Biomedical Engineering Reference
In-Depth Information
Staphylococcus aureus, and community-associated methicillin-resistant Sta-
phylococcus is becoming more common.
4,5,10-14
Left untreated, the secondary
bacterial infections can develop into cellulitis, streptococcal gangrene, or sepsis.
Long-term and continual infection has been associated with the development
of chronic diseases such as acute post-streptococcal glomerulonephritis
(APSGN),
15
Rheumatic Fever (RF) and Rheumatic Heart Disease (RHD).
16
High rates of ASPGN, RF, and RHD have been recorded in regions that also
show high rates of scabies infection.
17,18
Scabies is believed to play an impor-
tant role in contributing to such chronic disease development. Streptococcal
and staphylococcal species have been isolated in the mite burrow and in mite
fecal pellets alluding to the role that scabies plays in spreading pathogenic
bacteria.
19
Eradicating scabies could be a realistic means of reducing acute and
subsequent chronic disease burden, by reducing the opportunities for second-
ary infections. This has been demonstrated in scabies community treatment
control programs where treatment targeted at scabies reduced the pyoderma
incidence.
2
4.2 Host Immune Response to Scabies Infection
The classical symptoms of a scabies infestation consist of pruritus (itching)
that is more intense at night, the appearance of lesions, and in some cases a
generalized rash. Mite numbers are typically 10-12 per patient and are
usually self-limiting. The rash and pruritus can persist for several weeks
after infection clearance, possibly due to residual mite products within the
upper epidermal layers.
20
For reasons still unknown, some patients develop
a debilitating hyperinfestation of scabies mites called Crusted or Norwegian
scabies. Immunosuppression due to disease, medication, or substance abuse
has been postulated as a predisposing factor, but crusted scabies has also
been found in patients who are immunocompetent.
21,22
Immune deficiency
resulting from a genetic defect has also been proposed following reports of
familial clustering.
23,24
Streptococcal and staphylococcal infections are fre-
quently found in fissures that develop within crusts. These secondary
infections are associated with the high mortality rates seen in crusted scabies
patients.
25
Studies on the immune biology of scabies have been ongoing since 1944,
when initial work demonstrated that a patient experiencing a primary infes-
tation of scabies took up to 4 weeks to display symptoms.
26
Subsequent
infections resulted in symptoms arising within 24 h, but this hypersensitivity
was seen to wane 15 to 24 months after initial sensitization.
27,28
There is a
general consensus among researchers that this response results from a Type IV
delayed hypersensitivity reaction, a cell-mediated antibody-independent
immune response.
26,29-32
The symptoms presumably result from immune
responses to mite products such as saliva, eggs, and fecal pellets.
32
However,
the identification of the mite allergens responsible for these immune responses
is still unknown.
