Signs and symptoms of spontaneous bacterial peritonitis include fevers, chills, nausea, vomiting, abdominal tenderness, and general malaise. Affected individuals may complain of abdominal pain and worsening ascites. Thirteen percent of patients have no signs or symptoms. Hepatic encephalopathy may be the only manifestation of SBP; in the absence of a clear precipitant for the encephalopathy, all patients should undergo paracentesis, or sampling of the ascites fluid, in order to assess for SBP.

A pleural effusion is excess fluid that accumulates in the pleural cavity, the fluid-filled space that surrounds the lungs. This excess can impair breathing by limiting the expansion of the lungs. Various kinds of pleural effusion, depending on the nature of the fluid and what caused its entry into the pleural space, are hydrothorax (serous fluid), hemothorax (blood), urinothorax (urine), chylothorax (chyle), or pyothorax (pus). A pneumothorax is the accumulation of air in the pleural space, and is commonly called a "collapsed lung."

The main manifestations of peritonitis are acute abdominal pain, abdominal tenderness and abdominal guarding, which are exacerbated by moving the peritoneum, e.g., coughing (forced cough may be used as a test), flexing one's hips, or eliciting the Blumberg sign (a.k.a. rebound tenderness, meaning that pressing a hand on the abdomen elicits less pain than releasing the hand abruptly, which will aggravate the pain, as the peritoneum snaps back into place). Rigidity (involuntary contraction of the abdominal muscles) is the most specific exam finding for diagnosing peritonitis (+ likelihood ratio: 3.9). The presence of these signs in a patient is sometimes referred to as peritonism. The localization of these manifestations depends on whether peritonitis is localized (e.g., appendicitis or diverticulitis before perforation), or generalized to the whole abdomen. In either case, pain typically starts as a generalized abdominal pain (with involvement of poorly localizing innervation of the visceral peritoneal layer), and may become localized later (with the involvement of the somatically innervated parietal peritoneal layer). Peritonitis is an example of an acute abdomen.

Various methods can be used to classify pleural fluid.

By the origin of the fluid:

- Serous fluid (hydrothorax)

- Blood (haemothorax)

- Chyle (chylothorax)

- Pus (pyothorax or empyema)

- Urine (urinothorax)

By pathophysiology:

- Transudative pleural effusion

- Exudative pleural effusion

By the underlying cause (see next section).

In normal conditions, the peritoneum appears greyish and glistening; it becomes dull 2–4 hours after the onset of peritonitis, initially with scarce serous or slightly turbid fluid. Later on, the exudate becomes creamy and evidently suppurative; in dehydrated patients, it also becomes very inspissated. The quantity of accumulated exudate varies widely. It may be spread to the whole peritoneum, or be walled off by the omentum and viscera. Inflammation features infiltration by neutrophils with fibrino-purulent exudation.

Patients with miliary tuberculosis often experience non-specific signs, such as coughing and enlarged lymph nodes. Miliary tuberculosis can also present with enlarged liver (40% of cases), enlarged spleen (15%), inflammation of the pancreas (<5%), and multiple organ dysfunction with adrenal insufficiency (adrenal glands do not produce enough steroid hormones to regulate organ function). Miliary tuberculosis may also present with unilateral or bilateral pneumothorax rarely. Stool may also be diarrheal in nature and appearance.

Other symptoms include fever, hypercalcemia, chorodial tubercles and cutaneous lesions.

Firstly, many patients can experience a fever lasting several weeks with daily spikes in morning temperatures.

Secondly, hypercalcemia prevails in 16 to 51% of tuberculosis cases. It is thought that hypercalcemia occurs as a response to increased macrophage activity in the body. Such that, 1,25 dihydroxycholecalciferol (also referred to as calcitriol) improves the ability of macrophages to kill bacteria; however, higher levels of calcitriol lead to higher calcium levels, and thus hypercalcemia in some cases. Thus, hypercalcemia proves to be an important symptom of miliary tuberculosis.

