Causative agents of an Airborne bacterial infection

6. Neisseria meningitides (meningococci) Resistance

• Family: Neisseriaceae Meningococci do not survive in the environment, and
• Genus: Neisseria die upon drying, cooling, at a temperature above
• Species: Neisseria meningitidis 50 °C. They are sensitive to disinfectants.
Neisseria meningitidis is the causative agent of Epidemiology
meningococci disease. A natural reservoir of meningococci is the mucous
membrane of the human nasopharynx.
• Gram-negative
• round-shaped (diplococci) The main source of infection are healthy bacteria
• motionless carriers, as well as patients with meningococcal
• do not produce spores nasopharyngitis, rarely patients with a generalized infection.
• have 4 types of pili The transmission mechanism is aerogenic,
• form delicate capsule of polysaccharide nature transmission route – airborne.
• Grow on enriched nutrient media Pathogenesis
• blood agar, and chocolate agar The causative agent has a tropism to the mucous
membrane of the nasopharynx, which is under certain
conditions, it multiplies and is released with nasopharyngeal
• LPs (polysaccharides)
mucus into the external environment, which corresponds to
• Capsule
the most frequent form of infection - meningococcus.
• endotoxin
• antigens of 4 serogroups: A, C, Y and W-135
With a decrease in the activity of local immunity, the
• type IV pili violation of microbiocenosis, meningococcus can penetrate
• external membrane proteins deep into the mucous membrane, causing inflammation and
• aggression enzymes symptoms of nasopharyngitis.
• oxidase-test positive
• carbohydrate activate
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 Causative agents of an Airborne bacterial infection
Only 5% of patients with nasopharyngitis
meningococcus, overcoming the local barriers, penetrate the Treatment
vessels of the submucosa, and then spreads the hematogenous Benzylpenicillin and its derivatives (ampicillin,
way. oxacillin). In case of intolerance to penicillins,
chloramphenicol (Levomycetin) or rifampicin are
Immunity administered.
after a generalized infection is high-grade,
antibacterial, with prevalence of humoral protection Prevention (prophylaxis)
mechanisms (bactericidal antibodies). The immunity is group- Inactivated chemical meningococcal vaccine - contains
specific. capsular polysaccharides.
The vaccine, produced in the USA, contains antigens of
Specimen 4 serogroups: A, C, Y and W-135.
cerebrospinal fluid, blood, mucus from the
nasopharynx.
Laboratory Diagnosis
1. Microscopic
2. Bacteriological (oxidase-test positive)
3. Bacterioscopic (immunofluorescent)
4.Serological
o PCR or ELISA
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 Causative agents of an Airborne bacterial infection
7. Mycobacterium tuberculosis (tuberculosis)
• Family: Mycobacteriaceae
• Genus: Mycobacterium
• Species: Mycobacterium tuberculosis, M. bovis, M.
africanum
Mycobacterium tuberculosis is the predominant causative
agent of tuberculosis in humans.
• (Acid-fastness) cannot be classified as either
gram-positive or gram negative (Ziehl-Neelsen)
• straight rods
• non-capsulated
• non-flagellum
• aerobic
• cultivated on selective and special media
• grow on media containing eggs, glycerin, potatoes,
asparagine, vitamins, salts
• usually grows in warty dry colonies with cream-
colored «ivory» pigment
• oxidation-reduction enzymes
• reduces nitrates into nitrites
• express lecithinase, phosphatase and urease
• carbohydrates and proteins activated
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• cell wall insoluble polysaccharide antigens
• cytoplasmic soluble protein antigens
• LPs (polysaccharides)
• cytoplasmic protein antigens
• Tuberculin
• glycolipids
Resistance
Mycobacteria show high resistance in the environment.
They remain viable in water for 1 year, in soil for 6 months,
in the home dust and dried sputum for several months.
Heating at a temperature of 100°C readily kills all
mycobacteria. They susceptible to sunlight and UV
irradiation.
Epidemiology
The main sources of infection are persons with active
tuberculosis.
The infection is transmitted predominantly by the
airborne route and more seldom by contact route.
Pathogenesis
Inhaled mycobacteria are ingested by lung
macrophages and transported to regional bronchial lymph
nodes. Mycobacterium tuberculosis survives within
phagocytes, blocking phagolysosome fusion.
 Causative agents of an Airborne bacterial infection
Primary lung tuberculosis is characterized by acute
exudative lesion affecting lung acinary tissue with subsequent
rapid involvement of lymphatic vessels and regional
bronchial lymph nodes.
