Capsule can inhibit phagocytosis
PULMONOLOGY, MED II - 3RD YEAR
PNEUMONIA I & II: CAP & HCAP
( LECTURE OUTLINE DR LEE TRANS, MIDTERMS FEBRUARY 2017)
PNEUMONIA
 Inflammation of the lung parenchyma, the portion distal to the
terminal bronchioles and comprising the respiratory bronchioles,
alveolar ducts, alveolar sacs, and alveoli.
 Bronchitis – inflammation of the larger airways
 Bronchiolitis - <2um
ROUTES OF MICROORGANISM
Before infection can take place, the microorganism should be able to
reach the Lower Respiratory Tract (LRT). There are several routes wherein
microorganisms reach LRT. We have the inhalation route, aspiration from
the oropharyngeal area, hematogenous spread, contiguous extension
from an infected pleura or mediastinum so a direct spread from a nearby
structure causing Pneumonia. So which route is most common route
wherein microbe is able to cause Pneumonia? ASPIRATION.
And, aspiration is usually the mode of entry or route of entry of your what?
What are the different microorganisms that enters through your inhalation
route, aspiration route or your hematogenous route?
For your inhalation route, you have your TB. Q fever, Legionella, SARS and
fungal infection.
For your aspiration route, it would be your anaerobes, Strep. pneumoniae,
Chlamydia.
Your hematogenous route would usually be your Staph. aureus
In contiguous extension, what you usually see is your *****
1) Inhalation of microbes present in the air or contaminated droplets
2) Aspiration of organism from the nasopharynx or oropharynx
3) Hematogenous spread
4) Direct spread from a contiguous site of infection or penetrating injury
from infected pleura or mediastinum
5) Airborne – TB, Legionella, Fungal, Q fever
MICROBIAL FACTOR
There are several factors in the microbe that would increase their chance
of causing infection because they can counter the normal defense or
nonspecific defense of the host.
Chlamydia pneumonia, can cause the cilia to be static so nonfunctioning
or paralyze the cilia.
1) Chlamydia pneumonia
→ Has ciliostatic factor - inhibit activity
→ Causes ciliostasis; causes breakdown of mucociliary clearance
mechanism
2) Mycoplasma pneumonia – can destroy the cilia. Once the cilia is
destroyed, then it has to have some time for it to be rejuvenated.
When you have loss of your lining epithelium, after some time you will
have it regenerated. The same thing happens. It will take some time
for you to be able to regenerate your cilia.
→ common microorganism that causes CAP
→ Commonly destroy cilia
3) Influenza virus – inhibits ciliary motion for as long as 3 months. Let’s say
you have URTI caused by Influenza 1 month ago and you are still very
vulnerable for LRTI because your mucociliary defense is down.
→ inhibits ciliary motion (may last for 3 months)
→ In the 3 months period, there is a higher risk to develop
pneumonia that is why patients with CAP have history of viral
upper respiratory tract infection.
4) Neisseria meningitides – not common
→ split IgA
Your Neiserria meningitides can split IgA just like your Strep. pneumoniae.
5) Streptococcus pneumonia – most common microorganisms that
cause CAP - As I told you earlier, the most common cause of CAP that
leads to hospitalization is your Strep. pneumoniae. Why is this very
virulent? Because it produces protease that can split IgA and this will
promote their colonization and infection. It is encapsulated, so when
they colonzie, the phagocytic cells won’t be able to kill them. It
produces neuromanidase & hyaluronidase to protect themselves
against nonspecific defense.
→ produce proteases that can split IgA
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→
→ 53-kDa polypeptide pneumolysin ( a thiol-activated cytolysin
that interact with cell membrane with cholesterol)
→ Neuromanidase – inhibition of ciliary action
→ Hyaluronidase
→ IgA 1 protease
PREDISPOSING FACTOR
What are the different predisposing factors, let’s say even when you have
colonizations of your oropharyngeal area by your Chlamydia, that does not
mean that you have Pneumonia already. There are some factors that
increase the development of Pneumonia.
Risk factors to the development of pneumonia:
 Altered level of consciousness – can promote aspiration and every
CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER
time you go to sleep there is an alteration of level of consciousness.
Well of course, you have more waking hours compared to sleeping
time. So patients who really have alterations in the LOC like patients
who have CNS problem or patients with epilepsy, they are more prone
to aspiration and they are at a higher risk to develop Pneumonia.
 Cigarette smoking
 Hypoxemia
 Acidosis
 Alcohol
 Toxic inhalations
 Pulmonary edema
 Uremia
 Malnutrition
 Corticosteroids
 Immunosuppressive agents
 Viral infections – paralyses cilia
 Mechanical obstruction
 Hinder the clearance mechanism of the respiratory system – so
this will promote the possibility of infection
PREDISPOSING FACTORS TO RECURRENT INFECTION
So even if you have predisposing factor, generally you don’t have recurrent
Pneumonia. One of your classmate had Pneumonia before, how many
times? Once only, but sometimes you would encounter patients who have
recurrent Pneumonia so they may have Pneumonia 2-3 times a year so
that’s very common, frequent. So if you see patients who have recurrent
Pneumonia who had 2-3 times a year, they may have additional risk factor
aside from the risk factors that we have been talking about. Generally, they
may have congenital or acquired immunodeficiency or some problem with
the normal defense or nonspecific defense of the respiratory system just like
your ciliary activity or maybe your frequent aspiration because of a
esophagotracheal fistula. There are patients who are born with fistula. There
are 5 types of tracheoesophageal fistula. If you are taking care of babies,
and then there is frequent Pneumonia, then this is a problem that you have
to look into. But for adults, this cannot be congenital anymore. It is usually
an acquired problem, the fistula and this is usually due to a esophageal
malignancy that has invaded the trachea because the esophagus and the
trachea are very close to each other. The trachea is in front while the
esophagus is at the back. So if you have a problem in the esophagus, this
can easily affect the trachea. And, if you have an obstruction in the
esophagus, then this would tend to cause you to aspirate. So this will also
increase the chances for you to have recurrent infection of the LRT.
Recurrent alteration of the level of consciousness is usually seen among
patients who are epileptic. So every time they have seizure, they tend to
aspirate, and after that they also have loss of consciousness. Usually when
patients go into seizure, they do not know that they had a seizure attack.
Generally, they don’t know. These would predispose them with recurrent
Pneumonia, and we are seeing number of individuals with
immunodeficiency this is because of increased HIV infection that we have
here. In other countries, the incidence is already plateauing, but here we
are seeing increasing number of patients or individuals with HIV infection. I
think the last news was that we have 250 new cases every day. But we really
do see a lot of patients with HIV infection. That’s why before you seldom
encounter patients with HIV in most general hospitals, but now we see quite
a lot of them already with the immunodeficiency syndrome.
Some patients may develop pneumonia frequently. Recurrent pneumonia
is defined as having pneumonia 2-3 times a year. These patients may
have immunity problems:
1. Congenital defects in host defenses
2. Congenital defects in ciliary activity → Kartagener’s syndrome or
Dismotile cilia syndrome
3. Structural lung abnormalities
4. Acquired defects in host defenses
5. Bronchial obstruction → Bronchogenic CA
6. Esophageal abnormality → Anatomical abnormalities like achalasia
(causes regurgitation and esophageal fistula, do bronchoscopy) &
esophageal malignancies
7. Recurrent altered mental status → Chronic alcoholics & epileptics -
LOC
Stroke – affect muscle of deglutition
**AIDS – Acquired immune defects – impaired T cell function
HOST INFLAMMATORY REPONSE
Patients who have Pneumonia usually have clinical manifestation that’s
