COCCI  other species of CNS that may cause infection

1. S. lugdunensis
GRAM-POSITIVE COCCI 2. S. warneri
3. S. hominis
A. Family Micrococcaceae
 capable of producing catalase enzyme Cultural characteristics
 can be divided based on degradation of glucose  aerobic, facultative or micro-aerophilic
1. Genus Micrococcus  grow best at 37°C but pigments form best at RT
 degrade glucose by oxidation  Pigment production:
 usually saprophytic in nature a. S. aureus - golden yellow (due to
 not associated with human disease lipochrom)
 Modified oxidase test (Microdase) (+) b. S. citreus - lemon yellow
 free-living, found in the environment c. S. albus - porcelain white
 Obligate aerobe  colonies: round, smooth, raised and glistening
 colonies can be red, yellow and orange
 often resembles Staphylococci Growth Characteristics
 usually arrange in packets of 4’s or 8’s  strongly catalase (+)
 e.g. Gaffkya tetragenar  ferment many carbohydrates
 Sarcina lutea  produces lactic acid but no gas
2. Genus Staphylococcus  relatively resistant to drying and 9% NaCl
 degrade glucose by fermentation
 catalase (+) Pathogenicity
 pathogenic species are pus producers  haemolyze blood, coagulates plasma
a. Staphylococcus aureus – usually a creamy,  produces variety of extracellular enzymes and
golden color and is often beta hemolytic toxins
b. Coagulase-negative staphylococci – usually
appear as white to grey colonies on blood Staphylococcus aureus
agat and are not usually hemolytic  round, smooth, raised and gray to deep golden
(CNS): S. epidermides yellow colonies
S. saprophyticus Distribution:
B. Family Streptococcaceae skin eye
 catalase (-) urethra GIT
Genus Streptococci Respiratory Tract
 S. pyogenes  Coagulase, catalase,
 S. pneumoniae DNAse (+)
Gram-negative cocci
 Genus Neisseria TABLE 39.3 VARIOUS ENZYMES AND TOXINS
 Neisseria gonorrhoea PRODCED BY STAPHYLOCOCCI
 Neisseria meningitides Product Physiological Action
Staphylococcus 𝜷-lactamase Breaks down penicillin
 responsible for 80% of suppurative diseases in Catalase Converts hydrogen peroxide into
medical practice water and oxygen and reduces
 spherical (0.8 to 1.2micra in diameter), non-motile, killing by phagocytosis
usually arrange in grape-like cluster, non-capsulated, Coagulase Reacts with prothrombin to form a
non-spore former complex that can cleave fibrinogen
 around 35 species but only 3 are clinically important, and cause the formation of a fibrin
other species are important in Vet. Med. clot; fibrin may also be deposited
on the surface of staphylococci,
which may protect them from
destruction by phagocytic cells;
coagulase production is
synonymous with invasive
pathogenic potential
DNase Destroys DNA
Enterotoxins Are divided into heat-stable toxins 3. Enterotoxin protein in nature with the following
of six known types (A, B, C1, C2, antigenic Types:
D, E); responsible for the a. A and D
gastrointestinal upset typical of  associated with food poisoning
 emetic effect is due to reaction of
food poisoning
the toxin on neural receptors in the
Exfoliative Causes loss of the surface layers gut
toxins of the skin in scalded-skin b. B – associated with hospital infection
A and B syndrome c. F – Toxic Shock Syndrome (TSST-1)
(superantigens) TSST
Hemolysins Alpha hemolysins destroys  found in 20% of S. aureus isolates
erythrocytes and causes skin  associated with post-operative
destruction infection
Beta hemolysin destroys 4. Leukocidin
erythrocytes and sphingomyelin  kill white blood cells of humans and rabbits
 important virulence factor in community
around nerves
associated methicillin resistant S aureus
Gamma hemolysin destroys infections.
erythrocytes
Delta hemolysin destroys DISEASE ENTITIES
erythrocytes Skin
Hyaluronidase Also known as spreading factor; 1. Folliculitis
breaks down hyaluronic acid 2. Carbuncle (extend deeper to fibrous tissues)
located between cells, allowing for 3. Boil/Furuncles (involve the sub-cutaneous tissues)
penetration and spread of bacteria 4. Ritter's disease (Scalded skin syndrome)
Panton- Inhibits phagocytosis by  Exfoliativa Infantum
Valentine granulocytes and can destroy  characterized by postural dermatitis with
abundant flaking and red coloration of skin with
leukocidin these cells by forming pores in their fever and Gastrointestinal symptoms
phagosomal membranes 5. Impetigo (found in newborn)
Lipases Breaks down lipids  encrusted pustules on the surface of the skin
Nuclease Breaks down nucleic acids
Protein A Is antiphagocytic by competing
with neutrophils for the Fc portion
of specific opsonins
Proteases Breaks down proteins
Toxic shocks Is associated with the fever, shock,
syndrome and multisystem involvement of
toxin-1 (a toxic shock syndrome
superantigen)

