Lung disease results from clogging of the airways due to mucus build-up, decreased mucociliary clearance, and resulting inflammation. Inflammation and infection cause injury and structural changes to the lungs, leading to a variety of symptoms. In the early stages, incessant coughing, copious phlegm production, and decreased ability to exercise are common. Many of these symptoms occur when bacteria that normally inhabit the thick mucus grow out of control and cause pneumonia.

In later stages, changes in the architecture of the lung, such as pathology in the major airways (bronchiectasis), further exacerbate difficulties in breathing. Other signs include coughing up blood (hemoptysis), high blood pressure in the lung (pulmonary hypertension), heart failure, difficulties getting enough oxygen to the body (hypoxia), and respiratory failure requiring support with breathing masks, such as bilevel positive airway pressure machines or ventilators. "Staphylococcus aureus", "Haemophilus influenzae", and "Pseudomonas aeruginosa" are the three most common organisms causing lung infections in CF patients. In addition to typical bacterial infections, people with CF more commonly develop other types of lung disease. Among these is allergic bronchopulmonary aspergillosis, in which the body's response to the common fungus "Aspergillus fumigatus" causes worsening of breathing problems. Another is infection with "Mycobacterium avium" complex, a group of bacteria related to tuberculosis, which can cause lung damage and does not respond to common antibiotics.

Mucus in the paranasal sinuses is equally thick and may also cause blockage of the sinus passages, leading to infection. This may cause facial pain, fever, nasal drainage, and headaches. Individuals with CF may develop overgrowth of the nasal tissue (nasal polyps) due to inflammation from chronic sinus infections. Recurrent sinonasal polyps can occur in 10% to 25% of CF patients. These polyps can block the nasal passages and increase breathing difficulties.

Cardiorespiratory complications are the most common cause of death (about 80%) in patients at most CF centers in the United States.

Prior to prenatal and newborn screening, cystic fibrosis was often diagnosed when a newborn infant failed to pass feces (meconium). Meconium may completely block the intestines and cause serious illness. This condition, called meconium ileus, occurs in 5–10% of newborns with CF. In addition, protrusion of internal rectal membranes (rectal prolapse) is more common, occurring in as many as 10% of children with CF, and it is caused by increased fecal volume, malnutrition, and increased intra–abdominal pressure due to coughing.

The thick mucus seen in the lungs has a counterpart in thickened secretions from the pancreas, an organ responsible for providing digestive juices that help break down food. These secretions block the exocrine movement of the digestive enzymes into the duodenum and result in irreversible damage to the pancreas, often with painful inflammation (pancreatitis). The pancreatic ducts are totally plugged in more advanced cases, usually seen in older children or adolescents. This causes atrophy of the exocrine glands and progressive fibrosis.

The lack of digestive enzymes leads to difficulty absorbing nutrients with their subsequent excretion in the feces, a disorder known as malabsorption. Malabsorption leads to malnutrition and poor growth and development because of calorie loss. Resultant hypoproteinemia may be severe enough to cause generalized edema. Individuals with CF also have difficulties absorbing the fat-soluble vitamins A, D, E, and K.

In addition to the pancreas problems, people with cystic fibrosis experience more heartburn, intestinal blockage by intussusception, and constipation. Older individuals with CF may develop distal intestinal obstruction syndrome when thickened feces cause intestinal blockage.

Exocrine pancreatic insufficiency occurs in the majority (85% to 90%) of patients with CF. It is mainly associated with "severe" CFTR mutations, where both alleles are completely nonfunctional (e.g. ΔF508/ΔF508). It occurs in 10% to 15% of patients with one "severe" and one "mild" CFTR mutation where little CFTR activity still occurs, or where two "mild" CFTR mutations exist. In these milder cases, sufficient pancreatic exocrine function is still present so that enzyme supplementation is not required. Usually, no other GI complications occur in pancreas-sufficient phenotypes, and in general, such individuals usually have excellent growth and development. Despite this, idiopathic chronic pancreatitis can occur in a subset of pancreas-sufficient individuals with CF, and is associated with recurrent abdominal pain and life-threatening complications.

