Miliary tuberculosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Synonyms and keywords: Tuberculosis – disseminated; disseminated tuberculosis; disseminated TB; extrapulmonary tuberculosis

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Overview

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 X-ray 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. It is a complication of 1-3% of all TB cases.

Pathophysiology

Tuberculosis (TB) infection can develop after inhaling droplets sprayed into the air from a cough or sneeze by someone infected with the Mycobacterium tuberculosis bacteria. Small areas of infection, called granulomas (granular tumors), develop in the lungs.

Causes

Disseminated TB develops in the small number of infected people whose immune systems do not successfully contain the primary infection. It can occur within weeks of the primary infection. Sometimes, it does not occur until years after you become infected. Chances of having miliary tuberculosis is high if the immune system is weakened due to disease (such as AIDS) or certain medications. Infants and the elderly are also at higher risk.

Diagnosis

Symptoms

A patient with miliary tuberculosis will tend to present with non-specific signs such as low grade fever, cough, and generalized lymphadenopathy. Miliary tuberculosis can also present with hepatomegaly (40% of cases), splenomegaly (15%), pancreatitis (<5%), and multiorgan dysfunction with adrenal insufficiency.

Treatment

Secondary Prevention

TB is a preventable disease, even in those who have been exposed to an infected person. Skin testing for TB is used in high risk populations or in people who may have been exposed to TB, such as health care workers.

References

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Historical Perspective

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References

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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Overview

Tuberculosis (TB) infection can develop after inhaling droplets sprayed into the air from a cough or sneeze by someone infected with the Mycobacterium tuberculosis bacteria. Small areas of infection, called granulomas (granular tumors), develop in the lungs.

Pathophysiology

The usual site of TB is the lungs, but other organs can be involved. In the U.S., most people with primary tuberculous get better and have no further evidence of disease. Disseminated TB develops in the small number of infected people whose immune systems do not successfully contain the primary infection.

Disseminated disease can occur within weeks of the primary infection. Sometimes, it does not occur until years after you become infected. You are more likely to get this type of TB if you have a weaken immune system due to disease (such as AIDS) or certain medications. Infants and the elderly are also at higher risk.

Miliary tuberculosis is a form of tuberculous infection in the lung that is the result of erosion of the infection into a pulmonary vein^[1]. Once the bacteria reach the left side of the heart and enter the systemic circulation, the result may be to seed organs such as the liver and spleen with said infection. Alternately the bacteria may enter the lymph node(s), drain into a systemic vein and eventually reach the right side of the heart^[1]. From the right side of the heart, the bacteria may seed – or re-seed as the case may be – the lungs, causing the eponymous “miliary” appearance.

References

↑ ^1.0 ^1.1 Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 516-522 ISBN 978-1-4160-2973-1

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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Overview

Disseminated TB develops in the small number of infected people whose immune systems do not successfully contain the primary infection. It can occur within weeks of the primary infection. Sometimes, it does not occur until years after you become infected. Chances of having miliary tuberculosis is high if the immune system is weakened due to disease (such as AIDS) or certain medications. Infants and the elderly are also at higher risk.

Medication Causes

BCG vaccine

References

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Differentiating Miliary tuberculosis from other Diseases

Overview

Miliary tuberculosis is more common among immunocompromised patients who are at high risk for other fungal, bacterial, and viral infections.

Differentiating miliary tuberculosis from other diseases

Miliary tuberculosis is more common among immunocompromised patients who are at high risk for other fungal, bacterial, and viral infections. It should be differentiated from the following diseases:

Disease	Differentiating signs and symptoms	Differentiating tests
CNS lymphoma^[1]	Patient is immunocompetent Focal symptoms indicative of a mass lesion Seizure	Single solitary ring enhancing lesion on CT or MRI
Disseminated tuberculosis^[2]	Prior history of residence in an endemic area Chronic cough, weight loss, hemoptysis	PCR of CSF for tuberculosis Mycobacterial culture of CSF Brain biopsy for acid-fast bacilli staining Culture and acid stain positive for acid-fast bacilli CXR shows cavitations
Aspergillosis^[3]	Pulmonary lesions in addition to CNS lesions Symptoms may include cough, chest pain, and hemoptysis	CSF fungal culture, galactomannan
Cryptococcosis	Symptoms include cough, chest pain, and hemoptysis	Cryptococcal antigen from CSF and serum CSF fungal culture
Chagas disease^[4]	History of residence in Central or South America Acute infection is rarely symptomatic Encephalitis or focal brain lesions Myocarditis Chronic infections in immunocompromised patients develop into encephalitis with necrotic brain lesions causing a mass effect	Trypanosoma cruzi in blood, tissue, or CSF, PCR of tissue or body fluids, and serologic tests
CMV infection^[5]	Most common CNS opportunistic infection in AIDS patients Presents with encephalitis, retinitis, progressive myelitis, or polyradiculitis In disseminated disease, it involves both the liver and kidneys	Brain CT/MRI/biopsy: location of lesions is usually near the brain stem or periventricular areas PCR of CSF with detectable virus is diagnostic Brain biopsy with + staining for CMV or evidence of owl’s eyes is also diagnostic, but it is rarely performed because of the location of brain lesions
HSV infection^[6]	Seizures, headache, confusion and/or urinary retention can be seen in disseminated disease, which usually affects only the immunocompromised or acute infections In pregnant women, it may be associated with concurrent genital/oral lesions; can be spread to the neonate during acute infection in the mother, or via viral shedding in the birth canal Neonatal HSV can range from localized skin infections to encephalitis, pneumonitis, and disseminated disease	Brain CT/MRI/biopsy: location of lesions is usually the medial temporal lobe or the orbital surface of the frontal lobe. PCR of CSF with detectable virus is diagnostic
Varicella Zoster infection^[7]	Multifocal involvement has subacute course, usually only in immunosuppressed, with headache, fever, focal deficits, and seizures. Unifocal involvement is more typically seen in immunocompetent hosts, occurring after contralateral cranial nerve herpes zoster, with mental status changes, TIAs, and stroke Disseminated varicella zoster virus can occur in adults during primary infection, presenting with pneumonitis and/or hepatitis Disease is a vasculopathy with hemorrhage and stroke	PCR of CSF with detectable virus is diagnostic
Brain abscess^[8]^[9]	Associated with sinusitis (abutting the sinuses) or with bacteremia Signs and symptoms includes fever and necrotizing brain lesions with mass effect	CSF culture or culture of brain abscess
Progressive multifocal leukoencephalopathy^[10]	Symptoms are often more insidious in onset and progress over months. Symptoms include progressive weakness, poor coordination, with gradual slowing of mental function. Only seen in the immunosuppressed. Rarely associated with fever or other systemic symptoms	PCR of CSF for JC virus Biopsy reveals white matter lesions and not well-circumscribed lesions.

References

↑ Gerstner ER, Batchelor TT (2010). “Primary central nervous system lymphoma”. Arch. Neurol. 67 (3): 291–7. doi:10.1001/archneurol.2010.3. PMID 20212226.
↑ von Reyn CF, Kimambo S, Mtei L, Arbeit RD, Maro I, Bakari M, Matee M, Lahey T, Adams LV, Black W, Mackenzie T, Lyimo J, Tvaroha S, Waddell R, Kreiswirth B, Horsburgh CR, Pallangyo K (2011). “Disseminated tuberculosis in human immunodeficiency virus infection: ineffective immunity, polyclonal disease and high mortality”. Int. J. Tuberc. Lung Dis. 15 (8): 1087–92. doi:10.5588/ijtld.10.0517. PMID 21740673.
↑ Latgé JP (1999). “Aspergillus fumigatus and aspergillosis”. Clin. Microbiol. Rev. 12 (2): 310–50. PMC 88920. PMID 10194462.
↑ Rassi A, Rassi A, Marin-Neto JA (2010). “Chagas disease”. Lancet. 375 (9723): 1388–402. doi:10.1016/S0140-6736(10)60061-X. PMID 20399979.
↑ Emery VC (2001). “Investigation of CMV disease in immunocompromised patients”. J. Clin. Pathol. 54 (2): 84–8. PMC 1731357. PMID 11215290.
↑ Bustamante CI, Wade JC (1991). “Herpes simplex virus infection in the immunocompromised cancer patient”. J. Clin. Oncol. 9 (10): 1903–15. doi:10.1200/JCO.1991.9.10.1903. PMID 1919640.
↑ Hambleton S (2005). “Chickenpox”. Curr. Opin. Infect. Dis. 18 (3): 235–40. PMID 15864101.
↑ Alvis Miranda H, Castellar-Leones SM, Elzain MA, Moscote-Salazar LR (2013). “Brain abscess: Current management”. J Neurosci Rural Pract. 4 (Suppl 1): S67–81. doi:10.4103/0976-3147.116472. PMC 3808066. PMID 24174804.
↑ Patel K, Clifford DB (2014). “Bacterial brain abscess”. Neurohospitalist. 4 (4): 196–204. doi:10.1177/1941874414540684. PMC 4212419. PMID 25360205.
↑ Tan CS, Koralnik IJ (2010). “Progressive multifocal leukoencephalopathy and other disorders caused by JC virus: clinical features and pathogenesis”. Lancet Neurol. 9 (4): 425–37. doi:10.1016/S1474-4422(10)70040-5. PMC 2880524. PMID 20298966.