TOXINS PRODUCED
1. Exotoxin (cytolytic)
a. Alpha-toxin
 acts on broad spectrum of eukaryotic cell
membranes
 potent hemolysin
b. Beta-toxin
 degrades sphingomyelin
 toxic to many kind of cells including rbc
c. Gamma-toxin
 disrupts biological membranes

2. Epidermolytic toxin
 causes Staphylococcal scalded skin syndrome
(Impetigo) by dissolving the mucopolysaccharide
matrix of epidermides
 Epidermolytic enzyme A is chromosomal while
the B is plasmid mediated
 1. Halophilic
2. addition of 7.5% NaCl will inhibits normal flora but not
S. aureus

5. Animal Inoculation (bawal na

kuno)

Biochemical test
1. Coagulase test
 differentiate S. aureus from
other staphylococci
 use fresh human plasma or
reconstituted EDTA-rabbit
plasma, (+) test is clumping or
Resistance to Antibiotic clot formation.
 types
1. beta-lactamase production 1. Bound coagulase/Clumping factor
 under plasmid control either by transduction (slide test)
or conjugation 2. Free coagulase (detected using
2. Methicillin, Nafcillin and oxacillin resistance tube test)
 due to mecA gene which codes low-affinity 2. Catalase test
3. penicillin binding protein (PBP-2 orPBP-2a)  differentiate staphylococci from Streptococci
4. Vancomycin resistance  mediates breakdown of hydrogen peroxide
 due to vanA gene from Enterococci into water and oxygen
 use hydrogen peroxide (3% or 30%)
Laboratory Diagnosis  (+) test is indicated by bubbles or
Specimens: Blood, CSF effervescence or gas formation
Nasopharyngeal swab/washing  Staphylococcus (+)
Material from wound/skin lesions  Streptococcus (-)
Laboratory procedures/tests
1. Stained smear (Gram staining)
 morphology and arrangement
2. Serological test
 Antigen-Antibody reaction (not
common)
3. Molecular
 DNA hybridization/sequencing (Pulsed-
field gel electrophoresis, Multi-
locus sequence typing)
4. Culture 3. DNAse Test (DNA Hydrolysis Test)
a. Agar plate  determines the ability of organism to hydrolyze
 colonies are smooth, circular, opaque
DNA
 low convex, varying sizes  use DNAse Agar (Toluidine Blue/Methyl green)
 BAP, appears Beta-hymolytic, creamy,  reaction:
white - hydrolysis of DNA cause the release of
 pinhead colonies Toluidine
 MSA, S. aureus ferments mannitol or methyl green
indicated by yellow color of media  positive result:
 Loeffler’s serum slant, golden yellow  methyl green is converted to colorless
colonies  toluidine blue is converted to rose pink
b. other cultural and physiological color
characteristics
 non fastidious Epidemiology and Prevention
 aerobic/facultative anaerobe  S. aureus is frequent colonizer of skin and mucosa
 optimum temp. 30 – 37 C  80% carrier rates among hospital patient
 pH : 7.2 - 7.4  frequent pathogen in nosocomial infection
How one can be infected  ovoid or lancet-shaped cocci
 Droplet infection  (0.6 – 1.0 micra) often seen in pairs or in chain,
 contact with carrier (Nasopharynx) catalase (-)
 contact with patient and hospital workers  facultative anaerobic some are micro-aerophilic,
Prevention pinpoint colonies
 stay away from infected persons and carriers  non-motile, non-spore former
 proper disposal of contaminated materials
 avoid indiscriminate use of antibiotics
 Hand washing is the most important preventive
measures
Treatment
 penicillin still the drug of choice
 penicillin resistance is due to production of Beta-
lactamase

MRSA / ORSA
 Methicillin-Resistant S. aureus
 resistant to: B-lactam antibiotics, Cephalosporin
and Non -B-lactam antibiotics

