Primary Tuberculosis (Lecture)

8/18/2019 Primary Tuberculosis (Lecture)

1/24

Primary tuberculosisPrimary tuberculosis

LECTURELECTURE

docdoc.. KravchenkoKravchenko NN..SS..


2/24

Tuberculosis which develops in primary infected people is called

primary tuberculosis. It is diagnosed often in children and teenagers.

More rarely in young people.

Topical sings of primary tuberculosis are:

a) The intensity tuberculin test reaction;

b) lesion of lymphatic system (especially lymphatic nodes);

c) tendency to lymphogenous and hematogenous dissemination;

d) state of hypersensibilization of organism to pathogenic agent; e) possibility of spontaneous recovery.

Tuberculin intensifier is the appearance of first positive tuberculin reaction

after a negative one within a year or its increase in persons vaccinated.

Primary tuberculosis usually displays in three main forms:

- tuberculous intoxication in children and teenagers (tuberculosis without

established localization);

- primary tuberculous complex;

- tuberculosis of intrathoracic lymphatic nodes.


3/24

The clinical expression of disease caused by

Mycobacterium tuberculosisMycobacterium tuberculosis is greatly different in infants

children and adolescents than in adults. !hereas most adult

pulmonary tuberculosis is caused by a reactivation of dormant

organisms that are lodged in the apices of the lungs during

hematogenous dissemination at the time of infection pediatric

tuberculosis is usually a complication of the pathophysiologic

events surrounding the initial infection. The interval betweeninfection and disease is usually long - years to decades - in

adults but is often only wee"s to months in small children.

#hildren are more prone to extrapulmonary tuberculosis but

rarely experience infectious pulmonary disease. $s a result ofthe basic difference in pathophysiology of tuberculosis

between adults and children the approach to diagnosis

treatment and prevention of infection and disease in children

is very different.


4/24

TERMIN!"#

The terminology used to describe various stages and presentations

of pediatric tuberculosis often has been a source of confusion for

physicians. %t follows the pathophysiology but the stages are often lessdistinct in children.

E$posure means that the child has had significant contact with an

adult or adolescent with infectious pulmonary tuberculosis. The contact

investigation examining those persons close to a suspected case of

tuberculosis with a tuberculin s"in test chest radiograph and physicalexamination is the most important activity in a community to prevent

tuberculosis in children. The most fre&uent setting for exposure of a

child is the household but it can occur in a school day care center or

other closed setting. %n this stage the tuberculin s"in test result is

negative the chest radiograph appears normal and the child lac"s

signs or symptoms of disease. 'ome exposed children may have

inhaled droplet nuclei infected with M. tuberculosis and have early

infection but the clinician cannot "now it because it ta"es up to

months for delayed hypersensitivity to tuberculin a positive s"in test

result to develop.


5/24

Infection occurs when a person inhales droplet nuclei containing

M. tuberculosis, which becomes established intracellularly within the lung

and associated lymphoid tissue. The hallmar" of tuberculosis infection is a

reactive tuberculin s"in test. %n this stage the child has no signs or

symptoms and the chest radiograph either appears normal or reveals only

granuloma or calcifications in the lung parenchyma regional lymph nodes

or both. %n many countries all children with tuberculosis infection should

receive treatment usually with isoniazid (%*) to prevent the development

of disease in the near or distant future. %isease occurs when signs or symptoms or radiographic

manifestations caused by M. tuberculosis become apparent. The word

tuberculosis refers to disease. ot all infected patients have the same ris"

of developing disease. $n immunocompetent adult with untreated

tuberculosis infection has approximately a +, to , lifetime ris" of experiencing disease; one half of the ris" occurs in the first / to years after

infection. *istorical studies have shown that up to 0, of

immunocompetent infants with untreated tuberculous infection develop

disease often serious life threatening forms within to / years.


