Parascaris spp

                                                           Introduction

Parascaris equorum is the ascarid of horses. It is widespread and common in young horses; it may contribute to ill-thrift and occasionally causes death by obstruction. P. equorum is a large nematode, females being up to 50 cm long. The life cycle resembles that of A. suum. Similarly, hepatic and pulmonary lesions are associated with larval migration, and coughing may occur at the time larvae are in the lungs, particularly if infections are heavy. The prepatent period is ∼10-15 weeks. 
Host- Horse
Location- Smell intestine

Order	Ascaridida
Super Family	Ascaridoidea
Family	Ascarididae
Genus	Ascaris
Family character	Large nematode, buccal capsule is absent. Mouth is surrounded by 3 lips. Oesophagus is devoid of posterior bulb.

                                                     Morphology

• Parascaris equorum is large, cylindrical, and has a cuticle with three layers made of collagen and other compounds that protect the worm from the acids in the digestive tracts of animals. The adult male ranges from 15-28 cm. The tail end of male has numerous precloacal papillae and 5 pairs of postcloacal papillae. Median papillae also present. The females are much larger and can grow up to 50 cm. mouth is Surrounded by 3 lips. They are separated by intermediate lips. Each of these lips has a transverse groove or labial sinus on the lateral margins, which divide the lip into apical and basal regions. The eggs of Parascaris equorum are almost spherical and have a brownish color. The eggs contain a 1-celled zygote and are between 90-100 microns in size.

                                                       Life cycle

• A single female lays abo two lakhs eggs per day. Eggs are passed in the faeces of host and develop to infective stage in about 10 days or above depending upon the environmental temperature.
• The eggs are resistant to adverse conditions like drying, freezing and chemicals and remain viable for 5 years.
• The infection of host by ingestion of embryonated eggs containing L₂ larva. Ingested egg hatch in the intestine and liberate L₂.
• The liberated L₂ penetrate the intestinal wall reach the peritoneal cavity and then to liver. Majority of L₂ reach the liver via hepatoportal system.
• From the liver, the larvae carried to the right atrium via superior venacava by blood and then to lungs.
• In the lungs larvae are arrested in the capillaries where the L₂ moult to L₃. These L₃ break out of the alveolar capillaries and pass through alveolar duct and small bronchioles. Then the larvae gradually ascend the bronchial tree and reach the trachea. From the trachea the larvae migrate to pharynx and mouth and finally swallowed to reach the intestine. This migration is called as, “Tracheal migration”.
• Large number of L₃ reach intestine in about 7 to 8 days after infection.
• In the intestine L₃ moult to L₄ in about 14 to 21 days and L₄ to L₅ in about 21 to 29 days. The worms reach maturity in about 50 to 55 days. Eggs appear in faeces in about 62 days.
• In P. equorum, the worm reach maturity in 80 to 83 days

                                                         Pathogenesis

• Foals 3 to 9 months of age are commonly affected. Heavy infection causes coughing and circulating eosinophilia. Adult worm causes catarrhal enteritis and foetid diarrhoea.
• General malaise, debility and pot belly may occur. Hair Coat becomes very rough, sometimes the adult worms enter into the bile duct causing jaundice and also the adult worm enter into the intestinal wall causing generalized or localized peritonitis.

                                                           Diagnosis

• by identification of adult parasites.
• demonstration of eggs in faeces.

                                                            Treatment

• Thiabendazole – 44 mg/Kg b wt.
• Mebendazole – 10 mg/Kg b wt.

                                                              Control

• Foals must be kept in clean paddock and should not be allowed to graze along with the mother. The pregnant mare should be treated for ascaris before foaling.

Parascaris equorum is large, cylindrical, and has a cuticle with three layers made of collagen and other compounds that protect the worm from the acids in the digestive tracts of animals. The adult male ranges from 15-28 cm. The females are much larger and can grow up to 50 cm. Parascaris equorum has three very large lips. Each of these lips has a transverse groove or labial sinus on the lateral margins, which divide the lip into apical and basal regions.

Parascaris equorum is large, cylindrical, and has a cuticle with three layers made of collagen and other compounds that protect the worm from the acids in the digestive tracts of animals. The adult male ranges from 15-28 cm. The females are much larger and can grow up to 50 cm. Parascaris equorum has three very large lips. Each of these lips has a transverse groove or labial sinus on the lateral margins, which divide the lip into apical and basal regions.


