Some of the drugs associated with serum sickness are:

- allopurinol

- barbiturates

- captopril

- cephalosporins

- griseofulvin

- penicillins

- phenytoin

- procainamide

- quinidine

- streptokinase

- sulfonamides

- rituximab

- ibuprofen

- infliximab

Allergenic extracts, hormones and vaccines can also cause serum sickness.

The following factors increase some people's susceptibility to airsickness:

- Fatigue, stress, and anxiety, are some factors that can increase susceptibility to motion sickness of any type.

- The use of alcohol, drugs, and medications may also contribute to airsickness.

- Additionally, airsickness is more common in women (especially during menstruation or pregnancy), young children, and individuals prone to other types of motion sickness.

- Although airsickness is uncommon among experienced pilots, it does occur with some frequency in student pilots.

Morning sickness may be an evolved trait that protects the baby against toxins ingested by the mother. Evidence in support of this theory includes:

- Morning sickness is very common among pregnant women, which argues in favor of its being a functional adaptation and against the idea that it is a pathology.

- Fetal vulnerability to toxins peaks at around 3 months, which is also the time of peak susceptibility to morning sickness.

- There is a good correlation between toxin concentrations in foods, and the tastes and odors that cause revulsion.

Women who have "no" morning sickness are more likely to miscarry. This may be because such women are more likely to ingest substances that are harmful to the fetus.

In addition to protecting the fetus, morning sickness may also protect the mother. A pregnant woman's immune system is suppressed during pregnancy, presumably to reduce the chances of rejecting tissues of her own offspring. Because of this, animal products containing parasites and harmful bacteria can be especially dangerous to pregnant women. There is evidence that morning sickness is often triggered by animal products including meat and fish.

If morning sickness is a defense mechanism against the ingestion of toxins, the prescribing of anti-nausea medication to pregnant women may have the undesired side effect of causing birth defects or miscarriages by encouraging harmful dietary choices.

The cause of morning sickness is unknown. While some have claimed it to be due to psychological reasons, this is not supported by evidence.

Nausea and vomiting may also occur with molar pregnancy.

Travelers who are susceptible to motion sickness can minimize symptoms by:

- Choosing a window seat with a view of the ground or of lower clouds, such that motion can be detected. This will not work if the plane is flown in the clouds for a long duration.

- Choosing seats with the smoothest ride in regards to pitch (the seats over the wings in an airplane). (This may not be sufficient for sensitive individuals who need to see ground movement)

- Sitting facing forward while focusing on distant objects rather than trying to read or look at something inside the airplane.

- Eating dry crackers, olives or suck on a lemon, to dry out the mouth, lessening nausea.

- Drinking a carbonated beverage.

Although the occurrence of DCS is not easily predictable, many predisposing factors are known. They may be considered as either environmental or individual.

Decompression sickness and arterial gas embolism in recreational diving are associated with certain demographic, environmental, and dive style factors. A statistical study published in 2005 tested potential risk factors: age, gender, body mass index, smoking, asthma, diabetes, cardiovascular disease, previous decompression illness, years since certification, dives in the last year, number of diving days, number of dives in a repetitive series, last dive depth, nitrox use, and drysuit use. No significant associations with risk of decompression sickness or arterial gas embolism were found for asthma, diabetes, cardiovascular disease, smoking, or body mass index. Increased depth, previous DCI, larger number of consecutive days diving, and being male were associated with higher risk for decompression sickness and arterial gas embolism. Nitrox and drysuit use, greater frequency of diving in the past year, increasing age, and years since certification were associated with lower risk, possibly as indicators of more extensive training and experience.

Some clinical examples:

Other examples are:

- Subacute bacterial endocarditis

- Symptoms of malaria

The following environmental factors have been shown to increase the risk of DCS:

- the magnitude of the pressure reduction ratio – a large pressure reduction ratio is more likely to cause DCS than a small one.

- repetitive exposures – repetitive dives within a short period of time (a few hours) increase the risk of developing DCS. Repetitive ascents to altitudes above within similar short periods increase the risk of developing altitude DCS.