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Epidemiology and Demographics

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References

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Risk Factors

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Risk Factors

Immuno-compromised condition like AIDS
Immune system deficiencies
Malnutrition

References

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Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Complications

Complications of disseminated TB can include:

Adult respiratory distress syndrome (ARDS)

Liver inflammation

Lung failure

Relapse of the disease

Prognosis

Most forms of disseminated TB respond well to treatment.

References

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Diagnosis

Treatment

Medical Therapy | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case #1

Related Chapters

Tuberculosis

[Robbins-1] 1.0 ^1.1 Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 516-522 ISBN 978-1-4160-2973-1

[pmid20212226-1] Gerstner ER, Batchelor TT (2010). “Primary central nervous system lymphoma”. Arch. Neurol. 67 (3): 291–7. doi:10.1001/archneurol.2010.3. PMID 20212226.

[pmid21740673-2] von Reyn CF, Kimambo S, Mtei L, Arbeit RD, Maro I, Bakari M, Matee M, Lahey T, Adams LV, Black W, Mackenzie T, Lyimo J, Tvaroha S, Waddell R, Kreiswirth B, Horsburgh CR, Pallangyo K (2011). “Disseminated tuberculosis in human immunodeficiency virus infection: ineffective immunity, polyclonal disease and high mortality”. Int. J. Tuberc. Lung Dis. 15 (8): 1087–92. doi:10.5588/ijtld.10.0517. PMID 21740673.

[pmid10194462-3] Latgé JP (1999). “Aspergillus fumigatus and aspergillosis”. Clin. Microbiol. Rev. 12 (2): 310–50. PMC 88920. PMID 10194462.

[pmid20399979-4] Rassi A, Rassi A, Marin-Neto JA (2010). “Chagas disease”. Lancet. 375 (9723): 1388–402. doi:10.1016/S0140-6736(10)60061-X. PMID 20399979.

[pmid11215290-5] Emery VC (2001). “Investigation of CMV disease in immunocompromised patients”. J. Clin. Pathol. 54 (2): 84–8. PMC 1731357. PMID 11215290.

[pmid1919640-6] Bustamante CI, Wade JC (1991). “Herpes simplex virus infection in the immunocompromised cancer patient”. J. Clin. Oncol. 9 (10): 1903–15. doi:10.1200/JCO.1991.9.10.1903. PMID 1919640.

[pmid15864101-7] Hambleton S (2005). “Chickenpox”. Curr. Opin. Infect. Dis. 18 (3): 235–40. PMID 15864101.

[pmid24174804-8] Alvis Miranda H, Castellar-Leones SM, Elzain MA, Moscote-Salazar LR (2013). “Brain abscess: Current management”. J Neurosci Rural Pract. 4 (Suppl 1): S67–81. doi:10.4103/0976-3147.116472. PMC 3808066. PMID 24174804.

[pmid25360205-9] Patel K, Clifford DB (2014). “Bacterial brain abscess”. Neurohospitalist. 4 (4): 196–204. doi:10.1177/1941874414540684. PMC 4212419. PMID 25360205.

[pmid20298966-10] Tan CS, Koralnik IJ (2010). “Progressive multifocal leukoencephalopathy and other disorders caused by JC virus: clinical features and pathogenesis”. Lancet Neurol. 9 (4): 425–37. doi:10.1016/S1474-4422(10)70040-5. PMC 2880524. PMID 20298966.

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Miliary tuberculosis

Overview

Pathophysiology

Causes

Diagnosis

Symptoms

Treatment

Secondary Prevention

References

References

Overview

Pathophysiology

References

Overview

Medication Causes

References

Overview

Differentiating miliary tuberculosis from other diseases

References

References

Risk Factors

References

Complications

Prognosis

References

Diagnosis

Treatment

Case Studies

Related Chapters

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