Tropical Infection

Diseases
Gatot Sugiharto, MD, Internist
Internal Medicine Department
Faculty of Medicine, Wijaya Kusuma
University Surabaya

GSH - Tropmed - 2010 1

HIV / AIDS (cont)

Gatot Sugiharto, MD, Internist

Internal Medicine Department
Faculty of Medicine, Wijaya Kusuma
University Surabaya

GSH - Tropmed - 2010 2

 HIV Testing
Blood Detection Tests
Enzyme-Linked Immunosorbent
Assay/Enzyme Immunoassay (ELISA/EIA)
Radio Immunoprecipitation Assay/Indirect
Fluorescent Antibody Assay (RIP/IFA)
Polymerase Chain Reaction (PCR)
Western Blot Confirmatory test
Urine Western Blot
As sensitive as testing blood & safe way to
screen for HIV
Can cause false positives in certain people at
high risk for HIV
 Other tests for HIV-infection
PCR = polymerase chain reaction. Tests for
actual virus in the body.
PCR will be positive during the window period
Viral Load = measures how much virus is in the
body. Allows you to monitor stage of infection.
Very expensive test.
CD4 Count = how many CD4 cells in body
 What is the window period?
It takes about 3 months after infection, for the
antibody test to be positive
During the window period, a person will test
negativebut is really positive
They can pass the virus during the window
period !
Important to be clear on this and explain to
persons undergoing VCT
 Monitoring HIV-infection
Most clinics/hospitals in SA cant afford CD4 & VL
W.H.O. developed a staging system

STAGE 1: Early. Asymptomatic. Normal activity.

STAGE 2: Years later. Symptomatic. Lose weight, skin
problems, recurrent URIs, Herpes Zoster, etc.
STAGE 3: Frequent symptoms. Some activities, time in
bed. More weight loss, diarrhea, fever, thrush, vaginal
candida, TB, recurrent pneumonia
STAGE 4: Very ill. Bedridden for >half the day. Many
opportunistic infections. AIDS.
 Post Exposure Prophylaxis
(PEP) for Healthcare Workers(1)
Intact skin, mouth or nose:
immediately wash with soap and
water and rinse thoroughly to remove
all potentially infectious particles.
Cut or punctured skin: allow to bleed
fully.
Eye: flush immediately with water,
then irrigate with normal saline for 30
minutes.
Consider post exposure prophylaxis
Source: CDC 1996.

(PEP) if high risk of transmission: 22-7

 Post Exposure Treatment of
Healthcare Workers(2)

HIV testing immediately, 6 weeks, 6

months and 12 months
Treatment, if started, should continue
for 4 weeks. Any or all drugs may be
declined by exposed worker.
For lesser exposures, prophylaxis is
not recommended.

22-8
 HIV Prevention
Currently, there isno vaccine to
prevent HIV infection nor is there
acure for HIV/AIDS. To reduce risk of
becoming infected with HIV or
transmitting the virus to others:
Get tested regularly for HIV
Practice abstinence
Remain faithful to your spouse or
partner
Consistently use male latex or female
 Treatment
Antiretroviral drugs (ARVs)
Are not a cure
Slow down the process of replication
of HIV in the human body
Prevent and treat Opportunistic
Infections
Prevent mother-to-child-
transmission
During pregnancy and delivery
Safer infant feeding
Access to services / availability of
 Antiretroviral Drugs
Class:
Nucleoside Reverse Transcriptase inhibitors (NRTI)
Non-Nucleoside Transcriptase inhibitors (NNRTI)
Protease inhibitors (PI)
Do not cure people of HIV or AIDS rather,
they suppress the virus, even to undetectable
levels, but they do not completely eliminate
HIV from the body lead longer and
healthier lives can still transmit the virus
 Sinonym

