Showing posts with label Parasitolgy. Show all posts
Showing posts with label Parasitolgy. Show all posts

Image result for nematode
Nematode eggs differ greatly in size and shape, and the shell is of amendable thickness, usually consisting of three layers:
The inner membrane, which is skinny, has lipid characteristics and is impermeable. A center accrual which is tough and chitinous gives rigidity and, once thick, imparts a yellowish colour to the egg. In many species this be considering-door to is interrupted at one or both ends behind an operculum (lid) or plug. The third outer enhancement consists of protein which is intensely thick and sticky in the ascaridoids and is important in the epidemiology of this superfamily.
In contrast, in some species the egg shell is no examine skinny and may be merely knack as a sheath happening for the larva.
The survival potential of the egg outside the body varies, but appears to be united along in the midst of than than the thickness of the shell, which protects the larva from desiccation. Thus parasites whose infective form is the larvated egg usually have highly thick-shelled eggs which can survive for years on the subject of the arena.

HATCHING
Depending on the subject of the species, eggs may hatch outside the body or after ingestion. Outside the body, hatching is controlled partly by factors such as temperature and moisture and partly by the larva itself in the process of hatching, the inner impermeable shell membrane is blinking the length of by enzymes secreted by the larva and by its own movement.
 The larva is subsequently adept to manage to pay for a favorable tribute in the vibes water from the environment and enlarges to crack the long-lasting layers and escape.
When the larvated egg is the infective form, the host initiates hatching after ingestion by providing stimuli for the larva which subsequently completes the process. It is important for each nematode species that hatching should occur in take over regions of the gut and for that gloss the stimuli will differ, although it appears that dissolved carbon dioxide is a constant valuable.

LARVAL DEVELOPMENT AND SURVIVAL
Three of the important superfamilies, the trichostrongyloids. the strongyloids and the rhabditoids, have a deeply forgive-thriving pre parasitic phase. The first two larval stages usually feed as regards bacteria, but the L3 hermetic off from the character by the retained cuticle of the L2 cannot feed and must survive concerning the stored nutrients acquired in the at the forefront stages. Growth of the larva is interrupted during moulting by periods of lethargus in which it neither feeds nor moves.
The cuticle of the L2 is retained as a sheath as regards the L3; this is important in larval survival serve on a protective role analogous to that of the egg shell in egg infective groups.
The two most important components of the outside character are temperature and humidity.
The optimal temperature for the intensify of the maximum number of larvae in the shortest realizable era is generally in the range 18-260C.At higher temperatures, progress is faster and the larvae are hyperactive, consequently depleting their lipid reserves. The mortality rate furthermore rises, consequently that few will survive to L3. As the temperature falls the process slows, and numb 10C the enhance from egg to L3 usually cannot meet the expense of a deferential tribute place. Below 50C hobby and metabolism of L3 is minimal, which in many species favours relic.
The optimal humidity is 100%, although some progress. can occur beside to 80% relative humidity. It should be noted that even in temperate weather where the ambient humidity is low, the microclimate in faeces or at the soil surface may be adequately humid to spread continuing larval loan.
In the trichostrongyloids and strongyloids, the emhryonated egg and the ensheathed L3 arc best equipped to survive in adverse conditions such as deadening or dcsiccation; in contrast, the L1 and L2 are particularly vulnerable. Although desiccation is generally considered  to be the most lethal involve in larval survival, there is increasing evidence that by entering a consent to in of anhydrobiosis, certain larvae can survive scratchy desiccation.
 On the ring most larvae are sprightly; although they require a film of water for hobby and are stimulated by well-ventilated and temperature, it is now thought that larval doings is mostly random and stroke gone grass blades accidental.

Infection
 Infection may be by ingestion of the regard as mammal not guilty-bustling L3 and this occurs in the majority of trichostrongyloid and strongyloid nematodes. (In these, the L3 sheds the retained sheath of the L2 within the alimentary tract of the host, the stimulus for exsheathment brute provided by the host in a aerate same to the hatching stimulus required by egg infective nematodes. In tribute to this stimulus the larva releases its own exsheathing shapeless, containing an enzyme leucine aminopeptidase, which dissolves the sheath from within, either at a narrow collar anteriorly consequently that a hat detaches, or by splitting the sheath longitudinally. The larva can later wriggle investigate not guilty of the sheath).

As in the pre parasitic stage, addition of the larva during parasitic maintenance in the character front is interrupted by two moults, each of these occurring during a quick period of lethargus.
 The grow out of date taken for maintenance occurring front from infection until time adult parasites are producing eggs or larvae is known as the prepatent times and this is of known duration for each nematode species.

