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By Dr. Rakesh Prasad Sah
Assistant Professor, Microbiology
• Protozoan infections
• Cutaneous leishmaniasis
• Cutaneous amoebiasis
• Acanthamoeba skin lesions
• Trypanosoma chancre and
chagoma
• Sarcocystosis
• Cestode infections
• Muscular cysticercosis
• Trematode infections
• Cercarial dermatitis
• Ctaneous paragonimiasis
• Nematode infections
• Cutaneous filariasis
• Dracunculiaisis
• Trichinellosis
• Cutaneous larva migrans
• Apart from visceral leishmaniasis (VL), the leishmania
species  produce various cutaneous and mucocutaneous
manifestations.
• CL (Cutaneous leishmaniasis)
• Most common
• Global incidence 6-10 lakh new cases.
• 95% cases occur in America, Mediterranean basin, Middle East and
Central Asia
• MCL (Mucocutaneous leishmaniasis)
• Occur in Bolivia, Brazil, Ethiopia and Peru
• Cuased by Leishmania tropica complex
• Consist of three species
• L. tropica
• L. aethiopica
• L. major
• Life Cycle
• Is same as of L. donovani except that:
• Vector sandfly
• Habitat do not migrate to viscera
• Clinical Features
• Cutaneous leishmaniasis
• Condition known as “oriental sore”.
• Occurs on face and hands, begins with painless papule  nodular
 ulcerates.
• Leishmaniasis recidivans (LR):
• Granulomatous lesion  after healing of primary sore due to L. tropica
• Characterized by scaly, erythematous pappules and nodules, develop
in the centre or periphery of a previously healed sore.
• Diffuse cutaneou leishmaniasis
• Caused by L. aethiopica
• Characterized by lack of CMI response to parasite  widespread of CL
• May be confused with lepromatous leprosy (LL)
• Due to low CMI, montenegro test is negative
• Microscopy:- Amastigote form detected from active lesion
and touch preparation
• Culture
• Aspiration from the ulcers  NNN medium and Schneider’s Drosophila
medium  for isolation of promastigote forms
• Montenegro test
• Positive leishmanin skin test  delayed hypersensitivity,
• Negative  diffused CL
• Caused by
• Leishmania leishmania (L.L.) mexicana complex
• LL brziliensis complex
• LL chagasi
• Vector: Lutzomyia species
• Reservoir of infection: Dogs, foxes (Zoonotic)
• Amastigote form  R.E. cells of skin and mucous membrane
Leishmaina mexicana complex
• Causes CL and DCL
• Chiclero ulcer
• Specific form of CL
• Also called bay sore
• Characterized by persistent ulceration in pinna.
Leishmania viannia braziliensis complex
• Causes CL, similar to oriental sore but more severe, also
cause MCL
• Infects mucus membrane of nose, oral cavity, pharynx or
larynx
• Ulcerative lesion with erosion of the soft tissue and cartilages
 loss of lips, soft part of nose and soft palate (FIG)
• Gradually nasal septum destroyed  nasal collapse
• Lab diagnosis is same as Old world CL.
Loa Loa
• Causes infection of subcutaneous tissue and eyes
• Life Cycle
• Similar to W. bancrofti
• Clinical Feature
• Calabar swellings (repeated episodes of itchy swellings of the
body )
• Common form of loiasis.
• Also called fugitive swelling
• Swelling developing on extremities (knee or wrist)
• Ocular manifestations
• Conjunctival granuloma
• Edema of eye lid  proptosis (bulging)
• Complications
• Meningoencephalitis  occurs in DEC treated patients with
higher microfilaremia.
• Nephropathy
• Cardiomyopathy
• PBS
• Characteristics microfilarae.
• Blood collected at day time 10am to 3pm
• PCR
• Ab detection
• Causative agent of “river blindness”  endemic in west africa, south &
central America
• Dermatitis
• Onchocercoma :- formation of subcutaneous nodules, tend to develop
on head, neck and shoulders
• Ocular lesion:- bilateral blindness (river blindness), photophobia,
keratitis
• Lymphadeonopathy
• Also called as Guinea worm disease or dracunculiasis.
