STAPHYLOCOCCUS
Reservoir: normal flora of anterior nares, nasopharynx, perineal area, and skin | Sources of infection: nosocomial, autoinfection, contaminated fomites | zMode of transmission: traumatic introduction, contact with contaminated fomites
ORGANISM BIOLOGY
Gram(+), cocci in grape-like
clusters, nonmotile,
capsulated
Facultative anaerobe; prefers
aerobic
Temperature range for
Staphylococcus species: 6.5-
46oC,
optimal at 30-37oC
MOST RAPIDLY AT 37oC
Form pigment best at 20-25
pH range: 4.2-9.3
OPTIMUM: 7-7.5
SHEEP BLOOD AGAR IS
PRIMARY ISOLATION
MEDIA
Smears from pus – single,
pairs, short chains
Smears from cultures on
solid media – irregular
clusters
S. aureus Smears from broth culture –
short chains, diplococcal
Resistant to drying, heat,
NaCl
Readily inhibited by 3%
hexachlorophene
S.
epidermidis
S.
saprophyticu
s e.g., N. gonorrheae, S. aureus)
TESTS
Colony morphology
 Facultative anaerobe
 Smooth, opaque, round, low,
Biofilm formation convex, gray to golden yellow
 (carotenoids)
refractory to  BAP: cream/buff colored with B-
treatment LOGY hemolytic zone
Tests
 Catalase(+) (bubble formation,
detect cytochrome oxidase,
3% H2O2)
 Coagulase(+) (clot formation
within 1-4h)
o Slide: detect bound
coagulase (clumping factor)
o Tube: detect free coagulase
 Ferments carbohydrates –
produce lactic acid but not gas
 Mannitol fermenter (red to
yellow discoloration in mannitol
salt agar with 7.5% NaCl or
chromogenic media)
 Difference sa S. epid
 Penicillin G resistant  -
lactamase (+)
 35% of strains resistant to
nafcillin, oxacillin, and
methicillin (mecA gene)
 Resistance to vancomycin
(vanA)
 Serologic: antibodies against
teichoic acid
Host-specific to Colony Morphology
humans White. Nonhemolytic
Most frequent sites: Tests
axillae, head, arms, Catalase(+), coagulase(-),
legs, nares Mannitol non-fermenter
Novobiocin susceptible, Ferments
carbohydrates – produce lactic acid
but not gas; resistance to
methicillin and pen G
Colony Morphology
Nonhemolytic
Tests
CLINICAL MANIFESTATIONS VIRULENCE AND ANTIGENIC FACTORS TREATMENT
Habitat ANTIGENIC STRUCTURES Localized infection:
ANTERIOR NARES: MOST COMMON SITE  Capsule Drainage
Attachment: o Antiphagocytic, anti-complement, anti-chemotactic, Debridement
Capsule  Synthetic material adherence to synthetic materials B-lactamase if
Teichoic acid  Mucosal surfaces o Usual target of vaccines resistant to Penicillin
Protein A  Host cells  Peptidoglycan layer
o Chemoattractant, endotoxin-like activity Cutaneous infection:
Sources of infection o Confers rigidity Cloxacillin,
Fomites dicloxacillin
o Localized Schwartzman phenomenon: necrosis,
Respi tract Erythromycin (if
thrombosis, (+) complement, (+) humoral and cellular
use Nosocomial allergic to pen G)
immune response (Il-1 prod)
Methicillin
Mode of transmission  Protein A
o Antiphagocytic, anticomplement, Chemotaxis,
Traumatic Serious systemic
Person to person hypersensitivity, platelet injury disease
o Unique to S. aureus
Parenteral nafcillin
Localized skin infections o Five regions: 4 Fc binding domains, 1 C terminal domain or oxacillin(4-6wks)
o Binds @ Fc portion of IgG mols except IgG3
 Folliculitis (domed pustules around hair
o MSCRAMM (microbial surface components recognizing
follicles) Methicillin resistant
 Furuncles or boils (subcutaneous tissues adhesive matrix molecules)  IMPT VIRULENCE FACTOR (B lactam antibiotic
focal suppurative or abscess lesion)  Clumping factor (fibrinogen binding; unique to S. aureus; resistant
Vancomycin
 Carbuncles (coalescence of furuncles) MSCRAMM) AKA COAGULASE
Or in combo w
 Impetigo (macule  pus filled vesicle   Cytoplasmic membrane (osmotic barrier)
rifampicin
crust) DETERMINANTS OF PATHOGENICITY
 Surface receptors
Vanco if Hospitak
Deep and localized infections: o Polysaccharides (antiphagocytic) – capsule, PT, TA
Clinda if community
 Osteomyelitis – organisms localize at o Protein receptors  surface binding: fibronectin (adherence
diaphysis of vital cells), laminin (breach normal barrier), collagen
 Pyoarthrosis – destruction of articular  Extracellular enzymes
cartilage o Coagulase (binds and (+) prothrombin  clots plasma)
 Bacteremia o Lipase (survival in sebaceous areas)
 Endocarditis o Hyaluronidase (spreading)
 Pneumonia (necrosis + multiple abscesses) o Staphylokinase/fibrinolysin (fibrinolytic  dissolve clots)
 Metastatic infection o Nuclease (phosphodiesterase)
 Toxins
Diseased caused by Exotoxin: o Hemolysin toxins (α, β, γ, δ)
 TSS (via tampons; scarlatiniform rash   α (hemolytic, lethal, dermonecrotic) abscess formation
desquamation) TSST1  β (sphingomyelinase C; abscess formation; attacks
 Food poisoning (gastroenteritis w/o fever; lysophosphatidylcholine; heat labile)
vomit before diarrhea; onset 2-6h after  γ (hemolytic, Panton-Valentine leukocidin)
ingestion of food) Enterotoxin  δ (nonionic detergents: disrupts biologic membranes; (-)
 Scalded skin syndrome ileum water absorption) DELTA DETERGENT
o D/t exfoliatin toxin DIARRHEA
o Ritters dse / toxic epidermal o Leukocidin / Panton-Valentine (attack PML and
necrolysis / generalized exfoliative macrophages only)
dermatitis (painful erythema, bullous o Pyrogenic protein toxins (superantigens;
desquamation, (+) Nikolsky sign) immunosuppressive)
o Bullous impetigo (-) Nikolsky, in the  Enterotoxin (vomiting, diarrhea)  food poisoning
face) (frequently enterotoxin A); Enterotoxin B
o Scarlet fever (generalized) (pseudomembranous pseudocolitis
 Toxic Shock Syndrome Toxin-1/enterotoxin
F/pyrogenic exotoxin C (induce IL-2, T lymphocyte
prolif  fever, hypotension, desquamation, multi-organ
failure)
 Exfoliatin (desquamation  staphylococcal scalded
skin syndrome; toxin A heat stable, toxin B heat labile
 Teichoic acids (polysaccharide A: ribitol with N-acetyl D-
glucosamine; attachment to mucosa, antigenic)
ALL ARE HOSPITAL ACQUIRED  Teichoic acids (polysaccharide B: glycerol with glucosyl Aminoglycoside
Infections associated with implanted devices residues; attachment to mucosa, antigenic) (genta or tobramycin)
(e.g., cardiac valve, hip replacement)  Glycocalyx (adhesion to prosthetics, protection from antibiotics) + cephalotin +
Peritonitis penicillase
Bacteremia
UTI (elderly male) Vancomycin/
TSS vancomycin+
aminoglycoside
75% of coagulase-negative Staphylococcus
(CONS) infections
UTI in sexually active young women  Oligosaccharide receptor (adherence) Penicillin
 2nd most common  Extracellular enzyme complex (suppress growth of other bacteria, Cloxacillin, then
vancomycin if not
responding
 Catalase(+), coagulase(-)
Novobiocin resistant, agglutinate
sheep blood, Fail to ferment
glucose anaerobically

STREPTOCOCCUS

 GRAM (+) COCCI IN CHAINS, CAPSULATED (HYALURONIC ACID) o Beta: clear zone, complete hemolysis (beta = buo); classified by Lancefield
 Most species are facultative anaerobes, some are strictly anaerobic to capnophilic o Alpha: greenish-brown zone of discoloration, partial/incomplete hemolysis
 Complex nutritional requirements  blood/serum-enriched media for isolation
o Gamma: no zone of clearing, non-hemolytic
 Ferments carbohydrates, produce lactic acid but not gas
 Catalase negative (as opposed to Staphylococcus)  Diagnostic Laboratory Techniques
 Classified according to: colony morphology, hemolytic reaction, antigenic specificity of polysaccharide capsule, o Hippurate Hydrolysis Test: ninhydrin indicator; hydrolysis of sodium hippurate leads to formation of sodium
serologic specificity of cell wall substance (Lancefield groups A-H, K-U) benzoate and glycine (reacts with indicator to change into purple)
 Capsular polysaccharide: Groups A, B, and C  hyaluronic acid (impede phagocytosis) o CAMP Test: arrowhead-shaped enhancdement of beta hemolysis that occurs when hemolytic bacteria toxin
o Group A: Rhamnose-N-acetylglucosamine produced by Staphylococcus aureus synergistically with CAMP factor
o Group B: Rhamnose-glucosamine polysaccharide o Bile esculin slant: detect growth in the presence of bile (2% sodium deoxycholate) and hydrolysis of
o Group C: Rhamnose-N-acetylgalactosamine esculin (positive test: black)
o Group D: Glycerol teichoic acid containing D-alanine & glucose o 6.5% NaCl broth: growth indicated by turbidity and change in indicator from pink to yellow
o Group F: Glucopyranosyl-N-acetylgalactosamine o Optochin Suceptibility Test: paper disk with optochin (ethylhydrocupreine hydrochloride) applied to
 Cell wall: M, T, and R antigens surface of inoculated 5% sheep BAP  negative zone of inhibition
 Culture: discoid colonies (with capsule: mucoid); grow best at 37oC (Grp D: 15-45oC) o PYR Test: pyrolidonylarylamidase degrades L-pyrrolidonyl-2-naphthylamide; positive test  color change
to re
ORGANISM TESTS CLINICAL MANIFESTATIONS VIRULENCE AND ANTIGENIC FACTORS TREATMENT
Colony Morphology Pyogenic diseases (local):  M protein (antiphagocytic, anticomplementary)  Penicillin G
 Selective agar: with sulfamethoxazole and  Pharyngitis (5-15 y.o., beefy red tonsils, palata petechiae, hair-like projections on cell wall Erythromycin or azithromycin (Pen G
trimethoprim (TMP-SMX) posterior pharynx erythematous with exudates; via respiratory  T protein (trypsin resistant) allergy or necrotizing fasciitis)
 BAP: small colonies with B-hemolysis droplets; IP: 2-5d)  F protein (fibronectin binding: attachment to
 Impetigo/Pyoderma (vesicles to weeping lesions with amber crust epithelium)
Tests and purulent exudates; via direct contact; IP: 7-10d)  Lipoteichoic acid (adherence) [pharyngeal epi]
 Specimen: throat swab, pus, blood  Cellulitis (pink/red erythema, swelling, heat, pain, flat lesion, Toxins and Enzymes
 Catalase(-) indistinct borders; may lead to septicemia)  Hyaluronidase (spreading, antigenic)
 Group A antigen  Erysipelas (salmon/fiery red erythema in butterfly distribution,  Streptokinase (fibrinolysin, debridement) 
 B-hemolytic abrupt borders) transform plasminogen to plasmin
 PYR(+)  Necrotizing fasciitis/Strep gangrene  Streptodornase (DNase, debridement) 
 Bacitracin susceptibility (+) (zone of inhibition)  Puerperal fever depolymerize DNA
 Dick test (erythema) and Schultz Charlton reaction  Diphosphopyridine nucleotidase (leucocyte
Streptococcus pyogenes Toxigenic diseases (widespread):
(localized blanching) for exotoxin C killing)
(Group A)  Scarlet fever (diffuse erythema, circumoral pallor; exotoxin A-C)  Pyogenic toxins
 Streptococcal TSS (desquamation of skin, hypotension, o Exotoxin A (TSS)
erythoderma) o Exotoxin B (cysteine protease: necrotizing
fasciitis) BULOK
Immunologic (Post-streptococcal) diseases: o Exotoxin C (erythrogenic, rash in sCarlet
 Rheumatic fever (complication of pharyngitis; damage to heart fever)
muscles and valves d/t rxn between strep Ag and human heart  Hemolysins
tissue antigens  Aschoff bodies) most serious sequelae o Streptolysin S (oxygen stable), hemolytic
 Acute glomerulonephritis (complication of impetigo; edema of zones surrounding colonies on surface of
face and ankles, smoky urine; Ag-Ab complexes on glomerular BAP
basement membrane) o Streptolysin O (antigenic), hemolysis deep
into blood agar plate
 RECENT INFXN
Group C and G Streptococci -hemolytic Pharyngitis, sinusitis, bacteremia, endocarditis  Hemolysins
Resemble Group A strep Identified by reactions with specific antisera Post-streptococcal sequelae of acute glomerulonephritis  M proteins
Colony Morphology Neonatal group B step disease  DNase Penicillin G
5% sheep blood agar: large colonies, B-hemolytic zones Early Onset/In utero or at delivery:  Hyaluronidase (spreading) Ampicillin + Aminoglycoside
 < 7 d onset  Neuraminidase
Tests  Bacteremia, pneumonia, respiratory distress syndrome, fulminant  Protease
 Gram stain of vaginal secretion sepsis, meningitis  most common cause @ newborn  Hippurase
 Catalase (-)  High obstetric complications  Hemolysin
Streptococcus agalactiae  Group B antigen  High mortality rate  Capsule (antiphagocytic, antigenic)
(Group B)  B-hemolytic  Serotype Ia>III>V  Most important virulence factor
 CAMP(+)  arrowhead shaped enhancement
 Sodium hippurate (+) (purple) Late onset/Postpartum:
 Bile esculin (+)  1wk-3 months onset
 NaCl broth (+)  Bacteremia, meningitis, osteomyelitis
 Infrequent obstetric complications
 Low mortality rate

