KULIAH PARASITOLOGI

BLOK IMUNITAS DAN INFEKSI

KG

By Tri Wulandari K.

TOPICS• Opportunistic parasite

• Parasite causing allergy

IMMUNE RESPONSE TO PARASITE

• Generally, parasite infection can escape from immune system reaction, because:– Location: intracellular parasitic (plasmodium,

trypanosoma, leishmania) or live in lumen (intestinal helminth).

– Camouflage: change the surface antigent, so it can’t detect by host immun system (trypanosoma, plasmodium)

– Pressure the host immune system: damage limphoid cell, decrease the host immune response (larvae T. spiralis, schistosoma)

OPPORTUNISTIC PARASITE

• Definition – Parasite that pathogenic on

immunocompromise host

• Important species:– Toxoplasma gondii

MAMALIA, BURUNG

Trof. & sistadlm makanan

MANUSIA

KUCING

oosista

KUCING

oosista

Trof. & sistadlm makanan

oosista

Toxoplasma gondii

• Morphology– tachyzoite :

• crescent form/coma

– pseudocyst : • Group of tachyzoite; slinght positive with

PAS

– tissue cyst : • Cyst contain of bradyzoite; strong positive

with PAS

– oosista : • Double layer wall cyst, contain of 2

sporocyst that each contain of 2 sporozoite

TACHYZOITE PSEUDOCYST

TISSUE CYST OOCYST

• Pathogenesis– tachyzoite (intracell)→ multiplication → rupture of

host cell → invasion to other cell through circulation system (blood/lymph) → disturbance of host cell/tisue → manifestation or no manifestation with formed tissue cyst → reactivation of tissue cyst → manifestation

• Patologi - Gejala Klinis– Acquired Toxoplasmosis :

• immunoccompetent person→ no clinical manifestation• immunodeficiency → clinical manifestation

– lymphadenitis, fever, headache– myocarditis, meningoencephalitis, pneumonia– CNS disorder– Retinochoroiditis

– Congenital Toxoplasmosis

• Diagnosis– Serologic test

• antibody antitoxoplasma (IgM, IgG)• specimen : serum• Kind of test: (dye test,IHA,IFA,ELISA,ect)

– Biologic test• inoculation to lab. animal/ tissue culture → tachyzoite• specimen: tissue fluid, biopsy, blood.

– Histologic test• pseudocyst, tachyzoite, tissue cyst.• specimen: tissue biopsy/necropsy.

– Biomolecular approaches• PCR (polimerase chain reaction)

ALGORITHM FOR SERODIAGNOSIS OF TOXOPLASMOSIS

Test for toxoplasma-specific IgG antibodies

IgG negativeNot infected

IgG positive

IgM negativeInfected over 2 years ago

IgM low positive1. False positive2. Infection in past 2 years3. New infection

IgM high positiveInfected within past 3-6 months

Second sample 2 weeks later and retest both together

• Treatment– spiramycine :

• active against tachyzoite & intracellular form, safely for pregnant woman and fetus.

– pyrimethamine-sulphonamide : • synergistic action but cause severe side effect

and teratogenic → not recognized to pregnant woman.

– clindamycine : • Good for eye toxoplasmosis, with side effect :

– colitis ulcerative, – Not safely for children and pregnant woman.

• Epidemiology– Infected in man through:

• uncooked meat containing tissue cyst • swallow oocyst

– Cosmopilitely distribution.– No cases of congenital toxoplasmosis in infant,

much of congenital toxoplasmosis.• Prevention

– Washing hand before eat avoid ingest of oocyst– Cook completely of meat 66oC– Cat management

• Clean daily the litter pan; • Fed on dry, canned or boiled food; • Throw away the feces into WC; • Children sand’s boxes should be made cat proof

• Miscellaneous– Pneumocystis carinii– Cryptosporidium sp

PARASITE CAUSING ALLERGY

• Cutaneous form

• Respiratory form– Migratory larvae of worm in lung

• Hook Worm• Round worm

– Trigerred by mites

CUTANEOUS FORM

• Non human hook worm that infect to man by penetrate the skin cutaneous larva migrans

• Injurious arthropods : poison of the insects causing dermatitis up to fatal. – Stinging and biting do not affect every

person in the same manner (do not suffer local/general allergic manifestation)

– Flea, Mosquito, Cimex, Tick, Scorpion, Spider, Caterpillar, Fire ants, beetles, etc.

