VERSATILE

Allergic Contact Dermatitis (ACD)

2011-08-06T08:07:00.000-07:00

Allergic contact dermatitis (ACD) is a condition where patients develop inflammatory skin changes owing to contact with an allergen. Scientifically speaking allergic contact dermatitis is a delayed type of induced sensitivity. Manifestations of allergic contact dermatitis are redness of the skin (erythema), swelling (edema) and blistering (vesiculation). Allergic contact dermatitis is differ from contact dermatitis, which is due to the chemicals that directly damage the skin ( Irritant Contact Dermatitis).

Jadassohn was the first person who described allergic contact dermatitis (ACD). Sulzberger also contributed his knowledge to develop the patch test, which is used to identify the specific allergen.

Prevalence of different substances like pollens, chemicals and metals in the environment and genetic makeup of the individuals are the main determinants of allergic contact dermatitis (ACD).

Detailed history regarding allergies and patch test are important in identifying the allergen which causing allergic contact dermatitis. And avoidance of the identified allergen is the mainstay of the treatment. Topical corticosteroid and antihistamines play a big role in treatment of allergic contact dermatitis.

Amitriptyline hydrochloride (dose, side effects, indications)

2011-08-01T04:22:00.000-07:00

Amitriptyline hydrochloride is and antidepressant drug. It belongs to the tricyclic antidepressant group. It is one of the widely used tricyclic antidepressants.

Indications for Amitriptyline hydrochloride

Amitriptyline hydrochloride can be used in following conditions

Depressive illness
Nocturnal enuresis in children
Neuropathic pain
Migraine (as a prophylactic drug)

Prescribing physician should take extra precautions to avoid unnecessary side effects if a patient has a history of cardiac diseases, epilepsy, hepatic impairment, thyroid diseases, mania, angle closure glaucoma and urinary retention. It is advisable to avoid Amitriptyline hydrochloride in elderly and during breast feeding.

Contraindications for Amitriptyline hydrochloride

There are several conditions where Amitriptyline hydrochloride cannot be used. Recent heart attacks, arrhythmias, constipation and delirium are the commonest conditions where Amitriptyline hydrochloride is contraindicated.

Dose of Amitriptyline hydrochloride

Depression; initially 75 mg (elderly and adolescents 30–75 mg) daily in divided doses or as a single dose at bedtime increased gradually as necessary to 150–200 mg; CHILD under 16 years not recommended for depression
Nocturnal enuresis; CHILD 7–10 years 10–20 mg, 11– 16 years 25–50 mg at night; max. period of treatment (including gradual withdrawal) 3 months—full physical examination before further course
Neuropathic pain; initially 10– 25 mg daily at night, increased if necessary to 75 mg daily; higher doses under specialist supervision
Migraine prophylaxis; initially 10 mg at night.

Side effects of Amitriptyline hydrochloride

Common side effects of Amitriptyline hydrochloride are arrhythmias, heart block, drowsiness, dry mouth, blurred vision (very rarely precipitation of angle-closure glaucoma), constipation, and urinary retention (all attributed to antimuscarinic activity), and sweating

Benefits of Vitamin F

2011-07-31T22:50:00.000-07:00

Vitamin F is made up of unsaturated fatty acids (linoleic acid (LA) and alpha-linoleic acid (LNA)). Wheat germ, peanut oil, sunflower seeds, safflower, soybean, peanuts, walnuts, pecans, almonds and even avocados are the common foods rich in vitamin F.

Main benefit of vitamin F is the prevention of LDL plaque (bad cholesterol) formation in the arteries. In addition to that vitamin F helps healthy skin and hair as well.

Eczema, acne, and other skin or hair problems and diarrhea are the main results of vitamin F deficiency. Since vitamin F is nontoxic, supplements in the form of tablets can be taken. The excess amount of vitamin f can lead to weight gain.

Too much saturated fatty acids, oxygen and heat are the inhibitors of vitamin F.

Hormonal therapy for acne vulgaris

2011-07-29T09:51:00.000-07:00

Development of acne depends on follicular hyperkeratinization, sebum production, P. acnes growth, and inflammation. Hormones like androgens (male hormones) also play a part in the development of acne. Androgens increase the sebum production, which is one of the major determinants of acne development. Conditions like polycystic ovarian syndrome, congenital adrenal hyperplasia, and adrenal or ovarian tumors can result in increased level of androgen.
During prepubertal period, androgen production rises. Therefore prepubertal boys and girls can show evidence of increased acne.

Because of above reasons, hormonal therapy has a place in treatment of acne. Oral contraceptives and spironolactone are the commonest medications prescribed.Though the androgens play a role in development of acne, most of the patients with acne do not have increased levels of androgens in their blood. Still hormonal therapies are useful for the treatment of acne.

An oral contraceptive or anti-androgen can be used for women with moderate to severe acne who are not trying to become pregnant. Women with milder acne who choose oral contraceptives for the purpose of pregnancy prevention can also experience the ancillary benefit of improvement in their acne.

Hormonal therapy can be used as an adjuvant for moderate to severe acne. It can be combined with topical retinoid, topical and oral antimicrobial agent.Oral contraceptives preparations with a low androgenic progestin can be used for women with excessive ovarian androgen production (eg, polycystic ovarian syndrome) whereas Glucocorticoids are indicated for those with excessive adrenal androgen production, such as in classical congenital adrenal hyperplasia.

