Signs and symptoms of PCP include fever, non-productive cough (because sputum is too viscous to become productive), shortness of breath (especially on exertion), weight loss, and night sweats. There is usually not a large amount of sputum with PCP unless the patient has an additional bacterial infection. The fungus can invade other visceral organs (such as the liver, spleen, and kidney), but only in a minority of cases.

Pneumothorax is a well-known complication of PCP. An acute history of chest pain with breathlessness and diminished breath sounds is typical of pneumothorax.

"Pneumocystis" pneumonia (PCP) is a form of pneumonia, caused by the yeast-like fungus "Pneumocystis jirovecii".

"Pneumocystis" pneumonia is not commonly found in the lungs of healthy people, but, being a source of opportunistic infection, it can cause a lung infection in people with a weak immune system. "Pneumocystis" pneumonia is especially seen in people with cancer undergoing chemotherapy, HIV/AIDS, and the use of medications that suppress the immune system.

Pulmonary edema, connective tissue diseases, asbestosis, lymphangitic carcinomatosis, lymphoma, lymphangioleiomyomatosis, drug-induced lung diseases

- Lymphadenopathy

Sarcoidosis, silicosis, berylliosis, lymphangitic carcinomatosis, lymphoma, lymphocytic interstitial pneumonia

Pulmonary Langerhans cell histiocytosis, silicosis, coal workers pneumoconiosis, carmustine related pulmonary fibrosis, respiratory broncholitis associated with interstitial lung disease.

- Lower lung predominance

Idiopathic pulmonary fibrosis, pulmonary fibrosis associated with connective tissue diseases, asbestosis, chronic aspiration

- Central predominance (perihilar)

Sarcoidosis, berylliosis

- Peripheral predominance

Idiopathic pulmonary fibrosis, chronic eosinophilic pneumonia, cryptogenic organizing pneumonia

A primary spontaneous pneumothorax (PSP) tends to occur in a young adult without underlying lung problems, and usually causes limited symptoms. Chest pain and sometimes mild breathlessness are the usual predominant presenting features. People who are affected by PSPs are often unaware of potential danger and may wait several days before seeking medical attention. PSPs more commonly occur during changes in atmospheric pressure, explaining to some extent why episodes of pneumothorax may happen in clusters. It is rare for PSPs to cause tension pneumothoraces.

Secondary spontaneous pneumothoraces (SSPs), by definition, occur in individuals with significant underlying lung disease. Symptoms in SSPs tend to be more severe than in PSPs, as the unaffected lungs are generally unable to replace the loss of function in the affected lungs. Hypoxemia (decreased blood-oxygen levels) is usually present and may be observed as cyanosis (blue discoloration of the lips and skin). Hypercapnia (accumulation of carbon dioxide in the blood) is sometimes encountered; this may cause confusion and – if very severe – may result in comas. The sudden onset of breathlessness in someone with chronic obstructive pulmonary disease (COPD), cystic fibrosis, or other serious lung diseases should therefore prompt investigations to identify the possibility of a pneumothorax.

Traumatic pneumothorax most commonly occurs when the chest wall is pierced, such as when a stab wound or gunshot wound allows air to enter the pleural space, or because some other mechanical injury to the lung compromises the integrity of the involved structures. Traumatic pneumothoraces have been found to occur in up to half of all cases of chest trauma, with only rib fractures being more common in this group. The pneumothorax can be occult (not readily apparent) in half of these cases, but may enlarge - particularly if mechanical ventilation is required. They are also encountered in patients already receiving mechanical ventilation for some other reason.

Upon physical examination, breath sounds (heard with a stethoscope) may be diminished on the affected side, partly because air in the pleural space dampens the transmission of sound. Measures of the conduction of vocal vibrations to the surface of the chest may be altered. Percussion of the chest may be perceived as hyperresonant (like a booming drum), and vocal resonance and tactile fremitus can both be noticeably decreased. Importantly, the volume of the pneumothorax can show limited correlation with the intensity of the symptoms experienced by the victim, and physical signs may not be apparent if the pneumothorax is relatively small.

Although multiple definitions exist, a tension pneumothorax is generally considered to be present when a pneumothorax (primary spontaneous, secondary spontaneous, or traumatic) leads to significant impairment of respiration and/or blood circulation. Tension pneumothorax tends to occur in clinical situations such as ventilation, resuscitation, trauma, or in patients with lung disease.