CUTANEOUS LARVA MIGRANS

Pathophysiology

• Eggs are passed from animal feces into warm, moist, sandy soil larvae hatch infective third stage larvae penetrate through follicles, fissures, or intact skin of the new host (by using proteases) in the stratum corneum, the larvae shed their natural cuticle migration within a few days.

• In their natural animal hosts: the larvae penetrate into the dermis transported via the lymphatic and venous systems lungs break in alveoli migrate to the trachea swallowed mature sexually in intestine.

• Humans are accidental hosts: larvae are lack the collagenase enzymes disease remains limited to the skin.

Physical• Cutaneous signs include the following:

– Pruritic, erythematous, edematous papules and/or vesicles

– Serpiginous (snakelike), slightly elevated, erythematous tunnels that are 2- to 3-mm wide and track 3-4 cm from the penetration site

– Nonspecific dermatitis – Vesicles with serous fluid – Secondary infection – Tract advancement of 1-2 cm/d

• Systemic signs: peripheral eosinophilia, migratory pulmonary infiltrates and increased immunoglobulin E (IgE) levels (Loeffler syndrome), but are rarely seen.

• Lesions are typically : distal lower extremities: dorsa of the feet and the interdigital spaces of the toes, but can also occur in the anogenital region, the buttocks, the hands, and the knees.

Causes

• Common etiologies : – Ancylostoma braziliense (hookworm of wild and domestic dogs

and cats) is the most common cause. – Ancylostoma caninum (dog hookworm) is found in Australia. – Uncinaria stenocephala (dog hookworm) is found in Europe. – Bunostomum phlebotomum (cattle hookworm).

• Rare etiologies: – Ancylostoma ceylonicum – Ancylostoma tubaeforme (cat hookworm) – Necator americanus (human hookworm) – Strongyloides papillosus (parasite of sheep, goats, and cattle) – Strongyloides westeri (parasite of horses) – Ancylostoma duodenale

• Diagnosis– Based on the classic clinical appearance of the

eruption. – Eosinophilia and increased IgE levels on serum.– Biopsy may show a larva – Epidermal chronic inflammatory infiltrate with

many eosinophils.

• Medical Care– Even though self-limited the intense pruritus and

risk for infection should to be treated. – Topical : Soon: 10% thiabendazole susp. or

mebendazole cream– Thiabendazole agent of choice.– Alternatively drug: Mebendazole, Albendazole,

Ivermectin

• Complications– A secondary bacterial infection, usually with

Streptococcus pyogenes, may lead to cellulitis. – Allergic reactions may occur.

• Prognosis– The prognosis is excellent. This is a self-limiting

disease. Humans are accidental, dead-end hosts, with the larva dying and the lesions resolving within 4-8 weeks, as long as 1 year in rare cases.

• Patient Education– Persons who travel to tropical regions and pet

owners should be aware of this condition.

Scabies

• Etiology : Family Sarcoptidae

Species Sarcoptes scabiei

Morphology :- Oval body, dorso-ventrally flat,

- Leg : larvae : 3 pairs; adult: 4 pairs

- Differentiation ♂-♀ : leg (position of sucker) and size

- Mouth: celicera + palpus anteriorly

Life Cycle:Eggs Larvae Nympha Imatur adult

♀ matur adult

MP MP MP

♂ MP : moulting pocket

Special Characteristic:• Location stratum corneum; food: tissue • Btn burrowing in superficial layer of skin

curve apperence • Predelection smooth skin: interdigital,

penis, scrotum, axilla, knee, buttock, breast, ect .

• Children more area can infected

Clinical manifestation:- Curved burrow, black spot (deposit faeces)

predelection area- itch, especially at night scrathing lead to

secondary inf. pustula, eczema, impetigo contagiosa (mengaburkan gejala asli scabies)

- In individu with imunitas/hypersensitif crusta ceratotic (peeled off of non infection skin) crusted scabies/norwegian scabies

• Diagnosis

- characteristic clinical manifestation

- Dx. curry on the lesion skin exam microscopically

• Teatment - no resistance to drug

- 20-25% benzyl benzoate (emulsion) repeated 3 day later

- sulfur : tetmosol : 3x24 hours

tetmosol soap : prophylaxis/slow curatif

- 1% HCH (cream, lotion) repeated 2-7 days later

- 0,5% malathion ; 10% crotamion (cream/lotion) repeated 2-7 days later

Important : mass treatment !!!