 Mechanism
- Altered penicillin binding protein (PBP2) due to
acquisition of mec A gene carried by SCC mec,
through HGT
 Methicillin Resistance
 1961/1968 - first reported cases
 1980 - significant problem among hospitals
 CDC estimated 2.7% of population world wide
are carriers
 3 – 15% world wide hospital incidence

 Coagulase-negative Staphylococci (CNS)

 Classification
- normal flora of the skin and mucosa
- opportunistic microorganism A. Brown’s classification - based on the hemolytic activity
1. Alpha haemolytic
Staphylococcus epidermides  greenish zone around the colony
 comprise 70 – 80% of CNS infection  most common normal flora in throat culture
 mainly due to foreign body infection  e.g. S. pneumoniae
a. Endocarditis - implanted prosthetics (cardiac 2. Beta hemolytic
pacemaker)  clear zone around the colony (e.g. S. pyogenes)
b. Continuous Ambulant Peritoneal Dialysis  use of Todd-Hewitt broth for Fluorescence Mic.
(CAD) 3. Gamma hemolytic
Staphylococcus saprophyticus  no hemolytic zone (e.g. S. faecalis)
 associated with 10 - 20% of UTI
 acute bacteruria/UTI of young women B. Lancefield classification - based on the antigenic
 non-specific urethritis among sexually active characteristic of group; specific substances found in the
young men cell wall
 characterized by pus in urine and pain in a. Group A Streptococci (S. pyogenes)
urination b. Group B (S. agalactiae)
c. Group C (S. equisimilis)
Streptococcus d. Group D (Enterococcus)
Streptococci e. Group I (S. pneumoniae)
 widely distributed in nature, some are members f. Group J (Viridans group)
of the normal human flora, others are associated
with important human diseases
 Additional Information
1. S. agalactiae - found in female genetalia
2. Enteococci
a. E. faecalis (90%) is found in colon and GIT
of humans
b. E. faeceum (10%)
3. Oral streptococci – responsible for 50 – 70% of all
bacterial endocarditis

Streptococcus pyogenes
 gram positive cocci in chain
 Beta-haemolytic in BAP
 catalase (+), PYRase (+),
 Bacitracin sensitive, Sulfamethoxazole-Trimethoprin
resistant
 Streptococcus pyogenes - more than 20 extracellular  aids in the attachment of streptococcus at the point of
products that are antigenic are elaborated by S pyogenes, entry
including the following:  anti-phagocytic factor
Enzymes
 Streptokinase Streptococcal Sore Throat - most common infection due to
 conversion of plasminogen to plasmin hemolytic; S. pyogenes is streptococcal sore throat or
resulting to lyses of fibrin and CHON pharyngitis
 Streptodornase
 deoxyribonuclease that depolymerizes Streptococcal Pyoderma - common in
DNA children, called impetigo; consists of
3. Hyaluronidase superficial vesicles that break down and
 splits hyaluronic acid eroded areas whose denuded surface
4. Diphosphopyridine nucleotidase is covered with pus and later is
 lyses Leukocytes encrusted
Toxins
1. Erythrogenic/Pyrogenic toxin - responsible for Scarlet fever
rash in scarlet fever  disseminated infection by way of blood stream
2. Hemolysin – extracellular toxin produced by  caused by beta-hemolytic Streptococci due to
Streptococci production of erythrogenic toxins
a. Streptolysin O  characterized by fever, skin rashes, enlargement of
 produced by most strain of Group A lymph gland
Streptococci during active infection Serologic tests: (skin test)
 antigenic, oxygen labile a. Schultz-Charlton reaction – injected to the
 stimulates production of ASO rashes, (+) is indicated by fading or bleaching of
Antibody rashes
 clinically important in the
serological diagnosis Strawberry tongue
 toxic to WBC and myocardial cells in scarlet fever
b. Streptolysin S
 oxygen stable, non-antigenic
 produce hemolysis by direct cell to Streptococcal cellulitis - an acute,
cell contact rapidly spreading infection of the
 lytic for RBC, WBC and bacterial skin and subcutaneous tissues;
protoplast follows infection associated with
3. M- protein mild trauma, burns, wounds, or
 appears as hair-like projections of the surgical incisions; pain, tenderness,
streptococcal cell wall swelling, and erythema occur.
 a major virulence factor of group A
Spyogenes Erysipelas
 reddening of the skin
accompanied with fever
and enlargement of
lymph gland
 usually occurs in
children and the elderly.
 portal of entry is the skin
or outer mucous
membrane
 characterized by a
typical lesion: a raised,
demarcated, bright red
area of dermal and
subcutaneous
 often found affecting the face and orbit, extremities
 Necrotizing Fasciitis (Streptococcal Gangrene) utilize Sheep Agar Plate, Staphylococcus - S.

