Organ System Power Point

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Transcript Organ System Power Point

Topics in Microbiology
Organ Systems
2007
Respiratory Tract - Upper
RT
• Bronchioles branch to form the terminal
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bronchioles
The terminal bronchioles form the
respiratory bronchioles
The respiratory bronchioles branch into
alveoli
It is in the alveoli that gas exchange occurs
The surface of the lungs( pleura) and the
cavities that they occupy secrete a serous
fluid that lubricates
Infections are airborne and aerosolized in
Respiratory Tree
Ears
• Exposed to the environment
• Pinna - Flaps are somewhat protective
• Auditory canal contains hairs and secretes
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cerumen a product related to sebum.
Ceruminous glands in the ear produce this
product
Tympanic membrane separates the middle and
inner ear( compartmentalizaton)
Ear infections
• Most middle ear infections arise from the
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microorganisms that move up the Eustachian
tube from the nasopharynx
Younger children have more infections
because of the fact that their auditory tubes
are shorter and wider
Inner ear infections are rare - If the mastoid
area of the cranium becomes infected,
causing mastoiditis, there is danger that the
infection could reach the brain
Respiratory status
• Healthy lungs are sterile
• Organsims found in the trachea and
bronchi are normally transient
• Most are removed by the mucocilary
escalator( cilia roll bacteria into ball and
the microbes are pushed upward,
coughing and sneezing can expel the
organisms
Macrophages
• Macrophages are found in the
respiratory tree where they engulf both
organisms and debris
Elusive microbes in the respiratory tree
• Mycobacterium tuberculosis are able to
remain airborne through the trachea
and bronchi
• This organism can survive and multiply
inside of macrophages
• The organism can cause problems by
impairing the coughing reflex and can
even threaten the alveoli
Mycobacterium are Acid Fast
• Outer waxy cell wall
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made from mycolic
acid
A great proportion
of genome is
directed at cell wall
Slow grower
Eludes macrophages
Klebsiella pneumoniae
• Does not colonize
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upper respiratory
tract but may be
present
Passes down the
respiratory tract
Streptococcal Pharyngitis
• About 10% of cases of
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pharyngitis are caused by
Streptococcus pyogenes, Group
A Beta Hemolytic strep
Some individuals are carriers
Inhaled in the form of droplets
Adenoids and lymph nodes in the
neck swell
Pus like lesions are found in the
back of the throat
High fever
Scarlet fever can be caused by
the presence of a phage
Sinusitis - Inflammation of the sinuses
• Staphylococcus
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aureus
H. influenzae
Moraxella
catarrhalis
Streptococcus
pneumoniae
Bacteroides
• Chronic sinusitis may be
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caused by Bacteroides
Roots of the upper
teeth are very close to
the maxillary sinuses
Treatment may include
application of a warm
cloth, drainage, and
antibiotic therapy
Moraxella catarrhalis
• Moraxella
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catarrhalis is a gram
negative oxidase
positive bacterium
Affects people with
chronic condition
and smokers
Leads to
bronchopneumoniae
Diptheria
• Caused by
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Cornybacterium
diptheriae
Club shaped cells
Found in side by side
structures called
palisades
Diptheria
• Sequelae are adverse
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signs that accompany
diptheria
Diptheria basically
affects the nose and
the throat
Myocarditis inflammation of the
heart
Polyneuritis - an
inflammation of the
nerves
Paralysis can occur in
rare cases
Diptheria
• Caused by a
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bacteriophage prophage - lysogenic
phage
Produces an
exotoxin
Otitis media with effusion
• Passage of pharyngeal
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organisms through the
Eustachian tube
Fever and earache arise
from pressure the pus
creates in the middle
ear
The accumulation of
fluid in this area can
interfere with hearing
Tube can be inserted to
prevent middle ear
infections
The Common Cold
• Caused by Rhinoviruses
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and Coronaviruses
Most infections occur in
the spring and fall
Rhinoviruses grow best
in the epithelium of the
upper respiratory tract
113 Rhinoviruses have
been identified
Natural immunity is
rare
Corona virus
Fomites