Thickened secretions also may cause liver problems in patients with CF. Bile secreted by the liver to aid in digestion may block the bile ducts, leading to liver damage. Over time, this can lead to scarring and nodularity (cirrhosis). The liver fails to rid the blood of toxins and does not make important proteins, such as those responsible for blood clotting. Liver disease is the third-most common cause of death associated with CF.

Symptoms of DPB include chronic sinusitis (inflamed paranasal sinuses), wheezing, crackles (respiratory sounds made by obstructions such as phlegm and secretions in the lungs), dyspnea (shortness of breath), and a severe cough that yields large amounts of sputum (coughed-up phlegm). There may be pus in the sputum, and affected individuals may have fever. Typical signs of DPB progression include (enlargement) of the bronchiolar passages and hypoxemia (low levels of oxygen in the blood). If DPB is left untreated, bronchiectasis will occur; it is characterized by dilation and thickening of the walls of the bronchioles, inflammatory damage to respiratory and terminal bronchioles, and pooling of mucus in the lungs. DPB is associated with progressive respiratory failure, hypercapnia (increased levels of carbon dioxide in the blood), and can eventually lead to pulmonary hypertension (high blood pressure in the pulmonary vein and artery) and cor pulmonale (dilation of the right ventricle of the heart, or "right heart failure").

The term "bronchiolitis" generally refers to inflammation of the bronchioles. DPB is classified as a form of "primary bronchiolitis", which means that the underlying cause of bronchiolitis is originating from or is confined to the bronchioles. Along with DPB, additional forms of primary bronchiolitis include bronchiolitis obliterans, follicular bronchiolitis, respiratory bronchiolitis, mineral dust airway disease, and a number of others. Unlike DPB, bronchiolitis that is not considered "primary" would be associated with diseases of the larger airways, such as chronic bronchitis.

Some people with bronchiectasis may have a cough productive of frequent green/yellow mucus (sputum), up to 240 ml (8 oz) daily. Bronchiectasis may also present with coughing up blood (hemoptysis) in the absence of sputum, called "dry bronchiectasis". Sputum production may also occur without coloration. People with bronchiectasis may have bad breath indicative of active infection. Frequent bronchial infections and breathlessness are two possible indicators of bronchiectasis.

Crepitations and expiratory rhonchi may be heard on auscultation. Nail clubbing is rare.

Bronchiectasis has both congenital and acquired causes, with the latter more frequent. Cystic fibrosis is a cause in up to half of cases. The cause in 10-50% of those without cystic fibrosis is unknown; bronchiectasis without CF is known as non-CF bronchiectasis (NCBE).

Almost all patients have clinically diagnosed asthma, and present with wheezing (usually episodic in nature), coughing, shortness of breath and exercise intolerance (especially in patients with cystic fibrosis). Moderate and severe cases have symptoms suggestive of bronchiectasis, in particular thick sputum production (often containing brown mucus plugs), as well as symptoms mirroring recurrent infection such as pleuritic chest pain and fever. Patients with asthma and symptoms of ongoing infection, who do not respond to antibiotic treatment, should be suspected of ABPA.

Allergic bronchopulmonary aspergillosis (ABPA) is a condition characterised by an exaggerated response of the immune system (a hypersensitivity response) to the fungus "Aspergillus" (most commonly "Aspergillus fumigatus"). It occurs most often in patients with asthma or cystic fibrosis. "Aspergillus" spores are ubiquitous in soil and are commonly found in the sputum of healthy individuals. "A. fumigatus" is responsible for a spectrum of lung diseases known as aspergilloses.

ABPA causes airway inflammation, leading to bronchiectasis—a condition marked by abnormal dilation of the airways. Left untreated, the immune system and fungal spores can damage sensitive lung tissues and lead to scarring.

The exact criteria for the diagnosis of ABPA are not agreed upon. Chest X-rays and CT scans, raised blood levels of IgE and eosinophils, immunological tests for "Aspergillus" together with sputum staining and sputum cultures can be useful. Treatment consists of corticosteroids and antifungal medications.

Congenital absence of the vas deferens (CAVD) is a condition in which the vasa deferentia reproductive organs, fail to form properly prior to birth. It may either be unilateral (CUAVD) or bilateral (CBAVD).

Scrotal ultrasonography and transrectal ultrasonography (TRUS) are useful in detecting uni- or bilateral CBAVD, which may be associated with visible abnormalities or agenesis of the epididymis, seminal vesicles or kidneys.

