Special Microbiology

Special Microbiology
General template
Genus characteristics
Biochemical characteristics
General biochemical (diagnosis)
Morphology (gram+ shape):
Metabolism (aerobic/ anaerobic):
Ability to produce ATP (intracellular/ extracellular):
Growth requirements (simple/ fastidious):
Virulence factors (infection properties)

Improve pathogenicity course of disease
Motile (flagella)
Pathogenicity to humans (obligatory/ opportunistic):
Adhesion (pilli/ fimbriae)
Colonization
Invasion
Immune response inhibitors
Enzymes (e.g. degrading enzymes)
Toxins
Organelles (e.g. fibriae – adhesion)
Improve resistance treatment
Cell wall (e.g. myocolic acid)
Spores
Mechanism of ATB resistance
Laboratory tests
Clinically important species
ATB
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G+ cocci
1. Staphylococcus.
Staphylococci genus in general
Biochemical characteristics (diagnosis)

Morphology (gram+ shape): G+ cocci (1 micrometer in diameter), arranged in clusters
Metabolism (aerobic/ anaerobic): facultative anaerobes
Ability to produce ATP (intracellular/ not): extracellular
Growth requirements (simple/ fastidious): simple
Normal flora: skin & mucus membranes opportunistic pathogens
Lab tests
Genus:
• Agar: blood agar
• Catalase + (=bubbles appear) Staph Vs Strep + entero
S. Aureus:
• Coagulase + plasma become gelatinous instead of liquid (coagulation)
• Hemolysin + β-hemolysis typical yellow (golden); strep B
Species Hemolysis Coagulase Mannitol Nitrate Arginine Novobiocin Susceptibility
S. Aureus β + + + + +
S. Epidermidis γ - - + + +
S. γ - + - - -
Saprophyticus
Staph. Aureus

Enzymes/proteins
Protein A – bound to Fc region of IgG on cell wall prevents activation of classic complement
pathway prevents opsonization and phagocytosis (immune response inhibitors). It cleaves the Fab
part from the Fc part, thus it goes way from the bacteria and cannot oponize.
Bound Coagulase (=clumping factor): (agglutination – fibrinogen fibrin) – invasion, typical

localization (Vs Strep – spreading)
Leucocidin- makes pores in neutrophils thus kills them. In chronic granulomatous disease there is
deficiency in NADPH oxidase therefore inability to make oxidative burst and the bacteria wins.
Catalase- converts the neutrophil’s hydrogen peroxide into water and oxygen, thus disarming it.
Hyaluronidase, Fibrinolysin
Hemolysin + β-hemolysis typical yellow (golden); strep B
Mechanism of ATB resistance:
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• Deactivation enzymes: β-lactamase- breaks down β-lactam ring of ATB ineffective. (use
methicillin or amoxicillin clavulanate)
• Modifies PBP (MRSA strain)
(exo)Toxins (through lysogenic conversion)
• Enterotoxins – heat-resistance; food poisoning diarrhea short-time afterward. Also acts on

area postrema to induce vomiting.
• TSST-1 – superantigens – heat and proteolysis resistance- associated with highly absorbent
menstrual tampons which foster the growth. Causes the formation of IL-1 which acts as a
pyrogen and increases the hypothalamic set point.
• Exofoliative SSSS (Ritter’s disease) (superantigen?)- scaled skin syndrome.
Superantigen sepsis: Hypotension, tachypnea, disorientation 2/3 sepsis
Treatment
• 1st choice
o Oxacillin (methicillin), nafcillin.
o Cephalosporins 1st gen (cefazolin, cephalothin)
o Amoxicillin/ clavulanic a, ampicillin/ sulbactam
• 2nd choice
o Lincosamides (clindamycin)
o Glycopeptides (vancomycin)
• If MRSA- vancomycin
• If VISA/ VRSA- teicoplanin/ linezolid/daptomycin
Diseases
Food poisoning
• Caused by: enterotoxins (8)
• Main contaminated food = Processed Meats, Salads, Pastries, Milk-Products
• Incubation = 4 hours.
• Features (last 24h):
o Short-time after eating (toxins were already present in food)
o Severe Vomiting, Diarrhea, Abdominal Pain & Nausea
• Rx: rehydration
Staphylococcal Scalded-Skin Syndrome (SSSS, Ritter’s disease)
• Caused by: exfoliative toxin epidermal detachment (mediated by protease?)
• Features:
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o Diffuse eryhtema & blistering with nikolsky sign (skin is easily displaced by touch).
o Complication = same as skin burns (fluid & electrolyte loss, superinfections).
• ATB: methicillin or oxacillin (If MRSA vancomycin).
Toxic Shock Syndrome (TSS)
• Caused by: TSST-1 (superantigen) excessive immune response: cytokines storm
• Features:
o Fever
o Scarlatiniform rash that desquamates (esp. on palms and soles)
o Hypotension shock
o If 2/3: Hypotension, tachypnea, disorientation sepsis!
• Rx:
o Hemodynamic stabilization
o ATB: Ampicillin/Vancomycin + Gentamicin (aminoglycoside)
Other infections
Skin Infections abscess, cellulitis, folliculitis, furuncles, bullous impetigo.
After Trauma/Surgery septic (bacterial) arthritis, Osteomyelitis (#1 cause!!)
clindamycin (good bone penetration), Endocarditis (tricuspid valve).
Pneumonia mainly when immunity is compromised (esp. after viral infections), (patchy
infiltrations on X-ray).
Horedeulom- 95% by s. aureus. Treatment= chloramphenicol (sintomycin).
Other Staph species
Staph. Epidermidis
Coagulase (-)
Catalase (+)
Urease (+)
Mannitol (-)
Forms biofilms (polysaccharides) antibiotic resistant: stick and sleek metal and plastic surfaces.
Novobiocin susceptible
Mainly cause infection of artificial materials:

• Prosthetic valve endocarditis
• Prostheses infections
• Catheter-induced UTI
Treatment = Vancomycin.
Staph. Saprophyticus
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• Coagulase (-)
• Catalase (+)
• Urease (+)
• Novobiocin resistant
Mainly causes UTIs in newly sexually active females.
Treatment = amoxicillin. Or TMP/SMX
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2. Streptococcus
Streptococci family in general
Biochemical characteristics?
Morphology: (gram+ shape) G+ arranged in chains/ pairs (1 micrometer in diameter)- why in chains?
They keep dividing in the same plane and they don’t separate readily after they divide.
Metabolism (aerobic/ anaerobic): facultative anaerobe- create acidic environment (caries in

s.mutans)
Ability to produce ATP: (intracellular/ not)
Growth requirements (simple/ fastidious): blood enriched agar
M proteins?
Streptolysin O hemolysis (beta)
We use some strains of streptococci in cheese making.
Virulence (infection properties)

Motile (flagella)
Pathogenicity to humans: (obligatory/ oppurtonistic)
Adhesion (pilli)
Colonization
Invasion
Immune response inhibitors
Toxins
Cell wall
Spores
Mechanism of ATB resistance: modified PBPs.
Lab tests
Species Hemolysis Bacitracin Test CAMP Test Optochin Test Growth in 6.5% NaCl
S. Pyogenes (GAS) β + - - -
S. Agalactiae (GBS) β - + - -
S. Pneumoniae α - - + -
Viridans Streptococci α - - - -
Enterococci γ (/α/β) - - - +
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Streptococcus pneumoniae (pneumococci).
Lancet shaped diplococci
α hemolysis – partial hemolysis where the surrounding zone is greenish (viridation)
Polysaccharide capsule M phase. The capsule is very antigenic and thus it is used in vaccination.
Bile soluble doesn’t grow in bile
IgA protease can penetrate mucous membranes
C-substance (in the cell wall)-> binds with CRP to activate complement cascade.
Optochin sensitive
Sickle cell disease (asplenia) is particularly susceptible. Also Hodgkin, multiple myeloma.
Pneumococcal infections: #1 MOPS in children & adults

Transmission = via respiratory droplets (part of the normal nasopharyngeal flora) opportunistic
pathogen
- Community-Acquired Pneumonia (Lobar) (#1)
Occurs when S. Pneumoniae is aspirated to the lungs.
Productive Cough, Blood-Tinged (‚rusty‘) Sputum, Chest Pain (Pleurisy), Shivering, Fever.
Usually the infection is localized in the lower lobes.
Responsible for up to 50% of all CAP cases (followed by chlamidophila and mycoplasma).
Treatment
o 1st-line: amoxicillin- clavulanate/Augmentin
o 2nd-line: macrolides (Erythromycin, Azithromycin, clarithromycin), ceftriaxone
- Acute Otitis Media & Sinusitis (#1)
Mostly in children.
Usually they follow a viral URTI WBCs infiltrate obstruct the sinuses or ear-canal.
Otitis Media = Ear pain, bulging of eardrum, discharge from ear (if rupture of eardrum).
Sinusitis = sinus headache, nasal discharge.
Treatment = Amoxicillin/ augmantin or Erythromycin.
- Meningitis (#1)- one of the 3 (n.menengitidis, h.influenza type B)
S. Pneumoniae is a leading cause of meningitis (except of neonates).
Usually caused by pneumococcal CAP, Otitis Media or Sinusitis spreading of bacteria.
Treatment = Ceftriaxone or Cefotaxime.
- Sepsis
Occurs in 30% of pneumococcal pneumonias, and in 80% of pneumococcal meningitis.
Often, such bacteremia may cause endocarditis valvular damage.
Treatment = Ampicillin + Gentamicin.
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Prevention = Vaccination (Adults (23 Valent {types} +polysaccharide) IgM response, Children (13
valent {types}+ protein) IgG response).
Streptococcus pyogenes (A)
Virulence factors
Adherence: M protein, F protein, lipoteichoic acid
Inhibition of immunity (opsonization) and inhibition of phagocytosis: hyaluronic capsule
M protein prevents phagocytosis + initiates severe immune response (type II) RF
Invasiveness: hyaluronidase- paradoxically it breaks down both hosts and bacterial HA.
Streptolysin O β hemolysis (we generate ASO Ab to this)
Streptokinase- plasminogen plasmin
DNAase – depolymerize DNA resulted from the lysis of WBC extracellular traps. It is also a serologic
marker. The bacteria can also kill neutrophils (as s.aureus- leucocidin) by streptolysin O that lyse
cells by incorporating to the cholesterol sites. Hydrolytic enzymes from the lysosomes of the killed
neutrophils will contribute to the damage.
Toxins: exotoxins A, C (suprantigens) TSLS; exotoxin B necrotizing fasciitis
Scarlet fever by erythrogenic toxin. The toxin works on blood vessels and causes their dilation and
fluid leakage.
Bacitracin sensitive
Diseases:
- Transmission = respiratory droplets.
Respiratory tract, bloodstream, skin
Non-invasive: pharyngitis, skin infection (pyoderma)
Invasive: flesh-eating bacteria, TSLS
Purulent Tonsillopharyngitis (Strep Throat) (#1)

Incubation = 2-4 days.
Features = Sore throat, fever, headache, Redness of pharynx.
Treatment = Penicillin-V or Macrolides (Avoid Aminopenicillins as Mono may look similar).
Scarlet Fever
A Tonsillopharyngitis that occurs by pyogenic-toxinA (erythrogenic toxin )/C-forming
GAS (supraantigens).
2 days after onset, the toxin causes diffuse “sandpaper” rash which spares the face (lasts 5-
7 days).
A whitish coating first covers the tongue later sheds “strawberry tongue”.
Treatment = Penicillin-V or Macrolides (Avoid Aminopenicillins as Mono may look similar).
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Autoimmune Complications after Strep Throat (Develop 2 w after strep throat, treated with GCCs)
• Acute Rheumatic Fever (ARF)- there is an hypothesis that says that after ARF there are
autoantibodies against the heart myosin and sarcolemma.
M-protein generates antibodies that cross-react with autoantigens (type-2 reaction)
JONES:
♥ Joints
♥ Ab against myosin in cardiac muscle (molecular mimicry) damages mitral
valves
♥ Nodules on extensor surfaces
♥ Erythema marginatum
♥ Sydenham’s Chorea
Pharyngitis participates RF (not impetigo)
Post-Streptococcal Glomerulonephritis (PSGN)- onset after 2-3 weeks.
Formation of immune complexes (type-3 reaction) deposit in the glomeruli.
Puffy cheeks w. nephritis
Cola-coloured urine
Rx: penicillin- doesn’t help so much.. the disease is self limiting.
- Impetigo
A purulent skin infection of the face. Especially in children.
Stages = Vesicles Pustules (pus-filled vesicles) rupture crusting (drying).
Treatment = topical mupirocin.
- Erysipelas & Cellulitis
Erysipelas = infection of epidermis+ lymphatics. Leads to fever and septicemia.
Cellulitis = infection of the subcutis.
Occur commonly in young children & older adults (mainly in the legs).
Treatment = P.O/I.V. penicillins, erythromycin or clindamycin.
- Toxic-Shock-Like Syndrome (TSLS)
Cause = Pyogenic-toxin A/C-forming GAS (a superantigen) excessive immune response.
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Features = Fever, Hypotension ( Shock) & Scarlatiniform rash that desquamates.
Treatment = hemodynamic stabilization, ATBs (Ampicillin/Vancomycin + Gentamicin).
- Necrotizing Fasciitis
Caused by pyogenic-toxin B-forming GAS, which invades the deep tissues via breaks in the
skin.
First, it initiates cellulitis.
Eventually there is an extensive destruction of muscle & fat ( “flesh-eating bacteria”).
Treatment = surgical debridement + ATBs (Ampicillin + Clindamycin + Ciprofloxacin).
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Streptococcus agalactiae (B)
Virulence factors
β hemolysis
Positive hippurate test, hydrolyzes sodium Hippurate
Polysaccharide
CAMP (+) will have an increasing zone of hemolysis when plated w/ S. aureus
Bacitracin resistant
Diseases
- Reservoir = human vagina (15-20% of women) & GIT.

