Parasitic Infestations

By
Tonagaya, Sarah

Schistosomiasis
Schistosoma japonicum is an important
parasite and one of the major infectious agents
of schistosomiasis
Geog. Distribution:
Confined to Far East (Japan, China, Formosa,
Thailand and Philippines)

Schistosomiasis
Disease: Schistosomiasis/ Belharziasis/ Snail Fever
present in many countries and affect some 200 million
people with whom 120 million are symptomatic and
80 million suffer from severe disease
infection is transmitted in association with
implementation of water source project in most developi
ng countries can be acquired during activities like: bathi
ng, swimming,planting rice, fishing and doing laundry
involves contact with water infected with intermediate
snail host of the parasite free swimming cercaria attach
es to a vertebrate host and penetrate intact skin

Schistosomiasis
Schistosome Cercarial Dermatitis
Cercarial dermatitis, also called Swimmer's itch, is a
skin rash caused by an allergic reaction to infection
with certain parasites of birds and mammals.
These microscopic parasites are released from
infected snails who swim in fresh and salt water, suc
h as lakes, ponds, and oceans used for swimming an
d wading.
Infection is found throughout the world.
Swimmer's itch generally occurs during summer
months.

Schistosomiasis
signs and symptoms of swimmer's
itch:
Within minutes to days after
swimming in contaminated water, yo
u may experience tingling, burning,
or itching of the skin. Small reddish
pimples
appear within 12 hours. Pimples ma
y develop into small blisters. Itching

Schistosomiasis
If you have a rash, you may try the following for relief:
corticosteroid cream

cool compresses
bath with baking soda
baking soda paste to the rash
anti-itch lotion
Calamine* lotion
colloidal oatmeal baths, such as Aveeno

Try not to scratch. Scratching may cause the rash to become

infected. If itching is severe, your health care provider may p
rescribe lotion or creams to lessen your symptoms

Schistosomiasis

Swimmer's itch

Schistosomiasis

Papular dermatitis

Schistosomiasis
Visceral Schistosomiasis (Bilharziasis)
The cutaneous manifestation bilhaniasis may begin
with mild itching and a papular dermatitis of the
feet and other parts after swimming in polluted stre
ams containing Cercanae
After an asymptomatic incubation period, there may
be a sudden illness with fever and
chills,pneumonitis, and eosinophilia. Petechial hemo
rrhages may occur
Cutaneous schistosomal granulomas most
frequentiy involve the genitalia, perineum, and butt
ocks

Schistosomiasis
Treatment: Praziquantel

Ancylostomiasis
Ancylostomiasis (also anchylostomiasis or
ankylostomiasis) is the condition of infection by
Ancylostoma hookworms
Ancylostomiasis is caused when hookworms, present
in large numbers, produce an iron deficiency anemia
by sucking blood from the host's intestinal walls.
They commonly infect the skin, eyes, and viscera in
humans.

Ancylostoma brasiliensis causes cutaneous larva migrans.

Ancylostomiasis
CAUSE:
The infection is usually contracted by persons walking barefoot over
contaminated soil.
In penetrating the skin, the larvae may cause an allergic reaction. It is
from the itchy patch at the site of entry that the early infection gets its
nickname "ground itch".
Once larvae have broken through the skin, they enter the bloodstream
and are carried to the lungs (unlike ascarids, however, hookworms do n
ot usually cause pneumonia).
The larvae migrate from the lungs up the windpipe to be swallowed and
carried back down to the intestine. If humans come into contact with
larvae of the dog hookworm or the cat hookworm, or of certain other ho
okworms that do not infect humans, the larvae may penetrate the skin.
Sometimes, the larvae are unable to complete their migratory cycle in
humans. Instead, the larvae migrate just below the skin producing
snake-like markings. This is referred to as a creeping eruption or cutane
ous larva migrans.

