Первичный туберкулез.

2. Primary TB.
2.1. Motivation
2.2. Definition
2.3. Route and manner of infection
2.4. The lung changes after infection.
2.3.1. Basic types of tissue change
2.3. The lymph nodes at the root of the lung.
2.1. Motivation. TB disease in children under 15 years of age (also called
pediatric tuberculosis) is a public health problem of special significance
because it is a marker for recent transmission of TB. Also of special
significance, infants and young children are more likely than older
children and adults to develop life-threatening forms of TB disease (e.g.,
disseminated TB, TB meningitis). Among children, the greatest numbers
of TB cases are seen in children less than 5 years of age, and in
adolescents older than 10 years of age. BCG, or bacille Calmette-Guerin, is
a vaccine to prevent TB disease. BCG is used in many countries to prevent
childhood TB disease. However, the BCG vaccine is not generally used in
the United States, because of the low risk of infection with TB bacteria and
the variable effectiveness of the vaccine. The BCG vaccine should only be
considered for very select persons who meet specific criteria and in
consultation with a TB doctor.
2.2. Definition. The clinical form of primary tuberculosis, which is
characterized by specific inflammation in lungs (by primary affect), lesion
of intrathoracic lymphatic nodes (lymphadenopathy) and lymphangitis.
Lung localization occurs in 90 %, abdominal – in 10 % of primary
tuberculous complex cases.
2.3. Route and manner of infection. M. tuberculosis is a species of the
genus Mycobacterium, family mycobacteriaceae, order Actinomy-cetales.
The organisms are nonmotile, nonsporulating, aerobic, acid-fast rods.
Growth is slow, the organisms ordinarily not becoming visible for 2 weeks
or more, depending on the size of the inoculum and the medium. Colonies
are opaque, dry, off-white to cream-colored, with a nodular or wrinkled
surface and irregular edges. Optimum growth temperature is 37°C.
Multiplication does not occur at 25° or at 45°C. Ordinary laboratory
media do not support growth, and special substances such as egg,
potato, blood, or albumin are necessary for enrichment. A lipid substance
known as cord factor causes the bacilli to orient themselves parallel to one
another so that growth occurs in the form of serpentine cords, especially
on slide and membrane cultures and in liquid media without wetting
agents. Endogenous catalase is present in all strains except those resistant
to isoniazid. The human tubercle bacillus produces significantly greater
amounts of niacin than any other species of Mycobacterium.
M. tuberculosis is highly pathogenic for guinea pigs but not for rabbits or
chickens. Progressive disease can be produced in mice with the inoculation
of large numbers of bacilli. Many strains highly resistant to isoniazid lose
their pathogenicity for guinea pigs as well as their catalase activity.
In the vast majority of children, infection is acquired by inhaling
airborne infected droplet-nuclei derived from the sputum of an adult with
cavitary pulmonary tuberculosis. The source person need not be sick and
may not even be aware that he is dangerous to others. Most newly acquired
infections are from household contacts, especially in small children
exposed to adults with cavitary disease. Such factors as overcrowding and
an impoverished mode of living have an important effect upon the
infection rate. Numerous reports of "contained" or micro epidemics
tuberculosis support the concept of airborne infection as the chief mode of
transmission.
Tuberculosis organisms may also gain entrance into the body by
direct inoculation through the skin. Ingestion is rarely implicated since
pasteurization of milk and tuberculosis eradication among cattle have
become enforced public health measures. Infection is not transmitted by
fomites or by contact with clothing, bed linens, or personal articles of a
source person, as was once believed. Contaminated materials such as
urine, feces, fluid from draining sinuses, and sputum may serve as sources
of infection unless properly handled and disposed of. Children are often
infected from coughing or spitting adults. When an adult coughs many
small drops of liquid (spit) are forced into the air. If that adult has
tuberculosis in his or her lungs many of the drops carry bacilli. The largest
of the drops fall to the ground. But the smallest, which cannot be seen,
remain in the air and move with it. Out of doors or in well ventilated
rooms the small drops are carried away in the moving air. But in сlosed
rooms, huts or small spaces they remain in the air and increase in number
as the person continues to cough. Everyone sharing the room with the
'cougher' and breathing the same air runs the risk of breathing in tubercle
bacilli (ТВ). Those nearest to the person coughing are most likely to do so.
The danger is greatest when the 'cougher' does not take any care. He
should cover his or her mouth, turn away from the other persons or
children and spit into something which is then covered and kept closed.
So the infectious mother is a danger to her infant or children. Both
parents are dangerous in small living or sleeping spaces. Almost always
when young children are infected the infection comes dangerous in small
living or sleeping spaces. So would be an infectious teacher in the
classroom, an infectious doctor or dentist in the clinic or health center or
an infectious nurse or midwife or health worker in the home or hospital, a
shopkeeper in his shop or a bus driver in his bus. Almost always when
young children are infected the infection comes from a member of the
family group or a near neighbor. When older children are infected and the
immediate family is clear, look for a possible infector in school, in clinic,
in church, in public transport or wherever children come in contact with
adults inside buildings or small spaces. In these situations, the bacteria are
taken into the lungs with the breath and this is much the commonest way
of infection. But it is not the only way.
ТВ can reach children in milk or food and infection can then begin in
the mouth or intestine. Milk can carry bovine ТВ if cows in the area have
tuberculosis and the milk is not boiled before use. When that happens the
primary infection is in the intestine, or sometimes in the tonsils. But
human infection with bovine badly seems to be uncommon in many high
prevalence countries.
Unbroken skin seems to resist ТВ if they fall upon its surface. But if
there has been a recent cut or break ТВ may get in and cause an infection
as they do in the lungs. As might be expected, skin infection is most likely
on exposed surfaces such as the face or legs or feet or less often on the arm
or hand. These primary lesions are not common. But it is easy to forget
that such a lesion may be tuberculous, even when the nearest lymph nodes
are enlarged.
2.4. The lung changes after infection.. The concepts herein
presented have been gleaned in part from animal experimentation and from
the older records of pathologic observations on human autopsy material, to
which have been added more recent data from surgically resected
specimens as presented in die important monographs by Medlar and
Canetti. Aside from studies of pathologic tissues, we largely depend on
observations made on die behavior of pulmonary lesions as seen
roentgenographically for detecting the various patterns of development of
clinical tuberculosis. Newer information on cellular immunity has
provided some insight into the specific mechanisms underlying the tissue
changes subsequently described.
