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3 main types airborne transmission
infected to susceptible by cough, sneeze, talk
pathogen is attached to aerosolized mucus/saliva
dust contaminated with pathogen to susceptible person
from aerosols of water
AC, jacuzzi sprays
upper respiratory system parts
sinuses
nasal cavity
auditory tube opening
pharynx
uvula
lower respiratory parts
epiglottis
larynx
trachea
pleurae
bronchus
bronchiole
part of respiratory system but not included in upper or lower
diaphragm
3 diseases upper
Streptococcal pharyngitis
Scarlet fever
Diphtheria
3 diseases lower
Tuberculosis
Bacterial pneumonias
Legionnaires’ Disease
inflammation related
usually 1st part affected gets inflamed
red swell pain hot
rubor tumor dolor calor
Strep throat causative agent
Streptococcus pyogenes
G+ cocci
strep throat transmission
airborne droplets
Strep throat symptoms
fever but no runny nose
red pharyngeal tissues from tissue erosion
purulent (pus containing) abscesses covering tonsils
strep throat pathogenicity/virulence factors 3 brief
M protein
Streptokinase
Streptolysin
M protein
Strep throat virulence factor
destabilizes complement (C3b) which would form MAC
retards phagocytosis
>60 types immunity difficult
adhesin specific to S. pyogenes
Streptokinase
strep throat virulence factor
breaks blood clots
allows bacteria spread through damaged tissues
Streptolysin
strep throat virulence factor
lyses erythrocytes, leukocytes, platelets
classification of streptococci 2
blood agar - differential hemolytic properties
lancefield groups
3 hemolytic properties
gamma (y) no effect no change
alpha (a) partial destruction - olive green cells
beta (b) complete destruction - clear zone around cells/yellow
lancefield groups
serological classification of streptococci based on cell wall antigens designated groups A-O
group streptococci worst for humans
Group A beta (b) hemolytic
most common Group A, b hemolytic
Streptococcus pyogenes
worst for humans
other conditions resulting from pathogenic streptococcus
scarlet fever
erysipelas
scarlet fever picture
bright red tongue
scarlet fever
strep throat w skin rash caused by S. pyogenes with a lysogenized bacteriophage
scarlet fever bacteriophage
temperate bacteriophage genome encodes erythrogenic toxin
scarlet fever red rash
caused by blood leaking through walls of capillaries damaged by toxin
shows most in soft skin areas of mouth, neck, chest
erysipelas
acute infection of dermal layer with streptococcus
erysipelas symptoms
painful reddish patches recur periodically at same body site
erysipelas patients
infants/people >30 with history strep throat
erysipelas image
face red patch sharpie outline
Diphtheria causative agent
Corynebacterium diphtheriae
G+ rod w metachromatic granules (stains dark)
remains partially attached after division > chinese lettering/angular/palisade arrangement
diphtheria transmission
inhaling respiratory droplets near tonsils
diphtheria pathogenicity
exotoxin encoded by lysogenic corynephage (virus only infect corynebacterium)
lysogenic corynephage’s exotoxin
diphtheria pathogenicity
composed of 2 polypeps bind human growth factor receptor on human cell
triggers endocytosis
destroys euk elongation factor blocking protein synthesis
diphtheria symptoms
pseudomembrane
made of mucus, dead cells, fibrous material
respiratory blockage fatal
diphtheria treatment
target toxin - antitoxin and antibiotics
supportive treatment - tracheostomy tube
diphtheria prevention
vaccinate with DTaP
toxoid for diphtheria
tuberculosis
lower respiratory disease caused by Mycobacterium tuberculosis
in developing countries most deaths than from any other bacterial disease
pic: copper tubes grow cells
mycobacterium unique characteristics (4)
cell wall has waxy lipid mycolic acid
slow growth could not know for decade
protection from lysis after phagocytosis, not crunchy
capacity for intracellular growth