CULEX mosquitoes

2011-07-28T03:21:00.001-07:00

These mosquitoes are importance as vectors of Filariasis and arboviruses. Culex quinquefasciatus, Culex fatigans, Culex tritaeniorhynchus, Culex gelidus, Culex fuscocephala and Culex pseudovishnui are some importance members of this group.

Culex quinquefasciatus
Other Culex species

AEDES mosquitoes

2011-07-28T03:16:00.000-07:00

Aedes are world wide distribution extending up to the Arctic Circle where they are a serious biting nuisance to man during summer months. However their major medical importance is as vector of arboviruses. Aedes aegipti and Aedes albopictus are members of this family.

Aedes aegypti & Aedes albopictus

CULICINE MOSQUITOES

2011-07-28T03:10:00.000-07:00

Length of the palps of the females are much shorter than that of proboscis and palps of male are pointed ( not clubbed).Adults usually rests with body parallel to resting surface. Larvae hang down from water surface and have siphon tubes. Eggs may be in clusters or singly but do not have floats.
Culicine mosquitoes include around 30 genera of which the medically important ones are

Aedes
Culex
Mansonia
Armigeres

ANOPHELINES mosquitoes

2011-07-28T03:03:00.000-07:00

MORPHOLOGY

Length of the Palps of the females is equal to the length of the proboscis whereas palps of the male are clubbed in shape. Adults usually rest with body forming an angle to the resting surface. Larvae lie parallel to the surface of water with the help of palmate hairs on the abdomen. They do not have siphon tubes. Eggs are laid singly and usually have floats.

THE GENUS ANOPHELES

The genus Anopheles is the only mosquitoes that are medically important among Anophelines. Anopheles is the only known vectors of human malaria. In some countries they transmit Filariasis (Africa and SE Asia), and viruses as well (Africa).

Anopheles has world wide distribution. The genus contains about 400 species, but only about 30 species are efficient natural vectors of human malaria. Natural susceptibility of Anopheles to human malaria is largely unexplained. The frequency of feeding on man, mosquito density and longevity are some features of importance in determining the efficiency of a vector in nature. Further, the habits of a given species vary from country to country. Thus a particular species may be an important vector in one area and not in another.

Anopheles is crepuscular (around sunset) or nocturnal in habits such as mating, blood feeding and ovipositioning. They are generally not found at altitude above 2000-2500 m.

Anopheles culicifacies, Anopheles subpictus, Anopheles minimus, Anopheles vagus, Anopheles maculates and Anopheles annularis are some members of the genus Anopheles. They all are vectors of human malaria but distribution varies. Anopheles culicifacies is the only malarial vector in Sri Lanka whereas others are found as vectors in Africa.

MEDICALLY IMPORTANT MOSQUITOES

2011-07-28T02:55:00.000-07:00

INTRODUCTION

Mosquitoes are the most important group of insects. They are important as vectors of human diseases. In addition they cause a considerable biting nuisance to man. Mosquitoes are found world wide with over 3000 species included in 34 genera, distributed from the tropics to the arctic regions. However, the medically important species belong to only a few of these genera.

MORPHOLOGY

These are small slender flies with one pair of wings; forwardly projecting mouth parts; scales covered the body, legs and wings. The body is divisible to head, thorax and abdomen. The head bears the characteristic mouth pars suited for piercing and sucking. The mouth parts are collectively called the proboscis. It consists of a labium (lower lip), a labrum (upper lip) enclosing two pairs of cutting apparatus (mandibles and maxillae) and a stylet (hypopharynx) through which the salivary duct opens. The food channel is formed the labrum and the hypopharynx. The head bears a pair of palps and long segmented antennae. In the female the antennae have only few hairs, while in the males they are bushy and feathery. Internally trilobed salivary gland is situated ventrally in the thorax. Powerful flight muscles are also present in the thorax. The body cavity (hemocele) is bathed in fluid.

LIFE CYCLE
Only female mosquitoes suck blood, while the males thrive on plant and fruit juices. The blood meal is essential in providing nutrients for the maturation of eggs. The time taken from the blood meal to oviposition is referred to as the gonotrophic cycle (2-3 days in the tropic). The life cycle has a complete metamorphosis with egg, larva, pupa and adult stage.

EGG: A female mosquito carefully selects the breeding site, each species having its own preferred habit, 100-200 eggs are laid at a time on water or moist surface, either singly or in batches. Eggs hatch in around 2-5 days.
LARVA: Larvae are legless with prominent thorax. It is actively feeding with four larval stages (7-14 days). Larvae breathe air through spiracles found in the posterior ends. In general almost any collection of permanent or temporary water can be a larval habit, but larvae are not found in large expanses of water such as lakes and in fast flowing rivers (except at margins).
PUPA: They are ‘comma’ shaped with a large cephalothorax (fused head and thorax). Although non-feeding, they show active movements. Pupal stage lasts 2-3 days.
ADULT: They emerge by splitting the pupal skin. In the tropics adults live for 2-3 weeks but in colder climates they live much longer.

ADULT BEHAVIOUR

Mosquitoes are rather selective in their choice of hosts for their blood meals. Some species prefer human blood to animal and are called anthropophilic while others feeding only on animals are termed zoophilic. The biting and resting behavior of adults are important in the epidemiology of disease transmission.

Medically important mosquitoes can be divided into two groups;

1. Anophelines
2. Culicines

What are the phytohaemagglutinins?

