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Immuno mikro eng > Lower Respiratory Tract infections > Flashcards

Lower Respiratory Tract infections Flashcards

1
Q

What is the key determinant of pneumonia?

A

Age. Viruses predominate in childhood, and bacteria cause secondary infections

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2
Q

What are the two types of adult pneumonia + their risk factors?

A
  1. Community acquired - risk factors include alcohol abuse, occupational exposure, or underlying condition
  2. Nosocomial - immunocompromised or ventilation
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3
Q

What is “atypical pneumonia”?

A

Pneumonia caused by a pathogen other than Streptococcus pneumoniae

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4
Q

How is the capsule of pneumococcus involved in pathogenesis in the lungs?

A

Prevents C3b complement deposition and engulfment via alveolar macrophages. Capsule also facilitates evasion of lung surfactant

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5
Q

What is the function of pneumolysin and its role in pathogenesis of pneumonia?

A

Binds cholesterol, forms a large pore in cell membrane (similar to SLO of GAS or alpha-toxin of S. aureus)

Facilitates evasion of immune response, clearance from nasopharynx. Permits spread from alveoli to bloodstream for bacteremia. Also fixes complement, for immune response.

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6
Q

Other than pneumolysin, what is another major virulence factor that ellicits an inflammatory response?

A

Cell wall techoic acid and peptidoglycan

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7
Q

Of B. pertussis and S. pneumoniae, which one is only a human pathogen?

A

THEY BOTH ARE!!

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8
Q

How does pneumococcus relate to AIDS?

A

Recurrent pneumococcal pneumonia is a presenting manifestation of AIDS (along with Candida esophagitis from earlier)

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9
Q

Why are stroke, alcoholism, drugs, anesthesia, and viral infection all risk factors of pneumococcal pneumonia?

A

Compromised cough reflex allows pneumococcal entrance into lower respiratory tract

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10
Q

What antibody usually facilitates clearance of pneumococcus from the lower respiratory tract?

A

Anti-capsular

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11
Q

What is the primary cause of death in pneumococcal pneumonia?

A

Rusty lobar (sketchy) pneumonia occurs, with purulent material in alveoli. Inflammation leads to increase in vascular permeability -> fluid accumulation. Disrupted gas exchange due to fluid will suffocate patient

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12
Q

What are two secondary complications of pneumonia?

A
  1. Bacteremia from inflammation

2. Resultant meningitis due to vascular endothelial death and entrance across blood-brain barrier

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13
Q

What is the primary diagnostic tool of pneumonia and what is a common problem?

A

Sputum is gram-stained -> should be monomicrobial and contain PMNs

Problem: contamination with oropharynx microbes + saliva which can be polymicrobial and have squamous epithelium

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14
Q

What is a common radiological finding of pneumococcal pneumonia?

A

Bronchopneumia which consolidates to lobar pneumonia “rusty pneumonia”

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15
Q

How does encapsulated vs nonencapsulated Hemophilius influenza pneumonia differ?

A

Non-encapsulated (non-typable) - more common due to higher carrier rate, lower virulence

Encapsulated (type b) - less common, higher virulence and presents like S. pneumoniae, higher incidence of positive blood cultures vs non-typable

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16
Q

What is a hallmark presentation of Hib in 2-5 year old children?

A

Pneumonia and cherry red epiglottis (epiglottitis)

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17
Q

What are the predisposing factors of pneumonia via nontypable H. influenzae?

A
  1. COPD
  2. Emphysema
  3. Chronic bronchitis
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18
Q

What is the morphology and growth requirements of Hemophilus influenzae?

A

Small, gram negative coccobacillary rods

Requires factor 5 (nicotinamide) and factor 10 (hematin) for growth

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19
Q

What are the major virulence factors of Legionella pneumophila?

A
  1. Outer membrane proteins for macrophage entry
  2. Metalloprotease similar to elastase of P. aeruginosa
  3. dot locus
  4. Phospholipase C
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20
Q

What is the function of the dot locus in legionella?

A

dot = defect in organelle trafficking, prevents phagolyososome fusion in macrophages carrying Legionella, and recruits ribosomes to lysosome for nucleotides / amino acids

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21
Q

What is the function of PLC for Legionella?

A

Damages phospholipid membranes of eukaryotic cells, permitting engulfed bacteria to escape from phagocytic vesicle

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22
Q

How do Legionella species typically survive in the environment?

