Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2690_Библиотеки_им_академика_М_И_Перельмана
.pdf
10.6 Lipoatrophic–Lipodystrophic Syndromes 385
https://t.me/medicina_free
For Furth er Reading
1 . Oral EA. Lipoatrophic diabetes and other related syn-
dromes. Rev Endocr Metab Disord. 2003;4:61–77
2 . Premkumar A et al Lipoatrophic-lipodystrophic syn-
dromes: the spectrum of fi ndings on MR imaging. AJR Am
J Roentgenol. 2002;178:311–18
3 . Garg A et al Lipodystrophies: rare disorders causing meta-
bolic syndrome. Endocrinol Clin N Am. 2004;33:305–31
4 . Owen KR et al Mesangiocapillary glomerulonephritis type
2 associated with familial partial dystrophy (DunniganKobberling syndrome). Nephron Clin Pract. 2004;96:c35–8
5 . Spranger S et al Barraquer-Simon syndrome (with sen-
sorineural deafness): a contribution to the differential
diagnosis of lipodystrophy syndromes. Am J Med Genet.
1997;71:397–400
6 . Janaki VR et al Lawrence-Seip syndrome. Br J Dermatol.
1980;103:693
Fig. 10.6.6. An illustration demonstrates the facial features in
Parry-Romberg syndrome (PRS). Notice the hypoplasia of the
right side of the face with mouth deviation, reduced mandible
size, and eye size compared to the normal, unaffected left side of
the face
Histological examinations of the facial specimens
of the disease reveal proliferative interstitial neurovasculitis. PRS may be mistaken for an extensive form of
linear scleroderma.
Signs on MRI
The MRI in PRS usually shows cerebral hemiatrophy, cortical
calcifi cations, focal areas of white matter abnormalities, and
meningeal enhancement, all ipsilateral to the atrophic side of
the face.
7 . Lt Col Prasad AN. Berardinelli Seip syndrome. MJAFI.
2006;62:83–4
8 . Sheh JJ et al Mandibuloacral dysplasia caused by homozy-
gosity for the R527H mutation in lamin A/C. J Med Genet.
2003;40;854–57
9 . Babu P et al Berardinelli Seip syndrome in a 6-year-old boy.
Indian J Dermatol Venerol Leprol. 2008;74:644–46
10 . Kobashi Y et al Berardinelli Seip lipodystrophy. Skeletal
Radiol. 2007;36:999–1003
11 . Solanski M et al Talon cusps, macrodontia and aberrant
tooth morphology in Berardinelli Seip syndrome. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod. 2008; 105:e41–7
12 . Goldberg-Stern H et al Parry-Romberg syndrome: follow-
up imaging during suppressive therapy. Neuroradiology.
1997;39:873–76
13 . Mako SB et al Parry-Romberg syndrome: intracranial MRI
appearances. J Cranio-Maxillofacial Surg. 2003;31:321–24
14 . Mazzeo N et al Progressive hemifacial atrophy (Parry-
Romberg syndrome), case report. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. 1995;79:30–5
15 . Novelli G et al Mandibuloacral dysplasia is caused by a
mutation in LMNA -enconding lamin A/C. Am J Hum Genet.
2002;71:426–31
Chapter 11
https://t.me/medicina_free
Infectious Diseases and
Tropical Medicine
CONTENTS
11.1 Fever 388
11.2 Giardiasis 389
11.3 Amebiasis 390
11.4 Leprosy (Hansen Disease) 394
11.5 Toxoplasmosis 398
11.6 Brucellosis (Malta Fever) 401
11.7 Neurocysticercosis 403
Ascariasis 406
11.8
11.9 Guinea Worm Disease (Dracunculiasis) 408
11.10 Hydatid Cyst (Echinococcosis) 410
11.11 Chagas’ Disease (American Trypanosoma) 416
11.12 Schistosomiasis (Bilharziasis) 419
11.13 Tuberculosis 425
11.14 Typhoid Fever (Salmonellosis) 438
11.15 Malaria 440
11.16 Animal Bites and Stings 442
J. A. Al-Tubaikh: Internal Medicine – An Illustrated Radiological Guide
DOI: 10.1007/978-3-642-03709-2_11, © Springer-Verlag Berlin Heidelberg 2010
387
388 Chapter 11 Infectious Diseases and Tropical Medicine
https://t.me/medicina_free
11.1
11.1
Fever
Fever is a condition characterized by elevation of body
temperature above the normal daily variation, along
with an increase at the hypothalamic thermal set point.