- the rate of ascent – the faster the ascent the greater the risk of developing DCS. The US Navy Dive Manual indicates that ascent rates greater than about when diving increase the chance of DCS, while recreational dive tables such as the Bühlmann tables require an ascent rate of with the last taking at least one minute. An individual exposed to a rapid decompression (high rate of ascent) above has a greater risk of altitude DCS than being exposed to the same altitude but at a lower rate of ascent.

- the duration of exposure – the longer the duration of the dive, the greater is the risk of DCS. Longer flights, especially to altitudes of and above, carry a greater risk of altitude DCS.

- underwater diving before flying – divers who ascend to altitude soon after a dive increase their risk of developing DCS even if the dive itself was within the dive table safe limits. Dive tables make provisions for post-dive time at surface level before flying to allow any residual excess nitrogen to outgas. However, the pressure maintained inside even a pressurized aircraft may be as low as the pressure equivalent to an altitude of above sea level. Therefore, the assumption that the dive table surface interval occurs at normal atmospheric pressure is invalidated by flying during that surface interval, and an otherwise-safe dive may then exceed the dive table limits.

- diving before travelling to altitude – DCS can occur without flying if the person moves to a high-altitude location on land immediately after diving, for example, scuba divers in Eritrea who drive from the coast to the Asmara plateau at increase their risk of DCS.

- diving at altitude – diving in water whose surface altitude is above — for example, Lake Titicaca is at — without using versions of decompression tables or dive computers that are modified for high-altitude.

This depends on the degree of hepatocellular necrosis that has occurred. Decreases in the SDH and prothrombin time along with improvement in appetite are the best positive predictive indicators of recovery. GGT may remain elevated for weeks even if the horse is recovering. Horses that survive for greater than one week and that continue to eat usually recover. Cases with rapid progression of clinical signs, uncontrollable encephalopathy, haemorrhage or haemolysis have a poor prognosis. Horses that display clinical signs have a mortality rate of 50–90%.

All divers should be free of conditions and illnesses that would negatively impact their safety and well-being underwater. The diving medical physician should be able to identify, treat and advise divers about illnesses and conditions that would cause them to be at increased risk for a diving accident.

Some reasons why a person should not be allowed to dive are as follows:

- Disorders that lead to altered consciousness: conditions that produce reduced awareness or sedation from medication, drugs, marijuana or alcohol; fainting, heart problems and seizure activity.

- Disorders that substantially increase the risk of barotrauma injury conditions or diseases that are associated with air trapping in closed spaces, such as sinuses, middle ear, lungs and gastrointestinal tract. Severe asthma is an example.

- Disorders that may lead to erratic and irresponsible behavior: included here would be immaturity, psychiatric disorders, diving while under the influence of medications, drugs and alcohol or any medical disorder that results in cognitive defects.

Conditions that may increase risk of diving disorders:

- Patent foramen ovale

- Diabetes mellitus — No serious problems should be expected during dives due to hypoglycaemia in divers with well-controlled diabetes. Long-term complications of diabetes should be considered and may be a contrindication.

- Asthma

Conditions considered temporary reasons to suspend diving activities:

- Pregnancy—It is unlikely that literature research can establish the effect of scuba diving on the unborn human fetus as there is insufficient data, and women tend to comply with the diving industry recommendation not to dive while pregnant.

This condition most commonly occurs after the administration of a horse origin biological agent such as equine-derived antiserum, and usually occurs 4–10 weeks after the event. Diseases that have been vaccinated against using equine-origin antiserum, resulting in subsequent Theiler's disease, include: African horse sickness, Eastern and Western Equine Encephalitis, "Bacillus anthracis", tetanus antitoxin, "Clostridium perfringens", "Clostridium botulinum", "Streptococcus equi" subspecies "equi", Equine influenza, Equine herpesvirus type 1, pregnant mare's serum, and plasma. Although it occurs sporadically, It appears to be spreadable within a premises, and there have been outbreaks occurring on farms involving multiple horses over several months. In the Northern hemisphere it is most common between August to November. It is seen almost exclusively in adult horses, and lactating broodmares given tetanus antitoxin post foaling may be more susceptible.

