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PEDIATRIC

BACTERIAL INFECTIONS
Dra. Pauline Solis


OUTLINE
Gram-positive bacteria
Gram-negative bacteria
Anaerobic bacteria
Mycobacteria
Spirochetes
Mycoplasma
Chlamydia
Rickettsia
GRAM POSITIVE BACTERIA

I.
II.
III.
IV.
V.
VI.
VII.
VIII.

o
o


Staphylococcus epidermidis
Streptococcus pneumoniae
Epidemiology

Pathogenesis
Clinical Manifestations
Diagnosis
Treatment
Prognosis
Prevention

Group A Streptococci

Streptococcus pyogenes
Pathogenesis

Clnical Manifestation
Diagnosis
Tretment
Complication
Prognosis
Prevention
Rheumatic Heart Fever
Jones Criteria
Treatment

Non Group A or B Streptococci


Enterococci
Epidemiology

Virulence Factors
Teichoic acid cell wall structure that mediates
adhesion to mucosal cells
Slime layer - loose polysaccharide capsule which
interfere with opsonophagocytosis.
Coagulase and/or clumping factor - interacts
with fibrinogen to cause large clumps of
organisms, interfering with effective phagocytosis
o Causes plasma to clot by interacting with
fibrinogen and this may have an important
Protein A - present in most strains of S. aureus
o
o

Clinical Manifestations
Treatment

Listeria
Actinomyces
Nocardia

Aerobic
Grow in pairs and clusters
Ubiquitous
o

Heat and drying-resistant


Coagulase-positive: S. aureus
o

Part of normal flora of humans; found on


fomites, dust

produces a yellow or orange pigment

produce skin separation by splitting the


desmosome and altering the intracellular
matrix in the stratum granulosum
Serologically distinct proteins that produce
localized (bullous impetigo) or generalized
(SSSS, staphylococcal scarlet fever) skin
complications

Enterotoxins (types A, B, C1, C2, D, E)


o

STAPHYLOCOCCI

combines with the phospholipid of the


phagocytic cell membrane, producing
increased permeability, leakage of protein,
and eventual death of the cell

Exfoliatins A and B
o

Reacts specifically with immunoglobulin G1


(IgG1), IgG2, and IgG4.
Located on the outermost coat of the cell wall
and can absorb serum immunoglobulins,
preventing antibacterial antibodies from
acting as opsonins and thus inhibiting
phagocytosis.

Catalase - inactivates hydrogen peroxide,


promoting intracellular survival
Penicillinase or -lactamase - inactivates
penicillin at the molecular level and lipase
(associated with skin infection)
Panton-Valentine leukocidin (PVL) associated
with invasive skin disease

Diphtheria
Epidemiology

Pathogenesis
Clinical Manifestations
Diagnosis
Treatment
Prognosis
Prevention

Food poisoning, staphylococcal scarlet fever,


scalded skin syndrome, toxic shock syndrome
(TSS)

role in localization of infection (abscess


formation)

Group B Streptococci

Streptococcus agalactiae
Pathogenesis

Clinical Manifestations
Diagnosis
Treatment
Prognosis
Prevention

Primary and secondary


Associated with or result in osteomyelitis,
suppurative arthritis, deep abscesses,
pneumonia, empyema, endocarditis,
pyomyositis, pericarditis, meningitis

Toxin-mediated diseases
o

Impetigo
Furuncles
Cellulitis
Abscess
Lymphadenitis
Paronychia
Omphalitis
wound infection

Bacteremia is common
o
o

S. epidermidis - produces white pigment with


variable hemolysis. Less pathogenic unless
with indwelling catheters

Staphylococcus aureus
Most common cause of pyogenic infection of the
skin and soft tissue
o
o
o
o
o
o
o
o


Staphylococci

Staphylococcus aureus
Virulence factors

Epidemiology
Pathogenesis
Clinical Manifestations
Diagnosis
Treatment
Prognosis
Prevention

Coagulase-negative: S. epidermidis, S.
saprophyticus, S. haemolyticus
o

-hemolysis on blood agar


More virulent

Preformed toxins associated with food


poisoning vomiting, diarrhea, hypotension
By 10 yr of age, almost all individuals have
antibodies to at least 1 enterotoxin