This syndrome shows a wide range of abnormalities and symptoms. The main characteristics of the syndrome are exocrine pancreatic dysfunction, hematologic abnormalities and growth retardation. Only the first two of these are included in the clinical diagnostic criteria.

- Hematologic abnormalities: Neutropenia may be intermittent or persistent and is the most common hematological finding. Low neutrophil counts leave patients at risk of developing severe recurrent infections that may be life-threatening. Anemia (low red blood cell counts) and thrombocytopenia (low platelet counts) may also occur. Bone marrow is typically hypocellular, with maturation arrest in the myeloid lineages that give rise to neutrophils, macrophages, platelets and red blood cells. Patients may also develop progressive marrow failure or transform to acute myelogenous leukemia.

- Exocrine pancreatic dysfunction: Pancreatic exocrine insufficiency arises due to a lack of acinar cells that produce digestive enzymes. These are extensively depleted and replaced by fat. A lack of pancreatic digestive enzymes leaves patients unable to digest and absorb fat. However, pancreatic status may improve with age in some patients.

- Growth retardation: More than 50% of patients are below the third percentile for height, and short stature appears to be unrelated to nutritional status. Other skeletal abnormalities include metaphyseal dysostosis (45% of patients), thoracic dystrophy (rib cage abnormalities in 46% of patients), and costochondral thickening (shortened ribs with flared ends in 32% of patients). Skeletal problems are one of the most variable components of SDS, with 50% affected siblings from the same family discordant for clinical presentation or type of abnormality. Despite this, a careful review of radiographs from 15 patients indicated that all of them had at least one skeletal anomaly, though many were subclinical.

- Other features include metaphysial dysostosis, mild hepatic dysfunction, increased frequency of infections.

Shwachman–Diamond syndrome (SDS) or Shwachman–Bodian–Diamond syndrome is a rare congenital disorder characterized by exocrine pancreatic insufficiency, bone marrow dysfunction, skeletal abnormalities, and short stature. After cystic fibrosis (CF), it is the second most common cause of exocrine pancreatic insufficiency in children.

Symptoms of polyps include nasal congestion, sinusitis, loss of smell, thick nasal discharge, facial pressure, nasal speech, and mouth breathing. Recurrent sinusitis can result from polyps. Long-term, nasal polyps can cause destruction of the nasal bones and widening of the nose.

As polyps grow larger, they eventually prolapse into the nasal cavity resulting in symptoms. The most prominent symptoms of nasal polyps result blockage of the nasal passage.

People with nasal polyps due to aspirin intolerance often have symptoms known as Samter's triad, which consists of asthma worse with aspirin, a skin rash caused by aspirin, and chronic nasal polyps.

Nasal polyps (NP) are noncancerous growths within the nose or sinuses. Symptoms include trouble breathing through the nose, loss of smell, decreased taste, post nasal drip, and a runny nose. The growths are sac-like, movable, and nontender, though face pain may occasionally occur. They typically occur in both nostrils in those who are affected. Complications may include sinusitis and broadening of the nose.

The exact cause is unclear. They may be related to chronic inflammation of the lining of the sinuses. They occur more commonly among people who have allergies, cystic fibrosis, aspirin sensitivity, or certain infections. The polyp itself represents an overgrowth of the mucous membranes. Diagnosis may occur by looking up the nose. A CT scan may be used to determine the number of polyps and help plan surgery.

Treatment is typically with steroids, often in the form of a nasal spray. If this is not effective surgery may be considered. The condition often recurs following surgery, thus continued use of a steroid nasal sprays is often recommended. Antihistamines may help with symptoms but do not change the underlying disease. Antibiotics are not required for treatment unless an infection occurs.

About 4% of people currently have nasal polyps while up to 40% of people develop them at some point in their life. They most often occur after the age of 20 and are more frequent in males than females. Nasal polyps have been described since at least the time of the Ancient Egyptians.

Monocytosis often occurs during chronic inflammation. Diseases that produce such a chronic inflammatory state:

- Infections: tuberculosis, brucellosis, listeriosis, subacute bacterial endocarditis, syphilis, and other viral infections and many protozoal and rickettsial infections (e.g. kala azar, malaria, Rocky Mountain spotted fever).

