infectiousdiseases12-1226191746823718-8

8/7/2019 infectiousdiseases12-1226191746823718-8

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Infectious Diseases (1&2)Infectious Diseases (1&2)

INTRODUCTION

TUBERCULOSIS


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Spread & Dissemination of MicrobesSpread & Dissemination of Microbes

The bloodbloodis a hostilehostile environment to most microorganisms, thoseentering the blood are destroyeddestroyedrapidly

BACTEREMIA:BACTEREMIA:

Is the presence ofIs the presence of small numbersmall number ofof low virulencelow virulence bacteria in the bloodbacteria in the blood

of normal individualsof normal individuals without multiplicationwithout multiplication

Usually associated with severe localized infectionlocalized infection such as penumococcal

pneumonia, after tooth extractin

The bacteria detected by blood cultureculture &disappeardisappearfrom it when the local

infection subsides


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SEPTICEMIA:SEPTICEMIA:

Means theMeans the presence & multiplicationpresence & multiplication ofof highly pathogenichighly pathogenic

bacteria in the blood such as pyogenic cocci .bacteria in the blood such as pyogenic cocci .

The condition indicates a seriousserious infection with profound toxemia &

failure of the host defenses

Small hemorrhages due to capillarycapillary endothelial damage occur, high

counts ofneutophilsneutophils

, enlarged spleenenlarged spleen

It is rapidly fatalfatalwith rapid disseminationdissemination of the infection to various

sites in the body


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PYAEMIA:PYAEMIA:

MeansMeans puspus in the bloodin the blood

Associated with pyogenicpyogenic infection

Septic thrombusSeptic thrombus (infected by bacteria and infiltrated by neutrophils)

are fragmentedfragmentedand carried off in the blood as small micro-emboli

where they occlude smaller vesselsocclude smaller vessels, causing local injurylocal injury by the

obstruction and by the release of toxins from the bacteria

Results in eitherpyaemic abscessespyaemic abscesses or septic infarction


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TOXEMIA:TOXEMIA:

Is the presence of circulating bacterial toxins in theIs the presence of circulating bacterial toxins in the

bloodblood


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Infection DiseaseInfection Disease

Infection:Infection: Seeding of a focus with organisms,

which may or may not cause clinically

significant tissue damage i.e. disease Only a small fraction of those who contract anOnly a small fraction of those who contract an

infection develop active disease:infection develop active disease:

Generally, 3-4% of previously unexposed individuals

acquire active disease during the 1st year after

infection & no more than 15% do so thereafter


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TuberculosisTuberculosis

Is a communicable chronic granulomatous diseasecaused by Mycobacterium tuberculosisMycobacterium tuberculosis

It usually involves the lungs but may affect any

organ or tissue in the body

Typically results in caseating granulomas


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Tuberculosis

Tuberculosis EpidemiologyEpidemiology

~ 1.7 billion individuals are infectedworldwide ~ 1/3 of the worlds

population 3 million deaths / year

A leading cause of death globally

Accounts for~ 6% of deaths worldwide Is the most common cause of death

resulting from a single infectious agent


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Tube

rculosis

Tube

rculosis E

pidemiologyE

pidemiology

Until the midmid 19801980ss, in the USA& Western

countries there was a declinedecline in TB infection

The incidence in Western population increasedin HIV-infected persons & in immigrants from

high prevalence areas

The lunglung is the most common important

clinical site of infection


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Tube

rculosis

Tube

rculosis Routes of infectionRoutes of infection

1.1. Respiratory tract:Respiratory tract:

Most cases are acquired by direct person to person

transmission ofairborneairborne droplets with organismsfrom an active caseactive case to a susceptible host

2.2. Intestinal tractIntestinal tract

3. Skin by inoculation

4. Congenital by transplacental spread


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TuberculosisTuberculosis MicroorganismMicroorganism

