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416 Chapter 11 Infectious Diseases and Tropical Medicine
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11.11
11.11
Chagas’ Disease (American Trypanosoma)
Chagas’ disease (CD) is an infectious, multi-systemic
disease caused by Trypanosoma cruzi ( T. cruzi ), a
blood-borne fl agellate. T. cruzi was fi rst described in
Brazil by Carlos Chagas, in 1909. The disease is one of
the most common public health problems in South
America from Texas to Argentina.
CD often affects children and young adults living in
rural areas and mud huts. T. cruzi is transmitted to
humans by the defecation of a vector bug known as the
“kissing bug” (reduviid bug). The bite occurs around
the face, often at night, and the parasite is found in the
bug’s feces. The bite can be painless or painful depending on the toxins found in the bug’s saliva.
At the bite site, T. cruzi penetrates the skin and
travels via the blood to the body organs. The parasite
invades and enters the host cells, particularly the muscles, the glia, and the reticuloendothelial system.
Multiplication occurs by binary fi ssion until the cells
rupture, and the parasite enters the blood or invades
more tissues. At the site of multiplication, severe
infl ammatory reaction occurs with local lymphangitis, which is known as “ chagoma .” Soon after that,
lymphatic spread to regional lymph nodes occurs,
which is usually seen in the fi rst 2 weeks postinfection.
Although the parasite can be found in any body tissue, T. cruzi often has a distinct predilection for stri-
ated and cardiac muscles, glial, and nerve cells.
There are four distinct phases of CD, each with its
own pathological and radiological features.
Acute Chagas’s Disease
The main pathological process during this stage is
chagoma affecting the heart and the central nervous
system (CNS). The acute stage is frequently seen in
neonates, although it may occur at any age.
After an incubation period of 2 weeks, patients
often present with fever that can persist for months,
malaise, loss of appetite (anorexia), vomiting, diarrhea, and muscle pain.
In the heart, there is severe lymphocytic myocarditis with focal areas of endocardium and epicardium
infl ammation, which leads to dilated cardiomyopathy
and pericardial effusion. Hyaline necrosis of isolated
myocardial fi bers ( Magarinos-Torres’ lesion ) is a char-
acteristic feature of Chagas’ myocarditis.
In the CNS, encephalitis or meningoencephalitis is
often seen, and may be the primary manifestation of
CD. The trypanosomes may enter the conjuctiva in up
to 50% of patients, causing upper or lower eyelid
edema, conjuctiva chemosis, and preauricular lymph
nodes enlargement ( Romana’s sign ).
Hepatosplenomegaly, and pneumonia when the trypanosoma affect the lungs, may be seen.
ECG Abnormalities
The most common changes in electrocardiogram (ECG)
are prolonged P-R interval, low voltage in an ECG
rhythm showing electrical activity in the ventricles
(QRS complex), and prolonged Q-T interval.
Signs on Ultrasound
Hepatosplenomegaly that may persist for up to 5 months
from the onset of the disease.
Liver fatty infi ltration.
Regional lymph node enlargement.
Signs on Cardiac MRI
Chagas’ myocarditis is seen as focal, segmental high T2 signal
intensity areas, with contrast enhancement localized in the
mid-wall or the outer wall of the ventricle below the
pericardium (Fig. 11.11.1 ).
There are areas of wall motion abnormalities, along with
areas of aneurismal wall dilatation. Apical aneurysm with
thrombus formation is a common fi nding.
Subacute Chagas’ Disease
This stage is often seen in young adults, and the patient
presents without any fever, with severe heart failure
that does not respond to therapy.
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muscles results in marked esophageal dilatation. Food
may become lodged in the esophagus. Carcinoma and
esophageal abscess may develop in 7% of patients with
chronic CD.
In the colon, massive dilatation and chronic constipation is often seen. Sigmoid volvulus may occur in
10% of patients.
Signs on Plain Chest Radiograph
The dilated esophagus is seen as a medistinal mass along the
entire right side of the mediastinum with air or air–fl uid level.
The heart is often dilated due to dilated cardiomyopathy of
chronic CD.
Raised left hemidiaphragm due to splenic fl exture dilatation
may be found.
Fig. 11.11.1. Sagittal short-axis, T1W postcontrast cardiac MR
illustration demonstrates the type of myocarditis enhancement seen in Chagas’ disease (mid- to outer-wall enhancement)
( arrowhead )
Latent Chagas’ Disease
After the acute stage subsides, many patients completely recover, while others may pass into a latent or
chronic stage. In this stage, 2–5% of patients become
symptomatic annually.
