Otitis is a general term for inflammation or infection of the ear, in both humans and other animals.

It is subdivided into the following:

- "Otitis externa", external otitis, or "swimmer's ear" involves the outer ear and ear canal. In external otitis, the ear hurts when touched or pulled.

- "Otitis media" or middle ear infection involves the middle ear. In otitis media, the ear is infected or clogged with fluid behind the ear drum, in the normally air-filled middle-ear space. This very common childhood infection sometimes requires a surgical procedure called "myringotomy" and tube insertion.

- "Otitis interna" or labyrinthitis involves the inner ear. The inner ear includes sensory organs for balance and hearing. When the inner ear is inflamed, "vertigo" is a common symptom.

An integral symptom of acute otitis media is ear pain; other possible symptoms include fever, and irritability (in infants). Since an episode of otitis media is usually precipitated by an upper respiratory tract infection (URTI), there are often accompanying symptoms like a cough and nasal discharge.

Discharge from the ear can be caused by acute otitis media with perforation of the ear drum, chronic suppurative otitis media, tympanostomy tube otorrhea, or acute otitis externa. Trauma, such as a basilar skull fracture, can also lead to discharge from the ear due to cerebral spinal drainage from the brain and its covering (meninges).

Some common symptoms and signs of mastoiditis include pain, tenderness, and swelling in the mastoid region. There may be ear pain (otalgia), and the ear or mastoid region may be red (erythematous). Fever or headaches may also be present. Infants usually show nonspecific symptoms, including anorexia, diarrhea, or irritability. Drainage from the ear occurs in more serious cases, often manifest as brown discharge on the pillowcase upon waking.

The most common bacteria isolated from the middle ear in AOM are "Streptococcus pneumoniae, Haemophilus influenzae", "Moraxella catarrhalis," and "Staphylococcus aureus".

The main symptom of labyrinthitis is severe vertigo. Rapid and undesired eye motion (nystagmus) often results from the improper indication of rotational motion. Nausea, anxiety, and a general ill feeling are common due to the distorted balance signals that the brain receives from the inner ear.

In most cases, the condition tends to be self-limiting. In 95% or greater, vestibular neuritis is a one-time experience with most people fully recovering.

Recovery from acute labyrinthine inflammation generally takes from one to six weeks, but it is not uncommon for residual symptoms (dysequilibrium and/or dizziness) to last for a couple of months.

Recovery from a temporary damaged inner ear typically follows two phases:

1. An acute period, which may include severe vertigo and vomiting

2. approximately two weeks of sub-acute symptoms and rapid recovery

Mastoiditis is the result of an infection that extends to the air cells of the skull behind the ear. Specifically, it is an inflammation of the mucosal lining of the mastoid antrum and mastoid air cell system inside the mastoid process. The mastoid process is the portion of the temporal bone of the skull that is behind the ear which contains open, air-containing spaces. Mastoiditis is usually caused by untreated acute otitis media (middle ear infection) and used to be a leading cause of child mortality. With the development of antibiotics, however, mastoiditis has become quite rare in developed countries where surgical treatment is now much less frequent and more conservative, unlike former times. Additionally, there is no evidence that the drop in antibiotic prescribing for otitis media has increased the incidence of mastoiditis, raising the possibility that the drop in reported cases is due to a confounding factor such as childhood immunizations against Haemophilus and Streptococci. Untreated, the infection can spread to surrounding structures, including the brain, causing serious complications.

Vertigo that is caused by problems with the inner ear or vestibular system, which is composed of the semicircular canals, the vestibule (utricle and saccule), and the vestibular nerve is called "peripheral", "otologic" or "vestibular" vertigo. The most common cause is benign paroxysmal positional vertigo (BPPV), which accounts for 32% of all peripheral vertigo. Other causes include Ménière's disease (12%), superior canal dehiscence syndrome, labyrinthitis, and visual vertigo. Any cause of inflammation such as common cold, influenza, and bacterial infections may cause transient vertigo if it involves the inner ear, as may chemical insults (e.g., aminoglycosides) or physical trauma (e.g., skull fractures). Motion sickness is sometimes classified as a cause of peripheral vertigo.

