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Specific helminths can be identified through microscopic examination of their eggs (ova) found in faecal samples. The number of eggs is measured in units of eggs per gram. However, it does not quantify mixed infections, and in practice, is inaccurate for quantifying the eggs of schistosomes and soil-transmitted helmiths. Sophisticated tests such as serological assays, antigen tests, and molecular diagnosis are also available; however, they are time-consuming, expensive and not always reliable.
The clinical aspects of ancylostomiasis were first described in Europe as "miner's anaemia". During the construction of the Gotthard Tunnel in Switzerland (1871–1881), a large number of miners suffered from severe anaemia of unknown cause. Medical investigations let to the understanding that it was caused by "Ancylostoma duodenale" (favoured by high temperatures and humidity) and to "major advances in parasitology, by way of research into the aetiology, epidemiology and treatment of ancylostomiasis".
Hookworms still account for high proportion of debilitating disease in the tropics and 50-60,000 deaths per year can be attributed to this disease.
Control of this parasite should be directed against reducing the level of
environmental contamination. Treatment of heavily infected individuals is one
way to reduce the source of contamination (one study has estimated that 60% of
the total worm burden resides in less than 10% of the population). Other
obvious methods are to improve access to sanitation, e.g. toilets, but also
convincing people to maintaining them in a clean, functional state, thereby making
them conducive to use.
Diagnosis depends on finding characteristic worm eggs on microscopic examination of the stools, although this is not possible in early infection. Early signs of infection in most dogs include limbular limping and anal itching. The eggs are oval or elliptical, measuring 60 µm by 40 µm, colorless, not bile stained and with a thin transparent hyaline shell membrane. When released by the worm in the intestine, the egg contains an unsegmented ovum. During its passage down the intestine, the ovum develops and thus the eggs passed in feces have a segmented ovum, usually with 4 to 8 blastomeres.
As the eggs of both "Ancylostoma" and "Necator" (and most other hookworm species) are indistinguishable, to identify the genus, they must be cultured in the lab to allow larvae to hatch out. If the fecal sample is left for a day or more under tropical conditions, the larvae will have hatched out, so eggs might no longer be evident. In such a case, it is essential to distinguish hookworms from "Strongyloides" larvae, as infection with the latter has more serious implications and requires different management. The larvae of the two hookworm species can also be distinguished microscopically, although this would not be done routinely, but usually for research purposes. Adult worms are rarely seen (except via endoscopy, surgery or autopsy), but if found, would allow definitive identification of the species. Classification can be performed based on the length of the buccal cavity, the space between the oral opening and the esophagus: hookworm rhabditoform larvae have long buccal cavities whereas "Strongyloides" rhabditoform larvae have short buccal cavities.
Recent research has focused on the development of DNA-based tools for diagnosis of infection, specific identification of hookworm, and analysis of genetic variability within hookworm populations. Because hookworm eggs are often indistinguishable from other parasitic eggs, PCR assays could serve as a molecular approach for accurate diagnosis of hookworm in the feces.
In regions where helminthiasis is common, mass deworming treatments may be performed, particularly among school-age children, who are a high-risk group. Most of these initiatives are undertaken by the World Health Organization (WHO) with positive outcomes in many regions. Deworming programs can improve school attendance by 25 percent. Although deworming improves the health of an individual, outcomes from mass deworming campaigns, such as reduced deaths or increases in cognitive ability, nutritional benefits, physical growth, and performance, are uncertain or not apparent.
Evaluation of numerous public health interventions has generally shown that improvement in each individual component ordinarily attributed to poverty (for example, sanitation, health education and underlying nutrition status) often have minimal impact on transmission. For example, one study found that the introduction of latrines into a resource-limited community only reduced the prevalence of hookworm infection by four percent. However, another study in Salvador, Brazil found that improved drainage and sewerage had a significant impact (p<0.0001) on the prevalence of hookworm infection but no impact at all on the intensity of hookworm infection. This seems to suggest that environmental control alone has a limited but incomplete effect on the transmission of hookworms. It is imperative, therefore, that more research is performed to understand the efficacy and sustainability of integrated programs that combine numerous preventive methods including education, sanitation, and treatment.
