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Pyoderma/Impetigo
Pathophysiology
Impetigo is an infection caused by group A beta-hemolytic streptococci (GABHS) or S. aureus. The organisms are thought to enter through damaged skin and are transmitted through direct contact. After infection, new lesions may be seen on the patient with no apparent break in the skin. Some individuals colonized by S. aureus experience recurrent episodes of impetigo on the nose and lip. Bacteria can spread from the nose to normal skin within 14 days, with impetigo lesions appearing 7-14 days later. Approximately 10% of individuals are colonized by S. aureus in the perineum and more uncommonly, in the axillae, pharynx, and hands.
Pyoderma/Impetigo
Pathophysiology
Often these bacteria enter the body when the skin has already been irritated or injured because of other skin problems such as eczema, insect bites, chickenpox, burns, or cuts. Children may get impetigo after they have had a cold or allergies which have made the skin under the nose raw.
Pyoderma/Impetigo
Etiologic agents
S. aureus
Pyoderma/Impetigo
Epidemiology
Occurs worldwide esp. in countries with warm, humid climates
Incubation period
1-10 days
MOT
Trauma to skin (e.g. cuts, abrasions) Person to person via hands, nasal discharges, shared towels and toys
Pyoderma/Impetigo
s/sx
Red spots painless, pruritic blisters on skin, around nose and mouth, b/w upper lip and nose
Pyoderma/Impetigo
dx
med hx and PE (i.e. appearance of lesion)
Cx
rarely osteomyelitis, septic joints, or septicemia cellulitis in 10% of cases with strep may get lymphangitis, scarlet fever. post-streptococcal glomerulonephritis(rare) permanent skin damage and scarring
Tx
Antibiotics PO (Erythromycin or Cephalexin) or topical Bacitracin,Tee tree oil (topical)
Pyoderma/Impetigo
Nsg interventions
Assess the child's skin condition and document the location and appearance of lesions. Note any new lesion. Initiate and teach measures to prevent the spread of infection: frequent hand washing, use separate towels. daily bathing with soap and water. Regular laundering of contaminated bed linens, towels and clothing. Isolate the child from direct contact with other children until 24 hours after tx has started. engage the child in diversional activities to discourage scratching. Keep lesions covered
Pyoderma/Impetigo
Prognosis
Good, lesions heal slowly and seldom scar.
Acne
Pathophysiology
Acne is a disease that involves the pilosebaceous follicle (the hair follicle and sebaceous gland complex) of the nose, neck, chest, and upper back. Three pathophysiologic factors are involved in the development of acne: excessive sebum production, comedogenesis and the overgrowth of P. acne. Comedogenesis (formation of comedones) results in an inflammatory lesion that maybe either an open or closed comedo. Inflammation occurs with the proliferation of P. acnes, a benign organism always present on the skin, resulting in papules, pustules, nodules, and cysts.
Acne
Types of Acne: Acne vulgaris- commonly seen in adolescents, with lesions on the face, neck, and upper body; severe form of acne. Acne conglobata- chronic form resulting in scarring. Acne rosacea- chronic form occurring in older adults and resulting in reddening of the nose and cheeks; nose can also develop hyperplasia. Acne fulminans- is manifested by a sudden explosion of large inflamed lesions on the back and chest that ulcerate, heal and scar.
Acne
Other forms of Acne: Neonatal acne- occurs on newborn infants, mostly males. Typically, it is found in the nose and cheeks; it usually clears without treatment. Drug acne- occurs as an untoward reaction to certain pharmacologic agents most commonly steroids, iodides (in cough mixtures) and bromides (in sedatives). Occupational acne- acne that result from exposure to occupational compounds or chemicals. Acne cosmetica- is believed to be caused by womens use of cosmetics, cleaning and self-adornment products. The exact cause is unknown because of the variety of cosmetic agents used by women. Acne detergicans- is believed to be caused by compulsive washing of the face with soaps. Pomade acne- follows the hairline and is most commonly seen on African-American men.
Acne
Etiology
Increased proliferation of the keratinizing epidermal cells that form the sebaceous cells. Increased sebum production in relation to the severity of the disease. Decreased amount of linoleic acid in the sebum. The presence of Propionibacterium acnes. Precipitating factors may include use of certain cosmetics, ingestion of certain drugs, exposure to oil and grease,
Acne
s/sx
Non-inflammatory lesions:
Closed comedo or whitehead- plugged follicle stays below the surface of the skin. It usually appears on the skin as small, whitish bumps. Open comedo or blackhead- the plug enlarges and pushes through the surface of the skin. The dark appearance of the plug isnt due to dirt but due to build-up of melanin, the pigmentation of the skin.