why we would be able to take note of the possibility that the patients have
Pneumonia, and these clinical manifestations are usually the host response
to infection. If the patient does not respond to infection, usually they will not
have these clinical manifestations that generally you will recognize to
patients who have Pneumonia. Because when we talk about Pneumonia,
generally we would have patients who have cough and later on, the
patients will have high grade fever, the cough will be productive and if the
Pneumonia is extensive, then the patient will also have difficulty of
breathing. So the difficulty of breathing will only depend on how extensive
the Pneumonia is, it means how much segment or lobe of the lung has
infection. If it is just a small segment, then usually this will not cause much
problem with oxygenation and most patients would not be complaining of
difficulty of breathing. These are the usual manifestation of patients that
would make us suspect that they have Pneumonia. However, these
symptoms are NOT specific for Pneumonia. We also see these in patients
who have Bronchitis, Sinusitis. So these are non-specific and we have to
correlate these with our physical exam. However, even with good history
and physical examination, the sensitivity and specificity of these 2
combined is only 60%. So it is not very high, that’s why we really need
objective parameters to tell us whether the patient really has Pneumonia or
not, but usually we would suspect these if the patient has manifestations
suggestive of Pneumonia like fever & cough.
1. Fever
This fever is because of the defense or the host response to the infection. If
the patient does not have enough defense mechanism, does not respond
to invading microorganism, then you do not have fever. That’s why some
patients such as elderly patients have Pneumonia and yet they don’t have
fever because their immune response is already quite low. And this fever is
because of
 Release of inflammatory mediators→ IL-1, TNF
2. Leukocytosis and increased purulent secretions
Patients with Pneumonia especially those with co-bacterial infection usually
cough out purulent secretions. These purulent secretions are because of
your granulocyte colony stimulating factor and your chemokines and
interleukin 8 that causes the purulent sputum. This also causes the increase
in WBC count of the patients.
 Chemokines→ IL-8, GCST → (+) neutrophils
3. Alveolar Capillary Leak
Patients who have Pneumonia usually do not have pulmonary findings.
When we auscultate them, you will hear rales. These rales are due to the
leakiness of the pulmonary capillaries just like your ARDS, there would be
leakage of fluids into the interstitial space and alveoli. This leakiness of the
capillary is because of mediators released by your macrophages and the
recruited neutrophils. This capillary leakage can also lead to other
manifestation like hemoptysis. Some patients with Pneumonia can cough
out blood. Still remember the currant jelly sputum? The rustic colored
sputum? That we tackled in your 2nd year. These are part of the hemoptysis
and this is being caused by your capillary leakiness of the lungs in response
to the inflammation. This leakiness will also cause the hypoxemia and this is
the reason why you would hear rales when you try to auscultate the chest.
This would also cause the infiltrates that you see in the Chest X-ray to help
in the diagnosis of Pneumonia.
 Inflammatory mediators release by macrophage and recruited
neutrophils
 Increased permeability – Edema
 Hemoptysis
 Radiographic infiltrate
 Rales
 Hypoxemia from alveolar filling
4. Dyspnea
The difficulty of breathing of patients is due to hypoxemia and this
hypoxemia is due to the leakiness of the capillary. If the alveoli are filled up
with fluid, air would not be able to get in and there would be no gas
exchange. No gas exchange would lead to your hypoxemia. So, the lack
of oxygen would further drive your respiration to increase breathing. This
would further contribute to the feeling of difficulty of breathing. Aside from
this, the air would also inflame and there would be secretions lining the
airway causing airway obstruction. This airway obstruction is further
contributed by the inflammatory dilated bronchospasm causing more
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difficulty in the entry of air into the alveoli leading to the feeling of difficulty
of breathing or your dyspnea.
 Decrease in lung compliances, poor responses to
vasoconstriction – capillary leak
 Hypoxemia
 Increased respiratory drive
 Increased secretion
 Inflammation related bronchospasm
So these manifestations have reasons or explanation for it.
(+) peripheral chemoreceptors – aortic/ carotid bodies → pulmonary
shunting → severe hypoxemia → not responsive to supplemental oxygen
→ severe → death
Epithelial cells
 Barrier to dissemination of microorganism
CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER
 Produced antimicrobial molecules
 Recruit antiphagocytic cells
 Produce IL-8, macrophage-inflammatory protein 2, Granulocyte-
macrophage colony stimulating factor
 By products of arachidonic acid cascade
 Endothelial adhesion molecules
Host factor
 TNF alpha→ associated with fatal outcome
 Lymphotoxin alpha→ risk for septic shock
 TNF alpha 308: LT alpha + 250GC haptotype → protection against
septic shock
PATTERNS OF PNEUMONIA
When an individual keep infected of Pneumonia, they may have different
pattern of Pneumonia but in your Patho, the particular Pneumonia that
you settle would be your Lobar Pneumonia.
So aside from your Lobar Pneumonia, we have your Bronchopneumonia.
Initially manifesting as an airway infection and later on as your
pneumonia.
So your Lobar pneumonia is very typical with your Strep. pneumonia
infection while your Bronchopneumonia is usually of your Staph. aureus
infection. Interstitial Pneumonia would usually be that of your viruses or your
atypical microorganism. Although your typical microorganism also cause
to your Lobar Pneumonia. We also have your Miliary type of Pneumonia
wherein there is widespread. In the Philippines when we say Miliary type of
Pneumonia, we would be thinking of your TB.
 Patients with pneumonia may have different presentations. Some
patient may present with lobar pneumonia, bronchopneumonia,
interstitial pneumonia, or military pneumonia.
 The pattern of pneumonia will also depend on the microorganism that
causes the infection:
- Strep.pneumonia will cause lobar pneumonia
- Interstitial pneumonia is generally caused by viruses or atypical
microorganisms.
- Miliary pneumonia usually caused by TB (not common)
- Bronchopneumonia more commonly encountered in young
children rather than among young adults. Most of the time, lobar
pneumonia is seen among young adults.
So there are 4 phases in the pathology of your Pneumonia.
1. LOBAR PNEUMONIA (Typical pathological changes seen in patients
with pneumonia caused by S. pneumoniae)
a) CONGESTION (EDEMA)
 Initial phase
 Usually seen in the 1st 24 hours
 Not usually seen by the physician
 Grossly appears red & doughy – This is due to the protein, exudates
into the alveoli. When you aspirate fluid from the alveoli, you would
see a lot of bacteria in the fluid that you aspirated.
 Microscopically: (+) vascular congestion & alveolar edema +
microorganism can spread via pores of Kohn (within the alveoli)
 Proteinaceous exudates and often bacteria in alveoli
b) RED HEPATIZATION
 After 24 hours – The lung appears very red. This is because of the
increased number of RBCs in the alveolar exudates
 RBC in the cellular intraalveolar exudates
 ↑ neutrophil influx - Increasing number of neutrophils that would go
into the alveolar space and the number of bacteria will start to go
down because of the neutrophils and phagocytic cells.
 Bacteria occasionally seen in pathologic specimens
 Last for 2 days
c) GRAY HEPATIZATION – After 24-72 hours (of your red hepatization)
 No new RBC is extravasating and those already lysed and degraded
– No new RBC going into the alveolar space that’s why the RBCs will
now die out and this would cause the gray color.
 Predominant cell: neutrophil – Neutrophil will be the predominant cell
in the alveolar space & there will be no more bacteria.
 Abundant fibrin deposition
