This document provides information on various tropical diseases that may require surgery, including their pathogenesis, clinical features, investigations, and treatment options. It discusses amoebiasis, ascariasis, asiatic cholangiohepatitis, filariasis, hydatid disease, and leprosy. For each condition, it describes the causative organism, areas of prevalence, how the disease spreads in the body, potential symptoms, relevant tests, and medical and surgical management approaches.
3. AMOEBIASIS
• Entamoeba histolytica
• Indian subcontinent, Africa, parts of Central & South
America
• majority remain asymptomatic carriers
• mode of infection: faeco-oral route
• hygiene, sanitation, immunocompromised, alcoholic
6. Pathogenesis
• Incubation period (IP): 4 days-4 months
• intestinal amoebiasis: flask-shaped ulcers form in
submucosa
• abscess cavity contains chocolate-colored,
odourless, anchovy sauce-like fluid with mixture
of necrotic liver tissue and blood
• pus in abscess is sterile unless secondarily infected
7. Clinical Features
• young adult male
• insidious onset with non-specific symptoms;
abdominal pain, anorexia, fever, night sweats,
malaise, cough, weight loss
• gradually progress to more specific symptoms; pain
in the right upper abdomen, right shoulder tip,
hiccoughs, non-productive cough
• bloody diarrhea or travel to endemic area
8. Examination
• toxic, anaemic
• upper abdominal rigidity, tender hepatomegaly, tender,
bulging intercostal spaces
• skin edema
• pleural effusion
• basal pneumonitis
• occasionally, tinge of jaundice or ascites may be present,
rarely rupture into peritoneal, pleural or pericardial cavity
9. Amoeboma
• chronic granuloma arising in the large bowel (caecum)
• long-standing amoebic infection that has been treated
intermittently with drugs without completion of a full
course, a situation that arises from indiscriminate self-
medication
• can be mistaken for carcinoma
• suspect in endemic area with generalized ill health,
pyrexia, mass in right iliac fossa with hx if blood-stained
mucoid diarrhea
• altered bowel habit
11. Imaging Techniques
• Ultrasound; abscess cavity, hypoechoic or anechoic
lesion with ill-defined borders, internal echoes
suggest necrotic material or debris
• Computed tomography (CT scan); raised right
hemidiaphragm, pleural effusion, evidence of
pneumonitis
• Colonoscopy and biopsy
12.
13.
14.
15. Medical Treatment
• Intestinal & early hepatic amoebiasis: metronidazole
(800mg TID for 5-10days) or tinidazole/ornidazole (2g
OD for 3 days)
• Eliminate luminal cysts: diloxanide furoate or
paromomycin 500mg TID for 10 days
• Aspiration; imminent rupture of an abscess is
expected, helps penetration of the drugs *pleural cavity
pericardial sac or peritoneal cavity
• secondary infection, other drug treatment should be
added
16. Surgical Treatment
• rupture into pleural cavity, peritoneal or pericardial cavity
• intensive care unit
• resuscitation, drainage, appropriate lavage with vigorous
medical treatment
• large bowel, severe hemorrhage and toxic megacolon are rare
• resection of bowel with exteriorisation
• supportive therapy
• amoeboma not regressed -> colonic resection especially if
cancer cannot be excluded
17. ASCARIS LUMBRICOIDES
• Ascaris lumbricoides, roundworm,common intestinal
nematode to infest humans
• quarter of the world’s population
• larva-> pulmonary symptoms
• adult worm-> intestinal symptoms
18. • The eggs can survive in a hostile environment for a long time.
• hot and humid conditions in the tropics are ideally suited for the eggs to turn
into embryos. The fertilised eggs are present in soil contaminated with
infected faeces. Faeco-oral contamination causes human infection.
• As the eggs are ingested, the released larvae travel to the liver via the portal
system and then through the systemic circulation to reach the lung.
• The process of maturation takes up to 8 weeks
• The developed larvae reach the alveoli, are coughed up, swallowed and
continue their maturation in the small intestine.
• Sometimes, the young worm migrates from the tracheobronchial tree into the
oesophagus, thus finding its way into the gastrointestinal tract, from where it
can migrate to the common bile duct or pancreatic duct.
• The mature female, once in the small bowel, produces innumerable eggs
that are fertilised and thereafter excreted in the stool to perpetuate the life
Pathogenesis
20. Clinical Features
• Larval stage: pulmonary symptoms- dry cough, chest pain,
dyspnoea, fever (Loeffler's syndrome)
• Adult worm: malnutrition, failure to thrive, abdominal pain
• worms can migrate into CBD causing ascending cholangitis
& obstructive jaundice. Acute pancreatitis when worm in
pancreatic duct
• small intestine obstruction: bolus of adult worms
incarcerated in the terminal ileum -SURGICAL
EMERGENCY, rarely perforation may occur from
ischaemic pressure necrosis from the bolus of worms
21. Investigation
• eosinophilia
• stool examination: ova
• sputum or bronchoscopic washings: Charcot-Leyden crystals
or larvae
• CXR: fluffy exudates in Loeffler’s syndrome
• Barium meal and follow-through: bolus of worms in ileum or
lying freely within small bower
• USG: worm in CBD, pancreatic duct
• MRCP in obstructive jaundice: worms in CBD
22.
