The diagnosis of group A beta-hemolytic streptococcus (GABHS) tonsillitis can be confirmed by culture of samples obtained by swabbing both tonsillar surfaces and the posterior pharyngeal wall and plating them on sheep blood agar medium. The isolation rate can be increased by incubating the cultures under anaerobic conditions and using selective growth media. A single throat culture has a sensitivity of 90–95% for the detection of GABHS (which means that GABHS is actually present 5–10% of the time culture suggests that it is absent). This small percentage of false-negative results are part of the characteristics of the tests used but are also possible if the patient has received antibiotics prior to testing. Identification requires 24 to 48 hours by culture but rapid screening tests (10–60 minutes), which have a sensitivity of 85–90%, are available. Older antigen tests detect the surface Lancefield group A carbohydrate. Newer tests identify GABHS serotypes using nucleic acid (DNA) probes or polymerase chain reaction. Bacterial culture may need to be performed in cases of a negative rapid streptococcal test.

True infection with GABHS, rather than colonization, is defined arbitrarily as the presence of >10 colonies of GABHS per blood agar plate. However, this method is difficult to implement because of the overlap between carriers and infected patients. An increase in antistreptolysin O (ASO) streptococcal antibody titer 3–6 weeks following the acute infection can provide retrospective evidence of GABHS infection and is considered definitive proof of GABHS infection.

Increased values of secreted phospholipase A2 and altered fatty acid metabolism in patients with tonsillitis may have diagnostic utility.

It is hard to differentiate a viral and a bacterial cause of a sore throat based on symptoms alone. Thus often a throat swab is done to rule out a bacterial cause.

The modified Centor criteria may be used to determine the management of people with pharyngitis. Based on 5 clinical criteria, it indicates the probability of a streptococcal infection.

One point is given for each of the criteria:

- Absence of a cough

- Swollen and tender cervical lymph nodes

- Temperature >

- Tonsillar exudate or swelling

- Age less than 15 (a point is subtracted if age >44)

The McIsaac criteria adds to the Centor:

- Age less than 15: add one point

- Age greater than 45: subtract one point

The Infectious Disease Society of America however recommends against empirical treatment and considers antibiotics only appropriate following positive testing. Testing is not needed in children under three as both group A strep and rheumatic fever are rare, except if they have a sibling with the disease.

Optical fiber endoscopy can confirm the diagnosis in case of doubt, directly visualizing the inflamed adenoid.

Treatments to reduce the discomfort from tonsillitis include:

- pain and fever reducing medications such as paracetamol (acetaminophen) and ibuprofen

- warm salt water gargle, lozenges, or warm liquids

When tonsillitis is caused by a virus, the length of illness depends on which virus is involved. Usually, a complete recovery is made within one week; however, symptoms may last for up to two weeks.

Diagnosis is usually based on the symptoms. Medical imaging may be done to rule out complications. Medical imaging may include CT scan or MRI.

In cases of viral adenoiditis, treatment with analgesics or antipyretics is often sufficient. Bacterial adenoiditis may be treated with antibiotics, such as amoxicillin - clavulanic acid or a cephalosporin. In case of adenoid hypertrophy, adenoidectomy may be performed to remove the adenoid.

Gargling salt water is often suggested but evidence looking at its usefulness is lacking. Alternative medicines are promoted and used for the treatment of sore throats. However, they are poorly supported by evidence.

The pus can be removed by a number of methods including needle aspiration, incision and drainage, and tonsillectomy.

Treatment can also be given while a patient is under anesthesia, but this is usually reserved for children or anxious patients. Tonsillectomy can be indicated if a patient has recurring peritonsillar abscesses or a history of tonsillitis. For patients with their first peritonsillar abscess most ENT-surgeons prefer to "wait and observe" before recommending tonsillectomy.

A diagnosis can be made from clinical signs and symptoms, and treatment consists of minimizing the discomfort of symptoms. It can be differentiated from herpetic gingivostomatitis by the positioning of vesicles - in herpangina, they are typically found on the posterior oropharynx, as compared to gingivostomatitis where they are typically found on the anterior oropharynx and the mouth.