- Transmission = Vertical to neonate at birth.
- Early-Onset Disease (GBS-EOD) = occurs in 1st week of life (BMP)
Bacteremia (in 85% of cases) hypotension & shock + rash
Meningitis (in 33 of cases) lethargy
Pneumonia (in 33% of cases) respiratory distress
- Late-Onset Disease (GBS-LOD) = occurs 1 week to 3 months from birth
Meningitis lethargy, fever, poor feeding, seizures.
- Treatment = Ampicillin + Gentamicin.
- Prevention:
Prophylactic vaginal/rectal culturing for GBS at 35 weeks of gestation.
If culture is positive prophylactic intrapartum ATB (Penicillin-G or Cefazolin).
Viridans streptococci and Enterococcus. (viridis= green in latin)
• α-hemolysis
• They have no protective measures against the host’s immune system thus it is usually
cleared from the body. If it finds any protected niche it can cause endocarditis.
• Not encapsulated
• Optochin resistant
• Bile resistant
• Associated with dental caries- it is facultative anaerobe, thus lowering ph and creates caries.
• Synthesize dextran from glucose can adhere to platelets that has been damaged in heart
(most commonly mitral valve).
• Subacute endocarditis in damaged valves
ATB:
• 1st-choice: penicillin + aminoglycosides (added due to possible resistance)
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3. Enterococcus (group D strep)
G+ cocci, arranged in chains
Facultative anaerobic
Growth requirements: simple
γ hemolysis (no hemolysis)
They are Salt Tolerant (grow in 6.5% NaCl), Heat Tolerant (grow at 45oC) & Bile Tolerant (grow in
40% bile)
Glucose fermenters (Glucose L-Lactic Acid)
Normal flora: colon
Enterococci virulence is mainly due to:

1) They are inherently-resistant to many antibiotics (Cephalosporins, Oxacillin etc.).
2) They adhere to surfaces by forming a Biofilm (a sticky group made of many
individual microorganisms).
E. faecalis (more common), E. faecium (more dangerous)
• Enterococci – Main Diseases:

1) UTIs
It is most common site of Enterococcal infections.
Infections are frequently associated with urinary catheterization
These infections may be asymptomatic, uncomplicated cystitis, and/or
pyelonephritis.
2) Peritonitis
Occurs as a result of leakage of bacteria to the peritoneal cavity.
The leak of bacteria is mostly a result of trauma.
Peritonitis is usually Polymicrobic (involve many spp.).
3) Endocarditis
Enterococci reach the heart only by entering the blood from a primary infection site
(peritoneum or Urinary Tracts).
• Enterococci – Treatment:
Enterococci are resistant to many antibiotics (mainly Cephalosporins & Oxacillin).
Treatment then should be very precise: linezolid/tigecycline.
a) Most Frequent (For Serious Infections):
o Aminoglycosides + Cell-wall-synthesis-inhibitors (Penicillin or Vancomycin).
o Some enterococci even show resistant to Aminoglycosides or Vancomycin.
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G+ rods
Obligatory aerobic
4. Mycobacterium
Mycobacterium family in general
Morphology (gram+ shape): G+ rods; straight or slightly curved rods about 3x0.3 ųm in size
Metabolism (aerobic/ anaerobic): obligate aerobe
Ability to produce ATP (intracellular/ extracellular): intracellular
Growth requirements (simple/ fastidious): enriched media culture- Löwenstein-Jensen (only M. TB)
In liquid culture: “serpentine cords” (rope-like colonies)
Non-motile, nonsporeforming, non-capsulate
Normal flora: X (aerosols/ dust) obligate pathogen
Enzymes: prevent phagolysosome fusion- sulfatides.
Cord factor ↑TNF-α ↑granuloma formation
Cell wall: mycolic acid- LCFA hardy wall resistance to weak disinfectants and can survive for
months on dry surfaces. Can be stained by Zielh-Neelson stain (M. TB is stronger Acid fasts)
Laboratory tests
Like other mycobacteria, the tubercle bacilli are obligate aerobes but M. bovis grows better in
conditions of reduced oxygen tension. The mycobacteriae is a large family (bovis- cattle, marinum-
fish, avium- birds, leprae and tuberculosis- human)
Thus, when incorporated in soft agar media, M. Tuberculosis grows on the surface while M. bovis
grows as a band a few millimetres below the surface. This provides a useful differentiating test.
The human tubercle bacillus also differs from the bovine type in its ability to reduce nitrates to
nitrites, its production of large amounts of niacin, its sensitivity to pyrazinamide
Delayed type hypersensitivity (4) to tuberculin is highly specific for tubercle bacilli and this is the
basis of the tuberculin test. A positive test reveals previous mycobacterial infection but it does not
establish the presence of active disease. Reactivity appears about 1 month after infection and
persists for many years
Tuberculin (Mantoux) test – diagnostic test
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M. tuberculosis TB
Way of transmission: inhalation of M. tuberculosis in aerosols or dust lungs

Avoid mucus traps alveoli
Dust cells phagocytize them and package them inside their phagosome. M. TB produces enzymes
that inhibit phagosome-lysosome fusion M. TB avoid lysosomal hydrolytic enzymes survive! The
bacteria proceeds to the hilar lymph nodes within the macrophage and then begin to create
granulomas by cord factor (one of the waxes). There will be caseous necrosis in the lymph node and
tubercles in the lungs- Ghon complex.
Intracellular proliferation (generative time= 18h) localized infection = primary TB
Incubation period: 2-12 weeks
Pathogenesis: chronic granulomatous disease
Primary TB
Signs of infection after exposure
• Mostly asymptomatic
• Some have flu-like symptoms
3w later – cell mediated immunity:
• Granuloma – wall-off bacteria
• Caseous necrosis
• Granuloma + caseous necrosis (of lung parenchyma?) = Ghon focus
• Ghon focus + caseous necrosis of nearby l.n = Ghon complex
• Ghon complex is usually subpleural, occurs at lower lobes
• The tissue that is encapsulated by the granuloma undergoes fibrosis and calcification scar
tissue is visible on X-ray (“Ranke complex”)
Progression
• Some cases – the immune system overpowering M. TB resolution
• Other cases – remains viable latent
• If immunocompromised patient: reactivation of Ghon complex spreading to upper lobes
(greater oxygenation) memory T-cells release cytokines more caseous necrosis
cavitation dissemination to extra-pleural regions
o Via airways and lymphatics other parts of lungs Bronchopneumonia
o Via bloodstream systemic miliary TB
Secondary
Miliary – disease spread to extra-pulmonal sites generalized systemic infection
• Kidney sterile pyuria (WBC in urine)
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• Brain meningitis, tuberculoma
• Lumbar vertebra Pott disease: demineralization of lumbar vertebra, spinal weakness
• Adrenal gland Addison disease
• Liver hepatitis
• Cervical l.n. scrofula (=lymphadenitis in neck)
Immune-compromised patients cavitation
Secondary – can be as a consequence of impairment of the immune function. The reactivation
usually happens in the upper lobes (apex) because there is more oxygen there, thus the bacteria will
grow better. The symptoms are- fever, night sweats, hemoptysis, hey fever.
Symptoms
90-95% asymptomatic- contained inside macrophages (granulomas) latent (dormant) infection
If immunocompromised: AIDS, elderly, some immunodeficiency disease active infection
ATB therapy
Latent infection: rifampin or isoniazid for 9 months
Active infection:
1st-line: RIPES – “4 for 2, 2 for 4”
• Rifampin
• Isoniazid
• Pyrazinamide
• Ethambutol
• Streptomycin tuberculous meningitis
2nd-line: fluoroquinolone, linezolid, macrolides, aminoglycosides, thiacetazone, paraminosalycilate,
pyrazinamide.
• Levofloxacin
• Moxifloxacin
Strains
MDR TB (multi-drug resistant TB)
XDR TB (extremely drug resistant TB)
For effective Rx
• Make sure drugs work against specific strain
• Multiple medications used at the same time
• Medications used for full course of therapy
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M. leprae
General characteristics
(lab tests): can’t be grown in artificial culture media
Thrives in cold temperatures growth in extremities
Generation time: 10-20d
Leprosy- less contagious than tuberculosis!
Way of transmission: directly related to over-crowding places and poor hygiene
Armadillos are the major reservoirs (US) = Hanson’s disease
Pathogenesis
Intracellular pathogen: skin macrophages, endothelial cells, Schwann cells.
There are main 2 types- tuberculoid and lepromatous, although there are more intermediate types.
Tuberculoid stage – granulomatous lesions with epithelioid and giant cells, but without caseation
• TH1 stimulates macrophages to engulf the bacteria (cell-mediated immunity)
• Well demarcated hairless lesions on skin
• Usually self limiting disease but may proceed to lepromatous leprosy.
Lepromatous stage (skin and peripheral n)
• TH2 promotes humeral response
• Bacteria being unable to contained in macrophages
• Highly contagious
• Rash (mainly in thorax, no in soles and palms)
• Neuropathy due to thickening of nerves (loss of sensation) in soles and palms
• Facial deformity – leonine (facies) appearance in face- thickening of skin, nose
deformation, loss of sensation in face.
• Cutaneous form: large firm nodules are distributed widely
• Neural form: localized patches and anesthesia
ATB therapy
1st-line – for 6-9m
• Rifampin
• Dapsone
If in lepromatous stage – 2-5y
*if Dapsone-resistant clofazimine (expensive)
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5. Nocardia

Morphology (gram+ shape): G+ branching (filamentous, Aerial Hyphae) rods (like actinomyces)
Metabolism (aerobic/ anaerobic): obligate aerobe (unlike actinomyces)
Growth requirements (simple/ fastidious): Slow Growth.
Found in soil (but not a spore-forming) obligatory pathogenicity
Laboratory tests
• Weakly stained acid fast (short mycolic acids)
• Catalase (+) – patients with Chronic Granulomatous Diseases have ↑risk to have infection
• Urease (+)
• Hyphae of affected tissues
Nocardiosis
Epidemiology
• Primarily affect immunocompromised patients (HIV, transplanted, glucocorticoids, elderly),
especially impaired cell-mediated immunity)
• Affect more men
Pathogenicity of Nocardia:
Pathogenic Strains of Nocardia are able to evade phagocytosis:
• CAT & SOD Neutralize ROS of oxidative burst.
• Prevent Phagosome-Lysosome fusion.
• Avoids acid-phosphatase by using it as a carbon source.
Nocardiosis according to Sites of infection
1. Bronchopulmonary Disease
o Pneumonia-like symptoms: Cough, Dyspnea & Fever.
o Lung abscess formation
o Associated with cavity lesions in lungs.
o Spreading to the pleura is common!
2. Cutaneous Infections
o In general
- Activities that can cause open wounds that is exposed to dirt can lead to this
- Pyogenic response: indurated lesions and inflammatory reaction
o Mycetoma
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- Painless chronic infection of the feet.
- Local subcutaneous swelling.
- Involvement of underlying tissues (bones & mm.).
o Lymphocutaneous Infections
- Manifest as cutaneous nodules & Ulcerations along lymphatic tracts.
- May involve the entire regional lymph nodes.
o Chronic Cutaneous Lesions
- Painless & Disseminating.
3. Dissemination to CNS (Brain)
o Nocardia has affinity to neural tissues
o Can cause meningitis.
o Causes brain abscesses.
Treatment of Nocardiosis: Lymphocutaneous Infection
• Trimethoprim-Sulfamethoxazole (TMP-SMX) +
a. Pulmonary/Cutaneous infections Amikacin or Imipenem
b. CNS Infections Broad-Spectrum Cephalosporins (Ceftriaxone).
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6. Actinomyces
Morphology (gram+ shape): G+ rods, branching (filamentous, form hyphae) (like nocardia)
Metabolism (aerobic/ anaerobic): facultative anaerobe (ex. A. israelii and A. meyeri- both are
obligate anaerobe).
Growth requirements (simple/ fastidious): slow growth, fastidious
Normal flora: respiratory tracts, GI & female genital tracts opportunistic pathogen
Actinomyces multiply by fragmentation of filaments
Pathogenicity
• Actinomyces have low virulence.
• They only cause infections if the tissue is damaged (trauma, surgery, other infection).
• Infection is often associated with jaw trauma/ recent dental work.
• Infections by Actinomyces originate from ENDOGENOUS Actinomyces.
Actinomyces Infections - Actinomycosis:
• Characterized by chronic granulomatous lesions form abscesses.
• Morphological Features:
a. Colonies are seen on the abscess as “Sand” – yellow sulfur granules.
b. Tissue Swelling with fibrosis
c. Draining Sinus Tracts drainage thick yellow pus from infection.
• Locations of Actinomycosis:
o Cervicofacial (most of cases):
Slow course
Mainly develop as result of poor oral hygiene, or after invasive dental
procedure.
o Less common cases: thoracic, abdominal, pelvic, CNS
Actinomyces – Treatment:
a. 1st line – Penicillin G (IV)
b. Alternatives – Carbapenems, Macrolides, Clindamycin.
c. SURGICAL REMOVAL OF INVOLVED TISSUE IS REQUIRED!
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7. Corynebacterium
Corynebacterium genus characteristics
General Biochemical characteristics (diagnosis)

Morphology (gram+ shape): G+ pleomorphic rods (= able to change shape according to the
environment)
Metabolism (aerobic/ anaerobic): facultative anaerobe
Immotile, non-encapsulated. Catalase Positive.