Ascending slowly is the best way to avoid altitude sickness. Avoiding strenuous activity such as skiing, hiking, etc. in the first 24 hours at high altitude reduces the symptoms of AMS. Alcohol and sleeping pills are respiratory depressants, and thus slow down the acclimatization process and should be avoided. Alcohol also tends to cause dehydration and exacerbates AMS. Thus, avoiding alcohol consumption in the first 24–48 hours at a higher altitude is optimal.

Type III hypersensitivity occurs when there is an excess of antigen, leading to small immune complexes being formed that fix complement and are not cleared from the circulation. It involves soluble antigens that are not bound to cell surfaces (as opposed to those in type II hypersensitivity). When these antigens bind antibodies, immune complexes of different sizes form. Large complexes can be cleared by macrophages but macrophages have difficulty in the disposal of small immune complexes. These immune complexes insert themselves into small blood vessels, joints, and glomeruli, causing symptoms. Unlike the free variant, a small immune complex bound to sites of deposition (like blood vessel walls) are far more capable of interacting with complement; these medium-sized complexes, formed in the slight excess of antigen, are viewed as being highly pathogenic.

Such depositions in tissues often induce an inflammatory response, and can cause damage wherever they precipitate. The cause of damage is as a result of the action of cleaved complement anaphylotoxins C3a and C5a, which, respectively, mediate the induction of granule release from mast cells (from which histamine can cause urticaria), and recruitment of inflammatory cells into the tissue (mainly those with lysosomal action, leading to tissue damage through frustrated phagocytosis by PMNs and macrophages).

The reaction can take hours, days, or even weeks to develop, depending on whether or not there is immunological memory of the precipitating antigen. Typically, clinical features emerge a week following initial antigen challenge, when the deposited immune complexes can precipitate an inflammatory response. Because of the nature of the antibody aggregation, tissues that are associated with blood filtration at considerable osmotic and hydrostatic gradient (e.g. sites of urinary and synovial fluid formation, kidney glomeruli and joint tissues respectively) bear the brunt of the damage. Hence, vasculitis, glomerulonephritis and arthritis are commonly associated conditions as a result of type III hypersensitivity responses.

As observed under methods of histopathology, acute necrotizing vasculitis within the affected tissues is observed concomitant to neutrophilic infiltration, along with notable eosinophilic deposition (fibrinoid necrosis). Often, immunofluorescence microscopy can be used to visualize the immune complexes. Skin response to a hypersensitivity of this type is referred to as an Arthus reaction, and is characterized by local erythema and some induration. Platelet aggregation, especially in microvasculature, can cause localized clot formation, leading to blotchy hemorrhages. This typifies the response to injection of foreign antigen sufficient to lead to the condition of serum sickness.

The cause is the most mysterious aspect of the disease. Commentators then and now put much blame on the generally poor sanitation, sewage and contaminated water supplies of the time, which might have harboured the source of infection. The first outbreak at the end of the Wars of the Roses means that it may have been brought over from France by the French mercenaries whom Henry VII used to gain the English throne. However, the "Croyland Chronicle" mentions that Thomas Stanley, 1st Earl of Derby used the "sweating sickness" as an excuse not to join with Richard III's army prior to the Battle of Bosworth.

Relapsing fever has been proposed as a possible cause. This disease, which is spread by ticks and lice, occurs most often during the summer months, as did the original sweating sickness. However, relapsing fever is marked by a prominent black scab at the site of the tick bite and a subsequent skin rash.

Noting symptom overlap with hantavirus pulmonary syndrome, several scientists proposed an unknown hantavirus as the cause. A critique of this hypothesis included the argument that, whereas sweating sickness was thought to be transmitted from human to human, hantaviruses are rarely spread in this way. However, infection via human-to-human contact has been proven in hantavirus outbreaks in Argentina.

