SUBJECT: Pediatrics

TOPIC: Gram Positive Bacteria

Lecturer: Dr. Jindra H. Tetangco

Transcriber: Los
Editor: Tony
Number of Pages: 10

So hey. Remember Micro? This is pretty much a review. But

just like last year, lots of memory work going on here. Sorry if
I seem makulit in some parts, but thats just how I like to
memorize things haha. There wasnt too much emphasis on
morphology (thank god)so just focus on the clinics! She also
emphasizes a lot of keywords so take note of those too.
So here we go. Gram positive bacteria!
Staphylococcus
o S. aureus
o CONS
Streptococcus
o S. pneumonia
o GAS
o GBS
o Strep viridans
Enterococcus
Diphtheria
Listeria

STAPHYLOCOCCUS
G (+) cocci in pairs and clusters

pathognomonic!
Can be found in the body as normal flora, or on
fomites/dust

prevents phagocytosis by interacting with

fibrinogen, forms clumps of the organisms

o Abscess formationmost common

manifestation
o

*So again, when she says S. aureus, think pyogenic, teichoic

acid, and the 4 roles of the virulence factorsprotection,
localization of infection, tissue damage, toxins.

Virulence Factors
Protection
o Slime layer, interfering with
opsonophagocytosis
o EnzymesProtein A, catalase,
penicillinase, or B-lactamase, lipase
Emphasis on the Protein A inhibits opsonization,
phagocytosis by reacting to IgG

Again, S. aureuscauses most common

pyogenic infections. (remember?) This is
because of the coagulase/clumping factor,
which localizes the infection

Local tissue damage

o HemolysinsL-toxins, B-hemolysins
o PVL (panton-valentine leukocidin)

Coagulase (+) S. aureus

Coagulase (-)S. epidermidis,
saprophyticus, etc.

S. aureus
Coagulase (+)
More pathogenic than CONS (coagulasenegative staphylococcus)
Most common cause of pyogenic skin/soft
tissuee.g. SSSS, impetigo, furuncle,
cellulitis, abscess, wound infection
Adhesion mediated by teichoic aciddont
forget!!
Virulence factors have 4 roles:
o Protection
o Localize infection
o Local tissue damage
o Toxins affecting non-infected tissue
sites

Infection Localization
o Coagulase and Clumping factor

causes leukocyte death by interacting with

the phospholipids of their cell membranes,
producing increased permeability and
leakage of proteins
She says, dont be surprised if this comes
out in the exam, because these are mustknows. So alam na. Haha!

Toxins affecting non-infected tissue sites

o Exfoliatins A/B: localized,
generalized skin infxn
A: bullous impetigo
B: SSSS

Very important! Remember

ABBSSSS!

(+) Nikolsky sign

pathognomonic of bullous
impetigo and SSSS
o Enterotoxins: food poison
o TSST-1: toxic shock syndrome
Epidemiology
20-40% carry >1 strain in the anterior nares
So everyones got a bit of S. aureus (Staph
are NF, remember?), but symptoms only
appear after colonization
Transmitted from nose to skin
Spread via auto-inoculation or direct
contact with hands of colonized individuals

So always wash yo hands!!

Clinical Manifestations
Skin
o Impetigo contagiosum
o Ecthyma
o Bullous impetigo
o Folliculitis
o Hydradenitis
o Furuncles
o Carbuncles
o SSSS
o Wound infection
o

Again, pyogenic! Magsawa kayo!

Respiratory Tract
o Pneumoniaprimary
(hematogenous spread) or
secondary (after a viral infection e.g.
influenza)
o Rare, but is often associated in
patients with cystic fibrosis
o Necrotizing pneumonitis with
empyema, pneumatocoeles, etc.
o Children are very sick, admitted at
the ICU
Sepsis
o Primary or secondary to localized
infection
o Acute, with N/V, myalgia, fever,
chills
o Usually localize in heart valves,
lungs, joints bones, abscess
o Systemic manifestations!
Bones and Joints
o Most common cause of
Osteomyelitis, Suppurative arthritis
in children
Heart
o ACUTE Endocarditis
o In a case with an ACUTE onset of
symptoms pertaining to the heart,
consider S. aureus as a ddx
o

ACUTE ACUTE ACUTE=AUREUS AUREUS

AUREUS, ok?

