INFECTIOUS DISEASES

BY
DR ONOTA P.O
• SYPHILIS
• AMOEBIASIS
• TYPHOID
• SCHISTOSOMIASIS
• ONCHOCERCIASIS

07/18/2025 2
 SYPHILIS
• INTRODUCTION
• Syphilis is a chronic sexually transmitted disease
with varied clinical and pathologic
manifestations.
• The causative spirochete, Treponema pallidum subsp.
pallidum, hereafter referred to simply as T. pallidum, is
too slender to be seen in Gram stain, but it can be
visualized by silver stains and immunofluorescence
techniques

07/18/2025 3
 INTRODUCTION CTD
• Transplacental transmission of T. pallidum occurs
readily, and active disease during pregnancy results in
congenital syphilis
• T. pallidum cannot be grown in culture. Public health
programs and penicillin treatment reduced the number
of cases of syphilis in the United States from the late
1940s until the 1970s
• The number of cases has been relatively stable in
recent years, with approximately 14,000 being reported
in 2010.

07/18/2025 4
07/18/2025 5
PATHOGENESIS

• Proliferative endarteritis affecting small vessels with a

surrounding plasma cell-rich infiltrate is characteristic of
all stages of syphilis.
• Much of the pathology of syphilis can be ascribed to the
ischemia produced by the vascular lesions. The
pathogenesis of endarteritis is unknown.

07/18/2025 6
 PATHOGENESIS CTD
• The immune response to T. pallidum reduces the burden
of bacteria and can lead to resolution of local lesions
but does not reliably eliminate the systemic infection
• Superficial sites of infection (chancres and rashes) have
an intense inflammatory infiltrate that includes T cells,
plasma cells and macrophages that surround the
bacteria

07/18/2025 7
 PATHOGENESIS CTD
• The infiltrating CD4+ T cells are T 1 cells that may
H

activate macrophages to kill the bacteria.

• Treponeme-specific antibodies are detectable and these
activate complement in the lesion and opsonize the
bacteria for phagocytosis by macrophages

07/18/2025 8
PATHOGENESIS CTD
• In many patients, the organism persists despite these
host responses.
• A protein in the outer membrane of T. pallidum, TprK,
accumulates structural diversity during the course of
infection through gene conversion (recombination)
between silent donor sites and the tprK gene and this
might contribute to antigenic diversity that allows the
organism to persist.

07/18/2025 9
PATHOGENESIS CTD
• Syphilis is divided into three stages, with distinct
clinical and pathologic manifestations

07/18/2025 10
•

07/18/2025 11
PATHOGENESIS CTD
• PRIMARY SYPHILLIS; Occurs about 3 weeks after contact.
• A firm, non-tender, raised, red lesion(chancre) forms on the penis,
cervix, vaginal wall, or anus; this will heal even without therapy.
• Treponemes are plentiful, visualizable with silver or
immunofluorescent stains at the chancre surface; there is an exudate
composed of plasma cells, macrophages, and lymphocytes, with a
proliferative endarteritis.
• Treponemes spread lymphohematogenously throughout the body
even before the chancre appears.

07/18/2025 12
PATHOGENESIS CTD
• SECONDARY SYPHILIS; Occurs 2 to 10 weeks after the primary chancre
in 75% of untreated patients, due to spread and proliferation of
spirochetes in skin including palms and soles and mucocutaneous
tissues especially the mouth.
• Superficial lessions with erossions are painless and contain infectious
spirochetes. Mucocutaneous lessions show plasma cell infilterates
and obliterative endarteritis.
• Lymphadenopathy, mild fever, malaise, and weight loss are common.
• Secondary Syphilis lasts several weeks and then enters a long latent
phase.
07/18/2025 13
PATHOGENESIS CTD
• TERTIARY SYPHILIS; Occurs in one third of untreated patients after a
long latent period (>5 years).
• CARDIOVASCULAR SYPHILIS; (>80% of tertiary syphilis) results in
aortitis ( due to endarteritis of the aortic vasa vasorum) with aortic
root and arch aneurysms and aortic valve insufficiency.
• NEUROSYPHILIS; can be symptomatic (meningovascular disease, tabes
dorsalis, or diffuse brain parenchymal disease, so-called general
paresis) or asymptomatic (cerebrospinal fluid abnormalities only, with
pleocytosis, increased protein, and decreased glucose).

