An approach to dermatitis in Napkin area, with an emphasis on primary irritant type, with other differentials.

1. APPROACH TO DERMATITIS IN
NAPKIN AREA
Dr Sandeep Lal V

2. Napkin Dermatitis
■ Napkin dermatitis represents a descriptive phenotype for multiple
dermatoses that may affect the anogenital skin of napkin - wearing infants
■ These range from common problems such as a primary irritant dermatitis
directly caused by occlusion and friction, to rare diseases such as
Langerhans cell histiocytosis, unrelated to the wearing of a napkin
■ Thus, napkin dermatitis should be viewed not as a specific diagnostic
entity but rather as a regional diagnosis, like hand dermatitis, that
encompasses various skin diseases of multifactorial aetiology

3. Primary irritant contact napkin dermatitis- Definition
■ Napkin dermatitis (nappy rash, diaper dermatitis) is a dermatitis
exclusively localized, at least initially, in the area covered by napkins
■ Only observed when napkins are used
■ It is also observed in adults using large napkins because of urinary and
faecal incontinence

4. Etiology and Pathogenesis
■ Toxic contact dermatitits in napkin area
■ Primarily due to prolonged contact with feaces and secondarily to urine
with a host of other factors
■ Only 5% of napkin dermatitis is severe

5. Berg & Oranje model and modification by Atherton
Intact skin
Care taker intervention
Treatment
Frequent Napkin change
Activating factors
- Mix of faeces and urine
- Hydrated skin
- Occlussion
Napkin DermatitisCompromised skin
Irritation, friction
Inc Enzyme activity
Microbial infection
Pathogenesis

6. History
■ 20th cent – Ammonia from urine – primary irritant
■ Cooke described Bacterium ammoniagenes (Ammoniacal dermatitis)
■ Same incidence of urea - splitting bacteria in the napkins of babies with
and without rash
■ In 1977, Leyden et al. proved that ammonia did not cause skin irritation
when patch tested on the skin of adults and children
■ 1980s - complex etiology

7. History
■ Activated faecal lipases and proteases primarily damage the skin
■ These enzymes are activated in alkaline and hydrated conditions
■ Key approach to preventing napkin dermatitis is to keep the skin in the
napkin area protected from faeces and urine
■ Role of Candida albicans controversial due to the lack of typical clinical
features
■ The clinical features of cutaneous candidiasis in the napkin area were first
reported by Swift in 1956 as an exudative, erythematous plaque, with a
well - defined margin and often satellite lesions

8. History

9. Causative factors
■ Roles of faeces and urine
■ Friction
■ Hydration, temperature
■ Chemical irritants
■ Napkin itself (conventional)
■ Microbial infection

10. Napkins ( nappies, diapers)
■ Role of napkin – pivotal not irritant or allergic but the material
■ Ideal napkin - able to contain water without preventing air flow, and also
inform the carer (colour change) as soon as the baby urinates
■ Disposable napkins and new disposable napkins with superabsorbent gel
that is able to absorb 50 times its own weight of water

11. Napkins – modern disposable
■ 3 layers
■ Inner filtering layer
■ Intermediate layer able to absorb liquids – dec contact time of urine with
skin, low humidity
■ Outer waterproof layer - prevents perspiration - maintaining the
impermeability of the napkin
■ Elastic around the waist prevent the spread of gastrointestinal infection.
■ Increased occlusive effect - rare cases of allergic contact dermatitis
■ Traditional cotton napkin - characterized by significantly lower
absorbency and thus is associated with higher humidity in the napkin area

12. Napkins – modern disposable

13. Faeces
■ Prolonged contact with faeces - most irritant toxic factor on the skin – as
single factor can cause napkin dermatitis
■ Diarrhoea prolonged contact of faeces with skin incr hydration of the skin
■ Irritant capacity of faeces  ranging from acid stools burning the skin to
alkaline stools
■ Faecal proteases and lipases (?) – 100oc heating destroyed enzymes but
not irritant potential
■ ? Unidentified toxic substnaces ? Bile acids

14. Urine
■ Skin hydration  contribute to ND
■ Urine and ammonia as single factors fail to induce erythema
■ Unidentified factors responsible for skin irritation
■ Interaction between other factors