Unique composition of their cell-wall:
o Arabinose, Galactose.
o Meso-Diaminopimelic Acid (meso-DAP).
o Short-chain mycolic acids (but NOT ACID FAST because the chains are short).
Normal Flora: Skin, mucus membranes, Upper Respiratory Tract, GIT, Urogenital Tracts
Corynebacteria are Opportunistic Pathogens.
DD
Species Glucose Sucrose Urease Inverted CAMP
C. Diphtheria + - - -
C. Ulcerans + - + +
C. Pseudodiphtheriticum - - + -
C. diphteriae
Club-shaped, y/v formation
Metachromatic granules stained red with inulin dye (the rest of cell is stained blue)
Plated on: tellurite agar; Loeffler’s medium (horse serum) culturing bacteria
Elek’s test differentiate non/toxic strains.
Virulence factors: Diphtheria Toxin
Diphtheria
Way of transmission: respiratory droplets // enters to subcutaneous tissue via skin breaks
2-4 days incubation period, during which exotoxin starts to be produced:
1) Bacteriophage Lysogenic conversion acquiring Tox-gene encodes Tox Protein.
2) Proteolytic Cleavage of Tox A+B chains, connected by disulfide (A-B exotoxin).
3) A chain- Active subunit; B chain- Binding subunit
Pathogenesis
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1) Heparin-Binding Epithelial Growth Factor (HB-EGF) is present on the surface of eukaryotic
cells, mainly the heart & neurons.
2) B-chain binds to HB-EGF A-chain is inserted into the cell
3) The toxin act by ADP ribosylation inhibit: Elongation Factor 2 (EF2) ribosome function
protein synthesis cell death
Symptoms – local damage:

• Formation of pseudo-membrane- thick greyish exudate (similar to C. difficille in colon) over
mucosal surfaces of oropharynx colonization in thorax and tonsils
• Lymphadenopathy bull’s neck (characteristic thickening of the neck)
• Exudative pharyngitis, low-grade fever, sore-throat
• If cutaneous diphtheria: local nodule formation, characterized by a chronic non-healing ulcer
and covered by a grey-yellow membrane
Complications
• Extension of the Pseudomembrane to the larynx trachea airway obstruction
• If toxins get into bloodstream systemic effects
o Cardiotoxic effects: life-threating myocarditis, arrhythmia, heart block
o NS: local paralysis that begins at posterior oropharynx cranial nerves deficit (the
toxin damages myelin nerve fibers)
Rx
• Diphtheria antitoxin
• ATB: Penicillin or Erythromycin
• Prevention: DPT (Diphtheria, Pertussis (whooping cough, ‫)שעלת‬, Tetanus) vaccine – a toxoid
vaccine powerful IgG response
• If not vaccinated- passive immunization
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8. Listeria
General biochemical characteristics (diagnosis)
Morphology (gram+ shape): G+ short rods
Metabolism (aerobic/ anaerobic): facultative anaerobe
Ability to produce ATP (intracellular/ extracellular): facultative intracellular
Growth requirements (simple/ fastidious): salt tolerant
Can grow in a variety of temperatures (1oC – 45oC) – can survives and multiplies in near-freezing
temperature can contaminate diary products and milk even if refrigerated!
Important species: L. monocytogenes (10 species but only monocytogenes is important in human)
• Normal flora: X obligatory pathogen
• Motile
o Extracellular – “tumbling (‫ )מתגלגל‬motility” – by flagella
o Intracellular – “actin rocket” – rapidly polymerize actin filament against cell wall
propel along it in opposite directions (and even jump from cell to cell like that).
• Immune response inhibitors: Listerolysin O, PLC
• Causes weak β-hemolysis on blood agar.
• Catalase (+)
• It can be mistakenly diagnosed as S. Pneumoniae (!!) because:
o Short G+ rods that may appear in pairs similar morphology.
o Both can cause meningitis.
Listeriosis
Epidemiology
• Neonates & Elderly.
• Pregnant Women may lead to termination or disease in newborn
• Immunocompromised Patients.
Pathogenesis
1. Endocytosis into macrophages
a. The bacterium adheres to the cell via Internalins (InA or InB).
b. The bacterium is endocytosed into macrophages Phagosome.
c. It inherits double membrane from the host.
2. Phagolysosome Lysis
a. The Phagosome fuses with the lysosome Acid pH activation of 2 bacterial
enzymes: Listerolysin O, PLC.
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b. The enzymes cleave the phagolysosome Bacterium is released (from the double
membrane) to the cytosol.
c. Inside the cell cytoplasm, the bacterium replicates.
3. Directional Movement to the Cell Membrane
a. Actin assembly-inducing protein (ActA) = Actin polymerizing protein found on the
surface of L. Monocytogenes.
b. In a mammalian cell, the bacterial ActA interacts with actin monomers
polymerization on the bacterial surface generating a “comet-like tail”.
c. This new tail assists motility of the bacteria towards the cell membrane.
4. Moving to a nearby adjacent cell
a. The ActA protein assists the bacteria to pass the bacterial membrane and attach to
an adjacent cell.
b. After ingestion by the adjacent cell, the whole process (steps 1-4) occur again.
- Clinical Features in Adults:
Way of transmission: ingestion of contaminated food (milk products, meat, & cold salads).
Classically – Gastroenteritis flu-like symptoms with watery diarrhea. Usually it lasts for 48h
(unless immunocompromised)
In pregnant women sepsis w/o CNS involvement, or cause abortion. Mostly occur during
the 3rd trimester (in this time, immunity is most impaired).
In elderly & immunosuppressed pts. sepsis with meningoencephalitis. Can cause also
meningitis.
- Clinical Features in Neonates to infected mothers:
Way of transmission: Vertically- Mother to fetus during labor.
Early-onset
o Before birth abortion/ premature birth
o Shortly after birth Granulomatosis Infantiseptica (miliary microabscesses &
granulomas in the skin, liver & spleen).
Late-onset (2-3w after birth)
o Neonatal Meningitis – 3rd-most common agent (after GBS, E-coli)
o Meningoencephalitis + Septicemia
ATB therapy
Ampicillin for elderly meningitis caused by listeria (in general for adult meningitis- vancomycin (G-?)
and cenramycin (G+?)
• 1st choice- gentamycin (if immunocompromised?) + penicillin
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• Alternatives- linezolid, daptomycin, TMP-SMX.
• Prevention: pregnant women/ immunocompromised patients should not eat cold deli foods.
9. Bacillus.
Bacillus genus in general
Morphology (gram+ shape): G+ rods in chains
Metabolism (aerobic/ anaerobic): facultative aerobe
Pathogenicity to humans (obligatory/ oppurtonistic):
Spore-forming
B. Anthracis anthrax
Morphology of colonies: medusa head
immotile; no hemolysis
- Incubation = up to 2 months.
- Hosts = Herbivores (‫)אוכלי עשב‬, which eat the spores from soil esp. cows & sheep.
Pathophysiology:
pOX2 gene poly-D-glutamate capsule prevents phagocytosis.
pOX1 gene Protective Ag (PA); Edema Factor (EF); Lethal Factor (LF)
PA binds the host cell Host cell proteases cleave some of the PA (80 kDa 63 kDa)
allows entrance of Edema Factor (EF) & Lethal Factor (LF) EFs & LFs bind to PA Toxin
formation:
o EF: ↑AC ↑cAMP fluids in ECF edema inhibits host defense and prevents
phagocytosis
o LF: exotoxin- protease cleaves MAP kinase (signal protein which involved in cell
growth) tissue necrosis (black aschar)
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- Anthrax Forms (According to mode of Acquiring):
Cutaneous Anthrax by direct contact with spores found in soil, or via mosquito vector
Starts by development of painless nodule at the site of skin-inoculation.
Rapid progression into black ulceration (Eschar) surrounded by erythematous rim.
Symptoms: fever, malaise, painful lymphadenopathy, massive edema.
Mortality = 20%.
Inhalation Anthrax („Wool-Sorter Disease”) by inhalation of spores from soil
Prolonged incubation phase (2 months)
Nonspecific symptoms + non-productive (dry) Cough develop
Worsening of Symptoms: High Fever, Edema, Massive enlargement of mediastinal l.n.,
Pulmonary hemorrhage (on X-ray: widened mediastinum), Sepsis & respiratory failure
A life-threatening pneumonia with hypoxemia, shock with hemorrhagic Mediastinitis.
Such route may be used nowadays as a biological weapon
Does not pass between people by air, since the bacteria replicates in the bronchial
lymph nodes rather that inside the bronchi
Mortality = 100% (w/o treatment).
GI Anthrax (rare) by ingestion of contaminated meat
Causes ulceration & necrosis in site of infection bloody diarrhea and/or hematemesis.
Symptoms: Regional Lymphadenopathy, edema, nausea, vomiting, malaise, sepsis
Mortality = 20-60%.
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- Treatment = Ciprofloxacin or Doxycyclin + Amoxicillin (cutaneous)
- Prevention = vaccination (killed bacteria) of animals & high-risk people.
B. Cereus
Motile; hemolysis
Virulence factors
Hydrolytic Enzymes – damage cell membrane of host cells
1) Cereolysin
2) PLC
2 Enterotoxins which are:
a. Heat Stable
b. Resistant to Proteolysis
Gastroenteritis (Food Poisoning)
Can be 1 of 2 forms:
a. Vomiting Gastroenteritis (Emetic form):
Mostly results from consumption of contaminated rice by the Enterotoxin.
Shorter period of disease, severe vomiting, Abdominal cramps, nausea.
b. Diarrheal Gastroenteritis (Diarrheal form):
Mostly results from consumption of contaminated meat/vegetables by bacteria or
spores.
Cooking does not kill the spores!!!
Longer period of disease, severe diarrhea, Abdominal cramps, nausea.
Ocular Infections (Bacillus Ophthalmitis)
Occur after a traumatic-penetrating injury of the eye by a contaminated object.
Severe Pneumonia
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Such pneumonia mimics the symptoms of B. Anthracis.
ATB therapy
a. 1st choice: Ciprofloxacin, Clindamycin or Gentamycin
b. Series Cases: Vancomycin.
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Obligatory anaerobic, spores-forming
10. Clostridium
Clostridium genus in general
Morphology (gram+ shape): G+ rods
Metabolism (aerobic/ anaerobic): obligate anaerobe (some clostridia are Aerotolerant)
Spores-forming
Clostridium tetani.
Normal “flora”: found in soil (spore-forming) and in rusty nails obligatory pathogen
Toxin: Tetanospasmin – disrupts neuromuscular system by blockage of GABAergic neurons.
Diseases – tetanus (=being taut (‫))מתוח‬
Way of transmission: penetrate beneath skin via puncture wound (anaerobic conditions)
Pathogenesis
• Puncture wound occur with a foreign object that has tetani spores on it
• Spores embedded in flesh and organism vegetate
• Release of tetanus toxin- tetanospasmin retrograde transport of toxin moto-axons
spinal cord:
• Tetanospasmin acts as a protease- cleaves SNARE protein disrupts exocytosis of inhibitory
neurotransmitters (GABA & glycine) from Renshaw cells into moto-neurons synapse
• Uncontrolled firing of neurons spasm!
Symptoms (caused by the toxin, not by the bacteria itself)
• Spastic paralysis (VS placid paralysis, see “C. botulinum” below) – “too much” muscle
contraction rigidity
• Trismus = “Lockjaw”: spasm of masseter m prevents jaw from opening
• Risus Sardonicus (“evil grin”) = sustained spasm of facial mm.
• Tonic spasms, Opisthotonos – exaggerated arching (extension) of the back – due to powerful
spasm of back.
• SY overactivity: excessive diaphoresis, dysphagia, drooling, fever, irregular urination &
defecation
• Hyperreflexia.
Therapy
• ATB: Antitoxin (TIG) + Metronidazole. Consider Intubation.
• Vaccine – DPT vaccine (Diphtheria, Pertussis, Tetanus) has Tetanus toxoid = toxin
conjugated into protein to ↑↑immunity produce Ab response to toxin.
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Clostridium botulinum
Normal “flora”: mainly found in soil, fruits, vegetables & Honey obligatory pathogen
Fastidious
Motile (Flagellated Peritrichous).
Virulence factors: toxins
• There are 7 antigenically-different toxins (A-G), all act the same.
• Types A, B, E & F are associated with human disease.
• Blocks the release sites of ACh of the neuromuscular junction ↓↓muscle contraction.
• Small dose of it is used as Botox treatment
Diseases – botulism
Way of transmission: ingestion
• In adults – preformed toxins, which can be found in improper canning of food.
• In infants – spores, which can be found in honey.
Pathogenesis
• The toxin is spread via blood to PNS (no CNS because it can’t cross the BBB).
• The toxin is protease- it cleaves SNARE proteins prevent exocytosis of acetyl choline
(excitatory neurotransmitter) into pre-synaptic axon terminal.
• ACh muscle contraction flaccid paralysis.
Symptoms
• Flaccid paralysis – absence of muscle contraction
• Descending paralysis – from head to foot
• Early symptoms – eye problems: diplopia and ptosis, bulbar palsy (impairment of CN 9, 10,
11, 12) drooping eyelids, double vision, inability to make face expression, dysphagia
• In infants – “floppy baby syndrome”
• Main complication: involvement of Respiratory muscles Apnea
ATB therapy
• Against Toxin - Botulinum Antitoxin (passive immunization)
• Against Bacteria - Metronidazole or Penicillin-G
• Ventilation support.
• Prophylaxis: avoid giving honey to infants less than 12 months + monitor canning of food
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Clostridium perfringens.
Normal “flora”: found in soil obligatory pathogen
Clostridial myonecrosis (gas gangrene) (soft tissues infection)