M. tuberculosis hominisM. tuberculosis hominis

Transmitted by inhalation of infective droplets, coughed orsneezed into the air from patients with active open PTB

airborne or by exposure to contaminated secretions M. bovisM. bovis

Transmitted by milk from diseased cows intestinal &oropharyngeal TB

Rare

M. aviumM. avium--intracellulareintracellulare Very low virulence rarely cause disease in normal hosts

Cause disseminated infection in 10-30% ofAIDS pts


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TuberculosisTuberculosis Predisposing FactorsPredisposing Factors

A number of factors predispose to the

development of TB :

1.1. AccessAccess of organism: close contact with open

cases of disease, e.g. increased in crowded &

unhygienic working and living conditions

2.2. SusceptibilitySusceptibility of individual: the old, veryyoung, black&Asian populations have and

increased susceptibility


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TuberculosisTuberculosis Predisposing FactorsPredisposing Factors

3.3. NutritionNutrition: a disease of the undernourished & underprivileged poor

4.4. OccupationOccupation: increased incidence of TB in some types of

pneumoconiosis (silicosis & in health workers)5.5. Other DiseasesOther Diseases: such as;

pre-existing chronic lung disease, chronic renal

failure, Hodgkin diseases, diabetes mellitus,

alcoholism, corticosteroid, immunosuppressive &

cytotoxic drug therapy, immunodeficiencies; AIDS


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TuberculosisTuberculosis -- Characters of theCharacters of the

OrganismsOrganisms AerobicAerobic, acidacid--fast bacillifast bacilli

Has no known exotoxins, endotoxinsno known exotoxins, endotoxins

Has waxy coat high contents of complex lipidsthat causes them to retain the red dye when treated

with acid in acidacid--fast stainfast stain & resist decolorization


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TuberculosisTuberculosis -- PathogenesisPathogenesis

MacrophagesMacrophages are the primary cells infected by

M. tuberculosis.

EarlyEarly in infection, tuberculosis bacilli

replicate essentially unchecked, while laterlaterin

infection, the T-helper response stimulates

macrophages to contain the proliferation ofthe bacteria.


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M. tuberculosis entersenters macrophages by

endocytosisendocytosis mediated by several macrophage

receptors: Macrophages mannose receptorsMacrophages mannose receptors

Complement receptorsComplement receptors

Once inside the macrophage, M. tuberculosis

replicates within the phagosomereplicates within the phagosome by blockingblocking

fusionfusion of the phagosome& lysosome


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The earliest stage ofprimary tuberculosisprimary tuberculosis (


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The genetic makegenetic make--upup of the host may influence the course ofthe disease

In some people with polymorphisms in the NRAMP1 genepolymorphisms in the NRAMP1 gene,the disease may progress from this point without developmentof an effective immune response microbicidal function

NRAMP1 proteinNRAMP1 protein is a transmembrane proteintransmembrane protein found inendosomes and lysosomes & may have role in generation ofgeneration ofantianti--microbial oxygen radicalsmicrobial oxygen radicals

About3 weeksAbout3 weeks after infection, a Ta THH1 response1 response against M.tuberculosis is mounted that activates macrophages to becomebactericidalbactericidal


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TTHH00 cells are stimulated bycells are stimulated by mycobacterial antigens

drained to the lymph node, which are presented with

class II major histocompatibility proteins by antigenpresenting cells macrophages

Differentiation of TH1 cells depends on the presence

ofILIL--1212, which is produced by antigen presentingproduced by antigen presenting

cellscells that have encountered the mycobacteria

Mature TH1 cells, both in lymph nodes and in the

lung, produce IFNIFN--


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IFNIFN-- is the critical mediator which activates macrophages toactivates macrophages to

become competentbecome competentto contain the M. tuberculosis infection

IFN- stimulates formation of the phagolysosomesstimulates formation of the phagolysosomes in infectedmacrophages, exposing the bacteria to an inhospitable acidic

environment

IFN- also stimulates inducible nitric oxide synthasealso stimulates inducible nitric oxide synthase (iNOS),(iNOS),

which produces nitric oxide (NO)produces nitric oxide (NO)

NONO generates reactive nitrogen intermediatesnitrogen intermediates and otherfreefree

radicalsradicals capable ofoxidative destructionoxidative destruction of several

mycobacterial constituents, from cell wall to DNA.