Parascaris equorum is large, cylindrical, and has a cuticle with three layers made of collagen and other compounds that protect the worm from the acids in the digestive tracts of animals. The adult male ranges from 15-28 cm. The females are much larger and can grow up to 50 cm. Parascaris equorum has three very large lips. Each of these lips has a transverse groove or labial sinus on the lateral margins, which divide the lip into apical and basal regions.
Parascaris equorum is large, cylindrical, and has a cuticle with three layers made of collagen and other compounds that protect the worm from the acids in the digestive tracts of animals. The adult male ranges from 15-28 cm. The females are much larger and can grow up to 50 cm. Parascaris equorum has three very large lips. Each of these lips has a transverse groove or labial sinus on the lateral margins, which divide the lip into apical and basal regions.
Parascaris equorum is large, cylindrical, and has a cuticle with three layers made of collagen and other compounds that protect the worm from the acids in the digestive tracts of animals. The adult male ranges from 15-28 cm. The females are much larger and can grow up to 50 cm. Parascaris equorum has three very large lips. Each of these lips has a transverse groove or labial sinus on the lateral margins, which divide the lip into apical and basal regions.
Parascaris equorum is large, cylindrical, and has a cuticle with three layers made of collagen and other compounds that protect the worm from the acids in the digestive tracts of animals. The adult male ranges from 15-28 cm. The females are much larger and can grow up to 50 cm. Parascaris equorum has three very large lips. Each of these lips has a transverse groove or labial sinus on the lateral margins, which divide the lip into apical and basal regions.

Trichuris spp

                                                                             
                                                                       Introduction

• Trichuris ovis, commonly known as a whipworm, is a nematode belonging to the genus Trichuris. This whipworm species was first discovered in 1795 and is known to infect sheep and goats.   
• They have a direct life cycle, moving directly into the definitive host from the infective L1 egg stage. Once ingested the larva is freed from the egg casing due to digestion of the plugs at either end of the egg. The larvae then form mucosal nodules in which to develop before emerging into the lumen of the large intestine and caecum of the host. 

                                                                  Morphology 

• The anterior portion of the worm is long and slender, while the posterior part is short and stout.
• Male's tail end is spirally coiled and has single spicule enclosed in a spiny sheath.
• Female is oviparous.
• Eggs are brown in colour, barrel-shaped, transparent and have plug at both ends.
  
  

  

  Trichuris ovis

                                                            Life cycle

• Unembryonated egg passed in faeces of the host .Under favourable condition the infective stage(L1) is reached in about a weeks (infective stage is L1).
• The D/H acquires infection by ingestion of embryonated egg-containing L1.
• The eggs are hatched in the small intestine, the liberated L1 penetrate the intestinal mucosa, where all the moulting occurs.
• The adult worms reenter into the lumen and moves to the caecum. In the caecum the filamentous anterior end embedded in the caecal mucosa.
                                                          Pathogenesis
• Generally not pathogenic. But the heavy infection is causative for diphtheritic inflammation.
• Mainly occurs due to continuous moving of worm for attachment.
  
  
  
  
                                                         Diagnosis
  
  
• Diagnosis can be done by gross examination of adult parasites and identification of eggs in the faecal eggs.
• The eggs of Trichuris species are yellow/brown in colour and are bi-operculated (have a plug in each end). 

                                                                Treatment

• Levamisole - 7.5mg/Kg.b.wt
• Fenbendazole - 5mg/Kg. b.wt
• Methyridine - 200mg/Kg. b.wt
• Thiabendazole- 44mg/ Kg b.wt ( very effective ) 
• Mebendazole is also highly effected. 

Trichuris eggs

 video- https://youtu.be/Cn415GrJbt4 (Click here)

Heterakis gallinarum

                                                           Introduction

Heterakis gallinarum is a heavily prevalent poultry parasite that thrives in the ceca of various species of gallinaceous birds. It is a small roundworm, measuring between 4 and 15 mm long, in the family Heterakidae. Heterakis gallinarum has a direct life cycle not requiring an intermediate host to complete development, and it is generally believed that poultry raised at high density on litter are at greatest risk for accumulating large numbers of the nematode. This species typically only causes mild pathology that does not significantly affect bird performance. However, H. gallinarum is recognized as an economically important parasite by the poultry industry because its ovum serves as the vector for the protozoal parasite Histomonas meleagridis, the cause of histomonosis in poultry. Diagnosis of the nematode typically relies on fecal egg counts, which are prone to false negative diagnoses.

Common name	Caecal worm of poultry
Host	Fowl, Turkey, duck and Pea fowl
Location	Large intestine and Caecum

                                                        Gross

• Whitish small sized worm, 1.5 cm long.
• Large lateral alae extending down the side of the body.
• Oesophagus has strong posterior bulb having valvular apparatus.
• Tail end of male has large alae, circular precloacal sucker and 12 pairs of pedunculated papillare. Spicules are unequal, right one is slender and long. Left one is short and broad.
• Eggs are oval, smooth shelled.
                                                 Life cycle
    
  • Is direct, eggs developed into infective stage in 14 days. Infection of chicken by ingestion of egg containing L₂ stage.
  • L₂ hatch in the intestine move to caecal mucosa and remain there for 2 to 5 days and moult to L₃ in the lumen of caecum on 6^th day of infection.  
  • L₄ in 10 days and L₅ in 15 days. Prepatent period is 24 to 30 days, earthworm may act as transport host.
    