Way of transmission:
• Infections associated with dirt and soil ( spore-formation): Motorcycle accident, Military
combat wounds
• C. perfringens is introduced to body by trauma/ surgery (contamination of an open
wound) soft tissues infection
Pathogenesis
• After 1 week Toxin α activity (a phospholipase) direct cell damage local necrosis
(fasciae, muscles).
• It consumed CH gas is produced under the infected tissue
• Necrosis + gas = gas gangrene
• Clinically is manifested as “crackling sounds” on palpation
• The myonecrosis is caused by α-toxin (lecithinase) cleaves lecithin (PL) cell membrane
damage
o In vivo RBC hemolysis
o In vitro double zone β-hemolysis on blood agar (VS other bacteria that can
hemolyze blood agar (group A+ B strep, listeria…).
Symptoms
• Acute and extreme pain at wound site with locally-tense tissues (edema, gas) and
exudation.
• May affect RBCs hemolysis.
• Systemic symptoms = fever, tachycardia, diaphoresis, pallor, rapid progression to sepsis.
Therapy: Surgical Debridement + ↑↑ IV penicillin G + clindamycin + long exposure of wound to air
(hyperbaric room).
GI infection (food poisoning-associated diarrhea)
Transmission: ingestion of contaminated meat/chicken by spores
Pathogenesis:
Spores ingestion germinate in blood (takes time) produce toxins (CPE-enterotoxin, also takes
time) pores in enterocytes membrane food poisoning slow onset watery diarrhea which lasts
< 24 hrs (Self-limiting non-inflammatory).
VS B. cereus, C. botulinum – pre-formed toxins outside body, re-heating triggers germination.
Therapy: Rehydration. Antibiotic is not recommended, as diarrhea caused by food poisoning is
transient (it is self-resolved).
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C. difficile
Normal flora: GI (mainly colon) opportunistic pathogen
(lab tests)
• Assay to detect toxins in stool (not the actual bacteria)
• Produces variety of Volatile FAs “Barn-Yard” smell of the culture
Virulence factors: exotoxins: toxin A watery diarrhea; toxin B pseudomembranous colitis
Diseases
*Only toxin-producing strain will cause infection.
Way of transmission: nosocomial (Spores are easily transferred from patient to patient, low hygiene)
• Clindamycin ATB kill GI Floral Bacteria ↑proliferation of drug-resistant C. Difficile
• ↑↑ C. difficile Excessive Toxin Formation (A & B) Enterocytes Damage:
o Exotoxin A (enterotoxin) binds to intestinal brush border inflammation
watery Diarrhea
o Exotoxin B (cytotoxin) depolymerization of actin filaments disrupts
cytoskeleton integrity Necrosis detachment from surface yellowish-greyish
exudate pseudo-membrane that covers colonic mucosa – pseudomembranous
enterocolitis
ATB therapy
• 1st choice against Anaerobes Metronidazole.
• Series Infections oral Vancomycin
o IV isn’t as much as useful- we want to deliver AB where the bacteria are- intestinal
lumen
o Orally is poor absorption less side-effects.
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G- cocci
Obligate aerobe
11. Neisseria
Neisseria genus in general
General biochemical characteristics (diagnosis)

Morphology (gram+ shape): G- bean-shaped diplococci (arranged in pairs)
Metabolism (aerobic/ anaerobic): obligate aerobic (oxidase +); capnophilic (5%)
Growth requirements (simple/ fastidious): fastidious:
• Grows on chocolate agar (inhibited on blood agar)

• Selective agar: VPN (Thayer Martin) agar (enriched in Vancomycin, Polymyxin, Nystatin)
• Inhibition of C5-C9 MAC deficiency ↑infection (immune sys)
• IgA protease Cleaves IgA at hinge region facilitate survival along mucosal surfaces
(adhesion, immune sys)
• Fimbriae/ pilli
o Attachment to mucosal surfaces (adhesion)
o Frequent genetic rearrangement genetic variation make it more difficult for the
immune system to target it and prevent any lasting immune response (immune sys)
• Endotoxin (lipid A)
• Catalase + (immune sys)
DD
Species Glucose Maltose Sucrose Lactose ONPG Pigment Oxidase
N. Gonorrhea + - - - - - +
N. Meningitidis + + - - - - +
N. Lactamica + + - + + + +
Neisseria meningitidis.
Normal flora: upper respiratory tract opportunistic pathogen
Polysaccharide capsule (LOS- core of polysaccharide and lipid A) inhibits pathogenesis
Diseases
Epidemiology: Sickle cell & asplenic patients at higher risk of infection.
Way of transmission: human to human
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• Easily spread in close crowded spaces, like college dorms, military bases
• Transmitted by respiratory secretions (sneezing, coughing, kissing, sharing drinking).
• Colonize nasopharynx first (nasopharyngitis) invasive strains invade the bloodstream
through mucosa
Meningococcemia (sepsis)
LOS envelope proteins outgrow the bacteria massive (systemic) inflammatory reaction
• Fever
• Consumption of platelets and coagulation factors thrombocytopenia petechial/
purpuric rash – leakage of blood to subcutaneous indicates DIC
• ↑capillary permeability leakage of fluid into extravascular space hypovolemia shock
• Hypovolemia hypotension peripheral vasoconstriction (in attempt to maintain BP)
poor adrenal perfusion adrenal insufficiency/ infraction (“Waterhouse-Friderichsen
syndrome”, characterized by hemorrhage of adrenals) shock
May progress to meningitis or septic shock
Mortality = 50%. (even with ATB). Early treatment is still important and can improve outcome.
Other infections:
Meningococcal Meningitis w/o sepsis (most common pathologic presentation)
Result from hematogenous dissemination.
Neck Stiffness, Fever, Headache, Photophobia, Vomiting.
Mortality = 10%.
Meningococcal Meningitis with Meningococcemia
Meningitis is caused by meningococcemia.
Distinguishing sign = purpuric rash due to meningococcemia!
Mortality = 20%.
• Meningococcal Pneumonia, myocarditis, arthritis
Therapy
• 1st choice ATB- 3rd generation cephalosporins (ceftriaxone/ cefotaxime) (can penetrate BBB)
• Rifampin or ciprofloxacin prophylaxis in close contacts.
• Vaccine contains polysaccharide capsule (except type B capsule) most infections in
developed countries caused by type B strain.
Neisseria gonorrhoeae.
Normal flora: X obligatory pathogen
Ability to produce ATP (intracellular/ not): Facultative intracellular parasite in PMN’s (macrophages)
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Gonorrhea
Way of transmission: STD
Symptoms
• In general: characteristic white thick-purulent discharge (VS thin-watery- chlamydia)
• Men: urethritis – travel up the tract prostatitis, orchiditis, epididymitis. Most infections
are acute and symptomatic with dysuria (painful urination) after 2-5 d incubation period.
• Women: cervicitis, vaginitis; Pelvic Inflammatory Disease infertility, ectopic pregnancy.
Usually asymptomatic very dangerous; Disseminated Gonococcal Infection: skin lesions,
petechiae.
Complication
• Spread of PID to peritoneum – Fitz-Huge-Curtis syndrome- “violin string” like adhesions
(long and thin) to capsule the liver.
• Asymmetric arthritis, commonly at knee
• At joint tap – purulent synovial fluid that doesn’t gram-staining (intracellular infection)
Congenital infection in the newborn
Untreated expected mom pass on infection to baby during delivery via placenta Purulent
conjunctivitis that generally occurs within 5 first days of life – early onset (VS chlamydial neonatal
conjunctivitis – first 7 days of life)
ATB therapy
1st-line: ceftriaxone
Assume it’s a coinfection with chlamydia when treating (i.e. treat also with macrolides
(azithromycin) or tetracyclines (doxycycline)).
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G- rods
Obligatory aerobic
12. Bordetella.
Morphology (gram+ shape): G- coccobacilli, Small! (0.5x1 μm).
Metabolism (aerobic/ anaerobic): Obligate Aerobes
B. pertussis pertussis (whooping cough)
• PER = Severe, TUSSIS = Cough.

• Caused mainly by B. Pertussis (milder form by B. Parapertussis).
Normal flora: X obligate pathogen
Flagella motile
Encapsulated
Adhesins (Pertactin, Filamentous hemagglutinin, fimbriae) binding to the mucosa of the URT.
Toxins – damage respiratory epithelium “whooping cough”
• Endotoxin (G-)
• Tracheal Toxin paralyzes the cilia (damage) mucus accumulation strong cough
reflex. It is not a proteinous exotoxin but made of murein.
• Pertussis Toxin Ribosylation of Gi protein ↓regulation of AC ↑cAMP
Lymphocytosis + ↑capillary-sensitivity to histamine airway swelling restriction.
It is an AB toxin (B-binds, A- activates)
• Adenylate-Cyclase Toxin prevents chemotaxis + causes apoptosis of macrophages
Transmission = respiratory droplets.
Incubation Period = 1 week.
- Clinical Features:
1st phase = catarrhal (2 weeks) most contagious
Non-specific symptoms (low-grade fever, conjunctival infection with tearing, nasal
congestion, Rhinorrhea, Sneezing, Malaise, anorexia)
Bacterial number is at peak highest risk of infecting other people.
2nd phase = paroxysmal = reoccurrence (1-6 weeks)
Repetitive Coughs (40-50 times a day) with whooping noise (because it’s hard to breath)
The intense cough may cause rib fractures, vomiting, lung-collapse & facial petechiae.
May be life threatening in infants!! (cyanosis, apnea & hypoxia-induced seizures).
3rd phase = convalescence (2-3 months) = „100-day cough”
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Reduction of intensity & frequency of symptoms, until full healing.
There is an increased risk of pneumonia in this stage, due to damaged URT.
B. Pertussis - Treatment:
a) 1st choice – Macrolides (Azithromycin or Clarithromycin) – used during catarrhal or early
paroxysmal phases
b) Alternatives – Fluoroquinolones, Trimethoprim-Sulfamethoxazole (TMP-SMX).
c) Prevention - DTaP vaccine (contains pertussis toxoid & hemagglutinin; acellular vaccine using
purified Ag).
d) Important to prevent transmission to others (especially to infants and immunocompromised)
a. Isolate infected
b. ATB prophylaxis to close contacts
c. Infants monitored closely
d. Pregnant woman – vaccine in 3rd trimester (Ab cross placental barrier – passive
immunization)
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13. Legionella.
Legionella genus
Morphology (gram+ shape): G- rods (but needs silver stain to be visualized), small, pleomorphic
Metabolism (aerobic/ anaerobic): obligate aerobe (Oxidase +)
Ability to produce ATP (intracellular/ extracellular): facultative intracellular
Utilize AA as C source (not CH)
Growth requirements: fastidious – requires chocolate agar, cysteine & Fe // charcoal yeast extract

Motile (flagella)
Main source: cooling towers, water systems (showers, hot tubs) obligatory pathogen
Mechanism of ATB resistance: β lactamases (
• Zn metalloprotease – cytotoxic PMN production, SOD, IL-1, CD4, TNF
L. pneumophila
- Transmission = inhalation of infected aerosols.

- Risk Factors = smoking, immunosuppression.
Pontiac fever
An influenza-like disease (fever, headaches, malaise etc.) with mild pneumonitis.
Persist for 2-5 days, then self-resolves w/o ATB treatment.
Legionnaire disease
Very seriously and potentially fatal illness
Atypical pneumoniae – Unilobar pneumonia – x-ray shows patchy infiltrate with consolidation of one
lobe (but x-ray is highly variable and easily looks like other types of atypical pneumonia- not useful in
diagnosis of legionella).
Dyspnea, Fever, Chills, Myalgia, Dry-Cough, Headache.
Unique characteristics in clinical manifestation – helps differentiate it from other atypical
pneumoniae:
• Diarrhea ↓Na Neurologic symptoms: headache and confusion
• High fever + relative tachycardia
Complication Multiorgan involvement (CNS, GIT, Liver, Kidneys).