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In addition to stimulating macrophages to kill mycobacteria,the TTHH11 responseresponse orchestrates the formation of granulomasformation of granulomas& caseous necrosis& caseous necrosis

Activated macrophagesActivated macrophages, stimulated by IFN-, produce TNFTNF,which recruits monocytesrecruits monocytes

These monocytes differentiate into the "epithelioiddifferentiate into the "epithelioidhistiocytes"histiocytes" that characterize the granulomatous response

CDCD44+ T+ THH11 cellscells also facilitates development of CDalso facilitates development of CD88+ T+ T

cellscells,, which can kill the TB-infected macrophages

DefectsDefects in any of steps ofTTHH11 responseresponse result in poorlyformed granulomas, absence of resistance, & diseaseprogression


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In many peopleIn many people, this response contains the bacteriaand doesn't cause significant tissue destruction ordoesn't cause significant tissue destruction orillnessillness

In other peopleIn other people, the infection progresses and theongoing immune response results in tissueresults in tissuedestructiondestruction due to caseation &cavitation


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In summaryIn summary, immunity to M. tuberculosis is primarilymediated by TH1 cells, which stimulate macrophages to killthe bacteria

This immune response, while largely effective, comes at thecost of hypersensitivity and the accompanying tissuedestruction

Reactivation of the infection or re-exposure to the bacilli in apreviously sensitized host results in rapid mobilization of a

defensive reaction but also increased tissue necrosis


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TuberculosisTuberculosis Type IVType IV

Hypersensitivity ReactionHypersensitivity Reaction

It can be detected by tuberculin Mantoux testtuberculin Mantoux test: ~2-4 wks after infection, intracutaneous injection of

0.1 mL of PPD induces a visible & palpable

induration at least 5 mm in diameter that peaks in48-72 hrs

Positive testPositive testindicates cell-mediated hypersensitivity& doesnt differentiate between infection & disease

FalseFalse--negative testnegative testmay be produced by certain viral

infections, sarcoidosis, malnutrition, Hodgkindisease, immunosuppression& overwhelming activeTB

FalseFalse--positive testpositive testmay result from infection byatypical mycobacteria


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TuberculosisTuberculosis Natural History &Natural History &

SpectrumSpectrum

MajorityMajority


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PrimaryTuberculosisPrimaryTuberculosis

Occurs in previously unexposedpreviously unexposed& therefore

unsensitizedunsensitizedpersons

In non immunized childrennon immunized children

Elderly & profoundly immunosuppressedElderly & profoundly immunosuppressed

persons may lose their sensitivity to M.

tuberculosis& develop primary tuberculosis

Source of infection: exogenousexogenous

Only 5% will develop significant disease


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PrimaryTuberculosisPrimaryTuberculosis GrossGross

MorphologyMorphology

Typically; inhaled bacilli implant in the distal airspacesof the lower part of the upper lobelower part of the upper lobe orupper part of theupper part of thelower lobelower lobe, usually close to the pleuraclose to the pleura

As sensitization develops; 1-1.5 cm area of gray-whiteinflammatory consolidation forms Ghon focusGhon focus

In most cases the center of the focus develops caseousnecrosis

Tubercle bacilli either free or within macrophage draininto regional lymph nodelymph node caseating granulomacaseating granuloma


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Ghons complexGhons complex=

Parenchymal lesion +

Hilar lymph nodeinvolvement


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This is the gross appearance

of caseous necrosis in a hilar

lymph node infected withtuberculosis. The node has a

cheesy tan to white

appearance. Caseous necrosis

is really just a combination of

coagulative and liquefactivenecrosis that is most

characteristic of granulomatous

inflammation




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In most persons (95%),cell-mediated immunitycontrols infection & the

granulomatous diseasewill not progress. Overtime, the granulomasdecrease in size, fibrose,and can calcify, leaving a

focal calcified spot on achest radiograph thatsuggests remotegranulomatous diseaseRanke complexRanke complex