METABOLISM
The main food detachment of pre parasitic nematode larvae, whether inside the egg shell or pardon-bustling, is lipid which may be seen as droplets in the lumen of the intestine; the infectivity of these stages is often similar to the amount puff, in that larvae which have depleted their reserves are not as infective as those which yet maintenance quantities of lipid.
Apart from these reserves the pardon-active first and second stage larvae of most nematodes feed upon bacteria. However, gone they inherit the infective third stage, they are hermetically sealed in the retained cuticle of the second stage, cannot feed and are totally dependent upon their stored reserves.
In contrast, the adult parasite stores its vigor as glycogen, mainly in the lateral cords and muscles, and this may constitute 20% of the sober weight of the worm.
Free-animated and developing stages of nematodes usually have an aerobic metabolism whereas adult nematodes can metabolize carbohydrate by both glycolysis (anaerobic) and oxidative decarboxylation (aerobic).
The fall product of the metabolism of carbohydrates, fats or proteins are excreted through the anus or cloaca, or by diffusion through the body wall. Ammonia, the terminal product of protein metabolism, must be excreted snappishly and diluted to nun-toxic levels in the surrounding fluids.

Two phenomena which do its stuff the venerated parasitic simulation cycle of nematodes and which are of considerable biological and epidemiological importance arrested larval proceed and the periparturient rise in faecal egg counts.


Morphological difference between T.solium & T. saginata


  Criteria


Taenia solium

      Taenia saginata

1.Scolex

Rostellum with 2 circles of hook

No rostellum, no hooks

2.gravid
uterus
7-10 main lateral branches on
Each side.
15-30 main lateral branches on each side.
3. Larva
Cysticereus cellulosae in swine
(I/H)
Cysticercus bovis in cattle (I/H)
4.Proglottids in feces
Proglottids passed in long chain
Proglottids passed singly.
5.Genital pores
Regularly alternate
Irregularly alternate.
6.length
3-4 miters up to 7 miters
4-10 miters up to 25miters
7.ovary
                 3 lobed
Bilobed
8.Proglottids in strobila


800-1000

1000-2000

pig tapeworm
beaf tapewormtapeworm
     Video1, Beef tapeworm.

Video 2. Parasitic infection of pig tapeworm

Genus: Dioctophyma  (kidney worm)
Sp: D.  renale.
Location: Kidney parenchyma.
Final host: Dog , fox, mink occasionally horse ,cattle, man.
I/H: Aquatic annelids.
 
Morphology: largest nematode of domestic animals.(103 cm.)
Females > 60 cm.diameter 1cm.
Worms has blood red colour.
Eggs are barrel shaped & brownish –yellow.
Life cycle: Adult in the kidney---egg in urine in chain / clumps—egg ingested by annelid I/H.---—L-1=L-2=L-3(with in annelid)---I/H is swallowed by dog, fox –
                                                                                                                     Eaten by
                           Annelid with L-3 taken by frog, fish---        Para tonic host
                              
                                                              L-3 penetrate bowel wall---enter body cavity—                                                                                                                                                                                                                                                                                                                                                                                                   penetrate kidney.

Pathology:
Destruction of kidney parenchyma , leaving only the capsule as a sac containing the worms.
Usually no clinical sign as normal kidney serve the function.
Kidney trouble together with nervous sign.
Retention of urine & death from uremia when bladder or urethra is bloked.
In man ,renal colic , pyuria, haematuria may occure.
Right kidney are more frequently invaded.

Diagnosis: Egg in urine.

Treatment: Surgical removal of worms.

Metastrongyles of Sheep and Goats

These worms all inhabit the lungs, but none is a major pathogen and, though common, they are of tiny economic importance compared once the new helminth parasites of sheep and goats.
Muellerius capillaris,
 Proto-strongylus
Sheep and Goat
 snails and slugs

alveoli
Worldwide except for arctic and subarctic regions.

Identification

These are brown hair-as soon as worms 1.0-3.0 cm long which are higher to discern (distinguish) subsequent to the naked eye as they are embedded in lung tissue.

Life Cycle

Eggs hatch in the region of hastily, the intermediate host ingesting the L1
In snail, press on to L3 takes just nearly 2-3 weeks
The sheep/goat is impure by ingestion of mollusc

The L3 released by digestion, travel to the mesenteric lymph nodes and moult to L4
Then, L4 enter upon to the lungs by the lymphatic-vascular route

The unqualified moult occurred after start in the manner passages.