The most common findings in people with tension pneumothorax are chest pain and respiratory distress, often with an increased heart rate (tachycardia) and rapid breathing (tachypnea) in the initial stages. Other findings may include quieter breath sounds on one side of the chest, low oxygen levels and blood pressure, and displacement of the trachea away from the affected side. Rarely, there may be cyanosis (bluish discoloration of the skin due to low oxygen levels), altered level of consciousness, a hyperresonant percussion note on examination of the affected side with reduced expansion and decreased movement, pain in the epigastrium (upper abdomen), displacement of the apex beat (heart impulse), and resonant sound when tapping the sternum. This is a medical emergency and may require immediate treatment without further investigations (see below).

Tension pneumothorax may also occur in someone who is receiving mechanical ventilation, in which case it may be difficult to spot as the person is typically receiving sedation; it is often noted because of a sudden deterioration in condition. Recent studies have shown that the development of tension features may not always be as rapid as previously thought. Deviation of the trachea to one side and the presence of raised jugular venous pressure (distended neck veins) are not reliable as clinical signs.

The initial period following the contraction of HIV is called acute HIV, primary HIV or acute retroviral syndrome. Many individuals develop an influenza-like illness or a mononucleosis-like illness 2–4 weeks post exposure while others have no significant symptoms. Symptoms occur in 40–90% of cases and most commonly include fever, large tender lymph nodes, throat inflammation, a rash, headache, and/or sores of the mouth and genitals. The rash, which occurs in 20–50% of cases, presents itself on the trunk and is maculopapular, classically. Some people also develop opportunistic infections at this stage. Gastrointestinal symptoms, such as vomiting or diarrhea may occur. Neurological symptoms of peripheral neuropathy or Guillain–Barré syndrome also occurs. The duration of the symptoms varies, but is usually one or two weeks.

Due to their nonspecific character, these symptoms are not often recognized as signs of HIV infection. Even cases that do get seen by a family doctor or a hospital are often misdiagnosed as one of the many common infectious diseases with overlapping symptoms. Thus, it is recommended that HIV be considered in people presenting an unexplained fever who may have risk factors for the infection.

The initial symptoms are followed by a stage called clinical latency, asymptomatic HIV, or chronic HIV. Without treatment, this second stage of the natural history of HIV infection can last from about three years to over 20 years (on average, about eight years). While typically there are few or no symptoms at first, near the end of this stage many people experience fever, weight loss, gastrointestinal problems and muscle pains. Between 50 and 70% of people also develop persistent generalized lymphadenopathy, characterized by unexplained, non-painful enlargement of more than one group of lymph nodes (other than in the groin) for over three to six months.

Although most HIV-1 infected individuals have a detectable viral load and in the absence of treatment will eventually progress to AIDS, a small proportion (about 5%) retain high levels of CD4 T cells (T helper cells) without antiretroviral therapy for more than 5 years. These individuals are classified as HIV controllers or long-term nonprogressors (LTNP). Another group consists of those who maintain a low or undetectable viral load without anti-retroviral treatment, known as "elite controllers" or "elite suppressors". They represent approximately 1 in 300 infected persons.

HIV in pregnancy is the presence of the HIV virus in a woman while pregnant. There are concerns because women diagnosed with HIV/AIDS may transmit the infection to their child during pregnancy. The infection be transmitted to the infant during the pregnancy, childbirth, or breastfeeding. However, the risk of mother-to-child transmission of HIV may be reduced by the use of HIV medications known as antiretroviral therapy (ART). These medications may be used by women before, during, and after pregnancy. After delivery, children are also given the medication to reduce the risk of infection. Because HIV may be spread through breast milk, mothers with the infection are encouraged to avoid breastfeeding.

Infection with HIV/AIDS is not a contraindication to pregnancy. Women with the disease may choose to become pregnant if they desire, however, they are encouraged to talk with their doctors beforehand. Some women are unaware they have the disease until they become pregnant. In this case, they should begin antiretroviral therapy as soon as possible. With the appropriate treatment, the risk of mother-to-child infection can be reduced to below 1%. Without treatment, the risk of transmission is 15-45%.