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 Streptococcus bovis group/ Colony Morphology II: Penicillin or Vancomycin
Group D non-enterococci 5% Sheep BAP: raised, white to gray, non-hemolytic Hospital-acquired UTI and endocarditis
Colon carcinoma
DNA cluster I: Tests
S. equines  Bile esculin (+) (black slant)
DNA cluster II:  6.5% NaCl (-) (no growth)
S. gallolyticus  PYR(-)
DNA cluster III:
S. infantarius
DNA cluster IV:
S. alactolyticus

Usually non-hemolytic, occasionally alpha-hemolytic Nosocomial infections Aminoglycoside + cell wall-active

Tests Meningitis, bacteremia in neonates antibiotic (penicillin, ampicillin,
Enterococcus/Group D
 PYR (+) Endocarditis in adults vancomycin)
enterococci Linezolid, daptomycin, tigecycline,
 Growth in 6.5% NaCl
 Resistance to penicillin, vancomycin quinupristin/ dalfopristin
Colony Morphology
Streptococcus anginosus Variable hemolytic activity
group Minute colonies (<0.5mm diameter)
 S. milleri
Tests
 S. intermedius
PYR (-)
 S. constellatus Voges-Proskauer (+)
Butterscotch/caramel odor
Normal coagulation/souring of milk (N-Nido)
Group N Streptococci
DOGS/ANIMALS
Groups E-H K-U

Viridans Streptococci
 S. mitis
 S. salivarius
 S. sanguinis (Group H)
 S. mutans
Normal flora of upper
respiratory tract
S. pneumoniae, Diplococcus
pneumoniae, Pneumococcus
Nutritionally variant/Pyridoxal
dependent Streptococci
 S. defectives
 S. adjacens
Peptostreptococcus
NON-LANCEFIELD
Colony Morphology Normal flora or URTI Synthesis of glucan (virulence in producing caries) Penicillin
Produce green pigment on blood agar (virdis = green)
Bacterial endocarditis – MOST COMMON CAUSE
Tests Dental caries (S. mutans)
Optochin susceptibility(-) (no zone of inhibition)
Not soluble in bile
Colony Morphology Pneumonia (via aspiration)  RUSTY RED SPUTUM  Capsule (antiphagocytic, antigenic) Penicillin
 5% Sheep blood agar: young colonies round, Otitis media, sinusitis (precede viral infection of URT)  MOST IMPORTANT Erythromycin
complete edges, mucoid, alpha-hemolytic; older Bacteremia/sepsis  Pneumolysin (hemolysin, dermotoxic)
colonies with central indentation  flattened Meningitis  Purpura-producing principle (dermal hemorrhage) Vaccines:
 Chocolate agar: quite flat, alpha-hemolysis  Neuraminidase (spreading factor)  Polyvalent (23 type)
polysaccharide: long term (5 yr)
Tests  Amidase (autolysin for cell division)
protection
 Optochin susceptible (+) (clear zone >14 mm  IgA protease (enhance colonization)
diameter)  C-substance (reacts with CRP)  Pneumococcal conjugated vaccine
 Bile solubility(+)  Lipoteichoic acid (activates complement, induce (<2 yrs)
 Quellung reaction (capsule swelling; B cell inflammatory cytokine response)
response)
Colony Morphology Bacteremia
Grow as satellite colonies Endocarditis
Usually alpha-hemolytic
Require pyridoxal or cysteine for growth on blood agar
Variable hemolysis Mixed anaerobic infections in the abdomen, pelvis, lung, or brain
Pus has foul odor
Anaerobic
Microaerophilic

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Organism Biology
Bacteroides fragilis Gram-negative rods
Non spore forming
Bile resistant
Normal inhabitant of bowel
and other sites
Pigmenting G(-) bacilli Small coccobacilli
Yung prevotella sp.
Prevotella bivia  Small coccobacilli, in
pairs or short chains
Fusobacterium nucleatum  Most common
 Thin with pointed ends;
scattered wheat straw
 Very long, thin filaments
Fusobacterium necrophorium  Generally broad, usually
with rounded ends, and
may be short, long or
filamentous, often with
bulbous swellings and
round bodies.
 agents
4
Colony morphology
Broth Culture: Pleomorphic bacilli
with vacuoles and swelling
Colonies: low convex, white to gray,
semi-opaque and glistening, and some
strains may be hemolytic
Capable of surviving prolonged
exposures to O2, in the presence of
blood  produces Superoxide
dismutase and catalase (in the
presence of hemin)
Colonies on BAP: convex, smooth,
circular, sometimes β-hemolytic, and
usually pigmented, becoming tan to
black in 2 to 21 days
Vit. K and hemin – growth stimulants
 Hemin is required for growth
 Produce β-lactamase
Colonies: α-hemolytic, convex and
translucent with internal flecking or
mottling, or more umbonate, heaped,
dull and opaque
 Colonies: α- or β- hemolytic
Algorithm for identification of Gram-positive cocci .
Anaerobes
Disease
 
 P melaninogenica and similar species
are found in infections associated with
the upper respiratory tract.
 P bivia and P disiens occur in the female
genital tract.
 Prevotella species are found in brain and
lung abscesses, in empyema, and in
pelvic inflammatory disease and tubo-
ovarian abscesses.

 Part of the vaginal flora
 Bacterial vaginosis
 Genital tract infections, particularly
obstetric infections
 Part of normal flora of mouth; occ. in the
urogenital tract
 Oral infections, lung abscesses, other
pleuropulmonary infections, amniotic
fluid infections in the presence of intact
membranes and preterm gestation
 Causes Lemierre's syndrome
 Involved in abdominal infections and
liver abscesses
 Part of the normal flora of the GIT
 addition to the more
Virulence and Antigenic factors Treatment
Thermolabile protein
 Thermostable lipopolysaccharide Ags
 Species-specific capsular polysaccharide Ag
 Lipopolysaccharide lack the lipopolysaccharide structures with endotoxic activity
(including -hydroxymyristic acid)
 Polysaccharide capsule
o A unique feature of infections with B. fragilis is the ability of the organism to
induce abscess formation as the sole infecting organism.
 B. fragilis elaborates a number of enzymes important in disease:
o proteases and neuraminidases,
o two cytolysins that act together to cause hemolysis of erythrocytes.
An enterotoxin capable of causing diarrhea
 Polysaccharide capsular antigen –Porphyromonas gingivalis
 Lipopolysaccharide
 Collagenase
 Polysaccharide capsule
 β-lactamase


 Have lipase and leukocidal toxin (leukotoxin) Most are susceptible
 Other factors include a hemagglutinin, a hemolysin, and lipopolysaccharide (endotoxin). to Penicillin G and
 In addition, F. necrophorum is capable of causing platelet aggregation. other older
 cephalosphorins in
active anti-anaerobe
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G(+) ANAEROBIC BACILLI Anaerobic Organisms Associated With Different Conditions
 E. lentum: Most common isolate from non-oral clinical specimens Brain abscesses   Peptostreptococci, Fusobacterium nucleatum and others 
Eu o Coccobacilli
bacterium o Part of the normal flora of the GIT Oropharyngeal  Oropharyngeal anaerobes; Actinomyces, Prevotella
 E. brachy, E. timidum and E. nodatum infections  melaninogenica, Fusobacterium species 
o Periodontitis
Pleuropulmonary  Peptostreptococci; Fusobacterium species; Prevotella
 Slow growing infections  melaninogenica, Bacteroides fragilis in 20–25%; others 
 Actinomycesisraelii and Actinomyces gerencseriae
 Gram stain: short and club-shaped or long, thin, beaded filaments.
Intra-abdominal  Liver abscess: Mixed anaerobes in 40–90%; facultative
 prolonged incubation of the culture may be necessary before laboratory confirmation due
infections  organisms
Actino  Abdominal abscesses: Bacteroides fragilis; other
to slow growth
myces gastrointestinal flora 
 Some strains produce colonies on agar that resemble molar teeth.
 Some Actinomyces species are oxygen-tolerant (aerotolerant) Female genital  Vulvar abscesses: Peptostreptococci and others
and grow in the presence of air; these strains may be confused with Corynebacterium tract infections   Tubo-ovarian and pelvic abscesses: Prevotella bivia and
species Prevotella disiens; peptostreptococci; others 
 Actinomycosis is a chronic suppurative and granulomatous infection Skin, soft tissue,  Mixed anaerobic flora; Propionibacterium acnes 
 Normal inhabitants of the GIT and skin and bone
Propioni  Rarely cause infections infections 
bacterium  Closely resemble Actinomyces – pleomorphic: branched, Diphtheroidal or both Bacteremia   Bacteroides fragilis; peptostreptococci; propionibacteria;
acnes  Propionibacterium acnes, often considered an opportunistic pathogen, causes the disease
Fusobacteria; Clostridium; others 
acne vulgaris
Endocarditis   Bacteroides fragilis; Actinomyces 
Lacto  Normal flora in the mouth and GIT, and in women, predominant in the vagina
bacillus  Minimal pathogenic potential
 L. catenaforme – pleuropulmonary infections Veillonella: Little is known re: infection

