Diagnosis: Tuberculosis (Latent to Miliary))

Latent Tuberculosis Infection (LTBI)

This are people that has a small amount of TB bacteria in his/her body that are alive, but inactive. The process of LTBI begins when extracellular bacilli are ingested by macrophages and presented to other white blood cells. This triggers the immune response in which white blood cells kill or encapsulate most of the bacilli, leading to the formation of a granuloma. In some people, the tubercle bacilli overcome the immune system and multiply, resulting in progression from LTBI to TB disease.

Coinfection with human immunodeficiency virus is the most notable cause for progression to active disease, other factors, such as uncontrolled diabetes mellitus, sepsis, renal failure, malnutrition, smoking, chemotherapy, organ transplantation, and long-term corticosteroid usage, that can trigger reactivation of a remote infection are more common in the critical care setting.

Miliary tuberculosis

A fatal form of extrapulmonary tuberculosis is infection of the bloodstream by mycobacteria; this form of the disease is called disseminated or miliary tuberculosis. Miliary tuberculosis pro-gresses rapidly and can be difficult to diagnose because of its systemic and nonspecific signs and symp-toms, such as fever, weight loss, and weakness. Lymphatic tuberculosis is the most common extrapulmonary tuberculosis, and cervical adenopa-thy occurs most often. Other possi-ble locations include bones, joints, pleura, and genitourinary system

Pathogenesis:

TB arthritis- Musculoskeletal involvement with tuberculosis is relatively uncommon, representing approximately 1% to 3% of all cases. Tuberculosis bone and joint involvement (9%) is reported to be the fifth most common extra pulmonary location, following lymphatic (27%), pleural (21%), genitourinary (16%), and miliary (10%) locations. Musculoskeletal tuberculosis involves the spine in approximately one-half of patients. Sites more frequently affected are peripheral joints, followed by extra spinal tuberculosis osteomyelitis.

Because synovial tissue has no limiting basement plate, bacterial organisms quickly gain access to the synovial fluid characteristically creating acute-onset, and purulent joint inflammation.Acute septic arthritis usually presents with the abrupt onset of a single hot, swollen and very painful joint. Patients with septic arthritis typically present with a 1-2 week history of malaise, erythema, swelling, tenderness and a decreased range of motion of a single joint, although these symptoms may not always be present . The onset of fever in most cases is mild, with only 30%-40% of individuals having temperatures >39ºC.

Symptoms: Typical symptoms consist of slowly progressive joint pain, swelling and loss of function that progresses over weeks to months, rather than days. Constitutional symptoms, fever, and weight loss occur in about 30% of cases . A single joint is usually involved, but multiple lesions can occur.

Labs- In septic arthritis, SF usually has a turbid appearance with a WBC >50,000/mm

Loss of apetite- Anorexia

It is likely that several biological mechanisms, including the anorexia of in-fection, are contributing to wasting. Inflammatory cytokines are principal candidates as mediator of the metabolic changes resulting in tuberculosis-associatedwasting. Inflam-matory cytokines trigger the host’s acute phase response and possibly also the anorexia during infections.

Leptin concentrations may be low as a result of low body fat in tuberculosis or high as a result of the host inflammatory response. High leptin concentrations in tuberculosis patients could suppress appetite and food intake, which could be one of the contributing factors of weight loss and wasting. Low leptin concentrations may suppress immunity and worsen disease outcome.

Fever

Upon settlement in the alveolar space, after passes through the cough reflex and mucociliary clearence, mycobacterium tuberculosis (MTB) will initiate an immidiate acute inflammatory response. Detected foreign particle by macrophage through its distinctive mannose capped glycolipid, macrophage will start to engulf the MTB. Consequent to that, IL-1 will be released as soon as possible to stimulate the thermostat of the brain at the Organum Vasculasum of Lamina Terminalis (OVLT) to increase the level of body temperature with a hope to fight against the foreign particles. Through increasing the body temperature, iron serum level will drop significantly this will immobilize bacterial growth as most bacteria need iron for replication. Therefore, at the early stage of pulmonary TB, patient is presented with intermittent on and off low grade fever.

Calcified paratracheal lymph nodes

A lymph node that is "paratracheal" means that it is next to the trachea (the main windpipe). Lymph nodes in the chest commonly become enlarged due to previous chest infections. If lymph nodes remain enlarged for a long time, they can get calcium in them. Although lymph nodes can also become enlarged due to cancer, cancer does not cause calcium to be deposited in the lymph nodes. Therefore, if the lymph node contains calcium throughout the entire node, it is due to previous infection and not cancer.

The most common infections that cause lymph nodes to become enlarged are histoplasmosis (if you have traveled to or live in the Midwestern or Southern United States) and tuberculosis. We normally do nothing with calcified lymph nodes from histoplasmosis and these nodes rarely cause symptoms. It is

generally a good idea to get a tuberculosis test to be sure that the calcified lymph node is not from previous TB since that would necessitate treatment.

Bronchiectasis

Bronchiectasis may develop in any segment damaged by progressive caseating pneumonia. It develops as a result of tuberculous involvement of the bronchial wall and subsequent fibrosis. Although bronchiectasis in postprimary tuberculosis can be a result of cicatricial bronchostenosis. The symptoms of bronchiectasis are overshadowed and are usually regarded as part of the symptoms of tuberculosis.

Atelectasis

In chronic pulmonary infections, especially tuberculosis, the tendency of atelectasis is to remain permanent, with the consequent formation of a fibrotic lung. Cicatrization atelectasis is a common finding after postprimary tuberculosis. Up to 40% of patients with postprimary tuberculosis have a marked fibrotic response, which manifests as atelectasis of the upper lobe, retraction of the hilum, compensatory lower lobe hyperinflation, and mediastinal shift toward the fibrotic lung.

Hypercalcemia

Hypercalcemia manifests as polyuria, polydipsia, vomiting, dehydration, constipation and mental obtundation in absence of CNS disease. Regarding the mechanism of hypercalcemia, there is evidence that extra renal I-alpha hydroxylation of 25 hydroxy cholcalciferol to 1,25 dihydroxycholecalciferol (vitamin D) brought about by macrophages plays an important role in causing hypercalcemia in tuberculous patients. This enzyme (I-alpha hydroxylase) is under negative feedback control in normal tissues. However in granulomatous disorders (including TB), normal feedback inhibition is abolished, probably by the effects of interferon gamma.

Aspergilloma

Approximately 25%–55% of patients with aspergilloma have a history of chronic cavitary tuberculosis. The prevalence of aspergilloma associated with chronic tuberculosis has been reported to be 11% . Aspergilloma may exist for years without symptoms. It is usually located within a cavity or ectatic bronchus and consists of masses of fungal hyphae admixed with mucus and cellular debris

Dosoriented (Possible tuberculous meningitis)