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Primary tuberculosis is the pattern seen with initial infection

with tuberculosis, most often in children. Reactivation or

reinfection to produce secondary tuberculosis is more

typically seen in adult




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PrimaryTuberculosisPrimaryTuberculosis MicroscopicMicroscopic


The site of activeinvolvement shows

granulomatousinflammation with orwithout caseation&with multinucleatedgiant cells, that are

surrounded bylymphocytes &fibroblastic rim


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Well-defined non-caseating granulomas . Granulomas are composed of

transformed macrophages called epithelioid cells along with lymphocytes,

occasional PMN's, plasma cells, and fibroblasts.




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Caseous necrosis is characterized by acellular pink areas of

necrosis that is surrounded by a granulomatous

inflammatory process




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At high magnification, the granuloma demonstrates epithelioid macrophages

that are elongated with long, pale nuclei and pink cytoplasm. The

macrophages fuse to form giant cells. The typical giant cell for infectious

granulomas is called a Langhans giant cell and has the nuclei lined up along

one edge of the cell.




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This is the acid fast stain ofMycobacterium tuberculosis

(MTB). Note the red rods




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PrimaryTuberculosisPrimaryTuberculosis FateFate

1. Fibrosis & calcification healinghealing(9595%% of cases).

Only 5% of the newly infected persons are symptomatic

Scar may harborviable bacilliviable bacillifor years and perhaps for life:Act

as a nidus forreactivationreactivation at a later time when host defenses arecompromised

22 .. Progressive primary tuberculosisProgressive primary tuberculosis::

Occurs in immunosuppressed patients, malnourished children &

elderly

The primary focus enlarge:A.A. Acute pneumoniaAcute pneumonia--like picture:like picture:

Lower& middle lobe consolidation, pleural involvement

with effusion or empyema, hilar lymph node enlargement,

cavitation is rare


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B.B. Direct spreadDirect spread::

Erosion into bronchial tree produces:

Foci of infection in other parts of the lung

Laryngeal tuberculosis from coughed infected sputum

Intestinal tuberculosis from swallowing infected sputum


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C.C. Haematogenous spread into blood vessels:Haematogenous spread into blood vessels:

Will produce:

Isolated - organ tuberculosis in kidney, bone, meninges,

adrenal gland & fallopian tubes: The organisms are destroyedin all the organs but persist only in one organ

Systemic generlized miliary tuberculosis:

When the infective foci seed the pulmonary venous return to

the heart dissemination through systemic circulation to

different organs especially liver, bone marrow, spleen, adrenals,

meninges, kidneys, fallopiantubes and epididymis

Morphology:Morphology: Microscopic or small, visible (2mm) foci of yellow-

white consolidation scattered throughout the affected organs


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Secondary Reactivation orPostSecondary Reactivation orPost

PrimaryTuberculosisPrimaryTuberculosis

Tuberculosis that develops in a previously sensitized host

Causes:Causes:

1.1. ReactivationReactivation of dormant primary lesions when hostresistance is weakened most common main methodin low prevalence areas

2.2. Exogenous reinfectionExogenous reinfection due to: main in high prevalence

areas Waning of the protection offered by the primary disease OR

Large inoculum of virulent bacilli

Only


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PrimaryTuberculosisPrimaryTuberculosis -- MorphologyMorphology

Classic locationClassic location: the apex of one or both upper lobes

The initial lesion is usually a small focus ofsmall focus ofconsolidationconsolidation, less than 2 cm in diameter in the apexapex

Because ofpreexistent hypersensitivitypreexistent hypersensitivity, a rapid andrapid andmarked tissue responsemarked tissue response will start & will try to wall offwall offthis focus

Regional LNs are less prominently involved

Cavitation allow spread of infection via airways & isan important source of infectivity

Microscopically:Microscopically: Sharply circumscribed, firm, gray-white to yellow areas with central caseation & peripheralfibrosis


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PrimaryTuberculosisPrimaryTuberculosis Fate & CourseFate & Course