There are approximately 1.4 million HIV positive women who become pregnant and contribute to more than 300,000 neonatal and fetal deaths each year. With the use of ART, transmission of HIV from the mother to child has decreased according to reports by the World Health Organization (WHO). In 2009, there were an estimated 400,000 children born with HIV and by 2013, there were 240,000. Countries in Southern Africa are worst affected by the HIV/AIDS pandemic. In 2010, 30% of all pregnancies in the region were affected by HIV. In 2011, HIV was responsible for 50% of the deaths for children below the age of 5. In the United States, fewer than 200 babies are born with HIV every year.

As of 2015, Cuba has become the first country in the world to eradicate mother-to-child transmission of HIV. In 2010, the WHO partnered with the Pan American Health Organization (PAHO) to implement an initiative that would provide early prenatal care and HIV testing for all pregnant women in the country. For women who tested positive, ART was provided for both the mother and child, cesarean sections were performed, and alternatives to breastfeeding were provided. In implementing these measures, the country was successfully able to eradicate HIV transmission during pregnancy.

All people with ALPS have signs of lymphoproliferation, which makes it the most common clinical manifestation of the disease. The increased proliferation of lymphoid cells can cause the size of lymphoid organs such as the lymph nodes and spleen to increase (lymphadenopathy and splenomegaly, present in respectively over 90% and over 80% of patients). The liver is enlarged (hepatomegaly in 30 - 40% of patients).

Autoimmune disease is the second most common clinical manifestation and one that most often requires treatment. Autoimmune cytopenias: Most common. Can be mild to very severe. Can be intermittent or chronic. These include: Autoimmune hemolytic anemia, Autoimmune neutropenia, Autoimmune thrombocytopenia.

Other signs can affect organ systems similar to systemic lupus erythematosus (least common, affecting <5% of patients) Symptoms of the nervous system include: Autoimmune cerebellar ataxia; Guillain–Barré syndrome; transverse myelitis. Gastrointestinal signs like Autoimmune esophagitis, gastritis, colitis, hepatitis, pancreatitis can be found or (Dermatologic) Urticaria, (Pulmonary) bronchiolitis obliterans, (Renal) Autoimmune glomerulonephritis, nephrotic syndrome.

Another sign are cancers such as Hodgkin and non-Hodgkin lymphomas which appear to be increased, possibly due to Epstein–Barr virus-encoded RNA-positivity. Some carcinomas may occur. Unaffected family members with genetic mutations are also at an increased risk of developing cancer.

Among the presentation consistent with hyper IgM syndrome are the following:

- Infection/"Pneumocystis" pneumonia (PCP), which is common in infants with hyper IgM syndrome, is a serious illness. PCP is one of the most frequent and severe opportunistic infections in people with weakened immune systems. Many CD40 Ligand Deficiency are first diagnosed after having PCP in their first year of life. The fungus is common and is present in over 70% of healthy people’s lungs, however, Hyper IgM patients are not able to fight it off without the administration of Bactrim)

- Hepatitis (Hepatitis C)

- Chronic diarrhea

- Hypothyroidism

- Neutropenia

- Arthritis

- Encephalopathy (degenerative)

Autoimmune lymphoproliferative syndrome (ALPS), also known as Canale-Smith syndrome, is a form of lymphoproliferative disorder (LPDs). It affects lymphocyte apoptosis. It is a RASopathy.

It is a rare genetic disorder of abnormal lymphocyte survival caused by defective Fas mediated apoptosis. Normally, after infectious insult, the immune system down-regulates by increasing Fas expression on activated B and T lymphocytes and Fas-ligand on activated T lymphocytes. Fas and Fas-ligand interact to trigger the caspase cascade, leading to cell apoptosis. Patients with ALPS have a defect in this apoptotic pathway, leading to chronic non-malignant lymphoproliferation, autoimmune disease, and secondary cancers.

An early stage of hyperthermia can be "heat exhaustion" (or "heat prostration" or "heat stress"), whose symptoms include heavy sweating, rapid breathing and a fast, weak pulse. If the condition progresses to heat stroke, then hot, dry skin is typical as blood vessels dilate in an attempt to increase heat loss. An inability to cool the body through perspiration may cause the skin to feel dry.

Other signs and symptoms vary. Accompanying dehydration can produce nausea, vomiting, headaches, and low blood pressure and the latter can lead to fainting or dizziness, especially if the standing position is assumed quickly.

