Mucus, produced by
specialized cells lining the airway walls, is sticky
and traps a great deal of the inhaled dust, pollen, bacteria, and viruses.
Pneumonia is an infection that inflames the air sacs in one or both lungs. The air sacs may fill with fluid or pus, causing cough with phlegm or pus, fever, chills and difficulty breathing. A variety of organisms, including bacteria, viruses and fungi, can cause pneumonia. Pneumonia can range in seriousness from mild to life-threatening. It is most serious for infants and young children, people older than age 65, and people with underlying health problems or weakened immune systems.
Normal
immunological defense mechanism of the respiratory tract.
The lungs and the
airways leading to them are particularly vulnerable to infections.
Further down the
airway, in the trachea (about the diameter of a 25 cent piece), the bronchi,
(10 cent size) and and into the bronchioles (pencil diameter), the mucus is
lifted toward the throat by the constant waving of tiny hair-like projections
called cilia.
When the mucus secretions, together with its
trapped particles, reach the larynx, it is either coughed up or swallowed.
Alveoli look like
bunches of grapes hanging on their bronchioles, Their walls, which separate the
air from our blood, are only one cell layer thick. Their thinness allows macrophages from the blood to squeeze through
the capillary walls and into the air space of the alveoli where they eat
viruses, bacteria and dust (and are sometimes called dust cells once they are
full of dust or dead bacteria). These dust cells are then swept upwards into
the bronchi where they eventually get coughed out. Studies have demonstrated
that, when we're healthy, even very fine inhaled particles will be coughed out
in from 2-4 hours.
In addition to the
complex physical safeguards which the respiratory tree provides for us, there
are also countless islands of immune tissue along the way to protect us. The
tonsils - those little buds of lumpy tissue in the back of our mouth are one of
the first of these islands.They are the most visible of these collections of
lymph tissue referred to as MALT (mucosal associated lymph tissue) which are
found in the nose and all the way down to the the alveoli.
Streprococccus
pneumonia
is characterized by a
polysaccharide capsule that completely encloses the cell, and plays a key role
in its virulence. The cell wall of S. pneumoniae is composed of peptidoglycan, with
teichoic acid attached to every third N-acetylmuramic acid, and is about 6
layers thick. Lipoteichoic acid is attached to the membrane via a lipid moiety,
and both teichoic and lipoteichoic acid contain phosphorylcholine. Two choline
residues may exist on each carbohydrate repeat, which is important to S.
pneumniae because the
choline adheres to choline-binding receptors located on human cells.
The virulence factors of S.
pneumoniae include a plysaccharide
capsule that prevents phagocytosis by the host's immune cells, surface proteins
that prevent the activation of complement (part of the immune system that helps
clear pathogens from the body), and pili that enable S. pneumoniae to
attach to epithelial cells in the upper respiratory tract.
The polysaccharide capsule interferes
with phagocytosis through its chemical composition, resisting by interfering
with binding of complement C3b to the cell's surface.
Pili are long, thin extracellular organelles
that are able to extend outside of the polysaccharide capsule. They are encoded
by the rlrA islet (an area of a genome in which rapid mutation takes place)
which is present in only some isolated strains of S.
pneumoniae. These pili contribute to adherence and virulence, as well as
increase the inflammatory response of the host.
H.
Influenza
Most strains of H.
influenzae are
opportunistic pathogens; that is, they usually live in their host without
causing disease, but cause problems only when other factors (such as a viral
infection, reduced immune function or chronically inflamed tissues, e.g. from
allergies) create an opportunity. They infect the host by sticking to the host
cell using Trimeric Autotransporter Adhesins
(TAA). ( Bacteria
use TAAs in order to infect their host cells via a process called cell adhesion.
Staphylococcus
aureus
Staphylococcus aureus causes
a variety of suppurative (pus-forming) infections and toxinoses in humans. It
causes superficial skin lesions such as boils, styesand furuncules; more serious infections such
as pneumonia, mastitis,phlebitis, meningitis, and urinary tract infections; and deep-seated infections, such as osteomyelitis and endocarditis. S. aureus is a major cause of hospital acquired (nosocomial) infection of surgical wounds and infections
associated with indwelling medical devices. S. aureus causes food poisoning by releasing
enterotoxins into food, and toxic shock syndrome by release of superantigens into the
blood stream.
S. aureus expresses
many potential virulence factors: surface proteinsthat promote colonization of host tissues; invasins that promote bacterial spread in
tissues (leukocidin, kinases, hyaluronidase); surface factors that inhibit phagocytic
engulfment (capsule, Protein A); biochemical
properties that enhance their survival in phagocytes (carotenoids, catalaseproduction); immunological disguises (Protein A, coagulase); membrane-damaging toxins that lyse eucaryotic cell
membranes (hemolysins,leukotoxin, leukocidin; exotoxins that damage host tissues or otherwise
provoke symptoms of disease (SEA-G, TSST, ET); and inherent and acquired resistance to antimicrobial agents.
Opsonization
and Phagocytosis
Antibodies
coat microbes and promote their ingestion by phagocytes.
