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Summary List of essential microorganisms mechanisms of disease 1
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A fully detailed list of all essential microorganisms discussed in mechanisms of disease 1.
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Essential microorganismsWhat to know about the essential microorganisms?
- Structural characteristics (for parasites, focus on life cycle and morphology)
- Pathogenesis and main virulence factors
- Association with host defence disorders
- Epidemiology and transmission
- Common clinical presentation
- Which diagnostic tests are indicated
- The principles of antimicrobial therapy and choice of drug for a simple case
- Rational prevention and control measures
Bacteria
Microorganism Examples of infections
Staphylococcus aureus Boil, wound infection, sepsis
S. aureus is a gram+ staphylococcus. It’s catalase and coagulase positive. This type of bacteria is a primary pathogen, but
is present in around 30% of the population as colonizer of the nasal cavity.
Virulence factors:
Enzymes: coagulase is responsible for clotting of the blood which prevents phagocytosis.
Exotoxins:
- A-toxine: lysis of the cell membrane of host cells
- Superantigens: bind MHC class II molecules on APCs, which induces a massive production of cytokines →
associated with TSS
- Exfoliative toxins: cleave cell bindings in the epidermis
- Enterotoxins: responsible for infections in the intestines
Common clinical presentation:
Acute and local lesions of the skin. Redness. High fever and a low blood pressure might lead to fatal TSS. Diseases as a
result of s. aureus:
- Scalded Skin Syndrome (SSS): disease of the skin
- Toxic Shock Syndrome (TSS): symptoms like high fever, vomiting, diarrhea, a sore throat, muscle pain and low
blood pressure
- Sepsis
- Abscesses
Associated host defence disorders:
1. damage of the skin
2. granulocytopenia
Diagnostic tests:
Microscopy: gram stain (gram+, cocci, groups); Bacterial culture.
Transmission:
Skin → skin
Prevention:
Hand hygiene, anti-microbial profylaxe
Therapy:
Penicillin, or, when resistant, vancomycin
Coagulase- negative staphylococci, a.o. Infections of intravascular catheters and implanted prostheses.
Staphylococcus epidermidis
S. epidermidis is a commensal bacteria that turns out to be catalase positive and coagulase negative. Virulence factors:
Biofilms: PIA (polysaccharide intercellular adhesin) can bind to existing biofilms and form a huge biofilm that causes
,resistance against antibiotics.
Common clinical presentation:
Most infections with s. epididermis are a result of intravenous contamination caused by catheters, injections etc.
Associated host defence disorders:
1. damage of the skin
2. granulocytopenia
Diagnostic tests:
Microscopy: gram stain (gram+, cocci, groups)
Transmission:
Catheters and injections
Prevention:
Disinfection, sterilisation and hand hygiene
Therapy:
Vancomycin, due to the high resistance against antibiotics.
Streptococcus pyogenes Tonsillitis, scarlet fever, otitis media, erysipelas
S. pyogenes is a gram+ and bèta-hemolytic streptococcus. It’s a primary pathogen that colonizes the skin and throat.
Virulence factors:
Proteins: M-protein that takes care of adhesion to host cells.
Exotoxins:
- Streptolysin O: pore-forming cytokine that can lyse leukocytes.
- Superantigens: bind MHC class II molecules on APCs, which induces a massive production of cytokines →
associated with TSS
- C5a-peptidase: destroys the chemotactic signals by cleaving the complement component of C5A
Common clinical presentation:
An infection with S. pyogenes can be recognised by tonsillitis and pharyngitis. TSS can occur when toxins are spread to
other tissues (symptoms: high fever and a low blood pressure)
Associated host defence disorders:
1. Damage of the skin
2. Granulocytopenia
Diagnostic tests:
Microscopy: gram stain (gram+, cocci, strands); bèta-hemolytical signs
Transmission:
Sputum or saliva
Prevention:
Anti-microbial profylaxe
Therapy:
Penicillin
Streptococcus pneumoniae Pneumonia, otitis media, meningitis
S. pneumoniae is a capsulated, alpha-hemolytic primary pathogen. It’s a gram+ streptococcus that colonizes the upper
airways.
Virulence factors:
Capsule: prevents the binding of C3b that is responsible for opsonization.
Pneumolysin: destroys cilia and epithelial cells and lyses cells
Common clinical presentation
A pneumococcal pneumonia especially occurs in children under the age of two and adults above the age of 60. It’s
associated with alcoholism, diabetes mellitus, chronic renal disease and asplenia. One of the key symptoms are cold
shivers.
Associated host defence disorders:
1. Asplenia
2. X-linked agammaglobulinemia
3. Common variable immunodeficiency
4. Reduced coughing or dysfunction of the cilia
Diagnostic tests:
Microcopy: gram stain (gram+, diplococci); alpha-hemolytical signs
, Transmission:
Sputum, saliva or inhalation of sputum particles
Prevention:
Vaccination
Therapy:
Penicillin
Haemophilus influenzae Bronchitis, sinusitis, otitis media, meningitis
Haemophilus influenzae is a capsulated, gram- bacteria.
Virulence factors:
Capsule: prevents the binding of C3b that is responsible for opsonization.
Pili and HMW: take care of the adhesion to host cells
Common clinical presentation:
- Meningitis: especially in children under the age of two
- Epiglottitis and pneumonia: especially in children between the age of two and five. Pneumonia as a result of H.
influenzae is mainly caused by chronic bronchitis due to smoking.
- Cellulitis and arthritis
- Otitis media
Associated host defence disorders:
1. X linked agammaglobulinemia
2. Complement deficiency
3. Common variable immunodeficiency
4. Lack of tears
Diagnostic tests:
Microscopy: gram stain (gram-, very small, coccobacilli); blood cultures
Transmission:
Sputum and saliva
Prevention:
Vaccination and anti-microbial profylaxe
Therapy:
Cephalosporin
Mycobacterium tuberculosis Tuberculosis
M. tuberculosis is a mycobacteriaceae, which means that it’s a gram+, ‘acid-fast’ bacteria. Tuberculosis is associated
with the formation of granulomas. It’s an intracellular bacterium.
Virulence factors:
M. tuberculosis reproduces itself in alveolar macrophages as their cell wall is resistant to the acidification in
phagosomes. It is then carried to the lymph nodes where it can spread throughout the entire body.
ESAT-6: binds to the basal membrane in the alveoli.
Common clinical presentation:
- Primary tuberculosis: macrophages take in the bacteria and spread it.
- Latent tuberculosis: the bacteria is present, but inactive
- Reactivation tuberculosis: the tuberculosis gets reactivated and the formation of granulomas takes place.
- Chronic pneumonia: arises in the reactivated phase of tuberculosis. Symptoms: fever, coughing and weight loss.
Associated host defence disorders:
1. Impaired cellular immunity
2. Granulocytopenia
Diagnostic tests:
Serology; microscopy: Ziehl-Neelsen stain (granulomas)
Transmission:
Inhalation
Prevention:
Vaccination and care in an isolated room.
Therapy:
Isoniazid, ethambutol, rifampin, pyrazinamide
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