People with peripheral vertigo typically present with mild to moderate imbalance, nausea, vomiting, hearing loss, tinnitus, fullness, and pain in the ear. In addition, lesions of the internal auditory canal may be associated with facial weakness on the same side. Due to a rapid compensation process, acute vertigo as a result of a peripheral lesion tends to improve in a short period of time (days to weeks).

Vertigo that arises from injury to the balance centers of the central nervous system (CNS), often from a lesion in the brainstem or cerebellum, is called "central" vertigo and is generally associated with less prominent movement illusion and nausea than vertigo of peripheral origin. Central vertigo may have accompanying neurologic deficits (such as slurred speech and double vision), and pathologic nystagmus (which is pure vertical/torsional). Central pathology can cause disequilibrium which is the sensation of being off balance. The balance disorder associated with central lesions causing vertigo is often so severe that many patients are unable to stand or walk.

A number of conditions that involve the central nervous system may lead to vertigo including: lesions caused by infarctions or hemorrhage, tumors present in the cerebellopontine angle such as a vestibular schwannoma or cerebellar tumors, epilepsy, cervical spine disorders such as cervical spondylosis, degenerative ataxia disorders, migraine headaches, lateral medullary syndrome, Chiari malformation, multiple sclerosis, parkinsonism, as well as cerebral dysfunction. Central vertigo may not improve or may do so more slowly than vertigo caused by disturbance to peripheral structures.

Persistent tinnitus may cause anxiety and depression. Tinnitus annoyance is more strongly associated with psychological condition than loudness or frequency range. Psychological problems such as depression, anxiety, sleep disturbances and concentration difficulties are common in those with strongly annoying tinnitus. 45% of people with tinnitus have an anxiety disorder at some time in their life.

Psychological research has looked at the tinnitus distress reaction (TDR) to account for differences in tinnitus severity. These findings suggest that at the initial perception of tinnitus, conditioning links tinnitus with negative emotions, such as fear and anxiety from unpleasant stimuli at the time. This enhances activity in the limbic system and autonomic nervous system, thus increasing tinnitus awareness and annoyance.

There are two types of tinnitus: "subjective tinnitus" and "objective tinnitus". Tinnitus is usually subjective, meaning that others cannot hear it. Subjective tinnitus has also been called "tinnitus aurium", "non-auditory" or "non-vibratory" tinnitus. In very rare cases tinnitus can be heard by someone else using a stethoscope, and in less rare – but still uncommon – cases it can be measured as a spontaneous otoacoustic emission (SOAE) in the ear canal. In such cases it is objective tinnitus, also called "pseudo-tinnitus" or "vibratory" tinnitus.

Many patients will report a history of vertigo as a result of fast head movements. Many patients are also capable of describing the exact head movements that provoke their vertigo. Purely horizontal nystagmus and symptoms of vertigo lasting more than one minute can also indicate BPPV occurring in the horizontal semicircular canal.

Patients do not experience other neurological deficits such as numbness or weakness, and if these symptoms are present, a more serious etiology, such as posterior circulation stroke or ischemia, must be considered.

The spinning sensation experienced from BPPV is usually triggered by movement of the head, will have a sudden onset, and can last anywhere from a few seconds to several minutes. The most common movements patients report triggering a spinning sensation are tilting their heads upwards in order to look at something, and rolling over in bed.

In most cases AIT is characterized by onset of pain, firmness, tenderness, redness or swelling in the anterior aspect of the neck. Patients will also present with a sudden fever, dysphagia and dysphonia. Symptoms may be present from 1 to 180 days, with most symptoms lasting an average of about 18 days. The main issue associated with the diagnosis of AIT is differentiating it from other more commonly seen forms of thyroid conditions. Pain, fever and swelling are often much more severe and continue to get worse in patients who have AIT compared to those with other thyroid conditions. Patients who are suspected of having AIT often undergo tests to detect for elevated levels of white blood cells as well as an ultrasound to reveal unilobular swelling. Depending on the age and immune status of the patient more invasive procedures may be performed such as fine needle aspiration of the neck mass to facilitate a diagnosis.

In cases where the infection is thought to be associated with a sinus fistula it is often necessary to confirm the presence of the fistula through surgery or laryngoscopic examination. While invasive procedures can often tell definitively whether or not a fistula is present, new studies are working on the use of computed tomography as a useful method to visualize and detect the presence of a sinus fistula.