Food poisoning
o Ingestion of preformed
enterotoxinsespecially A (most
common) and B
o SSx develop after 2-7hrssudden
severe vomiting, watery diarrhea,
(+/-) low fever; usually resolves w/in
12-24hrs.
o Children take longer to recover,
sometimes >24hrs
o Management includes fluid and
electrolyte replacement; sometimes
(in severe cases) admitted and given
IV antibiotics
Toxic Shock Syndrome (TSS)
o TSST-1superantigen, in
menstruating women who use
tampons or vaginal devices
o Nonmenstrual TSS - Enterotoxins A
and B, nasal packing, or from other
localized infectionswound,
sinusitis, osteomyelitis, etc.
o Abscesses or other forms S. aureus
infectionstreat immediately with
DOC, otherwise they can go into
toxic shock
o Acute onset

o Induces production of IL-1 and TNF,

resulting in the ff. SSx:
High fever
Hypotension
Vomiting
Diarrhea
Sore throat
Headache
Myalgias
Diffuse erythematous
macular rash
Strawberry tongue
o Watch out for alterations in
consciousness, oliguria, or
hypotensionmay progress into
toxic shock and DIC
o e.g. septic abortiontake into
account salient symptoms such as
hypotension and signs of shock and
DIC; always consider TSS!
*The last 2 (food poisoning, TSS) are serious manifestations.

Diagnosis
Isolation of the organism from the site of
infectioncellulitis aspirate, abscess
cavities, etc.
Swab cultures NOT usefulwhy? Dont
forget that theyre part of the NF,
particularly in the anterior nares
Tissue samples or fluid aspiratebest
culture material
Testing for enterotoxins on food suspected
of contamination
Treatment
AbscessesIncision & Drainage
Antibiotics cannot pass through cell wall
because they are localized and
encapsulated
Drug to be used, dose, route, duration,
depends on site of infection
MSSA (methicillin-sensitive)semisynthetic
penicillin (nafcilin, DOC: oxacillin), 1st gen
cephalosporin (cephalexin, cefazolin)
MRSA (methicillin-resistant)vancomycin,
linezolid, daptomycin, dalfopristin,
vancomycin, TMP-SMX (Trimethoprimsulfamethoxazole)
*Doc breezed through the Rx, but said focus on the DOC in
the Phils. Dont forget!

MSSAoxacillin
MRSAvancomycin
Treat initially with IV vancomycin or
methi/nafci/oxaci, while awaiting sensitivity
resultstakes 5-7 days, but you gotta treat
immediately, especially for TSS
Quinolones not recommendedrapid
resistance
PEDIATRICS: Gram Positive Bacteria | Page 2 of 10

TMP-SMX for both MSSA and MRSA; cheap

and affordable
For less serious infections, oral DOC: TMPSMX (co-trimoxazole)

Coagulase Negative Staphyloccocus (CONS)

Low virulence (vs. S. aureus)
Infection in px with indwelling devicesIV,
foley catheters, etc.
Common cause of nosocomial neonatal
infection
NF skin, throat, mouth, vagina, urethra
S. epidermidismost common, 60-90% of
staph in the skin and mucous membranes
Colonization from hospital staff, or direct
inoculation during surgery precedes
infection
*So px with hx of prosthetic valve replacement,
cardiac pacemakers developing signs of
infection, CONS will be a ddx
Pathogenesis
Slime layerenhance adhesion to foreign
surfaces (i.e. catheters)

Remember, for S. aureus, teichoic acid enhances

adhesion

Very pathogenic because they resist

phagocytosis and impair penetration of
antibiotics

Clinical Manifestation
Immunocompromised
Previous/ongoing pneumonia, pyogenic
infections, asthma, foreign body
Two requirements: immunocompromised,
or foreign body!
S. epidermidismost common CONS;
common skin inhabitant

Wont be asked in the exambut she emphasized it.

