Oesophagostomum
Etiology
Oesophagostomum radiatum : Nodular worm
Clinical signs
The disease oesophagostomiasis is characterized by anemia and edema in addition to the explosive diarrhea.
Acute infections are the result of larval penetrations of the intestinal mucosa during the prepatent period. Diarrhea is the usual clinical sign in these cases and may be accompanied by weight loss and submandibular edema ("bottle jaw") in ruminants.
Chronic oesophagostomosis is most common in sheep and is due to repeated infections. Intermittent diarrhea accompanied by loss of appetite are the usual clinical signs and in more severe chronic cases sheep may become emaciated and anemia.
Infections in pigs may produce a range of clinical signs including acute diarrhea and a syndrome in adult females called the "thin sow syndrome" - a chronic infection with periodic acute flare-ups due to the resumption of development of hypobiotic larvae during spring farrowing. This syndrome shows as weight loss after farrowing and reduced milk production with adverse effects on the growth of litters.
Life Cycle
The preparasitic phase of Oesophagostomum is typically strongyloid, and infection is by ingestion of L3s
Adults in the intestine lay eggs which are passed in feces. Reaching the infective third-larvae stage in approximately 7 days. When ingested with herbage, the larvae penetrate the wall of the host's intestine, forming nodules anywhere between the stomach and the rectum. After 5 to 7 days they return to the intestinal lumen and travel to the colon, where they undergo a final molt and mature into adults. Eggs appear in the feces about 41 days after the larvae are ingested.
The prepatent period is 32 to 45 days, depending on the species. On reinfection with most species, the larvae may remain arrested as L4s, in nodules, for up to one year.
Location
Larvae in nodules in stomach and small and large intestines
adult worms in large intestine.
Pathogenesis
The most serious problems seen in Oesophagostomum infections arise from larvae penetrating the musosa of the intestine. After initial infections, small nodules about 1mm in diameter form around larvae in the mucosa. When larvae move back into the intestinal lumen the remaining nodules may be hemorrhagic particularly in acute infections but often they fill with pus, in which cases they are more properly described as small abscesses.
In heavy infections, the mucosa becomes inflamed and edematous and regional lymph nodes are often much enlarged. Chronic infections will produce an intestinal mucosa that is filled with nodules particularly if these repeat infections have been heavy. In these chronic cases tissue reactions are more severe and the nodules are much larger (up to 6mm in diameter) and creamy in color due to the development of connective tissue around them.
In chronic infections, most infecting larvae will be killed by host reactions. Therefore older animals will usually show extensively nodular intestines but with few, if any, adult worms in the colon.
Epidemiology
All domestic animals are infected by grazing pastures contaminated with L3s. Oesophagostomum radiatum in cattle is common throughout the world especially in tropical and subtropical areas and is also common in North America. In tropical areas with seasonal rainfall (such as Queensland in Australia) heavy infections with high mortalities may be seen in calves under natural grazing conditions during the rainy season.
Diagnosis
In acute infections clinical signs will occur during the prepatent period and diarrhea will occur without strongyle-type eggs being seen in the feces of infected animals. In chronic infections, strongyle-type eggs will be commonly seen but are indistinguishable from eggs produced by other strongyle nematodes. Necropsies will show the classic nodular lesions throughout the small and large intestines
Control
Pasture management
drenching cattle with ivermectin
the administration of an anthelmintic.
( source <Oesophagostomum)
Oesophagostomum radiatum : Nodular worm
Clinical signs
The disease oesophagostomiasis is characterized by anemia and edema in addition to the explosive diarrhea.
Acute infections are the result of larval penetrations of the intestinal mucosa during the prepatent period. Diarrhea is the usual clinical sign in these cases and may be accompanied by weight loss and submandibular edema ("bottle jaw") in ruminants.
Chronic oesophagostomosis is most common in sheep and is due to repeated infections. Intermittent diarrhea accompanied by loss of appetite are the usual clinical signs and in more severe chronic cases sheep may become emaciated and anemia.
Infections in pigs may produce a range of clinical signs including acute diarrhea and a syndrome in adult females called the "thin sow syndrome" - a chronic infection with periodic acute flare-ups due to the resumption of development of hypobiotic larvae during spring farrowing. This syndrome shows as weight loss after farrowing and reduced milk production with adverse effects on the growth of litters.
Life Cycle
The preparasitic phase of Oesophagostomum is typically strongyloid, and infection is by ingestion of L3s
Adults in the intestine lay eggs which are passed in feces. Reaching the infective third-larvae stage in approximately 7 days. When ingested with herbage, the larvae penetrate the wall of the host's intestine, forming nodules anywhere between the stomach and the rectum. After 5 to 7 days they return to the intestinal lumen and travel to the colon, where they undergo a final molt and mature into adults. Eggs appear in the feces about 41 days after the larvae are ingested.
The prepatent period is 32 to 45 days, depending on the species. On reinfection with most species, the larvae may remain arrested as L4s, in nodules, for up to one year.
Location
Larvae in nodules in stomach and small and large intestines
adult worms in large intestine.
Pathogenesis
The most serious problems seen in Oesophagostomum infections arise from larvae penetrating the musosa of the intestine. After initial infections, small nodules about 1mm in diameter form around larvae in the mucosa. When larvae move back into the intestinal lumen the remaining nodules may be hemorrhagic particularly in acute infections but often they fill with pus, in which cases they are more properly described as small abscesses.
In heavy infections, the mucosa becomes inflamed and edematous and regional lymph nodes are often much enlarged. Chronic infections will produce an intestinal mucosa that is filled with nodules particularly if these repeat infections have been heavy. In these chronic cases tissue reactions are more severe and the nodules are much larger (up to 6mm in diameter) and creamy in color due to the development of connective tissue around them.
In chronic infections, most infecting larvae will be killed by host reactions. Therefore older animals will usually show extensively nodular intestines but with few, if any, adult worms in the colon.
Epidemiology
All domestic animals are infected by grazing pastures contaminated with L3s. Oesophagostomum radiatum in cattle is common throughout the world especially in tropical and subtropical areas and is also common in North America. In tropical areas with seasonal rainfall (such as Queensland in Australia) heavy infections with high mortalities may be seen in calves under natural grazing conditions during the rainy season.
Diagnosis
In acute infections clinical signs will occur during the prepatent period and diarrhea will occur without strongyle-type eggs being seen in the feces of infected animals. In chronic infections, strongyle-type eggs will be commonly seen but are indistinguishable from eggs produced by other strongyle nematodes. Necropsies will show the classic nodular lesions throughout the small and large intestines
Control
Pasture management
drenching cattle with ivermectin
the administration of an anthelmintic.
( source <Oesophagostomum)
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