1 Infectious Diseases
PREVENTION 8 Active Immunization
Varicella vaccine (live attenuated).
IAPCOI opines that varicella vaccine is not recommended for universal immunization in India at present. One has to emphasize the benign nature of and rarity of complications with varicella in young children.
It may be offered to children of high socioeconomic status at 12 months to 12 years single dose and for person over 12 years of age, two doses, 4 to 8 weeks apart.
Other indications are children with chronic heart and lung diseases, HIV infection ( but with CD4 counts above 25% of age related norms), in leukemia (but in remission for at least 1 year), household contacts of immunocompromised children.
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Passive Immoprophylaxis
Varicella zooster immunoglobulin (VZIG).
Given to susceptible at risk of developing severe varicellaand in Immunocompromised children.8 To neonates whose mother experienced onset of varicella 5 days, or less before delivery or within 48 hours after delivery.
MOLLUSCUM CONTAGIOSUM (Fig. 1.9)
This is a skin infection caused by a poxvirus (DNA). It is a common infection in children.
It is transmitted by skin contact with an infected person.
The infection presents as small discrete, round, pearly-white growths, with central umblication on the skin. There may be single or multiple growths on the skin. These growths are usually symptomless.
Common sites of infection are the eyelids, neck, trunk and anogenital area.
Treatment- a) Trichloroacetic acid applications or b) Cryotherapy with liquid nitrogen applications or c) Light electrosurgery, d) Tretinoin gel for small lesion, e) Manual curettage of big lesions.
WARTS (VERRUCAE) (Figs 1.10A and B)
Warts are intraepidermal tumor of skin caused by human papilloma virus (HPV).
TYPES
Common wart (Verruca vulgaris): They are discrete flesh colored, single or multiple papules with a rough surface more common in hands but may occur anywhere.
Flat wart (Verruca plana): They are grouped as flat topped, flesh colored or pigmented papules with smooth surface, common on the face.
Anogenital wart (Condylomata accuminata): It is cauliflower like or pink filiform sessile papule with rough surface. It can be acquired from birth canal or acquired from sexual abuse.
Plantar wart.
Periungual wart.
TREATMENT
Conservative: No treatment spontaneous regression occurs within 2 years in most cases.
20 percent Podophylline is applied with a toothpick twice daily for 3 days. Podophylline is a plant extract, is a microtubule inhibitor that blocks the cell division. In excess doses it is neurotoxic and produces areflexic coma.
Fig. 1.9: Molluscum contagiosum
Figs 1.10A and B: (A) Condylomata in 7 months old child (B) Venereal wart in an adolescent boy
Use of salicylic acid and lactic acid locally.
Tretinoin gel locally at night.
Oral cimetidine 30 mg/kg/day in three divided doses for 3 months.
TUBERCULAR LYMPHADENOPATHY (Figs 1.11A to C)
Cervical and mediastinal glands are affected most commonly, followed by axillary and inguinal:
in 5 percent more than one regional group is involved.
Significant constitutional disturbance and evidence of associated tuberculosis is lacking.
The lymph nodes are painless, initially mobile, and occasionally discharge through the skin causing a “Collar-stud” abscess.
Diagnosis
• Ziehl-Neelsen microscopy (positive in only 25% cases).
• Histology revealing caseating granuloma.
• Culture on Lowenstein-Jensen or Bactec media.
A
Figs 1.11A to C: Tubercular lymphadenopathy. (A) Large solitary cervical lymph node proved to be tubercular on histopathological examination. (B) X-ray chest of the same patient depicting hilar adenopathy. (C) Scrufuloderma over cervical region
B
A B C
Treatment and Prevention
• Short course chemotherapy (as for Pulmonary TB).
• Paradoxical enlargement as a result of hypersensitivity reaction occurs occasionally during or even after completion of therapy.
• Surgical excision is sometime necessary.
• Prevention as for pulmonary tuberculosis.