Acne
s/sx
Inflammatory lesions
Papules- inflamed lesions that usually appear as small, pink bumps on the skin that can be tender to touch. Pustules (pimples)- papules topped by white or yellow pus-filled lesions that may be red at the base. Nodules- large, painful, solid lesions that are lodged deep within the skin. It is deep-seated structure and tends to remain as long as 8 weeks before finally resolving. Cysts- deep, painful, pus-filled lesions that can cause scarring. It forms as a result of the contents of the comedo spilling over the surrounding of the skin and due to the response of the local immune system in producing pus.
Acne
Dx
PE of affected areas Med hx regarding diet, skin care regimen and meds used.
Cx
Scarring Psychological trauma Social problems Anxiety Depression
Acne
Tx
Topical
Benzoyl peroxide Retinoids Antibiotics
PO
Antibiotics isotretinoin
Acne
Nsg intervention
Administer topical medications such as antibiotics or retinoic acid, as prescribed. Assess for the presence of secondary bacterial infx; if present, manage appropriately. Teach the patient about facial hygiene and management of pustules. Identify concerns regarding body images and encourage the patient to develop a positive self-image. Teach patient how to maintain a normal, wellbalanced diet.
Acne
Don't let acne define you. Remember that who you are goes beyond the condition of your skin.
Burn infx
Pathophysiology
The surface of a burn wound which contains a large amount of necrotic tissue and protein-rich wound exudates provides a rich growth medium. Burns are also associated with a generalized reduction in immunocompetency
Burn infx
EA
Pseudomonas aeruginosa primary cause of life-threatening burn infx. Staphylococcus aureus - pyogenic
Burn infx
Epidemiology
Each year in the United States between 10% and 30% of the approximately 60,000 people hospitalized for burn wounds die of infection, which is the major cause of death in persons hospitalized for burn wounds who have survived the first 48 hours.
Inc period
1-2 weeks from burn
Burn infx
MOT
Nosocomial/Health care-associated infx(HAIs) Autoinfx
Burn infx
s/sx
Redness Swelling Pain Peeling skin Shock Anorexia fatigue
Burn infx
Dx
PE but rather difficult to diagnose since burn induces inflam response indistinguishable from infx and because local s/sx may be absent or minimal.
Cx
Septicemia Pneumonia Meningitis Gas gangrene
Burn infx
Tx
for P. aeruginosa
Combinations(x2) of Ceftazidime (Ceflax, Fortax, Tecicef) Tobramycin (Nebcin) Gentamicin (Primaxin)
for S. aureus
Pen and flucloxacillin
Burn infx
Nsg interventions
Use aseptic tech in all aspects of patient care: Meticulous hand hygiene before and after patient care Use sterile gloves for wound care Wear isolation gown for patient care Wear mask and hair cover when wounds are exposed and during sterile procedures Screen visitors Remove plants in room Inspect wound for signs of infx Antibiotics as prescribed
Burn infx
Prognosis
Most burn infx can be successfully treated with antibiotics and surgery. If nursing intervention is done properly, prognosis will be good.
