Blood-and-Tissue-Nematode-new-to-post-updated.pptx

Toxocara spp. common ascarid roundworms of mammals. infection more commonly found in children than adults Primarily soil transmitted Toxocara spp. T. canis (presumed most common) cat roundworm T. cati (frequency not known). visceral larva migrans (VLM) and ocular larva migrans...

Toxocara spp. common ascarid roundworms of mammals. infection more commonly found in children than adults Primarily soil transmitted Toxocara spp. T. canis (presumed most common) cat roundworm T. cati (frequency not known). visceral larva migrans (VLM) and ocular larva migrans (OLM), covert toxocariasis (coTOX) Most infections are asymptomatic Humans are accidental hosts Life Cycle Patholog y Visceral Toxocariasis (Visceral Larval Larvae in liver Larvae in lungs Migrans) Migration and death of the larva in tissues causes an eosinophilic granuloma causing T. canis larva a variety of Hatching Larva Patholog y Visceral Toxocariasis (Visceral Larval Migrans) Migration and death of the larva in tissues causes an eosinophilic granuloma causing a variety of symptoms The liver, lungs, CNS and eyes are the most sensitive Wheezing is a common sign of VLM along with other lower respiratory symptoms May progress to eosinophilic Patholog y Visceral Toxocariasis (Visceral Larval Migrans) Usually associated with liver enlargement and necrosis. The heart may be affected causing myocarditis Patholog y Ocular Larval Migrans (OLM) May cause diffuse unilateral subacute neuroretinitis (DUSN) The most serious consequence is the invasion of the retina. May be the sole manifestation of toxocariasis Must be differentiated with Retinoblastoma. Patholog y CoTox (Covert Toxocariasis) May be asymptomatic Signs and symptoms are less specific Eosinophilia is seldom present coughing, wheezing, chronic or recurrent abdominal pain, hepatomegaly, sleep disturbances, headache, Patholog y Neural Toxocariasis (Neural Larval Migrans) Uncommon; may cause eosinophilic meningoencephalitis. Many are acquired food borne. Seizures and coma. Diagnosi s Definitive – biopsy (time consuming and difficult to perform Clinical and serologic Test TES – ELISA test wherein Toxocara excretory-secretory antigens are used to detect IgG antibodies Western Blot – more specific but cannot differentiate new and old infections Identification of the presence of typical clinical signs of OLM and VLM History of exposure to cats and dogs. Imaging (MRI) PCR Treatment albendazole or mebendazole, usually in combination with anti-inflammatory (steroids) medications. Diethylcarbamazine was found effective but had a lot of side effects so it is rarely used. Most patients recover without treatment, but if neurological/lung cardiac complications, anthelminthic treatment is mandatory. Dracunculus medinensis Dracunculiasis “Guinea worm disease” “Fiery serpent of the Israelites” Transmission is seasonal Animals can also be hosts (dogs) Usually grouped with filarial worms, but is not a true filarial disease. Epidemiology GWD only occurs in the poorest 10% of the world’s population who have no access to safe drinking water or health care. Therefore, GWD is both a disease of poverty and a cause of poverty. Prevalent in some places in Africa Endemic in West, Central, and East Africa Seasonal transmission (wet-dry, dry-wet) Pathogenesis and Clinical Manifestations Slight fever Itchy rash Nausea Vomiting Diarrhea Dizziness  (+) Blister, burning pain Ruptures after, exposing the worm to water Complications Redness and swelling of the skin (cellulitis) Boils (abscesses) Generalized infection (sepsis) Joint infections (septic arthritis) that can cause the joints to lock and deform (contractures) Lock jaw (tetanus) Physical Disability (sometimes permanent)  Management and Treatment No specific drug or vaccine Infected individual must NOT enter drinking water sources Wound cleaning Rinse with water may alleviate symptoms, and make worm removal easy Topical antibiotics Prevention Surveillance and Case containment Safe drinking water sources Drinking water treatment (Vector