 infection of the sub- agalactiae produces CAMP factor which acts
cutaneous tissues and synergistically with the beta-lysine of S. aureus
fascia. causing enhanced lysis of RBC’s
 extensive and very rapidly g. PYR Hydrolysis (+)
spreading necrosis of the  to determine if organism is capable of producing
skin and subcutaneous enzyme L-pyrroglutamylaminopeptidase
tissues. (PYRas)
 Group A streptococci that cause necrotizing fasciitis  PYR disk and N,N-
have sometimes been termed "flesh-eating bacteria." methylaminocennamaldehyde
 PYRase hydrolyze L-pyrrolidonyl-B-
 Post Streptococcal Complications naphthylamide
a. Acute Rheumatic fever (occurs 2 – 3 weeks after  Positive result: bright red
onset of Streptococcal infection (sore throat,
tonsillitis)  Mode of infection
b. Acute Glomerulonephritis - sometimes develops 3 - droplet infection (respiratory secretions)
weeks after S pyogenes skin infection - nosocomial infection
(pyoderma, impetigo)
c. Sepsis/Septic Shock  Treatment
 complication of invasive streptococcal disease - drug of choice: Penicillin G
associated with a widespread erythematous
rash, early onset of shock, and organ failure Streptococcus
pneumoniae
 Diagnosis  lancet-shaped,
 Stained smear  non-motile, capsulated
 Culture  Pneumococci
 BAP (Hemolytic activity) Antigenic structure
 Anaerobic condition  capsular
 Biochemical test polysaccharide
 Bacitracin test (specific solubility substance (SSS)
 Serological test
 Somatic antigen
 Anti-streptolysin O (ASO, ASOT, ASTO)
 C-polysaccharide, M-protein
 Biochemical tests  F- antigen (Forssmann antigen)
a. Catalase (-) Factors that contribute to pathogenicity
b. Growth tolerance test in 6.5% NaCl 1. Capsule
c. Bacitracin test ( Group A strep (+)) 2. Neuraminidase – acts on the structure of cell
 inhibited by bacitracin (0.02 – 0.04 membrane, glycolipids and glycoproteins of the
units) host
3. Hemolysin
d. Hippurate Hydrolysis (-)  Pneumolysin O (Cytolytic)
 determine the ability of organism to produce  Dermatotoxic
hippuricase which splits hippuric acid to glycine Clinical Significance
and benzoic acid 1. URTI (Upper Respiratory Infection)
 positive test is deep purple color 2. Lobar pneumonia/Bronchopneumonia
e. Bile esculin (-) 3. Sinusitis
 primary purpose is for identification of Group D 4. Otitis media
streptococci 5. Septicaemia
 Bile Esculin Agar (esculin, 40% bile, ferric citrate 6. Meningitis
organism hydrolyze esculin into esculentin which 7. Endocarditis
reacts with ferric citrate to form brown-black
precipitate Diagnosis
f. CAMP test (Christie, Atkins, Munch Petterson) Specimen: sputum, CSF , Blood
 negative 1. Stained smear
 purpose is to differentiate streptococcus 2. Culture (BHIA, Thioglycolate medium, BAP)
agalactiae from other Streptococci  fastidious (BAP, medium of choice)
 growth is enhanced with 5 -10% CO2
  optimum pH 7.4 - 7.8  Endocarditis, common blood isolate in colon
 colonies: circular, glistening, alpha hemolytic cancer
3. Biochemical (BOQUIA)  S. equinu, S. bovis