The number of ganglion cells in the Auerbach plexi
in the gastrointestinal (GI) tract starts to diminish in this
stage. All patients who recovered from the acute CD
stage, or live in endemic areas, have a positive complement fi xation test ( Machado-Guerreiro reaction ).
Chronic Chagas’ Disease
This stage develops after many years, and is characterized by dilated cardiomyopathy, with esophageal and
colonic dilatation. The main pathology is attributed to
reduction in the motor ganglia of the GI tract, resulting
in loss of motor function (aperistalsis), which results in
dilatation and fl accidity of the affected organs.
In the esophagus, early stages are characterized by
hypercontractility and hypertrophy of the circular
smooth muscles. Later, denervation of the esophageal
Signs on Barium Swallow and CT
The esophagus is massively dilated (>7 cm), with bizarre,
dysrhythmic contractions that mimic achalasia (Fig. 11.11.2 ).
Food may be found lodged within the esophagus.
On CT, megacolon with massive rectosigmoid dilatation is
usually found.
Fig. 11.11.2. Axial thoracic CT in a patient with chronic Chagas’
disease shows massive dilatation of the esophagus, with food
lodged inside the esophagus, mimicking achalasia
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11.11
For Further Reading
1. Felippe L et al Radiological diagnosis of Chagas’ disease
(American try panosomiasis). Semin Roentgenol. 1998;33(1):
26–46
2. Rochitte CE et al Myocardial delayed enhancement by mag-
netic resonance imaging in patients with Chagas’ disease: a
marker of disease severity. J Am Coll Cardiol. 2005;46:1553–
58. Originally published online 22 Sep 2005. doi: 10:1016/j.
jacc.2005.06.067
3. Barros MVL et al Doppler tissue imaging to access systolic
function in Chagas’ disease. Arq Bras Cardiol. 2003;80(1):
36–40
4. de Souza AP et al Magnetic resonance imaging in experimental Chagas disease: a brief review of the utility of the
method for monitoring right ventricular chamber dilatation. Parasitol Res. 2005;97:87–90
5. Ferreira-Santos R. Aperistalsis of the esophagus and
colon (megaesophagus and megacolon) etiologically
related to Chagas’ disease. Am J Digest Dis New Ser.
1961;6(8), 700–726
11.12 Schistosomiasis (Bilharziasis) 419
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11.12
Schistosomiasis (Bilharziasis)
Schistosomiasis is an infectious disease caused by
freshwater schistosoma. Schistosoma are fl atworms
that do not have a digestive tract, and are commonly
known as trematodes or blood-fl ukes. Schistosomiasis
is commonly known as “Bilharziasis,” after Bilharz,
the discoverer of the parasite in 1815.
Schistosoma Life Cycle
Schistosoma release their eggs in freshwater. Later, the
eggs are hatched into larvae, which maturate in freshwater snails. After maturation, the mature larvae (cercariae) leave the snails and enter into humans by
penetrating the exposed human skin in the freshwater.
After skin penetration, the parasites travel within the
lymphatic system through the thoracic duct to enter the
circulation. The parasites lie in the lymphatic system
for almost 21 days before they enter the hepatic portion of the portal venous system into the liver, where
they further mature and mate. Depending on the type
of the schistosoma, the parasites migrate into the intestinal or the bladder venous system to lay their eggs.
The adult worms are strictly intravenous and do not
evoke the immune system, while both the cercariae
and the eggs stimulate the immune system, resulting in
the formation of granulomas around the eggs and the
systemic cercariae, which will cause tissue fi brosis and
calcifi cation of the affected organ in advanced stages
of the disease. Dead worms can be embolized almost
anywhere within the body.
There are four types of Schistosoma worldwide:
Schistosoma japonicum is found within eastern Asia,
is located within the intestinal tract veins, and
releases its eggs in the feces.
Schistosoma mansoni is found within South America
and Africa, is located within the intestinal tract veins,
and releases its eggs in the feces.
Schistosoma haematobium is found within Africa
and the Middle East, is located within the bladder
and ureters venules, and releases its eggs in the
urine.
Schistosoma intercalatum is found only in equatorial
Africa, and mainly affects the intestinal tract and the
portal system.