Rubella
An acute mild, systemic viral dse that produces a distinct 3-day rash and lymphadenopathy caused by Rubivirus Togaviridae (rubella virus). Also German measles; 3-day measles The name rubella is derived from Latin term meaning little red Contagious, but is usually not dangerous Teratogenic to fetus(CRS)
Rubella
Pathophysiology
This disease produces no pathologic entities except those of the skin or the rare complications of the disease
Inc. period
14-21 days
Period of communicability
1 wk before to 5 days after appearance of rashes
Rubella
MOT
Nasopharyngeal secretions/droplet Direct contact Indirectly via freshly contaminated nasopharyngeal secretions or urine
Rubella
s/sx
Low grade fever;sore throat;headache; anorexia; posterior auricular and suboccipital lymphadenopathy;rash(first face then spreads downward to neck, arms, trunk, and legs. Forscheimers spots: small red lesions in the soft palate
Rubella
Dx Difficult because symptoms and rashes are similar to other viral infx Isolation of virus from nasal specimen, throat swab, urine, CSF lab test (e.g. serology) Lab data: inc. WBC Cx CRS Encephalitis 1/6,000 cases Otitis media(rare)
Rubella
Rubella
Tx Nonspecific, supportive Do not give ASPIRIN to children May lead to Reyes Syndrome (fatty degeneration of viscera, mainly affecting liver, brain, and kidneys) Malaise, cough, URI, fever, decreased LOC, hepatic and cerebral dysfunction, high mortality Nsg intervention advise bed rest Avoid exposure to pregnant women Increase fluid intake
Rubella
Immunization 2 doses of rubella vaccine to avoid CRS Immunize postpubertal individuals esp. college students and military recruits Women should avoid pregnancy within 3 mos of vaccine due to theoretical risk to fetus Rubella vaccine should be given as MMR routinely to 12-15mos of age, 2nd dose at 46yo,not later then 11-12yo Prognosis Generally good Bad for pregnant women at 1st tri
Rubeola
An acute viral dse caused by Morbilivirus Paramyxoviridae (measles virus) Also measles; 7-day measles Once considered as the most contagious childhood dse
Rubeola
Pathophysiology
Aside from the changes in the skin and mucous membranes of the mouth and respiratory tract; there is no lesion characteristic of measles other than of its complication
Epidemiology
Phil stat: 31.4/100,000 pop
Rubeola
Inc period
10-12 days
Period of communicability
3 days before to 5 days after appearance of rashes
MOT
Droplet/airborne
Rubeola
s/sx Prodromal(10-11 days): 3 Cs: coryza, cough, conjunctivitis. At the end of prodromal period, the appearance of Kopliks spots (whitish spots in the inner cheeks) Eruptive: maculopapular rashes from head to toe (may be pruritic) Convalescence(7-10days): desquamation of skin
Rubeola
Dx
Lab exam Lab data: inc WBC
Cx
Bronchitis Pneumonia Encephalitis Otitis media
Tx
supportive
Rubeola
Nsg interventions Observe respiratory/contact precautions throughout communicability period Isolation of aeg from dx until 5-7 days onset of rash Photophobia: darkened room and sunglasses Inc fluid intake Prevention Immunization (measles vaccine given at 9 mos SQ) Defer vaccination of persons having fever, severe acute illness Do not give when allergy to eggs is noted
Varicella
Contagious dse usually affecting children characterized by maculopapular rash caused by Varicella Zoster Virus (VZV) or Herpes Zoster Virus(Human Herpes Virus 3) Also chicken pox
Varicella
Pathophysiology After initial inhalation of respiratory droplets, the virus affects the conjunctiva or the mucosa of the upper respiratory tract. Viral proliferation occurs in the original lymph nodes of the upper respiratory tract . A second round of viral replication occurs in the bodys internal organs (the liver and spleen). This secondary viremia is characterized by diffuse viral invasion of capillary endothelial cells and the epidermis. Exposure to VZV in a healthy child initiates the production of immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies. Cell-mediated IR are important in limiting the scope and duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. VZV then remains latent in the dorsal ganglion cells of the sensory nerves.
Varicella
Epidemiology
Humans are the only reservoirs of this disease. estimated 3 million cases per year in US.
Inc period
2-3 wks (usually 10-14 days)
MOT
Direct contact; droplet spread; contact w/ contam objects or contact w/ skin lesions
Varicella
s/sx
Slight fever; malaise; anorexia (1st 24 hrs) Pruritic rash; macule to papule to vesicle to pustule Lesions crust over and usually heal without scarring
Varicella
Dx assessment
The childs fever goes above 39 degrees Celsius or lasts more than 4 days. The childs blisters appear to be infected. The child seems nervous, confused, unresponsive, or unusually sleepy
Varicella
Cx
Varicella pneumonia. Pneumonia can develop if the Chickenpox virus travels to the lungs. Pneumonia from Chickenpox is most common in teens, adults and pregnant women. It is more likely to develop in people who smoke cigarettes, have lifelong lung diseases, or have impaired immune systems. Acute Cerebellar Ataxia. This is treatable condition that causes poor muscle coordination when the virus affects the brain. This is most likely to affect older children. Encephalitis, meningitis, vision loss
Varicella
Cx
Reyes syndrome Arthritis Optic neuritis Nerve damage (facial) Thrombocytopenia Death (rare)
Varicella
Tx
Acyclovir (Zovirax) to lessen lesions Supportive Calamine lotion to reduce pruritus Acetaminophen
Varicella
Nsg interventions strict isolation until all vesicles and most scabs disappear Exclude children from school Focus on skin care to prevent infx Reduce pruritus Do not use aspirin VZIg effective in in modifying or preventing if given w/in 96hrs after exposure Active immunization: Varicella vaccine 1 dose SC for 12yo and younger and 2 doses 4-8 wk apart for older than 12yo
Varicella
Prognosis
Good One long term effect of Chickenpox is seen in about 20% of the population. This effect occurs most often in people over 50yo, and is known as Shingles.