 Motile, curved
Mo  Gram-positive type cell wall but frequently stain gram-negative or gram-variable
biluncus  M. mulieris and M. curtisii
o Highly associated with the presence of bacterial vaginosis
o Slow growth
Bifido  B. dentium
bacterium o Infrequently involved in infection
Bacillus

Laboratory Treat
Organism Biology Colony morphology Transmission Disease Virulence and Antigenic factors
Diagnosis ment
Bacillus (in Large  Have square ends Most are saprophytic organisms  Some are insect pathogens such as B. thuringiensis Pathogenic species possess virulence plasmids
general) GRAM POSITIVE  Spores are located in occurring in soil, water, air and on
SPORE-FORMER the center of the vegetation such as B. subtilis and  B. anthracis is the principal pathogen of the genus
Aerobic bacilli B. cereus and causes anthrax
 Round, “cut glass”
appearance in
transmitted light
Bacillus  Hemolysis is  Catalase test  Non-pathogenic to humans
subtilis uncommon with B. positive  May contaminate food but rarely causes food
Hay bacillus anthracis but  Model poisoning
or grass common with B. organism for  Spores can survive the extreme heating that is often
bacillus cereus and the laboratory used to cook food
saprophytic bacilli studies  Responsible for causing ropiness in food— a
sticky, stringy consistency caused by bacterial
production of long-chain polysaccharides
Bacillus  Motile  Non-  Found in many foods  Emetic syndrome is acquired by eating food with 1. Heat-stable toxin EMESIS!!!! Symp
cereus  Non- fastidious especially rice, pulses and preformed toxin most commonly fried rice or  Proteolysis-resistant enterotoxin tomat
encapsulated  Hemolysis vegetables recooked rice  Causes emetic form of the disease ic
on horse and  Ingestion of organism or  Disease result from eating food contaminated with  Produced in food associated with spore penetration
sheep blood toxin spores which produced enterotoxin in the GIT  Vomiting within 1-5 hours of ingestion DOC:
agar o Spore-associated disease is caused by Vanc
 Lecithinase contaminated meat or vegetables and 2. Heat-labile enterotoxin DIARRHEA!!! omyc
(+) manifest as diarrhea syndrome  After ingestion in
 Mannitol (-)  Invasive disease risk factors  Causes diarrheal form of the disease
EMETIC DIARRHEA SYNDROME  Diarrhea within 10-15 hours
SYNDROME  Similar to the enterotoxins produced by E. coli and V.
occurs at a short slightly longer incubation cholerae
incubation period (1-6 period 3. Necrotic toxin (heat-labile enterotoxin)
hours) and duration of 4. Cereolysin (a potent hemolysin named after the species)
illness is also short (24 5. Phospholipase C (a potent lecithinase)
hours)
nausea, vomiting, predominantly
abdominal cramps characterized by
moderate to severe
abdominal cramps and
watery diarrhea
diarrhea seen on one vomiting seen on one
third of patients fourth of patients
Both syndromes are mild, not associated with fever,

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 abate within 24 hours

Bacillus  Non-motile  Often have comma-  Definitive:  Spores remain viable in  Major disease threat to herbivores (cattle, sheep,  Exotoxins Ende
anthracis  Bamboo, shaped protrusions culture and soil for decades horses, hogs, goats)  pX01 plasmid-coded mic:
cane-like from colony edge ID o Source of  Humans infected by direct contact with diseased  heat-labile, heterogeneous protein complex made up of PEN
(“Medusa head” infection for animal, hides, wool, brushes, or bone meal 3 components: G
colonies) livestock through  Woolsorter’s disease – inhalation of infected dust 1. Edema factor (EF) – adenylate cyclase; with PA, it
ingestion  Ingestion of infected meat forms a toxin known as edema toxin (responsible for cell Terro

 Human infection is through ANTHRAX: SEE BELOW and tissue edema) rism:
contact with infected 2. Lethal factor (LF) – plus PA form lethal toxin, which is Cipro
animal or animal products a major virulence factor and cause of death in infected Doxy
 Outbreaks of GI anthrax animals and humans. When injected into laboratory
associated with ingestion animals, lethal toxin can quickly kill the animals by
of undercooked or raw impairing both innate and adaptive immunity, allowing
meat organism proliferation and cell death
 Can be used as a 3. Protective antigen (PA) – binds to specific cell
biological weapon receptors, and after proteolytic activation, it forms a
 Injection membrane channel that mediates entry of EF and LF
into the cell

CUTANEOUS ANTHRAX INHALATIONAL ANTHRAX GI ANTHRAX

 Accounts for more than 95% of human cases
 Spores enter the broken skin, germinate and rapidly proliferate at the site of
entry
 Vesicular pruritic papule at the site of infection
 Blue black edema
 Rupture will reveal a black eschar (malignant pustule)
 Generally, occurs on exposed surfaces of the arms or hands followed in frequency
by the face and neck
 A pruritic papule develops 1–7 days after entry of the organisms or spores through
a scratch
 Initially, it resembles an insect bite
 The papule rapidly changes into a vesicle or small ring of vesicles that coalesce,
and a necrotic ulcer develops
 AKA Woolsorter’s disease  Ingestion of infected meat
 Spore inhalation and phagocytosis  Proliferation within the GI tract (mucous membranes)
 Germination, replicated and infection of hilar lymph nodes  Fever, acute abdomen, vomiting, bloody diarrhea
 Hemorrhagic necrosis of lymph nodes  Intestinal eschar (similar to cutaneous lesion)
 Fever malaise, myalgia, and non-productive cough  Spread to mesenteric lymph nodes, septicemia, shock and death
 CXR – lobulated mediastinal widening, may have infiltrates
 Mediastinal widening and pleural effusion on chest x-ray in inhalational anthrax
 Spores from the dust of wool, hair or hides  inhaled  phagocytosed in the lungs
 transported by the lymphatic drainage to mediastinal lymph nodes 
germination  toxin production  development of hemorrhagic mediastinitis 
sepsis
Corynebacteria

Organism Biology Colony morphology Laboratory Diagnosis Transmission Disease Virulence and Antigenic factors Treatment
Corynebacterium (In CLUB SHAPED  Ubiquitous in  Normally colonize the skin, URT, UGT, GIT of Other coryneform bacteria
general) GRAM POSITIVE plants and humans Arcanobacteria – scarlet fever like
Bacilli animals  Can function as opportunistic pathogens but Rothia mucilaginosa – coccoid, mucoid,
Aerobic relatively few are associated with human sticky; endocarditis
non-motile, catalase disease Tropheryma whipelii – whipple disease
positive o Most famous is Corynebacterium
diphtheria
Most species ferment C. jeikeium - opportunistic
carbohydrates C. urealyticum – opportunistic; struvite calculi, renal
 Produce lactic stones
acid as C. amycolatum – resistant
byproduct C. pseudotuberculosis and C. ulcerans
- can carry diphtheria exotoxin gene; consumption
of raw milk
Corynebacterium Irregularly staining, Four biotypes based on Tinsdale medium is best  C.  HUMANS ARE ONLY KNOWN RESERVOIR DIPHTHERIA TOXIN DT
diphtheria pleiomorphic rod colonial morphology and diphtheria:  Clinical presentation is determined by: antitoxin
biochemical properties: Toxigenicity Testing maintained in o The site of infection 3 functional regions in the toxin molecule:
o o gravis C. diphtheria isolates the o The immune system of the patient
o mitis: most should be tested for toxin population by o The virulence of the organism Catalytic region on A subunit
diseases are production asymptomat  Exposure to C. diphtheriae may result to Receptor binding region on B subunit
caused by Gold standard for detection ic carriage o Asymptomatic colonization in fully Translocation region on B subunit
this biotype of diphtheria toxin: Elek in the
immune people
o intermedius test an immunodiffusion oropharync
o Mild respiratory disease in partially  Receptor for the toxin: heparin binding
o belfanti assay or skin of
immune patients; or epidermal growth factor which is
immune
o Fulminant, sometimes fatal present on surface of many eukaryotic
SCHICK TEST – swelling if people
disease in non-immune patients cells (heart and nerve cells)
not exposed  Transmission
is thru
Manifestations : Respiratory Diphtheria  Actions of the toxin:
respiratory
droplets or
skin contact o Symptoms develop after 2-4 days Host cell attachment
 Humans are incubation period (translocation region inserted into endosomal
the only o Organisms usually multiply locally on membrane)
known epithelial cells in the pharynx or adjacent
reservoir surfaces

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 o Initially cause localized damage due to
exotoxin activity Movement of catalytic region into the cell
o Sudden onset: malaise, sore throat, cytosol (a subunit inactivates EF2)
exudative pharyngitis, and low grade
fever
o Exudate is thick pseudomembrane of Termination of host cell protein synthesis
bacteria, lymphocytes, plasma cells,
fibrin, and dead cells
 Can cover tonsils, uvula, and * EF2 (Elongation Factor 2): required for
palate movement of nascent peptide chains on
 May extend up into nasopharynx or ribosomes. Toxin synthesis is regulated by
down into larynx diphtheria toxin repressor (DTxR): this
o Pseudomembrane firmly adheres to protein, activatd in the presence of high iron
underlying tissues concentrations, can bind to toxin gene
 Difficult to dislodge without operator and prevent toxin production.
making the tissue bleed (unique
to diphtheria)
o As patient recovers for around 1 week,
the membrane dislodges and is
expectorated
Complications

o Involve the heart and nervous system

o Myocarditis develops 1-2 weeks into the
illness and at the time when the
pharyngeal symptoms are improving
 Congestive heart failure, cardiac
arryhtmias, and death
o Neurotoxicity
 Neuropathy, initially localized to
the soft palate and pharynx
 Later involving oculomotor and
ciliary paralysis, with progression
to the peripheral neuritis

Manifestations : Cutaneous Diphtheria

o Acquired through skin contact with other

infected persons
o Papules develop first then evolves into a
chronic, nonhealing ulcer sometimes
covered with a grayish membrane
 Staphylococcus aureus or
Staphylococcus pyogenes also
frequently present in the wound

Clostridium

Virulence and Antigenic

Organism Biology Colony morphology Laboratory Diagnosis Transmission Disease Treatment
factors
Clostridium sp. GRAM POSITIVE  Some are commensals of animals and 
Bacilli human gut
Opportunistic  Causes diseases through toxins.
Spore former o Gas gangrene
Saprophyte o Tetanus
Anaerobic o Botulinum
o Pseudomembranous colitis
Employ butyric
fermentation pathways
to generate energy
(foul odor)

Clostridium Large rectangular  Can be identified by
perfringens spores BOXCAR Nagler reaction
Non-motile which exploits the
action of
phospholipases on
egg yolk medium
 Most common  Gas gangrene  Debridement
species of Clostria Rapidly spreading edema, myositis, tissue High dose antibiotics
isolated from necrosis, gas production, toxemia
clinical specimens Clostridial spores germinate in injured NO INNATE IMMUNITY
 Widely distributed in muscle
soil and sewage
 Commensals of the  Food poisoning (Enterotoxin 
lower GIT of animals diarrhea)

