King of pathology

By\King of pathology( Legand Hazem )

INFECTION
efinition!
invasion of ! living tissue by pathogenic microorganisms. These are ! viruses, bacteria, fungi, protozoa
& metazoan and development of pathological changes.
"ethod# of Infe$tion :
%) E&ogeno'# from patient or carrier via:
1-Sin or mucous membrane, in!ury facilitates ! infection.
e.g.sin T" #$upus vulgaris%, leprosy, & .
'- (ngestion #food or )ater%.
e.g. Typhoid fever, cholera, bacillary dysentery.
*- (nhalation:
- +irectly d.t inhaled droplets from patient.
- (ndirectly d.t inhalation of contaminated dust.
e.g. T" & other respiratory tract infection.
,- (n!ection & blood transfusion.
e.g. & , malaria, viral hepatitis, -(+S.
.- se/ual Transmission.
e.g. & , -(+S.
0- Transplacental from infected mother to ! fetus. e.g. congenital & , 1ubella, To/oplasmosis.
() Endogeno'# d.t
1- 2ommensals: "acteria normally present in ! body & under certain conditions, they turn pathogenic.
e.g.: Strept. viridans #in ! mouth%. 3neumococci #in 4asopharyn/%. 5 coli. #in ! intestine%.
infection occurs )hen ! body resistance - - 6 immunodeficient states #immune suppressive therapy,
prolonged antibiotic therapy% or, )hen these bacteria change their position. This is called
opportunistic infection
'- septic focus: as sinusitis, cholecystitis7etc
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)e#'lt# of Infe$tion (*a$te+ia i# ta,en a# an e&ample %:

(mmunity , )ea organism subclinical infection.
(mmunity , strong organism disease.
"ethod# of -p+ead of Infe$tion:
1-$ocal #+irect%: via tissue ,fluid and motility of macrophage.
'-$ymphatic :through the draining lymphatic.
*-"lood :through the )all of blood vessel 8r from lymphatic system )9 lead to to/emia,bacteremia,
septicemia and pyemia.
,--long the natural passage:5.g 1espiratory tract and lung alveoli.
I. To&emia
%.ef (.-o'+$e /.Type#0
%.ef!
2irculation of bacterial to/ins in ! blood )ith production of clinical & pathological manifestation.
(.-o'+$e# of To&in#!
1. produced by the organism itself:
:5/oto/ins from living gram ; ve bacteria. e.g. 4ecroto/in
:5ndoto/in from gram -ve bacteria.
2. released from the necrotic tissue
/.Type# of To&emia!
1) Acute Toxemia= Exotoxic toxemia :
$arge doses of to/ins reach ! blood )ithin a short period
e.g. acute infections such as diphtheria, bacillary dysentery, lobar pneumonia.
2) hronic Toxemia=Endotoxic toxemia :
Small doses of to/ins reach ! blood over long period e.g. chronic infections such as T", & .
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1Effe$t# of to&emia
I)Clini$al ($on#tit'tional #ign# 2 #ymptom#) : fever, headache, rigor, loss of appetite, loss of )eight,
tachycardia & ;; tissue metabolism
II)3athologi$al !
1-inflammation
'- degeneration: acute to/emia degeneration of parenchymatous organs # cloudy & fatty change%.
*- -myloidosis : in chronic to/emia
,-4ecrosis: acute to/emia hemorrhage of suprarenal glandsnecrosis & acute adrenal insufficiency
.--nemia: d.t depression of b.marro) by to/ins & hemolysis of 1"2s
N0B!-ap+emia! 6 to/in production by saprophytes on necrotic tissue e.g.retained placental products
after labor or abortion
II. Ba$te+aemia
%.ef (.-o'+$e# /.Effe$t#
%.ef!
2irculation of small number of bacteria e9out multiplication in the blood and e9out to/ins
(.-o'+$e# of *a$te+ia!
1) Endogenous :
-2ommensals : e.g. Strept veredans by tooth brushing, tooth e/traction%
-Septic foci as boil, otitis media, sinusitis7etc
2) Exogenous :
(n early stages of certain diseases as in typhoid fever & &
/.Effe$t#!
:2ommonly destroyed by body defense.
:$arge dose cause disease E0g:Subacute infective endocarditis #S(5%
Staph aureus cause 8steomylitis !"#$%& '()*
III. -epti$emia
%.ef (.Ca'#e# /.method# 4.effe$t# 5.O+gan affe$ted 6.C73 8.p+ogno#i# 9.po#tmo+tem0
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%.ef!
2irculation & multiplication of large number of virulent microorganism )ith their to/ins in ! blood
)ithout localization & )ith production of severe constitutional manifestations & structural changes.
(.Ca'#e# 2 pathogene#i#!
+),redisposing factors: +ecreased body defense due to immunodeficiency states
++)Exciting factors : 3yogenic microorganisms as:
: commonest is Strept. hemolyticus #in puerperal sepsis%.
:Staph. aureus #in acute 8steomyelitis%
:<eningococci #in septic meningitis%.
:=onococci #in gonorrhea%.
/."ethod#!
The micro- organisms reach ! blood by:
1-(nvasion of ! systemic arterial circulation from suppurative lesion of ! lungs or left side of ! heart
'-(nvasion of ! systemic venous circulation via:
a->inger pric by infected scalpel at operation or autopsy of septic cases.
b-Septic thrombophlebitis as in puerperal sepsis, cellulitis, osteomyelitis & septic meningitis.
c-from lymphatic system as in cellulitis.
4.Effe$t# of -epti$emia !(pathology)!
I)-e:e+e to&emia ;ith it# effe$t#!
a- 5rythrogenic 4ecroto/in act on ! capillaries producing necrosis of their )alls )hich leads to
multiple petechial hemorrhage in sin, mucous membranes & serous membranes
b- >atty change, cloudy s)elling of parenchymatous, organs & ?ener@s degeneration of muscles.
2- >ocal necrosis especially in:
- $ymphoid system.
- $iver & heart.
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- suprarenal gland - acute adrenal insufficiency.
II)Enzyme#!
a-Streptoinase & fibrinolysin: prevent blood coagulation.
b- Aemolysins #$ecithinase% dissolve ! cell membrane of erythrocytes.Aemolytic anemia
!aundice & ! intima of bl vesselsstained dar red color d.t released Ab.
5.O+gan# <ffe$ted!
I) -pleen! a$'te #pleni$ #;elling o+ t'mo+ (#epti$emi$ #pleen)!
N7E : :5nlarged, hyperemic, very soft, friable. C7- :bulging of red pulp )hich appears red-grey &
semifluid #)ashed under tap )ater%.
:$ymphoid follicles are ill defined.
"7E:+ilated congested sinusoids& atrophic lymphoid follicles & infiltration by neutrophils,
lymphocytes, macrophage & plasma cells& $ittoral cells sho) phagocytic activity
II) Lymph node#! Enla+ged 2 +e#em*le #pleen in "7E
III) Hea+t! =#epti$emi$ hea+t=!.
N7E 1 - Enla+ged, soft, flabby )ith dilated chambers. ! blood in ! dilated chambers & big blood
vessels does not coagulate #fluidity%.
'- The endo$a+di'm stained red.
*- The myo$a+di'm sho) foci of suppurations #abscesses%, necrosis and degenerations #fatty
change & cloudy s)elling%.
,- The pe+i$a+di'm: :is thic , dull ,opaBue and reticulated.
:the pericardial sac contain yello) pus.
.- The :al:e# sho) vegetations #-(5% acute infective endocarditis.
"7E! the endocardium&myocardium&pericardium&cusp vegetations sho) pi$t'+e of #'pp'+ati:e
inflammation #pus cells,$ongested blood vessel,e/udates rich in fibrin,neutrophils,necrosis%
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I>) Bone ma++o;!
-t first, there is increase of immature granular cell series then later, they decreased.
Therefore, ! blood picture sho)s leuocytosis follo)ed later by leucopenia.
6.C73
- 3atient is severely ill.#septicemic Shoc & fever%.
- 1ed color of sin #Ab%.
- Cello) color of eye #Daundice%.
8.3o#t mo+tem pi$t'+e: Sin is red, hot & Daundice may manifest.
<ultiple petechial hemorrhages. >luidity of blood in ! heart & big vessels.
9.3+ogno#i#!
Fatal in ho'+# o+ day# due to :acute heart failure,acute renal insufficiency and hypotension
I> 3yaemia
%.ef (.Type#.$a'#e# /.pathology 4.p+ogno#i#
%.ef! :2irculation of septic emboli #detached septic thrombi% e9 their localization in ! organs
:The responsible microorganism is usually Staph. aureus.
(.Type#:
I) 3'lmona+y pyemia!
Septic emboli coming from different organs & circulate in systemic venous blood then pulmonary
arterial circulation to be impacted in lung capillaries.
Common $a'#e#! puerperal sepsis or osteomyelitis or septic meningitis.
() -y#temi$ pyemia!
Septic emboli coming from suppurative lung lesions or from left side of ! heart & circulate in systemic
arterial blood to reach different body organs.
Common $a'#e#: suppurative lung lesion & acute bacterial endocarditis.
/) 3o+tal pyemia!
Septic emboli coming from suppurative lesion of =.(.T circulate in portal venous circulation to reach
liver.
Common $a'#e#: acute suppurative appendicitis , cholecystitis .
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4.3athology
(%) Capilla+y impa$tion p+od'$e# m'ltiple a$'te a*#$e##e# (pyemi$ a*#$e##e#)0
4E5:
:<ultiple abscesses
:8n outer & cut surface
:Cello)ish #pus%
:eBual in size #1-' mm%
:related to a blood vessel
:more or less rounded.
:5ach abscess is surrounded by zone of hyperemia.
<E5: as an abscess -./0 ? central bacterial colonies
(() <+te+ial impa$tion $a'#e# la+ge+ fo$i of #'pp'+ation (#epti$ infa+$t#)0
(/) Clo'dy #;elling 2 fatty $hange of @ pa+en$hymato'# o+gan#0
4.3+ogno#i#!
- 1apidly fatal.
- 2ommonly complicated by septicemia.
Infe$tion i# $la##ified to!
%.Ba$te+ial! (.3a+a#iti$ /.F'ngal 4.>i+al
1 T0B 2 A(#yphili#)0 1Bilhazia#i#0 1<$tinomy$o#i#
1Lep+o#y0 1 Hydatid 2 Fila+ia#i#0
1-a+$odo#i#(g+an'loma of 'n,no;n $a#'#e)0
>i+al infe$tion
3athologi$al effe$t# of :i+'#e# B ti##'e +ea$tion to :i+'# infe$tion in$l'de!
1 - 2ellular degeneration.
'- 2ellular necrosis.
*-2ellular proliferation as in sin )arts
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,->ormation of =iant cells.
. - (ntra-cellular inclusions bodies.
a%(ntracytoplasmic as: 2ouncilman bodies in viral hepatitis.
b% (ntranuclear & intracytoplasmic as: in cytomegalovirus.
0- 1elease of interferon.6 antiviral molecules
Type# Of >i+al Infe$tion
%. <$'te :i+al Infe$tion:
-s in influenza, measles, chicen po/ poliomyelitis, viral hepatitis.
<ethod of infection by inhalation or ingestion.
"e$hani#m!
The virus proliferates in ! cells at entrance site local lymph nodes cell death release to
blood stream.
3rimary viremia : ! virus circulate in the blood primary viremia constitutional symptoms
fever malaise, headache, vomiting, bone aching & lymphadenopathy%.
The virus multiply in all $.nodes )ith -- of constitutional symptoms.
Secondary viremia : ! virus released from all body lymph node to blood forming secondary
viremia )ith localization in specific organs.>or e/ample:
Firal hepatitis -, ", 2 to liver cell.
3oliomyelitis anterior horn cell.
2hicen po/ & Small po/ sin.
<easles lymphoid tissue.
(. Latent >i+al Infe$tion!
--Aerpes simple/ type(.
"-Aerpes zoster in young age ! organism becomes latent in dorsal root ganglion manifest in old age.
/.-lo; >i+al Infe$tion:
- 2rutz field =acop disease.
4. On$ogeni$ >i+'# infe$tion a#! !&123% 455)6%& 7"829:;%&
-- 3apova virus #papilloma virus%:
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2ondyloma accuminata.
2ommon )art.
Duvenile laryngeal polyp.
"- 5pstein "arr virus:
infectious mononucleosis .
"uritt@s lymphoma.
4asopharyngeal carcinoma.
2- A" Firus hepatoma.
+- Aerpes simples virus type (( cancer cervi/.
F'ngal Infe$tion
Ca'#e#!
>ungi & 3seudofungi #commensal type of bacteria%
Type#!
(- Superficial mycosis : tinea nigra, tinea vircecolour.
((- 2utaneous mycosis : 1ing )orm.
(((-+eep mycosis #subcutaneous mycosis%
a-$ocalized. b-Systemic.
<. Lo$alized a# :
<$tinomy$o#i# :
ef! -'pp'+ati:e g+an'loma )ith formation of multilocular abscess caused by pseudofungus
#actinomyces israeli, or actinomyces bovis%. (+y infe$tion may be ! cause of
#'pp'+ation
"ethod of infe$tion!
:3seudofungi are commensals in mout&intestine.
:(t invade tissue through mucosal abrasion.
: the superficial )ounds heal & the disease spread.
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-ite#!
a% 2ervicofacial #0GH%.
b%-bdominal #'GH%# iliocecal area% ma## in )t0 Ilia$ fo##a.
#blood spread but not lymphatic% to liver multiple lesions in ! liver.
c% 3ulmonary #1.H% aspiration from ! mouth abrasion lung or through diaphragm from
liver infection spread to surrounding #blood%.
d% Sin #.H%.
N7E!
%.-ite: a% 2ervicofacial #0GH%.
b%-bdominal #'GH%
c% 3ulmonary #1.H%
d%Sin #.H%.
(.-hape! Aard mass formed of multiple abscesses e9 multiple sinus discharging pus containing
Sulpher lie granules colonies of actinomyces israeli
"7E!
Suppurative granulomas formed of:
Cente+ : yello)ish bro)n fungus colonies )9 are formed of red stained clubs #rounded% and
hyphae #deep blue filaments%
3e+iphe+y : neutrophils ; pus cells ; macrophages ; lymphocytes ; fibrous tissue
Fate! a-1epair by fibrosis.
b-Spread:
1 . i+e$t. (t is the main method and donIt respect any structure.
'. Blood #p+ead #rare%.
*. Lymphati$ #p+ead not o$$'+.
"y$etoma ("ad'+a footC "ad'+amy$o#i#) it diffe+# f+om a$tinomy$o#i# in!
- 2aused by 4ocardia # live in soil %.
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- Spread only locally# direct %
N7E : %.-ite: in e/tremities #palm;foot%.
(.-hape:<# a$tinomy$o#i# e/cept only one difference:-
The $olonie# may *e ;hiti#hC*la$,C*+o;n o+ yello;0
"7E!-s actinomycosis -./0
3a+a#iti$ infe$tion
%.Hydatid di#ea#e
1efinition! (t is an infective parasitic disease transmitted from animal #dog% to man.
$a'#ed *y ingestion of contaminated food e9 egg of 5.granulosus by man hatch in ! intestine pass
)ith portal blood to ! liver mature into larval stage #hydatid cyst%.
-(t may pass to ! lung, systemic circulation brain, bone
-cyst may reach 'G cm in diameter. (t is composed of:
1% - lumen contains stra) -colored fluid.
'%(nner germinal layer:- that forms scolices.
*%8uter chitinous laminated layer.
,%Surrounding fibrous capsule.
1$ompli$ation#!
1 %3ressure on ! surroundings.
'% rupture anaphylactic shoc.
*% 'ry bacterial (nfection.
,%Spread of scolices directly or by blood.
(.Fila+ia#i#
1Etiology!
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King of pathology
The disease is transmitted by bites of ! 2ule/ pipiens mosBuitoes )hich inoculate micro-filaria of
Juchereia "ancrofti in ! sin. These microfilaria migrate to lymph nodes & lymphatics #mostly of !
lo)er limbs & e/ternal genitalia%)here they mature into adult )orms.
13athology! %.Lymphangiti# 2 lymphadeniti# #inguinal, femoral & popliteal lymph nodes%.
(nflammation is mainly produced by dead adult filaria )orms. (t starts allergic #eosinophils% then
becomes chronic granulomatous. 4ecrosis & liBuefaction may occur #filarial abscess%. >ibrosis )ill
finally cause lymphatic obstruction.
(.Lymphati$ o*#t+'$tion!. ! lymphatics distal to obstruction become dilated #lymphatic varices% &
may rupture leading to:
:2hylous ascites #$ymph in ! peritoneal sac%. :2hylothora/, chylocele.
:5lephantiasis: This is lymphatic edema #hard non pitting edema% of ! lo)er limb associated )ith
fibrosis. ! limb becomes maredly enlarged & ! sin is e/tremely thicened.
Ba$te+ial infe$tion
LE3)O-D
%.ef!infective granuloma caused by mycobacterium lepra.
(."ethod of infe$tion!
1bacteria enter via sin#commonly% or via 1s mucosa#rare%.
1infectivity is la) infection occur by long close contact.
1(ncubation period :.-1G days.
/.Type#! <)Ea+ly lep+o#y!
:manifestations: anesthesia &greenish maculed on the face and limbs.
:>ate: K.H recovery e9out tt.
'.H progressed to established leprosy.
B)E#ta*li#hed lep+o#y(Typia$l)!* types:
:$epromatous leprosy#nodular%.
:Tuberculoid leprosy#maculo-anasthetic%.
:"orderline leprosy:- :mi/ture of ' typical forms.
-unstable till change to one of the previous type
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Lep+omato'# lep+o#y B
nod'la+ lep+o#y
T'*e+$'loid lep+o#yB
Ne'+al lep+o#y0
%.in$iden$e!
(.Imm'nity!
4.infe$ti:ity
5.No0of
*a$illi!
/.Nat'+e!
6.Ne+:e
infilt+ation!
8.N7E!
9."7E!
E.3+ogno#i#
%F.iagno#i#!
commonest
high
high
high
progressive.
4o nerve infitration
. (t affects:
%)-,in! - multiple nodules on nose, eye
lids, eye bro)s
- ! lesion is symmetrical in both
sides
- leonine face#$oss of eye bro)s%
()e+mal #en#o+y ne+:e! - glove &
stocing anesthesia loss of sensation,
tissue atrophy autoamputation of
fingers & toes.
/) "'$o'# mem*+ane:sho) nodules in:
4ose bloced nose.
$aryn/ hoarseness of voice.
4)affe$tion of inte+nal o+gan# e&$ept
C0N0-0
)ea$tion! Lep+omato'# +ea$tion:-
:diffuse reaction.
: formed of dense infiltrate of
macrophages & lymphocytes.
: ma$+ophage#: contain lepra bacilli
foamy macrophages called #$epra
cells% & giant $ell#0
:lympho$yte#:scanty 8r absent.
:! reaction ends by fi*+o#i#0
:need tt.
:cause of death:renal failure.
$epramin test: -ve
$ess common.
lo)
lo)
lo)