THE COCKTAIL
COMBINATION THERAPY
ARVS (ANTI-RETROVIRALS)
ANTI-HIV THERAPY
HIV ANTI-RETROVIRAL DRUGS
HAART (HIGHLY ACTIVE ANTI RETROVIRAL
TX)
 ARVs
Common name research or brand name
AZT Zidovudine, retrovir
d4T Zerit, stavudine
3TC NRTI
Epivir, lamivudine
ddI Videx, didanosine

Efavirenz Sustiva, Stocrin, Efavir

NNRTI
Nevirapine Viramune, Neviral

Tenofavir Viread
Indinavir Crixivan
Nelfinavir PI
Viracept
Lopinavir / ritonovir Kaletra
 Opportunistic infection?
Also called OI
An infection or illness that takes the
OPPORTUNITY to cause an illness in a
person who is immunocompromised
Opportunistic infections are more common
in persons who have a lower CD4 count
HIV doesnt kill OIs kill
Most OIs are treatable/curable
Some are preventable
Early treatment for OIs prolongs life!
CD4 count and OIs

TB

PCP, thrush
Toxo,
Esoph
Below 200 thrush
PML
 Opportunistic Infections
associated with AIDS
Bacterial, parasitic, and other infections
Serious and recurrent bacterial infections, syphilis,
toxoplasmosis, crypto/microsporidiosis
Mycobacterial infections
MTB, MAC
Fungal infections
Pneumocystis jiroveci pneumonia, Candida,
cryptococcosis, histoplasmosis, coccidioidomycosis
Viral infections
CMV, HSV, HZV, HPV, HCV, HBV
16
 Management of TB in HIV pos
persons
If pts started ARV and TB therapy
together there was an increased risk
of progression to Aids
CD4 <200 where main problems
were seen and it was much better to
delay antiretroviral therapy start Tx
TB first
CD4 > 200 there was no difference
when it was started
Parasite
infestation
Gatot Sugiharto, MD, Internist
Internal Medicine Department
Faculty of Medicine, Wijaya Kusuma
University Surabaya

GSH - Tropmed - 2010 18

 The burden of some major parasitic
infections
Parasite Diseases No. people infected Deaths/yr
Plasmodium malaria 273 million 1.12 million
Soil transmitted 2 billion 200,000
helminths:
Pnemonitis, intestinal
Roundworm obstruction
(Ascaris)
Bloody diarrhoea, rectal
Whipworm prolapse
(Trichuris)
Coughing, wheezing,
Hookworm abdominal pain and
(Ancylostoma and anaemia
Necator)
Schistosoma Renal tract and intestinal 200 million 15,000
disease

Filariae Lymphatic filariasis and 120 million Not fatal but 40

elephantiasis million
disfigured
or
incapacitate
d
Trypanasoma cruzi Chagas disease 13 million 14,000
(cardiovascular)
African trypanosomes African sleeping sickness 0.3 0.5 million 48,000
Leishamania Cutaneous, mucocutaneous 12 million; 2 million 50,000
and visceral leishmaniasis new cases/yr
 Taxonomic classification of
Sub
helminths
Phylum Class Genus examples
kingdom
Metazoa Nematodes Ascaris (roundworm)
Round worms; appear round in Trichuris (whipworm)
cross section, they have body Ancylostoma (hookworm)
cavities, a straight alimentary Necator (hookworm)
canal and an anus Enterobius (pinworm or
threadworm)
Strongyloides

Platyhelminthes Cestodes Taenia (tapeworm)

Flat worms; dorsoventrally
flattened, no body cavity and, if
present, the alimentary canal is
blind ending
Adult tapeworms are found in the
intestine of their host
They have a head (scolex) with
sucking organs, a segmented body
but no alimentary canal
Each body segment is
hermaphrodite

Trematodes Fasciolopsis (liver fluke)

