Gatot Sugiharto, MD, Internist
Internal Medicine Department
Faculty of Medicine, Wijaya Kusuma
University Surabaya
GSH - Tropmed - 2010
1
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
• Orasure
– The only FDA approved HIV antibody  as accurate as
blood testing
– Draws blood-derived fluids from the gum tissue.
– NOT A SALIVA TEST!
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
negative…but 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 can’t 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 URI’s, 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
(1)
Healthcare Workers
• 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 (PEP) if
high risk of transmission:
– 4 week course of zidovudine (ZDV)
Source: CDC 1996.
– preferable to start within 1-2 hours
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 is no vaccine to prevent HIV
infection nor is there a cure 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
polyurethane condoms
• Do not share needles
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 drugs
• Availability, Coverage, Impact
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
• AZT
• d4T
NRTI
• 3TC
• ddI
research or brand name
Zidovudine, retrovir
Zerit, stavudine
Epivir, lamivudine
Videx, didanosine
• Efavirenz
• Nevirapine
Sustiva, Stocrin, Efavir
Viramune, Neviral
•
•
•
•
NNRTI
Tenofavir
Indinavir
Nelfinavir
Lopinavir / ritonovir
PI
Viread
Crixivan
Viracept
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 doesn’t kill  OI’s kill
• Most OIs are treatable/curable
• Some are preventable
• Early treatment for OIs prolongs life!
CD4 count and OIs
TB
PCP, thrush
Toxo, Esoph
thrush
Below 200
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
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
Plasmodium
Diseases
malaria
Soil transmitted helminths:
•
Roundworm (Ascaris)
Pnemonitis, intestinal obstruction
•
•
•
Whipworm (Trichuris)
Bloody diarrhoea, rectal prolapse
Hookworm (Ancylostoma
and Necator)
Coughing, wheezing, abdominal pain
and anaemia
No. people infected
Deaths/yr
273 million
1.12 million
2 billion
200,000
Schistosoma
Renal tract and intestinal disease
200 million
15,000
Filariae
Lymphatic filariasis and elephantiasis
120 million
Not fatal but 40
million
disfigured or
incapacitated
Trypanasoma cruzi
Chagas disease (cardiovascular)
13 million
14,000
African trypanosomes
African sleeping sickness
0.3 – 0.5 million
48,000
Leishamania
Cutaneous, mucocutaneous and
visceral leishmaniasis
12 million; 2 million new
cases/yr
50,000
Taxonomic classification of helminths
Sub
kingdom
Metazoa
Phylum
Class
Genus – examples
Ascaris (roundworm)
Trichuris (whipworm)
Ancylostoma (hookworm)
Necator (hookworm)
Enterobius (pinworm or
threadworm)
Strongyloides
Nematodes
Round worms; appear round in
cross section, they have body
cavities, a straight alimentary
canal and an anus
Platyhelminthes
Cestodes
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
Non-segmented, usually leafshaped, with two suckers but no
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
Taenia (tapeworm)
Fasciolopsis (liver fluke)
Schistosoma (not leaf
shaped!)
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 Brugia malayi and Brugia
timori
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 and
lymph glands
• Larvae develop into sexually mature adult worms
over 3-12 months depending on the species of
filarial worm
Microfilaria of B. malayi in thick blood film
(H&E stain; source: CDC)
Adult worms of B. malayi in section
in a lymph node (source: Univ South
Carolina)
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 swelling of the limbs
• Trauma and secondary bacterial
infection of affected tissues is
common
Elephantiasis of the leg (source:
WHO/TDR/Crump)
Symptoms - signs – 3 stages
Elderly male with massive
hydrocoele, and elephantiasis of
the leg. Also has nodules in the
groin due to onchocerciasis
(source: WHO/TDR/Crump)
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 tissue
resulting in severe deformities
• The legs are often affected and result in
inability to walk
• The scrotum is often affected in men and
the breasts and vulva in women
Diagnosis
• Microscopic examination of Giemsa stained thick blood films
for the presence of microfilariae
• W. bancrofti shows marked nocturnal periodicity, so it’s 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 allergictype reactions – add an antihistamine and aspirin to
treatment regimen
• Other treatment options are
– ivermectin
– combination of DEC and albendazole
Amebiasis
Entamoeba 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
Symptoms > 1 wk
Diarrhea
Dysentery
Abdominal pain
Weight loss
Fever >38oC
Heme (+) stool
Immigrant from or traveler
to endemic area
Prevalence (male/female)
% of Patients Affected
Most patients
94-100
94-100
12-80
44
10
100
>50
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 (212 weeks of symptoms) commonly
present with hepatomegaly and weight
loss
Amebic Liver Abscess
Sign or Symptom
Symptoms > 4 wks
Fever
Abdominal tenderness
Hepatomegaly
Jaundice
Diarrhea
Weight loss
Cough
Immigrant from or traveler
to endemic area
Prevalence (male/female)
90/10 in adults
% of Patients Affected
21-51
85-90
84-90
30-50
6-10
20-33
33-50
10-30
>50
50/50 in children;
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 cy
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 americanus
Ancylostoma 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 host’s
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 µm, 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 - (510 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