regressive.

presence of nerve infiltration.
. (t affects:
%) -,in!.hypopigmented anaesthetic
e9 flat macules.
- ! lesion is <symmetrical.
-sin ulceration;'ry infection.
() 3e+iphe+al (moto+ 2 #en#o+y
ne+:e#)!
Sho) :cord lie thicing.
:paralysis.
: anesthesia.
/)No affe$tion of inte+nal o+gan0
)ea$tion! T'*e+$'loid +ea$tion!.
$ocalized reaction:#tubercle lie granuloma
: Tubercle is similar to T." formed
of epithelioid cells, $anghans giant
cells and lymphocytes.
:giant $ell#:fe),small,e9 fe)
nuclei.
: lympho$yte#:plenty ,peripherally.
:4o caseation #non $a#eating t'*e+$le).
:! reaction ends by fi*+o#i#.
:spontaneous or stationary cure.
$epramin test: ;v
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-a+$odo#i# T0B
%.ef!
(.N7E!
/."7E!
4.
hype+$al$emia
5.+eti$'lin
F+ame;o+,!
6.3+ogno#i#!
8.iagno#i#!
:4on caseating granuloma of
Lnno)n cause.
:-ssociated e9 T-cell depression.
4on caseating lesions:-
a)L0N##hilar&mediastinal% :4ot
matted
*)L'ng! (Honey $om* appea+an$e%:
diffuse granulomas in alveolar )all
e/tensive fibrosis
compensatory dilatation of
surrouding bronchi.
:bacilli: 4o.#unno)n cause%.
:4o caseation.
:lymphocyte: Scanty.
: giant cells:- -fe).
-Schauman;asteroid inclusions
-mainly central nuclei.
:5pithrloid cells.
;;
(ntact
Lnpredictable: acute 8r chronic
Temorary 8r permanent.
Mveim test
:(nfective granuloma due to T." bacilli.
2aseating lesions:-
a) L0N##hilar&mediastinal%:matted.
*)L'ng:either:-# K%
:=honIs focus. :-ssmonIs simon
focus.
:2hronic fibrocaseous T.".
:T." bronchopneumonia.
:T." pneumonia. :<iliary T.".
:Tuberculoma.

: bacilli: present.
:central caseation.
:lymphocyte: plenty..
: giant cells:- -numerous.
-4o inclusions.
-peripheral nuclei.
Same.