The hells up with that?

Nosocomial bacteremia, usually associated

with central vascular catheters
May also cause CSF shunt meningitis,
because of the foreign body
S. saprophyticusUTI in sexually active
females

Mnemonic! SSxSaprophyticus=SeX. Thats just a

mnemonic, yeah? SSx still means signs and
symptoms when I write it down later.

Diagnosis
Difficult to differentiate true positive blood
culture (i.e. bacteremia) vs. contamination
(i.e. from a poorly collected specimen)
True bacteria:
o Rapid growth
o >2 cultures positive w same CONS
o SSx compatible with CONS sepsis

o S. epidermidis more common

contaminants
o

Emphasized, so take note.

Treatment
Methicillin-resistant, so use Vancomycin
Like in MRSA, Vancomycin is still DOC
Recap! Try to answer the questions yourselvesno
cheating!
1. Classified as coagulase positive
Staphylococcus
a. S. aureus
b. S. epidermidis
c. S. saprophyticus
d. S. haemolyticus
Answer: A

2. coagulase negative Staphylococcus?

a. S. aureus
b. S. epidermidis
c. S. saprophyticus
d. S. haemolyticus
Answer: B, C, D (Bonus question daw sa exam haha!)

3. A child was brought to the ER due to fever

& seizures. The doctor on duty suspects
that the patient has an infected VP shunt
inserted a month PTA. The most likely
etiologic gram (+) bacteria is:
a. S. aureus
b. S. epidermidis
c. S. saprophyticus
d. S. haemolyticus
Answer: B. Basta may catheter or nosocomial stuff,
think epidermidis!

4. A positive Nikolsky sign is pathognomonic of

this infection caused by S. aureus:
a. Erysipelas
b. Abscess
c. SSSS
d. TSS
Answer: C. (+) Nikolsky is pathognomonic for SSSS
and bullous impetigo. In SSSS, the s. granulosum is
affected, and when the skin is scratched, it peels off.
Doc says this is very painful, especially for kids.

5. A teenager was admitted at UMC due to

dyspnea. CXR showed the presence of
pneumatocoele and pneumothorax.
Diagnostic thoracentesis revealed pus. The
antibiotic of choice would be:
a. Vancomycin
b. Penicillin IV
c. 3rd gen cephalosporin
d. Oxacillin

PEDIATRICS: Gram Positive Bacteria | Page 3 of 10

Answer: D. By default, consider MSSA first before

trying Vancomycin, which is for MRSA. If oxacillin
doesnt work for 2-3 days, then consider MRSA and
give Vancomycin.

6. A 16y/o sexually active female was brought

to a private clinic due to fever and dysuria.
Upon work-ups, the diagnosis was UTI.
Among the gram (+) bacterial organisms,
the most likely etiology for this case is:
a. S. aureus
b. S. epidermidis
c. S. saprophyticus
d. S. haemolyticus
Answer: C. Again, SSx. Saprophyticus=SeX.

STREPTOCOCCUS
S. pneumoniae
Lancet-shaped, encapsulated diplococcus
Remember! Lancetpneumoniae
Individual cocci or in chains
Epidemiology
>90% children bet. 6mos-5yrs have S.
pneumoniae in nasopharynx
7 seroytpes4, 6B, 9V, 14, 18C, 19F, 23F

Treatment
Usually use penicillin, chloramphenicol, or
TMP-SMX
Know the pattern of resistance?
Resistance is decreasing

Children >1mo. w suspected pneumococcal

meningitisvancomycin + cefotaxime or
ceftriaxone
DOC for proven meningeal meningitis
o Penicillin G (for susceptible
organisms)
o Cefotaxime/Ceftriaxone (for
penicillin-resistant, treatment
failure)
Prevention/Vaccines
PCV13pneumococcal conjugate vaccine
o @ 2, 4, 6 mos
o Booster dose at 12-15
o

