Lung Flashcards
Community acquired pneumonia
Ok
Hospital acquired pneumonia
Ok
Healthcare acquired pneumonia
Ok
Ventilator associated pneumonia
Ok
Aspiration pneumonia
Ok
Right factors PNA
Ok
Patient population susceptible to PNA
Ok
Aspiration PNA
Ok
Local pneumonia
Alveoli
CXR/CT-dense consolidation , air bronchospasm
US-consolidation , dynamic air broncograms
Micro of lobar
Strep pneumonia
Klebsiella pneumonia
Legionella
Bronchopneumonia
Bronchi
CXR/CT-Patchy opacities
US-Patchy B lines
May have consolidation
Micro of bronchopneumonia
Wide variety (mycoplasma, chlamydia, staph, pseudomonas
Interstitial pneumonia
Interstitial
CT/CXR-diffuse hazy opacities, septal thickening
US-patchy B lines, may have some consolidation
Micro interstitial pneumonia
Viruses, PJP, mycoplasma
Discuss preventative practices for CAP. What are contraindications
Ok
Two indices used to determine if a patient needs to be admitted to the hospital for PNA
Ok
Outline the following in regards to aspiration PNA and lung abscesses: risk factors, patient presentation, common causative agents, lab findings, imaging, and a generic empiric treatment plan
Ok
Orthomyxovirus PNA
Ok
Adenovirus PNA
Ok
H5N1 PNA 240, 250
Avian flu virus great risk for human pandemics
MPV PNA 303 -paramimyxoviridaevirus
Second most common etiology of lower respiratory infection in young.
Upper and lower respiratory tract infections-young kids and old adults
Slightly older as than RSV, 1 year vs 6 months
Winter early spring
Bronchiolitis, croup, pneumonia in kids
Old-cold
Reverse transcriptase PCR
Supportive treatment
Hantavirus PNA 299, 308 a bunyviridae
New Mexico, Arizona, Colorado, Utah
Influenza like followed by sudden respiratory failure, lot causing death
In previously health adults
Hemorrhagic fever with renal failure , pulmonary syndrome
Deer mouse-sin nombre south west USA
Pulmonary syndrome-high fever, muscle aches, cough, nausea, vomiting, rapid HR and RR< high WBC, low platelets, elevated RBC
Diagnosis-IgM and IgG to sin nombre
Lung capillary permeability leak-need intubation
40% die
Young adults flu like symptoms who develop pulmonary edema*** just supportive therapy
Define antigenic drift and shift, provide an example of each
Ok
Outline diagnostic and treatment methods for influenza. Include in you discussion: supportive care and neuraminidase inhibitors
Ok
Strep pneumonia morphology, metabolism, clincial presentation, diagnostics 33, 38
Capsule
Smooth S colonies cause rapid death in mice
R-no capsule -lost virluence
India ink stain -no taken up by capsule appears as a transparent halo around the cell. Usually for crypto coccus
Quelling reaction-mixed with antibodies to bind to capsule
Optichin sensitivity
Most common cause of pneumonia in adults
Sudden-shaking chills , high fevers, chest pain with respiration’s, and SOB, alveoli in one or more lung lobes fill up with white blood cells, bacteria and exudate. Seen as white consolidation
Cough up yellow green phlegm
Gram positive lancet shaped diplococci
Most common cause of otitis media in kids and most common bacteria meningitis in adults
Haemophilus influenza morphology, metabolism, clincial presentation, diagnostics 96 ,100
Rod negative
HACEK
Blood loving, blood again
Hematin found in blood is necessary for the bacterium’s cytochrome system. Blood also contains NAD needed for metabolism
B bad-nonencapsulated strains can colonize UR tract of kids and adults. They lack the virluence invasiveness of their encapsulated cousins and can only cause local infection . Cause otitis media and respiratory disease in adults with weaker prezinsting lung disease
-COPD GET IT worsens wheezing and SOB
Antibodies not in infants 6 mo-3 years, window
B-meningitis , acute epiglottis, septic arthritis, sepsis,
Vaccination
Moraxella 68,71
Neisseriaceae
Causes otitis media, and URI in patients with COPD or old
COPD exacerbation
Staph aureus 43, 46
Enterotoxin-lipases, penicillinase, staphylokinase, leukocidin, exfoliation, factors that bind complement. Hydrolyzes lipids, destroying penicillins, activates plasminogen to lyse fibrin clots, loses white blood cells, epithelial cell loses,
Klebsiella 75, 94
Ok
Pseudomonas 92, 94
Ok
Coxiella burnetti 120
Ok
Typical pneumonia
Strep p, HE< moraxella cat, klebsiella, pseudomonas, coxiella burnetti
Atypical bacterial pneumonia
Mycoplasma, chlamydia pneumonia’s, legionella pneuophilia, chlamydia psittacosaurus, burkholderia cepacia
Mycoplasma pneumonia 156, 158
Ok
Chlamydia pneumoniae 115, 122
Atypical bacteria TWAR, which is transmitted from perso to person by the respiratory route and causes an atypical pneumonia in young adults worldwide.