Ancylostomiasis

creeping eruption or cutaneous larva

migrans

Ancylostomiasis

Treatment: mebendazole

Parasitic Systemic Infestations

Cutaneous And Mucocutaneous
Leishmaniasis

Trypanosomiasis
American Trypanosomiasis (AT)
Human African Trypanosomiasis (HAT)
Cutaneous Amebiasis And Acanthamebiasis

Cutaneous Amebiasis

Cutaneous Acanthamebiasis

Cutaneous And
mucocutaneous
Leishmaniasis

Cutaneous And
mucocutaneous Leishmaniasis

Etiology: Many species of obligate intracellular

protozoa Leishmania; predominant species are:
Old World: L.tropica, L.major, L. aethiopica
New World: L. Mexican complex, Viannia sub-genus

Cutaneous And
mucocutaneous Leishmaniasis
Vector: sandflies

Old World: Plebotomus

New World: Luzomyia

Cutaneous And
mucocutaneous Leishmaniasis
Infection of macrophage in skin (dermis), nasooropharyngeal mucosa, and
the reticuloendothelial system (viscera)
Diversity of clinical syndromes due to particular parasite, vector, and host
species.
Clinical syndromes: Cutaneous, mucosal, visceral
Cutaneous leishmaniasis (CL) characterized by development of single
or multiple cutaneous papules at the site of a sandfly bite, often evolvi
ng into nodules and ulcers, which heal spontaneous with a depressed s
car
Old World cutaneous leishmaniasis (OWCL)
New World cutaneous leishmaniasis (NWCL)
Diffuse (anergic) cutaneous leismaniasis (DCL)
Mucasal leishmaniasis (ML)
Visceral leishmaniasis (VL) ; kala-azar; post- kala- azar dermal
leishmaniasis (PKDL)

Cutaneous leishmaniasis

New World cutaneous leishmaniasis:

ulcer on thigh

Cutaneous leishmaniasis

New World cutaneous leishmaniasis:

chiclero ulcer

Mucocutaneous
leishmaniasis

Mucocutaneous leishmaniasis, South

American. Painful, mutilating ulceration

Cutaneous And
mucocutaneous Leishmaniasis
Treatment:
Cutaneous leishmaniasis

For certain types of cutaneous leishmaniasis

where the potential for mucosal spread is low, t
opical paromycin can be used.
For more invasive lesions (eg, those failing to
respond to topical treatment; metastatic sprea
d to the lymph nodes sodium stibogluconate or
pentamidine can be used.

Cutaneous And
mucocutaneous Leishmaniasis
Treatment:
Mucosal leishmaniasis

Pentavalent antimony for a course of 4

weeks has been recommended.
Amphotericin B deoxycholate may be
first-line therapy for advanced mucosal
disease.

Trypanosomiasis
American Trypanosomiasis (AT)
Human African Trypanosomiasis (HAT)

Trypanosomiasis

Zoonosis
Parasitic protozoa disease caused by three species o
f Trypanosoma

Trypanosomiasis
Vector: reduviid bugs

Epidermiology

Central and South America: T.cruzi

Africa: T.brucei gambiense, T.brucei
rhodesiense

Trypanosomiasis
Clinical findings:

Acute: Inoculation site nodule

Chronic: Cardiac, gastrointer, and
central nervous system involvment

Course: most infected persons

remain so far life. Heart, GI, and CNS
involvement associated with serious
morbidity

Trypanosomiasis
Treatment:
American trypanosomiasis is
currently treated with a variety of
antifungal agents, including
benznidazole and nifurtimox
. Melarsoprol is another drug which is
used for the treatment of T. b. gambi
ensie.

American Trypanosomiasis (AT)

American Trypanosomiasis (AT)

Synnonym: Chaga disease
Etiology: T.cruzi
Transmission: T.cruzi deposited in feces of
reduviid bugs onto the skin; enters host via
breaks in skin, mucous membranes, or con
junctivae. Chagoma can occur at inoculatio
n site. Can also be transmitted by transfusi
on of blood from infected persons, by orga
n transplantation, from mother to fetus

American Trypanosomiasis (AT)

Dissemination: Via lymphatics and
bloodstream to muscles.
Geography: Central and South
America
Clinical findings:
Acute AT
Chronic AT

American Trypanosomiasis (AT)