Wont be asked

Most frequent cause of bacteremia,

bacterial pneumonia, otitis media
2nd most common cause of pediatric
meningitis
Spreads via respiratory droplet
transmission, although usually occurs
sporadically
Pathogenesis
Interferes with normal defense mechanisms
caused by allergy, viral infections or irritants
(e.g. smoke)these allow colonization and
infection
What are normal defense mechanisms?
Mucus production, ciliary movement,
release of mucus. Once these are affected,
px will be affected by S. pneumonia, causing
SSx
The virulent pneumococci are resistant to
phagocytosis
So theyre very virulent, like staph
Lungsantiphagocytic properties of
pneumococcal capsule
Tissuelymphatics, bloodstream, direct
extension
Clinical Manifestations
SSx related to anatomic site
Otitis mediaesp. 6mos-5yrs
Sinusitis
Pneumoniamore severe form
Sepsis

Remember, theyre found mostly in the

nasopharynx, so SSx will mostly involve that area

Why? Remember that it affects children

6mos-5yrs. They gotta be protected during
that time!

PPV23
o vs. 23 serotypes responsible for
>95% of cases of invasive disease
o For high-risk children >2yrse.g.
asplenia, sickle cell dse,
immunofeicits, HIV, DM< chronic
lung, heart or kidney dse, CSF leak,
cochlear implants
o 2nd dose 5yrs. after 1st dose
o Supplemental to PCV13 for high-risk
children
o Doc didnt discuss the last 2 bullets,
so they might not be that important

Group A Streptococcus (S. pyogenes)

Common cause of URTI (pharyngitis), and
the skin (impetigo, pyoderma)
Causes scarlet fever, erysipelas, strep TSS,
necrotizing fasciitis
Potentially serious non-suppurative
complicationsrheumatic fever, acute GN
Etiology
Coccoid-shaped bacteria chains
Classified by degree of hemolysis
o -hemolytic (complete hemolysis)
most common; divided into >20
serogroups by the Lancefield
method
o -hemolytic (partial hemolysis)
o -hemolytic (non-hemolytic)
PEDIATRICS: Gram Positive Bacteria | Page 4 of 10

Epidemiology
Humans natural reservoir
Highly communicable
Highest incidence in 5-15yrs.

Remember, S. pneumonia6mos-5yrs; GAS515yrs

So basically, <5yrs: S. pneumonia
>5yrs: GAS

Spread by airborne salivary droplets and

nasal discharge
Incubation period: 2-5 days
Non-infectious after 24hrs antibiotic tx
Strep pyodermaimpetigo
o Occurs at the site of open lesions
o Spread skin to skin (not respiratory)
o Fingernails and perianal region
harbor GAS and play a role in
dissemination
o

So when playmates play with each other

;) Hahaha moving on

Usually affects low socioeconomic groups

Perianal regionchildren w parasites (i.e.
enterobious, ascaris, etc.)
They scratch their pwet then they scratch
their skin, inoculating the bacteria
Pathogenesis
M proteinresistance to phagocytosis;
stimulates type-specific Ab production
o Type 12 strain associated with
glomerulonephritis

Scarlet Fever
Upper respiratory tract infection associated
with characteristic rash (Exanthem)
Caused by pyrogenic (erythrogenic)
exotoxins
Clinical Manifestations
o (+) rash 24-48 hours after onset of
symptoms
o White strawberry tongue
o Bright red discoloration of the skin Diffuse, fine, erythematous papules
in neck, trunk, extremities which
blanches on pressure
o More intense along creases of the
elbows, axillae, groin
o Feels like gooseflesh or coarse
sandpaper
o Facial sparing, but cheeks are
erythematous with pallor around
the mouth (Circumoral Pallor)
o Desquamates after 3-4 days
cephalocaudally
o After desquamation, the reddened
papillae are more prominent = Red
Strawberry tongue

(Remember, Staphprotein A; GASM protein.

SAAM!)