N N
destroyed
=ood# healing % 8r "ad # spread %.
Tuberculin test.
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By\King of pathology( Legand Hazem )
TGBE)CGLO-I- ( T0B )
ef : 2hronic infective granuloma affecting nearly all body systems but mainly ! lungs.
Ca'#e# :-
<.3+edi#po#ing Fa$to+# !
En:i+onmental! 3e+#onal !
$o) socioeconomic level
2ontact e T" patient.
8ver cro)ding.
5nvironmental pollution.
4egroes.
"ad general hygieneG
<alnutrition.
+epletating #+<% & (mmune deficiency dse
B.mode of infe$tion : )ill be disscused.
$.Ca'#ati:e <gent# B E&$iting fa$to+# !
: TB *a$illi :
-t+'$t'+e of TB *a$illi !
* layers: 2A8, lipid & protein #tuberculoprotein%.
Type# of TB Ba$illi !
1- Auman type #<ycobacterium T"%: transmitted by inhalation from infected patient
'- "ovine type #<. "ovine%:transmitted by ingestion of infected co)@s mil
*- 8ther rare Types: -vian type.
Cha+a$te+ of TB *a$illi !
:)ea So sensitive to direct sunrays.
:aerobic O resist dryness.
:4on motile- 4on invasive.
:Not to&igeni$.
:highly antigeni$ :e+y i++itant to imm'ne #y#tem0
1Type# of T0B !
1-primary T."
'-secondary T."
)ea$tion of the *ody again#t *a$illiB t'*e+$le fo+mation B p+olife+ati:e +ea$tion B pa+en$hymato'#
le#ion0
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-3-TA8=545S(S
In %#t (4 h# from introduction of bacilli inside attraction of neutrophils to 2A8 layer of !
bacilli, but they can@t ill it & rapidly disappear.
F+om @ (
nd
day, attraction of macrophages & lymphocytes to lipid layer of ! bacilli.
macrophages engulf ! bacilli but can@t ill it # the organism multiply inside % as <acrophages at this
stage are unsensitized.
Fe; ;ee,# : T-lymphocytes are attracted to protein layer of bacilli # 33+ %,
T" granuloma is formed by the interaction # % macrophages & T cells
:Chemi$al mediato+# of g+an'loma fo+mation:
Fa$to+# +elea#ed *y ma$+ophage# Fa$to+# +elea#ed *y helpe+ T $ell#
($-1': ;; helper T cs to secrete
($-': ;; mitosis of other
lymphocytes
(4> : most important factor for
granuloma formation :
1- ;; production of monocytes from
bone marro).
'- ;; production of ($-1' from
macrophage
*- ;; all steps of phagocytosis
T4>:
1. 2hemotactic for macrophages
'. -ttrctive to other lymphocytes from
blood
*. Fasodilator # help more
macrophages & lymphocytes to reach the
area%
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The lipid part of ! engulfed bacilli changes ! characters of macrophages to cell similar to
epithelial 2s called epithelioid cells:a- "7E disscused later -./0
E": cell membranes sho) desmosomes # % 2s form a )all against spread of infection
$anghan@s giant 2s:-a-formed by fusion of epithelioid cells.
b- <E5 disscused later -./0
lymphocytes surround epithelioid 2s
>ibroblasts appear & encircle ! tubercle by fibrous tissue So The tubercle at this stage is
called Fi+m t'*e+$le
<fte+ ( . / ;,# a central caseation start in ! center & ! tubercle become #oft t'*e+$le
Ca#eation i# $a'#ed *y!.
1.lymphoines of sensitized lymphocytes.
'. 3roteolytic enzymes from dead neutrophils.
*.1elative central ischemia.
,.+elyed hypersensitivity reaction against tuberculoprotein.
N7E of TB +ea$tion! Size:1-*mm
2 -
Shape:at first granules then become cavity .
2olour:yello)ish .
(C
2onsistency:firm then after caseation become soft
"7E of t'*e+$le :
A< +f =on caseating tubercle :
Jell formed pale pin granuloma formed of , layers :
1 - Epithelioid $ell# :
* macrophage contain T." bacilli .
* ytoplasm : large, s)ollen, pale pin e9 ill defined border .
* =ucleus : vesicular, eccentric .
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: E":2ell membranes sho) desmosomes # % 2s form a )all against spread of infection.
(.Hiant $ell#!
: formed by fusion of epithelioid cells.
:it is of ' types:
LanghanI# type!
(n center of tubercle
4uclei are peripheral and may be
:Aorse-shoe lie
:"ipolar
:1ing form
Non.LanghanI# type!
4uclei in the center of cytoplasm.
/.T.Lympho$yte#!
:surround epithelioid cell and e/tend in P Q them.
:small rounded cells e9 dar stained rounded nucleus.
4.Fi*+o*la#t laye+ B Fi*+o#i# a+o'nd g+an'loma0
><+f caseating tubercle:
(t )ill be formed of . layers:
%.Cent+al $a#eation ne$+o#i# !
:(t occur due to JJJJJ0 ?"58@& -./*
:appear homogenous structurless pin area.
',*,,,.: Same cells as above e&$ept only one diffe+en$e!.
Little langerhans giant cells surround central caseation.
N0B : a-central caseation necrosis is directly proportional to hyperseitivity So:
Aypersensitivity caseation area
b->ibroblast layer is directly proportional to immunity# immunity fibroblast layer% .
18
King of pathology
: Type# of T0B !
1-primary T."
'-secondary T."
19
King of pathology
1ry T." 'ry T."
%.ef!
(."7I!
/.-ite#!
4.pathogene#i#
and +ea$tion
again#t T0B!
<.p+olife+ati:e
+ea$tionB
t'*e+$le
fo+mation!
B.E&'dati:e
+ea$tion!
5.N7E!
6."7E!
8.fate!
RSH
:T." of 1
st
e/posure.
:common in childhood period.
:occur in non immunized person.
(nhalation.
E&ogeno'#
(ngestion.
-liver tonsil
-nose 1are lung mainly.
-sin intestine
-mall +ea$tion occur.
:slo).
:>irm.
:)ell formed.
4o e/udative reaction.
Colo'+ :grey.
Con#i#ten$y :firm e9 no cavity.
T'*e+$le# eK minimal $a#eation.
<.good: Aealing by:
: Small lesionfi*+o#ed
:large lesion $al$ifi$ation2
en$ap#'lation.
:The organism may die or remain
dormant in ! healed lesion
:T." of '
nd
e/posure.
:less common in adulthood period.
-e&ogeno'#0
.endogeno'# do+mant fo$'#.
-ny organ but mainly lung.
(ntestine.
E&ten#i:e +ea$tion!at 1ry infection
8r at "2= vaccination the ptn
acBuire immunity and hypersensitivity
agains bacilli the immunity protect
ptn for some time then hypersensitivity
reaction of body against T.".
rapid occurrence,e/aggerated response
softer due to more liBuefaction of
caseating material.
59 more liBuefaction so it )ill form
cavity and may discharge from ulcer,
Sinus, fistula.
E&'dati:e +ea$tion !
:occur in serous covering and in soft
parenchymatous organs.
:The serous covering become studed e9
Tubercles associated e9 e/udates )9
may be: - serous.
-serofibrinous.
-T." pus.
* The E&'date Contain: neutrophils&
lymphocytes & macrophages & caseous
material. ! lymphocytes represent KGH
of ! inflammatory 2s. absent or little
<esothelial 2s.
Colo'+ :yello).
Con#i#ten$y :soft may fo+m $a:ity.
T'*e+$le# eK e&ten#i:e $a#eation0
<.good: Aealing by fibrosis,
calcification, encapsulation & cavity
formation e9 epithelialization.
B.*ad:
20
King of pathology

'H
+isscused in
pulmonaryT.".
-./0
do+mant fo$'#.
B.*ad: Spread by:
:local#direct%:by macrophage
Fia serous sac , cavities.
:lymphatics:via draining
$ymphatic.
:along natural passage:
-less than in 'ry T.".
- 5.g: lung alveoli.
respiratory tract.
:"lood#hematogenous%:
-more than in 'ry T.".
-(f:fe) number phagocytosed.
<oderate 4o isolated organ T."
$arge 4o <iliary T.".

:mainly by local spread.
4atural passage.
:4o role of lymphatics.
:minor role of blood spread.
The important complication here is:
(+y amyloido#i#.
N0B:def0 of do+mant fo$'#!
:(t is healed lesion in )9 organism still
dormant# . AB"C DE)0
:(t become activated in case of
immunity 'ry T." occur.
21
King of pathology
%+y T0B
(%).ef (().mode of infe$tion (/).#ite (4).Component (5).Fate0
(%).ef ! -s before0
(().mode of infe$tion ! -s before.
(/).-ite !-s before.
(5).Fate !-s before0
(4).Component of the %+y $omple&:-
1 p+olife+ati:e +ea$tionB t'*e+$le fo+mation in affe$ted o+gan!.
#pathogenesis-4E5-<E5% -s before.
1 TB lymphangiti# of lymphati$# d+aining the a+ea!
. (t forms a cord of multiple tubercles in ! )hole course.
.due to macrophage tae bacilli to draining $.4 along )ay of macrophage to $.4
The bacilli cause T." lymphangitis #inflammation of lymph vessels%.
:-fetr reaching $.4 bacilli cause T0B lymphadeniti#0
(+y T0B
i##$'#ed *efo+e0
"ilia+y TB! %+yL(+y. in any o+gan pyemi$ a*#$e##! FG H1"I
ef:due to blood#hematogenous%spread of large ef:due to circulation of small emboli infected
4o of T." bacilli e9 lo) immunity. e9 pyogenic bacteria.
"ethod of #p+ead: spread of bacilli from any lesion "ethod of #p+ead:by infected emboli )9 are
to the blood to reach any organ. (mpacted in capillaries and
N7E: small blood vessel in any organ
multiple N7E: -s before.
uniform small size #* mm% tubercles
separated from each other by normal tissue &
not surrounded by congestion &
present on outer & cut surface of organs
related to a bl.v.
(n lung,located mainly at the upper lobe.
(n serous membranes, are arranged diffusely.
"7E:-s tubercle but no giant cells or fibrosis#lo; imm'nity) "7E:-s abscess; central bacterial colonies
Fate: fatal Fate: fatal
%+y 3GL"ON<)D TB
(%).ef (().Etiology (/)."7E (4).Component (5).Fate0
3'lmona+y T0B i# Fa:o+a*le #ite fo+ TB ( ea#y inhalation %
22
King of pathology
(%).ef ! Jame as 1ry T.>.
(().Etiology !
a.p+edi#po#ing fa$to+# ! -s before0
*."7I ! 5/ogenous by inhalation0
$.E&$iting fa$to+# ! Auman type bacilli0
(/)."7E !
1"7E of t'*e+$le -./0 ? minimal $a#eation ne$+o#i#0
1T0B lymphangiti#! (t forms a cord of multiple tubercles in ! )hole course0
1T0B lymphadeniti#! (;ill *e di##$'#ed late+)0
(4).Component !
<. HhonI# fo$'# : parenchymatous lesion # disscused later %0
B. T0B lymphangiti#! (t forms a cord of multiple tubercles in ! )hole course0
C. T0B lymphadeniti# of hila+ O+ media#tinal L0N ( ;ill *e di##$'#ed late+ )0
M.HhonN# fo$'#!Oef N7E "7E Fate P

