parasitic infestions complete

Parasitic Infestations

ByTonagaya, 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 developing countries can be acquired during activities like: bathing, swimming,planting rice, fishing and doing laundry

• involves contact with water infected with intermediate snail host of the parasite free swimming cercaria attaches 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, such as lakes, ponds, and oceans used for swimming and 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, you may experience tingling, burning, or itching of the skin. Small reddish pimples appear within 12 hours. Pimples may develop into small blisters. Itching may last up to a week or more, but will gradually go away.

http://www.medicinenet.com/script/main/art.asp?articlekey=15781


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 prescribe 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 streams containing Cercanae

• After an asymptomatic incubation period, there may be a sudden illness with fever and chills,pneumonitis, and eosinophilia. Petechial hemorrhages may occur

• Cutaneous schistosomal granulomas most frequentiy involve the genitalia, perineum, and buttocks

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.

http://en.wikipedia.org/wiki/Ancylostoma

http://en.wikipedia.org/wiki/Hookworm

http://en.wikipedia.org/wiki/Iron_deficiency_anemia

http://en.wikipedia.org/wiki/Ancylostoma_brasiliensis



http://en.wikipedia.org/wiki/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 not 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 hookworms 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 cutaneous larva migrans.

Ancylostomiasis

creeping eruption or cutaneous larva migrans

Ancylostomiasis

Treatment: mebendazole

Parasitic Systemic Infestations

• Cutaneous And Mucocutaneous Leishmaniasis

• TrypanosomiasisAmerican Trypanosomiasis (AT)Human African Trypanosomiasis (HAT)

•Cutaneous Amebiasis And Acanthamebiasis Cutaneous AmebiasisCutaneous Acanthamebiasis

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


Vector: sandflies• Old World: Plebotomus• New World: Luzomyia


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 evolving into nodules and ulcers, which heal spontaneous with a depressed scar

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 LeishmaniasisTreatment: • Cutaneous leishmaniasis – For certain types of cutaneous leishmaniasis

where the potential for mucosal spread is low, topical paromycin can be used.

– For more invasive lesions (eg, those failing to respond to topical treatment; metastatic spread to the lymph nodes sodium stibogluconate or pentamidine can be used.


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

ZoonosisParasitic protozoa disease caused by three species

of 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 involvmentCourse: 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. gambiensie.

http://en.wikipedia.org/wiki/Antifungal

http://en.wikipedia.org/wiki/Benznidazole

http://en.wikipedia.org/wiki/Nifurtimox

American Trypanosomiasis (AT)


Synnonym: Chaga diseaseEtiology: T.cruziTransmission: T.cruzi deposited in feces of

reduviid bugs onto the skin; enters host via breaks in skin, mucous membranes, or conjunctivae. Chagoma can occur at inoculation site. Can also be transmitted by transfusion of blood from infected persons, by organ transplantation, from mother to fetus


Dissemination: Via lymphatics and bloodstream to muscles.

Geography: Central and South America

Clinical findings:• Acute AT• Chronic AT


Acute AT1. Inoculation chagoma • An indurated area of erythma and sweeling

(chagoma), at the portal of entry, occuring 7-14 days after inoculation.May be accompanied by local lymphadenopathy. Parasites located within leukocytes and cells of subcutaneous tissue. These initial local signs are followed by malaise, fever, anorexia, and edema of the face and lower extremities


An indurated area of erythma and sweeling (chagoma)


2.Romana sign• Unilateral painless edema of palpebrae

and periocular tissue – classic finding in acute AT


3.Edema of face and lower extremities


4.Trypanosomides • Morbilliform, urticariform, or

erythematopolymorphic eruptions


5.Hematogenic or metastatic chagomas• Nodule(s) caused by dissemination of

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


Chronic AT: In the immunocompromised host (HIV/AIDS disease, organ transplant recipient) • 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)


Synonym: Sleeping sicknessEtiology: complex of T.brucei • T.brucei gambiense causes West African

sleeping sickness• T.brucei rhodesiense cause East African

sleeping sicknessTransmission• Vector: tsetse flies • Transmission during human Blood meal from infected saliva


Preimary reservoir • West African sleeping sickness: humans• East African sleeping sickness: Antelope

and cattleEpidermiology:• Sub-saharan Africa • HAT in travelers: usually East African

trypanosomiasis


Clinical findings:• Acute HAT: Stage I Disease• Chronic HAT: Stage II Disease


Acute HAT: Stage I Disease 1. Trypanosomal chancre

Painful; 7-14 days after tsetse-fly bite. Occurs more commonly in travelers than in Africans. Typically 2-5 cm, indurated; may ulcerate; resolved in few weeks. Parasites can be seen in fluid expressed from chancre can buffy coat


Trypanosomal chancre


2. Hemolymphatic stage Marked by the onset of fever, arthralgia,

malaise, localized facial edema, and moderate splenomegaly. Lymphadenophthy is prominent in T.brucei gambiense trypanosomiasis

3. Macular-papular rash Occurs on the trunk 4. Pruritus


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


Chronic HAT: Stage II Disease1. CNS invasion

Characterized by insidious development of protean neurologic symptoms. Progressive indifference and daytime somnolence develops (“sleeping sickness”)


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

DiagnosisDetection of parasite in chancre, lymp node, blood, bone marrow.

Cutaneous Amebiasis And Acanthamebiasis

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 transplantation)

Cutaneous Amebiasis

Clinical finding: Cutaneous Amebiasis begins as an indurated

pustule that evolves to a painful ragged ulcer, foul-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 action (in the intestinal wall versus inside the intestine itself). Drugs may include metronidazole, paromomycin, iodoquinol, or diloxanide furoate.

• Occasionally, it may be necessary to drain a liver abscess.

• Follow-up care includes stool studies 2 to 4 weeks after completing treatment.

http://www.healthscout.com/ency/68/214/main.html

http://www.healthscout.com/ency/68/9/main.html

Cutaneous Acanthamebiasis

Caused • by free-living

Acanthamoeba

Clinical finding• Primary cutaneous Acanthamebiasis• Disseminated 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 swimming 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


• Granulomatous amebic encephalitis (GAE) is a subacute diffuse meningoencephalitis, usually with an insidious onset. The incubation period is unknown but is probably weeks to months.

http://emedicine.medscape.com/article/996227-overview


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


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.


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 therapy is discontinued, close observation is warranted to rule out recurrent disease.


Treatment:• Surgical Care– Keratitis: The abnormal epithelium is

débrided. Penetrating keratoplasty may be necessary in cases that do not respond to medical therapy.


Treatment:• Granulomatous amebic encephalitis – Ketoconazole, miconazole, itraconazole,

fluconazole,Pentamidine,Amphotericin Bparomomycin,Polymyxin,Trimethoprim-sulfamethoxazole,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. What’s the classic finding in acute American Trypanosomiasis (AT)?Answer ROMANA SIGN

2. What’s sign which is enlargement of the nodes of the posterior cervical triangle in the patient who was bitten by tsetse flies?Answer Winterbottom sign

parasitic infestions complete

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