Erythrogenic toxinsstreptococcal
pyrogenic exotoxin
o 3 types: A, B, C
o Causes the rash in scarlet fever
o Formation of type-specific antitoxin
Abs
o Immunity to 1 exotoxin does not
confer immunity to the other
(similar to dengue)possibility of
2nd attack of scarlet fever
o May be involved in strep TSS
Clinical Manifestations
Acute pharyngitisfever, sore throat,
dysphagia
Pneumoniamore common
Scarlet fever
Impetigo
Erysipelas
Vaginitis
Severe invasive diseases
o Strep TSS
o Necrotizing fasciitis
o Focal/systemic infection not
meeting the criteria of the above
nice to know

So it goes from white strawberry tongue to red strawberry

tongue, developing rashes in between. White. Rash. Red.
Yeah?

Impetigo
Bullous
o Fluid-filled
o Less common
o Sometimes whole body is affected
o (+) Nikolskyremember,
pathognomonic for bullous
impetigo and SSSS
o Usually in neonates and young
infants
o Flaccid, transparent bullae on
previously untraumatized skin,
usually around the face, buttocks,
trunk, perineum

PEDIATRICS: Gram Positive Bacteria | Page 5 of 10

Nonbullous
o More common
o Discrete papulovesicular lesions
which rapidly become purulent and
covered with a thick, confluent,
amber-colored crust
o

Just remember, non-bullous impetigo

more common, no fluid, purulent, and
crusty

Diagnosis
Throat swabpharyngitis
o Culture90-95% sensitive
o Rapid antigen detection testfaster
than culture
>95% specificity
<80-90% sensitivity
Positive test confirms
infection
Negative test prompts need
for throat culture
o

Basically, first youre supposed to do the

rapid antigen detection test, and if it tests
negative, do culture

o Culture is better, but takes a longer

time; gold standard!
Antibody titers
o ASOnot useful for impetigo
o Clinical features of impetigo very
pathognomonic, so not much need
for diagnostic tests
o

In other words, sobrang obvious na pag

nakita mo, so you dont really need to do
labs. REMEMBER: Honey-colored crusts

o Anti-DNAse
o Significant test: increase of >2
dilution between the acute and
convalescent phase
o

What does that mean? 2 tests are needed.

Treatment
DOC: penicillin
o Oral penicillin V
o IM penicillin G
*Penicillin G effective treatment for all Strep.
infections except Group-D Enterococci
*Aminoglycosides can be added for synergism =
efficacy (PHARMAAAA)
Penicillin-allergic:
o Cephalosporin
o Clindamycin
o Macrolides
Mild impetigo: topical mupirocin (e.g.
Bactroban)

So oral antibiotics arent always needed, especially if

the infection is localized.

Complications
Suppurative
o Peritonsillar abscess,
retropharyngeal abscess
o Cervical lymphadenitis
o Otitis media, mastoiditis, sinusitis

o
o
o
o
o

Pneumonia
Arthritis
Septicemia
Meningitis
Osteomyelitis (But S. aureus is a more
common cause)

Non-suppurative
o Acute rheumatic fever, post-strep
GNmore severe, more common
o Post-strep reactive arthritis
Rheumatic Fever

No questions in exam for RF

Just note than RF and post-strep GN are the

more common complications!
Diagnosis based on Jones criteria
major/minor

Group B Streptococcus (S. agalactiae)

One of the major causes of neonatal sepsis

Vaginal/rectal colonization in up to 30% of

pregnant womenthis is the usual source
for GBS transmission to newborns

In a newborn with a good APGAR score, but soon

develops SSx of dyspnea, tachypnea, always consider
GBS first

Tx: Penicillin G
Preventionintrapartum antibiotics to
women identified high risk (either by
culture or risk-factor)

And thats it for GBS. :-bd She just emphasized that

its the major cause of neonatal sepsis.