Parasitic infections can usually be treated with antiparasitic drugs.
Albendazole and mebendazole have been the treatments administered to entire populations to control hookworm infection. However, it is a costly option and both children and adults become reinfected within a few months after deparasitation occurs raising concerns because the treatment has to repeatedly be administered and drug resistance may occur.
Another medication administered to kill worm infections has been pyrantel pamoate. For some parasitic diseases, there is no treatment and, in the case of serious symptoms, medication intended to kill the parasite is administered, whereas, in other cases, symptom relief options are used. Recent papers have also proposed the use of viruses to treat infections caused by protozoa.
Biotechnology companies in the developing world have targeted neglected tropical diseases due to need to improve global health.
Mass drug administration is considered a possible method for eradication, especially for lymphatic filariasis, onchocerciasis, and trachoma, although drug resistance is a potential problem. According to Fenwick, Pfizer donated 70 million doses of drugs in 2011 to eliminate trachoma through the International Trachoma Initiative. Merck has helped The African Programme for the Control of Onchocerciasis (APOC) and Oncho Elimination Programme for the Americas to greatly diminished the effect of Onchocerciasis by donating ivermectin. Merck KGaA pledged to give 200 million tablets of praziquantel over 10 years, the only cure for schistosomiasis. GlaxoSmithKline has donated two billion tablets of medicine for lymphatic filariasis and pledged 400 million deworming tablets per year for five years in 2010. Johnson & Johnson has pledged 200 million deworming tablets per year. Novartis has pledged leprosy treatment, EISAI pledged two billion tablets to help treat lymphatic filariasis.
CLM can be treated in a number of different ways:
- Systemic (oral) agents include albendazole (trade name "Albenza") and ivermectin (trade name "Stromectol")).
- Another agent which can be applied either topically "or" taken by mouth is thiabendazole (trade name "Mintezol")), an anti-helminthic.
- Topical freezing agents, such as ethylene chloride or liquid nitrogen, applied locally can freeze and kill the larvae, but this method has a high failure rate because the larvae are usually located away from the site of the visible skin trails. Additionally, this is a painful method which can cause blistering and/or ulceration of the skin and it is therefore not recommended.
- It is recommended to use Benadryl or some anti-itch cream (i.e. Cortizone or Calamine lotion). This will help relieve some of the itch.
- Wearing shoes in areas where these parasites are known to be endemic offers protection from infection. In general, avoiding exposure of skin to contaminated soil or sand offers the best protection. In some areas dogs have been banned from beaches in an attempt to control human infection.
Inclusion of NTDs into initiatives for malaria, HIV/AIDS, and tuberculosis, as well as integration of NTD treatment programs, may have advantages given the strong link between these diseases and NTDs. Some neglected tropical diseases share common vectors (sandflies, black flies, and mosquitos). Both medicinal and vector control efforts may be combined.
A four-drug rapid-impact package has been proposed for widespread proliferation. Administration may be made more efficient by targeting multiple diseases at once, rather than separating treatment and adding work to community workers. This package is estimated to cost US$0.40 per patient. When compared to stand-alone treatment, the savings are estimated to be 26–47%. While more research must be done in order to understand how NTDs and other diseases interact in both the vector and the human stages, safety assessments have so far produced positive results.
Many neglected tropical diseases and other prevalent diseases share common vectors, creating another opportunity for treatment and control integration. One such example of this is malaria and lymphatic filariasis. Both diseases are transmitted by the same or related mosquito vectors. Vector control, through the distribution of insecticide treated nets, reduces the human contact with a wide variety of disease vectors. Integrated vector control may also alleviate pressure on mass drug administration, especially with respect to rapidly evolving drug resistance. Combining vector control and mass drug administration deemphasizes both, making each less susceptible to resistance evolution.
Mammals can get parasites from contaminated food or water, bug bites, or sexual contact. Ingestion of contaminated water can produce Giardia infections.
Parasites normally enter the body through the skin or mouth. Close contact with pets can lead to parasite infestation as dogs and cats are host to many parasites.
Other risks that can lead people to acquire parasites are walking barefeet, inadequate disposal of feces, lack of hygiene, close contact with someone carrying specific parasites, and eating undercooked foods, unwashed fruits and vegetables or foods from contaminated regions.