• Cold viruses spread by contact with touching
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anything that has come into contact with the
infected person
If a person blows his nose and then places a
Kleenex on the school desk, then the next
student who touches the desk, can get the
virus on his hands
Door handles
Shared drink bottles
Parainfluenza
• Paramyxoviruses
• Initially attack the mucous membranes of the
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nose and throat
Cough and hoarseness after two - three days
Barking cough
High pitched noise - stridor
Two of the four parainfluenza viruses can
cause Croup
Croup
• Acute inflammation of the larynx which can
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caused an obstruction to the airways
High pitched barking sound
Respiratory distress
By age ten most children have antibodies to
all four parainfluenza viruses
Whooping Cough
• Bordetella pertussis
• Incubation period of ten days
• Catarrhal phase - fever,sneezing vomiting, and
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cough
Paroxysmal- mucous and masses of bacteria
fill the airway and immobilize the cilia
Long strand of mucous in the airway causes
violent coughing
Cyanosis may result
Convalescent
Coughing
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Attacks of coughing are severe
Can break ribs
Vomiting
Hemorrhaging can occur
Electrolyte imbalance
Stages
Diagnosis
• Charcoal-blood agar medium
• Colonies can be fixed
• A fluorescent stain be used to identify
the organism
Mechanisms for Colonization
• Adherence mechanisms
of B. pertussis involve a
"filamentous
hemagglutinin" (FHA),
which is a fimbrial-like
structure on the
bacterial surface, and
cell-bound pertussis
toxin (PTx). Short range
effects of soluble
toxins play a role as well
in invasion during the
colonization stage.
Pertussis Toxin
• One of the toxins of B. pertussis, the pertussis toxin
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(PTx), is also involved in adherence to the tracheal
epithelium.
Pertussis toxin is a 105 kDa protein composed of six
subunits: S1, S2, S3, (2)S4, and S5. The toxin is both
secreted into the extracellular fluid and cell bound.
Some components of the cell-bound toxin (S2 and S3)
function as adhesins, and appear to bind the bacteria
to host cells.
S2 and S3 utilize different receptors on host cells.
S2 binds specifically to a glycolipid called
lactosylceramide, which is found primarily on the
ciliated epithelial cells. S3 binds to a glycoprotein
found mainly on phagocytic cells.
Filamentous hemagglutinin
• Filamentous hemagglutinin is a large (220 kDa)
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protein that forms filamentous structures on the cell
surface.
FHA binds to galactose residues on a sulfated
glycolipid called sulfatide which is very common on
the surface of ciliated cells.
Mutations in the FHA structural gene reduce the
ability of the organism to colonize, and antibodies
against FHA provide protection against infection.
However, it is unlikely that FHA is the only adhesin
involved in colonization. The structural gene for FHA
has been cloned and expressed in E. coli, raising the
possibility
Additional toxins
• Invasive adenylate cylclase
• Tracheal Cytotoxin
• Lethal toxin
Treatment of Whooping Cough
• Antitoxin - To combat toxin produced
by the bacterium
• Erythromycin to shorten the paroxysmal
stage
Classification of pneumonias
• Pleurisy - Inflammation of the pleura -
it causes painful breathing
• Bronchial pneumonia - Often appears as
a secondary infection
• Lobar pneumonia - Affects one of the
five lobes of the lung
Bronchial pneumonia
• Can follow exposure to chemicals
• Can follow aspiration fo vomitus or
other fluids
• Infants sometimes aspirate amniotic
fluid during birth
• Common in the elderly
• Transmitted by aerosolized droplets
Pneumococcal pneumonia
• Sudden infection
• Chest pain, cough, and sputum containing
blood, mucous, and pus
• High fever
• Fever may last for five to ten years
• Needs to be treated with antibiotics
Pneumococcal pneumonia
• Fourth leading cause of death in the
United States
• Chest pain
• Cough
• Congestion
Klebsiella pneumoniae
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Multiple serotypes
Patient can get reinfected
Lesions in the lungs
Cephalosporins are effective
Klebsiella Pneumoniae
Pathogenicity of Klebsiella
pneumoniae
• Klebsiella pneumoniae and Klebsiella oxytoca are both
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opportunistic pathogens found in the environment and
in mammalian mucosal surfaces;
They are commonly passed by hands of hospital
personnel. Common sites for nosocomial Klebsiella
infections inlcude the urinary tract, lower respiratory
tract, biliary tract, and surgical wound sites.