The heterophile antibody test works by agglutination of red blood cells from guinea pig, sheep and horse. This test is specific but not particularly sensitive (with a false-negative rate of as high as 25% in the first week, 5–10% in the second, and 5% in the third). About 90% of patients have heterophile antibodies by week 3, disappearing in under a year. The antibodies involved in the test do not interact with the Epstein–Barr virus or any of its antigens.

The monospot test is not recommended for general use by the CDC due to its poor accuracy.

About 10% of people who present a clinical picture of infectious mononucleosis do not have an acute Epstein–Barr-virus infection. A differential diagnosis of acute infectious mononucleosis needs to take into consideration acute cytomegalovirus infection and "Toxoplasma gondii" infections. Because their management is much the same, it is not always helpful, or possible, to distinguish between Epstein–Barr-virus mononucleosis and cytomegalovirus infection. However, in pregnant women, differentiation of mononucleosis from toxoplasmosis is important, since it is associated with significant consequences for the fetus.

Acute HIV infection can mimic signs similar to those of infectious mononucleosis, and tests should be performed for pregnant women for the same reason as toxoplasmosis.

People with infectious mononucleosis are sometimes misdiagnosed with a streptococcal pharyngitis (because of the symptoms of fever, pharyngitis and adenopathy) and are given antibiotics such as ampicillin or amoxicillin as treatment.

Other conditions from which to distinguish infectious mononucleosis include leukemia, tonsillitis, diphtheria, common cold and influenza (flu).

Treatment is usually supportive only, as the disease is self-limiting and usually runs its course in less than a week.

There is low or very-low quality evidence that probiotics may be better than placebo in preventing acute URTIs. Vaccination against influenza viruses, adenoviruses, measles, rubella, "Streptococcus pneumoniae", "Haemophilus influenzae", diphtheria, "Bacillus anthracis", and "Bordetella pertussis" may prevent them from infecting the URT or reduce the severity of the infection.

Diagnosis is usually made upon inspection. Differential diagnosis of tonsilloliths includes foreign body, calcified granuloma, malignancy, an enlarged temporal styloid process or rarely, isolated bone which is usually derived from embryonic rests originating from the branchial arches.

Tonsilloliths are difficult to diagnose in the absence of clear manifestations, and often constitute casual findings of routine radiological studies.

Imaging diagnostic techniques can identify a radiopaque mass that may be mistaken for foreign bodies, displaced teeth or calcified blood vessels. Computed tomography (CT) may reveal nonspecific calcified images in the tonsillar zone. The differential diagnosis must be established with acute and chronic tonsillitis, tonsillar hypertrophy, peritonsillar abscesses, foreign bodies, phlebolites, ectopic bone or cartilage, lymph nodes, granulomatous lesions or calcification of the stylohyoid ligament in the context of Eagle syndrome (elongated styloid process).

The Centers for Disease Control describe protocol for treating sinusitis while at the same time discouraging overuse of antibiotics:

- Target likely organisms with first-line drugs: Amoxicillin, Amoxicillin/Clavulanate

- Use shortest effective course: Should see improvement in 2–3 days. Continue treatment for 7 days after symptoms improve or resolve (usually a 10–14 day course).

- Consider imaging studies in recurrent or unclear cases: some sinus involvement is frequent early in the course of uncomplicated viral URI

Treatment comprises symptomatic support usually via analgesics for headache, sore throat and muscle aches. Moderate exercise in sedentary subjects with naturally acquired URTI probably does not alter the overall severity and duration of the illness. No randomized trials have been conducted to ascertain benefits of increasing fluid intake.

Typhlitis is a medical emergency and requires prompt management. Untreated typhlitis has a poor prognosis, particularly if associated with pneumatosis intestinalis (air in the bowel wall) and/or bowel perforation, and has significant morbidity unless promptly recognized and aggressively treated.