Toxic shock syndrome toxin-1 (TSST-1)


o
o
o

Superantigen that induces production of IL-1


and TNF resulting in hypotension, fever, and
multisystem involvement
Usually associated with menstruation
Enterotoxin A and enterotoxin B also may be
associated with nonmenstrual TSS

PEDIATRIC BACTERIAL INFECTIONS


Dra. Pauline Solis

Epidemiology
Many neonates are colonized within the 1st wk of
life
20-40% of normal individuals carry at least 1
strain of S. aureus in the anterior nares at any
given time
Colonizers nose, skin, umbilicus, vagina, perianal
area
Heavily colonized nasal carriers (often aggravated
by a viral URTI effective disseminators
Transmission: auto-inoculation or direct contact
hand washing is essential
Invasive disease may follow colonization
Factors that increase the likelihood of infection
o
o
o
o
o
o
o
o

Wounds
skin disease
VPS
Catheterization
Corticosteroid
Malnutrition
Azotemia
Influenza - predispose to secondary bacterial
infection with staphylococci

o
o

o
o

Neutropenia

Antibody to S. aureus toxins appears


protective but humoral immunity does not
necessarily protect against focal or
disseminated infection with the same
organisms

o
o

Clinical Manifestations
o
o
o

Pyogenic skin infections


o
o
o
o
o
o
o

Recurrent skin and soft tissue infections -


commonly associated with community-acquired
methicillin-resistant S. aureus (CA-MRSA)
Pneumonia
o
o

Impetigo contagiosa
Ecthyma
bullous impetigo
folliculitis
hydradenitis
furuncles, carbuncles
staphylococcal scalded skin syndrome, and
staphylococcal scarlet fever

1/hematogenous or 2 after a viral infection


Hematogenous - secondary to septic emboli
from right-sided endocarditis or septic
thrombophlebitis intravascular devices

Acute multisystem disease fever,


hypotension, erythematous rash with
desquamation of hands and feet; vomiting,
diarrhea, myalgias, nonfocal neurologic
problems, conjunctival hyperemia, strawberry
tongue
Caused by TSST-1producing and some
enterotoxin-producing strains of S. aureus,
which colonize the vagina or cause focal sites
of staphylococcal infection
Mostly in menstruating women who use
tampons or other vaginal devices (diaphragm,
contraceptive sponge)
Also in children, nonmenstruating women,
and men with an identifiable focus of S. aureus
infection
Clinical diagnosis (3 major + 3 minor
criteria)
Recovery in 7-10 days
Antibiotics, removal of vaginal devices, fluid
management

Diagnosis
Requires isolation of the organism from sterile
sites - cellulitis aspirates, abscess cavities, blood,
bone or joint aspirates
Swab cultures of surfaces are NOT useful - may
reflect surface contamination rather than the true
cause of infection
Tissue samples or fluid aspirates in a syringe
provide the best culture material.
Diagnosis of S. aureus food poisoning is made on
the basis of epidemiologic and clinical findings
o

Caused by ingestion of preformed


enterotoxins in contaminated foods
~ 2-7 hr after ingestion of the toxin sudden
severe vomiting watery diarrhea
Symptoms rarely persist longer than 12-
24 hrs

Toxic Shock Sydrome


o

chronic granulomatous disease


Transplacental transfer of humoral immunity in
infants
Older children- antibody development thru
colonization or minor infections.

S. aureus common cause of acute native-


valve endocarditis

Renal and perinephric abscess


Food poisoning
o

S. aureus as most common cause

Endocarditis
o

Job syndrome
Chediak-Higashi syndrome, Wiskott-
Aldrich syndrome

Primary or associated with any localized


infection
Organisms eventually localize at any site,
usually a single deep focus heart valves,
lungs, joints, bones, abscesses

Pyomyositis
o Localized staphylococcal abscesses in muscle
associated with elevation of muscle enzymes
sometimes without septicemia
Osteomyelitis and suppurative arthritis in
children
o

Inhalation pneumonia - alteration of


mucociliary clearance, leukocyte dysfunction,
or bacterial adherence initiated by a viral
infection.
Necrotizing pneumonitis - associated with
development of empyema, pneumatoceles,
pyopneumothorax, bronchopleural fistulas

