Table 47.
Organism
Aerobic and Facultatively Anaerobic Gram-Positive Cocci
Staphylococcus aureus
(beta hemolytic)
• GPC in clusters
• Facultative anaerobic
• non motile
• capsule
• catalase positive
• only S.aureus is
coagulase positive
(S.epidermidis and
saphrophyticus are
not)
Differentiating staph.
Aureus and epidermidis
Staph aureus: 1.) tests
positive on coagulase assay (it
forms a cloth) 2.) Shows up as
beta hemo, 3.) test positive for
mannitol plate--makes plate
turn yellow
Staph epidermis: 1.) Tests
negative on coagulase assay
(doesn’t form cloth) 2.) Shows
up as non-hemo 3.) test
negative for mannitol plate--
plate remains red as does not
Clinical Features Epidemiologic
Features &
Transmission
Cutaneous infections:
bullous impetigo from
bacteria paronychia,
folliculitis, acne, stye;
disseminated infections:
bacterimia-pneumonia,
empyema, osteomyelitis,
septic arthritis; toxin-
mediated infections-:
toxemia- scalded skin
syndrome, toxic shock
syndrome-Menstrual TSS,
Non-menstrual TSS;
community-acquired
infections
Virulence Factors Treatment
• Naturally occurring • Lipotechoic acid- Oxacillin; vancomycin (for
on skin binds to exterioir of oxacillin-resistant strains),
• Carriage-skin and epithelial wall cephalosporins.
nasal passage, • Fibronectin binding
airborne respiratory protein Penicillin resistant(PRSA),
droplets and • Laminin binding and MRSA(methicillin
desquamated cells, protein-can break resistant)
and disseminated into mucosa
by contact. • Sialoprotein binding VRSA arising
• Can grow in protein
extremely high
temp and saline Antiphagocytic factors:
conditions
• Capsule and thick
peptidoglycan layer
• Protein A-binds to
the Fc region
blocking
phagocytosis
• Coagulase-covers
bacteria in fibrin
• Hydrolytic Toxins-
hemolysins (alpha
major),
leukocydins(kills
leukocytes)
• Enterotoxin
1
Table 47.1

produce acid

S.aureus-Alpha hemolysin is
responsible for Beta hemolytic zone
in staph. Aureus

yellow in nutrient agar plate,

creamy white in blood agar plate
with clear zone.

Staphylococcus, coagulase
negative (CONS)
Opportunistic pathogen
causing infections on
foreign bodies (e.g.,
catheters, shunts,
prosthetic joints, and heart
valves); urinary tract
infections
Colonize human skin and Possess thick Oxacillin; vancomycin (for
mucosal surfaces; survive peptidoglycan layer and oxacillin-resistant strains)
on environmental surfaces; loose polysaccharide slime
able to grow at extremes layer; S. saprophyticus
temperatures produces high
concentrations of urease

Staph.epidermidis-causing
endocarditis and male
UTI’s in elderly

Staph. saphrophiticus-
causing female UTI’s

Streptococcus Suppurative infections: Diverse populations Adherence and Penicillin G, erythromycin

• GPC in chains
• Facultative anerobes
• Non-motile
• Catalase negative
• Alpha and beta
hemolytic zones
Streptococcus
pyogenes (group
A) beta hemolytic
pharyngitis, scarlet fever, virulence factors:
sinusitis, skin and soft-
tissue infection (impetigo, • capsuleM protein-
erysipelas(butterfly face), gives support to
cellulitis, necrotizing lipotechoic acid
fasciitis, toxic shock–like which is necessary
syndrome; nonsuppurative for adherence,
infections: rheumatic protects cell from
fever; glomerulonephritis phagocytosis & is a
factor for rheumatic
Streptoccal pharyngitis fever

2
Table 47.1
• F protein,
(Strep throat)-group A • G protein-fxns
• Group A is only B strep similar to prot A of
hemolysin, So if
you have a clear s. aureus-binds to
agar (Beta Complictaions: Fc region.
hemolysins) then
it’s Streptolysin S Scarlet fever, acute Toxins:
because it’s rheumatic fever, acute
resistant to the pyrogenic
oxygen
glomerulonephritis exotoxins;
environment of • Hemolysins;
the blood.
streptolysin O-
oxygen labile so
can be destroyed in
air
• Streptolysin S-
stable, resistant to
oxygen
• Streptokinase-
converts
plasminogen to
plasmin (inhibiting
clotting)
• deoxyribonuclease
(DNase); C5a
peptidase