control) Water filters → Fine-mesh cloth filters are given to households to strain out copepods (tiny “water fleas” too small to be clearly seen without a magnifying glass) from contaminated drinking water where there are no safe water supplies. Health Education  (Angiostrongylus) Parastrongylus cantonensis COMMON NAME: RAT LUNGWORM NATURAL HOST/ Definitive Host: RATS Intermediate host: Mollusks- Snail Pila luzonica (Kuhol) Brotia asperata (Suso) ACCIDENTAL HOST: Man MODE OF TRANSMISSION: Ingestion of INTERMEDIATE HOST by man containing the infective larvae  Parastrongylus cantonensis ➔ ADULT MALE: 16 to 22 mm in length and 0.25 to 0.35 mm in diameter → Well developed caudal bursa FEMALE: 19 to 33 mm in length and 0.28 to 0.50 mm in diameter. → Have uterine tubules that would spirally around the intestine. P. Cantonensis Adult  Parastrongylus cantonensis ➔ PATHOLOGY AND SYMPTOMS - Eosinophilia and symptoms of meningitis - May be fatal if left untreated - chief complaint in many cases is acute, severe, intermittent occipital or bitemporal headache. - stiffness of nech, paresthesia, vomiting, nausea, blurred vision/diplopia, body pain, fatigue - neurologic symptoms are also present - coma - intraocular hemorrhage and retinal detachment  Parastrongylus cantonensis ➔ Laboratory - Eosinophilia in CSF - Charcot-Leyden Crystals ➔ Prognosis and Treatment - Usually good - Infection is self-limited - No effective treatment (mebendazole and albendazole) - Surgical removal for ocular - Pain relievers - Steroids (Prednisone) for Cranial Nerve Involvement  Parastrongylus cantonensis ➔ Diagnosis - Difficult - Presumptive diagnosis (clinical, imaging, serology) - rule out other CNS infections - imaging - PCR - CT scan is usually unremarkable (differentiate it from neurocysticercosis) ➔ Prevention - proper eating habits and safe food preparation - discourage eating raw or poorly cooked mollusks or unwashed vegetables - Molluscicides (iron phosphate/metaldehyde)  Cutaneous Larval Migrans Caused by hookworm of cats and dogs Ancylostoma braziliense Ancylostoma caninum “Creeping Eruption”  Parasite Toxocara Toxocara Ancylostom Ancylostom canis cati a a caninum braziliense Common Dog Ascaris Cat Ascaris Cat Dog name hookworm hookworm MOT Ingestion of embryonated Skin penetration by filarial eggs larvae Clinical Visceral or ocular larva Cutaneous larva migrans or Manifestatio migrans CREEPING ERUPTION n Diagnostic EIA (enzyme immunoassay) –antibody testing technique Dirofilaria immitis COMMON NAME: DOG HEARTWORM Very common filarial parasite of Dogs In man = causes COIN LESION in the LUNGS 2 syndromes in man: Ocular/Subutaneous and Pulmonary VECTOR-BORNE Dirofilaria immitis COMMON NAME: DOG HEARTWORM Very common filarial parasite of Dogs In man = causes COIN LESION in the LUNGS 2 syndromes in man: Ocular/Subutaneous and Pulmonary VECTOR-BORNE  Anisakis spp. COMMON NAME: HERRING’S WORM Fish and Marine mammal roundworms Common in JAPAN Definitive host: Whales/Dolphins 1st Intermediate host: Copepods 2nd Intermediate host: Smaller fishes 3rd Intermediate Host: Larger fishes (Salmon) Mode of Transmission: Ingestion of raw fish infected with larvae. → SYMPTOMS AND PATHOLOGY Abdominal pain and granuloma around migrating larva in intestinal wall. BLOOD AND TISSUE DWELLING NEMATODES PPT originally by: Oliver C. Rayos, RMT Edited and Presented by: Robert Ubando Manansala III, RMT, MD  Filarial Parasites Slender, filiform, creamy white worms Range from 2 to 50 cm. long (adult) Females are 2x the size of males Arthropod transmitted Affect the circulatory, lymphatic and muscular systems, connective tissues and serous cavities  Lymphatic filariasis – Wuchereria bancrofti, – Brugia malayi – Brugia timori Subcutaneous filariasis – – Loa loa – Mansonella streptocerca – Onchocerca volvulus. Serous cavity filariasis – Mansonella spp. Wuchereria bancrofti Brugiya malayi Bancroftian filariasis, wuchereriasis Adult worms are located in the lymphatics Microfilaria  found in blood Sheathed microfilaria Nocturnal periodicity is very distinct More common