07/18/2025 14
PATHOGENESIS CTD
• ‘BENIGN’ TERTIARY SYPHILIS; is associated with necrotic, rubbery
masses, gummas due to delayed type hypersensitivity to the
organisms, which form in various sites, bone, skin, oral mucosa.
• CONGENITAL SYPHILIS; usually occurs when the mother has primary
or secondary syphilis.
• Intrauterine or perinatal death will occur in 50% of untreated cases.
• Early(infantile) congenital syphilis includes nasal discharge, a bullous
rash with skin sloughing, hepatomegaly, and skeletal
abnormalities(nose and lower legs are most distinctive). Diffuse lungs
or liver fibrosis can also occur.
07/18/2025 15
PATHOGENIS CTD
• Late(tardive) manifestations include notched central incisors,
deafness, and interstitial keratitis with blindness(Hutchinson triad).

07/18/2025 16
07/18/2025 17
 MORPHOLOGY
• In primary syphilis a chancre occurs on the penis
or scrotum of 70% of men and on the vulva or
cervix of 50% of women.
• The chancre is a slightly elevated, firm, reddened
papule, up to several centimeters in diameter, that
erodes to create a clean-based shallow ulcer.
• The contiguous induration creates a button-like mass
directly adjacent to the eroded skin, providing the basis
for the designation hard chancre

07/18/2025 18
MORPHOLOGY CTD
• On histologic examination, the chancre contains an
intense infiltrate of plasma cells, with scattered
macrophages and lymphocytes and a proliferative
endarteritis.
• The endarteritis starts with endothelial cell activation
and proliferation and progresses to intimal fibrosis

07/18/2025 19
MORPHOLOGY CTD
• The regional nodes are usually enlarged due to
nonspecific acute or chronic lymphadenitis, plasma cell–
rich infiltrates, or granulomas.
• In secondary syphilis widespread mucocutaneous
lesions involve the oral cavity, palms of the
hands, and soles of the feet.

07/18/2025 20
MORPHOLOGY CTD
• The rash frequently consists of discrete redbrown
macules less than 5 mm in diameter, but it may be
follicular, pustular, annular, or scaling.
• Red lesions in the mouth or vagina contain the most
organisms and are the most infectious.
• Histologically, the mucocutaneous lesions of secondary
syphilis show the same plasma cell infiltrate and
obliterative endarteritis as the primary chancre,
although the inflammation is often less intense.

07/18/2025 21
MORPHOLOGY CTD
• Tertiary syphilis most frequently involves the aorta;
the
• CNS; and the liver, bones, and testes.
• The aortitis is caused by endarteritis of the vasa vasorum of
the proximal aorta.
• Occlusion of the vasa vasorum results in scarring of the
media of the proximal aortic wall, causing a loss of elasticity.
• There may be narrowing of the coronary artery ostia caused
by subintimal scarring with resulting myocardial ischemia.

07/18/2025 22
MORPHOLOGY CTD

• Neurosyphilis takes one of several forms, designated

meningovascular syphilis, tabes dorsalis, and general
paresis

07/18/2025 23
07/18/2025 24
MORPHOLOGY CTD
• Syphilitic gummas are white-gray and rubbery, occur
singly or multiply, and vary in size from microscopic
lesions resembling tubercles to large tumor-like masses.
• They occur in most organs but particularly in
skin,subcutaneous tissue, bone, and joints.
• In the liver, scarring as a result of gummas may cause a
distinctive hepatic lesion known as hepar lobatum

07/18/2025 25
MORPHOLOGY CTD
• On histologic examination, the gummas have centers of
coagulated, necrotic material and margins composed of
plump, palisading macrophages and fibroblasts
surrounded by large numbers of mononuclear
leukocytes, chiefly plasma cells.
• Treponemes are scant in gummas and are difficult to
demonstrate.
• The rash of congenital syphilis is more severe than
that of adult secondary syphilis.