Taiwan and acute respiratory TWAR
Legionella pneumophilia 99-101, 102
Aerobic gram negative rod that is famous for causing an outbreak of pneumonia
Pontiac fever, legionnaires disease,
CAP, accounting for .2-10% of all admitted pneumonia cases
Local consolidation , but with fever with pulse temperature dissociation, (high fever, low HR), severe HA, confusion, myalgia, rhabdomyolysis, cough, hyponatremia, diarrhea,
Chlamydia psittacosaurus 115 122
Infects 130 species of birds
Human infected by inhaling chlamydia laden dust from feathers or dried out feces. This infection is an occupational hazard for breeders of carrier pigeons, veterinarians, and workers in pet shops or poultry slaughterhouse. Infection most commonly results in an atypical pneumonia called psittacosis, which occurs 1-3 weeks after
Burkholderia cepacia 93, 94-95
Gram negative rods in soil, water, plants, animals, lungs of CF, transmit on medical devices, hands of healthcare workers, between cystic fibrosis, oxidase positive, non lactose fermenter, antibiotic and disinfectant resistant
Pulmonary fungi
Aspergillus Histoplasma capsulatum Coccidiodes immitis Blastomycoses dermatidis -like Tb inhaled, primary infection int he lung, asymptomatic, mild, severe, or chronic lung infections, lung granulomas, calcifications and/or cavitation, can disseminate hematogenously to distant sites
Unlike-no person to person, fungi with spores not acid fast bacteria
Aspergillus 201, 2140215
Most common allergic bronchopulmonary aspergillosis, aspergillosis, invasive aspergillosis
Inhaling spores -ABPA, increase IgE, eosinophilia
Type IV,
Ppl with lung cavitation form TB can grow an aspergillus call called aspergillosis which needs surgery
Invasive-immunocompromised , bloody sputum may occur, due to blood vessel wall invasion by aspergillus hyphae (neutropenia after chemo or patients on highs teroids AIDS….multiple nodular infiltrateson chest CT, IgG mortality, voriconazole)
Mycotoxin-liver damage called AFLATOXIN…prob since grows in peanuts africa liver cancers
Histoplasma capsulatum 205-207, 212
Non encapsulated
Bird and bat droppings, (chicken cou)
AIDS disseminated \myxelial forms with spores at 25C, yeast at 37, no capsule,
Asymptomatic-most
Pneumonia-lesions calcific, which can be seen onc hest x ray (may look similar to tb)
Disseminated-can occur in almost any organ, espicially in the lung , spleen, or liver
Coccidiodes immitis 205-212
Mild pneumonia in normal southwest common in AIDS disseminated
Desert, respiratory transmitting
Mycelial forms at 25C, yeast at 37C
Asymptomatic most
Pneumonia
Disseminated-lints, skin, bones, meninges,
-erythema nodosum
Blastomycoses dermatidis 205-207
Soil, rotten wood, NOT MILD, weight loss, night sweats, lung involvement, skin ulcers, BBB
Mycelial forms 25 years 37
Asymptomatic-most
Pneumonia-lesions rarely calcify
Disseminated-present with weight loss, night sweats, lung involvement and skin ulcers
Cutaneous-skin ulcers
Harrisons 132 pneumonia Nd lung abscess,
101 influenza and other common viral respiratory infections
Ok
What is pneumonia
Infection of lung parenchyma, classified as community acquired (CAP) or health care-associated (HCAP)
HCAP
Hospital acquired and ventilator associated
Associated with current hospitalization for >48 h, hospitalization for > 2 days in the prior 3 months, chronic dialysis, home infusion therapy, home wound care, and contact with a family member who has multi drug resistant infection
How get pneumonia
Microorganisms gain access to the lower respiratory tract via microaspiration fromt he oropharyngeal (most common), inhalation of contaminated droplets, hematogenous spread , or contiguous extension from an infected pleural or mediastinal space
Before disease manifests, the size of the organism burden must overcome the ability of ___and other components of innate immunity (surfactant proteins A and D) to clear bacteria
Macrophages
Classic pneumonia presentation
Step p
Lobar pattern and evolves through four phases characterized by changes int he alveoli
Edema: proteinaceous exudates are present
Red hep-erythrocytes and neutrophils are present int he intraalveolar exudate
Gray hep-neutrophils and fibrin deposition are abundant
Resolution-macrophages are the dominant cel type
In VAP, respiratory bronchiolitis can __ a radiographically apparent infiltrate
Precede
Typical community acquired pneumonia
S pneumoniae, haemophilus influenza, staph aureus, and gram negative bacteria like klebsiella p and pseudomonas a
Atypical PNA
Mycoplasma pneumoniae, chlamydia pneumoniae, legionella, respiratory viruses (influenza, adenovirus, human metapneumovirus, RSV)
A virus may be responsible for a large proportion fo CAP cases that require ____, even in adults
Hospital admission
10-15% of PNA are ___
Polymicrobial
Combo of typical and atypical
When do anaerobes play a big role in CAP
Aspiration precedes presentation by days or weeks, often results in significant empyema
CAP epidemiology
> 5 million a year in US, 80% treated outpatient
> 55000 deaths annually
12 billion dollars
Who gets CAP most
<4 >60
Risk factors CAP
Alcoholism, asthma, immunosuppression, institutionalization, >70
Factors CPA
Tobacco smoke, copd, colonization with MRSA, recent hospitalization or antibiotic therapy-influence the types of pathogens that should be considered in etiology disease
Clincial manifestation CAP
Fevers, chills, sweat, cough, pleuritic chest pain, dyspnea
