Symptoms vary from none to severe diarrhea with poor absorption of nutrients. It can result in weakness, loss of appetite, stomach cramps, vomiting, bloating, excessive gas, and burping. Symptoms typically develop 9–15 days after exposure, but may occur as early as one day.

Symptoms are caused by "Giardia" organisms infecting the cells of the duodenum and jejunum of the small intestine and blocking nutrient absorption. Most people are asymptomatic; only about a third of those infected exhibit symptoms. If the infection is not treated, these symptoms may last for six weeks or more.

Symptomatic infections are well recognized as causing lactose intolerance, which, while usually temporary, may become permanent. Although hydrogen breath tests indicate poorer rates of carbohydrate absorption in those asymptomatically infected, such tests are not diagnostic of infection. It has been suggested that these observations are explained by symptomatic giardia infection allowing for the overgrowth of other bacteria.

Some studies have shown giardiasis should be considered as a cause of vitamin B deficiency as a result of the problems caused within the intestinal absorption system.

Giardiasis, popularly known as beaver fever, is a parasitic disease caused by "Giardia lamblia". About 10% of those infected have no symptoms. When symptoms occur they may include diarrhea, abdominal pain, and weight loss. Vomiting, blood in the stool, and fever are less common. Symptoms usually begin 1 to 3 weeks after exposure and without treatment may last up to six weeks.

Giardia usually spreads when "Giardia lamblia" cysts within feces contaminate food or water which is then eaten or drunk. It may also spread between people and from other animals. Risk factors include travel in the developing world, changing diapers, eating food without cooking it, and owning a dog. Cysts may survive for nearly three months in cold water. Diagnosis is via stool tests.

Prevention is typically by improved hygiene. Those without symptoms do not usually need treatment. When symptoms are present treatment is typically with either tinidazole or metronidazole. People may become temporarily lactose intolerant after an infection and therefore it is often recommended milk be avoided for a few weeks. Resistance to treatment may occur.

Giardia is one of the most common parasitic human diseases globally. In 2013, there were about 280 million people worldwide with symptomatic giardiasis. Rates are as high as 7% in the developed world and 30% in the developing world. The World Health Organization classified it as a neglected disease.

Physiological reactions to "Toxocara" infection depend on the host’s immune response and the parasitic load. Most cases of "Toxocara" infection are asymptomatic, especially in adults. When symptoms do occur, they are the result of migration of second stage "Toxocara" larvae through the body.

Covert toxocariasis is the least serious of the three syndromes and is believed to be due to chronic exposure. Signs and symptoms of covert toxocariasis are coughing, fever, abdominal pain, headaches, and changes in behavior and ability to sleep. Upon medical examination, wheezing, hepatomegaly, and lymphadenitis are often noted.

High parasitic loads or repeated infection can lead to visceral larva migrans (VLM). VLM is primarily diagnosed in young children, because they are more prone to exposure and ingestion of infective eggs. "Toxocara" infection commonly resolves itself within weeks, but chronic eosinophilia may result. In VLM, larvae migration incites inflammation of internal organs and sometimes the central nervous system. Symptoms depend on the organ(s) affected. Patients can present with pallor, fatigue, weight loss, anorexia, fever, headache, rash, cough, asthma, chest tightness, increased irritability, abdominal pain, nausea, and vomiting. Sometimes the subcutaneous migration tracks of the larvae can be seen. Patients are commonly diagnosed with pneumonia, bronchospasms, chronic pulmonary inflammation, hypereosinophilia, hepatomegaly, hypergammaglobulinaemia (IgM, IgG, and IgE classes), leucocytosis, and elevated anti-A and –B isohaemagglutinins. Severe cases have occurred in people who are hypersensitive to allergens; in rare cases, epilepsy, inflammation of the heart, pleural effusion, respiratory failure, and death have resulted from VLM.

Ocular larva migrans (OLM) is rare compared with VLM. A light "Toxocara" burden is thought to induce a low immune response, allowing a larva to enter the host’s eye. Although there have been cases of concurrent OLM and VLM, these are extremely exceptional. OLM often occurs in just one eye and from a single larva migrating into and encysting within the orbit. Loss of vision occurs over days or weeks. Other signs and symptoms are red eye, white pupil, fixed pupil, retinal fibrosis, retinal detachment, inflammation of the eye tissues, retinal granulomas, and strabismus. Ocular granulomas resulting from OLM are frequently misdiagnosed as retinoblastomas. "Toxocara" damage in the eye is permanent and can result in blindness.

A case study published in 2008 supported the hypothesis that eosinophilic cellulitis may also be caused by infection with "Toxocara". In this study, the adult patient presented with eosinophilic cellulitis, hepatosplenomegaly, anemia, and a positive ELISA for "T. cani"s.

The incubation period for "Toxocara canis" and "cati" eggs depends on temperature and humidity. "T. canis" females, specifically, are capable of producing up to 200,000 eggs a day that require 2-6 weeks minimum up to a couple months before full development into the infectious stage. Under ideal summer conditions, eggs can mature to the infective stage after two weeks outside of a host. Provided sufficient oxygen and moisture availability, "Toxocara" eggs can remain infectious for years, as their resistant outer shell enables the protection from most environmental threats.However, as identified in a case study presented within the journal of helminthology, the second stage of larvae development poses strict vulnerabilities to certain environmental elements. High temperatures and low moisture levels will quickly degrade the larvae during this stage of growth.