Conductive hearing loss makes all sounds seem faint or muffled. The hearing loss is worse in low frequencies.

Congenital conductive hearing loss is usually identified through newborn hearing screening or may be identified because the baby has microtia or other facial abnormalities. Conductive hearing loss developing during childhood is usually due to otitis media with effusion and may present with speech and language delay or difficulty hearing. Later onset of conductive hearing loss may have an obvious cause such as an ear infection, trauma or upper respiratory tract infection or may have an insidious onset related to chronic middle ear disease, otosclerosis or a tumour of the naso-pharynx. Earwax is a very common cause of a conductive hearing loss which may present suddenly when water gets behind the wax and this blocks the ear canal.

Fluid accumulation is the most common cause of conductive hearing loss in the middle ear, especially in children. Major causes are ear infections or conditions that block the eustachian tube, such as allergies or tumors. Blocking of the eustachian tube leads to decreased pressure in the middle ear relative to the external ear, and this causes decreased motion of both the ossicles and the tympanic membrane.

- acute or serous otitis media

- otitis media with effusion or 'glue ear'

- Perforated eardrum

- Chronic suppurative otitis media (CSOM)

- Cholesteatoma

- Otosclerosis, abnormal growth of bone in or near the middle ear

- middle ear tumour

- ossicular discontinuity as a consequence of infection or temporal bone trauma

- Congenital malformation of the ossicles. This can be an isolated phenomenon or can occur as part of a syndrome where development of the 1st and 2nd branchial arches is seen such as in Goldenhar syndrome, Treacher Collins syndrome, branchio-oto-renal syndrome etc.

- Barotrauma unequal air pressures in the external and middle ear. This can temporarily occur, for example, by the environmental pressure changes as when shifting altitude, or inside a train going into a tunnel. It is managed by any of various methods of ear clearing manoeuvres to equalize the pressures, like swallowing, yawning, or the Valsalva manoeuvre. More severe barotrauma can lead to middle ear fluid or even permanent sensorineural hearing loss.

Men with acute prostatitis often have chills, fever, pain in the lower back, perineum, or genital area, urinary frequency and urgency often at night, burning or painful urination, body aches, and a demonstrable infection of the urinary tract, as evidenced by white blood cells and bacteria in the urine. Acute prostatitis may be a complication of prostate biopsy. Often, the prostate gland is very tender to palpation through the rectum.

Paraproctitis is a purulent inflammation of the cellular tissues surrounding the rectum. The most frequent cause is penetration of bacterial flora from the rectum into the surrounding cellular tissues, which may occur through an anal fissure. The inflammation is sometimes limited to the formation of an abscess, and in some cases it spreads for a considerable distance and may be complicated by sepsis.

The symptoms are acute pain in the rectal region, tenderness during defecation, elevated body temperature, and the appearance of an infiltrate in the anal region or on the buttocks. An unlanced abscess may burst and a fistula form. The disease becomes chronic after recurrences. Treatment includes administration of antibiotics and anti-inflammatory agents and, in the suppurative stage, surgical lancing of the abscess.

Vertigo, a distinct process sometimes confused with the broader term, dizziness, accounts for about six million clinic visits in the United States every year; between 17 and 42% of these patients are eventually diagnosed with BPPV.

Other causes of vertigo include:

- Motion sickness/motion intolerance: a disjunction between visual stimulation, vestibular stimulation, and/or proprioception

- Visual exposure to nearby moving objects (examples of optokinetic stimuli include passing cars and falling snow)

- Other diseases: (labyrinthitis, Ménière's disease, and migraine, etc.)

Acute infectious thyroiditis (AIT) also known as suppurative thyroiditis, microbial inflammatory thyroiditis, pyrogenic thyroiditis and bacterial thyroiditis.

The thyroid is normally very resistant to infection. Due to a relatively high amount of iodine in the tissue, as well as high vascularity and lymphatic drainage to the region, it is difficult for pathogens to infect the thyroid tissue. Despite all this, a persistent fistula from the piriform sinus may make the left lobe of the thyroid susceptible to infection and abscess formation. AIT is most often caused by a bacterial infection but can also be caused by a fungal or parasitic infection, most commonly in an immunocompromised host.

