Staphylococcus aureus is a common cause of skin and soft tissue infections in pediatric patients. It can cause a variety of infections from mild to life-threatening. Newborns are especially at risk of developing serious infections due to immature immune systems. S. aureus produces virulence factors that help it evade the immune system and cause damage locally or systemically. Treatment depends on whether the strain is methicillin-resistant (MRSA) or methicillin-susceptible.

1. STAPHYLOCOCCAL
INFECTIONS IN PEDIATRICS
Dr. Hussein Ishak
Lecturer of Pediatrics – Al Azhar university

2. INTRODUCTION
• Staphylococci are hardy, aerobic, gram-positive bacteria that grow in
pairs and clusters and are ubiquitous as normal flora of humans and
present on fomites and in dust.
• They are resistant to heat and drying and may be recovered from non-
biologic environments weeks to months after contamination.

4. Strains are classified as
• (1) Staphylococcus aureus if they are coagulase positive or
• (2) coagulase-negative staphylococci (e.g., Staphylococcus epidermidis,
Staphylococcus saprophyticus, Staphylococcus haemolyticus ).
• S. aureus has many virulence factors that mediate various serious diseases,
whereas coagulase-negative staphylococci tend to be less pathogenic unless an
indwelling foreign body (e.g., intravascular catheter) is present.
• S. aureus strains resistant to β-lactam antibiotics, typically referred to as
methicillin-resistant Staphylococcus aureus (MRSA) , have become a
significant problem in both community and hospital settings.

5. Strains are classified as
• Staph infections can be either methicillin-resistant staph (MRSA) or methicillin-
susceptible staph (MSSA).
• MSSA infections are usually treatable with antibiotics.
• However, MRSA infections are resistant to antibiotics.
• Many staph infections are mild, but they can also be serious and life-threatening.
• S. aureus strains resistant to β-lactam antibiotics, typically referred to as methicillin-
resistant Staphylococcus aureus (MRSA) , have become a significant problem in both
community and hospital settings.
Methicillin was the first semisynthetic penicillinase-resistant penicillin.
It is a narrow-spectrum β-lactam antibiotic of the penicillin class.

6. Staphylococcus aureus
• Staph. aureus is the most common cause of pyogenic infection of the skin and
soft tissues.
• Bacteremia (primary and secondary) is common and can be associated with or
can result in osteomyelitis, suppurative arthritis, pyomyositis, deep abscesses,
pneumonia, empyema, endocarditis, pericarditis, and rarely meningitis.
• Toxin-mediated diseases , including food poisoning, staphylococcal scarlet fever,
scalded skin syndrome, and toxic shock syndrome (TSS), are caused by certain S.
aureus strains.

8. Etiology (virulence factors)
• Strains of S. aureus can be identified and characterized by the
virulence factors they produce.
• These factors tend to play 1 or more of 4 pathogenic roles in human
disease:
1. S. aureus protecting the organism from host defenses,
2. localizing infection,
3. causing local tissue damage, and
4. affecting noninfected sites through toxin elaboration.

10. Relationship of virulence factors and diseases associated with Staphylococcus aureus.
TSST-1, toxic shock syndrome toxin-1.

11. • Many strains of S. aureus release 1 or more exotoxins.
• Exfoliatins A and B are serologically distinct proteins that produce
localized (bullous impetigo) or generalized (scalded skin syndrome,
staphylococcal scarlet fever) dermatologic manifestations.
Staph. Toxins:

12. Staph. Toxins:
• S. aureus can produce >20 distinct enterotoxins (types A-V).
• Ingestion of preformed enterotoxin, particularly types A or B, can
result in food poisoning, resulting in vomiting and diarrhea and, in
some cases, profound hypotension.
• Toxic shock syndrome toxin-1 (TSST-1) is associated with toxic shock
syndrome (TSS).

13. Epidemiology
• Approximately 20–40% of normal individuals carry at least 1 strain of
S. aureus in the anterior nares at any given time.
• The organisms may be transmitted from the nose to the skin, where
colonization is more transient.
• Many neonates are colonized within the 1st week of life, usually by a
maternal strain.