Shingles
It is a reactivation of the varicella virus, often result of immunosuppression. Inflammation of the sensory ganglia of cutaneous sensory nerves, producing fluid-filled blisters, pain and paresthesia (numbness and tingling). It is a common disease that occurs at higher rates among the elderly and in patients with lymphomas, cancers and Hodgkins disease.
Shingles
Candidiasis
Candida species are ubiquitous fungi which are normal body flora. Unfortunately, candidiasis is also the most common mycotic infection, causing a variety of diseases. Also moniliais, oral thrush Candidiasis can range from superficial disorders such as diaper rash to invasive, rapidly fatal infections in immunocompromised hosts(AIDS,DM) Candida albicans, Candida tropicalis, Candida parapsilosis, Candida guilliermondi, and Torulopsis glabrata
Candidiasis
Pathophysiology
In immunocompetent persons, any warm, moist part of the body exposed to the environment is susceptible to infection (e.g vaginits, vulvar rash, oral thrush, conjuctivitis, diaper rash, infx of nail, rectum and skin folds. In immunocompromised aeg, systemic illnesses such as myocarditis, hepatosplenic abscess, pulmonary infection, and CNS infx may occur.
Candidiasis
Epidemiology
Thrush occurs in approximately 2-5 % of healthy newborns and occurs in a slightly higher percentage of infants during their first year of life. Most candidal nfections are superficial and are associated with a benign course and full recovery. Candida spp. colonize over 50% of healthy individuals. Up to 14% of patients with immunocompromising disease develop systemic candidiasis. C albicans is the most common cause of esophagitis (US). In countries where other fungi are endemic, Candida spp. have replaced Cryptococcus spp. as the most common fungi affecting the CNS of immunocompromised aeg.
Candidiasis
Predisposing factors
Prolonged use of broad-spectrum antimicrobials, indwelling IV catheters, parenteral hyperalimentation, prosthesis,GIT surgeries Corticosteroid, immunosuppressive drugs PEM DM, hypoparathyroidism, Addisons AIDS Leukemia Poor oral hygiene
Candidiasis
MOT
Vertical trans from infected mother to neonate(in-utero, or during passage thru vagina); autoinoculation; direct contact; sexual contact
Candidiasis
s/sx
patches of red, moist skin, sometimes with small pustules nearby. White patches around the mouth (thrush) In vaginal: pruritus, burning sensation, whitish-gray discharge
Candidiasis
Dx
Med hx, PE, lab test (blood, stool,wound), tissue bx(definitive) iso of organism from blood, CSF, bx specimen (BMA/tissue specimen)
Cx
Myocaditis, endophthalmitis, hepatosplenic abscess, chonic fatigue
Tx (topical)
Clotrimazole, nystatin, fluconazole, ketoconazole
Candidiasis
Nsg intervention
Admin antifugal drugs as prescribed Encourage proper nutrition, changing of underclothes frequently, good hygiene
Prognosis
Excellent for superficial infx Poor for systemic infx/cx (70% mortality)
Conjunctivitis
Inflam of conjunctiva Bacterial hyperacute, acute or chronic EA
Neisseria gonorrheae, Neisseria meningitidis, Streptococcus pneumoniae, Staphylococcus aureus, and Haemophilus influenzae
Conjunctivitis
Pathophysiology
Introduction of microbes into the eye and surrounding tissues initiates an inflammatory response that includes dilation of the blood vessels, swelling, antibody production and destruction of the offending agent by white blood cells.
