Often, a diagnosis can be made based on the patient's description of their symptoms, but other methods which may be used to verify gastritis include:

- Blood tests:

- Blood cell count

- Presence of "H. pylori"

- Liver, kidney, gallbladder, or pancreas functions

- Urinalysis

- Stool sample, to look for blood in the stool

- X-rays

- ECGs

- Endoscopy, to check for stomach lining inflammation and mucous erosion

- Stomach biopsy, to test for gastritis and other conditions

The following diagnostic methods are not routinely available to patients. Researchers have reported that they are more reliable at detecting infection, and in some cases can provide the physician with information to help determine whether "Blastocystis" infection is the cause of the patient's symptoms:

Serum antibody testing: A 1993 research study performed by the NIH with United States patients suggested that it was possible to distinguish symptomatic and asymptomatic infection with "Blastocystis" using serum antibody testing. The study used blood samples to measure the patient's immune reaction to chemicals present on the surface of the "Blastocystis" cell. It found that patients diagnosed with symptomatic "Blastocystis" infection exhibited a much higher immune response than controls who had "Blastocystis" infection but no symptoms. The study was repeated in 2003 at Ain Shams University in Egypt with Egyptian patients with equivalent results.

Fecal antibody testing: A 2003 study at Ain Shams University in Egypt indicated that patients symptomatically infected could be distinguished with a fecal antibody test. The study compared patients diagnosed with symptomatic "Blastocystis" infection to controls who had "Blastocystis" infection but no symptoms. In the group with symptoms, IgA antibodies to "Blastocystis" were detected in fecal specimens that were not present in the healthy control group.

Stool culture: Culturing has been shown to be a more reliable method of identifying infection. In 2006, researchers reported the ability to distinguish between disease causing and non-disease causing isolates of "Blastocystis" using stool culture. "Blastocystis" cultured from patients who were sick and diagnosed with "Blastocystis" infection produced large, highly adhesive amoeboid forms in culture. These cells were absent in "Blastocystis" cultures from healthy controls. Subsequent genetic analysis showed the "Blastocystis" from healthy controls was genetically distinct from that found in patients with symptoms. Protozoal culture is unavailable in most countries due to the cost and lack of trained staff able to perform protozoal culture.

Genetic analysis of isolates: Researchers have used techniques which allow the DNA of "Blastocystis" to be isolated from fecal specimens. This method has been reported to be more reliable at detecting "Blastocystis" in symptomatic patients than stool culture. This method also allows the species group of "Blastocystis" to be identified. Research is continuing into which species groups are associated with symptomatic (see Genetics and Symptoms) blastocystosis.

Immuno-fluorescence (IFA) stain: An IFA stain causes "Blastocystis" cells to glow when viewed under a microscope, making the diagnostic method more reliable. IFA stains are in use for Giardia and Cryptosporidium for both diagnostic purposes and water quality testing. A 1991 paper from the NIH described the laboratory development of one such stain. However, no company currently offers this stain commercially.

The diagnosis of CMV colitis is based on serology, CMV antigen testing and colonscopy with biopsy.

Clinical suspicion should be aroused in the setting of immunocompromised patient but it is much rarer in immunocompetent patient.

Although it is known that CMV colitis is almost always caused by reactivation of latent CMV infection in immunocompromised patients, new infection of CMV or reinfection of different strain of CMV can cause colitis in immunocompetent hosts.

Because asymptomatic CMV viremia and viruria is common and about 1/3 of symptomatic CMV infection is caused by reinfection of different strain of CMV, the diagnosis of CMV colitis needs more direct causality. It is practically achieved by colonoscopy or sigmoidoscopy tissue sampling and pathological evidence of CMV infection under microscope. Positive CMV IgG doesn't necessarily mean that it is reactivation of latent infection because of the possibility of reinfection of different strain.

Diagnosis is generally made by endoscopy with biopsy to evaluate histology. Review of symptoms and associated conditions is important.

Diagnosis is performed by determining if the infection is present, and then making a decision as to whether the infection is responsible for the symptoms. Diagnostic methods in clinical use have been reported to be of poor quality and more reliable methods have been reported in research papers.