Streptococcus Viridans
Non-group A or B streptococcus
Includes S. bovis, S. mitis, S. mutans, S.
sanguis
NF pharynx, nose, skin, gut
Subacute bacterial endocarditis, dental
caries, human bite infections
*So Subacute bacterial endocarditis is for
Streptococcus Viridans, while Acute endocarditis is
for S. aureus
Feeeeeedback!!
1. A 6y/o girl was brought to the OPD due to
fever and rash. On PE, the patient was
highly febrile with strawberry tongue,
hyperemic tonsils, erythematous cheeks,
and coarse, sandpaper-like skin. The most
likely gram(+) infection that she has is:
a. TSS
b. Scarlet Fever
c. Kawasaki disease
d. Measles
Answer: B. Remember, Scarlet feverStrawberry tongue.
Red. Rash. White.

PEDIATRICS: Gram Positive Bacteria | Page 6 of 10

2. A 3y/o female was brought to the ER due to

dyspnea. She had a history of cough and
colds for 5 days without treatment. She
only received DPT and polio vaccines. The
most likely gram(+) etiologic agent is:
a. S. aureus
b. S. epidermidis
c. S. saprophyticus
d. S. pneumoniae
Answer: D. Remember, <5yrsS. pneumonia, >5yrsGBS. S.
epidermidis usually in foreign bodies; S. saprophyticusSSx.
Saprophyticus. SeX.

3. Most common non-suppurative

complication of strep pneumonia
a. Rheumatic fever
b. Acute GN
c. Myocarditis
d. Post-strep arthritis
Answer: A/B. All are non-suppurative, but asks for the most
common. But RF is more common than AGN. Although she also
said that rheumatic fever and acute GN were the most
common complications for GAS, not S. pneumonia, so Im
confused

4. Responsible for the pathogenic virulence of

GAS.
a. Protein A
b. Erythrogenic toxins
c. Coagulase
d. Teichoic acid
Answer: B. Erythrogenic toxins and protein M. Remember,
Protein A is for S. aureus, and Protein M is for GAS. SAAM!

ENTEROCOCCUS

Catalase-negative facultative anaerobes

Grow in pairs and short chains
NF GIT
Often found in oral secretions, dental
plaque, URT, skin, vagina
E. faecalismost common (80% of
enterococcal infection)
E. faeciumaccounts for almost all the rest
Pathogenesis
Direct spread person to person or from
contaminated medical devices
Most common cause of nosocomial
infections
2ndpseudomonas
Nosocomial spread may lead to hospital
outbreaks
Notorious resistance to common
antibioticse.g. cephalosporins,
semisynthetic penicillins
Fatal!
Clinical Manifestations
Px w breakdown of normal physical
barriersGIT, skin, GUT
Prolonged hospitalization
Indwelling vascular catheters
Prior use of antibiotics
Compromised immunity
Keyword: NOSOCOMIAL
15% neonatal bacteremia/septicemia
Neonatal meningitis, usually as a
complication of septicemia
Accounts for ~15% of nosocomially acquired
UTIs

Risk increases w indwelling urinary catheter

Both Enterococcus and S. epidermidis are

nosocomial infections, but I guess what shes trying
to emphasize is that Enterococcus is more common.

Treatment
Ampicillin (DOC), Imipenem, Penicillin
Vancomycinfor those not responding to
first-line tx, and pencillin-allergic patients

Watch out for resistance! Always remember that

Vancomycin is used for resistant strains

CORYNEBACTERIUM DIPHTHERIAE
Aerobic, nonencapsulated bacilli
Most commonly isolated agent of
diphtheria
Exclusive inhabitant of human mucus
membranes and skin
Airborne spread! Respiratory droplets,
direct contact with respiratory secretions,
exudates from infected skin lesions
Asymptomatic carriage important in
transmission
Viable in dust or fomites up to 6 mos.
Pathogenesis
Diphteritic exotoxinmajor virulence
factor; inhibits protein synthesis, local
tissue necrosis
Formation of grayish peritonsilar
pseudomembranedense coagulum of
organisms, epithelial cells, fibrin, leukocytes
and erythrocytes
Toxin leads to paralysis of palate and
hypopharynx