The fi rst symptom of the disease starts when patients
develop itchy skin after larvae penetration, due to
hypersensitivity reaction type 1 and type 4 (cercarial
dermatitis or swimmer’s urticaria). Weeks later, systemic manifestations like hematuria, fever, weight loss,
diarrhea and abdominal pain arise.
The living worm lives between 4 and 30 years. The
living worm engulfs the red blood cells (RBCs) and
excretes them as hemozoin, which is engulfed later by
the macrophages. The other action by the living worm
is laying eggs (ova). As the ova penetrate the wall of
the intestine or the urinary bladder, they may cause
chronic bleeding (resulting in anemia), be trapped in
the wall of the organ, or enter the blood and circulate
as emboli. The dead worms initiate a severe infl ammatory reaction within the veins, causing thrombophlebitis, which can block the affected vein.
Diagnosis of schistosomiasis is confi rmed by identifying the schistosoma eggs in urine or feces, and
eosinophilia in the complete blood count (CBC).
The clinical and radiological manifestations of
schistosomiasis can be classifi ed according to the parasite type.
Schistosomiasis by S. japonicum
S. japonicum lives in the mesenteric veins, and mainly
affects the liver, small bowel, and lungs. In the small
bowel, the duodenum and the jejunum are mainly
affected.
In the liver, the parasite eggs are deposited in the
portal venules along the liver periphery. When the eggs
die, fi brosis within the venules results in a polygonal
network of periportal fi brosis that makes the liver look
like a “turtle back” on gross appearance (Fig. 11.12.1 ).
The eggs are also deposited within the liver capsule,
resulting in capsule thickening and fi brosis. There is a
high incidence of liver carcinoma with S. japonicum
infection.
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Fig. 11.12.1. An illustration demonstrates the gross turtle-back
appearance of S. japonicum liver schistosomiasis
Signs on Ultrasound
The liver shows an internal echogenic polygonal network due to
periportal fi brosis and calcifi cation, which causes a “fi sh-scale”
appearance (30% of cases).
Signs on Abdominal CT
There is internal periportal fi brosis (low-density bands) or
calcifi cation (high-density bands) within the liver parenchyma,
along with liver contour irregularities (turtle-back appearance)
(Fig. 11.12.2 ).
Fig. 11.12.2. Axial CT illustration of the liver in S. japonicum
schistosomiasis demonstrates the internal periportal calcifi cation and fi brosis causing the turtle-back appearance
Schistosomiasis by S. mansoni
S. mansoni mainly affects the liver, bowel, central ner-
vous system, and lungs. In the bowel, the parasite
causes granulomatous colitis, which causes loss of
haustration and strictures later on, mimicking Crohn’s
disease. If the small intestine is affected, regional ileitis and protein-losing enteropathy may develop. In
uncommon cases, when the calcifi cation is so severe as
to include all the layers of the colon wall, the ova start
to accumulate freely within the peritoneal cavity outside the wall. This causes infl ammation and fi brosis
within the peritoneal cavity and the pericolic region,
resulting in a pericolic mass that cannot be differentiated from carcinoma on imaging.
In the liver, the parasite deposits its eggs around the
main portal vein at the liver hilum, later resulting in
Symmer’s pipestem fi brosis. Symmer’s pipestem fi bro-
sis is a condition that arises when egg granulomas
aggregate around the portal vein, resulting in vascular
fi brosis that causes obstruction of the small veins and
presinusoidal cirrhosis. Portal hypertension (HTN),
esophageal varices, and splenomegaly are common
complications of this type of fi brosis.
In uncommon cases, angiomatoid lesions can
develop within the liver. These angiomatoid lesions
emerge as a secondary action taken by the body against
severe fi brosis of the hepatic veins and portal HTN.
The emergence of such lesions can be explained by the
fact that in severe portal HTN, the blood within the
veins cannot fl ow normally, which results in opening
of sideway channels and collaterals to decrease liver
congestion. This can result in angiomatoid formation
of lesions (e.g., hemangiomas). These lesions seen in
the liver represent a severe stage of portal HTN.
Splenomegaly in bilharziasis occurs at an early
stage due to antigen stimulation, causing splenic parenchymal hyperplasia, and later in the course of the disease due to portal hypertension.
If eggs are embolized into the pulmonary vessels
via the venous system, they damage the vascular wall
by initiating an infl ammatory reaction. The infl ammatory reaction results in a characteristic “dumbbell”
granuloma blocking the vessel, or forms a pseudoaneurysm. Pulmonary hypertension may develop in
advanced stages (20% of cases). All schistosoma species can affect the lungs.