14. Epidemiology
• Exposure to S. aureus generally occurs by autoinoculation or direct
contact with the hands of other colonized individuals.
• Outside the hospital setting, outbreaks of staphylococcal disease, in
particular disease caused by methicillin-resistant strains, have been
reported among athletes, military personnel, young children,
veterinarians, injection drug users, and inmates in correctional
facilities.
• Skin infections caused by S. aureus are considerably more prevalent
among persons living in low socioeconomic circumstances and
particularly among those in tropical climates.

15. Clinical Manifestations
• Signs and symptoms vary with the location of the infection, which is
usually the skin but may be any tissue.
• Disease states of various degrees of severity are generally a result of
local suppuration, systemic dissemination with metastatic infection,
or systemic effects of toxin production.

16. • S. aureus is an important cause of neonatal infections.
• Coagulase-negative staphylococci (CoNS) are the bacteria most frequently
recovered from blood cultures in neonates.
• Risk Factors for Neonatal Staph Infection:
1. Prematurity
2. Very low birth weight
3. Lengthy hospital stays
4. Invasive procedures
5. Use of venous catheters
Clinical Manifestations in Newborn

17. Signs of Neonatal Staph Infection
• Common signs of neonatal Staph infection include:
1. Hypothermia or hyperthermia
2. Tachycardia or bradycardia
3. Lethargy and irritability
4. Vomiting
5. Skin lesions
Untreated Neonatal Staph Infection leads to Sepsis and Meningitis.

18. Case:
• A 10-day-old male newborn was admitted to our unit with irritability,
poor feeding, and maculopapular lesions, but without fever. The skin
lesions were 10–15 in number, characterized by honey-colored crusts,
and distributed over the face, sparing the trunk, extremities, palms,
and soles. The mother reported that in the previous two days, the
maculopapular lesions transited into small vesicles and blisters that
rapidly ruptured, leaving erosions covered by honey-colored crusts.

20. • In term neonates, the most frequent hospital-acquired infection
is Skin infection due to Staphylococcus aureus (both methicillin-
sensitive and methicillin-resistant)
• In very-low-birth-weight (VLBW; < 1500 g) infants, gram-positive
organisms cause about 70% of infections, the majority being with
coagulase-negative staphylococci.
• Infection is facilitated by the multiple invasive procedures VLBW
infants undergo.
• The longer the stay in special care nurseries and the more
procedures done, the higher is the likelihood of infection.

21. Case of SSSS in a neonate, with diffuse erythema and skin exfoliation at the level of
the cubital fold and fluid-filled blisters that are thin-walled and easily ruptured.

22. A case of a neonate with severe Junctional Epidermolysis bullosa (A), with
Staphylococcal skin infection of the left leg (B) and the left hand (C).

23. • Case of burns in a neonate with overlapped Staphylococcal infection: the skin of
more than half of the body was initially injured (A), with the second to fourth
toes that appeared necrotic (B). Wounds healed after 38 days of therapy, with
serious scars at six months of life requiring numerous plastic surgical
interventions (C,D).

24. • Although we obtain blood cultures in preterm, low birth weight
neonates with localized pustulosis, if blood cultures were not
obtained, a five- to seven-day course of parenteral therapy is
reasonable, provided that the infant continues to be clinically well
and the pustulosis is completely resolved.
• We hospitalize neonates with skin and soft tissue infection (SSTI)
more severe than localized pustulosis (eg, multiple sites of pustulosis,
mastitis and other sites of cellulitis, abscess) for close monitoring and
parenteral antimicrobial therapy.
• In addition to provision of parenteral antimicrobial therapy, we
recommend drainage of purulent or fluctuant lesions (eg, cutaneous
abscess).
• The total duration of therapy for staphylococcal or streptococcal SSTI
confined to the skin and soft tissues in neonates depends upon
clinical response; a total of 7 to 14 days is usually adequate if there
are no complications

25. Suggested approach to initial antimicrobial therapy for suspected Staphylococcus aureus or
streptococcal skin and soft tissue infections in infants ≤28 days of age.
SSTI: skin and soft tissue infection.

28. NO

30. Skin
• S. aureus is an important cause of pyogenic skin infections:impetigo contagiosa,
folliculitis, hydradenitis, furuncles, carbuncles, and paronychia.
• Toxigenic infection with skin manifestations include staphylococcal scalded skin
syndrome and staphylococcal scarlet fever.
• S. aureus is a frequent cause of superinfection of underlying dermatologic conditions,
such as eczema or bug bites.
• Recurrent skin and soft tissue infections often are noted with community-associated
MRSA and affect the lower extremities and buttocks.
• S. aureus is also an important cause of traumatic and surgical wound infections and can
cause deep soft tissue involvement, including cellulitis and rarely, necrotizing fasciitis.