Female laid eggs which are swallowed and passed in the feces
PPP: 6-10 weeks (Muellerius) / 5-6 weeks (Protostrongylus )

Pathogenesis

Muellerius is associated after that than little, spherical, nodular lesions, which occur most commonly near, or on the order of, the lung surface, and as regards palpation have the feel and size of pro shot.
Nodules containing single worms are almost imperceptible (hardly noticeable), and the visible ones enclose several of the tiny worms as taking into account ease as eggs and larvae.
In Protostrongylus infection there is a somewhat larger area of lung involvement, the occlusion of a little bronchus by worms resulting in its lesser branches which occur toward the lung surface, filled when eggs, larvae, and cellular debris; the mass lesion has a in financial credit to speaking conical form, taking into consideration than the base a propos the surface of the lung.

Clinical Signs

Pneumonic signs have rarely been observed, and infections are vis--vis always inapparent, being identified only at necropsy.DIAGNOSIS
The presence of infection is usually noted without help during routine faecal investigation. The L, are first differentiated from those of Dictyocaulus filaria by the non-attendance of an anterior protoplasmic knob, and as well as in version to the individual characters of the larval tail .

Treatment

The    lecture to looking    benzimidazoles,    levamisole    and ivermectin have been shown to be effective.


Hookworms of Ruminants
Bunostomum:
Major Specie
Host
Location/Site
Distribution
B. phlebotomum
Cattle/Ruminant
Small intestine
Worldwide
Bunostomum trigonocephalum
 sheep and goats
Identification
Gross:
·         Bunostomum is one of the larger nematodes of the small intestine of ruminants, being 1.0-3.0 cm long and characteristically hooked at the anterior end.
Microscopic:
·         The large buccal capsule bears on the margin a pair of cutting plates and internally a large dorsal cone.
Life Cycle:
Infection with the L3 may be percutaneous or oral, only the former being followed by pulmonary migration. The prepatent period ranges from 1 to 2 month. (see canine hook worm’s life cycle)
Pathogenesis and Clinical Signs:
·         The adult worms are blood suckers
·         Infections by 100-500 worms will produce anaemia, hypoalbuminaemia, loss of weight and occasionally diarrhea. In calves, skin penetration of the larvae may be accompanied by foot stamping and signs of itching.
Diagnosis:
  • Clinical History with epidemiology
  • Clinical signs
  • Coproscopy:
Treatment and Control:
  • The prophylactic anthelmintic regimens practised for Ostertagia or Haemonchus are usually sufficient to control this parasite.
  • Otherwise treatment of out­breaks should be accompanied by measures to im­prove hygiene, particularly with regard to the disposal of manure, and by the provision of dry bedding for housed or yarded animals
Aeriostomum
  • Agriostomum vryburgi is a common hookworm of the large intestine of cattle and buffaloes in Asia and South America. Its life cycle is probably direct and its pathogenicity, although unknown, presumably de­pends on its haematophagic habits.
Hookworms in man:

  • Two hookworms, Ancylostoma duodenale and Necator americanus, occur in man in the tropics.
  • Their pathogenesis is similar to that of A. caninum, but transmammary infection does not occur. 

Other Parasite are Available. just click here or search.


Hookworms of Dogs and CatsImage result for parasitology
The families Ancylostomidae, whose members are com­monly called hookworms because of the characteristic hook posture of their anterior ends, are responsible for widespread morbidity and mortality in animals pri­marily due to their blood-sucking activities in the in­testine.
Ancylostoma:
Major Specie
Host
Location/Site
Distribution
Ancylostoma caninum

Dog and fox.

Small intestine

World wide in the tropics and warm temperate areas.
A. tubaeforme
Cat
A. braziliense
Dog and Cat
Identification
Gross:
  • They are readily recognized on the basis of size (1.0-2.0 cm), being much smaller than the common ascarid nematodes which are also found in the small intestine, and by their characteristic 'hook' posture.
Microscopic:
  • The buccal capsule is large with marginal teeth, there being three pairs in A. caninum and A. tubaeforme and two pairs in A. braziliense.
Ancylostoma caninum
Life Cycle
The life cycle is direct and given optimal conditions the eggs may hatch and develop to L3 in as little as five days.
                                                                                F/H becomes by two ways


infecInfection is by ingestion by L3


Directly pass to the intestine and de­velop to potency.
 