1ef ! parenchymatous lesion in 1ry pulmonary T.".
1N7E ! Size:1-'cm
.-ite:Sub-pleural lo)er part of upper lobe. .(-
Lpper part of lo)er lobe. Shape:oval or rounded.
.No:Single0 .%C 2olour:grayish yello).
1"7E : <E5 of tubercle -./0 ? minimal caseation necrosis0
1Fate :6>ate of 1ry pulmonary T." # disscused later %
(5).Fate!
<.good : RSH Aealing by:
: Small lesionfi*+o#ed
:large lesion $al$ifi$ation2 en$ap#'lation.
:The organism may die or remain dormant in ! healed lesion
do+mant fo$'#
B.*ad : 'H Spread by!
%.di+e$t #p+ead! pleurisy,pyothora/,pneumothora/,pyo pneumothora/
and haemoptysis.
(.Lymphati$ #p+ead::from hilar $.4 to hilar structure.
:from mediastinsal $.4 to mediastinal structure.
/.Blood #p+ead:#"acillemia% : spred of T." bacilli in blood.
: a$$o+ding to the do#e:-
If +ea$hed a :ein :
Small doseremoved by immune system
<oderate doseisolated organ T" 6 T'*e+$'loma.
$arge dose generalized milia+y TB
If +ea$hed a p'lmona+y a+te+y :
1eturn bac to the lung miliary T" of lung.
4.Nat'+al pa##age!
23
King of pathology
a<Endogenous passage : in lung tissue &bronchi
:T." bronchopneumonia: inflammation of bronchi surrounding lung tissue.
:T." pneumonia: inflammation of lung tissue.
:"roncho-pleural fistula.
:-cute tuberculous bronchopneumonia6-cute phthisis6=alloping consumption.
b<Exogenous passage : in structures above 8r outside lung:-
T =ohnIs focus enlarge& then open into bronchus
: T." laryngitis # T." in laryn/ %
: T." tonsillitis # T." in tonsils %
: T." ulcer in tongue.
: intestinal T." by s)allo)ing sputum.
K< Acute tuberculous bronchopneumonia =Acute phthisis = Lalloping consumption :<
%.ef!: bilateral consolidated patches around terminal bronchioles more in lo)er lobes.
:(t is rare complication of pulmonary T." occue )hen -- immunity &;; dose of bacilli e9 ;
;hypersensitivity
(.3athogene#i#!1 =honIs focus ulcerate in bronchial tree.
: (n ptn e9 -- immunity T." bacilli spread forming multiple tubercles#patches%
The patches fuse together forming large caseous area on evacuation Ca:ity fo+mation0
:2overing pleura sho) T." pleurisy.
:Ailar $.4 sho) hilar T." lymphadenitis.
/."7E!-s <E5 of tubercle -./0 B't No giant $ell# and No fi*+o#i# ( no imm'nity) 0
4.Fate! Fatal a# +'pt'+e of the $a:ity pneumothora/, pyo pneumothora/ and T." pleurisy.
T0B 'l$e+ in tong'e i# $hK *y :
N7E: No:single or multiple.
Size:variable in size.
'S
Shape:irregular in shape.
1 "a+gin: irregular, cyanotic.
1Edge : undermined # groove %
:Ba#e : hard, indurated.
:Floo+ : yello)ish covered e9 caseous material.
1d+aining L04 : mildly enlarged.
:It o$$'+ on tip spread deep parenchymatous glossitis. #"a$+oglo##ia ?"58& ME& %.
"7E: "7E of t'*e+$le0
(+y 3GL"ON<)D TB
(%).ef (().Etiology (/).In$iden$e0 (4).-ite (5).pathology0
%.ef! 1It i# ad'lthood type of p'lmona+y T0B0
24
King of pathology
1o$$'+ in %
#t
e&po#'+e in imm'no$omp+omized pe+#on
)e.e&po#'+e to T0B *a$illi0
(.Etiology!
a.p+edi#po#ing fa$to+#!-s before
*."7I! 5/ogenous by inhalation0
5ndogenos by )e-activation of dormant focus.
$.E&$iting fa$to+#!Auman type bacilli0
/.In$iden$e!Le## $ommon0
4.-ite! apical or sub-apical part especially in 1t than $t $ung due to:
1Hood :entilation(ae+o*i$ o+gani#m)0
1.. lymphati$# in api$al pa+t0
1na++o; )t p'lmona+y a+te+y than left .. *lood flo; ..+e#i#ten$e0


5.3athology!
a.<##man #imon fo$'#0
*.Ca:ita+y T0B0
$.Ch+oni$ fi*+o$a#eo'# p'lmona+y T0B0
a.<##man #imon fo$'#! (ef.ChK.fate)
1ef! 12hronic apical lesion.
:>ormed by fusion of many tubercles enlarge,caseate form large lesion e9
2entral caseation&fibrous capsule
:character:
:The lesion is variable in size.
:4ot associated e9 lymphangitis or lymphadenitis So it differ from =ohnIs focus.
:>ate: depend on amount of organism.
(mmunity.
Aypersensitivity.
<mo'nt of
o+gani#m
Imm'nity
hype+#en#iti:it
y
Effe$t
:Aealing by fibrosis 8r calcification.
:(t is less common.
Spread rapidly rapid destruction of lung tissue
# -cute T." bronchopneumonia %.
: (t is less common.
<oderate <oderate <oderate 2avitary pulmonary T" may # 2hronic fibrocaseous
pulmonary T" %.
:it is more common.
25
King of pathology
B. Ca:ita+y p'lmona+y TB!
- Softening & liBuefaction of caseous material coughed out 2avity formation.
-The cavity may be healed 81 pass to Ch+oni$ fi*+o$a#eo'# p'lmona+y TB .
C. Ch+oni$ fi*+o$a#eo'# p'lmona+y TB!.
( %.pathogene#i# (.N7E /."7E 4.Fate )
%.pathogene#i#!
a-the lesion e/tends from apical focus to ad!acent bronchi &lung tissue.
b- caseous material become discharged through bronchioles leaving a mother cavity
fo+mation of #mall $a#eo'# a+ea0
c-these areas on evacuation leaving small cavities called # a'ghte+ $a:itie# )B <$ina+ $a:itie#0
d- Fi*+o#i# o$$'+ 6 healing e/tends in # % ! cavities lung fibrosis & bronchiectasis0
e.These small foci may be formed in the )all of blood vessel . if rupture severe Aaemoptysis.
/."7E : m'ltiple $a#eating t'*e+$le# -./0 ? e/cess fibrosis ? epithelialization of cavities
?7. calcification.
(.N7 E!( of the mothe+ $a:ity):-
1No: Single #single mother caviyy surrounded by smaller ones%.
1-ite:apical 8r sub apical part of the 1t lung.
Size:large.
1(-
Shape:irregular.
: The lining is irregular & shreddy & yello)ish d.t caseous material.
: The ;all sho):a-raised bands of remnants of bl.vs & bronchi.
*-2aseation foci in )all of blood vessel if rupture cause
haemoptysis
:the #'++o'nding a+ea! the caviy is surrounded by:- a-fibrous tissue.
*-multiple small daughter cavities S8
- This arrangement of the large mother cavity &small daughter cavities gives )hat is called
( $lo:e+ leaf appea+an$e )0
4.Fate!.
<.good fate : healing by 5ncapsulation.
5pithelization.
+ystrophic calcification.
B.Compli$ation :-
1-due to tissue destruction: Aaemoptysis.
'ry amyloidosis.
"roncho O pleural fistula.
'-due to spread: +irect spraed.
"lood spread. +isscused before -./0
4atural spread.
No lymphati$ #p+ead.
*-due to fibrosis : (t cause 1t sided heart failure.
,-it cause peptic ulcer either by : -nti T." drugs
26
King of pathology
3sychic causes.
N0B : -ny chronic lung dse cause lung fibrosis
-ny diffuse lung fibrosis cause pulmonary hypertension.
-ny pulmonary hypertension cause 1t sided heart failure.
Jo No you OnoP Phy chronic fibrocaseous T.> cause Qt sided heart failure R

T B0 ENTE)ITI-
Inte#tinal T0B0
Type#:1ry intestinal T.".
'ry intestinal T.".
%+y inte#tinal T0B0 (Childhood type)
%.Etiology (.pathology /.Fate0
%.Etiology: :E&$iting fa$to+#: mainly bovine type. 1are Auman type
(.pathology:
< - pa+en$hymato'# le#ion!
1 m'ltiple t'*e+$le# eK minimal $ent+al $a#eation -./0
: bacilli are engulfed by macrophage of 3eyer@s patches proliferative reaction tiny ulceration.
: macrophage tae organism to draining $.4s T." lymphadenitis.
: along their course to $.4s, the bacilli taen by macrophage cause T." lymphangitis.
B. T0B lymphangiti#! (t forms a cord of multiple tubercles in ! )hole course0
C.T0B lymphadeniti#! :tubercles in the draining $.4s #mesenteric $.4s%
:this called #Ta*e# "e#ent+i$a%. ef: T." lymphadenitis of mesenteric $.4s
, as part of 1ry comple/.
* <esenteric $4s are enlarged & fused together 6matted #d.t inflam of perinodal tissue%
/.Fate
:Hood : healing
1Bad : spread.
$ocal # direct % T." peritonitis , T." salpingitis.
"lood spread a# *efo+e -./0

!"S ( +y inte#tinal T0 B0( $ommon in ad'lt# )
%.Etiology (.type# /."7E
%.Etiology!
a. E&$iting fa$to+# : mainly Auman type. 1are bovine type0
*."7I! in human type by s)allo)ing of infected sputum.
"lood transfusion.
(n bovine type by drining of infected mil.
27
King of pathology
(.type#!
I.Gl$e+ati:e Type! # pathogenesis T =UE T VUE %
1pathogene#i# of t'*e+$'l'# 'l$e+!
starts in peyer@s patches . T" reaction destruct submucosa & mucosa. ulcer )9 is at 1
st
parallel to
longitudinal a/is of ! intestine # tae the shape of peyer@s patches% but later d.t e/tension in lymphatic ,
! ulcer tae a girdle shape ulcer #encircle the bo)el% e9 its a/is perpendicular to that of intestine
:N7E B Cha+a$te+# of @ Gl$e+:
No:multiple.
-ite:terminal ileum.
Size: as payerIs patches.
(-
Shape:irregular transverse girdle ulcer.
"a+gin: irregular & cyanotic.
Edge: undermined #destruction is more in the deeper layers%
Ba#e:hard , indurated #fibrosis%.
Floo+:yello)ish covered e9 caseous material.
<&i#!perpendicular to longitudinal a/is of intestine.
+aining L0N : not enlarged #not affected%.
The pe+itoneal $o:e+ing is filled e9 multiple tubercles & appear thic dull & opaBue adhesions
1"7E! . m'$o#a ! 'l$e+ated0
. -'*m'$o#a!#ho; t'*e+$le# -./0