Life Cycle
• Definitive host Man
• Intermediate host  Cyclops
• Mode of transmission
• Drinking water from stagnant pools containing minute fresh water
crustaceans (Cyclops) infected with 3rd stage L3 larvae (infective form)
• Sign and symptoms appear approximately 1 year after the
infection when gravid adult female worm emerges near the
surface of the skin.
• Characterized by painful blister  female worm emerges 
local erythema, fever, nausea and pruritus.
• Most common sites  lower leg, ankle and foot
• Secondary bacterial infections may occur at the blister site.
• Detection of adult worm  blisters and X-ray for calcified
worms in deeper tissues
• Detection of L1 larvae
• When ulcerated leg  placed in container with cold water  large no.
of motile larvae discharged  which can be examined under
microscope.
• Ab detection
• PBS  Eosinophilia
• Trichinella spirallis causes trichinellosis.
• Is a zoonotic infection from domestic pigs or other carnivores.
• Life Cycle
• MOT by ingestion of raw or uncooked pork containing
infective form L1 larvae. 100-300 larvae req to initiate
infection.
• Clinical symptoms depends up on the phase of parasitic
invasion.
• Intestinal stage:
• Mostly asymptomatic
• Heavy load of parasite  watery diarrhoea  during 1st week after
infection
• Larval Migration (2nd week)
• Periorbital and facial edema is common
• Hemorrhages in the subconjuctiva, retina and nail beds (splinter
hemorrhages)
• Maculopapular rash
• Migration to heart, CNS and Lungs may occur but rare
• Muscle encystment
• Occurs 2-3 week after infection
• Common symptoms are myositis with myalgia, muscle edema and
weakness.
• Extraocular muscles most commonly involved, followed by biceps,
muslces of jaw, neck, lower back and diaphragm.
• Demonstration of larvae in Muscle biopsy obtained from
• Gastrocnemius
• Deltoid
• Biceps
• Direct slide technique
• Fresh muscle tissue  compressed between glass slides and
examined under low power microscope.
• Histological Examination
• Fresh muscle  digestion by pepsin
• Ab detection  IgG Ab
• Bachman intradermal test
• Prepared from Trichinella larvae  immediate induration & erythema
• Becomes positive in 2-3 weeks of infection and persist for life.
• Can not differentiate past and present infection.
• Other tests
• Blood tests
• Eosinophilia
• Elevated muscle enzymes  serum creatinine
• X-ray  calcified muscle cyst.
• CLM  skin lesions  produced by nematodes of lower animals
 infect man accidently.
• Agents
• Mainly by nonhuman hookworm species (A. brasiliensis, A. caninum and
A. ceylanicum)
• Rarely by strongyloides stercoralis, Ancylostoma duodenale and Nector
americanus.
• In lower animals: nematodes inf lower animals  larvae into
various organs (intestine) develop in adult worms  lay eggs 
cycle continues
• In humans: larvae of lower animal nematodes  accidently
infect man  not able to complete normal development (because
of unsulal host for them)  life cycle get arrested larvae wander
 skin & subcutaneous tissue producing a condition  called
cutaneous larva migrans (CLM) or creeping eruption.
• Another form of larvae migrans occurs called as “visceral larva
migrans”  life cycle arrested when larvae migrate to various
• Clinical Features
• Ground itch:- Pruritic maculopapular dermatitis and rashes (ground
itch) at the site of skin penetration of hookworm larvae.
• Larva currens:- Migrating strongyloides larvae produce the
pathognomic serpiginous urticarial rash called as larva currens near
the legs.
• Lab Diagnosis
• Larvae are usually not detected in skin biopsy.
• PCR
• Elevated Eosinophilia in PBS or sputum.
• Charcot-leyden crystals in sputum may be seen.
