2. Anatomy of the Respiratory System
• The dark caverns and tortuous passages of the respiratory
system are hot and humid, the atmosphere contains less
oxygen and more carbon dioxide than occurs in the air
• The eyes and the nose are the two gateways to the respiratory
system
• Respiratory system classified as Upper respiratory tract and
lower respiratory tract
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7. Microbial Diseases of URT
• Pharyngitis- inflammation of mucous membrane of the
throat, sore throat
• Laryngitis- when larynx is the infection site. This infection
affects ability to speak
• Sinusitis- infection of sinus involving heavy nasal discharge
of mucus.
• Epiglottitis- inflammation of epiglottis. Rapidly developing
disease that cause death with few hours
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8. Streptococcal pharyngitis
• Causative agent: S pyogenes; gram positive cocci, non-spore
former group A streptococci.
• Virulent factors: Protein F for attachment; Protein M interfers
with C3b; capsule inhibit phagocytosis; Protein G bind on Fc
region of antibody and prevent complement lysis; S and O
hemolytic enzymes; erythrogenic toxin etc
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9. Symptoms
• When the organism multiplies in the tonsils or pharyngeal
mucous membranes, causing redness, edema and enlargement,
and extreme tenderness, which make swallowing difficult and
painful.
• These symptoms are accompanied by fever, headache, nausea,
and abdominal pain. Other signs such as purulent exudate over
the tonsils, swollen lymph nodes, white, pus-filled abscess
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10. Scarlet Fever
• This is a complication of pharyngitis for the bacteria produce
erythrogenic (reddening) toxin that spread to the blood stream.
• The toxin results in skin hypersensitivity characterized by
pinkish red skin rash and high fever.
• The tongue has a spotted, strawberry like appearance and it
loses its upper membrane and becomes very red and enlarge.
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11. Post-infection sequel
• Rheumatic fever
• Glomeruli nephritis
• These complications is because of Ag-Ab complex.
• The S pyogens antigen protein moiety resembles human
cardiac and kidney skeletal muscles.
• Hence, the antibody cross react and damage heart and kidney
muscles ( autoimmune diseases)
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12. Otitis media
• It is uncomfortable complications of any infection of the nose
or throat, is infection of the middle ear, otitis media.
• The pathogens cause the formation of pus, which builds up
pressure against the ear drum and causes it to became inflamed
and painful.
• The condition is most frequent in early childhood because the
auditory tube connecting the middle ear to the throat is small
and more horizontal so easily blocked by the infection.
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15. Diagnosis
• Culturing the bacteria from throat swab on MSA;
• Rapid antigen detection using latex indirect agglutination and
enzyme immunoassay.
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17. Diphtheria
• Coryenebacterium diphtheriae; pleomorphic, non-motile,
aerobic, gram positive bacilli bacteria
• It is identified by its appearance after staining with methylene
blue dye, its colonial appearance, its biochemical activity, and
by demonstrating diphtheria toxin
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19. Sources of infection
• Humans are the primary reservoir for C diphtheriae.
• Sources of infection are carrier people and people with active
disease. Typically the organism can be carried by air and
acquired by inhalation.
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20. Virulence factors
• Attachment proteins that help it to establish itself on the
surface of throat, and larynx.
• Diphtheria exotoxin
• It is less invasive the disease is toxin-mediated
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21. Clinical Diseases
• Local infections (tonsils, pharynx, larynx and trachea)
• Toxin production and toxemia
• Cutaneous diphtheria because of secondary infection
manifesting as deep, erosive ulcers that are slow to heal
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22. Pathogenesis
• Diphtheria toxin affects the body in two levels.
• The local infection produces an inflammatory reaction , sore
throat, nausea, vomiting, enlarged cervical lymph nodes,
severe swelling in the neck, and fever.
• The inflammation results in pseudomembrane, greenish-gray
film develops in the pharynx from the solidification of fluid
expressed during inflammation.
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23. • The pseudomembrane is so leathery (diphtheria- Greek word
for leather) and tenacious that attempts to pull it away result in
bleeding; and if it forms in the air ways, it can cause
asphyxiation.
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24. toxemia
• It occurs when the toxin absorbed from the blood and carried
by blood to other organs such as heart and nerves; hence it can
cause myocarditis and cranial and peripheral nerve
involvement cause muscle weakness and paralysis.
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25. Symptoms
• Usually begins with a mild sore throat and slight fever,
accompanied by a great deal of fatigue and malaise.