Nausea, vomiting, diarrhea, fatigue, HA< myalgia, arthralgias
Old patients with CAP presentation
Atypical, with confusion but few other manifestations
PE CAP
Tachypnea, increased or decreased tactile fremitus; dull or flat percussion reflecting consolidation and pleural fluid, respectively; crackles; bronchial breath sounds ; pleural friction rub
Diagnose CAP-want bc empiric tratment better for specific , also public safety implications
Chest radiography (need sensitivity and specificity not perfect from PE)
- CT for postobstructive PNA or suspected cavitary disease
- some radiographically patterns suggest an etiology (pneumatoceles suggest s aureus)
Sputum samples must have WBC>25 and <10 squamous epithelial cells per high-power field to be appropriate for culture. The sensitivity of sputum cultures is highly variable; in cases of proven bacteremic pneumococcal pneumonia, the yield of positive cultures form sputum samples<50%
Blood cultures are positive in 5-14% of cases, most commonly yielding s pneumoniae. Blood cultures are optional for most CAP pots but should performed for high risk pts (pts with chronic liver disease or asplenia)
Urine antigen tests for S pneumiae and legionella pneumophila type 1 can be helpful
PCR of nasopharyngeal swabs has become the standard for diagnosis of respiratory viral infection and is also useful for detection of many atypical bacteria
Serology: a fourfold rise in titer of specific IgM antibody can assist in diagnosis of pneumonia due to some pathogens; however, the time required to obtain a final result makes serology of limited clincial utility
What are the two sets of criteria that identify pts who will benefit from hostpail care
Pneumonia severity index
CURB-65
Complications CAP
Respiratory failure, shock, multiorgan failure, coagulopathy, and exacerbation of comorbid disease. Metastatic infection occurs rarely and requires immediate attention
-lung abscess may occur in association with aspiration or infection from single CAP pathogen (P. Aeruginosa).
Any significant pleural effusion should be tapped for diagnostic and therapeutic purposes.
Pleura effusion pH<7, glucose<2.2 LDH >1000 or if bacteria seen or cultured
Fluid should be drained, a chest tube is usually required
Follow up CAP
CXR abnormalities may require 4-12 weeks to clear. Pts should receive influenza and pneumococcal vaccines, as appropriate
Ventilator associated pneumonia micro
Potential etiology agents include MDR and non MDR pathogens; the prominence of various pathogens depends not he lengthof hospital stay at the time of infection
Epidemiology VAP
-26-52 cases per 100 pts, with the highest hazard ration in the first 5 days of mechanical ventilation
Three factors important in the pathogenesis of VAP
Colonization of the oropharynx with pathogenic microorganisms, aspiration of these organisms to the lower respiration tract, and compromise of normal host defense mechanism
Clincial manifestation
Are similar to those in other forms of pneumonia
Diagnosis VAP
Application of clinical criteria consistently results in overdiagnsis of VAP. Use quantative culture to discriminate between coloniazation and true infection by determining bacterial burden may be helpful; the more distal int he respiratory tree the diagnostic sampling, the more specific the results
What if use wrong treatment
Higher mortality rate
Treatment failrue VAP
Common, espicially MRSA, P aeruginos
VAP complications
Prolonged mechanical ventilation, increased length of ICU stay and necrotizing pneumonia with pulmonary hemorrhage or bronchiectasis. VAP is associated with significant mortality risk
Hostpital acquired pneumonia
MDR usually
Anaerobes may also be more commonly involved in non-VAP pts bc of the increased risk of macro aspiration in pts who are not incubated
Bronchiectasis etiology
Irreversible airway dilation that involves the lung in either a focal or a diffuse manner
Epidemiology bronchiectasis
Older age women
25-50% idiopathic disease
Vicious cycle of bronchiectasis
Susceptibility to infection and poor mucocele are clearance results in microbial colonization of the bronchial tree.
Noninfections bronchiectasis
Immune mediated reactions that damage the bronchial wall and parenchymal distortion as a result of lung fibrosis
Clinical manifestation bronchiectasis
Persistent productive cough with ongoing production of thick, tenacious sputum
Crackles and wheezing on lung auscultation and occasionally reveals clubbing
Acute exacerbations are associated with increased purulent sputum production
Diagnose bronchiectasis
Clincial presentation with consistent radiographically findings such as parallel tram tracks a signet ring sign, lack of bronchial tapering, bronchial wall thickening or cysts emanating from bronchial wall
Treat bronchiectasis
Control of active infection and at improving in secretion clearance
Lung abscess what is it
Necrosis and cavitation of the lung following microbial infection -can be categorized as primary )80%) or secondary; alternatively, it can be categorized as acute (<4-6 weeks in duration) or chronic (40%)
What causes primary lung abscesses
Usually arise from aspiration int he absence of an underlying pulmonary or systemic condition, are often polymicrobial (primarily including anaerobic organisms and microaerophilic streptomcin) and occur preferentially in dependent segments (posterior upper and superior lower lobes) of the right lung.