Non-segmented, usually leaf- Schistosoma (not leaf
shaped, with two suckers but no shaped!)
distinct head
They have an alimentary canal and
are usually hermaphrodite and leaf
shaped
Schistosomes are the exception.
They are thread-like, and have
separate sexes
 Filariasis
Epidemiology
120m people infected in >80
countries in Africa, Asia, the Pacific
islands and South and Central
America
40m of those infected are disfigured
or severely incapacitated
95% cases due to Wuchereria
bancrofti, other species include
 Life cycle
Wuchereria bancrofti is mainly
transmitted by
Culex mosquitoes in India
Anopheline mosquitoes in Africa
B. malayi and B. timori are transmitted
mainly by Mansonia mosquitoes
Larval forms of the parasite (microfilariae)
are taken up by a female mosquito when
it takes a blood meal from a human
infected with adult worms
The microfilariae develop inside the
mosquito
When the mosquito takes another blood
meal the infective filariform larvae enter
the bite wound
Filariform larvae migrate to the lymphatics
 Adult worms of B. malayi in
section in a lymph node
Microfilaria of B. malayi in thick (source: Univ South Carolina)
blood film (H&E stain; source: CDC)
Pathology
Adult worms live in the
afferent lymphatic vessels
and cause severe disruption
to the lymphatic system
Scrotal damage and
massive swelling may occur
when adult Wuchereria
bancrofti lodge in the
lymphatics of the spermatic
cord
Late stage disease is
typified by elephantiasis
painful and disfiguring Elephantiasis of the leg
(source: WHO/TDR/Crump)

swelling of the limbs

 Symptoms - signs 3 stages
1. Asymptomatic stage
There is internal damage to the
lymphatics and kidneys
2. Acute stage Filarial lymphangitis
Characterised by bouts of fever
heat, redness, pain, swelling and
tenderness of the lymph nodes
and ducts
3. Chronic stage
Usually results in elephantiasis as
a result of chronic lymphoedema
There is a massive overgrowth of
Elderly male with massive
tissue resulting in severe
hydrocoele, and deformities
elephantiasis of the leg. The legs are often affected and
Also has nodules in the
groin due to result in inability to walk
Diagnosis
Microscopic examination of Giemsa stained thick
blood films for the presence of microfilariae
W. bancrofti shows marked nocturnal periodicity,
so its best to collect blood samples between
10pm and 1 am
Serology test
Treatment
Diethylcarbamazine (DEC) rapidly kills
microfilariae and will kill adult worms if given in
full dosage over 3 weeks
Release of antigens from dying microfilaria
causes allergic-type reactions add an
antihistamine and aspirin to treatment regimen
Other treatment options are
Entamoeba
Amebiasis
histolytica
Pseudopod-forming, non-flagellated protzoa

Most invasive parasite of the Entamoeba group

Only member that causes: Amebic colitis & liver abscess

Life Cycle consists of:

(1) Infectious cyst & (2) Invasive trophzoite

Trophozoites adhere to colonic mucin and epithelial
cells kill host epithelial & immune cells tissue
destruction
 Life cycle
Cysts are passed in feces(1).Infection by Entamoeba histolytica occurs by
ingestion of mature cysts in fecally contaminated food, water, or hands (2).
Excystation occurs in the small intestine(3) trophozoites released
migrate to the large intestine (4).Trophozoites multiply by binary fission and
produce cysts (5) passed in the feces.
Cysts (protected by their cell walls) can survive days to weeks in the external
environment and are responsible for transmission.
In many cases, trophozoites remain confined to the intestinal lumen
(noninvasive infection) of individuals who are asymptomatic carriers, passing
cysts in their stool.
In some patients trophozoites invade the intestinal mucosa (intestinal disease),
or, through the bloodstream, extraintestinal sites such as the liver, brain, and
lungs (extraintestinal disease), with resultant pathologic manifestations.
Invasive and noninvasive forms represent two separate species ( E. histolytica &
E. dispar respectively), however not all persons infected with E. histolytica will
have invasive disease. These two species are morphologically indistinguishable.
Transmission can also occur through fecal exposure during sexual contact
(cysts, & also trophozoites could prove infective).
Trophozoites of Entamoeba histolytica (Trichrome stain).
Two diagnostic characteristics: Two of the trophozoites have ingested
erythrocytes, and the nuclei have typically a small, centrally located
karyosome
 Clinical Manifestations
Amebic colitis
Sign or Symptom % of Patients Affected
Symptoms > 1 wk Most patients
Diarrhea 94-100
Dysentery 94-100
Abdominal pain 12-80
Weight loss 44
Fever >38oC 10
Heme (+) stool 100
Immigrant from or traveler
to endemic area >50
Prevalence (male/female) 50/50
 Clinical Manifestations