Bacteremia and sepsis

Phagocytosis and killing defects

Trauma
Surgery
foreign bodies
burns
Chemotaxis defects

Pathogenesis
Barriers to infection intact skin and mucous
membranes
o
o
o
o
o

Suspected contaminated food should be


cultured and can be tested for enterotoxin

Treatment
Abscesses incision and drainage
Foreign bodies removal
Antibiotics choice must be based on local
susceptibility patterns
o
o

Parenteral therapy for serious infections


Dose, route, and duration of treatment depend
on the site of infection, patient response,
susceptibility of organism recovered from
blood or from site of infection

PEDIATRIC BACTERIAL INFECTIONS


Dra. Pauline Solis

Oxacillin, 1st generation cephalosporin


(cefazolin), 2nd gen (cephalexin) methicillin-
susceptible
Clindamycin bacteriostatic not given for
endocarditis, brain abscess, meningitis

o
o

o
o

>90 serotypes identified by type-specific


capsular polysaccharides
Encapsulated strains cause most serious
disease in humans impede phagocytosis

Unpigmented, umbilicated colonies with


incomplete/-hemolysis.
Bile soluble and optochin-sensitive
Quellung reaction
o

blood cultures grow within 24 hr


2 blood cultures are positive with the same
CONS
clinical and laboratory Ssx compatible with
CONS sepsis and resolve with appropriate
therapy.
No blood culture that is positive for CONS in a
neonate or patient with intravascular catheter
should be considered contaminated without
careful assessment
Most CONS strains are resistant to methicillin.
Vancomycin as the drug of choice
rifampicin to increase antimicrobial efficacy
Removal of infected device to treat the
infection adequately.

STREPTOCOCCUS PNEUMONIAE
Pneumococcus
Gram-(+), lancet-shaped, polysaccharide
encapsulated diplococcus, singly or in chains
o

Prepared foods should be eaten immediately


or refrigerated appropriately

Staphylococcus epidermidis
Coagulase-negative Staphylococcus (CONS)
Cause infections in patients with indwelling
foreign devices - IV catheters, HD shunts and
grafts, CSF shunts, PD catheters, pacemaker wires
and electrodes, prosthetic cardiac valves, and
prosthetic joints
Common cause of nosocomial neonatal infection
Normal inhabitants of the human skin, throat,
mouth, vagina, and urethra
Colonization precedes infection
Direct inoculation during surgery
Produce an exopolysaccharide protective
biofilm, or slime layer surrounds the
organism, enhance adhesion to foreign surfaces,
resist phagocytosis, and impair antibiotic
penetration
True bacteremia should be suspected if
o
o

High morbidity and mortality in young infants


and in those with delayed treatment

Prognosis influenced by nutrition al status,


immunologic competence, and the presence or
absence of other debilitating diseases
Prevention
Proper handwashing techniques - most effective
Isolation precaution hospitalized patients
Hypochlorite and chlorhexidine wash
Nasal mupirocin t to prevent recurrences
Food poisoning - exclude individuals with S.
aureus infections of the skin from food
preparation and handling
o

Vancomycin, Linezolid, Trimethoprim-


sulfamethoxazole
Ceftaroline 4th gen ceph approved for adult
use (MRSA SSTI)

Prognosis
High fatality rate for untreated bacteremia
S. aureus pneumonia can be fatal at any age
o

Used to treat S. aureus toxinmediated


illnesses (TSS) to inhibit toxin production

Type-specific antisera combine with capsular


polysaccharide

o
o

Epidemiology
Most healthy individuals carry various S.
pneumoniae serotypes in their upper respiratory
tract
>90% of children 6 mos to 5 yrs harbor S.
pneumoniae in nasopharynx at some time
Carriage does not consistently induce local or
systemic immunity sufficient to prevent later
reacquisition of the same serotype
Carriage rate peaks on the1st and 2nd yr of life
gradually decline
Most frequent cause of bacteremia, bacterial
pneumonia, and otitis media
Second most common cause of meningitis in
children
Increased susceptibility to pneumococcal
infection
o
o

o
o

Sickle cell disease,


Asplenia,
Deficiencies in humoral (B cell) and
complement-mediated immunity
HIV infection
Malignancies - leukemia, lymphoma)
Chronic heart, lung, or renal disease
(nephrotic syndrome)
CSF leak
Cochlear implants

