Cysticerci can develop in any voluntary muscles in humans. Invasion of muscle by cysticerci can cause myositis, with fever, eosinophilia, and muscular pseudohypertrophy, which initiates with muscle swelling and later progress to atrophy and fibrosis. In most cases, it is asymptomatic since the cysticerci die and become calcified.

The term neurocysticercosis is generally accepted to refer to cysts in the parenchyma of the brain. It presents with seizures and, less commonly, headaches. Cysticerca in brain parenchyma are usually 5–20 mm in diameter. In subarachnoid space and fissures, lesions may be as large as 6 cm in diameter and lobulated. They may be numerous and life-threatening.

Cysts located within the ventricles of the brain can block the outflow of cerebrospinal fluid and present with symptoms of increased intracranial pressure.

Racemose neurocysticercosis refers to cysts in the subarachnoid space. These can occasionally grow into large lobulated masses causing pressure on surrounding structures.

Neurocysticercosis involving the spinal cord, most commonly presenting as back pain and radiculopathy.

"Taenia saginata" infection is asymptomatic, but heavy infection causes weight loss, dizziness, abdominal pain, diarrhea, headaches, nausea, constipation, chronic indigestion, and loss of appetite. It can cause antigen reaction that induce allergic reaction. It is also a rare cause of ileus, pancreatitis, cholecystitis, and cholangitis.

Clinical presentation of sparganosis most often occurs after the larvae have migrated to a subcutaneous location. The destination of the larvae is often a tissue or muscle in the chest, abdominal wall, extremities, or scrotum, although other sites include the eyes, brain, urinary tract, pleura, pericardium, and spinal canal. The early stages of disease in humans are often asymptomatic, but the spargana typically cause a painful inflammatory reaction in the tissues surrounding the subcutaneous site as they grow. Discrete subcutaneous nodules develop that may appear and disappear over a period of time. The nodules usually itch, swell, turn red, and migrate, and are often accompanied by painful edema. Seizures, hemiparesis, and headaches are also common symptoms of sparganosis, especially cerebral sparganosis, and eosinophilia is a common sign. Clinical symptoms also vary according to the location of the sparganum; possible symptoms include elephantiasis from location in the lymph channels, peritonitis from location in the intestinal perforation, and brain abscesses from location in the brain. In genital sparganosis, subcutaneous nodules are present in the groin, labia, or scrotum and may appear tumor-like.

Ocular sparganosis a particularly well-described type of sparganosis. Early signs of the ocular form include eye pain, epiphora (excessive watering of the eye), and/or ptosis (drooping of the upper eyelid). Other signs include periorbital edema and/or edematous swelling that resembles Romana’s sign in Chagas disease, lacrimation, orbital cellulitis, exophthalmos (protrusion of the eyeball), and/or an exposed cornea ulcer. The most common sign at presentation is a mass lesion in the eye. If untreated, ocular sparganosis can lead to blindness.

In one case of brain infestation by "Spirometra erinaceieuropaei", a man sought treatment on suffering headaches, seizures, memory flashbacks and strange smells. Magnetic resonance imaging (MRI) scans showed a cluster of rings, initially in the right medial temporal lobe, but moving over time to the other side of the brain. The cause was not determined for four years; ultimately a biopsy was performed and a 1 cm-long tapeworm was found and removed. The patient continued to suffer symptoms.

There are accidental consumptions of eggs of "T. solium" from contaminated vegetables or water. The eggs enter the intestine where they develop into larvae. The larvae enter the bloodstream and invade host tissues. This clinical condition, called cysticercosis, is the most frequent and severe disease caused by any tapeworm. It can lead to severe headaches, dizziness, occasional seizures, dementia, hypertension, lesions in the brain, blindness, tumor-like growths, and low eosinophil levels. It is the cause of major neurological problems, such as hydrocephalus, paraplegy, meningitis, convulsions, and even death.

Although tapeworms in the intestine usually cause no symptoms, some people experience upper abdominal discomfort, diarrhea, and loss of appetite. Anemia may develop in people with the fish tapeworm. Infection is generally recognized when the infected person passes segments of proglottids in the stool (which look like white worms), especially if a segment is moving.

Rarely, worms may cause obstruction of the intestine, and very rarely, T. solium larvae can migrate to the brain causing severe headaches, seizures and other neurological problems. Neurocysticercosis can progress for years before the patient displays symptoms.

In at least one case, cancer cells from a tapeworm spread to the human host in an immunocompromised man, producing swelling, obstructions, and other conventional symptoms of human-originated cancer.