• Cutaneous amoebiasis
• Acanthmoeba skin lesions
• Trypanosoma chancre
• Chagoma
• Muscular sarcocystosis
• Cysticercosis
• Sparganosis
• Cercarial dermatitis
• Cutaneous paragonimiasis
Parasitic infection of Skin, Soft tissue and Muskuloskeletal tissues.pptx
Parasitic infection of Skin, Soft tissue and Muskuloskeletal tissues.pptx

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Parasitic infection of Skin, Soft tissue and Muskuloskeletal tissues.pptx

  • 1. By Dr. Rakesh Prasad Sah Assistant Professor, Microbiology
  • 2. • Protozoan infections • Cutaneous leishmaniasis • Cutaneous amoebiasis • Acanthamoeba skin lesions • Trypanosoma chancre and chagoma • Sarcocystosis • Cestode infections • Muscular cysticercosis • Trematode infections • Cercarial dermatitis • Ctaneous paragonimiasis • Nematode infections • Cutaneous filariasis • Dracunculiaisis • Trichinellosis • Cutaneous larva migrans
  • 3. • Apart from visceral leishmaniasis (VL), the leishmania species  produce various cutaneous and mucocutaneous manifestations. • CL (Cutaneous leishmaniasis) • Most common • Global incidence 6-10 lakh new cases. • 95% cases occur in America, Mediterranean basin, Middle East and Central Asia • MCL (Mucocutaneous leishmaniasis) • Occur in Bolivia, Brazil, Ethiopia and Peru
  • 4. • Cuased by Leishmania tropica complex • Consist of three species • L. tropica • L. aethiopica • L. major • Life Cycle • Is same as of L. donovani except that: • Vector sandfly • Habitat do not migrate to viscera • Clinical Features • Cutaneous leishmaniasis • Condition known as “oriental sore”. • Occurs on face and hands, begins with painless papule  nodular  ulcerates.
  • 5. • Leishmaniasis recidivans (LR): • Granulomatous lesion  after healing of primary sore due to L. tropica • Characterized by scaly, erythematous pappules and nodules, develop in the centre or periphery of a previously healed sore. • Diffuse cutaneou leishmaniasis • Caused by L. aethiopica • Characterized by lack of CMI response to parasite  widespread of CL • May be confused with lepromatous leprosy (LL) • Due to low CMI, montenegro test is negative
  • 6. • Microscopy:- Amastigote form detected from active lesion and touch preparation • Culture • Aspiration from the ulcers  NNN medium and Schneider’s Drosophila medium  for isolation of promastigote forms • Montenegro test • Positive leishmanin skin test  delayed hypersensitivity, • Negative  diffused CL
  • 7. • Caused by • Leishmania leishmania (L.L.) mexicana complex • LL brziliensis complex • LL chagasi • Vector: Lutzomyia species • Reservoir of infection: Dogs, foxes (Zoonotic) • Amastigote form  R.E. cells of skin and mucous membrane Leishmaina mexicana complex • Causes CL and DCL • Chiclero ulcer • Specific form of CL • Also called bay sore • Characterized by persistent ulceration in pinna.
  • 8. Leishmania viannia braziliensis complex • Causes CL, similar to oriental sore but more severe, also cause MCL • Infects mucus membrane of nose, oral cavity, pharynx or larynx • Ulcerative lesion with erosion of the soft tissue and cartilages  loss of lips, soft part of nose and soft palate (FIG) • Gradually nasal septum destroyed  nasal collapse • Lab diagnosis is same as Old world CL.
  • 9. Loa Loa • Causes infection of subcutaneous tissue and eyes • Life Cycle • Similar to W. bancrofti • Clinical Feature • Calabar swellings (repeated episodes of itchy swellings of the body ) • Common form of loiasis. • Also called fugitive swelling • Swelling developing on extremities (knee or wrist)
  • 10. • Ocular manifestations • Conjunctival granuloma • Edema of eye lid  proptosis (bulging) • Complications • Meningoencephalitis  occurs in DEC treated patients with higher microfilaremia. • Nephropathy • Cardiomyopathy
  • 11. • PBS • Characteristics microfilarae. • Blood collected at day time 10am to 3pm • PCR • Ab detection
  • 12. • Causative agent of “river blindness”  endemic in west africa, south & central America • Dermatitis • Onchocercoma :- formation of subcutaneous nodules, tend to develop on head, neck and shoulders • Ocular lesion:- bilateral blindness (river blindness), photophobia, keratitis • Lymphadeonopathy
  • 13. • Also called as Guinea worm disease or dracunculiasis. Life Cycle • Definitive host Man • Intermediate host  Cyclops • Mode of transmission • Drinking water from stagnant pools containing minute fresh water crustaceans (Cyclops) infected with 3rd stage L3 larvae (infective form)
  • 14.
