Parasites Involved In Eye Infections PDF

Parasites involved in eye infections Department of Medical Microbiology T: +27(0)51 401 9111 | [email protected] | www.ufs.ac.za Objectives / Outcomes By the end of the lecture, the learner should be able to: Describe general features and classify protozoa, helminths and ectoparasites Describe the gene...

Parasites involved in eye infections Department of Medical Microbiology T: +27(0)51 401 9111 | [email protected] | www.ufs.ac.za Objectives / Outcomes By the end of the lecture, the learner should be able to: Describe general features and classify protozoa, helminths and ectoparasites Describe the general characteristics, life cycle, diseases caused and laboratory diagnosis of the following parasites: Toxoplasma gondii Acanthamoeba Onchocerca volvulus Toxocara canis Loa loa Lecture outline Definitions and terminology in Parasitology Modes of transmission of parasites Protozoa General characteristics Classification Examples of Protozoa: Toxoplasmosis Acanthamoebiasis Lecture outline Helminths General characteristics Classification Examples of Helminths: Onchocerciasis Toxocariasis Loiasis Ectoparasites Demodicosis Definitions and terminology in Parasitology Definitions and terminology in Parasitology Parasite: living organism which takes its nourishment and other needs from a host includes: Protozoa Metazoa (which includes Helminths and Ectoparasites) Parasitology: study of Protozoa & Metazoa – causing human disease Host: is an organism which supports the parasite 6 Definitions and terminology in Parasitology Reservoir: other animals that harbour some parasitic life stage Life cycle Simple – human to human transmission Complex – sexual & asexual stages involving 2 or more hosts Hosts then infect humans & other species Intermediate host – no sexual stage in host Definitive host – has sexual stage of life cycle in host 7 Modes of transmission of parasites Modes of transmission of parasites Faecal oral – e.g. Toxocariasis Penetration of mucous membranes and skin e.g. Acanthamoebiasis Sexually – e.g. Trichomonas vaginalis Vertical transmission – e.g. Toxoplasmosis Vector transmission – e.g. Simulium blackflies that causes Onchocerciasis 9 Protozoa Protozoa – general characteristics Diverse group of unicellular, eukaryotic organisms Most Protozoa divide by binary fission, but some have complex sexual and asexual lifecycles Only a few are pathogenic to humans that parasitize: Intestinal tract Urogenital tract Blood cells and tissues Protozoa – general characteristics Many intestinal protozoa develop cysts that are resistant to drying, cold and other environmental stresses Some protozoa have specialised structures Giardia – sucking discs Balantidium – mouth-like cytostome Classification of protozoa Protozoa can be classified by either the mode of locomotion or the site of the infection Classification according to mode of locomotion: Amoeba – Move by extending cytoplasmic projections Acanthamoebiasis Flagellates – Move by flagella Ciliates – Move by hair like cilia Sporozoa – Generally have non-motile adult forms Toxoplasmosis Di Reproduction of Protozoa Amoebae – binary fission of trophozoite or formation of trophozoites within multinucleate cyst Flagellates – binary fission Ciliates – binary fission Sporozoa & coccidia & microsporidia – complex asexual & sexual life cycles 15 Pathogenicity of Protozoa Not well understood Several surface attachment mechanisms (Giardia) Few known cytotoxins, e.g. Entamoeba histolytica (“tissue lysis”) Avoid host defences by several mechanisms Trypanosomes alter surface antigens which makes antibody formation/vaccine development difficult Leishmania produce superoxide dismutase that protects them from macrophage superoxide that allows them to survive within macrophages 16 Toxoplasmosis General characteristics of Toxoplasmosis Protozoa – one of the Sporozoa Caused by Toxoplasma gondii Cats are the definitive hosts Humans, birds and rodents are intermediate hosts Acquired by ingestion and trans-placental transmission Human infection is common, occurring worldwide, usually acquired from cats Toxoplasmosis Lifecycle Clinical manifestations of Toxoplasmosis Ocular manifestations Hallmark of ocular toxoplasmosis is necrotizing choroidoretinitis 75-80% of congenital toxoplasmosis bilateral in 85% of cases only 1-3% of patients with acquired infection believed to develop ocular toxoplasmosis Optic neuritis or papillitis associated with oedema, often called Jensen disease Clinical manifestations of Toxoplasmosis Non-ocular manifestations 80-90% of patients are asymptomatic Flu-like symptoms with lymphadenopathy Central nervous system – encephalitis, meningitis and mass lesions Myocarditis Pneumonitis Laboratory diagnosis of Toxoplasmosis Specimens Blood Ocular fluid Tissue Laboratory diagnosis of Toxoplasmosis Tests Indirect Serology: IgG and IgM antibodies against Toxoplasmosis can be used to confirm exposure Direct Microscopy: direct observation of Tachyzoites on hematoxylin and eosin stain Molecular techniques: Polymerase chain reaction Management of Toxoplasmosis Most healthy people recover without treatment Symptomatic individuals are treated with Co-trimoxazole Ocular toxoplasmosis treatment depends on: the size of the eye lesion the location characteristics of the lesion (acute active, versus chronic not progressing) Acanthamoebiasis General characteristics of Acanthamoebiasis Protozoa – one of the Amoebae It is caused by Acanthamoeba species They are ubiquitous free-living organisms commonly found in soil, water, sewage, ventilating and air conditioning systems Acanthamoeba exists in two forms: Active infective form: trophozoites Dormant form: hardy cyst Trophozoites produces enzymes which enable tissue penetration and destruction Able to survive in adverse environmental conditions as cysts Acanthamoebiasis Lifecycle Pathogenesis of Acanthamoeba keratitis Acanthamoeba invade the cornea though physical opening, e.g. minor abrasions in the corneal epithelium Contact lens wear facilitate direct inoculation into the eye Upon binding to glycoproteins in the corneal epithelium, Ancathamoeba secrete cytolytic proteins and proteases that facilitate penetration IgA proteases – degrade IgA that normally protect corneal epithelial cells Clinical manifestations of Acanthamoebiasis Ocular manifestations Keratitis most common manifest Acanthamoeba keratitis is a rare, potentially blinding infection 85% occur in contact lenses wearers Clinical manifestations of Acanthamoebiasis Risk risk factors for Acanthamoeba keratitis: Wearing contact lenses for long periods of time Use of nonsterile tap water in preparation of contact lens solutions is a well-recognized route of acquisition Contaminated commercial contact lens solutions have been associated with transmission Use of recalled contact lens solutions Daily use of soft contact lenses Use of all-in-one (also call multi-purpose) lens solutions Swimming, using a hot tub, or showering while wearing lenses Improper storing , handling and disinfecting lenses Previous corneal trauma Clinical manifestations of Acanthamoebiasis Non-Ocular manifestations Granulomatous amebic encephalitis (GAE) – subacute diffuse meningoencephalitis Skin infections – ulcers, nodules, or subcutaneous abscesses Sinusitis, pneumonitis, or a combination Other unusual manifestations of Acanthamoeba infections have included osteomyelitis, adrenalitis, and vasculitis Laboratory diagnosis of Acanthamoeba keratitis Specimens Corneal scrapings Tissue Contact lenses Saline solution Laboratory diagnosis of Acanthamoeba keratitis Tests Microscopy Stain corneal scrapings with calcofluor white (stains cyst walls) and examine specimen with fluorescent microscopy Detection of trophozoites and cysts on histopathology Corneal Culture Put scraping of the cornea onto lawn of E. coli – tracks in agar as the organism moves over agar Buffered charcoal yeast extract Molecular methods Polymerase chain reaction – most sensitive Management of Acanthamoeba keratitis Early diagnosis is essential for effective treatment Difficult to treat due to the resilient nature of cyst Therapy with topical cationic antiseptics Pain control Keratoplasty may restore visual acuity Steroid use is controversial Prevention: proper care of contact lens Helminths Helminths (Worms) – General characteristics Metazoa Diverse group of Multicellular, eukaryotic organisms Transmission Ingesting the ova or larvae Direct larval penetration of the skin Adult forms do not multiply in the human body; therefore, the number of adult worms present is related to the number of eggs or larvae ingested Adult forms usually visible with the naked eye 36 Helminths (Worms) – General characteristics Pathologic consequences and severity of infection are related to the number of adults present, commonly referred to as the worm burden Patients with only a few adult worms are usually asymptomatic, whereas a patient with a large number of adults shows clinical symptoms Most of the parasites inhabit the intestinal tract, but species also infect the liver, lungs, lymphatics, and blood vessels Different species have preferred site of infestation where they generally cause minimal damage These disseminate to vital organs and cause severe damage 37 Classification of Helminths (Worms) Belong to one of three groups: Nematodes (Roundworms) Onchocerciasis Toxocariasis Loiasis Cestodes (Tapeworms) Trematodes (Flukes) Onchocerciasis General characteristics of Onchocerciasis Helminth – one of the Nematodes (Round worms) Caused by Onchocerca volvulus Transmitted by vector, Simulium blackflies Cause of “River blindness” - the vector breeds in rapidly flowing streams and infection can cause blindness Onchocercal infections are found in tropical climates General characteristics of Onchocerciasis Risk factors for Onchocerciasis: >95% of infections occur in Sub Saharan Africa People living near streams or rivers where blackflies breed Blackflies are found mainly in rural agricultural areas in Africa Usually, many bites are needed before being infected, so people who travel for short periods to endemic areas have low risk Onchocerciasis Lifecycle Pathogenesis of Onchocerciasis Most symptoms of onchocerciasis are caused by the body’s response to dead or dying larvae Some people do not experience symptoms while infected Clinical manifestations of Onchocerciasis Ocular manifestations Punctate keratitis Relatively common acute, transient finding. White cell