In severe heat stroke, there may be confused, hostile, or seemingly intoxicated behavior. Heart rate and respiration rate will increase (tachycardia and tachypnea) as blood pressure drops and the heart attempts to maintain adequate circulation. The decrease in blood pressure can then cause blood vessels to contract reflexively, resulting in a pale or bluish skin color in advanced cases. Young children, in particular, may have seizures. Eventually, organ failure, unconsciousness and death will result.

The human disease occurs in two stages: an acute stage, which occurs shortly after an initial infection, and a chronic stage that develops over many years.

The acute phase lasts for the first few weeks or months of infection. It usually occurs unnoticed because it is symptom-free or exhibits only mild symptoms that are not unique to Chagas disease. These can include fever, fatigue, body aches, muscle pain, headache, rash, loss of appetite, diarrhea, nausea, and vomiting. The signs on physical examination can include mild enlargement of the liver or spleen, swollen glands, and local swelling (a chagoma) where the parasite entered the body.

The most recognized marker of acute Chagas disease is called Romaña's sign, which includes swelling of the eyelids on the side of the face near the bite wound or where the bug feces were deposited or accidentally rubbed into the eye. Rarely, young children, or adults may die from the acute disease due to severe inflammation/infection of the heart muscle (myocarditis) or brain (meningoencephalitis). The acute phase also can be severe in people with weakened immune systems.

If symptoms develop during the acute phase, they usually resolve spontaneously within three to eight weeks in approximately 90% of individuals. Although the symptoms resolve, even with treatment the infection persists and enters a chronic phase. Of individuals with chronic Chagas disease, 60–80% will never develop symptoms (called "indeterminate" chronic Chagas disease), while the remaining 20–40% will develop life-threatening heart and/or digestive disorders during their lifetime (called "determinate" chronic Chagas disease). In 10% of individuals, the disease progresses directly from the acute form to a symptomatic clinical form of chronic Chagas disease.

The symptomatic (determinate) chronic stage affects the nervous system, digestive system and heart. About two-thirds of people with chronic symptoms have cardiac damage, including dilated cardiomyopathy, which causes heart rhythm abnormalities and may result in sudden death. About one-third of patients go on to develop digestive system damage, resulting in dilation of the digestive tract (megacolon and megaesophagus), accompanied by severe weight loss. Swallowing difficulties (secondary achalasia) may be the first symptom of digestive disturbances and may lead to malnutrition.

20% to 50% of individuals with intestinal involvement also exhibit cardiac involvement. Up to 10% of chronically infected individuals develop neuritis that results in altered tendon reflexes and sensory impairment. Isolated cases exhibit central nervous system involvement, including dementia, confusion, chronic encephalopathy and sensory and motor deficits.

The clinical manifestations of Chagas disease are due to cell death in the target tissues that occurs during the infective cycle, by sequentially inducing an inflammatory response, cellular lesions, and fibrosis. For example, intracellular amastigotes destroy the intramural neurons of the autonomic nervous system in the intestine and heart, leading to megaintestine and heart aneurysms, respectively. If left untreated, Chagas disease can be fatal, in most cases due to heart muscle damage.

Hyper IgM syndromes is a group of primary immune deficiency disorders characterized by defective CD40 signaling; "via" B cells affecting class switch recombination (CSR) and somatic hypermutation. Immunoglobulin (Ig) class switch recombination deficiencies are characterized by elevated serum Immunoglobulin M (IgM) levels and a considerable deficiency in Immunoglobulins G (IgG), A (IgA) and E (IgE). As a consequence, people with HIGM have decreased concentrations of serum IgG and IgA and normal or elevated IgM, leading to increased susceptibility to infections.

In humans, hyperthermia is defined as a temperature greater than , depending on the reference used, that occurs without a change in the body's temperature set point.

The normal human body temperature can be as high as in the late afternoon. Hyperthermia requires an elevation from the temperature that would otherwise be expected. Such elevations range from mild to extreme; body temperatures above can be life-threatening.