31. Staphylococcal Scalded Skin Syndrome (Ritter disease )
• It is a disease characterized by denudation of the skin caused by
exotoxin producing strains of the Staphylococcus species, typically
from a distant site. It usually presents 48 hours after birth and is rare
in children older than six years.

32. 1- Fever: Temperature ≥38.9°C (102.0°F)
2- Hypotension: Systolic blood pressure less than 5th percentile by age for children <16 years of age.
3- Rash
• Diffuse macular erythroderma
• Desquamation
• 1 to 2 weeks after onset of illness, particularly involving palms and soles
4- Multisystem involvement (3 or more of the following organ systems)
A. Gastrointestinal: Vomiting or diarrhea at onset of illness
B. Muscular: Severe myalgia or creatine phosphokinase elevation >2 times the upper limit of normal
C. Mucous membranes: Vaginal, oropharyngeal, or conjunctival hyperemia
D. Renal: BUN or serum creatinine >2 times the upper limit of normal or pyuria (>5 white blood count/high power
field) in the absence of UTI.
E. Hepatic: Bilirubin or transaminases >2 times the upper limit of normal
F. Hematologic: Platelets <100,000/microL
G. CNS: Disorientation or alterations in consciousness without focal neurologic signs in the absence of fever and
hypotension
H. Negative results on the following tests, if obtained:
Blood or cerebrospinal fluid cultures for another pathogen (blood cultures may be positive for Staph. aureus)
Serologic tests for Rocky Mountain spotted fever, leptospirosis, or measles

33. • Criteria for a confirmed case include a patient with fever ≥38.9°C,
hypotension, diffuse erythroderm, desquamation (unless the patient
dies before desquamation can occur), and involvement of at least
three organ systems.
• A probable case is a patient who is missing one of the characteristics
of the confirmed case definition.
Staphylococcal Scalded Skin Syndrome (Ritter disease )

34. Respiratory Tract
• Infections of the upper respiratory tract (otitis media, sinusitis).
• Suppurative parotitis is a rare infection, but S. aureus is a common cause.
• A membranous tracheitis that complicates viral croup may result from infection with S. aureus,
although other organisms may also be responsible.
• Pneumonia caused by S. aureus may be primary or secondary after a viral infection such as
influenza.
• S. aureus often causes a necrotizing pneumonitis that may be associated with early development
of empyema, pneumatoceles, pyopneumothorax, and bronchopleural fistulas.
• Chronic pulmonary infection with S. aureus contributes to progressive pulmonary dysfunction in
children with cystic fibrosis.

36. • Pneumatocele formation. A, A 5 yr old child with Staphylococcus aureus pneumonia initially demonstrated
consolidation of the right middle and lower zones. B, Seven days later, multiple lucent areas are noted as
pneumatoceles develop. C, Two weeks later, significant resolution is evident, with a rather thick-walled
pneumatocele persisting in the right midzone associated with significant residual pleural thickening.

37. Muscle, Bones and Joints
• Localized staphylococcal abscesses in muscle sometimes without
septicemia have been called pyomyositis. This disorder is reported
most frequently from tropical areas and is termed tropical
pyomyositis.
• Multiple abscesses occur in 30–40% of cases.
• History may include prior trauma at the site of the abscess.
• Surgical drainage and appropriate antibiotic therapy are essential.
• S. aureus is the most common cause of osteomyelitis and
suppurative arthritis in children.

38. Central Nervous System
• Meningitis caused by S. aureus is uncommon; it is associated
with penetrating cranial trauma and neurosurgical
procedures (craniotomy, CSF shunt placement), and less
frequently with endocarditis, parameningeal foci (epidural or
brain abscess), complicated sinusitis, DM, or malignancy.
• The CSF profile of S. aureus meningitis is indistinguishable
from that in other forms of bacterial meningitis.

39. CVS:
• S. aureus is a common cause of acute endocarditis on native valves
and results in high rates of morbidity and mortality.
• Perforation of heart valves, myocardial abscesses, heart failure,
conduction disturbances, acute hemopericardium, purulent
pericarditis, and sudden death may ensue.