Severe cases WBC count may be low

o
o
o

High prevalence of colonization


Decreased ability produce antibody against
the T-cell independent polysaccharide
antigens in <2yrs old poor response to
polysaccharide vaccines

Transmission via respiratory droplet


Increased frequency and severity of
pneumococcal disease in:
o
o
o

Capsules become refractile seen


microscopically
Specific antibodies to capsular
polysaccharides confer protection on the host
opsonization and phagocytosis

Pathogenesis
Abnormal clearance mechanisms allergy,
irritants, viral infections
Resistance to phagocytosis
Poor prognosis - very large numbers of
pneumococci and high concentrations of capsular
polysaccharide in the blood and CSF
Greatest risk for invasive pneumococcal disease
(IPD) - infants <2 y/o poor antibody production
to most serotypes
Increased frequency of pneumococcal disease in
asplenia deficient opsonization and absence of
clearance by the spleen of circulating bacteria
Clinical Manifestations
Signs and symptoms are related to the anatomic
site of disease
IPD pneumonia, sepsis, meningitis
Otitis media, sinusitis, osteomyelitis, arthritis,
endocarditis
Diagnosis
Recovery of S. pneumoniae from the site of
infection or from blood
Blood cultures should be obtained in children
with pneumonia, meningitis, arthritis,
osteomyelitis, peritonitis, pericarditis, or
gangrenous skin lesions
Pronounced leukocytosis, WBC >15,000/mm3.
Treatment
Emperic therapy depends on local susceptibility
patterns
High-level -lactam resistance and MDR strains
Penicillins for susceptible strains

PEDIATRIC BACTERIAL INFECTIONS


Dra. Pauline Solis

Lincosamide (clindamycin) or macrolides


(erythromycin, clarithromycin, azithromycin for
penicillin allergic patients
Cephalosporins
o
o

Pneumococcal meningitis - sensorineural hearing


loss in 20-30%
o

o
o
o

o
o
o
o
o

Provoke protective antibody responses in


90% of infants given these vaccines at 2, 4, and
6 mo of age
Enhanced responses (e.g., immunologic
memory) are apparent after booster doses
given at 12-15 mo of age
Reduce nasopharyngeal carriage of vaccine
serotypes by up to 60-70%
13-valent vaccine (latest)

-hemolytic - complete hemolysis


-hemolytic - green or partial hemolysis
- nonhemolytic

M types commonly associated with


pharyngitis rarely cause skin infections
M types commonly associated with skin
infections rarely cause pharyngitis
Pharyngeal strains (M type 12) - associated
with glomerulonephritis,
Skin strains (M types 49, 55, 57, and 60)
nephritogenic
A few of the pharyngeal serotypes, but none of
the skin strains, have been associated with
acute rheumatic fever.
Rheumatogenic potential is not solely
dependent on the serotype but is a
characteristic of specific strains within several
serotypes

Humans - natural reservoir


Highly communicable
Can cause disease in normal individuals of all ages
who do not have type-specific immunity against
the particular serotype involved
Rate of pharyngeal infections highest in 5-15 y/o
Children with untreated acute pharyngitis spread
GAS via salivary droplets and nasal discharge.
Incubation period for pharyngitis - 2-5 days

Well-demarcated, perianal erythema with anal


pruritus, painful defecation, and blood-
streaked stools
Flat, pink to beefy-red perianal erythema with
sharp margins extending as far as 2 cm from
the anus w/o systemic SSx

Invasive GAS infection - isolation of GAS from a


normally sterile body site
o
o
o

acute GAS infection involving deeper layers of


the skin and connective tissue
The skin is swollen, red, and very tender with
sharply defined, slightly elevated border with
associated systemic symptoms

Perianal streptococcal disease


o

Rash of scarlet fever


Eaborated by streptococci that are infected
with a particular bacteriophage
appear to be involved in the pathogenesis of
invasive GAS disease including streptococcal
toxic shock syndrome.

