Zamia staggers is a fatal nervous disease affecting cattle where they browse on the leaves or fruit of cycads—in particular, those of the genus Zamia (thus the name). It is characterised by irreversible paralysis of the hind legs because of the degeneration of the spinal cord. It is caused by the toxins cycasin and macrozamin, β-glycosides (the sugars of which are glucose and primeverose, respectively) of methylazoxymethanol (MAM), and which are found in all cycad genera.

Following ingestion the sugar is removed by bacterial glycosidase in the gut, with the MAM being absorbed. The metabolized toxin produces tumours of the liver, kidney, intestine and brain after a latent period which may be a year or longer. The disease has been known in Australia since the 1860s and was the subject of a Queensland Government investigation during the 1890s.

Clinical signs are normally only seen in either piglets less than 3 weeks old or pregnant sows.

Signs in piglets include rhinitis, pneumonia, anaemia, fever and sudden death. Black discoloration around the eyes is often seen and gastrointestinal and neurological signs are also reported.

Signs in pregnant sows include reproductive failure, genital ulceration and agalactia.

Latent iron deficiency (LID), also called iron-deficient erythropoiesis, is a medical condition in which there is evidence of iron deficiency without anemia (normal hemoglobin level). It is important to assess this condition because it is accepted that individuals with latent iron deficiency will develop iron-deficiency anemia in the weeks or months following diagnoses of LID if they are not treated with iron supplementation. In addition, there is some evidence of a decrease in vitality and an increase in fatigue among individuals that have LID.

The clinical features of LID are in discussion, some studies have not shown a clear difference between individuals with LID and control a group of the same age, gender and origin without LID. But may be it is not wrong to say that the persons with LID have a mild decrease in vitality and increase of fatigue. What seems important for preventive healthcare is to detect this medical condition, because it will avoid the patient probably developing an iron-deficiency anemia.

Cadang-cadang is a disease caused by Coconut cadang-cadang viroid (CCCVd), a lethal viroid of coconut ("Cocos nucifera"), anahaw ("Saribus rotundifolius") buri ("Corypha utan"), and African oil palm ("Elaeis guineensis"). The name cadang-cadang comes from the word that means dying in Bicol. It was originally reported on San Miguel Island in the Philippines in 1927/1928. "By 1962, all but 100 of 250,000 palms on this island had died from the disease," indicating an epidemic. Every year one million coconut palms are killed by CCCVd and over 30 million coconut palms have been killed since Cadang-cadang has been discovered. CCCVd directly affects the production of copra, a raw material for coconut oil and animal feed. Total losses of about 30 million palms and annual yield losses of about 22,000 tons of copra have been attributed to Cadang-cadang disease in the Philippines.

Inclusion Body Rhinitis, also known as IBR or Cytomegalic Inclusion Disease, is a pig disease caused by porcine cytomegalovirus, which is a member of the herpesvirus family. It is a notifiable disease that is found worldwide. It is spread both vertically and horizontally and prevalence is high.

It is not a zoonosis but the risk to humans that receive pig organ transplants is currently under investigation.

Acute toxoplasmosis is often asymptomatic in healthy adults. However, symptoms may manifest and are often influenza-like: swollen lymph nodes, headaches, fever, and fatigue, or muscle aches and pains that last for a month or more. Rarely will a human with a fully functioning immune system develop severe symptoms following infection. People with weakened immune systems are likely to experience headache, confusion, poor coordination, seizures, lung problems that may resemble tuberculosis or Pneumocystis jiroveci pneumonia (a common opportunistic infection that occurs in people with AIDS), or blurred vision caused by severe inflammation of the retina (ocular toxoplasmosis) Young children and immunocompromised people, such as those with HIV/AIDS, those taking certain types of chemotherapy, or those who have recently received an organ transplant, may develop severe toxoplasmosis. This can cause damage to the brain (encephalitis) or the eyes (necrotizing retinochoroiditis). Infants infected via placental transmission may be born with either of these problems, or with nasal malformations, although these complications are rare in newborns. The toxoplasmic trophozoites causing acute toxoplasmosis are referred to as tachyzoites, and are typically found in bodily fluids.