PEDIATRICS: Gram Positive Bacteria | Page 7 of 10

Systemic toxin absorptionkidney tubule

necrosis, thrombocytopenia,
cardiomyopathy, nerve demyelination
Clinical Manifestations
Respiratory Tract Diphtheria
o Most commontonsils, pharynx
o 2ndnose, larynx
o Incubation period: 2-4days
o SSx inflammation develop
afterwards
Pseudomembrane formation
Bull-neck appearancewith
soft tissue edema and
lymphadenopathy; toxic,
severe respiratory
depression
Cutaneous Diphtheria
Infection at other sites:
o Otitis externa
o Purulent and ulcerative
conjunctivitis
o Purulent and ulcerative vulvovaginitis
o Less commonrespiratory is the
most common
Diagnosis
Culture speciments from the nose, throat,
or other mucocutaneous lesions
Complications
Toxic cardiomyopathy
o 10-25% px with respiratory
diphtheria
o 50-60% death
o Risk correlates w extent and severity
of oropharyngeal disease, w delay in
administration of antitoxin
o Usually occurs in the 2nd-3rd week of
illness
o Administer the antitoxin +
antibiotics and save a life!
o SSxtachycardia, prolonged PR
interval on ECG, ST-T wave changes,
dilated and hypertrophic
cardiomyopathy, seen in 2D Echos,
dysrhythmias or heart blocks
Toxic neuropathy
o 2-3wks, like cardiomyopathy
o Hyposthesia
o Local paralysis of soft palate
o Weakness of posterior pharyngeal,
laryngeal and facial nerves
o All in face!
o Nasal voice, Difficulty swallowing,
aspiration
o May eventually have diaphragmatic
paralysis
o VaccineDPT

o Cranial neuropathies by 5th week

oculomotor and ciliary paralysis (e.g.
strabismus, difficulty in
accommodation, etc.)

Recovery is slow but complete.

Treatment
Antitoxindont wait for culture results!
Must not delay tx!
Administered on the basis of clinical
diagnosis
Not recommended for asymptomatic
carriers
Halts toxin production, treats localized
infection, prevents transmission
DOC: erythromycin or penicillin
Prevention
Asymptomatic case contacts
o Persons living w the px; dont have
any symptoms
o Must be treated as well, otherwise
may develop SSx after 1-2wks
o 7-day monitoring
o Culture of nose, throat, and
cutaneous lesions
o Prophylaxis w erythromycin
x10dayshyperacidity in epigastric
o Or single dose pen g
o Diphtheria toxoid if no booster in
last 5yrs
o Prophylaxis + vaccination!
o continue vaccination for those
incompletely immunized
Asymptomatic carriers
o Prophylaxis w erythromycin or
penicillin
o Same with case contacts
o Diphtheria toxoid if no booster in
last 1yr
o Droplet precautions or contact
precautions until at least 2
subsequent cultures obtained 24hrs
apart post-treatment are negative
o Repeat cultures performed ~2wks
after completion of treatment for
both cases and carriersif culture
(+), repeat 10-day tx
o Antitoxin NOT recommendedonly
for symptomatic px!
VaccineDPT
o Children 6wks-7yrs
5 doses @ 2, 4, 6 mos old
4th dose at 9-12mos after 3rd
dose
Booster at 4-6yrs

Remember the PCV13 vaccine for

S. pneumoniae? Its also given @ 2,
4, and 6mos old. So both DPT and
PCV13 are given at 2, 4 and 6!
2,4,6!

PEDIATRICS: Gram Positive Bacteria | Page 8 of 10

o >7yrs

Those who have not received

the primary dose
2 doses 4-8wks apart
3rd dose 6-12mos after 2nd
dose
o Contraindicationhx neurologic or
severe hypersensitivity from a
previous dose
o Booster (Tdap) at 11-12yrs.