Successful treatment hinges on:

1. Early diagnosis provided by a high index of suspicion and the use of CT scanning

2. Nonoperative treatment for uncomplicated cases

3. Empiric antibiotics, particularly if the patient is neutropenic or at other risk of infection.

In rare cases of prolonged neutropenia and complications such as bowel perforation, neutrophil transfusions can be considered but have not been studied in a randomized control trial. Elective right hemicolectomy may be used to prevent recurrence but is generally not recommended

"...The authors have found nonoperative treatment highly effective in patients who do not manifest signs of peritonitis, perforation, gastrointestinal hemorrhage, or clinical deterioration. Recurrent typhlitis was frequent after conservative therapy (recurrence rate, 67 percent), however," as based on studies from the 1980s

Diagnosis is usually clinical. Smear for fusospirochaetal bacteria and leukocytes; blood picture occasionally. The important differentiation is with acute leukaemia or herpetic stomatitis.

Among individuals being treated in intensive care units, the mortality rate is about 30-50% when systemic candidiasis develops.

Typhlitis is diagnosed with a radiograph CT scan showing thickening of the cecum and "fat stranding".

The diagnosis can typically be made from the clinical appearance alone, but not always. As candidiasis can be variable in appearance, and present with white, red or combined white and red lesions, the differential diagnosis can be extensive. In pseudomembraneous candidiasis, the membranous slough can be wiped away to reveal an erythematous surface underneath. This is helpful in distinguishing pseudomembraneous candidiasis from other white lesions in the mouth that cannot be wiped away, such as lichen planus, oral hairy leukoplakia. Erythematous candidiasis can mimic geographic tongue. Erythematous candidiasis usually has a diffuse border that helps distinguish it from erythroplakia, which normally has a sharply defined border.

Special investigations to detect the presence of candida species include oral swabs, oral rinse or oral smears. Smears are collected by gentle scraping of the lesion with a spatula or tongue blade and the resulting debris directly applied to a glass slide. Oral swabs are taken if culture is required. Some recommend that swabs be taken from 3 different oral sites. Oral rinse involves rinsing the mouth with phosphate-buffered saline for 1 minute and then spitting the solution into a vessel that examined in a pathology laboratory. Oral rinse technique can distinguish between commensal candidal carriage and candidiasis. If candidal leukoplakia is suspected, a biopsy may be indicated. Smears and biopsies are usually stained with periodic acid-Schiff, which stains carbohydrates in fungal cell walls in magenta. Gram staining is also used as Candida stains are strongly Gram positive.

Sometimes an underlying medical condition is sought, and this may include blood tests for full blood count and hematinics.

If a biopsy is taken, the histopathologic appearance can be variable depending upon the clinical type of candidiasis. Pseudomembranous candidiasis shows hyperplastic epithelium with a superficial parakeratotic desquamating (i.e., separating) layer. Hyphae penetrate to the depth of the stratum spinosum, and appear as weakly basophilic structures. Polymorphonuclear cells also infiltrate the epithelium, and chronic inflammatory cells infiltrate the lamina propria.

Atrophic candidiasis appears as thin, atrophic epithelium, which is non-keratinized. Hyphae are sparse, and inflammatory cell infiltration of the epithelium and the lamina propria. In essence, atrophic candidiasis appears like pseudomembranous candidiasis without the superficial desquamating layer.

Hyperplastic candidiasis is variable. Usually there is hyperplastic and acanthotic epithelium with parakeratosis. There is an inflammatory cell infiltrate and hyphae are visible. Unlike other forms of candidiasis, hyperplastic candidiasis may show dysplasia.

Symptoms of vaginal candidiasis are also present in the more common bacterial vaginosis; aerobic vaginitis is distinct and should be excluded in the differential diagnosis. In a 2002 study, only 33% of women who were self-treating for a yeast infection actually had such an infection, while most had either bacterial vaginosis or a mixed-type infection.