Secondary cloud abscesses
In setting of underlying condition (post obstructive process, an immunocompromised condition) and can be due to a number of different organisms among which P aeruginosa and other gram negative rods are most common
Clinical manifestations lung abscess
Similar to pneumonia.
Anaerobic lung abscess presentation
More chronic and indolent presentation, with night sweats, fatigue, and anemia, in addition, pts may have discolored phlegm and foul tasting or foul smelling sputum
Lung abscess from non anaerobic organisms (s aureus)
Present with a more fulminant course characterized by high fevers and rapid progression
Diagnose lung abscess
Chest CT is the preferred radiographically study for precise delineation of the lesion
Secondary lung abscess diagnosis
Sample collection (lovage, CT guided percutaneous aspiration) are recommended for secondary lung abscesses or when empirical therapy fails
Treat primary lung abscess
Clindamycin or amoxacilllin
Secondary lung abscess treat
Specific pathogen
When stop treat lung abscess
When cleared or small scar
Influenza A< B, C
Viruses RNA and orthomyxoviridae that have different nucleoprotein and matrix protein antigens
Major human influenza
A and B (morphologically similar)
A or B more severe
A
Influenza A subtypes by ___ and ____
Hemagglutinin(H) and neuraminidase(N) antigens
How does influenza infect
Attaches to Salic acid cel receptors via the hemagglutinin.neuraminidase degrades the receptor and plays a role in the release of virus from infected cells after replication
What is major determinant of influenza a immunity
H antigen antibodies
N antibodies
Limit viral spread and contribute to reduction of the infection
How influenza a acquired
Aerosolized respiratory secretions of acutely ill individuals and possibly by hand to hand contact or other personal or fomoterol contact. Viral shedding usually stops 2-5 days after disease onset
Epidemiology influenza A
Each year an vary in extent/severity
Winter. In temperate climates
Year round in tropics
Epidemics begins abruptly, peak over2-3 weeks, last 203 months, and then subside rapidly
Global pandemics
2009 A H1N1
Multiple locations, high attack rates, beyond normal seasonality patterns, and are duein part to the propensity of the H and N antigens to undergo periodic antigenic variation
Major changes
Antigenic shirt (INFLUENZa a only
Minor variations
Antigenic drifts
Avian influenza virus A/H51
Cause sporadic human cases, but sustained human to human transmission has not been observed; infection is linked to direct contact with infected poultry
Swine
Can sustain simultaneous infection with swine, human, and avian
Thesis multiple. Virus infections facilitate reassortment of genetic segments of different viruses.
Pandemic A/H1N1 virus 2009-2010
Quadruple reassortment among swine, avian and human influenza viruses
Interpandemic outbreaked
226,000 hospitalizations and 23,000 deaths per year in US. Chronic cardiopulmonary disease and old age are the most prominent risk factors for severe illness
Clincial manifestation influenza
Mild cold like, abrupt HA< fever, chills, myalgia, malaise
Deserves every within 2-3 days, but respiratoy symptoms accompanied by sub sternal pain can persist for >1 week. Postinfluenza asthenia may persist for weeks, particularly int he elderly
Complications influenza
Pneumonia and extrapulmonary
Common patients under 5 and over 65, pregnant women, or patients with chronic disease
Pneumonia from influenza
Primary influenza pneumonia is the least OMMonday but most severe of the pneumonic complications, most often affecting patients with mitral stenosis and pregnant-pts with progressive pulmonary disease and high timers of virus in respiratory secretions
Secondary bacterial pneumonia
Usually due to strep pneumoniae, strep aureus, or haemophilus influenza and presenters as the reappearance of fever ANS respiratory symptoms after 2-3 days of clinical improvement
Most common pneumonic complication involves aspects of viral and bacterial pneumonia
Extrapulmonary complications : Reyes’s, myositis, rhabdomyolysis, myoglobinuria, and CNS disease can occur as complications of influenza infection
Reye’s syndrome
Serious complication in children that is associated with influenza B virus (and less commonly wth influenza A virus), varicella zoster virus, and asprin therapy for the antecedent viral infection
Diagnose influenza
Reverse transcription PCR of respiratory samples
Rapid tests that detect viral antigens
Fast results, can distinguish influenza a and b viruses, and are relatively specific but variably sensitive
Serologic testing
Requires availability of acute and convalescent phase sera and is useful only retrospectively
Prophylaxis influenza
Annual vaccination with either an inactivated or a live attenuated vaccine is the main public health measure for prevention
How make vaccine
Strains are generated from influenza a and b viruses that have circulated during the previous influenza season and whose circulation during the upcoming season is predicted
Inactivated vaccines
50-80% protection against influenza is expected if the vaccine virus and the currently circulating viruses are closely related
Who gets influenza vaccine
> 6 months
Chemoprophylaxis against influenza
Should be reserved for individuals at high risk of complications who have had close contact with a pt sick with influenza. Chemoprophylaxis can be administered simultaneously with inactivated-but not with live-vaccine
Acute viral respiratory illness
> 50% of all acute illnesses; adults have 3-4 cases per person per year.