15. Friction
■ Rubbing of the napkin on the skin or skin - to-
skin contact (friction) - chafing dermatitis
■ Predilection of napkin dermatitis for the convex
surfaces of the genitalia, the buttocks and the
waistline
■ Spares the depth of the folds
■ W - shaped napkin dermatitis in female infants

16. Hydration
■ Napkins that prevent evaporation and Urea facilitates hydration of skin
■ Excessive hydration  maceration of the skin  compromised barrier
properties of the epidermis  ideal environment for the proliferation of
microorganisms
■ Excessive hydration makes skin more susceptible to friction traumas

17. Temperature
■ Caused by napkins that prevent perspiration reducing heat loss
■ Increased temperature is responsible for vasodilation and promotion of
inflammation

18. Chemical irritants
■ Chemical compounds  direct toxic effect on the skin
■ Chemical irritants are deodorants, preservatives, creams and oils, in
particular when used frequently throughout the day
■ Many antimycotics are not well tolerated

19. Microorganisms
■ Candida albicans – most important organism
■ Bacterium ammoniagenes was seen as responsible for urea splitting and
free ammonia release, leading to the term ‘ ammoniacal dermatitis
■ Other microorganism - Proteus , Pseudomonas, Escherichia coli ,
Streptococcus , Staphylococcus and Enterococcus
■ Often, Staph. aureus and C. albicans were isolated simultaneously
■ The role played by anaerobic bacteria has been emphasized

20. Microorganisms
■ Severity and duration of napkin dermatitis - colonization by C. albicans
■ Three infantile disorders are definitively associated with C. albicans :
oral thrush, chronic mucocutaneous candidiasis and congenital
candidiasis but rarely coexist with napkin dermatitis
■ C. albicans can be isolated from the most intensely erythematous lesions
independent of the site involved and the type of lesions
■ C. albicans was rarely isolated before the appearance of napkin dermatitis
suggesting that C. albicans is a secondary invader of skin that is already
damaged
■ Under occlusive conditions, 10,000 organisms of C. albicans per square
centimetre could induce primary skin infection

21. Allergy
■ Misinterpreted as contact allergy to the napkin
■ Allergic contact dermatitis in the napkin area- possible sensitizers
including rubber, detergents, lanolin, preservatives, neomycin and
mercurial compounds
■ Disperse dye in diapers confirmed by epicutaneous patch testing
■ However, allergic contact dermatitis is uncommon, especially in the first
year

22. Clinical Features
■ Overlap in the clinical presentation of the conditions that cause napkin
dermatitis, and specific diagnosis may be difficult
■ Although history and correlating physical signs are often helpful, the
differential diagnosis is based primarily on the morphology and location
of the rash

23. Contact napkin dermatitis
■ Primary irritant contact napkin dermatitis
■ Allergic contact napkin dermatitis
■ Simple intertrigo
■ Granuloma gluteale infantum

24. Primary irritant contact napkin dermatitis
■ Most prevalent form
■ Glazed, confluent erythema, resembling burn
■ There may be erythematous papules, oedema and scaling of the involved
skin
■ When the eruption begins to resolve, a wrinkled parchment – like
appearance may be noted.
■ The rash, however, may wax and wane.
■ This form of napkin rash primarily involves the skin where contact with
the napkin is greatest, e.g. the convexities of the buttocks, medial thighs,
mons pubis and scrotum or labia majora. The intertriginous areas are
generally spared.
■ An early manifestation of this type of napkin dermatitis, especially in
infants less than 4 months of age, is mild perianal erythema

25. Primary irritant contact napkin dermatitis

26. Primary irritant contact napkin dermatitis
■ Two uncommon morphological subtypes –
■ Tide water mark dermatitis – erythematous macular eruption is band -
like and confined to the margins of the napkin area on the thighs or
abdomen
■ Exaggerated chafing at the edges of the napkin due to compromised Skin
integrity by the frequent cycles of wetting and drying combined with the
traumatic friction due to the plastic border of a disposable napkin
■ Jacquet dermatitis - presents with papuloerosive lesions that have a
punched - out or crater - like appearance. These ulcers have also been
referred to as ‘ ammoniacal ulcers ’ . This eruption, when it occurs, tends
to affect older, napkin - wearing children