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 and humans

Clostridium tetani Terminal spores No capsule TETANUS (SPASTIC PARALYSIS)  Common O antigen Human Ig
Squash racket, OBLIGATE ANAEROBE  Risus sardonicus  Tetanospasmin Penicillin or Metronidazole
drumstick, lollipop Peritrichous flagella  Trismus or lockjaw  Tetanus toxin Debridement
Motile  Opisthotonus This is what spreads to
spinal cord NOT organism IMMUNIZATION W Tetanus
 via motor nerves: CNS toxoid

TARGET: ANT HORN

CELLS
130 ng lethal dose
MOA: block glycine and
GABA

Clostridium botulinum Oval subterminal STRICT ANAEROBE  FLACCID PARALYSIS w respi failure Different strains produce 1 of Remove unabsorbed toxin
spores 8 exotoxin types from stomach/ Gastric
Motile MOST FATAL AMONG  Human Botulism A,B,C1,C2,D,E,F,G lavage
CLOSTRIDIA Fatal form of food poisoning  Types C and D
encoded by a Polyvalent antitoxin ABE
 INFANT Botulism bacteriophage
Honeeeey – Floppy baby syndrome AMONG MOST TOXIC DON’T EAT CANNED
SUBSTANCES KNOWN GOODS WC BULGE
MOA: block ACH
Clostridium difficile Oval subterminal Diarrhea  PSEUDOMEMBRANOUS COLITIS 2 toxins Discontinue antibiotics
spores Nosocomial  Diarrhea (Antibiotic assoc) Toxin A (enterotoxin)
Common @ neonatal feces Toxin B (cytopathic) Oral vancomycin/
Adhesin factor metronidazole

Mycobacteria

Organism Biology Colony morphology Laboratory Diagnosis Transmission Disease Virulence and Antigenic factors Treatment
Mycobacterium Waxy cell wall of Obligate aerobes Ziehl-Neelsen stain or Humans are the only Tuberculosis Serpentine cords (bacilli in DOTS: Isoniazid
tuberculosis mycolic acid, slender, Slow-growing, small, dry, Kinyoun: red rods in blue natural reservoir  Primary complex (usu. involve the right parallel) Rifampin
straight or curved, scaly, with uncorrugated background middle or lower lobe)  Trehalose dimycolate Pyrazinamide
nonmotile, non- surfaces Inhalation of infectious o Ghon focus – associated with  Catalase Ethambutol
sporogenous, non-  Growth is slower Tuberculin skin test aerosols through coughing, primary focus, lymphangitis, and  Tuberculoproteins
encapsulated, acid- than most (Mantoux): evokes a DTH sneezing, or speaking lymphadenitis Chemoprophylaxis
fast response, (+) for o Gibbus – deformation of vertebrae, Granuloma formation!! indications
individuals with active TB Resistant to drying and forming a wedge Malaise  Px with (+) PPD test
survive a long time in  Secondary / Post primary / Weight loss  Children exposed to risk of
Truant Fluorochrome dried sputum!!! Reactivation TB (begins at apex of Night sweats infection
Method: Uses fluorescent lung)  Px with (+) PPD who
auramine-rhodamine dyes;  Relapse TB (d/t treatment failure) undergo immune
yellow-orange fluorescence  Reinfection TB (infection by another TB suppression
strain)
 Extrapulmonary TB (result from
hematogenous spread of bacilli)
Mycobacterium leprae Waxy cell wall of Obligate intracellular: Lepromatous: (+) lepromin NOT highly infectious Leprosy (macules, papules, nodules, O-diphenoloxidase DAPSONE!!!
1st pathogen to be mycolic acid, acid requires armadillo tissue for skin test painless ulcers, rings without feeling inside Multidrug Therapy (MDT)
recognized fast, pleomorphic culture Common among household (peripheral neuritis)  Thalidomide: severe ENL
Tuberculoid: (-) lepromin contacts Types of leprosy reactions
Do not grow well above skin test Tuberculoid Lepromatous
30°C no systemic Non-progressing Progressive Both Multi and Paucibacillary:

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 diseases are caused at this NEVER been cultured in Inhalation of infectious Macules with few bacilli (Paucibacillary) Nodules with abundant bacilli Dapsone, Rifampin,
temperature the lab KASI agents (Multibacillary)
 Growth on cooler INTRACELLULAR SIYA CD4+ helper T-cells CD8+ suppressor T-cells Multi: ADD Clofazimine
surfaces of the body OK Insect bites, inoculation IL2, IFNγ, IL12 (+) healing IL4, IL10 (-) healing Single skin lesion (ROM):
through broken (intact) skin Sudden onset Slow onset Rifampicin, Ofloxacin,
Severe asymmetric nerve involvement Symmetric nerve involved Minocycline
Infectious: shed from nasal
mucous membranes esp. if Intact CMI Deficient CMI Prophylaxis: Dapsone
(+) ulceration  After tx  Erythema
nodosum leprosum NO VACCINE
(restn of CMI)
MOTT Group I: Yellow-orange when PPD (+) Produce lung and systemic disease Rifampin, Isoniazid,
 Mycobacterium Photochromogens exposed to LIGHT identical to Tb Ethambutol
kansasii
 Mycobacterium Group II: Produce pigment in DARK Scrofula: granulomatous adenitis enters Surgical resection of involved
scrofulaceum Scotochromogens through oropharynx cervical lymph nodes
Habitat
 Water sources
 Saprophyte from human
RT
 Mycobacterium Group III: Habitat: water and soil Portal of entry: respiratory or Most common bacterial cause of disease in Prophylaxis: rifabutin
avium-intercellulare Nonchromogens gastrointestinal tract AIDS (Ansamycin)
complex Smooth, soft, non- Treatment:
pigmented colonies  Highly resistant to anti-
MAC! tuberculous drugs
 Initial: macrolide
(clarithromycin or
azithromycin) + others
(clofazimine, rifabutin,
fluoroquinolones,
amikacin)
 Mycobacterium 3rd most common mycobacterial infection Surgical excision
ulcerans in humans

Buruli ulcer
 Mycobacterium Group IV: Diseases occur in: Resistant to anti-TB drugs
fortuitum-chelonei Rapidly growing  Immunocompromised patients
complex  Individuals with prosthetic hip joints Multiple drugs + surgical
and indwelling catheters excision

DOC: Amikacin and

Doxycycline
 Mycobacterium Chronic lung infections Highly antibiotic resistant
abscessus Infections of skin, bone, joints
 Mycobacterium Part of normal flora of smegma
smegmatis

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 Tuberculin skin test^

Spirochetes

Organism Biology Colony morphology Laboratory Diagnosis Transmission Disease Virulence and Antigenic factors Treatment
Treponema GRAM NEGATIVE, Pathogenic strain cannot be Darkfield microscopy Direct sexual Syphilis (disease of blood and perivascular areas): Lipids: keep proteins inaccessible DOC IS PEN G AT ALL
pallidum spiral rods cultured. Silver impregnation @ contact (most 1. Hard chancre (painless area of ulceration w/ hard to antibodies STAGES
motile Microaerophilic (1-4% O2) darkfield common) base) – PRIMARY LESION
central proplasmic Viable in blood at least 24 2. Condyloma lata (moist pale papules with red Hyaluronidase: enhances Penicillin: neurosyphilis,

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 cylinder, hrs at 4C Direct fluorescent
peptidoglycan, axial Motile for 3-6d at 25C antibody test congenitally or by
fibrils, endoflagella  Fluorescein-labeled transfusion with
Reiter strain: non- antitreponemal contaminated
pathogenic; saprophytic, antibodies are used to blood
cultured anaerobically in stain the bacteria
vitro
Antibody detection:
screening test
 Venereal Disease
Research Laboratory
(VDRL) Test
 Rapid Plasma Reagin
(RPR) Test
Treponemal tests
 Fluorescent treponemal
antibody–absorption
(FTA-ABS) test
 Treponema pallidum
particle agglutination
(TP-PA)
Acquired maculopapular rash) – SECONDARY LESION invasiveness by breaking down pregnant
3. Gummas (granulomatous lesions in skin, bones, hyaluronic acid
liver) Long acting benzathine
Outer membrane: penicillin: early stages
Congenital syphilis  Surrounds the periplasmic syphyilis
 Saddle nose, Hutchinson’s teeth, CNS anomalies space and peptidoglycan-
cytoplasmic membrane Penicillin G: congenital and
Early Congenital complex late syphilis
 Hydrops fetalis, Pemphigus symphiliticus (vesicular  Does not contain
eruptions of palms and soles) – HIGHLY INFECTIVE Doxycycline/Azithromycin:
lipopolysaccharide
SNUFFLES allergic to penicillin
Proteins:
Late Congenital
 Hutchinson’s triad: Hutchinson’s teeth, interstitial Membrane proteins
keratitis, 8th nerve deafness
 Clutton’s Joint: symmetrical joint swelling (common Endoflagella: composed of 3 core
in the knees) proteins; homologous to other
bacterial flagellin proteins plus an
 Mulberry molars: multiple rounded rudimentary
unrelated sheath protein
enamel cusps on the permanent first molars
(glycosaminoglycan)
 Higoumenaki’s sign: unilateral enlargement of the
sternoclavicular portion of the clavicle
Immunity
 Rhagades: fissures, cracks, or linear scars in the Cardiolipin: important component
skin, especially in the angles of the nose and mouth of treponemal antigens
 Saber shin, scaphoid scapula, saddle nose, and
relative protuberance of mandible Few antigens against T. pallidum
promote survival
Cardiovascular syphilis
Neurosyphilis
 Occurs at least 10 years after
 Asymptomatic neurosyphilis: CSF (+) for syphilis primary infection in 10% of
 Subacute meningitis: fever, stiff neck and untreated patients
headache, CSF with high lymphocyte count, high
 Aneurysm forms in ascending
protein, low glucose, (+) for syphilis
aorta or aortic arch
 Meningovascular syphilis: blood vessels in brain
and meninges (esp Circle of Willis) attacked,  Caused by chronic
cerebrovascular occlusion and infarction of nerve inflammatory destruction of
tissue in brain, spinal cord and meninges small arterioles (vasa vasorum)
supplying the aorta itself
 Tabes dorsalis: posterior column and dorsal roots;
disrupt vibratory and proprioceptive sensations
ataxia
 Dorsal root and ganglia damage loss of reflexes
and loss of pain and temperature sensation
 General paresis (of the insane): progressive disease
of neurons in brain, leading to mental deterioration
and psychiatric symptoms

Treponema Present in desert and Direct contact Endemic syphilis (Bejel)

pallidum subsp. temperate regions of
Endemicium North Africa and the Use of
BEJEL Middle East contaminated
eating utensils
Endemic bagel Disease of children
Trepanoma Present in tropical and Direct contact Yaws: primary lesion is seen as ulcerating papule in
subsp. Pertenue desert areas of South with infected skin arm or leg
YAWS America, Central lesions
Africa, and Indonesia
Person-to-person
Pertain to you contact in children
<15 years old
Treponema Present in tropical Direct contact Pinta: non-ulcerating and restricted to dark-skinned
carateum areas of Central and individuals;
PINTA South America depigmentation and hyperkeratosis