- Blood and immune causes: chronic neutropenia and myeloproliferative disorders.

- Autoimmune diseases and vasculitis: systemic lupus erythematosus, rheumatoid arthritis and inflammatory bowel disease.

- Malignancies: Hodgkin's disease and certain leukaemias, such as chronic myelomonocytic leukaemia (CMML) and monocytic leukemia.

- Recovery phase of neutropenia or an acute infection.

- Obesity (cf. Nagareddy et al. (2014), Cell Metabolism, Vol. 19, pp 821-835)

- Miscellaneous causes: sarcoidosis and lipid storage disease.

Pseudomonas infection refers to a disease caused by one of the species of the genus "Pseudomonas".

"Pseudomonas sp. KUMS3" could be considered

as an opportunistic pathogen, which can survive on the

fish surface or in water or in the gut and may cause disease

when unfavorable conditions develop.

"P. aeruginosa" is an opportunistic human pathogen, most commonly affecting immunocompromised patients, such as those with cystic fibrosis or AIDS. Infection can affect many different parts of the body, but infections typically target the respiratory tract (e.g. patients with CF or those on mechanical ventilation), causing bacterial pneumonia. In a surveillance study between 1986 and 1989, P. aeruginosa was the third leading cause of all nosocomial infections, and specifically the number one leading cause of hospital-acquired pneumonia and third leading cause of hospital-acquired UTI. Treatment of such infections can be difficult due to multiple antibiotic resistance, and in the United States, there was an increase in MDRPA (Multidrug-resistant "Pseudomonas aeruginosa") resistant to ceftazidime, ciprofloxacin, and aminoglycosides, from 0.9% in 1994 to 5.6% in 2002.

"P. oryzihabitans" can also be a human pathogen, although infections are rare. It can cause peritonitis, endophthalmitis, septicemia and bacteremia. Similar symptoms although also very rare can be seen by infections of "P. luteola".

"P. plecoglossicida" is a fish pathogenic species, causing hemorrhagic ascites in the ayu ("Plecoglossus altivelis"). "P. anguilliseptica" is also a fish pathogen.

Due to their hemolytic activity, even non-pathogenic species of "Pseudomonas" can occasionally become a problem in clinical settings, where they have been known to infect blood transfusions.

Monocytosis is an increase in the number of monocytes circulating in the blood. Monocytes are white blood cells that give rise to macrophages and dendritic cells in the immune system.

In humans, 950/μL is regarded as at the upper limit of normal; monocyte counts above this level are regarded as monocytosis.

Monocytosis has sometimes been called mononucleosis, but that name is usually reserved specifically for infectious mononucleosis.

Polycythemia (also known as polycythaemia or polyglobulia) is a disease state in which the hematocrit (the volume percentage of red blood cells in the blood) is elevated.

It can be due to an increase in the number of red blood cells ("absolute polycythemia") or to a decrease in the volume of plasma ("relative polycythemia"). Polycythemia is sometimes called erythrocytosis, but the terms are not synonymous, because polycythemia refers to any increase in red blood cells, whereas erythrocytosis only refers to a documented increase of red cell mass.

The emergency treatment of polycythemia (e.g., in hyperviscosity or thrombosis) is by phlebotomy (removal of blood from the circulation). Depending on the underlying cause, phlebotomy may also be used on a regular basis to reduce the hematocrit. Cytostatics such as busulfan and hydroxyurea are sometimes used for long-term management of polycythemia.

Only 10 to 15 percent of the cases diagnosed as SSHL have an identifiable cause. Most cases are classified as idiopathic, also called sudden idiopathic hearing loss (SIHL) and idiopathic sudden sensorineural hearing loss (ISSHL or ISSNHL) The majority of evidence points to some type of inflammation in the inner ear as the most common cause of SSNHL.

- Viral - The swelling may be due to a virus. A herpes type virus is believed to be the most common cause of sudden sensorineural hearing loss. The herpes virus lays dormant in our bodies and reactivates for an unknown reason.

- Vascular ischemia of the inner ear or cranial nerve VIII (CN8)

- Perilymph fistula, usually due to a rupture of the round or oval windows and the leakage of perilymph. The patient will usually also experience vertigo or imbalance. A history of trauma is usually present and changes to hearing or vertigo occur with alteration in intracranial pressure such as with straining; lifting, blowing etc.

