Skin infection

1. Skin infestations
(Parasitic Infestations)
BY Dr JERE A.MSHANA
DERMATOVENEROLOGIST
RDTC at KCMC
10.02.2017

2. contents
1. Scabies
2. Pediculosis
3. Tungiasis
4. Myasis
5. Larva migrants ( Creeping eruptions)
6. Larva currents
7. Papular urticaria
8. Onchocerciasis and lymphatic filariasis)

3. SCABIES
• What is scabies?
• Scabies is a very itchy rash caused by a
parasitic mite that burrows in the skin surface
The human scabies mite's scientific name is
Sarcoptes scabiei var. hominis

4. Sarcoptes scabiaei

5. Factors leading to spread of scabies
• Scabies affects families and communities worldwide
– It is most common in children, young adults and the elderly adults
and the elderly.
Factors leading to spread of scabies include:
• Poverty and overcrowding
• Institutional care, such as rest homes, hospitals, prisons
• Refugee camps
• Individuals with immune deficiency or that are immune
suppressed
• Low rates of identification and proper treatment of the
disease

6. What causes scabies?
• Scabies is nearly always acquired by skin-to-
skin contact with someone else with scabies
• The contact may be quite brief such as holding
hands with an infested child
• It is sometimes sexually transmitted
• Occasionally scabies is acquired via bedding or
furnishings

7. Cont…
• Typically, several scabies mites infest an
affected host
• After mating, the male mite dies
• The female scabies mite burrows into the
outside layers of the skin, where she lays up to
3 eggs each day for her lifetime of one to two
months
• The development from egg to adult scabies
mite takes 10–14 days

8. Skin manifestations of scabies
• Scabies causes a very itchy rash
• It’s important to search for burrows carefully
in a patient with severe itch, especially if the
rash is mild
• Contacts should be examined for burrows,
whether or not they are itchy

9. itchy
• If it is the first episode of scabies, itch arises 4–6 weeks
after transmission of a mite
• It may occur within a few hours of subsequent
infestation
• Itch is characteristically more severe at night,
disturbing sleep
• It affects the trunk and limbs, sparing the scalp.
• Itch is mild or absent in some patients with crusted
scabies
• Itch can persist for several weeks after successful
treatment to kill the mites

10. Burrows
• Scabies burrows appear as 0.5–1.5 cm grey
irregular tracks in the web spaces between the
fingers, on the palms and wrists
• They may also be found on or in elbows,
nipples, armpits, buttocks, penis, insteps and
heels
• Dermatoscopic or microscopic examination of
the contents of a burrow may reveal mites,
eggs or mite faeces

11. Generalised rash
• Scabies rash is a hypersensitivity reaction that arises several weeks after initial infestation. It
has a varied appearance
• Erythematous papules on the trunk and limbs, often follicular
• Diffuse or nummular dermatitis
• Urticated erythema
• Vesicles on Generalised rash
• palms and soles
• Acropustulosis (sterile pustules on palms and soles) in infants
• Papules or nodules in the armpits, groins, buttocks, scrotum and along the shaft of the penis
• Rare involvement of face and scalp

12. Complications of scabies
• Secondary infection
• Secondary infection is due to scratching and effect of
the mite on the skin's ability to fight bacteria
Staphylococcal or streptococcal infection results in
crusted plaques and pustules impetigo
• Streptococcal cellulitis results in painful swelling and
redness, and fever
• Systemic sepsis with staphylococci and/or streptococci
is potentially very serious
• Scabies outbreaks lead to cases of post-streptococcal
glomerulonephritis and rheumatic fever

13. Norwegian scabies
(Crusted scabies )
• Crusted scabies (previously called Norwegian
scabies )
• is a very contagious variant of scabies in which
an individual is infested by thousands or millions
of mites living in the surface of the skin
• The patient presents with a generalized scaly rash
• This is often misdiagnosed as psoriasis or
seborrhoeic dermatitis

14. Cont..
• Scale is often prominent in the finger webs, on
wrists, elbows, breasts and scrotum
• Itch may be absent or minimal
• Crusted scabies may affect the scalp

15. Crusted scabies

16. Risk factors for NORWEGIAN scabies
include
• Very old age
• Malnutrition
• Immune deficiency
• Intellectual deficit
• Neurological disease
• Specific inherited immune defect in some
otherwise healthy people