Typical symptoms of progressive pulmonary disease:
Intoxication, fever, productive cough with hemoptysis,
enlargement of lymph nodes and abnormal results of chest X-
ray examination.
Secondary tuberculosis is characterized by chronic
tissue lesions (tubercles, cavities with caseous necrosis, etc.),
followed by disseminated fibrosis.
Secondary lesions are very difficult in treatment
showing no tendency to self-recovery.
Immunity
in tuberculosis is predominantly cell-mediated and non-
sterile, maintained by viable mycobacteria.
Specimen
sputum, lymph nodes puncture contents, urine, pleural
or cerebrospinal fluid, etc.
Laboratory Diagnosis
1. Microscopic (Ziehl-Neelsen & dry colonies with
«ivory»-colored pigment) method
2. Bacteriological (produces urease, reduces nitrates
into nitrites)
3. Bacterioscopic (immunofluorescent)
4. Biological method
5. Serological
o PCR or ELISA
6. Tuberculin test Mantoux (Mantoux allergic test)
Treatment
The course of tuberculosis patient lasts from 6 to 12
months. Antimicrobial drugs in tuberculosis treatment are
(isoniazid, rifampicin, pyrazinamide, ethambutol,
streptomycin).
Prevention (prophylaxis)
Specific prophylaxis BCG vaccine contains live
avirulent mycobacteria obtained from M. bovis by perennial
passages on media containing bile.
Non-specific prophylaxis of the disease is achieved by
isolation and adequate treatment of tuberculosis patients.
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 Causative agents of an Airborne bacterial infection
8. Bordetella pertussis (Whooping cough) • Protein toxins
• Family: Alcaligenaceae o Tracheal toxin
• Genus: Bordetella o Pertussis toxin
• Species: Bordetella pertussis, B. parapertussis (mild o LPS endotoxin
infection), B. bronchiseptica (bronchitis and • Enzymes
pertussis-like illness) o Hyaluronidase
o Lecithinase
Bordetella pertussis is causative agent of Whooping cough. o Coagulase
• Gram-negative Resistance
• coccobacilli (oval-shaped) Bordetella pertussis is sensitive to environmental
• non-motile factors. It can withstand exposure to sunlight for about one
• non-spore forming hour. The bacterium is inactivated by heating at temperature
• capsulated of 56°С for 10 – 15 minutes. It is rapidly destroyed in
solutions of conventional disinfectants.
• aerobes
• grow on enriched media Epidemiology
• Bordet-Gengou medium (potato-blood-glycerol Whooping cough, caused by Bordetella pertussis, is a
agar) with penicillin or caseine- charcoal agar severe infectious disease of childhood.
The sources of infection are patients in the early
• does not ferment sugars, proteins catarrhal stage of disease and carriers.
• doesn’t reduce nitrates The infection is transmitted by air droplet route.
• catalase activity The incubation period is lasts about 3-14 days.
• oxidase positive
• Pili
• Capsule
• Filamentous hemagglutinin
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 Causative agents of an Airborne bacterial infection
Pathogenesis Treatment
After incubation period the disease takes a protracted antibiotics from macrolide or azalide groups during the
course comprising three stages: catarrhal stage of the disease fosters the elimination of
• catarrhal stages pathogens and may have prophylactic effect.
with mild coughing and sneezing. This stage continues
Prevention (prophylaxis)
11-14 days. The patient is highly infectious but not very ill.
For specific prophylaxis effective inactivated pertussis
• paroxysmal stages vaccine is used.
spasmatic cough is develops its explosive character and
characteristic “whoop” upon inhalation. This stage is
prolonged 2-8 weeks.
• convalescence stages
is slow (2-6 months).
Immunity
High grade humoral immunity acquired after whooping
cough is antimicrobial, which is stable and tense in character.
Specimen
nasopharyngeal aspirate or nasopharyngeal swabs.
Laboratory Diagnosis
1. Bacterioscopic (immunofluorescent)
2. Serological
o PCR or ELISA
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 Causative agents of an Airborne bacterial infection
9. Corynebacterium diphtheriae (Diphtheria) Resistance
• Family: Corynebacteriaceae Due to the presence of lipids, C. diphtheriae are highly
• Genus: Corynebacterium resistant to environmental factors. In droplets of saliva
• Species: Corynebacterium diphtheriae adhering to the walls of drinking glass, on door handles and
toys, they can persist for up to 15 days.
Bordetella pertussis is the causative agent of Diphtheria.