- Autoimmune - can be due to an autoimmune illness such as systemic lupus erythematosus, granulomatosis with polyangiitis

Sensorineural hearing loss (SNHL) is a type of hearing loss, or deafness, in which the root cause lies in the inner ear or sensory organ (cochlea and associated structures) or the vestibulocochlear nerve (cranial nerve VIII) or neural part. SNHL accounts for about 90% of hearing loss reported. SNHL is generally permanent and can be mild, moderate, severe, profound, or total. Various other descriptors can be used such as high frequency, low frequency, U-shaped, notched, peaked or flat depending on the shape of the audiogram, the measure of hearing.

"Sensory" hearing loss often occurs as a consequence of damaged or deficient cochlear hair cells. Hair cells may be abnormal at birth, or damaged during the lifetime of an individual. There are both external causes of damage, including noise trauma, infection and ototoxic drugs, as well as intrinsic causes, including genetic mutations. A common cause or exacerbating factor in sensory hearing loss is prolonged exposure to environmental noise, for example, being in a loud workplace without wearing protection, or having headphones set to high volumes for a long period. Exposure to a very loud noise such as a bomb blast can cause noise-induced hearing loss.

"Neural", or 'retrocochlear', hearing loss occurs because of damage to the cochlear nerve (CVIII). This damage may affect the initiation of the nerve impulse in the cochlear nerve or the transmission of the nerve impulse along the nerve into the brainstem.

Most cases of SNHL present with a gradual deterioration of hearing thresholds occurring over years to decades. In some the loss may eventually affect large portions of the frequency range. It may be accompanied by other symptoms such as ringing in the ears (tinnitus), dizziness or lightheadedness (vertigo). SNHL can be genetically inherited or acquired as a result from external causes like noise or disease. It may be congenital (present at birth) or develop later in life. The most common kind of sensorineural hearing loss is age-related (presbycusis), followed by noise-induced hearing loss (NIHL).

Frequent symptoms of SNHL are loss of acuity in distinguishing foreground voices against noisy backgrounds, difficulty understanding on the telephone, some kinds of sounds seeming excessively loud or shrill (recruitment), difficulty understanding some parts of speech (fricatives and sibilants), loss of directionality of sound, esp. high frequency sounds, perception that people mumble when speaking, and difficulty understanding speech. Similar symptoms are also associated with other kinds of hearing loss; audiometry or other diagnostic tests are necessary to distinguish sensorineural hearing loss.

Identification of sensorineural hearing loss is usually made by performing a pure tone audiometry (an audiogram) in which bone conduction thresholds are measured. Tympanometry and speech audiometry may be helpful. Testing is performed by an audiologist.

There is no proven or recommended treatment or cure for SNHL; management of hearing loss is usually by hearing strategies and hearing aid. In cases of profound or total deafness, a cochlear implant is a specialised hearing aid which may restore a functional level of hearing. SNHL is at least partially preventable by avoiding environmental noise, ototoxic chemicals and drugs, and head trauma, and treating or inoculating against certain triggering diseases and conditions like meningitis.

Primary polycythemias are due to factors intrinsic to red cell precursors. Polycythemia vera (PCV), polycythemia rubra vera (PRV), or erythremia, occurs when excess red blood cells are produced as a result of an abnormality of the bone marrow. Often, excess white blood cells and platelets are also produced. PCV is classified as a myeloproliferative disease. Symptoms include headaches and vertigo, and signs on physical examination include an abnormally enlarged spleen and/or liver. In some cases, affected individuals may have associated conditions including high blood pressure or formation of blood clots. Transformation to acute leukemia is rare. Phlebotomy is the mainstay of treatment. A hallmark of polycythemia is an elevated hematocrit, with Hct > 55% seen in 83% of cases. A somatic (non-hereditary) mutation (V617F) in the "JAK2" gene is found in 95% of cases, though also present in other myeloproliferative disorders.

Primary familial polycythemia, also known as primary familial and congenital polycythemia (PFCP), exists as a benign hereditary condition, in contrast with the myeloproliferative changes associated with acquired PCV. In many families, PFCP is due to an autosomal dominant mutation in the "EPOR" erythropoietin receptor gene. PFCP can cause an increase of up to 50% in the oxygen-carrying capacity of the blood; skier Eero Mäntyranta had PFCP, which is considered to have given him a large advantage in endurance events.

