HELMINTH PRELIM NOTES.pdf

Parasitology Prelim Lecture No. 1 : Introduction to Parasitology Facts which provide a better understanding of the biology of a parasite, its pathogenic effects and control measures against it. Study of the phenomenon of par...

Parasitology Prelim Lecture No. 1 : Introduction to Parasitology Facts which provide a better understanding of the biology of a parasite, its pathogenic effects and control measures against it. Study of the phenomenon of parasitism Harmful association where the parasite living at the expense of the host A state in which an organism (the parasite) is metabolically dependent to a greater or lesser extent on another (the host). Host - parasite compatibility is based on recognition mechanisms which are both host in origin and of exquisite specificity. Parasites can select sites and reorganize the local environment An important aspect of host - parasite specificity → evasion of the host response by parasites. Compete with the host for food → host may suffer specific deficiency syndrome Decreased food utilization by the host (reduced appetite or increased passage of food) Change in the absorptive surface of the intestine (alteration in the efflux and influx of water and sodium and chloride ions) Removal of host's tissue and fluids by parasites Destruction of the host's tissues (migration of larval stages and multiply in tissues or organs) Mechanism of host tissue destruction by parasites: ○ Bacterial infection of lesions caused by a parasite ○ Reaction of the host to the parasite Fibrosis of a lesion Excessive proliferation of epithelium, endothelium, lymphoid tissue or the initiation of malignant propensities Immunological response of the host (necrosis, dermatitis or edema) Free living or parasitic Unsegmented Usually cylindrical and elongate in shape (tapering at extremities) Alimentary canal is present Dioecious (few exceptions) Life cycle may be direct or include an intermediate host Cuticle is relatively thick (may be smooth or have longitudinal striations) May have special adhesive structures (hooks, thickenings, or a cephalic collar) Many species have cervical alae (lateral flattened cuticular expansion) In most species the males have cuticular expansions at the posterior extremity  Ascaris suum Muscular layer (lines the body cavity) is transversely striated Mouth is anterior (may be subdorsal or subventral) and is surrounded by the lips AMPHIDS → chemoreceptors (pair of depressions) that occur on each side of the head lying lateral to other specialized structures of the head PHASMIDS → chemoreceptors located on the posterior to the anus and glands Schematic overview of a plant-parasitic nematode. Amphids and phasmids are chemosensory organs. The stylet is a protrusible, hollow puncturing device, that is used to penetrate plant cell walls. Esophagus shows variations of structure that are used for the classification of species. ○ Triradiate lumen and thickly lined with cuticle ○ Wall contains three esophageal glands ○ Have a bulbar swelling (esophageal bulb) located posteriorly  Rhabditiform esophagus → Has a club - shaped anterior portion connected by a narrow neck with a pear - shaped posterior bulb Filariform esophagus → Club - shaped without a posterior bulb Genital papillae ○ Posterior extremity of the male ○ Paired and may have long stalks supporting the caudal alae or the copulatory bursae of the strongyles Male reproductive system, lateral view. Males ○ Single testis ○ Vas deferens (sometimes a seminal vesicle and a muscular ejaculatory duct) ○ One or two spicules lying in sheaths ○ Gubernaculum (thickening on the dorsal wall) ○ Telamon (thickening on the ventral wall) Female ○ Posterior vulva ○ 2 uteri and 2 ovaries ○ Some are oviparous, others are ovoviviparous or vivparous  Male Female Active, non - parasitic third stage larva (enters through its mouth) Passive infective egg contains a 2nd or third stage infective larva Intermediate host (infective larva develops) ○ IH is eaten by the definitive