Mycobacterium resistance to (4)
gram staining - only stained by acid fast procedure
detergents
many antimicrobial drugs
desiccation can survive in dried aerosol droplets for 8 months
2 types mycobacterium and disease they cause
Mycobacterium leprae: Leprosy/Hansen’s Disease
Mycobacterium tuberculosis: Tuberculosis
Tuberculosis transmission
M. tuberculosis inhaled into lungs
usually multiple exposures
see with chest xray
tuberculosis pathogenicity/virulence factors (2)
Mycolic acid - protects bacteria from lysis once phagocytosed
Cord factor - daughter cells remain attached to one another parallel alignment - inhibits migration neutrophils - toxic to mammalian cells
how tuberculosis starts
M. tuberculosis enters alveolus
10% ill in 3 months - cough, chest pain, fever, blood in sputum
90% only fever, weight loss
Tubercle formation - living bacteria, WBC, salts, fibrous materials
detect with xray
secondary/reactivated tuberculosis
body loses fight - reinfection of lungs
tubercles break, spread in lungs
common w immunosuppression
disseminated/miliary tuberculosis
tubercle break and spread bacteria via lymph and blood
to liver, kidneys, meninges, bone marrow
leads to consumption of tissues
development tuberculosis in lungs
respiratory droplets enter alveoli
phagocytosed by macrophage but not lysed
incipient tubercle - few macrophages with bacterium - 1° infection
macrophages stick together try wall off
inside tubercle dies - caseous necrosis - tubercle surrounded by collagen fibers
ruptured tubercle spreads out - 2° reactivated tuberculosis
tuberculosis diagnosis/detection
detect M. tuberculosis in sputum sample - long time wait 3 weeks
tuberculin skin test - inject 0.1mL M. tuberculosis cell wall antigens (just parts)
xray detect tubercles
tuberculosis treatment
common antimicrobials ineffective
combination therapy used for months treat disease
isoniazid, rifampin, ethambutol
6-9 months skip day lose pressure
DOT directly observed treatment
tuberculosis prevention
immunization with BCG vaccines where TB common
no vaccine in US
BCG bacille camille gueria - TB in cows
tuberculosis new threats
MDR-TB multi-drug resistant
XDR-TB extensively drug resistant
public health will track down
pneumonia
condition - inflammation of lungs - alveoli and bronchioles become filled w fluid
can be caused by bacteria, viruses, fungi
most prevalent - pneumococcal pneumonia
some patients
empynema - fluid in alveoli is pus
pleurisy - pleurae inflamed tight hard breathe
pneumococcal pneumonia causative agent
Streptococcus pneumoniae
G+ capsule diplococcus
pneumococcal pneumonia transmission and symptoms
airborne droplets
fever, fatigue, hacking cough
usually only compromised affected - elderly, malnourished, smokers, viral infected, hospital patients, chemo, transplants
most often secondary disease
pneumococcal pneumonia pathogenicity/virulence factors (3)
capsule - prevents phagocytosis
pneumolysin
IgA protease
pneumolysin
virulence factor pneumococcal pneumonia
binds cholesterol in ciliated epithelial cells cause lysis of cells
IgA protease
pneumococcal pneumonia virulence factor
destroys IgA in mucus
damage to lining alveoli allows fluid enter lungs
primary atypical pneumonia causative agent
mycoplasma pnuemoniae
no cell wall - if put in liquid change shape
pleomorphic
one of smallest bacteria cause human disease
causes epidemics in crowded places
primary atypical pneumonia who affect
primary disease - occurs in healthy people
mainly high school and college students
primary atypical pneumonia symptoms
fever, dry hacking cough, fatigue
primary atypical pneumonia pathogenicity
bacteria attach base of cilia cause cilia stop beating
colonization destroys epithelial cells lining respiratory tract
primary atypical pneumonia treatment
erythromycin or tetracycline
not penicillin bc no cell wall
legionnaire’s disease
aka legionellosis
1976 outbreak among