For identification of infection, the only method clinically available in most areas is the "Ova and Parasite" (O&P) exam, which identifies the presence of the organism by microscopic examination of a chemically preserved stool specimen. This method is sometimes called "Direct Microscopy". In the United States, pathologists are required to report the presence of "Blastocystis" when found during an O&P exam, so a special test does not have to be ordered. Direct Microscopy is inexpensive, as the same test can identify a variety of gastrointestinal infections, such as "Giardia", "Entamoeba histolytica", "Cryptosporidium". However one laboratory director noted that pathologists using conventional microscopes failed to identify many "Blastocystis" infections, and indicated the necessity for special microscopic equipment for identification. The following table shows the sensitivity of Direct Microscopy in detecting "Blastocystis" when compared to stool culture, a more sensitive technique. Stool culture was considered by some researchers to be the most reliable technique, but a recent study found stool culture only detected 83% of individuals infected when compared to polymerase chain reaction (PCR) testing.

Reasons given for the failure of Direct Microscopy include: (1) Variable Shedding: The quantity of "Blastocystis" organisms varies substantially from day to day in infected humans and animals; (2) Appearance: Some forms of "Blastocystis" resemble fat cells or white blood cells, making it difficult to distinguish the organism from other cells in the stool sample; (3) Large number of morphological forms: "Blastocystis" cells can assume a variety of shapes, some have been described in detail only recently, so it is possible that additional forms exist but have not been identified.

Several methods have been cited in literature for determination of the significance of the finding of "Blastocystis":

1. Diagnosis only when large numbers of organism present: Some physicians consider "Blastocystis" infection to be a cause of illness only when large numbers are found in stool samples. Researchers have questioned this approach, noting that it is not used with any other protozoal infections, such as "Giardia" or "Entamoeba histolytica". Some researchers have reported no correlation between number of organisms present in stool samples and the level of symptoms. A study using polymerase chain reaction testing of stool samples suggested that symptomatic infection can exist even when sufficient quantities of the organism do not exist for identification through Direct Microscopy.

2. Diagnosis-by-exclusion: Some physicians diagnose "Blastocystis" infection by excluding all other causes, such as infection with other organisms, food intolerances, colon cancer, etc. This method can be time consuming and expensive, requiring many tests such as endoscopy and colonoscopy.

3. Disregarding "Blastocystis" : In the early to mid-1990s, some US physicians suggested all findings of "Blastocystis" are insignificant. No recent publications expressing this opinion could be found.

Treatment is aimed at removing the irritant or infection. "Helicobacter pylori" infection is usually treated with antibiotics.

The diagnosis is mainly established based on the characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer. In some cases, doctors may treat ulcers without diagnosing them with specific tests and observe whether the symptoms resolve, thus indicating that their primary diagnosis was accurate.

More specifically, peptic ulcers erode the muscularis mucosae, at minimum reaching to the level of the submucosa (contrast with erosions, which do not involve the muscularis mucosae).

Confirmation of the diagnosis is made with the help of tests such as endoscopies or barium contrast x-rays. The tests are typically ordered if the symptoms do not resolve after a few weeks of treatment, or when they first appear in a person who is over age 45 or who has other symptoms such as weight loss, because stomach cancer can cause similar symptoms. Also, when severe ulcers resist treatment, particularly if a person has several ulcers or the ulcers are in unusual places, a doctor may suspect an underlying condition that causes the stomach to overproduce acid.

An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on people in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.

One of the reasons that blood tests are not reliable for accurate peptic ulcer diagnosis on their own is their inability to differentiate between past exposure to the bacteria and current infection. Additionally, a false negative result is possible with a blood test if the person has recently been taking certain drugs, such as antibiotics or proton-pump inhibitors.

The diagnosis of "Helicobacter pylori" can be made by:

- Urea breath test (noninvasive and does not require EGD);

- Direct culture from an EGD biopsy specimen; this is difficult to do, and can be expensive. Most labs are not set up to perform "H. pylori" cultures;

- Direct detection of urease activity in a biopsy specimen by rapid urease test;

- Measurement of antibody levels in the blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy;

- Stool antigen test;

- Histological examination and staining of an EGD biopsy.