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25.
26. Medical Treatment
• Pulmonary phase is self limiting disease so treat
symptomatically
• Single dose Albendazole 400mg, pyrantel pamoate
11mg/kg; max. 1 g, ivermectin (150-200
microgram/kg), or mebendazole 100 mg BD for 3
days *can precipitate intestinal obstruction
• intermittent/subacute intestinal obstruction; IV fluids,
NG suction. hypertonic saline enema
27. Surgical Treatment
• complications case
• intestinal obstruction that does not resolve with
conservative regimen
• laparotomy, bolus of worms at terminal ileum is milked
through ileocaecal valve into colon for natural passage in
stool. Post-op hypertonic saline enemas (extrusion of
worms)
• strictures, gangrenous, perforations: resection &
anastomosis
• healthy bowel wall: enterotomy and removal of the worms
28.
29. • Ileostomy: perforation in the presence of large number of
worms
• exteriorisation ideal in severe sepsis
• resection of diseased ileum, closure of distal bowerl and
end-to-side ileotransverse anastomosis
• Endoscopic removal: CBD, pancreatic duct *if endoscopic
fails, do open exploration
• Cholecystectomy
• * FULL COURSE ANTI-PARASITIC must follow any
surgical intervention
31. Pathogenesis
• In humans, the parasite matures into the adult worm in
the intrahepatic biliary radicles where they may reside for
many years
• intrahepatic bile duct: dilated with epithelial hyperplasia &
periductal fibrosis -> dysplasia -> cholangiocarcinoma
• eggs or dead worms as nidus for stone formation in gall
bladder or CBD, which may thickened & dilated in late
stage. produce mucin-rich bile
• *dilated intrahepatic bile duct can cause cholangitis, liver
abscess, hepatitis
32. Clinical Features
• may remain dormant for years
• non-specific: fever, malaise, anorexia, upper
abdominal discomfort
• specific: fever with rigors (ascending cholangitis,
obstructive jaundice due to stones, biliary colic and
pruritis), acute pancreatitis (obstruction of
pancreatic duct by adult worm)
33. Investigation
• LFT
• Examination of stool / duodenal aspiration; eggs or adult
worms
• USG:
uniform dilatation of small peripheral intrahepatic bile ducts
with only minimal dilatation of common hepatic & CBD.
Thickened duct walls (increased echogenicity, non-
shadowing echogenic foci in bile ducts representing worms
or eggs)
• ERCP for comfirmation
34. Treatment
• Drug of choice: praziquantel & albendazole
• Cholecystectomy with exploration of CBD when
indicated. repeated washouts are necessary
35. • choledochoduodenostomy: CBD dilated, stones, biliary
debris, sludge, mud (*some surgeon prefer
choledochojejunostomy to a Roux loop). Roux loop is
brought up to the abdominal wall,’access loop’-for IR to
remove stone
36. FILARIASIS
• Wuchereria bancrofti carried by mosquito
• variant parasites: Brugia malayi & B. timori
• affects >90 million people worldwide: 2/3rd in China,
India & Indonesia
• WHO: 2nd most common cause, after leprosy, of
long-term disability
37. Pathogenesis
• colonise lymphatic system
Once bitten by the
mosquito, the matured
eggs enter the human
circulation to hatch
and grow into adult
worms; the process of
maturation takes about
one year. The adult
worms mainly
colonise the lymphatic
system.
38. Clinical Features
• episodic attack of fever
• lymhadenitis
• lymphangitis…recurrent-> fibrosis of lymphatic channels
• massive lower limb deem
• skin thickening (obstruction of cutaneous lymphatics)
• secondary streptococcal infection
• B/L lower limb filariasis often associated with scrotal & penile elephantiasis
• chyluria
• chylous ascites
• mild respiratory symptoms: dry cough *tropical pulmonary eosinophilia
41. Treatment
• diethylcarbamazine 2mg/kg TID for 12 days or as a
single dose or albendazole 400mg with ivermectin
200microgram/kg in a single dose with or without
DEC (early stage-before gross deformities)
• intermittent pneumatic compression (early stage of
limb swelling)
• hydrocoele: excision & eversion of the sac with if
necessary excision of redundant skin
43. common source of infection
transmitted to the
intermediate hosts – humans,
sheep and cattle. In the dog,
the adult worm reaches the
small intestine, and the eggs
are passed in the faeces.
These eggs are highly
resistant to extremes of
temperature and may survive
for long periods. In the dog’s
intestine, the cyst wall is
digested, allowing the
protoscolices to develop into
adult worms. Close contact
with the infected dog causes
contamination by the oral
route, with the ovum thus
gaining entry into the human
44.