 Lung is dry, friable and gray-brown to yellow
 Start of the rebuilding / reconstitution of the lung
 Bacteria disappear
 Last 2-3 days
d) RESOLUTION – After 24-72 hours (of your gray hepatization) again
 Enzymatic digestion of alveolar exudates, resorption and
phagocytosis
 Macrophages reappears – predominant cell type – Macrophage now
would appear as the predominant cells in the alveoli and this will clear
out the debris, the waste products that is now in the alveoli - cleaning
out time.
 Lots of phagocytes
 Cleans up the debris of neutrophils, bacteria and fibrin
Those are the 4 phases of your Lobar Pneumonia.
Edema and usually it is in the first phase and the last phase of Pneumonia
wherein you would have very prominent rales when you auscultate.
During the gray hepatization, as the term implies, hepatization so the lung
becomes consolidated so there will be an increase, you may not hear
prominent rales – just a few rales maybe, but there will be increase
transmissions of breath sounds. Instead of vesicular breath sounds, you will
be able to hear bronchovesicular breath sounds or your bronchial breath
sounds.
In the 4 stages, you will have all your ergophony, increase tactile fremitus
because these are all consolidation.
2. Bronchopneumonia – margin usually poorly demarcated neutrophilic
infiltrates center in bronchi, and bronchiole
 White all over, patchy infiltrates on periphery
**most common in nosocomial pneumonia
Bronchopneumonia, pathologicallym it would be poorly demarcated
around the airways, more center in the bronchi, in the airways rather than
the alveoli.
3. Interstitial pneumonia – Inflammation in the interstitial space alveolar
wall and connective tissue space between the alveoli and the blood
vessels
4. Miliary Pneumonia – spread mildly and over both lung field
 Dots, coarse, smaller infiltrates
 Hematogenous spread
Miliary Pneumonia will be all over the lung due to the hematogenous
spread or an endobronchial spread.
*X-RAY & CT SCAN OF LOBAR PNEUMONIA*
This would be an example of patients who have an X-ray who have Lobar
Pneumonia. Why do we say this is a Lobar Pneumonia and not a mass? This
is because of the air bronchogram that you see. That’s why the alveoli are
filled up with secretions, debris, but the airway are patent so it will cast a
black shadow on chest x-ray. So within the consolidation, within the white
shadow, you will see lines of black – that is your air bronchogram. This is
because if you do a CT scan, you will see the alveoli are all filled up with
secretions causing whiteness and the airways are patent that’s why you
have lines of lucency. So that is your air bronchogram.
*CT SCAN OF BRONCHOPNEUMONIA*
This is what we call your Bronchopneumonia. It’s more in the airways,
demarcations, inflammations around the bronchi.
*CT SCAN OF MILIARY PNEUMONIA*
If you have your CT scan, you will have your spread, This also looks like
lymphangitic spread of malignancy when you have your cancer and you
have lymphangitic spread it will also look like that.
So you also have to correlate your anxillary findings to your clinical
manifestations of your patient.
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CLINICAL MANIFESTATIONS
Symptoms
 Fever, tachycardia
 Fatigue, headache, myalgia, arthralgia – viral cause, especially
if it is caused by your atypical microorganisms or viruses
 Chills and sweat – this is very typical of your Strep Pneumonia
 Cough – prominent in all the different microorganisms causing
Pneumonia but the sputum would differ if it is atypical type of
microorganism or your viruses, this would be more of mucoid. But
if this is a bacterial infection, generally it would be purulent.
 DOB – would depend on the extent of involvement of the lung
by infection. So just one look, the patient may not have much
difficulty but if it is multilobular, generally they would have severe
difficulty of breathing.
 Pleuritic Chest Pain – would only be present if the infection has
CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER
infection spread to the pleura. You know even the lung is
necrotizing, there would be no pain. Because there are no pain
fibers in the lungs. It is only the pleura that you have your pain
fiber so if the infection has spread to the pleura so the patients
will have pleuritic chest pain.
 GI symptoms in 20% of patients like nausea, vomiting and/or
diarrhea – this is especially true in patients with Legionella
Signs – What are the signs that we see when we do PE among patients
with Pneumonia?
 ↑ tactile fremitus - Because of the consolidation
 ↓ tactile fremitus, if there is effusion - If there is pleural effusion,
tactile fremitus is decreased over the area where you have
your effusion.
 Percussion is dull to flat
 Crackles, bronchial breath sounds, bronchovesicular sounds,
and pleural friction rub - & pleural friction rub if the infection has
spread to the pleura.
 Elderly – new onset confusion or worsening confusion – Among
elderly patients, they may manifest only with alterations of level
of consciousness or they will just manifest with anorexia without
fever
 Severely ill – organ failure, septic shock
DIAGNOSIS & TREATMENT
For us to be able to diagnose, whether the patients have Pneumonia or not,
usually we depend on the history, the complaints of the patients and the
physical examination findings. But as I told you earlier, even with a full
history and careful PE, the sensitivity and specificity is only around 60% so it
is not high so there is a high possibility that you will be make a mistake in
your diagnosis. For us to be able to diagnose whether our patients have
Pneumonia or not, we need a Chest X-ray so the only time that we will be
able to tell if the patent has Pneumonia or not would be chest x-ray findings
that shows that the patient has Pneumonia. Other diagnostic work-up
usually would be to help us determine the microbes that causes the
infection. So we can use differentially, gram stain & culture to help
determine the offending microorganism.
In very some patients, who are severely ill, and you have already given a
lot of antimicrobials, and yet the patient is not responding, then we have to
use a more invasive procedure to collect a specimen from the LRT like by
doing the Bronchopscopy, Protected Brush, Collection of Lung specimen or
transbronchial biopsy of the lungs in order to obtain the specific specimen.
Blood culture is really actually the GOLD STANDARD for us to determine
where the specific microbes.
The sputum cultures is NOT specific. It is ONLY PROBABLE or HIGHLY POSSIBLE.
But your blood culture, if you are able to culture the microbes then this is
the SPECIFIC microbes.
Serologic Testing is also helpful in including the antigen determination. This
would also be specific because this is specific for a particular
microorganism.
 History & PE → most important
 Sensitivity (58%) and specificity (67%)
 Radiologic examination (diagnosis of choice) – needed – efficient
o Chest X-ray (definitive)
o CT-scan →If chest x-ray in the 1st stage of pneumonia is
normal
 Sputum examination – gram stain → etiology
 Bronchoscopy – invasive
o Brush (protected)
o Transbronchial biopsy
 Lung biopsy – tissue Dictionary 2009), this is suggestive that the patient has Mycoplasma
 Blood culture serologic studies and antigen detection pneumoniae.
o Blood culture – wait for days; specific, seldom (+) – 30%,
etiology If the patient has alterations in the level of consciousness or the lack of gag
o Serological studies – specific – see increase in titer – only reflex that means they tend to aspirate – Anaerobic & Polymicrobial
used in research microorganism causing the lung infection.
o Ag detection – acute phase only
If the patient has Pneumonia and manifestations suggestive of Encephalitis,
 Diseases that may mimic pneumonia so there is alterations in the level of consciousness, then this is highly
o Bronchitis suggestive of atypical microorganism causing the infection such as your
o Patient with history of radiation Mycoplasma, Chlamydia, C. burmetti.
o Patient with congestion
o Pulmonary emboli The patients have Pneumonia and manifestations of cerebral Ataxia, then
you think of Mycoplasma pneumonia & Legionella pneumophilia.
PATHOLOGIC CHANGES IN THE LUNGS WHEREIN YOU WOULD HAVE