Rheumatic manifestations are uncommonly seen with
bilharziasis, resembling reactive arthritis or seronegative
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spondyloarthropathies and sacroiliitis. Rheumatoidlike disease affecting the metacarpophalangeal (MCP)
and proximal interphalangeal (PIP) joints, wrists,
ankles, and knees have been reported. Some of these
manifestations are due to immune complexes or direct
infection by the parasite.
In the central nervous system, S. mansoni produces
conus medullaris thickening and arachnoiditis ( bilhar-
zioma ).
Signs on Plain Chest Radiograph
Signs of pulmonary hypertension and enlarged pulmonary
trunk in advanced stages.
Localized bilharzias granulomas within the lung may be
mistaken for a neoplastic nodule or mass.
Calcifi cation of the bowel walls may be seen (rarely) on plain
Fig. 11.12.3. Plain abdominal radiograph shows calcifi cation of
the transverse colon walls in a patient with schistosomiasis
( arrowheads )
radiographs (Fig. 11.12.3 ).
Signs on Ultrasound
Hyperechoic lesions are noticed around the portal vein due to
Symmer’s pipestem fi brosis.
Thrombosis of the portal vein may be seen as loss of Doppler
signal fl ow within the portal main stem.
Signs of liver cirrhosis and portal hypertension (e.g.,
splenomegaly).
Gallbladder wall thickening is found in 80% of cases.
Fig. 11.12.4. Portal
cavography ( a ) and axial
CT-urography ( b ) in a patient
with schistosomiasis and
portal vein thrombosis shows
a severely dilated portal vein,
with development of
esophageal varices ( arrow-
head ) and splenic varices
( arrows )
Signs on Abdominal CT
The portal venous tracts are replaced by fi brous tissue, seen as
low-attenuation bands or rings, with peripheral fi brosis
radiating from the center of the liver around the main portal
vein branches. Marked enhancement is noticed on postcontrast images.
Shrunken liver, portal venous thrombosis, splenomegaly, and
esophageal varices are commonly noticed (Fig. 11.12.4 ).
Splenic siderotic nodules ( Gamna-Gandy bodies ) are
commonly seen within the enlarged spleen.
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Fig. 11.12.5. Sagittal T2W lumbar MR illustration demonstrates
enlarged conus medullaris with multiple high signal intensities
representing bilharzioma ( arrowhead )
Signs on Spinal Cord MRI
Bilharzioma is seen as localized conus medullaris thickening,
with high signal intensity on T2W images and heterogeneous
contrast enhancement postgadolinium injection (Fig. 11.12.5 ).
Schistosomiasis by S. haematobium
occur within the ureters, bladder, and seminal vesicles.
When the ureters are calcifi ed, obstructive uropathy
and renal hydronephrosis may occur.
Complications of the ova within the bladder and
intestinal walls:
Sandy patch occurs when a huge number of ova die
and calcify, causing the overlying mucosa to degenerate and atrophy.
Bilharzial polyp occurs due to localized deposi-
tion of a huge number of ova, with hyperplasia
of the wall. This is mainly seen in the intestine
( S. mansoni ).
Bilharzial ulcers can arise due to penetration of huge
numbers of ova, falling of the atrophic mucosa over
a sandy patch lesion, or due to detachment of a bilharzial polyp.
Fibrosis can arise as a consequence of chronic
infl ammation of the organ wall.
Urothilial changes (only seen in the bladder) com-
prise a chronic reactive infl ammatory disorder characterized by transitional epithelial hyperplasia in
the form of nests called von Brunn’s nests, due to an
irritant (e.g., schistosomal ova). These nests may
undergo central cystic degeneration, forming a condition called “cystitis cystica.” The cystitis cystica
transitional epithelium may undergo metaplasia
into columnar mucin-secreting epithelium, causing
another condition called “cystitis glandularis.” The
ova may cause squamous metaplasia of the transitional cell nest, causing leukoplakia, which may
transform into dysplasia and carcinoma in situ.
Leukoplakia is a thick, white patch of skin, com-
monly seen on the tongue, vulva, or the bladder. It is
composed of thick layers of stratifi ed epithelium
with keratin, with chronic infl ammation of the submucosa. Pathologically, it is explained by squamous
metaplasia followed by cellular hyperplasia.