17. Cont..
• A case of crusted scabies is the usual reason
for an outbreak of scabies in an institution.
Patients and staff in the institution may
present with
• Usual scabies
• Crusted scabies
• Hypersensitivity rash but no burrows, ie, not
infested

18. How to diagnose scabies
• The clinical suspicion of scabies in a patient with
an itchy rash especially when reporting itchy
household members
• And can be confirmed by
• Dermatoscopy (characteristic jet-plane or
appearance)
• Microscopic examination of the contents of a
burrow
• Skin biopsy(scabies histopathology usually
negative if taken from inflammatory rashes)

19. Dermoscopy of scabies burrows
Red arrow points to mite

20. Differential diagnosis of scabies
includes
• insect bites or papular urticaria
• skin infections
• dermatitis
• urticaria
• and bullous pemphigoid

21. treatment
• Management of a scabies outbreak involves
identification and treatment of individual
patients and household contacts with
insecticides
• Oral antibiotics are required for secondary
infection
• Careful attention to instructions is essential if
scabies is to be cured

22. Cont…treatments
• 25% Benzyl benzoate lotion, applied daily for 3
days rest for 8-10 then repeat for 3days
• 0.5% Aqueous malathion lotion, left on for 24
hours
• 2–10% Precipitated sulphur ointment
• Treatment should be repeated after 8–10 days
after the first application to catch mites that
have newly hatched

23. Cont..RX
• The chemical insecticides used to treat scabies
are called scabicides
• The scabicide is applied to the whole body
from the scalp to soles
• The usual topical treatment is 5% permethrin
cream, left on the entire skin for 8–10 hours
• It should be applied under fingernails using a
soft brush

24. Systemic treatments
• Oral ivermectin 200 mcg/kg is convenient, but
more expensive than topical permethrin or
• 0.2mgoral once repeat in two weeks and may be
combined with a topical scabicide
• It may be slightly less effective
• It is mainly used for mass treatments in
institutions, or in patients unable to use topical
therapy
• Gamma benzene hexachloride cream is no longer
recommended due to neurotoxicity

25. Additional management
• Bed linen, towels and clothing should be
laundered after treatment
• Non-washable items should be sealed in a
plastic bag and stored for one week
• Rooms should be thoroughly cleaned with
normal household products. Fumigation or
specialized cleaning is not required.
• Carpeted floors and upholstered furniture
should be vacuumed

26. Pediculosis
• Louse infestation remains a major problem
throughout the world, making the diagnosis
and treatment of louse infestation a common
task in general medical practice
• Lice are ectoparasites that live on the body
• Lice feed on human blood after piercing the
skin and injecting saliva, which may cause
pruritus due to an allergic reaction
• Lice crawl but cannot fly or hop

27. Incubation periods
• A mature female head louse lays 3-6 eggs, also
called nits, per day
• Nits are white and less than 1 mm long
Nymphs (immature lice) hatch from the nits
after 8-9 days, reach maturity in 9-12 days,
and live as adults for about 30 days

28. Feeding
• Different species of lice prefer to feed on certain
locations on the body of the host
types of lice
• Louse species include Pediculus capitis (head
lice), Pediculus corporis (body lice), and Pthirus
pubis (pubic lice, sometimes called “crabs
• Body lice infest clothing, laying their eggs on
fibers in the fabric seams
• Head and pubic lice infest hair, laying their eggs
at the base of hair fibers

29. Cont…
• Head and body lice are similarly shaped, but
the head louse is smaller
• Nevertheless, the 2 species can interbreed
• The pubic louse, or "crab," is morphologically
distinct from the other two

30. lice

31. Differences of the louse
• The head louse, Pediculus humanus capitis,
has an elongated body and narrow anterior
mouthparts
• Body lice look similar but lay their eggs (nits)
on clothing fibers instead of hair fibers

32. The pubic louse, Pthirus pubis, is
identified by its wide crablike body

33. Cont..
• Lice move from person to person through close
physical contact
• Spread through contact with fomites (eg, combs,
brushes, clothes, hats, scarves, coats, linens) used by
an infested person is uncommon
• Overcrowding encourages the spread of lice
• The body louse can be the vector of Rickettsia
prowazeki, which causes typhus
• Bartonella quintana, which causes trench fever
• and Borrelia recurrentis, which causes relapsing fever