27. Primary irritant contact napkin dermatitis
Tide water mark dermatitis Jacquet dermatitis

28. Allergic contact napkin dermatitis
■ Complicate another type of napkin rash or present de novo
■ Uncommon under 2 years of age
■ When to suspect - does not respond appropriately to treatment, application of a
potential allergen causes the napkin rash to become more intense or to spread
■ Begins with erythema and small vesicles that rupture which may not be evident,
leading to an eczematous eruption
■ Allergic contact napkin rash typically complicates a primary irritant napkin rash
and therefore follows the same distribution, i.e. the convex surfaces of the skin
under occlusion
■ Prominent flexural involvement, if the sensitivity is to a topical preparation
which concentrates within the skinfolds
■ Holster sign - contact dermatitis to rubber components around proximal thighs
and the waistline associated with disposable napkins

29. Allergic contact napkin dermatitis
the ‘holster sign

30. Simple intertrigo
■ Inflammatory process that occurs in areas where skin rubs against skin, as in the
folds of the groin, posterior thighs and intergluteal cleft.
■ Heat, moisture and sweat retention, coupled with friction, cause maceration,
inflammation and sometimes skin erosion.
■ Intertrigo may present with sharply demarcated moist erythema confined to the
skinfolds.
■ In contrast to a candidal napkin rash, there is little associated scale and no
satellite lesions.
■ As intertrigo is essentially due to friction and retained moisture, it may be
considered a subtype of irritant contact dermatitis. The tropical climate of the
napkin area makes the napkin - wearing child susceptible to the development of
simple intertrigo; however, it is most often seen in overweight infants

31. Granuloma gluteale infantum
■ Rare nodular eruption arising within an area of pre - existing irritant ND
■ Characterized by firm, painless, reddish - brown to purple nodules varying in
size from 0.5 to 4 cm appearing on the buttocks and inner thighs and
occasionally on the lower abdomen
■ Also outside the napkin area involving the folds of the axilla and neck.
■ These angioma - like swellings resembles lesions of Kaposi sarcoma or
lymphoma
■ Nodules may persist for weeks to months but eventually regress spontaneously
leaving behind atrophic scars
■ Over pre - existing ND localized cutaneous response to long - standing
inflammation
■ No correlation with severity of napkin
■ ?C. albicans, ?Fluorinated topical steroids

32. Granuloma gluteale infantum

33. Differential diagnosis
Eczematous/papulosquamous
• Primary irritant contact dermatitis
• Allergic contact dermatitis
• Candidiasis
• Intertrigo
• Seborrhoeic dermatitis
• Atopic dermatitis
• Psoriasis
• Kawasaki disease
• Langerhans cell
histiocytosis
(Letterer –Siwe)
• Perianal streptococcal
disease

34. Differential diagnosis
Vesiculobullous/ erosive
• Acrodermatitis enteropathica
• Biotin-responsive multiple carboxylase deficiency
• Cystic fibrosis
• Bullous impetigo
• Miliaria
• Scabies
• Other vesiculobullous disease (varicella, herpes simplex, hand,
foot and mouth disease, chronic bullous disease of childhood,
bullous mastocytosis, incontinentia pigmenti, epidermolysis
bullosa)
• Child abuse (burns)
• Laxative-induced dermatitis
• Human immunodeficiency virus

35. Differential diagnosis
Nodular
• Granuloma gluteale infantum
• Extrafacial periorificial granulomatous dermatitis
• Metastatic Crohn disease
Verrucous
• Congenital syphilis (condyloma lata)
• Perianal pseudoverrucous papules and nodules

36. Infectious napkin dermatitis
■ Candida napkin dermatitis
■ Perianal streptococcal disease and streptococcal intertrigo
■ Bullous impetigo
■ Scabies
■ Congenital syphilis
■ Human immunodefi ciency virus ( HIV)