6/24

EPI%EMI!"# %isease and InfectionEPI%EMI!"# %isease and Infection

1ecause most children with tuberculous infection and disease

ac&uired the organism from an adult in their environment the

epidemiology of childhood tuberculosis tends to follow that in adults.The ris" of a child ac&uiring tuberculous infection is environmental

determined by the li"elihood that he or she will be in contact with an

adult with contagious tuberculosis. %n contrast the ris" of a child

developing tuberculous disease depends more on host immunologic

and genetic factors. %t is estimated that the worldwide annual burden of tuberculosis

on children is .+ million cases and + deaths. $dult tuberculosis

case numbers have increased over the past decade in every region of

the world except !estern 2urope. There are no comparable data but it

is li"ely that childhood tuberculosis has grown in numbers as well.3ost children are infected with M. tuberculosistuberculosis in the home but

outbrea"s of childhood tuberculosis centered in elementary and high

schools nursery schools family day-care homes churches school

buses and stores still occur. %n most cases a high-ris" adult wor"ing in

the area has been the source of the outbrea".


7/24


8/24

TransmissionTransmission

#hildren usually are infected by an adult or adolescent in the

immediate household most often a parent grandparent orhousehold employee. #asual extrafamilial contact is the source of

infection much less often but babysitters schoolteachers music

teachers school-bus drivers parishioners nurses gardeners have

been implicated in individual cases and in hundreds of mini-epi

demics within limited population groups. !ithin the household of aninfectious adult the infants and toddlers almost always are infected.

$lso at high ris" are the older children and teenagers who help the

ailing adult. $dults with pulmonary disease who are receiving regular

appropriate chemotherapy probably rarely infect children; much more

dangerous are those with chronic tuberculous disease that is

unrecognized inade&uately treated or in relapse because of

development of resistance.

#hildren with tuberculosis rarely if ever infect other children.

3any children with the disease have tuberculin-negative parents.


9/24

!hen transmission of M. tuberculosis has been documented in

children7s hospitals it almost invariably has come from an adult with

undiagnosed pulmonary tuberculosis. %n tuberculous children M.

tuberculosis in endobronchial secretions are relatively sparse and

productive cough is not at all characteristic of endothoracic

tuberculosis or of miliary disease. !hen young children cough they

lac" the tussive force of adults.

$dolescents with typical reactivation-type pulmonary tuberculosismay be as infectious as adults. #hildren nevertheless play an

extremely important role in the transmission of tuberculosis not so

much because they are li"ely to contaminate their immediate

environment but because they harbor a partially healed infection that

lies dormant only to reactivate as infectious pulmonary tuberculosismany years later under the social emotional and physiologic stresses

arising during adolescence adulthood or old age. Thus children

infected with M. tuberculosis constitute a long-lasting reservoir of

tuberculosis in the population.


10/24

P&T'"ENE(I( IN )'I!%RENP&T'"ENE(I( IN )'I!%REN

8rimary tuberculosis is always result of exogenous infection.

The infection penetrates into organism by:

- aerogenic (the most often way of penetration) - alimentary;

- contact way.

. The primary complex of tuberculosis consists of local disease at the

portal of entry and the regional lymph nodes that drain the area of the

primary focus. %n more than 9+, of cases the portal of entry is thelung. M. tuberculosis within particles larger than (xm usually are

caught by the mucociliary mechanisms of the bronchial tree and are

expelled. 'mall particles are inhaled beyond these clearance

mechanisms. *owever primary infection may occur anywhere in the

body. /. %ngestion of mil" infected with bovine tuberculosis can lead to a

gastrointestinal primary lesion.

. %nfection of the s"in or mucous membrane can occur through an

abrasion cut or insect bite.


11/24

The number of M. tuberculosis re&uired to establish infection inchildren is un"nown but only several organisms are probablynecessary. The incubation period in children between the time theM. tuberculosis enter the body and the development of cutaneoushypersensitivity is usually / to / wee"s most often 0 to wee"s.The onset of hypersensitivity may be accompanied by a febrilereaction that lasts from to wee"s. uring this phase ofintensified tissue reaction the primary complex may becomevisible on chest radiograph. uring this time the primary focus

grows larger but does not yet become encapsulated. $shypersensitivity develops the inflammatory response becomesmore intense and the regional lymph nodes often enlarge. Theparen-chymal portion of the primary complex often healscompletely by fibrosis or calcification after undergoing caseous

necrosis and encapsulation.


