BACTERIAL INFECTIONS.pdf for derma residents

BACTERIAL INFECTIONS.pdf for derma residents

1. BACTERIAL
INFECTIONS
DR JYOSHMI EKKA

2. GRAM POSITIVE INFECTIONS ASSOCIATED
WITH TOXIN PRODUCTION:
•Caused by staph aureus and / or Group A streptococcus toxin
producing bacteria.
•Characteristic syndromes can be divided , depending upon the
predominant clinical presentation into:
❑predominantly cutaneous:
✓Local: bullous impetigo
✓Generalized : staphylococcus scalded skin syndrome

3. ❑Predominantly systemic
✓Generalized : toxic shock syndrome
staphylococcus (predominantly) or streptococcus
✓Scarlet fever: streptococcus (predominantly) or staphylococcus

4. BULLOUS IMPETIGO
•Caused by EXFOLIATIVE TOXINS producing Group
2 Staph aureus, mainly type II and phage type 71
without hematogenous dissemination.
•It’s a disease of children , although adult cases
can also occur.

5. •Early lesions: painless cloudy flaccid vesicle or
bullae surrounded by erythematous rim
•Late lesions: blisters rupture leaving behind moist
erosions and erythema
•Lesions are found around exposed parts of body
and around orifices.

6. •Diagnosis:clinical appearance.
•Blister fluid aspiration for gram stain: staph
aureus.
•Histopathology: intraepidermal cleavage
induced by toxin occurs within or just below
stratum granulosum.
inflammatory cells including neutrophils can
be visualized.
•Treatment: topical mupirocin ointment alone
and/or oral antibiotics.
•Prognosis : excellent

7. STAPHYLOCOCCAL SCALDED SKIN
SYNDROME
•Also k/o RITTER disease.
•SSSS is a generalized exanthematousdisease consisting of cutaneous
tenderness and widespread superficial blistering and denudation.
•Mainly seen in infants and children below the age of 5 years ,and
rarely in older children and adults.

8. ETIOLOGY AND PATHOGENESIS:
•Causative organisms: staph aureus group 2 phage
71 producing an exotoxin ( epidermolytictoxin ,
exfoliative toxin or epidermolysis).
•Staph reside in nasopharynx, conjunctiva , and
middle ear.

9. staph aureus
colonization or infection
production of exfoliative toxin A or B
Pre existing antibody Improper renal immunosuppression or
or proper renal excretion of ET excretion renal failure
No disease diseasein premature adult cases of
neonates and infants disease

10. •Exfoliative toxins are two serologically distinct proteins produced by
staph aureus.
•ETs( serine proteases) binds toDESMOGLEIN 1 loss of cell-
cell adhesion.
•Epidermolysis usually takes between stratum spinosum and
granulosum.
•This results in a very thin walled flaccid blister that is easily disrupted
exhibiting a positive nikolskysign.

12. CLINICAL FEATURES:
•Characterized by intensely erythematous
cutaneous eruptions following an URTI, or
purulent conjunctivitis.
•Initial site: face and proximal flexures but soon
process generalizes.
•Involvement of face, especially of paranasal
and perioral areas produces a distinctive facies.

13. •Presence of skin tenderness and positive
pseudo nikolskysign in early phase
followed by exfoliation in later phase.
•Painful erosions appear when
erythematous sheets of skin shrink and
shed (potato-chip desquamation).