Thirdly, chorodial tubercules, pale lesions on the optic nerve, typically indicate miliary tuberculosis in children. These lesions may occur in one eye or both; the number of lesions varies between patients. Chorodial tubercules may serve as important symptoms of miliary tuberculosis, since their presence can often confirm suspected diagnosis.

Lastly, between 10 and 30% of adults, and 20–40% of children with miliary tuberculosis have tuberculosis meningitis. This relationship results from myobacteria from miliary tuberculosis spreading to the brain and the subarachnoid space; as a result, leading to tuberculosis meningitis.

The risk factors for contracting miliary tuberculosis are being in direct contact with a person who has it, living in unsanitary conditions, and having an unhealthy diet. In the U.S., risk factors for contracting the disease include homelessness and HIV/AIDS.

Spontaneous bacterial peritonitis (SBP) is the development of a bacterial infection in the peritoneum causing peritonitis, despite the absence of an obvious source for the infection. It occurs almost exclusively in people with portal hypertension (increased pressure over the portal vein), usually as a result of cirrhosis of the liver. It can also occur in patients with nephrotic syndrome.

The diagnosis of SBP requires paracentesis (aspiration of fluid with a needle) from the abdominal cavity. If the fluid contains bacteria or large numbers of neutrophil granulocytes (>250 cells/µL) (a type of white blood cells), infection is confirmed and antibiotics are required to avoid complications. In addition to antibiotics, infusions of albumin are usually administered.

Mild ascites is hard to notice, but severe ascites leads to abdominal distension. Patients with ascites generally will complain of progressive abdominal heaviness and pressure as well as shortness of breath due to mechanical impingement on the diaphragm.

Ascites is detected on physical examination of the abdomen by visible bulging of the flanks in the reclining patient ("flank bulging"), "shifting dullness" (difference in percussion note in the flanks that shifts when the patient is turned on the side) or in massive ascites with a "fluid thrill" or "fluid wave" (tapping or pushing on one side will generate a wave-like effect through the fluid that can be felt in the opposite side of the abdomen).

Other signs of ascites may be present due to its underlying cause. For instance, in portal hypertension (perhaps due to cirrhosis or fibrosis of the liver) patients may also complain of leg swelling, bruising, gynecomastia, hematemesis, or mental changes due to encephalopathy. Those with ascites due to cancer (peritoneal carcinomatosis) may complain of chronic fatigue or weight loss. Those with ascites due to heart failure may also complain of shortness of breath as well as wheezing and exercise intolerance.

If left untreated, miliary tuberculosis is almost always fatal. Although most cases of miliary tuberculosis are treatable, the mortality rate among children with miliary tuberculosis remains 15 to 20% and for adults 25 to 30%. One of the main causes for these high mortality rates includes late detection of disease caused by non-specific symptoms. Non-specific symptoms include: coughing, weight loss, or organ dysfunction. These symptoms may be implicated in numerous disorders, thus delaying diagnosis. Misdiagnosis with tuberculosis meningitis is also a common occurrence when patients are tested for tuberculosis, since the two forms of tuberculosis have high rates of co-occurrence.

Hydrothorax is a type of pleural effusion in which transudate accumulates in the pleural cavity. This condition is most likely to develop secondary to congestive heart failure, following an increase in hydrostatic pressure within the lungs. More rarely, hydrothorax can develop in patients with cirrhosis or ascites. Hepatic hydrothorax is often difficult to manage in end-stage liver failure and often fails to respond to therapy.

Pleural effusions may also develop following the accumulation of other fluids within the pleural cavity; if the fluid is blood it is known as hemothorax (as in major chest injuries), if the fluid is pus it is known as pyothorax (resulting from chest infections), and if the fluid is lymph it is known as chylothorax (resulting from rupture of the thoracic duct).