A substance that induces fever is called a pyrogen.
Some infections produce exogenous toxins that
induce the synthesis of endogenous pyrogenic cytokines such as interleukin-1, interleukin-6, and tumor
necrosis factor. These endogenous pyrogens induce
the synthesis of prostaglandin E
vates the hypothalamic core temperature set point.
When the hypothalamic set point is raised, vasoconstriction occurs, decreasing heat loss from the skin.
Fever can be caused by infections (e.g., abscess and
septicemia), neoplasms (e.g., lymphoma), infl ammatory diseases (e.g., collagen vascular disease), and
other causes (e.g., Kawasaki syndrome).
Pyrexia of unknown origin ( PUO ) is defi ned as an
illness of more than 3 weeks’ duration, fever >38.3°C
on three occasions, and necessary initial investigations
that fail to reveal the cause of the fever. The necessary
initial investigations include detailed history and physical examination, complete blood count, antinuclear
antibodies, rheumatic factor, urinalysis, three blood
cultures, urine culture, chest radiograph, abdominal
sonography, and tuberculin skin test. In 25–35% of
PUO patients, a diagnosis cannot be made.
(PGE 2 ), which ele-
2
Central fever is a term used to describe fever that
arises after intracerebral hemorrhage, in the absence of
infection, infl ammation, or a tumor explaining the
fever. This fever has been attributed to cytokine-related
elevation of the hypothalamic set point.
Signs on CT and MRI
In patients with suspected central fever, the examination
classically shows bleeding into the thalamus and the hypothalamus (Fig. 11.1.1 ).
What is the difference between fever and hyperthermia?
Hyperthermia is a condition characterized by uncon-
trolled increase in body temperature that exceeds the
body’s ability to lose heat, in conjunction with a normal hypothalamic thermal set point.
Hyperthermia does not involve pyrogens, and does
not respond to antipyretics.
For Further Reading
1. Chantal PBR et al Fever. Medicine. 2009;37(1):28–34
2. Chantal PBR et al Pyrexia of unknown origin. Medicine.
2005;33(3):33–6
3. Rudd P. Pyrexia of unknown origin (PUO). Curr Paediatr.
1996;6:105–7
4. Deogaonkar A et al Fever is associated with third ventricle
shift after intracerebral hemorrhage: pathophysiological
implications. Neurol India. 2005;53(2):202–7
Fig. 11.1.1. Axial CT ( a ), MR-T1W ( b ), and MR-T2W ( c ) images
of a 26-year-old patient with intracranial bleeding after a car accident show multiple foci of intracranial bleeding. The patient
developed high-grade fever, with no signs of infection detected in
the serum or the cerebrospinal fl uid. The scans showed focal
intracranial hemorrhage involving the right lentiform nucleus
( arrowhead ) and the left thalamus ( arrow ). The patient was fi nally
diagnosed as having central fever and was managed accordingly
11.2 Giardiasis 389
https://t.me/medicina_free
11.2
Giardiasis
Giardiasis is an infectious disease inducing fatty diarrhea caused by the intestinal protozoa Giardia lamblia .
Protozoa are single-celled living organisms with two
cell layers: an outer layer (ectoplasm) and an inner
layer (endoplasm). In cases of environmental changes,
the protozoa secrete a protective coat and shrink into a
round, armored, infectious form called a “cyst.” When
humans ingest the cyst, it transforms again into the
motile form and is called “trophozoite.”
Giardiasis outbreak often occurs after sewage contamination of drinking water, or after drinking from
clear mountain streams contaminated with G. lamblia .
After ingestion of the cysts, the parasites transform
into trophozoites in the duodenum and jejunum, and
adhere to the intestinal wall. The parasites coat the
duodenal and jejunal walls and interfere with fat
absorption from the gut, resulting in fatty diarrhea.