 When the fine drops carrying the bacilli are breathed in they may
cross over defense mechanism of clearance and are carried through the air
passages to just under the surface of the lung. There they remain and the
ТВ slowly multiply in numbers. As that happens some are carried through
the Cohn’s pores into the interstitial tissue to begin travelling along the
lymph vessels to the nearest lymph nodes beside the bronchi. In BCG
vaccinated organism they meet with the place of hypersensitivity
surrounding BCG granulomata and may be broken forming the first
cockpit for struggle between TB and host defences. In well-nourished
children small quantity TB are swallowed by macrophages and
disintegrated without a trace (complete phagocytosis). In other cases the
presence of the bacilli causes a reaction and the defence cells of the body
begin to collect. In about 4-8 weeks there is a small area at the centre of
this process where the host tissues are dead (caseation) and around that
area is an increasing ring of defence cells. About this time most people
become sensitive to tubercle bacilli, as shown by a positive tuberculin skin
test. The changes in the lung and the same changes in the lymph nodes are
together known as the Primary Complex. In the immune body these
changes are small and can’t be recognized with the help of any known
techniques excluding the Mantoux test. From that time the result depends
upon the power of the child to resist the multiplication of the bacilli and
limit the amount of caseation.
That power varies with age, being least in the very young. It also
varies with nutrition. Poor nutrition lowers body defences. Most people
manage, slowly over many months, to heal both the focus in the lung and
that in the lymph nodes. But it takes time and ТВ can remain inactive but
living and capable of multiplication for many years.
The understanding of allergy and immunity in tuberculosis began
with the work of Lurie, followed by development of modern concepts of
delayed hypersensitivity and cellular immunity. The relation between
immunity and delayed hypersensitivity, however, remains controversial
even today. Immunity to tuberculosis may be either natural or acquired,
and it is the latter which is so intimately associated with the development
of allergy.
The former response presumably would be associated with a more
favorable outcome. Canetti has described the effects and histologic sites of
action of immune responses in humans in his quantitative studies on the
occurrence of tubercle bacilli in the various lesions and in the morphologic
patterns of disease as seen in surgically resected lungs and autopsy
specimens. The basic tissue elements thought to be responsible for
immunity are the macrophages, which phagocytize and destroy tubercle
bacilli, and caseation necrosis, in which bacilli are destroyed in large
numbers. There is now little doubt that the macrophages are an important
part of the complexity of chemical mechanisms involved in cellular
immunity to be described later.
More important basically than the places where tubercle bacilli are
destroyed are the mechanisms by which the bacillary destruction is
completed. The effectiveness of these immune mechanisms is influenced
by a number of environmental, hereditary, and developmental factors,
including age (infancy, puberty, and senility are periods of highest disease
ate), race, nutrition, stress, cellular immunodeficiency states, diabetes, and
silicosis. Essential to the patient's recovery is the predominance of immune
forces over tubercle bacilli, despite liquefaction of the caseum and spread
of the disease, so that ultimately the tissues may effectively contain or
preferably destroy bacilli.
From the time of infection bacilli escape into the blood stream and
are carried to other parts of the body. This is more probable in no
vaccinated body. Fortunately disease does not always result. The risk may
be small for any individual child. But in a community where there are
many adults spreading infection many children will become ill because
superinfection.
The Host Immune Response to Tuberculosis.
1) Organism is phagocytosed by macrophage which is not able to destroy
virulent microorganism.
2) In the early phase of primary tuberculosis, (in the unimmunized person),
there's uncontrolled proliferation of bacilli within pulmonary alveolar
macrophages with resulting bactremia and seeding of multiple sites.
3) After 3 weeks of infection, cell mediated immunity develops.
Macrophages process mycobacterial antigen and present it to unstimulated
CD4+Tн0 cells. Under effect of IL-12 secreted by macrophages,
CD4+Tн0 cells mature into CD4+Tн1 cells which secrete IFN-γ.
4)IFN-γ activates macrophages to secrete a group of mediators including:
-1-TNF... causing recruitment of monocytes, their activation,
differentiation to epithelioid cells. It also causes:
a. Increased NO production which generate free radicals able to destroy
the microorganism.
b. Secretion of IL-8 which is chemotactic for lymphocytes and monocytes.
2-IFN-γ.... which helps in
a. Macrophage activation for more phagocytosis, antigen presentation and
microbial killing.
b. Secretion of TGF-β which stimulate fibroblastic proliferation
We must now look at the serious changes which occur when the
infection progresses and the child becomes ill.
Primary tuberculosis complex.
Pathogenesis. After the penetration of MBT into the lungs,
primary lesion (primary affect), of the size from a millet grain to a section
of a lung, is predominantly localized subpleurally in the II, III, VIII, IX
segments. From the primary affect the infection spreads along lymphatic
vessels to intrathoracic lymphatic nodes. However, lymphadenopathy may
also be primary or develop simultaneously with the lung affect.
Pathomorphism. Primary tuberculous complex consists of three
components: primary affect (pneumonitis), lymphadenitis (lesion of
intrathoracic lymphatic node) and lymphangitis (a “path” which joins the
primary affect with lymphadenitis). Specific inflammation spreads to
pleura and causes pleurisy.
The clinic of primary tuberculous complex depends on spreading
pathomorphologic lung changes, intrathoracic lymphatic nodes, as well as
on various complications. There may be asymptomatic, little symptomatic,
pneumonia similar, influenza similar variants of the clinical course of
primary tuberculous complex. However, more often it develops and
proceeds like tuberculous intoxication.
Roentgenologically four phases (stages) of primary tuberculous
complex are discerned: pneumonic (infiltrative), suction (bipolarities),
scarring and calcification (petrification). At preantibacterial period
calcification processes started in a year and lasted for 2-3 years; under
present day antimycobacterial therapy they set in considerably earlier and
rather rarely, because suction and scarring processes prevail.
Complications: pleurisy, lympho-hematogenic dissemination, decay
(primary cavern on the site of lung component), bronchi tuberculosis,
atelectasis of a segment or a particle, caseous pneumonia, primary
tuberculosis with a chronic course, that develops as a result of considerable
complications or inferior treatment.
The diagnostics is based on the anamnesis (contact), tuberculin test
intensity, hyperergic reaction to Mantoux test, availability of intoxication
symptoms and paraspecific reactions, roentgenologic picture (primary
affect, lymphangitis, lymphadenitis), changes of haemogram (little
leucocytosis with an insignificant shift to the left, lymphopenia,
monocytosis, speeded up ESR), MBT are rarely to be found.
The differential diagnostics is performed, first of all, with
pneumonia, eosinophilic infiltration, peripheral or central cancer.
In etiology of segmentation pneumonia anchorwomen the part is
acted by respirator viral infections, adenovirus, rarer they complicate a
measles, whooping-cough, sepsis and other diseases. Segmentation
pneumonias can be and cleanly bacterial (streptococcus, staphylococcus,
caused by the Fridlendera stick, pneumococcus and i.e.).
The protracted flow is usually adopted by sharp segmentation
pneumonia at the children of early age, being often ill the sharp respiratory
diseases, having the hearths of chronic infection in nasopharynx tonsillitis,
adenoiditis) and allergic diseases. Primary tubercular complex at children
in modern terms, thanks to a number of factors cooperate to the rise of
reactivity of child's organism, and also under influencing of intensive
antituberculosis therapy can have the normal flow. In this connection the
protracted segmentation pneumonias and primary tubercular complex can
have a similar clinico-roentgenologic picture. At both diseases look after
small symptoms displays, similar segmentation localization, involving in
the process of intrathoracic lymphatic knots. In this connection distinctive
feature extraction, which it is possible to use for differential diagnostics of
these processes, is a necessity. For diagnostics of primary tubercular
complex it follows to follow next criteria.