A. Bile solubility test 4. Viridans Streptococci

 differentiate S. pneumoniae from Viridans group
 based on the presence of enzyme amidase that
cleaves the bond between lysine and NAM in the
peptidoglycan (causing bacteiolysis)
B. Optochin susceptibility test
 inhibit the growth of Pneumococci
 reagent: Ethylhydrocuprein hydrochloride
C. Neufeld Quellung reaction
 done by mixing the specimen with anti-
pneumococcal antibody and Methylene blue
 positive is indicated by swollen appearance of
bacterial capsule due to Ag – Ab reaction
D. Inulin fermentation
 growing the bacteria in medium containing inulin
E. Animal inoculation
 Intra-peritoneal injection of sample into the mice
 positive test is indicated by fatal infection of mice
after 16 – 48 hours
 Other Streptococci
 common species are : S. mutans, S. sanguis
and S. mitis
 can be isolated from the mouth, upper
respiratory, GIT and occasionally in skin
 Optochin-resistant, colonies not soluble in bile.
S. mutans
 responsible for the formation of dental caries
 has serologic type a,b,c, and d
 possess cellular and extracellular insoluble
dextran polymer which is an important
component of dental plaque
GRAM-POSITIVE ANAEROBIC COCCI
 strictly anaerobe
 Peptococcus niger, (black pigmented colonies)
Peptostreptococcus anaerobius (SPS sensitive)
 Mouth, colon, female genital tract
 Obligate anaerobes
 causes Abscesses (with multiple other bacterial
species)

1. Group B Streptococci Diseases

S. agalactiae
 is the only known species pathogenic to humans
(Neonatal sepsis and meningitis)
 could not be distinguished morphologically from
other Beta-hemolytic streptococci
 presumptive identification is the ability to
hydrolyze sodium hippurate
 (differentiate Group A from Group B Strep.)
- CAMP test (+)
1. sub-acute purulent infection
 cerebral abscess, Otitis media, necrotizing
pneumoniae, sinusitis, pulmonary abscess
2. Abdomen
 appendicitis, peritonitis, hepatic abscess
3. Genitals
 salphingitis
4. Post-operative wound infection

2. Group C Streptococci GRAM-NEGATIVE COCCI

S. equisimilis Neisseriaceae Coffee bean-
 is the most common type isolated from humans shaped
diplococci,
(found in the throat)
nonmotile,
 causes pharyngitis, pyogenic infections similar to oxidase (+),
group A streptococci catalase (-)
 morphologically similar to Group A, all are beta- Neisseria Cocci often in Gonorrhea
hemolytic except S. dysgalactiae gonorrheae phagocytes, acid
 rarely cause human diseases from fermentation
3. Group D Streptococci (found in the colon) of glucose
a. Enterococci group Neisseria Acid from Meningitis/sepsis
 Abdominal abscess, urinary tract infection, meningitidis fermentation of
endocarditis glucose and
 Growth in presence of bile, hydrolyze esculin, maltose
growth in 6.5% NaCl, PYR-positive
 S. faecalis, S. faecium, S. durans Non-pathogenic Neisseria
b. Non-eterococci group - Neisseria sicca
 Growth in presence of bile, hydrolyze esculin, no - Neisseria flavescence
growth in 6.5% NaCl, degrades starch - N. lactamica
Related organism (resembling Neisseria)
Moraxella (Branhamella)
Acinetobacter
Other genera under family Neisseriaceae
- Kingella - Eikenella
- Simonsiella - Alysiella
Neisseria meningitides
 Meningococci parasite of nasopharyngeal mucosa
 naso-pharynx (portal of entry)
 transmitted by airborne from patient with active
infection
 causes Meningococcemia (W135 strain and
Meningitis
 infection is characterized by excessive nasal
secretions, sore throat, fever, head ache, pain in
the back and neck, loss of mental alertness
 death could occur within 24 hours after
 onset of symptoms (Acute infection)
 drug of choice: Penicillin
Pathogenicity
 Determinant of pathogenicity is the capsular
polysaccharides which inhibits phagocytosis
 portal of entry of infection is by way of URT and
establishing in the membrane of naso-pharynx,
producing localized infection (carrier state)
 Invasion of the blood stream is manifested by high
fever, chills, malaise and severe headache and
haemorrhage (meningococcemia)
Laboratory Diagnosis
- specimen: nasopharyngeal swab,CSF, Blood,
petechial hemorrhage from skin
1. Catalase test (+)
2. Oxidase (+)
 reagent: 1% tetramethyl para-phenylene
diamine dihydrochloride
 positive is indicated by maroon-Violet color
 after 10-30 seconds
3. CHO utilization (glucose, maltose, sucrose)
 N. meningitides produce acids from
glucose and maltose
 N. gonorrhoea produces acids from
glucose
4. Culture (CAP and other special medium)
 smooth, raised, large, translucent and bluish
in color with no hemolysis
 requires 5 – 10% CO2
Susceptibility
 Meningococci remained susceptible to
Penicillin (except those Beta-lactamase
producers) and chloramphenicol
Serological type
- there are 8 (a,b,c,d,x,y,z and z’)
- only a is associated with cerebrospinal meningitis
Neisseria gonorrhoeae
 Gram-negative cocci in pairs, capsulated, non-
motile, non-spore former
 usually found intracellular, most strains are
Beta-lactamase producers
Antigenic structure
1. pilus protein
2. Polysaccharide component of cell wall
3. other membrane protein
Virulence factor
1. Capsule (anti-phagocytic)
2. Pili - attachment to human cells
- Anti-phagocytic
- facilitates genetic transformation
3. Protein I - surface antigen
4. Protein II – associated with nuclease
5. Lipopolysaccharide (Endotoxin activity)
6. Immunoglobulin A protease - destroys Ig A
7. Beta-lactamase - responsible for penicillin resistance
Methods of Beta-lactamase testing
1. Chromogenic cephalosporin method - indicated
by change in color
2. Acidimetric
3. Iodometric
Sample should be from primary isolation medium cause
plasmid coding for enzyme maybe lost in sub-culturing.
  Opthalmia neonatorum
 acquired by the neonates upon passage in the birth
canal during delivery by the infected mother
 the bacteria attach into the eye of the neonates
causing
 Inflammation of conjunctiva which may cause
blindness

