Staphylococcal infections

Bacteriology
1. Staphylococci are hardy, aerobic, gram-positive
bacteria that grow in pairs and clusters

2. Ubiquitous as normal flora of humans

3. Bacteriological culture of the nose and skin of normal

humans invariably yields staphylococci.

4. Present on fomites and in dust

 Classification
1. Coagulase positive: staphylococcus aureus;
more virulent
2. Coagulase-negative: less pathogenic;
infection of indwelling foreign body like
(intravascular catheter)
1. S. Epidermidis,
2. S. Saprophyticus,
3. S. Haemolyticus
 Viurlance of S.aureus

1. Staphylococcus aureus is coagulase positive and

has many virulence factors that mediate various
serious diseases.
2. Production of coagulase and/or clumping factor
interfering with effective phagocytosis.
3. Coagulase causes plasma to clot by interacting
with fibrinogen; this may have an important role
in localization of infection (abscess formation).
4. Coagulase positive Staphylococci produce
abscess formation
 S.Aureus
virulance factors
1. Panton-Valentine leukocidin (PVL) is an exotoxin causes leukocyte
destruction and tissue necrosis
2. Protein A, can absorb serum immunoglobulins, preventing
antibacterial antibodies from acting as opsonins and thus inhibiting
phagocytosis.
3. polysaccharide capsule, or slime layer, which may interfere with
opsonophagocytosis.
4. Catalase: inactivates hydrogen peroxide, promoting intracellular
survival of pathogens.
5. α toxin and β-hemolysin that cause local tissue destruction.
6. They produce B-lactamase which inactivates most penicillins
7. Methycillin resistant staphylococcus aureus (MRSA) are becoming
more prevalent
8. S. aureus is an important pathogen of pneumonia in patients with
cystic fibrosis
 Staphylococcus aureus
1. Superficial: impetigo, furuncles (boils), cellulitis,
abscess, lymphadenitis, paronychia, omphalitis, and
wound infection.
2. Deep: Bacteremia (primary and secondary) ,
osteomyelitis, suppurative arthritis, pneumonia,
empyema, endocarditis, pyomyositis, pericarditis, and
rarely meningitis.
3. Toxin-mediated: food poisoning, staphylococcal scarlet
fever, scalded skin syndrome, and toxic shock
syndrome (TSS) .
 Virulence factors
1. surface proteins that promote colonization of host tissues;
2. invasins that promote bacterial spread in tissues (leukocidin,
kinases, hyaluronidase);
3. surface factors that inhibit phagocytic engulfment (capsule,
Protein A);
4. biochemical properties that enhance their survival in
phagocytes (carotenoids, catalase production);
5. immunological disguises (Protein A, coagulase); and
6. membrane-damaging toxins that lyse eucaryotic cell
membranes (hemolysins, leukotoxin, leukocidin;
7. exotoxins that damage host tissues or otherwise provoke
symptoms of disease (SEA-G, TSST, ET
8. inherent and acquired resistance to antimicrobial agents.
 EPIDEMIOLOGY.
1. Neonates are colonized within the 1st week of life;
2. 20–30% of normal individuals carry at least 1 strain
of S. Aureus in the anterior nares at any given time.
3. The organisms may be transmitted from the nose to
the skin, where colonization can occur
4. Persistent umbilical, vaginal, and perianal carriage
occurs
5. Inoculation by auto-inoculation or direct contact
with the hands of other colonized individuals.
6. Invasive disease may follow colonization
Pathogenesis
 PATHOGENESIS.
1. Defects in the mucocutaneous barriers: trauma, surgery,
foreign surfaces (sutures, shunts, intravascular catheters),
and burns
2. Congenital or acquired defects in chemotaxis: Job, Chédiak-
Higashi, Wiskott-Aldrich syndromes),
3. defective phagocytosis and killing (neutropenia, chronic
granulomatous disease), and
4. defective humoral immunity (antibodies required for
opsonization) increase the risk for staphylococcal infections.
5. Impaired mobilization of polymorphonuclear leukocytes :
diabetic ketoacidosis ; after ingesting alcohol.
6. HIV : neutrophils are defective in their ability to kill S. aureus
 NB
• The most common source of postnatal
infections in hospitalized newborns is hand
contamination of health care personnel.
• Coagulase-negative staphylococci are the
most frequent neonatal nosocomial
pathogens.
 Skin
• Pyogenic skin infections, including impetigo
contagiosa, ecthyma, bullous impetigo, folliculitis,
hydradenitis, furuncles, carbuncles,
staphylococcal scalded skin syndrome, and
staphylococcal scarlet fever
• Superinfection of other noninfectious skin
disease (eczema)
 Features of Staph Pneumonia
1. Hematogenous pneumonia may be secondary to
septic emboli, right-sided endocarditis, or the
presence of intravascular devices.
2. Inhalation pneumonia is caused by alterations of
mucociliary clearance, leukocyte dysfunction, or
bacterial adherence initiated by a viral infection.
3. can occur both as community acquired and
hospital acquired infections and also ventilator
associated pneumonia (CAP, HAP and VAP)
 Clinical features
Infants:
1. abdominal distention, high fever, respiratory
distress, and toxemia.
2. occurs without predisposing factors or after
minor skin infections.
3. The organism is necrotizing, producing
bronchoalveolar destruction.
4. Pneumatoceles, pyopneumothorax, and
empyema are frequently encountered.
5. Rapid progression of disease is characteristic
 Older children
1. More common are high fever, abdominal pain,
tachypnea, dyspnea, and localized or diffuse
bronchopneumonia or lobar disease.
2. S. aureus often causes a necrotizing
pneumonitis;
3. Empyema, pneumatoceles, pyopneumothorax,
and bronchopleural fistulas develop frequently.
 Symptoms:

1. Starts as upper respiratory catarrh

2. Fever
3. Chills
4. Restlessness
5. Delirium
6. Pleuritic pain
 Signs
1. Tachypnoea
2. Grunt
3. Cyanosis
4. Chest retraction
5. Working of accessory muscles of respiration
6. Crackles and wheeze;
7. bronchial breathing
 Complications
1. Pneumatocoel formation
2. Pyopneumothorax
3. Bronchopulmonary fistulas
4. Lung abscess
5. Septicemia
6. Meningitis
7. Osteomyelitis
8. Metastasis
9. Empyema
10. pyopericardium
11. Death due to sepsis;
12. Resp.failure
 Diagnosis
• Staphylococcal pneumonia can be suspected on
the basis of chest roentgenograms that may
reveal pneumatoceles, pyopneumothorax, or
lung abscess.
• Indirect evidence:
– Skin abscess or cellulitis
– Skin pustules
 Treatment:
1. Antibiotic choice is decided by culture -
sensitivity patterns
2. Drugs: Empiric therapy
Community acquired staph pneumonia:
1. Co Trimoxazole: 8-12 (TMP) mg/kg/day
2. Clindamycin: 20-30 mg/kg/day
 Methicillin sensitive Staph aureus:
1. Penicillinase resistant antibiotics such as:
1. Oxacillin } 100-150 mg /kg/day/IV in 4
divided doses
2. Nafcillin }
3. Methicillin: 200-300 mg /kg/day/IV in 4
divided doses
2. Cephalosporins:
1. Cefazolin: 100-150 mg /kg/day/IV in 4
divided doses
2. Cephalexin: 50-100 mg /kg/day/orally in 4
divided doses
For methicillin resistant staph. aureus:
1. Vancomycin: 40 mg mg /kg/day/IV in 4 divided
doses
2. Linozolid is a recent drug
3. Rifampin may be added to vancomycin tharpy
Othyer measures:
1. Inter costal drainage of empyema
2. Fresh blood transfusion
 TOXIC SHOCK SYNDROME
1. TSS is caused by TSST-1-producing strains of S.
aureus, which may colonize the vagina or cause focal
sites of staphylococcal infection.
2. During mass vaccination with multi dose measles
vaccine; Staph.aureus contamination is possible due
to lack of specific preservative and TSS has been
reported in India as a complication of measles vaccine
3. Nonmenstrual TSS has occurred with S. aureus
infection of nasal packing or infections including
wound infections, sinusitis, tracheitis, pneumonia,
empyema, abscesses, burns, osteomyelitis, and
primary bacteremia.
 PATHOGENESIS
• S. Aureus strains produce a number of
extracellular toxins,
• TSST-1, which acts as a superantigen causing
causes massive loss of fluid from the
intravascular space directly or after
production of interleukin 1 and tumor
necrosis factor
 CLINICAL MANIFESTATIONS
• The onset is abrupt, with high fever, vomiting,
and diarrhea, and is accompanied by sore
throat, headache, and myalgias.
• diffuse erythematous macular rash
• strawberry tongue
• alterations in the level of consciousness,
oliguria, and hypotension, which in severe
cases may progress to shock and disseminated
intravascular coagulation
• Complications, include acute respiratory
distress syndrome, myocardial dysfunction,
and renal failure
• Recovery occurs within 7–10 days and is
associated with desquamation, particularly of
palms and soles
 DIAGNOSIS
• There is no specific laboratory test
• Bacterial cultures of the associated focus
(vagina, abscess) usually yield S. aureus,
although this is not a required element of the
definition
 Differential Diagnosis
• Group A streptococcus can cause a similar
TSS-like illness
• Kawasaki disease closely resembles TSS
clinically
• Scarlet fever
• Toxic epidermal necrolysis
 TREATMENT
• Nafcillin