Clinical Manifestations
Important cause of acute pharyngitis and
pneumonia
Nonbullous and bullous impetigo
Erysipelas
o

Toxic shock syndrome - shock + multiorgan


system failure early in the course
Necrotizing fasciitis - extensive local necrosis
of subcutaneous soft tissues and skin
Systemic infections not TSS or necrotizing
fasciitis - bacteremia with no identified focus,
meningitis, pneumonia, peritonitis, puerperal
sepsis, osteomyelitis, suppurative arthritis,
myositis, surgical wound infections
Exact pathogenesis unknown but pyrogenic
exotoxins are implicated superantigens

Scarlet Fever
o
o

-hemolytic streptococci - divided into groups by


a group-specific polysaccharide (Lancefield
carbohydrate C) located in the cell wall
Bacitracin test - a disk containing 0.04 U of
bacitracin inhibits the growth of most group A
strains
Serotyping based on M protein antigen
o

PPSV23
Unpredictable immunologic responsiveness
and efficacy following administration in
children <2 yr of age.
Contains purified polysaccharide of 23
pneumococcal serotypes responsible for
>95% of cases of invasive disease

GROUP A STREPTOCOCCI (GAS)


Streptococcus pyogenes
Gram-(+) coccoid-shaped, grow in chains.
Broadly classified by the zone of hemolysis on
blood agar
o
o
o

o
o

strains rich in M protein resist phagocytosis


M protein antigen stimulates the production of
type-specific protective antibodies

Streptococcal pyrogenic exotoxins A, B, and C

Pneumococcal conjugate vaccines (PCV)


o

Other serious neurologic sequelae - paralysis,


epilepsy, blindness, intellectual deficits

Prevention
Pneumococcal polysaccharide vaccines
o
o

Integrity of host defenses


Virulence and numbers of infecting organism
Age of host
Site and extent of the infection
Adequacy of treatment

Pathogenesis
Virulence of GAS depends primarily on the M
protein
o
o

Cefuroxime
Ceftriaxone/Cefotaxime

High dose amoxicillin (80-100mkday) for otitis


media. Others Vancomycin
Prognosis
Depends on
o
o
o
o
o

URTI associated with a characteristic rash


Caused by pyrogenic exotoxin
(erythrogenic toxin)-producing GAS in
individuals who do not have antitoxin
antibodies
Rash appears within 24-48 hours after onset
of symptoms: neck with facial
sparingtrunk, extremities

Diagnosis
Culture of a throat swab - remains the standard
for the documentation of GAS in URT and for
onfirmation of the clinical diagnosis of acute GAS
pharyngitis
Rapid antigen detection tests
Elevated or increasing streptococcal antibody titer
retrospective
o
o

diffuse, finely papular, erythematous,


blanching
often more intense along the creases of
the elbows, axillae, and groin
Fades with desquamation after 3 days
PE of pharynx - same findings as GAS
pharyngitis
Tongue with swollen papillae
porminent strawberry appearance

Antistreptolysin O assay (ASO)


Not specific to GAS

Treatment
Antibiotics for GAS pharyngitis - prevent acute
rheumatic fever, shorten clinical course, reduce
transmission, and prevent suppurative
complications
Penicillin as the drug of choice no resistance
reported yet

PEDIATRIC BACTERIAL INFECTIONS


Dra. Pauline Solis

o
o

o
o

No animal model
Cytotoxicity theory
Immune-mediated pathogenesis

o
o
o

2 major criteria OR 1 major + 2 minor


criteria and meets the absolute requirement
3 circumstances in which the diagnosis of
acute rheumatic fever can be made without
strict adherence to the Jones criteria

Chorea may occur as the only


manifestation of acute rheumatic fever.

During passage through the birth canal


aspiration of infected amniotic fluid
Ascending infection
Incidence of early-onset GBS infection
increases with the length of rupture of
membranes.
Late-onset infection - vertically transmitted or
acquired later from maternal or nonmaternal
sources

Capsular polysaccharide virulence factor


Clinical Manifestations
Early-onset neonatal GBS disease
o
o
o
o

Narrow zone of -hemolysis on blood agar


Resistance to bacitracin and cotrimoxazole
Lack of hydrolysis of bile esculin
Elaboration of CAMP factor (extracellular
protein)

Definite identification (+) Lancefield group B


carbohydrate antigen via latex agglutination
techniques
Strains classification based on distinct capsular
polysaccharides - important virulence factors and
stimulators of antibody-associated immunity
10 GBS capsular types
Pathogenesis
Maternal vaginal or rectal colonization by GBS
major risk factor for early neonatal infection
o

