Tuberculosis may infect any part of the body, but most commonly occurs in the lungs (known as pulmonary tuberculosis). Extrapulmonary TB occurs when tuberculosis develops outside of the lungs, although extrapulmonary TB may coexist with pulmonary TB.

General signs and symptoms include fever, chills, night sweats, loss of appetite, weight loss, and fatigue. Significant nail clubbing may also occur.

If a tuberculosis infection does become active, it most commonly involves the lungs (in about 90% of cases). Symptoms may include chest pain and a prolonged cough producing sputum. About 25% of people may not have any symptoms (i.e. they remain "asymptomatic"). Occasionally, people may cough up blood in small amounts, and in very rare cases, the infection may erode into the pulmonary artery or a Rasmussen's aneurysm, resulting in massive bleeding. Tuberculosis may become a chronic illness and cause extensive scarring in the upper lobes of the lungs. The upper lung lobes are more frequently affected by tuberculosis than the lower ones. The reason for this difference is not clear. It may be due to either better air flow, or poor lymph drainage within the upper lungs.

A diagnosis of latent tuberculosis (LTB), also called latent tuberculosis infection (LTBI) means a patient is infected with "Mycobacterium tuberculosis", but the patient does not have active tuberculosis. Active tuberculosis can be contagious while latent tuberculosis is not, and it is therefore not possible to get TB from someone with latent tuberculosis. The main risk is that approximately 10% of these patients (5% in the first two years after infection and 0.1% per year thereafter) will go on to develop active tuberculosis. This is particularly true, and there is added risk, in particular situations such as medication that suppresses the immune system or advancing age.

The identification and treatment of people with latent TB is an important part of controlling this disease. Various treatment regimens are in use to treat latent tuberculosis, which generally need to be taken for several months.

Symptoms are similar to tuberculosis (TB), and include fever, fatigue, and weight loss. Pulmonary involvement is similar to TB, while diarrhea and abdominal pain are associated with gastrointestinal involvement.

Urogenital tuberculosis may cause strictures of the ureter, which, however, may heal when infection is treated.

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.

The co-epidemic of tuberculosis (TB) and human immunodeficiency virus (HIV) is one of the major global health challenges in the present time. The World Health Organization (WHO) reports 9.2 million new cases of TB in 2006 of whom 7.7% were HIV-infected. Tuberculosis is the most common contagious infection in HIV-Immunocompromised patients leading to death. These both diseases become dreadful in combination as HIV declines the human immunity while tuberculosis becomes progressive due to defective immune system.This condition becomes more severe in case of multi-drug (MDRTB) and extensively drug resistant TB (XDRTB), which are difficult to treat and contribute to increased mortality. See Multi-drug-resistant tuberculosis. Tuberculosis can occur at any stage of HIV infection. The risk and severity of tuberculosis increases soon after infection with HIV. A study on gold miners of South Africa revealed that the risk of TB was doubled during the first year after HIV seroconversion. Although tuberculosis can be a relatively early manifestation of HIV infection, it is important to note that the risk of tuberculosis progresses as the CD4 cell count decreases along with the progression of HIV infection. The risk of TB generally remains high in HIV-infected patients above the background risk of the general population even with effective immune reconstitution with ART maintaining high CD4 cell counts.

Miliary tuberculosis is a form of tuberculosis that is characterized by a wide dissemination into the human body and by the tiny size of the lesions (1–5 mm). Its name comes from a distinctive pattern seen on a chest radiograph of many tiny spots distributed throughout the lung fields with the appearance similar to millet seeds—thus the term "miliary" tuberculosis. Miliary TB may infect any number of organs, including the lungs, liver, and spleen. Miliary tuberculosis is present in about 2% of all reported cases of tuberculosis and accounts for up to 20% of all extra-pulmonary tuberculosis cases.

The infection may affect the kidneys, ureter and bladder and may cause significant damage to each.

Multi-drug-resistant tuberculosis (MDR-TB) is a form of tuberculosis (TB) infection caused by bacteria that are resistant to treatment with at least two of the most powerful first-line anti-TB medications (drugs), isoniazid and rifampin. Some forms of TB are also resistant to second-line medications, and are called extensively drug-resistant TB (XDR-TB).

Tuberculosis is caused by infection with the bacteria Mycobacterium tuberculosis. Almost one in four people in the world are infected with TB bacteria. Only when the bacteria become active do people become ill with TB. Bacteria become active as a result of anything that can reduce the person’s immunity, such as HIV, advancing age, diabetes or other immunocompromising illnesses. TB can usually be treated with a course of four standard, or first-line, anti-TB drugs (i.e., isoniazid, rifampin and any fluoroquinolone).

