Non-pulmonary forms of tuberculosis – this term is conditional. It has taken root from the term showing a primary non-pulmonary affection of other organs – lymphatic system, kidneys, bones and joints, skin, genitalia, eye etc. Such affects can start during primary infection or at secondary tuberculosis. The development of any clinically isolated focus is based on the background of earlier general tubercular dissemination. As a rule, at primary dissemination the spread of an infection takes place simultaneously in all systems and organs, but sometimes dissemination gets character of repeated disseminations that entails chronic, long course of the disease and repeated occurrence of the affected focuses.
The reasons of the occurence of combined forms of tuberculosis among humans are not the same. There are many factors that are influencing the occurrence of this disease: massive and virulent infection, immuno-biological condition of a host, provoking factors of dissemination start, age, concomitant diseases
Tuberculosis of other organs rare – for example, liver, spleen, adrenal glands, heart muscle, pericarditis, poliserositis, etc.
Tuberculosis of meninges and central nervous system (CNS).
Tuberculosis of meninges and central nervous system (CNS) starts when MBT spread by the heamatogenous way and eventually reach nervous tissue bursting into the space surrounding the brain or spinal cord and causing meningitis. On the other hand, it may produce local reaction, which forms a tuberculoma in the brain. The younger the child the greater the risk and the more difficult it is to make the diagnosis.
Pathogenesis.
In the course of spread of the primary tuberculous focus, or as part of miliary tuberculosis spread, tiny tubercles are seeded into the brain and meninges. Occasionally they may also be seeded into the bones of the skull or the vertebrae. These tubercles may cause:
- inflammation of the meninges;
- formation of a grey jelly-like mass at the base of brain, and
- inflammation and narrowing of the arteries leading to the brain which may cause local brain damage.
These three processes cause the clinical picture of tuberculous meningitis. The most expressed path-morpholgical changes are found at the base of the brain (chiasma of optic nerves, hypophysis) in ependyma of vesicles, choroidal tissues. The other parts of nervous system – frontal lobes, Fissure of Sylvius, brain stem, spinal cord are also damaged. The proliferative reaction is usually expressed as the miliary tubercles, consisting of congestion of epithelial, plasmatic and lymphoid cells. In pathological process not only meninges and spinal cord membranes are involves but also vessels are included. All layers of wall of vessels are damaged, but to the greatest degree – the intima. These changes are considered by pathologists as display of hyperallergic inflammation. So, in the brain at tubercular meningitis the membranes and vessels are damaged first. The parenchyma of the brain in tuberculosis process participates in considerably smaller degree. The focuses of the specific inflammation are found out basically around the injured vessels in the cerebral cortex, subcortex, spinal cord.
Meningitis more often spread among children, especially at the early age, and much less often among adults.
Tuberculous meningitis among children occurs when a tuberculoma in the brain leaks or ruptures, living or dead bacilli escape into the surrounding space and around the base of the brain. There is a meningeal reaction and the blood vessels of the brain base become involved. Tuberculous meningitis often complicates into miliary, so that a chest X-ray can be helpful which may reveals military lung tuberculosis.
Clinical signs of the tubercular meningitis.
The tubercular meningitis develops gradually: headache, dizziness, nausea, sometimes vomiting, fever (subfebrile, less often – high temperature) appear firstly. Cases of development of illness are however known at normal temperature. Examination of the retina with an ophthalmoscope is useful. The diagnostic evidence is the presence of choroidal tubercles is diagnostic. There is usually a history of general illness for 2-8 weeks – malaise, tiredness, irritability, changes in behavior, loss of appetite, loss of weight and mild fever. Prodromal period of the tubercular meningitis ends with picture of full-scale clinical symptoms. At the patients with tubercular meningitis body temperature steadfastly raises up to 38-40 C.
The persistent on intensity headache, vomiting accrues. Meningeal symptoms develop: neck stiffness, Kernig’s symptom. At the patients adynamia and mental confusion occur. An inflammation of the brain base meninges causes paresis of the central type of the VII, IX, X, XII of cranial nerves pairs. Manifestations depending on localization of inflammative tubercular process.
- Inflammation of the meninges, there will be headaches, vomiting and neck stiffness.
- The serous exudates involving the base of the brain appear irritation of the cranial nerves giving some of the expected signs: deterioration of vision, paralysis of an eyelid, squint, unequal pupils, and deafness. Papilloedema is present in 40 per cent of patients.
- Involvement of the arteries to the brain can lead to fits, aphasia or weakness in a limb or limbs. Due to this occurence any area of the brain may be damaged.
- At hydrocaphaly Some degree the blocking by exudates of some of the cerebrospinal fluid connections within the brain. Hydrocephalus is the main reason for the loss of consciousness. Pathological manifestations may be permanent and probably accounts for the bad prognosis in patients who are unconscious.
- Spinal block by exudates may cause upper motor neuron weakness or paralysis of the legs.
As tuberculous disease can be found elsewhere in the body, then during inspection it is important to pay attention to the following:
- tuberculosis of the lymph nodes;
- X-ray evidence of lung disease especially miliary tuberculosis;
- enlargement of liver and/or spleen
- (choroidal) tubercles visible on examination of the retina.
The tuberculin test may be negative, especially in the advanced stages of the disease.
Diagnosis.
The main differential diagnosis to be distinguished are bacterial meningitis, viral meningitis, and HIV-related cryptococcal meningitis. In the first two of these the onset is much more acute. Cryptococcal meningitis may have a much slower onset. A family history of tuberculosis, or the finding of tuberculosis somewhere else in the body, makes tuberculosis much more likely. But the best evidence comes from examination of the cerebrospinal fluid (CSF) obtained by lumbar puncture.
The diagnostic cerebrospinal puncture:
- Pressure of CSF usually increases (the cerebrospinal fluid discharges by rapid drops or stream.
- Appearance: the CSF, at first, looks clear but may form a ‘spider’s web clot on standing. May be yellowish if there is spinal block.
- Cells: 200-800 per mm3 (norm 3-5). Lymphocites prevail.
- Glucose: low in 90 per cent of patients, but may be normal in the early stage of the disease or in AIDS. This is very helpful in differentiating from viral meningitis in which the glucose is normal.
- Increased protein content up to 6-10 g/l and higher.
- Bacteriology: smear positive only in 10 per cent unless large volume (10-12 ml) centrifuged long and hard. Culture examination should be carried out if possible. It is usually positive. But this procedure is to late confirmation of the diagnosis.
Treatment.
If there is suspicion of tuberculous meningitis, it is urgently necessary to send the patient to a hospital.
Prognosis:
Death is certain if the disease is untreated: the earlier it is diagnosed and treated, the more likely the patient recovers without serious permanent damage. The clearer the state of consciousness when treatment has started, the better the prognosis. If the patient is comatose the prognosis for complete recovery is poor. Unfortunately 10-30 per cent of survivors are left with some damage.