07/18/2025 26
MORPHOLOGY CTD
• It is a bullous eruption of the palms and soles of the feet
associated with epidermal sloughing.
• Syphilitic osteochondritis and periostitis affect all
bones,but lesions of the nose and lower legs are most
distinctive.
• Destruction of the vomer causes collapse of the bridge
of the nose and, later on, the characteristic saddle nose
deformity.
• Periostitis of the tibia leads to excessive new bone
growth on the anterior surfaces and anterior bowing, or
saber shin.
07/18/2025 27
MORPHOLOGY CTD
• There is also widespread disturbance in endochondral
bone formation.
• The epiphyses become widened as the cartilage
overgrows,and cartilage is found in displaced islands
within the metaphysis.
• The liver is often severely affected in congenital
syphilis.
• Diffuse fibrosis permeates lobules to isolate hepatic
cells into small nests, accompanied by the characteristic
lymphoplasmacytic infiltrate and vascular changes.
07/18/2025 28
MORPHOLOGY CTD
• Gummas are occasionally found in the liver, even in
early cases.
• The lungs may be affected by a diffuse interstitial
fibrosis
• In the syphilitic stillborn, the lungs appear pale and
airless (pneumonia alba).
• The generalized spirochetemia may lead to diffuse
interstitial inflammatory reactions in virtually any other
organ (e.g., the pancreas, kidneys, heart, spleen,
thymus, endocrine organs, and CNS).
07/18/2025 29
MORPHOLOGY CTD
• The late manifestations of congenital syphilis include a
distinctive triad of interstitial keratitis, Hutchinson
teeth, and eighth-nerve deafness.
• In addition to interstitial keratitis, the ocular changes
include choroiditis and abnormal retinal pigmentation.
• Hutchinson teeth are small incisors shaped like a
screwdriver or a peg, often with notches in the enamel.

07/18/2025 30
MORPHOLOGY CTD
• Eighth nerve deafness and optic nerve atrophy develop
secondary to meningovascular syphilis.

07/18/2025 31
 SEROLOGIC TEST FOR SYPHILIS
• Treponemal antibody tests measure antibodies reactive with
T.pallidum
• Non treponemal tests VDRL, rapid plasma reagin(RPR) measure
antibody to cardiolipin, a phospholipid in treponemes and normal
tissues.
• Both tests become positive approximately 6 weeks after infection but
are only moderately sensitive (70% to 85%) for primary syphilis; they
are >95% sensitive for secondary syphilis.

07/18/2025 32
SEROLOGIC TEST FOR SYPHILIS CTD
• Non treponemal test may become negative with time or treatment,
but treponemal antibody tests remain positive and are very sensitive
for tertiary and latent syphilis.

07/18/2025 33
AMOEBIASIS

• Amoebiasis is caused by Entamoeba hystolitica

• It has world wide distribution with more prevalence in tropical
countries
• ETHIOPATHOGENESIS
• Entamoeba has two forms
• Trophozoite(motile form)
• Cyst(immotile form)

07/18/2025 34
• Cysts are infectious forms which survive in the environment for weeks
to months
• MODE OF TRANSMISSION- direct fecal-oral route
• Ingested cysts resists gastric digestion and pass to the ileocecal region
• In the ileocecal region, they excyst and divide, giving rise to
trophozoites that then colonize the colon

07/18/2025 35
• Trophozoites produce enzymes(like glycosidase, galactosidase,
mannosidase, fucosidase, xylosidase, glucosidase, amylase and
hyaluronidase) which would degrade the mucosa and help the
organisms to attatch to the epithelial cells by adherence lectin
• This also protects the organism from the attack of complement
complex.
• Proteases causes the lysis of epithelial cells and degrade the
extracellular matrix, helping the organism to invade the tissue

07/18/2025 36
• Once the organism enters the tissue, it interacts with neutrophils and
macrophages
• It inhibits the migration of macrophages by producing macrophage
locomotion- inhibitory factor
• FACTORS WHICH AFFECT SEVERITY OF DISEASE;
• Poor nutrition
• Tropical climate
• Decreased host immunocompetence
• Integrity of mucosal barrier
07/18/2025 37
• Altered colonic bacterial flora
• Trauma
• Genetic differences in a cysteine proteases that serves as virulence
factor

07/18/2025 38
• CLINICAL FEATURES;
• All ages including infants are affected
• Many patients may remain asymptomatic
• Mild cases of amebiasis present with mild diarrhea, cramps or
abdominal discomfort often with mucus and blood in stools
• Intestinal amebiasis presents in 4 clinically recognized forms;
• Typical dysenteric infection with intermittent bloody diarrhea and
lower abdominal cramps