Patients with chronic, non-dysenteric

intestinal amebiasis may complain for
months to years of abdominal pain,
flatulence, intermittent diarrhea,mucus
in the stools, and weight loss
Chronic non-dysenteric intestinal
amebiasis has been mistakinly diagnosed
as ulcerative colitis
 Acute Fulminant or Necrotizing
Colitis
Unusual (about 0.5% of cases)
A complication that occurs more frequently in
patients inappropriately treated with
corticosteroid
Abdominal pain, distension, and rebound
tenderness are present in most patients
Indications for surgery:
Failure of response to anti-amebic drugs after
intestinal perforation/abscess formation
Persistence of abdominal distention after institution
of anti-amebic Rx
Toxic megacolon
 Ameboma
Segmented mass of granulation tissue in the
cecum or ascending colon
Occurs in 0.5% to 1.5% of patients with
intestinal amebiasis
Tender palpable abdominal mass
Concuurent amebic dysentery present in 2/3 of
patients
Apple-core lesions on barium enema study
Lesions resolve with anti-amebic chemotherapy
Intestinal constriction occurs in the colon in <1%
of patients
 Amebic Liver Abscess

Develops in about 10% of patients with

invasive E. histolytica infections
Few patients have concurrent dysentery
most report dysentery within the
preceding year
Occurs in any age group
Patients with a more chronic illness (2-
12 weeks of symptoms) commonly
present with hepatomegaly and weight
loss
 Amebic Liver Abscess
Sign or Symptom % of Patients Affected
Symptoms > 4 wks 21-51
Fever 85-90
Abdominal tenderness 84-90
Hepatomegaly 30-50
Jaundice 6-10
Diarrhea 20-33
Weight loss 33-50
Cough 10-30
Immigrant from or traveler
to endemic area >50
Prevalence (male/female) 50/50 in children;
90/10 in adults
Gross pathology of liver containing amebic abscess
 Laboratory Findings and Diagnosis
Differential Diagnosis of Amebic Dysentery :
IBD
Ischemic colitis
Other infectious causes of bloody diarrhea
Diagnostic Tests:
EIA is best for specific diagnosis of amebiasis
(Sensitivity & specificity of assay on stool >95%)
Colonoscopy remains important to evaluate for
other causes
Serology for antibodies: IHA
Positive in: 88% amebic dysentery, 70-80% liver
abscess, 50% of general population
 Laboratory Findings and Diagnosis

Differential Diagnosis of Amebic Liver

Abscess:
Pyogenic abscess
Echinococcal cyst
Hepatoma
Diagnostic Tests:
Ultrasonography
CT
MRI
None differentiate amebic from pyogenic abscess
Diagnosis is frequently a diagnosis of exclusion
Amebic liver abscesses
 Treatment

Asymptometic amebiais:
Luminal agent (paromomycin, diloxanide
furate, or iodohydroxyquin)
Amebic Colitis: Metronidazole & a
luminal agent
Amebic Liver Absces : Metronidazole &
a luminal agent
 Prevention

Prevention of E. hisolytca transmission requires

disruption of the fecal-oral spraed of amebic cysts

Individuals should be advised regarding:

Risk of traveling to endemic areas
Safeguards to prevent ingesting colonic
organisms