2011-07-28T02:46:00.000-07:00

Introduction

Haemagglutinins are proteins capable of agglutinating red blood cells. Such substances present in plants are called phytohaemagglutinins. They are present in all legumes. About 25% of the growth inhibition produced in rats (experiment level) by Soya beans is due to haemagglutinins. Significant level of haemagglutinins occur also in black beans and kidney beans (varieties of Phaseolus vulgaris).purified hemagglutinins from these two pulses, when fed to rats at a level0.5 to 1% result in 100% mortality within two weeks.

Mechanism of toxicity

Phytohaemagglutinins bind with the red cell membrane and make them more vulnerable to the hemagglutination

Common food items containing phytohaemagglutinins

Soya bean
Black beans and
Kidney beans

Removal of phytohaemagglutinins from those food items

The toxic factor can be destroyed completely by soaking the grain overnight and later autoclave.

The importance of such factors in human nutrition should not be discounted, as pulses form an important item in most diets.

Toxic substances in pulses

2011-07-28T02:32:00.000-07:00

Deleterious substances of various kinds are present in legume grain eaten by man. Among them are:

Trypsin inhibitors
Cyanogenic glucosides
Goitrogenic factors
Hemagglutinins/Haemagglutinins
Saponins
Alkaloids
Tannins
flatulent factors
Antivitamins
Aflatoxin

Contamination with microorganisms could result in the formation of toxins (aflatoxin) which produce adverse effects when ingested.

In most pulses these toxins are destroyed by adequate soaking, removal of the skin and ordinary methods of cooking. In some species removal of the skin and inactivation toxins require prolonged cooking time, pressure cooking or autoclaving, facilities that are available in few households. For any pulse to welcome in a household it should lend itself to ordinary methods of preparation, needing little fuel. Pulses form such an important item of the diet in developing countries that every effort should be made to encourage their consumption by increasing their digestibility.

In the preparation of whole grains, the seeds should be soaked for 24 to 36hoursin a small volume of water, changing the water every 8 to 12 hours. Skins can be removed by rubbing the seeds gently. The grain is then boiled in a little water till it softens. The cooking water should be consumed as it contains water soluble nutrients. When feeding young children, the seeds should be mashed to increase the digestibility. The dhal is more easily cooked than gram. Pulses are the one food that benefits by over boiling.

Azelaic acid for acne

2011-07-24T04:25:00.000-07:00

Azelaic acid is a saturated dicarboxylic acid. It is found as a white powder. Number of skin and hair conditioners contains azelaic acid as a component. Oleic acid is used as the precursor to produce azelaic acid industrially. Malassezia furfur (a Yeast) produces azelaic acid.

Mild to moderate acne can be treated with azelaic acid. Both comedonal acne and inflammatory acne is treatable with this compound.

Adapalene for acne

2011-07-24T03:43:00.000-07:00

Mild to moderate acne can be treated with adapalene. Adapalene is a retinoid (third generation). Adapalene is topically applied for acne vulgaris. It should be applied once a day basis. Before the application of adapalene, face should be washed with soap and water. Some patients may experience skin irritation.

ACTH stimulation test

2011-07-24T03:21:00.000-07:00

Introduction

The anterior pituitary is often referred to as the “master gland” because, together with the hypothalamus, it orchestrates the complex regulatory functions of multiple other endocrine glands. The anterior pituitary gland produces six major hormones: (1) prolactin (PRL), (2) growth hormone (GH), (3) adrenocorticotropin hormone (ACTH), (4) luteinizing hormone (LH), (5) follicle-stimulating hormone (FSH), and (6) thyroid-stimulating hormone (TSH)

ACTH secretion is pulsatile and exhibits a characteristic circadian rhythm, peaking at 6 A.M. and reaching a nadir about midnight. Adrenal glucocorticoid secretion, which is driven by ACTH, follows a parallel diurnal pattern.

ACTION

The major function of the HPA axis is to maintain metabolic homeostasis and to mediate the neuroendocrine stress response. ACTH induces cortical steroidogenesis by maintaining adrenal cell proliferation and function. The receptor for ACTH, designated melanocortin- 2 receptor, is a GPCR that induces steroidogenesis by stimulating a cascade of steroidogenic enzymes

LABORATORY INVESTIGATION

Biochemical diagnosis of pituitary insufficiency is made by demonstrating low levels of trophic hormones in the setting of low target hormone levels. The diagnosis of adrenalInsufficiency may be established by means of an ACTH stimulation test.

Test

This is a screening test (the so-called rapid ACTH stimulation test) which involvesthe administration of 25 units (0.25 mg) of cosyntropin intravenously or intramuscularly and measurement of plasma cortisol levels before administration and 30 and 60 min after administration, the test can be performed at any time of the day. The most clear-cut criterion for a normal response is a stimulated cortisol level of >500 nmol/L (>18 µg/dL), and the minimal stimulated normal increment of cortisol is >200 nmol/L (>7 µg/dL) above baseline. Severely ill patients with elevated basal cortisol levels may show no further increases following acute ACTH administration.

Acunol homeopathic medication for acne

2011-07-23T22:17:00.000-07:00

Acunol is a compound used in homeopathic system of medicine. Active constituents of acunol are Potassium Bromide, Sodium Bromide, Zinc Sulphate ,Sulphur and Nickel Sulphate. Whereas inactive ingredients are Lactose, Magnesium Stearate, and Copper. Acunol tablet is 600mg. it should be swallowed or chewed. Exact mechanism of action is not well understood. But its active ingredients may enhance phagocytic and bactericidal activity of neutrophils.