34. Nits
• The average nit (ie, ovum) of the 3 types of lice is 0.8
mm long. The nit attaches to the base of the hair shaft
(in the case of head or pubic lice) or to fibers of
clothing (in the case of body lice) with a strong, highly
insoluble cement; thus, nits are difficult to remove
• The nit is topped with a tough but porous cap known
as the operculum.
• This porous operculum allows for gas exchange while
the nymph develops in the casing Nit on a hair
• Note the thin, translucent cement surrounding the
hair shaft

35. Vectors?
• Pubic louse infestation is usually spread as a
sexually transmitted disease (STD).
• Thirty percent of infested individuals may
have other concurrent STDs (eg, HIV infection,
syphilis, gonorrhea, chlamydia, herpes, genital
warts

36. Nits

37. Prognosis
• Treatments are highly effective in killing
nymphs and mature lice, but less effective in
killing eggs.
•

38. Patient Education
• The social stigma associated with head lice
infestation must be addressed
• Poor hygiene is not a risk factor in acquiring
pediculosis capitis, although it is for body lice
• Management of head lice must include
examination of all individuals exposed (all
household members and other close contacts)
and treatment of all those who are infested
Individuals who have no evidence of infestation
should not be treated

39. education cont…
• Noncompliance is a common cause of treatment failure in
all 3 types of lice infestations
• Therefore, time is well-spent providing patients with
detailed instructions regarding the application and timing
of medications used in the treatment of lice
• During epidemics of head lice, children should be educated
not to share combs, brushes, headbands, hats, and scarves
• All sexual partners from within the previous month of a
person infested with pubic lice should be treated,
• infested clothing and towels need to be washed in hot
water and with a hot dryer; pediculicides are usually not
needed

40. DIFFERENCIAL DIAGNOSIS
• Dandruff
• Dried hairspray/gel
• Dermatophyte infection
• Piedra (black piedra from Piedraia hortae,
white piedra from Trichosporon asahii and
other species of Trichosporon)
• Hair shaft abnormalities (ie, monilethrix,
trichorrhexis nodosa

41. OTHER DIFFERENCIALS
• Folliculitis
• Insect Bites
• Scabies
• Acne
• Delusions of parasitosis
• Xerosis with excoriations
• Impetigo
• Postinflammatory hyperpigmentation

42. THERAPY
• Pesticides
• Occlusive and Nonpesticide Therapy
• Oral Agents:
– Oral anthelmintics, including ivermectin, levamisole, and albendazole
– have been found to be effective against head louse infestation, but are not
approved by the FDA to treat lice
Mechanical removal and shaving Nits
are cemented to hair shaft and unlikely to be successfully transferred to others
•

43. Tungiasis
• Is an infestation by the burrowing flea Tunga
penetrans or related species
• The flea has many common names, being
known in various locations as the
– chigger flea, sand flea, chigoe, jigger, nigua, pigue,
or le bicho de pe
Painful infections with T penetrans can cause
significant morbidity

44. Etiology Life cycle of the chigoe flea,
Tunga penetrans

45. Epidemiology
• Tungiasis was first reported in crewmen who
sailed with Christopher Columbus
• The flea is indigenous to the West
Indies/Caribbean/Central America region, but
it has spread to Africa, India, Pakistan, and
South America

46. Cont….
• To reproduce, the flea requires a warm-
blooded host
• In addition to humans, reservoir hosts include
pigs, dogs, cats, cattle, sheep, horses, mules,
rats, mice, and other wild animals

47. cycle of Tunga penetrans

48. Cont….
• The World Health Organization has listed
tungiasis as a neglected disease of
marginalized populations and has encouraged
more significant research of the disease
• Patient Education
Travelers to affected countries must be
advised to wear shoes (not sandals) when
walking along sandy areas in affected regions
and to refrain from sitting or lying in the sand

49. International occurrence
• Tungiasis is potentially endemic in 88
countries worldwide
• Tungiasis is especially prevalent in low-
resource communities
• Recent prevalence of tungiasis in rural and
urban resource-poor communities in Brazil,
Nigeria, and Madagascar was up to 60%