07/18/2025 39
• As fulminant amebic colitis
• Amebic appendicitis
• Localized mass lesion in the colon, the ameboma
• Dysenteric infection may lead to severe dehydration, abdominal pain
and hypotension
• Generalized peritonitis, toxic megacolon or rectal prolapse may
develop

07/18/2025 40
• Amebomas present as palpable mass, causes numerous symptoms
including alternating diarrhea and constipation, weight loss and low-
grade fever
• MORPHOLOGY
• GROSS FINDINGS
• Ulcerations are more often seen in cecum, followed by the sigmoid
colon, descending colon and rectum

07/18/2025 41
• Developing ulcers which have irregular, hyperemic mucosal outlines
with markedly undermined, overhanging edges, producing a
characteristic flask like shape
• Intervening mucosa is normal
• Ulcers may vary in size from few mm to several centimeters
• Amebomas present as localized, often circumferential areas of bowel
wall thickening, strictures, mucosal excrescences or large tumour like
masses

07/18/2025 42
• They result from persistent ulceration and granulation tissue
formation with fibroblastic proliferation and inflammation and may be
up to 15cms in diameter
• MICROSCOPIC FINDINGS
• Specific diagnostic finding is identification of the organism in either
the trophozoites or cyst formation
• Trophozoites are large round to ovoid structures, varying from 6um to
40um

07/18/2025 43
• They contain voluminous pinkish purple cytoplasm with distinctive
foamy, vacuolated or granular appearance
• Cytoplasm is PAS positive
• Amoebae contain ingested RBCs which can be demonstrated by
Heidenhain iron hematoxylin stain
• In tissue sections, amoebae may be surrounded by clear space, a
fixation induced shrinkage artefact

07/18/2025 44
• Amoebic ulcers are flask shaped with necrotic debris and fibrin
covering base of the ulcers
• Amoebae lie in the lamina propria surrounded by inflammatory
response. Some times organisms are found in tissue space and in
small vessels. In severe cases they are found in abdominal cavity and
serosal fat

07/18/2025 45
• Patient with long standing infections and exuberant tissue reactions
develop tumorous exophytic cicatrical, inflammatory masses known
as amoebomas. Histologically amoebomas consists of granulation
tissue with round cell infiltration and giant cells
• INVESTIGATION
• Stool examination
• Special stains used to identify trophozoites are; PAS, H&E, Trichrome,
Phosphotungstic acid hematoxylin
• Other tests; serological tests, DNA hybridization

07/18/2025 46
• TREATMENT AND PROGNOSIS
• Trophozoites may migrate to liver, producing amebic liver abscess
• They may also invade adjacent structures, including lungs,
peritoneum and pericardium
• Metronidazole along with diiodohydroxyquinoline or paramomycin

07/18/2025 47
07/18/2025 48
07/18/2025 49
TYPHOID
OUTLINE
 INTRODUCTION
 EPIDEMIOLOGY
 AETIOLOGY
 PATHOGENESIS
 CLINICAL FEATURES
 ORGAN CHANGES
TYPHOID
INTRODUCTION

 HUMAN INFECTIONS WITH

SALMONELLA ENTERICA RESULTS IN
TWO GROUPS OF DISEASES:

 1. GASTROENTERITIS

 2. TYPHOID FEVER
TYPHOID
EPIDEMIOLOGY
 INFECTS 21.6 MILLION PEOPLE EACH
YEAR

 KILLS 500,000 PEOPLE EACH YEAR

 65% IN ASIA AND 35% IN AFRICA

 TRANSMITTED THROUGH INGESTION OF

FOOD OR DRINK CONTAMINATED BY THE
URINE OR FEACES OF INFECTED
PERSONS
TYPHOID

EPIDEMIOLOGY

 INFECTION RESERVOIRS ARE USUALLY PATIENTS

WITH ACTIVE DISEASE AND APPARENTLY HEALTHY
CARRIERS
TYPHOID
TYPHOID
EPIDEMIOLOGY
 THE MOST NOTORIOUS CARRIER OF
TYPHOID FEVER