37. Candida napkin dermatitis
■ Warmth moisture C albicans penetrate Str corneum – alternative complement
pathway - inflammation
■ Most characteristic of the napkin rashes
■ Sharply marginated, intensely red, scaly plaques with satellite papules and
pustules with peripheral scales. Severe cases widespread skin erosion.
■ When candidiasis involves the genitalia, there is usually confluent erythema
involving the entire scrotum or labia, unlike psoriasis, in which genital
involvement is usually more localized and in which the lesions are more sharply
demarcated
■ KOH pseudo - hyphae
■ Scrapings negative, if taken from inflamed areas or in long - standing cases in
which the inflamatory response has led to the death of the Candida organism.
■ Yield on KOH is greatest from scrapes from the periphery of the rash or a fresh
papular or pustular lesion.

38. Candida napkin dermatitis
■ Recent history of treatment with broad - spectrum antibiotics, diarrhoea
■ Oral cavity should be examined to rule out concomitant thrush
■ Chronic or recurrent rash  seeding from the GI tract, maternal candidal
vaginitis, maternal mastitis

39. Candida napkin dermatitis

40. Candida napkin dermatitis
■ Psoriasiform skin reaction - complication of severe candida napkin rash
■ Shortly after therapy is initiated, scaly psoriasiform papules and plaques rapidly
develop on the trunk, usually sparing the extremities Which last for days to
weeks. C. albicans cannot be cultured from these plaques
■ However, active candidiasis of skinfolds in the neck and axilla, in addition to
the inguinal area, may be seen
■ The pathogenesis of this allergic skin eruption ? response to an antigenic
stimulus

41. Candida napkin dermatitis

42. Candida napkin dermatitis
■ Congenital candidal napkin dermatitis - manifestation of conge cut candidiasis.
■ Macerated areas of erythema in the anogenital region; may also present with
papulopustules, widespread erosions or a burn - like dermatitis
■ In term infants, congenital cutaneous candidiasis is typically a benign, self -
limited eruption attributed to vertical transmission from the colonized mother.

43. Perianal streptococcal disease and streptococcal intertrigo
■ Sharply demarcated, bright erythema in the perianal area. There may be
perirectal fissuring. Also involves other intertriginous areas, such as the neck,
axillae and inguinal folds
■ Itching and pain during defaecation and can lead to faecal hoarding
■ History of repeated streptococcal pharyngitis in family members
■ Diagnosis cotton swab bacterial culture of the affected perianal skin
■ Streptococcal intertrigo - involves bacterial infection of the inguinal creases and
other intertriginous areas, including the axillae, popliteal spaces and neck folds
of infants
■ Co – existent perianal disease may or may not be present.
■ The infection is characterized by a foul - smelling, macerated erythema of
intertriginous areas.
■ Occasionally, mixed infections with Staphylococcus aureus , Pseudomonas or
Proteus species

44. Perianal streptococcal disease and streptococcal intertrigo

45. Bullous impetigo
■ Caused by coagulase - positive, usually phage type II, Staph. Aureus which
produces an epidermolytic toxin that separates the upper layers of the epidermis
■ Bullous impetigo is characterized by the formation of large flaccid bullae
arising from apparently normal skin
■ The bullae rupture easily, leaving red, moist, denuded areas and honey -
coloured crusts
■ Multiple lesions involving the thighs, buttocks and lower abdomen, rapid
spread
■ Diagnosis can be confirmed with a Gram stain and bacterial culture

46. Bullous impetigo

47. Scabies
■ Pruritic papules, vesicles and vesiculopustules are seen. Intermingled with
eczematization, excoriation and crusting
■ Linear burrows are pathognomonic of scabies
■ Sites- fingerwebs, wrists, antecubital fossae, axilla, areolae and areas around the
umbilicus, lower abdomen, genitals and buttocks
■ In infant and young children, the palms, soles, head, neck and face may also be
affected. A high percentage of children with scabies may develop nodular
lesions
■ History of intense itching and pruritus in family members or caretakers