Positive throat culture or rapid streptococcal


antigen test
Elevated or increasing streptococcal antibody
titer

Treatment
Antibiotics for 10 days for initial attacks
Anti-inflammatory therapy aspirin. Steroids
Sedatives/anticonvulsants for sydenham chorea
Long term antibiotic prophylaxis to prevent
recurrences, infective endocarditis
GROUP B STREPTOCOCCI (GBS)
Streptococcus agalactiae
Major cause of neonatal bacterial sepsis in the
USA
Facultative anaerobic gram-positive cocci, in
chains or diplococci; small gray-white colonies on
solid medium
Presumptive identification
o
o
o
o

Clinical features: Arthralgia, Fever


Laboratory features: Elevated acute phase
reactants ESR, CRP
Prolonged PR interval

Supporting evidence of antecedent GAS infection


o

Carditis
Polyarthritis
Erythema marginatum
Subcutaneous nodules
Chorea

Minor criteria
o
o

Indolent carditis may be the only


manifestation in patients who 1st come to
medical attention months after the onset
of acute rheumatic fever
Most patients with recurrences of acute
rheumatic fever fulfill the Jones criteria,
but some may not

Jones Criteria
Major criteria
o
o
o
o
o

No clinical or laboratory finding is pathognomonic


for acute rheumatic fever
Jones criteria - intended only for the diagnosis of
the initial attack of acute rheumatic fever and not
for recurrences
o

not all of the serotypes of GAS can cause


rheumatic fever
serotypes of GAS (M types 1, 3, 5, 6, 18, 24) -
more frequently isolated from patients with
acute rheumatic fever

Pathogenesis
o
o
o

~2/3 patients with an acute RF have a history


of an URTI several weeks before
peak age and seasonal incidence of acute RF
closely parallel GAS infections
patients with acute RF almost always have
serologic evidence of a recent GAS infection,
with antibody titers higher than those seen in
patients with GAS infections without acute RF
Outbreaks of GAS pharyngitis in closed
communities, may be followed by outbreaks of
acute rheumatic fever
Antimicrobial therapy that eliminates GAS
from the pharynx also prevents initial
episodes of acute rheumatic fever, and long-
term, continuous prophylaxis that prevents
GAS pharyngitis also prevents recurrences of
acute rheumatic fever

Rheumatogenicity
o

A group of neuropsychiatric disorders


(particularly obsessive-compulsive disorders,
tic disorders, and Tourette syndrome) for
which a possible relationship with GAS
infections has been suggested

Prognosis
Excellent with complete recovery if properly
treated GAS pharyngitis
Treatment within 9 days of onset acute
rheumatic fever is prevented
No evidence that acute PSGN can be prevented
once pharyngitis or pyoderma with a
nephritogenic strain of GAS has occurred
Prevention
The only specific indication for long-term use of
antibiotics to prevent GAS infections is for
patients with a history of acute rheumatic fever or
rheumatic heart disease
No vaccine available yet
Rheumatic Fever
Considerable evidence to support the link
between GAS upper pharyngitis tract infections
and acute RF and RHD
o

Used to describe a syndrome characterized by


the onset of acute arthritis following an
episode of GAS pharyngitis in a patient whose
illness does not otherwise fulfill the Jones
criteria for the diagnosis of acute rheumatic
fever

Pediatric Autoimmune Neuropsychiatric


Disorders Associated with Streptococcus pyogenes
(PANDAS)
o

Macrolides for penicillin-allergic patients


Complications
Acute rheumatic fever
Acute poststreptococcal glomerulonephritis
Poststreptococcal reactive arthritis

presents within the 1st 6 days of life


associated with chorioamnionitis, prolonged
rupture of membranes, and premature labor.
Infants may appear ill at the time of delivery,
and most infants become ill within the 1st
24 hr of birth
most common manifestations - sepsis (50%),
pneumonia (30%), meningitis (15%)

Late-onset neonatal GBS disease


o
o

occurs on or after 7 days of life


most commonly manifests as bacteremia (45-
60%) and meningitis (25-35%)