 “TYPHOID” MARY MALLON A FOOD

HANDLER, INFECTED 47 PEOPLE AND
KILLING 3

 WORKED AS COOK IN NEWYORK CITY

IN THE EARLY 1907
TYPHOID
EPIDEMIOLOGY
 TRACED TO TWO TYPHOID OUT BREAKS
BY DR SARA JOSEPHINE BAKER

 SHE WAS TOLD TO STOP COOKING OR

HAVE HER GALL BLADDER REMOVED

 SHE REFUSED AND KEPT COOKING

UNDER A FALSE NAME

 PUT IN PRISON TWO TIMES WHERE SHE

DIED
TYPHOID

AETIOLOGY

 SALMONELLA ENTERICA IS A GRAM-NEGATIVE

ENTEROBACTERICIAE WHICH CAUSES INTESTINAL
INFECTION
TYPHOID
AETIOLOGY

 TYPHOID FEVER IS CAUSED BY

TYPHOIDAL SALMONELLA SEROVARS

S. enterica var typhi,

S. enterica var paratyphi A, B
AND C
TYPHOID
CLINICAL FEATURES OF
TYPHOID FEVER
EARLY FEATURES
 FEVER (STEP LADDER PATTERN)
 ANOREXIA
 EPISTAXIS
 MALAISE
 GENERAL ACHES AND PAIN
 HEADACHE
 VAGUE ABDOMINAL PAIN
 ROSE SPOTS
 NEUROPSYCHIATRIC SYMPTOMS
TYPHOID
CLINICAL FEATURES OF TYPHOID
FEVER
LATE FEATURES OCCUR IN UNTREATED
PATIENTS DURING THE 3RD AND 4TH WEEKS
 GASTROINTESTINAL
BLEEDING/PERFORATION
 HEPATITIS, HEPATIC AND SPLENIC ABSCESS
 PANCREATITIS
 NEPHRITIS
 CARDITIS
 MENINGITIS
 PNEUMONIA
 OSTEOMYLITIS
TYPHOID
TYPHOID
PATHOGENESIS OF TYPHOID
FEVER

 1. SALMONELLA TYPHI (TYPHOID FVER)

 2. PARATYPHI A,B AND C (PARATYPHOID

FEVER)

 PENETRATE ILEAL MUCOSA AND REACH

MESENTERIC LYMPH NODES VIA LYMPHATICS

 INCUBATION PERIOD VARIES BETWEEN 3 –

50 DAYS
TYPHOID
PATHOGENESIS OF TYPHOID
FEVER
 EVADE RECOGNITION BY THE PATHOGEN
RECOGNITION RECEPTOR (PRR)

 INVADE THE BLOOD STREAM THROUGH THE

LYMPHATIC DUCT

 INVOVLVEMENT OF PEYER’S PATCHES LEADS

TO INFLAMATORY REACTION, INFILTRATION
WITH MONONUCLEAR CELLS AND NECROSIS

 LEADING TO ULCERS AND PERFOFATIONS

TYPHOID
PATHOGENESIS OF TYPHOID FEVER

 INFECT THE LIVER, SPLEEN,

GALLBLADDER, KIDNEY AND BONE
MARROW

 AFTER MULTIPLICATION THEY PASS INTO

THE BLOOD CAUSING SECONDARY AND
HEAVIER BACTEREMIA

 FROM THE GALL BLADDER FURTHER

INVASION OF THE INTESTINE OCCURS
TYPHOID
ORGAN CHANGES
 SKIN- ROSE SPOTS: THROMBOSED
BLOOD VESSELS AND COLLECTION OF
BACILLI
 GALL BLADDER: CHOLECYSTITIS AND
FORMATION OF INFECTED GALL
STONES
 SPLEEN: SOFT AND ENLARGED
 KIDNEY: NEPHRITIS
 LIVER: ENLARGED WITH TYPHOID
NODULES AND STEATOSIS
TYPHOID
ORGAN CHANGES