Epidemiology
• Gram-positive + Diphtheria, an infection of local tissue of Upper
• not acid-resistant respiratory tract with production of toxin which causes
• rod-shaped with pointed or claviform ends systemic effects on Heart and Peripheral tissues
The source of infection is patients and carriers of toxic
• immotile
strains of C. diphtheriae.
• facultative anaerobe The infection is transmitted by airborne route. It can
• not grow in simple culture media also transmitted by contact, domestic and alimentary routes.
• hemolyzed blood The incubation period lasts 2 to 10 days
• forms black or black-grey colonies
• ferment glucose and maltose will acid formation Pathogenesis
• not produce urease The portal of entry of the infection are mucous
• not form indole membranes of the oropharynx, nose, larynx, trachea, as well
as mucous membranes of the eyes and genitals, damaged
• microcapsule K-antigen skin, wound or burn surface, intertrigo, an open umbilical
• polysaccharide antigen wound.
• histotoxin At the portal of entry of the infection, an inflammatory
reaction develops, accompanied by necrosis of epithelial
cells, edema, exit of fibrinogen from the vascular system into
the surrounding tissues and its transformation into fibrin
under the influence of thrombokinase, released by necrosis of
epithelial cells.
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 Causative agents of an Airborne bacterial infection
Diphtheritic inflammation occurs on the mucosa with Treatment
stratified squamous epithelium, all cells of which are firmly Diphtheria is a toxinemic infection. Therefore, in order
connected both among themselves and with the underlying to neutralize diphtheria histotoxin, diphtheria antitoxin is
connective tissue base. used (Purified concentrated diphtheria equine serum).
Croupous inflammation occurs when the pathological Prevention (prophylaxis)
For specific diphtheria prevention, diphtheria anatoxin
process develops in the lower respiratory tract, where the
is used, which is included in associated vaccines:
mucosa contains glands that secrete mucus and are covered
o diphtheria-tetanus-pertussis vaccine
with simple columnar epithelium.
o tetanus and diphtheria toxoids
o diphtheria toxoid
Immunity
Long-lasting, high-grade humoral antitoxic immunity
develops after the disease. In contrast, antibacterial immunity
in diphtheria is low-grade and serovar-specific.
The presence of antitoxic immunity does not prevent
carriage of toxic strains of C. diphtheriae.
Specimen
mucus and films from the foci of inflammation, as well
as secretions from the foci of the pathological process.
Laboratory Diagnosis
1. Bacterioscopic (immunofluorescent)
2. Bacteriological
3. Serological
o PCR or ELISA
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 Causative agents of an Airborne bacterial infection
10. Streptococcus pneumoniae (Pneumonia) Epidemiology
• Family: Streptococcaceae Streptococcus pneumoniae is a part of the transient
• Genus: Streptococcus normal microflora of the upper respiratory tract.
• Species: Streptococcus pneumoniae The source of infection is bacterial carriers.
The infection is transmitted by the airborne.
Streptococcus pneumoniae is the causative agent of The incubation period in diphtheria lasts from 2 to 10
pneumonia, sinusitis and otitis media, meningitis. days.
The risk group is children under 4 years old and
• Gram-positive + persons over 60 years.
• lancet-shaped cocci (diplococci)
• polysaccharide capsule Pathogenesis
• motionless Pneumococci are the main pathogens of acute and
• do-not form spores chronic inflammatory diseases of the lungs, which occupy
one of the leading places in the incidence, disability and
• facultative anaerobes mortality of the world's population.
• grow on a culture media with blood, serum and They also cause meningitis, creeping ulcer of the
carbohydrates cornea, otitis, endocarditis, peritonitis, septicemia and a
• When they growing on a solid medium they form number of other diseases.
small greyish or colorless colonies
Immunity
• catalase-negative After the infection, type-specific immunity is
• oxidase-negative established.
• alpha-hemolytic During the development of pneumonia, the appearance
• polysaccharide capsule of specific antibodies coincides with a crisis (a sharp drop in
• Toxins temperature) and the onset of recovery.
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 Causative agents of an Airborne bacterial infection
Specimen
Sputum, blood, endotracheal aspirate, bronchoalveolar
lavage, cerebrospinal fluid (CSF), pleural fluid, joint fluid,
abscess fluid, bones, and other biopsy material.
Laboratory Diagnosis
1. Bacterioscopic (immunofluorescent)
2. Bacteriological
3. Microscope
4. Serological
o PCR or ELISA
Treatment
Most pneumococci are susceptible to penicillin.
Prevention (prophylaxis)
For specific streptococcus pneumoniae prevention,
Pneumococcal vaccines, and polyvalent pneumococcal
conjugate vaccine.
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