Swollen lymph nodes are commonly found in the neck or under the chin, followed by the armpits and the groin. Swelling may occur at different times after the initial infection, persist, and recur for various times independently of antiparasitic treatment. It is usually found at single sites in adults, but in children, multiple sites may be more common. Enlarged lymph nodes will resolve within one to two months in 60% of cases. However, a quarter of those affected take two to four months to return to normal, and 8% take four to six months. A substantial number (6%) do not return to normal until much later.

Cortisone reductase deficiency is caused by dysregulation of the 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1), otherwise known as cortisone reductase, a bi-directional enzyme, which catalyzes the interconversion of cortisone to cortisol in the presence of NADH as a co-factor. If levels of NADH are low, the enzyme catalyses the reverse reaction, from cortisol to cortisone, using NAD+ as a co-factor.

Cortisol is a glucocorticoid that plays a variety of roles in many different biochemical pathways, including, but not limited to: gluconeogenesis, suppressing immune system responses and carbohydrate metabolism.

One of the symptoms of cortisone reductase deficiency is hyperandrogenism, resulting from activation of the Hypothalamic–pituitary–adrenal axis.

The deficiency has been known to exhibit symptoms of other disorders such as Polycystic Ovary Syndrome in women. Cortisone Reductase Deficiency alone has been reported in fewer than ten cases in total, all but one case were women. Elevated activity of 11β-HSD1 can lead to obesity or Type II Diabetes, because of the role of cortisol in carbohydrate metabolism and gluconeogenesis.

Chvostek's sign is not a very specific sign of tetany as it may be seen in 10% to 25% of healthy adults. It is therefore not a reliable clinical sign for diagnosing latent tetany. The sensitivity is lower than that in the corresponding Trousseau sign as it is negative in 30% of patients with hypocalcemia. Due to the combination of poor sensitivity and specificity the clinical utility of this sign is reduced.

Hitting a point between the middle third and upper third of the line joining the angle of the mouth to the zygomatic process gives rise to only a contraction of the muscles of the mouth and nose.

Warfarin-induced skin necrosis (or, more generally, Anticoagulant-induced skin necrosis) is a condition in which skin and subcutaneous tissue necrosis (tissue death) occurs due to acquired protein C deficiency following treatment with anti-vitamin K anticoagulants (4-hydroxycoumarins, such as warfarin).

Warfarin necrosis is a rare but severe complication of treatment with warfarin or related anticoagulants. The typical patient appears to be an obese, middle aged woman (median age 54 years, male to female ratio 1:3). This drug eruption usually occurs between the third and tenth days of therapy with warfarin derivatives. The first symptoms are pain and redness in the affected area. As they progress, lesions develop a sharp border and become petechial, then hard and purpuric. They may then resolve or progress to form large, irregular, bloody bullae with eventual necrosis and slow-healing eschar formation. Favored sites are breasts, thighs, buttocks and penis, all areas with subcutaneous fat. In rare cases, the fascia and muscle are involved.

Development of the syndrome is associated with the use of large loading doses at the start of treatment.

The olfactory system is the system related to the sense of smell (olfaction). Many fish activities are dependent on olfaction, such as: mating, discriminating kin, avoiding predators, locating food, contaminant avoidance, imprinting and homing. These activities are referred to as “olfactory-mediated.” Impairment of the olfactory system threatens survival and has been used as an ecologically relevant sub-lethal toxicological endpoint for fish within studies. Olfactory information is received by sensory neurons, like the olfactory nerve, that are in a covered cavity separated from the aquatic environment by mucus. Since they are in almost direct contact with the surrounding environment, these neurons are vulnerable to environmental changes. Fish can detect natural chemical cues in aquatic environments at concentrations as low as parts per billion (ppb) or parts per trillion (ppt).

Studies have shown that exposures to metals, pesticides, or surfactants can disrupt fish olfaction, which can impact their survival and reproductive success. Many studies have indicated copper as a source of olfactory toxicity in fishes, among other common substances. Olfactory toxicity can occur by multiple, complex Modes of Toxic Action.