Parasites can also be transferred to their host by the bite of an insect vector, i.e. mosquito, bed bug, fleas.
Visceral larva migrans (VLM) is a condition in humans caused by the migratory larvae of certain nematodes, humans being a dead-end host, and was first reported in 1952. Nematodes causing such zoonotic infections are "Baylisascaris procyonis", "Toxocara canis", "Toxocara cati", and "Ascaris suum". These nematodes can infect but not mature in humans and after migrating through the intestinal wall, travel with the blood stream to various organs where they cause inflammation and damage. Affected organs can include the liver, heart (causing myocarditis) and the CNS (causing dysfunction, seizures, and coma). A special variant is ocular larva migrans where usually "T. canis" larvae travel to the eye.
Only a few roundworm eggs are necessary to cause larva migrans in the human child or adult. However, visceral larva migrans seems to affect children aged 1–4 more often while ocular larva migrans more frequently affects children aged 7–8. Between 4.6% and 23% of U.S. children have been infected with the dog roundworm egg. This number is much higher in other parts of the world, such as Colombia, where up to 81% of children have been infected.
Cutaneous larva migrans is a condition where nematodes such as "Ancylostoma braziliense" migrate to the skin.
A list of causative agents of larva migrans syndromes is not agreed upon and varies with the author.
The infection causes a red, intensely pruritic (itchy) eruption. The itching can become very painful and if scratched may allow a secondary bacterial infection to develop. Cutaneous larva migrans usually heals spontaneously over weeks to months and has been known to last as long as one year. However, the severity of the symptoms usually causes those infected to seek medical treatment before spontaneous resolution occurs. Following proper treatment, migration of the larvae within the skin is halted and relief of the associated itching can occur in less than 48 hours (reported for thiabendazole).
This is separate from the similar cutaneous larva currens which is caused by "Strongyloides". Larva currens is also a cause of migratory pruritic eruptions but is marked by 1) migratory speed on the order of inches per hour 2) perianal involvement due to autoinfection from stool and 3) a wide band of urticaria.
Cat bites can often be prevented by:
- instructing children not to tease cats or other pets.
- being cautious with unfamiliar cats.
- approaching cats with care, even if they appear to be friendly.
- avoiding rough play with cats and kittens.
Rough play causes is perceived as aggressive. This will lead to the cat being defensive when approached by people. Preventing cat bites includes not provoking the cat.
The first step in treatment includes washing and then irrigating the bite wound.
Seek medical attention if: if the cat has not been vaccinated against rabies.
A tetanous booster is given to the person if It has been more than 5 years since their last tetanus shot. If a cat has bitten someone, and there is no evidence that the cat has been vaccinated against rabies, the person will be treated for rabies infection.
Nematode dermatitis is a cutaneous condition characterized by widespread folliculitis caused by "Ancylostoma caninum".
Löffler's syndrome or Loeffler's syndrome is a disease in which eosinophils accumulate in the lung in response to a parasitic infection.
It was first described in 1932 by Wilhelm Löffler in cases of eosinophilic pneumonia caused by the parasites "Ascaris lumbricoides", "Strongyloides stercoralis" and the hookworms "Ancylostoma duodenale" and "Necator americanus".
Although Löffler only described eosinophilic pneumonia in the context of infection, many authors give the term "Löffler's syndrome" to any form of acute onset pulmonary eosinophilia no matter what the underlying cause. If the cause is unknown, it is specified and called "simple pulmonary eosinophilia". Cardiac damage caused by the damaging effects of eosinophil granule proteins (ex. major basic protein) is known as Loeffler endocarditis and can be caused by idiopathic eosinophilia or eosinophilia in response to parasitic infection.