The breath test uses radioactive carbon to detect H. pylori. To perform this exam the person will be asked to drink a tasteless liquid which contains the carbon as part of the substance that the bacteria breaks down. After an hour, the person will be asked to blow into a bag that is sealed. If the person is infected with H. pylori, the breath sample will contain radioactive carbon dioxide. This test provides the advantage of being able to monitor the response to treatment used to kill the bacteria.

The possibility of other causes of ulcers, notably malignancy (gastric cancer) needs to be kept in mind. This is especially true in ulcers of the "greater (large) curvature" of the stomach; most are also a consequence of chronic "H. pylori" infection.

If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the person stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.

The systemic use of corticosteroids in the context of inflammatory bowel disease.

A gastric peptic ulcer is a mucosal perforation which penetrates the muscularis mucosae and lamina propria, usually produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: fibrinoid necrosis, inflammatory exudate, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.

Diagnosis is usually performed by submitting multiple stool samples for examination by a parasitologist in a procedure known as an ova and parasite examination. About 30% of children with "D. fragilis" infection exhibit peripheral blood eosinophilia.

A minimum of three stool specimens having been immediately fixed in polyvinyl alcohol fixative, sodium acetate-acetic acid-formalin fixative, or Schaudinn's fixative should be submitted, as the protozoan does not remain morphologically identifiable for long. All specimens, regardless of consistency, are permanently stained prior to microscopic examination with an oil immersion lens. The disease may remain cryptic due to the lack of a cyst stage if these recommendations are not followed.

The trophozoite forms have been recovered from formed stool, thus the need to perform the ova and parasite examination on specimens other than liquid or soft stools. DNA fragment analysis provides excellent sensitivity and specificity when compared to microscopy for the detection of "D. fragilis" and both methods should be employed in laboratories with PCR capability. The most sensitive detection method is parasite culture, and the culture medium requires the addition of rice starch.

An indirect fluorescent antibody (IFA) for fixed stool specimens has been developed.

1. One researcher investigated the phenomenon of symptomatic relapse following treatment of infection with "D. fragilis" in association with its apparent disappearance from stool samples. The organism could still be detected in patients through colonoscopy or by examining stool samples taken in conjunction with a saline laxative.

2. A study found that trichrome staining, a traditional method for identification, had a sensitivity of 36% (9/25) when compared to stool culture.

3. An additional study found that the sensitivity of staining was 50% (2/4), and that the organism could be successfully cultured in stool specimens up to 12-hours old that were kept at room temperature.

Neonatal sepsis of the newborn is an infection that has spread through the entire body. The inflammatory response to this systematic infection can be as serious as the infection itself. In infants that weigh under 1500 g, sepsis is the most common cause of death. Three to four percent of infants per 1000 births contract sepsis. The mortality rate from sepsis is near 25%. Infected sepsis in an infant can be identified by culturing the blood and spinal fluid and if suspected, intravenous antibiotics are usually started. Lumbar puncture is controversial because in some cases it has found not to be necessary while concurrently, without it estimates of missing up to one third of infants with meningitis is predicted.

Antacids are a common treatment for mild to medium gastritis. When antacids do not provide enough relief, medications such as H blockers and proton-pump inhibitors that help reduce the amount of acid are often prescribed.

Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. They include the medications sucralfate and misoprostol. If NSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is bismuth subsalicylate.

Several regimens are used to treat "H. pylori" infection. Most use a combination of two antibiotics and a proton pump inhibitor. Sometimes bismuth is added to the regimen.

"Campylobacter" organisms can be detected by performing a Gram stain of a stool sample with high specificity and a sensitivity of ~60%, but are most often diagnosed by stool culture. Fecal leukocytes should be present and indicate the diarrhea to be inflammatory in nature. Methods currently being developed to detect the presence of campylobacter organisms include antigen testing via an EIA or PCR.

Opportunistic infections caused by Feline Leukemia Virus and Feline immunodeficiency virus retroviral infections can be treated with Lymphocyte T-Cell Immune Modulator.

The methods used differ from country to country (definitions used, type of nosocomial infections covered, health units surveyed, inclusion or exclusion of imported infections, etc.), so the international comparisons of nosocomial infection rates should be made with the utmost care.