host (Metastrongylus) ○ IH conveys the infective larva then penetrates through the skin of the DH (Filarioidea) Without an intermediate host: ○ A. Eggs hatch outside the host Larvae are free - living and active Strongylidae and Trichostrongylidae MOT → through mouth with food and water, skin penetration ○ B. Eggs develop outside the host but do not hatch there Infective larvae are passive MOT → only through the mouth With an intermediate host: ○ A. Eggs hatch or the worms are viviparous Larva enters the IH after a short free existence MOT IH is eaten by the DH ○ B. Eggs do not hatch and ingested by the IH MOT→ IH is eaten by the DH ○ C. Worms are viviparous Larvae enter the blood and taken up by a blood - sucking IH (infective larva develops inside) MOT → penetration of the infective larvae (IH) to the DH during a blood meal  Parasitology Prelim Lecture No. 2 : Phylum Nematoda ( Ascaris, Parascaris, Toxascaris, Toxocara) Possess three large lips and caudal alae (laterally place) No buccal capsule Esophagus usually lacks posterior bulb Intestines may have ceca Females have blunt tails Males have coiled tails and has two spicules Direct or indirect life cycles Genera of medical importance: ○ Ascaris ○ Parascaris ○ Toxascaris ○ Toxocara Males → tail usually without a well-developed caudal alae, but bears numerous caudal papillae Females → oviparous, eggs are unsegmented when they are laid Ova → oval or sub-globular, thick shelled Ascaris suum ○ Pig ○ Previously considered synonymous with A. lumbricoides (humans) ○ Size: 15-25 cm (males) to 41 cm (females) ○ Dorsal lip bears 2 double papillae ○ Each ventrolateral lip has one double subventral and a small lateral papilla ○ Eggs are oval with thick shells, albuminous layer bears prominent projections ○ Life cycle Eggs passed in the feces of the host and develop to the infective stage in 10 days or longer Infective stage → L2 or L3 (Aranjo, 1972) MOT: Ingestion of the eggs with or water or from the soiled skin of the mother (sucking pigs) Eggs hatch in the intestine and larvae burrow into the wall of the gut → Peritoneal cavity → Liver → Heart and Lungs → Bronchial tree (tracheal route ) → Pharynx (swallowed) → Intestines Eggs appear in the feces at 60-62 days post infection/hatching ○ Pathogenesis Destruction of tissue and hemorrhage (liver and lungs) Desquamation of the alveolar epithelium Edema and infiltration of the surrounding pulmonary parenchyma with eosinophils and other cells Heavy infections → death from severe lung damage Interferes absorption of protein, fat and carbohydrate (malnutrition) Intestinal obstruction Biliary stasis or blockage of the bile ducts Perforation of the intestines (peritonitis) ○ Clinical signs Depends on the severity of the infection Pneumonia (newborn pigs) Stunted growth Diarrhea ○ Lesions Fibrosis of the liver (milk spots) Petechial hemorrhages in the lungs ○ Diagnosis Sputum examination → larvae Fecal examination → eggs ○ Treatment Anthelmintics (imidazole and benzimidazole) Levamisole Tetramisole (both mature and immature stages) Parbendazole Fenbendazole (also has ovicidal effect) Morantel tartrate Piperazine  Parascaris equorum ○ Small intestines of equines (cattle) ○ Size: 15-28 cm long (males) and can be up to 50cm long (females) ○ Rigid, stout with a large head ○ Three main lips are conspicuous ○ Tail (males) has a small lateral alae ○ Eggs are sub-globular with thick, pitted albuminous layer ○ Life cycle is similar to A.suum ○ Pathogenesis and Clinical signs Catarrhal enteritis → diarrhea (fetid and pale feces), flatulence Pot bellied appearance Heavy infections → coughing and eosinophilia Migration of adult worms to bile duct, bowel wall (peritonitis and obstruction) ○ Treatment Thiabendazole Mebendazole Fenbendazole Cambendazole Dichlorvos Haloxon  Esophagus lacks a posterior muscular bulb Anterior part with large cervical alae (bent dorsad) Toxascaris leonina ○ Small intestine of dog, cat, fox and wild Felidae and Canidae ○ Eggs are slightly oval with smooth sides (75- 85 x 60-75 um) ○ Life cycle Infective stage: Egg containing a 2nd stage larva Fourth stage larva are seen in the mucosa and the lumen of the intestine No migration of larvae occurs  Has posterior granular ventriculus at the base of the esophagus Intestinal caeca absent Toxocara canis ○ Small intestine of the dog and fox ○ Large cervical alae ○ Body is anteriorly bent ventrad ○ Male tail has a terminal narrow appendage and caudal alae ○ Eggs are sub-globular with thick, finely pitted shells ○ Life cycle May involve prenatal (transuterine) and colostral (lactogenic) transmission, direct transmission or paratenic host transmission. Has both somatic and tracheal routes Eggs hatch in the duodenum Enters the liver via the portal circulation Enters the lungs via the hepatic vein → trachea L3 are produced in the lungs, trachea or esophagus Somatic type of migration - L2 Tracheal type of migration - L3 Transmammary route of infection Neonatal infection of puppies from the nursing bitch Larvae are passed via the colostrum → develop directly to adult worms (intestine) Toxocara canis adult male and female. Toxocara cati ○ Small intestine of the cat and wild Felidae ○ Cervical alae are very broad and striated ○ Eggs are pitted (similar to T. canis) ○ Life cycle Prenatal infection does not occur Paratenic hosts play an important role in transmammary transmission MOT: Ingestion of eggs containing L2 Larval migration to the stomach wall, liver and lungs Tracheal route migration is present ○ Pathogenesis Poor hygiene → heavy infections Heavy prenatal infection (T. canis) → death of whole litter Migration to lungs → Progressive malaise + vomiting and diarrhea, pneumonia (uncommon) General unthriftiness, pot bellied appearance, intermittent diarrhea and anemia Acute intestinal obstruction Migration of adult worms to aberrant sites (bile duct or through the bowel wall) Nervous disorders (frequent) from irritation of the bowel or focal lesions in the CNS (aberrant larvae) ○ Clinical signs Unthrifty, either pot-bellied or with a tucked-up Dull and harsh coat Emaciation Anemia Restlessness Diarrhea or constipation  Parasitology Prelim Lecture No. 3 : Phylum Nematoda (Anikasidae & Oxyuridae) Esophagus with cylindrical ventriculus but intestinal cecum absent (Anisakis spp.) Posterior ventriculus and anterior cecum projecting forward along the esophagus (Porrocaecum) Posterior ventriculus, anterior cecum and posterior appendix projecting backwards from the ventriculus (Contracaecum) Host includes marine mammals, birds, fishes, reptiles and man (accidental) Zoonotic when fish is consumed by human Occur in marine animals Intestinal caecum is absent Anterior region of the lips form medial, bilobed processes Thinner and smoother than Ascaris Herring worm disease MOT (humans): Ingestion of raw or semi-raw fish containing larval stages Clinical signs: Symptoms associated with eosinophilic granuloma in the intestinal or stomach wall Mild cases are associated with slight irritation of the bowel MOT: larva, then develops to adult  A marine fish Has three inconspicuous lips Esophagus with a well developed posterior bulb Male bears a number of large papillae around the cloacal opening Females have long tapering tails Eggs are flattened on one side No IH needed Not prominent lips Oxyuris equi Large intestines of equine Esophagus is narrow at the middle and the bulb is not distinctly marked off Male has a single pin shaped spicule Eggs are elongate, slightly flattened on one side, provided with a plug at one pole Females are larger than males, same with ascaris Life cycle ○ Inhabit the cecum and large colon (L3) ○ Eggs are laid on the skin in the perineal region ○ MOT: Ingestion of the infective eggs on fodder and bedding ○ Itching happens during egg deposition (anal pruritus) Pathogenesis and Clinical signs ○ Anal pruritus (egg-laying females) ○ Restlessness and improper feeding (dull coat) ○ Ungroomed 'rat-tailed appearance Diagnosis ○ Examination of the perineal region (presence of eggs) ○ Fecal examination ○ Can use scotch tape method Treatment  ○ Mebendazole (5-10 mg/kg) ○ Cambendazole (20mg/kg) ○ Dichlorvos (26-52 mg/kg) Prominent plug Enterobius vermicularis (Kigwa) Pinworm or seat worm (human and other primates) Does not occur in dog and cat Cream - colored and slender Females has a long pointed tail (resembles O. equi) Adults occur in the cecum, appendix and ascending colon Gravid females migrate posteriorly and deposit eggs on the perianal and perineal regions MOT: Ingestion of infective embryonated eggs Itchy perianal region Treatment Dichlorvos (8-9 mg/kg/day) Pyrvinium pamoate (5 mg/kg) Piperazine (50 mg/kg) Thiabendazole (50 mg/kg x 2 days) lodine staining, not stained by bile, hence, coloriess Shape: Letter 'D'  Parasitology Prelim Lecture No. 4: Phylum Nematoda (Strongyloididae & Stephanuridae) Free living (saphrophytic) → Esophagus with a valvulated bulb Parasitic → Markedly elongated cylindrical esophagus Strongyloides stercoralis Parthenogenetic (parasitic forms) Small intestine of man and other primates, dog, fox and cat Females larger than males Parthenogenetic females - can reproduce without males Infective larvae (parasitic) can penetrate through the skin of the host and pass with the blood to the lungs → trachea → pharynx → intestines Eggs are large and have thin shells MOT: penetration through skin-unique Life cycle ○ Parthenogenetic female bury in the mucosa of the small intestine ○ Produce thin-shelled transparent eggs → hatch in the intestine (L1 in the feces) ○ Heterogonic cycle - NONPARASITIC: from L1 becomes free adult males and females, then produces larva ○ Homogonic - parasitic: L1 to L3 (infective stage) cannot survive the environment ○ MOT: Skin penetration, oral infection may occur ○ Migrate to the lungs → trachea→ esophagus→ intestines (maturity) Pathogenesis and clinical signs ○ Erosion of the intestinal mucosa and fluid gut contents ○ Catarrhal enteritis of the upper SI ○ Anorexia ○ Weight loss ○ Diarrhea ○ Moderate anemia ○ Erosion can cause irritation and microbleeding-anemia ○ Severe infection may occur in dogs (puppies) ○ Catarrhal inflammation of the SI ○ Necrosis and sloughing of the mucosa (severe diarrhea which may be blood stained) ○ Burrowing in the mucosa Diagnosis ○ Demonstration of eggs or larvae (dogs) in the feces Treatment ○ Thiabendazole (75 m/kg) ○ Diethlycarbamazine (100 mg/kg)  ○ Levamisole (5-10 mg/kg) ○ Cambendazole (20 mg/kg) ○ Fenbendazole (50 mg/kg) ○ Strongyloides is more known in horses- cambendazole ○ Pigs-levamisole ○ Dogs-diethylcarbamazine Cup-shaped buccal capsule containing teeth Parasites of the kidney and perirenal tissues Stephanurus dentatus Kidney-worm of swine Perirenal fat, pelvis of the kidney and walls of the ureters Erratic parasite in the liver or other abdominal organs (sometimes thoracic organs and spinal canal of pig) Females larger than males Males have a small bursa and 2 spicules Eggs are ellipsoidal and thin shelled Life cycle ○ Adult worms inhabit near the kidney (in cyst) ○ Eggs are passed out in the urine ○ MOT: Ingestion or through the skin ○ Larvae reach the liver (via portal vessels or lungs and systemic circulation) ○ Larva can migrate and penetrate soft tissues ○ Percutaneous infection → remain in pulmonary capillaries and become encapsulated in the lungs or reach the pleural cavity/other thoracic organs Pathogenesis ○ Nodules in the skin with enlargement of the superficial lymph nodes (percutaneous infection) ○ Acute inflammatory lesion in the liver ○ Abscess formation and extensive liver cirrhosis may occur ○ Thickened ureter ○ Cyst (containing the adults in pair) in kidney tissue ○ Cirrhosis develops in chronic infection Clinical signs ○ Stiffness of the leg (precrural nodules) ○ Posterior paralysis ○ Depressed growth rate, loss of appetite and emaciation ○ Ascites  Diagnosis ○ Presence of eggs in the urine ○ Definitive diagnosis by post mortem findings Treatment ○ Thiabendazole (inhibit the migration of larva) ○ No satisfactory treatment available