48. Primary and secondary
inflammatory conditions
■ Seborrhoeic dermatitis
■ Atopic dermatitis
■ Psoriasis
■ Mixed napkin dermatitis
■ Miliaria
■ ‘Perianal pseudo-verrucous papules and nodules’ entity
■ Perioral dermatitis with extrafacial genital manifestations and metastatic Crohn
disease
■ Kawasaki disease

49. Seborrhoeic dermatitis
■ Sharp Salmon - coloured, greasy yellowish scaly plaques that involve the
inguinal folds
■ In severe cases, there can be spread of the eruption from the skinfolds to convex
skin surfaces of the napkin area.
■ There may be associated fissuring, crusting and weeping.
■ Unlike candidiasis, there are no satellite lesions.
■ Clue to the diagnosis involvement of characteristic areas away from the
anogenital region
■ Scalp, face, primarily flexural areas, include the axilla, neck, postauricular folds
and umbilicus.
■ Assymptomatic commonly at 3 – 6 weeks of age. The prognosis is good and
resolves spontaneously by 3 – 6 months

50. Seborrhoeic dermatitis

51. Atopic dermatitis
■ Usually spares the napkin area
■ Appearance is similar to that of primary irritant napkin dermatitis
■ The rash, however, tends to be more chronic and refractory to treatment. There
may be oozing or crusting due to secondary infection with Staph. aureus
■ There may also be lichenification and excoriations
■ Pruritus is a cardinal feature of this disease
■ Pruritus usually do not occur until the child is 2 months of age and is able to rub
or scratch

52. Psoriasis
■ Rare in infancy
■ When it occur in the first year of life, it is likely to appear in the napkin area
because of the Koebner phenomenon caused by more common types of napkin
rash.
■ It typically presents as sharply demarcated, erythematous plaques of variable
size, with involvement of both the convex surfaces of the buttocks as well as the
inguinal
■ Unlike psoriatic plaques elsewhere on the body, there may be little or no scale
due to the constant hydration under the napkin
■ Psoriasis in the napkin area tends to be chronic and more resistant to treatment
with low - potency topical steroids
■ Topical corticosteroids that are slightly more potent than 1% hydrocortisone,
such as desonide 0.05% or aclometasone dipropionate 0.05%, may be necessary

53. Psoriasis

54. Mixed napkin dermatitis
■ Combination of factors
■ Irritant getting secondarily infected with C albicans – severe rash persisting for
more than 2-3 days , anti candidial tt inaddtion to steroids, occlusive creams and
frequent diaper change
■ Atopics more prone for secondary bacterial infection – crusting or bullae
■ Psoriasis – Isomorphic phenomenon of Keobner – dsitr characteristic of
primary condition – resistant to tt while primary condition responds

55. Perianal pseudo -verrucous papules and nodules
■ Perianal area of children in association with chronic faecal soiling
■ stool leakage was due to severe constipation with secondary encopresis or
followed surgical colonic reanastomosis in patients with Hirschsprung disease
■ 2 – 8 mm, red, moist, fl at – topped round papules and papulonodules

56. Perianal pseudo -verrucous papules and nodules

57. Neoplastic napkin conditions – LCH (Letterer Siwe )
■ Acute disseminative, potentially fatal form of LCH
■ Present with skin findings in the napkin area.
■ Although this is a rare disease, it should be considered in cases of intractable napkin dermatitis.
■ This infantile form of LCH usually occurs during the first year of life but may occur in children
up to the age of 3 years.
■ inguinal rash resembling Seborrhoeic dermatitis – but more erosive
■ Postauricular erosions and a scaly rash of the scalp and trunk. This eruption consists of
yellowish to reddish - brown infi ltrated papules, often with a purpuric component.
■ Lesions may show haemorrhagic crusting.
■ Petechiae and epidermal atrophy may also be seen.
■ The development of purpuric nodules of the palms and soles is associated with a poor
prognosis.
■ Systemic manifestations of the disease include fever, anaemia, diarrhoea, thrombocytopenia,
hepatosplenomegaly, lymphadenopathy and skeletal tumours