Paint a car Disease of young

adults (15 to 30 years
of age)
Leptospira GRAM NEGATIVE Aerobic, 28-30C Dark field examination, Human: Leptospirosis Penicillin: proven efficacy for
interrogans and obligate aerobe, Giemsa technique, PCR, accidental host  Mild: mud/swamp/sugar cane/bragg fever (anicteric preventing clinical disease
L. biflexa tightly coiled, Fletcher’s medium : ELISA, Lepto dipstick,  After contact syndrome) Doxycycline (wag sa kids)
(saprophytic) thin, septicemic stage in microcapsule agglutination with  Most characteristic clinical signs for early Tetracycline
flexible, blood/CSF, immune stage test, indirect water/material diagnosis
fine spirals in urine immunofluorescence test s o Febrile illness of sudden onset Mild: Ampicillin
contaminated o Severe general malaise Amoxicillin: alternative

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 with hook at one or Culture:
both ends, motile, Fletcher, EMJH
central proplasmic (Ellinghausen-McCullough-
cylinder, Johnson-Harris) ,
peptidoglycan, axial Tween 80-albumin
fibrils, endoflagella, (grow slowly, (+) within 2
catalase producing weeks)
Microscopic Agglutination
Test (MAT): reference
method; measure the ability
of the patient’s serum to
agglutinate live leptospires
Borrelia sp. Serologic tests: not useful,
organism undergoes
antigenic phase variation
Microscopy:
 Organism detected by
blood smears (taken
during febrile period)
stained with Giemsa
 most sensitive method
 Thin or thick blood
smears reveal large,
loosely coiled
spirochetes among the
red cells
Borrelia GRAM NEGATIVE Dx: Serological tests: IFA,
burgdorferi irregular spirals, ELISA, PCR
motile, Western blot: confirmatory
central proplasmic test
cylinder,
peptidoglycan, axial
fibrils, endoflagella,
microaerophilic
Organism Biology Colony morphology Laboratory Diagnosis
12
with excreta of o Muscular pain
animal hosts o Conjunctival suffusion Mod. to severe: Ampicillin
 Drinking,  Phases
swimming, o Septicemic phase: dehydration, muscle Pep: Doxycycline
bathing, or tenderness, conjunctival suffusion, generalized
food lymphadenopathy, hepatosplenomegaly, and
contamination rashes;
 Specimen positive during this phase: Blood, CSF
Principal sources
of human infection o Immune phase: Fever, uveitis, rash, headache,
 Rats, mice, and meningitis (hallmark of the immune phase of
wild rodents, anicteric leptospirosis); Specimen positive during
dogs, swine this phase: Urine
and cattle
 Severe: Weil’s disease (icteric syndrome):
jaundice, hemorrhage, proteinuria
o Blood & CSF specimen positive during first
week; urine specimen positive during second
week
Most striking property: capacity of Borrelia to undergo Tetracycline, erythromycin,
several antigenically distinct variations within a given penicilin
host
Relapsing fever
 Sudden onset, with chills and high fever (bacteremic
phase)
 Fever persists for 3-5 days and declines
 Afebrile period lasts 4-10 days, and followed by a
second attack of chills, fever, intense headache and
malaise
 There may be 3-10 such recurrences
 During the febrile stages the organisms are present
in the blood
Epidemic/Louse-borne relapsing fever: Borrelia
recurrentis; Vector: Pediculus humanus (human body
louse); Transmission: person to person
Endemic relapsing fever: Vector: soft ticks of genus
Ornithodoros
Bite of Ixodes tick Lyme disease (vector: Ixodes scapularis/dammini):  Undergoes several antigenically Doxycycline, amoxicilline /
 Stage 1 distinct variations! cefuroxime acetil
o Erythema migrans: begins 3 days to 4 weeks Arthritis: prolonged
after tick bite; flat reddened area near the tick doxycycline/amoxicillin, Pen G/
bite which slowly expands with central clearing ceftriaxone IV
 Stage 2
o Weeks to months later
o Arthralgia, arthritis, neuro manifestations +
meningitis, facial nerve palsy, cardiac disease
with conduction defects and myopericarditis
 Stage 3
o Months to years later
o Chronic skin, CNS, or joint involvement
Neisseria
Transmission Disease Virulence and Antigenic factors Treatment
of 20
 GRAM NEGATIVE Enriched media (Mueller-Hinton, Oxidation of Carbohydrates = Humans: only natural Ocular infections:  Pili (binding to epithelial cell, attachment to *Crede’s prophylaxis
diplococci, Thayer Martin): small, convex, Acid Production, NOT host  Ophthalmia neonotarium* host and resistance to phagocytosis by
non-motile, plasmid (+), glistening, elevated, mucoid, opaque FERMENTATION  blindness neutrophil killing) 3rd gen cephalasporins:
found inside PMNs, (Opa+), nonpigmented, nonhemolytic; Sexually transmitted,  Keratoconjunctivitis  Por or Protein I (reduce oxidative burst,  Ceftriaxone
fimbriae/pili, highly piliated on selective subculture Aerobic>anaerobic parturition Genital infections occurs in trimers to produce pores, binds to  Cefixime
branched ferment glucose,  Gonorrhea (scanty, clear or C3b and C4b for added resistance to
lipooligosaccharide (no O Grow best at aerobic environment, (+) acid, COMMUNICABLE AS cloudy to copious and humoral immune system, prevent Fluoroquinolone +
antigen) require cysteine and an energy source (+) oxidase test (dark LONG AS PERSON HAS purulent discharge; dysuria; phagolysosome formation)  Doxycycline (>8 yrs old)
Individual cocci are (e.g., glucose, pyruvate, lactate) for purple/black) ORGANISM 1-10 d incubation)  Opa or Protein II (invasion, adhesion to  Erythromycin (<8 yrs old)
kidney shaped growth [key test for Neisseria ID] colonies and eukaryotic receptors)  Ciprofloxacin
Neisseria gas (-) F: Cervix/vagina (salpingitis,  Rmp or Protein III (block bactericidal  Ofloxacin
gonorrhoeae Characteristics different fibrosis and obliteration of tubes antibodies against P.I and LOS, protection
from other Neisseriae: media with heated blood,  INFERTILITY IN 20%) of outer surface antigens)
 ONLY GLUCOSE hemin and animal protein, M: Urethra/penis (asym –  LOS (inflammation, toxicity of gonococci is
oxidation 5% CO2 dysuria) due to LOS endotoxic effect)
 Differ antigenically Tas may tulo pa  Tbp1&2 and Lbp (iron acquisition)
from others  IgA1 proteases
 Smaller colonies Disseminated infection (F>M)
 Dermatitis-arthritis
 Fitz-Hugh-Curtis (liver scar)
 Endocarditis
GRAM NEGATIVE, Enriched media (MH, TM): convex, Human: only natural host, Meningitis: MOST SERIOUS  Capsule (anti-phagocytic, antigenic) Penicillin
diplococci, non-motile, glistening, elevated, mucoid, 1-5um, only known reservoir  2nd leading cause  Outer membrane proteins (pilliated: do not Chloram-phenicol or 3rd gen.
found inside PMNs transparent or opaque – opa 6, form distinctive colony types) cephalasporins:
nonpigmented, nonhemolytic Person-to-person meningococcal pneumonia (URT),  Meningococcal LPS (toxic effect)  Cefotaxime
Capsulated transmission by  LOS (endotoxin, suppress leu B4)  Ceftriaxone
 Ito talaga diff nila 5% SBA: round, smooth, opaque, aerosolization of respiratory Fulminant meningococcemia Rifampin
and yung plasmid glistening, grayish/pink tract secretions in crowded (Waterhouse-Friederichsen
(+) sa taas conditions syndrome: most serious, Polyvalent vaccine
Neisseria Chocolate agar: gray>yellow, widespread purpura and
meningitides No distinct colony type transparent, nonpigmented, Close contact with echymosis)
nonhemolytic, greenish cast in older infectious person
Group A: meningitis in colonies meningococcemia (skin rash,
Baguio petechiae), primary meningococcal
Biochemical test: confirmatory; oxidize conjunctivitis
ACYW 135 – most impt in maltose and glucose
human dse
Specimen: blood, CSF, nasopharyngeal
secretions
GRAM NEGATIVE, Rough surface and friable in BAP or CAP, DNAse test Bacteremia, endocarditis, Amoxicillin
diplococci, non-motile, consistency using QuadFERM+ conjunctivitis, meningitis, LRTI,
non-fermentative, Pinkish-brown in color, and opaque otitis media + sinusitis (esp in Unresponsive cases:
Oxidase (+) Tolerates lower temperatures and children)  Coamoxiclav and
produces B-lactamase grow well at 28oC (whereas Neisseria Cephalosporins
spp. have an optimal growth  Macrolides and
temperature at 35-37°C) Cotrimoxazole
Moraxella
catarrhalis  Quinolones
Can be differentiated from other
Neisseriae by:
 Lack of carbohydrate fermentation
 Production of DNAse
 Also produces butyrate esterase
which forms the bases for rapid
fluorometric tests for identification
GRAM NEGATIVE rod, Isolation of organism from Habitat: human oropharynx Bone, joints, and tendon Penicillin
but diploccocal and the blood, synovial fluid, infections
coccobacillary forms are bone exudates, CSF, Enter the circulation
common, respiratory tract secretions through minor oral trauma Suppurative arthritis and
Oxidase (+), such as during brushing osteomyelitis in children < 5yrs of
Kingella kingae and non-motile organism that Organisms grow better in teeth age
Kingella denitrificans is hemolytic when grown aerobic conditions enhanced
on blood agar with CO2 Transmitted in day care Pyogenic arthritis
centers

GRAM NEGATIVE rod, PITS IN AGAR!!! HUMAN BITE!!! Part of gingival and bowel flora Resistant to clindamycin
Small,
oxidase (+), Eikin ka! Rawr! Occurs in infections from human Susceptible to ampicillin and
Eikinella corrodens bites the newer penicillin and
fastidious, requires CO2
for growth, does not cephalosporins
ferment carbohydrate
Acinetobacter GRAM NEGATIVE Species recovered from Often commensals, Gentamicin, amikacin, or
Aerobic, resemble genital tract has been sometime nosocomial tobramycin and to newer
neisseriae on smears mistaken for Neisseria penicillins or cephalosporins
diplococcal forms gonnorhoeae Patients with acinetobacter
predominate in body bacteremia: intravenous
fluids and on solid media Difference: Neisseriae catheters are almost always
produce oxidase, the source of infection