Eosinophilic pneumonia is diagnosed in one of three circumstances: when a complete blood count reveals increased eosinophils and a chest x-ray or computed tomography (CT) identifies abnormalities in the lung, when a biopsy identifies increased eosinophils in lung tissue, or when increased eosinophils are found in fluid obtained by a bronchoscopy (bronchoalveolar lavage [BAL] fluid). Association with medication or cancer is usually apparent after review of a person's medical history. Specific parasitic infections are diagnosed after examining a person's exposure to common parasites and performing laboratory tests to look for likely causes. If no underlying cause is found, a diagnosis of AEP or CEP is made based upon the following criteria. AEP is most likely with respiratory failure after an acute febrile illness of usually less than one week, changes in multiple areas and fluid in the area surrounding the lungs on a chest x-ray, and greater than 25% eosinophils on a BAL. Other typical laboratory abnormalities include an elevated white blood cell count, erythrocyte sedimentation rate, and immunoglobulin G level. Pulmonary function testing usually reveals a restrictive process with reduced diffusion capacity for carbon monoxide. CEP is most likely when the symptoms have been present for more than a month. Laboratory tests typical of CEP include increased blood eosinophils, a high erythrocyte sedimentation rate, iron deficiency anemia, and increased platelets. A chest x-ray can show abnormalities anywhere, but the most specific finding is increased shadow in the periphery of the lung, away from the heart.
Eosinophilic pneumonia due to cancer or parasitic infection carries a prognosis related to the underlying illness. AEP and CEP, however, have very little associated mortality as long as intensive care is available and treatment with corticosteroids is given. CEP often relapses when prednisone is discontinued; therefore, some people with CEP require lifelong therapy. Chronic prednisone is associated with many side effects, including increased infections, weakened bones, stomach ulcers, and changes in appearance.
If the nematode can be seen by an ophthalmologist, which occurs in less than half of cases, it should be treated with photocoagulation for extramacular location and surgical removal in case the larva is lying in the macula. After the worm is killed, visual acuity loss usually does not progress. Alternatively, Antihelminthic treatment such as high dose oral Albendazole and prednisolone may be used.
Anemia is often discovered by routine blood tests, which generally include a complete blood count (CBC). A sufficiently low hemoglobin (Hb) by definition makes the diagnosis of anemia, and a low hematocrit value is also characteristic of anemia. Further studies will be undertaken to determine the anemia's cause. If the anemia is due to iron deficiency, one of the first abnormal values to be noted on a CBC, as the body's iron stores begin to be depleted, will be a high red blood cell distribution width (RDW), reflecting an increased variability in the size of red blood cells (RBCs).
A low mean corpuscular volume (MCV) also appears during the course of body iron depletion. It indicates a high number of abnormally small red blood cells. A low MCV, a low mean corpuscular hemoglobin or mean corpuscular hemoglobin concentration, and the corresponding appearance of RBCs on visual examination of a peripheral blood smear narrows the problem to a microcytic anemia (literally, a "small red blood cell" anemia).
The blood smear of a person with iron-deficiency anemia shows many hypochromic (pale, relatively colorless) and small RBCs, and may also show poikilocytosis (variation in shape) and anisocytosis (variation in size). With more severe iron-deficiency anemia, the peripheral blood smear may show hypochromic, pencil-shaped cells and, occasionally, small numbers of nucleated red blood cells. The platelet count may be slightly above the high limit of normal in iron-deficiency anemia (termed a mild thrombocytosis), but severe cases can present with thrombocytopenia (low platelet count).
Iron-deficiency anemia is confirmed by tests that include serum ferritin, serum iron level, serum transferrin, and total iron binding capacity (TIBC). A low serum ferritin is most commonly found. However, serum ferritin can be elevated by any type of chronic inflammation and thus is not consistently decreased in iron-deficiency anemia. Serum iron levels may be measured, but serum iron concentration is not as reliable as the measurement of both serum iron and serum iron-binding protein levels (TIBC). The ratio of serum iron to TIBC (called iron saturation or transferrin saturation index or percent) is a value with defined parameters that can help to confirm the diagnosis of iron-deficiency anemia; however, other conditions must also be considered, including other types of anemia.
Further testing may be necessary to differentiate iron-deficiency anemia from other disorders, such as thalassemia minor. It is very important not to treat people with thalassemia with an iron supplement, as this can lead to hemochromatosis. A hemoglobin electrophoresis provides useful evidence for distinguishing these two conditions, along with iron studies.
It is unclear if screening pregnant women for iron-deficiency anemia during pregnancy improves outcomes in the United States. The same holds true for screening children who are "6 to 24 months" old.