58. Neoplastic napkin conditions – LCH (Letterer Siwe )

59. Metabolic napkin conditions – Acrodermatitis enteropathica
■ Inherited form of the disease as well as an acquired, transient form.
■ In the autosomal recessive inherited form of acrodermatitis enteropathica, there is an inborn
defect in the gastrointestinal absorption of zinc
■ Typically present when the affected infant is weaned from breastfeeding; breast milk is felt to be
protective because it contains a zinc ligand - binding protein
■ Transient form is due to nutritional zinc deficiency. It is seen in infants with severe
malabsorption, in premature infants who receive prolonged parenteral alimentation and in
breastfed infants when the zinc level in the mother ’ s milk is abnormally low
■ Periorificial and acral vesiculobullous eczematoid eruption. Scaly, sharply demarcated, crusted
plaques are seen in the folds of the napkin area, around the mouth, nose and eyes and on the
distal extremities
■ chronic, untreated cases, the lesions become lichenifi ed and psoriasiform in appearance
■ Other clinical characteristics include failure to thrive, photophobia, diarrhoea, alopecia,
paronychia, nail dystrophy, irritability or listlessness.
■ Diagnosis is confi rmed by a plasma zinc level less than 50 μ g/mL (normal values: 70 – 110 μ
g/mL), Low ALP

61. Management
■ Therapy should be closely linked to diagnostic and pathogenic considerations
■ Should specifically address assoc exogenous and endogenous contact irritants

62. Care of the napkin area
■ Highly absorbent napkins - acrylate gel
■ Non - disposable cloth napkins - antiseptics or fabric conditioners are not
recommended for washing napkins
■ Tumble drying preferred over air drying to make napkin soft
■ Adequate rinsing

63. Care of the napkin area – Prevention
■ Breast fed babies – less ND
■ Occlusive dressing avoided
■ Protective occlusive creams after direct irritation by faeces
■ Five aspects are important with respect to the prevention of napkin dermatitis.
1 The frequency of napkin change and cleaning of the napkin area
2 Absorbency of the napkins
3 Infection control at day - care centers
4 Underlying diseases/iatrogenic causes
5 Disposable versus washable cloth napkins

64. Frequency of napkin change
■ Frequent napkin changes (about seven times a day or every 3 – 4 hours) is the
most important preventive measure to avoid skin problems in the napkin area
■ The infant urinates about seven times a day at the age of 12 months. Neonates
urinate more than 20 times in 24 h . Therefore napkin changes should be more
frequent (more than seven times a day) in neonates.
■ Water has been the standard for cleansing the napkin area during changing

65. Absorbency of the used napkins
■ Acrylate gelling material (AGM) high molecular weight cross - linked sodium
polyacrylate polymer - Superabsorbent napkins
■ Hold up to 50 – 80 times its weight in liquid and form a gel when hydrated
■ Keeping the skin as dry as possible

66. Infection control in day-care centres and napkin types
■ Cloth vs Disopsable napkins
■ Coliform bacteria in fomites
■ Home care vs Day care centres
■ The most recent development in napkin technology is the disposable napkin
designed to deliver zinc - oxide petrolatum - based ointment continuously
■ Cloth napkins with several layers of the same fabric were less effective in
keeping the skin dry than cloth napkins that contained middle layers of different
non – woven components

67. Treatment
■ Napkin dermatitis is self - limiting
■ Children will outgrow this disorder after successful potty training
■ Never give parents the incorrect impression that napkin dermatitis is the result
of improper or negligent baby care
■ Ingredients of the medication are:
■ (a) protective compounds
■ (b) antimicrobial agent (s)
■ (c) other additives

68. Basic preventive treatment
■ Increased frequency of napkin changes and cleansing the skin.
■ The skin is cleaned gently and nursed with lukewarm tap water without
rubbing.
■ If faecal material is still present, a mild soap is used.
■ The activating factors must be minimized
■ A barrier cream containing zinc - oxide, titanium dioxide or white soft paraffin,
or a water – repellent substance such as dimethicone or other silicones, should
be applied.
■ The barrier agent selected should be non – toxic and as cosmetically acceptable
as possible.
■ The baby can be bathed once or twice daily with bath oil preparations