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 Acinetobacter does not

Bordetella

Virulence and Antigenic

Organism Biology Colony morphology Laboratory Diagnosis Transmission Disease Treatment
factors
GRAM NEGATIVE, Reversible phenotypic Species form acid (not in Other Bordetella sp.
coccobacilli modulation and reversible gaseous form) from B. avium – turkey coryza | B. holmesii – immunosuppd px
Bordetella sp. Extremely small phase variation glucose and lactose B. hinzii – bacteremia, respi illness, arthritis |
STRICTLY AEROBIC B. trematum – wound infx and otitis media
Non-motile When isolated from patients and Hemolysis of blood- HUMAN DISEASE most clinically important species because they cause ERYTHROMYCIN:
cultured on enriched media, B. containing medium is ONLY classic pertussis (whooping cough) EXOTOXINS (FAP) DOC
pertussis is in the hemolytic and associated with virulent B I. Incubation Filamentous
pertussis toxin-producing pertussis BLOOD IS NOT II. Catarrhal hemagglutinin Vaccine
virulent phase INVADED - TOXIN PRODUCTION OCCURS Adherence
Oxidize amino acids but - Rhinorrhea: PRIMARY FX
BORDET GENGOU MEDIUM do not ferment - Nonspecific findings such as malaise, low-grade fever, Adenylate cyclase toxin
Small transparent, hemolytic carbohydrates sneezing, and anorexia may also be present
colonies - Large numbers of organisms are sprayed in droplets, Pertussis toxin
BASED ON SYMPTOMS and the patient is highly infectious but not very ill (Pertussigen)
ANG DX - PEAK no. of bacteria occurs during this time A- Active
appearance of a persistent cough marks the transition B- Bind
ISOLATION BEST AT from the catarrhal to the paroxysmal coughing stage Responsible for
CATARRHAL KASI paroxysmal coughing
TOXIN PROD DUN III.Paroxysmal
- Ciliated epithelial cells are extruded from the PEPTIDOGLYCAN LIKE
CBC TEST: LEUKEMOID Tracheal toxin
respiratory tract and the clearance of mucus is
RXN Kill ciliary cells
impaired
- Characterized by the classic whooping cough
Saline nasal wash: HEAT LABILE
paroxysms
specimen Dermonecrotic toxin
- Toxins irritate surface cells
Bordetella pertussis Trachea necrosis
PCR IS MOST - Rapid exhaustion, vomiting, and cyanosis occur
SENSITIVE METHOD - Necrosis of epithelial cells with PMN infiltration and ENDOTOXIN
peribronchial inflammation Lipopolysaccharide
- The characteristic inspiratory whoop follows a
series of coughs as air is rapidly drawn through One locus on the B.
the narrowed glottis pertussis chromosome
- Vomiting frequently follows the whoop acts as a central regulator
- combination of mucoid secretions, whooping cough, of virulence genes
and vomiting produces a miserable, exhausted child - bvgS gene:
barely able to breathe responds to
- apnea may follow environmental
- INFANT: WHOOPING | CHILD: PAROXYSMAL signals
- bvgA gene:
IV. Paroxysmal transcriptional
- Secondary complications can occur factor of the
 The most common complication of pertussis is virulence genes
pneumonia caused by a superinfecting organism
such as Streptococcus pneumoniae (sometimes H.
influenzae)
 Atelectasis d/t mucus plugs
- Dse gradually fades
GROW MORE RAPIDLY w Silent copy of pertussis Cough resembling pertussis BUT LESS SEVERE
B. parapertussis LARGER COLONIES toxin

Silent copy of pertussis Respiratory disease and bacteremia in humans, esp. in

B. bronchiseptica toxin immunocompromised individuals; causes kennel cough in
dogs and snuffles in rabbits

Bordetella species Oxidase Urease

B. pertussis + -
B. parapertussis - +
B. bronchiseptica + +

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 Mycoplasma and Ureaplasma

Organism Biology Colony morphology Laboratory Diagnosis Transmission Disease Virulence and Antigenic factors Treatment
Smallest free-living bacteria Require complex media Stained by methylene blue and Part of normal flora Delayed type hypersensitivity  more severe  Glycolipids complete
Cell wall is absent so are azure of mouth Complement Fixation (alternative resistance to
pleomorphic (variant Fried-egg colonies  M. salivarium, Typical Species Diseases Caused pathway) antigen penicillin and
shapes)  M. hominis 1. Complement fixation - 4-6 M. orale in oral M. pneumonia  Upper respiratory tract vancomycin
ESPECIALLY weeks; 4-fold rise in titer cavity disease  Proteins
 M. pneumo: 2. Cold agglutinins- 1/3-2/3 of M. hominis in  Tracheobronchitis ELISA antigen Drug of choice
Has STEROLS like FUNGI
GRANULAR patients oropharynx  Atypical pneumonia in mycoplasmal
so MYCO!! (Walking pneumoniae)
 l Antigen  Joint infections
Pathogenic species have flask-like or pneumonia:
FACULTATIVE VERY SMOL  appear first M. genitalium  Non-gonococcal filamentous shapes with specialized Tetracyclines
ANAEROBES  non specific urethritis polar tip structures for adherence Erythromycins
Except M. pneumoniae: Have an affinity for  presumptive diagnosis M. hominis  Pyelonephritis Movement of cilia ceases
STRICT AEROBE mammalian cell membranes  (binding of IgM to I  Pelvic Inflammatory  Clearance mechanism stops
antigens on human disease resulting in cough
Mycoplasma Round colonies with granular erythrocytes at 4oC) is  Postpartum fever
 Salpingitis
surface & dark center, buried commonly used but not PROLINE RICH
Ureaplasma  Non-gonoccocal
in agar recommended due to urealyticum urethritis in men
poor sensitivity and  Lung disease in  Toxic metabolic products
CULTURE specificity premature infants with o Peroxide and superoxide
 Definitive diagnosis 3. ELISA- not commercially low birth weight o Inhibition of catalase
except M. genitalium available  Immunopathogenesis
 Sputum (Usually scant) or ** M. pneumoniae and M. o Activate macrophages
throat washings genitalium are o Stimulate cytokine
 Special transport medium serologically cross
production
needed reactive
- Must suspect M.  Antigen detection is rapid
pneumoniae but poor sensitivity and
Require glucose specificity Seasonal Cough is nonproductive, EXTRACELLULAR PATHOGEN
GRANULAR  PCR has excellent sensitivity variation – higher Initially but it is occasionally
but undefined specificity in summer and paroxysmal P1 pili (e.g. P1 adhesin)
 INDIRECT fall Blood-streaked sputum
IMMUNOFLUORESCENCE Later Superantigen
and chest pain
NOT PART OF Patient appears only
NORMAL FLORA moderately ill (WALKING
PNEUMONIA) nd physical
Common in Early in
signs of pulmonary
CHILDREN the
consolidation are often
course
negligible compared to the
M. pneumoniae Droplet striking consolidation seen
on x-rays
When the infiltration is at a
Later peak, the illness may be
severe
Resolution of pulmonary
infiltration and clinical
Resoluti
improvement occur slowly
on
over 1–4 weeks (rarely
fatal)
TRACHEOBRONCHITIS (70-80%)
Hemolytic pneumonia
Require arginine @ urinary tract  Women with salpingitis (uterine tube  Resistant to
Fried-egg infection) have increased antibodies both
post- partum or  Occasionally from patients with arthritis tetracycline
M. hominis post-abortal and
women erythromycin
 Treated with
clindamycin
M. genitalium DIFFICULT TO CULTURE  Non-gonococcal urethritis in men
 In women, causes cervicitis, and
infertility

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 T Strains Common in Nongonococcal, nonchlamydial urethritis Urethritis is associated with biovar 2  Resistant to
FEMALE infants in men tetracycline
U. urealyticum Require urea and sterols for  Treated with
growth Female genital Lung disease in low-birth-weight infants erythromycin
tract

Haemophilus

Organism Biology Colony morphology Laboratory Diagnosis Transmission Disease Virulence and Antigenic factors Treatment
GRAM NEGATIVE Fastidious: require heme X V Most are Haemophilus spp. Description Does not produce exotoxin
pleiomorphic organisms precursor in blood Fact Fact Hemolys indigenous flora H. influenza type B Important human pathogen
enriched media Species of the upper
or or is Sexually transmitted pathogen
reqt reqt respiratory tract H. ducreyi
causing chanchroid
H. - + +
H. aphrophilus and
parahemolyticu now Aggregatibacter aphrophilus
s H. paraphrophilus
Haemophilus H. haemolyicus + + + H. segnis now Aggregatibacter segnis
H. aegyptius + + - H. parainfluenzae
H. influenza + + -
H. - + - H. influenzae aegypticus
parainfluenzae Other species are among the normal microbiota of the mucus
H. ducreyi + - - membranes and occasionally cause disease
A. segnis - + -
A. aphrophilus - +/- -
coccobacillary or in long Fine refractile capsules in Grows best at 35 - 37°C Inhabit mucus Important cause of meningitis in children Antigenic types Drug of Choice:
threads and filaments Quellung reaction membranes of - Capsular polysaccharide Amoxicillin,
caused by swelling of the Carbohydrates fermented poorly and irregularly the upper - Lipooligosaccharide Ampicillin
URT and LRT infections in adults
Facultatively anaerobic cell wall (like Strep. respiratory tract (somatic)
Pneumo) of humans Outer membrane proteins Chemopx
Produce indole, ornithine decarboxylase, and -
H. influenzae type B DOC: Rifampicin
urease (somatic)
Medium: Levinthal agar Younger, more  Most common species serovar causing invasive
or Chocolate agar (Another basis for biotyping) susceptible Active
human disease
- 8 biotypes (I - VIII) ENCAPSULATED - typable immunization:
 Antibody to polyribitol ribose phosphate (PRP)
Growth in chocolate - Invasive infections: Biotypes I and II - Capsule confers type HIB vaccine
Disease occurs capsular antigen plays a key role in protection
agar: grayish colonies specificity PRP-OMPC
during age of against infection → bactericidal, promotes PRP-T
Marked tendency to lose its capsule and the relative humoral
Blood is added to agar opsonization
associated type specificity deficiency: 3 UNENCAPSULATED – non-
media and heated at 80°C months to 3 typable
- Non-encapsulated variants lack
(brown color)  Release years old KIDS
iridescence - Lack capsular
of Factor Heme (X) and (maturation of Infected children may be asymptomatic, or have respiratory polysaccharide
NAD (V) defenses) distress or meningitis - Respiratory tract
DNA from a given H. influenzae capable of
transferring type specificity to other cells inhabitants
Can also be detected Reservoir:
growing around colonies (transformation) ADULTS
humans (may be
of Staphylococcus aureus asymptomatic) Pneumonia or arthritis in H. influenzae in adults SOMATIC ANTIGENS
Haemophilus
influenzae on unheated blood agar These genes control resistance to ampicillin - Found on cell envelope
(satellite phenomenon) and chloramphenicol - LOS like Neisseria
Transmission: Immunity
respiratory Cross-reacting immunogen (Bactericidal)
Gram-stain specimen
droplets (for Capsule
CSF Natural resistance to Hib
invasive Polyribitol ribose phosphate
- Expectorated sputum diseases) Host defenses (Bactericidal)
(PRP): critical role in the
Middle ear aspirates Encapsulated (Hib) Non-Typable H. invasiveness of the disease
- Pus influenza
Outer membrane components
Thoracentesis SYSTEMIC HEENT Adherence
– Blood Bacteremia Otitis media IgA protease
Arthrocentesis Acute bacterial Sinusitis
meningitis Pneumonia
Acute bacterial Tracheobronchitis
epiglottitis
Conjunctivitis
Cellulitis
Osteomyelitis
Joint infections
Pneumonia

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 Classic microscopic appearance: Sexually transmitted disease characterized by painful genital Erythromycin
School of red fish ulcers
 Chancroid: ragged ulcer with mark swelling Recommended
H. ducreyi  Buboes: Characteristic suppurative inguinal treatment by
CDC: 1g
lymph nodes
azithromycin PO

Koch-Weeks bacillus Grows under the same conditions as H. Pink eye: communicable purulent conjunctivitis Erythromycin
(old name) influenza Brazilian purpuric fever: syndrome of fulminating illness
H. influenzae
characterized by nausea, vomiting, hemorrhagic skin lesions,
Aegyptus
fever, shock and death

usually occurs after dental procedures, dental disease, or oral Ampicillin

trauma
H. parainfluenzae
More commonly associated with endocarditis but may also be
associated with pneumonia, meningitis, bacteremia