PEDIATRIC BACTERIAL INFECTIONS


Dra. Pauline Solis

o

Diagnosis
Diagnosis of invasive GBS disease thru isolation
and identification of the organism from a normally
sterile site - blood, urine, CSF
Isolation of GBS from gastric or tracheal aspirates
or from skin or mucous membranes indicates
colonization and is NOT diagnostic of invasive
disease
Antigen detection methods using group B
polysaccharide-specific antiserum - latex particle
agglutination
o

o
o

Normal flora of pharynx, nose, skin, GU tract


Endocarditis, human bite infections

Penicillin as antibiotic of choice


ENTEROCOCCUS
Gram-(+), catalase-negative facultative anaerobes;
in pairs or short chains
Mostly nonhemolytic/ -hemolytic on sheep blood
agar
Grow in bile and hydrolyze esculin
Grow in 6.5% NaCl and hydrolyze L-pyrrolidonyl-
-naphthylamide (PYR)
o

Group C and G as most common cause of


human disease
Normal flora of pharynx, skin, GI and GU tracts
Wound infections, puerperal sepsis, cellulitis,
sinusitis, endocarditis, brain abscess, sepsis,
nosocomial infections

-hemolytic streptococci that cannot be classified


within a Lancefield group - the viridans
streptococci (S. bovis S. mitis S. mutans S. sanguis,
etc)
o
o

No vaccine developed yet

Non Group A or B Streptococci


-hemolytic streptococci of Lancefield groups C to
H and K to V
o

Administration of antibiotics to pregnant


women before the onset of labor does not
reliably eradicate maternal GBS colonization
and is not an effective means of preventing
neonatal GBS disease

Immunoprophylaxis - induction of protective


immunity
o

for broad coverage pending organism


identification and synergistic bactericidal
activity

features to distinguish them from group D


streptococcus
Identification at the species level is enabled by
differing patterns of carbohydrate
fermentation

Notorious for their frequent resistance to


antibiotics
Epidemiology
Normal inhabitants of GI tract of humans and
animals
Found in oral secretions, dental plaque, URT, skin,
vagina
E. faecalis - 80% of enterococcal infections,
E. faecium - ~20%

Indigenous flora presumed source of


enterococcal infection
Direct spread from person to person or from
contaminated medical devices nursery, ICU
Clinical Manifestations
Not aggressively invasive organisms
o
o

Prognosis
Neurodevelopmental delay due to meningitis
Favorable outcome for focal infections
Prevention
Chemoprophylaxis - elimination of colonization
from the mother or infant
o

Urine, blood, CSF samples

Non-specific CBC and CXR findings


Treatment
Penicillin G antibiotic choice for confirmed GBS
infection
Initial empirical therapy of neonatal sepsis -
ampicillin + aminoglycoside OR cefotaxime
o

focal infections (20%) - bone and joints, skin


and soft tissue, urinary tract, or lungs

Causing disease only in children with damaged


mucosal surfaces or impaired immune
response.
Emergence as a cause of nosocomial infection
is predominantly due to their resistance to
antibiotics commonly used in the hospital
setting

Neonatal septicemia, meningitis, endocarditis


UTI (nosocomial)
Catheter-related infections
Treatment
Highly resistant to cephalosporins and
semisynthetic penicillins (oxacillin)
Moderately resistant to extended-spectrum
penicillins such as ticarcillin and carbenicillin
Ampicillin, imipenem, and penicillin are the most
active -lactams against enterococci
o

Some strains of E. faecalis and E. faecium


demonstrate resistance due to mutations in
penicillin binding protein 5 or production of a
plasmid-encoded -lactamase (E. faecalis)
completely resistant to penicillins