1.1. Healing:Healing:

In favorable cases, having good immune response or afterRx

Progressive fibrous encapsulation and calcification

fibrocalcific scarfibrocalcific scar

Usually impossible to find tubercle bacilli within these

lesions


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2.2. Progressive pulmonary tuberculosis:Progressive pulmonary tuberculosis:

Apical lesion enlarges with expansion of the area of

caseation (progressive cavitating pulmonary tuberculosis)

Erosion into a bronchus evacuation of the caseous centeropen lesion ragged, irregular cavity lined by caseous

material that is poorly walled off by fibrous tissue

Erosion of blood vessels haemoptysis

Involvement of the pleural cavity

serous pleural effusion,tuberculous empyema or obliterative fibrous pleuritis


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With adequate treatmentWith adequate treatmentthe process may

be arrested, healing by fibrosis whichmight distort the pulmonary architecture

If treatment is inadequate or with impairedIf treatment is inadequate or with impaired

host defenses:host defenses: Spread of infection


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PrimaryTuberculosisPrimaryTuberculosis SpreadSpread

Direct expansion

Dissemination through the bronchial tree establish new

foci of infection in the lung and produce tuberculous

broncopneumomia Endobronchial, endotracheal and laryngeal tuberculosis:

When infected material spreads either through

lymphatic channels or from expectorated infectious

material

The mucosal lining studded with many minute

grnulomatous lesions

Dissemination through lymphatics or vascular system

miliary tuberculosis


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This is an example of granulomatous

disease of the lung. The pattern of

smaller nodules which have a

propensity for upper lobe

involvement suggests a

granulomatous process rather than

metastatic disease

SecondaryTuberculosisSecondaryTuberculosis GrossGross



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On closer inspection, the granulomas

have areas of caseous necrosis. This is

very extensive granulomatous disease.

This pattern of multiple caseatinggranulomas primarily in the upper lobes

is most characteristic of secondary

(reactivation) tuberculosis. However,

fungal granulomas (histoplasmosis,

cryptococcosis, coccidioidomycosis) can

mimic this pattern as well




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When there is extensive caseation and thegranulomas involve a larger bronchus, it

is possible for much of the soft, necrotic

center to drain out and leave behind a

cavity. Cavitation is typical for large

granulomas with tuberculosis. Cavitation

is more common in the upper lobes




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This is more extensive caseous

necrosis, with confluent cheesy tangranulomas in the upper portion of

this lung in a patient with

tuberculosis. The tissue destruction is

so extensive that there are areas of

cavitation (cystic spaces) being

formed as the necrotic (mainlyliquefied) debris drains out via the

bronchi




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IntestinalTuberculosisIntestinalTuberculosis

Due to drinking contaminated milkcontaminated milk

It was common, now is less frequent

Today in developed countries it is often a complication of

advanced secondary T.B & is due to swallowing of coughedswallowing of coughedupup infective material

It is accompanied by involvement of the oro-pharyngeal

lymphoid tissue and involvement of neck lymph nodes

The organisms are trapped in mucosal lymphoid aggregates

of small and large bowel inflammatory enlargement&ulceration of the overlying mucosa, particularly in ileum

Ulcers are rounded or oval, have undermined ragged edges

and soft yellow caseous floor


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HematogenousSpread:HematogenousSpread:

IsolatedIsolated--OrganTuberculosisOrganTuberculosis

Appear in any organ or tissue seeded via blood

Can be the presenting manifestation of T.B

The favored sites are: Bone: Tuberculous osteomyelitis

Vertebral involvement results in Potts disease

Lymph nodes, spleen, adrenals, kidneys, meninges,

fallopian tubes, epidydymis,


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Systemic MiliaryTuberculosisSystemic MiliaryTuberculosis

Via pulmonary venous return:Via pulmonary venous return:

The infective material return to the heart

disseminate theorganisms into the systemic arterial system

Most prominently involved organs are spleen, liver, bone

marrow, adrenals, kidneys, fallopian tubes, epididymis, and

meninges

NOTE:NOTE:

Tissues resistant to TB infection are: Heart, striated

muscle, Thyroid and pancreas

H S dH S d


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Miliary PulmonaryTuberculosisMiliary PulmonaryTuberculosis

Via lymphatics into lymphatic ducts:Via lymphatics into lymphatic ducts:

Empty into the venous return to right side of the heart

pulmonary arteries diffuse miliary T.B. of the lung


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When the immune response is poor

or is overwhelmed by an extensive

infection, then it is possible to see

the gross pattern of granulomatousdisease seen here. This is a "miliary"

pattern of granulomas because there

are a multitude of small tan

granulomas, about 2 to 4 mm in size,

scattered throughout the lung

parenchyma. The miliary pattern gets

its name from the resemblence of the

granulomas to millet seeds

MiliaryTuberculosisMiliaryTuberculosis GrossGross



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This is a caseating granuloma of tuberculosis in the

adrenal gland. Tuberculosis used to be the most

common cause of chronic adrenal insufficiency. Now,

idiopathic (presumably autoimmune)Addison's disease

is much more often the cause for chronic adrenal

insufficiency

Adrenal GlandTuberculosisAdrenal GlandTuberculosis


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This spleen shows a miliary pattern of granulomatous

inflammation, with numerous small tan granulomas. This suggests

a poor immune response. This patient had AIDS. The infection

turned out to be Mycobacterium avium-intracellulare (MAI), also

known as Mycobacterium avium-complex (MAC)

MiliaryTuberculosis inSpleenMiliaryTuberculosis inSpleen


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TuberculosisTuberculosis Clinical FeaturesClinical Features

Localized type may be asymptomatic

Low grade remittent fever, night sweats, malaise,

anorexia, weight loss Sputum at first mucoid and later purulent

Haemoptysis in half of the patients

Pleuretic pain


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TuberculosisTuberculosis DiagnosisDiagnosis

History, physical examination, radiological

findings consolidation & cavitationconsolidation & cavitation

Identification of the acid-fast bacilli in smears

and culture of sputum 10 weeks

PCR amplification ofM. tuberculosis DNA


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TuberculosisTuberculosis PrognosisPrognosis

Depends on:

The extent of the disease and the patient immune

status

Secondary amyloidosis may occur in persistent cases


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TuberculosisTuberculosis Chronic ConsequencesChronic Consequences

1.1. Pulmonary fibrosisPulmonary fibrosis

The lung lesions may heal with fibrosis at any stage, particularly with

treatment

This ranges from minor apical scarring to extensive and severe

widespread fibrosis producing localized to widespread honey-comb

appearance of the lung tissue. It is particularly seen in relapsing and

progressive untreated disease

This is complicated by respiratory failure & cor pulmonale

2.2. Pleural fibrosisPleural fibrosis Fibrosis commonly obliterate the pleural space

3.3. BronchiectasisBronchiectasis

Damage to the bronchial walls and scarring can cause distal pulmonary

collapse, secondary infection and bronchiectasis


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Infection in ImmunocompromisedInfection in Immunocompromised

IndividualsIndividuals

Mycobacterial infection of all types are increased in

immunocompromised individuals and is in most casesdue to reactivation of latent infectionreactivation of latent infection

Features are similar to infection in immunocompetent

individuals but disease usually progresses more rapidlyprogresses more rapidly due to

decreased host response


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Atypical Mycobacterial InfectionAtypical Mycobacterial Infection

These infections are caused by a group of non-tuberculous

mycobacteria of which the most important types are M.M.

aviumavium-- intracellulareintracellulare and M. kanasiiM. kanasii

The organisms are widely distributed in soil, water &soil, water &

domestic animalsdomestic animals

Infection is acquired directly from the environmentacquired directly from the environmentand

not by case to case contact

Infection by these organisms is seen inimmunocompromised patients particularlyAIDS