In addition to hand washing, gloves play an important role in reducing the risks of transmission of microorganisms. Gloves are worn for three important reasons in hospitals. First, they are worn to provide a protective barrier for personnel, preventing large scale contamination of the hands when touching blood, body fluids, secretions, excretions, mucous membranes, and non-intact skin. In the United States, the Occupational Safety and Health Administration has mandated wearing gloves to reduce the risk of bloodborne pathogen infections. Second, gloves are worn to reduce the likelihood that microorganisms present on the hands of personnel will be transmitted to patients during invasive or other patient-care procedures that involve touching a patient's mucous membranes and nonintact skin. Third, they are worn to reduce the likelihood that the hands of personnel contaminated with micro-organisms from a patient or a fomite can transmit those micro-organisms to another patient. In this situation, gloves must be changed between patient contacts, and hands should be washed after gloves are removed.

Wearing gloves does not replace the need for handwashing, because gloves may have small, undtectable defects or may be torn during use, and hands can become contaminated during removal of gloves. Failure to change gloves between patient contacts is an infection control hazard.

Individuals at higher risk are often prescribed prophylactic medication to prevent an infection from occurring. A patient's risk level for developing an opportunistic infection is approximated using the patient's CD4 T-cell count and sometimes other markers of susceptibility. Common prophylaxis treatments include the following:

Other radiological studies frequently used to assess patients with chronic stomach problems include a barium swallow, where a dye is consumed and pictures of the esophagus and stomach are obtained every few minutes. Other tests include a 24-hour pH study, CT scans or MRI.

Symptoms and the isolation of the virus pathogen the upper respiratory tract is diagnostic. Virus identification is specific immunologic methods and PCR. The presence of the virus can be rapidly confirmed by the detection of the virus antigen. The methods and materials used for identifying the RSV virus has a specificity and sensitivity approaching 85% to 95%. Not all studies confirm this sensitivity. Antigen detection has comparatively lower sensitivity rates that approach 65% to 75%.

The World Health Organization recommends the following:

- Food should be properly cooked and hot when served.

- Consume only pasteurized or boiled milk and milk products, never raw milk products.

- Make sure that ice is from safe water.

- If you are not sure of the safety of drinking water, boil it, or disinfect it with chemical disinfectant.

- Wash hands thoroughly and frequently with soap, especially after using the toilet and after contact with pets and farm animals.

- Wash fruits and vegetables thoroughly, especially if they are to be eaten raw. Peel fruits and vegetables whenever possible.

- Food handlers, professionals and at home, should observe hygienic rules during food preparation.

- Professional food handlers should immediately report to their employer any fever, diarrhea, vomiting or visible infected skin lesions.

Concomitant pinworm infection should also be excluded, although the association has not been proven. Successful treatment of the infection with iodoquinol, doxycycline, metronidazole, paromomycin, and secnidazole has been reported. Resistance requires the use of combination therapy to eradicate the organism. All persons living in the same residence should be screened for "D. fragilis", as asymptomatic carriers may provide a source of repeated infection. Paromomycin is an effective prophylactic for travellers who will encounter poor sanitation and unsafe drinking water.

People under 55 years without alarm symptoms can be treated without investigation. People over 55 years with recent onset dyspepsia or those with alarm symptoms should be urgently investigated by upper gastrointestinal endoscopy. This will rule out peptic ulcer disease, medication-related ulceration, malignancy and other rarer causes.

People under the age of 55 years with no alarm features do not need endoscopy but are considered for investigation for peptic ulcer disease caused by "Helicobacter pylori" infection. Investigation for "H. pylori" infection is usually performed when there is a moderate to high prevalence of this infection in the local community or the person with dyspepsia has other risk factors for "H. pylori" infection, related for example to ethnicity or immigration from a high-prevalence area. If infection is confirmed, it can usually be eradicated by medication.

Medication-related dyspepsia is usually related to NSAIDs and can be complicated by bleeding or ulceration with perforation of stomach wall.