Clincial presentation acute viral respiratory illness
Not specific enough to allow an etiology diagnosis, and viral illnesses are typically grouped into clinical syndromes
Microbiology rhinovirus
Non enveloped, SsRNA viruses int he family picornaviridae that together are the major cause of the common cold
Epidemiology rhinovirus
Spread by direct contact with infected secretions, usually respiratory droplets
Clinical manifestations rhinovirus
After an incubation period of 1-2 days, pts develop rhinorrhea, sneezing, nasal congestion and sore throat that lasts for 4-9 days. Fever and other systemic signs and symptoms are unusual in adults.
-severe disease, including fatal pneumonia, is rare but has been described in immunocompromised pts, particularly bone marrow transplant recipients
Diagnose rhinovirus
PCR and tissue availbe, but not ususlal attempted
Treat rhinovirus
Symptom-antihistamines and decongestants
Coronovirus
Pleomorphic, SsRNA viruses
What coronavirus cause
Common cold SARS
Incubation period coronavirus and duration
3 days
6-7 days
2002-2003
Coronavirus SARS developed in >8000 pts in 28 countries and was associated with 10% fatality rate, no case since 2004
SARS incubation period and duration
2-7 days after which patients develop fever, malaise, HA< myalgia, and then a nonproductive cough and dyspnea
SARS patients can develop what in second week of illness
ARDS and multiorgan dysfunction
Middle East respiratory syndrome coronavirus
First identified in 2012 and has caused more than 1600 cases, with a 36% case fatality rate. All cases have been associated with contact or travel to the Arabian peninsula
-after an incubation period of 5 days, patients develop cough and fever that progress to respiratory failure
Diagnose coronavirus
ELISA, IF< reverse transcription PCR
SARS and MERS detected by R-PCR or viral culture of respiratory samples
Treat coronavirus
Common cold-symptom relief
SARS MERS-aggressive supportive care is most important . No specific therapy has been established as efficacious
Human respiratory syncytial virus
Enveloped SsRNA and a member of the paramyxoviridae
Epidemiology HRSV
With an attack rate approaching 100% among susceptible individuals, HRSV is a major respiratory pathogen among young children (2-3 months) and the foremost cause of owner respiratory disease among infants
-30-35% of hospital admissions of young children for pneumonia and for 75% of cases of bronchiolitis in this age group
Transmission HRSV
Contact with contaminated fingers or fomites and by spread of coarse aerosols. Incubation 4-6 days
Clincial manifestation HRSV
Infants typically develop rhinorrhea, low grade fever, cough, and wheezing; 35-40% of infections resul in lower tract disease, including pneumonia, bronchiolitis and tracheobronchitis
In adults HRSV typically presents as the common cold, but is can cause
Lower respiratory tract disease with fever, including severe pneumonia in patients who are elderly or immunosuppressed or who have cardiopulmonary disease. HRSV pneumonia has a case-fatality rate of 20-80% among transplant pts
Diagnosis HRSV
Rapid viral diagnosis available IF, ELISA, RTPCR of nasopharyngeal washes, aspirates or swabs
Treat HSRV
Symptom based for upper tract disease and mild lower tract disease
Incubation-if severe lower tract disease
Prevention HRSV
Monthly give palivizumab <3 years old who have bronchopulmonary dysplasia or cyanosis heart disease or who were born prematurely. In settings with high transmission rates, contact precautions are useful to limit spread of the virus
Human metapneumovius
Pleomorphic, single stranded RNA virus of the family paramyxoviridae
Epidemiology Human metaneumovirus
1-5% of childhood upper respiratory tract infections and for 2-4% of acute respiratory illnesses in ambulatory adults
Clincial human metapneumovirus
Disease manifestations are similar to those caused by HRSV
Diagnose human HRSV
IF, PCR< tissue culture of nasal aspirates or respiratory secretions
Treat human metapneumovirus
Supportive and symptom based
Parainfluenza virus
Enveloped SsRNA virus of the family paramyxoviridae ranks second only to HRSV as a cause of lower respiratory tract disease among young children and is the most common cause of croup (laryngotracheobronchitis)
Clinical manifestations parainfluenza virus
Infections are milder among children and adults, but severe , prolonged and fatal infection has been reported among pts with severe immunosuppression, including transplant recipients
Diagnosis paramyxoviridae
Infections are milder among children and adults but severe prolonged and fatal infection has been reported among pts with severe immunosuppression, including transplant recipients
Diagnoses paramyxoviridae
Tissue culture, rapid testing with immunofluorescence or ELISA (both of which are less sensitive) or PCR of respiratory tract secretions, throat swabs, or nasopharyngeal washing can detect virus
Treat parainfluenza virus
Treat URI symptom based.