Scrufuloderma (Fig. 1.11C) results from enlargement, cold abscess formation, and breakdown of a lymph node, with extention to the overlying skin. Linear or serpiginous with dissecting fistulas and subcutaneous tracts studded with soft nodule may develop. Spontaneous healing may take years and eventually a cord like keloid scar results.
LUPUS VULGARIS (Figs 1.12A and B)
It is a rare chronic progressive form of tuberculosis of the skin that develop in an individual with moderate to high degree of tubercular sensitivity induced by previous infection. It is due to direct skin involvement from underlying joint and nodes. A solitary lesion consists of brownish red, soft papule that has an apple-jelly color when examined by diascopy. Chronicity is characteristic, and persistence and progression to plaque over many years are common.
Treatment consists of excision of small lesions and antitubercular drugs.
Figs 1.12A and B: Lupus vulgaris: (A) Lupus vulgaris in a nine-year-old boy. (B) Lupus vulgaris in different parts of the body. Courtesy-Dr Ranbir Pal, Dr Ankur Barua, Dr Pradeep Barua, Sikkim Manipal Institute of Medical Sciences
TETANUS (Figs 1.13A and B)
It is caused by C.tetani, which is a gram positive, spore forming anaerobic bacilli.
Although the incidence of tetanus is reducing due to wide coverage by vaccination, still tetanus neonatorum cases are seen in India due to practice applying mud and cowdung over cord.
From the contaminated wound the toxin tetanoplasmin travels proximally along the nerve to nervous system. It produces tetanus by two mechanisms; by blocking acetylcholine release
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at myoneural junction and by countering the inhibitory influence on muscle reflex arc. It results in increased activity of lower motor neuron, which produces muscle rigidity and spasm. Once fixed the toxin cannot be neutralized by antitoxin.
CLINICAL FEATURES
After an incubation period of 5 to 10 days painful stiff jaw muscle (trismus) appears followed by difficulty in opening the mouth (Lock jaw). Stiffness spreads to neck, back, chest and abdomen. This is rigid stage of the disease.
Intermittent painful contraction of the muscle then starts, the spasmodic stage. The spasm causes grimacing of face (risus sardonicus), and arching of neck and back (opisthotonus).
Spasm of respiratory and laryngeal muscle causes respiratory failure.
TREATMENT
Ideally should be treated in intensive care.
Human Tetanus Immunoglobulin (TIG) 3000 to 6000 IU IM followed by debridement of the wound. The role of ATS, i.e. antitetanus serum is now less important. It is only given when TIG is not available. It is given 50,000 to 100,000 units half IM and half IV.
Benzyl penicillin IV or IM for 10 days to eradicate the existing foci of infection and stop further toxin production.
Sedation by diazepam, but should be nursed in quit environment. Tracheostomy is indicated in severe cases, to guard against the life threatening laryngeal spasm.
Prevention: Tetanus is prevented by immunizing children by DPT under the age of five and by TT thereafter following the IAP immunizing schedule.
TETANUS NEONATORUM (Fig. 1.13B)
Tetanus neonatorum is potentially serious and fatal disease. It usually begins between 3 and 10 days. There is progressive difficulty in sucking, swallowing and excess crying is there.
The spasms and stiffness develops sometime opisthotonus posture is seen.
Prevention: It is prevented by immunizing pregnant mothers by two dose of tetanus toxoid between 16 and 36 week of pregnancy and only one dose of TT in the subsequent pregnancy.
Fig. 1.13A and B: (A) Tetanus in grown-up child, note the facial expression during the spasm (B) Spasm in neonate
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KAWASAKI DISEASE (Figs 1.14A to C)
The etiology of this condition is unknown. Search for an infective agent has so far proved unsuccessful. It is claimed to be an abnormal immunological response to variety of microbial agent including streptococci, rickettsiae, viruses and house dust mite. The greatest prevalence is in Japan. It occurs predominantly in children below five years of age.
Clinical Features and Diagnosis
• Five main features are recognized: fever for more than 5 days, non-purulent bilateral conjunctivitis, reddened lips and oral mucosa, raw red tongue, erythema of limbs including palms and soles, and edema may be present (later periungual or more generalized desquamation occurs), cervical adenopathy.