Conjunctivitis
Epidemiology
Bacterial conjunctivitis represents 25-50% of conjunctivitis in US
Inc period
1-3 days
MOT
Direct contact Contact w/ contam fingers, facial tissue, eye make-up, clothing
Conjunctivitis
s/sx
Purulent discharge Crusty eyelids after awakening Redness Swelling
Dx
aeg hx, symptomatic Microscopy(g/s), c/s, immunodx procedure
Conjunctivitis
Cx
Blindness (most severe)
Tx
antibiotics as ordered
Nsg interventions
Admin antibiotics as ordered Encourage proper hand washing Warm compress as ordered
Prognosis
Good w/ early tx
Trachoma
contagious eye dse which may result in blindness. one of the earliest eye afflictions, having been identified as early as 27 B.C. also called as granular conjunctivitis or Egyptian Ophthalmia associated with poverty and unhygienic conditions common in hot, dry, dusty climates in the developing world where water is scarce and sanitation is poor 2 stages of Trachoma: 1. active infection of the conjunctiva and 2. Damage to the cornea
Trachoma
Pathophysiology
this conjunctival infx causes inflam and scarring. Scar traction pulls and folds the eyelid inward so that the eyelashes rub against the conjunctiva and cornea, which causes corneal scarring, secondary bacterial infx, and ultimately blindness
Trachoma
Epidemiology
in 2k between 360 to 500 million people are affected by trachoma worldwide and that 6 million people are blind because of this dse (WHO est)
Inc period
5-12 days
MOT
Direct contact w/ eyes, nasal secretions or contam fomites
Trachoma
s/s Eye discharges, conjunctivitis, swollen eyelids, turned-in eyelashes, cloudy cornea Dx Lab assay Enzyme immunoassay conjunctival smear Monoclonal antibody assay
Trachoma
Cx
Chronic follicular conjunctivitis Conjunctival scarring Inversion of the eyelashes Corneal Ulceration Decreased vision Blindness Eye pain Conjunctivitis Keratitis
Trachoma
Tx
oral antibiotics (Erythromycin, Azithromycin) Antibiotic eye cream (Tetracycline) Corneal grafting
Nsg interventions
Good hygiene, public health, envtl sanitation, facial cleansing
Prognosis
Excellent w/ prompt tx The longer the period of infx, the greater the risk of corneal scarring
Gas gangrene
also called myonecrosis, is a subset of necrotizing myositis, an infectious dse emergency caused by Clostridium spp. The hallmark of this disease is rapid onset of myonecrosis, gas production, and sepsis. EA: C. perfringens (80-90% of cases) C. novyi, and C. septicum.
Gas gangrene
also called myonecrosis, is a subset of necrotizing myositis, an infectious dse emergency caused by Clostridium spp. The hallmark of this disease is rapid onset of myonecrosis, gas production, and sepsis. EA: C. perfringens (80-90% of cases) C. novyi, and C. septicum.
Gas gangrene
Pathophysiology
Clostridia are gram-positive, spore-forming, anaerobic rods normally found in soil and GIT of humans and animals. They most often cause disease in the setting of trauma or surgery but can also occur spontaneously in the absence of definite risk factors or exposures. Not all wounds contaminated with Clostridia develop gas gangrene; the myonecrosis seems to only develop when sufficient devitalized tissue is present to support anaerobic metabolism.
Gas gangrene
Epidemiology
Incidence highest in areas w/o access to proper wound care. Mortality from traumatic gas gangrene is greater than 25%. Mortality from non-traumatic gas gangrene caused by C. septicum ranges from 67-100%. Occurrence is not age specific. Diabetic peripheral vascular disease and other chronic immunocompromised states that can predispose individuals to gas gangrene are more prevalent in older populations.
Gas gangrene
Inc period
1-4 days after dirty wound
MOT
Non-transmissible from person-person; usually transmission via surgery or trauma.
Gas gangrene
s/sx
Moderate to severe pain around a skin injury Progressive swelling around a skin injury Moderate to high fever Blister filled with brownred fluid Tachycardia Diaphoresis Note: Symptoms usually begin suddenly and rapidly worsen.
Gas gangrene
Dx
Symptomatic, x-ray, CT scan, MRI to det extent of gangrene
Cx
Permanent tissue damage Jaundice with liver damage Kidney failure Spread of infection throughout the body Shock Stupor Delirium, coma
Gas gangrene
Tx
Debridement Amputation indicated to control spread of infx Antibiotics IV Hyperbaric oxygen
Nsg interventions
Thorough cleansing of wound Watch for signs of infx
Prognosis
Good if non-systemic 20-25% mortality rate for systemic cx
Scabies
contagious skin disease caused by small parasites called itch mites that infest the outer layers of the skin, where their waste products cause irritation. The most common itch mite is the female of Sarcoptes scabiei, a round, pearly white arachnid less than 0.05 cm (0.02 in) long. They are economically and medically injurious, because they carry diseases affecting livestock and humans.