Acunol is indicated in mild to moderate acne vulgaris, acne rosacea, peri-oral dermatitis, and folliculitis whereas allergy to ingredients of acunol is a contraidication.

Acunol should not be used during pregnancy but there are no evidence to suggest that it is harmful during pregnancy. Lactating mothers should use it with cautions as acunol can be secreted via breast milk. Dose should be adjusted in pediatrics practice.
Significant side effects are not reported but drug overdoe can give rise to gastrointestinal disturbances like nause, vomoting and diorrhea. Allergic reaction is a possible side effect.

Isotretinoin for acne

2011-07-23T21:38:00.000-07:00

Isotretinoin(Accutane) is a vitamin A derivative therefore it is a retinoid. Small amount of Isotretinoin(Accutane) is naturally present in the human body as well. Initially it was produced to treat cancers such as brain cancers and pancreatic cancers but now it is also useful as an acne treatment as well. Accutane, amnesteem, isotane and sotret are the few trade names. Oral preparations are available for the acne.

Topical treatment and oral antibiotics should be used for acne before isotretinoin. If those treatment fail, Isotretinoin can be used. Isotretinoin is indicated for the treatment of severe cystic acne vulgaris and severe acne rosacea.

Patient’s weight and the severity of the conditions are the determinats of isotretinoin dose. But usual dosage varies between 0.5 mg/kg/day to 2 mg/kg/day. Treatment should be continued for four to six months for a better result. 40% of patients will achieve complete cure while 20% will relapse. Isotretinoin is available in tablets and topical forms.

Common side effects are flaring up of acne, conjunctivitis, raised blood sugar and impotence. Teratogenicity is the most feared side effect of this drug therefore it should not be used during pregnancy.

Bence Jones protein

2011-07-11T01:49:00.000-07:00

The Bence Jones protein was described by the English physician Henry Bence Jones in 1847. Bence jones protein can be found in blood and urine. it is a monoclonal globulin protein. it's molecular weight i s 22-24 kDa. There are several conditions such as multipla myeloma can give rise to bence jones protein therefore detection of bence jones protein in the urine or blood can be used as a diagnostic test for those conditions. 2/3 of patients with multiple myeloma will be positive for bence jones protein test. Bence jones protein is produced by the neoplastic plasma cells (cancer cells).And these protens are immunoglobulin light chains

Human worm parasite infections

2011-06-25T21:25:00.000-07:00

HUMAN HELMINTH INFECTIONS

INTRODUCTION

Helminthes (worms) are among the major parasites of humans and are classified under two phyla;

Nemathelminthes ( Nematodes or Round worms)
Platyhelminthes (Cestodes or tape worms and Trematodes or flukes)

Majority of helminthes that infect humans belong to the following three classes.

Nematoda (round worms). They are elongated, cylindrical worms. The sexes are separate. A complete alimentary canal is present with some species having well developed buccal capsules. They possess a body cavity ( pseudocele)
Cestoda (tapeworms). They are flattened tape-like segmented worms. Sexes are not separate, each segment having a set of male and female reproductive organs. Alimentary canal is absent. The head end possesses suckers, often with hooks. The body cavity is absent.
Trematoda (flukes). They are flattened and leaf-like. Each fluke has a set of male and female reproductive organs (except blood flukes where sexes are separate). The alimentary canal is incomplete and there is no body cavity. They possess oral and ventral suckers.

Nematoda (round worms)
Trematoda (flukes)
Cestoda (tapeworms)

Roundworms (NEMATODES)

2011-06-25T21:21:00.000-07:00

This is a large and highly successful group of organisms found living in all types of habitats. Some are important parasites of human and animals. The parasitic nematodes are remarkable being similar to each other but vary widely in size. They are cylindrical with unsegmented bodies and have false body cavities (pseudocoelomes). The multi-layered cuticle is non-nucleated and allows contraction and expansion of the body. Inner to the cuticle is the muscle layer. Among the major organs are the alimentary, excretory and the reproductive systems, which are suspended in the ‘body cavity’. They have separate sexes.

The cuticle is shed (moulting) four times during development from egg to adult worm. Some species have direct life cycles while others need intermediate hosts. Nematodes do not multiply in humans (except in the form of auto infection with Strongyloides). Parasitic nematodes of humans are found in various tissues such as subcutaneous, muscle, lymphatic tissue and in organs such as the intestinal tract.

Nematode parasites of humans

Small intestine

Ascaris lumbricoides ( The large roundworm)
Necator americanus (Hook worm)
Ancylostoma duodenale (Hook worm)
Strongyloides stercoralis (Thread worm)
Trichinella spiralis (Trichina worm)

Large intestine

Trichuris trichiura (Whip worm)
Enterobius vermicularis (Pin worm)

Tissue nematodes

Subcutaneous tissue (filarial worm, Dracanculosis and animal hookworm larvae)
Muscle ( Trichinella spiralis)
Lymphatics ( Filarial worm)
Visceral organs (Toxocara)
CNS ( Angiostrongylus cantonensis and Toxocara)

Infections due to other nematodes

Dracunculus medinensis (Dracanculosis or Guinea worm disease)
Trichinella spiralis (Trichinosis)
Larva migrans

Cutaneous larva migrans
Visceral larva migrans

tapeworms (CESTODA)

2011-06-25T21:17:00.000-07:00

They are flat, ribbon-like worms inhabiting the intestinal tract of vertebrates. Their bodies are formed of chains of segments (proglottids) of varying sizes and shapes. The whole chain is called strobila. At the anterior end is the scolex or the ‘holdfast’ organ which is used for the attachment of the worm to the intestinal mucosa. Suckers aid the attachment to the mucosa in some while others use sucking grooves. Hooks also help when present. Behind the scolex is the undifferentiated ‘neck’ region from which growth of new segments takes place continuously. The end of the worm is comprised of gravid (pregnant) segments. They have no alimentary canals and nutrition is getting through the cuticle of the segments. Each segment has male and female reproductive organs (testes, ovaries and uteri).