For rapid diagnosis: urine antigen test
ATB
• Macrolides ((Azithromycin/Clarithromycin) (like other atypical pneumonia)
• Fluoroquinolone (Levofloxacin)
• Addition of Rifampin for immunosuppressed.
Prevention = routine decontamination of air-conditioner cooling tanks.
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14. Francisella tularensis.
Morphology (gram+ shape): G- rods (coccobacilli), Small (0.2 x 0.7 μm) (So small usually Gram-
Stain is Unsuccessful.)
Metabolism (aerobic/ anaerobic): Obligate Aerobe, immotile
Ability to produce ATP (intracellular/ extracellular): facultative intracellular recovery depends on
cell-mediated immunity; also helps facilitate its spread from site of infection to the rest of the body
Growth requirements (simple/ fastidious): Fastidious (requires chocolate agar & cysteine for growth
Virulence
• Form β-lactamases β-lactams are useless!
• Thin capsule
• Zoonotic Pathogen (rabbits, cats, rodents, Chicken, and deer) obligate pathogen
Tularemia (rabbit fever)
Way of transmission:
• Indirectly via vectors (ticks (dermacentor- not the same tick as in lime disease))
• Direct contact with infected animals (live or dead) or aerosolized and potentially to be use in
bioterrorism.
Pathogenesis: Francisella invades macrophages travels via lymph to RES cause granulomas+
caseating necrosis; regional lymphadenopathy spread systemically to other lymph nodes
Tularemia is subdivided into several forms, according to the clinical presentation:
Vector-Mediated Introduction (Commonest!) – Ulceroglandular = ulcer of location of injury
+ Lymphadenopathy.
Contact on the Eye – Oculoglandular = Eye involvement + Lymphadenopathy.
Ingestion - Typhoidal = GI-Symptoms. High risk of sepsis!
Inhalation - Pneumonic = Pneumonia resulting from inhalation of F. Tularensis.
Ingestion of Inhalation - Oropharyngeal = sore throat & tonsillitis, lymphadenopathy.
- Mortality = 7-50% (depending on form, most lethal are pneumatic & typhoidal).
ATB:
- 1st-line: Aminoglycosides (Streptomycin, gentamycin)

- 2nd-line: doxycycline
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15. Brucella.
Brucella genus
Morphology (gram+ shape): G- rods (coccobacilli), small (0.5X 1.5 µm)

Ability to produce ATP (intracellular/ extracellular): facultative intracellular (RES cells)
Growth requirements (simple/ fastidious): Brucella utilizes the sugar Erythritol prefers organs rich
in it (only in animals, not humans!). Capnophilic? Slow growth
Classification of Brucella is according to the morphology of their colonies, which is
determined by the serotype of the O-Antigen of their LPSs:
1) S-Phase Brucella much more virulent
2) R-Phase Brucella less virulent.
Diagnosis
• Extended Culture Incubation – at least 3 days (up to 2 weeks).
• Oxidase & Urease Positive; H2S positive,
• Serology (detection of antibodies).
Zoonotic (reservoir is cattle and other farm-animals) obligate pathogen
Immotile
Brucellosis (Malta fever, Undulant fever)
B. Abortus or B. Canis Mild disease.
B. Suis Destructive lesions + prolonged course.
B. Melitensis Severe Disease + Complications.
Way of transmission: direct contact or consumption of unpasteurized dairy products
Live inside RES cells by preventing phagolysosome fusion granuloma formation replicate
intracellularly host-cell lysis spread systemically:
Symptoms
Prodrome = non-specific symptoms: arthralgia, weakness, dry-cough, chills, anorexia, sweat,
with undulant (‫ )גלי‬fever
Later = Hepatosplenomegaly, General Lymphadenopathy, osteomyelitis, joint effusions.
Complications = respiratory/cardiac/GI/neurological impairments.
ATB
1st line: tetracycline (doxycycline) + rifampin for adjunctive therapy (VS Neisseria meningitidis or H.
influenza- which rifampin is used for prophylaxis for close contact).
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Obligate aerobe, Non-fermenting glucose
16. Pseudomonas.
Pseudomonas genus
G- rods, arranges in pairs, although it looks like just 1 (pseudomonas – like 1)

Obligate aerobe ( non-fermenter VS other enterobacteriacea (facultative anaerobe)!!))
Have simple growth-conditions, as it’s capable of using many organic compounds as a carbon source.
Opportunistic: After a broad-spectrum antibiotic therapy reduce intestinal flora easier growth.
P. Aeruginosa
Thrives in aquatic (pools, hot-tubs) environment “hot-tub folliculitis”

Often produces fruity grape-like odor
Virulence factors
Oxidase (+) (VS enterobacteriacea)

Catalase (+) Chronic Granuloma Diseases patients at risk
Motile – polar flagella
Capsule protection from phagocytosis.
Toxins:
• Endotoxin (Lipid A)
• Exotoxin A (ETA) – inactivates Elongation Factor 2 by ribosylation inhibition of protein
synthesis cell death (very similar to diphtheria toxins same MOA & targets):
o Skin wound infections Dermatonecrosis
o Ocular infections Corneal damage
o Pneumonia Pulmonary damage.
Pigments:
• Pyocyanin (Blue-green) ↑ROS formation (O2, H2O2)
• Pyoverdin (Yellow-green) binds host’s Fe for metabolism.
Secreted Enzymes:
a. Proteases degrade tissue Elastin & Complement-components.
b. PLC degrade cell membranes.
c. Exoenzymes S & T (ExoS & ExoT) act as exotoxins tissue destruction.
Mechanism of ATB resistance: Inactivation Enzymes/ modified PBPs/ altered permeability
Diseases
• #1 G- nosocomial late pneumonia in intubated patients – bilateral bronchopneumonia
CF - have mutated Cl channels
Immunocompromised.
40
Existing chronic pulmonary disease.
Previous Broad-Spectrum antibiotic treatment.
Use of ventilation equipment.
• Skin & Soft-Tissue Infections:
a. Burn-Wound Infection (most common)
Burn-wound infections necrotizing fasciitis & bacteremia.
Burn local vascular damage ↓WBC migration “immunocompromised-like”.
Fatal and not responding to ATB.
Folliculitis
b. Pseudomonal Folliculitis (“hot-tubs folliculitis”)
Burn-Wound Fasciitis Results from immersion in infected water (e.g. pools, hot-tubs).
Associated with people who use underchlorinated hot tubs
c. Osteochondritis – #1 cause of osteochondritis of the foot after a penetrating injury
• Osteomyelitis- epidemiology: IV drug users (direct contact with blood); diabetics (more
likely to develop traumatic injury, especially in foot, due to diabetic neuropathy, and then
pseudomonas can enter through these wounds)
• If get into circulation sepsis- release toxin that damages tissues and cause cutaneous
necrosis- “ecthyma gangrenenosum” (black necrotic lesions on skin)
• Nosocomial UTIs – usually occurs to patients with prolonged indwelling urinary catheter.
• Ear & Eye infections
o External Otitis (“Swimmer’s Ear”) by immersion in infected water (mainly pools).
o Chronic Otitis Media
o Purulent corneal ulcers by exposure of a post-traumatized cornea to infected water.
Rx
• P. aeruginosa is resistant to most antibiotics! (MDR pathogen)
• Often, treatment requires a combination of anti-pseudomonal drugs:
o 1st line: Anti-pseudomonas penicillin: piperacillin + tazobactam, (=Tazocin)
o Others: aminoglycosides (+ β-lactam), fluoroquinolones (especially for UTI):
ciprofloxacin, ofloxacin, 5th gen. cephalosporins (very powerful): Ceftobiprole,
Ceftolozane.
Antipseudomonal Drugs
41
Enterobacteria – fermenting glucose
• Enterobacteriaceae – General:
Gram-Negative Rods, Facultative anaerobes.
Non-spore-forming bacteria.
Most Enterobacteriaceae are motile (except Klebsiella, Shigella & Yersinia).
Are found in soil & water.
Normal Flora: Intestines.
All Enterobacteriaceae share a common O-Antigen (= “Enterobacterial common Ag”).
As G- bacteria, they contain an Endotoxin (Lipid A of the LPSs).
Inactivation Enzymes/ altered drug permeability
Diagnostic Features:
a. Glucose Fermenters (Glucose L-Lactic Acid).
b. Catalase-Positive
c. Oxidase-Negative ( used to differentiate from vibrio & pseudomonas spp.)
d. Nitrate Reducers
• Main antigens of Enterobacteriaceae:

1) Somatic O-Polysaccharide
Common to all Enterobacteriaceae (“Enterobacterial common Ag”).
O-Antigen is used to detect Enterobacteriaceae.
However, O-Antigens are strain-specific.
2) Capsular K-Antigen
Used to detect Salmonella.
K-Antigens may interfere with the detection of O-Antigen.
3) Flagellar H-Antigen
Heat-unstable Antigen.
H-Antigen is often found in pathogenic Enterobacteriaceae (E. coli, Salmonella etc.).
Species Glucose Lactose Mannitol Indole Urease Citrate H2S Motility DAF Nitrate ONPG Oxidase
E. Coli + + + + - - - + - + + -
Proteus + - - + + + + + + + - -
Salmonella + - + - - + + + - + - -
Shigella + - + + - - - - - + + -
Klebsiella + + + + + + - - - + + -
Pseudomonas - - - - + + - + - + + +
42
17. Escherichia coli.
Morphology (gram+ shape): G- rods
Metabolism (aerobic/ anaerobic): facultative anaerobes
Motile (flagella) – H Ag
Encapsulated (K Ag)
Toxins: LPS (O Ag) A endotoxin in outer cell membrane sepsis
Adhesion (pili/ fimbriae) UTI (80%)
Normal flora: GIT opportunistic pathogen
Laboratory tests
• As enterobacteriacea (glucose fermenter, catalase (+), oxidase (-), nitrate reducer, O Ag)
• Catalase (+)
• Lactose fermenter pink in MacConkey agar
• Green on EMB agar
• Encapsulated – K Ag neonatal meningitis
Gastroenteritis
Fecal-oral transmission
General symptoms
• Diarrhea
• Abdominal cramps
• Nausea & vomiting
• Low-grade fever
Entero-Toxigenic E-coli (ETEC)
• Special virulence factors
o Bacterial Surface-Attachment Proteins
o LT (heat labile) enterotoxin ↑cAMP (similarly to cholera toxin)
o ST (heat stable) enterotoxin ↑cGMP
• Main gastroenteritis: traveler’s diarrhea (diarrhea in developing countries, i.e. Mexico)
43
• Way of transmission: consumption of fecal-contaminated water or food
• General pathogenesis
o Exposure to bacteria Incubation period (1-2 days) Production of enterotoxins
o Hypersecretion of water and electrolytes watery diarrhea (3-5 d)
Entero-Hemorrhagic E-coli (EHEC)
• Special virulence factors: Shiga-like toxin (Stx1, Stx2)
• Main gastroenteritis (especially in children<10): bloody diarrhea; HUS
• Way of transmission: consumption of undercooked meat/ unpasteurized milk
• General pathogenesis
o Exposure to bacteria incubation period (3-4 days) production of shiga-like
toxins
Target the 60S subunit of ribosomes
Binds to intestinal epithelium endothelial destruction in enterocytes
malabsorption & bleeding bloody diarrhea
Hemolytic Uremic syndrome (HUS): damaged endothelial cell in
glomerulus become thrombogenic platelet aggregation
thrombocytopenia + RBCs lysis + RF
Enteropathogenic E. Coli (EPEC)
Special Virulence Factor(s):
A) E. coli Adherence Factor (EAF) A/E Histopathology (Attachment/Effacement of the
microvilli).
B) Bundle-Forming Pilli (BFP) aggregation of EPEC formation of colonies.
Main Gastroenteritis: Infant Diarrhea (mainly in developing countries).
Main Way of Exposure: Fecal-Oral exposure to contaminated surfaces or food.
General Pathogenesis:
a. Exposure to bacteria Short Incubation period
b. Destruction of Microvilli Malabsorption hypersecretion of water diarrhea.
Enteroaggregative E. Coli (EAEC)
Special Virulence Factor(s): Mainly Adhesins aggregation of EAEC on the intestinal epithelium.
Main Gastroenteritis: Chronic Diarrhea (mainly in developing countries).
Main Way of Exposure: Fecal-Oral exposure to contaminated surfaces or food.
a. Exposure to bacteria & Incubation period.
b. Aggregation on epithelium shortening of Microvilli Fluid Malabsorption diarrhea.
Enteroinvasive E. Coli (EIEC)
44
Special Virulence Factor(s): Plasmid-Mediated Bacterial Invasion Genes (pInv genes).
Main Gastroenteritis: Watery Diarrhea (rare).
Main Ways of Exposure:
- Uncooked food.
- Unpasteurized Milk or Juices.
a. Exposure to bacteria.
b. Plasmid-Mediated invasion to intestinal epithelial cells destruction watery diarrhea
(may progress to bloody stools).
Extraintestinal infections
UTI (#1)
E. coli can pass from the colon to the urethra by wrong cleaning of the anus.
Symptoms = urge to urinate, burning during urination.
Neonatal meningitis
Mainly by K-Antigen-Possessing E. coli can cross BBB.
Sepsis
• E. Coli is the commonest cause of G- Sepsis.
• LPS endotoxin.
• Mainly occurs as a secondary infection to an infection in the GIT or Urinary Tracts.
• Especially occurs in immunocompromised patients.
Rx
1st-line = Amoxicillin, Ciprofloxacin, TMP-SMX, Nitrofurantoin.
Others = Carbapenems (esp. For ESBL strains), Aztreonam (esp. For sepsis).
However, Enterobacteriaceae are preferred to be treated only to relieve symptoms &
prevent dehydration.
Several reasons for the low indication of antibiotics for Enterobacteriaceae:
1. High spectrum of Resistance (ESBLs, Carbapenemases etc.)
2. The basic infections end on their own (except meningitis).
45
18. Klebsiella
• Klebsiella - General:
It is an Enterobacteriaceae (G- Rods), Facultative Anaerobe.
It has a prominent polysaccharide capsule.
Immotile.
Klebsiella causes only 2% of all bacterial pneumonia cases (K. pneumoniae).
Diagnostic Features:
Mucoid growth in culture!
Positive for Citrate & Lysin-Decarboxylase.
Lactose fermenter – pink on MacConkey’s agar
Urease (+)
Alcoholics, Abscesses, Aspiration
• Main Klebsiella Infections:
1. Lobar Pneumonia
May be either Community-acquired (K. pneumoniae) or Hospital-acquired (K.
Oxytoca).
Accompanied by necrotic destruction of alveolar spaces Bloody Sputum.
Cavatary lesion on patient right lobe “TB-like”
2. Rhinitis
K. Rhinoscleromatis Granulomatous Rhinitis.
K. Ozanae Chronic-Atrophic Rhinitis.
3. Nosocomial UTI – by K. Ozanae
• Klebsiella – Treatment:
Treatment involves initial short-course of antibiotic therapy (48-72 hrs.).
Usable Antibiotics:
a. β-lactam + Anti-β-lactamase (Ampicillin/Sulbactam, Piperacillin/Tazobactam).
b. 3rd generation cephalosporins- ceftriaxone/cefotaxime.
c. Meropenem (for ESBL Klebsiella) / clindamycin?
d. Fluoroquinolones (Alternative)
46
19. Proteus.
Proteus genus
G- rods
Enterobacteriacea facultative anaerobe
Non-lactose ferments
H2S
Unique diagnostic features
Motile (!!!) – Rhauss phenomenon (=demonstrate swarming motility when plated)
Urease (+) ammonia UTI
Slow fermenters of glucose
Fishy odor
P. mirabilis
Diseases (also for P. vulgaris??)