The secondary stage most often occurs 10–30 days later, but can present up to six months later. The infection spreads to the lymph nodes through lymphatic drainage pathways. The most frequent presenting clinical manifestation of LGV among males whose primary exposure was genital is unilateral (in 2/3 of cases) lymphadenitis and lymphangitis, often with tender inguinal and/or femoral lymphadenopathy because of the drainage pathway for their likely infected areas. Lymphangitis of the dorsal penis may also occur and resembles a string or cord. If the route was anal sex the infected person may experience lymphadenitis and lymphangitis noted above. They may instead develop proctitis, inflammation limited to the rectum (the distal 10–12 cm) that may be associated with anorectal pain, tenesmus, and rectal discharge, or proctocolitis, inflammation of the colonic mucosa extending to 12 cm above the anus and associated with symptoms of proctitis plus diarrhea or abdominal cramps.

In addition, symptoms may include inflammatory involvement of the perirectal or perianal lymphatic tissues. In females, cervicitis, perimetritis, or salpingitis may occur as well as lymphangitis and lymphadenitis in deeper nodes. Because of lymphatic drainage pathways, some patients develop an abdominal mass which seldom suppurates, and 20–30% develop inguinal lymphadenopathy. Systemic signs which can appear include fever, decreased appetite, and malaise. Diagnosis is more difficult in women and men who have sex with men (MSM) who may not have the inguinal symptoms.

Over the course of the disease, lymph nodes enlarge, as may occur in any infection of the same areas as well. Enlarged nodes are called buboes. Buboes are commonly painful. Nodes commonly become inflamed, thinning and fixation of the overlying skin. These changes may progress to necrosis, fluctuant and suppurative lymph nodes, abscesses, fistulas, strictures, and sinus tracts. During the infection and when it subsides and healing takes place, fibrosis may occur. This can result in varying degrees of lymphatic obstruction, chronic edema, and strictures. These late stages characterised by fibrosis and edema are also known as the third stage of LGV and are mainly permanent.

Acute prostatitis is a serious bacterial infection of the prostate gland. This infection is a medical emergency. It should be distinguished from other forms of prostatitis such as chronic bacterial prostatitis and chronic pelvic pain syndrome (CPPS).

LGV may begin as a self-limited painless genital ulcer that occurs at the contact site 3–12 days after infection. Women rarely notice a primary infection because the initial ulceration where the organism penetrates the mucosal layer is often located out of sight, in the vaginal wall. In men fewer than 1/3 of those infected notice the first signs of LGV. This primary stage heals in a few days. Erythema nodosum occurs in 10% of cases.

The first symptom is a sudden onset of swelling of the face, which develops within two days into papules and pustues on the lips, nose, and around the eyes. These pustules release a purulent discharge, causing a crust to form on the skin. There is also lymphadenopathy (swelling of lymph nodes) in the main lymph nodes of the head. The feet, body, prepuce or perianal area may be affected. Pustular otitis externa can occur, with the pinnae (ear flaps) becoming thickened by edema. Affected areas are painful but not itchy. Approximately half of affected puppies have lethargy and depression. Less common symptoms include pyrexia, anorexia, and joint pain, caused by sterile suppurative arthritis.

Signs and symptoms of acute pyelonephritis generally develop rapidly over a few hours or a day. It can cause high fever, pain on passing urine, and abdominal pain that radiates along the flank towards the back. There is often associated vomiting.

Chronic pyelonephritis causes persistent flank or abdominal pain, signs of infection (fever, unintentional weight loss, malaise, decreased appetite), lower urinary tract symptoms and blood in the urine. Chronic pyelonephritis can in addition cause fever of unknown origin. Furthermore, inflammation-related proteins can accumulate in organs and cause the condition AA amyloidosis.

Physical examination may reveal fever and tenderness at the costovertebral angle on the affected side.

Pyelonephritis that has progressed to urosepsis may be accompanied by signs of septic shock, including rapid breathing, decreased blood pressure, shivering, and occasionally delirium.

Juvenile cellulitis, also known as puppy strangles or juvenile pyoderma, is an uncommon disease of dogs. Symptoms include dermatitis, lethargy, depression and lameness. When puppies are first presented with what appears to be staphylococcal pyoderma, juvenile cellulitis, a relatively rare condition, may not be considered.