In the life cycle the larval stages are found in the intermediate hosts. Some have only one intermediate host while others have two intermediate hosts. In humans pathology is caused by either adult worms or by larval stages.

Cestodes parasites in human

Human infection due to adult worms

Taenia saginata (beef tapeworm)
Taenia solium (pork tapeworm)
Hymenolepis diminuta (rat tapeworm)
Hymenolepis nana (The dwarf tapeworm)
Diphyllobothrium latum (fish tapeworm)
Dipylidium caninum (cat/dog tapeworm)
Bertiella studeri (monkey tapeworm)

Human infection due to larval stages

Cysticercosis cellulose (Cysticercosis)
Echinococcus garnulosus (Echinococcosis/Hadatid disease)

Flukes (TREMATODES)

2011-06-25T21:12:00.000-07:00

Several trematodes (also known as flukes) are capable of parasiting man. The most important of these are the schistosomes. Other trematodes are also of major medical significance, especially in the Far East, as parasites of the liver, lung and the intestinal tracts.

Trematodes are flat, leaf-like hermaphrodite helminthes (excluding schistosomes). These parasites vary in size from a few millimeters to around 7cm in length. They possess two suckers, one for attachment, and another into which the alimentary tract opens. The rest of the body is occupied by the gut, testes, uterus and yolk glands. The morphology of these structures is used in identification.

In all trematodes infections, man acts as the definitive host harbouring the adult worms. The life cycle is complex, with alternating sexual and asexual reproduction in different hosts. The first intermediate host, however, is always a freshwater snail. Each parasite is specific in the choice of a snail host. The life cycles of trematodes (excluding the schistosomes) are similar: the egg which is excreted by a definitive host needs to reach water/moisture, where the ciliated larva inside the egg (called the miracidium) escapes and finds its way into a snail host. There is prolonged development multiplication in the snail with the formation of sporocysts and radia (2nd stage larvae) stages. The final larval stages, which are known as cercaria, emerge from the snail and encyst as metacercaria on fish, crustacean or water plants. Human infection follows ingestion of these infected second intermediate hosts.

Trematodes parasites in human

Lung flukes

Paragonimus westermani

Liver flukes

Ophisthorchis (Clonorchis) sinensis (Chinese liver fluke)
Fasciola hepatica (sheep liver fluke)

Intestinal flukes

Fasciolopsis buski

Blood schistosomiasis

Intestinal schistosomiasis

Schistosoma mansoni
Schistosoma japonicum

Urinary schistosomiasis

Schistosoma haematobium

large roundworm( ASCARIS LUMBRICOIDES)

2011-06-25T21:04:00.000-07:00

GEOGRAPHICAL DISTRIBUTION

The worm has a world wide distribution but prevalence is high in warmer climates in tropical region where personal and environmental sanitation are poor. It is prevalent in countries like India, Nepal, Pakistan and Sri Lanka.

MORPHOLOGY

Adult female worms are 20-40 cm in length while the adult male worms measure 15-30 cm. The tail end of male is curved.

LOCATION IN THE HOST

The worms are found free in the lumen of the small intestine.

LIFE CYCLE

The fertilized female lays about 200.000 eggs per day. The eggs are oval in shape (65*45µm). The egg has an outer mammilated, ailbuminous coat that appears brown due to bile pigments. Some eggs may be decorticated (with outer coat missing). A certain portion of eggs (15%) is unfertilized and appear longer and rectangular (90*40µm) with no embryo. The embryo is unsegmented when eggs are passed in faeces.

The eggs develop further in soil with the first moult taking place (within the egg) to form the 1st stage larva in about 7 days. With the second moult the infective 2nd stage larva is formed inside the egg in 2-3 weeks under optimal conditions of development such as moist, warm (25-30 ºC) clay type soil. The infective eggs can remain viable in suitable soil for long periods of time.

When ingested the eggs hatch in the upper part of the small intestine liberating the larvae which penetrate the intestinal mucosa to enter the blood stream (or the lymphatics). The larvae are carried into the lungs via the liver and the heart. The larvae develop further in the lungs moulting twice (5th and 7th days). They penetrate the alveolar walls to move along the bronchioles, bronchi and trachea and are swallowed. On reaching the small intestine they mature into males and females. The time taken for an egg to develop into a mature is about 60 days. Adult worms may live up to 2 years.

PATHOGENESIS AND CLINICAL FEATURES

Many infected persons remain asymptomatic. However the presence of a small number of worms may lead to complications. The pathogenesis and clinical features can be categorized into; pulmonary ascariasis: intestinal ascariasis: complications of ascariasis and allergy to Ascaris species.