Proteus UTI – kidney stones
Proteus in UT cleaves urinary urea (by urease) ↑↑NH3 (+CO2) ↑↑pH precipitation of Mg,
NH3, PHO3 struvite stones formation (kidney stones) staghorn calculi pain; kidney damage;
act as _____ recurrent infection
Complication: bacteremia pneumonia
ATB
• 1st: amoxicillin / cotrimoxazole (sulfonamides) / nitrofurantoin
• 2nd: augmantin (amoxicillin + Clavulanic a) / cefuroxime, cefrozil (2nd gen)
• Severe Renal-Stone Cases: Surgery
• P. Vulgaris is generally more resistant to antibiotics than P. Mirabilis.
47
20. Salmonella.
Salmonella genus
Are Enterobacteriaceae (Gram-Negative Rods).
Facultative intracellular
Salmonella spp. AREN’T part of the normal flora of humans Absolute Pathogens!
Salmonella spp. are found in the GIT of non-human hosts.
Salmonella spp. have a pathogenicity island that allows them to evade the immune system!
Non-lactose fermenter white on MacConkey’s agar
Motile
H2S (+) colonies stain in black on hektoen agar
Indole (-)
Citrate (+) blue
Acid labile high doses are required in order to cause an infection (like V. cholerae); patients on
PPI are more susceptible
Capsulated spp: S. Typhi & S. Paratyphi enteric fever
Salmonellosis
1) Exposure to Salmonella:
Usually by ingestion of contaminated food products (mainly chicken, eggs & milk).
Salmonella growth on food products occur mainly in the warm months.
A large inoculum is required to develop a disease (10 6-108 bacteria).
2) The bacteria attach to the enterocytes of the small intestine
3) The bacteria invade the cells (by endocytosis)
Endocytosis “swallowed” by macrophages initiate inflammatory response.
Inside the macrophages, the bacteria begin to replicate (evade phagocytosis).
After invasion the bacteria may be released to the blood SEPSIS.
4) Inflammatory Response & Diarrhea
The response involves synthesis of prostaglandins ↑fluid secretion diarrhea.
Enteric/typhoid fever
- Endemic Areas = India, South Africa.
- Etiology = Salmonella Typhi (G- Rod)/ S. paratyphi
- Acquiring = ingestion of contaminated water/foods.
- Transmission = fecal-oral.
- Incubation = 7-14 days.
- Clinical Findings:
Flu-like symptoms (fever, dry cough, chills, myalgia, headache, anorexia)
Nausea
Abdominal discomfort with tenderness
‚Pea-Soup’ Diarrhea (a foul, green-yellow, liquid diarrhea)
Coated tongue
Hepatosplenomegaly
Abdominal Spotted-Rash (25% of cases)
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- Complications (after > 3 weeks from onset) = GI bleeding/perforation, Myocarditis, Typhoid
Encephalopathy, osteomyelitis (#1 among sickle-cell disease patients)
- Lethality = 2%.
- Dx. = blood & stool cultures, serology (Abs).
- Treatment = Ciprofloxacin or Azithromycin. Ceftriaxone in severe cases.
- Antibiotic treatment should continue for at least a week after fever is gone.
- Prevention = vaccination (attenuated), sanitation, hygiene.
**Fadget Sign = Paradoxical Combination of Fever + Bradycardia**
Typhoid Fever, Yellow Fever, Tularemia, Brucellosis, Brain Abscesses

Gastroenteritis
- Etiology = Salmonella Bongori or Enterica (G- Rod).
- Acquiring = Ingestion of Bacteria (contaminated chicken, eggs, or milk).
- Incubation = 6-48 hours.
Mild Fever
Headaches
Watery (inflammatory) Diarrhea
Abdominal Cramps
Nausea & Vomiting
Osteomyelitis (esp. in patients with sickle-cell disease)
- The symptoms of the Gastroenteritis may persist 2-7 days before Spontaneous Resolution.
- Diagnosis is by a stool culture.
- Treatment = only supportive by rehydration (if severe ciprofloxacin).
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21. Shigella
• Shigella - General:
Facultative intracellular
Non-capsulated, Immotile.
LPS type III secretion
In this genus there are main 4 species:
1. S. Dysenteriae (produces Shiga-Exotoxin).
2. S. Flexneri
3. S. Boydii
4. S. Sonnei
Shigella is an absolute human-pathogen, without any animal reservoirs.
Diagnostic Characteristics:
o Non-Fastidious
o Bile-Tolerant
o Non-Fermenters
o Immotile, non H2S
o Indole (+) green colonies on hektoin agar (Vs black salmonella)
Clinical Disease - Dysentery (S. Dysenteriae):

• Dysentery = a type of inflammatory gastroenteritis that results in diarrhea with fresh blood.
Primarily a pediatric disease.
Acid stable few (100-200) bacteria are enough to start a disease (VS salmonella, vibrio)
Way of Exposure: Fecal-Oral route (human to human only)
1. Ingestion stomach intestinal lumen intestinal mucosa Shigellosis:
2. Using its Gene-mediated-proteins, Shigella adheres & enters the colon’s enterocytes.
3. Shigella induce M-Cells in Peyer’s Patches of the ileum to phagocytose them
4. Escape from phagolysosome before degradation cytoplasm replication (1-4 d)
5. Cell-Cell Spreading: create a “tail” that helps to propel them from one cell to the other
(similar to “actin rocket” used by Listeria)
6. S. Dysenteriae forms Shiga-Exotoxin Block 60S subunit Necrosis & Ulceration
Signs & Symptoms (2-3 days after incubation period, last ~1w):
o Pus & Blood in the Stools (due to the inflammatory response).
o Diarrhea which begins watery, then becomes bloody (sometimes with mucus).
o In children < 10 YO toxin may cause Hemolytic-Uremic Syndrome (HUS).
o Toxin endothelial damage
o Renal glomeruli acute RF
o Platelet activation platelet aggregation RBCs hemolysis +
thrombocytopenia
o Fever, lower abdominal cramps, tenesmus.
Shigellosis – Treatment:
• Rehydration: Aimed to prevent dehydration as result of the diarrhea.
• Antibiotics (only in severe cases, since usually it self-resolving):
o 1st choice: Extended-Spectrum Penicillin (Pivmecillinam).
o Alternative: Ciprofloxacin, TMP-SMX (Co-Trimoxazole), macrolides?
• Prevention: proper sanitation (sewage, clean drinking water, hand washing).
50
22. Yersinia
• Yersinia - General:
Capsulated.
25oC – motile, 37oC - Immotile.
Resistant to cold temp (like listeria)
Stains heavily in both ends
- Yersenial Enterocolitis
Etiology = Y. Enterocolitica (G- Rod).
Transmission = fecal-oral (via contaminated food or water).
Large inoculum (108-109 bacteria) must first enter the GIT in order to cause disease
Host = doemstic animals (esp. dogs).
Pathogenesis = production of a heat-stable enterotoxin.
Incubation = 4-6 days.
Clinical Features:
In general: Abdominal pain + Diarrheal Disease + Fever (2 weeks). Possible
enlargement of mesenteric l.n.
In infants & young children febrile diarrhea with blood and pus.
In kids/ young adults pseudoappendicitis (mimics appendicitis).
In adults enterocolitis with postinfective sequelae like reactive arthritis.
Complication: Chronicization (months of occurrence)
Treatment = rehydration, ATBs (ciprofloxacin, cefotaxime/ceftriaxone).
- Black Plague
Etiology = Y. Pestis.
Virulence factors: endotoxin, exotoxin, neurotoxin, phagocytosis inhibition via type III
secretion
Transmission = via flea as a vector & human-human transmission by respiratory droplets.
Host = rats, squirrels.
2 Clinical Forms according to mode of transmission:

1) Bubonic Plague
o By flea-bite transmission.
o Incubation = < 1 week.
o High Fever + BUBU (= painful swelling of lymph nodes) in the axilla or groin.
o Rapid development of bacteremia necrosis of tissues
o Abscess, DIC
o 50% mortality without proper treatment
2) Pneumonic Plague
o Due to inhalation of Y. Pestis.
o Incubation period = 2-3 days
o High Fever + Malaise + Pulmonary dysfunction.
o 100% mortality w/o treatment!
Treatment = 1st: Streptomycin, 2nd: Doxycycline.

Prevention = avoid sick and dead animals, vaccination (killed vaccine).
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23. Vibrio.
Vibrio genus in general
Gram-Negative Curved Rods.

Facultative Anaerobes, Fermenters, Oxidase positive.
TCBS agar
Motile – have polar flagella Rapid movement (vibrio = vibrates, moves rapidly).
The flagella is often not seen well in gram-stain.
Tolerate pH of 8.5-9.0 are susceptible of gastric acid.
Clinically important vibrio: V. Cholerae, V. Parahemolyticus & V. Vulnificus.
Are classified into:
a. Halophilic (Require high NaCl for growth) – V. cholerae
b. Non-Halophilic
• Vibrio – Classification:
V. Cholerae is Halophilic (loves salt), and is divided into serotypes
Cholera In according to its O-
Antigen.
humans
• Vibrio – Pathogenicity:
52
Vibrio grow on the surface of water infections can occur by drinking contaminated
water.
Pathogenic vibrio is a part of the normal flora of brackish water (‫)מלוח במקצת‬.
Shellfish (oysters, mussels, clams) live in such waters Vibrio infections may occur
upon consumption.
V. cholerae
- Etiology = serotype O1 V. Cholerae (produces the cholera toxin).

- Endemic Areas = Developing countries (Asia, Africa)- poor sanitation of water
- Transmission = Fecal-Oral route of large dose (vibrio is acid-labile destroyed in stomach).
- Incubation = hrs.-days.
- Pathogenesis:
1) Vibrio is ingested & adheres to the gut mucosa (using toxin-coregulated pilli & flagella).
2) Vibrio form Cholera Toxin ↑cAMP activates CFTR channels massive Cl-efflux.
- Classic features: massive „rice-water” diarrhea (up to 20L/day) (formed due to high amount of
fluids & mucus in the stools), vomiting & abdominal cramps
- In severe cases:
o Hypovolemia or Dehydration (Water & electrolyte loss)
o Acidosis (HCO3 loss)
o Arrhythmias (Potassium loss)
- Treatment = rehydration, ATB in severe cases (Azithromycin? doxycyclin or ciprofloxacin).
- Prevention = adequate cooking of food, sanitation & hygiene.
1) V. Parahemolyticus acute Gastroenteritis

o Incubation period: 5-72 hrs. (24 hrs. is mean).
o The disease is characterized by an explosive watery diarrhea, mild fever & abdominal
cramps.
o No mucus or blood in the stools (except severe cases).
o Usually it is self-resolved.
2) V. Vulnificus fulminant Septicemia

o V. Vulnificus causes > 90% of vibrio-associated deaths in the US.
o It has a capsule & many proteases penetrates tissues very well and has easier spread.
o Septicemia results from:
a. Consumption of raw oysters.
b. Wound Infection by V. Vulnificus.
o Septicemia Fever, Chills, vomiting, diarrhea etc.
3) V. Parahemolyticus or Vulnificus Wound Infection

o Exposure of wound to contaminated seawater wound infection.
o V. Vulnificus has proteases local tissue necrosis (necrotic fasciitis).
53
24. Campylobacter.
Campylobacter – General:
Comma-Shaped (‫ )פסיק‬Gram-Negative Rods; Very small (0.2-0.5 μm).
Motile.
Growth requirements: Skirrow Agar; microaerophilic (5-7%), capnophilic (5-10%),
thermophilic (42 C)
Oxidase (+)
Campylobacters have lipoOLIGOsaccharides (LOSs) instead of LPSs.
There are 5 medically important Campylobacters:
a. C. Jejuni, C. Coli & C. Upsaliensis Gastroenteritis - diarrhea.
b. C. Fetus Septicemia (in immunocompromised patients), Vascular Infections, fetal
infections
c. C. Cinaedi & C. Fennelliae infections in homosexual man.
Campylobacter – Pathogenicity:
• C. Jejuni Exotoxins & Endotoxin cause damage to the jejunal mucosa Ulceration,
Abscess & Edema.
• Main reservoir: GIT of POULTRY (‫)עופות‬
• Way of transmission: eating infected chicken, raw milk, contaminated water, fecal-oral
Campylobacter – Main Clinical Diseases:
1) Gastroenteritis Diarrhea (mainly by C. jejuni, also: Coli & C. Upsaliensis)
o Ingestion of the bacteria colonization of intestinal mucosa attachment to epithelia
intracellular replication acute PMN response ulceration, abscess, edema.
o Symptoms: Diarrhea, Bloody Stools, fever, Appendicitis-like abdominal pain.
2) Autoimmune Complications
o Antibodies that are directed against the LOSs may damage Neurons or Joints:
a. Guillian-Barre Syndrome Autoimmune damage to myelin of PN ascending
paralysis, symmetric weakness.
b. Reactive Arthritis Autoimmune damage to the Joints swelling, redness & pain.
(arthritis, conjunctivitis, urethritis- can’t see, can’t pee, can’t climb a tree)
Campylobacter – Treatment:
FLUID REPLACEMENT!!!
Antibiotics are given only in severe cases, as gastroenteritis is usually self-resolved:
a. 1st choice – Erythromycin or Azithromycin (Macrolides).
b. Alternatives – Fluoroquinolones (Ciprofloxacin), Tetracyclins, Augmentin, Imipenem.
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Fastidious
25. Haemophilus.
Haemophilus genus
Small G- rods (coccobacilli)