Diagnosis of a yeast infection is done either via microscopic examination or culturing. For identification by light microscopy, a scraping or swab of the affected area is placed on a microscope slide. A single drop of 10% potassium hydroxide (KOH) solution is then added to the specimen. The KOH dissolves the skin cells, but leaves the "Candida" cells intact, permitting visualization of pseudohyphae and budding yeast cells typical of many "Candida" species.

For the culturing method, a sterile swab is rubbed on the infected skin surface. The swab is then streaked on a culture medium. The culture is incubated at 37 °C (98.6 °F) for several days, to allow development of yeast or bacterial colonies. The characteristics (such as morphology and colour) of the colonies may allow initial diagnosis of the organism causing disease symptoms.

Respiratory, gastrointestinal, and esophageal candidiasis require an endoscopy to diagnose. For gastrointestinal candidiasis, it is necessary to obtain a 3–5 milliliter sample of fluid from the duodenum for fungal culture. The diagnosis of gastrointestinal candidiasis is based upon the culture containing in excess of 1,000 colony-forming units per milliliter.

Treatment includes irrigation and debridement of necrotic areas (areas of dead and/or dying gum tissue), oral hygiene instruction and the uses of mouth rinses and pain medication. If there is systemic involvement, then oral antibiotics may be given, such as metronidazole. As these diseases are often associated with systemic medical issues, proper management of the systemic disorders is appropriate.

A determination of whether or not the person has dehydration is an important part of the assessment, with dehydration typically divided into mild (3–5%), moderate (6–9%), and severe (≥10%) cases. In children, the most accurate signs of moderate or severe dehydration are a prolonged capillary refill, poor skin turgor, and abnormal breathing. Other useful findings (when used in combination) include sunken eyes, decreased activity, a lack of tears, and a dry mouth. A normal urinary output and oral fluid intake is reassuring. Laboratory testing is of little clinical benefit in determining the degree of dehydration. Thus the use of urine testing or ultrasounds is generally not needed.

Oral candidiasis can be treated with topical anti-fungal drugs, such as nystatin, miconazole, Gentian violet or amphotericin B.

Underlying immunosuppression may be medically manageable once it is identified, and this helps prevent recurrence of candidal infections.

Patients who are immunocompromised, either with HIV/AIDS or as a result of chemotherapy, may require systemic treatment with oral or intravenous administered anti-fungals.

If candidiasis is secondary to corticosteroid or antibiotic use, then use may be stopped, although this is not always a feasible option. Candidiasis secondary to the use of inhaled steroids may be treated by rinsing out the mouth with water after taking the steroid. Use of a spacer device to reduce the contact with the oral mucosa may greatly reduce the risk of oral candidiasis.

In recurrent oral candidiasis, the use of azole antifungals risks selection and enrichment of drug-resistant strains of candida organisms. Drug resistance is increasingly more common and presents a serious problem in persons who are immunocompromised.

Prophylactic use of antifungals is sometimes employed in persons with HIV disease, during radiotherapy, during immunosuppressive or prolonged antibiotic therapy as the development of candidal infection in these groups may be more serious.

The candidal load in the mouth can be reduced by improving oral hygiene measures, such as regular toothbrushing and use of anti-microbial mouthwashes. Since smoking is associated with many of forms of oral candidiasis, cessation may be beneficial.

Other potential causes of signs and symptoms that mimic those seen in gastroenteritis that need to be ruled out include appendicitis, volvulus, inflammatory bowel disease, urinary tract infections, and diabetes mellitus. Pancreatic insufficiency, short bowel syndrome, Whipple's disease, coeliac disease, and laxative abuse should also be considered. The differential diagnosis can be complicated somewhat if the person exhibits "only" vomiting or diarrhea (rather than both).

Appendicitis may present with vomiting, abdominal pain, and a small amount of diarrhea in up to 33% of cases. This is in contrast to the large amount of diarrhea that is typical of gastroenteritis. Infections of the lungs or urinary tract in children may also cause vomiting or diarrhea. Classical diabetic ketoacidosis (DKA) presents with abdominal pain, nausea, and vomiting, but without diarrhea. One study found that 17% of children with DKA were initially diagnosed as having gastroenteritis.