Tapeworm infection is the infestation of the digestive tract by a species of parasitic flatworm (known as a cestode), called tapeworms. Live tapeworm larvae grouped in cysts (coenuri)are sometimes ingested by consuming undercooked meat. Once inside the digestive tract, a larva can grow into a very large adult tapeworm. Additionally, many tapeworm larvae cause symptoms in an intermediate host. For example, cysticercosis is a disease involving larval tapeworms in the human body.

Sparganosis is a parasitic infection caused by the plerocercoid larvae of the genus "Spirometra" including , "S. ranarum", "S. mansonoides" and "S. erinacei". It was first described by Patrick Manson from China in 1882, and the first human case was reported by Charles Wardell Stiles from Florida in 1908. The infection is transmitted by ingestion of contaminated water, ingestion of a second intermediate host such as a frog or snake, or contact between a second intermediate host and an open wound or mucous membrane. Humans are the accidental hosts in the life cycle, while dogs, cats, and other mammals are definitive hosts. Copepods (freshwater crustaceans) are the first intermediate hosts, and various amphibians and reptiles are second intermediate hosts.

Once a human becomes infected, the plerocercoid larvae migrate to a subcutaneous location, where they typically develop into a painful nodule. Migration to the brain results in cerebral sparganosis, while migration to the eyes results in ocular sparganosis. Sparganosis is most prevalent in Eastern Asia, although cases have been described in countries throughout the world. In total, approximately 300 cases have been described in the literature up to 2003. Diagnosis is typically not made until the sparganum larva has been surgically removed. Praziquantel is the drug of choice, although its efficacy is unknown and surgical removal of the sparganum is generally the best treatment. Public health interventions should focus on water and dietary sanitation, as well as education about the disease in rural areas and discouragement of the use of poultices.

Neurocysticercosis is a specific form of the infectious parasitic disease cysticercosis which is caused by infection with "Taenia solium", a tapeworm found in pigs. Neurocysticercosis occurs when cysts formed by the infection grow within the brain causing neurologic syndromes such as epileptic seizures. It has been called a "hidden epidemic" and "arguably the most common parasitic disease of the human nervous system".

The epidemiology of "Taenia solium" cysticercosis is solely associated with cultural values and poor sanitation and it is highly endemic in Sub Saharan Africa, Latin America, Asia, and Portugal (in Europe). Infection by "Taenia solium" cysticercosis, the pork tapeworm larvae in human, spares no ethnic group. Cysticercosis in the United States, which commonly presents in the form of neurocysticercosis, has been classified as a "neglected tropical disease", which commonly affects the poor and homeless. Neurocysticercosis most commonly involves the cerebral cortex followed by the cerebellum. The pituitary gland is very rarely involved in neurocysticercosis. The cysts may rarely coalesce and form a tree-like pattern which is known as racemose neurocysticercosis, which when involving the pituitary gland may result in multiple pituitary hormone deficiency.

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.

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.

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.

In adults, the most common symptom of meningitis is a severe headache, occurring in almost 90% of cases of bacterial meningitis, followed by nuchal rigidity (the inability to flex the neck forward passively due to increased neck muscle tone and stiffness). The classic triad of diagnostic signs consists of nuchal rigidity, sudden high fever, and altered mental status; however, all three features are present in only 44–46% of bacterial meningitis cases. If none of the three signs are present, acute meningitis is extremely unlikely. Other signs commonly associated with meningitis include photophobia (intolerance to bright light) and phonophobia (intolerance to loud noises). Small children often do not exhibit the aforementioned symptoms, and may only be irritable and look unwell. The fontanelle (the soft spot on the top of a baby's head) can bulge in infants aged up to 6 months. Other features that distinguish meningitis from less severe illnesses in young children are leg pain, cold extremities, and an abnormal skin color.

Nuchal rigidity occurs in 70% of bacterial meningitis in adults. Other signs include the presence of positive Kernig's sign or Brudziński sign. Kernig's sign is assessed with the person lying supine, with the hip and knee flexed to 90 degrees. In a person with a positive Kernig's sign, pain limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. Although Kernig's sign and Brudzinski's sign are both commonly used to screen for meningitis, the sensitivity of these tests is limited. They do, however, have very good specificity for meningitis: the signs rarely occur in other diseases. Another test, known as the "jolt accentuation maneuver" helps determine whether meningitis is present in those reporting fever and headache. A person is asked to rapidly rotate the head horizontally; if this does not make the headache worse, meningitis is unlikely.