Because humans and primates are the only known

reservoirs of E. histolytica, a successful vaccine
Could potentially eliminate this disease
 Intestinal Nematodes : Round
Worms
The most common parasitic infections in humans;
affect one quarter of the world population
Remain a major cause of physical growth delay,
cognitive delay, and malnutrition throughout the
world
In certain endemic populations, children are
disproportionately affected
Being increasingly encountered in the developed
world. In the USA, groups at increased risk
include: international travelers, recent
immigrants, refugees, and international adoptees
 Ascaris lumbricoides

The most common helminthic infection in humans

51 million children are currently estimated to be
infected
Commonly affects children living in economically
disadvantaged communities
Ascariasis still occurs frequently in the USA as an
imported infection in recent immigrants from Latin
America and Asia & internationally adopted children
Young children seem to be affected more severely
than adults (larger worm burden, parasite-induced
malnutrition)
 Life
cycl
 Life cycle
Adult worms live in the lumen of the small intestine (1). A female
may produce approximately 200,000 eggs per day, which are passed
with the feces (2) .
Unfertilized eggs may be ingested but are not infective. Fertile
eggs embryonate and become infective after 18 days to several
weeks(3) , depending on the environmental conditions (optimum:
moist, warm, shaded soil).
After infective eggs are swallowed (4) , the larvae hatch (5),
invade the intestinal mucosa, and are carried via the portal, then
systemic circulation to the lungs (6) .
The larvae mature further in the lungs (10 to 14 days), penetrate
the alveolar walls, ascend the bronchial tree to the throat (7), and
are swallowed .
Upon reaching the small intestine, they develop into adult worms
(1) . Between 2 and 3 months are required from ingestion of the
infective eggs to oviposition by the adult female. Adult worms can
live 1 to 2 years.CDC
Life cycle
 Clinical Manifestations

Larvae migration through the lung parenchyma

mechanical and immune-mediated damage:
Pulmonary microhemorrhages
Inflammation & exudation of fluid
Pulmonary infiltrates
Cough, dyspnea, wheeezing, mild hemoptysis (Loffler pneumonia)
Adult ascaris worms in the small bowel
Epigastric pain
Diffuse abdominal discomfort
Heavy infestation intestinal obstruction
Chronic infection malnutrition due partly to
malabsorption (proteins, fat & vitamin A)
 Ascaris
lumbricoides
 Laboratory Findings/Diagnosis

Diagnosis is established by stool examination

for characteristic ova. Each adult female
produces so many eggs that a single stool
specimen is adequate
Migration of larvae through the lungs is
assocaited with peripheral eosinophilia and
pulmonary infiltrates on chest radiograph
In endemic areas, any child presenting with
signs suggestive of intestinal obstruction
should be evaluated for Ascariasis
Ascaris egg
 Treatment

Mebendazole (100 mg twice daily X 3 days) or

Albendazole (400 mg as a single dose)
(The above are not generally given to children < 1 yr)
Pyrantel pamoate (11 mg/kg up to 1 gm/day, X 3 days)
In cases of partial bowel obstruction caused by
Ascaris: alternative therapy with piperazine citrate,
which paralyzes the worms may abrogate the need of
surgical intervention
Hookworms

Approximately 1 billion people harbor

hookworms in their gastrointestinal tract
A leading cause of iron deficiency anemia in
the developing world
Children are particularly vulnerable to the
morbid effects of hookworms infections
(often because dietary intake fails to
compensate for intestinal losses of iron and
serum proteins)
The most common hookworms

Ancylostoma duodenale & Necator americanus

Adult females:10-13 mm (A. duodenale), 9-11 mm (N.

americanus)
Adult males: 8-11 mm (A. duodenale), 7-9 mm (N.
americanus).

