Download Treatment

yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Neglected tropical diseases wikipedia , lookup

Microbicides for sexually transmitted diseases wikipedia , lookup

Anaerobic infection wikipedia , lookup

African trypanosomiasis wikipedia , lookup

Norovirus wikipedia , lookup

Middle East respiratory syndrome wikipedia , lookup

Traveler's diarrhea wikipedia , lookup

Cryptosporidiosis wikipedia , lookup

Sarcocystis wikipedia , lookup

Pandemic wikipedia , lookup

Clostridium difficile infection wikipedia , lookup

Trichinosis wikipedia , lookup

Leptospirosis wikipedia , lookup

West Nile fever wikipedia , lookup

Gastroenteritis wikipedia , lookup

Marburg virus disease wikipedia , lookup

Henipavirus wikipedia , lookup

Dirofilaria immitis wikipedia , lookup

Onchocerciasis wikipedia , lookup

Sexually transmitted infection wikipedia , lookup

Schistosomiasis wikipedia , lookup

Human cytomegalovirus wikipedia , lookup

Hepatitis C wikipedia , lookup

Oesophagostomum wikipedia , lookup

Herpes simplex virus wikipedia , lookup

Herpes simplex wikipedia , lookup

Lymphocytic choriomeningitis wikipedia , lookup

Shingles wikipedia , lookup

Coccidioidomycosis wikipedia , lookup

Neonatal infection wikipedia , lookup

Hospital-acquired infection wikipedia , lookup

Hepatitis B wikipedia , lookup

Chickenpox wikipedia , lookup

 The varicella zoster virus (VZV) is the cause
of both varicella (chickenpox) and zoster
Zoster is the result of reactivation of this
residual latent virus.
The virus is transmitted by droplet infection
from the nasopharynx.
Patients are infectious to others from about 2
days before to 5 days after the onset of the rash
Vesicle fluid contains a large amount of virus.
Completely dry scabs are not infectious.
 Varicella confers lasting immunity and
second attacks are uncommon, especially in
immunologically healthy subjects.
 Cell-mediated immunity (CMI) is more
important in both protection against and
control of the infection. If the primary
infection occurs when CMI is impaired, as in
organ-transplant patients,varicella may be
severe and occasionally fatal.
 Maternal varicella in the first 20 weeks of
pregnancy is associated with an approximate
2% risk of fetal damage.
 FVS including skin lesions, central nervous
system and ocular defects, and limb hypoplasia
with a 30% mortality within the first year of
 Maternal zoster in pregnancy is not associated
with intrauterine infection.
 If the mother has varicella within 4 days before
to 2 days after term, the neonate would have
no maternal antibody and is at risk of severe
varicella a mortality rate up to 30% in the
absence of treatment.
 Their distribution is centripetal, and on the
limbs the eruption is more profuse on thighs
and upper arms than on lower legs and
 Constitutional
proportionate to the fever. In some patients
pruritus is troublesome. After about 4 days, no
new crops of lesions appear and existing vesicles
dry and crust.
 Complications. These are rare in otherwise
healthy children, are less infrequent in neonates
and adults and are common in the
 Encephalitis ,pneumonia ,hepatitis ,secondary
infection, Reye’s syndrom,…
Chicken pox
 The first manifestation of zoster is usually pain,
which may be severe, and may be accompanied by
fever, headache, malaise and tenderness localized
to areas of one or more dorsal roots.
 Closely grouped red papules, rapidly becoming
vesicular and then pustular, develop in a
continuous or interrupted band in the area of one,
occasionally two and, rarely, more contiguous
 In uncomplicated cases recovery is complete in 2-3
weeks in children and young adults, and 3-4 weeks
in older patients.
 The thoracic (53%), cervical (usually C 2,3,4, 20%),
trigeminal, including ophthalmic (15%) and
lumbosacral (11%) .
 Trigeminal nerve zoster. In ophthalmic nerve
zoster the eye is affected in two-thirds of
cases, especially when vesicles on the side of
the nose indicate involvement of the
nasociliary nerve.
 Pressure on the facial nerve motor fibres adds
facial palsy, which with the ear pain and
associated vesicles completes the classical triad
of the Ramsay-Hunt syndrome;
 The commonest and most intractable sequel of
zoster is post-herpetic neuralgia, as persistence
or recurrence of pain more than a month after
the onset of zoster, but better considered after
3 months. It is unusual in childhood and
increases in incidence and severity with age.
 Varicella in the otherwise healthy child requires
only symptomatic treatment. Rest and analgesics
are sufficient for mild attacks of zoster in the
young. Soothing antiseptic applications may be
helpful and secondary bacterial infection will
require antibiotics.
 An antiviral is indicated for varicella in adults and
for severe varicella or zoster infections at any age
in the immunocompromised. typically 10 mg/kg
or 500 mg/m2 8-hourly intravenously or 4 g per
day orally . Courses of 5, 7 and 10 days have been
used and some advocate a change from
intravenous to oral drug after 48 hours. In general
practice, zoster is often treated with aciclovir 800
mg five times a day for 7-10 days.
 In the treatment of herpes zoster oticus
(Ramsay-Hunt syndrome), steroid therapy is
better established, probably because of the
central importance of inflammatory swelling
in its pathogenesis. A combination of aciclovir
plus prednisolone may give best results.
 For post-herpetic neuralgia: A tricyclic
antidepressant such as amitriptyline or nor
triptylene , sodium valproate (or other
capsaicin 0.025%.
Modes of transmission