Pre-acclimatization is when the body develops tolerance to low oxygen concentrations before ascending to an altitude. It significantly reduces risk because less time has to be spent at altitude to acclimatize in the traditional way. Additionally, because less time has to be spent on the mountain, less food and supplies have to be taken up. Several commercial systems exist that use altitude tents, so called because they mimic altitude by reducing the percentage of oxygen in the air while keeping air pressure constant to the surroundings.

Hazards in the underwater environment that can affect divers include marine life, marine infections, polluted water, ocean currents, waves and surges and man-made hazards such as boats, fishing lines and underwater construction. Diving medical personnel need to be able to recognize and treat accidents from large and small predators and poisonous creatures, appropriately diagnose and treat marine infections and illnesses from pollution as well as diverse maladies such as sea sickness, traveler's diarrhea and malaria.

The symptoms and signs, as described by physician John Caius and others, were as follows: the disease began very suddenly with a sense of apprehension, followed by cold shivers (sometimes very violent), giddiness, headache, and severe pains in the neck, shoulders and limbs, with great exhaustion. After the cold stage, which might last from half an hour to three hours, the hot and sweating stage followed. The characteristic sweat broke out suddenly without any obvious cause. Accompanying the sweat, or after, was a sense of heat, headache, delirium, rapid pulse, and intense thirst. Palpitation and pain in the heart were frequent symptoms. No skin eruptions were noted by observers including Caius. In the final stages, there was either general exhaustion and collapse, or an irresistible urge to sleep, which Caius thought to be fatal if the patient was permitted to give way to it. One attack did not offer immunity, and some people suffered several bouts before dying. The disease tended to occur in summer and early autumn.

Currently, no vaccine against relapsing fever is available, but research continues. Developing a vaccine is very difficult because the spirochetes avoid the immune response of the infected person (or animal) through antigenic variation. Essentially, the pathogen stays one step ahead of antibodies by changing its surface proteins. These surface proteins, lipoproteins called variable major proteins, have only 30–70% of their amino acid sequences in common, which is sufficient to create a new antigenic "identity" for the organism. Antibodies in the blood that are binding to and clearing spirochetes expressing the old proteins do not recognize spirochetes expressing the new ones. Antigenic variation is common among pathogenic organisms. These include the agents of malaria, gonorrhea, and sleeping sickness. Important questions about antigenic variation are also relevant for such research areas as developing a vaccine against HIV and predicting the next influenza pandemic.

Human milk sickness is uncommon today in the United States. Current practices of animal husbandry generally control the pastures and feed of cattle, and the pooling of milk from many producers lowers the risk of tremetol present in dangerous amounts. The poison tremetol is not inactivated by pasteurization. Although extremely rare, milk sickness can occur if a person drinks contaminated milk or eats dairy products gathered from a single cow or from a smaller herd that has fed on the white snakeroot plant. There is no cure, but treatment is available.

Space motion sickness is caused by changes in g-forces, which affect spatial orientation in humans. According to "Science Daily", "Gravity plays a major role in our spatial orientation. Changes in gravitational forces, such as the transition to weightlessness during a space voyage, influence our spatial orientation and require adaptation by many of the physiological processes in which our balance system plays a part. As long as this adaptation is incomplete, this can be coupled to motion sickness (nausea), visual illusions and disorientation."

Modern motion-sickness medications can counter space sickness but are rarely used because it is considered better to allow space travelers to adapt naturally over the first day or two than to suffer the drowsiness and other side effects of medication. However, transdermal dimenhydrinate anti-nausea patches are typically used whenever space suits are worn because vomiting into a space suit could be fatal, as it could obscure vision or block airflow. Space suits are generally worn during launch and landing by NASA crew members and always for extra-vehicular activities (EVAs). EVAs are consequently not usually scheduled for the first days of a mission to allow the crew to adapt, and transdermal dimenhydrinate patches are typically used as an additional backup measure.

Decompression Illness (DCI) describes a range of symptoms arising from decompression of the body.