Scabies
Pathophysiology
The scabies mite is an obligate parasite and completes its entire life cycle on humans. The skin is the main organ involved. The S. scabiei var hominis mite can be seen with the naked eye (0.3-0.4 mm long). The male fertilizes the female on human skin and then dies. Newly mated females burrow into human skin, using colytic enzymes to dissolve the stratum corneum of the epidermis. The mite has 4 pairs of legs and breathes and thus does not penetrate deeper than the outer layer of the epidermis.The female deposits eggs in the burrows and then the eggs incubate and hatch after 3-5 days (sometimes up to 8 days). About 90% of the hatched mites die, but those that survive go through various changing stages and reach maturity after a little more than 2 weeks. The female adults, who never leave the burrows, die after 1-2 months.
Scabies
Epidemiology
Endemic in many tropical and subtropical regions. Prevalence rates are extremely high in aboriginal tribes in Australia, in Africa, in South America, and in other developing regions of the world. Incidence in parts of Central America and South America and in one Indian Village approach 100%. Worldwide, the prevalence of scabies has been estimated at 300 million cases annually, although this figure may be an overestimate. No recent published data are available on its incidence in the United States. While scabies appears to be more common in the younger population, it certainly occurs in all ages, all ethnic groups, all socio-economic levels, and in both sexes, but is most common in school children. It is not directly related to hygiene, but is associated with poverty and crowding.
Scabies
Inc period
4-6 wk
MOT
mites are unable to fly or jump but crawl at a rate of 2.5cm/min Direct skin contact Sexually transmitted Indirect thru fomites
Scabies
s/sx Pruritus Hot and burning sensation Red raised lesions (Erythematous papules) Presence of burrow or gray or white threadlike line Skin rash, hand rash, nipple rash, etc. Fever, headache, malaise Pyoderma
Scabies
Dx
skin scrapings to demo mites Microscopy (mite, ova, feces)
Cx
Allergic dermatitis due to topical meds Acarophobia Delusional parasitosis Secondary infx
Scabies
Tx
Scabicide lotion containing permethrin or lindane Storax, semi liquid, grayish-brown balsam Ivermectin PO Thorough cleansing of body w/ soap and water
Scabies
Nsg interventions
Address nature of infx Address concurrent tx of sex partners and household contacts Machine wash(hot cycle) contam linens
Prognosis
excellent
Pediculosis
Lice infestation caused by Pediculus spp. Louse, common name for several species of small, wingless insects. EA: Pediculus humanus capitis (head louse-common among school-aged), Pediculus humanus corporis (body louse), and Pthirus pubis (pubic crab lousecommon among sexually active, found on pubic hair, chest hair, axillary hair, eyebrows, eyelashes, beards).
Pediculosis
Pediculosis
Pathophysiology
Lice have claws on their legs that are adopted for feeding and clinging to hair or clothing. The head and body lice are similar in shape, but the head louse is just smaller. The pubic or crab louse is quite distinct in appearance; it has claws same as those of sea crabs. Lice are blood sucking insects; they suck human blood several times a day. They stay close to the skin for moisture, food and warmth. They are capable of moving freely and quickly which explains their ease in transmission.
Pediculosis
Pathophysiology
A female louse lays about 10 eggs a day for a month because lice can only live for 30 days. The eggs (nits) are attached to the hair shaft, close to the skin surface for good temperature for its incubation.
6-10 days: Nits hatch and it becomes a nymph 10-12 days: The nymphs become mature lice. 15-20 hours: Time allotted for lice to live when outside or away from the host.
Pediculosis
Epidemiology
In the US: Pediculosis affects 6-12 million people annually. The head lice are common among school children. Internationally: Pediculosis has a world wide distribution and is endemic both in developing and developed countries. For example head lice were found 9.6% in adolescent school boys of Saudi Arabia. Pediculosis is more common in female than in male.
Pediculosis
Inc period
P. capitis 8 days P. corporis 6-10 days P. pubis 6-8 days
MOT
Direct Sharing of combs, clothes, hats Sexually
Pediculosis
s/sx
Pruritus Rashes Presence of nits Skin discoloration and thickening
Pediculosis
Dx
PE
Cx
secondary bacterial infx (impetigo, furunculosis)
Tx
Topical pediculocide
Permethrin (e.g. Nix) head/pubic Pyrethrins (e.g., RID, Pyrinate) head/pubic Lindane (e.g. Kwell) avoided in children
Pediculosis
Nsg interventions
encourage proper hygiene Health teaching is important (avoid sharing fomites, safe sex)
Prognosis
Good with prompt tx but reinfestation is common