Clinical syndromes caused by this bacteria include
pneumonia, bacteremia, thrombophlebitis, urinary
tract infection, cholecystitis, diarrhea, upper
respiratory tract infection, wound infection,
osteomyelitis, and meningitis
Vaccine
• The vaccine contains 23 serotypes
• Pneumovax
• The vaccine is protective against 80%
of pneumoccal infections
• Revaccination every 10 years is
currently recommended
Mycoplasma pneumoniae
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Primary atypical pneumonia
Mild onset
Some people have malaise and fever
Patients can be ambulatory - so it is also
called “ walking pneumonia”
Mycoplasma pneumoniae may cause 20% of all
noninfluenza community acquired pneumonias.
Mycoplasma
• Mycoplasma infections
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are most common in the
5 to 20 age range,
Although the disease is
usually more dangerous
among the middle-aged
and elderly.
An epidemic occurs
every three to five
years.
Mycoplasma genetics
• Interesting organism due to the degeneration of the
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genome.
During their evolutionary history multiple reductions
in genome size have occurred, the usual genetic code
has been altered, and the overall rate of evolution
uncharacteristically high.
One suggested reason for the reduction in genome
size is the evolution into strict parasites making much
of their metabolic machinery obsolete.
Mycoplasma also have unique use of the amino acid
codon UGA, which they use as an additional codon for
tryptophan, while other organisms use it as a stop
codon.
Mycoplasma as a parasite
• Mycoplasma are flask-shaped
and are most likely
descended from Grampositive bacteria.
• Due to their seriously
degraded genome they
cannot perform many
metabolic functions, such as
cell wall production or
synthesis of purines.
• They display the minimal
requirements for status as a
cell
Diagnosis
• Isolation of M. pneumoniae from sputum or
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from a nasopharyngeal swab
Growth of organisms is slow
Serological tests such as immunofluorescence,
latex agglutination, and Elisa are of value
during this
DNA probes are also of use
Azithromycin or a fluoroquinolone are drugs
of choice.
No vaccine is currently available
Laboratory Tests
Fluorescence
Legionnaires
• Legionella
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pneumophila
Gram negative rod
shaped bacteria with
an unusual
lipopolysaccharide
layer
35 serovars are
found
Legionella pneumophila
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Found in soil and water
Aerobic
Fastidious nutrient requirements
Does not ferment sugars
Life cycle quite unique
Some species can live as intracellular
parasites in Amoebas
Some of these colonize shower heads and
water systems
Legionella
• Enters the respiratory system as
aerosolized droplets
• Can be spread by humidifiers and
vaporizers in patient rooms
• These should be disinfected regularly
Pathogenicity
• These microbes are taken up by
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phagocytes
When they are placed in phaglysosomes
they thrive in the acidic environment
Eventually they break out
Lyse the cell
Spread
Symptoms
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Fever
Headache
Chills
Vomiting
Fluid in the lungs
Can be deadly
Nonpneumonic legionella is less severe and is
resolved in 5-7 days
Psittacosis
• Parrot fever
• Birds develop this in
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overcrowded situations
where the conditions
lead to spreading
Causative organism is
Chlamodophila psittoci
Disease is spread by
droplets as well as feces
Clamydophila psittaci
• Infection occurs in the
• Previously classified as
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epithelial mucosa
Infects macrophages
Mild to severe respiratory
symptoms result
No vaccine is available and
there is a 5% mortality
associated with infection
Antibiotic of choice is
Erythromycin
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Chlamydia
Exists as an EB body
between infections
When the EB body is taken
up by phagocytes and placed
in lysosomes it is
transformed into ad
Reticulate Body
The Reticulate body begins
to reproduce
The Reticulate Body is
transformed into an EB
before being passed to a new
host
Life Cycle
Q Fever – Coxiella burnetiisimilar to Rickettsiae
• This organism is a parasite
• It can survive long periods of times
without a cellular host
• It can be transmittted by ticks
• It exists as small and large varients
• It now appears as though it may form
and endospore
Pathogenicity of C. burnetii
• Bacterium is phagocytized
• The bacterium reproduces in lysosomes
• The acidic environment actually
stimulates their metabolism
Transmission
• The bacterium may be transmitted by
aerosolized droplets
• Farmers may be infected by delivering
livetock babies
• Animal hides may contain organism
• Transmitted by contaminated milk
Symptoms of Q fever
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Chills
Fever
Headache
Penumonia
Treated with Erythromycin or fluoquinolones
If untreated may result in recurring
symptoms
A vaccine is available for workers who are
continually exposed to livestock or products
Nocardia asteroides
• Found in soil and water
• Transmitted in aerosolized droplets
• Immunocompromised patients are
vulnerable to this organism
• High mortality rates treated with
sulfonamides in conjunction with
trimethoprim
Influenza
• Causative agent is an
Orthomyxovirus
• Influenza virus types A and B
are both common causes of
acute respiratory illnesses.