The parasites do not invade the intestinal wall, only
coat it. The ileum is rarely affected by giardiasis.
Most patients with giardiasis are asymptomatic.
Children and patients with low immunity may show
mild abdominal discomfort, along with fatty diarrhea
resembling celiac sprue or celiac disease diarrhea.
Rarely, G. lamblia may invade the gallbladder, causing
cholecystitis and jaundice. A concomitant infection
with Entamoeba histolytica may be overlooked in
cases of infection by a large number of G. lamblia .
There is an increased incidence of giardiasis in
patients with hypogammaglobulinemia. Intestinal lymphoid hyperplasia ( Peyer’s patches hyperplasia ) may
be found in cases of giardiasis infecting a patient with
hypogammaglobulinemia. Diagnosis of giardiasis is
confi rmed by identifying the cysts in the stool.
Fig. 11.2.1. Barium enteroclysis examination in a patient with
giardiasis shows some irregularity and mucosal thickening of
the second part of the duodenum. The proximal jejunum loops
show edema, irritability, and poor fi lling, with thickening and
separation of mucosal folds
Active male homosexuals may show cysts in the stool
in up to 20% of cases.
Signs on Barium enteroclysis
As giardiasis mainly aff ects the duodenum and jejunum, bowel
fold thickening, edema, and barium fi lling defects are usually
seen in the duodenum and jejunum. Occasional barium
segmentation or fragmentation may be seen (Fig. 11.2.1 ).
For Further Reading
Diff erential Diagnoses and Related Diseases
Gay bowel syndrome : there is an increased incidence
of giardiasis in male homosexuals with diarrhea.
1. Maurice MR. Radiological diagnosis of giardiasis. Semin
Roentgenol. 1997;32(4):291–300
2. Heymans HSA et al Giardiasis in childhood: an unnecessarily expensive diagnosis. Eur J Pediatr. 1987;146:401–3
3. David BH et al An update review on Cryptosporidium and
Giardia . Gastroenterol Clin N Am. 2006;35:291–314
390 Chapter 11 Infectious Diseases and Tropical Medicine
https://t.me/medicina_free
11.3
11.3
Amebiasis
Amebiasis is a parasitic infectious disease caused by
the protozoan Entamoeba histolytica . It is the second
most common cause of deaths from parasitic diseases
after malaria.
Amebiasis is endemic in Mexico, India, Central and
South America, and East and South Africa. There is a
high incidence of amebiasis among homosexual
patients.
The infectious form of the parasite is the “mature
cyst,” which is resistant to the gastric and gastrointestinal (GI) secretions. The mature cyst can survive harsh
environmental conditions, and is resistant to the conventional chlorine used to purify drinking water.
Amebiasis is initiated by ingestion of the mature
cyst from infected water or food. The disease is often
asymptomatic; however, multiple manifestations may
be seen throughout the body, including bloody diarrhea in a small percentage of patients. Diagnosis is
confi rmed by identifi cation of the amebic trophozoites
in the stool or by serological identifi cation of amebaspecifi c antibodies, usually 7 days after the initial
symptoms of amebiasis.
wall, measuring 5–30 cm. Ameboma is often solitary, but can be multiple. Patients complain of bloody
diarrhea, abdominal pain, and a colonic mass.
Amebic appendicitis : cannot be differentiated from
classic appendicitis, unless the patient’s history of
bloody diarrhea is known.
Fulminant colitis with toxic megacolon : a rapidly
progressing disease with up to 20 episodes of bloody
diarrhea within 24 h. Patients present with abdominal pain, anorexia, fever, rapid pulse, hypovolemia,
and intense, constant tenesmus. There is a high mortality rate, especially when massive thrombosis of
the colonic wall venules and intestinal ischemia
develop.
Chronic amebic colitis : this term is used to describe
patients with chronic, nonspecifi c abdominal pain
with occasional E. histolytica evidence in the stool.
Signs on Plain Abdominal Radiograph
Abdominal radiograph may show a dilated colon with loss of the
haustrations (0.5% of cases) (Fig. 11.3.1 ).