• Persistent leucocytosis, high erythrocytic sedimentation rate (ESR) or plasma viscosity and thrombocytosis (2nd week onwards) are characteristic laboratory features.
• Up to 20 percent of cases develops coronary aneurysm due to coronary arteritis during later phase of illness.
Diagnosis and Treatment
• Diagnosis is by clinical and laboratory features.
• Other diseases have to be ruled out like scarlet fever, TSS, erythema multiforme, juvenile stills.
• IV Gamma globulin and aspirin during the early stage reduces the risk of coronary aneurysm formation.
• Prolong follow-up should be advised.
Prognosis: usually benign, about one percent of cases ends fatally, mostly from cardiac complication.
Figs 1.14A to C: Kawasaki disease, note the exfoliation of palms and soles. Photographs by Dr KM Sahai, Jaipur
HYDATID DISEASE (Figs 1.15A and B)
The dog is the definitive host of the small tapeworm Taenia echinococcus that produces large number of eggs in the faeces, contaminating grass and infecting sheep, which are the usual intermediate hosts. The cycle is completed by the ingestion of infected raw sheep offal by dogs. Human becomes accidental intermediate host by close contact with dogs.
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In humans, the ingested ova develop to form embryo worms, which penetrate the gut wall and invade the tissues. Most of the embryos are destroyed, but one or more may survive and become encysted, usually in the liver.
Usually there is single cyst, but in 30 percent cases there are multiple cysts, usually in single organ. Cysts have been described in every organ but favored sites are liver, lungs, spleen, brain, eyes, heart, bone and genitourinary system.
Hydatid cysts reach a diameter of 1 cm in 5 months and continue to grow as large as 35 cm containing liters and ‘Hydatid sand’.
Clinical features: infection become manifest either because of expansion of cyst or by rupture and release of the cyst contents. Clinically the cyst present as a palpable, slowly growing liver tumor or as partially calcified lesion on chest X-ray. Large cysts in the liver may rupture spontaneously, causing sudden pain, fever allergic rash and eosinophilia. Cysts may calcify gradually with the death of all living worm tissue.
Diagnosis: Usually by radiography, ultrasongraphy and CT scan. Serological tests such as indirect hemogglutination or ELISA can be of value but false negatives occur, particularly in pulmonary disease and in children. The Casoni skin test is less reliable than serological test.
Treatment: Albendazole in three cycles of 28 days each may succeed in killing infective cysts. Hepatic Hydatid cysts are very slow growing and may not require any treatment unless large and causing compression. Operative removal of cyst under pre- and post albendazole treatment regimen is the mainstay of therapy. Calcified cysts should be left alone. Non-surgical aspiration of the cyst is dangerous and should be avoided.
ASCARIS LUMBRICOIDES (Figs 1.16A to C)
Ascaris lumbricoides is an intestinal round worm, and adult worm ranges from 20 to 35 cm long and is as thick as a pencil, although the male tends to be small. They are particularly more prevalent in condition of poor sanitation, with an individual patient harboring up to 1000 worms and mature female producing up to 20,000 eggs daily. The eggs need to
Figs 1.15A and B: Hydatid disease. (A) Contrast CT scan showing multiple hydatid cyst.
(B) CT chest showing hydatid cyst in lungs
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mature for 2 to 3 weeks in the soil. The spread is fecal-oral with an incubation period of 4 to 8 weeks.
The ingested embryonated eggs hatch in the duodenum and the larvae penetrates through the wall into the blood or lymphatics. They are carried to the liver, heart and thence to pulmonary circulation, here they penetrate through the capillaries into the alveoli. They then ascend the bronchial tree, enter the esophagus and pass down to the small intestine. Here they mature, mate and produces eggs 45 to 60 days after ingestion.