Pulmonary ascariasis: An intense host reaction occurs in the lungs as a result of larval migration, 5-6 days after the ingestion of infective eggs. Larval antigens released by moulting larvae elicit an inflammatory reaction associated with moderate eosinophilia, pneumonitis, bilateral pulmonary infiltration, cough, dyspnea, substernal pain, fever, skin rashes and often asthma. These signs and symptoms are collectively called the “Loffler’s Syndrome”. The severity of the host reaction depends on the number of larvae migrating and the previous infection history: hypersensitive individuals show severe reactions with other allergic manifestations. Loffler’s syndrome is usually transient, lasted about 2-5 days. Pulmonary pathology is primarily immunological in nature.
Intestinal ascariasis: Adult worms in the small intestine may cause mild abdominal pain and restlessness. Some asymptomatic persons are known to be harbour large worm loads. However, the clinical consequences of the infection are generally dependent on the number of worms present (worm load). It is difficult to say whether ascariasis is a direct cause of malnutrion as the infection is common in areas where malnutrion co-exist. But the infection certainly precipitates severe malnutrition (even kwashiorkor or marasmus) in undernourished children. Ascariasis as also known to lead to vitamin A deficiency. Improvement of growth in areas where protein energy malnutrition is prevalent has been demonstrated following worm treatment. Similarly worm treatment has been shown to improve physical fitness and educational abilities of malnourished children.
Complications of ascariasis: The commonest complication of ascariasis is intestinal obstruction, particularly in persons with heavy worm loads. They may also cause intestinal perforation leading to peritonitis. Adult worms may wander into orifices such as the opening of the bile duct, pancreatic duct causing obstruction bile and pancreatic secretion respectively. Some drugs, chemicals and food items may cause worms to get abnormally activated and migrate to distant site.
Allergy to Ascaris species: Allergic manifestations are common during the acute phase of larval migration and due to the presence of adult worms in the small intestine. Many allergic and infected persons experience asthma. The relationship of asthma, allergy and ascariasis is not clearly known. However it is well known that adult Ascaris worms are highly allergic and their handling may cause serious reactions in sensitive individuals.

DIAGNOSIS

The simplest diagnostic method is the demonstration of characteristic eggs in the faeces.

PREVENTION

Vegetable that are usually eaten raw or undercooked should be washed thoroughly. Fruits fallen under trees should be washed before eating. Washing of hands after working with soil helps in the prevention.

CONTROL

Prevention of indiscriminate defaecation, provision of sanitary latrines, elimination of parasite reservoir by worm treatment and health education are important.

TREATMENT

Broad spectrum antihelminthetic drugs like albendazole and mebandazole can be used. Usual drug course is 500mg stat for adults and the dose for children depends on the weight and the age.

Hookworms (NECATOR AMERICANUS & ANCHYLOSTOMA DUODENALE)

2011-06-25T20:58:00.000-07:00

GEOGRAPHICAL DISTRIBUTION

The parasite is widely distributed in the tropics and sub-tropics. In cold climates with suitable microclimates (such as in coal mines) the parasite may be found. Two species infect humans. Necator americanus is the species found in South Asia, Africa, pacific and in North and South America whereas Ancylostoma duodenale is the main hookworm of Eastern Europe, North Africa, India, Northern China and Japan. Both species can be found together in South East Asia, the pacific and West Africa.

MORPHOLOGY

The worms measure 1-2cm in length. The head ends of the worm are sharply bent backwards like a hook. In the case of N. americanus the buccal cavity bears a pair of ventral cutting plates used in biting the mucosa for feeding. A. duodenale is larger with the head end bending backwards smoothly. The buccal cavity has two pairs of curved teeth. In both species, the tail end of the male is flattened and expanded to form the copulatory bursa.

LOCATION IN THE HOST

The hookworms inhabit the small intestine of humans. Unlike Ascariasis it is attached to the mucosa of the intestine of the intestine with the buccal capsule.

LIFE CYCLE

Each female N.americanus lays about 3000-6000 eggs per day (A. duodenale lays about 10,000-20,000 per day). The eggs are oval in shape and have thin, glass-like egg-shells. The embryo is usually divided when the eggs are passed in faeces. On reaching soil and under optimum conditions the eggs hatch into L1 larva within 24 hours. The optimum conditions are; shade, warmth’ moisture and sandy type soil.

L1 is an actively feeding rhabditiform larva (esophagus with a posterior bulb, like in the Rhabtid species).These larvae grow rapidly and moult on about the 3rd day into L2 rhabditiform larvae. On or about the 5th day the second moult transform them into long, non-feeding L3 infective or filariform larvae. These larvae have long, narrow esophagi and retain the cuticle of L2 as a sheath. The infective larvae move on to the topsoil and on to low vegetation seeking hosts. Under favorable conditions they remain alive for 3-6 weeks. When they come into contact with human skin, the activated larvae shed the sheath and penetrate the skin (usually between toes).
The larvae are carried in the blood or lymphatics and finally reach the lungs. They penetrate the alveoli and start ascending along small bronchioles to bronchi and then to trachea (unlike Ascariasis there are no moults in the lungs). At the pharynx they are swallowed. On reaching the small intestine the final moult transform them in to young males and females. The time taken between larval penetration and the formation of mature worms is 4-7 to weeks. Infective A.duodenale larvae ingested with contaminated food can establish in the intestine without undergoing lung migration. Ancylostoma is a unique parasite as it can go into a phase of ‘arrested development’ when the external conditions are not favorable and restart the life cycle when the conditions are good.

