parasites cause skin and eyes infections

7/29/2019 Parasites Cause Skin and Eyes Infections

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BY

Sri Sundari Purbohadi


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Leishmania

Dracunculus medinensis


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1. Infectious Agent

Protozoan - Genus: Leishmania

Numerous species differ in

a . Natural habitat differ in various geographic

regions / countries

b . Different host / reservoirs

c . Type of disease produced a spectrum of

clinical syndromes from indolent self

resolving ulcer to fatal disseminated disease


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2. Reservoir / Host(animal, man or both)

Leishmania is primarily a parasite ofwild animals and man becomes

accidental host when intrudinginto the natural habitat of theseanimals i.e. ZoonoticLeishmaniasis.

Different Leishmania species mayhave different specific zoonotic

reservoirs ega. Dogs in Visceral Leishmaniasis

in Mediterranean basinb. Wild rodents in Mexican

cutaneous Leishmaniasis

c. Common reservoirs hosts:Rodents, dogs, foxes, jackals

d. Potential hosts include cattle,horses, wild canine, sloth


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3. Habitat

Physical geomorphological characteristics ofVector and Reservoir eg landscape, vegetation,

etc Environmental characteristics eg wind,

temperature, humidity, light etc


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4. Vector: female Phlebotomus sandflies.

Sandflies acquire infection from feeding oninfected animals.

Physiological age movements Time of activity

Flying range

Feeding habits

Reproductive activity

Condition of alimentary canal


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Sandfly bite Leishmania (promostigotes)phagocytosed by histiocytes reproducedwithin macrophage Daughter amastigotes

rupture from cell spread to othermacrophages

1. Immunological capabilities of the host

2. Infecting species of Leishmania


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LOCALISEDCUTANEOUSLEISHMANIASIS

PATHOLOGY

Amastigote-filled macrophagesulcerates overlying epidermis

Oval amastigotes 2m containing 2internal structures, a nucleus andkinetoplast

Amastigotes in macrophages appearas multiple cytoplasmic dotsLeishmanDonovan Bodies

Progressive development of CMI to theparasite Macrophages activated

Kill intracellular parasitesAmastigote-filled macrophagesGranulomatous reaction Ulcer

Lesion starts as small itching solitarypapule erodes to form shallow ulcer(sharp raised borders) Extension of

ulcer (6-8 cm) Satellite lesionsdevelop along draining lymphatics. Ulcer resolve in 3 6 months and

heals spontaneously


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Enormous numbers of macrophages containinglarge numbers of Leishmania

Develops in patients who lack specific cell-

mediated immune response to Leishmania. Begins as single nodule extensive ulceration

developing into satellites along draininglymphatics


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Late complication of cutaneous Leishmaniasis .

Species: L.Braziliensis

Geography: Central & South America

Reservoir: Rodents, sloth


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Early course and pathologic changes similar toLocalizes Cutaneous Leishmaniasis i.e. solitaryulcer appears, expands and then resolvesspontaneously.

Years after healing of primary ulcerdevelops at mucocutaneous junctions (e.g.nasal septum, anus, vulva) slowlyprogressive, highly destructive, disfiguring erodes mucosal surfaces and nearby tissues.

Destruction of nasal septumNose deformity

MCL ulcers may obstruct airways


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VISCERALLEISHMANIASIS(Kala-Azar)

Potentially fatal disseminatedinfection of macrophage /monocyte system caused by

several subspecies of L.donovani.

Reservoirs in susceptible agegroups vary in different parts

of the world egHumans in India

Foxes in S. France,Central Italy, S. America

Dogs in Mediteranean basin,China, S. America

Jackals M. East, Central Asia


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Sandfly bite localized collection of infected macrophagesulcer

95% infected persons can contain the disease, destroying L.Donovani by CMI.

5% Young children, malnourished persons failure to mountadequate CMI response

Mononuclear phagocytes full with proliferating L. amastigotes replacing normal architecture of liver, spleen, LN leading to theirmassive enlargement

BM is replaced by filled with proliferating amastigots

Eventually mononuclear phagocytes accumulate in other organse.g. heart, kidney.


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Normally develops


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Clinical signs & symptoms

Hypergammaglobulinemia

ELISA/Formol gel

Bone marrow biopsy

Spleen or liver biopsy

Culture & Histology


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Similar morphology

Isoenzyme profiles - Zymodemes

Monoclonal antibodies

DNA hybridisation - PCR


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Diet

Antibiotics

Pentavalent antimony

Pentamidine

New drugs - New delivery


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Vector control

Reservoir control

Treatment of active cases

Vaccination


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Pentavalent antimonial drug Not absorbed orally

Given IV/ IM for 20 days for cutaneousleishmaniasis & 28 days for visceral andmucocutaneous disease.

Distributed in extravascular compartement.

Partially metabolized

Excreted in urine


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Unknown

Production of oxygen free radicals


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GIT upset

Fever, headache, arthralgia , rash.

IMI----( local pain & sterile abscess).

QT prolongation.

Hemolytic anaemia


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Alternative to Na stibogluconate for thetreatment of visceral leishmaniasis.