S. haematobium mainly affects the bladder and the ure-
ters. The posterior part of the bladder is the most vascular area of the bladder, and it is the area where most
ova within the vesical veins are seen. S. haematobium
lays more ova than S. mansoni . The eggs are trapped
within the ureter and the bladder mucosa as they are
carried by the urine to be excreted. The immune system surrounds the eggs, and starts an aggressive granulomatous reaction that causes death and calcifi cation of
the eggs. As the disease advances, calcifi cation can
Signs on Plain Abdominal Radiographs
There is striking calcifi cation of the ureters or the bladder
(Fig. 11.12.6 ). The uniform and linear calcifi cation of the
schistosomiasis bladder is pathognomonic. In contrast,
bladder calcifi cation due to tuberculosis or radiation is often
patchy and focal.
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Signs on Ultrasound
Hyperechoic bladder wall, due to calcifi cation.
Bilateral, nonsymmetrical, hyperechoic dilated ureters are
often seen.
Signs on Intravenous Urography
Bilateral ureteric dilatation with hydronephrosis is often seen.
Marked bladder dilatation may be seen due to bladder neck
stenosis and hypertrophy of the trigon. This fi nding is only
reported in Egypt.
Fig. 11.12.6. Plain radiograph of the pelvis shows complete
bilateral calcifi cation of the ureters ( arrowheads ) and the blad-
der ( arrows ) in a patient with bilharziasis
Signs on CT and MRI
Fig. 11.12.7. Plain radiograph of the pelvis shows complete calcifi cation of the bladder with the seminal vesicles ( arrowheads )
in a patient with bilharziasis
Bilateral ureters calcifi cation (Fig. 11.12.6 ) with hydronephro-
sis is a common fi nding.
Calcifi cation of the seminal vesicles, testes, and spermatic
cords may be seen (Fig. 11.12.7 ).
Fallopian tubes or cervical calcifi cations may occur in women.
Cystitis cystica and cystitis glandularis are seen on MRI as
hypervascular polypoid tissue with low T1 and T2 signal
intensity, with central hyperintensity forming a branching
pattern. The branching central areas show contrast enhancement. The muscular layer of the bladder should be intact and not
disturbed or infi ltrated, a characteristic feature that distinguishes
cystitis cystica and cystitis glandularis from a real bladder tumor.
On CT, the scan shows irregular bladder wall thickening and
multiple polypoid masses arising, often from both the lateral
walls of the bladder and the base of the trigone (Fig. 11.12.8 ).
Fig. 11.12.8. Axial postcontrast CT illustration of the pelvis shows
multiple polypoid masses arising from the right lateral posterior
wall of the bladder with contrast enhancement representing the
radiological fi ndings in cystitis cystica and cystitis glandularis
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Diff erential Diagnoses and Related Diseases
Katayama syndrome is a disease characterized by
acute systemic immune reaction similar to the one
seen in schistosmiasis patients but is not caused by
mature worms or eggs. The patient typically has no
immunity, presenting with skin redness and irritation
or urticaria (swimmer’s urticaria) after 1–2 days of
swimming or washing in infected water. Weeks later,
the affected patient often presents with fever, headaches, chills, lack of appetite (anorexia), and abdominal pain. Neck stiffness and coma may occur. CBC
shows esinophilia in almost 90% of cases. Imaging
investigations are often nonspecifi c. The disease is
believed to be caused by esinophil-mediated toxicity
leading to vasculitis and small vessel thrombosis.
For Further Reading
1. Palmer PES. Schistosomiasis. Semin Roentgenol. 1998;33(1):
6–25
2. Manzella A et al Schistosomiasis of the liver. Abdom
Imaging. 2008;33:144–50
3. Maia ACM Jr et al Spinal cord compression secondary to epidural bilharzioma: case report. J Neuroimaging. 2007;17:367–70