14. •Cultures from intact blister are sterile, consistent with the
pathogenesis of a hematogenouslydisseminated toxin originating
from a distant focus of infection inducing the disease.
•Differential: TEN

15. CHARACTERISTICS SSSS TEN
Etiology S aureus group 2 phage 71 drugs
age Neonates and infants adults
Constitutional disturbancesmild severe
histopath Split in subcornealregion Epidermal necrosis
Mucous membrane Usually lips are involved Severe involvement
course Short ( 1-2 weeks) Long ( >2 weeks)
scarring absent Sometimes occur

16. characteristics SSSS TEN
Prognosis Good ( mortality 2-3 percent) Bad ( mortality 25-50 percent)
treatment Antistaphylococcalantibiotics Stop offending drug , IV Ig

17. •Treatment :
➢Hospitalization and iv antistaphylococcalantibiotics.
➢Suitable antibiotic + supportive therapy ( adequate hydration,
drainage of infective lesions) + management of potential fluid and
electrolyte abnormalities .
➢Neonates benefit from incubators to maintain body temperature and
humidity.
➢Topically mupirocin oinmentare effective.

18. •Complications: fluid and electrolyte disturbances
•Prognosis: mortality in uncomplicated pediatric SSSS is very low ( 2-3
percent).
adult mortality is higher as a result of concomitant morbidity factors
and sepsis .

19. TOXIC SHOCK SYNDROME:
•TSS is an inflammatory response characterized by fever ,
rash , hypotension and multiorgan involvement.
•It is superantigen mediated disease to be a/wtampon use
in mensturatingwomen.
•Presently occurrence of non menstrual form of TSS exceed
the menstrual form

20. •Etiology : toxins produced by either staph aureus or group A
streptococcus.
•Pathogenesis: colonization of infection by bacteria
production of toxins ( act as superantigen)
toxins absorbed systemically
massive release of cytokines, TNF, IL1 , IL6 ( cytokine storm)
capable of mediating shock and tissue injury and systemic
manifestation of TSS

21. •Predisposing factors:
influenza
sinusitis
tracheitis
intravenous drug use
HIV infection
cellulitis
burn wounds
allergic contact dermatitis
gynecologic infections
postpartum and postoperative sepsis

22. CLINICAL FINDINGS:
•STAPHYLOCOCCAL TSS:

23. STREPTOCOCCAL TSS:
•Caused by toxin producing Group A streptococci.
•Streptococcal pyrogenic exotoxin A (SPEA) .
•Very young and elderly individuals, diabetic and
immunocompromised are most susceptible.
•It has been a complications of wounds, varicella and influenza A.
•C/F is similar to TSS.

24. •Onset is usually as localized pain in extremities.
•The localized pain progresses to localized erythema and edema to
cellulitis a/wnecrotizing fasciitis and myocarditis with concomitant
streptococcal invasion of blolodstream.

25. DIFFERENTIAL DIAGNOSIS OF TOXIC SHOCK SYNDROME.
•Septic shock
•Staphylococcal exfoliative syndromes
•Rocky mountain spotted fever
•Viral hemorrhagic shock
•Measles
•Leptospirosis
•Steven johnsonsyndrome
•Kawasaki disease

26. DIAGNOSIS:
•No specific test can diagnose TSS.
•History taking
•Physical examination
•Blood culture
•Culture or throat secretion, vaginal culture
•RFT, LFT

27. MANAGEMENT:
•Assess BP , Temp, pulse, early signs and symptoms of shock.
•Rapid evaluation of condition of patient. Mechanical ventilation if
needed.
•Adequate hydration, vasopressors, antibiotics and drainage of
infective lesions.
•Topically mupirocin ointment and povidone iodine solutions are
effective.
•Antimicrobial coverage should be both for staphylococci and penicillin
resistant streptococci.
•Cephalosporin and macrolides such as erythromycin and clindamycin
are useful.
•Intravenous immunoglobulin is beneficial in STSS.

28. SCARLET FEVER:
•Syndrome characterized by exudative
pharyngitis, fever and rash.
•Causative organism : streptococcal pyogenes
( SPE-B, SPE-C)
•C/F: occurs shortly after an episode of
pharyngitis and is characterized by popular
erythematous sandpaper rash on trunk and
extremities accompanied by perioral pallor

29. •A linear petechial eruption ( pastia’s
line ) occurs in flexural areas.
•A white coating on tongue with
hypertrophied projecting papilla leads
to white strawberry tongue

30. THANKYOU