The analysis of sensitiveness to the tuberculin in a dynamics at
consumptive allows to set infected, in a number of cases the early period
of infected is determined — «conversion».
At most patients with pneumonia the analysis of sensitiveness to the
tuberculin specifies on a post-vaccine allergy, some patients negatively
react on a tuberculin. However it follows to take into account that in a
number of cases an infected by tuberculosis child can carry the unspecific
protracted bronco-pulmonary process. Exactly at infected by tuberculosis
children careful differential diagnostics for the exception of possibility of
development of tuberculosis must be conducted.

The origin of segmentation and by shares defeats at a child in the

period of conversion of tuberculin reactions in default of preceding
respirator disease testifies to the specific infection rather. At a child with
the protracted segmentation pneumonia, as a rule, in anamnesis are present
pointing on the frequent sharp respiratory diseases. For unspecific
segmentation pneumonia characteristically there is the sharp beginning. In
the clinical picture of sharp period of segmentation pneumonia accordance
is marked between weight of the state, prevalence of process and age of
child. At by shares hyper segmentation processes at the children of early
age the expressed of intoxication syndrome, respiratory symptoms is
looked after, the state of sick children is heavy. For a primary tubercular
complex characteristically there is the gradual beginning of disease, the
symptoms of intoxication and respiratory insufficiency is expressed in less
degree. At the roentgenological determined by shares, segmentation
process of tubercular etiology even at the considerable rise of temperature
of body there is relatively good health of child, he saves activity,
respiratory disorders are expressed insignificantly. At comparison of
clinical displays of primary tubercular complex and pneumonia
predominance of general symptoms at tuberculosis comes to light, while at
pneumonia are more than expressed cough, pains in a thorax, can become
separated from small thick sputum. At the physical inspection at a primary
complex the percussion changes are expressed, they prevail above
auscultation data. At pneumonia the auscultation changes prevail —
different moist wheezes on a background weakened, by the places of
bronchial, breathing. At unspecific processes the polysegmentation defeats
with primary localization in the lower segments of lung are characteristic,
simultaneous combination of defeats of two segments and more than and
the bilateral changes are possible.
At bronchoscopy research of patient with pneumonia widespread,
diffuse, usually bilateral hyperemia of mucous membrane of bronchial
tubes is marked, in the road clearance of them — mucous-festering secret.
In the difficult case for differential diagnostics conduct therapy by the
antibiotics of wide spectrum of action taking into account a bacterial
sensitiveness.
The Fridlender pneumonia. Roentgenologic determine vast,
sometimes plural one- or bilateral focuses of infiltration with the areas of
melting. More frequent the overhead stake of right lung, the volume of
which is multiplied, is struck, an upper border is disposed than due level
(approximately on the width of one intercostal) below, mediastinum is
displaced in an opposite side. Reactive adenitis with the increase of
volume, violation of structure and washed of contours of roots of easy out
accompanies to infiltration. Liquid is looked after also in pleura cavities.
Exudate of crimson color, contains microbes of sort of klebsiella.
Fridlender pneumonia at children meets as small flashes usually. This
heavy form of pneumonia begins usually sharply, the symptoms of
intoxication and respiratory disorders prevail in a clinical picture. For a
clinical picture are characteristic the persistent sickly cough attended with
the separation of sputum with the streaks of blood and smell of old meat.
In diagnostics characteristic disparity of grave common condition with
scanty data of physical inspection and moderate fever is used, ordinary for
this pneumonia thick ate from to look true-festering sputum at the children
of early age after difficultly. In spite of the protracted flow, Fridlender
pneumonia unlike tuberculosis is characterized by dynamic quality of
process with the displays of unfavorable local changes. The rapid forming
of cavities is looked after, elimination of content and partial transformation
of them in thin-walled. A similar rapid dynamics is not incident to primary
tuberculosis. Bilateral reactive adenitis and vascular hyperemia in the vital
organs are not typical also for tuberculosis.
Staphylococcus pneumonias differ by acuteness of flow and
expressed propensity to destruction. Development of disease often takes
place on a background ORVI, is characterized by the sharply expressed
symptoms of intoxication — getting up of temperature of body to the
febrile indexes, the shortness of breath, cough, appears, a child is languid,
pale, renounces a meal, vomiting can appear, sometimes liquid chair.
Staphylococcus pneumonias are characterized by magnitude of defeat,
quite often are accompanied by a festering bronchitis, festering pleurisy,
often there is development of air cavities with the level of liquid, which
from a valvular mechanism in bronchial tubes can achieve considerable
sizes.
Roentgenological staphylococcus pneumonia begins from the
inhomogeneous shading in lights, more frequent in right, with unclear
contours, which is quickly multiplied. The triad of characteristic symptoms
is known: focuses of infiltration, rounded cavities of disintegration, pleura
exudate.
Roentgenologic four phases (stages) of primary tubercular complex
are distinguished: pneumonic (infiltratition), sucction (bipolarity), scarring
and (petrification). In a before antibacterial period the processes of
scarring began through a year and 2-3 years proceeded; at modern
antimycobacterial therapy they come considerably earlier and enough
rarely, because the processes of sucction and scarring prevail.
Roentgenologic primary tubercular pneumonia in the period of active
phase of process is homogeneous, the contours of it were washed out, it
was related to the pathologically changed root by a «path» as unclear
outlined linear of shadows. Inflammatory transformation of lymphatic
ways and intermediate fabric on motion of bronchial tubes, vessels and
lobules is their morphological substratum lumens. Intensity of shade of
primary hearth is different, that is conditioned by not only a size but also
expressed of caseous component of necrosis.
Rupture of focus into the pleural space. We have already seen that the
primary focus forms just below the surface of the lung. Most do not
become larger than 10 mm. Sometimes the focus does get bigger still.
Then the surface of the lung may rupture allowing caseous material and
sometimes bacilli, to leak into the pleural space. The result seems to
depend on the child's nutrition and degree of tuberculin sensitivity. When
nutrition is good and sensitivity is strong much fluid is produced and a
large effusion results. When sensitivity is low in the young or
malnourished child the reaction is much less. The fluid of an effusion is
usually absorbed without difficulty. But occasionally if many bacilli are
present the fluid may become purulent and a tuberculosis empyema is the
result.
Acute cavitation of focus. When resistance is poor as in young or
malnourished children, the primary focus may increase in size. Instead of
leaking into the pleural space it may open into a small bronchus and the
caseous material is discharged by coughing. During this process there may
be a stage when air can enter the small cavity when the patient is breathing
in but cannot escape when he is breathing out. The result is the formation
of a small thin-walled cavity.
This process can speed infection to other parts of the lungs. Spread
may also occur by the erosion of the tuberculous nodes through the
bronchial wall. Caseous material and ТВ from the nodes may then spread
through the bronchi to other parts of the lung.