form of filariasis in the Philippines Concentration procedures may be necessary Wuchereria bancrofti Lymphatic Filariasis wide spectrum of clinical manifestations, with signs and symptoms different from one host to another. Acquired in childhood, manifests later Chronic LF → wide spectrum of clinical manifestations, with signs and symptoms different from one host to another. Probably due to defective transport of lymphatic fluid → Wuchereria bancrofti Hydrocele/chylocele results in the obstruction of the lymphatics of the tunica vaginalis Wuchereria bancrofti has a tropism in scrotal lymphatics Brugiya malayi Causative agent of malayan filariasis Adult and microfilaria closely resembles that of W. bancrofti Nocturnal periodicity is less distinct Rupture of lymphatics in the kidney may produce chyluria. B. malayi  MICROFILARIA DIFFERENTIATION POSTERIOR ANTERIOR  Life Cycle Adult females are viviparous Microfilariae migrate into the bloodstream and are ingested by mosquitoes during blood meal Microfilariae migrate to the muscles of the mosquito Larvae develop 6 – 20 days and force their way out of the muscles and migrate to the proboscis Developed larvae are transferred to another human host during blood meal Larvae pass to the lymphatic vessels and nodes and mature (6 months or more) Adults frequent the lymph vessels of the lower extremities, groin glands, epididymis or labial glands Mosquito vectors of W. bancrofti Aedes polynesiensis Brush mosquito Day biter, nondomesticated, rural, sylvatic Culex quinquefasciaticus Night biter, domesticated, urban mosquito Vectors of B. malayi Anopheles Aedes (Urban or sub-urban) (brush mosquito)  B. malayi Pistia Mansonia (breeding site of Night biters mansonia)  Epidemiology (W. bancrofti) Tropical and subtropical Africa, Asia, Philippines Correlated with the population density, presence of vector, and poor sanitation  Epidemiology (B. malayi) Sri Lanka, Indonesia, Philippines, China, Korea, Japan and other Asian countries Correlated with the population density, presence of vector, and poor sanitation  Pathology and Symptoms Bancroftian filariasis Malayan filariasis Caused mainly by living, dead and degenerating adult worms Microfilariae cause less pathologic response “Expatriate syndrome” When dead, these organisms may release their endosymbiotic bacteria  Course of Infection Pseudotubercu Adult lar granulomatous The walled degeneratin worms in reaction g worm around the occludes the the lymph trapped adult lymphatics worm Lakes of Dead worm is lymph fluids Lymphatic absorbed and develop in the s become replaced with lymph sinuses and lymph varicose hyalinized or nodes calcified scar tissue  Lymphatic filariasis disease spectrum Asymptomatic microfilariasis acute dermatolymphangioadenitis (ADLA), acute filarial lymphangitis (AFL), lymphedema and elephantiasis genitourinary lesions (e.g., hydrocele) tropical pulmonary eosinophilia (TPE). Lymphedema Elephantiasis Hydrocele Hydrocele Transillumination Test Negative transillumination test - Hernia Vulvar Lymphedema Staging of Elephantiasis Stage 1 – swelling increases during the day but reversible when lying in bed Stage 2 – no longer reversible overnight Stage 3 – shallow skin folds Stage 4 - knobs present in the affected area Stage 5 - deep skin folds, Stage 6 - mossy lesions are present Stage 7 - the patient is unable to adequately or independently perform activities of daily living  Classification of Filarial Infection Signs and symptoms Asymptomatic filariasis Inflammatory filariasis (acute filariasis) Obstructive filariasis (chronic filariasis)  Asymptomatic Filariasis When children are exposed to infection at an early stage Adults exhibit microfilariae in the blood without symptoms Moderate to general enlargement of the lymph nodes during physical examination Blood examination shows numerous microfilariae Adults die and microfilariae disappear without symptoms  Inflammatory Filariasis Immunologic phenomenon caused by sensitization to the product of living and dead adult worms (T-cell mediated responses) Characterized by