Ascites is the abnormal buildup of fluid in the abdomen. Technically it is more than 25 mL of fluid in the peritoneal cavity. Symptoms may include increased abdominal size, increased weight, abdominal discomfort, and shortness of breath. Complications can include spontaneous bacterial peritonitis.

In the developed world the most common cause is liver cirrhosis. Other causes include cancer, heart failure, tuberculosis, pancreatitis, and blockage of the hepatic vein. In cirrhosis the underlying mechanism involves high blood pressure in the portal system and dysfunction of blood vessels. Diagnosis is typically based on a examination together with ultrasound or a CT scan. Testing the fluid can help in determining the underlying cause.

Treatment often involves a low salt diet, medication such as diuretics, and draining the fluid. A transjugular intrahepatic portosystemic shunt (TIPS) may be placed but is associated with complications. Effects to treat the underlying cause, such as by a liver transplant may be considered. Of those with cirrhosis, more than half develop ascites in the ten years following diagnosis. Once ascites has developed in this group, average life expectancy is less than three years. The term is from the Greek "askítes" meaning "baglike".

Tuberculous pericarditis is a form of pericarditis.

Pericarditis caused by tuberculosis is difficult to diagnose, because definitive diagnosis requires culturing "Mycobacterium tuberculosis" from aspirated pericardial fluid or pericardial , which requires high technical skill and is often not diagnostic (the yield from culture is low even with optimum specimens). The Tygerberg scoring system helps the clinician to decide whether pericarditis is due to tuberculosis or whether it is due to another cause: night sweats (1 point), weight loss (1 point), fever (2 point), serum globulin > 40g/l (3 points), blood total leucocyte count <10 x 10/l (3 points); a total score of 6 or more is highly suggestive of tuberculous pericarditis. Pericardial fluid with an interferon-γ level greater than 50/ml is highly specific for tuberculous pericarditis.

There are no randomized trials which evaluate the length of anti-tuberculosis treatment required for tuberculous pericarditis. There is a small but not conclusive benefit for treatment with a schedule of steroids with anti-tuberculosis drugs. Open surgical drainage of fluid though effective in preventing cardiac tamponade was associated with more deaths.

Stages of tubercular lymphadenitis:

1. Lymphadenitis

2. Periadenitis

3. Cold abscess

4. 'Collar stud' abscess

5. Sinus

Tuberculous lymphadenitis is popularly known as collar stud abscess, due to its proximity to the collar bone and superficial resemblance to a collar stud, although this is just one of the five stages of the disease. The characteristic morphological element is the tuberculous granuloma (caseating tubercule): giant multinucleated cells (Langhans cells), surrounded by epithelioid cells aggregates, T cell lymphocytes and few fibroblasts. Granulomatous tubercules evolve to central caseous necrosis and tend to become confluent, replacing the lymphoid tissue.

Fever and headache are the cardinal features, confusion is a late feature and coma bears a poor prognosis. Meningism is absent in a fifth of patients with TB meningitis. Patients may also have focal neurological deficits.

Tuberculous lymphadenitis (or tuberculous adenitis) is a chronic specific granulomatous inflammation of the lymph node with caseation necrosis, caused by infection with "Mycobacterium tuberculosis" or "Mycobacterium bovis".

The characteristic morphological element is the tuberculous granuloma (caseating tubercule). This consists of giant multinucleated cells and (Langhans cells), surrounded by epithelioid cells aggregates, T cell lymphocytes and fibroblasts. Granulomatous tubercules eventually develop central caseous necrosis and tend to become confluent, replacing the lymphoid tissue.

Tuberculous gumma (also known as a "metastatic tuberculous abscess" and "metastatic tuberculous ulcer") is a cutaneous condition characterized histologically by massive necrosis. Restated, this is a skin condition that results from hematogenous dissemination of mycobacteria from a primary focus, resulting in firm, nontender erythematous nodules that soften, ulcerate, and form sinuses.