II.hype+pla#ti$ Type B Ileo.$ae$al T0 B!
%.-ite (.effe$t /.C73
%.-ite! 1Te+minal ile'm 1$ae$'m 1a#$ending $olon0
(.Effe$t! a.the )all of previous sites is thicened e9 narro) lumen chronic obstruction
b-the mucosa sho) foci of caseation and small ulcers.
/.C73: presence of )t ilia$ ma##.
Compli$ation of inte#tinal TB
1-inte#tinal fistula either internal PQ 'loops of intestine causing malabsorption.
5/ternal PQ loop of intestine&anterior abdominal )all
causing
>eacal matter goes out.
'-inte#tinal obstruction : # acute d.t adhesion or chronic in hyperplastic type %.
*-inte#tinal perforation : d'e to adhesions and fibrosis.
Thi# $a'#e septic peritonitis #4.":caused by 5coli bacteria not T."
bacilli as T." bacilli is not invasive%
,-Aemorrhage.
.-'ry amyloidosis.
0-Spread:
$ocal#direct% T." peritonitis , T." salpingitis # T." of fallopian tube %.
"lood spread as before -./0
28
King of pathology
%+y inte#tinal T0B (+y inte#tinal T0B
%.<ge!
(.Type
/.method
4.fo+m
5.L0N#
2hildren
bovine
drining diseased mil
tiny ulcers
enlarged#tabes mesentrica%
adults
human 8r bovine
-me 8r s)allo)ing of infected sputum.
La+ge t+an#:e+#e ulcers
4ot enlarged
29
King of pathology
T0 B0 3E)ITONITI-
8ccur in children & young adults.
"ethod of Infe$tion :
1-direct spread:from intestine , mesentry , fallopian tube.
'-lymphatic spread : from intestine , lung.
*-"lood spread:from T." of other organs.
Type#
<. lo$alized0
B. gene+alized 5/udative & depends on @ do#e of *a$te+ia & +e#i#tan$e of @ *ody0
1. Ascetic WmoistX Pet) type :
;; dose of bacilli &
- - resistance,
;; hypersensitivity
1 ?? #e+ofi*+ino'# e/udate, & ! peritoneal covering is studded e multiple tubercles.
'. aseous type :
- dose of bacilli.
-resistance moderate
-hypersensitivity
:5/udate formed of $a#eo'# mate+ial0
*- Nry Wplastic) type :
- - - dose
- ;; resistance
- - - hypersensitivity.
:$ittle tubercles, ;; fibrosis adhesion # % ! loops of intestine
:The omentum is thicened & contracted & rolled on itself (#a'#age #hape%
Compli$ation
- -dhesion acute intestinal obstruction.
- >ecal fistula.
- $ocalized T" peritonitis: caseous encysted type # % ! loops of intestine
<#$eti$ (moi#tC ;et) type +y (pla#ti$) type
%.$a'#e!
(.fl'id e&'date:
/.fi*+in!
4.No of t'*e+$le:
5.pe+itone'm!
6.ompli$ation#:
8.ChK #ign!
;; hypersensitivity, -- resistence
$arge amount
$ittle amount
:moderate 4o.
There is peritoneal distension
:rare
:------
-- hypersensitivity,;; resistence
$ittle amount
$arge amount
:large 4o.
There is peritoneal adhesions.
:8bstruction -fistula -'ry infection.
: #a'#age #haped ma##e#
30
King of pathology
T B0 LD"3H<ENITI-
ef! :(t accur as part of 1ry T.".
:$.4s arenIt affected in 'ry T." but it is affected only in 1ry T.".
(t is the 2ommon cause of lymphadenopathy in children.
"ETHO OF INFECTION! -ite#!
1. >orm part of 1ry comple/. :Ailar and mediastinal $.4s in pulmonaty T."
'. Spread through lymphatics. :<esentric $.4s in intestinal T.".
*. "lood spread # rare %. :2ervical $.4s in tonsillar T.".
N7E!
:$4 is enlarged .
:5arly T" lymphadenitis :-
<ultiple non caseating tubercles at periphery then go centrally. They are separated by thin rim of
nodal tissue.
:$ate T" lymphadenitis :-
- 2aseation starts in the tubercles fuse together replace the )hole $4 #if caseation is liBuefied by
enzymes of polymorphs it is called COL <B-CE-- %.
-The reaction e/tend to capsule perinodal tissue ! $4s become matted together form one mass
e9 central caseation.
"7E!
Ea+ly TB0 LN : non caseating tubercles -./*
Late TB LN : caseating tubercle -./*
Fery late:$.4s are transformed to caseous material enclosed e9in fibrous capsule COL <B-CE--
F<TE
YLood :Aealing by : fibrosis , calcification or encapsulation.
Y>ad : 1- spread according to its site:
--direct :
:cervical $.4s cold abscess retropharyngeal abscess open on the surface by sinus
31
King of pathology
)9 has undermined edge and discharge caseation.
:Ailar and mediastinal $.4s to hilar and mediastinal structures
:<esentric $.4s cause T." peritonitis.
"-"lood spread : as before -./0
'-'ry amyloidosis

Cold a*#$e##
%.ef (.Etiology /.N7E 4."7E 5.Effe$t
%.ef! (t is soft mass formed of caseous material surrounded e9 fibrous capsule.
(.Etiology: : very late T." lymphadenitis.
:3ottIs disease.
/.N7E: soft mass E encapsulated E UJ :sho) yello)ish , dry , friable material.
4."7E! "7E of t'*e+$le -./0 ; e/tensive fibrosis ; e/cess neutrophils.
5.effe$t! a :'ry amyloidosis.
*: in 2ervical region # vertebra % retropharyngeal abscess..
- in Thoracic region# vertebra % posterior mediastinal abscess.
-in $umber region# vertebra % psoas abscess.
$ :"lood spread: as before -./0
T'*e+$'loma
%.ef (.Etiology /.N7E 4."7E 5.Effe$t
%.ef:(t is tumor lie mass formed of caseating tuberculus reaction surrounded e9 fibrous#glial% capsule.
(.Etiology:due to blood spread of moderate dose of bacilli in patients e9 moderate immunity.
1T'*e+$'loma i# (+y B't it i# $ompli$ation of %+y01
/.N7E! No! single.
onNt fo+get! If it i# in *+ain In $e+e*ell'm2*+ain #tem -ingle0
32
King of pathology
In $e+e*+'m m'ltiple0
-ite :any organ .
1S -ize: ,. O 1G cm
-'+fa$e :nodular.
2olour:grayish yello) caseous material surrounded by grayish )hite capsule.
(C
2onsistency:firm.
Cap#'le :encapsulated.
C7- : sho) caseating center surrounded by fibrosis #o+ glio#i# if in *+ain)0
4."7E :t'*e+$le# eK e&ten#i:e $ent+al $a#eation -./* surrounded e9 fibrous# or glial if brain % capsule.
5.effe$t! :<ass effects: as pressure effect , obstructive effect ,edema,77..
:destruction of the affected organ.
:Spread of infection.

TB0 of C0 N0 -0
I) T0 B0 "eningiti#! Common0
%."ETHO OF INFECTION!
1. Blood #p+ead from a 1ry comple/.:
-- tubercles starts at brain corte/ & ventricles rupture reach 2.S.>.meningeal infection.
"-Through choroid ple/us.
2-3art of miliary T. ".
(. i+e$t #p+ead from vertebra# in 3ott@s disease%
(.3athogene#i#!
:yello;i#hCdiff'#e e&'date covers leptomeninges #pia-arachnoid% at ! base of ! brain due to irregular
brain surface at ! base; slo) 2. S. > circulation.
:T'*e+$le# fo+mation along the small blood vessel , choroid ple/us , and lining of ventricles.
33
King of pathology
:a+ea of $e+e*+al #oftening due to ischemia from 5-8.
:I++eg'la+ity of *a#e of *+ain 2ompression of eye nerves # *, ,, &0%.
/.N7E! 1- Thic dull opaBue leptomeninges0
'- subarachnoid space are studded e9 multiple tubercles.
*. 2S> circulation is a balance # % secretion & absorption #)ith no obstruction% .(f this
changes;; (2T dilated ventricles.
,-2hange of 2.S.>: :clear - lymphcytes - protein - pressure.
:"acilli presence - 2$ - sugar
:Sho) T." pus #thic, turbid , caseous%.
4."7E!
1-poo+ly fo+med tubercles in meninges Small e9 central caseation.
'-In$omplete transformation of macrophage to epitheloid cells.
*-#mall or fe) giant cells.
,- C0-0F : contain T" pus & bacilli.
.-E&'date formed of # caseation O $ymphocyte - 5pithiloid cells - >e) giant cells %.
5.Compli$ation!
:Fibrosis:hyrocephalus&cranial nerve palsy.
:(nfarction occur due to thrombosis&5-8.
:Spread:direct 81 blood.
II) T'*e+$'loma Le## $ommon
:N7E 2 "7E disscused before.
:Effe$t : there is increase intra-cranial pressure.