A smaller group of hookworms infecting animals can

invade and parasitize humans (A. ceylanicum) or can
penetrate the human skin (causing cutaneous larva
migrans), but do not develop any further (A.
braziliense, Uncinaria stenocephala).
 Life cycle
Eggs are passed in the stool (1), and under favorable conditions
(moisture, warmth, shade), larvae hatch in 1 to 2 days.
The released rhabditiform larvae grow in the feces and/or the
soil (2), and after 5 to 10 days (and two molts) they become
become filariform (third-stage) larvae that are infective (3).
These infective larvae can survive 3-4 weeks in favorable
environmental conditions. On contact with the human host, the
larvae penetrate the skin and are carried through the veins to
the heart and then to the lungs. They penetrate into the
pulmonary alveoli, ascend the bronchial tree to the pharynx, and
are swallowed (4).
The larvae reach the small intestine, where they reside and
mature into adults. Adult worms live in the lumen of the small
intestine, where they attach to the intestinal wall with resultant
blood loss by the host (5). Most adult worms are eliminated in 1
to 2 years, but longevity records can reach several years.
Geographic distribution of Ancylostoma duodenale
Geographic distribution of Necator americanus
 Hookworms
In the bowel, adults attach by their mouth to the
intestinal mucosa and begin to feed
Equipped with teeth, cutting plates or both, powerful
esophageal muscles, and hydrolytic enzymes, the
hookworm digests the plug of tissue within its buccal
capsule
Potent anticoagulants and inhibitors of platelet
function are released and cause profound bleeding
from lacerated capillaries in the lamina propria
Adult worms mate in the small intestine, and the
females deposit fertilized eggs in the lumen
Hookworms
Necator americanusAncylostoma duodenale
 Clinical Manifestations

Skin penetration by third stage larvae an intensely

pruritic dermatitis called ground itch (localized to
site of hookworm entry)
Adult hookworms in intestine:
Nonspecific GI tract symptoms
Blood loss secondary is proportional to worm burden and
develops 10-20 weeks after infection
A. duodenale infection is usually associated with greater loss
than occurs with N. amricanus
Hookworm anemia results when blood loss exceeds the hosts
iron reserve and dietary intake
Occasionally, severe hookworm anemia leads to heart failure
 Laboratory Findings and Ddiagnosiss

Characteristic rash of ground itch occurs on any skin

surface and can be erythematous, papular, or
vesicular
Intense prtutitis can lead to scratching, excoriation,
and secondary bacterial infection
In contrast to Ascaris, pulmonary symptoms are
usually not severe
Intestinal hookworm infection is detected by
identifying the characteistic egg in feces
The eggs of Ancylostoma & Necator amerianus are
similar under light microscope & cannot be easily
distinguished by morphology
 Ancylostoma duodenale & Necator americanus egg

Although the adult form of these intestinal nematodes can be distinguished, the
diagnostic form in humans, the ova, are essentially identicall, oval and measure about
60 X 40 m, typically a clear space between the embryo and the thin shell.
(unstained wet-prep)
 Treatment
Mebendazole (100 mg twice daily X 3 days) or
Albendazole (400 mg as a single dose)
Mebendazole is poorly absorbed and may not eradicate
developmentally arrested Ancylostoma larvae residing in
extraintestinal issues. Therefore periodic follow up stool
examination may be necesessary
Alternate Treatment:
Pyrantel pamoate (11 mg/kg up to 1 gm/day, X 3 days)
Re-infection in endemic areas occur so commonly that
the effect of single course of treatment is of
questionable benefit
Iron supplementaion reverses mild to modertae
hookworm anemis
 Tapeworms : Taenia saginata and Taenia solium

Segmented worms, called tape worms, cause human

illness in either of two stages in their life cycle:

(1) Adult stage: Cause gastrointestinal symptomatology

(2) Larval stage: Causes signs and symptoms referable to
enlarging larval cysts in a variety of tissues