Due to its asymptomatic nature, it is easy for a host to become infected with "Toxoplasma gondii" and develop toxoplasmosis without knowing it. Although mild, flu-like symptoms occasionally occur during the first few weeks following exposure, infection with "T. gondii" produces no readily observable symptoms in healthy human adults. In most immunocompetent people, the infection enters a latent phase, during which only bradyzoites (tissue cysts) are present; these tissue cysts and even lesions can occur in the retinas, alveolar lining of the lungs (where an acute infection may mimic a "Pneumocystis jirovecii" infection), heart, skeletal muscle, and the central nervous system (CNS), including the brain. Cysts form in the CNS (brain tissue) upon infection with "T. gondii" and persist for the lifetime of the host. Most infants who are infected while in the womb have no symptoms at birth, but may develop symptoms later in life.

Reviews of serological studies have estimated that 30–50% of the global population has been exposed to and may be chronically infected with latent toxoplasmosis, although infection rates differ significantly from country to country. This latent state of infection has recently been associated with numerous disease burdens, neural alterations, and subtle gender-dependent behavioral changes in immunocompetent humans.

Cortisol inhibition, and as a result, excess androgen release can lead to a variety of symptoms. Other symptoms come about as a result of increased levels of circulating androgen. Androgen is a steroid hormone, generally associated with development of male sex organs and secondary male sex characteristics The symptoms associated with Cortisone Reductase Deficiency are often linked with Polycystic Ovary Syndrome (PCOS) in females. The symptoms of PCOS include excessive hair growth, oligomenorrhea, amenorrhea, and infertility. In men, cortisone reductase deficiency results in premature pseudopuberty, or sexual development before the age of nine.

Long-term nonprogressors (LTNPs), sometimes also called "elite controllers", are individuals infected with HIV, who maintain a CD4 count greater than 500 without antiretroviral therapy with a detectable viral load. Many of these patients have been HIV positive for 30 years without progressing to the point of needing to take medication in order not to develop AIDS. They have been the subject of a great deal of research, since an understanding of their ability to control HIV infection may lead to the development of immune therapies or a therapeutic vaccine. The classification "Long-term non-progressor" is not permanent, because some patients in this category have gone on to develop AIDS.

Long-term nonprogressors typically have viral loads under 10,000 copies RNA/ml blood, do not take antiretrovirals, and have CD4+ counts within the normal range. Most people with HIV not on medication have viral loads which are much higher.

It is estimated that around 1 in 300 people with HIV are long-term nonprogressors. Without the symptoms of AIDS, many LTNP patients may not know they are infected.

Genetic traits that confer greater resistance or more robust immune response to HIV are thought to explain why LTNP patients are able to live much longer with HIV than patients who are not LTNP. Some LTNP are infected with a weakened or inactive form of HIV, but it is now known that many LTNP patients carry a fully virulent form of the virus. Genetic traits that may affect progression include:

- Gene mutation. A mutation in the FUT2 gene affects the progression of HIV-1 infection. 20% of Europeans who have that mutation are called "non secretor" because of their absence of a certain type of antigen that also provides strong resistance against norovirus.

- Mitochondrial DNA. Different mitochondrial DNA haplotypes in humans may increase or decrease rates of AIDS progression. Haplotypes associated with more loosely coupled mitochondrial respiration, with reduced ATP and ROS generation, have been associated with faster progression and vice versa.

- Receptor mutations. A low percentage of long-term nonprogressors have been shown to have inherited mutations of the CCR5 receptor of T cell lymphocytes. HIV uses CCR5 to enter these cells. It is believed that the Δ32 (delta 32) variant of CCR5 impairs HIV ability to infect cells and cause disease. An understanding of this mechanism led to the development of a class of HIV medicines, the entry inhibitors. The presence of this mutation, however, is not a unifying theme among LTNPs and is observed in an exceedingly small number of these patients.

- HLA type has also been correlated with long-term non-progressor cohorts. In particular, strong correlations have been found between possessing the class 1 HLA-B*5701, HLA-B*5703, and/or HLA-B*2705 alleles and ability to exert control over HIV.

- Antibody production. All individuals with HIV make antibodies against the virus. In most patients, broadly neutralizing antibodies do not emerge until approximately 2–4 years after the initial infection. At this point, the latent reservoir has already been established and the presence of broadly neutralizing antibodies is not enough to prevent disease progression. In some rare patients, these antibodies emerge earlier and can result in a delayed disease course. These patients, however, are not typically classified as LTNPs, but rather as slow progressors, who will eventually develop AIDS. Induction of broadly neutralizing antibodies in healthy individuals is a potential strategy for a preventive HIV vaccine, as is the elicitation of these antibodies through rationally designed immunogens. Direct production of these antibodies in somatic tissue through plasmid transfection also pose a viable method for making these antibodies available in a large number of humans.