 Warts are spread by direct or indirect contact.
For infection to occur, the wart virus particle
may need to come into contact with a stem cell
in the basal epidermal layer. Thus, impairment
of the epithelial barrier function, by trauma
(including mild abrasions), maceration or
both, greatly predisposes to inoculation of
virus, and is generally assumed to be required
for infection at least in fully keratinized skin.
 Iatrogenic transmission.
 both sexual and non-sexual routes are
significant in transmission of childhood
anogenital warts
 Common
warts are most commonly
situated on the backs of the hands and
fingers. New warts may form at sites of
isomorphic phenomenon is usually less
marked than in plane warts. About 65% of
warts disappear spontaneously within 2
 Periungual warts. Common warts around
the nails, specially at nail folds or beneath
the nail, can disturb nail growth.Nail biting
may increase the risk of infection at this site.
 plantar warts . Most are beneath pressure
points, the heel or the metatarsal heads.
Individuals may be affected by single or
numerous lesions. small bleeding points,
the tips of the elongated dermal papillae,
are evident.
 Plane warts (flat warts).they are round or
polygonal in shape
 The face and the backs of the hands and the
shins are the sites of predilection.
 Anogenital warts(condyloma acuminatum )
are common and are caused in 75% by HPV 6. The remainder are caused by HPV-11 or
more unusual, low-risk HPVs.
 Salicylic acid. The keratolytic effect of salicylic
acid helps to reduce the thickness of warts and
may stimulate an inflammatory response. A
preparation containing 12-26% salicylic acid,
possibly with additional lactic acid, in a quickdrying collodion or acrylate base, is the
treatment of first choice for common and
plantar warts.
 Podophyllin and podophyllotoxin.
contraindication in pregnancy
 Surgery. Excision is usually to be avoided since
scarring is inevitable and recurrences of the
wart in the scar are frequent.
 Cryotherapy. Carbon dioxide snow and
liquid nitrogen can both produce cold
thermal damage to the skin. Liquid N2 is
commonly used in hospital practice,
applied either by a cotton wool bud or from
a cryospray. The main disadvantage of
freezing is pain.
 laser. The carbon dioxide laser has been
used to treat a variety of different forms of
wart, both cutaneous and mucosa.
 Others. Cimetidine ,zinc ,retinoids,…
Herpes simplex
 There are two major antigenic types: type I, which
is classically associated with facial infections; and
type 2, which is typically genital, although there is
considerable overlap in disease manifestations.
 Both type 1 and type 2 HSV are acquired by direct
contact with, or droplets from, infected secretions
entering via skin or mucous membrane.
 Primary type 1 infections occur mainly in infants
and young children, when they are usually
minimal and often subclinical.
 Type 2 infections occur mainly after puberty, and
are often transmitted sexually. The primary HSV-2
infection is more commonly symptomatic.
 Herpetic gingivostomatitis . This is the most
common clinical manifestation of primary
infection by type 1. fever, which may be high,
malaise, restlessness and excessive dribbling.
Drinking and eating are very painful and the
breath is foul-smelling. The gums are swollen,
inflamed and bleed easily.
 Recurrent
infection.Itching or burning
precedes by an hour or two the development of
small, closely grouped vesicles on an inflamed
base. They usually become pustular and
crusted before healing in 7-10 days without
 Mild uncomplicated eruptions of herpes
simplex require no treatment. The use of a
topical antiseptic agent on affected skin may
help to reduce the risk of secondary bacterial
infection. In severe primary infection or
troublesome recurrent disease, antiviral
therapy should be instigated.
 Aciclovir . The usual dose is 5 mg/ kg 8-hourly
intravenously , The usual oral dose is 200 mg
five times daily for 5 or more days. Prophylaxis
against reactivation or spread of HSV may be
useful before cosmetic laser treatment of the
face, as widespread herpes has been reported
following such procedures.
 With
the eradication of smallpox,
molluscum contagiosum (Mc)became the
only remaining poxvirus infection to
specifically afflict humans. This disorder is
caused by the MC virus (MCV), a member
of the Molluscipox genus of Poxviridae. MC
is a common, benign, selflimited process in
children. It also occurs in adults, usually as
a sexually transmitted disease, and more
recently has been observed with increasing
frequency in immunocompromised hosts.
 Transmission is via skin-to-skin contact
and, less commonly,fomites. MC lesions
are firm, umbilicated pearly papules with a
waxy surface. They may occur anywhere on
the skin surface, but are most common in
skin folds and the genital region
deforming lesions may be seen in the
setting of immunosuppression, particularly
AIDS .An associated molluscum dermatitis
is common, especially in children with
atopic dermatitis.
molluscum contagiosum
 The differential diagnosis of MC may
include appendageal tumors, verrucae,
carcinoma, juvenile xanthogranuloma,
melanocytic nevi (especially Spitz nevi),
papular granuloma annulare, pyogenic
immunocompromised hosts, infectious
processes such as cryptococcosis or
histoplasmosis may mimic Mc.
 Most papules of MC resolve spontaneously,
but treatment may be requested when there
are numerous or cosmetically significant
lesions. There are many treatment options,
including curettage, manual expression,
liquid nitrogen, chemovesicants, topical
stripping and laser .