                                               Pathogenesis
  
  
  
  

  • Usually non pathogenic, but heavy infection cause thickening of caecal mucosa with petecheal haemorrhage on the surface.
  • The significance of the worm is that the protozoan viz. Histomonas meleagridis causing black head or entero hepatitis in turkeys is incorporated in the eggs of Heterakis galliarum.
    
    
                                      Diagnosis
    
    

    • Finding eggs in the feces.

    • gross examination of parasite
                                      Treatment
    
    
    

    • Phenothiazine is effective at the dose rate of one gram per bird.
    • Phenothiazine + Piperazine mixture is used to eliminate the mixed infections of H. gallinarum and A. galli.
    • Hygromycin B - 0.25% mix in feed is highly effective.
    • Mebendazole is also be used.

    
                                       Prevention
     
    
    

    • Strict sanitation of poultry houses is essential.
     
     

    

    Heterakis gallinarum egg

     
     
     
     
     
     

    
    

AMPHISTOMES

                                          Introduction

• Amphistomes, commonly referred to as 'stomach' or 'rumen' flukes because of the localization of these flukes in the stomach of ruminants.

                                             Gross

• small size, pinkish color when fresh, pomegranate seed like
• Body is thick, conical,elongate with blunt ends.
• Ventral sucker is situated at the posterior end, large and strongly developed.
• Intestinal caeca coiled (3-4 coils) and terminate at about the level of middle of ventral sucker.
• Testes lobed and tandem.
• Genital sinus enclosing genital opening. The cuticle is spineless. The vitelline glands are lateral and are strongly developed.

                                           Location

• present in rumen, reticulum and sometime bile duct of liver also.

Host	Cattle, buffalo, sheep and goat
Location	Adults in Rumen and reticulum,Immature flukes in Duodenum
Intermediate host	Indoplanorbis,Gyraulus,Lymnaea and Bulinus

                                                                 life cycle

• Eggs are composite, distinct operculum
• Metacercaria is dark in colour and remains viable for 3 months
• Infection of definitive host is by the ingestion of metacercaria along with the grass herbage.
• The ingested metacercaria gets excysted in the small intestine and gets attached to the mucosa of duodenum as immature flukes.
• After 6-8 weeks the immature flukes starts migrating through various parts of intestine.
• I part of development Intestine – migrate -- Rumen/Reticulum.

                                                         Pathogenesis

• The immature flukes are highly responsible for causing the pathogenesis by their presence in the small intestine.
• The immature flukes attach very strongly and get embedded in the mucosa of the intestine and they are commonly called as plug feeder.
• These immature flukes eats away pieces of mucosa through the sucker and pinch them off resulting in necrosis and severe hemorrhage in heavy infections the deeply placed immature flukes may reach the muscular coat of the intestine causing hemorrhagic duodenitis
• The adult flukes are normally non-pathogenic and are seen attached to the rumen feeding only on the seminal papillae resulting in loss of ruminal papillae.
• Due to the presence of the immature flukes in the intestine, extensive catarrhal hemorrhage occurs in the duodenum and jejunum with degeneration of intestinal glands. There will be anaemia, hypoproteinaemia,oedema and emaciation.

                                            Clinical signs and symptomes

• Infected animals are weak emaciated showing proper foetid foul smelling diarrhea along with immature flukes present in faces.
• Death may occur within 15-20 days after the onset of clinical symptom.
• Incase of immature amphistomosis the rate may go up to 80-90 %
• Affected animals feel thirsty and drink water frequently, the animal also shows in bottle jaw ( intermandibular swelling)which is characteristic of flukes infection.
• The immature amphistomes is  called  in Hindi as “gillor”, “pitto”
• PM lesions mucous membrane looks pale, subcutaneous fat is replaced by a gelatinous material, hydrothorax, hydro pericardium, and hemorrhagic deodenitis.
• The immature flukes are seen attached to duodenal mucosa in clusters which appear pink is colour.

                                                     
                                              Diagnosis

• By clinical signs and symptomes- as mentioned above
• By faecal examination- idetification of eggs
• Presence of snail Intermediate host near to infected animals.
• sometimes Immature flukes also passed in diahorrheal feaces of infected animals
• by Postmortem examination -finding of flukes in the rumen, reticulum and bileduct of liver.

