Bacteria Summary
Bacteria
By: Andrew Lukman (07120110067)
Normal Flora
All body surfaces possess a rich normal bacterial flora,
especially the mouth, nose, gingival crevice, large bowel,
skinVirulence
Quantitative ability of an agent to cause disease
Factors:
1. Adherence
2. Invasion
3. Toxin
4. Enzyme
5. Iron Binding Protein
6. Anti Phagocytic Factors
Gram Positive:
Staphylococcus Aureus
Gram Positive
Spherical cells
Grape-like structure
Ferment:
Carbohydrates Produce:
White to Deep yellow pigments Pathogenic Hemolyze blood
Coagulate plasma
Produce extracellular enzymes and toxins
Most common type of food poisoning (Heat-stable staphylococcal
enterotoxin)
Rapid resistance to antimicrobial agents and present difficult
therapeutic problems
Methicilin resistant staphylococcus aureus (MRSA) -> from
production of (-lactamaseMorphology
A. Culture
Grow most rapidly at 35C
Form pigment at room temperature (20-25C)
Gray to deep golden yellow colonies
B. Growth characteristics
Produce catalase -> differentiate from streptococcus
Ferment:
Carbohydrates -> produce lactic acid but not gas
Resistant to: Drying (Can withstand 6-14 weeks)
Heat (Can withstand 50C for 30 minutes)
9% Sodium Chloride
Antigenic Structure Contains:
Antigenic polysaccharide
Antigenic proteins
Protein A:
Cell wall component
Bacterial surface of protein -> characterized by adhesions
called microbial surface components recognizing adhesive matrix
molecules (MSCRAMMS)
Binds to Fc portion of IgG (except IgG3)
Fab portion of IgG bound to protein A is free to combine with a
specific antigen Inhibits the complement cascade
MSCRAMMS
Helps in bacterial attachment in host cell
Important virulence factor
Structural defense against Phagocytosis
Protein A:
Binds to Fc portion of IgG (except IgG3)
Fab portion of IgG bound to protein A is free to combine with a
specific antigen
Inhibits the complement cascade Clumping Factor (Bound
coagulase)
Converts the soluble blood protein fibrinogen in insoluble
fibrin molecules that form blood clots
Fibrin clots hide the bacteria from phagocytic cells
Synthesize loosely organized polysaccharide slime layers (often
called capsules)
Inhibit chemotaxis of and phagocytosis by leukocytes
Facilitates attachment of Staphylococcus to artificial
surfaces
Enzymes
Coagulase
Triggers blood clotting
Hyaluronidase
Breaks down hyaluronic acid, enabling the bacteria to spread
between cells
Staphylokinase
Dissolves fibrin threads in blood clots, allowing Staphylococcus
aureus to free itself from clots
Lipases
Digest lipids, allowing staphylococcus to grow on the skins
surface and in cutaneous oil glands
(-lactamase
Breaks down penicillin
Allows the bacteria to survive treatment with (-lactam
antimicrobial drugsToxins
Staphylococcus aureus produces toxins more frequently than
S.epidermidis Cytolytic toxins
Disrupts the cytoplasmic membrane of a variety of cells
Leukocidin can lyse leukocytes specifically
Exfoliative toxins Causes the patients skin cells to separate
from each other and slough off the body
Toxic-shock-syndrome toxin
Causes toxic shock syndrome
Enterotoxins
Stimulate the intestinal muscle contractions, nausea, and
intense vomiting associated with staphylococcal food poisoning
Diseases
Noninvasive Disease Food poisoning from the ingestion of
enterotoxin-contaminated food Cutaneous Disease Various skin
conditions including scalded skin syndrome, impetigo, folliculitis,
and furuncles
Systemic Disease Toxic shock syndrome-TSS toxin is absorbed into
the blood and causes shock Bacteremia-presence of bacteria in the
blood Endocarditis-occurs when bacteria attack the lining of the
heart Pneumonia-inflammation of the lungs in which the alveoli and
bronchioles become filled with fluid Osteomyelitis-inflammation of
the bone marrow and the surrounding bone
Diagnosis
Detection of Gram-positive bacteria in grapelike arrangements
isolated from pus, blood, or other fluids Specimen Smear Culture
Film Biochemical Reactions Antibiogram Typing
Treatment
Methicillin is the drug of choice to treat staphylococcal
infections
Is a semisynthetic form of penicillin and is not inactivated by
(-lactamasePrevention
Hand antisepsis is the most important measure in preventing
nosocomial infections
Also important is the proper cleansing of wounds and surgical
openings, aseptic use of catheters or indwelling needles, an
appropriate use of antiseptics
Staphylococcus epidermidis Normal flora in skin as oppose to
S.Aureus (pathogenic) Normal flora of:
Skin
Mucus Membrane
No protein A
No Coagulation
White in colorStreptococcus Pneumoniae
Gram Positive
Diplococcic
Normal: Upper Respiratory Tract
Cause:
Pneumonia
Sinusitis
Otitis
Bronchitis
Bacteremia
Meningitis
Morphology
A. Culture
Form round colonies
Enhanced by CO2B. Growth Characteristics
Energy from fermentation of glucose
Rapid production of lactic acid -> Limits growthAntigenic
Structure
Cell wall has: Peptidoglycan Teichoic acid Capsular
polysaccharide is covalently bound to the peptidoglycan and to the