• Both virus types may cause
epidemics of considerable
morbidity and mortality but
influenza B infections are
often limited to localized
outbreaks
• whereas influenza A viruses
are the principal cause of
larger epidemics including
worldwide pandemics.
Viral characteristics
• RNA virus
• Segmented genome
• Recombines to induce
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changes in
characteristics
Hemagglutinin is
resonsigble for
infectivity
It attaches to a
receptor on
erythrocytes or host
cells
Viral characteristics
• It takes about 6 hours for the replication of the
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Orthomyxovirus, killing the host cell in the process.
The virus attaches to the permissive cells via the
hemagglutinin subunit, which binds to cell membrane
glycolipids or glycoproteins containing Nacetylneuraminic acid, the receptor for virus
adsorption.
The virus is then engulfed by receptor mediated
endocytosis
It is capable of escaping from the endosome and is
released into the cytoplasm of the cell
Spread of virus
• The RNA enter the nucleus of the cell where
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fresh copies are made.
These return to the cytosol where some serve
as mRNA molecules to be translated into the
proteins of fresh virus particles.
Fresh virus buds off from the plasma
membrane of the cell (aided by the
neuraminidase) thus
spreading the infection to new cells.
Antigenic variations
• Antigenic drift – results from the mutations
that occur in the genes that code for
hemagglutinin and neuraminidase
• Antigenic shift occurs when two different flu
viruses are present in the same cell and then
reassortment and recombination can occur
( bird and human)
Characteristics
• Trasnmitted by respiratory secretion
• Inhalation of droplet
• Immediate invasion of the
oropharyngeal epithelial lining occurs
• Damages the cells that line the
respiratory pathways.( These are the
ciliated mucous producing cells)
Severe symptoms
• Cellular destruction of the respiratory
Epithelium
• Impaired phagocytosis
• Accumulation of fluid
• Fever, malaise,sore throat, and
gastroenteritis are common symptoms
Treatment of flu
• Flu vaccine ( Flu vaccine may prevent
heart attacks)
• Amantadine – effective against type A
influenza ( severe side effects)
SARS( sever acute respiratory
syndrome)
• First described in November, 2002
• Chinese reported numerous cases of an
atypial pneumonia
• Caused by a corona virus
• Causes high fevers, dry cough, and
pneumonia
Research on SARS
• http://www3.niaid.nih.gov/news/newsrel
eases/2004/sarsvax.htm
• http://www.nih.gov/news/pr/dec2004/n
iaid-13.htm
• http://www.ncbi.nlm.nih.gov/entrez/que
ry.fcgi?cmd=retrieve&db=pubmed&list_
uids=15024391&dopt=medline
H5N1
• HPAI A(H5N1) is an avian disease.
• There is no evidence of efficient human-to•
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human transmission or of airborne
transmission of HPAI A(H5N1) to humans.
In almost all cases, those infected with H5N1
had extensive physical contact with infected
birds.
Still, around 60% of humans known to have
been infected with the current Asian strain
of HPAI A(H5N1) have died from it
H5N1
Pandemic Possibility
• All influenza viruses have the ability to change
• Scientists are concerned that H5N1 virus one day
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could be able to infect humans and spread easily from
one person to another.
Because these viruses do not commonly infect
humans, there is little or no immune protection
against them in the human population.
If H5N1 virus were to gain the capacity to spread
easily from person to person, an influenza pandemic
(worldwide outbreak of disease) could beg