Other problems can produce symptoms similar to those above, but from non-meningitic causes. This is called meningism or pseudomeningitis.

Meningitis caused by the bacterium "Neisseria meningitidis" (known as "meningococcal meningitis") can be differentiated from meningitis with other causes by a rapidly spreading petechial rash, which may precede other symptoms. The rash consists of numerous small, irregular purple or red spots ("petechiae") on the trunk, lower extremities, mucous membranes, conjuctiva, and (occasionally) the palms of the hands or soles of the feet. The rash is typically non-blanching; the redness does not disappear when pressed with a finger or a glass tumbler. Although this rash is not necessarily present in meningococcal meningitis, it is relatively specific for the disease; it does, however, occasionally occur in meningitis due to other bacteria. Other clues on the cause of meningitis may be the skin signs of hand, foot and mouth disease and genital herpes, both of which are associated with various forms of viral meningitis.

Additional problems may occur in the early stage of the illness. These may require specific treatment, and sometimes indicate severe illness or worse prognosis. The infection may trigger sepsis, a systemic inflammatory response syndrome of falling blood pressure, fast heart rate, high or abnormally low temperature, and rapid breathing. Very low blood pressure may occur at an early stage, especially but not exclusively in meningococcal meningitis; this may lead to insufficient blood supply to other organs. Disseminated intravascular coagulation, the excessive activation of blood clotting, may obstruct blood flow to organs and paradoxically increase the bleeding risk. Gangrene of limbs can occur in meningococcal disease. Severe meningococcal and pneumococcal infections may result in hemorrhaging of the adrenal glands, leading to Waterhouse-Friderichsen syndrome, which is often fatal.

The brain tissue may swell, pressure inside the skull may increase and the swollen brain may herniate through the skull base. This may be noticed by a decreasing level of consciousness, loss of the pupillary light reflex, and abnormal posturing. The inflammation of the brain tissue may also obstruct the normal flow of CSF around the brain (hydrocephalus). Seizures may occur for various reasons; in children, seizures are common in the early stages of meningitis (in 30% of cases) and do not necessarily indicate an underlying cause. Seizures may result from increased pressure and from areas of inflammation in the brain tissue. Focal seizures (seizures that involve one limb or part of the body), persistent seizures, late-onset seizures and those that are difficult to control with medication indicate a poorer long-term outcome.

Inflammation of the meninges may lead to abnormalities of the cranial nerves, a group of nerves arising from the brain stem that supply the head and neck area and which control, among other functions, eye movement, facial muscles, and hearing. Visual symptoms and hearing loss may persist after an episode of meningitis. Inflammation of the brain (encephalitis) or its blood vessels (cerebral vasculitis), as well as the formation of blood clots in the veins (cerebral venous thrombosis), may all lead to weakness, loss of sensation, or abnormal movement or function of the part of the body supplied by the affected area of the brain.

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.

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

Eosinophilia and comparatively fewer cases of hypereosinophilia are associated with the following known diseases that are known or thought to have an allergic basis: allergic rhinitis, asthma, atopic dermatitis, eosinophilic esophagitis, chronic sinusitis, aspirin-induced asthma, allergic bronchopulmonary aspergillosis, chronic eosinophilic pneumonia, and Kimura's disease.

Certain types of food allergy disorders may also be associated with eosinophilia or, less commonly, hypereosinophilia. Allergic eosinophilic esophagitis and the Food protein-induced enterocolitis syndrome are commonly associated with increased blood eosinophil levels.

Helminths are common causes of hypereosiophilia and eosinophilia in areas endemic to these parasites. Helminths infections causing increased blood eosinophil counts include: 1) nematodes, (i.e. "Angiostrongylus cantonensis" and Hookworm infections), ascariasis, strongyloidiasis trichinosis, visceral larva migrans, Gnathostomiasis, cysticercosis, and echinococcosis; 2) filarioidea, i.e. tropical pulmonary eosinophilia, loiasis, and onchocerciasis; and 3) flukes, i.e. shistosomiasis, fascioliasis, clonorchiasis, paragonimiasis, and fasciolopsiasis. Other infections associated with increased eosinophil blood counts include: protozoan infections, i.e. "Isospora belli" and "Dientamoeba fragilis") and sarcocystis); fungal infections (i.e. disseminated histoplasmosis, cryptococcosis especially in cases with [[central nervous system]] involvement), and coccidioides); and viral infections, i.e. Human T-lymphotropic virus 1 and HIV.