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  • 17. • Sign and symptoms appear approximately 1 year after the infection when gravid adult female worm emerges near the surface of the skin. • Characterized by painful blister  female worm emerges  local erythema, fever, nausea and pruritus. • Most common sites  lower leg, ankle and foot • Secondary bacterial infections may occur at the blister site.
  • 18. • Detection of adult worm  blisters and X-ray for calcified worms in deeper tissues • Detection of L1 larvae • When ulcerated leg  placed in container with cold water  large no. of motile larvae discharged  which can be examined under microscope. • Ab detection • PBS  Eosinophilia
  • 19. • Trichinella spirallis causes trichinellosis. • Is a zoonotic infection from domestic pigs or other carnivores. • Life Cycle • MOT by ingestion of raw or uncooked pork containing infective form L1 larvae. 100-300 larvae req to initiate infection.
  • 20.
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  • 22.
  • 23. • Clinical symptoms depends up on the phase of parasitic invasion. • Intestinal stage: • Mostly asymptomatic • Heavy load of parasite  watery diarrhoea  during 1st week after infection • Larval Migration (2nd week) • Periorbital and facial edema is common • Hemorrhages in the subconjuctiva, retina and nail beds (splinter hemorrhages) • Maculopapular rash • Migration to heart, CNS and Lungs may occur but rare
  • 24. • Muscle encystment • Occurs 2-3 week after infection • Common symptoms are myositis with myalgia, muscle edema and weakness. • Extraocular muscles most commonly involved, followed by biceps, muslces of jaw, neck, lower back and diaphragm.
  • 25. • Demonstration of larvae in Muscle biopsy obtained from • Gastrocnemius • Deltoid • Biceps • Direct slide technique • Fresh muscle tissue  compressed between glass slides and examined under low power microscope. • Histological Examination • Fresh muscle  digestion by pepsin
  • 26. • Ab detection  IgG Ab • Bachman intradermal test • Prepared from Trichinella larvae  immediate induration & erythema • Becomes positive in 2-3 weeks of infection and persist for life. • Can not differentiate past and present infection. • Other tests • Blood tests • Eosinophilia • Elevated muscle enzymes  serum creatinine • X-ray  calcified muscle cyst.
  • 27. • CLM  skin lesions  produced by nematodes of lower animals  infect man accidently. • Agents • Mainly by nonhuman hookworm species (A. brasiliensis, A. caninum and A. ceylanicum) • Rarely by strongyloides stercoralis, Ancylostoma duodenale and Nector americanus. • In lower animals: nematodes inf lower animals  larvae into various organs (intestine) develop in adult worms  lay eggs  cycle continues • In humans: larvae of lower animal nematodes  accidently infect man  not able to complete normal development (because of unsulal host for them)  life cycle get arrested larvae wander  skin & subcutaneous tissue producing a condition  called cutaneous larva migrans (CLM) or creeping eruption. • Another form of larvae migrans occurs called as “visceral larva migrans”  life cycle arrested when larvae migrate to various
  • 28. • Clinical Features • Ground itch:- Pruritic maculopapular dermatitis and rashes (ground itch) at the site of skin penetration of hookworm larvae. • Larva currens:- Migrating strongyloides larvae produce the pathognomic serpiginous urticarial rash called as larva currens near the legs. • Lab Diagnosis • Larvae are usually not detected in skin biopsy. • PCR • Elevated Eosinophilia in PBS or sputum. • Charcot-leyden crystals in sputum may be seen.
  • 29. • Cutaneous amoebiasis • Acanthmoeba skin lesions • Trypanosoma chancre • Chagoma • Muscular sarcocystosis • Cysticercosis • Sparganosis • Cercarial dermatitis • Cutaneous paragonimiasis