The only symptoms in majority are the excretion of worms or eggs in the stool. In the small percentages of cases gastrointestinal or pulmonary symptoms may arise, probably related to the number of eggs. Loffler’s syndrome occurs when the larva migrates through the lungs. Cough, wheezing and breathlessness are the most important common presenting features. Heavy worm load in children may cause abdominal pain and features of intestinal obstruction and failure to thrive.
Diagnosis is usually by passage of adult worm in stool, detection of ova in stool. Barium meal examination, occasionally adult worm can be picked up in abdominal ultrasonogram.
Treatment consists of use of antihelminth drugs like albendazole, mebendazole, etc. No drug is effective in pulmonary phase of infection.
HERPES ZOSTER (Figs 1.17A and B)
Zoster results from reactivation of latent VZV in a dorsal root or extramedullary cranial nerve ganglion. The virus travels down the sensory nerve to the area of skin supplied by the nerve and produces the typical skin lesion. Zoster in the very young children is probably related to decreased CMI at the time of primary VZV infection.
Clinical features
• Prodromal pain: it persists for 2 to 3 days.
• Rashes initially red patches with vesicles progressing to pustule which scab and then separate. New lesions continue to occur for 3 to 5 days. Scabbing and separation are usually complete by 2 to 4 weeks. Single dermatome is usually involved, but lesion can be seen extending to adjoining dermatome due to overlapping innervations.
Figs 1.16A to C: Ascaris lumbricoides infestation. (A) Child harboring hundreds of roundworm (B) Adult worm in stool. (C) Abdominal USG revealed multiple horizontal streaks depicting worm body
A B C
• Dorsolumbar dermatomes are most frequently involved followed by trigeminal, cervical and sacral.
• Acute phase pain—common during rash evolution.
Complication depend on site of vesicles - ranging from skin infection, ocular, neuralgia, meningoencephalitis, Ramsay Hunt syndrome, cutaneous and visceral dissemination.
Treatment
• Antiviral drugs (acyclovir, famiclovir,valaciclovir) shortens the duration of acute illness.
• Analgesics
• In PHN amitrytylene topical cool spray and transcutaneous nerve stimulation are often helpful.
REFERENCES
1. Meyer HM et al. Am J.Dis. Child 1062; 103: 307.
2. Jes Persen CS et al. Acta Pediatri Scand 1977; 66: 376.
3. Measles: The urban Challenge, UNICEF NY. 1991.
4. WHO/UNICEF: Wkly Epidemiol Rew 1987; 62: 133.
5. IAP guide book on immunization 2004; 16-18.
6. CDC Data. Mumps surveillance Jan 1977, Dec 1982. US Dept of Health and Human Service 1984.
7. IAP guide book on immunization, 2004; 38.
8. IAP guide book on immunization, 2004; 25-26.
Figs 1.17A and B: Herpes zoster. (A) Note the red patche with vesicle over anterior and lateral chest.
(B) Note the same strip of vesicle on backside, the dermatomal distribution
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2 Dermatology
Chapter
ATOPIC DERMATITIS (Figs 2.1A and B)
DEFINITION
Atopic dermatitis or eczema is an itchy, dry, hypersensitive skin disorder affecting many people.
It is common in children but can occur at any age. It is not infectious or contagious.
The exact cause of atopic eczema is unknown. It may be hereditary. The patient or some family members may have other hypersensitive conditions like asthma or hay fever. Infections like Staphylococcus aureus, herpes simplex virus help in flaring of the dermatitis.
The rash may appear red, wet and weepy or dry, thickened and scaly. Scratching often aggravates the rash. The skin thickens and becomes darker. It is a chronic condition. It can affect any part of the body, particularly the elbow bends, back of the knees and the neck.
Infantile Type (seen from 2 months to 2 years). Classically cheeks and shin are involved.
It produces intense itching, lesion is dry, erythematous, excoriated plaques may then become lichenified and hyperpigmented. Spontaneous remission is common by 2 years.
Childhood Type—Seen above 5 years, seen at flexural area, neck, wrists antecubital and popliteal areas.
PATHOGENESIS