Treatment of AIT involves antibiotic treatment. Based on the offending organism found on microscopic examination of the stained fine needle aspirate, the appropriate antibiotic treatment is determined. In the case of a severe infection, systemic antibiotics are necessary. Empirical broad spectrum antimicrobial treatment provides preliminary coverage for a variety of bacteria, including "S. aureus" and "S. pyogenes." Antimicrobial options include penicillinase-resistant penicillins (ex: cloxacillin, dicloxacillin) or a combination of a penicillin and a beta-lactamase inhibitor. However, in patients with a penicillin allergy, clindamycin or a macrolide can be prescribed. The majority of anaerobic organisms involved with AIT are susceptible to penicillin. Certain Gram-negative bacilli (ex: "Prevotella", "Fusobacteria", and "Porphyromonas") are exhibiting an increased resistance based on the production of beta-lactamase. Patients who have undergone recent penicillin therapy have demonstrated an increase in beta-lactamase-producing (anaerobic and aerobic) bacteria. Clindamycin, or a combination of metronidazole and a macrolide, or a penicillin combined with a beta-lactamase inhibitor is recommended in these cases. Fungal thyroiditis can be treated with amphotericin B and fluconazole. Early treatment of AIT prevents further complications. However, if antibiotic treatment does not manage the infection, surgical drainage is required. Symptoms or indications requiring drainage include continued fever, high white blood cell count, and continuing signs of localized inflammation. The draining procedure is also based on clinical examination or ultrasound/CT scan results that indicate an abscess or gas formation. Another treatment of AIT involves surgically removing the fistula. This treatment is often the option recommended for children. However, in cases of an antibiotic resistant infection or necrotic tissue, a lobectomy is recommended. If diagnosis and/or treatment is delayed, the disease could prove fatal.

The tests, called assays, for detection of virus infection involve serum or blood tests that detect either viral antigens (proteins produced by the virus) or antibodies produced by the host. Interpretation of these assays is complex.

The surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection. However, early in an infection, this antigen may not be present and it may be undetectable later in the infection as it is being cleared by the host. The infectious virion contains an inner "core particle" enclosing viral genome. The icosahedral core particle is made of 180 or 240 copies of the core protein, alternatively known as core antigen, or HBcAg. During this 'window' in which the host remains infected but is successfully clearing the virus, IgM antibodies specific to the core antigen ("anti-HBc IgM") may be the only serological evidence of disease. Therefore, most diagnostic panels contain HBsAg and total anti-HBc (both IgM and IgG).

Shortly after the appearance of the HBsAg, another antigen called e antigen (HBeAg) will appear. Traditionally, the presence of HBeAg in a host's serum is associated with much higher rates of viral replication and enhanced infectivity; however, variants of the virus do not produce the 'e' antigen, so this rule does not always hold true. During the natural course of an infection, the HBeAg may be cleared, and antibodies to the 'e' antigen ("anti-HBe") will arise immediately afterwards. This conversion is usually associated with a dramatic decline in viral replication.

If the host is able to clear the infection, eventually the HBsAg will become undetectable and will be followed by IgG antibodies to the surface antigen and core antigen ("anti-HBs" and "anti HBc IgG"). The time between the removal of the HBsAg and the appearance of anti-HBs is called the window period. A person negative for HBsAg but positive for anti-HBs either has cleared an infection or has been vaccinated previously.

Individuals who remain HBsAg positive for at least six months are considered to be carriers. Carriers of the virus may have chronic hepatitis B, which would be reflected by elevated serum alanine aminotransferase (ALT) levels and inflammation of the liver, if they are in the immune clearance phase of chronic infection. Carriers who have seroconverted to HBeAg negative status, in particular those who acquired the infection as adults, have very little viral multiplication and hence may be at little risk of long-term complications or of transmitting infection to others.

PCR tests have been developed to detect and measure the amount of HBV DNA, called the viral load, in clinical specimens. These tests are used to assess a person's infection status and to monitor treatment. Individuals with high viral loads, characteristically have ground glass hepatocytes on biopsy.

Acute infectious thyroiditis is very rare, with it only accounting for about 0.1–0.7% of all thyroiditis. Large hospitals tend to only see two cases of AIT annually. For the few cases of AIT that are seen the statistics seem to show a pattern. AIT is found in children and young adults between the ages of 20 and 40. The occurrence of the disease in people between 20 and 40 is only about 8% with the other 92% being in children. Men and women are each just as likely to get the disease. If left untreated, there is a 12% mortality rate.