• Swelling of the neck is often dramatic.
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26. Diagnosis
• Presumptive diagnosis based on pseudomembrane
observation although it is equivocal it may suspect the
infection; epidemiological history; positive Schick test may
provide initial diagnosis to provide antitoxin before the
toxemia develops.
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27. Laboratory Diagnosis
• Simple stain using alkaline methylene blue reveals
pleomorphic granulated cells from throat swabs.
• Serology Elek test
• Molecular diagnosis using PCR
• It is advisable to distinguish C diphtheriae from normal floras,
C xerosis, and C pseudodiptheriticum, of the eye and
nasopharynx respectively
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28. Therapy
• Antitoxin serum therapy is the primary treatment and it must
commence as soon as possible
• This treatment is supplemented by administration of penicillin
and erythromycin
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31. Viral infections
• Common cold is typical URT viral infection
• Transmitted via droplets from coughs, sneezes, and respiratory
secretions
• Usually of short duration, lasting for a week or so with milder
symptoms
• Symptoms include rhinitis, nasal obstruction, watery nasal
discharge, muscle aches and general feeling of malaise without
fever
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34. Typical pneumonia
• It is caused by S pneumoniae; a gram positive cocci, non-spore
forming, capsulated bacteria
• It is a normal flora and infection is often acquired
endogenously from ones own microbiota.
• Predisposing factors for the infection are age, season (winter)
and other lung infections and immunosuppression
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36. • The inhaled bacteria multiply in the alveoli rapidly and cause
inflammatory response.
• Having capsule the bacteria are resistant to phagocytosis
interfering opsonization due to C3b
• Serum and phagocytic cells pour into the air sacs of the lung
and cause difficult in breathing.
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37. Symptoms
• Chills, shaking, rapid breathing, and fever. The patient can
experience severe pain in the chest wall, cyanosis, cough that
produced rusty colored sputum, and abnormal breathing
sounds.
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38. Complications
• The inflammatory response for the infection often involves
nerve endings, causing pain; the condition in which pain arises
from an inflamed pleura is called pleurisy.
• It enters bloodstream and cause septicemia
• It multiplies in CSF and cause meningitis
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39. Diagnosis
• Presumptive diagnosis by Gram staining
• Quellung reaction: serological test by mixing sputum with
anticapsular antisera and observe microscopically
• Differential test using hemolytic reactions
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40. Treatment and Prevention
• Penicillin, cephalosporin, sulfonamides, quinolones, and
erythromycin
• Vaccination
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41. Whooping Cough
• Bordetella pertussis: a tiny, encapsulated, strictly aerobic,
gram negative rod. They are sensitive to drying and sun light
so quickly dies outside the host.
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43. Epidemiology
• Primary infection route is direct contact with inhaled droplets
or aerosols given off during the coughing stage of infection.
• It is most common in children from birth to four years of age.
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44. Pathogenesis
• It attach with the ciliary respiratory epithelial cells and
colonize the nasopharynx, trachea, bronchi and bronchioles.
• It produces pertussis toxin that destroy and dislodged ciliated
cells. The loss of the ciliary escalatory leads to build up of
mucus and blockage of airways.
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45. • Catarrhal stage marked by nasal drainage and congestion,
sneezing, and occasional coughing.
• Paroxysmal stage is because of obstructed bronchioles that
result in areas of collapsed lung. Moreover, because of spasm
and mucous plugging, let air enter but not escape, causing
hyperinflation.
• Paroxysmal coughing causing hemorrhages in the brain, and
seizures can occur.
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46. Diagnosis
• The pathogen can only isolated and identified during the
catarrhal and early paroxysmal phases using nasopharynx
swabbing.
• Gram reactions, cellular morphology and motility are
identifying characters.
• Biochemical tests such as oxidase (positive); urease, nitrate
reductase, and citrate negative.
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47. Treatment and Prevention
• Antibiotic therapy can only be expected to be effective during
the catarrhal and early paroxysmal phases before the virulence
factors bound to the corresponding cell receptors. Macrolides
are the agents of choice.
• Vaccination (DPT)
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58. Diagnosis
• Tuberculin skin test for screening. This reaction appears as an
induration (hardening) and reddening of the area around the
injection site. It indicated active infection in young and
delayed hypersensitivity in old individuals.
• Nonetheless, it is an indication for further examination such as
chest X ray or CT examination
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59. Laboratory diagnosis
• Active infections diagnosed using microscopic examination of
sputum and AFB test
• According to recent medical opinion , the commonly used 125
year old microscopic exam routinely misses half of all cases.