Babies born to HIV-positive women should receive a 6-week course of zidovudine (AZT). The medication should be started within the first 6 to 12 hours of life. The baby should be tested for HIV at 14 to 21 days of life, at 1 to 2 months of age, and once more at 4 to 6 months of age. Usual antibody based testing is unreliable in infants due to the transmission of maternal antibodies. A qualitative HIV DNA PCR assay is recommended as it will detect pro-viral HIV DNA since HIV RNA may be suppressed by ART. In order to ensure the baby is HIV-negative, there must be two negative test results. Since zidovudine has been known to cause or worsen anemia, the baby's blood count should be routinely checked during AZT therapy.

To reduce the risk of developing "Pneumocystis jirovecii" pneumonia (PCP), all infants born to HIV-positive mothers should receive trimethoprim/sulfamethoxazole at age 4–6 weeks.

Although the risk is very low, HIV can also be transmitted to a baby through food that was previously chewed (pre-chewed) by a mother or caretaker infected with HIV. To be safe, babies should not be fed pre-chewed food.

The signs and symptoms for excited delirium may include:

- Paranoia

- Disorientation

- Dissociation

- Hyper-aggression

- Tachycardia

- Hallucination

- Diaphoresis

- Incoherent speech or shouting

- Seemingly superhuman strength or endurance (typically while trying to resist restraint)

- Hyperthermia (overheating)/profuse sweating (even in cold weather)

- Inappropriately clothed e.g. having removed garments

Chagas disease, also known as American trypanosomiasis, is a tropical parasitic disease caused by the protist "Trypanosoma cruzi". It is spread mostly by insects known as Triatominae, or "kissing bugs". The symptoms change over the course of the infection. In the early stage, symptoms are typically either not present or mild, and may include fever, swollen lymph nodes, headaches, or local swelling at the site of the bite. After 8–12 weeks, individuals enter the chronic phase of disease and in 60–70% it never produces further symptoms. The other 30 to 40% of people develop further symptoms 10 to 30 years after the initial infection, including enlargement of the ventricles of the heart in 20 to 30%, leading to heart failure. An enlarged esophagus or an enlarged colon may also occur in 10% of people.

"T. cruzi" is commonly spread to humans and other mammals by the blood-sucking "kissing bugs" of the subfamily Triatominae. These insects are known by a number of local names, including: "vinchuca" in Argentina, Bolivia, Chile and Paraguay, "barbeiro" (the barber) in Brazil, "pito" in Colombia, "chinche" in Central America, and "chipo" in Venezuela. The disease may also be spread through blood transfusion, organ transplantation, eating food contaminated with the parasites, and by vertical transmission (from a mother to her fetus). Diagnosis of early disease is by finding the parasite in the blood using a microscope. Chronic disease is diagnosed by finding antibodies for "T. cruzi" in the blood.

Prevention mostly involves eliminating kissing bugs and avoiding their bites. Other preventive efforts include screening blood used for transfusions. A vaccine has not been developed as of 2017. Early infections are treatable with the medication benznidazole or nifurtimox. Medication nearly always results in a cure if given early, but becomes less effective the longer a person has had Chagas disease. When used in chronic disease, medication may delay or prevent the development of end–stage symptoms. Benznidazole and nifurtimox cause temporary side effects in up to 40% of people including skin disorders, brain toxicity, and digestive system irritation.

It is estimated that 6.6 million people, mostly in Mexico, Central America and South America, have Chagas disease as of 2015. In 2015, Chagas was estimated to result in 8,000 deaths. Most people with the disease are poor, and most do not realize they are infected. Large-scale population movements have increased the areas where Chagas disease is found and these include many European countries and the United States. These areas have also seen an increase in the years up to 2014. The disease was first described in 1909 by the Brazilian physician Carlos Chagas, after whom it is named. Chagas disease is classified as a neglected tropical disease. It affects more than 150 other animals.

Other medical conditions that can resemble excited delirium are panic attack, hyperthermia, diabetes, head injury, delirium tremens, and hyperthyroidism.

Opioids, because of their effect on the part of the brain that regulates breathing, can during overdoses lead to the person not breathing (respiratory depression) and therefore result in death. Opiate overdose symptoms and signs can be referred to as the "opioid overdose triad": decreased level of consciousness, pinpoint pupils and respiratory depression. Other symptoms include seizures and muscle spasms. Sometimes a person experiencing an opiate overdose can lead to such a decreased level of consciousness that he or she won't even wake up to their name being called or being shaken by another person.