45. Classification
• WHO Informal Working Group on Echinococcosis (WHO-
IWGE)
• ultrasound classification
Group 1: Active group- cysts >2cm, often fertile
Group 2: Transition group- cysts starting to degenerate
& entering transitional stage because of host resistance
or treatment, but may contain viable protoscolices
Group 3: Inactive group- degenerated, partially or totally
calcified cysts; unlikely to contain viable protoscolices
46. Clinical Features
• liver hydatid cyst: enlarging painful mass in right upper
quadrant, liver swelling (dull pain- stretching of liver capsule)
• *daughter cysts communicate with biliary tree -> obstructive
jaundice
• pulmonary hydatid cyst: dyspnoea, travel through
tracheobronchial tree
• cerebral hydatid cyst: raised intracranial pressure symptoms
• anaphylactic shock (rare without any obvious cause)
47. Investigation
• high eosinophil count
• ELISA, immunoelectrophoresis
• USG; abnormality in gall bladder, bile ducts, liver
• CT scan; smooth space-occupying lesions with
several septa
48.
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53.
54. Treatment
• Tx depends on affected organ, tertiary unit,expert
hepatobiliary surgeon, experienced physician, and
where interventional radiologist available
• PAIR (puncture, aspiration, injection, reaspiration)
• approach decided by clinical team (activity of cysts,
anatomical position, number of cysts)
• albendazole 40mg BD for 3 months, praziquantel
20mg/kg BD for 14 days *lower ICP pressure before
treatment
55. • radical total or partial pericystectomy with
omentoplasty or hepatic segmentectomy
• scolicidal agents ; hypertonic saline (15-20%),
ethanol (75-95%), 1% povidone iodine
• inactive and asymptomatic patient may just be
observed
56.
57. Pulmonary Hydatid Disease
• second most affected organ
• cysts size varies
• right lung & lower lobes more often involved
• cyst usually single *but multiple cysts do occur &
concomitant hydatid cysts in other organs
• silent, incidental
• symptoms: cough, expectoration, fever, chest pain,
hemoptysis
58. • uncomplicated cysts: rounded or oval lesions on
CXR. erosion of bronchioles results in air being
introduced between pericyst and laminated
membrane and disease affecting both lungs or
recurrent or ruptured cysts
• CXR: meniscus or crescent sign
• CT-SCAN: water-lily sign
59.
60. • Treatment: preserve as much of viable lung tissue
as possible
cystotomy
capittonage (suturing together the walls)
pericystectomy
segmentectomy
pneumonectomy (occasionally)
61. LEPROSY
• Hansen’s disease, acid-fast bacillus,
Mycobacterium leprae
• India, Brazil, Nepal, Mozambique, Angola,
Myanmmar
• primary effect, social discrimination
• close contact over a long time of several years
causes the disease to spread
62. Pathogenesis
• bacillus inhibits the colder parts of the body -nasal
mucosa, skin in the region of the ears; facial nerve
as it exits from stylomastoid foramen
• transmit by nasal secretion
• infection being contracted in childhood or early
adolescence
• incubation periods for years
• skin, upper respiratory or neurological manifestation
65. • lepromatous leprosy: widespread dissemination of
abundant bacilli in the tissues with macrophages
and a few lymphocytes
• tuberculoid leprosy: scant bacilli in the tissues,
epithelioid granulomas, numerous lymphocytes and
giant cells
• tissue damage is inversely proportional to the host’s
immune response
66. Clinical Features
• slowly progressive affecting skin, upper respiratory tract,
peripheral nerves
• tuberculoid leprosy: damage to tissues occurs early &
localized to one part of the body with limited deformity of
that organ
• Neural involvement: thickening of nerves, which are
tender. asymmetrical well-defined anaesthetic
hypopigmented or erythematous macules with elevated
edge & a dry rough surface -lesions called leprids
67. • lepromatous leprosy: symmetrical & extensive. cutaneous
involvement- several pale macules that form plaques & nodules
called lepromas
• deformities
• primary: caused by leprosy or its reactions
• secondary: from effects such as anaesthesia of the hands &
feet
• leonine facies (nodular lesion),
• wrinkling of the skin, loss eyebrows, destruction of lateral
cartilages & septum of the nose with collapse of nasal bridge
& lifting of the tip of the nose
68. • paralysis of the branches of the facial nerve (in bony canal or zygomatic
branch)
• blindness (exposure keratitis or iridocyclitis)
• paralysis of orbicularis oculi (incomplete closure of the eye, epiphora,
conjunctivitis)
• claw hand, ulnar nerve at the elbow, median nerve at the wrist
• claw of the toes, posterior tibial nerve
• foot drop, lateral popliteal nerve -feel thickened nerve behind upper end
of fibula
• trophic ulceration, chronic infection, contraction & autoamputation
• testis atrophy, gynaecomastia
77. Surgical Treatment
• in advanced stages for functional disability of limbs,
cosmetic disfigurement of the face, visual problems
• major reconstructive surgery by plastic surgeon
• tendon transfer by specialist hand or orthopaedic surgeons
• amputation or emergency drainage of abscess by general
surgeon
• *all surgical procedures need to be done under anti-leprosy
drug treatment
• educate the patient and general public
78. REFERENCES
• Bailey & Love’s, Short Practice of Surgery, 26th
edition
• Davidson’s Textbook of Medicine, 22nd Edition
• CDC website
• youtube.com
