Respiratory Flashcards
Streptococcus pneumonae characteristics:
Gram + cocci
lancet shapped diplococci
Alpha hemolytic on blood agar
Catalase negative
colonizes upper respiratory tract, important cause of infection in normally sterile parts of tract
Streptococcus pneumonae immunity:
Antibody requires days to develop
90 different CPS that prevent phagocytosis (antigenic variation)
Streptococcus pneumonae Epidemiology:
Mucosal surface of nasopharynx, humans are the only host
most common in non-immune hosts (infants and elderly)
also common when there is impaired antibody production or defective clearance of opsonized bacteria
Diseases caused by Streptococcus pneumonae
-lobar pneumoina: most common community acquired pneumococcal pneumonia
shows patchy alveoli filled with acute inflammatory cells (structure in tact so usually clears with no damage)
Treatment of Streptococcus pneumonae:
altered penicillin binding proteins reduced affinity for penicillin
PBP confers resistance to most beta lactams
natural transformability exchanges these altered genes
resistant to most beta lactams - but can still be useful if concentration used is above organisms MIC (minimum inhibitory concentration)
Hemophilus influenzae characteristics:
- gram negative coccobacillus
- colonized upper respiratory tract
- requires two growth factors found in blood: hematin and NAD+
- 6 types of capsules, B most virulent
- resides in human nasopharynx
- encapsulated strains cause invasive infection
- nontypeable strains are unencapsulated, cause only upper respiratory tract infections
Hemophilus influenzae epidemiology:
- nontypeable is leading cause of acute otitis media and conjuctivitis in children
- COPD: chronic bronchitis in adults
Middle ear infections:
- common in children
- fluid in middle ear space
- becomes infected with organisms in the upper respiratory tract
Hemophilus influenzae type B:
- most virulent
- immunity based on antibody to CPS
- controlled by immunization to type B
Hemophilus influenzae treatment:
- most are still sensitive to penicillin
- when resistant it is due to expression of beta lactamase so cephalosporins still effective
Neisseria meningitidis characteristics:
- gram negative bean shaped diplococcus
- identical staining to neisseria gonorrhoeae
- ultrastructural level has a prominent antiphagocytic polusaccharide capsule
- 12 serogroups (A, B, C, Y and W-135 predominant)
- antigenic varriation
- DOES NOT CAUSE PNEUMONIA
Neisseria meningitidis epidemiology:
- nasopharynx
- older children, young adults (dorms, barracks)
- resides in the upper respiratory tract but DOES NOT CAUSE DISEASE THERE
Neisseria meningitidis treatment:
- penicillan
- third generation cephalosporin
- vaccine (none to serogroup B)
- antibiotic prophylaxis in outbreaks
Clinical diseases by Neisseria meningitidis:
- two presentations:
1) meningococcemia: skin lesions (petechiae and purpura), sepsis fulminant disease
2) acute bacterial meningitis
Bordetella pertussis characteristics:
- gram negative coccobacillus of upper respiratory tract
- whooping cough
- ciliated surfaces of the upper respiratory tract
Bordetella pertussis toxin:
- sense environmental signals such as temp which causes changes in gene regulation
- ADP ribosylates adenylate cyclase G regulatory protein which prevents inhibition of adenylate cyclase (increases cAMP)
- increased cAMP promotes respiratory secretions and reduces phagocytic activity
- toxin causes marked lymphocytosis (high lymphocytes) which is a hallmark of the disease
- toxin-mediated damage to the respiratory epithelium results in prolonged illness characterized by PAROXYSMAL COUGH
Bordetella pertussis stages of disease:
1) catarrhal stage: same as viral upper respiratory tract infection
2) paroxysmal stage: coughing, may not have whoop
3) convalescent stage: 100 day cough, complications in infants who may acquire pneumonia or apnea
Bordetella pertussis epidemiology:
- high mortality in infants, spread by adults
- HIGHLY contagious
Bordetella pertussis prevention:
- diagnosis by fluorescent antibody testing or culture swab with non-routine medium (Bordet-Gengou)
- treat with erythromycin or macrocodes
- treat close contact
- Immunization: acellular vaccine (DTaP), boosters for adults
mycoplasma pneumoniae:
- extracellular pathogen
- mollicutes class: NO CELL WALL, does not take up gram stain
- not killed by penicillins or beta lactam antibiotics
- “atypical” pneumonia
- test with serology or PCR, not routinely grown in labs
- intersitial infiltrates on multiple lobes
“WALKING PNEUMONIA”
Pseudomonas aeruginosa:
- ubiquitous, opportunistic pathogen
- gram negative rod
- aerobic
- minimal growth requirements, lives in many environments
- easy to grow in lab: oxidase positive, non-lactose fermenting, pigmented and smells sweet (smell of the locker room is this bacteria)
Pseudomonas aeruginosa epidemiology:
- thrives in warm, moist, air, damage
- environmental, not host
- many hospital sinks, basins, toilets, etc
Pseudomonas aeruginosa pathogenesis:
- limits neutrophil mediated clearance by contact dependent injection of toxins
- airways on CF patients become chronically infected
Pseudomonas aeruginosa diseases:
- Pulmonary: nosocomial pneumonia, chronic CF infections
- Skin: hot tub folliculitis, infections of burns
- otitis externea: swimmer’s eart
- corneal infections
- bacteremia: vascular catheter infections, neutropenic patients
biofilms:
bacteria growing on a surface
- dynamic microbial community encased in an extracellular matrix
- frequent mode of growth for pseudomonas
- enhanced resistance to antibiotics
Pseudomonas aeruginosa treatment:
- antibiotic resistance is major problem
- produce beta lactamases, mutations in porins reduce uptake, exchange of plasmids encoding resistance, reduced susceptibility of biofilms
- use anti-pseudomonal penicillins or 4th generation cephalosporins
- combinations for synergistic (IE) anti-pseudomonal penicillin and aminoglycoside
- no vaccine
Other difficult to treat gram negative rods:
- opportunistic respiratory
- burkholderia cepacia
- stenotrophomonas maltophilia
- acinetobacter species
- KPS: klebsiella pneumoniae produces extended sprectrum beta lactase
Legionela pneumophila:
- accidental human pathogen
- causes legionaires diseases
- gram negative motile coccobacilli
- non-fermentative
- poor gram stain
- parasite of aquatic protozoa (amoebae)
- falsely recognizes macrophages in human as natural host (survives in macrophage vacuole)
Legionela pneumophila epidemiology:
- water system outbreaks
- more common in elderly
- correlation with heavy tobacco/alcohol use
- men more likely to get infected
- no person to person spread
Legionela pneumophila diseases:
- infections
- pneumonia and extra-pulmonary complications
Legionela pneumophila treatment:
-macrolides or fluoroquinolones