However, beginning with the first antibiotic treatment for TB in 1943, some strains of the TB bacteria developed resistance to the standard drugs through genetic changes (see mechanisms.) Currently the majority of multidrug-resistant cases of TB are due to one strain of TB bacteria called the Beijing lineage. This process accelerates if incorrect or inadequate treatments are used, leading to the development and spread of multidrug-resistant TB (MDR-TB). Incorrect or inadequate treatment may be due to use of the wrong medications, use of only one medication (standard treatment is at least two drugs), not taking medication consistently or for the full treatment period (treatment is required for several months). Treatment of MDR-TB requires second-line drugs (i.e., fluoroquinolones, aminoglycosides, and others), which in general are less effective, more toxic and much more expensive than first-line drugs. Treatment schedules for MDR-TB involving fluoroquinolones and aminoglycosides can run for 2 years, compared to the 6 months of first-line drug treatment, and cost over $100,000 USD.If these second-line drugs are prescribed or taken incorrectly, further resistance can develop leading to XDR-TB.

Resistant strains of TB are already present in the population, so MDR-TB can be directly transmitted from an infected person to an uninfected person. In this case a previously untreated person develops a new case of MDR-TB. This is known as primary MDR-TB, and is responsible for up to 75% of cases. Acquired MDR-TB develops when a person with a non-resistant strain of TB is treated inadequately, resulting in the development of antibiotic resistance in the TB bacteria infecting them. These people can in turn infect other people with MDR-TB.

MDR-TB caused an estimated 480,000 new TB cases and 250,000 deaths in 2015. MDR-TB accounts for 3.3% of all new TB cases worldwide. Resistant forms of TB bacteria, either MDR-TB or rifampin-resistant TB, cause 3.9% of new TB cases and 21% of previously treated TB cases. Globally, most MDR-TB cases occur in South America, Southern Africa, India, China, and the former Soviet Union.

Treatment of MDR-TB requires treatment with second-line drugs, usually four or more anti-TB drugs for a minimum of 6 months, and possibly extending for 18–24 months if rifampin resistance has been identified in the specific strain of TB with which the patient has been infected. Under ideal program conditions, MDR-TB cure rates can approach 70%.

"Mycobacterium avium-intracellulare" infection (MAI) is an atypical mycobacterial infection, i.e. one with nontuberculous mycobacteria or NTM, caused by "Mycobacterium avium" complex ("MAC"), which is made of three mycobacteria species, "M. avium", "M. intracellulare", and "M. chimaera". This infection causes respiratory illness in birds, pigs, and humans, especially in immunocompromised people. In the later stages of AIDS it can be very severe. It usually first presents as a persistent cough. It is typically treated with a series of three antibiotics for a period of at least six months.

"M. avium", "M. intracellulare", and "M. chimaera" are each saprotrophic organisms present in soil and water; entry into hosts is usually via the gastrointestinal tract, but also can be via the lungs.

MAC infections can cause fevers, diarrhea, malabsorption, as well as loss of appetite and weight loss, and can disseminate to the bone marrow. Therapy for MAI is typically resistant to standard mycobacterial therapies.

Totally drug-resistant tuberculosis (TDR-TB) is a generic term for tuberculosis strains that are resistant to a wider range of drugs than strains classified as extensively drug-resistant tuberculosis. TDR-TB has been identified in three countries; India, Iran, and Italy. The emergence of TDR-TB has been documented in four major publications. However, it is not yet recognised by the World Health Organization.

TDR-TB has resulted from further mutations within the bacterial genome to confer resistance, beyond those seen in XDR- and MDR-TB. Development of resistance is associated with poor management of cases. Drug resistance testing occurs in only 9% of TB cases worldwide. Without testing to determine drug resistance profiles, MDR- or XDR-TB patients may develop resistance to additional drugs. TDR-TB is relatively poorly documented, as many countries do not test patient samples against a broad enough range of drugs to diagnose such a comprehensive array of resistance. The United Nations' Special Programme for Research and Training in Tropical Diseases has set up a TDR Tuberculosis Specimen Bank to archive specimens of TDR-TB.

Vietnamese tuberculosis refers to certain forms of chronic melioidosis that look clinically very similar to tuberculosis. It is derived from the clinical appearance of the disease in American soldiers returning from the Vietnam War.

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.

In humans, "Erysipelothrix rhusiopathiae" infections most commonly present in a mild cutaneous form known as erysipeloid or fish poisoning. "E. rhusiopathiae" can cause an indolent cellulitis, more commonly in individuals who handle fish and raw meat. It gains entry typically by abrasions in the hand. Bacteremia and endocarditis are uncommon but serious sequelae. Due to the rarity of reported human cases, "E. rhusiopathiae" infections are frequently misidentified at presentation.

Fish infected with typical BCWD have lesions on the skin and fins. Fins may appear dark, torn, split, ragged, frayed and may even be lost completely. Affected fish are often lethargic and stop feeding. Infection may spread systemically. Salmonid fish can also get a chronic form of BCWD following recovery from typical BCWD. It is characterised by erratic “corkscrew” swimming, blackened tails and spinal deformities.

In rainbow trout fry syndrome, acute disease with high mortality rates occurs. Infected fish may show signs of lethargy, inappetance and exopthalmos before death.

A presumptive diagnosis can be made based on the history, clinical signs, pattern of mortality and water temperature, especially if there is a history of the disease in the area. The organism can be cultured for definitive diagnosis. Alternatively, histology should show periostitis, osteitis, meningitis and ganglioneuritis.