Diffuse unilateral subacute neuroretinitis (DUSN) is a rare condition that occurs in otherwise healthy, often young patients and is due to the presence of a subretinal nematode.
Parasitic infestations, stings, and bites in humans are caused by several groups of organisms belonging to the following phyla: Annelida, Arthropoda, Bryozoa, Chordata, Cnidaria, Cyanobacteria, Echinodermata, Nemathelminthes, Platyhelminthes, and Protozoa.
- "Acanthamoeba" infection
- Amebiasis cutis
- Ant sting
- Arachnidism
- Baker's itch
- "Balamuthia" infection
- Bedbug infestation (bedbug bite, cimicosis)
- Bee and wasp stings
- Blister beetle dermatitis
- Bombardier beetle burn
- Bristleworm sting
- Centipede bite
- Cheyletiella dermatitis
- Chigger bite
- Coolie itch
- Copra itch
- Coral dermatitis
- Creeping eruption (cutaneous larva migrans)
- Cutaneous leishmaniasis (Aleppo boil, Baghdad boil, bay sore, Biskra button, Chiclero ulcer, Delhi boil, Kandahar sore, Lahore sore, leishmaniasis tropica, oriental sore, "pian bois, uta")
- "Cysticercosis" cutis
- Demodex mite bite
- Dogger Bank itch
- Dracunculiasis (dracontiasis, guinea worm disease, Medina worm)
- Echinococcosis (hydatid disease)
- Elephantiasis tropica (elephantiasis arabum)
- Elephant skin
- Enterobiasis (oxyuriasis, pinworm infection, seatworm infection)
- "Erisipela de la costa"
- Feather pillow dermatitis
- Funnel web spider bite
- Gamasoidosis
- Gnathostomiasis (larva migrans profundus)
- Grain itch (barley itch, mattress itch, prairie itch, straw itch)
- Grocer's itch
- Head lice infestation (cooties, pediculosis capitis)
- Hookworm disease (ancylostomiasis, ground itch, necatoriasis, uncinariasis)
- Human trypanosomiasis
- Hydroid dermatitis
- Irukandji syndrome
- Jellyfish dermatitis
- Ked itch
- Larva currens
- Latrodectism (widow spider bite)
- Leech bite
- Leopard skin
- Lepidopterism (Caripito itch, caterpillar dermatitis, moth dermatitis)
- Lizard bite
- Lizard skin
- Loaiasis (Calabar swelling, fugitive swelling, "loa loa", tropical swelling)
- Loxoscelism (brown recluse spider bite, necrotic cutaneous loxoscelism)
- "Mal morando"
- Millipede burn
- Mosquito bite
- Mucocutaneous leishmaniasis (espundia, leishmaniasis americana)
- Myiasis
- Nairobi fly dermatitis (Kenya fly dermatitis, Nairobi eye)
- Nematode dermatitis
- Norwegian scabies (crusted scabies)
- Onchocerciasis
- Ophthalmia nodosa
- Paederus dermatitis
- Pediculosis corporis (pediculosis vestimenti, Vagabond's disease)
- Pediculosis pubis (crabs, phthirus pubis, pthirus pubis, pubic lice)
- Pneumocystosis (often classified as fungal)
- Portuguese man-of-war dermatitis
- Post-kala-azar dermal leishmaniasis (post-kala-azar dermatosis)
- Protothecosis
- Pulicosis (flea bites)
- Reduviid bite
- Scabies (itch mite infestation, seven-year itch)
- Scorpion sting
- Sea anemone dermatitis
- Seabather's eruption (sea lice)
- Sea urchin injury
- Seaweed dermatitis
- Snake bite
- Sowda
- Sparganosis
- Spider bite
- Stingray injury
- Swimmer's itch (cercarial dermatitis, schistosome cercarial dermatitis)
- Tarantula bite
- Tick bite
- Toxoplasmosis
- Trichinosis
- Trichomoniasis
- Tungiasis ("bicho de pie", chigoe flea bite, jigger bite, "nigua, pique")
- Visceral leishmaniasis (dumdum fever, "kala-azar")
- Visceral schistosomiasis (bilharziasis)
- Viscerotropic leishmaniasis
- Wheat warehouse itch
Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.
The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.
The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.
The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.
Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.