Diagnosis
Specimen: swab from urethra, rectum
pharynx , cervix, vagina,
conjunctival discharge (neonates)
 Bacteremia Urethritis
1. Dermatitis 1. Prostatitis 1. Stained smear
2. Arthritis 2. Epididymitis  Gram (-) diplococci or cocci in pairs
3. Endocarditis 2. Biochemical : Catalase, Oxidase
4. Meningitis Cervicitis Sugar fermentation
5. Peri-hepatitis 1. Endometritis  ferment glucose, catalase (+), Oxidase(+)
6. Tenosynovitis 2. Salphingitis 3. Culture
3. Pelvic peritonitis MTM (Modified Thayer Martin)
 Vancomycin (inhibit enterics and Gram-
 Gonorrhoea positive cocci)
 most common among 20 – 24 years old  Nystatin (inhibits fungi and yeast)
 females are asymptomatic (85%)  Colisthemethate (inhibit Gram (-) bacilli
 males are symptomatic (95%) CAP (Chocolate Agar Plate)
 acquired through sexual contact with 4. Serological
 infected individual (multiple partner)  IFAT (Anti-pilus antibody test)
 infection occurs instantly due to pili (virulence factor)

Portal of entry
 columnar epithelium of the urethra
 peri-urethral ducts and glands
 - others: cervix
rectum
pharynx
conjunctiva
Signs and Symptoms
 Male : - 2 – 3 days after contact, itchy
sensation of urethral meatus and burning
sensation during urination
- purulent urethral discharge

 Female: Cultural and Biochemical characteristics

- frequency of urination
- purulent vaginal discharge
- fever and abdominal pain
Complications
 Male: - Prostatitis
- Epididymitis
 Female:
- Pelvic Inflammatory Disease (PID)
- Disseminated infection
- sub-acute bacterial endocarditis
and meningitis
 Fastidious, complex nutrients (usually lyzed blood
provided by CAP)
 starch, cholesterol and albumin should be added to
media
 to neutralize the inhibitory effect of fatty acids
 growth requirements: pH 7 – 7.4, moist aerobic
atmosphere with 5 – 10% CO2
 colonies: small, gray, and glistening, become
larger and
 opaque at 48 hours incubation
Susceptibility
 Penicillin is the drug of choice for Gonococci except
for Beta-lactamase producers and the (PPNG –
Penicillinase Producing N. gonorrhoea)

Prophylaxis – Rifampin (given in the US)

Prevention
 avoid sexual contact with multiple
 partners
 use of condom

Other Commensal Neisseria

 normally present in the mucous membrane of mouth,
nose and pharynx
 oxidase positive and can be differentiated from
pathogenic strain due to thief ability to grow in an
ordinary culture media
 e.g. N. flava and N sicca

Veillonella
- Gram- negative anaerobic cocci
- produces red fluorescence under U.V. light
Branhamella group
- B. catarrhalis/ Moraxella catarrhalis
- causes bronchitis, pneumonia, sinusitis. Otitis media
and conjunctivitis