight loss
look for choroid tubercles (patches in the eye during fundoscopy)
micronodular interstitial pattern on chest radiographs, maybe be NEGATIVE IN HIV AND THE ELDERLY
blood samples, transbronchial biopsy, bone marrow samples and liver biopsy may all yield positive cultures
treatment for all suspected cases using isoniazid rifampin ethambutol pyrazinamide
how is tuberculosis diagnosed
ziehl-Neelsen acid-fast stain can detect 10 to the power of 4 organisms per milliliter with 60% sensitivity
release of acid-fast bacilli from cavity lesions is intermittent. to ensure low infectivity, three negative smears are needed.
culture remains the most sensitive, it grows slowly (1/20th speed of normal bacteria), automated techniques detects within 9-16days
PCR should be performed
why should combination anti tuberculous therapy always be prescribed in active tuberculosis
reduce the selection into resistant strain (reduce resistance).
to reduce secondary resistance (resistance in someone who already received treatment before DOT is recommended [Directly observed therapy])
treatment for all suspected cases using
isoniazid
rifampin
ethambutol
pyrazinamide
what does having a positive PPD or interferon gamma test mean, and how should an individual with a positive test be treated
PPD (purified protein derivative) test[a test that says you’re positive for M. tuberculosis only if] the followig is met:
- positive test at more than 5mm in HIV or immunocompromised patients
- more than 10mm in people at over all risk of exposure
- more than 15 in people with no risk factors
Interferon gama test has similar sensetivity (watch a youtube about this whole card, im confused)
what are the characteristics pathogenesis of tuberculosis
no gram stainable because of the lipid mycolic acid. acid fast bacteria because it takes red dye fuchsine
lipid wall lets the M. tuberculosis survive disinfectant and macrophages thus they are transported within the macrophages to lymph nodes where a cell mediated immune response is generated
caseating granulomas forms as a consequence of cell mediated immunity and the accumulation of lipid rich bacteria
increase in IL1 causes fever and weight loss