Streptococcus agalactiae Neonatal disease (early Neonates; pregnant Similar to group A but no Penicillin and gentamycin
(group B) onset, late onset; women; patients with capsule
bacteremia, pneumonia, diabetes, cancer, or
meningitis, urinary tract alcoholism
infections

Type 3 most common in

neonatal meningitis

Streptococcus *lobar pneumonia; lower Diverse: neonates, • Alpha-hemolytic Penicillin, cephalosporins

pneumonia (alpha lobes children, adults with Evasion of Host (cefuroxime, cafataxime)
hemolytic) chronic diseases, elderly system:
Pneumonia and other Vaccination:23 valent
3
Table 47.1
• GPC
• capsule
• #1 pathogen for
community acquired
pneumonia
• #1 agent for Otitis
media (middle ear
infection)
• #1 gram positive
agent for Bacteremia
• #1 agent for
Meningitis in adults
Lab tests for S.pneumoniae: to
differentiate from other alpha-
hemolytic cocci
1) Optochin test
2) Quellung rxn(bile salt
solubility test)
Aerobic or Facultatively Anaerobic Gram-Positive Rod
Corynebacterium
diphtheria
• GPB
• Metachromatic
granules in a
palisade
arrangement
Aerobic Gram-Negative Cocci
Neisseria gonorrhoeae
respiratory tract infections;
meningitis; spontaneous
bacterial peritonitis,
endocarditis, septic
arthritis; bacteremia, otits
media(middle ear
infection)
Presence of upper resp
tract infection leads to
secondary infection-
pnemococcal disease:
Pneumonia, otitis media,
bacterimia, meningitis
Diphtheria: respiratory,
cutaneous infection
Gonorrhea, pelvic
• polysaccharide
persons capsule capsular
• IgA protease polysacharride/7valent
• Pneumolysin- conjugate vaccine
activates classical
complement path,
similar to
streptolysinO,
cytotoxic
• Pneumococcal
Surface Protein A
(PspA)- blocks the
binding of C3B
• Pneumococcal
Surface Protein C
(PspC)- similar to M
protein of group A.
strep (facilates the
degragation of C3B)
Toxins and enzymes:
autolysins, neuraminidase,
hydrogen peroxide
Spread by respiratory Diphtheria toxin which is Neutralizing exotoxin;
droplets to unimmunized an exotoxin encoded by penicillin or erythromycin
individuals bacterophage Beta. to eliminate organism and
terminate toxin
• Toxin inhibits production; immunization
protein synthesis with diphtheria toxoid
• Induces formation
of
pseudomembrane
Sexual transmission, Virulence factors: Cephalosporines or
4
Table 47.1
• GNDC inflammatory disease,
• Aerobic arthritis. Local infxns:
• Cytochrome oxidase conjunctivitis-opthalmia
positive neonatorum, pharyngitis,
• Ferments glucose procitis.
• Growth on chocolate
agar with carbon Males: symptomatic,
dioxide acute urethritis. purulent
exudates, dsyuria,
polyuria, headaches and
fevers. Chronic infxn could
lead to sterility.
Females: Generally
asymptomatic and affects
the lower tract. urethritis,
abdominal or pelvic pains.
Chronic infxn could lead to
inflammation of urethra
and genitourinary tract
and PID.
PID-affects upper genital
tract as infection ascends,
affects fallopian tubes,
uterus, ovaries, peritoneal
surfaces. Endometritis,
salpingitis, oophoritis.
Sterility may result.
Neisseria meningitides Community acquired
Meningitis, bacteremia
• GNDC (meningococcemia)-high
• Cytochrome oxidase fever, rash, vessel
positive blockage arthritis,
• Ferments glucose petechiae, pupura,
and mannitol nausea, vomiting.
• Growth on chocolate Sequelae- deafness,
agar with carbon mental retardation.
dioxide Fulminating
asymptomatic carriage
Endogenous infxn as
present in nasopharynx.
Carrier state, aerosol
transmission, most
common in children and
young adults, also
increased susceptibility in
individuals with
deficiencies in MAC
complex components.
• Pili fluroquinones (e.g
• OPA-for firm Ceftriaxone, ciprofloxacin)
adhesion
• Por-prevents
phagolysosome
fusion Penicillin, tertracyclin and
• LOS(sialyated LPS)- fluroqiuinone resistant
blocks antibody strains exist.
mediated killing
• IgA protease
• B-lactamase
Mechanisms:
• Phase and
antigenic variation
of pillin antigen
Virulence factors: 3rd gen cephalosporins,
rifampin.
• Has Capsule unlike
N.gonorrhoeae Mennactra vaccine best
making it anti- method of prevention
phagocytic
• Pili
• OPA-for firm
adhesion
• Por-prevents
5
Table 47.1
• #1 agent for teenage phagolysosome
meningitis Sepsis(waterhouse- fusion
frinderchsen syndrome)- • LOS(sialyated LPS)-
bilateral destruction blocks antibody
adrenal gland, leading to mediated killing
rapid collapse and death) • IgA protease
• B-lactamase

Invades epithelial barrier,

into blood stream and
becomes systemic.