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

PHYSICAL EXAMINATION FINDINGS OF There are manifestation like your Erythema Multiforme, this is suggestive of
Mycoplasma pneumoniae infection, Erythema Nodosum suggestive of
• Congestion → rales
Tuberculosis, Chlamydia pneumonia. And findings of your Erythema
• Hepatization (red/gray hepatization) Gangrenosum highly suggestive of Pseudomonas aeruginosa, Serattia
 Bronchial breath sounds marscenscens.
 Increase breath sounds
If the patient has Pneumonia and numerous cutaneous nodules & CNS
 Dullness on percussion manifestation, then it is highly suggestive of Nocardia infection.
• Hepatization state
 (+) minimal or no rales Periodontal disease with  Anaerobes or mixed aerobes
 (+) bronchial breath sounds foul smelling sputum & anaerobic infection
Bullous Myringitis  Mycoplasma pneumoniae
 Increased tactile fremitus Absent Gag reflex, altered  Polymicrobial (oral aerobic &
• Resolution state LOC or a recent seizure anaerobic bacteria) can be
 (+) rhonchi, rales macro or microorganism
aspiration
• Patient s coughing out the sputum (most of the time)
Encephalitis  M. pneumoniae
• Percuss → (+) flatness → (+) EFFUSION  C. burnetti
• Consolidation → (+) dullness on percussion
 L. pneumophilia
Cerebral Ataxia  M. pneumoniae
• Decreased TF – if complicated pneumonia  L. pneumophilia
Erythema Multiforme  M. pneumonia
Paraneumonic Effusion Erythema Nodosum  C. pneumonia
• Sometimes patient with pneumonia develops effusion  M. tuberculosis
Erythema Gangrenosum  P. aeruginosa
• On P.E. → (+) bronchial breath sounds, rales, wheezes (depending
 S. marscescens
on the stage of the pneumonia)
Cutaneous nodules  Nocardia species
• On percussion → (+) dull / flatness (abscesses) & CNS findings
• (+) dullness
DIFFERENTIAL DIAGNOSIS OF COMMON PATTERNS ON CHEST X-RAY
• Edema As I told you earlier, Chest X-ray is the basis for associating the patients
• Gray hepatization GERD with Pneumonia or not. Based on Chest X-rays, there are helpful in telling
us the possible offending microorganism. So if you have:
• Resolution
Focal Opacity –  S. pneumonia - #1 microbe you would
like your Lobar think about is Strep. pneumoniae
PHYSICAL FINDINGS
Pneumoniae  M. pneumonia – aside from strep.
So there are certain physical examination findings that may help us in
pneumo, there is a possibility of
determining the possible microorganism because when we do culture or
Mycoplasma pneumoniae,
gram staining it takes several days before the results would come in. And if
 Legionella penumophilia
your patient is severely ill, you cannot afford to wait very long. So at the start
 S. aureus
of the treatment, the patient would have Pneumonia generally this would
 C. pneumonia
be empirical treatment or educated guess treatment. We have to take the
 M. tuberculosis
possibility if the patient has Klebsiella infection so you have to give
 Blastomyces dermatitidis
antibiotics that would be able to cover the microbe because the mortality
- But of course the more common here would be
and the morbidity would depend on the initiations of your antibiotics. We
your Strep. pneumo, Mycoplasma or Staph.
found out that the mortality has decreased significantly if you are able to
aureus.
give the antibiotics within 6 hours of seeing the patient. Actually, they have
Interstitial  Viruses or atypical microorganisms
put it to 4 hours of seeing the patient. And, giving the correct medicine at
infiltrates such as your
the start of the treatment. So you have to have quite a good educated
 Mycoplasma pneumoniae
guess, and, of course, this would depend on the sensitivity of the different
 Pneumocystis jiroveci
pathogens of area of practice. Because different hospitals have different
 Chlamydia psittaci
sensitivity and resistance strain. So the microbes that we have in Fatima
- If this is a Pneumocystis jiroveci, then this is an
may not be necessarily the same microbe that we are seeing in PGH. And
AIDS-defining disease which means your patients
it may be the same with the resistance, resistance of certain
have acquired immune deficiency syndrome
microorganisms may be different. So this will also depend on the area you
already
are practicing.
Interstitial  EBV virus - #1 microbe
So if you examine a patient and you found out that the patient has foul pneumonia with  Francisella tularensis
smelling breath, lack of dental caries, gingivitis, most probably the infecting lymphadenopathy  Fungi
organism is Anaerobic microorganism. – enlargement of  Chlamydia psittaci
lymph nodes with  Mycoplasma pneumoniae
If you examine the ear, the patient has bullous myringitis (inflammatory interstitial
condition of the eardrum characterized by painful fluid-filled vesicles on the pneumo.
TM & the sudden onset of severe pain in the ear – Mosby’s Medical
Page 4 of 10
 Cavitation – Lung  Mixed aerobic & anaerobic (lung MICROBIAL CAUSES OF CAP
Abscess - abscess); aerobic gram (-) bacilli – We can guess the microorganism as to the site of care. If you think the
necrotizing microorganism can cause necrosis of patient can be taken care of in an outpatient basis, or need to be in the
the lung, gram (-) microorganism Intensive Care Unit (ICU), then there are highly possible microorganism
usually cause necrosis of the lung that we will have to consider.
parenchyma
 M tuberculosis So if the patient is not severely ill, that means the patient does not need
 Legionella pneumophilia to be hospitalized based on your assessment. We have different tools to
 Cryptococcus help us on the assessment.
 Nocardia asteroids
 Actinomyces israelii If the patient can be taken care of in an outpatient basis, then the #1
 Coccidioides immitis microorganism among patients who have CAP would be your Strep.
 Pneumocystis jiroveci pneumo. Aside from Strep. pneumo, would be your Mycoplasma, H.
– usually not that common but cavitations may influenza, Chlamydia pneumoniae & your respiratory viruses.
generally think of anaerobes, or polymicorbial