Intestinal Amebiasis
Amebic invasion of the GI tract can results in different
manifestations, each with its own radiological imaging
features:
Ulcerative amebic rectocolitis (ambulatory dysen-
tery) : in 10% of children, the trophozoites invade
and penetrate the intestinal mucosa, resulting in
intestinal erosions and bleeding. This is usually
day without systemic manifestations or fever.
Complications of ambulatory dysentery include anemia due to bloody diarrhea, intussception, and/or
rectal prolapse due to high-speed peristalsis.
Ameboma : a granulomatous colonic lesion of ameba,
with necrosis, edema, and infl ammation, resembling
a pseudotumor superimposed by secondary infection. It arises from the cecum or the ascending colon
Fig. 11.3.1. A plain abdominal radiograph of a patient with
chronic amebic dysentery shows toxic colonic dilatation of the
ascending and the transverse colon ( arrowhead )
11. 3 Amebiasis 391
https://t.me/medicina_free
Signs on Barium Enema
Ulcers : seen as fi ne granular appearance of the mucosa with
margin speculations. Deep ulcers penetrate the mucosa and
result in “collar-button” ulcers.
Thumbprinting : a term used to describe the shape of barium
distribution inside the intestinal or colonic lumen due to
edema. The barium will show fi lling defects at the mucosal
edges as if a person’s thumb has erased the barium from the
edges (Fig. 11.3.2 ).
Conical cecum : a term used to describe a rigid, ulcerated, and
conical-shaped cecum. Conical cecum is often seen in
intestinal tuberculosis, Crohn’s disease, and amebiasis,
because the cecum is aff ected in 90% of cases (Fig. 11.3.3 ).
Ameboma : seen as barium fi lling defect that resembles a
carcinoma.
Signs on CT
Colitis is seen as marked irregular thickening of the colonic wall,
with enhancement after contrast administration.
Fig. 11.3.3. Intestinal barium CGI shows the classical appearance of conical cecum ( arrowheads )
Hepatic Amebiasis
Occasionally, the amebic trophozoites can reach the
liver via the portal system and form an abscess (30% of
cases). GI invasion is often seen in children, with a mortality rate of 1%, while the formation of liver abscess is
often seen in adults, with a mortality rate of 0.2–2%.
Hepatic abscess may not be preceded by a history
of diarrhea (59% of cases). Patients often present with
sudden onset of right hypochondriac pain radiating to
the shoulder or the subscapular area. There is associated fever, anorexia, vomiting, and the pain is exacerbated by deep inspiration or sitting in the right lateral
decubitus position. The abscess is often seen in the
right lobe of the liver. Differentiation between amebic
and pyogenic hepatic abscess is important for proper
patient management.
Signs on Plain Chest Radiograph
Fig. 11.3.2. Intestinal barium CGI shows thumbprinting appearance ( arrowheads )
Hepatic abscess may often reveal itself in the form of a raised
right hemidiaphragm (Fig. 11.3.4 ).
392 Chapter 11 Infectious Diseases and Tropical Medicine
https://t.me/medicina_free
11.3
Fig. 11.3.4. A plain chest radiograph shows a raised right diaphragm due to hepatic abscess
a
b
Signs on US
Abscesses are seen as masses of heterogeneous echogenicity,
with irregular wall and poor peripheral defi nition. Internal
fl uid-fl uid level might be seen.
Signs on CT
Hepatic abscesses can be either pyogenic (bacterial) or amebic
(parasitic) in origin. It is often diffi cult to diff erentiate between
amebic and pyogenic liver abscesses based on CT appearance
alone, but some radiological clues may be of use:
Pyogenic abscess can present without any signs of infection,
shows uniform ring enhancement after contrast injection, air
fl uid level may be seen inside the abscess, and it shows
microabscesses (satellite lesions), which are occasionally seen
as hypodense lesions >2 cm around the main abscess. A
pyogenic abscess classically reveals yellowish fl uid after
aspiration.