DCI can be caused by two different mechanisms, which result in overlapping sets of symptoms. The two mechanisms are:

- Decompression sickness (DCS), which results from metabolically inert gas dissolved in body tissue under pressure precipitating out of solution and forming bubbles during decompression. It typically afflicts underwater divers on poorly managed ascent from depth or aviators flying in inadequately pressurised aircraft.

- Arterial gas embolism (AGE), which is gas bubbles in the bloodstream. In the context of DCI these may form either as a result of bubble nucleation and growth by dissolved gas into the blood on depressurisation, which is a subset of DCS above, or by gas entering the blood mechanically as a result of pulmonary barotrauma. Pulmonary barotrauma is a rupturing of lung tissue by expansion of breathing gas held in the lungs during depressurisation. This may typically be caused by an underwater diver ascending while holding the breath after breathing at ambient pressure, ambient pressure escape from a submerged submarine without adequate exhalation during the ascent, or the explosive decompression of an aircraft cabin or other pressurised environment.

In any situation which could cause decompression sickness, there is also potentially a risk of arterial gas embolism, and as many of the symptoms are common to both conditions, it may be difficult to distinguish between the two in the field, and first aid treatment is the same for both mechanisms.

The most common hypothesis for the cause of motion sickness is that it functions as a defense mechanism against neurotoxins. The area postrema in the brain is responsible for inducing vomiting when poisons are detected, and for resolving conflicts between vision and balance. When feeling motion but not seeing it (for example, in a ship with no windows), the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. As a result of the discordance, the brain will come to the conclusion that the individual is hallucinating and further conclude that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin. Treisman's indirect argument has recently been questioned via an alternative direct evolutionary hypothesis, as well as modified and extended via a direct poison hypothesis. The direct evolutionary hypothesis essentially argues that there are plausible means by which ancient real or apparent motion could have contributed directly to the evolution of aversive reactions, without the need for the co-opting of a poison response as posited by Treisman. Nevertheless, the direct poison hypothesis argues that there still are plausible ways in which the body's poison response system may have played a role in shaping the evolution of some of the signature symptoms that characterize motion sickness.

An alternative theory, also known as the Nystagmus Hypothesis, has been proposed based on stimulation of the vagus nerves resulting from the stretching or traction of extra-ocular muscles co-occurring with eye movements caused by vestibular stimulation. There are three critical aspects to the theory: first is the close linkage between activity in the vestibular system, i.e., semicircular canals and otolith organs, and a change in tonus among various of each eye's six extra-ocular muscles. Thus, with the exception of voluntary eye movements, the vestibular and oculomotor systems are thoroughly linked. Second is the operation of Sherrington's Law describing reciprocal inhibition between agonist-antagonist muscle pairs, and by implication the stretching of extraocular muscle that must occur whenever Sherrington's Law is made to fail, thereby causing an unrelaxed (contracted) muscle to be stretched. Finally there is the critical presence of afferent output to the Vagus nerves as a direct result of eye muscle stretch or traction. Thus, 10th nerve stimulation resulting from eye muscle stretch is proposed as the cause of motion sickness. The theory explains why labyrinthine defective individuals are immune to motion sickness; why symptoms emerge when undergoing various body-head accelerations; why combinations of voluntary and reflexive eye movements may challenge the proper operation of Sherrington's Law, and why many drugs that suppress eye movements also serve to suppress motion sickness symptoms.

Motion sickness is a condition in which a disagreement exists between visually perceived movement and the vestibular system's sense of movement. Depending on the cause, it can also be referred to as seasickness, car sickness, simulation sickness or airsickness.

Dizziness, fatigue and nausea are the most common symptoms of motion sickness. Sopite syndrome, in which a person feels fatigue or tiredness, is also associated with motion sickness. "Nausea" in Greek means seasickness ("naus" means ship). If the motion causing nausea is not resolved, the sufferer will usually vomit. Vomiting often will not relieve the feeling of weakness and nausea, which means the person might continue to vomit until the cause of the nausea is treated.

African horse sickness was diagnosed in Spain in 1987–90 and in Portugal in 1989, but was eradicated using slaughter policies, movement restrictions, vector eradication, and vaccination.