40. Renal:
1. S. aureus is a common cause of renal and perinephric abscess,
usually of hematogenous origin.
2. Pyelonephritis and cystitis caused by S. aureus are unusual.

41. GIT:
• Staphylococcal enterocolitis may rarely follow overgrowth of normal
bowel flora by S. aureus, which can result from broad-spectrum oral
antibiotic therapy.
• Diarrhea is associated with blood and mucus.
• Peritonitis associated with S.aureus in patients receiving long-term
ambulatory peritoneal dialysis usually involves the catheter tunnel.

42. Food poisoning
• It may be caused by ingestion of preformed enterotoxins produced by
staphylococci in contaminated foods.
• The source of contamination is often colonized or infected food workers.
• Approximately 2-7 hr after ingestion of the toxin, sudden, severe vomiting
begins, watery diarrhea may develop, but fever is absent or low.
• Symptoms rarely persist >12-24 hr.
• Rarely, shock and death may occur.

43. Differential Diagnosis
• Skin lesions caused by S. aureus may be indistinguishable from those
caused by group A streptococci, although the former usually expand
slowly, while the latter are prone to spread more rapidly and can be
very aggressive.

44. Differential Diagnosis
• Fluctuant skin and soft tissue lesions also can be caused by other
organisms, including Mycobacterium tuberculosis, atypical
mycobacteria, Bartonella henselae (cat-scratch disease), Francisella
tularensis, and various fungi.

45. Differential Diagnosis
• S. aureus pneumonia is often suspected in very ill-appearing children
or after failure to improve with standard treatment that does not
cover Staphylococcus, or on the basis of chest radiographs that reveal
pneumatoceles, pyopneumothorax, or lung abscess.
• Other etiologies of cavitary pneumonias include Klebsiella
pneumoniae and M. tuberculosis.

46. Differential Diagnosis
• In bone and joint infections, culture is the only reliable way to
differentiate S. aureus from other, less common etiologies, including
group A streptococci and in young children, Kingella kingae.

47. Diagnosis
• Gram stain, culture, and susceptibility testing of purulent material.
• The diagnosis of S. aureus infection depends on isolation of the
organism in culture from non-permissive sites, such as cellulitis
aspirates, abscess cavities, blood, bone, or joint aspirates, or other
sites of infection.
• Swab cultures of surfaces are not as useful, because they may reflect
surface contamination rather than the true cause of infection.
• Tissue samples or fluid aspirates in a syringe provide the best culture
material.

48. Diagnosis
• Cellulitic lesions may be cultured using a needle aspirate from the
most inflamed area after thorough skin cleansing.
• Isolation from the nose or skin does not necessarily imply causation
because these sites may be normally colonized sites.
• It is important to obtain a culture of any potential focus of infection as
well as a blood culture before starting antibiotic treatment.

49. Diagnosis
• After isolation, identification is made on the basis of Gram stain and
coagulase, clumping factor, and protein A reactivity.

50. Diagnosis
• Increasingly, molecular techniques such as PCR are used to supplement
traditional culture methods.
• Automated PCR systems may allow rapid species identification from positive
blood cultures and simultaneously identify genetic patterns associated with
methicillin resistance, such as expression of the MECA gene produced by MRSA.
• PCR-based determination of MRSA nasal colonization on admission to hospitals or
ICUs aids infection control procedures and identify patients at higher risk of
infection.

51. Diagnosis
• Diagnosis of S. aureus food poisoning is usually made on the basis of
epidemiologic and clinical findings.
• Food suspected of contamination may be cultured and can be tested
for enterotoxin

52. Treatment
1. Loculated collections of purulent material (abscesses) should be
relieved by incision and drainage.
2. Foreign bodies should be removed, if possible.
3. Therapy always should be initiated with an antibiotic consistent
with the local staphylococcal susceptibility patterns as well as the
severity of infection.

53. Treatment
• IV treatment is recommended until the patient has become afebrile and
other signs of infection have improved.
• Oral therapy is often continued for a time, especially in patients with
chronic infection or underlying host defense problems.
• Serious S. aureus infections, with or without abscesses, tend to persist and
recur, necessitating prolonged therapy.
• Initial treatment for serious infections thought to be caused by methicillin-
susceptible S. aureus (MSSA) should include semisynthetic penicillin (e.g.,
nafcillin) or a first-generation cephalosporin (e.g., cefazolin).