- APOBEC3G protein production. In a small number of people infected with HIV, the virus is naturally suppressed without medical treatment. These people may carry high quantities of a protein called APOBEC3G that disrupts viral replication in cells. APOBEC3G, or "A3" for short, is a protein that sabotages reverse transcription, the process HIV relies on for its replication. This process involves the virus transcribing its singe-stranded RNA genome into double-stranded DNA that is incorporated into the cell's genome. A3 usually stops dormant viruses in the human genome, called endogenous retroviruses, from reawakening and causing infections.

LID is present in stage 1 and 2, before anemia occurs in stage 3. These first two stages can be interpreted as depletion of iron stores and reduction of effective iron transport.

Stage 1 is characterized by loss of bone marrow iron stores while hemoglobin and serum iron levels remain normal. Serum ferritin falls to less than 20 ng/mL. Increased iron absorption, a compensatory change, results in an increased amount transferrin and consequent increased iron-binding capacity.

Stage 2 - Erythropoiesis is impaired. In spite of an increased level of transferrin, serum iron level is decreased along with transferrin saturation. Erythropoiesis impairment begins when the serum iron level falls to less than 50 μg/dL and transferrin saturation is less than 16%.

In stage 3, anemia (reduced hemoglobin levels) is present but red blood cell appearance remains normal.

Changes in the appearance of red blood cells are the hallmark of stage 4; first microcytosis and then hypochromia develop.

Iron deficiency begins to affect tissues in stage 5, manifesting as symptoms and signs.

Adult patients have worsening myalgias, bone pains and fatigue which are followed by recurrent fractures. Children present with difficulty in walking, stunted growth and deformities of the skeleton (features of rickets).

Symptoms of cadang-cadang develop slowly over 8 to 15 years making it difficult to diagnose at an early time. There are three main “stages” of defined series of characteristics: early, medium, and late stages. The first symptoms in the early stage develop within two to four years of infection. These symptoms include scarification of the coconuts which also become rounded. The leaves (fronds) display bright yellow spots. About two years later, during the medium stage, the inflorescences become stunted and eventually killed, so no more coconuts are produced. Yellow spots are larger and in greater abundance to give the appearance of chlorosis. During the final stage, roughly 6 years after the first symptoms are recorded, the yellow/bronze fronds start to decrease in size and number. Finally, all the leaves coalesce, leaving just the trunk of the palm “standing like a telephone pole”.

Palms under 10 years of age are rarely affected by cadang-cadang; the incidence of disease increases until about 40 years of age and then plateaus. "No recovery has ever been observed, and the disease is always fatal". African oil palm has similar symptoms as coconut but also have orange spotting on palms.

Euthyroid sick syndrome (ESS), sick euthyroid syndrome (SES), thyroid allostasis in critical illness, tumours, uremia and starvation (TACITUS), non-thyroidal illness syndrome (NTIS) or low T low T syndrome is a state of adaptation or dysregulation of thyrotropic feedback control where the levels of T3 and/or T4 are at unusual levels, but the thyroid gland does not appear to be dysfunctional.

This condition is often seen in starvation, critical illness or patients in intensive care unit. Similar endocrine phenotypes are observed in fetal life and in hibernating mammals The most common hormone pattern in sick euthyroid syndrome is a low total and unbound T3 levels with normal T4 and TSH levels.

Causes of euthyroid sick syndrome include a number of acute and chronic conditions, including pneumonia, fasting, starvation, anorexia nervosa, sepsis, trauma, cardiopulmonary bypass, malignancy, stress, heart failure, hypothermia, myocardial infarction, chronic renal failure, cirrhosis, and diabetic ketoacidosis.

Euthyroid sick syndrome (non-thyroidal illness syndrome) has been assumed closely related with a series of diseases, (such as inflammatory bowel disease).

Some fruit juices and fruits can interact with numerous drugs, in many cases causing adverse effects. The effect was first discovered by accident, when a test of drug interactions with alcohol used grapefruit juice to hide the taste of the ethanol.