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

infection or gram (-). The others are not really that If your patient is severely ill, and needs to be hospitalized in the ICU, then
common. Of course, we usually see TB & they the microbes would be your Strep pneuno, Staph aureus, Legionella,
tend to be in the upper lobe. Gram (-) bacilli, & H. influenza.
Bulging Fissure  Klebsiella pneumoniae (highly
suggestive of lobar) If the patient is very ill, but not as ill as those patients who are in ICU care,
 Legionella penumophilia that means they are not hypotensive, not severely hypoxemic, then that
- Now sometimes, we take CXR and see inifiltrates means they can care if only in the ward hospitalization is adequate, then,
at right upper lobe with bulging fissure. This is we think of Strep. pneumo, Mycoplasma, H influenza, Chlamydia pneumo,
highly suggestive of Klebsiella pneumoniae. Aside Legionella & respiratory viruses.
from Klebsiella is your Legionella pneumophilia, OPD IN-PATIENTS
but Klebsiella is more common. So this is how it NON-ICU ICU
looks, you have consolidation of your upper lobe S. pneumonia - #1 S. pneumoniae S. pneumoniae
and the minor fissure is bulging downward due to M. pneumoniae M. pneumoniae S. aureus
excessive secretions that the microorganism is H. influenza H. influenzae Legionella spp
able to produce. Your Klebsiella is also C. pneumoniae C. pneumoniae Gram (-) bacilli
encapsulated just like your Strep. pneumo. So the Respiratory Viruses Legionella spp. H. influenza
minor fissure instead of being straight, it bulges Respi viruses
down so even the radiologist would see this, they
would tell you that the patient possibly has EPIDEMIOLOGIC FACTORS SUGGESTING POSSIBLE CAUSE
Klebsiella pneumonia infection. This is quite FACTOR POSSIBLE PATHOGEN(s)
typical.
Alcoholism – prone to develop  Strep. Pneumonia
Multifocal  Staphylococcus aureus infection from Strep. pneumo,  Oral anaerobes
Opacities  Coxiella burnetti
Klebsiella,and they tend to  K. pneumonia
 Legionella pneumophilia aspirate.  Acinetobacter spp.
 Streptococcus pneumonia – tend to
 M. tuberculosis
present as lobar consolidatoin
 Aspiration –
Miliary Infiltrates  Mycoplasma tuberculosis - #1 oropharynx – aerobic +
In areas where fungal infections are common anaerobic
 B. dermatitidis
COPD and/or smoking  H. influenza
 H. capsulatum
 P. aeruginosa
 Coxiella immitis
 Legionella spp
 Varicella zoster
 S. aeruginosa
Segmental or  M. tuberculosis (Primary infection)  S. pneumonia
Lobar Pneumonia  Atypical rubeola  Moraxella catarrhalis
with LAD This would mean enlargedf lymph nodes, (most common in
possibility of primary complex or Ghon lesion, or COPD)
possibility of your atypical rubeola.  C. pneumoniae
Pneumatocoeles Sometimes in CXR, you will see a pneumatocele. Structural lung disease (ex.  P. aeruginosa - #1
If a radiologist, sees a pneumatocele, they would Bronchiectasis) Abnormality of  Burkholderia cepacia
tell you that it is highly suggestive of Staph. aureus. the lungs  S. aureus
Other microorganism may also lead to Dementia, stroke, decrease level  Oral anaerobes
pneumatocele such as Strep. pyogenes & of consciousness (aspiration)
Pneumocystis jiroveci. This is just like a bullae. There  Gram (-) enteric
is a capsule. Staph aureus is more common in
bacteria
pedia rather than the adult. The line if you look at
Lung abscess  CA-MRSA
the CXR, if you follow it, you will see the capsule
 Oral anaerobes
clearly, it is a very big bullae. This is not specific,
 Endemic fungi
there are other possibilities such as pyogenes and
 M. tuberculosis
jiroveci.
 Atypical mycobacteria
 Staphylococcus aureus
Travel to Ohio or St. Lawrence  Histoplasma
 Streptocoocal pyogenes
river valleys capsulatum
 P. jiroveci
Travel to Southwestern US –  Hantavirus
Round pneumonia  Coxiella burnetti
California  Coccidioldes spp
 Strep. pneumonia
Travel Southeast Asia – Be careful  Burkholderia
 Legionella pneumophilia
of your SARS pseudomallelei
 Staph. aureus
 Avian influenza virus
These are radiographic findings because you definitely need to get a
Stay in a hotel or cruise ship in  Legionella spp
Chest X-ray for you to say that the patient has Pneumonia. The feature of
previous 2 weeks
CXR may help in determining the offending microorganism.
Local influenza activity  Influenza virus
 S. pneumonia
 S. aureus
Exposure to bats or birds  H. capsulatum

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 Exposure to birds  Chlamydophila psittaci
or bird flu
Exposure to rabbits  Francisella tularensis
Exposure to cats – pregnant cat,  Coxiella burnetti
goat or sheep
HIV (early) – CD 4 count is  S. pneumonia
relatively good, around 200.  H. influenza
 M. tuberculosis
HIV (late) – CD4 is less than 200.  S. pneumonia
Think of atypical microorganisms  H. influenza
such as  M. tuberculosis
 P. jiroveci
 Cryptococcus
 Aspergillus
 M. kansai

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

 P. aeruginosa

PNEUMONIA SEVERITY INDEX

The more severe, the patient’s Pneumonia is, then the level of care would
be higher. If your patient has severe Pneumonia, then that means he needs
to be in the Intensive Care Unit, but if their Pneumonia Severity Index is low
then that means the mortality will also be low, then we may be able to take
care of them as an outpatient.