For cutaneous lesion


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Not absorbed orally

Given IV/ IM.

Accumulative drug & eliminated slowly in

urine ( elimination half-life 12 days). Not effectively cross blood brain barrier

Can be inhaled as a nebulized powder.


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Rapid IVI can lead to severe hypotension,tachycardia , dizziness, dyspnea ( should be givenslowly over 2 hours).

IMI pain & sterile abscess

Pancreatic toxicity( acute pancreatitis)

Hypoglycemia

Hyperglycemia Reversible renal insufficiency

Rash

Metallic taste


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Fever

Thrombocytopenia

Cardiac arrhythmias

GIT upset

Cough, dyspnea, bronchospasm ( with theinhaled drug )

Headache, Arthralgia


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Humans become infected by drinking unfiltered water containing copepods(small crustaceans) which are infected with larvae ofD. medinensis

Following ingestion, the copepods die and release the larvae, which penetrate thehost stomach and intestinal wall and enter the abdominal cavity andretroperitoneal space.

The worm molts again 20 days and 43 days post infection

After maturation into adults and copulation, the male worms die and the females(length: 70 to 120 cm) migrate in the subcutaneous tissues towards the skinsurface

Approximately one year after infection, the female worm induces a blister on theskin, generally on the distal lower extremity, which ruptures.

When this lesion comes into contact with water, which the patient seeks to relievethe local discomfort, the female worm emerges and releases larvae

The larvae are ingested by a copepod and after two weeks (and two molts) havedeveloped into infective larvae


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Dracunculiasis may result in three majordisease conditions Emergent adult worms Secondary bacterial infection Nonemergent worms When worms do not emerge they degenerate and release

antigens causing fluid filled abscesses or allergenic reactions.

If the worms become calcified they can cause inflammation

or if they remain in a joint, arthritis. Can cause paraplegia if it worm gets into the central nervous

system.


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None until the female worms cause an allergic reaction by releasingmetabolic wastes into host. This occurs at the onset of migration to theskin. a rash accompanied by severe itching

nausea

vomiting

diarrhea

dizziness

edema

Reddish papule-blister (local itching and intense burning).

Blister ruptures, becomes abscessed-very painful.

Secondary bacterial infections of opening possible. Retreating worm can draw bacteria under skin as well.

There may be later symptoms fibrosis of the skin, muscles, tendons and joints (may interfere with

locomotion or use of limbs)


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Adult in joint

Calcified lesion in soft

tissues


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DIAGNOSIS:

Diagnosis is made from the local

blister, worm or larvae.

The outline of the worm under

the skin.

Some people claim to be able tofeel the worm moving towards

the surface of the skin.

Finding Calcified worms.


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Drug TherapyMetronidazole

To help prevent bacterial infections

Anti-inflammatory to help reduce swelling

Treatment includes the extraction of the adult guinea worm

by rolling it a few centimeters per day

Usually takes weeks or months depending on how long the worm is.

Exposing area to cold water helps remove worm faster.

Preferably by multiple surgical incisions under local

anesthesia.

Infection does not make a person immune


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Filter, boil, or treat water with chlorine to kill intermediate host.

Finely-meshed cloth or, better still, a filter made from a 0.15 mm nylon mesh, is all

that is needed to filter out the copepods from the drinking water.

Avoid bathing or wading in drinking water.

Village-based volunteers demonstrating the use of cloth filter on a clay pot to

filter drinking water

Construction of copings around well heads or the

installation of boreholes with hand pumps.

Borehole is a deep and narrow well.

Coping is a cap/cover over a well

Key is to prevent copepod growth by controlling sunlight.

Light increases the food source of the copepod.


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Caused by the parasite Onchocerca volvulus. Affects 20 million people worldwide. Non-fatal dermal and ocular disease Human definitive host; fly intermediate host No animal reservoir ofO. volvulus Three main symptoms (occur 1-3 yrs after initial

infection): Skin lesions (microfilariae in dermis) Painless nodules (where tissues thin, bone) Eye lesions (blindness assoc. with dead mf)

Spread by blood-sucking blackfly Transmits parasite to the eye

Parasite invades the anterior chamber Causes corneal ulceration, fibrosis, and blindness


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Simuliumdamnosum


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History

Symptoms

Microfilaria in nodules


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Avoid black flies in endemic areas

Ivermectin

kills larvae but does not affect adult worms

Moxidectin currently in phase III clinical trials for treatment of

Onchocerciasis

kills both adults and microfilaria


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Loasis is similar to onchocercaisis

It can also cause blindness


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Deer flyCrysops


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Loa loa matures in its vector

the deer fly.

Worm migrates to the mouth of the fly.

Transmitted to a human when the fly bites

Microfilariae migrate through the subcutaneoustissue.

Cause inflammation

Settle in the cornea and conjunctiva

Worms can grow to more than an inch in length.


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A transient subcutaneous swelling markingthe migratory course through the tissues of

the adult filarial eye worm that appear most

frequently on the back of the hand or on the

arm.


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History

Symptoms

Microfilaria recovered from conjunctivae


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Avoid deer flies in endemic areas

Diethyl carbamazine kills larvae


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parasites cause skin and eyes infections

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