how to manage a case of recurrent skin abscesses

1. An approach to the patientAn approach to the patient
with recurrent superficialwith recurrent superficial
abscessesabscesses
Fawzeia abo ali
Ain shams faculty of medicine

2. INTRODUCTION
1. Recurrent mucocutaneous infection is a
common clinical problem.
2. S. aureus and the typical pathological
finding inabscess formation.
3. Leucocytes are the primary host defence
against S. aureus
4. Patients with quantitative or
qualitative defects in leucocyte function
are therefore at increased risk of staph.
disease .
a) Secondary
b) primary

3. Activity Mechanism
Adherence to host tissue
Tissue Destruction
Disruption of Host
Defense
Impaired Chemotaxis
Phagocyte Destruction
Impaired Opsonization
Impaired Intracellular
Killing
Staphylococcus aureus virulence
determinants

4. Immunodeficiency should be suspected
when recurrent infections are :

5. General considerations:
• Recurrent abscess formation in the same anatomic
location often arises from a local defect.
• Multiple or recurrent abscesses in a variety of
locations may be the result of autoinoculation in the
setting of drug abuse ("skin-popping") or
Munchausen syndrome
• Most patients who experience recurrent cutaneous
abscesses respond to treatment of staph.
eradications
• Don”t miss a treatable even uncommon diagnosis,
but don”t subject patients to the expense &
unnecessary investigations

6. History:
• Age at onset
• Other infections
• Family history
• Certain features
• Staph carrier
• Risk factor
• Secondary causes of impaired
neutrophil function

8. Common conditions associated
with recurrent skin abssesses
1. Staph carrier
2. Secondary conditions associated
with neutrophil dysfunction:
• Diabetes mellitus
• Hidradenitis suppurativa
• IBD
3. Primary neutrophil function defect.

9. Other Risk Factors :
• Injection drug use
• Chronic dermatologic conditions (e.g.,
eczema)
• Recent use of antimicrobial agents
• African-American race
• Previous SSTI
• Close contact with an SSTI patient
• Participation in contact sports
• Military personnel
• Prisoners

10. Management:

11. Diabetes mellitus
• Diabetes impairs several aspects of host
defence, the prevalence of infection
correlating with glycaemic control.
• Polymorphs show functional alterations
in chemotaxis and phagocytosis ,with
reduced chemotaxis most marked when
glycaemic control is poor.
• The killing activity of polymorphs is also
depressed by hyperglycaemia.

12. High colonization rates are found in patients
with DM, intravenous drug users, patients on
haemodialysis and surgery.
Staphylococcal carriage

13. Treatment of cutaneous staphylococcal carriage:
5-day decolonization regime
1. Mupirocin nasal ointment three times daily
2. Daily treatment of the skin and hair with an
octenidin-based wash solution
3. Daily disinfection of personal items
4. Hand disinfection after application of the nasal
ointment
5. Antiseptic treatment of the throat with 0·1%
chlorhexidine gargle tid
6. Daily changing and washing (at a temperature
of at least 60 degrees) of clothing

15. Hidradenitis suppurativa
Hidradenitis suppurativa is a common disorder
of the apocrine gland-bearing follicular epithelium, affecting
the axilla, perineum and groin, with a prevalence of up to
4·1%.
It usually develops in healthy post-pubertal individuals.
A recent study reported a reduction in natural killer cells
and a lower monocyte response to bacterial components
in patients with HS
 A genetic predisposition is likely, 26% of patients .
Risk factors include diabetes and smoking. Obesity,tight
clothing, poor hygiene, deodorant and chemical depilation,
although not causal, may aggravate HS,
Diagnosis is largely clinical. Medical treatment includes
early antibiotics, topical antiseptics and compresses.

