Pneumonia 2
Classification of Pneumonia:

Acute Pneumonia:
 Community acquired:
oPerson to person
• Classical bacterial pneumonia
• Atypical bacterial pneumonia
• Viral pneumonia
o Animal, or Environmental Exposure.
 Nosocomial acquired.
 Chronic Pneumonia.
Animal, or Environmental
Exposure:
o Legionellosis.
o Tularemia.
o Plague.
o Q fever.
o Anthrax.
Legionnaires' disease ( legionellosis)
History:
 Legionnaires' disease was diagnosed for the first
time in 1976 in Philadelphia among attendees of a
Legionnaires' convention held in a hotel, 182
attendees contracted the disease and 29 of them
died.
 It had caused several outbreaks. The last one was
in November 12 2014 in Portugal , 302 people
have been hospitalized and 7 died.
• Causative agent: Legionella pneumophila.
• Microscopy:
- Gram’s negative rod in nature,
coccobacilli in clinical specimens.
- Facultative intracellular parasites.
- Rods are motile by monotrichous flagella.
Transmission:
o Inhalation of contaminated water aerosols
from showers, humidifiers, air condition…..It
lives inside the free living protozoa.
o No person to person transmission.
o It had caused several outbreaks as well as
sporadic cases and nosocomial infections.
N
Pathogenesis:
- Engulfment by alveolar macrophages.
- Inhibition of phagosome-lysosome fusion.
- Replication inside the microphages until it
ruptures.
- Monocytic and neutrophils infiltration of
alveoli; TNF-α, and INF-γ production.
- Alveolitis (consolidation) and micro-abscess
and cavity formation.
- Bronchi are not affected.
N
Laboratory diagnosis:
-Staining of specimens (sputum, bronchial
aspirate) by gram stain and Giemsa stain.
-Cultured on buffered charcoal yeast extract agar
(BCYE; Enriched media: cysteine, iron) for 3- 5
days.
-Rapid identification:
Immunofluorescent microscopy.
PCR.
N
Pneumonic Tularemia (granulomatous
infection):
• Causative agent: Francisella tularensis.
• Gram negative capsulated coccobacilli with.
Facultative intracellular parasite. Obligate
aerobic bacteria.
Transmission: from animals (rabbit, birds) to man
(zoonosis) .Highly infectious.
• Arthropods bite; vector (ticks, mites).
• Skin penetration; handling infected animal
tissues.
• Inhalation of infectious aerosols.
• No person – person transmission.
N
Pathogenesis and clinical presentation:
N
Clinical presentations:
•
Ulceroglandular tularemia: (the most
common presentation). Infection of skin
macrophage; ulcerative papule at the site of
bite or entry; transmitted to regional lymph
nodes; lymphadenitis.
• Hematogenous dissemination: to the lungs.
liver, spleen, bone marrow.
• Pneumonic tularemia: By inhalation or
blood dissemination. Infection of alveolar
macrophage; granuloma in the lung.
Laboratory Diagnosis:
Cultured on buffered charcoal yeast extract
agar (BCYE) (Enriched media: cysteine,
iron).
N
Pneumonic Plague
• Causative agent: Yersinia pestis.
 Gram negative coccobacilli.
 In sputum: Gram negative bipolar-stained
(safety pin appearance).
• Virulence factors:
o Capsular antiphagocytic antigens: F1, V, and W.
o Lipopolysaccharide (LPS) endotoxin.
o Plasminogen activator: degrades fibrin.
Transmission:
• Vector-borne: insect bite (fleas) from rats.
• Skin penetration.
• Person-to-person: inhalation of droplets.
N
Infective dose: 100-500 cells.
Incubation: 2-8 days.
Three clinical presentations:
• Primary: Bubonic plague: Swollen tender
regional lymph node (buboes); lymphadenitis
(hemorrhagic necrosis).
• Septicemic plague: DIC, purpura and
ecchymosis.
• Pneumonic plague: (Bronchopneumonia):
o Primary: Inhalation of droplets.
o Secondary: Hematogenous spread.
N
Black death: ischemic lesion + cyanosis
Treatment of Plague:
• Pneumonic plague should be treated within 24 hours
of appearance of symptoms, (mortality rate
approaches100%).