Symptoms of peritoneal mesothelioma include weight loss and abdominal pain and swelling due to a buildup of fluid in the abdomen. Other symptoms of peritoneal mesothelioma may include bowel obstruction, blood clotting abnormalities, anemia, and fever. If the cancer has spread beyond the mesothelium to other parts of the body, symptoms may include pain, trouble swallowing, or swelling of the neck or face.

Rasmussen's aneurysm is a pulmonary artery aneurysm adjacent or within a tuberculous cavity. It occurs in up to 5% of patients with such lesions. It may lead to rupture and haemorrhage. It is named after Fritz Valdemar Rasmussen. It is quoted as the cause of hemoptysis in tuberculosis patients.

While the "classic" terminology relates the lesion to cavitary tuberculosis, the term is now used for the anatomic aneurysm associated with other destructive lung lesions. Even when the pulmonary aneurysm is present, the actual bronchial bleeding may be from the bronchial artery, rather than from the pulmonary artery.

Primary inoculation tuberculosis (also known as "Cutaneous primary complex," "Primary tuberculous complex," and "Tuberculous chancre") is a skin condition that develops at the site of inoculation of tubercle bacilli into a tuberculosis-free individual.

Mycobacterium tuberculosis of the meninges is the cardinal feature and the inflammation is concentrated towards the base of the brain. When the inflammation is in the brain stem subarachnoid area, cranial nerve roots may be affected. The symptoms will mimic those of space-occupying lesions.

Blood-borne spread certainly occurs, presumably by crossing the blood–brain barrier; but a proportion of patients may get TB meningitis from rupture of a cortical focus in the brain; an even smaller proportion get it from rupture of a bony focus in the spine.

Chronic diarrhea is almost always seen with lymphangiectasia, but most other signs are linked to low blood protein levels (hypoproteinemia), which causes low oncotic pressure. These signs include ascites, pleural effusion, and edema of the limbs and trunk. Weight loss is seen with long-term disease.

Scrofuloderma (also known as "Tuberculosis cutis colliquativa") is a skin condition caused by tuberculous involvement of the skin by direct extension, usually from underlying tuberculous lymphadenitis.

Pott disease or Pott's disease is a form of tuberculosis that occurs outside the lungs whereby disease is seen in the vertebrae. Tuberculosis can affect several tissues outside the lungs including the spine, a kind of tuberculous arthritis of the intervertebral joints. The disease is named after Percivall Pott (1714–1788), a British surgeon. The lower thoracic and upper lumbar vertebrae are the areas of the spine most often affected. The formal name for the disease is tuberculous spondylitis and it is most commonly localized in the thoracic portion of the spine.

Pott’s disease results from haematogenous spread of tuberculosis from other sites, often the lungs. The infection then spreads from two adjacent vertebrae into the adjoining intervertebral disc space. If only one vertebra is affected, the disc is normal, but if two are involved, the disc, which is avascular, cannot receive nutrients and collapses. In a process called caseous necrosis the disc tissue dies leading to vertebral narrowing and eventually to vertebral collapse and spinal damage. A dry soft tissue mass often forms and superinfection is rare.

Many lymphoceles are asymptomatic. Larger lymphoceles may cause symptoms related to compression of adjacent structures leading to lower abdominal pain, abdominal fullness, constipation, urinary frequency, and edema of the genitals and/or legs. Serious sequelae could develop and include infection of the lymphocele, obstruction and infection of the urinary tract, intestinal obstruction, venous thrombosis, pulmonary embolism, chylous ascites and lymphatic fistula formation.

On clinical examination the skin may be reddened and swollen and a mass felt. Ultrasonography or CT scan will help to establish a diagnosis.

Other fluid collections to be considered in the differential diagnosis are urinoma, seroma, hematoma, as well as collections of pus. Also, when lower limb edema is present, venous thrombosis needs to be considered.

Lymphadenopathy of the axillary lymph nodes can be defined as solid nodes measuring more than 15 mm without fatty hilum. Axillary lymph nodes may be normal up to 30 mm if consisting largely of fat.