Acute AT
1. Inoculation chagoma

An indurated area of erythma and sweeling

(chagoma), at the portal of entry, occuring
7-14 days after inoculation.May be accomp
anied by local lymphadenopathy. Parasites l
ocated within leukocytes and cells of subcut
aneous tissue. These initial local signs are f
ollowed by malaise, fever, anorexia, and ed
ema of the face and lower extremities

American Trypanosomiasis (AT)

An indurated area of erythma and

sweeling (chagoma)

American Trypanosomiasis (AT)

2.Romana sign

Unilateral painless edema of palpebrae

and periocular tissue classic finding in
acute AT

American Trypanosomiasis (AT)

3.Edema of face and lower extremities

American Trypanosomiasis (AT)

4.Trypanosomides

Morbilliform, urticariform, or
erythematopolymorphic eruptions

American Trypanosomiasis (AT)

5.Hematogenic or metastatic
chagomas

Nodule(s) caused by dissemination of

infection. Hard, painful, wine-colored
nodules; rarely soften or ulcerate

American Trypanosomiasis (AT)

Chronic AT: In the immunocompromised
host (HIV/AIDS disease, organ transplant r
ecipient)
Reactivation chagoma Nodule at inoculation
site
A cellulitis-mimicking plaque

Diagnosis

Acute AT : Detect parasites in blood

Chronic AT : Detect specific antibodies

Human African Trypanosomiasis (HAT)

Human African Trypanosomiasis (HAT)

Synonym: Sleeping sickness

Etiology: complex of T.brucei

T.brucei gambiense causes West African

sleeping sickness
T.brucei rhodesiense cause East African
sleeping sickness

Transmission

Vector: tsetse flies

Transmission during human
Blood meal from infected saliva

Human African Trypanosomiasis (HAT)

Preimary reservoir

West African sleeping sickness: humans

East African sleeping sickness: Antelope
and cattle

Epidermiology:

Sub-saharan Africa
HAT in travelers: usually East African
trypanosomiasis

Human African Trypanosomiasis (HAT)

Clinical findings:

Acute HAT: Stage I Disease

Chronic HAT: Stage II Disease

Human African Trypanosomiasis (HAT)

Acute HAT: Stage I Disease

1. Trypanosomal chancre
Painful; 7-14 days after tsetse-fly bite.
Occurs more commonly in travelers than i
n Africans. Typically 2-5 cm, indurated; m
ay ulcerate; resolved in few weeks. Parasi
tes can be seen in fluid expressed from ch
ancre can buffy coat

Human African Trypanosomiasis (HAT)

Trypanosomal chancre

Human African Trypanosomiasis (HAT)

2. Hemolymphatic stage
Marked by the onset of fever, arthralgia,
malaise, localized facial edema, and
moderate splenomegaly. Lymphadenop
hthy is prominent in T.brucei gambiense
trypanosomiasis
3. Macular-papular rash
Occurs on the trunk
4. Pruritus

Human African Trypanosomiasis (HAT)

5. Winterbottom sign
Enlargement of the nodes of the
posterior cervical triangle; cervical n
ode also enlarged

Human African Trypanosomiasis (HAT)

Chronic HAT: Stage II Disease

1. CNS invasion
Characterized by insidious development of
protean neurologic symptoms. Progressive
indifference and daytime somnolence
develops (sleeping sickness)

Human African Trypanosomiasis (HAT)

2. Cardiac disease
East African type may develop
arrhythmias and congestive heart failure
before CNS disease develops.
Diagnosis

Detection of parasite in chancre, lymp

node, blood, bone marrow.

Cutaneous Amebiasis And Acant

hamebiasis

Cutaneous Amebiasis

Cause :

By Entamoeba
histolytica, which
infects the GI tract and
rarely skin

Incidence : 10% of world population

infected with Entamoeba
Majority of infections caused by
noninvasive E. dispar

Cutaneous Amebiasis

More prevalent in tropics and in rural

areas: inadequate sanitation and
crowding
Skin involement is associated with
malnutrition and immunocompromise
(HIV/AIDS, solid organ transplantatio
n)

Cutaneous Amebiasis
Clinical finding:

Cutaneous Amebiasis begins as an indurated

pustule that evolves to a painful ragged ulcer, fou
l-smelling and coverd with pus or necrotic debris
Usually a consequence of an underlying amebic
abscess invading the skin
Typical sites are the perianal area (extension of
sigmorectal involvement) abdominal wall
(draining sinus from liver or colon)
Penis or vulva may become infected during
intercourse

Cutaneous Amebiasis

Cutaneous amebiasis: perineum

Perineal/perianal ulcer in a patient with
rectal amebiasis.