Normal flora: human mucus membranes opportunistic pathogen
Growth requirement: very fastidious
• Require blood for growth (Haemophilus = blood-lover)
• Require nutrient-rich media
o Chocolate agar – heated blood release of nutrients from RBCs + destroy inhibitors
of factor V
o Blood agar + S. aureus – hemolysis release of nutrients from RBCs
o Levinthal agar – filtrated chocolate agar
• Require addition of one or both GF
o Factor X – hematin
o Factor V – NAD
DD
Species X Factor V Factor X+V Hemolysis
H. Influenzae - - + -
H. Parainfluenzae - + + -
H. Hemolyticus - - + +
H. Parahemolyticus - + + +
H. Aphrophilus + - + -
H. influenzae
Virulence factors
Encapsulated
Strains: Serotypes A-F
Serotypes B (but also A since 2014) show the highest proportion of invasive infections
Diseases
High-Risk Patients = non-vaccinated children, asplenic patients, sickle-cell anemia pts (also at higher
risk for S. pneumoniae infection) sepsis, septic arthritis
Way of transmission: aerosols (respiratory) droplets
By serotype B (Such infection occurs mainly to non-vaccinated children)

• Pediatric Epiglottitis (obstructive laryngitis) (by serotype B)
o inflamed epiglottis (“cherry red epiglottis”), inspiratory strider, drooling
o Swelling of the epiglottis LIFE-THREATHENING SITUATION.
55
Pediatric Meningitis (by serotype B) esp. in nonvaccinated kids below age of 2 yrs.
Pediatric Cellulitis (by serotype B) Fever + Redness of Cheeks or Periorbital Areas.
• Arthritis – uncommon in older children & healthy adults.
Non-encapsulated serotypes
URTI: Acute Otitis Media, acute sinusitis
• LRTI: Pneumonia (in 1-24-month-old infants, and also in smokers); Bronchitis (exacerbations
of acute bronchitis in smokers with COPD).
ATB
1st choice Amoxicillin.
Alternatives = cephalosporins, fluoroquinolones.
Severe infections (meningitis, epiglottitis) cefotaxime or ceftriaxone.
Close contacts prophylaxis Hemophilus meningitis- rifampin (like as in N. meningitis)
Prevention
• Vaccination (serotype-B capsule Ag, the opposite in N. meningitidis vaccine) between age 2-
18 months
• Consists of polysaccharide of Hemophilus capsule, conjugated to diphtheria toxoid, which is
a protein that ↑immunogenicity of capsular polysaccharide the body can produce strong
IgG response T-cell dependent vaccine**
• Hemophilus meningitis is almost eradicated in the US
Other Haemophilus species
• H. Parainfluenzae, H. Hemolyticus & H. Parahemolyticus Mainly Opportunistic Infections.

• H. Aegyptius Acute & Purulent Conjunctivitis
• H. Ducreyi Chancroid (= Soft Chancre)
o Chancroid = STD that is most commonly diagnosed in men (because women can
have asymptomatic or inapparent disease).
o Course of disease:
a. Approximately 5 to 7 days after exposure, a tender papule with an
erythematous base develops on the genitalia or perianal area.
b. Within 2 days the lesion ulcerates and becomes painful.
c. Inguinal lymphadenopathy is commonly present.
o Other causes of genital ulcers (e.g. syphilis and herpes simplex disease) must be
excluded to confirm the diagnose Chancroid.
o ATB: Erythromycin (Macrolide)
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26. Obligatory anaerobic G- rods
Anaerobic Gram-Negative Rods – General:
• The most important G- Rods are Bacteroides & Fusobacterium.
• Respond weakly to gram stain.
Pathogenicity
• These anaerobes are mutualistic with humans, and are the predominant bacteria on most
mucosal surfaces & Colon opportunistic pathogens (cause disease only when they move
from their original site to a sterile site, spread as a result of trauma or disease)).
• Although they are G-, these bacteria have low/no activity of their endotoxin (lipid A).
Bacteroides vs. Fusobacterium:
Criterion Bacteroides Fusobacterium
Growth Speed Rapid Slow (3 days of incubation)
Growth Requirements Non-fastidious, Stimulated by Bile Fastidious
Capsule + -
Clinically Important spp. B. Fragilis Not a specific one
(some strains form enterotoxin)
Area of most dominancy GIT Head mucous membranes
Infections of specific -Gastroenteritis (Enterotoxin-Forming B. Sinusitis, Otitis
dominancy Fragilis; self-resolved watery diarrhea Brain Abscesses
(mainly in children))
-Intra-abdominal (sterile abdominal
organs (e.g. liver))
-Gynecological (Pelvic inflammations,
Endometritis, Abscesses)
-Aspiration Pneumonia (from GIT)
Skin & Wound Infections Biting skin wound infection myonecrosis (gas gangrene?) Life-
Threatening
Treatment a. 1st choice against anaerobes – Metronidazole, Carbapenems (Imipenem,
Meropenem).
b. Main alternative – β-lactam with β-lactamase inhibitor (piperacillin-
Tazobactam).
c. EXPOSURE TO AIR (IF POSSIBLE).
B. Fragilis - Liver Abscesses
57
Bacteroides fragilis-
• The bacteroides (fragilis, gingivalis, bivius) are part of the normal flora of the GIT.
• Gram negative rods, strict anaerobes.
• B. fragilis also takes part in vitamin K synthesis, therefore antibiotic treatment that kills the
bacteria may cause decrease in vitamin K and thus to coagulopathies.
• It is the main cause of appendicitis.
• When it spills out to the sterile peritoneal cavity it forms abscesses. The first to die during
the spilling out are the aerobes (due to low oxygen concentration). The facultative
anaerobes will finish the low amount of oxygen (as e.coli), and thus bacteroides, which is
anaerobe will prosper, cause abscess and bacteremia (the mechanism is unknown because it
lacks LPS).
• The treatment will be hemodynamic stabilization in sepsis and
metronidazole/clindamycin/carbapenem.
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G- Spirochete: ATB: Tetracyclines/ penicillin
Obligate aerobe
27. Leptospira.
Diagnostic characteristics
Morphology (gram+ shape): G- spirochete, small, thin, “?” giemsa stain
Specie: L. interrogans
Leptospirosis (Weil’s disease)
- Host = small mammals (esp. rats & domestic pets ).
- Transmission = contact with animal urine (esp. in water)/ Consumption of contaminated
water/food colonization with Leptospira leptospirosis
- Pathogenesis/ introduction =
o Has 2 periplasmic flagella motile (&thin) penetrates mucous membranes or enters
via small skin-breaks.
o Travels in bloodstream They easily spread to all tissues, including the CNS
o Clearance of Leptospira occurs only when humoral immunity against it develops.
- Incubation = 1-2 weeks.
- Highest-incidence area = Hawaii (endemic to tropical regions)
Initial Phase (1 week): Influenza-like illness: Fever, myalgia (muscle pain), chills, headache…
Second Phase
Severe worsening of the influenza-like symptoms.
GI symptoms & Conjunctival Suffusion (reddening of the eye, w/o puss).
Complications: Possible Hematogenous spread to:
o Vascular Collapse
o Thrombocytopenia & Hemorrhages
o Liver: Hepatitis Hepatic malfunction Jaundice.
o Kidney: Renal Malfunction ARF
o Brain: Aseptic Meningitis (= source of meningitis cannot be seen in the CSF).
- Dx. = microscopy isn’t reliable serology (Ab detection) (agglutinin test), blood-culture, PCR
- Treatment = Doxycycline, Azithromycin or Amoxicillin (if brain is involved ceftriaxone).
- Prevention = doxycycline after short-term exposure, vaccination of domestic pets, rat control.
59
Obligate anaerobe
28. Borrelia.
Borrelia genus

Morphology (gram+ shape): G- spirochete, large (poorly gram-stained (too thin wall), stained well in
Giemsa/ Wright; must be viewed using dark-stained microscopy).
Metabolism (aerobic/ anaerobic): most are obligate anaerobes, some are aerotolerant
(microaerophilic (B. Burgdorferi))
Growth requirements (simple/ fastidious): fastidious
Long replication time slow growth
Virulence
• Outer Surface Protein A (OspA) – mediates migration of the tick Borrelia from its gut to its
salivary glands.
• Outer Surface Protein C (OspC) – critical component of migration of the bacteria from tick’s
salivary glands into hosts.
Lyme disease
- Cause = Borrelia Burgdorferi (a G- Spirochete).
- Main reservoirs of the bacteria: Rodents (host of the tick larvae), Deer (obligatory host- host of
adult tick).
- Way of transmission: Transmitted by Hard Ticks- vectors (humans are an incidental host).
- Incubation Period = 3 – 28 days.
- Clinical Manifestation = 3 Stages:
Stage 1 = Localized
Erythema Migrans “bull’s eye rash” at the site of tick-bite + Flu-like symptoms (fever,
chills, sweating).
Can involve vesicle formation and central necrosis
Stage 2 = Early Disseminated
Occurs in untreated infections, several days-weeks from primary infection
Bacteria spread in the bloodstream to various locations, where elicit immune response:
o Heart Myocarditis AV-Blocks.
o CNS facial neuritis Bilateral Facial-nerve (Bell’s) Palsy.
o Meninges Meningitis.
o Joints Arthritis.
60
Stage 3 = Late Disseminated
Months-years from primary infection
Neuroborreliosis Encephalitis, Cognitive dysfunction, peripheral neuropathy. Memory
difficulty, lymphocytic meningitis.
Joints Chronic migratory poly-Arthritis.
- Treatment
Stage 1 Doxycycline (tetracycline) (Alternatives = Amoxicillin (penicillin), Cefotaxime).
Stages 2-3 IV Ceftriaxone.
- Prevention:
Vaccination (contains ospA)
Tick Removal (it takes 36-48 hrs for the bacterium to pass to the bitten person).
Prophylactic Doxycycline (up to 72 hrs from tick-removal).
Relapsing fever
B. Recurrentis, B. hermsii and B. duttonii
Transmitted by Lice (from humans) or Soft Ticks (from rodents & pets)
Incubation period = 1 week.
1) 1st phase – Abrupt Onset of Fever
o Shaking chills
o Headaches & muscle aches
o Fever
o Hepatosplenomegaly
2) 2nd phase – Relapsing
o After 1 week, initial fever is resolved.
o However, Worse (Relapsed) Febrile episodes start to occur (1-10 episodes).
3) Complication of febrile episodes
o Heart cardiac failure.
o Liver Hepatic failure.
o Brain cerebral hemorrhage.
ATB: penicillin, tetracyclines
Jarisch-Herxheimer’s Reaction (esp. In treatment of syphilis & Lyme disease) – indicates treatment is
working. =dying spirochetes releasing a bunch of cytokines fever, chills, sweating, muscle & joint
pain (h-d)
61
29. Treponema.
Treponema genus
Morphology (gram+ shape): G- spirochete (“spiral-shaped”); too thin can’t be stained with gram/
giemsa; dark-field microscopy is required for direct visualization
Metabolism (aerobic/ anaerobic): microaerophilic
Ability to produce ATP: obligate intracellular (depend on TCA cycle of host)
Growth requirements (simple/ fastidious): cannot be grown in culture, only in rabbit testes
Has 3 periplasmic flagella Motile in Dark-field microscopy.