It is still best-studied with grapefruit and grapefruit juice, but similar effects have more recently been seen with some (not all) other citrus fruits. One medical review advises patients to avoid all citrus juices until further research clarifies the risks. The interacting chemicals are found in many plants, and so many other foods may be affected; effects have been observed with apple juice, but their clinical significance is not yet known.

Normal amounts of food and drink, such as one whole grapefruit or a small glass () of grapefruit juice, can cause drug overdose toxicity. Fruit consumed three days before the medicine can still have an effect. The relative risks of different types of citrus fruit have not been systematically studied. Affected drugs typically have an auxiliary label saying “Do not take with grapefruit” on the container, and the interaction is elaborated on in the package insert. People are also advised to ask their physician or pharmacist about drug interactions.

The effects are caused by furanocoumarins (and, to a lesser extent, flavonoids). These chemicals inhibit key drug metabolizing enzymes, such as cytochrome P450 3A4 (CYP3A4). CYP3A4 is a metabolizing enzyme for almost 50% of drugs, and is found in the liver and small intestinal epithelial cells. As a result, many drugs are affected. Inhibition of enzymes can have two different effects, depending on whether the drug is either

1. metabolized by the enzyme to an inactive metabolite, "or"

2. activated by the enzyme to an active metabolite.

If the active drug is metabolized by the inhibited enzyme, then the fruit will stop the drug being metabolized, leaving elevated concentrations of the medication in the body, which can cause adverse effects. Conversely, if the medication is a prodrug, it needs to be metabolised to be converted to the active drug. Compromising its metabolism lowers concentrations of the active drug, reducing its therapeutic effect, and risking therapeutic failure.

Low drug concentrations can also be caused when the fruit suppresses drug absorption from the intestine.

The presentation of this condition includes a characteristic facies. The cardiac manifestations include patent ductus arteriosus, congenital hypertrophy of the left ventricle, and pericardial effusions.

Neurodevelopmental outcome appears normal, but obsessive traits and anxiety have been reported. It may also be associated with recurrent infections with low immunoglobulin levels and gastric bleeding, and additional possible associations include lymphoedema and heterochromia iridis.

The co-epidemic of tuberculosis (TB) and human immunodeficiency virus (HIV) is one of the major global health challenges in the present time. The World Health Organization (WHO) reports 9.2 million new cases of TB in 2006 of whom 7.7% were HIV-infected. Tuberculosis is the most common contagious infection in HIV-Immunocompromised patients leading to death. These both diseases become dreadful in combination as HIV declines the human immunity while tuberculosis becomes progressive due to defective immune system.This condition becomes more severe in case of multi-drug (MDRTB) and extensively drug resistant TB (XDRTB), which are difficult to treat and contribute to increased mortality. See Multi-drug-resistant tuberculosis. Tuberculosis can occur at any stage of HIV infection. The risk and severity of tuberculosis increases soon after infection with HIV. A study on gold miners of South Africa revealed that the risk of TB was doubled during the first year after HIV seroconversion. Although tuberculosis can be a relatively early manifestation of HIV infection, it is important to note that the risk of tuberculosis progresses as the CD4 cell count decreases along with the progression of HIV infection. The risk of TB generally remains high in HIV-infected patients above the background risk of the general population even with effective immune reconstitution with ART maintaining high CD4 cell counts.

Many conditions mimic or may be mistaken for warfarin necrosis, including pyoderma gangrenosum or necrotizing fasciitis. Warfarin necrosis is also different from another drug eruption associated with warfarin, purple toe syndrome, which usually occurs three to eight weeks after the start of anticoagulation therapy. No report has described this disorder in the immediate postpartum period in patients with protein S deficiency.

The BK virus is a member of the polyomavirus family. Past infection with the BK virus is widespread, but significant consequences of infection are uncommon, with the exception of the immunocompromised and the immunosuppressed.

Oncogenic osteomalacia or tumor-induced osteomalacia, also known as oncogenic hypophosphatemic osteomalacia or oncogenic osteomalacia, is an uncommon disorder resulting in increased renal phosphate excretion, hypophosphatemia and osteomalacia. It may be caused by a phosphaturic mesenchymal tumor.