Pneumonia 2

Classification of Pneumonia: Acute Pneumonia: Community acquired:oPerson to person

•Classical bacterial pneumonia

•Atypical bacterial pneumonia

•Viral pneumoniao 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; dark-red 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: Histology Lab:

Tuberculate macroconidia. 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 .