cell wall polysaccharidePathogenesis
A. Production of disease Pneumococci produce disease through
their ability to multiply in the tissues The virulence of the
organism is a function of its capsule, which prevents or delays
ingestion by phagocytes
A serum that contains antibodies against the type-specific
polysaccharide protects against infection
If such a serum is absorbed with the type-specific
polysaccharide, it loses its protective power Humans immunized with
a given type of pneumococcal polysaccharide are subsequently immune
to that type of pneumococcus and possess precipitating and
opsonizing antibodies for that type of polysaccharideB. Loss of
natural resistance Since 40-70% of humans are at some time carriers
of virulent pneumococci, the normal respiratory mucosa must possess
great natural resistance to the pneumococcus
Among the factors that probably lower this resistance and thus
predispose to pneumococcal infection are the following:
1. Viral and other respiratory tract infections that damage
surface cells; abnormal accumulations of mucus (eg, allergy), which
protect pneumococci from phagocytosis; bronchial obstruction (eg,
atelectasis); and respiratory tract injury due to irritants
disturbing its mucociliary function2. Alcohol or drug intoxication,
which depresses phagocytic activity, depresses the cough reflex,
and facilitates aspiration of foreign material3. Abnormal
circulatory dynamics (eg, pulmonary congestion, heart failure)4.
Other mechanisms, eg, malnutrition, general debility, sickle cell
anemia, hyposplenism, nephrosis, or complement deficiencyDiagnostic
Laboratory Tests
Blood is drawn for culture
CSF and sputum are collected for demonstration of pneumococci by
smear and culture
Sputum may be examined in several ways.
Stained smears A Gram-stained film of rusty-red sputum shows
typical organisms, many polymorphonuclear neutrophils, and many red
cells.
Capsule swelling tests Fresh emulsified sputum mixed with
antiserum causes capsule swelling (the quellung reaction) for
identification of pneumococci.
Culture The culture is created by sputum cultured on blood agar
and incubated in CO2 or a candle jar. A blood culture is also
taken.
Immunity
Immunity to infection with pneumococci is type-specific and
depends both on antibodies to capsular polysaccharide and on intact
phagocytic function. Vaccines can induce production of antibodies
to capsular polysaccharidesTreatment
Since pneumococci are sensitive to many antimicrobial drugs,
early treatment usually results in rapid recovery, and antibody
response seems to play a much-diminished role
Penicillin G is the drug of choice, but in the United States 15%
of pneumococci are penicillin-resistant (MIC 2g/mL) and about 18%
are moderately resistant (MIC 0.1-1 g/mL)
High-dose penicillin G with MICs of 0.1-2 g/mL appears to be
effective in treating pneumonia caused by pneumococci but would not
be effective in treatment of meningitis due to the same strains
Some penicillin resistant strains are resistant to
cefotaxime
Resistance to tetracycline and erythromycin occurs also
Pneumococci remain susceptible to vancomycin.Gram
Negative:Neisseria Gonorrhoeae Gram-negative Intracellular Aerobic
diplococcus Pathogenesis: It mainly affects the hosts columnar or
cuboidal epithelium Pili help in attachment of gonococci to mucosal
surfaces and contribute to resistance by preventing ingestion and
killing by neutrophils Opacity-associated (Opa) proteins: Increase
adherence between gonococci and phagocytes Promote invasion into
host cells Possibly down-regulate the immune response Porin
channels (porA, porB) In the outer membrane play key roles in
virulence Gonococcal strains with porA may have inherent resistance
to normal human serum An increased ability to invade into
epithelial cells, explaining their association with bacteremia
TEM-1type beta-lactamase (penicillinase) affects penicillin binding
and efflux pumps and confers resistance to penicillin TetM protects
the ribosome and confers resistance to tetracycline Alterations in
gyrA and parC genes result in fluoroquinolone resistance by efflux
activation and decreased antibiotic cell permeation Gonococci
attach to the host mucosal cell (pili and Opa proteins play major
roles) Within 24-48 hours, penetrate through and between cells into
the subepithelial space A typical host response is characterized by
invasion with neutrophils, followed by epithelial sloughing,
formation of submucosal microabscesses, and purulent discharge If
left untreated, macrophage and lymphocyte infiltration replaces the
neutrophils Some gonococcal strains cause an asymptomatic
infection, leading to an asymptomatic carrier state in persons of
either sex The ability to grow anaerobically allows gonococci, when
mixed with refluxed menstrual blood or attachment to sperm, to
secondarily invade lower genital structures (vagina and cervix)
Progress to upper genital organs (endometrium, salpinx, ovaries)
Treatment:Andrew Lukman (07120110067)