It can be seen also in immunocompetent individuals with

chronic pulmonary disease


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The lymph nodes in this mesentery, best seen at the left, are

enlarged and have cut surfaces that appear yellow-tan. These nodes

are filled with sheets ofMycobacterium avium-complex (MAC)

organisms, and the immune response is so poor in thisAIDS patient

that there is no focal granuloma formationno focal granuloma formation


Gross MorphologyGross Morphology


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Microscopically, Mycobacterium avium-intracellulare infection is

marked by numerous acid fast organisms growing withinnumerous acid fast organisms growing within

macrophagesmacrophages. Lots of bright red rods are seen, particularly in

macrophages, in this acid fast stain of lymph node


Microscopic MorphologyMicroscopic Morphology


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PRIMARYPRIMARY SECONDARYSECONDARY

Affect:

* Previously unexposed, unsensitized persons

* Non immune children

* Elderly & immuncomprised* Very young

Source:

* Exogenous

* 5% develop significant disease

Morphology & Site:* Primary T.B. mostly in lung rarely in

intestine, pharynx, larynx & skin

* Involve lower part of upper lobe or upper

part of lower lobe close to pleura

* Ghon-focus

A 1-1.5 cm gray white inflammatory

consolidation with involvement of hilarlymph node

* In 95% of cases the development of cell-

mediated immunity control the infection & no

lesion develops

Affect:

* Previously sensitized persons

Sources:* Develop from:

- Reactivation of dormant lesion

- Primary lesion if immunity of host is lowered

exogenous reinfection

- 5% of primary T.B. develop secondary T.B

Morphology & Site:* Localized at the apex of both or one upper

lobes because of better 02 tension

* Less lymph node involvement than the primary

* Cavitation is more common with dissemination

along air ways

- Cavitation is a source of infection by

sputum* Typically consolidating lesion 1-2 cm, firm

gray-yellow at apical pleura with central

caseation & peripheral fibrosis


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Histology:

* Typically granulomatous inflammation, both

caseating and non-caseating

Outcome:

* Hypersensitivity & increased resistance

* Healing & scarring ofGhon-focus but may

be still a focus for reactivation

*May progress to progressive primary T.B.

or disseminated T.B. especially in AIDS,

malnourished, very old, very young& Eskimos

Progressive primary T.BProgressive primary T.B.:

1. Progressive enlargement of the primary

focus with lung destruction & cavitation

2. Extension to the pleura pleural effusion

or empyema3. Enlarged lymph nodes obstruct bronchi

bronchiectasis

Histology:

* Same

Outcome:

* The apical lesion may heal spontaneously

Or with treatment and become a fibrocalcific

Scar

* Depress and pucker the pleural surface and can

cause pleural adhesion

Progressive pulmonary tuberculosis:Progressive pulmonary tuberculosis:

1. Apical lesion enlarge with expansion of

caseation.(cavitary fibrocaseous TB)

2. Erosion into bronchus with evacuation

forming irregular cavity poorly

delineated by fibrosis open lung lesion3. Erosion into blood vessels hemoptysis

4. Invasion of pleural space pleural

effusion, tuberculous empyema or

obliteraytive fibrous pleuritis


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Dissemination:

* Erosion into bronchi with spread of the

Infection

- Foci of infection in other parts of the lung

- Tuberculous pneumonia- Laryngeal T.B. from coughed sputum

- Intestinal T.B. from swallowing of

infected material

* Erosion of vessels

- Lymphatics foci of infection in the

lung lung miliary T.B.- Blood vessels systemic miliary T.B.

- Single-organ T.B. in bone, kidney, joint,

brain

Fate:Fate:

* With adequate treatment:

- The process is arrested by healing with

fibrosis & destruction of the lung architecture

If treatment is inadequate and host defence isimpaired:

- Spread of infection occurs

Spread:Spread:

* Dissemination via airways, lymphatics & BV

Miliary pulnmonary disease when bacilli drain

via lymphatics in lymphatic duct to the rightheart back to the lung and give miliary T.B.

Miliary systemic T.B. when infective foci seed

the pulmonary venous return to the heart to the

systemic circulation (liver, bone, spleen,

adrenals, fallopian tubes)

Endobronchial, endotracheal laryngeal miliary

granuloma Isolated organ T.B.

Intestinal T.B.


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