Chlamydia

Colony Virulence and

Organism Biology Laboratory Diagnosis Transmission Disease Treatment
morphology Antigenic factors
GRAM NEGATIVE Iodine- Culture: Cycloheximide- Person to person; Trachoma Heat-stable Tetracycline
 obligate intracellular (Reticulate bodies); staining treated McCoy cell culture mother to infant  Follicle or scar on conjunctiva lipopolysaccharides (adults)
 extracellular (Elementary bodies - inclusions (most specific) (LPS) Erythromycin
round); Urogenital infections (neonates)
 Single, round, vacuolar inclusion, Immunofluorescence: most Outer membrane Sulfonamides
 glycogen inclusion present, lack sensitive method Lymphogranuloma venereum proteins (endemic areas)
mechanisms for metabolic energy  STD characterized by suppurative inguinal adenitis Azithromycin
production and inability to synthesize ATP PCR  First stage: Painless vesicle (mass treatment)
Chlamydia
trachomatis  Has LPS (but weak endotoxin properties)  Second stage: Painful buboes, marked inflammation of
 No peptidoglycan (cell walls are not well- MULTIPLE SEROVARS draining LN
characterized)
Infant pneumonia: wheezing cough and pneumonia but no
Major Outer Membrane Protein (MOMP): fever
important structural component
Reiters Syndrome Triad:
Biphasic devtl cycle conjunctivitis, polyarthritis, genital or GI inflammation
Elementary body  reticulate body (grow) 
EBs released Serology: complement Airborne, bird Psittacosis (patchy inflammation of lungs) (Parrot Fever) Tetracycline or
- Lysis in C. psittaci fixation test excreta to humans erythromycin
- Extrusion in C. trachoma and C. pneumo Ornithosis
Chlamydophila
psittaci LORDE ANDAMING GANAP NETO BASAHIN Mental confusion and jaundice
MO YUNG TRANS IF MAY TIME (if wala ok na Common in animal handlers
to)

Serology: 4-fold titer Airborne, person to Atypical pneumonia (Walking pneumonia) Tetracycline or
increase person  LIKE MYCOPLASMA erythromycin
Microimmuno-fluorescence, Pharyngitis, bronchitis, sinusitis
IgG and IgM detection
Chlamydiophilia
Atherosclerosis
pneumoniae
Elementary bodies – pear-
shaped

ONLY 1 SEROVAR

SINGIT FROM NEISSERIA

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 NON-LACTOSE FERMENTERS

ORGANISM BIOLOGY
Shigella Slender Gram-negative rods,
non-motile
All shigellae ferment glucose
The inability to ferment lactose
distinguishes shigellae on
differential media
Form acid from carbohydrates
but rarely produce gas
Divided into those that ferment
mannitol and those that do not
TESTS CLINICAL MANIFESTATIONS VIRULENCE AND ANTIGENIC FACTORS TREATMENT
No gas production Shigellosis  Invasiveness (attachment and internalization) Ampicillin, amoxicillin
Sereny’s test for invasiveness  A form of bacillary dysentery: inflammation  Shiga toxin (exotoxin: enterotoxic, neurotoxic, cytotoxic) Trimethoprim-
Lysine(-), nonmotile, -/+ TSI, acetate(-), of the intestines due to bacterial infection  Intracellular survival and multiplication sulfameth-oxazole
lactose(-)  with invasion of host cells/tissuesMay be
with or without production of exotoxins
 Accompanied by:
Severe abdominal cramps
Tenesmus (straining to defecate)
Frequent, low volume stools
containing blood, mucus, and PMNs
Hemolytic uremic syndrome (due to Shiga toxin) can
develop in cases of infection by Sh. dysenteriae
Systemic invasion through bloodstream does not occur in
most cases

Salmonella Gram(-), rods Gas production Salmonellosis  Capsule ChloramphenicoI

Facultative intracellular, Typhidot test IgM(+), widal test (4x Enteritis, enteric fever, septicemia, asymptomatic carriage  Endotoxin Ampicillin
peritrichous flagella increase in titer), lysine(+), H2S(+), TSI (gall bladder)  Invasins Trimethoprim-sulfa
(-/+ with gas), indole(+), citrate(+),  Catalase Quinolones
ONPG(-), malonate(-)  Superoxide dismutase aminoglycoside
 Defensins
 Intracellular survival and multiplication
Proteus Ovoid or slightly curved rods, Deaminate Phe P. mirabilis: hospital acquired UTI, wound infection,  Endotoxin P. mirabilis-Ampicillin
peritrichous (swarming Urease(+ cerise color or hot); P. pneumonia, septicemia, eye and ear infection, pleuritis and Cephalosporins
phenomenon) mirabilis ornithine(+); P. vulgaris peritonitis, suppurative abscess, GIT infection, bacteremia P. vulgaris-
indole(+) Aminoglycoside
TMP-SMX
Morganella Indole(+), ornithine(+), citrate(+)  Nosocomial infections: UTI, Respiratory tract infections, wound Aminoglycoside
morganii infections TMP-SMX
Providencia Indole(+), H2S(-), citrate(+), lysine(-), Nosocomial infections: UTI, Respiratory tract infections,
lactose(-) wound infections
Yersinia pestis Microaerophilic or facultative Catalase(+), oxidase(-) Bubonic plague (with swollen and painful axillary and  Yops Ampicillin
anaerobe inguinal LN: buboes; rodent reservoir, arthropod vector)  Envelope F-1 antigen (antiphagocytic) Streptomycin
 Coagulase Tetracycline
 Fibrinogen activator
Protein V and W (proliferation)

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 RAPID LACTOSE FERMENTERS

ORGANISM BIOLOGY TESTS CLINICAL MANIFESTATIONS VIRULENCE AND ANTIGENIC FACTORS TREATMENT
Escherichia coli Gram(-), rods Sugar fermentation, TSI, IMViC(+ Urinary tract infection Type 1 common pili (mannose binding in the EPEC: gentamycin
+ --), lysine(+), acetate(+), host)
Smooth, flat, non-viscuous, distinct lactose(+); Sereny’s test for Neonatal meningitis P pili (agglutinate RBC) Fluid replacement all
edges, metallic sheen on differential invasiveness Adhesions cases
media Opportunistic infections ETEC: fluoroquinolones
MacConkey and EMB for isolation K1 capsule (antiphagocyte) and fluid restoration
EPEC Siderophores
 severe, watery diarrhea; vomiting; and fever, which is usually self- S fimbriae (binding to vascular endothelium
limited but can be prolonged or chronic and brain epith)
ETEC
 Adhesions (specialized pili called colonization factor antigens) Capsule
 Enterotoxin (heat labile – hypersecretion; hear stable – blocks fluid uptake) Hemolysins
EHEC: Siderophores
 Attachment Adherence pili
Shiga-like toxins / verotoxins
EIEC
 Closely resembles Shigella dysentery but does not produce toxin
 Cross react with Shigella antigens
 Much blood and mucus
Enterobacter Gram(-), rods, Peritrichous flagella TSI (A/A with gas), IMViC (-- ++), Nosocomial infections: UTI, bacteremia, sepsis resistance to cephalosporins (B-lactamase B-lactamase inhibitors –
lysine(+), ornithine(+) production) piperacillin
Facultative anaerobe Carbapenems
Raised, motile, viscous Aminoglycoside
Large, mucoid, pink to purple, no metallic
sheen on EMB

SLOW LACTOSE FERMENTERS

ORGANISM BIOLOGY
Gram(-), rod, motile, produces red
pigment (prodigiosin)
Serratia marcesens
Gram(-), nonspore forming rods,
peritrichous flagella
Citrobacter
Facultative anaerobes
Gray, opaque with strong fetid
odor
Gram(-), rod, motile
Edwardsiella tarda Facultative anaerobe
Produces hydrogen sulfide
Smooth, glistening, semitranslucent
Gram(-), rods, nonspore forming,
peritrichous
Arizona hinshawii Facultative anaerobe
Gram(-), rods
Facultative anaerobe
Hafnia alvei
Blood or MacConkey agar: gray-
white, slightly elevated, glistening,
strong scent of human feces
S. pneumoniae, Gram(+), lancet cocci in pairs or
Diplococcus short chains, capsulated
pneumoniae,
Pneumococcus
TESTS CLINICAL MANIFESTATIONS VIRULENCE AND ANTIGENIC FACTORS TREATMENT
Lysine(+), ornithine(+),citrate(+), indole(-), Pneumonia, nosocomial infections,  lipase Aminoglycoside
DNase(+) septicemia, UTI, wound infection,  gelatinase Chloram-phenicol
endocarditis Ciproflaxin
 DNase
Resistance to colistin and cephalothin Trimethoprim-sulfa
Ferment glucose with gas and acid production, UTI, wound infections, pneumonia, Third gen cephalosporins
oxidase(-), catalase and methyl red(+), voges- abscesses, septicemia, meningitis, Aminoglycoside
proskauer(-), lysine(-), citrate(+), hydrolyzes endocarditis Carbapenems
urea
H2S production, indole(+), nonfermenter of Bacterial gastroenteritis, wound B-lactams
mannitol, sucrose, arabinose, trehalose infections, systemic diseases CephalosporinsAminoglycoside
Fluoroquinolonechloram-phenicol
Urease(-), lysine(+), arginine(+), ornithine(+), Gastroenteritis Aminoglycoside + cell wall-active
lactose fermenter antibiotic (penicillin, ampicillin,
vancomycin)
Linezolid, daptomycin, tigecycline,
quinupristin/
dalfopristin
Indole(-), catalase(+), oxidase(-), lysine(+), Enteritis (diarrhea) Synthesis of glucan (virulence in producing caries) Third gen cephalosporins
ornithine(+), motile, ferments mannitol and Extraintestinal infections Aminoglycoside
maltose, no acid formation, no lipase or DNase Wound abscesses
Colony Morphology Pneumonia (via aspiration)  Capsule (antiphagocytic, antigenic) Penicillin
 5% Sheep blood agar: young colonies Otitis media, sinusitis (precede viral  Pneumolysin (hemolysin, dermotoxic) Erythromycin
round, complete edges, mucoid, alpha- infection of URT)  Purpura-producing principle (dermal hemorrhage)
hemolytic; older colonies with central Bacteremia/sepsis  Neuraminidase (spreading factor) Vaccines:
indentation  flattened Meningitis  Amidase (autolysin for cell division)  Polyvalent (23 type) polysaccharide:
 Chocolate agar: quite flat, alpha-hemolysis  IgA protease (enhance colonization) long term (5 yr) protection
 C-substance (reacts with CRP)  Pneumococcal conjugated vaccine
Tests  Lipoteichoic acid (activates complement, induce (<2 yrs)
 Optochin susceptible (+) (clear zone >14 inflammatory cytokine response)
mm diameter)

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  Bile solubility(+)
 Quellung reaction (capsule swelling; B cell
response)
Resemble Group A strep -hemolytic Pharyngitis, sinusitis, bacteremia,  Hemolysins
Group C and G Identified by reactions with specific antisera endocarditis  M proteins
Streptococci Post-streptococcal sequelae of acute
glomerulonephritis
Colony Morphology
Streptococcus anginosus Variable hemolytic activity
group Minute colonies (<0.5mm diameter)
 S. milleri
Tests
 S. intermedius
PYR (-)
 S. constellatus Voges-Proskauer (+)
Butterscotch/caramel odor
Nutritionally Require pyridoxal or cysteine for Colony Morphology Bacteremia
variant/Pyridoxal growth on blood agar Grow as satellite colonies Endocarditis
dependent Streptococci Usually alpha-hemolytic
 S. defectives
 S. adjacens
Anaerobic Variable hemolysis Mixed anaerobic infections in the
Peptostreptococcus Microphilic abdomen, pelvis, lung, or brain
Pus is has foul odor