A

They are parasites of freshwater and soil protozoa / amoeba (i.e. Acanthamoeba, Naeglaria), and thus live in reservoirs of amoeba/bacteria -> cooling towers of A/c systems, plumbing especially showerheads and faucet aerators, hospital respiratory therapy equipment

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23
Q

How is Legionella spread?

A

Typically via aerosolization through air conditioning ducts or shower heads and inhaled. Living inside amoeba makes it more resistant to disinfection. Cannot be spread person to person

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24
Q

What are the two diseases caused by Legionella? What are the clinical characteristics?

A
  1. Legionnaire’s Disease - severe lobar pnuemonia causing hyponatremia, diarrhea, headaches, confusion, and high fever
  2. Pontiac fever - Shorter incubation, self limiting, malaise which is less severe than the pneumonia (less virulent or dead strains)
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25
Q

What are the mechanisms by which Legionella enters the macrophage?

A
  1. Has surface protein for C3 binding and complement-mediated phagocytosis
  2. “Coiling phagocytosis” - induces alveolar macrophage uptake in the absence of opsonization via phagocytosis
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26
Q

How is Legionella rapidly diagnosed?

A

Urine soluble antigen testing, or need a direct lung biopsy since the organism is rarely found in the sputum

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27
Q

How is Legionella typically stained?

A

Gram stains poorly although it is a gram negative rod, can be visualized via silver staining

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28
Q

What does Acetinobacter cause?

A

Pneumonia or serious blood/wound infections in immunocompromised

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29
Q

What is significant about Acetinobacter and what is its morphology?

A

It is multiple-drug resistant and nosocomial, with a high incidence in U.S. Gulf War soldiers

Morphology: gram negative coccobacillus (similar to H. influenzae or B. pertussis)

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30
Q

What are the three major virulence factors of Mycoplasma pneumoniae?

A
  1. Adhesin - which binds sialic acid-containing glycolipids / proteins on bronchial epithelium
  2. Hydrogen peroxide and superoxide radicals to cause tissue damage
  3. Autoantibodies react with many body tissues due to homology between host cells and mycoplasma glycolipids
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31
Q

What type of pneumonia is characteristic of Mycoplasma and who gets it?

A

Highly infectious pneumonia often had by young people (<30 years) living in close quarters (i.e. military), called “walking pneumonia”

X-ray appears way worse than it actually is, with diffuse infiltrates

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32
Q

How is Mycoplasma cultured and detected?

A

Cultured on Eaton’s agar, lacks a cell wall and has a very small genome (Gram indeterminate). Sputum will not show organisms and organism grows very slowly.

Often detected via serodiagnosis for IgM antibodies

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33
Q

What are the two forms of Chlamydia pneumonia?

A
  1. Elementary body (EB) - enters the columnar epithelial cells of bronchioles
  2. Reticulate body (RB) - replicate and rely on host ATP before reorganizing into elementary bodies
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34
Q

What is the clinical presentation of Chlamydia pneumonia?

A

Atypical or walking pneumonia, similar clinical picture to Mycoplasma pneumoniae, presents in schoolchildren or young adults.

Can also cause pharyngitis and bronchitis

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35
Q

What is the morphology of Chlamydia pneumonia and how can it be told from Chlamydia trachomatis?

A

Gram negative outer membrane but no cell wall, coccobacillus

Can be told apart via RNA / PCR, or importantly does NOT form “glycogen-containing inclusion bodies” like C. trachomatis

36
Q

In what scenario does S. aureus cause pneumonia?

A

Secondary to some other lung insult such as influenza, with pathology similar to other bacterial pneumonias

37
Q

What is empyema?

A

Purulent infection of pleural space via Staph aureus. Can also cause lung abscess.

38
Q

What are the two main virulence factors of M. tuberculosis and how do they work?

A
  1. Mycolic acid (cord factor) - consists of long chain fatty acids >60C, provides resistance to disinfection and drying. Cord factor is a mycolic acid complex which promotes hypersensitivity granuloma via TNFalpha and tissue damage
  2. Lipoarabinomannan - glycolipid which suppresses T cell prolferation and prevents macrophage activation
39
Q

What are the symptoms of Mycobacterium avium complex and who does it infect?