funiculitis, epididymitis, orchitis, retrograde lymphangitis of extremities, localized swelling and redness of arms and legs May be accompanied by fever, headache, vomiting and malaise Most patients do not have microfilaremia Obstructive Filariasis Elephantiasis End result of filariasis (chronic) Develops slowly usually following years of continuous filarial infection Preceded by chronic edema and repeated inflammatory attacks Cellular reaction and edema are replaced by fibroblastic hyperplasia High protein content of the lymph stimulates the growth of dermal and collagenous connective tissue Over a period of time, the enlarged areas harden ADLA most common acute manifestation of LF localized pain, lymphadenitis and/or lymphangitis and/or cellulitis and local warmth, with or without systemic manifestations of fever, nausea, and vomiting. Similar to those of erysipelas and cellulitis Probably bacterial in origin Chronic Elephantiasis  Enlargement of Genitalia Epi dydimitis Hydrocele  Difference in Pathogenicity Lymphangitis, lymphadenopathy, abcess formation in the inguinal nodes occur more frequently with B. malayi Elephantiasis in B. malayi is generally confined to the distal extremities Involvement of the male genitalia (funiculitis and orchitis) is more common in W. bancrofti Rupture of the lymphatics of the kidney can occur in W. bancrofti resulting in chyluria  Diagnosis Identification of microfilariae in the blood History of exposure to endemic areas Place a drop of blood on a slide and examine under LPO for actively moving microfilariae Recommended time to collect blood: 8pm. – 4am. Best time: 10pm. – 2 am. To determine the species: stain thick or thin blood smear with Wright’s or Giemsa to bring about the differential characteristics W. bancrofti microfilariae may be present in urine  NO MICROFILARIAE IN THE BLOOD DOES NOT ALWAYS MEAN NO INFECTION Approximately 6-12 months may elapse from time of infection until worm matures and produce microfilariae Late in the disease (elephantiasis), adult worms and microfilariae may both have died  Other Diagnostic Methods Knott’s concentration nucleopore Used to detect light infection Slightly more sensitive 1ml. of night blood is laked in Filtration of 1 – 5 ml. of 10ml. of 2% formalin solution heparinized blood through a 5µ Sediment is examined directly of Nucleopore filter or may be dried and stained. The stained filter is placed on a slide and examined  Detection of circulating filarial antigens (CFA) is now the preferred method since it also detects latent infections. – Immunochromatography molecular xenomonitoring of parasites in pools of mosquitoes TREATMENT  Diethylcarbamazime (DEC, Hetrazan) The standard drug for treatment of most filariasis Dosage is 2 mg. per kg t.i.d. for 12 days Clears the blood of microfilariae but is also believed to affect adult worms Has the important disadvantage of producing significant/severe side effects Fever, arthralgia, adenopathy, headache, prostration May be the effect of the sudden death of large number of microfilariae Exact mechanism of side effects still unknown  Ivermectin Found to be almost equally effective as 12 days of DEC in rapid clearance of microfilaremia Unlike DEC, it is given in single dose only 10% to 20% recurrence occurs 3 to 6 months after treatment Has approximately the same side effects as DEC. Mechanical devices can be used to reduce edema Surgery to remove excess connective tissues in elephantiasis give short term benefits but long term complications  Other Albendazole Doxycycline and related antibiotics for Wolbachia For ADLA, – bed rest, cooling the affected area to relieve the pain, analgesics and antipyretics for pain and fever, topical antibiotics and antifungals for superficial bacterial and fungal infections, systemic antibiotics (e.g., penicillin) for moderate to severe cases, elevation of the involved extremity.  