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NEMATODOSIS. NEMATODOSIS at ABOMASUM RUMINANTS in INDONESIA Cause : ▹ Haemonchus sp. ▹ Mecistocirrus digitatus ⇨ >>> in Indonesia ▹ Trichostrongylus sp. ▹ Ostertagia sp. ⇨ sub tropical
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NEMATODOSIS at ABOMASUM RUMINANTS in INDONESIA Cause : ▹ Haemonchus sp. ▹ Mecistocirrus digitatus ⇨ >>> in Indonesia ▹ Trichostrongylus sp. ▹ Ostertagia sp. ⇨ sub tropical country
HAEMONCHIASIS CAUSE : Haemonchus sp. SENSITIVE ANIMAL : H. contortus & H. similis : sheep, goat,cattle and other ruminants, escpecially young ages H. placei : escpecially cattle & other ruminants and young ages PREDILECTION OF THE PARASITE: Abomasum, occasionally small intestine
ROUTE OF TRANSMISSION : ingest of infective larvae (3 rdstg.) by grass (per oral) PATOGENICITY : Depend on several factors: ∙ Sufferer ages ∙ Size and body weight ∙ Duration of infection ∙ Nutrition status ∙ Haematology status
PATOGENESIS&CLINICAL SYMPTOM : - 4 thstg larvae parasite characteristic ⇨ Blood sucking - Mature worm destroy the mucosae when absorb the blood (0,049 ml/ekr/hr) ⇨ anemia ⇨ decrease Hb ⇨ hypoproteinemia ⇨ increasing the permeability of the wal blood sirculation ⇨ leakage blood watery ⇨ oedema ⇨Bottle jaw - Mature worm secret anticoagulant at the mucosae of injury ⇨ iritated the mucosae - Decrease the capability: digesty, protein absorbtion– calium and phosphor - SELF CURE REACTION ⇨Rx. body defense ⇨ become at the day 10 –14 post infection
ACUTE SYMPTOM : Heavy infection at young sheep/goat ⇨ anaemia ⇨ death CHRONICS SYMPTOM: ۵Anaemia ۵ Oedema : Bottle jaw / watery poke ventral abdomen ۵Diarrhea/constipation occasionally ۵Variation of a desire to eat ۵Weakness & thinness
POST MORTEM CHANGES: -Mucosa membrane, skin & pale of visceral organ - Watery blood/hydraemis - Hydrothorax, hydropericard and ascites - Hepar light brown, fragile & fattening - The contents of abomasum were red brown, worm >> • Absces of mucosa, spot & ulcera & certain worms sticking at the ulcera
DIAGNOSE : - Clinical symptom:chronic of bottle jaw - Fecal examination by SEM 400 x
ELIMINATION : ~ Put the animals into a stall ~ Make a rotation for the meadow ~ Giving wormolas (phenothiazine 2,5 % inside molases) Periodic treatment by: * Phenothiazine single dose: 5- 40 gram/tail sheep/goat, p.o 40 – 80 gram/tail cattle, p.o * Levamisol HCl : 7,5 mg/kg BW/p.o 2 ml/50 kg BW/i.m * Parbendazole : 30 mg/kg BW Cattle 20 – 30 mg/kg BW sheep/goat ( ! : not for pregnant animals) * Doramectin/Avermectin : 1 ml/50 kg BW/im/sc
MECISTOCIRRUSIS CAUSE : Mecistocirrus digitatus PREDILECTION & SENSITIVE ANIMALS: Cattle abomasum, buffalo, rare at small ruminants DISTRIBUTION: especially in tropical area ROUTE OF INFECTION: Similar with Haemonchosis
PATOGENESYS & CLINICAL SYMPTOM : • Larva 4 th stage characterized parasitic, this stage quite long time • Adult worm hematophagous anaemia hypoproteinemia,oedema, bottle jaw • Decrease of BW, PCV at day 70 – 80 post infection
DIAGNOSE : ~ Clinical symptom ~ Fecal examination ELIMINATION: - Similar with Haemonchosis - Preferable cattle not to be tend similar with small ruminans
NEMATODOSIS AT THE SMALL INTESTINE OF GOAT & SHEEP, OTHER RUMINANTS CAUSE: ~Strongyloides papillosus ~Bunostomum sp. ~Gaigeria pachyscelis ~Trichostrongylus sp. ~Cooperia sp. ~Nemaodirus sp PREDILECTION & SENSITIVE ANIMALS : Small intestine of goat and other ruminants
ROUTE OF TRANSMISSION : Trichostrongylus sp., Cooperia sp., Nematodirus Ingest of infective larvae (L3) with ransum or water Bunostomum sp., Strongyloides sp. : Ingest of infective larvae (L3) with ransum or water (per oral), and skin penetration (per cutan) Gaigeria pachyscelis : L3 penetrated the skin (p.c)