A

TB-like disease causing fever and wasting, as well as diarrhea

Infects immunocompromised, especially AIDS patients with CD4 < 50 cells / mL

40
Q

What is Hansen’s disease?

A

Leprosy - degenerative disease of skin and nerves caused by Mycobacterium leprae

41
Q

Who most often gets TB?

A

AIDS patients (immunocompromised reactivation of primary infection) and immigrants (From developing world)

Outbreaks are in closed communities

42
Q

Where does reactivation TB most often grow and why?

A

In the apex of the lung, which has the highest oxygen tension (greatest relative ventilation / perfusion ratio, most available oxygen for M. tuberculosis to use)

43
Q

What are the symptoms of primary TB in most people and what can it progress to?

A

In 95% of people, infection is quickly resolved with a localized lung lesion.

In 5%, can cause disseminated infection with nodules forming around the body like millet seed, called “miliary TB”

44
Q

What is a Gohn complex?

A

The lung granuloma + enlarged hilar lymph nodes characteristic of primary TB infection

45
Q

What are the most common sites of miliary / disseminated TB and how does this happen?

A

Granulomas are broken up / necrotic tubercles erode, and TB disseminates into small granulomas around the body.

Common sites: Liver, spleen, bone, and meninges

46
Q

What are the common causes of reactivation TB?

A

Age, immunocompromised, alcoholism, diabetes

47
Q

Why does TB primarily grow in the lung?

A

It is an obligate aerobe

48
Q

How does TB grow in the lung?

A

Engulfed by alveolar macrophages and carried to lymph nodes, disallows phagolysosome fusion and grows intracellularly

49
Q

What is the cell-mediated response to TB?

A

Helper and cytotoxic T cells activate alveolar macrophages, which prevent replication of TB and wall off the bacteria, forming a granuloma. It has a caseous (cheesy) and necrotic consistency

50
Q

What causes the characteristic fever and weight loss of TB?

A

Cytokine response to organism (TNF). Loss of this will cause reactivation / disseminated TB

51
Q

Why is loss of DTH reaction to PPD a bad sign? How does the tuberculin test work?

A

It is a bad prognostic indicator because it means there is no immune response to the organism.

PPD / Tuberculin skin test is autolyzed bacteria containing antigens which are injected into skin and should cause DTH reaction. (Mantoux test)

52
Q

When does DTH first become positive?

A

About 6 weeks after primary infection, when the first hypersensitivity granulomas are being formed

53
Q

What stain is used for TB?

A

Ziehl-Neelsen - acid-fast stain which collects in the Mycobacterial mycolic acids

54
Q

When are IFNy-release assays used?

A

When patients are vaccinated with BCG or HIV Mantoux-test negative, uses a different TB antigen than BCG, measure T cell IFNy release in response to antigens.

55
Q

What is P. aeruginosa’s primary two virulence factors for survival in the lung?

A
  1. Alginate capsule - mucoid phenotype in lungs

2. Elastase - degradation of lung elastin

56
Q

How is P. aeruginosa MDR?

A

Mutations leads to loss of porin and decreased entry of antimicrobials, and LPS can be altered so it doesn’t bind Antibiotics

57
Q

What bacteria, other than S. aureus, can cause acute pneumonia, empyema, and abscess?

A

P. aeruginosa

58
Q

Who is most prone to P. aeruginosa pneumonia and what particular age group?

A

CF patients, because excess mucus provides physical barrier to drugs. Early in the disease they are haunted by S. aureus, later it’s multiple-drug resistant P. aeruginosa

59
Q

What are the defining characteristics of P. aeruginosa?

A

Gram negative rod
Oxidase positive
Identified by oxidative metabolism in OF dextrose tubes

60
Q

What causes Farmer’s lung?

A

Inhalation of large numbers of infectious conidia of Aspergillus, leading to acute pneumonia / lung abscess by the environmental mold

61
Q

What factors predispose someone to Aspergillus infection? What is the primary host defense?

A

Asthma, chronic bronchitis, TB (due to causing cavitation for aspergillosis), and immunosuppression

Primary host defense is neutrophils which act on invasive hyphae

62
Q

How is Aspergillus identified clinically?

A

Lung aspiration, bronchial lavage, or biopsy

-> will be easily identified, grows well

63
Q

How does Histoplasma capsulatum grow?

A

It is dimorphic, but its yeast form grows within human macrophages and survives oxidative bursts

64
Q

Where is Histoplasma found?

