There are no specific symptoms or signs of hookworm infection, but they give rise to a combination of intestinal inflammation and progressive iron-deficiency anemia and protein deficiency. Coughing, chest pain, wheezing, and fever will sometimes result from severe infection. Epigastric pains, indigestion, nausea, vomiting, constipation, and diarrhea can occur early or in later stages as well, although gastrointestinal symptoms tend to improve with time. Signs of advanced severe infection are those of anemia and protein deficiency, including emaciation, cardiac failure and abdominal distension with ascites.

Larval invasion of the skin (mostly in the Americas) can produce a skin disease called cutaneous larva migrans also known as "creeping eruption". The hosts of these worms are not human and the larvae can only penetrate the upper five layers of the skin, where they give rise to intense, local itching, usually on the foot or lower leg, known as "ground itch". This infection is due to larvae from the "A. Braziliense" hookworm. The larvae migrate in tortuous tunnels between the "stratum basale" and "stratum corneum" of the skin, causing serpiginous vesicular lesions. With advancing movement of the larvae, the rear portions of the lesions become dry and crusty. The lesions are typically intensely itchy.

Because the larvae are in an abnormal host, they do not mature to adults but instead migrate

through the skin until killed by the host's inflammatory response. This migration causes

local intense itching and a red serpiginous lesion. Treatment with a single dose of oral ivermectin results in cure rates of 94–100%.

The term "hookworm" is sometimes used to refer to hookworm infection. A hookworm is a type of parasitic worm (helminth).

Symptoms of parasites may not always be obvious. However, such symptoms may mimic anemia or a hormone deficiency. Some of the symptoms caused by several worm infestation can include itching affecting the anus or the vaginal area, abdominal pain, weight loss, increased appetite, bowel obstructions, diarrhea, and vomiting eventually leading to dehydration, sleeping problems, worms present in the vomit or stools, anemia, aching muscles or joints, general malaise, allergies, fatigue, nervousness. Symptoms may also be confused with pneumonia or food poisoning.

The effects caused by parasitic diseases range from mild discomfort to death.

The nematode parasites "Necator americanus" and "Ancylostoma duodenale" cause human hookworm infection, which leads to anaemia and protein malnutrition. This infection affects approximately 740 million people in the developing countries, including children and adults, of the tropics specifically in poor rural areas located in sub-Saharan Africa, Latin America, South-East Asia and China.

Chronic hookworm in children leads to impaired physical and intellectual development, school performance and attendance are reduced.

Pregnant women affected by a hookworm infection can also develop aneamia, which results in negative outcomes both for the mother and the infant. Some of them are: low birth weight, impaired milk production, as well as increased risk of death for the mother and the baby.

Although organisms such as bacteria function as parasites, the usage of the term "parasitic disease" is usually more restricted. The three main types of organisms causing these conditions are protozoa (causing protozoan infection), helminths (helminthiasis), and ectoparasites. Protozoa and helminths are usually endoparasites (usually living inside the body of the host), while ectoparasites usually live on the surface of the host. Occasionally the definition of "parasitic disease" is restricted to diseases due to endoparasites.

The signs and symptoms of helminthiasis depend on a number of factors including: the site of the infestation within the body; the type of worm involved; the number of worms and their volume; the type of damage the infesting worms cause; and, the immunological response of the body. Where the burden of parasites in the body is light, there may be no symptoms.

Certain worms may cause particular constellations of symptoms. For instance, taeniasis can lead to seizures due to neurocysticercosis.

Ancylostomiasis (also anchylostomiasis or ankylostomiasis) is a hookworm disease caused by infection with Ancylostoma hookworms. The name is derived from Greek ancylos αγκύλος "crooked, bent" and stoma στόμα "mouth".

Ancylostomiasis is also known as miner's anaemia, tunnel disease, brickmaker's anaemia and Egyptian chlorosis. Helminthiasis may also refer to ancylostomiasis, but this term also refers to all other parasitic worm diseases as well. In the United Kingdom, if acquired in the context of working in a mine, the condition is eligible for Industrial Injuries Disability Benefit. It is a prescribed disease (B4) under the relevant legislation.§

Ancylostomiasis is caused when hookworms, present in large numbers, produce an iron deficiency anemia by sucking blood from the host's intestinal walls.

In extreme cases of intestinal infestation, the mass and volume of the worms may cause the outer layers of the intestinal wall, such as the muscular layer, to tear. This may lead to peritonitis, volvulus, and gangrene of the intestine.

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.

