BACTERIA RESPIRATORY DISEASES

Respiratory disease, any of the diseases and disorders that affect human
respiration.
diseases of the respiratory system may affect any of the structures and organs that have to
do with breathing, including the nasal cavities, the pharynx (or throat), the larynx,
the trachea (or windpipe), the bronchi and bronchioles, the tissues of the lungs, and the
respiratory muscles of the chest cage.
The respiratory tract is the site of an exceptionally large range of disorders for three
main reasons: 1) it is exposed to the environment and therefore may be affected by
inhaled organisms, dusts, or gases; 2) it possesses a large network of capillaries through
which the entire output of the heart has to pass, which means that diseases that affect the
small blood vessels are likely to affect the lung; and 3) it may be the site of “sensitivity”
or allergic phenomena that may profoundly affect function.

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 Structure and Function of the Respiratory System
The upper respiratory system consists of the nose, pharynx, and associated
structures, such as the middle ear and auditory tubes. Coarse hairs in the nose filter large
particles from air entering the respiratory tract. The ciliated mucous membranes of the
nose and throat trap airborne particles and remove them from the body. Lymphoid tissue,
tonsils, and adenoids provide immunity to certain infections.
The lower respiratory system consists of the larynx, trachea, bronchial tubes, and
alveoli. The ciliary escalator of the lower respiratory system helps prevent
microorganisms from reaching the lungs. Microbes in the lungs can be phagocytized by
alveolar macrophages. Respiratory mucus contains IgA.

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 NORMAL MICROBIOTA OF THE RESPIRATORY SYSTEM
The normal flora of the nasal cavity and throat can include pathogenic
microorganisms.
Nasal Cavity:
 Diphtherias
 Staphylococci
 Micrococci
 Bacillus species
Throat:
 Streptococcus pneumoniae
 Haemophilus influenzae
 Neisseria meningitidis
The lower respiratory system is usually sterile because of the action of the ciliary
escalator.

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 Microbial diseases of the upper respiratory system
Specific areas of the upper respiratory system can become infected to produce
pharyngitis, laryngitis, tonsillitis, sinusitis, and epiglottis. These infections may be caused
by several bacteria and viruses, often in combination.
Most respiratory tract infections are self-limiting.
H. influenzae type b can cause epiglottitis.

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 BACTERIAL RESPIRATORY DISEASES
DIPTHERIA
Causes; Cornyebacterium diphtheria

Characteristic arrangements of Gram-stained cells of Corynebacterium diphtheriae

Mode of transmission; Airborne, and can be through gate. Gates may include; mucosal
of oral cavity, eyes in new-borns, wounds and genital areas.

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Mechanism; Bacteria never causes bacteraemia, instead they stay in the gates of the
injection. General manifestations arise due to toxins produced by the bacteria. Toxin is
very dangerous.

Target of toxins can be tissues near the gate such as tonsils. Severest oedema can
result due to high permeability and fibrinogen leakage from blood to tissues. This
fibrinogen is converted to fibrin and they cover mucosal. Epithelium doesn’t survive in
this case.

Heart – in toxaemia, toxins disturbs the heart, they cause blockage of respiratory
enzymes inside of cells, these cells cant breath, there would be no metabolism and then
necrosis develops, after, the cell dies. (Cardiomyocytes undergoes necrosis and heart
stops contractility)

Adrenals – necrosis

Tubular epithelial cells of kidney – necrosis

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MORPHOLOGY
There are 2 major types and they are classified as;

1. Diphtheria of fauces
2. Diphtheria of respiratory tract

Based on the type of inflammation that occurs, diphtheria of fauces is diphtheric

inflammation while the diphtheria of respiratory tract is croupous inflammation.

1. Diptheric fauces

Characteristics

 Develops in places of multi layered squamous epithelium.

 Film of fibrin is thick and densely adhered to mucosa
 Very contagious
 Ulceration after detachment
 Scarring in healing

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a) Necrosis zone with neutrophils b) survived epithelium

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 In the clinical picture, we see very severe edema, hyperemia. Usually, they estimate
the severity of the disease according to the spread of edema.

Grade I – edema in the submandibular region

Grade II – edema in the neck region
Grade III – edema in the thorax.

Complications.

Toxaemia; due to the dense adherence of the tissues, it leads to alterative toxic
myocarditis (necrosis predominates and toxins are responsible).

Cardiomyocytes lose their nuclei and becomes eosinophilic, it leads to stopping of

heart contractility which results in early paralysis of the heart. If patients survives
myocarditis, it will be cardiosclerosis.

Also, other complications are necrosis of tubules and necrosis of adrenal glands.

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Picture showing pseudomembrane in diphtheria
of fauces

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2. Diptheria of respiratory tract.