The process of coating particles for subsequent phagocytosis is called opsonization, and the molecules that coat microbes
and enhance their phagocytosis are called opsonins. When several antibody molecules bind
to a microbe, an array of Fc regions is formed projecting away from the
microbial surface. If the antibodies belong to certain isotypes (IgG1 and IgG3
in humans), their Fc regions bind to a high-affinity receptor for the Fc
regions of γ heavy
chains, called FcγRI (CD64), which is expressed
on neutrophils and macrophages. The phagocyte extends its plasma membrane
around the attached microbe and ingests the microbe into a vesicle called a
phagosome, which fuses with lysosomes. The binding of antibody Fc tails to FcγRI also activates the phagocytes, because the FcγRI contains a signaling chain that triggers numerous
biochemical pathways in the phagocytes. The activated neutrophil or macrophage
produces, in its lysosomes, large amounts of reactive oxygen species, nitric
oxide, and proteolytic enzymes, all of which combine to destroy the ingested
microbe. Antibody-mediated phagocytosis is the major mechanism of defense
against encapsulated bacteria, such as pneumococci. The polysaccharide-rich
capsules of these bacteria protect the organisms from phagocytosis in the
absence of antibody, but opsonization by antibody promotes phagocytosis and
destruction of the bacteria.
Humoral immune defense againts bacteria
Humoral immunity is due to
circulating antibodies in the gamma-globulin fraction of the plasma proteins.
It is composed of defense mechanism carried out by soluble mediators in the
blood plasma
The humoral system of immunity is also called the antibody-mediated system because of its use of specific
immune-system structures called antibodies.
The first stage in the humoral pathway of immunity is the ingestion (phagocytosis)
of foreign matter by special blood cells called macrophages. The
macrophages digest the infectious agent and then display some of its components
on their surfaces. Cells called helper-T cells recognize this presentation,
activate their immune response, and multiply rapidly. This is called the activation phase.
The next phase, called the effector phase,
involves a communication between helper-T cells and B-cells. Activated helper-T
cells use chemical signals to contact B-cells, which then begin to multiply
rapidly as well. B-cell descendants become either plasma cells or B
memory cells. The plasma cells begin to manufacture huge quantities of
antibodies that will bind to the foreign invader (the antigen) and prime it for
destruction. B memory cells retain a "memory" of the specific antigen
that can be used to mobilize the immune system faster if the body encounters
the antigen later in life. These cells generally persist for years.
Pneumonia Risk factor
While
most healthy children can fight the infection with their natural defences,
children whose immune systems are compromised are at higher risk of developing
pneumonia. A child's immune system may be weakened by malnutrition or
undernourishment, especially in infants who are not exclusively breastfed.
Pre-existing
illnesses, such as symptomatic HIV infections and measles, also increase a
child's risk of contracting pneumonia.
The
following environmental factors also increase a child's susceptibility to
pneumonia:
·
indoor air pollution caused by cooking and heating with biomass fuels
(such as wood or dung)
·
living in crowded homes
·
parental smoking.\
Clinical Manifestation of Pnuemonia
Like
other types of infection, pneumonia can trigger fever, chills, rapid heart
rate, body aches and weakness. Because pneumonia affects your lungs, it
typically causes rapid breathing and a cough, which may or may not produce
phlegm. The phlegm may be clear, yellow, greenish or blood-tinged. Pleuritic
pain -- sudden, sharp chest pain when you inhale -- is common in people with pneumonia.
When listening to your lungs, your doctor may hear crackles, pops, wheezes or
other unusual sounds from the infected lung, and the breath sounds on one side
may be quieter than the other.
Lab Exam
·
Chest X-rays, to confirm the presence of pneumonia and
determine the extent and location of the infection.
·
Blood tests, to confirm the presence of infection and to
try to identify the type of organism causing the infection. Precise
identification occurs in only about half of people with pneumonia.
·
Pulse oximetry, to measure the oxygen level in your blood.
Pneumonia can prevent your lungs from moving enough oxygen into your
bloodstream.
·
Sputum test. A sample of fluid from yours lungs (sputum)
is taken after a deep cough, and analyzed to pinpoint the type of infection.
Prevention
There are a number of steps you
can take to help prevent getting pneumonia.
·
Avoid
people who have infections that sometimes lead to pneumonia.
·
Stay
away from people who have colds, the flu, or
other respiratory tract infections.
·
If you
haven't had measles or chickenpox or
if you didn't get vaccines against these diseases, avoid people who have them.
·
Wash your hands often.
This helps prevent the spread of viruses and bacteria that may cause pneumonia.
Vaccines to help prevent
pneumonia are available. The vaccine for children is called the pneumococcal conjugate vaccine (PCV). The vaccine for older adults
(age 65 or older), people who smoke, and people who have some long-term
(chronic) conditions is called the pneumococcal polysaccharide vaccine (PPSV).
The pneumococcal vaccine may not
prevent pneumonia. But it can prevent some of the serious complications of
pneumonia, such as infection in the bloodstream (bacteremia) or throughout the
body (septicemia), in younger adults and those older than age 55 who have a
healthy immune system.