12/24

uring the development of the parenchymal lesion and the

accelerated caseation brought on by the development of hypersensitivity

M. tuberculosis from the primary complex spread via the bloodstream and

lymphatics to many parts of the body. The areas most commonly seeded

are the apices of the lungs liver spleen meninges peritoneum lymphnodes pleura and bone. This dissemination can involve either large

numbers of bacilli which leads to disseminated tuberculous disease or

small numbers of bacilli that leave microscopic tuberculous foci scattered in

various tissues. %nitially these metastatic foci are usually clinically

inapparent but they are the origin of both extrapulmonary tuberculosis and

reactivation pulmonary tuberculosis in some children.

The tubercle foci in the regional lymph nodes develop some

fibrosis and encapsulation but healing is usually less complete than in the

parenchymal lesions. 4iable M. tuberculosis may persist for decades after

calcification of the nodes. %n most cases of primary tuberculosis infection

the lymph nodes remain normal in size. *owever because of their locationhilar and paratracheal lymph nodes that become enlarged by the host

inflammatory reaction may encroach upon the regional bronchus. 8artial

obstruction caused by external compression may lead at first to hyperinfla

tion in the distal lung segment. 'uch compression occasionally causes

complete obstruction of the bronchus resulting in atelectasis of the lungsegment .


13/24

3ore often inflamed caseous nodes attach to the bronchial

wall and erode through it leading to endobronchial

tuberculosis or a fistulous tract . The extrusion of infected

caseous material into the bronchus can transmit infection to the

lung parenchyma and cause bronchial obstruction and

atelectasis. The resultant lesion is a combination of pneumonia

and atelectasis. The radiographic findings of this process have

been called epituberculosis, collapse-consolidation, and

segmental tuberculosis. =arely tuberculous intrathoracic lymphnodes invade other ad5acent structures such as the pericardium

or esophagus.

3assive lympho-hematogenous dissemination leading to

meningitis or miliary or disseminated disease occurs in .+, to

/, of infected children usually no later than to > months afterinfection. #linically significant lymph node or endobronchial

tuberculosis usually appears within to 9 months. ?esions of the

bones and 5oints usually ta"e at least a year to develop; renal

lesions may be evident + to /+ years after infection. %n general

complications of the primary infection occur within the first year.


14/24

'ow )hildren with Tuberculosis &re %iscovered'ow )hildren with Tuberculosis &re %iscovered

%n the developing world the only way children with

tuberculosis disease are discovered is when they present

with a profound illness that is consistent with tuberculosis.

*aving an ill adult contact is an obvious clue to the correct

diagnosis. The only available laboratory test usually is an

acid-fast smear of sputum which the child rarely produces.%n many regions chest radiography is not available. To aid in

diagnosis a variety of scoring systems have been devised

that are based on available tests clinical signs and

symptoms and "nown exposures. *owever the sensitivityand specificity of these systems can be very low leading to

both over- and under-diagnosis of tuberculosis.


15/24

%n industrial countries children with tuberculosis usually

are discovered in one of two ways.

)


16/24

Tuberculous into$icationTuberculous into$ication in children and teenagers is a

clinical form of primary tuberculosis which is characterized

by complex of symptoms of functional derangement without

local manifestation of disease.

3orfological substrat of tuberculous intoxication areminimal specific (tuberculous granuloma with areas of

microcaseose) and paraspecific changes usually in

lymphatic system.

) f


17/24

)linical manifestations.)linical manifestations.

ComplaintsComplaints on aggravation of appetite sweating not

constant subfebrile body temperature emotional instability

decreasing of memory.Objectively Objectively :: paleness decreasing of s"in turgor

micropoliadenitis (increasing of &uantity and sizes of periferal

lymphatic nodes more than five groups). uring percussion

changes over the lungs are absant. $uscultation: sometimesdry rales.

Laboratory and other methods of investigation.Laboratory and other methods of investigation.

%n hemogram can be slight leu"ocytosis with an insignificant

shift to the left lymphopenia eosinophilia monocytosis 2'= is

normal or increased.

Roengenological examination.Roengenological examination.

%n reviewable roentgenogram and tomogram of lungs there

are no changes usually. 'ometimes it can be strengthen of

lungs picture.


18/24

%ifferential diagnosis.%ifferential diagnosis.

%t is necessery to exclude diseases accompanied by

intoxication: chronical sourses of infection of oral cavity andepipharynx: chronical tonsillitis pielonephritis rheumatism

hepatocholecystitis helminthic invasions.

3ain diagnostic criterions of tuberculous intoxication are:

- tuberculin intensifier

- symptoms of intoxication

- absence of roentgenological changes

- excluding of intoxication with different ethiology

Treatment.