Croupous inflammation of tracheal mucosa

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Characteristics
 Fibrin covers mucosa of upper respiratory tract
 Croupous develops in place of columnar epithelium
 It is loosely attached, spontaneous detachment of fibrin (thin
film)
 Erosion after detachment of film
 Superficial defect arise and it is easily healed with regeneration
without a scar.

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a) Croupous exudate б) neutrophils in mucosa г) cartilage

Complications

Films are floating because they are loosely attached. Detachment can
cause irritation of vocal folds.

- Cough

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 - Cyanosis
- Asphyxia

MENINGOCOCCAL INFECTION
They cause purulent inflammation.

Transmission; Airborne

Gate; nasopharynx

It can pass through the blood brain barrier. It’s a sporadic, non-epithelial disease

Types
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 - Local meningococcal infection
- General meningococcal infection
- Atypical meningococcal infection
a) Local meningococcal infection

Latent cause; Carrier

Nasopharyngitis – just catarrhal inflammation of nasal mucosal characterized by

hyperaemia, oedema, mucous accumulation.

b) General meningococcal infection

o Purulent meningitis
o Meningoencephalitis
o Meningoccemia
o Fulminent meningocoocemia

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c) Atypical meningococcal infection
o Pneumonia
o Arthritis

Morphology

Nasopharyngtitis – Catarrhal inflammation

Histology – exudate and infiltrate (mucous or mucopurulent infiltrate)

Neutrophils is predominant in pus and inside the tissue

Purulent meningococcal

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 Picture showing brain in case of purulent meningocoocal meningitis

Grossly, meninges are thickened, swollen, non-transparent, and yellow-green in

colour (pus), all surfaces are covered with pus (patchery or diffused). Exudates can be
serous fibrinous then purulent.

Histology; it starts in the vessels of the brain, infiltrates in vascular wall and
meninges (neutrophilic infiltrates), meninges are thickened, subarachnoid spaces filled
with purulent exudate.
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 When pus and fibrin accumulate, infection can reach ventricles and cause
ventriculitis.

Outcome: Complete resolution of exudate. When exudate is not completely

reabsorbed, “organization” (ingrowth of connective tissue) occurs. Connective tissue can
block the outflow of cerebrospinal fluid/

If block is in in foramen of Monro, it will result in distention of ventricles which can

be unilateral or bilateral.

If block is in aqueduct, there would be distention of both lateral ventricles and 3 rd

ventricle

If blockage is in all the ventricles, we will see all cistern distention which results in
internal hydrocephaly.

External hydrocephaly results when there is distention of subarachnoid spaces

If local blockages, local hydrocephaly, cyst – like formation

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 When there is internal and external hydrocephaly, it’s referred to as total
hydrocephaly. If it develops in a child and head is big – “megacephaly” in which
cartilage can grow due to high pressure

If it develops in adults, it’s referred to as hydrocephaly. This results in an increase of

intracranial pressure which can lead to herniation of the brain into the foramen magnum
thereby compressing the medulla oblongata and can lead to death

MENINGOCOCCEMIA
Bacteria, toxins and immune complexes flow in blood and fix upon vessels causing
vasculitis and necrosis of the wall, “haemorrhagic rash”, the centre is usually dark and
necrotized.

Maximum manifestation of meningococcemia is observed in DIC (disseminated

intravascular coagulation)

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 Patient skin showing haemorrhagic rash in meningococcemia

Waterhouse-Friderichsen syndrome

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 This is also called haemorrhagic adrenalitis or fulminant meningococcemia. Is
basically defined as adrenal gland failure due to bleeding into the adrenal gland
commonly caused by severe bacterial infection.

Adrenal with haemorrhages and necrosis causing acute adrenal failure. Patient can’t
survive.

Shock can cause shock kidney with necrosis of tubules – necronephrosis.

SCARLET FEVER
Cause; Streptococcus (Bacterial Infection)
Usually due to decrease defence of immunity.
Complications: Infectious allergy
Transmission – Airborne
Gate – Nasopharynx
General manifestation

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a. Changes in the gates – flaming fauces, very bright red colour of fauces and
tonsils. It is the severest catarrhal inflammation.
b. Lymphadenitis – enlarged in submandibular, occipital, cervical
c. Rash – spontaneously appear all over the body. Background of the skin is red.
Multiple dark red spots upon skin, they don’t fuse each other. Nasolabial
triangle is white without rash.
d. Fever

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 Tongue of a child suffering from scarlet fever

Complications

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 The complications can be divided into the early ones and the late ones.

Early ones;

a) Retropharyngeal abscess - can protrude through the pharynx causing difficulty in

breathing. It should be cut to avoid entry the neck.
b) Sinusitis
c) Otitis
d) Meningitis
e) Phlegmon of the neck
f) Phlegmon of the mediastinum
g) Sepsis

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Late ones

a. Keratin discharges
b. Heart failure – myocarditis
c. Vasculitis
d. Rheumatism
e. Nephritis – glomerulonephritis

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