Skin infections are the commonest presenting problem in many clinics.18,19 These include a high incidence of scabies and tinea corporis (ringworm), boils and carbuncles, infected wounds, impetigo and cellulitis. A notably serious complication of skin infections is post-streptococcal glomerulonephritis secondary to S. pyogenes infection. Scabies is the most common skin infestation and commonly starts as an itchy rash with pinhead papules in the web spaces of the fingers.
Recommended treatment (in summary)6,19
Impetigo and other skin sores
Soak and remove crusts with saline or soap and water or povidone–iodine or potassium permanganate (Condy’s crystals) solution
Antibiotic treatment (if required)
benzathine penicillin, IM, statim dose
flucloxacillin/dicloxacillin (o) or cephalexin (o) or co-trimoxazole (o) for 3–7 days
Cellulitis (mild–moderate) and erysipelas
procaine penicillin IM daily for 5 days
benzathine penicillin IM on days 1 and 3 or daily for 3–5 days
If no improvement: flu/dicloxacillin (as below) plus probenecid
Boils, carbuncles, abscesses, bullous impetigo (Staphylococcus aureus infections)
Flu/dicloxacillin (o) 6 hourly for 5–10 days
Suppurative wound infections
Use local measures such as aseptic dressings and topical antiseptics
If necessary, add flu/dicloxacillin (as above); consider clindamycin
Tinea corporis (ringworm)
Use benzoic acid ointment, Whitfield’s ointment or one of the imidazole preparations: apply 1–3 times daily for 4–6 weeks or for 1 week after rash resolves
Systemic agents (e.g. griseofulvin (o) once daily) may be necessary
Apply permethrin 5% cream or benzyl benzoate 25% emulsion (see CHAPTERS 117 and 120). Treat household members.
For children less than 2 months use: sulphur 5% cream for 2–3 days
crotamiton 10% cream daily for 3–5 days
For infected scabies, use flu/dicloxacillin or erythromycin
Pityriasis versicolor (white spot)
Group A beta-haemolytic Streptococcus (GABHS) infections are a significant problem, causing diseases such as pharyngotonsillitis, impetigo, cellulitis, otitis media and scarlet fever. Two important immunological reactions to the streptococcus toxin are acute rheumatic fever and post-streptococcal glomerulonephritis (PSGN).2
Rheumatic fever and its effects are a serious cause of cardiovascular morbidity and mortality in Aboriginal and Torres Strait Islander peoples, who have the highest rate of acute rheumatic fever of any ethnic group in the world, with an incidence of 250–300 per 100 000 children.20 It is a classic hallmark of overcrowding, poverty and lack of hygiene, all of which facilitate streptococcal infection (see CHAPTER 35 for clinical features).
Treatment is with benzathine penicillin (IM).
There is an association between PSGN (see CHAPTER 76) and streptococcal skin and throat infections. Impetigo is the more frequent antecedent to PSGN. A study based on the fact that the Aboriginal and Torres Strait Islanders have an incidence of end-stage kidney failure 10 times greater than the general population found that people with a history of PSGN in childhood had a risk of overt albuminuria more than six times that of a control group.21 There is no simple treatment of PSGN and preventing streptococcal infection remains the most important control strategy. Penicillin is beneficial in preventing spread during epidemics.
Communicable diseases remain a problem, with an up to 10-fold increase over the non-Indigenous population for diseases such as hepatitis A, hepatitis B, meningococcal disease, Salmonella, Chlamydia and tuberculosis.3
The rate of TB in Aboriginal and Torres Strait Islanders is 10–15 times higher than for other people in the Northern Territory.2 This is related to poverty, overcrowding, malnutrition and homelessness. Early diagnosis and treatment is the key to its control. This includes detection of latent TB infection in those at risk and strategies to prevent transmission in acute cases. BCG immunisation in high-risk groups is a key preventive strategy and is recommended for newborns from high-risk communities (see CHAPTER 29).
Leprosy (see CHAPTER 15) has been endemic in Northern Australia for over 100 years, although the incidence is reducing. Control strategies include early diagnosis of new cases, treatment with multidrug therapy, monitoring of treatment to ensure its completion, and prevention of nerve function impairment (NFI). NFI is monitored by a brief voluntary muscle and sensory test. If detected early, it responds to anti-inflammatory medication such as prednisolone.
BCG vaccination, used to prevent TB, has probably had a protective efficacy against leprosy of approximately 50%.2