PATHOGENESIS AND CLINICAL FEATURES

In the acute infection the initial sings and symptoms are due to the penetration and migration of larvae in the skin. At the site of entry, a transient dermatitis with intense pruritus can result. This condition is called ‘ground itch’. The lesions may get secondarily infected. The lung migratory phase of hookworms is short and the pulmonary symptoms are either assent or minimum.

The pathogenesis of hookworm disease is directly related to the attachment of the worms to the mucosa. They attach to the mucosa by biting in plugs of mucosa (including 7-9 villi), which are stripped off the lamina propria. The pool of blood thus created is sucked in using the muscular pharynx. Only part of the sucked blood is used for food and oxygen, a large part being excreted continuously. This leads to blood loss and results in hypochromic, microcytic (iron deficiency) anemia. Each N.americanus sucks about 0.03 ml of blood per day while A.duodenale sucks about 0.26 ml per day.

The degree of anemia is related to the worm load and the nutritional status of the host. Hypoproteinemia seen in severe hookworm disease may be related to poor food intake (poverty, anorexia), impaired absorption, increased loss and a combination of all. Impairment of nutrient absorption, intestinal protein loss and lowered food intake collectively result in stunting (growth retardation). The pathogenesis of impaired mental and physical development in hookworm disease is not clear.

DIAGNOSIS

This is done by demonstrating characteristic eggs in the faeces. The eggs can be cultured into infective larval stage to distinguish between Necator and Ancylostoma.

PREVENTION AND CONTROL

Avoidance of indiscriminate defaecation and use of footwear help in prevention. Provision of hygienic latrines, chemotherapy of infected people and health education are important in control of the infection.

TREATMENT

Hookworm infection can be eradicated with several safe and highly effective antihelmintic drugs, including albendazole (400 mg once), mebandazole (500 mg once), and pyrantel pamoate (11 mg/kg for 3 days). Mild iron-deficiency anemia can often be treated with oral iron alone. Severe hookworm disease with protein loss and malabsorption necessitates nutritional support and oral iron replacement along with deworming.

Threadworm (STRONGYLOIDES STERCORALIS)

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GEOGRAPHICAL DISTRIBUTION

The parasite has a world wide distribution but more common in tropical and subtropical regions.

LOCATION IN THE HOST

It is found embedded on the mucosa of the small intestine

MORPHOLOGY

Only females are seen in the parasitic cycle (in the intestine of infected persons). These parasites measures 2-2.5 mm in length. In free-living cycle (outside the human body) both males and females are found. Free-living females are smaller and measure 0.95-1.5 mm in length. Males are smaller.

PARASITE

Strongyloides stercoralis is a unique parasite. It is the only nematode or helminth parasite that multiplies in the human body. A process known as ‘internal autoinfection’ accomplishes this. It differs from hookworms in that; no males in the parasitic cycle: no eggs are passed in the faeces but L1 rhabditiform larvae: internal and external autoinfection occurs when L1 larvae undergo accelerated development into rhabditiform L2 and then into L3 which is the filariform/infective larvae while moving down the intestinal tract: has a free-living cycle in the soil: may cause severe disseminated disease with larvae in vital organs in immunocompromised patients.

LIFE CYCLE

The parthenogenetic females lay eggs in the mucosa of the small intestine. Generally they have a low egg output per day. The eggs hatch in the mucosa itself and the L1 rhabditiform larvae enter the lumen and are excreted in the faeces.

The subsequent development and the rate depend on the internal and the external conditions. When external conditions are unfavorable L1 larvae rapidly develop into L2 and to the infective L3 larvae stage. The infective larvae develop into free-living males and females. The larvae produced by the free-living adults mature into free-living L3 stages. These larvae penetrate the skin of humans and once again start a parasitic cycle. The L3 larva of S.stercoralis differs from that of hookworms in; not having a sheath: having tri-radiate tip of tail.

PATHOGENESIS AND CLINICAL FEATURES

At the site of penetration of the skin, L3 larvae may cause ‘ground itch ( see hookworms). Pulmonary migration of larvae can cause lung symptoms and pneumonitis. But severe symptoms (as in ascariasis) are rare.

In mild infections, catarrhal enteritis is seen with increased amount of mucous secreted into the lumen. The mucosa is congested with hyperplasia of goblet cells with normal looking villi.
In heavy infections the villi become flattened and atrophied. Epigastric pain, nausea, anorexia and finally incessant diarrhea result.

In the hyperinfection syndrome seen in immunocompromised patients L1 develop rapidly to infective L3 stage, which penetrate the gut wall and enter the blood stream (internal autoinfection). Larvae in large numbers are carried into various organs resulting in serious damage to respective tissues. Organs and systems that can be damaged by larvae include brain, heart, pancreas, hepatobilliary system, lungs, genitourinary system and the skin.

In external autoinfection where L1 larvae develop into infective stage in soiled clothes, bed linen or around the anal verge the migrating larvae produce a characteristic epigenous dermatitis starting in the per anal region extending rapidly to the buttocks and lower abdomen. This condition is called ‘larva currens’.

DIAGNOSIS

Diagnosis is difficult. Because of low fecundity female worms produce only small numbers of larvae and it is also not regular. In cases suspected of having strongyloidiasis, negative report on a single wet smear of faeces does not exclude the infection. Several samples over period of 3-7 days may be necessary to exclude the infection. In the faeces rhabditiform larvae are looked for. In old samples sometimes hookworm larvae may be found. Then, the larvae have to be distinguished from those of Strongyloides. Duodenal intubation or ‘entero test’ may be used to obtain larvae directly from the small intestine.