For cases of croup with respiratory distress, intermittent racemis epinephrine and glucocorticoids are beneficial
Adenovirus
DsDNA virus 10% of acute respiratory infections among children and <3% of respiratory illness among civilian adults. Some serotypes are associated with outbreaks among military recruits. Transmission takes place primarily from fall to spring cia inhalation of aerosolized virus through inoculation of the conjunctival spaces, and probably via the fecal oral route
Clincial adenovirus
In children, causes upper and lower respiratory tract infections and outbreaks of pharyngojunctical fever
Adults-type 4 and 7 cause an acute respiratory disease consisting of a prominent sore throat, fever on the second or third day of illness, cough, Cory a, and regional adenoma they. Pharyngeal edema and tonsillar hypertrophy with little or no exudate may be seen
In addition to respiratory disease, adenovirus can cause diarrheal illness, hemorrhagic cystitis and epidemic keratoconjuctivitis. In patients who have received a solid organ transplant, adenovirus can affect the transplanted organ and disseminate to other organs
Diagnose adenovirus
Isolation fo the virus in tissue culture; by rapid testing of nasopharyngeal aspirates, conjunctival or respiratory secretions, urine, or stool, or by PCR testing
Treatment adenovirus
Supportive ribavirin cidofovir
Tb Harrison
Ok
Compare and contrast primary , progressice primary, latent and active Tb
Ok
Outline signs and symtpoms indicative of pulmonary Tb
Ok
Outline lab findings that are consistent with M Tb
Ok
Familiarize yourself with PPD skin testing, place emphasis on interpreting results, how the BCG vaccination affects PPD skin testing, and highlights false negative and false positive test results
Ok
Table 94-2
Ok
Describe imaging finding for primary Tb, active Tb, and Millard Tb
Ok
Define a nervy and discuss which patient populations are most likely to exhibit this phenomenon
Ok
Outline basic principles of anti Tb treatment, outline the 5 drugs used for the initial treatment of Tb . Include in your discussion potential side effects of each drug
Ok
In regards to monitoring treatment of TB, outline labs that are used to assess treatment progression and potential AE of medication
Ok
Define MDR-TB and XDR TB
List reasons for resistance
Mycobacterium TB
Acid fast
Mycotic acid, mycoside, cord factor , sulfatides, wax D MIKE WAX SURF CORD
Facultative intracellular growth in macrophages, cell mediated immunity, caseous necrosis
PPD skin test, type IV, (false positive BCG)
Mycobacterium Adium complex
AIDS-disseminated infection with fever, weight loss, hepatitis, and diarrhea
Immunocompromised-upper lung cavitary disease in elderly smokers, middle and lower lung nodular and bronchiectasis disease in middle aged femalenon smokes
Lymphadenitis-most commonly in kids
Mycobacterium kansaii
Gram positive acid fast, obligate aerobes, facultative intracellular organisms,
Pulmonary: upper lung cavitary disease
Disseminated disease in immunocompromised
Microbiology TB
Caused by organisms of the mycobacterium TB complex, which includes M Tb, most common and important agent of human mycobacteria disease, and M Boris, which is acquired via ingestion of unpasteurized milk. M Tb is a thin aerobic bacillus that is neutral on gram staining but that nice stained is acid fast. It cannot be decolonized by acid alcohol bc th cell walls high content of molecules acids and other lipids
Epidemiology TB
9 million new cases every year 1.5 million deaths-usually glow income, TB stable and falling worldwide
US T
HIV, immigrants, old, poor
MDR M TB
Resistant o at least rifampin and isoniazid and extensively drug resistant are increasing in frequency=480000 causes in 2013
How spread T
Droplet nuclei that are aerosolized by coughing, sneezing or speaking
<5-10 microV in diameter may be suspended in air for several hours
How determine intimacy of Tb and duration of contact with pt
Degree of infectiousness of the pt, and the shared environment
Cavitary or laryngeal disease
Most infectious, with as many as 10^5-10^7 acid fast bacilli in sputum
Risk factors for active TB
Recent acquisition, comobidity (HIV..), malnutrition, tobacco smoking, and presence of fibrotic lesions
Pathogenesis T
AFB that reach alveoli are ingested by macrophages. The bacilli impair phagosome maturation, multipl, lyse the macrophages, and spread to regional lymph nodes, reform which they may disseminate thought the body. Thesis initial stages of infection are generally asymptomatic and induce cellular and humoral immunity
2-4 weeks after Tb infection
A tissue damaging response resulting from delayed hypersensitivity destroys nonactivated macrophages that contain multiplying bacilli, and a macrophage activating response activates cells capable of killing AFB. A granuloma forms at the site of the primary lesion and at sites of dissemination. The lesions can then either heal by fibrosis or undergo further evolution. Despite helping, viable bacilli can remain dormant within macrophages or in necrotic material for years
______ confers partial protection against BT. Cytokines secreted by alveolar ___c ontribute to disease manifestations, granula formation and mycobacteria killing
Cell mediated immunity
Macrophages
Clinical T
Pulmonary, extrapulmonary or both
Extrapulmonary higher in HIV
Pulmonary TB primary disease
No or mild in contrast to prolonged disease course that is common in post primary or adult type
Primary Tb disease
Middle and lower lobes. Heal spontaneously, and calcified nodule (GHON FOCUS) remains
- transient hilar and paratracheal lymphadenopathy is common
- in immunosuppressed pts and children, primary disease may progress rapidly to significant clincial disease, with cavitation, pleural effusions and hematogenous dissemination (military)
Military disease
Hematogenous dissemination
Adult type TB
Initially with nonspecific and insidious signs and symptoms such as diurnal fever, night sweats, weight loss, anorexia, malaise, and weakness
- as progresses get cough, pursuant sputum with blood streaking, extensive cavitation may develop, with occasional massive hemoptysis following erosion of a vessel located int he wall of a cavity
- disease is usually localized to the apical and posterior segments of the upper lobes and superior segments of the lower lobes
Extrapulmonary T
Any site, usually lymph nodes, pleura, GU, bones, joints, meninges, peritoneum, and pericardium,
HIV and T
2.3 have extrapulmonary
Lymphadenitis T
35% extrapulmonary, esp in kids and HIV infected pts. Painless swelling of cervical and supraclavicular nodes (scrofula)
- nodes are discrete early on but can develop into a matter nontender mass with a fistulas tract
- fine needle aspiration or surgical excision biopsy of the node is requires for diagnosis. Cultures are positive 70=80%.