Insect bite reaction

• Clinical manifestation– minor swelling, redness, pain, and itching are

common reaction and may last from a few hours to a few days.

• Home treatment – needed to relieve the symptoms of a mild reaction to

common stinging or biting insects and spiders.– Some people have more severe reactions to bites or

stings. Babies and children may be more affected by bites or stings than adults.

Examples of problems that are more serious include:

• A severe allergic reaction (anaphylaxis). Severe allergic reactions are not common but can be life-threatening and require emergency care. Signs or symptoms may include: – Shock the circulatory system failure.– Coughing, wheezing, difficulty breathing, or feeling

of fullness in the mouth or throat. – Swelling of the lips, tongue, ears, eyelids, palms of

the hands, soles of the feet, and mucous membranes (angioedema).

– Nausea, diarrhea, and stomach cramps. – Hives and reddening of the skin. – A skin infection at the site of the bite or sting.

Treatment• Anaphylactic reaction

– Epinephrine injection is the main treatment.

• Local reactions – wash the area with soap and water.– an ice pack or cool compress. – a topical steroid cream Calamine lotion.– oral antihistamine diphenhydramine (Benadryl),– pain medications ibuprofen or acetaminophen.

• More extensive local reactions – oral steroid.

• If becomes infected– Antibiotics

RESPIRATORY FORM

LIFE CYCLE OF HOOK WORM

Life cycle of A. lumbricoides (Round worm)

Patogenesis-manifestation

Larvae migration effect• While larvae live in lung inflammation: >>

larvae pneumonitis.• Manifestation (Loeffler syndrome): dispnea,

nonproductive/productive cough, fever (39-40 oC), ronchi, eosinophilia

• Sputum: charcott leyden chrystal, eosinophil, larvae

Diagnosis• Migratory phase

– Loeffler syndrome in highly endemic area – Sputum / lavage of gastric material larvae– Sometimes eggs found in feces

• Treatment– Mebendazole– Pyrantel pamoate– Piperazine cytrate

• Epidemiology and prevention– Mass treatment– Using sanitation facility– Avoid using feces for fertilizer, although by a good processing– Personal hygiene mainly before feeding

Respiratory inflammation triggered by mites

• Dermatophagoides sp: – D. pteronyssinus (European dust mite)– D. farinae (American dust mite)

• Classification: Dust mites are arachnids, the class of arthropods which includes spiders, scorpions and ticks.

• Live in: cover bed, carpet, dust house, mattres, ect.• They live their whole lives in dark corner dust bunnies: hatching,

growing, eating, defecating, mating, laying eggs make us itch and wheeze (Many people develop severe allergies: difficulty breathing or even a severe asthma attack).

• Food: organic debris: dead skin, semen, ect. (and probably potato chips & cookie crumbs).

The mechanism of the inflammation triggered by dust mite

• Itchy red bumps on our skin due to how our mast cells respond to the allergen.

• Mast cells are covered with molecules of Immunoglobulin E antibody (IgE, ).

• There are antigens in dust mites, in their droppings and shed exoskeletons. Once these antigens get under the skin of an allergic host, the antigens cause mast cells to go angry.

• Antigens stick to the mast cell IgE antibodies, causing granules in the mast cell to fire their contents into the surrounding tissue.

• This releases inflammatory materials : leukotrienes, TNF, IL-4 and other cytokines.

• These materials cause fluid to leak from the capillaries and white cells including neutrophils, T cells and eosinophils to leave the circulation. The end result is a "local inflammatory response", a red, itchy welt.

Treatment (respiratory form): • bronchodilators, antihistamines, and corticosteroids.

Prevention: • Wash bedding at 55 oC to kill the mites and remove their allergen. • Regular washing of clothes and bedding in cool water will remove

food for dust mites .• Dry cleaning kills the mites (but 20-70 percent of the allergen will

remain) .• Leaving rugs and blankets in direct sunlight for 3 hours will kill mites

(not to allergen) .• Use mite allergen-proof mattress covers and pillow covers (vapor

impermeable) .• Store out-of-season clothes in plastic .• Consider using acaracides, which are chemicals that kill dust mites.

Benzyl benzoate is considered safe. • Use a vacuum cleaner that “keeps in” all the allergens in breeding

place, cover the mattres with plastics material, clean up the cover bed, ect.