A stye, also known as a hordeolum, is a bacterial infection of an oil gland in the eyelid. This results in a red tender bump at the edge of the eyelid. The outside or the inside of the eyelid can be affected.

The cause of a stye is usually a bacterial infection by "Staphylococcus aureus". The internal ones are due to infection of the meibomian gland while the external ones are due to an infection of the gland of Zeis. A chalazion on the other hand is a blocked oil gland without infection. They are typically in the middle of the eyelid and non painful.

Often a stye will go away without any specific treatment in a few days or weeks. Recommendations to speed improvement include warm compresses. Occasionally antibiotic eye ointment may be recommended. While these measures are often recommended, evidence to support them is poor. The frequency at which they occur is unclear. They may happen at any age.

The first sign of a stye is a small, yellowish spot at the center of the bump that develops as pus and expands in the area.

Other stye symptoms may include:

- A lump on the top or bottom eyelid

- Localized swelling of the eyelid

- Localized pain

- Redness

- Tenderness

- Crusting of the eyelid margins

- Burning in the eye

- Droopiness of the eyelid

- Scratchy sensation on the eyeball (itching)

- Blurred vision

- Mucous discharge in the eye

- Irritation of the eye

- Light sensitivity

- Tearing

- Discomfort during blinking

- Sensation of a foreign body in the eye

Vertigo is a medically recognized term for the symptom of vestibular system disturbance. It may include a feeling of rotation or illusory sensations of motion or both. The general term dizziness is used by nonmedical people for those symptoms but often refers to a feeling of light-headedness, giddiness, drowsiness, or faintness, all of which must be differentiated from true vertigo, since the latter symptoms might have other causes.

Motion sickness occurs more frequently in migraine patients (30–50% more than in controls). Benign paroxysmal vertigo of childhood is an example of migraine-associated vertigo in which headache does not often occur. Basilar artery migraine (BAM) consists of two or more symptoms (vertigo, tinnitus, decreased hearing, ataxia, dysarthria, visual symptoms in both hemifields or both eyes, diplopia, bilateral paresthesias, paresis, decreased consciousness and/or loss of consciousness) followed by throbbing headache. Auditory symptoms are rare. However, a study showed a fluctuating low-tone sensorineural hearing loss in more than 50% of patients with BAM with a noticeable change in hearing just before the onset of a migraine headache. The attacks of vertigo are usually concurrent with the headache and the family history is usually positive. The diagnostician must rule out: TIAs, and paroxysmal vestibular disorder accompanied by headache.

There is also a familial vestibulopathy, familial benign recurrent vertigo (fBRV), where episodes of vertigo occur with or without migraine headache. Testing may show profound vestibular loss. The syndrome responds to acetazolamide. Familial hemiplegic migraine (FHM) has been linked to mutations in the calcium channel gene. (Ophoff et al. 1966 cf. Lempert et al.)

In epizoology, an epizootic (from Greek: "epi-" upon + "zoon" animal) is a disease event in a nonhuman animal population, analogous to an epidemic in humans. An epizootic may be: restricted to a specific locale (an "outbreak"), general (an "epizootic") or widespread ("panzootic"). High population density is a major contributing factor to epizootics. Aquaculture is an industry sometimes plagued by disease because of the large number of fish confined to a small area.

Defining an epizootic can be subjective; it is based upon the number of new cases in a given animal population, during a given period, and must be judged to be a rate that substantially exceeds what is expected based on recent experience ("i.e." a sharp elevation in the incidence rate). Because it is based on what is "expected" or thought normal, a few cases of a very rare disease (like a TSE outbreak in a cervid population) might be classified as an "epizootic", while many cases of a common disease (like lymphocystis in esocids) would not.

Common diseases that occur at a constant but relatively high rate in the population are said to be "enzootic" ("cf." the epidemiological meaning of "endemic" for human diseases). An example of an enzootic disease would be the influenza virus in some bird populations or, at a lower incidence, the Type IVb strain of VHS in certain Atlantic fish populations.

An example of an epizootic would be the 1990 outbreak of Newcastle disease virus in double-crested cormorant colonies on the Great Lakes that resulted in the death of some 10,000 birds.