Hookworm eggs are shed in the infected dog (or other animal) feces to the ground and beach sand, where they then develop over a period of 1–2 weeks into the infectious larval form (filariform larvae). The filariform larvae can burrow through intact skin that comes into contact with soil or sand that is contaminated with feces. Although they are able to infect the deeper tissues of animals (through to the lungs and then the intestinal tract), humans are incidental hosts and the larvae are only able to penetrate the epidermis of the skin and thus create the typical wormlike burrows visible underneath the skin. These parasites apparently lack the collagenase enzymes required to penetrate through the basement membrane deeper into the dermal layers of the skin.

Neglected tropical diseases (NTDs) are a diverse group of tropical infections which are especially common in low-income populations in developing regions of Africa, Asia, and the Americas. They are caused by a variety of pathogens such as viruses, bacteria, protozoa and helminths. These diseases are contrasted with the big three diseases (HIV/AIDS, tuberculosis, and malaria), which generally receive greater treatment and research funding. In sub-Saharan Africa, the effect of these diseases as a group is comparable to malaria and tuberculosis. NTD co-infection can also make HIV/AIDS and tuberculosis more deadly.

In some cases, the treatments are relatively inexpensive. For example, the treatment for schistosomiasis is US$0.20 per child per year. Nevertheless, in 2010 it was estimated that control of neglected diseases would require funding of between US$2 billion and US$3 billion over the subsequent five to seven years. Some pharmaceutical companies have committed to donating all the drug therapies required, and mass drug administration (for example mass deworming) has been successfully accomplished in several countries. However, preventive measures are often more accessible in the developed world, but not universally available in poorer areas.

Within developed countries, neglected tropical diseases affect the very poorest in society. In the United States, there are up to 1.46 million families including 2.8 million children living on less than two dollars a day. In countries such as these, the burdens of neglected tropical diseases are often overshadowed by other public health issues. However, many of the same issues put populations at risk in developed as developing nations. For example, from poverty stem problems such as lack of adequate housing, thus exposing individuals to the vectors of these diseases.

Twenty neglected tropical diseases are prioritized by the World Health Organization (WHO), though other organizations define NTDs differently. Chromoblastomycosis and other deep mycoses, scabies and other ectoparasites and snakebite envenoming were added to the list in 2017. These diseases are common in 149 countries, affecting more than 1.4 billion people (including more than 500 million children) and costing developing economies billions of dollars every year. They resulted in 142,000 deaths in 2013—down from 204,000 deaths in 1990. Of these 20, two were targeted for eradication (dracunculiasis (guinea-worm disease) by 2015 and yaws by 2020), and four for elimination (blinding trachoma, human African trypanosomiasis, leprosy and lymphatic filariasis by 2020).

Lymphatic filariasis is also known as elephantiasis. There are approximately 120 million individuals infected and 40 million with deformities. Approximately two-thirds of cases are in Southwest Asia and one-third in Africa. Lymphatic filariasis is rarely fatal. Lymphatic filariasis has lifelong implications, such as lymphoedema of the limbs, genital disease, and painful recurrent attacks. Most people are asymptomatic, but have lymphatic damage. Up to 40 percent of infected individuals have kidney damage. It is a vector-borne disease, caused by nematode worms that are transmitted by mosquitoes.

It can be treated with cost-effective antihelminthic treatments, and washing skin can slow or even reverse damage. It is diagnosed with a finger-prick blood test.

Cat bites are usually considered as minor injuries but can result in serious infection. Not all infections that can be obtained from exposure to a cat are transmitted through a cat bite, like plague.

The diagnosis is aided by obtaining a history of the circumstances surrounding the bite. The time the bite was experienced, the location of the bite, and examination of the bite is noted. The person may have drainage from the site of the bite. They may also be febrile. Swelling may also occur. Because the wound from the bite may have healed over the punctures, the wound it may be opened and explored. The site is anesthetized prior to exploration of the wound for is examined for damage. Neurovascular status is assessed. Immune status may determine treatment as does

the presence of transplanted tissue or organs, rheumatic disease, diabetes, HIV/AIDS and sickle cell disease.

Swollen glands (lymph nodes) and red streaks radiating upward may be evident.

The diagnosis of a cat with rabies is evident by observing the cat. Cats with rabies may also appear restless, pant, and attack other animals, people, or objects. Animals with rabies typically die within a few days of appearing sick. Vaccination of the cat can prevent rabies being transmitted by the cat through a bite. If the cat is suspected of being infected with rabies, the person begins treatment with rabies vaccine.

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.

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.