• Cultural identification requires long period so it is less reliable
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60. Rapid diagnostic tests
• Use of PCR methods to detect the bacillus directly from the
sputum
• Quanti-FERON-TB GOLD (QFT-G) which detects IFN-
• TSPOT.TB, which enumerates the T cells that produce IFN-
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61. Treatment
• Multiple drug therapy includes four drugs, isoniazid,
ethambutol, pyrazinamide, and rifampin. (first line drugs)
• Because of the long generation time of M tuberculosis and its
resistance to destruction by body defenses, drug treatment
must be generally be continued for a minimum of 6 months to
cure the diseases
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62. Prevention
• BCG vaccine
• Since it causes positive tuberculin test eliminates an important
way of diagnosing tuberculosis early in the disease that can be
easily treated
• It is not safe to use in severely immunocompromised patients
• Control of tuberculosis is aided by identifying unsuspected
cases using skin tests and chest X ray
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65. • Influenza virus is RNA single stranded virus with envelope
• It is identified by a unique set of surface glycoprotiens (i.e.,
hemagglurtinin (HA or H) and neuraminidase (NA or N)
• Highly variable virus because of surface glycogen change,
antigenic drift.
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66. • The RNA genome of influenza is segmented, eight distinct
segments
• The genome packaging that result in intermix, hence a
genetically unique virus emerged, antigenic shift
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67. Symptoms
• Low grade fever, chills, fatigue, head and muscle aches, cough
sore throat, and general malaise
• The severe consequences occur not from the disease itself but
from bacterial secondary infections
• Treatment: using amantadine and rimantadine, oseltamivir
and zanamivir
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73. Epidemiology
• It is soil fungi commonly found in soil that contains high level
of avian fecal material
• Easily isolated from excrement of chicken houses and bat
caves
• Infection acquired by inhalation of conidia and there is no
human to human transmission
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74. Biology
• Histoplasma capsulatum is dimorphic fungi and intracellular
that preferentially attacks reticuloendothelial system. It does
not have capsule
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75. Pathogenesis
• Tissue damage by H capsulatum results in granulomatous
lesions but no toxin has been detected
• The virulence is associated with its ability to survive and
proliferate within macropages. In macrophages it prevents the
release of oxygen metabolites (superoxide, hydrogen per
oxide, etc) that normally destroy microbes
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76. • Pulmonary histoplasmosis sometimes become chronic and
indistinguishable from tuberculosis
• Untreated chronic disease may lead to dissemination of the
organism and invasion of the whole reticuloendothelial system
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78. Symptoms
• Fever with liver, spleen and lymph node enlargement
• The phagocytic cells found in these tissues are gorged with
small oval yeast cells. Mucocutaneous lesions appear in 50%
of infected individuals. The ulceration of oral lesions are often
painful and accompanied by regional lymph node enlargement
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79. Diagnosis
• On Sabouraud agar, mycelial growth reveals the characteristic
tuberculate conidia that develop from hypha
• The yeast cell can be demonstrated by growth on enriched
media
• 7-10 days required to grow sufficient amount of culture
• Exoantigen test for immuno-identification of the organism
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80. Treatment
• Amphothericin B is effective but must be sustained with
weekly infusions to prevent relapse.
• Itraconazole and fluconazole also appear to be highly effective
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82. • It is caused by Pneumocystis jerovecii
• It is harmless resident of upper respiratory tract of humans. It
is opportunistic pathogen
• In the human lung it mostly found in the lining of alveoli
• Diagnosis is usually made from sputum samples where cysts
detected
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83. Pathogenesis
• In immunocompetent individuals it is check by lung
macrophages and lymphocytes but in immunocompromised
human it multiplies intracellularly as well as extracellularly.
• The massive number of parasites adhere tenaciously to the
lung pneumocytes and cause inflammatory condition
• The lung epithelial cells slough off, and foamy exudate builds
up
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84. Symptoms
• Symptoms are non-specific and include cough, fever, shallow
respiration and cyanosis.
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86. • It dimorphic fungus commonly found in dropping of birds
• Particles containing dried yeast cells are readily scattered into
the air and dust
• The species sporadically isolated from dairy products, fruits
and healthy human body, tonsils and skin
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88. Pathogenesis
• It establishes infection first in the lung with no or mild
symptoms in most people and easily eliminated by defence
system
• In some cases it enters to bloodstream and disseminated to the
entire body.