Amoebic abscess characteristically shows a halo of hypoden-
sity surrounding the enhanced ring of the abscess, due to
peripheral edema (Fig. 11.3.5 ). After aspiration, an amebic
abscess classically reveals brown fl uid ( anchovy sauce
Fig. 11.3.5. Axial hepatic postcontrast-enhanced CT images in
two different patients with hepatic abscesses. In one patient ( a ),
an amebic liver abscess is illustrated with its characteristic halo
( arrowhead ). Notice the multiple splenic microabscesses. In the
other patient ( b ), a pyogenic liver abscess is demonstrated for
comparison. Notice the lack of the surrounding halo, with the
presence of multiple small satellite lesions ( arrows )
appearance ), although it may be a pyogenic abscess mixed
with hemorrhage from the needle. An acute amoebic abscess
can transform into a chronic abscess, which is characterized by
fi brosis and hard mass formation that can be mistaken for
hepatocellular carcinoma.
Diff erential Diagnoses and Related Diseases
Meleney’s synergistic gangrene is a rare complication
of progressive postoperative gangrene, which arises
after empyema or intra-peritoneal abscess drainage.
This complication can arise due to Staphylococcus
11. 3 Amebiasis 393
https://t.me/medicina_free
aureus infection or cutaneous amebiasis. Patients often
present 10–14 days post empyema or intraperitoneal
abscess drainage, with truncal ulcer and severe pain.
Pathologically, the ulcer is sharply demarcated, with
three zones of colors: an outer bright red zone, an inner
raised purple zone, and a central zone of red granulation tissue obscured by yellowish exudates.
Thoracic Amebiasis
Amebiasis from liver abscess may extend to the right
lower lung lobes via invading the diaphragm. This rare
complication is often seen in adults. Thoracic amebiasis
is almost always secondary to amebic hepatic abscess.
Empyema, pericarditis and medistinitis may occur due
to amebic extension into the thoracic structures.
Signs on Plain Chest Radiograph
Chest radiograph often shows a raised right hemidiaphragm
along with right basal pleural eff usion, pneumonic patch, or
atelectasis.
Brain Amebiasis
Brain amebiasis is a rare complication seen in 1% of
patients with amebic dysentery. The parasites often
reach the brain via the hematogenous route. Patients
often present with convulsions, hemiplegia, meningitis, or cranial nerve lesions.
Signs on Brain CT
Amebic abscess is seen as a nonspecifi c parenchymal hypodense
area with peripheral, uniform ring enhancement.
For Further Reading
1. Kimura K et al Amebiasis: modern diagnostic imaging with
pathological and clinical correlation. Semin Roentgenol.
1997;32(4):250–75
2. Yin LS et al Left lobe amoebic liver abscess mimicking a
perforated gastric tumor. Eur J Radiol Extra. 2008;66:e25–7
3. Davson J et al Diagnosis of Meleney’s synergistic gangrene.
Br J Surg. 1988;75:267–71
4. Cade D et al Amoebic perforation of the intestine in chil-
dren. Br J Surg. 1974;61:159–61
5. Avron B et al Biochemistry of Entamoeba : a review. Cell
Biochem Funct. 1988;6:71–86
394 Chapter 11 Infectious Diseases and Tropical Medicine
https://t.me/medicina_free
11.4
11.4
Leprosy (Hansen Disease)
Leprosy is a chronic, granulomatous, infectious disease that mainly affects the skin and the peripheral
nerves, and is caused by acid- and alcohol-fast bacilli
Mycobacterium leprae ( M. leprae ).
Leprosy is divided into different clinical subtypes
based on the capacity of the patient’s immune system
to resist the disease:
Indeterminate leprosy : the initial form that either
resolves spontaneously or progresses into the other
forms according to the degree of cell-mediated
immunity.
Tuberculoid leprosy ( TL ): a form of leprosy that
results from strong cell-mediated immune response
to the disease. This type is characterized by the formation of multiple skin and nerve granulomas
(tubercles), often restricted to a few locations. The
granulomatous reaction in TL mimics tuberculosis,
but is non-caseating.
Borderline leprosy : this form represents an interme-
diate state between the tubeculoid and the lepromatous forms of leprosy.