Prevention Control of mosquitoes and human sources of infection Spraying of houses with insecticides and larvicides are effective for domesticated mosquitoes only Protection of individual by screened quarters, bed nets, mosquito repellant and protective clothing (educational and economic problem)  Brugiya timori First reported in Timor, 1964 Microfilariae somewhat longer than those of B. malayi The cephalic space has a length-width ratio of approximately 2:1 in B. malayi but 3:1 in B. timori. Anopheles barbirostris – vector Humans are the only definitive host Loa loa “African eye worm” Human loiasis is confined to the rain forest and swamp forest areas of West Africa. It is especially common in Cameroon and on the Ogowe river. Loiasis is caused by the filarial nematode Loa loa which is transmitted to humans by day-biting Chrysops flies migrates actively throughout the subcutaneous tissues of the body More conspicuous and irritating when crossing conjunctiva  differ from the microfilariae of Wuchereria and Brugia in having body nuclei that are continuous to the tip of the tail. Diurnal periodicity Vector is Chrysops fly (Mango fly) The microfilariae development cycle is similar to Wuchereria  Life Cycle Once inside the body the infective larvae develop slowly into a mature adult (the process takes about a year). During this period it lives and moves around the fascial layers of the skin. Loa loa often makes frequent excursions through the subdermal connective tissues. Once they reach maturity (measuring 3-3.4 cm x 0.35-0.43 mm for males and 5.7 x 0.5 mm for females) the adults mate and produce sheathed microfilariae 298 x 7.5 micrometers in size. ctor: Chrysops fly (mango fly)  Pathology and Symptoms Damage is usually caused by migrating worm (rapid) Worm may migrate to the eye and damage the cornea Immune reactions to the worm may cause inflammation called Calabar swelling (also known as fugitive swelling): painful swelling usually in the extremities Recurrent swelling can lead to the formation of cyst like enlargements of the connective tissues around the tendon sheaths. Dying worms can also cause chronic abscesses followed by granulomatous reactions and fibrosis.  Lymphadenitis Edema of conjunctiva and eyelids if worms pass to that area Calabar swelling may appear in other places of the body Loaiasis in ectopic sites – Hydrocele – Orchitis – Colonic obstruction – Membranous glomerulonephritis – Loal encephalitis Loa loa Calabar Swelling  DIAGNOSIS History of Calabar swelling Appearance of worm in conjunctiva Detection of the microfilariae May be found in the blood, urine, sputum, and spinal fluid  Treatment Surgical removal of migrating adult worms DEC (contraindicated if microfilaria counts of >500 per 20 μL Ivermectin  Onchocerca volvulus is found in both the Old and New World but about 95% of all cases are in Africa. transmitted by the bite of Simulium flies – blackfly/buffalo gnat flies; can only breed in well oxygenated water because their larvae have an obligatory aquatic stage during which they require high oxygen tension associated with fast flowing rivers with rapids and onchocerciasis is often referred to as 'river blindness'  Life Cycle The infective larvae of Onchocerca enter the body through the wound made by the bite of its host fly. The larvae then move to the subcutaneous tissues where they become encapsulated nodules and mature into adults in approximately one year After mating the female vivipariously gives birth to microfilariae 300 mm in length and 0.8 mm in diameter. The microfilariae are sheathless with sharply pointed recurved tails. The microfilariae can be found free in the fluid within the nodules and in the dermal layers of the skin spreading centrifugally from the area where an adult lies. (onchcercoma) Microfilariae also can be found in the blood and eye during heavy infections. They infect their fly vectors while the flies are feeding on the human host and mature into stage three infective larvae in the flies' flight muscles Life Cycle O. volvulus in tissues  Pathogenesis and Symptoms Raised nodules under the skin around areas over bony prominence. (Onchocerchomata) – The larvae are immobilized in these locations (while the host is sleeping) In the skin