50. Epidermiology cont..
• Tungiasis has reemerged to epidemic levels in
many countries across sub-Saharan Africa
• In April 2012, a community-based cross-sectional
study was performed in 2 villages in Western
Tanzania
• A total of 586 individuals older than 5 years were
enrolled, and 249 (42.5%; 95% confidence
interval [CI], 38.5-46.5) were diagnosed with
tungiasis
• Those aged 45 years and older had the highest
prevalence of tungiasis at 71.1%

51. Clinical features
• most skin lesions appeared on the feet, where
lesions are most commonly found
• In rural and urban communities in Brazil,
tungiasis has been acquired peridomiciliar and
intradomiciliary
• In many countries with the greatest presence
of T penetrans, lack of health education, poor
housing, and close proximity to animals are
risk factors for tungiasis

52. Clinical features
• Uncomplicated infestation results in pain,
swelling, tenderness, and some limitation in
mobility (although sometimes lesions are
pruritic or even asymptomatic)

53. Prognosis
• The prognosis in tungiasis is excellent if proper
sterile methods are followed for the extraction
of fleas

54. complications
• complications can occur, including secondary
infections, such as bacteremia or septicemia,
lymphangitis, tetanus, and gas gangrene
(These infections may follow attempts to
extract the flea.)
• Autoamputation of digits or other extensive
soft tissue debridement is also a possibility
• Death from tetanus associated with tungiasis

55. Prevention and treatments
• To prevent superinfection, sand fleas should
be surgically extracted immediately after
penetration and the crater should be treated
with topical antibiotic

56. History
• Travel to areas with T penetrans
• Walking along beach areas with bare feet or in
sandals
• Pain or itching and papular or nodular
eruptions, usually on the feet

57. Physical Examination
• Typical areas of involvement include the plantar
surface of the foot, the intertriginous regions of
the toes, and the periungual regions
• the appearance of a white patch with a black dot
• More advanced infestation manifests as crusted,
erythematous papules; painful, pruritic nodules;
crateriform lesions; and secondary infections,
including lymphangitis and septicemia

58. A tungiasis lesion in sub stage 3a

59. differentials
• Cercarial dermatitis
• Creeping eruption due to Ancylostoma species
• Scabies
• Tick bite
• Flea bites
• Myiasis (Dermatobia hominis)
• Fire ant bites
• Ingrown toenails

60. investigations
• Dermoscopy may be helpful
• Histologic Findings
– Microscopically, the flea has a thick cuticle and a
band of striated muscle stretching from the head
to the abdominal orifice

61. topically
• Topical Treatments
• cryotherapy and electrodesiccation of the
nodules. Application of formaldehyde,
chloroform, or
dichlorodiphenyltrichloroethane (DDT) to the
infested skin has been used, but such
treatments are not recommended and may
cause patient morbidity

62. continuation
• Topical ivermectin, metrifonate, and
thiabendazole have been reported as effective
• Occlusive petrolatum suffocates the organism
Twenty-percent salicylated petroleum jelly
(Vaseline) applied 12-24 hours in profound
infestations caused the death of the fleas and
facilitated their manual removal

63. Cont…topical application
• The insect repellant Zanzarin, a lotion
consisting of coconut oil, jojoba oil, and aloe
vera, was shown to reduce the number of
newly embedded fleas and skin lesions, as
Deterrence and Prevention

64. Larva Migrans
• Larva migrans is a group of clinical syndromes
that result from the movement of parasite larvae
through host tissues
• The symptoms vary with the location and extent
of the migration
• Organisms may travel through the skin
(cutaneous larva migrans) or internal organs
(visceral larva migrans).
• Some larvae invade the eye (ocular larva migrans)
• Each form of the disease can be caused by a
number of organisms

65. Cutaneous Larva Migrans
• Larval migration in the skin of the host causes
cutaneous larva migrans
• These infections are often acquired by skin
contact with environmental sources of larvae,
such as the soil
• The larvae cause a pruritic, migrating
dermatitis as they travel through the skin
Many of these infections are self-limiting