It may be seen a child who suffocated from caseous material
suddenly blocking both main bronchi. Emergency bronchoscopy, if
available, could save such a child. If this is not available, we suggest
turning the child upside down and percussing the chest with the open hand
to try to help the child to cough up the material and clear the bronchi.
This type of progressive lung disease is particularly likely in
malnourished children. It can proceed so rapidly that the child may die
from tuberculous pneumonia before developing signs of blood spread
disease such as miliary tuberculosis or tuberculous meningitis.
Ring or coin shadowю Very occasionally in older children (and found only
by X-ray examination) a round coin-like lesion can be seen in the lung
field. Sometimes the edge is calcified or a series of zones of calcification
may be seen representing periods of healing and extension. This can
remain unchanged for long periods. It may then completely or partially
calcify.
The lymph nodes at the root of the lung are involved in the
inflammation and demonstrate more or less pronounced changes. Bacilli
from the primary focus reach the lymph nodes by direct drainage. These
nodes lie near to the air passages (bronchi). Both the nodes and the air
passages get larger towards the centre (root) of the lung. The bacilli in the
nodes cause a change which is the same as that in the focus in the lung and
the node becomes larger and may soften.
Tuberculosis of intrathoracic lymphatic nodes.
It is one of the most frequent clinical forms of primary tuberculosis,
that is characterised by specific injury of intrathoracic lymphatic nodes
(lungs root and mediastinum).
Pathogenesis. Infestation generally takes place by the air-droplet-dust
way, through the mucous membrane of tonsils and bronchi MBT penetrate
into lymphatic vessels, nodes, where a specific process develops.
Depending on the state of micro- and macroorganism, infiltrative-
inflammatory or necrotic changes in lymphatic nodes prevail.
Pathomorphism. One or some groups of lymphatic nodes may be
injured at tuberculosis. Paratracheal, tracheobronchial, bronchopulmonary,
bifurcating and other lymphatic nodes are hurt. The process may be uni- or
bilateral, predominantly asymmetric.
According to the character of pathomorphological changes,
hyperplastic and caseous forms of tuberculosis of intrathoracic lymphatic
nodes are discerned. Caseous form is characterized by a severe course and
is harder to treat.
The clinic of uncomplicated tuberculosis of intrathoracic lymphatic
nodes is analogous to that of primary tuberculous complex.
Clinico-roentgenological three forms of tuberculosis of intrathoracic
lymphatic nodes are discerned: “small”, infiltrative and tumors similar,
depending on the morphological substrate, first of all caseous. The “small”
form is characterized by a symptom-free or small symptomatic course. The
peculiarity of infiltrative bronchoadenitis is a small enlargement of
lymphatic nodes with perifocal inflammation in lung tissue, that
roentgenologically is manifested by the root shade dilation, bulging and
obscure contours; clinically – by intoxication symptoms. For
tumoursimilar bronchoadenitis the enlargement of one or some groups of
intrathoracic lymphatic nodes of mediastinum or lungs root with
polycyclic distinct outer contours is characteristic. Signs of intoxication
are more expressed, disposition to a complicated course.
The “small” form of tuberculosis is diagnosed on the basis of indirect
signs of enlargement of intrathoracic lymphatic nodes, in particular, of
local enrichment, deformation of the root lung picture, lowering of the root
shade structure, double contour of the middle shade at a certain level,
disappearance of the shade of the interstitial bronchus.
The course and complications of tuberculosis of intrathoracic
lymphatic nodes are almost analogous to those of primary tuberculous
complex and are connected with a specific affection of lymph nodes with
certain clinical-roengenologic signs: rshematogenic and lymphogenic
dissemination, exudative pleuritis, affection of an adjacent bronchus with
further bronchogenic dissemination or the violation of bronchial
passability and atelectasis.
The diagnostics is made on the basis of anamnesis, clinico-
roentgenologic picture in the period of intensity of tuberculin reaction,
laboratory, bacteriological and instrumental examination.
The differential diagnostics is made with sarcoidosis (I phase),
lymphogranulomatosis, lymphosarcoma, lympholeucolysis, central cancer,
unspecific adenopathies. For this the following procedures are performed:
roentgenograpgy in right and lateral projections, tomography on
bifurcation level (middle microscopic section), tuberculin tests,
bronchoscopy as well as punctured or operative biopsy.
Tumular bronhoadenit with the vast caseous changes in a few groups
of inrtathoracyc knots flows protractedly, saving activity. The phenomena
of infiltration diminish gradually. In place of expressed caseous can be
formed large calcification. Massive caseous bronchoadenitis can acquire
the protracted flow. Presently slowly current bronhoadenitis meet
infrequently. For slowly current bronhoadenitis are characteristic
undulating flow, expressed of symptoms of intoxication, increasing in the
period of intensification, and the expressed complications. Under
influencing of course of antytuberculosis therapy, in spite of duration of
flow, it is succeeded to obtain clinical recovery.
At differential diagnostics you should take into account the
roentgenoanatomic structure of mediastinum. Being part of pectoral cavity,
mediastinum at the front is limited by the back wall of breastbone and
costal cartilages, behind — by a vertebral post, from sides — by the
medium sheets of pleura, down — by a diaphragm, from above — by the
aperture of thorax.
 It’s useful the determination of localization of process. Expediently
to use a chart, in obedience to which by the frontal planes conducted on
the front and back walls of trachea, mediastinum divides by three
departments — front, back and middle.
Hyperplasia of thymus, thymoma. It meets in pectoral and early
child's age. Under the term of « thymoma» all types of tumors and cysts of
this gland are united. In considerable part of cases of defeat of thymus
flow asymptomatically. At development of tumor process there are the
clinical displays — symptoms of pressure on neighbor organs, and also
symptoms of hormonal activity. On X-ray thymoma is represented as
expansion of mediastimun from one or both sides. More frequent she is
disposed asymmetric. It’s favorite localization overhead and middle
departments of front mediastinum. On the sciagram of thymoma, it is
traced from the level of collar-bone, fills retrosternal space and, narrowing
down, depending on a size, can extend to the diaphragm. Shade is
homogeneous, has sharp, slightly protuberant in the sides of pulmonary
fabric contour. At displacement of megascopic stakes in one side extended
mediastinum has a bicyclic character. Sizes and form is knotty the
transformed stakes of forks gland, at the same time, vary widely. Specify
on the possible waviness of contours pear-shaped form, and also on the
inclusions of calcium salts. It creates likeness with large of intrathoracic
lymphatic knots.
The dermoid cysts and teratoma are also localized in front
mediactinum. The dermoid cysts are the vices of embryonic development
— derivative ectoderm; according to it in them such elements are found,
how a skin, hairs, sweat and greasy glands, is. Teratoma shows the
elements of all three embryonic sheets — ecto-, mezo- and entodermy;
skin with its appendages, muscles, nervous and bone fabric and even
elements of separate organs — teeth, jaws and etc. Dermoid cysts and
teratoma clinically, as a rule, show up nothing; usually they are exposed at
roentgenologic research. The clinical displays rely on sizes and direction
of growth. At localization of cyst in front mediastinum (in 30% cases)
more frequent a compression syndrome is looked after. Typical
localization of teratoma — middle department of front mediastinum. The
dermoid cysts differ by very slow growth. In youth age their growth
increases. Growth acceleration of cyst in the period of pregnancy,
pubescence is sometimes marked, after a trauma or infection.