 






PPP: 14-21 days (For any route)

Note:
  • The worms are prolific egg layers and an infected dog may pass millions of eggs daily for several weeks.
Epidemiology
  • In endemic areas, the disease is most common in dogs under one year old.
  • In older animals, the gradual de­velopment of age resistance makes clinical disease less likely, particularly in dogs reared in endemic areas whose age resistance is reinforced by acquired immunity.
  • The epidemiology is primarily associated with the two main sources of infection, transmammary in suckled pups and percutaneous or oral from the environment.
  • Transmammary infection for a period of 3 wks after whelping by L3 which remain dormant in skeletal muscle until the bitch is pregnant. (incase of percutaneous and penetration of oral mucosa)
  • Infection of the bitch on a single occasion has been shown to produce transmammary infections in at least three consecutive litters.
  • It also appears that dormant L3 in the muscles of both bitches and dogs can recommence migration months or years later to mature in the host's intestine.
  • Stress, severe illness or repeated large doses of corticosteroids can all precipitate these apparently new infections in dogs.
  • experimentally, L3 of some strains of A. caninum exposed to chilling before oral administration have been shown to remain in arrested development in the intestinal mucosa for weeks or months. The significance of this observation is still unknown, but it is thought that such larvae may resume development if the adult hookworm popula­tion is removed by an anthelmintic or at times of stress such as lactation.
Pathogenesis
·         This is essentially that of an acute or chronic haemorrhagic anaemia.
·         The disease is most commonly seen in dogs under one year old and young pups, in­fected by the transmammary route, are particularly susceptible due to their low iron reserves.
·         Blood loss starts about the eighth day of infection when the im­mature adult has developed the toothed buccal cap­sule which enables it to grasp plugs of mucosa containing arterioles. Each worm removes about 0.1 ml of blood daily and in heavy infections of several hundred worms, pups quickly become profoundly anaemic.
·         In lighter infections, common in older dogs, the anaemia is not so severe, as the marrow response is able to compensate for a variable period.
·         Ultimately however, the dog may become iron deficient and de­velop a microcytic hypochromic anaemia.
·         In previously sensitized dogs, skin reactions such as moist eczema and ulceration at the sites of percutaneous infection occur especially affecting the interdigital skin.
Clinical Signs:
In acute infections characterized by:
  • anaemia and lassitude (lethargy)  and
  • occasionally respiratory embarrassment.
  • In suckled pups the anaemia is often severe and is accompanied by diarrhoea which may contain blood and mucus.
  • Respiratory signs may be due to larval damage in the lungs or to the anoxic effects of anaemia.
chronic infections characterized by:
·         underweight, poor coat, and inappetite and perhaps pica.
·         Inconsistently, there are signs of respiratory embarrassment, skin lesions and lameness.
Diagnosis:
  • Clinical History with epidemiology
  • Clinical signs
  • Coproscopy:
    • High faecal worm egg counts are valuable confirma­tion of diagnosis
    • pups may show severe clinical signs before eggs are detected in the faeces
  • Haematological test
Treatment:
  • Anthelmintics therapy, such as mebendazole, fenbendazole and nitroscanate, (all of which will kill both adult and developing intesti­nal stages)
  • avermectins. (can kill both adult and larva)
  • If the disease is severe, it is advisable to give parenteral iron and to ensure that the dog has a pro­tein-rich diet. Young pups may require a blood transfusion.
Control:
  • A system of regular anthelmintic therapy and hygiene should be adopted.
  • Weaned pups and adult dogs should be treated every three months.
  • Pregnant bitches should be dosed at least once dur­ing pregnancy and the nursing litters dosed at least twice, at 1-2 weeks of age and again 2 weeks later (This will also help to control ascarid infections.)
  • The perinatal transfer of both Ancylostoma and Toxocara larvae may be reduced by the oral adminis­tration of fenbendazole daily from 3 weeks before to 2 days after whelping.
  • Kennel floors should be free of crevices and dry and the bedding should be disposed of daily.
  • Runs should preferably be of tarmac or concrete and kept as clean and dry as possible; faeces should be removed with a shovel before hosing. If an outbreak has occurred, earth runs may be treated with sodium borate which is lethal to hookworm larvae, but this also kills grass. A second possibility which is often "used in fox farms is the provision of wire-mesh flooring inLthe runs.
A. tubaeforme:
The life cycle and treatment of this hookworm of cats are similar to that of A. caninum in the dog, but there is no evidence of transmammary infection.
A. braziliense:
This hookworm occurs in both dogs and cats. Its life cycle is similar to that of A. caninum although evi­dence of transmammary infection is lacking. While it may cause a degree of hypoalbuminaemia through an intestinal leak of plasma, it is not a blood sucker and consequently is of little pathogenic significance in dogs, causing only mild digestive upsets and occasional diarrhoea. Treatment is similar to that for A. caninum.

The main importance of A. braziliense is that it is regarded as the primary cause of cutaneous larva migrans in man. This lesion, characterized by tortuous erythematous inflammatory tracts within the dermis and by severe pruritus, is caused by infective larvae of A. braziliense, and less frequently Uncinaria, penetrat­ing the skin and wandering in the dermis. These larvae do not develop, but the skin lesions usually persist for weeks.Similar lesions, although only transient and pin­point, may be caused by A. caninum larvae.

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