Pleural TB
20% extrapulmonary, from hypersensitivity response to mycobacteria antigens or contiguous spread of parenchymal inflammation
- pleural fluid is straw colored and exudative, with protein levels >50% of those in serum, normal to low glucose, and pH 7.3, and pleocytosis, the pleural concentration deaminase, of low, virtually excludes
- empyema is uncommon from rupture of a cavity with many bacilli into the pleural space. In these cases, direct smears and cultures are often positive, and surgical drainage us usually required in addition to chemo
GU T
Local symptoms predominate and 75% have a CXR with previous or concomitant pulmonary disease. Occasionally identified only after severe destructive lesions of kidney have developed.
- UA pyuria and hematuria with negative bacterial cultures
- mycobacteria culture of three morning urine specimens is diagnostic 90%
Weight bearing joints T
Most common spinal T(Potts)-often involves two or more adjacent vertebral bodies; in adults , lower thoracic/upper lumbar vertebrae are usually affected. Disease spreads to adjacent vertebral bodies, later affecting the intervertebral disk and causing collapse of vertebral bodies in advanced . Paravertebral cold abscess
Meningitis T
Kids and HIC,
1-2 weeks with paresis of CN, toward coma, with hydrocephalus and ICP high
-CSF can have high lymphocyte count an elevated protein level and a low glucose concentration. Cultures are positive in 8% of cases. PCR sensitive!!!!!
-glucocorticoids enhance survival
GI Tb
Can affect any portion of GI , ab pain, obstruction, hematochezia, palpable mass, peritonitis from ruptures lymph nodes
Pericarditis Tb
Acute or subacute onset of fever, dull retrosternal pain and friction rub, effusion common, chronic is potentially fatal,
Military disease
Hematogenous spread of M Tb through body. Small granulomas may develop in many organs. Hepatomegaly, splenomegaly, lymphadenopathy, and choroidal tubercles of eye
HIV associated TB
Partial Cell mediated compromised-typical upper lobe
Late HIV-diffuse interstitial or Millard infiltrate
Immune reconstitution inflammatory syndrome
1-3 mo after initiation antiretroviral, may exacerbate TB
Diagnose TB
AFB microscopy stained with Ziehl Neelsen basic fuchsin dyes of fluoresce microscopy of samples stained with auramine rhidamine-can provide a presumptive diagnosis in TB , two or three sputum samples need
Definitive diagnosis
Grow M Tb in culture or identification or the organisms DNA in clinical samples
-liquid media and speciation by molecular methods have decreased the time required for diagnostic confirmation 2-3 weeks
Nucleus acid amplification in AFB pos and neg
TST
Limited value active disease but mist widely used screening test for latent
Interferon gamma release assays
Measure the release of interferon gamma by T cells after stimulation with TB specific antigens and more specific for M Tb that TST
Prevent T
Vaccination
Treat latent infection
Tuberculin reaction size >5
HIV infected, recent contacts of a patient with TB , organ transplant recipients, persons with fibrotic lesions consistent with old TB on chest radiography, immunocompromised, persons with high risk medical conditions
Tuberculin reaction size >10 mm
Recent immigrants from high prevalence coutnries, injection drug users, mycobacteriology laboratory personnel; residents and employees of high risk congregate settings, children under 5, low risk
Leprosy
Nonfatal chronic infectious disease from m leprae, an obligate intracellular bacterial species indistinguishable microscopically from other mycobacteria. In humans, armadillos, and sphagnum moss
Can you culture M leprae
Not in vitro, has a doubling time in mice of 2 weeks
What is leprosy associated with
Poverty and rural residence, is a disease of developing world; its global prevalence is difficulty to assess and is variously estimated at .6-8 million
-400 in america
Transmission leprosy
Nasal drops maybe
Clinical leprosy
Polar tuberculoid to polar lepromatous disease is associated with an evolution from asymmetric localized Manuel’s and plaques to nodular and infuriated symmetric generalized skin manifestations, an increasing bacterial loss and loss of M leprae-specific cellular immunity.