Roentgenologic asymmetric expansion of mediastinum is determined.
The form of teratodermoid cysts is more frequent oval or half-round,
contours are sharp, sometimes wavy. Surrounding fabric at the small sizes
of cyst and absence of complications is not changed. In diagnostics the
reflection of inclusions of bone fabric is deciding (teeth, fragments of
jaws, phalanx). In default of visible inclusions a roentgenologic picture
corresponds to the of high quality tumor. In 15% cases the calcination is
looked after. In the case of necrosis of fabric appear chaotic or
calcifications in parenchim of cyst, growth of her is here halted.
Neurogenic formations is on the first seat among all tumors and cysts
of mediastinum. Meet in any age, including at new-born. More frequent all
this neurinoma — of high quality tumors developing from the Shwann
cells. Symptomatic of neurinoma is not typical, the flow is protracted,
without symptoms. More frequent they are exposed at the prophylactic
roentgenologic inspection, and at children — at the change of
sensitiveness to the tuberculin or concerning the bacillus contact. Dull and
aching pains in breasts which are the result of pressure of tumor on
neighbouring organs and fabrics can appear at the largenesses of
nevrinoma. A compression syndrome is possible. The structure of shade is
homogeneous, contours are clear, sometimes not sharply uneven.
Neurinoma rentgenofunctional symptoms are not peculiar — such, how
the change of form is at breathing. Neurinoma do not pulsate and move not
at the change of position of body of inspected. To the neurogenic tumors
the symptom of removing of mediastinal pleura a layer by a layer as
smooth transition of outlines of tumor in an overhead department in the
front contour of mediastinum is incident. Neurinoma cause destruction
bone elements. Determination of typical for neurinoma localization is the
basic criterion of difference from megascopic lymphatic knots.
Sarcoidosis. Tuberculosis of intrathoracic lymphatic nodes is
differentiated from the I stage of sarcoidosis. In obedience to modern
presentations, sarcoidosis — it is the chronic illness of indistinct etiology,
characterized by the defeat of the lymphatic system, internal organs and
skin with formation of specific granuloma surrounded by the layer of
gyalinous. Intrathoracic lymphatic nodes at sarcoidosis are struck in 100%
cases, and other organs may be involved too. From the published data,
women in age from 20 to 40 years are ill sarcoidosis in 2 times more
frequent than men. Sarcoidosis meets at the children of senior age and
teenagers.
At bronchologyc research for the I stage of sarcoidosis, characterized
by the defeat of intrathoracic lymphatic nodes, the indirect signs of their
increase are typical, and also the extended, coiled vessels of mucous
membrane. The last are the result of violation of haemo- and
lymphoflowing in connection with the considerable degree of adenopathy.
At tuberculosis the specific changes can be exposed in bronchial tubes or
limited catarrhal endobronchitis. At sarcoidosis simultaneously with the
defeat of intrathoracic lymphatic nodes are often observed uveitis,
iridocyclitis, shallow cavities in the hands and feet bones are sometimes
determined, salivary glands, liver, spleen, skin, heart, can be struck too.
Limfogranulematosis. The clinic-roentgenologic displays of
tuberculosis of intrathoracic lymphatic nodes have likeness with the
displays of lymphogranulematozsis. Such symptoms, how the decline of
mass of body, weakness, getting up of temperature of body to the subfebril
and febril sizes, determined roentgenologic megascopic intrathoracic
nodes, meet at both diseases. At differential diagnosticians of tubercular
bronhoadenitis and lymphogranulematosis is taken into account by next
positions.
Relevantly, primary tuberculosis may sometimes have chronic
undulatory course, with expressed phenomena of tuberculous intoxication
during the aggravation of specific process in lymphatic nodes or other
organs. Chemotherapy not always results in stable clinical recovery.
In very young children the nodes can press upon and narrow the soft
air passages and cause collapse of that part of the lung. In the older child a
node can break through the wall of the bronchus. When that happens the
soft contents of the node can leak into the air passage and as the child
breathes in the material containing bacilli can be drawn further into the
lung. So the disease is spread.
This is a common method of spread in young poorly nourished
children. If the child's defences are better, there is merely an extensive
exudate of fluid and cells into that part of the lung. This is due to
hypersensitivity to the ТВ or to tuberculoprotein in the caseous material.
This exudate later clears completely. Occasionally the contents of the
lymph nodes are firmer and simply stick into the bronchus so that when
the child breathes in, air can pass the narrowed space but when the child
breathes out the gap is closed and the air is trapped ('obstructive
emphysema'). This blows up the lung beyond the narrowing. In most cases
this does not last very long. The block becomes complete and the lung
beyond collapses.
Any of these forms of pneumonia, exudate or collapse may result in.
There is a group of large lymph nodes in the space where the main
windpipe (trachea) divides to supply a branch to each lung. At the front
this group is in dose contact with the back of the pericardium which
surrounds the heart. At the back they are near the gullet as it goes down to
pass through the diaphragm to the stomach. If this group of nodes enlarges
and softens with tuberculosis it may involve the pericardium. The node
contents may leak into the pericardium producing a pericardial effusion.
Very occasionally, instead of reaching to the front the mass of nodes
becomes attached to the gullet (oesophagus).
Blood spread of bacilli. During the time the primary complex is
forming and for some time afterwards bacilli escape into the bloodstream
from both the focus and the nodes. This may occur either by eroding a
blood vessel in the lesion or through the lymphatics. The bloodstream
carries the ТВ to distant parts of the body such as liver, spleen bones, brain
and kidneys. This process ceases as the child heals the primary focus and
its nodes but it can continue for many months. Most of these bacilli
although they form small tubercles do not cause any clinical illness and are
healed by the child's own defensive powers.
But in very young children defences are weak. They are also reduced
by malnutrition or by other infectious diseases, particularly measles and
whooping cough, in some countries HIV infection. In these children
primary infection may be rapidly followed by miliary tuberculosis
and/or tuberculous meningitis. These are still fatal diseases if not prop­
erly treated. If the child's defences are better, or fewer bacilli spread,
one of the more chronic lesions may show after months or years. These
include tuberculosis of bones, joints, kidneys etc.
Any of these lesions, including miliary or meningitis, may occur at
any time in life if there is a dormant (sleeping) lesion somewhere in the
body and the patient's resistance is lowered.
Tuberculosis of the cervical lymph nodes is common in Africa and
Asia. In Europe this was most frequently due to bovine bacilli acquired
from milk. The primary lesion (often invisible) was in the tonsil or
mouth. The lymph node component was in the draining nodes in the
upper part of the neck. Bovine ТВ have not been found in man in India,
and are probably rare elsewhere in Asia. In these areas it seems probable
that the disease, at least in the nodes above the clavicle, is due to spread
from intrathoracic lymph nodes associated with a primary lesion in
the lung. The frequency of bovine infection in Africa is still uncertain.