54. • For initial treatment for penicillin-allergic individuals and those with
suspected serious infections caused by MRSA, vancomycin is the
preferred therapy.
• Serum levels of vancomycin should be monitored, with serum trough
concentrations of 10-20 μg/mL, depending on the location and
severity of infection.

55. • For critically ill patients with suspected S. aureus, empirical therapy
with both vancomycin and nafcillin should be considered until
cultures results are available.

56. • Initial treatment with IV clindamycin, followed by a transition to oral
clindamycin, has been effective in bone, joint, and soft tissue
infection; however, not all strains of MSSA or MRSA are susceptible to
clindamycin.
• Clindamycin is bacteriostatic and should not be used to treat
endocarditis, persistent bacteremia, or CNS infections caused by S.
aureus.

57. • Linezolid and daptomycin are useful for serious S. aureus infections,
particularly those caused by MRSA, when treatment with vancomycin
is ineffective or not tolerated.

58. • Rifampin or gentamicin may be added to a β-lactam or vancomycin
for synergy in serious infections such as endocarditis, particularly
when prosthetic valve material is involved.

59. Oral Antibiotics
• In many infections, oral antimicrobials may be substituted to
complete the course of treatment, after an initial period of parenteral
therapy and determination of antimicrobial susceptibilities, or can be
used as initial treatment in less severe infections.

60. Oral Antibiotics
• Dicloxacillin (50-100 mg/kg/24 hr. divided 4 times daily PO) and
cephalexin (25-100 mg/kg/24 hr. divided 3-4 times daily PO) are
absorbed well orally and are effective against MSSA.
• Amoxicillin clavulanate (40-80 mg amoxicillin/kg/24 hr. divided 3
times daily PO) is also effective when a broader spectrum of coverage
is required.

61. Oral Antibiotics
• Clindamycin (30-40mg/kg/24 hr divided 3-4 times daily PO) is highly
absorbed from the intestinal tract and is frequently used for empirical
coverage when both MRSA and MSSA are possible, as well as for
susceptible MRSA infections or for MSSA in penicillin/cephalosporin-
allergic patients.

62. Oral Antibiotics
• Ciprofloxacin and other quinolone antibiotics should not be used in
serious staphylococcal infections, because their use is associated with
rapid development of resistance.
• Penicillin and ampicillin are not appropriate, because >90% of all
staphylococci isolated are resistant to these agents. Addition of a β-
lactamase inhibitor (clavulanic acid, sulbactam, tazobactam) to a
penicillin-based drug also confers antistaphylococcal activity but has
no effect on MRSA.
• Antistaphylococcal penicillins and most cephalosporins do not
provide activity against MRSA.

65. Prognosis
• Untreated S. aureus septicemia is associated with a high fatality
rate, which has been reduced significantly by appropriate
antibiotic treatment.
• S. aureus pneumonia can be fatal at any age but is more likely to
be associated with high morbidity and mortality in young infants
or in patients whose therapy has been delayed.
• Prognosis is influenced by numerous host factors, including
nutrition, immunologic competence, and the presence or absence
of other debilitating diseases.
• In most cases with abscess formation, surgical drainage is
necessary.

66. Prevention
• 1- Hand hygiene is the most effective measure for preventing the
spread of staphylococci from between individuals.
• Use of a hand wash containing chlorhexidine or alcohol is
recommended.

67. Prevention
• 2- In hospitals, all persons with acute S. aureus infections should be
isolated until they have been treated adequately.
There should be constant surveillance for nosocomial S. aureus
infections within hospitals.
When MRSA is recovered, strict isolation of affected patients has
been shown to be the most effective method for preventing
nosocomial spread of infection.

68. Prevention
• 3- Because of the potential severity of infections with S. aureus and
concerns about emerging resistance, much work has focused on
developing a staphylococcal vaccine for use in high-risk patients, but
to date, clinical trials have been disappointing.

69. Prevention
• 4- Food poisoning may be prevented by excluding individuals with S.
aureus infections of the skin from the preparation and handling of
food.
Prepared foods should be eaten immediately or refrigerated
appropriately to prevent multiplication of S. aureus that may have
contaminated the food.