PATHOGENESIS Larvae penetrated In the mucosa of SI Iritat, inflammd wall of SI, lesi, ulcera &bleedng, diarrheae Trichostrongylus, Nematodirus Not hematophagous Cooperia, G. pachyscelis, Bunostomum, Strongyloides Hematophagous G. pachyscelis & Bunostomum, if heavy infekct. ANAEMIA Bottle jaw Hipoproteinemia ►G. pachyscelis, Bunostomum & Strongyloides Skin penetrated Local reaction: inflammed, papula & skin rashl
CLINICAL SYMPTOM : * More clear at young animals: weakness, thin, anorexia , anaemia, gloomy of body hair, diarrhea, inhibited of the growth. * Heavy infection G. pachyscelis & Bunostomum : bottle jaw * Trichostrongylus at young animals & acute : didn’t want sucking, weakness & black scours worm *Cooperia and Nematodirus similar with Trichostrongylus * Strongyloides : diarrhea, anaemia, BW & anorexia
DIAGNOSIS : Clin sympt Fecal examine ELIMINATION : • Prevention : • ► to press down the worm population by doing : • - put animal in to a stable (intensive) • - make a rotation for the meadow • - high quality for the ransum • - put the ransum in a properly condition • - sanitation for the stable • - periodically treatment
Treatment : ~Methyridin : 180 mg/kg BW s.c ~Pyrantel tartrat : 25 mg/kg BW p.o ~Thiabendazol : 50 mg/kg BW ~Oxfendazol : 5 mg/kg BW ~Mebendazol : 15 mg/kg BW ~Bephenium carbonat : 250 mg/kg BW ~Phenothiazin : 20 – 30 gram/ekor sheep ~Neguvon : 110 mg/kg BW ~Avermectin : 1 ml/50 kg BW
NEMATODOSIS AT PIGS PULMO (METASTRONGYLOSIS) CAUSE: Metastrongylus apri⇨ seldom M. pudendotectus M. salmi PREDILECTION & SENSITIVE ANIMALS: Pulmo (trachea, bronchus & bronchioli) pig,wild pig, goat, deer and other ruminans.
INTER MEDIATE HOST: Blood worm • Octalaseum lacteum • Allolobophora calignosa • Lumbricus rubellus • Eisenia foetida • ROUTE OF TRANSMISSION: Ingest the earth worm which consist of larvae 3rd stage [could also by chance pig ingest the 3rd stage of larvae] • Infective larva be able to still alive inside the body of the earth worm: • 1,5 yr inside the body of Octalaseum lacteum • 2,5 yr inside the body of Allolobophora calignosa • 3 yr inside the body of Lumbricus rubellus • > 4,5 yr inside the body of Eisenia foetida
CLINICAL SYMPTOM : - Cough & braething hard - Inhibited of the growth - Weakness & pale of the mucosae ►Mild infection: bronchitis & pneumonia ►Heavy infection: be able death POST MORTEM CHANGES: • Macroscopics : • Red pale spot at pulmo pars inferior & occasionally pars superior • Decrease of the changes at the day 21 post infection • Mild emphysema • The area have a red color at the anterior part or at the lowest part of the lobus of diaphragma
Microscopics : • Young worms at the bronchioly at the day 10 - 20 post infection • Eosinophylia infiltration at the mucosa of bronchi, peribronchi • Early of hyperplasia at 2-3 weeks post infection • Adult worms inside the bronchi, with eosinophyl at the surrounding area DIAGNOSE : • CS/ be able confusing with Ascariasis & pig flu • Fecal examination ⇨eggs (consist of larvae)
ELIMINATION : • Good condition of the system of the stall Earth worm cannot growth Treatment for animals patients by : • Tetramisol : 15 mg/kg BW/s.c or mixed with ransum ▫ Levamisol HCl : 7,5 mg/kg BW/s.c ▫ Diethylcarbamacin : 22 mg/kg BW/s.c, 3 days ▫ Oxfendazol : 3mg/ kg BW for 7 days ▫ Doramectin/Avermectin : 1ml/50 kg BW/i.m/s.c
NEMATODOSIS AT COLON & RUMINANTS CAECUM CAUSE : ◊ Trichuris sp. ◊ Oesophagustomum sp. ◊ Chabertia sp.
Trichuriasis HABITAT & SENSITIVE ANIMALS : CAECUM of goat, sheep,cattle, dog , cat, pig,camel. ROUTE OF TRANSMISSION : Ingest the infektive eggs (stg. II) with ransum or water PATHOGENESIS, CLINICAL SYMPTOM & P.A : Sheep, pig, cattle natural infectionCS/ rare Adult worms cause of acute inflammed or chronics (sesitys) PA/ : sesitys, necrosys haemorrhagia, oedema of mucosae & adult worms >>.