T. Pallidum syphilis (Lues)
Way of transmission: STD
Incubation period: 3-12 w
Clinical manifestation- acquired syphilis
1) 1st Phase = Primary Syphilis (10-90 days from infection) – localized
o The bacteria locally invade small blood vessels causing ischemic necrosis and takes out
nerves Painless ulcer (= chancre) with raised borders at the site of infection (genitalia/
mouth). The ulcer is self-resolved after 3-6 weeks.
o Lymphadenopathy (enlargement of Lymph Nodes) develop after 1-2 weeks in most patients.
2) 2nd Phase = Secondary Syphilis (4-10 weeks from infection) – disseminated
o Results from dissemination of T. Pallidum
o Flulike Symptoms followed by widespread Maculopapular rash that starts on trunk and
spread palms, soles of feet, genitalia.
o Condyloma Lata (wart-like lesions on the genitals) may occur.
3) 3rd Phase = Tertiary Syphilis (3-15 years from infection) – systemic
o Causes granulomatous lesions = Gummas – soft growth with firm necrotic center
(coagulative)
o Endarteritis (inflammation in the vasovasorum- blood supply of the aorta) Aortitis
Aneurism of ascending aorta – “tree-barking” appearance.
o Tabes dorsalis (wasting of posterior column of the spinal cord) loss of vibration and
proprioception. (In rarer cases of damaged anterior spinal cord general paresis).
o Prostitutes pupil - Argyle Robertson: Ocular effects – pupils don’t react to light (but do to
accommodation).
o Other damaged organs: liver, joints, testes
62
Congenital syphilis – transmission is either via placenta or vertical
• Saber shins- an anterior bowing of tibia
• Saddle nose
• Hutchinson’s teeth: notched incisors or mulberry molars.
• Congenital deafness
Diagnosis:
ATB
• Penicillin – for all stages
• If allergic: desensitize them and give penicillin (especially if pregnant). Alternatively:
doxycycline (not if pregnant!!!)
• Jarisch-Herxheimer’s Reaction (esp. In treatment of syphilis & Lyme disease) – indicates
treatment is working. =dying spirochetes releasing a bunch of cytokines fever, chills,
sweating, muscle & joint pain (h-d)
Other diseases
Yaws (by T. Pertenue)
• Spread by contact with infected skin lesions.
• Early Phase: Granulomatous skin lesions.
• Late Phase: Destructive lesions of the skin, lymph nodes, and bones.
Pinta (by T. Carateum)
• Small pruritic papules develop on the skin surface after a 1- to 3-week incubation period.
• These lesions enlarge and persist for months-years before resolving.
• Disseminated, recurrent, hypopigmented lesions can develop over years, resulting in
scarring and disfigurement.
63
Undermined
ATB: Macrolides (atypical pneumonia)/ tetracyclines

30. Rickettsia.
Rickettsia genus – general biochemical (diagnosis)
Morphology (gram+ shape): G- (poor staining Giemsa staining), pleomorphic; 0.24-1 µm
Metabolism (aerobic/ anaerobic): obligate aerobe?
Ability to produce ATP (intracellular/ extracellular): obligate intracellular (unable to produce CoA
nor NAD, gets it from eukaryotes host)
Growth requirements (simple/ fastidious): slow growth inside the host cell (replication time = 9-12 h)
Weil Felix agglutination test for rickettsia infections
Incubation period: 2-14 d (no rash)
Prodrome (3-5 days) = flu-like disease (Headache, fever, myalgias) with or w/o nausea & vomiting
Pathogenesis
• Rickettsia bind to cell-surface Endocytosis (Phagosome).
• Rickettsia produce Phospholipase cleave phagosome bacteria is released to cytoplasm.
• Rickettsia adhere to the vascular endothelial cells using their Outer-Membrane-Protein-A
(OmpA).
• Rickettsia accumulate inside the host cytoplasm until cell membrane lyses bacteria are
released.
• Vascular Endothelium Damage Leakage of blood Hypovolemia & Hypoproteinemia.
Pathogenesis: Bacteria infect endothelial cells endothelial hyperplasia ↑vascular
permeability extravasation
Epidemic typhus by R. Prowazekii
Epidemiology: affects military camp recruits and prisoners of war (because poor hygiene lice!)
Way of transmission: human to human- vector via lice: lice defecate (bacteria is there) human
scratches feces in (+R. prowazekii).
Symptoms:
• Rash start at trunk spread outwards towards extremities (spares hands, feet, and head).
• Unremitting headache, high fever
• Myalgia (muscle pain) and arthralgia (joint pain)
• Skin eschar (necrosis)
• Pneumonia or pulmonary edema.
• Meningoencephalitis with dizziness and confusion seizures and coma
Treatment = Doxycycline (alternative = ciprofloxacin)
64
Rocky Mountains Spotted Fever (RMSF) by R. Ricketsii
Able to utilize host’s actin to achieve motility
Reservir = wild small rodent & domestic animals
Way of transmission: via (dermacentor) ticks – direct biting
Transmission = tick-bite (requires at least 6 hrs of feeding for transmission
Clinical Features: spotted fever rash + fever
Maculopapular rash which turns petechial after 6 days (due to extravasation).
The rash starts on the wrist & ankles and then spreads to the rest of the body.
Extravasation may cause swellings in the body (periorbital, neck, brain).
Complications:
o Extravasation Hypovolemia, pulmonary edema, renal failure, hepatic ischemia.
o CNS infection Encephalitis or Meningoencephalitis.
Treatment = doxycycline (vectors).
Prevention = tick-protection (clothing, repellants) & fast removal of tick.
65
31. Chlamydiaceae
Chlamydiaceae

Morphology (gram+ shape): poor gram staining (cell wall lacks muramic acid (component of
peptidoglycans) ATB); visualized with Giemsa stain
Metabolism (aerobic/ anaerobic): aerobic
Ability to produce ATP by its own (intracellular/ extracellular): obligate intracellular bacteria
Metabolism:
1st stage – Elementary body – Enters the cells – inactive dividing – infectious
2nd stage – Reticular body – Replicates (multiply by binary fusion) – active dividing – not infectious
Release of the newly replicated bacteria out of the cell …
Inclusion bodies (bunch of reticular bodies) visible within infected cells under microscope
Main Structural Proteins:

Each Spp. has a unique Major Outer Membrane Protein (MOMP).
All Chlamydiaceae have Outer Membrane Protein 2 (OMP2) – stability of EBs.
Immotile
Diagnosis: Giemsa stain ( intracellular inclusions) or NAAT (nucleic acid amplification test, like PCR)
Chlamydia trachomatis infections

A-C: trachoma
• Way of transmission: contact of contaminated secretions with the eye.

• Presents as acute follicuar conjunctivitis (= small lymphoid follicles in the conjunctiva) …
• … trichiasis (= turning inwards of the eyelashes) corneal scarring blindness (#1)
• Complication = Reiter’s Syndrome = Reactive Arthritis (ReA): Maladaptive autoimmune
response (as part of Ab response against infection, they also attack the body), especially at
sacroiliac joint and knee joint). Triad: uveitis (eye’s infection), urethritis, arthritis (can’t see,
can’t pee, can’t bend the knee).
D-K: urogenital infection, neonatal conjunctivitis, neonatal pneumonia
• Way of transmission: STD

• Characterized by watery discharge (VS thick purulent- gonorrhea)
• Asymptomatic urethritis dangerous! Remains untreatable and proceeds to complication
• PID: an ascending infection cervicitis, pelvic pain, abscess formation, scar tissues
infertility/ ectopic pregnancy.
66
• If a woman has an active infection during the baby delivery infected baby, but with
different presentation- neonatal conjunctivitis, neonatal pneumonia. Similar to N. gonorrhea
but in contrast- later onset, staccato cough (a cough with really short, sudden breaths).
L1-L3: LGV (Lympho-Granuloma Venereum)
• Way of transmission: STD

• Infection of lymphatics (inguinal especially)
• Starts with genital painless ulcer (similar to syphilis) but weeks-2m later
• Tender inguinal lymphadenopathy with draining lymph nodes
Chlamydophila.
Feature C. Pneumoniae C. Psitacci
Reservoir Human Respiratory Tract Birds, Parrots, Turkeys
Transmission Respiratory Droplets Inhaling dust of dried bird secretions and feces
Disease Walking Pneumonia Psitacossis („Parrot Fever”)
Clinical Features Similar to M. Pneumoniae (URTI LRTI) Atypical pneumonia with hepatitis, cough may be
absent
Complications x Hepatosplenomegaly, CNS & Cardiac involvement
Dx. Serology, CXR Serology, CXR, Liver functions
Treatment Erythromycin/ Doxycycline or Levofloxacin Doxycycline or Erythromycin
Prevention x Avoid birds
ATB
No muramic acid at cell wall penicillin is useless
If STD, trachoma 1st line: macrolides (azithromycin); 2nd line: tetracyclines (doxycycline)
If neonatal conjunctivitis/ trachoma? oral macrolides?
Atypical pneumonia 1st line: tetracyclines; 2nd line: macrolides
*always add ceftriaxone (in case of coinfection with gonorrhea)
Prevention = Erythromycin is effective in mothers to prevent vertical transmission neonate.
67
32. Mycoplasma.
Morphology (gram+ shape): smallest free-lining bacteria; no gram stained Microscopic diagnosis is
useless! (Serology is rather used: IgM cold agglutinins agglutination of RBCs hemolysis)
0.2-0.3 μm Coccoid/ 0.1-0.2 μm (width), short (1 μm length) Rod
Cell wall: no cell wall Resistance to Cell-Wall inhibitors (β-lactams, Vancomycin etc)
Cell membrane: contain cholesterol (the only bacteria to have this) stabilization and flexibility.
Metabolism (aerobic/ anaerobic): Facultative anaerobe (ex. M. pneumonia- obligatory aerobe)
Ability to produce ATP (intracellular/ extracellular): obligate extracellular
Growth requirements: sterol must be added to culture medium for proper growth
Slow Growth (Replication time = 1-16 hrs
Agar: eaton
M. pneumoniae
Obligate aerobe
High-Risk Population = young adults (< 30) in close-contact conditions (e.g. military
Transmission = respiratory droplets (inhalation or contact).
Pathogenesis (steps):
1. Bacteria are inhaled attach to respiratory ep. via complex of Adhesins (P1 is most
important) Strong Adherence
2. Inhibits ciliary action, produces H2O2 & superoxide radicals + cytolytic enzymes.
3. Eventually causing damage to the respiratory ep. Necrosis
Clinical Features = Walking Pneumonia (25% of all community-acquired pneumonias):
Acute stage = URTI (pharyngitis) with Tracheobronchitis & wheezing.
Up to 15% of cases progression to light patchy pneumonia (nonproductive cough).
Some cases show maculopapular skin-rash.
Self-Resolution after 2-3 wks (shorter with ATBs).
Secondary complications (Sepsis, Endocarditis, Meningoencephalitis)
Walking pneumonia – “the patient looks better than its lungs (patchy infiltrate in X-ray)” (VS typical
pneumonia (S. pneumoniae))
ATB
No cell-wall no β lactam (penicillin, cephalosporins, carbapenems, monobactams) nor
glycopeptides (vancomycin)
1st line: macrolides (Erythromycin, Azithromycin)
2nd-line: Doxycycline, Resp. Quinolones (Levofloxacin)
68

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Special Microbiology

Metabolism (aerobic/ anaerobic):

Ability to produce ATP (intracellular/ extracellular):

Growth requirements (simple/ fastidious):

Virulence factors (infection properties)

Pathogenicity to humans (obligatory/ opportunistic):

Adhesion (pilli/ fimbriae)

Immune response inhibitors

Enzymes (e.g. degrading enzymes)

Organelles (e.g. fibriae – adhesion)

Improve resistance treatment

Cell wall (e.g. myocolic acid)

Mechanism of ATB resistance

Clinically important species

Biochemical characteristics (diagnosis)

Metabolism (aerobic/ anaerobic): facultative anaerobes

Ability to produce ATP (intracellular/ not): extracellular

Growth requirements (simple/ fastidious): simple

Normal flora: skin & mucus membranes opportunistic pathogens

Virulence factors (infection properties)

Bound Coagulase (=clumping factor): (agglutination – fibrinogen fibrin) – invasion, typical

Hemolysin + β-hemolysis typical yellow (golden); strep B

Mechanism of ATB resistance:

(exo)Toxins (through lysogenic conversion)

• Enterotoxins – heat-resistance; food poisoning diarrhea short-time afterward. Also acts on

Superantigen sepsis: Hypotension, tachypnea, disorientation 2/3 sepsis

Mainly cause infection of artificial materials:

Metabolism (aerobic/ anaerobic): facultative anaerobe- create acidic environment (caries in

Ability to produce ATP: (intracellular/ not)

Growth requirements (simple/ fastidious): blood enriched agar

Streptolysin O hemolysis (beta)

We use some strains of streptococci in cheese making.

Virulence (infection properties)

Pathogenicity to humans: (obligatory/ oppurtonistic)

Immune response inhibitors

Improve resistance treatment

Mechanism of ATB resistance: modified PBPs.

Lancet shaped diplococci

α hemolysis – partial hemolysis where the surrounding zone is greenish (viridation)

Bile soluble doesn’t grow in bile

IgA protease can penetrate mucous membranes

Pneumococcal infections: #1 MOPS in children & adults

Adherence: M protein, F protein, lipoteichoic acid

Inhibition of immunity (opsonization) and inhibition of phagocytosis: hyaluronic capsule

M protein prevents phagocytosis + initiates severe immune response (type II) RF

Streptolysin O β hemolysis (we generate ASO Ab to this)

Streptokinase- plasminogen plasmin

Toxins: exotoxins A, C (suprantigens) TSLS; exotoxin B necrotizing fasciitis

Non-invasive: pharyngitis, skin infection (pyoderma)

Invasive: flesh-eating bacteria, TSLS

Purulent Tonsillopharyngitis (Strep Throat) (#1)

- Reservoir = human vagina (15-20% of women) & GIT.

• 1st-choice: penicillin + aminoglycosides (added due to possible resistance)

Growth requirements: simple

γ hemolysis (no hemolysis)

Glucose fermenters (Glucose L-Lactic Acid)

Normal flora: colon

Enterococci virulence is mainly due to:

• Enterococci – Main Diseases:

Way of transmission: inhalation of M. tuberculosis in aerosols or dust lungs

General biochemical (diagnosis)

Ability to produce ATP (intracellular/ extracellular):

Growth requirements (simple/ fastidious): slow growth, fastidious