• Cephalosporin
• Vancomycin
• Clindamycin
• Fluid replacement
• Inotropic agents
• Removal of any retained tampons
 STAPHYLOCOCCAL SCALDED SKIN SYNDROME
(RITTER DISEASE)
• caused predominantly by phage group 2
staphylococci
• staphylococcal epidermolytic or exfoliative
toxins A or B
• Foci of infection include the nasopharynx and,
less commonly, the umbilicus
• most common in infants and young children
 Clinical manifestation
• Localized bullous impetigo to generalized cutaneous
involvement with systemic illness
• The conjunctivae are inflamed and may become purulent
• Circumoral erythema
• Erythematous skin with sterile, flaccid blisters and
erosions
• Areas of epidermis may separate in response to gentle
shear force (nikolsky sign)
• Healing occurs without scarring in 10-14 days
Nikolsky sign.
 Differential Diagnosis
1. streptococcal scarlet fever: strawberry
tongue and palatal petechiae are absent
2. epidermolysis bullosa
3. drug eruption
4. erythema multiforme
5. drug-induced toxic epidermal necrolysis
 Treatment
1. Systemic therapy, given either orally or parenterally
with a semisynthetic penicillinase-resistant penicillin,
2. Clindamycin will inhibit bacterial protein (toxin)
synthesis.
3. The skin should be gently moistened and cleansed.
4. Application of an emollient provides lubrication and
decreases discomfort.
5. Topical antibiotics are unnecessary.
6. Recovery is usually rapid,
7. Complications: fluid loss, electrolyte imbalance, faulty
temperature regulation, pneumonia, septicemia, and
cellulitis
 Impetigo
• 2 classic forms of impetigo: nonbullous and bullous.
• GABHS and Staphylococcus aureus are the predominant
organism of nonbullous impetigo
• Staphylococci generally spread from the nose to normal
skin and then infect the skin
• Bullous impetigo is always caused by S. aureus strains
that produce exfoliative toxins which blister the
superficial epidermis by hydrolyzing human desmoglein
1, resulting in a subcorneal vesicle
 Nonbullous Impetigo
• Nonbullous impetigo accounts for > 70% of
cases.
• Lesions typically begin on the skin of the face or
on extremities that have been traumatized.
• Predisposing causes:
1. Insect bites,
2. Abrasions,
3. Lacerations,
4. Chickenpox,
5. Scabies
6. Pediculosis, and
7. Burns.
Miliaria
IBA
 Bullous Impetigo
• mainly an infection of infants and young
children
• bullous impetigo are a manifestation of
localized staphylococcal scalded skin syndrome
• Neonatal bullous impetigo can begin in the
diaper area
Bullous impetigo
 Differential diagnosis of bullous impetigo

• In neonates includes epidermolysis bullosa,

bullous mastocytosis, herpetic infection, and
early scalded skin syndrome.
• In older children, allergic contact dermatitis,
burns, erythema multiforme, linear
immunoglobulin (Ig) A dermatosis,
pemphigus, and bullous pemphigoid
 Complications
1. Osteomyelitis, septic arthritis, pneumonia, and
septicemia and Cellulitis
2. Lymphangitis, suppurative lymphadenitis,
3. Scarlet fever
4. Acute poststreptococcal glomerulonephritis
5. Acute rheumatic fever does not occur as a
result of impetigo
 Treatment
1. Topical therapy with mupirocin 2%, fusidic
acid, and retapamulin 1% is acceptable for
localized disease.
2. Cephalexin, 25-50 mg/kg/day for 7 days in
two divided doses, is an excellent choice
3. Appropriate drugs for MRSA