34
King of pathology
G+ina+y -y#tem TB
a),idney0 B)G+ete+ C)'+ina+y *lade+
%. Kidney T0 B!
"ETHO OF INFECTION!
:"lood spread :-
-as a part of military T.".
-T." in any organ.
:-scending from lo)er L.T.
Fo+m# of T0B le#ion in ,idney:
1< hronic T> pyelonephritis = surgical Oidney= hronic ulcerocaseous pylonephritis.
2<Viliary T. >. disscused before.
Z.Tuberculoma. disscused before.
1< hronic T. > pyelonephritis = surgical Oidney:<
1ef0 1-ite 13athogene#i#0 1N7E 1effe$t 1Compli$ation0
1ef: T." of idney in )9 tubercles present in the renal corte/ of the idney.
1-ite! start at pyrimdal ape/ or base.
: 3athogene#i#!
(nfection start in corte/ tubules & peritubular lymphaticsform multiple tuberclesmultiple
cavities caseous material discharge to calyces pelvis .
N7E! [M\"I (any di#ea#e o$$'e in ,idneyCit# N7E in$l'de '#'ally (-ize.-'+fa$e.Cap#'le.C7-)
-ize! enlarged
-'+fa$e: lobulated6 bossy
Cap#'le! thic adherent & difficult to be striped 9:]^* _/60 @ .
C7-! irregular cavities lined by & containing caseous material
35
King of pathology
; -hape! preserved.
Late!In T0B pyoneph+o#i#C ,idney *e$ome! : -ize! enlarged,
: -'+fa$e: lobulated6 bossy
: Cap#'le! thic &adherent & difficult to be striped .
:caseating material.
In (+y $ont+a$ted ,idneyC ,idney *e$ome !
1-ize! 1-'+fa$e!irregular.
1Cap#'le:thic& fi*+o'# :2aseating material:
:Fi*+o#i#:
Effe$t! depends on patency of ureter:
- (f 3atent ureter evacuation of caseous material fibrosis (+y $ont+a$ted ,idney.
-(f Lreteric obstruction accumulation of caseous material in idney T0B pyoneph+o#i#
Compli$ation !
Jpread
. di+e$t : to ureter urinary bladder #discending infection%.
.Blood #p+ead : a# *efo+e -./0
Qenal failure # if bilateral %
(0 T0 B G+ete+
a."ode of infe$tion : from idney 81 L." 81 "lood.
B.Effe$t !
5arly:<ainly )all of upper or lo)er 1E* become filled e9 tubercles.
$ate: <iddle part is affected.
36
King of pathology
/0 T0B0 '+ina+y *ladde+
a."ode of infe$tion :
-descending infection from idney infection start at Lreteric opening.
--scending infection from prostateinfection start at bladder nec. To trigone
B.Effe$t !
Tubercle formation then ulcerate discharging T" pus. (f heal by fibrosis $ont+a$ted *ladde+0
TB OF "<LE HENIT<L -D-TE"
"ethod of infe$tion!
1% (f ! infection is hematogenous epididymis is 1
st
site to be affected.
'%(f ! infection is descending from L T prostate is ! first site to be affected.
3athology!
%0 3+o#tate: -descending from L. bladder or ascending from epididymis. formation of multiple
tubercles fuse enlarged prostate.
-may result in urethral,rectal,or peritoneal fistula.
(0 -eminal :e#i$le!
(nfection from prostate or epididymismultiple tubercles & destruction of ! gland & hemospermia
# blood & bacilli & sperms%.
/0 T B0 #pe+mati$ Co+d (f'nni$'liti#)
- <ultiple T" nodules 6Tubercles.
. T'*e+$'loma `9]*
40 TB epididymiti#!
(nfection from blood 81 from spermatic cord
destruction of epididymis & formation of posterior scrotal sinus. & anterior
50 Te#ti# not affe$ted0
TB OF FE"<LE HENIT<L -D-TE"
%.T0B -alpingiti# B T0B of fallopian t'*e!
a."ode of infe$tion: :from surrounding structures.
:from blood spread.
*.N7E 2"7E!
T." salpingitis 4on T." salpingitis
%.ef!
(.N7E!
/."7E!
4.p+ogno#i#
Tubercle in )all of fallopian tube due
to direct or blood spread.
:the tube appear Sausage-shaped e9
3eri-tubal fibrosis and adhesion.
:)all thic.
:$umen contain caseating material.
-t'*e+$le eK $ent+al $a#eation -./0
:either heal or spread to near organs.
: (f ! fimberial end is patent
discharge caseous material to
peritoneal sac.
:(f ! fimberial end is closed d.t
adhesion TB pyo#alpin& (#a'#age
appea+an$e)
2hroic inflammation in fallopian tube.
:appear funnel shape.
:thin.
:contain pus.
.non #pe$ifi$ $h+oni$ inflammation -./0
:Aealing
37
King of pathology
(.TB Endomet+iti#!
+irect from ! tubes .
Q 3athology !
(f female in 2"3 ! tubercles are poorly formed e no caseation d.t shedding of endometrium every
month e menstruation.
"ut in old age tubercles are )ell formed & discharge caseous material in ! lumen T. ". pyometria.
/.O:a+ian TB!
Spread from fallopian tube or T" peritonitis.
BONE TB0
)o'te# of Infe$tion !
-"lood Spread.
->rom bone to !oints.
TB o#teomyeliti#!
Start in Aaversian canal & bone marro) destruction of bone e formation of seBustrum. a
granulation tissue is formed only# no callus% because ne) bone formation needs ostoblastic 2s an
involecurum is formed around. Aealing by fibrosis
TB >e+te*+ae (3ottI# di#ea#e)!.
%.ef :: it is T." of vertebrae
: it is the commonest T. ". of bone in children & adults.
(.Etiology : : mostly Aematogenous spread # blood spread %.
:rarely by other methods.
/.-ite#! -Thoracic vertebrae.
38
King of pathology
- $umbar vertebrae. Tho+a$o.l'm*a+ :e+te*+ae is the commonest site.
-2ervical vertebrae.
4.3athogene#i#: :T." start in vertebral body ad!acent to intervertebral disc then caseation necrosis
8ccur finally )ill involve the intervertebral disc.
:caseation material from destruction site )ill descend along vertebral columns till
3ara vertebral gutter.
: enclosure of caseous material e9in the fascia of the muscles 2old abscess formation
: The transverse process & spines of vertebrae are not affected.
5.Compli$ation B Effe$t!
a.efo+mity : yphosis, scoliosis, lordosis.
*.Cold a*#$e## !
: infection from vertebra periosteal covering neutrophils & fluid are ;; in caseous material
T" pus.
< pa+a:e+te*+al a*#$e## is formed in front & sides of ! vertebraeSpread under ! anterior vertebral
ligament to other vertebrae & under muscle sheath form abscesses in other areas.
< in eraical region Waertebra) retropharyngeal abscess..
< in Thoracic regionWaertebra) posterior mediastinal abscess.
<in bumber regionWaertebra) psoas abscess.
$.3a+aplegia !
:in 1G-'. Hof cases.
:$a'#e#: -2ompression of cord by collapsed vertebrae
-2ompression by:
T5/tradural cold abscess contain T" pus.
T(ntradural abscess
39
King of pathology
d. (+y amyloido#i#0
-ho+t Bone TB B TB0 da$tyliti#0
Start at medullary cavity of diaphysis.
Long Bone TB0
<etaphysis & epiphysis e/tend to !oints
Roint TB!.
-Fertebral , Mnee, hip, )rist !oint
- infection from neighboring epiphysis or hematogenous infection.
3athology!
T" synovitis e multiple studded tubercles #e/udative type% effusion is serous or serofibrinous or
pyogenic
- Aealing fibrous & bony anylosis.
"i#$ellaneo'#
T B0 )HINITI-
1ry: rare
'ry from infected sputum
T B0 -KIN B! L'p'# :'lga+i#
1ry infection from outside in "utchers
'ry: miliary
TB0 pe+i$a+diti#0
Serofibrinous inflammation - up to T" pus.
TB ton#illiti#
%+y TB ton#illiti#!
(nfection by bovine type from contaminated co)s mil,
40
King of pathology
1ry comple/ formed of :
- parenchymatous lesion in ! tonsil.
- T" lymphangitis.
- T" lymphadenitis of upper deep cervical $4s.
(+y ton#illa+ TB!
:'ry to fibrocaseous T" of lung.
:2ommon in adults
:3athology:T0B 'l$e+ ch9 by:
4o:single or multiple.
Size:variable in size.
'S
Shape:irregular in shape.
: "a+gin!Bl'i#h2nod'la+
:5dge:undermined #groove%
1Ba#e!-oft
:>loor: yello)ish covered e9 caseous material.
:draining $.4:mildly enlarged.
Finally Se #ay that : Fo+m# of T0B in l'ng# may *e ! (8)
:=honIs focus. :-ssmonIs simon focus.
:2hronic fibrocaseous T.". :T." bronchopneumonia.
:<iliary T.". :Tuberculoma.
41
King of pathology
:T." pneumonia.
Be#t ;i#he#

By7King of pathology0
42
King of pathology
By\King of pathology( Legand Hazem )
-D3HILI- (A)
ef! venereal 6 se/ually transmitted # ST+ % infective granuloma #chronic%due to treponema pallidum
"ode of Infe$tion!
+.Accuired infection : the organism penetrates ! intact mucous membranes & abraded sin.
1. #e&'al $onta$t
- genital organs # glans penis, vulva, cervi/ % .
- 5/tra genital organs as lip & tongue
(0 Non #e&'al $onta$t
- 4ipple of infected mother sucling infant.
- >inger #of a doctor% touch syphilitic lesion.
- "lood transfusion
++.ongenital +nfection :
The organism passes from infected mother to ! fetus via placenta after ! last * months of pregnancy.
3athogene#i# !
1-8rganism blood stream #bacteremia% to various organs & multiply in perivascular lymphatics
(t affects all ! organs.
'-the disease is divided to * #tage# #represent delayed hypersensitivity developed against organism
Separated by f+ee pe+iod# # represent developed immunity %.
*-1ry &'ry are highly infectious )hile *ry stage has very fe) organism.
A (-yphiliti$ )+ea$tion! !"S d;e0
1-peri-arteritis # acute then chronic % Thic,fibrosed adventitia.
'-5-8($on$ent+i$ endothelial 2 fi*+o*la#ti$ p+olife+ati:e thi$,ening of @ #mall :e##el#) thic,fibrosed intima.
43
King of pathology
*- perivascular infiltration # cuffing % by chronic inflammatory cells :
$ymphocytes, plasma cells (mainly) Cmacrophage and giant cells.
,-deposistion of mucopolysaccharides in the interstitial tissue hardness.
.-=ranulation tissue.
0-+raining $.4s: sho) follicular hyperplasia.

. %+y A! (%+y #o+eB $han$+eBha+d $han$+e) 4Gf"^%& 4e;g%& 9#C&
-not occur in blood transfusion infection & congenital &.
.(+y -tage 4Gf"^%& 4e;g%& 9#C&
./+y -tage!
:occur after 1G-*G years .
:(t has a favorable sites
cardiovascular system #SG-S.H%
2.4.S. #. - 1GH%.
1Type# of +ea$tion of Te+tia+y A!
%.iff'#e syphilitic reaction: :-ite : commonest in tongue , aorta , testis.
:N7E :sho) repeated necrosis & fibrosis.
1"7E : +iffuse & reaction.
(.lo$alized!(H'mma) 4Gf"^%& 4e;g%& 9#C&
Te+tia+y A OF C<)IO><-CRL<) -D-TE"
#SG-S.H of cases%
I . >a#$'la+ A (all #ize#)!.
44
King of pathology
- Small bl.vs #coronary% periarteriris.
- <edium bl.vs #limbs% 5ndoarteritis.
- $arge bl.vs #-orta% diffuse & aortitis
diff'#e -yphiliti$ <o+titi# B L'eti$ ao+titi# !
:8ccur after 'G years of 1ry infection & in male Q female *:1
:-ffect ! Thoracic aorta # -scending aorta & arch % 48T belo) ! diaphragm <the+o#$le+o#i# h/\
:occurs in this part d.t ;; vasa vasora & ;;lymph supply ;; 4o. of organisms.
%.3athogene#i#!
earliest changes are 5-8 ; perivascular cuffing of ! vasa vasorum by plasma 2s & lymphocytes.
narro)ing of these nutrient arteries ischemic destruction of ! ela#ti$ ti##'e 2 m'#$le of the media
stellate - shaped fibrous scars in ! media & fibrosis of ! adventitia. Cont+a$tion of @ median #$a+#
a transverse )rinling of the intima ( t+ee *a+, ) [9i]%& j"e% # appear as longitudinal )rinling %.
Sith de#t+'$tion of @ t'ni$a media, ! aorta loses its elastic support become dilated producing a
#yphiliti$ ane'+y#m ; 'ry atherosclerosis of damaged areas )eaening of ! )all diffuse
involvement by calcified atherosclerotic plaBue, )9 obliterates ! intimal tree barU pattern. ! presence
of atherosclerotic patches in this location #thora/% is not typical for atherosclerotic aneurysm )9 is
usually abdominal
(.Compli$ation!
a.Na++o;ing of $o+ona+y o#tia !.
: due to aortitis as & doesnIt affect coronaries # no lymphatic %.
: (f gradual &incomplete myocardial infarction and angina pectoris.
: (f sudden complete myocardial infarction.
*.<o+ti$ :al:e in$ompeten$e ( ao+ti$ +eg'+ge )!. volume overload $t ventricular hypertrophy &
dilatation# heart )eightQ1GGG gm %6 $o+. *o:in'm. A> death.
$.-yphiliti$ <o+ti$ <ne'+y#m!.
1ef :localized dilatation of arterial )all forming Sac.
:Ca'#e :due to stretching of fibrosed media by ".3 )9 is already lost its elasticity.
1Type# : may be saccular or fusiform
1 '#'ally contain mural thrombus
45
King of pathology
:;hen! aneurysmal dilation involve ! aortic valve ring -ortic valve incompetence volume
overload $t ventricular hypertrophy & dilatation# heart )eightQ1GGG gm%6 $o+. *o:in'm.
A> death.
:Compli$ation!
<ural thrombusembolization
1upturedeath.
3ressure on surrounding :- ##'pe+io+ media#tinal #ynd+ome %includes:-
yspnea & 1espiratory difficulties as a result of encroachment on lungs
ysphagia: difficulty in s)allo)ing due tocompression on ! esophagus
ysphonia & +ry cough due to pressure on recurrent laryngeal nerve eath
estruction & erosion of bone #vertebral bodies & ribs%.
istended nec veins due to pressure on SF2
II. Ca+dia$ A!
- 4arro)ing of coronary ostia.
- -ortic valve incompetence
- =umma of interventricular septum heart bloc & may septal defect.
- diffuse & pericarditis.
N0B! p+e$an$e+o'# le#ion of A a+e!. Le',opla,ia of tong'e 2 H'mmato'# 'l$e+0
Te+tia+y A of C0N0-!
:(t occurs in .-1GH of cases.
:(t is of ' types:
1< Veningo<aascular k.
2<parenchymatous k Wneuro k).
46
King of pathology
+<Veningo<aascular k :
:-yphiliti$ a+te+iti# of cerebral and spinal vessels lead to thrombotic occlusion and cerebral softening.
1-yphiliti$ meningiti# lead to fibrosis and compressing on emerging nerve lead to paralysis.
1"'ltiple g'mma0
++< =euro<k W parenchymatous neurok ):
male Q female after .-'G years ( T'a+tena+y #tage )0
<. Hene+aL 3a+aly#i# of in#ane ( H0 30 I ) ( ementia 3a+alyti$a )!
ef : sub-acute encephalitis due to & granulation tissue ending in gliosis.
N7E!
%-3ia.a+a$hnoid mem*+ane: is thic, fibrosed, adherent.
(.-'l$i 2 gy+i: flattened.
/.>ent+i$le#: dilated e9 compensatory in 2.S.>.
4.B+ain at+ophy motor , sensory , psychotic symptoms.
"7E!%.+od C# # long thic- microglial cells containing hemosiderin granules %.
(.A +ea$tion.
B.Ta*e# o+#ali# ( Lo$omoto+ <ta&ia )!
ef! "ilateral degeneration of dorsal horns of spinal cord & posterior roots of spinal nerves
=lial & fibrous tissue replace them.
It may *e: $umbar Tabes # atrophy % L$ atrophy.
2ervical Tabes )asting $$ atrophy.