Peritoneal tuberculosis is also common in high prevalence countries.
Where milk infection is rare, it must either be due to food contamination
with ТВ or to blood spread.
Tuberculosis should be suspected in these cases:
1. TB and malnutrition go together.
2. The slow onset of typhoid (enteric) fever or paratyphoid can be like
tuberculosis.
3. Chronic infections of the nose and lungs may be present at the
same time as tuberculosis.
4. Malaria and tuberculosis may be present together in the same child
or one may be mistaken for the other.
5. Swellings of lymph nodes such as lymphoma can resemble tuberculosis.
6. Your patient may have more than one infection or infestation and
different parasites are found in different regions - what types have
you in your locality?
7. Particularly in Africa it may be necessary to consider whether a
child may have tuberculosis complicating HIV infection. This may
be congenital or acquired from a contaminated needle or through
an open wound contaminated by someone's blood. AIDS in
children may closely resemble tuberculosis.
How TB shows in children.
More people become ill with tuberculosis in the lungs than in any
other part of the body. This is because the usual route of infection is by
breathing air containing bacilli and the extension of the primary complex
which follows the infection.
Despite the fact that this happens so often there are no physical
signs or symptoms which indicate without doubt that the child has
tuberculosis. The only complete proof is the finding of ТВ. That is
particularly difficult in children.
In the health centre or small hospital the diagnosis must often be made on
clinical grounds. This should be followed by a trial of treatment with
careful observation. So in these conditions the history and clinical
examination become all important. It is well worth while taking time
and trouble over the history, which is often the most important clue to
the diagnosis. Listen carefully to what the mother says. If there are
signs or symptoms of illness this usually indicates that the tuberculosis
is extending. The extension may be in the focus in the lung, in the
lymph nodes into which the focus drains, or in the body generally.
When first seen the complaint is frequently that the child has lost or
failed to gain weight or that he has lost his normal energy and activity.
He may sweat and may have a cough and/or a mild wheeze. But the
cough is usually unproductive so that sputum is hard to get. Children with
tuberculosis practically never cough blood or blood-stained spit. All this
has usually been present for some weeks before the child is brought to be
seen.
There may be signs of vitamin deficiency. These may have appeared either
before or after the general change in health was noticed.
The family history is important. Do the parents or grandparents have any
history of cough or have they had any treatment for tuberculosis?
Are any neighbours known to have a chronic cough or tuberculosis?
Sometimes a family history of tuberculosis may be suppressed. Have
there been any recent deaths in the family?
When you examine the child you must adapt yourself to his age.
Young children will usually be nursed or held by one or other parent.
Older children may stand or lie on a bed. Always remember that you may
learn far more by watching carefully than by any other way.
Train yourself to watch his behaviour, his physique (height and
weight by age), his skin and hair, his breathing (remember he may be
frightened).
Is there a wheeze, does he cough and if so is the cough loud or soft?
Does his chest move equally on both sides?
Does he seem to have any pain on breathing or elsewhere? If you
tap his chest with your finger can you feel any difference on one side
or the other - is there dullness which may show that there is fluid or
solid lung in that area?
If you listen with a stethoscope can you detect if more air is entering
one side of his chest than the other or can you hear a wheeze as when
there is narrowing of the air passages?
Sometimes you will hear moist or wet sounds if there is fluid in the
air passages.
But you must remember that whatever physical signs you find they
only help you to understand what is happening in one or both lungs in a
mechanical sense. The signs do not tell you the cause of these changes.
Every piece of information must be considered and that is where the plan
of action set out
Miliary tuberculosis. Miliary tuberculosis is the result of heavy
blood spread of bacilli which then seed into lungs, liver, spleen and brain.
At first only loss of energy and activity, loss of weight and fever are
caused. There may not be any signs in the eldest until the disease is far
advanced. But X-ray of the chest, if this is possible, may show miliary
shadows dotted throughout both lungs. This may not be obvious in the
early stages. If it is not, try shining a very bright light
behind the outer part of the intercostal spaces. This may pick up the
small early shadows.
2.3.1. Basic types of tissue change. Exudative lesion. The lung is most
often the site of the primary lesion. The earliest reaction of human tissue to
tubercle bacilli is thought to be a pre-exudative dilatation of alveolar
capillaries with moderate swelling of the alveolar endothelial cells, which
may contain limited numbers of phagocytized tubercle bacilli. The
exudative phase follows very rapidly and usually conforms to one of three
patterns, each of which bears a relationship to the number of tubercle
bacilli present in the lesion.
At first many tubercle bacilli may be seen within the mononuclear
macrophages in the alveolar lumen. Fibrin, some extracellular bacilli, and
occasional polymorphonuclear leukocytes are also found in the alveoli.
This lesion is very prone to caseate. So, the fist stage of TB infection is
polymorphonuclear alveolitis. With this type of alveolitis there is a
predominance of polymorphonuclear cells, with some fibrin and edema,
and invariably with a large number of tubercle bacilli seen throughout the
lesion. This type of alveolitis seldom caseates solidly but is more prone to
rapid liquefaction. It is rarely seen in primary tuberculosis.
fibrinous alveolitis (not seen in die primary infection). In this situation
fibrin with few or no cellular elements is present and tubercle bacilli are
rare. This lesion is also prone to caseate, despite a relative paucity of
organisms in die fibrin-filled alveoli.
The polymorphonuclear response is more often evoked when the
infection is massive or when the susceptibility of the host to the infection
is great, as in die guinea pig. Some of the pathologic descriptions of early
cellular changes have been taken from observations made in the
experimental animal, and there is in many writings a reference to initial
polymorphonuclear invasion, but this phenomenon may not necessarily
hold true for man in every instance.
The extent of the primary exudative response and its duration vary
with the number of bacilli present, the native resistance of the host, and the
onset of hypersensitivity. It is important to note that alveolar structure is
characteristically preserved and that bacilli are undergoing multiplication
to a greater or lesser extent. These lesions commonly undergo almost
complete resolution. With the onset of caseous necrosis, however, the
preservation of the underlying structures and reversibility of the process
ends; and it is generally agreed that with the appearance of caseation a
change in the reaction of the tissues toward the bacillus takes place. This
change indicates the beginning of hypersensitivity or allergy, and the battle
against the bacilli then acquires a different morphologic appearance and
behavior.
The second stage of TB infection is caseation and cavity formation.