Blastomycosis can present in one of the following ways:

- a flu-like illness with fever, chills, arthralgia (joint pain), myalgia (muscle pain), headache, and a nonproductive cough which resolves within days.

- an acute illness resembling bacterial pneumonia, with symptoms of high fever, chills, a productive cough, and pleuritic chest pain.

- a chronic illness that mimics tuberculosis or lung cancer, with symptoms of low-grade fever, a productive cough, night sweats, and weight loss.

- a fast, progressive, and severe disease that manifests as ARDS, with fever, shortness of breath, tachypnea, hypoxemia, and diffuse pulmonary infiltrates.

- skin lesions, usually asymptomatic, can be verrucous (wart-like) or ulcerated with small pustules at the margins.

- bone lytic lesions can cause bone or joint pain.

- prostatitis may be asymptomatic or may cause pain on urinating.

- laryngeal involvement causes hoarseness.

- 40% immunocompromised individuals have CNS involvement and present as brain abscess, epidural abscess or meningitis.

Blastomycosis (also known as "North American blastomycosis", "Blastomycetic dermatitis", and "Gilchrist's disease") is a fungal infection of humans and other animals, notably dogs and occasionally cats, caused by the organism "Blastomyces dermatitidis". Endemic to portions of North America, blastomycosis causes clinical symptoms similar to histoplasmosis. The disease occurs in several endemic areas, the most important of which is in eastern North America, particularly in the western and northern periphery of the Great Lakes Basin, extending eastward along the south shore of the St. Lawrence River Valley and southward in the territory spanned by the central Appalachian Mountains in the east, to the Mississippi River Valley in the west. Sporadic cases have been reported in continental Africa, the Arabian Peninsula and the Indian subcontinent.

Protein poisoning (also referred to colloquially as rabbit starvation, mal de caribou, or fat starvation) is a rare form of acute malnutrition thought to be caused by a complete absence of fat in the diet.

Excess protein is sometimes cited as the cause of this issue; when meat and fat are consumed in the correct ratio, such as that found in pemmican (which is 50% fat by volume), the diet is considered nutritionally complete and can support humans for months or more. Other stressors, such as severe cold or a dry environment, may intensify symptoms or decrease time to onset. Symptoms include diarrhea, headache, fatigue, low blood pressure, slow heart rate, and a vague discomfort and hunger (very similar to a food craving) that can be satisfied only by the consumption of fat.

Protein poisoning was first noted as a consequence of eating rabbit meat exclusively, hence the term, "rabbit starvation". Rabbit meat is very lean; commercial rabbit meat has 50–100 g dissectable fat per 2 kg (live weight). Based on a carcass yield of 60%, rabbit meat is around 8.3% fat while beef and pork are 32% fat and lamb 28%.

Given the lack of scientific data on the effects of high-protein diets, the US Food and Nutrition Board does not set a tolerable upper intake level nor upper acceptable macronutrient distribution range for protein.

Patients with idiopathic macular telangiectasia type 1 are typically 40 years of age or older. They may have a coincident history of ischemic vascular diseases such as diabetes or hypertension, but these do not appear to be causative factors.

Macular telangiectasia type 2 usually present first between the ages of 50 and 60 years, with a mean age of 55–59 years. They may present with a wide range of visual impact, from totally asymptomatic to substantially impaired; in most cases however, patients retain functional acuity of 20/200 or better. Metamorphopsia may be a subjective complaint. Due to the development of paracentral scotomota (blind spots), reading ability is impaired early in the disease course. It might be even the first symptom of the disease.

The condition may remain stable for extended periods, sometimes interspersed with sudden decreases in vision. Patients’ loss of visual function is disproportionately worse than the impairment of their visual acuity, which is only mildly affected in many cases. In patients with MacTel, as compared with a reference population, there is a significantly higher prevalence of systemic conditions associated with vascular disease, including history of hypertension, history of diabetes, and history of coronary disease. MacTel does not cause total blindness, yet it commonly causes gradual loss of the central vision required for reading and driving.

Macular telangiectasia describes two distinct retinal diseases affecting the macula of the eye, macular telangiectasia type 1 and macular telangiectasia type 2.

Macular telangiectasia (MacTel) type 1 is a very rare disease, typically unilateral and usually affecting male patients. MacTel type 2 is more frequent than type 1 and generally affects both eyes (bilateral). It usually affects both sexes equally. Both types of MacTel should not be confused with Age-related macular degeneration (AMD), from which it can be distinguished by symptoms, clinical features, pathogenesis, and disease management. However, both AMD and MacTel eventually lead to (photoreceptor) atrophy and thus loss of central vision.

The etiology of both types of MacTel is still unknown and no treatment has been found to be effective to prevent further progression. Because lost photoreceptors cannot be recovered, early diagnosis and treatment appear to be essential to prevent loss of visual function. Several centers are currently trying to find new diagnostics and treatments to understand the causes and biochemical reactions in order to halt or counteract the adverse effects.

Contemporary research has shown that MacTel type 2 is likely a neurodegenerative disease with secondary changes of the blood vessels of the macula. Although MacTel type 2 has been previously regarded as a rare disease, it is in fact probably much more common than previously thought. The very subtle nature of the early findings in MacTel mean the diagnoses are often missed by optometrists and general ophthalmologists. Due to increased research activity since 2005, many new insights have been gained into this condition since its first description by Dr. J. Donald Gass in 1982.