4. Jauréguiberry S et al Neurological involvement during
Katayama syndrome. Lancet Infect Dis. 2008;8(1):9–10
5. Wong-You-Cheong JJ et al Infl ammatory and nonneoplastic bladder masses: radiologic-pathologic correlation.
RadioGraphics. 2006;26:1847–68
6. Singh I et al Cystitis cystica glandularis masquerading as a
bladder tumor. Int Urol Nephrol. 2001;33:635–6
7. Lee G et al Case report: cystitis glandularis mimics bladder
tumor: a case report and diagnostic characteristics. Int
Urol Nephrol. 2005;37:713–5
8. Peng SL. Rheumatic manifestations of parasitic diseases.
Semin Arthritis Rheum. 2002;31:228–47
11.13 Tuberculosis 425
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11.13
Tuberculosis
Tuberculosis (TB) is a multi-systemic, granulomatous
disease caused by the bacilli Mycobacterium tubercu-
losis . There are two main groups of gram-negative
bacilli that infect humans: Mycobacterium tuberculo-
sis and Mycobacterium bovine . M. tuberculosis is an
infection from human to human. Humans are infected
by inhalation (pulmonary TB), by ingesting infected
food or drinks (tonsillar and intestinal TB), or by
wound contamination (rare). M. bovine , on the other
hand, infects humans who come into contact with an
infected mastitis cow.
TB bacteria have a body composed of protein with
an attached polysaccharide, and a capsule composed
of lipids. TB bacteria do not produce endotoxins and
are noninvasive. When neutrophils engulf the TB
bacilli, they do not digest the bacilli because neutrophils lack the enzyme lipase, which is necessary to dissolve the bacterial capsule. The bacteria remain alive
within the neutrophils until the neutrophils die, when
the bacteria are again released into the blood stream.
The pathogenesis of TB is due to the antibody reaction
evoked by the protein nature of the bacteria. The body
produces antibodies against the bacteria antigen,
resulting in a hypersensitivity reaction causing granulomas (tubercles).
Tubercle ( proliferative tissue reaction ) is the unit
reaction of TB. It is grossly composed of a grayish
nodule 1–2 mm in size. Microscopically, it is composed of caseating necrosis of epithelioid cells. The
epithelioid cells can join together to form large cells
with horseshoe-shaped peripheral nuclei, called
Langerhan’s giant cells. A tubercle is a granuloma
with a caseating center. An infected person becomes
tuberculin-test positive usually 1–2 months after initial
exposure. The caseous lesion has three prognoses: it
may heal, it may enlarge and spread to the lymphatic
or the blood stream, or it may form a cavity.
Necrotic TB lesions are the result of hypersensitive
immune reactions to the bacteria in different body systems (hypersensitivity necrosis), and ischemia, because
granuloma do not form angiogenesis, and the vessels
within the area of the granuloma develop endarteritis
obliterans due to the chronic infl ammatory reaction
(ischemic necrosis). Exodative tissue reaction is of a
special type and is seen in TB when the infl ammatory
reaction affects serosal tissue. This reaction is characterized by serous fl uid formation and a few epitheloid
cells and macrophages.
As TB is a multi-systemic disease, manifestations
of TB are different from organ to organ, with many
manifestations having characteristic radiological features that are best addressed separately.
Pulmonary TB
Patients with pulmonary TB classically present with
fever, weight loss, chills, night sweats, cough, and hemoptysis. Diagnosis is established by staining M. Tuberculosis
with acid-fast bacilli stain. Laboratory investigations
often show an elevated erythrocyte sedimentation rate
(ESR), anemia, mild hyponatremia (43%), moderate leucocytosis, and hypercalcemia (27%).
In the lungs, there are four outcomes of TB
infection:
TB clearance : the disease is cleared from the body
with dormant residuals, as long as the immune system is functioning properly.
Primary (acute) TB : this type is usually seen in chil-
dren with widespread disease and less tissue destruction. The rate of primary TB is 90%, and depends on
the body’s innate immunity and hypersensitivity.
The infection in primary TB is called “ primary com-
plex ,” composed of tuberculous focus, regional
lymphangitis, and lymphadenitis. It can occur in the
lung (by inhalation), the tonsils, or the intestine (by
ingestion), or (rarely) in the spleen (by wound infection via hematogenous spread). Primary pulmonary
TB is classically located in the apical segment of the
lower lobes or middle lobes. When the lesion is
healed, it results in a focal calcifi ed lesion known as
Ghon focus . Ghon focus is composed of multiple
aggregated tubercles, with TB lymphangitis due to
the spread of the bacteria in the nearby lymphatic
vessels. The disease can spread from one region of
the lung to another via the bronchi (bronchogenic
spread). It generally heals without sequelae, with
few cases of generalized spread.
Latent (chronic) infection : a condition characterized
by M. tuberculosis infection without any clinical
signs of active disease. The patient is at risk of
reactivation.
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