N7E!
%.3ia.a+a$hnoid mem*+ane: is thic, fibrosed, adherent.
47
King of pathology
(.o+#al #'+fa$e of #pinal $o+d: flattened.
/.Cent+al $anal: dilated e9 compensatory in 2.S.>.
4.o+#al $ol'mn at+ophy :-
$oss of deep sensation$ocomotor ata/ia.
$oss of pain sensation chronic ulcer& neuropathic arthropathy 6 2harcot@s !oint#hype+.mo*ility%.
"7E: . A +ea$tion.
Te+tia+y A of @ )e#pi+ato+y! -y#tem!
: 4ose destruction of nasal bridge saddle nose
:$aryn/ vocal cord destruction & stenosis of laryn/,
:$ung 5-8 pulmonary hypertension #-yerzas disease % =umma of lung is rare
Te+tia+y A of Ha#t+ointe#tinal T+a$t!
Tongue:
- leuoplaia
-+eep parenchymatous glossitis (ma$+oglo##ia) 0
-gumma occurs in midline on ! dorsum of ! tongue
hard palate:
-=umma perforation
$iver:
-<ultiple gumma heal by e/tensive fibrosis (rregular lobules # Aepar lobatum %
enla+ged nod'la+ li:e+0 ?"58l MEl
Te+tia+y A of @ Henital #y#tem!
Testis diffuse & reaction #bilateral small hard tests%
=umma hard large tests ante+io+ #$+otal #in'# ( TB h/\ )
2ervi/ =umma.
Te+tia+y A of '+ina+y #y#tem!
- nephrotic syndrome
Te+tia+yC A of Bone 2 Roint#!
Bone!
-+iffuse & reaction in diaphysis . (t is 8steosclerotic so pathological fracture rare
-=umma of flat bone )orm-eaten appearance
-4osesaddle nose
-palateperforation
Uoint#!
-=umma destroy synovial membrane & !oint structure
-Aydroarthrosis.
Congenital A!
(nfection from mother to fetus occur after ! 1
st
trimester # 1st * months %.
(f ! mother in 1
st
or '
nd
stage & stillbirth
(f mother in *rd stage & infantile or
tardive & .
48
King of pathology
I. ead fet'#B#till *i+thB
p+enatal o+ neonatal A!.
II.Infantile A! in %#t ( yea+0 III0 Ta+di:e A!$hildhood
ef!3remature labor of a
dead macerated heavily
infected fetus:
:#,in +a#h # macule,
papule, pustule,Fetilligo
& maceration %
:The inte+nal o+gan# :
enlarged, pale, )hitish
grey & firm.
:L'ng # pneumonia
alba%.
:Lymphadenopathy0
& appear during 1
st
' years of life.
:sOin lesion: as 'ry stage#a# *efo+e%
-./0 ?rhagades ! # radial scars at
angles of month & anus %.
YVucus Vb! as 'ry stage( a# *efo+e%
-./0 ? atrophic rhinitis.
YThe internal organs:
.Li:e+!
congenital & cirrhosis it is
pericellular cirrhosis6diffuse fibrosis
in PQ hepatocytes
# <onocellular fibrosis %.
.Bone 2 Roint# !
#1%Saddle nose # destruction of nasal
septum %.
#'% & epiphysitis.
#*% & periosteitis:
Head :become sBuare-shaped head.
3halange# :is fusiform & s)ollen.
Ti*ia :become thic-compressed
laterally-curved for)ard#s)ord tibia%
-L'ng #pneumonia alba%.
.Blood:3aro/ysmal cold hemoglobinuria.

& appear from '-'G years of life.
: mutchinsonns Triad:
a- Autchinson@s teeth:
incisors:)idely
separated&notched
2entrally.
b-+eafness.
c-Meratitis blindness.
Y=eurok WL. ,.+.)
Ymydroatherosis:
5ffusion of !oint cavity
# =lutton !oint %.
Y>one changes: as Zry stages.-./0
T'*e+$le H'mma
: occur in 1ry ;'ry T.".
:due to T." bacilli.
:Ca#eation:classical#complete tissue destruction%.
:Ne't+ophil#! present.
13+oteolyti$ enzyme: present.
:LiT'efa$tion: occurs.
:Ca:ity is formed.
:)ea$tion a+o'nd!.
-Epitheloid $ell# , lymphocyte , macrophage.
-$angerhanIs cells of $la##i$al type e9
3e+iphe+al nuclei & la+ge+ in size.
: <vascular lesion.
:Compli$ation: sinus-ulcer-fistula.
:occur in *ry & only.
:due to treponema pallidum.
:Ca#eation:-typical#No complete tissue destruction%.
absent.
absent.
4o liBuefaction.
4o cavity formation.
3la#ma $ell#,lymphocyte ,macrophage.
-$angerhanIs cells of <typi$al type e9
Cent+al nuclei & #malle+ in size.
Fascular lesion.
=ummatous ulcer.
49
King of pathology
Be#t Si#he#
By7King of pathology0
By\King of pathology( Legand Hazem )
Bilha+zia#i# B (-$hi#to#omia#i#)
ef : infective parasitic granuloma )9 is endemic in 5gypt.
/ #pe$ie# : J. haematobium #affects mainly ! urogenital system%, J. Vansoni o J. paponicum
#affects mainly ! digestive system%. 8nly ! first ' are present in 5gypt. #S.A all over ! country & S.<. in
! +elta%
"ode of infe$tion ! qr;s% [j&9I
-2ercariae #in ! )ater%penetrate ! sin reach ! capillaries & circulate e ! venous blood to lungs
systemic arterial circulation to different organs. 8nly ! cercariae reach ! abdominal organs
drained by ! portal blood can survive . they reach liver in ! intrahepatic portal branches to mature
male & female )orms. -dult )orms move as couples #male &females% from ! liver to rectal ple/us
#S. <ansoni%7.. S. haematobium reaches ! vesical, porstate & utero-vaginal ple/uses.
->emale shistosoma pass to submucosa capillaries and lying do)n the eggs.
-This eggs either :-
1- penetrate vein and )all of urinary blader )all then pass in urine.
'- 3enetrate vein only submucosa granulomatous reaction.
*- (mpact in liver "ilharzial preportal fibrosis.
3athogene#i# and +ea$tion of *ilha+zia#i#!.
a)<ntigeni$ity of *elha+zia :-
1 - Ce+$a+ia type ( hypersensitivity .
2 - So+m if living not antigenic
(f +ead antigenic vascular reaction .
3 - O:a if living antigenic vascular reaction .
(f +ead not antigenic no reaction of immune system .
4 - <'to.<g ;K de+i:e f+om the inflamed ti##'e .
!"S d;e0 *)pe+manent +ea$tion#!. H+an'lomato'# +ea$tion (delayed hype+#en#iti:ity type
5)
(t occur around living 8va and may be -:
1 - Fo$al +ea$tion B *ilha+zial g+an'loma B *ilha+zial p#e'do.t'*e+$le B *ilha+zial nod'le
= *ilha+zloma .
ef ! nodule of granulomatous reaction consist of bilharzial 8va surrounded by
$ymphocyte O plasma cells O macrophage O foreign body giant cells # chronic cells %
+ fibroblast O eosinophils .
The cells are not arranged in layers as in T.> and necrosis is minimal .
2 - iff'#e +ea$tion :
ef! heavy deposition of large number of 8va heal by fibrosis or even calcified .