there is destruction of the elastic tissues and the formation of redundant folds. Loss of pigmentation and the histological appearance of advance cases often resemble the skin of very old normal subjects Manifestations may differ in different places  mal morado or erisipela de la costa – Term in Western Hemisphere of onchodermatitis with patchy purplish or reddish eruption that characterizes acute attacks “Leopard Skin” in African patients - atrophy of the skin and subcutaneous lymphedema are also seen, along with depigmentation “Craw-craw” - papular to pustular nodules up to 1 cm in diameter, caused by inflammatory reactions to localized collections of microfilariae in the skin. “Leopard skin” craw-craw  River Blindness The microfilariae can also enter the eye They pass along the sheaths of the ciliary vessels and nerves from under the bulbar conjunctiva directly into the cornea, via the nutrient vessels into the optic nerve, and via the posterior perforating ciliary vessels into the choroid. Dead microfilariae in the eye lead to an inflammatory immune response and the eventual formation of secondary cataracts and ocular lesions  Infammatory Reactions The microfilariae can also cause inflammation of regional lymph glands. This inflammation along with the loss of tissue elasticity can lead to protruding lymph glands enfolded in pockets of skin. This condition is especially prominent in the areas around the scrotum (often called the 'hanging groin' effect) and in severe cases is classified as minor elephantiasis  Onchocercaiasis Raised nodules Hanging groin River Blindness  Diagnosis Skin snips – To be discussed in lab – Usually snipped in bottocks – 6 different sites Biopsy (therapeutic)  DEC Mazzotti reaction – Symptom complex after treatment of DEC – fever, urticaria, swollen and tender lymph nodes, tachycardia, hypotension, arthralgias, oedema, and abdominal pain that occur within seven days of treatment of microfilariasis. – Usually correlates to intensity of infection (Mazzotti Test) Ivermectin microfilaricidal effect = more slowly  Mansonella Ivermectin – kills only IMMATURE worms Doxycycline for Wolbachia  Mansonella ozzardi Only filarial worm parasitizing humans in South America Adult worms are found in the mesenteries and visceral fats Microfilaria are found in the blood and sometimes in the capillaries and intravascular spaces of the skin Usually asymptomatic May cause adenopathy, pruritic and maculopapular skin lesions, arthritis, fever, and marked eosinophilia Cullicoides, Simulium fly may also become a vector  Nuclei of the body of the microfilariae do not extend to the tip of the tail as in M. streptocerca, and the tail is shorter and less tapered than that of Onchocerca volvulus, the other microfilariae that may be found in skin biopsies.  Mansonella streptocerca Formerly Dipetalonema Infects both humans and monkeys in Africa (Congo) Microfilariae are found primarily in the skin, sometimes in the blood Posterior end of microfilaria resembles a shepherd’s crook Causes pruritic dermatitis with hypopigmented macules ans inguinal adenopathy Nuclei extend to the tip of the tail, which is characteristically bent in the form of a shepherd’s crook. Cullicoides  Mansonella perstans Common parasite of humans and apes in Africa May also be found in Latin and South America Adult worms are found in deep connective tissues Microfilariae are found in the blood, and in the skin Periodicity is not exhibited  Mansonelliasis perstans Majority of infections are benign May cause Calabar-like swellings, pruritis, hives, fever, and headache Causes Ugandan or Kampala eye worm condition when adult worms invade the conjunctiva and periorbital connective tissue Mansonella perstans microfilaria  Treatment DEC, Ivermectin (for M.streptocerca only) Asympomatic = no treatment Mebendazole, albendazone for M.perstans Summary  References Diagnostic Parasitology – Belizario Markell and Voge’s Medical Parasitology Harrison’s Internal Medicine 21th Edition CDC Robbin and Cotrans Pathology Vaughan and Ausbury Ophthalmology SECRET BOOK