Inhalation anthrax: Wool sorter's disease:
• Causative agent: Bacillus anthracis
Gram positive aerobic spore-forming bacilli.
• Transmission: inhalation of spores.
Clinical presentation of inhalation anthrax:
 Inhalation anthrax; hemorrhagic mediastinal
lymphadenitis: not a true pneumonia: alveolar
macrophages transfer the spores to the
mediastinal and peribronchial lymph nodes.
 Anthrax meningitis; in 50% of inhalation cases;
extensive hemorrhage in the leptomeninges; darkred appearance on autopsy “Cardinal’s cap” .
Treatment:
-Only if multiple intravenous antibiotics and passive
vaccine administered prophylactically after spore
exposure.
Hospital-acquired
Pneumonia (Nosocomial)
Nosocomial pneumonia: pneumonia acquired during
or after hospitalization (at least 72 hour after
admission)
Who are at Risk?
• Patients on mechanical ventilation (ICU).
• Immunocompromised patients.
• Other factors: malnutrition, heart and lung diseases.
Causative agents:
Aspiration of oropharyngeal and GIT flora &
hospital bacteria: methicillin resistant S. aureus
(MRSA), Pseudomonas, Enterobacter, Klebsiella,
Serratia, VRE and Acinetobacter (person-to person).
Chronic Pneumonias
(coccidioidomycosis,
histoplasmosis)
Chronic granulomatous pneumonia:
o Bacterial granulomatous pneumonia
Mycobacterium tuberculosis.
• Acid-fast bacilli (Mycolic acid waxy capsule).
• Cultured on Lowenstein-Jensen agar.
• Stained by Z.N stain.
• Fungal granulomatous pneumonia: Endemic
in America.
• Coccidioidomycosis.
• Histoplasmosis.
• Blastomycosis.
• Paracoccidioidomycosis
Coccidioidomycosis:
Caused by dimorphic fungi :Coccidioides immitis.
• In the environment; they are molds with hyphae
and arthroconidia (the infective stage).
• In the tissues, a large structure called spherule
filled with endospores (the diagnostic stage).
Pathogenesis and tissue damage:
- Arthroconidia engulfment by alveolar
macrophage; spherule.
- T cell mediated immunity and macrophage
activation.
N
Clinical presentations:
o Asymptomatic or mild flu like illness.
o Acute pulmonary infection; fever, dry
cough and chest pain (self-limited illness).
o Chronic pulmonary infection with
cavitation; in a small number of people.
o Chronic meningitis.
o Disseminated infection: in cell-mediated
immune deficiencies (e.g. AIDS):
cutaneous or systemic infection.
Histoplasmosis:
• Causative agent: the dimorphic fungus
Histoplasma capsulatum (non-capsulated).
• Pathogenesis and tissue damage:
-Inhalation of microconidia (infective stage);
engulfed by alveolar macrophage.
-Transferred into yeast form (diagnostic) that
modulate the phago-lysosomal pH.
-T cell mediated immunity; killing of yeast by
macrophage; Granuloma formation.
N
• Depending on pathogenic dose and T-cell
mediated response:
• Patchy pneumonitis.
• Mediastinal lymphadenopathy
• Chronic cavitary pulmonary
histoplasmosis, in patients with chronic
obstructive pulmonary disease (COPD).
• Acute disseminated histoplasmosis: in
immunocompromised:
hepatosplenomegaly, mucus membrane
ulcers, sepsis, and DIC.
N
Diagnosis:
Microbiology Lab:
Tuberculate macroconidia.
Histology Lab:
Macrophage with yeast cells.
Fungal Pneumonia in AIDS patients
• B - Cryptococcosis
• A - Pneumocystis pneumonia: (The most common).
-Caused by Pneumocystis jiroveci (P.carinii).
-Yeast lacking ergosterol in cell membrane and so can
not be treated by amphotericin.
-Encysted forms infects alveoli; exudate; blocks gas
exchange.
-Treatment: Sulfamethoxazole and trimethoprim.
Cysts of Pneumocystis carinii ; Sliver stain.
N
B- Cryptococcosis:
Causative agents: Cryptococcus neoformans.
-Yeast transmitted to man from birds (pigeon).
Capsulated microbe.
-Pneumonia and meningitis in
Immunocompromised host.
The Budding capsulated yeast
Cryptococcus neoformans
as shown in India ink wet
mount .