69. Further treatment
■ For napkin dermatitis that is not controlled by improved hygiene and use of
emollients or barrier creams
■ A topical anticandidal drug (such as nystatin or an imidazole) should be used,
best combined with 1% hydrocortisone in an ointment base.
■ A barrier cream should be used regularly, applied liberally at each napkin
change

70. Corticosteroids
■ The use of corticosteroids is controversial, but those of low potency such as 1%
hydrocortisone acetate are acceptable applied for a short period
■ Fluorinated and highly potent corticosteroids are contraindicated
■ Hydrocortisone can reduce the inflammation associated with napkin dermatitis.
■ It should be used not more than twice daily.
■ Corticosteroids have a markedly increased potency on the perineum and buttock
areas because of the napkin ’ s occlusive properties leading to an increased risk
of atrophy and striae, and even the possibility of adrenal suppression.

71. Tar
■ Controversial and conflicting, because of possible carcinogenic potential effects
■ Purified coal tar 10% in zinc - oxide ointment is effective, especially when
combined with sulphur 5%

72. Anticandida treatment and anti bacterial
■ Topical anticandida agents
■ for the more troublesome cases of napkin dermatitis, oral therapy (such as
Nystatin, fluconazole suspension) should be added
■ The rational for oral anticandidal therapy is that you need in addition to treat the
gut colonization, although the scientific proof for this approach is still lacking
■ Chemicals such as benzalkonium chloride and triclosan act as antimicrobial
agents

73. Home treatment
■ Egg - white can be applied in shaken form to the skin of the napkin area
■ Cornstarch powder reduces maceration and inhibits the growth of Candida
albicans

74. Preparations to avoid
■ Baby powder and other over - the - counter preparations should be discouraged
■ Potentially toxic compounds such as baking soda and boric acid should be
avoided because of the risk of absorption and toxicity
■ Use of baby powder (talcum powder) should be discouraged for two reasons.
■ First because of the risk of talcum powder granuloma
■ Secondly, because of toxicological aspects.
■ Accidental ingestion of baby powder and corn starch is dangerous and can lead
to severe aspiration pneumonia and even death

75. Complications of treatment
■ Poisoning of infants -improper antiseptics
■ Aniline poisoning has been described as a result of the use of marking inks.
This leads to methaemoglobinaemia.
■ Naphthalene - containing mothballs used for storage of napkins can lead to
haemolytic anaemia
■ Boric acid or camphor - containing products have been used in
ointments, but are potentially dangerous. These products
are readily absorbed through the compromised skin.

76. Thank you

77. HIV and Syphilis
■ Interaction between syphilis and HIV infection is complex and remains
incompletely understood
■ HIV can influence the course and presentation of Syphilis and vice versa
■ Impairment of both cell-mediated and humoral immunity by HIV may limit the
host's defenses against Treponema pallidum, thereby altering the clinical
manifestations or natural course of syphilis infection

78. HIV affecting Syphilis
■ Confusing clinical signs and symptoms
– Despite minor differences, syphilis presents similarly in HIV infected and
HIV-uninfected patients.
– In primary syphilis, HIV infected patients may present with >1 chancre (up
to 70% of patients) and with larger and deeper persistent lesions
– Atypical chancres have been reported, including lesions appearing as
fissures or abrasions. Two reports also described gummatous penile
ulceration. Unusual rashes include papular or nodular eruptions, nodular or
ulcerative lesions with necrotic centers (ie, lues maligna syphiliticum) and
keratoderma
– Approximately one-fourth of HIV-infected patients present with
concomitant lesions of both primary and secondary stages of syphilis at the
time of diagnosis
– Relapses of secondary syphilis symptoms and signs may occur early in the
latent stage

79. HIV affecting Syphilis
■ Telescoping of Disease
– HIV-induced meningeal inflammation may facilitate penetration of
spirochetes into the central nervous system (CNS) and thus contribute to
the development of symptomatic neurosyphilis.
– In contrast to HIV-uninfected patients, most of the new cases of clinical
neurosyphilis in HIV infected individuals are identified at the initial
presentation (early) -HIV infection may be associated with an increased
risk of development of neurological complications mainly acute syphilitic
meningitis and meningovascular neurosyphilis
– Persistent CSF abnormalities despite treatment - Higher cell counts, higher
protein levels, and lower glucose levels in the CSF are reported in HIV-
infected patients with syphilis