66. Cont..larva migrant
• Animal hookworms are the most common
cause of cutaneous larva migrans in humans
• Ancylostoma braziliense is the most
important species
• Less often, cutaneous larva migrans is caused
by A. caninum, A.,ceylanicum, A. tubaeforme,
Uncinaria stenocephala or Bunostomum
phlebotomum

67. Life cycles
• . In their usual hosts, the entry of hookworm larvae into the
skin is followed by penetration of the dermis.
• In the dermis, the larvae enter via veins or lymphatic
vessels, eventually reach the blood, and migrate through
the lungs before reaching the intestines, where they
mature into adults.
• In abnormal hosts such as humans, zoonotic hookworms
can enter the epidermis, but most species cannot readily
penetrate the dermis.
Instead, these larvae remain trapped in the skin. and migrate
for a time in the epidermis before dying. A. ceylanicum is an
exception to this pattern, in that the larvae migrate but are
able to establish patent infections in the human intestine

68. Cont…
• The threadworms Strongyloides papillosus, S. westeri,
S. stercoralis, S. procyonis and S. myopotami can cause
a very similar clinical syndrome
• Strongyloides spp. larvae move more rapidly in human
skin than hookworms, and some authors call this
infection larva currens (“racing larva”) rather than
cutaneous larva migrans.
• Other parasites such as Gnathostoma spinigerum and
Dirofilaria repens can travel through the skin and cause
dermatitis or swelling.
• Some authors consider these syndromes to be
cutaneous larva migrans

69. Cont….
• Parasites adapted to humans can cause some
cases of cutaneous larva migrans
• The human hookworms Ancylostoma
duodenale and Necator americanus migrate
through the skin to reach the intestinal tract
• In people who have been previously exposed,
an allergic reaction to the parasites results in a
pruritic dermatitis similar to that caused by
zoonotic hookworms

70. Visceral Larva Migrans
• Visceral larva migrans occurs when parasitic
larvae migrate through the internal organs of the
host
• Humans can acquire these infections by ingesting
parasite eggs, or by eating tissues from
intermediate or paratenic hosts that contain
larvae
• The symptoms vary with the number of parasites
and the tissue(s) invaded.
• Central nervous system (CNS) infections are often
the most serious form

71. Visceral migrants
• Toxocara canis and T. cati are the most important causes of
visceral larva migrans in humans
• In their normal canine or feline hosts, Toxocara eggs hatch
in the intestines, but the larvae leave the gastrointestinal
tract and migrate through the tissues
• .When they reach the intestines a second time, they
mature into adult worms
• In humans and other paratenic hosts, the larvae do not
complete this migration, and eventually encyst in the
tissues
• T. vitulorum (found in cattle) and T. pteropodis (found in
bats) may also be able to cause visceral larva migrans, but
these species have been less well studied.

72. Viscera migrants cont..
• Visceral larva migrans caused by Baylisascaris
procyonis, an ascarid of raccoons, has been
documented uncommonly in people
• However, most of the reported cases have been
serious, as the CNS and/or the eye were involved
• B. procyonis larvae can cause significant damage
because they migrate extensively,, continue to
grow, and become much larger than Toxocara spp

73. Ocular Larva Migrans
• Ocular larva migrans occurs when migrating larvae invade the eye
of the host
• Symptoms of visceral larva migrans may or may not be present at
the time
• Ocular larva migrans is often unilateral
• The symptoms vary with the location and activity of the larvae, as
well as the amount of inflammation, but can include blindness
• Zoonotic nematodes that have been found within the globe of the
eye include:
• Toxocara canis and T. cati. These species are the most common
cause of ocular larva migrans.
• Baylisascaris procyonis
• Ancylostoma spp. Ext.