PSEUDOMONDAS
ORGANISM BIOLOGY TESTS CLINICAL MANIFESTATIONS VIRULENCE AND ANTIGENIC FACTORS TREATMENT
 Gram negative, aerobic Colony Morphology  Endocarditis  Adhesins  Anti-pseudomonal
bacilli  Natural isolates from soil or water-  Respiratory Tract Infections o Glycocalyx (antiphagocytic) penicillin +
 Non lactose fer small, rough colonies o Primary pneumonia o Alginate slime (antiphagocytic, septicemia) - Aminoglycoside
menter  Clinical Samples: fried egg o Bacteremic pneumonia exopolysaccharide
 Single polar flagellum appearance, large, smooth, flat o LRT colonization of cystic fibrosis o N-methyl-Phe pili (type 4 – similar to N. gonorrhea and V. High rate of failure
 Optimal growth at 37oC, edges and elevated  Bacteremia and Septicemia (immunocompromised, cholerae Tcp pili; bind to GM1 of epithelial cells) (mortality can reach up
can grow at temp as high  Mucoid appearance: due to alginate hospital-acquired) o Non-pilus adhesions – bind to mucin only to 80%)
as 42oC slime  CNS infections (meningitis)  Invasins
 Ear infections (Otitis Externa  swimmer’s ear) o Pyocyanin (iron acquisition)
Tests  Eye infections (bacterial keratitis) o Elastase + Alkaline phosphatase (degrades ground
 Grows well on most lab media  Bone and Joint infections (osteomyelitis, substance, lyse fibrin (-) IFN-y and TNFs  degrade
 Non Lactose Fermenter osteochondritis) immune response)
 Oxidase (+)  Urinary Tract Infections (hospital-acquired UTI, d/t o Cytotoxin (leukocidin – lethal for WBC; pore forming)
 Beta-hemolytic catheterization) o Hemolysin (phospholipase C/lecithinase)
Pseudomonas  Characteristic odor (fruity – grapes)  Gastrointestinal infections (gastroenteritis, necrotizing o Siderophores
aeruginosa  Color: blue, fluorescence under UVL enterocolitis)  Flagella
 Skin and soft tissue, wound infections, pyoderma and  Toxins
dermatitis (abscesses, folliculitis, acne vulgaris) o LPS (antiphagocytic)
o Exoenzyme S (septicemia; impair phagocyte function)
o Exoenzyme A (tissue necorsis, (-) protein synthesis)
 Pigments
3 DISTINCT STAGES: o Pyocyanin: blue (suppress growth of other bacteria  aid
1. Attachment
colonization, impair action of cilia)
2. Local invasion
o Pyoverdin: green (fluoresce)
3. Disseminated systemic disease
o Pyochelin (siderophore)
o Pyorubin, pyomelanin
 Resistance plasmid and factors
 Adaptability to minimal nutrition
 Survival in various habitats
 Metabolic diversity
Stenotrophomonas  Gram (-) bacillus Colony Morphology  Predominantly cause colonization rather than  Few pathogenic mechanisms  Unnecessary if
maltophila  Aerobic Blood agar: lavender-green or gray inefction  Predominantly results in colonization rather than infection colonization only
 Non fermentative colonies  Frequent colonizer in respiratory tract in patients with  Invasive medical devices – vehicles by which the organism  Resistant to many
cystic fibrosis bypasses normal host defenses antibiotics considered

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 Tests  Catheter associated bacteruria effective for
(+) oxidation of glucose and maltose  IV line infections Pseudomonas
Distinguished from Pseudomonas:  Urosepsis  Resistant to
 (+) Lysine  Bacteremia aminoglycoside,
 (+) DNAase test  Pneumonia antipseudomonal
 (-) Oxidase  Pseudobacteremia penicillins,
antipseudomonal 3rd
SOURCES: gen cephalosporins
 Fluids in hospitals  Sensitive to TMP-SMX
 Respiratory equipment or Cefepime
 IV lines and fluids
 Urine

 Gram (-) bacillus Colony Morphology  Pneumonia  Has the ability to grow in wide range of microenvironment in the  TMP-SMX (Co-
 Aerobic  Non-wrinkled  Bacteremia (entry: respiratory tract, central venous hospital because of minimal growth requirements (e.g., povidone trimoxazole)
 Motile: polar tufts of  Culture B. cepacia from body fluids catheter) iodine catheters)  Chloramphenicol
flagella  Growth slower than enteric Gram(-)  Skin and Soft tissue infections (burns and wounds)  Low intrinsic virulence to healthy hosts  Cefepime
Burkholderia cepacia
rods  GUT infections  Increased vulnerability of cystic fibrosis patients  3rd gen
complex
 3 days before colonies are visible  Frequent colonizer of fluids in hospital (e.g.,  Glycocalyx: protection from antimicrobials/disinfectatns cephalosporins, esp.
 Also EO1/P.
irrigant solutions) ceftazidime
multivorans/P. kingie
Tests  Cepacia syndrome: in cystic fibrosis patients  Ureidopenicillin
 B. cenocepacia
 Weak, slow, (+) oxidase  Quinolones
 B. multivorans
 PCR- with genotyping  Meropenem
o 7 genovars  Imipenem
 Varying susceptibility
to fluoroquinolones
Gram (-) bacilli Colony Morphology Meliodiosis Tetracyclin,
Aerobic Cream to orange, mucoid. Smooth to  Abscesses sulfonamides,
Motile rough, wrinkled  Chronic infection mimics TB cotrimoxazole, 3rd gen
B. pseudomallei
 Infection through contamination of skin abrasions, cephalosporin
Growth at 42oC Tests inhalation/ingestion
(+) oxidase
Gram (-) bacilli Glanders Tetracycline +
Aerobic  Disease of horses, mules, donkeys aminoglycoside
B. mallei Non-motile  Transmissible to humans  ulcer of skin or mucous
Non-pigmented membranes followed by lymphangitis and sepsis
 Inhalation  primary pneumonia

VIBRIO, CAMPYLOBACTER, HELICOBACTER

Vibrio species:  Growth in estuarine and marine environments

 Differentiated from Enterobacteriaceae through: polar flagella, (+) oxidase  Pathogenic species  symbiotic with chitinous shellfish
 Growth at 18-87OC, pH 7.9-9.0; simple nutritional requirements
ORGANISM BIOLOGY TESTS CLINICAL MANIFESTATIONS VIRULENCE AND ANTIGENIC FACTORS TREATMENT
Vibrio cholerae  Comma-shaped bacilli Colony Morphology  Incubation period: 1-3 days  Cholera toxin (A2-5B) with A (active) and B (binding) subunits  Fluid and electrolyte
O1  Facultative anaerobe  Cary-Blair semi solid agar (transport)  High infectious dose  diarrhea d/t hypersecretion of electrolytes and fluids replacement
 Biotypes: El Tor,  Alkaline peptone broth (enrichment)  Cholera (major pandemics by O1 and  Somatic O antigen: >200 serogroups (O1 and O39  classic  Doxycycline (adult)
Classical/Cholerae  Growth even w/o salt  TCBS agar selective/differential): yellow O139; spread by consumption in high epidemic cholera)  TMP-SMX (pedia)
 Serotypes: Ogawa, colonies dose contaminated food and water)  Adherence factors (colonization)  Furazolidone (pregnant)
Inaba, Hikojima Tests o Rice-water stools, profuse loss of  Pilus  Killed parenteral vaccine
 Atypical/non-toxigenic:  (+) oxidase fluids and electrolytes  Mucinase/hemagglutination protease (inflammation and
does not produce  Ferments glucose o Death d/t hypovolemic shock, degeneration of tight junctions)
toxins  Diagnosis by culturing fresh stool metabolic acidosis  Siderophores (iron sequestration)
O139  Neuraminidase (inc. toxin receptors)
 Comma-shaped Colony Morphology  Explosive watery diarrhea (mild to  Kanagawa hemolysin: thermostable enterotoxin  Self-limited
 Facultative anaerobe  TCBS agar: yellow cholera-like)  Adhesion
 Wound infection
Vibrio parahaemolyticus  Halophilic Tests  Bacteremia
 (+) oxidase  Infection by consumption of
 Ferments glucose contaminated shellfish
 Diagnosis by culturing fresh stool
 Comma-shaped Colony Morphology  Infection associated with exposure of  Serum resistance  Minocycline/doxycycline +
 Facultative anaerobe  TCBS agar: yellow wound to contaminated sea water: may  Antiphagocytic polysaccharide capsule ceftriaxone or cefotaxime
progress to bullae and tissue necrosis  Cytolysin
 Halophilic Tests  Septicemia (via ingested contaminated  Collagenase
Vibrio vulnificus
 (+) oxidase shellfish)  Protease
 Ferments glucose  Siderophore
 Diagnosis by culturing wound or blood
specimen

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  Gram (-)
 Helical or corkscrew
 Long-sheathed polar flagellum
 “Gull wing” appearance
 Rapid darting motility
Campylobacter jejuni  Microaerophilic and
capnophilic (5% O2, 10% CO2,
35% N2)
 Thermophilic
 Reservoir: contaminated
poultry
 Gram (-)
 Helical
 Blunt/round ends
 Lophotrichous flagella 
highly motile
 Optimal growth at pH 6.0-7.0
Helicobacter pylori
(near epithelial surface of
stomach, since lumen side of
mucous layer is very acidic)
 Grows well at 37oC
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Tests  Gastroenteritis  Endotoxins  Fluid & electrolyte replacement
 Culture of stool specimen o Crampy abdominal pain  Flagella  motility  Erythromycin
 Non sugar fermenter or oxidizer o Profuse bloody diarrhea  Adhesions (attachment to mucosa)  Fluoroquinolones
 Oxidase (+)  Guillain-Barre syndrome  Cytopathic toxins  Azithromycin
 Catalase (+) o Low-incidence, potential sequel of
infection Infectious dose and host immunity determine whether disease
o Acute inflammatory demyelinating develops
neuropathy
o Acute axonal form d/t molecular
mimicry
o Serogroup O19
Colony Morphology  Gastritis  Flagella (motility)  Bismuth +
Skirrow’s medium or chocolate medium  Peptic ulcer disease  Adhesin, hemagglutinins (attachment)  Metronidazole
(isolation): translucent, 1-2 mm colonies  Mucinase (degradation of gastric mucus, local tissue damage)  Tetracycline
(stain: Giemsa or special silver stain)  Urease (acid neutralization)  Triple therapy: PPI (ex.
 Vacuolating cytotoxin (epithelial cell damage) omeprazole) + antibiotic (ex.
Tests  Superoxide dismutase and catalase (antioxidant, protect from clarithromycin, metronidazole,
 Detection in endoscopic antral gastric phagocytosis) amoxicillin) + bismuth
biopsy material
 Invasin (tissue damage) compound
 Non sugar fermenter of oxidizer
 Microaerophilic
 Urease (+) (rapid test; breath test)
 Oxidase (+)
 Catalase (+)
 Mucinase (+)
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