Step 1. First of all, we have to determine if the patient has Pneumonia or

not. 1st step is you have to take a CXR. The patient has manifestations
suggestive of Pneumonia, you take a CXR, there is Pneumonia. Then, if there
is Pneumonia. The next step is to take note of the age of the patient. Is the
patient more than 50 years old?
 If you need only to be at STEP 1, then obviously you belong at Risk
 If yes, then you go automatically to Step 2.
Class I. So that means the risk of mortality is very, very low and you can
 But if the patient is less than 50 years old, then you check if the
take care of the patient in an outpatient basis.
patient has other concomitant illness like malignancy, heart
 If your patient’s score is 70, then Risk Class 2. 71-90 is Risk Class 3. 91-
failure, cerebrovascular disease, congestive heart failure, renal
130 is Risk Class 4. More than 130 is Risk Class 5.
disease.
 In patients who are at Risk Class 1, the risk of mortality is almost 0. If the
 If yes, the patient has other concomitant illness, go
patient reached Risk Class 5, the mortality is really high at almost 30%.
immediately to Step 2.
 That means if the patient belongs to Risk Class 4, the patient has to be
 But if no, the patient does not have other concomitant illnesses,
hospitalized.
you further check the patient’s vital signs, is the pulse rate more
 If Risk Class 5, ICU.
than 125 bpm? RR is more than 30? Or your temp is less than 36
 If Risk Class I or 2, then the patient can be taken care of in outpatient
or more than 40˚C? Or your Systolic BP is less than 90 mmHg?
basis.
- If no, then you consider the patient automatically to the
 If patient belongs to Risk Class 3, a few days of hospitalization for
low risk class 1.
treatment and the patient can be discharged after 2-3 days stay at
 If yes, then the patient has to go to Step 2.
the hospital.
The Step 2 involves quite a lot so you have to check the age of the patient.
 This is a very tedious process and very long, but this is the guidelines
If the patient is a male, you put the age as is. So 70 years old, 70. That means
that is recommended by the American Thoracic Society and the
the patient has 70 points already.
Infectious Disease Society of America.
If the patient is female and she is 70 years old then deduct 10 from the age
RISK CLASSES NO. OF POINTS RECOMMENDATIONS
that means the patient now has 60 points (female = age-10).
FOR SITE OF CARE
Then, we check if the patient is living in a nursing home. If he/she is, add 10.
Does the patient have any coexisting illness, like I No predictors Outpatient
- Neoplasm: If the patient has Neoplasm, add 30. II <70 Outpatient
- Liver disease, add 20. III 71-90 Inpatient (briefly)
- CHF, Cerebrovascular Disease, Renal Disease, add 10. IV 91-130 Inpatient
- If the patient has all of these, you put it all together and V >130 Inpatient
add it all up.
2nd part of Step 2: Check the Physical Examination: MORTALITY RATE AT 30 DAYS AMONG PATIENT WITH CAP, ACCORDING TO
 Does the patient have altered level of consciousness? If PORT RISK CLASS
yes, add 20 points. RISK OPD IN PATIENTS
 Is the RR more than 30? If yes, add 20. CLASSES
 SBP of less than 90 mmHg, add 15. I 0 0.5 (HOME)
 Temp of less than 35˚C or more than 40 ˚C, add 15. II 0.4 0.9 (HOME)
 Pulse rate of more than 125, add 10. III 0 1.25 (HOSPITALIZATION, COMPLETE
- If no, don’t give any points. TREATMENT HOME SUPERVISION)
3rd part of your Step 2: Laboratory exam. IV 12.5 9.0
 Arterial pH is less than 7.35, add 30 V NA 27.1 (ICU)
 BUN of more than 30 or 11mmol/L, add 20 MEAN 0.6 8
 Serum Na less than 130, add 20.
 Glucose of more than 250, Hemoglobin of less than 9 g/dl CURB – 65
or Hematocrit of less than 30%, PaO2 less than 60 mmHg or There is an easier one with a total of 5 points. 5 points that means you
SaO2 less than 90% at room air, pleural effusion on CXR, all have very severe Pneumonia, you need to be in the intensive unit already
of these would have 10 points each. If there is none, do not automatically.
give any points. C – CONFUSION
Add all the points up and determine the risk class. U – UREA >7mmol/L
R – RESPIRATORY RATE > 30/min
B – BLOOD PRESSURE: SYSTOLIC <90 / DIASTOLIC <60
AGE > 65 – 65 stands for the age of the patient which is equal to 65 or
more than 65.

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 If the patient has 1 point, the patient’s risk of mortality is low so the  If yes, then check whether the patient has hypoxemia or
patient can be treated at an outpatient basis. hypoperfusion that means either of the 2, the patient
 2 points means the patient has to have close monitoring, a few days belongs to HIGH RISK GROUP. The patient has to be
in the hospital and then you can send the patient home. hospitalized in the ICU.
 If the patient has 3 points or more, it means the patient has Severe - If not, that means the patient has MODERATE RISK
Pneumonia, the patient has to be hospitalized. PNUEMONIA. The patient still has to be hospitalized, NOT in
 If the patient has 4 or 5 points, that means the patient has to be the ICU, but in the GENERAL WARD.
taken care for at the ICU.
0 0.7% No hospitalization
1 3.2 % Hospital (OPD)
2 13 % Hospital (assessment supervised)
3 17. 5 % Severe
4 41.5 % CAP
5 57 % Urgent Admission
So CURB-65 need a laboratory result. So if you are practicing for

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

outpatient because this is for Community Acquired Pneumonia, you may
not have the luxury to be attached to a laboratory so they put it now as
CRB-65, removing the U.
CRB - 65
 Applicable to office-based setting
 Score
0 Home treatment
1 Hospital – supervised
>2 Hospitalization
 The maximum point now would be 4. So if you have a point of 0,
then that means home treatment.
 1 point, hospital-supervised treatment and then if patient has 2 or
more than 2, then the patient has to be hospitalized because the risk
of CAP is very high.
 This is easier than PSI. This is the recommended by the British Thoracic
Society.