 GASTROINTESTINAL TRACT
HYPERPLASIA OF PEYERS
PATCHES,INFLAMMATION, NECROSIS
AND PERFORATION.
TYPHOID
TYPHOID
TYPHOID
DIAGNOSTIC METHODS
 BLOOD CULTURE/ BACTEK METHOD
 STOOL CULTURE
 URINE CULTURE
 BILE ASPIRATE CULTURE
 BONE MARROW CULTURE
 CO-AGGLUTINATION METHOD
 PCR
 WIDAL TEST (O > 1 IN 160, H > 1 IN
360 INSINGLE SAMPLE TESTS)
TYPHOID
TREATMENT
 99% OF PEOPLE WITH TYPHOID FEVER ARE
CURED WITH PROMPT ANTIBIOTIC
THERAPY
 CONVALESCENCE MAY LASTS SEVERAL
MONTHS
 ANTIBIOTICS
1.CHLORAMPHENICOL
2.TRIMETHOPRIM-SULPHAMETHOXAZOLE
3.FLOUROQUINOLONES(CIPROFLOXACIN/LE
VOFLOXACIN)
4.CEPHALOSPORIN( CEFTRIAZONE)
 SURGERY FOR COMPLECATED CASES
 SCHISTOSOMIASIS

 INTRODUCTION
 Schistosomiasis infects approximately 230
million persons
and kills more than 200,000 individuals
annually
 The affected organs and hence the site of
major disease vary with the species
 Shistosoma mansoni and S. japonicum affect
the liver and the gut predominantly
 Most deaths are due to hepatic cirrhosis, which
is caused by S. mansoni in Latin America,
Africa, and the Middle East and by S. japonicum
and S. mekongi in East Asia
 By contrast, S. haematobium, found in Africa,
causes chronic granulomatous bladder
inflammation that may lead to hematuria,
obstructive uropathy, and carcinoma
 Schistosoma flukes, like all trematodes, require
passage through freshwater snails that live in the
slow-moving water of tropical rivers, lakes, and
irrigation ditches, ironically linking agricultural
development with spread of the disease
 Acute schistosomiasis in humans can be a
severe febrile illness that peaks about 2
months after infection. Severe hepatic fibrosis
is a serious manifestation of chronic
schistosomiasis
 PATHOGENESIS

 Much of the pathology of schistosomiasis

is caused by host inflammatory reactions
to different stages of the parasite
 The life cycle of Schistosoma involves stepwise
infection of several human tissues, each
associated with host inflammatory responses
 After release from snails, ciliated miracidium
larvae mature into infectious schistosome
larvae (cercariae) that swim through fresh
water and penetrate human skin with the aid of
powerful proteolytic enzymes that degrade the
keratinized layer
 There is minimal skin reaction
 Schistosomes migrate through the skin into the
peripheral vasculature and lymphatics, travel
to the lungs and heart, from where they are
disseminated widely, including the mesenteric,
splanchnic and portal circulation, ultimately
reaching the hepatic vessels where they
mature (S. mansoni and S. japonicum
 Mature male-female worm pairs then migrate
once again and settle in the venous system
(commonly the portal or pelvic veins)
 Females produce hundreds to thousands of
eggs per day which secrete proteases and elicit
localized inflammatory reactions
 This inflammatory response to egg migration is
necessary for passive transfer across the
intestine and, in the case of S. haemtobium,
bladder walls, allowing the eggs to be shed in
stool or urine, respectively
 Infection of freshwater snails completes the life
cycle
 Eggs that are carried by the portal circulation
into the hepatic parenchyma can cause severe
chronic inflammation in the liver
 This immune response to S. mansoni and S.
japonicum eggs is responsible for the most
serious complication of schistosomiasis , liver
fibrosis
 The helper T-cell response in the early stage is
dominated by T 1 cells that produce IFN-γ,
H

which stimulates macrophages to secrete high

levels of the cytokines TNF, IL-1, and IL-6 that
cause Fever
 Chronic schistosomiasis is associated with a
dominant T 2 response, associated with the
H

presence of alternatively activated

macrophages
 Both types of helper T cells contribute to the
formation of granulomas surrounding eggs in
the liver
 Hepatic fibrosis is a serious manifestation of
chronic schistosomiasis in which T 2 cells and
H