= Past-E Question

LISTERIA MONOCYTOGENES
Facultative anaerobic motile
Catalase (+)
Epidemiology
Sewage, silage, soil (survives for >295 days)
No person to person spread except
maternal-fetal transmission
REMEMBER! Listeriamaternal-fetal
transmission
Food-borne transmissionaged cheese,
improperly pasteurized milk, raw beef,
pork, poultry, packaged meats, vegetables
in contaminated soil
More common is still through maternalfetal transmission
Enter through GIT
Clinical Manifestations
Pregnant women susceptible
Flu-like illnessleads to placenta listeriosis,
stillbirth, premature delivery
Neonatal listeriosis
o Early onset <7days
o Late onset >7days
o

These are Phil. stats! (In Nelson, its 5 days)

Post-Neonatal Infection
o In px w underlying malignancies or
immunosuppression
o May be associated with food-borne
outbreaks
o Meningitis, less commonly sepsis,
rarely other CNS involvement

Treatment
Ampicillin
Empiric treatment of sepsis or meningitis
Ampicillin included to cover for L.
monocytogenes

The end.
I wanted to throw my laptop, because MS Word is such a pain
in the ass to use! So I hope this helped, and know that a lot of
effort went into making this.

PEDIATRICS: Gram Positive Bacteria | Page 9 of 10

SUMMARY: GRAM (+) Infections

Organism
Characteristics Pathogenesis
S. aureus

CONS

S. pneumonia

gAS

gBS

Viridans Strep

Enterococcus
spp.

Corynebacterium
Diphtheriae

Listeria
Monocytogenes

Pyogenic
FORMS
ABSCESSES
NF in
anterior nares
Common in
immunocomp
romised or
patients with
foreign body

-hemolytic
Peak
Incidence
6mos-5yrs
Lancet
shaped,
encapsulated

-hemolytic
Peak
Incidence 515yrs

Adhesion mediated by
teichoic acid

Infection in px with
indwelling devices
Slime layerenhance
adhesion to foreign
surfaces
Most common CONS
S. epidermidis
Respiratory droplet
transmission, although
usually occurs
sporadically

Virulence Factors:
M protein
Erythrogenic toxins

Vaginal/rectal Vertical transmission

colonization in Maternal-fetal
up to 30% of
transmission
pregnant
women
NF of pharynx,
nose, skin, gut
MCC of
nosocomial
infections,
RESISTANCE
Aerobic, nonencapsulated

Catalase (+),
motile,
facultative
anaerobic

Clinical Manifestations/
Complications
Acute endocarditis
Bullous Impetigo, SSSS
(+) Nikolsky sign
Osteomyelitis
TSS
CSF shunt meningitis
Ventriculoperitoneal shunts

DOC

Most frequent cause of

bacteremia, bacterial
pneumonia, otitis media

Penicillin G (for
susceptible
organisms)
Cefotaxime/Ceftriaxo
ne (for penicillinresistant, treatment
failure)

Streptococcal pharyngitis
Scarlet Fever
Impetigo
Vaginitis
Erysipelas
Pneumonia
Non-suppurative:
Rheumatic Fever, Post strep
GN
Major cause of Neonatal
Sepsis

Subacute bacterial
endocarditis

Person-person spread

Destruction of skin, GUT, GIT

Contaminated Medical
Devices (indwelling of
catheters)
Major Virulence Factor
Diphtheric exotoxin

Neonatal meningitis,
bacteremia/septicemia

-NO person-person
spread
Spread via:
-Maternal-fetal
transmission (MC)
-Food-borne
transmission

Formation of Grayish
peritonsilar
pseudomembrane, Bull Neck
Appearance
Toxic cardiomyopathy,
neuropathy
Paralysis eventually of
diaphragm=death
Placenta Listeriosis

MSSA Oxacillin
MRSA - Vancomycin

Vancomycin

Prevention PCV13
PPV23
Penicillin G
Penicillin-allergic:
Cephalosporin
Clindamycin
Macrolides

Penicillin G
Prevention intrapartum Abs in
women IDed as high
risk
Penicillin G

Ampicillin

Antitoxin,
Erythromycin,
Penicillin
Prevention
DPT vaccine

Ampicillin

Neonatal listeriosis (Early vs.

Late)
Post Neonatal Listeriosis
Prematurity
Stillbirth

PEDIATRICS: Gram Positive Bacteria | Page 10 of 10