Humans are the only definitive hosts for T. saginata

(the beef tapeworm) and T. solium (the pork tapeworm)
 Life cycle
Eggs or gravid proglottids are passed with feces (1); eggs can survive for days to
months in the environment
Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation
contaminated with eggs or gravid proglottids (2). In the animal's intestine, the
oncospheres hatch(3), invade the intestinal wall, and migrate to the striated
muscles, where they develop into cysticerci. A cysticercus can survive for several
years in the animal
Humans become infected by ingesting raw or undercooked infected meat (4).In the
human intestine, the cysticercus develops over 2 months into an adult tapeworm,
which can survive for years.
The adult tapeworms attach to the small intestine by their scolex(5) and reside in
the small intestine (6).
Length of adult worms is usually <5 m for T. saginata (may reach up to 25 m) and 2 -
7 m for T. solium. The adults produce proglottids which mature, become gravid,
detach from the tapeworm, and migrate to the anus or are passed in the stool (~6
per day
T. saginata adults usually have 1,000 to 2,000 proglottids, while T. solium adults have
an average of 1,000 proglottids. The eggs contained in the gravid proglottids are
released after the proglottids are passed with the feces. T. saginata may produce up
to 100,000 and T. solium may produce 50,000 eggs per proglottid respectively
Taenia saginata - The Beef Tapeworm
Taenia solium - The Pork Tapeworm
 Epidemiology

T. saginata:
Widespread in cattle breeding areas of the world
Prevalence >10% in some independent states of the former
Soviet Union, in Near East, and in central and eastern Africa.
Lower rates : in Europe, Southeast Asia, & South America
T. solium:
Prevalent in Mexico, Central and South America, Africa,
Southeast, Asia,and the Philippines
Infections in USA and Canada are found in immigrants from
areas where taeniasis is endemic, and in travelers who consume
undercooked meats in endemic areas
 Pathology

Cysticercosis occurs in humans after the ingestion of T.

solium eggs
Embryonic metacestode migrates from the intestine
and can lodge in a number of tissue sites such as the
brain, muscle, and eyes with proclivity for the brain
The clinical course largely depends on the endurance of
the parasite inside the tissue and on the ensuing
inflammation
In the brain parenchyma, the intruding cysticercus
might be destroyed within a few days by host immune
mechanisms or remain viable in the brain for > 10 years
 Clinical Manifestations(1)
Affect humans at any age
Most common during the 3rd and 4th decades of life
About 10% occur in children
In infants initial signs of cysticecosis in infants is generalized
seizure
CT with contast or T2-weighted MRI isolated cystic lesion in
the brain parenchyma
Typically the lesion disappears spontaneously 2-3 months later,
but in some granuloma cacification (permanent sequela)
Isolated lesion is most common; some children have two-several
cysts
Cystcercotic encephalitis is a severe form of CNS cystcercosis
that occasionally occurs in children, particularly adolescent girls
 Clinical Manifestations(2)

In adults neurocysticercosis is quite different:

Multiple brain cysticerci, variable immune response, chronic
inflammation, chronic persistence of many active cysts,
vasculitis and protean clinical picture
Epilepsy occurs in 50% of cases; intracranial hypertension in 30%
Occular Cysticercosis: Subretinal area or
vitreous chamber
Muscular cystcercosis: Rare in both children and
adults; usually beign course
 Laboratory Findings/Diagnosis

CT and MRI are the most relaible tools for the

diagnosis of neurcysticercosis

Serologic tests are unreliable (cross reactivity with

antigens of other parasites)

Serology is highly specific for CNS inection when

tests are performed on CSF
 Treatment

Intestinal T. Solium infection : Praziquantel - (5-

10 mg/kg once)
Neurocysticercosis:
Albendazole - 15 mg/kg/day (maximum, 800 mg/day)
divided into two doses X 8 days
Two months later, if repeat imaging studies show
cysts :
Praziquantel in a total dose of 75mg/kg divided in three
doses for 15 days
Repeat imaging studies in two months
 Home work
Trypanosomiasis Africal sleeping
sickness tse tse fly
Leishmaniasis
Enterobius vermicularis
Trichuriasis
Strongyloidiasis
Shistosomiasis