%soniazidum mg@"g of weight A rifampicinum mg@"g or

etambutol /mg@"g for 0-> months vitamins 1 1> #.


19/24

Primary tuberculous comple$Primary tuberculous comple$

8rimary tuberculous complex is characterized by

development of specific general changes in lungs (primary

effect) lesion of intrathoracic lymphatic nodes and

lymphangitis.

8atological anatomy: zone of tuberculous granulations and

caseous necrosis is forming in lungs. Bone of perifocal toxicedema and serofibrinous inflammation is forming around zone

of specific inflammation. These changes form primary affect.

%nfection extence in lymphatic vessels from primary affect to

the root of lungs (lymphangitis) and in5ury of root lymphatic

nodes is ta"ing place (lymphadenitis).

fig.

)li i l if t ti)li i l if t ti


20/24

)linical manifestations.)linical manifestations.

$symptomatic course of disease can be present under little specific

changes in lungs. Complaints: subfebrile temperature decrease of

body weight bad appetite &uic" tiredness. #oughing happens seldom. Inspection: paleness decrease of s"in turgor paraspecific changes

micropolyadenitis. These changes can be absent.

Percussion: dullness over lung component with a big size.

!ea"end breathing with streached exhale.

*emogram: ?eucocytosis - T@l insignificant shift to the leftlymphopenia monocytosis ''2 /-/+ mm@h.

Tuberculin test - intensivity of tuberculin reaction hyperergic reaction.

31T are rarely to be found.

!ray diagnostics:

8hases: ) infiltrative or pneumonic;/) resorbtion (suctionbipolarities);

) scarring

0) calcification.fig. /


21/24

#omplications are connected with lung component:

- decomposition of primary affect with primary cavern forming

#omplications connected with regional lymphadenitis:- hematogenic dessimination

- lymphogenic dessimination

- pleuritis

- extencing of specific process from lymphatic node to

%tCs results:

a) formation of fistula

b) dispersion of caseous masses bronchogenic

dessemination c) disorder of bronchial permeability

fig.


22/24

"he differential diagnostics is performed #ith"he differential diagnostics is performed #ith ::

) 8neumonia;/) 2osinofilic infiltration;

) 8eripheral or central cancer.

6nspecific pneumonia usually beging sharply after

catching cold respiratory infection with the high body

temperature general wea"ness pespiration

considerable shortness of breath.

$uscultatorily is defned many dry and moist rales.

1lood examination: high leucocitosis and high 2'=.


23/24

Tuberculosis of intrathoracic lymphatic nodesTuberculosis of intrathoracic lymphatic nodes is specific

in5ury of lymphatic nodes of lungsC root and mediastinum.

8athomorphological forms:

a) hyperplastic b) caseous form

fig. 0f ig. 0

The clinic of uncomplicated tuberculosis of intrathoracic lymphaticnodes is similar to that of primary tuberculous complex.

#linical-radiological forms of tuberculosis of intrathoracic nodes:

) 'mall form D deformation and strengthening of pulmonary

picture near lung root decreasing of root structure. /) %nfiltrative D root shadow is widened with not clear contour

(ouyline).

) Tumorshaped D widening of mediastinum or lung root with

polycicle clear contour


24/24

%ifferntial diagnosis is conduction with:

?ymphogranulomatosis lymphosarcoma lymphoid leu"emia

unspecific adenopathy mediastinal cancer sarcoidosis.

Eor this the following procedures are performed:

) F-ray examination in right and lateral pro5ections;

/) Tomography on bifurcation level ( middle microscopic section);

) Tuberculin tests bronchoscopy as well as punctured or operative

biopsy.

Treatment of local forms of:

$tationary :

% months ! %soniazidum mg@"g of body weight * =ifampicinum

mg@"g of body weight A 8yrazinamidum /+ mg@"g of body weight.Under extend process, complications prescribe: A streptomycinum

+-/ mg@"g of body weight.

&ext ' months ! %soniazidum A rifampicinum or ethambutolum.

General course of treatment lasts for 6-9 mounths. 4itamins 1 1>

# desensibilizinig preparations are also prescribed.

Primary Tuberculosis (Lecture)

Documents

Transcript of Primary Tuberculosis (Lecture)