Caseation is a type of necrosis characteristic of tuberculosis. It has a gross
appearance somewhat like Roquefort cheese. As Canetti's quantitative
studies clearly show, the tubercle bacilli are eventually reduced in number
and many are destroyed within the caseum. The important physical and
chemical mechanisms that bring about this destruction both to the tissues
and to the bacilli are not entirely understood, but their occurrence is
characteristic of tuberculosis and certain other granulomatous processes
and is largely responsible for the permanent damaging effect of the
disease. The magnitude of the necrosis is influenced greatly by the
numbers of tubercle bacilli in the preexisting exudate and by the extent of
the exudate. Caseation is to be regarded as an expression of
hypersensitivity and cellular immunity, and die caseum is the site of
tremendous bacillary destruction. The subsequent behavior of the caseum
is very critical and largely determines whether or not tuberculosis will
become a progressive disease. These changes, briefly, are as follows:
1. The caseum may remain solid and may undergo localization,
resorption, hyaline degeneration, fibrosis, or, if large amounts of necrotic
material are present, calcification and even ossification. All these changes
are associated with reduction in tubercle bacilli and occasionally, but not
constantly or predictably, with eventual sterilization.
2. Less frequently, but more in association with larger areas of
caseation, polymorphonuclear invasion, and the appearance of proteolytic
enzymes, the caseum may soften and liquefy. Softening is accompanied by
intense multiplication of tubercle bacilli. The liquefied caseum usually
empties into a bronchus with intrabronchial dissemination of bacilli into
other parts of the lung.
The lesion which has sloughed its contents is now a cavity.
Atmospheric oxygen now has access to its lumen, where bacillary
proliferation continues in the necrotic inner zone. The capsule of
granulation tissue and fibrous tissue, which by this time surrounds die
necrotic inner zone, makes a contribution to the chronicity of die
tuberculous cavity. Without treatment few cavities heal of died own
accord, and they remain open sources of multiplying tubercle bacilli.
Tubercle formation may precede or follow necrosis. After the initial
polymorphonuclear invasion, mononuclear macrophages, which probably
come from blood monocytes, appear and continue to phagocytize tubercle
bacilli at the periphery of the lesion. The macrophages increase in size;
their cytoplasm acquires acidophilic-staining properties; the nuclei change
shape, become pale, and lose chromatin; and metaplasia into epithelioid
cells thus occurs.
The macrophages sometimes divide atypically or may coalesce to
form multinucleated giant cells of die Langhans type. This kind of
inflammatory response involving chiefly mononuclear cells is known as
granulomatous inflammation, in contrast to die polymorphonuclear
response to pyogenic organisms such as Streptococcus pneumoniae. More
or less simultaneously with these cellular reactions, new capillaries,
lymphocytes, fibroblasts, and collagenous tissue appear to encircle die
entire area, and caseation sooner or later appears in the center. The lesion
now contains all the morphologic elements of a classic tubercle. Canetti
has shown that tubercle bacilli are relatively scarce in mature tubercles, so
that tubercle formation of any extent is usually regarded as favorable to the
host. If tubercles occur in large numbers, the morphologic picture
resembles tumor formation; this pattern of tissue response, often seen in
the adult, has been called productive tuberculosis.
Nonspecific changes. In the lung more than in other organs, the basic
elements of the tuberculous focus are associated with other radiologic
changes that are nonspecific but may at times be considerably more
extensive than the specific lesions mentioned. These nonspecific changes
are usually inflammatory and accompany new tuberculous lesions. They
are regarded by most authorities as an expression of hypersensitivity to the
tuberculous focus or to the by-products of destroyed tubercle bacilli.
Canetti points out that tubercle bacilli are seldom found in these perifocal
inflammations, which are largely edematous and cellular but sometimes
hemorrhagic in appearance. Their importance will be apparent when it is
recognized that these inflammatory changes may involve an entire lobe or
lung and that it is possible but not common for them to caseate. They are
more often seen in young and middle-aged adults, frequently cause death,
but with treatment are usually the most reversible elements of the disease
process.
The primary complex . When the fine drops carrying the bacilli are
breathed in they are carried through the air passages to just under the
surface of the lung. There they remain and the ТВ slowly multiply in
numbers. As that happens some are carried in the lymph vessels to the
nearest lymph nodes beside the bronchi. In both places the presence of the
bacilli causes a reaction and the defence cells of the body begin to collect.
In about 4-8 weeks there is a small area at the center of this process
where the host tissues are dead (caseation) and around that area is an
increasing ring of defence cells. About this time most people become
sensitive to tubercle bacilli, as shown by a positive tuberculin skin test.
The changes in the lung and in the lymph nodes are together known as the.
From that time the result depends upon the power of the child to
resist the multiplication of the bacilli and limit the amount of caseation.
That power varies with age, being least in the very young. It also varies
with nutrition. Poor nutrition lowers body defenses. Most people manage,
slowly over many months, to heal both the focus in the lung and that in the
lymph nodes. But it takes time and ТВ can remain inactive but living and
capable of multiplication for many years. From the time of infection bacilli
escape into the blood stream and are carried to other parts of the body.
Fortunately disease does not always result. The risk may be small for
any individual child. But in a community where there are many adults
spreading infection many children will become ill. We must now look at
the changes which occur when the infection progresses and the child
becomes ill.
Rupture of focus into the pleural space. We have seen that the
primary focus forms just below the surface of the lung. Most do not
become larger than 10 mm. Sometimes the focus does get bigger still.
Then the surface of the lung may rupture allowing caseous material and
sometimes bacilli, to leak into the pleural space. The result seems to
depend on the child's nutrition and degree of tuberculin sensitivity. When
nutrition is good and sensitivity is strong much fluid is produced and a
large effusion results. When sensitivity is low in the young or
malnourished child the reaction is much less. The fluid of an effusion is
usually absorbed without difficulty. But occasionally if many bacilli are
present the fluid may become purulent and an empyema can become the
result.
Acute cavitation of focus may occur too. When resistance is poor as
in young or malnourished children, the primary focus may increase in size.
Instead of leaking into the pleural space it may open into a small bronchus
and the caseous material is discharged by coughing. During this process
there may be a stage when air can enter the small cavity when the patient
is breathing in but cannot escape when he is breaking out. The result is the
formation of a small thin-walled cavity. This process can seed infection to
other parts of the lungs. Spread may also occur by the erosion of the
tuberculous nodes through the bronchial wall. Caseous material and ТВ
from the nodes may then spread through the bronchi to other parts of the
lung. We have twice seen a child who suffocated from caseous material
suddenly blocking both main bronchi. Emergency bronchoscopy, if
available, could save such a child. If this is not available, we suggest
turning the child upside down and percussing the chest with the open hand
to try to help the child to cough up the material and clear the bronchi. This
type of progressive lung disease is particularly likely in malnourished
children. It can proceed so rapidly that the child may die from tuberculous
pneumonia before developing signs of blood spread disease such as
miliary tuberculosis or tuberculous meningitis.
Ring or coin shadow. Very occasionally in older children (and found
only by X-ray examination) a round coin-like lesion can be seen in the
lung field. Sometimes the edge is calcified or a series of zones of
calcification may be seen representing periods of healing and extension.
This can remain unchanged for long periods. It may then completely or
partially calcify.
Reaction of the lymph nodes at the root of the lung. Bacilli from the
primary focus reach the lymph nodes by direct drainage. These nodes lie
near to the air passages (bronchi). Both the nodes and the air passages get
larger towards the center (root) of the lung. The bacilli in the nodes cause
a change which is the same as that in the focus in the lung and the node
becomes larger and may soften.