Acute infection (200- 300 worms) : diarrhea, haemorrhagia, anaemia, if 6000 – 13000 : decrease of BW, weakness, inhibited of the growth ⇨ death OESOPHAGUSTOMIASIS CAUSE : Oesophagustomum sp. (=Nodular worm) PREDILECTION & SENSITIVE ANIMALS:Colon & Caecum, sensitive animals : O. columbianum: Sheep,Goat,Deer O.venulosum: Sheep, Goat, Camel O. radiatum: Cattle O. dentatum: Pig
ROUTE OF TRANSMISSION : Ingest of infected larvae (L3). PATHOGENESIS, C.S& P.A : - Pathogen : O. venulosum & O. columbianum - Occurs attacks by ages : 4 – 24 months - Young sheep & adult sheep which attacks with larvae migrated ⇨ didn’t have reaction of the body - Sensitive animals: larvae come in to the sub mucosae of lamina propria intestine Rx.local inflammed surrounding. Larvae, collecting the cell of EO, Lymphocyte, MO & Giant NODULES : Central nodules : Caseosa & calcification Outside`nodules : Capsules dan fibroblast Larvae can survive up to 3 months died
Chabertiasis • Cause: Chabertia sp • PREDILECTION &SENSITIVE ANIMALS: COLON (sheep, cattle, goat) * ROUTE OF TRANSMISSION: ingest eggs which coming out with faeces, hatch 24 hrs latter and growth to be infected larvae
GK/ :- Nodule >>> → rupture → peritonitis. - Diarrehea with mucus & black green colors (6 days p.i & similar with larvae that leave from the nodule). - Chronics : watery diarrhea dehydration,dry skin, hunchbacked pars posterior of the body, stiff and dirty. - Constipation because of the amount of worms >>> food appetite ↓↓ cachexia, BW ↓↓ & extended with died PA/ :- Emaciation & body fat <<< - Be found nodules >> at small intestine, colon & caecum,and worms at cacing di colon & caecum - Reddish of mucosae - Nodules green colors – yellow, cause of something like as a cheese
NEMATODOSIS ASCARIASIS
ASCARIASIS AT PIGS Cause: Ascaris suum Predilections and host: small intestine of pigs (main host), cattle, goat, sheep, dog and human Route of transmission: 1. Per oral (by ingest infective eggs) 2. Prenatal (through placenta⇨ v. umbilicalis foetus) 3. Nipples which contaminated by infective eggs
Pathogenesis and PA/ : - Larvae : larvae migrations ⇨ tissues organ damaged - At hepar: Acute : 1. bleeding surround v. intralobularis ⇨ eosinophyl infiltration ⇨ absorbtion and regeneration 2. Sticky of the hepar cells: the lobus sticky each others with increase of fibroblast Chronics : 1. Hepatitis interstitial focal chronics 2. if recovered ⇨ fibrocys (white spots) ⇨ milk spot liver
at the pulmo: 1. Laesi of the tissues cause of toxin 2. Mild bleeding at alveoli and bronchioli ⇨ destroyed of alveoli epithels, oedema, and eosinophyl infiltration surround the pulmo 3. Heavy infections ⇨ bronchioly obstruction - Adult worms: at the small intestine: 1. Adult worms ingest the content of intestines and destroy the mucosa of intestine 2. Heavy infection ⇨ obstruction of intestinal duct ⇨ annoying peristaltics of intestine & intestine perforations ⇨ peritonitis 3. Migration to the gastrium ⇨ vomite 4. Migration to the gall ducts ⇨ icterus
Clinical symptom: - Heavy infection at young pig: 1.pneumonia ⇨ coughing + exudate 2. sudden die Others general symptom: 1. Drooping of tail and ears 2. Decrease of food appetite 3. Difficulties in obtaining oxygen 4. Repeatedly rub the body on to the stable wall 5. Thiness 6. Diarrhea 7. Very weak animals ⇨ die - Mild infections ⇨ cough and inhibited of the bodies growth
- Heavy infections at the young pigs after has been weaned: 1.Heavy pneumonia ⇨ cough + exudate 2. Adult worms could be cause of die 3. Occasionally stiffness ⇨ paralysis 4. Obstruction of the gall ducts ⇨ GIT disturbances 5. Seldom accompany with secondary infections : pneumonia lobair an pig influenza - Heavy infections st the young pigs: 1. Short winded 2. Die cause of hepar functions disturbance 3. Adult worms migration to the gastrium ⇨ vomite, thiness, puff out and oedema 4. Icterus and anaemia
Diagnose : 1. Clinical symptom 2. Fecal examinations 3. Post mortem operating Disease elimination: 1. Take care of the healthy stabble especially suckled pigs mother 2. To take a bath for pigs mother before partus 3. To give anthelmintic for animals patients, especially before mating and at the middle of pregnant periods 4. Improvement the management of animal husbandry 5. Treatment of animal patients by: Piperazin : 120 mg/kg BW po ⇨ drug of choice Phenotiazin : 400 mg/kg BW po Thiabendazole : 0.1 – 0,4 % amount of feed animal Avermectin : 1 ml/50 kg BW, im, sc