Cutaneous Amebiasis

A male child with multiple ulcers by

amebiasis in the diaper area

Cutaneous Amebiasis
Treatment :
The choice of drug depends on the type of
clinical presentation and the site of drug a
ction (in the intestinal wall versus inside th
e intestine itself). Drugs may include
metronidazole
, paromomycin, iodoquinol, or diloxanide f
uroate.
Occasionally, it may be necessary to drain
a liver abscess.
Follow-up care includes stool studies 2 to 4

Cutaneous
Acanthamebiasis
Caused

by free-living
Acanthamoeba

Clinical finding
Primary cutaneous Acanthamebiasis
Disseminated cutaneous
Acanthamebiasis

Cutaneous
Acanthamebiasis

Primary cutaneous Acanthamebiasis

Occurs at site of trauma sustained in
adequatic environment.

- Keratitis is usually associated with a history

of improper cleaning of contact lenses and sw
imming in fresh water or a swimming pool,
especially while contact lenses are worn

Lesion begin as indurated red/violaceous

deep nodules or large pustules that soon
ulcerate

Cutaneous
Acanthamebiasis

Granulomatous amebic encephalitis

(GAE) is a subacute diffuse
meningoencephalitis
, usually with an insidious onset. The inc
ubation period is unknown but is probabl
y weeks to months.

Cutaneous
Acanthamebiasis

Disseminated cutaneous
Acanthamebiasis

Occurs in HIV/AIDS disease and solid

organ transplant recipients
Disseminates from nasal/sinus
colonization.
Present with multiple soft red nodule
that ulcerate

Cutaneous
Acanthamebiasis

Ulcerated lesions on the arm of a patient with disseminated

Acanthamoeba infection. Skin nodules with overlying erythema
underwent sequence of changes, characterized by central
darkening, crusting, and deep ulceration, which left a thin,
erythematous, indurated border.

Cutaneous
Acanthamebiasis

Treatment :
Keratitis

Medical treatment consists of topical antimicrobial agents, which can

achieve high concentrations at the site of the infection.
Because the cyst form may be highly resistant to therapy, a combination of
agents is generally used. Many authorities recommend a combination of
propamidine 0.1%, miconazole nitrate 1%,and neomycin.
combination of a diamide (propamidine isethionate) with a cationic antiseptic
(polyhexamethylene biguanide [PHMB] or chlorhexidine).
These topical antimicrobials are administered every hour immediately after corneal
debridement. These agents are then continued hourly during waking hours for 3 days
(at least 9 times/day is recommended).

The frequency is then reduced to every 3 hours. Two weeks may be

required before a response is observed, and the total duration of therapy is
a minimum of 3-4 weeks. Some advocate treating for 6-12 months. When t
herapy is discontinued, close observation is warranted to rule out recurrent
disease.

Cutaneous
Acanthamebiasis

Treatment:
Surgical Care

Keratitis: The abnormal epithelium is

dbrided. Penetrating keratoplasty may
be necessary in cases that do not respo
nd to medical therapy.

Cutaneous
Acanthamebiasis

Treatment:
Granulomatous amebic encephalitis

Ketoconazole, miconazole, itraconazole,

fluconazole,Pentamidine,Amphotericin
Bparomomycin,Polymyxin,Trimethoprim-sulfamethox
azole,Sulfadiazine,Flucytosine,Clotrimazole,Rifampin

Disseminated disease:

A case that involved only the skin was treated with

intravenous pentamidine, topical chlorhexidine
gluconate, and 2% ketoconazole cream, followed by
oral itraconazole.

Question
1. Whats the classic finding in acute
American Trypanosomiasis (AT)?
Answer ROMANA SIGN
2. Whats sign which is enlargement
of the nodes of the posterior cervical
triangle in the patient who was bitten
by tsetse flies?
Answer Winterbottom sign