alternatively activated macrophages may play

the major role
 MORPHOLOGY

 In early S. mansoni or S. japonicum

infections, white, pinhead-sized granulomas
are scattered throughout the gut and liver
 At the center of the granuloma is the
schistosome egg, which contains a miracidium;
this degenerates over time and calcifies
 The granulomas are composed of
macrophages, lymphocytes, neutrophils, and
eosinophils, which are distinctive for helminth
infections
 The liver is darkened by regurgitated heme-
derived pigments from the schistosome gut,
which, like malaria pigments, are iron-free and
accumulate in Kupffer cells and splenic
macrophages
 In late S. mansoni or S. japonicum
infections, inflammatory patches or
pseudopolyps may form in the colon
 The surface of the liver is bumpy, and cut
surfaces reveal granulomas and widespread
fibrosis and portal enlargement without
intervening regenerative nodules
 Because these fibrous triads resemble the stem
of a clay pipe, the lesion is named pipestem
Fibrosis
 The fibrosis often obliterates the portal veins,
leading to portal hypertension, severe
congestive splenomegaly, esophageal varices,
and ascites
 Schistosome eggs, diverted to the lung through
portal collaterals, may produce granulomatous
pulmonary arteritis with intimal hyperplasia,
progressive arterial obstruction, and ultimately
heart failure (cor pulmonale)
 On histologic examination, arteries in the lungs
show disruption of the elastic layer by
granulomas and scars, luminal organizing
thrombi, and angiomatoid lesions similar to
those of idiopathic pulmonary hypertension
 Patients with hepatosplenic schistosomiasis
also have an increased frequency of
mesangioproliferative or membranous
glomerulopathy
 The glomeruli contain deposits of
immunoglobulin and complement but rarely
schistosome Antigen
 In S. haematobium infection, inflammatory
cystitis due to massive egg deposition and
granulomas appears early, leading to mucosal
erosions and hematuria
 Later, the granulomas calcify and develop a
sandy appearance, which, if severe, may line the
wall of the bladder and cause a dense concentric
rim (calcified bladder) on radiographic films
 The most frequent complication of S.
haematobium infection is inflammation and
fibrosis of the ureteral walls, leading to
obstruction, hydronephrosis, and chronic
pyelonephritis
 There is also an association between urinary
schistosomiasis and squamous cell carcinoma
of the bladder
 ONCHOCERCIASIS

 INTRODUCTION
 Onchocerca volvulus is a filarial nematode that is
the leading cause of preventable blindness
in sub-Saharan Africa
 It is transmitted by black flies and affects 18
million people in Africa, South America, and Yemen
 An aggressive campaign of ivermectin treatment
has dramatically reduced the incidence of
Onchocerca infection in West Africa
 Since vector’s preferred habitat is near fast
moving water there is higher incidence of
human disease near rivers, accounting for the
name river blindness given to this disease
 It is estimated that there are 270,000 people
who are blind due to onchocerciasis
 PATHOGENESIS

 The disease attributable to onchocerciasis is

primarily due to inflammation induced by
microfilaria
 Adult O. volvulus parasites mate in the dermis,
where they are surrounded by a mixed infiltrate
of host cells that produces a characteristic
subcutaneous nodule (onchocercoma)
 Inseminated females produce microfilariae, which
accumulate in the skin and disseminate to the eye
chambers
 Ivermectin kills only immature worms, not adult
worms, so parasites repopulate the host a few
months after treatment
 Doxycycline treatment blocks reproduction of O.
volvus for up to 24 months by killing Wolbachia, a
symbiotic bacteria that are required for the fertility
of the filarial species
 MORPHOLOGY

 Onchocerca volvulus causes chronic, itchy dermatitis with

focal darkening or loss of pigment and scaling, referred to
as leopard, lizard, or elephant skin
 Foci of epidermal atrophy and elastic fiber breakdown
may alternate with areas of hyperkeratosis,
hyperpigmentation with pigment incontinence, dermal
atrophy, and fibrosis
 The subcutaneous onchocercoma is composed of a
fibrous capsule surrounding adult worms and a mixed
chronic inflammatory infiltrate that includes fibrin,
neutrophils, eosinophils, lymphocytes, and giant cells
 The progressive eye lesions begin with
punctate keratitis along with small, fluffy
opacities of the cornea caused by degenerating
microfilariae, which evoke an eosinophilic
infiltrate
 This is followed by a sclerosing keratitis that
opacifies the cornea, beginning at the scleral
limbus
 Keratitis is sometimes accentuated by
treatment with antifilarial drugs (Mazzotti
reaction)
 Microfilariae in the anterior chamber cause
iridocyclitis and glaucoma, whereas
involvement of the choroid and retina results in
atrophy and loss of vision