In very young children the nodes can press upon and narrow the soft
air passages and cause collapse of that part of the lung. In the older child a
node can break through the wall of the bronchus. When that happens the
soft contents of the node can leak into the air passage and as the child
breathes in the material containing bacilli can be drawn further into the
lung. So the disease is spread. This is a common method of spread in
young poorly nourished children.
If the child's defences are better, there is merely an extensive exudate
of fluid and cells into that part of the lung. This is due to hypersensitivity
to the ТВ or to tuberculoprotein in the caseous material. This exudate, as
seen on the X-ray, later clears completely. Occasionally the contents of the
lymph nodes are firmer and simply stick into the bronchus so that when
the child breathes in, air can pass the narrowed space but when the child
breathes out the gap is closed and the air is trapped ('obstructive
emphysema'). This blows up the lung beyond the narrowing. In most cases
this does not last very long. The block becomes complete and the lung
beyond collapses. Any of these forms of pneumonia, exudate or collapse
may result in. This is a common method of spread in young poorly
nourished children. If the child's defences are better, there is merely an
extensive exudate of fluid and cells into that part of the lung. This is due
hypersensitivity to the ТВ or to tuberculoprotein in the caseous material.
This exudate, as seen on the X-ray, later clears completely.
There is a group of large lymph nodes in the space where the main
windpipe (trachea) divides to supply a branch to each lung. At the front
this group is in dose contact with the back of the pericardium which
surrounds the heart. At the back they are near the gullet as it goes down to
pass through the diaphragm to the stomach. If this group of nodes enlarges
and softens with tuberculosis it may involve the pericardium. The node
contents may leak into the pericardium producing a pericardial effusion.
Very occasionally, instead of reaching to the front the mass of nodes
becomes attached to the gullet (esophagus).
Blood spread of bacilli. During the time the primary complex is
forming and for some time afterwards bacilli escape into the bloodstream
from both the focus and the nodes. This may occur either by eroding a
blood vessel in the lesion or through the lymphatics. The bloodstream
carries the ТВ to distant parts of the body such as liver, spleen, bones,
brain and kidneys. This process ceases as the child heals the primary focus
and its nodes but it can continue for many months. Most of these bacilli
although they form small tubercles do not cause any clinical illness and are
healed by the child's own defensive powers. But in very young children
defences are weak. They are also reduced by malnutrition or by other
infectious diseases, particularly measles and whooping cough, in some
countries HIV infection. In these children primary infection may be rapidly
followed by miliary tuberculosis and/or tuberculous meningitis. These are
still fatal diseases if not properly treated. If the child's defences are better,
or fewer bacilli spread, one of the more chronic lesions may show after
months or years. These inside tuberculosis of bones, joints, kidneys etc.
Any of these lesions, including miliary or meningitis, may occur at any
time in life if there is a dormant (sleeping) lesion somewhere in the body
and the patient's resistance is lowered.
Tuberculosis of the cervical lymph nodes is coming in Africa and
Asia. In Europe this was most frequently due to bovine bacilli acquired
from milk. The primary lesion (often invisible) was in the tonsil or mouth.
The lymph node component was in the draining nodes in the upper part of
the neck. Bovine ТВ have not been found in man in India, and are
probably rare elsewhere in Asia. In these areas it seems probable that the
disease, at least in the nodes above the clavicle, is due to spread from
intrathoracic lymph nodes associated with a primary lesion in the lung.
The frequency of bovine infection in Africa is still uncertain.
Peritoneal tuberculosis is also common in high prevalence countries.
Where milk infection is rare, it must either be due to food contamination
with ТВ or to blood spread.
Following the general statement given above we know something
about the usual timetable of tuberculosis by long observation of European
children whose time of infection was known. The common timetable of the
complications of primary tuberculosis can be set out in a diagram. This
diagram also gives some indication of the factors which increased the risk
of the most serious complications. These risks were found in children in a
well-nourished population before effective treatment was available. Risks
are likely to be greater in any population where malnutrition or HIV
infection is common. The time relationships of the development of the
primary complex after the child has been infected, and that most go on to
heal, but complications can arise from the focus in the lung, from the
lymph nodes and then spread to other organs, brain, bone and much later
the kidneys. It also gives an indication how long after infection
complications are most likely to occur and of the things which make a
primary infection more dangerous by reducing the body's power to resist
the multiplication of the tubercle bacilli.
Infection with Tuberculosis. Limited evidence from Africa and Asia
suggests (surprisingly) that the latent period between primary infection and
the development of pulmonary tuberculosis in adult life is much longer
than was found in Europe. Latent TB infection may occur in 90 % but is
needed in treatment is recommended for children to prevent them from
developing TB disease. Infants, young children, and immunocompromised
children with latent TB infection or children in close contact with someone
with infectious TB disease, require special consideration because they are
at increased risk for getting TB disease. Consultation with a pediatric TB
expert is recommended before treatment begins. Isoniazid is the anti-TB
medicine that is most commonly used for treatment of latent TB infection.
In children, the recommended length of treatment with isoniazid is 9
months.
The effect of age at infection, nutrition and other infections and
infestations. The power to resist infection is the power of the defences of
the body to overcome an invading organism. This depends on the age of
the person infected, upon his or her nutrition, upon the presence of other
infections (especially HIV infection) or infestations and upon the nature
of the infection itself whether it acts suddenly like cholera or very slowly
like leprosy. In tuberculosis the bacilli grow slowly over weeks and
months rather than days. So the effects and signs of the disease appear
slowly.
The changes which follow the first infection have been given above.
We also showed how most of those who have a first infection with
tuberculosis manage to heal it. Their bodies have indeed learned to
respond more quickly to future attacks by ТВ. If they should get another
infection the body's quicker defence prevents the spread of bacilli to other
organs, as occurs during the first infection.
This is the reason why BCG, a harmless form of primary infection,
reduces the frequency of miliary tuberculosis and tuberculous meningitis.
But the defences do not work so well at every age. They are poor at birth
and improve slowly for the first 10 years or so of life. Up to puberty the
child is not so good at preventing blood spread, though this gradually
improves with age. But a well nourished child seems good at preventing
the spread of disease within the lung itself. After puberty the body is better
at preventing blood spread, but much poorer at preventing spread in the
lungs. But badly nourished children may develop severe cavitation lung
disease at an early age.
Throughout life the body only responds to infection in the best way if
it is well nourished with an adequate supply of the proper food. At any age
insufficient food, leading to malnutrition, reduces the power of the body to
respond to its full capacity. This increases not only the seriousness of
disease but also the number of deaths. The other factor which reduces
resistance to tuberculosis is the presence of other infections. In children
this seems especially so with measles and whooping cough for if they
occur while the child has a primary infection with tuberculosis that disease
may extend and miliary tuberculosis or meningitis develops. In some areas
of the world HIV infection is the most important other infection. Severe
worm infestation, particularly with intestinal parasites, can be a cause of
malnutrition, particularly if the amount of food taken is only just enough.

Literature
J. Crofton. Text book.