infiltrates form around dead microfilariae in the cornea, causing "snowflake opacities," especially at the three and nine o'clock positions Punctate keratitis is reversible Sclerosing keratitis Chronic full-thickness fibrovascular change of the cornea and occurs in the setting of longstanding infection, particularly in Savanna regions These changes start typically at the three and nine o'clock positions and can extend across the entire cornea Clinical manifestations of Onchocerciasis Ocular manifestations continued Uveitis - In the setting of onchocerciasis typically presents with flare in the absence of an accompanying cell infiltrate Optic atrophy - Optic atrophy is a relatively chronic finding; optic disc pallor can occur following an episode of optic neuritis Onchochorioretinitis Common chronic finding The first layer damaged is the retinal pigment epithelium, and this is most frequently found just temporal to the macula. Subsequently, more extensive loss of the retinal pigment epithelium occurs with retinal death and atrophy and loss of the underlying choroid Clinical manifestations of Onchocerciasis Non-Ocular manifestations Subcutaneous nodules - typically appear over bony prominences Skin disease – Dermatitis and depigmentation Systemic disease - generalized musculoskeletal complaints, backache, and joint pains were more frequent in infected than uninfected individuals Laboratory diagnosis of Onchocerciasis Specimens Corneoscleral punch biopsy Tears –antigen testing Skin snips Urine Laboratory diagnosis of Onchocerciasis Tests Microscopy Demonstration of the microfilariae skin snip biopsy from iliac crest, scapula and lower extremities Incubate in normal saline at room temperature for 24 hrs to allow microfilariae to emerge H&E stain may be required for species identification, particularly in areas where other filarial species are also endemic Molecular – Polymerase chain reaction of the skin snip to detect DNA Laboratory diagnosis of Onchocerciasis Tests Serology - Not uniformly reliable. In addition, the prevalence of positive serology among non-endemic adults returned from endemic areas is extremely high in the absence of active infection and can remain positive for many years Antigen tests – May be more useful than antibody detection assays for the diagnosis of individual infections and for monitoring the success of therapy, since they are positive only in individuals with active infection Management of Onchocerciasis The recommended treatment is Ivermectin Ivermectin kills the larvae and prevents them from causing damage but it does not kill the adults Toxocariasis General characteristics of Toxocariasis Helminth – one of the Nematodes (Roundworm) Caused by Toxocara canis and Toxocara catis Zoonotic infection found in the intestines of dogs or cats Toxocara canis (dog roundworm) Toxocara catis (cat roundworm) Geographic range: Worldwide Definitive Host: Dogs and cats Intermediate Host: None Humans and other mammals are accidental hosts General characteristics of Toxocariasis Risk factors include: People living in hot , humid regions where eggs are kept viable in the soil Dog or cat owners are more like to be infected however, infection is often acquired in settings outside of the home (such as in public parks and playgrounds Children are more likely to be infected - especially those with exposure to playgrounds and sandboxes contaminated by dog or cat faeces Eating undercooked meat/viscera of infected paratenic hosts rabbit, chicken, cattle, or pigs Toxocariasis Lifecycle Pathogenesis of Toxocariasis The pathologic manifestations result from inflammation caused by the immune response directed against the excretorysecretory antigens of larvae Clinical manifestations of Toxocariasis Ocular manifestations Ocular larva migrans (OLM) Toxocara canis > Toxocara catis Occurs most commonly among older children and adolescents median patient age was 8.5 years The ocular lesion is due to larval localization in the eye and the granulomatous response around the larva with scar formation Common symptoms are unilateral visual impairment, causing failing vision and subsequent strabismus Clinical manifestations of Toxocariasis Ocular manifestations Ocular larva migrans (OLM) The typical lesion is a whitish elevated granuloma Occasionally, OLM may present as uveitis (often intermediate and posterior uveitis), papillitis, or endophthalmitis Ocular lesions may resemble retinoblastoma The most serious consequence of infection is invasion of the retina with granuloma formation in the periphery or posterior pole, leading to dragging of the retina and eventual retinal detachment, which can lead to blindness Clinical manifestations of Toxocariasis Non-Ocular manifestations Visceral larva migrans Liver – Hepatitis with/without hepatomegaly Peripheral nervous system - radiculitis, affection of cranial nerves Lungs – Pneumonitis Heart – Myocarditis, pericarditis and endocarditis Central nervous system – Meningoencephalitis, spaceoccupying lesions, myelitis, and cerebral vasculitis causing seizures Muscles Other Skin manifestations - Urticaria Laboratory diagnosis of Toxocariasis Specimen Serum for serology Aqueous fluid Vitreous fluid Tissue Laboratory diagnosis of Toxocariasis Tests