                                                         Egg characteristics

• Conical to oval shape, white to transparent, embryonic mass distinct and have operculum on both anterior and posterior ends.

Amphistome eggs

srtongyle

  strongyle egg

 

srtongyle egg

srtongyle egg

Video- https://youtu.be/CdPXX0FYKfY

MANGE

                                                               Demodex canis

                                                               Introduction
 Demodex canis is the common mite species causing demodicosis in dogs, is acquired by pups from their dams within the first days of life. As normal skin inhabitants, the mites reside in hair follicles without causing cutaneous changes in most dogs. Commonly young dogs develop localized demodicosis, defined by convention as five or fewer lesions. These are nonpruritic, alopecic lesions that often develop on the face or limbs, although other areas may be involved.

                                                   Morphology 

The general structure of Demodex consists of the head, or gnathosoma, with its mouthparts, the trunk (idiosoma) and the extremities. The idiosoma includes the podosoma, into which the legs are attached, and opistosoma, distal to the legs. The elongated, cigar-like idiosoma, the ring-like segmentation of opisthosoma and very short legs with claw-like hooks at the tips are characteristic Demodex features. The gnathosoma is trapezoid and wider than its length. The slit-like genital pore of the female is located ventrally at the level of the fourth pair of legs, extending slightly caudal past it. The male genital, or aedeagus, is located dorsally in the genital pore that is at the level of the second pair of legs. The width of female D. canis is about 40 μm and the length varies between 165 μm and 285 μm. Males are shorter (150–210 μm) with a shorter and sharper opisthosoma that that of females. D. injai is longer then D.canis (330–370 μm) and D. cornei is shorter (90–140 μm). Molecular biological studies have indicated that D. cornei may not be an independent species, but rather a morphological variant of D. canis. The egg is spindle-shaped and sized 80–105 μm × 32–54 μm.

Morphology

• 0.25 mm
• Female longer, elongate
• Cylindrical
• Body divided into head, thorax, and abdomen

Head

• Has three jointed pedipalp
• One pair chelicerae
• Single hypostome

Thorax

• Ventral side with four pairs of stumpy legs
• Each leg is three jointed, vulva in female on ventral side
• On the dorsal side in males there is a longitudinal slit which is the genital opening

Abdomen

• Transversely striated

                                             Effects on host

• Injury to host occurs when mites puncture with their stylet like chelicerae the epithelial cells lining the hair follicles and glands to feed on the cell contents
• The host response in most cases leads to thrombosis of internal infestations
• Pustules initially seen on abdomen, neck, legs, also feet, face and thigh regions
• Dogs have repulsive mousy odour / rancid odour
• Itching is less
• In dogs both forms are seen
• Clinical signs evident in dogs less than 1 year old- presumably immuno deficient
• 1^st appear as mildly erythematous patch above eyes and corners of mouth, associated typically with hair loss- then spreads to forelegs, trunk
• Most resolve without treatment
• Death occurs in severely infected animals
• In generally predisposed or immuno depressed animals and in case of secondary infection, it develops into chronically severe, moist, purulent dermatitis - "Pustular Demodicosis” - unpleasant odour - rancid/mousy
• If generalized, there is intense redness, tenderness of skin which easily bleeds-Death occurs  in heavily infested animals
• Mild and moderate hypertrophy of the affected epithelia
• In some cases marked hypertrophy and cell destruction occurs
• Opening of hair follicle and ducts of glands are blocked
• Dermal papule formation and nodules
• Hair loss-secondary bacterial infection-inflammation, pruritus and pustule formation (Staphylococcus)
• Lesions occur on face and head and then spread-if untreated, death due to emaciation and toxaemia occurs

                                                                  Clinical signs

There are two major forms of demodecosis
1- Scaly demodicosis
2- Papulonodular demodicosis

                                                     
                                                      Scaly demodicosis

• Most common form.
• Dry, scaly dermatitis
• Itching, thickening and wrinkling of skin
• Loss of hair, reddening of skin
• Sec infection-rupture of follicular cells, inflammation, purulent exudates
• Localized or Generalized
• Repulsive mousy odour
• Red skin-bluish green- coppery reddish colour
• Skin is tender, easily bleeds
                   
      
                                 Papulonodular demodicosis
  
  

  • Obstruction of hair follicles, gland ducts
  • Leads to palpable cyst like/nodular swellings in the skin - traps mites within. Common form in Cattle, Goats & Pigs
  • Lesions enlarge as the mites multiply along with cellular debris and glandular secretions
  • Eventually rupture -leads to secondary infections and abscesses
  • Can rupture internally- introduce mites into lymphatics.
     Video- https://youtu.be/a0w4zUfyxw0

demodex canis

Demodex canis in dog

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