ASCARIASIS AT CATTLE FAMILIES CAUSE : Toxocara vitulorum ROUTE OF TRANSMISSION : ~Through milk by early 3 wks lactation → milk born transmission ~Per oral (ingest infective eggs) ~prenatal infection PATHOGENESIS : Nyata terlihat at young cattle post natal infection & which born from infected mothers (prenatal infection)
CLINICAL SYMPTOM : Diarrhea, thiness The respiration smelt butiric acid, anorexia Weakness & bisa tjd anemia DIAGNOSE : Fecal examination from the young cattle (3-6 mths) Milk examination from the mothers induk menyusui (early 3 wks) Operated post mortem at the young cattle
ELIMINATION : 1. Pregnant cattle could be free from from worms, Tx/ anthelmintic before kawin → mid pregnant → post partus 2. Young cattle ages by 2 wks, which infected → treated Treatment and prevention : Piperazin (drug of choice) : 220 mg/kg BW/po Fenbendazole (Panacur) : 7.5 mg/kg BW Infected by T.vitulorum larvae at status dorman Mechanisms : • In activated parasite endocrine system → inhibited release the product suspension of hatching eggs at ecdysis periods • Blocking transcription material DNA gen template for perkembangan berikutnya
STATUS DORMAN → inhibited at 8–14 hr prepartus ↓ Penetration aktivation of fibrose tissue by larvae enzym for softening melunakkan tissue → L3 ENZYME PHENOMENA Because of prolactine hormon activity → they need Ca >> → immunosuppresive Prostaglandine hormone → immunosupp resive against immune respons → by infec tions mothers become sensitive
ASCARIASIS AT DOG CAUSE: Toxocara canis PREDILECTION OF ADULT WORM : Small Intestine CARA PENULARAN : - Per oral infection (ingests the infective eggs ) - Prenatal infection (through placenta) - Trans mammary infection = Lactogenic infection - Paratenic host → infective eggs ingests by i.h paratenic (rat, mouse) → L3 inside the muscle → ingests by host → L3 occur to be adult worm within 3 weeks without migration again
PATHOGENICITY & CLINICAL SYMPTOM : Puppies more sensitive & suffers than adult worm: Clinical symptom : Diarrhea, vomite Vomites materials → go into the pulmo → asphixia Puppies : inhibited of the growth,distended, vomite & diarrhea moreover constipation, death : 2-3 wks DIAGNOSE : Clinical symptom → fecal examination → eggs albumin sheet
albumin sheet DISEASE ELIMINATION : - Avoid mother & child from the sources of disease - Given a good quality of feed - Throw away the faces to the special area, if necessary can be burn - Sanitation the stable - Treatment with Piperazin for the child by ages 2,3,4 & 8 wks & treated the mother by 3 or 4 mg post partum
- to the dogs which don’t know the histosry (baru beli) : 3 – 6 mths: treated 2 x , repeated 1 wks > 6 mths: treated 1 x Anthelmintics : Piperazine adipate : 100 mg/kg BW/po Mebendazole 10 mg/kg BW/2 dd/ for 2 days
ASCARIASIS AT HORSES FAMILIES CAUSE : Parascaris equorum = Ascaris megalocephala PREDILECTION & HOST: Small intestine of horse, zebra & cattle TRANSMISSION : Ingest by infektive eggs PATHOGENESIS,CLINICal SYMPTOM & PA/ : Espec. at young horses by ages less than 6 mths
Heavy infection → catarrhalis enteritis → CS/ : putrisid smelt diarrhea & pale faecal. Others CS/: Weakness, thiness → BW drops. heavy infection: heavy colic, tachycardia, freq. resp., high febris & died after bbrp. hr. post infection Aktive worms → migration to the gall duct → obstruction PA/: ruptur ileum & peritoneum consist of intetine suspension & worm DIAGNOSE : Selain clinical symptom, feces examination → eggs
albumin sheet ELIMINATION : - To maintain and keep the stable clean & treat the young horses by ages 1 mth & seterusnya every 4 – 6 mths by piperazine 100 mg/kg BW - Pakan diletakkan palungan - Tempat pembuangan tinja → fermentasi → utk. pupuk → telur mati
THE EPIDEMIOLOGY OF GASTROINTESTINAL NEMATODA By Geographics : continous occur at the warm and mild climate areas Oesophagustomum sp. & Trichuris sp. Well growing at the temperature 10 - 25°C, wet environment, highly rainfal Chabertia sp.: cold environment DIAGNOSE - Clinical symptom → fecal examination - Post mortem examinations