Lepromatous leprosy ( LL ): this form results from
low immunity of the infected host, resulting in widespread, extensive disease damage. The granulomatous reaction in LL is characterized by the formation
of “lepromas,” which are granuloma formations
mediated by macrophages engulfi ng live bacteria
(lepra cells).
Skin Involvement
In TL, the early skin manifestation is hypopigmented
macules or plaques. A macule is a localized area with
textural or color change of the skin, while a plaque is a
palpable, plateau-like elevation of skin >2 cm in size.
TL is characterized by few skin lesions, which are
often dry, scaly, and hairless.
In LL, widespread symmetrically distributed macules are often seen as early skin changes. The macules
are poorly defi ned and show erythema (redness due to
vascular dilatation). If the macules are untreated, dermal infi ltration occurs, which causes skin thickening.
When skin thickness occurs in the face, it is called leo-
nine facies (Fig. 11.4.1 ). The eyebrows and the eye-
lashes may be lost ( madarosis ). Leprous alopecia is
characterized by scalp hair loss with preservation of
the hair over the course of scalp arteries. Dystrophic
nail changes, with development of peripheral edema of
the legs and ankles, often occur. Souza Campos nodule
is a rare form of TL seen in endemic areas of Brazil,
where leprosy infection may infect patients during a
kiss, and the highly resistant child develops a nodule at
the site of the inoculation. Lucio phenomenon is a very
rare reactional state of LL characterized by painful
irregular skin patches that become purpuric and form
bullae that break down, leaving widespread areas of
ulceration. Healing is with scar formation. Lucio phenomenon arises due to cutaneous vasculitis.
The clinical features of leprosy are determined by the
host response to M. leprae . Skin, nerves, eyes, mucosa,
and bone may all be affected by leprosy. Laboratory
results often show high erythrocyte sedimentation rate,
and increased fi nding of rheumatoid factor in LL (rheumatoid factor is positive in 58% of cases).
Diagnosis of leprosy is established via clinical
examination, and identifi cation of the acid- and alcohol fast bacilli on skin or buccal mucosa smears stained by
the Ziehl–Neelsen technique. Clinical diagnostic features of leprosy include skin lesions with defi nite sensory loss and thickened peripheral nerves.
Fig. 11.4.1. Forehead skin thickening and plaques (leonine facies)
with loss of the eyebrows (madarosis)
11.4 Leprosy (Hansen Disease) 395
https://t.me/medicina_free
Fig. 11.4.2. Bilateral
claw-hand deformities of
leprosy
Nerve Involvement
Nerve involvement in leprosy affects sensory, motor, and
autonomic peripheral nerves. The posterior tibial nerve is
mostly affected, resulting in anesthesia of the soles and
feet. Involvement of the peripheral autonomic fi bers
results in loss of skin sweating, with glove-and-stocking
hypohidrosis, a situation similar to the changes seen in
diabetic peripheral neuropathy. Loss of peripheral joint
sensation causes repetitive trauma and osteomyelitis, later
resulting in the development of Charcot’s joint. Motor
denervation of the hand causes progressive hand contracture deformity, known as “claw hand” (Fig. 11.4.2 ).
Eye Involvement
Blindness may occur in up to 5.3% of patients with
leprosy, due to an inability to close the eyes normally
( Lagophthalmos ), corneal ulceration, secondary cata-
ract, and chronic iridocyclitis.
The oral mucosa is affected in TL and LL patients,
who are often neglected and who receive delayed treatment. Oral mucosal lesions in LL include yellowishwhite plaques, nodular infi ltration of the tonsils, deep
ulceration of the soft palate, and elongation of the
uvula (Fig. 11.4.3 ).
Mucosal Involvement
Both the nasal and the oral mucosa may be affected by
LL. Nasal mucosa involvement results in sneezing
blood (epistaxis) due to ulceration, and nasal stuffi ness
due to formation of polyps.
Fig. 11.4.3. Oral mucosal involvement in leprosy. There is deep
ulceration of the soft palate, tonsillar abscess formation, and
elongation of the uvula
Соседние файлы в папке Библиотека им академика М.И. Перельмана