Incubacliniincubation leprosy
2-40 years, usually 5-7
Tuberculoid leprosy
At the less severe end of the disease spectrum, TT leprosy results in symptoms confined to the skin and peripheral nerves ,
- one or several hypopigmented macules or plaques with sharp margins that are hypesthetic and have lost sweat glands and hair follicles are present. AFB are few or absent
- there is asymmetric enlargement of one or several peripheral nerves-most often the ulnar, posterior auricular, peroneal and posterior tibial nerves-associated with hypesthesia and myopathy
LL leprosy
Pts develop symmetrically distributed skin nodules, raised plaques and diffuse dermal infiltration that can cause leonine fancies, loss of eyebrows and lashes, pendulous earlobes and dry scaling
- numerous bacilli are present in skin, nerves, and all organs except the lungs and CNE
- nerve enlargement and damage are usually symmetric and due to bacillary invasions
Complications leprosy
Reactional states-immune mediated inflammatory states(can be deadly)
-erythema nodosum -painful erythematous papules that resolve spontaneously in 1 week
Extremities-neuropathy (insensitive to stuff, and LOSE distal digits as result),
Eyes-CN palsies, legophthalmos and corneal insensitivity may complicate …blindness
Nerve abscess-urgent surgery
Diagnosis TT
Biopsy, even in normal skin
Others not good
What are nontuberculous mycobacteria
Mycobacteria not Tb or leprosy
Miepidemiology NTM
Cause disease in humans only rarely unless some aspect of host defense impaired
Mainly M kansasii, MAC M abscesses
Clincial manifestations NTM
Broad
Dieesminated
Pulmonary disease
Isolated cervical lymphadenopathy
Skin and ST
Disseminated NTM
Rare, HIV, spread from bowel to the bone marrow and bloodstream, but disease is indolent, and it can take weeks or months for the pt to present for medical attention with malaise, fever, weight loss, organometallic, and lymphadenopathy, >3 organ systems should be evaluated for interferon y pathway defect
Pulmonary NTM
Industrialized
MAC in North America
Present with months or years of throat clearing, nagging cough, and slowly progressice fatigue. M kanassii can cause a TB like syndrome with hemoptysis, chest pain and cavitary lung disease
Isolated cervical lymphadenopathy NTM
Most common in kids in NA, MAC
Nods typically firm and painless and develop in absence of systemic symptoms
Skin ST NTM
Requires break in skin for introduction of organisms. Different NTM associated with exposures
M fortuitous
Lined to pedicure bath-skin abrasions has imediatde pedicure (like if shaved legs before pedicure)
M marinum
Acquires from fish tanks
M ulverans
Waterborne tropical and africa
Diagnose NTM
Acid fast or fluorocarbons smears of clincial samples and cultured on mycobacteria medium. Isolation of NTM from a clincial specimen may reflect colonization and requires an assessment of the organisms clincial significance
Isolation of NTM from blood specimens is clear evidence of disease; many NTM species require special media and not grown on blood culture medium
MAC
Two of three sputum samples, a positive lovage, or a pulmonary parenchyma biopsy with granulomatous inflammation or mycobacteria found on section and NTM in culture.
Antibiotic NTM
Clarromycin, MAC
Kansassi-rifampin
MAC
Macrolides bc MDR
Kansassi
Isoniazid.
M Mary I’m
Rifamycin treat extrapulmonary disease
Pulmonary htn
Describe the common cause of pulmonary HTN
Outline clinical findings of patients with pulmonary HTN, and describe the basis for assigning patients to a group
Describe common management principles in patients with pulmonary HTN
Medication induced pulmonary HTN
Fen-phen, the weight loss drug that suppresses appetites
Releases serotonin
Fatigue dizzy, SOB, primary pulmonary HTN, idiopathic pulmonary arterial HTN, heart valve disease, HF
Causes pulmonary HTN and heart disease
.smoker, normal vitals, but low O2 sat. , bibasilar inspiratory crackles. No wheeze or prolongation of the expirations phase, no neck vein distention. S4
Normal vitals but low o2, has crackles, has s4 gallop
Hypovascularoty peripheral
Right descending pulmonary artery
prominent central artery
RV enlargement
X ray of PAH
Peripheral hypovascularity, prominent central pulmonary artery (right and left prominent), right descending pulmonary artery, RV enlargement(see on lateral)-from increased workload
Classic PFT pulmonary HTN
May have features of primary cause -severe COPD low DLCO
Low diffusion capacity for CO….
Classis PAH with no DLCO
Normal PFT except isolated reduction in DLCO
ECG PAH
RVH, RV strain, RAD
Right axis deviation, right ventricular hypertrophy
May see peaking of p wave—-right atrial enlargement .
Echo PAH
Increased estimated PA pressure
RA enlargement
RV enlargement
Is pulmonary HTN common
Pretty common
Idiopathic uncommon
Treat pulmonary HTN
Treatment is the treatment of underlying disease
Idiopathic HTN is common?
No…specific therapies are changing very rapidly
Group 1 pulmonary HTN
Idiopathic and CTD
Group 2 pulmonary HTN
Heart
Group 3 pulmonary HTN
Lung