Infection can cause subcutaneous haemorrhage that presents as reddening of the throat, mouth, gill tips, and fins, and eventual erosion of the jaw and palate. Hemorrhaging also occurs on internal organs, and in the later stages of the disease, the abdomen becomes filled with a yellow fluid - giving the fish a "pot-bellied" appearance. The fish often demonstrate abnormal behavior and anorexia. Mortality rates can be high.

A presumptive diagnosis can be made based in the history and clinical signs, but definitive diagnosis requires bacterial culture and serological testing such as ELISA and latex agglutination.

The infection in most instances presents as a painless lump just under the skin. In southern Australia, the presentation is more often as a pimple in the skin (dermis) rather than under it. The infection is mostly in the limbs, most often in exposed areas, but not on the hands or feet. In children, all areas may be involved, including the face or abdomen. A more severe form of infection produces diffuse swelling of a limb, which, unlike the papule or nodule, can be painful and accompanied by fever. Infection may frequently follow physical trauma, often minor trauma such as a small scratch.

Bacterial cold water disease (BCWD) is a bacterial disease of salmonid fish. It is caused by "Flavobacterium psychrophilum" (previously classified in the genus "Cytophaga"), a gram-negative rod-shaped bacterium of the family Flavobacteriaceae. The disease typically occurs at temperatures below 13⁰C, and it can be seen in any area with water temperatures consistently below 15⁰C. Salmon are the most commonly affected species. This disease is not zoonotic.

Asymptomatic carrier fish and contaminated water provide reservoirs for disease. Transmission is mainly horizontal, but vertical transmission can also occur.

BCWD may be referred to by a number of other names including cold water disease, peduncle disease, fit rot, tail rot and rainbow trout fry mortality syndrome.

Some fish species serve as vectors for the disease and have subsequently spread the pathogen to other parts of the world. An example is the fathead minnow ("Pimephales promelas") which is responsible for the spread of redmouth disease to trout in Europe. Other vectors include the goldfish ("Carassius auratus"), Atlantic and Pacific salmon ("Salmo salar"), the emerald shiner ("Notropis atherinoides"), and farmed whitefish ("Coregonus" spp.). Infections have also occurred in farmed turbot ("Scophthalmus maximus"), seabass ("Dicentrarchus labrax"), and seabream ("Sparus auratus"). It can now be found in North and South America, Africa, Asia, and Australia, as well as Europe.

Buruli ulcer is an infectious disease caused by "Mycobacterium ulcerans". The early stage of the infection is characterised by a painless nodule or area of swelling. This nodule can turn into an ulcer. The ulcer may be larger inside than at the surface of the skin, and can be surrounded by swelling. As the disease worsens, bone can be infected. Buruli ulcers most commonly affect the arms or legs; fever is uncommon.

"M. ulcerans" releases a toxin known as mycolactone, which decreases immune system function and results in tissue death. Bacteria from the same family also cause tuberculosis and leprosy ("M. tuberculosis" and "M. leprae", respectively). How the disease is spread is not known. Sources of water may be involved in the spread. As of 2013 there is no effective vaccine.

If people are treated early, antibiotics for eight weeks are effective in 80%. The treatment often includes the medications rifampicin and streptomycin. Clarithromycin or moxifloxacin are sometimes used instead of streptomycin. Other treatments may include cutting out the ulcer. After the infection heals, the area typically has a scar.

In 2015 about 2,000 cases were reported. Buruli ulcers occur most commonly in rural sub-Saharan Africa especially Cote d'Ivoire, but can also occur in Asia, the Western Pacific and the Americas. Children are most commonly infected. Cases have occurred in more than 32 countries. The disease also occurs in a number of animals other than humans. Albert Ruskin Cook was the first to describe buruli ulcers in 1897. It is classified as a neglected tropical disease.

A study conducted on 452 patients revealed that the genotype responsible for higher IL-10 expression makes HIV infected people more susceptible to tuberculosis infection. Another study on HIV-TB co-infected patients also concluded that higher level of IL-10 and IL-22 makes TB patient more susceptible to Immune reconstitution inflammatory syndrome (IRIS). It is also seen that HIV co-infection with tuberculosis also reduces concentration of immunopathogenic matrix metalloproteinase (MMPs) leading to reduced inflammatory immunopathology.

The treatment of choice is a single dose of benzathine benzylpenicillin given by intramuscular injection, or a five-day to one-week course of either oral penicillin or intramuscular procaine benzylpenicillin. Erythromycin or doxycycline may be given instead to people who are allergic to penicillin. "E. rhusiopathiae" is intrinsically resistant to vancomycin.

By the time a disorder reaches the point of causing dropsy, it can often be fatal and at the very least the fish is very ill and requires immediate quarantine and treatment.

An infection will usually first manifest in fish by causing frayed and ragged fins. This is followed by the appearance of ulcerations on the skin, and subsequent epidermal loss, identifiable as white or cloudy, fungus-like patches – particularly on the gill filaments. Mucus often also accumulates on the gills, head and dorsal regions. Gills will change colour, either becoming light or dark brown, and may also manifest necrosis. Fish will breathe rapidly and laboriously as a sign of gill damage. Anorexia and lethargy are common, as are mortalities, especially in young fish.