!"S d;e0 $)>a#$'la+ +ea$tion -:
50
King of pathology
* acute endophlebitis 81 acute endoarteritis .
* chronic endophlebitis 81 chronic endoarteritis .
* thrombus formation .
* organization .
* -rterio-venous shunt .
Biha+zial le#ion# of Hollo; o+gan#
. O:a in #'*m'$o#a if penetrate mucosa : petecial Age.
: ulceration.
: 1ed spots.
. O:a in #'*m'$o#a ( fe; n'm*e+ #) inable to penetrate mucosa Fo$al bilharzial +ea$tion0
.O:a in #'*m'$o#a (la+ge n'm*e+#) inable to penetrate mucosa 1-closed belharzial lesions.
'-bilharzial polyp.
*-sandy patches.
%. Le#ion# d'e to fi*+o#i#: # closed bilhartial lesion % :-
-(f there is severe fibrosis of ! submucosa & mucosa ova deposition in these sites stop. 4o ova pass
to urine or stool # 2losed lesion %. ! ova deposition continue in ! muscle, subserous & peritoneal layers
fibrosis & organ become small #contracted organ% e9 obstruction.
(.Le#ion# d'e to li:ing o:a: # Bilha+zial polyp %. 4Gf"^%& 4e;g%& 9#C&
/.Le#ion# d'e to dead o:a : # -andy pat$he# %. 4Gf"^%& 4e;g%& 9#C&
4. Bilha+zial 'l$e+# : 4Gf"^%& 4e;g%& 9#C&
N0B:- !"Sclosed bilhartial lesion = liaing oaa u fibrosis u negatiae urine. vhile
Jandy pathches = dead oaa u calcification u positiae urine.
"S")w* @ [M\"I "7E of any 'l$e+ B "7E of the le#ion $a'#ing it
51
King of pathology
G+ogenital Bilha+zia#i#! 4Gf"^%& 4e;g%& 9#C&
Epithealial $hange# in '+ina+y *ladde+ *ilha+zia#i# !.
:8ccur due to ".reaction & 'ry infection.
: these changes are:-
a.Epithelial hype+pla#ia : - >ocal increase in ! epithelial thicness.
- +ipping do)n of ! hyperplastic epithelium.

*. B+'nne+N# ne#t# ! 1- They are sheets of the hype+pla#ti$ t+an#itional epitheli'm )9 are
separated from surface epithelium & present in submucosa.
'- (schemia occur hyd+ophi$ degene+ation of the center cells compress the
Surrounding cells gi:e Cy#titi# $y#ti$a then glandular metaplasia of surface
epithelium occur give Cy#titi# gland'la+i#.
N0B! gland'la+ metapla#ia mean ( t+an#fo+mation of one type of epitheli'm to anothe+ ) -o !
The t+an#itional epitheli'm that line Cy#titi# $y#ti$a ;ill t+an#fo+m to gland'la+ epitheli'm ;K
I# lined *y ( $ol'mna+ epitheli'm ? go*let $ell# ) ;K line $y#titi# gland'la+i#0
$.Cy#titi# $y#ti$a d.$y#titi# gland'la+i#
.ef: hydrophic degeneration of
brunnerIs nest
-$arge size.
-$ined by transitional 2s # flat 2s %
-2ontains )atery secretion.
- is due to 'ry infection.
-(t is not precancerous.
-glandular metaplasia of surface
epithelium.
-Small size.
-$ined by columnar 2s ; goblet cells
-2ontains mucus.
-(t is due to bilharziasis.
-(t is precancerous.
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King of pathology
e. at+ophi$ $hange# o:e+ the #andy pat$he# .
f. #T'amo'# metapla#ia ( le',opla,ia ) : 1- eratinization very thic.
'- 4E5 :- )hitish irregular patches of mucus membrane.
*- <E5 :- eratinized stratified sBuamous epithelium.
,-type :- precancerous.
g. malignan$y : to : transitional cell carcinoma.
: sBuamous cell carcinoma.
: adenocarcinoma.
Othe+ '+ogenital B
%) B of @ '+ete+ !. common in ! lo)er third:
-8bstruction #hydroureter%.
-'ry infection #pyoureter%.
() B of @ ,idney !.
-8va are deposited in ! interstitial tissuepyelonephritis, pyonephrosis
/) B #eminal :e#i$le#: hemospermia.
4) B p+o#tate:- bladder nec obstruction.
5) B te#ti$le :- Aydrocele.
6) B #pe+mati$ $o+d:-+iffuse thicening.
8) B '+eth+a :- stricture & fistula formation.
Inte#tinal Bilha+zia#i# ! 4Gf"^%& 4e;g%& 9#C&
Hepati$ Bilha+zia#i#
Bilha+zial p+epo+tal fi*+o#i# in li:e+
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King of pathology
%.ef! it is diffuse hepatic affection by parasite emboli around dead )orms&living )orm of bilharzias.
(t occur as $ompli$ation of inte#tinal *ilha+zia#i#.
(.3athogene#i# : a) d+ained em*oli of li:ing o:a!
-re drained from the mesenteric vein portal vein liver portal tract then either:
:impacted in vein >a#$'la+ +ea$tion -./0
:penetration of vein Fo$al *ilha+zial +ea$tion -./0 ( x& D)w* @ angiomatoid# )

B) d+ained em*oli of dead ;o+m!
:<ild cases occlusion of the affected vein intimal and sub-intimal proliferation.
:Severe cases >a#$'la+ +ea$tion -./0
$)d+ained em*oli of li:ing ;o+m!
:contain pigment#haemosidrine% >ibrosis.
to/ins minimal tissue necrosis & minimal fatty change.
N0B: &My &My !"S angiomatoids6 small vascular spaces # in liver only %.
D%& z"{0 Fo$al +ea$tion D| }.~". Mw\ li:e+ and p'lmona+y only
/.N7E! &My !"S % - Size :-ea+ly :slightly enlarged # inflammation % E Late:shrunen # fibrosis %.
-'+fa$e : retracted.
Bo+de+ : sharp.
2onsistency: firm
(C
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King of pathology
2olour:: yello)ish bile & fatty change.
: bro)nish pigments.
: )hitish fibrosis.
Cap#'le : thicened and adherent to surface.
C7- : thicened , fibrosed portal tract.
4."7E! -Li:e+ a+$hite$t'+e : preserved.
-Hepato$yte#: either minimal cell necrosis E minimal fatty change.
-Blood #i'#oid#: normal.
-Bile $anali$'li: cholystasis.
-Cent+al :ein: normal.
->on ,'pffe+ $ell# #ho;: hyperplasia & hypertrophy.
-3o+tal t+a$t ( main pathology ) #ho;: :5nlarged O thicened O fibrosed.
:pigments O fibrosis.
:"ile duct proliferation.
: Fascular reaction -./0
: >ocal bilharzial reaction -./0 ( x& D)w* @ angiomatoid#)
5.Compli$ation ( effe$t )! a)po+tal hype+ten#ion0 *)li:e+ $ell fail'+e0
a) po+tal hype+ten#ion !.
Yauses : presinusoidal # >ibrosis E Thrombosis E -rterio-venous shunt %.
YEffect : 1- congestion of portal drained area Splenomegally O -scitis O 4ausea,vomiting.
'-opening of porto-systemic anastomosis esophageal varices O piles.
*) li:e+ $ell fail'+e0
6.Type# : Aepatic "ilharziasis is of ' types:- 1->ine. '-2oarse " hepatic fibrosis.
N0B: It i# $alled fi*+o#i# 2 not $i++ho#i# *e$a'#e @ le#ion i# +e#t+i$ted mainly to @ po+tal t+a$t#0
2nod'la+ a+$hite$t'+e of the li:e+ i# p+e#e+:ed
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King of pathology
Fine B0 fi*+o#i# Coa+#e B0 fi*+o#i#
-ite !
In$iden$e !
inte#tinal B !
3athogene#i#
:
1-8va
'-Jorm
*-1epetition
,-To/in
N7E !
Size
Surface
2apsule
2onsistency
2ut surface
"7E !
Effe$t# !
-Small portal tracts
-P than .GH of cases.
-<ild or moderate
->e) 4o. in small portal vein at one time
-4o )orm impaction.
-4o repetition of ! process.
-The same in both types
- decrease
- finely granular
- thic
- firm
- opaBue small portal tracts
Small portal tracts sho):
- >ibrosis & thicening
- 8va deposition
- $ittle liver cell necrosis
- 3ortal hypertension
- $iver cell failure
-$arge portal tracts.
-Q .GH of cases
-Severe.
-$arge 4o. in large portal vein or marginal vein
-Jorm impaction
-1epetition is found.
-the same
- mared decrease
- coarsely irregular
- thic
- firm
- opaBue, broad, irregular large portal tracts
large portal tracts sho):
- ;; fibrosis & thicening
- dead )orms ; ova
- very little liver cell necrosis
- 3ortal hypertension
- $iver cell failure
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King of pathology
Bilha+zia#i# of @ #pleen B Egyptian -plenomegaly
(t is a syndrome characterized by:- (ntestinal bilharziasis , ". hepatic fibrosis, Splenomegaly, -nemia,
leucopenia & fever. 1 -plenomegaly i# eithe+! .
Ea+ly #plenomegaly Late #plenomegaly
%.Ca'#e !
(.N7E !
-Size:
-Shape:
-capsule:
-consistency:
-2ES:
/."7E!
-
2apsule&trabeculae:
-Jhite pulp 6
$ymphoid follicle:
-1ed pulp:
4. Effe$t#!
:8ccur e9 both types of
S.haematobium & S.mansoni.
:d'e to immunological inflammation
response d'e to antigenic stimulation
<ildly enlarged.
3reserved.
: Tense.
>irm
1-$ymphoid follicle enlarged.
'-1ed pulp mild congestion.
4ormal.
Ayperplastic & e9 prominent
germinal centre.
1-<ildly congested.
'-5osinophilia.
*-Ayperplasia of littoral cells
#macrophage%.

4o effect
:8ccur e9 S.mansoni. only.
:Conge#ti:e d'e to portal hypertension
$a'#ed *y hepatic ". fibrosis.
Augely enlarged.
3reserved.
:Thicened. : )hitish due to fibrosis.
:adherent to surface.
:cartilaginous metaphases due to
subcapsular Age 8rganization.
>irm
1-$ymphoid follicle atrophied.
'-1ed pulp severly congested
Ayalined..
-trophied &e9 hyaline degeneration of the
arterioles.
1-Severly congested.
'-4o easinophilia.
*- =amna =andy 6 fibrosiderotic nodules:
:Component: as before #return to
circulatory disorder% -./0
- 2ompression of the surroundings organs
- Aypersplenism :-
ef! splenomegally ; pancytopenia
#anemia; leucopenia; thrombocyropenia%
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King of pathology
3'lmona+y Bilha+zia#i# ( Bilha+zial $o+.p'lmonale )
%.ef ! it is disease result from presence of ova & )orms in pulmonary circulation coming from
Lrinary bladder "ilharziasis SG H from S.haematobium E 'G H from S.mansoni
(.3athology!
I.O:a le#ion#:- (f
8va impaction in pulmonary vessels Fascular reaction -./0
3enetration of pulmonary vessels >ocal bilharzial reaction -./0 ( x& D)w* @
angiomatoid#)
II.So+m le#ion#!
The pulmonary arteries contain venous blood so )orms die rapidly necrosis of ! vessels &
surrounding lung tissue causing>e+mino'# pne'monia 6 focal consolidations e9 ;; necrosis &;;
eosinophils & foreign body reaction around )orm Fi*+o#i#0
/.Effe$t# 2 $ompli$ation#!
1% 3ulmonary hypertension 3ulmonary aneurysm.
Ycauses : due to # fibrosis O thrombosis O --F shunt %.
:Effect : Aypertrophy & dilatation of ! right side of ! heart 1.A.> # cor-pulmonale %
1ef of $o+.p'lmonale: 1t sided heart failure andEor hypertrophy )9 occur secondary to a disease in
the lung.

Be#t Si#he#
By\King of pathology( Legand Hazem )
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