Use of combination penicillin plus a -


lactamase inhibitor, imipenem or
vancomycin

Vancomycin-resistant enterococci
o

Use linezolid, daptomycin, tigecycline

o
o

Droplet precautions - pharyngeal diphtheria


Contact precautions cutaneous diphtheria

DIPHTHERIA
Acute toxic infection caused typically by
Corynebacterium diphtheriae
Aerobic, nonencapsulated, non spore-forming,
mostly nonmotile, pleomorphic, gram-positive
bacilli
Isolation is enhanced by use of a selective medium
(i.e., cystine-tellurite blood agar or Tinsdale agar)
that inhibits growth of competing organisms
gray-black colonies
The ability to produce diphtheritic toxin results
from acquisition of a lysogenic
Corynebacteriophage which encodes the
diphtheritic toxin gene and confers diphtheria-
producing potential
Demonstration of diphtheritic toxin production or
potential for toxin production by an isolate is
necessary to confirm disease
Toxigenic and nontoxigenic strains are
indistinguishable by colony type, microscopic
features, or biochemical test results
Epidemiology
Exclusive inhabitant of human mucous
membranes and skin
Transmission via respiratory droplets, direct
contact with respiratory secretions of
symptomatic individuals, or exudate from infected
skin lesions
Asymptomatic respiratory tract carriage is
important in transmission
Skin infection and skin carriage - silent reservoirs
of C. diphtheriae
Organisms can remain viable in dust or on fomites
for up to 6 mos
Pathogenesis
Both toxigenic and nontoxigenic strains cause
skin and mucosal infection

PEDIATRIC BACTERIAL INFECTIONS


Dra. Pauline Solis

o
o
o

o
o
o
o

Mechanical obstruction, myocarditis account for


most diphtheria-related deaths
Case fatality rate -10% for respiratory tract
diphtheria
At recovery, administration of diphtheria toxoid is
indicated to complete the primary series or
booster doses of immunization because not all
patients develop antibodies to diphtheritic toxin
after infection
Prevention
Antimicrobial prophylaxis for asymptomatic
household contacts and asymptomatic carriers
erythromycin or penicillin
Vaccination diphtheria toxoid containing
vaccines

Establishment of an artificial airway and


resection of the pseudomembrane can be
lifesaving


Detox your life in 4 easy
steps: Get rid of anyone
who:

indolent, non-progressive infection


superficial, ecthymic, non-healing ulcer with a
gray-brown membrane
Difficult to distinguish from streptococcal or
staphylococcal impetigo; may coexist
Extremities often affected than the trunk or
head
Pain, tenderness, erythema, and exudate
Respiratory tract colonization or symptomatic
infection with toxic complications occurs in
minority


1. Lies to you.
2. Disrespects you.
3. Uses you.
4. Puts you down.

(A Simple Reminder)

administered on the basis of clinical diagnosis


neutralizes only free toxin efficacy
diminishes with elapsed time after the onset
of mucocutaneous symptoms
equine diphtheria antitoxin is available in the
USA only from the CDC

Only erythromycin or penicillin is recommended


for treatment
o
o

Kidney tubule necrosis,


Thrombocytopenia
Cardiomyopathy,
Demyelination

Diagnosis
Specimens for culture nose, throat,
mucocutaneous lesion
A portion of membrane should be removed and
submitted for culture along with underlying
exudate
Use selective medium for C. diphtheriae
Culture isolates of coryneform organisms should
be identified to the species level, and toxigenicity
and antimicrobial susceptibility tests should be
performed for C. diphtheriae isolates
Treatment
Specific antitoxin - mainstay of therapy
o
o

Cutaneous diphtheria
o
o

virulence of the organism -subspecies gravis


has the highest fatality rate
patient age
immunization status,
site of infection
speed of administration of the antitoxin

The degree of local extension correlates directly


with profound prostration, bull-neck appearance,
and fatality due to airway compromise or toxin-
mediated complication
Laryngeal diphtheria - significant risk for
suffocation
o

o
o
o
o

Pseudomembrane - dense adherent necrotic


coagulum of organisms, epithelial cells, fibrin,
leukocytes, and erythrocytes
Bleeding edematous submucosa
Paralysis of the palate and hypopharynx is an
early local effect of diphtheritic toxin.

Tonsillar and pharyngeal diphtheria


Sore throat - universal early symptom
50% have fever, fewer with dysphagia,
hoarseness, malaise, or headache
Underlying soft tissue edema and enlarged
lymph nodes bull-neck appearance

Depends on:
o

Clinical Manifestations
Respiratory tract diphtheria
o
o
o

Toxin absorption can lead to systemic


manifestations
o
o
o
o

Prognosis

Organism remains in the superficial layers of skin


lesions or respiratory tract mucosa local
inflammatory reaction
Polypeptide exotoxin - major virulence factor
which inhibits protein synthesis local tissue
necrosis

Not a substitute for antitoxin therapy


Elimination of the organism should be
documented by negative results of at least 2
successive cultures of specimens from the
nose and throat (or skin) obtained 24 hr apart
after completion of therapy
Repeat treatment with erythromycin if either
culture yields C. diphtheriae.