16. Antimicrobi
al Agent
Recommended
Dose Range
(Oral)
Comments
Clindamycin 30–40 mg/kg/day
divided q6–8h
•Excellent bioavailability
•Noxious smell and taste of oral
suspension
Trimethoprim
-
Sulfamethox
azole
10–20 mg/kg/day
divided q12h
•Very low resistance rates
•Clinical data confirm effectiveness
•May have reduced activity
against S. pyogenes, though data
are not clear
Doxycycline 2.2 mg/kg/day
divided q12h
•Very low resistance rates
•Inappropriate for children <8
years of age
•Photosensitivity
Linezolid 30 mg/kg/day
divided q8h
•High susceptibility rates
•Excellent bioavailability
•Expensive, compared to other
agents

17. PRIMARY IMMUNE DEFICIENCIES ASSOCIATED
WITH RECURRENT SUPERFICIAL INFECTION
• Pediatric onset.
• Other infections
• Certain features
• Family history

18. PRIMARY IMMUNE DEFICIENCIES ASSOCIATED
WITH RECURRENT SUPERFICIAL INFECTION
• Chronic granulomatous disease (CGD)
• It is an inherited immune deficiency caused by
defects in the (NADPH) oxidase, the enzyme
complex that generates superoxide in
phagocytes .
• It is characterized by :
a)infection
b)granulomatous
c)autoimmune manifestations .
• Milder form may present at adult age with
recurrent skin infections.

19. Flow cytometry in chronic granulomatous disease (CGD). The upper two flow plots represent the
control sample, with evidence of a normal metabolic burst following granulocyte phagocytosis of
opsonized Escherichia coli (dihydrorhodamine oxidation − upper right second panel). The lower panels
represent the lack of metabolic burst obtained from a patient with autosomal recessive CGD.
Management includes appropriate antibiotic and anti-fungal prophylaxis −
cotrimoxazole and itraconazole. Non-myeloablative haematopoietic stem
cell transplantation .

21. Hyper-IgE syndrome
Eczema, abscesses, candidiasis, pneumonia,
eosinophilia and elevated levels of serum IgE were the
most common immunological features reported in
patients with the hyper-IgE syndrome [46].
Cold abscesses, with boils reported in 87% [47], and
candidiasis are the most common cutaneous
infections. These patients have difficulty in mounting
an adequate immune response to S. aureus. Some of
the earliest data implicated abnormal neutrophil
chemotaxis and an altered immunoglobulin profile as
the primary immune defect.
Diagnosis is important, as ongoing antibiotic
prophylaxis is required to reduce the associated
staphylococcal lung infections and risk of
pneumatocoele development.

24. OTHER NEUTROPHIL DISORDERS
• Cyclic neutropenia
• This is an AD disorder in which cyclic haematopoiesis
causes intervals of neutropenia and susceptibility to
opportunist infection [26]. A typical cycle is 21 days'
duration, with severe neutropenia lasting for 3–6 days
of this. Cycle length is, however, variable. Although
this may be asymptomatic, during the period of
severe neutropenia patients may develop aphthous
ulcers, gingivitis, stomatitis and cellulitis. Mutations in
the neutrophil elastase gene 2 (ELA2) have been
identified [24].

25. Laboratory
investigation
Specific features
FBC White cell differential − neutropenia or lymphopenia,
platelet
Blood film Abnormalities in neutrophil or platelet morphology and
platelet size (microthrombocytopenia in WAS)
IgE Elevated in atopic eczema, very high levels may
suggest hyper-IgE
CRP Evidence of active infection or ongoing inflammation
(IBD)
Blood glucose Diabetes confirmation
Microbiology Staphylococcal carriage/MRSA screen, culture and
PCR
Histology White cell infiltration (absence in LAD), granuloma
formation
Neutrophil function Metabolic burst by flow cytometry (NBT) test − CGD
Neutrophil
phenotyping
Adhesion molecule expression by flow cytometry −
LAD
Lymphocyte Surface expression of B, T and NK cell markers
Laboratory investigations to consider in the diagnosis of recurrent superficial abscesses

26. Take home messege
• The differential diagnosis of patients presenting with recurrent
superficial abscesses is broad;
• the majority of cases are not associated with an underlying
primary immune deficiency.
• Control secondary causes of impaired neutrophil functions
• Staph. Eradication is mandatory in all patients.
• The principle role of the immunologist is to recognize patients
with a specific immune deficiency and direct appropriate
investigation and management.