80. HIV affecting Syphilis
■ Telescoping of Disease
– HIV-infected patients with CD4 cell counts 200 cells/mL were 3.7 times
less likely to normalize CSF–Venereal Disease Research Laboratory
(VDRL) test results than were those with CD4 cell counts 1200 cells/mL,
suggesting, that HIVassociated immunedysregulation may account for the
impaired clearance of organisms from the CNS
– Certain studies recommend CSF examinations for HIV-infected patients
with a nontreponemal serum titer 1:32, regardless of the syphilis stage, or
for those with early-stage infection and a CD4 cell count !350 cells/mL,
regardless of titer But CDC guidelines say to follow clinical examination
and four fold rise in serology
– Although it remains unknown whether the lack of normalization of CNS
VDRL results among HIV-infected patients reflects treatment failure,
raising concerns regarding the adequacy of the current recommended

81. HIV affecting Syphilis
■ Serological tests abnormalities
– Unusual serologic responses have been reported in HIV-infected persons
with syphilis.
– Most reports involved higher than expected serologic titers in primary n
secondary
– False-negative serologic results and delayed appearance of seroreactivity
have also been reported
– Very high VDRL or RPR titers of greater than 1:64 have been reported in
HIV-infected patients without syphilis. These nontreponemal tests detect
antibodies directed against a cardiolipin-lecithin antigen. In patients with
immunoglobulin abnormalities, the RPR or VDRL test result may be
falsely positive. Many persons with HIV infection have both
anticardiolipin-lecithin antibodies and polyclonal gammopathy
– Slow reduction in titres of VDRL
– The serofast state is not uncommon among HIV-infected persons and refers
to the persistence of a reactive nontreponemal syphilis test, usually 1:16 or

82. HIV affecting Syphilis

83. HIV affecting Syphilis
■ Treatment
■ Persons with HIV infection who have early syphilis might be at increased risk
for neurologic complications and might have higher rates of serologic treatment
failure with recommended regimens. The magnitude of these risks is not
defined precisely, but is likely small. Although long-term (>1 year) comparative
data are lacking, no treatment regimens for syphilis have been demonstrated to
be more effective in preventing neurosyphilis in persons with HIV infection
than the syphilis regimens recommended for persons without HIV infection.
Careful follow-up after therapy is essential. The use of antiretroviral therapy as
per current guidelines might improve clinical outcomes in persons with HIV
infection and syphilis Unusual serologic responses have been reported in HIV-
infected persons with syphilis.
■ Persons with HIV infection and primary or secondary syphilis should be
evaluated clinically and serologically for treatment failure at 3, 6, 9, 12, and 24
months after therapy

84. Syphilis affecting HIV
■ Epidemiologic studies demonstrate that history of an STD, including syphilis, is
associated with an increased risk of HIV disease among both gay men and
heterosexuals because sexual behaviors that increase the risk of acquiring
STDs also increase the risk of acquiring HIV.
■ Furthermore, genital ulcerations and inflammation caused by STDs are
implicated as cofactors for acquiring or transmitting HIV infection.
■ Syphilitic ulcers disrupt epithelium and mucosa, thus aiding the passage of HIV.
■ HIV replication Oral routes being considered safe

85. Syphilis affecting HIV
■ CD4 count and syphilis
– Syphilis, like many other acute infections, causes transient increases in the
viral load and decreases in the CD4 cell count that resolve after the
infection is treated
– Syphilis infection, particularly the generalized stage of secondary syphilis,
may increase the immune activation of host cells, affect the secretion of
cytokines including TNFÆ, and upregulate transcription factors such as
nuclear factor kappa beta to alter cell cycles, and thus enhance HIV
replication.
– It is possible that these transient increases in viral load contribute to the
increased risk of HIV transmission among patients with concordant HIV
infection and syphilis
– Clinicians should be aware that syphilis may account for otherwise
unexplained decreases in CD4 cell counts or increases in the plasma viral
load in HIV-infected patients. Syphilis testing might be indicated in such
clinical scenarios.