Aerobic and Facultatively Anaerobic Gram-Negative Rods

Bordetella pertussis Pertussis (whooping Aerosol transmission; Virulence factors: Supportive therapy,
cough). Has 3 phases- severe diseases in infants, erythromycin (or other
• GNB catarrhal, convulsive, milder in adults • Fimbriae, macrolides) to decrease
convalescence adhesions-cause infectivity and prophylaxis
cilliary stasis for contacts;
• LPS fluoroquinolones
• Pertussis toxin-An
AB toxin of the
structure 1A5B, an
ADP ribosyl-
transferase , acts
upon the Gi protein,
increased cAMP cell
signaling by
inhibiting Gi protein
• adenylate cyclase
toxin
• Heat liable toxin

Haemophilus influenza Encapsulated type b Endogeneous pathogen. Virulence factor for HiB vaccine against type b
strains: systemic encapsulated strains: poly ribotol capsule
• GNCB infections-meningitis, Aerosol transmission in
• requires factor x- young, unimmunized • adhesion via
6
Table 47.1
heme and factor v-
NAD septicemia, septic arthritis.
• grows on chocolate Acute epiglotitis.
agar
• # 1 agent for toddler Unencapsulated strains:
meningitis otitis media, sinusitis,
conjunctivitis, bronchitis,
pneumoniae
H.influenza an etiological
agent of endemic
cinjuctivitis and brazillian
purpuric fever.
H.ducreyi Causes chancroid, soft
chancre, and accompanied
by regional
lymphadenopathy
Legionella pneumophilia Lobar consolidation of
upper lobes
• GNB
Legionnaires disease
(pneumonia), Pontiac fever
(flu like illness)
Moraxella catarrhalis Inusitis, otitis media,
COPD. Disharge from eyes
• Gram negative cocci and nose. Bronchitis.
(tetrad)??? Bronchopneumoniae
• Aerobic
• Cytochrome oxidase
positive
Anaplasma, Ehrlichia, Rickettsia, Coxiella, Mycoplasma, Chlamydia, and Chlamydophila
Mycoplasma pneumonia Atypical pneumonia,
children; spread from
upper respiratory tract in
elderly patients with
chronic respiratory disease
Increased susceptibility:
globulin deficiencies, sickle
cell, deficiencies C2,C3 and
factor I, COPD, pregnancy,
alcoholism, malignancy,
skull trauma
STD
Waterborne; elderly and
immunocompromised
patients
Normal flora of oral cavity
and upper respiratory tract
(endogenous infxn)
Children; patients with
compromised pulmonary
system
Symptomatic disease more
fimbriae Broad-spectrum
• Capsule(polyribitol cephalosporin ceftriaxone,
phosphate PRP) azithromycin,
• destruction of clarithromycin or
cilliary epithelium fluoroquinolone; many
• IgA protease strains resistant to
• LPS ampicillin
C3b adhesin, cytotoxins, Macrolides (erythromycin,
evasion of phagolysosome azithromycin,
fusion clarithromycin);
fluoroquinolones
(ciprofloxacin,
levofloxacin) used as
alternative therapy
Unknown Cephalosporins
Penicillin resistant
Virulence factor: Erythromycin, zithromycin,
7
Table 47.1

(walking pneumonia) patchy lung (affects common in children than • P1 adhesin protein- tetracycline
bronchioles) adults; special binds
• Facultative anaerobe susceptibility in patients M.pneumoniae to Penicillin ineffective
• Lacks peptidoglycan Fever, headache, malaise, with respiratory cells
• Pleomorphic muscle pain, non- hypogammaglobulinemia which Inhibits
• Cell memb’ has productive cough. and sickle cell cilliary action, by
sterols destruction and
• Small genome Also have presence of Transmission via loss of cilliary cells
serum, “cold agglutinins” respiratory droplets;
Incubation, 3 week period.