Prolonged hypoxia from respiratory depression can also lead to detrimental damage to the brain and spinal cord and can leave the person unable to walk or function normally, even if treatment with naloxone is given.

Alcohol also causes respiratory depression and therefore when taken with opioids can increase the risk of respiratory depression and death.

Symptoms and signs include abdominal discomfort, polyuria, polydipsia, incidental discovery of hypertension, abdominal mass. The classic presentation for ARPKD is systemic hypertension with progression to end-stage renal disease (ESRD) by the age of 15. In a typical presentation, a small number of ARPKD sufferers live to adulthood with some kidney function; but with significant deterioration in liver function. This outcome is postulated to result from expression of the polycystic kidney and hepatic disease gene PKHD1, which is located on chromosome 6p. In severe cases, a fetus will present with oligohydramnios and as a result, may present with Potter sequence.

Cycloid psychosis is a psychosis that progresses from normal to full-blown, usually between a few hours to days, not related to drug intake or brain injury. The cycloid psychosis has a long history in European psychiatry diagnosis. The term "cycloid psychosis" was first used by Karl Kleist 1926. Despite the significant clinical relevance, this diagnosis is neglected both in literature as in nosology. The cycloid psychosis has attracted much interest in the international literature of the past 50 years, but the number of scientific studies have greatly decreased over the past 15 years, possibly partly explained by the misconception that the diagnosis has been included incorporated in current diagnostic classification systems. The cycloid psychosis is therefore only partially described in the diagnostic classification systems used. "polymorph acute psychotic disorder", with or without schizophrenic symptoms. (F23.0 ICD 10). Cycloid psychosis is nevertheless its own specific disease that is distinct from both the manic-depressive disorder, and from schizophrenia, and this despite the fact that the cycloid psychosis can include both bipolar (basic mood shifts) as well as schizophrenic symptoms. The disease is an acute, usually self-limiting, functionally psychotic state, with a very diverse clinical picture that almost consistently is characterized by the existence of some degree of confusion or distressing perplexity, but above all, of the multifaceted and diverse expressions the disease takes. The main features of the disease is thus that the onset is acute, the multifaceted picture of symptoms and typically reverses to a normal state and that the long-term prognosis is good. In addition, diagnostic criteria include at least four of the following symptoms:

- Confusion

- Mood-incongruent delusions

- Hallucinations

- Pan-anxiety, a severe anxiety not bound to particular situations or circumstances

- Happiness or ecstasy of high degree

- Motility disturbances of akinetic or hyperkinetic type

- Concern with death

- Mood swings to some degree, but less than what is needed for diagnosis of an affective disorder

Cycloid psychosis occurs in people of generally 15–50 years of age.

An opioid overdose is toxicity due to excessive opioids. Examples of opioids include morphine, heroin, fentanyl, tramadol, and methadone. Symptoms include insufficient breathing, small pupils, and unconsciousness. Onset of symptoms depends in part on the route opioids are taken. Among those who initially survive, complications can include rhabdomyolysis, pulmonary edema, compartment syndrome, and permanent brain damage.

Risk factors for opioid overdose include opioid dependence, injecting opioids, using high doses of opioids, mental disorders, and use together with alcohol or benzodiazepines. The risk is particularly high following detoxification. Dependence on prescription opioids can occur from their use to treat chronic pain. Diagnosis is generally based on symptoms.

Initial treatment involves supporting the person's breathing and providing oxygen. Naloxone is then recommended among those who are not breathing. Given naloxone into the nose or as an injection into a muscle appears to be equally effective. Among those who refuse to go to hospital following reversal, the risks of a poor outcome in the short term appear to be low. Efforts to prevent deaths from overdose include improving access to naloxone and treatment for opioid dependence.

Opioid use disorders resulted in 122,000 deaths globally in 2015, up from 18,000 deaths in 1990. In the United States over 33,000 deaths occurred from opioids in 2015, 20,100 from prescription opioids and 13,000 from heroin. Opioid deaths represent more than 60% of all drug overdose related deaths in the United States. The opioid epidemic is believed to be in part due to assurances in the 1990s by the pharmaceutical industry that prescription opioids were safe.

People with psychosis normally have one or more of the following:

- hallucinations

- delusions

- catatonia

- thought disorder.

Impairments in social cognition also occur.