74. Papular urticaria
Dr Jere A.Mshana
DERMATOLOGIST

75. introduction
• Papular urticaria is a common and often
annoying disorder manifested by chronic or
recurrent papules caused by a hypersensitivity
reaction to the bites of mosquitoes, fleas,
bedbugs, and other insects

76. CONT…
• Although the overall incidence rate is
unknown, papular urticaria tends to be
evident during spring and summer months;

77. EPIDEMIOLOGY CONT…
• In addition, despite no known racial or sex
predisposition, certain ethnic groups
(specifically Asians) may be more predisposed
to more intense reactions, and
• a small Nigerian study reported a slight female
predominance for skin diseases such as
papular urticaria and atopic dermatitis

78. EPIDERMIOLOGY
• However, adults can be affected, at a much
lower rate

79. Etiology and Pathophysiology
• Papular urticaria is generally regarded to be
the result of a hypersensitivity or id reaction
to bites from insects,
• such as mosquitoes, gnats, fleas,mites,
bedbugs, caterpillars, and moths
• Varicella vaccines have also been implicated
However, it is unusual to identify an actual
culprit in any given patient

80. HISTOPATHOLOGICAL PATTERN
• The histopathologic pattern in papular
urticaria consists of mild subepidermal
edema, extravasation of erythrocytes,
interstitial eosinophils, and exocytosis of
lymphocytes
• These findings suggest a pathophysiologic
process that is immunologically based

81. CONT..PATHO- PHYS..
• Morphologic and immunohistochemical
evidence suggest that a type I hypersensitivity
reaction plays a central role in the
pathogenesis of papular urticaria
• The presence of immunoglobulin and
complement deposits in the skin of some
patients with papular urticaria suggests that
the lesions may be due to a cutaneous
vasculitis

82. CONT…
• The deposits were most frequently seen in
lesions within 24 hours of their development
• The presence of granular deposits of Clq, C3,
and immunoglobulin M (IgM) in superficial
dermal blood vessel walls suggests that
immune complexes (IgM aggregates) may be
primarily involved in the pathogenesis.

83. CONT..
• The deposits were most frequently seen in
lesions within 24 hours of their development
• The presence of granular deposits of Clq, C3,
and immunoglobulin M (IgM) in superficial
dermal blood vessel walls suggests that
immune complexes (IgM aggregates) may be
primarily involved in the pathogenesis.

84. CONT.PATH--PHYS
• with complement activation initiated by Clq
through the classic pathway
• A T helper 2 (Th2) shift may be present,
similar to what is observed in atopy
• In a study of the specific pattern of flea
antigen recognition by IgG subclass and IgE
during the progression of papular urticaria
caused by flea bite

85. CONT..
• variations in the antibody responses of both
subclasses to flea antigens were identified
• Among these 25 patients, those with 2-5 years
of papular urticaria had more IgE bands than
patients with shorter or longer durations of
symptoms
• Thus, the predominant specific antibody
isotypes appear to vary according to the time
elapsed from the onset of fleabite-induced PU

86. Clinical Evaluation
• Children, adult males, nonlocal inhabitants,
urban or periurban areas may be more
vulnerable to papular urticaria
• Patient reports chronic or recurrent episodes
of a papular eruption, that tends to occur in
groups or clusters associated with intense
pruritus

87. Clinical Evaluation
• The first appearance is of papules and
urticarial plaques in clusters
• over exposed and covered parts of the body
• The eruption is characterized by crops of
symmetrically distributed pruritic papules and
papulovesicles
• The lesions can also appear in an area
localized to the site of insect bites, but they
may occur on any body part

88. CLINICAL EVALUATION CONT..
• The lesions tend to be grouped on exposed
areas ,particularly the extensor surfaces of the
extremities
• Scratching may produce erosions and
ulcerations
• Secondary impetigo or pyoderma is common

89. DIFFERENTIALS
• Differential Diagnosis
• Dermatitis
Herpetiformis
• Id Reaction
(Autoeczematization)
• Impetigo
• Insect Bites

90. PAPULAR URTICARIA

91. PAPULAR URTICARIA

92. • Histologic Features
 acanthosis,
 mild spongiosis,
 exocytosis of
lymphocytes,
 mild subepidermal edema
 extravasation of
erythrocytes,
 superficial and deep
mixed inflammatory cell
infiltrate .
• Immunohistochemical
 abundant T lymphocytes
(CD45RO,CD3)
 macrophages (CD68)
 B lymphocytes (CD20)
 DC antigen presenting
cell.
•

93. Management and Prevention
• It should be symptomatic and conservative
• Mild topical steroids and systemic
antihistamines for relief of the itching
• severe enough to warrant the use of short-
term systemic corticosteroids
• If secondary impetigo occurs, topical or
systemic antibiotics may be needed

94. Thanks
• Thank you all