The clinical findings in this disease can be divided into acute and end-stage manifestations:

In the acute phase, patients often present with decreased visual acuity, vitritis, papillitis, and crops of gray-white or yellow-white outer retinal lesions. The clustering of the retinal lesions is important because this often helps to localize the causative nematode.

If left untreated, patients ultimately develop late sequel, which may include optic atrophy, retinal arterial narrowing, diffuse retinal pigment epithelial changes, and an abnormal electroretinogram. The late findings of this condition are often misinterpreted as unilateral retinitis pigmentosa.

Most types of eosinophilic pneumonia have similar signs and symptoms. Prominent and nearly universal signs and symptoms include cough, fever, difficulty breathing, and night sweats. Acute eosinophilic pneumonia typically follows a rapid course. Fever and cough may develop only one or two weeks before breathing difficulties progress to the point of respiratory failure requiring mechanical ventilation. Chronic eosinophilic pneumonia usually follows a slower course. Symptoms accumulate over several months and include fever, cough, difficulty breathing, wheezing, and weight loss. Individuals with CEP are often misdiagnosed with asthma before CEP is finally recognized.

EP due to medications or environmental exposures is similar and occurs after an exposure to a known offending agent. EP due to parasitic infections has a similar prodrome in addition to a host of different symptoms related to the variety of underlying parasites. EP in the setting of cancer often develops in the context of a known diagnosis of lung cancer, cervical cancer, etc.

Eosinophilic pneumonia (EP) is a disease in which an eosinophil, a type of white blood cell, accumulates in the lung. These cells cause disruption of the normal air spaces (alveoli) where oxygen is extracted from the atmosphere. Several different kinds of eosinophilic pneumonia exist and can occur in any age group. The most common symptoms include cough, fever, difficulty breathing, and sweating at night. EP is diagnosed by a combination of characteristic symptoms, findings on a physical examination by a health provider, and the results of blood tests and x-rays. Prognosis is excellent once most EP is recognized and treatment with corticosteroids is begun.

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.

Iron-deficiency anemia is characterized by the sign of pallor (reduced oxyhemoglobin in skin or mucous membranes), and the symptoms of fatigue, lightheadedness, and weakness. None of these symptoms (or any of the others below) are sensitive or specific. Pallor of mucous membranes (primarily the conjunctiva) in children suggests anemia with the best correlation to the disease, but in a large study was found to be only 28% sensitive and 87% specific (with high predictive value) in distinguishing children with anemia [hemoglobin (Hb) <11.0 g/dl] and 49% sensitive and 79% specific in distinguishing severe anemia (Hb < 7.0 g/dl). Thus, this sign is reasonably predictive when present, but not helpful when absent, as only one-third to one-half of children who are anemic (depending on severity) will show pallor.

Because iron-deficiency anemia tends to develop slowly, adaptation occurs to the systemic effects that anemia causes, and the disease often goes unrecognized for some time. In severe cases, dyspnea can occur. Pica may also develop; pagophagia has been suggested to be "the most specific for iron deficiency."

Other possible symptoms and signs of iron-deficiency anemia include:

Iron-deficiency anemia is anemia caused by a lack of iron. Anemia is defined as a decrease in the number of red blood cells or the amount of hemoglobin in the blood. When onset is slow, symptoms are often vague, including feeling tired, weakness, shortness of breath, or poor ability to exercise. Anemia that comes on quickly often has greater symptoms, including: confusion, feeling like one is going to pass out, and increased thirst. There needs to be significant anemia before a person becomes noticeably pale. Problems with growth and development may occur in children. There may be additional symptoms depending on the underlying cause.

Iron-deficiency anemia is usually caused by blood loss, insufficient dietary intake, or poor absorption of iron from food. Sources of blood loss can include heavy periods, childbirth, uterine fibroids, stomach ulcers, colon cancer, and urinary tract bleeding. A poor ability to absorb iron may occur as a result of Crohn's disease or a gastric bypass. In the developing world, parasitic worms, malaria, and HIV/AIDS increase the risk. Diagnosis is generally confirmed by blood tests.

Prevention is by eating a diet high in iron or iron supplementation in those at risk. Treatment depends on the underlying cause and may include dietary changes, medications, or surgery. Iron supplements and vitamin C may be recommended. Severe cases may be treated with blood transfusions or iron injections.

Iron-deficiency anemia affected about 1.48 billion people in 2015. A lack of dietary iron is estimated to cause approximately half of all anemia cases globally. Women and young children are most commonly affected. In 2015 anemia due to iron deficiency resulted in about 54,000 deaths – down from 213,000 deaths in 1990.

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