Serology Detection of specific antibodies to Toxocara antigen Result must be interpreted in the setting of compatible clinical symptoms and epidemiologic exposure Cross-reactivity of the ELISA assay with other parasite antigens is common, and the test may remain positive for several years even following treatment Positive ELISA result does not necessarily demonstrate the presence of active Toxocara infection or prove that clinical symptoms are attributable to Toxocariasis Histology - encapsulated larvae can be found in the liver, lung, brain, and/or enucleated eye Molecular – Polymerase chain reaction – not available commercially Management of Toxocariasis Treatment is generally based on clinical experience and expert opinion Ocular Toxocariasis Difficult to treat and consists of measures to prevent further damage Aggressive anti-inflammatory therapy with together with Albendazole is warranted for two to four weeks In complicated cases, surgical intervention may be warranted Visceral Toxocariasis Use anti-parasitic drugs in combination with anti-inflammatory medications Management of Toxocariasis Prevention: Treat dogs and cats regularly for worms Good hygiene practices when handling animals Don’t let children play in areas dogs are allowed to defecate Loiasis General characteristics of Loiasis Helminth – one of the Nematodes (Roundworm) Caused by Loa loa Vector is Chrysops fly (deerfly) Loa is endemic in West and Central Africa Microfilariae are produced 6 months after the bite and can persist for 17 years Adult worm can migrate through subcutaneous tissues, muscles and to the eye Loiasis Lifecycle Pathogenesis of Loiasis Host’s immune response to this migration causes many of the characteristic symptoms of Loiasis Clinical manifestations of Loiasis Ocular The adult worm migrates to the eye and crawls beneath the conjunctiva, causing transient conjunctivitis and oedema The worm may be visualized directly as it crosses the conjunctiva, which usually takes 10 to 20 minutes – definitive diagnosis Symptoms resolve spontaneously after the worm has left the eye, and usually there are no sequelae Rarely, adult worms invade the eye causing pain and intraocular inflammation Clinical manifestations of Loiasis Non-ocular Central nervous system – Encephalitis Cardiomyopathy due to Endomyocardial fibrosis Nephropathy Other: can migrate to any subcutaneous site, occasionally resulting in arthritis or lymphadenitis. Entrapment neuropathy related to inflammation and angioedema involving peripheral nerves may also be observed Laboratory diagnosis of Loiasis Specimens Blood for serology Definitive diagnosis can also be made by the pathologist reviewing the morphology of the worms recovered from tissue or the eye Laboratory diagnosis of Loiasis Tests Microscopy Peripheral blood smear (Thick and thin smear) Serology Antibodies against Loa loa are most useful for diagnosis of Loiasis among travellers and expatriates In endemic populations, serology is generally not useful since antibodies remain positive for prolonged periods following infection and thus cannot distinguish between active or prior infections or quantitate microfilaremia. However, a negative result can exclude the possibility of L. loa infection Laboratory diagnosis of Loiasis Tests Antigen testing Molecular Polymerase chain reaction Loop-mediated isothermal amplification Management of Loiasis Diethylcarbamazine – effective against adult worms and microfilariae Corticosteroids – to prevent severe allergic reaction Surgical removal Educations – regarding infection and its vector for people entering endemic areas Ectoparasites Ectoparasites Parasites that live on rather than in host One of the Metazoa Include animals varying in size and shape Falls under Phylum – Arthropoda Important Classes Insecta Fleas, flies, lice, mosquitoes and true bugs Arachnida Mites, ticks Including Demodicosis Demodicosis General characteristics of Demodicosis Arachnida Tiny mites that live on the hair follicle Found in facial skin especially eyelashes, forehead cheeks Genus: Demodex Two species typically found on humans: D. folliculorum D. brevis General characteristics of Demodicosis Up to 80 to 90% of humans may harbour the Demodex organism Demodex infestation usually remains asymptomatic and may have a pathogenic role only when present in high densities and also because of immunosuppression More common in the elderly Mode of transmission Direct contact with infested eyebrows, and sebaceous glands Clinical manifestations of Demodicosis Ocular Blepharitis Eyelid dermatitis Loss of lashes Non-ocular Rosacea-like inflammatory papules and pustules on the face Nodulocystic and conglobate (abscess-like) presentations on face Laboratory diagnosis of Demodicosis Specimens Skin scrapings Skin biopsy Diagnosis Microscopy – KOH preparation Clinical correlation is necessary for the interpretation of the KOH preparation because Demodex mites can be detected in normal skin and a definitive threshold for diagnosis has not been established Management of Demodicosis Topical Scrub with Mercury oxide Topical Permethrin 5% cream Topical sulphur Alcohol and tea tree oil Oral Oral Ivermectin, and oral Metronidazole are reasonable treatments for Demodex folliculitis