PREVENTION AND CONTROL

Avoidance of indiscriminate defaecation and use of footwear help in prevention. Provision of hygienic latrines, chemotherapy of infected people and health education are important in control of the infection.

TREATMENT

Even in the asymptomatic state, strongyloidiasis must be treated because of the potential for fatal hyperinfection. Ivermectin (200 µg/kg daily for 1 or 2 days) is more effective than albendazole (400 mg daily for 3 days, repeated at 2 weeks) and is better tolerated than thiabendazole (25 mg/kg twice daily for 2 days), whose common adverse effects include nausea, vomiting, diarrhea, dizziness, and neuropsychiatric disturbances. Because thiabendazole is not uniformly effective, stool examinations, eosinophil counts, and monitoring of clinical symptoms should be continued after treatment. For disseminated strongyloidiasis, treatment with Ivermectin should be extended for at least 5 to 7 days or until the parasites are eradicated.

TRICHINELLA SPIRALIS (Trichinosis/Trichinellosis)

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GEOGRAPHICAL DISTRIBUTION

The infection is seen in countries such as United States, countries of former Russian federation and Europe. It is rarely seen in tropics. It also occurs in east and west sub-Saharan African region.

MORPHOLOGY

The adult worms are small and measures 2-3mm (females) and 1-2mm (male).

LOCATION IN HOST

The worm is found embedded in the small intestine mucosa. The larval stages are also found in the same host. 9 example of man being both definitive and intermediate host)

LIFE CYCLE

Each female matures rapidly and following fertilization lays about 1500 larvae. The larvae make their way by way of lymphatics and the blood stream to reach striated muscles. Each larva enters a muscles fibre and converts it to a characteristic capsule called the ‘nurse cell’. Therefore the larvae can live for long periods. Later they usually get calcified. In humans the muscle phase is a dead end. When this happens in animals such as pigs and horses the meat becomes infective if not properly cooked. The muscle fibres entering the stomach are digested and the liberated larvae quickly gain entry into the small intestinal mucosa and mature rapidly into adult worms.

After about1 week, female worms release newborn larvae that migrate via the circulation to striated muscle. The larvae of all species except Trichinella pseudospiralis and Trichinella papuae then encyst by inducing a radical transformation in the muscle cell architecture. Although host immune responses may help to expel adult worms, they have little effect on muscle-dwelling larvae. Human trichinellosis is most often caused by the ingestion of infected pork products and thus can occur in almost any location where the meat of domestic or wild swine is eaten. Human trichinellosis also may be acquired from the meat of other animals, including dogs (in parts of Asia and Africa), horses (in Italy and France), and bears and walruses (in northern regions). Although cattle (being herbivores) are not natural hosts of Trichinella, beef has been implicated in outbreaks when contaminated or adulterated with trichinous pork.

ENCYSTED LARVA

PATHOGENESIS

In mild infections, adult worms cause minimal pathology. They may cause inflammation and congestion of the mucosa with cell destruction. Major pathology is by larvae due to their presence in the muscle or due to their migration through the central nervous system and the heart.

CLINICAL FEATURES

Clinical symptoms of trichinellosis arise from the successive phases of parasite enteric phase, invasive phase (larval migration), and encystment phase (muscle encystment)
1. Enteric phase (invasion of the intestine): patients develop nausea, vomiting and abdominal pain resembling an attack of acute food poisoning.
2. Invasive phase (larval migration): This phase is characterized by severe myalgia, periobital edema and eosinophilia. CNS or myocardial complications may occur during this phase.
3. Encysment phase (Encysment of larvae in the muscle): Severe infection leads to cachexia, edema and dehydration. Gram negative septicemia due to organisms. introduced by larvae may occur.

DIAGNOSIS

History of ingesting undercooked pork is suggestive. Often groups of people are affected as following parties.
Blood eosinophilia develops in_90% of patients with symptomatic trichinellosis and may peak at a level of 50% between 2 and 4 weeks after infection. Serum levels of IgE and muscle enzymes, including creatine phosphokinase, are elevated in most symptomatic patients.
Muscle biopsy can be used to demonstrate the encysted larvae. A definitive diagnosis requires surgical biopsy of at least 1 g of involved muscle; the yields are highest near tendon insertions. The fresh muscle tissue should be compressed between glass slides and examined microscopically, because larvae may be overlooked by examination of routine histopathologic sections alone.
In early infection serology may be useful (ELISA, western blot, Enzyme immunoassay.)

EPIDEMIOLOGY

Eating of undercooked pork or sometime horse meat is responsible. Feeding pigs with dead or killed rats should be avoided. This is the major avenue of transmission of the infection to pigs by rats, which maintain the infection.

PREVENTION AND CONTROL
Proper cooking of all meat will eliminate the infection. Cooking of all garbage fed to pig will also help. Deep freezing pork at -18º to -15º C is effective.

TREATMENT

Current antihelmintic drugs are ineffective against Trichinella larvae in muscle. Fortunately, most lightly infected patients recover uneventfully with bed rest, antipyretics, and analgesics. Glucocorticoids like prednisone (1 mg/kg daily for 5 days) are beneficial for severe myositis and myocarditis. Mebendazole and albendazole, like thiabendazole, appear to be active against enteric stages of the parasite, but their efficacy against encysted larvae has not been conclusively demonstrated.