31
Lower respiratory tract Lungs are axenic (no normal flora) – Pneumonia • Described by location, pathogen or way contracted – Pleurisy

Lower respiratory tract Lungs are axenic (no normal flora) –Pneumonia Described by location, pathogen or way contracted –Pleurisy

Embed Size (px)

Citation preview

Lower respiratory tract

• Lungs are axenic (no normal flora)– Pneumonia

• Described by location, pathogen or way contracted

– Pleurisy

Pneumococcal Pneumonia• Most common bacterial pneumonia• Causative agent

– Streptococcus pnuemoniae• Gram positive• Encapsulated, diplococci

• Signs and Symptoms– Cough; fever; congestion; chest pain; rust tinged sputum– Breathing becomes shallow and rapid– Skin becomes dusky due to poor oxygenation– Consolidation may occur

– Recovery is usually complete• Most strains do not cause permanent damage to

lung tissue

– Complications • Pleural effusions• Septicemia• Endocarditis • Meningitis

• Epidemiology– 75% of healthy individuals carry encapsulated

strain in their throat• Bacterial rarely reach lung • Risk of pneumonia rises when cilia destroyed

• Gram stain of sputum used for diagnosis • Pneumococci confirmed with quelling reaction

• Bacteria that reach alveoli cause inflammatory response

• Adhesions • Capsule• Phosphorylocholine in cell wall• Pneumolysin (cytotoxin)• IGA proteases

• Prevention – Pneumococcal vaccine

• Treatment– Antibiotics successful if given early

• Penicillin (some resistance) • Erythromycin, cephalosporin and chloramphenicol

Klebsiella Pneumonia

• Leading cause of nosocomial pneumonia

• Causative agent– Klebsiella pneumoniae

• Gram negative• Encapsulated, Bacillus• Produce mucoid colonies

• Signs and Symptoms:– Typical pneumonia symptoms combined with

a thick, bloody sputum and recurrent chills

– Organism causes tissue death• Leads to formation abscess in lung or other tissues • Endotoxin can trigger shock and disseminated

intravascular coagulation

• Epidemiology– Endogenous – Difficult for K. pneumoniae to infect lungs of

healthy persons • Leading causes of nosocomial death• Also causes UTI, meningitis and wound infections

– Diagnosed with chest x-ray and sputum culture

• Prevention – No vaccine available – Employ good aseptic technique

• Treatment– Antimicrobial treatment limited

• Cephalosporin combined with an aminoglycoside• Tissue damage and release of endotoxin can cause

permanent damage to lungs • High fatalities even with treatment

Mycoplasmal Pneumonia• “Walking pneumonia”

– Leading pneumonia in children

• Causative agent– Mycoplasma

pneumoniae• Small, pleomorphic,

Gram + • No cell wall• Prominent capsule

• Signs and Symptoms– Onset is gradual

• 1-4 week incubation period

– First symptoms include• Fever, headache, muscle pain, fatigue, sore throat

and excessive sweating • atypical for pneumonia• Persistent dry cough for several weeks

• Organism attaches to receptors on epithelium– Adhesion protein – Interferes with cilia, cells die and slough off– Capsule protects it from phagocytosis – Inflammation initiates thickening of bronchial and

alveolar walls• Causes difficulty in breathing

• Epidemiology– Spread through aerosol droplets

• Survive for long periods in secretions

– Grow slowly in culture • 2-6 weeks for “fried egg” colonies to appear

– Diagnosis difficult• Serological tests required

• Prevention and treatment– No practical prevention

• Avoid crowding in schools and military facilities• Aseptic technique

– Antibiotic treatment• Penicillins are ineffectual (WHY?)• Antibiotics of choice are tetracycline and erythromycin

Pertussis

• Whooping Cough• Causative agent

– Bordetella pertussis• Small, Gram negative• Encapsulated, coccobacillus

• Signs and Symptoms:– Catarrhal stage – cold symptoms (1-2 weeks)

– Paroxysmal stage – severe coughing (2-4 weeks)• Coughing followed by characteristic “whoop”• May cause vessels in eyes to rupture • Cyanosis• Vomiting, diarrhea and seizure may occur

– Convalescent phase –persistent cough (months)

• Pathogen enters respiratory tract and attaches to ciliated cells– Produces 2 forms of adhesions

• Colonizes upper and lower respiratory tract

– Produces numerous toxic products • Mucus secretion increases and cilia action decreases• Cough reflex is only mechanism for clearing

secretions• Decreased blood flow and WBC activity

• Epidemiology– Spreads via infected respiratory droplets– Highly contagious – Most infectious during runny nose period– Classically disease of infants– Often overlooked as a persistent cold in adults

– High risk of secondary infections!

• Prevention – Immunization

• Combined with Diphtheria and tetanus toxoids

• DTaP

• Treatment– Primarily supportive – Erythromycin may reduce infectivity if given early

Tuberculosis

• TB; Consumption • Causative agent

– Mycobacterium tuberculosis

• Gram positive• Acid fast, slender

bacillus• Cord factor

• Signs and Symptoms– Chronic illness– Initial symptoms:

• Minor cough and mild fever

– Progressive symptoms:• Fatigue; night sweats; weight loss; chest pain and

labored breathing • Chronic productive cough

– Sputum often bloody

• 3 types of tuberculosis:– Primary TB- initial case of tuberculosis disease– Secondary TB - reactivated – Disseminated TB- tuberculosis involving multiple

systems

• Primary TB– Transmitted through respiratory droplets – Pathogens taken up by alveolar macrophages

• fusion of phagosome with lysosomes prevented– Pathogen replicates inside macrophages slowly killing

them– Intense immune reaction occurs

• WBCs surround infected cells and release inflammatory chemicals

– Other body cells deposit collagen fibers

– macrophages and lung cells form tubercle

– Infected cells die producing caseous (cheesy) necrosis

– Body may deposit calcium around tubercles

• Ghon complex

– Secondary TB • tubercle ruptures and reestablishes active infection• More common in immunosupressed • Leading killer of HIV+ individuals

– Disseminated TB• Some macrophages carry pathogen through blood

and lymph to other sites of body• Bone marrow, spleen, kidneys, spinal cord and

brain

• Epidemiology– 1/3 of world population infected– Annual mortality of ~ 2 million – Estimated 10 million Americans infected

• Rate highest among non-white, elderly poor people– Small infecting dose

• As little as ten inhaled organisms• Not very virulent but high mortality

• Tuberculin test• Tuberculosis antigen injected

under skin• Injection site become red and

firm if positive• Positive test does not indicate

active disease• Definitive tests include sputum

samples and chest x-rays

• Prevention – Vaccination used in other parts of the world– Prophylactic antibacterial treatment for exposed

individuals

• Treatment– Antibiotic treatment

• Rifampin, Isoniazid, streptomycin and ethambutol

• MDR strains

• Therapy lasts up to 6 months (DOTS)