 Now the American Thoracic Society, not in collaboration with

Infectious Diseases Society of America, list down the minor and major
criteria.
CRITERIA FOR SEVERE COMMUNITY ACQUIRED PNEUMONIA
MAJOR  Invasive mechanical ventilation
CRITERIA
MINOR  RR > breaths/min → severe pneumonia
CRITERIA  PaO2/FiO2 ratio <250 LOW RISK CAP
 Multilobar infiltrates  MORTALITY RATE: <5%
 Confusion/ Disorientation  CLINICAL FINDINGS
 Uremia (BUN level, > 20 mg/dl)  Chest X-ray: localized infiltrates,
 Thrombocytopenia (Platelet, CT, <100,000 no evidence of pleural effusion
cells/mm3)  No progression within 24 hours
 Hypothermia (core temp, <36C)  DIAGNOSTIC WORK-UP
 Hypotension requiring aggressive fluid  Chest X-ray
resuscitation – Because some patients will  Sputum GS/CS - no need for you to give sputum exam or
have hypotension and if you give other diagnostic work up but if you want you can do the
intravenous fluid, the BP would elevate then sputum exam.
that’s okay already. However, some patient  POTENTIAL PATHOGENS
would not respond to your fluid challenge,  Strep. pneumonia
and you may have to give Inotropic agents  Chlamydia
(medicine to bring up the BP).  Moraxella catarrhalis
 Minor criteria would only need fluid resuscitiation.  Enteric gram (-) bacilli – esp. those with co-morbid conditions
 Major criteria would need medications to bring up the BP or need  M. pneumonia
mechanical ventilation.  H. influenza
 From your American Thoracic Society, if you have 1 major criterion  TREATMENT
already, that means the patient is already severe and you need to  Amoxicillin
be admitted to the ICU. Much easier than PSI.  Alternative: extended Macrolides (Azithromycin,
Clarithromycin) – If patient is allergic to Amoxicillin or cannot
MANAGEMENT – ORIENTED RISK STRATIFICATION OF CAP IN give Amoxicillin
IMMUNOCOMPETENT ADULTS  With stable co-morbid illness: Co-Amoxiclav, Sultamicillin, 2nd
 Philippines has our very own guidelines. generation cephalosporins – or extended macrolides
 First of all, we need to determine if our patients have Pneumonia or
not or what we all our Community Acquired Pneumonia. That means MODERATE RISK CAP
they need to have clinical manifestation and Chest X-ray showing  MORTALITY RATE: 21%
increased risk of highly suggestive of Pneumonia.  CLINICAL FINDINGS
 The vital signs of the patient, the RR of more than 30, PR of more than  Unstable vital signs:
125, Temp of more than or equal to 40 or less than 35 ˚C,  RR >30 bpm
extrapulmonary or manifestation of infection that means the patient  Temp – 35 ˚C / <40˚
may have sepsis, unstable co-morbid conditions which means the  PR > 125 cpm
patient may have Heart failure, Liver failure, Renal failure or have DM  Unstable co-morbid condition
that is uncontrolled, CXR if it is multilobar, pleural effusion, abscess,  DM, CAD, CHF, RF/dialysis, COPD uncomplicated, malignancy
progression of lesion of more than 50% within 24 hours.  Suspected aspiration
- If no that means the patient belongs to the LOW RISK  CXR: multilobar infiltrates
GROUP. We can take care of them in an outpatient basis.  (+) pleural effusion
 Progression of finding to >50% in 24 hours
Page 7 of 10
 POTENTIAL PATHOGENS Actually, it is easy to determine if the patient has Severe Pneumonia or not
 Additional to low risk PLUS: and we can just use the RR if the patient usually has a normal RR. That
 L. pneumophilia means, previously the patient does not have underlying lung problem. So
 Anaerobes that means the RR is within the normal range but now you have difficulty
 DIAGNOSTIC WORK-UP – CXR & Sputum GS/CS of breathing and if the RR is more than 30, please automatically tell the
 CXR patient has severe pneumonia and that he is at the high risk group.
 Blood culture
 Sputum GS/CS ANTIBIOTIC RESISTANCE
 When available: serologic test or antigen determination We are seeing increasing antibiotics. You have to be very careful when
for the atypical microorganism you give the antibiotics
- Part Agglutinin – M. pneumonia
- Microimmunofluorescence – C. pneumonia (elderly) S. pneumonae
- Direct Fluorescent Antibody (DFA) – L. pneumophilia There is a decrease in strep. pneumoresistance to antibiotics. This is
- Urine Ag. – L. pnuemophilia because of the immunity of the microorganism through the
 TREATMENT  Direct DNA incorporation and remodeling resulting from

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

 IV non-pseudomonal contact with closely related oral commensal bacteria
 B-lactamase with or without B-lactamase inhibitor plus  True or Natural transformation
macrolides or anti-pneumococcal fluoroquinolones (your  Genes
Levofloxacin) That’s why they are becoming resistant to the antibiotics we are giving.
That’s why infection control is very important.
HIGH-RISK CAP Pneumococcal Resistance to B-lactam drugs
 MORTALITY RATE: 36%  Low affinity penicillin-binding protein
 CLINICAL FINDINGS  Risk Factors
 Shock o Recent microbial therapy (< 3 months) – within 3 months
 Hypoxemia of antibiotic therapy
 POTENTIAL PATHOGENS o Young Age < 2 years old or elderly >65 years old
 Additional to moderate risk plus o Day care centers
 P. aeuruginosa o Recurrent hospitalization
 Staph. aureus o HIV infection
 DIAGNOSTIC WORK-UP o **MICs: <2ug/L - less than 2 or equal to 2 nanogram/mL
 ABG plus moderate risk Macrolides
 TREATMENT o Target site modification caused by ribosomal methylation
 No risk P. aeruginosa 23s rRNA encoded by ermB gene. MICs: 65ug/L – higher
- IV non-pseudomonal B-lactam with or without resistance to antimicrobial compared to efflux
B-lactamas inhibitor plus IV macrolide mechanism
- IV anti-pneumococcal fluoroquinolones o Efflux mechanism aided by ref genes (IV) phenotype is
 With Risk P. aeruginosa usually associated with low renal resistance, MICs: 132ug/L
- IV anti-microbial B-lactam with or without B- The resistance of your Strep. pneumonia to your macrolides is 45%.
lactamase inhibitor plus IV macrolide For the target site modifications, 65% for your influx mechanism
- IV anti-pneumococcal fluoroquinolones +/- Pneumococcal to fluoroquinolones
aminoglycoside or IV ciprofloxacin – Because o Change in one or both target sites in topoisomerase II and
your Ciprofloxacin is for your Pseudomonas IV result for mutation in the gyA and parC genes
infection o Efflux pump
o **Most important risk factor is use of specific antibiotic use
ANTI-PNEUMOCOCCAL FLUOROQUINOLONES within 3 months (should not be the same antibiotic) – We
 Levofloxacin do not want to repeat the antibiotics within 3 months of
 Moxifloxacin giving the antibiotics. That’s why it is important for us to be
NON-PSEUDOMONAL B-LACTAM asking what are the other drugs the patient has received
 IV β – lactams or has been taking for the past months especially if you
 2nd generation (cefuroxime sodium) want to give antibiotics.,
 3rd generation (ceftriaxone, cefotoxime)  We are also seeing nowadays, increasing incidence of Methicillin
 Anaerobic activity (cefoxitin, ceftizoxime, ertaperum) resistance Staph. aureus (MRSA.) This is due to the classical hospital
 IV β-lactams with β-lactamase acquired strain or recently we have seen in the community acquired
 Ampicillin strain. And it is because of the resistance to the SCCmec resistance.
 Anti-pseudomonal IV β-lactams For the hospital acquired resistance, it is usually the Type 2 or Type 3
 Those without anaerobic activity SCCmec element. But for the community acquired resistance, it is
 4th generation – Cefepime usually the Type 4 SCCmec resistance.
 Those with anaerobic activity  For the community acquired Staph. resistance, usually they would be
 Carbapenem (Imipenem – Cilastatin, Mepenem) susceptible to your oncomycin, Trimethopim-Sulfamethoxazole.
 IV β-lactams with β-lactamase inhibitor Gram negative bacilli
 Cefoperazone + sulbactam o Fluoroquinolones → E. coli resistance
 Ticarcillin + Clavulanic acid o Enterobacter spp. → DOC → fluoroquinolones
 Piperacillin + Tazobactam This is due to your health care associated Pneumoniae. This does not
mean that the patient has been hospitalized but has exposure to health
There are certain risk factors for early deterioration such as your CAP. And, care personnel. That would be your HCAP.
if this is present of the patients, then you have to be very watchful of the
higher mortality and morbidity of the patients. These are
 Lobar infiltrates seen in CXR
 Severe hypoxemia (O2 sat of less than 90%)
 Severe acidosis
 pH of less than 7.3
 Confusion
 Severe tachypnea, RR of more than 30
 Hypoalbuminemia
 Neutropenia
 Thromboyctopenia
 Hyponatremia
 Hypoglycemia