• Its capsule resist phagocytosis and chemotaxis of leukocytes
• Meningoencephalitis is the common infection by the pathogen
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89. • The tumor like masses formed in brain and meninges can
cause headache, mental changes, coma, paralysis, eye
disturbances, and seizures
• In some cases the infection disseminates into the skin, bones,
and viscera
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90. Diagnosis
• Negative staining to detect encapsulated budding yeast
• Negative nitrate assimilation, pigmentation on birdseed agar
• Serological tests and DNA probes
• Immediate treatment with amphothericin B and fluconazole
over a period of weeks or months
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92. • Pathogens are Aspergillus fumigatus, A flavus and A niger
• The respiratory tract is the principal portal entry
• Inhaled spores cause disease in healthy as well as
compromised individuals
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93. Pathogenesis
• Allergic aspergillosis respresented in the form of asthma like
response, an allergic rhinitis or sinusitis, or hypersensitivity
pneumonitis
• Asthma like illness is characterized by fever, cough, and
wheezing induced by the presence of reaginic IgE antibodies.
The syndrome may become severe and chronic with bronchial
plugging
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94. • Allergic rhinitis or hay fever may develop in individuals on
exposure to mold spores and mycelia. It resulted from the
interaction of allergens and IgE fixed to specific mast cells in
the epithelial surface of the nasal mucosa.
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95. • Hypersensitivity pneumonitis includes farmer’s lung,
bagassosis, and mushroom workers lung. It result from
exposure to thermophilic actinomycetes in hay, bagasse ( the
dry residue of sugar cane after the juice has been expressed)
• Symptoms develop after 4-8 hours after exposure and
symptoms persist for about 12 hours and recovery is
spontaneous
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97. Influenza
• Viruses in the influenza virus consists of eight separate RNA
segments of differing lengths enclosed by inner layer of
protein and an outer lipid layer
• The lipid layer characterized by numerous projections, the
main ones are haemagluttinin (HA) and neuraminidase (NA)
spikes
• HA and NA used for attachment and separation from the
infected cell respectively
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98. • Truly human adapted viruses are H1N1, H2N2, and H3N2
• Epidemics of influenza also occurs in animals such as birds,
seals, and pigs, and it is likely that antigenic variability of
influenza viruses is partly due to movement of viral genes
from one animal species to another
• Swine are good mixing vessel for antigenic variation of the
influenza virus
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99. • H1N1 strain is always of special interest because the lethal
1918 pandemic and 2009 epidemics was caused by it.
• Swine can function as something of a warm freezer for such
viral strain but mutations more likely occur in humans who
have a long life span
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100. Symptoms
• Flu is characterized by chills, fever, headache, and muscular
aches. Recovery normally occurs in a few days and cold like
symptoms appear as the fever subsides
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101. Prevention and treatments
• Vaccine
• The antiviral drugs amantadine and rimantadine significantly
reduce influenza type A if administered promptly
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103. • Serious lower respiratory tract infections of infants and young
children
• The virus is a member of paramyxovirus RNA virus
• Enters via inhalation and infects the respiratory tract
epithelium causing the death and slough of basement membrane
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104. Pathogenesis
• Bronchiolitis is common feature of the disease; the inflamed
bronchioles become partially plugged by sloughed cells,
mucus and clotted plasma that has oozed from the walls of the
bronchi
• The obstruction cause wheezing similar with asthma; the
inflammation extended to the alveoli and cause pneumonia
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105. Epidemiology
• Outbreaks common from late fall to late spring, peaking in mid
winter
• Weak acquired immunity after recovery so that infection can
recur throughout life
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106. Prevention and treatment
• Quarantine
• Inject monoclonal antibody called palivizumad for protection
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108. Causative agents
• Sin Nombre, Spanish for ‘no name’
• Enveloped virus of bunyavirus
• Its genome consists of three segments of ss ns RNA virus
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109. Pathogenesis
• Enters to the respiratory tract via inhalation
• By unknown mechanism enters circulation and carried through
out the body infecting the cells that line tissue capillaries
• The inflammatory response to the virus cause capillaries to
leak large amounts of plasma into the lungs, suffocating the
patient and cause blood pressure to fall, shock and death occur
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110. Symptoms
• Usually begins with fever, muscle aches (esp. in the lower
back), nausea, vomiting, and diarrhea.
• Unproductive cough and increasingly severe shortness of
breath appear within a few days, followed by shock and death
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