A

Grows in soil, especially with abundance of bird and bat droppings, in Ohio / Mississippi River Valleys

65
Q

What type of disease does Histoplasma cause and how common is this?

A

Causes TB-like disease, with primary lesions resembling pulmonary TB. Exposure is common but disease is rare. Activated macrophages via T cells will inhibit intracellular growth

66
Q

How is Histoplasma clinically identified?

A

Grows slowly over weeks on blood and Sabouraud agar. Typically has TB-like X-ray findings on exam. Sputum sample will not be useful - biopsy required

67
Q

What test is used to determine past Histo exposure?

A

Serological tests for DTH reaction with mycelial antigen - cross-reactive with other pathogens.

This can also be done by urine antigen testing.

68
Q

What is the major pathogenic difference of Blastomyces dermatitidis from H. capsulatum?

A

B. dermatitidis yeast cells are extracellular, not in macrophages

69
Q

What are the 3 B’s of Blastomyces?

A

Blastomyces - Broad Based Budding

They form large, thick-walled yeast cells with large buds

70
Q

What is the geographic distrubution of Blastomyces vs Histo?

A

Same area - middle / southeastern US

71
Q

What is the lung presentation of Blasto?

A

Chronic pneumonia may mimic pulmonary tumor or TB

72
Q

Where does Blasto typically disseminate to?

A

The skin very commonly (dermatiditis), but also the bone (osteomyelitis)

Leads to necrosis and fibrosis at infected area -> disfigurement

73
Q

What is the only good way to identify Blasto?

A

Via biopsy for yeast with broad buds -> there is no skin test and antigenic cross-reactivity is too high

74
Q

What are the growth phases of Coccidioides immitis? How do these evade immune response

A

Dimorphic

Infectious arthroconidia

Spherules are invasive tissue form which prevent phagolysosome fusion by neutrophils / macrophages. They reproduce via endospores.

Spores cause a large inflammatory response and cause formation of granulomas.

75
Q

What and where in the US is the infection caused by Coccidioides? What are the stages?

A

Valley fever - Southwestern US

cough, chest pain, and myalgia which can become chronic pneumonia in T-cell compromised and disseminate to skin and bones

76
Q

Are Histo and Coccidioides infections always obvious?

A

No, most cases are subclinical

77
Q

What T / B cell combinations indicate a poor vs good response to Coccidioides?

A

Immunity is primarily T-cell mediated
Good: Strong T cell response with little antibody
Bad: Increased non-protective B cell response (complement fixation does not work)

78
Q

What are the primary diagnostic methods of Coccidioides?

A
  1. Spherules on histological biopsy
  2. Coccidioidan DTH test - positive 1-4 weeks after onset
  3. Immunoassay
79
Q

How is Coccidioides spread?

A

Via dust carrying arthroconidia. Incidence has been increasing due to global warming

80
Q

What are the relative sizes of Histo, Blasto, and Coccidio?

A

Coccidio > Blasto > Histo

Blasto is ~ same size as RBC

81
Q

Is Pneumocystis jiroveci a common infection, and how can it be spread?

A

Yes, common infection with low virulence. 75% of people have antibodies by age 4.

Aerosol transmission, often from healthcare workers to immunocompromised like cancer wards and premature infants

82
Q

What is the most common opportunistic infection in AIDS?

A

Pneumocytosis - loss of T cell function when count falls below 200 cells / mL

83
Q

What is done to get a PCP sample?

A

Bronchoalveolar lavage for a sputum sample via hypertonic saline, especially in AIDS patients since they normally won’t produce sputum.

Can also biopsy

84
Q

How is PCP diagnosed once a sample is taken?

A

Histologically - extracellular cysts + trophozoites seen by fluorescence microscopy or Giemsa stain.

Can also immunofluoresce via monoclonal antibody, or PCR

85
Q

What are the clinical symptoms of pneumocystosis? How do patients die?

A

Mild or low grade fever
Typical signs of pneumonia absent - NONPRODUCTIVE COUGH
Progressive dyspnea and tachypnea with cyanosis due to hypoxia.

Patients die by asphyxiation

86
Q

What is seen on X-ray in PCP pneumonia?

A

Wispy, diffuse infiltrates -> no lobar consolidation or granulomas

Immuno mikro eng (56 decks)

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