Page 8 of 10
 For the EMPIRICAL TREATMENT recommended by the American Thoracic
Society together with the Infectious Disease Society of the America:
Or the patient may fail to improve because the pathogen or culprit is not
correct that’s why we gave the wrong antibiotics. We can give the correct
antibiotics with correct dosage if we have the correct microorganism. Or
the patient has already a superimposed nosocomial infection so the
patient may have Pneumonia because of Strep. pneumo because of the
hospital stay they acquired another microbe that causes Pneumonia. This
time it may be Pseudomonas, so we may be treating the patient who has
superinfection that we do not know about.

Usually we expect the patient to improve in 2-4 days.

We want prevent the recurrence of Pneumonia. We can prevent this by

giving vaccine. Around 70% of CAP may lead to hospitalization due to your
Strep. pneumoniae, so we give vaccine against your Strep. pneumonia,
and yearly Influenza vaccine. Influenza can cause problem and increase

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

vulnerability of the patient’s to the development of Pneumonia so we do
not want patients to develop Influenza infection. And, in case, you are not
able to give the vaccine and there is already the epidemic, then you have
to give chemoprophylaxis like your Oseltamivir or Zanavimir but we do not
have Zanamivir. We have Oseltamivir but it is very expensive and you have
to give it as soon as the patient has symptoms you have to give it.

Cigarette smoking may increase the risk of Pneumonia, alcohol may

increase the risk. We advise the patient to avoid these vices.

Sometimes patients who have CAP, may have clinical complications such
as: respiratory failure, mechanical ventilator, or they may develop septic
shock. So if the patient has severe infection, they may develop septic
shock, multiorgan failure. This can also cause problem with coagulability
and of course any illness can cause exacerbation of comorbid conditions
like heart failure, renal failure, liver failure. This may also lead to Strep
infection to other parts of the body, as well as typical lung abscess or
complicated bipleural effusion which we call as your PARAPNEUMO
EFFUSION.

PNEUMONIA II: HCAP

HCAP
 Incident of MDR pathogens is high as higher than HAP/HAV
 MDRSA was more common in HCAP than in the traditional HAP/HAV
or your ventilator-associated Pneumonia.

So what are the risk factors for the development of HCAP or at risk of
getting health-care related Pneumonia. These are patients who have
short hospital stay, hospitalized for more than 2 days in the last 3 months,
Out Patient those who have been taken care of in nursing home extended-care
o 5-7 days → antimicrobial facility residence, antibiotic therapy for the last 3 months, chronic dialysis,
Other treatment patient’s who have renal failure or diabetic foot, patients who have home
o Hydration – very important infusion therapy – let’s say they have problem with nutrition at home or
o Oxygen/mechanical ventilation – if patient is hypoxemic, has to be given antibiotics at home, they are at risk for HCAP or family
give supplemental O2. If the patient needs to be member with MDR infection.
connected to a mechanical ventilator, try to tie the patient Table 251-1 Clinical Conditions Associated with and likely pathogesn
over the in-sole to the lung, then we need to connect the in Health-Care Associated Pneumonia
patient to the mechanical ventilator. Condition Pathogen
o Adrenal sufficiency – glucocorticoids MRSA Pseudo Acine MDR
Sometimes they recommend giving Immunomodulin-lowering therapy monas aeru Tobac Entero-
such as your **** but we don’t get this here so this is recommended to ginosa ter spp. bacter
patient who have persistent septic shock, severely ill patients. iaceae
Failure to improve Hospitalization for X X X X
If we give the correct medicine or the medicine we give is effective, then 48 hrs
we expect the patient to be afebrile within 2-3 days. Generally, 3 days and Hospitalization for X X X X
the WBC count would also drop within this period of time. Clinically, the 2 days in prior 3
patient will improve, but do not expect the CXR to improve. There is always months
a radiologic lag just like sometimes we suspect Pneumonia, but when we Nursing home or X X X X
get the CXR and it would be normal. After 24 hours, you repeat the CXR, it extended-care
would already show Pneumonia. There would always be radiographic lag. facility residence
In the resolution, there would also be a radiologic lag, but if you take the Antibiotic therapy X X
CXR one month after the bout of Pneumonia and there is still infiltrates then in preceding 3
there is very big question to the radiographic lag already. Usually, in 1 months
month time the infiltrates should have resolved already so there may be Chronic dialysis X
another problem to consider. Like if your patient is not improving despite Home infusion X
the medications, you may have the wrong diagnosis because the patient therapy
may have the following: Home wound X
o Pulmonary edema care
o Pulmonary embolism
Family member X X
o Lung CA
with MDR
o Radiation and hypersensitivity pneumonitis
infection
o Tissues disorders molding the lungs

Page 9 of 10
Note: MDR, multidrug-resistant; MRSA – methicillin-resistant
Staphylococcus aureus

What are the pathogens we have to look out for? The most common
would be your Methicillin-Resistant Staph. aureus (MRSA), followed by your
Pseudomonas aeruginosa, and your multi drug resistance
Enterobacteriacaea, and then lastly would be your Acinetobacter.

- NEXT LECTURE: CONTINUATION OF HCAP &

BRONCHIECTASIS -

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

-LIGHT-
Please do not rely on this. Double check for any mistakes. Read
the book and study well. God bless, doctors! Thank you.
Thank you to JKCP Villarama Trans & Magallanes Marca ’12 Trans
for the lecture outlines.

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